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Intestinal perforation can occur as a complication of the neonatal small left colon syndrome. Four such infants are reported. Early diagnosis and treatment, utilizing water soluble contrast enema examination, are recommended to reduce the frequency of this complication.
16 cases of intestinal perforation following blunt abdominal trauma in children (14 boys and 2 girls from 3, 5 to 15 years old) are recorded in a 18 years period. We found 12 injuries of the small bowel, 2 of the colon and 2 of the duodenum. Except in the cases with hypovolemia or traumatic coma, the diagnosis is often made on abdominal physical findings and clinical evolution. Laboratory and radiological data were often useless. Then, surgical management was often delayed, principally in the most recent period with the non operative management of most pediatric blunt trauma. Simple closure (7 cases), resection and anastomosis (7 cases) or resection and double ostomy (2 cases) were performed. The result summarize 2 death and one complication (fistula). Complications do not increase with delay.
Over the past decade, nonoperative management of most pediatric blunt abdominal trauma has emerged as accepted practice. It is possible that treatment of associated hollow visceral disruption might be missed or delayed because of this nonoperative approach. In a review of all cases of intestinal perforation from blunt trauma seen over the past 6 years, we found 12 cases of intestinal disruption in more than 600 cases of significant blunt trauma. Child abuse caused eight cases and four were motor vehicle related (MVR). Seven of eight battered children had a delay of more than 48 hours from injury to hospital presentation. Three of four MVR patients had an 18-hour delay from injury to operation. Ten of 12 patients survived. The two children who succumbed were both battered and were moribund and unstable when first seen and failed to respond to aggressive stabilization and surgery. Serial physical examinations, contrast radiographic studies, and peritoneal lavage were the most helpful diagnostic modalities. There were no significant complications and no patient required more than one operation (except for ostomy closure). All surviving patients are well at followup and seven of ten have been followed for more than 3 years; two are not yet 1 year from surgery and one is lost to followup. Several principles have emerged from this review: 1) motor vehicle trauma and child abuse are the major etiologic factors in childhood blunt trauma; 2) accurate and rapid diagnosis of intestinal perforation in children is difficult; 3) recovery in the presence of stable vital signs can be expected, even with the long delays; and 4) abused children must be carefully evaluated for abdominal trauma.
A two-year-old boy underwent a laparatomy for an intestinal perforation due to eosinophilic gastroenteritis. He had marked peripheral blood eosinophilia and a small duodenal biopsy showed heavy eosinophilic infiltration in the mucosa. After 1 1/2 year on a restricted diet, a control duodenal biopsy showed only slight eosinophilia. Perforation of the small intestine is a rare but serious complication in eosinophilic gastroenteritis.
We present two cases of patients with acquired immunodeficiency syndrome who, in the course of their disease, suffered multiple intestinal perforations that were directly related to cytomegalovirus infection. Biopsy and surgical specimens and autopsy findings in both cases revealed extensive lesions of gastroenteritis; the gastroenteritis was characterized by randomly distributed deep ulcers, resulting in multiple perforations. The main characteristic histopathologic finding was the association of intestinal lesions with a severe form of cytomegalovirus-related occlusive vasculitis. This report provides evidence that supports the contention that cytomegalovirus is the primary causal agent of gastrointestinal lesions affecting immunocompromised patients.
Within 9 months we observed intestinal perforations in three very low birth weight (VLBW) infants undergoing indomethacin treatment for symptomatic patent ductus arteriosus (sPDA). The three patients exhibited striking similarities in their clinical courses and predisposing factors. Although clinical and histological criteria did not differentiate the perforations from necrotising enterocolitis (NEC), a well-known entity in premature infants, these events were remarkable to us since we had observed no other cases of NEC in recent years. From animal experiments and pathophysiological data, a role for indomethacin in gastrointestinal ischaemic damage must be considered. This communication is not meant to discredit indomethacin treatment. However, awareness of potential complications and careful monitoring during treatment is warranted.
This is a case report of focal intestinal perforation in a premature neonate following intravenous administration of indomethacin for patent ductus arteriosus.
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.
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.
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.
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.
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.
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Between 1982 and 1987 seven neonates ranging in age from 24 hours to 1 week were treated for idiopathic intestinal perforations at the Montefiore Medical Center, Albert Einstein College of Medicine. Four of the infants were born prematurely; three were full term. Five were being treated in an intensive care nursery when the perforation was diagnosed. All infants whose perforations were due to necrotizing enterocolitis, appendicitis, Hirschsprung's disease, meconium ileus, intestinal atresias, or drug therapy are excluded from the series. None of the infants had associated anomalies. The sites of the perforations were as follows: two in the jejunum, two in the ileum, one in the cecum, and two in the transverse colon. Six of the perforations were on the antimesenteric aspect of the bowel; one was on the mesenteric aspect. The sizes of the perforations ranged from pinhole to 1 cm in diameter. All the infants did well. Pathologic examination of the resected specimens failed to reveal an etiology for the perforations. There were no cases of duplication or muscular hypoplasia. We believe the etiology of this condition may be ischemic necrosis, secondary to a localized vascular accident in the wall of the affected viscus, but we do not have a good explanation for the upsurge in cases we are seeing.
The renal excretion of orally administered water-soluble contrast medium has been described in intestinal perforation (Mori and Barret, 1962). We present a case in which orally administered Diatrizoate methylglucamine (Gastrografin, Schering) was detected in the renal collecting system on computed tomography in a man with an ischaemic segment of small bowel associated with abscess formation but no evidence of intra-peritoneal perforation.
Although NSLCS has been considered to have a benign course, we have described an infant who had intrauterine intestinal perforation and meconium peritonitis associated with the NSLCS. Infants of diabetic mothers who are stillborn or who develop abdominal distention shortly after delivery should be suspected of having this complication of NSLCS. This disorder must also be considered in the differential diagnosis of infants who present with meconium peritonitis.
Female patient with multiple episodes of pelvic surgery and with radical cystopathy, treated by Neodymium: YAG laser photocoagulation with haemostatic purposes. During the post-operative she developed intestinal perforation with fatal evolution. The cases described on this serious and infrequent complication of laser endovesical application are reviewed, commenting the technical and anatomical elements that justify it.