Salon b 15 kasim 09.00 10.15 emel eryüksel

1. Inhalation Injury and Carbon
monoxide poisoning
EMEL ERYÜKSEL
Assoc. Prof.
Marmara University Medical School
Pulmonary and Critical Care, İstanbul

3. Inhalation Injury

4. lnhalation injury
• Upper airway injury (heat)
• Lower airway injury (local chemi cal)
• CO /cyanide poisoning (systemic toxicity)

5. Heat injury to the upper airway
• may cause massive
swelling of the tongue,
epiglottis, and
aryeepiglottic folds with
obstruction.
Therefore, intubation should not be delayed if
severe inhalation injury is present.
• as fluid resuscitation is
ongoing it can exacerbate
obstruction
• Initial evaluation is not a
good indicator of the
severity of obstruction
that may occur later
with permission from Dr. Yorgancı

6. Diagnosis of inhalation injury
• ıs a subjective decision
based on a history of
smoke exposure in a
closed space.
• Physical findings (facial
injury, singed nasal
hairs, soot in the
proximal
airways,changes in
voice ) support the diag

7. Airway management
• Common signs of the
potential need for
intubation include:
• Persistent cough, stridor,
or wheezing
• Hoarseness
• Deep facial or
circumferential neck
burns
• Nares with inflammation
or singed hair
with permission from Dr. Yorgancı

8. Airway management
• Intubation is justified if
any of the following signs
are present:
• Blistering or edema of the
oropharynx
• Depressed mental status
• Respiratory distress
• Hypoxia or hypercapnia
• Elevated carbon
monoxide and/or cyanide
levels
with permission from Dr. Yorgancı

9. INDICATIONS FOR INTUBATION
• “When in doubt,
intubate”
• altered mental status,
refractory hypoxemia,
and signs of airway
obstruction and
progressive facial
swelling.
laryngoscopic exam

10. • Patients who do not require intubation
should receive supplemental oxygen at a
fraction of inspired oxygen (FiO2) of 100
percent.
• The tissue hypoxia is multifactorial, including
the inspiration of air with an FiO2 of less than
0.15 during the fire and the impaired
delivery and utilization of oxygen by the
tissues due to carbon monoxide and cyanide
poisoning
• Tissue hypoxia can quickly lead to death.

11. Lung Injury

12. • Inhalation injury leads to
desuqamation of trachea
and bronchial tree followed
by atelectasis.
As a result, ARDS follows VALI
• Atelectasis causes ven/per
mismatch.
• Ventilator associated lung
injury occurs related to
cytokine release in over
ventilated regions.

13. INHALATION INJURY
• lnhalation injury is in part
a mechanical process
characterized by
secretions, can occlude
the airway leading to
atelectasis and
pneumonia.
• Aggressive use of
bronchoscopy is highly
effective in removing
foreign particles and
accumulated secretions

14. LATER TREATMENT CONSIDERATIONS

15. Management

16. ARDS

17. Carbon monoxide poisoning

18. CARBON MONOXIDE POISONING
• Competes with oxygen for
hemoglobin binding which shifts
the oxyhemoglobin dissociation
curve to the left
• Oxygen delivery is compromised
because of reduced oxygen
carrying capacity
• competitively inhibits
intracellular cytochrome P-450
resulting in inability of cellular
systems to utilize oxygen
• can also precipitate an
inflammatory cascade that results
in CNS lipid peroxidation and
delayed neurologic sequelae

19. Carbon monoxide and cyanide
• Standard pulse oximetry
is NOT reliable with
significant CO toxicity
(The absorbent spectrum
of Cohb and Ohb are very
similar)
• COhb level be obtained in
all patients with
moderate or severe
burns.

20. CO- Symptoms
Weaver LK. N Engl J Med 2009;360:1217-25.

21. Carboxyhemoglobin levels
• an elevated carboxyhemoglobin level
measured by cooximetry of an arterial blood
gas sample.
• Nonsmokers may have up to 3 percent
carboxyhemoglobin at baseline; smokers may
have levels of 10 to 15 percent.
• Levels above these respective values are
consistent with CO poisoning.

22. MANAGEMENT
• the most important
interventions in the
management of a CO-poisoned
patient are
prompt removal from the
source of CO and institution
of high-flow oxygen by face
mask.

23. Hyperbaric oxygen therapy
• Half-life of CO is 250
minutes in breathing
room air.
• This is reduced to 40 to
60 -minutes with
inhalation of 100%
oxygen
• Hyperbaric oxygen
treatment may be needed
if carbon monoxide levels
are high

25. • the more rapidly treatment is provided.
• Ideally, HBO should be initiated within six
hours.
• Benefit for patients treated more than 12
hours after their CO exposure is unproven

26. Cyanide
• produced during
combustion of multiple
household materials
• Cytochrome oxidase
• Lactic acidosis

27. Cyanide Intox-Symp
• Elevated lactat levels(>10mmol/L)
• Methabolic acidosis

28. Mechanical ventilation
• no ideal ventilator
strategy has emerged
• limit plateau pressures
to < 30 cm H2O
• allow Pco2 to increase if
needed to minimize
plateau pressures
• use the appropriate
level of positive end-expiratory
pressure

29. Noninvasive ventilation
• Without an ET tube,
patients communicate
more effectively,
require less sedation
and are more
comfortable

30. NIV : Keys of Success

31. NIV: Failure Rate
• %5-40
Brochard L, et al. N Engl J Med 1995;333(13):817–822.
Bott J, et al. Lancet 1993;341(8860):1555–1557..

32. NPPV failure eventually requires
intubation…
• Inability early to identify
patients will fail NPPV can
cause inappropriate
delay of intubation

33. Basic rules…….

34. NIMV – Noneligiable Patients
• Non-cooperable, agitated patients
• Hemodynamically unstable patients with
multiple organ failure
• Face/ Upper Airway Trauma
• Recent history of upper GI surgery
• Intestinal Obstruction
• Increased Secretion
• Presence of undrained pneumothorax

35. Noninvasive ventilation
• High secretions load are
often seen with II…
The most serious complication is failure to
recognize when should we stop?
Delayed entubation may cause continued
deterioration