Unit 4 Peds GI Disorders

Commonalities between adults and pediatrics

Vomiting

Weight loss

Dehydration

Abdominal distention

Changes in stools

Pain

GOALS

Gaining weight/passing stool

Family dealing & developmental needs met

Significance of Pediatric GI Disorders

Growth and development issues

Daily Weight

Sucking needs

Growth and Development Issues (Significance?)

Reason: Time frame of major growth and development unlike adults who have already went through their pediatric phases

Daily Weight (Significance?)

Reason: For the calculation and maintenance of fluids

Sucking (Significance?)

Reason: For nutrition, helps soothe the infant, development of muscles necessary for speech development

Rehydration in Pediatrics

You can’t replace large amounts at once in kids; lead to fluid overload

NPO Infant

Provide a pacifier

Cleft Lip & Cleft Palate

Ingestion is affected when a infant/child has these.

Detected on a 20-week ultrasound.

The Primary Palate

Includes the medial portion of the upper lip and the portion of the alveolar ridge that contains the central and lateral incisors.

The Secondary Palate

Includes the remaining portion of the hard palate (palatine processes of the maxilla and the horizontal plates of the palatine bones and all of the soft palate

Cleft Lip

Corrected: 6 - 12 weeks (2 - 3 months) with Z Plasty

It can be unilateral or bilateral, partial or complete. 

The child has problems with feeding, swallowing, and speech.

Z Plasty

Several staggered suture lines to minimize notching from scar and lengthen lip.

Cleft Lip Causes/Occurence

Caused by genetic and environmental factors (teratogens) influence in embryo.

Normally, the lips form between 7 - 8 weeks of gestation, but instead the maxillary and premaxillary processes don’t fuse in early embryonic life.

Cleft Palate

Corrected: 12 - 18 months to allow for palate growth

Occurs midline and may involve soft and hard palates

Bifid Uvula

The mildest form of a cleft palate with essentially no functional impact on speech or feeding.

Cleft Palate Causes/Occurence

Caused by genetic and environmental factors (teratogens) influence in embryo.

Normally, the palate forms between 7 - 12 weeks of gestation

Palate Expander

Worn to aid in palate growth and to make surgery easier

Cleft Lip/Palate (Pre-Op)

Risk for failed attachment

Inefficient suck

Feed upright

CLEFT PALATE: feeds may leak through nose

Special nipples: feeding devices: HABERMAN, BRECK FEEDER

Frequent burping: swallow lots of air during feeding

Formula may be mixed with cereal or spoon fed

Breastfeeding is encouraged (for cleft lip infant 

Feed Upright

45 Degrees for both cleft lip and palate, really the typical way to feed an infant in general.

Be alert for signs and symptoms of aspiration.

Risk For Failed Attachment (Cleft Lip/Palate)

Parents need emotional support due to the disfigurement

Encourage expression of parental grief and fear

Emphasize positive aspects of the infant’s appearance and optimism regarding surgical correction, also acknowledge concerns from parents

La Leche League International/Cleft Palate Foundation Recommendation

Pump breast milk and provide it using adapted feeder

Skin to skin

After bottle feeding- Nonnutritive Sucking

Breck Feeder

A syringe with a feeding tube extension. Used when the child cannot suck and post operatively when lips must heal. Formula is put on back of tongue, tube should be long enough to extend back into the mouth. 

The cleft lip infant can’t suck for a week postoperatively.

Haberman Feeder

Activated by tongue & gum pressure rather than by sucking

Imitates the mechanics involved in breastfeeding

Feeding Rules For Cleft Lip

Start with clear fluids then to formula thru Breck feeder- Do not allow infant to suck on tubing.

Rinse mouth with water after feeding.

Good aseptic technique- clean suture line with Q tip as per protocol (usually normal saline and ABT ointment).

