NITRIC OXIDE: THE SAVIOUR.

Nitric oxide (NO) is one of the nitrogen oxides and is synthesized within cells by an enzyme NO synthase. It  was formerly known as endothelium-derived relaxing factor (EDRF).  Being one of the fundamental mediators in physiological processes, this enzyme catalyses the oxidation of L-arginine to L-citrulline, producing NO, which diffuses into vascular smooth muscle, activating guanylate cyclase  which in turn converts guanosine triphosphate into cyclic guanosine monophosphate (cGMP),causing vascular relaxation.
                                 Nitric oxide synthetase is present in two forms a)The constitutive form (eNOS), which is present in vascular, neuronal, cardiac tissue, skeletal muscle and platelets, producing small quantities of NO continuously. Here NOS is Ca2+/calmodulin dependant and is stimulated by cGMP.and b)the inducible form (iNOS),present in endo thelium, myocytes, macrophages and neutrophils, which produces relatively large quatities of NO after exposure to endotoxins in sepsis.

Biological effects of Nitric oxide ;
• Vascular endothelium: producing vascular relaxation.
• Platelets: involved in aggregation and adhesion of platelets
• Brain tissue: acts as a neurotransmitter.
• Macrophages: involved in the response to infection.

RESUSCITATION IN PREGNANCY DURING AND AFTER

The overall incidence of cardiac arrest during late pregnancy is  estimated to be one in 30000,  however survival rate following such an event is extremely low. Most deaths are due to acute medical conditions associated with pregnancy rather than due to causes from pregnancy itself. Resusctation in pregnancy is different as we have two potential patients, the mother and the fetus. The best hope of fetal survival is maternal survival. Factors peculiar to pregnancy such as the anatomical, physiological and pathological changes make resuscitation difficult  in late pregnancy. The major considerations are :

Respiratory

• Increased  alveolar ventilaton and oxygen consumption
• Increased oxygen demand
• Reduced chest compliance
• Reduced functional residual capacity
• Increased risk of  aspiration
• Laryngeal edema
• Airway obstruction due to edema and soft tissue hypertrophy

Gastrointestinal

• Incompetent gastroesophageal (cardiac) sphincter
• Increased intragastric pressure
• Increased risk of regurgitation
• Increased acidity of gastric contents

Cardiovascular

• Physiological anemia
• Supine hypotension syndrome 

Anatomical

• Obesity, turning the patient to one side is difficult and requires assistance
• Hypertrophied breasts  cause difficulty in laryngoscopy  and prevents effective chest compression or defibrillation

Basic life support

•  Remove dentures or foreign body from airway
•  Suction and artificial airway,  if available
•  Ventilation by mouth to mouth or using an ambu bag. Remember to apply cricoid  pressure
• Turn the patient to get  lateral displacement of uterus and thereby preventing venacaval obstruction by the gravid uterus. A left lateral displacement is made by tilting the body to 30 degrees which can be  achieved with a cardiff wedge kept beneath the right buttock or a rolled towel  or pillow if wedge is not available. The other techniques to provide tilt are by manual displacement of uerus or by tilting onto the back of an upturned chair. A human wedge is the one where the patient is turned onto a rescuers knees to provide a stable position for BLS.
• Chest compressions at the rate of 30:2, consider the cephalad movement of the diaphragm, and so the hands should be kept at a higher level during compression

ACLS

• Early inyubation is recommended
• Airway is "difficult"
• Tracheal intubation difficult due to  anatomical changes like short neck, edematous soft tissues,  large tongue, and large breasts
• So isertion of laryngoscope is difficult hence,  short handle may be used  for the scope,  removing the blade and re attach after insertion into the oral cavity, or using a curved blade like Mc Coy, or polio blade etc are advised
• LMA classic or FAST TRACH  are advised  for emergency airway access if intubation fails.  Release cricoid pressure during insertion and re apply after insertion of LMA eventhough cricoid pressure  is not very effective with LMA insitu.
• Defibrillation  when needed should be done according to standard ACLS defibrillation doses. Remove all fetal or maternal monitors while giving shock. DC shocks are found to be not harmful to the fetus
• Immediate iv access and fluid resuscitation in case of hemorrage
• Consider low tidal volumes, enough to make a visible chest rise
• Consider early caesarean section  when standard rsuscitative measures fail to restore maternal circulation and shoul be done in less than 5 minutes.(even after mother's heart stops) caesarean section helps to relieve aortocaval compression and incrase venous return, thereby improve cardiac output.It also increases thoracic compliance
• Vaso pressors are also used as per standard ACLS protocols eventhough fetal blood flow is reduced

Differential diagnoses to be considered during or immediately after resuscitation

• Immediate abdominal ultrasound for concealed hemorrage
• Excess magnesium sulphate(may be iatrogenic). Administer calcium gluconate      1 gram or one ampoule.  Empirical therapy also is life saving.
• Acute coronary syndromes to be considered in elder patients.  Fibrinolytics  are  contra indicated hence percutaneous coronary intervention is the treatment of choice for STEMI
• Pre eclampsia, or eclampsia,  consider treatment of hypertension or emergency caesarean section
• Aortic dissection, a rare possibility
• Life threatening pulmonary embolism or stroke  here fibrinolytics must be administered as prognosis was found to be good ,in spite of risk, in  massive embolus
• Amniotic fluid embolism  consider  immediate CABG
• Trauma and drug overdose

Ref;   1) Circulation. 2005;112:IV-150 – IV-153. AHA guidelines for CPCR
         2) The abc of resuscitation,   BMJ

H1N1 PNEUMONIA, AN UPDATE

The outbreak of H1N1 influenza A virus infection was first detected in Mexico, in April 2009, with subsequent spread as pandemic to other countries .The diagnosis and management of H1N1 infection is of great concern to any health organisation so also its prevention. Patients having pneumonia  with prior symptoms of  H1N1 influenza, should be referred to intensive care units for further management, as prognosis is good except for the high risk patients.These high risk groups are

• Children younger than 5 years of age, but especially those younger than 2
• Individuals 65 years of age or older
• Pregnant women and women up to two weeks postpartum (including those who have had pregnancy loss)
• Individuals younger than 19 years of age who are receiving long-term aspirin therapy and who therefore might be at risk for Reye syndrome after influenza virus infection
• Individuals of any age with chronic medical conditions requiring ongoing medical care, including: chronic pulmonary disease,( including asthma) ,active malignancy  chronic renal insufficiency,chronic liver dise,diabetes mellitus,hemoglobinopathies such as sickle cell disease, immunosuppression, including HIV infection, immunoosuppressants, certain collagen vascular diseases, such as rheumatoid arthritis,antiphospholipid syndrome, etc
• Patients with inability to remove resp secretions due to inadequate cough reflex,  due to  spinal cord injury, neuromuscular diseases ,Children with metabolic diseases and Obesity are also cosidered under high risk. 

