Small Bowel Flashcards
Week 4 GI embryo
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
Week 5 GI embryo
Intestine elongates and midgut loop herniates through umbilical ring
Midgut loop continues to lengthen extracoelomically until about week 10
Week 10 GI embryo
Midgut loop rotates 270 degrees counterclockwise and returns back into the abdominal cavity
This is around axis of SMA
What is the SI derived from?
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
Vitelline duct
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)
Small bowel relation to peritoneum
Duodenum: First 2 cm is intraperitoneal. Rest is retro.
Jejunum and ileum: intraperitoneal
3 parts of SI
Duodenum (about 25cm)
Jejunum (100-110 cm)
Ileum (150-160 cm)
Total is 5-10m (6 avg)
Duodenum anatomy
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
Blood supply of duodenum
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
Jejunum and ileum anatomy
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.
Blood supply to jejunum and ileum
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
Lymphatics of SI
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
Anterior vs posterior ulcer rupture
Anterior = peritonitis. Leakage of duodenal contents into peritoneal cavity
Posterior = bleeding. Penetrated gastroduodenal artery.
Innervation
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
Peristalsis rate
1-2 cm/sec
SMA Syndrome
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
Which part of the small bowel is not supplied by branches of the SMA?
proximal duodenum (branches of celiac trunk)
Intestinal immune function
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)
SBO definition
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
SBO etiologies
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
Gastrin
From: Antrum
Action: Gastric acid secretion and cell growth
Stimulated by: Vagus, Food in antrum, gastric distention, calcium
Inhibited by: Antral pH
CCK
From: Duodenum
Action: GB contraction stimulates pancreatic acinar cell growth. Inhibits gastric emptying
Stim: Polypeptides, AAs, Fat, HCl
Inhib: Chymotrypsin, trypsin
Secretin
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
Somatostatin
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
Pancreatic polypeptide
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
Neurotensin
From: SI, Colon
Action: Pancreatic secretion, vasodilation, inhibits gastric acid secretion
Stim by: Fat
Peptide Y
From: SI, Colon
Action: Inhibits gastric acid secretion, pancreatic exocrine secretion, and migrating myoelectric complexes
Glucagon
From: SI, Colon
Action: Increases glycogenolysis, lipolysis, gluconeogenesis
Stim by: Lowe serum glucose
Inhib by: Somatostatin
Motilin
Action: Inhibits MMCs, increases gastric emptying, increases pepsin secretion alkaline enviornment
Stim by: Vagus, fat, intraduodenal
Inhib by: Pancreatic polypeptide
How do you differentiate btw jejunum and ileum?
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
Steatorrhea definition
Since > 93% of ingested fat is usually absorbed, >6g of fecal fat over 24h with 100g lipid per day diet is steatorrhea
Short chain fatty acid absorption
Large bowel
Can be used as alternative energy source for people who suffer from carb malabsorption
SBO vs LBO neoplasms
In SBO, neoplasm is rarely the cause. If it is, it is likely secondary to extrinsic compression as opposed to intraluminal obstruction
Risk factors for SBO
Pervious abdominal surgery Hernia IBD (Crohn's secondary to stricture formation) Diverticular disease Cholelithiasis Ingested foreign body
Signs/symptoms of SBO
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
Features associated with strangulated SBO
Tenderness Tachy Fever Markedly elevated WBC Acidosis with high lactate
These are NOT present in 5-15%, esp the elderly
Diagnostic process and tx for SBO
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.
Crohn’s Disease definition
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
Crohn’s epi
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.
Risk for Crohn’s
Jewish
FHx
Urban dwelling
Smoking
Signs/Symptoms of Crohn’s
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)
Extraintestinal manifestations of Crohn’s
Oral involvement (aphthous ulcers)
Joints (arthritis)
Ocular involvement
Derm involvement (erythema nodosum, pyoderma gangrenosum)
Hepatobiliary (sclerosing cholangitis)
Dx of Crohn’s
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
Tx of Crohn’s
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
Incidence of benign neoplasms of small intestine
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
Risk factors for benign neoplasms of small intestine
Hereditary syndromes
- Peutz-Jeghers (hamartomatous polyps)
- Gardner (adenoma)
- FAP (adenoma)
Consumption of red meat and salt-cured foods
Signs/symptoms of benign neoplasm of small bowel
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)
Dx of a benign neoplasm of small bowel
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
Enteroclysis
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
Tx of benign neoplasms
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)
Malignant neoplasms of intestine
Rare
Adenocarcinoma > Carcinoid > GI stromal tumor > lymphoma
Adeno risks: Crohn’s, Celiac, FAP, P-J Syndrome
Lymphoma: Celiac, immunodeficiency, autoimmune
Tx of malignant neoplasms
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
Prognosis of small bowel malignancies
Overal 5yr
Carcinoid definition
Malignant tumor of enterochromaffin cell origin, part of amine precursor uptake and decarboxylation (APUD) system
Most common in appendix
Carcinoid incidence
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
Signs/symptoms of Carcinoid
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)
Dx of Carcinoid
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
When do patients typically develop the Carcinoid Syndrome?
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
Tx for Carcinoid
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
Carcinoid prognosis
Overall 5 year = 54%
5 year after palliative resection = 25%
After curative resection = 70%
Fistula definition
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
Risk for fistula
Previous abdominal surgery (80%)
Diverticular disease
Crohn’s
Colorectal cancer
Signs of a fistula
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)
Proximal vs distal fistulas
Proximal causes more issues bc the draining contents are more acidic, more fluid/lytes are lost, and more absorptive area is lost
Dx of fistula
CT with enteral contrast shows leakage of contrast from intestinal lumen
Small bowel series
Enteroclysis
Fistulogram: contrast is injected directly into fistula tract
Tx of fistula
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
High output vs low output fistula
High: Drains > 500 ml/24h and are proximal (stomach, duodenum, prox small bowel)
Low:
Fistula prognosis
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
Mesenteric ischemia def
Reduction in blood flow to small bowel secondary to variety of things
Can result in 2 distinct conditions: Acute and chronic MI
Acute mesenteric ischemia def
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)
What are the factors that keep a fistula tract open?
FRIENDS
Foreign body Radiation Inflammation/Infx Epithelialization Neoplasm Distal obstruction Short segment fistula (
Risk factors for AMI
1) Cardiac - low CO states, cardiac arrhythmias, severe cardiac valvular disease, recent MI
2) Age
3) Atherosclerosis
4) Hypercoagulable states
Signs/symptoms of AMI
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
Dx of AMI
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
Tx or AMI
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
Prognosis of AMI
Acute arterial mortality = 59-93%
Acute mesenteric venous thrombosis mortality = 20-50% (30% recurrence if not anticoagulated)
Chronic Mesenteric Ischemia def
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
Risk factors for CMI
Atherosclerotic valvular disease (half of patients have history of peripheral vascular disease or CAD)
Smoking
Signs of CMI
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
Dx of CMI
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
Patients with acute mesenteric venous thrombosis should be evaluated for what?
Hereditary or acquired thrombophilias
Tx for CMI
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
Median arcuate ligament syndrome
“Celiac artery compression syndrome”
CMI due to compression of celiac artery by diaphragm
Tx = release of arcuate ligament and bypass of persistent stricture
Morbidity associated with TPN
Catheter sepsis
Liver/kidney failure
Venous thrombosis
prognosis of CMI
Periop mortality 0-16%
Initial relief of symptoms with surgery 90%
Recurrence following surgery
Short Bowel Syndrome
Presence of
Causes of SBS
Adults - AMI, Crohn’s, Malignancy
Peds - Volvulus, intestinal atresia, necrotizing enterocolitis
Pathophys of SBS
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
Tx for SBS
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
Prognosis for SBS
50-70% who initially require TPN can be completely weaned
Peds patients are more likely than adults to gain independence from TPN
