- Published on
Emergency And Acute Medicine - Gastritis
Basics Description
Inflammatory response of the gastric mucosa to injury, referred to as gastritis. The gastric mucosa is protected by three main defense mechanisms: a mucus layer that forms a protective pH gradient, surface epithelial cells capable of repairing small defects, and a postepithelial barrier that neutralizes acid that penetrates the first two layers. There is no definite correlation between histologic gastritis and dyspeptic symptoms. Epithelial cell damage without associated inflammation is termed gastropathy.
Etiology
Common causes of gastritis include infections, autoimmune disease, drugs such as cocaine, hypersensitivity reactions, and physiologic stress. Common causes of gastropathy include endogenous or exogenous irritants such as bile reflux, alcohol, aspirin and other NSAIDs, ischemia, stress, and chronic congestion. Acute gastritis may occur with severe stress states such as sepsis, burns, or trauma due to reduced splanchnic blood flow leading to decreased mucus production, bicarbonate secretion, and prostaglandin synthesis, resulting in mucosal erosions and hemorrhage. Alcohol induces leukotriene production, causing microvascular stasis and increased permeability with hemorrhage. NSAIDs, including aspirin, interfere with prostaglandin synthesis and cause similar mucosal injury. Steroids may also contribute. Chronic gastritis is most commonly caused by Helicobacter pylori, a gram-negative spiral bacterium found in the gastric mucus layer that produces urease, allowing alkalinization of its microenvironment.
Diagnosis Signs And Symptoms
Common symptoms include dyspepsia, bloating, nausea, vomiting, anorexia, epigastric tenderness, and heartburn. History often reveals episodic or chronic epigastric pain or discomfort, indigestion, eructation, flatulence, nausea or vomiting, and in severe cases hematemesis or melena.
Physical Exam Findings
Examination should include careful assessment of vital signs and orthostatics, stool Hemoccult testing, and evaluation for dehydration and tachycardia in patients with vomiting. Pallor may be present in hemorrhagic gastritis. Abdominal examination is often nonspecific but may reveal epigastric tenderness.
Essential Workup
Initial evaluation focuses on airway, breathing, and circulation, with hematocrit determination and assessment for dehydration or shock.
Diagnostic Tests And Interpretation
Laboratory studies are often normal in uncomplicated gastritis. CBC may reveal anemia in acute hemorrhagic gastritis or leukocytosis with infection. Electrolytes, BUN, creatinine, and glucose assess dehydration and metabolic disturbances. Amylase and lipase help exclude pancreatitis. Urinalysis evaluates dehydration or ketosis. Bilirubin may be elevated in hepatitis. ECG is recommended in elderly patients to evaluate for myocardial ischemia. Endoscopy is usually outpatient unless there is significant hemorrhage and allows visualization of bleeding sites, histologic confirmation, and detection of Helicobacter pylori. Noninvasive H. pylori testing includes urea breath tests, stool antigen testing, and serology. Serum pepsinogen isoenzyme ratios may suggest metaplastic atrophic gastritis.
Differential Diagnosis
Peptic ulcer disease, nonulcer dyspepsia, gastroesophageal reflux disease, biliary colic, cholecystitis, pancreatitis, hepatitis, abdominal aortic aneurysm, aortic dissection, and myocardial infarction should be considered.
Treatment Pre Hospital
Initial management includes airway support and intravenous fluid resuscitation as needed.
Initial Stabilization And Therapy
Patients with acute erosive or hemorrhagic gastritis and hemodynamic instability require aggressive fluid resuscitation with lactated Ringer solution or normal saline via two large-bore IV lines. Nasogastric tube placement is indicated for hematemesis or unstable patients, and Foley catheterization may be used to monitor volume status.
Emergency Department Treatment And Procedures
Symptom control includes antacids, gastrointestinal cocktail therapy, H2 receptor antagonists, proton pump inhibitors, and sucralfate. Narcotics should be avoided as they may mask serious illness. Acute hemorrhagic gastritis requires IV fluids, blood transfusion if indicated, and correction of underlying causes such as alcohol use, sepsis, NSAIDs, or trauma. Stress gastritis prevention in critically ill patients involves antacids or IV H2 blockers or proton pump inhibitors to maintain gastric pH above four. Chronic gastritis due to Helicobacter pylori requires eradication therapy with appropriate antibiotic regimens. Vitamin B12 supplementation is indicated in atrophic gastritis.
Medication
Therapeutic options include antacids, H2 blockers, proton pump inhibitors, sucralfate, bismuth subsalicylate, and misoprostol. First-line Helicobacter pylori treatment consists of triple therapy using a proton pump inhibitor with clarithromycin and amoxicillin or metronidazole. Sequential and bismuth-based quadruple therapies are used in high-resistance or treatment-failure settings.
Follow-Up Disposition
Admission is required for patients with acute hemorrhagic or erosive gastritis presenting with upper gastrointestinal bleeding, tachycardia, hypotension, uncontrolled pain or vomiting, or coagulopathy. Stable patients with normal examinations, laboratory results, and heme-negative stools may be discharged. Patients with heme-positive stools may be discharged only if vital signs and hematocrit are stable and nasogastric aspiration is negative.
Follow-Up Recommendations
Close outpatient follow-up with a gastroenterologist is recommended for endoscopy, biopsy, and Helicobacter pylori testing.
Clinical Pearls And Common Errors
Gastritis and gastropathy are common emergency department presentations characterized by dyspepsia, nausea, and vomiting. Management should include both diagnostic evaluation and targeted therapy. Treatment often involves Helicobacter pylori eradication, though antibiotic resistance is increasing. Early gastroenterology follow-up is essential to detect gastric dysplasia or malignancy.
