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. Infection TPN requires a chronic IV access for the solution to run through, and the most common complication is infection of this catheter. Infection is a common cause of death in these patients, with a mortality rate of approximately 15% per infection, and death usually results from septic shock. 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. Catheter complications include<unk> eumothorax, accidental arterial puncture, and catheter-related sepsis. The complication rate at the time of insertion should be less than 5%. Catheter-related infections may be minimised by appropriate choice of catheter and insertion technique. 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. Micrograph 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%. 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<unk> , 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<unk>  associated liver disease <unk> ALD). 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<unk>  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 normal oral diet. Administration of exogenous cholecystokinin (CCK) or stimulation of endogenous CCK by 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<unk> , 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<unk> , 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<unk>  therapy. First reported in 1965, the incidence of these reactions is speculated to be around one in 1.5 million patients who are provided<unk> . 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. Medications Patients who are receiving intravenous<unk>  may also need to receive intravenous medications as well using the same Y-site. It is important to assess the compatibility of the medications with the<unk>  components. Incompatibilities can be observed physically through discoloration, phase separation, or precipitation. 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 baby’s 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<unk>  administration begin after a period of natural<unk>  so doctors can properly calculate the<unk> al needs of the fetus. Otherwise, it should only be administered by a team of highly skilled doctors who can accurately assess the fetus’ needs.
Parenteral nutrition
Vegetarian nutrition
Assisted feeding
Human–animal breastfeeding
Clinical nutrition
Macrobiotic diet
Nutrition transition
Artificial digestion