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1/9. Nonketotic hyperglycemic hyperosmolar coma. Report of neurosurgical cases with a review of mechanisms and treatment.

    Seventy-eight critically ill patients who died while on the neurosurgical service were studied retrospectively to establish the prevalence of nonketotic hyperglycemic hyperosmolar coma (NHHC). All the patients had been comatose before death, and all underwent necropsy. Criteria for the diagnosis of NHHC included moderate-to-severe hyperglycemia with glucosuria, absence of significant acetonuria, hyperosmolarity with dehydration, and neurological dysfunction. This study revealed seven cases of unequivocal NHHC (9%), and six of hyperosmolarity but with incomplete records. Five of the seven confirmed cases of NHHC demonstrated no evidence of cerebral edema transtentorial herniation, or brain-stem damage, and showed central nervous system (CNS) lesions compatible with survival. Fatal complications of this syndrome, such as acute renal failure, terminal arrhythmias, and vascular accidents, both cerebral and systemic, were common in this series. The mechanism of coma in NHHC is believed related to shifts of free water from the cerebral extravascular space to the hypertonic intravascular space, with subsequent intracellular dehydration, accumulation of metabolic products of glucose, and brain shrinkage. It is uncertain whether injury to specific areas in the CNS is a predisposing factor to the development of NHHC. Factors documented to be significant in its development include nonspecific stress to primary illnesses, hyperosmolar tube feedings, dehydration, diabetes and mannitol, Dilantin, or steroid administration.
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2/9. Relationship of eye burns with calcifications of the cornea?

    INTRODUCTION: The clinical pattern of corneal calcification has been considered to be a part of chronic eye diseases, such as uveitis, severe glaucoma, keratitis and eye burns. Since, in some cases of eye burns, we have found corneal calcifications to be related to the initial calciferous caustic agents and to the use of phosphate-buffer-containing fluids, we have reviewed our files of clinical eye burns for the incidence and appearance of corneal calcification. methods: A total of 176 burnt eyes of 98 patients suffering from severe eye burns were retrospectively reviewed. The following data set was acquired: the type of caustic agent, the time of the burns, the delay and type of immediate treatment and the time and type of first aid, the subsequent medication, the clinical grading and the later results. RESULTS: Calciferous burning agents and corneal calcification are correlated (P<0.01). Initial single rinsing with phosphate does not produce corneal calcification (P=0.134). There is evidence that corneal calcifications are correlated with chronically administered phosphate-buffered eye drops (P<0.005). DISCUSSION: eye burns followed by calcifications follow two different major patterns: the corrosive substance contained calcium or the continued therapy was applied with phosphate-buffered eye drops. We present case reports of three different types of eye burns and later therapy resulting in corneal calcification. Corneal calcifications are presumably related to longer-lasting phosphate application. One suspicious mechanism is the low content of calcium ion stabilizing proteins such as hyaluronate or fetuin in treatments for severe eye burns. The exceeding of the solubility product of Ca(2 ) and PO(4) (-) results in the precipitation of calcium phosphates. In cases of chronic corneal disturbance, we recommend the elimination of phosphate-buffered medications to prevent corneal calcification.
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3/9. The use of continuous hemodiafiltration in a patient with diabetic ketoacidosis.

    A variety of fatal complications are associated with diabetes mellitus. Among these, diabetic ketoacidosis (DKA) figures largely in fatalities in young diabetics. Although hyperosmotic diuresis in DKA causes extreme fluid loss, acute renal failure is less common than expected in DKA. We treated a case of severe DKA with associated coma, acute respiratory failure, and acute renal failure in a 24-year-old man who had been diagnosed with type 1 diabetes mellitus at age 19. The comatose patient had been intubated before transfer to our hospital for intensive care. Despite infusion with isotonic saline and insulin, metabolic acidosis was refractory. On day 2, urine output decreased and pulmonary congestion developed, so we started continuous veno-venous hemodiafiltration (CVVHDF), which was effective against the metabolic acidosis; urine output increased gradually. CVVHDF was withdrawn on day 7, and the patient's renal function recovered completely. He was discharged from the intensive care unit (ICU) on day 14.
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ranking = 0.28571428571429
keywords = coma
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4/9. Acute metabolic crisis induced by vaccination in seven Chinese patients.

    Seven Chinese patients (5 males and 2 females) with vaccination-induced acute metabolic crisis were reported. Only one male with 21-hydroxylase deficiency had been diagnosed before vaccination. In the remaining six patients, the preexisting diagnoses were not confirmed before the vaccination. Acute metabolic crisis occurred in seven patients between 3 and 12 hours after the administration of Japanese encephalitis, diphtheria, and tetanus toxoids and acellular pertussis, hepatitis b, or measles vaccines. patients 1 and 2 displayed acute adrenal insufficiencies at the ages of 5 years and 3 months, respectively. Patient 3 had presented with mild motor retardation previously. patients 4 to 7 were previously healthy, but suffered from fever, seizures, coma, acidosis, and hypoglycemia after being vaccinated. Glutaric aciduria type 1 was evident in case 4. Leigh syndromes were present in patients 5, 6, and 7. They all died from respiratory failure before 2 years of age. Symmetric foci, cystic cavitations with neuronal loss, and vascular proliferation were observed by postmortem examination. Among the seven patients, although the vaccines were not the primary cause of the acute metabolic crisis, the severe acute episodes occurred coincidentally.
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ranking = 0.14285714285714
keywords = coma
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5/9. Hyperosmolar coma treated with intravenous sterile water. A study of three cases.

    Three patients with hyperosmolar coma were treated with intravenous isotonic saline, dextrose, and hypotonic saline solutions. The development of pulmonary edema and increasing hypernatremia precluded the further use of sodium solutions, and the presence of severe hyperglycemia made the further use of dextrose solutions undesirable. To provide further solute-free fluid, intravenous sterile water was administered through a central venous catheter. The hyperosmolar state improved, and all patients survived without biochemical evidence of hemolysis or clinical evidence of cerebral edema.
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keywords = coma
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6/9. Electrolyte abnormalities in lymphosarcoma after chemotherapy.

    A 12-year-old female with lymphosarcoma responding to treatment including vincristine and cyclophosphamide developed clinical and laboratory findings compatible with the syndrome of inappropriate secretion of antidiuretic hormone. Some additional findings were observed, i.e. uremia, hypopotassemia and alkalosis, that have not so far been recorded in that syndrome. All abnormalities were corrected upon water restriction. A similar episode occurred after a 2nd drug course. It too was corrected upon water restriction. The patient was clinically free from her malignancy in both episodes. It is suggested that our child had probably an expanded form of the syndrome of inappropriate secretion of antidiuretic hormone.
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ranking = 0.71428571428571
keywords = coma
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7/9. ethylene glycol poisoning: diagnosis based on high osmolal and anion gaps and crystalluria.

    We report a case of ethylene glycol poisoning in a 54-year-old man found comatose on the street. No history was available. The diagnosis was based on the findings of a high anion gap metabolic acidosis, a high osmolal gap, and the presence of oxalate and hippurate crystals in the urine. The diagnosis was confirmed later by an ethylene glycol level of 775 mg/dl. This case illustrates how these parameters can be used in the emergency department for rapid diagnosis and management.
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ranking = 0.14285714285714
keywords = coma
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8/9. The post-transurethral resection of prostate syndrome: therapeutic proposals.

    absorption of large volumes of irrigation fluid during transurethral resection of the prostate (TURP) can produce hyponatremia, coma, blindness, and cardiorespiratory depression. This has been termed the "post-TURP syndrome." The pathophysiology and management of this syndrome are controversial. A case of severe post-TURP syndrome due to the absorption of hypotonic glycine irrigant is reported. This patient developed severe hyponatremia, slight hypo-osmolality, hyperglycinemia, hyperserinemia, hyperammonemia, and hypocalcemia. He became comatose, profoundly hypotensive, bradycardic, and transiently blind. Because of this combination of severe biochemical, neurologic, and hemodynamic abnormalities, we elected to treat this patient with hemodialysis. The biochemical and clinical manifestations resolved completely. The pathophysiology and treatment of this disorder are discussed and a role for hemodialysis is suggested.
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ranking = 0.28571428571429
keywords = coma
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9/9. rhabdomyolysis due to hyperosmolarity leading to acute renal failure.

    Authors present the case of a 37-year-old man admitted to the emergency room of Universidade Federal de Sao Paulo-Escola Paulista de Medicina, with hyperosmolar coma, following progressive muscle discomfort and loss of renal function, with further need of dialysis therapy. Initial laboratory evaluation showed marked hyperglycemia, hypernatremia, hyperosmolarity, and high levels of creatinine. In the evolution he presented an elevation of creatino-phosphokinase levels in parallel with increasing levels of urea and creatinine. Urinalyses showed progressive increase in proteinuria and hematuria. A muscle biopsy was performed and confirmed the presence of muscular necrosis. The purpose of this paper is to emphasize hyperosmolarity as a newly described cause of rhabdomyolysis. The authors point out its multifactorial physiopathology and also stress the relatively common occurrence of acute renal failure (ARF) following an episode of rhabdomyolysis, and the poor prognosis that this complication represents.
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ranking = 0.14285714285714
keywords = coma
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