Cause Of Metabolic Acidosis Research Articles

Review article: Ketoacidosis in the emergency department.

Diabetic ketoacidosis, a life-threatening complication of type 1 diabetes mellitus, is a common cause of presentation to EDs. Two new drug classes have been found to cause ketoacidosis with distinctive presentations. The sodium-glucose transport protein 2 inhibitors used in the management of type 2 diabetes mellitus may present with ketoacidosis with normal glucose levels. Ketoacidosis with these medications may be prolonged and recur after initial resolution. Checkpoint inhibitors may present with fulminant diabetic ketoacidosis in individuals with previously normal glucose tolerance. Ketoacidosis may also occur as a result of starvation and alcohol excess, as well as a number of rare causes. Other causes of metabolic acidosis with both high and normal anion gap need to be considered in the differential diagnosis of ketoacidosis. Diabetic ketoacidosis may also present with biochemical changes suggestive of myocardial ischaemia and pancreatitis in the absence of these pathologies. The present paper reviews ketone body metabolism, ketone testing and the causes and differential diagnosis of ketoacidosis with particular relevance to emergency medicine.

Unexplained Severe Lactic Acidosis in Young Patient.

Case report: A 27-year-old previously healthy man was admitted to the ICU complaining nausea, vomiting and disorientation, after he ingested 1500 mg paracetamol, but its relatives explained that they possess in the house only metformin (maybe he ingested metformin instead of paracetamol). First blood gas showed moderate, and hours later severe lactic acidosis Ph 7,01, Lac 25 m mol/L, BE -26,4. Aggressive rehydration and hemofiltration was started, until full recovery after 24 hours of hospital admission. He was discharged after three days in healthy condition.
 Discussion: Lactic acidosis is a common cause of metabolic acidosis at the ICU. Type A is most common and caused by hypoperfusion or hypoxia, whilst type B has other causes including use of the antidiabetic drug metformin. Metformin associated lactic acidosis (MALA) is an important treatment-associated condition, and although rare, it is very serious.
 Conclusion: MALA should be strongly suspected in patients presenting with wide anion gap metabolic acidosis and high blood lactate concentration. Bicarbonate hemodialysis or continuous renal replacement therapy should be urgently arranged for patients with MALA.

Acidosis láctica asociada a metformina

La acidosis láctica severa asociada a metformina es una enfermedad grave, poco frecuente, pero con elevada mortalidad que se define en presencia de un pH < 7,35, Lactato > 2 mmol/L y una paCO2 en límites normales. Presentamos el caso de una paciente en tratamiento con metformina, hipertensa y dislipémica, polimedicada, con acidosis láctica grave ingresada en Reanimación, tras postoperatorio de laparotomía exploradora por sospecha de una isquemia intestinal. Llega en estado de shock circulatorio, con escasa respuesta a administración de volumen y drogas vasoactivas. Describimos algunos datos sobre su incidencia, la fisiopatología, el pronóstico y el tratamiento, así como la importancia de un diagnóstico precoz y diferencial con otras causas de acidosis metabólicas que eleven el anion GAP. ABSTRACT Lactic acidosis associated with metformin Metformin is an oral antidiabetic that belongs to the group of the biguainides. It is the drug of choice for the treatment of type II diabetes due to its efficacy and safety. It is a small molecule, whose elimination half-life is 8 to 20 hours in people with normal renal function. Severe lactic acidosis associated with metformin is a serious, infrequent disease (its incidence is estimated between 3-8 cases per 100,000 diabetic patients and year) but with high mortality (around 40% in accidental poisonings), which is defined in presence of a pH <7.35, lactate> 2 mmol / L and a paCO2 in normal limits. We present the case of a diabetic patient under treatment with metformin, hypertense and dyslipidemic, polymedicated, with severe lactic acidosis, in a Reanimation Care unit, after postoperative exploratory laparotomy due to suspicion of intestinal ischemia. He arrives in a state of circulatory shock, with little response to the administration of volume and vasoactive drugs. We describe some data about its incidence, pathophysiology, prognosis and treatment, as well as the importance of an early and differential diagnosis with other causes of metabolic acidosis that elevate the GAP anion.

