gastrointestinal disorders. embryonic development failure to fuse = cleft lip and palate failure to...

Gastrointestinal Disorders

Embryonic Development

Failure to fuse = cleft lip and palate

Failure to differentiate = duodenal stenosis

Atresia or abnormal closing of structure: Esophogeal atresia Anal-rectal malformation Biliary atresia

Fetal Development

Fistula is an abnormal connection

Tracheal esophageal fistula Anal-rectal malformations with fistula

Incomplete or abnormal placement Mal-rotation Diaphragmatic hernia

Prenatal History

Birth weight Prematurity History of maternal infection Polyhydramnios Down Syndrome

Health History

Congenital anomalies Growth or feeding problems 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 Fluid Gas Structural changes

Barium swallow or UGI Strictures Foreign body Motility disorder

Diagnostic Tests

Ultrasound Visualize organs Cysts Abscess appendicitis

CT scan = tumors, abscess, obstruction 24 hour probe = Gastro esophogeal reflux Biopsy of liver, esophagus, stomach, intestine

Stool and Blood

White blood cells Ova and Parasite Bacterial cultures Blood

Failure to Thrive

Inadequate growth resulting from inability

to obtain or use calories required for

growth.

Cleft Lip and Palate

Most common craniofacial anomaly 1 in 700 births 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

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Cleft Lip

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Post Surgery Care

Airway management Pain control Position in infant seat – upright position Elbow restraints Wound care as ordered by MD Minimizing crying Feeding techniques

Cleft Lip Repair

Cleft Palate

Cleft palate occurs when the palatine plates fail to migrate and fuse between the 7th and 12th week of gestation.

Diagnosed by looking into infants mouth.

Cleft Palate

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Cleft 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.

Palate Repair

Pre-surgery feeding Alternate nipple design

Breast feeding consultant

ESSR Enlarge / stimulate / swallow / rest

ESSR

TIP 18-2: Bowden Text

Devices For Feeding

Lamb’s nipple

Flanged nipple

Special nurser

Syringe with rubber tubing

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

Esophagus ends in a blind pouch.

Infant has a lot of mucous at birth.

The rationale for giving sterile water for the first feed.

E.A. Tracheo- esophageal Fistula

85 to 90% of defects

Failure of the esophagusto recanalize between 4th and 6th week of development.

Bowden Text

Esophageal atresia (or Oesophageal atresia) is a congenital medical condition (birth defect) which affects the alimentary tract.

It causes the esophagus to end in a blind-ended pouch rather than connecting normally to the stomach.

It comprises a variety of congenital anatomic defects that are caused by an abnormal embryological development of the esophagus. It is characterized anatomically by a congenital obstruction of the esophagus with interruption of the continuity of the esophageal wall.

Esophageal atresia (EA) is a birth defect in which part of your baby’s esophagus is missing. Instead of forming a tube between the mouth and the stomach, the esophagus grows in two separate segments that do not connect.

Children with esophageal atresia almost always have another birth defect called tracheoesophageal fistula, or TEF (a fistula is an abnormal connection). The esophagus and trachea should be two separate, unconnected tubes, but in TEF, they're connected.

There are four types of esophageal atresia:

Type A   The upper and lower segments of the esophagus end in

pouches, like dead-end streets that don’t connect. TEF is not present.

Type B The lower segment ends in a blind pouch. TEF is present on the upper segment. This type is very rare.

Type C The upper segment ends in a blind pouch. TEF is present on the lower segment. This is the most common type.

Type D TEF is present on both upper and lower segments. This is the rarest form of EA/TEF.

Clinical Manifestations

Excessive drooling / frothy mucus Inability to pass NG tube Choking and cyanosis with feeding High risk for aspiration of HCL from stomach

causing a chemical pneumonia.

