Cyclosporine enhances salt sensitivity of body water composition as assessed by impedance among psoriatic patients with normal renal function.

OBJECTIVE: Cyclosporine (CsA) therapy may be accompanied by a significant increase in blood pressure, either sodium (Na+) independent or Na+ dependent. The relationship between Na+ intake and body water distribution among patients treated with CsA has not been evaluated. We report the study, by bioelectrical impedance analysis (BIA), of water composition changes after dietary salt manipulations both before and during CsA treatment of psoriatic patients. METHODS: Ten normotensive psoriatic patients, ages 37 +/- 12 years (range, 19 to 54), with normal renal function were included. Each patient was assessed by BIA in 2 phases, before (phase 1) and during (phase 2) CsA therapy (3 mg/kg/day). In both phases, each patient was assessed in basal conditions (basal1 and basal2), on day 7 of a low-sodium diet (LS1 and LS2; 20 mEq/day) and on day 7 of a high-sodium diet (HS1 and HS2; 350 mEq/day). Plasma creatinine (Pcr), urinary volume excretion (Uv), urinary sodium (UNa+), urinary potassium (UK+), urinary osmolality (UOsmo), weight (Wt), resistance (R), reactance (Xc), total body water (TBW), extracellular water (ECW), intracellular water (ICW), Na:K exchangeable (Nae:Ke), phase angle (PA), and body cell mass (BCM) were evaluated. Blood pressure was monitored during 24 hours on the last day of each diet. Paired Student's t-test was used to analyze the different phases. RESULTS: Before CsA treatment, Wt, TBW and Nae:Ke were lower during LS1 than during basal1, whereas TBW was higher during HS1 than during LS1. During CsA, Wt, TBW, ECW, and Nae:Ke were lower during LS2 than during basal2, whereas ICW and PA were higher during LS2 than during basal2. HS2 showed higher TBW, ECW, and Nae:Ke and lower ICW, PA, and BCM than during LS2. Systolic blood pressure was higher during HS2 than during LS2 or HS1. In addition, diastolic blood pressure was higher during HS2 than during HS1. CONCLUSION: Body hydration status was more sensitive to dietary salt fluctuations during CsA treatment than without CsA, and a high-sodium diet seemed to enhance the CsA-induced hypertension side effect. Moreover, patients on low sodium intake under CsA treatment displayed neither any disturbance of body water composition nor any blood pressure change. Our data suggest that a low sodium intake might be very useful in preventing undesirable pressure and volume changes brought about by CsA treatment.     

Erythrocyte sodium and potassium in patients on peritoneal dialysis

Intracellular sodium and potassium concentrations were determined on erythrocytes obtained, before and after treatment, from patients with end-stage renal disease undergoing 48-hour intermittent peritoneal dialysis. Erythrocyte sodium increased from 7.5 +/- 0.3 to 8.6 +/- 0.4 mmol/L cells with a mean of 1.1 +/- 0.1 mmol/L cells (P less than .001), but erythrocyte potassium and cellular water content were virtually unchanged. Plasma potassium decreased during dialysis from 4.2 +/- 0.2 to 3.3 +/- 0.1 mEq/L (P less than .001). The increase in red-cell sodium correlated with this decrease in plasma potassium (r = .51, P less than .01). In contrast, erythrocyte sodium and potassium in undialyzed control patients with chronic renal failure did not change over a similar period, and plasma potassium was unchanged (4.3 +/- 0.1 mEq/L before and 4.3 +/- 0.2 mEq/L after 48 hours). Incubation of postdialysis erythrocytes from the dialysis patients in their own plasma at varying potassium concentrations showed that the rise in cell sodium was blunted as the plasma potassium was increased from 3.2 +/- 0.1 to 4.5 +/- 0.2 mEq/L. These results suggest that unlike hemodialysis, which is not associated with short-term changes in red-cell electrolytes, intermittent peritoneal dialysis results in a reversible increase in erythrocyte sodium. This change appears to be causally related to the decrease in extracellular potassium concentration.     

