A 50-year-old man with a long history of chronic alcohol use disorder is hospitalized due to nausea, vomiting, and epigastric pain lasting for 2 days. The patient was previously admitted with an episode of alcohol-induced acute pancreatitis. Temperature is 37 C (98.6 F), blood pressure is 102/70 mm Hg, pulse is 106/min, and respirations are 16/min. BMI is 17.5 kg/m2. On physical examination, he appears cachectic. He is alert and oriented. The chest is clear to auscultation. There is epigastric tenderness without rebound. Bowel sounds are present. Neurologic examination is normal. Laboratory results are as follows:
| Sodium | 132 mEq/L |
| Potassium | 3.2 mEq/L |
| Chloride | 90 mEq/L |
| Bicarbonate | 22 mEq/L |
| Blood urea nitrogen | 28 mg/dL |
| Creatinine | 0.8 mg/dL |
| Calcium | 9.6 mg/dL |
| Glucose | 70 mg/dL |
| Lipase | 32 U/L |
The patient is given thiamine, folic acid, and a multivitamin replacement, followed by 5% dextrose and normal saline with potassium replacement. A few hours later, he reports extreme weakness in all extremities. Deep tendon reflexes are absent. What is the most appropriate next step in management?
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This patient with chronic alcohol use disorder developed diffuse weakness and hyporeflexia hours after receiving dextrose-containing intravenous fluids, suggesting the development of refeeding syndrome. Refeeding syndrome occurs in the setting of hypophosphatemia, typically due to chronic malnutrition (eg, alcohol use disorder, anorexia). Patients with alcohol use disorders are at particularly elevated risk due to alcohol-induced chronic diarrhea (reduces intestinal phosphate absorption) and gastritis (calcium-based antacids bind intestinal phosphorus).
The reintroduction of carbohydrates (ie, 5% dextrose-containing intravenous fluids) in patients with chronic hypophosphatemia leads to increased insulin secretion. This stimulates the intracellular shift of electrolytes (ie, phosphate, potassium, magnesium) and increases phosphate utilization during glycolysis (eg, formation of ATP, 2-3 diphosphoglycerate), resulting in phosphate depletion and failure of cellular energy metabolism.
Manifestations include muscle weakness, hyporeflexia, rhabdomyolysis, hemolysis, arrhythmias, and congestive heart failure. In addition to hypophosphatemia, hypokalemia, hypomagnesemia, and elevated liver function studies are typical. The diagnosis is confirmed with low serum phosphorus levels, and management includes close laboratory monitoring of electrolytes with aggressive electrolyte repletion.
(Choice A) Acetylcholine receptor antibodies are used to evaluate for myasthenia gravis, which causes fluctuating, fatigable weakness that is most prominent in the facial and proximal muscles. Diffuse weakness that occurs after a dextrose infusion is more consistent with refeeding syndrome.
(Choice B) ACTH stimulation test is used to diagnose adrenal insufficiency, which also causes abdominal pain, nausea, and hyponatremia. However, although adrenal crisis can cause weakness, it typically also causes hypotension, hypoglycemia, and possibly hyperkalemia; areflexia is unexpected.
(Choice C) Lumbar puncture demonstrating albuminocytologic dissociation supports the diagnosis of Guillain-Barré syndrome, which can cause areflexia and weakness, but symptoms are typically ascending and follow an episode of gastroenteritis or upper respiratory infection.
(Choice D) MRI can evaluate for spinal cord compression, which could cause diffuse weakness, but would typically cause hyperreflexia rather than hyporeflexia. In addition, back pain is common and weakness from cord compression is often progressive over a course of days rather than the acute onset seen in this patient.
(Choice E) Severe hypothyroidism is confirmed with serum TSH and can cause weakness but typically causes delayed (not absent) reflexes. In addition, it is usually associated with other signs of hypothyroidism (eg, cold intolerance, bradycardia, myxedema). Acute onset is unlikely.
Educational objective:
Refeeding syndrome occurs after the reintroduction of carbohydrates in patients with chronic malnourishment. Clinical manifestations include hypophosphatemia and other electrolyte abnormalities, muscle weakness, hyporeflexia, arrhythmias, and/or congestive heart failure.