Effect of chloride level on outcome in critically ill patients

Background Chloride (Cl) abnormalities in the critical care units have received great attention, especially hyperchloremia as a cause of metabolic acidosis and hypochloremia as a cause of metabolic alkalosis. However, Cl abnormalities themselves have not been studied sufficiently. Aim The aim of this study was to show the effect of Cl abnormalities in critically ill patients. Settings The study was conducted in Critical Care Medicine Department in Alexandria University Hospital. Patients and methods A Prospective clinical study was conducted on 375 critically ill adult patients admitted to Alexandria University hospitals. All patients included were subjected to demographics, diagnosis and cause of admission, relevant medical history, calculated APACHE-II score, and laboratory data (days 1 and 3 after admission), including serum electrolyte level, ABG analysis (anion gap–gap/gap ratio–corrected anion gap), and serum albumin level. According to the recorded Cl levels at days 1 and 3 from ICU admission, patients were defined as normochloremic (99–110 mEq/l), hypochloremic ( 110). Outcome measures were all-cause mortality and length of stay (LOS) in ICU. Results Cl abnormalities at day 1 were associated with increased mortality. The mortality rate was significantly higher in hyperchloremic (67.3%) compared with hypochloremic (72.1%) and normochloremic patients (36.3%) (P Conclusion In a mixed general intensive care population, after careful controlling for confounders, Cl abnormalities (outside 99–110 mEq/l) were independent predictors for poorer outcomes such as ICU mortality and LOS.

ASSOCIATION OF ACID-BASE PARAMETERS WITH LACTATE LEVEL IN CRITICALLY ILL PATIENTS WITH METABOLIC ACIDOSIS

Metabolic acidosis is prevalent among critically ill patients and the common cause of metabolic acidosis in ICU is lactic acidosis. However, not all ICUs can provide lactate measurement. The traditional method that uses Henderson-Hasselbach equation (completed with BE and AG) and alternative method consisting of Stewart and its modification (BDEgap and SIG), are acid-base balance parameters commonly used by clinicians to determine metabolic acidosis in critically ill patients. The objective of this study was to discover the association between acid-base parameters (BE, AGobserved, AGcalculated, SIG, BDEgap) with lactate level in critically ill patients with metabolic acidosis. This was an analytical study with a cross-sectional design. Eighty-four critically ill patients hospitalized in the ICU department Dr. M. Djamil Padang Hospital were recruited in this study from January to September 2016. Blood gas analysis and lactate measurement were performed by potentiometric and amperometric method while electrolytes and albumin measurement were done by ISE and colorimetric method (BCG). Linear regression analysis was used to evaluate the association between acid-base parameters with lactate level based on p-value less than 0.05. Fourty five (54%) were females and thirty-nine (46%) were males with participant's ages ranged from 18 to 81 years old. Postoperative was the most reason for ICU admission (88%). Linear regression analysis showed that p-value for BE, AGobserved, AGcalculated, SIG and BDEgap were 119; 0.967; 0.001; 0.001; 0.689, respectively. Acid-base balance parameters which were mostly associated with lactate level in critically ill patients with metabolic acidosis were AGcalculated and SIG.

Competitive cation binding computations of proton balance for reactions of the phosphagen and glycolytic energy systems within skeletal muscle.

