Intestinal Failure
Intestinal failure (IF) was first described in 1981 by Fleming and Remington as the “reduction in gut mass resulting in the loss of the ability of digestion and absorption of food molecules
Functional Classification
Basis of onset, metabolic, and expected outcome criteria.
Type 1 transient intestinal failure
Type 2 long-term intestinal failure
Type 3 chronic intestinal failure
Type 1. Transient, frequent, usually self-limiting, lasting less than 28 days but may need treatment, supplementation or nutritional support. Ileus, by far the most frequently encountered version of IF, may be minimized, but there is no widely accepted single treatment for this commonly seen phenomenon amongst general surgeons. ex: post-operative ileus
Type 2. This type is severe, often complex and longer-term and requires nutritional support during expectant or conservative management. This type may arise from acute episodes of medical illness but increasingly from surgery or surgical complications. The outcome from this situation may include complete recovery, but the course of disease, treatment and restoration of function takes more than 28 days and should involve a multimodal, phasic approach and wherever possible, a multi-disciplinary team. This type of IF is of most interest to general surgeons since surgery is often pivotal in the etiology, stabilization and the ultimate rectification of the problem. Surgical issues giving rise to type 2 IF are anastomotic leak and ensuing sepsis, extensive resections for ischemia or trauma or entero-cutaneous fistulas arising from intraoperative bowel injury.
Surgical injuries resulting in short gut and high output stomas or fistulas are common causes for Type 2 IF
Type 3(chronic intestinal failure (CIF)
. This type describes a more chronic situation where the causative pathology or event has been stabilized or is slow-moving. Supplementation or chronic parenteral nutrition is required. It may be irreversible. Type 2 may progress to Type 3.
2016 ESPEN guideline statements for treatment of chronic intestinal failure with STRONG recommendations
| Statement of recommendation | Grade of evidence |
|---|---|
| Management of home parenteral nutrition for benign chronic intestinal failure | |
| 1. An HPN program should include evidence-based therapy, prevent HPN-related complications, and maximize quality of life. | Very low |
| 2. Perform regular audit of therapy and outcomes against standards to ensure safety and efficacy of HPN program. | Very low |
| 3. Patients selected for an HPN program should have confirmed intestinal failure that despite maximal medical therapy would lead to deterioration of nutrition and/or fluid status. | Very low |
| 4. Prior to discharge, patients should be metabolically stable, able to physically and emotionally cope with the HPN therapy, and have an adequate home environment | Very low |
| 5. HPN patients should have access to infusion pumps or devices with specified safety features together with ancillary products, safe compounding and delivery systems. | Very low |
| 6. Patient/caregiver training for HPN management should be patient-centered with a multidisciplinary approach, together with written guidelines. HPN training may take place in hospital or at home | Very low |
| 7. Regular contact by the HPN team with patients should occur, scheduled according to patients’ clinical requirements. | Very low |
| 8. Lab testing should be done on a regular basis using appropriate tests and timing relative to PN infusion. | Very low |
| 9. Quality of life for HPN patients should be regularly measured using validated tools as part of standard clinical care. Quality of care should be assessed regularly according to recognized criteria. | Very low |
| 10. A multidisciplinary team with skills and experience in intestinal failure and HPN management should care for CIF patients. | Very low |
| Parenteral nutrition formulation | |
| 11. Protein and energy requirements for CIF patients should be based on individual patient characteristics and specific needs and the adequacy of the regimen should regularly be evaluated through clinical, anthropometric, and biochemical parameters. | Very low |
| 12. HPN patients should have optimal blood glucose control, based on blood glucose <180 mg/dl (10.0 mmol/L) during HPN infusion and normal HbA1c levels (if diabetic), through regular monitoring. | Very low |
