Cases reported "Coma"

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1/9. Metabolic acidosis and coma following a severe acetaminophen overdose.

    OBJECTIVE: To report a case of metabolic acidosis and coma in a severe acetaminophen overdose. CASE SUMMARY: A 29-year-old white woman was admitted to the emergency department with a diminished level of consciousness and metabolic acidosis. The toxicology screen revealed a serum acetaminophen concentration of 1072 microg/mL, and she was consequently treated with intravenous acetylcysteine. Despite the elevated concentration, the patient did not manifest signs of hepatotoxicity. DISCUSSION: Metabolic acidosis and coma are rare manifestations in acetaminophen overdoses. In published case reports, severe acetaminophen ingestion independently causes metabolic acidosis and coma in the absence of hepatotoxicity. The mechanism by which metabolic acidosis occurs is not clearly defined. Studies conducted on animals demonstrated that in severe overdoses, acetaminophen may cause lactic acidosis by inhibiting mitochondrial respiration. The mechanism by which acetaminophen can cause coma is still unknown. CONCLUSIONS: Severe acetaminophen overdoses can independently cause metabolic acidosis and coma in the absence of hepatotoxicity.
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2/9. Carboxyatractyloside poisoning in humans.

    OBJECTIVE: Cocklebur (xanthium strumarium) is an herbaceous annual plant with worldwide distribution. The seeds contain the glycoside carboxyatractyloside, which is highly toxic to animals. We describe nine cases of carboxyatractyloside poisoning in humans which, to our knowledge, has not previously been reported. The clinical, laboratory and histopathological findings and our therapeutic approach are also discussed. SUBJECTS AND methods: The patients presented with acute onset abdominal pain, nausea and vomiting, drowsiness, palpitations, sweating and dyspnoea. Three of them developed convulsions followed by loss of consciousness and death. RESULTS: Laboratory findings showed raised liver enzymes, indicating severe hepatocellular damage. BUN and creatinine levels were raised, especially in the fatal cases who also displayed findings of consumption coagulopathy. CPK-MB values indicative of myocardial injury were also raised, especially in the fatal cases. Three of the patients died within 48 hours of ingesting carboxyatractyloside. Post-mortem histopathology of the liver confirmed centrilobular hepatic necrosis and renal proximal tubular necrosis, secondary changes owing to increased permeability and microvascular haemorrhage in the cerebrum and cerebellum, and leucocytic infiltrates in the muscles and various organs including pancreas, lungs and myocardium. CONCLUSIONS: Carboxyatractyloside poisoning causes multiple organ dysfunction and can be fatal. Coagulation abnormalities, hyponatraemia, marked hypoglycaemia, icterus and hepatic and renal failure are signs of a poor prognosis. No antidote is available and supportive therapy is the mainstay of treatment.
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3/9. Near-fatal amitraz intoxication: the overlooked pesticide.

    Amitraz is commonly used in agricultural industries throughout the world as a farm-animal insecticide. Despite its widespread use, amitraz intoxication is extremely rare and mainly occurs through accidental ingestion by young children. Severe, life-threatening amitraz intoxication in adults is very rarely recognized and reported. Described herein is a previously healthy 54-year-old patient who accidentally ingested a mouthful of liquid amitraz concentrate, and rapidly developed life-threatening clonidine-like overdose syndrome, manifested as nausea, vomiting, hypotension, bradycardia, bradypnoea, and deep coma. Supportive treatment, including mechanical ventilation, and atropine administration resulted in full recovery within 48 hr. Very few cases of near-fatal amitraz poisoning in adults have been described in the medical literature, leading to low awareness of physicians in general practice to the potential toxicity of amitraz. As a consequence, cases of amitraz poisoning are not recognised and therefore erroneously treated as the much more commonly recognized organophosphate and carbamate intoxication. In our discussion, we review the clinical and laboratory manifestations of amitraz poisoning, including clinical hints that aid in the recognition of this often-overlooked diagnosis. Differentiation of amitraz intoxication from the much more commonly seen pesticide-related organophosphate and carbamate intoxication is of utmost importance, in order to avoid erroneous, unnecessary, and often dangerous treatment.
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4/9. Effect of pyritinol on EEG and SSEP in comatose patients in the acute phase of intensive care therapy.

