Prevention of Thromboembolism in Spinal Cord Injury

Updated: Sep 07, 2015
  • Author: Dana McKinney, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Prevention of thromboembolism in spinal cord injury (SCI) is an important clinical issue, as deep vein thrombosis (DVT) and pulmonary embolism (PE) are not only common complications of acute spinal cord injury (SCI) but also major causes of morbidity and mortality. Morbidities from DVT include postphlebitic syndrome, prolonged edema, and pressure ulcers; those from PEs can cause arrhythmias, hypoxia, and death.

However, many patients with spinal cord injury do not receive DVT prophylaxis in the acute care setting, [1] perhaps secondary to concomitant medical problems that may enhance the risk of bleeding. In a retrospective study by Powell and colleagues, 38.6% of patients admitted to a rehabilitation hospital were receiving DVT prophylaxis. [2]

In prospective studies, the incidence of DVT following acute spinal cord injury has been reported at 18-100%, depending on the diagnostic technique used, time after injury, and concurrent risk factors. Overall incidence without prophylaxis is estimated to be 40% based on a meta-analysis of DVT in patients with acute spinal cord injury. [3]  A study by Chung et al of almost 48,000 patients with spinal cord injury found the adjusted hazard ratio for DVT in these patients to be 2.46-fold higher than that of controls. [4]

Clinically apparent DVT occurs in approximately 15% of patients with acute spinal cord injury, and PE develops in approximately 5% of these patients. The risk of DVT is highest within the first 2 weeks following injury, with peak occurrence between days 7 and 10. DVT has been detected as early as 72 hours postinjury; however, risk before this time appears to be low. A study by Alabed et al found the incidence of PE after the first 3 months post–spinal cord injury, and following the cessation of prophylactic anticoagulation therapy, to be lower than during the first 3 months after the injury, measuring 1.25% (eight out of 640 patients). [5]

For patient education information, see Lung Disease & Respiratory Health Center, as well as Deep Vein Thrombosis (Blood Clot in the Leg, DVT) and Pulmonary Embolism.

See also Spinal Cord Injuries, Autonomic Dysreflexia in Spinal Cord Injury, Functional Outcomes per level of Spinal Cord Injury, Heterotopic Ossification in Spinal Cord Injury, Hypercalcemia in Spinal Cord Injury, Osteoporosis and Spinal Cord Injury, Rehabilitation of Persons with Spinal Cord Injuries, and Spinal Cord Injury and Aging.



Patients with spinal cord injury (SCI) have a higher risk of thromboembolic disease related to the Virchow triad (ie, venous stasis, hypercoagulability, intimal injury). Stasis from paralyzed muscles and hypercoagulability remain the 2 major factors contributing to the development of thrombosis in this patient population. Other common risk factors for venous thromboembolism (VTE) include the following [6, 7, 8] :

  • Immobilization – The muscles in the legs act as pumps to maintain venous return from the lower extremities; inactivity of these muscles leads to venous stasis
  • Advanced age
  • Congestive heart failure – Cardiac output is reduced, as is venous return from the legs
  • Previous VTE
  • Surgical procedure of lower extremity/pelvis
  • Cancer/malignancy - Venous thromboembolism prophylaxis is not utilized fully in patients undergoing oncologic surgery a cohort study shows [9] ; appropriate prophylaxis is given more often to patients treated by high-volume surgeons at high-volume hospitals.
  • Oral contraceptive use/pregnancy
  • Trauma (eg, multiple trauma, spinal cord injury, burns, lower extremity fractures) – Direct mechanical injury to the lower extremities may lead to blood clot formation
  • Delayed initiation of thromboprophylaxis

Predisposing risk factors for the development of deep vein thrombosis (DVT) following spinal cord injury are found in the Virchow triad. Venous stasis results from loss of the pumping function normally provided by contracting limb muscles. Hypercoagulability results from the stimulation of thrombogenic factors following injury, with a resultant increase in platelet aggregation and adhesion. Intimal injury may occur directly, from vasoactive amines released in association with trauma or surgery, or it may result indirectly, from external pressure on the paralyzed leg.

Patients with DVT have higher levels of von Willebrand factor antigen and factor VIII–related antigen than do patients without thrombosis, and these individuals demonstrate hyperactive platelet aggregation responses to collagen and the appearance of circulating platelet aggregates.

Clinical factors believed to be associated with DVT include motor complete injuries, paraplegia, and male sex. [10] In a study by Powell and colleagues, no statistical difference in the incidence of DVT was found between patients with a motor complete injury and those with a motor incomplete injury, between patients with tetraplegia and those with paraplegia, or between patients with a traumatic cause of spinal cord injury and those with a nontraumatic cause. [2] Thus, all patients with spinal cord injury are at risk of developing a DVT.


Clinical Evaluation

In patients with spinal cord injury (SCI), clinical diagnostic signs and symptoms may differ from those found in noninjured patients, and these may be much more difficult to identify. The characteristics and diagnostic value of various clinical signs and symptoms include leg swelling and leg pain.

Typically, the hallmark of deep vein thrombosis (DVT) is a rapid onset of unilateral leg swelling; however, swelling of the lower extremities may be bilateral. Edema may be the only presenting symptom. Leg pain is nonspecific and includes a vast differential diagnosis. This is generally not a useful diagnostic symptom in patients with insensate lower extremities following spinal cord injury.

Unfortunately, overall, the diagnostic properties of the clinical examination are poor. Clinical findings are absent in 50% of patients with confirmed DVT. However, although it is virtually impossible to distinguish DVT from other processes, the following findings should raise clinical suspicion:

  • Leg swelling that is principally unilateral but may be bilateral, with a circumferential increase of the affected leg by at least 3 cm
  • Tenderness on compression of the calf muscles or over the course of the deep veins in the thigh
  • Increased temperature over the calf or thigh
  • Pain during forced dorsiflexion of the foot (Homan sign), although this is a nonspecific and insensitive test
  • Low-grade fever that cannot be explained after investigation of other possible sources
  • Superficial thrombophlebitis felt as a palpable cord and/or superficial venous distention at the knee, groin, or anterior abdominal wall

The clinical signs and symptoms of pulmonary embolism (PE) may be the primary manifestation in patients with confirmed DVT. Symptoms may include pleuritic chest pain, dyspnea, hemoptysis, and feelings of impending doom. Further physical signs of PE may include the following:

  • Tachycardia
  • Tachypnea
  • Hypoxia
  • Change in mental status
  • Pleural friction rub, pleural effusion
  • Fever
  • Cyanosis
  • Rales

Differential Diagnosis

As noted in Clinical Evaluation, the accurate diagnosis of deep vein thrombosis (DVT) by clinical signs and symptoms alone is unreliable at best. Signs of unexplained fever, unilateral leg swelling (although swelling can be bilateral), or erythema should alert the clinician to the possibility of DVT. The sudden onset of chest pain, tachycardia, tachypnea, hypoxia, hypotension, or cardiac arrhythmia should suggest pulmonary embolism (PE).

Conditions that should be also considered in a patient with spinal cord injury (SCI) and suspected thromboembolism include fractures, muscle or soft-tissue injury, dependent edema, ruptured Baker cyst, and hematoma. Other conditions in the differential diagnosis include the following:


Diagnostic Tests

D-dimer assays are a useful adjunct to noninvasive testing for suggested deep vein thrombosis (DVT). They are formed when crossed-linked fibrin contained in a thrombus is proteolyzed by plasmin, are highly sensitive, and have a high negative predictive value. D-dimer assays rule out DVT if the results are negative, but the assays are less helpful if the results are positive, especially in trauma patients. Impedance plethysmography (IPG) is a noninvasive test that generates no images, relying instead on unfamiliar technology. [11] This test is less sensitive than other tests for detecting DVT of the calf muscle, has less sensitivity and specificity than Doppler ultrasonography, and is less sensitive to incomplete obstruction of a vein by DVT. In addition, extrinsic compression may give a positive result.

Radiologic Studies

The following imaging studies may be used in the diagnosis of thromboembolic disease: radiocontrast venography, Doppler ultrasonography, I-125 fibrinogen scintigraphy, and ventilation/perfusion scanning.

