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Metabolic acidosis is a disorder that occurs when the body produces excessive amounts of acid, such as ketoacids or lactic acid; the kidneys are unable to remove enough acid produced from normal metabolism; or the body loses too much bicarbonate ion (HCO
3
).[1] If unchecked, metabolic acidosis can lead to acidemia, which is arterial blood pH lower than 7.37 due to increased production of hydrogen ions by the body or the loss and/or inability of the body to form bicarbonate (HCO
3
) in the kidney or gastrointestinal tract.[1] Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia.

Metabolic acidosis
Davenport Fig 12.jpg
Davenport diagram
SpecialtyNephrology

Terminology:

  • Acidosis refers to a process that causes a low pH in blood and tissues.
  • Acidemia refers specifically to a decrease in pH in circulating blood and is caused by acidosis.[1]

In most cases, acidosis occurs first for reasons explained below. Free H+
ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed.

Signs and symptomsEdit

Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur.

Extreme acidemia leads to neurological and cardiac complications:

Physical examination occasionally reveals signs of disease, but is otherwise normal. Cranial nerve abnormalities are reported in ethylene glycol poisoning, and retinal edema can be a sign of methanol intoxication. Longstanding chronic metabolic acidosis leads to osteoporosis and can cause fractures.

CausesEdit

Metabolic acidosis occurs when the body produces too much acid (e.g., lactic acidosis, see below section), changes in body fluid balance (e.g., diarrhea), or when the kidneys are not removing enough acid from the body.[2] Several types of metabolic acidosis occur. There are many causes for metabolic acidosis, but it is helpful to group them by the presence or absence of normal anion gap.[3]

The blood anion gap test can be performed by your healthcare provider to diagnose the type of metabolic acidosis.[4] The blood has both positively charged (cations) and negatively charged (anions) particles and they must be balanced at all times.[5] The blood contains cations such as sodium (Na+
) and potassium (K+
) and anions such as bicarbonate (HCO
3
) and chloride (Cl
).[6] The anion gap test measures the difference between cations and anions.[7]

Metabolic acidosis is marked by a decrease in HCO
3
in the blood. In metabolic acidosis with an increased anion gap, there is an increase in organic anions to compensate for the decreased HCO
3
. In metabolic acidosis with a normal anion gap, there is an increase in the Cl
to compensate for the decreased HCO
3
.[5]

The anion gap can be spuriously normal in sampling errors of the sodium level, e.g. in extreme hypertriglyceridemia. The anion gap can be increased due to relatively low levels of cations other than sodium and potassium (e.g. calcium or magnesium).

Increased anion gapEdit

Causes of increased anion gap include:

A mnemonic can also be used – MUDPILES[18]

  • M-Methanol
  • U-Uremia (chronic kidney failure)
  • D-Diabetic ketoacidosis
  • P-Paraldehyde (rare)
  • I-Infection, Iron, Isoniazid, Inborn errors of metabolism
  • L-Lactic acidosis (L-lactate and D-lactate)
  • E-Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic, as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.)
  • S-Salicylates

Normal anion gapEdit

Causes of normal anion gap include[19]

A mnemonic can also be used- HARDASS[20]

PathophysiologyEdit

Compensatory mechanismsEdit

Metabolic acidosis is characterized by a low concentration of bicarbonate (HCO
3
), which can happen with increased generation of acids (such as ketoacids or lactic acid), excess loss of HCO
3
by the kidneys or gastrointestinal tract, or an inability to generate sufficient HCO
3
.[5] The body regulates the acidity of the blood by four buffering mechanisms.

BufferEdit

The decreased bicarbonate that distinguishes metabolic acidosis is therefore due to two separate processes: the buffer (from water and carbon dioxide) and additional renal generation. The buffer reactions are:

 

The Henderson-Hasselbalch equation mathematically describes the relationship between blood pH and the components of the bicarbonate buffering system:

 

Using Henry's law, we can say that [CO
2
] = 0.03 × PaCO
2
(PaCO
2
is the pressure of CO
2
in arterial blood)
Adding the other normal values, we get

 

 
 

DiagnosisEdit

Although blood gas sampling is not always essential for the diagnosis of acidosis, a low pH (in either a venous or arterial sample) does support the diagnosis. If the pH is low (under 7.35) and the bicarbonate levels are decreased (<24 mmol/L), metabolic acidemia is present, and metabolic acidosis is presumed. Metabolic acidosis can be compensated by hyperventilation to decrease the PaCO
2
. The expected PaCO
2
in metabolic acidosis with the respiratory compensation is calculated with the following formula: PaCO
2
= (1.5 × [HCO
3
]) +8± 2.[21]  If the patient has other coexisting acid-base disorders, the pH may be low, normal or high in the setting of metabolic acidosis. If a setting of a cause for metabolic acidosis being noted in the patient's history, a low serum bicarbonate indicates metabolic acidosis even without measurement of serum pH.

