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Divisi Kardiologi Pediatrik & Penyakit Jantung Bawaan

Departemen Kardiologi & Kedokteran Vaskular

Fakultas Kedokteran Universitas Indonesia


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Inisial : An. AY

Jenis Kelamin : Laki-laki

Usia : 10 tahun 1 bulan

Alamat : Jakarta

Pembiayaan : Gakin DKI

MRS : 9 Februari 2010

Perut semakin membesar


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Keluhan perut membesar,

sesak (-)

Dirawat 4x di RSPP dan

dilakukan penghisapan

cairan perut 2x.

Terakhir dirawat bulan

Nov 2009: dikonsulkan ke

SpJP dikatakan krn

kelainan jantung. Pasien

pulang dalam keadaan

perut masih agak besar.

Pasien menjalani rawat

jalan. Terapi: Lasix

1x40mg, Letonal 1x25mg,

digoxin 1x1tab.

Juni-Jan 2009

Keluhan perut

semakin membesar,

lemas, tidak nafsu

makan dan mata

tampak kekuningan

Dirujuk ke PJNHK dg

D/ Perikarditis

konstriktif

Feb2010

Riwayat batuk lama disertai

dahak, nafsu makan kurang.

Sesak (-)

Dirawat dua minggu

keluhan demam disertai

batuk dan sesak.

Pemeriksaan CXR dan dahak

TB paru mendapat OAT

Dua bulan kemudian, perut

mulai membesar.

OAT dihentikan.

R

UJU

K

PJNHK

R

A

W

A

T

April 2009

Riwayat Perjalanan Penyakit


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Riw kehamilan: ANC teratur di dokter, ibu sakit berat (-),

perdarahan (-), keputihan (-), minum jamu/obat(-)

Riw persalinan: spontan, aterm, BL 3300 gram, langsung

menangis (+), biru (-) Pasien merupakan anak ke-3 dari 4 bersaudara, kakak dan

adik pasien sehat.

Usia ibu saat hamil 43 tahun dan ayah 42 tahun.

Ayah pasien sering batuk tanpa demam dan disertai dahak.

Ayah pernah mendapat OAT 8 bulan yll setelah diperiksarontgen dan dahak, namun obat dihentikan sendiri.


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KU: CM, tampak lemah

TD 86/48, HR115 x/mnt, RR 24 x/mnt, Sat 100%

BB 27 kg, lingkarperut: 74 cm

Mata: konjungtiva -/-, sklera ikterik +/+

Leher: JVP 5+2 cmH2O, Kusmaull sign (+)

Thoraks: simetris statis dinamis

Jantung: Iktus kordis di ICS IV 1 cm medialmidklavikula, BJ I N, BJ II N, murmur (-), gallop(-), friction rub (-), pericardial knock (-)

Paru: vesikuler, rhonki -/-, wheezing -/-

Abd:buncit, tegang, shifting dullness (+), hepar-

lien sulit dinilai Ekstremitas: akral hangat, edema -/-


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Hb : 13,7

Ht : 41

Leukosit : 4080

Trombosit : 217000

LED : 6 CRP : 4

GDS : 77

Ureum : 31

Creatinin : 0.7

Na : 135

K : 2,8

Ca total : 2,2

Cl : 94

Protein : 5,0

Albumin : 2,4

Globulin : 2,6

Bilirubin total : 0,74

Bilirubin indirek : 0,39 Bilirubin direk : 0,34

SGOT : 52

SGPT : 11


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ST, QRS axis N, QRS rate115 x/mnt, PR interval 0,12, QRS durasi 0,08, low voltage pada limb & precordial leads,

ST changes (-), T bifasik-inverted pada lead II, III, aVF, V2-V6.


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Inspirasi kurang, asimetris, eksposure cukup

CTR 48 %, segmen aorta normal, segmen pulmonal normal, pinggang jantung(-), apexdownward, kongesti (+), infiltrat (-), efusi pleura (-)


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Situs solitus, IVC >>>, RA besar,

All PV to LA

Fungsi LVEF 54% (Simpson)

Diskinesia IVS jerking movementposterior, mid anterior, anterolateralmenempelpada perikardium takbergerak

IVS intak

TR mild TVG 10 mmHg

Doppler : E/A >1,

Mitral inflow E-A variation >25% saat inspirasi & ekspirasi

Kontraktilitas RV ,TAPSE 8 mm

Kesimpulan: pericarditis konstriktif,fungsi RV terganggu.


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Dx fungsional : right heart failure

Dx anatomis : perikarditis konstriktif

Dx etiologi : susp TBC perikardium

Masalah: Asites

Hipoalbumin

Hipokalemia Gangguan fungsi hati


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R/jangka panjang :perikardiektomi

R/jangka pendek :perbaikan KU,

eksplore ke arah TBC,

evaluasi ggn fungsihati lebih lanjut

Tatalaksana:

Rawat IW Anak pemasangan vena dalam

Koreksi albumin

Koreksi kalium


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demam, batuk berdahak,

muntah

Paru: rhonki basah kasar

lobus tengah - bawah parukanan

Leu 6230, LED 6, CRP 7

BC -844 aldactone 1 x

50mg

Lasix 3mg/jam

Ranitidin 2x1/2ampVometa 3x1tab

Cefotaxime 2x500mg

Cek kultur darah

12 Feb 2010

Tes Mantoux (-),BTA 3x(-),

PCR TB darah(-),HBsAg (-)

Urin rutin: kuning jernih,

epitel (+), pH 6, BJ 1010,

eri (-), leu (-), silinder (-

), kristal (-), bakteri (-),

bilirubin (-), keton(-),

glukosa (-), protein (-),

urobilinogen


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21

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25

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Berat badan

Berat badan

60

62

64

66

68

70

72

74

76

Lingkarperut

Lingkar perut


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Temuan intraoperatif :

Pericardium menebal, tegang, kekuningan.

