Changes In Serum Sodium Concentration Research Articles

The epidemiology of intensive care unit-acquired hyponatraemia and hypernatraemia in medical-surgical intensive care units

IntroductionAlthough sodium disturbances are common in hospitalised patients, few studies have specifically investigated the epidemiology of sodium disturbances in the intensive care unit (ICU). The objectives of this study were to describe the incidence of ICU-acquired hyponatraemia and hypernatraemia and assess their effects on outcome in the ICU.MethodsWe identified 8142 consecutive adults (18 years of age or older) admitted to three medical-surgical ICUs between 1 January 2000 and 31 December 2006 who were documented to have normal serum sodium levels (133 to 145 mmol/L) during the first day of ICU admission. ICU acquired hyponatraemia and hypernatraemia were respectively defined as a change in serum sodium concentration to below 133 mmol/L or above 145 mmol/L following day one in the ICU.ResultsA first episode of ICU-acquired hyponatraemia developed in 917 (11%) patients and hypernatraemia in 2157 (26%) patients with an incidence density of 3.1 and 7.4 per 100 days of ICU admission, respectively, during 29,142 ICU admission days. The incidence of both ICU-acquired hyponatraemia (age, admission diagnosis, Acute Physiology and Chronic Health Evaluation (APACHE) II score, length of ICU stay, level of consciousness, serum glucose level, body temperature, serum potassium level) and ICU-acquired hypernatraemia (baseline creatinine, APACHE II score, mechanical ventilation, length of ICU stay, body temperature, serum potassium level, level of care) varied according to patients' characteristics. Compared with patients with normal serum sodium levels, hospital mortality was increased in patients with ICU-acquired hyponatraemia (16% versus 28%, p < 0.001) and ICU-acquired hypernatraemia (16% versus 34%, p < 0.001).ConclusionsICU-acquired hyponatraemia and hypernatraemia are common in critically ill patients and are associated with increased risk of hospital mortality.

Changes in serum sodium concentration after transurethral procedures

The aim of this study is to evaluate the changes in serum sodium concentration and the degree of correlation with factors such as the amount of intravenous fluid intake, the kind and the amount of irrigating fluids and the duration of the procedure. In this framework, 98 male patients who underwent transurethral procedure were studied and the correlation between the magnitude of hyponatraemia and the above-mentioned parameters was evaluated. All procedures were performed under spinal anesthesia and a solution of either manitol-sorbitol or sterilized water was used as irrigation fluid. Serum sodium concentration was measured before and after the procedure, while the kind and amount of the irrigating fluids, the amount of fluid intake and the duration of the procedure were also recorded. The patients were divided into three groups according to the duration of the procedure (i) <30 min, (ii) 30-60 min, and (iii) >60 min. Significant reduction in serum sodium concentration was found postoperatively (P < 0.001) and this was more profound in procedures longer than 1 h. This reduction was strongly correlated only with the duration of the transurethral procedure (P < 0.01). In conclusion, in transurethral procedures the reduction in serum sodium is postoperatively related to the duration of the procedure, while the intravenous and irrigating fluids to play no role on it.

The effect of prednisolone on serum sodium concentration

Background Glucocorticoids are widely used in clinical practice. In addition to their anti-inflammatory effects, they influence the salt and water homeostasis. Although parts of the latter action have been studied individually, there are no reports in stable outpatients on the net effect of glucocorticoids on serum sodium concentration. Methods A group of 23 patients on chronic prednisolone therapy was compared with a control population with respect to serum sodium concentration. Intra-individual changes in serum sodium concentration after the initiation of prednisolone therapy were studied separately in 14 patients. Results A significantly higher serum sodium level of 1.67 mmol/L ( P = 0.03) was observed in the prednisolone-treated patients, whereas initiation of prednisolone was accompanied by an increase of 2.61 mmol/L ( P = 0.004). The doses and duration of prednisolone therapy had no relation to the increase in serum sodium concentration. Conclusion Prednisolone therapy in stable outpatients results in a small, yet significant, increase in serum sodium concentration.

