Lactic acidosis

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Lactic acidosis Classification and external resources
Lactic acid
ICD-10	E87.2
ICD-9	276.2
DiseasesDB	29145
MedlinePlus	000391
eMedicine	med/1253
MeSH	C18.452.076.176.180

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Overview

Lactic acidosis is a condition caused by the buildup of lactic acid in the body. It leads to acidification of the blood (acidosis), and is considered a distinct form of metabolic acidosis.

The cells produce lactic acid when they use glucose for energy in the absence of adequate oxygen. If too much lactic acid stays in the body, the balance tips and the person begins to feel ill. The signs of lactic acidosis are deep and rapid breathing, vomiting, and abdominal pain. Lactic acidosis may be caused by diabetic ketoacidosis or liver or kidney disease, as well as some forms of medication (most notably the anti-diabetic drug metformin). Some anti-HIV drugs (antiretrovirals) warn doctors in their prescribing information to regularly watch for symptoms of lactic acidosis caused by mitochondrial toxicity.

Classification

The Cohen-Woods classification (1976) categorises causes of lactic acidosis as follows:

• Type A: Decreased perfusion or oxygenation
• Type B:
  • B1: Underlying diseases (sometimes causing type A)
  • B2: Medication or intoxication
  • B3: Inborn error of metabolism

Lactic acidosis is an underlying process of rigor mortis. Tissue in the muscles of the deceased resort to anaerobic metabolism in the absence of oxygen and significant amounts of lactic acid are released into the muscle tissue. This along with the loss of ATP causes the muscles to grow stiff.

Pathophysiology

• Lactic acidosis occurs when cells make lactic acid faster than it can be metabolized. ^{[1] [1]}

Reference Range
Capillary Blood	5-15 mg/dl
Deoxygenated Blood	-16 mg/dl
Cerebrospinal Fluid (CSF)	11-19 mg/dl

Differential Diagnosis

Increased

• Drugs, toxins
• End-stage renal failure
• Fetal emergency situations during childbirth
• Glycogen storage disease
• Heart failure
• Heavy exercise
• Hypothermia
• Hypoventilation with hypercapnia
• Hypovolemia
• Infusions
• Leukemia
• Liver failure
• Myocardial Infarction
• Postoperative
• Seizures
• Sepsis
• Severe anemia
• Severe thiamine deficiency
• Tumors
• Uncontrolled diabetes mellitus

See also

• Metabolic acidosis

References

Additional Resources

• Clinical Physiology of Acid-Base and Electrolyte Disorders by Rose, Post
• Intensive Care Medicine by Irwin and Rippe
• The ICU Book by Marino
• Cohen R, Woods H. Clinical and Biochemical Aspects of Lactic Acidosis. Blackwell Scientific Publications; 1976. ISBN 0-632-09460-5.

v • d • e Metabolic pathology / Inborn error of metabolism (E70-90, 270-279)
Amino acid	Aromatic (Phenylketonuria, Alkaptonuria, Ochronosis, Tyrosinemia, Albinism, Histidinemia) - Branched chain (Maple syrup urine disease, Propionic acidemia, Methylmalonic acidemia, Isovaleric acidemia, 3-Methylcrotonyl-CoA carboxylase deficiency) - Transport (Cystinuria, Cystinosis, Hartnup disease, Fanconi syndrome, Oculocerebrorenal syndrome) - Sulfur (Homocystinuria, Cystathioninuria) - Urea cycle disorder (N-Acetylglutamate synthase deficiency, Carbamoyl phosphate synthetase I deficiency, Ornithine transcarbamylase deficiency, Citrullinemia, Argininosuccinic aciduria, Hyperammonemia) - Glutaric acidemia type 1 - Sarcosinemia
Carbohydrate	Lactose intolerance - Glycogen storage disease (type I, type II, type III, type IV, type V, type VI, type VII) - fructose metabolism (Fructose intolerance, Fructose bisphosphatase deficiency, Essential fructosuria) - galactose metabolism (Galactosemia, Galactose-1-phosphate uridylyltransferase galactosemia, Galactokinase deficiency) - other intestinal carbohydrate absorption (Glucose-galactose malabsorption, Sucrose intolerance) - pyruvate metabolism and gluconeogenesis (PCD, PDHA) - Pentosuria - Renal glycosuria
Lipid storage	Sphingolipidoses/Gangliosidoses: GM2 gangliosidoses (Sandhoff disease, Tay-Sachs disease) - GM1 gangliosidoses - Mucolipidosis type IV - Gaucher's disease - Niemann-Pick disease - Farber disease - Fabry's disease - Metachromatic leukodystrophy - Krabbe disease Neuronal ceroid lipofuscinosis (Batten disease) - Cerebrotendineous xanthomatosis - Cholesteryl ester storage disease (Wolman disease)
Other lipid	Lipoprotein/lipidemias: Hyperlipidemia - Hypercholesterolemia - Familial hypercholesterolemia - Xanthoma - Combined hyperlipidemia - Lecithin cholesterol acyltransferase deficiency - Tangier disease - Abetalipoproteinemia Fatty acid: Adrenoleukodystrophy - Carnitine (Primary, I, II)
Mineral	Cu Wilson's disease/Menkes disease - Fe Haemochromatosis - Zn Acrodermatitis enteropathica - PO43− Hypophosphatemia/Hypophosphatasia - Mg2+ Hypermagnesemia/Hypomagnesemia - Ca2+ Hypercalcaemia/Hypocalcaemia/Disorders of calcium metabolism
Fluid, electrolyte and acid-base balance	Electrolyte disturbance - Na+ Hypernatremia/Hyponatremia - Acidosis (Metabolic, Respiratory, Lactic) - Alkalosis (Metabolic, Respiratory) - Mixed disorder of acid-base balance - H2O Dehydration/Hypervolemia - K+ Hypokalemia/Hyperkalemia - Cl− Hyperchloremia/Hypochloremia
Purine and pyrimidine	Hyperuricemia - Lesch-Nyhan syndrome - Xanthinuria
Porphyrin	Acute intermittent, Gunther's, Cutanea tarda, Erythropoietic, Hepatoerythropoietic, Hereditary copro-, Variegate
Bilirubin	Unconjugated (Gilbert's syndrome, Crigler-Najjar syndrome) - Conjugated (Dubin-Johnson syndrome, Rotor syndrome)
Glycosaminoglycan	Mucopolysaccharidosis - 1:Hurler/Hunter - 3:Sanfilippo - 4:Morquio - 6:Maroteaux-Lamy - 7:Sly
Glycoprotein	Mucolipidosis - I-cell disease - Pseudo-Hurler polydystrophy - Aspartylglucosaminuria - Fucosidosis - Alpha-mannosidosis - Sialidosis
Other	Alpha 1-antitrypsin deficiency - Cystic fibrosis - Amyloidosis (Familial Mediterranean fever) - Acatalasia

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .