SURGERY – SMALL INTESTINE

○​ Acidosis.
SMALL BOWEL OBSTRUCTION
DIAGNOSIS
●​ Mechanical small bowel obstruction is a common surgical issue.
●​ Causes are categorized as: ●​ Goals: differentiate mechanical obstruction from ileus, determine
○​ Intraluminal: Objects within the bowel (e.g., foreign bodies). etiology, distinguish partial from complete obstruction, and identify
○​ Intramural: Issues within the bowel wall (e.g., tumors). strangulation.
○​ Extrinsic: Problems outside the bowel pressing on it (e.g., ●​ History: prior abdominal surgeries, abdominal disorders.
adhesions). ●​ Physical exam: meticulous hernia search.
●​ Intra-abdominal adhesions from prior surgery are the leading cause (up ●​ Radiographic Examination:
to 75%). ○​ Abdominal series (supine, upright abdomen, and upright chest
●​ Hernias, malignant obstructions, and Crohn’s disease are less common. x-rays):
●​ Cancer-related obstructions are often due to external compression, not ■​ Specific finding: dilated small bowel loops (>3 cm), air-fluid
primary bowel tumors. levels (upright films), and minimal colon air.
●​ Congenital abnormalities can cause adult obstructions. ■​ Sensitivity: 70-80%; low specificity (ileus/colonic
●​ Superior mesenteric artery syndrome is a rare cause, compressing the obstruction mimic).
duodenum. ■​ False negatives: proximal obstruction, fluid-filled bowel (no
gas).

○​ Computed Tomography (CT) Scan:

■​ Preferred imaging test, ideally with oral contrast.
■​ Sensitivity: 80-90%; specificity: 70-90%.
■​ Findings: transition zone (dilated proximal, decompressed
distal), contrast not passing transition, minimal colon
gas/fluid.
■​ Detects closed-loop obstruction (U/C-shaped loop, radial
mesenteric vessels) and strangulation (thickened bowel
wall, pneumatosis intestinalis, portal venous gas,
mesenteric haziness, poor contrast uptake).
■​ Oral water soluble contrast can be used to predict non
PATHOPHYSIOLOGY
surgical resolution. Contrast in the colon within 24 hours is
●​ Obstruction leads to gas and fluid buildup proximal to the blockage. a good prognostic sign.
●​ Increased intestinal activity causes colicky pain and potential diarrhea. ■​ Limitations: low sensitivity (<50%) for low-grade/partial
●​ Gas comes from swallowed air and intestinal production. obstruction.
●​ Fluid includes swallowed liquids and gastrointestinal secretions.
●​ Bowel distension increases intraluminal and intramural pressure.
●​ Intestinal motility decreases.
●​ Normally sterile small bowel flora changes, with bacterial translocation
possible.
●​ High intramural pressure can impair blood flow, leading to intestinal
ischemia and necrosis(strangulated bowel obstruction).
●​ Partial small bowel obstruction allows some passage, with slower
progression.
●​ Closed loop obstruction (proximal and distal blockage) is dangerous,
causing rapid pressure increase and strangulation.
MANIFESTATION
●​ Symptoms: colicky abdominal pain, nausea, vomiting, and
obstipation.
●​ Proximal obstructions cause more prominent vomiting than distal ones.
●​ Feculent vomitus indicates bacterial overgrowth and established ○​ Small Bowel Series (Follow-Through):
obstruction. ■​ Contrast swallowed/instilled; serial abdominal radiographs.
●​ Continued flatus/stool passage (6-12 hours post-symptom onset) ■​ Water-soluble contrast used if perforation suspected.
suggests partial obstruction. ■​ More sensitive for luminal/mural etiologies (e.g., tumors).
●​ Signs: ○​ Enteroclysis:
○​ Abdominal distention (more pronounced in distal ileum ■​ Barium and methylcellulose instilled into jejunum via
obstruction) nasoenteric catheter.
○​ Altered bowel sounds (hyperactive initially, minimal later). ■​ Double-contrast technique for better mucosal assessment.
●​ Laboratory findings: ■​ Rarely used acutely; more sensitive for partial obstruction
○​ Hemoconcentration lesions.
○​ Electrolyte abnormalities ○​ CT Enterocolysis:
○​ Mild leukocytosis (due to volume depletion). ■​ Reported to be superior to plain film small bowel contrast
●​ Strangulated obstruction features: studies.
○​ Severe pain disproportionate to abdominal findings TREATMENT
○​ Tachycardia
●​ Fluid resuscitation is crucial due to intravascular volume depletion.
○​ Localized tenderness
Isotonic fluids are administered intravenously.
○​ Fever
●​ Bladder catheter monitors urine output.
○​ Marked leukocytosis
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 SURGERY – SMALL INTESTINE

