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.
Wednesday, March 31, 2010
ANAPHYLAXIS THE EXTREME HYPERSENSITIVITY!
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.
Tuesday, March 23, 2010
SEPSIS ON THE GO.
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.
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
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
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
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
Saturday, March 13, 2010
GUILLAIN-BARRE SYNDROME
Clinical Manifestations
- Rapidly evolving, progressive, ascending motor paralysis with or without sensory disturbance and with areflexia
- Lower cranial nerves are frequently involved and presented with difficulty in swallowing and maintaining airway
- Bulbar involvement is most frequently manifested as B/L facial paralysis
- Fever and other constitutional symptoms are usually absent
- Diminished DTR with absent proprioception. There may be marked sensory loss
- Bladder dysfunction is late and transient.
- Deep aching pain in muscles and back
- 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
- 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
- Metabolic derangements -Hyponatremia due to excessive ADH secretion
Friday, March 12, 2010
PREGNANT PATIENT WITH DVT IN PAIN
24 year old second gravida with 9 weeks of pregnancy reports to the emergency department with 1 day history of pain left loin spreading to left lower limb.The patient gives history of contraceptive injections. On examination the left lower limb appeared swollen and tender. The homan's sign was positive.Femoral and Popleateal pulsations were felt but dorsalis pedis feebly felt compared to right leg. The limb was not pale or cold. A provisional diagnosis of DVT is made and a venous doppler was ordered which showed DVTof the left lower limb extending upto left ileofemoral vein.
Patient is admitted in icu, heparin infusion started 5000units iv and then 1000units/hr keeping the APTT level 1.5 to 2 times than normal.Monitoring of Spo2, ECG, NIBP and temperature commenced. Serial ABG s were performed to asses the respiratory status. Lower limb mesurements were taken frequently and observed for development of compartmental syndrome.Arterial doppler showed no arterial insufficiency and echocardiogram showed normal study. The CXR also was normal
Anesthetic referral was sent for pain relief.
Providing pain relief to this patient was a real challenge before the anaesthetist He has to consider the following things before formulating the therapy
1) Patient is on thrombolytic therapy
2)Teratogenecity of anaesthetic agents
3)Effect of analgesic agents on uterine tone
4)Need of careful monitoring of the respiratory system as chance of pulmonary embolism is high.
NSAIDS including diclofenac sodium
Paracetamol
Paracetamol is considered to be safe and can be given intramuscular injection in case of
severe pain. But the efficacy is limited as continuous pain relief is not possible.The effects on maternal Liver like fatty liver or liver failure are of concern but are rare and occurs only on long term treatment.IV preparation is preferred as deep IM can cause hematoma formation as patient is on heparin
Patient is admitted in icu, heparin infusion started 5000units iv and then 1000units/hr keeping the APTT level 1.5 to 2 times than normal.Monitoring of Spo2, ECG, NIBP and temperature commenced. Serial ABG s were performed to asses the respiratory status. Lower limb mesurements were taken frequently and observed for development of compartmental syndrome.Arterial doppler showed no arterial insufficiency and echocardiogram showed normal study. The CXR also was normal
Anesthetic referral was sent for pain relief.
Providing pain relief to this patient was a real challenge before the anaesthetist He has to consider the following things before formulating the therapy
1) Patient is on thrombolytic therapy
2)Teratogenecity of anaesthetic agents
3)Effect of analgesic agents on uterine tone
4)Need of careful monitoring of the respiratory system as chance of pulmonary embolism is high.