Feeding Rules For Cleft Palate

Position lying on abdomen post-operation to facilitate drainage of secretions

Use Elbow Restraints

Nothing allowed into mouth (pacifiers, bottles, utensils)

Fed with cup (sippy cup) can also use side of spoon at the side of the mouth

Diet: Clear to soft/blended

No jello or peanut butter; sticks to roof of mouth due to high sugar content

No hard foods

Clean mouth after feeding

Post-Op Cleft Lip/Palate

Elbow restraints- for both

Steri strips- for both

Logan’s bow- for cleft lip

Medicate for pain/sedation to prevent crying and other facial movements

Position on the back except for the older infant who’s post op for cleft palate and just finished feeding— HOB elevated or on side to allow drainage

No tummy time until healed

Elbow Restraints

On at all times to protect operative site from tension and trauma, but are removed one at a time so we can perform range of motion and do a skin check.

Done every 2 hours.

Skin Check

Every 2 hours

Steri Strips

Used to close and support minor cuts, surgical incisions, and other wounds by holding the wound edges together while they heal

Logan’s Bow

Thin metal bar taped to cheeks to prevent tension on suture line and is only for cleft lip because it simply protects the lips from injury.

Difficulty Breathing Post Op

Cleft palate infant- has to adjust through breathing through nose

Place in mist tent

Mist Tent

Provides a cool, moist environment to help children with respiratory conditions.

Atresia

Absence of a normal body opening

Fistula

Abnormal passage between 2 internal organs

Esophageal Atresia

Absence of a normal opening in the esophagus

Tracheal Esophageal Fistula

Congenital incorrect anatomy connects trachea & esophagus

Esophageal Atresia & Tracheoesophageal Fistula

Congenital incorrect anatomy connects trachea & esophogus

Esophagus fails to develop as a continuous passage

Failure of trachea & esophagus to separate

Esophageal Atresia with Tracheoesophageal Fistula (TEF) Clinical Manifestations

Excessive drooling & salivation

Cyanosis/apnea

Choking, coughing, sneezing

Fluids returning to nose & mouth during feeds

Increased respiratory distress after feeding

Abdominal distention due to air

Infant Drooling

Starts at 4 Months

3 C’s of Esophageal Atresia with Tracheoesophageal Fistula (TEF)

Cyanosis, choking, coughing

Diagnosis (Esophageal Atresia with Tracheoesophageal Fistula Clinical Manifestations)

Failure to Pass Nasogastric Tube

Tube meets resistance and can only be advanced minimally

Cannot aspirate stomach contents

Definitive dx by Fluoroscopy

Fluoroscopy

Surgical Repair (Esophageal Atresia with Tracheoesophageal Fistula)

Required- 2 Stages

1. Get rid of the fistula, then get older for step 2

2. Put the esophagus back and use part of the small intestine to connect it like normal

Prognosis is usually good

Repair may be staged depending on severity

Cervical Esophagostomy

Nursing Diagnosis (Esophageal Atresia with Tracheoesophageal Fistula)

Aspiration/airway clearance

Impaired swallowing

High risk: infection related to surgery

Altered family process RT defect

Differences with Tracheoesophageal Fistula with Atresia

Monitor airway: aspiration, oxygen

Prevent reflux: HOB elevated 30°

G tube: 2-3 days postop

Gentle suction: with premeasured & marked catheter to prevent trauma

Oral feeds: slowly, initiated at day 10 – after healed

Pyloric Stenosis

Narrowed pyloric sphincter

Pylorous

Junction of the stomach and duodenum

Clinical Manifestations of Pyloric Stenosis

Healthy infant begins to vomit

Progresses to projectile, non bile stained

Ravenous hunger

Palpable pyloric “tumor”

Peristaltic waves observed

Scanty stools

Weight loss

Dehydration

Metabolic alkalosis

Differences with Pyloric Stenosis

Post-op: NO NGT NORMALLY: monitor I & O

POSTOP VOMITING may be from edema & decreased peristalsis-REFEED specified amount to PREVENT ADHESIONS

FEEDINGS: Specific times & amounts:

Clear –½ strength– full

Burp well

Position right side with HOB elevated, infant seat

Diapers below the incision site

Cystic Fibrosis

The lungs, pancreas, and small intestine are impacted.

