gastrointestinal disorder

GASTROINTESTINAL DISORDER

ISLAMIC University Nursing College

Gastrointestinal Tract

GI tract consists of a hollow muscular tube starting from the oral cavity, going through the rectum and is ended at the anus, where food is expelled.

Main function GI is turning food into nutrients which can be absorbed by the human body to provide energy needed for survival

Accessory organs that assist the tract by secreting enzymes to help break down food into its component nutrients (salivary glands, liver, pancreas and gall bladder)

Gastrointestinal Tract: Assessment

Health history Gestational age and birth weight. Nutritional history (length of BF, introduction of solid

food). Neonatal & infancy GI problems. Family factors (life style, hereditary problems. present changes in child’s life (start schooling, new

sibling or death in the family) Assessment of the digestive function in a 24hr (food

intake and elimination)

Gastrointestinal Tract: Physical Exam

physical parameter (Wt and Ht) Skin Color Inspection of oral cavity S & S of dehydration Abdominal and rectal assessment

PeristalsisAbdominal Tenderness Distended abdomen

Displaced heart (diaphragmatic hernia) Hair (loss of pigment or brittle)

Gastrointestinal Tract: Problems

Regurgitation(spitting-up) Vomiting.

Mechanical due to obstruction Reflexive due to infection or allergy Central due to CNS involvement (meningitis) or

sepsis Vomitous assessment includes:

Onset & frequencyQuantityDegree of forcefulness Presence of bile


Abdominal distention may be due to: Accumulation of fluid or gases

Congenital malformation

Constipation

Hernia

GI perforation

Cirrhosis Abdominal pain


Diarrhea Acute due to:

Infection.Stress.Drug reaction.

Chronic due to:Chronic infectionMalabsorptionObstruction inflammatory bowel disease.


Assessment of Diarrhea

Onset

Frequency Consistency & Quantity Odor, presence of blood mucus Combining factors (food, medication ..etc)

Gastrointestinal Tract: Diagnostic tests

CBC, ESR, Electrolytes Liver enzymes Pancreatic enzymes (amylase) Bilirubin Serum ammonia Stool testes

Stool culture/occult blood Stool fat Stool pH

Gastrointestinal Tract: Diagnostic procedures

Gastric Analysis Specimen is taken using NG tube pt should be NPO after midnight Stomach contents are examined for:

Hydrochloric acidOccult bloodMalignant cellsBacteria/parasites


Barium Swallow

Visualize esophagus, stomach and duodenum in upright position behind fluoroscopic screen

Pt should be NPO after midnight

Post-careEncourage fluid intake to prevent constipationWhite stools up to 72 hrs


Barium enema Examining rectum and colon Assist in the diagnosis of

Tumor PolypsDefects associated with

Crohn’s and ulcerative colitis diseases

PreparationWater enema to clear colon

and rectumNPO


Endoscopy Visualize the

upper and lower GI by fiberoptic

tube.


Colonoscopy Visualize large intestine Diagnosis of

constipation/diarrhea, anorexia, rectal bleeding, pain, polyps and tumors

Preparation NPO (8 hrs) Laxative a few days prior Enema the night before the

procedure Post

Cramps due to air in the colon Abdominal distention, bleeding

Gastrointestinal Tract: Nursing Care

Monitoring Caloric intake Daily wt Abdominal girth Intake and output Stool chart

Help family for lifetime adjustment to the disease by; Encouraging early family involvement in child’s care Educating family about the consequence of GI

alteration on child’s health and life style ( decrease oral gratification and availability of energy for mobility

GI Disorders

Anomalies &

Obstruction

Reflux Malabsorption &

Inflammatory Bowel Disease

Error of Metabolism

Anomalies & Obstruction

Pyloric Stenosi

sIntussuscepti

on Cleft lip & Cleft Palate

Hirschsprung’s Disease

Cleft Lip & Cleft Palate

Incomplete fusion of the embryonic structure surrounding the primitive oral cavity

Among the most common facial anomalies

Genetic basis is present (family history for presence of the defect in other siblings)

