Metabolic Acid-Base Disorders.

Metabolic acid-base disturbances are frequently encountered in the emergency department, and many of these patients are critically ill. In the evaluation of patients with these maladies, it is important for the emergency clinician to determine the cause, which can usually be elicited from a thorough history and physical examination. There are several mnemonics that can be used to form an appropriate list of potential causes. Most of the time, the management of these patients requires no specific treatment of the acid-base status but, rather, requires treatment of the underlying disorder that is causing the acid-base disturbance.

Spurious Electrolyte and Acid-Base Disorders in the Patient With Cancer: A Review.

Electrolyte and acid-base disorders are frequently encountered in patients with malignancy, either due to cancer itself or as a complication of its therapy. However, spurious electrolyte disorders can complicate the interpretation and management of these patients. Several electrolytes can be artifactually increased or decreased such that the serum electrolyte values do not correspond to their actual systemic levels, potentially resulting in extensive diagnostic investigations and therapeutic interventions. Examples of spurious derangements include pseudohyponatremia, pseudohypokalemia, pseudohyperkalemia, pseudohypophosphatemia, pseudohyperphosphatemia, and artifactual acid-base abnormalities. Correctly interpreting these artifactual laboratory abnormalities is imperative for avoiding unnecessary and potentially harmful interventions in cancer patients. The factors influencing these spurious results also must be recognized, along with the steps to minimize them. We present a narrative review of commonly reported pseudo electrolyte disorders and describe strategies to exclude erroneous interpretations of these laboratory values and avoid pitfalls. Awareness and recognition of spurious electrolyte and acid-base disorders can prevent unnecessary and harmful treatments.

Acid-Base Disorders in the Critically Ill Patient.

Acid-base disorders are common in the intensive care unit. By utilizing a systematic approach to their diagnosis, it is easy to identify both simple and mixed disturbances. These disorders are divided into four major categories: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Metabolic acidosis is subdivided into anion gap and non-gap acidosis. Distinguishing between these is helpful in establishing the cause of the acidosis. Anion gap acidosis, caused by the accumulation of organic anions from sepsis, diabetes, alcohol use, and numerous drugs and toxins, is usually present on admission to the intensive care unit. Lactic acidosis from decreased delivery or utilization of oxygen is associated with increased mortality. This is likely secondary to the disease process, as opposed to the degree of acidemia. Treatment of an anion gap acidosis is aimed at the underlying disease or removal of the toxin. The use of therapy to normalize the pH is controversial. Non-gap acidoses result from disorders of renal tubular H + transport, decreased renal ammonia secretion, gastrointestinal and kidney losses of bicarbonate, dilution of serum bicarbonate from excessive intravenous fluid administration, or addition of hydrochloric acid. Metabolic alkalosis is the most common acid-base disorder found in patients who are critically ill, and most often occurs after admission to the intensive care unit. Its etiology is most often secondary to the aggressive therapeutic interventions used to treat shock, acidemia, volume overload, severe coagulopathy, respiratory failure, and AKI. Treatment consists of volume resuscitation and repletion of potassium deficits. Aggressive lowering of the pH is usually not necessary. Respiratory disorders are caused by either decreased or increased minute ventilation. The use of permissive hypercapnia to prevent barotrauma has become the standard of care. The use of bicarbonate to correct the acidemia is not recommended. In patients at the extreme, the use of extracorporeal therapies to remove CO 2 can be considered.

Physicochemical properties of abnormal blood acid-base buffering.

