Q: Tromethamine (tris-hydroxymethyl aminomethane - THAM) buffers hydrogen ions and is an alternative for use in acidosis instead of 'bicarb'. THAM can be used in all of the following situations except? 

A) hypercapnic respiratory failure, 
B) drug intoxications, 
C) Acidosis with severe hypernatremia
D) renal failure
E)  mixed metabolic and respiratory acidosis



Answer: D

Tromethamine (THAM) is an alternative to NaHCO3 for use in acidosis. It buffers hydrogen ions by virtue of its amine (NH2) moiety

Bicarbonate generates CO2, 

THAM consumes CO2

 THAM get cleared by urinary route, thus is less effective when renal function is reduced. Also it may cause hyperkalemia and hypoglycemia. It has been used with success in acidosis associated with drug intoxications but in non-intubated patient it should be use with caution as rapid alkalization of the central nervous system may cause respiratory depression. THAM can be an excellent choice in hypercapnia as it clears CO2. It has also been used with success in diabetic ketoacidosis, RTA and gastroenteritis. Another advantage is that THAM does not cause a sodium load.


Reference:

Kallet RH, Jasmer RM, Luce JM, et al. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). Am J Respir Crit Care Med 2000; 161:1149.

Q: Chlordiazepoxide is a commonly used drug in ICUs for prevention and treatment of acute alcohol withdrawal. It has all the properties except?

A) amnestic,
B) anticonvulsant,
C) useful in myasthenia gravis,
D) anxiolytic,
E) skeletal muscle relaxant



Answer: C

Chlordiazepoxide is a drug of choice in ICUs to prevent and treat mild alcohol withdrawal symptoms due to its amnestic, anticonvulsant, anxiolytic and hypnotic effect. But as it has some skeletal muscle relaxant properties, it is not advised to be used in myasthenia gravis. 

Objective of above question is to highlight the muscle relaxant properties along with other known properties of  "Benzos" particularly chlordiazepoxide.

Q: All of the following can be parts of Ethylene Glycol toxicity except?

A) Intubation
B) Gastric lavage
C) Ethanol
D) Hemodialysis 
E) Fomepizole 


Answer: E

"Parent Alcohols" i.e., methanol and ethylene glycol get rapidly and fully absorbed after ingestion therefore mechanical maneuvers like activated charcoal, gastric lavage, or syrup of ipecac have no benefit in these toxic alcohol ingestions.

Ocular manifestations - an often ignored part in Methanol toxicity

"This 49-year-old male was sent to a municipal hospital because of sudden loss of consciousness for 1 day. At the emergency room, he was unresponsive with shallow respiration. He was intubated immediately and put on mechanical ventilation. Blood gas and biochemical analyses revealed severe metabolic acidosis (pH 6.8, HCO3 7 mEq/l), elevated liver enzymes and ammonia. Brain computed tomography images were unremarkable at that time. Initially, he was treated for metabolic acidosis. Under the impression of methanol intoxication, he underwent emergent haemodialysis. On the fourth day following exposure, blood methanol level was reported to be extremely high (811 mg/dl). The patient was transferred to our hospital for further management.......

He had had headache, nausea, vomiting, general weakness, visual disturbance, and shortness of breath 1 day before his admission. All the above symptoms occurred several hours after drinking an unknown amount of home-made herbal wine, which he obtained from a friend. He was successfully weaned from the respirator at our hospital. However, impaired consciousness, total blindness, and poor movement of his extremities were noted. An electroencephalogram showed diffuse cerebral dysfunction, compatible with the diagnosis of metabolic encephalopathy. The initial fundoscopic examination in both eyes showed moderately swollen, hyperaemic optic disc and dilated, unresponsive pupillary reflex. Visual-evoked potentials revealed marked suppression without identified waveform. Brain MRI performed on day 15 demonstrated multifocal necrosis in the bilateral putamen and frontal and occipital subcortical white matter regions, and marked perifocal vasogenic brain oedema. Intravenous corticosteroids were administered, initially with 300 mg hydrocortisone, and then 100 mg every 6 h. Intravenous osmotic diuretics were also used with 10% 300 ml glycerol every 8 h. Over the following 3–4 days, his consciousness gradually recovered, he became alert, and his motor function steadily improved. However, total blindness in both eyes persisted."


