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Chapter6 thoracic trauma
1. International Trauma Life Support
for Emergency Care Providers
CHAPTER
eighth edition
International Trauma Life Support for Emergency Care Providers, Eighth Edition
John Campbell • Alabama Chapter, American College of Emergency Physicians
Thoracic Trauma
6
Key Lecture Points
Briefly review the anatomy of the chest, particularly the great vessels.
Emphasize load-and-go conditions in particular the deadly dozen and discuss why these conditions are so critical:
Massive hemothorax with shock: Explain that when massive hemothorax has occurred, as evidenced by dullness to percussion and diminished breath sounds in the base of the affected lung, massive hemorrhage has occurred into the chest with major blood vessel disruption and massive blood loss. If these patients are not rapidly taken to surgery, they usually die.
Tension pneumothorax: Explain how the increased pressure in the chest reduces blood return to the heart, causing reduction in cardiac output, and thus producing shock. Stress the signs and symptoms of the tension pneumothorax (review the Primary Survey) and how critical it is not to leave out steps in the Primary Survey, which would prevent the identification of this problem.
Penetrating chest trauma with shock: Explain that the penetrating chest injury with resulting evidence of shock is a load-and-go situation because of the many serious and potentially lethal conditions that may result.
Discuss the mechanics of airflow during inspiration and expiration. Discuss how the presence of an open wound into the pleural space decreases air movement through the tracheobronchial tree.
Discuss the pathophysiology of the flail chest and the management of this problem: Assisted ventilation and prevention of movement of the flail segment if it is decreasing air movement through the tracheobronchial tree. Stress that hand stabilization is usually adequate until the patient is moved into the ambulance. Point out that nasotracheal intubation (patient usually has a gag reflex) is the most effective method to stabilize the flail and oxygenate the patient.
A review of the mechanism of injury in chest trauma is appropriate. Stress the importance of anticipating serious chest trauma or the potential for life-threatening injury even before deterioration has occurred. This is particularly important in those patients with evidence of major chest trauma.
Many vital organs are crowded into this area.
Trauma to this area is often life-threatening.
Bony cavity is formed by 12 pairs of ribs, which join posteriorly with the thoracic spine and anteriorly with the sternum.
Intercostal neurovascular bundle runs along inferior surface of each rib.
Inner side of cavity and lung itself are lined with thin layer of tissue, pleura. The space between pleural layers is normally only a potential space.
One lung occupies each thoracic cavity.
Between the two cavities is mediastinum, which contains heart, aorta, superior and inferior vena cava, trachea, major bronchi, and esophagus. (High potential for life-threatening injury because of vital cardiovascular and tracheobronchial structures within this area)
Spinal cord is protected by vertebral column.
Diaphragm separates thoracic organs from abdominal cavity. Upper abdominal organs, including spleen, liver, kidneys, pancreas, and stomach, are protected by lower rib cage.
In the trimodal distribution of trauma deaths (immediate, hours, weeks), injuries to the chest are responsible for most deaths at the scene (immediate deaths) and those within a few hours (early deaths).
Inadequate oxygen delivery to tissues secondary to airway obstruction
Hypovolemia from blood loss
Ventilation/perfusion mismatch from lung parenchymal injury
Changes in pleural pressures from tension pneumothorax
Pump failure from severe myocardial injury
Major symptoms are shortness of breath and chest pain.
Mechanism of injury is also a sign of chest injury or gives us a strong index of suspicion for the potential of major injury.
NOTE: Management of airway has been discussed in Chapter 4, so nothing further will be added here other than to stress its importance.
IMAGE: Figure 6-5: Flail chest anatomy.
IMAGE: Figure 6-6: Flail chest physiology.
NOTE: See also Figure 6-13.
Flail chest: Three or more adjacent ribs are fractured in at least two places, resulting in a segment of the chest wall that is not in continuity with thorax.
A lateral flail chest or anterior flail chest (sternal separation) may result.
With posterior rib fractures, heavy musculature usually prevents the occurrence of a flail segment.
If patient is breathing spontaneously, flail segment moves with paradoxical motion relative to rest of chest wall.
Multiple rib fractures with or without flail chest can cause hypoxia from mechanical ventilatory problems as well as pulmonary contusion. Patient, especially if older, must be closely monitored for hypoxia and respiratory failure.
Monitoring with pulse oximetry and capnography is very helpful.
Intubation and positive pressure ventilation are best stabilization. This is usually not possible, as patient is usually awake with an intact gag reflex.
Flail may contribute to development of pulmonary contusion, hemothorax, pneumothorax.
Consider intubation early in order to provide positive end-expiratory pressure.
Continuous positive airway pressure (CPAP) could be used in non-intubated patient.
NOTE: See also Figure 6-10.
Normal ventilation involves negative pressure being generated inside chest by diaphragmatic contraction.
As air is drawn through upper airway, lungs expand.
With a large open chest wound (larger than trachea or about size of patient's little finger), the path of least resistance for airflow is through the chest wall defect.
Air going in and out of this opening makes a sucking sound, and bubbles on expiration.
This air will enter only pleural dead space. It will not enter the lung and therefore will not contribute to oxygenation of blood. Ventilation is impaired, and hypoxia results.
