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Venous thromboembolism (VTE), which includes deep-vein thrombosis (DVT) and pulmonary embolism (PE), is a major cause of preventable morbidity and mortality in hospitalised patients. Hospital-acquired thrombosis (HAT) has been defined as any VTE event occurring during or within 90 days of hospitalisation. Acute VTE has an annual incidence of approximately one-to-two per 1,000 persons in the general population. However, this relative risk of VTE increases up to eight-fold in hospitalised medical patients, and to more than 100-fold for surgical patients. This augmented risk persists up to 90 days post-admission.
Prior to introduction of a national VTE prevention programme in the UK in 2010, it was estimated that more than 25,000 hospital deaths occurred annually from VTE.
HAT leads to a mortality rate that is greater than the combined total deaths from breast cancer, AIDS, prostate cancer and road traffic accidents.
Furthermore, VTE is responsible for the death of more than 500,000 people in Europe each year and is the third-leading cause of death from cardiovascular causes after myocardial infarction and stroke.
Pathogenesis and natural history of VTE
The symptoms of VTE are caused by obstruction of venous outflow by thrombi, causing inflammation of the vein wall, inflammation of the surrounding tissue or embolisation into the pulmonary circulation. DVT commonly presents with pain, erythema, tenderness and swelling of the affected limb. Clinical signs will show the circumference of the affected limb as larger than the unaffected side. Ruling out other causes for the same clinical presentation will depend on the presence or absence of risk factors for VTE. A two-level DVT Wells score helps to stratify patients for appropriate diagnosis.
Patients presenting with acute pulmonary embolism often complain of sudden onset of shortness of breath with haemoptysis and pleuritic chest pain. These patients can also present with collapse and shock. Similar to DVT, a clinical probability model for PE has been developed and is called the two-level PE Wells score.
Following treatment, the resolution of DVT is slower than PE. Complete resolution occurs more frequently in PE rather than DVT, where recanalisation is more common. The risk of recurrence is higher in unprovoked VTE, where risk factors are not yet established. The presence of persistent risk factors like cancer and antiphospholipid syndrome also increase the recurrence compared to patients with transient risk factors such as surgery. Long-term complications of VTE include recurrent VTE, post-thrombotic syndrome and chronic pulmonary hypertension.
Contrast enhanced CT thorax showing massive PE (arrows)
VTE risk factors
Risk factors for developing VTE in patients admitted in medical specialities are different than for those admitted for surgical or orthopaedic procedures. Medical patients often have multiple comorbidities and increased incidence of renal and hepatic dysfunction. According to the UK National Institute for Health and Care Excellence (NICE) guidelines, all patients admitted to hospital should be risk-assessed for VTE on admission, reassessed after 24 hours and after any change in clinical situation, as well as at the time of discharge. In the case where a patient has one or more risk factors for VTE, they should receive thromboprophylaxis.
Patient-related risk factors
- Active cancer or cancer treatment
- Age >60 years
- Known thrombophilias
- Obesity (BMI >30kg/m2)
- One or more significant medical comorbidities (eg, heart disease, metabolic, endocrine or respiratory pathologies, acute infectious diseases, inflammatory conditions)
- Personal history or first-degree relative with a history of VTE
- Use of hormone replacement therapy (HRT)
- Use of oestrogen-containing contraceptive therapy
- Varicose veins with phlebitis
- Pregnancy or <6 weeks post-partum
Admission-related risk factors
- Significant reduced mobility relative to normal state for >3 days
- Total anaesthetic + surgical time >90 minutes
- Surgery involving pelvis or lower limb, and total anaesthetic + surgical time >60 minutes
- Acute surgical admission with inflammatory or intra-abdominal condition
- Surgery with significant reduction in mobility
- Hip or knee replacement
- Hip fracture
- Critical care admission
Risk factors for bleeding
Assessment of all patients for risk of bleeding before offering pharmacological VTE prophylaxis is advised. No pharmacological VTE prophylaxis should be given to patients with any of the risk factors for bleeding, unless the risk of VTE outweighs the risk of bleeding.
Risk factors include:
- Active bleeding
- Acquired bleeding disorders (such as acute liver failure)
- Concurrent use of anticoagulants known to increase the risk of bleeding (such as warfarin patient with INR higher than 2)
- Lumbar puncture/epidural/spinal anaesthesia expected within the next 12 hours
- Lumbar puncture/epidural/spinal anaesthesia within the previous four hours
- Acute stroke
- Thrombocytopenia (platelets less than 75 x 109/L)
- Uncontrolled systolic hypertension (230/120mmHg or higher)
- Untreated inherited bleeding disorders (such as haemophilia and von Willebrand disease)
Assess the risk of VTE and bleeding of all hospitalised patients:
- At the time of admission
- Within 24 hours of admission
- Whenever a change occurs in clinical situation
- At discharge
VTE is an important cause of death in hospitalised patients and the economic burden of the disease is considerable in developed countries. An estimate of the combined direct and indirect cost of VTE in the UK is now placed at £640 million annually and the cost will further increase when long-term complications like post-thrombotic syndromes are taken into consideration. Therefore, it is highly recommended that efforts should be made to prevent the occurrence of VTE by risk-assessing all hospitalised patients and offering them thromboprophylaxis, as appropriate. Early mobilisation and adequate hydration are simple measures that should be applied to prevent VTE in all patients. However, more specific thromboprophylaxis measures are available, namely mechanical methods and pharmacological type.
