Faculty of medicine universitas brawijaya
Download
1 / 89

Faculty of Medicine Universitas Brawijaya - PowerPoint PPT Presentation


  • 141 Views
  • Uploaded on

Rheumatic Fever. Faculty of Medicine Universitas Brawijaya. Objectives. Etiology Epidemiology Pathogenesis Pathologic lesions Clinical manifestations & Laboratory findings Diagnosis & Differential diagnosis Treatment & Prevention Prognosis References. Etiology.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about ' Faculty of Medicine Universitas Brawijaya' - tamera


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Faculty of medicine universitas brawijaya

Rheumatic Fever

Faculty of Medicine

UniversitasBrawijaya


Objectives
Objectives

  • Etiology

  • Epidemiology

  • Pathogenesis

  • Pathologic lesions

  • Clinical manifestations & Laboratory findings

  • Diagnosis & Differential diagnosis

  • Treatment & Prevention

  • Prognosis

  • References


Etiology
Etiology

  • Acute rheumatic fever is a systemic disease of childhood,often recurrent that follows group A beta hemolytic streptococcal infection

  • It is a delayed non-suppurative sequelae to URTI with GABH streptococci.

  • It is a diffuse inflammatory disease of connective tissue,primarily involving heart,blood vessels,joints, subcut.tissue and CNS


Epidemiology
Epidemiology

  • Ages 5-15 yrs are most susceptible

  • Rare <3 yrs

  • Girls>boys

  • Common in 3rd world countries

  • Environmental factors-- over crowding, poor sanitation, poverty,

  • Incidence more during fall ,winter & early spring


Pathogenesis
Pathogenesis

  • Delayed immune response to infection with group.A beta hemolytic streptococci.

  • After a latent period of 1-3 weeks, antibody induced immunological damage occur toheart valves,joints, subcutaneous tissue & basal ganglia of brain


Strains that produces rheumatic fever - M types l, 3, 5, 6,18 & 24

Pharyngitis- produced by GABHS can lead to- acute rheumatic fever , rheumatic heart disease & post strept. Glomerulonepritis

Skin infection- produced by GABHS leads to post streptococcal glomerulo nephritis only. It will not result in Rh.Fever or carditis as skin lipid cholesterol inhibit antigenicity

Group A Beta Hemolytic Streptococcus


Diagrammatic structure of the group A beta hemolytic streptococcus

Antigen of outer protein cell wall of GABHS induces antibody response in victim which result in autoimmune damage to heart valves, sub cutaneous tissue,tendons, joints & basal ganglia of brain

Capsule

Cell wall

Proteinantigens

Group carbohydrate

Peptidoglycan

Cyto.membrane

Cytoplasm

…………………………………………………...


Pathologic lesions
Pathologic Lesions streptococcus

  • Fibrinoid degeneration of connective tissue,inflammatory edema, inflammatory cell infiltration & proliferation of specific cells resulting in formation of Ashcoff nodules, resulting in-

    -Pancarditis in the heart

    -Arthritis in the joints

    -Ashcoff nodulesin the subcutaneous tissue

    -Basal gangliar lesions resulting in chorea




Clinical features
Clinical Features streptococcus

1.Arthritis

  • Flitting & fleeting migratory polyarthritis, involving major joints

  • Commonly involved joints-knee,ankle,elbow & wrist

  • Occur in 80%,involved joints are exquisitely tender

  • In children below 5 yrs arthritis usually mild but carditis more prominent

  • Arthritis do not progress to chronic disease


Clinical features contd
Clinical Features (Contd) streptococcus

2.Carditis

  • Manifest as pancarditis(endocarditis, myocarditis and pericarditis),occur in 40-50% of cases

  • Carditis is the only manifestation of rheumatic fever that leaves a sequelae & permanent damage to the organ

  • Valvulitis occur in acute phase

  • Chronic phase- fibrosis,calcification & stenosis of heart valves(fishmouth valves)