X-ray Findings

Pre-surgery Care

NPO

Up in infant seat or HOB elevated

Continuous suction

G-tube to decompress stomach

Post Surgery Care

Post Operative Care

Respiratory support

Gastric decompression

Chest Tube

Gentle suctioning

TPN until taking PO’s

Antibiotics

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

Pyloric Stenosis

Ball & Bindler

Clinical Manifestations

Projectile vomiting Visible peristaltic waves Olive shape mass in the upper abdomen to

right of the midline Electrolyte imbalance

Management Pre-surgery

NPO / document any emesis

IV therapy / Correct electrolyte imbalance

Comfort infant and caretakers

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

Hernias

A hernia is a protrusion of an organ or

part of an organ through the wall of the

cavity in which it is contained.

Inguinal Hernia

Inguinal Hernia

Inguinal hernia is the most common congenital anomaly requiring surgical repair in infants: 80%

It is a protrusion of peritoneal sac into the processus vaginalis

Most common in males and pre-term infants.

Inguinal Hernia

Hydrocele

Hydrocele

Caused by peritoneal fluid communication with the scrotal area through a patent processus vaginalis.

Often will resolve on its own unless associated with an inguinal hernia.

Umbilical Hernia

More common in African

American infants.

Diaphragmatic Hernia

Congenital diaphragmatic hernia is the protrusion of abdominal contents into the chest cavity through a defect in the diaphragm.

1 in 5,000 births Mortality rate is 40 to 50%

Diaphragmatic Hernia

Clinical Manifestations

Chest appears barrel-like

Abdomen is sunken

Bowel sounds in chest

Breath sound decreased

Severe respiratory distress

Diaphragmatic Hernia

X-ray Diaphragmatic Hernia

Treatment

Ventilator support Chest tube Umbilical artery catheter NG tube Surgical correction when stable

Long Term Problems

Gastro Esophogeal Reflux

Respiratory infections

Obstructions

Abdominal Defects

Omphalocele

Gastroschisis

Intussusception

Telescoping of part of

intestine into an adjacent

distal portion.

History

Child appears with intermittent pain which is colicky, severe

Child will often draw legs up Episodes occur 2-3 times / hour Vomiting is prominent feature – bile stained

vomiting a late sign Bowel movements – bloody / mucous Classic current jelly stool is a late sign

Clinical Manifestation

Severe abdominal painInconsolable cryingDraw knees up Currant jelly-like stool is a late sign

Diagnostic X-ray

Management

Reduce the obstruction before the bowel becomes necrotic. Contrast Enema is diagnostic in 95% of cases

and therapeutic curative in most cases. Surgical reduction is radiologic reduction is not

achieved.

Surgical Intervention

IV fluids + antibiotics pre-operatively.

Manual reduction is attempted.

If bowel perforation is noted during operative procedure a temporary colostomy may be needed.

Hirschsprung Disease

Congenital abnormalitycaused by reducedmotility in colon.

Definition

Lack of ganglion cells in colon prevents

bowel from transmitting peristaltic

waves needed to move fecal material.

Clinical Manifestations

No meconium in the first 24 hours.

History of constipation or fecal mass.

Distended abdomen.

Diagnosis and Treatment

Rectal biopsy Removal of the aganglionic portion of the

colon. 1st stage surgery is often a colostomy 2nd stage is pull-through surgery to connect

the working colon to a point near the anus.

Typical X-ray

Colostomy at Birth

Pull-through Surgery

Surgery

Surgical repair done between 12 and 18 months

Long Term Complications

Anal stricture

Incontinence of stool

Short bowel syndrome

Appendicitis

Pathophysiology

Inflammation of the vermiform appendix.

Obstruction at base blocks outflow of mucus.

Pressure builds up

Blood vessels are compressed.

Perforation and rupture

Clinical Manifestations

Abdominal pain Generalized to localized Mc Burney’s point Rebound tenderness Loss of appetite Vomiting Low grade fever

Appendectomy

Appendectomy

Ruptured Appendix

Child developshigh fever aftera period of feelingbetter.

Perforation

Alert: With perforation of appendix, abdominal pain is suddenly relieved, but as peritonitis develops, it returns, along with signs of generalized acute abdomen.

