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J C Ayus

Publications and source records attributed to J C Ayus.

At least 19 recordsLinked to original sources
PubMed2006

Phosphorus balance and mineral metabolism with 3 h daily hemodialysis.

Poor control of mineral metabolism is independently associated with mortality in patients receiving hemodialysis. We analyzed data from a 12-month, prospective, non-randomized, controlled study of daily hemodialysis (DHD) (six sessions/week 3 h each) (n=26) vs conventional hemodialysis (CHD) (three sessions/week 4 h each) (n=51) for achievement of mineral metabolism goals and we performed a substudy of weekly dialytic phosphorus removal in DHD vs CHD. Phosphorus control was superior in the DHD group (% change from baseline to end-of-study -27+/-30% vs +7%+/-35% in the CHD group, P=0.0001). Percentage of patients using phosphate binders decreased from 77 to 40% among subjects on DHD, whereas these parameters did not change (76 vs 77%) in the CHD group (P=0.03 by Breslow-Day test for homogeneity of the odds ratios). Weekly mean phosphorus removal was higher in the DHD group (2452+/-720 mg/week vs 1572+/-366 mg/week, P=0.04). Mean normalized protein catabolic rate increased (0.90+/-0.43-1.22+/-0.26 g/kg/day, P=0.0013). DHD was also associated with an increase in the percent of subjects achieving three or more mineral metabolism goals (for phosphorus, calcium x phosphorus and parathyroid hormone) (15 vs 46%, P=0.046). In conclusion, DHD improves phosphorus control by increasing dialytic phosphorus removal while maintaining nutritional status and reducing the use of phosphate binders. The net effect allows for improved achievement of mineral metabolism goals.

Adult↗
PubMed2006

Hyponatremia with hypoxia: effects on brain adaptation, perfusion, and histology in rodents.

Hypoxia appears to be a prominent component of brain damage among patients with hyponatremic encephalopathy. Effects of hypoxia on brain in the presence of hyponatremia are not known. In order to evaluate the contributions of hypoxia to brain damage, three separate experiments were conducted in three groups of rodents. Experiment I evaluated the effects of hypoxia and acute (< 4 h) hyponatremia (plasma Na < 120 mmol/l) on brain adaptation in rabbits. Experiment II evaluated the effects of hypoxia and chronic (4 days) hyponatremia on cerebral perfusion in rats. Experiment III evaluated the effects of hypoxia and chronic hyponatremia on brain histology in rats. In experiment I, rabbits with acute hyponatremia demonstrated brain adaptation with significant falls in brain Na content (by 14.2%, P < 0.01) and osmolality (by 8.3%, P < 0.01), and a rise in brain water (by 10.6%, P < 0.05). Rabbits with combined hypoxia and hyponatremia failed to demonstrate brain adaptation. In experiment II, rats with chronic hyponatremia plus hypoxia had a decrease in cerebral perfusion index by more than 50% (P < 0.01). In experiment III, 23% of hypoxic rats had brain lesions, which were in the cerebellum, thalamus, reticular formation, and basal ganglia. Hyponatremia without hypoxia resulted in no brain lesions. Hypoxia in normonatremic animals results in cerebral edema and histopathologic lesions similar to those found in rats whose plasma Na was overcorrected. Hypoxia in hyponatremic animals aggravates cerebral edema, impairs brain adaptation, and decreases cerebral perfusion.

Adaptation, Physiological↗
PubMed2001

Infectious complications of the hemodialysis access.

Infectious complications of the vascular access are a major source of morbidity and mortality among hemodialysis (HD) patients. Numerous reports implicate the vascular access in up to 48 to 73% of all bacteremias in HD patients. The incidence of vascular access-related infection is highest when central venous dialysis catheters are employed. Native arteriovenous fistulas carry the lowest risk of infection. Unfortunately, prosthetic arteriovenous grafts, which represent the most common type of HD access in the United States, have been repeatedly shown to be a risk factor for bacteremic and nonbacteremic infections. Silent infection in old nonfunctional clotted prosthetic arteriovenous grafts has recently been recognized as a frequent cause of bacteremia and morbidity among HD patients. High proportions of infections related to the vascular access are caused by staphylococcal organisms, which carry high rates of mortality, recurrence, and metastatic complications. Management of vascular access-related infection has two aspects: The first relates to the choice, duration, and mode of administration of antibiotic therapy. Empiric antibiotic therapy, guided by demographic data and severity of illness, should be employed when the causative organisms are unknown. Prolonged administration of specific parenteral antibiotics is crucial in decreasing complications of infection, especially in cases of staphylococcal bacteremia. The second aspect relates to management of the vascular access. Efforts directed toward bacteriological cure should be concurrent with efforts to preserve native venous access sites whenever possible. Efforts to prevent vascular access-related infection should focus on increasing placement of arteriovenous fistulas and minimizing insertion of central venous dialysis catheters. Careful inspection and monitoring of the vascular access is of paramount importance in early detection of vascular access site-related infections. Several new approaches aimed at preventing catheter and prosthetic graft-related infection are being explored.

