metabolic acidosis
Jump to navigation
Jump to search
Etiology
increased anion gap
- osmolal gap > 15 mosm/kg; > 10 msom/kg[4]
- osmolal gap < 15 mosm/kg
- other
M - methanol
U - uremia
D - dehydration
P - paraldehyde (pharmacologic agents*)
L - lactic acidosis
E - ethanol
r - rhabdomyolysis
S - salicylates
* Pharmacologic causes:
- acetaminophen poisoning
- acetazolamide
- calcium channel blockers (overdose)
- cyanide (nitroprusside)
- isoniazid
- linezolid
- metformin
- nucleoside reverse transcriptase inhibitors
- paraldehyde
- propofol
- salicylate
- spironolactone
normal anion gap acidosis
- GI HCO3- loss
- diarrhea
- cholestyramine
- GI fistula
- ureterosigmoidostomy (ureteral diversion)
- renal HCO3- loss
- proximal renal tubular acidosis (RTA-2)
- carbonic anhydrase inhibitor (acetazolamide)
- Cl- infusion
- ammonium chloride ingestion
- toluene poisoning
- diabetic ketoacidosis (generally increased anion gap)[15]
- spironolactone
- renal H+ transport defects
- chronic renal failure (GFR < 25 mL/min/1.73 m2)[4]
- infusion of large volumes of normal saline[11]
- Addison's disease
pCO2 higher than expected*
- pCO2 higher than expected*
- respiratory & metabolic acidosis
- cardiac arrest
- post-ictal state
pCO2 lower than expected*
* Rules for predicting pCO2 (respiratory) compensation for pure metabolic acidosis (PaCO2, arterial)
- pCO2 (mm Hg) = digits to right of decimal point in pH
- pCO2 decreases by 1-1.3 mm Hg for each meq/L decrease in HCO3-
- pCO2 +/- 2 = 1.5 x HCO3- meq/L + 8[3]
- pCO2 (mm Hg) = HCO3- + 15 (chronic)
- compensation takes 12-24 hours to complete, thus no compensation may be present immediately after an acute drop in pH
- failure of the pCO2 to decrease by the expected value suggests complicating respiratory acidosis
- excessive decrease in the pCO2 suggests complicating respiratory alkalosis[4]
low anion gap acidosis
- low serum albumin
- unmeasured cations (Ig light chains)
urine anion gap:
- urine Na+ + urine K+ - urine Cl-
- large, negative urine anion gap suggests extrarenal origin of metabolic acidosis
- positive urine anion gap suggests renal origin of metabolic acidosis
Pathology
- increased susceptibility to cardiac arrhythmias
- decrease in myocardial contractility
- decreased response to inotropic agents
- secondary decrease in intracerebral pH may cause a diminished level of consciousness
- chronic metabolic acidosis
- loss of Ca+2 from bone
- skeletal muscle breakdown
Clinical manifestations
- difficult to separate from primary disease process, may involve respiratory system, cardiovascular system, nervous system & skeletal system systems
- nausea & abdominal pain may accompany intoxication
- respiratory compensation causes deep (Kussmaul) respirations, may result in fatigue & respiratory failure
- when pH < 7.2, arteriolar dilatation & hypotension
- cardiac arrhythmias[6]
- insulin resistance
Laboratory
- arterial blood gas (ABG)
- decreased pH
- diminished pCO2 secondary to compensatory respiratory alkalosis
- electrolytes
- diminished serum bicarbonate
- in normal anion-gap metabolic acidosis a decrease in serum bicarbonate is accompanied by an increase in serum chloride[11]
- serum K+: hyperkalemia
- if increased anion gap is present, measure
- serum creatinine to assess renal function
- osmolality: if calculated osmolal gap is increased, measure
- ethanol (blood alcohol level)
- methanol
- ethylene glycol
- isopropyl alcohol (anion gap not increased)
- urine ammonia is increased in hyperchloremic acidosis (seldom measured_[11]
- urinary anion gap (urine sodium + urine potassium - urine chloride) generally < 0 in normal anion-gap acidosis, but will become > 0 when excretion of urinary NH4Cl is impaired, in renal failure, distal renal tubular acidosis, or hypoaldosteronism[11]
