Necrotizing Enterocolitis

Occurs primarily in preterm babies with gestational age <32 weeks and weight < 1500gm

Etiology

Secondary to bowel ischemia and immaturity, probable bacterial invasion and premature oral feeding. Perinatal stress. The immature distal small and sometimes large intestine has a decreased ability to absorb substrate leading to stasis. Stasis encourages bacterial proliferation, which leads to local infection. The ischemia and infection may lead to necrosis of the intestinal mucosa, followed by perforation, and subsequently gangrene of the gut wall, fluid loss, peritonitis, septicemia, and disseminated intravascular coagulation.

Symptoms

Increased gastric residuals with feeding, abdominal distention, bilious vomiting, lethargy, occult or gross rectal bleeding, fever, hypothermia, abdominal mass, oliguria, jaundice, apnea and bradycardia, and fever

Diagnosis

X-ray showing fixed dilated intestinal loops, pneumatosis intestinalis (air in the bowel wall), portal vein air (a sign of advanced disease), ascites, and pneumoperitoneum

Management

Medical Management

Initial it is advisable to attempt medical mgt with cessation of oral intake, antibiotics, fluid and electrolytes, orogastric tube, and hemodynamic support before any surgical interventions

Surgical Management

If unresponsive to medical treatment, then an explorative laparotomy is needed to remove the gangrenous bowel and create an ileostomy

Preoperative Considerations

Surgical Time

1-2.5 hrs

EBL

10-100 mL

Mortality

20-25%

Morbidity

Respiratory failure, sepsis, stricture, intracranial hemorrhage

Pain Score

6-7

Pain Management

Morphine 0.05-0.1 mg/kg/IV q 1-2 hrs

Anesthetic considerations

Respiratory

Pulmonary insufficiency r/t prematurity - respiratory distress syndrome

Cardiovascular

Cardiac anomalies may need hemodynamic support – inotropes (dopamine)

Neurological

Intraventricular hemorrhage may be secondary to prematurity or birth asphyxia

This causes impaired autoregulation, and significant variations in BP (20-30 mmHg) can aggravate ischemia or cause hemorrhage

Renal

The presence of patent PDA and treatment with NSAIDs can lead to impaired renal perfusion (prostaglandins inhibited and thus less vasodilation in kidneys)

Other factors are aminoglycoside antibiotics, sepsis, and CHF

Metabolic

Metabolic acidosis secondary to sepsis and/or CHF will worsen cardiac function

Hematologic

DIC, thrombocytopenia, and anemia may be present

Hypothermia

Labs: ABG, Hb, glucose, electrolytes, coagulation profile

Anesthesia

GETA

Warm room and warming pad on OR table

Air/O₂ to maintain SpO₂ 92-94% (minimize the risk of retinopathy)

Correct hypovolemia – due to third spacing – albumin 5% (10 mL/kg/IV)

Warm fluids

Crystalloid >100 mL/kg/IV is not uncommon

Neonates may be fluid restricted in NICU to lessen incidents of PDA (this will cause R to L shunt)

IV access – a-line, and preferably a CVP

Atropine 0.02 mg/kg pre laryngoscopy – minimum dose 0.1 mg to avoid paradoxical slowing in the sinoatrial node

Need muscle relaxant and opioid - note issue with Succinylcholine due to hyperkalemia from dead bowel

Ketamine and opioid anesthesia

Avoid inhalational agents due to myocardial depressant effect

Continue 10% dextrose infusion from NICU to avoid hypoglycemia

Blood products if Hct below 30-35%

Have blood replacement ready in the room

The patient is transported to NICU, usually on the ventilator

Some develop short gut syndrome

• A malabsorption syndrome due to surgical removal of the small intestine