Prolonged bilateral reactive miosis as a symptom of severe insulin intoxication.

BACKGROUND: Miosis occurs following exposure to toxins that decrease the sympathomimetic tone, increase the cholinergic tone, or exert sedative-hypnotic effects, but has not been reported in insulin poisoning. CASE REPORT: A 64-year- old woman without co-morbidities was found unconscious next to an empty insulin pen. Her Glasgow Coma Scale was 3 with absent reflexes, bilateral reactive miosis, and injection marks across the abdominal wall. The patient was endotracheally intubated, mechanically ventilated, and transferred to this hospital. At admission, the blood glucose level was 34 mg/dL. Glasgow Coma Scale remained at 3, with persistent bilateral reactive miosis. The toxicology screening was negative for ethanol, barbiturates, tricyclic antidepressants, phenothiazines, amphetamines, cannabinoids, salicylates, acetaminophen, and cocaine. Cranial computed tomography with angiography and magnetic resonance imaging (MRI) did not show any structural brain lesions. Intravenous glucose was continued at 6-14 g/h for 3 days. On repeated neurological examinations, the patient remained deeply comatose, with partial loss of cranial nerve function. Bilateral reactive miosis persisted for 4 days. From day 5 on, the patient awoke progressively. At discharge, the patient was fully alert and orientated, without a focal neurological deficit. CONCLUSIONS: Prolonged bilateral reactive miosis can be a clinical symptom accompanying metabolic encephalopathy in severe insulin poisoning. Functional impairment of the pons due to relative hypoperfusion during hypoglycemia may serve as a reasonable pathophysiologic explanation for this phenomenon.

Severe hypoglycaemia in drug-treated diabetic patients needs attention: a population-based study.

OBJECTIVE: To study one-year incidence and risk factors of severe hypoglycaemias (SH) in adult drug-treated diabetic patients living in two Finnish communities. DESIGN: The episodes of SH and their risk factors were identified from local ambulance registers, from the databases of local health care units, and from patient questionnaires. SETTING: The target population consisted of all drug-treated diabetic patients from the two middle-sized communities in southern Finland, altogether 1776 patients. The study was retrospective. SUBJECTS: A total of 1469 patients (82.7% of the target population) gave informed consent for the use of their medical records and 1325 patients (74.6% of the target population) returned the detailed 36-item questionnaire. RESULTS: Of type 1 and type 2 insulin-treated diabetic patients, 14.6% and 1.0%, respectively, needed ambulance or emergency room care (incidence of 30.5 and 3.0 per 100 patient years). However, 31.0% of type 1 and 12.3% of type 2 diabetic patients reported at least one episode of SH (incidence of 72.0 and 27.0 per 100 patient years). Of all insulin-treated patients, 53 (7.8%) reported three or more episodes of SH. Significant independent risk factors for SH were depression, daily exercise, and nephropathy but not glycaemic control. CONCLUSION: The incidence of SH was high in both types of insulin-treated diabetic patients. However, the recurrent episodes of SH were clustered in a small minority of insulin-treated patients with diabetes. The risk of SH should be considered when assessing the treatment target for an individual diabetic patient.

[Diabetic emergencies]. / Diabetische Notfallsituationen.

Based on case reports pathogenesis and treatment of the following diabetic emergencies were discussed: 1. The hyperosmolar non-ketotic coma without or with only modest ketosis occurring mainly in type II diabetics and the severe ketoacidosis with or without disturbed consciousness occurring mainly in type I diabetics are the two forms of severe metabolic decompensation of diabetes mellitus. 2. Severe hypoglycaemia may be caused by treatment with sulfonylureas and insulin. 3. The most dangerous life threatening adverse effect of biguanides is lactic acidosis. The incidence of ketoacidosis is about 1-5% in type I diabetics with a mortality of 3-9%. Mortality rates of hyperosmolar non-ketotic comas are much higher, approaching 20-40%, and are explained by severe concomitant complications and older age. The most important triggering factors of diabetic coma are infections, insulin dispensing errors and non-compliance. Carefully instructing patients about the risks of loosing appetite and vomiting as early signs of ketoacidosis is essential. Adequate replacement of fluid, electrolyte and water are the most important therapeutical aspects of ketoacidosis and hyperosmolar non-ketotic coma. Early diagnosis and appropriate treatment of infection by antibiotics are important. Complication of therapy (hypokalemia, hypovolemia and rapid full of oncotic pressure) should be avoided by clinical and laboratory monitoring. Treatment of acidosis with bicarbonate has been found more dangerous than useful. Severe hypoglycaemia is the most important and most dangerous side effect of sulfonylurea and insulin. The incidence of severe hypoglycaemia under glibenclamide ist 3-5 fold higher than under treatment with tolbutamide or glibornurid. Glibenclamide should not be recommended anymore. Longterm experience of the therapeutic security of new sulfonylurea derivates like glimepirid is lacking. Blood-glucose-measurements in the afternoon are important for recognizing disposition to sulfonylurea hypoglycaemia, because at this time the blood-glucose-values tend to be lower than in the morning fasting state. Under insulin treatment the following risk factors for severe hypoglycaemia need to be considered: metabolic control in the near normal range, intensified treatment with rapidly decreasing HbA1c-levels, impaired renal function, unawareness o hypoglycaemia. When the renal function is impaired, biguanide treatment is not indicated because of the risk of lactic acidosis. Most of the diabetic emergency situations are avoidable by proper education of the patients.

