Hyponatremia acute

Unless severe central nervous system symptoms of acute hyponatremia persist after this level of correction (rarely encountered)... 

Amiry-Moghaddam M, Xue R, Haug FM, Neely JD, Bhardwaj A, Agre P, Adams ME, Froehner SC, Mori S, Ottersen OP (2004) Alpha-syntrophin deletion removes the perivascular but not endotheUeil pool of aquaporin-4 at the blood-brain barrier and delays the development of brain edema in an experimenUil model of acute hyponatremia. FASEB J 18 542-544 Anderson CM, Nedeigaard M (2003) Astrocyte-mediated control of cerebral microcirculation. Trends Neurosci 26 340-345... 

Improper proportioning of dialysate, due to either human or mechanical error, is still an important cause of neurological abnormality in dialysis patients (Bleumle, 1968). The usual effect of such dialysate abnormalities is the production of either hypo- or hypernatremia. Both of these abnormalities of body fluid osmolality can lead to seizures and coma, although different mechanisms are involved. In acute hypernatremia, there will be excessive thirst, lethargy, irritability, seizures, and coma, with spasticity and muscle rigidity. In acute hyponatremia there is weakness, fatigue, and dulled sensorium, which may also progress to seizures and coma,... 

A 24-year-old woman with a subependymoma in the fourth ventricle was given conivaptan 25 mg for acute hyponatremia her serum sodium increased by 16 mmol/1 over 8.5 hours without any deterioration in symptoms. 

Special risk Use with caution in the presence of cardiac disease, particularly in digitalized patients or in the presence of renal disease, metabolic acidosis, Addison disease, acute dehydration, prolonged or severe diarrhea, familial periodic paralysis, hypoadrenalism, hyperkalemia, hyponatremia, and myotonia congenita. 

Renal effects Acute renal insufficiency, interstitial nephritis with hematuria, nephrotic syndrome, proteinuria, hyperkalemia, hyponatremia, renal papillary necrosis, and other renal medullary changes may occur. 

Enuresis 10-40 ag qhs/bid Headache nausea Hyponatremia and water intoxication at toxic doses Can be useful for acute situations (e.g., sleepaways) or as maintenance treatment DDAVP 0.1, 0.2 mg t nasal spray 10 Hg/ spray... 

Case reports have indicated an association between SSRIs and the syndrome of inappropriate secretion of antidiuretic hormone. Symptoms include lethargy, headache, hyponatremia, increased urinary sodium excretion, and hyperosmotic urine. Acute treatment of this syndrome should consist of discontinuation of the drug as well as restriction of fluid intake. Patients experiencing severe confusion, convulsions, or coma should receive intravenous sodium chloride. Elderly persons may he at a higher risk for developing this syndrome. 

A group of nonpeptide antagonists of vasopressin receptors is being investigated for use in patients with hyponatremia or acute heart failure, which is often associated with elevated concentrations of vasopressin. Conivaptan has high affinity for both Vla and V2 receptors. Tolvaptan has a 30-fold higher affinity for V2 than for Vi receptors. In several clinical trials,... 

A 36-year-old woman who had undergone a standard course of gonadotrophin treatment for infertility developed severe pelvic pain and hyponatremia. She had a family history of porphyria and it was thought that the treatment had fired an acute attack of the condition. 

In an unusual case reported in detail from Saudi Arabia, a 28-year-old woman receiving gonadotropins developed acute respiratory distress, abdominal pain, and severe hyponatremia associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) (19). A multiple pregnancy nevertheless resulted and three fetuses went to term successfully. 

Hyponatremia, a condition wherein serum sodium concentration is < 135 mmol/L, is the most common electrolyte imbalance among hospitalized patients, occurring in up to 15% of in-patients.1,2 In addition to being a potentially life-threatening condition, hyponatremia is an independent predictor of adverse outcomes among patients with heart failure,3,4 acute ST-elevation myocardial infarction,5 and cirrhosis.6... 

Acute renal insufficiency has been reported as a severe complication of neuroleptic malignant syndrome (SED-13, 124) (SEDA-21, 49), and a patient who developed severe hyponatremia and progressed to neuroleptic malignant syndrome, myoglobinuria, and acute renal insufficiency deserves attention (355). 

Elizalde-Sciavolino C, Racco A, Proscia-Lieto T, Kleiner M. Severe hyponatremia, neuroleptic malignant syndrome, rhabdomyolysis and acute renal failure a case report. Mt Sinai J Med 1998 65(4) 284-8. 

The authors thought that this was the first report of acute transient proximal tubular injury with ecstasy. In contrast to SIADH, there was a high urine output in the presence of hyponatremia and solute diuresis. 

Ruby RJ, Burton JR (1977). Acute reversible hemiparesis and hyponatremia. Lancet i 1212 Sabolek M, Bachus-Banaschak K, Bachus R et al. (2005). Multiple cerebral aneurysms as delayed complication of left cardiac myxoma a case report and review. Acta Neurology Scandinavica 111 345-350 Sacco RL, Kargman DE, Gu Q et al. (1995). Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction. The Northern Manhattan Stroke Study. Stroke 26 14-20 Salgado AV (1991). Central nervous system complications of infective endocarditis. 

In contrast, published case reports and case series have provided more insight into the potential nephrotoxicity associated with COX-2-selective inhibitors. Taken together, these case reports suggest that COX-2 inhibitors, like non-selective NSAIDs, produce similar and consistent renal adverse effects in patients with one or more risk factors that induce prostaglandin-dependent renal function (that is patients with renal and cardiovascular disease and taking a number of culprit medications, such as diuretics and ACE inhibitors). Acute renal insufficiency, disturbances in volume status (edema, heart failure), metabolic acidosis, hyperkalemia, and hyponatremia have been commonly described. The duration of treatment with COX-2 inhibitors before the development of chnically recognized renal impairment ranged from a few days to 3-4 weeks. Withdrawal of COX-2 inhibitors and supportive therapy most often resulted in resolution of renal dysfunction, but in some patients hemodialysis was required (102,108-112). 

Acute renal insufficiency with severe hyponatremia has been attributed to vigorous diuretic treatment (metolazone, furosemide, spironolactone) with an ACE inhibitor (27). Because ACE inhibition impairs renal protection against reduced perfusion, the combination of an ACE inhibitor with high-dose furosemide causes a reduction in glomerular filtration rate linearly related to the change in blood pressure. 

Synergy between indometacin and cyclophosphamide has been advanced as the cause of a life-threatening acute water intoxication and severe hyponatremia observed in a patient with multiple myeloma and normal renal function (SEDA-15, 99). 

Four cases of acute renal insufficiency have been described in men aged 20-42 years who received mannitol 1172 (sd 439) g over 58 (sd 28) hours (7). The onset of acute renal insufficiency was detected 48 (sd 22) hours after the start of infusion. All the patients had dilutional hyponatremia (average 120 mmol/1) and serum hyper-osmolarity (osmolar gap 70 mosm/kg water). In the three anuric cases, in which hemodialysis was performed, there was immediate recovery of diuresis. This emphasizes the risk of renal insufficiency with mannitol and stresses the importance of early hemodialysis. Mannitol is dialysable and once its suppressive effect on renal perfusion is eliminated functional recovery is prompt. 

---