Rheumatic heart disease streptococcus. Abnormal mitral valve. Thick, fused chordae


Another view of thick and fused mitral valves in streptococcusRheumatic heart disease


Clinical features contd1

Occur in 5-10% of cases streptococcus

Mainly in girls of 1-15 yrs age

May appear even 6/12 after the attack of rheumatic fever

Clinically manifest as-clumsiness, deterioration of handwriting,emotional lability or grimacing of face

Clinical signs- pronator sign, jack in the box sign , milking sign of hands

Clinical Features (Contd)

3.Sydenham Chorea


Clinical features contd2
Clinical Features (Contd) streptococcus

4.Erythema Marginatum

  • Occur in <5%.

  • Unique,transient,serpiginous-looking lesions of 1-2 inches in size

  • Pale center with red irregular margin

  • More on trunks & limbs & non-itchy

  • Worsens with application of heat

  • Often associated with chronic carditis


Clinical features contd3
Clinical Features (Contd) streptococcus

  • Occur in 10%

  • Painless,pea-sized,palpable nodules

  • Mainly over extensor surfaces of joints,spine,scapulae & scalp

  • Associated with strong seropositivity

  • Always associated with severe carditis

5.Subcutaneous nodules


Clinical features contd4
Clinical Features (Contd) streptococcus

Other features (Minor features)

  • Fever-(up to 101 degree F)

  • Arthralgia

  • Pallor

  • Anorexia

  • Loss of weight


Laboratory findings
Laboratory Findings streptococcus

  • High ESR

  • Anemia, leucocytosis

  • Elevated C-reactive protien

  • ASO titre >200 Todd units. (Peak value attained at 3 weeks,then comes down to normal by 6 weeks)

  • Anti-DNAse B test

  • Throat culture-GABHstreptococci


Laboratory findings contd
Laboratory Findings (Contd) streptococcus

  • ECG- prolonged PR interval, 2nd or 3rd degree blocks,ST depression, T inversion

  • 2D Echo cardiography- valve edema,mitral regurgitation, LA & LV dilatation,pericardialeffusion,decreased contractility


Diagnosis
Diagnosis streptococcus

  • Rheumatic fever is mainly a clinical diagnosis

  • No single diagnostic sign or specific laboratory test available for diagnosis

  • Diagnosis based on MODIFIED JONES CRITERIA



Exceptions to jones criteria
Exceptions to Jones Criteria streptococcus

  • Chorea alone, if other causes have been excluded

  • Insidious or late-onset carditis with no other explanation

  • Patients with documented RHD or prior rheumatic fever,one major criterion,or of fever,arthralgia or high CRP suggests recurrence


Differential diagnosis
Differential Diagnosis streptococcus

  • Juvenile rheumatiod arthritis

  • Septic arthritis

  • Sickle-cell arthropathy

  • Kawasaki disease

  • Myocarditis

  • Scarlet fever

  • Leukemia


Treatment
Treatment streptococcus

  • Step I- primary prevention (eradication of streptococci)

  • Step II- anti inflammatory treatment (aspirin,steroids)

  • Step III- supportive management & management of complications

  • Step IV- secondary prevention (prevention of recurrent attacks)


STEP I: streptococcus Primary Prevention of Rheumatic Fever (Treatment of Streptococcal Tonsillopharyngitis)

Agent Dose Mode Duration

Benzathine penicillin G 600 000 U for patients Intramuscular Once 27 kg (60 lb) 1 200 000 U for patients >27 kg or

Penicillin V Children: 250 mg 2-3 times daily Oral 10 d (phenoxymethyl penicillin) Adolescents and adults: 500 mg 2-3 times daily

For individuals allergic to penicillin

Erythromycin: 20-40 mg/kg/d 2-4 times daily Oral 10 d Estolate (maximum 1 g/d)

or

Ethylsuccinate 40 mg/kg/d 2-4 times daily Oral 10 d (maximum 1 g/d)

