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• ISBN: 9781259835346
• Specialty: General Surgery
• 23 content blocks covering the full breadth of surgical science and practice

• Basic surgical principles - wound healing, hemostasis, surgical infections, fluid/electrolyte management
• Trauma and critical care
• Oncology - breast, colorectal, pancreatic, thyroid, and other cancers
• Abdominal surgery - stomach, small intestine, colon, liver, biliary tract, pancreas, spleen
• Vascular surgery
• Thoracic surgery
• Endocrine surgery
• Minimally invasive surgery & robotic surgery
• Transplantation
• Plastic and reconstructive surgery
• Orthopedics, neurosurgery, and more

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🫁 THE STOMACH & PEPTIC ULCER DISEASE

Schwartz's Principles of Surgery, 11th Ed. - Chapter 26

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PART 1: ANATOMY

Gross Morphology & Anatomic Relationships

• Proximally at the gastroesophageal (GE) junction (cardia)
• Distally at the pyloric sphincter (connects to the duodenum)

• The lesser curvature is on the right (shorter)
• The greater curvature is on the left (longer)
• The angle of His = where fundus meets the left side of GE junction
• The angularis incisura = where lesser curvature turns abruptly right, marking the start of the antrum

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Blood Supply

• Left gastric artery (from celiac) - supplies lesser curve
• Right gastric artery (from hepatic) - supplies lesser curve
• Left gastroepiploic artery (from splenic) - supplies greater curve
• Right gastroepiploic artery (from gastroduodenal) - supplies greater curve
• Short gastric arteries (from splenic) - supply fundus

Lymphatic Drainage

• N1 nodes = perigastric nodes along the lesser and greater curvature
• N2 nodes = nodes along the left gastric, common hepatic, splenic, and celiac arteries

Innervation

• Vagus nerve (parasympathetic) = stimulates acid secretion and motility
  • Left vagus = anterior trunk (mostly gastric branches)
  • Right vagus = posterior trunk (gives hepatic, celiac, gastric branches)
• Sympathetic = via celiac plexus; inhibits motility

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Histology - Epithelial Cell Types

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PART 2: PHYSIOLOGY

Acid Secretion - The Core of Everything

1. Acetylcholine - from vagally stimulated enteric neurons
2. Gastrin - from antral G cells (acts mainly via ECL cells to release histamine)
3. Histamine - from ECL cells (the main final mediator)

• Stored in intracellular tubulovesicles
• Final common pathway for gastric acid secretion
• When stimulated, tubulovesicles fuse with the apical membrane → acid is pumped into the lumen
• This is why PPIs (which block H+/K+-ATPase) are so effective

• Somatostatin (from antral D cells) - inhibits gastrin release; inhibited by vagus
• Secretin (duodenum) - released by acid in duodenum; inhibits gastric acid
• CCK, GIP - also inhibit acid secretion

Pepsinogen Secretion

• Chief cells secrete pepsinogens I and II
• Pepsinogen is activated to pepsin at pH < 3.5
• Pepsin begins protein digestion

Intrinsic Factor

• Secreted by parietal cells
• Binds vitamin B12 in the duodenum and is required for its absorption in the terminal ileum
• Loss of parietal cells (e.g., after total gastrectomy or in autoimmune atrophic gastritis) → pernicious anemia

Gastric Mucosal Barrier (Defense Mechanisms)

• Prostaglandins (this is why NSAIDs - which block prostaglandin synthesis - cause ulcers)
• Nitric oxide
• Epidermal growth factor (EGF)
• Calcitonin gene-related peptide (CGRP)

Gastric Hormones

• Produced by antral G cells
• Stimulated by: luminal peptides, amino acids, vagal input, alkaline pH
• Inhibited by: luminal acid (via somatostatin from D cells)
• Acts mainly via ECL cells → histamine → parietal cells
• Is trophic to gastric mucosa
• Molecular forms: Big gastrin (G34), Little gastrin (G17 - predominant in humans), Mini-gastrin (G14)

• From D cells; acts in a paracrine fashion
• Inhibits gastrin release from G cells
• Inhibits acid secretion directly

• Neurocrine peptide from the stomach
• "Hunger hormone" - stimulates appetite

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PART 3: DIAGNOSIS OF GASTRIC DISEASE

Alarm Symptoms - Mandate Urgent Upper Endoscopy

• Age >55 years with NEW onset dyspepsia
• Unintentional weight loss
• Persistent or recurrent vomiting
• Progressive dysphagia
• Recent onset odynophagia
• Unexplained iron deficiency anemia or GI bleeding
• Palpable abdominal mass or lymphadenopathy
• Family history of upper GI cancer

Diagnostic Tests

• Safe, accurate, performed under conscious sedation
• Can biopsy, assess H. pylori, perform endoscopic therapy
• All gastric ulcers found at EGD must have multiple biopsies of the base and rim to rule out cancer
• Complications: perforation (rare), aspiration, respiratory depression from sedation

• Better than EGD for fistula, tortuosity, stricture, hiatal hernia morphology
• Not a substitute - gastric ulcers always need biopsy

• Not routine for benign disease
• Mandatory for staging malignant gastric tumors

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PART 4: HELICOBACTER PYLORI INFECTION

• Gram-negative, spiral-shaped bacillus
• Colonizes the gastric mucosa
• Causes chronic active gastritis
• Causes >90% of duodenal ulcers and ~70% of gastric ulcers
• Is a class I carcinogen - strongly linked to gastric adenocarcinoma and MALT lymphoma

1. Damages the mucous layer (urease produces ammonia that injures cells)
2. Triggers inflammation → cytokine release → mucosal damage
3. Increases gastrin secretion (by inhibiting somatostatin from D cells) → increased acid
4. Directly reduces mucosal defenses

Always test and treat H. pylori when detected. Eradication dramatically reduces ulcer recurrence (see Figure 26-26 in the textbook).

