Episodes Of Hyponatremia Research Articles

Hyponatremia in Spinal Cord Injury

Hypoosmolar hyponatremia (serum Na+ less than 130 mmol/L) has proven a common and incompletely explained phenomenon in the spinal cord injured patient. When present, it has generally been preceded by excessive fluid intake and environmental/dietary factors which reversibly restrict free water excretion. We have attempted to more fully characterize the determinants of SCI-associated hyponatremia by retrospectively analyzing its features and treatment response in a series of 14 hyponatremic SCI patients. In most instances, hyponatremia could be attributed to uncontrolled fluid intake in the presence of an acute or semiacute illness and thus stimuli for non-osmotic releases of arginine vasopressin. Treatment measures generally included administration of 3% saline, with all patients recovering uneventfully from their episode of hyponatremia.

Life-threatening hyponatremia caused by vinblastine

Some days after the administration of a third bolus of ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) a patient affected by immunoblastic lymphoma underwent a neurotoxic crisis. The episode lasted 1 week and was followed by a dramatic fall in plasma sodium (104 mEq I-1), associated with a proportionally lesser decrease in plasma chloride and phosphate. Despite the lowest plasma osmolality, detectable levels of circulating ADH were present. After 36 h the hyponatremic episode improved after the infusion of hypertonic sodium chloride. Nevertheless the patient lapsed into a hypotonic coma. The urinary concentrations of the main tubular enzymes (gamma-glutamyltranspeptidase, N-acetyl-glucosaminidase, alpha-glucosidase) proved very high and successively decreased slowly. The most likely cause of such hyponatremic episode is vinblastine. The drug acted through: (a) an already known inappropriate release of ADH, and (b) a hitherto unreported tubular lesion, which impaired the reabsorption of sodium and other coupled solutes.

Extracellular fluid volume changes in very low birth weight infants during first 2 postnatal months

Serial extracellular volume (ECV) changes were measured in 18 infants of less than 32 weeks gestation. Results were compared with changes in body weight, fluid and sodium intake, urine output, and serum sodium concentration. Mean +/- SD ECV decreased from 550 +/- 116 mL/kg on day 1 to 359 +/- 66 mL/kg on day 14. Thereafter, mean ECV/kg remained between 336 +/- 42 and 349 +/- 54 mL/kg. Clinical hydration and serum sodium concentration usually remained normal during this reduction of stabilization of ECV/kg. Six episodes of hyponatremia occurred at 11 to 31 days of age. Mean ECV/kg was significantly lower in infants with hyponatremia compared with infants of similar age with normal serum sodium concentration (303 +/- 36 mL/kg vs 368 +/- 56 mL/kg, P less than 0.01). Sodium intake in the two groups was similar. We conclude that ECV in the VLBW infant decreases postnatally and is regulated within a range similar to that in older infants, and that postnatal natriuresis in the first 2 weeks of life represents physiologic reduction of the expanded ECV of the fetus. Late hyponatremia may indicate excessive sodium loss and ECV depletion.

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in small-cell lung cancer.

Review of clinical data from 350 patients with small-cell lung cancer (SCLC) revealed hyponatremia (sodium less than 130 mEq/L) attributable to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in 40 patients (11%). Although hyponatremia was severe in most instances (median, sodium 117 mEq/L), symptoms attributable to water intoxication were identified in only 27% of hyponatremic episodes. Development of SIADH showed no correlation with clinical stage, distribution of metastatic sites, sex, or histologic subtype of small-cell carcinoma. SIADH occurred most often with initial presentation (33 of 40), and resolved promptly (less than 3 weeks) with initiation of combination chemotherapy in 80% of evaluable patients. The presence of SIADH did not influence response to chemotherapy or overall survival as an independent variable. However, in five patients profound hyponatremia developed immediately following primary cytotoxic therapy (range, one to five days). Despite initial control of SIADH, dilutional hyponatremia recurred in 70% of patients with tumor progression. Our findings suggest that development of clinically demonstrable SIADH in patients with SCLC is dependent on functional properties of the neoplastic cells, rather than tumor burden or metastatic site. The potential for development of clinically significant hyponatremia early in the course of cytotoxic therapy emphasizes the need to closely monitor patients, particularly those receiving chemotherapy regimens requiring substantial intravenous hydration.

