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This is a case report of focal intestinal perforation in a premature neonate following intravenous administration of indomethacin for patent ductus arteriosus.
Phytobezoars are rare causes of acute abdomen cases. Here we are reporting two cases which were presented with acute abdomen symptoms and later were found to be small intestinal perforation due to bezoar.
BACKGROUND/PURPOSE: Laparotomy for peritonitis secondary to necrotizing enterocolitis (NEC) or focal intestinal perforation (FIP) has been supplanted by peritoneal drainage (PD) as the initial treatment in many institutions. Although proponents regard it as a safer alternative, early mortality is cited between 21% and 36%, with subsequent laparotomy required for worsening disease in 26% to 83% of patients. The current outcomes for initial laparotomy are analyzed and compared with those cited for PD. METHODS: A retrospective review of very small premature infants less than 1,500 g undergoing laparotomy for NEC or FIP between 1994 and 2000 was performed. RESULTS: Thirty-five neonates were identified with a median weight of 741 g (range, 460 g to 1,415 g) and a median age of 26 weeks (range, 23 to 33 weeks). Twelve patients had FIP and 23 had NEC including 5 with pan-intestinal necrosis (PIN). No deaths occurred during laparotomy or stoma closure. Seven (20%) patients died within the immediate 7-day postoperative period. Nine (26%) patients died in the 30-day postoperative period. CONCLUSIONS: With current peri-operative management, mortality rates for initial laparotomy and PD are comparable. Assessing the extent of disease and removing necrotic bowel at initial laparotomy can hasten recovery and eventual discharge while enabling informed surgical decision making and advice to parents.
Accidental ingestion of foreign bodies is common enough, especially in children, but is of relatively small importance as such objects readily pas through the body and no particular treatment is required. A more interesting and less frequent occurrence is the ingestion of objects such as bone fragments, fish bones, etc. that form part of ordinary food. Cases of intestinal perforation caused in this way are described, together with their clinical and surgical management.
We hereby report a case of fatal intestinal perforation in an immunocompetent old female. It was associated with invasive candidiasis.
The case of a male preterm baby who had congenital miliary tuberculosis with multiple intestinal perforations is reported. The patient was successfully treated with antituberculosis chemotherapy and surgical repair along with other supportive therapy. This is one of the rarest cases of the type described here.
One of the most serious complications of typhoid fever is intestinal perforation. Of 27 patients admitted to a provincial hospital in the Mekong Delta region of Vietnam who had gastrointestinal perforation secondary to suspected typhoid fever, 67% were male, with a median age of 23 years and a median duration of illness of 10 days. Salmonella enterica subspecies enterica serotype Typhi (S. Typhi) was isolated from 11 (41%) of 27 patients; of 27 patients, only 4 (15%) had positive cultures from gut biopsies. S. Typhi DNA was detected by polymerase chain reaction for all perforation biopsy samples. Detailed histological examination of the gastrointestinal mucosa at the site of perforation in all cases showed a combination of discrete acute and chronic inflammation. Acute inflammation at the serosal surface indicated additional tissue damage after perforation. Immunohistochemical results showed that the predominant infiltrating cell types at the site of perforation were CD68+ leukocytes (macrophages) or CD3+ leukocytes (T lymphocytes).
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Three premature neonates with a localized perforation of the intestine, but not associated with necrotizing enterocolitis (NEC) or gastrointestinal anomaly are reported. The birth weight of these babies was around 1500 g and they exhibited striking similarities in the clinical course. Before laparotomy, NEC was firstly impressed. Abdominal distension, refusal of feedings, poor activity and respiratory distress were the major manifestations. Pneumoperitoneum was all detected before operation. The perforate site was terminal ileum in one and anterior cecum in the other two babies. The gastrointestinal tract was otherwise normal. The first case received segmental resection of the perforation with end to end anastomosis and the other two underwent ileostomy. Bacteria was discovered from the peritoneal fluid in the second and third cases, including E. coli, Enterobacter cloacae and Klebsiella pneumoniae respectively. The postoperative course was complicated with wound infection and adhesion ileus in two patients. Rectal suction biopsy in the second and third cases showed normal histology. Until present all three patients were uneventful. We concluded that premature or very low birth weight infants with spontaneous, localized gastrointestinal perforation and peritonitis had milder course than NEC, and if promptly diagnosed and treated, the prognosis is excellent.
