21. Venous Thromboembolism Post Acquired Brain Injury
Summary
| Intervention | Key Point
Level of Evidence |
| Non-Pharmacological Interventions | |
| Mechanical Interventions | Intermittent pneumatic compression devices and low molecular weight heparin may have a similar effect in terms of the prevention of deep vein thrombosis post ABI when compared to each other.
– There is conflicting level 2 evidence (from one cohort study; Praeger et al., 2012; and one prospective controlled trial; Kurtoglu et al., 2004) and level 4 evidence (from one case series; Minshall et al., 2011) regarding the effectiveness of intermittent pneumatic compression devices compared to low-molecular-weight heparin or unfractionated heparin for the prophylaxis of DVT and PE. Intermittent compression devices may not aggravate intracranial hemodynamics in patients with severe ABI. – There is level 4 evidence (from one pre-post test; Davidson et al., 1993) that intermittent compression devices do not cause acute elevations in intracranial pressure in patients with severe ABI. When compared to VTE chemoprophylaxis., prophylactic inferior vena cava filters may worsen outcomes. – There is level 2 evidence (from one retrospective cohort study; Elkbulki et al., 2020a) that prophylactic inferior vena cava filters are associated with higher rates of DVT, nonfatal PE and longer hospital stays when compared to VTE chemoprophylaxis following severe TBI. Early placement of inferior vena cava filters (within 48 hours) may shorten hospital length of stay. – There is level 2 evidence (from one retrospective cohort study; Elkbuli et al., 2020) that IVC filter placement within 48hrs of admission significantly improves ICU and hospital length of stay in adult trauma patients. |
| Pharmacological Interventions | |
| Thromboembolic Prophylaxis | Administration of pharmacological thromboembolic prophylaxis within the first 72 hours post ABI may be effective for reducing the risk of developing venous thromboembolism.
– There is level 3 evidence that prophylactic anticoagulation is more effective than placebo in reducing the risk of developing deep vein thrombosis in patients post ABI.
Enoxaparin is effective for the prevention of venous thromboembolism development after elective neurosurgery and has not been found to cause excessive bleeding. – There is level 2 evidence that the administration of enoxaparin within the first 72 hours post ABI reduces the risk of developing deep vein thrombosis and pulmonary embolism post injury compared to unfractionated heparin.
|
Introduction
Venous thromboembolism (VTE) is a blood clot that forms within a vein. The most common place for a blood clot to form is a deep vein, which is called a deep venous thrombosis or DVT. If the clot breaks off and travels to the lungs, causing partial or full occlusion, it is called a pulmonary embolism (PE) (Office of the Surgeon et al., 2008). Together, DVT and PE are referred to as VTE. VTE remains a common complication in patients who have sustained an ABI (Raslan et al., 2010; Scudday et al., 2011); however the scientific literature specific to ABI is quite limited. The following section presents ABI specific research regarding the prevention and treatment of VTE. Additional information on clinical presentation and testing practices is presented, however, it should be noted that not all in-text citations refer to research that meets the specific ERABI ABI inclusion criteria (mixed populations, age, mixed ABI severity, etc.) and therefore should be interpreted with caution when considering the application of any tests or indicators of VTE to an ABI population.
Incidence of Venous Thromboembolism Post Head Injury
In a large sample study consisting of 38,984 individuals with TBI, the incidence of VTE at the time of admission was 1.31% (Olufajo et al., 2016). At one-month post injury, the incidence for VTE increased to 1.87% and by one year it was 2.83% (Olufajo et al., 2016). The reported incidence of DVT among patients with TBI ranges from 11% to 54% (Carlile et al., 2010; Cifu et al., 1996; Denson et al., 2007; Geerts et al., 1994). The risk of developing a DVT or PE, in the absence of prophylaxis, is estimated to be approximately 20% post TBI (Haddad & Arabi, 2012). Severity of injury is found to be associated with incidence of VTE in isolated patients with TBI (Van Gent et al., 2014). Decisions on how to treat, and when, are often made on a case-by-case basis (Tang & Lobel, 2009). Experts recommend beginning pharmacological prophylaxis as early as 48 to 72 hours post injury (INESSS-ONF, 2017; Norwood et al., 2001). Unless contraindicated, mechanical thromboprophlaxis and low-molecular-weight heparin (LMWH) are recommened in the acute phase of recovery (Haddad & Arabi, 2012).
