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BACKGROUND To evaluate the event rate of major adverse kidney events within 30 days (MAKE30) in acute pancreatitis (AP) and its potential risk factors. METHODS A retrospective analysis of a tertiary center data on all AP patients admitted within 72 h after onset of abdominal pain between June 2015 and June 2019 was conducted. MAKE30 - a composite of death, new renal replacement therapy (RRT), or persistent renal dysfunction (PRD) - and its individual components were retrieved at discharge or 30 days. Logistic regression analysis was used to assess the risk factors for MAKE30. RESULTS 295 patients were enrolled and 16% experienced MAKE30. For individual components, the incidence was 3% for death, 15% for new RRT, and 5% for PRD. In multivariate logistic regression analysis, hyperchloremia at admission [OR = 8.38 (1.07-65.64); P = 0.043] and SOFA score [OR 1.63 (1.18-2.26); P = 0.003] were independent risk factors in predicting MAKE30. Further analysis showed that patients with hyperchloremia had more requirements of RRT (57% vs. 10%, P

Objective Chloride is an important electrolyte in the body. In this study, we aimed to evaluate the associations between chloride levels on emergency department (ED) admission and neurologic outcomes by stratifying patients undergoing targeted temperature management (TTM) after out-of-hospital cardiac arrest (OHCA) into three groups (hyper/normo/hypochloremia); we also assessed the effect of changes in chloride levels from baseline over time on outcomes. Methods This retrospective, observational cohort study of 346 patients was conducted between 2011 and 2019. The chloride levels were categorized as hypochloremia, normochloremia, and hyperchloremia by predetermined definitions. The primary endpoint was poor neurologic outcomes after hospital discharge. We evaluated the associations between chloride levels on ED admission and neurologic outcomes and assess the effect of changes in chloride levels over time on clinical outcomes. Results On ED admission, compared with normochloremia, hypochloremia was significantly associated with unfavorable neurologic outcomes (OR, 2.668; 95% CI, 1.217–5.850, P = 0.014). Over time, unfavorable neurologic outcomes were significantly associated with increases in chloride levels in the hyperchloremia and normochloremia groups after ED admission. The rates of poor neurologic outcomes in the hyperchloremia and normochloremia groups were increased by 14.2% at Time-12, 20.1% at Time-24, and 9.3% at Time-48 with a 1-mEq/L increase in chloride levels. Conclusion In clinical practice, chloride levels can be routinely and serially measured cost-effectively. Thus, baseline chloride levels may be a promising tool for rapid risk stratification of patients after OHCA. For fluid resuscitation after cardiac arrest, a chloride-restricted solution may be an early therapeutic strategy.

Background The present study evaluated the relationships among perioperative hyperchloremic metabolic acidosis (HCA), hyperchloremia, and postoperative acute kidney injury (AKI) in patients who had undergone craniotomy for intracranial hemorrhage (ICH). Methods The present retrospective cohort study included adult patients who had undergone craniotomy for traumatic or spontaneous ICH from January 2005 to December 2017. The association of perioperative hyperchloremia (serum chloride [Cl−] >110 mmol/L during postoperative days 0–3), an increase in Cl− levels (maximum Cl− level in postoperative days 0–3 minus the baseline Cl− level before surgery), and perioperative HCA (Cl− >110 mmol/L; pH Results A total of 968 patients were included. Of these patients, 117 (12.1%) had postoperative AKI. The multivariable logistic regression analysis showed that the development of HCA was associated with a 1.850-fold increase in the incidence of postoperative AKI (odds ratio [OR], 1.850; 95% confidence interval [CI], 1.102–3.106; P = 0.020). However, hyperchloremia was not significantly related to the incidence of postoperative AKI (P = 0.207). Additionally, the presence of hyperchloremia and an increase in Cl− levels were both associated with an increased incidence of HCA (hyperchloremia group: OR, 2.162; 95% CI, 1.490–3.138; P Conclusions Perioperative HCA was independently related to an increased incidence of AKI after craniotomy for ICH. An increase in Cl− levels and perioperative hyperchloremia were associated with increased development of HCA but were not significantly related to the development of postoperative AKI.

Background: Acute diarrhea and severe dehydration (ADSD) is a common cause of under-5 mortality in low- and middle-income countries. There is a paucity of data on clinical profile of ADSD children presenting with severe non-anion gap metabolic acidemia (sNAGMA). Study was planned to delineate clinical profile, critical care needs, and outcome of these children. Methods: For this retrospective chart review, children (1mo-12yr) with ADSD and sNAGMA (pH

Hyperchloremic metabolic acidosis, particularly renal tubular acidosis, can pose diagnostic challenges. The laboratory phenotype of a low total carbon dioxide content, normal anion gap, and hyperchloremia may be misconstrued as hypobicarbonatemia from renal tubular acidosis. Several disorders can mimic renal tubular acidosis, and these must be appropriately diagnosed to prevent inadvertent and inappropriate application of alkali therapy. Key physiologic principles and limitations in the assessment of renal acid handling that can pose diagnostic challenges are enumerated.

Purpose The aim of this study was to determine whether serum chloride and changes in serum chloride over time were associated with acute kidney injury (AKI) or intensive care unit (ICU) mortality in a heterogenous critically ill population. Materials and methods The study was a retrospective observational study of 250 adult patients admitted to a multidisciplinary academic ICU. Serum chloride within 48 h of admission, changes in chloride, and other biochemical and clinical parameters were evaluated as predictors of AKI and mortality. Results Hyperchloraemia occurred in 143 (57.2%) patients within 48 h of ICU admission. Hyperchloraemia at 48 h was significantly associated with AKI, OR = 6.44 (95% CI 2.95–14.10) and mortality, OR = 2.46 (95% CI 1.22–4.94) on univariate analysis, with this association persisting on multivariable analysis. An increase in serum chloride was also associated with a significantly increased risk of AKI and mortality on univariate analysis. Hyperchloraemia on admission was, however, not associated with AKI or death. Of the 150 patients with AKI, 147 (98.0%) had developed AKI by 48 h. Conclusions Hyperchloraemia and increasing serum chloride are associated with adverse outcomes in critically ill patients. There is equipoise as to whether this represents an association, an epiphenomenon or causation.