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PART 5: PEPTIC ULCER DISEASE (PUD)

Definition

• Aggressive factors: acid, pepsin, H. pylori, NSAIDs, bile
• Defensive factors: mucus, bicarbonate, prostaglandins, mucosal blood flow, restitution

Epidemiology

• Prevalence: ~2% in the United States
• Lifetime cumulative prevalence: ~10%, peaking around age 70
• Costs exceed $8 billion/year in the US
• Hospital mortality: 3.7% for duodenal ulcer, 2.1% for gastric ulcer
• Emergency surgery rates have NOT decreased as dramatically as elective surgery

Causes of PUD

• ~75% H. pylori
• ~20% NSAIDs
• ~5% Zollinger-Ellison and other

• ~60-70% H. pylori
• ~25-30% NSAIDs
• Remainder: ZES, stress, idiopathic

In the US, more than 90% of serious peptic ulcer complications are attributable to H. pylori infection, NSAID use, and/or cigarette smoking.

Pathophysiology

• Higher mean BAO (basal acid output) and MAO (maximal acid output) than controls
• Normal fasting gastrin, but hyperresponsive to gastrin (parietal cell mass is hypersensitive)
• H. pylori causes increased gastrin secretion and accelerates gastric emptying → more acid delivered to duodenum per unit time
• Reduced duodenal bicarbonate buffering capacity

• Primarily a defect in mucosal defense (not excess acid)
• Bile reflux, NSAIDs, H. pylori all compromise the mucosal barrier
• Gastric acid is still required - acid suppression heals both DU and GU

Clinical Manifestations

• Epigastric pain - burning or gnawing; may be worse 2-3 hours after meals
• Duodenal ulcer: pain relieved by food and antacids ("hungry pain"); night pain common
• Gastric ulcer: pain may be worsened by food (due to acid secretion)
• Nausea, vomiting, belching
• Complications: bleeding, perforation, obstruction, intractability

Diagnosis

• Upper endoscopy (EGD) is the gold standard
• All gastric ulcers must be biopsied - cancer cannot be excluded on appearance alone
• Test for H. pylori at the same time
• Duodenal ulcers rarely need biopsy (malignancy is very rare)

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PART 6: COMPLICATIONS OF PUD

1. Bleeding Peptic Ulcer (Most Common Cause of Ulcer-Related Death)

• Most common complication
• ~25% of patients will rebleed in hospital
• All patients admitted with bleeding PUD should receive IV PPI immediately

• Based on: systolic BP, BUN, hemoglobin, pulse, melena, syncope, hepatic disease, cardiac failure
• Score ≥6 = high risk, needs urgent endoscopy

• Massive hemorrhage unresponsive to initial endoscopic control
• Recurrent hemorrhage despite endoscopic treatment
• Hemodynamic instability preventing safe endoscopy

• Suture ligation of the bleeder
• Suture ligation + definitive non-resective operation (HSV or vagotomy + drainage)
• Gastric resection (with vagotomy and ulcer excision)
• Gastric ulcer always requires biopsy if not resected

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2. Perforated Peptic Ulcer

• Sudden onset of severe, diffuse abdominal pain (chemical peritonitis from spilled gastric contents)
• Upright CXR or abdominal X-ray: pneumoperitoneum (free air under diaphragm) in ~70%
• CT scan is more sensitive if plain X-ray is negative

• NPO, NG decompression, IV fluids, antibiotics, IV PPI
• Surgery is usually required: laparoscopic or open
  • Graham patch repair (omental patch over perforation) - most common
  • Definitive ulcer operation (vagotomy) may be added if patient is stable and H. pylori negative

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3. Obstructing Peptic Ulcer (Gastric Outlet Obstruction)

• Results from edema and scarring near the pylorus or first part of duodenum
• Presents with: projectile vomiting, succussion splash, distension, weight loss
• Classic metabolic derangement: hypochloremic, hypokalemic metabolic alkalosis (due to loss of HCl in vomit)
• Gastric cancer must be excluded
• Initial management: NG tube decompression + IV fluids + IV PPI + H. pylori treatment
• Endoscopic balloon dilation may work for edematous obstruction
• Surgery (vagotomy + drainage, or resection) if scar obstruction does not respond

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4. Intractable / Nonhealing Peptic Ulcer

• Failure to heal after 12 weeks of adequate PPI therapy
• Always check: H. pylori status, NSAID/aspirin use, compliance, smoking
• Differential diagnosis of nonhealing ulcer:
  • Zollinger-Ellison syndrome (gastrinoma)
  • Malignancy (gastric cancer)
  • Crohn's disease
  • Chronic NSAID use
  • Tuberculosis, syphilis, CMV (in immunocompromised)
  • Systemic mastocytosis

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PART 7: MEDICAL TREATMENT OF PUD

Acid Suppression

• PPIs (Proton Pump Inhibitors) - mainstay of therapy
  • Block H+/K+-ATPase irreversibly
  • Most potent acid suppressants available
  • Patients hospitalized for ulcer complications: high-dose IV PPI; lifelong oral PPI on discharge unless definitive cause eliminated
• H2 Receptor Antagonists (H2RAs) - ranitidine, famotidine; less potent than PPIs; still effective
• Sucralfate - works locally on mucosal defects; useful as supplement

General Measures

• Stop NSAIDs and aspirin
• Stop smoking
• Stop alcohol
• If NSAIDs are unavoidable: always co-prescribe PPIs or high-dose H2RAs

H. pylori Eradication Regimens (10-14 days)

After H. pylori eradication is confirmed, acid suppression can generally be stopped after 3 months.

