This elderly man is obviously ill; aside from the history of subacute dyspnea, examination shows him to be hypotensive and tachycardic, with an elevated jugular venous pressure (JVP).
Note also the presence of pulsus paradoxus; this refers to a significant drop in systolic blood pressure and pulse amplitude during inspiration, which may be felt on palpation.
Relatively few conditions can give rise to this constellation of findings; in the context of recent trauma, those most pertinent are tension pneumothorax and cardiac tamponade.
While x-ray films obtained at the time of trauma showed no evidence of pneumothorax, this can still develop hours to days afterwards; furthermore, uncomplicated pneumothoraces can convert to tension pneumothorax down the line.
That said, points against this diagnosis include the absence of tracheal deviation, or a reduction in breath sounds, or hyper-resonance in the affected hemithorax. Note also that his oxygen saturation is 100% on room air.
other hand, cardiac tamponade is a strong possibility here; it is a well-known complication of blunt thoracic trauma, and can occur either acutely, or even several days afterwards.
Urgent bedside echocardiography is an essential next step; a portable chest x-ray should also be obtained in parallel, as this will rule out pneumothorax quickly and conclusively.
The echocardiogram subsequently reveals a pericardial effusion, while also showing signs suggestive of hemodynamic compromise, thus confirming the clinical diagnosis.
Pericardiocentesis should be performed as early as possible; this will result in immediate relief, while analysis of the aspirate will help determine the underlying etiology (i.e. hemorrhage vs. traumatic pericarditis).
Fluid resuscitation will help relieve the hypotension temporarily, en-route to pericardiocentesis; vasopressor medications can also be commenced to improve the perfusion pressure.
Note that there is no justification for intercostal tube placement.
In the United States, trauma is the leading cause of death in persons below 44 years of age, with injuries to the cardiovascular system being the second most common form of traumatic death.
With respect to the heart, blunt cardiac injuries (BCI) are far more common than penetrating injury; this is possibly due to the protection afforded by the thoracic cage.
Note also that the aforementioned protection by the thoracic cage implies that a significant amount of blunt force is usually required to give rise to BCI.
Motor vehicle collisions are the most common such cause. Other etiologies include direct impact injuries seen in explosions, occupational accidents, recreational activities, and even cardiopulmonary resuscitation.
Key forms of BCI include myocardial contusions, valve disruption, atrial rupture, ventricular rupture, septal rupture, cardiac herniation, and commortio cordis.
Myocardial contusions are typically asymptomatic, although some patients may develop tachycardia or arrhythmias. The right heart is more often injured in this manner, due to its anatomical proximity to the anterior chest wall.
Patients with valve disruption typically develop symptoms of heart failure, with the severity and time of onset depending on the degree of disruption; on auscultation, a murmur may be present.
Large atrial and ventricular ruptures are usually rapidly fatal; however, smaller ruptures may give rise to cardiac tamponade instead. Septal rupture is often asymptomatic initially, with affected persons developing heart failure later on.
Cardiac herniation is rare, occurring in 0.4% of cases of severe blunt trauma. This usually results in early death, with the diagnosis is being based on autopsy findings.
Commotio cordis is an unusual form of BCI; here, low-impact chest trauma causes sudden cardiac arrest in a patient without pre-existing structural heart disease; it is classically encountered in sportspersons.
The condition is believed to occur when a direct blow to the precordium coincides with the vulnerable phase of the cardiac cycle (i.e. the 'T' wave on an electrocardiogram).
There is no gold standard for the diagnosis for BCI in patients with trauma; electrocardiography (ECG), echocardiography, cardiac enzyme assays, and imaging studies such as chest radiography, ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) may all play a role.
There are no ECG findings pathognomonic for BCI; however, the presence of an arrythmia should prompt consideration of this; furthermore, ST segment changes which mimic an infarction may be seen in patients with myocardial contusions.
Cardiac biomarkers (such as troponins, and creatine kinase-MB) are another useful screening tool; BCI is unlikely in persons with normal levels of cardiac enzymes and a normal ECG.
Echocardiography is essential in all patients suspected to have BCI; this may reveal wall motion abnormalities, valvular disruption, chamber rupture, and pericardial fluid collections (i.e. suggesting at tamponade).
Note that in the emergency room setting, FAST (Focused Assessment with Sonography in Trauma) may also be helpful in rapidly diagnosing cardiac tamponade.
Furthermore, in patients who are hemodynamically stable, multidetector computed tomography (CT) with contrast will allow evaluation of the entire thoracic region, allowing for optimization of treatment.
Individuals with BCI may subsequently require more advanced studies, i.e. cardiac MRI to assess the extent of regional infarction, valvular dysfunction, wall motion abnormality and myocardial contusion; or coronary angiography to assess the coronary arteries.
Note that the severity of BCI can be quantified via the American Association for the Surgery of Trauma (AAST) organ injury scale; this defines six grades of injury from I to VI, depending on clinical and ECG criteria.
The initial management of these patients should follow advanced trauma life support (ATLS) guidelines; all patients should also undergo continuous cardiac monitoring.
Most individuals require supportive management alone; this includes treatment of any arrhythmias or heart failure. However, where atrial or ventricular rupture is present, or valvular disruption has occurred, surgical repair is required.
Note that given the great force required to usually cause BCI, other injuries may also be present, and should be managed appropriately.
It should also be appreciated that these patients may experience delayed complication days to weeks after the acute event; these include valvular dysfunction, outright valvular rupture due to necrosis of the papillary muscles, and delayed cardiac tamponade.
Overall, the majority of these patients have an excellent prognosis. Key causes of death include chamber rupture, cardiac herniation, and other associated injuries.
1. BCI is typically a sequela of significant blunt trauma to the chest.
2. A electrocardiogram (ECG) and cardiac enzyme levels are of value in screening for BCI; where positive, echocardiography will detect most forms BCI.
3. In hemodynamically stable individuals, computed tomography (CT) is highly useful for detecting mediastinal pathology and thus optimizing treatment
4. The majority of patients with BCI have an excellent prognosis.