Metabolic Acidosis

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

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

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

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

Lactic acidosis in diabetes mellitus in the practice of a family doctor

2020 ◽  
pp. 37-43
Author(s):  
Vsevolod Skvortsov ◽  
Ekaterina Skvortsova ◽  
Georgiy Malyakin ◽  
Elina Goliyeva
Keyword(s):  
Diabetes Mellitus ◽  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Chronic Hypoxia ◽  
Pathological Condition ◽  
Family Doctor ◽  
The Body ◽  
Anion Gap ◽  
The Moment

Lactic acidosis is a metabolic acidosis with a large anion gap (> 10 mmol/L) and a level of lactic acid in the blood > 4 mmol/L (according to some definitions, more than 2 mmol/L). This is a critical pathological condition of the body, accompanied by acute or chronic hypoxia, and even coma. The prognosis for the development of this condition is always severe, mortality is 50–80 %. Clear criteria for the diagnosis and treatment of this pathological condition are defined at the moment. This article focuses on the main issues that endocrinologists and resuscitators may encounter when identifying this complex of symptoms.

Acid-Base Disorders

2018 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Hydrogen Ions ◽  
Acid Base Balance ◽  
Acid Base ◽  
Renal Tubular

Under physiologic conditions, the acid-base balance of the body is maintained via changes in ventilation that eliminate carbon dioxide, buffering of acid loads, and renal excretion of hydrogen ions. Failure to maintain the pH of the blood between 7.35 and 7.45 can result in life-threatening conditions. This review details the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of acid-base disorders. Figures show the relationship between hydrogen ions and blood pH, proximal tubular bicarbonate reabsorption, the secretion of hydrogen ions, renal ammonia production, ammonium diffusion, metabolic alkalosis, electrocardiographic changes in hypokalemia and hyperkalemia, pseudoinfarction caused by hyperkalemia, and an algorithmic approach to suspected acid-base disorders. Tables list causes of high–anion gap metabolic acidosis, metabolic acidosis with a normal anion gap, type 1 renal tubular acidosis, type 4 renal tubular acidosis and aldosterone resistance, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis; treatment of hyperkalemia; and a stepwise approach for the evaluation of suspected acid-base disorders. This review contains 9 highly rendered figures, 9 tables, 64 references, and a list of pertinent Web sites.

Acid-Base Disorders

2015 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Hydrogen Ions ◽  
Acid Base Balance ◽  
Acid Base ◽  
Renal Tubular

Under physiologic conditions, the acid-base balance of the body is maintained via changes in ventilation that eliminate carbon dioxide, buffering of acid loads, and renal excretion of hydrogen ions. Failure to maintain the pH of the blood between 7.35 and 7.45 can result in life-threatening conditions. This review details the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of acid-base disorders. Figures show the relationship between hydrogen ions and blood pH, proximal tubular bicarbonate reabsorption, the secretion of hydrogen ions, renal ammonia production, ammonium diffusion, metabolic alkalosis, electrocardiographic changes in hypokalemia and hyperkalemia, pseudoinfarction caused by hyperkalemia, and an algorithmic approach to suspected acid-base disorders. Tables list causes of high–anion gap metabolic acidosis, metabolic acidosis with a normal anion gap, type 1 renal tubular acidosis, type 4 renal tubular acidosis and aldosterone resistance, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis; treatment of hyperkalemia; and a stepwise approach for the evaluation of suspected acid-base disorders. This review contains 9 highly rendered figures, 9 tables, 64 references, and a list of pertinent Web sites.

scholarly journals Metabolic acidosis in toluene sniffing

CJEM ◽  
2013 ◽  
Vol 15 (04) ◽  
pp. 249-252 ◽  
Author(s):  
Jon Tuchscherer ◽  
Habib Rehman
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Excretion Rate ◽  
Ammonia Excretion ◽  
Distal Renal Tubular Acidosis ◽  
Anion Gap ◽  
Renal Tubular ◽  
Conjugate Bases ◽  
Osmolal Gap ◽  
Ammonia Excretion Rate

ABSTRACT Toluene sniffing, frequently described under the generic category of “glue sniffing,” is a potential cause of normal anion gap metabolic acidosis due to distal renal tubular acidosis. Urine anion gap is used to diagnose metabolic acidosis of a normal anion gap variety; however, pitfalls exist when using urine anion gap in the setting of toluene sniffing. We present the case of a young woman who had a normal anion gap metabolic acidosis due to toluene sniffing and an unexpectedly low urine anion gap. In such a scenario, the urine anion gap will underestimate the rate of ammonia excretion when the conjugate bases of acids other than HCl are excreted in large quantities. Estimation of the urine osmolal gap will provide a more accurate ammonia excretion rate in these circumstances. The challenges in interpretation of the urine anion gap and ammonia excretion in the setting of distal renal tubular acidosis due to toluene toxicity are discussed.

