GROWTH AND DEVELOPMENT E– lectra complex

S– ame age group for room assignment

CONCEPTS IN GROWTH AND DEVELOPMENT C– astration anxiety
I–D H– ighly imaginative
N – o putting the baby on prone O– edipus complex
F – eeding O– ff limits to kitchen
 4 months – give cereals/ rice L– earn to imitate same sex parent
 6 months – fruits and vegetables S– upper ego
 9 months – meat, egg, and fish
A– nterior fontanel 12 – 18 months; diamond shaped PHYSICAL DEVELOPMENT
N– ote motor development  A security object and a night light help with sleepy
 3 months  At the beginning of the preschool period the eruption of the decidous (primary teeth) is
Good head contour complete
Good social smile
 6 months SCHOOL AGE
Sits with support; roll over S– TAGE OF INDUSTRY VS INFERIORITY
High chair will help in feeding C– OMPETITIVE PLAY
 9 months H–OMEWORKS
Stands with support; crawl O– BEYS TEACHERS THAN PARENTS
Pincer grasp O– BSSESSED WITH COLLECTIONS
T– rust vs mistrust Off limits to vehicles
S– tranger anxiety - 6 – 9 months L– OSS OF CONTROL IS A COMMON FEAR
 12 months – walks with support A– CCIDENTS (SPORTS AND MOTOR VEHICLE)
 15 months – walks alone G– AMES IN GROUPS
 9 months – mama, dada without meaning E– NVISIONS DEATH AS GHOST = 9 y/o and above – death is universal
 12 months – mama, dada with meaning
FEAR
PHYSICAL DEVELOPMENT AND CHARACTERISTICS  School Phobia
 Weight is doubled at 5 to 6 months and tripled at 12 months  Displacement from school
 At birth, head circumference is 2 – 3 cms more than chest circumference  Loss of Privacy
 Fear of Death
TODDLERS
T– OILET TRAINING (ANAL STAGE) 18 – 24mons PHYSICAL DEVELOPMENT
Bowel control first before bladder  Girls grow faster than boys
O– nset of tantrums  The first permanent (secondary) teeth erupt around age 6 and decidous teeth are lost
D– evelops ego gradually
D– evelops full set of teeth – 20mons
L– oves to say NO Significant Development
E– ngage in parallel play  Boys- Prone to bone fracture
R– ides a tricycle at 3  Mature vision 20/ 20
 3 y/o – rides a 3 wheeler
 6 y/o – rides a 2 wheeler/bicycle ADOLESCENT
S– eparation anxiety A– LTERATION IN BODY IMAGE (12 – 14 YEARS OLD)
INDEPENDENT: 15 – 20 y/o
PHYSICAL DEVELOPMENT D– EVELOPS SECONDARY SEXUAL CHARACTERISTICs
 Anterior fontanel closes between 12 to 18 mos  THELARCHE
 Lordosis (pot belly) is evident)  MENARCHE
 The toddler should seek a dentist soon after the 1st teeth erupt usually around 1 year of age O– BESE OR ANOREXIC
L– ADIES MATURE FIRST THAN BOYS
PRE SCHOOLERS E– NGAGE IN RISK TAKING BEHAVIOR
P– hallic S– UICIDE
Play is associative or cooperative C– ONFUSE ROLES OF IDENTITY
R– edirect attention E– NJOYS COMPARING BODY PART (BOYS)
N– EED FOR LOVE AND AFFECTION  Tonsillectomy
T– ALK ABOUT BOYS (GIRL) Removal of the palatine tonsils
Observe for signs of hemorrhage: frequent swallowing, increase PR, vomiting bright red
PHYSICAL DEVELOPMENT blood
 Puberty and secondary sex characteristics develops  Adenoidectomy
 Menstrual period occurs about 2 and ½ years after the onset of puberty Removal of the pharyngeal tonsils
* Tonsillectomy or Adenoidectomy is never done while the organs are infected
Significant Development
 Experiences conflict between his needs for sexual satisfaction and societies expectation Nursing Interventions
 Change of body image and acceptance of opposite sex After Surgery:
 Nocturnal emission  Place the child on the side or abdomen with a pillow under the chest
 Distinctive odor  Assess the subtle signs of hemorrhage
 Sperm is viable  If bleeding occurs, elevate the child’s head or turn him or her on the side
 Testes and scrotum increase  Offer frequent sips of clear liquid, popsicles or ice chips
 Breast and female genitalia increase  Avoid acid juices and red fluid

Personality Traits Adolescents Choanal Atresia

 Idealistic - Is a congenital destruction of the posterior nares by air obstructing membrane or bony
 Rebellious growth, preventing a newborn from drawing air through the nose and down into the
 Reformers nasopharynx
 Conscious with body image - Unilateral or bilateral
 Adventuresome -
Assessment -> Respiratory Distress
Problems
 Vehicular accident Diagnosis
 Smoking - Soft no. 8 or 10 French Catheter
 Alcoholism - Newborns mouth closed  compress one nostrils at a time
 Drug addiction
 Pre marital sex Treatment -> Surgical Removal of the Bony Growth