Acute and chronic changes in intra- and extracellular potassium and responses to neuromuscular blocking agents

The effects of acutely induced metabolic and respiratory alkalosis with reduction of serum potassium concentration as well as chronic total body potassium depletion induced by furosemide treatment were evaluated and correlated with alteration of neuromuscular blockade induced by d-tubocurarine, pancuronium, and succinylcholine in 12 mongrel dogs. Acute respiratory and metabolic alkalosis significantly reduced serum potassium by about 26%, while chronic furosemide treatment (1 mg/kg IV daily for 14 +/- 4 days) significantly reduced both serum potassium concentration (4.16 +/- 0.31 to 3.27 +/- 0.14 mEq/L) and skeletal muscle potassium content (80.9 +/- 5.6 to 58.7 +/- 4.1 mEq/kg). Succinylcholine neuromuscular blockages was essentially unchanged by acute respiratory or metabolic alkalosis or by chronic furosemide treatment, except for more rapid onset of blockade when 0.1 mg/kg succinylcholine was administered during metabolic alkalosis. Acute respiratory alkalosis shortened the duration of neuromuscular blockade induced by d-tubocurarine and pancuronium while acute metabolic alkalosis shortened the duration of pancuronium only and had no effect on d-tubocurarine. Chronic furosemide treatment had no effect on either d-tubocurarine or pancuronium neuromuscular blockage. Potassium concentration gradients between the intracellular and the extracellular compartments may be more important than cellular potassium depletion per se in affecting responses to neuromuscular blocking agents such as succinylcholine, d-tubocurarine, or pancuronium. Serum alkalemia and hypokalemia antagonize the duration of the neuromuscular blocking action of d-tubocurarine and pancuronium but not that of succinylcholine.     

Electrolyte and acid-base changes with massive blood transfusions.

The case records of 471 patients with massive transfusions of ten or more units of bank blood within 24 hours were reviewed to analyze the electrolyte and acid-base changes. The patients who lived had a less severe acidosis (7.23 +/- 0.15 vs 7.11 +/- 0.17) and the HCO3 was higher (19.8 +/- 15.2 vs 13.4 +/- 6.8) (P less than 0.001). The mean anion gap, despite the low HCO3, was 11.8 +/- 7.8 mEq/L. A combined metabolic and respiratory acidosis, often following bicarbonate therapy, was fetal in 83 per cent (39/47). Serum potassium values (K) were high in 22 per cent and low in 18 per cent of patients. If potassium levels were "corrected" by subtracting 0.5 mEq/L for each 0.1 pH of metabolic acidosis, only 5 per cent of patients were hyperkalemic. Patients dying within 48 hours of the massive transfusions had higher potassium levels (4.9 +/- 1.1 vs 4.4 +/- 0.9; P less than 0.001). Ionized calcium levels (Ca++) were less than normal (1.13-1.32 mmol/L) in 94 per cent of patients and were very low (less than 0.70 mmol/L) in 46 per cent (108/234). The mortality rate with severe ionic hypocalcemia was 71 per cent (vs 40% in patients with more normal values); P less than 0.0001. pH, PCO2, K, and Ca++ must be followed closely with massive transfusions. Rapid correction of volume and pH, without overcorrection, is essential.     

Sodium deficit causing decreased weight gain and metabolic acidosis in infants with ileostomy

The records of 11 infants, 25 to 38 weeks' gestation, with metabolic abnormalities induced by ileostomy fluid losses were reviewed. At operation for necrotizing enterocolitis (NEC) (9) or meconium ileus (MI) (2), they weighed between 1,100 and 3,100 g and were from one to 41 days old. All developed total body sodium depletion and metabolic acidosis from ileostomy bicarbonate loss. In seven, sodium depletion was severe enough to require supplementation; six initially lost or failed to gain weight despite being fed adequate diet and calories. However, after receiving sodium supplementation (three with NaCl and three with NaHCO3), these six patients gained weight and improved their metabolic acidosis. The other five subjects did not initially receive sodium supplementation. Four gained weight; one of these later received supplemental NaHCO3 for a metabolic acidosis. The fifth patient failed to thrive until his ileostomy was closed. All infants initially had urine Na less than 10 mEq/L and normal serum Na. All infants whose urine Na rose above 10 mEq/L and had serum HCO3- greater than or equal to 20 mEq/L grew adequately. A direct relationship existed between ileostomy output and sodium intake required for growth. This expressed mathematically (Na intake = 1.2 + [0.13 x ileostomy output] shows a basal sodium need (with no ileostomy output) of 1.2 mEq/kg/d and an additional requirement of 0.13 mEq/kg/d of sodium for each mL/kg/d of ileostomy output. We conclude that infants with ileostomies are at extreme risk of total body sodium depletion with resultant metabolic acidosis and inadequate weight gain. These infants require sodium supplementation with a combination of NaCl and NaHCO3.(ABSTRACT TRUNCATED AT 250 WORDS)     

The electrolytes in hyponatremia.

