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Peptic ulcers

now on peptic Section: UGI Sub-section: Gastric Curriculum: Curriculum, page 96

Definition

  • Peptic Ulcer disease
    • Defect of the mucosal barrier of the stomach or duodenum related to excess gastric juices
  • Ulcer
    • Breach of the mucosa of the GI tract, which extends through the muscularis mucosae into the submucosa or deeper
  • Simple or complicated

Incidence

  • Lifetime risk of developing a peptic ulcer in USA
    • 10% for men, 4% for women
    • Mortality now only 2.5% (was 4% in 1993)
  • Incidence markedly decreased over last 30 yrs
    • Decreasing both acute admissions and ulcer related pathology
  • M > F (3:1 in young pts; almost equal in older age)
  • More common in Māori & PI’s
  • In general DU > GU (but more NSAID-related GU in elderly)
    • GU: Peak Age > 55
    • DU: Peak age 20-45
  • Acute haemorrhage 3-4 x more common than perforation
    • 40/100,000 vs 10/100,00

Johnson Classification

Of gastric ulcers

Type 1

(60%)		Lesser curve (antral) near incisuraAcid UNRELATED

R/O malignancy
Type 2

(15%)		x2 gastric body and duodenal

(type 2, 2 ulcers)		Acid exposure
Type 3

(20%)		Prepyloric ulcerAcid exposure
Type 4

(10%)		Proximal GOJ - upper lesser curveAcid UNRELATED
Type 5Anywhere in gastric bodyNSAID induced

2x acid related = 2 + 3 2 ulcers lesser curve and duo Pre pyloric ulcers 2x non acid = 1 + 4 Lesser curve/antral → MALIG Proximal lesser curve 1x drugs = 5 = diffuse

Aetiology

  • Congenital:
    • Heterotopic / ectopic rests of gastric mucosa in the duodenum / distally can cause ulcers
      • E.g. Meckel’s ulceration
  • Inflammatory
  • Hiatus Hernias – Cameron Ulcer
  • Metabolic
    • ↑ Acid secretion – in DU pts only/type2/3 GU
    • ↓ Duodenal bicarbonate secretion / abnormal mucus
    • Low mucosal prostaglandins
    • ↑ Ca2+ → ↑ Gastrin secretion
  • Neoplastic
  • Drugs, poisons, toxic
    • NSAIDs → GU (or DU) – 10% on NSAIDs will get ulcer. Can act synergistically with H. pylori
    • Steroids
    • Smoking → impairs mucosal blood flow → ↑ ulcer recurrence/delayed healing
    • Association with EtOH

Presentation

  • Asymptomatic (50%)

  • Dyspepsia- aching / burning – Timing important!

    • GU: 15-20mins after eating; classically pain is exacerbated by food
    • DU: 2-3 hours after eating, so often described as starting before a meal / relieved by eating; may occur at night

  • Vomiting & anorexia – more common in GU

  • Zollinger-Ellison syndrome

  • Anaemia, weight loss, early satiety

  • Complications

    • Bleeding
    • Perforation
    • Obstruction

  • NOT Reflux – very rare to have PUD and volume reflux together

  • Zollinger-Ellison Syndrome

    • See Gastrinoma
    • Triad
      • Fulminant peptic ulcer disease
      • Acid hypersecretion
      • And resultant secretory diarrhoea
    • Non-beta Islet Cell Tumour of the Pancreas
    • Elevated serum gastrin with a pH < 2 in gastric aspirate is diagnostic of ZES
      • If pH > 3 without PPIs, is not ZES
      • Gastrin > 200 suggestive, > 1000 diagnostic
    • If diagnosis in question, can do secretin stimulation test
    • Treatment – localise and resect

