tag:blogger.com,1999:blog-87467267479573434332024-03-06T00:15:26.884-08:00ANAESTHESIA TODAYANAESTHESIA AND INTENSIVE CARE LECTURES,PROCEDURES CASE DISCUSSIONS AND OTHER TOPICS IN ANAESTHESIA AIMED AT PRACTISING ANAESTHETISTS AND RESIDENTSDR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.comBlogger47125tag:blogger.com,1999:blog-8746726747957343433.post-88101182649769100202014-12-30T11:45:00.000-08:002014-12-30T11:46:18.883-08:00ENHANCED RECOVERY, AN ENCHANTING EXPERIENCE!<div dir="ltr" style="text-align: left;" trbidi="on">
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The Science, art and practice of Anaesthesiology are changing day by day.The recent advances and researches in the field aim at a faster, safer and smoother recovery from anaesthesia, enabling patients to resume their normal day to day activities early..The elective, day care and office based anaesthesia services have improved so much and the concept of enhanced recovery is widely accepted for practice. Enhanced recovery practices aim fast but smooth recovery following surgery and anaesthesia thereby reducing patient discomfort, length of stay in hospital,prevent loss of manpower and increase productivity.This is achieved not just by cutting short anaesthesia or by providing inadequate or insufficient anaesthesia or by cutting short some surgical procedures but by avoiding certain medications or procedures by surgeons or anaesthetists which may actually delay recovery. It has been clearly shown by studies that enhanced recovery benefits much to colorectal, orthopedic urologic and gynae cological surgeries in terms of early mobilisation, reduction of complications and quality of life.<br />
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The single intervention or individual components of a certain surgical procedure, when implemented together as a group have a greater impact on the overall outcome of that procedure.This is the fundamental theory or concept behind enhanced recovery programmes.Even though the concept aims better and early post operative rehabilitation it gives utmost care to preoperative and intra operative assessment and care to make the morbidity less and to provide the highest possible quality of care to patients undergoing surgical procedures.<br />
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<span style="color: purple;"><span style="font-size: large;">The Components of Enhanced Recovery Programme.</span></span><br />
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<span style="color: blue;"><b>1. Referral from a general practitioner to specialist</b></span><br />
<ul style="text-align: left;">
<li>Evaluation of co morbidities like blood sugar and hypertension</li>
<li>Optimization of hemoglobin level</li>
<li>Advise to quit smoking</li>
<li>Advise on limitation of the use of alcoholol </li>
</ul>
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<span style="color: blue;"><b>2.Pre operative optimization by Anaesthetists, Physician, and Surgeon.</b></span><br />
<ul style="text-align: left;">
<li>Management of Hypertension or Diabetes </li>
<li>Informed consent and decision making by patient</li>
<li>Optimization of drug therapy, minimizing the current medications or medication reconciliation</li>
<li>Advise on postoperative oral intake or mobilization</li>
<li>Discharge planning should be explained with full instructions given about current medication and stoppage of medication. <br /><div class="separator" style="clear: both; text-align: center;">
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</li>
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<span style="color: blue;"><b>3.Pre operative preparation</b></span><br />
<ul style="text-align: left;">
<li>Admission on the day of surgery, Careful planning and advise to patients about preoperative preparation and procedures make it possible for them to get admitted on the day of surgery . The whole documentation including consent must be completed before admission.Preoperative optimization including all necessary investigations and review must be made.</li>
<li>Avoidance of bowel preparations; Bowel preparation adversely affects normal bowel recovery especially in colorectal surgeries.There is less risk of dehydration in colorectal and urological surgery when oral bowel preparation is not routinely used.It also helps in carbohydrate preloading.</li>
<li>Avoidance of prolonged fasting; Prolonged starvation adversely affect tissue hydration and serum electrolytes.Minimize fasting time and avoid overnight fasting orders.Fasting time of 2 hours for liquids and 6 hours for solids appropriate.Avoid over hydration too...</li>
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<ul style="text-align: left;">
<li>Carbohydrate drinks. Encouraging patients to take carbohydrate drinks (carbohydrate preloading) helps to prevent protein catabolism. It also helps to prevent insulin resistance due to stress response.Carbohydrates provide energy during the fasting period and during surgery and studies have proven that carbohydrate preloading has positive outcomes during recovery and better perioperative control of body metabolism.Use specially formulated oral fluids (complex carbohydrates) that are rapidly emptied from the stomach as they have a relatively low osmolality. CHO loading also helps to reduce patient anxiety, reduces inflammatory response and improve hydration.CHO preloading (drink) may be given 12 hours prior to surgery and up to two hours before reaching the operation suite.For patients with diabetes and delayed gastric emptying necessary precautions may be taken and the second dose may be avoided.</li>
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<li>Avoidance of sedative premedication.Sedative premedications especially long acting sedatives should be avoided as the residual effects can be avoided. To allay anxiety small dose of nonsedating anxiolytics preferred <div class="separator" style="clear: both; text-align: center;">
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<span style="color: blue;"><b>4.Intra operative care</b></span><br />
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<li>Always use minimally invasive techniques, especially laparoscopic resection.</li>
<li>If the abdomen needs to be opened a transverse incision is recommended than longitudinal cuts.This will reduce post operative pain and subsequent use of sedatives or narcotics</li>
<li>Avoid wound drains if possible. In colonic surgeries drains have been shown to be of no benefit.</li>
<li>Avoid nasogatric tubes as they increase morbidity in bowel surgeries </li>
<li>Individualized goal directed fluid therapy helps to avoid over hydration or dehydration. But central lines must be avoided.Fluid administration based on cardiac output monitoring recommended and esophageal doppler will be of great help in this. Judicial use of colloids helps to administer the right minimal amount to keep the cardiac output.</li>
<li><span style="font-family: Georgia,"Times New Roman",serif;">Anaesthetic care</span> : Use short-acting anaesthetic agents whenever possible.Fentanyl and propofol are chosen for intravenous induction and for maintenance desflurane or sevoflurane may be used.Midazolam may be avoided.Remifentanyl based total intravenous anaesthesia is found to be useful.For abdominal and colorectal surgeries epidural anaesthesia is preferred.They are also helpful to reduce stress response to surgery or may be beneficial to combine with General anaesthesia to reduce the dose of intravenous or inhalational agents.Epidurals also help to prevent post operative paralytic ileus by blocking sympathetic discharge.Excellent post op analgesia by epidural LAs without sedative effects helps early mobilisation or ambulation of post operative patients.Intraoperative use of ondansetron, droperidol or dexamethasone help to prevent PONV during emergence or in the post op period.Risk stratification of PONV using apfel scoring system and aggressive prophylaxis and treatment of PONV are recommended.Hypothermia may prolong recovery so intra operative warming devices and warm fluids must be used.Transverse abdominal plane block or TAP block is also an excellent choice for post operative pain relief especially in laparoscopic surgeries.Avoid the use of drains and nasogastric tubes as nasogastric tubes delay gastric emptying and may trigger nausea and vomiting. Nasogastric tubes and drains can affect a patient’s ability to mobilise as they always create a psychological barrier for early mobilisation attempts. Drains should be avoided If NGT is essential it may be removed immediately at the end of surgery.Even though early mobilisation reduces the risk of DVT, Thromboprophylaxis is recommended in selected cases especially limb surgeries.</li>
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<span style="color: blue;"><b> 5.Post operative care</b></span><br />
<ul style="text-align: left;">
<li>Active planned mobilization should be initiated within 24 hours.IV lines and catheters must be removed early.Patients must be encouraged to start early oral feeding which will prevent dehydration and reduce the chances of post op ileus.Also it is proven that early feeding helps to prevent surgical wound infections.Post operative hyperglycemia must be avoided in diabetic patients.Epidural catheters may be removed early after administration of parenteral NSAIDS.For moderate to severe pain oral opioid analgesics may also be supplemented along with NSAIDS.Physiotherapists have an active role in early patient mobilization.Regular follow up should should be done and the follow up process should extend to the post discharge period also. This is achieved by a dedicated clinical staff who can communicate to the patient over telephone who will be informing the clinician about the status of recovery. Discharge is planned as per protocols and criteria.</li>
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<span style="color: blue;"><b>Benefits of enhanced recovery programme</b></span> </div>
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<ul style="text-align: left;">
<li>In UK, the process is active and an ENHANCED RECOVERY PARTNERSHIP PROGRAMME (ERPP) has been formed with participation of department of health, NHS cancer team and the Royal colleges.The aim of the programme is to create awareness among Physicians, Surgeons and General public about the advantages and benefits of early recovery thereby improving patient care, improving productivity, reducing morbidity and cost.</li>
</ul>
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<ul style="text-align: left;">
<li>Improved clinical outcome and early detection of complications are possible.Earlier return to work or social activity improves productivity and social well being.Reduced hospital stay reduces cost and hospital acquired infections.Reduced waiting time for surgery as the patients are prepared early for surgery.Early mobilization helps to prevent bowel dysfunction and DVT.</li>
<li> Finally, there are improved relationsh ips between primary care and hospital trusts and better<br />Since a multidisciplinary team is involved in patient management improved communication and exchange of ideas improve patient care.Overall improvement in patient care and quality makes the process a nice experience for patient and health care team making enhanced recovery an enchanting experience.<div class="separator" style="clear: both; text-align: center;">
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<span style="color: #783f04;">References: </span><br />
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<span style="color: #783f04;">1.http://www.frca.co.uk/Documents/204%20Enhanced%20recovery%20after%20surgery%20%28ERAS%29.pdf</span></div>
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<span style="color: #783f04;"><br /></span>
<span style="color: #783f04;">2.http://www.medscape.org/viewarticle/579805_2</span><br />
<span style="color: #783f04;"><br /></span>
<span style="color: #783f04;">3.http://www.nhsiq.nhs.uk/media/2433399/ijoa_er_editorial_lucas_ijoa_april_2013.pdf</span><br />
<span style="color: #783f04;"><br /></span>
<span style="color: #783f04;">4.http://www.frca.co.uk/Documents/204%20Enhanced%20recovery%20after%20surgery%20%28ERAS%29.pdf</span><br />
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DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-54357967091739634252013-05-29T23:11:00.001-07:002014-12-30T11:45:54.733-08:00EGO, WHERE YOU GO?<div dir="ltr" style="text-align: left;" trbidi="on">
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Professional ego is commonly observed in medical profession.It is the basic nature of every
human being to claim the superiority over others thinking that he is more perfect and has got additional
capabilities over his fellow colleagues.Medical profession is no exception.Among the physicians ego is
more common among the anaesthesiologists because the choice and techniques to anaesthetise a particular patient are diverse and are based on individual experience and expertise<br />
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Several techniques and
methods are possible to anaesthetise a particular patient or to
perform a particular procedure, (with the procedural advantages or
complications specific to each of them) Often there will be debate on which technique is superior or suitable to the procedure.Individual experience may favour one to go for a particular procedure which may be deferred by others. Often the senior fellow or consultant will win in this argument as he is more powerful to execute his commands. In such instances it was advised to follow standard protocols or evidence based techniques,or majority opinion.Healthy discussions based on standard literature will help the clinicians to formulate an action plan and to proceed, which may help in their professional and academic improvement.<br />
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If the consultant is not successful with the procedure he proposed and
that too witnessed by his colleagues he may feel ashamed but
he may declare that the procedure is difficult but his ego does not permit him to allow his juniors to repeat the procedure and he may go for an
alternate procedure.As a result the patient may suffer as he is not able enjoy the advantage of that particular procedure.This is true when epidural anaesthesia is to be performed for a hypertensive patient or PIH patient where a change in hands may make the procedure less difficult and often successful and the patient is gaining the benefit of regional anaesthesia over GA. <br />
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The procedural ego unveils especially when
somebody fails to perform upto their self expectations.The physician will be tensed and nervous and keep on trying. During unsuccessful intubation he may not hand over the case to his fellow and instead keep on trying, introducing trauma and making the airway more difficult for others to manage.I have observed a
specialist attempting more than 8 times to insert a spinal needle in an
obstetric patiebnt for caesarean, while the consultant observing this
is advising him repeatedly to abandon the procedure and go for GA. The
specialist was not giving ears as he thought, failing the procedure in
front of staff and gynaecologists may affect his reputation badly.This
patient suffered severe post spinal head ache with nystagmus and
vomiting for several days post op.You may also find some instances in regional anaesthesia procedures where
the junior kept on praying that his senior should fail because he has already failed to perform.
He is seen depressed and withdrawn the whole day because the senior was
successful in single attempt.<br />
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Ego with investigations,was also observed among a few anaesthetists, when they delete or modify some of the preoperative investigations ordered by surgeons.The anaesthetist may ask for a fresh set of investigations just because the previous tests were ordered by a surgeon. This is because many feel interpreting investigations ordered by other doctors is an inferior job but they are not aware of the financial burden, physical strain and pain involved in repeating the lab tests.<br />
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Ego with paramedics and nursing staff, needs to be mentioned.The physician's ego doesn't permit him to accept minor mistakes by him, which are pointed out by nursing staff or technicians.Look at this incidence, A faint pneumothorax shadow in X ray was missed by an anaesthesia specialist but was observed by an X ray technician.The technician took the X ray and reported back to the specialist.Instead of admitting his mistake and attending the patient in ICU, the specialist filed a petition to higher authorities against the technician's rude behaviour! This is not appropriate as your ego should allow to appreciate and complement them.<br />
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Ego with patients,Here the physician fails to explain in detail about the anaesthetic procedure and about its complications.They just ask the patients a few serious questions during PAC and ask them to put their signature in the consent form.In fact they become restless and uncomfortable when the patient starts asking questions.On the contrary some physicians try to over exaggerate the complications and procedural details to make the patients feel that he will be doing something dangerous and great for patient's sake.Both of these are harmful practices as either the patient is unaware of the procedure or he will be too much nervous and tensed to face the situation.Pull out your ego and reassure the patient,explain about the possible complications, and gain the confidence and trust of patients and relatives.<br />
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It doesnt matter whether
the physician is an egoist or not,but denying treatment or harming patient's health on account of his ego, is strictly against medical ethics. One should identify his limitations and weakness as human beings and should have a helping mentality.He should be open to his colleagues, help them out in cases of difficulties, hear to them and should be willing to discuss with them.As we learn through mistakes,suppress your ego towards those who point out your mistakes. Since most of the procedures in anaesthesia are "blind
techniques" patient, positional or technical variations may affect them.
Luck also plays.So dont be hesitant to hand over the procedure to a
senior colleague or ask your junior to try out with a different hand,
when somebody fails in few attempts.The ultimate aim of ego less practise is Safe and Quality patient care.<br />
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<span class="userContent" data-ft="{"tn":"K"}">Ego is like your branded clothes.Its is important that you have it,but not necessary to show it always.</span>You may
have much of an ego in anesthesia because you aren't respected by the patient's relatives, you are not paid like surgeons and you have to work behind the curtains where no one understands how serious and risky is your job.But you may remember that Ego can be a great motivator and destroyer as well.Those who are successful in life know how to control their ego.No one is superior to others and the medical law states "You know only a fraction of what you are supposed to know" and no one can learn everything in medicine.Say good bye to ego and be part of the team work for better and quality patient care through dynamic decision making and individual participation which makes the practice of anaesthesia more
meaningful and sublime.<br />
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<span style="font-size: small;">Still interested to read on? visit the following links.</span><br />
<br />
1.<a href="http://www.dailymail.co.uk/news/article-2312847/Hospital-consultant-Jarrod-Homer-loses-tooth-fight-anaesthetist-Kamran-Abbas-Manchester-Royal-Infirmary.html" target="_blank">http://www.dailymail.co.uk/news/article-2312847/Hospital-consultant-Jarrod-Homer-loses-tooth-fight-anaesthetist-Kamran-Abbas-Manchester-Royal-Infirmary.html</a><br />
<br />
2.<a href="http://drsvenkatesan.wordpress.com/tag/doctors-ego/" target="_blank">http://drsvenkatesan.wordpress.com/tag/doctors-ego/</a></div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-21002746008275305722013-04-30T09:58:00.000-07:002013-04-30T09:58:56.510-07:00OBSTRUCTIVE SLEEP APNEA SYNDROME AND SLEEPLESS ANAESTHETIST!<div dir="ltr" style="text-align: left;" trbidi="on">
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Which is the most common form of apnea? Perhaps the most common apnea,which causes lot of physiological disturbances due to anatomical alteration of body size or tissues, leading to serious pathological changes in body systems, is Obstructive Sleep apnea.Obstructive sleep apnea
syndrome occurs when there are repeated episodes of complete or
partial blockage of the upper airway during sleep.<br />
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During episodes of sleep apnea,the diaphragm and respiratory muscles including the accessory muscles work hard to overcome the obstruction and the passage of air through the obstructed airway causes noisy breathing or snoring..Thus instead of getting a sound sleep for the victim, he falls into a "SOUND" sleep disturbing his partner or others.Thus due to obstruction the patient gradually stops his respiration momentarily and breathing usually resumes
with a loud gasp,snort,or body jerk.These episodes can interfere
with sound sleep[1]The physiological and pathological changes occurring in internal organs are due to relative deficiency of oxygen and retention of carbon dioxide. There is accumulating evidence that OSA is being considered as an independent risk factor for hypertension,diabetes mellitus,cardiovascular diseases and stroke, leading to increased cardiometabolic morbidity and mortality.<br />
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<span style="color: purple;">Definition:</span><b style="color: purple;"><span style="font-weight: normal;"> </span></b><b><span style="font-weight: normal;"> </span></b></h3>
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<b><span style="font-weight: normal;">An apnoea is defined as the complete
cessation of airflow for at least 10 sec.There three types of apnoea
found clinically are obstructive,central and mixed.The frequency of
apnoeas and hypopnoeas hourly is used to assess the severity of the
OSAHS and is called the apnoea/hypopnoea index (AHI) or the respiratory
disturbance index (RDI)According to the American Academy of
SleepMedicine recommendations,OSA is defined with AHI>5, and it
is classified as mild OSA with AHI of 5 to 15;</span></b>moderate OSA with AHI of 16 to 30; and severe OSA with AHI > 30.[2]</div>
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Respiratory effort–related arousal (RERA) is an event characterized by increasing respiratory effort for
10 seconds or longer leading to an arousal from sleep but one that does
not fulfill the criteria for a hypopnea or apnea. The criterion standard
to measure RERAs is esophageal manometry[12]<br />
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Symptoms:</h3>
<span style="color: purple;"><b>Adults:</b></span><br />
Snoring<br />
Daytime sleepiness or fatigue<br />
Headaches on awakening in the morning.<br />
Poor concentration,Loss of memory, Depression,or Mental irritability<br />
Dry mouth or sore throat upon awakening<br />
Night perspiration<br />
Restlessness during sleep<br />
Sexual dysfunction<br />
Sudden awakenings from sleep with a sensation of gasping or choking<br />
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<b><span style="color: purple;">In Children</span></b><br />
Drooling and often choking<br />
Excessive perspiration at night<br />
In drawing of the ribs while inspiration<br />
Learning and behavioral disorders<br />
Poor attention sleepiness and poor school performance<br />
Snoring<br />
Teeth grinding<br />
Restlessness during sleep<br />
Pauses or absence, cheyne stokes pattern of breathing<br />
Unusual sleeping positions, such as sleeping on the hands and knees, or with the neck hyperextended.<br />
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<b>Causes of obstruction:</b></h3>
In adults the causes for obstruction include thick or large necks.They may have a relatively smaller airway with edentulous soft tissues where patency is maintained by active contractions of pharyngeal dilators which are depressed with sleep, alcohol, or sedatives.Babies and small children may have sleep apnea that is caused by swollen tonsils or hypertrophy of the uvula and soft palate.A larger than average tongue can also block the airway in many people as well as a deviated septum in the nose.<br />
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<b>Risk factors: </b></h3>
<b><span style="color: #351c75;">Age:</span> </b>Prevalence is high in the middle aged reaching a plateau by around 60 years.[3].Older people with OSAS are found have increased fat deposition in parapharyngeal area, lengthening of the soft palate,and<br />
changes in body structures surrounding the pharynx.<br />
<b style="color: #351c75;">Sex:</b> OSAS is more common in men than women.<br />
<b style="color: #351c75;">Obesity:</b> BMI >30,Neck circumference more than 44 cm.The upper airway obstruction during sleep is attributed to increasing adiposity around the pharynx and body. Central obesity has been associated with reduction in lung volume,which leads to a loss of caudal traction on the upper airway, and hence, an increase in pharyngeal collapsibility.[4]<br />
<b style="color: #351c75;">Family history and genetic predisposition:</b> More common in first degree relatives of those with OSAS.<br />
<b style="color: #351c75;">Craniofacial anomalies:</b>Congenital or acquired alterations in the upper airway have been identified as risk factors for developing OSAS.Trauma, congenital anomalies like pierre robins syndrome.<br />
<b style="color: #351c75;">Smoking and alcohol consumption:</b> Cigarette smoking and alcohol have been shown to be risk factors for OSAS.Smoking induced airway inflammation is thought to be the causative factor while alcohol relaxes upper airway dilator muscles, increases upper airway resistance and may induce OSA in susceptible subjects<br />
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<span style="color: purple;">Pathophysiology: </span></h3>
People with sleep apnoea have a smaller pharyngeal airway than do matched controls.Also there will be alteration in bony structure and soft tissue surrounding the lumen.Due to the anatomical compromise,OSAS patients are susceptible to pharyngeal collapse during sleep or anaesthesia.Patients with OSA have increased pharyngeal dilator muscle activity which keep the airway patent during awake.Healthy individuals experience a loss of upper airway muscle tone at sleep onset (alpha-theta transition in the electroencephalogram) and experience some degree of breathing instability, an individual reliant on muscle tone due to an anatomical vulnerability will be particularly susceptible to apnoea when the dilator effect of pharyngeal muscles are lost.[5]Although pharyngeal dilator muscle responsiveness is likely impaired during NREM and REM sleep[6], the genioglossus can respond to both sustained mechanoreceptive (negative pressure) and chemo receptive stimuli, particularly when combined stimuli are present[7] The physiological response to this effect is a raise in CO2 due to respiratory obstruction and raise in negative intrathoracic pressure.The intrathoracic pressure appears to be a potent stimulus for genioglossal activation and maintaining airway patency.Elevated endexpiratory lung volume may lead to increased caudal traction on the diaphragm which may keep the airway stable and patent.<br />
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Thus the sequence is airway obstruction, hypoxia, increase CO2,increased EMG activity causing genioglossus and other pharyngeal muscle activation,negative intrathoracic pressure and chemoreceptor activation causing arousal.The pharyngeal muscle patency may be restored even before arousal.The mechanism of arousal is thought to be activation of parabranchial nucleus of pons due to neurohumoral activation by hypoxia and hypercarbia.A deeper stage of sleep, central nervous system depressants, prior sleep
fragmentation, and the presence of obstructive sleep apnea (OSA) have
been observed to increase the arousal threshold to airway occlusion.[8]<br />
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<span style="color: purple;">Systemic effects:</span></h3>
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<b style="color: purple;">Neurobehavioral and social:</b><span style="color: purple;"> </span> Excessive
daytime sleepiness, impaired vigilance, mood disturbances, and
cognitive dysfunctions are the features of OSAHS. The sleepiness may interfere with efficiency in work and may worsen interpersonal and social
relationships. The sleepiness may be dangerous when
driving and causes increase in road traffic accidents or injuries when
operating machinery.
Partners of patients with OSAS experience poor sleep,and will be the first one who takes the patient to a doctor for evaluation of his sleep disorder.[9]</div>
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<b style="color: purple;">Cardiovascular:</b><span style="color: purple;"> </span>The
intermittent hypoxia, Chronic hypercarbia, frequent negative intrathoracic pressure variations,and
sleep disturbance and arousals lead to increase in
blood pressure and lead on to sustained hypertension via chronically heightened
sympathetic nervous system activity and arterial baroreceptor
dysfunction.Myocardial infarctions are also common.The cerebrovascular system is also affected making the patient prone for CVAs and intracranial hypertension.Cardiac arrhythmias and cor pulmonale are commoner in these patients.[9]</div>
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<b style="color: purple;">Diabetes mellitus:</b><span style="font-weight: normal;"><span style="color: purple;"> </span>OSAS is an independent risk factor for development of Diabetes,associated with insulin resistance,</span><span style="font-weight: normal;">Obesity further increase the risk. Obesity associated changes in pharyngeal muscles may also contribute to OSAS.[9]</span> </div>
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<b style="color: purple;">Liver:</b><span style="color: purple;"> </span>Hepatic
dysfunction marked by raised liver enzymes,fatty liver and fibrosis are also associated with OSAS [9]</div>
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<span style="color: purple;">Perioperative and postoperative considerations:</span></h3>
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Patients
with OSAHS may have increased perioperative risks.<span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #403838; display: inline !important; float: none; font-family: 'Lucida Sans Unicode', Arial, 'Lucida Grande', Tahoma, Verdana, Helvetica, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 19px; orphans: auto; text-align: justify; text-indent: 0px; text-transform: none; white-space: normal; widows: auto; word-spacing: 0px;"><span style="color: black;"><span style="font-family: inherit;"><span style="font-size: small;">There is frequent prevalence of undiagnosed obstructive sleep apnea</span></span></span>.</span>Loss of control over airway, inability to mask ventilate, difficulty in intubation, intraoperative hypoxemia,abnormal raise in ETCO2 causing arrhythmias, intraoperative hypertension etc. are the problems anaesthesiologists face.The patients should be taken to OT adequately fasted and after acid aspiration prophylaxis.Fastrach LMA and fiberoptic bronchoscope are ideal for intubation and must be kept ready.It is advised to control the ventilations to match preoperative SPO2 and ETCO2.Spontaneous ventilations with LMA may cause hypoventilation and hypercarbia due to high rate of metabolism and increased thoracic mass.Whenever possible regional anaesthetic techniques or nerve blocks may be tried..Pre operative CPAP may be continued intra operatively also and extubation should be done when neuromuscular block is completely reversed and once the patient is fully conscious,communicative and able to generate adequate tidal volume.Semi sitting position or ramped position may be used to aid extubation, and the ETT may be pulled over a bougie or exchange catheter. Post operative respiratory depression is common and repetitive apnea may occur if the patient is somnolent.Monitor ETCO2 and SPO2 post operatively and if needed RBS and ABG may be performed frequently.Caution should be exercised when prescribing narcotics for post operative pain relief.</div>
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<span style="color: purple;">Diagnosis:</span> </h3>
<b style="color: purple;"> 1)A sleep test or polysomnogram( PSG):</b><span style="color: purple;"> </span>may be used for confirmation.Sleep testing is performed in a sleep lab and is supervised by a trained technologist. The test will measure various body functions, including:<br />
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Air flow<br />
Blood oxygen levels<br />
Breathing patterns<br />
Electrical activity of the brain<br />
Eye movements<br />
Heart rate<br />
Muscle activity<br />
For more information about polysomnography visit: <a href="http://classes.kumc.edu/cahe/respcared/cybercas/sleepapnea/trenpoly.html" target="_blank">http://classes.kumc.edu/cahe/respcared/cybercas/sleepapnea/trenpoly.html</a></div>
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The plysomnograph, Ref:[10]<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrz1j4Ci3IzOddBFDVnzxrd9SMVVkVPv_0U4vcGoqp04ndkxJ2Jatpp7CSt3L4LH291m4SRJDN4Pslt2yu9AXC0fUeXlT1YmyZLXOjbI-FS6ebMSkt-ls4YZQHq4r_0Mks8yNtKXLKIFqi/s1600/jpegggg.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="330" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrz1j4Ci3IzOddBFDVnzxrd9SMVVkVPv_0U4vcGoqp04ndkxJ2Jatpp7CSt3L4LH291m4SRJDN4Pslt2yu9AXC0fUeXlT1YmyZLXOjbI-FS6ebMSkt-ls4YZQHq4r_0Mks8yNtKXLKIFqi/s400/jpegggg.jpg" width="400" /></a></div>
UARS: upper airway resistance syndrome</div>
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<b style="color: purple;">2)Nocturnal sleep pulse oximetry:</b><span style="color: purple;"> </span> The oxygen desaturation index (ODI) measures the mean number of episodes of oxygen desaturation per estimated sleep hour and is sometimes used as a surrogate for the<br />
AHI.<br />
<b style="color: purple;">3)Epworth sleepiness scale (ESS):</b> Used to measure excessive day time sleepiness[10].<br />
<br />
<h3 style="text-align: left;">
<span style="color: purple;">Treatment:</span></h3>
<b><span style="color: purple;"></span><span style="font-weight: normal;"><span style="color: purple;"></span></span></b><b style="color: purple;">1) Continuous positive airway
pressure: </b><br />
Continuous positive airway
pressure:(CPAP) is the preferred treatment of choice for OSAHS.[9] The required CPAP is titrated to a level that
eliminates snoring, usually 5–20 cm Hg. A randomized placebo-controlled
trial showed that CPAP can improve breathing during sleep, sleep
quality, blood pressure,vigilance, cognition, and driving ability as
well as mood and quality of life in patients with OSAHS.The drug Modafinil is found to be effective in treating OSAS along with CPAP.It was also observed that CPAP therapy improves hypertension usually by about 10mmHg.[11]<br />
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<b>2) Mandibular repositioning splint:</b><br />
<div style="color: black;">
Mandibular repositioning splints (MRSs)or oral devices work by holding lower jaw and the tongue forward, thereby increasing the pharyngeal airway.</div>
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<b><span style="color: purple;">3) Surgery: </span></b></div>
<div style="text-align: left;">
Bariatric
surgery is useful and often curative in patients with morbid obesity. Tonsillectomy
is highly effective in children. Tracheostomy carries high morbidity and may be curative but rarely
used.[9]. Jaw advancement surgery, especially
maxilla-mandibular osteotomy, is effective in patients with
retrognathia.Somnoplasty uses radiofrequency energy to tighten the soft palate at the back of the throat.<br />
Nasal surgery may be considered for correction of nasal obstructions, such as a deviated septum.</div>
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Uvulopalatopharyngoplasty: A procedure that increases the width of the airway at the throat by removing soft tissue in the back of the throat and palate.</div>
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Mandibular/maxillary advancement surgery : The procedure involves surgically moving the jaw bone and face bones forward to make more room in the back of the throat, done in severe cases of OSAS and in patient with facial anomalies.<br />
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<b>Ref:</b></div>
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1). http://www.webmd.com/sleep-disorders<br />
2).AASM,Sleep 1999; 21 : 667-89.<br />
3).Young T, Skatrud J. Peppard PE. Risk factors for obstructive sleep apnea in adults. JAMA 2004; 291 : 2013-6.<br />
4).Schwartz AR, Patil SP, Laffan AM, Polotsky V, Schneider H,Smith PL. Obesity and obstructive sleep apnea – pathogenic mechanisms and therapeutic approaches. Proc Am Thorac Soc 2008; 5 : 185-92.<br />
5). Pathophysiology & genetics of obstructive sleep apnoea,Lisa Campana, Danny J. Eckert, Sanjay R. Patel† & Atul Malhotra.Indian J Med Res 131, February 2010, pp 176-187<br />
6).Shea S, Edwards J, White D. Effect of wake-sleep transitions and rapid eye movement sleep on pharyngeal muscle responseto negative pressure in humans. J Physiol 1999; 520 : 897-908.<br />
7).Stanchina ML, Malhotra A, Fogel RB, Ayas N, Edwards JK,Schory K, et al. Genioglossus muscle responsiveness to chemical and mechanical stimuli during non-rapid eye movement sleep.<br />
Am J Respir Crit Care Med 2002; 165 : 945-9.<br />
8).Respiratory arousal from sleep: mechanisms and significance.<span style="color: black;">Berry RB, Bleason, </span>Department of Medicine, Long Beach VA Medical Center, CA, 90822, USA.Sleep1997 Aug;20(8):654-75.<br />
9). GC Mbata and JC Chukwuka1,Obstructive Sleep Apnea Hypopnea Syndrome Ann Med Health Sci Res. 2012 Jan-Jun; 2(1): 74–77.<br />
10).<a href="http://www.sbu.se/upload/Publikationer/Content0/1/somnapne_fulltext.pdf" target="_blank">www.sbu.se/upload/Publikationer/Content0/1/somnapne_fulltext.pdf</a> <br />
11)Shiomi T, Sasanabe R, Ohtake K, et al. Cardiovascular complications,Obesity-induced hypertension and obesity heart failure accompanying obstructive sleep apnea. Journal of the Japanese Society of Internal Medicine. 2004;93(6):1114–1119.<br />
12)<a href="http://emedicine.medscape.com/article/295807-overview" target="_blank">http://emedicine.medscape.com/article/295807-overview</a> <br />
Image courtesy:<br />
1.Image header :<span class="irc_hd irc_iis"><a href="http://evelyngarone.wordpress.com/" target="_blank">evelyngarone.wordpress.com</a> </span><br />
<span class="irc_hd irc_iis"><span class="irc_dim"> 2. Image on diagnostic criteria and pathophysiology from Advances in Diagnosis and Treatment of Sleep Apnea Syndrome in Japan JMAJ 52(4): 224–230, 2009,Toshiaki and Ryujiro. </span></span><br />
<span class="irc_hd irc_iis"><span class="irc_dim">3.The multicolour circular flow chart..<a href="http://www.dentonsleepdisorderlab.com/obstructive-sleep-apnea.html" target="_blank">http://www.dentonsleepdisorderlab.com/obstructive-sleep-apnea.html</a> </span></span></div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-33991064359963917472013-03-29T03:56:00.000-07:002013-04-30T10:28:07.571-07:0010 COMMON 'PROCEDURAL BASICS' ANAESTHESIOLOGISTS MAY OVERLOOK!<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhJ8F6xoxcWWX3Dxl95T0GaJoEBa12JKqP-Ntsempeh0qEN64HizG7G6u5z_6-nPHkuHVwFut7TmxVwDuSDVrjvE0tUnEQHSa2A9W3DFZq0Gyv8GxdbDXlgSLRDU-9usl8dbT8RfL-L4y-y/s1600/345.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="190" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhJ8F6xoxcWWX3Dxl95T0GaJoEBa12JKqP-Ntsempeh0qEN64HizG7G6u5z_6-nPHkuHVwFut7TmxVwDuSDVrjvE0tUnEQHSa2A9W3DFZq0Gyv8GxdbDXlgSLRDU-9usl8dbT8RfL-L4y-y/s200/345.jpg" width="200" /></a></div>
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<span style="background-color: white;"><b style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #111111; font-family: Verdana, Geneva, sans-serif; font-size: small; font-style: normal; font-variant: normal; font-weight: bold; letter-spacing: normal; line-height: normal; orphans: auto; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: auto; word-spacing: 0px;">“To err is human;to forgive,divine.”</b><span style="font-family: inherit;"><span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #111111; display: inline !important; float: none; font-family: Verdana, Geneva, sans-serif; font-size: xx-small; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: auto; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: auto; word-spacing: 0px;">Remembering the famous poetry quote[1] by Alexander Pope (1688-1744).This means </span><span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #111111; display: inline !important; float: none; font-family: Verdana, Geneva, sans-serif; font-size: xx-small; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: auto; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: auto; word-spacing: 0px;">any
human can make a mistake,so we should try to forgive them, just as,God
said to show divine mercy to sinners and forgive them.Apart from
medication error and faulty techniques, anaesthesiologists rarely make
serious mistakes and any such mistake,if done may jeopardize the
patient's life.It is usual that anaesthesiologists forget to observe some basic procedural steps,which may lead to technical difficulties but usually the situation is overcome by timely intervention or by modifying the technique.Here are some situations, where an anaesthesiologist may encounter
difficulties during his routine anaesthesia practise when they fail to observe the basics.</span></span></span></h4>
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<span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #111111; display: inline !important; float: none; font-family: Verdana, Geneva, sans-serif; font-size: small; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: auto; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: auto; word-spacing: 0px;"><b style="background-color: white;">1)The importance of sniffing position with pillow under occiput</b></span><span style="font-family: inherit; font-size: small;">:</span></h3>
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The standard procedure for endotracheal intubation consists of keeping the head in sniffing position supported by pillow under head. <span style="font-family: inherit;">Successful tracheal intubation is achieved by obtaining a good glottic
view,which requires alignment of three optical axes corresponding to the
oral, pharyngeal and laryngeal planes. Extension at the atlanto occipital joint together with a head </span><span style="font-family: inherit; font-size: small;">elevation(</span><span style="font-family: inherit; font-size: small;"> <span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: Verdana; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 21.1875px; orphans: auto; text-align: justify; text-indent: 0px; text-transform: none; white-space: normal; widows: auto; word-spacing: 0px;"><span style="font-size: small;">m</span>oderate
head elevation 5–10 cm above the surgical table)</span> keeps the perfect axis for an easy intubation[2]</span><span style="font-family: inherit;">Infants may need a small towel roll under the "shoulders" to align the head.Obese patients [3]elevated head-up position or "ramp"position is used. In this position, the shoulders are elevated with several pads, the head and neck are extended, and the external auditory
meatus is in line with the sternal notch.Most the difficult airways arise due to defective positioning.</span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiZuw8jNrl4UZ0F2KvvYpdhsP8tNEmE90GbfYYCJ8ZtuSld-O-u2rw0pZt4xG2mwKUOgYp8ffaH_AoZv91NmrucFHwvBDUTFMNAzi0OGTSEFf9xzrK1v2HjsSVOrmH5xWzisInWLlicdYjZ/s1600/en_a10f03.gif" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="196" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiZuw8jNrl4UZ0F2KvvYpdhsP8tNEmE90GbfYYCJ8ZtuSld-O-u2rw0pZt4xG2mwKUOgYp8ffaH_AoZv91NmrucFHwvBDUTFMNAzi0OGTSEFf9xzrK1v2HjsSVOrmH5xWzisInWLlicdYjZ/s400/en_a10f03.gif" width="400" /></a> figure 1<br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgGzoRSihyphenhyphen_ZS5hoN8wy9CORjsVZTO2MoXr_saxEH_DjEVzUKPsGT4OaTT4CkjFpiZD1MZ8qpn4sLMvhu-uVbTfmGBPf_7BI-mQcmpA0vEiInD0Q3Y8JZcDzQo_6XUNf7hmOdqL3ihlH-mM/s1600/1-s2.0-S0733862708000874-gr3.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="193" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgGzoRSihyphenhyphen_ZS5hoN8wy9CORjsVZTO2MoXr_saxEH_DjEVzUKPsGT4OaTT4CkjFpiZD1MZ8qpn4sLMvhu-uVbTfmGBPf_7BI-mQcmpA0vEiInD0Q3Y8JZcDzQo_6XUNf7hmOdqL3ihlH-mM/s200/1-s2.0-S0733862708000874-gr3.jpg" width="200" /></a><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhwP4lM1lrp-uOSeNKydiO-Wz9db4H0jWae6ySClBH5rQPpMkyx0WRT-NyLcmCWZISNjNYSf2wX0S-yQ-MbRetHnYoNeItYC3-zfFHws4vxNaNMSp2TMclGJ5OiTXW1D0sRPiDI-A8Hqqns/s1600/Ramped.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhwP4lM1lrp-uOSeNKydiO-Wz9db4H0jWae6ySClBH5rQPpMkyx0WRT-NyLcmCWZISNjNYSf2wX0S-yQ-MbRetHnYoNeItYC3-zfFHws4vxNaNMSp2TMclGJ5OiTXW1D0sRPiDI-A8Hqqns/s320/Ramped.jpg" width="320" /></a></div>
