Complications of Home Parenteral and Enteral Nutrition: History
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Contributor:
John DiBaise

Although home parenteral and enteral nutrition (HPEN) can be life-saving therapies, they are also associated with complications that can be life threatening. An awareness of these complications and close monitoring is essential for prevention and identification of these problems.

  • home enteral nutrition
  • enteral nutrition
  • parenteral nutrition
  • complications

1. Central Venous Catheter-Related Complications

Complications of long-term central venous catheters (CVCs) include infection, thrombosis, and malfunction/breakage/dislodgement. One of the most common reasons for hospitalization in patients on HPN is catheter-related bloodstream infection (CRBSI) [1]. According to the most recent International Nosocomial Infection Control consortium surveillance data, there are approximately 4.1 central line-associated bloodstream infections per 1000 central line days [2]. Infection-related complications can be reduced with proper catheter insertion and care, as contamination of the catheter hub and migration of skin organisms into the catheter tract are the major events that lead to bacteremia [3]. Other sources of infection include contamination from infused substances or hematogenous spread from an unrelated infectious source [4]. The type of CVC and certain other catheter-related factors, including larger catheter caliber, absence of a cuff, and increased number of lumens, also correlate with increased infection risk [3]. Typical symptoms that suggest infection include fever, malaise, and tachycardia during CVC use, although these may not be present in all cases of catheter-related bloodstream infection (CRBSI) [5]. Elevation in leukocyte count and liver enzymes is often seen. Blood cultures should be obtained both from the CVC and from a peripheral vein prior to initiating empiric antibiotic therapy [6]. The most common causes of CRBSI include coagulase-negative staphylococci, Staphylococcus aureus, and Staphylococcus epidermidis. Gram-negative and fungal infections are less common.
If CRBSI is confirmed, the antibiotic therapy should be tailored to the identified pathogen. A 14-day course of intravenous antibiotic therapy is recommended in most uncomplicated cases. It has been recommended that PN be temporarily discontinued in the setting of a newly diagnosed CRBSI; the optimal number of days of discontinuation remains uncertain. Although CVC removal and replacement may be required as part of the treatment plan, repeated line removal and replacement procedures can threaten vascular access over time [7]. As such, for those patients on HPN and/or those who have existing vascular access challenges, an attempt at catheter salvage should be entertained. Catheter salvage success is primarily dependent on the culprit organism and therapeutic susceptibilities [5]. In a recent review and metaanalysis evaluating CVC salvage in adult patients on HPN, it was found that successful catheter salvage rates were highest in patients with coagulase-negative staphylococci followed by Gram-negative bacteria, while the lowest rates of successful catheter salvage were seen in patients with S. aureus and polymicrobial infections [8]. One technique for CVC salvage, as well as CRBSI prevention, has been the use of antibiotic lock therapy [5][9][10]. Attempted catheter salvage is not recommended for critically ill, unstable patients or those with fungal line infections [11]. Use of ethanol lock as a preventative and salvage agent has gained recent interest as an alternative to an antibiotic lock [12]. The decision to attempt line salvage may best be made with input from an Infectious Diseases specialist.
In addition to CRBSI, infection of the catheter tunnel and exit site can occur. Infections at the exit site generally present with purulent drainage, while tunnel infections manifest with erythema and tenderness along the catheter tunnel tract [13]. If drainage is present, culture of the site can be obtained to help target antimicrobial therapy. Exit-site infections often resolve with systemic antibiotics, and line removal can often be avoided. In contrast, infections of the catheter tunnel necessitate removal of the line in addition to systemic antibiotic treatment [13].
Deep venous thrombosis (DVT) is another common complication of indwelling CVCs. The reported incidence of this complication is variable due to the heterogeneity of the literature. Some studies suggest an incidence as high as 67%, while more recent studies report a rate of 14–18% [14][15]. Symptomatic DVT occurs less often, 1–5% of patients with a CVC, and may present with a variety of symptoms, including phlebitis, swelling, and catheter malfunction, depending on the severity of the thrombosis [16][17]. Risk factors for thrombus formation include catheter type, insertion site, tip location, and underlying patient factors such as the presence of a hypercoagulable state (e.g., malignancy, sepsis, critical illness, thrombophilia), prior venous thromboembolism, and concomitant use of certain medications such as oral contraceptives or hormone replacement therapies [15][18]. Several studies have shown that PICCs carry a higher risk for thrombosis compared to tunneled and subcutaneously implanted CVCs [19][20][21]. Other catheter-related factors that increase the risk of thrombosis include larger catheter diameter, tip location proximal to the superior vena cava, and access site, with femoral location being the highest risk [15]. Duplex ultrasonography typically is the diagnostic test of choice; however, venography is an option when suspicion remains high despite a negative ultrasound evaluation. Anticoagulation is typically recommended for the treatment of DVT when found; however, the duration may vary depending on other clinical circumstances [22][23][24]. Several guidelines suggest that CVCs can remain in place despite thrombus formation if the line is still needed, functional, well positioned, not infected, and symptom resolution occurs (if present) [22][25].
Damage to or deterioration of CVCs may occur over time due to normal wear and tear with prolonged use, repeated clamping, or use of high-pressure flushing in occluded catheters [26]. Catheter fracture may be minor, involving only the external sheath, or can involve full rupture of the catheter. Because repeated CVC loss can compromise vascular access over time, catheter salvage, when possible, should be considered. For catheters with minor damage involving the external sheath, catheter repair kits are available. This procedure can be done in the office by a trained provider. Data are emerging that repair is safe and can prolong the longevity of the CVC [26][27].

