CARDIAC Cardiac Assessment o Normal pediatric vital signs HR o Newborn 100-180 o 1 wk-3 mo 100-220 o 2 mo- 2 yr 60-150 o 2-10 yr 70-110 o 10 yr-adult 55-90 Cardiovascular disease has 2 major groups o Congenital heart disease (CHD) Primarily anatomic abnormalities present at birth that result in abnormal cardiac function 2 types Heart failure (HF) Hypoxemia o Acquired cardiac disorders Disease processes or abnormalities that occur after birth and can be seen in normal heart or the presence of genital heart defects Various factors: Infection Autoimmune responses Environmental factors Familial tendencies History & physical exam o HISTORY HISTORY HISTORY!!!! o Inspection Nutritional state- failure to thrive or poor weight gain is associated with heart disease Color- cyanosis common feature of CHD Pallor associated with poor perfusion Chest deformities- enlarged hears distorts chest configuration Unusual pulsations- visible pulsations of the neck veins are seen sometimes Respiratory excursion- refers to ease or difficulty of respiration Clubbing of fingers- associated with cyanosis o Palpation and Percussion Chest- maneuvers help discern heart size and other characteristics Abdomen hepatomegaly or spenomegaly 2 Peripheral pulses- rate, regularity, and amplitude o Auscultation Heart rate and rhythm- listen for fast heart rates, slow, and irregular rhythms Character of heart sounds- listen for distinct or muffled sounds, murmurs, and additional heart sounds o Diagnostic Electrocardiogram Nurse should assess the patient, not the monitor Echocardiography Most frequently used tests for detecting cardiac dysfunction Involves use of ultra-high-frequency sound waves to produce an image of hearts structure Transducer placed directly on chest wall delivers repetitive pulses of ultrasound and processes the returned signals
Cardiac Catheterization Invasive diagnostic procedure in which a radiopaque catheter is inserted thru a peripheral blood vessel into the heart Catheter is guided thru the heart with aid of fluoroscopy After tip of catheter is within a heart chamber, contrast material is injected, and films are taken of the dilution and circulation of the material (angiography) Types: o Diagnostic catheterizations: Used to diagnose congenital cardiac defects- particularly in symptomatic infants & before surgical repair Divided into right-sided catheterizations, in which cateheter is introduced through a vein & threaded into right atrium Left-sided catheterization- catheter is threaded thru an artery into aorta and into the heart o Interventional catheterizations: Therapeutic catheterization A balloon catheter or other device is used to alter the cardiac anatomy Interventions: Balloon atrioseptostomy o Transposition of great arteries o Some complex single-ventricle defects Balloon dilation o Valvular pulmonic stenosis o Branch pulmonary artery stenosis o Congenital valvular aoritic stenosis o Rheumatic mitral stenosis o Recurrent coarctations of aorta o Congential mitral stenosis Coil occlusion 3 o PDA (<4mm( Transcatheter device closure o ASD Amplatzer septal occluder o ASD VSD devices o VSDs Stent placement o Pulmonary artery stenosis o Coarctation of the aorta in adolescents o Use to treat other lesions RF ablation o Some tachydysrthymias o Electrophysiology studies Catheters with tiny electrode that record the impulses of the heart directly from conduction system are used to evaluate dysrthymias & sometimes destroy accessory pathways that cause some tachydsrthmias Possible side effects: o Acute hemorrhage from entry site o Low-grade fever o Nausea o Vomiting o Loss of pulse in catheterized extreme o Transient dysrhythmias Rare risks: o Stroke o Seiure o Tamponade o Death Preprocedural care: o Prepare child & fam for procedure o Use developmentally appropriate materials o Assess & mark pulses o Basline O2 sats o NPO for 4-6 hours before procedure Postprocedural: o Observe of the following for signs of complications: Pulses Temp & color of affected extremity Vital signs- q 15 minutes Blood pressure Dressing Fluid intake Bloog glucose levels- for hypoglycemia 4 Postpericardiotomy syndrome o Symptoms: Fever Pericardial friction rub Pericardial & pleural effusion o Occurs immediate post op o Also can occur later (day 7-21) o Cause=unknown
