Diagnosis and management of PUD

Ermias (MD)

History• Abdominal pain (epigatric burn)

– Common for DU, GU, NUD– 10% present with complications with out antecedent

pain, eg after NSAID– DU – 90min-3hr after meal, past midnight,

- relieve with food, antacids– GU – worse with meal, nausea and weight

loss are common

• Mechanism of pain– Acid induced chemoreceptor activation in duodenum– Enhanced duodenal sensitivity to bile acids and

pepsin– Altered gastro-duodenal motility

History conti…• Alterations in pain may show complications

– Persistent dyspepsia radiating to the back - penetrating ulcer to pancreas

– Sudden onset severe generalized pain – peritonitis due to perforation (6-7%)

– Worsening vomiting with meals – GOO (1-2%)

– Tarry stool, coffee ground vomits - bleeding (15%)

Physical examination

• Epigastric tenderness

• 20 % slightly to the right of the mid line

• In complications– Tachycardia, hypotension– Signs of peritonitis– Succussion splash

DDx

• NUD (functional, essential)

• Proximal GI tumors

• GERD

• Pancreaticobiliary diseases

• Crohn’s disease (gastro-duodenal)

diagnosis

• Empiric tx as NUD (<45 yrs age)• Ba studies

– Single contrast -80%, double contrast 90% sensitivity– See as well defined crater– Negative in <0.5cm ulcer, post op or scars

• Endoscopy– Photography, tissue biopsy, source of blood loss,

detection of small ulcers

• H. pylori• Serum gastrin, gastric acid analysis - ZES

H. Pylori detections– INVASIVE (ENDOSCOPY/BIOPSY REQUIRED)

• Rapid urease – (80–95/95–100) - Simple, false negative with recent use of PPIs, antibiotics, or bismuth compounds

• Histology – (80–90/>95) - Requires pathology processing and staining;

• Culture - Time-consuming, expensive, allows determination of antibiotic susceptibility

– NON-INVASIVE• Serology – (>80/>90) - Inexpensive, convenient; not

useful for early follow-up• Urea breath test – (>90/>90) - Simple, rapid; useful for

early follow-up; false negatives with recent therapy

– Stool antigen – (>90/>90) - Inexpensive, convenient; promising for eradication

treatment

• Schwartz – “no acid no ulcer” (old dictum)

• New concept– Eradication of H. pylori, – prevention of NSAID induced ds.

Acid neutralizing• Antacids – symptomatic relief

– Al(OH)3 Mg(OH)2– CaCO3, NaHCO3

• H2 receptor blockers – for active ulcer tx with H pylori eradication (4-6wk)– Antiandrogenic, cyt P450 inhibitor, – Elevation of transaminases, cr, prolactin;

pancytopenia

• Proton pump inhibitors– Irreversibly inhibit H+K+ATPase– Rapid onset and prolonged half life– Hypergastrinemia, carcinoid tumors (in animals),

hypochlorhydria (interfere with drug absorption)

Cytoprotective agents

• Sucralfate– Complex sucrose salt of Al(OH)3 and sulfate– Forms viscous paste in the stomach – Gives physicochemical barrier from further tissue

injury– Induce trophic effect on growth factors– Stimulate mucous and bicarbonate secretion– Enhance prostaglandin secretion– SE – constipation, neurotoxicity (Al) in renal

failure

• Bismuth preparations (colloidal bismuth subcitrate, subsalicylate)

– Anti H pylori effect– Mech. for ulcer not clear– Prostaglandin analogues – misoprostal – Enhance mucous bicarbonate secretion, stimulate

mucosal blood flow, decrease mucosal cell turn over

– Se – diarrhea, uterine bleeding and contraction– 200ug QID

Therapy of H pylori• Dramatic decrease in ulcer recurrence• GU 59% - 4%• DU 67% - 6%• Aim of initial eradication – 85-90%• Efficacy, pt tolerance, resistance pattern,

cost• dual tx not recommended < 80% eradication• Unnecessary tx – drug resistance• Infection recurrence in 6 mnth is likely from

recrudescence than reinfection

• TRIPLE THERAPY• 1.  Bismuth subsalicylate plus

    Metronidazole plus    Tetracycline

• 2.  Ranitidine bismuth citrate plus    Tetracycline plus    Clarithromycin or metronidazole

• 3.  Omeprazole (lansoprazole) plus    Clarithromycin plus    Metronidazole or    Amoxicillin

• QUADRUPLE THERAPY• Omeprazole (lansoprazole)

Bismuth subsalicylateMetronidazoleTetracycline

• 2 tablets qid250 mg qid500 mg qid

• 400 mg bid500 mg bid500 mg bid

• 20 mg bid (30 mg bid)250 or 500 mg bid500 mg bid1 gr bid

• 20 mg (30 mg) daily2 tablets qid250 mg qid500 mg qid

Tx of NSAID related gastric injury

• Stop the injurious agent

• Use acid inhibitory agent (PPI, H2 blocker)

• Prevention – misoprostol, PPI

• Use of COX -2 inhibitors

• Clinical Setting• Active ulcer    

– NSAID discontinued– NSAID continued

• Prophylactic therapy

• H. pylori infection

• Recommendation

• H2 blocker or PPIPPI

• MisoprostolPPISelective COX-2 inhibitor

• Eradication if active ulcer or a past history of peptic ulcer disease

UGIE

4wk

GU vs DU• GU (body, fundal) – likely to be malignant• Repeat endoscopy and biopsy at 8-12 wk• Non healing DU (8wk), GU (12wk) – refractory• Causes:

– Poor compliance– NSAID use– Cigarette smoking– Malignancy– Gastric hyper secretary state (ZES)– Ischemia, Crohn’s ds, Amyloidosis, Sarcoidosis,

Lymphoma, Eosinophilic gastroenteritis, CMV infection, Tuberculosis, syphilis

surgery

• Elective and emergency• Medically refractory ulcer and complicated

ulcers (bleeding, perforation and GOO)• Surgical mx decreased with increased

endoscopic interventions• Procedures:

– 1. vagotomy with drainage– 2. highly selective vagotomy– 3. vagotomy with antrectomy

complications• Depend on the extent of anatomic modification• Complications of intra abdominal procedure• Recurrent ulcerations• Afferent loop syndrome• Dumping syndrome• Post vagotomy diarrhea• Bile reflux gastropathy• Maldigestions and malabsorption• Gastric adenocarcinoma