Complications of Peptic Ulcer Disease

Overview

I. Gastrointestinal Bleeding (Hemorrhage)

Epidemiology

• The most frequent complication of PUD; annual incidence of ulcer bleeding ranges from 19–57 per 100,000 individuals (~0.02–0.06%)
• Bleeding peptic ulcers are the most common cause of upper GI bleeding in hospitalized patients
• NSAIDs are linked to 50–75% of bleeding peptic ulcers, one-third of hemorrhage deaths, and 30% of hospitalizations
• NSAIDs increase bleeding risk 3-fold under age 65 and 8-fold over age 75 — Mulholland & Greenfield's Surgery, 7e; Sleisenger & Fordtran's GI Disease

Clinical Manifestations

• Melena and/or hematemesis are the classic presentations
• Nasogastric aspiration confirms upper GI bleeding
• Abdominal pain is quite uncommon with bleeding ulcers
• Hypovolemic shock may be present in severe hemorrhage, necessitating aggressive resuscitation and blood transfusion
• Signs/symptoms of chronic anemia may precede acute events

Diagnostic Methods

• Early endoscopy (within 24 hours) diagnoses the bleeding source and guides hemostatic therapy
• The Forrest Classification stratifies endoscopic stigmata and prognosis:

• Active bleeding (Ia/Ib) and nonbleeding visible vessels (IIa) warrant endoscopic therapy
• Adherent clots (IIb): clot removal + endoscopic treatment lowers rebleeding risk from 30% → 5%
• Doppler endoscopic probe can detect arterial flow even under minor stigmata

• Glasgow Blatchford Score (GBS): uses BUN, Hgb, pulse, systolic BP, melena, syncope, cardiac/hepatic failure — predicts need for intervention; GBS ≤1 → outpatient management appropriate
• Rockall Score: composite pre- and post-endoscopy score predicting mortality (max 11; score ≤2 = low risk; score of 0 = negligible mortality, score of 5 = ~30% in-hospital mortality via AIMS65) — Schwartz's; Sleisenger & Fordtran's

Conservative (Medical) Management

• Nil by mouth + IV proton pump inhibitor (PPI): ~75% of patients stop bleeding spontaneously
• High-dose IV PPI (e.g., omeprazole 80 mg bolus → 8 mg/hr infusion) raises gastric pH, stabilizing clot
• Fluid resuscitation and blood transfusion as needed
• Treat H. pylori if positive — eradication dramatically reduces rebleeding risk
• Endoscopic hemostasis: epinephrine injection, electrocautery, hemoclips

Indications for Hospitalization

• Any significant upper GI bleed (hematemesis, melena, hematochezia with hemodynamic instability)
• Glasgow Blatchford Score ≥2 (score ≤1 may allow safe outpatient management)
• Hemodynamic instability: tachycardia, hypotension, shock
• Transfusion requirement
• Active bleeding or high-risk endoscopic stigmata (Forrest Ia, Ib, IIa)
• Significant comorbidities, advanced age, anticoagulant use

Surgical Management

• Indication: failure of 2 endoscopic attempts; persistent hemodynamic instability; transfusion >4 units/24 hours; rebleeding after initial control; deep ulcers on posterior duodenal bulb or lesser gastric curvature (erode the gastroduodenal artery — not amenable to endoscopy)
• Posterior duodenal ulcer: oversew the bleeding vessel (ligation of gastroduodenal artery), usually combined with pyloroplasty and truncal vagotomy (TV+D)
• Gastric ulcer: excision or distal gastrectomy (Billroth I or II)
• Operations for definitive treatment:
  • Truncal vagotomy + antrectomy (TV+A): lowest rebleeding rate
  • Truncal vagotomy + drainage (TV+D): pyloroplasty or gastrojejunostomy
  • Highly selective vagotomy (HSV): preserves pylorus, less side effects
• Elderly patients and those with multiple comorbidities may benefit from early elective surgery after initially successful endoscopy, particularly with high-risk lesions, as they do not tolerate repeated hemorrhagic episodes — Schwartz's; Mulholland & Greenfield's; Sleisenger & Fordtran's

