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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
Plasticsurgery.org
Cleft Lip
Plasticsurgery.org
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
Pedisurg.com
Cleft Palate
Pedisurg.com
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.