Patients with inflammatory bowel disease such as Crohn’s or ulcerative colitis are twice as likely to develop a DVT or PE than the general population, according to researchers in Denmark. This may help to further inform how VTE risk is calculated for patients, and for which patients thromboprophylaxis should be indicated.
Kappleman, M.D. Et al (2011) Thrombo-embolic risk among Danish children and adults with inflammatory bowel diseases: a population–based nationwide study. Gut. Doi 10.1136/gut.2011.228585
AE stockings are commonly used as a thrombolprophylaxis in secondary care settings. These may be prescribed after a patients’ risk of VTE has been assessed.
Patients are advised to wear them 24 hours daily from the time they are administered to the time the patient is no longer considered to be at an increased risk of developing VTE. AES may be prescribed in conjunction with pharmacological thromboprophylaxis for added protection in those assessed to be at greater risk.
Unless contraindicated, surgical patients are generally prescribed pharmacological thromboprophylaxis as well as mechanical thromboprophylaxis (AES or intermittent pneumatic compression – IPC).
CVA patient generally are not prescribed AES because they have not been shown to be effective in such patients and can increase the risk of skin breakdown.
Other patients to avoid AES are those with peripheral neuropathy or peripheral arterial disease, or friable skin.
AES need to be fitted correctly and the right size is essential. They work by exerting graduated circumferential pressure onto the legs which supports the veins and therefore improves venous return, which decreases venous stasis. They also decrease venous dilation and therefore help to prevent activation of clotting factors.
According to researchers from Kings College London, men with prostate cancer are at an increased risks of VTE (venous thromboembolism); this is further increased in patients receiving endcrine therapy – Lancet Oncology Online
Thrombophilia, as the name implies is a blood disorder that increases the risk of clotting and therefore increases the risk of venous thromboembolism. It can be acquired through conditions such as heart failure, irritable bowel syndrome and nephritic syndrome. Or it may be inherited. Up to half of those treated for VTE are thought to have hereditary thrombophilia. This is known because patients who have had VTE are routines screened to see if there was an inherited factor in their episode. If a family member has had a previous VTE, genetic screening can be offered to identify and deal with the risk in others. Tests are carried out a month after anticoagulant treatment has finished as these interact with the antithrombin, protein S and protein C that are screened for deficiencies.
The risk of developing VTE in patients with thrombophilia is increased with dehydration and immobility/inactivity, surgery (particularly major general surgery and orthopaedic surgery to the legs) leg fractures, hip fractures, spinal cord inury, varicose veins or congestive heart or respiratory failure. Some forms of contraception can also increase the risk of VTE, therefore they are not normally recommended for patients with hereditary thrombophilia. The progestogen only pill (POP) is generally used instead of combined oral contraceptives. Pregnancy is also a risk factor, particularly if the mother is obese or more mature. This is the biggest cause of maternal mortality, especially after Caesarean section. Cancer patients are at increased risk too, but there’s also a secondary risk with chemotherapy.
In the acute setting, patients will generally be prescribed five days of anti-coagulation treatment with low molecular weight heparin (LMWH) or unfractionated heparin (if in renal failure). This is then followed by six months of oral anticoagulants. Because of the increased risk of haemorrhage, anticoagulants are not normally continued in such cases after six months.
VTE is largely preventable in many cases. VTE is a term which includes PE and DVT. It doesn’t have ot be symptomatic.
DVT is most common in the lower leg, although it can occur further up or in the arms. It can be caused by several factors; they form Virchow’s triad:
- Pooling of blood (venous stasis) which occurs mainly in the extremities and is largely caused by immobility/inactivity
- Injury or dilation of the vein wall which releases tissue factor and enables clotting
- Hypercoaguability – increased ability for clotting – this may occur for a variety of reasons.
If any, or two, or all of the above factors are present the patient is at risk of VTE.
The thrombus becomes an embolus when it detaches and occludes a smaller vessel elsewhere, sometimes in the lung (PE). This prevents gaseous exchange, impeding the lung tissue’s blood supply which can cause chest pain, syncope, hypoxia, haemoptysis and shortness of breath. It is therefore important to monitory respiratory rate for tachpnea, tachycardia, and hypotension as PEs can be fatal.
Post-thrombotic syndrome (PTS) is cuased when a DVT causes long-term damage to venous values, this causes venous stasis which in turn increases the likelihood of developing a further DVT, causes erythema and swelling to the affected limb, discomfort, and sometimes venous leg ulcers. A third of DVT patients develop PTS.
On admission to hospital, all patients should be screened for their risk of developing TE and their care planned accordingly. This may involve anti-embolism stockings. Subcutaneous heparin, intermittent pneumatic compression (IPC), mobilisation as soon as possible or hydration.
Pharmacological prophylazis may involve low molecular weight heparin (LMMWH) fondaparinaz sodium, or if the patient has renal failure unfractionated heparin. Prophylaxis should begin as soon as possible and continue until the patient is no longer at the increased risk of VTE. As with all pharmacological thromboprophylaxis, the patient should be monitored for signs of bleeding/bruising. This needs to be documented and reported.