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Biomedical subjects

S N Chugh

Publications and source records attributed to S N Chugh.

At least 37 records · Page 2Linked to original sources
PubMed1994

Efficacy of magnesium sulphate in aluminium phosphide poisoning--comparison of two different dose schedules.

The results of an open randomised study on the efficacy of magnesium sulphate therapy in aluminium phosphide poisoning are presented. One hundred and fifty five patients divided in three groups and matched for age, sex, dose, duration and severity of poisoning constituted the subject matter. Significant hypomagnesemia was observed in patients who did not receive magnesium sulphate (group 1). Two dose schedules of MgSO4 therapy were tried. The dose schedule No.1 given to patients of group 2 did not raise the magnesium levels significantly as compared to controls (group 4). The difference in the mortality between groups 1 & 2 was also not significant. On the other hand, the dose schedule No.2 given to patients of group 3 raised the magnesium levels significantly and these remained above normal limits throughout the observed period. This dose schedule brought down the mortality significantly than dose schedule No.1 (p < 0.001). It was also found that dose schedule No.2 has been effective in reducing the mortality irrespective of dose of pesticide consumed and its efficacy was due to rapid rise in magnesium levels. It is suggested that hypomagnesemia might be responsible for high mortality of patients of aluminium phosphide poisoning and its correction has beneficial effect on the management and ultimate favourable outcome of the illness.

Adolescent↗
PubMed1993

Toxicity of exposed aluminium phosphide.

Poisoning by the partially or fully exposed compound of aluminium phosphide (ALP) is becoming common, Fifty patients with history of ingestion of ALP either in the form of broken tablets or granular powder were included in this study for analysis of systemic effects and outcome. Forty patients (Gr. I) consumed broken or granular form of tablets. Ten patients (Gr. II) consumed only powder form of tablets from an old container. 30 patients in group-I developed mild hypotension (BP 80-90 mm Hg). 4 patients (10%) developed ECG changes and mild metabolic acidosis. One patient died constituting 2.5% mortality rate. The patients of group-II neither developed any systemic effects nor showed any mortality. The aim of the study is to differentiate these cases from patients who consume active, fresh compound where mortality rate will be much higher.

Acidosis↗
PubMed1991

Magnesium levels in acute cardiotoxicity due to aluminium phosphide poisoning.

Significant hypomagnesemia and hypomagnocytia were observed in patients of aluminium phosphide (AIP) poisoning having evidence of acute cardiotoxicity while magnesium levels were normal in patients of AIP poisoning without shock or cardiotoxicity as well as in controls. There was a direct relationship between electrocardiographic findings and low magnesium levels. The mortality was also related directly to hypomagnesemia. The dose of pesticide also influenced the mortality adversely. Autopsied heart showed changes of toxic myocarditis on histopathology.

Acute Disease↗
PubMed1991

Incidence & outcome of aluminium phosphide poisoning in a hospital study.

A total of 418 patients with aluminium phosphide poisoning admitted during January 1981 to December 1987, were studied and analysed for various clinical parameters. A steady increase in the number of patients was seen during the last 7 yr. Maximum number belonged to the younger generation and nature of poisoning was suicidal in most of these patients. Dose of poison consumed varied, but most patients consumed two tablets (6 g). A wide range of symptoms and signs was seen, the commonest being gastrointestinal manifestations and shock. Cardiac arrhythmias and conduction disturbances were seen in 38.2 per cent patients. The overall mortality was 77.2 per cent. Indices of a bad prognosis included poor response to dopamine infusion and continuous increase in its dosage, chest infections, adult respiratory distress syndrome and disseminated intravascular coagulation. The complications noticed were pericarditis, congestive cardiac failure, acute gastrointestinal haemorrhage and acute respiratory arrest. Histopathology of various organs showed changes suggestive of cellular hypoxia but the mechanism of ECG changes and of the complications could not be elucidated.

Accidents↗
PubMed1991

Electrocardiographic abnormalities in aluminium phosphide poisoning with special reference to its incidence, pathogenesis, mortality and histopathology.