Anti-Bacterial Agents↗
PubMed2000

Hyponatremia.

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Female↗
PubMed2000

Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners.

BACKGROUND: Noncardiogenic pulmonary edema is often associated with increased intracranial pressure and can be the initial manifestation of hyponatremic encephalopathy. Marathon runners tend to develop conditions that lead to hyponatremia. OBJECTIVE: To describe the development and treatment of noncardiogenic pulmonary edema in marathon runners that was associated with hyponatremic encephalopathy. DESIGN: Case series. SETTING: One university hospital and two community hospitals. PATIENTS: Seven healthy marathon runners who had a history of nonsteroidal anti-inflammatory drug use. The runners collapsed after competing in a marathon and were hospitalized with pulmonary edema. MEASUREMENTS: Plasma sodium levels, chest radiograph, electrocardiogram, cardiac enzyme levels, and magnetic resonance imaging or computed tomographic scans of the brain. RESULTS: Patients had nausea, emesis, and obtundation. The mean (+/-SD) plasma sodium level was 121 +/- 3 mmol/L, and oxygen saturation was less than 70%. Electrocardiograms and echocardiograms were normal. Chest radiographs showed pulmonary edema with a normal heart. Creatine phosphokinase-MB bands, troponin levels, and pulmonary wedge pressure were not elevated. Scanning of the brain showed cerebral edema. All patients were intubated and mechanically ventilated. Treatment with intravenous NaCl, 514 mmol/L, increased plasma sodium levels by 10 mmol/L in 12 hours. Pulmonary and cerebral edema resolved as the sodium level increased. One patient had unsuspected hyponatremic encephalopathy and died of cardiopulmonary arrest caused by brainstem herniation. All six treated patients recovered and were well after 1 year of follow-up. CONCLUSIONS: In healthy marathon runners, noncardiogenic pulmonary edema can be associated with hyponatremic encephalopathy. The condition may be fatal if undiagnosed and can be successfully treated with hypertonic NaCl.

Adult↗
PubMed1999

The changing pattern of hypernatremia in hospitalized children.

OBJECTIVES: Past studies have revealed that hypernatremia occurs primarily in infants with diarrheal dehydration. With improved infant feeding practices and the advent of pediatric critical care medicine, the pattern of hypernatremia in children has likely changed. The purpose of this study was to evaluate the current pattern of hypernatremia in hospitalized children. METHODS: Medical records were reviewed for 68 patients admitted to a large urban children's hospital during a 3-year period, all with a serum sodium greater than 150 mEq/L. The etiologies, predisposing factors, and morbidity and mortality associated with hypernatremia were evaluated. RESULTS: The average patient age was 3.9 years (range, 1 day to 19. 7 years), and the peak serum sodium concentration was 159 mEq/L (range, 151-184 mEq/L). Hypernatremia was hospital acquired in 60% of children. The majority of children (71%) were admitted for reasons other than hypernatremia. In 76% of the patients, inadequate fluid intake was the main cause of hypernatremia. Gastroenteritis contributed to the hypernatremia in only 20% (14 out of 68) of children. Eleven of these were infants <1 year of age with hypernatremia on admission. Eighty-eight percent of patients (60 out of 68) suffered from neurologic impairment, critical illness, chronic disease, or prematurity before developing hypernatremia. The overall mortality was 16%. Patients in whom hypernatremia was not corrected had a significantly higher mortality than those in whom hypernatremia was corrected (4 out of 8 [50%] vs 7 out of 60 [12%]). Peak serum sodium was no different for survivors than nonsurvivors. No deaths were attributable to cerebral edema caused by correction of hypernatremia. Neurologic complications related to hypernatremia occurred in 15% of patients. CONCLUSIONS: Hypernatremia occurs in children of all ages, with the vast majority having significant underlying medical problems. Hypernatremia caused by gastroenteritis in infants has become much less common than previously reported. Hypernatremia is primarily a hospital-acquired disease, produced by the failure to administer sufficient free water to patients unable to care for themselves. Failure to correct hypernatremia may result in a high mortality rate.

Adolescent↗
PubMed1998

Dialysis therapy.

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Biocompatible Materials↗
PubMed1998

The patient with a clotted PTFE graft developing fever.

Haemodialysis access graft infection is easily recognizable when local symptoms (warmth, swelling, pain, or drainage) predominate, and endocarditis is a well established complication of infected grafts. We report a case of bacterial endocarditis complicating silent infection in clotted haemodialysis access graft. It is suggested that, clotted non-functioning grafts may be the harbingers of silent infection, and should be suspected as the source of infection in every haemodialysis patient that presents with fever, even in the absence of clinical signs of graft site infection.

Adult↗
PubMed1998

Silent infection in clotted hemodialysis access grafts.

