Normal Anion Gap Acidosis Research Articles

Sodium bicarbonate and intubation in severe diabetic ketoacidosis: are we too quick to dismiss them?

Management of diabetic ketoacidosis (DKA) has internationally established guidelines. However, management of severe, refractory DKA with multiple contributors to acidosis, and management of DKA in patients with altered mentation, remain ambiguous. Use of sodium bicarbonate and intubation in DKA are unpopular treatment practices, but warrant consideration in these unique clinical scenarios. This paper describes a 61-year-old Sri Lankan female who presented with severe DKA, seizures and altered level of consciousness. In her case, the acidosis was secondary to DKA, hyperlactatemia, hyperchloraemic acidosis and acute kidney injury (AKI). Intravenous sodium bicarbonate was used in the management of acidosis. She was intubated due to altered level of consciousness with inadequate respiratory drive to compensate for metabolic acidosis. The outcome in her case was favorable. Intravenous sodium bicarbonate in DKA should be considered for patients with severe, refractory acidosis with hemodynamic instability, hyperkalemia and compounding acidosis due to normal anion gap acidosis or AKI. Intubation should be considered for patients with obtunded mentation unable to achieve respiratory compensation and obtunded mentation where reversal of DKA is unlikely to improve consciousness. Both strategies should be personalized with consideration of individual risk vs benefit.

Managing Metabolic Acidosis in Chronic Renal Diseases

One of the most common side effects of chronic kidney disease is metabolic acidosis (CKD). It is associated with the development of CKD and various other functional disorders. Metabolic acidosis can be a common complication associated with progressive loss of kidney function. The form can be a metabolic acidosis with a non-anion gap or metabolic acidosis with a high or mixed anion gap. Reduced kidney ability to maintain acid-base homeostasis results in acid accumulation, causing various complications such as decreased nutritional status such as wasting muscle-hypoalbuminemia, inflammation, uremic bone disease and its association with increased mortality. In addition to the side effects associated with acid retention, metabolic acidosis can also cause kidney damage, possibly through stimulation of adaptive mechanisms aimed at maintaining acid-base homeostasis in the event of decreased renal function. chronic kidney disease (CKD), and therefore offers an effective, safe and affordable reno-protective strategy. This paper will discuss the physiology and pathophysiology of acid-base homeostasis in CKD, namely the mechanism of metabolic acidosis capable of impairing kidney function, and its relation to the benefits of alkaline therapy. based on clinical trials

Managing Metabolic Acidosis in Chronic Renal Diseases

One of the most common side effects of chronic kidney disease is metabolic acidosis (CKD). It is associated with the development of CKD and various other functional disorders. Metabolic acidosis can be a common complication associated with progressive loss of kidney function. The form can be a metabolic acidosis with a non-anion gap or metabolic acidosis with a high or mixed anion gap. Reduced kidney ability to maintain acid-base homeostasis results in acid accumulation, causing various complications such as decreased nutritional status such as wasting muscle-hypoalbuminemia, inflammation, uremic bone disease and its association with increased mortality. In addition to the side effects associated with acid retention, metabolic acidosis can also cause kidney damage, possibly through stimulation of adaptive mechanisms aimed at maintaining acid-base homeostasis in the event of decreased renal function. chronic kidney disease (CKD), and therefore offers an effective, safe and affordable reno-protective strategy. This paper will discuss the physiology and pathophysiology of acid-base homeostasis in CKD, namely the mechanism of metabolic acidosis capable of impairing kidney function, and its relation to the benefits of alkaline therapy. based on clinical trials