figure 2<br />
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<b>2)Bag and mask ventilation without oral airway and intubation without applying cricoid pressure. </b><br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjP-MmFr-O1NbYNFZZ73YKqrdX3djb8Skg6s3ri4X7IduBhJ-DAfv2ZL3RZ1VzjTCGgMQGV5hSmxpODwDGWFT_HIQOmRAPm-Ipq1vAriPtzGM8wNk8iatKSMl3UFEcu5vR2D0duyEupKQ95/s1600/ambu+bag+pt.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="196" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjP-MmFr-O1NbYNFZZ73YKqrdX3djb8Skg6s3ri4X7IduBhJ-DAfv2ZL3RZ1VzjTCGgMQGV5hSmxpODwDGWFT_HIQOmRAPm-Ipq1vAriPtzGM8wNk8iatKSMl3UFEcu5vR2D0duyEupKQ95/s320/ambu+bag+pt.jpg" width="320" /></a><b><br /></b>One 9 year old boy with respiratory distress was admitted to A and E following ARDS due to severe sepsis.The child was conscious but drowsy and dropping saturation. The anaesthesiologist was called in for intubation and he continued with initial bag and mask ventilation to maintain the saturation while preparing for intubation.An airway was not used and the air pumped into his lungs negotiated its way to stomach due to partial airway obstruction. While he did laryngoscopy, due to gag reflex he regurgitated and immediately aspirated. Further attempts to maintain saturation following intubation were not successful. Drowsy semiconscious patients with weak gag reflex may tolerate oral airway and definitely tolerate nasal airway which helps to direct the air into the lungs following ambu bag ventilation.[4].The basic rule states application of cricoid pressure with head down position will prevent aspiration.(application of cricoid pressure and its effectiveness is questioned and many controversies exist, but was found very useful practically)<br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhggfv2KrUhFpZN8VL6UzNusrWvBpjfCf9gT8rtHKzH-KGhiSYJi_TqSxp43iHdfNU8pcpTwaqGRcC7FOQc_5M2qSWe8ArFrkmh46uWT7C94MHwdsUTySY93tJZNt2GBgH9gljL3BwFr1CB/s1600/oral+airways.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="190" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhggfv2KrUhFpZN8VL6UzNusrWvBpjfCf9gT8rtHKzH-KGhiSYJi_TqSxp43iHdfNU8pcpTwaqGRcC7FOQc_5M2qSWe8ArFrkmh46uWT7C94MHwdsUTySY93tJZNt2GBgH9gljL3BwFr1CB/s200/oral+airways.jpg" width="200" /></a><br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwkUxZ71WGgkLtNQK_HXN3lKuPX5xkSNjgyzsW8hsUtywFwFLUX52HQBy_UJLZfqknePDzPxQOhgvXOpbwlzXPBdB2CHrDvSFpOkFrYlzum3Xsf3K_7eQipaZrEAJnPaDSFMuEhvIr3hVY/s1600/cricoid.gif" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="243" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwkUxZ71WGgkLtNQK_HXN3lKuPX5xkSNjgyzsW8hsUtywFwFLUX52HQBy_UJLZfqknePDzPxQOhgvXOpbwlzXPBdB2CHrDvSFpOkFrYlzum3Xsf3K_7eQipaZrEAJnPaDSFMuEhvIr3hVY/s320/cricoid.gif" width="320" /></a><br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjP-MmFr-O1NbYNFZZ73YKqrdX3djb8Skg6s3ri4X7IduBhJ-DAfv2ZL3RZ1VzjTCGgMQGV5hSmxpODwDGWFT_HIQOmRAPm-Ipq1vAriPtzGM8wNk8iatKSMl3UFEcu5vR2D0duyEupKQ95/s1600/ambu+bag+pt.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"></a><br />
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<b>3)Intubation using a bougie in difficult airway.</b><br />
Grades 2 and 3 glottic view may be managed by intubation over a bougie.Following laryngoscopy insert bougie into the glottis and then "rail road"the ETT over the bougie.The basic rule here is "dont remove the laryngoscope before railroading". Once you remove the scope after inserting bougie the epiglottis and pharyngeal soft tissues may come their way between the ETT and the bougie and cause intubation failure.Ask the assistant to pass the ETT over the bougie while the anaesthetist keeps the epiglottis elevated with his laryngoscope with one hand and stabilising the bougie with the other hand.<br />
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<b>4)Removal of a Laryngeal mask airway.</b><br />
Patients on spontaneous ventilation under LMA anaesthesia,it is advisable to remove the LMA in deep anaesthetic plane itself.If you wait till the patient is fully conscious,chance of biting the airway tube by patient is high which leads to total airway occlusion and any attempt to remove an LMA in this situation can cause damage to the LMA, laryngospasm or regurgitation by pharyngeal stimulation[5].The ideal sequence of removing LMA seems....remove in deep plane then cut down gases,insert oral or nasal airway,keep mask, turn head to one side, allow patient to recover by inhaling 100% oxygen.<br />
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<b>5)Treating laryngospasm during recovery.</b><br />
The treatment should be immediate,prompt and aggressive[6].Delay in treating laryngospasm may lead to serious morbidity.IPPV with 100% to break off the spasm is widely followed as the first line of management but there <i>should not be any delay </i>in administering suxamethonium.The most feared complications are hypoxia and negative pressure pulmonary edema.<br />
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<b>6)Exsanguinate before IVRA.</b><br />
Complete exsanguination of the upper limb is advocated before IVRA.Failure of proper exsanguination leads venous oozing during the procedure causing unsatisfactory operating conditions.Poor diffusion of the drug leads to 'patchy" anaesthesia or total failure of anaesthesia.The use of an esmarch or similar bandage is stressed.<br />
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<b>7)Extubating a difficult airway</b>.There are many gadgets available to deal with a difficult airway.With the introduction of fastrach LMA and fiberoptic bronchoscope, the success rate of intubation is high.Following ICU admission or surgical procedure many anaesthesiologists fail to observe the basic rule "while extubating a difficult airway take the same precaution and keep ready the same gadgets you used to intubate the case, since extubation failure or post extubation complications may necessitate immediate reintubation". Always use a guide wire or bougie over which the ETT is pulled out (extubation over bougie)and observe the vocal cord behaviour during extubation.<br />
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<b>8)Testing loss of resistance.</b> <span style="font-family: inherit;">While testing for loss of resistance during epidural anaesthesia always use saline instead of air to avoid complications like pneumocephalus[7],<span style="background-color: white; font-size: 13px; line-height: 17px;"> </span><span style="background-color: white; line-height: 17px;">spinal cord and nerve root compression, retroperitoneal air, subcutaneous emphysema, and venous air embolism[8] Alternatively saline with an air bubble technique also seems to be appropriate.</span></span><br />
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<span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"> Performing the LOR by saline, from NYSORA</span><br />
<span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"><br /></span>
<b>9)Nasal intubation in pediatrics. </b>Extreme caution should be taken while performing a nasal intubation in pediatric age group and any difficulty in ventilation should alert the anaesthetist of possibility of occlusion of the tip of ETT with a piece of adenoid tissue carried away in it. Any incidence of difficulty in ventilation, high airway pressure,abnormal tracing of capnogram or fall in saturation following nasal intubation in children,the anaesthetist should not hesitate to remove the ETT immediately and proceed with mask ventilation and oral intubation. Never attempt to overcome the resistance by forced ventilatory attempts or by passing catheters into ETT..[9][10]The obstruction by adenoid is usually distal to murphy's eye and other common causes for the obstruction are kinking of ETT and severe bronchospasm following intubation.<br />
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<b>10)Uncover during PAC!</b>The last but not the least, make a detailed physical examination during PAC.It was found on many occasions that gross physical deformities were overlooked by anaesthetists due to lack of proper exposure of body parts.Such deformities include pectus excavatum, pectus carinatum,scoliosis, thyroid swellings and other congenital abnormalities,.All these situations may lead to devastating intra operative complications.<br />
<br />
Ref:<br />
1)<a href="http://www.quotecounterquote.com/2010/12/to-err-is-human-to-forgive-divine.html" target="_blank">http://www.quotecounterquote.com/2010/12/to-err-is-human-to-forgive-divine.html</a><br />
2)<a href="http://www.anesthesia-analgesia.org/content/early/2011/05/18/ANE.0b013e31821c7e9c.full.pdf" target="_blank">http://www.anesthesia-analgesia.org/content/early/2011/05/18/ANE.0b013e31821c7e9c.full.pdf</a><br />
3)<a href="http://www.anesthesia-analgesia.org/content/102/5/1592.1.full" target="_blank">http://www.anesthesia-analgesia.org/content/102/5/1592.1.full</a><br />
4)<a href="http://www.acep.org/Clinical---Practice-Management/Focus-On---Bag-Valve-Mask-Ventilation/" target="_blank">http://www.acep.org/Clinical---Practice-Management/Focus-On---Bag-Valve-Mask-Ventilation/</a><br />
<a href="http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD007082/pdf" target="_blank"><span style="color: black;">5</span>)http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD007082/pdf</a><br />
6) <a href="http://www.respond2articles.com/ANA/forums/thread/1096.aspx" target="_blank">http://www.respond2articles.com/ANA/forums/thread/1096.aspx</a><br />
7)<a href="https://www.aana.com/newsandjournal/Documents/p449-453.pdf" target="_blank">https://www.aana.com/newsandjournal/Documents/p449-453.pdf</a><br />
8)<a href="http://www.ncbi.nlm.nih.gov/pubmed/9010941" target="_blank">http://www.ncbi.nlm.nih.gov/pubmed/9010941</a><br />
9)<a href="http://www.cas.ca/English/Page/Files/657_1344758.pdf" target="_blank">http://www.cas.ca/English/Page/Files/657_1344758.pdf</a><br />
10)<a href="http://www.thefreelibrary.com/Nasotracheal+tube+occlusion+from+adenoid+trauma.-a0188739844" target="_blank">http://www.thefreelibrary.com/Nasotracheal+tube+occlusion+from+adenoid+trauma.-a0188739844</a></div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com1tag:blogger.com,1999:blog-8746726747957343433.post-67851515637634048812013-02-26T12:53:00.000-08:002013-03-22T10:04:17.585-07:00POST DURAL PUNCTURE HEADACHE,A NEVER ENDING STORY!<div dir="ltr" style="text-align: left;" trbidi="on">
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“Toward the evening I was forced to take to bed and remained there for nine days, because all the manifestations recurred as soon as I got up. At midnight a violent headache set in that quickly became insupportable.” This was the first experience of spinal headache in the history and was experienced by the great August Bier in 1898,when he suffered severe headache after spinal anesthesia given to him by his colleague,on his request.The headache follows any diagnostic or therapeutic procedure of the spinal or epidural space.<br />
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According to Carrie and Collins [1] post dural puncture headache (PDPH) is "a headache occurring after dural puncture and has a significant effect on the patient's post operative well being i.e. headache which is not only postural but also continues for more than 24 hours at any level of intensity or so severe at any time that the patient is unable to maintain upright position.According to the International Headache Society, the criteria for PDPH [2] include a headache that develops less than seven days after a spinal puncture, occurs or worsens less than fifteen minutes after assuming the upright position, and improves less than thirty minutes in the recumbent position with at least one of the following (neck stiffness, tinnitus, hypacusia, photophobia, and nausea). The headache should disappear within fourteen days after a spinal puncture; if it persists, it is called a CSF fistula headache.The incidence[3] of PDPH is estimated to be between 30-50% following diagnostic or therapeutic lumbar puncture,0-5% following spinal anaesthesia and up to 81% following accidental dural puncture during epidural insertion in the pregnant woman.Other than spinal anaesthesia the procedures leading to PDPH include,diagnostic lumbar puncture( where a big sized needle is used) labour
analgesia with accidental dural puncture and therapeutic epidural
steroid injections.<br />
<br />
<b>Do the needle size and type matters?</b> Of course, researchers of the past 100 years have found that there is a definite relationship between the incidence of PDPH and needle size. Reducing the size of the spinal
needle has made a significant impact on the
incidence of post‐spinal headache. The incidence[4] is approx 40% with a 22G
needle; 25%
with a 25G needle; 2%–12% with a 26G Quincke needle; and less than 2% with a 29G needle. With needles of 29G or smaller, the technical difficulties may lead onto a failure of the procedure and multiple attempts may be required causing multiple dural puncture which in fact increase the incidence.Pencil point whitacre needles are now preferred.If the needle bevel is oriented parallel to the nerve
fibres during spinal anaesthesia the incidence can be lowered further.PDPH is rare in children owing to their low CSF pressure[5]<br />
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<b>Characteristic features of head ache: </b>Ninety per cent of headaches
will occur within 3 days of the procedure,[6]and 66% start within the first 48 h.[7] Rarely, the headache develops between 5 and 14 days after the procedure.The head ache is commonly distributed over the frontal and occipital areas
radiating to the neck and shoulders and sometimes the temporal, vertex
and nuchal areas also may be affected.Neck stiffness may be present. The pain is
exacerbated by movements of the head, standing position and relieved by supine position.Other symptoms include nausea,vertigo,tinnitus,visual disturbances and rarely cranial nerve palsies.The headache is usually relieved in seven days but cases were reported where it lasted upto 3 months.The cause for the head ache is CSF leak leading to intracranial hypotension<br />
<br />
<b>Diagnosis:</b> Mainly by clinical features and history of possible dural puncture.Additionally a diagnostic CSF tap may show, a low CSF opening pressure, minimally raised CSF protein, and a
rise in CSF lymphocyte count.The MRI may demonstrate diffuse dural
enhancement,
with evidence of a sagging brain or descent of the
brain.[8] Cisternography or CT myelography may be used for diagnosing a CSF leak.Untreated cases may develop intracranial hematoma due to rupture of bridging veins following intracranial hypotension.<br />
<br />
<h3 style="text-align: left;">
<b>Treatment: </b></h3>
1) <b><span style="color: purple;">Bed rest</span>:</b> No use at all [9] but along with other measures very effective in reducing headache.<br />
<br />
2) <span style="color: purple;"><b>Simple analgesics:</b><span style="color: black;"> Paracetamol and other NSAIDs for mild pain.</span></span><br />
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<span style="color: purple;"><span style="color: black;">3) <span style="color: purple;"><b>Posture:</b><span style="color: black;"> Supine position helps to maintain the CSF pressure and prone position increases intra abdominal pressure and the CSF pressure and gives instantaneous relief. However prone position may not be comfortable for the patient.</span></span></span></span>Supine position helps to avoid complications like intracranial hemorrhage and seizures due to low CSF pressure. <br />
<br />
<span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;">4)<span style="color: purple;"> <b>Abdominal binders:</b><span style="color: black;"><span style="color: black;"> Should be tight enough to increase the intra abdominal pressure.</span></span></span></span></span></span></span><br />
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<span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;">5)<b> <span style="color: purple;">Caffeine :</span></b> Caffeine is a CNS stimulant and cerebral vasoconstrictor.The recommended dose is 300-500 mg of oral caffeine once or twice in a day[10] [11]</span></span></span></span></span></span></span>It is assumed that caffeine acts through vasoconstriction of dilated cerebral vessels.Caffeine is associated with some adverse events like cardiac arrhythmias and maternal seizures and necessary precaution may be taken. High doses of the drug may reach the baby through breast milk and can cause neonatal irritability[12]<br />
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<span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;">6) <span style="color: purple;"><b>Sumatriptan:</b></span> </span></span></span></span></span></span></span><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;"> Sumatriptan is a 5‐HT<sub>1D</sub> receptor agonist that promotes cerebral vasoconstriction,<cite>acts in a similar way to caffeine</cite>. It increases the cerebral vascular tone.</span></span></span></span></span></span></span><br />
<br />
<span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;">7) <b><span style="color: purple;">Synthetic ACTH: </span></b>was first reported to be effective for treating PDPH in the 1990s. Postulated<br />mechanisms include CSF retention through increased mineralocorticoid mediated sodium reabsorption,<br />and a direct analgesic effect via its glucocorticoid activity[12]. A randomised controlled trial in 2004 found no effect of a single intramuscular injection of Synacthen compared with an intramuscular injection of normal saline.ACTH has been administered as an infusion [13] 1.5 microgram per kilogram. </span></span></span></span></span></span></span><br />
<br />
<span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;">8) <b><span style="color: purple;">Desmopressin(DDAVP):</span></b> injection intramuscularly before spinal injection has also proven to be effective but more reasearch is required to prove its efficacy.</span></span></span></span></span></span></span><br />
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<span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;">9)<b><span style="color: purple;">Adequate hydration</span></b>: was found to be helpful but overhydration must be avoided. </span></span></span></span></span></span></span><br />
<br />
<span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;">10)<span style="color: purple;"><b>Epidural Blood Patch:</b></span> Perhaps the most effective treatment for PDPH is epidural blood patch(EBP).the concept of EBP has developed following the observation that bloody taps were associated with reduced incidence of headache.The first epidural blood patch was performed in 1960 by theAmerican surgeon, Dr James Gormley.The mechanism is that once blood is introduced into the epidural space it coagulates and form a seal occluding the puncture site </span></span></span></span></span></span></span><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: purple;"><span style="color: black;"><span style="color: black;">preventing further CSF leak.The procedure is associated with high success rate and low incidence of complications and has become the standard mode of treatment for PDPH.Before initiating the treatment one has to look for the contraindications like coagulopathy, local infections, fever or patient refusal.A sample of the patient's blood may be sent to lab for culture[14].If symptoms of PDPH persist after 24-48 hours,or the headache is disabling,consider an epidural blood patch. </span></span></span></span></span></span></span><br />
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<b><span style="color: purple;"> Guidelines[15] for placement of epidural blood patch (St.George Hospital, London)</span></b><br />
<br />
The procedure must be carried out in theatre. Two anaesthetists are required, one of whom should be a consultant.<br />
1. Written, informed consent should be obtained from the woman following a careful explanation of the procedure. The discussion should also include the chances of success, significant side effects and the possibility of requiring a second blood patch(approximately 1 in 5).<br />
2. The epidural space is located with a Tuohy needle, by the first anaesthetist, at the level of the supposed dural puncture, or an intervertebral space above or below. CSF may be present in the epidural space. 20 – 30 ml of the patient’s blood (provided by the second anaesthetist) is then injected into the epidural space over 30 – 60 seconds. Dull, lower back pain may limit the volume injected, although pausing for a few seconds or slowing the rate of injection may allow the full amount to be injected.<br />
3. The second anaesthetist is responsible for drawing blood from the patient. As with the epidural, vene puncture must also be carried out using a full aseptic technique. After cleaning and draping the skin of the antecubital fossa, the skin should be anaesthetized with local anaesthetic prior to the insertion of a 14 or 16 gauge cannula. This should be done when the epidural needle is sited.<br />
4. It has previously been thought that samples of the blood should routinely be sent for culture. This is an area of much controversy, and is backed up by little evidence,however until we have a definitive answer to this question it would seem prudent to continue to send blood for screening purposes. There is no evidence for the routine use of prophylactic antibiotics following blood patch.<br />
5. The epidural blood patch should be carried out in the Obstetric theatre. Immediately following the procedure the patient should be taken to the recovery area for close observation. The patient is encouraged to lie still for one to two hours. After this time she can be transferred to the ward where she should be encouraged to walk.<br />
6. It is important that the patient has repeated clinical assessment while an inpatient,although she may well go home the same day. Prior to going home, advice must be given regarding the need to contact labour ward or present to an Accident and Emergency department in the case of any complications. Specifically patients should be told about presenting features of cauda equina syndrome and epidural abscess.Where<br />
possible written information should also be given. " During placing of EPB thus patient always should be asked about any acute occurrence of new pain, radiating pain and sharp shooting pain. Thus in EPB always a test dose of 2-3 ml of blood should be injected and patient should be evaluated. The total volume should be injected in increments of 2-3 mls".<br />
<br />
<span style="color: purple;"><b>Mechanism of action of EBP:</b></span> After injection the patient should remain supine and immobile for<br />
30 minutes to 2 hours to allow the blood to form a clot.Once injected the blood is distributed caudally
and cephalad regardless of the direction of the
bevel of the Tuohy needle. The blood also finds its distribution circumferentially
around
to the anterior epidural space. This has been proved [16] by using radiolabelled red cells or by MRI.There is evidence of thecal space compression and escape of blood through the intervertebral foramina and into the paravertebral space.The injected blood spreads up about six spinal
segments
cephalad and three segments caudad.The procoagulat property of CSF accelerates clotting of blood and the puncture site is sealed followed by an immediate relief of headache.At 7–13 h, there is clot resolution leaving a thick layer of mature
clot over the dorsal part of the thecal sac.[17]<br />
<br />
<span style="color: purple;"><b>Efficacy of blood patch:</b></span> EBP is likely to be most effective if performed at least 24 hours after the onset of PDPH.The success rate varies between 75-90% and about 40% patients may need second EBP.The technique is safe and the rare transient complications include radiculopathy,backache, neckache and bradycardia.Major complications are rare,and may include meningitis, subdural haematoma, seizures, arachnoiditis, spastic paraparesis, dural puncture,cauda equina syndrome etc.If an epidural blood patch fails to relieve a PDPH, it is advisable to consider radiological imaging of the head to exclude other pathology prior to repeating the blood patch.<br />
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<span style="color: purple;"><b>Prophylactic blood patch: </b></span>The beautiful explanation in this regard is by <cite>Dr Nicola Jane Campbell FRCA, Effective management of post dural
puncture headache Anaesthesia tutorial of the week 181, 31st may 2010.He says,</cite><br />
A potentially attractive option in the face of a recognised dural puncture with a Tuohy needle is to resite the epidural so that a prophylactic epidural blood patch (PEBP) can be provided in the hope of preventing a subsequent PDPH. The popularity of this technique has diminished recently for a number of reasons including the limited evidence that PEBP reduces the requirement for a therapeutic EBP, the increasing use of intrathecal catheter placement following dural puncture which may itself reduce the risk of subsequent PDPH and the recognition that some dural punctures don’t result in a PDPH and many PDPHs do not require a therapeutic EBP. Administering a PEBP to patients following duralpuncture may therefore expose these patients to an unnecessary procedure with associated risks.<br />
<b><span style="color: purple;">Epidural saline and Dextran:</span></b> theoretically a suitable alternative to EBP and thought to be safe as they are sterile solutions.These techniques are very useful in Jehovah witnesses patients or patient with bacteremia and HIV infection .They increase the CSF pressure by mass effect but formation of a coagulum and subsequent sealing effect over the dura are doubtful.Regimens include (i) 1.0–1.5 litre of epidural Hartmanns solution over 24 h, starting on the first
day after dural puncture;[18] (ii) up to 35 ml h<sup>–1</sup> of epidural saline or Hartmanns solution for 24–48 h, or after development of the headache; (iii) a single 30 ml bolus of
epidural saline after development of headache;[19] and (iv) 10–120 ml of saline injected as a bolus via the caudal epidural space.The tamponade effect of epidural dextran is also transient and similar to saline offering no advantage over saline.In neither of these an aseptic inflammatory response over the dura was found.<br />
<br />
<span style="color: purple;"><b>Epidural Morphine:</b></span> Administration of epidural morphine soon after inadvertent dural puncture as prophylactic measure to prevent PDPH has been advocated by many authors but evidence lack due to absence of large controlled trials.<br />
<br />
<b><span style="color: purple;">Fibrin glue:</span></b> As an alternetive to blood patch fibrin glue injection into the epidural space was found to be helpful..The procedure may be done blindly or by CT guided percutaneous injection.The failure rates are high. Chance of development of aseptic meningitis makes the procedure less acceptable to many.<b><span style="color: purple;"> </span></b><br />
<br />
<b><span style="color: purple;">Intrathecal catheters:</span></b>An alternative method of managing ADP by passing an epidural catheter through the needle into the subarachnoid space was described by Cohen in 1989. Since then, several studies have claimed a reduction in incidence of PDPH if the epidural catheter is inserted intrathecally at the time of dural puncture and removed after at least 24 h. Injection of a 10 ml bolus of normal saline into the intrathecal catheter before its removal further reduced the incidence of PDPH. [20]It was postulated that placement of <br />
a spinal catheter through
the perforation may provoke an inflammatory reaction that will seal the hole. However, neurological complications, such as cauda equina syndrome
and infection, should preclude the use of intrathecal catheters and keeping the catheter for more than 24 hours is also not advocated<br />
<br />
<b><span style="color: purple;">Surgical closure:</span></b> Surgical closure of the dural perforation is the last resort to treatment <br />
<br />
<span style="color: purple;"><b>Preventing PDPH;</b></span> Preventive measures like smaller needle size, shape of needles and direction of needle bevel in relation to dural fibers, should always be considered.For spinal blocks, pencil point needles of 25 G or smaller should be used, especially in the obstetric population.While performing Epidural anaesthesia Loss of resistance to saline performed with continuous pressure on the syringe plunger may have the effect of<br />
moving the dura anteriorly as the needle approaches thereby reducing the likelihood of dural puncture<br />
compared with an intermittent pressure technique with air.Other precautions should include ensuring an optimal patient position, slow controlled advancement of the needle and limiting patient movement during the procedure by using adequate local anaesthetic infiltration[12].When there is difficulty use of ultrasound guidance for epidural placement may be considered.<br />
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<b><span style="color: purple;">Differential diagnoses:</span></b> for PDPH:Tension Headache,Migraine Headache, Caffeine Withdrawal, Lactation Headache, Hypertension, Pneumocephaelus, Meningitis, Subarchnoid Heamorrahge, Spontaneous Intracranial Hypotension and eclampsia.<br />
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PDPH is the most distressing experience for post operative patient and can lead on to significant morbidity and death..Apart from increasing the duration of hospitalisation, it can cause auditory and visual disturbances, nausea, vomiting ,cranial nerve palsy and intracranial hemorrhage due to low CSF pressure.The treatment should be aggressive with conservative methods initially and in severe and resistant cases with CNS involvement EBP may be tried..Mostly the headache is benign and will be resolved spontaneously in 5-7 days<br />
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A current review about PDPH by Steve Schwalbe, MD is found to be interesting in this context..<a href="http://www.soap.org/media/newsletters/fall2000/pathophysiology_management.htm" target="_blank">http://www.soap.org/media/newsletters/fall2000/pathophysiology_management.htm</a><br />
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Ref:<br />
1) <i>Carrie Less, Collins PD. 29 guage spinal needle. Br J Anesth 1991; 66 :145-6.</i><br />
2) R. W. Evans, “Complications of lumbar puncture,” Neurologic Clinics, vol. 16, no. 1, pp. 83–105, 1998<br />
3)<a href="http://www.frca.co.uk/Documents/181%20Post%20dural%20puncture%20headache.pdf" target="_blank">http://www.frca.co.uk/Documents/181%20Post%20dural%20puncture%20headache.pdf</a><br />
4) <cite>Barker P. Headache after dural puncture. <span class="cit-source">Anaesthesia</span> <span class="cit-pub-date">1989</span>; <span class="cit-vol">44</span>: <span class="cit-fpage">696</span>–7</cite><br />
<cite>5) </cite><cite><cite>Carbajal R, Simon N, Olivier‐Martin M. Post‐lumbar puncture headache in children. Treatment with epidural autologous blood
(blood patch). <span class="cit-source">Arch Pediatr</span> <span class="cit-pub-date">1998</span>; <span class="cit-vol">5</span>: <span class="cit-fpage">149</span>–52</cite></cite><br />
6)<cite> Reynolds F. Dural puncture and headache. <span class="cit-source">Br Med J</span> <span class="cit-pub-date">1993</span>; <span class="cit-vol">306</span>: <span class="cit-fpage">874</span>–6</cite><br />
<cite>7) </cite><cite>Leibold RA, Yealy DM, Coppola M, Cantees KK. Post‐dural‐puncture headache: characteristics, management, and prevention. <span class="cit-source">Ann Emerg Med</span> <span class="cit-pub-date">1993</span>; <span class="cit-vol">22</span>: <span class="cit-fpage">1863</span>–70</cite><br />
<cite>8) </cite><cite><cite>Mokri B, Parisi JE, Scheithauer BW, Piepgras DG, Miller GM. Meningeal biopsy in intracranial hypotension: meningeal enhancement
on MRI. <span class="cit-source">Neurology</span> <span class="cit-pub-date">1995</span>; <span class="cit-vol">45</span>: <span class="cit-fpage">1801</span>–7</cite></cite><br />
<cite><cite>9) </cite></cite><cite>Spriggs DA, Burn DJ, French J, Cartlidge NE, Bates D. Is bed rest useful after diagnostic lumbar puncture? <span class="cit-source">Postgrad Med J</span> <span class="cit-pub-date">1992</span>; <span class="cit-vol">68</span>: <span class="cit-fpage">581</span>–3</cite><br />
<cite>10) </cite><cite>Sechzer PH. Post‐spinal anesthesia headache treated with caffeine. Evaluation with demand method. Part 2. <span class="cit-source">Current Therapeutic Research, clinical and experimental</span> <span class="cit-pub-date">1979</span>; <span class="cit-vol">26</span>: <span class="cit-fpage">440</span>–8</cite><br />
<cite>11) http://www.update-software.com/BCP/WileyPDF/EN/CD007887.pdf</cite><br />
<cite>12) Dr Nicola Jane Campbell FRCA, Effective management of post dural puncture headache Anaesthesia tutorial of the week 181, 31st may 2010</cite><br />
<cite>13) </cite><cite>Collier BB. Treatment for post‐dural puncture headache. <span class="cit-source">Br J Anaesth</span> <span class="cit-pub-date">1994</span>; <span class="cit-vol">72</span>: <span class="cit-fpage">366</span>–7</cite><br />
<cite>14)</cite><cite><cite>Crawford JS. Experiences with epidural blood patch. <span class="cit-source">Anaesthesia</span> <span class="cit-pub-date">1980</span>; <span class="cit-vol">35</span>: <span class="cit-fpage">513</span>–15.</cite> </cite><br />
<cite></cite><cite>15) <a href="http://www.oaa-anaes.ac.uk/assets/_managed/editor/File/Guidelines/PDPH/PDPH_diagnosis_management%20PDPH_Wendler_StGeorges.pdf" target="_blank">http://www.oaa-anaes.ac.uk/assets/_managed/editor/File/Guidelines/PDPH/PDPH_diagnosis_management%20PDPH_Wendler_StGeorges.pdf</a></cite><br />
<cite>16) </cite><cite>Szeinfeld M, Ihmeidan IH, Moser MM, Machado R, Klose KJ, Serafini AN. Epidural blood patch: evaluation of the volume and spread
of blood injected into the epidural space. <span class="cit-source">Anesthesiology</span> <span class="cit-pub-date">1986</span>; <span class="cit-vol">64</span>: <span class="cit-fpage">820</span>–2</cite><br />
<cite>17) D.K.Turnbull,D.B, shepherd,Post dural puncture headache, pathogenesis, prevention and treatment</cite><i> Br J Anaesth</i> 2003; <b>91</b>: 718–29<br />
18) <cite>Crawford JS. The prevention of headache consequent upon dural puncture. <span class="cit-source">Br J Anaesth</span> <span class="cit-pub-date">1972</span>; <span class="cit-vol">44</span>: <span class="cit-fpage">598</span>–600</cite><br />
<cite>19) </cite><cite>Moir DD. Recent advances in pain relief in childbirth. II: regional anaesthesia. <span class="cit-source">Br J Anaesth</span> <span class="cit-pub-date">1971</span>; <span class="cit-vol">43</span>: <span class="cit-fpage">849</span>–57</cite><br />
<cite>20) <a href="http://www.joacc.com/article.asp?issn=2249-4472;year=2011;volume=1;issue=2;spage=57;epage=66;aulast=Nath" target="_blank">http://www.joacc.com/article.asp?issn=2249-4472;year=2011;volume=1;issue=2;spage=57;epage=66;aulast=Nath</a></cite></div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-89438513144323336112013-01-29T23:21:00.002-08:002013-02-27T00:49:39.332-08:00THE GOLDEN RULES OF ANAESTHESIA<div dir="ltr" style="text-align: left;" trbidi="on">
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Back to the basics!!! Safe conduct of anaesthesia should be the priority when surgical cases are posted for procedures.The expertise and experience of the anaesthetist along with proper monitoring are essential in achieving this goal, but without considering the basics of anaesthesia practise even an experienced physician backed up by all essential monitors may turn to be a dangerous anaesthetist. Here are the ten golden rules of anaesthesia which stand immortal even in the midst of recent advances.<br />
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1.<b>Assess and prepare the patient adequately:</b>So that you will not anaesthetise anyone with multisystem disorders, heart disease,anemia or metabolic disorders.The physician should get sufficient information about the medications the patient is receiving as the drug interaction of these drugs with anaesthetic agents are complex and sometimes dangerous.Prepare the patient by correcting dehydration, severe anaemia,diabetes, heart failure,hyperthyroidism etc..Identifying pre existing diseases and correcting them help the anaesthetist for proper risk stratification of cases and a proper plan of anaesthesia technique can be made.The detailed explanation of the anaesthesia procedure must be offered to the patient and an informed consent must be obtained.</div>
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2.<b>Starve the patient even for local anaesthesia: </b>So that if the patient tries to vomit his stomach is less likely to be full. In case the local anaesthesia fails or a toxicity or CNS involvement by the local anaesthetics he may have to administer general anaesthesia or to resuscitate the patient.</div>
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3<b>.Anaesthetise him on a tipping table:</b> Because he may still vomit ,even if he is supposed to have been starved.So you must be able to tip him head down.If you do this, the chance of aspiration (even if he regurgitates)is very less.</div>
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4.<b>Check your drugs and equipment: </b>Before your start,especially if you are using less simple equipment. The equipment to preserve his airway must be ready beside you.All drugs including drugs for emergency use must be loaded and labelled.The anaesthesia machine and monitors should be checked as per routine checking protocols.</div>
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5.<b>Keep a sucker instantly ready:</b> Tested and working,so that if his pharynx fills with vomit,you can suck it out.You will also need suction catheters.A properly working suction catheter is mandatory for administering anaesthesia.</div>
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6.<b>Keep airway clear: </b>Because it can be easily obstructed.One way to do this is to use a Guedel's airway.You will need a range of different sizes. Alternatively you can use the triple manuevour too. Recently with the introduction of LMAs the airway management has become simpler and easier.</div>
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7.<b>If the patient needs ventilation:</b> Have a self inflating bag, non re breathing valve,and a face mask ready.You may need to intubate the patient.Have access to laryngoscope, tracheal tubes,an introducer and suction catheters.Intubation is the only way you can be sure to control his airway and prevent aspiration.</div>
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8.<b>Have a vein open: </b>Because if the patient has a drip,or an indwelling needle you can treat some of the complications ,that may arise during anaesthesia more easily, and give him both blood and fluids quickly.An open vein is an essential precaution in all major operations.</div>
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9<b>.Monitor pulse and blood pressure: </b>Continually during the operation and immediately after it,so that you are able to take the the necessary corrective action before it is too late.You must recognise cardiac arrest immediately.One of the most effective ways to do this is to strap a precordial stethescope to his chest and listen to the sounds.(we have advanced to the level of TEE now)</div>
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10.<b>Always have someone in the room who can apply cricoid pressure:</b> Some body who is experinced in giving cricoid pressure effectively must be available in the operating room.He should be either a second anaesthetist or a nurse anaesthetist.The practise is useful in emergency and to anaesthetise full stomach patients.Now the practise of cricoid pressure is a controversial issue as some physicians believe it will do more harm than good .They argue that the pharyngeal stimulation may result in regurgitation and it is difficult to estimate the required pressure.Also placement of LMA is difficult and chance of tracheal cartilage injury is high.. </div>
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These Golden rules were published in the beginning of anaesthesia practise aiming to help the anaesthetist to deliver safe anaesthesia but many of the rules stated are applicable to modern days of practise as well..The anaesthesiologist should not forget the directive primum non nocere (“first of all do no harm”) and should always observe the basics, guidelines and protocols in spite of advanced monitoring.Let us remember the saying </div>
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‘Provide good care with very few monitors’</div>
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‘More monitoring, however does not necessarily lead to better care’</div>
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‘No monitor can ever replace a human being as he has the 6th sense.’</div>
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‘The focus of attention for greater part of the time should be on the patient and the operation, not on monitors.’</div>
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- Wendell C. Stevens</div>
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Ref: 1) Primary Anaesthesia Edited by Maurice King, Oxford University Press 1992</div>
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2)<a href="http://books.google.co.in/books?id=rCvEJibQstcC&pg=PA22&lpg=PA46&ots=fsjiLMmdTp&dq=golden+rules+of+anaesthesia" target="_blank">http://books.google.co.in/books?id=rCvEJibQstcC&pg=PA22&lpg=PA46&ots=fsjiLMmdTp&dq=golden+rules+of+anaesthesia</a></div>
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DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com4tag:blogger.com,1999:blog-8746726747957343433.post-35786037226137690102011-03-31T04:27:00.000-07:002013-02-27T00:50:25.251-08:00ASA PHYSICAL STATUS CLASSIFICATION, NEEDS TO BE REVISED?<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-family: inherit; font-size: small;">The American Society of Anaesthesiology classification of physical status(ASA) is still used widely as a scoring system to assess the fitness of patients subjected to anaesthesia and surgery. The scoring system was devised to assess the physical status of patients before anaesthesia is planned and was applied uniformly for all patients.The grading system was useful for record keeping and for statistical analysis of patients' health status who were scheduled for administration of anaesthesia.This grading system is not indicated for prediction of operative risk.</span></div>
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<span style="font-size: small;">The evolution of ASA grading system[1]</span></div>
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<span style="font-size: small;">In 1940-41, ASA asked a committee of three physicians (Meyer Saklad, M.D., Emery Rovenstine, M.D., and Ivan Taylor, M.D.) to study, examine, experiment and devise a system for the collection and tabulation of statistical data in anaesthesia which could be applicable under any circumstances.[1] They were given the task to devise a grading system to assess the operative risk , but after detailed studies research and discussion they stated that "In attempting to standardize and define what has heretofore been considered 'Operative </span>Risk', it was found that the term ... could not be used. It was felt that for the purposes of the anesthesia record and for any future evaluation of anesthetic agents or surgical procedures, it would be best to classify and grade the patient in relation to his physical status only."They described a six-point scale, ranging from a healthy patient (class 1) to one with an extreme systemic disorder that is an imminent threat to life (class 4). The first four points of their scale roughly correspond to today's ASA classes 1-4, which were first published in 1963.[2] The original authors included two classes that encompassed emergencies which otherwise would have been coded in either the first two classes (class 5) or the second two (class 6).Two modifications were made in 1963 when the new classification is proposed ,the previous classes 5 and 6 were removed and a new class 5 was added for moribund patients not expected to survive 24 hours,with or without surgery.In addition emergency cases were designated by the letter 'E'.[3] The sixth class is a recent addition for declared brain dead organ donors. The six ASA classes for evaluation of physical status are </div>