2. HEN Complications

Patients receiving HEN may develop complications related to the tube or tube feeding. Although some complications are universal for each tube type and route of access (e.g., nasoenteral, percutaneous), including the risk of clogging and accidental displacement, each type of access also carries its own unique complications [28]. In the HEN scenario, placement of a percutaneous tube, either gastrostomy or jejunostomy, is more suitable than nasoenteral placement for obvious aesthetic and comfort reasons.
Percutaneous tube complications can result from their placement or subsequent long-term use. While the majority of complications related to percutaneous tube placement are minor, major complications may occur in up to 4% of procedures [29]. Potential problems during and after percutaneous placement include perforation/injury to surrounding organs, wound infection, hemorrhage, leakage at the tube site, and buried bumper syndrome.
Infection is one of the most common complications of percutaneous feeding tubes, ranging from 12 to 32% in gastrostomy tubes [30]. Infection can occur at any time after placement. Most infections are minor and typically present with symptoms of tenderness, erythema, and purulent drainage at the stoma site. Sometimes, however, it can be difficult to discern infection from other non-infectious causes of peristomal irritation. To help address this diagnostic dilemma, Mundi et al. have proposed objective criteria to help systematically evaluate patients for peristomal infections [31]. These criteria include an assessment of erythema, induration, and exudate at the stoma site, culminating in a score for risk stratification of the patient. Culture of the peristomal drainage is generally not advised as it typically includes skin contaminants. Treatment of peristomal infections with antibiotics, administered either orally or via the tube, is usually successful and hospitalization or use of intravenous antibiotics is uncommon. The tube rarely needs to be removed to facilitate infection control. Risk factors that predispose to the development of peristomal infection include underlying immune suppression and increased pressure from the bolster or traction on the tube [32]. Studies have shown that antibiotic prophylaxis given at the time of initial tube placement can reduce the incidence of peristomal infections [33].
Bleeding complications have been reported in up to 3% of percutaneous tube placement procedures [34]. Immediate postprocedural bleeding can result from injury to an abdominal wall vessel or originate within the tract itself, while delayed bleeding is usually related to gastric mucosal ulceration from a tight internal bumper. Other rare bleeding complications from percutaneous gastrostomy tubes that have been reported include rectus sheath hematoma, esophageal ulceration, intraabdominal vascular injury, and abdominal wall pseudoaneurysm formation [35][36][37][38][39]. Bleeding may manifest as oozing at the tube site or through the tube itself, hematemesis, melena, anemia, or hemodynamic instability [32]. Depending on the severity of bleeding, management may include applying external pressure or temporarily tightening the external bolster against the skin for a tamponade effect for peristomal oozing, or may require endoscopic, radiologic, or surgical intervention. For patients who use chronic antiplatelet and/or anticoagulant agents, guidelines put forth by the American Society of Gastrointestinal Endoscopy advise on length of medication held prior to tube placement [40].
Inadvertent feeding tube removal occurs in up to 12.8% of patients and can result from accidental traction applied to the tube or, in the case when an internal balloon bolster is present, if the balloon breaks and is no longer able to secure the tube in place [41]. If dislodgement of the tube occurs prior to tract maturation, which can take approximately 4 weeks, blind replacement should not be attempted due to the high risk of a misplaced tube as the stomach and abdominal wall may have separated. Patients should be treated with antibiotic therapy and monitored for peritonitis. If symptoms of peritonitis develop, surgical consultation should be requested. In asymptomatic patients, a new tube can be placed after a few days of monitoring. Immediate replacement, either endoscopically or radiologically, after inadvertent removal has also been reported but should be decided based on the individual clinical circumstances [42][43].
Percutaneous tube malposition and injury to internal organs can occur during tube placement. Reported injuries have involved the colon, small bowel, liver, and spleen [44]. Diagnosis can usually be achieved using computed tomography or fluoroscopic imaging with oral contrast or contrast injected through the tube [45]. In addition to malposition, in patients who have gastrojejunal tubes, the distal tip of the jejunal extension may displace back into the stomach. This frustrating, often recurrent, problem can be managed by tube repositioning and clipping into place or removal and replacement with a jejunostomy tube. Finally, buried bumper syndrome is an uncommon complication of percutaneous feeding tubes where the internal tube fixation device migrates into or through the abdominal wall. The estimated incidence of this complication is between 0.3 and 2.4% and often is related to increased tension between the external and internal bolsters [46]. Presenting symptoms can include pain with inability to manipulate the tube, leakage around the tube, and loss of tube patency and complications including bleeding, abscess, peritonitis, and perforation may occur. Endoscopic evaluation is sometimes needed to determine the depth of tube migration and most appropriate treatment option [46].
In addition to tube complications, it is also important to consider the potential gastrointestinal symptoms that can occur because of EN. Patients may develop bloating, diarrhea, constipation, flatulence, nausea, vomiting, and reflux. Some patients experience aspiration of tube feeding. These symptoms can limit a patient’s ability to tolerate EN and lead to undernourishment. The CAFANE study sought to evaluate variables that would impact the risk of these adverse events for patients receiving HEN and determined that type of enteral formula and route of administration were important contributing factors [47]. A variety of strategies may be helpful in mitigating these GI symptoms and include adjusting the infusion rate of enteral feeds, changing the enteral formula, and using medications such as antacids or antidiarrheals where appropriate.
Finally, inappropriate handling of the formula may lead to contamination or spoilage [48]. In order to prevent this from occurring, patients should be educated on appropriate formula handling and storage. Using effective hand hygiene during EN preparation and administration is crucial. Not only has a correlation been shown between healthcare staff hand cultures and EN contamination in the hospital setting, but there was also a reduction in contamination for patients who received an infection control program [49]. Other important strategies include using a clean workspace for EN preparation and using equipment dedicated only for EN use. Storing the EN formula according to the manufacturer’s instruction, following recommended hang times when using an open system, and avoiding “topping off” remaining formula can also reduce complications related to formula contamination or spoilage [50].

