care of child with cardiovascular disorders dr. manal kloub
TRANSCRIPT
Care of Child with Cardiovascular
Disorders
Dr. Manal Kloub
Outline
CHD CHF Hypoxemia
Acyanotic disorders Increased pulmonary
flow PDA ASD VSD
Cyanotic disorders Obstructive
AS PS COA
Decreased pulmonary flow TOF
Mixed defects TGV or TGA Hypoplastic heart
Heart Anatomy and Physiology
Cardiac Conduction
First Breath
• Pulmonary alveoli open up• Pressure in pulmonary tissues decreases• Blood from the right heart rushes to fill the
alveolar capillaries• Pressure in right side of heart decreases• Pressure in left side of heart increases• Pressure increases in aorta
Congenital Heart Diseases ♥
Definition: It includes primarily anatomic abnormalities
present at birth that results in abnormal cardiac functions
The newborn’s heart begins to beat at 28 days of gestation
The heart is completely developed on the 9th week of intrauterine life
Incidence: CHD
4 – 10/100 live births Major cause of death during 1st year of life
after prematurity Affect both sexes differently It is more likely to be with other congenital
anomalies e.g. T.E fistula, Renal agenecies and diaphragmatic hernia.
Etiology: CHD
Factors associated with increased incidence: Prenatal factors:
1. Maternal rubella
2. Radiation
3. Alcoholism
4. age >40 yrs
5. Insulin dependent diabetes
6. fetal intra uterine cardiac viral disease
Etiology: CHD
Genetic factors: although the influence is multifactorial there is high risk of CHD in children who have:
1. a sibling with a heart defect
2. a parent with CHD
3. chromosomal aberration e.g. Down’s syndrome
4. Born with other congenital anomalies
Altered Hemodynamics
1. Blood flows from high pressure to area of lower pressure and with lower resistance, in response to the pumping action of the heart
2. The higher the pressure gradient the greater the rate of flow
3. The higher the resistance the less the rate of flow
4. Normally the pressure in the Rt side is lower than the Lt side of the heart
5. The resistance in the pulmonary circulation and vessels entering or leaving these chambers have corresponding pressure
6. So if there is septal defect, blood will flow from Lt to Rt known as left to right shunt, and no desaturated blood flows directly into the Lt side of the heart so it is acyanotic defect
Cyanotic defects are due to:
Change in the pressure causing blood to flow Rt - to - Lt Shunt.
Due to increased pulmonary flow through the pulmonary vascular resistance
Or obstruction to the blood flow through the pulmonary valve and aorta
Or due to mixing of the blood between pulmonary and systemic circulation e.g. truncus arteriosus (the pulmonary artery and the aorta are one single vessel that overrides both ventricles
Classification and clinical consequences of congenital Heart Diseases:
Depending on the severity of the cardiac defect and the altered hemodynamics TWO principal clinical consequences can occur:
1st Consequence is Congestive Heart Failure
2nd Consequence is Hypoxemia
Congestive Heart Failure
It is the inability of the heart to pump adequate blood to the systemic circulation to meet the metabolic demands of the body.
It is a symptom caused by cardiac defect not a disease in itself, it is due to increased work load on normal myocardium
Congestive Heart Failure
Major manifestation of cardiac disease.
Under 1 year of age due to congenital anomaly.
Over 1 year with no congenital anomaly may be due to acquired heart disease.
In children failure of one chamber causes change in the opposite chamber
Pathophysiology of CHF
Two categories1. Rt sided failure; the Rt ventricle is unable to
pump blood to pulmonary artery resulting in increase in the pressure in the Rt atrium and systemic venous circulations leading to liver and spleen enlargement and occasionally edema.
2. Lt sided failure, the left ventricle is unable to pump blood into the systemic circulation leading to increased pressure in the Lt atrium and pulmonary veins. The lungs become congested leading to increased pulmonary pressure and pulmonary edema.