 
RECOMMENDATIONS

• Isolate all patients with respiratory signs suggestive of pneumonia
• Avoid use of fans as it causes air recirculation, normal icu air exhaust is enough
• Keep visitors to minimum
• Health care workers should wear, gloves, gown , FFP3 mask, eye protection as aerosol transmission is the major route of spread
• Hand hygiene
• Eye protection(goggles)

PROCEDURES  CAUSING INCREASED RISK OF TRANSMISSION BY AEROSOL

• Intubation and manual ventilation
• Tracheal suctioning
• Nasopharyngeal aspiration
• CPCR
• Bronchoscopy
• Autopsy procedures
• Nebulisation
• Nippv

DIAGNOSIS

• nasopharyngeal or throat swabs for viral culture or polymerase chain reaction

VENTILATION

• As far as possible consider non invasive ventilation, but intubation and ventilation may be considered if there is progressive increase in respiratory distress  and ABG is unsatisfactory.Following are the crieteria for invasive ventilation

1. Refractory hypoxemia,SpO2 < 90% on non-rebreathe mask @ 15L/min oxygen flow
2. Respiratory acidosis,pH < 7.2
3. Clinical evidence of impending respiratory failure,Respiratory rate > 40
4. Inability to protect or maintain airway
5. GCS <8

STRATEGY:

• Closed suctioning preferred
• Ventilatory strategies are similar to ARDS
• Consider inhaled nitric oxide and prone ventilation for better oxygenation
• High frequency oscillatory ventilation or ECMO should be considedered in refractory cases

ANTIVIRAL THERAPY

• H1N1 viruses are susceptible to neuramnidase inhibitors like osaltamivir and zanamivir(inhalation) but resistant to amantadine or rimantadine. Ideally treatment should start immediately to avoid viral replication but can be started at any stage of active  illness.The usual dosage in adults is 75 mg bid and 30-40mg bid for infants older than 1 year and children the dosage in critically ill is almost double than that used for influenza oseltamivir 150 mg bid through ryles tube may be used for 10 days. Dose adjustment required for creatinine clearance less than <30ml/mt.The recommended dose of zanamivir(above 5 yrs of age), is two inhalations(2 x 5mg) twice daily for 5 days.
• Rare but serious neuropsychiatric illness are reported as side effect for osaltam ivir.The adverse effects of  zanamivir include bronchospasm in asthmatics and gastrointestinal intolerance

SUPPORTIVE MANAGEMENT

• 20 percent of people require dialysis due to a/c renal failure
• Conservative fluid management advised
• Manage electrolyte abnormalities
• Secondary infection with streptococcal, staphylococcal and pneumococcal  bacteria  are common. appropriate culture and antibiotics administered.
• Control of hyperthermia by active cooling
• High flow oxygen therapy
• Low dose corticosteroid therapy is advantageous for treatment of septic shock, hypotension, or adrenal suppression but not recommended routinely(WHO)

Hypotension management shoul be aggressive and targeted

 • Systolic blood pressure < 90 mm Hg
 • Clinical evidence of shock:
 • Altered level of consciousness
 • Decreased urine output refractory to
 • Volume resuscitation
SOFA score  may be used for critical care assessment

Ref.links:
www.icmed.com/.../H1N1%20Influenza%20Management%20in%20the%20ICU%20gen...
http://www.utdol.com/home/content/topic.do?topicKey=pulm_inf/19054#

The United States Centers for Disease Control and Prevention
http://www.cdc.gov/h1n1flu/recommendations.htm

TRANSFER BY AIR

Patients, with dysfunction or failure of one or more organs can be categorised as critically ill patients. They depend on advanced monitoring and therapy to sustain their lives.When equipments, personnel or other facilities are not available or insufficient to deal with the critically ill patients, they should be transferred to a tertiary centre. Since these patients have reduced physiological reserves, even short trips can cause signi ficant adverse effects. Movements in the vehicle, temperature and pressure changes also affect them badly. The other problems to be faced are vehicle accidents and stress related health problems for the transporting personnel. Modes of transport that are available range from family car to fixed-wing aircraft. Here we are discussing the problems in transportation  by air with special referrance to helicopter or aircraft. Air lifting is appropriate if the transportation distance exceeds over 150 miles.Consider the following factors when air transportation is planned.

• Weather and climatic conditions, whether suitable or not.
• The time required >; to arrange the aircraft, to get permission to cross the borders of  a neighboring country, to arrange the staff and equipments.
• The risk benefit ratio.
• The condition of the patient, means the physiological tolerance
• The cost effectiveness

The advantages of air transport are

• Rapid transport (30-50% time of ground transport, 120-180 MPH covering up to 150 miles)
• Easy access to difficult locations
• Smoother flight
• Decreased incidence of accident, unless the craft is faulty

The disadvantages are

•    Helipad or aerodrome needed
•    Space and weight limits
•    Patient access limited
•    Increased noise level (90-110 dB)
•    Motion sickness 
•    Incorrect NIBP and SPO2 measurement due to movement and vibration
•    Weather restrictions
•    Altitude effects (>8000 ft) (mentioned below)
•    Cost to operate

A lower barometric pressure at high altitude can cause a reduction in the partial pressure of the oxygen in the alveoli. At 1500 meters Pao2 is about 75 mm of Hg. Also noise and vibration can cause autonomic dysturbances leading to nausea, vomiting, hypertension or tachycardia.Air contained in closed spaces and body cavities will get expanded due to low atm pressure. These problems are more with a helicopter and can be reduced significantly, if transportation is done by fixed wing aircraft as the cabin is pressurised to atmospheric pressure. The aircraft can offer more space, is fast, and can manage bad weather, cause less noise and vibration but are expensive.The other problems of air lifting include vibration leads to failure and inaccuracy of NIBP, limited Access to the patient ,accelaration and decelaration,hypothermia,etc. Pulse oxy meters may be un reliable in cold and moving patients.

