Case Tirotoksikosis

8/9/2019 Case Tirotoksikosis

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CASE REPORTNurhikmawati


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INTRODUCTION

It has long been recognized that thyroid diseasestates exert profound eects on the heart andcirculatory system

The close physiological relationship is armed bypredictable changes in cardiovascular functionacross the entire range of thyroid disease states


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INTRODUCTION

Thyrotoxicosis associated with a 50% decline insystemic vascular resistance

arterial resistance and venous tone venousreturn of blood to the heart

mean circulatory lling pressure

oxygen consumption in the periphery and metabolic demands blood supply and pumpingaction of the heart

atrial natriuretic peptide ! total proteinsynthesis "cardiac hypertrophy#


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PATIENT IDENTITY

$ame ! $n &

'edical (ecord ! )*+,0-

.ge ! // years old

.ddress ! 'aassar

.dmitted to hospital ! 1uly -,th/0--


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HISTORY TAKING

Chief complaint ! 2hortness of breath

Histor ta!in" !

It3s been felt since - day before admitted to the

hospital4 and worsening ) hours beforeadmission 2tarted with chest pain4 not radiated4and no cold sweat

pigastric pain "6#4 nausea "6#4 vomitting "6#4about ) times

7rination and defecation ! normal


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#EDICA$ HISTORY

8istory of 8yperthyroid "6#4 since / years

ago4 regularly on treatment "Thyrax4

maintate# 8istory of heart disease "9#


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PHYSICA$ E%A#INATION

:ital 2ign ! ;lood pressure ! -+0


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$A&ORATORY 'INDING

8b ! -+5 gr


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ADDITIONA$ E%A#INATION

>H !

9 2inus Tachycardia4 8( ! -50x


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ADDITIONA$ E%A#INATION chocardiography !


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/or!in" Dia"nosis

Thyroid 8eart isease


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Plannin"

Baboratorium examination ! 2HJTonsult to ndocrine and metabolic department


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'O$$O/ UP

2 ! 2hortness of breath "6#4 feels dicult to breath4 >hestpain "6#4 feels lie stabbed4 radiated to her bac

:ital 2ign ! ;lood pressure ! -)0


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'O$$O/ UP

B.;J(.TJ(I7'

-*


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'O$$O/ UP

B.;J(.TJ(I7'

/0


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'O$$O/ UP

B.;J(.TJ(I7'

/0


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'O$$O/ UP

B.;J(.TJ(I7'

/-


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'O$$O/ UP

B.;J(.TJ(I7'

/5


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ADDITIONA$ E%A#INATION

>T scan thoras with contrast !

;ronchopneumonia bilateral

>ardiomegaly

There3s no sign of .orta dissection


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/or!in" Dia"nosis

Thyroid 8eart isease

2usp 'yocarditis


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#ANAGE#ENT

J/ )9+ literl 0*% -0 dpm

'ethyprednisolone -/5 mg


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INTRODUCTION

.s early as -,0= 4 a persistent inAammatoryprocess following such an infection "eg4diphtheria# of the myocardium led to progressivecardiac damage and dysfunction

In -,)C4 the term myocarditiswas rst introducedas inAammation or degeneration of the heart bypostmortem

ndomyocardial biopsy in -*,0 allows thesampling of human myocardial tissue during life

and antemortem diagnosis of myocarditis


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INTRODUCTION

2tudies suggest that myocarditis is a ma1or causeof sudden"/0%#4 unexpected death in adults lessthan +0 years of age

&rospective and retrospective studies have

identied myocardial inAammation in - to *percent of routine postmortem examinations


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CAUSATION

. large variety of infections4 systemic diseases4drugs4 and toxins have been associated with thedevelopment of this disease

:iruses4 bacteria4 protozoa4 and even worms have

been implicated as infectious agents


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Pathophsiolo"

2everal mechanisms of myocardialdamage

"-# irect in1ury of myocytes by theinfectious agent"/# 'yocyte in1ury caused by a toxin suchas that

from Corynebacterium diphtheriae")# 'yocyte in1ury as a result of infection9 induced immune reaction orautoimmunity


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Pathophsiolo"

Triphasic disease process

Phase I( 0iral Infection an1 Replication

Phase 2( A,toimm,nit an1 in3,r

Phase 4( Dilate1 Car1iomopath


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Phase I( 0iral Infection an1Replication >oxsacievirus ;) causes an infectious phase4

which lasts C9-0 days4 and is characterized byactive viral replication

uring this phase initial myocyte in1ury taes

place4 causing the release of antigenicintracellular components such as myosin into thebloodstream


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Phase 2( A,toimm,nit an1in3,r

The local release of cytoines4 such asinterleuin9-4 interleuin9/4 interleuin9=4tumor necrosis factor "T$F#4 and nitric

oxide may play a role in determining the T9cell reaction and the subseNuent degree ofautoimmune perpetuation

These cytoines may also cause reversible

depression of myocardial contractilitywithout causing cell death


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Phase 2( A,toimm,nit an1in3,r Immune9mediated by >, lymphocytes and

autoantibodies against various myocytecomponents

.ntigenic mimicry4 the cross reactivity of

antibodies to both virus and myocardial proteins 'yocyte in1ury may be a direct result of >,

lymphocyte inltration


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Phase 4( Dilate1Car1iomopath

:iruses may also directly cause myocyteapoptosis

uring the autoimmune phase4 cytoine activatethe matrix metalloproteinases4 such as

gelatinase4 collagenases4 and elastases In later stages of immune activation4 cytoines

play a leading role in adverse remodeling andprogressive heart failure

>ardiomyopathy developed despite the absenceof viral

proliferation but was correlated with elevatedlevels of

cytoines such as T$F


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Clinical 'in1in"s

Smptoms an1 Si"ns9 &atients"5*%# freNuently present days to weesafter an acute febrile illness4 particularly a Au9liesyndrome

