A 43-year-old woman with hepatitis C, alcohol use, and liver cirrhosis is admitted to the hospital for severe vomiting over the last 2 days. The vomitus has appeared clear with no blood or coffee-ground material. She feels very weak but has no abdominal pain, fever, or diarrhea. The patient appears tired on examination. Temperature is 36.8 C (98.2 F), blood pressure is 100/70 mm Hg (while supine), pulse is 90/min, and respirations are 14/min. Lungs are clear to auscultation. There is mild epigastric tenderness but no abdominal distension. Extremities have no edema. Laboratory results are as follows: Which of the following is the most appropriate initial treatment for this patient?

Question

A 43-year-old woman with hepatitis C, alcohol use, and liver cirrhosis is admitted to the hospital for severe vomiting over the last 2 days.  The vomitus has appeared clear with no blood or coffee-ground material.  She feels very weak but has no abdominal pain, fever, or diarrhea.  The patient appears tired on examination.  Temperature is 36.8 C (98.2 F), blood pressure is 100/70 mm Hg (while supine), pulse is 90/min, and respirations are 14/min.  Lungs are clear to auscultation.  There is mild epigastric tenderness but no abdominal distension.  Extremities have no edema.  Laboratory results are as follows:  Which of the following is the most appropriate initial treatment for this patient?

Quizplus · Accepted Answer

Explanation: Repeated vomiting causes hypokalemic, hypochloremic, metabolic alkalosis. The pathogenesis can be separated into 2 phases: Generation phase: Repeated vomiting leads to depletion of total body acid (gastric contents are rich in hydrochloric acid) as well as loss of fluid, sodium, and chloride. Normally, acidic gastric secretions stimulate the pancreas and liver to excrete bicarbonate into the duodenum. However, in patients with recurrent vomiting, this bicarbonate excretion does not occur due to loss of gastric acid, leading to buildup of alkali (metabolic alkalosis). Maintenance phase: Although excess alkali are filtered in the glomerulus, they are also reabsorbed as a result of an activated renin-angiotensin-aldosterone system (RAAS). Fluid depletion from vomiting triggers RAAS in an attempt to conserve sodium and water. Aldosterone functions to retain water at the expense of excreting both potassium and acid in the urine, despite total body acid depletion (contraction alkalosis). Restoration of the extracellular volume with intravenous fluids (such as normal saline) removes the stimulus for RAAS activation, restoring the kidney's ability to excrete excess bicarbonate. Potassium supplementation should also be administered to treat hypokalemia (which should improve with normalization of the acid-base status); given her vomiting, intravenous formulations may be used. (Choices A and F) This patient is volume depleted, and diuretic therapy would worsen the contraction alkalosis. Acetazolamide, a diuretic that inhibits proximal renal bicarbonate reabsorption, may be used in patients with hypervolemia and metabolic alkalosis. Spironolactone, a potassium-sparing diuretic, is used in combination with furosemide for treatment of ascites. (Choice C) Intravenous sodium bicarbonate is used to treat severe metabolic acidosis and could worsen this patient's alkalosis. (Choice D) Oral lactulose is used to treat hepatic encephalopathy in patients with cirrhosis. This patient has no evidence of encephalopathy. (Choice E) Propranolol is used for both primary (ie, esophageal varices found on endoscopic screening) and secondary (ie, history of variceal bleed) prophylaxis of variceal hemorrhage in patients with liver cirrhosis. This patient has no evidence of a variceal bleed. Educational objective: Recurrent vomiting causes depletion of fluid, acid, and sodium chloride, leading to metabolic alkalosis, activation of the renin-angiotensin-aldosterone system, and increased urinary potassium loss. Volume resuscitation with normal saline corrects contraction alkalosis. Hypokalemia should be treated as well.

A 43-Year-Old Woman with Hepatitis C, Alcohol Use, and Liver