This paper describes two new features 1) development of physicochemically based, two-compartment models describing acid-base-state changes in normal and abnormal blood and 2) use of model results to view and describe physicochemical properties of blood, in terms of Pco2 as the causative independent variable and effected [H+] changes as the dependent variable. Models were derived from an in vitro experimental study, where normal blood was made both hypoproteinemic and hyperalbuminemic and then equilibrated with CO2. Strong-ion gap (SIG) values were selected to match model and experimental pH. The effect of individual physicochemical factors affecting blood acid-base-state were evaluated from their induced changes on buffer curve linearized slope (ßH+) and [H+] curve shift at 40 mmHg ([H+]40). Model findings were: 1) in severe hypoproteinemia, hemoglobin enhances buffering (decreases ßH+), whereas albumin compromises it, resulting in an almost unchanged ßH+; [H+]40 decreases (alkalemia) due to hypoalbuminemia. 2) Severe hyperalbuminemia greatly increases both ßH+ and [H+]40, hence, compromising buffering and causing a severe acidemia. 3) Pco2-induced changes in the electrical-charge concentration of hemoglobin are the principal factor responsible for maintaining normal buffering characteristics in hypoproteinemia and hyperalbuminemia. 4) SIG values are a third Pco2-independent characteristic of blood acid-base state and 5) the quantities, ßH+, [H+]40, and SIG, derived from a [H+] vs. Pco2 perspective, are a more informative and intuitive way to characterize blood acid-base state.NEW & NOTEWORTHY This study represents the most up-to-date, physicochemical, multi-compartment computer model of the processes involved in determining the acid-base buffering state of blood. Previous models lack this capability, notably by being single compartment and/or lacking electroneutrality and osmotic constraints. Model results, analyzed from a different perspective of dependent [H+] changes resulting from independent Pco2 changes, provide a new set of Pco2-independent parameters, characteristic of blood buffering properties.

Fluid Overload and Tissue Sodium Accumulation as Main Drivers of Protein Energy Malnutrition in Dialysis Patients.

Protein energy malnutrition is recognized as a leading cause of morbidity and mortality in dialysis patients. Protein-energy-wasting process is observed in about 45% of the dialysis population using common biomarkers worldwide. Although several factors are implicated in protein energy wasting, inflammation and oxidative stress mechanisms play a central role in this pathogenic process. In this in-depth review, we analyzed the implication of sodium and water accumulation, as well as the role of fluid overload and fluid management, as major contributors to protein-energy-wasting process. Fluid overload and fluid depletion mimic a tide up and down phenomenon that contributes to inducing hypercatabolism and stimulates oxidation phosphorylation mechanisms at the cellular level in particular muscles. This endogenous metabolic water production may contribute to hyponatremia. In addition, salt tissue accumulation likely contributes to hypercatabolic state through locally inflammatory and immune-mediated mechanisms but also contributes to the perturbation of hormone receptors (i.e., insulin or growth hormone resistance). It is time to act more precisely on sodium and fluid imbalance to mitigate both nutritional and cardiovascular risks. Personalized management of sodium and fluid, using available tools including sodium management tool, has the potential to more adequately restore sodium and water homeostasis and to improve nutritional status and outcomes of dialysis patients.

Regulation of Acid-Base Balance in Patients With Chronic Kidney Disease.

Normallly the kidneys handle the daily acid load arising from net endogenous acid production from the metabolism of ingested animal protein (acid) and vegetables (base). With chronic kidney disease, reduced acid excretion by the kidneys is primarily due to reduced ammonium excretion such that when acid excertion falls below acid porduction, acid accumulation occurs. With even mild reductions in glomerular filtration rate (60 to 90 ml/min), net acid excretion may fall below net acid production resulting in acid retention which may be initially sequestered in interstitial compartments in the kidneys, bones, and muscles resulting in no fall in measured systemic bicarbonate levels (eubicarbonatemic metabolic acidosis). With greater reductions in kidney function, the greater quantities of acid retained spillover systemically resulting in low pH (overt metabolic acidosis). The evaluation of acid-base balance in patients with CKD is complicated by the heterogeneity of clinical acid-base disorders and by the eubicarbonatemic nature of the early phase of acid retention. If supported by more extensive studies, blood gas analyses to confirm the acid-base disorder and newer ways for assessing the presence of acidosis such as urinary citrate measurements may become routine tools to evaluate and treat acid-base disorders in individuals with CKD.

Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis.