Therapeutic approach in patients with dysnatraemias

Rapid correction of dysnatraemias is frequently associated with increased morbidity and mortality. Therefore, it is important to estimate the proper volume and type of infusate required to change the serum sodium concentration predictably. The aim of this study is to evaluate the utility or/and the accuracy of the Adrogue-Madias formula in managing patients with hyponatraemia and hypernatraemia. Among the 317 patients who either on admission to our internal medicine clinic or during their hospitalization were found to have hyponatraemia or hypernatraemia, we studied 189 patients (59.6%) in whom the administration of intravenous solutions was required for the correction of dysnatraemias. Twelve hours after starting the administration of intravenous solutions the anticipated as well as the achieved serum sodium concentration were as follows: in volume depleted patients 130.2+/-4.1 vs 131.3+/-5.2 meq/l (n = 45; P = NS), in syndrome of inappropriate antidiuretic hormone secretion (SIADH) patients 127.4+/-5.7 vs 128.9+/-5.9 meq/l (n = 10; P = NS), in patients with diuretic-induced hyponatraemia 123.8+/-6 vs 125.5+/-5.6 meq/l (n = 29; P = NS), in patients with primary polydipsia 122.5+/-0.7 vs 129+/-1.4 meq/l (n = 2; P = 0.02), while in patients with hypernatraemia 153.6+/-7.5 vs 156.5+/-8.9 meq/l (n = 92; P = 0.021). Furthermore, 24 h from the initiation of the therapeutic intervention the expected and the achieved serum sodium concentrations were 130+/-4 vs 135.6+/-3.3 meq/l (n = 15; P = 0.002) in patients with volume depletion, 128.1+/-4.8 vs 130+/-4.5 meq/l (n = 15; P = NS) in patients with diuretic-induced hyponatraemia and 151.5+/-6.4 vs 153.3+/-8.3 meq/l (n = 67; P = NS) in patients with hypernatraemia. The formula that has been proposed by Adrogue and Madias predicted with relative accuracy the changes in serum sodium concentration in almost all patients. Thus, it should be considered as a very useful tool for the management of dysnatraemias. However, special attention should be paid when this equation is used in patients with hyponatraemia due to extracellular volume depletion after euvolaemia's restoration and primary polydipsia in order to avoid rapid correction of hyponatraemia.

The serum sodium concentration after surgical operation: precision permits predictions.

In view of previous conflicting reports, the distribution of a water overload was investigated in 6 healthy volunteers. The fall in serum sodium was predictable from prior measurement of total body water (tritium) confirming that the induced hyponatraemia was dilutional. Using a standard intravenous fluid regimen, a prospective study for 6 days on 50 patients undergoing major abdominal surgery established a confidence band for change in serum sodium concentration. This band not only enables precise prediction of whether observed sodium values in patients are "normal' for that point in their postoperative course, but also demonstrates that changes are more prolonged than was at first thought. Their dilutional nature following uncomplicated surgery is supported by linear relationships between serum osmolality and serum sodium (s-Osm = 1.86 [s-Na+] + 18:74; (P < 0.001) and between observed and calculated osmolality (Obs-Osm = 0.97 [Calc-Osm] + 15.11; P < 0.001). More detailed investigation of 14 patients by isotope dilution provided independent evidence of dilutional change. This conclusion is additionally supported by lesser changes in patients on a more restricted fluid regimen. As a practical confirmation of the utility of this approach, departures from the simple dilutional relationships were observed in 7 critically ill patients whose postoperative course was complicated. In this group osmolal "gags' of 20-50 mosmol/kg were identified. Current standard postoperative fluid regimens cause dilutional changes; these are predictable and provide a yardstick for use in management of both the healthy and the ill surgical patient.

