Q; Why Haldol (Haloperidol) should be use with caution in burn patients?
Answer: Neuropsychiatric complications are commonly seen in major burn patients. Haloperidol is frequently used to treat severe psychopathic behavior. There could be an increase tendency of severe muscle rigidity - an extrapyramidal side effect of the agent - in burn patients. Haloperidol causes a relative imbalance of dopaminergic and cholinergic neuronal activity in the basal ganglia with a relative increase in cholinergic activity being responsible for EPS. The burn patient may be more prone to extrapyramidal symptoms because of increased sensitivity of skeletal muscle neuromuscular junctions to acetylcholine after thermal injury.
Reference:Haloperidol Complications in Burn Patients. Journal of Burn Care & Rehabilitation. 8(4):269-273, July/August 1987
Tuesday, May 31, 2011
Monday, May 30, 2011
Q: 32 year old diabetic female is admitted with fever, chills, abdominal pain, nausea, vomiting, left flank pain with crepitation over left flank and urinary symptoms. What's your concern?
Answer: Emphysematous pyelonephritisEmphysematous pyelonephritis is a necrotizing acute nephritis with extension of the infection through the renal capsule. This leads to the presence of gas within the kidney and in the perinephric space.The mortality rate is 60% - 80% despite medical treatment and usually require surgical intervention with nephrectomy.
Answer: Emphysematous pyelonephritisEmphysematous pyelonephritis is a necrotizing acute nephritis with extension of the infection through the renal capsule. This leads to the presence of gas within the kidney and in the perinephric space.The mortality rate is 60% - 80% despite medical treatment and usually require surgical intervention with nephrectomy.
Sunday, May 29, 2011
Q: 22 year old female with severe peanut allergy presented to ER with asthma execerbation. Which commonly use drug should be avoided or at least be use with caution in this patient?
Answer: Atrovent
Actually, nebulized Atrovent doesn't pose a problem, but it was the soy lecithin additive in the propellant in the MDI's that could trigger a reaction in those with peanut and/or soy hypersensitivity.
Answer: Atrovent
Actually, nebulized Atrovent doesn't pose a problem, but it was the soy lecithin additive in the propellant in the MDI's that could trigger a reaction in those with peanut and/or soy hypersensitivity.
Friday, May 27, 2011
Thursday, May 26, 2011
Q: How pseudoaneurysm formed after traumatic femoral central line attempt?
Answer: A penetrating injury creates an opening in the artery and forms a hematoma. This hematoma develops a wall around it and the hematoma liquefies and forms a pulsating "bubble" on the artery. This is called a pseudoaneurysm. A pseudoaneurysm, like any aneurysm, can rupture and cause bleeding or loss of limb. The most common penetrating "injury" of the femoral artery occurs during cardiac catheterization performed via the femoral artery or after femoral central line attempt.
Answer: A penetrating injury creates an opening in the artery and forms a hematoma. This hematoma develops a wall around it and the hematoma liquefies and forms a pulsating "bubble" on the artery. This is called a pseudoaneurysm. A pseudoaneurysm, like any aneurysm, can rupture and cause bleeding or loss of limb. The most common penetrating "injury" of the femoral artery occurs during cardiac catheterization performed via the femoral artery or after femoral central line attempt.
Wednesday, May 25, 2011
Q: Why steroids remain mainstay of treatment in Neurocysticercosis?
Answer: Albendazole and Praziquantel are both effective in treatment of Neurocysticercosis. They are given under cover of steroids. Steroids are essentially needed as inflammatory reactions to the dying parasite could be life threatening with mental status changes and convulsions.
Also, Albendazole when co administered with a steroid (to treat inflammation) results in increased absorption of albendazole.
Both Albendazole and Praziquantel are recommended to give with fatty meal.
Monday, May 23, 2011
Sunday, May 22, 2011
Regarding binary toxin of C. difficile
So far Toxin A and Toxin B were known clinically significant for C.Diff. but recently some deadly strains of C. difficile are found to produce an additional toxin called binary toxin. This was first reported in 1988 but never considered clinically significant. Interestingly, binary toxin producers make up the majority of the C. difficile strains isolated in the recent large outbreaks. Also, a correlation between binary toxin production and severity of dirrhea has been demonstrated, and more community-acquired C. difficile-associated diarrhoea was found to be caused by binary toxin producers. The presence of the binary toxin in Clostridium difficile infection contributes to a marked increase in the risk of death, researchers reported. But still, it remains unclear whether the binary toxin itself causes increased virulence or is a marker for virulence.
