An Updated Review of Inhalation Injury

dr. Indi Esha, M.Si, Sp.P (K)

DEPARTMENT PULMONOLOGY AND RESPIRATORY

FACULTY OF MEDICINE, UNIVERSITY OF RIAU
INTRODUCTION

 EXPOSURE of TOXIC SUBSTANCE:

- Industry
- Home
- Public area

 WORKPLACE ACCIDENT

 DISASTERS

 FIRE ACCIDENT

 WAR
TYPE of TOXIC SUBSTANCE
 ABNORMALITY TYPE CAUSED by
TOXIC INHALATION DEPEND on SEVERAL FACTORS

 CHARATERISTIC of SUBSTANCE

 AMOUNT and CONCENTRATION

SUBSTANCE TOXIC INHALANT
 DURATION of EXPOSURE

IRITANT
 HOST FACTORS

ASPHYXIANT

SYSTEMIC TOXIN
 PATHOGENESIS

PATHOGENESIS of IRRITANT INJURY

 IRRITANT SUBSTANCE HAD EFFECT on VARIOUS AIRWAY ANATOMICAL

 HIGH HIGROSCOPIC (SOLUBLE WATER) SUBSTANCE  INJURY of UPPER AIRWAY

 LOW SOLUBLE WATER SUBSTANCE TOXIC in TERMINAL BRONCHIOLUS and ALVEOLI

 IRRITANT

ACID DEPOSITION BASE DEPOSITION ROS

CHLORIN OZONE
HIDROGEN CHLORIDA AMONIA
NITROGEN OXIDE NITROGEN OXIDE
FOSGEN NATRIUM DIOXIDE
SULFUR DIOXIDE CHLORINE

COAGULATION SOFTENING and MELT PEROXIDE LIPID

DESTRUCTION EFFECT
 IRRITANT SUBSTANCE

CYLIA ACTIVITY IMPAIRMENT MUCOCILLIARY CLEARANCE IMPAIRMENT

MUCUS HYPERSECRETION
EPITEL and PARENCYHME (BRONCHOREA)
INFECTION
DESTRUCTION & NECROSIS

BRONCHIAL EDEMA
PARTIAL or TOTAL OBSTRUCTION

ATELECTASIS

AIR TRAPPING and V/Q MISSMATCH

 PATHOGENESIS

PATHOGENESIS of ASPHYXIANT
 PATHOGENESIS of ASPHYXIANT

SIMPLE ASPHYXIANT
Substance simple asphyxiant:
 Helium, argon, xenon
 Aliphatic hydrocarbon Likemetana,
 Replace of oxygen in the air etana, propana and butana
 Decrease of FiO2  Carbondioxside (CO2)
 Oxygen did not adequate to haemoglobin saturation  Nitrogen
 Usually high concentration in the air and in the
closed room
 PATHOGENESIS of ASPHYXIANT

SYSTEMIC ASPHYXIANT
Substance systemic asphyxiant:
 Carbonmonoxide (CO)  CO Hb
 Cyanide  Oxidative enyzme
CAUSED PERIPHERAL HIPOXIA with  Hydrogen sulfide  Oxidative enyzme
IMPAIRMENT of DELIVERY

and UTILITY of OXYGEN

 PATHOGENESIS

PATHOGENESIS of SYSTEMIC TOXIN

Substance:
 Hydrocarbon
 Organophosphat
 LUNG as “PORT de ENTRE”  Metal fumes

 TARGETED  OTHER ORGAN

 SMOKE INHALATION

Smoke inhalation injury refers to injury due to inhalation or

exposure to hot gaseous products of combustion

Combination:
• Irritant particle
• Irritant gases
• Asphyxian gases
• Thermal injury
 SMOKE INHALATION

GAS PARTICLE THERMAL

FREE RADICALS
ASPHYXIANT IRRITANT THERMAL INJURY
ROS

ASPHYXIA DESTRUCTION EFFECT

 EXAMPLE SUBSTACDE RELEASE from FIRE ACCIDENT

Materials Combustionproducts
Wool Carbonmonoxide, hydrogenchloride, phosgene, cyanide
Nylon Ammonia, cyanide
Wood, cotton, paper Carbonmonoxide, formaldehyde
Plastics Cynaide, hydrogenchloride, aldehydes, ammonias, oxides of nitrogen, phosgene, chlorine
Polyvinyl chloride Carbonmonoxide, hydrogenchloride, phosgene, chlorine
Rubber Hidrogen sulfide, Sulfur doxide

