PNEUMONIA PADA ANAK :
DIAGNOSIS DAN TATA LAKSANA
DEFINISI
•
Pneumonia
adalah inflammasi
parenkim paru yg
disebabkan oleh
respon terhadap
invasi
mikroorganisme
FAKTOR RISIKO
FAKTOR SOSIAL EKONOMI /
LINGKUNGAN
- SOSIAL EKONOMI KURANG
- PENDIDIKAN IBU KURANG
- KESULITAN MENCAPAI FASKES
- POLUSI UDARA DALAM RUMAH
- MALNUTRISI
- TIDAK MENDAPAT ASI
- PAPARAN ASAP ROKOK
- PADA REMAJA : PENGGUNAAN
ALKOHOL, OBAT DAN ROKOK
FAKTOR PENYAKIT DASAR
- PENYAKIT JANTUNG BAWAAN
- PENYAKIT NEUROMUSKULAR (TERUTAMA
BILA DISERTAI KESADARAN MENURUN &
KETERLAMBATAN PERKEMBANGAN)
- DEFISIENSI UMUM PRIMER ATAU DIDAPAT
- GANGGUAN GIT (GER, TEF)
- ASMA
- BRONCHOPULMONARY DYSPLASIA
- DIABETES MELLITUS
- CYSTIC FIBROSIS
- ANEMIA SICKLE CELL
ETIOLOGI MIKROORGANISME
•
Dipengaruhi oleh faktor usia
Table 25.1
Most Common Agents Causing Community-Acquired Pneumonia
According to Age Group
Table 25.1
Most Common Agents Causing Community-Acquired Pneumonia
According to Age Group
Table 25.1
Most Common Agents Causing Community-Acquired Pneumonia
According to Age Group
Table 25.1
Most Common Agents Causing Community-Acquired Pneumonia
According to Age Group
Table 25.1
Most Common Agents Causing Community-Acquired Pneumonia
According to Age Group
KLASIFIKASI PNEUMONIA BERDASARKAN ASAL
MIKROORGANISME
•
PNEUMONIA KOMUNITAS
–
Pneumonia pada anak tanpa riwayat MRS dalam 2
minggu terakhir, atau
–
Pada anak yang MRS <48 jam
•
PNEUMONIA RUMAH SAKIT
–
Pneumonia pada anak dengan riwayat MRS dalam 2
minggu terakhir, atau
–
Pada anak yang MRS >48 jam dimana saat MRS tidak ada
gejala respirasi
PATOGENESIS
MIKROORGANISME
Aspirasi
Inhalasi isi
cavum oral atau
gaster
Inhalasi
melalui udara
Hematogenous
FAKTOR HOST
Sistem immunitas
paru menurun
FAKTOR LINGKUNGAN
Kepadatan
Usia
Sosial
ekonomi
KOLONISASI
MIKROORGANISME
INFEKSIUS DALAM SALURAN
NAPAS BAWAH
pathogenesis cont’d
KOLONISASI MIKROORGANISME PATOGEN DALAM SALURAN NAPAS
BAWAH
VIRUS
Akumulasi sel
mononuklear di
submukosa dan
perivaskular
Obstruksi jalan napas
partial/komplit
BAKTERI
1. Kongesti
2. Hepatisasi merah
3. Hepatisasi kelabu
4. Resolusi
1-2 hari
2-4 hari
4-7 hari
•
Kongesti kapiler diserta penggantian
udara dlm alveoli diganti oleh eksudat
selular (neutrofil, limfosit) & bakteri
•
Eritrosit >>, neutrofil, deskuamasi sel
epitel, dan fibrin dalam alveoli
•
Kapiler alveolar terisi darah (engorged)
è
konsistensi paru seperti hepar
•
Eritrosit mengalami disintegrasi/lisis &
dominasi eksudat fibrinopurulen
•
Makrofag mulai bermigrasi ke dalam
alveolus
•
Paru tampak abu-abu kekuningan
•
Resorpsi dan perbaikan struktur paru
•
Fagositosis sel asing oleh makrofag
alveolar
1-2 hari
3 minggu
PATOFISIOLOGI
path,cont’d
Efusi
pleura
udara ê
Aliran
Ventilasi
paru tdk
adekuat
MANIFESTASI KLINIS
GEJALA UMUM
GEJALA RESPIRASI
•
Irritable
•
Nafsu makan/minum menurun
•
Malaise
•
Keluhan saluran cerna
•
Bila berat : dehidrasi, kejang, kesadaran
menurun
manifestasi cont’d
•
Batuk DISERTAI demam dan distress napas
•
Distress napas :
–
Takipne è Batasan normal laju napas:
•
< 60 x/mnt : < 2 bulan
•
< 50 x/mnt : 2 sd 12 bulan