Tonsillitis and Adenoiditis Croup (Laryngotracheobronchitis)

Tonsillitis - infection and inflammation of the palatine tonsils - Inflammation of the larynx, trachea and major bronchi; 3months- 5 years of age
Adenoiditis - infection and inflammation of the adenoids (Pharyngeal) tonsils - Caused by usual inflammation such as Parainfluenza Virus
- Peak Age: 1-2 years old
 Group A beta- hemolytic Streptococcus- most common bacterial cause
 Common in school- age children Assessment
 Barking Cough (Croupy cough)
Assessment  Inspiratory Stridor
 Drooling of saliva  Marked Retractions
 Painful swallowing
 Increase Fever Therapeutic Management
 Pus  Take Vital Signs
 Nasal quality of speech  Instruct the parents of the child that coughing episodes may be relieved by taking the child
 Mouth breathing into cold night air or humid bathroom
 Sleep apnea  At ER: Cool moist air with a corticosteroid such as dexamethasone, or racemic epinephrine,
given by nebulizer
Diagnostic Evaluation -> Throat culture  Watch out for extreme restlessness and thrashing, increased stridor & increase HR, RR and
cyanosis
Therapeutic Management  Tracheostomy or ET
 Antipyretic  Do not elicit a gag reflex in any child with a croupy cough, barking cough
 Analgesic
 10- day course of antibiotic (ex. Penicillin) Foreign Body Aspiration
 • Swallowing and aspiration of a foreign body(ies) into the air passages 2 General Classes
• Mechanisms of airway obstruction by a Foreign Body (FB) a. Long- term control medication to achieve & maintain control of persistent asthma
• Most common offending foods are round in shapes b. Quick relief medications for immediate treatment of asthma symptoms

Assessment Long- term control medications

• Laryngeal obstruction  Corticosteroids
 Dyspnea  Cromolyn Na & Nedocromil
 Stridor  Mild to moderate antiinflammatory agents
 Cough  More commonly in children
 Hoarseness  Methylxanthines (e.g. theophylline)- for relief of nighttime asthma symptoms
• Bronchial Obstruction  Leukotriene Modifiers- new class of medications
 Cough  Ex. Montelukast (Singulair)
 Wheezing
 Asymmetrical breath sounds Quick Relief Medications
 Dyspnea  Short- acting beta 2- adrenergic agonists
Ex. Ventolin
Interventions  Anticholinergics
1. Emergency care Ex. Ipratropium Bromide (Atrovent)
a. Abdominal Thrusts
b. Back blows and chest thrusts Nursing Management
2. Nonemergency management entails removal by endoscopy • Assess the respiratory status
a. High- humidity air • Elevate HOB
b. Observe for signs and symptoms of airway edema • Teaching effective breathing techniques

Prevention Atelectasis
• Keep small objects out of reach of small children - An abnormal condition characterized by the collapse of lung tissue -> Preventing respiratory
• Avoid giving of round, food items exchange of CO2 & O2 occur due to occlusion of air (blockage) to a portion of the lung

Asthma Pathophysiology:
 Is a chronic inflammatory disease of the airways, resulting in airway hyper responsiveness, Reduced alveolar ventilation or Blockage that impedes the passage of air to & from the alveoli ->
mucosal edema & mucus production Trapped Air -> Becomes absorbed into the bloodstream -> Outside air cannot replace absorbed air ->
 An acute asthma attack is caused by an antigen- antibody reaction Isolated portion of the lung airless & shrinks

