Trauma
Question 161 of 216
A 17 year old is rushed to the Emergency Department by his friends who tell you he was stabbed in the chest 10 minutes ago. He is taken to the Resuscitation area and a trauma call is initiated. His primary survey findings are:
- Airway - patent, talking (anxious)
- Breathing - tachypnoea, equal air entry, equal chest expansion, 2 cm wound noted at the left sternal edge at the level of the 5th-6th intercostal space
- Circulation - tachycardia, hypotension, soft abdomen, distended neck veins
- Disability - GCS 15
Given these primary survey findings, what is the single most likely diagnosis?
Answer:
- Cardiac tamponade can develop slowly, allowing for a less urgent evaluation, or rapidly, requiring rapid diagnosis and treatment.
- The classic clinical triad of muffled heart sounds, hypotension, and distended veins is not uniformly present with cardiac tamponade. Muffled heart tones are difficult to assess in the noisy resuscitation room, and distended neck veins may be absent due to hypovolaemia.
- Kussmaul’s sign (i.e. a rise in venous pressure with inspiration when breathing spontaneously) is a true paradoxical venous pressure abnormality that is associated with tamponade.
- PEA is suggestive of cardiac tamponade but can have other causes.
Thoracic Trauma: Immediately Life-Threatening Injuries
Trauma
Last Updated: 27th February 2021
Major thoracic injuries that should be recognised and address during the primary survey are:
- Tracheobronchial tree injury
- Tension pneumothorax
- Open pneumothorax
- Massive haemothorax
- Cardiac tamponade
Tracheobronchial Tree Injury
- Pathophysiology:
- Injury to the trachea or a major bronchus is an unusual but potentially fatal condition.
- The majority of tracheobronchial tree injuries occur within 1 inch of the carina.
- These injuries can be severe, and the majority of patients die at the scene. Those who reach the hospital alive have a high mortality rate from associated injuries, inadequate airway, or development of a tension pneumothorax or tension pneumopericardium.
- Mechanism of injury:
- Rapid deceleration following blunt trauma produces injury where a point of attachment meets an area of mobility.
- Blast injuries commonly produce severe injury at air-fluid interfaces.
- Penetrating trauma produces injury through direct laceration, tearing, or transfer of kinetic injury with cavitation.
- Intubation can potentially cause or worsen an injury to the trachea or proximal bronchi.
- Diagnosis:
- Patients typically present with haemoptysis, cervical subcutaneous emphysema, tension pneumothorax, and/or cyanosis.
- Incomplete expansion of the lung and continued large air leak after placement of a chest tube suggests a tracheobronchial injury, and placement of more than one chest tube may be necessary to overcome the significant air leak.
- Bronchoscopy confirms the diagnosis.
- Management:
- If tracheobronchial injury is suspected, obtain immediate surgical consultation.
- Immediate treatment may require placement of a definitive airway.
- Intubation of patients with tracheobronchial injuries is frequently difficult because of anatomic distortion from paratracheal hematoma, associated oropharyngeal injuries, and/or the tracheobronchial injury itself.
- Advanced airway skills, such as fiber-optically assisted endotracheal tube placement past the tear site or selective intubation of the unaffected bronchus, may be required. For such patients, immediate operative intervention is indicated.
- In more stable patients, operative treatment of tracheobronchial injuries may be delayed until the acute inflammation and oedema resolve.
Tension pneumothorax
- Pathophysiology:
- Tension pneumothorax develops when a “one-way valve” air leak occurs from the lung or through the chest wall. Air is forced into the pleural space with no means of escape, eventually collapsing the affected lung. The mediastinum is displaced to the opposite side, decreasing venous return and compressing the opposite lung. Shock (often classified as obstructive) results from marked decrease in venous return, causing a reduction in cardiac output.
- Mechanism of injury:
- The most common cause of tension pneumothorax is mechanical positive-pressure ventilation in patients with visceral pleural injury.
- Tension pneumothorax also can complicate a simple pneumothorax following penetrating or blunt chest trauma in which a parenchymal lung injury fails to seal, or after attempted subclavian or internal jugular venous catheter insertion.
