Research Progress of the Death Caused by Insulin Intoxication / 法医学杂志

In recent years, with the sustained increase of the incidence of diabetes in humans and the wider use of exogenous insulin, the cases of inappropriate use and overdose of insulin is growing, even the cases of suicide and homicide using insulin. Through searching the literature at home and abroad about the mechanism, clinical and case report of poisoning and death caused by insulin intoxication, this paper reviews the mechanism, clinical manifestations, pathological changes, and forensic examination.

Forensic Analysis of 20 Dead Cases Related to Heroin Abuse / 法医学杂志

OBJECTIVES@#To perform retrospective analysis on 20 dead cases related to heroin abuse, and to provide references for the forensic assessment of correlative cases.@*METHODS@#Among 20 dead cases related to heroin abuse, general situation, using method of drug, cause of death and result of forensic examination were analyzed by statistical analysis for summarizing the cause of death and pathologic changes.@*RESULTS@#The dead were mostly young adults, with more male than female. The results of histopathological examinations showed non-specific pathological changes. There were four leading causes of death, including acute poisoning of heroin abuse or leakage （13 cases, 65%）, concurrent diseases caused by heroin abuse （3 cases, 15%）, inspiratory asphyxia caused by taking heroin （2 cases, 10%）, and heroin withdrawal syndrome （2 cases, 10%）.@*CONCLUSIONS@#The forensic identification on dead related to heroin abuse must base on the comprehensive autopsy, and combine with the qualitative and quantitative analysis of heroin and its metabolites in death and the case information, as well as the scene investigation.

Current views on antidotal therapy in managing cases of poisoning and overdose.

While it is an acknowledged dictum that in poisoning or overdose cases, the emphasis must be on general management comprising supportive measures than the use of specific antidotes in the vast majority of cases, it is nevertheless true that there are some instances where the timely use of a specific antidote or antagonist will dramatically reverse or at least halt the progression of toxicity. For this reason, and also because the indications and the exact manner in which antidotes must be used could be controversial or unfamiliar to the physician, an attempt has been made to review the current concepts on antidotal therapy of poisoning. There is enough evidence that the proper use of specific antidotes when combined with general supportive care does reduce the morbidity and mortality associated with severe poisonings. Common antidotes used in a hospital setting have been discussed in some detail.

Near-fatal amlodipine poisoning.

Amlodipine poisoning is very rare and only few cases have been reported in English literature. We report here a case of severe amlodipine poisoning with non-cardiogenic pulmonary edema.

Acute iron poisoning: clinical picture, intensive care needs and outcome.

In this retrospective study, we examined the prevalence of acute iron poisoning among children attending Pediatric Emergency service of a teaching hospital, and studied their clinical profile, treatment and outcome to define intensive care needs. During the 5 years' study period of 27125 patient visits to Pediatric Emergency, 337 (1.2%) were for accidental poisoning. Of these 21(7%) patients had iron poisoning; 18 were transferred to PICU. Three patients were asymptomatic, others had vomiting (n =15, 83%), diarrhoea (n =13, 72%), malena (n = 8, 44%), and hemetemesis (n=6, 33%) generally within 6 hours of ingestion. Nine progressed to shock and/or impaired consciousness; two had acute liver failure. Dose of ingested iron and clinical signs were most useful guide to iron toxicity and management decisions; serum iron did not help. Gastric lavage yielded fragments of iron tablets in 10 patients. On desferrioxamine infusion Vin-rose colour urine was not seen in 31% even in presence of high serum iron. Shock responded to normal saline (33 +/- 15 mL/kg) and dopamine (10 +/- 4 microg/kg/min) within 4-24 hours in 7 of 9 patients. Presence of shock or acute liver failure with coagulopathy and/or severe acidosis predicted all the four deaths. Desferrioxamine infusion and supportive care of shock was the mainstay.

Accidental dextropropoxyphene poisoning.

Dextropropoxyphene poisoning is an uncommon accidental poisoning in children. Presentation is similar to narcotic over dosage or poisoning. Convulsions, conduction disturbances, arrhythmias and hypoglycemia are common. Naloxone is the antidote. As it is uncommon and not documented in children in Indian literature we are reporting this case.

Paracetamol poisoning in children.

Paracetamol (acetaminophen) has become an antipyretic drug of choice. Due to its widespread use, toxicity secondary to overdose has increased in recent years. Children are especially vulnerable to accidental exposure due to non availability of child proof containers in India. The main clinical features of acute toxicity include anorexia, vomiting, abdominal pain, jaundice, hematuria and metabolic acidoses. Diagnosis is based on history and laboratory findings of acidosis and abnormal liver function tests. N-acetylcysteine is the specific antidote. This article reviews in detail the toxicokinetics, pathophysiology, clinical features and management of paracetamol poisoning in children.

Acute iron poisoning.

Accidental iron ingestion is not uncommon in children and has become a leading cause of unintentional pharmaceutical ingestion fatality. Difficulty in obtaining urgent serum iron levels in majority of hospitals in India, lack of objective indices for starting and stopping the chelation therapy and the cost of chelation therapy, all pose a significant challenge for a clinician in managing an acutely intoxicated patient. This review emphasizes the need for early recognition and correct intervention of a child with acute iron overdose to avoid undue morbidity and mortality.

El tratamiento de las intoxicaciones agudas causadas por carbamazepina, digoxina y ácido acetilsalicílico, mediante la administración de dosis repetidas de carbón activado / Treatment of acute intoxication caused by carbamazepine, digoxin and acetylsalycilic acid with repeated dose of activated charcoal

Se informa de doce pacientes pediátricos intoxicados en forma aguda, cuatro con carbamazepina, cuatro con digoxina y cuatro más con ácido acetilsalicílico. El tratamiento, además de las medidas generales de sostén y sintomáticas, consistió en la administración de dosis múltiples de carbón activado (superficie de adsorción aproximado de 950 m2/g), y un catártico salino al inicio, a la mitad y al final del tratamiento, cuya duración total fue de 24 a 36 horas. El procedimiento se consideró eficaz, pues además de la mejoría clínica de los pacientes, concomitantemente redujo las cifras plasmáticas de los fármacos responsables. Las cifras promediadas inicales de carbamazepina fueron de 21.64 ug/ml y las finales de 0.9 ug/ml, con un descenso neto de 95.8 por ciento (p<0.05). La digoxina de 5.14 y 1.1 ng/ml, con descenso de 78.6 por ciento (p<0.05), y finalmente, el ácido acetilsalicílico, cifra de 418.5 y 57.5 ug/ml respectivamente, con descenso de 86.3 por ciento (p<0.05). Estos resultados sugieren el papel del carbón activado en la depuración sistemática de los fármacos estudiados

Cardiovascular manifestations of aluminium phosphide intoxication.

Aluminium phosphide (ALP) a major suicidal agent in the developing countries is freely available as grain fumigant. It is highly toxic to lungs, heart and blood vessels causing pulmonary oedema, shock and arrhythmias. There is massive focal myocardial damage resulting in raised cardiac enzymes. Clinical manifestations were nausea and vomiting (32), dyspnoea and palpitations (25 each), cyanosis (12), hypotension (12) and shock (15). Cardiac arrhythmias were present in 28 cases and hypermagnesaemia in 13 patients. Mean serum magnesium level (1.95 +/- 0.2O, mEq/L) was significantly raised compared to mean magnesium level in control subjects (1.62 +/- 0.23 mEq/L). Hypermagnesaemia occurs due to myocardial and liver damage. Out of 32 cases studied, 22 died 18 within 24 hours of ALP ingestion. Thirty two cases of ALP were studied.