In the last years, casein nanoparticles have been proposed as carriers for the oral delivery of biologically active compounds. However, till now, no information about their possible specific hazards in vivo was available. The aim of this work was to assess the safety of casein nanoparticles when administered orally to animals through a 90 days dose-repeated toxicity study (OECD guideline 408), that was performed in Wistar rats under GLP conditions. After 90 days, no evidences of significant alterations in animals treated daily with 50, 150 or 500 mg/kg bw of nanoparticles were found. This safety agrees well with the fact that nanoparticles were not absorbed and remained within the gut as observed by radiolabelling in the biodistribution study. After 28 days, there was a generalized hyperchloremia in males and females treated with the highest dose of 500 mg/kg bw, that was coupled with hypernatremia in the females. These effects were related to the presence of mannitol which was used as excipient in the formulation of casein nanoparticles. According to these results, the No Observed Adverse Effect Level (NOAEL) could be established in 150 mg/kg bw/day and the Lowest Observed Effect Level (LOEL) could be established in 500 mg/kg bw/day.

Introduction: Diabetic ketoacidosis (DKA) often becomes the primary focus and in turn masks a similar serious condition like hyperchloremic metabolic acidosis. Case report: A 20 years old female with type 1 diabetes mellitus presented to the emergency department (ED) with signs and symptoms corresponding to DKA. Initial pH, HCO3, Na and Cl concentrations were 6.83, 3.6 mmol/l, 143 mmol/l and 122 mmol/l respectively; anion gap 17.4 mmol/l and absent urinary ketones. DKA regime showed no improvement in the measured parameters nor the patient. The diagnosis changed to hyperchloremic high-anion gap acidosis and treatment modifications were made by adding sodium bicarbonate infusion. There was significant improvement in the clinical status of the patient and the calculated parameters. Discussion: Hyperchloremic acidosis is associated with a non-anion gap, decrease in plasma bicarbonate and increase in plasma chloride. Rarely, as with this case, it may present with a high-anion gap. The use of bicarbonate therapy has shown improvement in cases of non-anion gap acidosis however there is very little data to support its role in high-anion gap hyperchloremic metabolic acidosis. Keywords: Diabetic ketoacidosis, Hyperchloremia, Non-anion gap metabolic acidosis, High-anion gap metabolic acidosis

Background 3 % hypertonic saline (HS) is a hyperosmolar agent often used to treat elevated intracranial pressure (ICP). However, the resultant hyperchloremia is associated with adverse outcomes in certain patient populations. In this study, HS solution buffered with sodium acetate (HSwSA) is used as an alternative to standard 3 % formulations to reduce overall chloride exposure. Our objectives are to establish whether this alternative agent – with reduced chloride content – is similar to standard 3 % HS in maintaining hyperosmolarity and investigate its effects on hyperchloremia. Methods A retrospective chart review was conducted from August 1, 2014 to August 1, 2017 on patients receiving hypertonic therapies for ICP management. Patients were categorized into three groups, those that received: (1) 3 % HS for at least 72 h, (2) HSwSA for at least 72 h, or (3) were switched from 3 % HS within 72 h of initiating therapy to HSwSA for at least 72 h. Results The average increase in serum osmolality after 72 h of therapy was 21.1 moSm/kg for those only on 3 % HS and 20.3 mOsm/kg for those only on HSwSA. Serum chloride levels after 24 h decreased on average by 2.5 mEq/L after switching from 3% HS to HSwSA and stayed below baseline, whereas matched patients only receiving 3% HS on average had serum chloride levels increase 4.3 mEq/L after 24 h and continued to rise. Conclusions Hyperchloremia has been associated with decreased renal perfusion, increasing the risk of acute kidney injury and hyperchloremic metabolic acidosis. Compared to standard 3% HS, our findings suggest an alternative hyperosmolar therapy with less chloride maintains similar hyperosmolarity while reducing overall chloride exposure.

Gordon's syndrome, or type II pseudo-hypoaldosteronism, is a rare cause of arterial hypertension in children. However, it is important to diagnose this syndrome because of the spectacular efficacy of thiazide diuretics. The typical clinical picture of Gordon syndrome includes, apart from arterial hypertension and dyskaliemia, hyperchloremia metabolic acidosis, hypercalciuria, a low rate of renin, and most frequently, a normal or high rate of aldosterone. Dental abnormalities and growth retardation can also be associated. In most cases, it is inherited in an autosomal dominant pattern. We report on a 7-year-old girl who was discovered with arterial hypertension during a consultation for chronic diarrhea. The association of growth retardation, hyperkaliemia, and metabolic acidosis oriented the diagnosis. Starting a thiazide diuretic helped control the arterial hypertension and the kaliemia in a spectacular manner. The genetic analysis proved the existence of a splice mutation on exon 9 of the CUL3 gene coding for cullin 3. This mutation is de novo.

Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance.

Intracranial hypertension (ICH) is the most important modifiable factor with predictive negative value in brain injury patients. Osmotherapy is the most important first level specific measure in the treatment of ICH. Mannitol 20%, and 3, 7.5, 10, and 23% hypertonic sodium chloride are the most commonly used osmotic agents in the neurocritical care setting. Currently, controversy about the best osmotic agent remains elusive. Therefore, over the past few years, half-molar sodium lactate has been introduced as a new osmotic agent to be administered in the critically ill. Lactate is able to prevent hyperchloremia, as well as its adverse effects such as hyperchloremic acidosis, systemic inflammation, and acute kidney injury. Furthermore, lactate may also be used by glia as energy substrate in brain injury patients. Half-molar sodium lactate would also have a more potent and long-lasting effect decreasing intracellular osmolarity and by inhibiting neuronal volume control mechanisms. Pioneering researches in patients with traumatic brain injury have shown a more significant effect than mannitol on the control of ICH. In addition, in this group of patients this solution appears to be beneficial in preventing episodes of ICH. However, future research is necessary to corroborate or not these promising results.