A Review of Bicarbonate Use in Common Clinical Scenarios

BackgroundThe use of sodium bicarbonate to treat metabolic acidosis is intuitive, yet data suggest that not all patients benefit from this therapy. ObjectiveIn this narrative review, we describe the physiology behind commonly encountered nontoxicologic causes of metabolic acidosis, highlight potential harm from the indiscriminate administration of sodium bicarbonate in certain scenarios, and provide evidence-based recommendations to assist emergency physicians in the rational use of sodium bicarbonate. DiscussionSodium bicarbonate can be administered as a hypertonic push, as a resuscitation fluid, or as an infusion. Lactic acidosis and cardiac arrest are two common scenarios where there is limited benefit to routine use of sodium bicarbonate, although certain circumstances, such as patients with concomitant acute kidney injury and lactic acidosis may benefit from sodium bicarbonate. Patients with cardiac arrest secondary to sodium channel blockade or hyperkalemia also benefit from sodium bicarbonate therapy. Recent data suggest that the use of sodium bicarbonate in diabetic ketoacidosis does not confer improved patient outcomes and may cause harm in pediatric patients. Available evidence suggests that alkalinization of urine in rhabdomyolysis does not improve patient-centered outcomes. Finally, patients with a nongap acidosis benefit from sodium bicarbonate supplementation. ConclusionsEmpiric use of sodium bicarbonate in patients with nontoxicologic causes of metabolic acidosis is not warranted and likely does not improve patient-centered outcomes, except in select scenarios. Emergency physicians should reserve use of this medication to conditions with clear benefit to patients.

An Infant Case of Transient Distal Renal Tubular Acidosis and Fanconi Syndrome Caused by Rotavirus Gastroenteritis.

We report an infant case of transient distal renal tubular acidosis and Fanconi syndrome caused by rotavirus gastroenteritis. A 10-month-old boy was admitted to the hospital because of frequent vomiting, lack of vitality, and dehydration. He was diagnosed with rotavirus gastroenteritis on account of his positive stool rotavirus antigen test. Although he presented with acidemia and severe mixed metabolic acidosis, he also had a urine pH of 6.0, indicating impaired urinary acidification. Therefore, he was diagnosed with distal renal tubular acidosis. On the third day of hospitalization, a relatively low %tubular reabsorption of phosphate level with hypophosphatemia, increased fractional excretion of uric acid with hypouricemia, and high urinary β2-microglobulin levels were observed. Moreover, he was diagnosed with Fanconi syndrome on account of multiple proximal tubular dysfunctions. After remission of rotavirus gastroenteritis, the signs of renal tubular dysfunction improved. This was a case of rotavirus gastroenteritis-caused transient distal renal tubular acidosis and Fanconi syndrome. Severe metabolic acidosis resulted from anion-gap metabolic acidosis due to acute kidney injury by rotavirus gastroenteritis and normal anion-gap acidosis due to renal tubular acidosis. When renal tubular acidosis is associated with a disease that causes anion-gap metabolic acidosis, mixed metabolic acidosis occurs and becomes exacerbated. Furthermore, it is important to consider the complications of renal tubular acidosis in the case of severe metabolic acidosis.

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.

Serum anion gap revisited: a verified reference interval for contemporary use

The anion gap (AG) is often used to evaluate acid-base disorders. The reference interval for normal AG is used to differentiate between raised (gap) or normal AG (non-gap) acidosis. Historically accepted AG values may not be valid with the evolution of modern analytical techniques and the reference interval requires revalidation. To determine the reference interval for AG based on current laboratory techniques. During a health-screening exercise, 284 participants with no major illnesses volunteered surplus blood for analysis. The samples were tested in an internationally accredited clinical laboratory. AG was calculated by [Na+ ] - [Cl- ] - [HCO3 - ] and AGK by [Na+ ] + [K+ ] - [Cl- ] - [HCO3 - ]. The reference interval was determined at 2.5th-97.5th percentiles. Analysis was further undertaken for a subcohort of 156 individuals with no suboptimal health indicators. Median age was 35 years, body mass index 23.4 kg/m2 and the glomerular filtration rate was 106 mL/min/1.73 m2 . Median AG was 13 mmol/L and the reference interval for normal AG is 10-18 mmol/L with a 99% level of confidence. Statistically significant differences in AG were detected for sex, race, obesity and serum albumin, but the difference was 1 mmol/L between subgroups. The reference interval was the same for the sub-cohort of 156 individuals. Median AGK was 17.7 mmol/L and reference interval was 14.6-22.5 mmol/L. The AG reference interval of 10-18 mmol/L is valid for laboratories with similar reference intervals for electrolytes. Lower values expected with current laboratory techniques were not observed. The median AG of 13 mmol/L may be used to differentiate gap acidosis, non-gap acidosis or mixed acid-base disorders.

