Thoracic Trauma

Reviewed and revised 3 May 2017

OVERVIEW

Assessment of thoracic trauma requires the identification of immediately life-threatening injuries on primary survey, and delayed life threats on secondary survey.

  1. Primary survey
  2. Resuscitation
  3. Secondary survey
  4. Diagnostic evaluation
  5. Definitive care

PRIMARY AND SECONDARY SURVEY

A widely used mnemonic for the 6 killer conditions to think of, and actively search for, during the primary survey is ATOM-FC:

  • Airway obstruction or disruption
  • Tension pneumothorax
  • Open pneumothorax
  • Massive haemothorax
  • Flail chest
  • Cardiac tamponade

With a little bit of contortion, potentially life-threatening chest injuries can also be remembered using ATOM-FC:

  • Aortic injury
  • Thorax injuries (non-massive hemothorax, simple pneumothorax)
  • Oesphageal perforation
  • Muscular diaphragmatic injury (a stretch this one, I know)
  • Fistula (bronchopleural) and other tracheobronchial injury
  • Contusion to the heart or lungs

Primary survey

AIRWAY OBSTRUCTION OR DISRUPTION

Recognition

  • External neck deformity or hematoma, crepitus from laryngeal fracture, surgical emphysema, hoarse voice or gurgling
  • Complete airway obstruction — silent chest, paradoxical chest movements
  • Partial airway obstruction — stridor, respiratory distress
  • Cyanosis

Management

  • High flow oxygen 15 L/min via non-rebreather mask
  • Use airway maneuvers and adjuncts to attempt to achieve airway patency (jaw-thrust, suction, oropharyngeal airway) and rapidly proceed to definitive airway if airway disruption confirmed
  •  Surgical airway may be required as endotracheal intubation with direct laryngoscopy may not be possible due to distorted anatomy
  • If a disrupted airway is visible through an open neck wound attempt to secure the distal trachea with forceps (retraction) and intubate through the wound (consider using a bougie)
  • Will need bronchoscopy / thoracotomy

TENSION PNEUMOTHORAX

  • Simple pneumothorax converts to a tension pneumothorax if the lung defect acts as a one way valve, which allows ongoing air leak into pleural space without letting it leak back out
  • Tension pneuothorax can be rapidly fatal as intra-thoracic pressure rises cause decreased venous return and kinking of great vessels resulting in obstructive shock
  • Have a high index of suspicion in any tachycardic and hypotensive patient — clinical features may not be obvious

Recognition

  • Anxiety and agitation
  • Respiratory distress
  • Tachycardia, hypotension
  • Neck vein distension
  • Ipsilateral hyperexpansion and decreased chest movement
  • Tracheal deviation to the contra-lateral side
  • Hyper-resonance ipsilaterally
  • Decreased breath sounds ipsilaterally
  • Bedside ultrasound can rapidly confirm pneumothorax

Management

  • High flow oxygen to maintain SpO2 target (e.g. 15L/min via non-rebreather mask)
  • Immediate needle thoracocentesis or finger thoracostomy (‘decompression’).
  • Proceed to formal intercostal catheter after needle decompression

OPEN PNEUMOTHORAX

  • Open pneumothorax is essentially a ‘sucking chest wound’
  • It is thought that once a chest wound is >2/3rds the diameter of the trachea, air will enter wound preferentially

Recognition

  • Open wound on chest wall
  • Anxiety and agitation
  • Respiratory distress
  • Tachycardia
  • Decreased chest movement ipsilaterally
  • Hyper-resonance ipsilaterally
  • Decreased breath sounds ipsilaterally
  • Bedside ultrasound can rapidly confirm pneumothorax

Management

  • High flow oxygen to maintain SpO2 target (e.g. 15L/min via non-rebreather mask)
  • Cover with occlusive 3-sided dressing to form a ‘flutter valve’ that allows the egress of air through the wound but prevents ‘sucking in’.
  • Place formal catheter in separate intercostal space
  • Will need formal exploration prior to closing

