AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are common complications of acute spinal cord injury (SCI) and a major cause of morbidity and mortality in this patient population. Many patients with SCI do not receive DVT prophylaxis in the acute care setting, perhaps secondary to concomitant medical problems that may enhance the risk of bleeding. In a recent retrospective study by Powell et al, 38.6% of patients admitted to a rehabilitation hospital were receiving prophylaxis. Clinically apparent DVT occurs in approximately 15% of patients with acute SCI, and PE develops in approximately 5% of these patients. The risk of DVT is highest in 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 prior to this time appears to be low.

Pathophysiology

Predisposing risk factors for the development of DVT following SCI can be classified with the Virchow triad (ie, venous stasis, hypercoagulable state, endothelial injury). Venous stasis results from loss of pumping function normally provided by contracting limb muscles. Hypercoagulability can occur as a result of stimulation of thrombogenic factors following injury, with resultant increase in platelet aggregation and adhesion. Intimal injury may result directly from the release of vasoactive amines with trauma or surgery, or indirectly from external pressure on the paralyzed leg.

Patients with DVT have higher levels of von Willebrand factor antigen and Factor VIII-related antigen and demonstrate hyperactive platelet aggregation responses to collagen and the appearance of circulating platelet aggregates compared with patients without thrombosis.

Clinical factors believed to be associated with DVT include motor complete injuries, paraplegia, and male gender. In the recent study by Powell et al, there was no statistical difference in incidence of DVT between motor complete versus motor incomplete injuries, tetraplegic versus paraplegic, or traumatic versus nontraumatic causes. Thus, all SCI patients are at risk of developing a DVT.

Frequency

United States

In prospective studies, the incidence of DVT following acute SCI has been reported at 18-100%, depending on the diagnostic technique used, time after SCI, and concurrent risk factors. Overall incidence without prophylaxis is estimated to be 40% based on meta-analysis of DVT in patients with acute SCI. Clinically apparent DVT occurs in approximately 15% and PE in approximately 5% of acute SCI patients.

Mortality/Morbidity

Due to the high incidence of thromboembolic disease in patients with acute SCI and the potential morbidity and mortality associated with this disease, use of effective prophylactic measures is of great importance and cannot be underestimated. Morbidities from DVT include postphlebitic syndrome, prolonged edema, and pressure ulcers. PE can cause arrhythmias, hypoxia, and death.

Sex

Preferential occurrence has been noted in males.

Age

Development of DVT is uniform over different age groups.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Clinical signs and symptoms for the diagnosis may be different than in noninjured patients and may be much more difficult to identify in SCI patients.

• Leg swelling
• • Typically, the hallmark of DVT is rapid onset of unilateral leg swelling.
  • Swelling of lower extremities may be bilateral.
  • Edema may be the only presenting symptom.
• Leg pain
• • This symptom is nonspecific and includes a vast differential diagnosis.
  • Leg pain generally is not a useful diagnostic symptom in patients with insensate lower extremities following SCI.
• Clinical signs and symptoms of PE may be the primary manifestation in patients with confirmed DVT. Symptoms may include pleuritic chest pain, dyspnea, hemoptysis, and feelings of impending doom.

Physical

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

• Leg swelling
• • Principally unilateral, but may be bilateral
  • Circumferential increase of the affected leg by at least 3 cm
• Tenderness upon 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), 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 distension at the knee, groin, or anterior abdominal wall
• As stated before, clinical signs and symptoms of PE may be the primary manifestation in patients with confirmed DVT. Further physical signs of PE may include the following:
• • Tachycardia
  • Tachypnea
  • Hypoxia
  • Change in mental status
  • Pleural friction rub
  • Fever
  • Cyanosis
  • Rales
  • Pleural effusion

Causes

Patients with 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 include the following:

• 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.
• Prior venous thromboembolism
• Surgical procedure of lower extremity/pelvis
• Cancer/malignancy
• Oral contraceptive use/pregnancy
• Trauma (eg, multiple trauma, SCI, burns, lower extremity fractures): Direct mechanical injury to the lower extremities may lead to blood clot formation.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Cellulitis
Fracture
Muscle or soft tissue injury
Superficial thrombophlebitis
Dependent edema
Lymphedema
Bursitis
Ruptured Baker cyst
Hematoma

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• D-dimer assays
• • Formed when crossed-linked fibrin contained within a thrombus is proteolyzed by plasmin
  • Useful adjunct to noninvasive testing for suggested DVT
  • Highly sensitive
  • High negative predictive value (rules out DVT if negative, but is less helpful if positive, especially in trauma patients)

Imaging Studies

• The accurate diagnosis of 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. Sudden onset of chest pain, tachycardia, tachypnea, hypoxia, hypotension, or cardiac arrhythmia should suggest PE. The following studies may be used in the diagnosis of thromboembolic disease:
• • Radiocontrast venography
    • The criterion standard for the diagnosis of DVT
    • Invasive procedure that may have adverse effects, including pain
    • Potential of contrast-mediated thrombosis and dye allergy
    • Costly procedure
• Doppler ultrasound
  • Noninvasive and sensitive (98-100%) method for the diagnosis of proximal DVT
  • Allows direct imaging of major veins and assessment of velocity of flow in these veins
  • The diagnostic accuracy of this technique compares favorably with venography.
  • Dependent on operator expertise
  • Has become the preferred test in the diagnosis of DVT
• I-125 fibrinogen scan
  • Greatest sensitivity for calf vein DVT
  • Rarely used in the clinical setting
  • Disadvantages include its cost, the 24-hour delay from injection to reading, failure to detect established thrombi, and the danger of viral transmission.
• Impedance plethysmography (IPG)
  • Noninvasive test
  • Generates no images and relies instead on unfamiliar technology
  • Less sensitive for detecting DVT of calf muscle
  • Less sensitivity and specificity than Doppler ultrasound
  • Less sensitive to incomplete obstruction of vein by DVT
  • Extrinsic compression may give positive result.
• Ventilation/perfusion lung scan
  • This scan is indicated as part of diagnostic evaluation of PE.
  • Definitive diagnosis occurs if results are normal or there is high probability, especially if clinical suspicion is confirmed by results.
  • Low or intermediate probability scan results require further evaluation, such as lower extremity Doppler ultrasound or pulmonary angiography.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

The high risk of thromboembolic complications makes routine prophylaxis in SCI patients essential. Prevention of DVT and its sequelae is an important aspect of the treatment of patients who have sustained SCI.

Mechanical modalities have been shown to be effective for reducing the incidence of DVT in acute SCI patients, although they must be used in conjunction with anticoagulation therapy. Prior to 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 (elastic stockings)
  • Apply a uniform distribution of pressure over the extremity
  • Improve lower extremity venous return
  • Help to control edema
  • Underlying skin should be examined daily for integrity.
  • Ineffective alone
  • Use with all patients for the first 2 weeks following injury.
  • No study is known to evaluate the difference in the incidence of thigh-length versus calf-length elastic stockings.
• External pneumatic devices
  • Mode of compression - Graded sequential, multicompartment uniform, or single-chamber uniform pressures
  • Improve lower extremity venous return
  • Ineffective alone
  • Use in all patients for the first 2 weeks following injury.
  • May be knee or thigh length
  • Contraindicated in patients with severe arterial insufficiency
• Venous foot pumps have not been studied in larger trials or in SCI patients, so efficacy in prevention of DVT in this population has not been established.
• Range of motion
  • Active and passive range of motion (ROM) reduces lower extremity stasis.
  • Some indirect evidence exists that ROM could be beneficial in the prevention of DVT.
  • Ineffective alone
• Electrical stimulation
  • Mechanically stimulates dorsiflexion and plantar flexion of lower extremity
  • Reduces lower extremity stasis
  • Ineffective alone
  • Must be used 24 hours/day, hindering the patient's ability to participate in therapies
  • Stimulation is painful in sensate patients.
  • This modality has not been established fully by medical literature.
• Pharmacologic prophylaxis: All patients should be on some type of anticoagulation therapy (see Medication for details).
  • Unfractionated heparin (fixed or adjusted dose)
  • Low molecular weight heparin
  • Warfarin

Surgical Care

• Vena cava filter
• • Indicated in patients who have not achieved success with anticoagulant prophylaxis or have a contraindication to anticoagulation
  • Not a substitute for thromboprophylaxis, due to morbidity related to DVT (eg, postphlebitic syndrome) and propagation of venal caval embolism
  • Possible complications include vena cava thrombosis, filter migration, and vena cava perforation.
• Thromboembolectomy is indicated when anticoagulant therapy is ineffective, unsafe, or contraindicated. This procedure can be performed to restore venous patency.

Activity

The amount of time needed for bedrest and for 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 on IV heparin with an INR goal of greater than 2.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The prevention of PE is the primary reason why diagnosis and treatment of venous thrombosis are urgent. Historically, low dose heparin has been used for DVT prophylaxis, but many studies demonstrate that low molecular weight heparin (LMWH) is superior in the prevention of thromboembolism. External pneumatic devices alone are not effective for DVT prevention. The Consortium for Spinal Cord Medicine developed clinical practice guidelines (CPG) for the prevention of thromboembolism in SCI, based on the best available scientific evidence.

Limited evidence exists to support the use of adjusted dose heparin versus LMWH therapy in patients with acute SCI. CPG recommends adjusted dose heparin or LMWH for anticoagulant prophylaxis. Studies have shown that the incidence of DVT is significantly lower when one of these anticoagulants is administered within 72 hours after SCI, provided there is no active bleeding, evidence of head injury, or coagulopathy. Low dose heparin 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 SCI.

Drug Category: Anticoagulants

Subcutaneous anticoagulants at specified intervals inhibit factors X and XI in the clotting cascade, resulting in decreased generation of thrombin and clot formation. In the case of already formed thrombosis, anticoagulation prevents further clot formation and allows the body's autolytic system to effectively lyse and heal DVT.

Drug Category: Thrombolytics

Thrombolytic therapy (eg, t-PA, urokinase, streptokinase) use in patients with SCI for the treatment of DVT and PE has not been established.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• The recommendation is that DVT prophylaxis be continued for a minimum of 8 weeks in patients with uncomplicated complete motor SCI following injury and 12 weeks for those with complete motor injury and other risk factors. If the patient is discharged from the hospital prior to 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 SCI who have recurrences of thromboembolic disease also may require prolonged therapy.

Complications

• Failure of DVT prophylaxis
• • PE is the most serious and fatal complication of DVT. Acute PE may occur despite adequate thromboprophylaxis.
  • Recurrence of DVT is a complication in patients with SCI.
  • Postphlebitic syndrome is a late complication of DVT and is associated with venous insufficiency.
• Hemorrhagic complications from anticoagulation

Prognosis

• The prompt and accurate diagnosis of DVT is vital so that proper treatment can be initiated to prevent more serious complications, such as clot progression and/or PE.
• For those patients with acute SCI, the risk of death due to PE is 210 times greater than that of a similar healthy population. This risk decreases to 19.1 times normal for years 2-5 and further decreases to 8.9 for those who survive more than 5 years, according to CPG.

Patient Education

• Patients, family members, and caregivers should be educated in the recognition and prevention of DVT.
• For excellent patient education resources, visit eMedicine's Circulatory Problems Center and Lung and Airway Center. Also, see eMedicine's patient education articles Blood Clot in the Legs and Pulmonary Embolism.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to provide adequate DVT prophylaxis in acute SCI patients based upon current literature
• Failure to consider the diagnosis of DVT/PE in symptomatic SCI patients and perform appropriate studies in a timely manner
• Failure of health care providers to understand the rate of incidence and risk factors of developing a thromboembolism in SCI patients because patients frequently are asymptomatic
• Failure to consider reinstitution of prophylactic measures in chronic SCI patients who have acute medical illnesses or surgical procedures if they are immobilized with bedrest for prolonged periods of time

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Akers SM, Bartter T, Pratter MR. Impedance plethysmography. It''s the clinical outcome that counts. Chest. Nov 1994;106(5):1317-8. [Medline].
• Anand SS, Wells PS, Hunt D, et al. Does this patient have deep vein thrombosis?. JAMA. Apr 8 1998;279(14):1094-9. [Medline].
• Clagett GP, Anderson FA, Heit J, et al. Prevention of venous thromboembolism. Chest. Oct 1995;108(4 Suppl):312S-334S. [Medline].
• Clagett GP, Anderson FA, Geerts W, et al. Prevention of venous thromboembolism. Chest. Nov 1998;114(5 Suppl):531S-560S. [Medline].
• Consortium for Spinal Cord Medicine Clinical Practice Guidelines. Prevention of Thromboembolism in Spinal Cord Injury. 2nd ed. Paralyzed Veterans of America;1999.
• Geerts WH, Jay RM, Code KI, et al. A comparison of low-dose heparin with low-molecular-weight heparin as prophylaxis against venous thromboembolism after major trauma. N Engl J Med. Sep 5 1996;335(10):701-7. [Medline].
• Green D. Prophylaxis of thromboembolism in spinal cord-injured patients. Chest. Dec 1992;102(6 Suppl):649S-651S. [Medline].
• Green D, Rossi EC, Yao JS, et al. Deep vein thrombosis in spinal cord injury: effect of prophylaxis with calf compression, aspirin, and dipyridamole. Paraplegia. Aug 1982;20(4):227-34. [Medline].
• Green D, Lee MY, Lim AC, et al. Prevention of thromboembolism after spinal cord injury using low- molecular-weight heparin. Ann Intern Med. Oct 15 1990;113(8):571-4.
• Merli GJ, Crabbe S, Paluzzi RG, Fritz D. Etiology, incidence, and prevention of deep vein thrombosis in acute spinal cord injury. Arch Phys Med Rehabil. Nov 1993;74(11):1199-205. [Medline].
• Merli GJ, Crabbe S, Doyle L, et al. Mechanical plus pharmacological prophylaxis for deep vein thrombosis in acute spinal cord injury. Paraplegia. Aug 1992;30(8):558-62. [Medline].
• Powell M, Kirshblum S, O''Connor KC. Duplex ultrasound screening for deep vein thrombosis in spinal cord injured patients at rehabilitation admission. Arch Phys Med Rehabil. Sep 1999;80(9):1044-6. [Medline].

Article Last Updated: Mar 22, 2006