    The extent and duration of acute disturbances of consciousness depend on the severity and localization of the underlying cerebral dysfunction. The glasgow coma scale (GCS) permits a relevant statement to be made on the course and recovery tendency of functional damage patterns in cerebral, mesencephalic, and brain stem structures. Therapy is directed at exerting a beneficial effect on the disturbed cerebral metabolism by administration of centrally active substances and at utilizing the available reserve plasticity of the brain for any possible recovery of mental performance. The bioavailability and profile of action of pyritinol have been well documented in animal experiments. We have studied the question as to the extent to which the substance influences the depth of coma in patients receiving acute intensive care therapy, and how this can be objectified electrophysiologically in the form of a specific central effect on basal brain structures. In a phase-II pilot study over five days the acute effect of intravenous 60-min. administration of 1,000 mg pyritinol on the depth of coma, the central conduction time (CCT) and the primary complex amplitude (N20/P25) of the SSEP, and on vigilance behavior (spectral edge frequencies and power) was investigated for 90 minutes in each case under intensive-medical steady-state conditions in 10 comatose patients. Because of the differences in the underlying brain damage, the primary depth of coma, age (30-89 years), sex (two female, eight male), as well as previous treatment (surgery, conservative), the significance of the results could not be evaluated by confirmatory statistical analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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5/9. Failure of therapeutic coma and ketamine for therapy of human rabies.

    The recent success in treating a human rabies patient in Milwaukee prompted the use of a similar therapeutic approach in a 33-year-old male Thai patient who was admitted in the early stages of furious rabies. He received therapeutic coma with intravenous diazepam and sodium thiopental to maintain an electroencephalographic burst suppression pattern, which was maintained for a period of 46 h, as well as intravenous ketamine (48 mg/kg/day) as a continuous infusion and ribavirin (48 to 128 mg/kg/day) via a nasogastric tube. He never developed rabies virus antibodies and he died on his 8th hospital day. At least three other patients have been treated unsuccessfully with a similar therapeutic approach. Because of the lack of a clear scientific rationale, high associated costs, and potential complications of therapeutic coma, the authors recommend caution in taking this approach for the therapy of rabies outside the setting of a clinical trial. More experimental work is also needed in cell culture systems and in animal models of rabies in order to develop effective therapy for human rabies.
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6/9. Cat scratch encephalopathy.

    Cat scratch disease is usually benign, self-limited and without sequelae. Margileth has established four clinical criteria, three of which must be satisfied to make the diagnosis: 1) a history of animal exposure, usually kitten, with primary skin or ocular lesions; 2) regional chronic adenopathy without other apparent cause; 3) a positive cat scratch disease antigen skin test; and 4) lymph node biopsy demonstrating noncaseating granulomas and germinal center hyperplasia. central nervous system involvement in cat scratch disease has been previously reported, although it is extremely uncommon. In a several-month period, we encountered two cases of cat scratch disease complicated by encephalopathy. The intents of this paper are twofold: 1) to briefly review the current literature on cat scratch disease, 2) to demonstrate that cat scratch disease complicated by encephalopathy presents acutely with seizures, posturing and coma and resolves rapidly with supportive care.
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7/9. Hypothalamic-midbrain dysregulation syndrome: hypertension, hyperthermia, hyperventilation, and decerebration.

    Certain decerebrate lesions of brain stem or hypothalamus induce pharmacologically reversible hypertension and hyperthermia in animals. We observed three young patients with episodic decerebration, hyperthermia, hypertension, and hyperventilation during recovery from comas of different etiologies. The shared pathology on neurologic examinations and computed tomographic scans was hypothalamic-mesencephalic dysfunction, suggesting a diencephalic-brain-stem disconnection syndrome or brain-stem release mechanism. propranolol was the most effective drug tested, but only two patients responded, one dramatically. This novel clinical syndrome may have localizing and therapeutic significance in pediatric coma that needs to be further defined in future studies.
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8/9. Recovery from vegetative state of six months' duration associated with Sinemet (levodopa/carbidopa).

    Certain pharmacologic interventions may improve outcome for brain injury in animals and humans. Medications affecting the dopaminergic pathway appear to be important. We present the case of a 24-year-old man with traumatic brain injury who remained unresponsive to commands and unchanged for six months despite periodic aggressive therapy. Within days of beginning Sinemet (levodopa/carbidopa), the patient became conversant and responsive. The reported low likelihood of spontaneous recovery of cognition in patients who are vegetative for six months suggests that Sinemet was responsible for this patient's recovery. In this case, the relatively small risk of side effects from Sinemet was greatly outweighed by the change in functional outcome.
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9/9. Clinical and anatomical observation of a patient with a complete lesion at C1 with maintenance of a normal blood pressure during 40 minutes after the accident.

    The authors report on their clinical observations concerning a patient with a complete spinal cord injury at the level of C1, followed by a cardiac hypoxic arrest, due to immediate respiratory paralysis after the accident. Normal cardiac activity was obtained as a result of rapid resuscitation measures, using only intubation and external cardiac massage without any drug administration. The blood pressure was maintained without any drugs at a level of 130 Torr during 40 minutes before it fell to a permanent level of 50--40 Torr on ventilation alone. The diagnosis during the first hours was believed to be that of an irreversible coma with no evidence of vertebral injury. The patient started to recover consciousness after a few days but died on the 15th day. The case is discussed in the light of the literature and of the recent physiological experiments concerning the rapid changes of blood pressure after spinal cord section in animals.
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