CONGENTIAL HEART DISEASE (CHD) Incidence: o 5-8 per 1000 live births o 2-3 are symptomatic in 1 st year of life o CHD=major cause of death in first year of life (after prematurity) o Most common anomaly= ventricular septal defect Causes: o Chromosomal/genetic 10-12% o Maternal/environmental 1-2% Maternal drug use Infants that have FAS- 5-% have CHD Maternal illness Rubella infection PDA & pulmonary branch stenosis Cytomegalovirus, toxoplasmosis, other viral illness Infants of diabetic mothers (IDMs) o Multifactorial 8%% Normal fetal circulation changes o When newborn takes 1 st breath, the fetal vascular system undergoes abrupt changes Umbilical vein & umbilical arteries Before birth, umbilical vein delivers O2 and nutrients to a fetus Foramen ovale Closes as pressure in left atrium exceed pressure in right atrium Ductus arteriosus Starts to close in presence of increased O2 o The following are NO LONGER NEEDED: Foramen ovale Shunts highly oxygenated blood from RA to LA & supplies upper extremities and head Ductus venosus Fetal blood vessel connecting UV to IVC Umbilical vessels o WITH THE FIRST BREATH Lungs expand causing dramatic fall in pulmonary vascular resistance 5 Market increase in pulmonary blood flow (raising LA pressure above that of IVC) A progressive thinning of the walls of pulmonary arteries occurs Blood pressure is now high in the aorta & the babys systemic circulation is well established The ductus arteriosus contstricts at birth, but there is often a small shunt of blood from the aorta to the Left Pulmonary Artery for a few days This decreases with increases PO2 which stimulates bradykinin release Umbilical arteries constrict functionally, later become fibrous o o History indicators of cardiac dysfunction Symptoms may appear 4-12 weeks after birth Failure to thrive, poor weight gain, activity intolerance Developmental delays Positive prenatal history Positive family history of cardiac disease o Physical indicators of cardiac dysfunction: Poor feeding Tachypnea, tachydardia Diaphoresis Crackles Hepatomegaly 6 Cyanosis Murmur Sternal lift Impaired myocardial function Tachycardia Fatigue Weakness Restlessness Pale Cool extremities Decreased BP Decreased output Pulmonary congestion Tachypnea Dyspnea Respiratory distress Exercise intolerance Cyanosis Systemic venous congestion Peripheral & periorbital edema Weight gain Hepatomegaly Neck vein distention Goals of management o Support maximal growth & nutrition o Reduce cardiac workload o Prevent & treat congestive heart failure o Maintain optimal cardiac output o Provide palliative procedures to protect lungs from too much bloow flow, or too little blood flow o Correct the underlying defect o Maintain fluid & electrolyte balance o Prevent secondary complications (failure to thrive, cardiogenic shock, infection, respiratory compromise, cardiac dysrthythmia, thromboembolism) Diagnostic tests: o H&P o Chest x-ray o Echocardiogram, EKG o Labs: ABGs CNC Electrolyte panel Therapeutic & diagnostic cardiac catheterization Therapeutic nursing management o Avoid situations that increase cardiac demands (fever, pain, agitation) o Avoid unnecessarily disturbing the infant 7 o Monitor weights o Small frequent feedings (increased calorie formula as needed) o O2 as needed o Administer pharmacologic agents as ordered; evaluate patient response to treatment o Portect from infection o Accurate I&O Pharmacology: o Depends on defect & MOST IMPORTANTLY patients clinical condition Digoxin Diuretics Prostaglandin Keep PDA open Indomethacin Close PDA Vasopressors Vasodilators Vaccinations as indicated Complications: o Heart failure o Postpericardiotomy syndrome Post-op period: fever, pericardial friction rub, pleural effusion o Cerebral thrombosis o Failure to thrive o Death Older Classifications of CHD o Acyanotic May become cyanotic o Cyanotic May be pink May develop congestive heart failure Newer classification of CHD o Hemodynamic characteristics (blood flow patterns within the heart): 1. Increased pulmonary blood flow 2. Decreased pulmonary blood flow 3. Obstruction of blood flow out of the heart 4. Mixed blood flow
Increased Pulmonary Blood Flow Defects Abnormal connection between the 2 side of the heart o Either the septum or great vessels Increase blood volume on RIGHT side of heart Increased pulmonary blood flow Decreased systemic blood flow 8 Defects: o Atrial Septal Defect (ASD) Acyanotic Hole between two atria Allowing blood from higher pressure left atrium to follow into the lower pressure right atrium Closes naturally, with therapeutic catheterization of surgery Loud, harsh murmur With fixed split second heart sound Enlarged right side of heart Increased oxygen saturiation in right atrium Mild congestive heart failure May be asymptomatc Surgical patch closure o Ventricular Septal Defect (VSD) Acyanotic Hole between right & left ventricles Most common cardiac defect Closes naturally or with surgical correction Loud, harsh murmur that begins at about 4-8 weeks of age O2 saturation is higher that normal in right ventricle Congestive heart failure Failure to thrive