NSAIDS including diclofenac sodium
Paracetamol
Paracetamol is considered to be safe and can be given intramuscular injection in case of
severe pain. But the efficacy is limited as continuous pain relief is not possible.The effects on maternal Liver like fatty liver or liver failure are of concern but are rare and occurs only on long term treatment.IV preparation is preferred as deep IM can cause hematoma formation as patient is on heparin
Thursday, March 11, 2010
ANAESTHESIA IN DENTAL CHAIR
As a rule patients should be premedicated with atropine to reduce oral secretions and to reduce the occurrence of vasovagal syncope.(In children this may be administered at the dose of 0.02mg/kg IV following induction and iv line placement) In a co operative child the IV cannula may be secured after topical application of EMLA cream also. Intravenous induction with Propofol and lidocaine may be condsidered for children above 3 yrs. A nasal mask or LMA may be used to protect the airway with additional pre op oral packing, particularly when nasal mask is used for delivering inhalational anaesthesia. Maintenance of anaesthesia is continued with oxygen, nitrous oxide with isoflurane allowing spontaneous ventilation. Alternatively inhalation induction with sevoflurane or halothane is preferred for children less than 3 yrs.The eyes should be protected. For maintenance, propofol or sevoflurane may be continued. Additional analgesia may be obtained by local nerve blocks by surgeon. If possible the child my be placed in the lateral position keeping the head low with proper stabilisation of head and neck.Use of nitrous oxide may be reduced or stopped with concurrent administration of short acting analgesics like fentanyl, to prevent hypoxia,provide analgesia and to make available 100% oxygen. Post op analgesia can be achieved with paracetamol or diclofenac suppositories or with intramuscular opioids.
Another technique called inhalational sedation is used for adults who are unwilling for local anaesthesia. Here conscious sedation is given using iv anaesthetic agents followed by analgesia supplemented with local anaesthetics once the sedative effect is established.Patients are given slow incremental doses of midazolam with oxygen and less than 50% nitrous oxide.A soft but weighted mask is put over the nostrils. It is essential that patient is conscious throughout the procedure and can control his airway. The patient should be able to communicate with the surgeon during the procedure. Mouth props are discouraged as they mask the patients inability to keep the mouth open, - an ominous sign of oversedation. Standard monitoring include NIBP, ECG, Temperature probe and Pulse Oximetry. Patient should be given 100 % oxygen following the procedure to avoid diffusion hypoxia and flumazenil should be available to reverse the residual effect of benzodiazepines effect, if required.
When to think of intubation?
- Difficult access as in impacted tooth, macroglossia, short neck
- Excessive uncontrolled bleeding
- maxillofacial or major dental surgery
- Mentally handicapped
- Obstruction of nasal passages, large adenoids where nasal mask is not effective
Problems in dental chair
- Reduced venous return, so more severe reaction to a vasovagal attack due to pain
- Increased chance of air embolism in sitting position
- Unprotected airway ie shared airway between surgeon and anaesthetist
- Aspiration of blood or mucus can cause laryngospasm,
- Adrenaline in local anaesthetic can cause arrhythmias in presence of halothane
- Higher incidence of arrhythmias due to stimulation of 5 th cranial nerve
- Nasal bleeding if nasal airway is used to deliver the anaesthetic
- Fainting due to cerebral hypoxia or cardiac arrest may be unrecognised
- Difficulty in initiating CPCR once cardiac arrest occurs
- Foreign body obstruction of the airway by needles or dentures,necessitating removal by bronchoscopy
- Uncontrolled and profuse bleeding into the airway in patients not screened for coagulopathies especially in out patients
- Higher incidence of infective endocarditis
- Anaphylaxis, to local anaesthetics or other drugs
- Malignant hyperpyrexia if halothane is used
- Difficulty in administering post op analgesia
Monday, March 8, 2010
MUSCLE RELAXANTS IN THE ICU.
Muscle relaxants are used in icu to facilitate mechanical ventilation of the critically ill patients.The drugs commonly used are pancuronium, vecuronium, atra curium, cisatra curium, and rocuronium. Muscle relaxants are essential in the management of tetanus, status epilepticus, to provide hyper ventilation in head injury, or after precise surgical intervention like tracheal anastomosis and vascular anastomosis.These agents are also used to reduce oxygen consumption or to reduce work of breathing in COPD and ARDS(where inflation pressures are high) patients.