Risk Factors for Venous Thromboembolism
The most recognized risk factors for VTE are venostasis, intimal damage of the vessel wall, and a hypercoagulable state (Virchow’s triad – see Figure 1) (Watanabe & Sant, 2001). Patients with a severe brain injury are commonly immobilized for periods of time as a result of extremity or spine fractures, they experienced at the time of their injury (Vergouwen et al., 2008). The incidence of DVT appears to be impacted by length of stay in the intensive care unit and the number of days a patient is on a ventilator. There does not appear to be a correlation between VTE incidence and initial Glasgow Coma Scale (GCS) scores, Injury Severity Scale scores, or the Abbreviated Injury Scale score (Denson et al., 2007). Those at highest risk post injury are those who remain on a ventilator longer than 3 days (Olufajo et al., 2016; Raslan et al., 2010). At 1-year post injury, risk of VTE is greatest for those discharged to extended care facilities compared to home, and for individuals who undergo an operation (Olufajo et al., 2016). Patients involved in trauma that does not specifically involve vessel injury are still at increased risk of thromboembolism, suggesting a trauma-induced hypercoagulable state (Geerts et al., 1994; Geerts et al., 1996). Therefore, persons who have sustained a TBI appear to be at increased risk of developing VTE for multiple reasons.
Figure 1 | Virchow’s Triad
Clinical Presentation of Deep Vein Thrombosis and Pulmonary Embolism
A study found that up to 91% of thrombi form below the iliac level (De Maeseneer et al., 2016). The most common symptoms reported when a DVT is present are pain, swelling of the legs, and discoloration of the region (Collins, 2009). The clinical presentation of PE is challenging. Many cases are clinically silent (66%) with only 30% having the clinical features of a DVT (Garcia-Fuster et al., 2014). Asymptomatic PE is discovered in 70% of patients with confirmed clinically symptomatic DVT (Browse, 1974; Corrigan et al., 1974; Hull & Hirsh, 1983). Clinically, PE presents with tachycardia, tachypnea, hemoptysis, pleuritic chest pain and fever. Radiographic findings might include signs of consolidation or pleural effusion (Worku et al., 2014). Massive PE may cause right heart failure, which can progress to cardiovascular collapse, coma, and death.
Diagnostic Testing for Deep Vein Thrombosis
A positive diagnosis of DVT can only be made if a venogram is positive or there is a positive venous ultrasound at two or more sites of the proximal veins. The diagnosis of DVT can be ruled out if there is a negative venogram, a negative D-dimer test or a normal venous ultrasound in patients with low clinical suspicion of DVT (Carlile et al., 2006).
D-Dimer Assay
D-dimer assay is a rapid, non-invasive, and inexpensive test. Fibrin is the main component of thrombus formation and fibrin degradation products include D-dimers (Gill & Nahum, 2000). A positive D-dimer test is highly sensitive for the presence of a thrombus but lacks specificity since D-dimers are found in other disease states, including cancer, congestive heart failure, and inflammatory conditions (Raimondi et al., 1993). As a result, D-dimer assays have a high negative predictive value but a poor positive predictive value. To illustrate, Akman et al. (2004) reported that the sensitivity and negative predictive values of the D-dimer test were high, at 95.2% and 96.2% respectively, in a group of 68 rehabilitation patients (stroke, spinal cord injury, TBI, hip arthroplasty). The specificity and positive predictive values were low at 55.3% and 48.7%, respectively.
Venography
Venography is considered a definitive test for DVT but it is an older, invasive test whereby contrast dye is injected into the leg veins. Diagnosis of DVT is made if an intraluminal-filling defect is noted.