2 Classification of Asthma Risk for Atelectasis

A. Extrinsic- caused by external factors • Postoperative patient
B. Intrinsic- caused by internal factors • Impaired cough mechanisms  obstruction by secretions
• Excessive pressure on the lung tissue  restricts normal lung expansion on inspiration
Clinical Manifestations • Clinical Manifestation
• Cough • Cough
• Dyspnea • Sputum Production
• Wheezing • Low- grade fever
• Chest Tightness • Fever
• Dyspnea  Fatigue
Diagnostic Tests • Increase HR, RR
• ABG & Pulse oximetry • Central Cyanosis
• CXR:
 lung hyperinflation related to air trapping; Assessment and Diagnostic Findings
 flat diaphragm related to intrathoracic volume • Decreased breath sounds & crackles over the affected area
• CBC: increase eosinophil count • CXR: Patchy or consolidated areas
• Blood sample to detect theophylline count • Pulse oximetry: decrease O2 saturation
• PCO2: normal or low
Medical Management
Pharmacologic Therapy: Management
Goal: To improve ventilation & remove secretions a. Steatorrhea- large, bulky & greasy stool
 Frequent turning b. Extremely foul odor stool
 Early ambulation c. Malnutrition - emaciated extremities & loose flabby folds of skin on buttocks
 Lung- volume expansion maneuvers d. Fat- soluble vitamin deficincy (Vit. A,D,E)
 Coughing
 Suctioning Lung Involvement
 CPT  Secondary Emphysema (over- inflated alveoli)
 Nebulization with bronchodilators  Bronchiectasis
 Thoracentesis or chest tube insertion  Pneumonia
 Clubbing of fingers and toes
TUBERCULOSIS  Barrel- shaped chest
• Contagious disease  Repsiratory Acidosis
• Mycobacterium tuberculosis
Sweat Gland Involvement
Assessment • Secretions contain excessive amount of Na and Cl, leading to excessive loss, especially with
• Malaise hot weather, fever or exertion
• Fever
• Cough Diagnostic Evaluation
• Weight loss Sweat Test - is a test for the chloride content of sweat
• Anorexia After the application of electrical current,
• Lymphadenopathy  Arm is washed & dried  filter paper is applied
 20 meqs/ L- Normal concentration of chloride in sweat”
Mantoux Test  > 60 meqs/ L- diagnostic of CF
• The test will produce a positive reaction 2 to 10 weeks after the initial reaction  50-60 meqs/ L- suggestive of lesions & call for a repeat of the test
• A positive reaction does not confirm the presence of active disease
• Once the child reacts positively, the child will always react positively Therapeutic Management
• TB testing should not be done at the same time as measles immunization Pulmonary Interventions
• Antimicrobial therapy for pulmonary infection
Sputum Culture • Bronchodilators & vasoconstrictors
• A definitive diagnosis is made by demonstrating the presence of mycobacterium in a culture • Aerosol, expectorants and mucolytic agents
• CPT for bronchial drainage
Intervention a. Postural drainage
• Medications b. Coughing & deep breathing exercises
 9 months course of INH
 To prevent a latent infection from progressing to clinically active TB and to Gastrointestinal Interventions
prevent initial infection in children in high-risk situations • Pancreatic enzyme supplementation is provided with each feeding
• Children with clinically active TB:
 Isoniazid (INH), Rifampin (Rifadin), Pyrazinamide daily = 2 months + Diet:
 Isoniazid and Rifampin twice weekly = 4 months • High- calorie, high CHON & moderate fat diet
• Airborne precaution • Extra salt may be added to food
• Adequate rest and adequate diet
CHF
Cystic Fibrosis • is the inability of the heart to pump a sufficient amount of oxygen to meet the metabolic
 Generalized dysfunction of the exocrine glands needs of the body
 Substances they secrete are abnormally viscous, affecting primarily the pulmonary and GI
Function Signs and Symptoms of CHF
 Autosomal recessive trait Left Sided Heart Failure
 Slightly more males than females are affected • Crackles and wheezes
• Cough
Pancreas Involvement: • Dyspnea
Thickened Enzyme Secretions -> Plug the Ducts -> Back- Pressure -> Non- production of Enzymes • Nasal flaring
• Orthopnea
Result: • Periods of cyanosis
 • Retractions b. loud, harsh systolic murmur
• Tachypnea (left sternal border, 3rd- 4th interspace)
c. thrill may be palpated
Right- sided Heart Failure • Echocardiography or MRI -> Right Ventricular Hypertrophy and possibly pulmonary artery
 Ascites dilatation
 Hepatosplenomegaly
 Jugular vein distention Therapeutic Management
 Oliguria • If small  close spontaneously
 Peripheral edema • Moderate in size, closed by interventional cardiac catheterization
 Weight gain • Large (over 3mm)- open heart surgery done before 2 years of age to prevent pulmonary
artery HPN
Interventions:
• Monitor for S/S of CHF • Postoperatively, be alert for arrhythmia
• Monitor for respiratory distress • May receive prophylactic antibiotics
• Monitor apical pulse • If defect is left open  infectious endocarditis and cardiac failure
• Strict I and O
• Monitor daily weight Atrial Septal Defect (ASD)
• Elevate HOB in a semi- fowler’s position Assessment
• Administer digoxin (Lanoxin) as prescribed • Harsh, systolic murmur over the 2nd or 3rd interspace
• Administer diuretics (furosemide) as prescribed • (fixed splitting)
• Echocardiography -> Enlarged right side of the heart and increase Pulmonary Circulation
Neonatal Congenital Heart Diseases
Classification Therapeutic Management
A. ACYANOTIC HEART DISEASE • Surgery
B. CYANOTIC HEART DISEASE If not, risk for infective endocarditis and eventual heart failure
Postoperatively, observe for arrhythmias
ACYANOTIC HEART DISEASE
 Involves heart or circulatory anomalies that involves either a stricture to the flow of blood or Atrioventricular Canal Defect
a shunt that moves blood from arterial to the venous system (oxygenated to unoxygenated Assessment
blood) or left- to – right shunts. • Same symptoms as ASD
• ECG: First Degree Heart Block
CYANOTIC HEART DISEASE • Echocardiography -> confirms the diagnosis
 occurs when blood is shunted from the venous to the arterial system as a result of abnormal
communication between the 2 (deoxygenated blood to oxygenated blood or right- to – left • Surgery is always necessary for a final repair
shunt). • Postoperatively, closely observe for jaundice
• Prophylactic anticoagulation and antibiotic therapy may be necessary
4 Classifications
A. Decreased Pulmonary Blood Flow Patent Ductus Arteriosus
B. Obstruction to Blood Flow Assessment
C. Mixed Blood Flow • Twice as common in girls
D. Decreased Pulmonary Blood Flow • Wide pulse pressure
• Continuous “machinery” murmur
Defects with Increased Pulmonary Blood Flow
A. Ventricular Septal Defect (VSD) Therapeutic Management
B. Atrial Sepal Defect (ASD) Medical Management
C. Atrioventricular Canal Defect (AVC)  Administration of oral or IV indomethacin
D. Patent Ductus Arteriosus ( PDA)  Indomethacin therapy: 12- 24 hours interval
Ductal Ligation
Ventricular Septal Defect (VSD) • If surgery is not done = at risk for heart failure and Infective Endocarditis
Assessment
• May not be evident at birth Defects with Obstruction to Blood Flow
• At about 4- 8 weeks A. Pulmonary Stenosis
a. Easy fatigue B. Aortic Stenosis
 C. Coarctation of the Aorta - No single artery originates from heart