RA dilatasi.

Perkijuan dan perlengketan di seluruh permukaan jantung

eksisi dan release restriksi perikard. Dibebaskan

perlengkatan yang hebat di aspek lateral, anterior, sertainferior. Sempat terjadi bleeding ketika membebaskan

permukaan lateral kanan jantung, bleeding dari RA

kanulasi dari arteri dan vena femoral, mesin jantung

dijalankan perdarahan dari RA diatasi.

Dilakukan pengambilan bahan untuk kultur dan

pemeriksaan PA


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Echo post op (1 Mar 2010):

Pericardial effusion (-),

IAS bulging ke LA,

LVEF 60% dengan jerking

movement septal,

TVG 15 mmHg,

RV fungsi TAPSE 1,2 cm,

E/A >2, restrictive

filling.


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Konsul pulmonologi:

INH 1 x 250mg

Rifampicin 1 x 350 mg

Pirazinamid 2 x 250 mg Etambuthol 1 x 400 mg

Prednison 3 x 4mg (1 bulan tappering off)

Ventolin expectorant 3 x cth 1


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An 10 tahun dengan right heart failure dengan sirosis

hepatis ec perikarditis konstriktif susp TB, telah dilakukan

tindakan perikardiektomi yang didapatkan hasil perikardium

menebal dengan perlengketan pus pada kavum

perikardium, diambil bahan untuk pemeriksaan kultur danhistologi PA. Pada pasien juga diberikan terapi koreksi

albumin dan kalium, aldactone 1x50mg, lasix drip 3 mg/jam,

dan terapi OAT.


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Fibrous sac surrounding heart-dense network of collagen

fibres

Serous membrane

two continuous layers

separated by a small amountof fluid lubricant (10-20mls )

Layers are :

Visceral is inner layer

(epicardium) Parietal is continuous with

diaphragm and outer walls

of great arteries


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Constrictive pericarditis is a condition in which

a thickened, scarred, and often calcified

pericardium limits diastolic filling of the

ventricles.

Idiopathic, acute pericarditis, cardiac trauma

and surgery, radiation therapy, renal

failure, and connective tissue diseases are mostcommon causes


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Guidelines on the Diagnosis and Management of Pericardial Disease.

European Heart Journal 2004


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Solomon SD. Essential Echocardiography


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Supportive care

Symptomatic patients require admission

and pericardiectomy


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Pericardiectomy forPericarditis in thePediatric Population

Ann Thorac Surg 2009;88:1546-1550

Conclusions: In properly selected pediatric patients, complete

pericardiectomy can be performed with good outcomes. Although theetiology of pericardial irritation is frequently elusive, resolution of

symptoms can be expected in most patients. Confronted with medically

refractory pericarditis, earlier consideration for pericardiectomy may be

warranted.


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A syndrome :

typical chest pain

a pathognomonic pericardial friction rub

specific ECG changes

Hurst's The Heart, 12th Edition


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Idiopathic Infection Viral (Coxsackievirus type B, Echovirus)

Tuberculosis

Pyogenic bacteriaNon infectious post myocardial infarction

Neoplastic

Radiation induce

Connective tissue diseases

Drugs

Lilly L.S, 2007, Pathophysiology of Heart Disease


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PERICARDITIS

Diffuse ST segment elevation with concavity upward in most leads

Diffuse P-R interval depression in most leads

T waves are upright (in contrast to ischemia)


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Pericardial friction rub :

superficial the sound of walking on dry snow / the

squeak of a leather saddle

between the lower left sternal edge and the

cardiac apex


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Idiopathic or viral pericarditis self

limiting disease (1 3 weeks)

Patients require bed rest

Colchicine initial attack

NSAID (aspirin 650 mg/3 hours, ibuprofen

300 to 800 mg/6 hours) relieving

symptoms of chest pain

Prednisone 60 to 80 mg/d (caution)

Antibiotics or antituberculosis


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Pericarditis is usually a benign disorder

Diagnosis relates to underlying cause

But any cause can lead to an effusion andtamponade which can lead to death

Pericarditis can also progress to pericardialconstriction and heart failure


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Accumulation of transudate, exudate, or

blood in the pericardial sac

Common complication of pericardial

disease

Should be sought in all patients with

acute pericarditis


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Asymptomatic cardiac tamponade symptom

Compression symptom :

Dysphagia (esophageal compression)

Dyspneu (lung compression) Hoarseness (N. recurrent laryngeal

compression)

Hiccups (N. phrenicus stimulation)

Soft heart sound

Reduce intensity of friction rub

Ewart sign dullness over posterior left lung


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ECG

Low voltage

Electrical alternans

CXR

May be normal silhouette

Volume >250 ml

enlarged cardiac silhouette

(flask shape)


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Confirms the clinical diagnosis

Can identify a small pericardial effusion (20 ml)

Quantify the volume

Determine ventricular filling

Help pericardocentesis


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If the cause is known underlying

disorder Tx

Pericardiocentesis

Relieve symptom

Establish etiology


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A hemodynamic condition

Equal elevation of atrial and pericardial

pressures

Pulsus paradoxus Arterial hypotension

The fluid accumulation severely impairs heart

filling

It is a medical emergency and must be treatedpromptly.

Risk of death depends upon speed of diagnosis,

treatment and underlying cause of the

tamponade


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Pericardialfluid pressure

Impaireddiastolic filling

Venous

pressureImpaired SV

Systemiccongestion

Pulmonarycongestion

CO

Hypotension


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IV Fluid Bolus-improves RV filling and

improves hemodynamics

Pericardiocentesis-therapeutic anddiagnostic

Admission to ICU or monitored setting

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