II. Perforation

Epidemiology

• Second most common complication; incidence 4–14 per 100,000 (0.004–0.014%)
• Now more common as an indication for operation than bleeding (as endoscopy controls most bleeding)
• Strongly associated with NSAID/aspirin use, especially in the elderly
• Many patients asymptomatic until perforation occurs

Clinical Manifestations

• Sudden, excruciating epigastric pain — patients can often give the exact time of onset
• Initially: chemical peritonitis from gastroduodenal secretions
• Within hours: bacterial peritonitis supervenes
• Obvious distress; board-like rigidity (involuntary guarding)
• Rebound tenderness on gentle examination
• Patient may lie motionless; any movement worsens pain
• Referred pain to shoulder (diaphragmatic irritation)
• Tachycardia, fever; hypotension in advanced cases (septic shock)
• Bowel sounds absent or diminished

Diagnostic Methods

• Upright chest X-ray or abdominal X-ray: free subdiaphragmatic air (pneumoperitoneum) in ~80% of cases — key finding
• If X-ray negative and suspicion remains: CT abdomen (more sensitive — detects small amounts of free air, localizes perforation, assesses peritoneal contamination)
• Water-soluble contrast study (Gastrografin): to confirm sealed perforation before nonoperative management
• Serum labs: leukocytosis, elevated amylase/lipase possible (pancreatic irritation), metabolic acidosis in advanced disease
• Endoscopy is contraindicated in suspected free perforation

Conservative Management

• Nonoperative (Taylor's method): reserved for highly selected cases only:
  • Hemodynamically stable patient
  • Radiologic (contrast study) evidence that the perforation has sealed spontaneously
  • Absence of clinical peritonitis
  • No signs of systemic sepsis
  • Requires: nasogastric decompression, IV fluids, IV antibiotics, IV PPIs, close monitoring
• If patient deteriorates → immediate surgery
• Surgery is almost always indicated for acute perforation with peritonitis

Indications for Hospitalization

• All suspected perforations require emergency hospitalization
• Emergency resuscitation: IV fluids (significant third-space sequestration into inflamed peritoneum), IV antibiotics, analgesia, NG decompression, urinary catheter

Surgical Management

• Preoperative: IV fluid resuscitation (mandatory — third-space losses can be massive), antibiotics, analgesia
• Approach: open or laparoscopic (laparoscopic approach is increasingly favored in stable patients)

1. Simple patch closure (Graham patch/omental patch): most commonly performed; procedure of choice for hemodynamic instability, exudative peritonitis (>24 hours), or significant contamination
   • A pedicle of omentum is sutured over the perforation
2. Patch closure + Highly Selective Vagotomy (HSV): in stable patients with chronic symptoms or failure of medical treatment
3. Patch closure + Truncal Vagotomy + Drainage (TV+D): acceptable definitive operation for perforated duodenal ulcer

• There is a clear trend in the US and Western Europe away from definitive anti-ulcer surgery at the time of perforation (patch + postoperative H. pylori eradication is standard)

• Distal gastric resection (preferred in stable patients): Billroth I gastroduodenostomy; vagotomy added for type II and III gastric ulcers
• Patch closure with biopsy or local excision and closure: for unstable/high-risk patients or unfavorable perforation location
• All perforated gastric ulcers must be biopsied (even prepyloric) — to exclude malignancy — Schwartz's Principles of Surgery, 11e; Sleisenger & Fordtran's

Algorithm for operation for bleeding peptic ulcer — Schwartz's Surgery

Algorithm for operation for perforated peptic ulcer — Schwartz's Surgery

III. Gastric Outlet Obstruction (for completeness)

• Occurs in ≤5% of PUD patients; caused by duodenal or prepyloric ulcer disease
• May be acute (inflammatory edema, dysmotility) or chronic (cicatrix/fibrosis)
• Presents with non-bilious projectile vomiting, weight loss, early satiety, distension
• Diagnosis: upper endoscopy, upper GI series, gastric emptying study
• Conservative: nasogastric decompression + IV PPIs (acute edematous obstruction)
• Endoscopic balloon dilation: immediate relief in 78–100%; many ultimately fail
• Surgical: vagotomy with drainage (pyloroplasty or gastrojejunostomy) or antrectomy

Summary Table: Complications at a Glance

• Schwartz's Principles of Surgery, 11th Edition
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease
• Mulholland and Greenfield's Surgery, 7th Edition