So far Toxin A and Toxin B were known clinically significant for C.Diff. but recently some deadly strains of C. difficile are found to produce an additional toxin called binary toxin. This was first reported in 1988 but never considered clinically significant. Interestingly, binary toxin producers make up the majority of the C. difficile strains isolated in the recent large outbreaks. Also, a correlation between binary toxin production and severity of dirrhea has been demonstrated, and more community-acquired C. difficile-associated diarrhoea was found to be caused by binary toxin producers. The presence of the binary toxin in Clostridium difficile infection contributes to a marked increase in the risk of death, researchers reported. But still, it remains unclear whether the binary toxin itself causes increased virulence or is a marker for virulence.
Saturday, May 21, 2011
Q: What is Pseudochylothorax?
Answer: Chylothorax must be distinguished from pseudochylothorax, or cholesterol pleurisy, which results from accumulation of cholesterol crystals in a chronic existing effusion. The most common cause of pseudochylothorax is chronic rheumatoid pleurisy, followed by tuberculosis and poorly treated empyema.
Answer: Chylothorax must be distinguished from pseudochylothorax, or cholesterol pleurisy, which results from accumulation of cholesterol crystals in a chronic existing effusion. The most common cause of pseudochylothorax is chronic rheumatoid pleurisy, followed by tuberculosis and poorly treated empyema.
Friday, May 20, 2011
Q: What is pseudo-pulmonary embolus syndrome?
Answer: The clinical scenario of collapse, shortly after an intravenous heparin bolus, most likely to be one of HIT type II is called ‘pseudo pulmonary embolus’. This is not due to a major pulmonary embolus, but is thought to be due to an endothelial injury, with sudden augmented release of IL-6, von Willebrand factor, and other adhesion molecules, resulting in an acute adult-type respiratory distress syndrome as a result of sudden vascular leak with hypoxia and hypotension.
Answer: The clinical scenario of collapse, shortly after an intravenous heparin bolus, most likely to be one of HIT type II is called ‘pseudo pulmonary embolus’. This is not due to a major pulmonary embolus, but is thought to be due to an endothelial injury, with sudden augmented release of IL-6, von Willebrand factor, and other adhesion molecules, resulting in an acute adult-type respiratory distress syndrome as a result of sudden vascular leak with hypoxia and hypotension.
Thursday, May 19, 2011
Lazarus Syndrome - after therapeutic hypothermia!
Interesting case report published in June 2011 issue of Critical Care Medicine1.
"A 55-yr-old man presented with cardiac arrest preceded by respiratory arrest. Cardiopulmonary resuscitation was performed, spontaneous perfusion restored, and therapeutic hypothermia was attempted for neural protection. After rewarming to 36.5°C, neurologic examination showed no eye opening or response to pain, spontaneous myoclonic movements, sluggishly reactive pupils, absent corneal reflexes, and intact gag and spontaneous respirations. Over 24 hrs, remaining cranial nerve function was lost. The neurologic examination was consistent with brain death. Apnea test and repeat clinical examination after a duration of 6 hrs confirmed brain death. Death was pronounced and the family consented to organ donation. Twenty-four hrs after brain death pronouncement, on arrival to the operating room for organ procurement, the patient was found to have regained corneal reflexes, cough reflex, and spontaneous respirations. The care team faced the challenge of offering an adequate explanation to the patient's family and other healthcare professionals involved".
Authors recommend caution in the determination of brain death after cardiac arrest when induced hypothermia is used. Confirmatory testing should be considered and a minimum observation period after rewarming before brain death testing ensues should be established.
Reversible brain death after cardiopulmonary arrest and induced hypothermia - Critical Care Medicine. 39(6):1538-1542, June 2011
Wednesday, May 18, 2011
Q: 48 year old male is brought to ED after V. fib. cardiac arrest. Cardiology wants to take patient to Cath lab. What are the recommendations regarding therapeutic hypothermia?
Answer: Therapeutic hypothermia should not be delayed particularly in clear cut cases of V.fib cardiac arrest and should be initiated in the emergency department. Cardiology interventions can be done and patients can continue to be cooled during percutaneous coronary intervention (PCI). As well, any medication necessary for primary cardiac condition like aspirin, antiplatelet compounds or even thrombolytics can be used.
