Necrotising fasciitis of the eyelid with toxic shock due to Pseudomonas aeruginosa.

Necrotising fasciitis is a rare and rapidly spreading soft tissue infection characterised by widespread necrosis of the superficial fascia and usually occurring in the limbs and the abdominal wall. Periocular necrotising fasciitis is unusual due to the excellent blood supply of the facial region. The usual pathogens are Group A beta-haemolytic Streptococcus and Staphylococcus aureus. We report a case of Pseudomonas necrotising fasciitis of the eyelid with septic shock, initially diagnosed as hordeolum in a young immunocompromised Chinese woman. Early recognition of the condition, followed by timely intervention with surgical debridement and intensive intravenous antibiotic treatment led to a favourable prognosis. It is important for general physicians to recognise the cardinal signs of necrotising fasciitis, as early treatment with timely surgical debridement and supportive medical therapy is the mainstay to successful management.

Charles Bonnet syndrome in Asian patients in a tertiary ophthalmic centre.

AIMS: To describe the epidemiology of Charles Bonnet syndrome (CBS) among patients in an Asian tertiary ophthalmic centre and to describe the characteristics of the hallucinations experienced. METHODS: 1077 consecutive patients aged 50 years and above were asked a standardised question to determine if they had ever experienced formed visual hallucinations. All patients who experienced these symptoms were further interviewed using a detailed, standardised questionnaire to ascertain if they met the diagnostic criteria established for CBS. RESULTS: There were 491 men (45.6%) and 586 women (54.4%). The best corrected visual acuity ranged from 20/20 to light perception in the better seeing eye and from 20/20 to no light perception in the worse seeing eye. Four patients (0.4%) were diagnosed with CBS; two men and two women. There were two Chinese and two Indians. The average age of the CBS patients was 76.3 years (range 65-90 years). Two patients had cataracts, one had glaucoma, and one had both cataracts and glaucoma. A wide variety of visual hallucinations were reported. Three out of four patients experienced a negative reaction to their hallucinations. Only one patient had discussed his symptoms with a doctor. CONCLUSIONS: This is the first report on the epidemiology of CBS in Asian patients. The prevalence rate of CBS (0.4%) is slightly lower than in comparable studies in non-Asian populations. The nature of the hallucinations experienced were similar to those previously reported.

Thyroid function in patients with chronic renal failure.

Chronic renal failure affects thyroid function in multiple ways, including low circulating thyroid hormone concentration, altered peripheral hormone metabolism, disturbed binding to carrier proteins, possible reduction in tissue thyroid hormone content, and increased iodine store in thyroid glands. Both plasma triiodothyronine (T(3)) and thyroxine (T(4)) are reduced. The low serum T(3) is not due to increased T(3) degradation or to decreased thyroidal T(3) secretion but is a result of impaired extrathyroidal T(4) to T(3) conversion. The reduction in T(4) is attributed to the presence of circulating inhibitors, which impair binding of T(4) to thyroxine-binding globulin. Despite decreased circulating T(4) and T(3), thyroid-stimulating hormone (TSH) is not elevated. This absence of TSH elevation is not due to dysfunction of the hypothalamo-pituitary axis, because truly hypothyroid renal failure patients can mount a high TSH response. Thyroid hormone losses during hemodialysis and peritoneal dialysis are trivial and do not require replacement. Serum inorganic iodide and thyroidal iodine content are increased in renal failure patients, and thyroid gland enlargement is frequently encountered. Experiments performed to correct the low serum T(3) level by administration of small doses of LT(3) to renal failure patients resulted in lesser nitrogen balance, greater leucine flux, and protein degradation. We speculate that the low thyroid state in uremia serves to defend against protein wasting and that misguided attempts to replete thyroid hormone stores may worsen protein malnutrition.

Protein intake in patients with renal failure: comments on the current NKF-DOQI guidelines for nutrition in chronic renal failure.

