Lecture

Inhalation injury
 Smoke inhalation is the primary cause of death
in about 60% to 80% of the 8,000 victims of burn in
juries each year in the United States . Airway injury
occurs in up to one third of those with major burns
and the risk of concurrent pulmonary damage is di
rectly related to the extent of surface burns presen
t
Inhalation injury greatly increases the incidenc
e of respiratory failure and acute respiratory distre
ss syndrome. It is also the cause of most early deat
hs in burn victims. The mortality rate following sm
oke inhalation ranges from 45% to 78% .
Definition
Inhalation trauma may be defined as an acute dam
age of the respiratory tract caused by the inhalation of
combustion products or steam, as a rule in a closed sp
ace.
Pathophysiology:
The 3 primary mechanisms that lead to injury are
thermal damage, asphyxiation, and pulmonary irritati
on.
1-Thermal damage (Damage from Heat Inhalation)
Thermal damage usually is limited to the orophary
ngeal area. This is due to the poor conductivity of air a
nd the high amount of dissipation that occurs in the u
pper airways. thermal injury is confined to the upper
airways.
2-Asphyxiation (Damage from Systemic Toxins):
Tissue hypoxia can occur secondary to decreasi
ng the ambient concentration of oxygen to as low
as 10-13%.
Carbon monoxide (CO) causes tissue hypoxia by
decreasing the oxygen-carrying capacity of the blo
od.
Toxin poisoning can cause permanent damage t
o organs including the brain.
Carbon Monoxide poisoning can appear sympt
omless up until the point where the victim falls int
o a coma.
3-Pulmonary irritation (Damage from Smoke Inhalati
on)
Irritants can cause direct tissue injury, acute br
onchospasm, and activation of the body's inflamm
atory response system. Activated leukocytes and/o
r humoral mediators, such as prostanoids and leuk
otrienes, produce oxygen radicals and proteolytic e
nzymes.
Mechanisms of injury
Pulmonary injury following smoke inhalation occur
s in two phases.
The initial cellular and exudative phase is characte
rized by an influx of neutrophils, elaboration of oxyge
n-free radicals, liberation of complement degradation
products
and production of inflammatory mediators.The co
nstituents of smoke can cause atelectasis by destroyin
g lung surfactant, increasing pulmonary vascular resist
ance, and contributing to edema.
Airflow limitation can result from bronchospasm,
upper airway narrowing from laryngeal edema, bronc
horrhea, ciliary dysfunction, and inspissation of desqu
amated cells.
CLINICAL PICTURE
After exposure to products of combustion, reac
tion occurs at three levels:
Supraglottic region: The latter responds by the rapid
development of oedema (within several minutes t
o three days
Symptoms: hoarseness, tendency to cough, respirato
ry insufficiency, imminent laryngospasm (Fig. 1).
Fig. 1 - Supraglottic region - pathophysiology; respira
tory insuficiency 5th hour - 3rd day.
2. Tracheobronchial damage: Slower development of
oedema. Greater risk of development of ARDS and
pneumonia, imminent bronchospasm.
Symptoms: urge to cough, bronchorrhoea, sings of re
spiratory insufficiency usually appear the third to fi
fth day (Fig. 2).
Fig. 2 - Tracheobronchial region - pathophysiology; re
spiratory insuficiency 3rd - 7th day postburn.
3. Intoxication by combustion products (most frequently
carbon monoxide C0): Carbon monoxid is linked very a
ctively to haemoglobin and thus takes up the binding s
ites for Oxygen. The transport capacity of haemoglobi
n for Oxygen is impaired even in the Gase of good part
ial Oxygen pressure in arterial blond and this results in
hypoxia.
N.B
inhalation injury usually appears within 2-48 hours
after the burn occurred. Indications may include:
 The patient faints
 Fire or smoke present in a closed area
 Evidence of respiratory distress or upper airway obstr
uction
 Soot around the mouth or nose
 Nasal hairs, eyebrows, eyelashes have been singed
 Burns around the face or neck Circumferential burns i
