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Flashcards in Small Bowel Deck (90)
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1
Q

Week 4 GI embryo

A

Primitive gut tube (made from endoderm) begins to develop into foregut, midgut, and hindgut

Endoderm becomes intestinal epithelium and glands

Mesoderm become connective tissue, muscle, and wall of intestine

2
Q

Week 5 GI embryo

A

Intestine elongates and midgut loop herniates through umbilical ring

Midgut loop continues to lengthen extracoelomically until about week 10

3
Q

Week 10 GI embryo

A

Midgut loop rotates 270 degrees counterclockwise and returns back into the abdominal cavity

This is around axis of SMA

4
Q

What is the SI derived from?

A

All of the SI is from midgut EXCEPT proximal duodenum (foregut)

Junction btw foregut and midgut is just distal to opening of common bile duct

5
Q

Vitelline duct

A

Initially, the primitive gut tube communicates with the yolk sac. This narrows by week 6 to form the vitelline duct.

If duct fails to obliterate by end of gestation, it persists as a Meckel’s diverticulum (2% of population)

6
Q

Small bowel relation to peritoneum

A

Duodenum: First 2 cm is intraperitoneal. Rest is retro.

Jejunum and ileum: intraperitoneal

7
Q

3 parts of SI

A

Duodenum (about 25cm)

Jejunum (100-110 cm)

Ileum (150-160 cm)

Total is 5-10m (6 avg)

8
Q

Duodenum anatomy

A

from pylorus to dudodenojejunal junction

4 parts

1 = superior - duodenal bulb: 5cm long. Site of most ulcers

2 = descending - 10cm. Curves around head of pancreas

3 = Transverse - 10cm. Crosses anterior to aorta and IVC and posterior to SMA and
SMV

4 = Ascending - 5cm. Ascends past left side of aorta, then curves anteriorly to meet with jejunum, forming the duodenojejunal junction, which is suspended by ligament of Treitz

Jejunum begins at Treitz

Since duodenum is retroperitoneal, it is tethered to posterior abdominal wall and has no mesentery at its posterior aspect

Plicae circulares (transverse mucosal folds in lumen) are most prominant in prox small bowel (duodenum and jejunum) than in distal small bowel

9
Q

Blood supply of duodenum

A

Arteries:
1) Prox (up to ampulla of Vader) = gastroduodenal (first branch of proper hepatic) bifurcates into anterior and posterior superior pancreaticoduodenals

2) Distal = inferior pancreaticoduodenal (first branch of SMA) bifurcates into anterior and posterior inferior pancreaticoduodenals

Venous:

1) Anterior and posterior pancreaticoduodenal veins drain into SMV. Joins splenic vein behind neck of pancreas to form portal vein
2) Prepyloric vein of Mayo is landmark of pylorus

10
Q

Jejunum and ileum anatomy

A

No anatomic boundary between the 2

Jejunum is prox 40% of SI distal to ligament of treitz while ileum is distal 60%

Combined length is 5-10m.

Mesentery tethers the jejunum and ileum to posterior abdominal wall.

11
Q

Blood supply to jejunum and ileum

A

Arteries:

1) Both jejunum and ileum supplied by branches of SMA which runs in mesentery
2) Arteries loop to form arcades that give rise to straight arteries - vasa recta

Venous:
SMV drains both

12
Q

Lymphatics of SI

A

Bowel wall - mesenteric nodes - lymph vessels parallel the corresponding arteries - cisterna chyli (retroperitoneal structure btw aorta and IVC) - thoracic duct - L subclavian vein

Participate in absorption of fat

13
Q

Anterior vs posterior ulcer rupture

A

Anterior = peritonitis. Leakage of duodenal contents into peritoneal cavity

Posterior = bleeding. Penetrated gastroduodenal artery.

14
Q

Innervation

A

1) Parasympathetic:
Fibers originate from vagus and celiac ganglia
- enhances bowel secretion, motility, and other digestive processes

2) Sympathetic:
Fibers from ganglion cells that reside in plexus at base of SMA
- opposes effects of para system on bowel

3) Enteric:
Consists of Meissner plexus at base of submucosa and Auerbach plexus between inner circumferential and outer longitudinal layers of muscle wall

15
Q

Peristalsis rate

A

1-2 cm/sec

16
Q

SMA Syndrome

A

Since 3rd part of duodenum runs behind SMA, compression of SMA on duodenum can lead to SBO.

