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Childhood Pneumonia

mtsdarmawandept anak fk uii

Pendahuluan

• Pneumonia & infeksi sal napas bawah :penyebab kematian utama di dunia.

Pendahuluan

• + 150 juta anak < 5 tn dunia

• + 10-20 million hospitalizations.

• Dx : made radiographic

• WHO : klinis dg inspeksi &frekuensi napas

Pendahuluan

• typical causes & presentations of pneumonia ininfants and children are variable, depending

upon the age & underlying condition.

Pembagian Lobus Paru

3 lobus

2 lobus

Definition

alveoli alami

inflamasi & terisi

cairan

Definition

• Konsolidasi(pemadatan) & terisinya rongga alveoli

dg exudate, sel-selinflammasi & fibrin

Pathophysiology

• Paru anak rawan thdpneumonia : berhubdengan dunia luar,

setiap saat difusi• udara bertebaran

bakteri, virus →

terhisap

Pathophysiology

• symptoms : caused by microorganisms & immune system's response

• > 100 strains of microorganism cause

pneumonia, only a few of them areresponsible

Pathophysiology

• Tubuh : proteksi alamiah thd peny• Bila ini terganggu, balance is broken →

• Awal : ISPA, "flu", bronkitis.• Bila Tx tdk adekuat, sistem imun lemah

→ mjd pneumonia.

Pathophysiology

• Inflammasi rongga alveolar → ganggu difusi O2 – CO2.

• often complicating other

LRTI (bronchiolitis orlaryngo-tracheobronchitis),

Pathophysiology

• via hematogenous oraspiration

• chemical injury, follow

direct lung injury (eg,near drowning).

Pneumonia

• Dapat mengenaihanya sebagian paru,or

• seluruhnya

Pathophysiology

The possible outcomes

–Resolution (diserap)

–Organization (mjd lobair pneu)

–Menjadi Abscess –Empyema

–Bacteremia

–Death –Risk Factors

Etiologi

• bakteri, virus, fungi (terbanyak).• parasit & mikroorganisme lain.

• Tersering Respiratory Syncial Virus (RSV): 40%

• Bakteri, terutama Streptococcus pneumoniae & Haemophilus influenzae type b (Hib).

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)

Classification

Based on• Etiology (pathogen type)

• Host reaction (duration)

• Gross anatomic distribution(pathologic morphology of several areas)

Classification

1.Pathological classification:The big-leaf is divided into

– bronchopneumonia,

– lobar (lobair) pneumonia, – bronchial pneumonia,

– interstitial pneumonia and

– bronchiolitis

Classification

2. Jenis pathogens : – bakterial,

– tersering :

• Streptococcus pneumoniae,• Staphylococcus aureus,

• Haemophilus influenzae and so on.

Classification

2. Jenis pathogens : – Virus,

– tersering

• respiratory syncytialvirus,

• influenza virus,

• parainfluenza virus,

• adeno virus.

Classification

2. Jenis pathogens : – fungi,

– mycoplasma,

– chlamydia.

Classification

3. Perjalanan penyakit – acute ,

– persistent &

– chronicpersistent :

- s/d 1 ~ 3 months

- > 3 months, compared with chronicpneumonia.

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.

Viral vs bacterial pneumonia

Perbedaan bronkopneumonia & lobar pneumonia

Lobar pneumonia• acute inflammation of the entire lobe or lung.

Lobar pneumonia

• = focal or non segmental pneumonia.

Lobar pneumonia

• Ro :nonsegmental,homogenousconsolidation, or

multiple lobes.

Lobar pneumonia

• Larger bronchi oftenremain patent with air :air bronchogram.

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

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.

Lobar pneumonia

4 stages of inflammatoryresponse :

3. Gray hepatization

(2-3 hari)

– progressive disintegration of RBC& the persistence of a

fibrin exudate

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.

Bronchopneumonia

• consolidation fromsuppurative,exudate that fills thebronchi, bronchioles,

and adjacentalveolar spaces.

Bronchopneumonia

• neutrophilic exudate centered in bronchi andbronchioles, with centrifugal spread to theadjacent alveoli.