MASSIVE HAEMOTHORAX

  • Massive hemothorax can result from either blunt or penetrating trauma
  • The source of bleeding can be from the lungs, major vessels, intercostal vessels or even the heart

Massive hemothorax is defined by the need for thoracotomy — the indications are:

  • Blood loss > 1,500 mL or 1/3rd of blood volume
  • Blood loss >200 mL/h (3 mL/kg/h) for 2-4 hours

Recognition

  • Anxiety and agitation
  • Hemorrhagic shock — pallor, tachycardia, hypotension, cool peripheries
  • External evidence of thoracic injury
  • Decreased chest movement ipsilaterally
  • Ipsilateral dullness
  • Decreased breath sounds ipsilaterally
  • Persistent blood loss following intercostal catheter insertion
  • Bedside ultrasound can rapidly confirm the presence of significant pleural fluid  — to see on erect chest requires 250mL of blood

Management

  • High flow oxygen to maintain SpO2 target (e.g. 15L/min via non-rebreather mask)
  • Treat with rapid restoration of blood volume combined with concurrent drainage of thorax
  • Immediate intercostal catheter insertion (re-expanding lung may tamponade the bleeding vessels)
  • Hemostatic resuscitation — activate massive transfusion protocol, use of an autotransfuser is ideal
  • Thoracotomy
  • If develops from blunt chest trauma may be able to consider embolisation

FLAIL CHEST

  • A flail chest is defined as fractures of 2 or more contiguous ribs in 2 or more locations
  • This results in a segment of the chest wall (the ‘flail’) that is no longer in continuity with the rest of the thoracic cage
  • Paradoxical movement results, the segment moves inwards on inspiration as the rest of the chest expands and outwards on expiration as the rest of the chest deflates
  • Rib fractures on opposite sides of the chest can result in a ‘central flail’ involving the sternum

Recognition

  • Chest pain
  • Respiratory distress
  • Boney crepitus
  • Paradoxical chest wall movements of the affected segment (not apparent if positive pressure ventilation applied)

Management

  • High flow oxygen to maintain SpO2 target (e.g. 15L/min via non-rebreather mask)
  • Analgesia
    • paracetamol 1g qid po, NSAIDs if not contraindicated, titrated opiates IV (e.g. fentanyl 25 micrograms q5min prn IV), ketamine infusion
    • consider adjunctive medications (e.g. pregabalin, tapentadol)
    • Early use of regional anesthesia (e.g. intercostal nerve blocks, paravertebral block, epidural anesthesia) due to risk of respiratory depression
  • Respiratory monitoring and support
    • close monitoring of SaO2, respiratory effort, and ABGs is important as patients tend to gradually deteriorate and may require intubation and mechanical ventilation
    • may benefit from non-invasive ventilation
  • Surgical intervention
    • selected patients may benefit from rib fixation (e.g. failure of analgesia and non-surgical interventions prior to intubation, or failure to wean from mechanical ventilation)

CARDIAC TAMPONADE

  • Pericardial tamponade is more common in penetrating thoracic trauma than blunt trauma
  • As little as 75 mL of blood accumulating in the pericardial space acutely can impair cardiac filling, resulting in tamponade and obstructive shock

Recognition

  • Anxiety and agitation
  • Obstructive shock — tachycardia, hypotension, cool peripheries
  • Beck’s triad: muffled heart sounds, hypotension and distended neck veins — not especially in a noisy trauma bay!
  • Pulsus paradoxus (drop in systolic blood pressure >10 mmHg on inspiration)
  • Very hard to differentiate clinically from tension pneumothorax and needs to be actively sought
  • Mostly diagnosed following identification of a pericardial effusion on bedside ultrasound as part of the FAST exam  leading to formal echocardiography