Attempted suicide using insulin by a non diabetic: a case study demonstrating the acute and chronic consequences of profound hypoglycemia.

This paper describes the case of a non diabetic physician with a prior psychiatric history in which there was overwhelming biochemical and clinical evidence that he had attempted suicide by injecting himself with an overdose of insulin. He was extensively monitored from the time of his admission to hospital in a coma, until he fully recovered consciousness 30 days later and during the next eight months of his rehabilitation. This case attests to the high level of morbidity which might follow profound hypoglycemia. It also illustrates some putative psychodynamics of suicidal behaviour--notably ambivalence and denial (at the time of writing, the patient never acknowledged that he had overdosed with insulin). A selective review on some of the more recent literature on the neuropathological effects of insulin overdose and profound hypoglycemia is presented.

[Functional neurologic studies in the diagnosis of coma]. / Place des explorations fonctionnelles neurologiques dans le diagnostic des comas.

Despite the development of medical imaging, functional exploration of the central nervous system by means of EEG and evoked potentials still plays an important role in the diagnosis and monitoring of coma. Together with clinical examination, these techniques contribute to the assessment of coma depth and inform, sometimes earlier than clinical signs, on the course of the coma. Finally, the data supplied by paraclinical explorations have a diagnostic value in cases of acute encephalitis, dysmetabolic diseases, drug poisoning or severe cerebral anoxia.

Insulin-induced factitious hypoglycemic coma.

Hypoglycemia due to the ingestion of oral hypoglycemic agents or injection of insulin is a common way for chronic factitious disorder to present to physicians. Despite this fact, factitious hypoglycemic coma is rare. Because hypoglycemia is potentially fatal, with numerous sequelae, physicians need to be aware of its occurrence and method of detection. A case of chronic factitious disorder presenting as hypoglycemic coma is presented and its implications discussed.

[Symptoms and incidence of hypoglycemia in 100 insulin dependent diabetics]. / Séméiologie et vécu des hypoglycémies chez 100 diabétiques traités par l'insuline.

The aim of this study was to discover the frequency and the symptoms of hypoglycaemic reaction and coma. One hundred type I diabetic patients answered an oral questionnaire and explained how they were awaken from their hypoglycaemicoma. The frequency of hypoglycaemic reaction was from one a day to one a year. 41 patients had nocturnal hypoglycaemic reactions. Our patients described 27 different symptoms of oncoming attack; however, not all of these symptoms was experienced by any one of the patients. Treatment of hypoglycaemic reaction was administered correctly but at the precise moment of the interview, 13% of patients had no carbohydrates with them. 42 patients had had hypoglycaemic reaction but no coma. Shared between 48 patients were 578 insulin years and 148 comas. Treatment of hypoglycaemic coma was variable: 20 patients remained at home receiving appropriate treatment; 33 were always hospitalised on attack and 20 were still comatous on each admission. The explanation of hypoglycaemic attack was variable; an emotional factor was given by 19% of patients. Both type I diabetic patients and their immediate entourage should be made aware of all the symptoms of oncoming attack and of the treatment of hypoglycaemic coma. Systematic glycemic auto control should testify to the existence of genuine hypoglycaemic reaction and perhaps diminish its supposed frequency.