Dysrthymias Small defects may be asymptomatic o Atrioventricular canal defect Combo of ASD & VSD Acyanotic Incomplete fusion of endocardium creating a large central AV valve that allows blood to flow between all four chambers of the heart Most common cardiac defect in children with Down syndrome Flow is determined by pulmonary and systemic resistance Surgical repair required 9 CHF Loud systolic murmur Cyanosis increases with crying Pulmonary vascular obstructive disease Increased blood volume is pumped into the lungs, which may eventually result in increased pulmonary vascular resistance o Patent Ductus Arteriosus (PDA) Acyanotic Fetal vessel between the pulmonary artery and the aorta that fails to close PDA is common in premature infants Closure occurs naturally, with Indomethacin, therapeutic catherization, or surgery Machinery-like murmur Patients at risk for BE and pulmonary vascular obstructive disease later in life from chronic excessive pulmonary blood flow Tachycardia Enlargement of left ventricle Wide pulse pressure Bounding pulses Tachypnea
OBSTRUCTIVE DEFECTS Blood exiting the heart meats an area of anatomic narrowing (stenosis) causing obstruction to blood flow The pressure in ventricle and in great artery before obstruction is increased, and the pressure in the area beyond the obstruction is decreased Location of narrowing is usually near the valve: o Vavlular- at site of valve o Subvalvular- narrowing in the ventricle below the valve (ventricular outflow tract) o Suprvalvular- narrowing in great artery above valve There is a pressure load on the ventricle and decreased cardiac output Clinically exhibit signs of HF Defects: o Coarctation of the Aorta Acyanotic Narrowing of the aorta due to a constricting band Increased blood pressure and oxygen saturation in the upper 10 extremities as compared with the lower extremities Headaches Vertigo Nosebleeds Absence of femoral pulses High blood pressure Leg pain Decreased cardiac output CHF Surgical repair & reconstruction is usually needed Cool lower extremities o Aortic Stenosis Acyanotic Narrowing of aortic valve Causing resistance to blood flow in left ventricle, decreased cardiac output, left ventricular hypertrophy, & pulmonary vascular congestion Left ventricular enlargement Systolic ejection murmur Faint pulses, hypotension, tachycardia, poor feeding Exercise intolerance, chest pain, and dizziness Decreased cardiac output Opened with balloon procedure or surgery Risk for: o BE, coronary insufficiency, & ventricular dysfunction o Pulmonic Stenosis Acyanotic Narrowing of the pulmonary valve or pulmonary artery Resistance to blood flow causes right ventricular hypertrophy & decreased pulmonary blood flow Right ventricular enlargement Systolic ejection murmur Exercise intolerance CHF, cyanosis Opened with balloon procedure or surgery
DECREASED PULMONARY BLOOD FLOW DEFECTS Tetralogy of Fallot o Cyanotic o Four anamolies are present: Pulmonary stenosis 11 VSD Dextroposition of aorta Enlargement of the right ventricle o Palliative shunt may be placed until child is able to have the surgical corrective repair o Systolic murmur o Cyanosis o Polycthemia o Clot formation o Severe dyspnea o Squatting position o Hypercyanotic spells (Tet Spells) o Acidosis o Clubbing of the fingers o Growth retardation o Failure to thrive Tricuspid Atresia o Cyanotic o Tricuspid valve is completely closed o Generally requires several complex surgeries o Incompatible with life if there is inadequate pulmonary blood flow o PGE infusion is used until an emergency shunt procedure can be performed o The Fontan procedure is the surgical repair o No blood flow from right atrium to right ventricle o Severe cyanosis within hours after birth (Increased as the PDA closes) o CHF o Failure to thrive
MIXED DEFECTS Transposition of the great arteries or transposition of the great vessels o Cyanotic o Aorta arises from the right ventricle instead of the left, and the pulmonary artery arises from the left instead of the right o Incompatible with life if there is no connection between right and left sides o Emergency septostomy is performed to create a connection between the right and left sides o The surgical repair is the atrial switch procedure 12 o Severe cyanosis hours to days after birth (as PDA closes) o Various murmurs o Presence of ASD and VSD o CHF Total anomalous pulmonary venous connection o Cyanotic o Total anomalous pulmonary venous return o Rare defect characterized by failure of pulmonary veins to join the left atrium; instead are connected with the venous system o Repaired surgically o Cyanosis (inversely related to amount to pulmonary blood flow) o May initially be asymptomatic o CHF, cardiac failure, death Truncus Arteriousus o Cyanotic o Failure of normal separation in development of the pulmonary artery and aorta, resulting in a single vessel that overrides both ventricles; mixing pulmonary & systemic circulations o Repaired in first few months of life (closing VSD and hemographs- modified Rastelli procedure) o CHF o Cyanosis o Poor growth o Activity intolerance o Murmur o Brain abscess o Bacterial endocarditis Hypoplastic heart syndrome o Left sided Cyanotic Left ventricle is NONFUNCTIONAL Requires several complex surgeries or cardiac transplantation for survival Right ventricular enlargement Severe cyanosis Severe decreases in cardiac output
