Short bowel syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Short bowel syndrome is a malabsorption disorder caused by the surgical removal of the small intestine. Most cases are acquired, although some children are born with a congenital short bowel. It does usually not develop unless a person has lost more than two-thirds of their small intestine. Intestine has the ability to adapt following resection. Adaptation depends on multiple factors including individual, intestinal and therapeutic measurements. Successful adaptation depends on the length of remaining intestine, portion of the resected intestine, and early introduction of nutrition therapy. Total intestinal adaptation defines as when patient is weaned from parenteral nutrition. The hallmark of short bowel syndrome is diarrhea. Complications might happen due to malnutrition, surgery and parenteral nutrition. Management of short bowel syndrome consists of medical and surgical therapy. Medical therapy consists of nutritional therapy and pharmacotherapy. Patients who have severe or worsened malabsorption might require surgery including intestinal transplant. Effective measures must be adopted for secondary prevention of complications following total parenteral nutrition including liver disease, cholelithiasis, kidney stone, small bowel bacterial overgrowth, lactic acidosis, lactic acidosis.

The first successful intestinal resection was performed in 1880. In 1935, Haymond following research on many patients with bowel resection, reported that 30 to 50% loss of bowel was well tolerated. Total parenteral nutrition (TPN) was introduced during 1960s which helped patients to survive following bowel resection.

Based on the length of the remaining bowel, short bowel syndrome may be divided into end-jejunostomy, jejunocolonic anastomosis, ileocolonic anastomosis. Severity varies from mild to severe. All of them require home parenteral nutrition except ileocolonic anastomosis which has excellent prognosis and rarely needs parenteral nutrition. Based on the etiology, short bowel syndrome may be divided into three categories such as vascular abnormalities, mucosal disease of intestine and causes without preexisting intestinal disease.

Short bowel syndrome occurrs as a result of bowel resection following various diseases of the gut such as Crohn’s disease, malignancies, ischemia, and trauma. Short bowel syndrome occurs when the length of the small intestine is less than 2 meters and requires nutritional therapy to prevent malnutrition. Post bowel resection, adaptation might occur which includes structural, motility and functional changes in the remaining intestine. Changes usually start in the first 24 hours following bowel resection and last for about two years. Adaptation depends upon multiple factors including individual, intestinal and therapeutic measurements. Following bowel resection, adaptation occurs in three phases including acute, adaptive, and maintenance phases. Successful adaptation depends on the length of remaining intestine, portion of the resected intestine, and early introduction of nutrition therapy. The term total intestinal adaptation is used when the patient is weaned from parenteral nutrition. The main reason for malabsorption following bowel resection is reduced absorptive capacity of the small intestine due to loss of surface area. On gross and microscopic examination, the resected bowel segment may show the underlying causes including Crohn’s disease, malignancies or ischemia.

Short bowel syndrome in adults is usually caused by surgical removal of the intestine due to different diseases including Crohn’s disease, mesenteric ischemia, malignancies or radiation enteritis. Less common causes include trauma, volvulus, adhesion and iatrogenic surgery on gastrointestinal system.

The incidence and prevalence of short bowel syndrome is difficult to estimate. All the data is derived from patients receiving home parenteral nutrition. Therefore, there are different distributions around the world. The incidence of short bowel syndrome was estimated to be 1-2 cases per 100,000 individuals worldwide per year. The prevalence of short bowel syndrome is approximately 0.3-4 per 100,000 individuals in the USA to 0.1-4 per 100,000 individuals in Europe. It affects all age groups. There is no racial predilection to short bowel syndrome and is reported worldwide. Short bowel syndrome affects men and women equally.

Common risk factor for the development of short bowel syndrome may be iatrogenic including any operation on the gastrointestinal system.

There is insufficient evidence to recommend routine screening for short bowel syndrome.

