A pulmonary embolism secondary to fracture tibia:a clinical case report

INTRODUCTION

Pulmonary embolism (PE) occurs when a thrombus blocks blood flow in a pulmonary artery, usually after it travels from a vein in the lower limb. The annual incidence of PE is estimated to range from 60 to 120 cases per 100,000 people.

Patients with long-bone fractures have a higher risk of developing PE early after the injury.¹ In 1856, Virchow described the classic triad of venous stasis, endothelial vascular damage, and hyper coagulability as key contributors to the development of deep vein thrombosis (DVT).

Given that venous stasis is considered the primary factor in DVT formation, and subsequently pulmonary embolism (PE) in trauma patients, it has traditionally been believed that these events typically occur five to seven days following the injury. Pulmonary embolism (PE) can be classified into three types: acute, subacute, and chronic.

Acute PE

Symptoms appear suddenly and can be challenging to diagnose. Acute PE typically requires urgent treatment, including thrombolytic therapy (clot-busting drugs) and anticoagulants.

Subacute PE

Symptoms develop gradually over a period of 2 to 12 weeks and are often more subtle, making diagnosis more difficult. Sub-acute PE carries a higher risk of mortality compared to acute PE.

Chronic PE

Symptoms progressively worsen over time, potentially leading to complications like heart failure. Chronic PE occurs when a small obstruction persists after an initial acute PE.

This case present to you show that even performing a simple nailing in fracture shaft tibia fracture one should be careful, pre op. Consideration of PTE and DVT should be done, necessary steps like venous colour Doppler imaging, echocardiography, D-dimer testing, and serum troponin I should be performed.

CASE REPORT

A patient age 34 years male adult came to our emergency department with complaint of pain and swelling rt leg since, 1 day. He had met a road side accident 1 day back. On examination there was gross swelling over rt leg with multiple blisters and there was gross deformity of the limb.

X ray was done. X-ray confirmed fracture both bone of right leg. Below knee slab was applied and was admitted. Next day further investigation was done and patient was posted for surgery. External fixator was applied and he was advised for definitive surgery after 15 days.

After 15 days he came back for definitive surgery. During surgery while we were inserting the nail patient felt breathlessness, chest pain and suddenly there was drop in pulse and after some time no vitals could be assessed.

He was revived by CPR. The surgery was continued. During closure he again developed same features. He was pulse less and his could not be monitored for more than 10 minutes. He was revived by CPR again then he was intubated and shifted to ICU.

He was advised for CT pulmonary angiography, HRCT Thorax, and NCCT HEAD And report showed “cute pulmonary thromboembolism of segmental branches of B/L pulmonary arteries with? pulmonary infarct”, NCCT head was normal. He was in ICU for 5 days and was in ventilator for 2 days. He was discharged after 7 of surgery.

DISCUSSION

During the past 3 decades, the incidence of colorectal Pulmonary embolism occurs in 1-5% of patients with tibial fracture. we normally don’t practice duplex imaging in our routine for lower leg fractures. But as we show in our case it seems it has its own importance. Performing duplex should be mandatory for the patient with fractures of lower limb specially when there is gross swelling of the limb and you are planning for 2 stage surgery (external fixator-nailing/plating).

Long bone fractures can lead to various complications, including fat embolism, shock, compartment syndrome, deep vein thrombosis (DVT), pulmonary thromboembolism (PTE), disseminated intravascular coagulation (DIC), impaired wound healing, coagulopathy, and infection. Among these, pulmonary thromboembolism is particularly noteworthy as a leading cause of mortality in individuals with long bone fractures.

The majority of complications resulting from long bone fractures, approximately 99%, are typically manageable.

However, in about 1% of cases, these complications can be fatal. Causes of death associated with bone fractures can be grouped into five categories: cardiovascular, infectious, respiratory, malignancy-related, and miscellaneous causes. Cardiovascular causes include myocardial infarction, heart failure, and cerebrovascular accidents. Infectious causes often involve conditions such as sepsis and pneumonia. Respiratory causes include pulmonary thromboembolism and respiratory failure. Other causes involve renal failure and multiple organ failure.

The mortality rate in cases of bone fractures is influenced by factors such as gender, smoking habits, body mass index (BMI), congestive heart failure, dementia, moderate to severe renal disease, and history of a malignant tumor. The incidences vary from 0.5% to 0.7%. This, variability can be attributed to differences in population characteristics, the severity of injuries, and screening protocols. The computed tomography pulmonary angiogram (CTPA) is regarded as the gold standard for diagnosing PTE, offering high predictive value and detailed visualization of the pulmonary arteries.