3. Intestinal-Failure-Associated Liver Disease

Intestinal-failure-associated liver disease (IFALD) describes patients with chronic intestinal failure, usually receiving long-term PN, who develop liver dysfunction. Patterns of liver injury include steatosis, cholestasis, or a combination of these [51]. Cholelithiasis and gallbladder sludge are also common. The diagnosis should be based on the presence of abnormal liver biochemical tests and/or evidence of radiological and/or histological liver abnormalities occurring in an individual with intestinal failure, in the absence of another cause [52]. Risk factors for IFALD include overfeeding, type and amount of intravenous lipid emulsion administered, duration of PN use, lack of enteral stimulation, and recurrent sepsis [51]. Optimizing the PN formula, using non-soy-based lipid emulsions and limiting the amount of intravenous lipid to <1 g/kg/day, encouraging oral intake/enteral stimulation, normalizing micronutrients, and cycling the delivery of PN are all recommended to prevent and treat IFALD [53]. For those with refractory liver injury in the setting of intestinal failure, combined intestine-liver transplantation may be needed.

4. Metabolic Bone Disease

As mentioned previously, patients receiving chronic PN and EN are at risk of developing metabolic bone diseases including osteomalacia, osteopenia, and osteoporosis. Bone loss in patients on chronic HPN may be related to the nutrient composition of the PN with an often-negative calcium balance and vitamin D deficiency [54][55]. Other factors that may contribute or predispose patients to this condition include previously existing metabolic bone disease, malabsorption, medications such as corticosteroid use, and hypercalciuria [56][57]. Regular screening with DXA can help identify patients with metabolic bone disease and determine when treatment with specific osteoporosis therapy is appropriate [58].

