PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “INTESTINAL ATRESIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1988

New observations on the pathogenesis of multiple intestinal atresias.

It has been suggested that multiple intestinal atresias result from multiple ischemic infarctions of the intestinal tract. We have studied surgical material from 59 neonates with intestinal atresias seen at our hospital between 1975 and 1986. Forty (68%) patients had single intestinal atresias and 19 (32%) had multiple atresias. There were seven cases of hereditary multiple atresias seen in three families and 12 cases of nonhereditary multiple atresias. All hereditary cases had numerous type I or type II gastrointestinal atresias but none had type IIIa atresia. Six of the seven hereditary cases had multiple atresias in the small as well as large bowel. The 12 patients with nonhereditary atresias had various types of atresias but mesenteric or intestinal interruption was observed in only two patients. All patients with hereditary multiple intestinal atresias showed identical microscopic appearances in the small and large intestine, consisting of sieve-like multiple lumina, each surrounded by its own mucosa and muscularis mucosae but sharing a common muscle coat. There was no evidence of lanugo, bile pigments, or squames within the lumen distal to atretic segments in any of these patients. Six nonhereditary cases who had multiple septal atresias affecting only the small bowel demonstrated essentially similar lesions on microscopic examination as seen in hereditary cases. There was no evidence of arterial occlusion in the mesentery and lanugo, bile pigments, and squames could not be found distally in the intestinal contents in any of these cases. These pathologic findings suggest that all cases of hereditary multiple intestinal atresias and some cases of nonhereditary multiple intestinal atresias are a consequence of a malformative process of the gastrointestinal tract rather than an ischemic process.

Abnormalities, Multiple↗
PubMed1977

Gastroschisis complicated by intestinal atresia.

Gastroschisis complicated by intestinal atresia is a complex problem. Six cases are presented. A review of the literature and of our own cases shows a high mortality rate. Success or failure is related more to the pathology present than to any specific method of operative management. Resection and primary anastomosis is the favored method of treatment, as the intestine heals well in spite of its appearance. Primary closure of the abdominal wall musculature and skin is done whenever possible. A gastrostomy is used uniformly. Intravenous hyperalimentation is critical to survival of these babies and should be used early. The use of this therapeutic modality allows for the onset of gastrointestinal function spontaneously (often over prolonged periods of time) without nutritional deprivation. Intestinal atresias almost always are easy to identify in babies with gastroschisis. Extensive dissection and mobilization of this friable intestine is contraindicated in those babies in whom an atresia is not obvious but only suspected. In such cases the gastroschisis defect should be managed by whatever method is deemed appropriate and the baby observed while receiving intravenous nutritional support. If an atresia is present, it can be managed later in the baby's course by resection and primary anastomosis.

Abdominal Muscles↗
PubMedDate not supplied

[Treatment of intestinal atresia].

Thirteen cases of intestinal atresia are described: 9 jejunal and 4 ileal. The duration of pregnancy was significantly shorter and the birthweight significantly lower in jejunal than in ileal atresia. The proximal intestine was strongly dilated in 8/9 cases with jejunal atresia. This group also contains several complex and extended varieties of atresia. The postoperative mortality was 8%. Gastrointestinal functional disturbances occurred only in the group treated for jejunal atresia. These disturbances were temporary and occurred postoperatively in 2 cases but reoperation was mandatory in another 2 cases, once without functional success. There were no problems in the other cases. Ileal atresia is easy to treat and the result is always good. In contrast, the situation is much more challenging in cases of jejunal atresia: prematurity, higher incidence of complex and extended gastrointestinal malformations, impossibility to resect the dilated proximal segment, presence of a long under-developed distal segment. No problems have been observed after construction of a double stoma and restoration of the intestinal continuity. However a proximal stoma leads to important fluid and electrolyte losses, necessitating total parenteral nutrition. Functional gastrointestinal disturbances are frequently observed after end-to-side anastomosis in Y with mucous fistula. An end-to-end anastomosis can be combined with enteroplasty of the proximal distended bowel segment, eventually including the duodenum. Although the enteroplasty technique is an important progress in the treatment of neonates with extended types of jejunal atresia, transit problems cannot always be prevented by this procedure.

Birth Weight↗
PubMedDate not supplied

A very rare type of multiple intestinal atresias: "a string of pearls".

Intestinal atresia is the most frequently encountered cause of ileus in the neonate. Of all atresias combination of small and large bowel atresias is extremely rare. In 1973, Guttman presented a case with multiple, widespread atresias of small and large bowel, intraluminal calcifications and a hereditary nature. This paper describes the detailed pathological findings of a similar case of multiple intestinal atresias and discusses for the pathogenesis of this rare condition.