How to manage transport?

• Increase fio2 if cabin is open
• Drainage of pneumothoraces
• All tubes eg, NG tube should be kept open
• Split plaster casts, as these may cause ischemic injury of the limb due to swelling up of tissues

According to General Surgeon, Neel, (commanding officer of the helicopter, medical evacuation program in Vietnam) The helicopter must be incorporated into an integrated medical system. Such a system must include centralized control, adequate, reliable communications, methods for locating and reporting casualties, and skilled medical personnel to provide attention at the site of the injury, during flight, and at the arrival of the the hospital.

Thanx to: Dr.Babji Kalapati, Anaesthetist, ARMED FORCES HOSPITAL, MUSCAT, for sharing the information

Ref:   Oxford handbook of critical care, 3rd edition page 648

THE MYSTERIOUS SOUL!

Believe it or not, it happened  and it is true...........
During my tenure as lecturer in a teaching institution, i was posted on  rotation to emergency OT. The busy OT list went upto 3 am early morning and i was too sleepy and tired,to attend the last patient for appendicectomy. I told my junior to proceed with the case and then took rest for some time.  Immediately i fell asleep. Now i could see somebody trying to wake me up from sleep.I got up,  half asleep and, surprised to see a new face, a middle aged man with beard, in  khaki coloured pants  and white shirt. I thought he may be a newly appointed ward attendant or any staff from some other department,whom i have not met before.  Since the lights were switched off ,and  the corridoor lights were not powerful, his identity was also not very clear. and.......
he was telling,  Doctor;  you rush immediately to A and E, there is a serious case admitted with head injury, who just had a  road traffic accident. This time i am really confused and i checked my pager for any missed call registration but nothing was there. But as a routine the A and E staff is calling the anaesthetist over phone, to attend the emergencies, in case the pager fails. Rarely do they send a person to OT, and persons coming to OT are  supposed to  change their  dress also. But this person was not in OT uniform at all! After all it is impossible for some body to come inside the OT  without the permission from  the staff as the doors are closed and locked from inside, and if this is the case the staff should have called me  first. I thought i might have missed the phone call from emergency department as i was in deep sleep, and so they sent this person. I opened my cupboard to take  my stethescope and emergency kit and turned to him but... he had already disappeared. I rushed to A and E  and noticed on the way that all doors were still remaining closed.
                               I had a totally different experience when i reached A and E as i couldnt find any patient and the atmosphere is totally silent. One sister is sleeping on the desk and she has not even noticed the  loud alarm from a steriliser. I woke up the sister and asked, any emergency?  She was very much angry and told me,  what happened to you doctor? are you crazy? did you receive any code alert? why you are disturbing others at this time?  I cursed my fate, may be it is a dream, and expressed sorry to sister,and walked out. But suddenly one ambulance arrived and stopped, and the attendants took out a body soaked with blood. Now  i could hear the sister shouting , doctor your patient has come;  attend and go., so i immediately attended.
I was shocked and trembling to look at the face, and i couldnt believe my eyes!!         IT WAS THE SAME PERSON WHOM I MET IN OT! He was gasping and had sustained severe  head injury. Immediate intubation , CT scan and evacuation of extradural hematoma was done.Patient was on ventilator for 5 days and discharged after3 weeks  but couldnt recall anything following the accident.
                        Your mind or thoughts can be influenced by others , especially during emergencies.The already dead or dying can also control your mind or consciousness. But how? nobody knows. Psychologists call this phenomenon as telepathic transmission of thoughts or dual personality or multiple personality.The scientific basis is still unknown. Have you heard that people are conversing with souls using ojo board? how it is possible?     Still i dont know.

OT:     Operation Theatre
keen about ojoboard? watch the link: http://ojoboards.blogspot.com/      

CENTRAL VENOUS CANNULATION. WHICH ROUTE?

Central venous cannulation is an indispensable monitoring tool in intensive care.Central lines  are used for fluid resuscitation  and cvp monitoring, trans venous pacing, administration of irritant drugs, parenteral nutrition,venovenous hemodialysis, and as vascular access when peripheral cannulation is impossible.Veins used for cannulation are  internal jugular, subclavian, and femoral. The advantages of subclavian cannulation over internal jugular are : absence of valves, larger vein,and low rate of catheter related infection (2). Also the patency can be maintained as chance of kinking the catheter is less.Care of the catheter by the staff also is easy as the location is more convenient.

Subclavian cannulation is attempted by supraclavicular or infraclavicular approach, the second approach is more common and often described as classic. To our observation the supraclavicular route offers and excellent alternate way of subclavian cannulation and is associated with fewer side effects compared to infraclavicular approach, and is also relatively easy. The advantages of  this approach are,

• There is a well defined anatomical landmark, the angle formed by the clavicular head of sternomastoid with the clavicle,
• A straighter course to the IJV
• Away from apex of lung
• Less chance of arterial puncture
• Can be inserted during cpcr, without interruption.
• And is useful in obese patients and pregnant ladies, where land mark is obscure

TECHNIQUE:  The needle is inserted 1 cm lateral to the lateral head of the sternocleidomastoid muscle and 1 cm posterior to the clavicle and directed at a 45-degree angle to the sagittal and transverse planes. Aim towards the contralateral nipple. The needle  is advanced in an avascular plane, away from the subclavian artery and the dome of the pleura, entering the junction of the subclavian and internal jugular veins.a trendlenberg position is advised to avoid the risk of air embolism and distend the vein.  ref :(1)

CXR showing central line placed through Rt.subclavian by supraclavicular route

According to published literature  the overall complication rate  of supraclavicular route is around 0.56%.The author recommends supraclavicular route as the first choice of approach for central venous cannulation.
 
