Pulmonary Contusion

Etiology

Any chest trauma, blunt, penetrating, or a combination of both, can cause a pulmonary contusion. Other identified causes include explosions, assaults, falls from great heights, motor vehicle accidents, and sports collisions.[4][5] Severe chest injuries often lead to sternal fractures. However, minor chest trauma in older adults tends to produce lung contusions.[6] Pulmonary contusion is a common complication of rib fractures.[7] 

Epidemiology

The true prevalence of pulmonary contusions is unknown, as most studies may have selection bias due to the inclusion of small server case samples. However, pulmonary contusions are the most commonly identified lung injuries (30% to 75%) in blunt chest trauma cases, with a mortality rate of 10 to 25%.[8] Blunt thoracic injuries are the second leading cause of death after head and spinal cord injuries.[9][10] Pulmonary contusion is the second leading injury associated with sternal fractures, accounting for a third of cases.[11][12] Though scapular fractures are rare, more than 90% are associated with severe injuries and pulmonary contusion.[13]

Pathophysiology

The pathophysiology of pulmonary contusion is poorly understood. What is known, however, is that the injury disrupts the blood-air barrier, resulting in leakage of blood and interstitial fluids into the alveolar and interstitial spaces. Fluid in the alveolar space produces alveolar edema and decreases the amount of lung surfactant, resulting in alveolar collapse and atelectasis. Decreased lung compliance, ventilation-perfusion mismatch, and intra-pulmonary shunting result from the tissue damage.[14]

Ventilation of the affected lung is impaired as oxygenated air cannot enter the fluid-filled alveoli during inspiration. Reduced oxygenation leads to reflex vasoconstriction and decreased perfusion, resulting in hypoxemia and hypercapnia.[15][16]

Pulmonary contusion activates the immune system, resulting in tissue macrophage activation and leucocyte migration. The production of cytokines, chemokines, arachidonic acid metabolites, oxygen radicals, and complement in the injury site increases. The coagulation cascade is also activated.[17] 

The increased inflammatory response impairs neutrophilic apoptosis and increases alveolar epithelial apoptosis. Severe inflammation may cause Acute Respiratory Distress Syndrome (ARDS). Edema and inflammation may also develop in the contralateral intact chest. Concurrent aspiration of gastric acid can complicate a pulmonary contusion by further injuring the lungs and worsening ARDS.[18]

Pulmonary contusion has three possible mechanisms:[19]

• The spalling effect - occurs when a pressure wave encounters a liquid-gas interface like the alveolar wall, thus disrupting the cells' lipid membranes and increasing membrane permeability.
• The inertial effect - tissues with different densities accelerate or decelerate pressure waves at different rates, stripping lighter alveoli away from denser bronchial tissue.
• The implosion effect - happens when a pressure wave encounters tissues with air bubbles and compresses the gas within the tissues. The rebound force overstretches and tears tissues.

Pulmonary contusions can lead to respiratory failure and death.

Histopathology

Pulmonary hemorrhage may be associated with pulmonary contusion. Alveolar or interstitial fluid accumulation was found in World War II soldiers' lung tissue samples, though this finding was initially attributed to fluid resuscitation. Recent animal models have identified interstitial hemorrhage with edema and inflammatory cell infiltration in patients with lung contusion.[20]

History and Physical

Patients with severe chest injuries may present unresponsive, apneic, and pulseless. After a quick primary survey, resuscitation must be started for these individuals regardless of the cause. Once stable, a secondary survey may be initiated.

Pulmonary contusion presents variably, depending on the severity of the condition. Breathing difficulty, chest pain, and hemoptysis may be elicited in patients with severe pulmonary contusion. Individuals with mild injury may be asymptomatic. A history of trauma typically precedes the symptoms, warranting an investigation for concurrent injuries. 

Patients with severe pulmonary contusion are tachypneic, tachycardic, and visibly in respiratory distress in the early stages. Oxygen saturation is low. Chest retractions, jugular distension, and cyanosis may also be observed. Auscultation will reveal decreased breath sounds. Injuries to other parts of the body may also be noted. Cardiorespiratory decompensation may occur in the advanced stages of a pulmonary contusion. Patients may present with hypotension, bradypnea or apnea, altered sensorium, and bradycardia.

In severe contusion, symptoms appear within hours. In mild injury, symptoms may develop gradually over 24 to 48 hours.[21][37]

Evaluation

A detailed history of the injury, thorough physical examination, and imaging can aid in diagnosing pulmonary contusion. The imaging techniques include radiography of the chest, computer tomography (CT) scans, and ultrasound.