Venous Ultrasound
Venous ultrasound is often used to diagnose a DVT. There are several types of venous ultrasonography. They include compression ultrasound, duplex ultrasound, and color Doppler imaging. Although these types of venous ultrasonography are sometimes used interchangeably, their sensitivities and specificities for detecting acute DVT vary (Zierler, 2004). The sensitivity and specificity of compression ultrasonography for detecting DVTs is 43% and 85%, respectively (Girard et al., 2005). The weighted mean sensitivity and specificity of venous ultrasonography for the diagnosis of symptomatic proximal DVT are 97% and 94%, respectively; the sensitivity falls to 73% for distal DVT (Kearon et al., 1998; Zierler, 2004). Importantly, distal DVTs do not confer the same risk of extension to PE as do proximal DVTs. Typically, if a distal clot is going to extend proximally, this occurs within one week of its development. Consequently, serial ultrasound could be used in symptomatic patients in whom the test is initially negative as the test would become positive with the clot extension.
Diagnostic Testing for Pulmonary Embolism
The diagnostic work-up for a suspected PE is a step-wise decision algorithm consisting of clinical likelihood and D-dimer testing (Di Nisio et al., 2016; Moore et al., 2018). Patients with low clinical suspicion of PE have D-dimer testing. If the D-dimer is negative, PE is ruled out in patients with low clinical suspicion of PE; if positive, patients move to imaging for PE. Patients with high clinical suspicion of PE do not have D-dimer testing and move straight to imaging. Patients with ABI are most often considered high-risk for PE. Computed Tomography Pulmonary Angiogram (CTPA) is the preferred imaging modality for diagnosis of PE (Di Nisio et al., 2016; Moore et al., 2018). Ventilation/Perfusion Scanning (V/Q Scan) can be used when CTPA is contraindicated. Combining imaging with pre-test clinical decision rules increases the predictive power in the diagnosis of PE.
Computed Tomography Pulmonary Angiogram
CTPA is the preferred imaging modality for diagnosing PE (Di Nisio et al., 2016; Moore et al., 2018). It has become first line at most centers because it is fast, highly sensitive and specific, and can detect other causes of chest pain such as pneumonia, musculoskeletal injuries or pericardial abnormalities (Di Nisio et al., 2016). Combined with clinical probability rules there is a very high positive predictive value (Gottschalk et al., 2002; Stein et al., 2006). CTPA carries risks associated with radiation exposure, bleeding, adverse reaction to contrast medium, and is contraindicated in renal insufficiency. V/Q scan is used for investigating potential PE when CTPA is contraindicated (Di Nisio et al., 2016).
Ventilation/Perfusion Scanning
Palmowski et al. (2014) reported the sensitivity and specificity of V/Q scanning as 95.8% and 82.6%, respectively, with false negative rates of 4.2% and false positive rates of 17.3%. Hence, a normal scan virtually excludes a PE (high negative predictive value). Identified perfusion defects are non-specific and only represent true PE in about one-third of cases. The probability that a perfusion defect represents a PE increases with the size, shape, and number of defects as well as the presence of a normal ventilation scan.
TABLE 1 | Probability of Pulmonary Embolism Based on Ventilation-Perfusion Scan Results and Clinical Suspicion in the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED Investigators) Study
| Ventilation-Perfusion Scan Results | Clinical Suspicion of Pulmonary Embolism* | ||
| Low | Intermediate | High | |
| High Probability | 56% | 88% | 96% |
| Intermediate Probability | 16% | 28% | 66% |
| Low Probability | 4% | 16% | 40% |
| Normal/Near-Normal Probability | 2% | 6% | 0% |
*Percentage of patients with pulmonary embolism; adapted from the PIOPED Investigators (Gill & Nahum, 2000; PIOPED Investigators, 1990).
The Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED Investigators) study demonstrated that a low-probability or normal ventilation-perfusion scan with a low clinical suspicion of PE essentially excludes the diagnosis of PE (negative predictive values of 96% and 98% respectively) (Gill & Nahum, 2000; PIOPED Investigators, 1990). When clinical suspicion is high and the scan indicates a high probability of PE, the positive predictive value is 96% (Gill & Nahum, 2000; PIOPED Investigators, 1990), and these patients should be treated. The majority of ventilation perfusion scans have non-diagnostic results, requiring further testing (PIOPED Investigators, 1990). For this reason, in addition to limited availability of V/Q scans, CTPA is the preferred investigation for PE imaging.