BACKGROUND: Early aggressive hydration is widely recommended for the management of acute pancreatitis, but evidence for this practice is limited. METHODS: At 18 centers, we randomly assigned patients who presented with acute pancreatitis to receive goal-directed aggressive or moderate resuscitation with lactated Ringer's solution. Aggressive fluid resuscitation consisted of a bolus of 20 ml per kilogram of body weight, followed by 3 ml per kilogram per hour. Moderate fluid resuscitation consisted of a bolus of 10 ml per kilogram in patients with hypovolemia or no bolus in patients with normovolemia, followed by 1.5 ml per kilogram per hour in all patients in this group. Patients were assessed at 12, 24, 48, and 72 hours, and fluid resuscitation was adjusted according to the patient's clinical status. The primary outcome was the development of moderately severe or severe pancreatitis during the hospitalization. The main safety outcome was fluid overload. The planned sample size was 744, with a first planned interim analysis after the enrollment of 248 patients. RESULTS: A total of 249 patients were included in the interim analysis. The trial was halted owing to between-group differences in the safety outcomes without a significant difference in the incidence of moderately severe or severe pancreatitis (22.1% in the aggressive-resuscitation group and 17.3% in the moderate-resuscitation group; adjusted relative risk, 1.30; 95% confidence interval [CI], 0.78 to 2.18; P = 0.32). Fluid overload developed in 20.5% of the patients who received aggressive resuscitation and in 6.3% of those who received moderate resuscitation (adjusted relative risk, 2.85; 95% CI, 1.36 to 5.94, P = 0.004). The median duration of hospitalization was 6 days (interquartile range, 4 to 8) in the aggressive-resuscitation group and 5 days (interquartile range, 3 to 7) in the moderate-resuscitation group. CONCLUSIONS: In this randomized trial involving patients with acute pancreatitis, early aggressive fluid resuscitation resulted in a higher incidence of fluid overload without improvement in clinical outcomes. (Funded by Instituto de Salud Carlos III and others; WATERFALL ClinicalTrials.gov number, NCT04381169.).

Trauma-related electrolyte disturbances: From resuscitation to rhabdomyolysis.

Traumatic injury results in drastic changes to a patient's normal physiology. The hormonal stress response, as well as some treatment strategies, lead to significant disruptions in electrolyte homeostasis that are important for clinicians to understand. In addition, advances in fluid resuscitation and modern transfusion practices have led to their own unique set of consequences, which we are just beginning to appreciate. Special attention is placed on rhabdomyolysis, as this distinct entity represents an extreme example of injury induced electrolyte derangements. This review describes the physiologic response to trauma and highlights some of the important electrolyte abnormalities that can be encountered while caring for the injured patient.

Association between anion gap and mortality of aortic aneurysm in intensive care unit after open surgery.

BACKGROUND: There has not been a well-accepted prognostic model to predict the mortality of aortic aneurysm patients in intensive care unit after open surgery repair. Otherwise, our previous study found that anion gap was a prognosis factor for aortic aneurysm patients. Therefore, we wanted to investigate the relationship between anion gap and mortality of aortic aneurysm patients in intensive care unit after open surgery repair. METHODS: From Medical Information Mart for Intensive Care III, data of aortic aneurysm patients in intensive care unit after open surgery were enrolled. The primary clinical outcome was defined as death in intensive care unit. Univariate analysis was conducted to compare the baseline data in different groups stratified by clinical outcome or by anion gap level. Restricted cubic spline was drawn to find out the association between anion gap level and mortality. Subgroup analysis was then conducted to show the association in different level and was presented as frost plot. Multivariate regression models were built based on anion gap and were adjusted by admission information, severity score, complication, operation and laboratory indicators. Receiver operating characteristic curves were drawn to compare the prognosis ability of anion gap and simplified acute physiology score II. Decision curve analysis was finally conducted to indicate the net benefit of the models. RESULTS: A total of 405 aortic aneurysm patients were enrolled in this study and the in-intensive-care-unit (in-ICU) mortality was 6.9%. Univariate analysis showed that elevated anion gap was associated with high mortality (P value < 0.001), and restricted cubic spline analysis showed the positive correlation between anion gap and mortality. Receiver operating characteristic curve showed that the mortality predictive ability of anion gap approached that of simplified acute physiology score II and even performed better in predicting in-hospital mortality (P value < 0.05). Moreover, models based on anion gap showed that 1 mEq/L increase of anion gap improved up to 42.3% (95% confidence interval 28.5-59.8%) risk of death. CONCLUSIONS: The level of serum anion gap was an important prognosis factor for aortic aneurysm mortality in intensive care unit after open surgery.