The symptoms of short bowel syndrome usually develop immediately following bowel resection. Diarrhea may cause massive fluid and electrolyte loss. Immediately after surgery, intestinal adaptation develops in three phases, including acute, adaptive and maintenance phase. During the adaptation, structural, motility and functional changes occur. Patients need hydration and nutritional support via parenteral, enteral and oral routes. Length of remaining small bowel is the most important prognostic factor. Patients with more than 200 cm length of small bowel, usually do not need parenteral nutrition. Patients with shorter small bowel may not wean off from parenteral nutrition support. Complications might occur due to malnutrition, surgery and parenteral nutrition. Malnutrition presents with vitamin, mineral and essential fatty acids deficiencies. Complications related to surgery including thrombosis, infection, hemorrhage, atelectasis and anastomosis disruption might occur. Small intestinal bacterial overgrowth due to stasis and obstruction might also occur. Chronic liver disease following parenteral nutrition is a common complication in short bowel syndrome. There is no definite cure for short bowel syndrome. However, medications and nutritional therapy significantly improve the quality of life and survival of the patients. Prognosis of short bowel syndrome depends on the location and size of the bowel resection, underlying pathology, nutrition support, pharmacotherapy, and extent of intestinal adaptation. The 2 and 5-year survival rate of patients with short bowel syndrome are approximately 80% and 70%, respectively.

Short bowel syndrome is mainly diagnosed based on clinical presentation. There are no established criteria for the diagnosis of short bowel syndrome. History of bowel resection and clinical manifestation including diarrhea and malnutrition would confirm the diagnosis.

The hallmark of short bowel syndrome is diarrhea. A positive history of operation on gastrointestinal system and symptoms of malabsorption is suggestive of short bowel syndrome. The most common symptoms of short bowel syndrome include dehydration, abdominal pain, and fatigue.

Patients with short bowel syndrome usually appear weak and tired. Physical examination of patients with short bowel syndrome is usually remarkable for signs of malabsorption, dehydration and abdominal tenderness.

Laboratory findings consistent with the diagnosis of short bowel syndrome include anemia, hypoalbuminemia, low level of vitamins, minerals, and micronutrients. Level of acute phase reactants is high. Abnormal liver function tests including elevated liver enzymes and bilirubin might be seen. Fluid and electrolyte imbalance might be present. Fecal fat test is usually positive.

There are no ECG findings associated with short bowel syndrome. In case of malnutrition and electrolyte imbalance, an ECG may be helpful. Hypokalemia might present with arrhythmia, ST segment depression, low T wave, prominent U waves and QRS prolongation. Hypocalcemia might present with QT interval prolongation. Hypomagnesemia might present with QT interval prolongation and ventricular and supraventricular arrhythmia.

An abdominal x-ray may be helpful in the diagnosis of short bowel syndrome. Abdominal x-ray helps to rule out ileus or intestinal obstruction. Upper gastrointestinal series might demonstrate strictures and dilation of the bowel.

There are no abnormal echocardiographic findings associated with short bowel syndrome. Ultrasound may be helpful in the diagnosis of complications of short bowel syndrome including gallstones and liver diseases. Doppler ultrasound might be used to diagnose venous thrombosis.

Abdominal CT scan with contrast may be helpful in the diagnosis of short bowel syndrome complications including dilation, obstruction of the bowel and signs of liver diseases.

There are no MRI findings associated with short bowel syndrome.

There are no other imaging findings associated with short bowel syndrome.

There are no other diagnostic studies associated with short bowel syndrome.

Management of short bowel syndrome is complicated and requires close collaboration of all medical team members including the physician, nutritionist, and nurse with the patient and their families. Medical therapy consists of nutritional therapy and pharmacotherapy. Nutritional therapy is essential for short bowel syndrome and to restore the intestinal adaptation. It could be provided through oral, enteral and parenteral routes. The ultimate goal is to provide necessary nutrients via oral route other than parenteral or enteral routes. All patients require enough fluid, electrolytes, supplements and calories. Medications are used to control symptoms of short bowel syndrome include antimotility agents, antisecretory agents, and trophic agents. Lifelong follow-up is usually needed.

Surgery is not the first-line treatment option for patients with short bowel syndrome. Surgery is usually reserved for patients with the goal to wean them off parenteral nutrition. Patients who have severe or worsened malabsorption might require surgery including intestinal transplant. Transplant is contraindicated in patients with active infection or malignancies. Approximately half of the patients with short bowel syndrome will require surgery. Bianchi procedure and serial transverse enteroplasty (STEP) are performed to lengthen dilated bowel. Stricturoplasty might be necessary. Intestinal transplant is reserved for patients who have life-threatening complications of intestinal failure, irreversible permanent total parenteral nutrition requirement and episodes of sepsis or loss of venous access.

There are no established measures for the primary prevention of short bowel syndrome. However, treating underlying causes including Crohn’s disease and malignancies might prevent short bowel syndrome.