n the cervical area cause extrinsic upper airway occlusi
on from encircling eschars.
Management
Diagnosis
. Clinical manifestations vary among victims depending o
n their susceptibility to injury and degree of exposure.
Injury may be limited to the upper airways (eg, nasop
haryngeal irritation, hoarseness, stridor, cough)
may extend distally with tracheobronchial and alv
eolar destruction (eg, dyspnea, chest discomfort, hem
optysis).
Inhalation injury is likely in the presence of facial a
nd upper cervical burns, singed eyebrows and nasal vi
brissae, bronchial breath sounds, wheezing, rales, cya
nosis, and carbonaceous sputum.
1-Chest films taken soon after smoke inhalation injury ar
e often normal, but abnormalities ranging from patchy
atelectasis to diffuse interstitial and alveolar involvem
ent may be seen 24 to 36 hours later..
2-Pulmonary function testing can confirm obstructive or
restrictive ventilatory defects.
3-Bronchoscopy is considered the "gold standard" for ea
rly evaluation of upper airway injury, but the best resu
lts are obtained within the first 24 hours.
4-Bronchoalveolar lavage, which typically reveals an incr
eased number of polymorphonuclear cells and alveola
r macrophages,
5-Transbronchial biopsy, which can be used to diagnose
bronchiolitis obliterans and interstitial fibrosis
 TREATMENT
Treatment of patients with Inhalation injuries i
nvolves supportive treatment apart from the speci
fic treatment of some intoxications.In the majority
of Gases, Inhalation trauma is associated with exte
nsive dermal burns.
Immediately after injury and on admission to a
specialized department, basic measures are essenti
al to take:
1. Ensuring free airways - prompt endotracheal intubatio
n:In case of deep skin burns on the neck and trunk, rel
easing incisions must be made as soon as possible.
2. Ensuring adequate ventilation and oxygenation of peri
pheral tissues: moistened oxygen, artificial pulmonary
ventilation in case of respiratory insufficiency.
3. Treatment of shock, involving haemodynamic stabiliza
tion of the patient , it means adequate intravenous vol
ume resuscitation as a prevention of hypovolaemic sh
ock. In inhalation trauma, during the first 24 hours the
need of crystalloids is 40-75 % greater than in patients
with dermal burns only.
4. Careful analgosedation is essential.
5. Specific antibodies (if known) and oxygen therapy.
6. Promotion of mobilization and evacuation of secretio
ns and detritus from the tracheobronchial tree and lun
gs (airway suction and lavage, humidification, chest ph
ysiotherapy, regular positioning of the patient, mucoly
tics, bronchodilatating substances).
7. Antioedematous treatment (elevation of head and tru
nk on the bed, escinum etc.).
8.Maintenance of airway patency,
9.Adequate oxygenation and ventilation,aggressive pul
monary toilet, and stabilization of hemodynamic statu
s are the cornerstones of therapy for smoke inhalation
injury.
10.Patients with altered mental status or documented u
pper airway injury are at risk for airway obstruction.
11.Early intervention and respiratory support are essenti
al.

12.The cervical spine must be protected during endotrac

heal intubation in neurologically impaired patients. In
haled bronchodilators help reduce bronchospasm, and
humidification can relieve excessive airway drying or
mucous plugging.

13.High-flow oxygen should be administered to all patie

nts with smoke inhalation. In severe cases, mechanical
ventilatory support,

14.Chest physiotherapy, early ambulation to reduce post

-injury atelectasia, consolidation, and pneumonia
 Prognosis
Patients with smoke inhalation injury may have
complications caused by a number of pulmonary s
equelae, including persistent chest tightness and s
hortness of breath.
Chronic cough and wheezing may reflect underl
ying hyperreactive airways.
Chronic bronchitis, bronchiectasis, bronchial ste
nosis, pulmonary fibrosis, and bronchiolitis obliter
ans may also occur.