9 'yocarditis is most commonly asymptomatic4with no evidence of left ventricular dysfunction9 fever4 malaise4 fatigue4 arthralgias4 myalgias4and sin rash9>ardiac symptoms may result from systolic or

diastolic left ventricular dysfunction or fromtachyarrhythmias or bradyarrhythmias "dyspnea4fatigue4 decreased exercise tolerance4palpitations #


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Clinical 'in1in"s

Smptoms an1 Si"ns

9 >hest discomfort")5%# is a commonsymptom

and is typically pericardial in nature9 'yocarditis may present as suddendeath4 as a result of malignant ventricular

arrhythmias orcomplete heart bloc

92ystemic and pulmonary thromboembolihavealso been noted


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Clinical 'in1in"s

Phsical E5amination9Tachycardia4 hypotension4 fever and tachycardiamay be disproportionate to the degree of fever9;radycardia is seen rarely4 and a narrow pulse

pressure is occasionally detected9'urmurs of mitral or tricuspid regurgitation arecommon 4 2) and 2+ gallops may also be heard9istended nec veins4 pulmonary rales4 wheezes4gallops4 and peripheral edema may be detected


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Cate"or I( Clinical Smptoms

Clinical heart fail,re

'e7er

0iral pro1rome 'ati",e

Dspnea on e5ertion

Chest pain

Palpitations Presncope or sncope


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Cate"or II( E7i1ence of Car1iacStr,ct,ral-',nctional Pert,r9ation in the AbsenceofRe"ional Coronar Ischemia

Echocar1io"raph e7i1ence

Re"ional 8all motion a9normalities

Car1iac 1ilation

Re"ional car1iac hpertroph

Troponin release Hi"h sensiti7it ;


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Cate"or III( Car1iac #a"netic Resonance Ima"in"

Increase1 mocar1ial T2si"nal on in7ersion

reco7er se@,ence

Delae1 contrast enhancement follo8in"

"a1olini,m?DTPA inf,sion

Cate"or I0( #ocar1ial &iopsPatholo"ical or#olec,lar Analsis

K Patholo" Bn1in"s compati9le 8ith Dallas criteria

K Presence of 7iral "enome 9 polmerase chainreaction or in sit, h9ri1iation


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Dia"nostic St,1ies

Electrocar1io"raph

The most common abnormality is sinustachycardia

may show ventricular arrhythmias or heart

bloc4 or it may mimic the ndings in acutemyocardial infarction or pericarditis

(elations between these clinical and laboratoryndings


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Dia"nostic St,1ies

Chest ra1io"raph9'ild to moderate cardiomegaly fromdilatation of the left or right ventricular

cavity9The cardiac silhouette may also beglobular when a pericardial eusion ispresent

9 :enous congestion and pulmonaryedema may be seen in more severe cases


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Dia"nostic St,1ies

Echocar1io"raph

myocardial contractility 4 chambersizes 4valvular function

Beft ventricular systolic dysfunction4regional wall motion abnormalities 4global hypoinesis

B: may be normal in size or minimallyenlarged

'itral or tricuspid regurgitation

'ural thrombi in -5% of cases


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Dia"nostic St,1ies

- helpful in demonstrating abnormalities ofdiastolic lling that mimic restrictivecardiomyopathy and indistinguishingventricular dilatation from pericardial

eusion- monitor the course of the illness and to

evaluate therapy


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Dia"nostic St,1ies

#ocar1ial ima"in"9Hallium9=C imaging 9G active inAammation of themyocardium and pericardium9Indium9--- monoclonal antimyosin antibody imaging 9G detecting myocyte in1ury in patients

9>ontrast media9enhanced '(I 9Gdetecting myocardial inAammation


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Dia"nostic St,1ies

Car1iac catheteriation9 elevated left ventricular end9diastolic pressure4a depressed cardiac output4 and increasedventricular volumes

9 >oronary angiogram typically demonstratesnormal coronary arteries


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Dia"nostic St,1ies

En1omocar1ial 9iops9 gold standard for the diagnosis ofmyocarditis

9Dallascriteria"an inAammatory inltrate of the

myocardium 6in1ury to the ad1acent myocytes#9borderline myocarditis is made when the

inltrate is not accompanied by myocytein1ury


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Others test

levated erythrocyte sedimentation rate "2(# 4 mild tomoderate leuocytosis

>E9'; 4 >ardiac troponin9I

Jther laboratory analyses that may be useful include a'ono9spot test4 pstein9;arr virus titers4 hepatitis serology4

and urine and serum for cytomegalovirus ">':#

T i h i 1i


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Triphasic 1isease process=


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#ana"ement of mocar1itis

'anagement is dictated by clinical signsand symptoms

'.$O proposed therapies4 most have onlya theoretical basis 2ome have beentested in animal models

>onventional heart failure therapy iscurrently the only accepted therapy formyocarditis including .> inhibitors4angiotensin receptor blocing agents4diuretics4 P9blocers or amiodarone


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Diet an1 $ifestle

(estrict salt intae to /9)g of sodium perday

xercise especially during the acute phase

of >oxsacie virus ;) murine myocarditisenhances viral replication rate4 enhancesimmune mechanisms and increasesinAammatory lesions and necrosis(esumption of physical activity can taeplace within / months of the acutedisease


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T8.$E OJ7

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Case Tirotoksikosis