These pts are thin and have lost the fat pad between SMA and duodenum leading to recurrent symptoms of SBO

17
Q

Which part of the small bowel is not supplied by branches of the SMA?

A

proximal duodenum (branches of celiac trunk)

18
Q

Intestinal immune function

A

Largest immune organ in body

IgA is most common type of Ig in lumen of GI tract

Lymphoid nodules, mucosal lymphocytes, and isolated lymphoid follicles in appendix and mesenteric lymph nodes together constitute the mucosa-associated lymphoid tissue (MALT)

19
Q

SBO definition

A

1 cause = adhesions from prior abdominal surgery (#2 = hernia)

Cessation, impairment or reversal of physiologic transit of intestinal contents secondary to a mechanical or functional cause

20
Q

SBO etiologies

A

1) Mechanical
Adhesions, hernia, cancer, abscess, congenital

Gallstone ileus, foreign body, intussusception

Crohn’s, lymphona, radiation enteritis

2) Functional (paralytic ileus)
Postop

Lyte issues (hypoK)

Peritonitis

Meds (opiates, anticholinergics)

Hemoperitoneum/ retroperitoneal hematoma

21
Q

Gastrin

A

From: Antrum

Action: Gastric acid secretion and cell growth

Stimulated by: Vagus, Food in antrum, gastric distention, calcium

Inhibited by: Antral pH

22
Q

CCK

A

From: Duodenum

Action: GB contraction stimulates pancreatic acinar cell growth. Inhibits gastric emptying

Stim: Polypeptides, AAs, Fat, HCl

Inhib: Chymotrypsin, trypsin

23
Q

Secretin

A

From: Duodenum

Action: Stimulates pancreatic secretion of H2O and HCO3. Bile secretion of HCO3. Pepsin secretion. Inhibits gastric acid secretion

Stim by: Low pH, intraluminal duodenal fat

Inhib by: High duodenal pH

24
Q

Somatostatin

A

From: Pancreas

Action: Increases SI absorption of H2O and lytes. Inhibits cell growth, GI motility, GB contraction, pancreatic/biliary/enteric secretion of gastric acid, secretion/action of all GI hormones

Stimulated by: Intraluminal fat, gastric and duodenal mucosa, catecholamines

Inhibited by: ACh release

25
Q

Pancreatic polypeptide

A

From: Pancreas

Action: Clinical usefulness of pancreatic polypeptide is limited to being a marker for other endocrine tumors of the pancreas

Stimulated by: Cephalic - vagus. Gastric - reflexes. Intestinal - food in small bowel

26
Q

Neurotensin

A

From: SI, Colon

Action: Pancreatic secretion, vasodilation, inhibits gastric acid secretion

Stim by: Fat

27
Q

Peptide Y

A

From: SI, Colon

Action: Inhibits gastric acid secretion, pancreatic exocrine secretion, and migrating myoelectric complexes

28
Q

Glucagon

A

From: SI, Colon

Action: Increases glycogenolysis, lipolysis, gluconeogenesis

Stim by: Lowe serum glucose

Inhib by: Somatostatin

29
Q

Motilin

A

Action: Inhibits MMCs, increases gastric emptying, increases pepsin secretion alkaline enviornment

Stim by: Vagus, fat, intraduodenal

Inhib by: Pancreatic polypeptide

30
Q

How do you differentiate btw jejunum and ileum?

A

Jejunum has larger diameter, thicker wall, more prominent plicae circulares

Jejunum has few arcades (1-2) with long vasa recta

Ileum has many arcades with short vasa recta

Ileum has fatty mesentery

31
Q

Steatorrhea definition

A

Since > 93% of ingested fat is usually absorbed, >6g of fecal fat over 24h with 100g lipid per day diet is steatorrhea

32
Q

Short chain fatty acid absorption

A

Large bowel

Can be used as alternative energy source for people who suffer from carb malabsorption

33
Q

SBO vs LBO neoplasms

A

In SBO, neoplasm is rarely the cause. If it is, it is likely secondary to extrinsic compression as opposed to intraluminal obstruction

34
Q

Risk factors for SBO

A
Pervious abdominal surgery
Hernia
IBD (Crohn's secondary to stricture formation)
Diverticular disease
Cholelithiasis 
Ingested foreign body
35
Q

