Metabolic alkalosis
Metabolic alkalosis: Excerpt from Professional Guide to Diseases (Eighth Edition)
A clinical state marked by decreased amounts of acid or increased amounts of base bicarbonate, metabolic alkalosis causes metabolic, respiratory, and renal responses, producing characteristic symptoms (most notably hypoventilation). This condition is always secondary to an underlying cause. With early diagnosis and prompt treatment, prognosis is good; however, untreated metabolic alkalosis may lead to coma and death.
Causes
Metabolic alkalosis results from loss of acid, retention of base, or renal mechanisms associated with decreased serum levels of potassium and chloride.
Causes of critical acid loss include vomiting, nasogastric (NG) tube drainage or lavage without adequate electrolyte replacement, fistulas, and the use of steroids and certain diuretics (furosemide, thiazides, and ethacrynic acid). Hyperadrenocorticism is another cause of severe acid loss. Cushing’s disease, primary hyperaldosteronism, and Bartter’s syndrome, for example, all lead to retention of sodium and chloride, and urinary loss of potassium and hydrogen.
Excessive base retention can result from excessive intake of bicarbonate of soda or other antacids (usually for treatment of gastritis or peptic ulcer), excessive intake of absorbable alkali (as in milk-alkali syndrome, often seen in patients with peptic ulcers), administration of excessive amounts of I.V. fluids with high concentrations of bicarbonate or lactate, or respiratory insufficiency — all of which cause chronic hypercapnia from high levels of plasma bicarbonate.
Signs and symptoms
Clinical features of metabolic alkalosis result from the body’s attempt to correct the acid-base imbalance, primarily through hypoventilation. Other manifestations include irritability, picking at bedclothes (carphology), twitching, confusion, nausea, vomiting, and diarrhea (which aggravates alkalosis). Cardiovascular abnormalities (such as atrial tachycardia) and respiratory disturbances (such as cyanosis and apnea) also occur. In the alkalotic patient, diminished peripheral blood flow during repeated blood pressure checks may provoke carpopedal spasm in the hand — a possible sign of impending tetany (Trousseau’s sign). Uncorrected metabolic alkalosis may progress to seizures and coma.
Diagnosis
Confirming diagnosis Blood pH level greater than 7.45 and bicarbonate levels above 29 mEq/L confirm the diagnosis. A partial pressure of carbon dioxide above 45 mm Hg indicates attempts at respiratory compensation. Serum electrolyte studies show low potassium, calcium, and chloride levels.
Other characteristic findings include:
❑ Urine pH is usually about 7.0.
❑ Urinalysis reveals alkalinity after the renal compensatory mechanism begins to excrete bicarbonate.
❑ Electrocardiogram may show low T wave, merging with a U wave (secondary to hypocalcemia from metabolic alkalosis), and atrial or sinus tachycardia.
Treatment
Treatment aims to correct the underlying cause of metabolic alkalosis. Therapy for severe alkalosis may include cautious administration of ammonium chloride I.V. or hydrochloric acid to release hydrogen chloride and restore concentration of extracellular fluid and chloride levels. Potassium chloride and normal saline solution (except in the presence of heart failure) are usually sufficient to replace losses from gastric drainage. Electrolyte replacement with potassium chloride and discontinuing diuretics correct metabolic alkalosis resulting from potent diuretic therapy.
Oral or I.V. acetazolamide, which enhances renal bicarbonate excretion, may be prescribed to correct metabolic alkalosis without rapid volume expansion. Because acetazolamide also enhances potassium excretion, potassium may have to be administered before giving this drug.
Special considerations
Structure the care plan around cautious I.V. therapy, keen observation, and strict monitoring of the patient’s status.
❑ Dilute potassium when giving I.V. containing potassium salts. Monitor the infusion rate to prevent damage to blood vessels; watch for signs of phlebitis. When administering ammonium chloride 0.9%, limit the infusion rate to 1 L in 4 hours; faster administration may cause hemolysis of red blood cells. Avoid overdosage because it may cause overcorrection to metabolic acidosis. Don’t give ammonium chloride with signs of hepatic or renal disease; instead, use hydrochloric acid.
❑ Watch closely for signs of muscle weakness, tetany, or decreased activity. Monitor vital signs frequently and record intake and output to evaluate respiratory, fluid, and electrolyte status. Remember, respiratory rate usually decreases in an effort to compensate for alkalosis. Hypotension and tachycardia may indicate electrolyte imbalance, especially hypokalemia.
❑ Observe seizure precautions.
❑ To prevent metabolic alkalosis, warn patients against overusing alkaline agents. Irrigate NG tubes with isotonic saline solution instead of plain water to prevent loss of gastric electrolytes. Monitor I.V. fluid concentrations of bicarbonate or lactate. Teach patients with ulcers to recognize signs of milk-alkali syndrome: a distaste for milk, anorexia, weakness, and lethargy.
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.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
» Next page: Metabolic syndrome (Professional Guide to Diseases (Eighth Edition))
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