Introduction Metabolic acidosis is common post cardiac surgery. The incidence of hyperchloremic metabolic acidosis (HCMA) post cardiac surgery was 56% in our previous audit . There was a huge correlation with the use colloid 4 % gelatin in these patients. The purpose of the present audit was to assess the current incidence of HCMA and contributing factors as part of quality improvement. Methods A prospective audit, data collected from all cardiac surgical patients over a period of two months. Incidence of HCMA on admission to ICU and its course over the first 24 hours was analysed. The duration of CPB, amount of cardioplegia used, perioperative chloride level and amount and type of perioperative fluids used were analysed. Results On Admission to ITU, 30 patients (56%) had metabolic acidosis, of whom19 (63%) patients were hyperchloremic, giving an incidence of HCMA as 36% .Hyperchloremia without acidosis was seen in 43% patients, making the overall incidence of hyperchloremia on admission as 55%. Hyperchloremia persisted in 61% patients on day 1 post surgery. No relation was found between perioperative fluids used and hyperchloremia. Maintenance fluid had changed to hartmann's solution & use of colloid 4% gelatin had decreased by 75% following the previous audit. Among the patients with persistent hyperchloremia, 57% had CPB time greater than 120 minutes and 61% had more than 2 litres of cardioplegia. Discussion HCMA post cardiac surgery has been related to the CPB prime and perioperative fluids. Our CPB prime is normochloremic and there was no relation between hyperchloremia and the intravenous fluids used. There was a direct relationship between hyperchloremia and the duration of CPB and the volume of cardioplegia used because cardioplegia contains 160 mmols/L of chloride. Thus, we conclude that increasing volumes of cardioplegia used with longer cardiopulmonary bypass times might be a significant contributor to increasing incidence of hyperchloremic metabolic acidosis. This is the first report implicating cardioplegia in the pathogenesis of HCMA.

To determine the severity, duration, and contributing factors for metabolic acidosis after deep hypothermic circulatory arrest (DHCA).Retrospective observational study.University hospital.Eighty-seven consecutive patients undergoing elective thoracic aortic surgery with DHCA.Regression analysis was used to test for relationships between the severity of metabolic acidosis and clinical and laboratory variables.Minimum pH averaged 7.27±0.06, with 76 (87%) having a pH7.35; 55 (63%), a pH7.30; and 7 (8%), a pH7.20. The mean duration of metabolic acidosis was 7.9±5.0 hours (range: 0.0 - 26.8), and time to minimum pH after DHCA was 4.3±2.0 hours (1.0 - 10.0 hours). Hyperchloremia contributed to metabolic acidosis in 89% of patients. The severity of metabolic acidosis correlated with maximum lactate (p0.0001) and hospital length of stay (LOS) (r = 0.22, p0.05), but not with DHCA time, DHCA temperature, duration of vasoactive infusions, or ICU LOS. Patient BMI was the sole preoperative predictor of the severity of postoperative metabolic acidosis.This retrospective analysis involved short-term clinical outcomes related to pH severity and duration, which indirectly may have included the impact of sodium bicarbonate administration.Metabolic acidosis was common and severe after DHCA and was attributed to both lactic and hyperchloremic acidosis. DHCA duration and temperature had little impact on the severity of metabolic acidosis. The severity of metabolic acidosis was best predicted by the BMI and had minimal effects on short-term outcomes. Preventing hyperchloremic acidosis has the potential to decrease the severity of metabolic acidosis after DHCA.

Background The infusion of crystalloid solutions is a fundamental part of the management of critically ill patients. These solutions are used to maintain the balance of water and essential electrolytes and replace losses when patients have limited gastrointestinal intake. They also act as carriers for intravenous infusion of medication and red cells. The most commonly used solution, 0.9% saline, has equal concentrations of Na + and Cl − even though the plasma concentration of Na + normally is 40 meq/L higher than that of Cl − . The use of this fluid thus can produce a hyperchloremic acidosis in a dose-dependent manner, but it is not known whether this has clinical significance. Approach The first part of this article deals with the significance of Na + and Cl − in normal physiology. This begins with examination of their roles in the regulation of osmolality, acid–base balance, and generation of electrochemical gradients and why the concentration of Cl − normally is considerably lower than that of Na + . The next part deals with how their concentrations are regulated by the gastrointestinal tract and kidney. Based on the physiology, it would seem that solutions in which the concentration of Na + is "balanced" by a substance other than Cl − would be advantageous. The final part examines the evidence to support that point. Conclusions There are strong observational data that support the notion that avoiding an elevated Cl − concentration or using fluids that reduce the rise in Cl − reduces renal dysfunction, infections, and possibly even mortality. However, observational studies only can indicate an association and cannot indicate causality. Unfortunately, randomized trials to date are far too limited to address this crucial issue. What is clear is that appropriate randomized trials will require very large populations. It also is not known whether the important variable is the concentration of Cl − , the difference in concentrations of Na + and Cl − , or the total body mass of Cl − .

Hypokalemic respiratory paralysis in Sjogren's syndrome (SS) with distal renal tubular acidosis (RTA) is very rare. In the literature, only five such cases have been reported. We report a 48-year-old lady, who presented with respiratory paralysis, bulbar weakness, and flaccid quadriplegia. She had severe hypokalemia (1.11 mEq/L), metabolic acidosis (pH = 7.09), hyperchloremia (120.8 mEq/L), and normal anion gap (11.2). An ammonium chloride test was consistent with the diagnosis of distal RTA. She recovered completely with potassium and alkali supplementations. Clinical features, positive Schirmer's test, and autoantibody screening were suggestive of diagnosis of SS. Hypokalemic periodic paralysis and respiratory involvement may occur as a first and rare complication of SS with distal RTA. Immunosuppressive therapy is not indicated except in the presence of systemic vasculitis. Potassium and alkali supplementations are the mainstay of the therapy. Patients with secondary hypokalemic periodic paralysis should be investigated for this possibility.

Objectives To analyze the mechanism of acid–base disorders in liver transplant recipients and to examine the relationship between these disorders and the fluids administered during surgery. Methods This prospective study in a university-affiliated hospital intensive care unit (ICU) included 52 patients admitted to the ICU from December 2009 to January 2011. We examined the contributions of inorganic ion differences, lactate, unmeasured anions, phosphate, and albumin to metabolic acidosis. In addition to laboratory variables, we collected demographic and clinical data. Results Metabolic acidosis (standard base excess ≤ −2.0 mmol/L) was identified in 37 (71.2%) patients during the immediate postoperative period. The inorganic ion difference was the main determinant of acidosis, accounting for −6.17 mEq/L of acidifying effect. The acidemia was attenuated mainly by the alkalinizing effect of albumin reduction, which contributed +6.03 mEq/L. There was an inverse proportional relationship between the quantity of saline solution used during surgery and the inorganic ion difference during the immediate postoperative period. Conclusions Hyperchloremia is the primary contributor to metabolic acidosis in liver transplant recipients. Possibly the use of chloride-rich solutions increases the incidence of this disorder.