Venous Thromboembolism Prophylaxis Post ABI
Several interventions have been examined for the prevention of DVT after an ABI, including mechanical therapy, pharmaceuticals, or a combination of both. In a systematic review, Hachem et al. (2018) found rates of VTE in patients with severe TBI not receiving anticoagulation prophylaxis were near 30%, compared to 5-10% of patients with prophylaxis. However, there is no agreement on the administration of these medications in terms of timing, dose, and/or which anticoagulation medication.
Non-Pharmacological Prophylaxis
Key Points
Intermittent pneumatic compression devices and low molecular weight heparin may have a similar effect in terms of the prevention of deep vein thrombosis post ABI when compared to each other.
Intermittent compression devices may not aggravate intracranial hemodynamics in patients with severe ABI.
When compared to VTE chemoprophylaxis., prophylactic inferior vena cava filters may worsen outcomes.
Early placement of inferior vena cava filters (within 48 hours) may shorten hospital length of stay.
Non-pharmacological, mechanical interventions used to prevent the development of DVT post ABI include: the insertion of inferior vena cava filters, thromboembolism deterrent stockings, and intermittent pneumatic compression devices including arteriovenous foot pumps and sequential compression devices (SCDs). These devices operate primarily through two distinct mechanisms of action. The first is mechanical, in which the device increases the velocity of venous return to decrease venous stasis, thus reducing the opportunity for clot formation. The second, and perhaps more important mechanism, involves the systemic activation of the fibrinolytic system which, during compression, leads to the breakdown of fibrin clots associated with thromboembolism (Macatangay et al., 2008). The exception is vena cava filters, which operate by another method of mechanical VTE prevention (Watanabe & Sant, 2001). These filters are inserted into the inferior vena cava to prevent the passage of distal emboli into the lungs. Some reports have demonstrated success rates as high as 96% in the prevention of pulmonary emboli (Greenfield & Michna, 1988). However, the use of vena cava filters carries some associated risks. They can become blocked or dislodged which can increase the risk of an embolism. Some have also reportedly increased risks for repeated DVT compared with patients without such devices (Decousus et al., 1998).
Discussion
Gersin et al. (1994) investigated the effectiveness of SCDs. Of 32 patients admitted to the surgical intensive care unit with severe TBI, a total of eight patients developed DVT or PE following injury, half of whom had received prophylactic SCDs (showing no significant difference between SCDs and no intervention). The effectiveness of prophylactic SCDs in the prevention of post-TBI DVT or PE thus remains questionable.
Davidson et al. (1993) conducted a study to evaluate the possibility that intermittent pneumatic compression could aggravate intracranial hemodynamics in patients with severe brain injury. The authors reported that the use of intermittent compression devices to prevent the occurrence of DVT was not associated with any significant changes in intracranial pressure or cerebral perfusion pressure in stable patients in whom intracranial pressure was controlled by conventional measures (Davidson et al., 1993). These findings suggest that there is no contraindication to the use of pneumatic compression for the prevention of DVT in severe acute patients with brain injury who are responsive to conventional intracranial management measures.
When intermittent pneumatic compression devices were compared to prophylactic LMWH for the prevention of VTE, no significant differences in the development of PEs or DVTs were found between groups (Kurtoglu et al., 2004). However, Minshall et al. (2011) found that mortality was higher in the group of patients receiving sequential compression devices alone compared to LMWH or UFH.
Conclusions
There is conflicting level 2 evidence (from one cohort study; Praeger et al., 2012; and one prospective controlled trial; Kurtoglu et al., 2004) and level 4 evidence (from one case series; Minshall et al., 2011) regarding the effectiveness of intermittent pneumatic compression devices compared to low-molecular-weight heparin or unfractionated heparin for the prophylaxis of DVT and PE.
There is level 4 evidence (from one pre-post test; Davidson et al., 1993) that intermittent compression devices do not cause acute elevations in intracranial pressure in patients with severe ABI.
There is level 2 evidence (from one retrospective cohort study; Elkbulki et al., 2020a) that prophylactic inferior vena cava filters are associated with higher rates of DVT, nonfatal PE and longer hospital stays when compared to VTE chemoprophylaxis following severe TBI.
There is level 2 evidence (from one retrospective cohort study; Elkbuli et al., 2020) that IVC filter placement within 48hrs of admission significantly improves ICU and hospital length of stay in adult trauma patients.