Democlocycline improves hyponatremia in chronic schizophrenics

Serum sodium concentration increased significantly in eight hyponatremic schizophrenic subjects treated with demeclocycline. The incidence of severe hyponatremic episodes was significantly reduced. The authors argue that mild impairments in urinary dilution contribute to water intoxication in most chronic psychotics who develop this syndrome. Demeclocycline may help these patients.

Tobacco Smoking and Hyponatremia in Psychiatric Patients

To the Editor.— In his article, Dr Blum 1 states that in his study of ten compulsive drinkers he found that episodes of hyponatremia developed only in heavy smokers. We have previously looked at this question of heavy smokers and hyponatremia and polydipsia. 2 In our study, we found that most of the patients who presented with hyponatremia and severe neurological dysfunction were heavy smokers. However, when compared with normonatremic schizophrenics, the rate of smoking was not different. Many studies concerning hyponatremia and schizophrenia do show that these patients may have inappropriate release of antidiuretic hormone (ADH) associated with their polydipsia. Factors that cause this release of ADH remain uncertain. Studies with ADH levels and their relationship to smoking would be helpful to settle this matter.

The Possible Role of Tobacco Cigarette Smoking in Hyponatremia of Long-term Psychiatric Patients

HYPONATREMIA in psychiatric patients is found infrequently, but it may represent a medical emergency with an occasionally lethal outcome.¹Once gastrointestinal tract sodium loss, adrenal gland insufficiency, renal disease, congestive heart failure, hepatic cirrhosis, or use of diuretics are ruled out as causes of true low serum sodium concentration, there is still a group of patients with episodes of hyponatremia for which the causality is elusive. Low levels of serum sodium in these cases are usually ascribed to psychotropic drug—induced syndrome of inappropriate antidiuretic hormone secretion (SIADH) and excessive fluid intake. An SIADH induced by postulated neuroendocrine mechanisms triggered through the emotional stress of psychosis has been described in the literature. Excessive fluid intake is frequently observed among hospitalized psychiatric patients. A study of 241 such patients identified 41 (17.5%) with polydipsia. Their estimated fluid intake ranged from 4 to 10 L/day, and 24-hour urine volumes from 2,120 to

Instable osmoreceptors and deficient thirst in hypothalamic hypopituitarism

A unique abnormality of osmoreceptors is reported in a child with hypothalamic hypopituitarism. Anterior pituitary testing revealed deficiency of GH, TSH and ACTH. The clinical course was characterized by fluctuation between dehydration of diabetes insipidus and coma of water intoxication. Plasma/Urine osmolality ranged from 263/110 mOsm/kg to 325/187 mOsm/kg. Osmotic threshold (OT) was determined by isovolemic infusion of hypertonic saline. An abrupt decrease of 30% or more of free water clearance defined the OT. During a hyponatremic episode the OT was detected at 263mOsm/kg. While hypernatremic OT was found at 300 mOsm/kg. These values are significantly different from the 286.6± 0.9 (M±SD) mOsm/kg found in 6 healthy volunteers. The presence of endogenous vasopressin, and the normally functioning volume receptors was demonstrated by the normal urine concentration when dehydrated. With plasma osmolality as high as 3O7mOsm/kg the child denied any feeling of thirst. The data indicate an instability of the osmoreceptors and a deficiency of thirst mechanism with intact volume receptors.