Signs/symptoms of SBO

A
Colicky abdominal pain
Distention
N/v
Obstipation
Hyperactive BS
Signs of low volume (hemoconcentration, lyte issues) bc of low PO intake, vomiting, and accumulation of fluid in bowel lumen and wall (third spacing)

(+) flatus and BM initially then later on obstipation

early on borborygmi matching up with colicky pain. Later on no BS

36
Q

Features associated with strangulated SBO

A
Tenderness
Tachy
Fever
Markedly elevated WBC
Acidosis with high lactate

These are NOT present in 5-15%, esp the elderly

37
Q

Diagnostic process and tx for SBO

A

Colicky abd pain with borborygmy and/or obstipation - get KUB then CT with barium

KUB - look for Air fluid levels
CT - if barium can enter rectum it is not completed obstructed
- if it pools somewhere we know it’s total and know it’s location

If complete - surgery

If strangulated - IVF then surgery

If partial/stable patient - medical management with NPO, IVF, NGT suction, Foley, monitor lytes for hypoK, metabolic acidosis (sign of ischemia)

If they get worse or signs of peritoneal signs develop take to OR. If there is no change in 24h then surgery.

38
Q

Crohn’s Disease definition

A

IBD characterized by transmural inflammation involving ANY part of the GI tract from mouth to anus

Inflammation is discontinuous (Skip lesions)

Often leads to fibrosis and ultimately obstruction as well as fistulae

39
Q

Crohn’s epi

A

80% have involvement of SI, usually distal ileum (33% of these patients just have ileitis)

50% of patients have involvement of ileum AND colon

20% have involvement of colon only - diff from UC bc Crohn’s patients tend to have rectal sparing

33% have perianal disease

Diagnosis most common btw ages 15 and 40, second peak btw 50-80.

40
Q

Risk for Crohn’s

A

Jewish

FHx

Urban dwelling

Smoking

41
Q

Signs/Symptoms of Crohn’s

A

Crampy abdominal pain (RLQ usually), diarrhea, weight loss

Fever, fatigue

Bleeding (hemoccult + stools common, but gross lower GI bleed less common than in UC)

Perianal disease including skin tags, anal fissures, perirectal abscesses, and anorectal fistulae

Signs/symptoms of intestinal perf and/or fistula formation (combo of localized peritonitis, fever, ab pain, tenderness, palpable mass)

42
Q

Extraintestinal manifestations of Crohn’s

A

Oral involvement (aphthous ulcers)

Joints (arthritis)

Ocular involvement

Derm involvement (erythema nodosum, pyoderma gangrenosum)

Hepatobiliary (sclerosing cholangitis)

43
Q

Dx of Crohn’s

A

History of prolonged diarrhea with abdominal pain, weight loss, and fever with or without gross bleeding

PE can be nonspecific or be suggestive with perianal skin tags, sinus tracts, or palpable abdominal mass

Colonoscopy with bx, visualization of terminal ileum may reveal focal ulcerations adjacent to areas of normal mucosa along with cobblestone appearance of mucosa

EGD for proximal disease

Imaging (small bowel contrast studies) helpful in characterizing length of involvement and areas of stricture, especially in parts of small bowel that can’t be reached via colonoscopy

Rads: mucosal nodularity, narrowed lumen, ulceration, string sign, presence of abscesses or fistulae

44
Q

Tx of Crohn’s

A

1) Medical - Corticosteroids, aminosalicylates (sulfasalazine, 5-ASA), immune modulators (azathrioprine, 6MP, cyclosporine), infliximab (anti-TNFa), metronidazole
- Many patients require surgery to relieve symptoms that do not respond to drugs or to treat complications such as obstruction, abscesses, fistulae, perf, perianal disease or cancer

Surg should be avoided if possible since Crohn’s is not curable by surgery like UC is

About 80% will eventually require some intervention

Increased risk of colon cancer with long-standing crohn’s colitis

45
Q

Incidence of benign neoplasms of small intestine

A

1 cause of adult intussusception

Adenomas > leiomyomas > lipomas

Leiomyomas most likely to cause symptoms tho

Most SI benign neoplasms are found in duodenum

Most patients in 5th or 6th decade of life

46
Q

Risk factors for benign neoplasms of small intestine

A

Hereditary syndromes

  • Peutz-Jeghers (hamartomatous polyps)
  • Gardner (adenoma)
  • FAP (adenoma)