Caused by a mutation in the CFTR (cystic fibrosis transmembrane conductance regulator) gene. Development of thick, sticky mucus production, obstructing various

Cystic Fibrosis Gastrointestinal Overview

Generalized dysfunction of the exocrine (mucus producing) glands

Inherited autosomal-recessive trait

Mechanical obstruction occurs due to increased viscosity of mucus gland secretions

Passages in pancreas & bronchioles become obstructed (GI & Resp Systems)

Pancreatic ducts become blocked causing degeneration & fibrosis of pancreatic lobes

Pancreatic enzymes are prevented from reaching the duodenum: impairing digestion & absorption

UNABLE TO DIGEST FATS, PROTEINS & SOME SUGARS: excreted in stool

Median lifespan 37.4 years in the US

Normal Lung Function

Responsible for gas exchange, where oxygen enters the bloodstream, and carbon dioxide is expelled. This process occurs in the alveoli, which are kept clear by a thin layer of mucus to trap and eliminate pathogens and debris.

Lungs (Cystic Fibrosis)

Causes the mucus in the airways to become thick and sticky, leading to obstruction, chronic respiratory infections, and inflammation. The inability to clear mucus effectively results in frequent bacterial infections, bronchiectasis, and progressive damage

Normal Pancreas Function

Pancreas produces enzymes (lipase, amylase, proteases) that aid in the digestion of fats, carbohydrates, and proteins. It also regulates blood sugar levels by secreting insulin and glucagon

Pancreas (Cystic Fibrosis)

Blocked pancreatic ducts prevent enzymes from reaching the intestines. This leads to malabsorption of nutrients (especially fats and fat-soluble vitamins) and contributes to failure to thrive. Over time, damage to the pancreas can result in insulin-dependent diabetes due to loss of insulin-producing cells

Normal Liver Function

Processes nutrients, produces bile to aid in fat digestion, detoxifies substances, and stores glycogen. It also plays a role in blood clotting by producing clotting factors

Liver (Cystic Fibrosis)

Blocked bile ducts, leading to biliary cirrhosis and liver disease. This obstructs the normal flow of bile, which impairs fat digestion and absorption and may cause jaundice or liver scarring.

Small Intestines Functions

The intestines absorb nutrients from digested food and facilitate waste excretion. The normal mucosal lining secretes mucus to facilitate the passage of food and stool

Small Intestines (Cystic Fibrosis)

Blockages leading to conditions like meconium ileus in newborns or chronic constipation and bowel obstruction in older patients. Nutrient malabsorption occurs due to the lack of pancreatic enzyme secretion, resulting in poor growth and weight gain.

Cystic Fibrosis Risk Factors

Genetic mutation (CFTR gene)

Family history

Ethnicity:

Newborn (Issues with Cystic Fibrosis)

Meconium ileus: small intestine is blocked with meconium: abdominal distention, vomiting, failure to pass stools, dehydration

Fecal impaction & intussusception are common

Steatorrhea: large, frothy, foul smelling, fatty, loose stools

Voracious appetite: early in disease

Cystic Fibrosis Clinical Manifestations

Appetite: Loss of appetite – Failure to thrive, Anemia – growth stops----- later in disease

Protuberant abdomen: due to bulk of intestinal stool

Tissue wasting: thin extremities

Deficiency of fat soluble vitamins – ADEK

Prolapse of rectum: most common gastrointestinal adaptation

Pulmonary involvement possible: lungs fill with mucus the cilia cannot clear, air is trapped in small airways causing atelectasis, increased upper respiratory infections, decreased O2, hypercapnea & acidosis

Cystic Fibrosis Diagnostic Test

Sweat Test: Elevated sodium and chloride in sweat

Cystic Fibrosis Nursing Diagnoses

Altered nutrition

Altered G&D

Altered family process

Anticipatory grieving

Differences with Cystic Fibrosis

Diet : ↑calorie, protein, moderate fat

Pancreatic enzymes with food/formula: no hot food

↑ protein formula to infants

Monitor stools: SHOULD IMPROVE: Weight GAIN

SALT supplements PRN

Water soluble preps of fat soluble vitamins

? tube feedings/ supplements?

Emotional support

Celiac Disease

A disease of the proximal SI characterized by abnormal mucosa and intolerance to gluten (protein in wheat, rye, barley & oats)

Etiology- idiopathic, inherited predisposition, autoimmune

Previously believed to be a pediatric diease: symptoms present when cereal is introduced at 6-18 months

Diarrhea: steatorrhea

FTT: anorexia, vomiting, diarrhea

Celiac Disease Clinical Manifestations

Abdominal distention

Muscle wasting– buttocks, extremities

Vomiting

Deficiency of fat soluble vit (ADEK)

Behavioral changes: apathetic, fretful, irritable

Celiac Crisis

Acute, severe episodes of vomitting & diarrhea

Causes: infection, prolonged fasting, gluten ingestion, anticholinergic drugs

Rapidly causes fluid and electrolyte imbalance

Celiac Disease Planning & Implementation

PERMANENT GLUTEN FREE DIET

Increase calories, increase protein, simple CHO’s (fruits, vegetables), decrease fats.

Substitute rice and corn

Avoid high fiber during inflammation

Corticosteroids

Diet teaching: label reading

Stress permanence of disease

Comorbidities: Diabetes mellitus, thyroid, CA

Intussusception

Telescoping of one portion of the intestine into another

Intussuception Clinical Manifestations

Sudden onset

Pulls up legs, cries, inconsolable

Severe spasmodic abdominal pain

Distended abdomen * Vomiting

Currant- jelly stools

Palpable sausage-shaped mass: RUQ

Intussception Management

Hydrostatic pressure to push bowel back (air, barium enema)

Surgery if unsuccessful

Maintain F&E

ASSESS ALL STOOLS: normal brown stool-resolution has occurred- begin clear liquids

Parent education- infection, reoccurrence

Hirschsprung’s Disease

Also known as congenital aganglionic megacolon

Obstruction caused by inadequate motility in part of the intestine

RT absence of autonomic parasympathetic ganglion cells within the muscular wall of the rectum & proximal portion of large intestine (no peristalsis)

Accumulation of intestinal contents and distention of bowel proximal to defect

Hirschsprung’s Disease Clinical Manifestations

Neonate fails to pass meconium in 1st 24-48 hrs

Abdominal distention

Vomiting

Constipation & ribbon like stools

Palpable fecal mass

Poor appetite/Failure to thrive & Malnutrition & anemia in long-standing cases

Hirschsprung’s Disease Planning & Implementation

Diet: Decrease fiber, increase calorie, increase protein (keep stools soft)

TPN PRN

Enemas- colonic irrigations- saline only to prevent H20 intoxication

Abdominal girth

Monitor hydration status

Bowel prep- saline enemas, antibiotics, colonic irrigations with antibiotic solution

Routine post-op care

Colostomy/skin care

Teach parents – discharge planning

Imperforate Anus

Also known as anorectal malformation

Congenital malformation in which the outside opening of the rectum & location of the rectum are affected

3 categories, depending upon extent of rectal involvement

May have fistulas to urethra (male) or vagina (female)

No apparent rectal opening – small opening

No passage of meconium within 24-48 hrs

Meconium may be present abnormally in urine or vagina

Ribbonlike stools, abdomen distention with anal stenosis

Imperforate Anus Planning & Treatment

Depends on severity

Dilation alone may help stenosed opening

Surgery with temporary colostomy to rest bowel after reconstruction for 6-12 months

gentle daily dilations

No rectal temps

NGT to decompress stomach

Good anal & perineal care

Monitor stool patterns

Imperforate Anus Post OP Planning

Monitor vitals

Wound care – esp. around stoma

Monitor hydration status

Remove pressure from suture line: Side lying or prone with hips elevated, or supine with legs suspended at 90° to trunk

Teach parents – discharge planning