Bronchopneumonia

• lesions + 3-4 cm,dry, granular & grayish-red to yellow

• = multifocal orlobular pneumonia,

Bronchopneumonia

• Sejalan dg penybertambah berat, tjdkonsolidasi(pemadatan) pd

bronkiolus terminal& alveoli

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.

Bronchopneumonia

• pathogens known to cause : particularlydestructive :

– abscesses,

– pneumatoceles, &

– pulmonary gangrene

Bronchopneumonia

Mixed Lobar & Bronchopneumonia

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.

Ro :• edema &

inflammatory cellularinfiltrate into the

interstitial tissue of the lung.

• reticular or

reticulonodularpattern

• 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.

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)

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 .

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

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

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

Aspiration pneumonia

• specifically to the development of an infectious infiltrate

in patients who are at increased risk of oropharyngealaspiration.

• inhalation of oropharyngeal secretions& colonized organisms :

– Haemophilus influenzae

& – Streptococcus

pneumoniae,

• Bacterial pathogens of pneumonia and somenotable features

• Atypical organisms:

generally associatedwith a milder form of pneumonia

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.

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

Gram-positive bacteria

• S pneumoniae:S aureus: MRSA

• Enterococcus (Enterococcus faecalis,Enterococcus faecium):

- Actinomyces israelii:

Gram-negative bacteria

• Pseudomonas aeruginosa:• Klebsiella pneumoniae:

• Haemophilus influenzae:

• Escherichia coli:

• Moraxella catarrhalis

• Acinetobacter baumannii:

• Francisella tularensis: Yersinia pestis:

• 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.

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).

Pleuritis

• may result if underlying inflammationextends to the pleural surface of thelung

Frequency

• In the USA, acute lower respiratory tractinfections (ALRTI = ISPA) cause more diseaseand death than any other infection

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

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.

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

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

Cli i l Hi

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

Symptoms

• alveoli filled with fluid,keeping oxygen fromreaching thebloodstream.

Cli i l Hi t

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

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

Dif i O2 C 2 di l l

A i ti i k

Aspiration risks

• Alcoholism• Altered mental status

• Anatomic abnormalities, congenital oracquired

• Dysphagia

• GERD

• Seizure disorder

Ph i l & R i ti

Physical & Ro examination

• takipneu,hipoksemia,distres respirasi

• Ronki basah halus

(krepitasi) : khas• Ronki basah kasah

• Ro : a ground-glassappearance & air

bronchograms

Air bronchogram

Physical examination

Sangat tergantung pd• tipe mikroorganisme,

• Derajat penyakit

• Adanya komplikasi

• Hipertermia (demam, >38°C) or hipotermia(<35°C)

• Takipnea (> 30 x)

• Penggunaan otot bantu pernapasan• Takikardia (>120 bpm) or bradikardia (<60

• Central cyanosis

• Altered mental status

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

• 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 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

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

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

• > bacterial than viral• The most important : Respiratory &

circulatory failure

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

1. Imunitas rendah :- penderita HIV/AIDS (ODHA)- peny kronik : jantung, DM

- kemoterapi & immunosupressant lama.

Cara penularan

2. Perokok dan peminumalkohol.

• iritasi bronchial :• sekresi mukus bila

mengandung bakteri :pneumonia

• alkohol berdampak buruk terhadap lekosit

melawan suatu infeksi.

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

5. Pasien yang lama

berbaring. Pascaoperasi besar → lama

immobilisasiberbaring : statis → dahak berkumpul di

rongga paru : mediaberkembangnya bakteri

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

• Anak dg GER berat mudah mjd pneumoniakarena aspirasi berulang.

• Inhalasi zat kima tertentu or smoke : → pulmonary inflammation.

Treatment

Typically,• AB oral, istirahat, cairan

• Simptomatik

• Pd anak : TIDAK ADA TEMPAT BAGIMUKOLITIK, EKSPEKTORAN. Berikanbronkodilator !!!

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

Terima Kasih

• mtsdarmawan@yahoo.co.id Fb Mt d

penykt ank

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