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ACUTE NASOPHARYNGITIS (CORYZA)
Most frequent infectious disease in children Average of 10-12 colds/ year Incubation period- 2-3 days ETIOLOGIC AGENT:
1. rhinovirus-most common cause 2. coxsackie virus 3. respiratory syncitial virus (major etiologic agent) 4. adenovirus 5. parainfluenza/ influenza virus
SIGNS AND SYMPTOMS
1. nasal congestion 2. watery rhinitis 3. low grade fever 4. mucus membrane is edematous 5. cervical lympnode may be swollen and palpable 6. body malaise
initial pathology is submucosal edema of nasal mucosa followed by shedding of ciliated epithelial cells( 5th day) nasal mucopurulent discharge, then release of interferon (play major role in recovery)
Common colds is self-limiting supportive care relief of nasal obstruction - use of isotonic saline drops and aspiration antipyretic or analgesic agents antitussive is sometimes used for persistent cough
> caused by group A beta-hemolytic streptococcus (GABS) > can lead to cardiac and kidney damage > more severe than viral infection Signs and symptoms: 1. marked erythema of the back of throat and palatine tonsils 2. tonsils are enlarged and (+) white exudates in the tonsillar crypts 3. high grade fever 4. difficulty swallowing Dx: throat swab and culture
1. antibiotics- 10 days course of oral antibiotics (pen G or clindamycin) 2. high fluid intake 3.relief of pain COMPLICATION:
1. Rheumatic fever 2. Glomerulonephritis
- term commonly used to refer to infection and inflammation of palatine tonsils palatine tonsils - located on both side of pharynx Adenitis - refers to infection and inflammation of the adenoids ( pharyngeal) tonsils adenoids - located in the nasopharynx Tubal tonsils - located at entrance to the Eustachian tube lingual tonsils - located at base of tongue
SIGNS AND SYMPTOMS
1. difficulty of swallowing 2. fever 3. lethargy 4. mouth breathing (post pharyngeal) 5. difficulty hearing (Eustachian tube) 6. halitosis 7. sleep apnea
<3 years old - often viral school age children
1. antipyretic 2. analgesics 3. Antibiotics ( 10 day course - usually penicillin but may be erythromycin if allergic to penicillin) is prescribed for bacterial infections to prevent the complication of rheumatic fever. 4. Surgical – tonsillectomy with adenoidectomy
Post –op Care: 1.Observe for, & report unusual bleeding ( frequent swallowing) 2. Help prevent bleeding by discouraging the child from coughing & clearing the throat. 3. Position the child on the side or the abdomen to facilitate drainage from the throat 4.Provide appropriate teaching . Instruct the child & parents to:
a.Observe activity restrictions, including when the child can return to school. b. Avoid persons with known infections c. Avoid acidic & other irritating foods d. Monitor the child for bleeding, especially immediately postoperatively& 5 to 10 days post op when tissue sloughing occurs.
1. chronic tonsillitis (not done if inflamed because may spread infection) 2. Recurrent tonsillitis (4-6x/year) 3. Sleep apnea Nursing diagnosis: pain related to surgical procedure
keep pt in upright position with head tilted slightly forward to minimize the amount of blood pressure in nasal vessels, keep blood moving forward not back to nasopharynx apply pressure to the side of the nose with your fingers
3. keep the child quiet and stop crying because crying increases pressure in the blood vessels of the head and prolonged bleeding 4. control of bleeding, can give epinephrine (1:1000) to constrict blood vessels 5. can put nasal packing for continuous pressure
CROUP (LTB) Acute Laryngotracheobronchitis) - Inflammation & narrowing of the larynx, trachea,
and major bronchi. Most common form of croup & usually affects children younger than 5 years old. - one of the most frightening diseases of early childhood for both parents and children. Tends to occur at night & recur with respiratory tract infections. - common cause is viral infection usually parainfluenza virus, influenza virus.
signs and symptoms
1.Gradual onset from upper respiratory tract infection , which progresses to signs of distress. 2. Hoarseness 3. low grade fever 4. barking cough at night 5. inspiratory stridor 6. Retractions 7.Severe respiratory distress 8. Restlessness& Irritability 9. Wheezing, rales, rhonchi, & localized areas of diminished breath sounds
MANAGEMENT - Assess for airway obstruction by evaluating
respiratory status. Note color, respiratory effort, evidence of fatigue, & VS. provide warm, moist environment-give o2 to alleviate hypoxia Keep emergency equipment ( tracheostomy & intubation tray) near the bedside. give corticosteroids & epinephrine (nebulizer) reduce inflammation and bronchodilation intravenous hydration
Nursing dx: Ineffective airway clearance related to edema
Health Teachings 1.When the child awakens with a barklike cough, tell the parents to place the child in the bathroom & to run hot water to produce steam. 2.Instruct the parents to stay in the bathroom with the child to prevent accidental injury.
>an acute , severe inflammation of the epiglottis.( flap of tissue that covers the opening to larynx to keep out food and fluids) > it is considered an emergency because the swollen epiglottis can’t rise and allow the airway to open. > This emergency situation occurs most commonly in children between 3 and 6 years of age.
