What happens when a stomach ulcer ruptures

History and Physical Examination

With extensive hemorrhage, vomiting, diarrhea, or ulcer perforation, patients with GI hemorrhage may be presented in a state of shock resulting from blood loss, hypovolemia, endotoxemia, or sepsis. Examination findings consistent with shock include tachycardia, diminished or thready arterial pulses (particularly peripheral), cool extremities, prolonged capillary refill time, and pale mucous membranes. Immediate resuscitative therapies to reverse the state of shock take precedence (see Chapters 5 and 60), and localization of the site of hemorrhage and tailored therapies may have to be delayed until the cardiovascular system is stable.

Once resuscitative efforts have commenced, a complete history and physical examination should be performed. Hematemesis (vomitus with the appearance of coffee grounds or frank blood), hematochezia (passage of bright red or frank blood with or without stool), or melena (black, tarry stool) suggests the GI tract as a source of hemorrhage. However, these signs are not always evident clinically and may not appear until significant GI hemorrhage has occurred.3,4,11 With duodenal hemorrhage, if reflux of duodenal contents into the stomach is insufficient, blood may not be visible in the vomitus.12 However, when it is present, hematemesis suggests ongoing blood loss.13 Diseases of the nasal cavity and oropharynx occasionally can cause hematemesis and melena from swallowing blood of epistaxis or hemoptysis (coughing of blood). In addition, activated charcoal, metronidazole, bismuth (Pepto-Bismol), and diets high in iron (liver, unsweetened baking chocolate) can result in dark stools and should not be confused with melena.14

A history of aspirin or other NSAID administration is not uncommon.4,11,15 Case reports exist of GI ulceration, hemorrhage, and GI perforation occurring in veterinary patients that have received selective cyclooxygenase inhibitors at recommended therapeutic dosages.11 Decrease or loss of appetite with or without other signs of GI disease should prompt consideration of GI side effects in any patients receiving NSAIDs. The medication should be discontinued and the patient should be examined. In cases of thrombocytopenia or coagulation disorders, there may be a history of bleeding from other sites of the body, including the nasal cavities or urinary tract. Thorough examination of the mucosal surfaces may reveal petechiae in severely thrombocytopenic patients. A search for subcutaneous nodules or masses may detect underlying mast cell tumors.

Because GI hemorrhage may be insidious in onset, especially when chronic, the abdomen should be examined carefully. Abdominal palpation may localize areas of pain (tenderness, voluntary or involuntary guarding) or induce nausea, identify masses or foreign objects, or detect abdominal distention or a fluid wave. Splenomegaly or hepatomegaly may be identified in patients with mastocytosis, other neoplasia, or hepatic diseases. A careful rectal examination should be performed to detect frank blood or melena and to look for masses or foreign bodies.

Localizing the site of GI hemorrhage is important because the cause, diagnostic tests, and therapies for upper and lower GI hemorrhage may vary.5,14 Although hemorrhage from any site in the GI tract can be serious, upper GI hemorrhage tends to be more severe.13,14 Hematemesis or melena suggests upper GI hemorrhage.14 However, it is the amount of time the blood remains in the GI tract and not necessarily the site of bleeding that determines its color.14,15 Delayed GI transit time and retention of blood in the colon could result in melena associated with a lower GI tract lesion.14,16 Hematochezia is usually reflective of large intestinal, rectal, or anal hemorrhage; however, severe acute intestinal hemorrhage can act as a cathartic, significantly decreasing GI transit time.13-15 This may result in the passage of frank blood in the stool after significant blood loss into the upper GI tract.13,15

HISTORY AND PHYSICAL EXAMINATION

With extensive hemorrhage, vomiting, diarrhea, or ulcer perforation, patients with GI hemorrhage may present in a state of shock due to blood loss, hypovolemia, endotoxemia, or sepsis. Examination findings consistent with shock include tachycardia, diminished or thready arterial pulses (particularly peripheral), cool extremities, prolonged capillary refill time, and pale mucous membranes. Aggressive resuscitative therapies to reverse the state of shock take precedence (see Chapters 10 and 65, Shock and Shock Fluids and Fluid Challenge, respectively), and localization of the site of hemorrhage and tailored therapies may need to be delayed until the cardiovascular system is stable.

Once resuscitative efforts have commenced, a complete history and physical examination should be performed. Hematemesis (vomitus with the appearance of coffee grounds or frank blood), hematochezia (passage of bright red or frank blood with or without stool), or melena (black tarry stool) suggests the GI tract as a source of hemorrhage. However, these signs are not always evident clinically and may not appear until significant GI hemorrhage has occurred.3,4,10 With duodenal hemorrhage, if reflux of duodenal contents into the stomach is insufficient, blood may not be visible in the vomitus.11 However, when it is present, hematemesis suggests ongoing blood loss.12 Diseases of the nasal cavity and oropharynx occasionally can cause hematemesis and melena from swallowing blood of epistaxis or hemoptysis (coughing of blood), and these causes should be considered. In addition, activated charcoal, bismuth (Pepto-Bismol), and diets high in iron can result in dark stools and should not be confused with melena.13