Congestive heart failure leads to:
cardiac muscles damage decrease the cardiac output decrease the flow of blood to the kidneys increase the reabsorption of Na and water
and increase blood volume increase systemic congestion Distention in neck veins and peripheral
veins Edema and hepatomegaly Forehead sweating due to sympathetic
response
Clinical S & S of CHF
Cardiac Congestion: Tachycardia Cardiomegaly Pale cool extremities Weak peripheral pulses Low blood pressure Gallop Rhythm heart
beats
Pulmonary Congestion: Tachypnea Dyspnea Cyanosis Wheezing Grunting Retractions with flaring
nares Cough and hoarseness of
voice
Clinical S & S of CHF
Exercise intolerance Orthopnea Sweating Decreased urine output Weakness Fatigue Restlessness Anorexia
Systemic Venous Congestion:• Weight gain (due to edema)• Hepatomegaly• Peripheral edema
especially periorbital area• Ascites• Neck vein distension
♥ Therapeutic management
Goals: Improve cardiac function Remove accumulated
fluid and Na Decrease cardiac
demands Improve tissue
oxygenation and decrease O2 consumption
Interventions
Fluid restriction Diuretics – Lasix (potassium wasting) or
Aldactone (potassium sparing) Bed rest Oxygen therapy Small frequent feedings – soft nipple with
supplemental NG for adequate calorie intake Pulse oximeter Sedatives if needed
Improving Myocardial efficiency
By giving: Digitalis glycosides (Lanoxin /Digoxin) Increase cardiac output Decrease heart size Decrease venous pressure Decrease edema Regulate heart rate
Digoxin increases the force of the myocardial contraction.
Digoxin Therapy
Take an apical pulse with a stethoscope for 1 full minute before every dose of digoxin. If bradycardia is detected. < 100 beats / min for infant and toddler < 80 beats in the older child < 60 beats in the adolescent
Nursing alert* Call physician before administering the drug*
Signs of Digoxin Toxicity
Extreme Bradycardia Arrhythmia Nausea, vomiting, anorexia Dizziness, headache Weakness and fatigue
Supplemental Feeding
Infants with cardiacconditions often requiresupplemental feeding to provide sufficientnutrients for growth.
Angiotensin-converting enzyme (Captopril/capotin):
Inhibit the normal function of rennin angiotensin in the kidney and vasodilatation occur, decrease pulmonary and systemic vascular resistance which decreases B/P and cardiac after load
Remove accumulated fluid and Na: Diuretics. frusamide (Lasix). Thiazide and
Spironolactone. Possible restriction of fluids and decrease Na Observe fluid intake and out put and Signs of
dehydration Potassium supplement, because Diuretics
increase potassium loss
Decrease cardiac demand: Decrease physical activities, by bed rest, observe
body temp. Treat any infections Improve breathing ; semi sitting position and sedate
irritable children
Increase tissue oxygenation and decrease O2 consumption by applying the mentioned measures and giving humidified cool O2
2nd Consequence Hypoxemia Referred to arterial O2 tension (or pressure PaCo2), that
is less than normal can be identified by ↓ SaO2 or ↓PaO2
Hypoxia: Reduction in tissue oxygenation that results from
↓oxygen saturation and PaO2 which results in impaired cellular process
Cyanosis: Blue discoloration of mucus membrane, skin nail
beds due to reduced O2 saturation, results from the presence of deoxygenated hemoglobin in a concentration of 5g/dl of blood or more.