1. Bacterium H-Influenza type b 2. pneumococci, streptococci most common cause 3. echovirus 4.respiratory syncitial virus
Sign and symptoms: 1. begins as mild URTI 2. restlessness & anxiety 3. hyperextension of the neck, drooling, & severe sore throat with refusal to drink 4 rapid, thready pulse 5. characteristic “tripod: position: child sits in upright position, with chin thrust out & tongue protruding. 6. sudden onset of high fever, lethargy, & dyspnea & dysphygia 7. Red & inflamed throat with
NURSE ALERT!!! “ Never illicit gag reflex-may cause complete obstruction” Laboratory findings: 1. leukocytosis ( 20,00030,000 mm3)
MANAGEMENT: 1.Closely monitor respiratory status to ensure patent airway. If a child presents with sx of epiglottitis, ensure that appropriate personnel perform a throat examination & that emergency equipment is at hand. 2. Prepare for emergency hospitalization = after dx is confirmed, an endotracheal intubation or tracheostomy is performed to maintain a patent airway. Swelling usually
3. After the child is intubated, monitor
closely & maintain a patent airway by suctioning as needed& providing oxygen therapy as prescribed. 4. Administer prescribed medications ( antibiotics, anti-inflammatories.) 5. Recommend that all children receive H. Influenzae type B ( Hib) conjugate vaccine beginning at 2 months of age, because H.Influenzae is the most common cause of epiglottitis.
. Provide warm, moist environment
8. o2 therapy 9. Intravenous therapy
> chronic, reversible , obstructive airway disease, characterized by wheezing. It is caused by smooth muscle spasm w/ hypertrophy of the bronchial tubes, or swelling of the bronchial mucosa, after exposure to various stimuli. Hypersecretion of mucus Most common chronic disease in childhood. Most children experience their first sx by 5yo exercise, nocturnal occurrence, seasonal, hx of allergy, stress
Etiology: 1.Commonly results from hyperresponsiveness of the trachea & bronchi to irritants. Common irritants include: 1.Allergens = dust mites, molds, animal danders 2. Viral infections 3. Irritants = air pollution, smoke, perfumes, laundry detergents 4. Certain foods ( food additives,
5. Rapid changes in environmental factors 6. Exercise 7. Psychological stress
Pathophysiology: * Release of inflammatory mediators from bronchial mast cells,epithelial cells, & macrophages >>> activation of inflammatory cells >>>bronchial spasm >>> inflammation >>> edema of the mucosa >>> production of thick mucus>>> inc. airway resistance >>>closure of airways >>>dyspnea & wheezing
allergy skin test, pulse oximetry, peak flow meter
Clinical Assessment of Asthma
MILD breathless walking talks in sentences Alertness may be agitated RR accessory wheeze pulse Inc (-) audible <100 MOD talking Phrases usually agitated inc (+) audible SEVERE at rest words agitated
>30 (+) audible w/o steth 100-120 >120
Intermittent Mild Moderate Severe Persistent Persistent Persistent
Am sx Pm sx
Daily; aff Daily; dec activ activ > 1x/wk
</= 2x/mo >/= 2x/mo >1x/wk
Management B2 agonists ( Bronchodilators), Theophylline, Steroids( anti inflammatories), Cromolyn Na, O2 Orthopneic position Monitor VS, hydration Adequate nutrition and non allergenic diet Environmental modification Health education
Progression of acute, severe, prolonged asthma attack unresponsive to therapy Preceding upper respiratory tract infection, allergen, cigarette smoke HR and RR inc, dec breath sounds, cyanosis Mx: cont B2 agonist and IV steroid, O2, coughing, fluids, monitor I and O
>sudden, unexpected death of any infant for whom a postmortem exam fails to determine the cause of death > Death occurs during sleep >most common cause of death (1 mo-1 year old, peaks 2-4 mos) Preterm / infants with apneic episodes, with prenatal drug exposure, siblings of infants who died of SIDS, exposed to smoking, infants of adolescent mothers, infants of closely spaced pregnancies, underweight the victim seems healthy sleeping on prone position Theories of causation: abnormalities in the brain and metabolic disorder
Sudden Infant Death Syndrome >sudden, unexpected death of any infant for
Maternal risk factors - cigarette smoking during pregnancy, maternal age < 20 yo, poor prenatal care, low weight gain, anemia, use of illegal drugs and alcohol, low socioeconomic status Newborn risk factors – cyanosis, tachycardia, respiratory distress, irritability, hypothermia, poor feeding
Nsg Dx: Dysfunctional grieving r/t loss of a child Management assist psychologically - intense grief and guilt for parents
Cleft Lip and Palate
failure of fusion of maxillary and median nasal process hereditary unilateral/bilateral males Mx: surgery - Cheiloplasty Rule of 10’s-10 wks, 10 lbs, Hgb 10 gm
MX : Surgical repair ( Cheiloplasty)
LIP : 6 weeks – 12 weeks PALATE : 12-18 months PREOP = feed upright / burp frequently
use large holed nipple
POSTOP = Position : on side / use cup/ avoid straw. ELBOW restraint, give water after each feeding to clean suture line .