A history of aspirin or other NSAID administration is not uncommon.4,10,14 There are case reports of GI ulceration, hemorrhage, and GI perforation occurring in veterinary patients that have received selective cyclooxygenase inhibitors at recommended therapeutic dosages.10 Decrease or loss of appetite with or without other signs of GI disease should prompt consideration of GI side effects in any patients receiving NSAIDs. The medication should be discontinued and the patient should be examined. In cases of thrombocytopenia or coagulation disorders, there may be a history of bleeding from other sites of the body including the nasal cavities or urinary tract. Thorough examination of the mucosal surfaces may reveal petechiae in severely thrombocytopenic patients. A search for subcutaneous nodules or masses may detect underlying mast cell tumors.

Because GI hemorrhage may be insidious in onset, especially when chronic, the abdomen should be examined care-fully. Abdominal palpation may localize areas of pain (tenderness, voluntary or involuntary guarding) or induce nausea, identify masses or foreign objects, or detect abdominal distention or a fluid wave. Splenomegaly or hepatomegaly may be identified in patients with mastocytosis, other neoplasia, or hepatic diseases. During initial evaluation or resuscitation of the patient, a careful rectal examination should be performed to detect frank blood or melena and to look for masses or foreign bodies.

Although hemorrhage from any site in the GI tract can be serious, upper GI hemorrhage tends to be more severe.12,13 In addition, the etiology as well as the diagnostic tests and therapies for upper and lower GI hemorrhage may vary, making localization of the site of hemorrhage important.5,13 Hematemesis or melena suggests upper GI hemorrhage.13 However, it is important to remember that it is the amount of time the blood remains in the GI tract and not necessarily the site of bleeding that determines its color.13,14 Delayed GI transit time and retention of blood in the colon could result in melena associated with a lower GI tract lesion.13,15 Hematochezia is usually reflective of large intestinal, rectal, or anal hemorrhage; however, severe acute intestinal hemorrhage can act as a cathartic, significantly decreasing GI transit time.12-14 This may result in the passage of frank blood in the stool following significant blood loss into the upper GI tract.12,14

Peptic ulceration

There is a higher incidence of gastric ulcers in cocaine users, both perforated ulcers and giant gastroduodenal ulcers, thought to be due to localized ischemia secondary to vasoconstriction [226,227]. Two reports have afforded data on gastrointestinal ulcers and cocaine. In one study the authors observed that since the advent of crack cocaine they had seen more than 70 cases of crack-related perforated ulcers [228]. They suggested that an ischemic process rather than an acid-producing mechanism was to blame. They described three patients, all of whom had laparoscopic omental patches for ulcers, with good results. In a longitudinal assessment of patients with endoscopically diagnosed gastric ulcers (n = 98) or duodenal ulcers (n = 116) users of cocaine or metamfetamine were nearly 10 times more likely to have giant gastric or duodenal ulcers (over 2.5 cm) compared with non-users [229]. The authors speculated that cocaine and amfetamine-induced catecholamine stimulation of α-adrenoceptors may cause intense vasoconstriction and thus a reduced blood supply to an ulcer, resulting in a giant ulcer.

Five cases of gastric perforation (rather than the more common duodenal perforation) have been reported in young male smokers of crack, all of whom had only brief histories of prodromal symptoms and none of whom had long-standing peptic ulcer disease [230].

Intraabdominal Infections

The main causes of abdominal sepsis in postoperative cardiac surgery patients are mesenteric infarction, perforated peptic ulcer, cholecystitis, and diverticulitis. These conditions, with the exception of diverticulitis, are discussed in Chapter 34. Pseudomembranous colitis is due to bacterial overgrowth by toxin-producing Clostridium difficile; it too is discussed in Chapter 34.

Infections are commonly polymicrobial, and empiric antimicrobial therapy should be directed against enteric gram-negative bacilli (i.e., Enterobacteriaceae), Enterococcus species, and enteric anaerobes (e.g., Bacteroides fragilis). This may be achieved by means of “triple” therapy: gentamicin (for gram-negative bacilli), metronidazole (for anaerobes), and amoxicillin (for Enterococcus species). Aztreonam may be substituted for gentamicin in patients with renal failure. Depending on local resistance patterns, alternative strategies include the use of meropenem or piperacillin/tazobactam. In high-risk patients, treatment with theconazole may decrease mortality as infection with Candida may occur.58

Imaging Studies

An initial plain X-ray of the abdomen helps more to exclude the diagnosis of perforated ulcer or intestinal obstruction rather than to diagnose pancreatitis. Dilated loops of small bowel (“sentinel loop”) or transverse colon (“colon-cut off sign”) are nonspecific and infrequent. Chest X-ray helps to evaluate the lungs and to diagnose pleural effusion. An initial abdominal ultrasound is a must in all cases except when an alcoholic etiology is quite clear. The main purpose is to look for gallstones or sludge, and assess the CBD size. Contrast enhanced CT helps in assessing severity of AP.

