Q: All of the following are causes of Antithrombin (AT) deficiency except?

A)  Liver cirrhosis
B) Nephrotic syndromes 
C) Extracorporeal membrane oxygenation (ECMO) 
D) Hemodialysis 
E) Normal pregnancy


Answer: E

Objective of above question is to highlight the fact that patients on ECMO and HD may have lower AT deficiency. This may be related to cannula itself. As these patients, while in ICU frequently requires heparin, deficiency of AT may cause ineffective anticoagulation. In such scenarios administration of AT may be required. Normal pregnancy does not cause any AT deficiency but may be present in preeclampsia or eclampsia.

Cirrhosis and Nephrotic syndrome are understandably the causes of AT deficiency.  


References:

1. Alegre A, Vicente V, Gonzalez R, Alberca I. Effect of hemodialysis on protein C levels. Nephron 1987; 46:386. 

2. Weenink GH, Treffers PE, Vijn P, et al. Antithrombin III levels in preeclampsia correlate with maternal and fetal morbidity. Am J Obstet Gynecol 1984; 148:1092.

Q: What is one simple (and probably only) advantage of impedance plethysmography over compression ultrasonography in the diagnosis and follow-up of Deep Venous Thrombosis (DVT)?


Answer:  Impedance plethysmography normalizes relatively more quickly after a previous episode of DVT, and can be more helpful in patients with recurrent DVT or in the follow-up of present DVT.



Reference:

1. Huisman MV, Büller HR, ten Cate JW. Utility of impedance plethysmography in the diagnosis of recurrent deep-vein thrombosis. Arch Intern Med 1988; 148:681.

Q; Which one precaution should be taken while administrating lidocaine as local anesthetic during talc procedure for pleurodesis?


Answer:  Talc slurry may get adsorp to lidocaine, so it should be administer a few minutes before the talc slurry administration. Lidocaine is usually given as a spray of 25 mL (250 mg) of 1 percent lidocaine intrapleurally. Beside lidocaine, patient should also receive intravenous analgesic and midazolam for comfort.


Reference:  

 Lee P, Colt HG. A spray catheter technique for pleural anesthesia: a novel method for pain control before talc poudrage. Anesth Analg 2007; 104:198.

Q: Which of the following found to be having some role in treatment of hepatic encephelopathy

A) Methadone
B) Flumazenil
C) Naloxone
D) Fomepizole
E) ETOH


Answer:  B

There is some evidence of an increase in benzodiazepine receptor ligands in patients with hepatic encephalopathy, so multiple attempts have been made to use benzodiazepine receptor antagonists to treat hepatic encephalopathy with various levels of success. But still evidence is far from enough to label it as a strong agent for use as a standard of treatment. It may be used in acute situations to buy some time and/or as temporizing measure for two to four hours. On positive note, those patients who respond to flumazenil usually have a favorable prognosis. 


References:

1.  Basile AS, Harrison PM, Hughes RD, et al. Relationship between plasma benzodiazepine receptor ligand concentrations and severity of hepatic encephalopathy. Hepatology 1994; 19:112. 

2. Gyr K, Meier R, Häussler J, et al. Evaluation of the efficacy and safety of flumazenil in the treatment of portal systemic encephalopathy: a double blind, randomised, placebo controlled multicentre study. Gut 1996; 39:319. 

3. Cadranel JF, el Younsi M, Pidoux B, et al. Flumazenil therapy for hepatic encephalopathy in cirrhotic patients: a double-blind pragmatic randomized, placebo study. Eur J Gastroenterol Hepatol 1995; 7:325. 

4. Pomier-Layrargues G, Giguère JF, Lavoie J, et al. Flumazenil in cirrhotic patients in hepatic coma: a randomized double-blind placebo-controlled crossover trial. Hepatology 1994; 19:32. 

5. Als-Nielsen B, Kjaergard LL, Gluud C. Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy. Cochrane Database Syst Rev 2001; :CD002798. 

