Cases reported "Coma"

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1/113. pituitary apoplexy after cardiac surgery presenting as deep coma with dilated pupils.

    Acute clinical deterioration due to infarction or haemorrhage of an existing, often previously unrecognized, pituitary tumour is a rare but well-described complication. It can occur spontaneously or may be caused e.g. by mechanical ventilation, infection or surgical procedures. We report on a case of pituitary apoplexy occurring in a 64-year-old patient 3 weeks after cardiac surgery. The patient presented with deep coma and dilated pupils. magnetic resonance imaging revealed a haemorrhagic pituitary tumour. After prompt endocrinologic replacement therapy with levothyroxine and hydrocortisone the patient regained consciousness. Neurological examination revealed right oculomotor nerve palsy and bilateral cranial nerve VI palsy. Subsequent trans-sphenoidal removal of a nonfunctional macroadenoma with large necrotic areas was performed. The patient recovered completely. To our knowledge, pituitary tumours presenting with a combination of deep coma and dilated pupils must be considered exceedingly rare. Possible pathophysiologic mechanisms are discussed. As our case illustrates, even in severe cases complete recovery is possible if the diagnosis is suspected, and diagnostic and therapeutic measures are initiated in time.
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2/113. Favourable prognosis of prolonged coma associated with large doses of diazepam in severe tetanus.

    A report is made of five tetanus patients who were treated with large repetitive doses of diazepam and became comatose. The period of impaired consciousness varied from thirteen to twenty-one days. None had significant respiratory depression, and full recovery occurred in all. It is proposed that diazepam-induced prolonged coma should be regarded as a side-effect rather than a toxic effect and should caution rather than contra-indicate further use of large doses of the drug in the management of tetanus.
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3/113. Early rebleeding from intracranial dural arteriovenous fistulas: report of 20 cases and review of the literature.

    OBJECT: In this study the authors sought to estimate the frequency, seriousness, and delay of rebleeding in a homogeneous series of 20 patients whom they treated between May 1987 and May 1997 for arteriovenous fistulas (AVFs) that were revealed by intracranial hemorrhage (ICH). The natural history of intracranial dural AVFs remains obscure. In many studies attempts have been made to evaluate the risk of spontaneous hemorrhage, especially as a function of the pattern of venous drainage: a higher occurrence of bleeding was reported in AVFs with retrograde cortical venous drainage, with an overall estimated rate of 1.8% per year in the largest series in the literature. However, very few studies have been designed to establish the risk of rebleeding, an omission that the authors seek to remedy. methods: Presenting symptoms in the 20 patients (17 men and three women, mean age 54 years) were acute headache in 12 patients (60%), acute neurological deficit in eight (40%), loss of consciousness in five (25%), and generalized seizures in one (5%). Results of the clinical examination were normal in five patients and demonstrated a neurological deficit in 12 and coma in three. Computerized tomography scanning revealed intracranial bleeding in all cases (15 intraparenchymal hematomas, three subarachnoid hemorrhages, and two subdural hematomas). A diagnosis of AVF was made with the aid of angiographic studies in 19 patients, whereas it was a perioperative discovery in the remaining patient. There were 12 Type III and eight Type IV AVFs according to the revised classification of Djindjian and Merland, which meant that all AVFs in this study had retrograde cortical venous drainage. The mean duration between the first hemorrhage and treatment was 20 days. Seven patients (35%) presented with acute worsening during this delay due to radiologically proven early rebleeding. Treatment consisted of surgery alone in 10 patients, combined embolization and surgery in eight, embolization only in one, and stereotactic radiosurgery in one. Three patients died, one worsened, and in 16 (80%) neurological status improved, with 15 of 16 AVFs totally occluded on repeated angiographic studies (median follow up 10 months). CONCLUSIONS: The authors found that AVFs with retrograde cortical venous drainage present a high risk of early rebleeding (35% within 2 weeks after the first hemorrhage), with graver consequences than the first hemorrhage. They therefore advocate complete and early treatment in all cases of AVF with cortical venous drainage revealed by an ICH.
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4/113. Recurrent psychogenic coma following tracheal stenosis repair.