Recommendations of American Heart Association

Dr.Said Alavi


Step II: streptococcusAnti inflammatory treatment

Clinical condition Drugs


Bed rest streptococcus

Treatment of congestive cardiac failure: -digitalis,diuretics

Treatment of chorea: -diazepam or haloperidol

Rest to joints & supportive splinting

3.Step III: Supportive management & management of complications


STEP IV : streptococcus Secondary Prevention of Rheumatic Fever (Prevention of Recurrent Attacks)

Agent Dose Mode

Benzathine penicillin G 1 200 000 U every 4 weeks* Intramuscular

or

Penicillin V 250 mg twice daily Oral

or

Sulfadiazine 0.5 g once daily for patients 27 kg (60 lb Oral 1.0 g once daily for patients >27 kg (60 lb)

For individuals allergic to penicillin and sulfadiazine

Erythromycin 250 mg twice daily Oral

*In high-risk situations, administration every 3 weeks is justified and recommended

Recommendations of American Heart Association

Dr.Said Alavi


Duration of Secondary Rheumatic Fever Prophylaxis streptococcus

Category Duration

Rheumatic fever with carditis and At least 10 y since last residual heart disease episode and at least until (persistent valvar disease*) age 40 y, sometimes lifelong prophylaxis Rheumatic fever with carditis 10 y or well into adulthood, but no residual heart disease whichever is longer (no valvar disease*)

Rheumatic fever without carditis 5 y or until age 21 y, whichever is longer

*Clinical or echocardiographic evidence.

Recommendations of American Heart Association


Prognosis
Prognosis streptococcus

  • Rheumatic fever can recur whenever the individual experience new GABH streptococcal infection,if not on prophylactic medicines

  • Good prognosis for older age group & if no carditis during the initial attack

  • Bad prognosis for younger children & those with carditis with valvar lesions


Thank You streptococcus


Valvular heart disease

VALVULAR HEART DISEASE streptococcus

MITRAL STENOSIS

G


Etiology rheumatic valvular disease
ETIOLOGY streptococcusRHEUMATIC VALVULAR DISEASE

  • MOST COMMON CAUSE OF M ITRAL STENOSIS

    • Pure mitral stenosis 25%

    • Pure mitral regurgitation 35%

    • Combined MS and MR 40%

  • 15 TO 20 YEAR LATENCY PERIOD


Etiology other causes
ETIOLOGY streptococcusOTHER CAUSES

  • CONGENITAL

  • MALIGNANT CARCINOID

  • SLE OR RHEUMATOID ARTHRITIS

  • AMYLOID

  • METHYLSERGIDE THERAPY


Pathology symptomatic mitral stenosis
PATHOLOGY streptococcusSYMPTOMATIC MITRAL STENOSIS