Treatment of recurrent syndrome of inappropriate secretion of antidiuretic hormone with lithium

The usual treatment for recurrent syndrome of inappropriate secretion of antidiuretic hormone has been fluid restriction. Recently White and Fetner described an adult with SIADH successfully managed with lithium carbonate. Described here is a child with recurrent SIADH who was diagnosed as having an acute hyponatremic episode and who then relapsed twice in a two-month period while chronic fluid restriction was attempted. He has now been maintained on 300 mg/day of lithium carbonate and is asymptomatic with normal serum sodium concentration and urine osmolalities. Lithium appears to be effective in the management of recurrent SIADH and may allow control in a patient who cannot comply with long-term fluid restriction.

Pseudohypoaldosteronism due to Sweat Gland Dysfunction

Pseudohypoaldosteronism is an uncommon disorder characterized by urinary sodium wasting and is attributed to a defect in distal renal tubular sodium handling with failure to respond to endogenous aldosterone. Sweat electrolyte values in other reported patients, when measured, have been normal. A 3.5-year-old girl developed repeated episodes of dehydration, hyponatremia, and hyperkalemia during the first 19 months of life. Serum sodium was as low as 113 mEq/liter and potassium as high as 11.1 mEq/liter. Her plasma and urinary aldosterone levels were persistently elevated (Figs. 1-4). Unlike patients with classic pseudohypoaldosteronism she demonstrated no urinary sodium wasting (Figs. 2 and 3). During episodes of hyponatremia and reduced sodium intake her urinary sodium was less than 5 mEq/liter. In addition, her sweat sodium concentration was consistently above 125 mEq/liter and salivary sodium concentration above 58 mEq/liter. Her chest x-ray, 72-hr fecal fat excretion, serum and urinary pancreatic amylase (amy-2) were normal, providing no evidence for cystic fibrosis. It is proposed that this patient represents a new variant of pseudohypoaldosteronism with excessive loss of sodium from the sweat and salivary glands instead of the kidneys.

Pseudohypoaldosteronism due to Sweat Gland Dysfunction

Extract: Pseudohypoaldosteronism is an uncommon disorder characterized by urinary sodium wasting and is attributed to a defect in distal renal tubular sodium handling with failure to respond to endogenous aldosterone. Sweat electrolyte values in other reported patients, when measured, have been normal. A 3.5-year-old girl developed repeated episodes of dehydration, hyponatremia, and hyperkalemia during the first 19 months of life. Serum sodium was as low as 113 mEq/liter and potassium as high as 11.1 mEq/liter. Her plasma and urinary aldosterone levels were persistently elevated (Figs. 1–4). Unlike patients with classic pseudohypoaldosteronism she demonstrated no urinary sodium wasting (Figs. 2 and 3). During episodes of hyponatremia and reduced sodium intake her urinary sodium was less than 5 mEq/liter. In addition, her sweat sodium concentration was consistently above 125 mEq/liter and salivary sodium concentration above 58 mEq/liter. Her chest x-ray, 72-hr fecal fat excretion, serum and urinary pancreatic amylase (amy-2) were normal, providing no evidence for cystic fibrosis. It is proposed that this patient represents a new variant of pseudohypoaldosteronism with excessive loss of sodium from the sweat and salivary glands instead of the kidneys. Spectulation: Aldosterone is known to control sodium and potassium excretion by kidneys, sweat glands, and salivary glands. In patients with classic pseudohypoaldosteronism there is a defect in renal tubular response to aldosterone action. Studies in the present patient suggest that there may be variants of this syndrome in which the end organ defect is in the sweat and salivary glands instead of the renal tubule. In addition, it is possible that new variants will be found in which end organ defect is in still other organs concerned with electrolyte transport.

Late hyponatremia in very low birthweight infants. (less than 1.3 kilograms).