Pulmonary Stenosis Therapeutic Management -> Restructuring of the common trunk to create separate vessels
Assessment:
 Asymptomatic or signs of mild (right side) heart failure Hypoplastic Left Heart Syndrome
 Cyanosis • Rare Defect
 Systolic Murmur LV nonfunctional -> RV Hypertrophy
• Prostaglandin Therapy
Therapeutic Management -> Balloon Angioplasty - procedure of choice • Limited success at surgery
• Heart Transplant
Aortic Stenosis
Assessment Defects with Decreased Pulmonary Blood Flow
• Asymptomatic A. Tricuspid Atresia
• Typical murmur B. Tetralogy of Fallot
• Thrill at suprasternal notch
Tricuspid Atresia
Assessment -> When the child is active, Chest pain similar to angina • IV Infusion of PGE
• Fontan Procedure (sometimes termed a Glenn Shunt Baffle)
Therapeutic Management
• Beta- Blocker or Calcium Channel Blocker Tetralogy of Fallot
• Balloon Valvuloplasty 4 Anomalies
A. Pulmonary Stenosis
Coarctation of Aorta B. VSD (Usually Large)
Assessment C. Dextroposition (Overriding of the Aorta)
• Absence of palpable femoral pulses- only symptom if coarctation is slight D. Hypertrophy of RV
• Diminished pulses in the extremities
• Leg pain Assessment
• BP in the arms at least 20 mmHg higher than in legs • As the child becomes active  Cyanosis begins
• Headache and vertigo • Polycythemia
Complications of Polycythemia
Therapeutic Management -> Interventional Angiography or Surgery a. Thrombophlebitis
b. Embolism
Defects with Mixed Blood Flow c. CVA
• Transposition of the Great Arteries • Squatting position or knee- chest position when resting
• Total Anomalous Pulmonary Venous Return • Syncope (Fainting)
• Truncus Arteriosus • Hypoxic Episodes (Tet Spells)
• Hypoplastic Left Heart Syndrome
Therapeutic Management
Transposition of the Great Arteries • Hypoxic Episode:
Assessment O2 Administration, Knee- chest position
• Cyanotic from birth • Give Propanolol (Inderal, a Beta Blocker); Digoxin as prescribed
• Decrease O2 Saturation • Blalock- Taussig Procedure

Therapeutic Management -> Arterial Switch Procedure: Major vessels are switched in position Children
• Rheumatic Fever
Total Anomalous Pulmonary Venous Return • Kawasaki Disease
- All four pulmonary veins connects to the SVC • Endocarditis