Вплив альтерації гомеостазу глюкози на водно-електролітний баланс та кислотно-основний стан у пацієнтів із цукровим діабетом

Незважаючи на успіхи в терапії цукрового діабету, частота виникнення ускладнень, зокрема порушення водно-електролітного та кислотно-основного стану, останніми роками не зменшилась. Цікаво відмітити той факт, що клінічні прояви такого грізного ускладнення, як діабетичний кетоацидоз, уперше описав Дрешфельд у 1886 році. Відтоді і до початку застосування інсуліну (в 1922 р.) смертність від цього ускладнення сягала 100 %. Широке впровадження в практику інсулінотерапії знизило смертність до 30 %, а з удосконаленням методів лікування, зокрема інфузійної терапії, відбулось подальше її зниження. На сьогодні рівень летальності пацієнтів із порушеннями водно-електролітного та кислотно-основного стану залишається високим (близько 5 % у спеціалізованих центрах). Тільки в США щорічно від цього ускладнення помирає близько 4000 хворих на цукровий діабет. Прогноз перебігу захворювання значно погіршується з віком, при розвитку коми та артеріальної гіпотензії. Поширеність цукрового діабету стрімко зростає і на сьогодні становить від 20 до 50 % випадків вперше виявленого захворювання в молодих людей. Порушення електролітів є частими в пацієнтів із даною патологією і можуть бути результатом зміненого розподілу електролітів, пов’язаного з індукованою гіперглікемією осмотичних зрушень рідини, або загального дефіциту, спричиненого осмотичним діурезом. Ускладнення від пошкодження органів-мішеней і методи лікування цукрового діабету можуть також сприяти електролітним порушенням. Порушення регуляції гомеостазу глюкози призводить до великої кількості прямих і непрямих впливів на електролітний і кислотно-основний баланс, оскільки велика поширеність діабету гарантує, що лікарі практично кожної спеціальності мають справу з пацієнтами, хворими на цукровий діабет, а знання, пов’язані зі змінами електролітів, є необхідними. У статті розглянуто, як впливають зміни гомеостазу глюкози при цукровому діабеті на водно-електролітний баланс та кислотно-основний стан пацієнта.

Time-updated anion gap and cardiovascular events in advanced chronic kidney disease: a cohort study.

ABSTRACTBackgroundStudies examining associations between metabolic acidosis and cardiovascular events in chronic kidney disease (CKD) have shown conflicting results and have not differentiated between normal anion gap (hyperchloremic) acidosis and high anion gap acidosis. We aimed to examine the impact of normal and high anion gap acidosis, separately, on the risk of cardiovascular events among patients with CKD.MethodsThis retrospective cohort study included 1168 patients with an estimated glomerular filtration rate (eGFR) of 10–60 mL/min/1.73 m2 and available data on anion gap. We analyzed the association of time-updated high anion gap (anion gap ≥9.2) with the rate of cardiovascular events using marginal structural models (MSMs) to account for time-dependent confounding. We also analyzed the association between time-updated normal anion gap acidosis (anion-gap-adjusted bicarbonate level ≤22.8 mEq/L) and cardiovascular events.ResultsThe mean baseline eGFR of the cohort was 28 mL/min/1.73 m2. The prevalence rates of high anion gap in CKD stages G3a, G3b, G4 and G5 were 20%, 16%, 27% and 46%, respectively. During a median follow-up period of 2.9 years, 132 patients developed cardiovascular events (3.3/100 patient-years). In MSMs, high anion gap was associated with a higher rate of cardiovascular events [hazard ratio (HR) 1.87; 95% confidence interval (95% CI) 1.13‒3.09; P = 0.02] and the composite of cardiovascular events or all-cause death (HR 3.28; 95% CI 2.19‒4.91; P < 0.001). Normal anion gap acidosis was not associated with cardiovascular events (HR 0.74; 95% CI, 0.47‒1.17; P = 0.2).ConclusionsAmong patients with advanced CKD, high anion gap was associated with an increased risk of cardiovascular events.

A Rare Case of Renal Salt Wasting Associated with Metabolic Acidosis and Hyperkalemia

In the evaluation of patients presenting with chronic hyperkalemia hyponatremia and normal anion gap acidosis, pseudohypoaldosteronism types I and II are within the spectrum of differential diagnosis. Recognition of these patients is important to prevent inappropriate mineralocorticoid therapy. Using clinical scenarios we aim to illustrate clinical mimics and dissimilarities to differentiate theses disorders.

Anion-gap metabolic acidemia: case-based analyses.

Not all metabolic acidosis is associated with an elevated chloride replacing the low bicarbonate concentration. When other acids, usually non-Cl organic acids are introduced into the blood an "Anion Gap" metabolic acidosis exists. The serum anion gap is calculated as [Na+] - ([Cl-] + [HCO3-]) = Unmeasured anions - Unmeasured cations. The normal gap is mostly due to negatively charged albumin: (Normal range: 8-12 meq/l) as the unmeasured anions, since albumin is usually reported in grams per liter (not meq/l). For diagnostic purposes, calculating the serum anion gap allows determination of coexisting acid-base processes in a patient. Assuming a 1:1 fall in bicarbonate compared with rise in anion gap in a usual gap acidosis, one can compare the Δ anion Gap/ΔHCO3-: Δ gap = observed anion gap - normal anion gap and the Δ HCO3- = normal HCO3- - observed HCO3-. A ratio of 1 suggests a simple anion gap acidosis; if <1 a superimposed non-gap acidosis is lowering HCO3- and if >1 a superimposed metabolic alkalosis is raising HCO3-. Comparing the anion gap and osmolar gap can narrow the differential diagnosis to include toxic alcohol ingestions with acidic metabolites such as ethylene glycol and methanol. Not all metabolic acidosis is associated with an elevated chloride replacing the low bicarbonate concentration. When other acids, usually non-Cl organic acids are introduced into the blood an "Anion Gap" metabolic acidosis exists. This review will consider the generation of anion-gap acidoses through case discussions.

SUN-507 Fueling the Fire: A Case of Hypokalemic Periodic Paralysis Associated with Type I Renal Tubular Acidosis and Thyrotoxicosis in Pregnancy

Background: Hypokalemic periodic paralysis (HPP) related to thyrotoxicosis, though rare, is more often seen in Asian males. Type 1 renal tubular acidosis (T1 RTA), which can also cause HPP, is typically managed with alkali therapy and potassium supplementation, though there are no well-established guidelines for management in pregnancy.Clinical Case: A 27-year-old Puerto Rican woman, at 32 weeks gestation, presented to the hospital with sudden onset muscle weakness, and was found to have 1/5 muscle strength in her lower extremities. She had no personal or family history of similar illness. Laboratory analysis revealed hypokalemia (potassium 2.0 mmol/L, range: 3.5 – 5); non-gap metabolic acidosis (sodium 137mmol/L, range 136 – 145; chloride 113 mmol/L, range 98- 107; and bicarbonate 8 mmol/L, range 22 – 29); and an arterial pH of 7.09. Urine studies demonstrated a urine pH of 6.5 and a urine sodium of 32 mmol/L which was diagnostic of T1 RTA in the context of her metabolic derangements. She was treated emergently with potassium and bicarbonate infusions, with improvement in her symptoms. Subsequent thyroid function testing revealed: a low TSH of 0.01 uIU/ml, normal free T4 of 1.66 (range: 0.9 - 1.7) ng/dl, normal free of T3 3.7 (range: 2.0 -4.4) pg/ml and elevated total T4 of 16.5 (range: 4.5 - 11.7) ug/dl. Renal ultrasound demonstrated medullary nephrocalcinosis. She was discharged on potassium and sodium citrate tablets. At 37 weeks, the patient was readmitted for induction of labor due to pre-eclampsia, and delivered a healthy male baby. Several months later, she presented to the Endocrinology clinic with symptoms of increased frequency bowel movements, palpitations and heat intolerance, which had been ongoing since pregnancy. On review, a metabolic panel prior to pregnancy had demonstrated non-gap acidosis and mild hypokalemia. Further testing demonstrated the following: TSH < 0.01 uIU/ml, Free T4 1.71 ng/dl, Free T3 4.8 pg/ml, TSI 280%, and a thyroid uptake scan with homogenous radiotracer uptake, with a 24-hour uptake of 40%. She was started on methimazole therapy, and continued on potassium and sodium citrate tablets with clinical and biochemical improvement.Conclusion: Thyrotoxicosis can augment hypokalemia in T1 RTA, and can increase the risk of HPP. Our patient had biochemical evidence of RTA prior to pregnancy, though without episodes of HPP, and we believe that her hyperthyroidism, triggered by pregnancy, may have been the additional insult that precipitated her paralysis. This is the first reported case of HPP related to co-existing thyrotoxicosis and T1 RTA in a pregnant individual.Reference:1. Tu ML, Fang YW, Leu JG, Tsai MH. An atypical presentation of high potassium renal secretion rate in a patient with thyrotoxic periodic paralysis: a case report. BMC Nephrol. 2018;19(1):160. Published 2018 Jul 4. doi:10.1186/s12882-018-0971-9