It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).     

Salt and fluid intake in the development of hypertension in peritoneal dialysis patients

BACKGROUND: Although fluid overload contributes to hypertension in CAPD patients, less attention has been paid to the role of excess salt and fluid intake. Therefore, we investigated the role of salt and fluid intake in the development of hypertension in CAPD patients. METHODS: A total of 165 stable CAPD patients were included into this study. Based on the blood pressure in three consecutive months, they were divided into three groups: persistent hypertensive (PH; n = 33), intercurrent hypertensive (IH; n = 58) and persistent normotensive (PN; n = 74). The IH group was further divided into two phases: normotensive and hypertensive. Fluid status was evaluated by clinical assessment and bioimpedance analysis (BIA). RESULTS: There were no differences in age, gender, and duration of dialysis among groups. Patients were more fluid overloaded in the PH group. Extracellular water (ECW), total body water (TBW), and normalized extracellular water by height (NECW) were higher in the PH group than the PN group (16.77 +/- 3.62 L vs. 14.61 +/- 2.92 L for ECW, p < 0.01; 32.22 +/- 8.23 L vs. 28.98 +/- 6.00 L for TBW, p < 0.05; and 10.28 +/- 1.86 L/m vs. 9.08 +/- 1.63 L/m for NECW, p < 0.01). However, patients in the PH group also had more total fluid removal (TFR) and total sodium removal (TSR) compared with the PN group (1346.82 +/- 431.27 mL/d vs. 1139.28 +/- 412.65 mL/d for TFR, p < 0.05; and 141.52 +/- 61.57 mmol/d vs. 102.42 +/- 62.51 mmol/d for TSR, p < 0.01). The same trend was demonstrated when compared values of hypertensive and normotensive phase in IH group; patients had higher ECW, TBW, NECW, TSR, and PNa when they were in hypertensive phase than in the normotensive phase. CONCLUSIONS: This study confirmed that fluid overload was closely associated with the development of hypertension in CAPD patients. It also showed that hypertensive patients were in general more fluid overloaded despite a higher fluid and sodium removal as compared with normotensive patients.     

Body composition and nutritional status in patients on continuous ambulatory peritoneal dialysis (CAPD)

Total body water (TBW), extracellular water (ECW), exchangeable potassium pool (EKP), and alkali-soluble nitrogen in skeletal muscle tissue (N) were determined in 9 CAPD patients on treatment from 5 to 14 months (mean 8.6 months). The parameters were reevaluated in 6 of these patients 5 to 13 months later (mean 8.6 months). The mean value of TBW was normal and directly correlated to body weight (BW), but TBW was abnormally distributed between extracellular and intracellular space. ECW volume was significantly lower than the predicted value (12.1 +/- 1.4 versus 16.8 +/- 1.9 l) and out of proportion to TBW (34.8 +/- 3.9% versus 47.8 +/- 1.5%). The calculated intracellular water, therefore, appeared clearly hyperexpanded. The mean value of EKP was slightly reduced, but in three patients there was a 25% reduction. N content was low in 5 out of 9 patients. When the parameters were re-evaluated BW and TBW were unchanged in two subjects. A third patient showed a simultaneous increase in both BW (12.7%) and TBW (19%). TBW variations (+19%, -23%, -24%) without changes in BW were seen in three patients. The mean value of EKP was unchanged, but there was a 25% reduction in one patient. N content improved in two and worsened in one of the three patients in whom it was determined. The data suggest that cell overhydration was the distinctive feature in our CAPD patients, and that the evolution of the nutritional status was variable, since the patients could remain stable, gain or loose body fat, and probably change their lean body mass.     

Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in haemodialysis patients.

