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Stress ulcers are a well-known clinical entity described as stress-induced gastritis or gastropathy. The gastric and sometimes esophageal or duodenal mucosal barrier is disrupted secondary to a severe acute illness. It may present as erosive gastritis ranging from asymptomatic superficial lesions and occult gastrointestinal (GI) bleed to overt clinically significant GI bleeding. This activity reviews the cause, pathophysiology, and presentation of Curling ulcers and highlights the role of the interprofessional team in its management. Objectives: Review the etiology of Curling ulcers. Describe the pathophysiology of Curling ulcers. Summarize the treatment of Curling ulcers. Outline modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by Curling ulcers. Access free multiple choice questions on this topic.

Stress ulcers are stress-induced gastritis or gastropathy, in which the gastric and sometimes esophageal or duodenal mucosal barrier is disrupted secondary to a severe acute illness. It may present in the form of erosive gastritis, ranging from asymptomatic superficial lesions and occult gastrointestinal bleed to overt clinically significant gastrointestinal bleeding. The stress ulcers secondary to systemic burns are known as Curling ulcers. Stress ulcers in patients with acute traumatic brain injury are known as Cushing ulcers. The gastric body and fundus are common locations for stress ulcerations, but they can also occur in the antrum and duodenum.[1][2]

The major risk factors for the development of stress ulcerations include: Mechanical ventilation for more than 48 hours Abnormal coagulation profile, such as platelet count less than 50,000, INR greater than 1.5, and PTT greater than 2 times the control value Sepsis or septic shock Use of vasopressors Use of high-dose systemic corticosteroids (more than 250 mg or the equivalent of hydrocortisone per day) Hepatic failure Renal failure Multiorgan failure Burns of more than 30% of the body surface area Head trauma Lack of sanitation during intensive care unit stay History of gastrointestinal bleeds within a year [3][4][5]

The incidence of stress ulcers is unknown but is thought to almost always occur in severe acute illness. The most common presentation of stress ulceration is in the form of upper gastrointestinal bleeding, and gastrointestinal bleed secondary to stress ulcerations may range from 1.5% to 15%, depending on whether or not patients received stress ulcer prophylaxis. The incidence of stress ulceration and its complications is declining with the advent of active prophylaxis methods for preventing stress-related gastritis. Patients with gastrointestinal bleeding secondary to stress ulceration have increased morbidity and mortality compared to those who do not have gastrointestinal bleeding. Hence, stress ulcer prophylaxis has been the center of many randomized clinical trials. Very rarely (less than 1% of the time), stress ulcers can cause perforation and perforation-related complications.[2]

Stress ulceration results from damage to the mucosal barrier secondary to systemic stress, resulting in multiple superficial erosions of the gastric mucosa. Possible pathological changes leading to ulceration include an impaired mucosal barrier. The mucosal glycoprotein is denuded by increased refluxed bile salts or uremic toxins due to a critical illness. Increased gastric acid secretion in response to increased gastrin secretion in patients is also thought to be responsible for stress ulceration. However, this is more commonly seen in patients with acute neurological trauma than in other stress-related diseases. Helicobacter pylori infection has also been associated with stress ulcers, though the evidence is limited. There could be a subgroup of critical care patients who may present with overt gastrointestinal bleeding without stress ulceration or stress-related mucosal damage (SRMD), such as a patient with variceal bleeds, vascular anomalies, or diverticulosis. Hence, these gastrointestinal bleeds may not respond adequately to stress ulcer prophylaxis (SUP) or to antireflux therapy with proton pump inhibitors (PPIs) or antihistamines.[6] Patients with acute respiratory distress syndrome (ARDS) who receive positive pressure ventilation (PPV) for more than 3 days are especially susceptible to mucosal damage due to splanchnic hypoperfusion, which is more pronounced at positive end-expiratory pressure (PEEP) levels of 15-20 cm of water (H2O).[7][8]

Ulcers are covered with slough and inflammatory debris. Sometimes, hemorrhagic spots are seen. These are usually less than 1 cm, with a brown, circular base due to digested blood. Beneath the ulcer base, there is neutrophilic infiltration and active granulation with mononuclear infiltration. Fibrinoid necrosis may also be found. In chronic forms, lymphocytes, monocytes, and plasma cells infiltrate the mucosa and submucosa.

The most common mode of presentation of stress ulcers is the onset of acute upper gastrointestinal bleeding, such as hematemesis or melena, in a patient with an acute critical illness. The patient may or may not have hemodynamic instability in the presence of bleeding, and most of these patients have a drop in hemoglobin concentration that requires blood transfusion. The clinician should maintain a high index of suspicion for patients in intensive care who have decreased hematocrit. The following signs and symptoms are present in typical cases: Coffee ground vomitus Hematemesis Melena Abdominal pain Nausea Orthostasis in severe cases

Before the diagnostic evaluation for stress ulceration, patient stabilization should take priority. Monitor the need for fluid resuscitation and blood transfusion and reversal of coagulopathy if needed. Gastric lavage can be used to confirm whether blood is present in the upper gastrointestinal tract or not. It also helps to quantify the amount of blood if found. Esophagogastroduodenoscopy should be performed. Stress ulcers are small, superficial mucosal erosions or ulcerations in the gastric body and fundus. Testing for H. pylori infection, such as the urease breath test or stool antigen test, can also be undertaken in cases of refractory stress ulceration.