Answer: Therapeutic hypothermia should not be delayed particularly in clear cut cases of V.fib cardiac arrest and should be initiated in the emergency department. Cardiology interventions can be done and patients can continue to be cooled during percutaneous coronary intervention (PCI). As well, any medication necessary for primary cardiac condition like aspirin, antiplatelet compounds or even thrombolytics can be used.
Tuesday, May 17, 2011
Q: What is the treatment of Q fever in Pregnancy?
Answer: co-trimoxazole
Q fever is caused by infection with Coxiella burnetii. This organism is found in cats, dogs, cattle, sheep, goats and other domestic mammals. Infection results from inhalation of endospores, and from contact with the milk, urine, feces or body fluid of infected animals.
Q fever can be treated with antibiotics - doxycycline, tetracycline, chloramphenicol, ciprofloxacin, ofloxacin, and hydroxychloroquine.
Q fever in pregnancy may cause abortions particularly in the first trimester. As doxycycline and ciprofloxacin are contraindicated in pregnancy, the preferred treatment is co-trimoxazole for the duration of pregnancy.
Answer: co-trimoxazole
Q fever is caused by infection with Coxiella burnetii. This organism is found in cats, dogs, cattle, sheep, goats and other domestic mammals. Infection results from inhalation of endospores, and from contact with the milk, urine, feces or body fluid of infected animals.
Q fever can be treated with antibiotics - doxycycline, tetracycline, chloramphenicol, ciprofloxacin, ofloxacin, and hydroxychloroquine.
Q fever in pregnancy may cause abortions particularly in the first trimester. As doxycycline and ciprofloxacin are contraindicated in pregnancy, the preferred treatment is co-trimoxazole for the duration of pregnancy.
Q fever during pregnancy: diagnosis, treatment, and follow-up - Arch Intern Med. 2002 Mar 25;162(6):701-4.
Monday, May 16, 2011
Sunday, May 15, 2011
The Challenge of the ICU
In one recent article 4 keys have been identified for success against challenges of the ICU
Success Key No.1: Overcoming sepsis
Success Key No.2: Rapid response team
Success Key 3: Reducing CLABSIs (central line–associated bloodstream infections).
Success Key No. 4: Improving care with intensivists
Read full article here
Saturday, May 14, 2011
Q: Deficiency of which vitamin may cause lactic acidosis?
Answer: Thiamine (Vitamin B1)
Clinically it may become significant in patients who have prolong NPO status or have TPN without essential vitamins in it. It should also be considered in patients who alcohol abuse and poor intake.
Severe lactic acidosis and thiamine deficiency during total parenteral nutrition--case report. Hepatogastroenterology. 2004 Jan-Feb;51(55):253-5.
Friday, May 13, 2011
Thursday, May 12, 2011
Q; 52 year old female with history of hypertension - but controlled with Lisinopril developed UTI (urinary tract infection). What should be your worry to treat her with Bactrim (TMP-SMX)?
Answer: Hyperkalemia
The mechanism of Bactrim induced hyperkalemia is via Trimethoprim inhibition of the sodium channel located on the luminal surface of the principal cells. This decreases sodium reabsorption and the electro negativity in the lumen thus decreases the driving force for the secretion of potassium through an apically located potassium channel on the same principal cells.
This side effect is most common in HIV infected patients who are treated with high doses of TMP-SMX. However hyperkalemia can occur with lower doses in patients with preexisting renal dysfunction or in those taking medications such as angiotensin-converting enzyme inhibitors or potassium-sparing diuretics. It may exacerbate hyperkalemic effect to potentially dangerous levels.
Answer: Hyperkalemia
The mechanism of Bactrim induced hyperkalemia is via Trimethoprim inhibition of the sodium channel located on the luminal surface of the principal cells. This decreases sodium reabsorption and the electro negativity in the lumen thus decreases the driving force for the secretion of potassium through an apically located potassium channel on the same principal cells.
This side effect is most common in HIV infected patients who are treated with high doses of TMP-SMX. However hyperkalemia can occur with lower doses in patients with preexisting renal dysfunction or in those taking medications such as angiotensin-converting enzyme inhibitors or potassium-sparing diuretics. It may exacerbate hyperkalemic effect to potentially dangerous levels.
Wednesday, May 11, 2011
Q: 32 year old male with sickle cell disease presented to ER with severe episode of priapism. What should be considered?