Basics Description
Inflammatory response of the gastric mucosa to injury, referred to as gastritis. The gastric mucosa is protected by three main defense mechanisms: a mucus layer that forms a protective pH gradient, surface epithelial cells capable of repairing small defects, and a postepithelial barrier that neutralizes acid that penetrates the first two layers. There is no definite correlation between histologic gastritis and dyspeptic symptoms. Epithelial cell damage without associated inflammation is termed gastropathy.
Etiology
Common causes of gastritis include infections, autoimmune disease, drugs such as cocaine, hypersensitivity reactions, and physiologic stress. Common causes of gastropathy include endogenous or exogenous irritants such as bile reflux, alcohol, aspirin and other NSAIDs, ischemia, stress, and chronic congestion. Acute gastritis may occur with severe stress states such as sepsis, burns, or trauma due to reduced splanchnic blood flow leading to decreased mucus production, bicarbonate secretion, and prostaglandin synthesis, resulting in mucosal erosions and hemorrhage. Alcohol induces leukotriene production, causing microvascular stasis and increased permeability with hemorrhage. NSAIDs, including aspirin, interfere with prostaglandin synthesis and cause similar mucosal injury. Steroids may also contribute. Chronic gastritis is most commonly caused by Helicobacter pylori, a gram-negative spiral bacterium found in the gastric mucus layer that produces urease, allowing alkalinization of its microenvironment.
Diagnosis Signs And Symptoms
Common symptoms include dyspepsia, bloating, nausea, vomiting, anorexia, epigastric tenderness, and heartburn. History often reveals episodic or chronic epigastric pain or discomfort, indigestion, eructation, flatulence, nausea or vomiting, and in severe cases hematemesis or melena.
Physical Exam Findings
Examination should include careful assessment of vital signs and orthostatics, stool Hemoccult testing, and evaluation for dehydration and tachycardia in patients with vomiting. Pallor may be present in hemorrhagic gastritis. Abdominal examination is often nonspecific but may reveal epigastric tenderness.
Essential Workup
Initial evaluation focuses on airway, breathing, and circulation, with hematocrit determination and assessment for dehydration or shock.
Diagnostic Tests And Interpretation
Laboratory studies are often normal in uncomplicated gastritis. CBC may reveal anemia in acute hemorrhagic gastritis or leukocytosis with infection. Electrolytes, BUN, creatinine, and glucose assess dehydration and metabolic disturbances. Amylase and lipase help exclude pancreatitis. Urinalysis evaluates dehydration or ketosis. Bilirubin may be elevated in hepatitis. ECG is recommended in elderly patients to evaluate for myocardial ischemia. Endoscopy is usually outpatient unless there is significant hemorrhage and allows visualization of bleeding sites, histologic confirmation, and detection of Helicobacter pylori. Noninvasive H. pylori testing includes urea breath tests, stool antigen testing, and serology. Serum pepsinogen isoenzyme ratios may suggest metaplastic atrophic gastritis.
Differential Diagnosis
Peptic ulcer disease, nonulcer dyspepsia, gastroesophageal reflux disease, biliary colic, cholecystitis, pancreatitis, hepatitis, abdominal aortic aneurysm, aortic dissection, and myocardial infarction should be considered.
Treatment Pre Hospital
Initial management includes airway support and intravenous fluid resuscitation as needed.
Initial Stabilization And Therapy
Patients with acute erosive or hemorrhagic gastritis and hemodynamic instability require aggressive fluid resuscitation with lactated Ringer solution or normal saline via two large-bore IV lines. Nasogastric tube placement is indicated for hematemesis or unstable patients, and Foley catheterization may be used to monitor volume status.
Emergency Department Treatment And Procedures
Symptom control includes antacids, gastrointestinal cocktail therapy, H2 receptor antagonists, proton pump inhibitors, and sucralfate. Narcotics should be avoided as they may mask serious illness. Acute hemorrhagic gastritis requires IV fluids, blood transfusion if indicated, and correction of underlying causes such as alcohol use, sepsis, NSAIDs, or trauma. Stress gastritis prevention in critically ill patients involves antacids or IV H2 blockers or proton pump inhibitors to maintain gastric pH above four. Chronic gastritis due to Helicobacter pylori requires eradication therapy with appropriate antibiotic regimens. Vitamin B12 supplementation is indicated in atrophic gastritis.
Medication
Therapeutic options include antacids, H2 blockers, proton pump inhibitors, sucralfate, bismuth subsalicylate, and misoprostol. First-line Helicobacter pylori treatment consists of triple therapy using a proton pump inhibitor with clarithromycin and amoxicillin or metronidazole. Sequential and bismuth-based quadruple therapies are used in high-resistance or treatment-failure settings.
Follow-Up Disposition
Admission is required for patients with acute hemorrhagic or erosive gastritis presenting with upper gastrointestinal bleeding, tachycardia, hypotension, uncontrolled pain or vomiting, or coagulopathy. Stable patients with normal examinations, laboratory results, and heme-negative stools may be discharged. Patients with heme-positive stools may be discharged only if vital signs and hematocrit are stable and nasogastric aspiration is negative.
Follow-Up Recommendations
Close outpatient follow-up with a gastroenterologist is recommended for endoscopy, biopsy, and Helicobacter pylori testing.
Clinical Pearls And Common Errors
Gastritis and gastropathy are common emergency department presentations characterized by dyspepsia, nausea, and vomiting. Management should include both diagnostic evaluation and targeted therapy. Treatment often involves Helicobacter pylori eradication, though antibiotic resistance is increasing. Early gastroenterology follow-up is essential to detect gastric dysplasia or malignancy.
0 Comments
