Cases reported "Coma"

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1/45. Acute adrenal insufficiency during pregnancy and puerperium: case report and literature review.

    Acute adrenal dysfunction during pregnancy is rare. Nevertheless, adrenal insufficiency can present as an adrenal crisis, and may be life threatening. There is a wide range of clinical symptoms and signs, and the differential diagnosis is challenging. A full adrenal and pituitary evaluation, both structural and hormonal, must be performed to reach the correct diagnosis, and appropriate treatment must not be delayed. A case is presented of acute adrenal insufficiency that occurred 24 hours after a cesarean delivery. The initial symptoms included hypoglycemic seizures and coma. The workup, both hormonal and structural, revealed isolated adrenocorticotrophic hormone deficiency. This considers this case and reviews the differential diagnosis, diagnostic workup, and the treatment of adrenal dysfunction in pregnancy and the puerperium, as well as the obstetric outcome in women suffering from this disorder. TARGET AUDIENCE: Obstetricians & Gynecologists, family physicians. learning OBJECTIVES: After completion of this article, the reader will be able to understand the various presentations of hypopituitarism, the various etiologies of this condition, and the appropriate work up and management of a patient with hypopituitarism.
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2/45. 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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3/45. 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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4/45. A case of neonatal-onset carbamoyl-phosphate synthase I deficiency treated by continuous haemodiafiltration.

    This is the first case of fulminant neonatal-onset carbamoyl-phosphate synthase I deficiency treated by continuous hemodiafiltration indicating that this is an available and effective procedure for neonates with hyperammonemic coma.
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5/45. Postoperative coma in a child with carnitine palmitoyltransferase I deficiency.

    IMPLICATIONS: We describe prolonged drowsiness proceeding to hepatic encephalopathy in a child with sickle cell trait and carnitine palmitoyltransferase deficiency. The latter defect of fatty acid metabolism is associated with striated muscle dysfunction and hepatic failure.
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6/45. Type II (adult onset) citrullinaemia: clinical pictures and the therapeutic effect of liver transplantation.

    OBJECTIVE: adult onset type II citrullinemia is an inherited disorder of amino acid metabolism caused by a deficiency of liver specific argininosuccinate synthetase activity. Most of the patients with this disease were reported in japan and therefore, this disease has not been well recognised outside this country. The detailed clinical pictures of the patients with type II citrullinaemia are reported and their outcomes after liver transplantation referred to. methods: Ten patients with this disease were evaluated. Seven of them underwent liver transplants using a graft obtained from a healthy family member. RESULTS: There were six men and four women; the age of onset of encephalopathy ranged from 17 to 51 years. The initial symptom in nine patients was sudden onset disturbance of consciousness, and one patient had long been regarded as having a chronic progressive psychotic illness. High concentrations of plasma citrulline and ammonia were commonly seen on admission. Although brain CT or MRI lacked any consistent findings, the EEG was abnormal in all patients, showing diffuse slow waves. Additionally, in five patients chronic pancreatitis preceded the onset of encephalopathy. After liver transplantation the metabolic abnormalities, including abnormal plasma concentrations of citrulline and ammonia, were immediately corrected and all neuropsychic symptoms soon disappeared, except for impaired cognitive function in one patient. Six out of these seven patients returned to their previous social lives, including work. CONCLUSIONS: The clinical concept of adult onset type II citrullinaemia coincides well with the range of hepatic encephalopathy, and liver transplantation is a very promising therapeutic approach.
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7/45. nature and nurture in vitamin B12 deficiency.

    We report on a child in whom severe nutritional vitamin B12 deficiency was exacerbated by a genetic impairment of the folate cycle, causing reduced CSF concentrations of the methyl group donor 5-methyltetrahydrofolate. Some patients with vitamin B12 deficiency may benefit from high dose folic acid supplementation, even if plasma concentrations are high.
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keywords = deficiency
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8/45. Reversible coma caused by risperidone-ritonavir interaction.

    Medications that act on the central nervous system are frequently used in people infected with human immunodeficiency virus (hiv). Actually, drug interactions are an important factor in the treatment of patients with (hiv) infection and because of the complexity of the current drug regimens, clinicians should be trained in order to recognize and manage drug interactions. Herein, we present an hiv infected male admitted for manic behavior and treated with risperidone who developed a profound coma secondary to increased levels of risperidone because of a possible drug interaction with ritonavir and indinavir. Subsequently, we discuss this interaction, rarely described in the literature. risperidone is a cytochrome P450 (CYP2D6) enzyme substrate and weak inhibitor and a CYP3A4 substrate. Possible interactions with CYP2D6 inhibitors (amiodarone, fluoxetine or ritonavir) and CYP3A4 inhibitors (indinavir and ritonavir) can increase its serum concentrations and produce significant adverse effects. In conclusion, this drug combination should be administered with caution and routinely examined for signs and symptoms of risperidone toxicity. Dosages should be reduced as needed. Finally, we think that in patients taking multiple medications, plasma levels of risperidone should be monitored especially if drug interactions are possible.
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9/45. Late-onset presentation of ornithine transcarbamylase deficiency in a young woman with hyperammonemic coma.

    ornithine transcarbamylase deficiency (OTCD) is an X-linked inherited disease and the most common inborn error in urea synthesis in human patients. In adult heterozygous patients, OTCD can be responsible for life-threatening hyperammonemic coma. We report the case of a 32-year-old woman admitted to our hospital with seizures after a recent high protein load. Her parents related a history of recurrent episodes of vomiting, meat refusal, lethargy, and convulsions since childhood, and measurement of plasma ammonemia levels was the key to early diagnosis of OTCD. We report the pathophysiologic characteristics, clinical features, clinical course, and differential diagnosis of OTCD and discuss the therapeutic options, including continuous venovenous hemodiafiltration and pharmacologic therapy for reduction of plasma ammonemia levels. A diagnosis of OTCD should be considered in adult nonhepatic patients with hyperammonemic coma, particularly if they have a history of protein avoidance and neurologic symptoms. Early recognition and appropriate treatment are critical to avoid severe brain damage and death.
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ranking = 32621.197932966
keywords = ornithine transcarbamylase deficiency, transcarbamylase deficiency, ornithine transcarbamylase, transcarbamylase, ornithine, deficiency
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10/45. A young woman with persistent hypoglycemia, rhabdomyolysis, and coma: recognizing fatty acid oxidation defects in adults.

    OBJECTIVE: To describe an acutely decompensated adult patient with very-long-chain acyl-coenzyme a dehydrogenase (VLCAD) deficiency. DESIGN: Case report. SETTING: Medical intensive care unit of the University Hospital Hamburg-Eppendorf, germany. PATIENT: A 32-yr-old female comatose patient with persistent hypoglycemia, rhabdomyolysis, and acute cardiomyopathy after a prolonged history of recurrent muscular weakness. INTERVENTIONS AND MEASUREMENTS: Treatment in the intensive care unit for 20 days. The combination of symptoms led to the detection of increased dicarboxylic acids in her urine and an abnormal profile of acylcarnitines in her blood. In cultured fibroblasts, the oxidation of palmitate, measured as the production of acetylcarnitine, was reduced. Direct measurement of VLCAD activity proved to be 30% of normal. dna analysis showed two different mutations in the VLCAD gene of the patient. RESULTS: The patient fully recovered. CONCLUSIONS: Genetic defects of fatty acid oxidation should be suspected, even in previously healthy adults, when typical symptoms such as nonketotic hypoglycemia, rhabdomyolysis, cardiomyopathy, or unexplained organ steatosis point to such a disorder of energy metabolism.
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