Metabolic acidosis laboratory findings

Resident Survival Guide

Metabolic acidosis Microchapters
Home
Patient Information
Overview
Classification
Pathophysiology
Causes
Differentiating Metabolic Acidosis from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Metabolic acidosis laboratory findings On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Metabolic acidosis laboratory findings All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Metabolic acidosis laboratory findings
CDC on Metabolic acidosis laboratory findings
Metabolic acidosis laboratory findings in the news
Blogs on Metabolic acidosis laboratory findings
Directions to Hospitals Treating Metabolic acidosis
Risk calculators and risk factors for Metabolic acidosis laboratory findings

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Metabolic acidosis is present when the blood bicarbonate concentration is decreased (<24 meq/L). In order to determine the underlying etiology of the metabolic acidosis, several laboratory measurements are needed, such as arterial blood gas sampling , anion gap, electrolytes basic metabolic panel), serum lactate and ketone concentrations, as well as toxicological screening, salicylate level (methanol or ethylene glycol). The analysis of the urine electrolytes concentration might be useful with normal anion gap metabolic acidosis.

Laboratory Findings

Metabolic acidosis is present when the blood bicarbonate concentration is decreased (<24 meq/L). In order to determine the underlying etiology of the metabolic acidosis, the following laboratory measurements are needed to specify whether metabolic acidosis is an isolated or combined process and to calculate the plasma anion gap:

• Plasma bicarbonate
• PCO2
• Arterial pH
• Plasma Na+
• Plasma Cl-

In normal anion gap metabolic acidosis, additional measurement of urinary Na+, K+, and Cl- is needed in order to calculate urinary anion gap.

In high anion gap metabolic acidosis, the osmolal gap needs to be calculated; and therefore, blood sodium concentration, blood glucose, and BUN are needed.

Shown below is an algorithm depicting the series of laboratory tests needed to evaluate metabolic acidosis.

❑ Anion Gap (Na+ - Cl- - HCO3-) ❑ Consider measurement of albumin, Ca2+, K+, and Mg2+)

High anion gap ❑ Screen for ketonuria (dipstick acetoactetae or plasma beta hydoxybutarate) ❑ Renal function ❑ Lactate concentration ❑ Toxin screen ❑ Osmolal gap

Normal-low anion gap ❑ Urinary anion gap (Na+ + K+ - Cl-)

Anion Gap

Calculation of Anion Gap

The anion gap can be calculated as follows:

Anion gap = Na+ - (Cl- + HCO3-)

Interpretation of Anion Gap

Anion gap (AG) is: unmeasured anions - unmeasured cations

• Unmeasured anions include plasma proteins
• Unmeasured cations include calcium, potassium, magnesium

When an anion decrease, another anion must increase as a compensation to keep the electrolyte balance. In metabolic acidosis, a decrease in the bicarbonate is associate with an increase in another anion. For example, when bicarbonate decreases, chloride might increase as a compensation. In that case the anion gap remains within normal limits. If chloride does not increase following the decrease of bicarbonate, another unmeasured anion must increase leading to an increase in the anion gap.

Shown below is a table that summarizes the interpretation of the anion gap results. Note that a change in the unmeasured cation might lead to a change in the anion gap without any alteration in the acid base status.

Anion gap	Interpretation
High	Increased in unmeasured anions, OR Decrease in unmeasured cations such as calcium, potassium, magnesium
Low	Laboratory mistake (the most common etiology) Low albumin level: There is a decrease of the AG by 2.5 for every 1 g/dL decrease in plasma albumin, OR Increase in unmeasured cations such as calcium, potassium, magnesium Elevated cationic paraprotein (immunoglubulin G gammopathy) Ingestion of pyridostigmine bromide (used to treat myasthenia gravis)

Urinary Anion Gap

Calculation of Urinary Anion Gap

The urinary anion gap must be calculated in normal anion gap metabolic acidosis. The anion gap can be calculated as follows:

Urinary anion gap = (Na+ + K+)- (Cl-

Interpretation of Urinary Anion Gap

Urinary anion gap= Unmeasured anion- unmeasured cations

The major unmeasured cation is NH₄⁺.

Urinary anion gap	Interpretation
U (AG) < 0	Increased NH4+ production to accompany the increased Cl- which reflects that the kidneys are not the cause of the metabolic acidosis
U(AG) ≥ 0	Impaired NH4+ production as in the case of renal failure, renal tubular acidosis type 1, renal tubular acidosis type 4

Plasma Osmolar Gap

Calculation of Plasma Osmolar Gap

The plasma osmolar gap can be useful in high anion gap metabolic acidosis. The plasma osmolar gap can be calculated as follows:

Plasma osmolar gap = plasma calculated osmolal gap - plasma measured osmolal gap Plasma osmolality= (2 x Na+) + (Glucose/18) + (BUN/2.8)

Interpretation of Plasma Osmolar Gap

The plasma osmolar gap is considered high if >20. A high osmolal gap represents an increase in unmeasured osmoles, such as in the cases of:

• Ingestion:
  • Alcohol
  • Methanol
  • Ethylene glycol
  • Formaldehyde
• Ketoacidosis
  • Diabetic ketoacidosis
  • Alcoholic ketoacidosis
• Lactic acidosis

Hypochloremia vs Hypercholremia

The following equation can be used to assess the variation in chloride concentration in response to the metabolic acidosis: Na⁺/ Cl^-

• If Na⁺/ Cl^- < 1.4: Hyperchloremia (usually associated with normal anion gap metabolic acidosis)

• If Na⁺/ Cl^- > 1.4: Hypochloremia

Respiratory Compensation

In metabolic acidosis, there is respiratory compensation that starts within a short period of the onset of the acid-base disturbance. Respiratory alkalosis (through hyperventilation) occurs in order to decraese PaCO2 and therefore compensate for the metabolic acidosis.

The expected change in PaCo2 is as follows:

Expected respiratory compensation: Δ PaCO2 = 1.2 [1 to 1.5] x Δ HCO3-

Note that compensation increases the pH but does not bring it to normal. If bicarbonate concentration is low and the pH is normal, this suggests a combined acid-base abnormality.

Pure vs Combined Metabolic Acidosis

Pure vs combined metabolic acidosis can be estimated using the following values: plasma HCO3^-, PCO2, and arterial pH. Shown below is a table summarizing the findings in the different scenarios.

Acid base status	Plasma bicarbonate (meq/L)	Arterial pH	PCO2 (mmHg)
Normal	24	7.4	40
Pure metabolic acidosis	↓	↓	↓
Combined metabolic and respiratory acidosis	↓	↓	↔
Combined metabolic and respiratory alkalosis	↓	↔	↓

Pure high anion gap metabolic acidosis can be differentiated from combined metabolic acidosis by using the following equation: Δ Anion gap (AG)/ Δ HCO3^-

Δ AG/ Δ HCO3-	Interpretation
1-2	Pure high anion gap metabolic acidosis
<1	High anion gap metabolic acidosis PLUS normal anion gap metabolic acidosis
>2	High anion gap metabolic acidosis PLUS metabolic alkalosis

Associated Potassium Disorders

Metabolic acidosis is commonly associated with hyperkalemia. As the H+ is low, K+ moves from inside the cell to the blood to ensure electrical neutrality.