Consumption of red meat and salt-cured foods

47
Q

Signs/symptoms of benign neoplasm of small bowel

A

Most asymptomatic until they are large

(#1 symptom) Intermittent obstruction - crampy ab pain, distention, nausea, vomiting

Occult or overt bleeding

Palpable abdominal mass

Obstructive jaundice (periampullary lesion)

48
Q

Dx of a benign neoplasm of small bowel

A

1) EGD - can see prox duodenum. Most duodenal neoplasms are found by accident
- Endo US. Can tell us depth of invasion too

2) Rads - small bowel series (low sensitivity)
- CT
- Enteroclysis** can detect tumors in distal small bowel

3) Majority of patients: Small bowel series with follow-through followed by enteroclysis
4) High risk patients: Enteroclysis

49
Q

Enteroclysis

A

double contrast study involving passing a tube into prox small bowel and injecting barium and methylcellulose.

Can detect tumors missed on conventional small bowel follow-through

50
Q

Tx of benign neoplasms

A

All symptomatic lesions = resection (surg or endo)

Tumors in prox duodenum, even asymptomatic ones should be removed endo (2)

Tumors in second portion of duodenum, near ampulla, may require Whipple (pancreaticoduodenectomy)

51
Q

Malignant neoplasms of intestine

A

Rare

Adenocarcinoma > Carcinoid > GI stromal tumor > lymphoma

Adeno risks: Crohn’s, Celiac, FAP, P-J Syndrome

Lymphoma: Celiac, immunodeficiency, autoimmune

52
Q

Tx of malignant neoplasms

A

1) Wide resection of involved intestine
2) For adeno - wide local excision with its accompany mesentery along with regional nodes
3) GISTS usually treated with segmental resection of affected intestine and Gleevec (tyrosine kinase inhib)
4) Duodenal lesions may need Whipple
5) Bypass may be required for palliation
6) Localized lymphoma is treated with segmental resection of intestine and mesentery
7) Diffuse lymphoma is only situation where chemo (not surg) should be primary

53
Q

Prognosis of small bowel malignancies

A

Overal 5yr

54
Q

Carcinoid definition

A

Malignant tumor of enterochromaffin cell origin, part of amine precursor uptake and decarboxylation (APUD) system

Most common in appendix

55
Q

Carcinoid incidence

A

29-40% of primary small bowel malignancies

Peak incidence btw 50-70yrs

More than 90% diagnosed in GI system

Appendix is most common GI carcinoid site followed by small bowel followed by rectum

56
Q

Signs/symptoms of Carcinoid

A

Slow growing; therefore frequently asymptomatic and found incidentally

In symptomatic patients, vague abdominal pain is #1 symptom

Intermittent obstruction in 25% of patients

Rectal bleeding (from rectal carcinoid), pain, weight loss

Carcinoid syndrome - 10% of cases

  • Due to production of serotonin, bradykinin, tryptophan by tumor and exposure of these products to systemic circulation prior to breakdown by liver
  • cutaneous flushing, sweating, watery diarrhea, wheezing, dyspnea, valvular lesions (R>L)
57
Q

Dx of Carcinoid

A

Most found incidentally during rads studies, appendectomy, or surgery for intestinal obsruction

If patient has the syndrome:

  • 5HIAA in 24h urine collection
  • plasma chromogranin A - independent predictor of prognosis
  • Pentagastrin provocation test (pentagastrin induces flushing)
  • Otherwise diagnosed as any other small bowel neoplasm
58
Q

When do patients typically develop the Carcinoid Syndrome?

A

Typically, appendiceal and SI carcnoids cause the syndrome only after they have metastasized to liver

Thus, not surgical candidates due to extensive mets

Wheezing = endobronchial lesion maybe

59
Q

Tx for Carcinoid

A

Medical: Serotonin antagonists (cyproheptadine) or somatostatin analogues for sumptoms

Surg:

  • Appendiceal 2cm = R hemicolectomy
  • Small intestinal = resect tumor with mesenteric lymph nodes as well as inspect entire small bowel for synchronous lesions

Otherwise, resect tumor and any solitary liver mets

60
Q

Carcinoid prognosis

A

Overall 5 year = 54%

5 year after palliative resection = 25%

After curative resection = 70%

61
Q

Fistula definition

A

Communication btw 2 epithelialized surfaces. It can form btw 2 parts of the GI or GU tract, an internal fistuala (choledocho-duodenal or colo-vescical)