6. Goulenok C, Bernard B, Cadranel JF, et al. Flumazenil vs. placebo in hepatic encephalopathy in patients with cirrhosis: a meta-analysis. Aliment Pharmacol Ther 2002; 16:361.

Q; In recent years prophylaxis for infective endocarditis has been curtailed down significantly  prior to various dental, urologic, gastrointestinal and invasive procedures. What is the reason behind it?

Answer:  In experimental animals as well as long term studies have shown that it is almost impossible to induce/have endocarditis unless the valvular endocardium is first damaged. Endocardial injury is the 101 requisite to develop infective endocarditis. Without any previous history of endocarditis or evidence of congenital or acquired endocardial lesions, prophylaxis is usually not recommended.

Please refer elsewhere to see guidelines from various societies in this regard.

Q: Why auscultation of heart is an important component in the evaluation of hemoptysis?


Answer: To rule out mitral stenosis or mitral regurgitation as a cause of hemoptysis

Though not high on the list, but the presence of murmur of mitral valve should raise the possibility of the cardiac source of hemoptysis. This can be supplemented with echocardiography and evaluation of upper lobes of lungs via radiological workup.


References and further readings:

1. Ramsey HW, de la Torre A, Bartley T, et al: Intractable hemoptysis in mitral stenosis. Ann Intern Med 1967; 67:588-593

2. P. A. Schnyder, A. M. Sarraj, B. E. Duvoisin, L. Kapenberger, and M. J.-M. Landry, “Pulmonary edema associated with mitral regurgitation: prevalence of predominant involvement of the right upper lobe,” The American Journal of Roentgenology, vol. 161, no. 1, pp. 33–36, 1993.

3. H. W. Ramsey, A. de la Torre, T. D. Bartley, and J. W. Linhart, “Intractable hemoptysis in mitral stenosis treated by emergency mitral commissurotomy,” Annals of Internal Medicine, vol. 67, no. 3, pp. 588–593, 1967.

4. T. H. Spence and J. C. Connors, “Diffuse alveolar hemorrhage syndrome due to “silent” mitral valve regurgitation,” Southern Medical Journal, vol. 93, no. 1, pp. 65–67, 2000.

5. K. Woolley and P. Stark, “Pulmonary parenchymal manifestations of mitral valve disease,” Radiographics, vol. 19, no. 4, pp. 965–972, 1999.

 6. A. W.-T. Yeung, H. P. Shum, G. S.-M. Lam, K. K.-C. Chan, S. K. Li, and W. W. Yan, “Diffuse alveolar hemorrhage and intravascular hemolysis due to acute mitral valve regurgitation,” Critical Care and Shock, vol. 16, no. 1, pp. 3–7, 2013.

7. U. Kim HG, D. H. Kim, S. H. Lee et al., “Diffuse alveolar hemorrhage due to acute mitral regurgitation,” Journal of Cardiovascular Ultrasound, vol. 15, no. 1, pp. 16–18, 2007.

8. J. M. Roach, K. C. Stajduhar, and K. G. Torrington, “Right upper lobe pulmonary edema caused by acute mitral regurgitation: diagnosis by transesophageal echocardiography,” Chest, vol. 103, no. 4, pp. 1286–1288, 1993.

A note on Diuretics and Thiamine deficiency

A very under-appreciated cause of thiamine deficiency is use of diuretics as well as any polyuria in ICU, and/or accompanied by poor nutrition. Loss of thiamine via diarrhea, dialysis and vomiting is well known but in ICU setting loss via diuretics become a significant factor. Polyuria for any reason may cause thiamine deficiency, and should be supplemented. CHF patients who are on chronic diuretic therapy are particularly prone to thiamine deficiency.


References:

1. Wooley, JA. Characteristics of thiamin and its relevance to the management of heart failure. Nutr Clin Pract. Oct-Nov 2008. 23:487-93. 

