Fatality due to paraquat intoxication: confirmation by postmortem tissue analysis.

A brief case report is presented describing a patient who unknowingly ingested a fatal amount of paraquat, presumably mixed in some illicit moonshine alcohol. Despite an initial clinical presentation typical of paraquat intoxication, the herbicide was absent upon analysis of multiple urine and blood specimens, and the diagnosis was confirmed only postmortem after determination of high paraquat tissue concentrations in all the major organs. Autopsy results are presented along with a discussion of the histopathologic changes observed in the lungs, liver, and kidneys. Because the combination of toxicologic sequelae attributable to acute paraquat poisoning is fairly unique to this agent, the diagnosis must be suspected highly early in the clinical course of such cases and appropriate therapy initiated, despite the inability to isolate paraquat on preliminary laboratory screening.

Massive pulmonary embolism: treatment with full heparinization and topical low-dose streptokinase.

Three patients with massive pulmonary embolism were treated with low-dose streptokinase (delivered topically via the pulmonary artery) and simultaneous full-dose heparin. In two patients with acute emboli, rapid but incomplete lysis was observed over 15-30 hours. In one patient with recurrent embolization over three weeks, the major embolus shrank considerably. Pulmonary artery pressure and angiographic findings improved significantly in both patients with acute emboli. In the patient with old embolus, pulmonary artery pressure did not improve despite considerable improvement in angiographic findings and arterial PO2. These data suggest that early topical administration of low-dose streptokinase plus full-dose heparin may be the treatment of choice for patients with massive pulmonary embolism, particularly those with compromised cardiopulmonary status.

Cardiac output measurement using N2O uptake: a method to subtract cardiogenic oscillations.

Plethysmographic (box) methods using N2O uptake to measure pulmonary capillary blood flow, right ventricular stroke volume, and pulmonary arterial flow pulse conduction time have been complicated by the presence of so-called "cardiogenic oscillations" in the box flow records on air and N2O breathing. The exact cause of these oscillations is unknown but believed to be secondary to instantaneous changes in net blood flow into and out of the thorax during the cardiac cycle. We examined these oscillations and pulmonary capillary blood flow in normal human subjects in a flow plethysmograph using a pressure compensation circuit to extend the frequency response. The cardiogenic oscillations in flow recorded at the mouth (with glottis open) are much greater in amplitude and 90 degrees out of phase from those recorded from the plethysmograph. We derived a theoretical analysis of this and designed an analogue electrical circuit to enable us to eliminate these oscillations by electrical subtraction from the box flow record generated by N2O uptake in the pulmonary capillary bed. Measurements of pulmonary capillary blood flow and ventricular stroke volume using our method correlate with measurements made with acetylene-rebreathing blood flow measurements performed sequentially at the same sitting.