Use impervious material taped on three sides.
Consider the collection of drainage when deciding which sides to tape.
The Asherman chest seal can be used to seal a sucking chest wound or can be placed over a decompressing needle.
Monitor SaO2 and eTCO2.
IMAGE: Figure 6-14: Massive hemothorax.
NOTE: See also Table 6-1.
Discuss pathophysiology and diagnosis.
Blood in pleural space is a hemothorax.
A massive hemothorax occurs as a result of at least a 1,500 mL blood loss into thoracic cavity. Each thoracic cavity may contain up to 3,000 mL of blood.
As blood accumulates within the pleural space, the lung on the affected side is compressed. If enough blood accumulates (rare), the mediastinum will be shifted away from the hemothorax. The inferior and superior vena cava and contralateral lung are compressed. Thus, ongoing blood loss is complicated by hypoxemia.
Fluid administration to increase blood pressure may increase bleeding.
Titration of fluid resuscitation is important.
If tension hemopneumothorax develops, acute chest decompression is required.
IMAGE: Figure 6-15: Tension pneumothorax.
NOTE: See also Figure 6-19.
Tension pneumothorax is a circulatory (obstructive) emergency.
Occurs when a one-way valve is created from either blunt or penetrating trauma. Air can enter but not leave pleural space.
This causes an increase in intrathoracic pressure, which will collapse the affected lung and will then exert pressure on the mediastinum.
This pressure will eventually collapse the superior and inferior vena cava, resulting in a loss of venous return to the heart.
A shift of the trachea and mediastinum away from the side of the tension pneumothorax will also compromise ventilation of other the lung, although this is a late phenomenon and usually cannot be detected except by x-ray.
NOTE: Decompression is discussed in skill station.
Stress that loss of breath sounds on one side does not make a diagnosis of tension pneumothorax.
A needle decompression is a temporary, but life-saving, measure.
If within scope of practice, consider chest tube, chest decompression catheter or finger thoracostomy.
IMAGE: Figure 6-17: Cardiac tamponade.
Discuss pathophysiology and diagnosis.
The pericardial sac is an inelastic membrane that surrounds the heart. If blood collects rapidly between heart and pericardium from a cardiac injury, ventricles of the heart will be compressed. A small amount of pericardial blood may compromise cardiac filling. As compression of ventricles increases, the heart is less able to refill, and cardiac output falls.
Fluid administration may increase bleeding.
If available, perform a 12-lead ECG (including V4R).
IMAGE: Figure 6-20: Myocardial contusion.
Myocardial contusion is a potentially lethal lesion resulting from blunt chest injury.
The chest pain may be difficult to differentiate from associated musculoskeletal discomfort that patient also suffers as a result of injury.
If available a 12-lead ECG should be performed.
Traumatic thoracic aortic tears usually are due to deceleration injury with heart and aortic arch moving suddenly anteriorly (third collision), transecting the aorta where it is fixed at ligamentum arteriosum.
In 10%–20% of patients who do not exsanguinate (promptly) suggest immediately, the aortic tear will be contained temporarily by surrounding tissues and adventitia. However, this will usually rupture within hours unless surgically repaired.
NOTE: Hypertension in upper extremities and hypotension in lower extremities (as assessed by pulse strength) are rare.
NOTE: This may be one occasion when a main stem intubation would be beneficial.
NOTE: Scaphoid: “sucked in,” comma shaped.
Tears in diaphragm may result from a severe blow to abdomen.
A sudden increase in intra-abdominal pressure, such as a seat-belt injury or kick to abdomen, may tear diaphragm and allow herniation of abdominal organs into the thoracic cavity.
Occurs more commonly on left than right, as the liver protects right hemidiaphragm.
Blunt trauma produces large radial tears in diaphragm.
Penetrating trauma may also produce holes in diaphragm, but these tend to be small.
A very common chest injury resulting from blunt trauma, a pulmonary contusion takes hours to develop and rarely develops during prehospital care, unless very long transport times or delayed discovery of victim occurs.
Contusion of lung may produce marked hypoxemia.
Management consists of intubation and/or assisted ventilation if indicated, oxygen administration, transport, and IV insertion.
With the increase in terrorism, understanding blast injury is important. The magnitude of the blast wave depends on the size of the explosion and the environment in which it occurs. Closed spaces, such as buses, produce highly lethal blast injury.
The mechanism of injury by explosions is due to three and potentially five factors:
Primary—initial air blast
Secondary—shrapnel
Tertiary—body thrown
Quaternary—thermal burns
Quinary—hyperinflammatory state (dirty bomb)
IMAGE: Figure 6-21: Traumatic asphyxia. Cervical collar can cause compression of the swollen neck and should be avoided.
Pneumothorax is caused by accumulation of air within the potential space between visceral and parietal pleura.
Lung may be totally or partially collapsed as air continues to accrue in thoracic cavity.
In a healthy patient, this should not acutely compromise ventilation, if there is not a large pneumothorax or a tension pneumothorax does not evolve.
Patients with less respiratory reserve may not tolerate even a simple pneumothorax.