There are several ways to prevent complications of short bowel syndrome. Management strategies and regular follow-up are needed to find and treat complications accordingly. Effective measures must be done for secondary prevention of complications following total parenteral nutrition including liver disease, cholelithiasis, kidney stone, small bowel bacterial overgrowth, lactic acidosis, lactic acidosis. Hydration, consuming supplements, antibiotic therapy, and regular monitoring with blood tests, ultrasound and scans are recommended.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

The first successful intestinal resection was performed in 1880. In 1935, Haymond following research on many patients with bowel resection, reported that 30 to 50% loss of bowel was well tolerated. Total parenteral nutrition (TPN) was introduced during the 1960s, which lead to increased survival following bowel resection.

• In 1880, Koeberle performed the first successful intestinal resection.^[1]
• In 1935, Haymond reported the association between the size of intestinal resection and survival of the patients. He concluded that patients who had less than 30% bowel loss would develop near normal intestinal function. The upper limit of safety was considered to be less than 50% bowel loss.^[2][3]
• During the 1960s, Dudrick and Wilmore introduced total parenteral nutrition (TPN) which lead to increased survival following bowel resection.^[4][5]

• In 1960, total parenteral nutrition (TPN) was developed by Dudrick and Wilmore to manage short bowel syndrome.^[4][5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Based on the length of the remaining bowel, short bowel syndrome may be divided into end-jejunostomy, jejunocolonic anastomosis, ileocolonic anastomosis. Severity varies from mild to severe dysfunction. All of them require home parenteral nutrition except ileocolonic anastomosis which has excellent prognosis and rarely needs parenteral nutrition. Based on the etiology, short bowel syndrome may be divided into cases occurring secondary to vascular abnormalities, mucosal disease of intestine and cases without preexisting intestinal disease.

Based on the length of the remaining bowel, short bowel syndrome may be divided into three types:^[1][2][3][4]

• End-jejunostomy (type I): Most severe form and less intestinal adaptation
• Jejunocolonic anastomosis (type II): Greater degree of intestinal adaptation
• Ileocolonic anastomosis (type III): Uncommon, excellent prognosis and parenteral nutrition is rarely needed

Based on the etiology, short bowel syndrome may be divided into three categories:^[5][6][7][8]

• Vascular abnormalities
  • Mesenteric vessel thrombosis 
  • Mesenteric vessel occlusion
  • Volvulus
  • Adhesions
  • Internal hernia

• Mucosal disease of intestine
  • Crohn’s disease
  • Radiation enteritis
• Without preexisting intestinal disease
  • Malignancy
  • Jejunoileal bypass surgery to treat obesity
  • Trauma to the small intestine

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Short bowel syndrome occurrs as a result of bowel resection following various diseases of the gut such as Crohn’s disease, malignancies, ischemia, and trauma. Short bowel syndrome occurs when the length of the small intestine is less than 2 meters and requires nutritional therapy to prevent malnutrition. Post bowel resection, adaptation might occur which includes structural, motility and functional changes in the remaining intestine. Changes usually start in the first 24 hours following bowel resection and last for about two years. Adaptation depends upon multiple factors including individual, intestinal and therapeutic measurements. Following bowel resection, adaptation occurs in three phases including acute, adaptive, and maintenance phases. Successful adaptation depends on the length of remaining intestine, portion of the resected intestine, and early introduction of nutrition therapy. The term total intestinal adaptation is used when the patient is weaned from parenteral nutrition. The main reason for malabsorption following bowel resection is reduced absorptive capacity of the small intestine due to loss of surface area. On gross and microscopic examination, the resected bowel segment may show the underlying causes including Crohn’s disease, malignancies or ischemia.

The small intestine has an average length of 5.5-6 meters and is responsible for digestion and absorption of food and nutrients. Three portions of small intestine are duodenum, jejunum, and ileum. There is an anatomic gradient for absorption throughout the gastrointestinal tract.^[2][3]

• Duodenum is the first part of the intestine located after the stomach and receives partially digested acidic chyme from the stomach. Brunner’s glands, which secrete alkaline rich mucin are also found in the duodenum. This alkaline rich mucin plays a protective role against the acidic contents received from the stomach.
• The jejunum (second portion of small intestine) is responsible for absorption of nutrients. The inner surface of the jejunum is covered with villi, which increase the surface area of tissue available to absorb nutrients from the gut contents. The villi in the jejunum are much longer than in the duodenum or ileum. It has many large circular folds in its submucosa called plicae circulares, which increase the surface area for nutrient absorption.
• The ileum (third portion of small intestine) is responsible for absorption of vitamin B12 and bile salts and whatever products of digestion that were not absorbed by the jejunum. Its surface is made up of folds, mainly villi and microvilli. Therefore the ileum has an extremely large surface area both for the adsorption of enzymes and for the absorption of products of digestion. The diffuse neuroendocrine system (DNES) cells that line the ileum contain protein and carbohydrate digesting enzymes (gastrin, secretin, cholecystokinin), which are responsible for the final stages of protein and carbohydrate digestion.

