eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Prevention of Thromboembolism in Spinal Cord Injury

Author: Dana McKinney, MD, Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Kansas Medical Center
Coauthor(s): Susan V Garstang, MD, Assistant Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey; Attending Medical Staff, Director of Spinal Cord Injury Program, Department of Physical Medicine and Rehabilitation, University Hospital
Contributor Information and Disclosures

Updated: Jan 13, 2009

Introduction

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 patients with SCI. Many patients with SCI 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 prophylaxis.² 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 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 prior to this time appears to be low.

Related eMedicine topics:
Deep Venous Thrombosis
Deep Venous Thrombosis and Thrombophlebitis
Deep Venous Thrombosis, Lower Extremity
Deep Venous Thrombosis Prophylaxis in Orthopedic Surgery
Deep Venous Thrombosis, Upper Extremity
Perioperative DVT Prophylaxis
Pulmonary Embolism [Emergency Medicine]
Pulmonary Embolism [Pulmonology]
Spinal Cord Injuries
Spinal Cord Injury: Definition, Epidemiology, Pathophysiology
Spinal Cord Trauma and Related Diseases
Thromboembolism [Orthopedic Surgery]
Thromboembolism [Pediatrics: General Medicine]

Pathophysiology

Predisposing risk factors for the development of deep vein thrombosis (DVT) following spinal cord injury (SCI) are found in the Virchow triad (ie, venous stasis, hypercoagulable state, endothelial injury). Venous stasis results from loss of the pumping function normally provided by contracting limb muscles. Hypercoagulability result 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 they 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 gender.³ In the 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 SCI and those with a nontraumatic cause.² Thus, all patients with SCI are at risk of developing a DVT.

Related eMedicine topics:
Factor VIII
von Willebrand Disease [Hematology]
Von Willebrand Disease [Pediatrics: General Medicine]

Frequency

United States

In prospective studies, the incidence of deep vein thrombosis (DVT) following acute spinal cord injury (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 the meta-analysis of DVT in patients with acute SCI. Clinically apparent DVT occurs in approximately 15% of patients with acute SCI, and PE develops in approximately 5% of acute SCI cases.

Mortality/Morbidity

Because of the high incidence of thromboembolic disease in patients with acute spinal cord injury and owing to the potential morbidity and mortality associated with this disease, the use of effective prophylactic measures is of great importance. Morbidities from DVT include postphlebitic syndrome, prolonged edema, and pressure ulcers. Pulmonary embolisms can cause arrhythmias, hypoxia, and death.

Sex

A higher prevalence has been noted in males.

Age

No age prevalence has been found for deep vein thrombosis.

Clinical

History

In patients with spinal cord injury (SCI), clinical diagnostic signs and symptoms may differ from those found in noninjured patients and may be much more difficult to identify. The characteristics and diagnostic value of various clinical signs and symptoms are as follows:

• Leg swelling
  • Typically, the hallmark of deep vein thrombosis (DVT) is a rapid onset of unilateral leg swelling.
  • Swelling of the 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.
• The clinical signs and symptoms of pulmonary embolism 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 deep vein thrombosis (DVT). However, although it is virtually impossible to distinguish DVT from other processes, the following findings should raise clinical suspicion:

• Leg swelling
  • Principally unilateral, but may be bilateral
  • 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), 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 pulmonary embolism (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 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 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.

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