1.West J Emerg Med. 2009 May; 10(2):110–114.PMCID:PMC2691520,Supraclavicular Subclavian Vein Catheterization: The Forgotten Central Line
2. McGee DC, Gould MK. Preventing complications of central venous catheterization. N Engl J Med. 2003;348:1123–33. [PubMed]

ACUTE PAIN IN CHILDREN

YES CHILDREN ARE AFRAID OF NEEDLES AND INJECTIONS! A CHILD CRYING OF PAIN DUE TO INJURY, FRACTURE ,SICKLE CELL CRISIS OR DUE TO EVEN  DECAYED TOOTH, IS A CONCERN FOR THE MOTHER AS WELL AS FOR THE ATTENDING PHYSICIAN. IT IS HIGHLY IMPOSSIBLE AND CRUEL TO RESTRAIN A CRYING CHILD FOR INTRAVENOUS ACCESS, IN ORDER TO ADMINISTER ANALGESICS ESPECIALLY IN A&E AND IN WARDS. ALSO IV ANALGESICS LIKE MORPHINE  CAN CAUSE  IMMEDIATE SIDE EFFECTS DUE TO RAPID SYSTEMIC ABSORPTION. THE ANXIETY, APPREHENSION AND TENSION OF THE MOTHER ALSO TO BE CONSIDERED WHEN IV CANNULATION IS ATTEMPTED. ALL THESE CAN BE SURMOUNTED WITH THE INTRODUCTION OF DIAMORPHINE, WHICH IS FOUND TO BE EFFECTIVE WHEN ADMINISTERED INTRANASALLY, WHICH IS SLOWLY ABSORBED INTO THE SYTEMIC CIRCULATION THEREBY PRODUCING LESS SIDE EFFECTS, BUT PROVIDING EFFECTIVE PAIN RELIEF.

DIAMORPHINE IS A SEMISYNTHETIC DERIVATIVE OF MORPHINE AND CAN BE CONSIDERED AS A 'PRO-DRUG',EXERTING ITS EFFECTS BY ACTIVE METABOLITES.THE HALF LIFE IS 3-5 MINUTES AND IS HYDROLYSED AND DE ACETYLATED TO 6 MONO ACETYL MORPHINE AND THEN TO MORPHINE. MORPHINE IS THEN CONJUGATED AND EXCRETED.THE PHARMACOLOGICAL ACTION IS MAINLY DUE TO MORPHINE.

IT HAS BEEN SHOWN THAT DIAMORPHINE GIVEN INTRANASALLY 0.1 MG/KG ACHIEVED ADEQUATE PLASMA CONCENTRATIONS OF MORPHINE, COMPARABLE TO THE SAME DOSE GIVEN BY IV ROUTE. ALSO INTRANASAL DIAMORPHINE ADMINISTERED AS NASAL DROPS PRODUCED SIGNIFICANTLY ATTENUATED AND DELAYED PEAK PLASMA LEVELS OF MORPHINE COMPARED TO IV ROUTE, AND IS EFFECTIVE IN SICKLERS WHERE IV CANNULATION ITSELF IS DIFFICULT.

REF:S KIDD, S BRENNAN, R STEPHEN, R MINNS, T BEATTIE, COMPARISON OF MORPHINE CONCENTRATION TIME PROFILES FOLLOWING IV AND IN DIAMORPHINE, ARCHIVES OF DISEASE IN CHILDHOOD, DEC 2009 VOL94, ISSUE 12, THANX TO GOOGLE  IMAGE

COMMUNICATION AND PATIENT CARE

HOW IMPORTANCE IS COMMUNICATION WITHIN HEALTH CARE TEAMS? IT HAS BEEN OBSERVED THAT IN ANY HOSPITAL PROPER CARE TO THE CRITICALLY ILL PATIENTS WHO ARE NEARING DEATH, IS NOT GIVEN DUE TO A LACK  OF  COMMUNICATION BETWEEN  DOCTORS  OR BETWEEN DOCTORS AND STAFF.THIS IS BECAUSE OF THE WRONG CONCEPTION THAT THE CRITICALLY ILL PATIENT WHO IS NEARING TO DEATH IS AT "NO POINT OF RETURN" AND SPENDING TIME AND EFFORT ARE FUTILE. ACCORDING TO THE SURVEY BY THE NATIONAL CONFIDENTIAL ENQUIRY INTO PATIENT OUTCOME AND DEATH, CARING TO THE END IS NOT PROPERLY CARRIED OUT TO PATIENTS GOING TO DIE, AND MOST OF THESE CASES PROPER 'HAND OVER' IS NOT GIVEN BETWEEN THE STAFF OR THE CONSULTANTS NEVER VISITED THEM, DENYING THESE PATIENTS OF PROPER 'END LIFE CARE'

READ MORE AT.....http://www.rcoa.ac.uk/index.asp?PageID=65&NewsID=727
post you comments at comments

MAC OR MAC?

WHAT YOU MEAN BY MAC?  IN ANAESTHESIA MAC REFERS TO EITHER MONITORED ANAESTHESIA CARE OR MINIMUM ALVEOLAR CONCENTRATION.
According to the American Society of Anesthesiologists (ASA), a monitored anesthesia care (MAC) is a planned procedure during which the patient undergoes local anesthesia together with sedation and analgesia. The three fundamental components  and purposes of a conscious sedation during a MAC are: a safe sedation, the control of the patient anxiety and the pain control.The patient should be consciously sedated and remain without pain or discomfort.This procedure can be performed with patient controlled sedation techniques or with continued intravenous infusion or with target controlled infusion.using anaesthetic agents which have a fast half life.Just connecting to monitor and asking surgeon to give blocks cannot be called MAC,in the ideal sense. But how conscious sedation monitored? The Internet Journal of Health, suggests bi spectral index for this purpose.Drugs to control PONV and other drugs for co morbid conditions like DM etc are advised to be given and their activity monitored.The patient may be observed in PACU for about thirty minutes, eventhough fast tracking is possible. Anaesthetic agents used are midazolam, propofol, remifentanyl,and alpha2adrenergic drugs.
                                         Minimum alveolar concentration means,the concentration of inhalational anaesthetic agent that prevents movement in response to a skin incision in 50 % of individuals at 1 atmosphere in 100 % oxygen.The anaesthtic potency can be calculated from MAC based on the fact that, at equilibrium the alveolar concentration equates brain concentration and alveolar concentration can be  easily measured.It has been observed that sex, weight, height and anaesthetic duration will not affect MAC . MAC values of different agents are additive, and it has been observed that 1.3 times MAC of any anaesthetic agent prevents movement in 90% of individuals.       MAC values
* Halothane 0.74 %
* Enflurane 1.68 %
* Isoflurane 1.15 %
* Desflurane 6.3 %
* Sevoflurane 2.0 %
* Nitrous oxide 104 %
 