| 13. Insulin should not be added to HPN admixtures due to lack of evidence-based data regarding insulin prescription for HPN patients who have hyperglycemia. | Very low |
| 14. Regular monitoring should be performed for signs and symptoms of dehydration, fluid balance, laboratory tests, and 24-h urine output as well as a timely adjustment of fluid supplementation to prevent chronic renal failure. | Very low |
| 15. The HPN formula should be adjusted to normalize laboratory tests related to fluid, electrolytes, and mineral balance. | Very low |
| 16. Regular monitoring of acid-base status should occur in patients on long-term HPN. | Very low |
| 17. Baseline serum vitamin concentrations should be measured at the onset of HPN and then at least once per year. | Very low |
| Intestinal rehabilitation strategy-medical: short bowel syndrome | |
| 18. SBS patients should consume regular whole foods and be encouraged to compensate for malabsorption by hyperphagia. | Low |
| 19. SBS patients with a preserved colon should consume a diet high in complex carbohydrates and low in fat; the fat to carbohydrate ratio seems of less importance in patients without a colon. | Low |
| 20. In SBS patients consuming a low fat diet or where the long-chain triglycerides have been replaced by medium-chain triglycerides, attention should be paid to the potential deficiency in essential fatty acids and fat-soluble vitamins. | Low |
| 21. Do not add soluble fiber (e.g., pectin) to the diet to enhance overall intestinal absorption. | Low |
| 22. Do not add glutamine, probiotics, or other supplements to the diet in the aim of promoting intestinal rehabilitation. | Low |
| 23. Use H2-receptor antagonists or PPIs in reducing fecal wet weight and sodium excretion, especially during the first 6 months after surgery, mainly in those SBS patients with a fecal output exceeding 2 l/day. | Moderate |
| 24. Patients treated with octreotide should be carefully monitored to prevent fluid retention and other adverse events. | Strong |
| 25. Oral loperamide should be used to reduce wet weight and sodium fecal excretion in SBS patients with an ostomy. | Moderate |
| 26. Loperamide is preferred to opiate drugs because it is not addictive or sedative. | Moderate |
| 27. In SBS patients with high ostomy output, the use of loperamide should be guided by objective measurements of effect. | Moderate |
| 28. Consider occasional antibiotic treatment in SBS patients with motility disorders and symptoms of bacterial overgrowth. | Very low |
| 29. Do not use routine antibiotics in SBS patients with a preserved colon. Malabsorbed carbohydrates are fermented to short-chain fatty acids by colonic bacteria and may provide additional energy. | Very low |
| 30. Patients with CIF due to SBS should be carefully informed of the potential benefits and risks associated with growth factor treatments; information should deal with the probability of weaning from HPN, the probability of quality of life improvement, the expected duration of treatment, the expected effects after cessation of the treatment, the potential adverse effects and risks of the treatment, the cost-effectiveness of the treatment, and the need for careful monitoring. | Low |
| 31. The efficacy of growth factor treatment should be evaluated according to standardized protocols measuring fluids, electrolytes, and, whenever possible, energy balance. | Low |
| 32. Intestinal growth factors should only prescribed by experts who are experienced in the diagnosis and management of SBS patients and who have the ability and the facilities to objectively evaluate and balance the benefit and clinical meaningfulness of the interventions versus the inconveniences, adverse effects, potential risks, and cost-effectiveness. | Low |
| 33. Drugs should be prescribed on an individual basis to patients with SBS following a careful evaluation of the absorptive capacity of the remnant bowel, knowledge of the physiochemical characteristics of the drug, and an evaluation as to if the drug can be titrated according to an objectively measured effect or according to measurements of plasma concentrations. The use of parenteral and transdermal routes and the use of suppositories should also be considered in SBS patients with limited intestinal absorption. | Very low |
| Chronic intestinal pseudo-obstruction | |
| 34. In patients with CIPO, no specific diet should be prescribed; patients should eat according to individual tolerance. | Very low |