The National Kidney Foundation Clinical Practice Dialysis Outcomes Quality Initiative (DOQI) guidelines recently recommended dietary protein intake for patients with chronic renal failure as follows: predialysis patients should receive 0.60 g/kg/day of protein and increase intake to 0.75 g/kg/day for subjects who cannot follow such a diet. For stable maintenance hemodialysis patients, the recommended protein intake is 1.2 g/kg/day, and for chronic peritoneal dialysis patients, 1.2-1.3 g/kg/day. We differ with these recommendations and believe that a dietary protein intake of 0.8 g/kg/day is appropriate for the predialysis population; an intake of 0.9-1.0 g/kg/day and 1.0-1.1 g/kg/day for maintenance hemodialysis patients and peritoneal dialysis patients, respectively, should be adequate. The rationale and the evidence supporting our arguments are outlined and discussed.

Protein metabolism in patients with chronic renal failure: role of uremia and dialysis.

Individuals with chronic renal failure (CRF) have a high prevalence of protein-energy malnutrition. There are many causes for this condition, chief among which is probably reduced nutrient intake from anorexia. In nondialyzed patients with CRF, energy intake is often below the recommended amounts; in maintenance dialysis patients, both dietary protein and energy intake are often below their needs. Although a number of studies indicate that rats with CRF have increased protein catabolism in comparison to control animals, more recent evidence suggests that increased catabolism in CRF rats is largely if not entirely due to acidemia, particularly if these animals are compared to pair-fed control rats. Studies in humans with advanced CRF also indicate that acidemia can cause protein catabolism. Indeed, nitrogen balance studies and amino acid uptake and release and isotopic kinetic studies indicate that in nondialyzed individuals with CRF, who are not acidemic, both their ability to conserve body protein when they ingest low protein diets and their dietary protein requirements appear to be normal. For patients undergoing maintenance hemodialysis or chronic peritoneal dialysis, dietary protein requirements appear to be increased. The increased need for protein is due, in part, to the losses into dialysate of such biologically valuable nitrogenous compounds as amino acids, peptides, and proteins. However, the sum of the dietary protein needs for CRF patients (of about 0.60 g/kg/day) and the dialysis losses of amino acids, peptides and proteins do not equal the apparent dietary protein requirements for most maintenance dialysis patients. This discrepancy may be due to a chronic state of catabolism in the clinically stable maintenance dialysis patient that is not present in the clinically stable nondialyzed individual who has advanced CRF. Possible causes for such a low grade catabolic state include resistance to anabolic hormones (for example, insulin, IGF-1) and a chronic inflammatory state associated with increased levels of pro-inflammatory cytokines.

The effect of uraemia, acidosis, and dialysis treatment on protein metabolism: a longitudinal leucine kinetic study.

BACKGROUND: Uraemia and dialysis are viewed as catabolic processes resulting in malnutrition in chronic renal failure (CRF) patients. To sort out the effects of uraemia, acidosis, and dialysis on protein metabolism, we measured leucine flux in CRF patients before and after initiation of maintenance dialysis. SUBJECTS AND METHODS: Whole-body leucine flux was measured by primed-constant infusion of L[1-(13)C] leucine in nine CRF patients longitudinally; twice before and once after initiation of maintenance dialysis (D). Before dialysis, one leucine flux was measured when the patients were acidotic (A), and the other, when acidosis was corrected with NaHCO, (NA). Five normal subjects underwent one single leucine flux measurement to serve as control (N). Both patients and normal subjects consumed a constant diet for 6 days and leucine flux was measured on the 7th day 12 h post-absorption. Diet for the CRF patients was identical during the three periods. Plasma L[1-(13)C] leucine and L[1-(13)C]KIC were measured by gas chromatography/mass spectrometry and expired 13CO2 by isotope ratio spectrometry. Leucine kinetics were calculated using standard equations. RESULTS: Plasma CO2 levels were 19, 26 and 31 mmol/l in A, NA and D periods respectively. All kinetic results (micromol/kg/h) are presented as means +/- SD in the order of A, NA, D, and N, and CRF values that are statistically different from N are identified (*). The amounts of leucine release from endogenous protein breakdown (Ra or Q) were 101 +/- 12* 95 +/- 9* 113 +/- 22 and 117 +/- 6. Leucine oxidation (C), quantities of leucine irreversibly oxidized to CO2, were 16.5 +/- 5.4, 9.7 +/- 3.7*, 12.3 +/- 3.0*, and 23.2 +/- 3.1. Leucine protein incorporation levels (S) were 85 +/- 10, 85 +/- 8, 101 +/- 19 and 94 +/- 6. The S of 101 in CRF patients at period D was statistically higher than those during A and NA periods. CONCLUSIONS: These data indicate that when acidosis was corrected, CRF patients adapted to lower protein intake by reducing amino-acid oxidation and protein degradation, and maintained protein synthesis at normal levels. Metabolic acidosis impaired the downregulation of amino-acid oxidation. Maintenance dialysis treatment longitudinally restored protein flux to normal and increased protein synthesis. The general notion that uraemia and dialysis are protein catabolic is not supported by this work.

