Cases reported "Coma"

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1/66. Acute isoniazid intoxication: seizures, acidosis and coma.

    isoniazid (INH) is the most widely used of the antituberculosis drugs. An acute overdose is potentially fatal and is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. The diagnosis of INH overdose should be considered in any patient who presents with an unexplained metabolic acidosis and convulsions. The cornerstone of therapy consists in pyridoxine (vitamin B6) and the dose should be equal to the amount of INH ingested. When conservative therapy fails or in case of renal insufficiency, dialysis must be considered. Severe central nervous toxicity can also be caused by chronic ingestion of higher than therapeutic doses of INH. In those cases pyridoxine-therapy can be useful as well. In the present paper a case of acute overdose of INH is reported, followed by a review of the literature.
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ranking = 1
keywords = intoxication
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2/66. High-efficiency dialysis for carbamazepine overdose.

    BACKGROUND: carbamazepine intoxication is associated with seizures, coma, arrhythmias, and death. In acute intoxications, charcoal hemoperfusion enhances removal of the drug but is associated with thrombocytopenia, coagulopathy, hypothermia, and hypocalcemia. Alternatively, high-efficiency hemodialysis can be used without the side effects of charcoal hemoperfusion. CASE REPORT: We report an 18-month-old comatose, convulsing child with plasma carbamazepine 27 microg/mL treated with high efficiency hemodialysis. Therapeutic carbamazepine levels were obtained after 4.5 hours of high-efficiency hemodialysis. The patient developed no untoward side effects, improved clinically, and was subsequently discharged home without sequelae. We conclude that high-efficiency hemodialysis is a safe, effective alternative to charcoal hemoperfusion in the pediatric population.
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ranking = 0.5
keywords = intoxication
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3/66. diffusion-weighted magnetic resonance imaging in a case of methanol intoxication.

    BACKGROUND: methanol intoxication is an uncommon clinical problem leading to profound metabolic acidosis with serious neurological deterioration. We describe methanol induced brain lesions on diffusion-weighted MR images and discuss the pathophysiology of these lesions in light of diffusion changes. CASE REPORT: brain imaging was performed in a 32 year-old man in a coma with focal neurological signs. Bilateral putaminal [hyperintensity] was seen on fast spin echo T2-weighted sequences, on Fluid Attenuated Inversion Recovery (FLAIR) and on diffusion weighted images. Decreased ADC values were observed bilaterally in the putamina. In addition, FLAIR images showed diffuse hypersignal in the subarachnoidal space. The patient showed rapid neurological deterioration while blood chemical tests revealed a severe metabolic acidosis and plasma methanol levels of 21 mmol/L. The patient died from hepatic failure thirty six hours after admission. CONCLUSION: Although decreased ADC values on diffusion-weighted imaging are commonly associated with arterial ischemic stroke, this pattern can also be observed in the case of putaminal necrosis following methanol ingestion.
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ranking = 1.25
keywords = intoxication
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4/66. coma and seizures due to severe hyponatremia and water intoxication in an adult with intranasal desmopressin therapy for nocturnal enuresis.

    Desmopressin, a synthetic analogue of the antidiuretic hormone, is an effective medication for primary nocturnal enuresis for both children and adults. Its safety is well established. Although it has a favorable side effect profile, because of its pharmacological effect, intranasal desmopressin can rarely induce water intoxication with profound hyponatremia if given without adequate restriction of water intake. The authors describe an adult patient with water intoxication and severe hyponatremia accompanied by loss of consciousness and seizures after 2-day intranasal administration of desmopressin. The present and the previously reported cases emphasize the need for greater awareness of the development of this serious and potentiallyfatal complication. In addition, to adjust the drug to the lowest required dosage, adequate restriction of water intake is recommended, and serum levels of sodium should be measured periodically to allow for early detection of water intoxication and hyponatremia.
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ranking = 1.75
keywords = intoxication
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5/66. Severe intoxication from xylazine inhalation.

    We present the first documented case of overdose from xylazine inhalation. The patient developed findings consistent with alpha 2 adrenergic agonist toxicity, eg coma, miosis, apnea, bradycardia, hypothermia, and dry mouth 2 hours after exposure. Standard dose naloxone did not reverse these effects. The patient fully recovered after appropriate supportive measures. A review of prior reports of xylazine exposure is provided.
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ranking = 1
keywords = intoxication
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6/66. Hospital-acquired salicylate intoxication. report of a case with psychosis, acidosis, and coma.