5. Fluid and Electrolyte Derangements

Fluid disturbance can present as either hypovolemia/dehydration or hypervolemia. Patients at risk for developing dehydration are those with increased GI losses, intestinal malabsorption, fluid restrictions, advanced age, or altered mental status [54][59]. For those who have underlying cardiac, liver, or renal disease, hypervolemia may be of more concern [60]. It is important for patients and their caregivers to be educated on monitoring fluid intake and output and signs and symptoms of dehydration and fluid overload. Nutrition support can be adjusted to help optimize the fluid balance by changing fluid volume administered, adjusting the formula and/or electrolyte content administered, and using medications and/or supplemental oral rehydration solution or parenteral fluids when appropriate [54].
Electrolyte derangements, particularly involving sodium, potassium, magnesium, and phosphorus, are common in the setting of HPEN, especially in the early stages of therapy. Electrolytes are involved in several essential bodily functions and when derangements are severe, there can be significant clinical consequences including fatality [61]. Several factors can contribute to electrolyte abnormalities such as renal function, underlying disease process, changes in disease acuity, and medications [54]. A comprehensive understanding of these complex processes is required to effectively manage electrolytes. As noted previously, routine laboratory monitoring allows identification and correction of any disturbances that might occur. This can be done more frequently when first starting EN or PN or when making changes to the formula. Once stabilization of electrolyte levels has been established, the monitoring interval can be spaced out.

6. Vitamin and Trace Element Disturbances

Micronutrient deficiencies are encountered regularly in patients receiving HPEN; however, they are often clinically silent. Thus, a high index of clinical suspicion and periodic laboratory monitoring is needed to identify, as mentioned previously. Since the introduction of home PN infusions, commercially available lipid, multivitamin, and trace element preparations have undergone substantial modifications in order to provide the essential nutrients and reduce the potential for micronutrient deficiencies. Consequently, micronutrient deficiencies described in the early years of PN such as iron, selenium, copper, zinc, thiamine, copper, vitamin A, vitamin E, vitamin D, and essential fatty acid are now less common. Importantly, most commercial trace element solutions only provide the recommended daily nutrient need without consideration of replacement of deficient micronutrient stores, and additional supplementation may be necessary. In addition, when HPN patients are completely or incompletely weaned from PN, they are at risk for developing deficiencies as determined by their underlying bowel condition and clinical status, and life-long oral supplementation and monitoring of micronutrient levels are necessary. This is particularly important considering recent shortages in parenteral individual and MTE preparations available for use in PN.
Manganese toxicity is a rare complication that can occur with long-term HPN use and can lead to accumulation in various organs over time such as the liver, brain, and bone [62]. Neurotoxicity from hypermanganesemia is well documented with patients exhibiting symptoms including motor function deficits, mood destabilization, and cognitive impairment. The recent availability of a multiple trace element product for PN that does not contain manganese may lower the risk of this complication, but periodic monitoring is still recommended.

7. Refeeding Syndrome

As alluded to previously, refeeding syndrome can be defined as metabolic and electrolyte alterations occurring because of the reintroduction and/or increased provision of calories after a period of decreased or absent caloric intake [63]. Refeeding syndrome can be life threatening and is a risk for patients receiving both PN and EN. Because there is no standardized definition, the true incidence is uncertain [64]. Hypophosphatemia, hypokalemia, and hypomagnesemia are the classical electrolyte disturbances that occur in refeeding syndrome, although patients may also develop thiamine deficiency and alterations in fluid, glucose, protein, and fat metabolism [65]. Several risk factors for the development of refeeding syndrome have been identified and include low body mass index, unintentional weight loss of at least 10–15% body weight, little or no nutritional intake, and low levels of potassium, phosphate, or magnesium prior to initiation of nutrition support (Table 1) [66]. Recommendations on how to reduce the risk of refeeding syndrome include gradually initiating and advancing the nutrition support along with adequate monitoring and replacement of electrolytes [66][67][68][69]. Importantly, patients at risk of refeeding syndrome should also receive thiamine supplementation, and electrolyte deficiencies should be repleted both prior to and after initiation of feeding. If refeeding syndrome does occur, nutrition and fluid administration should be reduced, and metabolic derangements addressed prior to advancing the formula [70].
Table 1. Risk factors for refeeding syndrome.
  • BMI < 18.5
  • Unintentional weight loss > 10% of total body weight
  • Little or no nutritional intake
  • Low levels of potassium, magnesium, or phosphate prior to feeding
  • Comorbidities that predispose to malnutrition including anorexia nervosa, malignancy, advanced age, alcohol/substance misuse or abuse

