Metabolic acidosis
Metabolic acidosis: Excerpt from Professional Guide to Diseases (Eighth Edition)
Metabolic acidosis is a physiologic state of excess acid accumulation and deficient base bicarbonate produced by an underlying pathologic disorder. Symptoms result from the body’s attempts to correct the acidotic condition through compensatory mechanisms in the lungs, kidneys, and cells. Metabolic acidosis is more prevalent among children, who are vulnerable to acid-base imbalance because their metabolic rates are faster and their ratios of water to total-body weight are lower. Severe or untreated metabolic acidosis can be fatal.
Causes
Metabolic acidosis usually results from excessive fat burning in the absence of usable carbohydrates. This can be caused by diabetic ketoacidosis, chronic alcoholism, malnutrition, or a low-carbohydrate, high-fat diet — all of which produce more keto acids than the metabolic process can handle. Other causes include:
❑ anaerobic carbohydrate metabolism: a decrease in tissue oxygenation or perfusion (as occurs with pump failure after myocardial infarction, or with pulmonary or hepatic disease, shock, or anemia) forces a shift from aerobic to anaerobic metabolism, causing a corresponding rise in lactic acid level
❑ renal insufficiency and failure (renal acidosis): underexcretion of metabolized acids or inability to conserve base
❑ diarrhea and intestinal malabsorption: loss of sodium bicarbonate from the intestines, causing the bicarbonate buffer system to shift to the acidic side. For example, ureteroenterostomy and Crohn’s disease can also induce metabolic acidosis.
Less frequently, metabolic acidosis results from salicylate intoxication (overuse of aspirin), exogenous poisoning, or Addison’s disease with an increased excretion of sodium and chloride, and retention of potassium ions.
Signs and symptoms
In mild acidosis, the underlying disease’s symptoms may obscure any direct clinical evidence. Metabolic acidosis typically begins with headache and lethargy, progressing to drowsiness, central nervous system depression, Kussmaul’s respirations (as the lungs attempt to compensate by “blowing off” carbon dioxide), stupor and, if the condition is severe and goes untreated, coma and death. Associated GI distress usually produces anorexia, nausea, vomiting, and diarrhea, and may lead to dehydration. Underlying diabetes mellitus may cause fruity breath from catabolism of fats and excretion of accumulated acetone through the lungs.
Diagnosis
Confirming diagnosis Arterial pH below 7.35 confirms metabolic acidosis. In severe acidotic states, pH may fall to 7.10, and the partial pressure of arterial carbon dioxide may be normal or below 34 mm Hg as compensatory mechanisms take hold. Bicarbonate may be below 22 mEq/L.
A metabolic panel can help reveal the cause and severity of metabolic acidosis. A complete blood count can be done to help assess possible causes as well. Supportive findings include:
❑ urine pH: below 4.5 in the absence of renal disease
❑ serum potassium levels: above 5.5 mEq/L from chemical buffering
❑ glucose levels: above 150 mg/dl in diabetes
❑ serum ketone bodies: elevated levels in diabetes mellitus
❑ serum osmolarity: increased levels, as in hyperosmolar hyperglycemic nonketotic acidosis or dehydration
❑ plasma lactic acid: elevated levels in lactic acidosis
❑ anion gap: greater than 14 mEq/L indicating metabolic acidosis (diabetic ketoacidosis, aspirin overdose, alcohol poisoning). (See Anion gap.)
Treatment
In metabolic acidosis, treatment consists of administration of sodium bicarbonate I.V. for severe cases, evaluation and correction of electrolyte imbalances and, ultimately, correction of the underlying cause. For example, in diabetic ketoacidosis, a low-dose continuous I.V. infusion of insulin is recommended.
Special considerations
❑ Keep sodium bicarbonate ampules handy for emergency administration. Monitor vital signs, laboratory results, and level of consciousness frequently because changes can occur rapidly.
❑ In diabetic acidosis, watch for secondary changes due to hypovolemia, such as decreasing blood pressure.
❑ Record intake and output accurately to monitor renal function. Watch for signs of excessive serum potassium — weakness, flaccid paralysis, and arrhythmias, possibly leading to cardiac arrest. After treatment, check for overcorrection to hypokalemia.
❑ Because metabolic acidosis commonly causes vomiting, position the patient to prevent aspiration. Prepare for possible seizures with seizure precautions.
❑ Provide good oral hygiene. Use sodium bicarbonate washes to neutralize mouth acids, and lubricate the patient’s lips with lemon and glycerin swabs as indicated.
❑ To prevent metabolic acidosis, carefully observe patients receiving I.V. therapy or who have intestinal tubes in place as well as those suffering from shock, hyperthyroidism, hepatic disease, circulatory failure, or dehydration. Teach the patient with diabetes how to routinely test urine for glucose and acetone, and encourage strict adherence to insulin or oral hypoglycemic therapy.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
More About Metabolic disorders
More Medical Textbooks Online about Metabolic disorders
Review other book chapters online related to Metabolic disorders:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
» Next page: Metabolic alkalosis (Professional Guide to Diseases (Eighth Edition))
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
