Q; 24 year old female 2 weeks post partum developed severe headache of one week followed by seizure. While you start workup what would be your presumptive diagnosis and line of mangement?


Answer: Postpartum cerebral vasospasm would be high on list

Cerebral angiography or Magnetic resonance imaging/angiography should be perform as soon as possible to rule out vasospasm. IV fluid should be started with atleast 125 cc/hour and goal to keep BP high. Treatment consist of hyperosmolar, hypervolemic therapy and nimodipine.

Neuro-Critical Care

Q; Beside it's use in prevention of vasospasm in Subarachnoid hemorrhage - what could be the other less known uses of Nimodipine?

Answer: Though not as effective but it can be use as an alternative or an adjuvent to magnesium for seizure prophylaxis in women with severe preeclampsia.

Also it has an adjuvent value in the treatment of intractable seizure.

Please note that FDA warned against using Nimodipine capsules as IV.

Nimodipine has been originally designed for the treatment of high blood pressure but is not used for this indication anymore.

Trivia!

Q; Do you know the meaning of word "sepsis" (word origin)?


Answer: Sepsis is derived from a Greek word "sepo" meaning “I rot”. Historically first time described in the poems of Homer.

Reference:

Historical perspective of the word Sepsis - Intensive Care Medicine(2006), Volume 32, Number 12, page 2077

Q; After successful completion of Transjugular Intrahepatic Porto-systemic Shunt (TIPS) for variceal bleeding - hepatic encephalopathy __________ ?

A) tends to get better
B) tends to get worse
C) It has nothing to do with TIPS


Answer is B

Hepatic encephalopathy tends to get worse after successful completion of TIPS as due to shunting, blood flow to the liver is reduced, which might result in increase toxic substances reaching the brain without being metabolized first by the liver. It can be treated medically such as diet, lactulose or by narrowing of the shunt by insertion of a reducing stent.

Back to Basic - MoA ACE inhibitors

Drug interaction

Q: Which 2 commonly used cardiac medicines may interact negatively?

Answer: Aspirin and ACE inhibitors

Effects of ACE inhibitors are attenuated by aspirin.

ACE inhibitors decrease angiotensin II production and inhibit breakdown of bradykinin. Bradykinin stimulates vasodilator prostaglandins via a cyclo-oxygenase–dependent pathway.

Aspirin inhibits cyclo-oxygenase-1 (COX-1), thereby reducing synthesis of vasodilatory prostaglandins.

Above interaction may be of more academic interest. In clinical practice - there are no firm guidelines for use of both drugs simultaneously.

New Brain Death Guidelines!

The American Academy of Neurology has released new guidelines for determining brain death in adults. The recommendations provide step-by-step instructions to help guide clinical decision making.

The guidelines are published in the June 8 issue of Neurology.

Among other the notable thing is that more than 1 exam is not required in the new brain death guidelines. Clinicians usually perform 2 exams. In new guidelines one time brain death exam is sufficient.

Click here to get full update.

On Friday the 13th!

Q: What is the possible explanation behind Lazarus Syndrome?

Answer: Lazarus Syndrome is a generic term use in hospitals when patient shows sign of life after clinically declared dead, like a patient that develops vital signs after cessation of resusitative efforts or organ-donation team arrives to find a live person.

Possible explanation is that a chief factor is the buildup of pressure in the chest as a result of cardiopulmonary resuscitation (CPR). The relaxation of pressure after resuscitation efforts have ended is thought to allow the heart to expand, triggering the heart's electrical impulses and restarting the heartbeat.

The syndome is named after bible story in which Jesus brought back to life a dead person named Lazarus from his tomb. Term became very popular after publication of book "The Lazarus syndrome: Burial alive and other horrors of the undead" (Rodney Davies - 1978).

In recent years, 'Lazarus Syndrome' has also been use for HIV/AIDS patients who feel having new chance of living with new HIV medications.

Q: 24 year old male presented with syncope. Patient has family history of sudden cardiac deaths in family and you strongly suspect Brugada syndrome. Which drug can be use to elicit specific EKG patterns for diagnosis of Brugada syndrome?

