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PubMed1978

[Hyponatremia and hypoglycemia after treatment with chlorpropamide. Case histories with review of the literature on 18 cases of chlorpropamide induced hyponatremia].

A case of chlorpropamide-induced, symptomatic hyponatremia in a diabetic patient is reported. The hyponatremia was associated with loss of appetite, nausea, and vomiting. These symptoms caused reduced food intake which provoked severe hypoglycemia with disturbed consciousness. The hyponatremia developed when the chlorpropamide doses were increased from 400 to 600 mg/day. Withdrawal of chlorpropamide was followed by remission of hyponatremia. Chlorpropamide-induced hyponatremia is a rare complication and is due to an antidiuretic effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of adiuretin in the tubuli of the kidney. This case report and the analysis of 18 published cases in the literature show the following characteristics for chlorpropamide-induced hyponatremia: (1) Hyponatremia is a rare complication in the treatment of diabetics with chlorpropamide. The patients typically are female and over sixty. The dosage of chlorpropamide usually was 500 mg daily or even more. (2) Hyponatremia is often unrecognized for a long time because the symptoms are not specific. The characteristic symptoms include loss of appetite, nausea, vomiting, abdominal pain, confusional state and, rarely, convulsions and coma. Recovery occurs spontaneously after withdrawal of the drug. (3) The incidence of this type of hyponatremia is increased in cases of preexisting tendency to water retention such as heart failure and renal failure, and in cases of diuretic therapy. In the light of these findings, the authors believe that chlorpropamide is no longer a drug of choice in the treatment of diabetic women, especially in cases of preexisting tendency to water retention and in diuretic therapy. In such cases, a sulfonylurea without antidiuretic effect is to be preferred.

Adult↗
PubMed1994

Normal acid-base equilibrium in acute hyponatremia and mixed alkalosis in chronic hyponatremia induced by arginine vasopressin or 1-deamino-8-D-arginine vasopressin in rats.

The effects of acute and chronic water intoxication induced by the administration of oral water and arginine vasopressin (AVP) or 1-deamino-8-D-arginine-vasopressin (DDAVP) on blood acid-base equilibrium and aldosterone, corticosterone, and thyroxine secretion were studied in rats. Acute hyponatremia (3 hours) was associated with normal bicarbonate and blood acid-base equilibrium and a decrease in aldosterone and thyroxine concentrations, while corticosterone was increased. When similar levels of hyponatremia (serum sodium 110 mEq/L) were maintained for 24 or 72 hours, a normal serum bicarbonate concentration was observed, but blood acid-base equilibrium showed a mixed respiratory and metabolic alkalosis. Blood pH was negatively correlated with serum sodium concentration (R = -0.65; p < 0.001), as was the metabolic alkalosis (base excess; R = -0.64; p < 0.001) and the aldosterone concentration (R = -0.52; p < 0.01), while the PCO2 was positively correlated (R = +0.49; p < 0.01). Hyperaldosteronism was similar whether hyponatremia was induced with AVP or DDAVP and was observed even for mild hyponatremia. When hyponatremia was induced by a high water and salt intake (2.5% D-glucose, 0.45% NaCl; 15% body weight), aldosterone concentration was as high (about three times control values) as in rats with similar levels of hyponatremia but with a salt-free diet. The high salt intake was associated with a more severe metabolic alkalosis (base excess +5,5 mEq/L). In chronic hyponatremia, corticosterone and thyroxine values were normal. In hyponatremia related to syndrome of inappropriate secretion of antidiuretic hormone, the normal serum bicarbonate level is an expected observation; as in acute water intoxication, it stays normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

Neuropsychological manifestations of hyponatremia in chronic schizophrenic patients with the syndrome of psychosis, intermittent hyponatremia and polydipsia (PIP).

We examined the neuropsychological sequelae of water intoxication in nine schizophrenic patients with the syndrome of psychosis, intermittent hyponatremia and polydipsia (PIP). Patients were assessed using a standardized test battery on two occasions following laboratory blood work: once during hyponatremia (serum sodium < 130 mmol/l) and once during normonatremia (serum sodium > 136 mmol/l). Results revealed significant deficits during hyponatremia involving complex information processing skills such as mental flexibility and verbal fluency. In contrast, short-term memory was intact and no deficits in sustained attention or visual-motor scanning were observed. Our results underscore the dramatic fluctuations in neuropsychological functioning due to metabolic and osmotic changes during water loading in PIP syndrome patients. In addition, we found that the neuropsychological effects of hyponatremia are remarkably consistent across patients. These complications, if not recognized, are likely to contribute to worsening of psychosis despite appropriate pharmacological treatment while severely limiting patient ability to actively participate in behavioral interventions.