ANAMNESE  EXPOSURE
SHORT EXPOSURE
• Quick onset (second until minute)
• Sign :
- Mouth pain, nose and pharinx
- Mucous edema, cough and stridor
- Conjunctive injection, skin iritation
- Airway obstruction
DIAGNOSE
HISTORY
LONGTERM EXPOSURE
• There is no sign of quick onset
• Inhale until lower respiratory tract
• Tracheobronchitis,bronchiolitis,
bronchospasm
• Acute lunginjury, noncardiogenic
pulmonary edema
• Dispnea, chest thigtness,cough,
wheezing, rhonchi
• Chest x ray : alveolar infiltrate
• Arterial hipoxemia
CLINICAL SYMPTOMS
SUGESTED INHALATION INJURY
Indications and symptoms of inhalation injury:
• Facial and neck burns
• Burned lips and vibrissae
• Soot-containing airway secretions
• Pathological respiration patterns (coughing,
stridor and hoarseness)
• Dyspnea
• Cyanosis
• Neurological symptoms (current or past
unconsciousness, dizziness, nausea and
vomiting)
 DIAGNOSE

ANAMNESE  EXPOSURE HISTORY CLINICAL SYMPTOMS

• Depend on type of substance

inhalant (iritant, asphyxia or
IRITANT sistemic toxin)
• As a “sign “ to suggest type of
substance inhalant
ASPHYXIANT

SYSTEMIC TOXIN
 CLINICAL SYMPTOMS

IRRITANT

 Burning sensation in nose, throat, trachea and main bronchus

 Dry cough, hemoptisis, mocous secretion, dispneu, wheezing, apnea
 Nasal obstruction, epistaxis, pharyngitis and laryngitis
 Lung edema
 Respiratory failure  some cases reported in 5 hrs – 7 hrs after exposure
 CLINICAL SYMPTOMS

ASPHYXIANT

Decreased oxygen in blood (hypoxemia)

 Cephalgia, hyperventilation, nausea, tachycardia, convulsion

 Decreased of concious, cardiac arrest, apnea and death

COHb levels in blood and the corresponding clinical manifestation :
 CLINICAL SYMPTOMS

SYSTEMIC TOXIN

 Depend on type of substance inhalant  mostly case was

organophosphat inhalation
 Usually effect on central and peripheral nervous system  decrease of
conciousness and weakness
 CNS narcosis, anesthetic stats, diffuse gastrointestinal symptoms,
peripheral neuropathy with weakness, coma, sudden death, chemical
pneumonitis, CNS abnormalities, gastrointestinal irritation,
cardiomyopathy, renal toxicity
 DIAGNOSTIC APPROACH

THORACIC X-RAY

BLOOD GASES ANALYSIS

LARYNGOSCOPY

BRONCHOSCOPY, BAL
In case of chemical asphyxiant, there are
certain kinds of laboratory test (CO-
LABORATORY oxymeter, pulse oxymetry, CO-Hb, MetHb
level, lactate) can be used to aid in confirm
diagnosis
X-RAY  A R DS
BRONCHOSCOPY for INHALATION INJURY
GRADING SCALE for INHALATION INJURY
DIAGNOSTIC PATHOLOGY
DIAGNOSTIC PATHOLOGY
DIAGNOSTIC PATHOLOGY
 TREATMENT

GENERAL TREATMENT SPESIFIC TREATMENT

 Suportive treatment
 Goal :
1. Vital sign monitoring
2. Decreased of toxic
substance exposure
3. Increased elimination of
substance toxic
 TREATMENT

GENERAL TREATMENT

1.a. FIRST and EMERGENCY TREATMENT

1.b. MAINTENANCE TREATMENT

(NON-SPESIFIC)
 TREATMENT

GENERAL TREATMENT SPESIFIC TREATMENT

 Evaluated severity of inhalation injury and degree of hypoxemia

 Still observation 4-12 hours
 Airway obstruction and respiratory distress could worse in 24- 48 hours
 Bronchoscopy  clearing and removing of secret, debris or carbon
 Tracheostomi, intubation & ventilator support if respiratory failure
 EVALUATE

Group Sign/Symptoms Action

Low risk person no clinical symptoms Usually be observed for 4-12 hours and
discharged with close follow-up and
instructions to return if symptomatic.

High-risk person only minimal Observed for 4-12 hours

symptoms

High-risk person any symptoms or admit to the hospital for further

concerns arise observation and oxygenation monitoring.

