Trauma
This was previously featured in an exam
This was previously featured in an exam
Question 199 of 216
A 65 year old man is brought into ED by an air ambulance following a gas explosion at his home. Primary survey demonstrates the following.
- Airway - hoarse voice, drooling
- Breathing - RR 28 breaths/min, SpO2 99% on 15L NRB, decreased air entry left base
- Circulation - BP 98/55, HR 112 bpm
- Disability - GCS 12/15 (E3 M5 V4)
- Exposure - Bleeding laceration left thigh, full thickness burns over hands and arms, gross deformity to left wrist, tender RUQ with guarding
What is the most appropriate immediate management?
Answer:
- 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.
- Signs of upper airway injury
- Dyspnoea
- Hoarseness or dysphonia
- Facial burns
- Upper airway oedema
- Stridor
- 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
Inhalation Injury
Trauma
Last Updated: 8th September 2021
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 |
