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6.pneumonia (New)
6.pneumonia (New)
6.pneumonia (New)
K-3B
DEFENSE
Physical, Humoral & Cellular
FAKTOR RISIKO CARA
• Alkohol • I NOKULASI langsung
•
• Merokok •
INHALASI
HEMATOGEN
• Peny. kronik: • KOLONISASI (terbanyak)
- Jantung & Paru
• Obstruksi bronkus - Red hepatization : 2 – 4 days
• Immunosupressi - Gray hepatization : 4 – 8 days
• Drug abuse - Resolution : > 8 – 10 days
Figure : Host defense in the respiratory tract
Figure : Factor that interfere with host defence of respiratory tract
kongesti
Red hepatization
(Udara di alveolus hilang diganti
dengan eksudat yang membeku
Gray
hepatization
Resolusi
STADIUM PATOLOGI ANATOMI KLINIK
• Cara penularan
1. Pneumococcus species
2. Haemophilus influenzae
2. Bakteri Penyebab
a. Pneumonia bakterial/ tipikal
b. Pneumonia atipikal penyebab: Mycoplasma, Legionella dan Chlamydia
c. Pneumonia virus
d. Pneumonia jamur infeksi sekunder pd pend immunocompromised
3. Berdasarkan predileksi infeksi
a. Pneumonia (Pneumonia lobaris)
- Sering pada pneumonia bakterial
- Jarang pada bayi dan orang tua aspirasi benda asing
Respiratory features
cough 90
sputum 70
dyspnea 70
chest pain 65
upper respiratory tract symptoms 33
hemoptysis 13
Nonrespiratory
vomiting 20
confusion 15
diarrhea 15
rash 5
abdominal pain 5
Typical clinical features of bacterial pneumonia
Clinical features Incidence (%)
Signs
80 – 90
fever
80 – 90
tachypnea
80 – 90
tachycardia
80 – 90
abnormal chest signs
20
hypotension
15
confusion
10
herpes labialis
DIAGNOSIS
2. Pemeriksaan Penunjang
a. Gambaran radiologis
Foto toraks (PA / lateral) penunjang utama diagnosis :
infiltrat – konsolidasi dg “air bronchogram”, interstisial serta gambaran kaviti.
Foto toraks petunjuk kearah diagnosis etiologi :
- Pneumonia lobaris Streptokokus pneumoniae
-Infiltrat bilateral/bronkopneumonia Pseudomonas aeruginosa
b. Pemeriksaan laboratorium
- Leukosit > 10.000 - 30.000 atau 4.500
- Hitung jenis leukosit pergeseran ke kiri dan peningkatan LED
- Diagnosis etiologi : dahak, kultur darah, dan serologi
- Kultur darah positif : 20 -25 % penderita tidak terobati
- Analisa gas darah hipoksemia dan hipokarbia
- Stadium lanjut asidosis respiratorik
• Lobar pneumonia
Refers to a homogeneous radiologic density that involves a distinct anatomic segment of the lung.
Infection originates in the alveoli. As it spreads, this form of infection respects the anatomic boundaries
of the lung and does not cross the fissures. Most commonly seen with S. pneumoniae, H. influenzae, and
Legionella.
• Bronchopneumonia
The bronchopneumonia form of pulmonary infection originates in the small airways and spreads to adjacent areas.
Infiltrates tend to be patchy, to involve multiple areas of the lung, and to extend along bronchi. Infiltrates are not
confined by the pulmonary fissures. Commonly observed with S. aureus, gram-negative bacilli, Mycoplasma, Chlamydia,
and respiratory viruses.
• Interstitial pneumonia
Infection causing inflammation of the lung interstitium result in a fine diffuse granular infiltrate. Influenza and
cytomegalovirus commonly present with this CXR pattern. In AIDS patients, Pneumocystic jirovecii infection results in
interstitial inflammation combined with increased alveolar fluid that can mimic cardiogenic pulmonary edema. Miliary
TB commonly presents with micronodular interstitial infiltrates.
• lung abscess
Anaerobic pulmonary infections often cause extensive tissue necrosis, resulting in loss of tissue and formation of
cavities filled with inflammatory exudate. S. aureus also cause tissue necrosis and can form cavitary lesions.
• noduler lesions
Histoplasmosis, coccidiomycosis, and cryptococcosis can present as nodular lung lesions (multiple or single) on CXR.
Hematogenous pneumonia resulting from right-sided endocarditis commonly presents with “cannonball” lesions that
can mimic metastatic carcinoma
PNEUMONIA KOMUNITI
(DIDAPAT DI MASYARAKAT)
ETIOLOGI
- Kepustakaan : Gram pos. & bakteri atipik
- Indonesia : Gram negatip (beberapa kota)
- Klebsiella pneumoniae 45,18 % - Pseudomonas aerugenosa 8, 56 %
- Streptococcus pneumoniae 14,04 % - Streptococcus hemolyticus 7,89 %
- Streptococcus viridans 9,21 % - Enterobacter 5, 26 %
-Staphylococcus aureus 9, 00% - Pseudomonas spp 0, 90 %
-
-
Essential of diagnosis
• Symptoms and signs of an acute lung infection:
fever or hypothermia, cough with or without
sputum, dyspnea, chest discomfort, sweats,or
rigors.