BACKGROUND: It is speculated, but unconfirmed, that the usual electrocardiographic manifestations of hyperkalaemia are less frequent and less pronounced in persons with end-stage renal disease (ESRD) than in those with normal renal function. We studied 74 consecutively selected stable haemodialysis patients to determine the prevalence of electrocardiographic changes of hyperkalaemia in stable persons with ESRD receiving haemodialysis. METHODS: Pre-dialysis serum potassium concentration and other electrolytes were measured and simultaneous 12-lead electrocardiogram obtained. RESULTS: The 74 study subjects (45 men, 29 women) comprised 63 blacks (85%), four Hispanics (6%), four whites (6%), and three Asians (4%) of mean+/-standard deviation age 55.5+/-14.7 years. Mean pre-dialysis potassium concentration was 4.9+/-0.71 mEq/l (range 3.3-6.7). No study subject evinced arrhythmia or any of the typical electrocardiographic changes associated with hyperkalaemia. There was no significant difference in T wave amplitude (F statistic=2.1; P=0.11) or T wave to R wave ratio (F statistic=2; P=0.12) between quartiles of serum potassium concentration. Also, T wave amplitude was equivalent in patients with serum potassium concentration >5.5 mEq/l (7.1+/-4.1 mm) or < or =5.5 mEq/l (5.2+/-3.5 mm) (P=0.13). Linear regression analysis showed that the total serum calcium concentration had an inverse relation with T wave amplitude (P=0.03) after adjustment for other factors (a high total serum calcium concentration was associated with a low T wave amplitude). CONCLUSION: Haemodialysis patients with hyperkalaemia may not exhibit the usual electrocardiographic sequella of hyperkalaemia, possibly due in part to fluctuations in serum calcium concentration. Thus, the absence of electrocardiographic changes in hyperkalaemic haemodialysis patients should be interpreted with caution.     

Temporal relationship of hepatocellular dysfunction and ischemia in sepsis

To determine whether hepatic dysfunction in sepsis results from hypoperfusion or direct cellular injury, Sprague-Dawley rats underwent either cecal ligation and puncture or sham operation. After either two or six hours, effective hepatic blood flow was measured using the galactose clearance method. Hepatocytes were isolated and intracellular sodium and potassium and glucose production were measured. Hepatic blood flow in septic rats decreased as early as two hours after sepsis when compared with sham-operated rats (3.8 +/- 1.4 vs 8.7 +/- 3.1 mL/min/100 g body weight). Intracellular sodium and potassium levels and glucose production in septic rats were not significantly different when compared with controls at two hours. After six hours, hepatic blood flow remained depressed and intracellular sodium level was increased compared with sham-operated rats (41.7 +/- 10.4 vs 31.4 +/- 5.9 mmol/L [41.7 +/- 10.4 vs 31.4 +/- 5.9 mEq/L]) and potassium decreased compared with controls (90.7 +/- 7.9 vs 111.5 +/- 6.7 mmol/L [90.7 +/- 7.9 vs 111.5 +/- 6.7 mEq/L]). Glucose production was decreased in septic rats after six hours when compared with controls (4.7 +/- 1.5 vs 15.4 +/- 6.4 mumol/g hepatocytes). These data suggest that hepatic blood flow is decreased before alterations in intracellular sodium and potassium as well as glucose production.     

Bone histology and bone mineral density after correction of acidosis in distal renal tubular acidosis