Limited research and data has been published for the H+ coefficients for the metabolites and reactions involved in non-mitochondrial energy metabolism. The purpose of this investigation was to compute the fractional binding of H+, K+, Na+ and Mg2+ to 21 metabolites of skeletal muscle non-mitochondrial energy metabolism, resulting in 104 different metabolite-cation complexes. Fractional binding of H+ to these metabolite-cation complexes were applied to 17 reactions of skeletal muscle non-mitochondrial energy metabolism, and 8 conditions of the glycolytic pathway based on the source of substrate (glycogen vs. glucose), completeness of glycolytic flux, and the end-point of pyruvate vs. lactate. For pH conditions of 6.0 and 7.0, respectively, H+ coefficients (-‘ve values = H+ release) for the creatine kinase, adenylate kinase, AMP deaminase and ATPase reactions were 0.8 and 0.97, -0.13 and -0.02, 1.2 and 1.09, and -0.01 and -0.66, respectively. The glycolytic pathway is net H+ releasing, regardless of lactate production, which consumes 1 H+. For glycolysis fueled by glycogen and ending in either pyruvate or lactate, H+ coefficients for pH 6.0 and 7.0 were -3.97 and -2.01 (pyruvate), and -1.96 and -0.01 (lactate), respectively. When starting with glucose, the same conditions result in H+ coefficients of -3.98 and -2.67, and -1.97 and –0.67, respectively. The most H+ releasing reaction of glycolysis is the glyceraldehyde-3-phosphate dehydrogenase reaction, with H+ coefficients for pH 6.0 and 7.0 of -1.58 and -0.76, respectively. Incomplete flux of substrate through glycolysis would increase net H+ release due to the absence of the pyruvate kinase and lactate dehydrogenase reactions, which collectively result in H+ coefficients for pH 6.0 and 7.0 of 1.35 and 1.88, respectively. The data presented provide an extensive reference source for academics and researchers to accurately profile the balance of protons for all metabolites and reactions of non-mitochondrial energy metabolism, and reveal the greater role of glycolysis in net H+ release than previously assumed. The data can also be used to improve the understanding of the cause of metabolic acidosis, and reveal mechanistic connections between H+ release within and from muscle and the electrochemical neutrality concepts that further refine acid-base balance in biological solutions.

Relationship of at Admission Lactate, Unmeasured Anions, and Chloride to the Outcome of Critically Ill Patients.

To investigate the association between the concentration of the causative anions responsible for the main types of metabolic acidosis and the outcome. Prospective observational study. Teaching ICU. All patients admitted from January 2006 to December 2014. None. Four thousand nine hundred one patients were admitted throughout the study period; 1,609 met criteria for metabolic acidosis and 145 had normal acid-base values. The association between at admission lactate, unmeasured anions, and chloride concentration with outcome was assessed by multivariate analysis in the whole cohort and in patients with metabolic acidosis. We also compared the mortality of patients with lactic, unmeasured anions, and hyperchloremic metabolic acidosis with that of patients without acid-base disorders. In the whole population, increased lactate and unmeasured anions were independently associated with increased mortality, even after adjusting for potential confounders (odds ratio [95% CI], 1.14 (1.08-1.20); p < 0.0001 and 1.04 (1.02-1.06); p < 0.0001, respectively). In patients with metabolic acidosis, the results were similar. Patients with lactic and unmeasured anions acidosis, but not those with hyperchloremic acidosis, had an increased mortality compared to patients without alterations (17.7%, 12.7%, 4.9%, and 5.8%, respectively; p < 0.05). In this large cohort of critically ill patients, increased concentrations of lactate and unmeasured anions, but not chloride, were associated with increased mortality. In addition, increased unmeasured anions were the leading cause of metabolic acidosis.