  • THICKENED MITRAL CUSPS

    • +/- CALCIFIC DEPOSITS

  • FUSION OF VALVE COMMISSURES

  • SHORTENING OF CHORDAE WITH FUSION

  • “FISH MOUTH” OR FUNNEL ORIFICE


History
HISTORY streptococcus

  • PRINCIPLE SYMPTOM IS DYSPNEA

    • Reduces compliance of the lung

  • PULMONARY EDEMA

    • Effort, emotional stress, infection, fever, pregnancy

  • ATRIAL FIBRILLATION

    • Increased rate causes increased LA to LV gradient


History1
HISTORY streptococcus

  • CHEST PAIN

    • 15% DUE TO RV HTN, EMBOLIZATION

  • THROMBOEMBOLISM

    • 20% HISTORICALLY INVOLVED

    • CORRELATES INVERSELY WITH CARDIAC OUTPUT

    • CORRELATES DIRECTLY WITH LA SIZE AND AGE OF PATIENT


Physical examination
PHYSICAL EXAMINATION streptococcus

  • ARTERIAL PULSE NORMAL OR DIMINISHED

  • JUGULAR PRESSURE PROMINENT a WAVE

  • PALPATION

    • INCONSPICUOUS LV, RV HEAVE IN PULMONARY HTN


Physical examination auscultation
PHYSICAL EXAMINATION streptococcusAUSCULTATION

  • ACCENTUATED S1

    • PROLONGED Q-S1 INTERVAL

  • OPENING SNAP

    • SUDDEN TENSING OF VALVE LEAFLETS

    • A2-OS INTERVAL SHORTENS WITH SEVERITY

  • DIASTOLIC MURMUR


Pathophysiology
PATHOPHYSIOLOGY streptococcus

  • NORMAL VALVE AREA 4 TO 6cm2

  • NORMAL MEAN LA TO LV PRESSURE GRADIENT 2 TO 4mmHg

  • MILD MITRAL STENOSIS 2cm2

  • CRITICAL MITRAL STENOSIS 1cm2 or less

    • 20MMhg GRADIENT REQUIRED FOR FLOW


Management natural history
MANAGEMENT streptococcusNATURAL HISTORY

  • 20 TO 25 YEAR ASYMPTOMATIC PERIOD

  • 5 YEARS FOR PROGRESSION CLASS II-IV

  • SURVIVAL

    • CLASS III 62% 5 YR SURVIVAL

    • CLASS IV 15% 5 YR SURVIVAL

  • ASYMPTOMATIC CLASS 1 40% WORSENED OR DIED IN 10 YEARS


Management medical treatment
MANAGEMENT streptococcusMEDICAL TREATMENT

  • RHD PCN AND SBE PROPHYLAXIS

  • SYMPTOMATIC PATIENTS

    • ORAL DIURETICS AND ACTIVITY RESTRICTION

    • BETA BLOCKERS AND LOW HEART RATE

    • DIGOXIN IN AF AND WITH PULM HTN

  • ANTICOAGULATION FOR LA SIZE >5.5cm, EMBOLISM OR ATRIAL FIBRILLATION


Management surgical treatment
MANAGEMENT streptococcusSURGICAL TREATMENT

  • OPERATE FOR SEVERE SYMPTOMS

    • CLASS III OR GREATER (SYMPTOMS WITH LESS THAN USUAL ACTIVITY)