FACTORS AFFECTING MAC
 
INCRASE IN  MAC

 Hyperthermia
 Hypernatraemia
 Sympathoadrenal stimulation
 Chronic alcohol abuse
 ? Chronic opioid abuse
 Increases in ambient pressure
 Hypercapnia
 Decreasing age
 Thyrotoxicosis

DECREASE IN MAC

 Nitrous oxide
 Hypothyroid/myxoedema
 Hypocapnia
 Hypothermia-decrease is roughly linear
 Hyponatraemia
 Increasing age
 Hypotension
 Anaemia
 Pregnancy
 Hypoxia
 CNS depressant drugs including alcohol,lithium, magnesium,clonidine etc

Ref: a brief history of MAC, anaesthesiology 2002,96(1), & anaesthesia uk,  Intnt journl of health,2000,vol.1,no1

THE TRACHEOSTOMY DREAM!

DO ANAESTHETISTS DRAEM? OFCOURSE, THEY DO. AFTER FINISHING A BUSY PEDIATRIC LIST, AND WHEN THE END TIDAL SEVOFLURANE CONCENTRATION EQUATES MAC, ANAESTHETISTS MAY TAKE A DOZE AND DREAM. HERE IS AN INTERESTING DREAM "STORY", BY AN ANAESTHETIST.

I was sleeping..... and i heard some noice outside my duty room, its like shouting or banging at the door by some one, i got up cursing my time, opened the door and found three people, one female and two males, gazing at me,furiously.I could see all of them were covering their neck with their hands. I asked, whats the matter? they said, "we are already dead and reached our final destination, means to GOD almighty, and we were sent back to earth. We were treated by you in icu, when we were critically ill on ventilator. Its you!  its you!, who made these holes on our necks, and they removed their hands covering neck. I was surprised to see that, all of them were tracheostomised with the holes still persisting! They then told me that, all of them were allowed to enter heaven by god, but the god's assistants refused their entry just because of their holes on neck as such a deformity is not expected for anybody coming to heaven, and told them we can go to hell if we wish. We were asked by these servants of god, to go back to earth and meet those people who made this deformity to us and find a solution, So we are sure, you are responsible for this as you gave consent for tracheostomy and so should find the solution also.

I was totally confused, and i tried to convince them that, eventhough i gave the consent, the decision to operate was taken by the ENT surgeon and he did the procedure, and i just supported him thinking that this will improve your clinical condition.But unfortunatelly all of you were critically ill and we couldnt save your lives. So please go to the ENT surgeon and ask for help.

They nodded their heads and immediately disappeared, after sometime again i heard knocking sounds at the door, i opened the door , and i found them again. this time one more person also present with them, and that was the ENT surgeon. The surgeon told me, some how it happened, and now we have to find a solution. only you can help me. We asked our visitors to wait for some time mean while discussed the possible ways to correct the deformity. We came to a conclusion to put an endotracheal tube to cover up the deformity as lost tissues cannot be made. So we took them to OT again and intubated. they were very happy and left.

Again after some time, all the three appeared in front of my room, and said this is also not accepatable there as it is artificial. This time me and the ENT surgeon were in a dilemma on what to do? At last we were forced to do a full tracheal reconstruction surgery to all of them, with the help of our thoracic surgery colleague. Again they left happily and never reappeared!

         WATCH  TRACHEOSTOMY VIDEO

"SUGAMMADEX" A NOVEL REVERSAL AGENT

THE QUEST FOR AN IDEAL NEUROMUSCULAR REVERSAL AGENT IS STILL GOING ON. THE RECENT INTRODUCTION OF THIS NOVEL AGENT SUGAMMADEX  WOULD BE AN ANSWER FOR THIS? WHY THIS DRUG IS UNIQUE IN ITS CLASS IS THAT, UNLIKE THE OTHER REVERSAL AGENTS WHICH ACT BY NATURAL DEGRADATION OR COMPETITIVE ANTGONISM ,  SUGAMMADEX  USES THE ENCAPSULATION METHOD TO TERMINATE THE EFFECTS OF NEUROMUSCULAR BLOCKING AGENTS. THE COMPLETE AND RELIABLE BINDING OF NM AGENTS  IS ASSOCIATED WITH EXCELLENT CLINICAL RECOVERY AS WELL AS FEW SIDE EFFECTS.SUGAMMADEX PREVIOUSLY KNOWN AS Org 25969, WORKS WELL AGAINST TWO AMINOSTEROID NMBS, Ie. ROCURONIUM AND VECURONIUM, BOTH THESE ARE HAVING AN INTERMEDIATE DURATION OF ACTION.

MECHANISM OF ACTION: (ref 1)

Binding of the steroidal molecule of rocuronium by a cyclodextrin is a new concept for reversal of neuromuscular block. Sugammadex is a modifiedcyclodextrin.Cyclodextrins are naturally occurring rings of glucose that geometrically resemble a truncated cone. The cavity created by the ring is lipophilic while the exterior is hydrophilic. Cyclodextrins may encapsulate lipophilic drugs  like rocuronium,  yet remain soluble in water.
Sugammadex is synthesized from a gamma cyclodextrin modified with eight carboxyl thioether extensions added at the narrow rim.This modification enlarged the cavity size increasing its affinity for two specific lipophilic NMBAs, rocuronium and vecuronium. The ability of sugammadex to encapsulate and non-covalently bind rocuronium and vecuronium terminates their paralytic effects and effectively reverses their action.Once encapsulated, the NMBAs are no longer able to diffuse across tissue membranes to exert their action at the neuromuscular cleft.after iv administration,Plasma encapsulation causes a reversal of concentration gradient and extracts NMBA molecules back into plasma  from neuromuscular junction terminating  the  neuromuscular blockade and restoration of normal motor function. and the  NMBA molecules which are pulled into the plasma are quickly encapsulated with high affinity, preventing any further drug effect.With adequate doses the reversal process occurs in minutes and then  the resultant sugammadex bound NMBA (inclusion complex) is then excreted by the kidneys.

