Paraquat poisoning treated by forced diuresis.

Abstract

Bruce, 1968Examination on admission showed epigastric tenderness and guarding. The liver edge was just palpable below the costal margin. There was no evidence of pre-existing cardiac, pulmonary, or renal disease. Shortly after admission gastric lavage was performed and no solid Weedol particles were visible in the aspirate. Forced diuresis was begun.Next day he complained of anterior chest tightness, frontal headache, and photophobia. Chest auscultation revealed generalized bilateral sibilant rhonchi. The abdominal pain disappeared by the eighth day and tenderness by the tenth day. The liver edge remained palpable throughout. He remained free of oral and pharyngeal ulceration. Clinical examination of the chest showed disappearance of rhonchi by the tenth day and there was no evidence of pulmonary hypertension at any time. The temperature rose on only one occasion to 99°F. (37.2°C.). A five-day course of intramuscular penicillin was started on admission and was followed by a five-day course of prednisolone, begun on the fifth day.Investigations.-Daily chest x-ray films and electrocardiograms performed from time of admission showed no abnormality. The haemoglobin and absolute values were found to be normal. The white cell count was 6,650/cu. mm. on admission and 13,500/cu. mm. on the twelfth day. The E.S.R., blood urea, urine urea, serum electrolytes, serum bicarbonate, standard liver function tests, and arterial blood gas values were all persistently normal. Occult blood was not found in the stools. Creatinine clearance just before discharge was 58 ml./min.Forced diuresis was performed by the method of Linton, Luke, Speirs, and Kennedy (1964) and continued for 24 hours. Throughout the forced diuresis two-hourly aliquots of urine were collected and blood samples were obtained at intervals. The concentrations of paraquat in each of these specimens and in one specimen of gastric aspirate were determined by the method of Daniel and Gag. (1966). The lower limit of sensitivity by this method is 10 pg. of paraquat. This quantitative method is efficient but time-consuming. The urine cell counts were performed by the method of McGeachie and Kennedy (1963).

Paraquat Poisoning--Lung Transplantation

“…The youth took the paraquat on an empty stomach and unfortunately did not vomit for at least five hours, thus despite slow absorption a Paraquat Poisoning-Matthew et al BRmSH MEDICAL JOURNAL considerable amount was taken up. Though repeated forced diuresis as suggested by Kerr et al (1968) was undertaken, the toxic effects later became evident in the liver, kidneys, and especially the lungs. The damaged liver and kidneys steadily improved, and at no time was any neurological change evident.…”

“…Detection and quantification of the small amounts likely to be encountered in the urine during the second and following days after ingestion may prove difficult. The procedure using a cation exchange resin described by Tompsett et al (1961) and Tompsett (1968) has proved effective in these circumstances.…”

Two survivors of severe paraquat intoxication by ?continuous hemoperfusion?

“…No mucosal ulcerations were detectable in the mouth or throat. Paraquat intoxication was established by a rapid diagnostic test on the urine [5]. The physical examinations showed no pathological changes.…”

Two autopsy cases of paraquat poisoning.

“…Survival periods of paraquat poisoning varied from 7 to 20 days (Bullivant 1966;Feenelly et al 1968) and the cause of death is usually respiratory distress except for only one case, in which the patient died of cardiac arrest (Oreopouls et al 1968). Although most cases were fatal (Bullivant 1966;Almog and Tal 1967;Campbell 1968;Feenelly et al 1968;Matthew and Logan 1968), recovered cases without respiratory symptoms were reported (Kerr et al 1968;Mckean 1968;Fisher et al 1971). The periods from paraquat ingestion to the development of lung dysfunction were different, but death occurred 8 to 10 days after the onset of clinical signs (Smith et al 1974).…”