Adult↗
PubMed1997

Reduction of hyponatremia in a schizophrenic with polydipsia-hyponatremia syndrome by surgical intervention.

In a chronic schizophrenic with polydipsia-hyponatremia syndrome, we observed physiological data consecutively before and after a successful LAPIDES vesicostomy for his bladder retention. Although his polydipsia was unchanged, frequency of hyponatremia was significantly reduced after the operation. We found that bladder retention might be one of the factors relevant to the prediction of hyponatremia from diurnal weight gain.

Adult↗
PubMed2006

Hyponatremia in Kawasaki disease.

Although hyponatremia frequently occurs in Kawasaki disease (KD), the clinical characteristics of KD patients with hyponatremia and the pathogenesis of hyponatremia in KD remain unknown. The aims of this study were to define the clinical characteristics of KD patients with hyponatremia (serum sodium <135 mEq/l) and to determine the factors associated with its development. One hundred and fourteen patients with KD were included in this study. Fifty-one patients (44.7%) had hyponatremia. Coronary artery lesions and dehydration were significantly more common in patients with hyponatremia. The duration of fever was significantly longer in patients with hyponatremia. Pyuria and hematuria were present significantly more often in patients with hyponatremia. The serum concentrations of potassium, chloride and total cholesterol were significantly lower in patients with hyponatremia. Serum C-reactive protein and alanine aminotransferase were significantly higher in patients with hyponatremia. Some patients with pyuria and hyponatremia exhibited increased excretion of urinary tubular epithelial cells and urinary casts. There was no difference in the incidence of diarrhea between patients with hyponatremia and patients without hyponatremia. These results indicate that hyponatremia in KD occurs in patients exhibiting severe inflammation. Further studies will be necessary to confirm the pathogenic mechanisms of hyponatremia in patients with KD.

Child↗
PubMed2006

Hyponatremia after transsphenoidal surgery for hypothalamo-pituitary tumors.

Transient diabetes insipidus is a well-known complication after transsphenoidal surgery (TSS). On the other hand, transient hyponatremia has been reported as being a delayed complication of TSS. Transient hyponatremia has been attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but the details of hyponatremia have not been clarified. In the present study, we retrospectively reviewed 110 consecutive patients (39 males and 71 females, age 9-80 years) operated on transsphenoidally for pituitary and hypothalamic tumors. We investigated the frequency, time of onset, duration of hyponatremia after TSS, and analyzed possible factors associated with it. A postoperative sodium concentration <135 mEq/l was observed in 29 (26%) patients. Five patients were excluded from this study because their hyponatremia could be due to either overdose of desmopressin or SIADH for meningitis. Therefore, we investigated 24 (22%) patients with hyponatremia in this study. The sodium levels in the patients with hyponatremia ranged from 110 to 134, with a mean of 126.2 +/- 5.3 mEq/l. Hyponatremia was observed on average on postoperative day 9.5 +/- 2.4, the serum sodium levels normalized within 3.8 +/- 1.7 days. Hyponatremia occurred in patients with non-functioning pituitary adenoma (26%, 11/42), Rathke's cleft cyst (29%, 5/17), prolactinoma (31%, 4/13) and acromegaly (15%, 4/27). 18 patients (75%, 6/24) who developed hyponatremia had macrotumor (>10 mm), and 6 patients (25%, 6/24) had microtumor. The plasma arginine vasopressin (AVP) levels in the patients with hyponatremia ranged from 0.21 to 2.1, with a mean of 0.79 +/- 0.46 pg/ml, and the levels were inversely correlated with plasma osmolality (r = -0.80, p = 0.002). The urine to plasma osmolality ratios were >1. All the patients received appropriate hormonal replacement, including hydrocortisone. These data showed that postoperative hyponatremia after TSS was not rare, and the hyponatremia was mainly associated with SIADH. As the hyponatremia could be a life-threatening complication, all patients should be screened for serum electrolytes after TSS.