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PART 8: SURGICAL TREATMENT OF PUD

Indications for Surgery (in order of decreasing frequency today)

1. Perforation
2. Obstruction
3. Bleeding
4. Intractability / Nonhealing

Gastric cancer must always be excluded in patients with gastric ulcer or gastric outlet obstruction.

Vagotomy - The Core Surgical Principle

Reconstruction After Antrectomy

• Billroth I (gastroduodenostomy): Gastric remnant sutured directly to duodenum. Physiologic; preferred when feasible.
• Billroth II (gastrojejunostomy): Gastric remnant to jejunum; duodenal stump closed. Used when tension on anastomosis or when duodenum is inflamed.
• Roux-en-Y gastrojejunostomy: Used to prevent bile reflux into the gastric remnant.

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PART 9: POSTGASTRECTOMY PROBLEMS

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PART 10: ZOLLINGER-ELLISON SYNDROME (ZES)

• Caused by a gastrinoma (neuroendocrine tumor of pancreas or duodenum)
• Massive hypergastrinemia → extreme acid hypersecretion → refractory ulcers
• Ulcers may be multiple, in unusual locations (distal duodenum, jejunum)
• Associated with MEN-1 (Multiple Endocrine Neoplasia type 1) in ~25% of cases
• Diagnosis: Fasting serum gastrin > 1000 pg/mL is virtually diagnostic; secretin stimulation test
• Treatment: High-dose PPIs (often very high doses needed); tumor resection when possible

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SUMMARY TABLE - Key Surgical Decisions in PUD

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COMPLICATIONS OF PUD - Initial Management & Definitive Treatment

Schwartz's Principles of Surgery, 11th Edition - Chapter 26

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THE KEY TABLE (Table 26-12) - Surgical Options in PUD Complications

Footnotes from Schwartz:

• Unless the patient is in shock or moribund, a definitive procedure should be considered.
• "Operation of choice in low-risk patient" = the most definitive option listed.
• HSV = Highly Selective Vagotomy | V+A = Vagotomy + Antrectomy | V+D = Vagotomy + Drainage | GJ = Gastrojejunostomy

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COMPLICATION 1: BLEEDING PEPTIC ULCER

Initial Management (Step-by-Step)

• Large-bore IV access, aggressive IV fluid resuscitation
• Type and crossmatch blood; transfuse if hemoglobin <7 g/dL (or <9 in cardiac patients)
• Start IV PPI immediately (high-dose) - most patients stop bleeding with resuscitation + PPI alone
• NG tube insertion
• Surgical consultation is mandatory

• Uses: age, shock (HR/BP), comorbidities, endoscopic diagnosis, stigmata of recent hemorrhage
• Score ≥5 = high risk for rebleed and death

• Identifies the bleeding source
• Apply the Forrest Classification to predict rebleed risk and guide therapy:

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Indications for Emergency Surgery

• Massive hemorrhage unresponsive to initial endoscopic control
• Recurrent hemorrhage requiring multiple transfusions after two attempts at endoscopic control
• Ongoing hemorrhage with limited blood availability or no therapeutic endoscopist available
• >4 units blood in 24 hours or >8 units in 48 hours
• Ulcer >2 cm in diameter
• Shock on presentation
• High-risk vessel: posterior duodenal ulcer eroding gastroduodenal artery; lesser curvature ulcer eroding left gastric artery
• Concurrent perforation or obstruction

Mortality for surgery for bleeding peptic ulcer is approximately 20% - reflecting the very high-risk selection of patients who reach the OR today.

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Definitive Surgical Treatment - Bleeding DU

1. Pylorotomy/duodenotomy → identify the bleeder
2. U-stitch / figure-of-8 sutures with heavy material to secure the gastroduodenal artery at the base of the posterior duodenal ulcer. Multiple sutures usually required. Kocher maneuver allows digital control while suturing.
3. Once hemostasis is secure → pyloroplasty (closes the opening, also drains the stomach)
4. If patient is stable and surgeon experienced → add vagotomy (truncal vagotomy + pyloroplasty = V+D)
5. If patient is stable and low-risk → V+A (vagotomy + antrectomy) = most definitive, lowest recurrence rate

• Oversew + biopsy (if unstable)
• Distal gastrectomy (if stable, low-risk) - operation of choice; removes the ulcer, pathology confirmed, and reduces acid

Note: Oversewing alone has a higher rebleed rate but lower operative mortality. Definitive operation has lower rebleed rate but higher operative mortality. In the shocked/unstable patient - just oversew. In the stable patient - add vagotomy.