Fatal Outcome↗
PubMed1987

Myoelectric activity differences in acute and chronic models of lamb intestinal atresia.

Clinical and experimental investigations of intestinal atresia have reduced mortality and clarified etiology. However, the morbidity of this lesion remains excessive and its pathophysiology uncertain. The purpose of this project was to produce the first long-term model of intestinal atresia and thereby to study the motility of the adapting bowel. Intestinal atresia was induced in nine fetal lambs at midgestation by mesenteric avulsion. At term, this experimental group and eight control lambs underwent resection with anastomosis, decompression gastrostomy, and implantation of electrodes proximal and distal to the anastomosis. Vigorous resuscitation and constant intensive care were critical for survival. Slow wave activity (SWA) and spike potential activity (SPA) were recorded in the first 24 hours and every 48 hours thereafter for a 6-hour interval. Three of nine lambs with atresia and five of the eight control animals survived over 48 hours (chronic). Analysis of 220 hours of recording showed, in the first 24 hours of life, a statistically significantly different SWA of 16.4 cycles/min (+/- 1.15 SD) in the chronic atretic survivors compared with 13.1 cycles/min (+/- 2.6 SD) in the acute (died less than 48 hours) atretic group (P less than .05). The SWA of the chronic atretic survivors was similar to the SWA of the chronic nonatretic control animals, 15.1 cycles/min (+/- 1.4 SD). SPA was present on the first day of life in the microintestine of the chronic atresia group in contrast to the acute animals of this study and of Doolin and Hill's previous study. Delayed function has been attributed to the absence of SPA in the microintestine of acute models.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1999

Alterations of the intramural nervous distributions in a chick intestinal atresia model.

The postoperative intestinal dysmotility seen in intestinal atresia (IA) is usually found in association with a dilatation of the proximal intestinal segment, but the etiology of this disorder is not yet fully understood. A chick IA model was made by cutting the postumbilical midgut on d 11 in ovo. The operated chicks were euthanized 2 d after hatching. The samples were divided into two groups according to the extent of the dilatation of proximal ileal segments. Cryostat sections were processed for immunohistochemistry by the use of antisera to protein gene product 9.5, vasoactive intestinal polypeptide, substance-P, and alpha-smooth muscle actin and were also stained by NADPH-diaphorase. Tn highly dilated proximal segments, a decreased number of protein gene product 9.5-positive fibers was found in both the circular muscle and submucous layers. The number of nerve fibers positive for vasoactive intestinal polypeptide, substance-P, and NADPH-diaphorase also decreased in the circular muscle layer, particularly in the deep muscular plexus. Hypertrophy and an alteration of the staining intensities in the circular muscle layer were also revealed by a-smooth muscle actin staining. The nerve distribution of the distal segments was indistinguishable from that of the age-matched controls and the sham-operated group. Abnormalities in the intramural nerves are only found in the proximal ileal segment of the IA models. The abnormal nerve distribution of the proximal segment might thus be implicated in the postoperative dysmotility of the intestine in IA.

Actins↗
PubMed2001

Inherited thrombophilia: a possible cause of in utero vascular thrombosis in children with intestinal atresia.

BACKGROUND: Congenital atresia of the small and large intestine is thought to evolve from in utero mesenteric vascular occlusion of the corresponding intestinal segment. Because spontaneous thrombosis recently has been described in association with inherited thrombophilia, the authors wondered if inherited thrombophilia also might be found in babies with intestinal atresia. METHODS: Genetic analysis was done on 28 children treated for congenital intestinal atresia. DNA was analyzed for point mutations to detect the 2 most common types of inherited thrombophilia, the G1691A mutation in the factor V gene (factor V Leiden) and the G20210A mutation in the prothrombin gene. In addition, other genetic risk factors for thrombosis were analyzed including the C677T mutation in the methylenetetrahydrofolate reductase gene (MTHFR) and 2 polymorphisms of the factor VII gene (the R353Q and the hypervariable region 4 polymorphisms). RESULTS: The factor V Leiden mutation was present in 5 of 28 (18%) children treated for congenital intestinal atresia. This is increased significantly when compared with the reported carrier frequency of 3% to 7% in the general population and a reported carrier rate of 4.2% in the local population (P <.005). The R353Q polymorphism of the factor VII gene, specifically the RR genotype, was noted in 85% of patients with atresia with an expected frequency of 64% (P <.008). There were no significant associations noted between mutations in the prothrombin gene, the MTHFR gene, or the hypervariable region of the factor VII gene. CONCLUSIONS: The factor V Leiden mutation and the RR subtype of the R353Q polymorphism of the factor VII gene are seen at an increased frequency in children with congenital intestinal atresia. This suggests that inherited thrombophilia may play a role in the etiology of these in utero mesenteric thrombotic events.