Cyanosis occurs when O2 saturation is 75% - 85%
May not reflect arterial hypoxemia because both O2 saturation and amount of circulating hemoglobin are involved
In severe anemia no cyanosis despite severe hypoxemia, because hemoglobin level may be too low to produce blue color
On the contrary, in polycythemia there is cyanosis and normal PaO2
In Heart defects Hypoxemia and Cyanosis result from desaturated venous blood entering the systemic circulation
Clinical manifestations of Hypoxemia
Squatting (rarely seen)
Polycythemia (increased number of RBC)
Clubbing of the finger Hypercyanotic spells
Hypercyanotic spells
Hypercyanotic spells: Cyanosis Hyperapneia (increased depth of breathing) ↑Rt -to-Lt Shunt. Rare < 2 months of age More common in >1year of age increase in the
morning and during feeding, crying and defecation Possible consequences :
1. CVA2. Brain abscess
3. ↓Development
Congenital Heart Diseases TYPES OF DEFECTS and Classification
1st Acyanotic ♥ 2nd Cyanotic ♥ ↑Pulmonary Obstruction to ↓Pulmonary Mixed blood flow blood flow flow flow
↓ ↓ ↓ ↓ ASD Tetralogy TPOGA VSD Coarctation of of Fallots Truncus the aorta arteriosis. PDA Tricuspid Hypoplastic Pulmonic stenosis Artesia Lt Heart syndrome
Right to Left Shunts
Occurs when pressure in the right side of the heart is greater than the left side of the heart. Resistance of the lungs in abnormally high Pulmonary artery is restricted
Deoxygenated blood from the right side shunts to the left side
Right to Left Shunt
Hole in septum + obstructive lesion =
Deoxygenated blood from the right side of the heart shunts to the left side of the heart and out into the body.
Clinical Manifestations
Hypoxemia = the result of decreased tissue oxygenation.
Polycythemia = increased red blood cell production due to the body’s attempt to compensate for the hypoxemia.
Increase viscosity of the blood = heart has to pump harder.
Potential Complications
Thrombus formation due to sluggish circulation.
Brain abscess or stroke due to the un-oxygenated blood bypassing the filtering system of the lungs.
Left to Right Shunt
Pressures on the left side of the heart are normally higher than the pressures in the right side of the heart. If there is an abnormal opening in the septum between the right and left sides, blood flows from left to the right.
Clinical Manifestations
The infant is not cyanotic.
Tachycardia due to pushing increased blood volume.
Cardiomegaly due to increased workload of the heart.
Clinical Manifestations
Dyspnea and pulmonary edema due to the lungs receiving blood under high pressure from the right ventricle.
Increased number of respiratory infections due to blood pooling in the the lungs promoting bacterial growth.
♥ Acyanotic Defects:
Lt – to – Rt shunting through an abnormal opening or obstructive lesions leading to decrease blood flow to various parts of the body.
The most common clinical manifestation is heart failure. Some of them may be asymptomatic (ASD, VSD, PDA)
Patent Ductus Arteriosus
Patent Ductus Arteriosus: (PDA)
The fetal ductus artery connecting the aorta and the pulmonary artery fails to close within few weeks after birth, so the blood flows from the high pressure of the aorta to the lower pressure of the pulmonary artery (Lt – to –Rt shunt
Ductus normally closes within hours of birth Connection between the pulmonary artery
(low pressure) and aorta (high pressure)
Patent Ductus Arteriosus
Incidence: Incidence 10% It is most common cardiac anomaly One of the most common benign defects The ratio is: 2 ♀: 1♂ High risk for pulmonary hypertension
Clinical Manifestations: PDA
Might be asymptomatic Show signs of CHF Machinery - like murmur Widened pulse pressure Bounding pulses resulting from runoff of
blood from aorta to pulmonary artery Risk of bacterial endocarditis and pulmonary
vascular obstructive disease in later life from chronic excessive pulmonary blood flow
Diagnosis tests
Diagnosis by Chest x-ray – enlarged heart and dilated
pulmonary artery Echo-cardiogram – show the opening between
pulmonary artery and aorta
Treatment: PDA
Medical management by using Endomethacin (Prostaglandin inhibitor) which constricts the muscle in the wall of the PDA and promotes closure
Nonsurgical treatment where coil is placed in the open duct and acts like a plug used during catheterization procedure
Surgical Management via small incision made between ribs on left hand side and PDA is ligated or tied and cut off
Prognosis is good with less than 1% mortality
Atrial Septal Defect (ASD)
Atrial Septal Defect (ASD)
An abnormal opening between atria with a Lt-to-Rt Shunt. Blood in left atrium flows into right atrium.