Metabolic Acidosis

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

Metabolic Acidosis

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

Acetaminophen, the missing anion gap in the patient with metabolic acidosis

Acetaminophen intake is well-known but an often missed cause of high anion gap (AG) metabolic acidosis, and physicians must understand the metabolic pathway which increases the AG. Multiple mnemonics for common causes of metabolic acidosis have been developed and are widely taught in medical schools. Some of them, such as MUDPILES and KUSMAE, may not lead to an adequate workup and miss the diagnosis for the acidosis. More recently developed memory tools, such as GOLDMARK, provide a complete differential diagnosis for high AG metabolic acidosis. Pyroglutamic acid accumulates after alterations of the gamma-glutamyl cycle mediated by acetaminophen and glutathione deficiency in some patients. The lower capacity of 5-oxiprolinase to metabolize pyroglutamic acid into glutamate results in the gradual accumulation of oxoproline/pyroglutamic acid. Treatment is mainly supportive with the major aim of restoring glutathione levels, optimizing nutrition, and using N-acetylcysteine as needed. Different modalities of renal replacement therapy have also been used in these patients.

Pyroglutamate (5-oxoproline) measured with hydrophilic interaction chromatography (HILIC) tandem mass spectrometry in acutely ill patients

BackgroundPyroglutamic acid (PGA) is challenging to quantify in plasma and is a rare cause of metabolic acidosis that is associated with inherited disorders or acquired after exposure to drugs. MethodWe developed a hydrophilic interaction liquid chromatography tandem mass spectrometry method with a short analysis time. We established a reference interval and then measured PGA in acutely ill patients to investigate associations with clinical, pharmaceutical and laboratory parameters. ResultsThe assay limit of the blank was 0.14μmol/L and was linear to 5000μmol/L with good precision. In-source formation of PGA from glutamate and glutamine was avoided by chromatographic separation. The PGA in controls had a reference interval of 22.6 to 47.8μmol/L. The median PGA concentration in acutely ill patients was similar (P=0.21), but 18 individuals were above the reference interval with concentrations up to 250μmol/L. We detected an association between PGA concentration and antibiotic and acetaminophen administration as well as renal impairment and severity of illness. Elevations of PGA in this unselected cohort were small compared to those reported in patients with pyroglutamic acidosis. ConclusionThe method is suitable for routine clinical use. We confirmed several expected associations with PGA in an acutely ill population.

Minding the Gap: Utility of the Anion Gap in the Differential Diagnosis of Metabolic Acidosis.

The anion gap, in conjunction with other laboratory results, can be a useful clue in the differential diagnosis of metabolic acidosis. There are three primary causes of metabolic acidosis: loss of base, decreased renal excretion of acid, and increased acid production. Depending on the cause of metabolic acidosis, the anion gap may be elevated or normal.

Lactic acidosis, hyperlactatemia and sepsis

Among hospitalized patients, lactic acidosis represents the most common cause of metabolic acidosis. Lactate is not just a metabolic product of anaerobic glycolysis but is triggered by a variety of metabolites even before the onset of anaerobic metabolism as part of an adaptive response to a hypermetabolic state. On the basis of such considerations, lactic acidosis is divided into two classes: inadequate tissue oxygenation (type A) and absence of tissue hypoxia (type B). Lactic acidosis is characterized by non-specific symptoms but it should be suspected in all critical patients who show hypovolemic, hypoxic, in septic or cardiogenic shock or if in the presence of an unexplained high anion gap metabolic acidosis. Lactic acidosis in sepsis and septic shock has traditionally been explained as a result of tissue hypoxia when whole-body oxygen delivery fails to meet whole body oxygen requirements. In sepsis lactate levels correlate with increased mortality with a poor prognostic threshold of 4 mmol/L. In hemodynamically stable patients with sepsis, hyperlactatemia might be the result of impaired lactate clearance rather than overproduction. In critically ill patients the speed at which hyperlactatemia resolves with appropriate therapy may be considered a useful prognostic indicator. The measure of blood lactate should be performed within 3 h of presentation in acute care setting. The presence of lactic acidosis requires early identification of the primary cause of shock for the best appropriate treatment. Since most cases of lactic acidosis depend on whole-body oxygen delivery failure, the maximization of systemic oxygen delivery remains the primary therapeutic option. When initial resuscitation does not substantially or completely correct lactic acidosis, it is also essential to consider other causes. The treatment of acidosis with buffering agents (specifically bicarbonate) is generally advocated only in the setting of severe acidosis. Ongoing research into lactate clearance and probable noninvasive surrogate measures may add further insight into outcome-based practices.