2. Sica DA. Loop diuretic therapy, thiamine balance, and heart failure. Congest Heart Fail. 2007 Jul-Aug. 13(4):244-7.

3. Hanninen SA, Darling PB, Sole MJ, et al. The prevalence of thiamin deficiency in hospitalized patients with congestive heart failure. J Am Coll Cardiol. 2006 Jan 17. 47(2):354-61.

Q: Patients with chron disease are prone to which of the following complications in hospital (select one)

A) Pulmonary Embolism
B) Acute MI
C) Intracranial bleed
D) Upper GI bleed
E) Acute liver failure


Answer: A

Patients with inflammatory bowel disease (IBD) are more prone to venous thromboembolism as well as pulmonary embolism. It is of critical importance that patients with acute exacerbation of IBD in hospitals should not miss DVT prophylaxis.


References:

1. Miehsler W, Reinisch W, Valic E, et al. Is inflammatory bowel disease an independent and disease specific risk factor for thromboembolism? Gut 2004; 53:542. 

2. Nguyen GC, Sam J. Rising prevalence of venous thromboembolism and its impact on mortality among hospitalized inflammatory bowel disease patients. Am J Gastroenterol 2008; 103:2272. 

Q: All of the following are recommended to pursue during acute exacerbation of Idiopathic Pulmonary Fibrosis (AE-IPF) except?

A)  High-flow oxygen
B) Anti-acid/reflux treatment
C) Invasive mechanical ventilation
D) Broad spectrum antibiotic 
E) High dose steroids


Answer: C

 Invasive mechanial ventilation has an extremely high mortality in acute execerbation of IPF, and should be pursue only if patient or family insist despite full discussion and disclosure of potential harm, and high probaility of its failure as a salvage therapy.

Choice B may look surprising but reflux has been described as a possible cause of AE-IPF.


References:

1. Gaudry S, Vincent F, Rabbat A, et al. Invasive mechanical ventilation in patients with fibrosing interstitial pneumonia. J Thorac Cardiovasc Surg 2014; 147:47. 

2. Mallick S. Outcome of patients with idiopathic pulmonary fibrosis (IPF) ventilated in intensive care unit. Respir Med 2008; 102:1355. 

3. Raghu G, Collard HR, Egan JJ, et al. An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management. Am J Respir Crit Care Med 2011; 183:788.

4. Lee JS, Collard HR, Anstrom KJ, et al. Anti-acid treatment and disease progression in idiopathic pulmonary fibrosis: an analysis of data from three randomised controlled trials. Lancet Respir Med 2013; 1:369.

Q: One unit of cryoprecipitate (cryo) raises the fibrinogen level by how much?


Answer: Plasma fibrinogen level rise by approximately 7 to 10 mg/dL, with each unit of cryo transfusion. The usual formula to calculate the requirement of cryo is 1 unit of cryo per 10 kg of body weight. In massive surgical bleed, it should be calculated as 1 unit per 5 kg of body weight. One unit of cryo is about 10 to 15 mL in volume and is obtained from one unit of whole blood, and is about 200 to 400 mg in each unit of cryo.

Q: All of the following are risk factors for re-intubation except?

A) weak cough strength
B) requiring frequent suctioning
C) a rapid shallow breathing index (RSBI) more than 58 breaths/min per L, 
D) a negative fluid balance during the 24 hours preceding extubation, 
E) Intubation secondary to pneumonia 


Answer: D

Below 15 percent of failed planned extubations is a acceptable number for any ICU. There are many factors which may lead to failure of planned extubation including choice A, B and C.

Choice C is interesting as conventional teaching is RSBI less than 100 breaths/min per L is acceptable. It is true in most situations but risk of extubation failure start to rise once it goes above 58 breaths/min per L 2. It is actually a positive fluid balance particularly in preceding 24 hours which may be a problem. Also, patient's baseline cardiopulmonary health plays an important role in success of extubation.



References: 

1.  Frutos-Vivar F, Ferguson ND, Esteban A, et al. Risk factors for extubation failure in patients following a successful spontaneous breathing trial. Chest 2006; 130:1664. 

