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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The water and electrolyte status was studied in 26 children with acute asthma, 8 of whom required hospital admission. Patients were evaluated before therapy, during hospital management, and at least 10 days after symptoms had subsided. Laboratory evaluation included serum electrolytes, BUN, sOsmo, urinalysis, and uOsmo. Data were analyzed for the manifestations of SI-ADH. Mild serum hyposmolarity was noted initially in only two patients and during the hospital stay in one patient for a short time, but none of the patients fulfilled the criteria of SIADH. At the time of presentation at the emergency room, none of the 26 patients had clinical signs of dehydration, yet some degree of hypertonicity seemed to be present in most patients. This study shows that children with acute asthma are ordinarily not at high risk of SIADH and fluid therapy should be included in the management. Nevertheless, because such patients may be at risk of pulmonary edema, vigorous fluid administration should be discouraged, except to correct dehydration.
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PMID:Water and electrolyte status in children with acute asthma. 673 70

We report two cases with complex partial and secondarily generalized seizures, both on oxcarbazepine and vigabatrin, with additional lamotrigine in one case. Both died in a manner resembling SUDEP, i.e. suddenly, unexpectedly, probably following a seizure with pulmonary oedema at autopsy. Both had SIADH. A number of drugs may cause SIADH, among them carbamazepine and oxcarbazepine. A search for SIADH in patients on carbamazepine and oxcarbazepine, and in cases of sudden death in epilepsy, is recommended.
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PMID:Sudden death in two patients with epilepsy and the syndrome of inappropriate antidiuretic hormone secretion (SIADH). 980 22

Hyponatraemia is the most common electrolyte imbalance in neurosurgical patients. Acute hyponatraemia is particularly common in neurosurgical patients after any type of brain insult, including brain tumours and their treatment, pituitary surgery, subarachnoid haemorrhage or traumatic brain injury. Acute hyponatraemia is an emergency condition, as it leads to cerebral oedema due to passive osmotic movement of water from the hypotonic plasma to the relatively hypertonic brain which ultimately is the cause of the symptoms associated with hyponatraemia. These include decreased level of consciousness, seizures, non-cardiogenic pulmonary oedema or transtentorial brain herniation. Prompt treatment is mandatory to prevent such complications, minimize permanent brain damage and therefore permit rapid recovery after brain insult. The infusion of 3% hypertonic saline is the treatment of choice with different rates of administration based on the severity of symptoms and the rate of drop in plasma sodium concentration. The pathophysiology of hyponatraemia in neurotrauma is multifactorial; although the syndrome of inappropriate antidiuresis (SIADH) and central adrenal insufficiency are the commonest causes encountered. Fluid restriction has historically been the classical treatment for SIADH, although it is relatively contraindicated in some neurosurgical patients such as those with subarachnoid haemorrhage. Furthermore, many cases admitted have acute onset hyponatraemia, who require hypertonic saline infusion. The recently developed vasopressin receptor 2 antagonist class of drug is a promising and effective tool but more evidence is needed in neurosurgical patients. Central adrenal insufficiency may also cause acute hyponatraemia in neurosurgical patients; this responds clinically and biochemically to hydrocortisone. The rare cerebral salt wasting syndrome is treated with large volume normal saline infusion. In this review, we summarize the current evidence based on the clinical presentation, causes and treatment of different types of hyponatraemia in neurosurgical patients.
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PMID:Diagnosis and treatment of hyponatraemia in neurosurgical patients. 2696 74