●​ Central-venous or pulmonary-artery catheters are used in patients with ○​ Adhesions cause obstruction in 25-33% of cancer patients,
cardiac disease and severe dehydration. requiring appropriate therapy.
●​ Broad-spectrum antibiotics are used if bowel ischemia is suspected ○​ Palliative resection or bypass can improve quality of life in
and surgery is planned. recurrent malignancy cases.
●​ Nasogastric (NG) tube is used for continuous stomach evacuation, ○​ Surgical morbidity can be high (fistula, leak, mortality).
reducing nausea, distention, and aspiration risk. ○​ Patients with carcinomatosis and multifocal obstruction have
○​ Longer nasoenteric tubes are rarely used due to higher limited prognoses.
complication rates and no proven greater efficacy. ○​ Management is tailored to individual prognosis and desires.
●​ Partial obstruction is often managed nonoperatively. ○​ Bypass procedures are preferred to avoid difficult resections.
●​ Complete obstruction traditionally required surgery ○​ Palliative gastrostomy tubes can help with nausea and vomiting.
○​ Nonoperative approaches are now considered if closed-loop ILEUS AND OTHER DISORDERS OF INTESTINAL MOTILITY
obstruction and ischemia are ruled out.
●​ These are syndromes of impaired intestinal motility.
●​ Conservative therapy (NG decompression, fluid resuscitation) is
●​ They present with obstruction symptoms without a mechanical blockage.
common for initial management of nonischemic obstruction.
●​ Ileus is temporary and reversible.
●​ Surgery is considered if partial obstruction symptoms don't improve
●​ Chronic intestinal pseudo-obstruction involves irreversible dysmotility.
within 48 hours.
●​ Ileus is a significant morbidity factor in hospitalized patients, especially
●​ Water-soluble oral contrast is used for diagnosis, therapy, and
post-surgery.
prognosis, often reducing the need for surgery and hospital stay.
●​ Prolonged postoperative ileus increases hospital stays and costs.
○​ Operative procedure varies based on etiology (adhesions lysed,
tumors resected, hernias repaired).
○​ Affected intestine is examined; nonviable bowel is resected.
○​ Viability assessed by color, peristalsis, and arterial pulsations.
○​ Doppler probes or fluorescein dye can be used for borderline
cases, but clinical judgment is usually adequate.
○​ Short lengths of questionable bowel are resected in stable
patients, with primary anastomosis performed.
○​ Large areas of questionable viability may require a "second-look"
operation after 24-48 hours.
●​ Laparoscopic surgery is increasingly used, with lower complication
rates and shorter hospital stays, but higher surgical time.
●​ Proximal obstructions from single adhesive bands are best suited for
laparoscopic approach.
●​ Distended bowel and multiple adhesions increase difficulty and
conversion rates.
OUTCOMES
●​ Perioperative mortality for nonstrangulated obstruction is <5%, primarily
in elderly patients with comorbidities.
●​ Mortality for strangulated obstruction is higher, emphasizing the need for
prompt intervention.
●​ Long-term prognosis depends on obstruction etiology. PATHOPHYSIOLOGY
●​ Most patients treated conservatively for adhesive obstruction do not
●​ Factors causing ileus: abdominal surgery, infections, inflammation,
require readmission.
electrolyte abnormalities, and drugs.
●​ Recurrence risk for adhesive obstruction after surgical intervention is
●​ Post-abdominal surgery:
5.5% at 1 year, 11.3% at 3 years, and 13.5% at 5 years.
○​ Dysmotility from surgical stress reflexes, inflammatory mediators,
●​ Standard hospital policies can improve care, reducing time to surgery
and anesthetic/analgesic effects.
and hospital stay.
○​ Normal motility return: small intestine (24 hours), stomach (48
PREVENTION hours), colon (2-5 days).
●​ Preventing postoperative adhesions is crucial due to the burden of ○​ Bowel sounds are not a reliable resolution indicator; passing
adhesive small bowel obstruction. flatus/bowel movement is better.
●​ Good surgical technique, careful tissue handling, and minimal foreign ○​ Resolution delayed by intra-abdominal abscesses or electrolyte
body exposure are fundamental. imbalances.
●​ Laparoscopic surgery is strongly recommended over open surgery to ●​ Chronic intestinal pseudo-obstruction causes:
reduce adhesion risk. ○​ Visceral myopathies: degeneration and fibrosis of intestinal
○​ Open surgery has a fourfold increased risk of small bowel muscle.
obstruction within 5 years. ○​ Visceral neuropathies: degeneration of myenteric and
●​ Hyaluronan-based agents (e.g., Seprafilm) have shown some success in submucosal plexuses.
reducing postoperative bowel adhesions in open surgeries. ○​ Sporadic and familial forms exist.
○​ Their impact on reducing actual small bowel obstruction is less ○​ Systemic disorders (sclerosis, muscular dystrophy, Parkinson’s)
defined. can cause it.
○​ Use is at surgeon's discretion. ○​ Viral infections (cytomegalovirus, Epstein-Barr) can also be
○​ Wrapping intestinal anastomosis with these products is causative.
discouraged due to increased leak rates. MANIFESTATION
OTHER CAUSES OF SMALL BOWEL OBSTRUCTION ●​ Ileus:
●​ Early Postoperative Bowel Obstruction: ○​ Resembles small bowel obstruction.
○​ Occurs within 30 days of surgery (0.7-9% of patients, higher in ○​ Symptoms:
pelvic/colorectal surgery). ■​ Intolerance to oral intake
○​ CT or small bowel series are needed for diagnosis. ■​ Nausea
○​ Usually partial; rarely strangulated. ■​ Lack of flatus/bowel movements.
○​ Extended nonoperative therapy (2-3 weeks: bowel rest, hydration, ○​ Signs:
TPN) is often warranted. ■​ Vomiting
○​ Immediate reoperation is needed for complete obstruction or ■​ Abdominal distention
peritonitis signs. ■​ Diminished/absent bowel sounds (unlike hyperactive
●​ Crohn’s Disease sounds in mechanical obstruction).
●​ Malignant Small Bowel Obstruction: ●​ Chronic Intestinal Pseudo-obstruction:
○​ Often indicates advanced disease with poor prognosis. ○​ Variable nausea