Changes in acid-base status in oxygen toxicity at 230 kPa oxygen as a function of exposure time.

Breathing less than 50 kPa of oxygen over time can lead to pulmonary oxygen toxicity (POT). Vital capacity (VC) as the sole parameter for POT has its limitations. In this study we try to find out the changes of acid-base status in a POT rat model. Fifty male rats were randomly divided into five groups, exposed to 230 kPa oxygen for three, six, nine and 12 hours, respectively. Rats exposed to air were used as controls. After exposure the mortality and behavior of rats were observed. Arterial blood samples were collected for acid-base status detection and wet-dry (W/D) ratios of lung tissues were tested. Results showed that the acid-base status in rats exposed to 230 kPa oxygen presented a dynamic change. The primary status was in the compensatory period when primary respiratory acidosis was mixed with compensated metabolic alkalosis. Then the status changed to decompensated alkalosis and developed to decompensated acidosis in the end. pH, PCO2, HCO3-, TCO2, and BE values had two phases: an increase and a later decrease with increasing oxygen exposure time, while PaO2 and lung W/D ratio showed continuously increasing trends with the extension of oxygen exposure time. Lung W/D ratio was significantly associated with PaO2 (r = 0.6385, p = 0.002), while other parameters did not show a significant correlation. It is concluded that acid-base status in POT rats presents a dynamic change: in the compensatory period first, then turns to decompensated alkalosis and ends up with decompensated acidosis status. Blood gas analysis is a useful method to monitor the development of POT.

Alterações hidroeletrolíticas em pessoas com cirrose / Hydroelectrolytic alterations in cirrhotic patients

O objetivo deste estudo foi evidenciar e discutir as principais alterações hidroeletrolíticas em pessoas com cirrose. Trata-se de uma revisão integrativa, de natureza qualitativa. Os artigos foram selecionados por meio da plataforma Medical Literature Analysis and Retrievel System Online. Os principais achados identificados a partir dos artigos selecionados foram a ocorrência de hiponatremia, o mau prognóstico diante da presença de distúrbios hidroeletrolíticos em relação à sobrevida em pessoas com cirrose e a importância da albumina. Indivíduos com cirrose são suscetíveis ao desenvolvimento de distúrbios hidroeletrolíticos devido às mudanças fisiopatológicas da doença e às condições clínicas apresentadas. A hiponatremia e a hipocalemia são os mais recorrentes, destacando, porém, a necessidade de atenção aos demais distúrbios. (AU)

The objective of this study was to show and discuss the main hydroelectrolytic alterations in cirrhotic patients. This is an integrative review, a qualitative study, in which articles were selected at the Medical literature Analysis and Retrieval System Online. The main findings identified in the articles selected were the occurrence of hyponatremia, the poor prognostic, due to the presence of hydroelectrolytic disorders, regarding cirrhotic individuals survival and the importance of albumin. Individuals with cirrhosis are susceptible to the development of hydroelectrolytic disorders due to the pathophysiological alterations of the disease and because of the clinical status presented. Hyponatremia and hypokalemia are the most recurrent, but attention shall be given to the other disorders too. (AU)

Modulation of the Association of Hypobicarbonatemia and Incident Kidney Failure With Replacement Therapy by Venous pH: A Cohort Study.