Acute Intestinal Obstruction

I. Classification

A. By Mechanism

• Divided by location relative to the bowel wall:

• No physical blockage; failure of normal coordinated peristalsis
• Causes: post-laparotomy, metabolic disease (especially hypokalemia), narcotics, retroperitoneal/pelvic/intrathoracic infection, abdominal trauma

• Massive colonic dilation without mechanical cause; disruption of interstitial cells of Cajal pacemaker activity; associated with neurogenic/autonomic dysfunction

B. By Degree

• Partial (incomplete): some luminal content passes; less urgent
• Complete: no flatus or stool passes distally; requires prompt intervention

C. By Vascular Status

• Simple obstruction: no compromise of blood supply
• Strangulating obstruction: vascular compromise → ischemia → necrosis → perforation; mortality is double that of simple obstruction
• Closed-loop obstruction: bowel obstructed at two points (e.g., volvulus, internal hernia); intraluminal pressure rises rapidly; arterial obstruction → infarction — surgical emergency

D. By Location

• Small bowel obstruction (SBO): most common; predominantly due to adhesions
• Large bowel obstruction (LBO): most commonly due to colorectal carcinoma, volvulus (sigmoid > cecal), diverticular disease

E. By Acuity

• Acute (rapid onset, full obstruction)
• Chronic (gradual, partial, recurrent)

II. Pathophysiology

III. Methods of Examining Patients

History

• Onset, character, and location of pain (colicky vs. continuous)
• Vomiting (bilious, feculent?)
• Last bowel movement and flatus passage
• Abdominal distension
• Prior abdominal surgeries, hernias, malignancy, IBD

Physical Examination

• Inspection: abdominal distension, visible peristalsis (advanced obstruction), surgical scars, hernias
• Auscultation: high-pitched, tinkling/rushing bowel sounds (mechanical obstruction early); absent bowel sounds (ileus or late strangulation)
• Percussion: tympany over distended loops
• Palpation: tenderness (peritoneal signs suggest strangulation), palpable hernias, masses
• Vital signs: tachycardia, fever, hypotension suggest strangulation/sepsis
• Rectal exam: impaction, blood, rectal mass

Red flags for strangulation / urgent surgery (from imaging + exam):

IV. Diagnosis

Laboratory Studies

• CBC: leukocytosis (strangulation, perforation); anemia
• Metabolic panel: electrolyte imbalances (K⁺, Na⁺, Cl⁻, HCO₃⁻), BUN/Cr (renal failure, dehydration)
• Serum lactate: elevated → ischemia / strangulation
• Amylase/lipase: may be elevated (not specific)
• ABG: metabolic alkalosis (proximal) or acidosis (distal, strangulation)
• Type & screen (pre-op preparation)

Imaging

• First-line, rapid, available
• SBO: dilated small bowel loops (>3 cm) with multiple air-fluid levels ("step-ladder pattern"), absent colonic gas
• LBO: dilated colon proximal to obstruction (cecum >9 cm = risk of perforation; >12–14 cm = surgical emergency)
• Free air under diaphragm (erect film) → perforation
• Sigmoid volvulus: "coffee bean" sign; cecal volvulus: kidney-bean shape

• Most sensitive and specific modality
• Identifies: site and cause of obstruction, transition point, degree (partial vs. complete), strangulation (mesenteric edema, fat stranding, pneumatosis, portal gas), free fluid, perforation
• Differentiates benign (smooth transition zone, mesenteric vascular changes) from malignant (mass, adenopathy, abrupt transition, irregular thickening) causes
• CT enteroclysis: water-soluble contrast via naso-enteric tube → better definition of low-grade or partial SBO
• Ultrasound: sensitivity ~85%, no radiation; useful in pregnancy; inferior to CT for defining transition zone

• Oral Gastrografin: both diagnostic (appearance of contrast in colon within 24 h predicts resolution of adhesive SBO) and therapeutic (hyperosmolar effect draws fluid into lumen, reduces edema)
• Contrast enema: for LBO — identifies site, distinguishes from pseudo-obstruction

• Flexible sigmoidoscopy/colonoscopy: in LBO, useful to decompress sigmoid volvulus or place colonic stent
• Contraindicated if peritonitis or perforation suspected