Sodium Balance And Sweat Loss During The Hawaii IRONMAN Triathlon

PURPOSE To determine the variability in sweating rate and sweat sodium concentration (sweat-Na) and its relationship to changes in serum sodium concentration (serum-Na) in ultra-endurance triathletes competing in the 2003 Ironman Triathlon World Championship. METHODS During the sweat analysis trial, seventy-one heat-acclimatized males and females (22–74y) exercised on a stationary bicycle at 70–75% of HRmax for 30 minutes following an 8 minute warm-up. All trials took place in warm conditions (26.4 ±0.2°CWBGT, 28.5 ± 0.2°C dry bulb, 66.0 ± 0.0% RH) in an outdoor field laboratory in Kailua-Kona, HI, 3–7d prior to the race. Serum-Na and skin-fold thickness were measured prior to exercise. Sweating rate, determined via change in body mass, and sweat-Na were measured during the 30 min exercise bout. Forty-six male and female subjects who participated in the sweating analysis trial were also studied on race-day. Pre- and post-race serum-Na and body mass were measured and race nutritional intake was also recorded. RESULTS The subjects exhibited a large amount of variability in absolute and relative sweating rate (1.39±0.05 L/hr, coefficient of variation (CV) = 30.8%; 19.4 ± 0.7 ml/kg/hr, CV = 28.5%), sweat-Na (43.4±2.1 mEq/L, CV = 40.0%), and absolute and relative sweat-Na loss(61.6±4.1 mEq/hr, CV = 56.0; 0.87 ± 0.06 mEq/kg/hr, CV = 54.2%). In males, the decline in race-day serum-Na was correlated with relative sweat rate, relative rate of sweat-Na loss, and body mass change (r=−0.413, p<0.05; r=−0.457, p<0.05; r=−0.549, p<0.01). Together, the rate of relative sweat-Na loss and body mass change were highly related to changes in serum-Na (r=0.686, p<0.05). In females, body mass changes alone were highly associated with declines in serum-Na (r=0.614, p<0.05). Females had a significant relationship between rate of absolute sweat-Na loss and Na intake (r=0.637, p<0.05), while males did not (r=0.280, p=0.466). CONCLUSIONS Changes in serum-Na during an ultra-endurance triathlon were related to the interactions of sweat-Na loss, sodium ingestion, and fluid balance. Supported by the Gatorade Sports Science Institute.

Sodium Balance And Sweat Loss During The Hawaii IRONMAN Triathlon

PURPOSE To determine the variability in sweating rate and sweat sodium concentration (sweat-Na) and its relationship to changes in serum sodium concentration (serum-Na) in ultra-endurance triathletes competing in the 2003 Ironman Triathlon World Championship. METHODS During the sweat analysis trial, seventy-one heat-acclimatized males and females (22–74y) exercised on a stationary bicycle at 70–75% of HRmax for 30 minutes following an 8 minute warm-up. All trials took place in warm conditions (26.4 ±0.2°CWBGT, 28.5 ± 0.2°C dry bulb, 66.0 ± 0.0% RH) in an outdoor field laboratory in Kailua-Kona, HI, 3–7d prior to the race. Serum-Na and skin-fold thickness were measured prior to exercise. Sweating rate, determined via change in body mass, and sweat-Na were measured during the 30 min exercise bout. Forty-six male and female subjects who participated in the sweating analysis trial were also studied on race-day. Pre- and post-race serum-Na and body mass were measured and race nutritional intake was also recorded. RESULTS The subjects exhibited a large amount of variability in absolute and relative sweating rate (1.39±0.05 L/hr, coefficient of variation (CV) = 30.8%; 19.4 ± 0.7 ml/kg/hr, CV = 28.5%), sweat-Na (43.4±2.1 mEq/L, CV = 40.0%), and absolute and relative sweat-Na loss(61.6±4.1 mEq/hr, CV = 56.0; 0.87 ± 0.06 mEq/kg/hr, CV = 54.2%). In males, the decline in race-day serum-Na was correlated with relative sweat rate, relative rate of sweat-Na loss, and body mass change (r=−0.413, p<0.05; r=−0.457, p<0.05; r=−0.549, p<0.01). Together, the rate of relative sweat-Na loss and body mass change were highly related to changes in serum-Na (r=0.686, p<0.05). In females, body mass changes alone were highly associated with declines in serum-Na (r=0.614, p<0.05). Females had a significant relationship between rate of absolute sweat-Na loss and Na intake (r=0.637, p<0.05), while males did not (r=0.280, p=0.466). CONCLUSIONS Changes in serum-Na during an ultra-endurance triathlon were related to the interactions of sweat-Na loss, sodium ingestion, and fluid balance. Supported by the Gatorade Sports Science Institute.

