Nursing responsibilities on Inhalation Injury

1. INHALATION
INJURY
CONTENTS :
1. Introduction
2. Etiology
3. Pathophysiology
4. Assessment
5. Diagnosis
6. Management
7. Nursing Diagnosis

2. Inhalation injuries are acute injuries to your
respiratory system and lungs. They can happen if
you breathe in toxic substances, such as smoke
(from fires), chemicals, particle pollution, and
gases.
Respiratory tract injuries resulting from inhalation
of smoke or chemical products are the leading
causes of death in thermally injured patients.

3. ETIOLOGY
Inhalation injury is classified in three types:
UPPER AIRWAY
LOWER AIRWAY
METABOLIC
ASPHYXIATION

4. Upper Airway
• Upper airway injuries caused primarily by thermal injury to
the mouth, oropharynx, and larynx;
• Super-heated air usually injures only the airway structure
above the vocal cords because of low heat capacity of air,
efficient heat dissipation in the upper respiratory tract, and
reflex closure of the upper airway.

5. Lower airway
• Lower airway and parenchymal injuries caused by chemical
and particulate constituents of smoke
• Lower airway
• The lower airway is damaged by smoke-related toxins, which
are generated from the incomplete combustion of certain
products. Burning cotton, rubber, and plastic produce many
injurious substances such as the aldehydes, nitrogen
dioxide, sulfur dioxide, ammonia, and chlorine, which turn
into strong acids or alkalis when combined with water in the
lower airway.

6. Metabolic Asphyxiation
• Metabolic asphyxiation, which is the process by which
certain smoke constituents, such as carbon monoxide (CO)
and cyanide, impair oxygen (O2) delivery to the tissue.
• It should be noted that these often overlap and that even
patients without inhalation injury may develop massive facial
edema requiring intubation during the resuscitation process.

7. • CO is a colorless, tasteless, inodorous, non-irritative gas
produced by incomplete hydrogen combustion. CO poisoning is a
major cause of morbidity in burn patients. It binds to hemoglobin
with approximately 240 times greater affinity than O2.
• Hydrogen cyanide
• is produced during combustion of household materials containing both
carbon and nitrogen. These include synthetic polymers, acrylonitrile, nylon,
melamine, wool, and cotton
• Cyanide poisoning is almost impossible to confirm without clinical
suspicion. A low threshold should be maintained to empirically treat
cyanide toxicity. The severity of cyanide poisoning depends on the amount
of exposure, duration, and route.

8. Pathophysiology

9. ASSESSMENT
Assess breathing by respiratory rate, chest wall motion, and auscultation of air
movement. Assess circulation by level of consciousness, pulse rate, blood
pressure, capillary refill, and by symmetry and strength of pulses.
Perform a brief neurological evaluation, including a determination of the
Glasgow Coma Scale, pupil size and reactivity, and any focal findings. Remove
all clothing to expose traumatic injuries/burns and to prevent on going
thermal injury from smouldering clothes. Evaluate patient's back and perform
a log roll if appropriate.
Identification of signs or symptoms of airway compromise is important
to permit early and aggressive treatment before rapid progression to
upper airway obstruction and respiratory failure ensues.
The secondary survey continues in a complete head-to-toe examination as in any
other trauma evaluation. Burns on the face, soot marks, and singed eyebrows or
facial hair are indicative of smoke inhalation. Large cutaneous burns indicate an
inability to escape flame and a risk for smoke inhalation injury.