CT patterns of closed-loop SBO: (A) typical, (B) collapsed, (C) flat-belly pattern — Current Surgical Therapy 14e

V. Principles of Conservative (Non-Operative) Treatment

• Partial (incomplete) SBO without peritonitis or hemodynamic instability
• Adhesive SBO (most resolve with non-operative management)
• Post-operative ileus
• Early post-operative SBO (within 4–6 weeks of surgery — adhesion edema likely)
• Patient with multiple prior surgeries and known adhesive disease

1. Nil per os (NPO) — bowel rest
2. Nasogastric tube (NGT) decompression
   • Removes swallowed air and gastric secretions, reduces distension, relieves vomiting
   • Most useful in complete SBO and ileus; role debated in partial SBO
3. IV Fluid resuscitation — isotonic crystalloids (NS or Lactated Ringer's) to correct volume depletion and electrolyte deficits
4. Electrolyte replacement — especially potassium
5. Analgesia — opioids acceptable; do not withhold pain relief
6. Antiemetics
7. Urinary catheter — to monitor urine output (target ≥0.5 mL/kg/hr)
8. Serial clinical reassessment — vital signs, abdominal exam, fluid balance every 4–6 hours
9. Water-soluble contrast (Gastrografin) challenge: in adhesive partial SBO — both diagnostic and therapeutic; appearance of contrast in colon within 24 h predicts resolution; also reduces need for surgery and length of stay

VI. Indications for Hospitalization

• IV resuscitation and monitoring
• Serial examination
• Surgical availability if clinical deterioration occurs
• Any complete obstruction
• Any partial obstruction with risk factors for strangulation

VII. Indications for Surgical Treatment

• Peritonitis or signs of bowel strangulation/ischemia (fever, tachycardia, leukocytosis, lactic acidosis, peritoneal signs)
• Complete obstruction with no improvement after 24–48 h resuscitation
• Closed-loop obstruction (on CT or clinically suspected)
• Non-reducible (incarcerated/strangulated) hernia
• Cecal dilation >12–14 cm (risk of perforation)
• Sigmoid or cecal volvulus not reducible endoscopically
• Perforation (free air)
• Hemodynamic instability attributable to obstruction

• LBO due to colorectal cancer (resection + stoma or primary anastomosis)
• Recurrent adhesive SBO with multiple hospital admissions
• Failure of non-operative management after 48–72 hours

VIII. Surgical Tactics

Principles of Surgery for SBO

1. Exploration and identification of the transition point (cause of obstruction)
2. Assessment of bowel viability: pink color, peristalsis, bleeding at cut edge, Doppler signal in mesentery; if doubtful → warm saline packs + 10–15 min waiting → re-assess; if still not viable → resect
3. Relief of obstruction:
   • Adhesiolysis: division of adhesive bands (sharp or harmless energy)
   • Bowel resection with primary anastomosis (if well-perfused, non-contaminated field) or stoma formation (if ischemic bowel, contamination, hemodynamically unstable → Hartmann's procedure or loop stoma)
   • Manual reduction of volvulus ± fixation (pexia) or resection
   • Hernia repair with bowel reduction or resection
4. Decompression of grossly dilated bowel if needed (milking content proximally into stomach → NGT, or enterotomy decompression)
5. Laparoscopic approach: increasingly used for adhesive SBO; reduced morbidity, shorter hospital stay; convert to open if bowel is distended, dense adhesions, or if bowel viability uncertain

SBO with Strangulation

• Urgent resection of non-viable bowel
• Primary anastomosis if: hemodynamically stable, non-contaminated, adequate tissue perfusion
• Stoma if: unstable, contaminated, ischemic/necrotic bowel, nutritionally depleted patient

LBO Surgical Options

• Right-sided obstruction (cecum → transverse colon): right hemicolectomy + primary ileocolic anastomosis (generally safe)
• Left-sided obstruction (descending → sigmoid):
  • Hartmann's procedure: resection of sigmoid/left colon, end-colostomy, rectal stump closure — safest in emergency; stoma reversal later
  • Primary resection + anastomosis ± on-table lavage: in selected stable patients
  • Loop colostomy + deferred resection: for high-risk patients
  • Endoluminal stenting: self-expanding metal stent (SEMS) as a bridge to elective surgery — decompresses, allows bowel prep; reduces stoma rate
• Sigmoid volvulus: initial endoscopic decompression/detorsion via rigid sigmoidoscopy or colonoscopy; if successful → elective sigmoid resection to prevent recurrence; if fails or gangrenous → emergency resection + Hartmann's