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○​ Vomiting
○​ Abdominal pain
○​ Distention.
DIAGNOSIS
●​ Routine postoperative ileus needs no diagnostic evaluation.
●​ Prolonged postoperative ileus (persists beyond 5 days) requires
evaluation.
○​ Defined as "interval from surgery until passage of flatus/stool AND
tolerance of an oral diet”.
○​ Prolonged is defined as having two or more of the following:
■​ Nausea/vomiting
■​ Inability to tolerate oral diet over 24 h
■​ Absence of flatus over 24 h
■​ Distension
■​ Radiologic confirmation occurring on or after day 4
postoperatively without prior resolution of postoperative
ileus.
●​ Prolonged ileus occurs in 10-15% of intestinal surgery patients.
○​ Evaluation includes:
■​ Reviewing medications (especially opiates).
■​ Measuring serum electrolytes.
■​ Abdominal radiographs (difficult to distinguish from
mechanical obstruction).
■​ CT scanning (preferred; detects abscesses and excludes
mechanical obstruction).
●​ Chronic pseudo-obstruction diagnosis:
○​ Clinical features, radiographic, and manometric studies.
○​ Laparotomy/laparoscopy with full-thickness biopsy for neural
disorders.
TREATMENT
●​ Ileus management:
○​ Limiting oral intake.
○​ Correcting underlying cause.
○​ Nasogastric tube for vomiting/distention.
○​ Intravenous fluids and electrolytes.
○​ Total parenteral nutrition (TPN) for prolonged ileus.
●​ Strategies to reduce ileus duration: CROHN’S DISEASE
○​ Nonsteroidal anti-inflammatory drugs (ketorolac). ●​ Chronic, idiopathic transmural inflammation with skip lesions.
○​ Perioperative thoracic epidural anesthesia/analgesia. ●​ Affects any part of the alimentary tract, especially the distal small bowel.
○​ Limiting intra- and postoperative fluids. ●​ Nearly 80% of patients have small bowel involvement; 30% have terminal
○​ Early postoperative feeding. ileitis exclusively.
○​ Early Recovery After Surgery (ERAS) pathways. ●​ Prevalence: approximately 241 cases per 100,000 in the U.S.
●​ Prokinetic agents have unfavorable efficacy-toxicity profiles. ●​ Higher incidence in Western nations and northern latitudes (Canada has
●​ Alvimopan (peripheral mu-opioid receptor antagonist) reduces ileus the highest rates).
duration, hospital stay, and readmissions. ●​ Lower prevalence in countries like China, but rates are increasing.
●​ Chronic intestinal pseudo-obstruction therapy: ●​ Incidence varies among ethnic groups:
○​ Palliative symptom management. ○​ Ashkenazi Jewish population (Eastern European) has a two- to
○​ Fluid, electrolyte, and nutritional management. fourfold higher risk.
○​ Surgery avoided if possible. ●​ Slightly more prevalent in females.
○​ Prokinetic agents (metoclopramide, erythromycin) have poor ●​ Bimodal distribution: peak diagnosis in the third and sixth decades of life.
efficacy. ●​ Genetic and environmental factors contribute.
○​ Cisapride (limited availability due to cardiac toxicity). ○​ First-degree relatives have a 14-15 times higher risk.
○​ Refractory cases: ○​ Monozygotic twin concordance rate: up to 67%.
■​ TPN ●​ Higher socioeconomic status is associated with increased risk.
■​ Decompressive gastrostomy ●​ Breastfeeding is protective.
■​ Small bowel resection ●​ Smoking increases prevalence and postsurgical relapse risk.
○​ Small-intestinal transplantation (role still being defined). PATHOPHYSIOLOGY
●​ Sustained inflammation of unknown cause.
●​ Genetic susceptibility and gut microbiome play a role.
●​ Abnormal epithelial barrier function or immune dysregulation.
●​ Mucosal T-cell over-responsiveness leads to defective immune tolerance.
●​ Genetic defects:
○​ NOD2 gene (IBD1 locus on chromosome 16): 40-fold increased
risk with allelic variants.
○​ IBD2 on chromosome 12q, and IBD3 on chromosome 6 are under
investigation.
●​ Appendectomy does not increase Crohn's disease risk.
●​ Pathological lesions:
○​ Aphthous ulcers (early lesions).
] ○​ Noncaseating granulomas (up to 70% of surgical specimens).
○​ Stellate-shaped ulcers, linear/serpiginous ulcers, cobblestoned
mucosa.
○​ Transmural inflammation: fibrosis, strictures, abscesses, fistulas,
rare perforation.
○​ Skip lesions (discontinuous inflammation).