10. SIGNS AND SYMPTOMS
• Tachypnea
• Dyspnea
• Cough
• Decreased breath
sounds
• Wheezing
• Rales
• Rhonchi
• Retractions

11. DIAGNOSIS
Traditionally, the diagnosis of
inhalation injury has rested on both
subjective and objective measures.
History and physical are important
factors as they may help
prognosticate the host response and
co-morbidities.
• carboxyhemoglobin
measurements,
• chest computed
tomography (CT),
• fiberoptic bronchoscopy
(FOB),
• radionuclide scan with
133 Xenon,
• and pulmonary function
testing.
Laboratory values used to
determine severity include
PaO2/FiO2 and alveolar-
arterial gradients but
these can be arbitrarily
high or low depending upon
ventilation modes and
other clinical parameters

12. MANAGEMENT
Initial management
Immediate and directed assessment of the respiratory or
circulatory status of patients with smoke inhalation is
required similar to standard assessment and management
for all trauma patients.
Intubation
Intubation should be considered if any of the following signs exist:
respiratory distress, stridor, hypoventilation, use of accessory
respiratory muscles, blistering or edema of the oropharynx, or deep
burns to the face or neck.
O2
Any patients who have suspicious inhalation injuries should receive
supplemental O2 at an FiO2 of 100%. Any comatose patients who have
suspicious CO or cyanide poisoning should be ventilated mechanically
using 100% O2.
Mechanical ventilation
Patients who require intubation because of upper airway edema,
pulmonary dysfunction, or impaired mental status generally
require mechanical ventilation.

13. MANAGEMENT
-PHARMACOLOGY
• Patients require aggressive pulmonary toilet, chest physiotherapy, airway suctioning,
therapeutic serial bronchoscopies, and early aggressive ambulation. This defines our
current treatment options.
• Bronchodilators
Bronchodilators decrease airflow resistance and improve airway compliance. β2-adrenergic
agonists such as albuterol and salbutamol decrease airway pressure by relaxing smooth
muscle and inhibiting bronchospasm thereby increasing the PaO2/FiO2 ratio36.
• Muscarinic receptor antagonists
Muscarinic receptor antagonists such as tiotropium decrease airway pressures and mucus
secretion and limit cytokine release by causing smooth muscle constriction within the
airways, and stimulation of submucosal glands
• Inhaled (nebulized) Mucolytic agents and Anticoagulants
The airway obstruction secondary to mucus, fibrin cast formation, and cellular debris
subsequent to inhalation injury are addressed by mucolytic agents, specifically, N-
acetylcysteine (NAC)40

14. • Respiratory support
Without consistent reproducible data to support the use of the above pharmacologic
adjuncts, other centers have focused on the risks and benefits of different modes of
ventilation. Ideally, aggressive pulmonary toilet without the use of mechanical
ventilation improves outcomes.
• Airway pressure release ventilation (APRV)
APRV is an inverse ratio, pressure controlled mode of ventilation that allows for
spontaneous breaths. It has been shown to recruit alveoli, imprve oxygenations and
hemodynamics and potentially lung protective.
• Extracorporeal membrane oxygenation (ECMO)
A systematic review and meta-analysis on the use of ECMO in inhalation injury is
currently limited by the number of available studies.

15. NURSING DIAGNOSIS
1.Risk for Ineffective Tissue
Perfusion
Related to:
O reduction/interruption of
arterial/venous blood flow
O Hypovolemia
2. Risk for Ineffective Airway Clearance
related to:
O Tracheobronchial obstruction: mucosal
edema and loss of ciliary action (smoke
inhalation
O Trauma: direct upper-airway injury by
flame, steam, hot air, and chemicals/gases
O Fluid shifts, pulmonary edema, decreased
lung compliance

16. Reference
• https://nurseslabs.com/11-burn-injury-nursing-care-plans/11/
• https://www.dovepress.com/assessing-inhalation-injury-in-the-emergency-
room-peer-reviewed-fulltext-article-OAEM
• https://www.sciencedirect.com/science/article/pii/B978032347661400016
2
• https://ccforum.biomedcentral.com/articles/10.1186/s13054-015-1077-4
• https://www.studocu.com/en-us/document/american-career-
college/intermediate-med-surg/concept-map-inhalation-injury/10655532
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722076/
•

17. Thank You