    • PULMONARY HTN DEMANDS OPERATION

  • ROUTINE CATHETERIZATION MEN>45

  • MILDY SYMPTOMATIC PATIENTS

    • CONSIDER SIZE OF MV ORIFICE, LIFESTYLE AND HISTORY OF COMPLICATIONS


Management balloon valvuloplasty
MANAGEMENT streptococcusBALLOON VALVULOPLASTY

  • PROCEDURE OF CHOICE IN RIGHT PT

    • TRANSESOPHAGEAL ECHO HELPFUL IN SORTING OUT WHICH PATIENT

    • ECHO SCALE OF PREDICTORS RELATES TO THICKENING AND CALCIFICATION OF VALVE

  • RESULTS COMPARABLE TO SURGERY

  • MORTALITY 2-3%, MORBIDITY 8-12%


Valvular heart disease1

VALVULAR HEART DISEASE streptococcus

MITRAL INSUFFICIENCTY


Etiology acute vs chronic
ETIOLOGY streptococcusACUTE VS CHRONIC

  • INFLAMMATORY

  • DEGENERATIVE

  • INFECTIVE

  • STRUCTURAL

  • CONGENITAL


Etiology degenerative
ETIOLOGY streptococcusDEGENERATIVE

  • MYXOMATOUS DEGENERATION OF LEAFLETS

    • MITRAL VALVE PROLAPSE

    • MOST COMMON CAUSE OF ACUTE MR IN US ADULTS

  • MARFAN SYNDROME

  • CALCIFICATION OF MV ANNULUS


Etiology inflammatory
ETIOLOGY streptococcusINFLAMMATORY

  • RHEUMATIC HEART DISEASE

    • ACUTE RHEUMATIC FEVER VS CHRONIC

  • SYSTEMIC LUPUS ERYTHEMATOSUS

  • SCLERODERMA


Etiology structural
ETIOLOGY streptococcusSTRUCTURAL

  • RUPTURED CHORDAE TENDINAE

  • RUPTURE OR DYSFUNCTION OF PAPILLARY MUSCLES

  • DILATATION OF MITRAL VALVE ANNULUS

  • PARAVALVULAR PROSTHETIC LEAK


Anatomy of mitral valve
ANATOMY OF MITRAL VALVE streptococcus

  • VALVE LEAFLETS

    • ANTERIOR AND POSTERIOR

  • MITRAL ANNULUS

    • DILATATION

  • CHORDAE TENDINAE

  • PAPILLARY MUSCLES


Pathophysiology volume overload
PATHOPHYSIOLOGY streptococcusVOLUME OVERLOAD

  • IMPEDENCE TO VENTRICULAR EMPTYING IS REDUCED

    • LV DECOMPRESSES INTO LA

  • VOLUME OF REGURGITANT FLOW

    • DEPENDENT ON SIZE OF REGURGITANT ORIFICE

      • AND LV TO LA PRESSURE GRADIENT


Pathophysiology hemodynamics
PATHOPHYSIOLOGY streptococcusHEMODYNAMICS

  • FORWARD CARDIAC OUTPUT USUALLY DEPRESSED

    • TOTAL LV OUTPUT (FORWARD AND BACKWARD) INCREASED

  • NORMAL LA COMPLIANCE (ACUTE MR)

    • LITTLE ENLARGEMENT OF LA, HIGH LA PRESSURE

  • LOW LA COMPLIANCE (CHRONIC MR)

    • ENLARGED LA, MINIMALLY INCREASED LA PRESSURE


Clinical manifestations natural history
CLINICAL MANIFESTATIONS streptococcusNATURAL HISTORY

  • VARIABLE AND DEPENDS ON MR VOLUME

  • MILD MR STABLE IN MAJORITY FOR YEARS

    • MINORITY DEVELOP SEVERE MR

  • MORE RAPIDLY WITH DEGENERATIVE DISEASE THAN RHEUMATIC


Clinical manifestations
CLINICAL MANIFESTATIONS streptococcus

  • SYMPTOMS USUALLY NOT UNTIL LV STARTS TO FAIL

  • LONGER TIME INTERVAL IN MR THAN MITRAL STENOSIS

  • RIGHT HEART FAILURE IN END STAGE MR


Physical examination1
PHYSICAL EXAMINATION streptococcus

  • CAROTID UPSTROKE SHARP, RAPID FALLOFF

  • S1 USUALLY SOFT, WIDELY SPLIT S2

  • HOLOSYSTOLIC MURMUR

    • APEX TO AXILLA

  • SYSTOLIC EJECTION MURMUR

    • ISCHEMIC MR


Physical examination2
PHYSICAL EXAMINATION streptococcus

  • MITRAL VALVE PROLAPSE

    • MID TO LATE SYSTOLIC EJECTION MURMUR

    • MID SYSTOLIC NON-EJECTION CLICK

    • VALSALVA PROLONGS MURMUR AND BRINGS IT TO START CLOSER TO S1


Laboratory examination
LABORATORY EXAMINATION streptococcus

  • CHEST XRAY

    • CARDIOMEGALY (ECCENTRIC HYPERTROPHY)