• Bronchial breath sounds or rales are freqent
auscultary findings.
• Parenchymal infiltrate on chest radiograph.
• Occur outside of the hospital or less than 48 hours
after admission in patient who is not hospitalized
or residing in a long-term care facility for more
than 14 days before the onset of symptoms.
DIAGNOSIS PASTI
Batuk-batuk bertambah
Perubahan karakteristik dahak/purulen
Suhu ≥ 38 °C (aksila)/ riwayat demam
Fisik : tanda konsolidasi, bronkial & ronki
Leukosit ≥ 10.000 atau < 4.500
Faktor modifikasi meningkatkan risiko infeksi
mikroorganisme patogen
spesifik
Tidak
Adakah R/ ko-morbid
- Neoplasma Pasien masuk dalam kelas
- Gagal jantung kongestif ……………Ya…………………. resiko II-IV sesuai langkah
- Peny. Serebrovaskuler ke 2/ sistim skor rumus
- Peny. Ginjal prediksi
- Peny. Hati
Tidak
I
Low II 70 total points
III 71-90
Moderate IV 91-130
High V 130
Kriteria indikasi rawat inap PK berdasarkan kesepakatan PDPI:
2. Skor PORT ≤ 70 tetap dirawat inap jika ada satu dari kriteria:
If three criteria are present, the patient is at an even greater risk of dying
and may need admission to the ICU. This rule is simple to use and is
based on clinical criteria that are generally available when the patient is
first evaluated
CURB-65
Clinical features Score
Age 65 years 1
Penatalaksanaan berdasarkan CURB-65
Score Group Treatment Options
Temperature ≤ 37,8 °C
Heart rate ≤ 100 beats/min
Respiratory rate ≤ 24 times/min
Systolic blood pressure ≥ 90 mmHg
Arterial saturation oxygen ≥ 90 % or ≥ 60 mmHg on room air
Ability to maintain intake
Normal mental status
Anamnesis, pemeriksaan fisis, foto toraks
Di tatalaksana sbg diagnosis Evaluasi untuk kriteria rawat jalan/ rawat inap
lain
Rawat jalan Rawat inap
Terapi empiris
Terapi
Membaik Memburuk
Terapi empiris dilanjutkan kausatif
TERAPI EMPIRIK PK
1. Sehat : Gram (Kota besar : ada Gram )
2. Komorbid : Gram ditambah Gram
3. Faktor modifikasi :
a. Pneumokokus resisten terhadap penisilin
b. Bakteri enterik Gram
c. Pseudomonas aerogenosa
• Pneumonia Nosokomial
- Angka kematian = 33 – 50 % jadi 70 % terkait penyakit dasar.
Penyebab kematian biasanya ok bakteriemia - Ps. Aerugenosa
- Acinobacter spp.
PROGNOSIS
• Umumnya : baik.
(Excelent with appropriate antimicrobial and supportive care)
penderita antibiotik
bakteri penyebab
KOMPLIKASI
The pathogen stimulates host defenses and alveolar airspaces become filled with eosinophilic edematous fluid
containing neutrophil polymorphs. The edema transport, organisms through the pores of Kohn into the alveoli.
in days 2 – 4; a red hepatization occurs; there is accumulation in alveolar spaces of polymorps,
lymphocytes, and macrophages. The alveolar exudate contains a fine network of fibrin and large numbers of
extravasated red cells. The lung is red, solid, and ariless. Red hepatization corresponds to an area of edema and
hemorrhage.
In days 4 – 8; a gray hepatization occur. Fibrinous pleurisy is present. Alveolar spaces are microscopically
distended and filled by a dense network of fibrin-containing neutrophil polymorphs. Gray hepatization
represents a zone of advanced consolidation with destruction of red and white blood cells. The lung is gray or
brown and solid.
Resolution occurs after 8 – 10 days in untreated cases. When bacteria has been eliminated, macrophages
enter and replace granulocytes. The exudate is liquefied by fibrinolytic enzymes and coughed uo or absorped.
ETIOLOGY
S. Pneumoniae is the causative organism in 55 – 75% of cases.
Causes and features of community acquired pneumia
Organism Features of pneumonia % cases
Streptococcus pneumoniae Gram-positive alpha-hemolytic; polysaccharide capsule determines virulence and 55 - 75
is detectable serologically; responsible for a high mortality (esp. in the setting
bacteremia) unless treated appropriately; vaccine available
Mycoplasma pneumoniae Epidemics every 3-4 years usually in young patients, 50% have cold agglutinins; 5 – 18
associated with many extrapulmonary manifestations; penicillin ineffective as no
bacterial cell wall
influenzo Epidemics common; affects patients with underlying lung disease; can be severe; 8
S. aureus, S. pneumoniae, H. influenzae occur secondarily; a vaccine is available
Legionella pneumophila Gram-negative; found in cooling towers and air-conditioning; causes very severe 2–5
pneumonia with high mortality and is frequently associated with extrapulmonary
features; antigen may help in diagnosis
Chlamydia pneumoniae Headache very common; usually serological diagnosis 2–5
Haemophilus influenzae Gram-negative rod; more commonly associated with exacerbations of COPD 4–5
Staphylococcus aureus gram-positive coccus; often follow flu; alcoholics and patient with mitral valve 1–5
disease are susceptible; often causes severe; often cavitating pneumonia;
commonly fatal
Klebsiella pneumoniae Gram-negative; seen in alcoholics; severe and often cavitates 1
Complications Management
Antibiotic treatment should be started immediately, without
The key of complications are:
waiting for microbiology results.
