|
| Theory | Theory mechanism | Associated disease and theory strength | Theory weakness |
|
| Mechanical theory | | | |
| (i) Mechanical GI theory | (i) Increased intraluminal pressure (obstruction)
(ii) Intestinal wall injury | (i) Intestinal obstruction (tumor, GOO, SV, and pseudo-obstruction)
(ii) Secondary wall injury (IBD, diverticulitis, colitis, enteritis, ischemic bowel disease, peptic ulcer, and celiac sprue)
(iii) Iatrogenic wall injury (blunt abdominal trauma, endoscopy, postsurgical intestinal anastomosis, enteric tube placement, barium enema, and bowel preparation) | Cannot explain how the cysts are maintained once they have formed |
| (i) Mechanical pulmonary theory | Pulmonary alveolar rupture:
(i) Pneumomediastinum
(ii) Dissect retroperitoneum
(iii) Mesenteric vessels
(iv) Bowel wall | (i) COPD, asthma, and bronchitis
(ii) Interstitial pneumonia
(iii) Emphysema
(iv) Pulmonary and cystic fibrosis
(v) PEEP ventilation | (i) Unable to explain the finding that hydrogen may comprise up to 50% of the gas content of the cysts
(ii) Many patients show no accompanied lung disease
(iii) The gas is caused by accompanied increase in intra-abdominal pressure, with a reduced barrier function caused by corticoid therapy |
| Bacterial theory | Gas-forming bacteria:
(i) Enter mucosal barrier
(ii) Produce the gas within the bowel wall | This mechanism is supported by the following:
(i) Successful treatment of PCI with antibiotics
(ii) Theory of counter perfusion supersaturation
(iii) Pneumatosis observed near blood vessels along mesenteric border | The presence of an aerogenic bacteria in the cysts has not yet been proven |
| Biochemical theory | Carbohydrate metabolism:
(i) Increased production of hydrogen gas
(ii) Raises intraluminal pressure
(iii) Force the gas into the weakened bowel wall | (i) The cessation of α-GI therapy is the key to the successful treatment of PCI
(ii) Malnutrition can prevent the digestion of carbohydrates and increased bacterial fermentation in the intestine | |
| Others | Chemotherapy, hormonal therapy, and connective tissue disease | Lupus, polymyositis, polyarteritis nodosa, scleroderma, sarcoidosis, and celiac sprue | |
|