Leucine turnover in patients with nephrotic syndrome: evidence suggesting body protein conservation.

Whole-body leucine flux was measured in eight patients with nephrotic syndrome and in five healthy subjects by primed-constant infusion of L-[1-13C leucine]. Plasma enrichment of 13C leucine and 13C alpha-keto-isocaproate (13C KIC) was measured by gas chromatography/mass spectrometry, and expired 13CO2 was measured by isotope ration mass spectrometry. Leucine kinetics, calculated from the primary pool enrichment [13C leucine], showed no difference between the nephrotic patients and the control subjects. Kinetics derived from the reciprocal pool [1-13C KIC] enrichment, however, showed that leucine turnover rates were reduced in the nephrotic patients. The values (mumol/kg per h, means +/- SD) comparing the patients and the control subjects are as follows: rate of leucine release from protein degradation, 99 +/- 6 and 117 +/- 12 (P = 0.007); leucine oxidation rate, 15 +/- 7 and 22 +/- 3 (P = 0.04); rate of leucine incorporation into body protein [S], 84 +/- 10 and 95 +/- 6 (P = 0.04); protein turnover rate, 3.99 +/- 0.49 and 4.72 +/- 0.25 g/kg per d (P = 0.007). Nitrogen balance, measured only in the nephrotic patients, showed a mean positive balance of 0.5 g/d. In the nephrotic and control subjects, protein intake levels were 0.84 +/- 0.16 and 1.17 +/- 0.18 g/kg per d (P = 0.002), respectively, and energy intake levels were 33.3 +/- 8.5 and 33.9 +/- 2.4 kcal/kg per d, respectively. Linear correlations between leucine turnover rates and protein intake were highly significant. This study found that nephrotic patients given a modestly protein-restricted diet were able to maintain positive nitrogen balance. Moreover, leucine flux measurements showed downregulation of protein degradation and amino acid oxidation, reflecting appropriate adaptation to a lower protein intake.

Dialysate sodium delivery can alter chronic blood pressure management.

Low dialysate sodium concentrations can reduce postdialysis thirst and serum sodium activity, but patients typically experience dialysis hypotension, fatigue, disequilibrium, and cramps. "High-sodium" hemodialysis minimizes dialysis disequilibrium but increases the serum sodium activity of most patients. Programmed "variable-sodium" dialysis can minimize dialysis discomfort but may also alter the sodium kinetics from those of "high-sodium" dialysis. We designed a cross-over study with random order assignment to determine whether a "variable-sodium" dialysis program could reduce the blood pressure of dialysis patients without increasing dialysis morbidity. Dialysis with a dialysate sodium of 140 mEq/L was compared with dialysis with a programmed exponential decrease of dialysate sodium from 155 mEq/L to 135 mEq/L. Dialysate sodium was then held constant at 135 mEq/L for the final half hour of dialysis. Eighteen patients completed the 7-month study, each receiving 3.5 months of experimental and 3.5 months of standard therapy. Programmed "variable-sodium" dialysis resulted in a reduction in antihypertensive drug use without alterations in predialysis blood pressure, interdialytic weight gain, ultrafiltration tolerance, or the frequency of symptomatic dialysis cramps or hypotension. Patients did, however, have lower postdialysis standing blood pressures and higher postdialysis target weights during programmed "variable-sodium" dialysis.

