A 55-year-old man is brought to the emergency department after a motor vehicle collision. Due to severe, blunt trauma to the chest and abdomen the patient develops acute respiratory distress syndrome and requires intubation with mechanical ventilation. He receives enteral tube feeding for several days, but has high gastric residuals due to ileus. On hospital day 8, total parenteral nutrition is initiated. Temperature is 36.5 C (97.7 F), blood pressure is 110/60 mm Hg, pulse is 85/min, and respirations are 16/min. Physical examination shows moist mucous membranes and normal jugular venous pressure. Breath sounds are coarse bilaterally and heart sounds are normal. Multiple scattered ecchymoses are present on the chest and abdomen. There is mild pedal edema in the bilateral lower extremities. Laboratory results are as follows:
| Complete blood count | ||
| Hemoglobin | 11.2 g/dL | |
| Platelets | 200,000/mm3 | |
| Leukocytes | 4,100/mm3 | |
| Serum chemistry | ||
| Sodium | 134 mEq/L | |
| Potassium | 3.6 mEq/L | |
| Creatinine | 1.2 mg/dL | |
| Calcium | 9.6 mg/dL | |
| Glucose | 97 mg/dL | |
| Liver function studies | ||
| Albumin | 3.7 g/dL | |
To prevent further complications, which of the following laboratory tests should be monitored closely both before and after initiation of total parenteral nutrition?
Patients who are critically ill frequently develop intracellular phosphate deficiencies due to poor oral phosphate intake. This deficiency is usually clinically silent until patients receive caloric supplementation with intravenous dextrose, a component of total parenteral nutrition (TPN). Dextrose stimulates insulin secretion, and insulin drives serum phosphate into cells to be used for oxidative phosphorylation. The shift of serum phosphate into the intracellular space and the subsequent usage of phosphate to generate adenosine triphosphate can rapidly deplete serum phosphate levels and cause hypophosphatemia. As such, critically ill patients initiated on TPN should have serum phosphate closely monitored so that phosphate can be administered if a deficiency develops.
Hypophosphatemia after the initiation of TPN is a prominent manifestation of refeeding syndrome, a condition that develops due to fluid and electrolyte shifts when chronically malnourished patients are reinitiated on adequate nutrition. If fluid and electrolyte abnormalities are not carefully managed, patients with refeeding syndrome are at risk of developing seizures, rhabdomyolysis, and life-threatening cardiovascular complications (eg, arrhythmia, congestive heart failure).
(Choice A) Vitamin D levels drop in patients who are critically ill. Although low vitamin D levels are associated with increased mortality in the intensive care unit, supplementation with vitamin D does not seem to improve outcomes. As such, close vitamin D monitoring is not usually required.
(Choice B) Low-density lipoprotein cholesterol is typically monitored as part of risk assessment for atherosclerotic disease. Although lipid formulations are usually part of TPN, ongoing monitoring of low-density lipoprotein is not typically used to guide therapy.
(Choice C) Serum B-type natriuretic peptide is used primarily in patients with heart failure. This patient has normal heart sounds and jugular venous distension as well as mild pedal edema; heart failure is unlikely.
(Choice E) Zinc deficiency can develop in patients on chronic TPN so zinc is often included in TPN formulations. Routine zinc monitoring is not typically necessary.
Educational objective:
Patients on total parenteral nutrition are at high risk for hypophosphatemia. Serum phosphate levels must be closely monitored.