Metabolic Acidosis in Emergency Medicine Workup

Updated: Sep 29, 2022
  • Author: Antonia Quinn, DO; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Laboratory Studies

Arterial blood gas analysis

A low HCO3 level found on an automated sequential multiple analyzer (SMA) (eg, serum chemistries) is often the first clue to the presence of a metabolic acidosis; however, it cannot be the only consideration in the diagnosis of metabolic acidosis. A low HCO3 level can be caused by metabolic acidosis, a metabolic compensation of a respiratory alkalosis, or a laboratory error.

The HCO3 level that is calculated by the arterial blood gas (ABG) machine, which uses the Henderson-Hasselbalch equation, represents a more accurate measure of the plasma HCO3 level than the SMA measurement. It is suggested that the HCO3 level that is determined from the ABG be used in the anion gap calculation instead of the HCO3 level found using the SMA.

Measurement of pH and PCO2 by ABG in a patient with a low HCO3 level makes it possible to differentiate a metabolic compensation of a respiratory alkalosis from a primary metabolic acidosis. Measurement of PCO2 also makes it possible to judge the appropriateness of respiratory compensation of a metabolic acidosis, and to detect respiratory acidosis, which is signified by an elevated PCO2 level.

Oxygenation does not affect the acid-base status of a patient and generally should not be part of the discussion unless severe hypoxia is leading to ischemia. In that case, measurement of PO2 can identify severe hypoxia as a precipitant of lactic acidosis.

ABGs also measure base excess/base deficit (BE/BD), which is the best indicator of the degree of acidosis/alkalosis. BE/BD is measured by gauging the amount of acid or base that is required to titrate the patient's blood sample to a pH of 7.40, given a PCO2 level of 40 mm Hg at 37 degrees Celsius. BE/BD is a more accurate reflection of the body's state, and it is recommended over calculations using the HCO3 level.

Serum chemistry

Sodium, potassium, chloride, and bicarbonate levels are used in the calculation of serum anion gap (SIG). Phosphate and magnesium levels, as well as serum albumin levels, are used to calculate the SIG.

Hyperkalemia often complicates metabolic acidosis. It commonly is seen with inorganic acidosis (ie, non-AG). Diabetic ketoacidosis (DKA) often presents with hyperkalemia that does not parallel the acidosis; in this case, hyperkalemia results from insulin deficiency and the effects of hyperosmolality. Lactic acidosis and other forms of organic acidosis generally do not present with a significant potassium shift.

Glucose level is commonly elevated in DKA, and it may be low, normal, or mildly elevated in alcoholic ketoacidosis.

The BUN and creatinine levels are elevated in uremic acidosis.

CBC count

An elevation of the WBC count is a nonspecific finding, but it should prompt consideration of septicemia, which causes lactic acidosis.

Severe anemia with compromised O2 delivery may cause lactic acidosis.


A urine pH is normally acidic at < 5.0. In acidemia, the urine normally becomes more acidic. If the urine pH is above 5.5 in the face of acidemia, this finding is consistent with a type I RTA. Alkaline urine is typical in salicylate poisoning.

Ethylene glycol toxicity may present with calcium oxalate crystals, which appear needle shaped, in the urine.


Imaging Studies

If iron ingestion is suspected, perform imaging studies on the abdominal area, including the kidneys, ureters, and bladder.


Other Tests

Anion gap (AG)

Calculation of the AG is often helpful in the differential diagnosis of metabolic acidosis. [6] The AG is equal to the difference between the plasma concentrations of the measured plasma cation (ie, Na+) and the measured anions (ie, chloride [Cl-], HCO3-). It exists because standard electrolyte panels do not measure all the anions present in the serum.

AG calculation = (Na+) - ([Cl-] + [HCO3-])

A normal AG is traditionally listed as 8-16 mEq/L, with an average value of 12. This value may vary, depending on the instrumentation used to measure electrolyte levels, and recent data suggest a normal range of 5-11 mEq/L. Some authors add K+ to measured cations; then, the traditional normal range is 12-20 mEq/L. The anion gap allows for the differentiation of 2 groups of metabolic acidosis. Metabolic acidosis with a high AG is associated with the addition of endogenously or exogenously generated acids. Metabolic acidosis with a normal AG is associated with the loss of HCO3 or the failure to excrete H+ from the body.

