Metabolic acidosis: Difference between revisions

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'''Metabolic acidosis''' is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of [[bicarbonate]], and a reduced ability of the [[Kidney|kidneys]] to excrete excess acids.<ref name=":2">{{Cite web|url=https://www.uptodate.com/contents/approach-to-the-adult-with-metabolic-acidosis|title=Approach to the adult with metabolic acidosis|last1=Emmett|first1=Michael|last2=Szerlip|first2=Harold}}</ref> Metabolic acidosis can lead to [[Acidemia|acidemia]], which is defined as arterial blood [[pH]] that is lower than 7.35.<ref name=":0">{{Cite book|title=Physiology|last=Costanzo|first=Linda|publisher=Elsevier|year=2010|isbn=978-1-4160-6216-5|location=Philadelphia, Pennsylvania}}</ref> Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low, normal, to high.
 
Acute metabolic acidosis, lasting from minutes to several days, often occurs during serious illnesses or hospitalizations, and is generally caused when the body produces an excess amount of organic acids ([[Ketoacidosis|ketoacids]] or [[Lactic acidosis|lactic acid]]). A state of chronic metabolic acidosis, lasting several weeks to years, can be the result of impaired kidney function ([[Chronic kidney disease|Chronic Kidney Disease]]) and/or bicarbonate wasting. The adverse effects of acute versus chronic metabolic acidosis also differ, with acute metabolic acidosis impacting the cardiovascular system in hospital settings, and chronic metabolic acidosis affecting muscles, bones, kidney and cardiovascular health.<ref name=":3">{{Cite journal|last1=Kraut|first1=Jeffrey A.|last2=Madias|first2=Nicolaos E.|date=2010-05-01|title=Metabolic acidosis: pathophysiology, diagnosis and management|journal=Nature Reviews Nephrology|language=en|volume=6|issue=5|pages=274–285|doi=10.1038/nrneph.2010.33|pmid=20308999|s2cid=205512465|issn=1759-5061}}</ref>
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* Intoxication:
**Salicylates, [[methanol]], [[ethylene glycol]]<ref name="DeGowin's diagnostic examination"/>
**Organic acids, [[Paraldehyde|paraldehyde,]], [[ethanol]], [[formaldehyde]]<ref>{{Cite book|title=Critical care|others=Oropello, John M.,, Pastores, Stephen M.,, Kvetan, Vladimir|isbn=9780071817264|location=[New York]|oclc=961480454|date = 2016-11-22}}</ref>
**[[Carbon monoxide]], [[cyanide]], [[ibuprofen]], [[metformin]]<ref>{{Cite book|title=Current medical diagnosis & treatment 2020|others=Papadakis, Maxine A.,, McPhee, Stephen J.,, Rabow, Michael W.|isbn=9781260455281|edition= Fifty-eighth |location=New York|oclc=1109935506|date = 2019-09-02}}</ref>
* [[Propylene glycol]] (metabolized to L and D-lactate and is often found in infusions for certain intravenous medications used in the [[intensive care unit]])<ref>{{Cite book|title=Harrison's principles of internal medicine.|others=Jameson, J. Larry,, Kasper, Dennis L.,, Longo, Dan L. (Dan Louis), 1949-, Fauci, Anthony S., 1940-, Hauser, Stephen L.,, Loscalzo, Joseph|isbn=9781259644030|edition= 20th |location=New York|oclc=1029074059|date = 2018-08-13}}</ref>