Cases reported "Hypernatremia"

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1/14. peritoneal dialysis in an infant with type 1 diabetes and hyperosmolar coma.

    Hyperosmolar coma which is characterized by severe hyperglycemia in absence of chetosis is very rare in pediatric age with only 11 cases reported in the literature. The outcome of the condition is usually poor with mental retardation being the most common event. Here a case of hyperosmolar coma is described in a female of three months of age who was treated with peritoneal dialysis 11 hours after admittance to hospital. This female patient has been receiving insulin from three months of age and today at the age of 10 years she leads a normal life despite being on insulin therapy. A very low level of c-peptide (<0.3 ng/ml) clearly confirms she is affected by Type 1 diabetes. To our knowledge this is the first case report of hyperosmolar coma in a neonate with Type 1 diabetes who survived this condition without late neurological consequences.
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2/14. Hypernatraemia induced by sodium polystyrene sulphonate (Kayexalate) in two extremely low birth weight newborns.

    Hyperkalaemia is a life-threatening electrolyte disorder that can occur in the first week of life in almost 50% of preterm infants with a birth weight less than 1000 g [extremely low birth weight (ELBW)]. serum potassium values higher than 7 mmol x l-1 are associated with cardiac arrhythmias and an increased incidence of intraventricular haemorrhage and periventricular leucomalacia. Therapeutic options to treat this dangerous imbalance comprise calcium gluconate, insulin plus glucose, albuterol/salbutamol inhalation. Administration of cation-exchange resin such as sodium polystyrene sulphonate (Kayexalate) is effective in lowering plasma potassium, although complications following oral or rectal administration are reported in newborns. We describe two ELBW infants affected by hyperkalaemia, treated with Kayexalate, who developed serious hypernatraemia, that has never been reported before in preterm infants.
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3/14. rhabdomyolysis associated with cranial diabetes insipidus.

    rhabdomyolysis has been reported to be associated with hyperosmolality in diabetic ketoacidosis and non-ketotic hyperosmolal state. Whether the rhabdomyolysis was due to hyperosmolality per se or whether hyperglycaemia also played a role is not clear. We hereby report a case of cranial diabetes insipidus with hypernatraemia and hyperosmolality complicated by rhabdomyolysis. None of the known risk factors, such as coma, hypokalaemia, hypophosphataemia, diabetic ketoacidosis or non-ketotic hyperosmolality, were present in this patient. We believe that severe hyperosmolality per se is an important predisposing factor for non-traumatic rhabdomyolysis, and serum muscle enzymes should be closely monitored in the management of patients with diabetes insipidus.
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4/14. Hyperosmolality due to antacid treatment.

    magnesium trisilicate mixture is an antacid used commonly in our intensive care Unit in the prevention and treatment of stress ulcers. In this case the administration of large doses over a period of time led to the development of massive hyperosmolality, cerebral dehydration and coma. Management with hypotonic fluid resulted in complete recovery.
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5/14. Lateral pontine and extrapontine myelinolysis associated with hypernatremia and hyperglycemia.

    Efforts to understand and prevent pontine and extrapontine myelinolysis have focused on the correction of hyponatremia, but controversy persists. We report a woman who presented in hyperosmolar diabetic coma with hypernatremia (169 mEq/l) and hyperglycemia (954 mg/dl). plasma sodium rapidly increased to 188 mEq/l before gradually returning to normal. She remained obtunded and died 21 days later. autopsy showed widespread, symmetrical demyelination involving the subcortical white matter, corpus callosum, anterior commissure, extreme, external, and internal capsules, fornix, thalamus, cerebellum, and lateral pons. The central pons and lateral geniculate nuclei were uninvolved. This case illustrates that lateral pontine and extrapontine myelinolysis can be associated with hypernatremia and hyperosmolality. In both hypo- and hypernatremic states, the significant event may be an increase in serum sodium or serum osmolality of sufficient rapidity and magnitude.
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6/14. indomethacin treatment in a patient with lithium-induced polyuria.

    lithium intoxication causes polyuria, central nervous system manifestations, and ultimately stupor progressing to coma. Moreover, polyuria leading to hypernatraemia itself can progress to convulsions and coma. We present a patient with lithium intoxication who remained polyuric, hypernatraemic and somnolent despite normal serum lithium concentrations. After institution of indomethacin orally, polyuria and hypernatraemia disappeared and patient regained consciousness.
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7/14. survival with severe hypernatremia.

    In a 74-year-old woman, excessive insensible water loss developed secondary to a period of hot, humid weather, associated with an underlying inability to obtain adequate water replacement. On admission to the hospital she was comatose, clinically dehydrated, and had laboratory values consistent with a water deficit of approximately 30% (9 L) of body water. serum sodium concentration was 202 mEq/L. serum osmolality was 430 mOsm/L. The patient remained comatose for seven days, during which time she was vigorously treated with fluids, and she gradually recovered. This case represents what we believe is a unique report in the literature of the severity of hypernatremia developing via this pathogenic mechanism and survival in an adult with this degree of disturbance of sodium and water homeostasis.
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8/14. Hypernatremic hemorrhagic encephalopathy.

    A 12-year-old juvenile diabetic was inadvertently given 500 ml of hypertonic saline intravenously. He developed hypernatremia, hyperosmolality, metabolic acidosis, and hyperglycemia. seizures and stupor ensued, followed by coma and death. Computerized cranial tomography revealed numerous small subcortical hemorrhages that were verified postmortem.
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9/14. Hyperosmolar non-ketotic coma in diabetic stroke patients.

    Hyperosmolar non-ketotic coma in diabetes is a life-threatening condition. We describe three patients, aged 59-67 years, who developed hyperosmolar coma during the first ten days after admission for stroke. Common to all three were normal plasma osmolality and slightly elevated plasma creatinine levels on admission, treatment with diuretics, parenteral dextrose administration before and low urinary glucose output during the coma. In the five days preceding the coma, total fluid deficits were 3.8, 6.5 and 9.4 1, respectively. In one patient the rate of glucose delivery had clearly exceeded utilization during adequate insulinization, in another a marked reduction in urinary glucose output preceded extreme hyperglycaemia and coma. Two of the three patients died, both from extensive thrombus formation in cerebral arteries and multiple emboli to the lungs. We conclude that enhanced endogenous glucose production and reduced renal clearance of glucose may contribute to precipitate hyperosmolar non-ketotic coma. A close monitoring of fluid and dextrose administration seems mandatory in diabetic stroke patients, in particular if renal function is impaired or if diuretics are given. insulin treatment should be considered in all diabetic patients during the first days after a stroke.
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10/14. Constant low-dose insulin infusion in severe diabetes mellitus.

    Eight patients with diabetic ketoacidosis and two patients with hyperosmolar non-ketotic coma have been treated with a constant low-dose insulin infusion technique (2-4 units/hour). In all cases a rapid, smooth control of blood glucose levels was obtained in conjunction with a similar improvement in clinical status and remedying of other biochemical defects. At no stage of therapy did hypoglycaemia or hypokalaemia occur. In the majority of cases control of the patient's metabolic state was achieved within eight to 12 hours. The insulin regime is simple to institute and maintain.
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