Incidence rate of cleft lip is 1:7800 Incidence rate of cleft palate alone in 1:2000 May result in communication between the nasal and

oral cavities


Cleft lip may be unilateral or bilateral

Cleft lip may be accompanied with cleft palate

Cleft palate may be present without cleft lip (non-visible): early sign is dripping milk from nose


Assessment should be focused on;

In newborn: compromised sucking ability

Respiratory status Family reaction


Management Surgical repair for cleft lip during

the first few weeks of life

Initial repair for cleft palate during 4-6 months of age and the surgical correction between 6-18 months


Nursing care Provide

adequate nutrition and prevent aspiration and infection (otitis media)

During feeding Upright positionFeed slowlyBurp frequently


After the surgical operation Restrains may be necessary to prevent

disturbance of the surgical site No straws, tooth brushing Prevent infection follow-up assessment of

GrowthSpeechTeeth development


Complications

Makes sucking weaker: altered nutrition

Speech difficulties May affect development of teeth and

jaw Affect the bite More frequent ear infection


Nursing diagnosis: Altered nutrition related to physical

defect / difficulty eating Risk for aspiration Risk for infection Risk for impaired verbal

communication Altered family process

Hypertrophic Pyloric Stenosis


An overgrowth of the circular muscle of the pylorus, results in obstruction/ partially / narrowing of the pyloric sphincter

Cause is unknown, however there is a hereditary component

The stomach contractions increase in frequency and force to empty the stomach content.


Usually develops in the first few weeks of life Clinical Manifestation:

Regurgitation small amounts of milk immediately after feeding.

Projectile vomiting. Vomiting may occur during feeding or shortly

after feeding Vomitus contain NO bile Gastritis due to prolonged stay of stomach

content Wt loss and dehydration Metabolic alkalosis Failure to thrive


Assessment Olive-like mass at right epigastrium

under the edge of the liver. Peristaltic waves can be noted after

feeding moving from left to right. Ultrasoundgraphy.

Treatment is by surgery: to allow better passage of milk.


Nursing diagnosis: Fluid volume deficit.

Nursing Care:Monitor intake and output.Assess vomitus.Prevent dehydration.Monitor Wt and Ht.

Intussusception

Intussusception

Is an invagination of part of the intestine into an adjacentdistal portion of the intestine.

Occurs in healthy infants around 6 months of age and rarely occur before 3 months or after 3-years of age

More common in male infants The cause is unknown. The most common type is near the ileocecal

valve pushing into the cecum and onto the colon.

Intussusception

The involved intestine become inflamed and edematous with bleeding from the mucosa

Untreated intussusception can lead to intestinal gangrene, peritonitis and death

Diagnosis by barium enema ( if there is intraperitoneal air from a bowel perforation thus enema is contraindicated)

Intussusception

Assessment is focused on:

Stool inspection (currant-jelly stools)

CM such as Pain Abdominal palpation

Intussusception

Early symptoms Crampy abdominal pain and a drawing up of the knees to the

chest periods of apathy Poor feeding and vomiting

Late symptoms Worsening vomiting, becoming bilious Abdominal distension/ Palpable abd. Mass (sausage-shaped) Heme positive stools Followed by “currant jelly” stools: Jelly stools due to leaking

of blood and mucus into the intestinal lumen as a result of venous engorgement

Dehydration If untreated, necrosis and perforation are possible

Intussusception

Treatment

Supportive therapy (Fluid; Antibiotics)

Hydrostatic barium

Operation ManualResection and reanastamosis

Hirschsprung’s Disease (aganglionic megacolon)

A congenital anomaly resulting from an absence of ganglion cells in the colon (lack of nerve ending in the sigmoid colon)

Autosomal dominant genetic mutataions

More common in male & children with down syndrome

peristalsis can not occur


CM Newborn:

failure to pass meconium after birth (during the firs t 24 hr)

Poor feeding and spitting up Visible bowel loops Bile-stained vomitus Abdominal distention

Infancy Failure to thrive Constipation & Abdominal distention Diarrhea & vomiting/ Explosive watery stool fever


CM Childhood (more chronic:

constipation Ribbon-like & foul smelling stools Abdominal distention Palpable fecal masses Poorly nourished Lethargy, nausea and anorexia

Treatment by surgery (removal of non-motile part) Colostomy/ileostomy care after surgery After surgery high fiber diet is established Prevent enterocolitis