This entry is adapted from the peer-reviewed paper 10.3390/nu14132558

References

  1. Corrigan, M.L.; Pogatschnik, C.; Konrad, D.; Kirby, D.F. Hospital readmissions for catheter-related bloodstream infection and use of ethanol lock therapy: Comparison of patients receiving parenteral nutrition or intravenous fluids in the home vs a skilled nursing facility. J. Parenter. Enter. Nutr. 2013, 37, 81–84.
  2. Rosenthal, V.D.; Al-Abdely, H.M.; El-Kholy, A.A.; AlKhawaja, S.A.A.; Leblebicioglu, H.; Mehta, Y.; Rai, V.; Hung, N.V.; Kanj, S.S.; Salama, M.F.; et al. International nosocomial infection control consortium report, data summary of 50 countries for 2010-2015: Device-associated module. Am. J. Infect. Control. 2016, 44, 1495–1504.
  3. Dreesen, M.; Foulon, V.; Spriet, I.; Goossens, G.A.; Hiele, M.; De Pourcq, L.; Willems, L. Epidemiology of catheter-related infections in adult patients receiving home parenteral nutrition: A systematic review. Clin. Nutr. 2013, 32, 16–26.
  4. Kornbau, C.; Lee, K.C.; Hughes, G.D.; Firstenberg, M.S. Central line complications. Int. J. Crit. Illn. Inj. Sci. 2015, 5, 170–178.
  5. Dibb, M.J.; Abraham, A.; Chadwick, P.R.; Shaffer, J.L.; Teubner, A.; Carlson, G.L.; Lal, S. Central venous catheter salvage in home parenteral nutrition catheter-related bloodstream infections: Long-term safety and efficacy data. J. Parenter. Enter. Nutr. 2016, 40, 699–704.
  6. Mermel, L.A.; Allon, M.; Bouza, E.; Craven, D.E.; Flynn, P.; O’Grady, N.P.; Raad, I.I.; Rijnders, B.J.; Sherertz, R.J.; Warren, D.K. Clinical practice guidelines for the diagnosis and management of intravascular catheter-related infection: 2009 Update by the Infectious Diseases Society of America. Clin. Infect. Dis. 2009, 49, 1–45.
  7. Varayil, J.E.; Whitaker, J.A.; Okano, A.; Carnell, J.J.; Davidson, J.B.; Enzler, M.J.; Kelly, D.G.; Mundi, M.S.; Hurt, R.T. Catheter salvage after catheter-related bloodsream infection during home parenteral nutrition. J. Parenter. Enter. Nutr. 2017, 41, 481–488.
  8. Gompelman, M.; Paus, C.; Bond, A.; Akkermans, R.P.; Bleeker-Rovers, C.P.; Lal, S.; Wanten, G.J.A. Comparing success rates in central venous catheter salvage for catheter-related bloodstream infections in adult patients on home parenteral nutrition: A systematic review and meta-analysis. Am. J. Clin. Nutr. 2021, 114, 1173–1188.
  9. Snaterse, M.; Ruger, W.; Scholte Op Reimer, W.J.; Lucas, C. Antibiotic-based catheter lock solutions for prevention of catheter-related bloodstream infection: A systematic review of randomised controlled trials. J. Hosp. Infect. 2010, 75, 1–11.
  10. Zacharioudakis, I.M.; Zervou, F.N.; Arvanitis, M.; Ziakas, P.D.; Mermel, L.A.; Mylonakis, E. Antimicrobial lock solutions as a method to prevent central line-associated bloodstream infections: A meta-analysis of randomized controlled trials. Clin. Infect. Dis. 2014, 59, 1741–1749.
  11. Guenezan, J.; Drugeon, B.; Marjanovic, N.; Mimoz, O. Treatment of central line-associated bloodstream infections. Crit. Care 2018, 22, 303.
  12. Zhang, J.; Wang, B.; Wang, J.; Yang, Q. Ethanol locks for the prevention of catheter-related infection in patients with central venous catheter: A systematic review and meta-analysis of randomized controlled trials. PLoS ONE 2019, 14, e0222408.
  13. DiBaise, J.K.; Scolapio, J.S. Home parenteral and enteral nutrition. Gastroenterol. Clin. N. Am. 2007, 36, 123–144.
  14. Rooden, C.J.; Tesselaar, M.E.; Osanto, S.; Rosendaal, F.R.; Huisman, M.V. Deep vein thrombosis associated with central venous catheters—A review. J. Thromb. Haemost. 2005, 3, 2409–2419.
  15. Wall, C.; Moore, J.; Thachil, J. Catheter-related thrombosis: A practical approach. J. Intensive Care Soc. 2016, 17, 160–167.
  16. Geerts, W. Central venous catheter-related thrombosis. Hematol. Am. Soc. Hematol. Educ. Program. 2014, 2014, 306–311.