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COMPLICATION 2: PERFORATED PEPTIC ULCER

Initial Management

• NPO immediately
• Nasogastric tube - decompress the stomach and stop spillage
• IV fluid resuscitation
• Broad-spectrum IV antibiotics (covering gram-negatives and anaerobes)
• IV PPI (high-dose)
• Urinary catheter for urine output monitoring
• Upright CXR - free air under diaphragm (~70% sensitive). If negative and high clinical suspicion → CT abdomen (most sensitive)
• Surgical consultation immediately - surgery is almost always required

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Definitive Surgical Treatment - Perforated DU

Perforated DU
    ↓
Hemodynamically unstable / Peritonitis >24 hrs old?
    YES → Simple Graham Patch closure only
    NO  ↓
        Chronic ulcer symptoms / Failed medical treatment?
            YES → Patch + HSV  (or Patch + V+D)
            NO  → Simple Patch closure (rely on PPI + H. pylori treatment post-op)

1. Simple patch closure (Graham patch) - omentum sutured over the perforation. Operation of choice in unstable/moribund patient or perforation >24 hours old (exudative peritonitis). Simple, fast, safe.
2. Patch + HSV (highly selective vagotomy) - add in stable patients with chronic symptoms or failed prior medical therapy. Appealing because no drainage procedure needed.
3. Patch + V+D (vagotomy + drainage) - acceptable definitive operation. Faster to perform than HSV. Good for perforated DU in stable patient.

There is a clear trend away from definitive operation for perforated duodenal ulcer in the US and Western Europe. Most surgeons rely on Graham patch + postoperative H. pylori eradication + lifelong PPI.

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Definitive Surgical Treatment - Perforated GU

• Stable, low-risk patient: Distal gastric resection (best option - removes the ulcer, confirms pathology, and treats the underlying disease)
• Unstable or high-risk or awkward location: Biopsy + patch; or local excision + closure; or biopsy + closure + truncal vagotomy + drainage
• All perforated gastric ulcers must be biopsied if not resected - even prepyloric ones - because gastric cancer cannot be excluded.
• Vagotomy is added for Type II and Type III gastric ulcers (which have high acid).

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COMPLICATION 3: OBSTRUCTING PEPTIC ULCER

Initial Management

• NG tube decompression (large-bore, to drain the distended stomach)
• IV fluid and electrolyte replacement - correct the hypochloremic, hypokalemic metabolic alkalosis (from repeated vomiting of HCl)
• IV PPI (high-dose)
• H. pylori testing and treatment
• Total parenteral nutrition (TPN) if malnourished
• After 72 hours of NG decompression → trial without NG tube
• Many acute obstructions resolve with intensive antisecretory therapy + NG suction

• Endoscopic balloon dilation - can transiently improve obstructive symptoms, but many ultimately fail and come to operation
• Surgery if no improvement

Definitive Surgical Treatment - Obstruction

1. V+A (Vagotomy + Antrectomy) - standard operation, operation of choice
   • Removes the obstructed segment
   • Eliminates the gastrin source
   • Lowest recurrence rate
2. V + Gastrojejunostomy (GJ) - preferred when a difficult duodenal stump is anticipated (inflamed, friable duodenum makes resection hazardous). Bypasses the obstruction.
3. HSV + GJ - appealing because it can be done laparoscopically and does not complicate future resection. May be comparable to V+A for obstruction.
   • Caution: Potentially curable gastric or duodenal cancers can be missed with HSV+GJ alone - always biopsy.

Gastric cancer must always be excluded as a cause of gastric outlet obstruction before assuming it is benign PUD.

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COMPLICATION 4: INTRACTABLE / NONHEALING PEPTIC ULCER

Initial Management - Always Ask "Why?"

1. Confirm compliance with PPI - consider supervised high-dose PPI
2. Repeat H. pylori testing; if any doubt → empiric re-treatment (false-negatives are common)
3. Stop all NSAIDs, aspirin, cocaine, alcohol, smoking
4. Check fasting serum gastrin → rule out ZES (if >1000 pg/mL, virtually diagnostic)
5. Repeat EGD with multiple biopsies → rule out malignancy
6. Nutritional assessment - optimize nutritional status before any surgery

Definitive Surgical Treatment - Intractability

• Multiple recurrences
• Large ulcers (>2 cm)
• Complications (obstruction, perforation, or hemorrhage)
• Suspected malignancy

1. HSV (Highly Selective Vagotomy) - operation of choice in low-risk patient. Zero mortality, lowest side-effect profile.
2. V+D (Truncal vagotomy + drainage)
3. V+A (Truncal vagotomy + antrectomy)

1. HSV + Wedge excision of the ulcer
2. Distal gastrectomy - operation of choice in low-risk patient

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SUMMARY: APPROACH TO EACH COMPLICATION

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🏥 MOCK ORAL EXAM - Stomach & PUD

Format: 2 Cases | 4 Questions Each | 2.5 pts/question | 7 minutes total

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📋 CASE 1

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❓ Question 1

✅ Click to reveal answer

Diagnosis: Perforated peptic ulcer (most likely perforated duodenal ulcer given his risk factors).

Underlying cause: Chronic NSAID use + smoking → disruption of gastric mucosal barrier → peptic ulceration → perforation. NSAIDs block prostaglandin synthesis, which is the key mediator of mucosal defense (mucus, bicarbonate, microcirculation).

Key findings pointing to perforation:

• Sudden onset "worst pain of his life" = chemical peritonitis from spillage of gastric contents
• Board-like rigidity + generalized guarding = generalized peritonitis
• Free air under diaphragm on CXR = pneumoperitoneum (confirms perforation)

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❓ Question 2

✅ Click to reveal answer

Immediate management (all simultaneously):

1. NPO - nothing by mouth
2. Nasogastric tube insertion - decompress stomach, stop further spillage of gastric contents
3. Large-bore IV access × 2 - aggressive fluid resuscitation (Normal Saline / Ringer's Lactate)
4. IV PPI - high dose (e.g., omeprazole 80 mg bolus then 8 mg/hr infusion)
5. Broad-spectrum IV antibiotics - covering gram-negatives and anaerobes (e.g., ceftriaxone + metronidazole)
6. Urinary catheter - monitor urine output (target >0.5 mL/kg/hr)
7. Bloods: FBC, U&E, LFTs, coagulation, blood group and crossmatch, serum amylase (rule out pancreatitis)
8. Analgesia (IV opioids - do NOT withhold in surgical emergency)
9. Surgical consult → prepare for emergency surgery
10. Consent and mark the patient

The CXR already confirms pneumoperitoneum - no need to delay with CT if diagnosis is clear. CT is done only if CXR is negative and clinical suspicion remains.

