Venous thromboembolism (VTE) refers to thrombotic and embolic disease of the venous system. In terms of anaesthetic and clinical practice, the key forms are:
Deep vein thrombosis (DVT)
Pulmonary embolism (PE)
These conditions are closely linked, but with the primary focus of these notes being on DVT. PE is discussed elsewhere.
DVT refers to a clot (thrombus) within the deep veins of the legs and/or pelvis. As well as causing potential problems in themselves, their risk of breaking off and travelling to the lungs (embolism) makes them of particular concern.
The term deep vein is important to distinguish from superficial veins, in whom thrombosis is considered a different clinical entity. The deep veins are the larger, valved veins that run between muscle and are so are acted on by the muscular pump to return blood centrally.
Distal DVT - refers to thrombosis of the veins of the calf Proximal DVT - refers to thrombosis including the popliteal vein and higher
Essentially this is a case of clot development when it shouldn’t occur. When we understand the physiology of haemostasis, we can see that this is likely due to a disturbance in the balance between pro and anti-coagulant factors.
As such, the pathophysiology of VTE is classically described in relation to Virchow’s triad:
These are the 3 factors that highlight how this imbalance occurs.
Stasis refers to the impact that venous blood stasis has on thrombus development. Whilst on its own it does not seem to be sufficient to allow thrombus formation, when combined with the other components of the triad it makes a significant contribution. In DVTs this stasis often refers to a notably reduced blood flow around the valves of the deep veins. The pathophysiology is thought to reflect a degree of hypoxia that occurs locally here, and which may result in downregulation of some of the protective endogenous anticoagulant factors.
Hypercoagulative states are fairly self-explanatory as to how they contribute to VTE development. There exist many conditions where there is an imbalance of the procoagulants and anticoagulants at a more systemic level. This trend towards the procoagulant state makes a clot more likely to form in any given scenario.
Trauma causes disruption of the endothelium that usually has a strong antithrombotic effect, as well as separating the blood from the powerfully prothrombotic factors found outside. Conditions that can result in endothelial trauma include smoking and venous instrumentation e.g. cannulas.
Can be broken down into risk groups: Patient Factors:
Family history of VTE
Increased age (>60 years)
High BMI (>30)
Trauma to vein e.g. cannulation
Drugs: oestrogens, chemotherapy
The site for DVTs is most commonly in the legs. It’s annual incidence is thought to be around 1 in 1000 people.
The presentation can be very varied, from asymptomatic to very symptomatic - this contributes to the frequent difficulty in diagnosis. Symptoms and signs are generally arising as a result of the obstruction to venous flow that the thrombosis causes. ‘Classic’ symptoms include:
Skin discoloration (erythema, cyanosis)
These will generally be unilateral, in the thrombosed leg, but propagation up to the iliac vessels and across to the contralateral side can occur.
‘Classic’ signs include:
Measurable leg swelling (difference in calf circumference)
Tenderness on palpation of deep venous system
Superficial venous distension
Palpable cord (hardened and thickened vein)
Secondary infection (e.g. overlying cellulitis) can further complicate the clinical picture. Initial presenting symptoms may be vague and mild e.g. cramping.
Some of these may coexist
Ruptured Baker’s cysts
Generalised oedema (if bilateral)
The gold standard tool for diagnosis (contrast venography) has significant practical limitations, and as such is rarely used in clinical practice. Other investigations have a different set of limitations that prevent them simply being used in every possible case of DVT. The assessment process therefore involved a combination of clinical risk assessment alongside additional investigations to create an overall risk analysis.
This can perhaps be best thought of as a step wise decision tree, obviously occurring after full history and examination. This first step of clinical risk assessment is usually done using a validated tool. This is because of the great difficulty with diagnosing DVT on clinical grounds, although experience clinicians may be able to categorise the patient into an appropriate risk group via gestalt. It is important to be aware that some tools are primarily designed for specific populations e.g. the Well’s score for outpatient or A&E patients rather than inpatients. As such, if there is strong clinical grounds for believing a DVT is present, imaging should be undertaken.
This score allocates a numerical value to some key clinical findings (and a negative score to allow for clinical impression of a likely alternative diagnosis).
There are different ways of using this. One example is described here.
If the score is 0, then the risk of DVT is low (around 5%). Combination of this with a negative D-Dimer test rules out DVT to a high degree of confidence (<1%).
If the score is 1 or 2, the risk category is moderate. If combined with a negative high sensitivity D-Dimer, then the risk can also be said to be very low (<1%).
If the D-Dimer is positive in either of these cases, they should proceed to ultrasound (US) imaging.