The perioperative benefits of a direct acting, complete, and reliable NMBA reversal drug had been the dream of both surgeons and anaesthetists. The improved ability to reverse NMBAs will allow the anaesthetist to administer the maximum dose of relaxant facilitating excellent operating conditions for the surgeon especially orthopedic surgeons

Sugammadex provides faster reversal of  NM blockade, but without the adverse effects like  MH,  hyperkalemia , muscle pains or prolonged apnea of succinyl choline(depolarising agents) or without residual blockade or bradycardia , as of other non depolarisers.  rocuronium  is comparable to scoline for rapid sequence intubation in trauma patients, and the effects can be easily reversed with sugammadex, in case of a failed intubation, and this reversal of blockade takes place faster than scoline metabolism,(by plasma esterases) and patient can be made awake without persisting side effects of scoline. Thus rocuronium may replace scoline for use with rapid sequence induction  in conjunction with sugammadex. Residual paralysis is not seen with sugammadex reversal.blockade,  IV administration of sugammadex creates a concentration gradient favoring the movement of rocuronium molecules from the neuromuscular junction back into the plasma, which results in a fast recovery of neuromuscular function, a unique mechanism owned by this drug.  No additional anticholinesterase or anticholinergic drugs are needed for antagonism of residual neuromuscular blockade, which means that the cardiovascular and other side effects of anticholinesterases or anticholinergics can be avoided.

study by  H. D. de Boer1,et al,  from   Radboud University Medical Centre Nijmegen Nijmegen,showed thatSugammadex caused a rapid and complete reversal of rocuronium-induced neuromuscular block but not atrcurium or mivacurium induced block, but the drug is found to be effective against vecuronium.   The drug has a  favourable pharmacological profile as it is inactive, does not bind to plasma proteins, and appears to be safe and well tolerated. Additionally, it has no effect on acetylcholinesterase or any receptor system in the body. The compound's efficacy as an antagonist does not appear to rely on renal excretion of the cyclodextrin-relaxant complex.
The effectiveness of sugammadex is dose dependant.  At a  dose of 0.6mg/kg of rocuronium at induction (T2), 1-3 mt rapid return of TOF ratio to >0.9 requires 2-4 mg of the drug iv. At deeper levels, (PTC2), 8-16 mg is required for the same  effect.
Special thanx to : Anthony M. Harris M.D. et al, department of anaesthesia and dept  of orthopedic surgery,University of Florida & Shands
  Ref: The Internet Journal of Orthopedic Surgery 2007 : Volume 7 Number 2
          British Journal of Anaesthesia 2006 96(4):473-479; doi:10.1093/bja/ael013
          Anesth Analg 2007;104:575-581
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TRANSFUSION ASSOCIATED LUNG INJURY

TRALI IS A RARE  COMPLICATION FOLLOWING BLOOD TRANSFUSION. THE ESTIMATED INCIDENCE IS  1:5000. ANY EPIDSODE  OF ACUTE RESPIRATORY FAILURE FOLLOWING TRANSFUSION CAN BE  CATEGORISED AS TRALI. SINGLE TRANSFUSION IS ENOUGH TO TRIGGER THE REACTION

PATHOPHYSIOLOGY: Anti Leukocyte antibodies in donor blood bind to circulatory  granulocytes in the recipient, and promote leukocyte sequestration in the pulmonary microvasculature. this then lead to  granulocyte mediated lung injury which presents as acute   respiratory distress syndrome or non cardiogenic pulm edema

CLINICAL FEATURES: Fever chills dyspnea hypoxemia, tachypnea tachycardia some times with  hypotension., within a few hrs of transfusion CXR shows diffuse pulmonary infiltrates, usually resolved in a week

TREATMENT:  Stop transfusion immediately,  consider mechanical ventilation if picture simulates ARDS, diuretics , morphine to reduce pulm edema, physiotherapy, antibiotics. and steroids
FUTURE TRANSFUSIONS: Either by washed rbcs, or autologous transfusion
Image courtesy:  www.scielo.br/scielo.php?pid=S0034-7094200900...

Canadian Consensus Conference proposed criteria for transfusion-related acute lung injury (TRALI).
Criteria for TRALI

•       Acute lung injury (ALI)
•       Acute onset, Hypoxemia

In research setting:      Ratio of PaO2/FiO2 300 or    SpO2 < 90% on room air

Non-research setting:   Ratio of PaO2/FiO2 300 or    SpO2 < 90% on room air

Other clinical evidence of hypoxia

• Bilateral infiltrates on frontal chest radiograph
• No evidence of left atrial hypertension (i.e., circulatory overload)
• No preexisting ALI before transfusion
• During or within 6 hours of transfusion; and
• No temporal relationship to an alternative risk factor for ALI

Criteria for possible TRALI

• ALI
• No preexisting ALI before transfusion
• During or within 6 hours of transfusion; and
• A clear temporal relationship to an alternative risk factor for ALI

THE ANAESTHESIA MUSEUM

Do you know about the anaesthesia museum in London?What all things are displayed there? Try out the web site link at the bottom. The following information is from the Association of Anaesthetists of Great Britain and Ireland and  produced by Jane Rugg BA as  teachers handbook for students!! The picture shows morton's inhaler used for public demonstration in 1846, kept in the museum.The museum is known as:

THE ANAESTHESIA HERITAGE CENTRE

The Association of Anaesthetists of Great Britain and Ireland has brought together theAssociation’s museum, archives and library in an Anaesthesia Heritage Centre for specialists as well as interested members of the public

The Anaesthesia Heritage Centre comprises the archives, library and museum of the Association. The collections work together to help date, explain and illustrate each other and are therefore a unique resource for research into the history of anaesthesia. The museum collection contains over 3000 objects relating to the story of anaesthesia. Its collections date from 1774 to the present day and provide a detailed insight into the

history of medicine relating to anaesthesia and anaesthetic equipment as well as pain relief and resuscitation.

Additionally, the museum also contains pull-out drawers for smaller objects and flipbooks giving biographies of the pioneering anaesthetists who made important contributions to anaesthesia as well as details of the larger machines in the collection that are not on display.

Museum Details

Anaesthesia Heritage Centre

Association of Anaesthetists of Great Britain and Ireland

21 Portland Place

London

W1B 1PY

Tel.02076318806/8811

Opening times

The heritage centre is openmonday to friday from 09:30 am to 05 pm

There is no entrance charges

For more informations:  e mail heritage@aagbi.org

web site  http://www.aagbi.org/heritage/museum.htm

YOU KNOW ABOUT ANY OTHER MUSEUM SOLELY FOR ANAESTHESIA?