midline opening of palate usually w/ Cleft lip Female surgery 12-18 mos allow anatomic changes <1 yo ie formation of palatine arch and tooth buds
Ndx: Risk for imbalanced nutrition, less than body requirements r/t feeding problems Risk for ineffective airway clearance r/t oral surgery Risk for infection during post op period
Nursing mx: Adequate nutrition; sips of fluid btw feeding in semiupright position; use rubber tipped syringe Direct the formula away from the cleft & toward the side & back of the mouth to prevent aspiration. Provide special nipples or feeding devices ( ex. Soft pliable bottle with soft nipple with enlarged opening) Feed the infant slowly & burp frequently to prevent excessive swallowing of air & regurgitation. Prevent ear and upper respiratory tract infection Address body image and speech concerns Reassurance to parents
1.Surgical correction of the cleft lip usually occurs at 1-3 mos. Repair of the cleft palate is usually performed between 6-18 mos. Repair of the cleft palate may require several stages os surgery as the child grows. 2. Early correction of the CL enables development of more normal speech pattern 3. Delayed closure or large defects may require the use of orthodontic appliances
Postop monitor respiratory distress d/t edema, hemorrhage Use mist tent , if prescribed, to minimize edema, liquefy secretions & minimize distress. Suction mucus and blood gently dropper feeding 1st 3 weeks; regular feeding after Use elbow restraints to maintain suture line integrity. Remove them every 2 hours Position side lying or back in cleft lip to avoid injury to the operative side; prone in cleft palate to facilitate drainage.
Gastrointestinal Esophageal atresia / tracheoesophageal atresia anomalies
EA is a condition in which the proximal and distal portions of the esophagus do not communicate. TEF is an abnormal communication between the trachea and esophagus
> Communication of the esophagus and trachea > maternal hydramnios and prematurity S/sx:coughing, choking, cyanosis, dyspnea, excessive secretion, abdominal distention Dx: Ba swallow
Preop Suction regularly Elevate the head Gastrostomy feeding hydration O2 Postop 1. Observe for respiratory distress 2. Proper positioning –avoid hyperextension of neck 3. Continue suction 4. Prevent wound infection 5. Provide pacifier
Hirschsprung disease ( Aganglionic Megacolon) – is a congenital anomaly characterized by absence of nerves( innervation) to a section of the intestines ( usually the rectosigmoid) 4x more common in boys ( esp. with Down’s syndrome) It can be acute & life threatening or chronic familial, congenital
No peristalsis in the affected area. Pathophysiology: 1. Absence of ganglion cells in one segment of the colon >>> lack of innervation >>> absence of propulsive movements >>> accumulation of intestinal contents & distention of the bowel proximal to the defect >>> enterocolitis ( inflammation of the small bowel & colon – leading cause of death in children with hirschsprung)
S/SX: 1.Newborns – failure to pass meconium, reluctance to ingest fluids, abdominal distention, bile stained emesis. 2. Infants – failure to thrive, constipation, abdominal distention, vomiting& episodic diarrhea 3. Older children – anorexia, chronic constipation, foul smelling & ribbon like stools, abdominal distention,,
Rectal exam reveals a rectum empty of stool, a tight anal sphincter, & stool leakage. Ominous sign signifying enterocolitis include explosive, bloody diarrhea, fever, & severe prostration. DX : > Barium enema reveals megacolon > Rectal biopsy reveals absence of ganglionic cells which confirms the diagnosis.
Preop Nursing Care 1. Daily cleansing enemas w/ 0.9% NaCl *Tap/hypotonic water will cause cardiac congestion or cerebral edema 2. Manual dilatation of the anus 2. Minimal residue diet w/ vitamin supplementation 3. Position semi fowlers to relieve dyspnea from distended abdomen Postop 1. Observe for abdominal distention 2. Small frequent feedings after NGT removal 3. Colostomy care 4. Assist parents to cope with children’s feeding problems
Surgery is done in 3 Stages: 1.Temporary colostomy before definitive surgery to allow the bowel to rest & the child to gain weight. 2. Reanatomosis by means of abdominoperineal pull-through about 912 mos later. 3. Closure of the colostomy about 3 mos after the pull through procedure.
invagination or telescoping of one portion of the intestine into an adjacent portion, causing obstruction. One of the most frequent causes of intestinal obstruction in children ages 3 mos to 5 yrs, most commonly bet 312 mos of age. If tx is delayed for longer than 24 hrs, bowel strangulation may occur, leading to necrosis, hemorrhage,
Cause: > unknown > maybe associated with viral infections, intestinal polyps,lymphoma Pathophysiology: Invagination because of hyperperistalsis in an intestinal segment usually the ileocecal valve >>>peristalsis continues to pull the invaginated segment along the bowel >>> intestinal edema >>>obstruction occur >>> blood supply is cut off
Ndx: Pain r/t abnormal abdominal peristalsis Risk for deficient fluid volume r/t bowel obstruction DX: Barium enema for dx & therapeutic treatment tool ( reduction by hydrostatic pressure) Sonogram reveals “ coiled spring “ MX: surgery
S/Sx: 1.Severe paroxysmal abdominal pain, causing the child to scream & draw his knees to the abdomen. 2. Vomiting of gastric contents 3. Tender, distended abdomen with palpable sausage shaped mass. 4. “ Currant jelly stools”containing blood & mucus 5. Bile stained or fecal emesis, &
Provide comfort measures pacifier for infants NPO Adequate hydration via IV therapy Promote parent-infant bonding
Pyloric Stenosis – is the narrowing of the pyloric sphincter at the outlet of the stomach d/t hypertophy or hyperplasia. > Common in males Cause: unknown ; may be hereditary Pathophysiology: Pylorus narrows bec of hyperplasia/ hypertrophy>>>obstruction of the pyloric sphincter >>>gastric distention >>> dilatation >>>hypertrophy
S/SX: 1.Projectile vomiting 2. Non bile stained emesis 3. No signs of anorexia, good appetite & feeding patterns. 4. No evidence of pain, weight loss, upper abdominal distention 5. Palpable olive shaped mass in the epigastrum (RUQ) just to the right of the umbilicus.
