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S P I N A L C O R D M E D I C I N E

Prevention ofThromboembolismin Spinal CordInjury

Second Edition

Consortium for Spinal Cord MedicineAdministrative and financial support provided by Paralyzed Veterans of AmericaC

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C L I N I C A L P R A C T I C E G U I D E L I N E S

S P I N A L C O R D M E D I C I N E

Prevention ofThromboembolism inSpinal Cord Injury

Second Edition

Consortium for Spinal Cord MedicineAdministrative and financial support provided by Paralyzed Veterans of America©Copyright 1999, Paralyzed Veterans of AmericaNo copyright ownership claim is made to any portion of these materials contributed bydepartments or employees of the United States Government.

This guideline has been prepared based on scientific and professional information availablein September 1999. Users of this guideline should periodically review this material toensure that the advice herein is consistent with current reasonable clinical practice.

September 1999

ii Foreword

iii Preface

iv Acknowledgments

v Panel Members

vi Contributors

1 Summary of Treatment Recommendations

GUIDELINES FOR THE PREVENTION OF THROMBOEMBOLISM IN SPINAL CORD INJURY CLINICAL DECISION TABLE

3 Introduction

6 The Spinal Cord Medicine Consortium

GOALS OF THE GUIDELINES

NEED FOR THE GUIDELINES

FRAMEWORK FOR THE GUIDELINES

METHODOLOGY

EVIDENCE ANALYSIS

8 Treatment Recommendations

MECHANICAL METHODS OF PROPHYLAXIS

ANTICOAGULANT PROPHYLAXIS

PROPHYLAXIS BASED ON PATIENT STRATIFICATION FOR RISK

FAILURE OF PROPHYLAXIS

EXERCISE, PASSIVE MOVEMENT, AND EARLY MOBILIZATION

EDUCATIONAL PRIORITIES FOR HEALTH CARE PROFESSIONALS

14 Directions for Future Research

15 References

17 Glossary of Terms

19 Index

Contents

C lots in the leg veins and pulmonary arteries occur frequently in persons with spinalcord injuries (SCI) and are a major cause of death and disability. Unfortunately,there does not appear to be a decline in either the rate of deep vein thrombosis

(DVT) or of fatalities from pulmonary embolism (PE). Because a variety of methodshave been recommended for thromboprophylaxis, some practitioners feel uncertain asto which method should be implemented and under what circumstances. As a result,considerable confusion exists in the medical community.

Prevention of these diseases requires both an awareness of the problem andimplementation of safe and effective deterrents. To this end, panelists from a varietyof disciplines—including medical specialties, physical therapy, and nursing—met underthe auspices of the Paralyzed Veterans of America (PVA) to draft recommendations forthe prevention of thromboembolism. This group, which consisted of representativesfrom 17 organizations concerned with the health of patients with spinal cord injury,commissioned a group of experts to develop clinical practice guidelines (CPGs), withrecommendations specifically for thromboprophylaxis. The panel was assisted by amethodologist, who searched the medical literature for relevant articles on this topic.These publications then were reviewed, evaluated, and placed in a database to supportdevelopment of the recommendations.

The guidelines that grew out of this process are designed to focus attention onthe issues of awareness and prevention and to provide the best medical and scientificknowledge available to those entrusted with the care of patients who are at specialrisk. The guidelines include a statement on the prevalence of venous thromboem-bolism and on the impact of thrombotic disease on rehabilitation and recovery, as wellas on mortality. Recommendations are provided on the use of local measures, such aspassive leg motion, elastic hose, compression boots, and vena cava filters. Other rec-ommendations concern the use of anticoagulants, such as the low molecular weightheparins, and combined modalities.

The concept of selecting prophylactic measures on the basis of risk is introduced,with risk being defined in terms of such factors as obesity, age, location of lesion, com-pleteness of motor paralysis, prior history of thromboembolism, concurrent surgicalprocedures, and use of agents to decrease spasticity. Recommendations for when pro-phylaxis should be initiated as well as discontinued are provided. Finally, future direc-tions for investigation are delineated, because informational gaps in the literaturebecame evident through the process of developing the guidelines.

The panelists recognize that these guidelines are but a first draft in what must bean ongoing dialogue among patients, members of the medical community, andresearchers and practitioners who prepare documents such as this. Although everyeffort has been made to provide a comprehensive statement of the problem, someissues may have been overlooked or not dealt with completely. Some areas are contro-versial and clearly require further study. And some of the recommended devices andmedications may soon become obsolete as other, safer, more effective agents take theirplace. In 1999, the panel considered three new references in the literature and modifiedappropriate recommendations accordingly. It is our fervent hope that these guidelineswill stimulate new research into the pathophysiology, management, and prevention ofthromboembolism in spinal injury and will lead to improved patient outcomes.

David Green, MD, PhDChairmanGuidelines Development Panel

ii PREVENTION OF THROMBOEMBOLISM IN SPINAL CORD INJUR Y

Foreword

Thromboembolic disorders continue to be a significant threat to the person with arecent spinal cord injury. Less well recognized is the threat of recurrent throm-boembolic disorders in people who are living with the after effects of SCI. New

research and publications have expanded the state of our knowledge since the publica-tion of the first edition of Prevention of Thromboembolism in Spinal Cord Injuryin February 1997.

Since its inception the Steering Committee of the Consortium for Spinal CordMedicine has been committed to publication of clinical practice guidelines and theirperiodic updating, so that the health-care providers who serve people with SCI willhave access to the current thinking, while maintaining the benefits of established sci-entific evidence. The second edition of Prevention of Thromboembolism in SpinalCord Injury presents such an update in our attempt to disseminate the current con-cepts of prevention of this deadly complication.

Controversies remain in this field. What about new approaches to anticoagula-tion? As risk stratification is further refined, how long should prophylaxis be contin-ued in specific clinical circumstances? What is the most cost-effective protocol thatcombines the use of the various agents that are available?

The recent increase in use of inferior vena cava filters, both temporary and per-manent, may yield benefits in prevention of pulmonary emboli, but the long-term con-sequences of their use in people with spinal cord injury must be monitored. Willassisted coughing with abdominal compression (AKA “quad cough”) dislodge a filteror cause further trauma to the inferior vena cava? Should prophylaxis be continuedindefinitely, since the presence of the filter may increase the risk of lower body throm-bosis? It is my hope that prospective studies will be published that address these ques-tions. Then there will be new material for incorporation in future editions of thisimportant guideline.

Once again I must express my gratitude to David Green, MD, PhD, for his willing-ness to lead and champion this cause for the specific population that we serve. Heand his panel have proved that endurance and effort bring continued success by pub-lishing this, the first of our second editions. I am also grateful to Dawn M. Sexton andJ. Paul Thomas at PVA as they continue to shepherd the process that leads to our pub-lications. Their excellence is manifested daily! For the leadership, membership, andsupporters of the Paralyzed Veterans of America, I reserve my highest praise: withoutyou all, this would not have been possible.

Kenneth C. Parsons, MDChairmanConsortium for Spinal Cord Medicine Steering Committee

CLINICAL PRACTICE GUIDELINES iii

Preface

T he chairman and members of the panel wish to express special appreciation to theindividuals and the professional organizations that were involved in the spinalcord medicine consortium, to the expert health care providers who reviewed the

draft documents, and to the consumers, the advocacy organizations, and the staffs ofthe numerous medical facilities and spinal cord injury rehabilitation centers who con-tributed their time and expertise to the development of these guidelines.

Kit N. Simpson, Andrea K. Biddle, and their fine staff in the Health Policy andAdministration Department at the University of North Carolina at Chapel Hill masterfullyconducted the initial and secondary-level literature searches, evaluated the quality andstrength of evidence of the scientific investigations, constructed evidence tables, and per-formed meta-analyses of the benefits and effects of the various preventive and therapeu-tic modalities and interventions.

Members of the Consortium Steering Committee, representing 17 professionalorganizations, were joined by 50 expert reviewers in providing outstanding scientificand clinical analysis. Through their valuable comments, they helped to refine the rec-ommendations and to identify additional supporting evidence from the scientific litera-ture. The quality of the technical assistance from these dedicated reviewerscontributed significantly to the professional consensus building that is hopefullyachieved through the guidelines development process.

The guidelines development panel is grateful for the many technical support ser-vices provided by the various departments of the Paralyzed Veterans of America. Inparticular, the panel recognizes the organizational and managerial skills of J. PaulThomas and Dawn M. Sexton in the Research, Education, and Practice GuidelinesDepartment; the guidance in writing, formatting, and art work provided by James A.Angelo, Patricia E. Scully, and Christine Campbell in the Communications Department;the excellent technical review of the clinical practice guidelines provided by medicalwriter Joellen Talbot; and the intensive efforts of both PVA staff and consultants whodeveloped the glossary, standardized the nomenclature, and indexed the guidelines.Appreciation is expressed for the steadfast commitment and enthusiastic advocacy ofPVA’s senior officers, including National President Joseph L. Fox, Sr., Executive Direc-tor Delatorro L. McNeal, Deputy Executive Director John C. Bollinger, and the entirePVA Board of Directors. Their generous financial support has made the CPG consor-tium and guidelines development process a successful venture.

iv PREVENTION OF THROMBOEMBOLISM IN SPINAL CORD INJUR Y

Acknowledgments

David Green, MD, PhD (Chair)Rehabilitation Institute of ChicagoNorthwestern University Medical CenterChicago, Illinois

Andrea K. Biddle, PhD, MPH (Methodologist)Department of Health Policy & AdministrationSchool of Public HealthUniversity of North CarolinaChapel Hill, North Carolina

Victoria Fahey, RN, MSNDivision of Cardiac and Vascular ServicesNorthwestern Memorial HospitalChicago, Illinois

Geoffrey A. Gardiner, Jr., MDRadiology DepartmentThomas Jefferson University HospitalPhiladelphia, Pennsylvania

Russell Hull, MDUniversity of Calgary & Calgary General HospitalsCalgary, Alberta

Michael Y. Lee, MDDepartment of Physical Medicine & RehabilitationUniversity of North CarolinaChapel Hill, North Carolina

Geno J. Merli, MDDepartment of Internal MedicineThomas Jefferson University HospitalPhiladelphia, Pennsylvania

Kurt Mossberg, PT, PhDDepartment of Physical TherapyUniversity of Texas Medical Branch/

School of Allied Health SciencesGalveston, Texas

Graham Pineo, MDUniversity of Calgary & Calgary General HospitalsCalgary, Alberta

Kristjan Ragnarsson, MD (Steering Committee Liaison)Department of Rehabilitation MedicineMt. Sinai Medical CenterNew York, New York

David Rosenbloom, DPharmDirector of Pharmaceutical ServicesChedoke-McMaster HospitalsHamilton, Ontario

Kit N. Simpson, PhD (Methodologist)Department of Health Policy & AdministrationSchool of Public HealthUniversity of North CarolinaChapel Hill, North Carolina