Thrombotic and infectious complications are frequent causes of hemodialysis vascular access failure and contribute considerably to the cost of care for chronic hemodialysis patients. Although there is clear indication for removal of patent grafts in unresolved bacteremia, there are no guidelines for the management of clotted nonfunctioning grafts. To evaluate for the existence and clinical relevance of silent infection in clotted nonfunctioning hemodialysis grafts, a study was conducted with a series of 20 hemodialysis patients who presented with fever (15 patients), or fever and clinical signs of sepsis (five patients), in whom the source of infection was not immediately localized to any organ system. Comparison was made with 21 asymptomatic patients with clotted grafts who served as control subjects. All patients and control subjects came from a pool of 115 chronic hemodialysis patients in an outpatient hemodialysis unit in the Houston metropolitan area, who were on hemodialysis for a period of time ranging from 3 to 15 yr. Indium scans were performed, followed by removal of the clotted grafts in all patients and control subjects. Bacterial cultures of the recovered surgical material and blood were done concomitantly in all study participants. Indium scans showed positive uptake in or around the clotted grafts in all of the patients and in 15 of the control subjects. Purulent material was found in the grafts in all patients and in 13 of 15 indium scan-positive control subjects. When positive, blood culture pathogens were identical to those cultured from the graft material in all instances. The predominant pathogens were Staphylococcus aureus, followed by Staphylococcus epidermidis. There was no evidence of graft infection in the control subjects if indium scan was negative. Chart review dating back to the start of dialysis revealed five past infectious episodes in the patient group, compared with four in the control group. These findings suggest that clotted nonfunctioning grafts are frequent harbingers of infection. They should be suspected as the source of infection in every hemodialysis patient that presents with fever, even in the absence of clinical signs of graft site infection.

Adult↗
PubMed1997

Glycine-induced hypo-osmolar hyponatremia.

BACKGROUND: Hyponatremia is commonly observed following transurethral resection of the prostate or endometrial resection when the operative field is irrigated with hypotonic glycine. Although glycine-induced hyponatremia has been associated with brain damage, the mortality is low, and it has been suggested that the condition might not be hypo-osmolar and thus might not cause brain edema. OBJECTIVE: To determine if glycine-induced hyponatremia is a hypo-osmolar condition. METHODS: The study was a retrospective evaluation of 13 men who underwent transurethral resection of the prostate and 5 women who underwent transcervical endometrial resection at 2 university medical centers. In all patients, hypotonic glycine (200 mmol/L) was the irrigating solution. Measurements were made of the plasma sodium, osmolality, glucose, urea, glycine, and ammonia; and arterial pH, PO2 and PCO2. Mortality and the occurrence of respiratory arrest were recorded. Data are given as mean (+/- SE). RESULTS: The plasma sodium in 18 patients was 106 +/- 2 mmol/L and the measured osmolality was 235 +/- 5 mOsm/kg H2O. Glycine was measured as the difference between measured and calculated plasma osmolality and was 18 +/- 2 mmol/L. Four patients suffered respiratory arrest; all died. One patient had elevated blood ammonia (130 mumol/L) with a plasma sodium level of 110 mmol/L. She was treated with endotracheal intubation and respiratory support plus hypertonic sodium chloride, and recovered. The other 14 surviving patients were treated with hypertonic sodium chloride. CONCLUSIONS: Patients who undergo transurethral resection of the prostate or endometrial resection with hypotonic glycine as the irrigating medium can experience symptomatic hyponatremia that is hypo-osmolar and can be fatal. Therapy with hypertonic sodium chloride was associated with survival in 14 of 14 patients. Ammonia intoxication also can develop, and can be managed with respiratory support.

Adult↗
PubMed1996

Effects of hypernatraemia in the central nervous system and its therapy in rats and rabbits.

1. We studied the effects of acute (1 or 4 h) and chronic (1 week) hypernatraemia (plasma [Na+], 170-190 mM) on brain histology, and brain water and solute contents in rats and rabbits. 2. In rabbits with acute hypernatraemia, there was significant loss of intracellular brain water, with increases in brain [Na+ + K+], amino acid concentration, and undetermined solute (idiogenic osmole). After 1 week of recovery, brain intracellular water content had returned to normal. 3. In hypernatraemic rats there was myelinolysis of brain white matter, with karyorrhexis and necrosis of neurons. 4. Hypernatraemic rabbits were treated with 77 mM NaCl (i.v.) to normalize plasma [Na+] over 4-24 h intervals. Therapy of either acute or chronic hypernatraemia resulted in significant brain oedema because brain osmolality failed to decrease at the same rate as plasma osmolality. 5. It is concluded that: (a) untreated hypernatraemia results in brain lesions demonstrating myelinolysis and cellular necrosis; (b) normalization of hypernatraemia over 4-24 h results in cerebral oedema, due primarily to failure of brain amino acids and idiogenic osmoles to dissipate as plasma [Na+] is decreased to normal.

Amino Acids↗