10% of defects Reduced blood volume in systemic
circulation
Clinical Manifestations (ASD)
May be asymptomatic May develop CHF Characteristic murmur Pt is at risk for atrial dysrythmia ( may be due to atrial
enlargement and stretching of conduction fibers) At risk for pulmonary vascular obstructive disease, and
emboli formation later in life due to chronic increased pulmonary blood flow
If left untreated may lead to pulmonary hypertension, congestive heart failure or stroke as an adult.
Diagnosis: (ASD)
Heart murmur may be heard in the pulmonary valve area because the heart is forcing an unusually large amount of blood through a normal sized valve.
Echocardiogram is the primary method used to diagnose the defect – it can show the hole and its size and any enlargement of the right atrium and ventricle in response to the extra work they are doing.
Treatment: (ASD)Nonsurgical treatment: might use techniques and
devices during cardiac catheterization to close the opening
Surgical treatment: using surgical dacron patch closure of moderate to large defects. After closure in childhood the heart size will return to
normal over a period of four to six months. No restrictions to physical activity post closure
Prognosis very low operative mortality, <1%
Ventricular Septal Defect (VSD)
Ventricular Septal Defect (VSD)
It is an abnormal opening between right and left ventricles, may vary in size ; small pinhole to the absence of the septum, resulting in common ventricle. Frequently associated with other defects
Lt –to – Rt Shunt 30% of defects May be classified according to defect
location
Ventricular Septal Defect (VSD)
Small holes generally are asymptomatic Medium to moderate holes will cause problems
when the pressure in the right side of the heart decreases and blood will start to flow to the path of least resistance (from the left ventricle through the VSD to the right ventricle and into the lungs)
May be associated with other defects such as (PS, TGV,PDA…)
Many VSD closes spontaneously 1st year of life
Clinical Manifestations: VSD
May develop CHF Characteristic murmur Right ventricular hypertrophy Deficient systemic blood flow High risk of bacterial endocarditis and
pulmonary vascular obstruction disease May develop Eisenmenger syndrome
refers to the combination of systemic-to-pulmonary communication, pulmonary vascular disease and cyanosis
Diagnostic tests: VSD
Diagnosis – heart murmur – clinical pearl a louder murmur may indicate a smaller hole due to the force that is needed for the blood to get through the hole.
Electrocardiogram – to see if there is a strain on the heart
Chest x-ray – size of heart Echocardiogram – shows size of the hole and
size of heart chambers
Management: VSD
Palliative: placing band on pulmonary artery to decrease pulmonary blood flow
Complete repair: small defects are reparied with purse-string. Large defect require knitted Dacron patch sewn over the opening.
Post – operative complication include conduction system disturbances
Nonsurgical treatment: closure during cardiac catheterization are still under study
Prognosis: risk depend on location of the defect,
number of defects and other cardiac factors. Mortality rate ranges from 5% to 20%
Surgical Repair
Over a period of years the vessels in the lungs will develop thicker walls – the pressure in the lungs will increase and pulmonary vascular disease
If pressure in the lungs becomes too high the un-oxygenated blood will cross over to the left side of the heart and un-oxygenated blood will enter the circulatory system.
If the large VSD is repaired these changes will not occur.
Medical Treatment: VSD
CHF: diuretics of help get rid of extra fluid in the lungs
Digoxin if additional force needed to squeeze the heart
FTT or failure to grow may need higher calorie concentration
Will need prophylactic antibiotics before dental procedures if defect is not repaired
♥ Major Cyanotic Defects
Cyanotic defects result from:
1. Obstructive defects (PS, AS, COA)
2. And Mixing of desaturated blue venus blood with fully saturated red arterial blood within the chambers of the heart (TOF, TGV / TGA, Hypoplastic heart)
Pulmonary stenosis
Pulmonary Stenosis (PS)
It is narrowing at the entrance of the pulmonary artery (pulmonary valve) leads to narrowing and obstruction between the right ventricle and the pulmonary artery.
