Produced by the Royal College of Physicians of Edinburgh and Royal College of Physicians and Surgeons of Glasgow

DVT in hospitals: guideline implementation

Hospital beds in ward | ©istockphoto.com/Stefan Klein

  • Dr K Hogg, SpR Emergency medicine, NorthWest England rotation training scheme
  • Dr S Jones, Consultant in Emergency medicine and Intensive Care, Manchester Royal Infirmary, Oxford Rd, Manchester, England
  • Professor K Mackway-Jones, Professor in Emergency medicine, Manchester Royal Infirmary, Oxford Rd, Manchester, England

Summary

While much media coverage of DVT has focussed on long-distance travel, it is perhaps less publicly-known that many patients develop DVTs whilst in hospital and that DVT is the most common form of preventable death in hospital. A number of clinical guidelines have been developed to tackle this problem, but how extensively are they being implemented? Dr Kerstin Hogg, Dr Steve Jones and Professor Kevin Mackway-Jones review the evidence.

Key Points

  • 60% of diagnoses of DVT occur during hospital admissions for unrelated conditions.
  • 10% of hospital deaths are due to venous thromboembolic disease (VTE).
  • Medical as well as surgical patients are at risk.
  • Several evidence-based guidelines exist for prevention of VTE.
  • Compliance to these guidelines is variable.
  • The key challenge is the implementation of the guidelines.

Declaration of interests: No conflict of interests declared

Introduction

Deep vein thrombosis and pulmonary embolism co-exist as part of the thromboembolic disease process. In 1976, the mortality of recognised and treated pulmonary embolism was 8%.1 Despite increased awareness of this disease and changes in prevention, diagnosis and treatment there has been little improvement in the prognosis with recent registries reporting the mortality to be 7%.2

Sixty per cent of all patients diagnosed with DVT develop the condition during hospital admission for an unrelated illness and 10% of hospital deaths are caused by VTE.3 Whilst certain surgical procedures, such as major joint replacement, colorectal surgery and surgery for cancer, have long been associated with a high risk of VTE, recent studies have demonstrated that older medical patients hospitalised with acute illness have a comparable risk. In 2004 the American College of Chest Physicians (ACCP) stated that ‘PE is the most common preventable cause of hospital death and is the number one strategy to improve patient safety in hospitals’.4 Those patients who develop PE during hospital admission are not only at risk of death but also a prolonged hospital stay and anticoagulant therapy. Patients who develop DVT are at risk of PE (either in hospital or at home following discharge) as well as post-thrombotic syndrome of the affected leg.

There are several evidence-based guidelines for the prevention of VTE. These have been produced by specialty organisations such as Investigators Against Thromboembolism (INATE), and the ACCP as well as national organisations, for example the Scottish Intercollegiate Guideline Network (http://www.sign.ac.uk). Despite the publication of these guidelines, the use of VTE prophylaxis varies markedly.

This short review attempts to collate evidence for the inpatient risk of VTE, optimal prevention strategies and their implementation. The referenced studies used a variety of techniques to verify primary endpoints of DVT and PE. The authors acknowledge this and accept the heterogeneous nature of the summated endpoints. Many studies (in particular surgical inpatient studies) assess the incidence of both symptomatic and asymptomatic DVTs. The clinical relevance of an asymptomatic DVT remains unclear, however evidence suggests that interventions reducing the incidence of asymptomatic DVTs produce a similar reduction in PE.5,6

Patients undergoing surgical procedures

Patients undergoing operations for joint replacement and hip fracture are at high risk of VTE. About 50% of patients undergoing hip fracture surgery without prophylaxis develop VTE.4,7 Twenty percent of deaths following orthopaedic surgery are caused by PE.8 When treated with prophylactic low molecular weight heparin (LMWH), the rate of DVT following knee replacement surgery is 33%, and hip replacement is 14%.4 These patients are at risk because they tend to be elderly, the operative procedure obstructs lower limb venous return, and postoperative mobility can be poor.

There are a few small studies suggesting that mechanical methods such as pneumatic compression boots reduce the incidence of post-operative DVT.7 One multicentre study has demonstrated that aspirin can reduce VTE following hip fracture surgery by 36% and knee or hip replacement surgery by 18%.9 Following major orthopaedic surgery the use of warfarin, low dose unfractionated heparin or LMWH reduces the incidence of VTE to around half of that observed without prophylaxis.7 There is little evidence that blood loss is increased, however blood loss reporting in existing studies is generally poor.7 Overall LMWH appears to be more efficacious in reducing the incidence of DVT than either warfarin or unfractionated heparin.10 The synthetic pentasaccharide Fondaparinux is at least as effective as LMWH in reducing postoperative thromboembolism following hip fracture repair or knee replacement surgery.4 Prolonged prophylactic therapy for up to 30 days post surgery is recognised to further reduce thromboembolic complications.