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○​ Fat wrapping (encroachment of mesenteric fat) is pathognomonic. ●​ No single diagnostic test; based on clinical presentation, radiographic,
●​ Differentiation from ulcerative colitis: endoscopic, and pathologic findings.
○​ Inflammation depth (transmural in Crohn’s, mucosa/submucosa in ●​ Blood tests: full blood count, electrolytes, renal and liver function, iron,
ulcerative colitis). B12, ESR, CRP.
○​ Longitudinal extent (discontinuous/rectum-sparing in Crohn’s, ○​ May show anemia (nondiagnostic).
continuous/rectum-affecting in ulcerative colitis). ●​ Colonoscopy with terminal ileum intubation: main diagnostic tool.
○​ Ulcerative colitis can include backwash ileitis. ○​ Reveals focal ulcerations, cobblestone appearance, skip areas,
MANIFESTATION and pseudopolyps.
●​ Imaging: barium small bowel follow-through, CT enterography, MR
●​ Common symptoms: abdominal pain, diarrhea, and weight loss.
enterography.
●​ Highly variable clinical features based on affected GI segment,
○​ Reveals strictures or ulcer/fissure networks.
inflammation intensity, and complications.
○​ CT scan for intra-abdominal abscesses and to rule out other
●​ Misdiagnosis as irritable bowel syndrome or celiac disease is possible.
abdominal disorders.
●​ Patients classified by predominant manifestation:
●​ Esophagogastroduodenoscopy (EGD) for proximal alimentary tract
○​ Fibrostenotic disease.
disease.
○​ Fistulizing disease.
●​ Capsule endoscopy for small bowel imaging.
○​ Aggressive inflammatory disease.
●​ Antibody tests:
●​ Insidious symptom onset with waxing and waning severity.
○​ ASCA+/pANCA– (Crohn’s disease).
●​ Constitutional symptoms: weight loss, fever, or growth retardation.
○​ ASCA–/pANCA+ (ulcerative colitis).
●​ 80% of cases affect the small bowel; 20% affect the colon alone.
○​ High specificity, low sensitivity.
●​ Majority of small bowel disease is ileocecal.
●​ Stool tests (fecal calprotectin, lactoferrin) can identify intestinal
●​ 5-10% have isolated perineal and anorectal disease.
inflammation, but are not routinely used.
●​ Uncommon sites: esophagus, stomach, and duodenum.
●​ Diagnosis often delayed due to insidious presentation.
●​ 25% have extraintestinal manifestations (some common ones include
●​ Acute presentations: diagnosis during surgery (laparotomy/laparoscopy).
erythema nodosum, and peripheral arthritis).
○​ Right lower quadrant pain mimicking appendicitis.
○​ 25% of those affected will have more than one manifestation.
○​ Acute abdomen from small bowel obstruction, abscess, or
perforation.
○​ Perianal abscesses/fistulas.
TREATMENT
●​ Goal: palliate symptoms, not cure.
●​ Medical therapy: induce and maintain remission.
●​ Surgery: specific indications.
●​ Nutritional support: enteral or parenteral nutrition.
MEDICAL THERAPY
●​ Agents: antibiotics, aminosalicylates, corticosteroids,
immunomodulators, biologic therapies.
●​ Antibiotics: adjunctive role; perianal disease, fistulas, colonic disease.
●​ Disease activity assessment: Crohn’s disease Activity Index or
Harvey-Bradshaw Index.
●​ Mild/moderate disease: outpatient management.
●​ Severe/fulminant disease: hospitalization, bowel rest, nutritional support.
●​ Treatment approaches:
○​ Top-down: potent agents initially, then tapered.
○​ Step-up: less potent drugs initially, then advanced.
●​ 5-ASA drugs (mesalamine): used for mild small bowel disease.
●​ Glucocorticoids: mild/moderate disease; intravenous for severe disease.
○​ Tapered once remission achieved; steroid dependence/resistance
DIAGNOSIS requires immunomodulators.
●​ Diagnosis based on endoscopic findings and clinical history. ○​ Budesonide: oral steroid with fewer systemic effects.
●​ Considered in patients with: ●​ Thiopurine antimetabolites (azathioprine, 6-mercaptopurine): severe
○​ Acute/chronic abdominal pain disease, remission maintenance, steroid tapering.
(especially right lower ○​ Response in 3-6 months; can cause bone marrow suppression.
quadrant). ●​ Methotrexate: alternative for thiopurine non-responders.
○​ Chronic diarrhea. ●​ Infliximab (anti-TNFα antibody): biologic therapy for remission induction
○​ Radiographic/endoscopic and fistula closure.
evidence of intestinal ○​ Adalimumab and certolizumab pegol are other anti-TNFα
inflammation. antibodies.
○​ Bowel stricture or fistula. ○​ Vedolizumab (anti–α4β7 integrin): intestine specific
○​ Inflammation/granulomas on anti-inflammatory effect.
intestinal histology. ●​ Perianal disease: metronidazole or ciprofloxacin; azathioprine for relapse.
●​ Differential diagnoses: ulcerative ●​ Fistulas: infliximab and azathioprine.
colitis, irritable bowel syndrome, SURGICAL THERAPY
mesenteric ischemia, collagen
●​ Decreased need with new treatments.
vascular diseases,
●​ Reserved for unresponsive disease or complications.
carcinoma/lymphoma, diverticular
●​ Indications:
disease, and infectious
○​ Failed medical management
enteritides.
○​ Medication complications
○​ Acute ileitis
○​ Growth retardation.
(Campylobacter, Yersinia).
○​ Intestinal obstruction: Most common indication
○​ Typhoid enteritis
○​ Abscesses: percutaneous drainage.
(Salmonella typhosa).
○​ Fistulas: surgery if symptomatic or metabolic derangements.
○​ Intestinal tuberculosis
○​ Less common: hemorrhage, perforation, cancer.
(Mycobacterium
tuberculosis).
○​ Cytomegalovirus (CMV).