    • LEFT ATRIAL ENLARGEMENT

  • REGURGITANT VOLUME

    • MILD 25%, MODERATE 40%, SEVERE 75%


Echocardiography
ECHOCARDIOGRAPHY streptococcus

  • GOOD ANATOMICAL DETAIL

  • LA SIZE, THROMBUS, LV FUNCTION

  • UNDERLYING ETIOLOGY OF MR

  • INFECTIVE ENDOCARDITIS

  • DOPPLER

    • SEVERITY OF MR, SIZE OF MR JET


Management medical management
MANAGEMENT streptococcusMEDICAL MANAGEMENT

  • AFTERLOAD REDUCTION

    • REDUCES IMPEDENCE TO EJECTION IN AORTA

    • ACE INHIBITORS AND HYDRALAZINE

  • ACUTE MR

    • IV NITROPRUSSIDE CAN BE LIFESAVING

  • DIGOXIN, DIURETICS IN CHRONIC MR

  • FOLLOW LV SIZE AND FUNCTION


Surgical treatment
SURGICAL TREATMENT streptococcus

  • OPERATE FOR SYMPTOMS

  • ENLARGING LEFT VENTRICULAR SYSTOLIC DIMENSION (>5.5CM), EJECTION FRACTION <55% ARE PREDICTORS OF BAD OUTCOME

  • OPERATIVE MORTALITY 2 TO 7% IN CLASS II TO III PATIENTS

  • RECONSTRUCTION IS BETTER THAN REPLACEMENT IF POSSIBLE


Valvular heart disease2

VALVULAR HEART DISEASE streptococcus

AORTIC STENOSIS


Etiology obstruction to lv outflow
ETIOLOGY streptococcusOBSTRUCTION TO LV OUTFLOW

  • HYPERTROPHIC CARDIOMYOPATHY

  • SUPRAVALVULAR

  • SUBVALVULAR

  • CONGENITAL

  • ACQUIRED


Etiology congenital aortic stenosis
ETIOLOGY streptococcusCONGENITAL AORTIC STENOSIS

  • UNICUSPID

    • SEVERE AND DEADLY IN INFANCY

  • BICUSPID

    • MANIFESTED LATER IN LIFE

    • MOST COMMON CONGENITAL CARDIAC ANOMALY IN LIVE BIRTHS (1%)

  • TRICUSPID

    • CUSPS OF UNEQUAL SIZE


Etiology acquired aortic stenosis
ETIOLOGY streptococcusACQUIRED AORTIC STENOSIS

  • RHEUMATIC HEART DISEASE

  • DEGENERATIVE

  • ATHEROSCLEROTIC

  • CALCIFIC DUE TO PAGET’S DISEASE

  • RHEUMATOID


Etiology degenerative calcific aortic stenosis
ETIOLOGY streptococcusDEGENERATIVE CALCIFIC AORTIC STENOSIS

  • PRIMARY CAUSE OF ADULT AORTIC STENOSIS

  • YEARS OF MECHANICAL STRESS

  • DEPOSITION OF CALCIUM AT CUPAL BASE

  • PRESERVED COMMISSURES

  • RISK FACTORS

    • DIABETES AND HYPERLIPIDEMIA


Etiology rheumatic aortic stenosis
ETIOLOGY streptococcusRHEUMATIC AORTIC STENOSIS