2. Thille AW, Harrois A, Schortgen F, et al. Outcomes of extubation failure in medical intensive care unit patients. Crit Care Med 2011; 39:2612.

3. Esteban A, Anzueto A, Frutos F, et al. Characteristics and outcomes in adult patients receiving mechanical ventilation: a 28-day international study. JAMA 2002; 287:345.

Q: Harvey-Bradshaw Index (HBI) is a grading system for the severity of which disease? 

A) Crohn Disease
B) Ulcerative Colitis
C) Acute appendicitis
D) Acute Peritonitis
E) Diverticulitis

Answer: A

Crohn's Disease Activity Index (CDAI) is a commonly used grading system to measure the severity of Crohn disease. Harvey-Bradshaw Index (HBI) is created as a simplified version of CDAI.

0-149 points: Asymptomatic remission
150-220 points: Mildly to moderately active Crohn's disease
221-450 points: Moderately to severely active Crohn's disease
451-1100 points: Severely active to fulminant disease

A Harvey-Bradshaw Index of less than 5 correlates with clinical remission.

References:

1. Harvey RF, Bradshaw JM. A simple index of Crohn's disease activity. Lancet. 1980 Mar 8;1(8167):514.

2. Best WR. Predicting the Crohn's disease activity index from the Harvey-Bradshaw Index. Inflamm Bowel Dis. 2006 Apr;12(4):304-10. 

3. Best WR, Becktel JM, Singleton JW, Kern F Jr. Development of a Crohn's disease activity index. National Cooperative Crohn's Disease Study. Gastroenterology. 1976 Mar;70(3):439-44.

Q: All of the following are considered as risk factors associated with a poor outcome in acute colonic ischemia except?

A) male gender,
B) SBP less than 90 mm Hg
C) BUN more than 20 mg/dL
D) Hgb less than 8 g/dL
E) LDH more than 350 units/L


Answer: D

As per The American College of Gastroenterology, following are considered as risk factors associated with a poor outcome in acute colonic ischemia and risk stratifications may help in decreasing morbidity and mortality. The risk factors associated with poor outcome described are 

• male gender, 
• hypotension (SBP less than 90), 
• tachycardia (heart rate more than 100 beats/minute), 
• abdominal pain without rectal bleeding, 
• blood urea nitrogen (BUN) more than 20 mg/dL, 
• hemoglobin (Hgb) less than 12 g/dL, 
• LDH more than 350 units/L, 
• serum sodium less than 136 mEq/L, and 
• WBC more than 15,000/mm3

Reference:

Brandt LJ, Feuerstadt P, Longstreth GF, et al. ACG clinical guideline: epidemiology, risk factors, patterns of presentation, diagnosis, and management of colon ischemia (CI). Am J Gastroenterol 2015; 110:18.

A note on lactic acid clearance

The two components of lactic acid may very well predict and correlate with ICU mortality.

1) Duration, and
2) Degree

Abramson et al showed more than 23 years ago that if lactic acid normalizes within 24 hours following multiple trauma, survival is 100% predicted. But if it takes more than 48 hours to normalize, survival prediction gets down to only 14%.

Similarly other works have shown that if lactic acid remains elevated more than 4 mmol/L after 24 hours of ICU admission, likelihood of survival is only 11%.



Reference:

1. Abramson D, Scalea TM, Hitchcock R, Trooskin SZ, Henry SM, Greenspan J. Lactate clearance and survival following injury. J Trauma. 1993 Oct. 35(4):584-8. 

2.  Jones AE. Point: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy? Yes. Chest. 2011 Dec. 140(6):1406-8. 

3. Jones AE, Shapiro NI, Trzeciak S, Arnold RC, Claremont HA, Kline JA. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA. 2010 Feb 24. 303(8):739-46.

Q: What are the potential treatment options for Digoxin's Non-Occlusive Mesenteric Ischemia?


