Post on 04-Apr-2018
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Childhood Pneumonia
mtsdarmawandept anak fk uii
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Pendahuluan
• Pneumonia & infeksi sal napas bawah :penyebab kematian utama di dunia.
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Pendahuluan
• + 150 juta anak < 5 tn dunia
• + 10-20 million hospitalizations.
• Dx : made radiographic
• WHO : klinis dg inspeksi &frekuensi napas
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Pendahuluan
• typical causes & presentations of pneumonia ininfants and children are variable, depending
upon the age & underlying condition.
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Pembagian Lobus Paru
Kanan
3 lobus
Kiri
2 lobus
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Definition
alveoli alami
inflamasi & terisi
cairan
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Definition
• Konsolidasi(pemadatan) & terisinya rongga alveoli
dg exudate, sel-selinflammasi & fibrin
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Pathophysiology
• Paru anak rawan thdpneumonia : berhubdengan dunia luar,
setiap saat difusi• udara bertebaran
bakteri, virus →
terhisap
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Pathophysiology
• symptoms : caused by microorganisms & immune system's response
• > 100 strains of microorganism cause
pneumonia, only a few of them areresponsible
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Pathophysiology
• Tubuh : proteksi alamiah thd peny• Bila ini terganggu, balance is broken →
sick.
• Awal : ISPA, "flu", bronkitis.• Bila Tx tdk adekuat, sistem imun lemah
→ mjd pneumonia.
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Pathophysiology
• Inflammasi rongga alveolar → ganggu difusi O2 – CO2.
• often complicating other
LRTI (bronchiolitis orlaryngo-tracheobronchitis),
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Pathophysiology
• via hematogenous oraspiration
• chemical injury, follow
direct lung injury (eg,near drowning).
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Pneumonia
• Dapat mengenaihanya sebagian paru,or
• seluruhnya
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Pathophysiology
The possible outcomes
–Resolution (diserap)
–Organization (mjd lobair pneu)
–Menjadi Abscess –Empyema
–Bacteremia
–Death –Risk Factors
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Etiologi
• bakteri, virus, fungi (terbanyak).• parasit & mikroorganisme lain.
• Tersering Respiratory Syncial Virus (RSV): 40%
• Bakteri, terutama Streptococcus pneumoniae & Haemophilus influenzae type b (Hib).
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Severity of pneumonia
• Tergantung mikroorganisme penyebab• Viral : tidak begitu serius,
- tapi bisa mengancam jiwa pada balita & manula &
orang dg imunitas rendah
• Bahkan severe acute respiratory syndrome(SARS), mortalitas hanya (+ 3- 4% of all cases)
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Classification
Based on• Etiology (pathogen type)
• Host reaction (duration)
• Gross anatomic distribution(pathologic morphology of several areas)
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Classification
1.Pathological classification:The big-leaf is divided into
– bronchopneumonia,
– lobar (lobair) pneumonia, – bronchial pneumonia,
– interstitial pneumonia and
– bronchiolitis
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Classification
2. Jenis pathogens : – bakterial,
– tersering :
• Streptococcus pneumoniae,• Staphylococcus aureus,
• Haemophilus influenzae and so on.
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Classification
2. Jenis pathogens : – Virus,
– tersering
• respiratory syncytialvirus,
• influenza virus,
• parainfluenza virus,
• adeno virus.
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Classification
2. Jenis pathogens : – fungi,
– mycoplasma,
– chlamydia.
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Classification
3. Perjalanan penyakit – acute ,
– persistent &
– chronicpersistent :
- s/d 1 ~ 3 months
- > 3 months, compared with chronicpneumonia.
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Perbedaan bronkopneumonia & lobar pneumonia
Bronkopneumonia
• patchy foci of consolidation (pus in
many alveoli andadjacent air passages)scattered in one or
more lobes of one orboth lungs.
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Viral vs bacterial pneumonia
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Perbedaan bronkopneumonia & lobar pneumonia
Lobar pneumonia• acute inflammation of the entire lobe or lung.
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Lobar pneumonia
• = focal or non segmental pneumonia.
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Lobar pneumonia
• Ro :nonsegmental,homogenousconsolidation, or
multiple lobes.
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Lobar pneumonia
• Larger bronchi oftenremain patent with air :air bronchogram.
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Lobar pneumonia
4 stages of inflammatory response : 1. Congestion
– intraalveolar fluid & numerous bacteria;
– the lung is heavy, boggy & red. – within 24 hours of infection,
– Microscopic : vascular congestion & alveolar
edema – Many bacteria & few neutrophils
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Lobar pneumonia
4 stages of inflammatory response : 2. Red hepatization (2-3 hari)
- massive exudation,
- RBC, leukosit, and fibrin filling the alveolarspaces; the affected area appears red, firm,and airless, with a liverlike consistency.