Therapeutic Management Rheumatic Fever

• Reimplanting the pulmonary veins into the LA • Is an autoimmune disease that occurs as a reaction to a group A beta- hemolytic
• Continuous IV infusion containing PGE streptococcal infection
• Most first attacks of ARF occur 2-3 weeks after streptococcal infection of throat or upper
Truncus Arteriosus respiratory tract
 • Aneurysm may form in coronary arteries
Assessment • Sudden Death
Major Manifestations •
a. Carditis Stage III: Convalescent Stage
b. Polyarthritis • Child appears well ( Days 21- 60)
c. Chorea • ESR returns to normal
d. Erythema Marginatum
e. Subcutaneous Nodules Therapeutic Management
Minor Manifestations • Acetylsalicylic Acid (Aspirin) or Ibuprofen- decrease inflammation and blocks platelet
a. History of previous rheumatic fever/ evidence of preexisting RHD aggregation
b. Arthralgia • Abciximab- is a platelet receptor inhibitor specific for kawasaki disease
c. Fever • IV immune globulin can be administered to reduce the immune response
d. Lab. Abnormalities • Steroids are contraindicated
e. ECG changes- PR interval (Prolonged)
Nursing Interventions
Therapeutic Management • Observe the child for signs of heart failure
• 6-8 weeks- course of rheumatic fever • Provide Comfort Measure
• Penicillin Therapy or a single IM injection of Benzathine Penicillin • Applying lip balm
• Erythromycin- for children sensitive to penicillin • Offer extra fluids
• Prophylactic antibiotic • Keep child free from heavy blankets or clothing and prevent overexertion
• Oral Acetylsalicylic Acid (Aspirin) or Ibuprofen- to reduce inflammation and joint pain
• Corticosteroids to reduce inflammation for children not responding to salicylate therapy Anemia
alone • A condition of a lower- than- normal level of hemoglobin, reflects fewer than normal RBCs
• Mitral Valve Replacement, if needed within the circulation
Nursing Interventions
• Explain the importance of taking the full- course of Penicillin A. Iron Deficiency Anemia
• Provide Bed rest during acute febrile phase B. Pernicious Anemia
C. Folic Acid Deficiency
Kawasaki Disease D. Aplastic Anemia
• Is a febrile, multisystem disorder that occurs before the age of puberty
• More common in boys than in girls Iron Deficiency Anemia
• Microcytic, Hypochromic
* Vasculitis is the principal finding, leading to formation of aneurysm and MI • Inadequate Iron in the diet (children, adolescent, pregnant women)
• Blood Loss ( Adults)
Inflammation of Blood Vessels -> Aneurysms, platelet accumulation and formation of thrombi ->
Obstruction in the Heart and Blood Vessels Clinical Manifestation
A. Physical
Assessment • Headache
Stage I: Acute Phase • Dizziness
• High fever (102- 104 F) (39.0- 40.0C) • Tinnitus
• Lethargic &/ or Irritable • Palpitations
• Reddened & Swollen hands & feet • Dyspnea on exertion
• Conjunctivitis • Pallor of skin and mucous membrane
• “ Strawberry” tongue, & red, cracked lips • Smooth, sore tongue
• Rashes
• Cervical lymph nodes enlarged B. Behavioral
• Abdominal Pain, anorexic and Diarrhea • Fatigue
• Swollen, Reddened Joints • Pica
• WBC & ESR are elevated
Diagnostic Evaluation
Stage II: Subacute Phase (10 days after onset) • CBC & Iron Profile
• Desquamation of palms and soles of the feet • Decrease Hgb & Hct, serum iron & ferritin
• Platelet count rises
Medical Management Management
Iron Supplementation • Oral folic acid replacement
• Oral ferrous sulfate • Inclusion of foods rich in folic acid: beef, liver, peanut butter, red beans, oatmeal, broccoli,
• Parenteral therapy of Iron Dextran (DexFerrum) asparagus

Nursing Intervention Aplastic Anemia

• Preventive Education • Is a disorder characterized by bone marrow hypoplasia or aplasia resulting in pantocytopenia
• Food sources high in Iron • Can be caused by medications, chemicals, radiation damage, infection
• Organ meats (Chicken liver); beans; leafy green vegetables; raisins
• Medicine administration Clinical Manifestation
• Iron is best absorbed by an empty stomach • From anemia: pallor, weakness, fatigue, exertional dyspnea, palpitations
• Iron salts may color the stool dark green or black • From infection associated with neutropenia: fever, headache, malaise, adventitious breath
sounds, abdominal pain, diarrhea
Pernicious Anemia • From thrombocytopenia: bleeding gums, nose, GI, GUT, petechiae, ecchymosis
• Megaloblastic Anemia
• Deficiency of Vitamin B12 Diagnostic Evaluation
• Rare, but can develop in strict vegetarians • CBC: Decrease RBC, WBC and platelets
• Absence of intrinsic factor • Bone Marrow Aspiration and Biopsy: Bone marrow is hypocellular or empty with greatly
reduced or absent hematopoiesis
Clinical Manifestation
• Of anemia- pallor, fatigue, dyspnea on exertion, palpitations Medical Management
• Of underlying GI dysfunction- sore mouth, glossitis, anorexia, N&V, epigastric discomfort, • Allogeneic BMT (Bone Marrrow Transplantation)
recurring diarrhea or constipation • Immunosuppresive Treatment
• Of neuropathy- paresthesias in extremities (particularly numbness and tingling in the feet &
lower legs) Nursing Intervention
• Minimize Risk of Infection
Diagnostic Evaluation • Minimize Risk of Bleeding
• CBC: Decrease Hgb and Hct
• Schilling Test Sickle Cell Disease
• Determine the cause of vitamin B12 deficiency • Genetically determined, inherited disease- Autosomal Recessive
• Intrinsic factor added to the oral radioactive vitamin B12 • Presence of abnormally shaped (elongated) RBCs.
• Almost exclusively for African Americans
Medical Management
• Vitamin B12 Replacement Erythrocytes  elongated and crescent- shaped (sickled) when….
• If due to defective absorption and absence of intrinsic factor- replacement is by monthly IM a. Low O2 concentration
injection of Vitamin B12 b. Low blood pH (acidosis)
c. Increased blood viscosity (Dehydration or Hypoxia)
Nursing Intervention
• Careful neurologic assessment Sickled RBCs -> Not move freely through vessels -> Stasis & Further sickling occur (Sickle- cell crisis) ->
• Pay particular attention to ambulation & patient’s gait & stability Blood Flow Halts -> Ischemic Tissue -> Acute Pain & Cell Destruction

