History
Metabolic acidosis can result in a variety of nonspecific changes in several organ systems, including, but not limited to, neurologic, cardiovascular, pulmonary, gastrointestinal, and musculoskeletal dysfunction. Symptoms are often a result of and specific to the underlying etiology of the metabolic acidosis.
Head, eyes, ears, nose, throat (HEENT) findings include the following:
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Tinnitus, blurred vision, and vertigo can occur with salicylate poisoning.
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Visual disturbances, dimming, photophobia, scotomata, and frank blindness can be seen in methanol intoxication.
Cardiovascular findings include the following:
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Palpitations
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Chest pain
Neurologic findings include the following:
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Headache
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Visual changes
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Mental confusion
Pulmonary findings include subjective dyspnea from the patient's observation of hyperventilation.
GI findings include the following:
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Nausea and vomiting
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Abdominal pain
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Diarrhea
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Polyphagia
Musculoskeletal findings include the following:
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Generalized muscle weakness
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Bone pain
Physical
Neurologic
Cranial nerve palsies may occur with ethylene glycol intoxication.
Retinal edema may be seen in methanol ingestions.
Lethargy, stupor, and coma may occur in severe metabolic acidosis, particularly when it is associated with a toxic ingestion.
Cardiovascular
Severe acidemia (ie, pH < 7.10) can predispose a patient to potentially fatal ventricular arrhythmias, and it can reduce cardiac contractility and the inotropic response to catecholamines, resulting in hypotension and congestive heart failure.
Pulmonary
Patients with acute metabolic acidosis demonstrate tachypnea and hyperpnea as prominent physical signs.
Kussmaul respiration, an extremely intense respiratory effort, may be present.
Hyperventilation, in the absence of obvious lung disease, should alert the clinician to the possibility of an underlying metabolic acidosis.
Musculoskeletal
Chronic metabolic acidosis (eg, uremia, renal tubular acidosis [RTA]) is associated with substantial bone disease from bone buffering of calcium carbonate. [4]
Long bone malformations in pediatric patients (eg, vitamin D resistant, rickets) and fractures in adult patients are noted.
Causes
Causes of inability to excrete the dietary H+ load are as follows:
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Renal failure - Diminished NH4+ production
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Hypoaldosteronism - Type 4 RTA
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Diminished H+ secretion - Type 1 (distal) RTA
Causes of increased H+ load include the following:
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Lactic acidosis - Numerous causes, including circulatory failure, drugs and toxins, and hereditary causes (see Lactic Acidosis) [12]
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Ketoacidosis - Diabetes, alcoholism, and starvation
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Ingestions - Salicylates, methanol, ethylene glycol, isoniazid, [13] iron, paraldehyde, sulfur, toluene, ammonium chloride, phenformin/metformin, [14] and hyperalimentation fluids
GI HCO3- loss is caused by the following:
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Diarrhea
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Pancreatic, biliary, or intestinal fistulas
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Ureterosigmoidostomy
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Cholestyramine
Renal HCO3- loss may be caused by type 2 (proximal) RTA.
Acetazolamide may also be a cause of metabolic acidosis.
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Approach for evaluating metabolic acidosis.