Fluid balance during and after an ironman triathlon.

To record weight changes, fluid intake and changes in serum sodium concentration in ultradistance triathletes. Descriptive research. Ironman triathlon (3.8 km swim, 180 km cycle, 42.2 km run). Air temperature at 1200 h was 21 degrees C, (relative humidity 91%). Water temperature was 20.7 degrees C. 18 triathletes. None. Subjects were weighed and had blood drawn for serum sodium concentration [Na], hemoglobin, and hematocrit, pre-race, post-race, and at 0800 h on the morning following the race ("recovery"); subjects were also weighed at transitions. Fluid intake during the race was estimated by athlete recall. Median weight change during the race = -2.5 kg (p < 0.0006). Subjects lost weight during recovery (median = -1.0 kg) (p < 0.03). Median hourly fluid intake = 716 ml/h (range 421-970). Fluid intakes were higher on the bike than on the run (median 889 versus 632 ml/h, p = 0.03). Median calculated fluid losses cycling were 808 ml/h and running were 1,021 ml/h. No significant difference existed between pre-race and post-race [Na] (median 140 versus 138 mmol/L) or between post-race and recovery [Na] (median 138 versus 137 mmol/L). Plasma volume increased during the race, median + 10.8% (p = 0.0005). There was an inverse relationship between change in [Na] pre-race to post-race and relative weight change (r = -0.68, p = 0.0029). Five subjects developed hyponatremia ([Na] 128-133 mmol/L). Athletes lose 2.5 kg of weight during an ultradistance triathlon. most likely from sources other than fluid loss. Fluid intakes during this event are more modest than that recommended for shorter duration exercise. Plasma volume increases during the ultradistance triathlon. Subjects who developed hyponatremia had evidence of fluid overload despite modest fluid intakes.

MRI changes during water loading in patients with polydipsia and intermittent hyponatremia.

Patients with polydipsia and intermittent hyponatremia have greater ventricle-brain ratios (VBRs) than matched patients without polydipsia and intermittent hyponatremia and normal subjects. Unlike previous studies, this study controlled for the impact of water loading when examining the volume of intracranial structures. Under controlled conditions, eight male schizophrenic patients with polydipsia and intermittent hyponatremia were first assigned to either normal fluid intake or oral water loading and then the alternative condition the following day. Magnetic resonance imaging (MRI) volumetric measurements were made with the use of a standardized protocol. During water loading, total VBR and lateral ventricle volume significantly decreased by 13.1% and 12.6%, respectively. A strong association between change in serum sodium concentration and change in VBR was noted across conditions. These findings indicate that 1) water loading does not account for the diminished brain volume observed in patients with polydipsia and intermittent hyponatremia in previous studies, and 2) hyponatremia can significantly alter brain morphology on MRI.

Evaluation of an ultrasonic blood volume monitor.

Hypotension complicates approximately 30% of all dialysis treatments. Although the genesis of hypotension is multifactorial, hypovolaemia is thought to play a major role as a direct result of decreased blood volume, particularly during ultrafiltration. The described blood volume monitor enables blood volume to be measured continuously by a non-invasive technique. The blood volume monitor is based on the principle that the total protein concentration, the sum of haemoglobin and plasma proteins in the vascular space, changes during ultrafiltration. Changes of total protein concentration are determined from the velocity of sound waves in blood, measured using a cuvette in the extracorporeal circuit designed for this purpose. The precision of the blood volume monitor was evaluated in 180 dialysis treatments in 49 patients. The relative blood volume obtained by the monitor was compared with a standard reference method involving calculation of relative blood volume from serial measurements of haemoglobin. A very good agreement between the two methods was achieved (SD = 1.70%, r > 0.96). The results showed no sensitivity to changes in serum sodium concentration (range 130-145 mmol). The 'noise' introduced in the blood volume signal was low (< or = 0.2%, sampling rate 10 s) allowing subtle blood volume changes to be detected with high resolution. In addition the device enabled the measurement of haematocrit (Hct) and haemoglobin (Hb) to be made since this is the largest blood component determining total protein concentration. A comparison with the centrifuge method revealed an accuracy of +/-2.9 Hct-%, and a comparison with the photometer an accuracy of +/-0.8 g Hb/dl. In summary the blood volume monitor allows precise and reliable measurement of relative blood volume. It provides the instrumentation essential for feedback control of relative blood volume during dialysis.

