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Child with Altered Gastrointestinal Status Jan Bazner-Chandler CPNP, CNS, MSN, RN
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Developmental and Biologic Variances Suck and swallow reflex develops at 34 weeks Stomach capacity is 10-20 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
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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
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Prenatal History Birth weight Prematurity History of maternal infection Polyhydramnion
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Focused Health History Congenital anomalies Growth or feeding problems Travel Economic status Food preparation General hygiene Family history of allergies
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Present Illness Onset and duration of symptoms Weight loss or gain Recent changes in diet
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Vomiting Reflexive = infection or allergy Central = central nervous system head trauma meningitis CNS tumor
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Nursing Assessment Abdominal distention Abdominal circumference Abdominal pain Acute / diffuse / localized Abdominal assessment Inspect / auscultation / palpation / measure
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Measuring Abdominal Girth Bowden Text
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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
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Abdominal x-ray
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UGI Series with Barium 5-year-old s/p MVA Diagnosis: hematoma of duodenum Treatment: NG tube, IV fluids, electrolyte maintenance
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Diagnosis of appendicitis, tumors, abscess
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CT of liver with metastasis
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EndoscopyColonoscopy
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Stool Sample White blood cells Ova and Parasite Bacterial cultures Fecal fat Stool pH Rotazyme (rotovirus) Blood
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Blood Values Liver function tests: ALT, AST, GGT, ALP, ammonia levels Bilirubin direct and indirect Hepatitis antigens Total protein, albumin levels
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Treatments Endoscopy Surgical interventions Ostomy Nutritional therapy Modified diet Enteral nutrition
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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
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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
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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
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Cleft Lip and Palate Most common craniofacial anomaly Males 3 to 1 Higher in Asians Familial history Often diagnosed in utero by ultrasound
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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
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Feeding
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Cleft Lip Plasticsurgery.org
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Cleft Lip Repair Plasticsurgery.org
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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
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Arm Immobilizer
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Cleft Lip Repair
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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.
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Note disruption of tooth development in D. A. Cleft Lip B. Complex Cleft Lip C. Cleft Lip and palate
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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.
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Post Surgery Repair Position on side NPO for 48 hours Suction with bulb syringe only Avoid injury to palate with syringes, straws, cups etc.
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Long Term Referrals Hearing Speech Dental Psychological Team approach to care
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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)
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Esophageal Atresia
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Tracheal Esophageal Fistula TEF TEF results from failure of the trachea and esophagus to separate. Fistula
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Assessment- Prenatal Clinical manifestations may be noted prenatally History of polyhydramnios Stomach cannot be easily identified on ultrasound
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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.
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Diagnostic Tests Feeding tube is passed into the esophagus but resistance will be felt. Diagnosis confirmed by radiographs
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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
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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
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Esophageal Repair
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Long Term Complications 5 to 15% experience leaking at operative site. Aspiration Dysphagia / difficulty swallowing Stricture of esophagus Coughing Regurgitation
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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
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Hypertrophic Pyloric Stenosis Most common cause of gastric outlet obstruction in infants. More common in males 2 to 4 per 1,000 births
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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.
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Pyloric Stenosis
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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
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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
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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
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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
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