Resistance to blood flow cause Hypertrophy of right ventricle
Thickened tissue become less pliable and increases the obstruction
Right ventricle must work harder to eject blood into the pulmonary artery.
7% of defect
Clinical Manifestations: (PS)
Some might be asymptomatic Some might have mild cyanosis or CHF Newborns with severe narrowing will be
cyanotic Characteristic murmur Cardiomegally is evident in chest X-ray ↑ Risk of Bacterial Endocarditis with
progressive narrowing lead to increase symptoms
Diagnostics: PS
Diagnosis: heart murmur is heard – clicking sound when the thickened valve snaps to an open position.
Chest x-ray, enlarged heart Electrocardiogram would be normal Echocardiogram most important non-invasive test to
detect and evaluate pulmonary stenosis Cardiac Catheterization – to measure pressures and
measure the stenosis
Management: PS Surgical correction:
Infants: Transventricular valvotomy Bock procedure
Children: Valvotomy with cardiopulmonary bypass
Nonsurgical treatment: Cardiac catheterization to dilate the valve and
open up the obstruction by using a balloon angioplasty
Prognosis: less than 2% mortality
Aortic stenosis
Aortic Stenosis (AS)
Narrowing of aortic valve causing resistance to blood flow in the Lt ventricle, decrease cardiac output, Lt ventricular hypertrophy and pulmonary vascular congestion.
Causes obstruction to blood flow between the left ventricle and aorta.
Most common form is obstruction of the valve itself
Aortic Stenosis 6% of defects, 30% incidence of sudden death
Aortic valve: has two rather than three leaflets. Leaflets are thickened or fused.
When the aortic valve does not open properly the left ventricle must work harder to eject blood into the aorta.
Left ventricular muscle becomes hypertrophied.
Clinical Manifestations: (AS)
Infants with severe defects: Signs of decreased cardiac output and faint pulses Hypotension and tachycardia Poor feeding Exercise intolerance Chest pain and dizziness Characteristic murmur Risk for endocarditis, ventricular dysfunction, and
coronary insufficiency
Diagnostics: AS
Heart murmur of turbulent like noise caused by ejection of blood through the obstructed valve.
Electrocardiogram is usually normal Echocardiogram will show the obstruction
and rule out other heart anomalies Exercise stress test – provides information on
impact of the stenosis on heart function
Management: AS Surgical correction: - valvotomy if the closed procedure does not work – often
done when patient is older when severe calcium deposits further obstruct the valve.
Nonsurgical correction: - Dilating narrowed valve with balloon angioplasty in the cath
lab
Prognosis: Newborn critical conditions mortality 10% - 20% Older children elective valvotomy has lower risk
Complication: Recurrent valve obstruction is a complication and if valve replacement is done too early the child may outgrow the valve. Prophylactic antibiotic needed
Coarctation of the Aorta (COA)
Coarctation of Aorta: (COA)
There is localized narrowing near the insertion of ductus arteriosus resulting in: Increased pressure in proximal structures to
the defect (Head and upper extremities) Decreased pressure distal to obstruction (body and lower extremities)
Congenital narrowing of the descending aorta 7 % of defects 80% have aortic-valve anomalies Difference in BP in arms and legs (severe
obstruction)
Clinical manifestations: (COA)
High B/P and bounding pulses in arms Weak or absent femoral pulses Cool lower extremities with low B/P Signs of CHF in infants Older children may experience dizziness,
headaches, fainting and epistaxis due to hypertension
Risk of hypertension, ruptured aorta, aortic aneurism or stroke
Diagnostics: COA
In 50% the narrowing is not severe enough to cause symptoms in the first days of life.
When the PDA closes a higher resistance develops and heart failure can develop.
Pulses in the groin and leg will be diminished
Echocardiogram will show the defect in the aorta
Management: COA
Surgical correction: Resection of narrowed portion and end - to - end anastomosis or graft replacement via thoracotomy incision
Nonsurgical treatment: balloon angioplasty may be successful in some cases but risk of aneurysm formation is present
Prognosis: less than 5% mortality rate in isolated coarctation
- high risk in infants with other complex cardiac defects
Medical Treatment: Prostaglandin may given to keep the PDA open to
reduce the pressure changes Antibiotic prophylactic need due to possible aortic valve
abnormalities.