Pharmacological Prophylaxis
Key Points
Administration of pharmacological thromboembolic prophylaxis within the first 72 hours post ABI may be effective for reducing the risk of developing venous thromboembolism.
Enoxaparin is effective for the prevention of venous thromboembolism development after elective neurosurgery and has not been found to cause excessive bleeding.
Oral agents have been investigated for their prophylactic potential against DVT. Warfarin (Coumadin), a well-established anticoagulant with a predictable duration of action, is sometimes avoided as a prophylactic alternative for DVT due to its elevated bleeding side effects (Watanabe & Sant, 2001). Albrecht and colleagues (2014) report that warfarin use is associated with lower rates of DVT and PE, but comes at the cost of the risk of increased hemorrhagic bleeding. However, some experts felt the use of warfarin was advisable, especially for high-risk patients due to its benefit in treating undetected thrombosis; the therapeutic dose range for prophylaxis and treatment of thromboembolism are the same (Hirsh et al., 1992; Hyers et al., 1992; Landefeld & Goldman, 1989).
In a multicenter observational study of DVT prophylaxis with a mixed TBI population sample of 932 patients treated with anticoagulation drugs, 71% were given LMWH, 23% unfractionated heparin, 1% Coumadin, and 3% were given both LMWH and Low-dose unfractionated heparin, none of which were associated with increased intracranial or systemic hemorrhage (Carlile et al., 2010). The Institut national d’excellence en santé et en services sociaux (INESSS) and Ontario Neurotrauma Foundation clinical practice guidelines for the rehabilitation of moderate to severe TBI recommend initiating thromboprophylaxis as soon as medically appropriate (level B evidence), and physical methods of thromboprophylaxis (i.e., compression stockings) should be used when pharmacological prophylaxis is delayed or contraindicated (level B evidence)(INESSS-ONF, 2017). There is also evidence from a meta-analysis that aspirin has positive effects in the reduction of both DVT and PE, by 40% and 60% respectively (BMJ, 1994). A systematic review on anticoagulation in patients with severe TBI found 30% rate of VTE among patients not receiving anticoagulation compared to 5-10% in patients receiving anticoagulation therapy (Hachem et al., 2018).
Overall, there is a lack of persuasive evidence to guide decisions about when to administer anticoagulant prophylaxis in those who sustain traumatic intracranial hemorrhage. Clinicians often make decisions based on their own assessments of the risks and benefits (Scales et al., 2010). To date no national standard of care exists for the administration of the pharmacological prophylaxis treatment of DVT post TBI (Phelan, Eastman, et al., 2012).
Differences in medications used for pharmacological thromboprophylaxis of patients with ABI is another important consideration. Subcutaneous heparin in low doses has been reported to be both safe and effective as prophylaxis against DVT development post ABI (Watanabe & Sant, 2001). The route of delivery may also affect the efficacy of anticoagulant prophylaxis (Watanabe & Sant, 2001). For this reason, intravenously delivered heparin may be more effective in the prevention of thromboembolism compared with subcutaneous administration, although this method of delivery might increase the risk of bleeding (Green et al., 1988). LMWH, which is injected subcutaneously, has gained popularity due to the ease of administration and dosage adjustment. Of note, low-molecular weight variants of unfractionated heparin are more expensive but the advantages are such that they have become the standard of care. Carlile et al. (2006) found that 15 of the 16 rehabilitation centers surveyed reported routinely initiating treatment with either LMWH or Low-dose unfractionated heparin. In a study with a mixed trauma population, low-dose unfractionated heparin was compared to enoxaparin (LMWH) for the treatment of DVT (Geerts et al., 1996). Of those receiving low-dose unfractionated heparin, 44% suffered a DVT compared to 31% of patients receiving enoxaparin (p=0.014) (Geerts et al., 1996). These results are consistent with Byrne et al. (2017) matched analysis in patients with isolated severe TBI, where patients who received LMWH had an adjusted odds ratio of 0.49 (95% CI=0.29-0.82) of developing a PE compared to patients who were treated with unfractionated heparin. The INESSS and Ontario Neurotrauma Foundation clinical practice guidelines for the rehabilitation of moderate to severe TBI recommends LMWH over unfractionated heparin after TBI (level C evidence), although these guidelines are mostly based on evidence in general trauma patients, and not TBI specifically (INESSS-ONF, 2017).