- its similarity to the consistency of liver,
- many erythrocytes, neutrophils, desquamatedepithelial cells, and fibrin within the alveoli.
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Lobar pneumonia
4 stages of inflammatoryresponse :
3. Gray hepatization
(2-3 hari)
– progressive disintegration of RBC& the persistence of a
fibrin exudate
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Lobar pneumonia
4 stages of inflammatory response : 4. Resolution (final stage)- consolidation exudate within the alveolarspaces undergoes progressive enzymaticdigestion to produce debris that is laterresorbed, ingested by macrophages, coughedup, or becomes organized by fibroblastsgrowing into it.- resorpsi & restorasi arsitektur paru.
- Fibrinous inflammation may extend into thepleural space, causing a rub heard byauscultation, and it may lead to resolution or toorganization and pleural adhesions.
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Bronchopneumonia
• consolidation fromsuppurative,exudate that fills thebronchi, bronchioles,
and adjacentalveolar spaces.
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Bronchopneumonia
• neutrophilic exudate centered in bronchi andbronchioles, with centrifugal spread to theadjacent alveoli.
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Bronchopneumonia
• lesions + 3-4 cm,dry, granular & grayish-red to yellow
• = multifocal orlobular pneumonia,
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Bronchopneumonia
• Sejalan dg penybertambah berat, tjdkonsolidasi(pemadatan) pd
bronkiolus terminal& alveoli
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Bronchopneumonia
→ jd sentrilobular nodular opak or air-space nodules
→ dpt berlanjut kmd & mjd
pola lobular or lobar.• Onset + 7 hari sejak batuk,TIDAK MENDADAK sesak.
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Bronchopneumonia
• pathogens known to cause : particularlydestructive :
– abscesses,
– pneumatoceles, &
– pulmonary gangrene
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Bronchopneumonia
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Mixed Lobar & Bronchopneumonia
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Interstitial pneumonia
• Skrg diklasifikasi sbg focal or diffuse.• pathologic : 1 dr 2 bentuk :
1. insidious infectious course results in
lymphatic infiltration of alveolar septawithout parenchymal abnormality or
2. acute or rapidly progressive diseasethat results in diffuse alveolar damage affecting the interstitial and air spaces.
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Interstitial pneumonia
Ro :• edema &
inflammatory cellularinfiltrate into the
interstitial tissue of the lung.
• reticular or
reticulonodularpattern
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Interstitial pneumonia
• interstitial picture.
• Alveolar septa :
widened & edematous
and usually have
a mononuclear inflammatoryinfiltrate of lymphocytes,histiocytes & plasma cells;neutrophils may also
be present in acute cases.
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Interstitial pneumonia
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Community-acquired pneumonia (CAP)
• in outpatient setting or within 48 hours of admission to a hospital,
• should not meet the criteria for health care –associated pneumonia (HCAP)
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Community-acquired pneumonia (CAP)
• Tjd pd orang yg tidak dirawat di RS.• most common type of pneumonia.
• S. pneumoniae : penyebab tersering
• Gram (-) > sering• is the 4th most common cause of death
in the UK and the sixth in the USA .
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Hospital-acquired pneumonia
• Tjd setidaknya 48 jam sejak masuk RS (MRS)Risk factors :
• Tx AB dlm 90 hari krn nosokomial• Setidaknya setelah perawatan 5 hari di RS
• Frekuensi tinggi penggunaan AB• Memikili peny immunosuppresif or terapi
imunosupresif
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Hospital-acquired pneumonia
• = nosocomial pneumonia,• Didapatkan selama atau setelah perawatan di RS• The causes, microbiology, treatment and prognosis
are different from those of community-acquiredpneumonia.
• + 5% dari kasus dirawat di RS krn penyebab lain
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Nosocomial pneumonia
• may include resistant bacteria such as MRSA,Pseudomonas, Enterobacter, and Serratia.
• Risiko > CAP
• Ventilator-associated pneumonia (VAP) is a
subset of hospital-acquired pneumonia.• VAP occurs after at least 48 hours of ET &
ventilation
• Salah satunya dicirikan dg penggunaan alat2
canggih di RS, penggunaan alat invasif
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Aspiration pneumonia
• specifically to the development of an infectious infiltrate
in patients who are at increased risk of oropharyngealaspiration.
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Aspiration pneumonia
• inhalation of oropharyngeal secretions& colonized organisms :
– Haemophilus influenzae
& – Streptococcus
pneumoniae,
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Aspiration pneumonia
• Bacterial pathogens of pneumonia and somenotable features
• Atypical organisms:
generally associatedwith a milder form of pneumonia
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Mycoplasma pneumonia
• the smallest known free-living organisms inexistence;
• they lack cell walls (and
therefore are notapparent after Gramstain) but do haveprotective 3-layered cell
membranes.