    A case of salicylate intoxication from repeated therapeutic doses of aspirin is reported in an adult with impairment of salicylate elimination. Evolution of acid-base disturbance from respiratory alkalosis to metablic acidosis is documented. serum salicylate levels during several years of therapy demonstrate the acquisition of impaired elimination of the drug. This case illustrates the practical importance of special features of salicylate accumulation kinetics emphasized in a recent review.
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ranking = 1.25
keywords = intoxication
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7/66. coma blisters in a case of fatal theophylline intoxication.

    A case of fatal poisoning caused by theophylline toxicity (serum level 127 micro g/ml) is presented. At external examination, skin blisters on regions exposed to pressure were distinctive. Histologic examination demonstrated subepidermal bullae with eosinophilic necrosis of the eccrine sweat gland coil but no epidermal necrosis, vascular changes, or inflammatory infiltrate. To the authors' knowledge, this is the first description of coma blisters in a case of theophylline intoxication.
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ranking = 1.25
keywords = intoxication
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8/66. Hyponatraemic coma induced by desmopressin and ibuprofen in a woman with von Willebrand's disease.

    A middle-aged woman was admitted to the hospital after being found unconscious at home. A brain CT scan excluded an intracranial bleed or other focal abnormality. Laboratory analysis showed hyponatraemia (sodium: 121 mmol L(-1)) and a low plasma osmolality, with normal sodium excretion and urine osmolality. A diagnosis of hyponatraemic coma was made. The patient was treated with water restriction; 24 h later the sodium was 135 mmol L(-1) and the patient was neurologically fully recovered. The patient, who suffered from von Willebrand's disease, had received desmopressin and ibuprofen for analgesia 2 days before after a dental intervention. She had received desmopressin several times in the past without any complications. A few patients treated with desmopressin for coagulation abnormalities have been reported to develop water intoxication and severe hyponatraemia resulting in seizures and coma. By inhibiting prostaglandin synthesis, non-steroid anti-inflammatory agents (NSAIDs) potentiate the effect of water reabsorption in the renal tubules of vasopressin, therefore enhancing water retention. Desmopressin and NSAIDs should not be used in combination in patients with bleeding disorders, but it is often followed in clinical practice. In addition, this is probably not an unusual situation in patients treated with desmopressin for other 'non-haemorrhagic' indications. This report emphasizes the need for practitioners to be aware of this rare but severe complication.
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ranking = 0.25
keywords = intoxication
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9/66. Long lasting impaired cerebral blood flow after ecstasy intoxication.

    Four hours after having taken 10 ecstasy tablets a Grand Mal seizure occurred in a 19-year-old woman followed by coma, hyperthermia, tachycardia, tachypnea, and renal failure. After awakening she was oriented but presented with helplessness, disconcertion, hallucinations, panic attacks, and amnesic syndrome. Computed tomography and magnetic resonance imaging scans of the brain were normal. [99Tc]-hexamethylpropyleneamine oxime (HMPAO)-single photon emission computed tomography (SPECT), 20 days after intoxication, showed reduced, inhomogeneous, supratentorial tracer uptake bilaterally. electroencephalography (EEG) disclosed diffuse slowing and occasionally generalized sharp waves. valproic acid was begun. Except for slight amnesia, neuropsychological deficits had disappeared and [99Tc]-HMPAO-SPECT normalized, 29 days later. Decreased cortical blood flow was explained by vasoconstriction following ecstasy-induced depletion of serotonin.
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ranking = 1.25
keywords = intoxication
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10/66. Pyrimidifen intoxication.

    We present a case of lethal ingestion of pyrimidifen, a new insecticide with an unclear mode of action. The primary manifestations were coma and circulatory shock, leading to irreversible multiorgan failure. Pyrimidifen was detected in the patient's blood, urine, brain tissue, and gastric content samples. Minimal structural homology exists between pyrimidifen and organochlorines. Currently, no antidote is available, and therapy is primarily supportive.
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ranking = 1
keywords = intoxication
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