• Short bowel syndrome is the result of bowel resection following Crohn’s disease, malignancies, ischemia, and trauma.^[4]
• The small intestine has a very good adaptation following bowel resection of up to half of the small bowel length. However, a small intestine length less than 2 meters is considered as short bowel syndrome and requires nutritional therapy to prevent malnutrition.^[5]

• Adaptation is the specific ability of the intestine to increase its capacity to absorb nutrients following loss of its surface area and length.^[6][7]
• There will be structural, motility and functional changes in the remaining intestine to compensate its loss.^[2][5]
• Changes usually starts in the first 24 hours following bowel resection.^[8]

Change	Main features
Structural changes	Increase in the absorptive surface area Small bowel dilation Crypt cells hyperplasia Villous hypertrophy Local angiogenesis Increased production of enteral hormones and pancreaticobiliary secretions
Motility changes	Greater motility during the initial phase Reduced motility during the adaptive phase
Functional changes	Increased activity of enzymes Increased level of trophic factors Increased level of carrier proteins

• Adaptation depends on multiple factors including individual, intestinal and therapeutic measurements.^[6]
• Adaptation usually occurrs during the first two years after the bowel resection.
• Successful adaptation depends on the length of remaining intestine, portion of the resected intestine, early introduction of nutrition therapy. Total intestinal adaptation defines as when patient is weaned from parenteral nutrition.^[9]
• Following the bowel resection, adaptation occurs in three phases including acute, adaptive, and maintenance phases.^[10]

Intestinal adaptation
Phase	Duration	Main feature
Acute phase	1 to 3 months	Fluid loss Poor absorption of all nutrients, including carbohydrates, proteins, fat, electrolytes, minerals and trace elements Dysmotility Hypergastrinemia
Adaptive phase	1 to 2 years	Reaching 90% to 95% of the bowel adaptation potential Enterocyte and villous hyperplasia Increased mucosal surface area Converting unabsorbed carbohydrates into absorbable short-chain fatty acids Gaining weight Stabilization of fluid and electrolyte levels
Maintenance phase	Following adaptive phase	Reaching the maximum bowel adaptation potential

• There are factors which stimulate the intestinal adaptation, including:^[11]
  • Oral nutrients
  • Soluble fibres such as polysaccharides present in pectin and soy
  • Hydrolysed or whole protein formula
  • Polyamines
  • Long-chain triglycerides and short-chain fatty acids
  • Glucagon-like peptide 2 (GLP-2)
  • Secretin
  • Cholecystokinin
  • Neurotensin
  • Insulin-like growth factor I
  • Glutamine
• There are factors which decrease the intestinal adaptation, including:
  • Starvation
  • Absence of luminal nutrients 
  • Absence of pancreato-biliary secretions 
  • Monosaccharides

• The main reasons for malabsorption following bowel resection include:
  • Reduced absorption capacity of the small intestine due to loss of surface area, leading to:
    • Loss of fluid and dehydration 
    • Electrolyte imbalance
    • Loss of Macronutrients including carbohydrates, lipids and proteins
  • Disturbance in production of enzymes and hormones, leading to:
    • Diarrhea
    • Steatorrhea
    • Loss of vitamins
  • Resection of specific sites, leading to:
    • Loss of absorption of vitamin B12 and bile salts
    • Reduced capacity of fluid retention
  • Loss of ileocecal valve, leading to:
    • Small bowel bacterial overgrowth
    • Increased gastric and intestinal transit
  • Compromised production of gastrointestinal regulators including cholecystokinin, secretin, gastric inhibitory polypeptide and peptide YY, leading to:
    • Increased gastric and intestinal transit
    • Hypergastrinemia

Short bowel syndrome might be associated with following pathologies:

• Mesenteric vascular events including thrombosis or occlusion of the superior mesenteric artery or vein
• Crohn’s disease
• Malignancy
• Radiation enteritis
• Volvulus
• Adhesions
• Jejunoileal bypass surgery to treat obesity
• Trauma to the small intestine
• Internal hernia

• On gross pathology, the resected bowel may show the underlying causes including Crohn’s disease, malignancies or ischemia.