  17. Citla Sridhar, D.; Abou-Ismail, M.Y.; Ahuja, S.P. Central venous catheter-related thrombosis in children and adults. Thromb. Res. 2020, 187, 103–112.
  18. Saber, W.; Moua, T.; Williams, E.C.; Verso, M.; Agnelli, G.; Couban, S.; Young, A.; De Cicco, M.; Biffi, R.; van Rooden, C.J.; et al. Risk factors for catheter-related thrombosis (CRT) in cancer patients: A patient-level data (IPD) meta-analysis of clinical trials and prospective studies. J. Thromb. Haemost. 2011, 9, 312–319.
  19. Chopra, V.; Anand, S.; Hickner, A.; Buist, M.; Rogers, M.A.; Saint, S.; Flanders, S.A. Risk of venous thromboembolism associated with peripherally inserted central catheters: A systematic review and meta-analysis. Lancet 2013, 382, 311–325.
  20. Winters, J.P.; Callas, P.W.; Cushman, M.; Repp, A.B.; Zakai, N.A. Central venous catheters and upper extremity deep vein thrombosis in medical inpatients: The Medical Inpatients and Thrombosis (MITH) Study. J. Thromb. Haemost. 2015, 13, 2155–2160.
  21. Bonizzoli, M.; Batacchi, S.; Cianchi, G.; Zagli, G.; Lapi, F.; Tucci, V.; Martini, G.; Di Valvasone, S.; Peris, A. Peripherally inserted central venous catheters and central venous catheters related thrombosis in post-critical patients. Intensive Care Med. 2011, 37, 284–289.
  22. Kearon, C.; Akl, E.A.; Comerota, A.J.; Prandoni, P.; Bounameaux, H.; Goldhaber, S.Z.; Nelson, M.E.; Wells, P.S.; Gould, M.K.; Dentali, F.; et al. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012, 141, e419S–e496S.
  23. Kearon, C.; Akl, E.A.; Ornelas, J.; Blaivas, A.; Jimenez, D.; Bounameaux, H.; Huisman, M.; King, C.S.; Morris, T.A.; Sood, N.; et al. Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report. Chest 2016, 149, 315–352.
  24. Debourdeau, P.; Farge, D.; Beckers, M.; Baglin, C.; Bauersachs, R.M.; Brenner, B.; Brilhante, D.; Falanga, A.; Gerotzafias, G.T.; Haim, N.; et al. International clinical practice guidelines for the treatment and prophylaxis of thrombosis associated with central venous catheters in patients with cancer. J. Thromb. Haemost. 2013, 11, 71–80.
  25. Farge, D.; Bounameaux, H.; Brenner, B.; Cajfinger, F.; Debourdeau, P.; Khorana, A.A.; Pabinger, I.; Solymoss, S.; Douketis, J.; Kakkar, A. International clinical practice guidelines including guidance for direct oral anticoagulants in the treatment and prophylaxis of venous thromboembolism in patients with cancer. Lancet Oncol. 2016, 17, e452–e466.
  26. Wouters, Y.; Vissers, R.K.; Groenewoud, H.; Kievit, W.; Wanten, G.J.A. Repair of damaged central venous catheters is safe and doubles catheter survival: A home parenteral nutrition patient cohort study. Clin. Nutr. 2019, 38, 1692–1699.
  27. Velapati, S.R.; Schroeder, S.; Kuchkuntla, A.R.; Salonen, B.R.; Bonnes, S.L.; Hurt, R.T.; Mundi, M.S. Repair of Central Venous Catheter in a Single-Center Adult Home Parenteral Nutrition Cohort. J. Parenter. Enter. Nutr. 2020, 44, 265–273.
  28. DeLegge, M.H. Enteral access and associated complications. Gastroenterol. Clin. N. Am. 2018, 47, 23–37.
  29. McClave, S.A.; Chang, W.K. Complications of enteral access. Gastrointest. Endosc. 2003, 58, 739–751.
  30. Lim-Teodoro, A.; Sarita, M.A.; Semeniano, R.; Ramos, M., Jr. Incidence of percutaneous endoscopic gastrostomy site wound infection among frail elderly patients admitted in a tertiary medical center. J. Infect. Dis. Epidemiol. 2019, 5, 89.
  31. Mundi, M.S.; Seegmiller, S.; Davidson, J.; Schneckloth, J.; Saied, J.; Hurt, R.T. Prospective Assessment of Peristomal Infections Using Objective Criteria. J. Parenter. Enter. Nutr. 2018, 42, 877–884.
  32. Hucl, T.; Spicak, J. Complications of percutaneous endoscopic gastrostomy. Best Pract. Res. Clin. Gastroenterol. 2016, 30, 769–781.