Regional hemodialysis anticoagulation: hypertonic tri-sodium citrate or anticoagulant citrate dextrose-A.

Regional citrate anticoagulation should be a simple process of substituting hypertonic (1.6 mol/L) citrate for heparin and adjusting the infusion to obtain an arterial activated clotting time of 150 to 200 seconds. Serious, documented complications of citrate anticoagulation involve citrate intoxication during isolated ultrafiltration; hyperaluminemia, hyperammonemia, and hypernatremia during sorbent dialysis; and profound alkalosis, paresthesias, arrhythmia, and cardiac arrest during bicarbonate dialysis. We suspected that some of these complications could be avoided by using anticoagulant citrate dextrose-A (ACD) rather than hypertonic tri-sodium citrate (TSC) as the anticoagulant. In a cross-over study with random assignment order eight adults underwent mid-week dialyses with ACD (0.113 mol/L citrate) and TSC (1.6 mol/L citrate) regional citrate anticoagulation. Predialysis to postdialysis changes in Na (mEq/L), Ca (mg/dL), ionized Ca (mg/dL), pH, and HCO3 (mEq/L) are listed below. [Table in journal] Using continuous blood flow and avoiding isolated ultrafiltration and sorbent dialysis should prevent the delivery system complications of regional citrate anticoagulation. During this evaluation isotonic and hypertonic citrate resulted in similar serum sodium changes, and standard dialysate effectively reversed the citrate/calcium interaction of both hypertonic and isotonic citrate infusions to restore homeostasis without a separate calcium infusion. The combination of TSC and bicarbonate dialysate does produce a profound metabolic alkalosis, which is lessened by using ACD. In general, regional citrate anticoagulation is simplified by using standard dialysate with a hypertonic rather than an isotonic citrate infusion, and dangerous complications are further evaded by adjusting the dialysate bicarbonate to 25 to 30 mmol/L or substituting a mixture of citric acid and TSC (ACD) for TSC.

The significance of protein intake and catabolism.

Diet and nutrition are integral to the management of individuals with renal disease. Uremia engenders anorexia, nausea, meat aversion, and emesis, disturbances that ultimately reduce appetite and cause weight loss and malnutrition. Protein restriction can alleviate these uremic symptoms and improve patient health and vigor, but overly zealous protein restriction may, itself, produce malnutrition. This is particularly likely when energy intake is restricted by either design or anorexia. End-stage renal disease patients require renal replacement therapy for survival, and although dialysis is life sustaining, it neither replaces normal kidney function nor obviates the need for dietary management. In this setting of controlled, persistent uremia, undernutrition can develop surreptitiously. Dialysis physicians have long regarded malnutrition as a sign of uncontrolled uremia and failing health. This supposition has now been validated by epidemiologic studies demonstrating that serum albumin and protein catabolic rate (PCR) discriminate between dialysis patients at high and low risk of death or illness. This correlation of undernutrition with health and survival persists across wide ranges of age, medical diagnoses, and dialysis prescriptions. Because PCR is readily measured using urea kinetic analyses, it has been promoted as a patient monitoring tool and under steady-state conditions it is a reliable method of determining protein intake. Although a single PCR measurement does not integrate day-to-day dietary and metabolic fluctuations and contains an inherent uncertainty of +/- 20%, sequential measurements can be used to assess changes in an individual's dietary protein intake. PCR defines nitrogen losses and, when normalized to a realistic index of metabolic activity (metabolically active body size), it can disclose subtle individual variances in nitrogen utilization. These normalized protein catabolic rates (NPCR) do not, however, measure or describe overall nutrition. The normalization schemes employed are based on population averages and only approximate an individual's true metabolic activity. Thus, using NPCR to define nutritional needs can result in overfeeding obese and underfeeding wasted subjects. Instead, nutritional adequacy should be defined by clinical inspection and comparison with defined standards. Once that state is defined, and desirable protein and calorie intakes are determined, NPCR can be used to monitor the patient's ability to maintain homeostasis.