Background: Channelopathies, defined as diseases that are caused by mutations in genes encoding ion channels, are associated with a wide variety of symptoms and have been documented extensively over the past decade. In contrast, despite the important role of chloride in serum, textbooks in general do not allocate chapters exclusively on hypochloremia or hyperchloremia and information on chloride other than channelopathies is scattered in the literature. Study design: To systematically review the function of chloride in man, data for this review include searches of MEDLINE, PubMed, and references from relevant articles including the search terms "chloride," "HCl," "chloride channel" "acid-base," "acidosis," "alkalosis," "anion gap" "strong anion gap" "Stewart," "base excess" and "lactate." In addition, internal medicine, critical care, nephrology and gastroenterology textbooks were evaluated on topics pertaining the assessment and management of acid-base disorders, including reference lists from journals or textbooks. Conclusion: Chloride is, after sodium, the most abundant electrolyte in serum, with a key role in the regulation of body fluids, electrolyte balance, the preservation of electrical neutrality, acid-base status and it is an essential component for the assessment of many pathological conditions. When assessing serum electrolytes, abnormal chloride levels alone usually signify a more serious underlying metabolic disorder, such as metabolic acidosis or alkalosis. Chloride is an important component of diagnostic tests in a wide array of clinical situations. In these cases, chloride can be tested in sweat, serum, urine and feces. Abnormalities in chloride channel expression and function in many organs can cause a range of disorders. (C) 2011 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.

The aim of this study was to define the nature of metabolic acidosis in patients with septic shock on admission to intensive care unit (ICU) using Stewart method. We also aimed to compare the ability of standard base excess (SBE), anion gap (AG), and corrected AG for albumin and lactate (AGcorr) to accurately predict the presence of unmeasured anions (UA).Thirty consecutive patients with septic shock were prospectively included on ICU admission. Stewart equations modified by Figge were used to calculate the strong ion difference and the strong ion gap (SIG).Most patients had multiple underlying mechanisms explaining the metabolic acidosis. Unmeasured anions and hyperchloremia were present in 70% of the patients. Increased UA were present in 23% of patients with normal values of SBE and [HCO3-]. In these patients, plasma [Cl-] was significantly lower compared with patients with low SBE and increased UA (103 [102-106.6] vs 108 [106-111] mmol/L; P=.01, respectively). Corrected AG for albumin and lactate had the best correlation with SIG (r²=0.94; P.0001) with good agreement (bias, 0, and precision, 1.22) and highest area under the receiver operating characteristic curve (0.995; 95% confidence interval, 0.87-1) to discriminate SIG acidosis.Patients with septic shock exhibit a complex metabolic acidosis at ICU admission. High UA may be present with normal values of SBE and [HCO3-] as a result of associated "relative" hypochloremic alkalosis. Corrected AG for albumin and lactate offers the most accurate bedside alternative to Stewart calculation of UA.

OBJECTIVE: Intravenous infusion of crystalloid solutions is a cornerstone of the treatment of hemorrhagic shock. However, crystalloid solutions can have variable metabolic acid-base effects, perpetuating or even aggravating shock-induced metabolic acidosis. The aim of this study was to compare, in a controlled volume-driven porcine model of hemorrhagic shock, the effects of three different crystalloid solutions on the hemodynamics and acid-base balance. METHODS: Controlled hemorrhagic shock (40% of the total blood volume was removed) was induced in 18 animals, which were then treated with normal saline (0.9% NaCl), Lactated Ringer's Solution or Plasma-Lyte pH 7.4, in a blinded fashion (n = 6 for each group). Using a predefined protocol, the animals received three times the volume of blood removed. RESULTS: The three different crystalloid infusions were equally capable of reversing the hemorrhage-induced low cardiac output and anuria. The Lactated Ringer's Solution and Plasma-Lyte pH 7.4 infusions resulted in an increased standard base excess and a decreased serum chloride level, whereas treatment with normal saline resulted in a decreased standard base excess and an increased serum chloride level. The Plasma-Lyte pH 7.4 infusions did not change the level of the unmeasured anions. CONCLUSION: Although the three tested crystalloid solutions were equally able to attenuate the hemodynamic and tissue perfusion disturbances, only the normal saline induced hyperchloremia and metabolic acidosis.

Background Neurological manifestations secondary to extrapontine myelinolysis and rhabdomyolysis caused by hypernatremia are infrequently reported. Occurrence of neurological manifestations due to spontaneous hypernatremia during postpartum period producing rhabdomyolysis and cerebral parenchymal MRI changes has not been previously reported. Objective Evaluation of clinical and radiological profile of postpartum hypernatremia. Methods Clinical, laboratory and radiological data of eleven women in postpartum period presenting with hypernatremic encephalopathy with or without muscle weakness were reviewed. Results Eleven puerperal women presented with encephalopathy due to hypernatremia from 2007 to 2009. Consciousness was altered in all the patients ranging from confusion to deep coma. Nine patients had quadriparesis, eight had corticospinal and corticobulbar dysfunction, six had ataxia, and seizures occurred in four patients. The patients had hypernatremia ranging from 158 to 199 mEq/l with hyperchloremia, markedly elevated serum CK levels (2572 to 61,107 U) and azotemia. Ten patients underwent MRI which revealed hyperintensity of corpus callosum in all the patients in T2, FLAIR and diffusion weighted sequences. Symmetrical hyperintensities were seen also in internal capsule, corona radiata, cerebellar peduncles and hippocampus in various combinations. Seven patients improved neurologically with reduction of serum sodium and CK levels while four patients died. Conclusion Hypernatremia is a potentially lethal condition which can produce encephalopathy, osmotic demyelination and rhabdomyolysis. Prompt identification and appropriate management can improve the outcome in these patients.

Purpose This study aimed to test the hypothesis that intensive care unit survivors and nonsurvivors differ with regard to type and severity of acid-base disorders. Materials and Methods Prospective, observational, cohort study of 107 consecutive patients admitted in a 7-bed intensive care unit during a 6-month period that stayed at least 4 days. All acid-base variables for the first 3 days and the day of discharge were analyzed. Results Survivors had significant metabolic acidosis upon admission, which was due to hyperlactatemia, an excess of unmeasured anions, and principally, hyperchloremia. A progressive decrease in these anions in the presence of constant hypoalbuminemia led to normal standard base excess at discharge. Nonsurvivors had greater metabolic acidosis upon admission with acidifying variables in similar proportions to that of the survivors. On the day of death, nonsurvivors had a similar degree of metabolic acidosis but a different proportion of the anions (less chloride and more lactate) compared with the day of admission. Unmeasured anions were greater in nonsurvivors both on the day of admission and on the day of death. Conclusions Intensive care unit survivors and nonsurvivors differed in the severity of metabolic acidosis; however, the proportion of the different anions causing the acidosis on admission was similar between these 2 groups.