Radiocontrast venography

Radiocontrast venography is the criterion standard for the diagnosis of deep vein thrombosis (DVT). This is a costly, invasive procedure that may have adverse effects, including pain. There is potential for contrast-mediated thrombosis and dye allergy.

Doppler ultrasonography

Doppler ultrasonography has become the preferred test in the diagnosis of DVT. It is a noninvasive and sensitive (98-100%) method for the diagnosis of proximal DVT. Doppler ultrasonography allows direct imaging of major veins and assessment of flow velocity in these veins. Its diagnostic accuracy compares favorably with that of venography, but it is dependent on operator expertise.

I-125 fibrinogen scintigraphy

Iodine-125 (125 I) fibrinogen scanning has the greatest sensitivity for calf vein DVT. However, this imaging modality is rarely used in the clinical setting. Disadvantages include cost, a 24-hour delay from injection to reading, failure to detect established thrombi, and the danger of viral transmission.

V/Q scanning

Ventilation/perfusion lung scanning is indicated as part of the diagnostic evaluation of pulmonary embolism (PE). A definitive diagnosis occurs if the results are normal or if there is a high probability, especially if clinical suspicion is confirmed by results. Low or intermediate probability scan results require further evaluation (with, for example, lower extremity Doppler ultrasonography or pulmonary angiography).


Mechanical Prophylaxis

The high risk of thromboembolic complications makes routine prophylaxis in spinal cord injury (SCI) patients essential. [12] The prevention of deep vein thrombosis (DVT) and its sequelae is an important aspect of treatment for patients who have sustained spinal cord injury.

Mechanical prophylaxis modalities (eg, compression hose, external pneumatic devices, electrical stimulation, venous foot pumps, range of motion [ROM] exercises) have been shown to be effective for reducing the incidence of DVT in acute spinal cord injury, [13] although they must be used in conjunction with anticoagulation therapy. [12] Before applying mechanical compression, tests to exclude the presence of lower extremity DVT should be undertaken if thromboprophylaxis has been delayed for more than 72 hours after injury.

Compression hose

Compression hose (elastic stockings) distribute pressure uniformly over the extremity, improve lower extremity venous return, help to control edema, require that the integrity of underlying skin be examined daily, and are ineffective alone.

Use compression hose with all patients for the first 2 weeks following spinal cord injury. No known study has evaluated whether the incidence of DVT is different in patients wearing thigh-length elastic stockings than it is in those wearing the calf-length type.

External pneumatic devices

External pneumatic devices have a mode of compression that is graded sequential, multicompartment uniform, or single-chamber uniform pressures. These devices improve lower extremity venous return but are ineffective alone.

Use in all patients for the first 2 weeks following spinal cord injury. External pneumatic devices may be knee or thigh length. These devices are contraindicated in patients with severe arterial insufficiency.

Electrical stimulation

Electrical stimulation mechanically stimulates dorsiflexion and plantar flexion of the lower extremity. This modality reduces lower extremity stasis but is ineffective alone.

Electrical stimulation must be used 24 hours per day, hindering the patient's ability to participate in therapies. Stimulation is painful in sensate patients. This modality has not been fully established by the medical literature.


Venous foot pumps have not been studied in larger trials or in patients spinal cord injury, so their efficacy in the prevention of DVT in this population has not been established.

Active and passive ROM exercises reduce lower extremity stasis. Some indirect evidence exists that ROM could be beneficial in the prevention of DVT. ROM is ineffective alone.

The amount of time needed for bedrest and for the discontinuation of lower extremity ROM has been debated in the literature. Most widely accepted evidence suggests mobilization of the patient 24-72 hours after the injury and maintenance of the individual on intravenous (IV) heparin, with an international normalized ratio (INR) goal of greater than 2.



As noted in Mechanical Prophylaxis, routine prophylaxis in spinal cord injury (SCI) patients essential owing to the high risk of thromboembolic complications in these patients. [12] The prevention of pulmonary embolism (PE) is the primary reason why the diagnosis and treatment of venous thrombosis are urgent. Mechanical methods alone are ineffective in preventing thromboembolism.