•
< 40 x/mnt : 1 sd 5 tahun
–
Retraksi dinding dada : subkostae, interkostae,
suprasternal
–
Napas cuping hidung
–
Head nodding (kepala mengangguk-angguk), grunting
•
Auskultasi : crackle/rhales basah halus dapat disertai
wheezing
GEJALA RESPIRASI
KLASIFIKASI DERAJAT PNEUMONIA WHO
BUKAN PNEUMONIA
PNEUMONIA : Batuk, demam, takipne, crackle
PNEUMONIA BERAT :
Gejala PNEUMONIA disertai salah satu dari
- Retraksi dinding dada - Napas cuping hidung
- Head nodding - Grunting - Sianosis
- Dehidrasi - Lethargi - Kejang
Rawat jalan
Rawat inap
PEMERIKSAAN PENUNJANG
•
Saturasi oksigen
•
Darah lengkap
•
Rontgen dada PA/AP :
–
Konsolidasi lobaris
–
Bercak infiltrat tersebar pada lapangan paru
(bronkopneumonia)
–
Interstitial
•
Biakan sputum dan/atau darah
RONTGEN DADA
•
Indikasi rontgen dada :
–
Gejala pneumonia berat
–
Gambaran klinis meragukan
–
Menyingkirkan kemungkinan penyebab distress napas
lain (benda asing, penyakit kardiopulmonal lain)
–
Pada setiap anak dengan demam berkepanjangan dan
leukositosis tanpa sebab yang jelas walaupun telah diberi
antibiotika empirik adekuat
•
Ro dada tidak rutin dilakukan pada anak dengan
pneumonia yang dapat dilakukan rawat jalan
RONTGEN DADA
Konsolidasi lobar
Retikular interstitial
Posisi : bila berumur >
4 thn dan sudah bisa
berdiri : PA
Pada anak lbh muda :
AP
Lateral dekubitus bila
ada kecurigaan efusi
pleura
Bronkopneumonia
Pneumatocele
Normal
Air
bron-
cho-gram
Bercak2
opasitas
multipel
yang
konfluen
Tampak air
broncho-
gram
Opasitas
tersebar
sampai ke
perifer,
bilateral,
dan tidak
simetris
BRONKOPNEUMONIA
BERCAK
BERBENTUK
SEPERTI BENANG
(LINEAR,
RETIKULAR)
YANG TERSEBAR
SAMPAI KE
PERIFER
AERASI MASIH
TERLIHAT
INTERSTITIAL
Massa
kistik
berdin-ding tipis
berisi
udara
berbagai
ukuran
PENATALAKSANAAN
•
Oksigenasi
•
Hidrasi
•
Antibiotika
•
Bila wheezing : inhalasi salbutamol
•
Terapi supportif: antipiretika, mukolitik
OKSIGENASI
•
Semua gejala pneumonia berat
•
Saturasi oksigen <90%
•
Konjungtiva pucat (anemia berat)
INDIKASI
CARA PEMBERIAN:
- Nasal kanul, masker, CPAP, ventilator
LAJU ALIRAN MAKSIMUM MELALUI NASAL
KANUL
- ½ L/mnt : 0-2 bln - 1 L/mnt : 2-12 bln
- 2 L /mnt : 1 – 5 tahun -max 4 L/mnt
ANTIBIOTIKA
–
Rawat jalan : Antibiotika selama 3-5 hari
•
Amoksisilin 80-100 mg/kgBB/hari dibagi 2 dosis
atau
•
Eritromisin 40-60 mg/kgBB/hari dibagi 3-4 dosis
–
Rawat inap :
•
Lini pertama: ampisilin 50 mg/kgBB @6 jam dan
gentamisin 7.5 mg/kgBB @ 24 jam selama 5 hari
•
Lini kedua: ceftriaxone 25-50 mg/kgBB @ 12 jam
selama 5 hari
•
Bila ada kecurigaan infeksi oleh S. aureus : Kloksasilin
50 mg/kgBB/6 jam
INDIKASI PULANG
•
Distres napas teratasi
•
Tidak ada hipoksia (saturasi oksigen >90%)
pada suhu ruang
•
Dapat makan dengan baik
•
Dapat minum obat oral atau telah
menyelesaikan terapi antibiotik parenteral
•
Orang tua memahami gejala pneumonia,
faktor risiko dan kapan harus kembali
KOMPLIKASI
•
Gagal napas
•
Effusi pleura
•
Empiema
•
Pneumotorak, pneumomediastinum
•
Abses paru
•
Sepsis
61 Journal of the Scientific Society, Vol 41 / Issue 1 / January-April 2014
Management
of spontaneous