BACKGROUND: The association between chronic metabolic acidosis and alterations in bone cell functions has been demonstrated in vitro and in animal studies. However, the causal role of acidosis and the effects of alkaline therapy on bone histology and bone mineral density in chronic metabolic acidosis have never been systematically demonstrated in humans. This study was conducted to examine the alterations in bone mineral density and bone histology before and after correction of acidosis among patients with distal renal tubular acidosis (dRTA) METHODS: Correction of metabolic acidosis by potassium citrate was done in non-azotemic dRTA patients, 6 females and 4 males, who had never received long-term alkaline therapy before enrolling into this study. Blood chemistries, serum intact parathyroid hormone, and 24-hour urine collection for the determination of urinary calcium, phosphate, sodium, potassium, bone mineral density determination, and transiliac bone biopsy were done in all patients at baseline and after one year of potassium citrate therapy. RESULTS: Significant elevations in serum bicarbonate (16.5 +/- 3.0 vs. 24.6 +/- 2.8 mEq/L, P < 0.05) and urinary potassium excretion (35.2 +/- 7.9 vs. 55.4 +/-3.5 mEq/L, P < 0.05) were observed after potassium citrate therapy. No significant alterations in other serum and urine electrolytes were found after the therapy. Serum intact parathyroid hormone level was also significantly elevated after one year of treatment (12.8 +/- 7.3 vs. 26.2 +/- 8.7 pg/mL, P < 0.05). Bone formation rate was significantly suppressed at baseline and was normalized by the treatment (0.02 +/- 0.02 vs. 0.06 +/- 0.03 microm(3)/microm(2)/day, P < 0.05). There were non-significant elevations in trabecular bone volume, osteoblastic and osteoclastic numbers. Bone mineral densities in dRTA patients were also significantly decreased below normal values in most studied areas at baseline and were significantly elevated at the trochanter of femur (0.677 +/- 0.136 vs. 0.748 +/- 0.144 g/c m(2), P < 0.05) and total femur (0.898 +/- 0.166 vs. 0.976 +/- 0.154 g/c m(2), P < 0.05) after the treatment. CONCLUSIONS: This study demonstrates that alkaline therapy corrects abnormal bone cell function and elevates bone mineral density in dRTA patients, indicating the causal role of acidosis in the alterations of bone cell functions and reduction in bone mineral density. Parathyroid gland activity also may be involved in the adaptation of the body to chronic metabolic acidosis.     

Comparison of point-of-care versus central laboratory measurement of electrolyte concentrations on calculations of the anion gap and the strong ion difference

BACKGROUND: Clinicians calculate the anion gap (AG) and the strong ion difference (SID) to make acid-base diagnoses. The technology used is assumed to have limited impact. The authors hypothesized that different measurement technologies markedly affect AG and SID values. METHODS: SID and AG were calculated using values from the point-of-care blood gas and electrolyte analyzer and the central hospital laboratory automated blood biochemistry analyzer. Simultaneously measured plasma sodium, potassium, and chloride concentrations were also compared. RESULTS: Mean values for central laboratory and point-of-care plasma sodium concentration were significantly different (140.4 +/- 5.6 vs. 138.3 +/- 5.9 mm; P < 0.0001), as were those for plasma chloride concentration (102.4 +/- 6.5 vs. 103.4 +/- 6.0 mm; P < 0.0001) but not potassium. Mean AG values calculated with the two different measurement techniques differed significantly (17.6 +/- 6.2 mEq/l for central laboratory vs. 14.5 +/- 6.0 mEq/l for point-of-care blood gas analyzer; P < 0.0001). Using the Stewart-Figge methodology, SID values also differed significantly (43.7 +/- 4.8 vs. 40.7 +/- 5.6 mEq/l; P < 0.0001), with mean difference of 3.1 mEq/l (95% limits of agreement, -3.4, 9.5 mEq/l). For 83 patients (27.6%), differences in AG values were as high as 5 mEq/l or more, and for 46% of patients whose AG value was outside the reference range with one technology, a value within normal limits was recorded with the other. CONCLUSIONS: Results with two different measurement technologies differed significantly for plasma sodium and chloride concentrations. These differences significantly affected the calculated AG and SID values and might lead clinicians to different assessments of acid-base and electrolyte status.     

Improved efficiency of hypervolemic therapy with inhibition of natriuresis by fludrocortisone in patients with aneurysmal subarachnoid hemorrhage

OBJECT: To reduce the risk of ischemic complications in patients with subarachnoid hemorrhage (SAH), hypervolemic therapy is generally advocated. However, such conventional treatment cannot always ensure the maintenance of an effective intravascular volume expansion, because excessive natriuresis and osmotic diuresis occur after SAH. In this prospective study the authors examined the effects of inhibition of natriuresis with fludrocortisone acetate on intravascular volume expansion during hypervolemic therapy. METHODS: Thirty patients with SAH were randomized and divided into two groups: controls (Group 1, 15 patients) and patients treated with 0.3 mg/day of fludrocortisone (Group 2, 15 patients). In all patients sodium and fluid intake levels were in excess of maintenance requirements in an attempt to maintain a positive water balance and a central venous pressure (CVP) of 8 to 12 cm H2O. The mean sodium and water intake levels for 14 days after SAH were significantly reduced by fludrocortisone in Group 2 (487+/-34.52 mEq/day and 5159.2+/-249.29 ml/day, respectively; p<0.01) compared with Group 1 (634.2+/-42.86 mEq/day and 6611.7+/-365.67 ml/day). Fludrocortisone significantly reduced the urinary sodium excretion (p<0.01) and urine volume (p<0.01) in parallel, and effectively prevented a negative shift in the sodium as well as water balance (p<0.01). The serum sodium level tended to decrease in Group 1, reaching 135 mEq/L on average, but not in Group 2 (p<0.01). Hyponatremia in Group 1 was always observed at the optimal range of CVP values. A decrease in serum potassium level within the range of 2.8 to 3.5 mEq/L was transiently noted in 11 patients (73.3%) of Group 2, but was easily corrected. Possible side effects of fludrocortisone, such as pulmonary edema, were not encountered. CONCLUSIONS: Intravascular volume expansion in the presence of excessive natriuresis requires a large sodium and water intake and is often associated with hyponatremia. Inhibition of natriuresis with fludrocortisone can effectively reduce the sodium and water intake required for hypervolemia and prevent hyponatremia at the same time.     

Safety and efficacy of low-potassium dialysate

To evaluate the safety and efficacy of low-potassium dialysate, 11 patients with stable end-stage renal disease and with no history of arrhythmia or digitalis use were studied. All were treated with hemodialysis three times per week. Dialysates with potassium concentrations of 2 mEq/L, 1 mEq/L, or 0 mEq/L were compared. Each patient (exceptions noted in text) was studied once at each bath potassium concentration. Cardiac rhythm was recorded by Holter monitor during and for six hours following dialysis. Single PVCs and APCs were common with all potassium concentrations. Only one patient had high-grade ventricular ectopy. It was seen with each of the three potassium concentrations, but was most severe with the potassium-free dialysate. The potassium-free dialysate removed significantly more potassium (78.5 +/- 2.6 mEq) than the 1-K dialysate (62.9 +/- 5.1 mEq) or the 2-K dialysate (50.6 +/- 6 mEq), and the 1-K dialysate removed significantly more potassium than the 2-K dialysate. There were small but significant differences in serum potassium concentrations with the three different dialysates. It was concluded that (1) in all but one of our patients potassium-free dialysate did not produce new ectopy; (2) potassium-free dialysate was 24% more effective than 1-K dialysate and 50% more effective than 2-K dialysate in removing body potassium; and (3) 1-K dialysate was 20% more effective than 2-K dialysate in removing body potassium.     

Hypertonic sodium resuscitation is associated with renal failure and death.

OBJECTIVE: The use of hypertonic sodium solutions (HSS) and lactated Ringer's (LR) solution in the resuscitation of patients with major burns was compared. SUMMARY BACKGROUND DATA: Hypertonic sodium solutions have been recommended for burn resuscitation to reduce the large total volumes required with isotonic LR solution and their attendant complications. METHODS: To evaluate the efficacy of this therapy in our adult burn center, we resuscitated 65 consecutive patients with HSS (290 mEq/L Na) between July 1991 and June 1993 and compared them with 109 burn patients resuscitated with LR (130 mEq/L Na) between July 1986 and June 1988 (LR-1). A subsequent 39 patients were resuscitated with LR between September 1993 and August 1994 (LR-2). RESULTS: Patients receiving hypertonic sodium solutions versus LR-1 were similar with respect to age (46.0 vs. 43.6 years), total burn size (39.2% vs. 39.9%), incidence of inhalation injury (41.5% vs. 47.7%), and predicted mortality (34.6% vs. 30.2%). Total resuscitation volumes during the first 24 hours were lower among patients treated with HSS than those in the LR-1 group (3.9 +/- 0.3 vs. 5.3 +/- 0.2 mL/kg/% body surface area [BSA], p < 0.05). After 48 hours, however, cumulative fluid loads were similar (6.6 +/- 0.6 vs. 7.5 +/- 0.3 mL/kg/%BSA), and total sodium load was greater with the HSS group (1.3 +/- 0.1 vs. 0.9 +/- 0.1 mEq/kg/%BSA, p < 0.002). During the first 3 days after burn, serum sodium concentrations were moderately elevated in the HSS patients (153 +/- 2 vs. 135 +/- 1 mEq/L, p < 0.001). Patients resuscitated with HSS had a fourfold increase in renal failure (40.0 vs. 10.1%, p < 0.001) and twice the mortality of LR-1 patients (53.8 vs. 26.6%, p < 0.001). In patients resuscitated with HSS, renal failure was an independent risk factor (p < 0.001, by logistic regression). Analysis of these results prompted a return to LR resuscitation (LR-2). Age (41.6 +/- 2.9 years), burn size (37.8 +/- 3.9 %BSA), and incidence of inhalation injury (51.3%) were similar to the earlier groups. Total sodium load was less among LR-2 patients than the HSS group (0.7 +/- 0.1 mEq/kg/%BSA, p < 0.01), but similar to the LR-1 patients. Renal failure developed in only 15.4%, and 33.3% died, similar to the LR-1 group and significantly lower than patients treated with HSS (p < 0.001 and p < 0.05, respectively). CONCLUSION: Hypertonic sodium solution resuscitation of burn patients did not reduce the total resuscitation volume required. Furthermore, it was associated with an increased incidence of renal failure and death. The use of HSS for burn resuscitation may be ill advised.     