Postmortem biochemistry in suspected starvation-induced ketoacidosis

Significantly increased blood ketone body levels can be occasionally observed in the forensic setting in situations other than exposure to cold, diabetic or alcoholic ketoacidosis. Though infrequent, these cases do occur and deserve thorough evaluation in order to establish appropriate differential diagnoses and quantify the role that hyperketonemia may play in the death process. Starvation ketoacidosis is a rare cause of metabolic acidosis and is a phenomenon that occurs normally during fasting, as the body switches from carbohydrate to lipid energy sources. The levels of ketonemia in starvation ketoacidosis is usually mild in comparison to those seen in diabetic or alcoholic ketoacidosis. In the clinical setting, several cases of starvation-induced ketoacidosis mainly associated with gastric banding, pregnancy, malnutrition and low-carbohydrate diets have been reported. However, starvation ketosis causing severe metabolic acidosis has been rarely described in the medical literature. In the realm of forensic pathology, starvation-induced hyperketonemia has been rarely described. In this paper we present the postmortem biochemical results observed in situations of suspected starvation-induced hyperketonemia that underwent medico-legal examination. In all these cases, the diagnosis of starvation induced-hyperketonemia and the subsequent ketoacidosis was established per exclusionem based on all postmortem investigation findings. A review of the literature pertaining to the clinical diagnosis of starvation ketoacidosis is also provided.

Severe Ketoacidosis in a Patient with an Eating Disorder.

Severe ketoacidosis with a blood pH below 7.0 is only rarely seen in other diseases except type 1 diabetes. This paper reports a case of severe ketoacidosis secondary to an eating disorder. A 46-year-old woman presented to the emergency department with an acute onset of shortness of breath. She has a history of an eating disorder, an anxiety disorder, and hypothyroidism. Her body mass index was 19. Examination of the initial vital signs revealed the following: pulse, 91 beats/min; body temperature, 34.9℃; respiratory rate, 35 breaths/min; oxygen saturation, 100% on room air; and blood pressure, 130/70 mmHg. Urinalysis revealed specific gravity of >1.030, pH of 5.5, negative results for glucose, and positive results for ketone bodies (>150 mg/dL). Her serum glucose level was 4.9 mmol/L. Venous blood gas analysis revealed the following: pH, 6.96; HCO3−, 5 mmol/L, pCO2, 22 mmHg; base deficit, 27 and anion gap, 21. the patient showed a high anion gap metabolic acidosis with proper respiratory compensation. Results of the blood analysis are shown in Table 1. The osmolar gap was 20, which suggested unmeasured anions. However, tests for ethanol, salicylate, ethylene glycol, and methanol levels were negative. The serum ketone test was positive. These laboratory parameters made us rule out diabetic ketoacidosis and alcoholic ketoacidosis as the cause of the metabolic acidosis. Initially, the patient received a 5% dextrose solution in normal saline (D5W NS). After 12 hours of hospitalization on D5W NS, venous blood gas analysis revealed improved results: pH, 7.18; HCO3−, 5 mmol/L; and pCO2, 13 mmHg, with a base deficit of 23. TABLE 1 Biochemical markers Initially, the family and the patient told us that the patient had been doing much better in the last 2 weeks regarding her eating habits. We asked her repeatedly and she finally admitted to giving her food to her dog underneath the table. Moreover, she had been taking stool laxatives. In a patient with ketonemia, low glucose levels excluded diabetic ketoacidosis as the cause of severe metabolic acidosis.1 Negative results for laboratory tests for toxicology and toxic alcohol levels led us to consider starvation as the etiology of the acid-base imbalance.2 Ketoacidosis secondary to starvation is due to diminished insulin secretion that leads to an increase in lipolysis and ketogenesis.3 Eating disorders not otherwise specified are a category of eating disorder that includes patients with early aberrant eating patterns and weight management habits who do not meet the criteria for anorexia or bulimia nervosa.4 It occurs in approximately 3-5% of women aged between 15 and 30 years in Western countries.5 Patients with bulimia ten to abuse laxatives. It prevents the absorption of calories, which may aggravate starvation ketoacidosis.6 In conclusion, starvation should be considered as one of the causes of severe ketoacidosis in individuals with an eating disorder, even when the patient denies diet restriction.

