[Pneumatosis cystoides intestini caeci--a pseudotumor presented at autopsy]. / Pneumatosis cystoides intestini caeci-- pseudotumor zjistený pri pitve.

A large focus of cystic intestinal pneumatosis appeared as an accidental finding in a 59-year-old man suffering from obstructive lung disease, with cor pulmonale as the cause of death. The gas pseudocysts were found in the submucosa, muscularis propria and in the subserosal space. The pseudocysts were lined by flattened cells of connective tissue origin with presence of occasional macrophages. We believe that the lesion started by focal damage of the mucosal membrane, which was followed by penetration of stool particles with microbes into the submucosa. E. coli and Morganella morgani are the probable producers of the gas bullets.

Candida jejunitis: a rare cause of intestinal pneumatosis in the immunocompromised patient.

A case of fatal necrotizing jejunitis caused by Candida albicans is described in a patient with acute myeloid leukaemia undergoing chemotherapy. The diagnosis was made at autopsy. Computed tomography findings were of small bowel dilatation with pneumatosis.

Pneumatosis cystoides intestinalis and high breath H2 excretion: insights into the role of H2 in this condition.

Patients with pneumatosis cystoides intestinalis have been reported to excrete excessive H2 because of a lack of H2-consuming intestinal bacteria. This study describes a patient with bacterial overgrowth and pneumatosis of the small intestine whose colonic flora avidly consumed H2 but whose small bowel flora produced but did not consume H2. There is no commonly accepted mechanism whereby excessive luminal H2 causes intramural gas. An explanation is proposed in which an initial, transitory source of intramural gas is distinguished from the mechanism that results in the persistence of the gas. Independent of the initial source of gas, rapid diffusion of H2 from the lumen into an intramural gas bubble would cause N2, O2, and CO2 to diffuse from the blood into the bubble. As a result, the bubble would expand and then persist indefinitely as long as H2 continued to diffuse from the lumen to the intramural gas collection.

Pneumatosis intestinalis and active cytomegaloviral infection after lung transplantation. Groningen Lung Transplant Group.

Pneumatosis intestinalis occurred in a patient with a primary cytomegaloviral (CMV) infection with pneumonitis 6 weeks after single lung transplantation for primary pulmonary hypertension. The possible causal relationship between pneumatosis intestinalis, an uncommon disorder with an obscure pathogenesis, and active CMV infection has been observed before; however, to our knowledge, this is the first report of this combination after lung transplantation. The patient had no abdominal complaints, and after treatment of the CMV infection, the pneumatosis intestinalis resolved spontaneously. The early diagnosis of active CMV infection and the prevention of unnecessary abdominal surgery were essential in this case.

Impaired hydrogen metabolism in pneumatosis cystoides intestinalis.

BACKGROUND: Pneumatosis cystoides intestinalis (PCI) is characterized by high levels of breath hydrogen. Clinical features of PCI may be due to abnormal H2 metabolism. METHODS: Breath levels of H2 and CH4 were measured in 3 patients and total gas in 2 patients with PCI on a polysaccharide-free (basal) diet and after administration of 15 g of lactulose. Metabolic activities and counts of methanogenic (MB) and sulfate-reducing (SRB) bacteria were measured in feces. Ten volunteers were also studied. RESULTS: Total H2 levels in patients were 383-420 mL/day on the basal diet and 1430-1730 mL/day after lactulose administration compared with 35 +/- 6 mL/day and 262 +/- 65 mL/day, respectively, in controls. Basal breath H2 levels in controls were 27 +/- 6 vs. 214 +/- 27 mL/day in patients and after lactulose ingestion, 115 +/- 18 vs. 370 +/- 72 mL/day. Four controls were methanogenic and had high fecal MB counts. The other controls had high SRB counts and sulfate reduction rates. All patients were nonmethanogenic and had low sulfate reduction rates. CONCLUSIONS: Patients with PCI excrete more H2 than controls. In normal subjects, H2 is consumed by MB or SRB; the activity of these bacteria is virtually absent in PCI. This may explain the gas accumulation in these patients.

Differences in the clinical and radiologic patterns of rotavirus and non-rotavirus necrotizing enterocolitis.

We analyzed retrospectively 32 successive infants who developed necrotizing enterocolitis (NEC), 13 with rotavirus (RV) infection (RV+) and 19 RV-negative (RV-). All patients showed at least pneumatosis intestinalis. All patients except one had risk factors for perinatal asphyxia. Our study demonstrated significant differences between RV+ NEC and RV- NEC cases: RV+ NEC infants had a higher birth weight and were born at a later gestational age. Oral feeding was started earlier and symptoms developed later and more insidiously in RV+ patients than in RV- NEC babies. Radiology revealed a less severe and more distal colon involvement in RV+ NEC infants, whereas the RV- NEC patients mostly had small intestinal or ileocecal changes and more frequent complications of pneumoportogram and intestinal perforations. These latter infants often had a rapidly deteriorating clinical course; 84% needed surgical treatment. In conclusion RV may be a cause of NEC in susceptible infants. Historic and clinical data and a more distal colonic pneumatosis allow a differentiation of RV+ NEC from other forms of NEC.

Breath hydrogen in pneumatosis cystoides intestinalis.

Pneumatosis cystoides intestinalis (PCI) is an uncommon condition of unknown aetiology. Bacterial gas production may be an important aetiological factor, but experimental evidence in humans has been lacking. We have studied breath hydrogen excretion as an index of bacterial gas production in 12 patients with PCI and have shown that four out of five with demonstrable cysts produced unusually high levels of hydrogen while fasting. This abnormality has not been previously reported. One patient showed resolution of PCI after antibiotic treatment. These findings confirm the importance of bacterial gas production in the pathogenesis of PCI.

High flow oxygen therapy for pneumatosis coli.

Symptomatic and radiological resolution of pneumatosis coli was achieved by intermittent high flow oxygen therapy in five patients. In each case the extent of the disease was defined by colonoscopy and contrast radiography before treatment. Despite the confirmation of pneumocyst resolution, recurrence of colonic gas cysts was noted in two patients at six months and one year after treatment. Bacteriological studies indicated that resolution of the disease, induced by oxygen therapy, was not associated with eradication of anerobic bacteria from stool and colonic mucosa. The clinical features and response to treatment of this group of patients are discussed, with particular reference to previously reported methods of oxygen administration.

Pneumatosis cystoides intestinalis.

Pneumatosis cystoides intestinalis (PCI) is an uncommon disease of previously unknown etiology, characterized by the presence of gas-filled cysts in the walls of some portion of the gastrointestinal tract. This investigation showed that PCI was readily produced in the germfree rat by inoculating its peritoneal cavity with a pure culture of either C. perfringens or C. tertium. Similar inoculation of the germfree animal with any one of eight other clostridia species did not result in the formation of PCI. The bacterial theory for the formation of at least some cases of PCI is now established. This work suggests that part of the treatment of those fulminating diseases known to be frequently associated with PCI should be directed at controlling a possible clostridial infection.

Etiology of pneumatosis cystoides intestinalis.

Pneumatosis cystoides intestinalis is an uncommon condition of previously unknown etiology. Experimental work is discussed which proves that either one of at least two clostridial species can produce PCI after relatively atraumatic contamination of the peritoneal cavity of germfree animals. This work strongly supports the bacterial etiology of PCI. It further suggests that vigorous and early treatment be directed toward control of the clostridial organisms in those cases where fulminating conditions associated with PCI are present.