Cases reported "Coma"

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1/14. 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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2/14. Isolated medulla oblongata function after severe traumatic brain injury.

    The objective was to report the first pathologically confirmed case of partly functionally preserved medulla oblongata in a patient with catastrophic traumatic brain injury.A patient is described with epidural haematoma with normal breathing and blood pressure and a retained coughing reflex brought on only by catheter suctioning of the carina. Multiple contusions in the thalami and pons were found but the medulla oblongata was spared at necropsy. In conclusion, medulla oblongata function may persist despite rostrocaudal deterioration. This comatose state ("medulla man") closely mimics brain death.
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3/14. Management of unexplained coma in children.

    coma in children is uncommon and can pose difficulties in diagnosis and management. resuscitation should concentrate on management of the airway, breathing and circulation and on rapid exclusion of easily correctable conditions, e.g. hypoglycaemia. Common causes of coma are considered and the diagnostic evaluation of these children is discussed. A case of a toddler in coma is discussed from the perspective of the accident and emergency department to illustrate the management of these challenging but uncommon patients.
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4/14. pyridoxine-dependent seizures responding to extremely low-dose pyridoxine.

    We report on a male infant with pyridoxine dependency and seizures from birth, controlled with pharmacological doses of pyridoxine at 4 months of age. seizures stopped between 30 and 80 days of age when very-low doses of pyridoxine were given in a multivitamin supplement. Daily dose was 0.5 mg that corresponded to 0.08 to 0.16 mg/kg/day when weight gain is considered. In previous reports doses have ranged from 0.2 to 30 mg/kg/day. Another distinctive feature was that this infant went into a coma and developed hypotonia and irregular breathing when pyridoxine was given by enteral tube which has usually been reported when the vitamin is given intravenously. Use of low doses of pyridoxine in multivitamin supplements could be a confounding factor for early diagnosis and appropriate treatment of pyridoxine-dependent seizures.
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5/14. Myxoedema coma.

    Myxoedema coma is a medical emergency, which must be treated immediately. Otherwise the mortality is high. It is important to administer L-triiodothyronine and corticosteroids early. If hypoventilation occurs, artificial respiration may be necessary. In the two cases of described here the outcome was successful, probably owing to quick substitution. The causes of myxoedema and the symptomatology are discussed.
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6/14. methemoglobinemia as a cause of coma.

    A 50-year-old man presented to the emergency department in a coma with fixed and dilated pupils. skin and mucous membranes were noted to be an ashen grey color. Initial vital signs were blood pressure of 104/70 mm Hg; pulse, 110; and respirations, 12. Initial arterial blood gases were pH of 7.25; PaCO2, 26.6 mm Hg; PaO2, 22.1 mm Hg; oxygen saturation, 15.2%; and methemoglobin level, 81.5%. Venous and arterial blood samples were chocolate brown, and it was noted that the color did not change when 100% oxygen was bubbled through the blood. methylene blue 140 mg was given intravenously, and the patient gradually became more responsive. He was discharged three days later with no neurologic deficits. A comprehensive literature search revealed no reported cases of complete patient recovery with this high a methemoglobin level.
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7/14. The complete apallic syndrome--a case report.

    In six patients with apallic syndrome the EEG was isoelectric, although the patients were breathing spontaneously and vegetative functions remained stable for a long period of time. No cortical somatosensory evoked potentials could be recorded in four of the patients examined. Cranial CT performed in three patients revealed extensive hypodensity of the cortex, whereas the brain stem showed no major damage. This syndrome is labelled a "complete apallic syndrome". None of our patients, and none of the 23 patients described in the literature, recovered.
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keywords = breathing
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8/14. A delayed drowning death with histological findings of shock.

    A delayed drowning death case with histological findings of shock was described. The person was sustained by continuous positive-pressure respiration and died 2 days after resuscitation from drowning. The histological findings were intravascular microthrombi, hyaline bodies and fibrin thrombi in the brain, multiple megakaryocytes in the pulmonary capillaries, hyaline membranes of the lung, multiple small hyaline bodies in the liver sinusoids, and erosion of the mucous membrane of the stomach as well as histological findings of shock kidney. drowning and systemic hypotension during resuscitation seemed to cause irreversible oxygen debt of the organs and the tissues to lead to shock.
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9/14. Aspiration pneumonia and coma--an unusual presentation of dystrophic myotonia.

    A 30-year-old female patient presented in a comatose state with clinical and radiographic signs of aspiration pneumonia 16 hours following elective surgery. Subsequent clinical assessment and investigations revealed the characteristic facies, proximal muscle weakness, lenticular opacities, pulmonary function defects, arterial desaturation and abnormal breathing during rapid eye movement (REM) sleep often associated with myotonia dystrophica. Although these characteristic features were evident on clinical examination postoperatively they were not noted in the preoperative assessment. The aspiration pneumonia and coma were unusual presenting features of this disease. Unsuspected myotonia dystrophica should be considered in the differential diagnosis of unexplained respiratory depression, aspiration or comatose state following surgery. Recognition of the disorder during the preoperative assessment is the key to avoiding complications during the perioperative management of such patients.
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keywords = breathing
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10/14. Neocortical death in infants: behavioral, neurologic, and electroencephalographic characteristics.

    Neocortical death is a form of the persistent vegetative state characterized by the maintenance of sleep/wakeful cycles and spontaneous respirations and the lack of cognitive function. It is difficult to diagnose in neonates and young infants because their cognitive skills are limited by inexperience and by immaturity of the central nervous system. Because neocortical death has not been described previously for this age group, we report the neurologic, behavioral, electroencephalographic, and computed tomographic characteristics of three infants who survived in the persistent vegetative state following severe brain injury. Each infant appeared to exhibit some complex behaviors, including interaction with the environment and the examiners, although the electroencephalograms documented no electrical activity of cerebral origin. Computed tomography revealed extensive destruction of the cerebral hemispheres. Infants and newborns with a history suggesting brain injury and with the neurologic and behavioral characteristics described here should be evaluated with serial electroencephalograms and computed tomography to diagnose the syndrome of neocortical death.
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