13 CHF IN CHILDREN Impaired myocardial function o Tachycardia o Fatigue o Weakness o Restlessness o Pale o Cool extremities o Decreased blood pressure o Decreased urinary output Pulmonary congestions o Tachypnea o Dyspnea o Respiratory distress o Exercise intolerance o Cyanosis Systemic venous congestions o Peripheral & periorbital edema o Weight gain o Ascites o Hepatomegaly o Neck vein distention
ENDOCARDITIS Bacterial endocarditis (BE) and subacute endocarditis (SBE) are now referred to as infective endocarditis (IE) Often a sequela of bacteremia in children with CHD or AHD Most common causative agents: o Streptococcus viridans or Staphylococcus aureus o Fungal agents such as Candida albicans Prophylaxis for 1 hour before procedures (IV) or may use PO in some cases o Antibiotics Clinical manifestations: o Onset usually insidious o Unexplained fever o Anorexia o Malaise o Weight loss o Characteristic findings caused by extracardiac emboli formation Splinter hemorrhage (think black lines) under the nails Osler nodes Janeway lesions Petechiae on oral mucous membranes o May be present: 14 Heart failure Cardiac dysrthmias New murmur
RHEMATIC FEVER (RF) & RHEMATIC HEART DISEASE (RHD) Rheumatic Fever o Inflammatory disease occurring after group A B-hemolytic stremptococcal pharyngitis (GABHS) o Infrequently seen in US o Self-limiting Affects joints, skin, brain, serous surfaces, & heart Rheumatic heart disease o Most common complication of RF o Damage to valves as a result of RF Clinical manifestations: o Jones criteria (Presence of 2 major manifestations or one major manifestation & two minor manifestations) Carditis Polyarthritis Erythema Marginatum Subcutaneous Nodes Chorea (St. Vitus Dance, Sydenham Chorea) Treatment o Prevention of GABHS o Tx of streptococcal tonsillitis and pharyngitis Penicillin G IM once Penicillin V by mouth for 10 days Sulfa by mouth for 10 days Erythromycin (if patient is allergic to the above agent) by mouth for 10 days o Tx of recurrent RF Same as above
KAWASAKI DISEASE (KD); Mucocutaneous lymph node syndrome An acute systemic vasculitis of unkown cause 75% of cases, the child is younger than 5 years of age 3 phases: o Acute phase Sudden high fever, unresponsive to antipyretics & antibiotics o Subacute phase Lasts from end of fever thru end of all KD clinical signs o Convalescent phase: Clinical signs have resolved, but laboratory values have not returned to normal 15 Ends when normal values have returned (6-8 weeks) Diagnostic criteria for Kawasaki disease o Changes in extremities In acute phase: edema, erythema of palms and soles Subacute: periungual desquamation (peeling) of hands & fet o Bilateral conjuctival injection (inflammation) without exudation o Changes in the oral mucous membranes o Polymorphous rash o Cervical lymphadenopathy Treatment of KD o Acetylsalicyclic acid (ASA) 80-11 mg/kg/day for fever o IV immunoglobulin (IVIG) o Then 3-5 mg/kg/day antiplatelet
Hyperlipidemia Identify kids at risk & treat early Tx is lifestyle modifcation o Restrict intake of cholesterol & fats o Increase intake of whole grains, fruits, & veggies o Exercies for 60 min a day 5 days a week o Stop smoking and avoid second-hand smoke If there is no response to diet changes & meds: o Colestipol (Colestid) o Cholestyramine (Questran)
Systemic Hypertension Essential hypertension has no known cause Secondary has an identifiable cause Pediatric hypertension is generally secondary to structural abnormality or an underlying pathologic condition o Renal disease o Cardiovascular disease o Endocrine or neurologic disorders Pharmacologic treatment: o B-blockers o Calcium channel blockers o Angiotensin-converting enzyme (ACE) inhibitors o Angiotensin receptor blockers o Diuretics
MS
Immobilized patient 16 Atrophy Joint contracture Major musculoskeletal consequences of immobilization are: o Significant decrease in muscle size, strength, and endurance o Bone demineralization leading to osteoporosis o Contractures and decreased joint mobility DVT