Objectives To investigate whether colocystoplasty has resulted in metabolic changes in the growing child during long-term follow-up according to whether cecum with ascending or sigmoid colon was used. Methods Twenty-eight patients (mean age at surgery 11 years) were included in the study and divided into two groups: group 1, cystoplasty with cecum and ascending colon (12 patients) and group 2, sigmoid cystoplasty (16 patients). Patients' linear growth, body mass index, and the following parameters were estimated before surgery and at 3, 6, and 12 months, and then yearly after surgery: blood and urine electrolytes (sodium, potassium, chloride, calcium, phosphorus, magnesium), creatinine, urea, blood gases, blood pH, urine pH, and blood alkaline phosphatase (ALP). All the data were statistically analyzed. Results In group 1, the blood ALP increased significantly ( P = 0.026) during follow-up. Severe metabolic acidosis with or without hyperchloremia was found in 7 patients. In group 2, the serum sodium and serum calcium levels decreased significantly ( P = 0.014 and P = 0.003, respectively); however, the blood ALP, urine sodium, and urine phosphorus levels increased significantly ( P = 0.033, P = 0.027, and P = 0.026, respectively) during follow-up. A statistically significant decrease in blood pH ( P = 0.022) was found after surgery. Severe metabolic acidosis with or without hyperchloremia was detected in 5 patients. The average linear growth decreased significantly ( P = 0.001 and P = 0.016, respectively) 1 and 2 years postoperatively. Conclusions The statistically significant increase in blood ALP and decrease in serum calcium indicate bone demineralization after colocystoplasty. Our investigations in children suggest that bone demineralization is more frequent after sigmoid cystoplasty than after the use of cecum and ascending colon.

Background At our institution, we began using sodium acetate for resuscitation of trauma patients in 2005. Sodium acetate is used as an alternative to normal saline to help prevent hyperchloremic metabolic acidosis as well as to help buffer metabolic acidosis. Discussion Here we present a case of a 29-year-old trauma patient who began to have severe lactic acidosis after the infusion of sodium acetate. This is the first reported case of lactic acidosis caused by sodium acetate infusion. Up to this point, we have not experienced any adverse events and patients have tolerated sodium acetate well. Conclusion This unique case report presents the first case of lactic acidosis from sodium acetate infusion. The lactic acidosis seen in this patient reminds us of the complex regulation of pyruvate dehydrogenase and the potential for down regulation of the enzyme shunting substrates to formation of lactate.

Diabetic ketoacidosis is an infrequent complication of gestational diabetes but results in fetal loss. It usually occurs in the later stages of pregnancy. We report two young pregnant women who were admitted because of newly diagnosed diabetes with ketoacidosis. One patient presented with intrauterine fetal demise.

A 71 year old hypertensive, non insulin-dependent diabetic patient with moderate renal insufficiency taking 500 mg/d of metformin and 5 mg/d of enalapril, developed metabolic acidosis characterized by fairly elevated anion gap, hyperchloremia, severe hyperkaliemia, normal plasma level of 3-hydroxybutyric acid, absence of ketonuria and high plasma level of lactic acid. This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis, both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture). The patient was dehydrated and lethargic; the ECG revealed the presence of nonparoxysmal junctional tachycardia. The clinical evolution was favorable under the treatment with an infusion of isotonic saline solutions, mild alkalinizing solutions, low-dose regular insulin and antibiotics. It is likely that metformin and enalapril, regularly taken by this nephropathic patient, could have played an iatrogenic role, even if the doses were low. This case highlights the importance of complying with the contraindications of these drugs, to avoid the rare but reported life-threatening complications of metformin administration.

Resume Une pseudohyperchloremie a fait suspecter une intoxication par les bromures chez un patient presentant des troubles psychiques. Le diagnostic a ete confirme par une bromuremie superieure a 20 mmoL·L–1. La seule rehydratation a permis de baisser le taux de brome sanguin et de normaliser la chloremie. Dans ce type d’intoxication, une hyperchloremie associee a un trou anionique negatif constitue la cle du diagnostic.

A retrospective analysis of 130 cases of cystectomy and urinary diversion for bladder carcinoma was performed. A logistic regression analysis found preoperative irradiation to be associated with early complications (p = 0.014), whereas no such association was observed with late complications. Metabolic evaluation in 51 surviving patients revealed hyperchloremia in 17 patients (33%) and hyperchloremic acidosis in 2 cases (4%). Vitamin B12 deficiency was found in 11 patients (22%), all of whom had preoperative irradiation or reservoir procedures performed. Routine evaluation of vitamin B12 serum levels should be carried out at follow-up in these groups of patients.

Tissue glycogen and blood glucose concentrations, blood chloride values, and eight hematological parameters were determined in groups of common Indian freshwater catfish, Heteropneustes fossilis, held at four different loading densities, namely, 0.99, 1.485, 1.98 and 2.475 fish cm/l (biomass densities of 3.42, 5.13, 6.84 and 8.55 kg/m3) of water and compared to parallel control groups with a desirable loading density of 0.495 fish cm/l (1.71 kg/m3) of water. High loading densities induced both liver and muscle glycogenolysis with concomitant hyperglycemia, hyperchloremia, significant decrease in the size of red blood cells, erythrocytosis, significantly increased hemoglobin content and hematocrit, markedly decreased erythrocyte sedimentation rate, leucopenia (due to lymphopenia), thrombocytopenia, and hypocoagulability of the blood.