  33. Sharma, V.K.; Howden, C.W. Meta-analysis of randomized, controlled trials of antibiotic prophylaxis before percutaneous endoscopic gastrostomy. Am. J. Gastroenterol. 2000, 95, 3133–3136.
  34. Seo, N.; Shin, J.H.; Ko, G.Y.; Yoon, H.K.; Gwon, D.I.; Kim, J.H.; Sung, K.B. Incidence and management of bleeding complications following percutaneous radiologic gastrostomy. Korean J. Radiol. 2012, 13, 174–181.
  35. Lau, G.; Lai, S.H. Fatal retroperitoneal haemorrhage: An unusual complication of percutaneous endoscopic gastrostomy. Forensic. Sci. Int. 2001, 116, 69–75.
  36. Sekmenli, T.; Gunduz, M.; Akbulut, H.; Emiroglu, H.; Koplay, M.; Ciftci, I. Massive hemorrhage: A late complication of replacement percutaneous endoscopic gastrostomy: Case report. Arch. Argent. Pediatr. 2018, 116, e315–e318.
  37. Lee, S.H.; Moon, H.S.; Park, J.H.; Kim, J.S.; Kang, S.H.; Lee, E.S.; Kim, S.H.; Sung, J.K.; Lee, B.S.; Jeong, H.Y. Percutaneous endoscopic gastrostomy tube insertion-induced superior mesenteric artery injury treated with angiography. Korean J. Gastroenterol. 2018, 72, 308–312.
  38. Ubogu, E.E.; Zaidat, O.O. Rectus sheath hematoma complicating percutaneous endoscopic gastrostomy. Surg. Laparosc. Endosc. Percutan. Tech. 2002, 12, 430–432.
  39. Fujita, T.; Tanabe, M.; Iida, E.; Matsunaga, N.; Ito, K. Successful percutaneous treatment for massive hemorrhage due to infectious pseudoaneurysm in the abdominal wall after percutaneous endoscopic gastrostomy: A case report. BMC Res. Notes 2014, 7, 354.
  40. Committee, A.S.O.P.; Acosta, R.D.; Abraham, N.S.; Chandrasekhara, V.; Chathadi, K.V.; Early, D.S.; Eloubeidi, M.A.; Evans, J.A.; Faulx, A.L.; Fisher, D.A.; et al. The management of antithrombotic agents for patients undergoing GI endoscopy. Gastrointest. Endosc. 2016, 83, 3–16.
  41. Rosenberger, L.H.; Guidry, C.A.; Davis, J.P.; Hranjec, T.; Johnston, V.K.; Wages, N.A.; Watson, C.M.; Sawyer, R.G. Reducing accidental dislodgement of the percutaneous endoscopic gastrostomy: A prospective trial of the “safetybreak” device. Surg. Innov. 2016, 23, 62–69.
  42. Galat, S.A.; Gerig, K.D.; Porter, J.A.; Slezak, F.A. Management of premature removal of the percutaneous gastrostomy. Am. Surg. 1990, 56, 733–736.
  43. Soliman, Y.; Kurchin, A.; Devgun, S. ‘Re-PEGing’: An endoscopic approach to inadvertent early removal of PEG tube. J. Community Hosp. Intern. Med. Perspect. 2020, 10, 194–198.
  44. Rahnemai-Azar, A.A.; Rahnemaiazar, A.A.; Naghshizadian, R.; Kurtz, A.; Farkas, D.T. Percutaneous endoscopic gastrostomy: Indications, technique, complications and management. World J. Gastroenterol. 2014, 20, 7739–7751.
  45. Milanchi, S.; Wilson, M.T. Malposition of percutaneous endoscopic-guided gastrostomy: Guideline and management. J. Minim. Access Surg. 2008, 4, 1–4.
  46. Cyrany, J.; Rejchrt, S.; Kopacova, M.; Bures, J. Buried bumper syndrome: A complication of percutaneous endoscopic gastrostomy. World J. Gastroenterol. 2016, 22, 618–627.
  47. Wanden-Berghe, C.; Patino-Alonso, M.C.; Galindo-Villardon, P.; Sanz-Valero, J. Complications Associated with Enteral Nutrition: CAFANE Study. Nutrients 2019, 11, 2041.
  48. Darlene, G.; Kelly, J.K.D.; Megan, B. Home parenteral and enteral nutrition. In Clinical Management of Intestinal Failure; Christopher, P., Duggan, T.J., Kathleen, M.G., Eds.; CRC Press: Boca Raton, FL, USA, 2011; pp. 419–440.
  49. Ho, S.S.; Tse, M.M.; Boost, M.V. Effect of an infection control programme on bacterial contamination of enteral feed in nursing homes. J. Hosp. Infect. 2012, 82, 49–55.
  50. Boullata, J.I.; Carrera, A.L.; Harvey, L.; Escuro, A.A.; Hudson, L.; Mays, A.; McGinnis, C.; Wessel, J.J.; Bajpai, S.; Beebe, M.L.; et al. ASPEN safe practices for enteral nutrition therapy . J. Parenter. Enter. Nutr. 2017, 41, 15–103.