  • FUSION OF COMMISSURES AND CUSPS

  • RETRACTION OF CUSPAL BORDERS

  • REDUCE ORIFICE TO TRIANGULAR OPENING

  • ASSOCIATED WITH AORTIC INSUFFICENCY

  • MITRAL DISEASE COMMON

  • ISOLATED AORTIC STENOSIS RARE


History2
HISTORY streptococcus

  • ANGINA

    • MEDIAN SURVIVAL 5 YEARS

  • SYNCOPE

    • MEDIAN SURVIVAL 3 YEARS

  • CONGESTIVE HEART FAILURE

    • MEDIAN SURVIVAL 2 YEARS


Physical examination3
PHYSICAL EXAMINATION streptococcus

  • PULSUS PARVUS AND TARDUS

    • IN CAROTID PULSE

  • REDUCED PULSE PRESSURE

  • SUSTAINED CARDIAC IMPULSE

  • DELAYED A2 OR DIMINISHED

  • HARSH SYSTOLIC EJECTION MURMUR


Pathophysiology1
PATHOPHYSIOLOGY streptococcus

  • GRADUAL DEVELOPMENT OF OBSTRUCTION TO LV OUTFLOW

  • LV OUTPUT MAINTAINED BY LV HYPERTROPHY

  • LV HYPERTROPHY MAY SUSTAIN A LARGE PRESSURE GRADIENT FROM THE LV TO AORTA OVER YEARS

  • ATRIAL CONTRACTION IMPORTANT

    • ATRIAL FIBRILLATION MAY CAUSE ABRUPT AND SEVERE SYMPTOMS


Pathophysiology2
PATHOPHYSIOLOGY streptococcus

  • INCREASE IN AFTERLOAD

  • INCREASED LV WALL STRESS COMPENSATED BY THE INCREASED LV HYPERTROPHY

  • ULTIMATELY LOSS IN CONTRACTILITY OF LV MASS AND DEVELOPMENT OF HEART FAILURE


Laboratory
LABORATORY streptococcus

  • EKG

    • LEFT VENTRICULAR HYPERTROPHY IS PROMINENT FINDING

  • CHEST XRAY

    • MAY BE ENTIRELY NORMAL BECAUSE THE HYPERTROPHY OF LV IS CONCENTRIC (CENTRAL) NOT ECCENTRIC LIKE MR OR AORTIC INSUFFICIENCY