Symptomatic person any signs of airway admitted to the hospital for appropriate
obstruction, monitoring because edema and obstruction
bronchospasm, typically worsen over the next 24-48 hours.
respiratory distress,
or concurrent burns
 INDICATION for HOSPITALIZATION

Patients with any of the following should be strongly considered for hospitalization :

 History of closed space exposure for longer than 10 minute

 Carboneous sputum production
 Arterial PO2 less than 60 mmHg
 Metabolic acidosis
 COHb > 15%
 Arteriousvenous oxygen difference (on 100% oxygen) greater than 100 mmHg
 Bronchospasm
 Odynophagia
 Face burn
 In HOSPITAL TREATMENT

 Reevaluated  airway management and oxygenation status of the patient

 The bronchoscopical examination of the airway represents the gold standard to detect a
pathognomonic mucosalhyperemia

 Chest X-ray
 During the initial period, the degree of injury is usually underestimated based on the
chest x-ray, as the injury is mainly confined to the airways
 Diffuse atelectases, pulmonary edema or bronchopneumonia

 Appropriate fluid resuscitation of patients with smoke inhalation injury is still subject to
controversial debates.

 Fluid resuscitation should be guided by urine output and hemodynamic parameters

of the individual patient
 NEBULIZED TREATMENTS

 β2-agonists, improve respiratory mechanics by decreasing airflow resistance and

peak airway pressures. β2-agonists are associated with improved airspace fluid
clearance and stimulation of epithelial repair
 Inhaled NO is thought to improve oxygenation and to reduce increased
pulmonary vascular resistance by reversing the ventilation-perfusion
mismatch in ARDS owing to selective vasodilation in well-ventilated lung
areas  ???
 Heparin nebulization had only partial or no beneficial effects in ovine ARDS
after combined burn and smoke inhalation injury
 CORTICOSTEROID

 For suppressing inflammation and reducing edema.

 Their effects on various forms of chemical pneumonitis are disappointing.
 No direct data support their use in smoke inhalation.
 Prolonged use of steroids is discouraged.
 Consider a brief course of steroids in those patients with otherwise
unresponsive severe lower airway obstruction.
 Suggested as having some value in exposure to the following : NOx, Zinc
Oxide, Red Phosporus, Sulfur trioxide, Titanium tetrachloride,
polytetrafluoroethylene
 PULMONARY TOILET

 As with many diseases, the utility of chest physiotherapy is widely accepted but
remains unproven in controlled trials.
 The use of percutaneous cupping and postural drainage seem reasonable to clear
airways of cellular debris and soot, thereby preventing atelectasis and obstruction.
 Encourage extubated patients to cough and deep breathe.
 In intubated patients, use gentle suctioning to remove mucus, debris, and sloughed
epithelium.
 Fiberoptic bronchoscopy may be helpful in removing the debris and in facilitating
pulmonary toilet.
 HIPERBARIC OXYGEN (HBO)

 Neurologic abnormalitie and history of loss consciousness are the

primary clinical feature of asphyxian toxicity (CO toxicity)

 HBO use is indicated in patients with :

• Base escess < -2 mmol/L
• CO level greater than 25%( 0r >15% in pregnancy)
• Signs of cerebellar dysfunction
• Cardiovascular dysfunction
• Pulmonary edema
• Extremes of age
 If ARDS MANIFEST

ARDS management in acute toxic inhalation :

 Not different in usuallyARDS management

 Corticosteroid stil controversial

 Bronchodilatorif proven bronchospasm

 Profilactic antibiotic ????

 Antidotum in spesific case

 MECHANICAL VENTILATION STRATEGIES

 Low tidal volume ventilation with associated permissive hypercapnia

has been shown to effectively reduce ventilator- induced lung injury.
 Positive pressure ventilation with low tidal volumes (3-5 mL/kg) and
positive end-expiratory pressure (PEEP) and maintenance of plateau
pressures below 30 cm water significantly increases short-term
survival and is associated with decreased tracheobronchial cast
formation
 Increase the intensive care unit (ICU) survival rate from 29% to 62%.
 ANTIDOTUM SPESIFIC

Antidotum Toxic substance

Sodium nitrite H2S inhalation

Ethyleneediaminic tetraacetic acid Cadmium inhalation

Natrium tiosulfat, hydroxocobalamin and Cyanide inhalation

dicobalt ethylenediaminetetraacetic acid
(EDTA)

Amyl nitrit, continue by natrium iv Hydrogen cyanide

and natrium tiosulfat inhalation
 CONCLUSION
1.Acute toxic inhalation divided on type of substance : aphyixiant, iritant or systemic toxic

2.On case smoke inhalation there were multicomponent iritant particle, iritant gases,
asphyxian gases and thermal injury

3.Inhalation injury usually hapenned in case irritan substance component

4.Management of acute toxic inhalation including first and emergency treatment and continue by
maintenance treatment

5.Observation for airway obstruction and respiratory distress must be doing in case sugessted
Inhalation injury

6.The initial bronchoscopy on smoke inhalation injury performed within the 18-72 hours of
admission to the hospital and repeated till the airways became clear from soot and
carbonaceous secretions
THANK YOU