Answer: Digoxin (cardiac glycosides) has shown to cause contraction of vascular smooth muscles, particularly arteriolar vessels. Studies have demonstrated that rapid IV push of digoxin may causes constriction of the splanchnic bed. This effect may get enhanced in the presence of hypokalemia, so inhibition of the Na+-K+-ATPase is suspected as underlying mechanism. As digoxin has slow elimination (not cleared by dialysis either), infusion of papaverine (vasodilator) under angiography guide is recommended as a treatment. Another, relatively simple antidote described is glucagon, which is known to  decrease mesenteric vascular resistance. Similarly, diltiazem is also recommended as a treatment.



References:

1. Bynum TE, Hanley HG (1982) Effect of digitalis on estimated splanchnic blood flow. J Lab Clin Med 99:84–91 

2. Ferrer MI, Bradley SE, Wheeler HO, Enson Y, Presig R, Harvey RM (1965) The effect of digoxin in the splanchnic circulation in ventricular failure. Circulation 32:524–537

3. Hess T, Scholtysik G, Salzmann R, Riesen W (1983) Digoxin-specific antibody fragments and a calcium antagonist for reversal of digoxin-induced mesenteric vasoconstriction. J Pharm Pharmacol 35:647–651 

4. Levinsky RA, Lewis RM, Bynum TE, Hanley HG (1975) Digoxin induced intestinal vasoconstriction. The effects of proximal arterial stenosis and glucagon administration. Circulation 52:130–136 

5. Gasic S, Korn A, Eichler HG (1987), Diltiazem counteracts digitalis-dependent splanchnic vasoconstriction in man. Int J Clin Pharmacol Ther Toxicol 25:553–557

Q; 52 year old male with history of renal transplant 2 weeks ago is now in ICU for worsening renal failure. The ultrasound report reads "ureteral jets noted in bladder". What does it means? 


Answer: Obstructive uropathy is a common cause of acute kidney injury (AKI) in patients with transplanted kidneys, and one of the common cause is ureteral strictures. For this reason ureteral stents are placed during kidney transplantation. If ultrasound reads that "Ureteral Jets" (pulsatile movement of urine into the bladder) is present, it rules out ureteral obstruction, proved otherwise.

Q: Why it is important to delay bladder catheterization in hemodynamic compromise secondary to suspected right ventricular infarct?

Answer: Bladder catheterization may increase the vagal tone and can decrease preload acutely, leading to cardiogenic shock. Mechanism supposed to be associated is an induction of a parasympathetic autonomic reflex (bradycardia and hypotension) due to a sudden decrease of bladder volume via bladder catheter, while patient is lying supine. 


References: 

Mary DA. The urinary bladder and cardiovascular reflexes. Int J Cardiol. 1989;23:11–17

Q: During thoracentesis, which of the following sign is more predictive of Re-expansion Pulmonary Edema (REPE)  - (Select one)?

A) Chest pain
B) Cough


Answer: A

Usually patients tolerate large volume thoracentesis without REPE. But development of anterior chest pain could be an indicator of REPE. Cough is a very frequent sign during thoracentesis or resolution of pneumothorax but is not as highly associated with REPE as anterior chest pain. In any case, it is recommended to keep volume of thoracentesis less than 1.5 Liters.


Reference: 

Doelken P, Huggins JT, Pastis NJ, Sahn SA. Pleural manometry: technique and clinical implications. Chest 2004; 126:1764.

Q: All of the following predicts difficult bag-mask ventilation (BMV) except? 

A) Mask seal
B) Obstruction or Obesity
C) Age over 55 (due to loss of tissue elasticity)
D) presence of teeth
E) Stiff lungs


Answer:  D

Difficult bag-mask ventilation (BMV) can be predicted during intubation with mnemonic MOANS© 

• Mask seal 
• Obstruction or Obesity
• Age over 55 
• No teeth
• Stiff lungs

Another Mnemonic commonly used is ROMAN

• Radiation or Restriction 
• Obstruction or Obesity or Obstructive Sleep Apnea 
• Mask Seal or Mallampati or Male 
• Age 
• No teeth 

The objective of above question is to highlight the importance of presence or absence of dentures during intubation/BMV. Contrary to popular belief, the presence of teeth is a good sign during intubation for BMV. Teeth provide a good anatomical framework against which the mask can be sealed properly. Patients with denture should be bag mask ventilated with dentures still on and should be removed when an operator is ready to proceed for blade/video laryngoscopy.


