UCONN Emergency Medicine Interest Group

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Pearl/Pitfall: Cyanide

In PEARL/PITFALL on October 2, 2011 at 8:00 AM

Based on discussion/lecture from Dr. O`Toole, Emergency Physician and Medical Toxicologist at Hartford Hospital:

In the case of a patient presenting with new onset seizures, tachycardia and hypotension with elevated lactate and acidosis, always consider cyanide poisoning as a potential etiology.

In brief, a lethal dose to adults of potassium cyanide is ~200 mg. Cyanide inhibits many enzymes, perhaps most importantly cytochrome oxidase at cytochrome a3 in the electron transport chain, inducing cellular asphyxia by preventing aerobic metabolism. This results in movement towards anaerobic metabolism, ultimately producing lactic acidosis.

Cyanide is also a neurotoxin by several mechanisms, including impairment of metabolism as above, as well as increased release of excitatory neurotransmiters and increasing/activation of NMDA receptor activity, producing a number of CNS s/s including seizures.

It should be noted that cyanide does cause variable cardiovascular effects depending on when in the course of the exposure the patient is observed. Initially, cyanide causes bradycardia and hypertension, followed by hypotension and reflex tachycardia, and finally, bradycardia and hypotension leading to death.

As there is now a very safe antidote, hydroxocobalamin available, which essentially binds cyanide to become cyanocobalamin (ie. vitamin B12), early recognition of this poisoning may be life-saving.


Hoffman, Robert. Goldfrank’s Manual of Toxicologic Emergencies. New York: McGraw-Hill, 2007.

Pearl/Pitfall: Hypoglycemia

In PEARL/PITFALL on July 25, 2011 at 2:15 PM

Based on two discussions I had with Dr. Nowicki and Dr. Price:

Always check a blood glucose level in patients with altered mental status or neurologic deficits. The clinical presentations of hypoglycemia are protean; Dr. Nowicki told me about a case in which a patient presented with an isolated unilateral CN VII palsy in a patient with no prior neurologic history, which completely resolved after the hypoglycemia was corrected. It is both embarassing to the provider as well as potentially dangerous for the patient for delay in diagnosis of this condition. It is very simple and fast for this to be ruled out as a likely cause of the patient’s symptoms, and the stakes are high. However, there are several things that should be considered as pitfalls here.

First, the blood glucose level at which nondiabetic patients and diabetic patients display symptoms may differ considerably. In one study in NEJM (reference provided below), poorly controlled diabetics first developed symptoms at a mean glucose of 78 mg/dL, while nondiabetics developed symptoms at a mean glucose of 53 mg/dL. The implication is that a so-called “normal” glucose level, which may not be flagged as abnormal by the lab (which has no knowledge of the patient’s history) may actually be hypoglycemic in terms of their body’s altered metabolism.

Second, it is important not to undertreat hypoglycemia. The initial treatment, of course, is IV dextrose; adult patients typically require 0.5-1.0 g/kg D50. Since an amp of D50 has 25 g of dextrose, a single amp of D50 will usually not be sufficient to match this requirement (consider that the “standard” patient is 70 kg; this implies that they will need at minimum 35 g, and up to 70 g of dextrose, which implies they will need at least 2 and potentially 3 amps). Once the patient is able, this initial bolus of dextrose should then be followed by a meal; this provides sustained calories over time (if the patient cannot eat, dextrose infusions may be necessary). Otherwise, the patient may rebound back into hypoglycemia!


Boyle PJ, Schwartz NS, Shah SD, et al. Plasma glucose concentrations at the onset of hypoglycemic symptoms in patients with poorly controlled diabetes and in nondiabetics. N Engl J Med. 1988;318:1487-1492.

Pearl/Pitfall: Right-sided MI

In PEARL/PITFALL on July 11, 2011 at 12:40 AM

From didactics with Dr. Regan:

Understanding the presentation of posterior MI on EKG is not that complicated, and need not require any mirrors or special tricks! It can be relatively easily understood simply by recalling the coronary anatomy and lead placement. Remember that anatomically, the right coronary artery takes a path that goes to the posterior portion of the heart, then the inferior portion of the heart. This means that a posterior MI must* have an associated inferior MI; if the inferior leads (II, III, aVF) do not show signs of MI on EKG, then there is no posterior MI. Recall also that the chest leads V1-V6, just like the other leads, measure a vector of electrical activity pointing anteriorly. This implies that the vector goes from posterior to anterior. So, it should be expected that posterior MI should show reciprocal ST-T changes in the anterior chest leads. If they do not, this implies that the MI is a more distal pure inferior MI (which has a significantly better prognosis). If the chest leads do show reciprocal changes, right sided chest leads should be placed to obtain a right-sided EKG to determine if the obstruction is more proximal, resulting in a complete right sided MI, or more distal, resulting in a posteroinferior MI. In other words, the right-sided EKG should demonstrate ST-T changes consistent with MI if there is a complete right-sided MI (eg. ST elevation).  If they do not, the diagnosis is posteroinferior MI (again, remember that a posterior MI requires there to be an accompanying inferior MI).

* Note: as with everything in medicine, there are exceptions to the rule, and so it is possible for variants in coronary anatomy to make this idea not always hold. However, Dr. Regan informs me that he has only seen this occur several times in his nearly 20 years of practicing EM.

** Note: please remember that not all MI present with EKG changes. In fact, the sensitivity of the first EKG in acute MI is only 13-69%, and considering the evolution of all EKG abnormalities (ST, T, Q waves, LBBB) over time, the sensitivity is  87%.


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