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Three cases of pneumatosis coli (PC) in adult patients with acute myeloid leukaemia seen over the last five years in Hammersmith Hospital are reported. Although definite conclusions are impossible, we suggest that that pneumatosis could be due to damage to the bowel mucosa as a result of the disease or the treatment. The literature is reviewed and discussed in an inconclusive attempt to discover the source of the gas.
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We reviewed pathology specimens from 84 patients seen during a 10-year period with neonatal necrotizing enterocolitis, and these findings were correlated with clinical features. Coagulation (ischemic) necrosis, inflammation, and bacterial overgrowth were all present in the intestine of nearly all patients but with individual variability in the severity of these findings. Overall, coagulation necrosis was more severe than any other finding in most infants, indicating the importance of ischemia in the pathophysiology of necrotizing enterocolitis. Reparative tissue changes such as epithelial regeneration, granulation tissue formation, and fibrosis, found in two thirds of cases, suggested ongoing tissue injury of at least several days' duration. Birth weight, Apgar score, age, feeding status, and the presence of respiratory distress syndrome were not correlated with any particular histologic feature. The pathologic changes of necrotizing enterocolitis suggest that its cause is multifactorial, with ischemia, inflammation, bacterial overgrowth, and reparative tissue changes all playing important roles.
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A distinctive form of necrotizing enterocolitis was observed in seven newborn infants in a 4 1/2-year period. Characteristically these patients had gross blood in the stools, but other local and systemic signs were mild or absent. Radiography mainly revealed submucosal intramural intestinal gas which was limited to the colon (pneumatosis coli). There was no evidence of small bowel involvement as judged by the absence of small intestinal pneumatosis or distension. This form of colonic disease should be recognized as a benign variety of neonatal necrotizing enterocolitis that carries a favorable prognosis and responds to medical management without sequelae.
We report six episodes of pneumatosis intestinale (PI) in children with primary combined immunodeficiency. PI was generally benign and responded to conservative therapy. Increased risk of infection or disruption of gastrointestinal mucosa are probable predisposing factors. A diagnosis of PI should be considered in children with primary combined immunodeficiency who experience otherwise unexplained gastrointestinal symptoms, particularly in the early post-transplant period.
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The pathogenesis of pneumatosis cystoides coli remains obscure in the absence of an explanation for why pockets of gas should form in the first place and why they should be maintained in the wall and mesentery of the colon. Counterperfusion supersaturation could explain the formation and location of the gas cysts, which occur mostly near blood vessels on the mesenteric border of the colon, and the absence of methane gas in them. The hypothesis can be tested by treating patients with pneumatosis cystoides coli with heliox.
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As part of the ongoing effort to minimize health care expenses, mothers and newborns are being discharged after shorter hospital stays. Problems that previously would have been noticed in the hospital nursery are now being seen in the emergency department. We report the case of a 1-day-old infant who was brought to our ED with grossly bloody stool. An Apt test was performed to determine whether the blood was of infant or maternal origin. After determining that the blood was the infant's, we transferred the child to a pediatric specialty center, where a diagnosis of necrotizing enterocolitis was made.
INTRODUCTION: Though impairment of the gastrointestinal tract is commonly encountered in patients with systemic sclerosis, the most frequent abnormalities are esophageal and anorectal disorders. Involvement of the small intestine is also common, reaching a 40-80% prevalence. It often leads to life-threatening complications. CURRENT KNOWLEDGE AND KEY POINTS: The occurrence of small intestine impairment and its potential relationships with other organ impairment is still unknown. However, it rarely indicates the existence of the disease (10%) which remains asymptomatic for a long period. As clinical symptoms are non-specific and radiological tests (upper intestinal tract barium meal, gastrointestinal transit times of radiolabeled meal, computerized tomography scan) not sensitive enough to detect the symptoms, diagnosis of small intestine impairment is delayed, i.e., when severe complications such as malabsorption or pseudo-obstruction are present. The physiopathology of small intestine disorders is still unclear, leading to both collagenous fibrosis and atrophy of muscle fibers. As well, its treatment is difficult. FUTURE PROSPECTS AND PROJECTS: Knowledge of the mechanisms at the origin of small intestine impairment in the course of systemic sclerosis is important for the development of efficacious therapies. Manometry of the small intestine would be a useful tool to assess the various motor abnormalities that may occur in patients presenting with systemic sclerosis associated with either malabsorption or pseudo-obstruction. It would also provide a useful test in selecting patients whose treatment require somatostatin analogs.
Two cases are presented of benign pneumatosis coli diagnosed on digital fluoroscopic barium enema examinations, in which the gas-filled cysts in the colonic wall were only recognized by postprocessing of the images (i.e. increasing the brightness and contrast settings) at the computer workstation. When digital barium enemas are performed, we therefore recommend image postprocessing to evaluate polypoid lesions in order to differentiate pneumatosis coli from true colonic neoplasms.
Gastrointestinal involvement is frequent in systemic sclerosis (SSc), occurring in 75 to 90% of patients with diffuse or limited cutaneous SSc. Although all regions of the gut may be affected, the esophagus is the most common gastrointestinal localization of this disease. If not diagnosed at an early stage, resulting complications may include esophagitis (leading to stenosis, strictures, and Barrett's esophagus) and increased risk of interstitial lung disease. Esophageal manometry is the most sensitive test for accurate diagnosis of motor dysfunction. Antisecretory agents (mainly proton-pump inhibitors) are effective for treating esophageal manifestations. Gastrointestinal involvement is reported in 50-88% of patients with SSc. It remains associated with a poor prognosis and leads to death in 6 to 12% of cases. Gastrointestinal impairment may lead to life-threatening complications, including severe dyspepsia, hemorrhage related to watermelon stomach (gastric antral vascular ectasia), malabsorption syndrome (related to bacterial overgrowth), and intestinal pseudo-obstruction. Treatment for the latter two remains difficult, although octreotide has proven to be effective in SSc patients. Small bowel manometry is useful for careful selection of SSc patients who will benefit from this treatment. Anorectal involvement is frequent in SSc patients (50-70%) and causes fecal incontinence and rectal prolapse. Other digestive manifestations, including liver impairment, are less common in SSc.