Specialized studies such as magnetic resonance imaging (MRI), magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasound (EUS) have only limited value in the routine management, but may be needed to exclude a CBD stone in the presence of a dilated duct or persistently abnormal liver enzymes.

Upper GI Events

From clinical trials the benefit of COX-2 selective inhibitors regarding upper GI complications (such as ulcers, bleeding, and perforations) over nsNSAIDs was demonstrated. It was therefore not surprising, that high-risk patients (i.e. those subjects with at least one risk factor of developing upper GI complications: (1) age ≥65 years; (2) history of upper GI event; (3) concomitant use of anticoagulants; (4) concomitant use of antiplatelets (low-dose aspirin, LDA); and (5) concomitant use of corticosteroids) were preferentially prescribed COX-2 selective inhibitors instead of nsNSAIDs. However, concurrent prescription of a PPI to a nsNSAID might be just as ‘safe’ as prescribing a COX-2 selective inhibitor. Clinical trials were not able to demonstrate superiority of one of these preventive strategies over the other, not only because of selective inclusion and exclusion of patients with co morbid diseases, but also because of composite endpoint definition. When comparing COX-2 selective inhibitors with nsNSAIDs in an observational study, confounding by indication should be taken into account. By matching on the probability that a subject receives one drug over the other (such as a COX-2 selective inhibitor over a nsNSAID), confounding by indication should be dealt with as the underlying treatment indication should be similar between those matched subjects. In a cohort study of new users of COX-2 selective inhibitors and nsNSAIDs, the risk of upper GI complications was estimated. By applying a high-dimensional propensity score the risk of upper GI complications was reduced for use of COX-2 selective inhibitors compared to nsNSAIDs (RR 0.62; 95%CI: 0.43–0.91) [6c]. This study did not take concurrent prescription of a gastroprotective agent (GPA, such as a PPI) into account, while this may results in similar risk of upper GI events for COX-2 selective inhibitors and nsNSAIDs plus GPAs. This question was addressed by another observational study which tried to identify which of these strategies (COX-2 selective inhibitor or nsNSAID + GPA) should be preferred in the daily clinical setting. A case–control study nested within an NSAID user cohort among three European primary care databases was performed. To mitigate against confounding by indication, only highly adherent GPA users were included (≥80% coverage of GPA during use of nsNSAID). Overall, the risk of upper GI events (n = 398 cases) and upper GI bleeding (n = 225) was equivalent (OR: 1.02; 95%CI: 0.77–1.37). However, in those subjects using corticosteroids, the risk of upper GI events was significantly higher for those using nsNSAID + GPA compared to COX-2 selective inhibitor users (OR:9.01; 95%CI: 1.61–50.50). As is known from previous studies, concurrent use of LDA eliminates the benefit of COX-2 selective inhibitors over nsNSAIDs [7c].

Still a considerable proportion of users continue to experience upper GI events; around 3.7–8.9%. So even despite the beneficial effect of COX-2 selective inhibitors further gastroprotective measures may be indicated in certain COX-2 selective inhibitor users was demonstrated in another observational study. In a case–control study nested within a COX-2 selective inhibitor plus concomitantly GPA users cohort, the risk of upper GI events was compared in relation to GPA adherence. It showed that for every 10% decrease in GPA adherence, the risk of upper GI events increased by 9% (OR 1.09; 95%CI: 1.00–1.18) [8c].

A systematic review and meta-analysis of observational studies on individual NSAIDs and the risk of upper GI complications included 28 studies. It demonstrated increased risks ranging from 1.43 for aceclofenac (95%CI: 0.65–3.15) up to 18.45 for azapropazone (95%CI: 10.99–30.97) (Table 1). Higher doses of NSAIDs were associated with a 2–3 times higher risk than lower doses [9M]. Another systematic review pooled randomized trials comparing GI adverse effects between COX-2 inhibitors and NSAIDs plus PPIs. A total of nine trials involving 7616 patients from 2002 to 2011 were included. All trials were randomized, double-blind and placebo-controlled trials. Pooled analysis showed that COX-2 inhibitors were associated with a reduced risk of major GI events (including perforation, obstruction and bleeding) with an risk ratio (RR) of 0.38; 95%CI: 0.25–0.56) compared to nsNSAIDs. However, the benefit of coxibs over nsNSAIDs + PPIs was only seen for high-risk patients and in long-term users [10M].

Table 1. Risk of Upper Gastrointestinal Complications for Individual NSAIDs

NSAIDPooled relative risk95% Confidence intervalRankAzapropazone18.511.0–31.01Ketorolac11.55.6–23.82Piroxicam7.45.2–10.63Diflunisal4.41.1–17.84Indometacin4.12.9–5.95Naproxen4.13.2–5.26Tenoxicam4.12.2–7.87Ketoprofen3.92.7–5.78Nimesulide3.83.2–4.69Meloxicam3.52.2–5.510Diclofenac3.32.8–4.011Sulindac2.91.9–4.412Rofecoxib2.31.9–2.913Ibuprofen1.81.5–2.214Celecoxib1.51.2–1.815Aceclofenac1.40.7–3.216

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