Jonathan R. Strayer, MDThe Institute for Rehabilitation & ResearchHouston, Texas

CLINICAL PRACTICE GUIDELINES v

Panel Members

Consortium Member Organizations and SteeringCommittee Representatives

American Academy of Orthopedic SurgeonsRobert Waters, MD

American Academy of Physical Medicine and RehabilitationMargaret Turk, MD

American Association of Neurological SurgeonsPaul McCormick, MD

American Association of Spinal Cord Injury NursesNahid Veit, RN, MSN

American Association of Spinal Cord Injury Psychologists and SocialWorkers

Helen Bosshart, LCSW

American Congress of Rehabilitation MedicineMarilyn Pires, MS, RN

American Occupational Therapy AssociationSusan Garber, MA, OTR, FAOTA

American Paraplegia SocietyTodd Linsenmeyer, MD

American Physical Therapy AssociationMontez Howard, PT, MEd

American Psychological AssociationJ. Scott Richards, PhD

American Spinal Injury AssociationKenneth C. Parsons, MD

Association of Academic PhysiatristsKristjan Ragnarsson, MD

Association of Rehabilitation NursesAnaise Theuerkauf, MEd, RN, CRRN

Congress of Neurological SurgeonsPaul McCormick, MD

Insurance Rehabilitation Study GroupDolores Hynes, RN

Paralyzed Veterans of AmericaR. Henry Bodenbender, MD

U.S. Department of Veterans AffairsMargaret C. Hammond, MD

Expert Reviewers

American Academy of Orthopedic SurgeonsRobert Waters, MD

American Academy of Physical Medicine and RehabilitationMurray Brandstater, MDDiana Cardenas, MDDavid Chen, MDBenjamin Eng, MDIb Odderson, MD, PhDMichael Priebe, MD

American Association of Spinal Cord Injury NursesKathleen Dunn, RN, MSKeri Jaeger, RN, MBAKelly Johnson, RN, MSNSylvia McDonald, RN, MSSusan Thomason, RN, MS

American Association of Spinal Cord Injury Psychologists and SocialWorkers

Mickey Ginsburg, PhDJayne Kleinman, MS, CRC

American Congress of Rehabilitation MedicineR. Edward Carter, Jr., MDRobert R. Menter, MDSamual L. Stover, MD

American Occupational Therapy AssociationTheresa Gregorio, MA, OTR

American Paraplegia SocietyMichael Y. Lee, MDJames Schmidt, MD

American Physical Therapy AssociationCynthia Shewan, PhD

American Psychological AssociationJ. Scott Richards, PhD

American Spinal Injury AssociationRodney H. Adkins, PhDDirk H. Alander, MDSam C. Colachis III, MDErica L. Druin, MPTMarilyn R. Emerich, RPTMel B. Glenn, MDMichael Y. Lee, MDSteven M. Moskowitz, MDKenneth C. Parsons, MDJay V. Subbarao, MDAnn T. Vasile, MDClaire O. Weeks, MDGale Whiteneck, PhDGary M. Yarkony, MD

Association of Academic PhysiatristsSteven Kirschblum, MDMichael Y. Lee, MDMichael Priebe, MD

Association of Rehabilitation NursesJoseph Adamski, Jr., MS, RN, CRRNSusan Dangler, MSN, CRRNLinda Hennig, EdD, RNJeanne Mervine, MS, RN, CRRNNancy Thibault Wiemers, RN, MSN, CRRN

Insurance Rehabilitation Study GroupDolores Hynes, RN

Paralyzed Veterans of AmericaR. Henry Bodenbender, MD

U.S. Department of Veterans AffairsMeena Midha, MDArundhati Perkash, MD, PhDVidya Sridharan, MD

vi PREVENTION OF THROMBOEMBOLISM IN SPINAL CORD INJUR Y

Contributors

CLINICAL PRACTICE GUIDELINES 1

Mechanical Methods of Prophylaxis

1. Whenever possible, compression hose or pneumaticdevices should be applied to the legs of all patientsfor the first 2 weeks following injury. External pneu-matic compression devices may be knee or thighlength with single or sequential chamber compres-sion. The effectiveness of these devices may beenhanced by combining them with pharmacologicantithrombotic agents.

2. During every nursing shift, compression modalitiesshould be inspected for proper placement and theunderlying skin examined for evidence of abrasions,ecchymoses, or injury. In patients whose thrombo-prophylaxis has been delayed for more than 72 hoursafter injury, tests to exclude the presence of legthrombi should be performed prior to applying com-pression devices.

3. Vena cava filter placement is indicated in SCI patientswho have failed anticoagulant prophylaxis or whohave a contraindication to anticoagulation, such asactive or potential bleeding sites not amenable tolocal control (e.g., the central nervous system, gas-trointestinal tract, or lungs). Filters should also beconsidered in patients with complete motor paralysis due to lesions in the high cervical cord (C2, C3),

with poor cardiopulmonary reserve, or with throm-bus in the inferior vena cava despite anticoagulantprophylaxis. However, filter placement is not a sub-stitute for thromboprophylaxis, which should becommenced as soon as feasible. Furthermore, filterplacement may increase the risk of future develop-ment of deep vein thrombosis, so the use of remov-able filters should be considered.

Anticoagulant Prophylaxis

4. Anticoagulant prophylaxis with either low molecularweight heparin or adjusted dose unfractionatedheparin should be initiated within 72 hours after SCI,provided there is no active bleeding or coagulopathy.

5. Anticoagulants should be continued until dischargein patients with incomplete injuries, for 8 weeks inpatients with uncomplicated complete motor injury,and for 12 weeks or until discharge from rehabilita-tion for those with complete motor injury and otherrisk factors (e.g., lower limb fractures, a history ofthrombosis, cancer, heart failure, obesity, or age over70). This recommendation also applies to those withinferior vena cava filters, because such persons areat increased risk for deep vein thrombosis.

Summary of Treatment Recommendations

TABLE 1Guidelines for the Prevention of Thromboembolism in Spinal Cord Injury

Clinical Decision Table

Level of Risk Motor Incomplete Motor Complete Motor CompleteWith Other Risk*

Intensity of Prophylaxis

Low Compression hose Compression hose Compression hoseCompression boots Compression boots Compression boots

and and and

Intermediate UH+: 5000 U q 12h; UH+: Dose adjusted to UH+: Dose adjusted to or LMWH+++ high normal aPTT++; or high normal aPTT++; or

LMWH+++ LMWH+++

andHigh — — Inferior vena cava filter in

certain situations

Duration of ProphylaxisCompression boots: Compression boots: Compression boots:2 weeks; 2 weeks; 2 weeks;Anticoagulants: while Anticoagulants: Anticoagulants: in hospital for ASIA at least 8 weeks 12 weeks or untilclass D and up to 8 discharge fromweeks for ASIA class C rehabilitation

*Other risk factors: lower limb fracture, previous thrombosis, cancer, heart failure, obesity, age over 70+UH—Unfractionated heparin++activated partial thromboplastin time+++LMWH—Low molecular weight heparin, prophylactic dose as recommended by the manufacturers.

2 PREVENTION OF THROMBOEMBOLISM IN SPINAL CORD INJUR Y

Prophylaxis Based on Patient Stratificationfor Risk

6. Patients with complete motor and/or incomplete non-functional motor involvement should be on prophy-lactic measures for venous thromboembolism asearly as possible.

7. Spinal cord injured patients with functional motormovements or with no significant motor/neurologicaldeficits should be on prophylactic measures as earlyas possible.

8. The duration of the prophylaxis for thromboem-bolism should be individualized, depending on theneed, medical condition, functional status, supportservices, and risk of the patient.

9. Reinstitution of prophylactic measures should beconsidered in chronic SCI patients if they are immo-bilized with bed rest for a prolonged period of time,are readmitted for medical illnesses or altered med-ical conditions, or undergo surgical procedures.

Failure of Prophylaxis

10. In symptomatic patients, perform ultrasound of thelower extremities and/or tests for pulmonary emboli.If clinical suspicion is strong but the tests are nega-tive or indeterminate, obtain venography of the legs,spiral computerized tomography of the lungs, ormagnetic resonance/contrast angiography.

Exercise, Passive Movement, and Early Mobilization

11. Early mobilization and passive exercise should beinitiated as soon as the patient is medically and sur-gically stable. These activities should be coordinatedwith other preventative modalities. With documentedDVT, mobilization and exercise of the lower extremi-ties should be withheld 48 to 72 hours until appro-priate medical therapy is implemented.

Educational Priorities for Health CareProfessionals

12. Health care professionals should be aware of thesigns and symptoms of DVT and should performphysical assessment to detect this complication.Appropriate prophylactic measures, including appli-cation of mechanical devices and administration ofanticoagulant agents, should be implemented.Patients, family members, and significant othersshould be educated in the recognition and preventionof DVT.


T he high incidence, insidious onset, and potential-ly lethal consequences make venous thromboem-bolic disease a leading cause of mortality and

morbidity following acute spinal cord injury. Themajor factors predisposing persons with acute SCI tovenous thromboembolism include venostasis due tofailure of the venous muscle pump with paralysis(Seifert et al., 1972) and a transient hypercoagulablestate (Rossi et al., 1980).

Alterations in hemostasis seen after acute SCIhave included reduced fibrinolytic activity (Petaja etal., 1989) and increased blood factor VIII activity(Myllynen et al., 1987), despite normal values onroutine coagulation measures. This situation may beaggravated by dehydration, administration of bloodproducts, and concomitant injury to the soft tissue orlong bones. Because deep vein thrombosis (DVT)may progress proximally in 20 percent of cases(Davies and Salzman, 1979) and may embolize in upto 50 percent (Carabasi et al., 1987), it is importantto regard venous thromboembolism as a continuumof pathology, of which DVT and pulmonary embolism(PE) are subgroups. PE has been found to lead todeath in as many as 35 percent of patients not treat-ed for thrombosis (Davies and Salzman, 1979). Theneed for aggressive medical prophylaxis for throm-boembolic disease has become increasingly apparent,and to this end the term “thromboprophylaxis” hasbeen suggested to refer to all measures, medical andotherwise, that act to prevent thromboembolic disease.

Studies examining the incidence of venousthromboembolism in acute SCI vary greatly, princi-pally due to variation in surveillance technique (table2). Studies based on clinical parameters alone typi-cally estimate the incidence of DVT in acute SCI at14 to 16 percent (Watson, 1978–79; Myllynen et al.,1985; Waring and Karunas, 1991). The advent ofnewer technology in the detection of DVT, particular-ly noninvasive measures, combined with protocols ofroutine surveillance of acute SCI patients have led toa new appreciation of the high frequency of throm-boembolic disease in acute SCI without medical pro-phylaxis for DVT.

Using sensitive measures such as doppler ultra-sonographic imaging and 125–I fibrinogen scan, cou-pled with the traditional contrast dye venography,studies employing serial examination have shown theincidence of DVT in acute SCI to be from 47 to 100percent (Myllynen et al., 1985; Merli et al., 1988;Geerts et al., 1994; Clagett et al., 1995). Myllynen etal. (1985) reported on a limited series of 9 patients,all of whom developed DVT when examined using125–I fibrinogen scans confirmed with venography.The study of a placebo control group by Merli et al.(1988) documented DVT in 47 percent (8 of 17) ofacute SCI patients without prophylactic measures.

More recently, Geerts et al. (1994) presented aseries of 26 acute unprophylaxed SCI patients, 81percent of whom developed DVT confirmed onvenography. Clagett et al. (1995) published a meta-

Introduction

TABLE 2Incidence of objectively diagnosed DVT in patients with acute spinal cord injury

Source and Year Number of Number of Incidence EndpointPatients Patients (%)

With DVT

Bors et al. (1954) 99 58 59 Venography

Silver (1974) 100 18 18 FUT*

Brach et al. (1977) 10 9 90 FUT*/IPG+

Rossi et al. (1980) 18 13 72 FUT*

Myllynen et al. (1985) 9 9 100 FUT*

Merli et al. (1988) 17 8 47 FUT*

Petaja et al. (1989) 9 7 78 FUT*

Yelnik et al. (1991) 127 29 23 Venography

Gunduz et al. (1993) 30 16 53 Venography

Overall incidence 419 167 40

Notes: Reprinted with permission from Clagett, G.P., F.A. Anderson, Jr., and J. Heit et al., Prevention of venous thromboembolism, Chest 108 (4 Suppl) (1995): 312S–34S.

