quiz spontaneous intestinal perforation

[Ahmed Nabil]

You are consulted on a 10-day old 900-gm premature infant who has suddenly developed intraperitoneal free air. There is no obvious pneumatosis intestinalis on recent imaging studies.

Factors associated with spontaneous intestinal perforation include all of the following except

A early postnatal indomethacin

B early postnatal steroids

C maternal drug use

D Staphylococcus epidermidis

E Candida

[Admin]

C

correct

Spontaneous, or focal, intestinal perforation (SIP or FIP) occurs primarily in premature infants with very low birth weight (VLBW, birth weight less than 1500 g) and extremely low birth weight (ELBW, birth weight less than 1000 g). SIP is generally believed to be a separate clinical entity from necrotizing enterocolitis. A number of risk factors have been identified including early postnatal indomethacin, steroids and the synergistic effect of both together. Although it is not clear whether enteral Staphylococcus epidermidis and Candida are causative agents, their presence in peritoneal cultures is high. Chorioamnionitis has also recently been identified as a risk factor for SIP.

Animal models of SIP suggest that risk factors converge on a collection of signaling pathways - nitric oxide synthases (NOS), insulin like growth factors and epidermal growth factors. Many of these factors skew trophism of the ileum - defined as thinning of the submucosa concomitant with hyperplasia of the muscosa. Global depletion of NOS is associated with disturbed intestinal motility and diminished transforming growth factor alpha in the muscularis externa. This constellation of insults seems to make the distal intestine vulnerable to perforation during recovery of motility. There is also evidence that congenital or acquired ischemia induces absence of intestinal muscularis.

There is no evidence that suggests that maternal drug abuse is associated with SIP.

[Sharon]

C

[Basma Waseem]

D

[Admin]

C

correct

Spontaneous, or focal, intestinal perforation (SIP or FIP) occurs primarily in premature infants with very low birth weight (VLBW, birth weight less than 1500 g) and extremely low birth weight (ELBW, birth weight less than 1000 g). SIP is generally believed to be a separate clinical entity from necrotizing enterocolitis. A number of risk factors have been identified including early postnatal indomethacin, steroids and the synergistic effect of both together. Although it is not clear whether enteral Staphylococcus epidermidis and Candida are causative agents, their presence in peritoneal cultures is high. Chorioamnionitis has also recently been identified as a risk factor for SIP.

Animal models of SIP suggest that risk factors converge on a collection of signaling pathways - nitric oxide synthases (NOS), insulin like growth factors and epidermal growth factors. Many of these factors skew trophism of the ileum - defined as thinning of the submucosa concomitant with hyperplasia of the muscosa. Global depletion of NOS is associated with disturbed intestinal motility and diminished transforming growth factor alpha in the muscularis externa. This constellation of insults seems to make the distal intestine vulnerable to perforation during recovery of motility. There is also evidence that congenital or acquired ischemia induces absence of intestinal muscularis.

There is no evidence that suggests that maternal drug abuse is associated with SIP.