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ASA I</div>
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An immediate green flag: Normal healthy patients are coming under this group.Ptients can walk one flight of stairs or two level city blocks without distress.No clinical co morbidity , no significant past or present medical or surgical history.<br />
ASA II<br />
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Patients have mild to moderate systemic disease which is well controlled.Patients are able to walk up one flight of stairs or two level city blocks,but with moderate levels of exertional distress. History of well-controlled disease states including non-insulin dependent diabetes,Patients with anginal symptoms less than once a week,High blood pressure treated with a single type of medicine,[4],or asthma controlled by inhalers. ASA III</div>
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Patients with severe systemic disease that limits activity, but is not incapacitating.Angina symptoms more than <span class="Apple-style-span" style="font-family: inherit;">once a week,</span><span class="Apple-style-span" style="font-family: inherit;">Taking more than one blood pressure tablet </span><span class="Apple-style-span" style="font-family: inherit;">Having complications of diabetes such as kidney failure or poor circulation,</span><span class="Apple-style-span" style="font-family: inherit;">Asthma requiring frequent hospital admissions</span><span class="Apple-style-span" style="font-family: inherit;">,</span><span class="Apple-style-span" style="font-family: inherit;">Respiratory disease [COPD / COAD] causing breathlessness climbing a single flight of stairs</span><span class="Apple-style-span" style="font-family: inherit;">,</span><span class="Apple-style-span" style="font-family: inherit;">Someone with a raised creatinine of less than 200 micro mol/L,without dehydration, are all examples.[5]</span></div>
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<span class="Apple-style-span" style="font-family: inherit;">ASA IV</span></div>
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<span class="Apple-style-span" style="font-family: inherit;">A Patient with severe systemic disease that is a constant threat to life:Advanced liver disease, severe COPD, ARDS, History of unstable angina pectoris, myocardial infarction or cerebrovascular accident within the last six months, severe congestive heart failure, , and uncontrolled diabetes, hypertension, epilepsy,etc.</span></div>
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<span class="Apple-style-span" style="font-family: inherit;">ASA V</span></div>
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<span class="Apple-style-span" style="font-family: inherit;">A moribund patient not expected to survive 24 hours with or without surgery, eg;Severe gangrenous intestine in septic shock or terminally ill patients.</span></div>
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<span class="Apple-style-span" style="font-family: inherit;">ASA VI</span><br />
<span class="Apple-style-span" style="font-family: inherit;">A brain dead donor for organ harvestation.</span></div>
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The prefix 'E' is added to emergency operation of any class eg; ASA I E, for emergency caesarean section in an ASA I patient.<br />
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The inconsistency and inadequacy of ASA grading system has been questioned for many years. The major drawbacks of this grading system are<br />
<ul style="text-align: left;">
<li>Inconsistency of grading between anesthetists.[6],Research by Haynes, S. R. and Lawler, P. G. P, showed that so much variation was observed between individual anaesthetist's assessments when describing common clinical problems and that the ASA grade alone cannot be considered to satisfactorily describe the physical status of a patient.</li>
<li>Age; is not considered as an influencing factor,extremes of age like elderly patients and neonates may have poor tolerance to surgery and anaesthesia in the absence of systemic illness and cannot be considered as ASA 1 patients.</li>
<li>The grading system is not well suited for assesing physical status of special clinical conditions like burns,trauma and metabolic disorders</li>
<li>No grade was available to describe moderate systemic illness.</li>
<li><span class="Apple-style-span" style="font-family: inherit;">The ASA Grading System shows poor interrater reliability in pediatric practice[7]</span></li>
</ul>
<span class="Apple-style-span" style="font-family: inherit;">Here comes the importance of revising the ASA physical status system.An attempt was made by Tomoaki Higashizawa M.D., Ph.D. and Yoshihisa Koga M.D.,who revised the score and introduced a 7 graded scoring system.This was done by modification of the original ASA grading system as below.[8] The authors claim r</span>eevaluation of ASA physical status (7-grade) can provide a better grading outcome for predicting the incidence of intra- and postoperative complications in surgical patients compared with the conventional ASA's.<br />
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With 2 subclasses 1a 1b,2a,2b this classification seems to be appropriate to fill up the gap between the severity of systemic illness but difficult to apply for routine use because of its complex nature.We expect that a revision of ASA grading system will be implemented soon by ASA.<br />
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Many anaesthetists are concerned more with the morbidity and mortality of associated risk conditions, The physical status evaluation alone was not useful for risk stratification and many other grading systems were devised to evaluate the perioperative risk.eg; E-PASS and POSSUM score.<br />
Reference:</div>
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<span class="Apple-style-span" style="font-family: inherit;">1)</span><span class="Apple-style-span" style="line-height: 17px;"><span class="Apple-style-span" style="font-family: inherit;">Saklad M. Grading of patients for surgical procedures. Anesthesiology 1941; 2:281-4.(by courtesy of WIKIPEDIA)</span></span><br />
<span class="Apple-style-span" style="line-height: 17px;"><span class="Apple-style-span" style="font-family: inherit;">2)</span></span><span class="Apple-style-span" style="line-height: 17px;"><span class="Apple-style-span" style="font-family: inherit;"> </span><span class="citation Journal" style="font-style: normal; word-wrap: break-word;"><span class="Apple-style-span" style="font-family: inherit;">Little JP (1995). "Consistency of ASA grading". </span><i><span class="Apple-style-span" style="font-family: inherit;">Anaesthesia</span></i><span class="Apple-style-span" style="font-family: inherit;"> </span><b><span class="Apple-style-span" style="font-family: inherit;">50</span></b><span class="Apple-style-span" style="font-family: inherit;"> (7): 658–9. pubmed.</span></span></span><br />
<span class="Apple-style-span" style="line-height: 17px;"><span class="citation Journal" style="font-style: normal; word-wrap: break-word;"><span class="Apple-style-span" style="font-family: inherit;">3)</span></span></span><span class="Apple-style-span" style="line-height: 17px;"><span class="Apple-style-span" style="font-family: inherit;">New classification of physical status. Anesthesiology 1963; 24:111</span></span><br />
<span class="Apple-style-span" style="line-height: 17px;"><span class="Apple-style-span" style="font-family: inherit;">4)</span></span><span class="Apple-style-span" style="font-family: inherit;">Margaret J. Fehrenbach, RDH, MS, from the American Society of Anesthesiologists, Medical Emergencies in the Dental Office (Malamed, Mosby, 2008), </span><br />
<span class="Apple-style-span" style="font-family: inherit;">5)<a href="http://www.nhfd.co.uk/003/hipfractureR.nsf/">http://www.nhfd.co.uk/003/hipfractureR.nsf/</a> (National hip fracture database)</span><br />
<span class="Apple-style-span" style="font-family: inherit;">6)Haynes, S. R. and Lawler, P. G. P. (1995), An assessment of the consistency of ASA physical status classification allocation. Anaesthesia, 50: 195–199.</span><br />
<span class="Apple-style-span" style="font-family: inherit;">7)Aplin S, Baines D,Lima, Use of the ASA physical status grading system in pediatric practice.,Pediatric Anaesthesia,</span>2007 Mar;17(3):216-22.<br />
<span class="Apple-style-span" style="font-family: inherit;">8)</span>T. Higashizawa & Y. Koga : Modified ASA Physical Status (7 grades) May Be More Practical In Recent Use For Preoperative Risk Assessment . <i> The Internet Journal of Anesthesiology. </i> 2007 Volume 15 Number 1.</div>
</div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com4tag:blogger.com,1999:blog-8746726747957343433.post-11373404435181006162011-01-30T04:10:00.000-08:002011-01-30T04:10:25.267-08:00LOCAL ANAESTHETIC TOXICITY, WHAT INTRALIPID CAN OFFER?<div dir="ltr" style="text-align: left;" trbidi="on"><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiCnLfxju0wBS2kz_RH8RFYR_-rdlQtNyWCUlcFoXV4RhoA0l1qfv5Qtlg1jqeKcQLw1WraJBRa9MR2-H2LGYGY1yvdfKYrkCKzLQS9QrT88vpro0tyJ4GkKmJOkmGkf0bEQu2eNuufWL2E/s1600/injection.jpgsciencemuseum.org.uk.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiCnLfxju0wBS2kz_RH8RFYR_-rdlQtNyWCUlcFoXV4RhoA0l1qfv5Qtlg1jqeKcQLw1WraJBRa9MR2-H2LGYGY1yvdfKYrkCKzLQS9QrT88vpro0tyJ4GkKmJOkmGkf0bEQu2eNuufWL2E/s200/injection.jpgsciencemuseum.org.uk.jpg" width="181" /></a></div>A 30 year old ASA 1 patient weighing 70 kg is scheduled for open reduction and internal fixation of fracture both bones on right upper limb. The pre anaesthetic check up was unremarkable except for mild nasal allergy.The patient received 3 mg intravenous midazolam in operation theatre for sedation and an interscalene brachial plexus block was attempted by the anaesthetist using 20 ml 1% lignocaine along with 20 ml 0.25% bupivacaine.Analgesia was adequate and almost complete after 10 minutes of the block and the surgeon was about to operate. The patient complained of dizziness and vomited once.The blood pressure dropped below70 mm Hg systolic and the pulse was felt slow, feeble and thready. The chest on auscultation revealed equal and bilateral air entry. Later on he complained of numbness of the face and began to convulse. Immediate support of airway and ventilation provided by mask ventilation and intubation after intravenous thiopental. Intravenous fluids administered and intravenous ephedrine given at increments . Blood pressure dropped further down and patient had a cardiac arrest following asystole. CPR given as per ACLS protocols and a lipid emulsion was requested. The patient responded to resuscitative efforts and intralipid administration was not necessary. He was shifted to intensive care unit for close monitoring of vitals and has fully recovered without any neurologic sequelae.<br />
<br />
<b style="color: purple; font-family: Georgia,"Times New Roman",serif;">Local anaesthetics</b> are drugs used to prevent or relieve pain in specific regions of the body without producing unconsciousness. They block pain sensation by blocking conduction of pain impulses through nerves.Motor blockade and autonomic blockade are also observed as part of local anaesthetic action.Local anaesthetic drugs are widely used in dentistry and surgical specialities for providing surface anaesthesia, infiltrative anaesthesia or for nerve block. They are indispensable for the anaesthetist, in providing Regional Anaesthesia.The drug lignocaine find an unique place in crash cart for CPR and in emergency medicine trolley for treating arrhythmias.No pain management services can run without using local anaesthetics.However precaution must be taken while using them as chances of toxicity or side effects are high and may even be fatal. Manifestations of toxic reaction may range from minor urticaria or edema to very severe neurological toxcity or severe cardiovascular collapse.So basic resuscitation equipments and essential drugs should be kept ready before administering LAs to any patient. A brief review of local anaesthetic toxicity and its management, is given here.<br />
<div class="separator" style="clear: both; text-align: center;"></div> <b style="color: #990000;">Pharmacology:</b> Structurally, all local anaesthetics are similar and consist of three parts: a lipiophilic (aromatic) end, a hydrophilic (amine) end, and a link between the two ends.[1] This intermediate link can be either an aminoester or an aminoamide bond, which classifies the local anaesthetics into two different groups: amides and esters. Esters include Procaine, Cocaine, Chlorprocaine, Amethocaine, etc .Amides include Lignocaine, Bupivacaine, Levobupivacaine, Ropivacaine etc.<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgRPza-bvfY6i-oVBvjbcPe7-yUUvu2Q7eYBwz922ITvf_289XN6FFUGYVPC80ZeCmoXp7stEvJkbu61bsTBI4W1XavfpFOq4QXV9oDRrcEYFNuQv20W7GXqWqvqpUR7-xiXfX25dNFED3v/s1600/834279-873879-25.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="316" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgRPza-bvfY6i-oVBvjbcPe7-yUUvu2Q7eYBwz922ITvf_289XN6FFUGYVPC80ZeCmoXp7stEvJkbu61bsTBI4W1XavfpFOq4QXV9oDRrcEYFNuQv20W7GXqWqvqpUR7-xiXfX25dNFED3v/s400/834279-873879-25.jpg" width="400" /> </a> </div><div class="separator" style="clear: both; text-align: left;">All local anaesthetic drugs are weak bases and exists in an equilibrium between ionised and non ionised forms in solution.The non-ionised form diffuses readily across the neuronal membranes into the axoplasm, where it ionises and blocks sodium channels within the cell. </div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;"></div>Factors affecting the anaesthetic activity of local anaesthetics include the dissociation constant (pKa),[2]<br />
protein binding, lipid solubility, pH, and vascularity at the injection site.The pH at which the amount of ionised and nonionised drug is equal is known as the pka or diffusion constant , (the pKa of lignocaine is 7.8 but at a pH of 7.4, more than half of the drug exist as charged cation) The onset of action of the drug is determined by the dissociation constant and pH of the medium. Anaesthetic with a pKa value near the physiological pH has a greater proportion of drug in the non-ionised form. The non ionised form diffuses more readily across the nerve sheaths and membrane to its site of action. Therefore, local anaesthetics with pKa values close to physiological pH tend to have a more rapid onset of action as the non ionised content of the drug is more. Factors that promote local extracellular acidosis (eg: infection) increase drug ionisation and therefore reduce local anaesthetic diffusion and penetration of the nerve membrane. Addition of sodium bicarbonate (1 ml 8.4% sodium bicarbonate per 19 ml 1 % lignocaine)to local anaesthetics increases the pH of the solution, which increases the ratio of non-ionised to ionised form,resulting in a more rapid onset of action. The potency of local anaesthetics is affected by its lipid solubility A highly lipid-soluble drug readily penetrates cell membranes and thus have higher potency compared to drugs having lower lipid solubility<br />
<br />
The degree of protein binding( alpha 1 acid glyco protein) and vascularity also affects the local anaesthetic’s<br />
duration of action. Those with high plasma protein binding have longer durations of action. Addition<br />
of a vasoconstrictor like epinephrine to lipid soluble local anaesthetics decreases vascularity at the injection site, which prolongs the duration of action (via reduced absorption of the drug into the systemic circulation).<br />
<br />
<div style="color: #990000;"><b>Mechanism of action:</b></div>LAs are membrane-stabilising drugs that reversibly decrease the rate of depolarisation and repolarisation of excitable membranes.Local anaesthetics block sensory and motor function by impeding the permeability of<br />
neuronal cell membranes to sodium. This action prevents the rapid influx of sodium during the depolarisation phase of the action potential and its onward transmission.LAs selectively bind to inactivated closed sodium channels and stabilise them in order to prevent channel opening due to nerve stimulation and subsequent propagation of action potential.The primary electrophysiological effect of these compounds is to cause a local decrease in the rate and degree of depolarisation of the nerve membrane such that the threshold potential for transmission is not reached and the electrical impulse is not propagated down the nerve.[2] <br />
<br />
Metabolism: The ester type local anaesthetics are hydrolysed by esterases in tissues and blood, while the amide types are metabolised primarily in the liver by cytochrome P450 enzymes and then excreted through kidney. Dosage adjustments may be made in hepatic and renal failure.[2]<br />
<br />
<div style="color: #990000;"><b>Calculation of percentage and dosage:</b></div><br />
Concentration. Drug concentration is expressed as a percentage, i.e. grams per 100ml (e.g. 1%=1 g/100 ml (1 000 mg/100 ml) or 10 mg/ml). (Bupivacaine 0.25%=2.5 mg/<br />
ml; lignocaine 1%=10 mg/ml.)<br />
Dilution. When adrenaline is combined in an anaesthetic solution the result is expressed as a dilution (e.g. 1:100 000):<br />
• 1:1 000 means 1 mg/1 ml (0.1%)<br />
• 1:10 000 means 1 mg/10 ml (0.01%)<br />
• 1:2 000 means 1 mg/2 ml (0.05%)<br />
• 1:20 000 means 1 mg/20 ml (0.005%)<br />
• 0.1 ml of 1:1 000 adrenaline added to 10ml of anaesthetic solution = 1:100 000 dilution or 0.01 mg/ml<br />
• 50 ml of lignocaine 1% with adrenaline 1:100 000 contains lignocaine 500 mg and adrenaline 0.5 mg.<br />
Adrenaline is the most commonly used vasoconstrictor, it is added to local anaesthetic solutions in concentrations ranging from 1 in 80,000 to 1 in 300,000, although most are usually prepared to contain a 1 in 200,000 (5 microgram /ml) concentration of adrenaline.[3]<br />
<br />
<div style="color: #741b47;"><i>Practical Point</i><i> </i></div><div style="color: #741b47;"><i>Adrenaline 1:1000 contains 1 gram of adrenaline per 1000mls solution i.e. 1mg/ml. To prepare a 1 in 200,000 solution the 1:1000 must be diluted 200 times. This is achieved by taking 0.1ml (= 0.1mg) and adding 19.9 mls of local anaesthetic solution. </i></div><br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg9W9B95M0dIZY_Vu11EAMBdJYUDsCBjWyzjc2Yq9lS9V_WX7E1Y8iPaCsxiY1nlgb1U1rM28SVo08l61LoA54bOq0VxAVBni71qFtNK4mVQIZIAQ8KVtXEDHOhgSzOtriHbUWXpNDm_7ic/s1600/Untitled.jpg23.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="192" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg9W9B95M0dIZY_Vu11EAMBdJYUDsCBjWyzjc2Yq9lS9V_WX7E1Y8iPaCsxiY1nlgb1U1rM28SVo08l61LoA54bOq0VxAVBni71qFtNK4mVQIZIAQ8KVtXEDHOhgSzOtriHbUWXpNDm_7ic/s640/Untitled.jpg23.jpg" width="640" /></a></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><b style="color: #990000;">Etiology of toxic reactions to Local Anaesthetics</b>:[1]<br />
<ul style="text-align: left;"><li>Systemic: CNS and CVS toxicity, termed as local anaesthetic systemic toxicity or LAST</li>
</ul><ul style="text-align: left;"><li>Local toxicity: Neuronal damage or skeletal muscle damage </li>
</ul><ul style="text-align: left;"><li>Others: Methemoglobinemia (prilocaine) Hydrolysis of prilocaine initially leads to the formation of o-toluidine products that bind to haemoglobin and oxidises Hb to ferric form and cause methaemoglobinaemia.</li>
</ul><ul style="text-align: left;"><li> Allergy: Allergic reactions are rare even though IgE mediated reactions can occur and may be seen with ester linked LAs.</li>
</ul><ul style="text-align: left;"><li>Addiction: Cocaine may lead to drug dependance. </li>
</ul><ul style="text-align: left;"><li>Reaction to vasoconstrictors: Tachycardia, hypertension, headache,apprehension, which usually need no treatment.</li>
</ul><ul style="text-align: left;"><li>Vasovagal reaction: Rapid onset of bradycardia, hypotension, pallor,faintness.Usually seen when patient assumes sitting position.</li>
</ul><ul style="text-align: left;"><li>Anaphylaxis: Hypotension, bronchospasm, urticaria, oedema, needs treatment as per anaphylaxis algorithm </li>
</ul><ul style="text-align: left;"><li>Transient nerve damage like persisting paraesthesia, prolonged anaesthesia etc will resolve spontaneously and permanent nerve damage is rare. </li>
</ul><div style="color: #cc0000;"><b style="font-family: Georgia,"Times New Roman",serif;">Local anaesthetic systemic toxicity (LAST)</b></div><div style="color: #cc0000;"><br />
</div><span style="font-family: Georgia,"Times New Roman",serif;">Toxicity may occur due to</span>[2]<br />
<ol style="text-align: left;"><li>Accidental intravascular or intrathecal injection</li>
<li>Relative overdosage of drug used</li>
<li>Rapid systemic absorption from the injected site </li>
</ol><span style="font-family: Georgia,"Times New Roman",serif;"><span style="color: #990000;">CNS Toxicity:</span> </span>Symptoms and signs of CNS toxicity are manifested as initial excitation followed by depression. The pre excitation phase is characterised by tinnitus, light headedness ,confusion and circum oral numbness and paraesthesia. This progresses on to the excitation phase where the signs are shivering, tremor muscular twitchings and convulsions .The final stage of depression is fatal as patients may loose consciousness and may go in for respiratory arrest. Blockade of inhibitory pathways and inhibition of release of glutamate in cerebral cortex produce initial excitation.Blockade of inhibitory pathways allows facilitatory neurons to function in an unopposed fashion, which results in an increase in excitatory activity leading to convulsions. A further increase in the dose of local anesthetic leads to inhibition of activity of both the inhibitory and facilitatory circuits, which results in a generalized state of CNS depression.Respiratory or metabolic acidosis increases CNS toxicity by increased cerebral blood flow and resulting in rapid delivery of anaesthetic agents to brain.Acidosis also decreases intracellular pH resulting in iron trapping, decreases the plasma protein binding making available more free form of the base. Seizures produce hypoventilation and a combined respiratory and metabolic acidosis, which further exacerbates the CNS toxicity. Hence immediate support of airway with proper ventilation and meticulous control of seizures advised,in LA toxicity<br />
<br />
<span style="color: #990000; font-family: Georgia,"Times New Roman",serif;">CVS Toxicity</span><span style="color: #990000;">:</span> Direct cardiovascular effects and direct peripheral vascular effects are observed .The direct CVS effects include bradycardia due to action on sodium channels which reduces action potential duration and effective refractory period.They increase PR interval and QRS complex duration resulting in prolongation of conduction time.They also exert dose-dependant negative inotropic action on cardiac muscle.Local anesthetics may depress myocardial contractility by affecting calcium influx and triggered release from the sarcoplasmic reticulum,[2] The direct peripheral vascular effects include a biphasic response on vascular smooth muscles characterised by initial vasoconstriction followed by vasodilatation.Thus there will be a reduction in blood pressure. The toxic effects are more pronounced with bupivacaine and remain sustained.Ventricular arrhythmias including fibrllation are more common with bupivacaine and cardiac resuscitation is more difficult after bupivacaine-induced cardiovascular collapse, and acidosis and hypoxia markedly potentiate the cardiotoxicity of bupivacaine.(4)<br />
<br />
<div style="color: #cc0000;"><b>Treatment of LAST:</b></div>In 2007, the Association of Anaesthetists of Great Britain and Ireland published guidelines for the<br />
management of severe local anaesthetic toxicity.[5] In 2008, the American Society of Critical Care Anesthesiologists and the American Society of Anesthesiologists Committee on Critical CareMedicine,[6] as well as the Resuscitation Council of the United Kingdom[7] also published protocols for the treatment of LAST. In 2010, the American Society of Regional Anesthesia and Pain Medicine published its practice advisory on LAST.[8] These guidelines emphasise the importance of airway management and early cardiopulmonary resuscitation, They also strongly advise use of lipid emulsions along with resuscitative measures and have incorporated the use of lipid emulsion therapy in their guidelines, in the management of LAST. The AAGBI algorithm is shown below.<br />
<br />
<div class="separator" style="clear: both; text-align: center;"></div><br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh_whEzwWGQvkcZ8hSPWDucb4NMu5kQ4pSYkU1KW1brANHh_QaX7EsH_DU7mPrNNY1KPgXRarK8a4HFGx4ih_5PXq3ev-tqaSA_Wx4RiXPWEPUpprSvAGmlP0kJfvyB9n-MquNUlwIv7okx/s1600/GUIDE1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh_whEzwWGQvkcZ8hSPWDucb4NMu5kQ4pSYkU1KW1brANHh_QaX7EsH_DU7mPrNNY1KPgXRarK8a4HFGx4ih_5PXq3ev-tqaSA_Wx4RiXPWEPUpprSvAGmlP0kJfvyB9n-MquNUlwIv7okx/s640/GUIDE1.jpg" width="448" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcn1dhAWK3ws1Ca13ylQBY51JPzKoS-z8UcxKUSfwhMRo9trjr65c5bgZvSFhvcjog8LmJ6_nGtJ95PWY9N2982vFDy_AZWg15VmSxMfePgEyJBDlrCt8gLYXDk3wW7yTtThPscSdCBnQl/s1600/pdf+2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjcn1dhAWK3ws1Ca13ylQBY51JPzKoS-z8UcxKUSfwhMRo9trjr65c5bgZvSFhvcjog8LmJ6_nGtJ95PWY9N2982vFDy_AZWg15VmSxMfePgEyJBDlrCt8gLYXDk3wW7yTtThPscSdCBnQl/s640/pdf+2.jpg" width="432" /></a></div><div style="color: #741b47;"><b>What is intra lipid? How it helps?</b></div><b>Intralipid</b> is a brand name for the first safe fat emulsion for human use, approved in 1962 in Europe and invented by Professor Arvid Wretlind, Sweden. It is used as a component of parenteral nutrition for patients who are unable to get nutrition via an oral diet. It is an emulsion of soy bean oil, egg phospholipids and glycerin. It is available in a 10%, 20% and 30% concentration. The 30% concentration is not approved for direct intravenous infusion, but should be mixed with amino acids and dextrose as part of a total nutrient admixture.Intralipid provides essential fatty acids, Linolenic acid (LA), an omega-6 fatty acid,alpha-linolenic acid(ALA), an omega-3 fatty acid. Some preparations of the anaesthetic drugs propofol and etomidate (the vehicle for etomidate is propylene glycol) are supplied using Intralipid as a vehicle.[9] Intralipid is widely and freely available in all hospital intensive care units as this is one of the major constituent of parenteral nutrition<br />
<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi9LyU4gCoYMsCeM0xsHGUzKKZzEtzCit47FW3Y-3uzFknLBpmm8PmG4ktU374lZxUMb7t99x2RAOWNIka5da2lMRZqtoJ_jGpPpOkeF-3X2gLLVCwP4FkSm6nDfDgn415TMzNWB3D2UzvR/s1600/Untitled.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi9LyU4gCoYMsCeM0xsHGUzKKZzEtzCit47FW3Y-3uzFknLBpmm8PmG4ktU374lZxUMb7t99x2RAOWNIka5da2lMRZqtoJ_jGpPpOkeF-3X2gLLVCwP4FkSm6nDfDgn415TMzNWB3D2UzvR/s400/Untitled.jpg" width="318" /></a></div><br />
<br />
<br />
In 1998 Weinberg et al[10] first reported that lipid emulsion infused during resuscitation increased the<br />
median lethal dose (LD50) of bupivacaine in rats by 50%. Followed by in 2006 Rosenblatt et al[11] and<br />
Litz et al[12] reported successful clinical use of lipid emulsion to reverse local anaesthetic induced cardiac<br />
arrest.Many clinical reports released after this supported the use of lipid emulsion in the management of LAST[13,14,15] caused due to bupivacaine, levobupivacaine, and ropivacaine.<br />
<br />
The exact mechanism of action of lipid emulsion therapy is not known. It may serve as a“lipid sink”, providing a large lipid phase in the plasma, enabling capture of the local anaesthetic molecules and making them unavailable to tissues.Alternatively they prevent impaired fatty acid delivery caused by local anaesthetics in the mitochrondria, and enhance energy production. The commonly used lipid emulsion preparation is Intralipid 20%, and the efficacy of other preparations is not studied in detail . Propofol is not asuitable substitute for Intralipid. It is formulated in a 10% lipid emulsion as the amount of lipid emulsion is less compared to the concentration of propofol and higher doses of propofol have direct cardiovascular depressant effects. The recommended Intralipid regimen as given by AAGBI, entails an initial intravenous bolus injection of a 20% emulsion at 1.5 mL/kg over 1 minute, followed by an infusion of 15mL/kg/h. Cardiopulmonary resuscitation should be continued. If cardiovascular stability is not restored after 5minutes or if haemodynamics deteriorate, a maximum of two repeated boluses (1.5 mL/kg) may be given at 5-minute intervals. The intravenous infusion rate should also be doubled to 30 mL/kg/h. A maximum of three boluses can be given, and a cumulative dose of 12 mL/kg should not be exceeded.<br />
<br />
It is seen that increasing the dose beyond 8 mL/kg is unlikely to be useful and in practice, resuscitation of an adult weighing 70 kg is as follows:<br />
<ol><ol><li>Use a 500-mL bag of fat emulsion (Intralipid 20%) and a 50-mL syringe.</li>
<li>Draw up 50 mL and give it stat intravenously, and then draw up and give another 20 mL.</li>
<li>Do exactly the same thing up to twice more as the epinephrine is given—if necessary or appropriate.</li>
<li>Then, attach the fat emulsion bag to a giving set and administer it intravenously over the next 15 minutes.</li>
</ol></ol><br />
Contra-indications to lipid emulsion therapy include lipid metabolism disorders and egg allergy, and caution is required for patients with anaemia, severe liver disease, coagulopathy, and pulmonary disease. Potential complications include allergic reaction, fluid overload, impaired liver function, hypercoagulability and pancreatitis.<br />
<br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEifhdB9wFxHKf-tHmy_jNSSzFlnTrfwzqgBiLMyT9fGwPA3x_nHc6CoDJZND80oUwZxydj34G7vJC1BdWjkD3TPHsBkpkXhzCrBiQL1K68NaDYhNJyJD0b9XpXETXFXjVBe-acl_l_IGbSi/s1600/weinberg_guy_007.jpg+another+version.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEifhdB9wFxHKf-tHmy_jNSSzFlnTrfwzqgBiLMyT9fGwPA3x_nHc6CoDJZND80oUwZxydj34G7vJC1BdWjkD3TPHsBkpkXhzCrBiQL1K68NaDYhNJyJD0b9XpXETXFXjVBe-acl_l_IGbSi/s200/weinberg_guy_007.jpg+another+version.jpg" width="200" /></a>Here is the great and eminent personality whom i admire and salute, Dr. Weinberg,a pioneer behind this experimentation and who first postulated that lipid emulsion has a role in the treatment of LA toxicity. Following his second report in 2003 stating that "Lipid emulsion infusion rescues dogs from bupivacaine-induced cardiac toxicity"., published in Regional Anesthesia and Pain Medicine 2003; 28: 198-202, many case reports have been published in support of the efficacy of lipid emulsions for reversing local anaesthetic toxicity.[13,14,15] He himself has designed a web site and shared his experience knowledge and invited people from all over the world for contributions in this regard .The site deals with local anaesthetic toxicity, literature, case reports,experiments, and treatment regimen.He has designed the lipid rescue kits and is running a laboratory for further research on this issue watch this site: <a href="http://www.lipidrescue.org/">www.lipidrescue.org</a><br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjlndG1yl5OTB2RjXqRJkHmRu4BhODF2a7QqF7pOmKt_ECPc5TLz5NE3g-tPJZHIsD83XsNwGuklnqwlWFBY3BAWch11ydgqHGwkyEQ56TYLuYUxCwtEAVLsHzDT7R7q7NxIEvYk8TCTA8r/s1600/lipidrescue1+kit.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjlndG1yl5OTB2RjXqRJkHmRu4BhODF2a7QqF7pOmKt_ECPc5TLz5NE3g-tPJZHIsD83XsNwGuklnqwlWFBY3BAWch11ydgqHGwkyEQ56TYLuYUxCwtEAVLsHzDT7R7q7NxIEvYk8TCTA8r/s320/lipidrescue1+kit.jpg" width="240" /></a>This figure shows a Home made lipid rescue kit .This kit designed by Mike Alway, RPh, from BonSecours Hospital. "The container for the kit is a blue storage bin that has a clear hinged lid. It contains the 20% Lipid bag (500 ml), IV tubing, 60cc Syringes (2), and needles. The protocol is attached to the Lipid bag inside the kit and also pasted it on the outside.<br />
<div class="description"></div><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg2cnVxhlSiRcnOARzLV4oqK3MZeXpRVxSKOTBO1iCLnBY7b_exwdDgVrHRaZgpr6_cWG9omG0mkR4pUK7quIF8gYlq3sZKXr0bq_DRWs_ld7xD-Rtp4xE-NmwR0FIbUl3ZLnM1aGSEiU10/s1600/lipidrescue3+kit.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg2cnVxhlSiRcnOARzLV4oqK3MZeXpRVxSKOTBO1iCLnBY7b_exwdDgVrHRaZgpr6_cWG9omG0mkR4pUK7quIF8gYlq3sZKXr0bq_DRWs_ld7xD-Rtp4xE-NmwR0FIbUl3ZLnM1aGSEiU10/s320/lipidrescue3+kit.jpg" width="240" /></a><br />
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So make your own rescue kits today and keep them in OR within your reach.<br />
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</div><div style="color: #990000;"><b>Reference:</b></div>1.KC Lui;YF Chow, Safe use of local anaesthetics: prevention and management of systemic toxicity; Hong Kong Med J 2010;16:470-5<br />
2. Miller's Anaesthesia,7th edition, R D Miller et al , Churchil Livingston<br />
3.René du Plessis, MB ChB,Specialist Anaesthetist,Bloemfonte, Local anaesthetics: Characteris tics, uses<br />
and toxicities;CME September 2009 Vol.27 No.9<br />
4.<a href="http://www.blogger.com/post-edit.g?blogID=8746726747957343433&postID=1137340443518100616" name="4-u1.0-B978-0-443-06959-8..00030-3--bib104"></a>Englesson S: The influence of acid-base changes on central nervous system toxicity of local anaesthetic agents. An experimental study in cats. <i>Acta Anaesthesiol Scand</i> 1974; 18:79-87. <br />
5.Guidelines for the management of severe local anaesthetic toxicity. The Association of Anaesthetists of Great Britain &Ireland; 2007.<br />
6.Gabrielli A, O’Connor MF, Maccioli GA. Anesthesia Advanced Circulatory Life Support. The American Societyof Critical Care Anesthesiologists & The American Society of Anesthesiologists, Committee on Critical care Medicine;2008.<br />
7.Cardiac arrest or cardiovascular collapse caused by local anesthetic. Resuscitation Council (UK); 2008.<br />
8.Neal JM, Bernards CM, Butterworth JF 4th, et al. ASRA practice advisory on local anesthetic systemic toxicity. RegAnesth Pain Med 2010;35:152-61.<br />
9.Wikipedia, <span id="search" style="visibility: visible;"><span class="f"><cite>en.wikipedia.org/wiki/<b>Intralipid.</b></cite></span></span><span id="search" style="visibility: visible;"><span class="f"></span></span><br />
<span id="search" style="visibility: visible;"><span class="f"><cite></cite></span></span>10.Weinberg GL, VadeBoncouer T, Ramaraju GA, Garcia-Amaro MF, Cwik MJ. Pretreatment or resuscitation with a lipid infusion shifts the dose-response to bupivacaineinduced<br />
asystole in rats. Anesthesiology 1998;88:1071-5.<br />
11. Rosenblatt MA, Abel M, Fischer GW, Itzkovich CJ, EisenkraftRosenblatt MA, Abel M, Fischer GW, Itzkovich CJ, Eisenkraft JB. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest.Anesthesiology 2006;105:217-8.<br />
12.Litz RJ, Popp M, Stehr SN, Koch T. Successful resuscitation of a patient with ropivacaine-induced asystole after axillary plexus block using lipid infusion. Anaesthesia 2006;61:800-1.<br />
13.Julio A. Warren, MD,R. Brian Thoma, MD, Alexandru Georgescu, MD,Saurin J. Shah, MD<br />
Intravenous Lipid Infusion in the Successful Resuscitation of Local Anesthetic-Induced Cardiovascular<br />
Collapse After Supraclavicular Brachial Plexus Block (Anesth Analg 2008;106:1578 –80)<br />
14.Meg A. Rosenblatt, M.D., Mark Abel, M.D., Gregory W. Fischer, M.D.,Chad J. Itzkovich, M.D.,James B. Eisenkraft, M.D; Successful Use of a 20% Lipid Emulsion to Resuscitate a Patient after a Presumed Bupivacaine-related Cardiac Arrest<br />
15. R. J. Litz,M. Popp,S. N. Stehr, Anaesthesia, Volume 61, Issue 8, pages 800–801, August2006, Successful resuscitation of a patient with ropivacaine-induced asystole after axillary plexus block using lipid infusion.</div>DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com3tag:blogger.com,1999:blog-8746726747957343433.post-36274301554311820152010-12-19T09:02:00.000-08:002010-12-20T04:04:24.570-08:00CAUDAL EPIDURAL BLOCK, A REVIEW.<div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTqJlEuC9JSYmJgfebWlFS69tUXCdcaxP2ammTsVRch9wBUZEu9XqgV-6aCY4sU5Sbvmy0k1Iv4qyAXzKRfCLBYFnxeCV7nOmjwLrrzxuiTNoA4JFnqXT8t1G9s-5jx3mLJs2QomxizRUz/s1600/4.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="168" n4="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTqJlEuC9JSYmJgfebWlFS69tUXCdcaxP2ammTsVRch9wBUZEu9XqgV-6aCY4sU5Sbvmy0k1Iv4qyAXzKRfCLBYFnxeCV7nOmjwLrrzxuiTNoA4JFnqXT8t1G9s-5jx3mLJs2QomxizRUz/s200/4.jpg" width="200" /></a></div><div style="text-align: justify;">CEB is a commonly performed anaesthetic procedure to provide intra operative and postoperative analgesia in children undergoing lower limb and abdominal surgeries. It is a simple and highly effective technique useful for most of the surgical procedures of the lower half of the body, like urinary tract surgeries,circumcision, herniorrhaphies, orthopedic surgeries on the lower limb and pelvis, or operations of the anus or rectum.Excellent surgical conditions are obtained in congenital talipus equino varus(CTEV) surgery when combined with light general anaesthesia.The technique can be successfully used in children, as the fluidity of the epidural fat is more compared to adults, allowing easy spread of the deposited solution. Moreover if lumbar or thoracic anaesthesia is required, an epidural catheter can be threaded and advanced easily to achieve analgesia at the desired dermatomal level.</div><br />
<div style="color: #741b47; font-family: "Helvetica Neue",Arial,Helvetica,sans-serif;">Anatomical Landmarks:</div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh3R2Y0B7iEP83-kV3gEV25s-etGyNVXA-wFi2JF3kFXGy57JS5Lm4otv9MQLUbaFfcuxayKJZdQrjqZ460_IbjLdmaNaUYdEHXj1Nzls7Fr037yXbXUFVAN23UQQlAdTV1ESAS8Ks0GGSZ/s1600/CaudalPicture3.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="261" n4="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh3R2Y0B7iEP83-kV3gEV25s-etGyNVXA-wFi2JF3kFXGy57JS5Lm4otv9MQLUbaFfcuxayKJZdQrjqZ460_IbjLdmaNaUYdEHXj1Nzls7Fr037yXbXUFVAN23UQQlAdTV1ESAS8Ks0GGSZ/s400/CaudalPicture3.jpg" width="400" /></a></div>The sacrum is a large triangular piece of bone formed by fusion of the 5 sacral vertebrae. The lamina of the fifth and mostly of the 4th vertebra fails to fuse in the midline creating a deficiency known as sacral hiatus, which can be palpated by running your finger upwards tracing the segments of the coccyx from below. The hiatus can be easily palpated in children as the land marks are more clear. The contents of the sacral canal include[1]<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjGVdYlghyphenhyphenBeMRuLWAvP33jl9Zi4MbF6N7CgsnxxYHEzkrbQCZFYsIL5bXdFnUSAulGCXk02AHyheNcl_j-mWIdxPz7JEwK4a79j4BF6Jg6hSErYe0pEkb65NwbH4I8LCT44d7ORO-l2Zh9/s1600/121111.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjGVdYlghyphenhyphenBeMRuLWAvP33jl9Zi4MbF6N7CgsnxxYHEzkrbQCZFYsIL5bXdFnUSAulGCXk02AHyheNcl_j-mWIdxPz7JEwK4a79j4BF6Jg6hSErYe0pEkb65NwbH4I8LCT44d7ORO-l2Zh9/s1600/121111.jpg" /></a></div><ul><li>The sacral and coccygeal nerves with their dorsal root ganglia</li>
<li>The terminal part of the dural sac which ends between S1 and S3 and from where the pia mater extends downwards as filum terminale.</li>
<li>A venous plexus formed by the extension of internal vertebral plexus. </li>
<li>loose areolar and fatty tissue.</li>
<li>The filum terminale - the terminal fibres of the spinal cord which does not contain nerves. This exits through the sacral hiatus and is attached posterior to coccyx. </li>
</ul>Pediatric considerations: In infants or small children sacrum is cartilaginous which can allow for inadvertent intra-osseous injection.Also the spinal cord reaches L3-4 in the neonate and the dural sac can be found at S3-4. This increases the risk of inadvertent dural puncture or spinal cord injury. Adult levels of L1 and S1 are usually reached by 1 year of age. Up to 6-7 years of age good results are observed.As the age advances the axis of the sacrum in relation to the lumbosacral spines changes and the hiatus is difficult to access or even fuse. The sacrococcygeal ligaments are tough or calcified.Hence the procedure may be difficult in adulthood.<br />
The volume of the sacral canal averages 14.4 mL, but varies from 9.5 to 26.6 mL. <br />
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Drugs and dosages: Most commonly used drugs are lignocaine and bupivacaine Additives may be used to enhance analgesia, relaxation or prolongation of effect.For practical purposes the dosage suggested by Armitage may be used which is simple and easy to remember.<br />
<div style="color: #741b47;"><b>Armitage Formula:</b></div><br />
Bupivacaine, max dose 2.5 mg/kg without adrenaline and 3mg/kg with adrenaline(1:200000)<br />
0.5 ml/kg for a lumbosacral block<br />
1 ml/kg for a thoraco-lumbar block<br />
1.25 ml/kg for a midthoracic block<br />
(0.25% Bupivacaine up to a maximum of 20ml, for analgesia and 0.5% if motor block is desired.) <br />
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Lignocaine max dose 7mg/kg without adrenaline and 10 mg/kg with adrenaline<br />
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0.5 ml/kg for lumbosacral block<br />
1ml/kg for thoracolumbar block<br />
1.5 ml/kg for mid thoracic block<br />
(Maximum of 20ml, 1% for analgesia and 2 % for motor block)<br />
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If more than 1ml/kg (to a maximum of 20 ml) needs to be given it is preferable to avoid caudal route and go for a higher epidural route(for lesser volume of drug) as it is observed that large volumes of caudal drug spread rostrally above T4. According to bromage;[2] anesthetic dose requirements are about 0.1 mL/ segment/year of age for 1% lidocaine or 0.25% bupivacaine.<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiNd31_BwUdpbE8Eu2HktxKw1OuVSjUyfZqQcXg5810BJuKrjwryIS5k80uiYOa23Od2-37iQPKWham6QxRA6dF74xmXEqOeygnaT_zOBuiTA0VxdnUqUw8-m-vhJMOEUI1crtN76CbZQxY/s1600/12121.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiNd31_BwUdpbE8Eu2HktxKw1OuVSjUyfZqQcXg5810BJuKrjwryIS5k80uiYOa23Od2-37iQPKWham6QxRA6dF74xmXEqOeygnaT_zOBuiTA0VxdnUqUw8-m-vhJMOEUI1crtN76CbZQxY/s1600/12121.jpg" /></a></div><br />
<div style="color: #741b47;"><b>Scott’s Calculation:</b></div>Calculates the dose based on the child’s age and/or weight table.If the child is of average weight for his or her height, both figures will be the same.Avoid this formula in obese children to prevent overdosage.<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiUAHCT9t4wiOlhvgCRX8YmlhIrc6Z2MpGe7MKOiEre6tBH68j17ZVxHDBlMej3-4Bv4U6MQkEyWvN7TfVSrWo2TYtjIvy1RCblO4pnk0kElW0oX_YPoSZgvFDIDaB8EqwIuuzgF7HAz_PE/s1600/13.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" n4="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiUAHCT9t4wiOlhvgCRX8YmlhIrc6Z2MpGe7MKOiEre6tBH68j17ZVxHDBlMej3-4Bv4U6MQkEyWvN7TfVSrWo2TYtjIvy1RCblO4pnk0kElW0oX_YPoSZgvFDIDaB8EqwIuuzgF7HAz_PE/s1600/13.jpg" /></a></div>In premature infants successful caudal anaesthesia can be performed with 1 mL/kg of 0.375% bupivacaine, for surgeries like inguinal herniorrhaphy, orchiopexy, and circumcision.<br />
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<div style="color: #741b47;"><b>Identification of the sacral hiatus and the procedure of the block:</b></div>The procedure must be carried out under strict aseptic precautions, <br />
<div style="color: #741b47;"><b>Patient position:</b></div>Lateral position in children or prone position (desirable) for adults.The pelvis is elevated with the help of a pillow and the thighs are little extended The legs turned in wards,(internally rotated ). This makes the identification of the hiatus more easy by relaxing gluteal muscles. Look at figure 2B.<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj7YP9U2vSw3iYsZogekCbiOKBRcnHeF02PbqKSFSuaUo0bz7soXy05JzxhduiPQmuObHLQB7JATN_u4rCLmbhhNhotSPqAVv_s4pikEDnZEO7qTiSIBqFxsPK3haLElWGDqHJFXwWEu_a3/s1600/15.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="252" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj7YP9U2vSw3iYsZogekCbiOKBRcnHeF02PbqKSFSuaUo0bz7soXy05JzxhduiPQmuObHLQB7JATN_u4rCLmbhhNhotSPqAVv_s4pikEDnZEO7qTiSIBqFxsPK3haLElWGDqHJFXwWEu_a3/s320/15.jpg" width="320" /></a></div><span id="goog_1073700273"></span><span id="goog_1073700274"></span><br />
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</b></div><div style="color: #990000; font-family: Georgia,"Times New Roman",serif;"><b>The standard technique as described by Miller is shown below:[3]</b></div>Caudal anesthesia requires identification of the sacral hiatus. The sacrococcygeal ligament (i.e.,extension of ligamentum flavum) overlying the sacral hiatus lies between the sacral cornua. To facilitate locating the cornua, the posterior superior iliac spines should be located and, by using the line between them as one side of an equilateral triangle, the location of the sacral hiatus should be approximated After the sacral hiatus is identified, the index and middle fingers of the palpating hand are placed on the sacral cornua,<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi811rN2qVBzWKGZtgJt-qJEPbWYxRcCnF08_o2pZSJbN6tHASHGeAK0jDgZPYjJlCjiQq9cIFitzDikMX8PE7X4UTbs0D-G4MFBqIB6HILjwLmYCa5dmUqWBBQKAOQtjKysEADDl6nvq-n/s1600/Untitled.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi811rN2qVBzWKGZtgJt-qJEPbWYxRcCnF08_o2pZSJbN6tHASHGeAK0jDgZPYjJlCjiQq9cIFitzDikMX8PE7X4UTbs0D-G4MFBqIB6HILjwLmYCa5dmUqWBBQKAOQtjKysEADDl6nvq-n/s400/Untitled.jpg" width="372" /></a></div><br />