Use of Bicarbonate in Patients With Metabolic Acidosis

Please elaborate on why bicarbonate is not used unless the ph is 7.2 or less. Many nurses, particularly cardiovascular nurses, have difficulty understanding this when the patient’s blood pressure is low and the patient is acidotic with large negative base excesses. Please explain the physiological basis for the deci

A novel bedside diagnostic test for methanol poisoning using dry chemistry for formate

Background. The standard diagnostic approach to methanol poisoning is chromatographic measurement of methanol on centrally placed stationary equipment. Methanol poisoning in places where such equipment is unavailable is thus often not diagnosed. Methanol is metabolized to a toxic metabolite, formate; the presence of this compound indicates methanol poisoning. We have developed an enzymatic test for formate and modified it into a portable dry chemistry system that could be used anywhere. Methods. The method consists of two enzymatic steps: Formation of NADH from NAD by formate dehydrogenase, and subsequent use of NADH as a reductant of a tetrazolium into a formazan dye that can be quantified photometrically or visually. Results. The photometer gave a good correlation of R2 = 0.9893 in serum and R2 = 0.9949 in whole blood, showing an instrumental detection limit of less than 1 mM (4.5 mg/dL). The visual readings showed a correlation of R2 = 0.8966. Users experienced some difficulty in separating the negative control from the low positives. Conclusions. We have documented the feasibility of an affordable formate strip test for bedside diagnosis of methanol poisoning and for screening of metabolic acidosis of unknown origin. Visual reading is possible, but a reader will improve reliability at lower levels of formate. Future studies are necessary to study the sensitivity and specificity towards other causes of metabolic acidosis and other acids present in human blood.

Protocolo diagnóstico de la acidosis metabólica

Metabolic acidosis is an acid-base disorder tends to produce acidemia (decrease in pH) for the primary changes in bicarbonate concentration. It is classified into normochloremic or hyperchloremic by the value of anion gap (AG) of the plasma; parameter representing the difference between the main positive charge (cations) and negative (anions). The cause of metabolic acidosis should be assessed by history and clinical context, but any assessment of acidosis should include blood gas, electrolyte determination, measuring response and compensatory respiratory, AG and ΔAG/ΔHCO▪.

Cétose de jeûne chez une femme allaitante

IntroductionBovine ketosis is a rare cause of metabolic acidosis. It is a starvation ketosis that appears in lactating woman. Case reportA 29-year-old woman had a previous gastric surgery one month ago while breastfeeding her 6-month child. She presented to emergency with dyspnea, fatigue, weight loss and anorexia. The explorations revealed a serious metabolic acidosis with a high anion gap, for which all other causes have been eliminated. ConclusionA restrictive diet in lactating patients is a major risk of ketosis or bovine ketosis. Medico-surgical treatment of obesity during lactation seems unreasonable. Breastfeeding should be systematically sought before a medical and surgical management of obesity. With the spread of bariatric surgery, starvation ketosis is a cause of metabolic acidosis not to ignore.

The anion gap

The growing availability of cage-side blood gas and electrolyte analysers allows easy measurement of bicarbonate, and calculation of the anion gap. Potentially, the anion gap can provide valuable insights into the causes of metabolic acidosis in companion animals. However, in order to use this information to improve diagnosis and treatment, it is important to consider several other factors about the patient, sample collection and analyser performance. This article summarises the clinical value of the anion gap and these potential pitfalls.