Apart from the beneficial effects the complications of these agents are also of concern and are investigated. These can be classified as complications due to short term use and long term use
Short term use
- Side effects atracurium causing histamine release or hyperkalemia due to suxamethonium
- Inadequate analgesia or sedation as these components are under estimated when relaxants are used
- Immobility : DVT decubitus ulcers, peripheral nerve injuries.
- Inability to cough: retained secretions, atelectasis and infection
- Persistent paralysis on stoppage of the drugs "Critical Illness Neuropathy and Critical Illness Myopathy", Steroid induced myopathy.
- CNS effects of drugs eg: laudanosine causing convulsions
Wednesday, March 3, 2010
H1N1 AND HAND HYGIENE
There is a raising concern and anxiety about the spread of H1N1 influenza among people and health care personnel, as the number of reported cases are on the hike. Eventhough the mode of transmission is by droplet spread, transmission through conta minated hands are also considered to be significant. Along with personal protection devices like N-95 mask, goggles, apron, and gloves the importance of hand hygiene is also stressed, as prevention is the major goal for the control of spread. Several studies conducted on this issue have proved that practise of safe and appropriate hand hygiene is an important public health initiative to reduce pandemic H1N1 influenza transmission.
The commercially available hand sanitisers are alcohol based with the addition of various antiseptics and emollients.They are available both in liquid form and gel form. The advantages of alcohol based sanitisers are.
Research by (Ref), Grayson ML, Melvani S, Druce J, Barr IG, Ballard SA, Johnson PD, Mastorakos T, Birch C., Infectious Diseases Department, Austin Health, Heidelberg, Victoria 3084, Australia, showed that hand hygiene with soap and water or alcohol-based hand rub is highly effective in reducing influenza A virus on human hands, although washing with soap and water is the most effective intervention.
Following the" NO FEAR, FIGHT INFLUENZA" campaign, instant hand sanitisers are made available everywhere, including supermarkets,restaurants, clinics, schools, factories etc.One danger of alcohol based sanitisers is that they are flammable and can cause burns.It happened in one hospital where the hospital cleaner used hand wash gel after cleaning the toilets and immediately lighted up a cigarette, holding up his hands to protect the flame from the wind, and his hands burst into flames.Anoher incidence reported from a birthday party where the children were playing with a sanitiser spray and their dress caught fire from candles. So it is advised that after sanitiser use one should make sure that the hands are dry before lighting gas stove,cigarettes or candles and when handling fire or dealing with any job which produces spark for example welding works.
Agents that reduce skin microflora are called antiseptics, whereas agents that reduce microflora on non living objects are called disinfectants. Antibiotic creams or dettol(chlorhexidine) are considered antiseptics, while glutaraldehyde (cidex) or floor cleaners like lysol(phenol based) are categorised as disinfectants. The efficacy of disinfectants or antiseptics are determined by Rideal Walker coefficient and is obtained by dividing the figure indicating the degree of dilution of the disinfectant that kills a microorganism in a given time by that indicating the degree of dilution of phenol that kills the organism in the same space of time under similar conditions.
Ref: Clin Infect Dis. 2009 Feb 1;48(3):285-91.
Watch a video on H1N1
The commercially available hand sanitisers are alcohol based with the addition of various antiseptics and emollients.They are available both in liquid form and gel form. The advantages of alcohol based sanitisers are.
- Instant in action , effective in less than 15 seconds
- Reliable, almost 99% of pathogens including viruses are killed(actiton on spores doubtful)
- Easy to use as it immediately dries up and hand washing is not necessary
- leaves less stain than other agents
Research by (Ref), Grayson ML, Melvani S, Druce J, Barr IG, Ballard SA, Johnson PD, Mastorakos T, Birch C., Infectious Diseases Department, Austin Health, Heidelberg, Victoria 3084, Australia, showed that hand hygiene with soap and water or alcohol-based hand rub is highly effective in reducing influenza A virus on human hands, although washing with soap and water is the most effective intervention.
