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Biomedical subjects

J C Ayus

Publications and source records attributed to J C Ayus.

At least 37 records · Page 2Linked to original sources
PubMed1996

Abnormalities of water metabolism in the elderly.

Hypernatremia is a frequent problem at the extremes of age, but particularly so in elderly individuals. Changes in the physiological responses to water deprivation with increasing age may be of particular interest in understanding the pathogenesis of hypernatremia in the elderly. When comparing healthy elderly men to younger controls, there are differences in the response to water deprivation. In older men, there are deficits in both the intensity and threshold of the thirst response. The ability to concentrate the urine also declines with age. There is both a decline in glomerular filtration rate and an increased incidence of renal disease with advancing age, which may contribute to impaired ability to conserve water. Because of a decrease in the percent total body water with age, equal volumes of fluid loss in young and old individuals may represent more severe dehydration in the elderly. Hyponatremia is seen in all age groups, but there are important differences in the elderly. When compared with postmenopausal women, menstruant (of childbearing age) women are over 25 times more likely to suffer permanent brain damage as a complication of hyponatremic encephalopathy. Furthermore, menstruant women suffer seizures or respiratory arrest at far higher levels of plasma sodium (110 to 130 mmol/L) than occurs in postmenopausal women (95 to 123 mmol/L).

Aged↗
PubMed1995

Age, gender, and vasopressin affect survival and brain adaptation in rats with metabolic encephalopathy.

Children and menstruant women are far more likely than men to develop metabolic brain damage from hyponatremia. We evaluated brain adaptation and mortality from hyponatremia in male and female rats of three different age groups. With acute hyponatremia, the mortality was 84% in prepubertal rats vs. 15% in adults and 0% in elderly rats. With chronic hyponatremia, mortality was 13% in adult males vs. 62% in females. Testosterone pretreatment significantly decreased mortality (from 62 to 9% in adult females, and from 100% to zero in prepubertal rats), but estrogen significantly increased mortality (from 13 to 44% in adult males). With acute hyponatremia in adult rats, brain sodium was significantly decreased (-17%), but in prepubertal rats it was actually increased (+ 37%). Cerebral perfusion during chronic hyponatremia was significantly impaired in adult females vs. males or controls (P < 0.01). Neither vasopressin administration nor chronic hyponatremia induced with desmopressin resulted in any mortality or decrement of cerebral perfusion. Thus age, gender, and the cerebral effects of vasopressin are major determinants of mortality in experimental metabolic encephalopathy.

Adaptation, Physiological↗
PubMed1995

Pulmonary complications of hyponatremic encephalopathy. Noncardiogenic pulmonary edema and hypercapnic respiratory failure.

OBJECTIVE: To determine the causes of hypoxia in patients with hyponatremic encephalopathy. DESIGN: Retrospective cohort study. SETTING: Consultation and referral service of two university medical centers and community hospitals. PATIENTS: Forty adults with postoperative hyponatremic encephalopathy and hypoxia of whom 30 had noncardiogenic pulmonary edema and 10 had hypercapnic respiratory failure. MAIN MEASUREMENTS: We evaluated the chest radiographs and measured plasma electrolytes, arterial blood gas values, pulmonary artery pressure, pulmonary capillary wedge pressure (PCWP), cardiac output, and net fluid retention. RESULTS: Forty patients with hyponatremic encephalopathy had hypoxia (arterial PO2 below 70 mm Hg), of whom 30 had pulmonary edema and 10 had hypercapnia (PCO2 above 50 mm Hg). Among the 30 patients with pulmonary edema, the serum sodium (+/- SD) was 114 +/- 7 mmol/L, arterial pH was 7.24 +/- 0.16, PCO2 was 45 +/- 15 mm Hg, and PO2 was 42 +/- 16 mm Hg. The cardiac index was 3.6 +/- 0.4 L/min/M2, pulmonary artery pressure was 26/16 mm Hg, and PCWP was 12 +/- 6 mm Hg. There was pulmonary edema, with normal heart size. The hypoxic patients who did not have pulmonary edema had significant hypercapnia (PCO2 = 91 +/- 29 mm Hg, p < 0.001). CONCLUSIONS: Patients with postoperative hyponatremic encephalopathy can develop hypoxia by at least two different mechanisms: noncardiogenic pulmonary edema or hypercapnic respiratory failure.