Ninety-five patients out of total 190 cases of aluminium phosphide (ALP) poisoning, who exhibited ECG changes were studied for incidence, type and pattern of ECG abnormalities, their effect on mortality and their relationship with histopathology of heart. Its incidence in the present study was 50%. The arrhythmias, conduction disturbances and ischaemic pattern occurred more or less in equal frequency. Certain ECG abnormalities which had not been reported previously ie, early repolarisation syndrome, varied sino-atrial blocks, bradycardia-tachycardia syndrome and electrical alternans were observed in this study. The clinical profile of these cases was similar irrespective of whether patients had ECG abnormalities or not. Shock was the cardinal feature. There was no effect of ECG abnormalities on mortality. The mortality which was otherwise high, depended upon severity of poisoning, dose of poison consumed, duration of shock, failure of response of shock to resuscitative measures and severe hypomagnesaemia. The pathogenesis of ECG abnormalities is still obscure. Hypomagnesaemia was observed in all the 18 cases studied, irrespective of ECG abnormalities. However, these were common when hypomagnesaemia was severe. Hypoxaemia and shock were not the contributory factors for these abnormalities. Autopsy revealed stereotyped histopathological changes of toxic myocarditis independent of ECG findings.

Adolescent↗
PubMed1990

Plasma renin activity in shock due to aluminium phosphide poisoning.

Plasma renin activity (PRA) was estimated in 30 patients with aluminium phosphide (AIP) poisoning (study group) admitted in shock. Ten patients in shock other than due to AIP poisoning (Group II A) and 20 normal healthy subjects (Group II B) served as controls. The PRA was significantly higher in the study group and group II A as compared to normal healthy subjects (p less than 0.001). Significantly higher PRA was found in the study group as compared to Group II A (p less than 0.001). The initial higher PRA continued to rise further in the study group but it started decreasing in Group II A as the duration of shock advanced. Continuation of shock in AIP poisoning was probably due to slow release of toxic PH3 gas, which was detected by positive silver nitrate paper test. The rise in PRA was directly proportional to the dose of pesticide consumed. There was direct relationship of mortality with increased PRA. Angiotensin converting enzyme inhibitors may have a role in combating shock in AIp poisoning.

Adolescent↗
PubMed1989

Adult respiratory distress syndrome following aluminium phosphide ingestion. Report of 4 cases.

Four cases of adult respiratory distress syndrome (ARDS) following aluminium phosphide ingestion (ALP) are being reported. The dose of the intoxicant varied from 2 tablets (6.0 gm) to 3 tablets (9.0 gm). All patients had shock at admission and developed ARDS within 6 hours. The exhalation of Phosphine, (PH3) detected by positive silver nitrate paper test, was the possible noxious triggering factor in our cases. The cases are being reported because of their rare occurrence.

Adolescent↗
PubMed1989

Adrenocortical involvement in aluminium phosphide poisoning.

The effect of aluminium phosphide (AlP) which is a systemic poison on the adrenal cortex was studied in 30 patients of AlP poisoning. A significant rise in the plasma cortisol level (greater than 1048 nmol/l) was observed in the twenty patients. Mortality was 50 per cent. Autopsy study could be undertaken only in 10 patients. Histopathology showed mild to moderate changes. In the rest (10 patients), the adrenal cortex was critically involved and the cortisol level failed to rise beyond normal levels (less than 690 nmol/l). The histopathology revealed severe changes (complete lipid depletion, haemorrhage, necrosis etc.) and all these patients died. In the critically ill patients, the cortisol levels remained low because of severe adreno-cortical involvement. The changes in the adrenal cortex could be due to shock or to cellular toxic effect of phosphine. The histopathological changes in various viscera showed congestion, edema and cellular infiltration. In the heart, there were patchy areas of necrosis, while the liver showed fatty changes and the lungs showed, in addition areas of gray/red hepatization. There was no adrenal apoplexy or extensive haemorrhage that could explain shock in these patients. Cardiogenic shock could not be confirmed due to lack of facilities for haemodynamic monitoring, but there was histopathological evidence in support of cardiovascular shock.

Adolescent↗