Download Case Study: Metabolic Alkalosis in Chronic Respiratory Alkalosis Patient and more Exams Biology in PDF only on Docsity! Quiz of the Month Answer The patient’s mental status deteriorated because of metabolic alkalosis induced by oral alkali therapy given to a patient with chronic respiratory alkalosis. The ar terial blood gas on admission showed a pH of 7.41, pCC>2 25 mm Hg, pC>2 85 mm Hg. The initial serum total CO2 was low, and the serum chloride level was high because of metabolic compensation of chronic respiratory alkalosis due to liver disease rather than to metabolic acidosis. Since his arterial pH was normal to start with, treating him with alkali made him acutely alkalemic which caused his mental status to decline. An arterial blood gas, drawn after alkali therapy was initiated, showed a pH of 7.57 and a PCO2 of 26 mm Hg at a time when his serum bicarbonate was normal (24 mEq/1). The normal total CO2 in this case did not indicate the resolution of an acidosis, but rather an acute metabolic alkalosis due to oral bicarbonate therapy. Since a low serum bicarbonate may be present with either respiratory alkalosis or meta bolic acidosis, a blood gas must always be obtained with the serum electrolyte measurements to determine the patient’s true acid-base status. All patients with severe liver disease will have a chronic respiratory alkalosis with metabolic compensa tion; if uncomplicated they will always present with a low serum bicarbonate and a high chloride level. If serum electrolyte analysis shows a normal bicarbonate level, then another metabolic disturbance must be looked for such as a metabolic alkalosis from persistent vomiting or diuretic use or a rarely coexistent state of primary hyper aldosteronism, Cushing’s disease, or Bartter’s syn drome. Other mistakes were made in this patient's manage ment: (1) Furosemide is usually inappropriate treatment for edema secondary to cirrhosis. Since such patients have decreased effective arterial blood volume, furosemide can precipitate an acute fall in serum potassium and blood pressure further decreasing effective arterial blood volume and worsening mental status. (2) The ibuprofen should have been discontinued. Nonsteroidal anti-inflammatory agents can exacerbate renal failure by decreasing renal blood flow and glomeru lar filtration rate. A recent study of patients with chronic glomerulonephritis showed that sulindac, a selective cy clooxygenase inhibitor, did not decrease renal blood flow or glomerular filtration rate in patients with mild renal impairment and may be a safe substitute for other non steroidal anti-inflammatory drugs in patients with com promised kidney function. (3) The dose of cimetidine should have been de creased. Cimetidine dosage must be adjusted to the level of renal function. (4) Mylanta should not be given to patients with renal failure because of the possibility of magnesium toxicity; aluminum gel antacids should be used instead. References 1 Cogan, M.C.; et al.,: Metabolic alkalosis. Med. Clins. N. Am. 67: 903-914 (1983). 2 Epstein, M.: Rena! sodium handling in cirrhosis. Semin. Ne phrol. 3: 225-240 (1983). 3 Zipser, R.D.; et al.: Prostaglandins: modulators of renal function and pressor resistance in chronic liver disease. J. clin. Endocr. Metab. 48: 895-900 (1979). 4 Clive, D.M.; Stoff. J.S.: Renal syndromes associated with nonste roidal anti-inflammatory drugs. New Engl. J. Med. 310: 563-572 (1984). 5 Ciabattoni, G.; et al.: Effects of sulindac and ibuprofen in patients with chronic glomerular disease. New Engl. J. Med. 310:279-283 (1984).