Type 1 Diabetes Mellitus Presenting as Distal Renal Tubular Acidosis (RTA Type 1)

Background: Type 1 Diabetes Mellitus (DM) is an autoimmune process which causes destruction of b-cells and absolute insulin deficiency. This insulin deficiency prone patient to hyperglycemia and resultant early micro-vascular and macro-vascular complications. Macro-vascular complication seen early in diabetes are CAD, CVA and PAD. In micro-vascular complications, we have retinopathy, neuropathy and nephropathy. In diabetic nephropathy, usually glomerular injury is widely described in literature but little is known about the tubular changes. We report a case which has tubular damage in the form of distal tubular damage causing renal tubular acidosis. Patient has classical bilateral nephrocalcinosis, normal anion gap acidosis and persistently low HCO3. This entity in type 1 DM is not reported in literature.&#x0D; Case: Patient S, 42 yr Male with Type 1 DM for 15 years on Inj. Insulin mixtard presented to emergency with swelling of bilateral lower limb associated with pain/tingling and numbness for 3 months.&#x0D; Conclusion: In a patient with type 1 DM, acidosis can occur due to causes other than DKA and workup should be done if acidosis persists even after treatment.

Acid-Base Disturbances in Patients with Asthma: A Literature Review and Comments on Their Pathophysiology.

Asthma is a common illness throughout the world that affects the respiratory system function, i.e., a system whose operational adequacy determines the respiratory gases exchange. It is therefore expected that acute severe asthma will be associated with respiratory acid-base disorders. In addition, the resulting hypoxemia along with the circulatory compromise due to heart–lung interactions can reduce tissue oxygenation, with a particular impact on respiratory muscles that have increased energy needs due to the increased workload. Thus, anaerobic metabolism may ensue, leading to lactic acidosis. Additionally, chronic hypocapnia in asthma can cause a compensatory drop in plasma bicarbonate concentration, resulting in non-anion gap acidosis. Indeed, studies have shown that in acute severe asthma, metabolic acid-base disorders may occur, i.e., high anion gap or non-anion gap metabolic acidosis. This review briefly presents studies that have investigated acid-base disorders in asthma, with comments on their underlying pathophysiology.

Normal anion gap metabolic acidosis secondary to topiramate intake: case report

Introducción. El topiramato es un medicamento que se usa en el tratamiento de varios tipos de epilepsia y como profilaxis en casos de cefalea migrañosa. Entre sus mecanismos de acción, la inhibición de la anhidrasa carbónica en el riñón desencadena la excreción de orina alcalina ocasionando acidosis metabólica. Presentación del caso. Paciente femenino de 17 años procedente de la Ciudad de México con antecedente de consumo de topiramato, quetiapina y sertralina para manejo de síndrome depresivo, quien desarrolla acidosis metabólica de anión restante normal secundaria a ingesta de topiramato. La joven requiere soporte ventilatorio invasivo por deterioro del estado de conciencia y síndrome de dificultad respiratoria y presenta adecuada respuesta a manejo con catártico y bicarbonato sin compromiso renal y sin secuelas neurológicas. Discusión. La acidosis metabólica es la alteración ácido base más frecuente en la práctica clínica. La diferencia entre cationes y aniones medibles, conocida como anión restante o brecha aniónica, permite clasificar este tipo de acidosis. Las pérdidas de bicarbonato o trastornos de la función tubular renal generan acidosis de anión restante normal; por el contrario, la acidosis causada por sobreproducción de ácido endógeno o por insuficiencia renal genera anión restante elevado. El topiramato es una causa poco conocida de acidosis metabólica con anión restante normal; al inhibir la anhidrasa carbónica, se ocasiona una acidosis tubular renal mixta o tipo 3 debido a una incapacidad de secreción de hidrogeniones en el túbulo colector y una limitación en la reabsorción del bicarbonato en el túbulo proximal. Conclusión. El topiramato en dosis terapéutica o en sobredosis puede generar acidosis metabólica de anión restante normal debido a la inhibición de la anhidrasa carbónica a nivel renal. Se trata de un cuadro reversible en el cual el manejo con bicarbonato ha mostrado buenos resultados clínicos.