Mechanical thromboprophylaxis serves as the preferred alternative in patients who are ineligible for pharmacologic therapy but are at high risk in developing VTE. These methods also serve as a valuable adjunct to pharmacological methods in others.
Currently-available mechanical thromboprophylaxis methods include graduated compression stockings (GCS), intermittent pneumatic compression devices (IPCD) and venous foot pump (VFP) devices.
A number of pharmacological agents are available for thromboprophylaxis and their effectiveness varies, depending upon the clinical procedure and patient-related risk factors. They include:
- Unfractionated heparin (UFH)
- Low molecular weight heparin (LMWH)
- Novel oral anticoagulants (NOACs)
LMWHs produced by various methods of depolymerisation of standard UFH have become the standard first-line thromboprophylaxis agents. LMWHs have proven to be more efficacious in preventing VTE without increasing risk of bleeding in comparison with UFH. Side-effects such as injection-site haematoma, heparin-induced thrombocytopaenia and osteoporosis are less likely with LMWHs as compared to UFH.
NOACs have been approved for thromboprophylaxis following orthopaedic surgery. Fondaparinux, a synthetic pentasaccharide, indirectly inhibits factor Xa and has been shown to be effective in all cases of thromboprophylaxis, ie, medical, surgical and orthopaedic.
Current practice of preventing VTE
Although evidence-based consensus guidelines for VTE prophylaxis have been available for more than 20 years, VTE prophylaxis continues to be under-utilised. Despite its proven efficacy and safety, the uptake of thromboprophylaxis nationally has been disappointing, and the Irish outcome from the ENDORSE study suggested that over half of patients admitted to Irish hospitals are at risk for VTE and only 57 per cent of these are receiving recommended prophylaxis.
Seven years on from the ENDORSE study, the use of VTE prophylactic measures remain sub-optimal in Ireland where, like many other countries, we have yet to implement mandatory risk assessment tools and thromboprophylaxis policy nationally.
The safety and efficacy of VTE prophylaxis is well established, but adherence to guidelines is poor. Mandatory risk assessment and penalties for failing to implement thromboprophylaxis have been shown to significantly reduce the incidence of HAT in the UK. Perhaps it is time we considered such measures in Ireland.
References available on request
Case report 1
A 59-year-old man was admitted with chest pain. His past medical history included ischemic heart disease, hypertension, cerebrovascular accident and history of deep venous thrombosis (DVT) 10 years earlier. He was readmitted six weeks’ post discharge with shortness of breath and chest pain and was found to have bilateral PE.
This case highlights that the risk period for development of a clot is not just while a patient is in hospital but can remain up to 90 days post-hospitalisation and discharge. Multiple risk factors were present for VTE in this scenario including IHD, HTN and past history of DVT.
Case report 2
A 54-year-old man, who weighed 118kg, was admitted following a crush injury. He had a prolonged hospital stay with multiple surgical procedures, including below-knee, followed by above-knee amputations. Risk assessment was carried out on admission and he received standard thromboprophylaxis with low molecular weight heparin. Despite this, he developed an above-knee extensive DVT on day 40 of his admission.
This patient was at high risk for developing VTE and despite thromboprophylaxis, he developed extensive above-knee DVT. His increased BMI may have been an additional risk factor and perhaps weight-adjusted thromboprophylaxis could have been considered in his situation.
Case report 3
A 65-year-old male with a history of obesity, hypertension, hypothyroidism, left ventricular dysfunction, ischemic heart disease, dermatomyositis and previous pulmonary embolism, currently on warfarin therapy, was admitted with a gastrointestinal (GI) bleed. His haemoglobin fell from a baseline of 12.0g/dl to 7.5g/dl. International normalised ratio (INR) was 3.6 on admission. Warfarin was discontinued and INR reversed to normal within 24 hours. He received two units of red cells and after upper and lower GI work-up, was discharged without any anticoagulation. He was readmitted two weeks later with a massive bilateral PE with right heart strain and pulmonary hypertension.
This was a complex case where the risk of bleeding and thrombosis would require ongoing risk assessment on a daily basis and particularly on discharge.