No abstract

Methanol ingestion is an uncommon form of poisoning that can cause severe metabolic disturbances, blindness, permanent neurologic dysfunction and death. While methanol itself may be harmless, it is converted in vivo to the highly toxic formic acid. The diagnosis is sometimes elusive and requires a high index of suspicion. Because antidotal treatment is available it is important to recognize methanol poisoning promptly. The presence of metabolic acidosis associated with an increased anion gap and increased osmol gap are important laboratory findings. Specific therapeutic measures include correction of the metabolic acidosis with sodium bicarbonate and administration of enteral or parenteral ethanol to competitively inhibit the metabolic breakdown of methanol to formic acid. Hemodialysis accelerates the elimination of both methanol and formic acid and also assists in correction of the metabolic acidosis. Experimental data suggests that administration of folic acid may be of benefit by hastening the metabolism of formic acid to carbon dioxide. Prompt institution of specific therapy can probably decrease the morbidity and mortality associated with this form of poisoning.

In early severe sepsis and septic shock, within the first 3 hrs of hospital presentation, distinct biomarker patterns emerge in response to hemodynamic optimization strategies. A significant association exists between temporal biomarker patterns in the first 72 hrs, severity of global tissue hypoxia, organ dysfunction, and mortality. These findings identify global tissue hypoxia as an important contributor to the early inflammatory response and support the role of hemodynamic optimization in supplementing other established therapies during this diagnostic and therapeutic "window of opportunity."