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and the caudal needle is inserted at an angle of approximately 45 degrees to the sacrum.<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhAOCJkG3VB66D6_to61dLvMVLhZrOlMT9Daea9WFqYk4cNmJ0buZIk-Qg7bsDOl6D80gD5orV8nnXMlCqCWS3dscbvHLxl6wUoQJ4cPpwdW-J0wJxsYVudkKc2wFKZTY8kGVi26T-iVz6y/s1600/7.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhAOCJkG3VB66D6_to61dLvMVLhZrOlMT9Daea9WFqYk4cNmJ0buZIk-Qg7bsDOl6D80gD5orV8nnXMlCqCWS3dscbvHLxl6wUoQJ4cPpwdW-J0wJxsYVudkKc2wFKZTY8kGVi26T-iVz6y/s1600/7.jpg" /></a></div><br />
While advancing the needle, a decrease in resistance to needle insertion should be appreciated as the needle enters the caudal canal. The needle is advanced until bone (i.e., dorsal aspect of the ventral plate of the sacrum) is contacted and then slightly withdrawn, and the needle is redirected so that the angle of insertion relative to the skin surface is decreased. In male patients, this angle is almost parallel to the coronal plane; in female patients, a slightly steeper angle (15 degrees) is necessary. During redirection of the needle and after loss of resistance is again encountered, the needle is advanced approximately 1 to 2 cm into the caudal canal.<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEim1u_EvMebuinMZKzhEBEQa8rq6AV5szEEzG761J3C8F6xqLJ87DEGnaviAvbITeZwE4adwhHhxvfN32ttxs7Stksi13h4AeldVebPLYffqhblaxFlo-eCj4gD_T8Ph234jKG9pRUQrBzY/s1600/2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEim1u_EvMebuinMZKzhEBEQa8rq6AV5szEEzG761J3C8F6xqLJ87DEGnaviAvbITeZwE4adwhHhxvfN32ttxs7Stksi13h4AeldVebPLYffqhblaxFlo-eCj4gD_T8Ph234jKG9pRUQrBzY/s1600/2.jpg" /></a></div><br />
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Performance of caudal block.[6] SC, sacral cornua; PSIS, posterior superior iliac spine; SH, sacral hiatus; TC, tip of coccyx. Note that an equilateral triangle is formed with the fingertips from PSIS to PSIS to needle insertion at SH.(<i>By courtesy of Cristian TANASE,Clinical Emergency Hospital for Children “Grigore</i> <i>Alexandrescu” Bucharest.)</i><br />
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Further advance is not attempted because dural puncture and unintentional intravascular cannulation become more likely. One method of increasing the likelihood of correct caudal needle placement is to inject 5 mL of saline rapidly through the caudal needle while palpating the skin overlying the sacrum. If no midline bulge is detected, the needle is probably positioned correctly. In contrast, if a midline bulge is detected during saline injection, the needle is positioned incorrectly.<br />
<div style="color: #741b47;"><b><br />
</b></div><b style="background-color: #741b47; color: #741b47;"></b><b style="color: #741b47;"><span style="background-color: white;"></span>S</b><b style="color: #741b47;">imple teaching: </b>[2] The sacral hiatus can be located by first palpating the coccyx, and then sliding the palpating finger in a cephalad direction until a depression in the skin is felt. Once the sacral hiatus is identified the area above is carefully cleaned with antiseptic solution, and a 22 gauge short bevelled cannula or needle is directed at about 45° to skin and inserted till a "click" is felt as the sacro-coccygeal ligament is pierced. The needle is then carefully directed in a cephalad direction at an angle approaching the long axis of the spinal canal. <br />
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1).Palpate the coccyx with the index finger of the left hand<br />
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2).Slide the palpating finger cephalad<br />
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3).Feel the depression.<br />
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4).Keep the finger at the hiatus and turn the hand at 80 degrees anchoring the index finger at the hitus<br />
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5).Hold the syringe filled with the drug in right hand.<br />
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1)Pierce the SC ligament by entering into it at 45 degree angle<br />
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2)Carefully advance and feel for the "click"<br />
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3)Once the click is felt lower the needle almost parallel to the coronal plane (along the long axis of the spinal canal)<br />
4)Advance the needle further 1-2 cm into the caudal canal.<br />
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<div class="separator" style="clear: both; text-align: center;"></div>Instead of using the needle alone , a syringe filled with 1-2 ml saline may be attached to it.Once the caudal canal is entered, the saline can be injected freely without any resistance. Air should not be used for this loss of resistance technique as the incidence of air embolism is high in children.Once the canal is identified local anaesthetic test dose may be given to rule out accidental intravascular or dural puncture.<br />
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Continuous caudal anaesthesia may be given by inserting an epidural catheter through an indwelling cannula or a 20 gauge touhy needle used to puncture.Remember that the catheter can be threaded easily because of the fluidity of loose areolar tissues in children and catheter tip in mid thoracic or higher level may lead on to a higher level of block.Measuring the catheter with the length of spine may be used as a rough guide to decide on how far the catheter to be inserted.Tunnelling the catheter on the back using a touhy needle helps to secure the catheter and prevent fecal contamination of the entry site as well.<br />
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<div style="color: #741b47; font-family: "Helvetica Neue",Arial,Helvetica,sans-serif;"><b><i>How to identify the caudal space and to ensure the correct placement of catheter.</i></b></div><ul><li>Ease of injection by loss of resistance technique</li>
<li>Absence of a cutaneous bulging over the injection site</li>
<li>Test dose, A small amount of local anaesthetic should be injected as a test dose (2-4mls).Look for peri oral tingling or numbness,or hypotension Also look for lower lumbar segment motor block. If the test is negative proceed with injection. </li>
<li>Aspiration test for either CSF or blood.[2] A negative aspiration test does not exclude intravascular or intrathecal placement. The injection rate should not exceed 10 ml/30 seconds.[3] During injection also watch for acute toxicity</li>
<li>The whoosh test and modified swoosh test(see below)</li>
<li>Flouroscopy(see below)</li>
<li>Nerve stimulation test,the presence or absence of anal sphincter contraction to electrical stimulation is used as a guide for correct needle placement (using epidural nerve stimulators)</li>
<li>Ultrasound.(see below)</li>
</ul><div style="color: #990000;"><b>The whoosh test and modified swoosh test:[4]</b></div><br />
The whoosh test is done by injection of air into the caudal epidural space with simultaneous auscultation over the thoracolumbar spine for an audible "whoosh" sound.Injection of air is associated with side effects like neurological complicaions and air embolism. So is being replaced by swoosh test where saline or the LA solution is used instead of air.1-1.5 ml of air or saline is used.<br />
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<b><span style="color: #990000;">Fluoroscopy:</span></b> is most commonly used in interventional spine procedures and is frequently used in confirming the location of caudal epidural needle[6]. It is necessary that caudal epidural needle placement should be confirmed by fluoroscopy alone or by epidurography when the procedure is used for caudal epidural injection of steroids for treating chronic pain syndromes.<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEigNERKnqU5IzNDjHpiwpi3VHM94XvlWR4A7d0O6qrGTMl_6JtQhSibnTSMdEgNSpVzNTYDYwCvizsUKp8t4swIN1Cg-lv7kKvJQf7cdr_iX-icNwS3buGnWftTsxOcp3zXEGjKE3Advljv/s1600/ultra+3.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEigNERKnqU5IzNDjHpiwpi3VHM94XvlWR4A7d0O6qrGTMl_6JtQhSibnTSMdEgNSpVzNTYDYwCvizsUKp8t4swIN1Cg-lv7kKvJQf7cdr_iX-icNwS3buGnWftTsxOcp3zXEGjKE3Advljv/s1600/ultra+3.jpg" /></a></div>Exposure to radiation is one hazard of flouroscopic confrmation and proper precautions to be taken.This include proper schielding, reducing exposure time and using pulsed imaging.<br />
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<b><span style="color: #990000;">Ultrasound:</span> </b>Combined with fluoroscopy ultrasound gives almost 100% accuracy in placement of the needle.As an adjuvant tool ultrasound is useful along with other methods in difficult cases and when successful placement is mandatory.Ultrasound is radiation free, is easy to use, and can provide real-time images in guiding the caudal epidural needle into the caudal epidural space.[6]Sterile precautions are taken before probe placement and a transverse view of the sacral hiatus is made first by placing the transducer transversely at the midline over hiatus.The hiatus is seen as a hypoechoic region between two hyper echoic shadows, the SC ligament and the dorsal bony surface. Then a longitudinal view is made by keeping the transducer between the sacral cornua,and a needle is inserted and advanced under sonographic guidance in real time.The portion of the needle which entered into the canal may not be seen clearly.Again the transducer is rotated to view the transverse axis where the needle tip may be visualised as a small round hyper echoic structure between the two hyperechoic cornua and within the two hyper echoic bands formed by the SC ligament and the dorsal bony wall of sacrum.<br />
<i>Images below are reproduced from Chen, Carl P. C. M.D.; Tang, Simon F. T. M.D,Anesthesiology:July 2004 - Volume 101 - Issue 1 - pp 181-184[7] where a detailed description of the procedure is available</i><br />
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<i style="color: #741b47; font-family: Georgia,"Times New Roman",serif;">Adjuvants used along with Local Anaesthetics:</i><span style="color: #741b47;"> </span> Adjuvants are used to intensify the block ,to reduce systemic absorption or to prolong the action.The commonly used adjuvants are,<br />
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<b>Opioids </b>:Prolong analgesia in infants and children but with attendant risks of respiratory depression and side effects like nausea vomiting and itching. It can produce urinary retention also. Hence morphine administration should be done under monitoring of vitals. Catheterization may sometimes be required. A dose of 50mcg/kg of preservative free morphine or diamorphine 30mcg/kg can be added to the local anesthetic solution[8].The optimal dose is between 33-50 μg/kg.[9] This will provide 12 to 24 hours of analgesia.Fentanyl 1-2 ug/kg may be also used but with unpredictable duration of action.<br />
<b>Clonidine:</b> An α2-adrenergic agonist,. A dose of 0.5-1.0 microgram/kg improves the quality and duration of analgesia without significant side effects[8]The analgesia may last upto 12 hours.Sedation and bradycardia are noted at doses above 5mic/kg.<br />
<b>Ketamine:</b> An NMDA antagonist. In doses of 0.25 - 1.0 mg/kg, causes significant prolongation of post operative analgesia, without significant side effects. May be combined with 0.25%bupivacaine.Preservative free ketamine is preferred. Higher doses (>0.5mg/kg) may produce neuroleptic side effects<br />
Epinephrine: 5 mic/ml of epinephrine is used to detect intravascular placement of catheter or needle.It also prolongs the duration of action of LA by local vasoconstriction and thereby delaying uptake and metabolism.<br />
<b>C<span style="font-family: "Helvetica Neue",Arial,Helvetica,sans-serif;">ontinuous epidural anaesthesia:</span> </b> is possible by inserting a catheter into the caudal space, through an indwelling cannula or a touhy needle.The initial dose may be 0.05ml/seg/kg[10]<br />
<ul><li>Less than 1 year of age 0.1-0.2ml/kg/hr of 0.1% bupivacaine</li>
<li>more than 1 year 0.1% bupivacaine with 3 microgram/ml of fentanyl at the rate of 0.1-0.4ml/kg/hr, (less than 0.5microgram/kg/hr of fentanyl to start with.)[11]Ropivacaine is used at the dose of 0.4mg/kg/hr</li>
</ul><div style="color: #741b47; font-family: "Helvetica Neue",Arial,Helvetica,sans-serif;"><b><i>Pharmacological Considerations: </i></b></div><br />
Local anaesthetics are classified into two groups, amides and esters. the amides are metabolised in liver while the esters are hydrolysed by esterases in the plasma.Since newborn and pediatric liver functions are immature and not fully functional the metabolism of amides is not complete and the un metabolised fraction can produce toxic reactions. Another factor which contributes to toxicity is the reduction in plasma proteins like albumin and alpha 1 acid glycoprotein resulting in excess free fraction of the drugs in plasma. On the contrary the volume of distribution of local anaesthetics is more in children compared to adults causing a reduction plasma concentrarion of these drugs and which may nullify the effect of reduced elimination allowing higher doses.For eg:The maximum safe dose of bupivacaine in neonates is 1.5mg/kg.Other Local anaesthetic drugs which may be used for caudal include Ropivacaine 0.2- 2 mg/kg and Levobupivacaine 0.25- 1 mg/kg with slight increase in duration of action.Pregnant patients need 25-35% reduction in dose requirements for labour analgesia due to engorged epidural veins reducing space.Caudal blockade in pediatrics is used primarily for perioperative pain control, whereas in adults it is primarily for chronic pain management. [12]<br />
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Combination with GA: For intra and post operative pain relief and to reduce the requirement of depressant general anaesthetic agents for rapid and smooth recovery, caudal is combined with GA, The procedure is ideal for children as positioning after induction is easy and the success rate is high. Inhalational or iv induction then securing airway with LMA or ETT, is followed by caudal injection.The disadvantage being, failure of detection of LA toxicity or high block in an anaesthetised child.Careful monitoring of vitals mandatory.The effectiveness of the block is determined by "loss of anal sphincter tone".[13]<br />
Indications(Uses) :<br />
<ul><li>Apart from the usual indications mentioned above the caudal block is highly useful for emergency surgical procedures like,testicular torsion, omphalocele correction,strangulated hernias,high risk neonates for anorectal and abdominal surgeries,biliary tract surgeries and operative procedures on stomach (especially when a catheter is threaded to deposit the drug at higher dermatomes)</li>
<li>Ambulatory and day care minor surgeries where fast-traching is desired.</li>
<li>For combining with General anaesthesia to provide stable hemodynamics, adequate analgesia and to reduce the requirement of general anaesthetic agents, in surgeries of abdomen, lower thorax or even open heart procedures.</li>
<li>Continuous epidural analgesia can be provided with a catheter in caudal space for long surgical procedures like orthopedic corrective surgeries or plastic surgery procedures of the lower limb. </li>
<li>Percutaneous epidural neuroplasty is a technique of administering local anesthetics, corticosteroids, hyaluronidase, and hypertonic saline through a caudal catheter for the purpose of lysing epidural adhesions. [13]</li>
</ul><div style="color: #741b47; font-family: "Helvetica Neue",Arial,Helvetica,sans-serif;"><b><i>Advantages over conventional epidural anaesthesia:</i></b></div><ul><li>Easy location because of the prominent anatomical landmarks, helps to establish the block faster</li>
<li>Reduced incidence of failed or patchy blocks</li>
<li>Predictable distribution of LA solution </li>
<li>Easy to place a catheter</li>
</ul><div style="color: #990000;"><b>Side effects:</b></div><ul><li>Failed block , the incidence is as high as 5-20%.Ultrasound guidance helps to increase the success rate</li>
<li>Predominant unilateral block or patchy block. Lateralisation is due to rapid injection.</li>
<li>Dural puncture: due to anatomic variation and low lying dura in infants. Sequale is, a total spinal block with dilated pupils, apnea, and unconsciousness.</li>
<li>Local anaesthetic toxicity can be either due to intravascular injection or due to overdose resulting in excess plasma concentrations.Since the extradural veins have no valves, retrograde flow is fast once the drug is injected intravascularly.</li>
<li>Intra osseous injection</li>
<li>Bleeding</li>
<li>Introduction of infection.</li>
</ul><div style="color: #cc0000;"><b>Contraindications: </b></div><ul><li>Patient refusal</li>
<li>local infections,eg: dermattis, pilonidal sinus </li>
<li>Coagulation disorders</li>
<li>Neurologic diseases,Poliomyelitis</li>
<li>Sensitivity to local anaesthetics</li>
<li>Increased intra cranial tension like meningitis, hydrocephalus etc.</li>
<li>Congenital malformations of lower meninges or spine eg: spina bifida, meningo myelocele</li>
<li>Unstable cardiovascular system, valvular heart diseases</li>
</ul><div style="color: #cc0000;"><b>Management of Local Anaesthetic toxicity( in general:)[4]</b></div><ul><li>Oxygenation, intubation, cardiac massage </li>
<li>Sodium bicarbonate hypertonic 4.2%(through central vein preferably) 2ml/kg/10 mts.(1mmol/kg/10mt) or isotonic 1.4% through peripheral vein 6ml/kg/10 mts(1mmol/kg/10mts)</li>
<li>IV midazolam or diazepam for seizures</li>
<li>IV atropine 0.02mg/kg</li>
<li>IV vasoactive agents, epinephrine 0.1ml/kg1/10000 solution (10 microgram/kg) or isoprenaline 0.1 mic/kg</li>
<li>Dopamine or dobutamine infusion 2-10 mic/kg/mt,</li>
<li>Calcium chloride 10-30 mg/kg</li>
<li>Treatment of VF/VT as per ACLS guidelines</li>
<li>Lipid emulsions IV.</li>
</ul><div style="color: #741b47; font-family: "Helvetica Neue",Arial,Helvetica,sans-serif;"><b><i>Role of caudal block in pain management: </i></b></div>In radiculopathies refractory to routine management this route is adopted for pain relief. Percutaneous epidural neuroplasty uses a caudal catheter left in place for up to 3 days to inject hypertonic solutions into the epidural space to treat radiculopathy with low back pain and epidural scarring, typically from previous lumbar spinal surgery.[12]After confirmation of epidural space by fluoroscopy a mixture of drugs consisting of Local anaesthetics, steroids, hyaluronidase, and saline is injected.Initially1500 units ofhyaluronidase in 10mLof preservative-free saline is injected rapidly. This is followed by an injection of 10 mL of 0.2% ropivacaine and 40 mg of triamcinolone, An additional injection of 9 mL of 10% hypertonic saline is infused over 20 to 30 min. On the second and third days, the local anesthetic (ropivacaine) injection is followed up by the hypertonic saline solution. Antibiotic coverage is provided to reduce the possibility of epidural abscess formation.[12]. The video below illustrates how to conduct an ultrasound guided epidural instillation of steroids to treat chronic pain syndromes.<br />
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<div style="color: #741b47;"><b> <span style="font-family: "Helvetica Neue",Arial,Helvetica,sans-serif;">Reference:</span></b></div>1).NJH Davies, JN Cashman, Lee's Synopsis of Anaesthesia 13 th edition, Butterworth Heineman<br />
<div style="border: medium none;">2).Bromage PR: Epidural Analgesia. WB Saunders, 1978, pp 258-282<br />
<span style="font-size: medium;">3).Dr.Bela Vadodaria and Dr David Conn,</span> "Update in Anaesthesia" Issue 8 (1998) Article 3: <a href="http://www.nda.ox.ac.uk/wfsa/html/u08/u08_011.htm">http://www.nda.ox.ac.uk/wfsa/html/u08/u08_011.htm</a> <br />
4).Ronald D Miller; Millers anaesthesia, 7th edition, Churchil Livingstone <br />
<span id="main" style="visibility: visible;"><span id="search" style="visibility: visible;"><i>5).</i></span></span><span id="main" style="visibility: visible;"><span id="search" style="visibility: visible;">Anaesthesia.</span></span><span id="main" style="visibility: visible;"><span id="search" style="visibility: visible;"><i>1998 Aug</i>;<i>53</i>(<i>8</i>):<i>829</i>. <a href="http://www.ncbi.nlm.nih.gov/pubmed/9797541">http://www.ncbi.nlm.nih.gov/pubmed/9797541</a></span></span></div><div style="color: black;"><span class="Apple-style-span" style="border-collapse: separate; font-family: arial,sans-serif; font-size: x-small; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;"><span class="Apple-style-span" style="line-height: 15px;">6)</span></span>. Cristian TANASE,<span class="Apple-style-span" style="border-collapse: separate; font-family: arial,sans-serif; font-size: x-small; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;"><span class="Apple-style-span" style="line-height: 15px;"> <a href="http://www.umftgm.ro/d_ati/.../Neuraxial%20blocks_engl.pdf">www.umftgm.ro/d_ati/.../Neuraxial%20blocks_engl.pdf</a></span></span></div>7)..Chen, Carl P. C. M.D.; Tang, Simon F. T. M.D, Pain and Regional AnesthesiaUltrasound Guidance in Caudal Epidural Needle Placement, Anesthesiology:July 2004 - Volume 101 - Issue 1 - pp 181-184<br />
8).Alice Edler MD, MA,Vinit G.Wellis, MD, Caudal Epidural Anaesthesia for paediatric patients,Update in Anaesthesia 1998 No. 8<br />
9).Krane EJ, Tyler DC, Jacobson LE. The dose response of caudal morphine in children. Anesthesiology 1989; 71:48-52.<br />
10.Amr aboulesh(anesthesiology 79:400,1993,) <a href="http://www.cmuh.org.tw/HTML/dept/.../20081119_pedi_regional.pp">www.cmuh.org.tw/HTML/dept/.../20081119_pedi_regional.pp</a><br />
11).Amr aboulesh(anesthesiology 79:400,1993,) <a href="http://www.cmuh.org.tw/HTML/dept/.../20081119_pedi_regional.pp">www.cmuh.org.tw/HTML/dept/.../20081119_pedi_regional.pp</a>.(anesthesia analgesia 75:164, 1992)<br />
12).Kenneth D. Candido, MD and Alon Winnie, MD, Caudal Anaesthesia,;Paediatr Anaesth 2003; 13:31 1317.<br />
<div class="MsoNormal" style="font-family: inherit; line-height: normal; margin-bottom: 0.0001pt;"><span style="font-size: small;">13).Verghese S, Mostello L, Patel R: Testing anal sphincter tone predicts the effectiveness of caudal analgesia in children. Anesth Analg<span style="font-size: x-small;"> 2002:94:1161-1164</span>.</span></div><div class="MsoNormal" style="font-family: inherit; line-height: normal; margin-bottom: 0.0001pt;"><br />
</div><span class="status action"><b>AERW79Q8FZH3 </b></span><ul></ul>DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com7tag:blogger.com,1999:blog-8746726747957343433.post-76844577286181295502010-11-05T10:18:00.000-07:002010-11-05T10:18:26.216-07:00AHA CPR GUIDELINES 2010<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEho0hmmWQxb8ceP60peuZkyu11GKa60HyryfOfVZhn9eyGPBWXsUXB-xvZBAnsBJw60aE2u34wOzSQPSpsKuCMdwY4AD2flpYiQZ13_Jo3n2KZseP0-yq3OUXAde9QAsm5ayFxi5BMa-ogq/s1600/CPR%252520Image%2525201.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEho0hmmWQxb8ceP60peuZkyu11GKa60HyryfOfVZhn9eyGPBWXsUXB-xvZBAnsBJw60aE2u34wOzSQPSpsKuCMdwY4AD2flpYiQZ13_Jo3n2KZseP0-yq3OUXAde9QAsm5ayFxi5BMa-ogq/s200/CPR%252520Image%2525201.jpg" width="200" /></a></div><div style="text-align: justify;">Cardiopulmonary Resuscitation is an emergency life saving procedure consisting of delivering effective chest compressions and effective ventilations to a victim of cardiac arrest. The American Society of Anesthesiology and European Resuscitation Council have made evidence based guidelines for the efficient and proper conduct of high quality CPR.These guidelines, being revised from time to time according to newer evidences, research and outcome help the primary care provider to offer the best care for the victims of cardiac arrest.The 2010 AHA Guidelines for CPR and ECC are based on an international evidence evaluation process that involved hundreds of international resuscitation scientists and experts who evaluated, discussed, and debated thousands of peer reviewed publications. Here is the new" guidelines(2010) in nutshell' for CPR from AHA .The major changes have been highlighted.A detailed information of both ERC and AHA Guidelines, is available from the resuscitation council links given below.</div><br />
<b>BASIC LIFE SUPPORT</b><br />
<b>1</b>.<b>Continued Emphasis on High-Quality CPR:</b><br />
The 2010 AHA Guidelines for CPR and ECC once again emphasize the need for high-quality CPR, including<br />
<br />
<ul><li>A compression rate of at least 100/min (a change from“approximately” 100/min) </li>
<li>A compression depth of at least 2 inches (5 cm) in adults and a compression depth of at least one third of the anteroposterior diameter of the chest in infants and children(approximately 1.5 inches [4 cm] in infants and 2 inches[5 cm] in children). Note that the range of 1½ to 2 inches is no longer used for adults, and the absolute depth specified for children and infants is deeper than in previous versions the AHA Guidelines for CPR and ECC</li>
<li>Allowing for complete chest recoil after each compression</li>
<li>Minimizing interruptions in chest compressions</li>
<li>Avoiding excessive(hyper) ventilation</li>
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There has been no change in the recommendation for a compression-to-ventilation ratio of 30:2 for single rescuers of adults, children, and infants (excluding newly born infants). The 2010 AHA Guidelines for CPR and ECC continue to recommend that rescue breaths be given in approximately 1 second. Once<br />
an advanced airway is in place,rescue breaths can be provided at about 1 breath every 6 to 8 seconds (about 8 to 10 breaths/minute) and need not be synchronised with chest compressions which can be<br />
continuous (at a rate of at least 100/min)<br />
<b>2</b>.<b>A Change From A-B-C to C-A-B</b><br />
The major change made in BLS, from airway, breathing,and circulation the sequence has been changed to compression,airway and breathing .This is to aviod delay in delivering fast and effective chest compressions. Securing airway as the initial priority is time consuming and may not be 100% successful, especially by lone rescuers or paramedics.The vast majority of cardiac arrests occur in adults and the commonest causes for arrest are VF or pulseless VT. A witnessed cardiac arrest in these cases can be efficiently reverted with immediate defibrillation and cardiac compressions, which is life saving, and should be the goal in BLS.. In the A-B-C sequence, chest compressions are often delayed while the responder opens the airway to give mouth-to-mouth breaths, retrieves a barrier device,or gathers and assembles ventilation equipment.After initiating the emergency response system the next important thing is to start chest compressions.Only infant cpr is an exception to this protocol,where the previous sequence remains unchanged. That means no more looking, listening and feeling,as this component of assessment is removed from the guidelines. In the C-A-B sequence,chest compressions will be initiated sooner and ventilation only minimally delayed until completion of the <i>first cycle of chest compressions</i>. It was observed that the bystanders of the arrested victims do not actively participate in CPR as they find the first step of a-b-c sequence is difficult to perform. A-B-C starts with the most difficult procedures: opening the airway and delivering rescue breaths and that is the reason why less than one third of the victims in cardiac arrest receive by stander CPR in a witnessed cardiac arrest.. Hence a change in sequence to C-A-B<br />
<b>3.Compression rate:</b> Should be at least 100/min (rather than“approximately” 100/min). The number of chest compressions delivered per minute during CPR is an important determinant of return of spontaneous circulation (ROSC) and survival with good neurologic function<br />
<b>4.</b>C<b>ompression depth:</b> For adults has been changed from the range of 1½ to 2 inches to at least 2 inches (5 cm).(The motto is push harder and faster) Effective compressions generate critical blood flow and oxygen and energy delivery to the heart and brain.<br />
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5.<b>Hands Only CPR: </b>Hands Only CPR. This is technically a change from the 2005 Guidelines, but<b> </b>AHA<br />
endorsed this form of CPR in 2008. The Heart Association still wants untrained lay rescuers to do Hands Only CPR on adult victims who collapse in front of them.Hands-Only (compression-only) CPR is easier for an untrained rescuer to perform and can be more readily guided by dispatchers over the telephone.It was documented that survival rates from cardic arrest of cardiac origin are same irrespective of compressions alone(hands only cpr) or compressions with ventilations<br />
<b>5.Dispatcher Identification of Agonal Gasps:</b> It is important that the rescuer shoul be well trained to identify between normal respirations from agonal breaths, in order to proceed with CPR. The lay rescuer should be taught to begin CPR if the victim is “not breathing or only gasping.” The healthcare provider should be taught to begin CPR if the victim has “no breathing or no normal breathing (ie, only gasping).”This rapid breathing check should be done before activation of emergency response system.<br />
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<b>6.Cricoid Pressure:</b> Routine use of cricoid pressure is not recommended as it may impede ventilation. Studies showed that cricoid pressure can delay or prevent the placement of an advanced airway and some aspiration can still occur even with proper application.In addition, it is difficult to appropriately train rescuers in use of this maneuver.<br />
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<b>7.Activation of Emergency Response System:</b> Should be made after assessment of the patients' responsiveness and breathing but should not be delayed. The 2005 guidelines states immediate activation of EMS after finding an unresponsive victim.(or send someone to do so), If the healthcare provider does not feel a pulse within 10 seconds, the provider should begin CPR and use the AED when it is available.<br />
<b>8. Concept of team resuscitation:</b> For better and efficient delivery of resuscitation,is emphasized.<br />
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<b>ELECTRICAL THERAPIES INCLUDING USE OF AED AND DEFIBRILLATOR.</b><br />
<br />
<div style="font-weight: bold;">1.AED Use in Children Now Includes Infants</div>For attempted defibrillation of children 1 to 8 years of age with an AED, the rescuer should use a pediatric<br />
dose-attenuator system if one is available. If the rescuer provides CPR to a child in cardiac arrest and does not have an AED with a pediatric dose-attenuator system, the rescuer should use a standard AED. For infants (<1 year of age), a manual defibrillator is preferred. If a manual defibrillator is not available,an AED with pediatric dose attenuation is desirable. If neither is available, an AED without a dose attenuator may be used. Automated external defibrillators with relatively high-energy doses have been used successfully in infants in cardiac arrest, with no clear adverse effects. No other major changes have bee made in electrical therapies including AED and defibrillator.<br />
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<b>ADVANCED CARDIAC LIFE SUPPORT</b><br />
<b>1.Capnography Recommendation:</b> Quantitative waveform capnography is recommended for confirmation of endotracheal tube placement and for monitoring CPR quality and detecting return of spontaneous circulation based on end tidal CO2. Because blood must circulate through the lungs for CO2 to be exhaled and measured, capnography can also serve as a physiologic monitor of the effectiveness of chest compressions and to detect return of spontaneous circulation. Ineffective chest compressions (due to either patient characteristics or rescuer performance) are associated with a low Petco2 and return of spontaneous circulation is associated with an abrupt increase in ETCO2. Previously an exhaled carbon dioxide (CO2) detector or an esophageal detector device was recommended to serve this purpose.<br />
<b>2.Simplified ACLS Algorithm and New Algorithm: </b> The new circular algorithm is introduced in 2010<br />
The conventional ACLS Cardiac Arrest Algorithm has been simplified and streamlined to emphasize<br />
the importance of high-quality CPR. The 2010 AHA Guidelines for CPR and ECC note that CPR is ideally guided by physiologic monitoring and includes adequate oxygenation and early defibrillation while the ACLS provider assesses and treats possible underlying causes of the arrest. There is no definitive clinical evidence that early intubation or drug therapy improves neurologically intact survival to hospital discharge.The algorithm focusses on to the basics with an increased emphasis on what is known to work: high quality CPR.<br />
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<b>3.New Medication Protocols:</b><br />
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<ul><li>Atropine is not recommended for routine use in the management of PEA/asystole and has been removed from the ACLS Cardiac Arrest Algorithm.</li>
<li>The algorithm for treatment of tachycardia with pulses has been simplified. Adenosine is recommended in the initial diagnosis and treatment of stable,undifferentiated regular, monomorphic wide-complex tachycardia (this is also consistent in ACLS and PALS recommendations). It is important to note that adenosine should not be used for irregular wide-complex tachycardias because it may cause degeneration of the rhythm to VF.</li>
</ul><div><div><b>4.Organized Post–Cardiac Arrest Care: </b>2010 (New): Post–Cardiac Arrest Care is a new section<br />
<div><div>in the 2010 AHA Guidelines for CPR and ECC. To improve survival for victims of cardiac arrest who are admitted to a hospital after ROSC, a comprehensive, structured, integrated,multidisciplinary system of post–cardiac arrest care should be implemented in a consistent manner.Treatment should include cardiopulmonary and neurologic support. Therapeutic hypothermia and percutaneous coronary interventions (PCIs) should be provided when indicated.Because seizures are common after cardiac arrest, an electroencephalogram for the diagnosis of seizures should be performed with prompt interpretation as soon as possible and should be monitored frequently or continuously in comatose patients after ROSC.</div></div></div></div><div><b>5.Initial and Later Key Objectives of Post–Cardiac Arrest Care:</b></div><div>1. Optimize cardiopulmonary function and vital organ perfusion after ROSC</div><div>2. Transport/transfer to an appropriate hospital or critical care unit with a comprehensive post–cardiac arrest treatment system of care</div><div>3. Identify and treat ACS and other reversible causes</div><div>4. Control temperature to optimize neurologic recovery</div><div>5. Anticipate, treat, and prevent multiple organ dysfunction.This includes avoiding excessive ventilation and hyperoxia.</div><div><b>6.Tapering of Inspired Oxygen Concentration:</b></div><div>After ROSC Based on Monitored Oxyhemoglobin Saturation, ie, SPO2. New recommendation</div><div><br />
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</div><div><b>ETHICAL ISSUES</b></div><div><div>The ethical issues relating to resuscitation are complex,occurring in different settings (in or out of the hospital) and among different providers (lay rescuers or healthcare personnel) and involving initiation or termination of basic and/or advanced life support. All healthcare providers should consider the ethical, legal, and cultural factors associated with providing care for individuals in need of resuscitation. Although providers play a</div><div>role in the decision-making process during resuscitation, they should be guided by science, the preferences of the individual or their surrogates, and local policy and legal requirements.</div><div><b>Terminating Resuscitative Efforts in Adults With Out-of-Hospital Cardiac Arrest</b></div><div>• Arrest not witnessed by EMS provider or first responder</div><div>• No ROSC after 3 complete rounds of CPR and AED analyses</div><div>• No AED shocks delivered</div><div><b>For situations when ACLS EMS personnel are present to provide care;</b> for an adult with out-of-hospital cardiac arrest, an “ACLS termination of resuscitation” rule was established to consider</div><div>terminating resuscitative efforts before ambulance transport if all of the following criteria are met:</div><div>• Arrest not witnessed (by anyone)</div><div>• No bystander CPR provided</div><div>• No ROSC after complete ALS care in the field</div><div>• No shocks delivered</div><div>Implementation of these rules includes contacting online medical control when the criteria are met. In 2005 guidelines,no specific criteria were established</div></div><div><br />
</div><div><b>THE PEDIATRIC ADVANCED CARDIAC LIFE SUPPORT</b></div><div><div>Many key issues in the review of the PALS literature resulted in refinement of existing recommendations rather than new recommendations; </div><div>1. Monitoring capnography/capnometry is again recommended to confirm proper endotracheal tube position and may be useful during CPR to assess and optimize the quality of chest compressions.</div><div>2.The PALS cardiac arrest algorithm was simplified to emphasize organization of care around 2-minute periods of uninterrupted CPR.</div><div>3.The initial defibrillation energy dose of 2 to 4 J/kg of either monophasic or biphasic waveform is reasonable but for ease of teaching, a dose of 2 J/kg may be used (this dose is the same as in the 2005 recommendation). For second and subsequent doses, give at least 4 J/kg. Doses higher than 4 J/kg (not to exceed 10 J/kg or the adult dose) may also be safe and effective, especially if delivered with a biphasic defibrillator.</div><div>4.On the basis of increasing evidence of potential harm from high oxygen exposure, a new recommendation has been added to titrate inspired oxygen (when appropriate equipment is available), once spontaneous circulation has been restored, to maintain an arterial oxyhemoglobin saturation ≥94% but <100% to limit the risk of hyperoxemia.</div><div>5.New sections have been added on resuscitation of infants and children with congenital heart defects,including single ventricle, palliated single ventricle, and pulmonary hypertension. The use of extracorporial membrane oxygenation , if facilities are available is stressed.</div><div>6.Several recommendations for medications have been revised. These include, not administering calcium except in very specific circumstances like hypocalcemia, calcium channel blocker overdose,</div><div>hypermagnesemia, or hyperkalemia. and limiting the use of etomidate in septic shock. Routine calcium</div><div>administration in cardiac arrest provides no benefit and may be harmful.</div><div>7.Indications for postresuscitation therapeutic hypothermia have been clarified somewhat.(see below)</div><div>8.New diagnostic considerations have been developed for sudden cardiac death of unknown etiology.</div><div>9.Providers are advised to seek expert consultation, if possible, when administering amiodarone or procainamide to hemodynamically stable patients with arrhythmias.</div><div>10.The definition of wide-complex tachycardia has been changed from >0.08 second to >0.09 second.</div><div><br />
</div><div>When a sudden, unexplained cardiac death occurs in a child or young adult, obtain a complete past medical and family history (including a history of syncopal episodes, seizures, unexplained accidents/drowning, or sudden unexpected death at <50 years of age) and review previous ECGs. All infants, children, and young adults with sudden, unexpected death should, where resources allow, have an unrestricted complete autopsy, </div><div>preferably performed by a pathologist with training and experience in cardiovascular pathology. Tissue should be preserved for genetic analysis to determine the presence of channelopathy. It is explained as ;There is increasing evidence that some cases of sudden death in infants, children, and young adults may be associated with genetic mutations that cause cardiac ion transport defects known as channelopathies. These can cause fatal arrhythmias, and their correct diagnosis may be critically important for living relatives</div></div><div><br />
</div><div><b>NEONATAL RESUSCITATION</b></div><div><div style="font-weight: bold;"><br />
</div><div>1.Once positive-pressure ventilation or supplementary oxygen administration is begun, assessment should consist of simultaneous evaluation of 3 clinical characteristics:heart rate, respiratory rate, and evaluation of the state of oxygenation (optimally determined by pulse oximetry rather than assessment of color)</div><div>2. Anticipation of the need to resuscitate: during elective cesarean section</div><div>3. Ongoing assessment</div><div>4.Supplementary oxygen administration; For babies born at term, it is best to begin resuscitation with air rather than 100% oxygen.Administration of supplementary oxygen should be regulated by blending oxygen and air, and the amount to be delivered should be guided by oximetry.</div><div>5.Suctioning : There is no evidence that active babies benefit from airway suctioning, even in the presence of meconium, and there is evidence of risk associated with this suctioning. The available evidence does not support or refute the routine endotracheal suctioning of depressed infants born through meconium-stained amniotic fluid.</div><div>6.Ventilation strategies (no change from 2005)positive airway pressure may be helpful in the transitioning of the preterm baby. Use of the laryngeal mask airway should be considered if face-mask ventilation is unsuccessful and tracheal intubation is unsuccessful or not feasible.</div><div>7.Recommendations for monitoring exhaled CO2. Exhaled CO2 detectors are recommended to confirm endotracheal intubation.</div><div>8.Compression-to-ventilation ratio remains the same: The recommended compression-to-ventilation ratio remains 3:1. If the arrest is known to be of cardiac etiology, a higher ratio (15:2) should be considered.</div><div>9.Thermoregulation of the preterm infant should be considered (no change from 2005)</div><div>10.Postresuscitation therapeutic hypothermia: It is recommended that infants born at ≥36 weeksof gestation with evolving moderate to severe hypoxic-ischemic encephalopathy should be offered therapeutic hypo thermia.</div><div>11.Delayed cord clamping : There is increasing evidence of benefit of delaying cord clamping for at least 1 minute in term and preterm infants not requiring resuscitation. There is insufficient evidence to support or refute a recommendation to delay cord clamping in babies requiring resuscitation.</div><div>12.Withholding or discontinuing resuscitative efforts (Reaffirmed 2005 Recommendation): In a newly born baby with no detectable heart rate, which remains undetectable for 10 minutes, it is appropriate to consider stopping resuscitation,considering factors such as the presumed etiology of the arrest, the gestation of the baby, the presence or absence of complications, and the potential role of therapeutic hypothermia.</div><div><br />
</div><div><b>THERAPEUTIC HYPOTHERMIA</b></div><div>In adult post–cardiac arrest patients treated with therapeutic hypothermia, it is recommended that clinical neurologic signs, electrophysiologic studies, biomarkers, and imaging be performed where available, at 3 days after cardiac arrest. Currently, there is limited evidence to guide decisions regarding withdrawal of life support. The clinician should document all available prognostic testing 72 hours after cardiac arrest treated </div></div><div><div>with therapeutic hypothermia and use best clinical judgment based on this testing to make a decision to withdraw life support when appropriate. Explained as; on the basis of the limited available evidence, potentially reliable prognosticators of poor outcome in patients treated with therapeutic hypothermia after cardiac arrest include bilateral absence of N20 peak on somatosensory evoked potential more than or equal to 24 hours after cardiac arrest and the absence of both corneal and pupillary reflexes >3 days after </div><div>cardiac arrest. Limited available evidence also suggests that a Glasgow Coma Scale Motor Score of 2 or less at day 3 after sustained return of spontaneous circulation and presence of status epilepticus are potentially unreliable prognosticators of poor outcome in post-cardiac arrest patients treated with therapeutic hypothermia. Similarly, recovery of consciousness and cognitive functions is possible in a few post-cardiac arrest patients treated with therapeutic hypothermia despite bilateral absent or minimally present N20 responses of median nerve somatosensory evoked potentials, which suggests they may be unreliable as well. The reliability of serum biomarkers as prognostic indicators is also limited by the relatively few patients who have been studied. </div></div><div class="separator" style="clear: both; text-align: center;"><iframe allowfullscreen='allowfullscreen' webkitallowfullscreen='webkitallowfullscreen' mozallowfullscreen='mozallowfullscreen' width='320' height='266' src='https://www.blogger.com/video.g?token=AD6v5dzMnCsLadDFE3uDllwedOZrL00ggHZKVJIi1cRiDyy7g23eXiZ_0aCZWMpF48FtqD-oA2d322nAkayxLj7Waw' class='b-hbp-video b-uploaded' frameborder='0'></iframe></div><div><br />