| 35. HPN should not be delayed in malnourished CIPO patients with chronic gastrointestinal motility dysfunctions when oral/enteral nutrition is obviously inadequate. | Very low |
| 36. Attempt a trial with prokinetics in patients with chronic gastrointestinal motility dysfunctions. | Very low |
| 37. Use antibiotic therapy to treat intestinal bacterial overgrowth and to reduce malabsorption in patients with chronic gastrointestinal motility dysfunctions. | Very low |
| Radiation enteritis | |
| 38. The nutritional regime in chronic radiation enteritis patients follows the same criteria adopted for the HPN of patients with other causes of CIF. | Very low |
| 39. HPN should not be delayed in malnourished radiation enteritis patients if oral nutrition/enteral tube feeding is inadequate. | Very low |
| Intestinal rehabilitation strategy-non-transplant surgery | |
| 40. Bowel length should be conserved to the fullest extent possible to avoid dependence on HPN. | Low |
| 41. In patients with SBS, restoration of intestinal continuity should be realized when possible to decrease HPN. | Moderate |
| 42. When considering non-transplant surgery, bowel-lengthening procedures can be considered in selected SBS patients. | Very low |
| 43. In patients with SBS, management is performed through a multidisciplinary approach. | Low |
| Intestinal transplantation | |
| 44. Consider HPN as the primary treatment for patients with CIF and the early referral of patients to intestinal rehabilitation centers with expertise in both medical and surgical treatment for CIF, to maximize the opportunity of weaning off HPN, prevent HPN failure, and ensure timely assessment of candidacy for intestinal transplant. | Very low |
| 45. Assess candidacy for intestinal transplantation, when one of the following indications exists: 1. Failure of HPN: a. Impending or overt liver failure because of intestinal failure-associated liver disease (IFALD) b. Central venous catheter-related thrombosis of two or more central veins c. Frequent central line sepsis i. Two or more episodes per year of systemic sepsis secondary to line infections requiring hospitalization d. Single episode of line-related fungemia e. Septic shock and/or acute respiratory distress syndrome f. Frequent episodes of severe dehydration despite intravenous fluid in addition to HPN 2. High risk of death attributable to the underlying disease a. Invasive intra-abdominal desmoid tumors b. Congenital mucosal disorders (i.e., microvillus inclusion disease, tufting enteropathy) c. Ultra short bowel syndrome (gastrostomy, duodenostomy, residual small bowel <10 cm in infants, < 20 cm in adults 3. Intestinal failure with high morbidity or low acceptance of HPN a. Need for frequent hospitalization, narcotic dependency, or inability to function b. Patient’s unwillingness to accept long-term HPN (i.e., young patients) | Very low |
| 46. Patients with impending or overt liver failure due to IFALD and those with an invasive intra-abdominal desmoid tumor should be listed for a life-saving intestinal transplantation (with or without liver transplantation). | Very low |
| 47. We do not recommend listing for a life-saving intestinal transplantation of patients with CIF having any of the indications for assessment of candidacy other than IFALD-related liver failure, intra-abdominal desmoids or CVC-related multiple vein thrombosis. | Very low |
| 48. Whenever possible, patients listed for intestinal transplantation should undergo the procedure while they are in stable clinical condition (i.e., not requiring hospitalization while waiting for transplant). For patients listed for a combined intestinal and liver transplantation, the mechanisms to prioritize patients on the waiting list for liver transplantation should be adopted in order to minimize the risk of mortality while on waiting list and after transplantation. | Very low |
| Prevention/treatment of CVC-related complications CVC-related infection | |
| 49. The choice of central venous catheter type and location of exit site be made by a multidisciplinary HPN team, along with an experienced specialist and the patient. | Low |
| 50. Access to the upper vena cava is the first choice for CVC placement, via internal jugular vein or subclavian vein. | Moderate |
| 51. The tip of the catheter should be placed at the level of the right atrial-superior vena cava junction. | Moderate |