Cohort Studies↗
PubMed1974

Hereditary multiple intestinal atresia.

FIVE CASES OF INTESTINAL ATRESIA IN THREE FAMILIES WHO HAD COMMon ancestors are reported. Consanguinity was present in two of the sibships. The lesions were located at multiple sites of the gastrointestinal tract, from the stomach to the anal margin. Intraluminal calcifications were also observed in the intestine. The authors suggest that this well-delineated congenital defect has an autosomal recessive mode of inheritance.

Calcinosis↗
PubMed2002

Maternal medication use and risks of gastroschisis and small intestinal atresia.

Gastroschisis and small intestinal atresia (SIA) are birth defects that are thought to arise from vascular disruption of fetal mesenteric vessels. Previous studies of gastroschisis have suggested that risk is increased for maternal use of vasoactive over-the-counter medications, including specific analgesics and decongestants. This retrospective study evaluated the relation between maternal use of cough/cold/analgesic medications and risks of gastroschisis and SIA. From 1995 to 1999, the mothers of 206 gastroschisis cases, 126 SIA cases, and 798 controls in the United States and Canada were interviewed about medication use and illnesses. Risks of gastroschisis were elevated for use of aspirin (odds ratio = 2.7, 95% confidence interval: 1.2, 5.9), pseudoephedrine (odds ratio = 1.8, 95% confidence interval: 1.0, 3.2), acetaminophen (odds ratio = 1.5, 95% confidence interval: 1.1, 2.2), and pseudoephedrine combined with acetaminophen (odds ratio = 4.2, 95% confidence interval: 1.9, 9.2). Risks of SIA were increased for any use of pseudoephedrine (odds ratio = 2.0, 95% confidence interval: 1.0, 4.0) and for use of pseudoephedrine in combination with acetaminophen (odds ratio = 3.0, 95% confidence interval: 1.1, 8.0). Reported fever, upper respiratory infection, and allergy were not associated with risks of either defect. These findings add more evidence that aspirin use in early pregnancy increases risk of gastroschisis. Although pseudoephedrine has previously been shown to increase gastroschisis risk, findings of this study raise questions about interactions between medications and possible confounding by underlying illness.

Acetaminophen↗
PubMed2004

Hereditary multiple intestinal atresia: thirty years later.

BACKGROUND: Hereditary multiple intestinal atresia (HMIA) is an unusual form of intestinal atresia with a presumed autosomal recessive mode of inheritance. The aim of this study was to review the authors' experience with this disease, 30 years after its first description. METHODS: All cases of HMIA treated at the authors' institution were reviewed with a particular focus on presence of close consanguinity in the families, prenatal diagnosis, radiologic and surgical findings, pathology report, and outcome. RESULTS: Sixteen cases were identified. Two patients were siblings (1 newborn and 1 aborted foetus) and close consanguinity was proven in 1 other case. Bowel obstruction was suspected on prenatal ultrasound scan in 6 patients, but HMIA could not be diagnosed specifically. Radiologic, surgical, and pathologic findings were compatible with the standard description of this disease in the literature. All the patients died. Mean survival time was 50 days. CONCLUSIONS: Thirty years after its first description, HMIA remains a disease without reliable prenatal diagnosis nor effective surgical therapy. An autosomal recessive mode of inheritance is suspected. Until accurate in utero diagnosis becomes available, children with HMIA should be oriented toward palliative care.

Fatal Outcome↗
PubMed2002

Pyloric atresia associated with multiple intestinal atresias and pylorocholedochal fistula.

Although congenital pyloric atresia commonly occurs in isolation, it has rarely been reported in association with other alimentary tract atresias. This is a report of a newborn with congenital pyloric atresia associated with duodenal atresia, jejunal atresia, apple-peel ileal atresia, and pylorocholedochal fistula. Preoperative diagnosis was duodenal atresia because of bilious vomiting, and erect radiogram showed double bubble sign. The presented case is the first report of such an association.

Abnormalities, Multiple↗
PubMed2003

Epidemiological investigations of an outbreak of intestinal atresia in two Israeli dairy herds.

