1/14. Prehospital cardiac arrest in diabetic ketoacidemia: why brain swelling may lead to death before treatment.An adolescent is reported with type 1 diabetes mellitus and diabetic ketoacidemia (DKA) who died from brain herniation prior to treatment with intravenous fluids and intravenous insulin. The pathophysiology of raised intracranial pressure (ICP) and water intoxication is discussed. As DKA evolves, water and electrolyte losses are replaced by very hypotonic fluids taken orally, leading to a physiologic excess of free water that would cause brain swelling prior to treatment. central nervous system acidosis may interfere with normal compensatory mechanisms that help prevent small increases in ICP. The pathophysiology of pre-treatment brain swelling has important implications for rehydration with intravenous fluids and treatment with insulin. Prevention of DKA is paramount as well as complete postmortem evaluation of patients who die from this disease.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/14. Unexplained drowsiness and progressive visual loss: methanol poisoning diagnosed at autopsy.A patient was admitted to the emergency department with a reduced level of consciousness and deteriorating vision. Her pupils became fixed and dilated and she developed a third nerve palsy with extensor posturing of her limbs. biochemistry profile showed an increased serum osmolar gap with a raised anion gap metabolic acidosis. Supportive treatment was instituted, but she made no recovery and brainstem death was later confirmed. Post mortem examination and toxicology screen confirmed the cause of death as methanol poisoning leading to cerebral oedema and transtentorial herniation. We highlight some of the diagnostic difficulties associated with treating a patient with a reduced level of consciousness. The clinical and biochemical findings that are critical in establishing a diagnosis of methanol intoxication are discussed. The definitive management of methanol poisoning is reviewed.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
3/14. Renal transplants from non-heart beating paracetamol overdose donors.INTRODUCTION: Non-heart beating donors (NHBD) are widely encouraged to avert the critical shortage in the kidney donor pool. Ischaemic injury at the time of cardiac arrest in the NHBD is more pronounced and therefore the kidneys resulting are considered marginal. This review describes our experience with four kidneys from two controlled NHBDs who were exposed to paracetamol intoxication and subsequently were treated with mannitol prior to organ donation. MATERIALS AND METHOD: Two patients with fulminant liver failure following paracetamol overdose were referred as 'withdrawal of treatment' NHBD. As the two patients had developed hepatic encephalopathy they were treated with mannitol to reduce intra-cerebral oedema. The two donors were oligoanuric for at least 24 h prior to cardiac arrest. Following cardiac arrest, in situ perfusion was carried out and the kidneys were removed. One pair of kidneys were machine perfused while the second pair of kidneys were cold stored prior to transplantation. RESULTS: Pre-transplant assessment of NHBD kidneys resulted in three of four kidneys being transplanted. The NHBD kidneys exhibited a period of delayed graft function (DGF). The early transplant biopsies showed evidence of diffuse cytoplasmic vacuolation. These histological features disappeared with time and the renal function improved until the time of discharge. DISCUSSION: Non-heart beating donor kidneys are considered marginal and the effect of mannitol and paracetamol drug intoxication will induce reversible sub-lethal injury. A period of dialysis is inevitable in clearing the reactive intermediates of mannitol and paracetamol. The kidneys behaved as traditional controlled NHBD at time of discharge.- - - - - - - - - - ranking = 2keywords = intoxication (Clic here for more details about this article) |
4/14. pica-associated cerebral edema in an adult.Acute cerebral edema due to lead intoxication is an unusual presentation in an adult. Here we describe an adult with pica presenting with severe encephalopathy due to extremely high lead levels (>200 microg/dl) with marked cerebral edema and mild hyperammonemia. Rapid initiation of chelation therapy led to a reduction in serum lead and ammonia levels and a resolution of the cerebral edema and encephalopathy, suggesting a close relationship between lead toxicity and hepatic dysfunction.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