Liver transplantation in hyponatremic patients with emphasis on central pontine myelinolysis

Patients awaiting liver transplantation may suffer from severe hyponatremia. It has been suggested that hyponatremia or its treatment. might be associated with central pontine myelinolysis (CPM), a serious complication that can be seen after orthotopic liver transplantation. (OLT). We undertook this study to assess the outcome of hyponatremic patients after OLT and to evaluate the risk factors in the development of CPM. A total of 379 adult OLT performed in 347 patients between March 1993 and December 1995 was studied using a prospectively‐collected data base and retrospective chart review. The following risk factors for the development of CPM were analyzed: primary liver disease, nutritional status, alcoholism, diuretic use, hepatic encephalopathy, United Network for Organ Sharing (UNOS) status, preoperative serum sodium, magnesium and cholesterol levels, increase in serum sodium concentration during surgery, and immunosuppressive treatment. Overall 12 patients (3.5%) underwent OLT in a hyponatremic state (serum sodium 127 meq/L). At a median follow‐up of 14 months, 8 patients were alive without any neurological sequel. Six of the 12 patients developed neurological complications in the early postoperative period including CPM in 3, confusion in 2, and seizure in 1. The 3 patients who developed CPM expired within 3 months of OLT. The changes in serum sodium concentration during OLT in patients with and without CPM were 20.78.1 and 7.0 5.1 meq/L, respectively (p = 0.005). No other risk factor could be identified in the development of CPM. It is concluded that prognosis of hyponatremic patients after OLT is poor if they develop CPM. Slow correction of hyponatremia perioperatively may be critical in preventing this devastating complication.

The Effect of Fluvoxamine on Serum Prolactin and Serum Sodium Concentrations

Hyperprolactinemia and hyponatremia are adverse drug reactions regularly reported for selective serotonin reuptake inhibitors. Results from animal studies suggest that serotonin receptors of different subtypes are involved in the mediation of these effects. We have investigated to what extent fluvoxamine alters serum prolactin and serum sodium levels and whether these effects are related to platelet 5-hydroxytryptamine 2A (5-HT2A) receptor status, as studied by [3H]lysergic acid diethylamide ([3H]LSD) binding. Eight healthy subjects were given fluvoxamine in increasing dosage from 25 mg/day to 200 mg/day during 4 weeks, and serum sodium and serum prolactin concentrations were obtained weekly. All subjects had normal prolactin and sodium levels before start of treatment. Two subjects had substantial increases in serum prolactin levels (up to 35 microg/L) during fluvoxamine treatment, and these two subjects had higher Bmax for platelet [3H]LSD binding before fluvoxamine treatment than the six other subjects (32.7 vs. 23.1 fmol/mg protein). There was a small, nonsignificant decrease (mean 1.0 mmol/L) in serum sodium levels after institution of fluvoxamine but a significant increase (mean 1.9 mmol/L) in serum sodium levels after discontinuation of the drug (p = 0.02). Bmax for [3H]LSD binding and change in serum sodium concentration after institution of fluvoxamine showed a significant positive correlation (r = 0.85;p = 0.007). The results indicate that fluvoxamine affects serum prolactin as well as serum sodium concentrations and lend indirect support to the suggestion that 5-HT2A receptors might be involved in the mediation of these effects.