In order to elicit the pathogenesis of focal intestinal perforation in preterm infants we contrasted 8 infants who developed this disease with 16 gestation-matched controls. The cases were found to have lower birthweights for gestation (median standard deviation score of -1.02 in cases versus -0.08 in controls), and more frequently had pre-existing patent ductus arteriosus and intraventricular haemorrhage (88 and 63% in cases versus 25 and 6% in controls, respectively). There were similar rates of other perinatal variables in the two groups, including indomethacin and umbilical arterial catheter use. Conditions associated with fetal or neonatal hypoxia are important antecedents for this emerging distinct clinical entity.
The appropriate therapy for intestinal perforation in typhoid fever has been controversial since the late 1880s. Around the turn of the century, surgery became the established mode of therapy, with a mortality of 69% based on 166 patients in the English-language medical literature, and continued to be the preferred treatment until the advent of chloramphenicol in 1948. At this time the surgical mortality was approximately 50%. Following the recovery of a few patients with perforation treated only with antimicrobial agents (six initially, then eventually 22), nonsurgical therapy became the accepted mode of treatment. This change was never justified and this review demonstrates this. Appropriate therapy is virtually always surgical, usually consisting of simple closure and irrigation. Chloramphenicol alone is inadequate antimicrobial therapy in a patient with perforation and must be supplemented by other antimicrobials directed against enteric aerobic gram-negative bacilli and enteric anaerobes.
Among 36 neonates with intestinal perforations (IP) between 1975 and 1996, 5 had necrotizing enterocolitis (NEC IP) and 10 had focal IPs (FIP). A histologic review of the bowel near the perforations was made to see if there was any difference between cases of NEC IP and FIP. In 1 case of NEC IP, a defect in the musculature was found in addition to disappearance of the mucosal villi and dilated vessels or hemorrhage in the submucosa. Thinning or absence of the intestinal musculature and short villi in the mucosa was observed in 3 cases of FIP, but the acute ischemic changes in FIP were much less than in NEC IP. Hypothesizing that the defective musculature in FIP may be acquired by a vascular accident either before or after birth, we examined the histology of the latest consecutive infants diagnosed as having meconium peritonitis (MP) due to in-utero volvulus and perforation. In the tissue near the perforation, there was an identical focus of thinning and interruption of the musculature while the acute ischemic changes were minimal. We speculate that thinning or absence of the intestinal musculature in FIP may be a result of a transient ischemic event occurring in-utero and that FIP may develop in the damaged intestine after birth when it is fully dilated.
In recent 11 years, 5 cases of severe high voltage electrical burn with intestinal perforations were successfully treated. They showed obvious whole layer necrosis of abdominal wall, exudation, intestinal prolapse and peritonitis. On the basis of antishock therapy and protection of renal function, acute laparotomy was done early. Resection of the small intestine with necrosis and perforation and end-to-end anastomosis were done in 4 cases (5 regions). Colon resection and colostomy were done in 2 cases, and immediate end-to-end anastomosis in 2 cases. Bowel segment with external fistulae was left in 1 case (2 regions). If the abdominal wall defect could not be sutured directly, skin grafting on the residual tissue and omentum may be temporarily effective. And myocutaneous pedicle flap should be repaired secondarily. After operation, parenteral nutrition and anti-infection are important for patient recovery. No complication occurred in this group.
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Explore the source record for details and available documents.
Four very-low-birth-weight infants developed localized intestinal perforations after enteral administration of indomethacin. The clinical picture and histologic findings were unlike those seen in necrotizing enterocolitis.
Two cases of colitis due to Salmonella enteriditis which later developed a toxic megacolon with intestinal perforation are presented and the probable pathogenesis is discussed. This exceptional clinical course which has not been previously described forces to perform a differential diagnosis with chronic intestinal inflammatory disease which must be based on microbiologic, serologic and/or histologic criteria. Moreover, the authors warn about the unsuitability of using anticholigernic drugs in gastroenteritis since they could be related to the ethiopathogenical basis of the disease's unfavorable course in the described patients.