    

RESPIRATORY CRIPPLE WITH CIRRHOSIS

CASE HISTORY:
60 YEAR OLD PATIENT,C/C SMOKER , KNOWN COPD, OSTEOPOROSIS, BPH, WITH NO H/O DM OR HTN IS ADMITTED WITH H/O RESP DISTRESS AND TYPE 2 RESP FAILURE. THE PATIENT WAS GETTING RECURRENT CHEST INFECTION AND DYSPNEA FOR THE LAST 10 YEARS. PREVIOUS CXR SHOWED B/L APICAL OPACITIES SUGGESTIVE OF FIBROSIS. PREVIOUS SPUTUM EXAMINATION FOR MYCOBACT.TB AND MANTOUX TEST WERE NEGATIVE. SUBSEQUENT CT SCAN SHOWED HONEY COMB LUNG WITH APICAL FIBROSIS WITH MULTIPLE CYSTS AND THICKENED PLEURA. CLINICALLY THE PATIENT IS DROWSY, DISORIENTED AND CHEST ON AUSCULTATION REVEALED B/L CREPITATIONS AND RHONCHI, ABDOMINAL EXAM- SPLENOMEGALY WITH ASCITIS . BLOOD INVESTIGATIONS SHOWED, AST-490, ALT-1067, NORMAL COAG PROFILE AND RFT. PATIENT WAS INTUBATED AND VENTILATED IN VIEW OF LOW SPO2 LOW PO2 AND RAISED PCO2 WITH RESP ACIDOSIS. A DIAGNOSIS OF CIRRHOSIS WITH HEPATIC ENCEPHALOPATHY WAS MADE.

CXR  SHOWED   RT APCAL FIBROSIS WITH DEVIATION OF TRACHEA TO THE RIGHT

ISSUES TO BE DISCUSSED ARE
1. HOW AND WHAT AGENTS CAN BE USED FOR SEDATION IN ICU IN VIEW OF HEPATIC DERRANGEMENT?

2. WHAT SHOULD BE THE VENTILATORY MODE?

3.FLUID MANAGEMENT WITH CONSIDERATION TO HEPATORENAL SYNDROME?

4. MANAGEMENT OF NUTRITION IN ICU ESPECIALLY PARENTERAL NUTRITION?

1.SEDATIVE AGENTS OF CHOICE--> THE DRUG OF CHOICE OF SEDATION FOR CIRRHOTICS IS PROPOFOL 0-3 MG/KG/HR , SINCE METABOLISM BY REDISTRIBUTION AND EXTRAHEPATIC MECHANISMS OF METABOLISM ARE HELPFUL. OPIOIDS OF CHOICE ARE MORPHINE 1-3 MG/HR (DUE TO PHASE 2 METABOLISM) MIDAZOLAM INFUSION ALSO SUGGESTED BUT AT A REDUCED DOSE. 0.5-1 MG/HR



2. EVENTHOUGH ASSIST CONTROL OR CONTROLLED MODE VENTILTION ARE USED AS THE STARTING VENTILTORY MODES IN COPD PATIENTS, A CIRRHOTIC PTIENT WITH ALVEOLAR EDMA AND V/Q MSMATCH MAY REQUIRE BIPAP MODE TO AVOID EXCESSIVE AIRWAY PRESSURE AND HYPERINFLATION OR VOLUTRAUMA. A LOW RESP RATE WITH ADEQUATE EXP TIME RECOMMENDED FOR EXAMPLE;  A RR OF 8/MT WITH 1:2 RATIO WILL GIVE 5 SECONDS FOR EXPIRATION AND A RATE OF 6/MT EXP TIME,  6.7 SECS, THUS ALOWING ADEQUATE TIME FOR EXPIRATION TO AVOID AUTO PEEP. IT IS SUGGESTED THAT ADDITION OF EXTRINSIC PEEP UPTO 80% OF INTRINSIC PEEP REDUCES THE PATIENT'S INSPIRATORY EFFORT;    SHOULD WE USE PEEP? AND IF SO HOW MUCH? WHY?
3. FLUID MANAGEMENT: ADEQUATE INTRAVASCULAR FILLING IS NEEDED FOR MAINTAINING PERFUSION TO OTHER ORGANS.--> SALT AND VOLUME RESTRICTION ADVISED TO REDUCE ASCITIS, 0.25% SALINE TO BE USED INSTEAD OF .5% SALINE . APPROXIMATELY 1.5 LITRES OF FLUID/DAY WITH SALT SUPPLEMENTATION OF 88 MEQ/DAY IS RECOMMENDED. COTROLLED SPIRONOLACTONE THERAPY TO PUMP OUT FLUIDS WHILE MAINTAINING POTASSIUM LEVEL IS SUGGESTED.  A CVP CATHETER IS NEEDED FOR FLUID MANAGEMENT AND FOR PARENTERAL NUTRITION(THROUGH A PERIPHERAL ROUTE IF COAGULATION IS DERRANGED).FLUID OVERLOAD IS POORLY TOLERATED AND MAY LEAD ON TO PULM EDEMA, AS DILATED RT VENTRICLE (COR PULMONALE) COMPROMISE THE FUNCTION OF LEFT VENTRICLE. CVP READING MAY BE UN RELIABLE IN PRESENCE OF PULMONARY HYPERTENSION, AND SHOULD BE CAREFULLY FOLLOWED UP
4. MANAGEMENT OF NUTRITION: PARENTERAL NUTRITION RECOMMENDED INTHE CRITICALLY ILL

