Name : Ida Bagus Sila Wiweka

Place / Date of Birth : Denpasar, 01st Juni 1967

Academic Qualification :
• Medical Doctor in Faculty of Medicine, University of Udayana,
Denpasar, 1993
• Pulmonologist in Faculty of Medicine, University of Indonesia, Jakarta,
2003
Academic / Clinical Appointment:
Department of Pulmonology, The National Medical for Infectious Disease
Prof. Dr. Sulianti Suroso and Pertamina Center Hospital, Jakarta
Acute inhalation injury

Sila Wiweka

Department of Pulmonology
The National Medical Center for Infectious
Disease Prof.Dr. Sulianti Saroso /
Pertamina Center Hospital, Jakarta
Sources of Exposure
Introduction
• Definition :
• Damage to the airways and lung parenchyma
following ‘smoke’inhalation
• Insiden:
• 8000 per years
• Mortality:
• Smoke inhalation  60-80%
• Combined with burns  40-100%
• Bomb
• Increase morbidity and mortality
Mechanism of inhalation injury
• Inhaled exposure
forms:
• Fog, Mist, Fume, Dust,
Gas, Vapor, Smoke
• Determinants of
inhalation
pulmonary toxicity:
• upper, lower, terminal
airway
Mechanism of inhalation injury:
*Simple asphyxiants, chemical asphyxiants, pulmonary irritants
*Two phases:
- the initial cellular and oxidative phase
- the repair and proliferation phase
Clinical presentation

• Largely by the physical

characteristics of the gas
and duration of exposure
• Symptom:
– Upper airways
• irritation, hoarseness,
stridor, cough
– Tracheobronchial and
alveolar destruction
• dyspnea, chest
discomfort, hemoptysis
– Sudden death
Diagnostic
• History:
• Based on the mechanism of injury,
location of the thermic affection and
the patient’s symptoms
• Physical examination:
• Facial and upper cervical burns,
singed eyebrows and nasal vibrissae,
bronchial breath sounds, wheezing,
rales, cyanosis, and carbonaceous
sputum.
Bronchoscopy: “gold standard”
Early evaluation mucosal erythema, edema,
erosions, necrosis, and presence of
particulate matter
• Laboratory:
• Complete lab. standard: AGDA, Carboxy
hemoglobin level
• BAL :
– PMN cells and alveolar macrophages, cytology, level of
albumin, surfactant, and procollagen III
• Radiology:
• Chest X-ray
• CT scan (HRCT)
• Xenon 133, TC 99m DTPA
• Lung function test:
• Obstructive : diffuse bronchospasm
• Restrictive : decreased vital capacity and reduced
lung compliance
 Radiology

Mr., victims bomb Marriot hotel

CT scan Mr., victims bomb Marriot hotel
• Laboratory:
• Complete lab. standard: AGDA, Carboxy
hemoglobin level
• BAL :
– PMN cells and alveolar macrophages, cytology, level of
albumin, surfactant, and procollagen III
• Radiology:
• Chest X-ray
• CT scan (HRCT)
• Xenon 133, TC 99m DTPA
• Lung function test:
• Obstructive : diffuse bronchospasm
• Restrictive : decreased vital capacity and reduced
lung compliance
Management
• ABCs
• airways patency, adequate
oxygenation and ventilation,
aggressive pulmonary toilet and
stabilization of hemodynamic status
• Maintenance of optimal fluid status
• Antibiotics and corticosteroids
• Observed closely for several hours
• Antidote therapy
Complication
• Acute
– Acute lung injury
– ARDS
– Sepsis
• Chronic
• COPD, Bronchiectasis, bronchial stenosis,
fistula, pulmonary fibrosis, cor pulmonale
ARDS before therapy
ARDS post therapy
Complication
• Acute
– Acute lung injury
– ARDS
– Sepsis
• Chronic
• COPD
• Bronchiectasis
• Bronchial stenosis
• Fistula
• Pulmonary fibrosis
• Cor pulmonale
Bronchiectasis

fistula
Conclusion

• Symptom and sign are often

nonspecific
• Good management best
prognostic
• Difficult to manage because
occur infrequently and the
exact toxic agents
• Prevention is best