Neurologic symptoms with electrolyte and water imbalance.
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A male quadriplegic (C6--complete) with persistent chronic hyponatremia (serum sodium values ranging consistently from 117-132 mmol/L) developed acute hyponatremia with a serum sodium concentration of 98 mmol/L. This extreme hyponatremia related, in part, to a reversible defect in the excretion of a water load, while on a low (46 mmol/day) sodium diet. Subsequent ingestion of a normal sodium diet (150 mmol/day), with or without 0.1 mg of fludrocortisone (Florinef), reestablished his ability to excrete a water load normally. The etiology of this patient's hyponatremia is discussed as well as the unique concordance of factors which make hyponatremia a common occurrence among spinal-cord injured patients.
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Bedside evaluation of a patient's intravascular volume status is challenging, even for the seasoned practitioner. There is no single diagnostic test to determine whether a patient is hypovolemic, hypervolemic, or euvolemic. Often, underlying or concomitant disease states, medications, and other therapeutics can make available data difficult to interpret. Therefore, a combination of clinical evaluation, laboratory studies, and other diagnostics are required to make a clinical judgment regarding volume status. Patients who demonstrate alterations in their volume status are likely to have electrolyte abnormalities as well, and assessment of serum electrolyte values and potential therapeutic interventions is a vital piece in caring for critically ill patients.
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1. The relation between water loading and electrolyte excretion in dogs fed on a meat diet proved impossible to evaluate owing to the large variability in electrolyte excretion rates in control experiments.2. In animals fed a synthetic diet of constant and known composition the administration of a water load of 2.5% of body weight caused significant increases in the rate of excretion of sodium (P < 0.01) and potassium (P < 0.05). The chloride excretion rate also increased in the one animal tested.3. The significance of these results is discussed.
Our previous studies in rats have suggested a role for renomedullary hyaluronan (HA) in water homeostasis. The gerbil is known for its unique ability to conserve water. In the present study renal papillary and intestinal HA were compared between groups of anaesthetized gerbils and rats before and after up to 6 h of I.V. water loading. Baseline papillary HA in gerbils was only 37 % of that in the rat. Water loading in rats increased the papillary HA content. Elevation was maximal (+27 %, P < 0.05) after 2 h of water loading and then declined to control levels after 6 h of water loading (+3 %, n.s.). In contrast, the gerbil responded with a decreased papillary HA content during water loading. The depression was maximal after 2 h (-49 %, P < 0.05) and was still 41 % below the control values after 6 h (P < 0.05). The urine flow rate increased rapidly in the rat and its maximum, 21 times above the control level (P < 0.05), occurred at the HA peak, i.e. after 2 h of water loading while in the gerbil, the urine flow rate increased slowly and slightly and was only six times above control values after 6 h of water loading (P < 0.05). The HA content along the intestine was similar in the two species: lowest in the duodenum and jejunum and highest in the distal colon. To conclude, in the rat, the elevation of papillary interstitial HA during acute water loading would counteract water reabsorption by changing the physico-chemical characteristics of the interstitial matrix favouring rapid water diuresis. This would work as a complement to the powerful regulation by ADH. The gerbil has a diametrically different regulation of papillary HA turnover during water loading. The decreased papillary HA level during water loading and the slow and small diuretic response may represent a genetic difference in adaptation to enhance the ability to conserve water in an arid environment.
Sixty-four infants and children showing signs of decerebrate rigidity admitted to a paediatric unit have been studied. Cases of head injury, myelomeningocoele, and tumours were excluded from the series. The aetiological factors causing decerebration in the remainder fell into four main groups: infections, hypoxia, metabolic disease, and intracranial haemorrhage. Increased intracranial pressure was diagnosed in 87%. Defects in homeostasis occurred in 75%, respiratory abnormalities were present in 66%, cardiovascular in 33%, hypothermia in 30%, and hyponatraemia in 17%. Early recognition and treatment of raised intracranial pressure and defects in homeostasis are of the utmost importance if morbidity and mortality are to be minimized. There was a 31% mortality from the acute illness: 30% of the survivors were normal at follow-up examination; the remainder showed varying degrees of handicap. The severity of decerebration showed no correlation with aetiology or prognosis. The study shows that a wide range of disorders can lead to the clinical picture of decerebration in the young child, and that the prognosis is probably much better than in adults showing the same symptoms and signs.