Abnormal endocrine tests in a hemodialysis patient.

A home hemodialysis patient with abnormal thyroid function tests and hyperprolactinemia is presented. Abnormal thyroid tests included low total triiodothyronine and low total thyroxine and free thyroxine; the latter was documented by the use of both RIA and direct dialysis equilibrium techniques. Serum thyroid-stimulating hormone was normal, and the thyroid-stimulating hormone response to thyrotropin-releasing hormone stimulation was in the low-normal range. Serum prolactin was elevated to more than twice the normal level, and the prolactin response to thyrotropin-releasing hormone was also blunted. The interpretation, pathogenesis, physiologic significance, and management of these abnormalities are discussed.

Is 8 hours of nightly peritoneal dialysis enough?

Eight hours of nightly tidal peritoneal dialysis (TPD) theoretically can provide uremia control equal that of continuous cyclic peritoneal dialysis (CCPD). To assess the in vivo validity of this prediction, six patients underwent mass transfer area coefficient (MTaC) measurements and dialysis using CCPD and TPD. CCPD consisted of five nighttime exchanges of 40 ml/kg and a daytime exchange of 20 ml/kg. TPD used an initial fill of 40 ml/kg and hourly tidal flows of 30 or 50 ml/kg. The nocturnal portion of CCPD lasted 9.7 hr (range 9.5-10 hr). TPD lasted 8.5 hr (range 8-9 hr) and was devoid of daytime dialysis. The patients consumed a diet containing 1.2 +/- 0.07 g protein/kg body weight (range 0.7-1.7 g/kg) and had a pre dialysis blood urea nitrogen concentration of 52 mg/dl (range 18-82 mg/dl). The dialysate clearances of urea and creatinine were indexed to patient size and extrapolated to weekly values. CCPD provided a weekly creatinine clearance of 50 L/1.73 m2 and a Kt/Vurea of 2.06. TPD with an hourly dialysate flow of 30 ml/kg achieved a weekly creatinine clearance of 42.8 L/1.73 m2 and a Kt/Vurea of 1.73. When the hourly dialysate flow was increased to 50 ml/kg, these values improved to 53.3 L/1.73 m2 and 2.15, respectively. Dialysis efficiency equal to that of CCPD can be obtained using 8 hr of TPD when membrane characteristics (mass transfer area coefficient) and dialysate flow rates are appropriate. Patients with normal or above normal mass transfer area coefficients can obtain a weekly Kt/Vurea exceeding 2.0 using nightly high flow TPD.

Continuous ambulatory peritoneal dialysis catheter infections: diagnosis and management.

PURPOSE: To develop diagnostic and treatment strategies for peritoneal dialysis catheter exit-site and tunnel infections. POPULATION: All consenting peritoneal dialysis patients performing home dialysis through the University of Iowa Hospitals and Clinics Home Dialysis Training Center. This is a state-owned teaching hospital serving a rural population of approximately one million people in Iowa and western Illinois. METHODS: Four dialysis nurses collected information on a prospectively designed data acquisition tool. Patients were randomly assigned to one of two treatment groups, intraperitoneal vancomycin plus oral rifampin or oral trimethoprim/sulfamethoxazole (TMP/SMX), and their initial antibiotic therapy determined by that assignment. If the infection was gram-negative, the initial antibiotics were discontinued and an alternative therapy begun. Therapy was initiated by the nursing staff and required physician notification within 48 hours. RESULTS: There were 126 recorded catheter infections (exit-site, tunnel, or cuff infection) resulting in a rate of 0.67 episodes per patient year of exposure. Staphylococcus aureus was isolated from the majority (60%) of these events. Pseudomonas aeruginosa was the next most common isolate and accounted for 21% of infections. Rubor, dolor, and turgor are the classic signs of inflammation, and at least one of these was present in 79% of the episodes. Isolated pericatheter erythema or serous discharge was associated with a minimal risk (< 2%) of catheter loss. The presence of a purulent exit-site discharge identified patients who had a 30% chance of failing systemic antibiotic therapy and a 20% risk of catheter loss. The concurrent presence of exit-site tenderness or swelling identified the most severe infections. Staphylococcal infections responded equally well to local cleaning and vancomycin plus rifampin (86% cured) or oral trimethoprim/sulfamethoxazole (89% cured) therapy. Gram-negative infections were frequent (27%) and appeared to respond best to a combination of tobramycin and ciprofloxacin. CONCLUSION: Exit-site/tunnel inflammation is detectable by patients and can be used to guide therapy. An isolated finding of erythema or serous discharge is not indicative of an acute infection and may not require systemic antibiotics. The presence of purulence identifies patients at risk for catheter loss, and these patients benefit from systemic therapy. The combination of a purulent exit-site discharge plus pericatheter tenderness or swelling identifies patients likely to suffer treatment failure and require subsequent catheter removal. The cure rate of gram-positive catheter infections treated with vancomycin plus rifampin was indistinguishable from that achieved with oral trimethoprim/sulfamethoxazole (p = 0.99).