    • CALCIFICATION OF AORTIC VALVE MAY BE SEEN


Echocardiography1
ECHOCARDIOGRAPHY streptococcus

  • CALCIFIED VALVE WITH THICKENED LEAFLETS OR COMMISSURES

  • DECREASED OPENING OF AORTIC VALVE SEEN

  • LEFT VENTRICULAR HYPERTROPHY

  • DOPPLER

    • VALVE PRESSURE GRADIENT CALCULATED

    • VALVE AREA FROM THIS MEASUREMENT


Medical history
MEDICAL HISTORY streptococcus

  • EDUCATION IN SYMPTOMS AND REPORTING

  • OPERATE FOR SYMPTOMS WHEN VALVE IS SEVERLY NARROWED

    • <1CM2 IN AREA

  • DO NOT OPERATE ON SEVERE NARROWING IF ASYMPTOMATIC

  • ENDOCARDITIS PROPHYLAXIS


Surgical management results
SURGICAL MANAGEMENT streptococcusRESULTS

  • 5 YEAR ACTUARIAL SURVIVAL 85%

  • REDUCTION IN LV MASS

  • IF PATIENTS HAVE CONGESTIVE HEART FAILURE THEN VALVE REPLACEMENT HAS 10-25% MORTALITY

  • NORMAL 3-5% MORTALITY IN OR

  • PORCINE VALVE FOR AGE > 70


Surgical management
SURGICAL MANAGEMENT streptococcus

  • ASYMPTOMATIC PATIENTS

    • MORTALITY WITHOUT OPERATION IS <5% PER YEAR

    • FOLLOW EVERY 6 MONTHS IN OFFICE

    • COUNSEL ON DEVELOPMENT OF SYMPTOMS OF ANGINA, CHF, SYNCOPE


Aortic stenosis in the elderly
AORTIC STENOSIS IN THE ELDERLY streptococcus

  • OPERATIVE MORTALITY IN THE ELDERLY

    • 1.8% AGE < 50

    • 5.1% AGE 50 - 60

    • 7.1% AGE 60 – 70

  • ISOLATED AV REPLACEMENT IN PTS AGE 80 TO 89

    • 94% HAD GOOD RESULTS

    • APPROPRIATE SELECTION


Aortic insufficiency

AORTIC INSUFFICIENCY streptococcus

VALVULAR HEART DISEASE


Etiology1
ETIOLOGY streptococcus

  • ¾ OF PATIENTS WITH PURE AI ARE MALES

  • 2/3 OF PATIENTS FROM RHEUMATIC FEVER

    • THICKENING AND DEFORMATION OF INDIVIDUAL VALVE CUSPS

  • INFECTIVE ENDOCARDITIS

    • VARIOUS PREVIOUSLY DAMAGING ETIOLOGIES


Etiology2
ETIOLOGY streptococcus

  • PROLAPSE OF AN AORTIC CUSP

  • CONGENITAL FENESTRATIONS OF CUSP

  • TRAUMATIC RUPTURE

  • ASCENDING THORACIC AORTA DISSECTION

  • MARKED AORTIC ROOT DILATATION

  • SYPHILIS, ANKYLOSING SPONDYLITIS


Pathophysiology3
PATHOPHYSIOLOGY streptococcus

  • MARKED INCREASE IN STROKE VOLUME OF LEFT VENTRICLE

    • EXTRA BLOOD FROM LEAKING BACK INTO LV TO EJECT

  • CONTRAST TO MITRAL INSUFFICIENCY

    • AI: EJECTING BLOOD INTO HIGH AFTERLOAD (AORTA)

    • MI: EJECTING BLOOD INTO LOW AFTERLOAD (LEFT ATRIUM)


Pathophysiology4
PATHOPHYSIOLOGY streptococcus

  • DILATATION OF LEFT VENTRICLE

    • TO MAINTAIN ADEQUATE FORWARD CARDIAC OUTPUT

    • COR BOVINUM

  • REVERSE PRESSURE GRADIENT FROM AORTA TO LV IN DIASTOLE CAUSES BACK FLOW

  • ACUTE VS CHRONIC INSUFFICIENCY


History3
HISTORY streptococcus

  • FAMILY HISTORY WITH MARFAN SYNDROME

  • INFECTIVE ENDOCARDITIS

  • SYPHYLIS

  • AWARENESS OF HEARTBEAT

  • ORTHOPNEA, DOE LATE OR IN ACUTE

  • ANGINA

  • EDEMA


Physical findings
PHYSICAL FINDINGS streptococcus

  • INSPECTION

    • BOBBING HEAD OR JARRING OF BODY

  • PALPATION

    • ARTERIAL JACK HAMMER PULSE

    • CAPILLARY PULSATIONS

    • VARIOUS SIGNS

    • WIDENED PULSE PRESSURE


Physical findings1
PHYSICAL FINDINGS streptococcus

  • MURMURS

    • DIASTOLIC HIGH PITCHED BLOW

    • LOUD SYSTOLIC AORTIC EJECTION FLOW MURMUR

    • DIASTOLIC RUMBLE AUSTIN FLINT MURMUR

      • MISTAKEN FOR MITRAL STENOSIS


Laboratory1
LABORATORY streptococcus

  • EKG

    • LEFT VENTRICULAR HYPERTROPHY

      • WITH STRAIN

    • ECHOCARDIOGRAM

      • FLOW INTO LV FROM AORTIC VALVE

      • LV SIZE

      • FLUTTERING OF MITRAL LEAFLET

    • BLOOD CULTURES IN ENDOCARDITIS


Treatment1
TREATMENT streptococcus

  • CONGESTIVE HEART FAILURE TREATMENT

    • DIGOXIN, DIURETICS, AFTERLOAD REDUCTION

      • IV NITROPRUSSIDE MAY BE LIFESAVING


Treatment2
TREATMENT streptococcus

  • SURGERY

    • SYMPTOMATIC PATIENTS SHOULD BE OPERATED UPON

    • ASYMPTOMATIC PATIENTS FOLLOWED FOR LEFT VENTRICULAR ENLARGEMENT AND SYSTOLIC DIMENSIONS ON ECHOCARDIOGRAM

    • YEARLY ECHOCARDIOLOGY

    • MORTALITY <5% IF GOOD LV

    • MORTALITY 5-10% IF POOR LV FUNCTION


Thank You streptococcus


ad