IX. Pre-Operative and Post-Operative Management

Pre-Operative Management

1. Resuscitation: aggressive IV fluids (isotonic crystalloids), correct electrolyte deficits (especially hypokalemia)
2. NGT decompression: decompress stomach, reduce aspiration risk, facilitate anesthesia
3. Urinary catheter: monitor urine output
4. Blood tests: CBC, electrolytes, coagulation, group & screen, lactate, ABG
5. IV antibiotics: broad-spectrum cover for gram-negative and anaerobes (e.g., cefazolin + metronidazole or piperacillin-tazobactam) before operation — especially for strangulation, perforation, or prolonged obstruction with bacterial translocation risk
6. Analgesia: do not withhold; opioids acceptable
7. Thromboprophylaxis: low-molecular-weight heparin (if time permits)
8. Informed consent and marking for possible stoma

Post-Operative Management

1. Fluid balance: maintain IV fluids until return of bowel function
2. NGT: continue decompression until return of bowel function (passage of flatus/stool); remove when output <200–300 mL/day
3. Early mobilization: reduces ileus, DVT risk
4. Nutrition: early enteral feeding when feasible; TPN for prolonged ileus or short bowel
5. Analgesia: multimodal (epidural, regional blocks, NSAIDs, paracetamol) to minimize opioids → reduces post-op ileus
6. Antibiotics: continue post-operatively if contaminated field, until clinical improvement
7. Monitor for complications: anastomotic leak (day 3–7: fever, tachycardia, peritonism, rising CRP), wound infection, stoma dysfunction, DVT/PE, respiratory complications
8. Enhanced Recovery After Surgery (ERAS) pathways: early feeding, early mobilization, minimize opioids, restrict fluids → significantly reduce length of stay
9. Stoma care: if formed, educate patient; mark pre-operatively with stoma nurse; reversal planned at 3–6 months

X. Chronic Intestinal Obstruction

Definition

Causes

• Adhesions (most common) — recurrent partial SBO from prior surgery or peritonitis
• Colorectal/small bowel malignancy — progressive luminal narrowing
• Crohn's disease — strictures from chronic inflammation + fibrosis
• Radiation enteritis — fibrotic strictures following pelvic/abdominal radiation
• External hernias — intermittent incarceration
• Diverticular disease — stricturing from recurrent diverticulitis
• Extrinsic compression — lymphoma, retroperitoneal fibrosis, endometriosis
• Pseudo-obstruction (Ogilvie's) — functional, no mechanical cause

Clinical Presentation

• Recurrent colicky abdominal pain, often post-prandial (food aversion)
• Abdominal distension — episodic, partially relieving with passage of gas/stool
• Nausea and vomiting — often intermittent, not as acute as in complete obstruction
• Altered bowel habit — alternating constipation and diarrhea; incomplete evacuation
• Weight loss — due to food avoidance (fear of pain), malabsorption
• Borborygmi — loud, hyperactive bowel sounds
• Episodes may partially resolve spontaneously or with conservative measures, only to recur

Diagnosis

• Clinical history is key — recurrent episodes, prior surgeries
• CT abdomen/pelvis: identifies strictures, transition point, degree of dilation, cause (adhesion vs. mass vs. inflammatory)
• Barium small bowel follow-through / CT enterography: excellent for mapping small bowel strictures (especially Crohn's); shows "string sign," mucosal detail
• CT enteroclysis: superior small bowel distension and visualization of partial strictures
• Colonoscopy / flexible sigmoidoscopy: for colonic causes (cancer, diverticular stricture, Crohn's colitis)
• Gastrografin challenge: diagnostic + therapeutic
• Laboratory: CBC (anemia, leukocytosis if active IBD), inflammatory markers (CRP, ESR), nutritional status (albumin, pre-albumin)