Tidal peritoneal dialysis: kinetics and protein balance.

Some patients find automated peritoneal dialysis preferable to continuous ambulatory peritoneal dialysis (CAPD). Unfortunately, automated peritoneal dialysis prescriptions are time consuming and can impede rehabilitation. We wished to determine whether an 8-hour tidal peritoneal dialysis (TPD) prescription could maintain the time averaged blood urea nitrogen at 60 mg/dL or less while patients consumed a diet containing approximately 1.2 g protein/kg body weight/d. Ten home dialysis patients previously stabilized on continuous cyclic peritoneal dialysis volunteered for a metabolic balance study conducted at the University of Iowa's Clinical Research Center. A peritoneal equilibration test was conducted and mass transfer area coefficients (MTaCs) were derived for each subject. Nitrogen balance was measured during the last 5 days of a 12-day constant diet while patients underwent a series of monitored nocturnal dialyses. Mass transfer area coefficient measurements were reproducible and independent of the filling volume and ultrafiltration, but varied between subjects (normalized MTaCurea = 33.6 +/- 16.3 mL/min, normalized MTaCcrt = 16.3 +/- 9.5 mL/min). Tidal peritoneal dialysis urea and creatinine clearances could be predicted by these MTaC values (r2 = 0.70 urea, r2 = 0.91 creatinine). Nitrogen balance assumptions predicted, and we confirmed, a relationship between dietary protein intake and urea nitrogen generation (r2 = 0.82) during TPD. A normalized protein catabolic rate of 1.2 g/kg/d resulted in a urea nitrogen generation rate of approximately 100 mg/kg/d. If a patient's protein intake was approximately 1.2 g/kg/d, then TPD with a weekly urea clearance normalized to body volume (Kt/V(urea)) of approximately 2.1 (urea clearance, approximately 0.35 mL/kg/min) could maintain a time averaged blood urea nitrogen of approximately 60 mg/dL.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of hemodialysis on protein metabolism. A leucine kinetic study.

To assess the effect of hemodialysis on protein metabolism, leucine flux was measured in seven patients before, during, and after high efficiency hemodialysis using cuprophane dialyzers and bicarbonate dialysate during a primed-constant infusion of L-[1-13C]leucine. The kinetics [mumol/kg per h, mean +/- SD] are as follows: leucine appearance into the plasma leucine pool was 86 +/- 28, 80 +/- 28, and 85 +/- 25, respectively, before, during, and after dialysis. Leucine appearance into the whole body leucine pool, derived from plasma [1-13C]alpha-ketoisocaproate enrichment, was 118 +/- 31, 118 +/- 31, and 114 +/- 28 before, during, and after dialysis, respectively. In the absence of leucine intake, appearance rate reflects protein degradation, which was clearly unaffected by dialysis. Leucine oxidation rate was 17.3 +/- 7.8 before, decreased to 13.8 +/- 7.8 during, and increased to 18.9 +/- 10.3 after dialysis (P = 0.027). Leucine protein incorporation was 101 +/- 26 before, was reduced to 89 +/- 23 during, and returned to 95 +/- 23 after dialysis (P = 0.13). Leucine net balance, the difference between leucine protein incorporation and leucine release from endogenous degradation, was -17.3 +/- 7.8 before, decreased to -28.5 +/- 11.0 during, and returned to -18.9 +/- 10.3 after dialysis (P < 0.0001). This markedly more negative leucine balance during dialysis was accountable by dialysate leucine loss, which was 14.4 +/- 6.2 mumol/kg per h. These data suggest that hemodialysis using a cuprophane membrane did not acutely induce protein degradation. It was, nevertheless, a net catabolic event because protein synthesis was reduced and amino acid was lost into the dialysate.