Answer: Flecainide

The Brugada syndrome is a genetic disorder characterised by abnormal EKG findings and an increased risk of sudden cardiac death particularly in young men without known underlying cardiac disease.

Brugada syndrome can be detected by observing characteristic patterns on an EKG, which may be present all the time, or in clinical suspicion can be elicited by the administration of Class IC antiarrhythmic drugs (like flecainide) that blocks sodium channels and causing appearance of ECG abnormalities.

Review on Brugada Syndrome at emedicine.com

The End of the Code

"When I was but an EMT lad in an ED I witnessed something I’ve incorporated into my own practice, and I think every doc should do it. When it’s ‘that time’, time to stop the resuscitation, in every instance I say something along the lines of “Okay, we’ve been coding this person for xx minutes, and there’s been (brief summary): does anyone here want to do anything else? If so, tell me now”. This does two things which are important for everyone in the room who isn’t dead: it makes them part of the decision making process, and it empowers them to very easily object should they wish, for whatever reason, to continue. “I’d like to give some (whatever)” is then totally fine, and they’re not having to object in a vague way that they’re not done yet with what can be a terrifically personal struggle to save someone none of us has met, or knows as anyone other than a patient. We give the whatever, and after a while, given the persistence of death, I’ll give my speech as many times as it takes (so far, twice has been all, but I’d be perfectly willing to go on for a long time), because it’s important for everyone involved to acknowledge that they did what they could, and to be comfortable with stopping.

Codes end, very occasionally with a happy outcome, more often than not with a patient under a sheet, but the people who were there need to feel like they had a chance to do all they could.

Death is forever, and so is guilt; I want to make certain the dead don’t take the living with them"

Taken from blog of GruntDoc

Q: Describe the significance of "Herald Bleeding" in Primary aortoenteric fistula (PAEF)?

Answer: One of the known characteristic of PAEF is of a "herald" bleeding followed hours, days, or even weeks later by a catastrophic bleeding. The herald bleeding is the result of a small fistula tamponaded by thrombus formation. If the fistula continues to expand or the occluding thrombus is removed, massive hemorrhage results.

Clinical significance: This is probably the only window of opportunity to salvage the patient before massive bleed takes over. Emergency exploratory laparotomy should be done as soon as the diagnosis is considered clinically. Mortality is 100% without surgical intervention.

Communications between the aorta and the intestine resulting from disease at either site are referred to as primary aortoenteric fistulas. Causes include untreated aortic aneurysm, infectious aortitis, erosion of the intestine by prosthetic vascular grafts, esophageal cancer etc. Refer other texts for more detailed descriptions.

Q: Whats the best measure of titrating Atropine drip in Organophosphate poisoning?

Answer: Control of hypersecretions served as the best monitoring parameter for titration of the drip rate. Organophosphate (OP) toxicity itself is a clinical diagnosis. There is no clinical lab value which can be followed except for above clinical objective finding. Following mnemonic can be used to remember the muscarinic effects of organophosphates.

SLUDGE: salivation, lacrimation, urination, diarrhea, GI upset, emesis

DUMBELS: diaphoresis and diarrhea; urination; miosis; bradycardia, bronchospasm, bronchorrhea; emesis; excess lacrimation; and salivation.

Q: Which vitamin deficiency may cause life threatening lactic acidosis?



Answer: Thiamine (Vitamin B1) deficiency

Thiamine is part of the pyruvate-dehydrogenase (PDH) complex. Its deficiency inhibits pyruvate entry into mitochondria.

Clinical implication: It is important to add Thiamine on patients requring long term parentral nutrition (TPN).


Reference: Click to get references

1. Thiamine deficiency as a cause of life threatening lactic acidosis in total parenteral nutrition - Klin Wochenschr. 1991;69 Suppl 26:193-5.

2. Metabolic acidosis and thiamine deficiency - Mayo clinic Proceedings, March 1999 vol. 74 no. 3 259-263

3. Severe Lactic Acidosis Related to Acute Thiamine Deficiency - Journal of Parenteral and Enteral Nutrition, Vol. 15, No. 1, 105-109 (1991)

Q: Despite being an old player Sucralfate is still very well indicated in stress ulcer prophylaxis. What is the mechanism of action of sucralfate?

Answer: Sucralfate act by multiple mechanisms

1. Sucralfate acting locally that in an acidic environment , reacts with hydrochloric acid in the stomach to form a cross-linking, viscous, paste-like material capable of acting as an acid buffer for as long as 6 to 8 hours after a single dose.

2. It also attaches to proteins on the surface of ulcers, such as albumin and fibrinogen, to form stable insoluble complexes. These complexes serve as protective barriers at the ulcer surface, preventing further damage from acid, pepsin, and bile.

3. It prevents back diffusion of hydrogen ions.

4. It adsorbs both pepsin and bile acids.

5. Sucralfate also stimulates the increase of prostaglandin E₂, epidermal growth factors (EGF), bFGF, and gastric mucus.

Q: How Dexilant (Dexlansoprazole) is different from other PPIs (Proton Pump Inhibitors)?


Answer: Dexilant has a DUAL DELAYED RELEASE mechanism. It contains two different types of granules for two releases of medicine. Dexilant works by releasing one shift of medicine within an hour of taking it to decrease the amount of acid in stomach. Around 4–5 hours later, Dexilant releases a second shift of medicine.

How much advantage does it provide over other PPIs has yet to be determine in independent studies.

Thursday August 5, 2010


Q: What is the difference between available synthetic thyroid hormone replacement and natural thyroid hormone replacement in market?


Answer: Synthetic thyroid hormone contains T4 only and is therefore largely ineffective for patients unable to convert T4 to T3. Also some patients may develop allergy to synthetic thyroid hormone.

Natural thyroid treatments hormones are still available. Armour Thyroid is the most popular brand available and is a natural, porcine-derived thyroid replacement containing both T4 and T3. The ratio of Thyroid T4 to T3 is 4.22:1.

Armour thyroid is available in strengts as grains (1/4, 1/2, 1 grains).

1 grain of Armour is approximately equal to 100 mcg of levothyroxine.

Q: Why Prealbumin is called Prealbumin?


Answer: Prealbumin is called prealbumin because it ran faster than albumins on electrophoresis gels in contrast to general belief that its a precursor of albumin. It should not be confused with albumin.

The right name for Prealbumin is Transthyretin (TTR). TTR is a serum and cerebrospinal fluid carrier of the thyroid hormone thyroxine (T4) and retinol. This is how transthyretin gained its name, transports thyroxine and retinol.

Nutritional status can be assessed by measuring concentrations of prealbumin in the blood. Prealbumin is preferred because of its shorter half-life, although this means that its concentration more closely reflects recent dietary intake rather than overall nutritional status.

Q: In human body for measurement , each 1 g/dL decrease of albumin will raise the serum Calcium by what level?

Answer: Each 1 g/dL decrease of albumin raises the serum calcium (Ca) level by 0.8 mg/dL in human body. Remember the formula for calcium correction from internship days?

Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 (4.0 - serum albumin [g/dL])

Pleural calcification in asbestos exposure

Pleural calcification occurs in about 50% with asbestos-related disease, especially along the diaphragmatic pleura. (White arrow)The overall appearance of the plaque has been likened to a holly leaf. (Black arrows) point to many of the calcified pleural plaques.

Q: 78 year old male presented with severe abdominal pain. Patient is taking huge amount of over the counter NSAIDs and you suspect perforated peptic ulcer. As an initial workup you ordered upright KUB. Looking at portable screen of technician you didn't see any free air. What should be your next step?


Answer: Take a left lateral decubitus film.

Plain x-rays of the abdomen with the patient in the upright position have been used in diagnosing perforated ulcer. However, in 30% to 50% of patients, the x-ray may be negative for free air, particularly in the elderly. A left lateral decubitus film has been shown to be most sensitive in detecting pneumoperitoneum. Placing the patient in the upright or left lateral decubitus position for 10 minutes before taking the x-ray may help detect the condition. Similarly, use of water-soluble contrast medium with an upper gastrointestinal tract series or computed tomography scan may increase the diagnostic yield.