6. Visible gastric peristalsis moving from left to right across the epigastrum. 7. Decreased frequency & volume of stools. 8. Signs of malnutrition & dehydration DX: x-ray “ string sign”, Endoscopy MX: Surgery ( pyloromyotomy) fredet ramstedt procedure
Ndx: Risk for deficient fluid volume r/t inability to retain food Risk for infection at site of surgical incision r/t danger of contamination from feces d/t proximity of incision to diaper area
Hydration Pacifier may give thickened feedings on upright position then NPO just before surgery Monitor I and O, weight, and vomiting Postop 1. dropper feeding 4-6 hrs after surgery 45 min- 1 hr duration; oral rehydration soln then half strength breastmilk/formula at 24 hr interval 2. Side lying position 3. Monitor weight and return of peristalsis 4. Wound care 5. Pacifier for oral needs
Herniation of intestinal content into the thoracic cavity Left side S/sx:respiratory difficulty, cyanosis, retractions, (-) breath sounds affected side, scaphoid abdomen Cx: pulmonary HPN Mx:’E’ surgery
Ndx: Risk for ineffective airway clearance r/t displaced bowel Risk for imbalanced nutrition, less than body requirements, r/t NPO status
Preop Elevate head Low intermittent suction Postop 1. Semi-fowlers 2. Maintain warm, humidified envt – lung fluid drainage 3. Suction prn 4. Chest pptx 5. NPO – prevent pressure on diaphragm
Malabsorption syndrome that occurs when the mucosa of the proximal small intestine is sensitive to gluten. (wheat, rye, oats, barley) inability to absorb fat, thus steatorrhea, def fat soluble vitamins, malnutrition and distended abdomen S/Sx appears bet 1-5 yo after introduction of gluten in the diet. S/sx:diarrhea, wt loss, anorexia, irritable, anemic (Fe deficiency)
Celiac Disease/Gluten sensitive enteropathy/Celiac sprue
Intolerance for or inability to digest gluten >>>accumulation of the amino acid glutamine>>>toxic to intestinal mucosal cell>>> intestinal villi atrophy >>>reduction of absorptive surface of the small intestine.
CELIAC CRISIS (due to ingestion of gluten, infections, prolonged fasting) = acute vomiting and diarrhea & may lead to F & E imbalance & rapid dehydration. Dx: Biopsy of the jejunum reveals the mucosal surface with hyperplastic villus atrophy. ( Definitive diagnosis of celiac disease). This characteristic lesion return to normal after dietary restriction of gluten which helps confirm the dx. Mx: hydration, gluten free diet, vitamin & Fe supplementation , avoid cereals, bread, cake, cookies, spaghetti, pizza, instant soup, some chocolates, some ice cream, donuts, pies, hotdogs,
Foods allowed: 1.Meats: beef, pork, poultry & fish 2. Eggs 3. Milk & dairy products: milk, cheese, cream 4. Fruits & veg: all 5. Grains: rice, corn, gluten free wheat flour, corn flakes, corn meal & gluten free pre-cooked cereals
Autosomal recessive Chronic multisystem disorder of the exocrine glands characterized by abnormally thick pulmonary secretions. Affects lungs, pancreas, intestines and sweat glands, salivary glands, reproductive tract.
S/SX: GI - meconium ileus, rectal prolapse,( most common GI sign); loose, bulky, fatty stools (steatorrhea,) malnutrition ( vit ADEK deficiency), failure to thrive; marked tissue wasting; distended abdomen thin extremities. Respiratory –wheezing, recurrent infection,cough, dyspnea, clubbing, cyanosis, atelectasis, generalized obstructive emphysema, chronic sinusitis, bronchitis, ear, nose, throat problems.
Reproductive – Female – delayed puberty & decreased fertility ( from decreased viscosity of cervical mucus which blocks the entry of sperm) Male – infertile, sterility is due to blockage of the vas deferens with abnormal secretions. Cardiovascular – Cor Pulmonale, right sided heart enlargement, CHF d/t obstruction of pulmonary flow S/SX of hyponatremia – rapid IV
Integumentary – > Increased concentrations of sodium & chloride in sweat; parents report “salty” taste when they kiss their babies. > Failure to thrive may result in hypoalbuminuria, which causes edema.
Dx: > “Sweat test” (Chloride 2-5x the normal), > absence of pancreatic enzymes, >immunoreactive trypsinogen in blood > stool analysis – steatorrhea > xray – patchy atelectasis & generalized obstructive emphysema. Mx: chest physiotherapy, antibiotics, pancreatic enzymes, vitamins, lung or pancreas transplant
Hi calorie, Hi CHON, moderate fat diet Nebulization and physiotherapy Frequent Position changes when in bed Oral care Adequate rest and comfort
Congenital club foot
clubfoot, or talipes equinovarus is a birth The foot is twisted in (inverted) and down.