Ventilatory and metabolic changes during high efficiency hemodialysis.

Ventilatory and metabolic changes were measured in seven patients undergoing high efficiency hemodialysis using a cuprophane dialyzer and bicarbonate-containing dialysate. At an HCO3 concentration of 35 mEq/liter and a mean in vivo urea clearance of 3.6 ml/kg/min, hypoxemia was not detected during dialysis (PaO2 was 14.00 and 13.60 kPa before and during dialysis). The new findings, related to high efficiency bicarbonate dialysis, include a sustained rise in minute ventilation (VE, 6.1 to 6.8 liter/min, P less than 0.01), an increase in CO2 excretion (VCO2, 194 to 214 ml/min, P less than 0.05), and O2 consumption (VO2, 215 to 246 ml/min, P less than 0.05). The increment in VE and VCO2 was attributed to the high flux rate of bicarbonate while the rise in VO2 is likely the result of metabolic alkalosis. Arterial pH rose from 7.40 to 7.49 mm Hg and serum HCO3 increased from 23.8 to 29.2 mEq/liter, while pCO2 remained normal at 5.07 kPa throughout the study. The acid-base status of the blood changed from that of a metabolic acidosis to that of a respiratory acidosis across the dialyzer where the pH decreased from 7.47 to 7.41 and pCO2 rose from 5.31 to 7.72 kPa. These data indicate that a healthy ventilatory response is needed to excrete the excess CO2 generated during high efficiency bicarbonate hemodialysis. The significance and etiology of the elevated O2 consumption is undetermined.

Tidal peritoneal dialysis: preliminary experience.

OBJECTIVES: To determine the feasibility of home tidal peritoneal dialysis (TPD) and to assess whether eight hours of TPD can achieve uremia control and urea removal equal to that of continuous cycling peritoneal dialysis (CCPD). DESIGN: An open enrollment pilot study. SETTING: The Home Dialysis Training Center of the University of Iowa Hospitals and Clinics, a tertiary care teaching hospital. PATIENTS: Nine patients experienced with CCPD and living 80 km to 280 km from the dialysis center began TPD, because they wished to decrease their dialysis time. INTERVENTIONS: Following baseline measurements, each patient was taught to perform TPD. TPD consisted of an initial fill volume of 40 mL/kg, a residual volume approximately 20 mL/kg, and tidal exchanges of 10 to 20 mL/kg to achieve the desired hourly flow rate. Clinic assessments took place every four to six weeks, and prescriptions were subsequently altered to attain urea removal equal to that of CCPD. MEASUREMENTS: Patient interviews were used to determine TPD acceptance. Prior to each clinic visit, dialysate effluent volume and dialysis duration were recorded, and a sterile sample of the effluent was obtained for urea, creatinine, and total nitrogen measurement. RESULTS: Urea and creatinine clearances increased with dialysate flow. Dialysate nonurea nitrogen was 3.0 +/- 0.2 mmol/kg/D and changed minimally with increasing dialysate volumes. Eight hours of TPD (initial fill: 40 mL/kg; residual volume: 20 mL/kg; tidal inflow: 20 mL/kg) with hourly tidal flow exceeding 40 mL/kg/hr and no daytime volume achieved urea removal equal to that of the patient's prior CCPD prescription. CONCLUSION: TPD can provide dialysis equal to that of CCPD within a shorter amount of time (eight vs ten hours), but uses a greater volume of dialysate (16.0 L for TPD vs 9.5 L for CCPD).