Complications: Surgical complications – kidney damage due to
clamping off of blood flow during surgery High blood pressure post surgery – may need to be on
antihypertensives
Tetralogy of Fallot (TOF)
Tetralogy of Fallot (TOF)
6% of defects
Most common cardiac malformation responsible for cyanosis in a child over 1 year
TOF Four Components
Ventricular Septal defect - VSD Pulmonary stenosis – narrowing of pulmonary
valve Overriding of the aorta – aortic valve is enlarged
and appears to arise from both the left and right ventricles instead of the left ventricle
Hypertrophy of right ventricle – thickening of the muscular walls because of the right ventricle pumping at high pressure
Clinical Manifestations: TOF
Dependent on degree of right ventricular outflow obstruction.
Some infants are acutely cyanosed at birth, others have mild cyanosis that progresses over the 1st year as the pulmonary stenosis worsen
Children are at risk of developing emboli, C.V disease, brain abscess, Seizures and loss of consciousness, or sudden death following an anoxic spell.
Clinical Manifestations: TOF
• Acute episodes of cyanosis and hypoxia (blue spells) usually during crying or after feeding
• With increased cyanosis increased clubbing of fingers, Squatting, Poor growth
• Severe irritability due to low oxygen levels
• “tet” spells - treated by flexing knees forward and upward
Knee-chest Position
Child with a cyanotic heartdefect squats (assumes a knee-chest position) to relievecyanotic spells. Some times called “tet” spells.
Nurse puts infant in knee-chest position.
Diagnostic tests: TOF
Cyanosis Oxygen will have little effect on the cyanosis Loud heart murmur Echocardiogram – demonstrates the four
defects characteristic of tetralogy
Management: (TOF)
Palliative: to increase blood flow back to the pulmonary artery from right or left subclavian artery by doing modified blalock taussig shunt
If oxygen levels are extremely low prostaglandins may be administered IV to keep the PDA open
Prognosis: less than 5% total operative mortality rate
Surgical Treatment
Corrective: Elective reparit in 1st year of life based on increased symptoms.
Correction includes Closure of the VSD with dacron patch The narrowed pulmonary valve is dilated Coronary arteries will be repaired Hypertrophy of right heart should remodel within a
few months when pressure in right side is reduced
Long Term Outcomes
Leaky pulmonary valve that can lead to pulmonary insufficiency
Arrhythmias after surgery Heart block – occasionally a pacemaker is
necessary Periodic echocardiogram and exercise stress
test or Holter evaluation
Transposition of Great Vessels
Transposition of Great Arteries
Transposition of Great Arteries or Vessels (TGA or TGV)
Pulmonary artery leaves the Lt ventricle Aorta exits from the Rt ventricle With no communication between systemic
and pulmonary circulation Males are affected more than females Associated defects such as Septal defects or
patent ductus arteriosus permits blood to enter the systemic circulation and or pulmonary circulation for mixing of saturated and nonsaturated blood
Clinical manifestations: TGV/TGA
It depends on the type and size of the associated defects.
If minimum communication present, then children are severely cyanosed
If PDA or septal defect is present, less cyanosis symptoms present but might show signs of CHF.
Heart sounds vary according to defects Cardiomegally occur after few weeks of life
Surgical Palliative treatment (To provide intracardiac mixing):
1. Administration of IV prostaglandin E1 to keep the ductus arteriosus open to temporary increase in blood mixing and provide O2 saturation of 75% or to maintain cardiac output.
2. Rashkin procedure: Enlarge septal defect
Complete repair: Switching the great vessels to their correct anatomic
position.