  51. Nowak, K. Parenteral nutrition-associated liver disease. Clin. Liver Dis. 2020, 15, 59–62.
  52. Lal, S.; Pironi, L.; Wanten, G.; Arends, J.; Bozzetti, F.; Cuerda, C.; Joly, F.; Kelly, D.; Staun, M.; Szczepanek, K.; et al. Clinical approach to the management of Intestinal Failure Associated Liver Disease (IFALD) in adults: A position paper from the Home Artificial Nutrition and Chronic Intestinal Failure Special Interest Group of ESPEN. Clin. Nutr. 2018, 37, 1794–1797.
  53. Woodward, J.M.; Massey, D.; Sharkey, L. The Long and Short of IT: Intestinal failure-associated liver disease (IFALD) in adults-recommendations for early diagnosis and intestinal transplantation. Frontline Gastroenterol. 2020, 11, 34–39.
  54. Davila, J.; Konrad, D. Metabolic Complications of Home Parenteral Nutrition. Nutr. Clin. Pract. 2017, 32, 753–768.
  55. Haderslev, K.V.; Tjellesen, L.; Haderslev, P.H.; Staun, M. Assessment of the longitudinal changes in bone mineral density in patients receiving home parenteral nutrition. J. Parenter. Enter. Nutr. 2004, 28, 289–294.
  56. Ferrone, M.; Geraci, M. A review of the relationship between parenteral nutrition and metabolic bone disease. Nutr. Clin. Pract. 2007, 22, 329–339.
  57. Seidner, D.L. Parenteral nutrition-associated metabolic bone disease. J. Parenter. Enter. Nutr. 2002, 26, S37–S42.
  58. WHO Scientific Group. Assessment of Osteoporosis a the Primary Health-Care Level; University of Sheffield: Sheffield, UK, 2007; pp. 53–69.
  59. Dickerson, R.N.; Brown, R.O. Long-term enteral nutrition support and the risk of dehydration. Nutr. Clin. Pract. 2005, 20, 646–653.
  60. Metheny, N. Fluid and Electrolyte Disturbances Associated with Tube Feedings. In Fluid and Electrolyte Balance, 5th ed.; Jones & Bartlett LEarning, LLC: Sudbury, MA, USA, 2012; pp. 179–189.
  61. Rhoda, K.M.; Porter, M.J.; Quintini, C. Fluid and electrolyte management: Putting a plan in motion. J. Parenter. Enter. Nutr. 2011, 35, 675–685.
  62. Hamdan, M.; Puckett, Y. Total parenteral nutrition. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2022.
  63. Da Silva, J.S.V.; Seres, D.S.; Sabino, K.; Adams, S.C.; Berdahl, G.J.; Citty, S.W.; Cober, M.P.; Evans, D.C.; Greaves, J.R.; Gura, K.M.; et al. ASPEN consensus recommendations for refeeding syndrome. Nutr. Clin. Pract. 2020, 35, 178–195.
  64. Braun, K.; Utech, A.; Velez, M.E.; Walker, R. Parenteral Nutrition Electrolyte Abnormalities and Associated Factors Before and After Nutrition Support Team Initiation. J. Parenter. Enter. Nutr. 2018, 42, 387–392.
  65. Friedli, N.; Odermatt, J.; Reber, E.; Schuetz, P.; Stanga, Z. Refeeding syndrome: Update and clinical advice for prevention, diagnosis and treatment. Curr. Opin. Gastroenterol. 2020, 36, 136–140.
  66. Nutrition Support for Adults: Oral Nutrition Support, Enteral Tube Feeding and Parenteral Nutrition Clinical Guideline . Available online: https://www.nice.org.uk/guidance/cg32 (accessed on 13 March 2022).
  67. Boland, K.; Solanki, D.; O’Hanlon, C. Prevention and Treatment of Refeeding Syndrome in the Acute Care Setting. Available online: https://www.irspen.ie/professional-resources-2/irspen-professional-resources/ (accessed on 14 March 2022).
  68. McCray, S.; Parrish, C.R. Refeeding the malnourished patient: Lessons learned. Pract. Gastroenterol. 2016, 155, 56–66.
  69. Mehanna, H.M.; Moledina, J.; Travis, J. Refeeding syndrome: What it is, and how to prevent and treat it. BMJ 2008, 336, 1495–1498.
  70. Friedli, N.; Stanga, Z.; Culkin, A.; Crook, M.; Laviano, A.; Sobotka, L.; Kressig, R.W.; Kondrup, J.; Mueller, B.; Schuetz, P. Management and prevention of refeeding syndrome in medical inpatients: An evidence-based and consensus-supported algorithm. Nutrition 2018, 47, 13–20.
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