- CBC: a leukemoid reaction may occur
- see ARUP consult[7]
Management
- correct underlying primary disease process
- NaHCO3
- consider if pH < 7.2
- consider if serum bicarbonate is chronically < 22 meq/L[4]
- HCO3- deficit = 0.5 x LBM* (desired - measured) [[[A18927|HCO3-]]]
- excess HCO3- can cause seizures, tetany, cardiac arrhythmias
- HCO3- should be discontinued when pH > 7.20
- with lactic acidosis, correction of pH to > 7.2 can result in overshoot alkalosis since metabolism of lactate generates bicarbonate
- NaHCO3 reduces need for hemodialysis in critically ill patients with metabolic acidosis[12]
- metabolic acidosis associated with chronic renal failure
- bicarbonate supplements slow progression of chronic renal failure[4][8]
- maintain serum bicarbonate > 22 meq/L (see chronic renal failure)
- consider if pH < 7.2
- fomepizole to inhibit alcohol dehydrogenase for ethylene glycol toxicity & methanol toxicity
- supplementary K+
- monitor Ca+2
- increasing pH decreases ionized Ca+2
- hemodialysis, epecially for dialyzable etiology
* lean body mass in kg
More general terms
More specific terms
- D-lactic acidosis
- diabetic ketoacidosis (DKA)
- ketoacidosis
- lactic acidosis
- pyroglutamic acidosis
- renal tubular acidosis (RTA)
Additional terms
References
- ↑ Harrison's Principles of Internal Medicine, 13th ed. Companion Handbook, Isselbacher et al (eds), McGraw-Hill Inc. NY, 1995, pg 831
- ↑ Manual of Medical Therapeutics, 28th ed, Ewald & McKenzie (eds), Little, Brown & Co, Boston, 1995, pg 58-62
- ↑ 3.0 3.1 Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 602-603
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 16, 17, 18, 19. American College of Physicians, Philadelphia 1998, 2006, 2012, 2015, 2018, 2021
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ Harrison's Principles of Internal Medicine, 14th ed. Fauci et al (eds), McGraw-Hill Inc. NY, 1998, pg 280
- ↑ 6.0 6.1 Prescriber's Letter 11(3):14 2004
- ↑ 7.0 7.1 ARUP Consult: Metabolic Acidosis The Physician's Guide to Laboratory Test Selection & Interpretation https://www.arupconsult.com/content/metabolic-acidosis
- ↑ 8.0 8.1 de Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM. Bicarbonate supplementation slows progression of CKD and improves nutritional status. J Am Soc Nephrol. 2009 Sep;20(9):2075-84. PMID: https://www.ncbi.nlm.nih.gov/pubmed/19608703
- ↑ Kraut JA, Kurtz I. Toxic alcohol ingestions: clinical features, diagnosis, and management. Clin J Am Soc Nephrol. 2008 Jan;3(1):208-25. PMID: https://www.ncbi.nlm.nih.gov/pubmed/18045860
- ↑ Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010 May;6(5):274-85 PMID: https://www.ncbi.nlm.nih.gov/pubmed/20308999
- ↑ 11.0 11.1 11.2 11.3 11.4 Berend K et al Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med 2014; 371:1434-1445. October 9, 2014 <PubMed> PMID: https://www.ncbi.nlm.nih.gov/pubmed/25295502 <Internet> http://www.nejm.org/doi/full/10.1056/NEJMra1003327
- ↑ 12.0 12.1 Jaber S, Paugam C, Futier E et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): A multicentre, open-label, randomised controlled, phase 3 trial. Lancet 2018 Jul 7; 392:31. PMID: https://www.ncbi.nlm.nih.gov/pubmed/29910040
Kraut JA, Madias NE. Sodium bicarbonate for severe metabolic acidaemia. Lancet 2018 Jul 7; 392:3. PMID: https://www.ncbi.nlm.nih.gov/pubmed/29910039 - ↑ Kraut JA, Madias NE. Metabolic Acidosis of CKD: An Update. Am J Kidney Dis. 2016 Feb;67(2):307-17. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/26477665
- ↑ Rastegar M, Nagami GT. Non-Anion Gap Metabolic Acidosis: A Clinical Approach to Evaluation. Am J Kidney Dis. 2017 Feb;69(2):296-301. PMID: https://www.ncbi.nlm.nih.gov/pubmed/28029394
- ↑ 15.0 15.1 NEJM Knowledge+ Nephrology/Urology