Anion gap and cancer mortality: Insight from NHANES database.

e13068 Background: The serum anion gap is an effective tool to analyze acid- base disorders for the past 40 years. Anion gap and non-anion gap acidosis is prevalent in cancer patients and contributes to morbidity and mortality The aim of the present study was to investigate the independent association of serum anion gap with cancer mortality. Methods: We examined the 34,370 participants ( ≥ 20years of age) using National Health and Nutrition Examination survey data (1999-2010) combined with National Death Index for mortality status through December 2011.The serum anion gap was calculated by subtracting sum of chloride and bicarbonate from sodium concentrations in meq/l. We divided the data set in to four quartiles of serum anion gap. Cox proportional hazard models were made to estimate the hazard ratios for cancer mortality for each unit increase in serum anion gap. The models were adjusted from demographic and confoundig variables. Results: The mean age of participants was 49.59±18.42 years. Out of total population 33,717(98.1%) were alive and 651 (1.9%) were dead secondary to cancer. The mean period of follow up was 5.55±3.53 years. In univariate regression model using serum anion gap as continuous variable, we found 6% (HR-1.06;95%CI,1.0-1.1), increase in cancer mortality with each unit increase in serum anion gap. After adjusting for potential confounders using multivariate regression model we found 8%(HR-1.08;95%CI,1.03-1.14), increase in cancer mortality with each unit increase in serum anion gap. In univariate regression model using quartiles, we found 47% (HR-1.47;95%CI,1.04-1.93), increase in cancer mortality with each unit increase in serum anion gap in highest quartile compared to the lowest quartile. After adjusting to the potential confounders the risk for cancer mortality increases to 60% in highest quartile comparison to lowest quartile (HR-1.60;95%CI,1.12-2.26). Conclusions: We found a linear association between serum anion gap and cancer mortality. A high serum anion gap is associated with increase in cancer mortality and may be the prognostic indicator of cancer mortality in general population. This should be validated by performing further investigation.

Acute Hypophosphatemia and Non-Anion Gap Acidosis After Living Donor Renal Transplant

Acute Hypophosphatemia and Non-Anion Gap Acidosis After Living Donor Renal Transplant

Ileal Neobladder: An Important Cause of Non-Anion Gap Metabolic Acidosis

BackgroundThe differential diagnosis for a non-anion gap metabolic acidosis is probably less well known than the differential diagnosis for an anion gap metabolic acidosis. One etiology of a non-anion gap acidosis is the consequence of ileal neobladder urinary diversion for the treatment of bladder cancer. Case ReportWe present a case of a patient with an ileal neobladder with a severe non-anion gap metabolic acidosis caused by a urinary tract infection and ureteroenterostomy. Why Should an Emergency Physician Be Aware of This?Part of the ileal neobladder surgery includes ureteroenterostomy and predisposes patients to several clinically significant metabolic derangements, including a non-anion gap metabolic acidosis. These patients have an increased chronic acid load, bicarbonate deficit, and hypokalemia, which should be appreciated when resuscitating these patients.

Distal renal tubular acidosis with hypokalemic paralysis as primary presentation of Sjogren's syndrome without sicca symptoms: An unusual case presentation

Abstract Sjogren's syndrome is a systemic autoimmune disorder characterized by chronic inflammation of the exocrine glands with extra-glandular manifestations. Renal involvement occurs in 18–67% of cases, with chronic tubulo-interstitial nephritis being the most frequent pathology which can lead to distal renal tubular acidosis characterized by normal anion gap acidosis with hypokalemia and alkaline urinary pH. Hypokalemic periodic paralysis can be primary or secondary to potassium deficiency which can arise from several causes. Primary Sjogren's syndrome is a rare cause which can lead to renal involvement producing distal renal tubular acidosis with hypokalemic paralysis.

Treatment of acute non-anion gap metabolic acidosis.

Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acid–base disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide might be less frequent than in high anion gap metabolic acidosis because of better tissue perfusion and the ability to eliminate carbon dioxide. Further basic and clinical research is needed to facilitate development of evidence-based guidelines for therapy of this important and increasingly common acid–base disorder.