scholarly journals SUN-185 Severe Hyponatremia and Type 4 Renal Tubular Acidosis (Functional Hypoaldosteronism) Secondary to Trimethoprim

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Yun Qing Koh ◽  
Kian Ming Jeremy Hoe ◽  
Timothy Peng Lim Quek
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Chloride ◽  
Sodium Bicarbonate ◽  
Renal Tubular Acidosis ◽  
Anion Gap ◽  
Aortic Graft ◽  
Acid Base ◽  
Severe Hyponatremia ◽  
Renal Tubular ◽  
Oral Sodium

Abstract Introduction: Trimethoprim-sulfamethoxazole (TMP-SMX) is a commonly used antibiotic. We present a case of severe hyponatremia and Type 4 renal tubular acidosis (functional hypoaldosteronism) in a patient treated with TMP-SMX. Clinical Case: A 62 year old gentleman with hypertension, dyslipidemia and a surgically repaired abdominal aortic aneurysm developed an aortic graft infection. He was admitted to hospital for acute right lower limb ischemia with embolic phenomena, and underwent surgical graft explantation. He required multiple courses of antibiotics post operatively. He was initially referred to Endocrinology for severe hyponatremia, deemed likely to be from a salt losing nephropathy secondary to polymyxin. Thyroid function and morning cortisol levels were normal. He was managed with intravenous hypertonic saline and oral salt tablets. The hyponatraemia resolved a week after polymyxin was stopped. Intravenous TMP-SMX was commenced the next day at 240 mg BD. A week later, the hyponatremia recurred, with concomitant hyperkalemia and a normal anion gap metabolic acidosis. The serum sodium was 126 mmol/L (reference interval (RI) 135-145) and the serum osmolality 275 mmol/kg (RI 275- 305). Urine studies showed a high urinary sodium (154 mmol/L) and osmolality (481 mmol/kg), consistent with renal salt wasting. The serum potassium rose to a peak of 6.1 mmol/L (RI 3.5 - 5.0), with a normal anion gap metabolic acidosis (bicarbonate 17 mmol/L (RI 21 – 31)). A paired urine pH of 8 pointed to an inability to acidify the urine. Given the clinical course and laboratory investigations, the diagnosis of TMP-associated hyponatremia and Type 4 RTA was made. Oral resonium was started to correct hyperkalemia, with a combination of oral sodium chloride and sodium bicarbonate used to treat the hyponatremia and metabolic acidosis. Fludrocortisone was not used given the concerns of causing hypertension in a patient with a diseased aortic graft. The dose of TMP-SMX was gradually reduced with improvement of the acid-base and electrolyte abnormalities, lending weight to our diagnosis. After the dose of the TMP-SMX was reduced to 80 mg BD, the hyperkalemia and metabolic acidosis resolved. The oral sodium chloride and sodium bicarbonate were gradually tailed off and stopped after cessation of the TMP-SMX. Clinical Lesson: Trimethoprim blocks the epithelial sodium channel (ENaC) of the principal cells in the terminal portion of the nephron, similar to potassium sparing diuretics like amiloride and triampterene. The resulting hyponatremia, hyperkalemia and metabolic acidosis can be life threatening. Therefore, monitoring of electrolytes and acid base status is important, particularly in susceptible patients or in those where a high dose of trimethoprim is required.

Glue-sniffing and distal renal tubular acidosis: sticking to the facts.

1991 ◽  
Vol 1 (8) ◽  
pp. 1019-1027 ◽  
Author(s):  
E J Carlisle ◽  
S M Donnelly ◽  
S Vasuvattakul ◽  
K S Kamel ◽  
S Tobe ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Extracellular Fluid ◽  
Distal Renal Tubular Acidosis ◽  
Anion Gap ◽  
Acid Base ◽  
Major Question ◽  
The Subject ◽  
Renal Tubular ◽  
Sodium And Potassium

An index case is presented to introduce the subject of the acid-base and electrolyte abnormalities resulting from toluene abuse. These include metabolic acidosis associated with a normal anion gap and excessive loss of sodium and potassium in the urine. The major question addressed is, what is the basis for the metabolic acidosis? Overproduction of hippuric acid resulting from the metabolism of toluene plays a more important role in the genesis of the metabolic acidosis than was previously believed. This conclusion is supported by the observation that the rate of excretion of ammonium was not low during metabolic acidosis in six of eight patients, suggesting that distal renal tubular acidosis was not an important acid-base abnormality in most cases where ammonium was measured. The excretion of hippurate in the urine unmatched by ammonium also mandates an enhanced rate of excretion of the cations, sodium and potassium. The loss of sodium causes extracellular fluid volume contraction and a fall in the glomerular filtration rate, which may transform the normal anion gap type of metabolic acidosis into one with a high anion gap (accumulation of hippurate and other anions). Continuing loss of potassium in the urine leads to hypokalemia. An understanding of the metabolism of toluene provides the basis for the unusual biochemical abnormalities seen with abuse of this solvent.