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PATHOPHYSIOLOGY
●​ Manifestations depend on involved structures.
●​ Enteroenteric fistulas: malabsorption.
●​ Enterovesicular fistulas: recurrent urinary tract infections.
●​ Enterocutaneous fistulas: skin excoriation, dehydration, electrolyte
abnormalities, malnutrition.
●​ Spontaneous closure inhibitors: malnutrition, sepsis, inflammatory bowel
disease, cancer, radiation, distal obstruction, foreign bodies, high output,
short fistulous tract (<2 cm), epithelialization.
MANIFESTATION
●​ Iatrogenic enterocutaneous fistulas: evident 5-10 days postoperatively.
●​ Initial signs:
○​ Fever
●​ Intraoperative discovery of terminal ileum inflammation: medical
○​ Leukocytosis
treatment; appendectomy (unless cecum inflamed).
○​ Prolonged ileus
●​ Planned surgery: examination of entire intestine; note skip lesions.
○​ Abdominal tenderness
●​ Segmental intestinal resection with primary anastomosis: standard
○​ Wound infection.
procedure.
●​ Diagnosis: enteric material drainage through wound or drains.
○​ Microscopic Crohn’s at margins does not compromise
●​ Often associated with intra-abdominal abscesses.
anastomosis.
○​ Margin length does not affect recurrence. DIAGNOSIS
○​ End to end sutures and side to side staples have similar ●​ CT scan with enteral contrast: initial test; detects contrast leakage and
outcomes. abscesses.
●​ Stricturoplasty: alternative for obstructing lesions; preserves intestinal ●​ Small bowel series or enteroclysis: fistula origin and distal obstruction.
surface. ●​ Fistulogram: contrast injection into fistula tract; used when other
○​ Heinecke-Mickulicz or Finney pyloroplasty; side-to-side methods fail.
isoperistaltic enteroenterostomy. TREATMENT
○​ Metallic clips mark sites.
●​ Steps:
○​ Recurrence rates similar to resection; cancer risk is theoretical.
○​ Stabilization: fluid/electrolyte resuscitation, parenteral nutrition,
○​ Contraindicated: abscesses, fistulas.
sepsis control, skin protection.
○​ Investigation: fistula anatomy definition.
○​ Decision: treatment options and timeline.
○​ Definitive management: surgical procedure.
○​ Rehabilitation.
●​ Goal: spontaneous closure.
●​ TPN; oral/enteral nutrition for low-output distal fistulas.
●​ Octreotide: adjunct for high-output fistulas.
●​ Negative pressure wound therapy: manages fistula output.
●​ Surgical intervention:
○​ 2-3 months of conservative therapy.
○​ Fistula tract and originating intestine resection.
○​ Simple closure has high recurrence.
○​ Challenging due to adhesions.
○​ Biologic sealants: alternative therapies.
OUTCOMES
●​ 50% spontaneous closure.
●​ “FRIEND” mnemonic:
○​ Foreign body
○​ Radiation
○​ Infection/Inflammation
○​ Epithelialization
○​ Neoplasm
○​ Distal obstruction.
○​ ●​ Surgical treatment:
●​ Intestinal bypass: intramesenteric abscesses, dense inflammatory mass, ○​ High percentage of fistulas originate from the small bowel, and are
duodenal strictures. iatrogenic.
●​ Laparoscopic surgery: less pain, shorter ileus, shorter hospital stay; ○​ 30-day mortality: ~4%; 1-year mortality: 15%.
similar recurrence rates. ○​ Morbidity: >80%.
OUTCOMES ○​ First surgical repair success: 70%; overall closure: 84%.
●​ Complication rates: 15-30% (wound infections, abscesses, leaks). ○​ Abdominal fascia closure reduces refistulization and mortality.
●​ Surgery is not curative; recurrence is common. ○​ Recurrence: 30%; associated with high output and non-resection
●​ Endoscopic recurrence: 70% at 1 year, 85% at 3 years. surgery.
●​ Clinical recurrence: 60% at 5 years, 94% at 15 years.
●​ Reoperation: one-third by 5 years.
●​ Smoking is a risk factor for recurrence.
INTESTINAL FISTULAS
●​ Abnormal communication between epithelialized surfaces.
●​ Internal fistula: between two GI tract parts or adjacent organs.
●​ External fistula: involves skin or external surface.
●​ Enterocutaneous fistulas:
○​ Low-output: <200 mL/day.
○​ High-output: >500 mL/day.
●​ 80% are iatrogenic (enterotomies, anastomotic dehiscences).
●​ Spontaneous fistulas: Crohn’s disease, cancer.