Management

  • High flow oxygen to maintain SpO2 target (e.g. 15L/min via non-rebreather mask)
  • May transiently respond to fluid challenge
  • Needle pericardiocentesis, preferably ultrasound guided, may be lifesaving may be life-saving but may fail due to clotted blood
  • Pericardotomy is definitive treatment
  • Emergency thoracotomy may be necessary in the event of cardiac arrest

Secondary survey

AORTIC AND GREAT VESSEL INJURY

  • Aortic disruption in trauma typically involves a tear on the aortic wall due to acceleration-deceleration forces
  • May result from penetrating (usually succumb in the field) or blunt injury
  • Those that make it to hospital may only have the outer aortic wall layer, the adventitia, intact containing a hematoma

Recognition

  • Conscious patients may experience tearing chest and back pain. Neurological deficits may also be present (e.g. dissection involvement origins of carotid arteries, spinal arteries, etc)
  • Clinical signs (such as differences in blood pressure and pulses between the upper limbs) are unreliable.
  • Suspect based on mechanism and the presence of other injuries (e.g. fractures of the sternum, upper ribs and scapula)
  • Look for features of aortic dissection on CXR (especially widened mediastinum) — though these are often absent
  • Essential to have a low threshold for definitive test: CT angiogram of the aorta
  • Pericardial tamponade or an aortic dissection flap may be seen on echocardiography (TOE is more sensitive than TTE)

Management

  • High flow oxygen 15L/min via non-rebreather mask
  • Avoid excessive fluid resuscitation
  • Lower the pulse rate to decrease aortic shear forces by commencing beta blockade (e.g. titrated esmolol infusion) then commence GTN infusion to aiming for systolic blood pressure of 90-100 mmHg and adequate tissue perfusion
  • Definitive treatment is surgery, stenting or both

SIMPLE PNEUMOTHORAX

Recognition

  • Evidence of thoracic trauma
  • Hyper-resonance ipsilaterally
  • decreased breath sounds ipsilaterally
  • Bedside ultrasound can rapidly confirm pneumothorax
  • CT chest may diagnose small pneumothoraces not seen on CXR

Management

  • High flow oxygen 15L/min via non-rebreather mask
  • Small traumatic pneumothoraces may only require observation
  • Significant simple pneumothoraces require intercostal catheter insertion, especially if the patient require intubation due to the risk of conversion to tension pneumothorax.

NON-MASSIVE HAEMOTHORAX

Recognition

  • Respiratory distress, ipsilateral dullness
  • On supine CXR films will appear as simply a veiling
  • Bedside ultrasound can rapidly confirm fluid in the pleural space

Management

  • High flow oxygen 15L/min via non-rebreather mask
  • Intercostal catheter insertion (re-expansion of the ipsilateral lung may help tamponade bleeding vessels and ongoing blood loss can be monitored)

OESOPHAGEAL PERFORATION

  • Traumatic esophageal perforation is usually caused by penetrating trauma

Recognition

  • Chest or epigastric pain, dysphagia, hematemesis
  • Neck and/or chest wound
  • Surgical emphysema
  • Pleural effusion, especially on left side (CXR or bedside ultrasound)
  • Drainage of gastrointestinal contents from an intercostal catheter
  • Shock (sepsis ensues if delayed presentation due to GI contents in the thoracic cavity)

Management

  • High flow oxygen 15L/min via non-rebreather mask
  • Fluid resuscitation
  • Nasogastric tube on free drainage
  • Broad spectrum antibiotics
  • Formal surgical repair

DIAPHRAGMATIC INJURY

  • Diaphragmatic injuries may occur from either blunt or penetrating trauma (especially on the left side) and are easily missed.
  • Blunt injury causes radial tears that tend to allow herniation of abdominal structures into the thoracic cavity early.
  • Penetrating injuries can cause small defects that don’t present with herniation until years later.