*FUT—Fibrinogen uptake test, confirmed by venography where positive+IPG—Impedance plethysmography


analysis of 9 studies examining the incidence ofobjectively measured (using venography or 125–I fibrinogen scan) DVT following acute SCI; of 419unprophylaxed patients, 167 showed DVT, for anoverall incidence of 40 percent.

Several studies have examined the occurrence ofDVT relative to time postinjury. DVT has been report-ed as soon as 72 hours postinjury; however, risk priorto this time appears to be low (Green et al., 1990). Instudies of unprophylaxed patients, researchers havefound that over 80 percent of DVTs occur within thefirst 2 weeks of injury (Rossi et al., 1980; Merli et al.,1993). Evidence documenting the duration of thisheightened risk is less clear. Incidence of DVTdeclines after week 2, and one report suggests a 6-percent incidence of DVT at week 8 with discontin-uation of medical prophylaxis (Green, 1994).

Studies of longer term risk for venous throm-boembolism are rare, but overall suggest a muchlower rate of occurrence. Data from the federallydesignated Model Spinal Cord Injury Systems suggestthat the risk for DVT among chronic SCI patients(1–6 years postinjury) is much lower than that foracute SCI patients (1.1 percent), and the risk for PEis even lower (0.3 percent). However, the sample sizedecreases dramatically, from 2791 at year 1 to 45 foryear 6, suggesting significant data loss (Ragnarssonet al., 1995). Kim et al. (1994) looked prospectivelyat 22 asymptomatic chronic SCI patients and foundthat only 1 patient (7.0 percent) had chronic DVT.Interestingly, among 21 admissions of chronic SCIpatients with clinical signs suggestive of DVT, only 6turned out to have DVT on venography, yielding anincidence of 28.6 percent among symptomaticpatients.

Other clinical factors have been associated withthe onset of DVT. Reporting on 2186 acute admis-sions, Ragnarsson et al. (1995) found a higher rateof occurrence of DVT among those with motor com-plete injuries (16.6 percent) and lower rates ofoccurrence among those with incomplete injuries(12.5 percent) and with minimal deficit (6.4 per-cent). Considering the level of injury as it influencesvenous thromboembolism risk, Ragnarsson reportedthat those with paraplegic SCI have a greater risk forDVT than tetraplegic patients (16 and 11.9 percent,respectively). Furthermore, he found that the inci-dence of PE was not influenced by the degree orlevel of injury. The same study described the effectsof age on the onset of venous thromboembolism,with DVT showing a relatively uniform incidence overthe years (15–17 percent), while PE displayed amarked peak in years 61–75. Additionally, both PEand DVT exhibited preferential occurrences in males(M:F roughly 5:3). Finally, a significant associationwas seen between heterotopic ossification and DVTin a limited retrospective study (Colachis and Clin-chot, 1993).

It is not uncommon for DVT to evolve to achronic stage—postthrombotic syndrome, evidencedby degrees of chronic edema, induration, pain, andskin ulceration. Although clinicians generally agreethat postthrombotic syndrome is prevalent amongthe chronic SCI population, it remains poorly studiedamong persons with SCI. Prospective studies of unse-lected patients reveal that DVT progresses to post-thrombotic syndrome in one-half to two-thirds ofpatients (Monreal et al., 1993). These investigatorsfound that 12 percent of patients followed for a 3-year period after DVT were disabled due to post-thrombotic syndrome alone. Chronic skinbreakdown, pain, refractory edema, recurrent DVT,frequent hospitalization, and at times pulmonaryhypertension and cor pulmonale have all been seenin conjunction with postthrombotic syndrome(Davies and Salzman, 1979).

The most striking evidence for the necessity ofeffective prevention of thromboembolic diseasecomes from studies of mortality in the first year afterSCI. Autopsy investigations into the deaths of acuteSCI patients have shown as high as a 37-percent inci-dence of death due to PE (Tribe, 1963). Reportingon the first years of Model Systems care of SCI,Stover and Fine (1986) reported that PE ranked asthe fifth leading cause of death from 1973 to 1985,accounting for 8.5 percent of deaths. In the 1995Model Systems report, DeVivo and Stover (1995)reported that PE was the third leading cause of deathamong those with paraplegia, and it was tied for sec-ond leading cause of death in those with Frankel D(neurologically incomplete) lesions. Furthermore, PEwas found to be the third leading cause of death forall SCI patients in the first postinjury year, account-ing for 14.9 percent of deaths in this group. Forthose with acute SCI, the risk of death due to PE is210 times greater than that of a similar healthy pop-ulation. This risk decreases to 19.1 times normal foryears 2–5 and further decreases to 8.9 for those whosurvive more than 5 years.

The toll exacted by thromboembolic disease onsociety is difficult to calculate, particularly for thosewith SCI. As a whole, the economic cost of SCI in theUnited States has been estimated at $7.2 billion peryear (DeVivo et al., 1995). In a conservative investi-gation, Tator et al. (1993) found that thromboembol-ic disease can increase length of hospital stay by 46percent and costs by 35 percent. The development ofDVT can mean an additional 1 to 2 weeks of acutehospital care, with costs ranging from $19,000 to$38,000 (DeVivo et al., 1995). Given an annual inci-dence rate for SCI of 30 to 40 cases per million(DeVivo et al., 1995), and a conservative incidenceof clinically significant DVT of 47 percent, annualdirect costs for hospital care alone can run as highas $178 million. These figures do not take intoaccount the economic cost of lives lost to throm-


boembolic disease. For the individual person with aspinal cord injury, thromboembolic disease causesconsiderable discomfort and a delay in recovery.Weeks are lost from physical rehabilitation, an unwel-come interruption in an era when physical rehabilita-tion time is doled out parsimoniously. In summary,venous thromboembolism causes chronic disfigure-ment, disability, pain, and too often, death. Knowl-edgeable medical practitioners can play a significantrole in reducing the incidence of this disease.


C linical practice guidelines are a new trend in medi-cine. They are derived from the National Institutesof Health Consensus Conference format, which

enables scientists and clinicians to make statementsabout clinical conditions based on evidence publishedin the scientific literature. In June 1995, 17 organiza-tions joined the Paralyzed Veterans of America to cre-ate a formal consortium for the development ofclinical practice guidelines in spinal cord medicine.After studying the guidelines development process,the PVA Health Policy Department recognized thatthe success of its CPG process would require that alldisciplines and specialties involved in clinical deci-sionmaking, including payers and consumers, partici-pate and that the development process would have tobe based on scientific evidence in order to be credi-ble in the community of practice.

The consortium asked each participating organi-zation to select a representative with guidelinesdevelopment experience to sit on a steering commit-tee. That committee serves as the consortium gover-nance. To ensure a standardized frame of referencefor all organizational representatives, PVA conductedan orientation workshop featuring experts from anumber of leading professional organizations withextensive guidelines development experience. Theworkshop faculty included senior staff members fromthe Academy of Family Practice, the Academy ofPediatrics, the Agency for Health Care Policy andResearch (AHCPR), the American Academy of Oto-laryngology—Head and Neck Surgery, the AmericanCollege of Cardiology, and the American MedicalAssociation.

After extensive study of the processes used todevelop numerous types of guidelines, the consor-tium steering committee unanimously agreed on anew, modified scientific evidence-based modelderived from AHCPR. The model was:� Interdisciplinary, to reflect the multiple informa-

tion needs of the spinal cord medicine practicecommunity.

� Responsive, with a time line of 12 months for thecompletion of the guidelines.

� Reality-based, to make the best use of the timeand energy of the busy clinicians who were serv-ing as panel members and field reviewers.

Both administrative and financial support were pro-vided by PVA.

The Spinal Cord Medicine Consortium wasunique to the practice guidelines field in that itemployed highly effective management strategiesbased on the availability of resources in the health

care community, it was coordinated by a recognizednational consumer organization with a reputation forproviding effective service and advocacy for personswith spinal cord injury and disease, and it includedthird-party and reinsurance payer organizations inevery level of the development and disseminationprocess.

Goals of the Guidelines

The primary goal of these guidelines is to improveoutcomes for individuals with spinal cord injury bydecreasing the frequency and severity of thromboem-bolic complications. The specific goals are to:� Provide a rationale for the implementation of

thromboprophylaxis.

� Make available to providers the best currentknowledge and expert consensus regarding safeand effective prophylaxis procedures.

� Encourage providers to reexamine their practicepatterns and to individualize treatment based onpatient characteristics.

� Stimulate future research to fill gaps in knowledgeregarding thromboprophylaxis for spinal cordinjury.

The focus is on persons who have sustained a spinalcord injury and who require appropriate interven-tions to prevent deep vein thrombosis and pulmonaryembolism. The guidelines apply not only to the peri-od immediately following injury, but also to themonths and years when longer term prophylaxis isneeded. Attempts are made to tailor the approachesto persons with a broad variety of risk factors forthrombosis, such as complete motor paralysis,advanced age, obesity, or a prior history of thrombo-sis. It is hoped that the recommendations have beenoptimized by combining published evidence with clin-ical experience.

Need for the Guidelines

Concerns about thromboembolism arise during thecare of nearly every patient with acute spinal cordinjury. Centers collecting data on the incidence ofdeep vein thrombosis and pulmonary embolism con-tinue to report high rates of these complications.Methods of prevention vary widely—from the simpleapplication of elastic hose to the insertion ofmechanical filters in the vena cava. Such broad varia-tions in clinical practice reflect the uncertainty andconfusion among health care providers regardingoptimal management. Thus, there is a need for clini-cal guidelines based on the best available scientificevidence.

The Spinal Cord Medicine Consortium


Framework for the Guidelines

The outcome measures used in preparing theseguidelines included the endpoints of deep veinthrombosis—pulmonary embolism, hemorrhagicepisodes, and mortality. Quality-of-life considerationswere also included. The scope of the guidelines cov-ers all patients with spinal injury, although the focusis predominantly on persons with spinal cord injury.

Methodology

To prepare the guidelines, a panel of nine personswas selected: three specialists in internal medicine,two in physical medicine and rehabilitation, and onespecialist each in nursing, physical therapy, pharma-cology, and radiology. All of the panelists had exten-sive clinical experience working with persons eitherwith spinal cord injury or venous thrombosis.

In addition, a methodologist, Kit N. Simpson, ofthe Department of Health Policy and Administration,University of North Carolina School of Public Health,Chapel Hill, conducted an extensive literature search.Sources included MEDLINE and several other data-bases and covered materials published in English aswell as in most European languages. The search strat-egy included MeSH heading and key word searchesand focused on SCI and DVT or other thromboembol-ic (TE) events. The time period from 1975 to 1999was examined; more than 126 articles were reviewed.Information was extracted from each article and com-piled into summary tables according to epidemiologyof DVT/TE, diagnosis of DVT/TE, prophylactic therapyfor DVT/TE, and therapy/management approaches forDVT/TE. A separate search was conducted for venacava filter; some 30 articles published from 1990 to1999 were retrieved and reviewed.