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RADIATION ENTERITIS MECKEL’S DIVERTICULA

●​ Undesired side effect of radiation therapy for abdominal/pelvic cancers. ●​ Most common congenital GI anomaly, affecting ~2% of the population.
●​ Two distinct syndromes: ●​ True diverticula: all small intestine
○​ Acute radiation enteritis: transient, occurs in ~75% of patients. wall layers present.
○​ Chronic radiation enteritis: inexorable, occurs in 5-15% of ●​ Usually in ileum, within 100 cm of
patients. ileocecal valve.
PATHOPHYSIOLOGY ●​ ~60% contain heterotopic mucosa
(gastric most common).
●​ Radiation induces cellular injury via free radicals, leading to apoptosis.
●​ “Rule of twos”: 2% prevalence, 2:1
●​ Rapidly proliferating small-intestinal epithelium is highly susceptible.
male predominance, 2 feet proximal
●​ Acute injury: villus blunting, leukocyte/plasma cell infiltrate, mucosal
to ileocecal valve, half symptomatic
sloughing, ulceration, hemorrhage.
under 2 years.
○​ Intensity related to radiation dose (>4500 cGy).
○​ Risk factors: limited splanchnic perfusion (hypertension, diabetes,
coronary artery disease), adhesions. PATHOPHYSIOLOGY
○​ Potentiated by chemotherapy (doxorubicin, 5-fluorouracil, ●​ Incomplete obliteration of omphalomesenteric (vitelline) duct during 8th
actinomycin D, methotrexate). week of gestation.
○​ Resolves after radiation cessation due to epithelial regeneration. ●​ Other abnormalities: omphalomesenteric fistula, enterocyst, fibrous band
●​ Chronic injury: progressive occlusive vasculitis, chronic ischemia, to umbilicus.
fibrosis (all intestinal wall layers). ●​ Mesodiverticular band (remnant of left vitelline artery) can tether
○​ Leads to strictures, abscesses, fistulas. diverticulum to mesentery.
MANIFESTATION ●​ Bleeding: ileal mucosal ulceration near acid-producing gastric mucosa.
●​ Intestinal obstruction mechanisms:
●​ Acute: nausea, vomiting, diarrhea, crampy abdominal pain.
○​ Volvulus around fibrous band.
○​ Transient, subsides after radiation cessation.
○​ Entrapment by mesodiverticular band.
○​ CT scan if peritonitis signs.
●​ Chronic: evident within 2 years (can be months to decades later).
○​ Diarrhea, partial small bowel obstruction (nausea, vomiting,
distention, pain, weight loss).
○​ Terminal ileum most affected.
○​ Complete obstruction, hemorrhage, abscess, fistula.
DIAGNOSIS
●​ Chronic:
○​ Review radiation treatment records (dose, fractionation, volume).
○​ Enterocolysis: most accurate imaging (>90%
sensitivity/specificity). ○​ Intussusception (diverticulum as lead point).
○​ CT scan: rule out recurrent cancer. ○​ Stricture from chronic diverticulitis.
●​ Littre’s hernia: diverticulum in inguinal or femoral hernia sac.
MANIFESTATION
●​ Usually asymptomatic unless complications arise.
●​ Lifetime complication incidence: ~4-6%.
●​ Complications: bleeding, intestinal obstruction, diverticulitis.
●​ Bleeding: most common in children (<18 years); rare in adults >30 years.
●​ Intestinal obstruction: most common in adults.
●​ Diverticulitis: mimics acute appendicitis (~20% of symptomatic cases).
●​ Neoplasms: Carcinoid tumors (.5-3.2% of resected symptomatic cases)
DIAGNOSIS
●​ Often incidental finding (radiography, endoscopy, surgery).
●​ Difficult to diagnose before surgery (except bleeding).
●​ CT scan: low sensitivity.
●​ Enterocolysis: 75% accuracy; not for acute cases.
TREATMENT ●​ Radionuclide scan (99mTc-pertechnetate): detects ectopic gastric
mucosa; 90% accurate in children, <50% in adults.
●​ Acute: self-limited; antiemetics, parenteral fluids (dehydration).
●​ Angiography: localizes bleeding during acute hemorrhage.
○​ Rarely requires radiation therapy reduction.
●​ Chronic: challenging.
○​ Antidiarrheals, low-residue diet (obstructive symptoms).
○​ Surgery: high morbidity; reserved for high-grade obstruction,
perforation, hemorrhage, abscess, fistula.
■​ Goal: limited resection with primary anastomosis.
■​ Difficult due to diffuse fibrosis and adhesions.
■​ High leak rates with anastomoses between irradiated
segments (~50%).
■​ Intestinal bypass if limited resection not possible (except
hemorrhage).
■​ Short bowel syndrome may occur.
OUTCOMES & PREVENTION
●​ Outcomes:
○​ Acute injury: self-limited; no correlation with chronic enteritis.
○​ Chronic: high surgical morbidity; ~10% mortality.
●​ Prevention:
○​ Radiation exposure <5000 cGy.
○​ Multibeam radiation techniques, tilt tables. TREATMENT
○​ Oral sulfasalazine (limited evidence). ●​ Symptomatic diverticula: diverticulectomy with band removal.
○​ Surgical techniques to keep small bowel out of pelvis (absorbable ●​ Bleeding: segmental ileal resection (diverticulum and ulcer).
mesh sling). ●​ Segmental resection: tumor, inflamed/perforated diverticulum base.

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●​ Asymptomatic diverticula: Controversial.