Answer: For priapism in sickle cell disease, early exchange transfusion is indicated, meanwhile pain can be controlled with epidural analgesia. Exchange transfusions may be required to increase hemoglobin concentration to higher than 10% and decrease hemoglobin S to less than 30%. Before any intervention urology consult should be obtiained for possible use of terbutaline and pseudoephedrine. Some studies suggest that the use of terbutaline orally, at a dose of 5-10 mg, followed by another 5-10 mg 15 minutes later, if required, produces resolution in about one third of patients. Oral pseudoephedrine, 60-120 mg orally has also been suggested as a potential therapy due to its alpha-agonist effect. The exact efficacy of this medication orally is unknown.
Answer: For priapism in sickle cell disease, early exchange transfusion is indicated, meanwhile pain can be controlled with epidural analgesia. Exchange transfusions may be required to increase hemoglobin concentration to higher than 10% and decrease hemoglobin S to less than 30%. Before any intervention urology consult should be obtiained for possible use of terbutaline and pseudoephedrine. Some studies suggest that the use of terbutaline orally, at a dose of 5-10 mg, followed by another 5-10 mg 15 minutes later, if required, produces resolution in about one third of patients. Oral pseudoephedrine, 60-120 mg orally has also been suggested as a potential therapy due to its alpha-agonist effect. The exact efficacy of this medication orally is unknown.
Tuesday, May 10, 2011
Q; Nimodipine has strong 'black box' warning against IV administration but still there are reports of IV administration of Nimodipine 'by error'. How?
Answer: Intravenous nimodipine can result in death, cardiac arrest, due to acute fall in blood pressure.
When PO administration is not feasible it is given via nasogastric tube. The recommended way is to make a hole in both ends of the capsule with an 18 gauge needle, and the contents of the capsule extracted into a syringe. This may be the reason of 'by error' administration of Nimodipine via IV route.
FDA advise that the syringe be labeled "Not for IV Use." The needle should be removed from the syringe and the contents should then be emptied into the patient's in situ nasogastric tube and washed down the tube with 30 mL of normal saline (0.9%).
Source: FDA (here)
Answer: Intravenous nimodipine can result in death, cardiac arrest, due to acute fall in blood pressure.
When PO administration is not feasible it is given via nasogastric tube. The recommended way is to make a hole in both ends of the capsule with an 18 gauge needle, and the contents of the capsule extracted into a syringe. This may be the reason of 'by error' administration of Nimodipine via IV route.
FDA advise that the syringe be labeled "Not for IV Use." The needle should be removed from the syringe and the contents should then be emptied into the patient's in situ nasogastric tube and washed down the tube with 30 mL of normal saline (0.9%).
Source: FDA (here)
Monday, May 9, 2011
Sunday, May 8, 2011
Saturday, May 7, 2011
Ice test in Myasthenia Gravis
Most of the Myasthenia patients along with other symptoms of weakness usually exhibits ptosis. While at bedside place an ice cube over eye lids for 2 minutes. Cooling improves neuromuscular transmission. Resolution of ptosis with cooling is a positive test for Myasthenia Gravis and reported upto 80% reliable to diagnose ocular myasthenia.
Most of the Myasthenia patients along with other symptoms of weakness usually exhibits ptosis. While at bedside place an ice cube over eye lids for 2 minutes. Cooling improves neuromuscular transmission. Resolution of ptosis with cooling is a positive test for Myasthenia Gravis and reported upto 80% reliable to diagnose ocular myasthenia.
Friday, May 6, 2011
Q: What is MELAS Syndrome?
Answer: It stands for
Early symptoms include muscle, headaches, vomiting, and seizures and lately stroke-like episodes.
"MELAS episode" or attack appears as temporary hemiparesis, altered consciousness, vision abnormalities, seizures and severe headaches like migraines. Most people with MELAS buildup of lactic acid due to mitochondrial error.
There is no treatment known but it is described that Riboflavin (vitamin B2) may help.
Answer: It stands for
- Mitochondrial myopathy,
- Encephalopathy,
- Lactic Acidosis, and
- stroke like episodes
Early symptoms include muscle, headaches, vomiting, and seizures and lately stroke-like episodes.
"MELAS episode" or attack appears as temporary hemiparesis, altered consciousness, vision abnormalities, seizures and severe headaches like migraines. Most people with MELAS buildup of lactic acid due to mitochondrial error.