Complications

  • Bleeding
    • Haemetemesis, Melaena, Haematochezia (Rapid transit UGIB!)
  • Perforation
    • Pain may begin in epigastrium but move to RLQ (due to tracking along paracolic gutter) = Valentino’s Syndrome
    • Radiation to back – suggests posterior perforation
    • Early (within first 4-6hrs)
      • May have mild tenderness only
      • Then initially feels better / pain may transiently ↓
      • Due to dilution of irritants by a peritoneal reaction
    • Later (> 12 hours)
      • Peritonitis
      • ↑ Pain & abdominal signs / guarding
      • Loss of liver dullness on percussion, due to free air
  • Obstruction – late complication; usually DU
    • May be reversible with medical treatment
    • Sx: Anorexia, vomiting, succussion splash
    • Hypokalaemic, hypochloraemic metabolic alkalosis

Pathophysiology

  • Increase in damaging (aggressive) factors or decrease in protective factors
    • Leads to mucosal damage and ulceration
  • Location
    • GU: Most benign ulcers are found on the lesser curve (and 60% within 6cm of pylorus)
    • Ulcers NOT along the lesser curve are more likely to be malignant
    • DU usually within duodenal cap, within 2cm of pylorus
  • Chronic gastritis
    • Virtually universal in pts with PUD, especially GUs - often due to H pylori
    • In stress ulceration adjacent mucosa is usually normal
    • NSAID ulcers only 25% have gastritis
  • Ulcers are usually punched out
    • Compared to malignant ulcers that have elevated edge
  • Multiple ulcers in 10-20% of cases
  • Cancer is more common when GU > 2cm (10% malignant)
    • Ca is related to presence of associated chronic gastritis rather than PUD itself

Protective Factors

  • Mucosal bicarbonate secretion
  • Mucus production
  • Blood flow
  • Growth factors
  • Epithelial cell renewal
  • Endogenous prostaglandins
    • ↑ Mucosal blood flow
    • ↑ Mucus secretion
    • ↑ Mucosal bicarbonate secretion

Aggressive Factors

  • Acid secretion
  • Pepsins
  • ETOH/Smoking
  • Duodenal reflux of bile
  • Ischaemia / Hypoxia
  • H. pylori infection
  • NSAIDs
    • Inhibit prostaglandin synthesis
    • Usually no associated gastritis
    • Increased risk of ulcer with concurrent steroids or anticoagulants

Investigations

  • History and exam
  • Bloods – FBC, LFTS, Lipase, Creatinine, Coags
    • Serum gastrin for pts with multiple ulcers or refractive disease (fasting & stimulated)
  • X-ray
    • Erect CXR → Free air in a perforation in >90%
    • AXR: Riggler’s sign (= Both sides of bowel wall visible)
  • OGD
    • Biopsy + rapid urease assay
    • GU: Ulcer edge biopsies – must exclude gastric malignancy!
    • Gives options of tx for bleeding ulcers
  • CT if concerned about posterior perforation
  • H. pylori testing

Helicobacter Pylori Testing

  • Invasive
    • Histological biopsy – sens 95%- Gold Standard
    • Rapid urease assay (CLO) – detects urease in gastric biopsy – sens 90%/spec 98%
      • Urea (orange) in membrane is converted to ammonia (red) by urease and changes pH which is detected by reagent similar to litmus paper (orange to red)
      • Rapid result in 1 hour but may take up to 24 hours
    • Culture – sens 80%. 3-5 days till dx & expensive
  • Non-invasive
    • Serology (ELISA) to detect IgG antibody
      • 90% sensitivity/spec but titre can remain high for up to 12 months after eradication therefore not good to test eradication
    • Carbon-13 Urea breath test
      • Carbon labeled urea is hydrolyzed by H. pylori to CO2 and exhaled – sens/spec = 95%
        • Best performed 4 weeks after eradication as can give false –ve if too early
    • Stool antigen testing
      • Monoclonal immunoassay to detect H. pylori antigens. Sens 95%
      • Can test eradication early but false neg may occur so recommended to wait 4 weeks and off PPI for at least 2 weeks

Management

  • Medical
  • Lifestyle modification
  • Treatment of acidic environment
  • Eradication of H. pylori
  • Surgical (management of complications)
    • Only required in 20%

