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Questions Answered: 216

Final Score 84%

181
35

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Trauma

Question 69 of 216

A 23 year old woman is brought to the Emergency Department by paramedics following a house fire in a nearby property. She is alert and talking with a hoarse voice. You note stridor and singed nasal hair. She has full thickness burns to an estimated 30% of her total body surface area. What treatment does this patient require as a priority?

Answer:

An airway should be immediately secured with an endotracheal tube (ETT) if the patient has diminished mental status with poor airway reflexes or history and examination suggestive of injury with threatened patency. Patients with inhalation injury often have difficult airways to secure, and preparations for a surgical airway should be made in anticipation of ETT placement failure.

Inhalation Injury

Pathophysiology

Inhalation injury typically results from an obvious exposure to harmful inhaled substances, resulting from, for example, an industrial accident or a residential fire. Common causative factors in residential fires are heat, inert gases that displace oxygen (e.g. nitrogen, hydrogen, methane), toxic gases (e.g. carbon monoxide, hydrogen cyanide, ammonia, sulfur dioxides), and particulate matter (dust and smoke). Broad categories of injury include direct thermal injury, local irritant injury, asphyxiation, and systemic toxic effects.

  • Upper airway injury
    • Thermal and toxic exposure can induce direct upper airway injury and oedema that can lead to airway compromise, leading to rapid clinical deterioration. A comprehensive evaluation to ensure that the airway is not threatened should be performed on all patients.
  • Cellular asphyxia
    • Carbon monoxide (CO) and hydrogen cyanide are by-products of residential fires that cause cellular asphyxia by disrupting cellular oxygen transport. CO toxicity is much more common and all patients exposed to an explosion or fire should be assessed for CO toxicity. If historical factors (burning home furnishings) or hypoxia suggest cyanide toxicity, the patient should be assessed for metabolic acidosis with an ABG, serum bicarbonate, and serum lactate level. However, these findings are not specific to cyanide toxicity, and are more commonly seen as a result of CO toxicity or shock.
  • Lower airway injury
    • There are numerous inhaled gases and particulates that can cause direct injury to the cells in the conducting airways, leading to bronchoconstriction, oedema, epithelial cell death with sloughing, diminished airway clearance, and airway obstruction. Like upper airway injury, lower airway injury may be delayed, emphasising the importance of frequent reassessment.
  • Lung parenchymal disease
    • Inhalation injury and commonly associated conditions (cutaneous burns and trauma) are associated with acute respiratory distress syndrome (ARDS). These complications may be evident on presentation, or may develop in the initial hours of treatment, unmasked by resuscitation of circulating volume. Patients will demonstrate an increasing oxygen requirement, and chest radiographs will commonly show diffuse airspace opacities.

Clinical features

  • Known inhalation exposure
  • Similarity of symptoms to those of others at site of exposure
  • Signs of upper airway injury
    • Dyspnoea
    • Hoarseness or dysphonia
    • Facial burns
    • Upper airway oedema
    • Stridor
  • Signs of lower airway injury
    • Cough
    • Dyspnoea
    • Tachypnoea
    • Wheezing
    • Diminished breath sounds or crackles
  • Signs of carbon monoxide poisoning
    • Nausea
    • Headache
    • Dizziness
    • Confusion
    • Seizures

