Metabolic Acidosis Clinical Presentation
- Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
Symptoms of metabolic acidosis are not specific. The respiratory center in the brainstem is stimulated, and hyperventilation develops in an effort to compensate for the acidosis. As a result, patients may report varying degrees of dyspnea. Patients may also report chest pain, palpitations, headache, confusion, generalized weakness, and bone pain. Patients, especially children, also may present with nausea, vomiting, and decreased appetite.
The clinical history in metabolic acidosis is helpful in establishing the etiology when symptoms relate to the underlying disorder. The age of onset and a family history of acidosis may point to inherited disorders, which usually start during childhood. Important points in the history include the following:
Diarrhea - GI losses of HCO 3 -
History of diabetes mellitus, alcoholism, or prolonged starvation - Accumulation of ketoacids
Polyuria, increased thirst, epigastric pain, vomiting - Diabetic ketoacidosis (DKA)
Nocturia, polyuria, pruritus, and anorexia - Renal failure 
Ingestion of drugs or toxins - Salicylates, acetazolamide, cyclosporine, ethylene glycol, methanol
Visual symptoms, including dimming, photophobia, scotomata - Methanol ingestion
Renal stones - RTA or chronic diarrhea
Tinnitus, blurred vision, and vertigo - Salicylate overdose
The best recognized sign of metabolic acidosis is Kussmaul respirations, a form of hyperventilation that serves to increase minute ventilatory volume. This is characterized by an increase in tidal volume rather than respiratory rate and is appreciated as deliberate, slow, deep breathing.
Chronic metabolic acidosis in children may be associated with stunted growth and rickets.
Coma and hypotension have been reported with acute severe metabolic acidosis.
Other physical signs of metabolic acidosis are not specific and depend on the underlying cause. Some examples include xerosis, scratch marks on the skin, pallor, drowsiness, fetor, asterixis, and pericardial rub for renal failure, as well as reduced skin turgor, dry mucous membranes, and fruity smell for DKA.
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|Characteristics||Proximal (Type 2)||Distal (Type 1)||Type 4|
|Primary defect||Proximal HCO3 - reabsorption||Diminished distal H+ secretion||Diminished ammoniagenesis|
|Urine pH||< 5.5 when serum HCO3 - is low||>5.5||< 5.5|
|Serum HCO3 -||>15 mEq/L||Can be < 10 mEq/L||>15 mEq/L|
|Fractional excretion of HCO3 - (FEHCO3)||>15-20% during HCO3 - load||< 5% (can be as high as 10% in children)||< 5%|
|Serum K+||Normal or mild decrease||Mild-to-severe decrease*||High|
|Associated features||Fanconi syndrome||...||Diabetes mellitus, renal insufficiency|
|Alkali therapy||High doses||Low doses||Low doses|
|Complications||Osteomalacia or rickets||Nephrocalcinosis, nephrolithiasis||...|
|*K+ may be high if RTA is due to volume depletion.|