Read full report and discussion here:  C-S Yang, W-J Tsai and J-F Lirng - Ocular manifestations and MRI findings in a case of methanol poisoning - Eye (2005) 19, 806–809

Link: http://www.nature.com/eye/journal/v19/n7/full/6701641a.html

Q: What is the clinical significance of calculating Maddrey discriminant function (DF) in acute alcoholic hepatitis?



Answer:  Patients with a score of  DF value more than or equal to 32 may have high  mortality and may need institution of glucocorticoids, whereas those with lower scores may get treated only with enteral nutrition!!

Formula to calculate 

DF = (4.6 x [prothrombin time (sec) - control prothrombin time (sec)]) + (serum bilirubin)


For bilirubin in système international (SI) units (micromol/L): 
DF = (4.6 x [prothrombin time (sec) - control prothrombin time (sec)]) + (serum bilirubin/17.1)

Q: 47 year old male with CKD 3 is admitted to ICU with severe sepsis. Patient post-24 hours admission labs are relatively stable with creatinine rising from 1.2 to 1.4. Patient is on 'minimal dose' of norepinephrine. Patient is making about 15-30 cc/hr of urine. Patient's K is 5.2 mmol/L. You received call from lab that patient's Phosphate is 7 mmol/L. What would be your 'line of discussion' with nephrology service?



Answer: Possible initiation of CRRT 

Severe hyperphosphatemia is a sign that patient has developed acute on chronic renal failure despite 'reasonable' creatinine and potassium, and it would be appropriate to initiate renal replacement therapy. This is probably a sign that GFR has fallen below 20 to 25 mL/min. This is due to diminished phosphate excretion.

Q: Why it is important to administer calcium in symptomatic hyperkalemia while treating it with other modalities like insulin, glucose, bicarb., albuterol or cation exchange resin?


Answer: All other modalities take its "own sweet time" to exert effect, like even insulin and glucose  'combo' will take 30 to 60 minutes to act. If patient start showing signs of EKG changes like flattening of P waves or widening of QRS, calcium should be administered to have cardiac protection. Also, be aware of the danger of using calcium along with bicarbonate.  Administering bicarbonate after calcium, may bind calcium and may render it ineffective. This is why we don't prepare "bicarb drip" in LR (Lactated Ringer’s). Preferably, if required sodium bicarbonate should be given before calcium. 

Q: Why intravenous potassium replacement should be given in non-dextrose solution?


Answer:  Non-dextrose solution like saline should be used for potassium replacement therapy because dextrose tends to stimulate insulin release, and insulin is known to drive extracellular potassium into the cells, exacerbating hypokalemia. 

 Reference: 

KUNIN AS, SURAWICZ B, SIMS EA. Decrease in serum potassium concentrations and appearance of cardiac arrhythmias during infusion of potassium with glucose in potassium-depleted patients. N Engl J Med 1962; 266:228.

Q:  ACE inhibitors have documentation to cause hallucinations via central effect, particularly in elderly patients. Which drug may reverse this effect?



Answer:  Naloxone

Aging process is the biggest risk factor for ACE inhibitor–induced visual hallucinations.  Also, This may be a diagnosis of exclusion or may require challenge with drug again to prove the diagnosis! ACE inhibitors that cross the blood brain barrier include captopril, fosinopril, lisinopril, perindopril, ramipril, and trandolapril. Benazepril, enalapril, moexipril, and quinapril do not cross the blood-brain barrier. Ironically, captopril has been researched for slowing of Alzheimer's disease but also said that the development of visual hallucinations in elderly patients may suggest underlying Alzheimer's disease!