| 52. The exit site of the catheter should be easily visualized and accessible for patients doing self-care and the preferred site should be marked by clinicians experienced with HPN. | Low |
| 53. Tunneled central venous catheters or totally implanted devices should be used for long-term HPN. | Very low |
| 54. Do not use PICC lines for expected long-term HPN because of the higher risk of thrombosis and issues related to self-administration of HPN. | Low |
| 55. CVC-related infections should be diagnosed according to current guidelines on catheter-related infections. | Very low |
| 56. CVC-related infections should be managed according to current guidelines on long-term intravascular catheters. | Moderate |
| 57. For prevention of central venous catheter-related infections, consider the following: • Education of staff and patients/caregivers • Implementation of an adequate policy of hand washing and disinfection by patients and staff • Hand washing and disinfection by patient and caregivers before touching central venous catheter as well as after catheter care • Disinfection of the hub connector every time it is accessed • Use of tunneled single-lumen catheters whenever possible • Use of chlorhexidine 2 % for antisepsis of hands, catheter exit site, stopcocks, catheter hubs, and other sampling ports • Regular change of i.v. administration sets | HIgh |
| 58. For prevention of CVC-related infections do NOT use: • In-line filters • Routine replacement of catheters • Antibiotic prophylaxis • Use of heparin lock | Low |
| 59. Do not perform catheter locking with 70 % ethanol to prevent CVC-related infections because its use is associated with systemic toxicity, catheter occlusion and catheter damage. | High |
| 60. In patients who repeatedly present with CVC-related infections, consider re-education of the patient and/or caregiver and/or use of an antimicrobial catheter lock. | Low |
| CVC-related occlusion/thrombosis | |
| 61. Treat HPN patients with CVC-related venous thrombosis with anticoagulation; the duration of this treatment should be chosen on an individual basis and the decision to maintain the catheter be dependent on individual factors. | Low |
| 62. For the primary prevention of CVC-related venous thrombosis, perform insertion of the catheter using ultrasound guidance and placement of the tip at the superior vena cava-right atrium junction. | Low |
| 63. Do not use routine thromboprophylaxis as primary prevention of CVC-related venous thrombosis for all adults | Low |
| Prevention/treatment of intestinal failure-associated liver disease | |
| 64. For prevention of intestinal failure-associated liver disease: • Prevent or manage sepsis if present • Preserve small intestinal length and retain the colon in continuity with small bowel • Maintain oral/enteral intake • Cycle PN • Avoid overfeeding with PN • Limit the dose of soybean-oil based lipid to less than 1 g/kg/day | Low |
| Prevention/treatment of gallbladder sludge and stones | |
| 65. For the treatment of gallbladder sludge and stones, perform cholecystectomy and/ or endoscopic procedures in case of biliary complications as for the general population. | Low |
| Prevention/treatment of intestinal failure-associated renal failure and stones | |
| 66. For the primary prevention of renal failure and of renal stones, perform regular monitoring of renal function and fluid balance as well and adjust fluid supplementation to avoid episodes of dehydration. | Low |
| 67. For the primary prevention of renal failure, acute and chronic infections and dehydration should be addressed. | Low |
| 68. Treat renal failure and renal stones in patients with CIF according to the standards for these conditions. | Very low |
| Prevention/treatment of intestinal failure-associated metabolic bone disease | |
| 69. For routine purposes, the diagnosis of metabolic bone disease is based on a combination of bone densitometry scanning and biochemistry. | Low |
| 70. The HPN population should be routinely monitored for metabolic bone disease by bone densitometry scanning and biochemistry. | Low |
| 71. General risk factors for developing osteoporosis be promptly addressed in all patients on long-term HPN. | Very low |
| 72. The primary step for treatment of metabolic bone disease is to optimize the program for PN with the required supplements of vitamin D, calcium, and phosphate. Further, medical treatment may be useful to increase bone mineral density and lower fracture risk. | Low |
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