Q: Your Diagnosis?

Answer: Bilateral Pneumothoraces Bilateral pneumothoraces can be very deceiving as there is no deviation of trachea, and percussion and breath sounds seems equal on both sides. Clinically these patients are usually haemodynamically compromised and on CXR you may see the characteristic 'disappearing heart' with bilateral tension pneumothoraces.

Q: 78 year old DNR patient is in Atrial fibrillation with RVR (Rapid Ventricular Rate) causing borderline hypotension. Patient did not respond to Digoxin and Amiodarone. Patient is on chronic coumadin therapy with INR of 2.8. Echo ruled out any thrombus. Patient refuses any sort of cardioversion but oked any drug treatment. Cardiologist on consult informed you that he will be using ibutalide this afternoon to see if that works. To minimize the associated ventricular arrhythmia what could be your preventive strategy?

Answer: Administer Magnesium before ibutalide use

The risk of developing torsade de pointes with ibutilide is about 4% but it can reduced with intravenous infusion of high-dose magnesium sulfate and having potassium level around 4.5 range.

Reference: Patsilinakos S, Christou A, Kafkas N, et al. Effect of high doses of magnesium on converting ibutilide to a safe and more effective agent. Am J Cardiol 2010; 106: 673–6

Q: Lorazepam(Ativan) and Diazepam(Valium) both have been used as first line treatment of Status Epilepticus. What advantage Lorazepam have over Diazepam?

Answer: Lorazepam and diazepam both have been used as a first line drugs in the management of Status Epilepticus. Though diazepam acts slightly faster than lorazepam its effective duration of action may be only 5-10 min - and may require repeated doses or quick followup with administration of phenytoin (or fosphenytoin). On the other hand once effective dose(s) of lorazepam is given, the effective duration of action of lorazepam is 8-10 hours, and so is more recommended for initial treatment of status epilepticus.

Q: Is Amniotic fluid embolism (AFE) a anaphylactoid reaction?

Answer: Yes

Amniotic fluid embolism (AFE) is a misnomer as clinical picture is more or less like acute collapse from pulmonary embolism but in fact it is an allergic type reaction. Amniotic fluid embolism (AFE) is a rare obstetric emergency in which amniotic fluid, fetal cells, hair, or other debris enters the mother's blood stream and triggers an allergic reaction - which results in cardiorespiratory collapse. Another hallmark of the disease is severe coagulopathy.

Diagnosis: In a patient who is suspected of having AFE, a sample should be obtained by aspiration of the distal port of a pulmonary artery catheter. If sample contains fetal squamous cells it is highly suggestive of AFE syndrome - but does not completely rule in or rule out other causes too.

Treatment: Immediate delivery of baby. Support coagulopathy and hemodynamics as per standard.

Q: What is Hamman's syndrome?

Answer: Hamman's syndrome is a clinical condition and frequently requires ICU admission for observation. It is a spontaneous pneumomediastinum with subcutaneous emphysema. It occurs mostly in young females peripartum or postpartum. It is named after the physician (Louis Hamman 1877–1946), who described it.

Hamman's syndrome usually occurs in the second stage of labor but can be delayed to the postpartum phase. An association with prolonged labor has been proposed (increase intrathoracic pressure) with rupture of alveoli.

Treatment is supportive and course is usually benign.

Dudley DK, Patten DE. Intrapartum pneumomediastinum associated with subcutaneous emphysema. CMAJ 1988;139:641-2

Q: Patient developed lower GI bleed in ICU. GI service after scope diagnosed anal fissure and prescribed Cardizem. Is this a mistake?

Answer: No

Cardizem (Diltiazem) is frequently used in the treatment of anal fissures - either via oral route or can be applied topically!

It has a very good short term success rates and provide temporary relief till surgical intervention is done, if required. Local application of it relaxes the sphincter muscle, and allows the healing to proceed.

Q: Enteral feeding is always preferred over parenteral feeding (TPN) in ICUs - as enteral feeding also prevents a very dangerous ICU entity - acalculous cholycystitis. What is the mechanism?

Answer: There are 2 synergistic components to this pathophysiology.

1. Bile Stasis: Absence of oral/enteral feeding results in a decrease or absence of cholecystokinin-induced gallbladder contraction.

2. Increase Bile Viscosity: Increased bile viscosity due to fever and dehydration causes acalculous cholycystitis.