Mgt : long leg cast q2 wks 6-12 weeks
Denis browne splint (bar shoe)
surgical correction- 3-6 mos
Congenital Hip Dysplasia
Imperfect hip development affecting femoral head and acetabulum Female Unilateral more common Inc frequency w/ breech delivery
A. Lower right leg B. asymmetric skin
Etiology: Unknown Possible Causes: a. Abnormal Development of the joint caused by: > Fetal position > Genetic factors b. Abnormal relaxation of the capsule & ligaments of the joint caused by hormonal factors. c. Environmental factors such as breech delivery
S/sx: limited abduction of affected hip shortening of leg on affected side ( Galeazzi / Allis sign ) asymmetric thigh and gluteal folds buttocks on affected side will flatten on prone pelvis dips on normal side when standing on affected leg ( Trendelenburg ) palpable click ( Ortolani’s click)
. Leg length Inequality with unilateral complete dislocation. . Delayed walking . Limp > Trunk dips when the child puts weight on his involved leg. > Waddling gait is observed in children with bilateral dislocation.
maintaining hip in abduction traction and casting
Goal: To restore as closely as possible anatomic alignment of the hip while maintaining pain-free function. Early recognition is the key to successful treatment. 1. Tx varies with age & extent of the defect. 2. Early Stage ( Birth – 3 months) a. Reduction by gentle manipulation. b. Splinting the hip by means of
3. Later Stages ( 3-18 months) a. Preliminary traction b. Closed reduction c. Immobilization in a hip spica cast or splint or Pavlik harness 4. Older child ( 18 mos – 4 yrs old) a. Preliminary traction b. Possible need for open reduction or osteotomy. c. Immobilization in a hip spica
some splinting devices used for DDH
principle: normal development of the femoral head and the acetabulum depends on reestablishing a normal acetabulofemoral relationship that is sufficiently stable to permit early motion von Rosen
Collective term for all SC disorders
Spina Bifida Occulta – posterior laminae fail to fuse - dimpling, abnormal tufts of hair Meningocoele - meninges herniate through unformed vertebrae; protrusion covered by a layer of skin - usually occurs in the lumbar region - protrusion is covered by a skin layer or only the clear dura mater
Myelomeningocoele – SC and meninges protrude through the vertebrae defect
- absent motor and sensory function
- flaccidity, lack of sensation in LE - loss of bowel and bladder control - may be accompanied by hydrocephalus Dx: sonography
Types of Hydrocephalus? Congenital hydrocephalus -is present at birth
and may be caused by environmental influences during fetal development or by genetic factors.
Acquired hydrocephalus -develops at the time of
birth or at some point afterward. This type of hydrocephalus can affect individuals of all ages and may be caused by injury or disease.
Communicating hydrocephalus -occurs when
the flow of cerebrospinal fluid (CSF) is blocked after it exits the ventricles . the CSF can still flow between the ventricles, which remain open
Non-communicating hydrocephalus-also called
"obstructive" hydrocephalus -- occurs when the flow of CSF is blocked along one or more of the narrow pathways connecting the ventricles.
S/sx: head enlargement, ant fontanel wide and bulging, scalp veins dilated, broad forehead, sclera shows above iris, brisk tendon reflexes, spasticity, irritability, lethargy, poor appetite, cracked pot sound on percussion
Congenital Heart Defects -CHD are structural defects of the heart, great vessels, or both that are present at birth. -Children with CHD are more likely to have associated defects such as tracheoesophageal fistula. - CHD is second only to prematurity as a cause of death in the first year of life.
1.Acyanotic Heart Disease – conditions that interfere with normal blood flow through the heart either by slowing it down or by L R shunt high pressure to low pressure oxygenated to unoxygenated blood 2. Cyanotic Heart Disease – allow unoxygenated blood into the systemic circulation R L shunt
4 Classifications of Congenital Heart Defects: Defects with increased pulmonary blood flow: a. Atrial Septal Defect (ASD) b. Ventricular Septal Defect (VSD) c. Patent Ductus Arteriosus (PDA) 2. Defects with Decreased pulmonary blood flow: a. Tetralogy of Fallot (TOF) b. Tricuspid Atresia ( TA)
3. Obstructive Defects: a. Coarctation of the Aorta ( COA) b. Aortic stenosis ( AS) c. Pulmonic stenosis ( PS) 4. Mixed Defects: a. Transposition of the Great Vessels ( TOGV) b. Truncus Arteriosus c. Hypoplastic left Heart Syndrome ( HLHS)
ACYANOTIC HEART DISEASE
1. Atrial Septal Defect
Opening between 2 atria Atrial septal tissue does not fuse properly during embryonic development S/sx: cyanosis(CHF), dyspnea on exertion, fatigue, failure to thrive, split S2 Mx: surgery 1-3 yo Cx: endocarditis, heart failure Postop: monitor arrhythmia, administer antibiotics
Pathophysio: Pressure is higher in the left atrium than the right >>>blood shunts from the left to the right >>>RV & pulmonary artery enlarge ( they are handling more blood). Notes: >Most infants are asymptomatic until early childhood; many defects close spontaneously by 5 yo. DX: Echocardiography –reveals enlarged right side of the heart & inc. pulmonary circulation.