If the score is 3 or higher then the risk category is high (17-53% likelihood) This means that US imaging is needed for assessment. A D-dimer may still be take, as the result may help with further assessment in the case of diagnostic uncertainty (i.e. a negative US)
This is a blood test which measures the breakdown products of clots. As such, it is a sensitive but non-specific test when testing for VTE (i.e. a negative result tells you more information that a positive one). The use of a D-Dimer should be considered in the context of the clinical picture and risk score, as described above. Patients with a likely DVT and a positive D-dimer should be considered at high risk for actually having a DVT, and even in the context of a negative US scan, this scan should generally be repeated after a week in these patients.
Duplex ultrasound is generally the first line imaging of choice. It has a high degree of sensitivity (98.7%) and specificity (100%) for above knee DVTs, although the sensitivity drops to 85.2% for below knee DVTs. It is also non-invasive and with no ionising radiation. The quality of the images obtained, and the protocol used may impact on the sensitivity and specificity.
Other imaging modalities can include:
Combining the above approach allows guidance on further management.
Wells’ score 0 + negative D-Dimer = No further imaging needed Wells’ score 0 + positive D-Dimer + negative US = DVT ruled out
Wells score 1-2 + negative HS D-Dimer = No further imaging needed Wells score 1-2 + positive HS D-Dimer + negative US = DVT ruled out
Wells’ score 3 + negative US + negative D-Dimer = DVT ruled out Wells’ score 3 + negative US + positive D-Dimer = DVT not fully ruled out (repeat US within 1 week)
Any positive US = Highly likely DVT
In cases where high sensitivity D-Dimer is not available, NICE describe separation into likely and unlikely groups. A Wells’ score of 0 or 1 is unlikely. A Wells' score of 2 or more is likely.
DVT unlikely Perform a D dimer If negative, DVT is unlikely. If positive perform US.
DVT likely Perform an US (and usually D dimer) If negative, and D dimer negative, DVT unlikely. If negative and D-Dimer positive, repeat imaging should be performed.
If US imaging is not available within 4 hours, patients can commence treatment with LMWH and have the imaging within 24 hours.
In those patients without a clear trigger for a DVT, a cause should be investigated for. In older patients (over 40) this investigation will primarily investigate for malignancy:
In younger patients (under 40) the investigations will be directed at thrombophilia.
Patients with confirmed DVT require anticoagulation. Initially this is with LMWH or fondaparinux whilst a regular oral anticoagulant is commenced. Traditionally this has been warfarin, but there has been an increased used of the NOACs/DOACs in this role. The benefits of anticoagulation should obviously be balanced against the increased bleeding risk for the patient.
Treatment should be continued for at least 3 months, at which point the risk/benefit ratio should be reviewed. In cases of a clear trigger for the VTE being present, no further anticoagulation may be needed. In cases of ongoing risk, longer treatment durations may be needed.
In patients with active cancer, continued treatment with a LMWH for 6 months should be considered.
Unfractionated heparin should be considered in those patients with a higher bleeding risk. Temporary IVC filters may be considered in those patients in whom anticogulation is contraindicated.
Patients with isolated distal DVT can be challenging to manage. These patients are at a lower risk of PE, but the risk is of propagation to more proximal vessels, and then an increased risk of complications. About 25% will propagate, so ongoing management is required. Evidence is scanty, but one possible management approach:
Lower risk (minor symptoms, no risk factors for extension) - serial imaging of legs to assess for propagation
Higher risk (severe symptoms, risk factors for extension) - treat with anticoagulation
Risk factors for extension include:
Extensive thrombosis (length and proximity to proximal veins)
No reversible risk factors
History of VTE
Admitted to hospital
Catheter directed thrombolysis of the DVT has been described, but has an associated bleeding risk. It may be useful in those patients with an early (under 2 weeks) symptomatic iliofemoral DVT who have a low bleeding risk. The benefit is of a reduced risk of post thrombotic syndrome.
Post thrombotic syndrome
Post thrombotic syndrome occurs in about 50% of cases of DVT. It refers to a syndrome of venous hypertension in the leg following the thrombosis, due to damage to the vein and its valves.
Preventing VTE from developing in the first place is a very important step, and has become a key part of inpatient safety.
Patients should be advised on considering stopping oestrogen containing drugs (contraceptive pill or HRT) 4 weeks before elective surgery.
All patients should be risk assessed for VTE at admission to hospital. This includes an assessment of their thrombotic risk and their bleeding risk. NICE report that this can be done using any appropriate published tool, with the Department of Health VTE risk assessment tool being the most commonly used (available https://www.nice.org.uk/Guidance/NG89/resources). This identifies common risk factors for thrombosis, and if present should prompt consideration of pharmacological thromboprophylaxis.
This risk should be reassessed at 24 hours and whenever the clinical picture changes.
Intermittent pneumatic compression device
Pharmacological Low molecular heparin (LMWH) is generally the first line pharmacological agent. It’s use will be a balance of the thrombotic risks and bleeding risks which will be impacted on by patient and surgical factors.