- Occasionally, traumatic defects in the chest wall cause a tension pneumothorax when occlusive dressings are secured on four sides or the defect itself constitutes a flap-valve mechanism.
- Rarely, tension pneumothorax occurs from markedly displaced thoracic spine fractures.
- Diagnosis:
- Patients who are spontaneously breathing often manifest extreme tachypnoea and air hunger, whereas patients who are mechanically ventilated manifest haemodynamic collapse.
- Tension pneumothorax is characterised by some or all of the following signs and symptoms:
- Chest pain
- Air hunger
- Tachypnoea
- Respiratory distress
- Tachycardia
- Hypotension
- Tracheal deviation away from the side of the injury
- Unilateral absence of breath sounds
- Unilateral hyperresonant note on percussion
- Elevated hemithorax without respiratory movement
- Neck vein distention
- Cyanosis (late manifestation)
- When ultrasound is available, tension pneumothorax can be diagnosed using an extended FAST (eFAST) examination. However tension pneumothorax is a clinical diagnosis; do not delay treatment to obtain radiologic confirmation.
- Management:
- Tension pneumothorax requires immediate decompression and may be managed initially by rapidly inserting a large over-the-needle catheter into the pleural space.
- Due to the variable thickness of the chest wall, kinking of the catheter, and other technical or anatomic complications, needle decompression may not be successful. In this case, finger thoracostomy is an alternative approach.
- Recent evidence supports placing the large, over-the-needle catheter at the fifth intercostal space, slightly anterior to the midaxillary line (rather than the second intercostal space in the midclavicular line).
- Successful needle decompression converts tension pneumothorax to a simple pneumothorax. However, there is a possibility of subsequent pneumothorax as a result of the manoeuvre, so continual reassessment of the patient is necessary.
- Tube thoracostomy is mandatory after needle or finger decompression of the chest.
Open pneumothorax
- Pathophysiology:
- Large injuries to the chest wall that remain open can result in an open pneumothorax, also known as a sucking chest wound. Equilibration between intrathoracic pressure and atmospheric pressure is immediate. Because air tends to follow the path of least resistance, when the opening in the chest wall is approximately two-thirds the diameter of the trachea or greater, air passes preferentially through the chest wall defect with each inspiration. Effective ventilation is thereby impaired, leading to hypoxia and hypercarbia.
- Diagnosis:
- Open pneumothorax is commonly found and treated at the scene by prehospital personnel.
- The clinical signs and symptoms are pain, difficulty breathing, tachypnoea, decreased breath sounds on the affected side, and noisy movement of air through the chest wall injury.
- Management:
- For initial management of an open pneumothorax, promptly close the defect with a sterile dressing large enough to overlap the wound’s edges.
- Any occlusive dressing (e.g. plastic wrap or petrolatum gauze) may be used as temporary measure to enable rapid assessment to continue. Tape it securely on only three sides to provide a flutter-valve effect. As the patient breathes in, the dressing occludes the wound, preventing air from entering. During exhalation, the open end of the dressing allows air to escape from the pleural space. Taping all four edges of the dressing can cause air to accumulate in the thoracic cavity, resulting in a tension pneumothorax unless a chest tube is in place.
- Place a chest tube remote from the wound as soon as possible.
- Subsequent definitive surgical closure of the wound is frequently required.
Massive haemothorax
- Pathophysiology:
- Massive haemothorax results from the rapid accumulation of more than 1500 mL of blood or one-third or more of the patient’s blood volume in the chest cavity.
- Mechanism of injury:
- It is most commonly caused by a penetrating wound that disrupts the systemic or hilar vessels, although massive haemothorax can also result from blunt trauma.
- Diagnosis:
- In patients with massive haemothorax, the neck veins will be flat due to severe hypovolaemia. Rarely will the mechanical effects of massive intrathoracic blood shift the mediastinum enough to cause distended neck veins.
- A massive haemothorax is suggested when shock is associated with the absence of breath sounds or dullness to percussion on one side of the chest.
- Management:
- Massive haemothorax is initially managed by simultaneously restoring blood volume and decompressing the chest cavity.