2. Ventricular Septal Defect Opening in ventricular
septum, most common S/sx: respi infections, failure to thrive, dyspnea, fatigue, pansystolic murmur Mx:close spontaneously otherwise surgery <2 yo Cx:pulmonary HPN, endocarditis, heart failure Postop: monitor arrhythmia, administer antibiotics
Ventricular septal defect
Sometimes called a hole in the heart most common congenital heart defect occurs when the septum, the muscular wall separating the right and left ventricles, fails to fully form The hole allows oxygen-rich blood to leak from the left ventricle into the right ventricle, instead of moving into the aorta and on to the body. Too much blood may flood the lungs. This defect can lead to heart failure, excessive blood pressure in the lungs (pulmonary hypertension), infections of the heart (endocarditis), irregular heartbeats (arrhythmias) and delayed growth. Small holes may heal on their own or cause no symptoms. Larger holes may require surgical repair by stitching together or covering with a patch.
Congenital Heart Defect
3. Patent Ductus Arteriosus Aorta to pulmonary artery
Fetal ductus arteriosus fails to close after birth Common in prematurity, high altitude, maternal rubella females S/sx:clubbing, dyspnea, “machine like murmur” (2nd-3rd ICS) Cx:heart failure, endocarditis, pulmonary artery stasis/HPN Mx:Indomethacin, surgery/2-3yo
Patent ductus arteriosus
Before birth, a temporary blood vessel called the ductus arteriosus connects the pulmonary artery and the aorta. This allows blood to bypass the lungs because oxygen is delivered to the fetus through the placenta and umbilical cord. The temporary vessel normally closes within a few hours or days of birth since the lungs take over. If it remains open (patent), some blood that should circulate through the body is misdirected to the lungs. This defect can cause heart failure or endocarditis. In infants, it can be closed with medications. In older children and adults, plugs, coils or surgery can be used to close the vessel.
Congenital Heart Defect
CYANOTIC HEART DISEASE
1. Tetralogy of Fallot
Localized narrowing of the aorta. TOF consists of 4 major anomalies: 1. VSD 2. Right Ventricular Hypertrophy 3. Pulmonic Stenosis 4. Aorta overriding the VSD
Tetralogy of Fallot
This defect is a combination of four (tetralogy) congenital abnormalities. The four defects typically are ventricular septal defect (VSD), pulmonary stenosis, a misplaced aorta and a thickened right ventricular wall (right ventricular hypertrophy). They usually result in an insufficient amount of oxygenated blood reaching the body. Complications of tetralogy of Fallot (fuh-LOE) include cyanosis — sometimes called "blue baby syndrome," since the lips, fingers and toes may have a bluish tinge from lack of oxygen — as well as poor eating, inability to tolerate exercise, arrhythmias, delayed growth and development, and stroke. Surgical repair of the defects is required early in life. Tet spells- irritability, pallor and blackouts or convulsions,
Pathophysio: PS impedes flow of blood to lungs>>>inc pressure in the rt ventricle ( causes hypertrophy)>>>forces deoxygenated blood thru the septal defect to the left ventricle >>>overriding aorta receives blood from both rt & left ventricles.
1.Acute episodes of cyanosis ( “ Tet spells”). Tet spells are characterized by irritability, pallor & blackouts or convulsions. Cyanosis occuring at rest as PS worsens clubbing, exertional dyspnea, fainting, fatigue slowness due to hypoxia Squatting,( a characteristic posture of older children that serves to decrease the
return of poorly oxygenated venous blood from the lower extremities & to increase systemic vascular resistance, which increases pulmonary blood flow &
DX: Echocardiography – shows enlarged rt chamber & dec in pulmonary artery size > Cardiac catheterization & Angiography – allows definitive evaluation Cx: thromboembolism,CVA Mx: 1. Surgical repair when infant is 1 yo Blalock Taussig: anastomose SC and pulmonary artery - avoid BP and venipuncture in right arm
2. Tricuspid - Tricuspid valve fails to develop Atresia
-Without the tricuspid valve, there is no communication between the right atrium & the right ventricle -Involves complete mixing of oxygenated & unoxygenated blood on the left side of the heart resulting in pulmonary obstruction. Blood flows thru a patent foramen ovale to the left side of the heart & thru the VSD, to the right ventricle & to the lungs.
S/S: 1.Cyanosis in NB 2. Chronic hypoxia, clubbing in older children DX: Echocardiography MX: 1.Palliative procedures such as pulmonary to systemic artery anastomosis ( for children w/ CHF) 2. Corrective surgery may be performed
1. Transposition of the Great Vessels
Pulmonary artery leaves the L ventricle, Aorta exits the right ventricle. No communication bet systemic & pulmonary circulations This defect results in 2 separate circulatory patterns. Rt heart – systemic circulation Left heart – pulmonary circulation.
Transposition of the great vessels/ arteries:
With this defect, the positions of the aorta and the pulmonary artery (the great arteries) are reversed (transposed). The aorta arises from the right ventricle instead of the left and the pulmonary artery arises from the left ventricle instead of the right. This creates a circulatory pattern that prevents nourishing oxygenated blood from reaching the body. This condition would quickly be fatal to a newborn except it's generally accompanied by another defect — commonly a septal defect or patent ductus arteriosus — that does allow oxygen-rich blood to get to the body. Surgical repair is usually necessary shortly after birth.