All patients with spinal cord injury should be on some type of anticoagulation therapy, such as the following:

  • Unfractionated heparin (fixed or adjusted dose) [14, 15]
  • Low–molecular weight heparin (LMWH) [13, 14, 15, 16, 17]
  • Warfarin [13, 14, 15]

The Consortium for Spinal Cord Medicine developed clinical practice guidelines for the prevention of thromboembolism in spinal cord injury based on the best available scientific evidence. [18, 19]


Historically, low-dose heparin (LDH) has been used for deep vein thrombosis (DVT) prophylaxis, but many studies demonstrate that LMWH is superior for the prevention of thromboembolism. [13, 14, 15, 16, 17]

Limited evidence exists to support the use of adjusted-dose heparin versus LMWH therapy in patients with acute spinal cord injury. [14, 15] A meta-analysis of nonsurgical patients at risk for DVT concluded that the frequency of LDH dosing (bid versus tid) did not differ in the effect of DVT, PE, major bleeding, or mortality. Furthermore, either of the two dosing regimens of LDH or LMWH appeared to be a reasonable strategy for thromboprophylaxis in medical patients. [20]

Clinical practice guidelines recommends adjusted-dose heparin or LMWH for anticoagulant prophylaxis. [18, 19] Studies have shown that the incidence of DVT is significantly lower when one of these anticoagulants is administered within 72 hours after spinal cord injury, provided that there is no active bleeding, evidence of head injury, or coagulopathy.

LDH therapy, external pneumatic devices, or compression stockings provide inadequate protection when used alone, but they are of benefit when used in combination in patients with spinal cord injury. [21]

Subcutaneous anticoagulants

Subcutaneous anticoagulants at specified intervals inhibit factors X and XI in the clotting cascade, resulting in a decrease in the generation of thrombin and a reduction in clot formation. In the case of an already formed thrombosis, anticoagulation prevents further clot formation and allows the body's autolytic system to effectively lyse and heal DVT. [14, 15, 22, 23, 24, 25]

Thrombolytic therapy

The use of thrombolytic therapy (eg, tissue plasminogen activator [t-PA], urokinase, streptokinase) in patients with spinal cord injury for the treatment of DVT and PE has not been established.

Duration of prophylaxis

The recommendation is that DVT prophylaxis be continued for a minimum of 8 weeks following injury in patients with uncomplicated, complete motor spinal cord injury and for 12 weeks in patients with complete motor injury and other risk factors.

If the patient is discharged from the hospital before the recommended time, then DVT prophylaxis can be continued on an outpatient basis, provided that adequate home care and close medical follow-up can be arranged.

Patients with spinal cord injury who have recurrences of thromboembolic disease may also require prolonged therapy.


Surgical Intervention

Placement of a vena cava filter is indicated in patients who have not achieved success with anticoagulant prophylaxis or who have a contraindication to anticoagulation. [26] This procedure is not a substitute for thromboprophylaxis, due to the morbidity related to deep vein thrombosis (DVT) (eg, postphlebitic syndrome) and the propagation of vena caval embolisms. Possible complications include vena caval thrombosis, filter migration, and vena caval perforation.

Thromboembolectomy is indicated when anticoagulant therapy is ineffective, unsafe, or contraindicated. A thromboembolectomy can be performed to restore venous patency.


Complications and Prognosis

Pulmonary embolism (PE) is the most serious and fatal complication of deep vein thrombosis (DVT); acute PE may occur despite adequate thromboprophylaxis.

Recurrence of DVT is a complication in patients with spinal cord injury (SCI). Postphlebitic syndrome is a late complication of DVT and is associated with venous insufficiency.

Hemorrhagic complications from anticoagulation are also possible.

The prompt and accurate diagnosis of DVT is vital to the initiation of proper treatment; such treatment can prevent more serious complications, such as clot progression and/or PE. Therefore, patients, family members, and caregivers should be educated in the recognition and prevention of DVT.

For patients with acute spinal cord injury, the risk of death due to PE is 210 times greater than that for a similar, healthy population. According to clinical practice guidelines, this risk decreases to 19.1 times the normal risk during years 2-5; it further decreases (to 8.9 times the normal risk) in patients who survive longer than 5 years. [18, 19]