OR btw an internal organ and an outer epithelialized surface (enterocutaneous) - external fistual

62
Q

Risk for fistula

A

Previous abdominal surgery (80%)

Diverticular disease

Crohn’s

Colorectal cancer

63
Q

Signs of a fistula

A

Iatrogenic fistulae usually appear 5-10 days postop

If associated with an abscess, can be with fever and leukocytosis

Drainage of succus entericus (bowel contents) from skin (enterocutaneous fistula)

Diarrhea, usually secondary to malabsorption (entero-enteric; esp btw prox and distal small bowel or colon since a large portion of small bowel absorptive surface is bypassed)

Pneumaturia and symptoms of urinary tract infection (colovesicular fistula)

64
Q

Proximal vs distal fistulas

A

Proximal causes more issues bc the draining contents are more acidic, more fluid/lytes are lost, and more absorptive area is lost

65
Q

Dx of fistula

A

CT with enteral contrast shows leakage of contrast from intestinal lumen

Small bowel series

Enteroclysis

Fistulogram: contrast is injected directly into fistula tract

66
Q

Tx of fistula

A

1) Stabilize - manage lytes, fluid losses, and nutritional status
2) Drainage of abscesses if present

3) Allow time for spontaneous closure
- bowel rest
- provide nutrition (TPN)
- Consider octreotide for high output and pancreatic fistulas

4) If 6-8w pass without improvement, then surgery should be performed to resect the fistula tract, together with the segment of small bowel from which it originates

67
Q

High output vs low output fistula

A

High: Drains > 500 ml/24h and are proximal (stomach, duodenum, prox small bowel)

Low:

68
Q

Fistula prognosis

A

Enterocutaneous fistulas have 15-20% mortality related to complications of sepsis and underlying disease

Surgery is associated with considerable morbidity and a high recurrence rate

69
Q

Mesenteric ischemia def

A

Reduction in blood flow to small bowel secondary to variety of things

Can result in 2 distinct conditions: Acute and chronic MI

70
Q

Acute mesenteric ischemia def

A

Rapid onset of intestinal hypoperfusion

Can be caused by arterial occlusion (usually a single artery)

  • SMA embolism = 50%
  • SMA thrombosis = 15-25%
  • Vasospasm (nonocclusive AMI) = 20-30%
  • Venous obstruction (thrombosis or strangulation usually of SMV) = 5%

Regardless of cause, AMI can lead to mucosal sloughing within 3hrs of onset and to intestinal infarction within 6hrs of onset

SMA is most common vessel involved. Most emboli that cause AMI come from heart (LA or LV). 95% of patients with AMI have history of cardio disease (AFib or MI)

71
Q

What are the factors that keep a fistula tract open?

A

FRIENDS

Foreign body
Radiation
Inflammation/Infx
Epithelialization
Neoplasm
Distal obstruction
Short segment fistula (
72
Q

Risk factors for AMI

A

1) Cardiac - low CO states, cardiac arrhythmias, severe cardiac valvular disease, recent MI
2) Age
3) Atherosclerosis
4) Hypercoagulable states

73
Q

Signs/symptoms of AMI

A

Abdominal pain out of proportion to exam

Pain is colicky and diffuse, typically in mid abdomen

Can be associated with nausea and vomiting and diarrhea

Following infarction, peritonitis (rebound and rigidity), abdominal distention and passage of bloody stools occurs

74
Q

Dx of AMI

A

1) High clinical suspicion especially if history of cardiac disease or hypercoagulopathy
2) No lab test is sensitive for diagnosis. Findings may include leukocytosis, acidosis, hemoconcentration, occult blood in stool
3) If there are peritoneal signs, then patient should undergo emergent laparotomy

4) Otherwise pursue diagnostic tests
- Mesenteric angiography: most sensitive and specific but it’s invasive
- CT scan: good initial test. Can rule out other causes of abdominal pain. Can reveal evidence of ischemia. Can reveal occlusion/stenosis of vasculature
- if high suspicion get MA after a negative CT bc CT can’t see an arterial AMI. Great sensitivity for venous thrombosis tho

75
Q

Tx or AMI

A

Stabilize patient - hemodynamic monitoring and fluids. Correct lytes. Broad spectum Abx. Place NGT for decompression

Patient with peritoneal signs - surgery

  • embolic causes = intraoperative embolectomy
  • For CA/SMA thrombosis - bypass site of obstruction using saphenous graft

