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[Intestinal perforation secondary to impaction of a retained endoscopic capsule].

We present the first documented case of intestinal perforation due to impaction of an endoscopic capsule. The capsule was used to investigate anemia in an 80-year-old woman and was retained in the intestinal lumen for 2 months without producing symptoms. The patient presented to the emergency service with sudden, intense, diffuse abdominal pain. Hollow viscus perforation was suspected and surgery was performed. The diagnosis was distal ileum perforation secondary to an impacted endoscopic capsule in an area of severe postsurgical adhesions under a subcostal cholecystectomy incision performed 10 years previously. After reviewing the literature, we believe it important to report this exceptional complication of capsule endoscopy and suggest the possible management of capsules retained in the digestive tract.

Aged, 80 and over↗

Ascitic fluid carcinoembryonic antigen and alkaline phosphatase levels for the differentiation of primary from secondary bacterial peritonitis with intestinal perforation.

BACKGROUND/AIMS: In cirrhotic patients, spontaneous bacterial peritonitis (SBP) may be difficult to distinguish from secondary peritonitis with occult intestinal perforation; Runyon's criteria (based on ascitic fluid glucose, protein and lactate dehydrogenase levels) are sensitive but not specific. Ascitic fluid carcinoembryonic antigen (CEA) and alkaline phosphatase (AP) are potential markers for secondary peritonitis. METHODS: Ascitic fluid CEA and AP levels were prospectively compared among three subject groups--cirrhotic patients with sterile ascites, cirrhotic patients with SBP, and patients (cirrhotic and non-cirrhotic) with perforation-related secondary peritonitis. RESULTS: The secondary peritonitis group (n = 38 including 11 cirrhotic patients) had significantly higher mean CEA and AP levels than the SBP (n = 34) and sterile ascites patients (n = 63). Of secondary peritonitis patients, 92% fulfilled predetermined criteria (either CEA >5 ng/ml or AP >240 units/l) versus only 12% of SBP patients; sensitivity was 92% and specificity 88% for differentiating secondary peritonitis from SBP. Runyon's criteria had a sensitivity of 97% and specificity of 56%. Stratification of secondary peritonitis patients by the presence or absence of cirrhosis did not alter our results. CONCLUSIONS: Ascitic fluid CEA or AP elevations appear to be sensitive and specific markers for perforation-related secondary peritonitis in cirrhotic as well as non-cirrhotic patients.

Adult↗

Spontaneous localized intestinal perforation in very-low-birth-weight infants: a distinct clinical entity different from necrotizing enterocolitis.

BACKGROUND: Idiopathic spontaneous intestinal perforation (SIP), a distinct clinical entity different from necrotizing enterocolitis (NEC), has an increasing prevalence in very-low-birth-weight infants. The aims of our study were to define patient characteristics and potential risk factors for premature infants with SIP compared with infants subjected to surgical treatment for NEC. STUDY DESIGN: The medical records of 29 premature infants with either SIP (n = 13) or NEC (n = 16) were reviewed retrospectively. RESULTS: Infants who experienced SIP were smaller at birth, had lower Apgar scores, and required more intensive neonatal resuscitation. An increased rate of premature rupture of membranes in infants with SIP (8/13 versus 6/16) was not associated with a higher rate of infection in mothers or infants. The onset of illness in SIP was significantly earlier than in NEC (p = 0.022). In contrast to patients with NEC (7/16), 11 of 13 patients in the SIP group had received indomethacin (p = 0.02). Bluish discoloration of the abdomen (8/13), a gasless abdomen (8/13), and the absence of pneumatosis intestinalis (0/13) were further significant markers in infants with SIP. At operation, SIP was always located in the terminal ileum in an antimesenteric position (13/13), and the remaining bowel appeared grossly normal. In most cases of SIP (10/13), the histologic investigation revealed an area of hemorrhagic necrosis without the typical coagulation necrosis seen predominantly in NEC. CONCLUSIONS: Based on clinical presentation and radiologic and intraoperative findings, SIP is a distinct pathologic entity in very-low-birth-weight infants and can be differentiated from classic NEC. Detected early, SIP can be treated by simple procedures (sutures, or resection and primary anastomosis) with a low rate of morbidity and mortality.

Chi-Square Distribution↗

Concurrent use of indomethacin and dexamethasone increases the risk of spontaneous intestinal perforation in very low birth weight neonates.

BACKGROUND: Dexamethasone or indomethacin predisposes very low birth weight (VLBW) neonates to spontaneous intestinal perforation (SIP). However, no study has specifically investigated the role of the concurrent use of indomethacin and dexamethasone in SIP. OBJECTIVE: To test whether the concurrent use of indomethacin and dexamethasone increases the risk of SIP. METHODS: In this single center, retrospective, 2:1 matched, case-control study, the odds of SIP were assessed using univariate and multivariate logistic regression analysis in < or =14-day old VLBW infants. RESULTS: Sixteen VLBW infants with SIP were matched to 32 controls by birth weight. After adjusting for clinically relevant variables, patients who received > or =3 doses of indomethacin for ductal closure or intraventricular hemorrhage prophylaxis and > or =3 doses of low-dose dexamethasone (0.3 mg/kg cumulative dose over 3 days) for refractory hypotension during the first postnatal week, were 9.6 times more likely to develop SIP [95% CI 1.22, 75.71]. CONCLUSIONS: The combined use of indomethacin and dexamethasone increases the risk of SIP in VLBW neonates.

Case-Control Studies↗

[Ischemia-related small intestine perforation 15 days after car accident. Fate or avoidable complication?].