Developmental Dysplasia of the Hip (DDH)x Wide range of abnormal development of the hip leading to hip instability 1 per 100 live births 80% are female Lift hip affected most commonly Caucasion children most often affected Degrees of DDH o Acetabular dysplasia Acetabular rool shallow; mildest form o Subluxation Head of femur is partially displaced Flattened socket; most common form o Dislocation Femoral head not in contact with acetabulum Clinical manifestations of DDH o Infant: Shortened limb on affected side Restricted abduction of hip on affected side Unequal gluteal folds when infant prone Positive Ortolani test Positive Barlow test o In older infant & child Affected leg shorter than other Telescoping or piston mobility of joint Trandelenburg sign Trandelenburg gait Greater tochanter is prominent and appears above line from anterosuperior iliac spine to tuberosity of ischium Marked lordosis if bilateral dislocations Waddling gait if bilateral disclocations Sign of gluteus medius weakness or relative inhibition Sign is elicited by asking patient to stand on involved leg If sign is positive, the pelvis will drop on uninvolved side Ortolani & Barlow tests o Barlow test shows that hip has potential to dislocate o Ortolani test confirms its dislocation 17 o o Never do at the same time; do one knee then the other Diagnosis o Newborn assessment tools most reliable in early infancy o X-ray not reliable in infancy due to incomplete ossification of femoral head o Ultrasound as adjunct to abnormal physical findings Therapeutic management of DDH o Importance of early intervention o Newborn to age 6 months: Palvik harness for abduction of hip o Age 6-18 months: Dislocation unrecognized until child begins to stand and walk; use traction and cast immobilization (spica) o Older child: Operative reduction Tenotomy (muscle contracture) Osteotomy (rebuild acetabular roof) Difficult after 4 years Management: 0-6 months o Splinting: Palvik harness Worn continuously x 3-5 months until hip stable Straps checked q 1-2 weeks for adjustment o 95% effective if hips reducible at birth o prevent adduction o Nursing care of child in palvik harness Newborn hip assessment Management of reduction device Teaching application/use of harness o Removal, adjustment discouraged Prevent skin breakdown o Clothing, diaper under straps 18 o Check for reddening under straps often Management: 6-18 months o Gradual reduction by traction x 3 weeks o Closed/open reduction under anesthesia o Hip spica cast x 3 months Management: Older child o Operative reduction o Construction of acetabular roof o Post-operative casting o Successful reduction difficult after 4 years
TALIPES: Congenital Clubfoot Includes multiple foot, ankle deformity and malposition, and soft tissue contractures Incidence: 1-2: 1000 live births Male: female= 2:1 50% are bilateral increase risk of hip dysplasia Etiology o Not well identified o Strong family disposition Q:10 if parent affected o Possible arrested fetal development of skeletal & soft tissue (9-10 weeks gestation) o Associated with other syndrome (myelomeningocele) o Idiopathic clubfoot most common form 19 o o Talipes varus: inversion, or bending inward o Talipes valgus: eversion, or bending out o Talipes equinus: plantar flexion with toes lower than the heel o Talipes calcaneus: dorsiflexion with toes higher than the heel o Talipes equinovarus: when the foot turns inward and downward; most common form Classification of clubfoot o Mild or postural May correct spontaneously or require passive exercise or serial casting o Tetralogic Associated with other congenital anomalies Usually requires surgical correction with high incidence or recurrence o Idiopathic Bony abnormality almost always requiring surgical intervention Treatment o Started as a neonate 20 o Serial casting of affected leg(s) o Recasting frequent until maximum correction achieved (~8-12 weeks) o X-Ray to evaluate efficacy of casting o If casting unsuccessful, surgery @6-12 months & casting/brace after surgery
Metatasus Adductus Most common Treatment usually not needed Due to abnormal intrauterine positioning Associated with pigeon toed gait Different from Talipes deformities because foot has full ROM