Following the" NO FEAR, FIGHT INFLUENZA" campaign, instant hand sanitisers are made available everywhere, including supermarkets,restaurants, clinics, schools, factories etc.One danger of alcohol based sanitisers is that they are flammable and can cause burns.It happened in one hospital where the hospital cleaner used hand wash gel after cleaning the toilets and immediately lighted up a cigarette, holding up his hands to protect the flame from the wind, and his hands burst into flames.Anoher incidence reported from a birthday party where the children were playing with a sanitiser spray and their dress caught fire from candles. So it is advised that after sanitiser use one should make sure that the hands are dry before lighting gas stove,cigarettes or candles and when handling fire or dealing with any job which produces spark for example welding works.
Agents that reduce skin microflora are called antiseptics, whereas agents that reduce microflora on non living objects are called disinfectants. Antibiotic creams or dettol(chlorhexidine) are considered antiseptics, while glutaraldehyde (cidex) or floor cleaners like lysol(phenol based) are categorised as disinfectants. The efficacy of disinfectants or antiseptics are determined by Rideal Walker coefficient and is obtained by dividing the figure indicating the degree of dilution of the disinfectant that kills a microorganism in a given time by that indicating the degree of dilution of phenol that kills the organism in the same space of time under similar conditions.
Ref: Clin Infect Dis. 2009 Feb 1;48(3):285-91.
Watch a video on H1N1
Monday, March 1, 2010
AIRWAY MANAGEMENT IN A PATIENT WITH HUGE THYROID
Airway management of a patient with a huge thyroid swelling is a real challenge to the anaesthetist. The anaesthetic concerns and the management of airway are discussed here.
60 year old female patient is admitted to the A&E department with history of neck swelling and stridor. She is a known case of medullary carcinoma thyroid with lymph node metastases.
The patient assumed a sitting position as stridor exacerbated on lying supine and looks distressed .She was oriented conscious and responding to comm ands. Examination of the chest revealed b/l basal creps and oxygen saturation was 88% with oxygen mask. ABG showed resp acidosis with hypoxemia.The pulse rate was regular and ECG was normal.The thyroid swelling was huge and completely occupying the anterior neck with the trachea not at all palpable at any point and with evidence of possible retrosternal extension.Oxygen by mask administered and patient postioned sitting, leaned forward.
Investigations done:
Additional investigations (may be deferred here as this patient requires emergency airway access)
1) Induction or any anaesthetic intervention should be done with the patient in sitting position, as supine position further compromises airway.
2)Emergency tracheostomy, minintracheostomy or retrograde tracheostomy cannot be
performed here due to tumour extension.
3)Distorted airway anatomy makes intubation impossible even with fiber optic bronchoscopy.
4)Ventilation through Fastrach may not be adequate and may not be effective due to tracheal compression, if intubation through Fastrach fails.
5)Airway blocks like trans tracheal or superior laryngeal nerve blocks cannot be performed.
6) Tracheostomy malfunction may occur post operatively due to tracheal collapse because of tracheomalacia.
The ideal management in this case would be a fiberoptic trial of intubation through the nasal or oral route, in the sitting position with topical airway anaesthesia, followed by palliative debulking of the tumor and then tracheostomy.
following rigid fiber optic bronchoscopy and inhalation induction using sevoflurane in the sitting postition followed either by blind intubation or fiberoptic aided intubation.
Anaesthetist should be vigilant, careful and well prepared while dealing with neck masses compromising airway. Management should done in operation theatre set up with all available equipments ready to tackle the difficult situation. The ENT and General surgeon also should be available to deal with emergency.
Thanx to Dr.Santhosh Kumar Sathiarajan, Radiologist, Ibri hospital, Muscat.
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60 year old female patient is admitted to the A&E department with history of neck swelling and stridor. She is a known case of medullary carcinoma thyroid with lymph node metastases.
The patient assumed a sitting position as stridor exacerbated on lying supine and looks distressed .She was oriented conscious and responding to comm ands. Examination of the chest revealed b/l basal creps and oxygen saturation was 88% with oxygen mask. ABG showed resp acidosis with hypoxemia.The pulse rate was regular and ECG was normal.The thyroid swelling was huge and completely occupying the anterior neck with the trachea not at all palpable at any point and with evidence of possible retrosternal extension.Oxygen by mask administered and patient postioned sitting, leaned forward.
