Care of Child with Cardiovascular Disorders Dr. Manal Kloub.

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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