TPN fully bypasses the GI tract and normal methods of nutrient absorption. Possible complications, which may be significant, are listed below. Other than those listed below, common complications of TPN include hypophosphatemia, hypokalemia, hyperglycemia, hypercapnia, decreased copper and zinc levels, elevated prothrombin time (if associated with liver injury), hyperchloremic metabolic acidosis and decreased gastrointestinal motility. When using central venous access, the subclavian (or axillary) vein is preferred due to its ease of access and lowest infectious complications compared to the jugular and femoral vein insertions.
Blood clots Chronic IV access leaves a foreign body in the vascular system, and blood clots on this IV line are common. Death can result from
pulmonary embolism wherein a clot that starts on the IV line breaks off and travels to the lungs, blocking blood flow. of
periportal fatty liver as may arise due to TPN.
Trichrome stain. Patients on TPN who have such clots occluding their catheter may receive a
thrombolytic flush to dissolve the clots and prevent further complications.
Fatty liver and liver failure Fatty liver is usually a more long-term complication of TPN, though over a long enough course it is fairly common. The pathogenesis is due to using
linoleic acid (an
omega-6 fatty acid component of soybean oil) as a major source of calories. TPN-associated liver disease strikes up to 50% of patients within 5–7 years, correlated with a mortality rate of 2–50%. The onset of this liver disease is the major complication that leads TPN patients to requiring an
intestinal transplant.
Intralipid (
Fresenius-Kabi), the US standard lipid emulsion for TPN nutrition, contains a 7:1 ratio of n-6/n-3 ratio of
polyunsaturated fatty acids (PUFA). By contrast,
Omegaven has a 1:8 ratio and showed promise in multiple clinical studies. Therefore, n-3-rich fat may alter the course of parenteral nutrition associated liver disease (PNALD).
Hunger Because patients are being fed intravenously, the subject does not physically eat, resulting in intense
hunger pangs (pains). The brain uses signals from the
mouth (
taste and
smell), the
stomach and
gastrointestinal tract (fullness) and
blood (
nutrient levels) to determine conscious feelings of
hunger. In cases of TPN, the taste, smell and physical fullness requirements are not met, and so the patient experiences hunger, although the body is being fully nourished. Patients who eat food despite the inability can experience a wide range of complications, such as
refeeding syndrome.
Cholecystitis Total parenteral nutrition increases the risk of acute
cholecystitis due to complete disuse of the gastrointestinal tract, which may result in bile stasis in the
gallbladder. Other potential
hepatobiliary dysfunctions include
steatosis,
steatohepatitis,
cholestasis, and
cholelithiasis. Six percent of patients on TPN longer than three weeks and 100% of patients on TPN longer than 13 weeks develop
biliary sludge. The formation of sludge is the result of stasis due to lack of enteric stimulation and is not due to changes in bile composition. Gallbladder sludge disappears after four weeks of a normal oral diet. Administration of exogenous
cholecystokinin (CCK) or stimulation of endogenous CCK by a periodic pulse of large amounts of amino acids has been shown to help prevent sludge formation. These therapies are not routinely recommended. Such complications are suggested to be the main reason for mortality in people requiring long-term total parenteral nutrition, such as in
short bowel syndrome. In newborn infants with short bowel syndrome with less than 10% of expected intestinal length, thereby being dependent upon total parenteral nutrition, five-year survival is approximately 20%.
Gut atrophy Infants who are sustained on TPN without food by mouth for prolonged periods are at risk for developing gut atrophy.
Hypersensitivity Hypersensitivity is a rarely described but significant complication of parenteral nutrition therapy. First reported in 1965, the incidence of these reactions is speculated to be around one in 1.5 million patients who are provided parenteral nutrition. There is a wide range in how and when these reactions manifest.
Cutaneous manifestations are the most common presentation. Hypersensitivity is thought to occur to the individual components of TPN, with the
intravenous lipid emulsion being the most frequently implicated component, followed by the
multivitamin solution and the
amino acid solution.
Metabolic complications Metabolic complications include the
refeeding syndrome characterised by
hypokalemia,
hypophosphatemia and
hypomagnesemia.
Hyperglycemia is common at the start of therapy, but can be treated with insulin added to the TPN solution. Hypoglycaemia is likely to occur with abrupt cessation of TPN. Liver dysfunction can be limited to a reversible cholestatic jaundice and to fatty infiltration (demonstrated by elevated transaminases). Severe hepatic dysfunction is a rare complication. Overall, patients receiving TPN have a higher rate of infectious complications. This can be related to hyperglycemia.
Pregnancy Pregnancy can cause major complications when trying to properly dose the nutrient mixture. Because all of the fetus' nourishment comes from the mother's blood stream, the doctor must properly calculate the dosage of nutrients to meet both recipients' needs and have them in usable forms. Incorrect dosage can lead to many adverse, hard-to-guess effects, such as
death, and varying degrees of
deformation or other
developmental problems. It is recommended that parenteral nutrition administration begins after a period of natural nutrition so doctors can properly calculate the nutritional needs of the
fetus. Otherwise, it should only be administered by a team of highly skilled doctors who can accurately assess the fetus' needs. ==Total parenteral nutrition==