Other tests relevant in this context are electrolytes (including chloride), glucose, kidney function, and a full blood count. Urinalysis can reveal acidity (salicylate poisoning) or alkalinity (renal tubular acidosis type I). In addition, it can show ketones in ketoacidosis.

To distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is considered very useful. It is calculated by subtracting the sum of the chloride and bicarbonate levels from the sum of the sodium and potassium levels. As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions. Normally, this concentration is about 8–16 mmol/L (12±4). An elevated anion gap (i.e. > 16 mmol/L) can indicate particular types of metabolic acidosis, particularly certain poisons, lactate acidosis, and ketoacidosis.

As the differential diagnosis is made, certain other tests may be necessary, including toxicological screening and imaging of the kidneys. It is also important to differentiate between acidosis-induced hyperventilation and asthma; otherwise, treatment could lead to inappropriate bronchodilation.[22]

TreatmentEdit

The goals of the treatment are to treat underlying disorders, improve renal perfusion and increase acid excretion. A pH under 7.1 is an emergency, due to the risk of abnormal heart rhythms, and may warrant treatment with intravenous bicarbonate. The dose (in milliequivalents) of NaHCO
3
may be calculated as: Weight (kg) × Base deficit × 0.3.[23] Bicarbonate should be given at a time under scrupulous monitoring of the arterial blood gas readings. This intervention, however, has some serious complications in lactic acidosis, and in those cases, should be used with great care. The potential risks of giving bicarbonate may include potassium and calcium shift, increased lactate production and generation of carbon dioxide.[24]

If the acidosis is particularly severe and/or intoxication may be present, consultation with the nephrology team is considered useful, as dialysis may clear both the intoxication and the acidosis.