RATIONALE & OBJECTIVE: Studies showing an association between lower bicarbonate levels and worse kidney disease prognosis have not accounted for the influence of pH. It remains unknown whether this association is consistent across a wide range of blood pH values. This study sought to assess how pH modifies the relationship between hypobicarbonatemia and incident kidney failure requiring kidney replacement therapy (KFRT). STUDY DESIGN: Retrospective cohort study. SETTING & PARTICIPANTS: 1,058 Japanese patients with estimated glomerular filtration rates<60mL/min/1.73m2. EXPOSURE: Baseline venous bicarbonate levels and venous pH. OUTCOME: KFRT defined as initiation of kidney replacement therapy (hemodialysis, peritoneal dialysis, and kidney transplantation). ANALYTICAL APPROACH: Cox proportional hazards model assessing the interaction between baseline bicarbonate levels and venous pH on incident KFRT. RESULTS: In the lowest bicarbonate quartile (≤21.5 mEq/L), 59% of patients had acidemia (pH<7.32), whereas 38% had venous pH within the normal range and 3% had alkalemia (pH>7.42). During a median follow-up of 3.0 years, 374 patients developed KFRT. Venous pH modified the association between bicarbonate level and rate of KFRT (P for interaction=0.04). After adjustment for potential confounders, including capacity for respiratory compensation, the lowest (vs the highest) bicarbonate quartile was associated with a 2.29-fold (95% CI, 1.10-4.77; P=0.03) higher rate of KFRT among patients with acidemia (pH<7.32). In contrast, among patients without acidemia (pH≥7.32), no significant association was found between bicarbonate level and KFRT. In an exploratory analysis, patients with higher respiratory compensation capacity had a lower rate of KFRT (HR per 0.1 increase in respiratory compensation capacity, 0.90; 95% CI, 0.87-0.94; P<0.001). LIMITATIONS: Observational study design; blood gas measurements were performed in a select patient population. CONCLUSIONS: Venous pH modified the association of hypobicarbonatemia with progression of chronic kidney disease to KFRT. Measurement of venous pH may be valuable for identifying patients with chronic kidney disease and hypobicarbonatemia and may inform treatment.

Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review.

Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid-base abnormality. In patients with excessive loss of salt in the sweat or poor salt intake, the maintenance of metabolic alkalosis is crucially modulated by the chloride-bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the salt content of foods as part of an effort to minimize the tendency towards systemic hypertension. Hence, the baby food industry decided to remove added salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a chloride content of only 2-4 mmol/L), were admitted with failure to thrive, constipation, food refusal, muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic alkalosis, hypokalemia, hypochloremia, and a reduced urinary chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal chloride content. Since 1982, 13 further publications reported additional cases of dietary chloride depletion. It is therefore concluded that the dietary intake of chloride, which was previously considered a "mendicant" ion, plays a crucial role in acid-base and salt balance.

Tackling acid-base disorders, one Twitter poll at a time.

Understanding and interpretation of acid-base disorders is an important clinical skill that is applicable to the majority of physicians. Although this topic is taught early in medical school, acid-base disturbances have been described as challenging by postgraduate trainees. We describe the use of Twitter, an online microblogging platform, to augment education in acid-base disturbances by using polls in which the user is shown laboratory values and then asked to select the most likely etiology of the disorder. The answer and a brief explanation are then shared in a subsequent tweet. Both polling questions and answers are shared from the account for the online, mobile-optimized, nephrology teaching tool NephSIM (https://www.nephsim.com/). An anonymous survey was administered to assess attitudes toward these polls. Using Twitter as an approach to enhance teaching of acid-base disturbances was both feasible and an engaging way to teach a challenging topic for trainees and physicians. Moreover, the coronavirus disease 2019 (COVID-19) pandemic has demonstrated the importance of incorporating virtual learning opportunities in all levels of medical education.

Acid-Base Balance Disorders During Kidney Preservation in Cold Ischemia.

BACKGROUND: Acid-base balance disorders are a crucial element of ischemia-reperfusion injury during organ transplantation. Hypoxia during organ procurement and storage cause cellular homeostasis imbalance with impact on further graft function. Acidosis in preserved kidney caused by lactate accumulation may have an important role as a common denominator of various pathways leading to cellular damage. METHODS: Our trial sought to answer questions regarding a range of pH alterations in the kidney before the transplantation, their potential cause, and how this may affect further outcome of the kidney transplantation procedure. Perfusion fluid for pH analysis was obtained from perfusion pump (PP) or through kidney flushing at the end of preservation depending on the storage method. RESULTS: A total of 66 sample results were collated with the data from the transplant registry, hospitalization, and outpatient department. Statistical analysis was conducted linking pH results with factors related to donor, recipient, preservation, and outcome according to designed schematics. Mean perfusate pH was significantly lower in simple hypothermia (SH) vs the PP storage group (6.77 vs 7.11; P < .001). All samples of perfusate pH in the SH group were below physiological values (<7.35), and in 10% of samples in the SH group, pH >7.00. CONCLUSIONS: We concluded that kidney storage in cold ischemia is associated with organ acidosis independent of preservation method and that SH is correlated with significantly bigger acidosis than storage in PP, which is an important procedure removing an excessive amount of hydrogen ions from kidney microcirculation, decreasing cell damage.

Distúrbios ácido-base nas doenças hepáticas / Acid-base disorders in liver diseases

O objetivo deste artigo foi abordar as controvérsias científicas acerca dos distúrbios ácido-base nas doenças hepáticas. Nos estágios avançados da doença hepática, os distúrbios ácido-base atuam de forma complexa, comprometendo a qualidade de vida do paciente e desafiando o manejo clínico. A literatura apresenta a alcalose respiratória como uma das principais alterações, porém há uma longa discussão sobre o mecanismo fisiopatológico; em especial, citam-se a hipóxia, a hipocapnia e o nível de progesterona. Nas desordens metabólicas, com destaque para a acidose, os estudos apontam principalmente o lactato, os unmeasured ions ou íons não medidos e as alterações hidroeletrolíticas, mas cada componente desse sobressai-se dependendo da fase da doença estudada, compensada ou descompensada. As controvérsias dos distúrbios ácido-base nas doenças hepáticas devem-se ora à complexidade da fisiopatologia da própria doença, ora à necessidade de mais estudos esclarecedores.

The aim of this study is to address the scientific controversy about acid-base disorders in liver diseases. In the end stage of liver diseases, the acid-base disorder has a complex performance, impairing the patient's quality of life and challenging the clinic management. Although the literature shows respiratory alkalosis as one of the main alterations, there is a long discussion about the pathophysiological mechanism, specially regarding hypoxia, hypocapnia, and progesterone level. In metabolic disorders, especially acidosis, the studies mainly indicate the lactate, unmeasured ions, and hydroelectrolytic alterations, but, depending on the disease phase, either compensated or decompensated, each element has a particular action. The controversy about acid-base disorders in liver diseases is associated with the complexity of this condition, as well as with the necessity of more specialized research.

Electrolyte and acid-base disorders in cancer patients and its impact on clinical outcomes: evidence from a real-world study in China.

Background: This study aims to delineate the incidence of electrolyte and acid-base disorders (EAD) in cancer patients, to figure out the risk factors of EAD, then to assess the impact of EAD on patients' in-hospital clinical outcomes.Methods: Patients with the diagnosis of malignancies hospitalized during 1 October 2014 and 30 September 2015 were recruited in Zhongshan Hospital, Fudan University in Shanghai of China. Demographic characteristics, comorbidities, and clinical data, including survival, length of stay and hospital cost, were extracted from the electronic medical record system. Electrolyte and acid-base data were acquired from the hospital laboratory database.Results: Of 25,881 cancer patients with electrolyte data, 15,000 (58.0%) cases had at least one electrolyte and acid-base abnormity. Hypocalcemia (27.8%) was the most common electrolyte disorder, followed by hypophosphatemia (26.7%), hypochloremia (24.5%) and hyponatremia (22.5%). The incidence of simple metabolic acidosis (MAC) and metabolic alkalosis (MAL) was 12.8% and 22.1% respectively. Patients with mixed metabolic acid-base disorders (MAC + MAL) accounted for 30.2%. Lower BMI score, preexisting hypertension and diabetes, renal dysfunction, receiving surgery/chemotherapy, anemia and hypoalbuminemia were screened out as the major risk factors of EAD. In-hospital mortality in patients with EAD was 2.1% as compared to those with normal electrolytes (0.3%). The risk of death significantly increased among patients with severe EAD. Similarly, the length of stay and hospital cost also tripled as the number and grade of EAD increased.Conclusion: EAD is commonly encountered in cancer patients and associated with an ominous prognosis. Patients with comorbidities, renal/liver dysfunction, and anti-tumor therapy have a higher risk of EAD. Regular monitoring of electrolytes, optimum regimen for intravenous infusion, timely correction of modifiable factors and appropriate management of EAD should not be neglected during anti-tumor treatment.