Adolescent↗
PubMed1990

Management of severe hyponatremia: rapid or slow correction?

Case reports and the literature on the treatment of severe hyponatremia were reviewed. It appeared that the conflicting opinions with respect to the rate of correction of severe hyponatremia could be reduced to not differentiating between acute and chronic hyponatremia, to using different criteria for this distinction, and to differences in treatment strategy. After reviewing the available data in the literature, it is suggested that hyponatremia should be classified as acute whenever the rate of decrease of serum sodium exceeds 0.5 mmol/L/hour. If it is unknown at which rate the hyponatremia has developed, it can be assumed to be acute if within a short period of time (two to three days), large quantities of fluid are ingested orally or administered parenterally, especially hypotonic fluids in the presence of impaired water excretion. In other cases, chronic hyponatremia is probable. It is concluded that acute hyponatremia should be treated without delay and rapidly at a rate of at least 1 mmol/L/hour, to prevent severe neurologic damage or death. With respect to chronic hyponatremia, it appeared that severe neurologic complications almost exclusively occurred in patients who were treated with hypertonic or isotonic saline without the addition of furosemide or an osmotic diuretic agent, resulting in a (rapid) correction rate of 0.5 mmol/L/hour or more. In contrast, patients with severe chronic hyponatremia treated with furosemide and isotonic or hypertonic saline almost uniformly did well after rapid correction. Uneventful recovery is also the rule when severe chronic hyponatremia is corrected slowly, at a rate less than 0.5 mmol/L/hour. On pathophysiologic grounds, and bearing in mind that slow correction was used in the majority of reported patients in the literature with severe chronic hyponatremia who recovered without neurologic complications, this treatment modality is preferable. Whenever the available data do not permit a differentiation between acute or chronic hyponatremia, rapid correction has to be pursued by means of administration of hypertonic or isotonic saline together with furosemide.

Acute Disease↗
PubMed2006

Patterns of ecstasy-associated hyponatremia in California.

STUDY OBJECTIVE: We describe the clinical characteristics of patients with ecstasy- (3,4-methylenedioxymethamphetamine [MDMA]) associated hyponatremia (serum sodium level <130 mmol/L) reported to the California Poison Control System during a 5-year period and determine whether a sex difference exists among patients with ecstasy-associated hyponatremia and hyponatremia-associated adverse outcomes. METHODS: We performed a retrospective review of cases involving ecstasy intoxication reported to the California Poison Control System and recorded in its computerized database from January 1, 2000, through October 9, 2005. We excluded cases that did not involve MDMA exposure or in which there were no symptoms or were minimal effects only. Confirmation of exposure to MDMA was based on history of use and, when available, urine toxicology testing results positive for MDMA or amphetamine derivatives. Hyponatremia was defined as a measured serum sodium level less than 130 mmol/L. RESULTS: A total of 1,436 cases potentially involving ecstasy were reported to the California Poison Control System during the 5-year study period, of which 891 were excluded according to the criteria described above. Of the 545 cases that met inclusion criteria, 296 (54.3%) were women and 249 (45.7%) were men. There were 188 cases (34.5%) with a documented serum sodium level, of which 73 (38.8%) reported hyponatremia (Na <130 mmol/L). Of the 73 subjects with hyponatremia, 55 (75.3%) were women and 18 (24.7%) men; of the 115 nonhyponatremic subjects, 50 (43.5%) were women and 65 (56.5%) were men. Among patients with a documented serum sodium level, female sex was associated with increased odds of hyponatremia (odds ratio [OR] 4.0; 95% confidence interval [CI] 2.1 to 7.6). Among women, those with hyponatremia demonstrated increased odds of coma (OR 3.9; 95% CI 1.2 to 12.9), whereas among men, no increased odds of hyponatremia-associated coma were observed (OR 0.8; 95% CI 0.15 to 4.0). CONCLUSION: Female sex was associated with increased odds of hyponatremia and increased odds of hyponatremia-associated coma among persons with ecstasy intoxication and a documented serum sodium level reported to the California Poison Control System from 2000 to 2005. Multiple potential confounders, including spectrum bias, incomplete laboratory data, and individual differences in study subject characteristics, prevent determination of causality about sex differences in the incidence of ecstasy-associated hyponatremia and its complications.