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Kyphosis o Abnormally increased convex angulation of the curvature of the thoracic spine o Most common form is postural o Can result from tuberculosis, arthritis, osteodystrophy, or compression fracture o PT w/ strengthening excercises o Not associated with pain Lordosis o Accentuation of the cervical or lumbar curvature beyond physiologic limits o May be idiopathic or secondary complication or trauma o May occur with flexion contractures of hip, congenital dislocated hip o In obese children, abdominal fat alters center of gravity, causing lordosis o Treat cause ie excess weight and manage pain; associated with pain Scoliosis o Most common spinal deformity o Complex spinal deformity in 3 planes: Lateral curvature Spinal rotation causing rib asymmetry Thoracic kyphosis o Congenital or develop during childhood 22 Congenital associated w/ myelomeingocele o Idiopathic scoliosis during growth spurt of early adolescence most common form o Early manifestations of Idiopathic scoliosis Seldom apparent before preadolescent growth spurt May be picked up in school screening Uneven pants length Rarely painful Right curvature is usually scoliosis Left curvature often associated with disorders and have a neurologic component o Diagnosis Physical exam Asymmetry of shoulder, hip height; flank, scapular shape when standing Asymmetry of ribs & flanks with bend at waist Stand & twist to evaluate flexibility of curve X-Ray of spine to measure curve magnitude MRI if indications of other spinal abnormalities Spinal curvature and treatment o 10 degree normal postural variation o 10-20 mild, no treatment if no progression o 20-40- bracing o >40 surgery Bracing/exercise o Bracing can slow or stop progression of curvature o TLSO (thoracolumbarsacral orthosis) Wear 16-23 hours per day; adjusted periodically Milwaukee brace; Boston brace (less visible) o Daily exercises to prevent atrophy of spinal and abdominal muscle Operative management o Curves >40, difficult sitting, breathing, pain require surgery o Realignment and internal fixation with bony fusion or realigned spine o Harrington rod system Immobilized postoperatively Post-Op Nursing care o Pain management Considerable pain 2-3 days post-op o Neurologic dysfunction Post-op paralysis a risk o GI dysfunction Paralytic ileus o GU dysfunction Urine retention & hypoperfusion possible o Respiratory dysfunction 23 Anesthesia & immobility atelectasis o Immobility consequences High potential for skin breakdown Potential for phlebitis Discharge education o Recommended physical activity o Pn meds & side effects o Psychological adjustment to brace, altered body image o Assess family, peer support o Schooling o National Scoliosis Foundation
Fractures Bone structure in a child o Ossification incomplete until 18-21 years o Epiphyseal plate Growth plate o Periosteum Vascular membrane Critical for growth and healing of bone Bone healing in children o Generally faster in children due to thick vascular periosteum o Healing of bone Neonate: 2-3 weeks Early childhood: 4 weeks Later childhood: 5-8 weeks Adolescence: 8-12 weeks Adult: 10-16 weeks o Remodeling Fractures in infant & small child: o Infancy: Birth trauma MVA Child abuse (twisting, rough handling, pulling) Periosteal bleeding not visible on x-ray for weeks after injury o Small child: Multiple fractures at varied stages of healing warrants investigation for abuse Causes: o Breaking a fall- clavicle, forearm o Auto vs peds- femoral neck or femur Most commonly seen in 4-7 years old Triad of auto vs peds injuries: Femur fracture Trunk trauma 24 Head injury
Epiphyseal fractures o Epiphyseal plate weakest point of long bones o Normally heals quick and completely o Risk of damage to growth plate o Can be mistaken for dislocation o Early identification critical to minimize growth problems & angular deformities Clinical course of fracture o Muscles contract to splint broken bone o Contusion or severe hemorrhage of surrounding soft tissue may occur o Stable bone due to intact periosteum o Neurovascular damage less common than in adults 25 o o 5 Ps of ischemia from vascular injury: Pain Pallor Pulselessness Paresthesia Paralysis o Slight rise in WBC due to inflammation & hgb decreases Management o Usually closed reduction & casting o Femur, humerus fractures may require hospitalization and traction o Internal fixation more quickly stabilizes injury (ORIF) o Casting Bone will grown in the direction in which stress is placed on it- Wolffs law Critical to check for skin injury prior to application of cast Check for neurovascular compromise TRACTION o Primary goals of traction To fatigue involved muscle and reduce muscle spasm To realign distal and proximal bone ends to promote satisfactory bone healing To immobilize fracture until realignment has occurred and boen has healed well enough to cast or splint o Complications of fractures Circulatory impairment Nerve compression Compartment syndrome Epiphyseal damage Non union or malunion of bone Osteomyelitis Pulmonary emboli