Multiple electrolyte imbalances and mixed acid-base disorder posing a diagnostic dilemma: a case report.

BACKGROUND: In clinical practice, both the history and laboratory testing are paramount to making an accurate diagnosis. Situations in which laboratory findings and patient history are not congruent pose a diagnostic dilemma. We report a case of a young woman presenting with a myriad of electrolyte and acid-base disorders. Difficulty in reaching a unifying diagnosis persisted due to discordant patient history. We believe this case shows that lab findings will clearly portray the problems a patient has and should be given more credence in a case where the history is discordant with lab findings. CASE PRESENTATION: A 28-year-old Hispanic American woman presented to the emergency room of our institution with a complaint of painless and sudden onset of stiffness in her upper and lower limbs. Associated weakness worse in the distal limbs was also reported. She experienced shortness of breath with minimal exertion, diaphoresis, and anxiety. Her vital signs revealed tachycardia without corresponding fever. She was conscious, oriented, and alert. Her physical exam revealed dry mucous membranes and warm extremities. She denied recent consumption of a large carbohydrate meal, diarrhea, vomiting, use of laxatives, and use of alcohol or recreational drugs. She vaguely described two previous similar episodes in the last 7 months that spontaneously resolved. Her medical history was significant only for hypothyroidism treated with daily levothyroxine tablets. Laboratory analysis revealed the following abnormalities: an elevated anion gap with significant lactate, hypokalemia, hypomagnesemia, elevated mean corpuscular volume, elevated mean cell hemoglobin, and elevated liver enzymes with aspartate aminotransferase/alanine aminotransferase ratio > 2. She was hydrated with balanced crystalloids, and her electrolyte deficiencies corrected. The etiology of her multiple electrolyte abnormalities was unclear because alcohol use was vehemently denied. Extensive evaluation for causes of electrolyte disorder was undertaken, which was unrevealing. On further interrogation, she admitted to recent alcohol intoxication and several episodes of vomiting before presentation. She was advised to refrain from alcohol use and discharged afterward. CONCLUSION: Both patient history and laboratory analysis have a role in identifying and confirming a diagnosis. In cases in which laboratory tests are incongruous with reported history, making a unifying diagnosis can be challenging or delayed. The importance of taking a comprehensive history cannot be overemphasized, but history provided by patients may be prone to intentional or unintentional distortion, whereas laboratory findings are more objective. The case presented underscores why the lab findings should be given credence in cases in which there is discordance between lab results and the provided patient history.

Association of serum chloride level alterations with in-hospital mortality.

BACKGROUND: We aimed to assess the association between alterations in serum chloride levels during hospitalisation and mortality. METHODS: We reviewed all adult patients admitted to our hospital from the year 2009 to 2013, who had at least two serum chloride measurements during hospitalisation. The serum chloride change during hospitalisation, defined as the absolute difference between the highest and lowest serum chloride levels, was categorised into seven groups; 0-2, 3-4, 5-6, 7-8, 9-10, 11-12 and ≥13 mEq/L. Multivariable logistic regression was performed to assess the independent association between serum chloride change and in-hospital mortality, using the serum chloride change of 0-2 mEq/L as the reference group. RESULTS: A total of 57 880 patients, with median serum chloride change of 5 (IQR 3-9) mEq/L, were studied. The in-hospital mortality was progressively increased with larger chloride change, from 0.6% in group of 0-2 mEq/L to 5.9% in group of ≥13 mEq/L (p<0.001). In adjusted analysis, serum chloride change of ≥7 mEq/L was significantly associated with increased in-hospital mortality. For upward trend, serum chloride change of ≥3 mEq/L was significantly associated with increased in-hospital mortality, whereas, for downward trend, serum chloride change was not consistently associated with in-hospital mortality. CONCLUSION: Alterations in serum chloride during hospitalisation were associated with increased hospital mortality. The association was more prominent with upward than downward trend of serum chloride.