Adult↗
PubMed1994

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairs brain adaptation to hyponatremia, worsening brain edema, we performed in vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or hypoxic hypoxia. Mortality with hypoxic hypoxia was 0%; with hyponatremia, 22%; and with hyponatremia+hypoxia, 100%. Hyponatremia in cats produced brain edema, with a compensatory decrease of brain sodium. Ischemic hypoxia also resulted in brain edema, but with elevation of brain sodium. However, when ischemic hypoxia was superimposed upon hyponatremia, there was elevation of brain sodium with further elevation of water. Outward sodium transport in cat cerebral cortex synaptosomes was measured via three major pathways through which brain osmolality can be decreased. After hyponatremia, sodium transport was significantly altered such that brain cell osmolality would decrease: 44% increase in Na(+)-K(+)-ATPase transport activity (ouabain inhibitable); 26% decrease in amiloride-sensitive sodium uptake. The change in veratridine-stimulated sodium uptake was not significant (P > 0.05). When ischemic hypoxia was superimposed upon hyponatremia, all of the cerebral adaptive changes induced by hyponatremia alone were eliminated. Thus, hypoxia combined with hyponatremia produces a major increase in brain edema and mortality, probably by eliminating the compensatory mechanisms of sodium transport initiated by hyponatremia that tend to minimize brain swelling.

Amiloride↗
PubMed1993

Endometrial ablation complicated by fatal hyponatremic encephalopathy.

OBJECTIVES: To investigate the occurrence of hyponatremic encephalopathy and the effects of therapy for symptomatic hyponatremia on outcome in women undergoing endometrial ablation. DESIGN AND SETTING: Consultations from university-affiliated and community hospitals from June 1991 to June 1992. PATIENTS: Four generally healthy women who underwent elective endometrial ablation for dysfunctional bleeding and developed hyponatremic encephalopathy. INTERVENTIONS: Three patients were promptly treated with hypertonic (514 mmol/L) sodium chloride such that the serum sodium level increased from 102 to 123 mmol/L within 24 hours. The fourth patient was not treated until after suffering grand mal seizures followed by respiratory arrest. MAIN OUTCOME MEASURES: Of the four patients who developed hyponatremic encephalopathy, the diagnosis was established before respiratory arrest occurred in three. The operative procedure was terminated and all three were aggressively treated with intravenous hypertonic sodium chloride, which raised the serum sodium level to modestly hyponatremic levels (120 to 130 mmol/L). All three completely recovered without sequelae. The fourth patient suffered respiratory arrest before therapy could be initiated. The patient remained comatose, and central diabetes mellitus and insipidus developed. She never regained consciousness and died after several days. Autopsy revealed cerebral edema and tonsillar herniation. RESULTS: The mean (+/- SD) preoperative serum sodium level was 138 +/- 1 mmol/L; at the time of diagnosis of hyponatremia, it was 107 +/- 13 mmol/L. In two patients, hyponatremic encephalopathy was diagnosed intraoperatively because of tremulousness and either hypothermia or hypoxemia. In the other two patients, the diagnosis was made postoperatively because of headache, nausea, emesis, and in one of these patients, respiratory arrest. CONCLUSIONS: Women undergoing elective endometrial ablation can develop severe symptomatic hyponatremia, which can be fatal. The presence of symptoms suggesting hypo-osmolality should lead to immediate measurement of plasma sodium level. If hyponatremia with hypo-osmolality is present, early and appropriate therapy for the hyponatremia should be instituted before respiratory insufficiency occurs.

Adult↗
PubMed1993

Pathogenesis and prevention of hyponatremic encephalopathy.

Hyponatremia is the most common in-hospital electrolyte abnormality, and it has recently become apparent that there are at least two hyponatremia-associated mechanisms that may induce brain injury. They are hyponatremic encephalopathy and brain damage associated with therapy. The diagnosis of hyponatremia is established easily at virtually no risk to the patient by evaluation of plasma electrolytes. Rapid and appropriate therapy with hypertonic NaCl is indicated prior to respiratory insufficiency to prevent brain damage.

Brain Diseases, Metabolic↗
PubMed1992

Postoperative hyponatremic encephalopathy in menstruant women.

OBJECTIVES: To determine factors associated with the development of encephalopathy and with its clinical course in patients with postoperative hyponatremia. SETTING: Consultation and referral services of two university medical centers and community hospitals. DESIGN: Case-control study (risk factors for encephalopathy) and cohort study (clinical course among patients with encephalopathy). PATIENTS: Case patients included 65 adults with postoperative hyponatremic encephalopathy; controls included 674 adult patients who had postoperative hyponatremia without encephalopathy and who were selected from 76,678 consecutive adult surgical inpatients. MEASUREMENTS: Age, gender, menstrual status, neurologic symptoms, time to development and degree of hyponatremia, arterial blood gas determinations, serum chemistries, morbidity and mortality. RESULTS: Case patients included 40 women (62%) and 25 men (38%) (P > 0.05); controls included 367 women (54%) and 307 men (46%) (P > 0.1). Of the 34 case patients who developed permanent brain damage or died, 33 (97%) were women (P < 0.001). Among the women with brain damage, 25 (76%) were menstruant (P < 0.001). The relative risk for death or permanent brain damage from hyponatremic encephalopathy in women compared with men was 28 (95% Cl, 5 to 141) and in menstruant women compared with postmenopausal women, 26 (Cl, 11 to 62). Arterial PO2 at diagnosis was significantly lower in female than in male case patients (34 +/- 5 compared with 91 +/- 3 mm Hg; P < 0.001). Further, of the 38 case patients who had respiratory arrest before the diagnosis of hyponatremic encephalopathy, 36 (95%) were women. Extent of or time to development of hyponatremia did not correlate with subsequent brain damage (P > 0.1). CONCLUSIONS: Women and men are equally likely to develop hyponatremia and hyponatremic encephalopathy after surgery. However, when hyponatremic encephalopathy develops, menstruant women are about 25 times more likely to die or have permanent brain damage compared with either men or postmenopausal women.

Adult↗
PubMed1992

Hyponatraemia and death or permanent brain damage in healthy children.

OBJECTIVE: To determine if hyponatraemia causes permanent brain damage in healthy children and, if so, if the disorder is primarily limited to females, as occurs in adults. DESIGN: Prospective clinical case study of 16 affected children and a review of 24,412 consecutive surgical admissions at one medical centre. PATIENTS: 16 children (nine male, seven female; age 7 (SD 5) years) with generally minor illness were electively hospitalised for primary care. Consultation was obtained for the combination of respiratory arrest with symptomatic hyponatraemia (serum sodium concentration less than or equal to 128 mmol/l). MAIN OUTCOME MEASURES: Presence, gender distribution, and classification of permanent brain damage in children with symptomatic hyponatraemia in both prospective and retrospective studies. RESULTS: By retrospective evaluation the incidence of postoperative hyponatraemia among 24,412 patients was 0.34% (83 cases) and mortality of those afflicted was 8.4% (seven deaths). In the prospective population the serum sodium concentration on admission was 138 (SD 2) mmol/l. From three to 120 inpatient hours after hypotonic fluid administration patients developed progressive lethargy, headache, nausea, and emesis with an explosive onset of respiratory arrest. At the time serum sodium concentration was 115 (7) mmol/l and arterial oxygen tension 6 (1.5) kPa. The hyponatraemia was primarily caused by extrarenal loss of electrolytes with replacement by hypotonic fluids. All 16 patients had cerebral oedema detected at either radiological or postmortem examination. All 15 patients not treated for their hyponatraemia in a timely manner either died or were permanently incapacitated by brain damage. The only patient treated in a timely manner was alive but mentally retarded. CONCLUSIONS: Symptomatic hyponatraemia can result in high morbidity in children of both genders, which is due in large part to inadequate brain adaptation and lack of timely treatment.

Adolescent↗
PubMed1992

Case report: severe symptomatic hyponatremia associated with lisinopril therapy.

A 63-year-old white female who was being treated for hypertension with lisinopril presented with seizures, altered mental status, and a serum sodium of 101 mEq/L. Serum sodium prior to initiation of lisinopril therapy was 137 mEq/L. The hyponatremia was corrected and did not recur after lisinopril was stopped. The hyponatremia may have been a result of polydipsia and inappropriate antidiuresis secondary to ACE-inhibitor therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Symptomatic hyponatremia in rats: effect of treatment on mortality and brain lesions.

Hyponatremia was induced in rats over 3 days with dextrose in water and vasopressin. Eighty-five percent of the rats survived for 5 mo after spontaneous correction of mild hyponatremia. However, spontaneous correction of symptomatic hyponatremia (serum sodium less than 120 meq/l) resulted in 32% survival. Rapid correction of symptomatic hyponatremia by hypertonic saline with an absolute change in serum sodium of greater than 14 and less than 25 meq/l in the first 24 h allowed 100% of the rats to survive for 5 mo without brain lesions. On the other hand, correction of symptomatic hyponatremia with an absolute change in serum sodium of greater than 25 meq/l in the first 24 h resulted in 12% survival and development of brain lesions. We conclude that rapid correction of symptomatic hyponatremia improves survival and is safe if the absolute change in serum sodium is between 14 and 25 meq/l in the first 24 h. Increased mortality and brain lesions are associated with an absolute change in serum sodium of greater than 25 meq/l in the first 24 h.

Animals↗
PubMed1987

Treatment of symptomatic hyponatremia and its relation to brain damage. A prospective study.

We studied the effects of replacement therapy in two groups of patients with symptomatic hyponatremia. Thirty-three patients, who were studied prospectively, had no evidence of cerebral demyelinating lesions. Their hyponatremia (mean serum sodium concentration [+/- SE], 108 +/- 1 mmol per liter) was increased to 126 +/- 1 mmol per liter with hypertonic saline (856 mM) delivered at a rate of 1.3 +/- 0.2 mmol per liter per hour. The serum sodium concentration did not rise to normal or hypernatremic levels in the first 48 hours of therapy, and none of these patients had a respiratory arrest or other hypoxic episode. Twelve patients, evaluated retrospectively, had evidence of cerebral demyelinating lesions at autopsy or on computerized axial tomography. The rate of correction of hyponatremia (1 +/- 0.2 mmol per liter per hour) was similar to the rate in the patients in Group I. However, at least one of four characteristics was present: an increase in serum sodium to normal or hypernatremic levels in the first 48 hours, a change in the serum sodium concentration of more than 25 mmol per liter in the first 48 hours, a hypoxic-anoxic episode, and an elevation of serum sodium to hypernatremic levels in patients with hepatic encephalopathy. Although these four features were associated with demyelination, our observations suggest that this complication does not depend on the rate of correction of hyponatremia.

Adolescent↗
PubMed1985

Changing concepts in treatment of severe symptomatic hyponatremia. Rapid correction and possible relation to central pontine myelinolysis.

Severe symptomatic hyponatremia (serum sodium level below 120 meq/liter) is often a life-threatening emergency that can result in permanent neurologic damage or death if left untreated. Early recognition and rapid correction to mildly hyponatremic levels by the administration of hypertonic saline are important in order to reduce the potential mortality and morbidity. If the serum sodium level is more than 105 meq/liter, it can be corrected to a value of 125 to 130 meq/liter. However, if the serum sodium level is less than 105 meq/liter, it may be safe to raise the value by only 20 meq/liter. Care should be taken to avoid acute correction to normonatremia or hypernatremia. Moreover, it is also of equal importance to avoid development of hypernatremia in the subsequent days following the correction to mild hyponatremia.

Alcoholism↗
PubMed1985

Rapid correction of severe hyponatremia in the rat: histopathological changes in the brain.

The purpose of the present studies was to examine the effects of rapid correction of severe hyponatremia (serum sodium less than 120 meq/liter) either to mildly hyponatremic levels (serum sodium = 130 meq/liter) or to normonatremic levels (serum sodium = 150 meq/liter) on the brain histology of rats. In group I, 13% of the rats revealed brain lesions following correction to mildly hyponatremic levels by the administration of 855 mM NaCl. All the rats (100%) in group II had brain lesions following correction to normonatremic levels by 24 h of water restriction. Similarly, all the rats in group III showed brain lesions following correction to normonatremic levels by the administration of 855 mM NaCl. Severe hyponatremia by itself did not cause any brain lesions in another group. We conclude that rapid correction of severe hyponatremia to mildly hyponatremic levels by the administration of 855 mM NaCl does not cause significant brain lesions. On the other hand, rapid correction to normonatremic levels either by water restriction or by the administration of 855 mM NaCl results in significant brain lesions.

Animals↗