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Biomedical subjects

P M Palevsky

Publications and source records attributed to P M Palevsky.

13 recordsLinked to original sources
PubMed1998

Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines.

BACKGROUND: Hyperkalemia is a common, potentially life-threatening disorder. Electrocardiograms are considered to be sensitive indicators of the presence of hyperkalemia. Since the treatment of hyperkalemia involves relatively few maneuvers and because its success can be objectively scored, we investigated how physicians manage this disorder and how successful their prescribed therapy is. We also sought to determine whether treatment could be improved by providing the treating physicians with therapy guidelines on a real-time basis. METHODS: Consecutive patients with hyperkalemia were identified by review of laboratory records. During the observation-only phase of the study, demographic data, contributing causes, electrocardiogram findings, treatments used, compliance with prescribing guidelines, and patient outcome were recorded. During the subsequent notification phase of the study, treatment recommendations were sent to the patient's ward when the elevated potassium value was noted. The same outcome data were collected. RESULTS: There were 127 episodes of hyperkalemia during the observation-only phase and 115 during the notification phase. No patients died or had life-threatening cardiac arrhythmias. Electrocardiographic abnormalities consistent with hyperkalemia were observed in only 14% of episodes. Renal failure (77%), drugs (63%), and hyperglycemia (49%) contributed to most episodes. Treatments used were exchange resin (51%), insulin (46%), calcium (36%), bicarbonate (34%), and albuterol (4%). The agents were equally efficacious. The time to first treatment was shorter in patients with potassium levels of 6.5 mmol/L or more than in patients with lower values (2.1 +/- 2.2 vs 2.8 +/- 2.4 hours; P<.05). Treatment was better in the intensive care unit than on regular wards. Only 39% of episodes during the observation-only period met the predetermined criteria for monitoring and diagnosis, initial treatment, and follow-up. During the notification period, physician performance was no better; only 42% of episodes met all criteria. The laboratory transmitted a copy of the guidelines to the patient's ward only 38% of the time. In a separate analysis of these episodes, there was no improvement in treatment. Physicians who did not receive the notification fulfilled all treatment criteria more often than physicians who did (50% vs 30%; P<.05). CONCLUSIONS: Although treatment of hyperkalemia was frequently suboptimal, no serious arrhythmias and no deaths complicated management of 242 episodes of severe hyperkalemia. A narrowly targeted effort to improve physician management of a disorder with discrete treatment options did not improve therapy.

Adolescent↗
PubMed1998

Determinants of vancomycin clearance by continuous venovenous hemofiltration and continuous venovenous hemodialysis.

The clearance of vancomycin is significantly reduced in patients with acute, as well as, chronic renal failure. Although multiple-dosage regimen adjustment techniques have been proposed for these patients, there is little quantitative data to guide the individualization of vancomycin therapy in acute renal failure patients who are receiving continuous renal replacement therapy (CRRT). To determine appropriate vancomycin dosing strategies for patients receiving continuous venovenous hemofiltration (CVVH) and continuous venovenous hemodialysis (CVVHD), we performed controlled clearance studies in five stable hemodialysis patients with three hemofilters: an acrylonitrile copolymer 0.6 m2 (AN69), polymethylmethacrylate 2.1 m2 (PMMA), and polysulfone 0.65 m2 (PS). Patients received 500 mg of vancomycin intravenously at least 12 hours before the start of the clearance study. The concentration of vancomycin in multiple plasma and dialysate/ultrafiltrate samples was determined by EMIT (Syva, Palo Alto, CA). The diffusional clearance and sieving coefficient (SC) of vancomycin were compared by a mixed-model repeated-measures analysis of variance (ANOVA) with filter and blood (Q(B)), dialysate inflow (Q(DI)), or ultrafiltration rate (Q(UF)) as the main effects and patient as a random effect. Vancomycin was moderately protein bound in these patients; free fraction ranged from 49% to 83%. The SCs of the three filters were similar and significantly correlated with the free fraction of vancomycin (P = 0.01; r2 = 0.465). Significant linear relationships were observed between the diffusional clearance of vancomycin and Q(DI) for all three filters: AN69 (slope = 0.482; r2 = 0.880); PMMA (slope = 0.853; r2 = 0.966); and PS (slope = 0.658; r2 = 0.887). The slope of this relationship for the PMMA filter was significantly greater than that of the AN69 and PS filters. The clearance of vancomycin, urea, and creatinine, however, was essentially constant at all Q(B)s for all three filters. Thus, the clearance of vancomycin was not membrane dependent during CVVH. However, during CVVHD, membrane dependence of vancomycin clearance was noted at a Q(DI) greater than 16.7 mL/min; vancomycin clearance with PMMA at a Q(DI) of 25 mL/min was 66% and 43% greater than that with the AN69 and PS filters, respectively. CVVH (62% to 262%) and CVVHD (90% to 540%) can significantly augment the clearance of vancomycin in acute renal failure patients. Dosing strategies for individualization of vancomycin therapy in patients receiving CVVH and CVVHD are proposed.