There are case reports of hallucinations from angiotensin receptor blocker(ARBs) too. 



References:

1. Gillman M, Sandyk R. Reversal of captopril-induced psychosis with naloxone. Am J Psychiatry. 1985;142:270.

2. Sink K, Leng X, Williamson J, et al. Angiotensin-converting enzyme inhibitors and cognitive decline in older adults with hypertension: results from the Cardiovascular Health Study. Arch Intern Med. 2009;169:1195–1202. 

3. Gorelick P, Nyenhuis D, On behalf of the American Society of Hypertension Writing Group. ASH Position Paper: blood pressure and treatment of persons with hypertension as it relates to cognitive outcomes including executive function. J Am Soc Hypertens. 2012;6:309–315. 

Q: In recent years, use of prepared fibrinogen concentrate ((RiaSTAP) has been on rise in ICU for active bleeding where hypofibrinogenemia is suspected. Though expensive, it is quickly available and have instant effect in comparison to availability and infusion of cryoprecipitate. What is the formula to calculate its dose?




Answer:

Dose (mg) = [Target fibrinogen level (mg/dL) – measured fibrinogen level] ÷ 1.7 x body weight (kg) 

If fibrinogen level is not known, One vial should be administered, which is usually a dose of 70 mg/kg for an average adult.




Reference:

Franchini M, Lippi G. Fibrinogen replacement therapy: a critical review of the literature. Blood Transfus 2012; 10:23.

Q: 58 year old male with ESRD (End Stage Renal Disease) is status post cardiac bypass (CABG) surgery. Patient continue to have generalized "oozing". All coagulation profiles and blood counts including platelet count are normal. You decided to try DDAVP to counter effect of impaired platelet function . You repeated dose twice and it helped partially. Your next step?

A) Repeat DDAVP to get full effect 
B) Transfuse FFP
C) Transfuse pRBC if hemodynamic instability
D) Try low dose Factor 7
E) Perform Hemodialysis



Answer: C

Objective of this question is to emphasis that Desmopressin (DDAVP) though counter impaired platelet function resulting from uremia and common in ESRD patients, but should not be repeated more than twice for two reasons. Firstly, tachyphylaxis quickly develops after 2 doses of DDAVP. Secondly, further DDAVP administration may cause symptomatic hyponatremia.

Choice B is wrong as all coagulation profile is normal so FFP is not required.

Choice is acceptable as a supportive treatment.

Choice D should be used with very very high caution only in life-threatening (life and death) situations as it may thrombose the bypass grafts!

Choice E has no role in immediate post-op CABG patients and actually may be harmful.

Practically, in above situation continuous close observation or prophylactic transfusion of platelet may be carried out.

Q: 33 year old morbidly obese female presented to ER with shortness of breath. CT scan confirmed pulmonary embolism (PE). Echo confirmed severe right heart strain with clinical hemodynamic instability. Patient has been started on 2 hours regimen of thrombolytic (tPA 100 mg) intravenously, and transferred to ICU. What would be your approach to initiate heparin therapy?


Answer: 3 "rules of thumb" to follow while initiating Heparin post thrombolytic therapy in PE are 

1. Loading dose should be avoided

2. aPTT should be measured at the end of the infusion of the thrombolytic therapy. 

3. Heparin should be started with weight based calculation of 18 units/kg/hour only when the aPTT is less than twice its upper limit of normal.

Q: All of the following can be used in monitoring of Diabetic Ketoacidosis (DKA) except? 

A) hourly glucose measurement 
B) periodic venous pH
C) direct measurement of beta-hydroxybutyrate 
D) serum anion gap
E)  nitroprusside testing



Answer:  E

DKA requires very close monitoring of metabolic status which includes every hour glucose measurement (correction neither too slow nor too fast!) as well as closing of anion gap. Arterial ABGs are not required as periodic venous ABGs should be enough to guide resolution of acidosis. Also, periodic direct measurement of beta-hydroxybutyrate guides resolution of DKA. Nitroprusside testing has been used in monitoring of DKA but its not a reliable method as it reacts with acetoacetate and acetone. Acetone is biochemically neutral and does not contribute to the ketoacidosis. 



