Short-term complications of PN therapy may be divided into three classes: mechanical, infectious, and metabolic. Longer term complications can include overfeeding, hepatobiliary complications, and metabolic bone disease.
Central catheter placement can be associated with serious mechanical complications, including pneumothorax, arrhythmias, catheter-related thrombosis, and catheter occlusion. Radiologic confirmation of line placement is necessary before initiating PN therapy. Catheter occlusion is the most common mechanical complication and may require thrombo-lytic treatment or line replacement. Catheter flushing protocols should be carefully followed to reduce risk of occlusion.
Infection due to catheter-related sepsis is another serious complication of PN that is associated with appreciable morbidity and cost. Prudent and meticulous catheter care and sterile technique should be emphasized. Catheter infections comprise a significant percentage of all nosocomial infections. Fever and unexplained hyperglycemia may be potential warning signs of catheter-related sepsis. It is important to note that there are frequently no external signs of catheter infection visible at the insertion site. Aseptic technique in manipulating the central line and related administration lines can help prevent introduction of infectious sources such as endogenous skin flora or contamination of the catheter hub. Appropriate methods and a sterile environment in compounding PN will reduce chances of contamination of the PN admixture during preparation. Treatment of catheter-related sepsis often includes access device removal and administration of appropriate antibiotic or antifungal therapy. With selected pathogens in patients with limited access options, salvage antimicrobial therapy may be considered to prevent the necessity of line removal.
The incidence of metabolic complications in PN patients is estimated to be 5-10%. Metabolic complications may include intolerance to fluid or macro-nutrients, or imbalances in electrolyte or vitamin and trace element homeostasis or function. Hyperglycemia is the most common complication associated with PN therapy.
Refeeding syndrome is a potential phenomenon of metabolic complications that may be observed when severely malnourished patients are re-fed in an overzealous manner. The rapid provision of macronutrients is associated with serum depletion and intracellular shifts of phosphorus, potassium, and magnesium as well as fluid retention and vitamin derangements. These abnormalities may result in the development of clinical sequellae such as arrhythmias, heart failure, respiratory failure, and death. Prevention of this phenomenon is achieved by identifying the patient at risk, repletion of electrolytes prior to initiation of nutrition support, and the slow advancement of PN with careful daily monitoring of electrolytes, including phosphorus and magnesium levels, as well as weights and fluid intake and output.
Electrolyte adjustments warrant close clinical evaluation. For example, hyponatremia can represent sodium deficiency or water excess. Electrolyte loss or shifts may occur from renal or gastrointestinal losses, hormonal imbalances, medication use, or acid-base disturbances. Accumulation of electrolytes may occur with fluid or acid-base shifts, renal insufficiency, or overzealous exogenous replacement. Generally, a consistent PN formula is recommended, with additional acute electrolyte replacements provided separately from the PN. Lower concentrations or even elimination of selected electrolytes from PN are often indicated in patients with renal failure.
Hepatobiliary complications, including steatosis and cholestasis, are associated with PN patients due to the lack of enteral stimulation and limited gastrointestinal motility. Cholestasis is universal in patients receiving PN for more than 6 weeks without enteral feedings. Transition to enteral or oral feedings will help prevent the potential development of gallstones associated with cholestasis. In adults, hepatic steatosis, or fatty liver, is generally associated with normal or mildly increased bilirubin levels and mild elevations in alkaline phosphatase and hepatic transaminases. In rare cases, hepatic steatosis may progress to steatohepatitis. In order to reduce the potential for hepatobiliary complications, the practitioner should attempt enteral feedings as soon as possible. Overfeeding with excessive lipid and dextrose loads should be avoided. The PN infusion can also be cycled to provide a rest period for the liver's macronutrient processing. Administration of a cholecystokinin-octapeptide may also help to reduce cholestasis.
Osteoporosis or osteomalacia may develop in long-term PN patients. Metabolic bone disease may develop due to underlying disease, inadequate intakes or malabsorption of calcium and vitamin D, corticosteroid therapy or other medications, and hypercalciuria. For selected long-term PN patients, treatment with bisphosphonates, calcium, and vitamin D should be considered to prevent the development of complications.
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