Acrylic Resins↗
PubMed1998

Duodenal obstruction in polycystic kidney disease. Case report and review of the literature.

Polycystic kidney disease in a common inherited disorder accounting for 8-10% of cases of end-stage renal disease. The enlarged kidneys often produce pain and hematuria but rarely obstruction of surrounding organs. We report a case of autosomal dominant polycystic kidney disease producing symptomatic duodenal obstruction and malnutrition. Duodenal obstruction should be considered in the differential diagnosis of a patient with polycystic kidney disease and intermittent or persistent nausea and vomiting.

Adult↗
PubMed1998

Hypernatremia.

Renal water conservation minimizes the progression of hypernatremia, but the ultimate defense against progressive hypernatremia is the stimulation of thirst by hypertonicity with a resultant increase in water ingestion. Defects in thirst may result from focal lesions involving the hypothalamic osmoreceptors, but more commonly are the result of lesions that impair higher cortical processes required for thirst perception and water ingestion. In response to hypernatremia, the brain undergoes adaptive responses to minimize osmotic shrinkage. Initially there is a rapid uptake of electrolytes, while a slower adaptive phase involves the accumulation of organic osmolytes. The rate at which these solutes can be extruded from the brain dictates the rate at which water replacement can be safely administered during treatment. The incidence of hypernatremia ranges from less than 1% to more than 3% in clinical series. While hypernatremia in nonhospitalized patients is predominantly a disease of the elderly, and is commonly a manifestation of infection or inadequate nursing care, hospital-acquired hypernatremia occurs in a patient population more closely resembling the general hospitalized population and results from inadequate water prescription to patients who are unable to self-regulate water intake. Mortality rates range from approximately 40% to more than than 60%.

Adaptation, Physiological↗
PubMed1997

Hyponatremia and hypernatremia.

Hyponatremia and hypernatremia are common electrolyte disorders resulting from disorders in water homeostasis. Hyponatremia usually results from defects in free water excretion, although increased intake may also contribute. The treatment of hyponatremia has been controversial because of the high associated morbidity and mortality and the observation that rapid correction of hyponatremia is associated with the development of central pontine myelinolysis. Mild hyponatremia should be treated with water restriction alone, whereas severe acute or symptomatic hyponatremia should initially be corrected rapidly until symptoms resolve followed by more gradual correction. In all cases, treatment should be individualized on the basis of severity, cause, and duration of the hyponatremia. Hypernatremia results from impaired water ingestion, although increased water losses are often contributory. Hospital-acquired hypernatremia is usually iatrogenic because of inadequate water prescription and is therefore preventable. Hypernatremia is also associated with high morbidity and mortality, both as a result of the underlying disease and inadequate treatment. The primary treatment of hypernatremia is water replacement-repleting water deficits and replacing ongoing losses. Additional treatment should be directed at eliminating excess water losses.

Body Water↗
PubMed1996

Regulation of a sodium channel-associated G-protein by aldosterone.

The action of aldosterone to increase apical membrane permeability in responsive epithelia is thought to be due to activation of sodium channels. This channel is regulated, in part, by G-proteins, but it is not known if this mechanism is regulated by aldosterone. We report that aldosterone stimulates the expression of the 41-kDa alphai3 subunit of the heterotrimeric GTP-binding proteins in A-6 cells. Both mRNA and the total amount of this protein are increased by aldosterone. The G-protein is palmitoylated in response to the steroid, and the newly synthesized subunit is found to co-localize with the sodium channel. Aldosterone stimulation of sodium transport is significantly inhibited by inhibition of palmitoylation. These results suggest that aldosterone regulates sodium channel activity in epithelia through stimulation of the expression and post-translational targeting of a channel regulatory G-protein subunit.

Aldosterone↗
PubMed1996

Hypernatremia in hospitalized patients.

OBJECTIVE: To determine the incidence, clinical characteristics, and outcome for general medical-surgical hospital patients with hypernatremia. DESIGN: A prospective cohort study. SETTING: A 942-bed urban university hospital. PATIENTS: All patients who developed a serum sodium concentration of 150 mmol/L or greater during a 3-month observation period. MEASUREMENTS: Daily fluid balance, mental status, and serum and urine electrolytes and osmolality. RESULTS: 103 patients were identified. Eighteen patients were hypernatremic on hospital admission, and 85 developed hypernatremia during hospitalization. Patients who developed hypernatremia during hospitalization were younger than patients who developed hypernatremia before hospital admission (mean age +/- SD, 58.9 +/- 19.2 years compared with 76.6 +/- 16.6 years; P < 0.01) but did not differ in age from the patients of the general hospitalized population. Eighty-nine percent of patients who developed hypernatremia during hospitalization had urine concentrating defects, primarily as the result of the use of diuretics or of solute diuresis, whereas only 50% of patients who were hypernatremic on admission could be shown to have concentrating defects (P < 0.01). Fifty-five percent of all hypernatremic patients had increased insensible water losses, and 35% had increased enteral water losses. Eighty-six percent of patients with hospital-acquired hypernatremia lacked free access to water, 74% had enteral water intake of less than 1 L/d, and 94% received less than 1 L of intravenous electrolyte-free water per day during the development of hypernatremia. No supplemental electrolyte-free water was prescribed during the first 24 hours of hypernatremia in 49% of patients. The duration of hypernatremia was shorter in patients who were hypernatremic on admission (median duration, 3 days) than in patients with hospital-acquired hypernatremia (median duration, 5 days; P < 0.05). Mortality was 41% for all patients, but hypernatremia was judged to have contributed to mortality in only 16% of patients. CONCLUSIONS: Although the development of hypernatremia before hospital admission occurs primarily in geriatric patients, hospital-acquired hypernatremia was more common in our cohort and had an age distribution similar to that of the general hospitalized population. Hospital-acquired hypernatremia was primarily iatrogenic, resulting from inadequate and inappropriate prescription of fluids to patients with predictably increased water losses and impaired thirst or restricted free water intake or both. Treatment of hypernatremia is often inadequate or delayed. Efforts to manage hypernatremia better and altogether avoid hospital-acquired hypernatremia should focus on both physician education and the development of hospital systems to prevent errors in fluid prescription.