** To sustain life, the child must have an associated defect ( VSD, ASD, PDA)- which permits oxygenated blood into the systemic circulation, but cause increased workload. S/SX: 1.In infants w/ no associated defects, severe respiratory depression & cyanosis 2. In infants w/associated defects, less cyanosis but may have sx of CHF Mx: PGE for PDA, Balloon catheter to create ASD, Arterial switch procedure-
Total Anomalous Pulmonary Venous Return
Pulmonary v. drain to SVC or R atrium PDA or foramen ovale essential S/sx :cyanosis, fatigue CX: R heart failure Mx: PGE, surgery
This is a defect in which the normally distinct pulmonary artery and aorta merge into one single great vessel (truncus) arising from the right and left ventricles. In addition, there's usually a large ventricular septal defect, essentially turning the right and left ventricles into a single chamber. This allows oxygenated and unoxygenated blood to mix. Too much blood may flow to the lungs, flooding them and making it difficult to breathe. It can also result in life-threatening pulmonary hypertension. Surgery is needed to close the septal defect with a patch and to separate the pulmonary arteries from the trunk. A conduit is placed to connect the right ventricle to the pulmonary artery. Because the conduit doesn't grow with the child, repeat surgery may be necessary over time.
Hypoplastic left heart syndrome
Hypoplastic left heart syndrome
In this condition, the left side of the heart is underdeveloped (hypoplastic), including the aorta, aortic valve, left ventricle and mitral valve. As a result, the body doesn't receive enough oxygenated blood. In the first few days after a baby is born, the ductus arteriosus remains open (patent), allowing normal circulation, so the baby may seem fine initially. But when the ductus arteriosus naturally closes, signs and symptoms begin, including a bluish cast to the skin from lack of oxygen, difficulty breathing and poor feeding. This condition may be accompanied by an atrial septal defect. Treatment options for this life-threatening condition are a heart transplant or a multistage surgical procedure done during the first few years of life.
Atrioventricular canal defect
Atrioventricular canal defect This is a combination of defects, including a large hole in the center of the heart and a single common valve instead of the separate tricuspid and mitral valves. Also called atrioventricular septal defect, this defect is classified by whether it's only partial, involving only the upper chambers of the heart, or complete, in which blood can travel freely among all four chambers of the heart. Both forms allow extra blood to circulate to the lungs, causing the heart to enlarge. The condition is often associated with Down syndrome. Infants may also have trouble breathing and not grow well. Surgery is often done in infancy to close the hole and reconstruct the valves.
1. Coarctation of the Aorta
males Constriction of aorta S/sx: asymptomatic HPN, irritability, headache, epistaxis, dyspnea, bounding UE pulses, higher BP in upper extremities, dec femoral and distal pulses,systolic murmur Cx:chronic HPN Mx:surgery 2 yo Postop: monitor abdominal pain, antihypertensives
Coarctation of the aorta
This is a narrowing (coarctation), or constriction, in a portion of the aorta. Coarctation forces the heart to pump harder to get blood through the aorta and on to the rest of the body. This defect can cause several life-threatening complications, including severe hypertension, aortic aneurysm, dissection or rupture, endocarditis, brain hemorrhage, stroke, heart failure and premature coronary artery disease. Repair is typically recommended before age 10, either by surgically removing the affected portion or widening it through balloon angioplasty and placement of a stent.
defect that narrows or obstructs the aortic valve opening, making it difficult for the heart to pump blood into the aorta. Mild cases may not have symptoms initially, but they can worsen over time. The defect can cause heart enlargement, left-sided heart failure, arrhythmias, endocarditis and fainting. Treatment includes surgical repair or replacement of the valve or, in young children, widening through balloon valvuloplasty
2. Aortic Stenosis
-Involves an obstruction of the ventricular outflow of the blood S/SX: faint pulse, hypotension, tachycardia, poor feeding, exercise intolerance, chest pains DX; ECG, Echocardiography reveals left ventricular hypertrophy. MX: -Surgical aortic valvutomy or prosthetic valve replacement.
the flow of blood from the right ventricle to the pulmonary artery is obstructed by narrowing at the pulmonary valve. When there's an obstruction (stenosis), the right ventricle must pump harder to get blood into the pulmonary artery. The defect may occur along with other defects, such as thickening of the muscle of the right ventricle immediately below the valve.
in many cases, pulmonary stenosis is mild and doesn't require treatment. But because it can cause heart failure, arrhythmias or enlargement of the right heart chambers, surgery may be necessary to repair the stenosis or replace the valve. Special balloons to widen the valve (balloon valvuloplasty) may also be used.
