To the Editor:
We agree that low vascular resistance may be contributory to refractory hypotension in severe organophosphate poisoning as clinically we note these patients to be generally vasodilated (similar to septic shock as opposed to haemorrhagic shock). They also respond extremely poorly to inotropes. We find intermittent intravenous normal saline boluses (10 mL/kg) to be helpful in refractory hypotension to maintain an acceptable level of blood pressure (e.g., 90–100 mmHg systolic). The limitation of this practice is the rising inhaled oxygen requirements to maintain oxygenation even when the patient is mechanically ventilated with a PEEP. Thus, our hypothesis is that global myocardial impairment is the cause of death in this subcategory of patients. On the other hand, other groups of less severe organophosphate-poisoned patients on some occasions display higher levels of blood pressure (160–180 mmHg systolic) initially, suggesting that organophosphates may also be active at ganglion level, triggering a predominant autonomic vasoconstrictor response.
C. D. A. Goonasekera