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</div><div>EUROPEAN RESUSCITATION COUNCIL GUIDELINES:</div><div><a href="http://aim.code.nl/article/S0300-9572(10)00447-8/pdf/european-resuscitation-%20%20council-guidelines-for-resuscitation-2010-section-1-executive-summary">http://aim.code.nl/article/S0300-9572(10)00447-8/pdf/european-resuscitation- council-guidelines-for-resuscitation-2010-section-1-executive-summary</a></div><div>Reference:</div><div>1.<a href="http://circ.ahajournals.org/content/vol122/18_suppl_3/">http://circ.ahajournals.org/content/vol122/18_suppl_3/</a></div><div>2.<a href="http://www.heart.org/HEARTORG/CPRAndECC/Science/Guidelines/2010-AHA-%20%20Guidelines-for-CPR-ECC_UCM_317311_SubHomePage.jsp">http://www.heart.org/HEARTORG/CPRAndECC/Science/Guidelines/2010-AHA- Guidelines-for-CPR-ECC_UCM_317311_SubHomePage.jsp</a></div><div>3.<a href="http://www.heart.org/HEARTORG/CPRAndECC/CPR_UCM_001118_SubHomePage.jsp">http://www.heart.org/HEARTORG/CPRAndECC/CPR_UCM_001118_SubHomePage.jsp</a></div><div>4.<a href="http://circ.ahajournals.org/content/vol112/24_suppl/">http://circ.ahajournals.org/content/vol112/24_suppl/</a></div>DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com5tag:blogger.com,1999:blog-8746726747957343433.post-19969154294302652102010-10-15T13:00:00.000-07:002010-10-24T12:17:35.327-07:00EVOLUTION THROUGH REVOLUTION, COMMEMORATING ETHER DAY!<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgn6nAfvvpNoER97s3LpXINSGpbeRyI0t2BwiMzr7HDpRhcvCHcMQQmVOCLxiYXIAGFHtyNCheO_SQhWIQP0YH9vEOisnQaMr8eEateMopU2Y80ZDiLFGQfuA9WLXsrEdDgm_fvwgzxBE79/s1600/first-anaesthetist.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" ex="true" height="156" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgn6nAfvvpNoER97s3LpXINSGpbeRyI0t2BwiMzr7HDpRhcvCHcMQQmVOCLxiYXIAGFHtyNCheO_SQhWIQP0YH9vEOisnQaMr8eEateMopU2Y80ZDiLFGQfuA9WLXsrEdDgm_fvwgzxBE79/s200/first-anaesthetist.jpg" width="200" /></a></div><span id="goog_1689331754"></span><span id="goog_1689331755"></span>So the LORD God caused a deep sleep to fall upon the man, and he slept; then He took one of his ribs and closed up the flesh at that place.( Genesis 2:21) Who is the first Anaesthesiologist then? its Lord,The God almighty. Adam was first formed, then Eve and she was made of the man, out of his bone, and for the man (1 Co. 11:8, 9), Thus the speciality of Anaesthesiology is divine and .... Anaesthesiologists are followers of God.! According to the law of equations, following Anaesthesiologist is as equivalent as following God!! .... Of course what is of more glorified act than giving pain relief to whom who suffer from severe physical and mental agony? Even Eve was not lucky enough to have a painless labour, a luxury and privilege enjoyed by her descendants, made possible by this blessed branch of medical sciences. The history of anaesthesia dates back and starts from here.<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEghgnkz_6vZjVgjk7HnsoQRuRpPzMO9y1sM7P_CIGo43rAIQHVFCwglFnPhXvx0HgJfzxRwLrDahJQPAXFBd8bhA-3iQ0-Q1WQQc_5rp4g7MRu04rNulPZPPlQ9bebRJtynw2I2VBZF8Sdg/s1600/Mesmertn.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" height="136" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEghgnkz_6vZjVgjk7HnsoQRuRpPzMO9y1sM7P_CIGo43rAIQHVFCwglFnPhXvx0HgJfzxRwLrDahJQPAXFBd8bhA-3iQ0-Q1WQQc_5rp4g7MRu04rNulPZPPlQ9bebRJtynw2I2VBZF8Sdg/s200/Mesmertn.jpg" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #af0000; font-family: inherit; font-size: x-small;">Mesmer practising animal magnetism</span></td></tr>
</tbody></table><div style="text-align: justify;">Before the advent of anaesthesia, surgery was a terrifying prospect. Many approached surgery as if they are facing execution and many suffered pain, hemorrage, shock, infection and death, due to inappropriate assessment, lack of proper agents or equipments.The pre anaesthetic era witnessed the application of physical means and herbal remedies for pain relief eg: local application of cold water, ice or pressure. Plants and extracts,Coca leaves chewed and saliva dripped into injured areas or open wounds -Inca Shamans, Alcohol with opium or hemp –“soporific sponge" (mentioned around 1200 by Nicholas of Salerno ) , Hypnosis (Its eponymous originator was Anton Mesmer (1734-1815)). etc. Amputations were performed by giving alcohol and patients were made intoxicated (Apuleius, a 5th century compiler) or the legs were frozen by applying ice(Refrigeration anaesthesia by Marco AvrelioSeverino). Egyptian surgeons apparently half-asphyxiated children undergoing circumcision by first almost strangling them. This practice sounds almost as barbarous as the operation itself. </div><div style="border: medium none;"><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiTGZ8uaard0cKhD9ExPzx21ljMZFFQiZ4B-8SNhvWgugEoCh1a1xJLTOlXvoxHA6-b8PjoTYxGm68HJyEuGN_AK6zJSYxhPvGZFfw0eh2W40sLg1LH1iVVD7gB9cyDq_l_GOrXEhHNcyqk/s1600/opium.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiTGZ8uaard0cKhD9ExPzx21ljMZFFQiZ4B-8SNhvWgugEoCh1a1xJLTOlXvoxHA6-b8PjoTYxGm68HJyEuGN_AK6zJSYxhPvGZFfw0eh2W40sLg1LH1iVVD7gB9cyDq_l_GOrXEhHNcyqk/s1600/opium.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Opium</span></td></tr>
</tbody></table></div><div style="border: medium none;">The discovery that plant extracts, like opium (papaver somniferum), mandragora from atropa, belladona (morning glory) Marijuana (cannabis indica) can provide pain relief, helped the primitive physicians to conduct surgeries and threw light into the pharmacological and physiological principles of pain transmission and pain management.While the physicians across the atlantic enjoyed the benefits of coca (Viennese ophthalmologist Karl Koller used cocaine locally for ophthalmic surgeries)(1857-1944),the chinese were focussing on acupuncture</div><div style="border: medium none;"><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj5rtAFjQqYXAZD5UaoqcJb5jShq_rTdqZ-Xx-xcwZw504zzr0J4aMSsCU8OxUGA6f7kNLxSSXVlUA68uuE0SAyC_7WqyhcSZj3BCwHzUx0jQkDj2PCNdsScw6ZZ-kJT9GJ7u7t81TfkyHF/s1600/h+d.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj5rtAFjQqYXAZD5UaoqcJb5jShq_rTdqZ-Xx-xcwZw504zzr0J4aMSsCU8OxUGA6f7kNLxSSXVlUA68uuE0SAyC_7WqyhcSZj3BCwHzUx0jQkDj2PCNdsScw6ZZ-kJT9GJ7u7t81TfkyHF/s1600/h+d.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Humphry Davy</span> </td></tr>
</tbody></table><div style="border: medium none;">The 19th century stood as an important mile stone in the history of anaesthesia with the synthesis and use of atmospheric gases and nitrous oxide by early scientific luminaries such as Black, Priestley, and Lavoisier.Of which the first gas recognised to have anaesthetic powers was nitrous oxide (N2O) which is inert, colourless, odourless and tasteless. Nitrous oxide was first isolated and identified in 1772 by the English chemist, Joseph Priestley (1733-1804). The exhilarating effects of inhaling nitrous oxide were noted by English chemist Sir Humphry Davy (1778-1829).The term laughing gas was given to it and N2O was used widely for recreational purposes.It was Davy who suggested N2O for pain relief during surgery." Nitrous Air, and Its Respiration (1800)" Davy described the different planes of anaesthesia as stage 1: analgesia; stage 2: delirium; stage 3: surgical anaesthesia; stage 4: respiratory paralysis, though without appreciating the significance of each stage.. In 1824, English country doctor Henry Hill Hickman (1800-30), performed painless operations by inhalation of CO2 but was not widely recognised. </div><table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjoJX5O4icuLRJgbbLzq2AgCARORF7YErgugh9m61Ajhxd1PKWWXEiMW_5w7xtNlEKqPkFMr-DtTKu84P7XBSaKquSfEo6VciLEpw8rBI1bqw4doY_X9EkkUwB05O25b7hExYmZdxb9d3tz/s1600/Crawford_Long.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjoJX5O4icuLRJgbbLzq2AgCARORF7YErgugh9m61Ajhxd1PKWWXEiMW_5w7xtNlEKqPkFMr-DtTKu84P7XBSaKquSfEo6VciLEpw8rBI1bqw4doY_X9EkkUwB05O25b7hExYmZdxb9d3tz/s1600/Crawford_Long.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Crawford Williamson Long</span> </td></tr>
</tbody></table>Ether was first discovered by Catalan philosopher chemist Raymundus Lullius (1232-1315). Lullius called it "sweet vitriol", it was produced by distilled sulfuric acid fortified with wine and sugar.Paracelsus observed that chickens who were given vitriol fell asleep and awaken unharmed.The first use of general anaesthesia probably dates to early nineteenth century in Japan. On 13th October 1804, a japanese physician [1]Seishu Hanaoka (1760-1835) removed a breast tumour uneventfully for which he used "Tsusensan", a herbal preparation.The first successful use of ether anaesthesia is by Crawford Williamson Long (1815-78).who may be called as the "discoverer of anaesthesia".He removed a cyst from the neck of Mr James Venable under ether anaesthesia but this was remained unpublished.<br />
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<tr><td style="text-align: center;"> <a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgGqDcfshYLnPPVqEoZHmY2WLWbW8laqm-FH0VV-c5Z36RSS611fPSfPHwFhHcMy-Ch5D__u_AlrWRd4IsncXdtKfnNmIfhX-GYw6hrzham7-gXeho2sdqJNY73gW2m-9WlN0DV_U9fugFK/s1600/horace.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgGqDcfshYLnPPVqEoZHmY2WLWbW8laqm-FH0VV-c5Z36RSS611fPSfPHwFhHcMy-Ch5D__u_AlrWRd4IsncXdtKfnNmIfhX-GYw6hrzham7-gXeho2sdqJNY73gW2m-9WlN0DV_U9fugFK/s1600/horace.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Horace Wells</span> </td></tr>
</tbody></table> The anaesthetic revolution set a pace, Horace Wells (1815-1848) demonstrated that injuring leg under N2O inhalation is painless. He himself was subjected to N2O anaesthesia for dental extraction without pain.Later on he attempted a public demonstration with N2O in january 1845 which was a failue.There was laughter and cries of "humbug". <br />
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The era of surgical anaesthesia unveils, William Thomas Green Morton (1819-1868). discovered the quality of ether that it can produce surgical anaesthesia without profound respiratory or circulatory depression. He found that a slow rate of induction allowed high margin of safety for ether. He was received an invitation to give a public demonstration at Massachussets General Hospital on friday <span style="color: #990000;">16 oct 1846.</span> The patient was Edward Gilbert Abbot and the surgeon was John Collins Warren.<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEizu3NSmMeO83DdvRX-JS_RJOm9XEyRgK8FyYdqiq-vqTbGCKSHnJP3FhR7F4566A9CRiM_sVgmBb6qy8lG5PTkUG-o_UQiUgDiaR3PgdfuTl1dxf0873-c0lnongELCOGmCHkUQb3ppD3g/s1600/william-morton.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" ex="true" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEizu3NSmMeO83DdvRX-JS_RJOm9XEyRgK8FyYdqiq-vqTbGCKSHnJP3FhR7F4566A9CRiM_sVgmBb6qy8lG5PTkUG-o_UQiUgDiaR3PgdfuTl1dxf0873-c0lnongELCOGmCHkUQb3ppD3g/s320/william-morton.jpg" width="235" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">William Thomas Green Morton</span> </td></tr>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrJrJNE1gGzDHSjv1oQsNCG0wpbWeHX67JtXdd7wHxt83UDgoCKDmp-rCElJIXwoSU4PkgkrMgwyKTU5EnLwUa-zJzCPszgCkouP-L19lpyZlWvG9sDFHlpIlRG-NEVm9C_LERPHuybm_N/s1600/ether-inhaler.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrJrJNE1gGzDHSjv1oQsNCG0wpbWeHX67JtXdd7wHxt83UDgoCKDmp-rCElJIXwoSU4PkgkrMgwyKTU5EnLwUa-zJzCPszgCkouP-L19lpyZlWvG9sDFHlpIlRG-NEVm9C_LERPHuybm_N/s200/ether-inhaler.jpg" width="136" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Morton's inhaler</span></td></tr>
</tbody></table>The surgeon excised a vascular swelling from the neck successfully. Morton used a draw over vapouriser designed by him. on Completion of surgery Warren announced "Gentlemen this is no humbug" A great discovery ,a golden mile stone in the history of anaesthesiology,the day being celebrated worldwide as "ether day".Oliver wendel homes(1809-94). suggested the name anaesthesia for this painless state.[2]<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhbOpO6e8m2grRbYoY6AVOeEJtzZxjhyphenhyphenWGr1kavutuA62G2kQJckWt9_dWXd-5jY0d5RVNWGnmvxc6OveZzvnca9i6b6ktQJuNyp9fijrhC9oBi7Wzo5cmKnQcbV3XJ62t8B3WIBpwYesFi/s1600/Ether+Day+by+hinkley.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" ex="true" height="273" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhbOpO6e8m2grRbYoY6AVOeEJtzZxjhyphenhyphenWGr1kavutuA62G2kQJckWt9_dWXd-5jY0d5RVNWGnmvxc6OveZzvnca9i6b6ktQJuNyp9fijrhC9oBi7Wzo5cmKnQcbV3XJ62t8B3WIBpwYesFi/s400/Ether+Day+by+hinkley.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Ether Day</span></td></tr>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhp_kCssXwOpQDa5uO0bIOpI2qy08AIK7YQOw14mbA8bLYJpKxIhUJLAjUy2VLsVIK6JQXL0PXu2t1-YVb1-L5jW_0BRa4Ld29ZeOnUBJ0nKFHnaqQ8mwrtrZftSm29DeJKLoVxKAcrgZGn/s1600/250px-MGH_Ether_Dome_29Jan2008.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhp_kCssXwOpQDa5uO0bIOpI2qy08AIK7YQOw14mbA8bLYJpKxIhUJLAjUy2VLsVIK6JQXL0PXu2t1-YVb1-L5jW_0BRa4Ld29ZeOnUBJ0nKFHnaqQ8mwrtrZftSm29DeJKLoVxKAcrgZGn/s1600/250px-MGH_Ether_Dome_29Jan2008.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Ether dome</span></td></tr>
</tbody></table>The amphitheatre at MGH, where this demonstration took place is honoured by giving the name "ether dome"This is now a national shrine.the Morton's grave in Mount Auburn Cemetery near Boston bears the inscription: <br />
WILLIAM T. G. MORTON<br />
Inventor and Revealer of Anaesthetic Inhalation<br />
Before Whom, in All Time, Surgery Was Agony<br />
By Whom Pain in Surgery was Averted and Annulled<br />
SinceWhom Science Has Control of Pain <br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_lUDmZQtwW2cJtfNvXT46Dj7A0q1-1mdW-jFMkf3kjTEQ5UB_F-6imwMObpLLAZBR9robmDVFDab2SAkM0c4dcCxd9Ac34rS6H-9z26s_lkeVuglgiLss3kZRFJnnAH4_vBFzno6kYJsb/s1600/simpson.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_lUDmZQtwW2cJtfNvXT46Dj7A0q1-1mdW-jFMkf3kjTEQ5UB_F-6imwMObpLLAZBR9robmDVFDab2SAkM0c4dcCxd9Ac34rS6H-9z26s_lkeVuglgiLss3kZRFJnnAH4_vBFzno6kYJsb/s1600/simpson.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">James young simpson</span></td></tr>
</tbody></table>In Scotland, Sir James Young Simpson (1811-1870), used Ether for the first time for relieving labour pain(1846) He was experimenting on chloroform and proved the efficacy of chloroform by giving it to those who attended a dinner party He also tried the drug himself and published his findings in Lancet. Later he himself defended the use of chloroform for pain relief in labour as it was against religion and belief. Chloroform use also had a short history. It is a colourless volatile liquid with a characteristic smell and a sweet taste.It was discovered in1831 by American physician Samuel Guthrie (1782-1848); <br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEitaBJOmCMTxWBOdR8GHnPi0rM1NIYUs4-vzzO5DkekWUr1gO5x8Y1xRMYyE45Fn2-qFxiPP4uL6e57FGwqZERJV8pc1ujDFO5qGaDEIeeSZ3jOYTe6LXJaIAR2qCHsYjLluJwRacLKo02y/s1600/snow.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEitaBJOmCMTxWBOdR8GHnPi0rM1NIYUs4-vzzO5DkekWUr1gO5x8Y1xRMYyE45Fn2-qFxiPP4uL6e57FGwqZERJV8pc1ujDFO5qGaDEIeeSZ3jOYTe6LXJaIAR2qCHsYjLluJwRacLKo02y/s1600/snow.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">John snow</span></td></tr>
</tbody></table>In England, at least, the practice of anaesthesia during childbirth won greater respectability following its widely-publicised use on Queen Victoria. The delivery in 1853 of Victoria's eighth child and youngest son, Prince Leopold, was successful: chloroform was administered by Dr John Snow (1813-1858) of Edinburgh, the world's first anaesthesiologist/anaesthetist. He used chloroform in a hand kerchief for inhalation and Queen victoria never had pain during child birth.The contributions of John snow include<br />
<ul><li>Description of stages of anaesthesia based on patient's responsiveness</li>
<li>Developed ether inhalers, and an ether vapouriser which is thermocompensated.</li>
<li>Development of agent specific chloroform vapouriser</li>
<li>Described the minimum anaesthetic concentration to prevent movement which led to the future discovery of MAC</li>
<li>Published books and journals on chloroform and ether</li>
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj2Quw9lj9ZaQcE-9EViBqCW_f2woW2KyauWZCPupM6SnKxuNeTSC6a4Ldp9825uBpX6IvHkWjYep0UfvQ2_0-IZ63IgNhn2FKtjlXKQ1ZHChbrFM6w-vAYBd8aC4AP3OOtQmy0LseLEOvM/s1600/clover.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj2Quw9lj9ZaQcE-9EViBqCW_f2woW2KyauWZCPupM6SnKxuNeTSC6a4Ldp9825uBpX6IvHkWjYep0UfvQ2_0-IZ63IgNhn2FKtjlXKQ1ZHChbrFM6w-vAYBd8aC4AP3OOtQmy0LseLEOvM/s1600/clover.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Joseph clover</span></td></tr>
</tbody></table><li>Conducted epidemiological surveys and proved that cholera is transmitted by water.</li>
</ul> Dr Joseph Clover (1825-1882) developed the first apparatus to provide chloroform in controlled concentrations; in 1862 and a "portable regulating ether-inhaler" in 1877. This was to minimise the complications associated with the use of chloroform<br />
<br />
The other Inhalation Anaesthesia landmarks include <br />
<ul><table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhpLOIDWo1zw4t04q6MKkBGZ5xq_6bF23_av01sCkRPm10Fze9G7Pz2JbTPaBQAq2uH6DN_leI2qvNW3YHEZffPfohDaP8aiYGthskyRXS63grSVRuqxayuuUP_qd-1q_dqV4uj92CWV3tG/s1600/boyl.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhpLOIDWo1zw4t04q6MKkBGZ5xq_6bF23_av01sCkRPm10Fze9G7Pz2JbTPaBQAq2uH6DN_leI2qvNW3YHEZffPfohDaP8aiYGthskyRXS63grSVRuqxayuuUP_qd-1q_dqV4uj92CWV3tG/s1600/boyl.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Boyles apparatus</span></td></tr>
</tbody></table><li>Introduction of first anaesthesia machine in 1917 by Henry Boyle</li>
<li>CO2 absorption canister in 1924 by Rudolf Waters</li>
<li>Endotracheal intubation in 1920 by Ivan Magill.</li>
<li>Introducton of halothane in 1950 </li>
</ul><br />
<object height="385" width="640"><param name="movie" value="http://www.youtube.com/v/_j7MUhwlfQw?fs=1&hl=en_US"></param><param name="allowFullScreen" value="true"></param><param name="allowscriptaccess" value="always"></param><embed src="http://www.youtube.com/v/_j7MUhwlfQw?fs=1&hl=en_US" type="application/x-shockwave-flash" allowscriptaccess="always" allowfullscreen="true" width="640" height="385"></embed></object><br />
<ul></ul>Epoch of Regional Anaesthesia[3]<br />
<ul><li>Karl Koller( 1857-1944) an ophthalmologist from vienna introduced cocaine for topical ophthalmic anaesthesia</li>
<li>William Halstead, described nerve blocks of face and arm 1886,</li>
<li>Description of spinal anaesthesia by Leonard Corning. He coined the term spinal anaesthesia. He used cocaine into the spinal canal</li>
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjJP8j0M2-iorAxm19NQA5rX5-rgi31wWiKZaXJcypY39Xjg236w4YfD5aGNfGvaVaW7xSeMf94uCffyzGM7OQlSbISzgiqml3TTgELTdQpeaPKEbD-5CRDvt8i1th4ByuFxc_cLeKfUFeO/s1600/spin.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" ex="true" height="164" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjJP8j0M2-iorAxm19NQA5rX5-rgi31wWiKZaXJcypY39Xjg236w4YfD5aGNfGvaVaW7xSeMf94uCffyzGM7OQlSbISzgiqml3TTgELTdQpeaPKEbD-5CRDvt8i1th4ByuFxc_cLeKfUFeO/s200/spin.jpg" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="color: #990000;">Regional Anaesthesia</span></td></tr>
</tbody></table><li>August Bier, further research on spinal anesthesia in 1898.</li>
<li>Virginia Apgar promotes Regional analgesia in childbirth 1930.</li>
<li>Arthur Barker hyperbaric spinal anaesthesia by addition of glucose 1935</li>
<li>August Bier, intravenous regional anaesthesia in 1908</li>
<li>Martinez Curbelo from cuba continuous epidural anaesthesia 1949</li>
</ul>Intravenous Anaesthesia<br />
<ul><li>1903 Barbitone synthesis by Fischer, Berlin, Nobel Prize.</li>
<li>1932 Evipan used IV by Weese Schraff, & Rheinoff. </li>
<li>1934 Lundy, Mayo Clinic, used Sodium Pentothal.</li>
<li><span style="color: black; font-family: TimesNewRoman; font-size: small;">1942 Curare first used clinically by Griffith and Enid johnson in Montreal</span></li>
<li>1857 Claude Bernard published that curare blocked the NMJ.</li>
<li>1940 Bennett used curare to modify seizures induced by metrozol.</li>
</ul>Modern anaesthesia<br />
<ul><li>Starts from 1980</li>
<li><span style="color: #ebebeb; font-family: TimesNewRoman;"><span style="color: black; font-size: small;">Standards for Basic Anesthetic Monitoring ASA, House of Delegates 10/21/1986.</span></span></li>
<li><span style="color: #ebebeb; font-family: TimesNewRoman;"></span><span style="color: black;"><span style="font-family: TimesNewRoman;"><span style="font-size: small;">Anesthesia Patient Safety Foundation 1984.</span></span></span></li>
<li><span style="color: black;"><span style="font-family: TimesNewRoman;"><span style="font-size: small;">International anaesthesia research society 1922 by mcMechaan</span></span></span></li>
<li>BJA 1923</li>
<li>Association of anaesthetists of great britain and ireland 1932. </li>
</ul><br />
<ul><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEghxM-72WnKo0Z3l2oP3e8-vUumufvuOpi_D7vmFPs_1weyIpzqQXezyK5D4C8otuzXhEad3rNfX22jIF_UzVnKzj0UdQYlfJp3P-AJstgrowposJjVbgwaWQGUAPtaOdtSWwY6FCU-JLRZ/s1600/2254769323_4908aeb483.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" ex="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEghxM-72WnKo0Z3l2oP3e8-vUumufvuOpi_D7vmFPs_1weyIpzqQXezyK5D4C8otuzXhEad3rNfX22jIF_UzVnKzj0UdQYlfJp3P-AJstgrowposJjVbgwaWQGUAPtaOdtSWwY6FCU-JLRZ/s1600/2254769323_4908aeb483.jpg" /></a></div></ul>The modern Anaesthesiologist is a physician and primary care provider who is concerned with the total wellbeing of his patients. Other than the safety and comfort of patient in operation theatre, the anaesthesiologist's services extend outside the operating room as well. They are routinely asked to monitor or sedate patients for lithotripsy, MRI, cardiac catheterisation, electroconvulsive therapy, fluroscopy etc. They are considered to be the pioneers in cardiopulmonary resuscitation. The anaesthesiologist is actively involved in Intensive care, Trauma care, Pain management and complex specialised surgical procedures<br />
<br />
<table><tbody>
<tr><td valign="top" width="4%"></td><td><span class="text">Reference:</span></td></tr>
</tbody></table>1). Matsuki A: Seishu Hanaoka, Japanese pioneer in anesthesia. Anesthesiol1970; 32:446-50 Fenster J M: <br />
2). Sykes: Essays on the First Hundred Years of Anaesthesia. Robert E. Kreiger Publishing Co. 1972. <br />
Wolfe & Menczer: I Awaken to Glory. Boston Medical Library, 1994. <br />
3) An article on Anesthesiology yesterday, today and tomorrow by Mr.Adolph H. Giesecke MD.UTX Southwestern Medical Center, Dallas T<br />
4) Wylie and Churchil Davidson Practise of Anesthesia. 7th edition.; Pp 01-15<br />
5) Images :<br />
<a href="http://en.wikipedia.org/wiki/Ether_Dome">http://en.wikipedia.org/wiki/Ether_Dome</a><br />
<a href="http://www.general-anaesthesia.com/images/ether-inhaler.html">www.general-anaesthesia.com/images/ether-inhaler.html</a> <br />
<a href="http://www.bmj.com/content/2/4475/536.full.pdf+html">http://www.bmj.com/content/2/4475/536.full.pdf+html</a>DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-33128224828411212792010-09-22T23:35:00.000-07:002013-02-27T00:51:01.300-08:00THE ROLE OF CLASSIC LMA IN DIFFICULT AIRWAY.<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhF4BKaTE8rYVs15fMziz0Pjki0vM21yYLMxDJVvrcstHVlWbevGfHZGx1olE-3HkKp9Lv9JsPHtebXKB8e5wWbaAXr_Yuh4AawmTMybYKrcWVa3bhopGrkkqn9vusB_kPHfgFNG-lUekvV/s1600/13466_135512893136439_100000331885975_250650_527566_s.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" bx="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhF4BKaTE8rYVs15fMziz0Pjki0vM21yYLMxDJVvrcstHVlWbevGfHZGx1olE-3HkKp9Lv9JsPHtebXKB8e5wWbaAXr_Yuh4AawmTMybYKrcWVa3bhopGrkkqn9vusB_kPHfgFNG-lUekvV/s320/13466_135512893136439_100000331885975_250650_527566_s.jpg" /></a></div>
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The recent development in the management of "difficult airway" is the incorporation of LMA into its algorithm. Since the introduction of LMA in 1981 they have been widely evaluated for their efficacy in managing difficult airways and have been proven effective in CICV situations.According to the 'Practice Guidelines for Management of the Difficult Airway' by the ASA task force, the use of supraglottic airway devices including LMA, Combitube or other suitable supraglottic airway as rescue devices in the “cannot intubate cannot ventilate” situation, is highly recommended. The advice switches from an earlier emphasis on laryngoscopy and intubation to an emphasis focusing on ventilation and oxygenation.The present topic concentrates only on the algorithm where LMA can be used as an intubation conduit. Eventhough intubating LMA is widely used to manage difficult airway, classic LMA alone is included in the algorithm because of its simplicity and safety in inexperienced hands. Watch the following flow charts, photographs, and a video which are self explanatory.</div>
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<b>Classic LMA</b></div>
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<ul>
<li>Developed by Dr. Archie I J Brain, a British anesthetist in 1981.</li>
<li>First successful use of prototype LMA in failed intubation situation in a 114 kg patient in February 1983. </li>
<li>Dr. Archie Brain publishes his first series of 23 patients undergoing routine airway management by the LMA in 1983.</li>
<li>21 cases of difficult intubations were managed by the LMA and reported in literature between 1983 - 1987.LMAs are commercially available since 1987.</li>
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<img border="0" bx="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgUohkYXZmGNhyphenhyphenlCiKTMsSoKGdSc2XLanO7EkdusttCvWFQzVQzdRziI0w-LpbCyGRmJxoD_IQqVTMfTC3wBj0a4_1TT6fTdccTbhOsgKeO3i3Sc9R4oJSO__2hdl5aOa7sO1Sw2CMGnNPS/s320/classic+lma.jpg" /></div>
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<b><span style="color: #cc0000;">How to insert:</span></b></div>
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<span style="color: #741b47;"><b>The standard technique:</b></span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhupf6nb8Vif4NLGqWymE7APm5iXAVYuG4W6nyVL_TxE1crLzuhhS6PqD1Vb1t3HJi1y4y4z8zZLlW_J63G-AAf5wqNolMu58PmTyoE2I2MewQKYjEbmf8ZCcMkLCOmyS3cp8GQi8qHO2KH/s1600/lma+inse.bmp" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" bx="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhupf6nb8Vif4NLGqWymE7APm5iXAVYuG4W6nyVL_TxE1crLzuhhS6PqD1Vb1t3HJi1y4y4z8zZLlW_J63G-AAf5wqNolMu58PmTyoE2I2MewQKYjEbmf8ZCcMkLCOmyS3cp8GQi8qHO2KH/s320/lma+inse.bmp" /></a></div>
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Why and how LMA has found a unique place in Algorithm?</div>
<li>Simple to use </li>
<li>Non-invasive design as it does not invade trachea</li>
<li>An easy to learn & easy to teach quality. </li>
<li>Improved success rate with minimal tissue trauma in first attempt </li>
<li>Ability to be used as a ventilatory device as well as an aid to intubation.</li>
<li>Immediate airway access compared to invasive techniques</li>
<li>Less gastric inflation and subsequent regurgitation.</li>
</ul>
<b><span style="color: #741b47;">Alternate methods for placement of LMA:</span></b><br />
<br />
<ul>
<li>Insert the deflated LMA with the laryngeal aperture facing cephalad and rotate it 180º as the cup enters the pharynx, Specially useful in patients with restricted mouth opening or hindrance to placement by tongue.</li>
<li>Insert the LMA from the side of the mouth in emergency for example from bedside using thumb</li>
<li>Insert the LMA with the cuff partially inflated when the deflated cuff gets folded.</li>
<li>Insert the LMA with the aid of a laryngoscope again in difficult insertion due to large tongue, edentulous airway or due to restricted mouth opening.</li>
<li>Insert LMA with the aid of stylet or a bougie as guide.</li>
<li>In patients with a restricted mouth opening, LMA can be placed retro molar and subsequently the LMA tube is brought forward to lie centrally</li>
</ul>
<b><span style="color: #cc0000;">The Algorithm: Click on the image to enlarge.</span></b><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgMrmCbh1BEsUlYqweQs1rKb4zgTht3mOg1RqWixFQ0z4zAZNveFpXGq4zkS8CX_OVeg75doX6L-Ks0aMByfgZe-BvpMBJx7ig9avPQ7aPJwr9IpHk-361EErTTZ5VOiKPZgAN6s2P9iacL/s1600/algorithm.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" bx="true" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgMrmCbh1BEsUlYqweQs1rKb4zgTht3mOg1RqWixFQ0z4zAZNveFpXGq4zkS8CX_OVeg75doX6L-Ks0aMByfgZe-BvpMBJx7ig9avPQ7aPJwr9IpHk-361EErTTZ5VOiKPZgAN6s2P9iacL/s400/algorithm.jpg" width="350" /></a></div>
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<span style="color: #cc0000;"><b> <span style="color: #cc0000;">ALGORITHM EXPLAINING THE ROLE OF LMA (EXPANDED)</span></b></span><br />
<b><span style="color: #cc0000;"> Click on the image to enlarge</span></b><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj8JicUPonz1ctvkSv4-CxPIfSvW9nmrZ6U9S9zOHsQCDTIrBHn10sawdWKbWIGqRadOrS1TW6j07ODA5kd1521WPU6UJNGVJMj4lgKq_u7ePz1xv7FPkrKF8odrjDKKCp_qn6bDFKQNY5H/s1600/algorithm+corr.bmp" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="300" px="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj8JicUPonz1ctvkSv4-CxPIfSvW9nmrZ6U9S9zOHsQCDTIrBHn10sawdWKbWIGqRadOrS1TW6j07ODA5kd1521WPU6UJNGVJMj4lgKq_u7ePz1xv7FPkrKF8odrjDKKCp_qn6bDFKQNY5H/s400/algorithm+corr.bmp" width="400" /></a></div>
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<b>LMA AS AN INTUBATION CONDUIT:</b><br />
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<ul>
<li><b>Blind passage of ETT through LMA:</b> After placement of LMA by any one of the above techniques, the lubricated endotracheal tube is passed blindly through LMA and placement confirmed by auscultation, chest movement or by capnogram. The following table helps you to choose the correct size of ETT to be passed.</li>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijNEg-Jd92Z97DpPmOswVNJkX6xEvv0sHligzLBcWDaUvnxwrg9fUWvP1hh_3Sj-Rr7csZYG1VSvQ5ZCwHC_FDRqbjldu9_uWSyPszSUFh7hmbdck4P7m41EMISFDdLgz4SvH1hNa7qtYM/s1600/table+for+lma+size.bmp" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" px="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijNEg-Jd92Z97DpPmOswVNJkX6xEvv0sHligzLBcWDaUvnxwrg9fUWvP1hh_3Sj-Rr7csZYG1VSvQ5ZCwHC_FDRqbjldu9_uWSyPszSUFh7hmbdck4P7m41EMISFDdLgz4SvH1hNa7qtYM/s320/table+for+lma+size.bmp" /></a></div>
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In an attempt to insert the LMA blindly one may encounter 2 levels of obstruction within the LMA.The first one is at the level of the aperture bar and the second one is at the level of glottic opening. </div>
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To overcome the first level of obstruction, the ETT is slightly bend and turned to one side while passing. The second level of obstruction is overcome by flexing the neck while insertion</div>
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<li><b>Premounted ETT in LMA with insertion:</b>To avoid the problems associated with obstruction, the ETT is premounted on LMA and inserted. Subsequently manipulated to enter the glottis.<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhuLHGDggQOlffY_E2_DHjJRg5PZ3_vGIycfuryuz1809ccW1noNzLjCk5ifLTa-uU0I823O2rJJcjrK8SjBU35U0k5rq0Jo4-fucrZ6gMKWSjWQHknCzBYAPR-AcVjtv3ro2PUOMkN2QS0/s1600/premou.JPG" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" px="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhuLHGDggQOlffY_E2_DHjJRg5PZ3_vGIycfuryuz1809ccW1noNzLjCk5ifLTa-uU0I823O2rJJcjrK8SjBU35U0k5rq0Jo4-fucrZ6gMKWSjWQHknCzBYAPR-AcVjtv3ro2PUOMkN2QS0/s320/premou.JPG" /></a></li>
<li><b>Bougie aided intubation through LMA: </b>The LMA is inserted cuff inflated and placement confirmed. A bougie is passed through the ETT and manipulated into the larynx. The LMA is deflated and removed and a lubricated ETT is passed over the bougie into the trachea</li>
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<li><b>Trachlight aided intubation via LMA: </b>After placement of LMA a trachlight (lighted wand) is used to identify the laryngeal inlet and ETT is passed over it.</li>
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<li><b>Fiberoscope aided intubation via LMA:</b> Similar to trach light, a fiberoptic bronchoscope is passed into the LMA to reach the trachea and subsequent intubation over bronchoscope is done.</li>
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<span style="color: #741b47;">Video showing blind intubation over LMA</span><br />
<iframe allowfullscreen='allowfullscreen' webkitallowfullscreen='webkitallowfullscreen' mozallowfullscreen='mozallowfullscreen' width='320' height='266' src='https://www.blogger.com/video.g?token=AD6v5dxEOBfWNCHErbQwW40ymMb3L-hZSHrx34N1vvfWFHXcuvlN6JOWgqZxP8StuQQxsyCInutoivsOZzse921olA' class='b-hbp-video b-uploaded' frameborder='0'></iframe><br />
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When no aids are available in CVCI situation the algorithm advises on cricothyrotomy and transtracheal jet ventilation.An anteriorly placed larynx can be managed, in the absence of stylet or bougie by simple manipulation of the ETT, by anchoring it on middle finger to bring forward the tip of ETT.<br />
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The <span style="color: black;">video and a few photographs are reproduced with permission from Dr.Rashid M Khan and Dr.Naresh Kaul of Khoula hospital Muscat, who conducted a workshop on "difficult airway" at ibri hospital in March 2010. The author is much thankful to them.</span></div>
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<span style="color: black;"><b>Ref:</b>1)ASA, Practice guidelines for the management of difficult airway -2003 . <a href="http://www.asahq.org/publicationsAndServices/Difficult%20Airway.pdf">www.asahq.org/publicationsAndServices/Difficult%20Airway.pdf</a></span><a href="http://www.asahq.org/publicationsAndServices/Difficult%20Airway.pdf"><span style="color: black;"> </span></a><br />
<span style="color: black;"> 2)Leader GL, facilitation of insertion of Laryngeal mask, Anaesthesia 1991;46:987 </span><br />
<span style="color: black;"> 3)The <b>Difficult Airway</b> in Adult Critical Care.: Supraglottic Airway <b>,www.medscape.com</b></span></div>
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DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-88190869050290946612010-08-31T10:41:00.000-07:002010-08-31T10:41:42.361-07:00ANAESTHESIA FOR STRABISMUS SURGERY.<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh12DyN8TlEEiWAoJKK0ImJA31kRCw8XAVv1ijkwaunA4tNgLFtZrMUfZYmQ7crnrXiBKwvfmTIszKYeFnJQZF3EwRrkPZVfwVnNvZTLagd6xQK6y2JFMUWNjlXQtCdmZ56Q7bzlmPNacF-/s1600/2.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" ox="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh12DyN8TlEEiWAoJKK0ImJA31kRCw8XAVv1ijkwaunA4tNgLFtZrMUfZYmQ7crnrXiBKwvfmTIszKYeFnJQZF3EwRrkPZVfwVnNvZTLagd6xQK6y2JFMUWNjlXQtCdmZ56Q7bzlmPNacF-/s320/2.jpg" /></a></div>One of the commonly performed ophthalmic surgery in the pediatric age group.The surgical procedure is simple and short but often associated with unexpected peri operative complications, but most of them can be successfully managed by immediate intervention by a vigilant anaesthetist.The anaesthetic concerns include controversial use of suxamethonium for induction, difficult airway, high incidence of post operative nausea and vomiting, systemic effect of topical medications,other associated congenital mal formations, oculocardiac reflex, need for post op analgesia and propensity for malignant hyperpyrexia.<br />
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<strong>Suxamethonium:</strong> Suxamethonium if used for induction can cause sustained contracture of intraocular muscles and this may affect the forced duction test performed by surgeons during surgery to estimate the amount of restriction in movement of extraocular muscles. Hence to ensure patient immobility during surgery non depolarising agents like atracurium, vecuronium or rocuronium are considered. But because of its faster action,effective relaxation of laryngeal muscles and that raise in intra ocular pressure is not very significant in strabismus surgery,some anaesthetists still prefer[1] suxamethonium for induction.The use of suxamethonium also helps the surgeon, as the globe adducts exposing a large bare area of sclera allowing for easy re insertion of cut lateral rectus[2]<br />
<strong>Incidence of Difficult Airway: </strong>Patients with squint may have associated congenital malformations like Down's syndrome,Marfans syndrome or Muscular dystrophies, with involvement of airway. Careful assessmemt of airway is mandatory before planning anaesthetic management.<br />
<strong>Effect of medications placed on eye:</strong> Eye drops are readily absorbed through hyperemic, incised conjunctiva causing systemic effects<em> Phenylephrine</em> is placed in the eye to produce mydriasis and haemostasis, however absorption of the phenylephrine can cause profound systemic vasoconstriction and hypertension.It can also cause arrhythmia and head ache. To prevent systemic hypertension only 1 to 2% phenylephrine should be used and only one drop should be put into each eye.<em>Adrenaline</em>(2%) cause hypertension & arrhythmias <em>Timolol</em> (B-blocker) causes bradycardia, hypotension & exacerbation of asthma <em> Phospoline iodide</em>(echothiophate iodide) is a long acting anti-cholinesterase used in glaucoma prolongs suxamethonium induced muscle relaxation.A patient who has been treated with echothiophate iodide can retain low blood levels of pseudocholinesterase for weeks or even months after discontinuing the medicine.Thus the use of suxamethonium is contraindicated when phospholine iodide is used for fear of post op apnea.[3]systemic effects of <em>cyclopentolate hydrochloride</em> include disorientation dysarthria and seizures.<br />
<strong>Oculocardiac reflex:</strong> Bernard Ashner and Guiseppe Dagnini first described this reflex in 1908.This reflex is a trigemino vagal reflex and is triggered by pressure on the globe or by traction on the extraocular muscles. The reflex is also triggered by ocular trauma, retrobulbar block, severe pain or by orbital compression due to hematoma or edema. the afferent impulse travels via the long and short ciliary nerves to the ciliary ganglion, then continues to the gasserian ganglion along the ophthalmological division of the trigeminal nerve and terminates at the main trigeminal sensory nucleus in the floor of the fourth ventricle. The efferent impulse travels by way of of the nucleus of the vagus nerve to the vagal cardiac depressor nerve, producing negative inotropic and conduction effects consisting of bradycardia, nodal rhythm, ectopic beats, ventricular fibrillation and rarely asystole.The surgeon should be informed immediately when this arrhythmia develops, to remove pressure or traction on the globe.<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhCNdzQzXkt5lhSLLdysfXl6teF177ukD5frcxnPulS6iRF66opFJD04UJACdtDVImQY895U-vfnPPWq_0Cykgnpfglc_6MxRNP8_96KeQMOyoc3OHcR1lt89PD6sKO0MyVrDkm_3mYuVh0/s1600/ocr.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" ox="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhCNdzQzXkt5lhSLLdysfXl6teF177ukD5frcxnPulS6iRF66opFJD04UJACdtDVImQY895U-vfnPPWq_0Cykgnpfglc_6MxRNP8_96KeQMOyoc3OHcR1lt89PD6sKO0MyVrDkm_3mYuVh0/s320/ocr.jpg" /></a></div>The treatment of oculocardiac reflex should be immediate and with intravenous injection of atropine at doses of 0.005 to 0.4 mg/kg. Anticholinergic premedication helps to prevent occurence of this reflex.Recurrent episodes require local infiltration of lignocaine near the extrinsic muscles.IV Epinephrine 6-12 mg is used for patients with cardiovascular collapse. IV Lidocaine 1.5-2 mg/kg is given for Ventricular arrhythmias along with cardiac massage. Retrobulbar block with 1 to 3 ml of 1% or 2% lidocaine (Xylocaine) may prevent oculo cardiac reflex by blocking the afferent limb of trigeminal vagal reflex. <br />
<strong>Malignant hyperpyrexia:</strong> Patients with strabismus have a higher incidence of malignant hyperthermia<strong>.</strong>In cases where susceptibility to malignant hyperpyrexia or a family history is suspected pre-treatment with dantrolene is required[3]. Study of phenylketopyruvate serum levels can be useful in predicting susceptibility to malignant hyperthermia in a patient with a questionable family history[3].The triggering agents include suxamethonium and halothane and hence the preferred general anesthetic regimen for patients with susceptibility to malignant hyperthermia is propofol,fentanyl, nitrous oxide, and a non depolarising muscle relaxant.Classicaly malignant hyperthermia occurs intraoperatively and results in rapid rise in temperature, muscle rigidity, dysrrythmias, rhabdomyolysis, acidosis and hyperkalemia. Approximately, one half of patients who develop muscle rigidity after succinylcholine are susceptible to malignant hyperthermia by the muscle biopsy and contracture test. In these patients, if creatinine phosphokinase level is more than 20,000 IU, malignant hyperthermia susceptiblity is strongly suggested. If massester muscle spasm occurs, a muscle biopsy and contacture test is indicated to confirm malignant hyperthermia.[4].The treatment of malignant hyperpyrexia include discontinuation of all anaesthetic agents, 100% oxygen,dantrolene 2.5mg/kg IV,rapid cooling to bring down body temperature correction of acidosis and hyperkalemia, and ventilatory support.<br />
<strong>Post operative nausea and vomiting:</strong>is<strong> </strong>very common following strabismus correction. The exact mechanism is not known. It may be secondary to altered visual perception or an oculoemetic reflex, which is analogous to the oculocardiac reflex.It is more common in opioid premedicated patients.Oral midazolam 0.5 mg/kg seems to be a better premedicant for strbismus cases.Intraoperative use of metoclopramide 0.1-0.15mg/kg IV,droperidol 70 mic/kg,ondansetron 0.1mg/kg, and intravenous induction of anaesthesia by propofol etc, helps to reduce the incidence of PONV.[5]<br />
<strong>Post operative pain management:</strong>is also equally important to reduce pain and discomfort in children.rectal paracetamol or diclofenac suppositories are commonly used for this purpose.Pre operative subtenon's instillation of levobupivacaine is also helpful.<br />
<span style="font-family: Georgia, "Times New Roman", serif;"><em><strong>Anaesthetic management:</strong></em></span> Strabismus surgery in adult can be performed under local anaesthesia(retrobulbar or peribulbar block) with or without sedation. Adult Un-coperative patient can be managed with total intravenous anaesthetic technique with sedative and narcotic drugs. Children will always require general anaesthesia for corrective surgery. Premedication may be given with oral midazolam 0.5 mg/kg along with atropine 0.02 mg/kg. Inhalational induction with sevoflurane in oxygen and nitrous oxide,fentanyl 1mg/kg IV,rocuronium 1 mg/kg IV or atrcurium 0.5 mg/kg IV, proseal LMA/ETT, controlled ventilation.Intravenous induction is with fentanyl 1mg/kg, propofol 2.5mg/kg,vecuronium/atracurium with nitrous oxide in oxygen and isoflurane.The use of neuromuscular monitoring is strongly advised and ECG monitoring is mandatory. It is essential to maintain normocarbia throughout the procedure.Extubation or removal of LMA attempted in deep plane of anaesthesia.Intraop prophylaxis for PONV with ondansetron or metoclopramide in suggested doses should be administered.<br />
<strong>References:</strong><br />
1)J.C Stanley, Hand Book of Clinical anaesthesia, Chrchill livingstone, 1996.<br />
2)D Abrams, British Journal of Ophthalmology,1984,64:218<br />
3)Eugene M. Helveston, M.D.Surgical Management of Strabismus: A practical and updated approach, 5th edition;<a href="http://telemedicine.orbis.org/bins/content_page.asp?cid=1-2161">http://telemedicine.orbis.org/bins/content_page.asp?cid=1-2161</a><br />
4)Practical case notes;Dr. R.C. Agarwal,Dept. of Anaesthesiology & Critical Care, Bhopal Memorial Hospital & Research Centre, Raisen by-pass Road Karond, Bhopal.<br />
5)Kenneth Davison, Clinical Anaesthesia Procedures of MGH, fifth edition.<br />
Image cortesy: <a href="http://www.nysora.com(subspeciality/ophthal">www.nysora.com(subspeciality/ophthal</a>)DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com1tag:blogger.com,1999:blog-8746726747957343433.post-76609112834651928722010-07-15T13:14:00.000-07:002013-03-10T04:04:41.156-07:00WIRELESS PAC CLINIC, THE SCOPE!<div dir="ltr" style="text-align: left;" trbidi="on">