AIMS:
a. PROVIDE ADEQUATE AMOUNT OF CALORIES WITH MINIMAL VOLUME

b. AVOID AMINO ACID IMBALANCE

c. SHOULD NOT CAUSE ANY ELECTROLYTE IMBALANCE

d. SHOULD NOT AGGRAVATE NEUROLOGICAL STATUS

HEPATIC ENCEPHALOPATHY IS CHARACTERISED BY IMBALANCE OF MONOAMINE NEUROTRANSMITTERS LIKE TRYPTOPHAN TYROSIN, AND PHENYL ALANINE AND REDUCED LEVELS OF BRANCHED CHAIN AMINOACIDS LIKE LEUCINE, ISOLEUCINE AND VALINE( DUE TO PERIPHERAL UPTAKE IN MUSCLE) SO INCREASE BRANCHED CHAIN AMINOACID CONTENT(AS THEY COMPETE WITH LONG CHAIN AMINOACIDS TO CROSS BBB AND THEREBY REDUCE THE CONTENT OF MONOAMINES IN BRAIN. BRANCHED CHAIN AMINO ACIDS ALSO HELPS TO REDUCE THE CATABOLIC RESPONSE AND PROMOTES HEPATIC PROTEIN SYNTHESIS AND LIVER REGENERATION. SUPPLEMENTATION OF POTASSIUM PHOSPHATE ALSO NEEDED TO HELP INCREASE PRODUCTION OF ATP.      EXAMPLE:  HEPATAMINE SOLUTION

DO CORTICOSTEROIDS PREVENT EXTUBATION FAILURE?

EXTUBATION FAILURE MEANS, THE NEED FOR REINTUBATION SOON AFTER EXTUBATION, IS ASSOCIATED WITH SIGNIFICANT MORTALITY IN ICU PATIENTS.

THE COMMON CAUSES BEING RESIDUAL NEURO MUSCULAR BLOCKADE, RESIDUAL SEDATION OR NARCOSIS,LARYNGOSPASM, LARYNGEAL EDEMA DUE TO PROLONGED MECHANICAL VENTILATION, HEMODYNAMIC INSTABILITY AND VOCAL CORD PALSY. IT IS PROVEN THAT CORTICOSTEROIDS CAN REDUCE AIRWAY INFLAMMATION AND LARYNGEAL EDEMA AND SUBSEQUENTLY REDUCE THE RATE OF RE INTUBATION, BUT WHAT REGIMEN TO BE USED, THROUGH WHICH ROUTE, AND HOW MANY HOURS BEFORE EXTUBATION ETC. STILL REMAIN UNCLEAR



REVIEWING THE STUDY MADE BY MC. CAFFERY ET AL (JOURNAL OF INTENSIVE CARE MEDICINE, VOL 35, NO, 6, JUNE 2009), STEROIDS HELP TO REDUCE THE RATE OF EXTUBATION FAILURE, MAINLY DUE TO A REDUCTION IN LARYNGEAL EDEMA, ESPECIALLY IN PATIENTS UNDERGONE PROLONGED MECHANICAL VENTILATION. ALSO THE EFFECTS OF STEROIDS MAY BE MORE PRONOUNCED WHEN THE TREATMENT IS COMMENCED 12 HRS PRIOR TO EXTUBATION. IN NEONATAL AND PEDIATRIC POPULATIONS DEXAMETHASONE AT DOSES OF 0.25 TO 0.5 MG/KG IS SUGGESTED. BUT FOR ADULTS DIFFERENT REGIMENS ARE PROPOSED. DEXAMETHASONE 8 MG 1 HR PRIOR FOR PATIENTS VENTILATED FOR LESS THAN 36 HRS, IS FOUND TO BE EFFECTIVE. ALSO DEXAMETHASONE 5 MG 24 HRS PRIOR TO EXTUBATION IN 6 DIVIDED DOSES AND CONTINUED POST EXTUBATION FOR ANOTHER 24 HRS, FOR A DURATION OF MECHANICAL VENTILATION OF 7-8 DAYS. OR HYDROCORTISONE 100 MG 1 HR PRIOR, FOR PATIENTS VENTILATED LESS THAN 5 DAYS, ARE FOUND TO BE EFFECTIVE.

PULSELESS ELECTRICAL ACTIVITY OR SILENT ELECTRICAL ACTIVITY?

CASE HISTORY:
70 YEAR OLD PATIENT WITH NO PREVIOUS MEDICAL ILLNESS IS ADMITTED TO THE ACCIDENT AND EMERGENCY DEPARTMENT WITH CHEST DISCOMFORT.  HIS PULSE RATE IS 64/MT, BP 90/50 MMHG AND ECG SHOWED ST SEGMENT ELEVATION.  A DIAGNOSIS OF ACUTE MI IS ESTABLISHED AND PATIENT WAS SHIFTED TO ICU FOR THROMBOLYTIC THERAPY. PATIENT IS CONSCIOUS BUT SEDATED DUE TO THE EFFECT OF MORPHINE AND OBEYING COMMANDS, CHEST ON AUSCULTATION REVEALED B/L FINE BASAL CREPS. OXYGEN ON FLOW 8L/MT BY FACE MASK. THE ECG SHOWED

AFTER ABOUT 20 MINUTES THE ICU STAFF NOTICED A FALL IN SPO2 AND PATIENT IS UNRESPONSIVE. CODE BLUE ALERT GIVEN. THE MONITOR SHOWED COMPLEXES SIMILAR TO THE PREVIOUS ECG AND NIBP SHOWED 80/60 MMHG WHICH WAS SET AUTOMATIC AT 3 MINUTES INTERVAL. PATIENT WAS GASPING AND THE ANAESTHETIST IMMEDIATELY INTUBATED THE PATIENT AND CPCR CONTINUED AS PER ACLS PROTOCOLS BUT COULD NOT BE REVIVED



PATIENT WENT INTO PEA IMMEDIATELY FOLLOWING LAST BP MEASUREMENT AND WAS IN CARDIORESPIRATORY ARREST FOR FOR MORE THAN TWO MINUTES. SINCE FRC IS ENRICHED WITH INITIAL HIGH CONCENTRATION OF OXYGEN, FALL IN OXYGEN SATURATION WAS SLOW AND THE MONITOR SHOWED NOISY SIGNAL WITH LOW AMPLITUDE PLETHISMO WAVES AND HEART RATE PICKED UP FROM  ECG, AS IT IS SET. ABSENT PULSE WAS UN NOTICED.



PEA CAN FOLLOW A/C MI BUT MAY BE UNRECOGNISED. SINCE MOST PEAs CAN BE SUCCESSFULLY TREATED WITH EFFECTIVE CPCR AND DRUGS,  ESPECIALLY IN YOUNG PATIENTS, CAREFUL AND CLOSE MONITORING OF POST MI PATIENTS IN ICU IS RECOMMENDED