The ACCP does not recommend use of anticoagulant prophylaxis following routine knee arthroscopy.

Studies of general surgical patients without prophylaxis established the prevalence of DVT to be 15% to 30%. A variety of factors influence the risk of thromboembolic disease: the type of surgery, patients’ risk factors (such as cancer, previous history of thromboembolism, obesity), patients age, type of anaesthesia and postoperative care.4 The ACCP recommend the use of anticoagulant prophylaxis for all general surgical patients except those categorized as low risk.4 Low risk is defined as a patient under 40 years of age with no risk factors who is undergoing a minor operative procedure (day surgery). The incidence of thromboembolism following uncomplicated laparoscopic surgery is thought to be small, but the exact risk remains unclear. As yet there remains no clear consensus for the approach to patients undergoing laparoscopic intervention. There is little evidence on the risk of surgery in patients taking the oral contraceptive pill or hormone replacement therapy (HRT). One prospective population study has demonstrated no increased incidence of VTE following surgery in patients using the oral contraceptive.11 In contrast, another prospective study showed a significant increased risk of VTE in those taking HRT who underwent surgery (hazard ratio of 4•9).12

In general surgical patients, unfractionated and LMWH are similarly efficacious (reducing the rate of thromboembolism by at least 60%4) and have a similar risk of bleeding postoperatively, this risk increasing with higher doses.4 The combination of graded elastic compression stockings and heparin is better at preventing VTE than using heparin alone.13 Studies have failed to demonstrate that fondaparinux confers greater protection than LMWH in this group.

A summary of the ACCP analysis of risks and successful prevention strategies is summarised in table 1. The ACCP have also published recommendations for vascular, gynaecological, urological, spinal, trauma surgery and neurosurgery.2

Medical inpatients

The risk of DVT following surgery has been known for many years although the majority of DVTs diagnosed during hospital admission are among medical inpatients, and 75% of fatal inpatient PEs occur in the medical population.3 It has recently been estimated that fatal PE occurs in around 5% of medical inpatients.14 A variety of factors are identified as increasing the risk of thromboembolism in medical inpatients, in particular: age over 75, cancer, recent myocardial infarction, congestive cardiac failure, ischaemic stroke, chronic obstructive airways disease and acute infectious disease. Around half of medical inpatients with recent stroke and a quarter of patients with recent myocardial infarction develop DVT.14 The ACCP recommends anticoagulant prophylaxis in acutely ill medical patients who are admitted to hospital with congestive heart failure, severe respiratory disease, acute ischaemic stroke (with reduced mobility) and myocardial infarction. In addition, those who are confined to bed and have one or more additional risk factors, including active cancer, previous VTE, sepsis, acute neurologic disease, or inflammatory bowel disease, should receive prophylaxis.

It is generally accepted that graduated elastic compression stockings reduce the incidence of thromboembolism in the inpatient medical population, although very few studies have addressed this. Both unfractionated and LMWH have similar efficacy, but LMWH is associated with less bleeding.14 Unfractionated heparin recommended as a twice daily treatment reduces the incidence of VTE by around 60%.4 When given three times daily the incidence reduces by around 70% but there is a twofold higher incidence of major bleeding. Low molecular weight heparin administered once daily reduces VTE in acutely unwell medical inpatients by a half to two thirds3,4,14 as does fondaparinux 2•5 mg once daily (without an increased rate of bleeding compared to placebo).1,2,6

Appropriate heparin prophylaxis for inpatients will reduce the morbidity and mortality of VTE associated with hospital admission, but it is important to recognise that heparin treatment causes heparin-induced thrombocytopenia in up to 1% of patients treated. Although unfractionated and LMWH may perform equally for prophylaxis in surgical and medical inpatients, LMWH may have additional advantages including a once daily dose and a lower incidence of heparin-induced thrombocytopenia.

Guideline compliance

Despite the publication of guidelines and the evidence base behind them, the use of prophylaxis for VTE is variable. This variation is across specialty areas as well as geographic boundaries. One study of surgical patients reports prophylaxis rates of up to 93% for patients undergoing total hip replacement, but only 84% for patients undergoing colectomy and 66% for hysterectomy. Despite the ACCP guideline highlighting the risk to medical patients, another study found that prophylaxis had been given to only 46% of appropriate medial inpatients. Variation also exists between countries; one study indicated that the majority of patients in one Australian hospital received no prophylaxis at all, but in a study from the USA, up to 89% of patients did. The authors of this paper concluded that publication of consensus statements or guidelines alone may be insufficient to ensure the incorporation of important new clinical information into routine practice.

