Smoke inhalation injury

Question 1

What physical examination findings are most indicative of smoke inhalation injury in small animals?

Answer 1

Facial burns, soot in nostrils or oropharynx, harsh lung sounds, coughing, respiratory distress, and hyperemic mucous membranes.

Question 2

What clinical signs differentiate carbon monoxide toxicity from cyanide toxicity in small animals?

Answer 2

CO Toxicity: Bright red mm, neuro signs, and cardiac arrhythmias.
Cyanide Toxicity: Almond-like breath odor, acute onset of seizures, and metabolic acidosis.

Question 3

What are the most common delayed carbon monoxide poisoning?

Answer 3

Seizures, ataxia, blindness, and behavioral changes due to hypoxic brain injury and delayed neurotoxic effects.

Question 4

Why are standard two-wavelength pulse oximeters unreliable in detecting oxygenation levels in smoke inhalation patients?

Answer 4

They cannot differentiate between oxyhemoglobin and carboxyhemoglobin, falsely elevating SpO2 readings.

Question 5

What is the half-life of carboxyhemoglobin at room air, 100% oxygen, and hyperbaric oxygen therapy?

Answer 5

Room air: ~4–6 hours.
100% oxygen: ~40–60 minutes.
Hyperbaric oxygen: ~15–30 minutes.

Question 6

What are the potential benefits of nebulized heparin and N-acetylcysteine in treating upper airway edema?

Answer 6

Nebulized heparin reduces fibrin deposition and airway obstruction. N-acetylcysteine decreases mucus viscosity and acts as an antioxidant, mitigating oxidative stress.

Question 7

What factors influence the decision to perform a tracheostomy in smoke inhalation patients?

Answer 7

Severe upper airway obstruction, laryngeal edema, or failure of intubation warrants a tracheostomy.

Question 8

What prognostic factors influence survival in dogs and cats suffering from smoke inhalation?

Answer 8

Severity of CO exposure, presence of concurrent burns, response to oxygen therapy, and development of secondary infections.

Question 9

What are the most common long-term respiratory complications in survivors of smoke inhalation injuries?

Answer 9

Chronic bronchitis, fibrosis, and restrictive lung disease are common sequelae.

Question 10

Why is hydroxocobalamin (vitamin B12a) a preferred antidote for cyanide poisoning in smoke inhalation cases?

Answer 10

Hydroxocobalamin binds cyanide to form cyanocobalamin, which is excreted in urine. It is effective, rapid, and has minimal side effects compared to sodium nitrite or thiosulfate.

Question 11

How does carbon monoxide toxicity affect the oxygen-hemoglobin dissociation curve, and why? what are the clinical implications of this shift?

Answer 11

L shift. CO increases Hb’s O2 affinity, impairing oxygen unloading in tissues, exacerbating cellular hypoxia despite normal oxygen levels in arterial blood.

Question 12

Compare the mechanisms by which carbon monoxide (CO) and hydrogen cyanide (HC) cause cellular hypoxia.

Answer 12

CO binds to hemoglobin with high affinity, reducing oxygen delivery and causing functional anemia + inhibits cytochrome
oxidase enzyme systems resulting in intracell
inability to utilize O2.
HC inhibits cytochrome c oxidase in the mitochondrial electron transport chain, blocking oxidative phosphorylation.

Question 13

How does the size of particulate matter in smoke determine its site of deposition in the respiratory tract?

Answer 13

Particles >5 μm are trapped in the upper airway. Particles 1–5 μm deposit in the trachea and bronchi. Particles <1 μm reach the alveoli, where they cause the most significant damage.

Question 14

Describe the cascade of inflammation following thermal injury to the upper airway.

Answer 14

Thermal injury triggers epithelial necrosis and release of cytokines (IL-1, IL-6, TNF-α). This activates neutrophils, leading to oxidative stress, edema, and further airway damage.

Question 15

Explain the role of nitric oxide (NO) in the pathophysiology of smoke inhalation injury.

Answer 15

NO reacts with superoxide to form peroxynitrite, a potent oxidant that damages endothelial cells, disrupts the alveolar-capillary barrier, and worsens inflammation and edema.

Question 16

How does smoke inhalation lead to a V/Q mismatch in the lungs?

Answer 16

Smoke inhalation causes bronchoconstriction, alveolar edema, and impaired surfactant production, leading to alveolar collapse (atelectasis) and increased shunting (low V/Q areas). Concurrently, airway obstruction causes areas of dead space (high V/Q areas).

Question 17

What are the three stages of ARDS, and how are they characterized histologically and clinically?

Answer 17

Exudative Stage (0–7 days): Diffuse alveolar damage (DAD), hyaline membrane formation, pulmonary edema, and inflammatory cell infiltration. Clinically, dyspnea, hypoxemia, and reduced lung compliance are common.
Proliferative Stage (7–21 days): Resolution of edema, proliferation of fibroblasts, and early interstitial fibrosis. Symptoms may plateau or improve slightly.
Fibrotic Stage (>21 days): Persistent fibrosis and scarring, leading to restrictive lung disease and poor prognosis.

Question 18

Why is direct thermal injury to the lower airways uncommon, and what mechanisms contribute to lower airway damage following smoke inhalation?

Answer 18

Direct thermal injury to the lower airways is uncommon because the upper airway effectively dissipates heat, preventing high temperatures from reaching the lower respiratory tract.
Lower airway damage primarily occurs due to the inhalation of chemical irritants present in smoke.

These irritants stimulate the bronchial system, which is densely innervated with vasomotor and sensory nerve endings. Chemical exposure triggers the release of neuropeptides, such as neurokinins and calcitonin gene-related peptide, by activating vagal nerve sensory fibers. This results in a cascade of inflammatory responses, including:

Bronchoconstriction: Narrowing of the airways due to smooth muscle contraction.
Pulmonary vasoconstriction: Reduced blood flow in the pulmonary vasculature.
Airway fluid accumulation: Increased permeability and secretion lead to edema and mucus buildup.
These processes exacerbate respiratory distress and contribute to hypoxemia in smoke inhalation injuries.

Question 19

When does the severity of edema peak?

Answer 19

24h post exposure

Question 20

List the effects of CO intoxication.

Answer 20

• 250x higher affinity for Hb
• L shift of the oxy-Hb dissociation curve
• inhibition of cytochrome
  oxidase enzyme systems= intracell inability to utilize O2, electron chain dysfunction, electron
  leakage, superoxide production, and mitoch oxidative stress (=neuronal necrosis/apoptosis)
• increased platelet adherence-> risk of
  thromboembolic events

Question 21

What are the organs mostly affected by CO intox and why?

Answer 21

• brain
• heart
  Compared with other organs, the brain and heart have a significantly
  higher oxygen extraction, and consequently are majorly affected during
  COHb circulation

Question 22

The combustion of what substences is most likely to cause HC production? And what about CO?

Answer 22

HC: wool, silk, cotton, paper, plastic and other polymers
CO: all materials

Question 23

T/F: CO and HC are odorless

Answer 23

F: CO is odorless but HC smells like bitter almonds