GI Disorders

Anomalies &

Obstruction

Reflux Malabsorption &

Inflammatory Bowel Disease

Error of Metabolism

Celiac Disease

Celiac Disease

A disease of malabsorption & abnormal immune reaction to gluten

Celiac disease is a hereditary intolerance of gluten (protein found in wheat, barely, oats, rye)

Gluten protein (gliadin) causes inflammation and damages villi in the small bowel Enzyme insufficiency (peptidase) causes

accumulation of toxic gluten peptide Gluten toxicity results from alteration in

immunologic response It is the second cause of malabsorption

after CF

Celiac Disease

CM (related to malabsorption and malnutrition) Problem starts after the introduction of solid food Diarrhea; Steatorrhea (stool is bulky, fatty foul

smelling) Wt loss (due to poor absorption of protein, CHD,

vit and iron) Weakness; Abdominal pain & distention Bone & joint pain Anemia (malabsorption of iron) Vit. Deficiency Failure to thrive ( without S&S of GI problems) Behavioral changes: irritability, apathy and

uncooperative

Celiac Disease

Assessment Family history Child’s dietary history

Diagnostic test anti-tissue transglutaminase antibodies (tTGA)

or anti-endomysium antibodies (EMA). Malabsorption test CBC Biopsy of jejunal (atrophy of villi) Serum protein & immunoglobulin decreased

Celiac Disease

Dietary management a gluten-free diet

In acute phase; corticosteroid fluid replacement N/G to decrease the

distention

Celiac Disease Family education:

Diet regimen: free of wheat and barley

Monitor growth and development Complications (if not treated)

Iron deficiency anemiaOsteoporosisinfertility or recurrent miscarriagedepression or anxietytingling numbness in the hands and feetseizures

Inflammatory bowel diseases: Ulcerative colitis & Crohn’s

disease Inflammatory bowel disease (IBD) refers to

chronic conditions that cause inflammation in some part of the intestines.

The intestinal walls become swollen, inflamed, and develop ulcers

IBD can cause discomfort and serious digestive problems

Symptoms depend on which part of the digestive tract is involved

Causes of the inflammation in IBD involves a complex interaction of several factors:

the genes the patient has inherited, the environment and the immune system.

antigens in the environment may cause of the inflammation or they may stimulate the body's defenses to produce inflammation


disease

Symptoms of IBD The symptoms of ulcerative colitis and

Crohn's disease are similar: Abdominal pain or cramping Diarrhea multiple times per day Bloody stools Weight loss Mouth sores and skin problems Arthritis Eye problems that affect vision


disease

Crohn's Disease is characterized by a chronic inflammatory process that may affect any segment of the gastrointestinal tract, from mouth to anus.

The inflammatory process usually extends through all layers of the intestinal wall

Skip lesions Treated by medication to decrease

inflammation and usually control the symptoms but does not provide a cure

Inflammatory bowel diseases: Crohn’s disease

Ulcerative Colitis is characterized by continuous inflammation confined to the large intestine.

Inflammation is limited primarily to the mucosa and does not extend through all layers.

Treated by; The primary treatment options are medications that

decrease the abnormal inflammation in the colon lining and control the symptoms..

Ulcerative colitis is potentially curable if the colon is removed

Inflammatory bowel diseases: Ulcerative colitis

Inborn errors of metabolism55

GalactosemiaPhenylketonuriaCongenital hypothyroidism

Inborn errors of metabolism56

Clinical manifestations Neurological symptoms ( lethargy, poor feeding, vomiting

and irritability) In severe cases coma, seizureUnexplained metabolic acidosisEpisodes of hypoglycemia/ hyperglycemia, ketonuriaHeart failureLiver diseaseDysmorphic featuresDevelopmental delay

Inborn error of metabolism: Galactosemia

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Lack of galactose-1-phosphate uridyl-transferase enzyme. Inherited as autosomal recessive. Failure of conversion of galactose to glucose,

accumulation of galactose leads to damage of the liver & brain.

Should be suspected in any infant who vomits, refuses feeds, fails to thrive & become jaundiced in the first week

Long term effect: ovaries damage, speech delay, learning difficulties

Treatment may include stopping BF & replacement by a special low-lactose milk.