High AG warrants the following:

  • Lactic acidosis - Lactate, D-lactate

  • Ketoacidosis - Beta-hydroxybutyrate, acetoacetate

  • Renal failure - Sulfate, phosphate, urate, and hippurate

  • Ingestions - Salicylate, methanol or formaldehyde (formate), ethylene glycol (glycolate, oxalate), paraldehyde (organic anions), sulfur (SO4-), phenformin/metformin

  • Pyroglutamic acidemia (5-oxoprolinemia)

  • Massive rhabdomyolysis (release of H+ and organic anions from damaged muscle)

Several mnemonics are used to prompt recall of the differential diagnosis of high anion gap acidosis. Two, neither of which is completely comprehensive, are as follows:

  • MUDPILES: M-methanol; U-uremia; D-DKA, AKA; P-paraldehyde, phenformin; I-iron, isoniazid; L-lactic (ie, CO, cyanide); E-ethylene glycol; S-salicylates

  • DR. MAPLES: D-DKA; R-renal; M-methanol; A-alcoholic ketoacidosis; P-paraldehyde, phenformin; L-lactic (ie, CO, HCN); E-ethylene glycol; S-salicylates

Normal AG (ie, hyperchloremic acidosis) indicates the following:

  • GI loss of HCO3-, diarrhea

  • Pancreatic fistula

  • Renal HCO3- loss - Type 2 (proximal) RTA

  • Renal dysfunction

  • Some cases of renal failure

  • Hypoaldosteronism (ie, type 4 RTA)

  • Hyperventilation

  • Ingestions - Ammonium chloride, acetazolamide, hyperalimentation fluids, some cases of ketoacidosis, particularly during treatment with fluid and insulin

The AG can rise because of increases in unmeasured anions or decreases in unmeasured cations (eg, hypokalemia, hypocalcemia, hypomagnesemia). AG can also increase, secondary to an increase in albumin or an increase in negative charges on albumin, which is caused by alkalosis.

AG can be decreased by an increase in unmeasured cations (eg, hyperkalemia, hypercalcemia, hypermagnesemia, lithium intoxication, high immunoglobulin G [IgG] levels), or by a decrease in unmeasured anions (eg, hypoalbuminemia).

Finally, laboratory errors can also affect the AG. Hyperproteinemia, hyperlipidemia, and hyperglycemia resulting in underestimation of serum sodium level can falsely depress AG. In addition, bromide intoxication can be mistaken for Cl-, which can result in an inappropriate depression of the AG.

The osmolal gap is the measured plasma osmolality minus calculated osmolality. The serum osmolality is composed of all osmotically active substances including ionic and nonionic substances such as serum ions, glucose, and BUN. Other substances such as alcohols, excess serum lipids and proteins, and delivered substances such as mannitol all contribute to the serum osmolality. The calculated osmolality is 2 X plasma [Na+] + [glucose]/18 + BUN/2.8.

Normal osmolal gap is 10-15.

Metabolic acidosis with elevated osmolal gap indicates methanol and ethylene glycol ingestions.

Ketone level

Elevations of ketones indicate diabetic, alcoholic, and starvation ketoacidosis.

The nitroprusside test is used to detect the presence of ketoacids in the blood and the urine. This test only measures acetoacetate and acetone; therefore, it may underestimate the degree of ketonemia and ketonuria because it will not detect the presence of beta-hydroxybutyrate (BOH). This limitation of the test can be especially problematic in patients with ketoacidosis who cannot convert BOH to acetoacetate because of severe shock or liver failure.

An assay for BOH is unavailable in some hospitals. An indirect method to circumvent this problem is to add a few drops of hydrogen peroxide to a urine specimen. This enzymatically will convert BOH into acetoacetate, which will be detected by the nitroprusside test.

Serum lactate level

For a complete discussion of the differentials of lactic acidosis, refer to Lactic Acidosis.

The normal plasma lactate concentration is 0.5-1.5 mEq/L.

Lactic acidosis is considered present if the plasma lactate level exceeds 4-5 mEq/L in an acidemic patient.

Salicylate levels

Therapeutic salicylate levels range up to 20-35 mg/dL.

Plasma levels exceeding 40-50 mg/dL are in the toxic range.

Plasma levels provide some information as to the severity of intoxication: 40-60 mg/dL is considered mild; 60-100 mg/dL is moderate; and greater than 100 mg/dL is considered severe.

Iron levels

Iron toxicity is associated with lactic acidosis.

Iron levels greater than 300 mg/dL are considered toxic.


An ECG may be used to detect abnormalities that result from the effects of electrolyte imbalances (eg, hyperkalemia).