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Do you think the PAC clinics have started disappearing? Are they essential for pre anaesthetic evaluation? This issue has recently been emerged as a topic for discussion in some Anaesthesia conference. Eventhough at first thought, you may feel this is an absurd statement,those who support this notion give some valid reasons. They strongly argue that ASA 1 and 2 patients are not benefitted from PAC as they are in good health or in mild systemic illness which is well controlled.These patients can be directly admitted to the ward by surgeons or they can report as day care cases, which will reduce the work strain of staff and doctors and that this is cost effective.This method also helps to reduce the waiting time of patients in PAC clinic. For ASA 3 and 4 pre anaesthetic check up and follow up are done in ward on a multidisciplinary approach.</div>
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The author somehow feels this is inappropriate. A well conducted PAC clinic is essential for the proper assessment of all types of patients including ASA 1 and 2. Now office based and day care surgeries are commonplace everywhere and patients seen in PAC clinic can be sent to office or day care suite direct,on the day of surgery without getting them admitted to the hospital.Even in a properly conducted preanaesthetic check up, the clinician missed certain vital informations in ASA 1 and 2 cases, which led to serious intra operative complications.Thus the necessity of a thorough and proper evaluation aided by available investigations is stressed.. Look into some of the following clinical scenario.<br />
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<b>Scenario 1,</b> <br />
A10 year old ASA 1, boy was posted for sebaceous cyst excision under GA. He was induced with propofol fentanyl and sevoflurane. LMA was inserted for airway control and left him on spontaneous. Soon after induction of anaesthesia he developed hypertension inspite of adequate depth of anaesthesia.The search for a possible cause could not reveal anything.A post op follow up by echocrdiogram and CT scan revealed mild co arctation of aorta which remained undetected. In this case a preop BP check was not performed by the anaesthetist, which was not practised as routine for ASA 1 children, in that hospital.The child had no intraoperative adverse outcome as it was a minor surgery without much hemodynamic disturbance.<br />
<b>Scenario 2,</b><br />
A 23 year old patient was posted for D&C .The PAC was unremarkable except for a tachycardia of rate 110/mt.A referral to physician was made from the surgical side for a possible cause, and a diagnosis, anxiety induced tachycardia was made.The anaesthetist gave fitness as ASA 1 and advised sedative premedication. On the day of surgery the case was reviewed and the mild proptosis with tachycardia made the second anaesthetist to think of the possibility of a thyrotoxicosis, and blood sample was sent for thyroid function tests.Meanwhile the patient had a bout of bleeding and was taken to OT for emergency curettage.A thyroid function test result after 1 hour showed severe thyrotoxicosis but patient sustained surgery without any adverse outcome.<br />
<b>Scenario 3,</b><br />
A 16 year old boy was sent for pre anaesthetic check up for excision of dermoid cyst of scalp. He had no past h/o illness and was given fitness by anaesthesia.General anaesthesia was given and he was intubated. The tumour was tightly adherent to the scalp and the surgeon was not able to remove it completely. On extubation the boy showed muscular rigidity, hypertonicity followed by generalised convulsions for 1 minute. The child remained un conscious and reintubated. Blood sample sent for electrolytes measurement. A CT scan done which showed erosion of the dermoid into the skull vault with intracranial extension.The child was shifted to a tertiary centre for neurosurgical evaluation.<br />
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Thus running a PAC clinic is a must for the proper evaluation and follow up of all pre operative patients irrespective of their ASA status, and this evaluation should include complete physical and laboratory examination with inter departmental referrals, on an outpatient basis.<br />
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The realm of anaesthesiology is now expanding. Apart from their role as perioperative physicians, anaesthesiologists are actively involved in trauma management, intensive care and pain management. Several hospitals have already integrated pain clinics to the PAC clinic for the effective delivery of pain management services. Some of this clinics are even equiped with facilities to institute nerve blocks under monitoring and even minor surgeries.Thus hospital admission and and the health risks associated,such as nosocomial infections, work load on the staff etc. can be reduced and this is found to be cost effective. Thus the need for running a full fledged PAC clinic is emphasized.<br />
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Consultation by an anaesthesiologist is essential for the proper assessment of a patient prior to anaesthesia for surgery or other procedures. The purpose is to make sure that the patient is in optimal physical state for anaesthesia and surgery and is not affected by systemic illness, and if at all affected, stable in a controlled state.The visit also helps in risk stratification according to various scoring systems and ASA physical status. Anaesthesia management is planned and informed consent for the anaesthesia procedure is obtained during the visit after fully explaining the advantages and disadvantages of a particular anaesthetic procedure. Certain guidelines have been published by various societies and associations for a proper conduct of pre anaesthetic check up. The notable one include the canadian society recommendations.[1]<br />
<b><span style="font-family: inherit;">Test Indications</span></b> :<br />
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<b>Complete blood count: </b> Major surgery requiring group and screen or group and match, Chronic cardiovascular, pulmonary, renal or hepatic disease,Malignancy ,known or suspected Anemia, Bleeding diathesis or Myelo-suppression,Patient less than 1 year of age. <br />
<b>Sickle cell screen:</b> Genetically predisposed patient (hemoglobin electrophoresis if screen is positive) <br />
<b>International normalized ratio (INR),</b> : (Activated partial thromboplastin time) Anticoagulant therapy <br />
Bleeding diathesis,Liver disease,<br />
<b>Electrolytes and creatinine levels:</b> Hypertension ,Renal disease,Diabetes Pituitary or adrenal disease, Digoxin or diuretic therapy, or other drug therapies affecting electrolytes <br />
<b>Fasting glucose level</b>: Diabetes, (should be repeated on day of surgery) <br />
<b>Pregnancy: </b> (Beta-HCG), Women who may be pregnant. <br />
<b>Electro-cardiograph:</b> Heart disease, Hypertension, Diabetes,Other risk factors for cardiac disease (may include age) Subarachnoid or Intracranial hemorrhage, Cerebrovascular accident, Head trauma <br />
<b>Chest radiograph:</b> Cardiac or pulmonary disease,Malignancy .<br />
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<b>Fasting policies:</b> Must vary, to take into account of age and pre-existing medical conditions and should apply to all forms of anesthesia, including monitored anesthesia care. Emergent or urgent procedures should be undertaken after considering the risk of delaying surgery versus the risk of aspiration of gastric contents. The type and amount of food ingested should be considered in determining the duration of fasting. Before elective procedures, the minimum duration of fasting should be <br />
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<ul>
<li>8 hours after a meal that includes meat, fried or fatty foods </li>
<li>6 hours after a light meal (such as toast and a clear fluid), or after ingestion of infant formula or nonhuman milk </li>
<li>4 hours after ingestion of breast milk </li>
<li>2 hours after clear fluids. </li>
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Premedication, when indicated, should be ordered by the anesthesiologist. Orders should be specific as to dose, time and route of administration. <br />
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According to National Institute of Clinical Excellence UK gudelines, the preop investigations are planned with due consideration of their ASA physical status and type of surgery. According to the type of surgery different grades have been proposed.[2]<br />
Grade 1: (minor) Excision of lesion of skin; drainage of breast abscess<br />
Grade 2: (intermediate) Primary repair of inguinal hernia; excision of varicose vein(s)of leg; tonsillectomy / adenotonsillectomy; knee arthroscopy<br />
Grade 3: (major) Total abdominal hysterectomy; endoscopic resection of prostate; lumbar discectomy; thyroidectomy<br />
Grade 4: (major+) Total joint replacement; lung operations; colonic resection; radical neck dissection<br />
Grade >4: Neurosurgery, Cardiovascular surgery <br />
<br />
ASA Grades: <br />
ASA Grade 1 “Normal healthy patient” (that is without any clinically important comorbidity and without clinically significant past/present medical history) <br />
ASA Grade 2 “A patient with mild systemic disease”<br />
ASA Grade 3 “A patient with severe systemic disease”<br />
ASA Grade 4 “A patient with severe systemic disease that is a constant threat to life”<br />
<br />
For eg ASA 1 patient for grade 1 surgery less than 16 years of age no investigations are required but for adults(>16 years) ECG is required above 40 years, CBC and renal function required above 60 years and urine analysis for all. CXR is not at all required.For ASA 2,3 and 4 patients for grade2,3 and 4 surgeries more detailed evaluation and risk strtification are necessary. A detailed information can be obtained from ref [2] <br />
<br />
In general the following recommendation which is widely followed in UK can be used for requesting pre op investigations, which are evidence based. <br />
<br />
<b>Urine analysis: </b>All patients,for sugar, blood and protein <br />
<b>ECG:</b> Age >50 years, History of heart disease, Lung disease or Hypertension <br />
<b>Complete blood count:</b> Males greater than 40 years, All females,All major surgery and when Anemia is suspected <br />
<b>Renal function tests:</b> Age >60 years, All major surgery, Diuretic drugs, Previous renal disease <br />
<b>Blood glucose:</b> Diabetic patients, Glycosuria <br />
<b>Coagulation screen:</b> History of bleeding tendency <br />
<b>Sickle cell screening:</b> Races where the disease is common and status unknown, if positive Hb electrophoresis should be done <br />
<b>Pregnancy:</b> Whenever there is a chance or suspicion of pregnancy <br />
<b>CXR:</b> Not routine H/o Cardiac or pulmonary disease or h/o Tuberculosis. H/o Malignancy <br />
<b>HIV status:</b> Not routine <br />
<br />
Thus for children posted for tonsillectomy, the essential investigations include Hb% and blood grouping and sickle cell status if there is a racial significance or predilection and nothing else. For circumcision in ASA 1 no investigations are necessary. <br />
<br />
The domain of PAC clinic has extended outside the anaesthetist's rooms. With the advent of third generation communication means and high speed wireless access, the concept of a wireless PAC clinic has emerged. This adds to the importance of running a well equipped PAC clinic with all facilities to deliver proper pre anaesthetic care and other services, including pain management.The components of a wireless PAC clinic include mobile phones equipped with 3G facilities,computers and high speed internet connection. A wireless communication is established between patients and physician and data related to history, investigations, and examination findings can be transferred. Advise regarding medications, consent, and other pre operative instructions can be sent to patients.The physician can verify all investigation reports and previous examination findings. CT or Ultrasound scan procedures can be visualised in real time. The exercise tolerance can be assessed using a web cam. The respiratory and heart sounds can be heard through a microphone attached to patient's chest. This process is highly useful for ASA 1 and 2 patients and for patient referral from peripheral hospital to tertiary centres.The need for patient education on computers and internet and the cost of implementation are the limiting factors.[3]<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhUAifBNrx8Jp4SD_Hre681CLev3J3TOtljJSoZgNnfaswm2hZK3mLpzXdds4TuwwHw28f5QRp0z6yFbKQZeqHDAtDOuEaNjuHcq01KVuurPw8bYljrwYthwQla3FFpKQVw3RvJxTshjA25/s1600/wirepp.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="412" rw="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhUAifBNrx8Jp4SD_Hre681CLev3J3TOtljJSoZgNnfaswm2hZK3mLpzXdds4TuwwHw28f5QRp0z6yFbKQZeqHDAtDOuEaNjuHcq01KVuurPw8bYljrwYthwQla3FFpKQVw3RvJxTshjA25/s640/wirepp.gif" width="640" /></a></div>
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<b>Ref:</b><br />
1) The Canadian Anesthesiologists' Society; <a href="http://www.cas.ca/members/sign_in/guidelines/practice_of_anesthesia/default.asp?load=preanesthetic">http://www.cas.ca/members/sign_in/guidelines/practice_of_anesthesia/default.asp?load=preanesthetic</a> <br />
2) National Institute of Clinical Excellence,UK; <a href="http://www.nice.org.uk/nicemedia/live/10920/29090/29090.pdf">www.nice.org.uk/nicemedia/live/10920/29090/29090.pdf</a> <br />
3) An article on wireless prescription by Jay Srage, Qualcomm; Arab health issue 2, 2010<br />
4) Image courtesy:<a href="http://ipcl.ee.queensu.ca/information.html"> ipcl.ee.queensu.ca/information.html </a></div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com4tag:blogger.com,1999:blog-8746726747957343433.post-52614569624699498942010-06-30T07:34:00.000-07:002010-07-27T09:23:30.507-07:00MISDIRECTED CENTRAL VENOUS CATHETER<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj6gjDDHIYbqvz1g88-OC3-k952qJIdilq0PnQc_JjlOEbAoNo2dmZBNVLdKSFp0ZZqcXaHEcpsXKBI5AUeGbdyJe2JDc7n2JdXbmleH2OhvvL4a5NW66jZdJY4Rx-xBDZbT_4WFMP6PXwT/s1600/aaaaaaaaaaaaaaaa.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" ru="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj6gjDDHIYbqvz1g88-OC3-k952qJIdilq0PnQc_JjlOEbAoNo2dmZBNVLdKSFp0ZZqcXaHEcpsXKBI5AUeGbdyJe2JDc7n2JdXbmleH2OhvvL4a5NW66jZdJY4Rx-xBDZbT_4WFMP6PXwT/s320/aaaaaaaaaaaaaaaa.jpg" /></a></div><div style="text-align: justify;"><strong>Scenario 1</strong>. A 23 yr old patient with antepartum hemorrhage was taken to OT for Caesarean section. She had profuse bleeding on table but could be controlled following delivery of baby, with blood transfusion and colloids. The chest on auscultation revealed fine basal creps and she had persistent hypotension.A central venous catheter was introduced through the right internal jugular vein. Confirmation of placement done by aspiration for free flow and rapid infusion of fluids.But the free flow was not obseved at a catheter length of 14 cm or13 cm but free flow observed at 11 cm.The patient remained ventilated and was shifted to the icu and CXR was taken The tip of the catheter appeared to be in the right subclavian vein with a slight angulation. A repeat procedure was deferred as the patient had coagulopathy and that the clinical confirmatory tests are satisfactory. The next day afternoon patient was complaining of raspiratory distress with tachypnea and pain on right side of chest. Auscultation revealed absent breath sounds on right side with dullness on percussion. A repeat CXR showed displacement of catheter tip, with massive pleural effusion on the right side which was drained subsequently.<br />
<a name='more'></a></div><br />
<strong>Scenario 2</strong>. A 30 year old patient was admitted with h/o road traffic accident.His GCS was 13 and he complained of abdominal pain. A tender and rigid abdomen was noted the pulse rate was 122/mt and BP was 90/50.A diagnosis of blunt injury abdomen was made USG abdomen was done and fluid resuscitation started.Soon he collapsed and was taken for emergency laparotomy. Central venous catheter inserted through right internal jugular and free flow confirmed. Blood and fluids were infused at moderate speed. Surgery over, resuscitation was complete and patient was shifted to icu for post operative care. CXR ordered. In the icu he had bleeding from the site of insertion of central line and infusion of fluids got obstructed.Aspiration and bright red colour of the blood raised the suspicion of arterial cannulation. ABG was confirmatory. Central line was removed and a right subclavian line secured <br />
<br />
<strong>Scenario 3</strong>. An 80 year old patient with h/o CVA and unconsciousness required central line as she had ischemic changes in ECG and because the peripheral veins are flimsy.Post procedure CXR showed the catheter tip in Rt. internal jugular vein.<br />
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<div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZEswzc6PZnoGBVQzbHe4GvylkxMb014y-5xyBgmTbjUlB1fSwJHngylW2d3R_iiWXV3zUX5BAlP8-_Nt2SAZQYUZpbamsyKF_AcsT3qeVRyfyhTiNuA1iahBDOsVRhCBgfndcQV3Vvffk/s1600/Image070.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" ru="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZEswzc6PZnoGBVQzbHe4GvylkxMb014y-5xyBgmTbjUlB1fSwJHngylW2d3R_iiWXV3zUX5BAlP8-_Nt2SAZQYUZpbamsyKF_AcsT3qeVRyfyhTiNuA1iahBDOsVRhCBgfndcQV3Vvffk/s320/Image070.jpg" /></a></div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: center;"><br />
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</div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;">In the first Scenario, the possible explanation for catheter migration into the pleural cavity could be as follows:</div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;">The catheter was in right subclavian artery and as the systemic pressure was very low it allowed free flow of fluid and back flow. The oxygen saturation will be obviously low in severe hemorrage so bright red colour of the blood was masked .As the systemic pressure improved with fluid resuscitation and with infusion of inotrops, the ejection force transmitted to the catheter by aorta made a dislodgement of the catheter and subsequent erosion into the pleural cavity and the IV infusion caused a massive pleural effusion.The same mechanism ie. internal carotid artery cannulation, operated in the second scenario but leak around the catheter when BP improved with bright red colour of the blood lead to early detection of misplacement.The third scenario shows procedure related migration of central venous catheter into the right IJV.</div><br />
<div style="text-align: justify;">Central venous cannulation is an indispensable monitoring tool in the management of critically ill patients. Of the several approaches for insertion, the subclavian route is considered as the classic procedure.During the procedure misdirection or migration of the catheter, eventhough rare, can cause some complications.</div><div style="text-align: justify;">The most commonly observed malpositioning is, the catheter is directed cephalad into the ipsilateral internal jugular vein .Other sites for malpositioning mentioned in literature include the azygos vein, left superior intercostal vein, hemiazygos vein, lateral thoracic vein, inferior thyroid vein, left superior intercostal vein, thymic vein, and pleural cavity [1] . Contralateral subclavian is an extremely unusual site for malpositioning Malpositioning may not serve the purpose of insertion and most often needs revision of the procedure.It is both time and resource consuming. Misplacement of the catheter tip can enhance the risk of clot formation and cause thrombophlebitis. The other complication is catheter migration, which is uncommon but dangerous . The catheter can erode into the pleural cavity as in the first case or a catheter abutting the wall of superior vena cava can cause perforation and profuse hemorrhage.It was seen that carotid artery puncture occurred in 8.3% of patients undergoing internal jugular vein cannulation.[2]<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1JXUyrguz-wXVSE1vqsBzXbDoqWT5OXahJAImul5TXzDu1SltAvsC9RK9edG63qHT0ltz_SVCq_g_SbeWbgkRLIXVARyFAqm-yPqku7lrK3RzcPF_M8NOiSqz6xk2lQP1ylNUmrlM-kkT/s1600/24072010052000.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="300" hw="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1JXUyrguz-wXVSE1vqsBzXbDoqWT5OXahJAImul5TXzDu1SltAvsC9RK9edG63qHT0ltz_SVCq_g_SbeWbgkRLIXVARyFAqm-yPqku7lrK3RzcPF_M8NOiSqz6xk2lQP1ylNUmrlM-kkT/s400/24072010052000.jpg" width="400" /></a></div><div class="separator" style="clear: both; text-align: center;">CXR showing catheter malposition into contralateral subclavian vein in a trauma victim.</div><strong>How to prevent Malposition during the procedure?</strong></div> The positioning of guidewire has a role. A randomized, controlled study, suggest that keeping the guide wire J-tip directed caudad increased correct placement of central venous catheters towards the right atrium [3]. It was also postulated that there is a relationship between the length of the guidewire and catheter malposition. Some authors implicate excessive guidewire length as cause for this complication and recommends a guidewire length of 18 cm which should be considered as the upper limit [4].It is also seen that a steep head low to fill the central lines is associated with increased venous pressure which preferentially direct the floating guidewire to the neck veins.<br />
<br />
<strong>How to detect Malposition while placing?</strong><br />
<ul><li>Aspiration of blood; free flow should be tested using a syringe of at least 20 mL in volume,and the aspiration of blood should be without resistance (or back flow into the infusion aided by gravity.)</li>
<li>Rapid infusion of saline,unobstructed flow</li>
<li>Observing the ECG tracings during guidewire placement, configuration of 'p' wave.</li>
<li>Observing the classic central venous pressure tracings</li>
<li>Using the real-time ultrasound guided technique for puncturing and cannulating the internal jugular vein [5] It has been shown that under ultrasound guidance, the jugular vein could be entered on the first attempt in 83.3% of patients.</li>
<li>Using a doppler probe (the one used by obstetricians for fetal monitoring may suffice)[6] </li>
<li>Endocavitory ECG , can guide correct placement of catheter in superior vena cava.Here the catheter is connected to the ECG recorder wire to record ECG in Lead II, considered as an alternate method to check the position of the catheter. When the catheter enters the right atrium, there is a large increase in the amplitude of P wave.This technique is cheaper, and of similar efficacy to the radiological method. Endocavitary ECG can replace chest X-rays to check the position of the catheter in more than 90% of cases[7]</li>
<li>Fluoroscopic guidance during the procedure helps to assess the position of the catheter, any vascular abnormalities or stenosis and can be used to find out misplaced catheter.</li>
<li>The simple technique for detection is called The IJV occlusion test: After placement occlude the IJV by external pressure over the neck(in the supraclavicular area for approximately 10 sec.A flattened trace and increase in CVP of approximately 5 mmHg suggests misplacement of catheter into IJV.This is especially useful for subclavian vein cannulation[8]</li>
<li>Another simple and sensitive bed side method for detection is the 'Saline flush test'.Used to detect subclavian catheter malposition in IJV. Flush test was performed by injecting 10 ml of normal saline in the distal port of catheter, while anterior angle of ipsilateral neck was palpated by an independent observer. A thrill of fluid elicited on the palm of hand (positive test) was suggestive of catheter misplacement.This may be confirmed by fluroscopy[9]</li>
</ul> Fig: demonstrating the saline flush test, By courtesy of Ref [9] <br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiIWMtgk64tmceU2wkERul1pQCWBcIPcESLt3e6x3W5lq6Lw70S-aLE1cyuOx8fXE05JnA1eH5FmWYtJnCJwcjKRYOmbByD18tK2pxHks4LK2RFp4cO_0Idm-ggLMdnUz0hvJqhOmuoFWx6/s1600/saline+flush.gif" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="168" ru="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiIWMtgk64tmceU2wkERul1pQCWBcIPcESLt3e6x3W5lq6Lw70S-aLE1cyuOx8fXE05JnA1eH5FmWYtJnCJwcjKRYOmbByD18tK2pxHks4LK2RFp4cO_0Idm-ggLMdnUz0hvJqhOmuoFWx6/s200/saline+flush.gif" width="200" /></a></div><div></div><ul><li>CXR: A post procedural CXR is the most commonly used method to find catheter malposition.A positon at the junction of the the superior vena cava and right atrium is considered ideal, where the catheter tip is imaged just above the carina.In suspected cases of catheter migration a lateral CXR is also indicated.The unusual position of catheter as in the internal mammary vein will be located more laterally, the pericardio phrenic vein will follow the left cardiac border,and the superior intercostal vein will follow the aortic knob and frequently reveal an aortic nipple,while the superior intercostal vein will occupy the posterior mediastinal position in lateral view.</li>
<li>Other techniques for detection of malposition are CT scan or venography but are employed when other measures are failed</li>
</ul><strong> How to correct Malpositioning or Misdirection after placement?</strong> <br />
<strong></strong> <br />
The author prefers the following procedure.The patient may be positioned semirecumbent my minimal elevation of the head end of the cot. The central venous catheter (CVC) is withdrawn upto 4-5 cm mark A fresh guidewire is inserted through the catheter but advanced upto12-14 cm only.The new CVC is then reinserted after applying pressure over the ipsilateral IJV.Always use a new CVC as guidewire can damage the previous catheter while insertion.Subsequently a flush test or IJV occlusion test may be performed to assess the positon.The CXR is now repeated.A risk of air embolism is there associated with minimal head up position but rare and all precautions should be taken.<br />
<br />
<strong>Related post: Supraclavicular CVC insertion, <a href="http://anaesthesiatoday.blogspot.com/2010/02/central-venous-cannulation-which-route.html">http://anaesthesiatoday.blogspot.com/2010/02/central-venous-cannulation-which-route.html</a></strong><br />
<br />
<div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;"><strong>Ref:</strong>1) Currarino G. Migration of jugular or subclavian venous catheters into inferior tributaries of the brachiocephalic veins or into the azygos vein, with possible complications. Pediatr Radiol 1996 ;26:439-49. </div> 2) Denys BG, Uretsky BF, Reddy PS. Ultrasound-assisted cannulationof the internal jugular vein. A prospective comparison to the externallandmark-guided technique. Circulation 1993;87:1557-62.<br />
3) Tripathi M, Dubey PK, Ambesh SP. Direction of the J-tip of the guidewire, in seldinger technique, is a significant factor in misplacement of subclavian vein catheter: a randomized, controlled study. Anesth Analg 2005 ;100:21-4.<br />
4) Andrews RT, Bova DA, Venbrux AC. How much guidewire is too much? Direct measurement of the distance from subclavian and internal jugular vein access sites to the superior vena cava-atrial junction during central venous catheter placement. Crit Care Med 2000 ;28:138-42.<br />
5) Farrell J, Gellens M. Ultrasound-guided cannulation versus the landmark-guided technique for acute haemodialysis access. Nephrol Dial Transplant 1997;12:1234-7.<br />
6) Paul Marino The ICU Book 3rd edition<br />
7)Calabuig R, Sueiras A, Galera MJ, Ortiz C, Pi F, Sierra E. Central venous catheter location by endocavitary ECG: an alternative to chest radiography Med Clin (Barc). 1997 Sep 20;109(9):324<br />
8)Ambesh SP, Pandey JC, Dubey PK, Internal jugular vein occlusion test for rapid diagnosis of misplaced subclavian vein catheter into the internal jugular vein. Anesthesiology. 2001 Dec;95(6):1377-9.<br />
9)G P Rath, P K Bithal, G R Toshniwal, H Prabhakar, H H Dash Rath GP, Bithal PK, Toshniwal GR, Prabhakar H, Dash HH."Br J Anaesth. 2009 Apr;102(4):499-502. Epub 2009 Feb 25".Saline flush test for bedside detection of misplaced subclavian vein catheter into ipsilateral internal jugular vein. <br />
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<em><span style="font-family: Times, "Times New Roman", serif;"><strong>Post image by courtesy of AZ Rainman;</strong></span></em> <a href="http://www.freakingnews.com/Necks-Pictures--1489-0.asp">www.freakingnews.com/Necks-Pictures--1489-0.asp</a>DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com1tag:blogger.com,1999:blog-8746726747957343433.post-87458261707933254502010-06-21T11:39:00.000-07:002010-07-27T09:25:22.858-07:00ARTIFICIAL BLOOD, HOPE FOR THE FUTURE?<div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiuxc2R1jU8BuGBTiumzLcRGrW-3dogG6-_vKkn2QLgil5lOnCT7OtTtLeHQ5ZtSQt64Vvml_XR95ytPpUmMkuCTfPBXVoYo5iduuusOPoWmg4mce6hx65S_T507Oa8f45nToq-PE36juyN/s1600/_45591818_blood_new203.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" qu="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiuxc2R1jU8BuGBTiumzLcRGrW-3dogG6-_vKkn2QLgil5lOnCT7OtTtLeHQ5ZtSQt64Vvml_XR95ytPpUmMkuCTfPBXVoYo5iduuusOPoWmg4mce6hx65S_T507Oa8f45nToq-PE36juyN/s320/_45591818_blood_new203.jpg" /></a></div>A sigh of relief, the tension is relieved as the gynaecologist took the baby out with great difficulty through the incision. The indication for caesarean section was severe fetal distress and the OT atmosphere has now turned pleasant as the paediatrician reported that the APGAR score is 9. The anaesthesiologist is busy preparing oxytocin infusion and sedation.The patient who was given regional anaesthesia is now anxious to see her baby.But the enjoyment did not last long as the surgical team noted profuse bleeding with a flabby uterus not responding to ergometrine or oxytocin.A request for issuing blood was sent to blood bank but the request was returned ,stating that the husband refused any kind of blood transfusion as he is a strict <em>Jehovah's witness</em> which he didn't mention at the time of taking the consent!<br />
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<div> Jehovah's witnesses, a fellowship of more than 1 million americans, object to the administration of blood in any form for any indication.This objection is based on "THE HOLY BIBLE" Acts 15:28,29 which states "For it has seemed good to the Holy Spirit and to us to lay on you no greater burden than these requirements: that you abstain from what has been sacrificed to idols, and from <strong>blood</strong>, and from what has been strangled, and from sexual immorality. If you keep yourselves from these, you will do well. Farewell.” According to them blood removed from the body should be discarded "You should pour it upon the ground as water" (Deuteronomy 12:24.)This makes pre operative blood conservation technique like preoperative phlebotomy and storage impractical</div>The search for an oxygen carrying blood substitute started with world war II as the military realized the difficulties of whole blood transport and storage.Subsequently several trials were made to bring out an ideal blood substitute using chemicals which can carry oxygen.<br />
<span style="font-family: Georgia, "Times New Roman", serif;"><strong>1<em>)Perfluorocarbon compounds</em></strong></span>:Of the various substances that carry or facilitate the transport of oxygen the perfluorocarbons gave the most promising results.They were created by replacing H2 atoms of hydrocarbons with flurine. This was following the first real success in "fluid breathing system" proposed by Leland Clark in 1966. He found that oxygen and carbondioxide are very much soluble in fluorocarbon liquids and can be used for artificial ventilation of the lungs which are immersed in these compounds where satisfactory oxygen uptake and giving out of CO2 takes place by the alveoli through the liquid media, in the absence of external oxygen supply.He performed his experiment in anaesthetised rat where the animal is paralysed intubated and immersed in PF liquid.After bubbling oxygen through the liquid this is pumped into the animal's lungs and recirculated. Most of the animals kept in the fluid for upto an hour survived for several weaks. Subsequently trials were made in humans during war time.<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEge28GTXHLLWUexd5_MJqMaXSQXb3QpM1_G-WWmg2_IKCXm9XJmxEIKuzI_xbKTSJl2Ky3DHqtFWfyPZysiWGg_N0O_wBwjOKWuETrf__dJioZrD18sIyn5SucwCQQR0s1Yfvs8G21n9kYN/s1600/mouse.JPG" imageanchor="1" style="clear: right; cssfloat: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" qu="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEge28GTXHLLWUexd5_MJqMaXSQXb3QpM1_G-WWmg2_IKCXm9XJmxEIKuzI_xbKTSJl2Ky3DHqtFWfyPZysiWGg_N0O_wBwjOKWuETrf__dJioZrD18sIyn5SucwCQQR0s1Yfvs8G21n9kYN/s320/mouse.JPG" /></a> Figure: Demonstrating a living mouse immersed in perfluorocarbon compound along with a goldfish.<br />
<ul><li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong>Fluosol-DA</strong> was the most notable compound among PFCs, regarded as a <strong>first generation</strong> PFC.It contained perfluorodecalin and perfluorotripropylamine emulsified with Pluronic F-68 It was approved by the FDA for use in percutaneous transluminal coronary angioplasty initially but was subsequently withdrawn(see below)</li>
<li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;">They have high affinity for oxygen approximately 10-20 times greater than plasma.The oxygen content of PFCs is directly proportional to oxygen partial pressure and are most efficient as oxygen carriers at a partial pressure of more than 300mmHg, which limited their use, as patients needed high inspired oxygen concentration. A short intravascular half life, unstable at extreme temperatures, Low oxygen carrying capacity ,poor shelf life and adverse effects such as acute complement activation and disruption of pulmonary surfactant, all lead to their withdrawal from the market. But still these compounds have found some place in "Liquid ventilation" of lungs in ARDS. <a name='more'></a></li>
<li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;">Perfluorocarbons demonstrate a linear oxygen dissociation curve in contrast to the sigmoid dissociation curve of blood and oxygen transport is enhanced by elevated PO2. Because of this linear relationship the oxygen delivery to the capillaries remained unsatisfactory as most of the oxygen get dissociated before the blood reaches the capillaries.</li>
<li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong>Second generation</strong> PFCs: A mixture of perfluorooctyl bromide and perfluorodecyl bromide was introduced later on, which used egg yolk lecithin as emulsifier.This compound was termed <strong>Oxygent</strong>. The oxygen carrying capacity was 2-3 times that of Fluosol-DA and was more stable at room temperature. This product is now under phase 3 clinical trial.Febrile reactions, cerebrovascular insufficiency and transient thrombocytopenia are the adverse reactions observed with oxygent.</li>
<li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;">Other PFC emulsions that have been developed include Perftoran; Oxycyte ( entering phase II trials), and Oxyfluor</li>
</ul><div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong>2)<span style="font-family: Georgia, "Times New Roman", serif;">Hemoglobin based oxygen carriers;(HBOC) or Stroma free Hb. </span></strong></div><ul><li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><span style="font-family: inherit;">The finding that native Hb is not antigenic, led to the development of <strong>hemoglobin solutions</strong> or <strong>stroma</strong> <strong>free hemoglobin</strong>.The red cells are removed and hemoglobin isolated and maintained as solution.They withstood sterilisation and had a shelf life of 2 years.Rapid administration (as they are not antigenic) and easy availability were other advantages. But they are not as effective at oxygenation as packed RBCs because of their high affinity to oxygen.They have a reduced circulatory half life as the Hb tetramers are split to dimers and are cleared from blood stream by glomeruar filtration and uptake by RE system.They are hyperosmolar solutions and significantly increase plasma oncotic pressure. Renal dysfunction,coagulopathy and liver dysfunction are the other side effects observed.They bind to nitric oxide and can cause hypertension. Several approaches were made to prevent the toxicity and to decrease the avidity of Hb to oxygen ,and as a result modified hemoglobins were introduced.</span></li>
<li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong>Crosslinked hemoglobins:</strong> Diaspirin cross-linked hemoglobin (DCLHb) is the prototype molecule of this category of blood substitutes. Stability of the molecule is achieved by cross-linking between the two alpha chains and thus dissociation is prevented and the circulating half life is extended. Both intermolecular and intramolecular crosslinkage was experimented. It was found that a bifunctional agent, 2-Nor-2-formylpyridoxal 5-phosphate which is also a 2,3-DPG analogue can intramolecularly crosslink the 2 beta subunits of the hemoglobin molecules and the resulted compound has less oxygen affinity and high oxygen carrying capacity.Diaspirin cross linked Hb(DCLHb) made from outdated human blood has a shelf life of approximately 9 months when frozen and 24 hours when refrigerated. The intravascular half-life is 2-12 hours and is dose dependant but the raise in colloid oncotic pressure was a concern. Eventhough it increased blood oxygen content, intense vasoconstriction causing high vascular resistance, reduced cardiac output, and high heart rate were undesirable for the critically ill patients and the manufacturers halted further development of DCLHb in 1998.</li>
<li style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong>Polymerised Hemoglobins:</strong> The next step in the development was to polymerise the crosslinked tetramers to reduce oncotic pressure and to avoid filtration by kidneys.The crosslinking agent was glutaraldehyde. Since it was difficult to control the Hb-glutaraldehyde polymerization reaction which yielded products of various molecular sizes and the viscosity of the solution was high, the results were not promising.The polymerisation reaction is as below</li>
</ul><div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"> H-CO-(CH2)3-CO-H + HB-NH2 = HB-NH-CO-(CH2)3-CO-NH-HB</div><div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"> glutaraldehyde hemoglobin Crosslinked Hemoglobin </div><ul><li><br />
<div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><span style="font-family: Georgia, "Times New Roman", serif;"><em>PolyHeme:</em></span> is a first-generation pyridoxylated polymerized hemoglobin made from outdated human blood and is currently being evaluated in a phase III clinical trial that is enrolling patients.The purified Hemoglobin is chemically modified into a polymerised form and incorporated into solution. 1 gram of Polyheme contains 50 grams of modified hemoglobin.which is almost same as that of blood and the use of a 2,3-DPG analogue, pyridoxal phosphate, to crosslink hemoglobin improved the P50. It has a half-life of 24 hours, a shelf life longer than 12 months when refrigerated, and a p50 of 28-30 mm Hg.Polymerised polynitroxyl Hb, (Hemozyme) is a vasodilator, an antioxidant and an antiinflammatory agent and can be used in ischemia reperfusion and inflammation.Also beneficial in post reperfusion multi organ dysfunction syndrome.Other first-generation polymerized hemoglobin products include HbOC-201, <span style="font-family: Georgia, "Times New Roman", serif;"><em>Hemopure and HemoLink</em></span>. <span style="font-family: Georgia, "Times New Roman", serif;"><em>Hemopure</em></span> is a polymerized form of bovine hemoglobin with a p-50 of 30 mm Hg that is closer to human hemoglobin compared to stroma-free hemoglobin. It has an intravascular half-life of 8-23 hours and a shelf life of 36 months at room temperature. <span style="font-family: Georgia, "Times New Roman", serif;"><em>Hemopure</em></span> is approved in South Africa for the treatment of anemic patients for surgery to avoid or reduce transfusion needs but following phase II trials the US withhold its use due to adverse reactions including strokes and myocardial infarction.</div></li>
<li><br />
<div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong>Conjugated Hemoglobins:</strong>Conjugation of Hb is done by covalent binding of Hb to a biocompatible polymer, such as polysaccharide, in order to increase its overall size.This process achieved same results as that of polymerisation with regard to stability and improved oxygenation. Polyethylene glycol modified Human Hb (Hemospan) has the advantage of low affinity and increased oxygen transport capacity.Pegylation(using poly ethylene glycol) of hemoglobin prevents immunological reactions and these compounds claim the longest circulating half life of upto 12-20 hrs.</div></li>
</ul><br />
<div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong><span style="font-family: Georgia, "Times New Roman", serif;">3) Encapsulated hemoglobin:</span></strong> Artificial red blood cells. Efforts have been made to encapsulate hemoglobin within a lipid-membrane to create a compound capable of carrying oxygen while not being associated with significant vasoconstriction. These liposomes appear to be retained in plasma for a significant period. These have P50 and oxygen dissociation curve similar to red blood cells, since 2-3-DPG is reatained inside Hemoglobin also stays inside as tetramers. These artificial red blood cells do not have blood group antigens on the membrane and therefore do not participate in antigen antibody reactions.The major problem with these artificial cells is that they are rapidly cleared off the circulation by the reticuloendothelial system resulting in reduced circulatory half life.Preparation of smaller submicron lipid membrane artificial red blood cells resulted in improvements in circulation time.Other than activation of the reticuloendothelial system these artificial cells are difficult to produce and they stimulate the complement pathway. They also activate platelets. </div><div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><strong><span style="font-family: Georgia, "Times New Roman", serif;">4) Recombinant human hemoglobin:</span></strong> </div><div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;">The next generation HBOCS.The first recombinant hemoglobin product, rHb 1.1 (Optro, Somatogen and Eli Lilly) was a genetically engineered variant of human hemoglobin, Hemoglobin Presbyterian, with modifications to decrease its oxygen affinity. The human gene responsible for producing Hb is copied and modified with the intent to enhance the stability and and functionality of the Hb including reduced side effects.Copies of this gene are then inserted into the DNA of a highly controlled population of E-Coli and the bacteria produce Hb which is subsequently purified.The product had an intravascular half-life of 2-19 hours and a shelf life of 18 months when refrigerated. The adverse effect profile was similar to DCLHb and consisted of vasoconstriction, GI distress, fever, chills, and backache. Currently, the production of this compound has been discontinued due to safety concerns.</div><div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"></div><div><strong>Ideal blood substitute:</strong> Should satisfy the following criteria</div><ul><li>High oxygen carrying capacity</li>
<li>lack of antigenecity</li>
<li>Stable shelf life</li>
<li>Stable and prolonged intravascular half life of weeks to months.</li>
<li>Free of infectious complications</li>
<li>Free of adverse effects or systemic toxicity</li>
<li>Easy to produce in large scale</li>
<li>Cost effective</li>
</ul><strong>Advantages of blood substitutes:</strong><br />
<br />
<ul><li>Universal compatibility; helpful in emergency</li>
<li>Purity and non toxicity; free of infectious agents and allergens</li>
<li>Storage and shelf life; need not be refrigerated and ideal in remote areas, fields, and disaster situations.</li>
<li>Availability; readily available in large quantities</li>
<li>predictability; has ingredients which are known and understood and the effects can be predicted</li>
</ul><strong>Adverse Effects Related to Blood Substitutes(In general)</strong><br />
<br />
<ul><li>Adverse effects associated with hemoglobin-based oxygen carriers include hypertension, abdominal pain, skin rash, diarrhea, jaundice, hemoglobinuria, oliguria, fever, stroke, and laboratory anomalies such as an elevation in lipase levels. Although most of these side effects were transient and clinically asymptomatic, many clinical trials involving these agents have been discontinued or held due to the associated adverse effects</li>
</ul><strong>The general benefits of HBOCs over transfused red bloodcells:</strong><br />
<ul><li>No prior planning needed eg emergency use</li>
<li>Faster & better O2 distribution </li>
<li>Ready to use </li>
<li>No equipment needed</li>
<li>Long shelf life </li>
<li>No refrigeration required</li>
<li>Universally compatible </li>
<li>Immediately offloads oxygen</li>
<li>No 2,3-DPG </li>
<li>Can be used by <em>Jehovah's Witnesses</em> </li>
</ul><strong>Other applications of PFCs:</strong>Other than oxygen carrying agents in hemorrhage or anaemia, they could be incorporated into solutions used in open heart surgery, and in supplying devascularized organs with oxygen prior to transplantation.They may be used to perfuse the myocardium or brain tissue in heart attacks and strokes, oxygenating obstructed regions due to capillary blockage and for mechanical ventilation in ARDS.In cancer therapy they are helpful to increase oxygenation of tumours which may help radiation therapy. Chemotherapeutic drugs could be added to the PFC and delivered to the target organ affected by cancer.It was also observed that toxic doses of PFCs resulted in necrosis of tumour cells.They had promising results in the treatment of fungal or bacterial infections of skin and GI tract, carbon monoxide poisoning, Alcheimer's disease and medical imaging.Clinical conditions like a/c MI, cardiac failure,thromboembolism, air embolism,hepatic failure, a/c renal failure and preservation of donor organs etc also make use of the oxygen carrying capacity of these compounds.<br />
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In spite of many years of research, the ideal blood substitute continues to elude researchers.Continued research helped them to reduce the complications and limitations associated with HBOCs. Initial problems in the development which were related to potential toxicity, poor half life, poor oxygen carrying capacity and limitations with animal studies.( which may not reflect human response). Most of the recent attempts are focussed to bridge this gap to prove the safety of these agents in humans and many of these problems have now been solved by extensive basic studies on Hemoglobin. Crosslinked hemoglobin would be the first modified hemoglobin available for routine clinical use.Hopefully, as better blood substitutes are developed and enter routine clinical use, the need for blood transfusions in the operative and trauma settings will decrease. <br />
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<strong>Recent advances:</strong> Researchers are hunting around stem cells for the possible production of hemoglobin. Major research is underway in the UK and US to utilize stem cells to generate blood without a donor. That is, stem cells can be used to generate synthetic blood in a lab which is very much identical to human blood in all aspects.The blood taken from newly cut umbilical cords or adult stem cells, such as induced pluripotent stem cells (iPSCs) can be used to generate Hb. .According to <em><strong>telegraph,</strong></em> The British scientists are planning a ground-breaking research project to create synthetic human blood from embryonic stem cells, The three-year project will be led by the Scottish National Blood Transfusion Service and includes NHS Blood and Transplant and the Wellcome Trust, the world's biggest medical research charity. The artificial blood will be made from the stem cells of human embryos left over from IVF treatment.Such blood produced from stem cells would have the benefit of not being at risk of infected with viruses such as HIV and hepatitis.The project lead Professor Marc Turner stated "We could provide an unlimited supply of blood in this way" The idea is to produce O -ve red cells in the laboratory from stem cells. Fig. by courtesy of BBC UK<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzxNrWpkhZ6Da7hA7-cT9mQpmxtchSISu_z-1UrPwXlM4-G0nO49UUs-dhQTrMi0j9RdNbx9Qewk_CbPyzJxVZfRC2t5zm7uv7jS7H8-y77psDLbvaenkPzcnIUKrpWiJYhH_4sTVPcdDa/s1600/_45592390_stem_cells_226.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" ru="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzxNrWpkhZ6Da7hA7-cT9mQpmxtchSISu_z-1UrPwXlM4-G0nO49UUs-dhQTrMi0j9RdNbx9Qewk_CbPyzJxVZfRC2t5zm7uv7jS7H8-y77psDLbvaenkPzcnIUKrpWiJYhH_4sTVPcdDa/s320/_45592390_stem_cells_226.gif" /></a></div><br />
<strong>1</strong>) Embryo created from IVF is tested for O-negative blood group, then allowed to develop for several days until stem cells can be extracted<br />
<strong>2</strong>) Stem cells are cultured in laboratory with nutrients to stimulate red blood cell creation<br />
<strong>3</strong>) Nuclei are removed in final stage to produce oxygen-carrying mature blood cells. Trillions of these will be needed to build up a blood bank.<br />
<strong>References:</strong><br />
1) Sara J Grethlein, MD, Arun Rajan, MD, Blood substitutes:<br />
<a href="http://emedicine.medscape.com/article/207801-overview">http://emedicine.medscape.com/article/207801-overview</a><br />
2) <a href="http://www.telegraph.co.uk/.../British-scientists-to-create-synthetic-blood-from-embryonic-stem-cells.html">http://www.telegraph.co.uk/.../British-scientists-to-create-synthetic-blood-from-embryonic-stem-cells.html</a><br />
3) <a href="http://www.onenewspage.co.uk/news/Health/.../Synthetic-blood-from-embryos-bid.htm">www.onenewspage.co.uk/news/Health/.../Synthetic-blood-from-embryos-bid.htm</a><br />
4) <a href="http://community.advanceweb.com/.../artificial-blood-why-and-when.aspx">community.advanceweb.com/.../artificial-blood-why-and-when.aspx</a><br />
5) Benesch R, Benesch RE, Yung S, Edalji R. Hemoglobin covalently bridged across the polyphosphate binding site. Biochem Biophys Res Commun 63:1123, 1975.<br />
6) Blood substitutes excerpt:eMedicine.com,inc.<br />
7) Scott MG, KucikDF,GoodnoughLT: Blood substitutes evolution and future applications, ClinChem 1997; sept43(9);1724-31<br />
8) Cohn SM: Blood substitutes in surgery.Surgery2000;127(6):599-602<br />
9) Anaesthesia UK web site.DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com2tag:blogger.com,1999:blog-8746726747957343433.post-6337636140458884212010-05-14T13:58:00.000-07:002010-07-27T09:27:10.103-07:00HOW TO WEAN AND WHEN?<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjUkFmRPvbxg2oStqWqqQtYQCVwNu-GbKYOwJ0iQoEsGQb9_IyMOYYdBGWebEfzBAlX8BC1fcxUZv_VxO-XW7MZqxT5wp8f3lM4etCxPtL60SRvTItl-jjF-WGYPmABu1Ip-Drk4UZZS4jo/s1600/images10.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjUkFmRPvbxg2oStqWqqQtYQCVwNu-GbKYOwJ0iQoEsGQb9_IyMOYYdBGWebEfzBAlX8BC1fcxUZv_VxO-XW7MZqxT5wp8f3lM4etCxPtL60SRvTItl-jjF-WGYPmABu1Ip-Drk4UZZS4jo/s320/images10.jpg" wt="true" /></a></div>A patient is considered fit for weaning from ventilator when he is conscious responsive and hemodynamically stable and when the pathology which necessitated mechanical ventilation has been resolved adequately.Improved patient outcomes and decreased costs are two benefits of implementing a protocol for early weaning from ventilator.A simplified approach to weaning off ventilator is described below.<br />
<br />
<strong>1)<em>.<span style="font-family: Georgia, "Times New Roman", serif;">Criteria to determine whether a patient can be given a trial of spontaneous breathing.</span></em></strong><br />
<strong>Repiratory criteria:</strong><br />
<ul><li>PaO2 > 60 mmHg on Fio2 40-50% and peep less than 5-8 cmH2O</li>
<li>PaCO2 normal or baseline</li>
<li>Adequate inspiratory effort</li>
</ul><strong>Cardiovascular criteria:</strong><br />
<ul><li>No evidence of myocardial ischemia</li>
<li>Heart rate less than 140/mt.</li>
<li>Blood pressure normal without inotrops or minimal inotropic support eg: dopamine <5 mic/kg/mt</li>
</ul><strong>Adequate mental status:</strong><br />
<ul><li>GCS >13 and arousable</li>
</ul><strong>Absence of correctable comorbid conditions:</strong><br />
<ul><li>Afebrile</li>
<li>No significant electrolyte abnormalities</li>
</ul><strong>2)</strong> <em><strong><span style="font-family: Georgia, "Times New Roman", serif;">Criteria to determine whether patients can tolerate spontaneous breathing trial</span></strong></em><br />
<ul><li><span style="font-family: inherit;">Tidal <em>volume</em> 5-7 ml/kg threshold >4-6 ml/kg</span></li>
<li>Respiratory rate 10-18beats/mt threshold <30/mt.</li>
<li>RR/VT ratio 20-40 /LTR threshold 100/LTR</li>
<li>Max insp. pressure -90to -120 cm H2O threshold -15 to -30 cm H2O</li>
</ul>The RR/VT ratio or rapid shallow breathing index is a useul predictor. Value above 105/LT, 95% of the attempts are successfull.<br />
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<strong>3)</strong> <strong><span style="font-family: Georgia, "Times New Roman", serif;"><em>Spontaneous breathing trials (SBT)</em></span></strong><br />
<ul><li><span style="font-family: inherit;"><strong>Breathing through ventilator:</strong> The advantage is TV and RR can be monitored and apnea ventilation mode is utilised to detect apnea.The disadvantage is extra work of breathing offered by the circuits and valves.</span></li>
<li><strong>Pressure support ventilation: </strong>A positive pressure of 5-7 cm of H2O is kept to overcome the problems due to increased resistance and increased work of breathing (helps to gradually assume more more work of breathing)</li>
<li><strong>Breathing through T Piece:</strong> Known as the T piece trial,The advantage is reduced work of breathinge the disadvantage is the inability to monitor TV and RR and to provide the desired FIO2</li>
<li><strong>Airway pressure release ventilation: </strong>The patient breaths with a high continuous positive airway pressure and at a point the expiratory valve opens and pressure drops down to a lower level or baseline.It remains there for 1-2 seconds and again the original CPAP is reapplied.It is claimed that APRV provides good gas exchange at lower mean airway pressures and thus weaning is thought to be easy.</li>
</ul><strong><em><span style="font-family: Georgia, "Times New Roman", serif;">Protocol for weaning</span></em></strong><br />
<ul><li><span style="font-family: inherit;">Initial trial shuold be for 30-120 mts and if tolerates higher chance for permanent weaning</span></li>
<li>For short term ventilatory suport, ie for post op ventilation one hour is enough</li>
<li>In case of prolonged ventilatory support for eg: more than 'days' a trial for upto 8-24 hours may be given</li>
</ul><strong><em><span style="font-family: Georgia, "Times New Roman", serif;">Failure to wean</span></em></strong><br />
<ul><li><span style="font-family: inherit;"><strong>Dependance: </strong>The only possible way to treat ventilator dependancy is by frequent weaning trials</span></li>
<li><strong>Low cardiac output:</strong> Due to high intrathoracic pressure causing reduced venous return or more negative intrathoracic pressure preventing ventricular emptying.CNS blood supply and diaphragmatic blood supply and thereby oxygenation are affected due to low cardiac output</li>
<li><strong>Over feeding:</strong> Excess CO2 produced due to metabolism of carbohydrates stimulate ventilation and increase the work of breathing So calorie intake should match calorie requirement.</li>
<li><strong>Neuromuscular weakness:</strong> due to hypoproteinemia or critical illness neuromyopathy may affect the intercostal muscles or diaphragm</li>
<li><strong>Metabolic:</strong> Hypomagnesemia or hypocalcemia may affect the proper functioning of respiratory muscles</li>
</ul><strong><em><span style="font-family: Georgia, "Times New Roman", serif;">Other points to note:</span></em></strong><br />
<ul><li><span style="font-family: inherit;">Optimum hemoglobin</span></li>
<li>Absence of arrhythmias</li>
<li>PaO2/FiO2 >150</li>
<li>Normal ABG values.</li>
</ul><strong>References:</strong><br />
1). Esteban A, Alia I, Gordo F, et al. Extubation outcome after spontaneous breathing trials with T-tube or pressure support ventilation. The Spanish Lung Failure Collaborative Group. Am J Respir Crit Care Med. 1997;156(2 pt 1):459-465<br />
2) Manual of Intensive Care Medicine, James Ripple<br />
3) Paul L Marino The ICU Book 3rd edition<br />
4) Oxford Hand Book of Critical Care<br />
5)CHEST: 120/ Number 6/ Dec 2001/suppl evidence based guidelines for weaning <br />
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<a href="http://ccforum.com/content/4/2/72">http://ccforum.com/content/4/2/72</a> discontinuing ventilatory supportDR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-46719193511852829892010-05-07T05:41:00.000-07:002010-05-20T12:04:18.814-07:00STRESS AND ANAESTHETIST<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTwijjhiSHKKeUFzE252PzEcL6D36KmekkVjGFC4C3gGgcCgUiLtzxdCIKm_vtQaMF8u_DLPrDbyve4-gXBRjB9hmqlzR-X9CiZfRWaaLbe5wYcpROrCKTUP3j8eIphvqIxJs6mASVT3ox/s1600/cw_14_mainpict.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="143" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTwijjhiSHKKeUFzE252PzEcL6D36KmekkVjGFC4C3gGgcCgUiLtzxdCIKm_vtQaMF8u_DLPrDbyve4-gXBRjB9hmqlzR-X9CiZfRWaaLbe5wYcpROrCKTUP3j8eIphvqIxJs6mASVT3ox/s200/cw_14_mainpict.jpg" tt="true" width="200" /></a></div>The previous night duty was so busy and i was tired out.The exploratory laparotomy went upto 2 am in the morning.Today i got up late and found my bus just leaving.My colleague staying next door offered me a lift but i reached hospital late.The morning ICU rounds already started and i tried to hide my self behind the team members, in order to escape notice of the consultant.The rounds finished and it was my turn to present the previous day's cases.It didnt go smooth as I was drowsy and was not able to concentrate. The consultant asked me to attend the elective cases in surgery OT where the list was also heavy with 3 major cases. While preparing for the cases, the hospital clerk handed over the university notification for the venue and timings for final masters exam, scheduled next month.The second case in my OT had a stormy recovery with laryngospam and agitation which was so difficult to control, and finally i am totally upset when the school principal telephoned and conveyed the message that my daughter is sick and will be brought to OPD.<br />
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Stress can be defined as mental, emotional or physical strain or tension which is an integral part of everyone's life.Even though moderate stress is necessary for the optimal function of human beings undue stress may have physiological and psychological impact(1) Stress occurs when there is a perceived imbalance between the demands being made and the ability to meet those demands.It is a pattern of strain produced by excessive urgency or pressure. According to Cooper stress is negatively perceived quality which could cause physical and mental ill health. <br />
<br />
Most of the doctors are found to have Type A personality featuring insecurity of status and a high amount of anxiety. This personality type is often associated with increased aggression and a constant sense of time urgency and mental tension.They are more prone for stress related responses.They also tend to have a higher incidence of coronary artery disease and may have problems coping with and responding to difficult situations. This may lead on to psychiatric problems in the future.<br />
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In the specialty of anaesthesia it is now well recognised that anaesthetists do suffer from stress. In a recent survey (4) 30% of anaesthetists felt stressed a lot of the time while 5% felt stressed all the time; 33% described themselves as severely stressed and 7% felt their stress was more than severe. In the work related environment the stressful elements were lack of control (42%), strained professional relationships (25%), work overload (24%), difficult work (6%) and potential litigation (3%). In the area of administrative and social factors, administrative responsibilities (42%) and work-home conflict (35%) were the most stressful while money (14%), teaching responsibilities (6%) and peer review (4 %), were less so.<br />
<strong>Responses to excessive stress are categorised as;</strong> <br />
<strong>Behavioural Response:</strong><br />
<ul><li>incrased irritability</li>
<li>destructive behaviour</li>
<li>obscessive compulsive disorder</li>
<li>increase in substance abuse ,(easy availability of drugs for anaesthetists) smoking, or alcoholism </li>
</ul><strong>Physical Response</strong><br />
<br />
<ul><li>Hypertension</li>
<li>Loss of weight</li>
<li>Sleep disturbance</li>
</ul><strong>Personal Response </strong><br />
<ul><li>Intellectual impairment</li>
<li>Poor concentration memory and judgement</li>
</ul><strong>According to one survey( 3) the consequences of stress are found to be</strong><br />
<br />
<ul><li>Difficulty in sleeping 70%</li>
<li>loss of libido 40%</li>
<li>Physical illness 35%</li>
<li>Incresed alcohol intake 35%</li>
<li>Contemplated suicide 21% </li>
<li>Drug misuse 4%</li>
</ul>Some of the sources of stress as far as Anaesthesiologists are concerned are<br />
<br />
<ul><li>Difficulty to cope with work pattern including irregular working hours and emergency work</li>
<li>Frequent CME programs</li>
<li>Sleep deprivation</li>
<li>Bad professional relationship with colleagues</li>
<li>Family problems</li>
<li>Chronic illness</li>
<li>Unstable employment</li>
<li>Time pressure</li>
<li>Fear of Litigation, eventhough, 'Anesthesia' today is considered to be more safe.</li>
</ul><strong>Stress Management Strategies:</strong><br />
<br />
<ul><li>Modifying response to stress:Developing self esteem; Identify your strength and weakness.Realise the concept that something can be changed but something cannot be.So better change yourself and adjust.</li>
<li>Developing coping strategies, try to develop existing ones and implement new strategies.</li>
<li>Developing communication skills. Effective communication is in fact a best reliever of stress.They help to avoid misunderstandings and help to allay anxiety and fear.</li>
<li>Time management effective time management strategies identify goals, set priorities, and manage time.</li>
<li>Improve professional and personal relationships.</li>
<li>Hobbies; indulging in favourite hobbies, achieve balance between work exercise relaxation and personal development.</li>
<li>Attending stress relieving workshops,accident and incident conferences, in which anaesthetists present the critical situations they encountered, could also help.They play a role in the social and emotional support to be given to the stressed.</li>
<li>Improving social support in the professional setting,by maintaining personal relationship</li>
<li>The simulator, which is increasingly used for crisis-management training, can be of some help in the management of stress for those who have excessive response to it. </li>
</ul> <a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhQ1JhxbBUcwBSAZAmBvewONQl5UqGujAvjoDH83e9mQ_FmVDGI4ereM6tuZg3i4jpeql713Bi676aJ88FoZvTt9_Qgv7l1xT4n5ycEZ3WuItDYGCN-PJT2WKSHIMjOPKpQq7oa_IXufxTe/s1600/Copy+of+IMG_1678.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhQ1JhxbBUcwBSAZAmBvewONQl5UqGujAvjoDH83e9mQ_FmVDGI4ereM6tuZg3i4jpeql713Bi676aJ88FoZvTt9_Qgv7l1xT4n5ycEZ3WuItDYGCN-PJT2WKSHIMjOPKpQq7oa_IXufxTe/s400/Copy+of+IMG_1678.jpg" tt="true" width="400" /></a> Recreational activities and gathering help to reduce stress. <br />
<br />
<br />
<strong>Other measures</strong> <br />
<br />
<ul><li>Positive thinking, the ability to degree or disagree or say yes or no without overt hostility whenever appropriate</li>
<li>Avoidance of stressful situation by logical thinking. Don't try to manage a problem which could have been avoided.</li>
<li>Avoid isolation, develop friendship, join 'facebook' and <em>add me as friend</em></li>
<li>Keep your knowledge updated. Follow Mary Ann's Journal watch <a href="http://www.anaesthesiacases.com.au/">http://www.anaesthesiacases.com.au/</a> regularly.</li>
<li>Maintaining good health, regular exercise, nutritious and timely diet, regular sleep pattern, Meditation etc.</li>
</ul>One recent study( 4) among anaesthesiologists has shown that the mean stress level was 50.6 which is no higher than we found in other working populations. The three main sources of stress reported were a lack of control over time management, work planning and risks. About 40.4% of the study group were suffering from high emotional exhaustion (burnout); the highest rate was in young trainees under 30 years of age.<br />
<br />
SUMMARY OF REPORT ON STRESS BY AAGBI ( Ref.1)<br />
<br />
<ul><li>A stressed doctor is not necessarily a bad doctor but difficulties may occur when the stress gets out of control.</li>
<li>The multiplicity of support groups attests to the fact that problems are widespread and solutions complex.</li>
<li>The organisational difficulties in the workplace lead to an inability to reach desired goals and produce frustration. It is clear that lack of control and the problems of administrative responsibilities figure most highly as stressful factors.</li>
<li>Consultants are responsible for each other by moral obligation and for trainees and non consultant grades by convention. In stressful situations discussions with a friendly, understanding colleague may be all that is required to resolve difficulties. </li>
<li>The skills of stress management are integral to the management of many conditions at work and in everyday life.</li>
<li>Communication skills are basic in our personal and professional lives and the ability to stand up for one’s rights without violating the rights<br />
of others is important in the practice of assertiveness. It is necessary<br />
to learn to say no, when appropriate, in a constructive and non confro ntational manner and there is need to be able, politely, to resist<br />
unrealistic demands from others. Some distorted beliefs may be longstanding and encouraged by our environment.</li>
<li>When problems occur the first action of the Clinical Director must be<br />
to discuss the situation with the person involved or to get another senior colleague to do so. Any reported problems should be approached with diplomacy and confidentiality must be respected.However documentation, statements and witnesses are also important.It must always be remem bered that patient safety is paramount.</li>
<li>At any stage in a consultant career support and advice may be needed.It is not widely understood how the various support systems work. All directorates should practise their methodology of dealing with problems and of providing support for colleagues. A mentor system may be worthy of exploration.</li>
<li>All doctors should be discouraged from self diagnosis and, especially,self treatment.</li>
<li>Support and treatment should always be on a confidential basis</li>
</ul>For those in UK and Ireland ,The Association of Anaesthetists of Great Britain and Ireland can provide confidential guidance in all these matters<br />
Ref (1) STRESS IN ANAESTHETISTS<br />
The Association of Anaesthetists of Great Britain and Ireland,<br />
9 Bedford Square, London WC1B 3RA, UK.<br />
Telephone 0171 631 1650; Fax 0171 631 4352;<br />
E-mail: aagbi@compuserve.com<br />
(2) Wylie Churchil Davidson, A practise of Anaesthesia; 7th edition.<br />
(3)coulson J, Stress in doctors, BMA News Review 1996; April 24,<br />
(4) A. S.Nyssen, I.Hansez, P.Baele, M.Lamy and V.De Keyser; Occupati onal stress and burnout in anaesthesia; British Journal of Anaesthesia, 2003, Vol. 90, No. 3 333-337DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com2tag:blogger.com,1999:blog-8746726747957343433.post-62671373218371536292010-04-28T14:03:00.000-07:002010-04-28T20:41:57.147-07:00DIFFUSION HYPOXIA<div class="separator" style="clear: both; text-align: left;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhsVTTTZ5PmY0FKNp0Z2b6g6wzXtZuWVWGlPxCmfjnpYr0WGd39WSAsunU3D850-UnY_LHXTzG_o2e_mtssm90N5iyEG7vGF5PTiE3OHktsnwLyss9mbzcCi7xgjmSTeCSdqWto4POddBOW/s1600/imagesDR354.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhsVTTTZ5PmY0FKNp0Z2b6g6wzXtZuWVWGlPxCmfjnpYr0WGd39WSAsunU3D850-UnY_LHXTzG_o2e_mtssm90N5iyEG7vGF5PTiE3OHktsnwLyss9mbzcCi7xgjmSTeCSdqWto4POddBOW/s320/imagesDR354.jpg" tt="true" /></a>More than pain, he was worried of the disfigurement it caused.A small nevus just above the right eyebrow was a source of worry and disappointment which made him think of a cosmetic repair for better appearance. Mathew Davids,a 38 year old software engineer from India and employed in USA flew to his home country eventhough one of the US hospitals (with the best facil ities in world) offered a cosmetic cum plastic repair for him within affordable cost.He thought he will be more comfortable amidst of friends and relatives.</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;">After 2 days he was scheduled for surgery. The pre anaesthetic check went smooth except for an elevated diastolic BP record of 94 mmHg. He was given GA spontaneous following propofol induction and fentanyl infusion using classic LMA. Maintenance of anaesthesia was with 4-6% sevoflurane in oxygen and nitrous oxide.Intra operative BP, SPO2, ETCO2 and HR were within normal limits. Surgery completed in 32 minutes, LMA removed and he was shifted to recovery room.He was drowsy but arousable.</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;">The recovery nurse who was busy with the management of some major post operative cases thought that his surgery is too short and doesn't require intensive monitoring.The oxygen mask was applied to his face but the other end of the tubing got disconnected on patient movement and was un noticed</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;">There is a fall in saturation and SPO2 low alarm on monitor alerted the staff nurse. She rushed to his trolley and found him unresponsive and cyanosed.The monitor showed severe bradycardia and ST elevation on ECG. Immediate mask ventilation, CPCR and intubation followed.Patient was shifted to ICU where a 12 lead ECG showed STEMI and the troponin value was raised.A decision to thrombolyse was made and initiated. He was on ventilator for three days and got discharged without any neurological deficit.The probable cause for this incidence was thought to be diffusion hypoxia with hypercarbia.Who is the cul prit here? The anaesthesiologist who kept the patient in deep inhalational plane maintaining spontaneous ventilation for 32 minutes or the recovery nurse who neglected the importance of administering oxygen for a GA case?</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;">Diffusion hypoxia (fink effect) means outpouring of large volumes of nitrous oxide into the lung during recovery from general anaesthesia and subsequent hypoxia.This is due to</div><div class="separator" style="clear: both; text-align: left;">1) Direct replacement of oxygen from lung</div><div class="separator" style="clear: both; text-align: left;">2) Diluting alveolar carbon dioxide causing decreased drive for ventilation. </div><ul></ul><div class="separator" style="clear: both; text-align: left;">This effect is seen in first 5-10 minutes of recovery when large volumes of nitrous oxide is released into the lung.The blood gas solubility of nitrous oxide is 0.42 which is less than that of any other inhalational agents.So rapid alveolar concentration following inhalation.But N2O is more soluble than nitrogen in blood. Hence blood and body fluids are rich in N2O.At the end of anaesthesia N2O diffuses back into alveoli from blood down a concentration gradient and this diffusion back is rapid than uptake of nitrogen from the alveoli by blood. This leads to replacement of all alveolar gases by nitrous oxide and subsequent hypoxia.</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgC7kDsqpFaLjoQdF0hd5zlMOXU7qL0h22WdK4wQkQWqsU3BCpCJfMniZB3JtXaS8qmY7m28m_wRU6ZKlpt_1xEgsLXjfM6r2-v6cbEvpty-iX8Y_OnRfIDz8KB2Uclnk_0J_SYrcCudQt8/s1600/22310033.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="368" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgC7kDsqpFaLjoQdF0hd5zlMOXU7qL0h22WdK4wQkQWqsU3BCpCJfMniZB3JtXaS8qmY7m28m_wRU6ZKlpt_1xEgsLXjfM6r2-v6cbEvpty-iX8Y_OnRfIDz8KB2Uclnk_0J_SYrcCudQt8/s400/22310033.gif" tt="true" width="400" /></a></div><div class="separator" style="clear: both; text-align: left;">Fig. showing relationship between O2 and N2O following recovery.</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;">So it is mandatory that 100% oxygen should be given for all GA cases following recovery for about 5-10 minutes to avoid the occurrence of diffusion hypoxia</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;">Ref: 1) Millers Anaesthesiology 7th edition</div><div class="separator" style="clear: both; text-align: left;"> 2John L.Bezzant,M.D, <a href="http://library.med.utah.edu/kw/derm/nitrous/05ni.htm">http://library.med.utah.edu/kw/derm/nitrous/05ni.htm</a></div>DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com3tag:blogger.com,1999:blog-8746726747957343433.post-19566990107527858362010-04-19T03:08:00.000-07:002013-02-27T00:52:04.903-08:00CELIAC PLEXUS BLOCK<div dir="ltr" style="text-align: left;" trbidi="on">
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Celiac plexus lies anterior to the aorta at the level of the first lumbar vertebra, between the origin of celiac and superior mesenteric arteries The adre nal glands lie lateral to the plexus and stomach and pancreas lie anteriorly. The connections include Preganglionic sympathetic fibres from splanchnic nerves, Preganglionic parasympathetic from vagus, Sensory fibres from phrenic and vagus, Afferent fibres concerned with nociception <br />
The three pairs of splanchnic nerves descending to the celiac plexus are<br />
1) Greater splanchnic nerves from T5-T9<br />
2) Lesser splanchnic nerves from T10 and T11 segments<br />
3) Least splanchnic from T12<br />
<div>
<br />
The three pairs of ganglia in the plexus are </div>
<div>
1)Celiac ganglia</div>
2)Superior mesenteric ganglia<br />
3)Aorticorenal ganglia <br />
<div>
</div>
The nociceptive afferent fibres travel from viscera along with the sympathetic fibres, through the ganglia, splanchnic nerve, sympathetic chain, white rami communicans and then synapse in the dorsal root ganglia.The proximal axon of these bodies synapse in the dorsal horn of the spinal cord <br />
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</div>
The blockade of the celiac pleexus causes blockade of pain transmission from the visceral structures including Pancreas, Liver, Gall bladder, Omentum, Mesentery, Alimentary tract, and complete blockade of the Sympathetic fibres causing increased Parasympathetic activity manifested as increased intestinal motility and relaxed sphincters. The sympathetic blockade to the splanchnic vessels cause vasodialatation and hypotension <br />
<br />
Agents used for blockade are 0.5% bupivacaine with adrenaline1:200000 around 30ml, 15 ml on either side with or without steroids(dexamethasone) for chronic pain. Neurolytic blockade is indicated in abdominal malignancies where alcohol 50-100% or 10% phenol is used. The pain on injection of alcohol can be minimised with combination of bupivacaine 1:1 ratio <br />
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<b>Indications: </b></div>
<ul>
<li>Pain relief in upper abdominal malignancies from stomach, pancreas, gall blader, and liver.(Indication for neurolytic block)</li>
<li>Pain after multiple abdominal surgeries. Local anesthetic and steroids indicated.</li>
<li>For evaluation of upper abdominal pain, local anaesthetic alone used</li>
<li>Chronic inflammatory conditions like chronic pancreatitis, neurolytic block advised.</li>
</ul>
<b>Technique</b><br />
1) Informed consent<br />
2) IV access monitors<br />
3) Prone position with pillow beneath hip to minimise lumbar lordosis<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjdS9AFK14WfYAgZjel3KiA5cuPrISwRBaejE5EV73JpIpfCFC3Li6ySbx3ef0iMi3e62iRokcPl5smeP7aMHb6SMidIesk_NVMitVuh4d4LbQE2wi_rJ6AgRVBrWN3LfjR83qOe-XEVIhG/s1600/Image081000.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="240" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjdS9AFK14WfYAgZjel3KiA5cuPrISwRBaejE5EV73JpIpfCFC3Li6ySbx3ef0iMi3e62iRokcPl5smeP7aMHb6SMidIesk_NVMitVuh4d4LbQE2wi_rJ6AgRVBrWN3LfjR83qOe-XEVIhG/s320/Image081000.jpg" width="320" wt="true" /></a></div>
<span style="font-family: Georgia, "Times New Roman", serif;"><i>Classic approach: </i>M</span>ark the inferior edge of T12 (A) and L1 spinous processes and the inferior edge of the 12th rib at a point 7-8cm lateral of the midline(points B and C). Connect these points to form a triangle, the base of which is passing over the inferior edge of the L1 spinous process <br />
<br />
Aseptic preparation of the skin, infiltrate the skin and muscle with local anaesthetic use a 12-18 cm long ,20-22 gauge needle and introduce(the left side needle first) at a 45degree angle relative to the sagittal plane running through the spine. The direction is towards the L1 spine and proceeds to hit on the L1 vertebral body.(more superficial bony contact may be the L1 transverse process)The needle contacts the L1 vertebral body at a depth of. 7-10 cm. A skin marker is placed on the needle. The needle is then withdrawn deep to the subcutaneous plane and re introduced laterally until it just slips from the lateral border of the vertebral body Slowly advance the needle further, feeling for the transmitted pulsations of the aorta and stop advancing once pulsations are felt. On the right side advance further 1 cm. <br />
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Lateral X-ray taken and a negative aspiration test for blood done.A test dose containing 2-3 mlof local anae sthetic with adrenaline is given to exclude intravascular or sub arachnoid placement. Inject 20-25 ml local anaesthetic through each needle. Fluroscopy or CT scan guidance may be undertaken for high precision in case of therapeutic blocks.The signs of successful block is hypotension and the patient may feel an urge to empty bowel.<br />
<br />
<div>
<b>Paramedian approach:</b> Needle is inserted caudad to 12 th spinous process at a point 3 cm lateral to the midline in a plane perpendicular to the skin </div>
<br />
<b>Anterior approach:</b> Through the anterior abdominal wall under fluoroscopic and ultrasound guidance. <br />
<br />
<div>
<b>Direct block:</b> Retroperitoneal surgeries, pancreatectomy or whipples resection block given by surgeon for post op analgesia or neurolytic block for malignant conditions.</div>
<br />
<b>Endoscopic Ultrasound Guided Method: </b>See Ref: below.<br />
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<div>
</div>
<b>Complications:</b><br />
<br />
<ul>
<li>Hypotension due to sympathetic blockade minimised by giving 500-1000 ml of RL before the block.</li>
<li>Orthostatic hypotension may persisit after a neurolytic block for about one week.but self limiting.</li>
<li>Other complications are back ache due to retroperitoneal hamatoma or injury to lumbar plexus, injury to kidney, bowel, retroperitoneal hematoma ,intrathecal injection, pneumothorax.,infection, aortic dissection, paraplegia or local anaesthetic toxicity. </li>
</ul>
<b>Ref:</b> An endoscopic ultrasound guided technique(Michaels AJ, Draganov PV, Endoscopic ultrasound guided celiac plexus block... World J gastroenterology2007:13(26):3575-80) <br />
Wylie Churchil Davidson Practise of Anaesthesia Seventh edition pp1261-62<br />
<div>
Michael Mulroy,Christopher Bernards, et al; A Practical approach to Regional Anaesthesia, Fourth Edition</div>
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DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com2tag:blogger.com,1999:blog-8746726747957343433.post-49286989625790837632010-04-14T07:39:00.000-07:002010-05-20T12:44:11.015-07:00THE 'JALAKANYAKA TRAGEDY'<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgEsFKUweeVnBUFHNfkVVIc31S2VBlLcw5G6maEVTIC-fdOPAgHhUk7RNrfa_rGQgH4MsnpfK-dU5vgJojeO6bjeOctnsXDAOZfUe2wrAeaJLo5u6Io3g_uTab5z8xjqup2JpO2fPxLgJJC/s1600/photo404.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="182" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgEsFKUweeVnBUFHNfkVVIc31S2VBlLcw5G6maEVTIC-fdOPAgHhUk7RNrfa_rGQgH4MsnpfK-dU5vgJojeO6bjeOctnsXDAOZfUe2wrAeaJLo5u6Io3g_uTab5z8xjqup2JpO2fPxLgJJC/s200/photo404.jpg" width="200" wt="true" /></a></div>September 30, 2009; was a day of agony, sorrow and mourning for the people of Kerala,"The Gods Own Country." A tourist boat capsized in Thekkady lake, Kerala when 46 passengers drowned (nearly half of them were children) and lost their lives.The double decker boat ‘Jalakanyaka’ operated by Kerala Tourism Development Corporation (KTDC). capsized at a depth of 40 to 50 feet in Periyar Lake, at Periyar Wildlife Sanctuary, Thekkady around 17:30 hrs IST. It was one of the major accidents in the history of Kerala, and the authorities were not prepared to face such a tragedy as it was sudden and unexpected.<br />
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The accident happened when the boat "Jalakanyaka" tilted after several tourists moved to one side on sighting elephants on the banks of the lake and the driver lost control. This happened around sunset making rescue operations dfficult. It was shocking to note that none of the passen gers were wearing life jackets and there were no prior instructions to passengers on safety aspects by the boat crew before the journey. Also there were no life guards in the boat. <br />
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<div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgqAoRTgwlYy6y56dbuhvVo0_YvIBByrIJ3eZ8Yg3QRkp48Ku0P0xqP3x_OF6wEFhNB60crLbo4bSnYPkeu8Pc9pkh8arJjv9Op7n1GHs_-j8yAXKzcHdhMaEQINVbWSzjaW3_oDp5H-om1/s1600/full+2.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="250" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgqAoRTgwlYy6y56dbuhvVo0_YvIBByrIJ3eZ8Yg3QRkp48Ku0P0xqP3x_OF6wEFhNB60crLbo4bSnYPkeu8Pc9pkh8arJjv9Op7n1GHs_-j8yAXKzcHdhMaEQINVbWSzjaW3_oDp5H-om1/s400/full+2.jpg" width="400" wt="true" /></a></div><br />
Drowning means death due to suffocation with or without aspiration of water while submerged in water.Near drowning means suffocation and asphyxia but with possible survival. Asphyxia due to submersion or hypoxia due to aspiration of water or a combination of both occur in drowning leading to death. Drowning can be either fresh water (well, lakes) or sea water.Also classified as dry or wet drowning. In dry drowning the victim is subjected to severe reflex laryngospasm and hypoxia following accidental contact with cold water and death is primarily due to asphyxia ( lungs are free of water). In wet drowning water enters the lung and cause alveolar flooding, alveolar edema, loss of surfactant, ventilation perfusion mismatch ,bronchospasm and hypoxia. Disruption of the alveolocapillary membranes lead on to ARDS.<br />
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In fresh water drowning the hypotonic water aspirated is rapidly absorbed into the pulmonary circulation an amount of more than 500-800 ml can cause hemodilution, hyponatremia and hemolysis. In salt water drowning water is drawn into the alveoli from pulmonary circulation causing hemoconcentration and hypernatremia.Hypermagnesemia and hypercalcemia are also seen in salt water drowning The patient may lose consciousness in cold water drowning if body temperature is below 32 deg.C.Ventricular fibrillation may occur. It is stated that hypothermia has protective effects on brain and favourable neurological outcome following successful resuscitation is possible.<br />
<br />
<strong>Clinical manifestations:</strong> Patients present with hypoxia, hypercarbia and metabolic acidosis.Injury to cerv ical spines to be considered in divers or in victims of "water accidents" The recovery may be complicated by permanent neurologic sequealae or ARDS.<br />
<br />
<strong>Emergency management:</strong><br />
<br />
<ul><li>Call for help emergency response system</li>
<li>The victim should be removed from the water early as possible with attention to cervical spine </li>
<li>Open the mouth and clear the airway of mud, weed, other foreign bodies or vomitus using finger sweep technique.Rescue breathing should be performed while the individual is still in water, or on board in a boat.But chest compressions are inadequate because of buoyancy issues.. Do not attempt to deliver abdominal thrusts to expel water as it can cause aspiration of water or induce vomiting.</li>
<li>Alternately bag and mask ventilation using 100% oxygen with airway and cricoid pressure can also be performed if resuscitation equipments are available nearby.</li>
<li>Cardiac compressions shoul be initiated. Advanced cardiac Life support by intubation and drugs to be followed, if the victim is still unresponsive. </li>
</ul>Most of the near drowned patients respond to appropriate initial resuscitative efforts and the efforts should be continued in case of cold water drowning until the patient is fully assessed and under tretment in a hospital.<br />
<br />
<strong>In hospital management:</strong> <br />
<br />
Immediate rewarming measures initiated to prevent ventricular fibrillation if body temperature is below 25 deg. Hypothermia improves neurological oucome so rapid rewarming to room temperature is to be avoided if body temp is above 30 deg and patient is hypoxic. Core rewaming can be performed with warm oxygen, continuous bladder lavage with fluid at 40°C, and intravenous (IV) infusion of isotonic fluids at 40°C and warm fluids through Ryles tube. <br />
<br />
Recent investigations In 2002, by the American Heart Association, followed in 2003 by the European Resuscitation Council, based on the results of blinded, randomized, multicenter clinical trials, suggest induced hypothermia(Therapeutic hypothermia (TH)) improves oxygen supply to ischemic brain areas, decreases cerebral metabolic demand, and decreases increased intracranial pressure.But the danger of hypoperfusion, acidosis and cardiac complications of hypothermia are also to be considered.<br />
<br />
Intubation may be required in order to provide adequate oxygenationif 100% oxygen by face mask is ineffective to maintain oxygenation.Protect the cervical spines in cervical collar or apply manual in line traction during intubation. Criteria for ET intubation include the following:<br />
<ul><li>PO2 less than 60-70 mm Hg (>80 mm Hg in children) on 100% oxygen by mask</li>
<li>Impaired consciousness and inability to protect airway or handle secretions</li>
<li>High alveolar-arterial (A-a) gradient - PaO2 of 60-80 mm Hg or less on 15 L oxygen by non rebreathing mask</li>
<li>Respiratory failure - PaCO2 >45 mm Hg</li>
<li>Unsatisfactory ABG results</li>
</ul>A trial of bilevel positive airway pressure (BiPAP)/CPAP, may be considered in conscious patients before intubation. Intubated victims of submersion injury may require PEEP with mechanical ventilation to maintain adequate oxygenation. PEEP imroves ventilation in non compliant lung by<br />
<ol><li>Shifting interstitial water into the pulmonary capillaries,</li>
<li> Prevention of alveolar collapse, </li>
<li>Adequate alveolar ventilation and decreasing capillary permeability and </li>
<li>Increasing the diameter of both small and large airways to improve distribution of ventilation.</li>
</ol>ECMO (Extracorporeal Membrane Oxygenation) has been shown to be helpful in individuals who remain hypoxic despite aggressive mechanical ventilation. Bronchoscopy may be needed to remove foreign material, such as aspirated debris or vomitus plugs from the airway.<br />
Thoracotomy with open heart massage and warm mediastinal lavage may be required in selected patients as the hypothermic heart is typically unresponsive to pharmacotherapy ,cardioversion or defibrillation<br />
Extracorporeal blood rewarming may be considered in severe hypothermia unresponsive to above measures. Do not abandon resuscitation of a submersion victim until the patient has been warmed to a minimum of 30°C because of the reasons mentioned above<br />
<br />
<strong>Other treaments include:</strong><br />
<br />
<ul><li>Beta 2 agonists as Nebulization Albuterol 1.25-2.5 mg diluted in 2-5 mL sterile saline or water Q8</li>
<li>Inotropic support dopamine 10-20 mic/kg/mt</li>
<li>Treatment of hemolysis by blood transfusion</li>
<li>Correction of electrolyte abnormalities</li>
<li>Antibiotic therapy</li>
<li>Decompression of stomach using ryles tube</li>
<li>Raised intracranial tension management according to protocols</li>
<li>Ventilatory management of ARDS</li>
</ul><strong>Prevention:</strong><br />
<ul><li>Children, especially toddlers, should be under supervision when they are around water, including a bathtub or bucket full of water. </li>
<li>All individuals involved in boating activities water sports or recreational activities in beach should be able to swim, and should wear life jackets while onboard </li>
<li>Avoid alcohol or drugs while boating or swimming</li>
<li>Individuals with underlying medical illnesses such as seizure disorder, diabetes mellitus,or coronary artery disease, should swim only under supervision</li>
<li>All tourists should make sure that boating facilities are provided by an authorised authority.Thet should see whether adequate life saving equipments including life jackets and trained rescuers are available while boating</li>
</ul> <br />
Ref: Article on Drowning from emedicine medscape; by Suzanne Moore Shepherd, MD, William H Shoff, MD, Professors, Department of Emergency Medicine, Hospital of the University of Pennsylvania; <br />
<a href="http://emedicine.medscape.com/article/772753-overview">http://emedicine.medscape.com/article/772753-overview</a><br />
Oxford Handbook of Critical Care 3rd edition<br />