A systematic review has been undertaken to look at what measures can be undertaken to improve the use of prophylaxis for VTE.15 Thirty studies passed the inclusion criteria and the majority of these reported an audit cycle before and after the introduction of VTE guidelines. Strategies for increasing the uptake of VTE prophylaxis included passive dissemination, audit and feedback, computer-based decision aids, documentation aids, continuing education, quality assurance activities, advertising, appointment of specific implementation staff and recruitment of local change agents or opinion leaders.

The design of these studies meant that the quality of the evidence produced was ‘average’ and the outcomes were mostly related to changing physician behaviour rather than patient outcomes. What was clear was that in those studies that relied on passive dissemination alone, adherence to guidelines and the provision of adequate prophylaxis was poor. The most effective single measure was the use of computer-based clinical decision support systems although, in general, the use of multiple measures was more effective. The most effective strategies incorporated a system for reminding clinicians to assess patients for VTE risk (either electronic decision-support systems or paper-based reminders) and used audit and feedback to facilitate the iterative refinement of the intervention. The authors’ recommendation for improving VTE prophylaxis is in Table 2.

Conclusion

Despite irrefutable evidence that primary thromboprophylaxis reduces all VTE, the most common cause of preventable hospital death is still PE. There are a number of evidence-based guidelines to assist prescribing for the patient groups at risk, although the challenge for today’s clinician is less about deciding which guideline to follow and more about how to implement it.

Notes

Sources of patient orientated information can be found at: http://www.medicinenet.com/deep_vein_thrombosis/article.htm
http://www.nhsdirect.nhs.uk/articles/article.aspx?articleId=122

References

  1. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet 1999; 353:1386–9.
  2. Alpert J, Smith R, Carlson J, Ockene I, Dexter L, Dalen J. Mortality in patients treated for pulmonary embolism. JAMA 1976; 236:1477–80.
  3. Goldhaber SZ, Turpie AG. Prevention of venous thromboembolism among hospitalized medical patients. Circulation 2005; 111(1):1–3.
  4. Geerts WH, Pineo GF, Heit JA et al. Prevention of Venous Thromboembolism: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004; 126:338–400.
  5. Mismetti P, Laporte S, Darmon JY, Buchmuller A. Decousus H. Meta-analysis of low molecular weight heparin in the prevention of venous thromboembolism in general surgery. Br J Surg 2001; 88:913–30.
  6. Turpie AGG, Bauer KA, Eriksson BI, Lassen MR. Relevance of venographic distal thrombus assessment in venous thromboembolism (VTE) prophylaxis studies: lessons from the fondaparinux (Arixtra) database in major orthopedic surgery. J Thromb Haemost 2003; 1(suppl):P2066.
  7. Handoll HH, Farrar MJ, McBirnie J, Tytherleigh-Strong G, Milne AA, Gillespie WJ. Heparin, low molecular weight heparin and physical methods for preventing deep vein thrombosis and pulmonary embolism following surgery for hip fractures. The Cochrane Database of Systematic Reviews 2002; (4):CD000305.
  8. Bhattacharyya T, Iorio R, Healy WL. Rate of and risk factors for acute inpatient mortality after orthopaedic surgery. J Bone Joint Surg Am 2002; 84-A(4):562–72.
  9. Anonymous. Prevention of pulmonary embolism and deep vein thrombosis with low dose aspirin: Pulmonary Embolism Prevention (PEP) trial. Lancet 2000; 355(9212):1295–302.
  10. Conduah A, Lieberman JR. Venous thromboembolic prophylaxis after elective total hip arthroplasty. Clin Orthop Relat Res 2005; 441:274–84.
  11. Tosetto A, Frezzato M, Rodeghiero F. Prevalence and risk factors of non-fatal venous thromboembolism in the active population of the VITA Project. J Thromb Haemost 2003; 1(8):1724–9.
  12. Grady D, Wenger NK, Herrington D et al. Postmenopausal hormone therapy increases risk for venous thromboembolic disease. The Heart and Estrogen/progestin Replacement Study. Ann Int Med 2000; 132(9):689–96.
  13. Wille-Jorgensen P, Rasmussen MS, Andersen BR, Borly L. Heparins and mechanical methods for thromboprophylaxis in colorectal surgery. The Cochrane Database of Systematic Reviews 2003; (4):CD00121.
  14. Spyropoulos AC. Emerging strategies in the prevention of venous thromboembolism in hospitalized medical patients. Chest 2005; 128(2):958–69.
  15. Tooher R, Middleton P, Pham C et al. A systematic review of strategies to improve prophylaxis for venous thromboembolism in hospitals. Ann Surg 2005; 241(3):397–415.