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Chlamydophila species
(Chlamydophila psittaci, Chlamydophilapneumoniae):
• Psittacosis, also known as parrot disease orparrot fever, is caused by C psittaci and is
associated with the handling of various typesof birds.
• Legionella species
• Coxiella burnetii• Typical organisms
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Gram-positive bacteria
• S pneumoniae:S aureus: MRSA
• Enterococcus (Enterococcus faecalis,Enterococcus faecium):
- Actinomyces israelii:
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Gram-negative bacteria
• Pseudomonas aeruginosa:• Klebsiella pneumoniae:
• Haemophilus influenzae:
• Escherichia coli:
• Moraxella catarrhalis
• Acinetobacter baumannii:
• Francisella tularensis: Yersinia pestis:
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• Anaerobic organisms associated withaspiration pneumonia:
• due to anaerobes typically results fromaspiration of oropharyngeal contents, as
previously mentioned.• polymicrobial & may consist of : Klebsiella,Peptostreptococcus, Bacteroides,Fusobacterium, and Prevotella.
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Pathology of pneumonia
• migration of neutrophils out of capillaries andinto the air spaces, forming a marginated pool of neutrophils that is ready to respond whenneeded.
• They phagocytize microbes & kill them with
reactive oxygen species, antimicrobial proteins,and degradative enzymes; they also extrude achromatin meshwork containing antimicrobialproteins that trap and kill extracellular bacteria,known as neutrophil extracellular traps (NETs).
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Pleuritis
• may result if underlying inflammationextends to the pleural surface of thelung
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Frequency
• In the USA, acute lower respiratory tractinfections (ALRTI = ISPA) cause more diseaseand death than any other infection
h l f
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The most common etiologies of community-acquired pneumonia (CAP)
Listed in descendingorder of frequencyare as follows :
Outpatient
• S pneumoniae
• M pneumoniae
• H influenzae
• C pneumoniae
Inpatient, non-ICU• S pneumoniae
• M pneumoniae
• C pneumoniae
• H influenzae
• Legionella species
• Respiratory viruses
li / bidi
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Mortality/Morbidity
WHO :• LTRI 2nd leading cause of death in children < 5
years (+ 2.1 million [19.6%]).
• Most children are treated as outpatients and
fully recover.• young infants & immunocompromisedindividuals, mortality is higher.
• In studies of adults with pneumonia, a higher
mortality rate is associated with abnormal vitalsigns, immunodeficiency, and certainpathogens.
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Mortality/Morbidity
• In 2006, lama dirawat di RS 5-19 hari • In 2005 : 61.189 people died
• age-adjusted death rate of 19.7 deaths per100,000 people.
• Pneumonia and influenza together were the 8leading cause of death in the United
li / bidi
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Mortality/Morbidity
• In 2005, black men 14% > likely to die (26.6deaths per 100,000 people vs 23 deaths per100,000 people),
• black and white women were almost equallylikely to die from pneumonia (17.4 deaths per
100,000 people and 18.2 deaths per 100,000people).
• deaths has been higher among females since1980s.
Clinical History
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Clinical History
Cli i l Hi
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Clinical History
Symptoms • cough, productive of sputum :
the most consistent symptom.
• Sputum suggests the pathogen:
– Rust-colored (warna karat)sputum – S. pneumoniae
– Currant-jelly ( jelly kismis) sputum- Klebsiella species
S t
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Symptoms
• alveoli filled with fluid,keeping oxygen fromreaching thebloodstream.
Cli i l Hi t
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Clinical History
Symptoms , spesifik : • Foul-smelling (busuk) or bad-tasting sputum :
infeksi anaerob
• Dada terasa sakit
• Sesak napas,
• hemoptisis,
• ↓ kemampuan fisik &
• abdominal pain from pleuritis
Cli i l Hi t
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Clinical History
Symptoms , nonspecific symptoms :• demam or menggigil
• Rigor (“kaku”), & malaise
• Nyeri otot, pening, mual muntah, diare & altered sensorium.
• Potential exposures - Travel, pets, occupation,environment
Difusi O2 ~ Co2 di alveolus
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Difusi O2 ~ Co2 di alveolus
Dif i O2 C 2 di l l
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Difusi O2 ~ Co2 di alveolus
A i ti i k
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Aspiration risks
• Alcoholism• Altered mental status
• Anatomic abnormalities, congenital oracquired
• Dysphagia
• GERD
• Seizure disorder
Ph i l & R i ti
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Physical & Ro examination
• takipneu,hipoksemia,distres respirasi
• Ronki basah halus
(krepitasi) : khas• Ronki basah kasah
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• Ro : a ground-glassappearance & air
bronchograms
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Air bronchogram
Physical examination
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Physical examination
Sangat tergantung pd• tipe mikroorganisme,
• Derajat penyakit
• Adanya komplikasi
Physical examination
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Physical examination
Signs
• Hipertermia (demam, >38°C) or hipotermia(<35°C)
• Takipnea (> 30 x)
• Penggunaan otot bantu pernapasan• Takikardia (>120 bpm) or bradikardia (<60
bpm)
• Central cyanosis
• Altered mental status
Physical examination
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Physical examination
Physical findings • Suara paru tambahan: ronki basah, wheezing
• Khas : ronki basah halus : krepitasi : kresek-kresek.