26 Sprains & Strains Sprain: o Ligament stretched or torn by force created as joint twisted Vessel, tendon, nerve damage common Joint laxity best indicator of severity of sprain Strain: o Microscopic tear of tendon Painful & swollen Usually do not occur immediately but over time Management of soft tissue injuries o RICE Rest Ice (some controversy about icing) Compression Elevation First 6-12 hours critical for treatment
Shin Splints Extensive running pressure on tibia Ligaments tear away from shaft of tibia Painful but rarely serious
Nursemaids elbow Most common dislocation in young children Usually <5 Sudden jerk and pull of arm Tx: pop back into place just like a shoulder
Osgood-Schlatter disease Painful inflammatory disorder of proximal tibia at point of insertion of patellar tendon Repeated stress and overuse of quadriceps causes irregularities of growth Presentation: o Knee pain, inflammation at tibial tubercle o Prominent tibial tubercle o Pn exacerbated by activity, improved with rest o Hip examination necessary to rule out hip abnormalities o Knee x-ray findings variable Treatment: o Self-limiting o When growth of proximal tibia ceases, pain disappears o Rest, avoiding activity that contract quadriceps
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Osteogenesis Imperfecta (OI) Group of heterogenous inherited disorders of connective tissue Characterized by excessive fragility and bone defects Defective periosteal bone formation and reduced cortical thickness of bones Hyperextensibility of ligaments Therapeutic management o Primarily supportive care o Drugs of limited benefit o May rule out OI if multiple fractures occur o Nursing care management: Caution with handling to prevent fractures Fam education Occupational panning and genetic counseling
Legg-Calve-Perthes disease Self-limiting, idiopathic, occurs in juveniles ages 3-12 , more cmmon in males 4-8 yo Avascular necrosis of femoral head 10-15% of cases have bilateral hip involvement Most have delayed bone age Pathophysiology: o Cause is unkown but involved disturbed circulation to the femoral head with ischemic aseptic necrosis Treatment goal: o Keep head of femur in acetabulum o Containment with various appliances/devices o Rest, no weight bearing initially o Surgery in some cases o Home traction in some cases Prognosis o Self-limiting o Outcome has wide variations due to multiple factors Nursing care management: o Identification of affected children & referral teaching care and management o Compliance issues with child and family
OSTEOMYELITIS Inflammation and infection of bony tissue May be caused by exogenous or hematogenous sources Signs and symptoms begin abruptly, resemble symptoms of arthritis and leukemia Marked leukocytosis Bone cultures obtained from biopsy or aspirate Early x-rays may appear normal Bone scans for diagnosis Exogenous Osteomyelitis 28 o Infectious agent invades bone following penetrating wound, open fracture, contamination in surgery, or secondary from extension from abscess or burn Hematogenous osteomyelitis o Preexisting infection o Source may be furuncles, skin infections, upper respiratory tract infection, abscessed teeth, pyelonephritis o Any organism can cause osteomyelitis o Infective emboli travel to artiers in bone metaphysis, causing abscess formation and bone destruction Therapeutic management of osteomyeleitis o May have subacute presentation with walled off abscess rather than spreading infection o Prompt, vigorous IV antibiotics for extended period (3-4 weeks or up to several months) o Monitor hematologic, renal, hepatic responses to treatment Nursing care: o COMPLETE bed rest & immobility of limb o Pn management concerns o Long-term IV access (for antibiotic administration) o Nutritional considerations o Long-term hospitilzation, therapy o Psychosocial needs Juvenile Idiopathic Arthritis (JIA) AKA juvenile rheumatoid arthritis, juvenile chronic arthritis, or idiopathic arthritis of childhood Possible causes Peak ages: 1-3 years and 8-10 years Often undiagnosed Actually a heterogenous group of diseases: o Pauciarticular onset involves 4 or more joints o Polyarticular onset- involves 5 or more joints o Systemic onset- high fever, rash, hepatosplenomegaly, pericarditis, pleuritis, lymphadenopathy) Symptoms may burn out and become inactive Chronic inflammation of synovium with joing effusion, destruction of cartilage, and ankylosis of joints as disease progresses Symptoms: o Stiffness o Swelling o Loss of mobility in affected joints o Warm to touch, usually without erythema o Tender to touch in some cases o Symptoms increase with stressors o Growth retardation Diagnostic evaluation of JIA 29 o No definitive diagnostic tests o Elevated sedimentation rate in some cases o Antinuclear antibodies common, but not specific for JIA o Leukocytosis