Contemporary Surgery

Gastric Pneumatosis

From the Department of General Surgery, The Cleveland Clinic Foundation,  Cleveland, Ohio.

Fred Brody, MD, Department of General Surgery, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Desk A80, Cleveland, Ohio 44195; telephone (216) 444-6668; fax (216) 445-7653 (e-mail: Brodyf@ccf.org).

Introduction

Gastric pneumatosis is a rare finding with few cases reported in the literature. Traditionally, gastric pneumatosis has variously been called pneumatosis intestinalis, gastric emphysema, and emphysematous gastritis. Currently, gastric pneumatosis is defined as air or gas within the wall of the stomach.

Air. Gastric pneumatosis resulting from a violation of mucosal integrity followed by forceful entry of air between the gastric layers is called noninfectious gastric pneumatosis.

Gas. Infectious gastric pneumatosis, also known as emphysematous gastritis, is caused by gas-forming organisms within the gastric wall. This condition was first described by Fraenkel in 1889 in a 35-year-old male with bloody vomitus and epigastric pain.¹ At autopsy, Fraenkel described the patient’s stomach as edematous with diffusely scattered, gas-filled blebs. In addition, the submucosa was densely infiltrated with rod-like organisms. Since then, multiple organisms, including Escherichia coli and species of Clostridium, Staphylococcus, Pseudomonas, and Strongyloides, have been associated with gastric pneumatosis.^2-7

Etiology

When gastric pneumatosis is encountered, it is important to distinguish between noninfectious and infectious etiologies. Because the pathophysiology for each is different, each form of gastric pneumatosis can be elucidated by careful history and physical examination.

Noninfectious gastric pneumatosis. Gastric pneumatosis has been reported in patients with obstructing gastrointestinal lesions. Elevated intraluminal gastric pressures secondary to distal obstruction coupled with any type of mucosal injury facilitates gastric pneumatosis. A variety of different clinical presentations including pyloric obstruction, volvulus, impacted duodenal gallstones, and carcinoma can induce an obstruction and cause elevated gastric pressures.^2,5,21-24 Within the pediatric population, gastric pneumatosis has resulted from hypertrophic pyloric stenosis.²¹

To date, no cases of gastric pneumatosis have been linked to gastric ischemia or stress gastritis. In some cases, as in ours (page opposite), where the etiology is obscure, the endoscopic findings of diffuse inflammation with rapid resolution of signs and symptoms may suggest a transient ischemia. Cordum et al described a patient with diffusely friable, edematous mucosa with mucopurulent exudate throughout the antrum and duodenum. In their patient, as in ours, nonoperative management and nasogastric decompression resulted in resolution of pneumatosis in 72 hours.¹² In these cases of transient ischemia, the mucosa may be injured or compromised during decreased perfusion thus allowing air to penetrate and dissect into the gastric wall.

Several noninfectious etiologies exist for gastric pneumatosis, including peptic ulcer disease, a ruptured pulmonary bleb, gastroscopy, or gastric outlet obstruction secondary to cancer. In all cases, a violation in the gastric mucosa allows luminal air to dissect into the gastric wall. Gastric pneumatosis has been described in patients with pulmonary emphysema. Clinically, this was observed by Plachta and Speer who described 4 post-mortem cases of gastric pneumatosis secondary to ruptured pulmonary blebs.¹³ All 4 patients had ruptured bullae with distal dissection through their esophageal wall creating gastric pneumatosis. Experimentally, this concept was demonstrated by hyperinflating the alveoli of cats and rabbits by stretching and straining their alveolar walls. As a result, air dissected along the perivascular and perilymphatic sheaths of the lung parenchyma.¹⁴ The air ultimately dissected caudally along the esophagus to the stomach.

Insufflation during gastroscopy is responsible for the majority of cases of benign, noninfectious gastric pneumatosis. Similar to Macklin’s cat model, insufflated air can dissect through all layers of the stomach without causing a perforation.¹⁵ Although the mucosa appears intact, air under pressure is forced through either microscopic or ulcerative mucosal defects which allow the air to eventually track into the omentum, mediastinum, retroperitoneum, and subcutaneous tissues.^16,17 This was demonstrated clinically by Myhre and Wilson after obtaining routine abdominal radiographs following uncomplicated gastroscopy. These investigators discovered 2/119 (1.7%) such patients with asymptomatic gastric pneumatosis.¹⁸ In 1949, Fierst reviewed 7 cases of pneumoperitoneum following uneventful gastroscopies.¹⁹ In all cases, subsequent laparotomy revealed no evidence of gross perforation. In several instances, however, an ulcer crater was identified following gastrotomy.^17,20