• On microscopic histopathological analysis, the resected bowel may show the underlying causes including Crohn’s disease, malignancies or ischemia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Short bowel syndrome in adults is usually caused by surgical removal of the intestine due to different diseases including Crohn’s disease, mesenteric ischemia, malignancies or radiation enteritis. Less common causes include trauma, volvulus, adhesion and iatrogenic surgery on gastrointestinal system.

Short bowel syndrome in adults is usually caused by surgical removal of the intestine due to:^{[1][2][3][4][5]}

• Mesenteric vascular events including thrombosis or occlusion of the superior mesenteric artery or vein
• Crohn’s disease
• Malignancy
• Radiation enteritis

Less common causes of short bowel syndrome include:

• Volvulus
• Adhesions
• Jejunoileal bypass surgery to treat obesity
• Trauma to the small intestine
• Internal hernia

Cardiovascular	Mesenteric vascular events
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	Adhesions, Crohn’s disease, internal hernia, radiation enteritis, volvulus
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	Post gastrointestinal operations, jejunoileal bypass surgery to treat obesity
Infectious Disease	No underlying causes
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Malignancy
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	Trauma to small intestine
Urologic	No underlying causes
Miscellaneous	No underlying causes

List the causes of the disease in alphabetical order.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

The incidence and prevalence of short bowel syndrome is difficult to estimate. All the data is derived from patients receiving home parenteral nutrition. Therefore, there are different distributions around the world. The incidence of short bowel syndrome was estimated to be 1-2 cases per 100,000 individuals worldwide per year. The prevalence of short bowel syndrome is approximately 0.3-4 per 100,000 individuals in the USA to 0.1-4 per 100,000 individuals in Europe. It affects all age groups. There is no racial predilection to short bowel syndrome and is reported worldwide. Short bowel syndrome affects men and women equally.

• The incidence and prevalence of short bowel syndrome is difficult to estimate. Data is derived from patients receiving home parenteral nutrition.^[1]
• The incidence of short bowel syndrome was estimated to be 1-2 cases per 100,000 individuals worldwide per year.^[2]
• The incidence of short bowel syndrome is approximately 0.07-1.5 per 100,000 individuals in Europe.^[3]

• The prevalence of short bowel syndrome is approximately 0.3-4 per 100,000 individuals in the USA.^[4]
• The prevalence of short bowel syndrome is approximately 0.1-4 per 100,000 individuals in Europe.^[3]

• Patients of all age groups, from neonates to elderly may develop short bowel syndrome.

• There is no racial predilection to short bowel syndrome.

• Short bowel syndrome affects men and women equally.

• Short bowel syndrome is reported worldwide.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Common risk factor in the development of short bowel syndrome may be iatrogenic, including any operation of the gastrointestinal system.

Common risk factor in the development of short bowel syndrome may be iatrogenic, including any operation of the gastrointestinal system.^[1][2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

There is insufficient evidence to recommend routine screening for short bowel syndrome.

There is insufficient evidence to recommend routine screening for short bowel syndrome.

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

The symptoms of short bowel syndrome usually develop immediately following bowel resection. Diarrhea may cause massive fluid and electrolyte loss. Immediately after surgery, intestinal adaptation develops in three phases, including acute, adaptive and maintenance phase. During the adaptation, structural, motility and functional changes occur. Patients need hydration and nutritional support via parenteral, enteral and oral routes. Length of remaining small bowel is the most important prognostic factor. Patients with more than 200 cm length of small bowel, usually do not need parenteral nutrition. Patients with shorter small bowel may not wean off from parenteral nutrition support. Complications might occur due to malnutrition, surgery and parenteral nutrition. Malnutrition presents with vitamin, mineral and essential fatty acids deficiencies. Complications related to surgery including thrombosis, infection, hemorrhage, atelectasis and anastomosis disruption might occur. Small intestinal bacterial overgrowth due to stasis and obstruction might also occur. Chronic liver disease following parenteral nutrition is a common complication in short bowel syndrome. There is no definite cure for short bowel syndrome. However, medications and nutritional therapy significantly improve the quality of life and survival of the patients. Prognosis of short bowel syndrome depends on the location and size of the bowel resection, underlying pathology, nutrition support, pharmacotherapy, and extent of intestinal adaptation. The 2 and 5-year survival rate of patients with short bowel syndrome are approximately 80% and 70%, respectively.