Therapy via angiography includes vasodilators (papaverine) or thrombolytic agents (streptokinase, urokinase, tPA), angioplasty, placement of a stent, embolectomy

Venous thrombosis requires heparin

76
Q

Prognosis of AMI

A

Acute arterial mortality = 59-93%

Acute mesenteric venous thrombosis mortality = 20-50% (30% recurrence if not anticoagulated)

77
Q

Chronic Mesenteric Ischemia def

A

Insidious, episodic, or constant state of intestinal hypoperfusion

Rarely leads to infarction of small bowel due to development of collateral circulation

Can be caused by:

1) Arterial ischemia (#1) - associated with atherosclerosis of more than one mesenteric and splanchnic vessels
2) Venous thrombosis - portal or splenic veins leading to portal HTN with subsequent varices and splenomegaly
3) Vasculitis

78
Q

Risk factors for CMI

A

Atherosclerotic valvular disease (half of patients have history of peripheral vascular disease or CAD)

Smoking

79
Q

Signs of CMI

A

Intestinal angina - dull, crampy, postprandial ab pain leading to food aversion and weight loss

Patients with chronic venous thrombosis may be asymptomatic due to collateral formation or may present with variceal bleeding

80
Q

Dx of CMI

A

High clinical suspicion

Must rule out other causes of chronic ab pain, weight loss, and food aversion (malignancy)

Diagnosis is supported by demonstration of high-grade stenoses in multiple mesenteric vessels

Diagnostic tests:

  • Angiography = Gold standard
  • CT and MRA - good initial tests since they can ID a stenosis and serve as guide for angiography
  • mesenteric duplex US - can be used for screening to detect stenosis of celiac and SMA
81
Q

Patients with acute mesenteric venous thrombosis should be evaluated for what?

A

Hereditary or acquired thrombophilias

82
Q

Tx for CMI

A

Arterial CMI:

1) surgical revasculatization
- aortoesenteric bypass graft
- mesenteric endarterectomy

2) Percutaneous transluminal angioplasty (PTA) with or without placement of a stent
- less relief of symptoms and less durability than surgery
- serves as alternative to surgery for those patients who are not optimal surgical candidates due to comorbidiites

Chronic venous mesenteric thromboses:
1) Anticoagulation with heparin

83
Q

Median arcuate ligament syndrome

A

“Celiac artery compression syndrome”

CMI due to compression of celiac artery by diaphragm

Tx = release of arcuate ligament and bypass of persistent stricture

84
Q

Morbidity associated with TPN

A

Catheter sepsis
Liver/kidney failure
Venous thrombosis

85
Q

prognosis of CMI

A

Periop mortality 0-16%

Initial relief of symptoms with surgery 90%

Recurrence following surgery

86
Q

Short Bowel Syndrome

A

Presence of

87
Q

Causes of SBS

A

Adults - AMI, Crohn’s, Malignancy

Peds - Volvulus, intestinal atresia, necrotizing enterocolitis

88
Q

Pathophys of SBS

A

Malabsorption occurs following resection of 50-80% of small bowel

presence of intact colon, as well as an ileocecal valve lowers severity of malabsorption

Resection of ileum is associated with higher malabsorption secondary to inability to absorb bile salts and vitamin B12

Small bowel adaptation period is about 1-2 years following surgery

89
Q

Tx for SBS

A

Medical:

1) Repletion of fluid and lytes. Initially, most patients require TPN
2) PPI/H2 blockers to lower gastric acid secretion
3) Antimotility agents to lower transit time through small bowel
4) Octreotide to lower intestinal secretions

Surgical:
1) Restoration of intestinal continuity in patients with stomas in order to increase absorptive capacity

Surgeries aimed at slowing transit through small bowel:

1) Segmental reversal of the small bowel
2) Placement of a segment of colon between 2 segments of small bowel
3) Creation of artificial small bowel valves

Surgeries aimed at lengthening the small bowel:

1) Longitudinal intestinal lengthening and tailoring (LILT)
2) Serial transverse enteroplasty procedure (STEP)
3) Small bowel transplant
- indicated for patients with life-threatening intestinal failure or complications from TPN
- Risk = rejection and CMV infection
- Good results with no need for TPN

90
Q

Prognosis for SBS

A

50-70% who initially require TPN can be completely weaned

Peds patients are more likely than adults to gain independence from TPN