Cases reported "Coma"

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1/78. 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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2/78. Successful use of alternate waste nitrogen agents and hemodialysis in a patient with hyperammonemic coma after heart-lung transplantation.

    BACKGROUND: Lethal hyperammonemic coma has been reported in 2 adults after lung transplantation. It was associated with a massive elevation of brain glutamine levels, while plasma glutamine levels were normal or only slightly elevated. In liver tissue, glutamine synthetase activity was markedly reduced, and the histologic findings resembled those of reye syndrome. The adequacy of therapy commonly used for inherited disorders of the urea cycle has not been adequately evaluated in patients with this form of secondary hyperammonemia. OBJECTIVE: To determine whether hemodialysis, in conjunction with intravenous sodium phenylacetate, sodium benzoate, and arginine hydrochloride therapy, would be efficacious in a patient with hyperammonemic coma after solid-organ transplantation. DESIGN: Case report. SETTING: A children's hospital. PATIENT: A 41-year-old woman with congenital heart disease developed a hyperammonemic coma with brain edema 19 days after undergoing a combined heart and lung transplantation. methods: Ammonium was measured in plasma. amino acids were quantitated in plasma and cerebrospinal fluid by column chromatography. The effectiveness of therapy was assessed by measuring plasma ammonium levels and intracranial pressure and performing sequential neurological examinations. RESULTS: The patient had the anomalous combination of increased cerebrospinal fluid and decreased plasma glutamine levels. To our knowledge, she is the first patient with this complication after solid-organ transplantation to survive after combined therapy with sodium phenylacetate, sodium benzoate, arginine hydrochloride, and hemodialysis. Complications of the acute coma included focal motor seizures, which were controlled with carbamazepine, and difficulty with short-term memory. CONCLUSIONS: The aggressive use of hemodialysis in conjunction with intravenous sodium phenylacetate, sodium benzoate, and arginine hydrochloride therapy may allow survival in patients after solid-organ transplantation. An acute acquired derangement in extra-central nervous system glutamine metabolism may play a role in the production of hyperammonemia in this illness that resembles reye syndrome, and, as in other hyperammonemic disorders, the duration and degree of elevation of brain glutamine levels may be the important determining factors in responsiveness to therapy.
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3/78. Right median nerve electrical stimulation to hasten awakening from coma.

    Electrical stimulation of the right median nerve may hasten the awakening of closed head injured, comatose patients. A series of 25 comatose patients have been treated. These patients made better recoveries than similar individuals reported in the literature. In a double-blind pilot project patients in the treated group scored better on interval glasgow coma scale scores, spent fewer days in the intensive care unit, and showed better Glasgow Outcome Scores at 1 month post-injury. Peripheral electrical stimulation of the right median nerve, through activation of the ascending reticular activating system, may be sufficient to arouse the moderate to severely comatose patient.
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4/78. 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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5/78. family intervention strategies when dealing with futility of treatment issues: a case study.

    As multidisciplinary medical team members, we are sometimes confronted by cases that frustrate us because they do not proceed well, and our desired outcome goal of healing and restoration cannot be achieved. A case like this may stay in our memories due to our regrets regarding the inability to intervene in a manner that is effective. The following case is an example of this. This case is one that challenges health care professionals to revisit our thinking regarding intervention strategies for families confronted with terminal illness. The case also allows us to examine how systemic issues within a health care organization can sometimes impede the goal of achieving the most optimal outcome for the patient and family.
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6/78. kearns-sayre syndrome presenting as 2-oxoadipic aciduria.

    A patient with 2-oxoadipic aciduria and 2-aminoadipic aciduria presented at 2 years of age with manifestations typical of organic acidemia, episodes of ketosis and acidosis, progressive to coma. This resolved and the key metabolites disappeared from the urine and blood. At 9 years of age she developed typical kearns-sayre syndrome with complete heart block, retinopathy, and ophthalmoplegia. Southern blot revealed a deletion in the mitochondrial genome.
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7/78. Adrenal crisis presenting as hypoglycemic coma.

    An 18-month-old male infant presented with hypoglycemic coma and clinical signs of bronchopneumonia. He was suspected of suffering from septic shock. The patient progressed to irreversible multiple organ failure before the diagnosis of adrenal crisis was established. plasma levels of ACTH and cortisol remained undetectable. renin and aldosterone were normal. An autopsy failed to demonstrate any adrenal gland cortical tissue. Immunohistochemical staining demonstrated the presence of all pituitary hormones except ACTH, establishing the diagnosis of isolated ACTH deficiency. intensive care clinicians should consider adrenal crisis in non-diabetic children with hypoglycemia and rapid circulatory deterioration.
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8/78. 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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9/78. Coma as an acute presentation of adrenoleukodystrophy.

    X-linked adrenoleukodystrophy is a metabolic disorder with broad clinical variations. A 4-year-old male admitted to the hospital with fever, hypotension, and coma as the presenting signs of adrenoleukodystrophy is reported. The initial presentation followed by rapidly developing disseminated intravascular coagulopathy and multiorgan failure suggested an initial diagnosis of septic shock. However, bronze skin pigmentation and a cranial computed tomography scan demonstrating posterior demyelination consistent with adrenoleukodystrophy led to the final diagnosis. The diagnosis was confirmed by the findings of elevated very-long-chain fatty acid levels and an elevated C24/C16 ratio in plasma and fibroblast cultures. Atypical presentations of the disease require a high index of suspicion to initiate treatment before the appearance of irreversible sequelae.
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10/78. guillain-barre syndrome occurring in two women after ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus.

    We report two women who presented with a guillain-barre syndrome just after a ketoacidosic comatose state disclosing an insulin-dependent diabetes mellitus. One had characteristic clinical signs and the other had major motor involvement. At neurophysiologic investigations, one had typical demyelinating neuropathy whereas the second had mainly axonal degeneration. At ultrastructural examination of a peripheral nerve biopsy, features of macrophage-associated demyelination were present in both nerve specimens, thus confirming the diagnosis of acute inflammatory demyelinating polyneuropathy, i.e., guillain-barre syndrome. Prominent axonal involvement was also present in the motor nerves of the second patient. insulin therapy had to be permanently continued and these two cases are quite different from the transient diabetes sometimes observed in certain cases of guillain-barre syndrome. Both the latter and insulin-dependent diabetes mellitus probably have auto-immune mechanisms. It is likely that in our two patients both auto-immune diseases were triggered by a common event. Such cases of guillain-barre syndrome have to be distinguished from other acute diabetic neuropathies.
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