Mineralocorticoid-resistant renal hyperkalemia without salt wasting (type II pseudohypoaldosteronism): Role of increased renal chloride reabsorption. A rare syndrome has been described in which mineralocorticoid-resistant hyperkalemia of renal origin occurs in the absence of glomerular insufficiency and renal sodium wasting and in which hyperchloremic acidosis, hypertension, and hyporeninemia coexist. The primary abnormality has been postulated to be a defect of the potassium secretory mechanism of the distal nephron. The present studies were carried out to investigate the mechanism of impaired renal potassium secretion in a patient with this syndrome. When dietary intake of sodium chloride was normal, renal clearance of potassium was subnormal (CK/GFR = 3.6 ± 0.2%; normal subjects, 9.0 ± 0.9%, N = 4) despite high normal or supernormal levels of plasma and urinary aldosterone. The fractional clearance of potassium remained subnormal (CK/GFR = 5.1 ± 0.2%) during superimposed chronic administration of superphysiologic doses of mineralocorticoid hormone. Little increase in renal potassium clearance occurred when the delivery of sodium to distal nephron segments was increased further by the i.v. infusion of sodium chloride, despite experimentally sustained hypermineralocorticoidism. But potassium clearance increased greatly when delivery of sodium to the distal nephron was increased by infusion of nonchloride anions: sulfate (sodium sulfate infusion, low sodium chloride diet; CK/GFR = 63.7 ± 0.4%) or bicarbonate (sodium bicarbonate plus acetazolamide infusion; CK/GFR = 81.7 ± 1.7%). These findings indicate that mineralocorticoid-resistant renal hyperkalemia in this patient cannot be attributed to the absence of a renal potassium secretory capability or to diminished delivery of sodium to distal nephron segments; instead it may be dependent on chloride delivery to the distal nephron. We suggest that the primary abnormality in this syndrome increases the reabsorptive avidity of the distal nephron for chloride, which (1) limits the sodium and mineralocorticoid-dependent voltage driving force for potassium and hydrogen ion secretion, resulting in hyperkalemia and acidosis and (2) augments distal sodium chloride reabsorption resulting in hyperchloremia, volume expansion, hyporeninemia, and hypertension.Hyperkaliémie rénale résistant aux minéralocorticoïdes sans perte de sel (pseudohypoaldostéronisme de type II): Rôle de l'augmentation de la réabsorption de chlore. Un syndrome rare a été décrit dans lequel une hyperkaliémie d'origine rénale résistant aux minéralocorticoïdes survient en l'absence de diminution du débit de filtration glomérulaire et de perte rénale de sodium et dans lequel une acidose hyperchlorémique, une hypertension et une hyporéninémie coexistent. L'anomalie primaire qui a été postulée est un déficit du mécanisme de sécrétion de potassium du néphron distal. Ce travail a été entrepris pour étudier le mécanisme de la modification de la sécrétion rénale de potassium chez un malade atteint de ce syndrome. Quand l'apport alimentaire de chlorure de sodium était normal, la clearance rénale du potassium était inférieure à la normale (CK/GFR = 3,6 ± 0,2%; sujets normaux 9,0 ± 0,9%, N = 4) malgré des niveaux á la limite supérieure ou franchement élevés d'aldostérone plasmatique et urinaire. La clearance fractionnelle du potassium était inférieur à la normale (CK/GFR = 5,1 ± 0,2%) au cours de l'administration de doses supra-physiologiques de minéralocorticoïdes. Une augmentation faible de la clearance du potassium a été observée quand le débit de sodium aux segments distaux du néphron a été encore augmenté, par l'administration intraveineuse de chlorure de sodium, malgré l'hyerminéralocorticisme expérimentalement maintenu. La clearance du potassium, cependant, a considérablement augmenté quand le débit de sodium au néphron distal a été augmenté par la perfusion d'anions différents du chlore: sulfate (perfusion de sulfate de sodium, régime pauvre en chlorure de sodium: CK/GFR = 63,7 + 0,4%) ou en bicarbonate (perfusion de bicarbonate de sodium et perfusion d'acetazolamide: CK/GFR = 81,7 ± 1,7%). Ces constatations indiquent que l'hyperkaliémie rénale résistant aux minéralocorticoïdes chez ce malade ne peut être attribuée à l'absence de capacité sécréter le potassium ou à une diminution du débit de sodium aux segments distaux. Par contre elle peut dépendre du débit de chlore au néphron distal. Nous suggérons que l'anomalie initiale dans ce syndrome est une augmentation de la capacité réabsorption du chlore par le néphron distal qui (1) limite la force électro-motrice, dépendant du sodium et des minéralocorticoïdes, de sécrétion des ions hydrogène et potassium, ce qui a pour résultat l'hyperkaliémie et l'acidose et (2) augmente la réabsorption distale de chlorure de sodium ce qui a pour résultat l'hypercholorémie, l'expansion volémique, l'hyporéninémie et l'hypertension.

In order to assess the frequency and severity of lactic acidosis and 3-hydroxybutyric acidosis in ethanol abusers, 29 patients who presented to an emergency room with acute intoxication were tested. Most were also chronic ethanol abusers but were not otherwise seriously ill. Their serum ethanol concentrations averaged 226.5 +/- 94.8 mg/dl (range 98 to 426 mg/dl). In 20 patients, the plasma lactate level was elevated only mildly or not at all (1.1 to 3.0 mmol/liter). Seven patients had plasma lactate levels between 3.5 and 4.3 mmol/liter, and only two patients had moderately elevated levels, 5.1 and 8.7 mmol/liter. Thus, severe lactic acidosis was uncommon in these ethanol-intoxicated patients. Only two patients had even trivially elevated plasma levels of 3-hydroxybutyrate, 1.0 and 1.2 mmol/liter. Thus, these patients did not have unrecognized "alcoholic ketosis" manifested mainly as 3-hydroxybutyric acidosis. An unexpected and unexplained finding was the presence of hyperchloremia in 10 of the 29 patients, with serum chloride levels of more than 110 mmol/liter.

The charts of 70 successive patients presenting for dialysis therapy for end-stage renal disease (ESRD) were evaluated for their serum electrolyte values. The "classical" pattern of low total CO2 (tCO2), elevated anion gap ("delta"), and normal chloride was found in a minority of patients (14 of 70, or 20%). Hyperchloremia was noted in 46%; in 21 patients (30%), this was associated with a normal delta and in 11 (16%), hyperchloremia was accompanied by an elevated delta. Fourteen patients (20%), most with diabetic nephropathy, had normal serum electrolytes. Patients with chronic glomerulonephritis had a hyperchloremic pattern as often as not, and two of four patients with interstitial nephritis demonstrated hyperchloremia without an elevated delta. We conclude that the previously held thesis that hyperchloremia is a rare or absent finding by the time renal failure progresses to ESRD is no longer tenable. Furthermore, a significant minority of ESRD patients may require the initiation of dialysis at a time when their serum electrolytes are still normal.