The chest x-ray is the most commonly used diagnostic imaging technique (see Image. Pulmonary Contusion Radiograph). However, the image's interpretation may be difficult as lung anatomical boundaries do not limit pulmonary contusions. The presence of a pneumothorax or hemothorax may obscure other injuries. Contusion signs may not appear on chest x-rays immediately after the injury and may be delayed for 6 to 48 hours.[22]

A mild contusion appears as ground-glass haziness on a chest x-ray, while severe disease may mimic pneumonia consolidation.[23] However, pneumonia consolidation is confined to specific areas, while pulmonary contusions can cross fissures. Computed tomography (CT) is recommended if the chest x-ray is equivocal.[24] 

A chest CT scan is more sensitive in diagnosing pulmonary contusion than plain films. A higher CT resolution can detect contusion immediately after trauma.[25] A three-dimensional chest CT reconstruction can quantify the contusion volume and help identify individuals at higher risk of ARDS. Patients with contusion volumes of at least 20% have severe disease and are more likely to develop ARDS and pneumonia than patients with contusion volumes of less than 20%.[26] 

An ultrasound is a vital bedside imaging tool that can help clinicians quickly identify pulmonary contusion if a chest x-ray or CT cannot be obtained immediately (see Image. Pulmonary Contusion On Ultrasound). The focused assessment with sonography for trauma (FAST) exam is a normal part of the initial trauma assessment but is limited to the pericardium and peritoneum. Extended FAST (E-FAST) includes a chest exam.[27] E-FAST can help expedite management planning for patients with pulmonary contusions.[28]

Electrocardiography (ECG) is indispensable when evaluating patients with blunt chest injuries, with or without suspicion of a pulmonary pathology. Cardiac contusion, which is rapidly fatal, is also likely in such cases. For example, a precordial blow during a sports collision can trigger an arrhythmia such as ventricular fibrillation, resulting in a fatal condition called "commotio cordis."[29] 

Treatment / Management

Most pulmonary contusions require supportive therapy until the injury heals. Continuous close monitoring is necessary because contusions can evolve even 24 to 48 hours after trauma. The management goal should be respiratory insufficiency prevention. Patients must be given appropriate pain control to avoid splinting chest muscles and allow lung expansion. 

Supportive Care

Postural drainage, suctioning, chest physiotherapy, incentive spirometry, encouraging coughing, and deep breathing help prevent atelectasis. Addressing associated injuries like rib and sternal fractures is also paramount. Pain control can reduce pulmonary morbidity by allowing lung expansion and preventing atelectasis.[30]

Pulmonary contusion is an independent predictor of the need for tracheal intubation in chest trauma.[31] Ventilation settings must be chosen carefully to keep the alveoli patent and recruit more alveoli while preventing barotrauma. Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) may be provided to patients who do not require intubation. (B2)

Prone positioning of the patient with contusion reduces pressure on the diaphragm. Additionally, positioning the contused lung in a non-dependent position helps recruit alveoli. Noninvasive ventilation (NIV) is relatively contraindicated in patients with impaired consciousness, as it can cause gastric distention and aspiration.[32]  

Invasive ventilation is required if positive pressure ventilation fails. However, large tidal volumes can increase the risk of barotrauma. Starting with a low tidal volume is recommended.[33] 

Diuretics can reduce pulmonary venous resistance and pulmonary capillary hydrostatic pressure. If fluid therapy is required to maintain euvolemia, measuring pulmonary artery pressure can help avoid pulmonary edema.

Surgery

Patients with multiple rib fractures or flail chest may require surgical stabilization to correct pulmonary mechanics. Rib fracture surgery reduces ventilator days in patients with mild-to-moderate pulmonary contusions.[34] Hypoxia refractory to all conventional therapies has been successfully managed by venovenous extracorporeal membrane oxygenation (vv-ECMO).[35]

Differential Diagnosis

The differentials of breathing difficulty after a traumatic injury include the following:

• Pulmonary disorders: lung laceration, pneumonia, hemothorax, pneumothorax, pulmonary edema, pulmonary embolism, transfusion-associated lung injury (TRALI), asthma 
• Cardiac conditions: cardiac contusion, myocardial infarction, pneumomediastinum, myocarditis, aortic dissection, cardiac tamponade
• Musculoskeletal pathology: rib fractures, foreign body injury, muscular contusion 
• Psychiatric conditions: panic attack, hyperventilation, anxiety disorder
• Systemic disorders: poisoning, anaphylaxis, acidosis

A detailed medical evaluation will help clinicians distinguish these conditions from pulmonary contusions.

Staging

The Murray score for acute lung injury can help assess lung injury severity.[36] This system has four variables: hypoxemia (PaO2/FiO2), atelectasis, lung compliance, and PEEP. Each variable is assigned a score from 0 to 4. The sum of the scores is divided by the number of examined variables. The final score is interpreted as follows:

• 0 - no lung injury
• 0.1 to 2.5 - mild to moderate lung injury
• Greater than 2.5 - lung injury with ARDS

The Murray Score helps clinicians determine the appropriate ventilator settings for managing patients with acute lung injury or ARDS.

Prognosis

Most pulmonary contusions heal within 5 to 7 days with good supportive care. In a study involving 73 patients with pulmonary contusion, 38.4% were diagnosed with pneumonia, while 6.8% developed ARDS. About 52.1% had greater than 20% pulmonary contusion volume.[38] Individuals who recover from severe pulmonary contusions may develop chronic pulmonary disease, manifesting as diminished functional residual capacity.[22] The mortality rate for lung contusions varies from 14% to 40%, depending on the severity of associated injuries.[39]

Complications

Pulmonary contusions may result in pneumonia, ARDS, and respiratory failure. Patients with polytrauma are more likely (78%) to develop ARDS than those with only pulmonary contusions (17%). The leading causes of mortality within the first month of sustaining a pulmonary contusion are ARDS (44.1%) and respiratory infection (26.5%).