CTPA is favored for its superior diagnostic accuracy, enabling precise identification of the location and extent of clots, which aids in treatment planning and patient risk stratification. Historically, screening for asymptomatic pulmonary thromboembolism was not feasible. However, recent research, including a study by Schultz, has revealed a higher prevalence of occult PTE than previously recognized.¹ Schultz reported a 24% incidence of asymptomatic PTE in a cohort of 90 moderately-to-severely injured trauma patients using systematic contrast-enhanced helical CT scanning Advances in CT technology, particularly the development of multi-detector scanners, have significantly enhanced the accuracy of PTE detection.^2,6

Additional investigations for the workup of pulmonary thromboembolism (PTE) include chest X-ray, ECG, arterial blood gas analysis, the 2-level PE Wells score, bedside echocardiography, color Doppler ultrasound of the leg veins, D-dimer testing, and serum troponin I measurement. Assessing Tissue Plasminogen Activator (tPA) 20 resistance can provide early indications of post-traumatic PTE. Factors such as fibrinolysis shutdown and tPA resistance further increase the risk of early PTE. Detecting a hypercoagulable 20 state through tPA resistance testing within 12 hours of admission is critical, offering a window for timely intervention and management to mitigate the risk of PTE.

The management of pulmonary embolism includes anticoagulation therapy, thrombolytic treatment, surgical interventions, and the use of caval filters. Prophylactic measures to prevent PTE involve the administration of anticoagulants such as heparin, low-molecular-weight heparins (LMWH), warfarin, and apixaban.⁷ As mentioned earlier, long bone fractures significantly increase the risk of early pulmonary thromboembolism (PTE). Traditionally, PTE was thought to occur most frequently between days 5 and 7 following trauma, with occurrences before day 4 considered rare.^2-5 This belief was based on the conventional understanding that post-traumatic PTE primarily arises from deep vein thrombosis (DVT) in the lower extremities and pelvis stasis, a key factor in DVT formation, was thought to delay the development of PTE until 5 to 7 days after the injury.^2-7

A review of the literature indicates that lower limb fractures are commonly associated with early pulmonary thromboembolism (PTE).^1,5,6 Several risk factors impact the timing of post-traumatic pulmonary thromboembolism (PTE), including advanced age, obesity severe injury characteristics, compromised hemodynamic status, sepsis, and hypoxemia.^{5,10-12,14,15}In this case, pulmonary thromboembolism was identified as the immediate cause of death, with histopathological examination revealing thrombi in the pulmonary arterioles. Post-traumatic pulmonary thromboembolism is a life-threatening condition that typically develops within a week of a long bone fracture, and in some cases, within 72 hours.

However, in this particular instance, pulmonary thromboembolism occurred within 6 hours of the trauma, which is considered rare. Early pulmonary thromboembolism is linked to risk factors such as a history of surgery, hospitalization, pregnancy, cancer, and a family history of blood clots, including Factor V Leiden. The occurrence of early post-traumatic pulmonary embolism (PTE) is influenced by factors related to the fracture's location and the patient's individual characteristics.

Several pathophysiological mechanisms contribute to the early onset of PTE. These include undiagnosed congenital or acquired prothrombotic disorders, hypercoagulable 20 states within the initial four days following trauma, the presence of pulmonary clots, the independent risk posed by long bone fractures, and molecular processes associated with the fracture that led to the formation of new thrombi in the pulmonary circulation. Together, these factors significantly increase the risk of early PTE in patients with long bone fractures.

The adrenergic response to trauma may also contribute to early pulmonary thromboembolism (PTE) by inducing vascular endothelial inflammation and promoting the synthesis of circulating adhesion molecules, which facilitate thrombosis and rapid vascular occlusion. Risk factors for PTE include obesity, advanced age, sepsis, acute renal failure, and congenital prothrombotic disorders. Early PTE is more frequently observed in cases involving a higher incidence of lower extremity fractures and severe extremity trauma.^17-19,22

In summary, the pathophysiology of PTE is multifaceted. The "lethal triad" of hypothermia, acidosis, and coagulopathy creates a prothrombotic environment. Systemic inflammatory response syndrome (SIRS) and compensatory anti-inflammatory response syndrome (CARS) contribute to endothelial dysfunction, further promoting thrombosis. Stress mechanisms enhance hypercoagulability by increasing platelet activation and aggregation. The primary hit mechanism initiates clot formation, while the secondary hit exacerbates the prothrombotic state. Disseminated intravascular coagulation (DIC) also plays a role, with widespread activation of coagulation leading to microthrombi formation and subsequent PTE.

CONCLUSION

This case shows that every trauma Patient specially fracture of lower leg should be examined, investigated and treated (surgery) properly, e.g., even simple nailing should not be performed before knowing their vascular status of the limb. Various methods like duplex imaging, echo etc should be done. The acute onset of pulmonary thromboembolism (PTE) may result from a hypercoagulable state triggered by the multi-site fracture, potentially acting as a physiological response to minimize excessive blood loss. However, the imbalance in the coagulation-anticoagulation system proved harmful. So, comprehensive screening for PTE should be prioritized in patients with long bone fractures, along with the implementation of proactive strategies to reduce the risk of its occurrence.