Adult↗
PubMed1996

FK-506 and rapamycin but not cyclosporin inhibit aldosterone-stimulated sodium transport in A6 cells.

The immunosuppressants cyclosporin A (CyA), FK-506, and rapamycin (RAP) have multiple actions on target cells that appear to be mediated by interaction of drug-binding protein complexes. Both FK-506 and CyA, but not RAP, inhibit the Ca2(+)-dependent phosphatase, calcineurin, and in so doing have been found to inhibit Na(+)-K(+)-ATPase activity in various nephron segments. Of interest, FK-506 and RAP, but not CyA, are bound by the steroid receptor-associated FK-506-binding heat shock protein of 56 kDa, HSP56. To determine the physiological effect of this interaction on a steroid-mediated phenomenon, the effect of these agents on steroid-mediated Na+ transport in A6 cells was investigated. Aldosterone stimulation of Na+ transport and Na(+)-K(+)-ATPase activity are significantly inhibited by prolonged incubation with FK-506 and RAP. Although CyA inhibits basal Na(+)-K(+)-ATPase activity, it has no effect on aldosterone-induced Na+ transport or the aldosterone-induced increase in Na(+)-K(+)-ATPase activity. FK-506 inhibits the aldosterone-induced synthesis of G alpha i-3 protein but has no effect on glucocorticoid receptor number as quantified by Western blotting. The results suggest that FK-506 and RAP inhibit steroid-mediated Na+ transport at some pretranslational site. The common interaction of these agents with the steroid receptor-associated HSP56 might account for these findings.

Aldosterone↗
PubMedDate not supplied

Dialysate and blood flow dependence of diffusive solute clearance during CVVHD.

To define the flow dependence of diffusive solute clearance (Kd) during continuous venovenous hemodiafiltration (CVVHD), urea, creatinine, and phosphate clearance were measured during CVVHD, while ultrafiltration was minimized. Studies were performed using AN69, polyacrylonitrile (PAN), and polyamide (PA) hollow fiber hemofilters. To assess the dialysate flow dependence of Kd, clearances were measured at constant blood flow (QB), while dialysate inflow (QDi) was increased incrementally from 8.3 to 33.3 ml/min. Kd increased linearly for all three solutes using all membranes. To assess its blood flow dependence, Kd was measured at blood flows of 50, 75, 100, and 150 ml/min, while QDi was held constant at 33.3 ml/min. The PA membrane showed no flow dependence; for the other membranes, Kd was flow independent for QB > 100 ml/min. At all values of QB and QDi, clearances for the AN69 and PAN membranes were two to three times that of the PA membrane (p < 0.01). Lactate uptake increased with increasing QDi for all three membranes, but did not result in blood lactate accumulation. It is concluded that: 1) small molecule clearance is dialysate flow limited during CVVHD; 2) increasing QB beyond 100 ml/min is unnecessary for maintaining solute clearance; and 3) the PA membrane is unsuitable for CVVHD because of its low diffusive solute clearance.

Biological Transport, Active↗
PubMedDate not supplied

Failure of low molecular weight dextran to prevent clotting during continuous renal replacement therapy.

Clotting of the extracorporeal circuit during continuous renal replacement therapy results in decreased ultrafiltration rates, impaired solute clearance and, ultimately, occlusion of the extracorporeal circuit. The authors conducted an open-label randomized controlled trial to determine whether low molecular weight dextran could prevent hemofilter clotting in patients undergoing continuous venovenous hemodialysis. Eleven patients were randomized to receive a continuous infusion of 10% low molecular weight dextran at 25 mL/hr; 8 patients served as control subjects. No differences in the frequency of hemofilter clotting or hemofilter lifespan were detected. The authors concluded that continuous infusion of low dose low molecular weight dextran is not effective in preventing clotting during continuous renal replacement therapy.

Adult↗