See alsoEdit

ReferencesEdit

  1. ^ a b c Costanzo, Linda (2010). Physiology. Philadelphia, Pennsylvania: Elsevier. ISBN 978-1-4160-6216-5.
  2. ^ McPhee, Stephen J.; Hammer, Gary D.; Kwok, Yeong (2019). Pathophysiology of disease: An introduction to clinical medicine (8th ed.). New York, N.Y.: McGraw-Hill Education. ISBN 9781260026504. OCLC 1083234878.
  3. ^ Stern, Scott D. C.; Cifu, Adam S.; Altkorn, Diane (2015). Symptom to diagnosis: an evidence-based guide (3rd ed.). New York: McGraw-Hill Education. ISBN 9780071803441. OCLC 896866189.
  4. ^ "Anion Gap (Blood)". Health Encyclopedia. University of Rochester Medical Center. Retrieved 2019-08-31.
  5. ^ a b c Costanzo, Linda S. Physiology (6th ed.). Philadelphia, PA: Elsevier. ISBN 9780323511896. OCLC 965761862.
  6. ^ Laposata, Michael, ed. (2019). Laposata's Laboratory Medicine: The Diagnosis of Disease in the Clinical Laboratory (3rd ed.). New York, N.Y.: McGraw-Hill Education. ISBN 9781260116793. OCLC 1083234456.
  7. ^ Cameron, John L.; Cameron, Andrew M. (eds.). Current surgical therapy (12th ed.). Philadelphia, PA: Saunders. ISBN 9780323376914. OCLC 966447396.
  8. ^ Quinn, Gene R.; Gleason, Nathaniel W.; Papadakis, Maxine A.; McPhee, Stephen J., eds. (2016). Current medical diagnosis & treatment study guide (2nd ed.). New York: McGraw-Hill. ISBN 9780071848053. OCLC 910475681.
  9. ^ a b DeGowin's diagnostic examination. LeBlond, Richard F.,, Brown, Donald D., 1940-, Suneja, Manish,, Szot, Joseph F., (Tenth ed.). New York. ISBN 9780071814478. OCLC 876336892.CS1 maint: extra punctuation (link) CS1 maint: others (link)
  10. ^ Morgan & Mikhail's clinical anesthesiology. Butterworth, John F., IV,, Mackey, David C.,, Wasnick, John D.,, Morgan, G. Edward,, Mikhail, Maged S.,, Morgan, G. Edward. (Sixth ed.). New York. ISBN 9781259834424. OCLC 1039081701.CS1 maint: others (link)
  11. ^ Poisoning and drug overdose. Olson, Kent R. (Kent Russell),, Anderson, Ilene B.,, Benowitz, Neal L.,, Blanc, Paul D., 1951-, Clark, Richard F.,, Kearney, Thomas E., (Seventh ed.). [New York]. ISBN 9780071839808. OCLC 1013928560.CS1 maint: extra punctuation (link) CS1 maint: others (link)
  12. ^ Critical care. Oropello, John M.,, Pastores, Stephen M.,, Kvetan, Vladimir,. [New York]. ISBN 9780071817264. OCLC 961480454.CS1 maint: extra punctuation (link) CS1 maint: others (link)
  13. ^ Current medical diagnosis & treatment 2020. Papadakis, Maxine A.,, McPhee, Stephen J.,, Rabow, Michael W., (Fifty-eighth ed.). New York. ISBN 9781260455281. OCLC 1109935506.CS1 maint: extra punctuation (link) CS1 maint: others (link)
  14. ^ Harrison's principles of internal medicine. Jameson, J. Larry,, Kasper, Dennis L.,, Longo, Dan L. (Dan Louis), 1949-, Fauci, Anthony S., 1940-, Hauser, Stephen L.,, Loscalzo, Joseph, (20th ed.). New York. ISBN 9781259644030. OCLC 1029074059.CS1 maint: extra punctuation (link) CS1 maint: others (link)
  15. ^ Morgan & Mikhail's clinical anesthesiology. Butterworth, John F., IV,, Mackey, David C.,, Wasnick, John D.,, Morgan, G. Edward,, Mikhail, Maged S.,, Morgan, G. Edward. (Sixth ed.). New York. ISBN 1259834425. OCLC 1039081701.CS1 maint: others (link)
  16. ^ Katzung, Bertram G.,. Katzung & Trevor's pharmacology : examination & board review. Kruidering-Hall, Marieke,, Trevor, Anthony J., (Twelfth ed.). New York. ISBN 1259641023. OCLC 1052466341.CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  17. ^ Levitzky, Michael G. (2007). Pulmonary physiology (7th ed.). New York: McGraw-Hill Medical. ISBN 9780071437752. OCLC 75713147.
  18. ^ "Anion Gap: Acid Base Tutorial". University of Connecticut Health Center. Archived from the original on 2008-11-21. Retrieved 2015-02-25.
  19. ^ Field, Michael J.; Pollock, Carol A.; Harris, David C. (2010). The renal system: basic science and clinical conditions (2nd ed.). Edinburgh: Churchill Livingstone/Elsevier. ISBN 9780702033711. OCLC 319855752.
  20. ^ Le, Tao (2019). First aid for the USMLE Step 2 CK. McGraw-Hill Education. ISBN 9781260440294. OCLC 1057446864.
  21. ^ "American Thoracic Society - Interpretation of Arterial Blood Gases (ABGs)". www.thoracic.org. Retrieved 2019-08-30.
  22. ^ Meert, K. L; Clark, J; Sarnaik, A. P (2007). "Metabolic acidosis as an underlying mechanism of respiratory distress in children with severe acute asthma". Pediatric Critical Care Medicine. 8 (6): 519–23. doi:10.1097/01.PCC.0000288673.82916.9D. PMID 17906597.
  23. ^ Hay, William W.; Levin, Myron J.; Deterding, Robin R.; Abzug, Mark J. Current diagnosis & treatment: pediatrics (24th ed.). New York: McGraw-Hill Education. ISBN 9781259862915. OCLC 1039891466.
  24. ^ Rice, Mike; Ismail, Bashar; Pillow, M. Tyson (2014-05-01). "Approach to Metabolic Acidosis in the Emergency Department". Emergency Medicine Clinics of North America. Endocrine and Metabolic Emergencies. 32 (2): 403–420. doi:10.1016/j.emc.2014.01.002. ISSN 0733-8627.

External linksEdit