Medical Management

  • Vast majority will only need medical management
  • Always remember life-style modification
    • Stop smoking
    • Reduce ETOH/coffee
    • Stop NSAIDS
  1. Treat high acidic environment to enable stabilization of early healing factors
  • Proton pump inhibitor
    • Most potent antisecretory agents
    • Provide a more complete and prolonged acid suppression than H2 blockers
    • Ulcer healing 85% at 4 weeks, 95% at 8 weeks
    • Require acidic environment to become activated therefore should not use with H2 antagonists or antacids
  • Antacids
    • Reduce gastric acidity by reacting with HCL
    • Magnesium based antacids are best but cause diarrhea
    • Work best when taken after a meal as retained in stomach for longer
    • ~ 80% ulcer healing in one month but compliance issues
  • H2 receptor antagonists
    • Similar structure to histamine and bind to histamine receptor and block it - preventing acid secretion.
    • Can get Tachyphylaxis after 4-6 weeks (less effective over time)
    • Resolution of ulcers in 70-80% in 4 wks, up to 90% at 8 wks
  • Sucralfate
    • Effective for ulcers but unknown mechanism ? protective barrier by binding of sucrose polymers to ulcer crater
  • Stop NSAIDs – usually don’t recur, if have to use – Misoprostol
  1. H pylori eradication
  • Reduces recurrence to < 2%
  • Healing in > 90%
  • Can follow local guidelines (BPAC)
  • Initially triple therapy for one week
    • PPI, Clarithromycin and either Amoxicillin or metronidazole
      • If has had metronidazole recently, don’t use that
      • If has had macrolide recently, uses PPI, Amoxil and metronidazole
    • If penicillin allergic use PPI, Clarithromycin and Amoxil
    • Consider Bismuth for refractory disease
  • Retest to ensure eradication if the patient has had a peptic ulcer

Perforated Peptic Ulcer

  • Mortality up to 15%
  • Highest of PUD complication

Initial Management

  • Resuscitate while investigating
    • IV fluids
  • NBM and NG Tube
  • IV antibiotics
  • IDC
  • Analgesia, antiemetics
  • IV PPI
  • Reverse anticoagulants
    • If abnormal post resuscitation
  • Theatre
  • If normal observations, consider CT to see where perforation is

Conservative Management

  • Taylor’s method (rarely used)

  • May have a role in

    • Very fit patients
    • Admitted within 24hrs of perforation
    • Not shocked
    • And can be carefully monitored
    • Stable patients, presenting ≥ 3 days after perforation (self-sealed)
    • Patients too old/frail for surgery

  • NG suction, IV Abx, IVF, IV PPI, H. pylori eradication if +ve, close monitoring

  • Patients who fail to improve within 24hrs → Operation

  • 50% successful

  • Need OP scope in 6 weeks

  • In trials mortality was the same, but morbidity & length of hospital stay greater in conservative group

  • Failure likely if:

    • Significant pneumoperitoneum
    • Tachycardic
    • Abdo distension
    • Age > 60

Surgical Management

  • Consider laparoscopy to identify where perforation is and how much contamination
  • Consider Lap vs Open and appropriate skill set
    • In experienced hands, laparoscopy superior approach
    • Less pain and narcotic use
    • Earlier time to discharge
    • Conversion rate 10-15%

Gastric Ulcer

  • Lavage, lavage, lavage
  • Leave NGT
  • Resect ulcer for histology or biopsy
    • Wedge resection and direct closure
  • May require distal gastrectomy if large
  • If very unwell could consider omental patch only
    • Still need to biopsy ulcer
    • If don’t, will need gastroscopy 6/52
  • No role for acute acid reducing procedure

Duodenal Ulcer

  • Lavage, lavage, lavage
  • Leave NGT
  • Main repair strategy is patch
  • If > 50% of lumen -
    • May require pyloric exclusion
      • Options for management of duodenal stump
        • Nissen closure- Management of the Difficult Duodenal Stump , page 2
        • Bancroft closure - Management of the Difficult Duodenal Stump , page 3
        • Duodenostomy - Management of the Difficult Duodenal Stump , page 3
      • Options for management of stomach
      • Place many drains