during exacerbations o Diagnosis based on criteria of American College of Rheumatology Their diagnostic criteria: Age of onset <16 years 1 or more affected joints Duration of arthritis >6 weeks Exclusion of other forms of arthritis Therapeutic management: o No cure o Goals of therapy: Preserve function Prevent deformities Relieve symptoms o Iridocyclitis, uveitis: Inflammation of iris & ciliary body Unique to JIA Requires opthalmologist MEDS o NSAIDs o SSARDs o Corticosteroids o Cytotoxic agents o Immunologic modulators Management of JIA o Therapy individualized to child o Physical & occupational therapy o Nutrition, exercise o Splinting devices o Pn management o Prognosis Systemic Lupus Erythematosus (SLE) A chronic, multisystem, autoimmune disease of the CT and blood vessels characterized by inflammation on potentially any body issue Course and symptoms: unpredictable, mild to life threatening complications o Clinical manifestations of systemic lupus erythematosus related to tissues involved: Constitutional- fever, fatigue, weight loss, anorexia Cutaneous- erythematous butterfly rash over bridge of nose and across cheeks, discoid rash, photosensitivity, mucocutaneous ulceration, alopecia, periungual telangiectasias Musculoskeletal- arthritis, arthralgia, myositis, myalgia, tenosynovitis 30 Neurologic- headache, seizure, forgetfulness, behavior change, change in school performance, psychosis, chorea, stroke, cranial and peripheral neuropathy, pseudotumor cerebri Pulmonary and cardiac- pleuritis, basilar pneumonitis, atelactasis, pericarditis, myocarditis, endocarditis Renal- Glomerulonephritis, nephritic syndrome, hypertension GI- abdominal pain, NV, blood in stool, abdominal crisis, esophageal dysfuntion, colitis Hepatic, splenic, and nodal- hepatomegaly, splenomegaly, lymphadenopathy Hematologic- anemia, cytopenia Ophthalmologic- cotton wool spots, papilledema, retinopathy Vascular- Raynaud phenomenon, thrombophleitis, livedo reticularis o Diagnostic Criteria for SLE: 1. Malar rash- fixed malar erythema 2. Discoid rash- patchy erythematous lesions 3. Photosensitivity- pain with sun exposure 4. Oronasal ulcers- painless ulcers in mouth or nose 5. Arthritis- swelling, tenderness, or effusion in two or more peripheral joints (nonerosive) 6. Serositis- pleuritis, pericarditis 7. Renal disorder- proteinuria, casts 8. Neuro disorder- psychosis, seizures 9. Hematologic disorder- hemolytic anemia, thrombocytopenia, leucopenia, lymphopenia 10. Immunologic disorder- anti double stranded DNA, anti Sm, antiphospholipid antibodiesl lupus anticoagulant; false positive syphilis test (rapid plasma reagin [RPR]) 11. Antinuclear antibodies Neonatal lupus: another form of lupus, which occurs when maternal auto antibodies cross the placenta and cause transient lupus like symptoms in a newborn, with potential complications of heart block Therapeutic management o Ensure childs health by balancing meds necessary to avoid exacerbation and complications while preventing or minimizing treatment associated morbidity. o MEDS Corticosteroids-to control inflammation administered in doses sufficient to control and then taper to lowest suppressive dose Antimalarial (rash and arthritis) NSAIDS (relieve muscle and joint inflammation) Immunosuppressive agents such as cyclophosphamide- renal and CNS disease mycophenolate, azathioprine, and methotrexate-effective, may be used to control SLE and allow steroids to be reduced 31 Antihypertensives, aspirin, antibiotics, may be needed to treat or avoid complications General supportive care: sufficient nutrition, sleep and rest, exercise. o Limit exposure to sun and ultraviolet B (UVB) light is limited bc of association with SLE exacerbation Sunscreens, wearing sun resistant clothes, and altering outdoor activities; must be provided with great sensitivity to ensure compliance while minimizing the associated feeling of being different from peers Nursing Care Management o Principal nursing goal: help child and fam positively adjust to disease and therapy o Learn S/S of exacerbation o Key issues: Therapy compliance, body-image problems associated with rash, hair loss, and steroid therapy; school attendance; vocational activities, social relationships; sexual activity; and pregnancy. Maintain reg med supervision, seek attention quickly when ill, or before elective surgical procedures, such as dental extraction, bc of potential needs for increasd steroids or prophylactic antibiotics o Carry ID for disease and steroid dependence
A Comparative Study of Intelligence in Children of Consanguineous and Non-Consanguineous Marriages and Its Relationship With Holland's Personality Types in High School Students of Tehran