Child with Altered Gastrointestinal Status Jan Bazner-Chandler CPNP, CNS, MSN, RN

Developmental and Biologic Variances Suck and swallow reflex develops at 34 weeks Stomach capacity is mL in the infant up to 3 liters by adolescence Coordinated oral pharyngeal movements necessary to swallow solids develops after age 2 months Stool frequency is highest in infancy Control of stool is achieved by 18 months to 4 years

Developmental and Biologic Variances Liver edge is palpable 1-2 cm in infants and young children Abdominal distension can cause respiratory distress Pancreatic amylase secretion does not begin until age 4 months

Prenatal History Birth weight Prematurity History of maternal infection Polyhydramnion

Focused Health History Congenital anomalies Growth or feeding problems Travel Economic status Food preparation General hygiene Family history of allergies

Present Illness Onset and duration of symptoms Weight loss or gain Recent changes in diet

Vomiting  Reflexive = infection or allergy  Central = central nervous system head trauma meningitis CNS tumor

Nursing Assessment Abdominal distention  Abdominal circumference Abdominal pain  Acute / diffuse / localized Abdominal assessment  Inspect / auscultation / palpation / measure

Measuring Abdominal Girth Bowden Text

Diagnostic Tests Flat plate of abdomen Upper Gastrointestinal series (UGI) Barium swallow / enema Gastric emptying study Abdominal ultrasound CT scan with or without contrast MRI Endoscopy

Abdominal x-ray

UGI Series with Barium 5-year-old s/p MVA Diagnosis: hematoma of duodenum Treatment: NG tube, IV fluids, electrolyte maintenance

Diagnosis of appendicitis, tumors, abscess

CT of liver with metastasis

EndoscopyColonoscopy

Stool Sample White blood cells Ova and Parasite Bacterial cultures Fecal fat Stool pH Rotazyme (rotovirus) Blood

Blood Values Liver function tests: ALT, AST, GGT, ALP, ammonia levels Bilirubin direct and indirect Hepatitis antigens Total protein, albumin levels

Treatments Endoscopy Surgical interventions Ostomy Nutritional therapy Modified diet Enteral nutrition

Failure to Thrive Inadequate growth resulting from inability to obtain or use calories required for growth. FTT is failure to grow at a rate consistent with standards for infants and toddlers younger than 3 years of age. Symptom – not a diagnosis

FTT Organic  Physical cause identified: heart defect, GER, renal insufficiency, malabsorption, endocrine disease, cystic fibrosis, AIDS. Non-organic  Inadequate intake of calories  Disturbed mother-infant bonding  No associated medical condition

Interdisciplinary Interventions If no medical cause is found focus of care is on environmental / developmental / behavioral cause Occupational therapy to determine infant ability to suck / swallow Observation of infant / caretaker interaction Calorie count to determine actual calories consumed Monitoring of height / weight / HC

Cleft Lip and Palate Most common craniofacial anomaly Males 3 to 1 Higher in Asians Familial history Often diagnosed in utero by ultrasound

Cleft Lip Incomplete fusion of the primitive oral cavity Obvious at birth Infant may have problems with sucking Surgery in 2 to 3 months Goals of surgery Close the defect Symmetrical appearance of face

Feeding

Cleft Lip Plasticsurgery.org

Cleft Lip Repair Plasticsurgery.org

Post Surgery Care Airway management Pain control / minimize crying Position with HOB elevated 30 degrees Elbow immobilizers Suture line care as ordered by MD  Cleanse with saline or dilute hydrogen peroxide to remove crusts and minimize scarring

Arm Immobilizer

Cleft Lip Repair

Cleft Palate Cleft palate occurs when the palatine plates fail to migrate and fuse between the 7 th and 12 th week of gestation. Diagnosed by looking into infants mouth.

Note disruption of tooth development in D. A. Cleft Lip B. Complex Cleft Lip C. Cleft Lip and palate

Cleft Palate Repair Babies should be weaned from bottle or breast prior to the surgical procedure. Done around 1 year of age after teeth have erupted and before the child is talking to promote better speech outcomes Poor speech outcomes if done after 3 years of age.

Post Surgery Repair Position on side NPO for 48 hours Suction with bulb syringe only Avoid injury to palate with syringes, straws, cups etc.

Long Term Referrals Hearing Speech Dental Psychological Team approach to care

Esophageal Atresia EA Congenital anomaly that results from failure of the esophagus to develop normally. The proximal esophagus ends in a blind pouch instead of communicating with the stomach. EA is often associated with a tracheal esophageal fistula (TEF)

Esophageal Atresia

Tracheal Esophageal Fistula TEF TEF results from failure of the trachea and esophagus to separate. Fistula

Assessment- Prenatal Clinical manifestations may be noted prenatally  History of polyhydramnios  Stomach cannot be easily identified on ultrasound

Assessment at Birth CaREminder: Excessive drooling of saliva may be first symptom of TEF. When fed, the infant sucks well but then chokes and coughs as the feeding enters the lungs.

Diagnostic Tests Feeding tube is passed into the esophagus but resistance will be felt. Diagnosis confirmed by radiographs

Interdisciplinary Interventions Pre-surgery Care Sump catheter in upper esophageal pouch to provide continuous suction of pooled secretions Gastrostomy may be performed to provide gastric decompression Respiratory support Antibiotics for aspiration pneumonia

Interdisciplinary Interventions Repair done within 24 to 72 if infants condition is stable Done through a thoracotomy or thoracoscopic repair Antibiotics Acid suppression therapy Chest tube, gastric decompression and continued respiratory support TPN

Esophageal Repair

Long Term Complications 5 to 15% experience leaking at operative site. Aspiration Dysphagia / difficulty swallowing Stricture of esophagus  Coughing  Regurgitation

Pyloric Stenosis Most common cause of gastric outlet obstruction in infants. 1 in 500 More common in males 3 weeks to 2 months of age History of regurgitation and non-bilious vomiting shortly after feeding. Vomiting becomes projectile

Hypertrophic Pyloric Stenosis Most common cause of gastric outlet obstruction in infants. More common in males 2 to 4 per 1,000 births

Pathophysiology Hypertrophy and hyperplasia of the circular smooth muscle of the pylorus of the stomach. The lumen of the pylorus narrows and lengthens and the gastric outlet is progressively obstructed.

Pyloric Stenosis

Assessment History of regurgitation and nonbilious vomiting during or shortly after feeding. Within a week vomiting becomes projectile Olive shape mass in the upper abdomen to right of the midline Weight loss and FTT Because of persistent vomiting will often present with dehydration

Interdisciplinary Interventions Initial goal of therapy is to correct any fluid and electrolyte imbalance NPO / NG tube insertion to empty and decompress stomach Comfort infant and caretakers

Interdisciplinary Interventions After fluid and electrolyte balance is re- established surgery is the definitive treament. Postoperative care:  IV fluids  Oral feeding Starting with small amounts of pedialyte Advance to full formula feedings as tolerated

Feeding Post-operatively Give 10 ml oral electrolyte solution after recovered from anesthesia Start pyloric re-feeding protocol. Increase feeding volumes from clear fluids to dilute to full-strength formula. Keep feeding record Assess for vomiting Discharged when taking full-strength formula