5/14. Acute endosulfan poisoning with cerebral edema and cardiac failure.BACKGROUND: Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide with several deaths. Despite their widespread use in agriculture during the 1940s to 1960s and the well-known signs and symptoms of intoxication, the clinical picture in case of poisoning varies. We report two cases of acute intentional endosulfan intoxication with cerebral edema and cardiac failure. case reports: Both cases developed life-threatening signs like epileptic state, respiratory insufficiency and hemodynamic instability soon after ingestion. The survivor developed severe myocardial insufficiency and pulmonary edema documented by echocardiography and x-ray of the chest. The deceased patient developed severe cerebral edema and multiorgan failure ten days after ingestion of Thiodan 35. The peak serum concentration of endosulfan in the survivor was 0.12 mg/L approximately 23 hours after ingestion, whereas the peak blood concentration in the fatal case was 0.86 mg/L approximately 25 hours post-ingestion. Post-mortem endosulfan levels in different organs were determined. CONCLUSION: endosulfan is a highly toxic organochlorine insecticide that produces well-known neurological symptoms of tonic-clonic convulsions, headache, dizziness and ataxia but also can cause gastrointestinal symptoms and metabolic disturbances. life-threatening cerebral edema and hemodynamic instability may occur. Treatment is symptomatic and supportive.- - - - - - - - - - ranking = 3keywords = intoxication (Clic here for more details about this article) |
6/14. Severe ethylene glycol intoxication mimicking acute basilar artery occlusion.We report a patient with severe ethylene glycol poisoning initially mimicking acute basilar artery occlusion and elucidate the importance of immediate diagnosis and treatment: a previously healthy 59-year-old truck driver presenting with hallmarks of basilar artery syndrome after having consumed an unknown substance. Immediate application of intravenous ethanol and hemodialysis could not prevent the development of a malignant brain edema within hours. This report describes a new clinical presentation of severe ethylene glycol intoxication mimicking acute basilar artery occlusion with the development of a fatal brain edema within hours, despite adequate treatment.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
7/14. A case of valproate intoxication with excessive brain edema.A 29-year-old man, who had been treated with sodium valproate for 3 years because of generalized cerebral seizures, ingested a large amount of this drug in an attempt to suicide. The exact amount he had swallowed could not be determined. The patient arrived in the intensive care unit in a deep coma, was intubated, and artificially ventilated. He developed a massive cerebral edema, as proved by computerized tomography (CT). This was supported by electroencephalography (EEG). The measured value for the concentration of valproate in serum was markedly elevated on the day of admission (2300 mumol/l; therapeutic range 350-700 mumol/l). Treatment with sodium thiopental, glycerol, and glucocorticoids was initiated. A second CT scan performed 9 days after admission showed a complete normalization and the EEG yielded a markedly improved pattern. At this point the patient slowly regained consciousness. We conclude that in patients with an acute sodium-valproate intoxication, care should be taken with regard to the development of a severe cerebral edema, which in the reported case could be treated successfully.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
8/14. Acute methanol intoxication: a survey of patients requiring intensive therapy.A survey of patients suffering from severe acute methanol intoxication who required admission to an Intensive Therapy Unit was carried out. The clinical features of 25 patients admitted during an 18-month period are presented, together with case histories of the two patients most severely affected. The investigation and management of such patients are discussed.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
9/14. Lead encephalopathy: symptoms of a cerebellar mass lesion and obstructive hydrocephalus.The neurologic signs and symptoms of lead intoxication are quite varied. We review a case of lead poisoning in a 9-month-old child who presented clinically and radiographically with a posterior fossa mass effect and obstructive hydrocephalus. The predominance of edema of the cerebellum sufficient to achieve obstruction of the ventricular system represents a particularly unusual presentation of this disease process. review of the literature for similar cases of lead encephalopathy is included.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
10/14. Periventricular leukomalacia in adults. Clinicopathological study of four cases.The pathological findings in four patients with courses characterized by acute coma and respiratory insufficiency occurring in obscure circumstances are presented. carbon monoxide intoxication was excluded. After an early partial recovery from coma, the patients remained in a persistent vegetative state, with a tetrapyramidal syndrome. Pathologic changes consisted of infarction and demyelination of periventricular white matter, with associated necrotic foci in the basal ganglia in some cases. We propose that the prolonged hypoxia and ischemia produce a "no reflow" phenomenon causing brain edema (more pronounced in the white matter); this resulted in infarctions of white matter in the periventricular arterial end and border zones.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
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