Investigations

  • Pulse oximetry
    • May show hypoxaemia (however will appear normal even in the setting of significantly elevated CO-Hb levels)
  • Arterial blood gas
    • May show severe metabolic acidosis which may suggest hypoperfusion from shock, carbon monoxide poisoning or cyanide toxicity
  • Serum lactate
    • May be elevated which could indicate hypoperfusion, carbon monoxide poisoning or cyanide toxicity
  • Carboxyhaemoglobin (CO-Hb) level
    • A CO-Hb level > 15% are seen in carbon monoxide poisoning (normal levels are 1 - 3% and up to 10% in smokers)
  • Chest x-ray
    • May show air trapping and atelectasis suggesting airway injury, obstruction and collapse, or pulmonary oedema suggesting ARDS
  • ECG and cardiac telemetry monitoring
    • Increased cardiac demand, inflammation, and systemic and cellular hypoxia all predispose to cardiac ischaemia or arrhythmias
  • Urine toxicology screen and serum ethanol level
    • May show evidence of ethanol or illicit drug use (there is a high incidence of intoxication among victims of residential fires)
  • Pulmonary function tests
    • Allows characterisation and serial measurement of airflow obstruction; may show decreased FEV1 or forced vital capacity, and a flow-volume loop suggesting obstruction
  • Laryngoscopy and bronchoscopy
    • Allows more advanced assessment of airway oedema, burns or ulcerations and debris in airways
  • Cyanide level
    • A level greater than 11.62 micromol/L (0.5 mg/L) seen in cyanide poisoning

Management

  • Upper airway management
    • Early assessment
    • Early intubation if indicated (diminished mental status with poor airway reflexes or history and examination suggestive of injury with threatened patency)
    • Frequent reassessment if intubation not immediately indicated
  • Treatment of carbon monoxide toxicity
    • High-flow supplemental oxygen therapy
    • Hyperbaric oxygen
  • Treatment of cyanide toxicity
    • Hydroxocobalamin and sodium thiosulfate
  • Supportive treatment of lower airway injury or parenchymal lung disease
    • Inhaled beta-agonists to relieve bronchoconstriction
    • Oxygen therapy
    • Non-invasive positive pressure ventilation
    • Intubation with mechanical ventilation
  • General measures
    • Analgesia and sedation
    • Hand hygiene
    • Head-of-bed elevation
    • Catheter care
    • DVT prophylaxis
    • Treatment of burns

Complications

  • Infection
  • Barotrauma
  • Pneumothorax
  • Neurocognitive deficit secondary to carbon monoxide poisoning
  • Chronic respiratory disease

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  • Biochemistry
  • Blood Gases
  • Haematology
Biochemistry Normal Value
Sodium 135 – 145 mmol/l
Potassium 3.0 – 4.5 mmol/l
Urea 2.5 – 7.5 mmol/l
Glucose 3.5 – 5.0 mmol/l
Creatinine 35 – 135 μmol/l
Alanine Aminotransferase (ALT) 5 – 35 U/l
Gamma-glutamyl Transferase (GGT) < 65 U/l
Alkaline Phosphatase (ALP) 30 – 135 U/l
Aspartate Aminotransferase (AST) < 40 U/l
Total Protein 60 – 80 g/l
Albumin 35 – 50 g/l
Globulin 2.4 – 3.5 g/dl
Amylase < 70 U/l
Total Bilirubin 3 – 17 μmol/l
Calcium 2.1 – 2.5 mmol/l
Chloride 95 – 105 mmol/l
Phosphate 0.8 – 1.4 mmol/l
Haematology Normal Value
Haemoglobin 11.5 – 16.6 g/dl
White Blood Cells 4.0 – 11.0 x 109/l
Platelets 150 – 450 x 109/l
MCV 80 – 96 fl
MCHC 32 – 36 g/dl
Neutrophils 2.0 – 7.5 x 109/l
Lymphocytes 1.5 – 4.0 x 109/l
Monocytes 0.3 – 1.0 x 109/l
Eosinophils 0.1 – 0.5 x 109/l
Basophils < 0.2 x 109/l
Reticulocytes < 2%
Haematocrit 0.35 – 0.49
Red Cell Distribution Width 11 – 15%
Blood Gases Normal Value
pH 7.35 – 7.45
pO2 11 – 14 kPa
pCO2 4.5 – 6.0 kPa
Base Excess -2 – +2 mmol/l
Bicarbonate 24 – 30 mmol/l
Lactate < 2 mmol/l
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