Inappropriate vasopressin secretion (SIADH) in burned patients

To determine if concentration of plasma arginine vasopressin (AVP) is inappropriate for the plasma Na+ concentration in hyponatremic burned patients, we obtained 32 plasma samples from 20 patients with total burn size (TBS) 15 to 80% of body surface on or after postburn day (PBD) 4 in the morning following all-night recumbency. In the 25 samples (17 patients) with hyponatremia, AVP was elevated, 1.6 to 14.3 (normal less than 0.5) pg/ml. Most patients with normal serum Na+ had normal AVP values. Out of the total, nine patients (12 samples) without renal failure or sepsis, selected also for hyponatremia and urinary Na+ greater than or equal to 20 mEq/L, were considered separately. BUN of 11.7 +/- 1.8 mg/dl and plasma glucose of 130 +/- 5.6 mg/dl, Na+ of 130 +/- 1.1 mEq/L, calculated osmolality of 272 +/- 1.6 mosm/kg, and cortisol of 20.4 +/- 1.6 micrograms/dl were associated with a 24-hour fluid intake of 4.3 +/- 0.26 L and urinary output of 2.7 +/- 0.33 L, Na+ of 80 +/- 14 mEq/L, and osmolality of 520 +/- 73 mosm/kg (mean +/- SE). In all of the plasma samples, AVP was markedly elevated (6.9 +/- 1.1 pg/ml). In another study, four hyponatremic burned patients were given a standard water load. Excretion of the water was delayed, and further dilution of the initially hypotonic plasma resulted in a fall of urinary osmolality and plasma AVP. Cutaneous thermal injury can cause resetting of the mechanism linking plasma tonicity and AVP secretion resulting in dilutional hyponatremia. This syndrome occurs in the absence of gross physiologic perturbations such as volume depletion or adrenal insufficiency.     

Insulin and mineralocorticoids influence on extrarenal potassium metabolism in chronic hemodialysis patients.

Insulin-mineral corticoids effects on extrarenal K+ metabolism in dialysis patients. During the inter-dialytic interval in dialyzed patients, hydrogen and potassium ions are regulated by extrarenal mechanisms. We studied the hormonal and acidotic effects on the extrarenal potassium metabolism, in selected, anuric and stable, hemodialysis patients. Fifteen patients, were grouped according to the mean mid-week pre-dialysis K+ over the past 12 months: > 6.0 mEq/L (G1, n=5), = 5.1-6.0 mEq/L (G2, n=5), < or = 5.0 mEq/L (G3, n=5). After a mid-week hemodialysis session and 12 h fasting, they received 1 g/Kg glucose p.os (A). Insulin, aldosterone, renin, pH, HCO3-, glucose, body weight, blood pressure and heart rate were measured before and 60' after the meal. We recorded the same parameters, except insulin, in 15 patients, similarly grouped, before hemodialysis (T0) and on 3 consecutive off dialysis days (T1-T3); G1 received fluorohydrocortisone (FHC) 0.1 mg-0.3 mg/day, according to body weight and G3 spironolactone (SLT) 200 mg per day. G2 were controls (B). (A) A significant rise in glycemia (81 +/- 23 to 157 +/- 52 mg/dL, P<0.001) and insulin (11.8 +/- 6.2 to 46.8 +/- 19.5 microU/mL, P<0.001), with a drop in K+ (5.1 +/- 0.6 to 4.8 +/- 0.7 mEq/L, P=0.001) and aldosterone (453 +/- 373 to 383 +/- 364 pg/mL, P<0.01), were noted at T60 vs. T0, in all groups. Insulin levels correlated negatively (r=-0.54, P<0.04) to serum K+ at T60, in all patients. (B) No major pH, HCO3 and aldosterone changes were observed in the 3 groups. Despite that, K+ dropped in G1 by FHC (6.7 +/- 0.9 to 5.9 +/- 0.6 mEq/L, P<0.05), rose in G3 by SLT (4.4 +/- 0.4 to 5.4 +/- 0.3 mEq/L, P<0.05) and remained unchanged in controls (5.8 +/- 0.2 to 5.8 +/- 0.6 mEq/L), (T0 vs T3 pre-dialysis values). Glucose significantly lowered K+ by promoting adequate insulin secretion. Drugs affecting aldosterone action significantly influenced potassium metabolism. Acid-base balance was not important in K+ handling in steady state anuric dialysis patients.     