Inborn error of metabolism: Phenylketonuria

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autosomal recessive genetic disorder causing mutation of the gene that producing phenylalanine hydroxylase enzyme that is necessary to metabolize the amino acid phenylalanine to tyrosine.

Phenylalanine is converted into phenylketone which is detected in the urine

the disease may present clinically with Seizures excessively fair hair and skin "musty odor" to the baby's sweat and urine


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Early cases of PKU were treated with a low-phenylalanine diet. Children with PKU must adhere to a special diet

low in Phe for optimal brain development. The diet requires severely restricting or eliminating

foods high in Phe, such as meat, chicken, fish, eggs, nuts, cheese, milk & dairy products.

If PKU is left untreated, it can cause problems with brain development, including mental retardation, brain damage and seizures.


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Gastroesophageal Reflux

Back flow of the gastric content to the esophagus

It becomes Gastroesophageal Reflux Disease (GERD) when it is associated with complications such as FTT, bleeding and dysphagia

GER is caused by dysfunction of the lower esophageal sphincter

(LES) Delay in gastric emptying Poor clearance of esophageal acid Susceptibility of esophageal mucosa to acid injury


Factors may cause variation in the pressure of the lower esophageal sphincter (LES)

Increased volume (after meal)

Position ( bending/lying)

Delay in gastric emptying

Increased gastric pressure (coughing, obesity, tight clothing)

CNS disease hernia


Children at risk of GER Premature infants Bronchopulmonary dysplasia Children with tracheoesophageal/esophageal atresia repair Asthma, CF; CNS disorder /CP

CM Regurgitation Heartburn after meals (bending) Sore throat with hoarseness Bronchospasm and laryngospasm Poor Wt gain Heme-positive emesis/stool


Diagnostic test 24-hour pH monitoring Barium swallow Upper endoscopy

Management Medication:

antiacids; maalox0 H2 receptor blocker ; decrease acid production

(ranitidine) Reduce gastric secretion ( omeprazole (prilosec)) Pro-motility agent (metoclopramide( reglan))


Diet modifications Eliminate acid food (citrus juice, tomatoes, carbonated

fluid) Avoid food that relax esophageal sphincter (fatty foods,

peppermint, chocolate) thickened formula & Small meals Elevate the head of the bed when sleeping (infant in prone

position)

Avoid feeding at bedtime Wear loss cloth Maintain ideal body weight Surgery to tighten the lower esophageal sphincter

Appendicitis Inflammation of the appendix

Caused by an obstruction. Fecalith (hard feces) Lymphoid obstruction Infection

Swelling of the appendix reduces blood flow causing

Ischemia necrosis

Perforation (rupture) may occur which may cause peritonitis, sepsis or abscess

Appendicitis

CM PAIN (pain is the first sign)

starts around the belly and moves to the lower right quadrant of the abdomen

Right lower quadrant localized tenderness Right lower quadrant rebound tenderness

fever, nausea, vomiting & diarrhea WBC over 15,000 Elevated C-reactive protein

Appendicitis

CM In neonate (non specific)

Irritability/ lethargy Abdominal distention & abdominal mass Vomiting

In infants and older children Vomiting & diarrhea; Pain & fever

Appendicitis

S & S of appendix perforation Fever Sudden relief from pain Subsequent increase in pain and rigidity

guarding of the abdomen Progressive abdominal distention Tachycardia, rapid-shallow breathing Pallor , chills and irritability

Appendicitis

Nursing Diagnosis

Pain R/T inflammation process

Risk for fluid volume deficit R/T decrease intake (loss of appetite) and excessive loss via vomiting

Risk for infection ( possibility of rupture)

Appendicitis

Nursing care (pre-op care) Avoid administering laxative, enema or heat application to

avoid increase the bowel motility which may lead to perforation

Cold packs on the abdomen/pain killer

Monitor I & O

IV fluid

Monitor S & S of appendix rupture/peritonitis

Post operative care

gastrointestinal disorder

Documents

gastrointestinal tractgi

factors food

hr food intake

diagnostic tests cbc

introduction of solid

hereditary problems

problems diarrheaacute

neonatal infancy gi