Management of stress-induced gastritis includes prompt identification and prevention of complications related to stress ulceration. The management can be divided into pharmacological and non-pharmacological interventions. The nonpharmacological interventions include early enteral feeding, NG tube placement, intravenous fluid resuscitation, blood transfusion, and reversal of coagulopathy with platelet transfusion, fresh frozen plasma, or cryoprecipitate.[9][10] The medical management of patients with stress ulcers is more or less similar to the management of peptic ulcer disease in general. The medication targeting acid peptic disease includes proton pump inhibitors, antihistaminic, and ulcer-healing drugs like sucralfate. Patients with overt gastrointestinal bleeding from ulceration require endoscopic evaluation and management of the stress ulcers. Endoscopic therapies may include epinephrine injection, electrocauterization, or clipping of the bleeding vessels. Bleeding ulcers refractory to localized endoscopic treatment may need embolization of the culprit vessel or, rarely, surgical intervention as a last resort. Surgical interventions are commonly indicated for patients with refractory bleeding despite endoscopic or angiographic treatment or for patients with unstable hemodynamics to undergo endoscopic or angiographic procedures. Surgeries are performed as a last resort to save lives.[11] Sometimes, the ulcers can be deep enough to cause perforation of the gastric wall, leading to acute peritonitis requiring urgent laparotomy. Compared with other forms of stress ulcerations, perforations are most likely to occur with Cushing and Curling ulcers, as they tend to be deep and can cause extensive necrosis. Mortality without surgical intervention in these patients who develop free-wall gastrointestinal perforation is almost 100%.[6][12]

The following should also be considered in the differential diagnosis: Peptic ulcer disease Nonsteroidal anti-inflammatory drug (NSAID)–induced gastritis Alcoholic gastropathy Gastroesophageal reflux disease (GERD) Gastric or esophageal cancer Gastroparesis Pancreatic cancer Biliary pain Uremic gastropathy Dyspepsia

Proton pump inhibitors (PPIs) have traditionally been considered superior to histamine receptor-2 (H2) blockers to prevent stress ulceration in critically ill patients at risk. Recent studies have raised the concern of increased mortality in patients who receive PPIs for stress-ulcer prophylaxis. Large trials directly comparing the agents for stress ulcer prophylaxis are lacking, and further studies are needed to determine whether PPIs are harmful.

The Forrest classification is used to stage gastric ulcers and is largely based on endoscopic findings. Acute Hemorrhage Forrest Ia - Active spurter Forrest Ib - Active oozing Signs of Recent Hemorrhage Forrest IIa - Non-bleeding visible vessel Forrest IIb - Adherent clot Forrest IIc - Flat pigmented haematin on ulcer base Lesions Without Active Bleeding Forrest III - Lesions without active bleeding

Patients with stress ulceration usually have a poor prognosis, secondary to the underlying critical illness. Moreover, gastrointestinal bleeds in these patients secondary to stress-related mucosal disease are independently associated with increased morbidity and mortality. These patients are often too unstable for advanced endoscopic or surgical procedures to suppress gastrointestinal bleeding, leading to worse outcomes. Hence, aggressive prophylactic measures for the appropriate patient population at risk of developing stress ulceration remain the cornerstone in the management of stress-induced gastropathy.[13][14]

Stress ulceration can be associated with the following complications: Bleeding Anemia Strictures Perforation Peritonitis Gastrocolic fistula Gastric outlet obstruction due to strictures Hemorrhagic shock Increased length of intensive care unit stay Death

Patients with stress ulceration are usually managed in intensive care units. The gastroenterology service should be consulted if there are any signs or symptoms related to ulcer development. Neurosurgery and general surgery teams should be consulted if stress ulceration arises in the setting of head injury or burns, respectively. Interprofessional teamwork improves mortality and morbidity outcomes in the setting of stress ulceration.

Stress ulcers are sores in the digestive tract that can cause stomach upset and bleeding. Symptoms include upper abdominal pain, nausea, vomiting, or blood in the stool. In stressful situations, excess acid in the system breaks down the protective layer of mucus on the lining, making it more susceptible to damage. Prophylactic treatment in intensive care units leads to decreased recurrence of stress ulcers. Healthcare providers are the best source of information for concerns related to stress ulcer formation.

SUP has been a subject of debate among various national and international critical care societies. SUP has been shown to be of benefit in preventing gastrointestinal bleeding related to stress ulceration, but the guidelines regarding the indications, drug selection, and duration of SUP are not clear.[15] Surviving Sepsis Campaign recommends SUP for patients on mechanical ventilation for more than 48 hours and patients with coagulopathy. The other indications for SUP include sepsis and septic shock, severe burn injuries, use of high-dose steroids, and neurological trauma. Surviving Sepsis Campaign recommends the use of PPI over antihistamines for SUP. Even though multiple studies have challenged the superiority of one over the other, PPIs are the most common agents used in the intensive care and burn unit as SUP. Sucralfate, an ulcer-healing drug, can also be used for SUP. It is shown to be less effective than PPI and histamine blockers but safer regarding adverse reactions. Cytoprotective agents such as prostaglandin analogs (eg, misoprostol) can also be used for SUP. They suppress acid secretion via a cyclic AMP pathway and enhance the mucosal barrier of the gastric epithelium. However, they are still under investigation and lack adequate evidence for use in SUP. The adverse effects of PPIs' frequent use in this population, including but are not limited to, Clostridium difficile-associated diarrhea, pneumonia, and adverse drug interactions.[8][16] The duration of stress ulcer prophylaxis is usually for the period of critical illness or mechanical ventilation, and sometimes it can be continued until the patient begins to tolerate an oral diet.[17]

The major part of the management of stress ulcers is its prevention in the critical care population with high-risk factors, as the outcomes associated with stress-induced gastritis and the gastrointestinal bleed are worse but preventable. An interprofessional team comprising the critical care nurse and the critical care specialist physician can minimize risk and achieve optimal patient outcomes. Pharmacists evaluate medication use for prophylaxis and check for drug-drug interactions. Nursing staff monitor patients and update the team when the patient's status changes.