 Reference: 

 Conlon NP, Sullivan RP, Herbison PG, et al. The effect of leaving dentures in place on bag-mask ventilation at induction of general anesthesia. Anesth Analg 2007; 105:370.

Q: What is MacCallum's patch? 


 Answer: During mitral regurgitation, where the regurgitant jet strikes back the atrial wall, results in endocardial thickening and it is called MacCallum's patch. They are also called MacCallum plaques and also considered as a hallmark in rheumatic heart disease. They are described as "map-like areas of thickened, roughened, and wrinkled part of the endocardium in the left atrium", usually associated with dilated left atrium.

Clinical significance: They are more prone to have vegetations in infective endocarditis.

Q: Which set of arteries usually a cause of massive hemoptysis (select one) 

A) BRONCHIAL 
B) PULMONARY 


Answer: A 

Though most of the circulation requires passing through the pulmonary vasculature bed but the cause of hemoptysis is usually bronchial arteries, proved otherwise. This is due to the high systolic pressure because of their origin from the aorta (sometimes from the intercostal or vertebral arteries). Another reason is their vital supply to hilar lymph nodes, visceral pleura, and to the mediastinum.



Reference:

Cahill BC, Ingbar DH. Massive hemoptysis. Assessment and management. Clin Chest Med 1994; 15:147.

Q: Passive Leg Raise (PLR) testing gives more reliable result when initial hemodynamic data {Cardiac Output (CO) or Pulse-Pressure-Variation (PPV) } is obtained by putting patient at 45 degrees, and obtain hemodynamic data again by

A) Lowering the patient's head to the horizontal position and raise the legs at 45 degrees for about 60-90 seconds

B) Lowering the patient's head to the horizontal position and raise the legs at 90 degrees for about 60-90 seconds

C) Lowering the patient's head to the horizontal position and raise the legs at 45 degrees for about 10-15 seconds.

D) Keep the patient's body to 45 degrees and lower the legs at 90 degrees for about 60-90 seconds

E) PLR testing should be preceded by 500 cc Albumin bolus over 15 minutes, otherwise data is not reliable

Answer: A

PLR test, though easy to perform but is a complex hemodynamic maneuver. It requires proper testing. Answer A is correct as maximal effect occurs at 30-90 seconds. If performed incorrectly, it may lead to erroneous conclusion and may harm the patient. Also, it should be read in conjunction with other maneuver like Pulmonary artery catheter (PAC) data, PPV on arterial line or bedside point of care echo-cardiogram. Also, it should be understand that PLR is more about predicting patient responsiveness to fluid, rather total volume status or ventricular function, though they may important roles. Answer E is wrong as PLR better be performed before IVF bolus.

By definition, a 10 percent increase in CO or decrease in PPV predicts volume responsiveness.

Références and further reading: 

1.  Préau S, Saulnier F, Dewavrin F, Durocher A, Chagnon JL. Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis. Crit Care Med. 2010 Mar;38(3):819-25

2. Marik PE, Monnet X, Teboul JL. Hemodynamic parameters to guide fluid therapy. Ann Intensive Care 2011; 1:1. 

3. Mandeville JC, Colebourn CL. Can transthoracic echocardiography be used to predict fluid responsiveness in the critically ill patient? A systematic review. Crit Care Res Pract 2012; 2012:513480. 

4. Cherpanath TG, Hirsch A, Geerts BF, et al. Predicting Fluid Responsiveness by Passive Leg Raising: A Systematic Review and Meta-Analysis of 23 Clinical Trials. Crit Care Med 2016; 44:981. 

5. Bentzer P, Griesdale DE, Boyd J, et al. Will This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? JAMA 2016; 316:1298.

Q: On bedside echo which one other finding may help to rule in cardiac tamponade beside fluid around the heart and diastolic collapse of right ventricle?



Answer: Inferior Vena Cava (IVC) dilatation  without respiratory variations.

IVC dilatation without respiratory variations, reflects the elevated right atrium pressure.

One of the non-pharmacologic strategy to treat atrial fibrillation

Editors' note: icuroom.net has no collaboration with any company. This video is solely for educational purpose

Q: In Intra-Cranial Hemorrhage (ICH) - which area is more prone to cause seizure?

A) lobar  hemorrhage
B) deep hemorrhage


Answer: A

Contrary to popular belief, seizures are more common in lobar hemorrhage as compared to deep hemorrhage. Monitoring is essential as non-convulsive seizure is not uncommon.


Reference:

1. Kuramatsu JB, Sauer R, Mauer C, et al. Correlation of age and haematoma volume in patients with spontaneous lobar intracerebral haemorrhage. J Neurol Neurosurg Psychiatry 2011; 82:144.

2. Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 2007; 38:2001.

Q: what is the physiology behind "alimentary hypoglycemia" in patients with dumping syndrome after gastric bypass surgery?



Answer: In patients with gastric surgery, the rapid "dumping" of food triggers the pancreas to release excessive amounts of insulin and to cause "alimentary hypoglycemia." To note, it has also been reported without any history of gastric surgery 1.


Reference:

1. M. Alan Permutt, M.D., John Kelly, M.D., Robert Bernstein, M.D., David H. Alpers, M.D., Barry A. Siegel, M.D., and David M. Kipnis, M.D. - Alimentary Hypoglycemia in the Absence of Gastrointestinal Surgery -  N Engl J Med 1973; 288:1206-1210 - June 7, 1973

Q: Which antihypertensive medicine has shown to reverse the myoclonus effect of opioid analgesics?


Answer: Nifedipine

Nifedipine, also popularly known by its trade name Procardia is known to reverse the myoclonus effect of opioids. The Dose is 10 mg three times per day. Another drug which may help is Clonazepam in a dose of 0.5 mg three times per day.

Q: After new year night fireworks, 20 year old male is admitted via ED with partial-thickness burns greater than 10% of Total Body Surface Area (TBSA). Why it is important to give constant rate of IVF depending upon calculated fluid requirement (using either Parkland or the modified Brooke formula), and avoid intermittent IV fluid boluses? 


 Answer: Giving IVF boluses instead of constant rate IVF for volume resuscitation in burn patients, may cause vascular collapse and increase the edema. 


 Reference:

 Gueugniaud PY, Carsin H, Bertin-Maghit M, Petit P. Current advances in the initial management of major thermal burns. Intensive Care Med 2000; 26:848.

cocaine toxicity

Q: All of the following can be used in cardiac complications of cocaine toxicity except?

A) nitroglycerin
B) benzodiazepines
C) aspirin  
D) phentolamine
E) beta-blocker 


Answer: E

The objective of the above question is to reinforce the contraindication of beta-blockers in acute cocaine ingestion, as well as to highlight the benefit of phentolamine. Phentolamine is an alpha-adrenergic antagonist and is very effective as a second agent in reversing cocaine-induced coronary artery vasoconstriction in unresponsive benzodiazepines. It is given as an IV bolus in a dose of 1 to 2.5 mg every 5 to 10 minutes on a PRN basis.

#toxicology


References: 

1. Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med 2001; 345:351.

2. Hollander JE. The management of cocaine-associated myocardial ischemia. N Engl J Med 1995; 333:1267. 

3. Albertson TE, Dawson A, de Latorre F, et al. TOX-ACLS: toxicologic-oriented advanced cardiac life support. Ann Emerg Med 2001; 37:S78.