Nearly seventy articles are cited in these guide-lines. The primary emphasis is on experimental studies,although review articles and observational studies alsoare included if they provide information critical tounderstanding the natural history of thromboembolismin SCI. This database was sent to all members of thepanel, who were asked to prepare a brief summary ofthe issues in their areas of expertise based on thepublished literature and on their own clinical experi-ence. Next, a meeting of the panel was convened, andthe summaries drafted by each panelist were thorough-ly discussed. These discussions led to specificrecommendations for management. Over a period of 2months, panelists revised their drafts and recommen-dations, which were then forwarded to the Chair to beedited and incorporated into the complete document.Copies of the full draft guidelines were then submittedto representatives of each Consortium member organi-zation for critique and amendment. As a result, therecommendations are based on the best currentknowledge, although they undoubtedly will undergorevision as new information becomes available.

Evidence Analysis

Each guideline recommendation is justified in termsof the level of evidence supporting it, with level Ibeing the strongest evidence and level V the weakest.Unfortunately, randomized, controlled clinical trials—level I evidence—have been conducted infrequentlyin patients with SCI. However, such studies havebeen done in patients undergoing joint replacementsurgery, hip fracture, and stroke so that surrogateevidence for safety and efficacy is available. In addi-tion, observational studies and clinical experience doprovide important, though by no means infallible,support for some recommendations. The levels ofevidence used in these guidelines (Sackett, 1989) areas follows:

I. Large randomized trials with definite results.

II. Small randomized trials with uncertain results.

III. Nonrandomized studies with concurrent controls.

IV. Nonrandomized studies with historic controls.

V. Case series with no controls.

Next, each of the guideline recommendations wasclassified depending upon the level of scientific evi-dence supporting the specific recommendations. Theschema used by the panel is:

A Guideline recommendation is supported by one or more Level I studies

B Guideline recommendation is supported by one or more Level II studies

C Guideline recommendation is supported only by Level III, IV, or V studies

In situations where no published literature existed,consensus of the panel members and outside expertreviewers was used to develop the guideline recom-mendation and is indicated as “expert consensus.”

After deliberation and discussion of each guidelinerecommendation and the supporting evidence, thelevel of panel agreement with the recommendationwas assessed as either low, moderate, or strong. Inthis assessment, each panel member was asked toindicate his or her level of agreement on a 5-pointscale, with 1 corresponding to “neutrality” and 5 rep-resenting “maximum agreement.” The scores wereaggregated across the panel members and an arith-metic mean was calculated. This mean score wastranslated into low, moderate, or strong, as follows:

Low—1.0 to less than 2.33Moderate—2.33 to less than 3.67Strong—3.67 to 5.0


Mechanical Methods of Prophylaxis

1. Whenever possible, compression hose or pneu-

matic devices should be applied to the legs of

all patients for the first 2 weeks following

injury. External pneumatic compression devices

may be knee or thigh length with single or

sequential chamber compression. The effective-

ness of these devices may be enhanced by com-

bining them with other antithrombotic agents.

(Scientific evidence—level I; Grade of recommenda-tion—A; Strength of panel opinion—strong)

2. During every nursing shift, compression modali-

ties should be inspected for proper placement

and the underlying skin examined for evidence

of abrasions, ecchymoses, or injury. In patients

whose thromboprophylaxis has been delayed for

more than 72 hours after injury, tests to exclude

the presence of leg thrombi should be performed

prior to applying compression devices. (Scientificevidence—NA; Grade of recommendation—expertconsensus; Strength of panel opinion—strong)

A number of mechanical modalities have beenshown to be effective in reducing the incidence ofdeep vein thrombosis in acute SCI. These modalitiesimprove lower extremity venous return, whichreduces stasis, a major cause for thrombus develop-ment in this patient population. Active and passiverange of motion reduces lower extremity stasis bysimulating flexion and extension of the gastrocne-mius and soleus muscle groups, resulting in empty-ing of the calf veins. Centripetal massage alsoenhances venous drainage by manual compression. Alevel III study compared active and passive range ofmotion twice per day (group A) with lower extremitymassage plus elastic bandages (group B) (Van Hove,1978–79). The incidence of clinical DVT was 40 per-cent in group A and 0 percent for group B. Becausethe efficacy of these modalities was assessed by clini-cal examination, conclusions about the effectivenessof this intervention are not firm.

Several mechanical methods are available forimproving lower extremity venous return. A level IIstudy of 15 patients evaluated the rotation of treat-ment tables as a modality for reducing stasis and pre-venting DVT (Becker et al., 1987). Although theauthors concluded that the method was effective,their mode of assessing the endpoint of thrombosiswas limited and their sample size was small, suggest-ing that the results must be interpreted with caution.Gradient elastic stockings (GES) reduce venouscapacitance by applying a uniform distribution ofpressure over the extremity. Calf-length stockings are

the most frequently prescribed because of their easeof application. No study indicates a difference in theincidence of DVT with thigh-length versus calf-lengthGES. This modality has been shown to be effective inlow-risk surgery (Wells et al., 1994).

Electrical stimulation (ES) was developed tomechanically simulate dorsi and plantar flexion of thelower extremity (Merli et al., 1988). To accomplishthis, stimulation at a pulse duration of 50 µs and afrequency of 10 HZ was required. The contractionswere 4 seconds, with a rest period of 8 seconds. Themuscle groups were activated 5 times per minute for23 hours daily. This modality was evaluated in a levelI trial comparing a saline placebo, low-dose heparin,and ES plus low-dose heparin. Patients had acuteSCI; were in American Spinal Injury Association(ASIA) class A, B, and C; and were treated during thefirst 30 days following trauma. The incidence of DVTwas 47 percent, 50 percent, and 6.7 percent in theplacebo, heparin, and heparin plus ES group, respec-tively. Despite the effectiveness of ES, it has not beenfurther developed because the stimulation is painfulin sensate patients and difficult in patients with lowerextremity edema. Additionally, frequent maintenanceof the equipment is required.

External pneumatic compression offers a moresustained method of augmenting lower extremityvenous return (Salzman et al., 1987). Various devicesare commercially available. External pneumatic com-pression sleeves (EPCS) may be thigh and/or kneelength, and the mode of compression may be eithergraded sequential, multicompartment uniform, or sin-gle-chamber uniform pressures. Although the multi-chambered sequential pressure devices showimproved flow velocity, volume flow rate, shearstress, residual volume, and stimulation of fibrinolysis(Salzman et al., 1987), greater antithrombotic effec-tiveness has not been demonstrated clinically.

EPCS and EPCS plus antiplatelet agents (aspirin300 mg twice daily and dipyridamole 75 mg 3 timesdaily) were studied in ASIA A, B, and C acute SCI byGreen et al. (1982). Thrombosis was detected byradiolabeled fibrinogen leg scanning; a previousstudy by the authors using this method recorded a72-percent frequency of DVT in patients not treatedwith EPCS or antiplatelet agents. The incidence ofDVT was 40 percent in the EPCS group and only 25percent in the combination therapy group, but bleed-ing occurred in some patients receiving aspirin. Merliet al. (1992) demonstrated a reduction in DVT in asimilar population by combining EPCS with GES andlow-dose heparin (5,000 U subcutaneously every 8hours).

Treatment Recommendations


Another mechanical device is the venous footpump. It functions by rapidly flattening the plantararch, which causes an increase in venous return, aswell as turbulence in the valve pockets, as demon-strated by video phlebography. In a study of patientshaving total hip replacement, Fordyce and Ling(1992) demonstrated DVT in 40 percent of a controlgroup compared to 5 percent in those using thevenous foot pump. Wilson et al. (1992) evaluated theefficacy of this same device in total knee replacement,but found no significant differences in the incidenceof DVT (68.7 percent for the control group versus 50percent for the venous foot pump group). These weresmall level II studies, and larger trials will be requiredto justify the use of these devices in the SCI population.

Only a few studies have examined the safety andeffectiveness of combining pneumatic compressiondevices with anticoagulants. In a very recent trial,more than 2000 patients undergoing cardiac surgerywere fitted with pneumatic compression boots on arandom basis (Ramos et al., 1996); all were treatedwith unfractionated heparin (UH), 5000 U every 12hours. Pulmonary emboli occurred in 1.5 percent ofthose with boots, as compared to 4 percent withoutboots (p<0.01). The investigators concluded that theaddition of the devices to standard heparin prophy-laxis was of significant benefit.

3. Vena cava filter placement is indicated in SCI

patients who have failed anticoagulant prophy-

laxis or who have a contraindication to antico-

agulation, such as active or potential bleeding

sites not amenable to local control (e.g., the

central nervous system, gastrointestinal tract,

or lungs). Filters should also be considered in

patients with complete motor paralysis due to

lesions in the high cervical cord (C2, C3), with

poor cardiopulmonary reserve, or with throm-

bus in the inferior vena cava despite anticoagu-

lant prophylaxis. However, filter placement is

not a substitute for thromboprophylaxis, which

should be commenced as soon as feasible. Fur-

thermore, filter placement may increase the risk

for future development of deep vein thrombosis.

(Scientific evidence—level IV; Grade of recommenda-tion—C; Strength of panel opinion—moderate)

No randomized controlled trials of vena cava fil-ters in SCI patients have been reported, and very fewstudies have specifically addressed the use of filtersin these patients. In one prospective series of 63high-risk trauma patients prophylactically treatedwith filters (Rogers et al., 1995), the incidence ofsymptomatic pulmonary embolus was significantlyreduced, compared with historical controls treatedwith heparin and/or venous compression boots. Thistrial included 25 SCI patients. In a consecutive seriesof 15 SCI patients treated prophylactically with filters(Wilson et al., 1994), there were no symptomaticpulmonary emboli, compared to an incidence of 6.3

percent in a historical group of 111 SCI patientstreated with heparin and/or venous compressionboots (with no statistical difference). Some or all ofthese patients may have been included in the abovestudy. In a third level IV study (Khansarinia et al.,1995), 108 patients with severe trauma were treatedprospectively with filter placement as well as withcontinued DVT prophylaxis. This group was com-pared to a matched historical series of 216 patients.There was no clinical evidence of pulmonaryembolism in the filter treated group, compared to 13in the historical control group, including 9 PE–relat-ed fatalities. This difference was statistically signifi-cant. Although SCI patients were included in thisstudy, the specific numbers were not noted.

Recently, 400 patients with deep vein thrombosisconsidered at risk for pulmonary embolism were ran-domized to receive a vena cava filter or no filter(Decousus et al., 1998). All patients were givenheparin or LMWH acutely and continued on warfarinfor at least three months. Evaluation at day 12showed a significant reduction in the frequency ofpulmonary emboli (1.1 percent in those with filters;4.8 percent in those without filters). However, attwo years, 20.8 percent of those with filters, but only11.6 percent of those without filters, had experi-enced recurrent deep vein thrombosis. There was nodifference in mortality between the two groups. Theinvestigators concluded that the beneficial effect ofthe vena cava filters was counterbalanced by theexcess of deep vein thrombosis.

Adverse experiences reported with vena cava fil-ters include cava thrombosis, filter migration, perfo-ration of the vena cava, and complications at the skininsertion site. The frequency of these problems usingthe newer small caliber systems and percutaneousinsertion is low. Filter malposition is usually due topoor insertion technique, but also can be related toanomalies involving the cava or renal veins or to thepresence of intracaval thrombus. This complicationcan be largely eliminated by the use of routine prein-sertion inferior vena cavagrams and fluoroscopicguidance, which should be a prerequisite to filterplacement. A followup plain film of the abdomenshould always be obtained immediately after the pro-cedure to document filter position. Recurrent pul-monary embolism (defined as embolization with thefilter in place) is reported in 2 percent to 5 percentof patients (Balshi et al., 1989; Becker et al., 1992).

Anticoagulant Prophylaxis

4. Anticoagulant prophylaxis with either low mole-

cular weight heparin (LMWH) or adjusted dose

unfractionated heparin should be initiated with-

in 72 hours after SCI, provided there is no active

bleeding or coagulopathy. (Scientific evidence—onelevel II study; Grade of recommendation—B; Strengthof panel opinion—strong)


5. Anticoagulants should be continued for 8 weeks

in patients with uncomplicated complete motor

injury and for 12 weeks or until discharge from

rehabilitation for those with complete motor

injury and other risk factors (e.g., lower limb

fractures, a history of thrombosis, cancer, heart

failure, obesity, or age over 70). This recommen-

dation also applies to those with inferior vena

cava filters, because such persons are at increased

risk for deep vein thrombosis. (Scientific evidence—level IV studies; Grade of recommendation—C;Strength of panel opinion—strong)

The evidence that low-dose unfractionatedheparin (5000 U 2 or 3 times a day) may be benefi-cial comes from small studies, some retrospective,with inadequate outcome measures. To determinewhether higher doses of unfractionated heparin wouldbe more effective, Green et al. (1988) conducted alevel I unblinded trial comparing UH 5000 U every 12hours, with doses of heparin adjusted to prolong theactivated partial thromboplastin time (aPTT) into theupper normal range. Doses averaging 13,200 U every12 hours were required to maintain the aPTT at 1.5times control values. One-third of patients receivinglow-dose UH had thrombosis, compared to 7 percentreceiving adjusted dose UH (p<0.05). However, notonly was the adjusted dose UH difficult to implementlogistically, but 7 of 29 patients had bleeding suffi-cient to require withdrawal of the heparin.

Green et al. (1990) then compared low molecularweight heparin (tinzaparin) 3,500 U once daily with ahigher fixed dose of UH (5000 U 3 times daily), alsoin a level I trial. This trial was blinded for thrombosisbut not for bleeding. The regimens were commencedwithin 72 hours of injury. Thrombi detected by nonin-vasive tests were confirmed venographically. The trialwas stopped after 41 patients because 7 patients inthe UH group but no one in the tinzaparin group hadan event (p=0.006). These events included 5 inci-dents of thrombosis (2 involving fatal pulmonaryemboli) and 2 incidents of bleeding.

Subsequent uncontrolled experience with tinza-parin in 60 patients suggested that thrombosis devel-oped at a rate of 10 percent over 8 weeks but bleedingwas infrequent; only 1 patient bled in the immediatepostoperative period (Green et al., 1994). Experiencewith another low molecular weight heparin, enoxa-parin, has been similar. This anticoagulant was givento 105 spinal injury patients in a dose of 30 mg subcu-taneously every 12 hours (Harris et al., 1996). Nopatient developed clinical evidence of thromboem-bolism, and bleeding attributed to the low molecularweight heparin was reported in only 3 patients.

Geerts et al. (1995) compared the safety andeffectiveness of low-dose UH (5000 U twice daily) andLMWH (enoxaparin, 30 mg twice daily) in patientswith major trauma, including a few with SCI. Treatmentwas initiated 36 hours after injury. The overall rate of

venous thrombosis (44 percent versus 31 percent;p=0.014) and proximal vein thrombosis (15 percentversus 6 percent; p=0.009) was significantly higher inthe UH group. Furthermore, there was 1 nonfatal PEand 2 episodes of heparin-induced thrombocytopenia inthis group. Major bleeding occurred in 2.9 percent ofpatients receiving LMWH and 0.6 percent receivingUH. Thus, LMWH was significantly more effective witha relatively low rate of bleeding. There were 23 patientswith spinal injury in this study; 10 of 15 (67 percent)receiving UH but only 4 of 8 (50 percent) treated withLMWH developed deep vein thrombosis. Table 3 sum-marizes the results of preventive anticoagulant regimesin patients with acute spinal cord injury.

At the time these guidelines were prepared,LMWHs were approved by the U.S. Food and DrugAdministration for prophylaxis of thrombosis inpatients undergoing surgical procedures on theabdomen, pelvis, hip, and knee.

Prophylaxis Based on Patient Stratification for Risk

6. Patients with complete motor and/or incomplete

nonfunctional motor involvement should be on

prophylactic measures for venous thromboem-

bolism as early as possible. (Scientific evidence—

TABLE 3Thromboembolism after acute spinal cord injury

Agent, Author, and Year Untreated Treated EndpointControls

Low-Dose Heparin

Frisbie and Sasahara (1981) 1/17 (6%) 1/15 (7%) IPG

Green et al. (1988) None N9/29 (31%) IPG

Merli et al. (1988) 8/17 (47%) 8/16 (50%) FUT

Green et al. (1990) None 5/21 (24%) IPG

Intermittent Pneumatic Compression

Green et al. (1982) None 6/15 (40%) FUT, IPG

Adjusted Dose Heparin


Low Molecular Weight Heparin


Green (1994) None 5/60 (8%) IPG, DU, VEN

Geerts et al. (1996) None 4/8 (50%) VEN

Combined Prophylaxis With IPC, ASA, and DIP

Green et al. (1982) None 4/12 (33%) FUT, IPG

Combined Prophylaxis With IPC, ES, and LDUH

Merli et al. (1992) 6/17 (35%) 1/19 (5%) FUT

Notes: Modified with permission from Clagett, G.P., F.A. Anderson, Jr.,and J. Heit et al., Prevention of venous thromboembolism, Chest 114(Suppl) (1998): 531S–560S.

ASA—Aspirin IPC—Intermittent pneumatic compressionDIP—Dipyridamole IPG—Impedance plethymographyDU—Duplex ultrasound LDUH—Low-dose unfractionated heparinES—Elastic stockings VEN—VenographyFUT—Fibrinogen uptake test


level I; Grade of recommendation—A; Strength ofpanel opinion—strong)

Many studies have shown that the risk of throm-boembolism in SCI increases rapidly following injury andis maximal between days 7 and 10 (Geerts et al., 1994;Green et al., 1982; Merli et al., 1988). Anticoagulantsmay be withheld during the first 24 to 48 hours afterinjury because of concern for bleeding complicationsand for potential neurological deterioration. The inci-dence of venous thromboembolism within the first 72hours is probably small, but measures such as mechani-cal devices and physical modalities should be imple-mented to prevent thromboembolism. If surgicalintervention such as spinal stabilization is required,heparin or low molecular weight heparin may be with-held the morning of the procedure and resumed the nextday. Physical modalities, including compression devices,should be continued if possible during this period.

7. Spinal cord injured patients with functional

motor movements or with no significant motor/

neurological deficits should be on prophylactic

measures as early as possible. (Scientific evidence—level I; Grade of recommendation—A; Strength ofpanel opinion—strong)

Because of prolonged bed rest and concomitantinjuries, these patients should be on prophylacticmeasures, at least until they are ambulatory (Geertset al., 1994).

8. The duration of the prophylaxis for thromboem-

bolism should be individualized, depending on the

need, medical condition, functional status, sup-

port services, and risk of the patient. (Scientificevidence—level II; Grade of recommendation—B;Strength of panel opinion—strong)

The duration of prophylaxis after SCI is contro-versial. Many practitioners continue prophylacticmeasures for about 3 months postinjury (Green etal., 1994). Although some evidence of decreased inci-dence of thromboembolism after 3 months exists inthis patient population, there are many clinical reportsof the incidence of thromboembolism after 3 months(Perkash et al., 1993). With changes in the provisionof health care and improvements in managementthroughout acute and rehabilitation settings, manypatients are discharged from the hospital settingbefore 3 months. If a minimum of 3 months for pro-phylactic measures is recommended, many issuesneed to be addressed regarding patients who arebeing discharged from institutional settings earlierthan 3 months. The patient’s functional ability, levelof neurological injury, access to nursing and medicalcare at home and other sites and family support,cost, appropriate use of recommended measures, andpatient and family education and training are justsome of the issues that need to be considered beforerecommending continuation of prophylactic measures.

Is there a need for prophylactic measures after 3months? The role of spasticity in the reduction of inci-

dence of venous thromboembolism in this populationis not clear. Spasticity of muscles of lower extremitiesin the spinal cord injured may cause increased venousflow, which may reduce the development of venousthromboembolism. Theoretically, treatment of spastici-ty could increase the risk of venous thromboem-bolism. Other factors, such as limited participation intherapy programs, recurrent infections, heterotopicossification, or history of thromboembolism, may sug-gest the need to continue prophylactic measuresbeyond 3 months (Perkash and Perkash, 1990). Thebenefits of continuing prophylactic measures versusthe risks—including bleeding complications and thedevelopment of osteoporosis with long-term use ofheparin—as well as the cost should be considered.Some of the nursing measures and physical modali-ties, including turning, use of stockings, physical ther-apy, and range-of-motion exercises, could becontinued without significant risk or cost, although itis not clear whether these measures decrease thedevelopment of thromboembolism in SCI patients.

9. Reinstitution of prophylactic measures should be

considered in chronic SCI patients if they are

immobilized with bed rest for a prolonged peri-

od of time, are readmitted for medical illnesses

or altered medical conditions, or undergo surgi-

cal procedures. (Scientific evidence—level I; Gradeof recommendation—A; Strength of panel opinion—strong)

SCI patients who have acute medical illnesses orwho require surgical procedures are at similar orincreased risk for the development of venous throm-boembolism as any other patient (Kim et al., 1994).Prophylaxis with either mechanical devices or antico-agulants may be appropriate, depending on the clini-cal situation.

Failure of Prophylaxis

10. In symptomatic patients, perform ultrasound

of the lower extremities and/or tests for pul-

monary emboli. If clinical suspicion is strong

but the tests are negative or indeterminate,

obtain venography of the legs, spiral computerized

tomography of the lungs, or magnetic reso-

nance/contrast angiography. (Scientific evidence—level I; Grade of recommendation—A; Strength ofpanel opinion—strong)

Failure of prophylaxis should be suspected inindividuals with unexplained fever; unilateral legswelling, pain, or erythema; or sudden onset ofhypotension, tachycardia, tachypnea, chest pain, car-diac arrhythmia, or hypoxemia. Although ultrasoundexamination of the lower extremities is highly sensi-tive and specific in symptomatic persons, it is lesssensitive in those who are asymptomatic, and venog-raphy may be necessary to establish a diagnosis.

Ventilation/perfusion lung scans are interpretedas normal or high, intermediate, or low probability of


pulmonary embolism. Only normal or high proba-bility lung scans are regarded as definitive; scans inthe other categories offer no assurance that patientshave or do not have thromboses, and therefore furtherevaluation, such as spiral computerized tomography ofthe chest or pulmonary angiography, is required ifthere is strong clinical suspicion of thromboembolism.

Exercise, Passive Movement, and EarlyMobilization

11. Early mobilization and passive exercise should be

initiated as soon as the patient is medically and

surgically stable. These activities should be coordi-

nated with other preventative modalities. With

documented DVT, mobilization and exercise of the

lower extremities should be withheld 48 to 72

hours until appropriate medical therapy is imple-

mented. (Scientific evidence—Grade of recommen-dation—expert consensus; Strength of panelopinion—strong)

Physical therapy has been a routine part of acuteSCI treatment for decades. The physical therapyassessment and treatment focuses on respiratory func-tion, muscle strength, joint range of motion, and skincondition. Orientation to the vertical position and initi-ation of functional activities begin when spinal stabilityhas been established. In terms of prevention of deepvein thrombosis, it is widely held that early mobiliza-tion and movement of the extremities are essentialparts of treatment (Frost, 1993; Keppler, 1987).

In the acute phase of SCI management, physicaltherapy intervention can begin immediately in theintensive care unit (McBride and Rodts, 1994). Thegoal of range-of-motion activities is to prevent jointcontractures. However, because of spinal instability,certain precautions may be necessary. Range-of-motion activities of the shoulder and arms must belimited in patients with cervical injuries. Similarly, hipflexion and extension should be limited in individualswith low thoracic and lumbar injuries. Movement ofthe extremities occurs passively or, if possible, active-ly. With incomplete injuries, active muscle contrac-tion may be possible. Movement and strengtheningactivities can become more vigorous as the patient iscleared for more functional activity and as he or shemoves into the postacute phase.

The role of physical therapy intervention in theprevention of deep vein thrombosis has not beenexamined rigorously. Because physical therapy is rou-tinely applied, controlled studies examining the spe-cific effects of early mobilization activities have notbeen undertaken. In addition, in studies that haveexamined other treatment modalities, little if anymention is made of the type and frequency of theseroutine procedures. No mention is made as towhether exercise, passive movement, or early mobi-lization activities have been controlled by proper ran-domization and control groups.

Some evidence suggests indirectly that a vigor-ous program of passive and, if possible, active exer-cise could be beneficial in the prevention of DVT.Myllynen et al. (1985) compared the incidence ofDVT in individuals immobilized due to spinal frac-tures. The group without paralysis had no detectableDVT, whereas nearly 80 percent of the paralyzed indi-viduals developed DVT. This would suggest thateither preserved motor function or preserved sympa-thetic input to the veins was responsible for thedecreased incidence of DVT in the nonparalyzedpatients. If inherent muscle tone and small sponta-neous movements were responsible for the decreasedincidence, then one might extrapolate that a persis-tent passive exercise program might produce a sig-nificant reduction in DVT. However, the intactsympathetic system may play the more significantrole. These factors need further investigation.

In addition to improvements in venous return asa result of changes in intrathoracic pressure, eleva-tion of the lower extremities utilizes the effects ofgravity to reduce venous stasis. Positioning of thelower extremities higher than the level of the heartcould prove beneficial and very cost effective. Closemonitoring of arterial perfusion would be necessaryin those individuals with hypotension and bradycar-dia. This intervention would require no equipment,and the legs could be positioned for specified periodsof time and comparisons made to electrical stimula-tion (Merli et al., 1988) and to external compressionstockings and boots (Green et al., 1982; Merli et al.,1992). Unfortunately, use of this simple interventionhas not been formally examined.

In summary, very few controlled studies havebeen performed examining the effectiveness of earlymobilization, and many areas need research. It wouldbe of benefit to more closely monitor and documentthe type, duration, and frequency of physical therapyintervention. Given the absence of side effects andcomplications (except for the precautions mentionedabove), early mobilization and physical therapydeserve closer attention.

Educational Priorities for Health CareProfessionals

12. Health care professionals should be aware of the

signs and symptoms of DVT and should perform

physical assessment to detect this complication.

Appropriate prophylactic measures, including

application of mechanical devices and adminis-

tration of anticoagulant agents, should be imple-

mented. Patients, family members, and

significant others should be educated in the

recognition and prevention of DVT. (Scientific evi-dence—NA; Grade of recommendation—expert con-sensus; Strength of panel opinion—strong)

With an understanding of the rate of incidence,risk factors, pathophysiology, clinical presentation,


and treatment strategies, health care professionalscan be instrumental in preventing and treating DVT.Physical assessment should be performed on eachpatient twice daily (Herzog, 1992). All extremitiesshould be inspected for the following signs of DVT:� An increase in the circumference of the calf or

thigh (unilateral edema).

� An increase in the venous pattern of collateralveins in the affected extremity.

� Pain, tenderness, and/or heaviness of the affectedextremity.

� A low-grade fever of unknown origin.

The patient also should be monitored for clinicalmanifestations of pulmonary embolus, which includechest pain, breathlessness, apprehension, fever, andcough. The neurovascular status of the extremitiesalso should be assessed. The physician should benotified if there is a change in baseline signs andsymptoms, and the patient should be immobilizeduntil seen by a physician.

Because patients are frequently asymptomatic,health care professionals need to understand whatfactors increase the risk of developing a thrombo-embolism. In persons with SCI, immobilization due to paralysis or to concomitant injuries, such as lowerlimb fractures, greatly increase the risk of throm-bosis. Other risk factors include dehydration, obesity,age over 40, malignancy, congestive heart failure,estrogen therapy, pregnancy, and a history ofthrombosis.

Additional interventions should include the per-formance of active and passive range-of-motion exer-cises and the application of elastic support hose andmechanical devices (Fowler, 1995; Spoltore andO’Brien, 1995). Elastic support—such as elastic ban-dages or compression stockings—should be worn topromote venous return and to control edema. Thedevices should be removed twice daily and the legsand feet carefully inspected for signs of erythema,ecchymoses, or skin breakdown. Hose must beapplied so that tight bands around the limb areavoided. If pneumatic compression systems areimplemented, they must be monitored regularly toassure correct placement of the sleeves and properfunction of the pump. The extremities must be exam-ined before and after the application of stockings andsleeves to make certain that the integrity of theunderlying skin is not compromised from pressureexerted by the devices. Pneumatic compression sys-tems—intermittent or sequential—are contraindicat-ed in patients with severe arterial insufficiency.

A baseline partial thromboplastin time, pro-thrombin time, and platelet count should be obtained

before heparin and/or warfarin therapy are initiated.Patients receiving heparin should be observed forsigns of heparin-induced thrombocytopenia, whichusually appear 5 to 7 days after initial exposure toheparin, or sooner with reexposure to heparin(Fahey, 1994). The diagnosis is suspected if theplatelet count declines by 50 percent or more and/orif signs of venous or arterial occlusion occur: stroke,myocardial infarction, or acute arterial or venousthrombosis. Patients also should be monitored forsigns of bleeding, including epistaxis, hematoma,hematuria, melena, and/or decrease in hemoglobinand hematocrit.

Intake and output should be monitored and flu-ids administered as needed to maintain fluid balanceand avoid dehydration (Fahey, 1994). The legs shouldbe elevated above the level of the heart. Elevation ofthe knees—using either pillows or the bed adjust-ment—should be avoided, as this creates a jackknifeposition that can promote venous obstruction,venous hypertension, and thrombus formation. If ele-vation of the foot gatch is required, the knee sectionof the bed also should be raised to prevent hyperex-tension of the leg.

Comprehensive patient and staff educationalprograms should include information about the signsand symptoms of thromboembolism, the importanceof physician notification if thrombosis is suspected,and the common risk factors that increase the likeli-hood of clotting (Fowler, 1995). Interventions thatprotect against thrombosis should be emphasized:� Exercise

� Weight loss

� Cessation of smoking

� Good elastic support

� Avoidance of constricting garters, leg bag straps,tight knee-high boots, girdles, or overly tightpantyhose or slacks

If the patient is receiving anticoagulant therapy,instructions should include the purpose of the drug,the side effects (e.g., bleeding), potential drug andfood interactions, and the need for regular laboratorymonitoring and medical followup. Written instruc-tions should be provided whenever possible, and doc-umentation of drugs, dose, and instructions in themedical record is always advisable.


O ur review of the literature of the past decadeidentified many areas in need of further study.The factors leading to thromboembolism remain

incompletely understood. Fatal pulmonary embolimay occur even in patients thought to be at low risk.The interplay of clotting factor activation and inhibi-tion, vessel wall injury, and fibrinolytic activity needscareful examination using contemporary methodssuch as measurement of molecular markers of coagu-lation, studies of platelet-derived microvesicles, andassessment of endothelial cell integrity.

Another understudied area is the detection ofthromboembolism. Because of impaired sensationand horizontal leg position, clinical signs of deepvein thrombosis such as leg pain and swelling areusually lacking, and signs associated with pulmonaryembolization such as shortness of breath are usuallyattributed to atelectasis or lung infection. Althoughthe clinician may have a high index of suspicion forthromboembolism, studies such as venous ultrasoundand ventilation/perfusion scanning are less sensitivein asymptomatic patients. Therefore, laboratorymethods with adequate sensitivity for the detection ofthrombosis, such as some of the newer d-dimer tests,need to be studied in the SCI population. Positiveresults obtained with these tests will need to be con-firmed by advanced imaging modalities such as spiralcomputerized tomography (CT) and ultrafast CT andmagnetic resonance imaging.

Evaluation of methods of prophylaxis is incom-plete. Randomized controlled trials of various physi-cal modalities used for thrombosis prevention, suchas advanced models of sequential compression

devices and foot pumps, have not been done, nor arethere randomized studies of vena cava filters,although these are in widespread use. The risks andbenefits of such filters and their appropriate use inSCI require urgent attention. With regard to antico-agulant therapy, there is a multicenter, randomizedtrial comparing low-dose heparin, 5000 U every 8hours plus compression boots with low molecularweight heparin, 30 mg twice daily for 2 weeks. Forthe next 6 weeks, patients continue on either thelow-dose heparin or on low molecular weightheparin, 40 mg once daily. This study, by Geno Merli,MD, at Jefferson Medical College, Philadelphia, hasbeen submitted for publication.

The optimal duration of thromboprophylaxisalso needs to be clarified. Clearly, patient characteris-tics are important and such factors as location of thecord lesion; extent of paralysis; associated injuries,especially to the long bones; age; obesity; and con-comitant illnesses need study. If a leg thrombus isdetected, when is it safe to resume physical andother therapies? No data on thrombus stability exist,to our knowledge. Treatment for thromboembolismhas traditionally been intravenous heparin and war-farin. However, the benefits of low molecular weightheparins for thrombosis therapy are now being rec-ognized; these include administration by the subcuta-neous route, no requirement for monitoring, andfewer complications such as bleeding, osteoporosis,and heparin-induced thrombocytopenia. Whether lowmolecular weight heparins or other new anticoagu-lants will be as safe and effective in the managementof SCI as in other indications needs to be examined.

Directions for Future Research


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Becker, D., M. Gonzalez, A. Gentili et al. Prevention ofdeep venous thrombosis in patients with acute spinalcord injuries: Use of rotating treatment tables. Neuro-surgery 20 (1987): 675-77.

Becker, D.M., J.T. Philbrick, and J.B. Selby. Inferior venacava filters, indications, safety, effectiveness. Archives ofInternal Medicine 152 (1992): 1985–94.

Bors, E., C.A. Conrad, and T.B. Massell. Venous occlusionof lower extremities in paraplegic patients. Surgery,Gynecology, and Obstetrics 99 (1954): 451–54.

Brach, B.B., K.M. Moser, and L. Cedar et al. Venousthrombosis in acute spinal cord paralysis. Journal ofTrauma 17 (1977): 289–92.

Carabasi, R.A., M.J. Moritz, and B.E. Jarrell. Complica-tions encountered with the use of the Greenfield filter.American Journal of Surgery 154 (1987): 163–68.

Clagett, G.P., F.A. Anderson, Jr., and J. Heit et al. Preven-tion of venous thromboembolism. Chest 108 (4 Suppl)(1995): 312S–34S.

Clagett, G.P., F.A. Anderson, Jr., W. Geerts, et al. Preven-tion of venous thromboembolism. Chest 114 (Suppl)(1998): 531S–560S.

Colachis, S.C., and D.M. Clinchot. The associationbetween deep venous thrombosis and heterotopic ossifi-cation in patients with acute traumatic spinal cord injury.Paraplegia 31 (1993): 507–12.

Davies, G.C., and E.W. Salzman. “The pathogenesis ofdeep vein thrombosis.” In Venous and Arterial Throm-bosis: Pathogenesis, Diagnosis, Prevention, and Thera-py, edited by J.H. Joist and L.A. Sherman, 1–22. NewYork: Grune and Stratton, 1979.

Decousus, H., A. Leizorovicz, F. Parent, et al. A clinicaltrial of vena caval filters in the prevention of pulmonaryembolism in patients with proximal deep-vein thrombosis.New England Journal of Medicine 338 (1998):409–15.

DeVivo, M.J., and S.L. Stover. “Long-term survival andcauses of death.” In Spinal Cord Injury: Clinical Out-comes From the Model Systems, edited by S.L. Stover,J.A. DeLisa, and G.G. Whiteneck, 289–316. Gaithersburg,Md.: Aspen Publishers, 1995.

DeVivo, M.J., G.G. Whiteneck, and E.D. Charles, Jr. “Theeconomic impact of spinal cord injury.” In Spinal CordInjury: Clinical Outcomes From the Model Systems,edited by S.L. Stover, J.A. DeLisa, and G.G. Whiteneck,234–71. Gaithersburg, Md.: Aspen Publishers, 1995.

Fahey, V.A. “Venous thromboembolism.” In VascularNursing, edited by V.A. Fahey, 405–31. Philadelphia: W.B.Saunders, 1994.

Fordyce, M., and R. Ling. A venous foot pump reducesthrombosis after total hip replacement. Journal of Boneand Joint Surgery 74 (1992): 45-49.

Fowler, S.B. Deep vein thrombosis and pulmonary emboliin neuroscience patients. Journal of Neuroscience Nurs-ing 27 (1995): 224–28.

Frisbie, J.H., and A.A. Sasahara. Low-dose heparin pro-phylaxis for deep venous thrombosis in acute spinal cordinjury patients: A controlled study. Paraplegia 19(1981): 343–46.

Frost, F.S. Role of rehabilitation after spinal cord injury.Urologic Clinics of North America 20 (1993): 549–59.

Gardner, A.M.N., R.H. Fox, C. Lawrence, et al. Reductionof post-truamatic swelling and compartment pressure byimpulse compression of the foot. Journal of Bone JointSurgery 72-B (1990): 810–15.

Geerts, W.H., K.I. Code, R.M. Jay et al. A prospectivestudy of venous thromboembolism after major trauma.New England Journal of Medicine 331 (1994):1601–6.

Geerts, W.H., R.M. Jay, K.I. Code et al. Thromboprophy-laxis after major trauma: A double-blind RCT comparingLDH and the LMWH, enoxaparin. Thrombosis andHaemostasis 73 (1995): 973 (abstract).

Geerts, W.H., R.M. Jay, K.I. Code, et al. A comparison oflow-dose heparin with low-molecular-weight heparin asprophylaxis against venous thromboembolism after majortrauma. New England Journal of Medicine 335(1996): 701–7.

Green, D. Prophylaxis of thromboembolism in spinalcord-injured patients. Chest 102 (Suppl) (1994):649S–51S.

Green, D., D. Chen, J.S. Chmiel et al. Prevention ofthromboembolism in spinal cord injury: Role of low mole-cular weight heparin. Archives of Physical Medicineand Rehabilitation 75 (1994): 290–92.

Green, D., M.Y. Lee, V.Y. Ito et al. Fixed versus adjusteddose heparin in the prophylaxis of thromboembolism inspinal cord injury. Journal of the American MedicalAssociation 260 (1988): 1255–58.

Green, D., M.Y. Lee, and A.C. Lim. Prevention of throm-boembolism after spinal cord injury using low molecularweight heparin. Annals of Internal Medicine 113(1990): 571–74.

Green, D., E. Rossi, J. Yao et al. Deep vein thrombosis inspinal cord injury: Effect of prophylaxis with calf com-pression, aspirin, and dipyidamole. Paraplegia 20(1982): 227-34.

Gunduz, S., E. Ogur, H. Mohur et al. Deep vein thrombo-sis in spinal cord injured patients. Paraplegia 31 (1993):606–10.

Harris, S., D. Chen, and D. Green. Enoxaparin for throm-boembolism prophylaxis in spinal injury. American Jour-nal of Physical Medicine and Rehabilitation 75(1996): 1–3.

Herzog, J.A. Deep vein thrombosis in the rehabilitationclient. Rehabilitation Nursing 17 (1992): 196–98.

Jones, B.T., and J.A. Fink. A prospective comparison ofthe status of the deep venous system after treatment withintracaval interruption versus anticoagulation. Journal ofthe American College of Surgery 178 (1994): 220–22.

Keppler, J.P. Rehabilitation in spinal cord injury. CriticalCare Clinics 3 (1987): 637–54.

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Abrasion: an excoriation or circumscribed removal of thesuperficial layers of skin or mucous membrane.

Anticoagulant: a drug or substance that prevents clotting, theprocess of changing from a liquid to a solid, said espe-cially of blood.

Antithrombotic agent: a drug that prevents occlusion ofblood vessels by clots.

aPTT (activated partial thromboplastin time): a test used tomonitor the activity of anticoagulant medications such asheparin.

Arterial perfusion: the flow of blood through arteries toorgans.

ASIA class C: incomplete: motor function is preserved belowthe neurological level, and the majority of key musclesbelow the neurological level have a muscle grade lessthan 3.

ASIA class D: incomplete: motor function is preserved belowthe neurological level, and the majority of key musclesbelow the neurological level have a muscle grade greaterthan or equal to 3.

Atelectasis: absence of gas from a part or the whole of thelungs, due to failure of expansion or resorption of gasfrom the alveoli.

Blood factor VIII activity: a clotting protein important inblood coagulation.

Bradycardia: slowness of the heartbeat, usually defined (byconvention) as a rate under 60 beats per minute.

Clot: coagulate, said especially of blood; or, a soft, nonrigid,insoluble mass formed when a liquid gels.

Collateral vein: a vein that forms to convey blood around anoccluded blood vessel.

Contrast dye venography: radiographic demonstration of avein after the injection of contrast medium.

Cor pulmonale: failure of the right side of the heart, usuallydue to obstruction of blood flow through the lungs.

Deep vein thrombosis: displacement of thrombi (clots) fromthe leg veins to the arteries of the lung (pulmonaryembolism). If there is a hole in the heart, the clots maycross into the arterial circulation and deposit in the brain,causing a stroke.

Dipyridamole: a coronary vasodilator that also has a weakaction to reduce platelet aggregation; commonly used inplace of exercise for radionuclide studies of the myocardi-um.

Doppler ultrasonographic imaging: application of theDoppler effect in ultrasound to detect movement of scat-ters (usually red blood cells) by analysis of change in fre-quency of the returning echoes.

Early mobilization: exercising as soon as possible aftersurgery or injury.

Ecchymosis (plural, ecchymoses): a purplish patch caused byextravasation of blood into the skin, differing from apetechia only in size (larger than 3 mm diameter).

Electrical stimulation (ES): electrical charge to cause musclecontraction.

Erythema: redness of the skin due to capillary dilatation

Evidence table: a chart prepared by methodologists thatreports the strength of evidence of literary cited in prac-tice guideline development.

Fibrinolysis: dissolution of an elastic filamentous proteinderived from fibrinogen by the action of thrombin, whichreleases fibrinopeptides A and B from fibrinogen in coag-ulation of the blood.

Fibrinolytic activity: denoting, characterized by, or causingfibrinolysis.

Frankel D (neurologically incomplete) lesion: a level ofinjury under the Frankel method of classifying spinal cordinjury based on severity of nerve damage; D indicatespersisting neurological function.

FUT (fibrinogen uptake test): a test which uses fibrinogenwith a radioactive tag (125I) to detect blood clots in thelower extremities.

Gradient elastic stockings (GES): rubberized hose appliedsnugly to provide uniform compression of the veins ofthe lower limb.

Hemostasis: the arrest of bleeding, the arrest of circulation ina part.

Heterotopic ossification: deposition of calcium in the mus-cles, usually occurring after injury and nerve damage.

Hypercoagulable state: characterized by abnormallyincreased coagulation.

Hypotension: subnormal arterial blood pressure, reducedpressure or tension of any kind.

Hypoxemia: subnormal oxygenation of arterial blood, short ofanoxia.

I-125 fibrinogen scan: a test that uses fibrinogen with aradioactive tag (125I) to detect blood clots in the lowerextremities.

Impedance plethysmography: a technique used to determinewhether there are clots blocking the major veins of thelegs.

Inferior vena cava: the main vein of the abdomen, transport-ing blood from the lower extremities to the heart.

Joint contractures: usually permanent deformity of a jointcausing limited mobility.

Glossary of Terms


Low molecular weight heparin (LMWH): a fragment ofheparin prepared by enzymatic or chemical processing,having many advantages over heparin including betterabortion after injection, longer persistence in the blood,and fewer side effects.

Meta-analysis: a statistical technique for combining theresults of many studies, giving greater weight to the finalconclusion.

Methodologist: an individual who reviews published data andretrieves the salient information.

Microvesicle: a fluid-filled space formed within the epidermisthat is too small to be recognized as a blister.

Morbidity: the ratio of sick to well in a community.

Mortality: pertaining to death or causing of death.

Paraplegic: relating to or having paralysis of both lowerextremities and generally the lower trunk.

Passive exercise: movement of an extremity by someoneother than the patient.

Pathophysiology: derangement of function seen in disease;alteration in function as distinguished from structuraldefects.

Placebo: an inert compound identical in appearance to materi-al being tested in experimental research, which may ormay not be known to the physician and/or patient.

Placebo control group: a group of patients to which a place-bo is administered in experimental research, to distin-guish between drug action and suggestive effect of thematerial under study.

Pneumatic compression devices: bladders that are intermit-tently filled with air and are applied to an extremity torhythmically compress the veins.

Postthrombotic syndrome: a complication of deep veinthrombosis consisting of chronic swelling of the leg,cramping, itching, skin discoloration, and often skinulceration.

Potential bleeding sites: breaks in the lining of blood vesselsin various organs such as the brain, lung, stomach, orbladder that may bleed when a patient is treated withanticoagulant drugs.

Pulmonary arteries: the two terminal branches of the pul-monary trunk, which pierces the pericardium to enter thehilus of the lungs. Branches are distributed with thebronchi, frequent variations occurs.

Pulmonary angiography: radiography of vessels in the lungsafter the injection of a radiopaque contrast material; usu-ally requires percutaneous insertion of a radiopaquecatheter and positioning under fluoroscopic control.

Pulmonary embolism: obstruction or occlusion of a vessel byan embolus of the pulmonary arteries, most frequently bydetached fragments of thrombi from a leg or pelvic vein,commonly when thrombosis has followed an operation orconfinement to bed.

Pulmonary hypertension: an increase in the blood pressurein the arteries of the lung, often due to clots in the small-er branches of these arteries.

Randomized: by chance; method for allocation of individualsto groups for experimental and control regimens.

Range of motion: a statistical measurement of a dispersionor variation of change of place or position.

Refractory edema: an accumulation of an excessive amountof watery fluids in cells, tissues, or serous cavities that isresistant to treatment.

Spasticity: an state of increased muscular tone with exaggera-tion of the tendon reflexes.

Tachycardia: rapid beating of the heart, conventionally appliedto rates over 100 per minute.

Tachypnea: rapid breathing.

Tetraplegic: pertaining to the paralysis of all four limbs.

Thrombocytopenia: a condition in which there is an abnor-mally small number of platelets in the circulating blood.

Thromboembolism: displacement of thrombi (clots) from theleg veins to the arteries of the lung (pulmonaryembolism). If there is a hole in the heart, the clots maycross into the arterial circulation and deposit in the brain,causing a stroke.

Thrombotic disease: a disorder of body functions caused by aclot in the cardiovascular system formed during life fromconstituents of blood.

Ultrasound: a technique for visualizing thrombi in the veins,usually using Doppler methodology.

Vena cava filter: a device that is introduced into the venacava to prevent thrombi from passing from the legs tothe lungs.

Venography: radiographic demonstration of a vein after theinjection of contrast medium.

Venostasis: abnormally slow motion of blood in veins, usuallywith venous distention.

Venous thromboembolism: embolism from a clot in the car-diovascular system formed during life from constituentsof blood relating to the veins.

Ventilation/perfusion lung scanning: using a combination oftracers to measure airflow and blood flow in the lungs.The demonstration of airflow in tissue that is not receiv-ing blood flow suggests that the blood vessels to the tis-sue are blocked by clots (pulmonary emboli).

Abrasions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 8American Spinal Injury Association . . . . . . . . . . . . . . . . .1, 8Anticoagulants . . . . . . . . . . . . . . . . . . . . . . . .ii, 1, 9, 11, 14

anticoagulant agents . . . . . . . . . . . . . . . . . . . . . . . .2, 12anticoagulant prophylaxis . . . . . . . . . . . . . . . . . . . .1, 10antiplatelet agents . . . . . . . . . . . . . . . . . . . . . . . . . . . .8antithrombotic agents . . . . . . . . . . . . . . . . . . . . . . . .1, 8

Apprehension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Arterial insufficiency . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Arterial perfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12Aspirin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12Atelectasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14Bed rest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2, 11Blood

active bleeding sites . . . . . . . . . . . . . . . . . . . . . . . . .1, 9blood products . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3blood factor VIII activity . . . . . . . . . . . . . . . . . . . . . . . .3hematocrit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13hematuria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13hemoglobin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13hemostasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3platelet count . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13potential bleeding sites . . . . . . . . . . . . . . . . . . . . . . .1, 9venostasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3

Breathlessness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13, 14Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 9Cardiac

bradycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12cardiac arrhythmia . . . . . . . . . . . . . . . . . . . . . . . . . . .11cardiopulmonary reserve . . . . . . . . . . . . . . . . . . . . . .1, 9chest pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11, 13congestive heart failure . . . . . . . . . . . . . . . . . . . . . . . .13heart failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 9tachycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11myocardial infarction . . . . . . . . . . . . . . . . . . . . . . . . .13

Centripetal massage . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8Clots . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .ii, 13Clotting factor activation . . . . . . . . . . . . . . . . . . . . . . . . .14Coagulopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 9Collateral veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Compression devices . . . . . . . . . . . . . .ii, 1, 8, 11, 12, 13, 14Computerized tomography (CT) . . . . . . . . . . . . . . . . . . . .14Controlled clinical trials . . . . . . . . . . . . . . . . . . . . .7, 10, 14

controls . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3, 7, 10evidence tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .6placebo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3randomized . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7strength of evidence . . . . . . . . . . . . . . . . . . . . . . . . . .7

Coumadin (see Warfarin therapy)D-dimer tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14

Deep vein thrombosis (DVT) . . . .ii, 1, 3, 4, 6, 7, 8, 9, 12, 14recurrent DVT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4

Dehydration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3, 13Dipyridamole . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8Early mobilization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12Ecchymoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 8, 13Edema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4, 8, 13

lower extremity edema . . . . . . . . . . . . . . . . . . . . . . . . .8Elastic bandages . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8, 13

elastic hose . . . . . . . . . . . . . . . . . . . . . . . . . . . .ii, 6, 13external stocking and boots . . . . . . . . . . . . . . . . . . . . .12gradient elastic stockings (GES) . . . . . . . . . . . . . . . . . .8

Electrical stimulation (ES) . . . . . . . . . . . . . . . . . . . . . .8, 12Endothelial cell integrity . . . . . . . . . . . . . . . . . . . . . . . . .14Enoxaparin (LMWH) . . . . . . . . . . . . . . . . . . . . . . . . . . . .10Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7Epistaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Erythema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11, 13Estrogen therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2, 11, 12, 13

active exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12range of motion . . . . . . . . . . . . . . . . . . . . . . . .8, 12, 13range-of-motion exercises . . . . . . . . . . . . . . . . . . . . . .11passive exercise . . . . . . . . . . . . . . . . . . . . . . . . . . .2, 12

External pneumatic compression . . . . . . . . . . . . . . . . . .1, 8IPC-intermittent pneumatic compression . . . . . . . . . . .10pneumatic compression devices . . . . . . . . . . . .1, 8, 9, 13

Fever . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11, 13Fibrinolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8

fibrinolytic activity . . . . . . . . . . . . . . . . . . . . . . . . .3, 14Flexion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8, 12

dorsi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8plantar . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8, 9

Functional status . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11Gastrocnemius . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8Heparin . . . . . . . . . . . . . . . . . . . . . . . . .8, 9, 10, 11, 13, 14

adjusted dose unfractionated heparin . . . . . . . . . .1, 9, 10LDUH (low-dose unfractionated heparin) . . . . . . .1, 9, 10LMWH (low molecular weight heparin) . .ii, 1, 9, 10, 11, 14low-dose heparin . . . . . . . . . . . . . . . . . . . . . . . . . .8, 14unfractionated heparin (UH) . . . . . . . . . . . . . . . . . .9, 10

Hematoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Heterotopic ossification . . . . . . . . . . . . . . . . . . . . . . .4, 11Hypercoagulable state . . . . . . . . . . . . . . . . . . . . . . . . . . . .3Hypotension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11, 12Hypoxemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11I-125 fibrinogen scan . . . . . . . . . . . . . . . . . . . . . . . . . . . .3

fibrinogen leg scanning . . . . . . . . . . . . . . . . . . . . . . . . .8FUT-fibrinogen uptake test . . . . . . . . . . . . . . . . . . .3, 10

Impedance plethysmography . . . . . . . . . . . . . . . . . . . .3, 10


Index

Inferior vena cava . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 9inferior vena cava filters . . . . . . . . . . . . . . . . . . . . . .1, 9inferior vena cavagrams . . . . . . . . . . . . . . . . . . . . . . . .9

Intrathoracic pressure . . . . . . . . . . . . . . . . . . . . . . . . . . .12Legs . . . . . . . . . . . . . . . . . . . . . . . . .ii, 1, 8, 11, 12, 13, 14

circumference of the calf . . . . . . . . . . . . . . . . . . . . . . .12hyperextension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13joint contractures . . . . . . . . . . . . . . . . . . . . . . . . . . . .12leg thrombi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 8leg swelling . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11, 14leg veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .iilower limb fractures . . . . . . . . . . . . . . . . . . . . . .1, 9, 13passive leg exercise . . . . . . . . . . . . . . . . . . . . . . . . . . .ii

Mechanical devices . . . . . . . . . . . . . . . . . . . . . .9, 11, 12, 13Mechanical filters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .6Meta-analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3Methodologist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7Microvesicles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14Model SCI Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4Mortality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .ii, 3, 4, 7, 9Morbidity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3Neurologic Classification

ASIA class C . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1, 8ASIA class D . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1Frankel D (neurologically incomplete) lesions . . . . . . . . .4

Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . .ii, 1, 6, 9, 13, 14Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11, 14Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4, 5, 11, 13, 14Paraplegic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4

complete motor paralysis . . . . . . . . . . . . . . . . . .ii, 1, 6, 9incomplete motor paralysis . . . . . . . . . . . . . . . . . . . . . . . .1Partial thromboplastin time . . . . . . . . . . . . . . . . . . . . . . .13

activated partial thromboplastin time . . . . . . . . . . . .1, 10Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . .ii, 12-13Perforation of the vena cava . . . . . . . . . . . . . . . . . . . . . . . .9Physical assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Physical therapy . . . . . . . . . . . . . . . . . . . . . .ii, 7, 11, 12, 14Placebo

placebo control group . . . . . . . . . . . . . . . . . . . . . . . . . .3saline placebo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8

Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12Postthrombotic syndrome . . . . . . . . . . . . . . . . . . . . . . . . .4Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Prevalence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .iiPrevention . . . . . . . . . . . . . . . . . . . . . . . . . . .ii, 1, 4, 12, 14

Prophylactic measures . . . . . . . . . . . . . . .ii, 2, 3, 10, 11, 12Prophylaxis . . . . . . . . . . . . . . . . .ii, 1, 3, 6, 8, 9, 10, 11, 14Prothrombin time . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13Proximal vein thrombosis . . . . . . . . . . . . . . . . . . . . . . . . .10Pulmonary

cor pulmonale . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4cough . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13pulmonary angiography . . . . . . . . . . . . . . . . . . . . . .2, 12pulmonary arteries . . . . . . . . . . . . . . . . . . . . . . . . . . . .iipulmonary embolism . . .ii, 3, 4, 6, 7, 9, 10, 11-12, 13, 14pulmonary hypertension . . . . . . . . . . . . . . . . . . . . . . . .4

Sequential chamber compression . . . . . . . . . . . . . . . . . .1, 8Soleus muscle groups . . . . . . . . . . . . . . . . . . . . . . . . . . . .8Spasticity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .ii, 11Spinal stabilization . . . . . . . . . . . . . . . . . . . . . . . . . . .11, 12Spiral computerized tomography . . . . . . . . . . . . . . .2, 11, 12Stasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8, 12Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7, 13Surgical procedures . . . . . . . . . . . . . . . . . . . . . . . .2, 10, 11Surveillance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3Tachypnea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11Tetraplegic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4Thromboembolism . . . . . . . . . .ii, 1, 6, 7, 10, 11, 12, 13, 14

history of . . . . . . . . . . . . . . . . . . . . .ii, 1, 6, 7, 9, 11, 13thromboprophylaxis . . . . . . . . . . . . . .ii, 1, 3, 6, 8, 9, 14thrombocytopenia . . . . . . . . . . . . . . . . . . . . . .10, 13, 14thromboemobolic disease . . . . . . . . . . . . . . . . .ii, 3, 4, 5

Tinzaparin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .10Ultrasound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2, 11

Doppler ultrasonographic imaging . . . . . . . . . . . . . . . . .3DU-duplex ultrasound . . . . . . . . . . . . . . . . . . . . . . . .10venous ultrasound . . . . . . . . . . . . . . . . . . . . . . . . . . .14magnetic resonance imaging . . . . . . . . . . . . . . . . . . . .14

VEN-Venography . . . . . . . . . . . . . . . . . . . . . .2, 3, 4, 10, 11contrast dye venography . . . . . . . . . . . . . . . . . . . . . . . .3

Vena cava filter . . . . . . . . . . . . . . . . . . . . . .ii, 1, 6, 7, 9, 14filter malposition . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9

Venous thrombosisvenous thromboembolism . . . . . . . . .ii, 3, 4, 5, 10, 11, 13venous thromboembolism disease . . . . . . . . . . . . . . . . .3

Venous foot pump . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9Ventilation/perfusion lung scanning . . . . . . . . . . . . .2, 11, 14Video phlebography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9Warfarin therapy . . . . . . . . . . . . . . . . . . . . . . . . . .9, 13, 14


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August 2002

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