Megaloblastic Anemia: Folic Acid Anemia Assessment

• Folic Acid- a vitamin that is necessary for normal RBC production • Hemoglobin electrophoresis- used to diagnose sickle- cell anemia
• Found in green vegetables & liver • Fever
• Anemia
Clinical Manifestation • Protruding Abdomen
• Of anemia: fatigue, weakness, pallor, dizziness, headache, tachycardia • Enlarged Liver
• Of folic acid deficiency: sore tongue, cracked lips • Enlarged Spleen
• Blood Stasis & Infarction may occur in any body part
Diagnostic Evaluation • Hand- foot syndrome
• Decreased folic acid • Kidney function decreased
• CBC: decrease RBC, Hgb, Hct • Icteric Sclera
• Decreased Vision
 • Priapism • Dizziness
• Fatigue
Sickle- cell Crisis • Blurred vision
• Most common form of crisis • Hepatosplenomegaly
• A sudden, severe onset of sickling • Increase risk of CVA and MI
• Pooling of the many new sickled cells in vessels & consequent hypoxia (A vaso occlusive crisis)
• Occurs when… Collaborative Management
Dehydration or a Respiratory Infection  Decrease O2 Concentration • Increase fluid intake
Extremely strenuous exercise  Tissue Hypoxia • Monitor for s/s of bleeding
• If CVA occurs from a blocked artery, the CNS will be affected & the child may have coma, • Monitor for s/s of thromboembolism
seizures & even Death • Angina
• Claudication
Therapeutic Management in Sickle- cell Disease • Thrombophlebitis
• 3 Primary Needs • Administer analgesic as ordered
a. Pain Relief • Administer antihistamine
b. Adequate Hydration • Therapeutic phlebotomy
c. Oxygenation • Chemotherapy
• Acetaminophen (Tylenol) • Radiation Therapy
• Narcotic Analgesic (IV Morphine) • Pt. teaching: avoid high altitude
• Intensive IVF Replacement Therapy
a. Electrolyte replacement Hemophilia “The Royal Disease"
• Infection treated with antibiotics • An inherited, congenital bleeding disorder characterized by a lack of blood clotting factors,
• Blood Transfusion esp. factors VIII & IX
• Hydroxyurea, an antineoplastic agent Hemophilia A (Factor VIII Deficiency)
• Children who receive frequent BT should not be given supplementary iron or iron- fortified Hemophilia B (Factor IX Deficiency, Christmas Disease)
formula or vitamin or they may receive too much iron. • Sex- linked, Recessive trait- caused by a gene carried on the x- chromosome
• Appears primarily in males, but is transmitted by females
Beta- Thalassemia Major • May appear in females if a female carrier bears offspring with a male hemophiliac
• Autosomal recessive disorder characterized by the reduced production of one of globin chains
in the synthesis of hemoglobin Assessment
• Bleeds excessively after circumcision
ASSESSMENT: • Joints: Swollen and warm
• Frontal bleeding • Heavily bruised lower extremities
• Maxillary prominence • Severe bleeding: GI, Peritoneal cavity or CNS
• Wide- set eyes with a flattened nose • Platelet count and PT are Normal
• Greenish- yellow skin tone • Whole blood clotting time is markedly prolonged or normal.
• Hepatosplenomegaly
• Severe Anemia Management
• Microcytic , hypochromic RBCs • Replace missing coagulation factors (VIII or IX)
• Splenectomy = infection • Immobilization of affected joint
• Genetic counseling • Desmopressin (DDAVP) for mild to moderate factor VIII- deficient hemophiliacs

Polycythemia Von Willebrand Disease

• Increase RBC and Hgb production • A hereditary bleeding disorder characterized by a deficiency of or defect in a protein termed
• Compensatory response to chronic hypoxia von Willebrand Factor (vWF)
• The vWF protein serves as a carrier protein or factor VIII
Polycythemia Vera • It is characterized by an increased tendency to bleed from mucous membranes
• Hyperplasia of the bone marrow
• Cause is unknown; associated with genetics ASSESSMENT:
 Epistaxis
S/S:  Gum Bleeding
• Ruddy complexion  Easy Bruising
• Headache  Excessive menstrual bleeding
 Pyloromyotomy - an incision through the muscle fibers of the pylorus that may be performed by
INTERVENTIONS -> Similar to hemophilia laparoscopy