There is no treatment known but it is described that Riboflavin (vitamin B2) may help.
Thursday, May 5, 2011
Q: Name the organism after knowing following 5 tips
1. Usually happen in warm-weather months
2. Assosicated with eating Raw oyster
3. Common in immunocpromised patients
4. Also common in patients with liver insufficiency secondary to alcohol or hepatitis
5. One of the clinical sign is cutaneous bullae?
Answer: Vibrio vulnificus
Vibrio vulnificus is a Gram-negative, motile, curved, rod-shaped bacteria of the Vibrio Genus. It can cause rapidly expanding cellulitis and septicemia. It is present in marine environments and causes an infection often after eating seafood, especially raw or undercooked oysters; the bacteria can also enter the body through open wounds when swimming in infected waters. Symptoms include vomiting, diarrhea, abdominal pain, and a blistering dermatitis. It is common in immunocpromised patients and in patients with liver insufficiency.
1. Usually happen in warm-weather months
2. Assosicated with eating Raw oyster
3. Common in immunocpromised patients
4. Also common in patients with liver insufficiency secondary to alcohol or hepatitis
5. One of the clinical sign is cutaneous bullae?
Answer: Vibrio vulnificus
Vibrio vulnificus is a Gram-negative, motile, curved, rod-shaped bacteria of the Vibrio Genus. It can cause rapidly expanding cellulitis and septicemia. It is present in marine environments and causes an infection often after eating seafood, especially raw or undercooked oysters; the bacteria can also enter the body through open wounds when swimming in infected waters. Symptoms include vomiting, diarrhea, abdominal pain, and a blistering dermatitis. It is common in immunocpromised patients and in patients with liver insufficiency.
Wednesday, May 4, 2011
Q: One most important thing to know about Candida Glabrata?
Answer: Diflucan (fluconazole) does not cover it.
Candida Glabrata once thought to be rare in hospital patients is now increasingly more common. C. glabrata possesses an 'evolved resistance' to the azole drugs (fluconazole and ketoconazole). Drug of choices are amphotericin B and caspofungin.
Answer: Diflucan (fluconazole) does not cover it.
Candida Glabrata once thought to be rare in hospital patients is now increasingly more common. C. glabrata possesses an 'evolved resistance' to the azole drugs (fluconazole and ketoconazole). Drug of choices are amphotericin B and caspofungin.
Tuesday, May 3, 2011
Mnemonic for Ranson criteria of Acute Pancreatitis
Ranson criteria is a clinical prediction rule severity of acute pancreatitis.
At admission: "GA LAW"
Glucose; more than 200 mg/dL
AST: more than 250 IU/L
LDH: more than 350 IU/L
Age: more than 55 years
WBC: more than 16000 cells/mm3
At 48 hours: "C Hobbs"
Calcium: less than 8.0 mg/dL
Hematocrit fall more than 10%
Oxygen: PO2 less than60 mmHg
BUN increased by 1.5 or more mg/dL after IV fluid hydration
Base deficit: more than 4 mEq/L
Sequestration of fluids: more than 6 L
Score 0 to 2 : 2% mortality
Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality
Score 7 to 8 : 100% mortality
Ranson criteria is a clinical prediction rule severity of acute pancreatitis.
At admission: "GA LAW"
Glucose; more than 200 mg/dL
AST: more than 250 IU/L
LDH: more than 350 IU/L
Age: more than 55 years
WBC: more than 16000 cells/mm3
At 48 hours: "C Hobbs"
Calcium: less than 8.0 mg/dL
Hematocrit fall more than 10%
Oxygen: PO2 less than60 mmHg
BUN increased by 1.5 or more mg/dL after IV fluid hydration
Base deficit: more than 4 mEq/L
Sequestration of fluids: more than 6 L
Score 0 to 2 : 2% mortality
Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality
Score 7 to 8 : 100% mortality
Monday, May 2, 2011
Q: 34 year old female with no significant past medical history is admitted with urosepsis. EKG was ordered as 'routine'. What is your diagnosis?
Answer: Wolff-Parkinson-White syndrome
Wolff–Parkinson–White syndrome (WPW) is a syndrome of pre-excitation of ventricles of the heart due to an accessory pathway called bundle of Kent. WPW syndrome gets diagnosed in asymptomatic people on EKG via delta wave, which is a slurred upstroke in the QRS complex associated with a short PR interval. (see above in EKG.
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