The impact of residual renal function and total body water volume on achieving adequate dialysis in CAPD.

AIMS: The objective is to evaluate the impact of residual renal function (RRF) and total body water (TBW) on achieving adequate dialysis. METHODS: Sixty three CAPD patients performing four 2 liter exchanges daily were evaluated for RRF, total weekly Kt/V (TWKt/V), total weekly creatinine clearance (TWCC) and TBW. RESULTS: In patients with residual renal function (N = 41), TWKt/V and TWCC were 2.2 +/- 0.8 and 77.4 +/- 24.5 L, respectively. In patients without RRF (N = 22), TWKt/V was 1.6 +/- 0.4 and TWCC 42.6 +/- 9.2 L. TBW correlated negatively with TWKt/V in the group without RRF (r = -0.75, P<0.001). CONCLUSION: It is not possible for larger patients without RRF treated with CAPD (2L x 4 exchanges) to achieve the acceptable targets for TWKt/V and TWCC due to TBW.     

Hyponatremia in patients with the acquired immunodeficiency syndrome

Of 103 patients with the acquired immunodeficiency syndrome (AIDS) admitted for acute opportunistic infections, 36 had serum sodium less than or equal to 130 mEq/l (130 mmol/l). In 12 the hyponatremia was associated with volume depletion and corrected with saline replacement therapy. In 23 it was associated with the syndrome of inappropriate antidiuretic hormones secretion (SIADH). One patient had adrenal insufficiency and the serum sodium corrected after steroid replacement. We conclude that hyponatremia is a common electrolyte abnormality in AIDS patients suffering acutely from opportunistic infections and that SIADH and volume depletion are important contributing factors.     

Comparison of Point-of-Care Versus Central Laboratory Measurement of Electrolyte Concentrations on Calculations of the Anion Gap and the Strong Ion Difference

Background: Clinicians calculate the anion gap (AG) and the strong ion difference (SID) to make acid-base diagnoses. The technology used is assumed to have limited impact. The authors hypothesized that different measurement technologies markedly affect AG and SID values.

Methods: SID and AG were calculated using values from the point-of-care blood gas and electrolyte analyzer and the central hospital laboratory automated blood biochemistry analyzer. Simultaneously measured plasma sodium, potassium, and chloride concentrations were also compared.

Results: Mean values for central laboratory and point-of-care plasma sodium concentration were significantly different (140.4 +/- 5.6 vs. 138.3 +/- 5.9 mm;P < 0.0001), as were those for plasma chloride concentration (102.4 +/- 6.5 vs. 103.4 +/- 6.0 mm;P < 0.0001) but not potassium. Mean AG values calculated with the two different measurement techniques differed significantly (17.6 +/- 6.2 mEq/l for central laboratory vs. 14.5 +/- 6.0 mEq/l for point-of-care blood gas analyzer;P < 0.0001). Using the Stewart-Figge methodology, SID values also differed significantly (43.7 +/- 4.8 vs. 40.7 +/- 5.6 mEq/l;P < 0.0001), with mean difference of 3.1 mEq/l (95% limits of agreement, -3.4, 9.5 mEq/l). For 83 patients (27.6%), differences in AG values were as high as 5 mEq/l or more, and for 46% of patients whose AG value was outside the reference range with one technology, a value within normal limits was recorded with the other.