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❓ Question 3

✅ Click to reveal answer

Operation: Simple Graham Patch closure (omental patch)

Why: In a hemodynamically unstable patient with exudative peritonitis (signifying perforation >24 hours old or severe contamination), the operation of choice is simple patch closure only. This is:

• Fast
• Safe
• Achieves the primary goal: seal the perforation and stop contamination

Technique: A tongue of mobile omentum is sutured over the perforation using interrupted sutures. The peritoneal cavity is then thoroughly washed out.

You do NOT add vagotomy in this unstable setting because:

• Adds operative time and risk
• The patient cannot tolerate a prolonged procedure
• Postoperative IV PPI + H. pylori eradication is equally effective at preventing recurrence in the modern era

Remember Schwartz: "Simple patch closure is the procedure of choice in patients with hemodynamic instability and/or exudative peritonitis signifying a perforation >24 hours old."

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❓ Question 4

✅ Click to reveal answer

Before discharge:

1. Test for H. pylori (if not done intra-op - biopsy at time of surgery is ideal)
2. If H. pylori positive → eradicate with triple or quadruple therapy (10-14 days)
3. Confirm eradication with urea breath test or stool antigen test at 4 weeks post-treatment
4. Stop NSAIDs permanently - switch to alternative analgesia
5. Stop smoking - counsel strongly

Long-term plan:

• Lifelong PPI should be considered in all patients admitted to hospital with ulcer complications (per Schwartz)
• If NSAIDs are unavoidable in future (e.g., arthritis), always co-prescribe PPI
• Repeat EGD in 6-8 weeks to confirm healing (mandatory for gastric ulcers to exclude malignancy; less critical for duodenal ulcers)
• If H. pylori negative and not on NSAIDs → rule out ZES (check fasting serum gastrin)

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📋 CASE 2

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❓ Question 5

✅ Click to reveal answer

Diagnosis: Upper GI bleeding secondary to peptic ulcer disease (bleeding peptic ulcer). Coffee-ground vomiting = altered blood in stomach. Melena = digested blood = upper GI source.

Severity assessment:

• HR 115 bpm = tachycardia → compensatory response to hypovolemia
• BP 95/60 = hypotension → she has lost significant circulating volume; this is hemodynamic instability
• Hb 7.2 g/dL = significant anemia from acute blood loss

This is a high-risk presentation (hemodynamic instability = shock). She needs immediate resuscitation and urgent endoscopy.

Blatchford Score calculation for this patient:

• SBP <90: 3 pts
• HR ≥100: 1 pt
• Hb <10 g/dL (female): 6 pts
• Melena: 1 pt = Score ≥11 → extremely high risk → mandatory urgent inpatient endoscopy

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❓ Question 6

✅ Click to reveal answer

Immediate management:

1. 2 large-bore IV cannulas → aggressive fluid resuscitation
2. Blood transfusion - Hb is 7.2 g/dL and she is in shock; transfuse packed red blood cells. Threshold for transfusion in hemodynamically unstable patient = transfuse regardless of Hb number
3. IV PPI immediately - high dose bolus + infusion (reduces rebleed risk; stabilizes clot over the ulcer)
4. Type & crossmatch - have blood ready
5. NG tube - assess ongoing bleeding, clear stomach for endoscopy
6. Urinary catheter - monitor output
7. Urgent endoscopy (EGD) - once resuscitated sufficiently. Identifies source + Forrest classification + endoscopic therapy

Regarding aspirin:

• Do NOT stop aspirin permanently - she is on it for a cardiac indication (stroke/MI prevention). Stopping abruptly in a cardiac patient risks a thrombotic event which can be more deadly than the GI bleed.
• Hold aspirin temporarily during the acute bleeding episode
• Restart aspirin as soon as possible (within 1-3 days) once endoscopic hemostasis confirmed and hemodynamically stable, with concomitant PPI cover
• Long-term: she should be on PPI co-prescription permanently whenever on aspirin/NSAIDs

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❓ Question 7

✅ Click to reveal answer

She now has indications for emergency surgery:

• Active bleeding unresponsive to two attempts at endoscopic control
• Requiring >4 units of blood in 24 hours
• Forrest Ia = highest rebleed risk (~90%)

Before surgery, consider: Angiography and embolization of the gastroduodenal artery (GDA) is an option in some centers, especially in very high-risk surgical patients. However, if she can tolerate surgery, operate.

In the OR - Operation for Bleeding Posterior Duodenal Ulcer:

1. Pylorotomy (longitudinal incision through the pylorus) → access the bleeding posterior duodenal ulcer
2. Kocher maneuver → mobilize duodenum; allows digital compression of the GDA if needed
3. U-stitch / figure-of-8 sutures with heavy suture material → ligate the gastroduodenal artery at the superior, inferior, and medial aspects of the ulcer base (3-point ligation)
4. Confirm hemostasis absolutely
5. Close as pyloroplasty (Heineke-Mikulicz)

Is she stable enough for a definitive operation?

