eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Prevention of Thromboembolism in Spinal Cord Injury

Dana McKinney, MD, Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Kansas Medical Center
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

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.

Differential Diagnoses

Achilles Tendon Injuries and Tendonitis
Bursitis
Cellulitis
Heterotopic Ossification
Lymphedema
Superficial Thrombophlebitis

Other Problems to Be Considered

Fracture
Muscle or soft tissue injury
Dependent edema
Ruptured Baker cyst
Hematoma

Workup

Laboratory Studies

• D-dimer assays
  • Formed when crossed-linked fibrin contained in a thrombus is proteolyzed by plasmin
  • Useful adjunct to noninvasive testing for suggested deep vein thrombosis (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 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). 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 ultrasonography
  • 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
  • Diagnostic accuracy compares favorably with that of venography
  • Dependent on operator expertise
  • Has become the preferred test in the diagnosis of DVT
• ¹²⁵ I fibrinogen scan
  • Greatest sensitivity for calf vein DVT
  • Rarely used in the clinical setting
  • Some disadvantages - These include cost, a 24-hour delay from injection to reading, failure to detect established thrombi, and the danger of viral transmission.
• Impedance plethysmography (IPG)⁴
  • Noninvasive test
  • Generates no images, relying instead on unfamiliar technology
  • Less sensitive for detecting DVT of calf muscle
  • Less sensitivity and specificity than Doppler ultrasonography
  • 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 the diagnostic evaluation of 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).

Related eMedicine topic:
Bedside Ultrasonography, Deep Vein Thrombosis

Treatment

Medical Care

The high risk of thromboembolic complications makes routine prophylaxis in spinal cord injury (SCI) patients essential.⁵ The prevention of deep vein thrombosis (DVT) and its sequelae is an important aspect of treatment for 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.⁵ 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. Mechanical modalities include the following⁶ :

• 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
  • Are ineffective alone
  • Use with all patients for the first 2 weeks following injury.
  • No known study evaluating 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
  • Mode of compression - Graded sequential, multicompartment uniform, or single-chamber uniform pressures
  • Improve lower extremity venous return
  • Ineffective alone
  • For 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 - Because these have not been studied in larger trials or in SCI patients, their efficacy in the prevention of DVT in this population has not been established.
• Range of motion (ROM)
  • Active and passive ROM reduce lower extremity stasis.
  • Some indirect evidence exists that ROM could be beneficial in the prevention of DVT.
  • ROM is ineffective alone
• Electrical stimulation
  • Mechanically stimulates dorsiflexion and plantar flexion of the lower extremity
  • Reduces lower extremity stasis
  • Is ineffective alone
  • 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.
• Pharmacologic prophylaxis - All patients should be on some type of anticoagulation therapy (see Medication for details).
  • Unfractionated heparin (fixed or adjusted dose)^7,8
  • Low–molecular weight heparin^6,7,8,9,10
  • Warfarin^6,7,8

Surgical Care

• Vena cava filter¹¹
  • Indicated in patients who have not achieved success with anticoagulant prophylaxis or who have a contraindication to anticoagulation
  • Not a substitute for thromboprophylaxis, due to the morbidity related to deep vein thrombosis (eg, postphlebitic syndrome) and the propagation of vena caval embolisms
  • Possible complications include vena caval thrombosis, filter migration, and vena caval perforation.
• Thromboembolectomy - This is indicated when anticoagulant therapy is ineffective, unsafe, or contraindicated. A thromboembolectomy can be performed to restore venous patency.

Activity

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 IV heparin, with an international normalized ratio (INR) goal of greater than 2.

Medication

The prevention of pulmonary embolism is the primary reason why the diagnosis and treatment of venous thrombosis are urgent. Historically, low-dose heparin has been used for deep vein thrombosis (DVT) prophylaxis, but many studies demonstrate that low–molecular weight heparin (LMWH) is superior for the prevention of thromboembolism.^6,7,8,9,10  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 spinal cord injury (SCI), based on the best available scientific evidence.^12,13

Limited evidence exists to support the use of adjusted-dose heparin versus LMWH therapy in patients with acute SCI.^7,8 The CPG recommends adjusted-dose heparin or LMWH for anticoagulant prophylaxis.^12,13 Studies have shown that the incidence of DVT is significantly lower when one of these anticoagulants is administered within 72 hours after SCI, provided that 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.

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 deep vein thrombosis.^7,8,14,15,16

Related eMedicine topics:
Factor X
Factor XI Deficiency

Heparin

Augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin.

Dosing

Adult

Fixed dose: Usually 5,000 U SC q12h-q8h; ineffective alone for DVT prophylaxis
Adjusted dose: Based on patient's weight and requires monitoring of prothrombin time to maintain at 1.5-2 times control (doses averaging 13,200 U SC q12h); increased risk for hemorrhage; IM use not recommended
Treat uncomplicated complete motor patients for 8 wk; treat complete motor injury patients with other risk factors for 12 wk

Pediatric

Not established

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, ASA, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity

Contraindications

Documented hypersensitivity; subacute bacterial endocarditis, active bleeding, history of heparin-induced thrombocytopenia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in severe hypotension and shock; monitor blood coagulation tests, platelets, hematocrit, and for occult blood in stool

Enoxaparin (Lovenox)

Enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, enoxaparin preferentially increases the inhibition of factor Xa. This product has been FDA approved for the prophylaxis of thrombosis in patients undergoing surgical procedures on the abdomen, pelvis, hip, and knee; it is more efficacious for prophylaxis than is low-dose unfractionated heparin. Enoxaparin has fewer bleeding complications, as well as a longer half-life and more bioavailability, than does unfractionated heparin. Because there is no requirement for monitoring, enoxaparin is suitable for home treatment.

Dosing

Adult

30 mg SC q12h

Pediatric

Not established

Interactions

Oral anticoagulants or platelet inhibitors, such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine, may increase risk of bleeding

Contraindications

Documented hypersensitivity to heparin or pork products, major bleeding, and thrombocytopenia associated with antiplatelet antibody in presence of enoxaparin

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

If thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate alternate therapy; elevation of hepatic transaminases may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated LMWH; 1 mg of protamine sulfate will reverse effect of approximately 1 mg of enoxaparin if significant bleeding complications develop; caution in thrombocytopenia, severe uncontrolled hypertension, bacterial endocarditis, bleeding disorders, hemorrhagic stroke, and recent brain, spinal, or ophthalmic surgery

Dalteparin (Fragmin)

Enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, dalteparin preferentially increases the inhibition of factor Xa.

Dosing

Adult

5000 IU SC qd

Pediatric

Not established

Interactions

Platelet inhibitors or oral anticoagulants, such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine, may increase risk of bleeding

Contraindications

Documented hypersensitivity to heparin or pork products, major bleeding, and thrombocytopenia

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

If thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate alternate therapy; elevation of hepatic transaminases may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated LMWH; 1 mg of protamine sulfate will reverse effect of approximately 1 mg of dalteparin if significant bleeding complications develop; caution in thrombocytopenia, severe uncontrolled hypertension, bacterial endocarditis, bleeding disorders, hemorrhagic stroke, and recent brain, spinal, or ophthalmic surgery

Warfarin (Coumadin)

Interferes with the hepatic synthesis of vitamin K – dependent coagulation factors. Warfarin is used for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Adjust the dose as needed to maintain an INR in the range of 2 to 3.

Dosing

Adult

2-5 mg/d PO qd initial dose; 2-10 mg/d PO maintenance dose; adjust dose according to desired INR

Pediatric

Not established

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate; medications that may increase anticoagulant effects of warfarin include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity; severe liver or kidney disease; open wounds or GI ulcers

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Fondaparinux (Arixtra)

Selectively binds to antithrombin III and potentiates the neutralization of factor Xa. The neutralization of factor Xa interrupts the blood coagulation cascade and thus inhibits thrombin formation and thrombus development.

Dosing

Adult

2.5 mg SC qd

Pediatric

Not established

Interactions

None reported; increased risk of bleeding possible with concurrent administration of platelet inhibitors, oral anticoagulants, or thrombolytic agents

Contraindications

Documented hypersensitivity; seriously impaired kidney function (CrCl <30 mL/min) or in patients who weigh <110 lb; patients given spinal anesthesia or spinal puncture; active bleeding, bacterial endocarditis, thrombocytopenia associated with positive in vitro test for antiplatelet antibody in presence of fondaparinux therapy

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

When spinal anesthesia or spinal puncture is used, may develop blood clot in spine, which can result in long-term or permanent paralysis (holding 2 doses prior to LP or surgery is recommended); major bleeding risk increased when initiated before 6 h following surgery; elimination decreased in elderly and renal impairment

Thrombolytics

The use of thrombolytic therapy (eg, t-PA, urokinase, streptokinase) in patients with spinal cord injury for the treatment of deep vein thrombosis and pulmonary embolism has not been established.

Urokinase (Abbokinase)

Direct plasminogen activator that acts on the endogenous fibrinolytic system and converts plasminogen to the enzyme plasmin, which in turn degrades fibrin clots, fibrinogen, and other plasma proteins.

Dosing

Adult

Loading dose: 4400 U/kg IV over 10 min and increase to 6000 U/kg/h
Maintenance dose: 4400-6000 U/kg/h IV

Pediatric

Not established

Interactions

Thrombolytic enzymes, alone or in combination with anticoagulants and antiplatelets, may increase risk of bleeding complications

Contraindications

Documented hypersensitivity; internal bleeding, recent trauma, history of intracranial or intraspinal surgery or trauma, cerebrovascular accident, intracranial neoplasm, AV malformation, aneurysm, bleeding diathesis, severe uncontrolled hypertension

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients receiving intramuscular administration of medications, severe hypertension, trauma, or surgery in previous 10 d; avoid dislodging possible deep vein thrombi, do not measure blood pressure in lower extremities; monitor therapy by performing PT, aPTT, TT, or fibrinogen approximately 4 h after initiation of therapy

Streptokinase (Kabikinase, Streptase)

Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots, as well as fibrinogen and other plasma proteins. An increase in fibrinolytic activity that degrades fibrinogen levels for 24-36 h takes place with IV infusion of streptokinase.

Dosing

Adult

Loading dose: 250,000 U IV over 30 min
Maintenance: 100,000 U/h IV for 24-72 h

Pediatric

Not established

Interactions

Antifibrinolytic agents may decrease effects of streptokinase; heparin, warfarin, and aspirin may increase risk of bleeding

Contraindications

Documented hypersensitivity; active internal bleeding, intracranial neoplasm, aneurysm, diathesis, and severe uncontrolled arterial hypertension

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in severe hypertension, intramuscular administration of medications, trauma, or surgery in the previous 10 days; measure hematocrit, platelet count, aPTT, TT, PT, or fibrinogen levels before therapy is implemented; either TT or aPTT should be less than twice the normal control value following infusion of streptokinase and before (re)instituting heparin; do not take blood pressure in the lower extremities, as it may dislodge a possible deep vein thrombus; PT, aPTT, TT, or fibrinogen should be monitored 4 h after initiation of therapy

Alteplase (Activase)

Tissue plasminogen activator used in the management of acute myocardial infarction, acute ischemic stroke, and pulmonary embolism.

Dosing

Adult

Infuse 0.9 mg/kg (not to exceed 90 mg) over 60 min, with 10% of total dose administered as initial IV bolus over 1 min

Pediatric

Not established

Interactions

Drugs that alter platelet function (eg, aspirin, dipyridamole, abciximab) may increase risk of bleeding prior to, during, or after alteplase therapy; may give heparin with and after alteplase infusions to reduce risk of recurrence of thrombosis; either heparin or alteplase may cause bleeding complications

Contraindications

Documented hypersensitivity; active internal bleeding, cerebrovascular accident or stroke within last 2 mo, intracranial or intraspinal surgery or trauma, intracranial hemorrhage on pretreatment evaluation, suspicion of subarachnoid hemorrhage, intracranial neoplasm, AV malformation or aneurysm, bleeding diathesis, or severe uncontrolled hypertension

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following alteplase administration (when managing acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH

Follow-up

Further Inpatient Care

• The recommendation is that deep vein thrombosis (DVT) prophylaxis be continued for a minimum of 8 weeks following injury in patients with uncomplicated, complete motor spinal cord injury (SCI) and for 12 weeks in patients 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 deep vein thrombosis (DVT) prophylaxis
  • Pulmonary embolism (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 deep vein thrombosis (DVT) is vital to the initiation of proper treatment; such treatment can prevent more serious complications, such as clot progression and/or pulmonary embolism (PE).
• 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 the CPG, 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 more than 5 years.^12,13

Patient Education

• Patients, family members, and caregivers should be educated in the recognition and prevention of deep vein thrombosis (DVT).
• For excellent patient education resources, visit eMedicine's Circulatory Problems Center and Lung and Airway Center. Also, see eMedicine's patient education articles Deep Vein Thrombosis (Blood Clot in the Leg, DVT) and Pulmonary Embolism.

Miscellaneous

Medicolegal Pitfalls

• Failure to provide adequate deep vein thrombosis (DVT) prophylaxis in acute spinal cord injury (SCI) patients, based on current literature
• Failure to consider the diagnosis of DVT/pulmonary embolism in symptomatic SCI patients and to perform appropriate studies in a timely manner
• Failure of health care providers to understand the rate of incidence of and the risk factors for thromboembolism development in SCI patients, because patients frequently are asymptomatic
• Failure to consider the 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

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13. Consortium for Spinal Cord Medicine Clinical Practice Guidelines. Prevention of Thromboembolism in Spinal Cord Injury. 2^nd ed. Washington, DC: Paralyzed Veterans of America; 1999.

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Keywords

deep venous thrombosis, embolism, DVT, pulmonary embolism, spinal cord injury, clot, blood clot, blood clots, paralysis, spinal cord, spinal, platelet, platelets, thromboembolism, vein thrombosis, deep vein thrombosis, venous thrombosis, anticoagulation, paraplegia, thromboembolic disease, vein thrombosis treatment, venous thrombosis treatment

Contributor Information and Disclosures

Author

Dana McKinney, MD, Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Kansas Medical Center
Dana McKinney, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Paraplegia Society, and National Medical Association
Disclosure: Nothing to disclose.

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
Susan V Garstang, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Medical Editor

Milton J Klein, DO, MBA, Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital, Allegheny General Hospital, and Ohio Valley General Hospital.
Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds Novaritis; Novaritis  Novaritis; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

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