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ALUMINIUM PHOSPHIDE: WORSE THAN BHOPAL

SIR,-Dr Bajaj and Dr Wasir (April 9, p 820) deserve thanks forhaving drawn attention to the tragedy of aluminium phosphidedeaths in India. Aluminium phosphide deaths first became publicknowledge in 1983 when 37 cases at Udaipur Medical CollegeHospital in one year were reported by one of us (S.G.K.) to thePress Trust of India, whose despatches were carried by all theleading daily newspapers in the country. The response of localauthorities was lukewarm; moreover, they were, surprisingly,unaware of the statutory provision (in the manufacturers’ licence)that aluminium phosphide was to be supplied to large warehousesonly. The pesticide was not only freely available but it was activelypromoted by the manufacturers for use in the home. A team offorensic experts and lawyers confirmed that open sale of the

pesticide was prohibited by law. Yet, there were several who sworethat the pesticide was safe. In one macabre case, a local politicalparty stalwart died after swallowing a tablet of aluminium

phosphide. He was demonstrating his conviction that if the

pesticide was indeed dangerous, his party’s government would nothave permitted its availability (Times of India, Jaipur; April 20,1986: 3).Most deaths are suicidal but fatal accidents and even homicides

are known. According to the forensic science department, SMSMedical College, Jaipur, a history of aluminium phosphideingestion has been found in 26 unnatural deaths in the past 3 years.18 of these 26 cases were in young women, reflecting the readyavailability of this deadly poison in Indian households. As Bajaj andWasir rightly state, many cases go unreported in medical journals.We know of 319 published fatal cases, and reports appear almostdaily in local newspapers. The few survivors were those fortunateenough to have consumed exposed tablets that had lost much oftheir potency. The number of people killed by phosphine (liberatedfrom ingested aluminium phosphide) every year in India may wellbe greater than the methyl isocyanate deaths in the Union Carbidetragedy at Bhopal in 1984.

Department of Surgery,Santokba Durlabhji Memorial Hospital,Jaipur 302 015, Rajasthan, India

S. G. KABRA

RAMJI NARAYANAN

SEVERITY INDEX OF PARAQUAT POISONING

SiR,—The prognosis in acute paraquat poisoning is largelydetermined by the time between ingestion and treatment and byserum paraquat concentrations before treatment. However, in theabsence of an objective index for severity, predictions will beinaccurate and it will also be impossible to evaluate the results oftreatment. We have developed such an index.30 patients with acute paraquat poisoning (19 males and 11

females, mean age 45) were admitted to our hospital betweenNovember, 1985, and September, 1987. The serum paraquat levelswere measured at admission by colorimetry and the time elapsedbefore intensive treatment began was recorded. All patients weretreated in the same way. Deaths were attributed to circulatoryfailure! or to respiratory failure ("paraquat lung"2).

10 patients (33%) survived, 9 died in respiratory failure and 11 incirculatory failure.The accompanying figure is a plot of time from ingestion (x)

against log serum paraquat concentration (y) and survivors and fatalcases are shown separately. The boundary between survival anddeath that can be expressed by y = A/x, A being the severity index ofparaquat poisoning (SIPP). Thus SIPP is time to treatment sinceingestion of paraquat multiplied by the serum levels at admission.The boundary SIPP = 10 (for survival versus death from eithercause). SIPP = 50 separated deaths from respiratory failure anddeaths from circulatory failure. The curve for SIPP = 10 enclosesProudfoot and colleagues’ survival curve3 (dotted line).When we plotted log survival time (y) against log SIPP (x) for

fatal cases (ie, SIPP above 10) the result was a straight line: logy=-l’251ogx+4’14(r- - 0-875, p < 001 ).

In paraquat poisoning the prognosis is usually gloomy and tosome extent it is predictable at the time of admission. Proudfoot etap showed that survival is determined by time elapsed since

Relation between serum paraquat and time since ingestion.

ingestion and serum paraquat levels. Nevertheless such survivalcurves3.4 are of limited use in the quantitative evaluation of theseverity of poisoning. Our SIPP gives an accurate prognosis andpredicts the duration of survival. We also find that the indexpredicts changes in lung function, haemodynamics and thefunctions of other organs terminally (eg, kidneys). It should alsoprove useful in planning treatment, in studying the pathology ofparaquat poisoning, and in comparing the results of differenttreatments.

Department of Emergency Medicine,School of Medicine,Kogoshima University,Kogoshima- hi, 890 Japan

YUHSUKE SAWADAISOTOSHI YAMAMOTOTAMINORI HIROKANEYOSHIKAZU NAGAI

YOHJI SATOHMASASHI UEYAMA

1. Satoh Y, Yamamoto I, Sawada Y, et al. Haemodynamics of paraquat poisoning inacute phase. J Clin Exp Med 1987; 143: 867-68 (summary in English).

2. Spencer H. Paraquat lung. In Pathology of the lung: Vol II, 4th ed Oxford: PergamonPress, 1985. 719-21

3. Proudfoot AT, Stewart MJ, Levitt T, et al Paraquat poisoning. Significance ofplasma-paraquat concentrations. Lancet 1979; ii: 330-32

4. Heart TB, Nevitt A, Whitehead A. A new statistical approach to the prognosticsignificance of plasma concentrations. Lancet 1984, ii 1222-23

FALSE POSITIVE IN PRENATAL DIAGNOSIS OFCYSTIC FIBROSIS

SIR,-Dr Sharples and colleagues (March 13, p 595) report that afetus, shown at 17 weeks’ gestation to have an echogenic bowel andabnormal microvillar enzyme levels in amniotic fluid, was normal atbirth. We had an almost identical experience with a woman who hada detailed ultrasound scan because of a distant family history ofcystic fibrosis. Echogenic bowel was seen and amniotic fluidmicrovillar enzyme levels were reduced within the range associatedwith cystic fibrosis in the fetus.

This mother’s prior risk of having a child with cystic fibrosis wasonly 1 in 640 and is seems possible that the microvillar enzyme assaywas confirming the ultrasound finding of bowel obstruction ratherthan providing new information. We were also aware that similarultrasound findings had been reported in fetuses subsequently