• She is in shock pre-op → do NOT add gastric resection in an unstable patient
• If she stabilizes intra-operatively → consider adding truncal vagotomy (V+D) to reduce recurrence
• Per Schwartz Table 26-12: Oversew alone (option 1) is appropriate in shock; V+D or V+A in stable low-risk patients

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❓ Question 8

✅ Click to reveal answer

Diagnosis: Gastric outlet obstruction (obstructing peptic ulcer)

This is likely due to scarring/fibrosis at the pylorus/duodenal bulb from her chronic peptic ulcer disease (edema and inflammation from her recent ulcer episode may have now scarred down).

Succession splash = fluid sloshing in a dilated stomach hours after eating = hallmark of gastric outlet obstruction.

Initial management:

1. NG tube decompression - drain the distended, food-filled stomach (large-bore Ryles tube)
2. IV fluids - correct dehydration
3. Correct electrolytes - classic metabolic abnormality is hypochloremic, hypokalemic metabolic alkalosis (from repeated vomiting of HCl - replace with normal saline + KCl supplementation)
4. IV PPI - high dose
5. Nutritional support - she is likely malnourished; consider TPN
6. H. pylori testing and eradication if not already confirmed
7. EGD - confirms obstruction, takes biopsies to rule out gastric cancer as cause
8. If edematous → endoscopic balloon dilation can be attempted

If no improvement → Surgery:

• V+A (vagotomy + antrectomy) = standard operation, operation of choice
• If difficult duodenal stump anticipated (inflamed, friable) → V + Gastrojejunostomy
• Per Schwartz Table 26-12: For gastric ulcer obstruction → Biopsy + HSV + GJ, or Distal gastrectomy (operation of choice in low-risk)

Always exclude gastric cancer before assuming benign obstruction.

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📊 SCORING GUIDE

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1. What complication is this? (bleeding / perforation / obstruction / intractability)
2. What do I do in the first 30 minutes? (ABCDE + specific steps)
3. What is the operation if I need surgery, and does the patient's stability change my choice?
4. What is the definitive long-term plan? (H. pylori / PPI / stop NSAIDs / follow-up EGD)

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When Do We Do CT in PUD / Stomach Disease?

🔴 Perforated Peptic Ulcer

Rule: CXR first. CT only if CXR is negative or diagnosis is unclear. Plain CXR catches ~70% of perforations. CT catches nearly all.

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🟡 Gastric Cancer / Malignant Tumors

• CT chest + abdomen + pelvis
• Assesses: local invasion, lymph nodes, liver mets, peritoneal spread

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🟢 Uncomplicated / Benign Gastric Disease

Schwartz states directly: "Usually, significant gastric disease can be diagnosed without these sophisticated imaging studies."

• EGD and barium studies are sufficient for most benign conditions
• MRI may have a future role in quantifying gastric emptying but is not routine

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One-Line Exam Answer:

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Labs to Order - Each PUD Complication

🔴 BLEEDING PEPTIC ULCER

Exam pearl: Elevated BUN with normal creatinine = upper GI bleed. The blood is digested and absorbed as protein → raises BUN. This is why Blatchford score uses BUN as a parameter.

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🔵 PERFORATED PEPTIC ULCER

Exam pearl: Serum amylase is ordered to rule out pancreatitis, but remember - perforation itself can cause a mildly elevated amylase. It does NOT confirm pancreatitis.

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🟡 OBSTRUCTING PEPTIC ULCER

Exam pearl: The classic metabolic picture in obstruction is: ↓ Na, ↓ K, ↓ Cl, ↑ HCO3, ↑ pH = Hypochloremic, Hypokalemic Metabolic Alkalosis Caused by repeated vomiting of gastric juice (HCl). The kidney tries to compensate by retaining H+ and excreting K+ → worsens hypokalemia. Fix with normal saline + KCl before any surgery.

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🟢 INTRACTABLE / NONHEALING PEPTIC ULCER

Exam pearl: Always check fasting serum gastrin in any nonhealing ulcer. Stop PPIs for at least 1-2 weeks before testing (PPIs raise gastrin falsely). If fasting gastrin is borderline → do Secretin Stimulation Test (gastrin paradoxically rises in ZES; it stays flat or drops in normal patients).

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QUICK SUMMARY TABLE

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• Bleeding → BUN:Cr ratio + coagulation
• Perforation → amylase + lactate
• Obstruction → electrolytes + ABG (metabolic alkalosis)
• Intractability → fasting serum gastrin

Table 26-12 - Surgical Options in PUD

Schwartz's Principles of Surgery

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The Logic Before the Table

1. What complication is it? (Bleeding / Perforation / Obstruction / Intractability)
2. Is the patient stable or unstable?

Rule from Schwartz: "Unless the patient is in shock or moribund, a definitive procedure should be considered."

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The Table - Built Step by Step

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🔴 BLEEDING

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🔵 PERFORATION

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🟡 OBSTRUCTION

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🟢 INTRACTABILITY / NONHEALING

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🧠 THE MASTER TABLE (Full View)

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Abbreviations (Must Know)

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One Pattern to Remember Everything

UNSTABLE PATIENT → Always the simplest option (Option 1)
   Bleeding    → just Oversew
   Perforation → just Patch
   
STABLE / LOW-RISK → Always the definitive option (last option)
   Duodenal    → V+A (bleeding/perforation/obstruction) or HSV (intractability)
   Gastric     → Distal Gastrectomy (for all 4 complications)

Gastric ulcer rule: Distal Gastrectomy is the operation of choice in low-risk patients for ALL 4 complications.