Adult↗
PubMed2000

High incidence of hyponatremia in patients with ruptured anterior communicating artery aneurysms.

We studied the incidence and timing of hyponatremia (Na < 135 mEq l-1) after subarachnoid hemorrhage (SAH) with special reference to ruptured anterior communicating artery (A-com) aneurysms. Hunt and Kosnik (HK) grading, symptomatic vasospasm in A-com aneurysm, and hydrocephalus were analyzed for connections to hyponatremia in 55 patients with ruptured A-com aneurysms, 65 with ruptured internal cerebral artery (ICA) aneurysms, and 49 with ruptured middle cerebral artery (MCA) aneurysms. Hyponatremia occurred in 28 (51%) of 55 patients with A-com aneurysms and in nine (18%) of 49 patients with MCA aneurysms. Severe hyponatremia (Na < 130 mEq l-1) occurred in 16 patients (29%) in the A-com group, four patients (6%) in the ICA group, and three patients (6%) in the MCA group. The A-com aneurysm group had a significantly higher incidence of mild hyponatremia (p < 0.01) and severe hyponatremia (p < 0.001) than other groups. Among A-com cases, hyponatremia occurred significantly more often in HK grade III and IV cases (p < 0.05), in cases with vasospasm (p < 0.001), and in cases with hydrocephalus (p < 0.01). Respective days of onset for symptomatic vasospasm and for hyponatremia were day 7.6 +/- 4.4 and day 10.6 +/- 5.8 following SAH, representing a 3-day delay for hyponatremia (p < 0.05). In most patients hyponatremia resolved within 28 days following SAH. Hyponatremia occurred more often with A-com aneurysms, possibly because of vasospasm around the A-com or hydrocephalus causing hypothalamic dysfunction. Since hypervolemic therapy can cause hyponatremia, particularly careful observation is required during such therapy in patients with A-com aneurysm.

Aneurysm, Ruptured↗
PubMed2006

Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage.

BACKGROUND: Hyponatremia develops in approximately a third of patients with aneurysmal subarachnoid hemorrhage (SAH). Studies have been conflicting about the association between hyponatremia and cerebrovascular spasm (CVS). AIMS: To investigate whether hyponatremia can signal the onset of CVS. SETTINGS AND DESIGN: Retrospective chart review of all patients with SAH treated at a tertiary-care university hospital from January to May 2002. MATERIALS AND METHODS: 106 patients were included in the study. Serum sodium levels were recorded from days 1 to 14 of hospitalization. Hyponatremia was defined as serum sodium level<135 meq/l and a fall in sodium level of >4 meq/l from the admission sodium level. The presence of CVS was determined by transcranial doppler sonography. Patients were assigned to one of four groups based on the presence or absence of CVS and hyponatremia. STATISTICAL ANALYSIS: Student's t-test was used for comparison of means. A logistical regression model was constructed and odds ratios (OR) were calculated. RESULTS: 41 patients developed hyponatremia and 44 developed CVS. Among the 41 with hyponatremia, 22 (54%) had evidence of CVS, whereas among the 65 patients without hyponatremia, 22 (34%) had evidence of CVS (P=0.023). Among those with hyponatremia, the mean sodium drop was 7.9 meq/L in those with CVS compared to 7.0 meq/L in those without CVS (P=0.068). More than half of those with hyponatremia and CVS (13/22) developed hyponatremia at least a day before CVS was diagnosed. CONCLUSION: In patients with SAH, hyponatremia is associated with a significantly greater risk of developing CVS and may precede CVS by at least one day.

Adolescent↗
PubMed2003

Validity of hospital discharge International Classification of Diseases (ICD) codes for identifying patients with hyponatremia.