An epidemiological investigation of an outbreak of intestinal atresia in Israeli Holstein-Friesian newborn calves showed a linkage with rectal palpation for early pregnancy diagnosis, performed less than 42 days after insemination. The odds of an exposed calf, i.e., one born to a dam that was diagnosed by early palpation as having intestinal atresia were 119.7 times higher than one born in normal control herds (95% CI; 7.4-1946.3). A total of 682 calves-at-risk was recorded from mid-1998 to mid-2000 and a total of 47 calves (6.9%) were born with intestinal atresia during this period. Two forms of intestinal atresia were recognized at post-mortem: atresia coli and atresia ilei.

Animals↗
PubMed1994

Increased risk of small intestinal atresia among twins in the United States.

OBJECTIVE: To compare the prevalence of small intestinal atresia among twins and singletons in the United States. DESIGN: Descriptive analysis. MEASUREMENTS: The McDonnell Douglas Health Information System (MDHIS), a national registry of newborn diagnoses, 1982 through 1988; and the Metropolitan Atlanta Congenital Defects Program (MACDP), a registry of defects among infants in Atlanta, 1968 through 1989. PATIENTS: Live-born infants with small intestinal atresia. INTERVENTIONS: None. MAIN RESULTS: In both systems, the rate of small intestinal atresia was higher among twins than singletons (MDHIS: 5.5 per 10,000 vs 2.0, relative risk [RR] = 2.8, 95% confidence interval [CI] = 1.9 to 4.0; MACDP: 7.3 vs 2.5, RR = 2.9, 95% CI = 1.5 to 5.7). The increase was more notable among same-sex twins than opposite-sex twins, suggesting an increase among monozygotic twins. It was also more notable among twins with jejunoileal atresia than those with duodenal atresia, suggesting a vascular cause in many cases. CONCLUSION: Twins have a higher rate of small intestinal atresia than singletons, possibly due to vascular disruption in monozygotic twins.

Databases, Factual↗
PubMedDate not supplied

Association between multiple intestinal atresia and omphalocele: a case report.

Multiple intestinal atresia is a rare disorder with vascular or hereditary etiology. So far, the occurrence of this malformation along with omphalocele has not been reported. We describe a boy born from a nonconsanguineous gypsy couple with intrauterine growth retardation, omphalocele, and multiple intestinal atresia from the pylorus to the rectum. The microscopic examination of the intestine shows multiple small lumina with a sieve-like appearance. This is characteristic of the hereditary atresias and suggests development of a defect in (re)canalization during embryogenesis. The association with omphalocele indicates a common developmental defect may be present.

Hernia, Umbilical↗
PubMed1990

Congenital intestinal atresia.

Surgery for infants with intestinal atresia has evolved along with the development of specialized neonatal surgical units. This once fatal condition now carries a better than 85% chance of survival and an excellent long-term prognosis. Recent advances in bowel preservation techniques have reduced morbidity and improved gut function in both the long and the short term.

Anastomosis, Surgical↗
PubMed1975

The pathogenesis of intestinal atresia.

The records of 28 patients with duodenal and 31 with jejunoileal intestinal atresia or stenosis were studied. Vomiting and abdominal distention were the most prominent symptoms; an unusual colon may be present in jejunal as well as ileal obstruction and is not pathognomonic for ileal obstruction. Intestinal atresia is associated with a high incidence of preterm babies but with a low incidence of intrauterine growth retardation. Fifty-three infants were operated upon; the overall survival rate was 79 per cent. The high percentage of mortality in duodenal obstruction is due to associated malformations. Theories of the pathogenesis of intestinal atresia do not seem to fit current clinical and experimental evidence in all patients. Possibly, different factors play a role in separate situations.

Abnormalities, Multiple↗
PubMed1986

Intestinal atresia and stenosis: a review comparing its etiopathogenesis.

Two theories were proposed originally to describe the development of congenital intestinal atresia. The theory of imperfect recanalization, the theory of vascular insufficiency, and studies which have been performed to validate each of these theories were reviewed. Specific causes of the development of vascular insufficiencies in different species were reviewed if literature was available. In utero vascular accidents have been incriminated as the major cause of congenital intestinal atresia distal to the duodenum. There was relatively little evidence to show that intestinal atresia is inherited in any species. Duodenal atresia may be caused by either an embryologic defect for which there is some evidence of inheritance or by a vascular accident. The pathogenic mechanism for intestinal atresia may be similar in most species.

Animals↗