• Intensitas suara paru menurun
• Egophony : “wolu-wolu” → “wele-wele”
• Suara spt “berbisik -bisik” (whispery
pectoriloquy)• Perkusi pekak
• Tracheal deviation
Egophony
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Egophony
Physical examination
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Physical examination
• Auscultation : the most important portion of the examination of the child with respiratorysymptoms.
• The examination often is very difficult in
infants and young children for severalreasons.
• Additionally, not all children with pneumoniahave crackles/ ronki.
Physical examination
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Physical examination
Physical findings• Lymphadenopathy
• Bradycardia -Legionella
• Periodontal disease - Anaerobic and/orpolymicrobial infection
• Bullous myringitis -Mycoplasma pneumoniae
• Physical evidence of risk for aspiration (eg,
decreased gag reflex)• Cutaneous nodules (especially in the setting of
CNS findings) -Nocardia
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Tabel: Pedoman Perhitungan Frekuensi Napas (WHO)
Umur Anak Napas Normal Takipnea (Napas cepat)
0 – 2 Bulan 30-50 per menit > 60 x per menit
2-12 Bulan 25-40 per menit > 50 x per menit1- 5 Tahun 20-30 per menit > 40 x per menit
Diagnosis
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Diagnosis
Doctor rely on :
• symptoms & physical examination.
• chest X-ray, blood tests & sputum cultureshelpful
• chest X-ray : used in hospitals
community setting : based on symptoms & physical examination alone.
• Occasionally a chest CT scan or other testsmay be needed to distinguish pneumonia fromother illnesses.
Complications
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Complications
• > bacterial than viral• The most important : Respiratory &
circulatory failure
Complications
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Complications
• can also cause respiratory failure bytriggering acute respiratory distress syndrome( ARDS).
• The lungs quickly fill with fluid and becomevery stiff .
• → ventilator mekanik.
Cara penularan
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Cara penularan
1. Imunitas rendah :- penderita HIV/AIDS (ODHA)- peny kronik : jantung, DM
- kemoterapi & immunosupressant lama.
Cara penularan
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Cara penularan
2. Perokok dan peminumalkohol.
• iritasi bronchial :• sekresi mukus bila
mengandung bakteri :pneumonia
• alkohol berdampak buruk terhadap lekosit
melawan suatu infeksi.
Cara penularan
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Cara penularan
3.Pasien di ICU
ventilator & ET :Saat batuk keluarkan isi lambung kekerongkongan, bakteri pindah ke ventilator,potensial pneumonia.
4. Inhalasi udara tercemar polusi zat kemikal
Cara penularan
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Cara penularan
5. Pasien yang lama
berbaring. Pascaoperasi besar → lama
immobilisasiberbaring : statis → dahak berkumpul di
rongga paru : mediaberkembangnya bakteri
Gastroesophageal Reflux Disease (GERD)
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Gastroesophageal Reflux Disease (GERD)
• Asam lambungreflux ke esophagus• Hub (+) antara GERD & bbrp masalah occured
in the sinuses, ears, nasal passages & airways• Risiko tinggi terkena chronic bronchitis, chronic
sinusitis, emphysema, pulmonary fibrosis (lungscarring), and recurrent pneumonia.• contribute by triggering inflammation in these
upper passages
Gastroesophageal Reflux Disease (GERD)
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Gastroesophageal Reflux Disease (GERD)
• Anak dg GER berat mudah mjd pneumoniakarena aspirasi berulang.
• Inhalasi zat kima tertentu or smoke : → pulmonary inflammation.
Treatment
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Treatment
Typically,• AB oral, istirahat, cairan
• Simptomatik
• Pd anak : TIDAK ADA TEMPAT BAGIMUKOLITIK, EKSPEKTORAN. Berikanbronkodilator !!!
Treatment
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Treatment
AB broad spectrum :
• Gol penisilin, cefalosporin gol III & IV.
• Oral – Amoksisilin, kotrimokzasole, eritromisin,
cefadroksil,
• Inj. – Combined AB : ampi : kloramp
– Ampi + cefotaxim – ceftriaxone
T i K ih
7/29/2019 penykt ank
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Terima Kasih
• mtsdarmawan@yahoo.co.id Fb Mt d