Duodenal ulcer rule: V+A is the operation of choice for bleeding, perforation, and obstruction. HSV is preferred for intractability.

When to Do EGD in PUD / Stomach Disease

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By Complication

🔴 BLEEDING — EGD is the FIRST thing you do (after resuscitation)

• At least 2 large-bore IVs in
• Resuscitation started
• Blood available

• Identify source
• Apply Forrest classification
• Perform endoscopic hemostasis (cautery + epinephrine injection + clipping)
• Biopsy for H. pylori (CLO test)

Exam rule: Resuscitate FIRST, scope SECOND. But do not delay endoscopy unnecessarily - the longer you wait, the more blood they lose.

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🔵 PERFORATION — EGD is CONTRAINDICATED acutely

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🟡 OBSTRUCTION — EGD after initial resuscitation

• Confirm obstruction and its level
• Biopsy - rule out gastric cancer as the cause
• Attempt endoscopic balloon dilation if edematous obstruction (may avoid surgery)
• Assess H. pylori status

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🟢 INTRACTABILITY / NONHEALING — EGD is mandatory and repeated

• Multiple biopsies of base AND rim of gastric ulcer — mandatory every time (cancer cannot be excluded on appearance)
• H. pylori testing (CLO test + histology)
• If ulcer not healed at 6-8 weeks → repeat biopsy again

Critical rule from Schwartz: "All patients with gastric ulcer diagnosed on upper GI series or found at EGD should have multiple biopsy specimens of the base and rim of the lesion." Duodenal ulcers do NOT routinely need biopsy (malignancy is very rare there).

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Alarm Symptoms — EGD is Mandatory Regardless

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Quick Summary Table

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One-Line Exam Answer

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🏛️ ANAL ANATOMY, ANAL ABSCESS & COMPLICATIONS

Schwartz's Principles of Surgery - Chapter 29: Colon, Rectum & Anus

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PART 1: ANATOMY OF THE ANAL CANAL

The Anal Canal - Basic Structure

• Begins at the anorectal junction
• Ends at the anal verge (skin)

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The Dentate Line - THE Most Important Landmark

Exam pearl: Cancer above the dentate line → spreads to inferior mesenteric/internal iliac nodes. Cancer below the dentate line → spreads to inguinal nodes. This changes staging and management completely.

Pain pearl: Procedures below the dentate line (e.g., banding hemorrhoids) are VERY painful - need local anesthesia. Procedures above it - much less painful.

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The Columns of Morgagni & Anal Crypts

• Columns of Morgagni = longitudinal folds of mucosa in the upper anal canal, running from the dentate line upward
• Anal crypts = small pockets at the base of the columns, AT the dentate line
• Anal glands = 6-8 glands that open into the anal crypts. Their ducts traverse the internal sphincter and the glands sit in the intersphincteric space
• This is the origin of ALL cryptoglandular (anal gland) infections → anal abscesses

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The Sphincter Complex - Must Know

Internal Anal Sphincter (IAS)

• Formed by the thickened inner circular smooth muscle of the distal rectum
• Involuntary - autonomic control
• Innervated by sympathetic + parasympathetic fibers (both inhibit contraction, so the IAS is tonically contracted at rest)
• Responsible for ~80% of resting anal tone
• The IAS is what keeps you continent at rest (while sleeping, etc.)
• Cannot be voluntarily controlled

External Anal Sphincter (EAS)

• Striated (skeletal) muscle - voluntary control
• Three parts: subcutaneous, superficial, and deep
• The deep external sphincter is a direct extension of the puborectalis muscle
• Innervated by the inferior rectal branch of the internal pudendal nerve
• Responsible for squeeze pressure - voluntary continence when you need to defer defecation

Puborectalis Muscle

• Part of the levator ani (pelvic floor) complex
• Forms a U-shaped sling around the anorectal junction
• Creates the anorectal angle (~90°) which is critical for continence
• When it relaxes during defecation → anorectal angle straightens → stool can pass

Levator Ani Muscle

1. Puborectalis
2. Pubococcygeus
3. Iliococcygeus

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Perianal & Perirectal Spaces - THE Key to Understanding Abscesses

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Blood Supply Summary

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Lymphatic Drainage Summary

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PART 2: ANAL ABSCESS (ANORECTAL ABSCESS)

Etiology - Cryptoglandular Theory

"The majority of anorectal suppurative disease results from infections of the anal glands (cryptoglandular infection) found in the intersphincteric plane." - Schwartz

1. Anal gland (in intersphincteric space) becomes infected - usually with gut bacteria
2. The duct of the gland opens into an anal crypt at the dentate line
3. Obstruction of the duct → infection accumulates → abscess forms in the intersphincteric space
4. Abscess enlarges and spreads along the path of least resistance into the perianal spaces
5. Where it ends up determines the type of abscess

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Classification - 4 Types Based on Location

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1. 🔴 PERIANAL ABSCESS (Most Common ~60%)

• Severe, constant anal pain
• Obvious visible, tender swelling at the anal verge
• Fluctuant mass
• Patient cannot sit comfortably
• Fever may or may not be present

• Most can be drained under local anesthesia in the ER/clinic/office
• Cruciate or elliptical skin incision → excise a disk of skin to prevent premature closure
• No packing needed
• Start sitz baths next day

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2. 🟠 ISCHIORECTAL ABSCESS (~20%)