The simultaneous time courses of hydromineral hormones (renin-aldosterone system, arginine vasopressin, and atrial natriuretic peptide) and renal responses were examined during and after the completion of hyperhydration induced by glycerol and fluid ingestion. Eight healthy young male Caucasian subjects participated in two separate trials, each including three consecutive phases in a thermoneutral environment. Phases 1 and 3 involved a 90-min period at rest, while phase 2 involved a 120-min period at rest designed to provide either (i) euhydration (control trial) or (ii) hyperhydration induced by ingestion of glycerol (1.1 g/kg body mass) and fluid (21.4 mL/kg body mass). During the 2-h time period of glycerol and fluid ingestion, urine flow, urine osmolality, and plasma levels of hydromineral hormones remained at basal values. In contrast, after hyperhydration completion during phase 3, the diuresis increased markedly together with a dilution of the urine (p < 0.05) while hormonal responses did not change. These results indicate significant differences in renal responses during and after hyperhydration completion and suggest that these changes are independent of fluid-regulating hormonal responses.
Heart failure is a leading cause of morbidity and mortality. In the United States, there are more than 5 million patients with heart failure and over 500,000 newly diagnosed cases each year. Numerous advances have been made in our understanding of the pathophysiologic mechanisms contributing to sodium and water retention in this condition. Important alterations in the sympathetic nervous system and the renin-angiotensin-aldosterone system have been described in heart failure, allowing the use of mechanism-specific treatments such as beta-adrenergic receptor antagonism and angiotensin-converting enzyme inhibition. As our understanding of the roles of the natriuretic peptides and the arginine vasopressin-aquaporin-2 system in the pathophysiology of heart failure evolves, treatments directed toward the alterations in these systems in heart failure can be further developed.
Body weight and fluid input/output are usually monitored for checking fluid balance in case of intravenous hyperhydration during nephrotoxic chemotherapy. The reliability of measuring fluid input/output is uncertain. Moreover, this measurement is redundant, complex, labour-intensive and represents an occupational hazard for nurses and other health-care workers handling fluids or body excreta. In a prospective cohort study, we determined the concordance between body weight and fluid intake/output. We also examined the clinical consequences with respect to the safety of selecting only body weight measurement as a parameter for fluid overload. A total of 591 combined observations of fluid balances and body weights were collected. We observed a higher increase in body weight than in fluid balance. The Pearson correlation between fluid balance and body weight was relatively low (r = 0.28). With regard to the safety of measuring body weight only, we found 4 cases (0.6%) who might not have received furosemide if the fluid input/output had not been measured, without clinical consequences, however. After standardization, body weight can safely be used as the only parameter for monitoring fluid retention in case of hyperhydration during chemotherapy.
In the present study, the effect of selective glucocorticoid deficiency on renal water excretion was investigated in conscious, trained, adrenalectomized dogs. The animals were studied before and after a water load while on replacement therapy of desoxycorticosterone acetate, 5 mg/day, and dexamethasone, 0.8 mg/day (group I), and while off dexamethasone for 5-9 days (group II). Before the water load the weight, inulin space, cardiac output, blood pressure, glomerular filtration rate, renal blood flow, plasma osmolality, and plasma antidiuretic hormone measured by radioimmunoassay were similar in both groups I and II. However, after a 40 ml/kg water load a marked impairment in renal water excretion in the glucocorticoid deficient dogs became apparent. Maximal free water clearance was -0.046+/-0.16 vs. 6.51+/-0.72 ml/min (P < 0.001) and minimal urinary osmolality was 425+/-56 vs. 82+/-3.5 mosmol/kg H(2)O (P < 0.001) in group II as compared to group I. Plasma antidiuretic hormone was maximally suppressed during the water load in group I to 0.34+/-0.08 pg/ml but remained elevated at 9.18+/-1.79 pg/ml (P < 0.005) in group II. This nonsuppressibility of plasma antidiuretic hormone during water loading in group II was associated with a significant tachycardia of 145+/-6 vs. 87+/-6 beats/min (P < 0.001) in group I and a significantly lower stroke volume of 27+/-0 vs. 59+/-0.5 ml/beat (P < 0.001). In conclusion, our results implicate a persistent secretion of antidiuretic hormone as an important factor in the impaired water excretion of glucocorticoid deficiency. A deleterious effect of glucocorticoid deficiency on cardiac function was observed and this hemodynamic alteration could be involved in initiating a nonosmolar, baroreceptor-mediated release of vasopressin.