Discussion
Results indicate that early anticoagulation treatment (within the first 72 hours) may reduce the risk of developing DVT post injury (Brandi et al., 2020; Byrne et al., 2016; Farooqui et al., 2013; Kim et al., 2002; Kim et al., 2014; Norwood et al., 2008; Saadi et al., 2018; Salottolo et al., 2011; Scudday et al., 2011) without increasing the risk of intracranial hemorrhagic injury (Baharvahdat et al., 2019; Byrne et al., 2016; Koehler et al., 2011; Scudday et al., 2011; Stormann et al., 2019) or deterioration on neurological examination (Kim et al., 2002). However, these results are in conflict with Meyer et al. (2016) and Hachem et al. (2018), which found no increased risk of ICH worsening, but found no benefit regarding VTE incidence.
Patients with ABI who were started on unfractionated heparin within three days of injury onset, compared to those who started after this time period, did not differ significantly in terms of the number of thromboembolic events (Kim et al., 2002; Kim et al., 2014). However, those who received heparin earlier had greater cumulative neuro improvement and lower injury severity scale scores (Kim et al., 2014).
Norwood and colleagues conducted two studies examining the benefits of administering enoxaparin (LMWH) prophylaxis to those who sustain a severe ABI within the first 48 hours post injury (Norwood et al., 2008; Norwood et al., 2002). Results from both studies indicate that administering enoxaparin post ABI reduces the risk of developing DVT and PE, without increasing the risk of bleeding post injury. Scudday et al. (2011) also found that patients who received chemical prophylaxis within 72 hours of injury had a significantly lower incidence of developing VTE post ABI (p<0.019) compared to those not receiving chemical prophylaxis (Kim et al., 2014). Overall, a meta-analysis by Jamjoom and colleagues (2013) concluded that individuals who begin pharmacological thromboprophylaxis within 72 hours of injury have half the risk of VTE without significantly increased risk of intracranial hemorrhage progression, compared to those who start prophylaxis more than 72 hours after their injuries.
On the contrary, a few studies have demonstrated that these medications may not be beneficial or superior treatments. In one study with individuals who underwent a craniotomy post ABI, indicative of a more severe brain injury, no significant differences were reported for rate of DVT and PE when comparing those who received enoxaparin prophylaxis to those who did not (Daley et al., 2015). Further, Kwiatt et al. (2012) reported that patients receiving LMWH were at higher risk for hemorrhage progression and the risk of using LMWH may exceed its benefit. Similarly for heparin, Lin et al. (2013) did not find a reduction in DVT or PE once individuals with a severe TBI were administered a heparin prophylaxis protocol.
A systematic review of twelve studies reported that overall evidence supported the use of enoxaparin for reduction of DVT and unfractionated heparin for decreased mortality rates compared to no chemoprophylaxis (Chelladurai et al., 2013). Furthermore, a retrospective study of 20 417 patients with isolated TBI reported less likelihood of VTE with LMWH compared to unfractionated heparin (Benjamin et al., 2017).
Conclusions
There is level 3 evidence that prophylactic anticoagulation is more effective than placebo in reducing the risk of developing deep vein thrombosis in patients post ABI.
There is level 2 evidence that the administration of enoxaparin within the first 72 hours post ABI reduces the risk of developing deep vein thrombosis and pulmonary embolism post injury compared to unfractionated heparin.
Conclusion
The most well studied intervention for the prevention of VTE is pharmacological thromboprophylaxis. There is moderate evidence that pharmacological prophylaxis with heparin, particularly LMWH helps reduce the risk of developing a VTE post ABI, without increasing the risk of intracranial bleeding in patients with TBI. Compression stockings are not more effective than LMWH. Unfortunately, the evidence in ABI specific populations is limited; the timing, agent and methods of anticoagulation therapy would benefit from more research.
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TABLE OF CONTENTS:
Summary
Introduction
Clinical Presentation of Deep Vein Thrombosis and Pulmonary Embolism