Post-Operative Management

  • NGT to decompress stomach until bowel activity returns
  • Keep drains until eating and no evidence of increase in volumes
  • No evidence of leak
  • Routine contrast studies not required before initiating eating
  • If signs of leak, can be used to evaluate if actually is leak or quality of drainage
  • Eradicate H pylori if positive
  • Continue PPI

Gastroduodenal Haemorrhage

  • 70% non-variceal bleeding due to PUD
  • Majority will stop spontaneously and require no definitive management
  • However persistent bleeding is associated with mortality of up to 10%

Initial Management

  • Resuscitation
    • Large bore IV access x2,
    • Restore intravascular volume with IVF and blood products if required
    • Consider massive transfusion protocol
  • Bloods including U+E, LFTs, Coags, G + x-match
  • NG tube
  • IDC
  • IV omeprazole (80mg)
  • Reverse anticoagulants
  • All patients should have endoscopy < 24hrs
  • Test H pylori status (non-urgent)

Risk Stratification

  • Predictive factors of persistent/re-bleeding:
    • Age
    • Decreased Hb (100)
    • Shock at presentation (SBP<100, HR>100)
    • Melena
    • Requirement for blood transfusion
  • Glasgow Blatchford Score
  • Rockall score (ABCDE)
    • Useful predictor of rebleed and in hospital mortality
    • Helpful in determining if surgical intervention may be required after initial resuscitation and evaluation
  • AIMS65

Glasgow-Blatchford

  • Predicts need for clinical intervention, rebleed, and mortality
    • Similar to Rockall score but doesn’t use endoscopic information
  • Can use on initial presentation
  • Score of 0-1 is low risk
  • Any score above 0 predicts need for transfusion, endoscopy, or surgery
    • Sensitivity 99%
    • Better sensitivity than pre-endoscopy Rockall score for detecting patients that can be discharged Screen Shot 2020-10-17 at 4.16.20 PM.png

Rockall Score

  • A - Age
  • B - Blood pressure
    • Presence of shock
  • C - Co-morbidities
  • D – Diagnosis
  • E – Endoscopic stigmata of bleeding
  • Score out of 11 to predict risk of re-bleed after endoscopic intervention
    • 1-2 = Low risk

    • 8 = High risk

Screen Shot 2020-10-17 at 4.07.24 PM.png

Endoscopic Management

  • Consent, including possible need for surgery
  • Preferably in theatre with anaesthetist
    • GA if unstable due to risk of aspiration
    • Can move to surgery quickly
  • Experienced endoscopy team
    • Appropriate haemostatic options
    • Mechanical lavage
  • Assess the ulcers, describe using Forrest Classification
    • Endoscopic appearance helps determine which lesions need therapy or at risk of rebleeding
    • Forrest 1A, 1B, 2A should have intervention as high risk of rebleed
  • Endoscopic control of bleeding
  • Biopsy for H pylori
  • Monitoring post-endoscopy Screen Shot 2020-10-17 at 4.42.30 PM.png Forrest Classification of Peptic Ulcers

Endoscopic Control of Bleeding Ulcer

  • 90% successful, use dual therapy
    • Adrenaline injection (1 in 1000)
      • Primary haemostasis rates high
      • But up to 30% rebleed if used alone - don’t use as monotherapy
    • Clips
    • Coagulation/APC
    • Fibrin sealants/haemostatic agents
    • < 1% complication rate (necrosis, perforation)
  • Dual therapy (adrenaline and another) has relative risk of re-bleed compared to monotherapy of 0.3

Monitoring after Endoscopic Therapy

  • Monitor in HDU/ICU until all bleeding has stopped for 24hrs
  • Place on IV PPI
    • Bolus then infusion or intermittent IV doses
    • For at least 72 hrs (stabilises clot)
    • PPI better than H2 Blockers
      • Rebleed rates, rate of emergency surgery, mortality
  • If Re-bleeds
    • Repeat endoscopic management if tolerated
      • Also if remain haemodynamically stable
    • Does not increase mortality
    • Could consider angiographic embolisation
      • Can be tricky due to rich vascular plexus of stomach
  • 5-10% have ongoing bleeding that requires surgery
    • Haemodynamically unstable patients
    • Ongoing transfusion requirements (> 6 units RBCs)