Recognition

  • Suspect with any penetrating injury that could extend to between the T4 and T12 levels
  • Suspect with severe blunt trauma to the torso, especially if there were compressive or rapid deceleration forces
  • May be asymptomatic initially
  • Abdominal pain, guarding and/or rigidity
  • Cardiovascular and/or respiratory compromise may occur if abdominal contents herniate into the thoracic cavity
  • Herniation may be detected by hearing bowel sounds on chest auscultation, or by CXR (NG tube tip may extend into the thoracic cavity) or bedside ultrasound
  • Diagnosis of diaphragmatic rupture is usually on multidetector CT, though even a normal CT does not rule out the diagnosis
  • Laparoscopy or open exploration are the gold standard for diagnosis

Management

  • Laparoscopy or thoracoscopy if suspected
  • Most require formal surgical repair

TRACHEOBRONCHIAL INJURY

  • Tracheobronchial injury usually occurs close to the carina, and is associated with severe blunt trauma

Recognition

  • Hemoptysis, cough and respiratory distress
  • Subcutaneous emphysema
  • Pneumothorax with persistent air leak after correct placement of an intercostal catheter (continues to bubble vigorously with little resolution of pneumothorax)

Management

  • High flow oxygen 15 L/min via non-rebreather mask
  • Multiple intercostal catheters may be required
  • Urgent bronchoscopy and operative intervention

PULMONARY CONTUSION AND OTHER INJURIES

  • Pulmonary contusion can occur with any significant thoracic injury.
  • Lung hemorrhage and pulmonary edema leads to impaired gas exchange and respiratory insufficiency.
  • Lesions may progress over hours to days (e.g. peak at 72 hours then resolve over 7 days) then gradually improve.

Recognition

  • Suspect in any significant thoracic trauma
  • May occur in small children in the absence of fractures due to the high compliance of the chest wall
  • Respiratory distress, hemoptysis, cyanosis
  • Decreased breath sounds and crackles in the affected lung area
  • Hypoxia and/ or hypercapnia on ABG
  • Pulmonary contusions are detectable on bedside ultrasound
  • Alveolar opacities on CXR
  • MAy be complicated by nosocomial pneumonia

Management

  • High flow oxygen 15 L/min via non-rebreather mask
  • ‘Fluid restriction’ may reduce size of contusion but may not affect outcomes
  • Analgesia for pain from associated thoracic injuries, which may impair respiratory function
  • Respiratory support — severe cases require intubation and mechanical ventilation
  • Pulmonary lacerations may be managed conservatively with an intercostal catheter, thoracotomy and lung repair may be required

CARDIAC CONTUSION AND OTHER INJURIES

  • spectrum of injury from minor enzyme rises to fulminant cardiac failure and lethal cardiac rupture

Recognition

  • Suspect if severe blunt trauma with fractures of the sternum, ribs and/ or thoracic vertebrae
  • Chest pain
  • Persistent unexplained tachycardia
  • pericardial injury: can produce herniation and cardiac dysfunction
  • valvular: aortic > mitral > tricuspid + pulmonary valves; results in murmurs and heart failure
  • septal injury: loud holosystolic murmur
  • Suspect cardiac contusion if any underlying ECG abnormality, including any arrhythmia, conduction defect or ischaemic changes such as ST segment deflections and T wave changes
  • Troponin doesn’t alter management

Management

  • Cardiology consult and admission for cardiac monitoring and echocardiogram
  • medical management/PCI/stent/ CABG for coronary artery injury
  • cardiac surgery may be required for valvular dysfunction and penetrating injuries
  • emergency thoracotomy may be required in the event of a cardiac arrest

OTHER CHEST WALL INJURIES

Rib fractures

  • multiple rib #’s, 1st and 2nd rib and scapular fractures = high energy -> need good analgesia

Sternal fracture

  • consider cardiac injury, though rare with isolated sternal fractures

References and Links

LITFL

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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