Perforated peptic ulcer

Abstract

Perforated peptic ulcer is a common emergency condition worldwide, with associated mortality rates of up to 30%. A scarcity of high-quality studies about the condition limits the knowledge base for clinical decision making, but a few published randomised trials are available. Although Helicobacter pylori and use of non-steroidal anti-inflammatory drugs are common causes, demographic differences in age, sex, perforation location, and underlying causes exist between countries, and mortality rates also vary. Clinical prediction rules are used, but accuracy varies with study population. Early surgery, either by laparoscopic or open repair, and proper sepsis management are essential for good outcome. Selected patients can be managed non-operatively or with novel endoscopic approaches, but validation of such methods in trials is needed. Quality of care, sepsis care bundles, and postoperative monitoring need further assessment. Adequate trials with low risk of bias are urgently needed to provide better evidence. We summarise the evidence for perforated peptic ulcer management and identify directions for future clinical research.

Figure 1. Peptic ulcer disease burden globally

Years of life lost (YLL) and years of life with disability (YLD) presented for quintiles of the Human Development Index (HDI). Age-standardised estimates for peptic ulcer disease were retrieved from the Global Burden of Disease Study 2010 repository (http://ghdx.healthdata.org/record/global-burden-disease-study-2010-gbd-2010-results-cause-1990-2010-country-level). Proportion of deaths (bubble size), rate of years of life lost (YLL) and rate of years of life with disability (YLD) for both sexes and year 2010 were analysed. Data are presented by United Nations Development Programme Human Development Index quintiles (http://hdr.undp.org/en/content/human-development-index-hdi)

Figure 2. Mechanisms and factors in pathogenesis of perforated peptic ulcer [sketch, to be redrawn]

(A) an imbalance between between hostile and protective factors start the ulcerogenic process, and (B) although many cotributors are known, helicobacter infection and use of non-steroidal anti-inflammatory drugs appear of importance in disturbing the protective mucosal layer and (C) expose the gastric epithelium to acid. Several additional factors (D) may augment the ulcerogenic process (such as smoking, alcohol and several drugs) that lead to erosion (E). Eventually, the serosal lining is breached (F), and when perforated, the stomach content, including acidic fluid, will enter the abdominal cavity giving rise to intense pain, local peritonitis that may become generalized and eventually lead to a systemic inflammatory response syndrome and sepsis with the risk of multiorgan failure and mortality.

Figure 3. Preoperative adverse prognostic factors for mortality in PPU disease

Adjusted preoperative prognostic factors for motality. Data derived and developed from Møller et al ^[47]. ASA, denotes American Society of Anesthesiologist risk score COPD, denotes chronic obstructive pulmonary disease S-albumin, denotes serum albumin NSAIDs, denotes non-steroidal antiinflammatory drugs RR, denotes relative risk CI, denotes confidence interval