DIC
- Is a widespread hypercoagulation within arterioles and capillaries throughout the body
- It is characterized by 2 opposing manifestations:
1. Diffuse fibrin deposition with resultant widespread clotting
2. Hemorrhages from kidneys, brain, adrenals, heart & other organs
- Etiology is unknown, possibly linked with thromboplastic substances entering blood

Pathophysiology Cleft Lip and Cleft Palate

Release of Thromboplastic Substances -> Deposition of Fibrin through microcirculation -> Microthrombi
- Congenital anomalies that occurs as a result of failure of soft tissue or bony structure to fuse
in Brain, Kidneys, Heart -> Microinfarcts & Tissue Necrosis -> Red Cells trapped in Fibrin strands are
during embryonic development
destroyed (Hemolysis) -> Platelets, Prothrombin and other Clotting Factors consumed in the Process ->
Free Bleeding -> Excessive Clotting activates Fibrinolytic Mechanisms -> Production of Fibrin split
products -> Fibrin split products Inhibit Clotting Formation -> Further Bleeding

Signs and Symptoms

- Prolonged PT/ PTT, abnormal bleeding times
- Decreased platelets
- Increase fibrin split products
- Decreased fibrinogen
- Petechiae, ecchymosis in skin, mucous membrane, lungs (Microhemmorhages)
- Patients may develop organ dysfunction

Treatment C- ommon among males

- Centered on underlying cause L- arge soft nipples or dropper
- FFP E- ncourage feeding
F- eed in upright position
HYPERTROPHIC PYLORIC STENOSIS T- each about the surgery
Hypertrophy of the Pylorus -> Narrowing of the Pyloric Canal
- Elbow restraints postoperatively
- Closure of cleft lip defect precedes that of the cleft palate

Post-op Repair of Cleft Lip

- Sidelying position
- Feed away the suture line
- Logan Bar- to reduce the tension on suture line
- Feeding through a cup
Assessment - Position the patient on prone / on the abdomen
 Forceful and projectile vomiting
 Peristaltic waves are visible ESOPHAGEAL ATRESIA AND TRACHEOESOPHAGEAL FISTULA
 Olive- shaped mass The esophagus terminates before it reaches the stomach, ending in a blind pouch, and / or a
fistula is present that forms an unnatural connection with the trachea
 DHN and malnutrition
 Electrolyte imbalances
Assessment
 Metabolic alkalosis
- Frothy saliva in the mouth and nose and drooling
- 3 C’s- coughing & choking during feedings, cyanosis
Interventions
- Regurgitation and vomiting
 Monitor VS and I and O
- Abdominal distention
 Obtain daily weights
- Inability to pass a small- gauge orogastric feeding tube via the mouth into the stomach
 Monitor for signs of DHN and electrolyte imbalances
Interventions
 - Maintain on NPO status - Prepare the patient for surgery
- Maintain IVF as prescribed - Provide colostomy care
- Monitor respiratory status closely
- Maintain the gastrostomy tube GASTROESOPHAGEAL REFLUX
- Administer broad spectrum antibiotics as prescribed Incompetence of the lower esophageal or cardiac sphincter -> Backflow of gastric contents into the
esophagus
INTUSSUSCEPTION
- Telescoping of the bowel Assessment
- The condition results in an obstruction to the passage of intestinal contents - Poor weight gain
- - Hematemesis
- Melena
- Passive regurgitation or emesis
- Irritability
- Heartburn (in older children)
- Anemia from blood loss

Interventions
- Small, frequent feedings
Assessment
- Small frequent thickened feedings
- Colicky pain with knees drawn up
- Burp the infant frequently when feeding and handle the infant minimally after feedings
- Vomiting of gastric contents
- For toddlers, feed solids first followed by liquids
- Bile- stained fecal emesis
- Currant jelly- like stools
Positioning
- Hypoactive or hyperactive bowel sounds
- Infants: Non prone position (sleep) Prone (if awake)
- Sausage- shaped mass
- > 1 y/o: Left side with HOB elevated
Interventions
Meds
- Monitor for signs of perforation
- Histamine 2 (H2) Antagonists
- Barium Enema- may reduce intussusceptions by Hydrostatic pressure
- Acetaminophen (Tylenol)
HIRSCHSPRUNG’S DISEASE
Surgery
- Also known as congenital aganglionosis or aganglionic megacolon
- Fundoplication - a wrap to the stomach fundus is made around the distal esophagus
- Absence of parasympathetic ganglion cells in a portion of the large colon resulting to
decreased motility in that portion and obstruction CONSTIPATION AND ENCOPRESIS
CONSTIPATION - is the infrequent and difficult passage of dry, hard stools
Assessment ENCOPRESIS - is constipation with fecal incontinence
Newborn infants
- Failure to pass meconium stool * If the child does not have a neurological or anatomical disorder, encopresis is usually the result of fecal
- Abdominal distention impaction and an enlarged rectum caused by chronic constipation
Children
- Abdominal distention Assessment
- Constipation alternating diarrhea  Constipation
- Ribbon- like and foul- smelling stools  Abdominal pain and cramping without distention
 Palpable movable fecal masses
Laboratory Data:  Normal or decreased bowel sounds
- Biopsy reveals absence of ganglion cells  Malaise and headache