○​ Historically, prophylactic removal was not recommended.
○​ Meta-analysis showed a very high number needed to treat to
prevent one death.
○​ Some advocate for removal, citing low morbidity and potential
underestimation of complication risk.
○​ Selective approach: removal in younger patients (<50 years),
those with bands/ectopic tissue, or diverticula >2 cm.
●​ There is a lack of controlled studies to support or refute the selective
approach.
ACQUIRED DIVERTICULA
TREATMENT
●​ False diverticula: walls lack complete muscularis (mucosa and
●​ Asymptomatic: leave alone.
submucosa only).
●​ Bacterial overgrowth: antibiotics.
●​ Duodenum: periampullary, juxtapapillary, perivaterian (near ampulla);
●​ Jejunum/ileum complications (bleeding, diverticulitis): segmental
75% on medial wall.
intestinal resection.
●​ Jejunum/ileum: jejunoileal diverticula; 80% jejunum, 15% ileum, 5%
●​ Lateral duodenal diverticula complications: diverticulectomy.
both.
●​ Medial duodenal diverticula complications: nonoperative (endoscopy) if
○​ Jejunum: large, multiple diverticula.
possible.
○​ Ileum: small, solitary diverticula.
○​ Emergent bleeding: lateral duodenotomy and oversewing.
●​ Duodenal diverticula prevalence: 0.16-6% (upper GI), 5-27% (ERCP),
○​ Perforation: wide drainage.
23% (autopsy); increases with age.
●​ Biliary/pancreatic symptoms: diverticulectomy is controversial and not
●​ Jejunoileal diverticula prevalence: 1-5%; increases with age (6th-7th
routine.
decades).
MESENTERIC ISCHEMIA
PATHOPHYSIOLOGY
●​ Two distinct syndromes: acute and chronic.
●​ Herniation of mucosa/submucosa through weakened muscularis due to
●​ Acute Mesenteric Ischemia:
intestinal smooth muscle abnormalities or dysregulated motility.
○​ Four pathophysiologic mechanisms:
●​ Bacterial overgrowth: vitamin B12 deficiency, megaloblastic anemia,
■​ Arterial embolus (most common, >50%).
malabsorption, steatorrhea.
■​ Arterial thrombosis.
●​ Periampullary duodenal diverticula: can compress common
■​ Vasospasm (nonocclusive mesenteric ischemia or NOMI).
bile/pancreatic ducts (obstructive jaundice, pancreatitis).
■​ Venous thrombosis.
●​ Jejunoileal diverticula: intestinal obstruction via intussusception or
○​ Embolus: usually cardiac origin (left atrial/ventricular thrombi,
compression.
valvular lesions).
MANIFESTATION ■​ Superior mesenteric artery most common site.
●​ Usually asymptomatic unless complications arise (6-10%). ■​ Thrombosis: usually at proximal mesenteric arteries,
●​ Complications: superimposed on atherosclerosis.
○​ Intestinal obstruction ■​ NOMI: vasospasm, in critically ill patients (vasopressor
○​ Diverticulitis agents).
○​ Hemorrhage ■​ Venous thrombosis: superior mesenteric vein (95% of
○​ Perforation cases).
○​ Malabsorption ●​ Primary (no identifiable cause) or secondary
●​ Periampullary duodenal diverticula may be associated with : (coagulation disorders).
○​ Choledocholithiasis ○​ Leads to mucosal sloughing (3 hours) and full-thickness infarction
○​ Cholangitis (6 hours).
○​ Pancreatitis ●​ Chronic Mesenteric Ischemia:
○​ Sphincter of Oddi dysfunction ○​ Insidious development, collateral circulation, rarely infarction.
●​ Jejunoileal diverticula (10-30%): ○​ Arterial: atherosclerotic lesions in splanchnic arteries (celiac,
○​ Intermittent abdominal pain superior mesenteric, inferior mesenteric).
○​ Flatulence ■​ At least two arteries stenosed/occluded.
○​ Diarrhea ○​ Venous: portal/splenic veins, portal hypertension (varices,
○​ Constipation splenomegaly, hypersplenism).
DIAGNOSIS MANIFESTATION
●​ Often incidental finding (radiography, endoscopy, surgery). ●​ Acute:
●​ Duodenal diverticula: ultrasound/CT can mimic other abdominal ○​ Severe abdominal pain (out of proportion to tenderness).
masses. missed by forward viewing endoscopes, best seen on upper GI ○​ Colicky pain, midabdomen.
radiographs. ○​ Nausea, vomiting, diarrhea.
○​ Early: few physical findings.
○​ Late (infarction): distention, peritonitis, bloody stools.
●​ Chronic:
○​ Insidious onset.
○​ Postprandial abdominal pain (“food fear”), weight loss.
○​ Chronic venous thrombosis: often asymptomatic, variceal
bleeding.
MISCELLANEOUS CONDITIONS
OBSCURE GI BLEEDING
●​ GI bleeding with no source found by EGD and colonoscopy.
●​ Overt GI bleeding: hematemesis, melena, hematochezia.
●​ Occult GI bleeding: detected by lab tests (anemia) or stool tests (guaiac).
●​ 20% of obscure GI bleeding is occult.
●​ Small bowel is the most common location of lesions.
●​ Jejunoileal diverticula: enterocolysis (most sensitive).
○​ Angiodysplasias (adults, ~75%).
○​ Neoplasms (adults, ~10%).
○​ Meckel’s diverticulum (children).
○​ Other causes: Crohn’s, infections, NSAID ulcers, vasculitis,
ischemia, varices, diverticuli, intussusception.