Interdialytic Weight Gain Correlates With Glycosylated Hemoglobin in Diabetic Hemodialysis Patients

Most of the excess mortality and morbidity in diabetic end-stage renal disease patients is ascribed to diabetes associated cardiovascular disease, which is accelerated by uremia. We compared the interdialytic weight gain in 33 diabetic patients (group 1) undergoing maintenance hemodialysis in an ambulatory facility retrospectively over 3 months, with 25 randomly selected nondiabetic hemodialysis patients (group 2); in addition, we assessed glycemic control in the diabetic subjects using glycosylated hemoglobin (HbA1c). Interdialytic weight gain was expressed as a percentage of the immediately preceding postdialysis weight, and a mean was calculated for each subject. In all subjects, predialysis serum aldosterone, plasma renin activity, and the interdialytic change in serum sodium were measured. Both groups received an equivalent amount of dialysis using a cellulose membrane (mean ± SD of thrice weekly dialysis: group 1 = 3.8 ± 0.35 hours, group 2 = 3.86 ± 0.3 hours; P < 0.5) and had similar predialysis serum creatinine, hematocrit, and serum albumin levels. Group 1 patients had a mean age of 56.5 ± 11.4 years (age range, 30 to 71 years) and group 2 had a mean age of 55.8 ± 15.4 years (age range, 29 to 76 years) (P < 0.84). Mean (±SD) duration on maintenance hemodialysis was 18.7 ± 15.3 months (range, 2 to 84 months) for group 1 and 21 ± 28.9 months (range, 3 to 156 months) for group 2 (P < 0.9). Interdialytic weight gain was 30% greater in group 1 (4.2% ± 0.19%) than in group 2 (3.2% ± 0.2%) (P < 0.001). Those diabetic patients (n = 5) with poor glycemic control as measured by a mean HbA1c of 11.96% ± 3.9% had a higher mean (±SEM) interdialytic weight gain (5.6 ± 0.4) than did those diabetic patients (n = 18) with good control (3.9 ± 0.2; HbA,c = 5.78% ± 0.93%) (P < 0.01). Insulin-treated group 1 patients (n = 7) gained more weight (5.3 ± 0.37) than those (n = 13) on oral hypoglycemic agents (4.4 ± 0.19) or dietary control (n = 13) (3.3 ± 0.23) (P by ANOVA < 0.001). Median interdialytic change in serum sodium concentration was -3 mEq/L for diabetic patients and +2 mEq/L for nondiabetic patients. Diabetic subjects had a higher mean (±SEM) predialysis serum aldosterone concentration (43.9 ± 9.5 ng/dL) than did nondiabetic subjects (18.4 ± 5.8 ng/dL) (P < 0.05). The mean plasma renin activity level, however, did not differ significantly between diabetic (3.6 ± 1.2 ng/mL/hr) and nondiabetic subjects (3.7 ± 2.1 ng/mL/hr) (P < 0.96). We conclude that hyperglycemia-induced thirst, and perhaps elevated aldosterone or uremia itself, stimulate increased fluid ingestion, resulting in excess interdialytic weight gain in dialyzed diabetic patients.

Early detection of absorption of irrigating fluid during transurethral resection of the prostate with alcohol gas detector tube

Nineteen patients (mean age, 70 years; range, 58-80 years) undergoing elective transurethral resection of benign hypertrophy of the prostate (mean weight of resectate, 25 g; range 10-59 g; mean resection time, 61 min; range 45-80 min) under spinal anesthesia were studied for early detection of absorption of irrigating solution by means of expired breath alcohol analysis. The irrigating fluid used in all resections was tenfold diluted Urigal solution containing 1% ethanol. Expired breath was collected into a rubber bag every 10 min during the surgery, and the concentration of ethanol was analyzed using a gas detector tube (GASTEC LTD.). Hemodynamic parameters including central venous pressure were routinely measured at the same intervals. The volumetric fluid balance was measured every 20 min. Blood was collected preoperatively, at the same 20-min intervals during the resection, and 4-6 hours after the end of the operation. Serum electrolytes, hemoglobin and total plasma protein concentration were measured, and blood gas tension was analyzed. Mean arterial pressure, central venous pressure, blood gas tension showed no significant changes at these observed time intervals. Heart rate decreased 120 min after the start of the operation. Ethanol was detected in the expired breath 10 min after the start of the surgery, and showed progressive increase in concentration until the end of the surgery. Serum electrolyte concentrations and hemoglobin content showed gradual decrease proportional to the increase in irrigating fluid volume. The ethanol concentration in the expired breath was significantly correlated with the change in serum sodium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis

To determine whether correction of acidemia using bicarbonate improves hemodynamic variables and tissue oxygenation in patients with lactic acidosis. Prospective, randomized, blinded, cross over study. Each patient sequentially received sodium bicarbonate and sodium chloride. The order of the infusions was randomized. Ten patients with metabolic acidosis, increased arterial plasma lactate concentrations (greater than 2.45 mmol/L), and no severe renal failure (creatinine less than 250 mumol/L [less than 2.3 mg/dL]). Sodium bicarbonate (1 mmol/kg body weight) or equal volume of sodium chloride was injected iv at the beginning of two successive 1-hr study periods. Period order was randomized. Arterial and venous blood gas measurements, plasma electrolytes (sodium, potassium, chloride), osmolality and lactate, 2,3-diphosphoglycerate (DPG), and oxygen hemoglobin affinity, hemodynamic variables, oxygen delivery, and oxygen consumption measurements were obtained before and repeatedly during the 1-hr period after the injection of bicarbonate or sodium chloride. Sodium bicarbonate administration increased arterial and venous pH, serum bicarbonate, and the partial pressure of CO2 in arterial and venous blood. Hemodynamic responses to sodium bicarbonate and sodium chloride were similar. Tissue oxygenation (as estimated by oxygen delivery, oxygen consumption, oxygen extraction ratio, and transcutaneous oxygen pressure) was not modified. No changes in serum sodium concentration, osmolality, arterial and venous lactate, red cell 2,3-DPG levels, or hemoglobin affinity for oxygen were observed. Administration of sodium bicarbonate did not improve hemodynamic variables in patients with lactic acidosis, but did not worsen tissue oxygenation.

Central Pontine Myelinolysis following Correction of Hyponatremia: MRI Diagnosis

A 37-year-old woman with hepatic failure developed a locked-in syndrome after correction of a severe symptomatic hyponatremia. Magnetic resonance imaging showed a lesion involving the basis pontis and extending into the midbrain, consistent with central pontine myelinolysis. In this patient the rate of correction of hyponatremia was within the range considered sure by several authors, but factors such as hepatic encephalopathy, a single generalized seizure and correction of hyponatremia in 42 h with a change in serum sodium concentration of 34 mmol/l were present, and they could have been etiologically relevant. This case, like other recent reports, suggests new views about the pathogenesis of cerebral demyelinating lesions in patients with hyponatremia.

Sodium balance and extracellular volume regulation in very low birth weight infants

We assessed sodium balance and extracellular volume regulation in very low birth weight infants by examining the effect of differences in sodium intake on postnatal sodium homeostasis and body water composition. Twenty infants (mean birth weight 1103 +/- 216 gm, mean gestation 28.5 +/- 1.7 weeks) were randomly assigned to receive sodium in doses of either 1 or 3 mmol.kg-1.day-1 for the first 10 postnatal days. Extracellular volume (estimated by the bromide dilution method), sodium excretion, creatinine clearance, fractional sodium excretion, plasma atrial natriuretic factor level, urine aldosterone concentration, and vasopressin excretion were measured on postnatal days 1, 5, 10, 20, and 30. The corrected bromide space was large at birth and decreased in both groups during the first 5 days of observation, concomitant with a negative sodium balance. After 5 days of age, sodium excretion decreased in both groups so that sodium balance became positive and the corrected bromide space increased in proportion to increasing body weight. Differences in sodium intake were associated with differences in tubular sodium reabsorption; corrected bromide space and net sodium balance were similar in the two groups. Serum sodium concentration was significantly lower in the low-sodium intake group. Creatinine clearance, plasma atrial natriuretic factor level, and excretion of aldosterone and vasopressin were not significantly different between the two groups. We conclude that very low birth weight infants are able to regulate sodium balance by altering renal sodium excretion. However, the renal response to sodium intake may be insufficient to prevent changes in serum sodium concentration. The roles of specific renal and hormonal mechanisms regulating sodium excretion in very low birth weight infants remain incompletely defined.