Intrarenal prostaglandin release: Effects of arachidonic acid and hyperchloremia. We measured the release of PGE2, 6kPGF1α, PGF2α, and TXB2 into urine (U) and renal hilar lymph (L) to assess the possible roles of intrarenal prostaglandins (PGs) in arachidonic acid (AA)-induced renal vasodilation and Cl-induced renal vasoconstriction, (a model of tubuloglomerular feedback, TG). AA caused an ipsilateral fall in renal vascular resistance (RVR) and diuresis and increased release of all PGs into U; release of 6kPGF1α into L increased ninefold. Hypertonic NaCl infusion caused ipsilateral vasoconstriction and decreased GFR; the release of TXB2 into U and L increased, but other PGs were not altered consistently. During a background infusion of AA, hypertonic NaCl infusion again evoked TXB2 release into U and L without significant changes in other PGs. AA attenuated the NaCl-induced renal vasoconstriction in dogs with the highest rates of PGE2 release into L. Changes in RVR correlated with the ratio of excretion of vasodilator PG (PGE2 + 6kPGF1α) to TXB2 (r = -0.74). Indomethacin administration blunted, but did not abolish, the Cl-induced increase in RVR. In conclusion, (1) AA evokes the release of PGs, especially prostacyclin, into renal cortex; (2) hyperchloremia increases RVR and evokes a rather selective release of renal TX; (3) the production of vasodilator PGs by AA may attenuate Cl-induced renal vasoconstriction; (4) renal vasodilator and vasoconstrictor PGs can be released relatively independently—their balance could modulate RVR during activation of the TG response. Relargage intrarenal de prostaglandines: Effets de l'acide arachidonique et de l'hyperchloremie. Nous avons mesure le relargage de PGE2, 6kPGF1α, et TXB2 dans les urines (U) et la lymphe (L) hilaire renale pour preciser les roles possibles des prostaglandines intrarenales (PGs) sur la vasodilatation renale induite par l'acide arachidonique (AA) et sur la vasoconstriction renale induite par Cl (un modele de feedback tubulo-glomerulaire, TG). AA a entraine une chute ipsilaterale des resistances vasculaires renales (RVR) et de la diurese et a augmente le relargage de toutes les PGs dans U; le relargage de 6kPGF1α dans L a augmente de 9 fois. Une perfusion de NaCl hypertonique a entraine une vasoconstriction ipsilaterale et a diminue GFR; le relargage de TXB2 dans U et L a augmente, mais les autres PGs n'etaient pas notablement modifiees. Au cours d'une perfusion continue d'AA, une perfusion de NaCl hypertonique a encore entraine un relargage de TXB2 dans U et L sans changements significatifs des autres PGs. AA a attenue la vasoconstriction renale induite par le NaCl chez les chiens ayant les vitesses de relargage de PGE2 dans L les plus grandes. Les modifications de RVR etaient correlees au rapport d'excretion de PG vasodilatatrices (PGE2 + 6kPGF1α) sur TXB2 (r = -0,74). L'administration d'indomethacine a diminue, mais n'a pas aboli l'elevation de RVR induite par Cl. En conclusion, (1) AA entraine un relargage de PGs, surtout de prostacycline, dans le cortex renal; (2) l'hyper-chloremie augmente RVR et induit un relargage relativement selectif de TX renal; (3) la production de PGs vasodilatatrices par AA pourrait attenuer la vasoconstriction renale induite par Cl; (4) les PGs vasodilatatrices et vasoconstrictrices renales peuvent etre relarguees de facon relativement independante. Leur equilibre pourrait moduler RVR au cours de l'activation de la response TG.

Type II pseudohypoaldosteronism is an uncommonly reported disorder. The authors recently evaluated a patient who in many respects appeared to have this syndrome. He had hyperkalemia, a normal glomerular filtration rate, “normal” serum and urinary aldosterone levels, and low plasma renin activity. In addition, he had a hyperchloremic metabolic acidosis and hypertension. Fractional excretion of potassium was reduced in response to sodium chloride loading. However, renal potassium excretion in response to administration of sodium sulfate was normal. Thiazide diuretic restored the serum potassium, the low bicarbonate, and blood pressure to normal. He developed marked natriuresis and kaliuresis in response to high-dose exogenous mineralocorticoid. The magnitude of the kaliuretic response achieved to exogenous mineralocorticoid has been reported only once previously.

1.1. A classification of the clinical features of renal acidosis is presented together with a clarification of the terms under which the disease has been described. 2.2. Two additional patients with the disease are reported. 3.3. Observations on the family of one patient are offered as the first known demonstration that this disease can exist on a familial basis. 4.4. Pathogenesis of the disease is discussed.

Summary We report a group of four infants and one child who showed a strikingly similar syndrome characterized by persistent dehydration, acidosis with hyperchloremia, and extensive diffuse deposits of calcium salts in and around the renal tubules.

A detailed summary is given of the fluid and electrolyte therapy used in the early phases of treatment of twenty-nine episodes of severe diabetic ketoacidosis. There was little difference in the volume of fluid retained when repair solutions of varying tonicity were employed. Hyperosmolarity of the serum was present in 52 per cent of the patients on entry and in 46 per cent of the patients after twelve hours of therapy. When hypertonic fluids were used there was more hyperosmolarity of the serum after twelve hours of therapy than with hypotonic fluids, and hypernatremia and hyperchloremia were frequently noted. This indicates the need for use chiefly of hypotonic fluids. Factors influencing the correction of acidosis included the lactatechloride ratio of the intravenous fluids used (considered to be best at a ratio over 1.0), the entry serum chloride level, the use of hypertonic solutions, large loads of 0.9 per cent sodium chloride and the rate of fall of the blood ketone levels. Detailed balance studies in eight patients correlated well with previous estimates of 5 to 10 per cent body fluid loss and with balances of certain ions. From these studies we believe that the average range of intake in the early, more acute phases of treatment should be 70 to 120 ml. H 2 O/Kg.; 7 to 10 mEq. Na/Kg.; 5 mEq. Cl/Kg.; 2 to 3 mEq. K/Kg.; 0.2 mEq. Mg/Kg.; 1 mM P/ Kg.; and 4 to 5 mEq. HCŌ 3 /Kg.

