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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
22
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24
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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Guidelines on the Diagnosis and Management of Pericardial Disease.
European Heart Journal 2004
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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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Guidelines on the Diagnosis and Management of Pericardial Disease.
European Heart Journal 2004
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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