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Metabolic acidosis
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Davenport diagram
Community portal Metabolic acidosis is a condition that occurs when the
Recent changes Classification and external resources
body produces excessive quantities of acid or when the
Contact page Specialty Endocrinology
kidneys are not removing enough acid from the body. If
Patient UK Metabolic acidosis
Tools
unchecked, metabolic acidosis leads to acidemia, i.e.,
[edit on Wikidata]
blood pH is low (less than 7.35) due to increased
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production of hydrogen ions by the body or the inability of
Upload file the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be
Special pages serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of
Permanent link acidemia.
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Terminology :
Wikidata item
Cite this page Acidosis refers to a process that causes a low pH in blood and tissues.
Acidemia refers specifically to a low pH in the blood.
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Create a book In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the
Download as PDF blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is
Printable version present, acidosis is presumed.

In other projects Contents [hide]

Wikimedia Commons 1 Signs and symptoms
2 Causes
Languages
2.1 Increased anion gap
‫اﻟﻌﺮﺑﻴﺔ‬
3 Pathophysiology
Deutsch
3.1 Compensatory mechanisms
Español
3.2 Buffer
Français
Bahasa Indonesia 4 Diagnosis
Italiano 5 Treatment
Bahasa Melayu 6 See also
Português 7 References
Русский
8 External links
8 more
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Signs and symptoms [ edit ]

Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for
arterial blood gas sampling. Symptoms may include chest pain, 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:

Neurological: lethargy, stupor, coma, seizures

Cardiac: Abnormal heart rhythms (e.g., ventricular tachycardia) and decreased response to epinephrine,
both leading to low blood pressure

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.

Causes [ edit ]

Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing
enough acid from the body. Several types of metabolic acidosis occur. The main causes are best grouped by
their influence on the anion gap.

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 gap [ edit ]

Main article: High anion gap metabolic acidosis

Causes of increased anion gap include:

Lactic acidosis
Ketoacidosis
Chronic kidney failure (accumulation of sulfates, phosphates, urea)
Transient 5-oxoprolinemia due to long-term ingestion of high-doses of acetaminophen (often seen with
sepsis, liver failure, kidney failure, or malnutrition)
Intoxication:
Organic acids, salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, isoniazid
Sulfates, metformin
Propylene glycol (metabolized to L and D-lactate and is often found in infusions for certain intravenous
medications used in the intensive care unit)
Massive rhabdomyolysis

A mnemonic can also be used - MUDPILES[1]

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

Pathophysiology [ edit ]

Compensatory mechanisms [ edit ]

Metabolic acidosis is either due to increased generation of acid or an inability to generate sufficient
bicarbonate. The body regulates the acidity of the blood by four buffering mechanisms.

Bicarbonate buffering system

Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins,
phosphates and carbonate in bone.
Respiratory compensation. Hyperventilation will cause more carbon dioxide to be removed from the body
and thereby increase pH.
Kidney compensation

Buffer [ edit ]

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 [CO2]=0.03xPaCO2

(PaCO2 is the pressure of CO2 in arterial blood)
Adding the other normal values, we get

Diagnosis [ edit ]

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. 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.[2]

Treatment [ edit ]

A pH under 7.1 is an emergency, due to the risk of abnormal heart rhythms, and may warrant treatment with
intravenous bicarbonate. Bicarbonate is given at 50-100 mmol 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.

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 also [ edit ]

Trauma triad of death

Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Winters' formula
Delta ratio

References [ edit ]

1. ^ "Anion Gap: Acid Base Tutorial" . University of Connecticut Health Center. Archived from the original on
2008-11-21. Retrieved 2015-02-25.
2. ^ 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 .

External links [ edit ]

Classification ICD-10: E87.2 · ICD-9-CM: 276.2 · MeSH: D000138 · DiseasesDB: 92 D

External MedlinePlus: 000335 · eMedicine: emerg/312 med/1458 ped/15 · Patient UK: Metabolic
resources acidosis

· · Electrolyte imbalance and acid–base imbalance (E86–E87, 276) [hide]

Volume status Volume contraction (dehydration/hypovolemia) · Hypervolemia

Sodium High (Hypernatremia · Salt poisoning) · Low (Hypotonic · Isotonic)

Potassium High · Low

Electrolyte
Chloride High · Low

Calcium High · Low

Metabolic: High anion gap (Ketoacidosis · Diabetic ketoacidosis ·

Acidosis Alcoholic ketoacidosis · Lactic) · Normal anion gap (Hyperchloremic · Renal tubular)
Respiratory
Acid–base
Metabolic (Contraction alkalosis)
Alkalosis
Respiratory

Both Mixed disorder of acid-base balance

Categories: Acid–base disturbances

This page was last edited on 21 August 2018, at 15:58 (UTC).

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