pneumothorax in
a newborn: A rare
clinical entity
Sir,The sudden unexpected development of spontaneous pneumothorax in a full-term, apparently healthy infant is rarely seen, though it is a well-known complication of the respiratory distress syndrome and its therapy.[1] Spontaneous pneumothorax that
occurs during this period is mostly associated with assisted ventilation, birth trauma, meconium aspiration or prematurity.[2] We report the occurrence
of spontaneous pneumothorax in a 3.5 kg healthy neonate born by spontaneous vaginal delivery at 38 weeks gestation in the absence of any known predisposing factors. The prenatal course was unremarkable with no evidence of chorioamnionitis, oligohydramnios or any systemic infection. Amniotic fluid did not show any staining with meconium and Apgar scores were eight and nine at 1 and 5 min, respectively. After delivery, the baby was active and showed no sign of respiratory distress, but the baby suddenly became lethargic and pale without any preceding clinical event 6 h after birth.
On admission to neonatal emergency unit, the neonate was lethargic, pale and had a respiratory rate of 72 breath/min, heart rate 172 beats/min, CFT <3 s, but peripheral pulses were palpable. On examination, the anterior fontanelle was normal, SpO2 was 75% on room air and decreased breath sounds on the right side of the chest. The chest X-ray revealed pneumothorax on the right side with the shift to the left [Figure 1] while brain and abdominal sonograms were normal. The initial sepsis screen was negative, blood sugar and electrolytes were normal. The chest tube was inserted immediately on the right side and the baby had sudden improvement with SpO2 >92% and respiratory rate <60 breaths/min and patient started accepting breast feeds. The repeat chest X-ray revealed normal findings and the child was discharged after 5 days [Figure 2]. The occurrence of spontaneous pneumothorax in a healthy newborn is a rare entity.[3] Most neonatal
pneumothorax, pneumomediastinum and surgical emphysema in the neck occurs as a result of birth injury, shoulder dystonia, prematurity, pneumonia, meconium aspiration syndrome or assisted ventilation.[3-5]
However, during normal delivery, when the term baby passes through the vagina, there are potential chances of his thoracic cage being over-compressed during the delivery. Under such circumstances, the pressure gradient between the alveolar and perivascular space can increase abnormally for a transient period that may possibly lead to the rupture of the alveoli. However, this condition may manifest several hours after birth and respiratory distress may develop, which is considered to be the most important presenting sign, as has been noted in the present case. Though renal anomalies are commonly associated in neonates with
Figure 1: Chest X-ray revealing pneumothorax on the right side with the shift to the left
Figure 2: Chest X-ray revealing normal bilateral lung fields without any shift of the heart
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