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DIAGNOSIS ○​ Endoscopic repairs are sometimes possible if the iatrogenic

perforation is recognized immediately.
●​ Tailored to bleeding severity and available technology.
●​ Jejunum/ileum perforation: peritoneal cavity, overt symptoms (pain,
●​ Enteroscopy: increasingly important.
tenderness, distention, fever, tachycardia).
○​ Push enteroscopy: visualizes proximal jejunum; diagnostic yield
○​ Plain abdominal radiographs: free intraperitoneal air.
3-65%; allows cauterization.
○​ CT scan: if perforation suspected but not obvious.
○​ Sonde enteroscopy: peristalsis-driven; visualization during
○​ Jejunal/ileal perforations: surgical repair or segmental resection.
withdrawal; no biopsy/therapy capability; abandoned due to
capsule endoscopy. SHORT BOWEL SYNDROME
○​ Wireless capsule enteroscopy: high success rate in identifying ●​ Significant malabsorption due to extensive intestinal resection.
small bowel pathology; no biopsy/therapy; does not improve ●​ Anatomically: <200 cm residual small bowel in adults.
outcomes. ●​ Adult causes:
○​ Enterocolysis: used if push/capsule enteroscopy is negative. ○​ Mesenteric ischemia
○​ 99mTc-pertechnetate scintigraphy: Meckel’s diverticulum (low ○​ Malignancy
yield in adults >40). ○​ Crohn’s Disease
○​ Angiography: detects angiodysplasia and vascular tumors; used ●​ Pediatric causes:
for persistent or overt bleeding. ○​ Intestinal atresias
○​ Exploratory laparoscopy/laparotomy with intraoperative ○​ Volvulus
enteroscopy: for undiagnosed, persistent, or recurrent bleeding. ○​ Necrotizing enterocolitis.
■​ Endoscope inserted perorally or via enterotomy. PATHOPHYSIOLOGY
■​ Transillumination helps identify angiodysplasias.
●​ <50% resection: generally tolerated.
■​ Lesions marked with sutures for resection.
●​ 50-80% resection: significant malabsorption.
■​ Examination during insertion (not withdrawal) to avoid
●​ Adults without colon: lifelong TPN if <100 cm residual bowel.
confusing trauma with lesions.
●​ Adults with colon: lifelong TPN if <60 cm residual bowel.
●​ Management Algorithm:
●​ Infants: TPN independence with as little as 10 cm residual bowel.
○​ Push/capsule enteroscopy (if bleeding stopped).
●​ Factors affecting malabsorption:
○​ Enterocolysis (if enteroscopy negative).
○​ Intact colon: absorbs fluid, electrolytes, short-chain fatty acids.
○​ 99mTc-pertechnetate scintigraphy (Meckel’s diverticulum).
○​ Ileocecal valve: delays transit, increases absorption.
○​ “Watch-and-wait” or angiography (if no diagnosis).
○​ Healthy residual intestine.
○​ Laparoscopy/laparotomy with intraoperative enteroscopy (if
○​ Jejunum resection better tolerated than ileum (bile salt, B12
persistent or recurrent bleeding).
absorption).
●​ Intestinal adaptation (1-2 years): decreased bowel movements, increased
absorption, reduced TPN.
●​ Hypergastrinemia: increased gastric acid, inhibits absorption.
TREATMENT
●​ Medical:
○​ TPN initially.
○​ Enteral nutrition gradually introduced.
○​ H2 blockers/proton pump inhibitors: reduce gastric acid.
○​ Antimotility agents (loperamide, diphenoxylate): slow transit.
○​ Octreotide: reduces GI secretions (inhibits adaptation).
○​ TPN titration during adaptation.
●​ Nontransplant Surgical:
○​ Restore intestinal continuity (stomas).
○​ Lengthening procedures:
■​ Longitudinal intestinal lengthening and tailoring (LILT).
■​ Serial transverse enteroplasty procedure (STEP).
○​ Procedures that slow intestinal transit have unclear efficacy.
●​ Intestinal Transplantation:
○​ Indications: TPN complications (liver failure, venous thrombosis,
SMALL BOWEL PERFORATION sepsis, dehydration).
●​ Historically: duodenal perforation from peptic ulcer disease. ○​ Types: intestine-alone, intestine/liver, multivisceral.
●​ Currently: iatrogenic injury during endoscopy (most common). ○​ High graft function, but high morbidity (rejection, CMV,
●​ Other causes: infections (tuberculosis, typhoid, CMV), Crohn’s, ischemia, lymphoproliferative disease).
drug-induced ulcers, radiation injury, Meckel’s and acquired diverticuli, ●​ Alternative Therapies:
neoplasms, foreign bodies. ○​ GLP-2, glutamine/growth hormone with high-carbohydrate diet.
●​ Iatrogenic: duodenal perforation during ERCP with ES (most common). OUTCOMES
○​ Incidence decreasing, ~0.5%. ●​ 50-70% achieve TPN independence.
Stapfer Type Classification ●​ Pediatric prognosis better than adults.
●​ Poor survival with end-enterostomies and <50 cm residual bowel.
I Free bowel wall perforation
●​ Transplant survival: variable based on type of transplant.
II Retroperitoneal duodenal perforation (periampullary injury)

III Pancreatic or bile duct perforation

IV Retroperitoneal air alone

○​ Type II most common; often managed nonsurgically.
○​ Manifestations can mimic pancreatitis (hyperamylasemia).
○​ CT scan: most sensitive; pneumoperitoneum (free perforations),
retroperitoneal air, contrast extravasation, paraduodenal fluid.
○​ Asymptomatic retroperitoneal air after ERCP: common, no
treatment needed.
○​ Retroperitoneal perforations: nonoperative management if no
progression/sepsis.
○​ Intraperitoneal perforations: surgical repair (pyloric exclusion,
gastrojejunostomy, tube duodenostomy).

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