Conservative Treatment

• Dietary modification: low-fiber diet to reduce bulk; small, frequent meals
• Liquid/elemental diet: during acute exacerbations to reduce intestinal load
• IV fluids during flares with vomiting
• Corticosteroids (in active Crohn's strictures with inflammatory component): oral prednisolone or IV methylprednisolone
• Biologic therapy: for Crohn's (infliximab, adalimumab) — can reduce inflammatory component of stricture
• Octreotide: reduces GI secretions; useful in malignant partial obstruction
• Endoscopic balloon dilation: first-line for accessible short fibrous strictures (Crohn's, anastomotic, post-radiation); effective in 78–100% immediately; many require repeat sessions
• SEMS (self-expanding metal stents): for malignant colonic strictures as palliation or bridge to surgery

Surgical Treatment

• Adhesiolysis: for adhesive recurrent SBO — laparoscopic preferred if feasible
• Intestinal resection with primary anastomosis: for fibrotic/malignant strictures
• Strictureplasty (Crohn's disease — bowel-sparing):
  • Heineke-Mikulicz: for strictures <7 cm — longitudinal incision closed transversely
  • Finney: for 8–15 cm strictures — U-shaped closure
  • Michelassi (side-to-side isoperistaltic): for long/multiple strictures — advanced technique
• Diverting stoma: palliative decompression in inoperable malignant obstruction
• Colonic resection (for diverticular stricture, cancer): Hartmann's or primary anastomosis based on patient fitness

XI. Adhesive Disease (Peritoneal Adhesions)

Definition

Pathogenesis

• Normal healing of peritoneal injury involves fibrinous exudate → fibrin deposition → organization by fibroblasts → fibrous adhesion
• Failure of normal fibrinolysis (peritoneal fibrinolytic activity is suppressed by surgery, infection, ischemia, foreign bodies) allows permanent adhesion formation
• Adhesions may be:
  • Filmy / avascular: easily divided
  • Dense / vascular: difficult, risky to lyse; risk of enterotomy

Causes / Risk Factors

• Prior abdominal surgery (accounts for ~60% of all SBO; ~75% of SBO following colorectal surgery)
• Intra-abdominal infection / peritonitis
• Pelvic inflammatory disease
• Endometriosis
• Abdominal/pelvic radiotherapy
• Inflammatory bowel disease
• Prior peritoneal adhesions (self-perpetuating)

Clinical Consequences

• SBO (acute or recurrent chronic)
• Chronic abdominal/pelvic pain
• Female infertility (pelvic adhesions)
• Difficult re-operative surgery

Diagnosis

• CT scan: shows transition point at adhesion band (no mass lesion); mesenteric vascular changes; may show fixed, angulated bowel loop
• "Diagnosis of exclusion" — no mass, no hernia, history of prior surgery

Treatment

• NGT, IV fluids, bowel rest (as above for SBO)
• Gastrografin challenge: therapeutic + diagnostic; if contrast reaches colon within 24 h → 97% resolve without surgery
• Success rate of non-operative management for adhesive SBO: 70–80% overall

• Adhesiolysis: sharp or energy-device division of adhesive bands
• Laparoscopic adhesiolysis: preferred for limited adhesions; shorter hospital stay, faster recovery; technical difficulty increases with dense adhesions or prior multiple laparotomies
• Open adhesiolysis: for complex, dense adhesions; allows tactile feedback; safer for enterotomy repair
• Noble plication / Baker tube plication: rarely used historical operations to stent bowel in organised position and prevent re-adhesion
• Bowel resection only if bowel is non-viable

• Meticulous peritoneal hemostasis
• Minimizing tissue trauma and foreign material (e.g., powder-free gloves, minimal suture)
• Irrigation of peritoneal cavity
• Anti-adhesion barriers: hyaluronic acid–carboxymethylcellulose membrane (Seprafilm) — placed over bowel at closure; shown to reduce adhesion formation and SBO incidence
• Laparoscopic approach (vs. open) significantly reduces adhesion burden

Prognosis

• After a single episode of adhesive SBO requiring surgery: ~30% risk of recurrence within 10 years
• Each reoperation increases adhesion burden and operative risk
• Goal of management is to avoid unnecessary surgery and prevent recurrence

Summary: Acute vs. Chronic Obstruction

• Rosen's Emergency Medicine, 10th Edition
• Current Surgical Therapy, 14th Edition
• Harrison's Principles of Internal Medicine, 22nd Edition
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease