Metabolic acidosis
Metabolic acidosis is a primary fall in serum bicarbonate that is first confirmed with an arterial or venous blood gas, then classified by the serum anion gap into an increased anion gap process (unmeasured organic anion, most often lactate) or a normal anion gap process (bicarbonate loss from the gut or kidney). The urine anion gap and clinical context localize the cause, and management targets the underlying disease, reserving intravenous sodium bicarbonate for severe acidemia (pH less than 7.1-7.2) or specific indications such as chronic kidney disease and renal tubular acidosis.
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What this article covers
- Overview
Metabolic acidosis is a primary process defined by a low serum bicarbonate, distinguished from a compensatory fall in bicarbonate for chronic respiratory alkalosis by a concurrently low arterial or venous pH.
- Epidemiology
Lactic acidosis is the most common cause of increased anion gap metabolic acidosis, from tissue hypoperfusion (type A) or drug/toxin-related impairment of metabolism without hypoperfusion (type B).
- Risk factors
Reduced GFR (CKD): impaired ammoniagenesis and, at lower GFR, retention of organic and inorganic anions.
- Pathophysiology
An increased anion gap reflects accumulation of an unmeasured anion that replaces bicarbonate consumed buffering an acid load: lactate, ketoacids, glycolic acid (ethylene glycol), formic acid (methanol), or salicylate itself.
- Clinical features
Signs track the etiology more than the acidemia itself: Kussmaul respirations and fruity breath odor in DKA; abdominal pain and vomiting in alcoholic ketoacidosis or salicylate toxicity; flank pain…
- Differential diagnosis
Lactic acidosis (type A or B): distinguished from ketoacidosis and toxic-alcohol ingestion by serum lactate 4.0 mEq/L with a normal ketone panel and normal osmolal gap.
- Diagnosis
The diagnosis is established by a blood gas showing pH below 7.37 with a low serum bicarbonate (below about 22 mEq/L), confirming a primary metabolic acidosis rather than a purely compensatory fall…
- Management
First, treat the underlying cause identified on workup, since most morbidity comes from the etiology rather than the pH itself: aggressive fluid resuscitation and source control for…
- Complications
Arrhythmia and impaired cardiac contractility with severe acidemia (pH <7.1-7.2).
- Prognosis
Prognosis tracks the underlying cause, not the degree of acidemia alone: hypoperfusion-driven lactic acidosis resolves with resuscitation, while type B lactic acidosis from an irreversible malignancy is a poor sign.
- Prevention
Start alkali therapy in CKD once serum bicarbonate is chronically below 22 mEq/L, titrated to a normal range (about 22-26 mEq/L), per KDIGO.
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Related articles
- Renal tubular acidosis
Renal tubular acidosis is a normal anion gap metabolic acidosis caused by impaired renal bicarbonate reabsorption (type 2, proximal) or impaired distal acid excretion (type 1, hypokalemic distal, or type 4, hyperkalemic distal from aldosterone deficiency or resistance). The urine anion gap, serum potassium, and urine pH distinguish the three types, which are treated respectively with alkali replacement plus a thiazide, potassium citrate, and correction of the underlying cause plus mineralocorticoid replacement when appropriate.
- Lactic acidosis
Lactic acidosis is a high anion gap metabolic acidosis from a serum lactate above 4.0 mmol/L, most often type A from tissue hypoperfusion (septic, cardiogenic, or hypovolemic shock) or type B from impaired metabolism (metformin, mitochondrial toxins, malignancy). Diagnosis rests on the anion gap plus lactate level; management treats the underlying cause, since bicarbonate is reserved for arterial pH below 7.1-7.15.
- Diabetic ketoacidosis
Diabetic ketoacidosis is a life-threatening hyperglycemic crisis of near-absolute insulin deficiency, most common in type 1 diabetes, producing an anion-gap ketoacidosis from unrestrained lipolysis and osmotic diuresis from severe hyperglycemia. It is diagnosed by hyperglycemia, ketonemia, and an anion-gap metabolic acidosis, and treated with intravenous isotonic saline, an intravenous regular insulin bolus and infusion, and aggressive potassium repletion guided by frequent electrolyte monitoring.
- Acute kidney injury
Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
- Metabolic alkalosis
Metabolic alkalosis is a primary rise in serum bicarbonate generated by acid loss or alkali retention (usually vomiting, nasogastric suction, or diuretic use) and sustained by a maintenance state, most often volume contraction, hypokalemia, or mineralocorticoid excess. The urine chloride level is the key diagnostic branch point, separating chloride-responsive (saline-responsive) causes, treated with isotonic saline and potassium repletion, from chloride-resistant causes driven by mineralocorticoid excess, treated with potassium repletion and correction of the underlying endocrine or genetic disorder.
- Respiratory acidosis
Respiratory acidosis is retention of arterial carbon dioxide from impaired alveolar ventilation, producing hypercapnia and a low pH that is buffered acutely and partially corrected over 3 to 5 days by renal bicarbonate reabsorption. Management corrects the underlying ventilatory mechanism, escalating from treatment of the precipitant to noninvasive and then invasive mechanical ventilation based on the degree of acidosis, mental status, and hemodynamic stability.