Kawasaki Disease/ Mucocutaneous Lymph Node Syndrome Before puberty, peaks 4 yo
S/sx:spiking fever x 5 days, bilateral conjunctivitis, reddened pharynx, dry lips, strawberry tongue, cervical lymphadenopathy, peripheral edema, erythema and desquammation, truncal rash, arthritis Patho: Respi infection immune complex systemic vasculitis Unwanted Cx: aneurysm and MI Dx:clinical Mx: Salicylates and Immunoglobulins given via IV
Other Measures: Protect edematous areas Record intake and output Offer soft food Administer prescribed medication
Rheumatic Fever Autoimmune
Grp A Beta hemolytic strep 6-15 yo, peaks 8 yo 1-3 wks after untreated infection Dx: 5 major criteria – polyarthritis, carditis, subcutaneous nodules, erythema marginatum, sydenham’s chorea minor – fever, polyarthralgia, hx of RF, inc ESR, antecedent strep infection
N. E. S.
S/SX: 1.Carditis – sx include tachycardia, cardiomegaly, murmur, muffled heart sounds, precordial pain. 2.Polyarthritis – consists of swollen, hot, painful joints 3.Syndenham Chorea or St. Vitus dance – demonstrated by sudden, aimless, irregular movements of the extremities, involuntary facial grimaces, speech disturbances. 4. Erythema marginatum – clear centered,transitory, nonpruritic
MX: 1.Child may receive monthly injections of benzathine penicillin, 2 daily oral doses of penicillin ( to prevent recurrent streptococcal infections CX:= Mitral valve insufficiency & myocarditis To diagnose: = either 2 major or I major 2 minor criteria present
Nursing Care Monitor vital signs Provide adequate nutrition Promote safety to prevent chorea related injuries
Inflammation of glomeruli or kidney Follows infection with strep 10-14 days 5-10 yo Males
S/sx:sudden onset of edema and hematuria, proteinuria, hypertension Dx: urinalysis and 24 hour urine hypoalbuminemia inc ESR, BUN, Crea, antistreptolysin O
Mx: semi fowlers diuretics, antibiotics O2 antihypertensives Nsg Care: quiet play activities diet – normal CHON, mod salt restriction, fluid restriction daily weight and output
Altered glomerular permeability(autoimmune); inc permeability to albumin 3 yo Males Minimal change syndrome
S/sx: proteinuria, edemaperiorbital area, hypoalbuminemia, hyperlipidemia Dx:urinalysis and 24 CHON, inc ESR hr
Mx:steroids, immunosupressant NDx: Risk for decreased fluid volume r/t CHON and fluid loss Imbalanced nutrition: less than BR r/t CHON and fluid loss Nsg care: Adequate nutrition proper diet – dec salt Weigh daily, monitor I and O Protect edematous areas Administer prescribed drugs Health teaching
Malignant tumor of the kidney Associated with other anomalies 6 mos-5 yo, peaks 3-4 yo Good prognosis S/sx:abdominal mass, hematuria, low grade fever, anemia, wt loss Dx: CT scan Mx: Nephrectomy, radiotherapy avoid abdominal palpation
Inflammation of glomeruli or kidney Follows infection with strep (10-14 days) 5-10 yo, peak 6-7 yo Males Etiology : GABS ( Group A Beta Hemolytic Streptococcus) Poststreptococcal infection ( usually of the skin- impetigo or upper respiratory tract.
S/SX: >history of infection about 10 – 14 days before the onset of sx. >irritablity, fatigue & lethargy >anorexia, pallor , hypertension > sudden onset of edema ( periorbital) and hematuria ( urine is brown (tea or cola colored) Dx: urinalysis and 24 hour urine mild hypoalbuminemia inc ESR, BUN, Crea, antistreptolysin O
Mx: semi fowlers diuretics, antibiotics, O2 antihypertensives – calcium channel blockers, B- blockers, ACE inhibitors ( Angiotensin converting enzyme) Nsg Care: quiet play activities diet – normal CHON, mod salt restriction, fluid restriction daily weight and output
Altered glomerular permeability(autoimmune); inc permeability to albumin 3 yo Males Minimal change syndrome S/sx: proteinuria, edemaperiorbital area, significant hypoalbuminemia, hyperlipidemia Dx:urinalysis and 24 hr CHON, inc ESR
Mx: steroids, immunosupressant NDx: Risk for decreased fluid volume r/t CHON and fluid loss Imbalanced nutrition: less than BR r/t CHON and fluid loss Nsg care: Adequate nutrition, proper diet – dec salt Weigh daily, monitor I and O Protect edematous areas Administer prescribed drugs Health teaching
Wilms tumor( nephroblastoma)
is the fifth most common pediatric malignancy and the most common renal tumor in children. NURSE : post a sign DO NOT PALPATE THE ABDOMEN on the bed
A cancer of the bone that usually affects the large bones of the arm or leg. common site : epiphyseal plate of the long bones (femur) It occurs most commonly in young people and affects more males than females.
Atopic Dermatitis 2 mos-3 yo
R/t food allergy S/sx: papular and vesicular skin eruptions w/ erythema, pruritus, dry,flaky scales upon healing Mx: reduce allergen, topical steroids NDx: Impaired skin integrity r/t eczematous lesion Nsg care: Reduce allergen Prevent skin dryness and pruritus
Protein Energy Malnutrition
Marasmus Low calorie, low CHON 0-2 yo (-) edema “all skin and bone” (+) growth retardation Apathetic, quiet Good appetite Infrequent skin/hair changes Anemia uncommon
Kwashiorkor Low CHON 1-3 yo (+) edema Wasting variable Growth retardation variable Irritable, moaning Poor appetite (+) skin and hair changes (+) anemia