Clinical Anaesthesiology, Morgan, Mikhail, third edition, Mc Graw HillDR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-25617206999103669432010-04-07T12:29:00.000-07:002010-04-10T10:19:29.082-07:00DILATED CARDIOMYOPATHY<div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;"><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhgqF0XjRYifhkTIvcrVFP3b225-lpZoUGaai_I7jm4Bk031oYf6aguC_Vtd4JyyBpVeKspv4z6W0ocW4AgMo8hlr7c-KshYaDKIDIDU4Hjn0W6E-TEjd2y0fbsnrTCtXHktITkr2qTleBO/s1600/images[13].jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" nt="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhgqF0XjRYifhkTIvcrVFP3b225-lpZoUGaai_I7jm4Bk031oYf6aguC_Vtd4JyyBpVeKspv4z6W0ocW4AgMo8hlr7c-KshYaDKIDIDU4Hjn0W6E-TEjd2y0fbsnrTCtXHktITkr2qTleBO/s320/images%5B13%5D.jpg" /></a></div><div style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none;">A 7 year old boy is presented with chest discomfort and palpitation. He is also complaining of right iliac fossa pain.The pulse rate is 174/mt, BP 94/50 with mild elevated JVP. The monitor showed supraventricular tachycardia which responded to carotid sinus massage. He is febrile and has pallor.Chest is clear and CVS examination revealed an ejection systolic murmur of grade 2/4 radiated along left parasternal border and tachycardia. Abdominal examination showed Rt. iliac fossa tenderness with guarding.Lab findings were normal except for a high WBC count and Hb value of 9 Gms%. Previous records showed one ER admission with palpitation and the diagnosis was marked as suspected Cardiomyopathy(unclassified) with a probable viral etiology.The monitor again showed rapid pulse rate and the ECG is characteristic of supraventricular tachycardia with no response to carotid sinus massage this time.The patient was shifted to ICU for stabilisation, Oxygen by mask applied and cardiovascular status monitored. Inj. adenosine was given 2.6 mg iv and the heart rate slowed down initially to 100/mt but raising,so an immediate second bolus of adenosine 5.2 mg was given.Controlled fluid management started and temperature was maintained.The heart rate reduced to 132/mt and a second ECG showed SVT with QRS duration of .08 with QT 0.45 secs </div></div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: center;"></div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: center;"></div><div class="" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;"><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjrscLNSQm4V7jfg_AIQivNz8m67QL1fetWGhYBc-r5DIAGj9kRKsn9MqHPZkvFR4UGEjYkBt-f_5JNxn9uDI5n_Jp5kqp50aEwicTVZ25XLwWu9Xm8QiOUAaDxYBh-5gna3KPU-QKyTn91/s1600/Image034.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="300" nt="true" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjrscLNSQm4V7jfg_AIQivNz8m67QL1fetWGhYBc-r5DIAGj9kRKsn9MqHPZkvFR4UGEjYkBt-f_5JNxn9uDI5n_Jp5kqp50aEwicTVZ25XLwWu9Xm8QiOUAaDxYBh-5gna3KPU-QKyTn91/s400/Image034.jpg" width="400" /></a></div>The HGT was 5.5 and ABG showed mild respiratory alkalosis.Abdominal examination revealed acute appendicitis and was confirmed by ultrasonography.A decision to operate was made.The patient was administered amiodarone 5mg/kg and infusion 2.5 mic/kg/mt followed.The CXR showed cardiomegaly and an echocardiogram showed dilated left ventricle with global hypokinesia and impaired systolic function, posteriorly displaced mitral valve with MR, ejection fraction of 40%, all suggestive of a dilated cardiomyopathy.The heart rate is now stabilised on amiodarone and the cardiologist was consulted for the management of any intraoperative adverse events and to prepare for a temporary pacemaker insertion as an emergency intervention.Aspiration prophylaxis was given, Midazolam 1mg was given IV and the patient was shifted to operation theatre. </div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;"><br />
</div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;">ECG, Oxygen saturation,Temperature ,NIBP etc were monitored. Anaesthesia was induced with IV ketamine 1 mg/kg and propofol 1mg/kg, along with IV fentanyl 1mcg/kg supplemented with oxygen, nitrous oxide and 1-1.5% isoflurane.Vecuronium was used to facilitate intubation at the dose of 1.5 mg/kg.(1) The heart rate and BP were stable throughout the procedure and a baseline infusion of amiodarone 1-2mic/kg/mt was on flow.Anaesthesia was maintained with O2/N2O in isoflurane (MAC 1-1.5) and intermittent boluses of vecuronium bromide IV, An arterial line and central venous catheter were inserted.TEE was not available. An esophageal stethescope was introduced. The capnogram waveforms are carefully observed.A central venous pressure of 6-8 cm of H2O was maintained by controlled fluid administration. Ideally a pulmonary artery catheter is indicated to monitor the filling pressures along with TEE. The reversal of neuromuscular block was achieved with neostigmine and glycopyrrolate and the postoperative period was uneventful.The child is stabilised on amiodarone 125 mg bid dose and was discharged with a maintenance dose of atenolol 25 mg so as to prevent the long term complications of amiodarone like thyroid dysfunction and pulmonary toxicity.</div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;"><br />
</div><div class="separator" style="border-bottom: medium none; border-left: medium none; border-right: medium none; border-top: medium none; clear: both; text-align: left;">Dilated cardiomyopathy is characterised by left ventricular or biventricular dilatation and impaired ventricular contractility.The most common complication of dilated cardiomyopathy is progressive congestive cardiac failure.The commonest etiology is idiopathic or viral infections in children and alcohol abuse in adults.Most of the patients are asymptomatic with cardiomegaly and minimal CVS symptoms and present later in the course with cardiac failure, when the mortlity rate is high.The predictors of poor prognosis are(2) an ejection fraction of less than 0.25 (as seen on Echo, during the acute presentation of heart failure), left ventricular end diastolic dilatation, a hypokinetic left ventricle, the presence of mitral and tricuspid regurgitation</div><br />
The goals (3) of anaesthetic management are <br />
<ul><li>Myocardial depression should be avoided</li>
<li>Normovolemia is maintained</li>
<li>To avoid overdose of drugs during induction as the circulation time is slow.</li>
<li>Ventricular afterload is avoided</li>
<li>Avoid sudden hypotension when regional anaesthesia is the choice</li>
</ul>Alternate anaesthetic techniques are <br />
<ul><li>Induction by midazolam/nitrous oxide/ vecuronium /isoflurane for GA</li>
<li>Graded epidural anaesthesia with sedation using midazolam.The advantages are adequate post operative analgesia and less hemodynamic alteration.The changes in preload and afterload produced by epidural anesthesia mimic the pharmacological goals of treatment.(3) Here an anaesthetic level upto T4 is required and a well relaxed abdominal muscles are preferred.To achieve this goal the dosage of local anaesthetic requirement would be high which may precipitate sudden change in hemodynamics and the treatment of hypotension with ephedrine further worsens the CVS status.Phenylephrine if used to treat hypotension may cause increase in afterload which is detrimental.Hence the decision to administer GA.</li>
</ul>Ref:<br />
1)Yamaguchi S, Wake K, Mishio M, et al. Anesthetic management of a patient with dilated cardiomyopathy under total intravenous venous anaesthesia with propofol and ketamine combined with continuous epidural analgesia. Masui 1999;48: 1232-34. <br />
<a href="http://www.ncbi.nlm.nih.gov/pubmed/10586558">http://www.ncbi.nlm.nih.gov/pubmed/10586558</a><br />
2 WILLIAM G, VALENTIN FUSTER: Idiopathic dilated Cardiomyopathy. New England Journal of Medicine; 331:1564-75, 1994.<br />
3. ROBERT STOELTING K, STEPHEN F: Anesthesia And Co-Existing Disease, 4th Edition Lippincott-Raven; Ch. 7:117-120.DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-87948389241828986672010-03-31T21:45:00.000-07:002013-02-27T00:52:29.982-08:00ANAPHYLAXIS THE EXTREME HYPERSENSITIVITY!<div dir="ltr" style="text-align: left;" trbidi="on">
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A 5 year old female child was admitted in the ER with h/o wasp sting. She is drowsy and has facial and lip edema.She is also in respiratory distress with stridor. She has a rapid thready pulse with urticarial rashes all over the body. An attempt for endotracheal intubation under suxamethonium and sedation failed due to extensive edema of the tongue and oropharynx and the vocal cords were not visualised. Emergency airway access obtained by a classic LMA with positive pressure ventilation but desaturation persisted and the ENT surgeon was called in for emergency tracheostomy</div>
<br />
Anaphylaxis is an acute, severe, potentially life threatening allergic reaction (type 1 hypersensitivity) characterised by severe bronchospasm, angio neurotic edema and cardiovascular collapse following repeated exposure to an allergen to which the individual is already sensitised. Anaphylaxis can be caused by a variety of allergens. <br />
<a name='more'></a><br />
<ul>
<li>Food, (Peanuts Tree nuts (walnuts, pecans, pistachios, filberts, cashews, almonds, etc.) </li>
<li>Shellfish (crab, crayfish, prawns, shrimp, lobster, etc.)</li>
<li>Proteins in Fish Milk, Soyabean, Wheat, Eggs </li>
<li>Medications(Penicillin, Sulfa antibiotics, Allopurinol, IV contrast material )</li>
<li>Insect venom (including bees, wasps, ants )</li>
<li>Latex.</li>
</ul>
<i><b>Pathophysiology</b></i><br />
At the time of first exposure to the antigen,allergen or drug the immunoglobulin IgE(antibody) is sensitised by the allergen.The IgE antibody is now fixed to its receptors on tissue mast cells or circulating basophils.Re exposure to the same antigen causes direct bridging of cell surface Ig E receptors.This causes activation of membrane associated enzymes causing complex biochemical cascades that lead to efflux of Ca++ ion with release of granule associated mediators and generations of new mediators from cell membrane phospho lipids.The important mediator is Histamine which dilate terminal arterioles and increase the permeability of venules, causing extravasation of fluid, increased airway resistance,cutaneous vasodilatation, resulting in pruritus and urticaria. Other mediators are Prostaglandins,ECF - A [ Eosinophil Chemotactic Factor - A]NCF [ Neutrophil Chemotactic Factor ],Slow Reacting Substance of Anaphylaxis ( SRS – A ), Leukotriens and Platelet Activating Factor ( PAF ). These chemical mediators are responsible for the systemic manifestations of anaphylaxis including vasidilatation and flushing, bronchospasm, itching, urticaria angioedema and hypotension.<br />
<br />
<b><span style="font-family: Georgia, "Times New Roman", serif;">Clinical manifestations:</span></b><br />
General : The patient will be apprehensive, anxious and may c/o dizziness, loss of consciousness, tightness of chest, dysphagea,throat pain,abdominal pain, nausea or vomiting. There may be tachycardia, numbness of tongue sneezing or muscle cramps.<br />
<br />
The major systemic manifestations are<br />
<b>Cutaneous</b><br />
<br />
<ul>
<li>The classic skin manifestation is itching and urticaria, commonly called as hives. These lesions are red and raised, and they sometimes have central blanching. Intense pruritus is associated with the lesions. This can be generalised or localised. Localised lesions are common in insect bites, where the involved area is erythematous, edematous, and pruritic.Angioedema is also often asociated with anaphylaxis manifesrted as cutaneous nonpruritic edematous lesions in the skin and mucosa typically seen around the eyes, lips, palms, soles, and genitalia.</li>
</ul>
<b>Pulmonary.</b><br />
<ul>
<li>Mucosal edema of the upper airway including oropharynx, tongue and larynx can occur.This may lead on to stridor,severe airway obstruction and hypoxia. Lower airway involvement is manifested as severe boronchospasm (wheezes). Angioedema alone can cause severe edema of the tongue and lips causing severe airway obstruction.</li>
</ul>
<b>Cardiovascular</b><br />
<br />
<ul>
<li>Intravascular volume depletion may take place as a consequence of capillary leakage. There will be associated tachycardia and severe hypotension, termed as anaphylactic shock.Various arrhythmias are also reported and may be worsened by treatment with adrenaline</li>
</ul>
<b><span style="font-family: Georgia, "Times New Roman", serif;">Emergency management</span></b><br />
<ul>
<li>Progression to severe bronchospasm or laryngeal edema can occur within few minutes to hours in sensitised individuals and so early treatment is advised. Adrenaline injection 0.3 to 0.5 mg should be given deep intramuscular immediately on diagnosis. IM route preferred as absorption will be better and reliable.</li>
<li>In case of severe laryngeal edema; nebulised adrenaline is administered (0.25 ml 1:100 epinephrine added to 2 ml saline)</li>
<li>Glucagon 5-15 mic/mt intravenous is also tried in refractory hypotension or in patients already on treatment with beta blockers.</li>
<li>Histamine blockers like diphenhydramine 25-50 mg PO/IM/orIV may be given to block the effects of histamine.</li>
<li>Ranitidine 50 mg IV or 150 mg orally may be given for blocking H2 receptors</li>
<li>Steroids; Prednisolone 50 mg PO or Methyl prednisolone 125mg IV sixth hourly may be administered</li>
<li>Albuterol 2.5 ml 0.5% solution nebulised, is useful for relieving severe bronchospasm</li>
</ul>
<b>Anaphylactic shock</b><br />
<ul>
<li>Epinephrine 0.3 to 0.5 mg intravenous followed by infusion 2-8 mic/mt</li>
<li>Volume resuscitation as massive fluid shifts are common. Colloids like hetastarch are preferred.</li>
<li>Persistent hypotension is managed with infusion of dopamine 5-15 mic/kg/mt or nor epinephrine 2-8 mic/mt</li>
</ul>
<b>Prevention</b><br />
<ul>
<li>Identify the cause of allergy and avoid exposure, Food, Dust, Drugs etc.</li>
<li>Epi Pen: It is essential that anyone with a history of anaphylaxis or allergy should keep epinephrine auto-injectors, such as EpiPen® with them at all times and be prepared to use them whenever a reaction occurs.These are available in 0.15mg and 0.3 mg doses for subcutaneous injections by using a pen device</li>
</ul>
<b><span style="font-family: Georgia, "Times New Roman", serif;">Anaphylaxis during Anaesthesia:</span></b><br />
<br />
Evaluation and management of anaphylaxis is difficult and challenging in OT set up as multiple drugs are given repeatedly and that the general warning symptoms are absent under anaesthesia.Patients are unconscious and in deep levels of anaesthesia masking the symptoms and signs of anaphylaxis. The anaesthetist has to look for cardiovascular and respiratory signs like unexplained hypotension and increase in airway resistance with desaturation. Increased or decreased ETCO2 is observed and there will be hemoconcentration. CVS collapse is the most common manifestation under anaesthesia and is seen in around 80% of cases with the reported incidence of cardiac arrest in 10% cases.On table management is the same as described above.Stop all anaesthetic agents keeping the minimum of inhalational agents.Unintubated patients should be intubated, airway pressures are monitored, and nebulised adrenaline or albuterol administered via T piece attached to the breahting circuit.CPCR should be activated as per ACLS protocols If you notice facial swelling and lip edema with the above findings extubation is deferred and patient may be ventilated until systemic manifestations like laryngeal edema bronchospasm and hypotension are treated.A simple test to find residual airway edema on table is absence of leak following deflation of ETT cuff. <br />
<b>Lab findings intra op</b><br />
<ul>
<li>Serum histamine and mast cell tryptase lavel within ten minutes of onset of signs and symptoms.</li>
<li>Detection of N methyl histamine a breakdown product of histamine in urine is also helpful</li>
</ul>
<b>Differential Diagnoses intra op:</b><br />
<br />
<ul>
<li>Myocardial infarction</li>
<li>Exacerbation of bronchospasm in asthmatics</li>
<li>Pulmonary embolism</li>
<li>Pulmonary aspiration</li>
<li>Acute pulmonary edema</li>
<li>Pneumothorax</li>
</ul>
<b>Some Anaphylaxis situations encountered by anaesthesiologists:</b><br />
<ul>
<li>Opioid administration for acute painful conditions like trauma: due to histamine release mild anaphylactic reactions are observed. Manifested as itching and hypotension and are treated with antihistamines and IV fluids.</li>
<li>Barbiturates due to non immunologically mediated mechanisms</li>
<li>Local anaesthetics mainly ester linked local anaesthetics are involved</li>
<li>Radiocontrast media. In radiology suite anaesthetists are called to treat patients with anaphylactic reactions.Reactions to radiocontrast usually are mild (most commonly urticarial), and rarely serious reactions can occur. Risk of a fatal reaction has been estimated at 0.9 cases per 100,000 exposures and the incidence is 5-8%.The reaction is said to be anaphylactoid and may be due to complement activation.Pretreatment with antihistamines or corticosteroids and use of LMW agents can significantly reduce the incidence. A suggested protocol for prevention of reactions to IV contrast is given below.</li>
</ul>
Use low osmolality contrast media<br />
Administer hydrocortisone (200 mg IV), wait 1-2 hours <br />
if time permits.<br />
Administer diphenhydramine (25-50 mg IM) immediately<br />
before the procedure. <br />
<ul>
<li>Protamine used for heparine reversal in CPB cardiac catheterisation or hemodialysis and can cause fatal anaphylactic reactions sometimes.The patients who are more prone are diabetics on subcutaneous insulin,vasectomised patients or those allergic to fish. In this situation it is better to reverse the effect with hexadimethrine</li>
<li>Methyl methacrylate is another agent commonly implicated in allergic reactions and anaphylaxis.Methyl methacrylate otherwise known as bone cement is used to attach a prosthetic joint to raw bone and is widely used in hip and knee replacement surgeries. Hypotension hypoxemia and pulmonary edema are observed during implant fixation.Prior corticosteroids rae found to be useful to prevent this reaction.</li>
<li>Mannitol is known to cause release of histamine from basophil degranulation due to a direct reaction</li>
<li>Streptokinase and Eurokinase are also responsible for rare anaphylactic reactions</li>
<li>Neuromuscular blocking agents are also involved in anaphylaxis due to non immunologic mechanisms eg pancuronium and vecuronium.Cross sensitivity is also noted</li>
</ul>
<b>Sensitivity testing</b><br />
<br />
Pre op diagnosis of allergic drugs or antigens in susceptible individuals: Intradermal skin tests using 0.01 -0.02 ml of the allergen. An intradermal weal of more than 8 mm is considered postive. Obtain informed consent and all necessary precautions are taken to deal wth an emergency situation as even test dose can precipitate severe allergic reactions.Testing for sensitivity to penicillin antibiotics may be useful when a penicillin or cephalosporin antibiotic is the drug of choice for a serious infection in a patient who has a history of severe reaction.Here Incremental doses of intradermal doses of the drug are administered while observing the patient for pruritus, flushing, urticaria, dyspnea, hypotension, or other manifestations of anaphylaxis. If no reactions are observed a full dose can be given safely As per, Richard S Krause, MD, Ref (4) A suggested protocol for IV testing begins with 0.001 mg of the chosen drug. At 10-min intervals, incrementally increase the dose (eg, 0.001 mg, 0.005 mg, 0.01 mg, 0.05 mg, 0.1 mg, 0.5 mg, 1 mg, 10 mg, 50 mg, 100 mg, full dose), while observing the patient. Sensitivity testing along with desensitisation occurs here but can be rarely fatal.<br />
<br />
<b>Desensitization regimens</b><br />
<br />
Desensitization regimens for certain antibiotic allergy have been shown effective. A typical desensitization regimen involves administering the antibiotic of choice at an initial dose of 0.01 mg. While observing the patient, double the dose every 10-15 minutes until a full dose has been administered.This is the basis of administering immunotherapy to sensitised individuals where an allergist or other physician who has been trained in the therapy administers immunotherapy by injecting a small, precisely calibrated amount of purified extract of the identified allergen under the skin of a patient's arm. Patients then are given injections of gradually increasing doses of the allergen at intervals that typically range from 1 to 8 weeks over the course of 3 to 5 years. The dosage, regimen intervals, and duration of therapy vary depending on the type and severity of the person's allergy.<br />
The other useful tests used to detrmine the hypersensitivity are Radioallergosorbent test (RAST) which determines antigen specific IgE antibodies in serum and Basophil Activation test,by flow cytometric analysis of basophil membranes following activation<br />
<br />
<b>Anaphylactoid reactions</b>Some drugs (Non steroidal anti inflammatory drugs,polymyxin, morphine, x-ray dye, and others) may cause an anaphylactic-like reaction (anaphylactoid reaction) when people are first exposed to them. This is usually due to a non immunologically mediated toxic reaction(directly causing the release of mediators from mast cells and basophils )rather than the immune system response that occurs with "true" anaphylaxis.<br />
<b><span style="font-family: Georgia, "Times New Roman", serif;">The Anaphylaxis Algorithm:</span></b><br />
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<br />
<br />
Ref:<br />
<a href="http://acta%20anaesthesia%20belgica%202004/;55,229-237/">acta anaesthesia belgica 2004;55,229-237</a><br />
<a href="http://www.wikipedia.org/">http://www.wikipedia.org/</a><br />
<a href="http://www.anaphylaxis.org/">http://www.anaphylaxis.org/</a><br />
<a href="http://emedicine.medscape.com/article/756150-overview">http://emedicine.medscape.com/article/756150-overview</a><br />
Paul Marino the icu book 3rd edition<br />
Tinkers anaesthesiology<br />
<a href="http://www.resuscitation.org.uk/">http://www.resuscitation.org.uk/</a> <br />
<i>image</i><br />
<a href="http://www.naturfoto-cz.de/">http://www.naturfoto-cz.de/</a><br />
Thanks to Mr.Nisar Abdulla, Nisar Manzil Ponkunnam for technical assistance</div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com2tag:blogger.com,1999:blog-8746726747957343433.post-48185921196971832562010-03-23T09:23:00.000-07:002010-05-20T12:47:20.060-07:00SEPSIS ON THE GO.<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgivpNj5UwQ_jebgmNx2hHwYciT2Yn7Yw9QL2sW_Quc0C9_k0zQLWmEUBKrF-2399EKdJC40_OgrnUDA7olalLp7JrpW4OB2nY7o5066iLxVdvCpy3sZvG21q8XOWzZ4XeFNwobQdPO4TzI/s1600-h/Image041.jpg" imageanchor="1" style="clear: left; cssfloat: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="150" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgivpNj5UwQ_jebgmNx2hHwYciT2Yn7Yw9QL2sW_Quc0C9_k0zQLWmEUBKrF-2399EKdJC40_OgrnUDA7olalLp7JrpW4OB2nY7o5066iLxVdvCpy3sZvG21q8XOWzZ4XeFNwobQdPO4TzI/s200/Image041.jpg" vt="true" width="200" /></a></div>Will you be careless about a lacerated sports injury or an unknown bite on your leg? Have you ever neglected a skin abrasion by a metal piece or thorn? Do insect bites need attention? Here is the story of a young labourer, a worker from a farm, who succumbed to death following sepsis due to an unattended injury/bite on his leg about which he was totally unaware. <br />
This man was complaining of pain on his left hip and leg for two days.The left thigh appeared swollen with mild bluish discolouration on the anterolateral aspect.. He had no past history of any systemic illness and was in good health while joining the farm. Since 1 day he had low grade fever and there was progre ssive increase in difficulty of breathing. Examination showed tachypnea, dyspnea, Pulse: 122/mt, BP: 88/64 mm Hg, SPO2: 78% on room air, Pallor +, ABG: mild metabolic acidosis, Chest: b/l crepitations,CVS: tachycardia, CNS: alert and conscious, ABD: mild splenomegaly and abdominal wall edema, Swollen, warm and tender left leg with knee effusion and normal dorsalis pedis pulsation.A definite or identifiable mark of injury was not observed on the limb. A provisional diagnosis of cellulitis with septicemia or DVT with pulmonary embolism, was made. Patient was shifted to ICU for close observation of vitals and cardiorespiratory support. IV fluids started and oxygen by mask applied, dopamine 10-15 mic/kg/mt and dobutamine 5-10 mic/kg/mt were on flow. Blood investigations were ordered.Fluid aspirated from thigh and knee was serosanguinous in nature and awaited culture reports. Empirical broad spectrum antibiotics were started.Doppler ultrasound ruled out DVT or limb ischemia due to thrombus.X ray of left femur was normal.ECG showed sinus tachycardia, and CXR was normal. CT chest, abdomen and limb were considered but deferred as contrast could not be given due to derranged RFT, hypotension and abnormal coagulation profile. The echo cardiogram revealed Dilated left ventricle and impaired systolic function with EF 40%, and global hypokinesia, consistent with myocarditis.Fresh blood transfusion and FFP commenced. The blood investigations now showed<br />
<br />
Hb 12.9 gm/dl, Platelet 100 K/UL, Derranged coagulation, RBS 120 mg/dl,CRP ++, ESR 70mm/hr, WBC 16K/uL, Uric acid 417 micmol/Lt.,LDH 820 u/l, CK 9495u/l, Liver function elevated bilirubin total and direct with high ALP and AST . RFT : creatinine 200 mic mol/ltr, Hypoalbuminemia, FDP 80 mic gram/ml, Urine Hemoglobin +++ and myoglobin + peripheral smear --> WBC more than 17% bands with toxic changes along with 10% atypical lymphocytes, Microcytic Hypochomic Anemia and Megakaryocytes <br />
<a name='more'></a><br />
<br />
A diagnosis of septicemia with multi organ failure was confirmed. Central line was not attempted as coagulation was persistently derranged. Oxygenation was adequate on non invasive ventilatory strategies and guided by frequent ABGs.The patient's condition deteriorated in next 8 hours as there was progressive tachypnea, dyspnea, hypotension non refractory to blood and fluid resuscitation, peripheral cyanosis, reduced or nil urinary output and restlessness and agitation . Chest b/l crepitations and CVS sinus tachycardia with absent peripheral pulses and cold extremities. Immediate intubation and ventilatory support initiated. The CXR showed ARDS <br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEigDu8JydsyRWjHZrnVBxzFxycLY4Re13ZXYjY6skeGBV2pc1V6C8DpGKpMu81njlvUdweZuheUCONHAUX2dyucvqK3WVHWeCrNZGqqun8vdtNOlsieJ3vdHeNORjmUMuCb9VjnSjdVLCkE/s1600-h/20100320049.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEigDu8JydsyRWjHZrnVBxzFxycLY4Re13ZXYjY6skeGBV2pc1V6C8DpGKpMu81njlvUdweZuheUCONHAUX2dyucvqK3WVHWeCrNZGqqun8vdtNOlsieJ3vdHeNORjmUMuCb9VjnSjdVLCkE/s320/20100320049.jpg" vt="true" /></a></div>Central line placement attempted irrespective of derranged coagulation as benefit outweighs risk(Paul Marino suggests derranged coagulation is not a contraindication to central venous cannulation)Inspite of all active interventions the patient developed asystole and expired in another 2 hours. <br />
<br />
<br />
Sepsis means systemic inflammatory response to infection particularly by gram negative bacteria like klebsiella, pseudomonas,enterococci or e-coli. Coagulase negative staphylococci are also implicated.The other agents responsible are fungi and viruses. Infetion leads to activation of neutrophils, endothelial injury, tissue parenchymal injury, organ damage and multiorgan failure.The noxious substances released due to infection including proteolytic enzymes and metabolites are responsible for this systemic inflammatory response and can be harmful to the body when the natural defence mechanisms of the body are overwhelmed.Thats why antibiotics are not much useful and corticosteroids are playing hide and seek in sepsis management. <br />
<br />
<strong>Sepsis Syndromes: </strong>According to ACCC (society of critical care consensus conference (critical care medicine 1992;20:864-74) sepsis syndromes can be classified as <br />
<br />
Stage 1) Systemic Inflammatory Response Syndrome (SIRS) if 2 or more of the following criteria are met<br />
a) Temp >38deg or less than 36degree<br />
b) Heart rate greater than 90/m<br />
c) Respiratory rate greater than 20/mt or paCO2 less than 32mmHg<br />
d) WBC count greater than 12000/micltr or less than 4000micltr or greater than 10% bands<br />
<br />
Stage 2) Sepsis; SIRS with a culture documented infection<br />
<br />
Stage 3) Severe sepsis; sepsis plus organ dysfunction, hypotension or hypoperfusion(lactic acidosis,oliguria,hypoxemia or acute alteration in mental status)<br />
<br />
Stage 4) Septic shock; hypotension despite fluid resuscitation plus evidence of hypoperfusion <br />
<br />
The features of severe sepsis include ARDS, Lactic acidosis, ATN, Liver dysfunction Septic shock, Altered mentation and DIC.The risk factors for acquiring infection are <br />
<br />
Diabetes, Anemia, Invasive procedures, Immunocompromised state ( AIDS TB or chemotherapy) Antibiotic abuse, Genetic predisposition, Drug addiction and severe road traffic accidents.<br />
<br />
<strong>Investigations:</strong> should be aimed at identifying the source or site of infection. Unfortunately all lab findings are nonspecific to sepsis diagnosis.Those which are helpful are <br />
<br />
<ul><li>Elevated WBCs with bands</li>
<li>ABG for respiratory compromise</li>
<li>Plasma lactate for tissue hypoxia </li>
<li>Coag profile for DIC</li>
<li>Blood culture: 40% cases organism can be isolated, Gram study and culture of serosanguinous fluids or bronchial aspirates are carried out.</li>
<li>RFT for renal failure</li>
<li>LFT hepatic derrangement</li>
<li>CXR: to find out pneumonia</li>
<li>CT or MRI to locate the septic focus of infection eg: retroperitoneal or intra abdominal abscess</li>
</ul><strong>Differential Diagnosis:</strong> Pulm embolism, MI, metabolic diseases, severe burns or trauma <br />
<br />
<strong>Treatment</strong><br />
<em><span style="font-family: Georgia, "Times New Roman", serif;">Oxygenation</span></em><br />
Remember that tissue oxygenation is not impaired in sepsis as the defect is in cellular oxygen utilisation a condition called cytopathic hypoxia. So tissue concentration of oxygen is high in severe sepsis. (Fink MP, Cytopathic hypoxia, mitochondrial dysfunction as mechanism for organ dysfunction in sepsis, criti care clinics 2001;17: 219-237). Keep SPO2 more than 90-95%. Permissive hypercapnea is allowed.Consider low tidal volume and low inspiratory pressure if on ventilator<br />
<span style="font-family: Georgia, "Times New Roman", serif;"><em>General principles:</em></span><br />
<ul><li>Rapid and prompt initial resuscitation</li>
<li>Good glycemic control</li>
<li>Stress ulcer prophylaxis</li>
<li>DVT prophylaxis; Elastic stockings if LMWH contra indicated</li>
<li>Strict infection control</li>
<li>Adequate nutrition, preferably early enteral route</li>
<li>Maintenance of normothermia</li>
<li>Early mobilisation </li>
</ul><em><span style="font-family: Georgia, "Times New Roman", serif;">Initial resuscitation</span></em><br />
<br />
Central venous pressure: 8–12 mm Hg<br />
Mean arterial pressure 65 mm Hg<br />
Urine output 0.5ml/kg/hr<br />
Central venous (superior vena cava) or mixed<br />
venous oxygen saturation 70%<br />
<br />
Fluid challenge: <br />
1)Infuse 50-100ml crystalloid or 300-500ml colloid over 30 minutes<br />
2)Repeat as needed until goal reached or fluid overload imminent<br />
5% albumin preferred in sepsis as hypoalbuminemia is usually associated with sepsis(Marik PE treatment of hypoalbuminemia in the critically ill patients, Heart Lung 1993; 22, 166-170)<br />
<br />
<em><span style="font-family: Georgia, "Times New Roman", serif;">Vasopressors:</span></em> Dopamine 5-20 mic/kg/mt,or norepinephrine 0.2 -1.3 mic/kg/mt(1-10 mic/mt for 70 kg patient)<br />
Still refractory consider vasopressin, a pure vasoconstrictor at the dose of 0.01 to 0.04 units/mt<br />
<br />
<em><span style="font-family: Georgia, "Times New Roman", serif;">Steroids:</span></em> previously not considered for sepsis management but evidence shows that low doses are beneficial especially in adrenal shut down, low dose Hydrocortisone 6th hrly or 200-300mg IV OD for 7 days improved survival in 'pressor unresponsive' sepsis(if administered in less than 8 hrs of presentation)<br />
<em><span style="font-family: Georgia, "Times New Roman", serif;">Norepinephrine:</span></em> greater than 0.4mic/kg is anNalternative for pressor resistant septic shock.<br />
<em><span style="font-family: Georgia, "Times New Roman", serif;">Activated protein C</span></em> if given before 48 hrs of onset improves outcome<br />
Anti inflammatory antibodies agaist endotoxins, TNF, IL-1etc. under trial, Polyclonal<br />
intravenous immunoglobulin has been reported to reduce mortality rate and is a promising adjuvant in the treatment of sepsis and septic shock.<br />
<em><span style="font-family: Georgia, "Times New Roman", serif;">Surgical drainage</span></em> of pus<br />
<span style="font-family: Georgia, "Times New Roman", serif;"><em>Granulocyte colony stimulating factors</em></span> improves immunity<br />
<em><span style="font-family: Georgia, "Times New Roman", serif;">Anti oxidant therapy:</span></em><br />
Free radicals produced during inflammation are thought to be the cause for tissue injury. Hence Antioxidants act as "free radical scavengers" and prevent and repair damage done by these free radicals. eg: Coenzyme Q10 (CoQ10) ,Glutathione superoxide dismutase (SOD) ,catalase glutathione peroxidase etc Now under experimental trial<br />
<span style="font-family: Georgia, "Times New Roman", serif;"><em>Others:</em></span> Plasmapheresis, GIK regimen, Hemofiltration<br />
<strong>Sepsis resuscitation bundles</strong><br />
<em><strong>complete within 6 hours</strong></em><br />
Measures serum lactate<br />
Obtain blod cultures prior to antibiotic administration<br />
Administer broad spectrum antibiotics within 3 hours of emergency department admission and within 1 hour on emergency department admission<br />
In the event of hypotension or serum lactate more than 4 mmol/L20ml/Kg of crystalloid or equal volume of colloid then use vasopressors to keep mean BP more than 65mmHg if not responding to fluid.<br />
If still hypotensive achieve CVP more than 8mmHg and SCvo2 more than 70 or SVo2 more than 65<br />
<em><strong>complete within 24 hours</strong></em><br />
Give low dose steroid for shock<br />
Administer activated protein C <br />
Maintain glucose between 70-150 mg/dl<br />
Mean insp plateau pressure less than 30 cm of water<br />
<br />
Ref: R. Phillip Dellinger, MD; Jean M. Carlet, MD; Henry Masur, MD;et al; Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock, Critical Care Med 2004 Vol. 32, No. 3<br />
<a href="http://www.survivingsepsis.org/">http://www.survivingsepsis.org/</a><br />
Paul Marino; The ICU Book, second and third editions.<br />
Current critical care diagnosis and treatment second edition<br />
Mervin Singer, Andrew Web; Oxford Hand Book of Critical Care, 3rd edition<br />
<br />
<strong>Other sites of interest:</strong><br />
Advances in Sepsis<br />
<a href="http://www.advancesinsepsis.com/">http://www.advancesinsepsis.com/</a><br />
European Society of Intensive Care Medicine<br />
<a href="http://www.esicm.org/">http://www.esicm.org/</a><br />
International Sepsis Forum Website<br />
<a href="http://www.sepsisforum.org/">http://www.sepsisforum.org/</a><br />
Society of Critical Care Medicine<br />
<a href="http://www.sccm.org/">http://www.sccm.org/</a>DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com0tag:blogger.com,1999:blog-8746726747957343433.post-57059769960490207352010-03-13T06:34:00.000-08:002013-02-27T00:53:47.085-08:00GUILLAIN-BARRE SYNDROME<div dir="ltr" style="text-align: left;" trbidi="on">
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Acute, frequently severe and fulminant, poly radiculopathy,which is auto immune in nature.Males and females equally affected. More frequent in adults than in children.Variants involving the cranial nerves, pure motor involvement etc are also found. In severe cases, muscle weakness may lead to respiratory failure,with auto nomic involvement and unstable hemodynamics, necessitating ventilatory management<br />
<b>Clinical Manifestations</b><br />
<br />
<ul>
<li>Rapidly evolving, progressive, ascending motor paralysis with or without sensory disturbance and with areflexia</li>
<li>Lower cranial nerves are frequently involved and presented with difficulty in swallowing and maintaining airway</li>
<li>Bulbar involvement is most frequently manifested as B/L facial paralysis</li>
<li>Fever and other constitutional symptoms are usually absent</li>
<li>Diminished DTR with absent proprioception. There may be marked sensory loss</li>
<li>Bladder dysfunction is late and transient. </li>
<li>Deep aching pain in muscles and back</li>
<li>Difficulty in swallowing due to pharyngeal muscle weakness and impaired ventilation due to intercostal muscle paralysis in 30% of cases and they require ventilatory support </li>
<li>Marked autonomic dysfunction leads to Wide fluctuations in blood pressure – hypo / hyper tension, Sudden profuse diaphoresis,Peripheral vasoconstriction Resting tachycardia,Cardiac conduction abnormality, Orthostatic hypotension – severe, Thromboembolism due to immobilisation, & sudden death</li>
<li>Metabolic derangements -Hyponatremia due to excessive ADH secretion <a name='more'></a></li>
</ul>
<b>Pathophysiology </b><br />
The condition is preceded 1-3weeks by a/c infections affecting the respiratory tract or GIT (60-75% cases). Commonly implicated organisms include CMV, Epstein Barr, HIV, Viruses or Mycoplasma pneumoniae or crampylobacter jejuni bacteriae. GBS is also found to be associated with lymphoma and hodgkin’s disease. The basic pathophysiology is, Immune responses to nonself antigens - auto antibodies - misdirected to host nerve tissue - ganglioside damage - demyelination - conduction block.Secondary axonal degeneration rare, except in chronic cases.<br />
<br />
<b>Diagnosis </b><br />
<br />
<i><span style="font-family: Georgia, "Times New Roman", serif;">Essential Criteria</span></i><br />
<br />
<ul>
<li>Progressive weakness of more than one limb due to neuropathy</li>
<li>Areflexia</li>
<li>Duration of progression less than 4 weeks</li>
</ul>
<i><span style="font-family: Georgia, "Times New Roman", serif;">Supportive Criteria</span></i><br />
<ul>
<li>Relative symmetry </li>
<li>Mild sensory signs or symptoms </li>
<li>Cranial nerve involvement, especially bilateral facial weakness </li>
<li>Recovery begins 2 to 4 weeks after progression ceases </li>
<li>Autonomic dysfunction </li>
<li>Absence of fever at onset </li>
<li>Typical CSF and EMG/nerve conduction studies features. <br />
<b></b></li>
</ul>
<b>Clinical Features</b><br />
<br />
<ul>
<li>Weakness is usually symmetrical</li>
<li>Sensory signs are mild</li>
<li>Cranial nerve involvement common</li>
<li>Autonomic dysfunction common</li>
</ul>
<b>Laboratory Features</b><br />
<br />
<ul>
<li>CSF after 1st week, total protein content is increased (80%)</li>
<li>White cell count near normal (90%)</li>
<li>EMG--nerve conduction slowed, suggesting demyelination </li>
</ul>
<i><span style="font-family: "Courier New", Courier, monospace;"><b>Antibodies in GBS</b></span></i><br />
GM1 - Associated with severe, pure, motor variant<br />
GM1b - Campylobacter jejuni -- severe progression<br />
GQ1b - Miller Fischer variant<br />
<br />
Permanent Neurological sequalae in 7-15% of patients<br />
1) Foot drop 2) Intrinsic muscle weakness3) Sensory ataxia 4) Dysarthria<br />
<br />
<b>Differential diagnosis for GBS</b><br />
<br />
<ul>
<li>Transverse Myelitis</li>
<li>Myasthenia Gravis</li>
<li>Poliomyelitis</li>
<li>Periodic Paralysis</li>
<li>Polymyositis</li>
<li>Acquired hypokalemia</li>
<li>Botulism</li>
<li>Porphyric neuropathy</li>
<li>Toxic neuropathies</li>
<li>Meningo radiculopathies</li>
<li>Lyme’s disease,and radiculopathies due to CMV, HIV</li>
</ul>
<b>Treatment in nutshell.</b><br />
<ul>
<li>Symptomatic</li>
<li>Good general medical and nursing care including monitoring </li>
<li>Monitoring of vital capacity and when it is less than 15ml/kg or pharyngeal muscle weakness - early intubation and ventilatory support indicated</li>
<li>Measurement of ABG - adequacy of ventilation</li>
<li>Suction clearance of secretions</li>
<li>Tracheostomy if prolonged ventilation is needed</li>
<li>Measures to prevent DVT and pulmonary embolism- heparin s/c, graded elastic stocking etc</li>
<li>Skin care--frequent turning to prevent bed sore</li>
<li>Chest physiotherapy and correction of electrolytes</li>
<li>Steroids are not much useful</li>
<li>Plasmapheresis; Accelerates recovery if performed within 2 weeks of onset of the disease. Within 1 week - most useful. 40-50ml/kg plasma exchange for 4 to 5 days </li>
<li> I/V immunoglobulins 2g/kg 5 daily infusions</li>
</ul>
ICU monitoring and elective intubation should be considered if Vital capacity less than 20 mL/kg , Maximal inspiratory pressure worse than -30 cmH2O, Maximal expiratory pressure less than 40 cmH2O, Reduction of 30% in vital capacity, Maximal inspiratory pressure or Maximal expiratory pressure. <br />
<br />
<b>Recovery</b><br />
85 to 90% patients recover completely in a few weeks, Death is Mainly due to secondary pulmonary complications, ARDS, emboli etc.Mortality rate is 3 to 8%<br />
<br />
<b>Anesthetic Considerations</b><br />
Patients usually present for elective tracheostomy and are already intubated<br />
<br />
<i><span style="font-family: Georgia, "Times New Roman", serif;">Preoperative assessment</span></i><br />
<br />
<ul>
<li>If unintubated assess airway, month, dentition and neck</li>
<li>Assess bulbar function to prevent aspiration during induction</li>
<li>Assess respiratory muscle function – vital capacity, mouth occlusion pressures, cough</li>
<li>Assess autonomic function – ECG, postural hypo tension, excessive sweating</li>
<li>Correct electrolyte imbalance/hyponatremia </li>
</ul>
<i><span style="font-family: Georgia, "Times New Roman", serif;">Perioperative Management</span></i><br />
<br />
Monitoring : ECG, BP , Invasive and Noninvasive SPO2, PNS Rapid sequence induction if bulbar function is poor, using vecuronium suggested.But suxamethonium is avoided as wide spread denervation may result in hyperkalemia.Controlled ventilation is indicated. Altered function of ANS so compensatory CVS responses may be absent and can cause Profound hypo tension, when there is blood loss, changes in posture or application of positive pressure ventilation.Similarly noxious stimulus can cause hypertension for example laryngoscopy or painful stimulus. Vasopressor adminis tration may cause exaggerated response. Non depolarizing relaxants requirement is less, and if needed vecuronium is preferred. Regional anaesthetic techniques contraindicated and if at all graded epidural may be beneficial.<br />
<br />
<b>Post Operative Management</b> <br />
<ul>
<li>Adequate pain relief</li>
<li>Post operative ventilation continued</li>
<li>Care of bowel, bladder and skin</li>
<li>Physiotherapy/prevention of DVT</li>
</ul>
Ref: <a href="http://bestpractice.bmj.com/best-practice/monograph/176/diagnosis/criteria.html">http://bestpractice.bmj.com/best-practice/monograph/176/diagnosis/criteria.html</a>, Millers anaesthesia 6th edition, Harrisons principles 17 th edition, Stoelting anaesthesia and co existing disease 4th edition, E- med; <a href="http://www.emedicine.medscape.com,gbs/">http://www.emedicine.medscape.com,gbs/</a><br />
<br />
<b><span style="background-color: white; color: red;">HOT ISSUES NOW!</span></b><br />
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The recent H1N1 pandemic has brought concern and fear about Guillain Barre syndr ome once more. The issues raised were whether swine flu itself can cause GBS? and whether vaccination agaist H1N1 is associated with increased risk of Guillain Barre syndrome? Let us see what CDC, media, authorities, and experts say about this. Like other viral infections, H1N1 infection itself has the potential for triggering an immune reaction leading on to GBS, but the estimated incidence is unknown. The available literature supports the safety of vaccine.This is a controversial issue and the blogger has no personal opinion about this. Follow the links and arrive at a conclusion.<br />
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<a href="http://www.cdc.gov/h1n1flu/vaccination/gbs_qa.htm">http://www.cdc.gov/h1n1flu/vaccination/gbs_qa.htm</a><br />
<a href="http://www.phac-aspc.gc.ca/alert-alerte/h1n1/faq/faq_rg_h1n1-fvv-eng.php">http://www.phac-aspc.gc.ca/alert-alerte/h1n1/faq/faq_rg_h1n1-fvv-eng.php</a><br />
<a href="http://www.cbsnews.com/stories/2009/11/20/earlyshow/health/main5723397.shtml">http://www.cbsnews.com/stories/2009/11/20/earlyshow/health/main5723397.shtml</a><br />
<a href="http://www.cdc.gov/eid/content/16/3/pdfs/09-1699.pdf">www.cdc.gov/eid/content/16/3/pdfs/09-1699.pdf</a><br />
<a href="http://www.flutrackers.com/forum/showthread.php?p=343548">http://www.flutrackers.com/forum/showthread.php?p=343548</a><br />
<a href="http://www.reuters.com/article/idUSTRE50R6IK20090128">http://www.reuters.com/article/idUSTRE50R6IK20090128</a></div>
DR.M.KHAN SHERIEF http://www.blogger.com/profile/11660784689085374264noreply@blogger.com3