Infectious gastric pneumatosis. The pathophysiology of infectious gastric pneumatosis is unclear. However, some have suggested that an initial insult creates a portal into the gastric wall, allowing bacterial invasion through the mucosa and submucosa. Often, this is secondary to ingestion of a corrosive or caustic substance, although nonsteroidal anti-inflammatory drugs (NSAIDs) and alcohol also have been implicated in infectious gastric pneumatosis.^3,8-10

Clinically, patients with infectious gastric pneumatosis appear septic and complain of fever, chills, and abdominal pain. Patients can vomit blood or even an entire gastric mucosal cast.^1,11 Physical exam usually reveals epigastric tenderness. Laboratory data is nonspecific but may reveal leukocytosis or a hypokalemic, hypochloremic, metabolic alkalosis secondary to vomiting. Radiologically, “mottled” gas bubbles are seen within a thickened gastric wall.² Early gastroscopy and biopsy are advocated to facilitate a diagnosis.¹² Endoscopic evidence of submucosal abscesses or exudative gastritis suggests an infectious etiology while endoscopic biopsies demonstrating organisms histologically unequivocally establishes an infectious etiology.¹²

Differential Diagnosis and Treatment

Gastric pneumatosis was first radiologically described by Weens in 1946, and the radiologic findings of infectious and noninfectious gastric pneumatosis may be as indistinguishable today as they were then.²⁵ In both entities, cystic lucencies appear within the gastric wall. In noninfectious gastric pneumatosis, the air is often described as curvilinear streaks of air within a nonthickened, distended stomach.¹² On the other hand, infectious gastric pneumatosis is often characterized as having “mottled” gas bubbles within a thickened gastric wall. In both cases, air or gas lies within the gastric submucosa or subserosa and does not change location with patient movement.²⁶ Computed tomography clearly reveals linear lucencies within the gastric wall²⁷(see Figure 2 on page 255).

Although implicated as a cause of gastric pneumatosis, early upper endoscopy is also useful in the diagnosis and management of gastric pneumatosis.¹² Gastroscopy provides visual evaluation of the mucosa and provides tissue for histologic and microbiologic analysis. Noninfectious gastric pneumatosis might reveal submucosal gas bubbles, a nonspecific exudative gastritis, or a grossly intact mucosa. Gastric pneumatosis is confirmed histologically by demonstrating numerous empty spaces within the lamina propria.¹² A noninfectious etiology of gastric pneumatosis may be difficult to determine on inspection alone; therefore, repeated endoscopy may be needed to demonstrate resolution if biopsies are inconclusive.

The treatment of gastric pneumatosis depends on the patient’s clinical presentation. Initially, nonoperative management is indicated for noninfectious gastric pneumatosis. Treatment consists of nasogastric decompression, intravenous hydration, and observation. Initially antibiotics are not required. Air forced into the wall of the stomach appears to be self-limiting and resolves with nasogastric tube decompression.⁵ If, however, a patient develops worsening abdominal pain, increasing leukocytosis, fever, or peritonitis, exploration may be required.

On the other hand, the majority of patients with infectious gastric pneumatosis present with septic shock and the initial treatment is supportive with intravenous fluids and broad spectrum antibiotics in a monitored setting.

Although few cases are reported, surgery is not recommended in the acute setting due to the extensive inflammation and friability of the gastric wall. Exploration is warranted if the patient shows no improvement or if symptoms and signs worsen. At exploration, the stomach may appear crepitant, inflamed, and adherent to other structures.¹¹ A variety of operations have been performed for infectious gastric pneumatosis; however, no standard procedure currently exists. It should be noted that most authors recommend a subtotal or total gastrectomy to completely eradicate involved tissue.

At present, we found little data regarding the morbidity or mortality following operative intervention for infectious gastric pneumatosis. In the largest review of infectious gastric pneumatosis, Moosvi reported a 61% mortality in 29 patients. Subsequently, 6 of the 11 surviving patients developed strictures within the stomach.¹¹ Overall, infectious gastric pneumatosis, or emphysematous gastritis, is a highly lethal condition with significant morbidity.

Gastric pneumatosis from gastrointestinal obstruction usually requires surgery directed towards the cause of the obstruction. In 1982, Kussin reviewed 11 cases of gastric pneumatosis secondary to gastric obstruction. In 6 cases (55%), the obstruction was secondary to a distal gastric lesion.²⁶ These patients were surgically managed with distal gastric resections or were palliated with a gastrojejunostomy for advanced disease.

Conclusion

Although gastric pneumatosis is rarely seen, surgeons must be aware of the entity and the clinical implications of both etiologic forms. Gas within the gastric wall is secondary to infectious organisms within the wall of the stomach; air within the gastric wall is a result of forceful entry through a mucosal defect.

While the clinical course of noninfectious gastric pneumatosis is either self-limiting or surgically correctable, infectious gastric pneumatosis can be fatal. Surgeons must be cognizant of the spectrum of gastric pneumatosis in order to determine the timing and the potential efficacy of surgical intervention.

References

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