1. Respiratory failure • Empirical treatment with macrolide, doxycycline, or
2. Parapneumonic effusions fluoroquinolone (outpatients)
3. Empyema • Fluoroquinolone or an extended-spectrum cephalosporin
in combination with a macrolide (hospitalized patients)
4. Lung abscess
• Ceftriaxone, cefotaxime, ampicillin-sulbactam, or
5. Pulmonary fibrosis, after resolution piperacillin-tazobactam combined with a fluoroquinolone
or macrolide (ICU patients)
Laboratory tests • Pathogen-spesific therapy when the pathogen is identified
• Sputum-culture and Gram stain
In addition, pleuritic pain should be relieved with simple
• Blood-full blood count, blood culture (low analgesia and oxygen therapy administered if appropriate.
sensitivity, high specificity)
• Pleural fluid-culture and Gram stain Prognosis
• Chest radiography It is important to assess the severity of CAP as this impacts
on prognosis and therefore treatment planning. Prognosis
• Bronchoscopy with BAL if diagnosis uncertain
may range from full recovery to death.
• Assessment of oxygenation
The key adverse prognostic features are:
• Other specific tests – Mycoplasma, Legionella, • New mental confusion
and Chlamydia antibodies; pneumococcal antigen
• Urea > 7 mmol/L
testing by counter-immunoelectrophoresis (CIE)
of the sputum, urine, and serum. • Respiratory rate ≥ 30/min
• Systolic blood pressure < 90 mmHg / diastolic ≤ 60 mmHg
Patient with two or more of these features are at high risk
of mortality and should be managed aggressively.
INDIKASI VENTILATOR MEKANIK PADA PNEUMONIA
Etiology
Factors predisposing to hospital-acquired infections are:
1. Intubation
2. Suppressed cough leading to aspiration (e.g., postoperatively)
3. Reduced host defenses
4. Long stay in hospital, with associated exposure to pathogens
Pathogens
Gram-negative bacteria (Escheruchia, Klebsiella, and Pseudomonas spp.) are the cause of
hospital-acquired pneumonia in many cases, although Staphylococcus aureus (particularly drug-
resistant strains) is also common
Clinical features & laboratory tests similar to those described above under CAP.
Management
Good Gram-negative coverage is achieved with an aminoglycoside plus anti pseudomonal penicillin
or a third-generation cephalosporin. Most hospital-acquired pneumonia is serious, and these drugs
are frequently given intravenously.
Pneumonia in the immunocompromised patient
1. Pneumocystis carinii pneumonia (PCP)
Is a fungal infection that is largely confined to the lung. It is the most common
opportunistic infection in the immunocompromised.
Infection occurs by inhalation of the organism. The patient presents with an insidious
or abrupt onset of dry cough, fever, and dyspnea. Pleural effusions rare.
Pathology
There is an interstitial infiltrate of mononuclear cells and alveolar airspaces are filled with
foamy eosinophilic material.
Diagnosis
Bilateral pneumonia in an immunocompromised patient should raise suspicion of PCP.
Diagnosis in 90% of cases is by staining using Giemsa, methanamine-silver, Papanicocoau, or Gram-
Weigert stains with monoclonal antibodies.
Chest radiography shows diffuse bilateral alveolar and interstitial shadowing, beginning in
peripheral regions and spreading in a butterfly pattern.
Treatment
Trimethoprim-sulfamethoxazole is given, intravenously at first. Prophylaxis is recommended in
patients with low CD4 counts or where previous infection has occurred. Mortality of untreated
patients is 100%; in treated patients, mortality is 20 – 50%
Pneumonia in the immunocompromised patient
2. Cytomegalovirus (CMV)
Is a DNA virus in the herpes group. Of patient with AIDS, 90% are infected with CMV. CMV also occurs in
recipients of bone marrow and solid organ transplants. Only occasionally does CMV cause pneumonia.
Usual symptoms are a nonproductive cough, dyspnea, and fever. Disseminated infection occurs, causing
encephalitis, pneumonitis, retinitis, and diffuse involvement of the gastrointestinal tract.
Pathology
• Interstitial inflammatory infiltrate of mononuclear cells
• Scattered alveolar hyaline membranes
• Protein-rich fluid in alveoli
• Intranuclear inclusion bodies found in alveolar epithelial cells.
Diagnosis
CMV infection can be diagnosed by the identification of characteristic intranuclear owl’s eye inclusions in tissue
and by direct immunofluorescence.