scholarly journals Rickets with hypophosphatemia, hypokalemia and normal anion gap metabolic acidosis: not always an easy diagnosis

2020 ◽  
Vol 13 (1) ◽  
pp. e233350
Author(s):  
Saurav Shishir Agrawal ◽  
Chandan Kumar Mishra ◽  
Chhavi Agrawal ◽  
Partha Pratim Chakraborty
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Potassium Citrate ◽  
Anion Gap ◽  
Tubular Dysfunction ◽  
Diagnostic Challenge ◽  
Primary Defect ◽  
Proximal Tubular Dysfunction ◽  
Proximal Tubular ◽  
Renal Tubular

Rickets other than those associated with advanced kidney disease, isolated distal renal tubular acidosis (dRTA) and hypophosphatasia (defective tissue non-specific alkaline phosphatase) are associated with hypophosphatemia due to abnormal proximal tubular reabsorption of phosphate. dRTA, however, at times is associated with completely reversible proximal tubular dysfunction. On the other hand, severe hypophosphatemia of different aetiologies may also interfere with both distal tubular acid excretion and proximal tubular functions giving rise to transient secondary renal tubular acidosis (distal and/or proximal). Hypophosphatemia and non-anion gap metabolic acidosis thus pose a diagnostic challenge occasionally. A definitive diagnosis and an appropriate management of the primary defect results in complete reversal of the secondary abnormality. A child with vitamin D resistant rickets was thoroughly evaluated and found to have primary dRTA with secondary proximal tubular dysfunction in the form of phosphaturia and low molecular weight proteinuria. The child was treated only with oral potassium citrate. A complete clinical, biochemical and radiological improvement was noticed in follow-up.

Metformin-Associated Nonketotic Metabolic Acidosis

1997 ◽  
Vol 31 (1) ◽  
pp. 53-55 ◽  
Author(s):  
Mark R Jurovich ◽  
John D Wooldridge ◽  
Rex W Force
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Early Recognition ◽  
Normal Serum ◽  
Anion Gap ◽  
Diabetic Patients ◽  
Strict Adherence ◽  
Arterial Blood

OBJECTIVE: To document a case of anion gap, nonketotic metabolic acidosis occurring in a patient with acute renal failure who was receiving metformin. CASE SUMMARY: A 67-year-old white man presented with a 9-day history of weakness, nausea, dizziness, and difficulty moving; he had also not eaten during the previous 2 days. The patient had numerous abnormalities on his serum chemistry panel and arterial blood gases, including a pH of 7.1 and an anion gap of 21 mEq/L. No ketones were detected in the urine. The patient was treated with intravenous fluids, sodium bicarbonate, insulin, and hemodialysis. All medications were discontinued. The acidosis resolved shortly after hemodialysis. The hospital course was complicated by the onset of atrial fibrillation occurring on day 2 that did not respond to chemical cardioversion. On day 6 the patient was discharged home with resolving acute renal failure and normal serum pH. CONCLUSIONS: The mortality rate of biguanide-induced lactic acidosis is approximately 50%; thus, early recognition and treatment are essential. Suspicion of lactic acidosis should be high when diabetic patients who are taking a biguanide present with acidosis. The majority of cases of metformin-induced lactic acidosis have occurred in patients with contraindications to the drug (i.e., renal dysfunction). Thus, it is important to maintain strict adherence to these contraindications and monitor patients for deteriorating renal function.

Growth failure and metabolic acidosis due to total body sodium depletion in an infant with an ileostomy

2021 ◽  
Vol 14 (3) ◽  
pp. e241570
Author(s):  
Christina Marie Zarraga ◽  
Stephen Mark Borowitz
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Intake ◽  
Significant Risk ◽  
Growth Failure ◽  
Sodium Depletion ◽  
Body Sodium ◽  
Essential Nutrient ◽  
Sodium Loss ◽  
Total Body ◽  
Renal Tubular

Sodium is an essential nutrient and inadequate sodium intake and/or excessive sodium losses can result in suboptimal growth. Infants with ileostomies are at significant risk of developing growth failure as a result of excessive sodium loss in their ileostomy effluent. Chronic sodium depletion can also limit the kidney’s ability to excrete hydrogen and potassium ions, mimicking electrolyte abnormalities found in type 4 renal tubular acidosis. This report describes an infant with an ileostomy with severe growth failure, hyperkalaemia and metabolic acidosis—all of which promptly resolved with sodium supplementation.

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