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Parts
A. Esophagus
Only portion of GIT that has neither digestive nor abortive function Serves only as a conduit between mouth and stomach that function to prevents reflex (gastroesophageal junction)
Parts
B. Stomach Permit complex mixing and churning movements that help begin the process of digestion C. Small intestine Major digestive and absorptive portion of GIT D. Colon Absorption of water and electrolytes The storage and elimination of feces
Meconium Syndrome
Meconium Plugs Believed to be related to colonic hypomotility Alternatively termed as functional inertia of prematurity or neonatal small left colon syndrome Usually seen among infants of diabetic mothers, maternal use of opiates and MgSO4, and among those with rectal aganglionosis Maybe evacuated by glycerin suppository or rectal irrigation with isotonic solution.
Meconium Syndrome
Meconium Ileus Usually associated with cystic fibrosis (CF) The absence of fetal pancreatic enzymes in CF limits normal digestive activities Usually concentrated in the lower part of ileum Clinically, maybe patterned to GI obstruction with/out perforation
Meconium Syndrome
Meconium Peritonitis Perforation of the intestine may occur in utero This causes meconium leakage into the peritoneal cavity Usually has calcification in abdominal x-ray Symptoms: abdominal distention, vomiting, absence of stools Treatment: elimination of intestinal obstruction and drainage of peritoneal cavity
Meconium Peritonitis-Calcification
Necrotizing Enterocolitis
Most common life threatening emergency in neonatal period Characterized by various degrees of mucosal and transmural necrosis Cause is multifactorial
Pathophysiology
1. Prematurity 90% or more occur in preterm infants The lower the gestational age and birth weight, the higher the risk for NEC Studies have shown that prematurity may alter multiple components of intestinal host defense, motility, blood flow, and inflammatory response that may contribute to intestinal injury resulting to NEC.
Pathophysiology
2. Enteral feeding Most cases of NEC occur after introduction of enteral alimentation among premature infants and low birthweight infants. Decreased NEC incidence:
Trophic or hypocaloric feeding with small volumes and slow rates of increase
Pathophysiology
2. Enteral feeding - Breastmilk - contains multiple bioactive factors: - secretory IgA - polyunsaturated fatty acid - leukocyte - epidermal growth factors - lactoferrin - platelet actively factor - lysozyme - macrophages - mucin
Pathophysiology
3. Intestinal Ischemia/Asphyxia Ischemia leads to intestinal necrosis Hypothesis: In period of stress, blood flow was diverted away from splanchnic circulation resulting to bowel injury
Pathophysiology
4. Bacterial Colonization Most cases occur endemically and demonstrate a variety of bacterial isolates (E. coli, Klebsiella, Clostridium, Staph epid) Blood culture is positive in 20-30% At birth, intestine is a sterile environment: This supports the importance of bacterial colonization
Pathophysiology
4. Bacterial Colonization Hypothesis:
Evidence suggests that bacterial cell wall products activate specific receptors on intestinal epithelium and activate the inflammatory cascade leading to intestinal injury
Diagnosis
Presents with:
Abdominal distention Gastric residuals/vomiting Lethargy Neutropenia/thrombocytopenia Guaiac (+) (stool occult)
Diagnosis
Stages (Modified Bell Staging)
Stage
I
Classification
Clinical Signs
Radiologic signs
Ileus/dilatation
Suspected NEC Abdominal distention Bloody stools Residual/vomiting Proven NEC Stage I + -Abdominal tenderness acidosis Thrombocytopenia Stage III + -Hypotension -Significant acidosis -DIC -Neutropenia/Thrombo
II
III
Advanced NEC
Stage II + Pneumoperitoneum
Pneumatosis Intestinalis
Treatment
No specific treatment Mostly supportive: Fluids/electrolyte Withhold feeding Antibiotics (gm (+), (-), anaerobes) Indication for surgery: perforation
Gastrointestinal Anomalies
A. Abdominal Wall Defects 1. Omphalocele - Results from failure in folding mechanisms that starts at about 5 weeks AOG. - The liver and small intestine usually occupy a portion of the sac with other abdominal contents. - Usually associated with a syndrome
Omphalocele
Gastrointestinal Anomalies
A. Abdominal Wall Defects 2. Gastroschisis - May involve a rupture of umbilical stalk during midgut herniation - There might be thromboembolic infarction of the developing abdominal wall. - sac is absent
Gastroschisis
Obstruction Lesions
1. Esophageal Atresia - vomiting occurs in the 1st feeding - drooling from the mouth - resistance is encountered upon OGT insertion
Obstruction Lesions
2. Malrotation and Midgut Volvolus - describe as an anomaly of intestinal fixation and rotation - at 6th-12th weeks AOG, bowel undergoes two independent 270 degrees counter clockwise rotation
- Vomiting is very common (bilious) - Dx: UGIS (volvolus: birds beak/corkscrew configuration) - malrotation: duodenal-jejunal junction and small intestine should be right of the midline
Obstruction Lesions
Treatment: Surgery
Obstruction Lesions
4. Hirschsprungs Disease - congenital intestinal aganglionosis - most common cause of intestinal obstruction in neonates - M:F = 3.4:1 - Presentation: - abdominal distention - vomiting - failure to pass meconium - rectal exam: (+) explosive stool
Obstruction Lesions
4. Hirschsprungs Disease - Diagnosis: - Biopsy: (+) aganglionosis and hypertrophy of nerve trunks - Treatment: Surgery