    Medication, intracranial hemorrhage, infarction, infection, hypoxia, organ failure, and nutritional deficiency may cause unconsciousness following successful emergence from anesthesia. A 39-year-old woman with a history of tracheal stenosis, depression, and anxiety had complete unconsciousness on 3 separate occasions following surgical repair of her tracheal stenosis. In each case, the patient's endotracheal tube had been removed; she was alert and oriented to person, time, and place; and she was admitted to the hospital for observation. Within a few hours after the tube was removed, the patient became abruptly unconscious for periods of 36, 18, and 30 hours. Each time, the results of cardiac, pulmonary, metabolic, and neurologic examinations and radiological studies were normal. We hypothesize that the patient's apparent comas were the result of an underlying conversion disorder precipitated by unresolved psychological conflict surrounding a long history of abuse in which she was repeatedly smothered by a pillow.
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5/113. Recurrent episodes of coma: an unusual phenotype of familial hemiplegic migraine with linkage to chromosome 1.

    Over a period of ten years, a boy had several episodes of coma, lasting three to five days. Each episode was preceded by hemiparesis or paresthesias, aphasia, headaches and behavioural changes, with subsequent loss of consciousness. Partial seizures occurred during the first episode. A history of migraine or hemiplegic migraine was found in several members of the family. Linkage to chromosome 1q21-23, where a gene for familial hemiplegic migraine has been mapped, was shown in this family.
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6/113. 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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7/113. anaphylaxis should be considered to be a potential cause of stuporous state.

    anaphylaxis is not considered to cause stupor. We studied the case of a 69-year-old woman who lost consciousness after eating seafood. On her admittance to hospital she was in a state of stupor and elevated serum tryptase levels led us to the diagnosis of anaphylaxis.
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8/113. Predicting outcome from coma: man-in-the-barrel syndrome as potential pitfall.

    The glasgow coma scale motor score is often used in predicting outcome after hypoxic-ischemic coma. Judicious care should be exerted when using this variable in predicting outcome in patients with coma following hypotension since borderzone infarction can obscure the clinical picture. We describe a patient who underwent skull base surgery for a schwannoma of the left facial nerve. The operation, which lasted for 10 h, was conducted under controlled hypotension. After the intervention the patient remained comatose with absent arm movements upon painful stimuli. An absent motor score usually carries a poor prognosis. However, magnetic resonance inversion recovery imaging of the brain showed bilateral hyperintense lesions in the arm-hand area indicative of borderzone ischemic damage. The patient received optimal supportive care and after 17 days he regained consciousness with 'man-in-the-barrel syndrome', which also further improved over time.
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9/113. myxedema coma of both primary and secondary origin, with non-classic presentation and extremely elevated creatine kinase.

    myxedema coma is a rare, often fatal endocrine emergency that concerns elderly patients with long-standing primary hypothyroidism; myxedema coma of central origin is exceedingly rare. Here, we report a 37-year-old woman in whom classical symptoms of hypothyroidism had been absent. Six years earlier, she had severe obstetric hemorrhage and, shortly after, two subsequent episodes of pericardial effusion. On the day of admission, pericardiocentesis was performed for the third episode of pericardial effusion. Because of the subsequent grave arrhythmias and unconsciousness, she was transferred to our ICU. Prior to the endocrine consultation, a silent myocardial infarction had been suspected, based on the extremely high serum levels of creatine kinase (CK) and isoenzyme CK-MB. However, based on thyroid sonography, pituitary computed tomography, elevated titers of antithyroid antibodies and pituitary stimulation tests, the final diagnosis was myxedema coma of dual origin: an atrophic variant of Hashimoto's thyroiditis and post-necrotic pituitary atrophy (Sheehan syndrome). Substitutive therapy caused a prompt clinical amelioration and normalization of CK levels. Our patient is the first case of myxedema coma of double etiology, and illustrates how its presentation deviates markedly from the one endocrinologists and physicians at ICU are prepared to encounter. In addition, cardiac problems as those of our patient should not discourage from substitutive treatment (using L-thyroxine and the gastrointestinal route of absorption), if the age is relatively low.
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10/113. Pure acute subdural haematoma without subarachnoid haemorrhage caused by rupture of internal carotid artery aneurysm.

    A 52-year-old female presented with disturbance of consciousness and clinical signs of tentorial herniation. Computed tomography showed a pure acute subdural haematoma (SDH) over the left convexity without subarachnoid haemorrhage. cerebral angiography showed a saccular aneurysm at the junction of the left internal carotid artery and the posterior communicating artery. Surgery to remove the haematoma and clip the aneurysm showed the rupture point was located in the anterior petroclinoid fold (subdural space). The patient recovered without neurological deficits. Pure SDH caused by ruptured aneurysm is rare. rupture of an aneurysm adhered to either the dura or falx and located in the subdural space may cause pure SDH. Therefore, ruptured intracranial aneurysm should be considered as a cause of non-traumatic SDH. Immediate removal of the SDH and aneurysmal clipping is recommended in such patients, even those in poor neurological condition.
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