Child will guard area of pain Abdominal distension High fever May appear dehydrated

Interventions for Perforation

Extra fluids may be needed – a bolus of normal saline

NG may be inserted to decompress the stomach

IV antibiotics prior to surgical procedure Fever control

Post Operative Care

NPO

IV therapy

IV Antibiotics

Nursing Interventions

Monitor I & O Assess for bowel sounds Dressing change as ordered Ambulate ! Ambulate ! Ambulate ! Cough and deep breath Pain Management

Inflammatory Bowel Disease

A virus or bacteria interacts with the body’s immune system to trigger an inflammatory reaction in the intestinal wall.

Inflammatory Bowel Disease

Refers to two chronic diseases that cause inflammation of the intestines. Ulcerative Colitis Crohn’s Disease

Causes

Most likely a genetic link that affects the immune system.

Ulcerative Colitis

Inflammatory disease of the large intestine. The inner lining or mucosa becomes inflamed, swells and ulcers develop.

Affects the lining of the bowel. Most severe in the rectal area and anus.

Crohn’s Disease

Differs from ulcerative colitis in the areas of the bowel affected.

Most often affects the small intestine and parts of the large intestine.

Inflammation that extends deeper into the layers of the intestinal wall than ulcerative colitis.

Clinical Manifestations

Diarrhea Rectal bleeding Abdominal pain Weight loss Anemia

Diagnostic Tests

Erythrocyte sedimentation rate ESR

Stool for gross or occult blood

Colonoscopy evaluation and biopsy

Genetic marker / family history

Drug Therapy

Corticosteroids during acute phase Mesalazine – anti-inflammatory drug for mild

to moderate cases. Immunosuppression drugs: Azathioprine,

methotrexate, 6-mercaptopurine Remicade has been approved in severe

cases

Long Term

Surgical removal of bowel if not managed by medical management.

Complications: Alteration in body image due to steroids Arthritis Osteoporosis Increase risk of colorectal cancer

Gastro-esophageal Reflux

GER

Incompetence oflower esophogealsphincter, whichallows return of stomachcontents into esophagus.

GER

Common condition involving regurgitation, or “spitting-up” which is the passive return of gastric contents retrograde into the esophagus.

Peaks between one to four months. Usually resolved by 12 months.

Clinical Manifestations GER

Regurgitation of formula after feeding No weight loss

Conservative Management GERPositioning: upright, semiprone after feeding to

promote gravity resistance to reflux

Dietary: thicken feedings

Feeding modifications: small feedings with frequent burping to decrease gastric distention

GERD: Gastro-esophageal Reflux Disease Infant older than 6 months, infant / child with

congenital or neurological problems. GER not relieved by simple measures. Clinical Manifestations: Regurgitation of feedings with slow growth /

poor weight gain Esophagitis = excessive crying Apnea / Respiratory problems Anemia

Diagnostic Work-up for GERD Upper GI series

Esophageal pH monitoring

Endoscopic exam

Pharmacologic Therapy

Medications to reduce symptoms including

antacids or histamine-2 blocking agents Histamine 2 blocker: cimetadine Reglan or metaclopramide to enhance gastric

emptying

Surgical Management: GERD

Fundoplication Pedisurg.com

Celiac Disease

Malabsorption caused by a permanent intolerance to dietary gluten.

1 in 3000 in USA 1 in 300 in European countries Genetic predisposition

Celiac Disease

Small villi lining

the intestine are

damaged by the

Body’s immune

system.

Celiac.com

Assessment

Chronic diarrhea Foul smelling, greasy stools Abdominal distention Anemia Muscle wasting

Management

Gluten free diet Limit the intake of wheat, barley, rye

containing foods

Management

Dietary Restrictions

Lactose Intolerance

Inability to digest significant amounts of lactose.

Lactose that is not broken down can cause abdominal distention and bloating.

Lactose tablets to help breakdown lactose containing foods.