Prognosis: Operative mortality about 5 – 10%
Management: TGV/TGA
ACUTE RHEUMATIC FEVERACUTE RHEUMATIC FEVER
Acute rheumatic fever (ARF) is a systemic disease characterized by inflammatory lesions of connective
tissue and endothelial tissue. It is a primary type of acquired heart
disease.
Etiology/Incidence The pathogenesis is thought to be an autoimmune response
to group A beta-hemolytic Streptococcus.
Most attacks of ARF are preceded by an untreated streptococcal infection of the throat or upper respiratory tract at an interval of 2 to 6 weeks.
ARF is not caused by direct infection of the organism.
ARF is commonly seen in children 5 to 15 years of age, during winter months, and in poorer living conditions.
Incidence is greater in underdeveloped countries, although it is on the rise in the United States.
Altered Physiology
There is cross-reactivity between cardiac tissue antigens and streptococcal cell wall components.
The Streptococcus may no longer be present, but auto antibodies attack one's heart (myocardium, pericardium, or valves)
The unique pathologic lesion of rheumatic fever is the Aschoff body, a collection of reticuloendothelial cells surrounding a necrotic center on some structure of the heart.
The inflammatory process involves the heart, joints, skin, and central nervous system.
The inflammation may involve the leaflets or chordae tendinae of the heart valves, most frequently THE MITRAL or aortic valves, resulting in sclerosis and fusion of valve margins
Valvular incompetence results There is a high recurrence rate. Of those with ARF, 75% progress to rheumatic
heart disease in adulthood. ARF is a preventable condition with penicillin
treatment of the primary infection. Erythromycin is treatment for those with penicillin sensitivities.
Complications:
♥ Significant chronic heart failure ♥ Pericarditis, pericardial effusions♥ Aortic/Mitral valve regurgitation ♥ Permanent cardiac damage
Major Manifestations:
1. CARDITIS: manifested by significant murmurs, signs of Pericarditis, cardiac enlargement, or CHF
2. POLYARTHRITIS: almost always migratory and is manifested by:
a. swelling,
b. heat,
c. redness and tenderness
d. or by pain and limitation of motion of two or more joints.
(The synovial fluid is sterile (
Cont. Major Manifestations
3. Chorea, a CNS disorder that lasts 1 to 3 months purposeless, involuntary, rapid movements often are associated with muscle weakness, involuntary facial grimaces, speech disturbances, and emotional liability
Cont. Major Manifestations
4. Erythema marginatum: are temporary nonpruritic,pink rash.
The erythematus areas have pale centersand round or wavy margins, vary greatly in
size, And occur mainly on the trunk and extremities.
Erythema is transient, migrates from place to place, and may be brought out by the application of heat.
(Erythema marginatum)
Cont. Major Manifestations
5. Subcutaneous nodules are firm, painless nodules seen or felt over the extensor surface of certain joints, particularly elbows, knees, and wrists, in the occipital region, or over the spinous processes of the thoracic and lumbar vertebrae; the skin overlying them moves freely and is not inflamed.
(Subcutaneous nodule)
Minor Manifestations :
1. History of previous rheumatic fever or evidence of preexisting rheumatic heart disease
2. Arthralgia—pain in one or more joints without evidence of inflammation, tenderness to touch, or limitation of motion
3. Fever—temperature in excess of 38°C
4. Elevated erythrocyte sedimentation rate (ESR)
5. Positive C-reactive protein (CRP)
5. ECG changes—mainly PR interval prolongation
Supporting Evidence of Streptococcal Infection:
Increased titer of streptococcal antibodies (Antistreptolysin O or ASO titer)
Positive throat culture for group A beta-hemolytic streptococci or recent scarlet fever
Treatment: Treatment of streptococcal infection—
generally intramuscular (IM) penicillin G (Penicillin L-A); erythromycin for patients with penicillin allergy
Prevention of permanent cardiac damage corticosteroids for patients with Carditis
Palliative management of other symptoms—Salicylates prescribed for patients with arthritis (but not while on high-dose corticosteroids due to risk of gastrointestinal bleeding); antipyretics after diagnosis has been established
Prevention of recurrences of ARF
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