Funding: No funding sources

Conflict of interest: None declared

Ethical approval: Not required

REFERENCES

1. 1. Benns M, Reilly P, Kim P. Early pulmonary embolism after injury: a different clinical entity. Injury. 2014;45(1):241-4.
2. 2. Coleman JJ, Zarzaur BL, Katona CW, Plummer ZJ, Johnson LS, Fecher A, et al. Factors associated with pulmonary embolism within 72 hours of admission after trauma: a multicentre study. J Am Coll Surg. 2015;220(4):731-6.
3. 3. Brakenridge SC, Toomay SM, Sheng JL, Gentilello LM, Shafi S. Predictors of early versus late timing of pulmonary embolus after traumatic injury. The American Journal of Surgery. 2011;201(2):209-15.
4. 4. Kazemi Darabadi F, Jafari Zare MA, Torabi Goodarzi Z, Namdar P. Prevalence and main determinants of early post-traumatic thromboembolism in patients requiring ICU admission. Euro J Trauma Emerg Surg. 2018;44:133-6.
5. 5. Owings JT, Kraut E, Battistella F, Cornelius JT, O'Malley R. Timing of the occurrence of pulmonary embolism in trauma patients. Arch Surg. 1997;132(8):862-7.
6. 6. Sing RF, Camp SM, Heniford BT, Rutherford EJ, Dix S, Reilly PM, Holmes JH, Haut E, Hayanga A. Timing of pulmonary emboli after trauma: implications for retrievable vena cava filters. J Trauma and Acute Care Surg. 2006;60(4):732-5.
7. 7. Menaker J, Stein DM, Scalea TM. Pulmonary embolism after injury: more common than we think. J Trauma Acute Care Surg. 2009;67(6):1244-9.
8. 8. Menaker J, Stein DM, Scalea TM. Incidence of early pulmonary embolism after injury. J Trauma Acute Care Surg. 2007;63(3):620-4.
9. 9. Cambien B, Wagner DD. A new role in hemostasis for the adhesion receptor P-selectin. Trends Mol Med. 2004;10(4):179-86.
10. 10. Lentz SR. Thrombosis in the setting of obesity or inflammatory bowel disease. Hematology 2014, the American Society of Hematology Education Program Book. 2016;2(1):180-7.
11. 11. Howard VJ, Cushman M, Pulley L, Gomez CR, Go RC, Prineas RJ, et al. The reasons for geographic and racial differences in stroke study: objectives and design. Neuroepidemiol. 2005;25(3):135-43.
12. 12. Blokhin IO, Lentz SR. Mechanisms of thrombosis in obesity. Curr Opin Hematol. 2013;20(5):437-44.
13. 13. Donzé JD, Ridker PM, Finlayson SR, Bates DW. Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study. BMJ. 2014;3:49.
14. 14. Levine RL, LeClerc JR, Bailey JE, Monberg MJ, Sarwat S. Venous and arterial thromboembolism in severe sepsis. Thrombosis Haemostasis. 2008;99(11):892-8.
15. 15. Brill GL Suidan DD Wagner. Hypoxia, such as that encountered at high altitudes, promotes deep vein thrombosis in mice. J Thromb Haemost. 2013;119:17-9.
16. 16. Blaisdell FW, Graziano CJ. Assessment of clotting by the determination of fibrinogen catabolism. Am J Surg. 1978;135(3):436-43.
17. 17. Chakroun-Walha O, Samet A, Jerbi M, Nasri A, Talbi A, Kanoun H, et al. Benefits of the tranexamic acid in head trauma with no extracranial bleeding: a prospective follow-up of 180 patients. Euro J Trauma Emerg Surg. 2019;45:719-26.
18. 18. Schreiber MA, Differding J, Thorborg P, Mayberry JC, Mullins RJ. Hypercoagulability is most prevalent early after injury and in female patients. J Trauma and Acute Care Surg. 2005;58(3):475-81.
19. 19. Velmahos GC, Spaniolas K, Tabbara M, Abujudeh HH, De Moya M, Gervasini A, et al. Pulmonary embolism and deep venous thrombosis in trauma: are they related. Arch Surg. 2009;144(10):928-32.
20. 20. HB Moore EE Moore BR Huebner M Dzieciatkowska GR Stettler GR Nunns Fibrinolysis shutdown is associated with a fivefold increase in mortality in trauma patients lacking hypersensitivity to tissue plasminogen activators. J Trauma Acute Care Surg. 2017;83(6)1014-22.