The etiology of gastrointestinal perforations in the newborn

Lloyd, James R.

doi:10.1016/0022-3468(69)90186-9

Cited by 254 publications

(69 citation statements)

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“…Before the realization that extreme prematurity, steroids and indomethacin were risk factors for SIP, the surgical literature contained reports of a congenital absence of the muscularis as the presumed etiology for intestinal perforations in near term infants. 5 As evidence for this hypothesis, previous authors had noted the same pathologic findings subsequently found in SIP of the ELBW infant. 6,7 Our ability to capture this subset of patients, who are significantly more likely to be male and seem to have perforations in transit out of the womb, reinvigorates the postulate that SIP can be acquired congenitally.…”

Section: Discussionmentioning

confidence: 62%

“…Before the improved survival of ELBW infants, SIP was thought to be a congenitally acquired disease that affects term and near term infants (old SIP). [5][6][7] These case reports described segmental absence of the muscularis in the distal intestine either as an isolated or multifocal process, with some infants having a single occurrence and others having recurrent presentations. The difference in presumed etiology between the old SIP and the new SIP has never been resolved but reports of the old SIP have declined in recent years.…”

Section: Introductionmentioning

confidence: 99%

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New insights into spontaneous intestinal perforation using a national data set: (2) two populations of patients with perforations

et al. 2006

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Background: Spontaneous intestinal perforation (SIP) is increasingly common in the premature infant and has been demonstrated to be associated with early postnatal administration of glucocorticoids and indomethacin. Before survival of the extremely low birth weight (ELBW) infant, SIP was thought to be a rare, congenitally acquired disease sporadically affecting the muscularis of the distal intestine. These disparate views of etiology have not been previously reconciled in the literature.Objectives: (1) To establish a cohort of SIP patients in a national data set. (2) To use timing of diagnosis as a unique data element and thereby differentiate between SIP cases which are susceptible to postnatal risk factors versus those occurring at or immediately after birth (and therefore not exposed to postnatal risk factors).Methods: A large deidentified national data set was used to retrospectively look at timing of diagnosis and then the cohort was divided into postnatal treatment groups for further subanalyses. This analysis resulted in the division of the cohort into early and late diagnosis SIP subcohorts. These were then queried retrospectively by univariate analysis to look for differences in demographics between the two (using a P-value < 0.05) Results: There were 633 patients with SIP evaluated in this data set. The early SIP cohort (0-3 days) was made up of 116 infants with a median BW of 1.401 kg, whereas the late cohort (4-14 days) held 386 infants with a median BW of 775 g. Infants with early SIP were significantly more likely to: be male, have higher Apgar scores, have not received antenatal steroids, surfactant or required mechanical ventilation.Conclusions: Two populations of infants acquire SIP: ELBW infants acquire SIP on average between 7 and 10 days of life after exposure to indomethacin and glucocorticoids (either endogenous or exogenous), and infants with early SIP (0-3 days) who are significantly less likely to have been exposed to postnatal risk factors and are less premature.

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Section: Discussionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

New insights into spontaneous intestinal perforation using a national data set: (2) two populations of patients with perforations

et al. 2006

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“…Death usually was caused by chemical or bacterial peritonitis. The gastric contents in the first 24 hr of life are highly acid, increasing the chance of inflammation (10,14).…”

Section: Materials and Methods Discussionmentioning

confidence: 99%

Spontaneous Rupture of the Stomach in the Newborn: Clinical and Experimental Evaluation

et al. 1976

Pediatr Res

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Extractwhen the infants were taking formula orally, the gastrostomy tubes were vented to a large coll~cting balloon aboveeach patient (15). o u r study presents an experimental model for studying gastric ~h~ air swallowed into the stomach was readily measured with this rupture in the newborn. w e showed that gastric rupture could be system (Fig. I ). Because spontaneous rupture usually occurs when produced in eight newborn rodents and in three puppies less than 10 an infant is supine (6), these infants were fed in this position, which days old after injection of 120 ml air at 100 mm Hg pressure in the also prevented eructation. Initially, the infants were fed standard rodents and ml air at 240 inin Hg pressure in the puppies. formula, but after two gastrostomy tubes partially obstructed, Gastric rupture occurred with animals supine and with approxi-they were fed with sugar water only. Larger volumes of air were mately 20 ml barium injected into the stomach. Positioning of the collected from this latter group.animal in the supine position permitted the barium to pool in the To explore Hood's theory (6). that the antrum acts as a "fluid antral-pyloric region of the stomach.trap." the following experiment was performed. After intramuscular anesthesia. a thin nasogastric tube was placed in either rats', Speculation guinea pigs', or puppies' stomachs under fluoroscopic control.we believe that spontaneous gastric rupture occurs as a result o f a With the animal supine, either standard infant formula or an pooling of liquid barium or food in the pylorus equivalent volume of thin (25%) barium sulfate suspension (appermits a physio~ogic outlet obstruction of the stomach. our proximately 20 ml in each instance) was instilled into the stomach.observations indicate that normal infants accumulate considerable The animal was positioned SO that the liquid ~o o l e d in the amounts of air in the stomach while feeding. the stomach antral-pyloric region (as checked fluoroscopically in the animals distends reflux of air into the esophagus is impeded by an air-fluid given the barium suspension). A "Y" connector was placed in the trap at the esophageal-gastric junction. Thus, our study suggests proximal end of the nasogastric tube. o n e end of the Y connector that increased intraluminal pressure the stomach is sufficient Was joined with a 50-cc syringe. permitting increments of air to be to cause gastric rupture in the newborn and that the fluidmair trap is introduced; the other end was connected to a gauge that measured an important mechaism in gastric rupture. pressure after each injection (Fig. 2). Eight rodents (five rats and three guinea pigs) and six puppies were used for this study. After this procedure the animals were Spontaneous rupture of the stomach characteristically occurs in autopsied and the stomachs examined. the first days of life as a linear tear high on the stomach wall. Since the original description by Siebold in 1825. there has been a great RESULTS

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“…This is the mostt acceptable 1heory of pathogenesis which is based on "the master switch of life" (Scholander,, 1963), and which occurs as a physiologic and protective mechanism in diving mammals and birds. This was emphasized by Lloyd (1969) as an important etiology of gastroi.ntestinal perforations of the newborn infant. The high incidence of infection found in NEC has been reported by many authors which is mostly caused by gram-negative microorganisms such as, Salmonella (Stein et al, 1972), Klebsiella (Hill et al,, and E. coli (Speer et al, 1976).…”

Section: Et!iology and Pathogenes·1smentioning

confidence: 99%

Neonatal Necrotizing Enterocolitis

Tjandra

2017

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Neonatal Necrotizing Enterocolitis (NEC) is a highly lethal disease of the newborn infant, which has aroused great interest in the past decades. It is characterized by ischemic necrosis of th'e intestinal wall, frequ®tly /'{fading to perforation and death. Unlike most neonatal emergencies, it is acquired and can be wccessfully treated without op,eration in most cas(!S.The etiology is still obscure and is considered to be multifactorial. Intesti11al ischemi.a, infections, cow's milk, and hyperosmolar

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The etiology of gastrointestinal perforations in the newborn

Cited by 254 publications

References 4 publications

New insights into spontaneous intestinal perforation using a national data set: (2) two populations of patients with perforations

New insights into spontaneous intestinal perforation using a national data set: (2) two populations of patients with perforations

Spontaneous Rupture of the Stomach in the Newborn: Clinical and Experimental Evaluation

Neonatal Necrotizing Enterocolitis

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