Intraabdominal organ lesions after blunt abdominal injuries often are missed, especially in the contest of a polytrauma because of the absence of obvious clinical injury signs, difficult examination conditions of an intubated patient and the possibility of secondary development of lesions. For an exact recognition of the abdominal injuries a standard diagnostic procedure is necessary. Clinical and laboratory parameters which determine the circulatory situation, initial abdominal ultrasound, x-ray and follow up examinations are indispensable. In equivocal situations CAT scan respectively angiography are recommended. The correct initial diagnosis of intestinal perforations still is problematic and requires repeated examinations. We report the case of a patient with initial blunt abdominal injury and a non dislocated Weber-A-fracture after a car accident. 15 days after trauma the patient was seen with the clinical signs of an acute abdomen. After emergency laparotomy an ischemic necrosis of the ileum, covered with net, was seen.

Abdominal Injuries↗

Intracerebral sepsis due to intestinal perforation by ventriculo-peritoneal shunts: two cases.

Two cases of ventriculo-peritoneal (V-P) shunt infection attributable to intestinal perforation are reported. One patient developed a brain abscess, the other ventriculitis. Microbiology consisted of faecal flora and the peritoneal catheter was found to be faecally stained in both cases. There were no abdominal symptoms or signs. It is likely that infection developed via the ascending route.

Adult↗

Idiopathic intestinal perforations in premature infants without evidence of necrotizing enterocolitis.

In the past three years five premature very low birth weight infants (VLBW, birth weight 720-1,300 g) developed spontaneous localized perforations of the small intestine during the second week after birth. There was no evidence of intestinal obstruction or necrotizing enterocolitis (NEC). The clinical presentation and laboratory values as well as the radiologic, intraoperative and histologic findings were different from those of NEC. In four cases the initial symptoms presented as a gray-green discoloration of the flank and inguinal region with an otherwise unremarkable general condition. All patients exhibited a leukocytosis (range 14,700-19,300) and increased neutrophil count (range 9,900-14,800). Additionally, a pronounced increase in the activity of alkaline phosphatase (> 2.000 U/l in 3 cases) and a renewed increase of serum bilirubin was observed. Four of the five infants survived following laparotomy with ileostomy (n = 2) or primary anastomosis (n = 3).

Female↗

[Intestinal perforation by a fish bone. Apropos of a case and review of the literature].

We report a case of transverse colon perforation by a fish bone (Grouper) in a toothless-old female. A review of the literature revealed a great variety of foreign bodies which may cause perforations at variable sites of the gastrointestinal tract. Fish bones were responsible for 46% of intestinal perforations in a review of 24 cases collected in 1984. Advanced age and poor patient dentition, as well as mental debility constitute predisposing factors for the swallowing of foreign bodies. Emergency radiology may be required. An exaggerated inflammatory reaction may give rise to a misleading pseudo tumor appearance. We agree that a well conducted and well analysed clinical history associated with a careful pathologic examination are very helpful in the diagnosis.

Aged↗

Technetium-99m-pyrophosphate scintigraphic findings of intestinal perforation in dermatomyositis.

Gastrointestinal complications are more common in children than in adults and present a serious problem with dermatomyositis. We report on a 66-yr-old man with dermatomyositis who suffered from intestinal perforation. The abdominal plain radiograph revealed only dilatation of the intestinal loops; increased radioactivity, however, was clearly demonstrated in the early 5-min and delayed 3-hr 99mTc-pyrophosphate images.

Aged↗

Intestinal perforation in newborn following intrauterine meconium peritonitis.

A newborn infant, who had suffered intrauterine perforation and had developed peritoneal calcification, showed no sign of pneumoperitoneum on the first radiograph taken 3 hours after delivery. At that time air was present in the stomach only. Subsequently pneumoperitoneum developed as air passed down the gut to the point of perforation. Thus, the absence of pneumoperitoneum on a radiograph taken very early in life does not exclude an intestinal perforation.

Colonic Diseases↗

[Allergic granulomatosis and angiitis associated with intestinal perforation and eye movement disorder].

A perforation in the small intestine and one and a half syndrome were observed in 45-year-old male with allergic granulomatosis and angiitis (AGA). The patient was first admitted to our hospital in 1988 with complaints of bronchial asthma and an abnormal density on his chest X ray. The diagnosis of PIE syndrome was made based on marked peripheral blood eosinophilia. He was successfully treated with prednisolone and had been well on the maintenance therapy of small doses of it. In May 1990, peripheral neuropathy occurred in his bilateral lower legs and it was followed by nausea and vomiting. The laboratory findings on admission showed leukocytosis (19,300/mm3) with 43% eosinophilia and elevated blood level of IgE (3000 IU/ml). On the tenth day of admission, ileus symptom and subsequently a perforation of the small intestine were observed. The mesenterial specimens obtained during the emergency operation showed the findings compatible with AGA. Remission of AGA was induced by the treatment with 60 mg prednisolone and 100 mg cyclophosphamide per day following methylprednisolone pulse therapy. He was well on maintenance prednisolone until June 1991, when he suddenly developed one and a half syndrome. Although cranial CT scan and MRI showed no abnormal findings, cyclophosphamide therapy was resumed and prednisolone was increased because microangiopathy due to AGA was thought to be the cause of this central nervous system symptom. The one and a half syndrome improved with this therapy. This case suggests that the long term treatment with prednisolone and cyclophosphamide would be indicated in the severe AGA with close monitoring of the symptoms and peripheral blood eosinophilia.

Churg-Strauss Syndrome↗