• The symptoms of short bowel syndrome usually develop immediately following bowel resection.^[1]
• Short bowel syndrome may cause diarrhea which presents with massive fluid and electrolyte loss.^[2]
• It is important to manage the patient following surgery, to hydrate and receive enough nutrients through parenteral or enteral routes.^[3]
• Immediately after surgery, intestinal adaptation develops in three phases, including acute, adaptive and maintenance phase.^[4]
• Structural, motility and functional changes occur to adapt intestine to the new situation.^[5]
• Patients with remaining small bowel of more than 120 cm length, usually do not need parenteral nutrition and may be adapted easily.^[6][4]
• It is not common for patients who have small bowel length of less than 50 to be weaned off from parenteral nutrition.^[7][8]
• Efforts must be applied to wean the patients from parenteral nutrition to enteral nutrition and if it is possible to oral nutrition.^[9]
• However, complications might happen even if all the precautions are done.^[10]

Common complications of short bowel syndrome may be classified to different categories, including malnutrition, surgery related, and chronic complications.^{[2][4][8][10][11][12][13][14][15]}

Malnutrition

• Vitamin deficiency
  • Vitamin A deficiency that presents with night blindness
  • Vitamin B12 deficiency that presents with megaloblastic anemia
  • Vitamin C deficiency that presents with bleeding tendency
  • Vitamin D deficiency that presents with osteomalacia
  • Vitamin E deficiency that presents with neuropathy
  • Vitamin K deficiency that presents with bleeding
• Mineral deficiency
  • Iron deficiency
  • Folic acid deficiency
  • Calcium deficiency
  • Zinc deficiency
  • Magnesium deficiency
  • Selenium deficiency
  • Copper deficiency
• Essential fatty acid deficiency

Surgery related complications

• General complications of surgery
  • Thrombosis
  • Hemorrhage
  • Wound infection
  • Postoperative pulmonary atelectasis
  • Acute kidney injury
  • Pulmonary embolism
  • Deep vein thrombosis
• Surgery on gastrointestinal system
  • Anastomotic disruption
  • Anastomotic bleeding

Catheter related complications:

• Infection of the central venous line
• Occlusion of the catheter due to thrombosis, fibrin formation, or precipitations
• Breakage of the central line

Post bowel transplant complications:

• Acute rejection
• Chronic rejection
• Hepatic, portal, or mesenteric vein thrombosis
• Opportunistic infection, such as CMV, ….

Chronic complications

• Gastrointestinal complications
  • Small intestinal bacterial overgrowth due to stasis
  • Bowel obstruction
  • Bowel motor abnormalities
  • Stasis of intestinal contents
  • Parenteral nutrition liver disease from steatosis to fibrosis and cirrhosis
  • Bowel necrosis
  • Peptic ulcers due to gastric hypersecretion
  • Gallstones due to altered bile salt and bilirubin metabolism
  • Hepatobiliary disease
  • Lactose intolerance
  • Permanent intestinal failure
• Extra-intestinal complications
  • Kidney stone due to hyperoxaluria
  • Metabolic bone disease
  • Lactic acidosis 

• There is no definite cure for short bowel syndrome. However, medications and nutritional therapy significantly improve the quality of life and survival of the patients.^[16]
• Prognosis of short bowel syndrome depends on the location and size of the bowel resection, underlying pathology, nutrition support, pharmacotherapy, and extent of intestinal adaptation.^[11][14][5]
• The quality of life for patients with short bowel syndrome depends on their ability to previous activities. Majority of them on effective treatment could have an excellent quality of life.^[17]
• The 2 and 5-year survival rate of patients with short bowel syndrome are approximately 80% and 70%, respectively.^[12]
• The 6-year survival rate of patients with short bowel syndrome is approximately 65% for patients who have remaining short bowel of more than 50 cm.^[5]
• Much hope is vested in Omegaven, a type of lipid TPN feed, in which recent case reports suggest the risk of liver disease is much lower.^[18]
• Although promising, the small intestine transplant has a mixed success rate, with a postoperative mortality rate of up to 30%. One-year and 4-year survival rates are 90% and 60%, respectively.^[4]

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