The Gastrointestinal Tract

The Gastrointestinal Tract

This system is a complex combination of organs whose function is to digest and absorb nutrients. Other function: Endocrine (pancreas)

The Gastrointestinal Tract

Embryology Alimentary canal is the folding of endoderm and splanchnic mesoderm at 3-4 wks. AOG The head of the yolk sac becomes the foregut and the caudal part of yolk sac becomes the hindgut The midgut remains in between the foregut and hindgut and remains within the yolk sac until it closes to form the digestive tube at 10th weeks.

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

Common symptoms of GI disorders

A. Vomiting This may be frequent during the neonatal period in the 1st few hours after birth They may vomit mucus or occasionally blood streaked. This is may be due to irritation of mucosa or swallowed materials during the delivery. If vomiting persists and is bile stained, GI disorders may be considered

Common symptoms of GI disorders

A. Vomiting Persistence of vomiting may mean GI obstruction, metabolic disorders or increased intracranial pressure A history of polyhydramnios suggests UGI obstruction. Bile stained emesis suggests obstruction beyond the duodenum

Common symptoms of GI disorders

B. Constipation More than 90% of term infants pass meconium in 24 HOL Possibility of obstruction maybe suspected if an infant does not pass meconium in 24-36 HOL. Differentials: intestinal atresia or stenosis: Hirschsprungs disease; meconium ileus; or meconium plugs. Constipation during the 1st month may be a sign of aganglionic megacolon; hypothyroidism or strictures from NEC

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

Pneumatosis intestinalis Portal venous gas

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

Omphalocele and 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

3. Duodenal Atresia/Stenosis - There is bilious vomiting within 24 HOL in

an otherwise stable infant with non distended abdomen - Plain radiograph: double bubble sign - Treatment: Surgery

double bubble sign

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