Alterations in serum sodium in relation to atrial natriuretic factor and other neuroendocrine variables in experimental pacing-induced heart failure

The pathophysiologic role of atrial natriuretic factor and other neuroendocrine variables in relation to serum sodium and renal function was evaluated in 15 conscious dogs with severe chronic ventricular pacing-induced heart failure (250 beats/min for 5.1 ± 0.4 weeks). Six sham-operated dogs observed over an 8 week period served as controls. Development of heart failure was characterized by a progressive increase in plasma norepinephrine, renin activity and aldosterone from control values of 293 ± 15 pg/ml, 1.4 ± 0.4 ng/ml per h and 124 ± 42 pg/ml, respectively, to 1,066 ± 96 pg/ml,10.2 ± 2.4 ng/ml per h and 577 ± 151 pg/ ml (all p < 0.01), respectively, at severe heart failure.In contrast to other neuroendocrine variables, plasma atrial natriuretic factor increased from a control level of 243 ± 74 pg/ml to a peak concentration of 724 ± 149 pg/ml (p < 0.01) at 2 weeks, then declined and plateaued at twice the level of the control value as severe heart failure developed. At severe heart failure, serum sodium decreased from 147 ± 0.6 to 141.8 ± 2.1 mmol/liter (p < 0.05), whereas urea increased from 6.0 ± 0.5 to 7.8 ± 0.6 mmol/ liter (p < 0.05). The change in serum sodium concentration correlated with plasma renin activity and aldosterone (r = −0.77, −0.88, respectively, both p < 0.01), but not with norepinephrine or atrial natriuretic factor. When sinus rhythm was restored, 14 dogs were observed for 48 to 72 h and 8 dogs were followed up for another 4 weeks after cessation of pacing. Recovery from heart failure was characterized by a return of all neuroendocrine variables, serum sodium and urea levels to control values by 48 to 72 h.The unique time profile of atrial natriuretic factor during the developing heart failure suggests that the circulating level of this hormone may not be sufficient to maintain circulatory homeostasis in advanced heart failure. The strong negative correlations among the change in serum sodium and plasma renin and aldosterone support the hypothesis proposed by previous clinical studies that hyponatremia in congestive heart failure is in part mediated by the activation of the renin-angiotensin system.

Pharmacokinetics of iothalamate in endstage renal disease.

Some nephrologists make alterations in routine peritoneal and hemodialysis schedules after diagnostic studies that use radiographic contrast agents. A study to determine the pharmacokinetics of one contrast agent, iothalamate, is reported. The plasma (total body) clearance of iothalamate was measured in seven patients who had endstage renal disease (ESRD) and who received maintenance hemodialysis. During an interdialytic period, plasma clearance of iothalamate varied from 0.7 to 5.2 mL/min (3.1 +/- 1.8 mL/min, mean +/- SD) with an elimination rate constant (beta) of 0.0164 +/- 0.01 hr-1, a terminal half-life of 61 +/- 42 hours, and an estimated distribution volume of 11 +/- 3.9 L. Hemodialysis clearance of iothalamate was 104 +/- 54 mL/min. With the assumption that iothalamate is mainly distributed in the extracellular fluid (ECF) compartment, the theoretical fluid shift from the intracellular fluid (ICF) compartment to the ECF compartment was 323 mL after administration of the largest dose (2.1 mL/kg or 1.6 mmol/kg of body weight) of 60% meglumine iothalamate solution. The average maximum serum osmolarity change was less than expected, suggesting some type of internal buffering of meglumine iothalamate. In the first few hours after radiocontrast administration in four patients, the average change in serum osmolarity was 5 mmol/L; the average change in serum sodium concentration during this same time was a decrease of 0.5 mmol/L. The minor increase in ECF volume induced by hyperosmolar contrast agents does not require immediate dialysis in most patients. When needed, however, for contrast-related adverse effects, hemodialysis is efficient in rapidly removing iothalamate.

Diuretic effect of metoprolol

Metoprolol caused a significant ( P < 0.001) increase in urine output in rabbits. There was no change in serum sodium concentration but serum potassium levels increased significantly. The most probable mechanism of action was increase in renal blood flow and glomerular filtration rate.