Surgical Management

Gastric Outlet Obstruction

  • Due to oedema/inflammation/stricture at ulcer
  • If prolonged vomiting patients develop
    • Hypochloraemic, Hypokalaemic Metabolic Alkalosis
    • Paradoxical acidic urine due to profound losses of HCl
      • Vomiting = Loss of Gastric HCl
      • Dehydration and Metabolic Alkalosis
      • Progressive dehydration – Kidneys preferably keep Na+ over K+
      • Hypokalaemia develops
      • Kidney then switches and keeps K+ and loses H+
  • Need to exclude malignancy (a more common aetiology)
  • Management

Intractable PUD

  • Definition
    • Failure of an ulcer to heal after 8-12 weeks of treatment, or relapse after treatment discontinued
    • Need to confirm adequate treatment/compliance, H. pylori eradication and ceased NSAIDS
      • Check Serum gastrin for PPI compliance
        • Increased levels (quickly normalises after cessation of PPI)
      • Can do NSAID assays
    • R/O Gastrinoma
  • Rarely require surgical intervention for intractable disease
  • Indications:
    • Intractable disease where H.pylori negative
    • NSAID related that cannot stop NSAIDS
  • Goal = Reduce acid secretion
  • Two methods:
    • Reduce vagal stimulation (vagotomy)
    • Reduce parietal cells/gastrin production with antrectomy

Highly Selective Vagotomy

  • Cuts branches only to body and fundus in attempt to prevent stasis
    • Leaves hepatic and coeliac branches
    • Leaves antral and pyloric branches intact (Nerve of Latarjet)
  • Divides “crow’s feet” up to 7cm proximal to pylorus and 5cm proximal to GOJ up oesophagus including the proximal, dividing the “Criminal Nerve of Grassi” from posterior Vagus
  • NB: Leaves supply to G cells
    • Gastrin will increase, but no response
  • Recurrence 10-15%
  • Not recommended for pre-pyloric ulcers (these recur)
  • Side effects
    • Diarrhoea 30-70% - most resolve,
    • If not can use Cholestyramine 4g/ meal – takes up to a month to act
      • anion exchange resin that binds bile salts rendering them unabsorbable & inactive
    • May need 10cm reversed segment jejunum interposition
      • 70-100cm from ligament of Treitz
  • Gastric atony
    • Not seen in highly selective
    • Loss of antral function will reduce ability to empty solids
    • Diagnose with scintigraphy to confirm delayed emptying, contrast study & endoscopy to exclude mechanical obstruction
  • Rx: Pro-kinetics

Gastric antrectomy

  • 50% distal gastrectomy
    • Reconstruct with Billroth I or II
    • ± vagotomy (add if Type 2 or 3 – acid related ulcers)
  • Best results in recurrent ulcers (2%)
  • 20% get post-gastrectomy syndromes
  • Billroth I = Antrectomy + Gastroduodenostomy
    • Avoids duodenal stump
    • Avoids duodenal stump leak
    • Avoids afferent limb syndrome
  • Billroth II = Antrectomy + Gastrojejunostomy
    • Billroth II takes more stomach therefore would be operation of choice if malignancy suspected

Prognosis/ Natural History

  • Eradication of H pylori
    • Ulcer recurrence rates of < 5% (after 5yrs f/up)
    • More effective cf no Rx
  • After vagotomy
    • Ulcer recurrence ≈ 10% at 10yrs
  • After perforated ulcer → Mortality rate ≈ 15%
  • Follow-up
    • Gastric ulcers:
      • Need re-scope & re-biopsy in 6-12/52
      • Ideally should be off PPI for 2/52 prior
    • If patient has been treated for H. pylori:
      • PPI for 2/12, then repeat H. pylori faecal Ag test to see if clearance (should have been off PPI for 2/52 prior)

H. Pylori

Non-steroidal anti-inflammatory drugs

Graph View

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