Nursing Diagnosis -> Altered bowel elimination pattern Encopresis
 Evidence of soiling of clothing
Interventions
 Scratching or rubbing of the anal area
- Administer stool softeners as ordered
 Fecal odor
- Maintain a low residue diet

- Measure abdominal girth
Interventions
 Maintain a diet high in fiber and fluids for simple constipation Therapeutic Management:
 Decrease sugar and milk intake - D/C feedings
 Administer enema as prescribed - IV or TPN
 Encourage the child to sit on the toilet for 5-10 minutes approximately 20- 30 minutes after - Solutions
breakfast and dinner - Antibiotics
- Handle abdomen gently
APPENDICITIS
- Inflammation of the appendix CELIAC DISEASE
- Gluten- sensitive enteropathy
Inflamed Appendix ->Perforation ->Peritonitis, sepsis, septic shock ->Death - Permanent inability to tolerate dietary gluten in the small intestines

Assessment Assessment
 Pain in periumbilical area that descends to the RLQ - Acute or insidious diarrhea
 Referred pain= peritoneal irritation - Steatorrhea
 Rebound tenderness and abdominal rigidity - Anorexia
 Side- lying position with abdominal guarding - Abdominal pain and distention
 Lab data: Elevated WBC - Muscle wasting
- Vomiting
Interventions - Anemia
 Unruptured appendix: any position of comfort - Irritability
 Ruptured: high- fowler’s
 Avoid applying hot compress on the RLQ Laboratory Data -> Small bowel biopsy
 Administer antibiotics as ordered
 Prepare the patient for surgery Interventions
- Lifetime avoidance of:
NECROTIZING ENTEROCOLITIS B- arley
- The bowel develops necrotic patches, interfering with digestion & possibly leading to a R- ye
paralytic ileus O- ats
- Result from ischemia or poor perfusion of blood vessels in sections of bowel W- heat
- Highest in immature infants - Foods which are allowed:
Corns
3 Factors in the Development of NEC: Cereals
1. Intestinal ishemia Soybeans
2. Colonization by pathogenic bacteria Rice
3. Substrate (formula feeding) in the intestinal lumen
LACTOSE INTOLERANCE
Pathophysiology: - Inability to tolerate lactase as a result of an absence or deficiency of lactase
Decreased Blood supply to mucosal cells -> Mucosal cells die-> Stop secreting protective, lubricating
mucus-> Proteolytic enzymes attack bowel wall -> Bowel wall swell and break down-> Unable to Assessment
synthesize protective lgM -> Mucosa is permeable to macromolecules -> Hamper intestinal defenses - Abdominal distention
Gas-forming bacteria -> Intestinal Pneumatosis - Crampy, abdominal pain; colic
- Diarrhea and excessive flatus
Assessment:
- Distended abdomen Interventions
- Gastric residuals - Eliminate the offending dairy product or administer an enzyme replacement
- Blood in the stools - Substitute soy- based formulas for cow’s milk formula or human milk
- Signs of blood loss - Calcium and Vitamin D supplements
- Increase abdominal girth - Encourage consumption of hard cheese, cottage cheese, or yogurt
- Abdominal x- ray: sausage- shaped dilation of the intestine that progresses to marked - Encourage consumption of small amounts of dairy foods daily
distention & the characteristic intestinal pneumatosis
- Perforation: air in the abdominal cavity INGESTION OF POISONS
 1. LEAD POISONING
2. ACETAMINOPHEN
3. ACETYLSALICYLIC ACID

Poisoning
1. Determine substance taken, assess LOC
2. Unless poison is corrosive, caustic or a hydrocarbon, vomiting is the most effective way to
remove poison
3. Universal antidote: charcoal, milk of magnesia & burned toast
4. Never administer charcoal before Ipecac

LEAD POISONING
- Excessive accumulation of lead in the blood

Risk Factors
- Children who live in houses built before the 60’s
- Contaminated water
- Refurnishing old furniture

* When lead enters the body, it affects the erythrocytes, bones and teeth, and organs and tissues,
including the brain and nervous system

Initial Manifestation
 Vomiting
 Abdominal Pain
 Colic

Laboratory Data
Blood lead level test - used for screening and diagnosis
Erythrocyte protoporphyrin test - initial test; indicator of anemia
Normal value (child): 35 mcg/ 100mL of whole blood or lower

Antidote:
 Dimercaprol in peanut oil (BAL in oil)
 Calcium disodium edetate (EDTA)

Interventions
 Ensure adequate urine output before administering the medication
 Provide adequate hydration and monitor kidney function for nephrotoxicity
 Instruct the parents to eliminate lead hazards at home

ABDOMINAL WALL DEFECTS:

 OMPHALOCELE
 GASTROSCHISIS