Investigations done:
- Routine hemogram
- CXR showed severe narrowing and deviation of the trachea to the right side, by compression from the mass
- CT scan showed narrowed tracheal orifice(the black round hole) with compression of the esophagus and nodular metastases
Additional investigations (may be deferred here as this patient requires emergency airway access)
- Pulmonary function tests may show a restrictive defect with high FEV1/FVC ratio
- Carotid angiogram to assess the vessels
1) Induction or any anaesthetic intervention should be done with the patient in sitting position, as supine position further compromises airway.
2)Emergency tracheostomy, minintracheostomy or retrograde tracheostomy cannot be
performed here due to tumour extension.
3)Distorted airway anatomy makes intubation impossible even with fiber optic bronchoscopy.
4)Ventilation through Fastrach may not be adequate and may not be effective due to tracheal compression, if intubation through Fastrach fails.
5)Airway blocks like trans tracheal or superior laryngeal nerve blocks cannot be performed.
6) Tracheostomy malfunction may occur post operatively due to tracheal collapse because of tracheomalacia.
The ideal management in this case would be a fiberoptic trial of intubation through the nasal or oral route, in the sitting position with topical airway anaesthesia, followed by palliative debulking of the tumor and then tracheostomy.
- Lignocaine jelly or gargle may be used to anaesthetise the posterior tongue
- Glossopharyngeal nerve block can be performed intra orally by injecting local anaesthetic into the base of the palatoglossal fold.
- Nasal passages may be anaesthetised by lignocaine jelly using swabs or catheter.
- Excellent anaesthesia of the larynx and trachea can be achieved with topical aerosolised lignocaine.
- Intravenous sedation can be given with midazolam or fentanyl in titrated doses during the procedure, if patient is uncomfortable.
- A smaler sized re inforced tube is preferred for intubation
following rigid fiber optic bronchoscopy and inhalation induction using sevoflurane in the sitting postition followed either by blind intubation or fiberoptic aided intubation.
Anaesthetist should be vigilant, careful and well prepared while dealing with neck masses compromising airway. Management should done in operation theatre set up with all available equipments ready to tackle the difficult situation. The ENT and General surgeon also should be available to deal with emergency.
Thanx to Dr.Santhosh Kumar Sathiarajan, Radiologist, Ibri hospital, Muscat.
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Thursday, February 25, 2010
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.
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.
Monday, February 22, 2010
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
2) The abc of resuscitation, BMJ
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
- Incompetent gastroesophageal (cardiac) sphincter
- Increased intragastric pressure
- Increased risk of regurgitation
- Increased acidity of gastric contents
- Physiological anemia
- Supine hypotension syndrome
- 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
- 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
- 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
- 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
2) The abc of resuscitation, BMJ
Friday, February 19, 2010
H1N1 PNEUMONIA, AN UPDATE
- 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)
- Intubation and manual ventilation
- Tracheal suctioning
- Nasopharyngeal aspiration
- CPCR
- Bronchoscopy
- Autopsy procedures
- Nebulisation
- Nippv
- nasopharyngeal or throat swabs for viral culture or polymerase chain reaction
- 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
- Refractory hypoxemia,SpO2 < 90% on non-rebreathe mask @ 15L/min oxygen flow
- Respiratory acidosis,pH < 7.2
- Clinical evidence of impending respiratory failure,Respiratory rate > 40
- Inability to protect or maintain airway
- GCS <8
- 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
- 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
- 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)
• 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
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
Thursday, February 18, 2010
TRANSFER BY AIR

- 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 648Wednesday, February 17, 2010
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/
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/
Monday, February 15, 2010
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,
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]
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
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]
Friday, February 12, 2010
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
Thursday, February 11, 2010
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
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
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
Monday, February 8, 2010
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
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
Sunday, February 7, 2010
"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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Thursday, February 4, 2010
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
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
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
• 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
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
• 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
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