- Establish large caliber intravenous lines, infuse crystalloid, and begin transfusion of uncrossmatched or type-specific blood as soon as possible.
- When appropriate, blood from the chest tube can be collected in a device suitable for autotransfusion.
- A single chest tube (28-32 French) is inserted, usually at the fifth intercostal space, just anterior to the midaxillary line, and rapid restoration of volume continues as decompression of the chest cavity is completed.
- The immediate return of 1500 mL or more of blood generally indicates the need for urgent thoracotomy.
- Patients who have an initial output of less than 1500 mL of fluid, but continue to bleed, may also require thoracotomy. This decision is based on the rate of continuing blood loss (200 mL/hr for 2 to 4 hours), as well as the patient’s physiologic status and whether the chest is completely evacuated of blood. Again, the persistent need for blood transfusion is an indication for thoracotomy.
- During patient resuscitation, the volume of blood initially drained from the chest tube and the rate of continuing blood loss must be factored into the resuscitation required.
- Colour of the blood (indicating an arterial or venous source) is a poor indicator of the necessity for thoracotomy.
- Penetrating anterior chest wounds medial to the nipple line and posterior wounds medial to the scapula (the mediastinal “box”) should alert the practitioner to the possible need for thoracotomy because of potential damage to the great vessels, hilar structures, and the heart, with the associated potential for cardiac tamponade.
- Do not perform thoracotomy unless a surgeon, qualified by training and experience, is present.
Cardiac tamponade
- Pathophysiology:
- Cardiac tamponade is compression of the heart by an accumulation of fluid in the pericardial sac. This results in decreased cardiac output due to decreased inflow to the heart. The human pericardial sac is a fixed fibrous structure, and a relatively small amount of blood can restrict cardiac activity and interfere with cardiac filling.
- Mechanism of injury:
- Cardiac tamponade most commonly results from penetrating injuries, although blunt injury also can cause the pericardium to fill with blood from the heart, great vessels, or epicardial vessels.
- Diagnosis:
- Cardiac tamponade can develop slowly, allowing for a less urgent evaluation, or rapidly, requiring rapid diagnosis and treatment.
- The classic clinical triad of muffled heart sounds, hypotension, and distended veins is not uniformly present with cardiac tamponade. Muffled heart tones are difficult to assess in the noisy resuscitation room, and distended neck veins may be absent due to hypovolaemia.
- Kussmaul’s sign (i.e. a rise in venous pressure with inspiration when breathing spontaneously) is a true paradoxical venous pressure abnormality that is associated with tamponade.
- PEA is suggestive of cardiac tamponade but can have other causes.
- Focused assessment with sonography for trauma (FAST) is a rapid and accurate method of imaging the heart and pericardium that can effectively identify cardiac tamponade. Remember that tamponade can develop at any time during the resuscitation phase, and repeat FAST exams may be necessary. Providers experienced in ultrasonography may also be able to assess myocardial dysfunction and ventricular filling.
- Additional methods of diagnosing cardiac tamponade include echocardiography and/or pericardial window, which may be particularly useful when FAST is unavailable or equivocal.
- Management:
- When pericardial fluid or tamponade is diagnosed, emergency thoracotomy or sternotomy should be performed by a qualified surgeon as soon as possible.
- Administration of intravenous fluid will raise the patient’s venous pressure and improve cardiac output transiently while preparations are made for surgery.
- If surgical intervention is not possible, pericardiocentesis can be therapeutic, but it does not constitute definitive treatment for cardiac tamponade.
- When subxiphoid pericardiocentesis is used as a temporising manoeuvre, the use of a large, over-the needle catheter or the Seldinger technique for insertion of a flexible catheter is ideal, but the urgent priority is to aspirate blood from the pericardial sac.
- Because complications are common with blind insertion techniques, pericardiocentesis should represent a lifesaving measure of last resort in a setting where no qualified surgeon is available to perform a thoracotomy or sternotomy.
- Ultrasound guidance can facilitate accurate insertion of the large, over-the-needle catheter into the pericardial space.
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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 |
