A driver of a car was presented with worsening chest pain and shortness of breath following a road traffic accident. He was diagnosed to be having PE within 12 h from the injury both clinically and radiologically, without evidence of DVT.
Though chest pain and shortness of breath can be due to chest trauma, myocardial infarction, and PE in this case, clinical and radiological examination and ECG could exclude chest trauma and myocardial infarction with a reasonable degree of accuracy. Cardiac troponins are the most sensitive and the most specific biochemical marker indicating myocardial injury. But troponin can also get elevated in a few non-cardiac causes such as acute PE, sepsis, and acute renal failure. Elevation of Troponin in PE is attributed to the increased mechanical load on the right ventricle caused by the increased pulmonary vascular resistance due to pulmonary artery obstruction (Kilinc et al., 2012). In this patient, the rise in creatinine kinase, a compact enzyme that is found in tissues where energy demands are high, may be elevated due to either the muscle injury following femur fracture (Baird et al., 2012) or due to the PE having a deleterious effect on the cardiac muscle of the right ventricle (Adams III et al., 1992).
According to research, up to 30% of people with PE have them restricted to subsegmental or smaller arteries (Oser et al., 1996). In the absence of a central PE, the clinical relevance of peripheral emboli in subsegmental or smaller pulmonary arteries is yet unknown. Additionally, there is a debate over how these minor peripheral emboli should be treated and whether doing so will lead to better results (Novelline et al., 1978). In a study conducted by Menaker et al. (2009), majority of PE were located in the main, lobar and segmental arteries, and most of the emboli were clinically significant. There is no such thing as clinically minor PE (Handler & Feied, 1995).
While Menaker et al. (2009) and Brakenridge et al. concluded through studies that a PE can occur as early as 4 days from the onset of injury, Coleman et al. (2015) found in 2015 that 42.9% of patients with PE following trauma, was diagnosed within 72 h of hospitalization. According to the most recent study by Gelbard (2016) more than half of the early PEs occurred within 24 h of trauma. On the ground of these studies, we can suspect that an ‘early’ PE may be associated with a different pathophysiological mechanism. However, much more research is needed to come to a conclusion.
There can be several possibilities for early pulmonary embolism following trauma. One is an undiagnosed congenital or acquired prothrombotic conditions. Hypercoagulable state becomes more prominent in the first 4 days following trauma (Schreiber et al., 2005). Another could be, as Velmahos (2009) proposed, patients with early post-traumatic PE in the absence of DVT, could be due to pulmonary clots that are generated within the lungs. Furthermore, Brakenridge (2011) postulated that a long bone fracture alone is an independent risk factor of early PE. He stated that there could be an underlying molecular phenomenon linked to fractures causing early PE.
Furthermore, the literature survey reveals that fat embolism appears to be more commoner than thromboembolism following long bone fractures, with its incidence widely ranging from 47% to 100% distinguished by advanced diagnostic tools (Gurd & Wilson, 1974), whereas fat embolism has been diagnosed through autopsy examination in 68% to 82% (Mudd et al., 2000) who succumbed to major trauma. Accurate incidence of thrombembolism following long bone fractures remains unclear in the literature survey.
Bahloul et al. (2020) in a narrative review list four possibilities of early PE in the absence of DVT. They are (i) rapidly developing post-traumatic hypercoagulable disorders (ii) clots that form in the lower extremity veins completely embolizing to the pulmonary circulation without leaving any residues behind (iii) screening errors and undetected upper extremity DVTs and (iv) thrombi in the pulmonary circulation are “de novo” and not generated from the peripheries.
Chest trauma is also an identified risk factor for the development of early or late pulmonary embolism. Velmahos et. al (2009) theorized that in the absence of DVT, there can be other pathophysiology that resulted in PE. Knudson (2011) has reported a case of PE following a severe chest injury and suggested localized inflammation, occult vascular injury, and low flow state occurring following chest trauma as a likely aetiopathogenesis for “in situ” formation of thrombus in the pulmonary circulation. This is a probability in the case under discussion in the view of the history of chest impact though there were no demonstratable external or internal chest injuries.
Other risk factors for PE such as obesity, old age, sepsis, and acute renal failure (Paffrath et al., 2010) did not exist in our patient. The possibilities of congenital prothrombotic conditions were also minimal in this case.
Additionally, the development of pulmonary thrombosis may be influenced by the action of the post-traumatic adrenergic response, which causes vascular endothelial inflammation and the synthesis of circulating adhesion molecules, leading to localized thrombosis and rapid occlusion (Morris et al., 2007). More research is required on this topic.
