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Peptic Ulcer Disease (PUD)

Anesthesia Implications

Updated On: July 22, 2026

Anesthesia Implications

Elective versus emergent is the whole story - An outpatient on a proton pump inhibitor for uncomplicated PUD is a routine anesthetic. A perforation or an actively bleeding ulcer is a resuscitation that happens to involve an operation. Sort out which one you have before anything else.

Perforation is a full stomach and a sepsis case - Plan an RSI. These patients arrive tachycardic, often hypotensive, with diffuse tenderness progressing to guarding and rigidity, and free air on an upright chest film or CT. A nasogastric tube, IV proton pump inhibitor and broad-spectrum antibiotics covering gram-negative rods and anaerobes should already be running. Delay beyond 24 hours from perforation drives mortality, so resuscitate on the way to the room rather than instead of going.

Volume-load before induction - Roughly 30% to 35% of perforated ulcer patients are already septic on arrival in the OR. Gastric acid leaking into the peritoneum causes a chemical peritonitis that third-spaces a large volume before food particles and bacterial peritonitis follow. Induction on top of an empty tank drops the pressure hard.

Labs that change the plan - CBC, chemistry panel, liver function tests, coagulation profile and lipase (to exclude pancreatitis), plus blood type and screen. In anyone meeting SIRS criteria add blood cultures and a lactate — the lactate is what tells you whether there is coexistent ischemia.

Anticipate anemia in the bleeder - Upper GI bleeding is the most common complication of PUD. Chronic occult bleeding shows up as melena, an elevated BUN and a positive fecal occult blood test. Get a hemoglobin rather than assuming a normal starting point, and have blood in the room for an active bleed.

Risk-stratify with the scores the surgeons use - The Boey score (concomitant severe medical illness, preoperative shock, perforation duration over 24 hours) and ASA physical status are the validated predictors in perforated ulcer. All three Boey factors positive predicts 38% mortality and 77% morbidity — that is the conversation to have before induction, not after.

This is usually an older, sicker patient - 60% of patients with PUD are over 60. Age over 65, comorbidity, shock at admission, metabolic acidosis, acute renal failure, hypoalbuminemia and delayed presentation all independently raise mortality. Correct the acidosis and the volume deficit as far as the clock allows.

Skip the NSAIDs in your multimodal plan - The drug class that caused the ulcer does not belong in the analgesic plan. Ketorolac and piroxicam have the highest mucosal-injury profile in the NSAID family. In a patient with a PUD history, COX-2 selective agents are preferred because COX-2 is not expressed on gastric mucosa.

Keep the PPI running - IV proton pump inhibitor creates a more neutral gastric pH, which supports platelet aggregation and helps a bleeding or perforated ulcer seal. It continues postoperatively to prevent recurrence.

Plan the disposition for sepsis, not for the incision - Laparoscopic and open omental patch repair show no meaningful difference in mortality, so the approach does not change your risk estimate. More than 25% of these patients develop septic shock within the first month after surgery, with 50% to 60% mortality. In an ASA I or II patient the opposite is true — early removal of tubes and early oral intake shortened hospital stay by about three days.

Pathophysiology

Peptic ulcer disease (PUD) is a break in the mucosa of the stomach or proximal duodenum that extends past the muscularis mucosae. Lesions under 5 mm are erosions; over 5 mm they are ulcers. Two causes account for most of it. Helicobacter pylori colonizes the gastric epithelium, inflames it and impairs bicarbonate secretion — it is behind 90% of duodenal and 70% to 90% of gastric ulcers. NSAIDs, including low-dose aspirin, block COX-1 prostaglandins and so cut gastric mucus, bicarbonate and mucosal blood flow. Corticosteroids, bisphosphonates, potassium chloride, smoking, alcohol and Zollinger-Ellison syndrome contribute.

About 70% of patients are asymptomatic, so PUD itself rarely brings anyone to the OR. Its complications do: bleeding (the most common), perforation and gastric outlet obstruction. Perforation carries a 30-day mortality around 24%, and sepsis accounts for roughly half of those deaths.


Suggested Reading

Hsieh HH, Lee WY, Lin CL, et al. Impact of anti-peptic ulcer disease (PUD) medications on hyperlipidemia risk in patients with PUD: a population-based retrospective cohort study. Ther Adv Endocrinol Metab. 2026. PMID: 42027967.
Hemmings HC Jr, Yao FF, Goldstein PA, et al, eds. Yao & Artusio's Anesthesiology: Problem-Oriented Patient Management. 10th ed. Wolters Kluwer; 2025.
Gropper MA, Eriksson LI, Fleisher LA, et al, eds. Miller's Anesthesia. 10th ed. Elsevier; 2024.
Eftekhari A, Masjedi Arani A, Bakhtiari M, et al. Efficacy of emotion regulation training on pain intensity and life quality in patients with peptic ulcer disease (PUD). Gastroenterol Hepatol Bed Bench. 2023. PMID: 38313358.
Hines RL, ed. Stoelting's Anesthesia and Co-Existing Disease. 8th ed. Elsevier; 2021.
Molaoa SZ. Prevalence of Helicobacter pylori infection and the incidence of the associated malignant and peptic ulcer disease (PUD) at Nelson Mandela Academic Hospital: a retrospective analysis. J Drug Assess. 2021. PMID: 34104536.