Emphysematous Gastritis: Clinical and Diagnostic Insights

Emphysematous gastritis is a rare but life-threatening condition characterized by gas within the stomach wall due to infection. It differs from gastric emphysema, which is non-infectious and typically benign. Prompt diagnosis and intervention are critical, as delayed treatment significantly increases mortality.

Early recognition is essential due to the rapid progression and potential for severe complications. Imaging and endoscopy play key roles in differentiating emphysematous gastritis from other gastrointestinal disorders.

Mechanisms Involved

The disease results from gas-forming bacteria invading the gastric wall, leading to tissue damage and systemic toxicity. A compromised gastric mucosa—due to ischemia, ulceration, or recent surgical interventions—provides an entry point for these pathogens. Once inside, bacteria metabolize glucose anaerobically, producing hydrogen and carbon dioxide. This gas accumulation within the stomach lining distinguishes emphysematous gastritis from other gastric conditions.

Factors such as prolonged NSAID use, alcohol consumption, and corrosive ingestion weaken the gastric mucosa, increasing susceptibility to bacterial infiltration. Diabetes mellitus and immunosuppression further impair host defenses, allowing unchecked bacterial proliferation. The resulting overgrowth exacerbates inflammation, leading to necrosis and additional gas production.

Vascular compromise also plays a critical role. Reduced blood flow—due to atherosclerosis, shock, or thrombosis—creates an environment conducive to anaerobic bacterial growth. Ischemic injury weakens the stomach’s ability to clear infections, facilitating deeper bacterial penetration. As infection progresses, bacterial toxins, gas accumulation, and ischemic damage contribute to full-thickness necrosis, increasing the risk of perforation and sepsis.

Symptoms And Clinical Signs

Patients typically present with acute, progressive abdominal pain, often diffuse rather than localized. Nausea and persistent vomiting, sometimes with hematemesis due to mucosal ulceration, are common. Despite severe symptoms, early physical examination findings may be relatively mild. As infection advances, peritoneal signs such as guarding and rebound tenderness suggest deeper gastric wall involvement or impending perforation.

Systemic manifestations develop quickly. Fever is common, though hypothermia may occur in septic shock. Tachycardia and hypotension often indicate systemic inflammatory response syndrome (SIRS) and evolving sepsis. In severe cases, multi-organ dysfunction ensues, with acute kidney injury and altered mental status reflecting declining perfusion.

Marked abdominal distension and tympany on percussion result from intramural gas accumulation, a distinguishing feature from other forms of gastritis. Some patients experience diarrhea due to bacterial translocation or toxin-mediated effects. Disease progression may lead to gastric perforation, signaled by abrupt worsening of pain, abdominal rigidity, and free air under the diaphragm on imaging.

Endoscopic Observations

Endoscopy reveals severe mucosal inflammation, with patchy or diffuse necrosis. Affected areas often appear mottled or blackened, indicating ischemic injury and bacterial infiltration. Unlike other gastritis forms, which typically present with erythema and superficial erosions, emphysematous gastritis features extensive ulceration and sloughing mucosa, reflecting deep tissue involvement.

A hallmark finding is submucosal gas bubbles—irregular, translucent pockets produced by bacterial fermentation. These gas collections distinguish emphysematous gastritis from non-infectious gastric emphysema. The distribution often extends beyond the antrum into the body and fundus. Endoscopic insufflation can worsen mucosal separation, emphasizing the need for careful technique to avoid iatrogenic perforation.

In advanced cases, the gastric wall may appear friable, with spontaneous bleeding upon minimal contact. Purulent exudate or fibrinous debris further supports an infectious etiology. While endoscopic biopsy can confirm bacterial infiltration, tissue fragility often limits sampling.

Radiological Insights

Imaging is crucial for diagnosis, with CT scans providing the most definitive findings. Intramural gas appears as radiolucent streaks or pockets within the stomach wall, typically along the greater curvature. Unlike gastric emphysema, where gas is uniformly distributed without inflammation, emphysematous gastritis features mural thickening and surrounding fat stranding, indicating an infectious process.

CT often shows gastric wall thickening, ranging from mild to severe, with heterogeneous contrast enhancement reflecting ischemia and inflammation. Non-enhancing areas suggest impending perforation or full-thickness necrosis. Free air in the abdominal cavity, though less common early on, signals perforation and necessitates immediate surgical evaluation.

Laboratory Findings

Laboratory tests help assess infection severity and systemic impact. A complete blood count (CBC) typically shows leukocytosis with neutrophil predominance, though leukopenia may occur in overwhelming sepsis. Elevated C-reactive protein (CRP) and procalcitonin levels reflect systemic inflammation and bacterial proliferation.

Metabolic acidosis is common due to tissue necrosis and septic shock, with elevated serum lactate indicating impaired perfusion. Blood cultures may identify gas-forming bacteria like Clostridium perfringens, Escherichia coli, or Klebsiella pneumoniae, guiding antimicrobial therapy. Renal function tests often reveal acute kidney injury in septic patients, while electrolyte imbalances such as hyperkalemia and hypocalcemia may result from systemic toxicity. Serial laboratory assessments are essential for tracking disease progression and treatment response.

Microbial Profiles

The bacteria implicated in emphysematous gastritis are predominantly anaerobic or facultatively anaerobic, producing gas through fermentation. Clostridium perfringens is a frequent pathogen, known for generating large amounts of hydrogen and carbon dioxide. Its potent exotoxins contribute to extensive tissue destruction and systemic toxicity.

Gram-negative enteric bacteria such as Escherichia coli, Klebsiella pneumoniae, and Enterobacter species are also common. These organisms produce gas and release endotoxins that trigger severe inflammation. Polymicrobial infections can exacerbate tissue damage through synergistic bacterial interactions. Fungal co-infections, though rare, may complicate management in immunocompromised individuals. Identifying the causative pathogens via blood cultures and gastric biopsy samples is essential for targeted antibiotic therapy, as resistance patterns vary based on bacterial strain and patient history.