Late hyponatremia (plasma Na+ less than 130 mEq/liter) occurred frequently (on 54 of 159 occasions) in 46 very low virthweight (VLBW) infants (less than 1.3 kg at birth) between 2 and 6 weeks of age while receiving a sodium intake of less than or equal to 2 mEg/kg/24 hr. To elucidate possible pathogenetic mechanisms five groups of such infants were studied while receiving a commercially available formula reconstituted to give two different volumes and two different Na+ concentrations. Sodium intake in the nonsupplemented (NS) infants (n = 23) was less than 2 mEq/kg/24 hr. Supplemented (S) infants (n = 16) received approximately 3 mEq Na+/kg/24 hr. A further group of seven infants given a high volume (200 ml/kg/24 hr), high caloric (100 cal/dl) formula and Na+ supplementation (to 3 mEq/kg/24 hr) was also included. Infants were studied from age 14 days until they weighed 1.80 +/- 0.05 kg at a mean age of 47 days. At the time of start of the study, 6 of 20 NS and 6 of 19 S infants were hyponatremic. After supplementation only two episodes of hyponatremia occurred in S infants, both during the first study week, whereas the high incidence of hyponatremia in NS infants period. During baseline urine collections all infants excreted between 80 and 100 ml/kg/24 hr urine, but those receiving 150 ml/kg/24 hr formula decreased their urinary output rapidly to 50 ml/kg/24 hr, whereas infants receiving high volume feeds (200 ml/kg/24 hr) did not decrease their urinary output until the third balance at an average age of 45 days. All infants excreted between 1.0 and 1.2 mEq/kg/24 hr of sodium in their urine during the initial collection. Nonsupplemented infants reduced their urinary Na+ excretion more rapidly than supplemented babies (NS: from 1.03 to 0.55 mEq/kg/24 hr, first vs second balance; S: from 1.00 to 0.80 mEq/kg/24 hr, first vs third balance). Mean potassium excretion remained unchanged in NS and S infants during the study period and was not affected by the volume or caloric content of the formula. Extracellular volume (ECV) and total body water (TBW) were measure serially, and there were no differences between S and NS infants in the distribution of body water. The percentage of TBW and ECV decreased in all groups with increasing postnatal age.

PSEUDO-HYPOALDOSTERONISM DUE TO SWEAT GLAND DYSFUNCTION

14 mo. old white female has experienced repeated spontaneous episodes of hyponatremia, hyperkalemia, dehydration and shock since birth. Serum Na has been as low as 113 mEq/L and serum K as high as 11.1 mEq/L. Physical examination, growth and development have been normal.Balance Studies 3-5 Days after following Diets were:Urinary 17-keto, 17-OH and pregnanetriol baseline and with ACTH stimulation were normal. Renal function has been normal. Salivary Na was 70 and K 16 mEq/L. Chest X-ray and 72 hour fecal fat excretion have been normal. There is no family history of cystic fibrosis.Aldosterone is known to control Na and K secretion by kidney, sweat and salivary glands. It is proposed that this patient presents a new syndrome of pseudo-hypopoaldosteronism with the end organ defect in sweat glands instead of the kidneys.

Inappropriate secretion of antidiuretic hormone secondary to vincristine therapy

A transient severe episode of the syndrome of inappropriate antidiuretic hormone secretion (IADHS) developed in a fifty-four year old white man with acute leukemia following the first and only intravenous injection of 4 mg of vincristine (0.065 mg/ kilo). In retrospect, the findings directly attributable to the syndrome were apparent on the eighth day after this treatment. By the twenty-second day the symptoms and abnormal biochemical findings disappeared and did not recur for the remaining two and a half years of his life. The clinical events, biochemical findings and response to therapy were typical for the syndrome of IADHS. The responsible agent was most likely vincristine. Evidence of this cause and effect relationship was suggested by (1) the known neurotoxicity of vincristine, (2) the interval between administration of the drug and development of the syndrome, (3) the subsequent course of the patient and (4) the exclusion of other known causes for IADHS. This is the first case reported in an adult. Three hyponatremic episodes in children have been described, temporally related to vincristine therapy and thought to represent transient IADHS.