Ten patients who were hospitalized because of flaccid quadriplegia and hypokalemia were found to have renal tubular disease. Nine had typical renal tubular acidosis with hyperchloremia and persistently alkaline urine. One had an as yet poorly understood renal tubular disease characterized by excessive renal sodium, potassium and chloride loss, alkalosis, hydronephrosis, nephrocalcinosis and mental deficiency. Balance studies in several patients demonstrated a large negative potassium balance with abnormal urinary potassium losses even during hypokalemic episodes. Other clinical and laboratory features included polyuria, polydipsia, nephrocalcinosis, hyposthenuria, hypouricemia and pyelonephritis, with occasional findings, during the hypokalemic phase, of normocalcemic tetany, hyperdynamic circulation, pulsus alternans and hypophosphatemia. Of possible etiologic significance was the presence or history of pyelonephritis in eight patients. Histamine achlorhydria in one patient studied suggested a possible generalized defect in carbonic anhydrase activity. This patient's red blood cells were found to contain normal carbonic anhydrase activity, and her arterial alveolar pCO 2 gradient was normal at rest and after exercise. Although these results fail to support a generalized deficiency of this enzyme, they do not exclude a localized deficiency within the renal tubular cells. Each patient responded well to potassium and alkali therapy and paralysis has not recurred. Renal function as measured by blood non-protein nitrogen, phenolsulfonphthalein excretion, urinalysis and intravenous pyelograms has remained normal in all subjects, six of whom have been under observation for five years or longer. Three patients no longer require potassium supplements, and one patient appears to have had a complete remission from her renal tubular disease.

When total cystectomy is necessary during pelvic exenteration to remove cancer in this region, an isolated short segment of terminal ileum functions well as a conduit for the urine. The ureters are anastomosed to the side of the ileal segment, the proximal end of which is closed and the distal end opening on the abdominal wall. The segment spontaneously empties at intervals by peristalsis into a receptacle attached to the abdominal skin around the ileostomy. Careful attention to the technical details of the operation, especially the ureteroileal anastomoses, heralds good results. The hazards of acidosis, hyperazotemia, hyperchloremia, and ascending urinary tract infection, the distressing continuous discharge of a liquid mixture of feces and urine which attends the “wet” colostomy, and the almost certain lethal outcome due to nephropathy are avoided. A personal experience with fifty-seven cases underscores the virtues of an isolated ileal segment with its fewer complications as the best available method of conducting the urine from the ureters to an external appliance when pelvic evisceration is performed.

long been recognized as one of the common manifestations of renal insufficiency. Considerable clinical interest has been generated by reports appearing in the past few decades describing acidosis of renal origin occurring without significant azotemia or other signs of impairment of glomerular filtration. This isolated disturbance has been called "renal tubular acidosis" to distinguish it from that seen with azotemia, so-called "uremic acidosis." Butler, Wilson, and Farber, in t936,1 reported the occurrence of persistent unexplained acidosis with hyperchloremia in 4 infants who had no underlying renal disease or any history of significant abnormal losses from vomiting or diarrhea. All of the infants had a similar clinical history of failure to thrive, anorexia, and recurrent bouts of mild vomiting. All of them ultimately developed signs of marked dehydration and hyperpnea that led to clinical recognition of the disturbance. All of these infants died, and calcification of variable degrees was found in the renal medullary parenchyma at postmortem. These authors included in this report a description of a similar biochemical disturbance (hyperchloremic acidosis) observed in a 10-year-old boy who presented a different clinical course. The

During a fifteen year interval, thirty-five patients with primary hyperparathyroidism were treated surgically. The increased incidence during the last seven years of this period was attributed to an increased awareness of the vagaries of this disease by the physician plus the use of routine blood screening procedures on admission. As evidence of the latter, 62 per cent of the patients were admitted to the hospital with complaints unrelated to parathyroid overactivity. Females predominated in this series by a ratio of 2.5 to 1. The largest number of patients presented between the ages of fifty-one and seventy years. Hypercalcemia was present in every case. Hypophosphatemia, hyperchloremia, hyperuricemia, and hypomagnesemia were found in occasional patients. Thirty-one of the thirty-five had either adenomas or hyperplasia and they responded to surgical excision. There was a significant (20 per cent) incidence of concurrent thyroid disease.

duct.' The effects of a thoracic duct fistula are proportional to the duration and volume of the lymph drainage and include fever, hypoalbuminemia, and hypoglobulinemia,' chylofibrosis, and malnutrition. a Additional potential problems include respiratory distress,' salt and water depletion, and lymphocytopenia. To this list of possible complications we add metabolic acidosis. The normal anion gap suggested that this infant's acidosis was due to the loss of bicarbonate rather than the addition of acid. Comparing the cations (Na,K) with the anions (HCO" Cl) normally reveals a cation preponder­ ance of approximately 11 to 19 mSq/l.' This anion gap is comprised of unmeasured anions, largely negatively charged plasma proteins. The addition of an acid (e.g., lactate or ,B-hydroxybutyrate) lowers the bicarbonate concentration without raising the concentration of other measured anions, and increases the gap. With acidosis secondary to bicarbonate loss, there is renal retention of chloride. The resulting hyperchloremia off-sets the low serum bicarbonate concentration, and the normal cation­ anion difference (gap) is maintained. As the electrolyte composition of lymph approximates that of plasma," s and as this infant's lymph loss averaged 700 nil/day (184 nil/kg/day), his water and electrolyte losses were substantial. Moreover, the magnitude of the infant's bicarbonate loss is impressive, considering that his normal total bicarbonate stores were only about 42 mEq (assuming bicarbonate's space of distribution to approxi­ mate 50%of body weight and a normal serumbicarbonate concentration to be 22 mfiq/l). Although the daily volume and bicarbonate concentration of the thoracic drainage varied, on some days the bicarbonate loss approximated SO% of the infant's normal body stores. Controversy does exist regarding the management of postoperative chylothorax. Many lymphatic leaks will seal spontaneously and can be managed with thoracentesis or chest-tube drainage. Additional conservative measures include intravenous administration of albumin, and a medium-chain triglyceride diet.' There is general agree­ ment, however, that thoracic duct ligation is necessary when profuse lymphatic drainage persists for more than a week or two.'

Chlorine gas Inhalation is usually accompanied by pulmonary toxicity and hypoxemia; the associated acidemia, when present, has been attributed to lactic acidosis. This case report describes the development of hyperchloremic metabolic acidosis following accidental chlorine gas exposure. The mechanism postulated for the production of this acidosis is the absorption of hydrochloric acid following the reaction of chlorine gas with tissue water. This may be the first case of chlorine toxicity in which the mechanism of the acidosis has been determined.