• Diffuse, indurated swelling in the ischiorectal fossa
• May be large and NOT visible at the anal verge (can be missed on inspection)
• Deep, brawny induration lateral to the anus on DRE
• Fever and systemic signs more common (large space)
• Can involve both sides → "horseshoe abscess" (via the deep postanal space)

• Drain through an incision in the overlying skin
• Horseshoe abscess: Requires drainage of the deep postanal space posteriorly (Hanley procedure) + counterincisions over one or both ischiorectal spaces

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3. 🟡 INTERSPHINCTERIC ABSCESS (~5%)

• Notoriously difficult to diagnose - no visible external swelling, no perianal signs of infection
• Pain described as deep, "up inside" the anal area
• Pain worsened by coughing or sneezing (increased intra-abdominal pressure)
• Pain so intense that DRE is often impossible without anesthesia
• Diagnosis requires high index of suspicion + Examination Under Anesthesia (EUA)

• Requires EUA
• Drained internally through the rectum - internal sphincterotomy to open the intersphincteric space
• Do NOT drain externally (would create a complex fistula)

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4. 🔵 SUPRAELEVATOR ABSCESS (~4%) - Most Complex

• Upward extension of an intersphincteric abscess through the rectal wall
• Upward extension of an ischiorectal abscess through the levator ani
• Downward extension of intra-abdominal disease (e.g., Crohn's, diverticulitis, appendicitis)

• Uncommon; can mimic intra-abdominal conditions (pain, fever, elevated WBC)
• DRE may reveal indurated, bulging mass above the anorectal ring
• Diagnosis often requires CT or MRI

This is a classic exam question: "Where do you drain a supraelevator abscess?" Answer depends entirely on where it came from.

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Summary Table - All 4 Abscess Types

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PART 3: COMPLICATIONS OF ANAL ABSCESS

Complication 1: FISTULA IN ANO (Most Common Complication - 50%)

"Drainage of an anorectal abscess results in cure for about 50% of patients. The remaining 50% develop a persistent fistula in ano." - Schwartz

• Internal opening = at the infected crypt at the dentate line
• External opening = at the site of prior abscess drainage on the perianal skin

• Posterior external opening → curved tract → internal opening in posterior midline (at 6 o'clock)
• Anterior external opening → straight (radial) tract → internal opening in the closest anterior crypt
• Exception: anterior openings >3 cm from the anus follow the posterior rule

• Low fistula (below or through lower 1/3 of EAS) → Fistulotomy (lay it open) - safe, effective
• High fistula (involving significant sphincter) → Seton placement (a thread through the tract) - staged approach to preserve continence
• Complex fistulas → may need multiple procedures, advancement flaps, or fibrin glue

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Complication 2: RECURRENCE

• About 10-20% of abscesses recur after drainage
• Recurrence usually means either incomplete drainage or an underlying fistula that was not treated
• Recurrent or complex abscesses should raise suspicion for: Crohn's disease, malignancy, tuberculosis, actinomycosis, radiation injury, chlamydia

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Complication 3: NECROTIZING SOFT TISSUE INFECTION (Fournier's Gangrene)

• Immunocompromised patients
• Diabetics
• Inadequately drained or missed anal abscess
• Occasionally post-hemorrhoidectomy

• Necrotic skin, bullae, crepitus (gas in tissues - pathognomonic)
• Severe systemic toxicity - septic shock
• Perineal signs may be MINIMAL despite extensive deep infection → high index of suspicion is essential

1. Emergency wide surgical debridement of ALL nonviable tissue - the most important step
2. Multiple operations may be necessary to clear all necrotic tissue
3. Broad-spectrum IV antibiotics (adjunct - NOT a substitute for surgery)
4. Colostomy if extensive sphincter resection required, or if stool contamination prevents wound healing
5. ICU support

Mortality: ~50% despite early recognition and adequate surgery.

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Complication 4: FECAL INCONTINENCE (Iatrogenic)

• Can occur if the sphincter is damaged during drainage or during fistula surgery
• The internal sphincter provides resting tone (most important for passive continence)
• The external sphincter provides squeeze pressure
• Aggressive surgery (e.g., wide fistulotomy for a high fistula) → division of sphincter → incontinence
• This is why high fistulas are treated with setons instead of single-stage fistulotomy

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Complication 5: PERIANAL SEPSIS IN THE IMMUNOCOMPROMISED

• Immunocompromised patients (chemotherapy, AIDS, leukemia) may have NO cardinal signs of inflammation (no redness, no fluctuance, no fever) despite serious infection
• Leukopenia masks the inflammatory response
• Any perianal pain in an immunocompromised patient → do not delay EUA
• Antibiotics alone may cure some, but examination under anesthesia should not be delayed
• Any indurated area must be:
  1. Incised and drained
  2. Biopsied (to exclude leukemic infiltrate)
  3. Cultured (to guide antibiotics)

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QUICK SUMMARY

ANAL GLAND INFECTION (intersphincteric space)
         ↓
   Abscess forms and spreads...

   ↙          ↓          ↘           ↘
Perianal  Ischiorectal  Intersphincteric  Supraelevator
(60%)      (20%)          (5%)             (4%)
Visible   Lateral DRE   Deep pain        Above levator
Drain     Drain skin    Drain internally  Drain = depends on origin
locally   ± horseshoe   (sphincterotomy)

         ↓ After drainage ↓

    50% cured       50% develop FISTULA IN ANO
                    
                    ↓ Complications ↓
    
    Fistula in ano | Recurrence | Fournier's Gangrene | Incontinence

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