Reference:

Savage MW, Dhatariya KK, Kilvert A, et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med 2011; 28:508.

Q: All of the following may cause false negative positron emission tomography (PET) except?

A) tumor with low metabolic activity,
B) a small tumor,
C) hyperglycemia.
D) SIRS (Systemic Inflammatory Response System)
E) mucinous bronchioloalveolar cell carcinomas



Answer: D

PET scan should be read with caution as there may be very variables causing false positive and false negative results.

False positive results may occur due to active sepsis/SIRS, inflammatory lesions, or in rare case metabolically active brown fat or thymic tissue. In contrast, false negative tests may occur due to a tumor with low metabolic activity, a small size tumor, or hyperglycemia.


References: 

1. Jung Min Chang, MD, Hyun Ju Lee, MD, Jin Mo Goo, MD, Ho-Young Lee, MD, Jong Jin Lee, MD, -  False Positive and False Negative FDG-PET Scans in Various Thoracic Diseases -  Korean J Radiol. 2006 Jan-Mar; 7(1): 57–69. Published online 2006 Mar 31 

2. Cronin CG, Prakash P, Daniels GH, et al. Brown fat at PET/CT: correlation with patient characteristics. Radiology 2012; 263:836. 

3. Ferdinand B, Gupta P, Kramer EL. Spectrum of thymic uptake at 18F-FDG PET. Radiographics 2004; 24:1611.

A note on Diaphragmatic dysfunction after Cardiac surgery

Diaphragmatic dysfunction commonly occurs postoperatively in patients post cardiac surgery. Phrenic nerve injury may occurs from cold cardioplegia or mechanical stretching during open-heart surgery. It has also been attributed to pleurotomy in order to harvest internal mammary artery (IMA) grafts. IMA dissection may reduce blood supply to ipsilateral intercostal muscles and may cause mechanical injury to the phrenic nerve. Previously, phrenic nerve injury was mostly blamed from cold-induced injury, though now warm cardioplegia is a regular practice. Most patients with post–cardiac surgery diaphragmatic dysfunction improve with conservative measures such as chest physiotherapy. Also, patients develop compensatory mechanisms. The definitive surgical option is plication of diaphragm. Off-pump CABGs said to reduce the incidences.


References:

Yatin Mehta, Mayank Vats, Ajmer Singh, and Naresh Trehan - Incidence and management of diaphragmatic palsy in patients after cardiac surgery - Indian J Crit Care Med. 2008 Jul-Sep; 12(3): 91–95. 

Vanishing Lung Syndrome

Q; What is Vanishing Lung Syndrome?

Answer: Vanishing Lung Syndrome or Shrinking Lung Syndrome is a complication of systemic lupus erythematosus (SLE). Most prominent complain is episodic pleuritic chest pains. Interestingly, and as name implied, there is no evidence of interstitial fibrosis on radiological workup. Various explanations have been sought but so far no concrete mechanism has been established. Most accepted theory is the myopathy causing diaphragmatic weakness, resulting in elevation of the diaphragms, impaired deep inspiration followed by parenchymal reorganization resulting in decrease lung compliance. PFT usually shows a restrictive ventilatory defect. It is a dignosis of exclusion. Treatments described include steroids, theophylline and immunosuppressive therapy.


References:

1. Karim MY, Miranda LC, Tench CM, et al. Presentation and prognosis of the shrinking lung syndrome in systemic lupus erythematosus. Semin Arthritis Rheum 2002; 31:289. 

2. Warrington KJ, Moder KG, Brutinel WM. The shrinking lungs syndrome in systemic lupus erythematosus. Mayo Clin Proc 2000; 75:467. 

Q: 54 year old male with severe COPD is admitted to ICU with A.fib. with RVR. You decided to avoid B-Blocker in view of his COPD. Patient also has CKD-4. You want to avoid Digoxin. You tried intravenous Cardizem bolus with continuous infusion - but patient remained in Heart rate around 160-180. Finally, you decided to 'bite the bullet' and start Amiodarone infusion after few IV boluses - and patient responded well. 3 days post admission, as patient is getting ready for transfer out of ICU, developed acute episode of dyspnea, cough, and bout of hemoptysis. CXR showed diffuse ground glass opacities. Patient required intubation and bronchoscopy. BAL confirmed 'Diffuse Alveolar Hemorrhage' (DAH) by Hemosiderin-laden macrophages. You suspect Amiodarone induced DAH. What would be the next step after stopping Amiodarone?



Answer: IV Steroids

Diffuse alveolar hemorrhage (DAH) is a rare but a life-threatening complication of amiodarone. It usually occur abruptly and may take clinicians with surprise. The most vital and difficult aspect is diagnosis. Discontinuation of Amiodarone is the most important step, followed by relatively high dose systemic steroids up to 500 mg every 6 hours for 5 days! which is gradual tapered, but may require low dose maintenance for few weeks depending on clinical scenario.



References:

1. Iskandar SB, Abi-Saleh B, Keith RL, et al. Amiodarone-induced alveolar hemorrhage. South Med J 2006; 99:383.

2. Tanawuttiwat T, Harindhanavudhi T, Hanif S, Sahloul MZ. Amiodarone-induced alveolar haemorrhage: a rare complication of a common medication. Heart Lung Circ 2010; 19:435.

Q: You were called to evaluate a patient. On arrival at bedside you find a fairly obese patient in impending respiratory failure. As you start preparing and to perform intubation, you asked Respiratory Therapist to apply "cricoid pressure". As soon as he is in process of applying cricoid pressure, patient had a huge forceful vomiting. You quickly  get the bed's head down, turned patient's head to the side, and suctioned the mouth.  Your next step? (Next best)

A) Continue to apply cricoid pressure
B) Let go of cricoid pressure
C) Abandon the whole procedure
D) Start rapid mask bag ventilation
E) Insert Orogastric tube, clean the stomach and then proceed with intubation



Answer: B

In case should patient shows active forceful vomiting, further cricoid pressure should be avoided as it may cause esophageal rupture. 

Choice 'C' is wrong as patient may 'code' and die. Instead preferably patient should be quickly  intubated taking all safe precautions with inflation of the endotracheal tube cuff as quickly as possible.

Choice 'D' is not a good choice as further bag mask ventilation may further inflate the stomach. If oxygenation is sufficient to pass the intubation phase, it should be avoided.

Choice 'E' may be applied if you have luxury of time, which is unfortunately not the case in such situation.

Q: 52 year old female is in ICU after Carotid Endarterectomy (CEA). Nurse called you to bedside and reports that patient tongue is deviated. Your diagnosis?


 Answer: Hypoglossal nerve injury

The hypoglossal nerve supplies motor function to the tongue. Injury to  hypoglossal is one of the more common cranial nerve injury associated with CEA. It is manifested as tongue deviation towards the side of surgery (CEA). Risk factors include inadvertent retraction or transection. 

Q: What length of dialysis catheter is appropriate for insertion via femoral vein?


Answer: 20-24 cm

Insertion of hemodialysis catheters less than 15-17 cm may cause higher recirculation rates as tip of the catheter is probably positioned in the iliac vein. Similarly, contrary to popular belief very long catheter like more than 30-32 cm is not appropriate either as flow rate decreases with increasing length of catheter. A dialysis catheter of more than 20-22 cm should be adequate for most adults to position the tip of the catheter in the inferior vena cava, which minimizes recirculation.


Reference:

Little MA, Conlon PJ, Walshe JJ. Access recirculation in temporary hemodialysis catheters as measured by the saline dilution technique. Am J Kidney Dis 2000; 36:1135.

Q: 48 year old male with ESRD is in ICU with recent Pulmonary Embolism. Patient is on IV heparin drip. Patient's central line is sluggish! Flushing with saline didn't work. You asked nurse to flush one time with Heparin. Which one mistake should be avoided?



Answer: Flushing via running IV Heparin drip

 Heparin solution in IV drip should not be used to flush catheter locks, ports or intervenous lines, because the solutions intended for intravenous heparin therapy are significantly more concentrated than the solutions used for catheter flushes.

Note:  For the sake of question, flushing of CVC with heparin is described but is should not be a standard practice.

Q: All of the following are or can be parts of Acute Chest Syndrome (ACS) management except?

A) empiric antibiotic therapy
B) IVF
C) DVT prophylaxis
D) Exchange transfusion
E) Hemodialysis



Answer: E

Acute chest syndrome (ACS) is a life threatening complication for patients with sickle cell disease. It is defined as a new infiltrate on CXR accompanied by respiratory symptoms. Objective of above question is to highlight few important aspects of ACS which may get ignored under narrow focus of diagnosis.

As well known, IV fluid is mainstay of treatment. But, many times it is hard to distinguish or rule out community acquired pneumonia which may co-exist with ACS. Prophylactic antibiotics is recommended. Chances of DVT is very high and prophylaxis is as important as ruling out PE or existing DVT. Severe cases may require management with exchange transfusion and should kept available as backup. Hemodialysis has no role in ACS.

A Doctor at His Daughter’s Hospital Bed

".............I know about stuff like septic shock because for more than 20 years I was a transplant surgeon, and some of our patients got incredibly sick after surgery. So when I’m sitting in an I.C.U. in Omaha terrified that Natalie, my 17-year-old daughter, might die, I know what I’m talking about. I tell the nurse that Natalie needs to get another slug of intravenous fluids, and fast. 

 The nurse says she’ll call the doctor. Fifteen minutes later I find her in the lounge at a computer, and over her shoulder I see a screen full of makeup products. When I ask if we can get that fluid going, I startle her. She says she called the resident and told him the vital signs, but that he thought things were stable.

 “He said to hold off for now,” she says. 

 “Get me two bags of saline. Now,” I tell her. 

 She says, “I’m calling my supervisor,” and she runs out of the lounge.

......................................."

Read beautiful article: here

(link: http://www.nytimes.com/2015/09/06/opinion/sunday/a-doctor-at-his-daughters-hospital-bed.html?_r=1 )

Q: What are the four major components of  Critical Illness Polyneuropathy (CIP)?


Answer:  Critical Illness Polyneuropathy (CIP) is a distinct entity from Critical Illness Myopathy (CIM) - though both may usually exists together. Critical Illness Polyneuropathy (CIP) has four distinct properties which distinguish it from CIM.

• limb muscle weakness which proceeds to atrophy, 
• decrease  or absent deep tendon reflexes, 
• loss of distal peripheral sensation, and 
• relative preservation of cranial nerve function

Reference: 

 Latronico N, Shehu I, Seghelini E. Neuromuscular sequelae of critical illness. Curr Opin Crit Care 2005; 11:381.

Q: What is Transcatheter Potts shunt (TPS)?


Answer: It is probably more of academic interest or at least a weapon used in refractory and very advanced pulmonary hypertension. Data is very scarce and procedure itself can be of very  high risk. It is surgically placed  right to left shunt between the left pulmonary artery and the descending aorta. It can also be attempted at high tertiary care center by interventional radiology under  fluoroscopic guidance. Procedure itself involves retrograde needle perforation of the aorta, with subsequent placement of a stent between the aorta and left pulmonary artery.



Reference:

Esch JJ, Shah PB, Cockrill BA, et al. Transcatheter Potts shunt creation in patients with severe pulmonary arterial hypertension: initial clinical experience. J Heart Lung Transplant 2013; 32:381.

Q: What is the acceptable ischemic time between procurement and re-implantation of donor lung to recipient body? (select one)

A) Less than 2 hours
B) Less than 4 hours
C) Less than 6 hours
D) Less than 8 hours
E) There is no time limit (as far as organ is good)




Answer: D

Recommended optimal acceptable ischemic time between procurement and re-implantation of donor lung to recipient body is up to 8 hours, though institutions may accept  ischemic times of up to 12 hours. Studies have shown that the risks of primary graft dysfunction and 30 day mortality increase with more than 8 hours of ischemia.




Reference:

1.  de Perrot M, Liu M, Waddell TK, Keshavjee S. Ischemia-reperfusion-induced lung injury. Am J Respir Crit Care Med 2003; 167:490. 

2. Thabut G, Mal H, Cerrina J, et al. Graft ischemic time and outcome of lung transplantation: a multicenter analysis. Am J Respir Crit Care Med 2005; 171:786.

Q: Ultrasound technician called you to bedside to show images while doing sonography of Right Upper Quadrant (RUQ). On screen you see "pulsatile flow within the portal vein". What is your concern?


Answer: Tricuspid regurgitation and Right sided heart failure

In patients with portal hypertension due to right-sided heart failure with tricuspid regurgitation, flow within the portal vein usually appears pulsatile, unless patient is  cirrhotic which may make the portal wave-form flattened. This finding should be co-related with other clinical findings.

Picture Diagnosis

Q: 32 year old male is transferred from outside hospital for transplant evaluation for acute liver failure. Medical student on exam wrote "unusual ring in the eyes". Diagnosis?

Answer: Kayser-Fleischer rings

Kayser-Fleischer ring is a hallmark of Wilson disease. The dense brown copper deposits encircle the iris. It requires slit-lamp examination. Though very highly suggestive of Wilson disease, Kayser-Fleischer rings are not specific for Wilson disease as they have been reported in cholestatic diseases, like primary biliary cirrhosis.

Clinical significance: Kayser-Fleischer rings gradually disappear with medical treatment for Wilson disease or if liver transplantation carried out. Their reappearance suggests either noncompliance or failed treatment.

Q: ICU resident had needle stick while performing a procedure in an HIV positive patient. Resident decided not to take post-exposure prophylaxis. What are her or his chances to contract HIV?
 

Answer: The average risk of seroconversion after a needle stick injury is about 3 per 1000 with no prophylaxis.  To be precise, it is between 0.23 to 0.36 percent.

 References: 

Tokars JI, Marcus R, Culver DH, et al. Surveillance of HIV infection and zidovudine use among health care workers after occupational exposure to HIV-infected blood. The CDC Cooperative Needlestick Surveillance Group. Ann Intern Med 1993; 118:913.

Baggaley RF, Boily MC, White RG, Alary M. Risk of HIV-1 transmission for parenteral exposure and blood transfusion: a systematic review and meta-analysis. AIDS 2006; 20:805.

Q: 52 year old female from Cambodia, who just migrated to United States is admitted to ICU with exacerbation of Asthma. It was noticed that patient's symptoms get worse, every time she receives corticosteroids. Knowing her country of origin and above observation, which infectious disease should be considered? (choose one)

A) Strogyloidiasis 

B) Malaria

C) Ebola

D) HIV

E) Yellow Fever

 

Answer: A

Strongyloidiasis is common in many parts of world where sanitation can be an issue. We choose Cambodia in above question as disease is very prevalent in that area and could be a hint to answer. On interesting note, patients with chronic Strongyloidiasis may also develop asthma that paradoxically may worsens with corticosteroid use.

 References: 

 Sen P, Gil C, Estrellas B, Middleton JR. Corticosteroid-induced asthma: a manifestation of limited hyperinfection syndrome due to Strongyloides stercoralis. South Med J 1995; 88:923. 

Wehner JH, Kirsch CM, Kagawa FT, et al. The prevalence and response to therapy of Strongyloides stercoralis in patients with asthma from endemic areas. Chest 1994; 106:762.