Medical diagnosis can be studied using various sources of information, such as medical and hospital discharge records and laboratory measurements. These sources do not always concur. The objective of the present study was to assess the sensitivity, specificity, and positive and negative predictive values of hospital discharge diagnosis compared with clinical laboratory data for the identification of hyponatremia. Patients with hyponatremia were selected from a hospital information system determined by the International Classification of Diseases, 9th edition (ICD-9). The validity parameters for hyponatremia (ICD code 276.1) were estimated by comparison with accurate serum sodium (Na+) levels. A total of 2632 cases of hyponatremia were identified using laboratory measurements (Na+ < or =135 mmol/L). The sensitivity of ICD coding for hyponatremia was maximally about 30% for patients with very severe hyponatremia (Na+ < or =115 mmol/L). Corresponding specificities were high (>99%). In 87% of the cases with severe hyponatremia (Na+ < or =125 mmol/L), other discharge ICD codes reflecting severe morbidity were found. This study suggests that ICD codes for hyponatremia represent only one third of the patients admitted to the hospital and experiencing hyponatremia. About two thirds of the patients with hyponatremia were classified as hospitalized for other reasons. To assess the validity of case finding of patients with hyponatremia, the use of analytical techniques, such as certain laboratory measurements, is advisable.

Female↗
PubMed2006

Hyponatremia impairs early posttransplantation outcome in patients with cirrhosis undergoing liver transplantation.

BACKGROUND & AIMS: Hyponatremia is associated with reduced survival in patients with cirrhosis awaiting liver transplantation. However, it is not known whether hyponatremia also represents a risk factor of poor outcome after transplantation. We aimed to assess the effects of hyponatremia at the time of transplantation on posttransplantation outcome in patients with cirrhosis. METHODS: Two-hundred forty-one consecutive patients with cirrhosis submitted to liver transplantation during a 4-year period (January 2000-December 2003) were included in the study. The main end point was survival at 3 months after transplantation. Secondary end points were complications within the first month after transplantation. RESULTS: Patients with hyponatremia (serum sodium lower than 130 mEq/L) had a greater incidence of neurologic disorders, renal failure, and infectious complications than patients without hyponatremia (odds ratio; 4.6, 3.4 and 2.7, respectively) within the first month after transplantation. By contrast, hyponatremia was not associated with an increased incidence of severe intra-abdominal bleeding, acute rejection, or vascular and biliary complications. Hyponatremia was an independent predictive factor of early posttransplantation survival. Three-month survival of patients with hyponatremia was 84% compared with 95% of patients without hyponatremia (P < .05). Survival was similar after 3 months. CONCLUSIONS: In patients with cirrhosis, the presence of hyponatremia is associated with a high rate of neurologic disorders, infectious complications, and renal failure during the first month after transplantation and reduced 3-month survival. In cirrhosis, hyponatremia should be considered not only a risk factor of death before transplantation but also a risk factor of impaired early posttransplantation outcome.

Adult↗
PubMed2006

Cost of illness of hyponatremia in the United States.

BACKGROUND: Hyponatremia is a disorder of fluid and electrolyte balance characterized by a relative excess of body water relative to body sodium content. It is the most common electrolyte disorder encountered in clinical medicine and is associated with negative outcomes in many chronic diseases. However, there is limited information in the literature about health care resource use and costs attributable to the effects of the condition. The purpose of this analysis was to estimate the annual cost of illness of hyponatremia in the United States. METHODS: The study utilized a prevalence-based cost of illness framework that incorporated data from publicly available databases, published literature and a consensus panel of expert physicians. Panel members provided information on: classification of hyponatremia patients, treatment settings for hyponatremia (i.e., hospital, emergency room, doctor's office), and health care resource use associated with the diagnosis and treatment of hyponatremia. Low and high prevalence scenarios were estimated and utilized in a spreadsheet-based cost of illness model. Costs were assigned to units of resources and summarized across treatment settings. RESULTS: The prevalence estimate for hyponatremia ranged from 3.2 million to 6.1 million persons in the U.S. on an annual basis. Approximately 1% of patients were classified as having acute and symptomatic hyponatremia, 4% acute and asymptomatic, 15%-20% chronic and symptomatic, and 75-80% chronic and asymptomatic. Of patients treated for hyponatremia, 55%-63% are initially treated as inpatients, 25% are initially treated in the emergency room, and 13%-20% are treated solely in the office setting. The direct costs of treating hyponatremia in the U.S. on an annual basis were estimated to range between $1.6 billion and $3.6 billion. CONCLUSION: Treatment of hyponatremia represents a significant healthcare burden in the U.S. Newer therapies that may reduce the burden of hyponatremia in the inpatient setting could minimize the costs associated with this condition.

Journal Article↗