Venous
thrombosis
2. Diminished rate of blood flow in the veins. In modern medical
practice this occurs during and after operations, and in debilitating conditions
such as strokes and myocardial infarction.
Much more is now understood about the
clotting cascade that results in the deposition of thrombus, as well as the
fibrinolytic system that removes thrombus. Congenital deficiencies in either of
these systems may result in increased susceptibility to thrombosis in that
individual (Table 16.2).
Severe deficiencies of antithrombin III, protein C or
protein S lead to severe or fatal episodes of venous thrombosis at an
Spontaneous
venous thrombosis may occur following injury to the leg such as a severely
sprained ankle, as the consequence of an infection or following a period of
immobility. Long-haul air travel is recognised as the cause for venous
thrombosis in a number of people who are obliged to spend long periods in
conditions permitting little movement of the legs. Long car journeys may also
cause venous thrombosis in the lower limbs in susceptible individuals. In a
proportion of patients an underlying malignancy appears to be the precipitating
factor. In a patient who develops venous thrombosis in the absence of any
identifiable cause clinical examination and special investigations should be
arranged to detect common malignancies (leg, lung, stomach, large bowel).
Patients
receiving treatment in hospital are at increased risk of venous thrombosis. This
includes patients being treated surgically or for medical conditions. The
factors which result in increased risk of venous thrombosis include advancing
age and greater complexity of surgical treatment. Orthopaedic operations on the
lower limbs (hip and knee replacements) are especially likely to result in
venous thrombosis. The risk of venous thrombosis associated with particular
surgical procedures is summarised in Table
16.3. However, medical patients are
also at risk, particularly those being treated for strokes and other
neurological conditions. Any patient with myocardial infarction or any serious
illness runs the risk of venous thrombosis of the lower limb. Should this
thrombus detach and become a pulmonary embolism, the result may be fatal. A
large number of medical conditions, in addition to those mentioned above, may
lead to venous thrombosis. These are listed in Table
16.4.
Prevention
of deep vein thrombosis
All patients admitted to hospital or being treated for a serious illness
should be assessed for the risk of deep vein thrombosis. These patients may he
considered at low risk, moderate risk or high risk:
• moderate risk — patients over the age of 40 years with
debilitating illnesses, undergoing major surgery but no additional risk factors;
• high risk — patients over the age of 40 years with serious medical
conditions, such as stroke and myocardial infarction, and undergoing major
surgery with additional risk factor, such as a past history of venous
thromboembolism, extensive malignant disease or obesity.
Pharmacological
methods evaluated include: low-dose heparin, low-molecular-weight heparin,
dextran and adjusted dose warfarin. There is now good scientific evidence that
low-dose heparin is effective in reducing the incidence of deep vein thrombosis
and pulmonary embolism. Most studies suggest that the use of 5000 units of
heparin, given subcutaneously two or three times a day, is effective. This
should be continued for at least 5 days. The risk of developing a deep
vein thrombosis following hospital discharge has now been recognised, and deep
vein thrombosis prophylaxis probably ought to be extended into the postdischarge
period. Low-molecular-weight heparin is effective in reducing the incidence of
deep vein thrombosis. It has been shown to be more effective than low-dose
heparin in orthopaedic patients and as effective in patients undergoing general
surgical procedures. The advantages of low-molecular-weight heparin over
standard heparin include once a day administration and a lower risk of bleeding
complications, making it more suitable for out of hospital use.
Pulmonary
embolism
Pulmonary embolism is a potentially fatal complication of lower limb
deep vein thrombosis. A clot from the lower limb veins becomes detached from its
site of formation and passes via the inferior vena cava and right heart to the
pulmonary arteries. Here it may totally occlude the perfusion to part or all of
one or both lungs. This leads to collapse or sudden death in some patients and
is a medical emergency. Treatment includes full, immediate anticoagulation with
intravenous heparin combined with standard methods of resuscitation. Large emboli
may be treated by infusion of fibrinolytic drugs into the pulmonary
arteries via catheters inserted via arm or leg veins.
Diagnosis
of deep vein thrombosis
The symptoms and clinical features of a lower limb deep vein thrombosis
are listed in Table 16.5. The most significant findings are tenderness in
the calf and oedema at the ankle. However, these may also be attributable to
other conditions. Pain in the calf on dorsiflexion of the ankle (Homan’s sign)
has been described in many textbooks. However, this is a very misleading
clinical sign and provides no useful information about the presence or
otherwise of a lower limb venous thrombosis. It should no longer be used. Some
patients with deep vein thrombosis of the lower limb may have no symptoms in the
leg, but present with severe dyspnoea due to pulmonary embolism.
Treatment
of deep vein thrombosis
In treating an established deep vein thrombosis it is important to make
the correct diagnosis. Twenty per cent of patients with clinical signs and
symptoms of a deep vein thrombosis have normal deep veins. The differential
diagnosis includes ruptured Baker’s cyst, superficial thrombophlebitis, calf
muscle haematomas and a ruptured plantaris tendon. All of these diagnoses can be
demonstrated on ultrasonography, which has the advantage of allowing the
examination of the soft tissues, something which venography is unable to do.
Having
made the diagnosis of a deep vein thrombosis and confirmed it by duplex
ultrasound imaging or venography, treatment should be instituted. Standard
treatment involves intravenous heparin with the dose adjusted according to the
weight of the patient and controlled by the activated partial thromboplastin
time (APTT). The duration of heparin treatment should be at least 5 days.
The aim is to minimise the risk of pulmonary embolism and encourage the thrombus
to resolve. At the same time, the patient should be commenced on warfarin. The
aim here is to reduce the risk of a further recurrence of venous thrombosis.
Warfarin does not remove the clot from blocked veins and the duration of
treatment (usually 3—6 months) is selected to prevent further episodes of
venous thrombosis. Warfarin dosage is controlled by measuring the
international normalised ratio (INR) by regular blood tests. The INR should be
prolonged to between 2.5 and 3.5 times the control value. Patients
with recurrent venous thromboembolic problems should be anticoagulated for life.
The
use of subcutaneous injections of low-molecular-weight heparin for the treatment
of deep vein thrombosis is an alternative method of anticoagulation. The dose is
based on the patient’s weight and treatment given without blood tests to
control the dose. This has been found to produce reliable anticoagulation
without the risk of haemorrhage. This may in future become a very convenient way
to manage patients with acute deep vein thrombosis, either in hospital or at
home. Warfarin treatment is commenced at the same time and controlled using the
INR in the same way as for the intravenous heparin regime.
Venous
thrombectomy
In some patients the risk of pulmonary embolism is very great, e.g. a
large venous thrombosis in the lower limb where anticoagulation is
contraindicated (e.g. following a haemorrhagic stroke). In others, pulmonary
embolism occurs despite full anticoagulation with warfarin. Pulmonary embolism
may be prevented by the insertion of an inferior vena cava filter which traps
large thrombi in its wires and prevents them from occluding the pulmonary
arteries. These filters are usually placed by a radiologist via the femoral or
jugular vein under X-ray control without the need for an open surgical procedure
(Fig. 16.35).
Superficial
vein thrombosis
Venous thrombosis (thrombophlebitis) often occurs in superficial veins.
This is a frequent complication of varicose veins and may follow cannulation of
a vein for an intravenous infusion. Spontaneous superficial thrombophlebitis
may occur in the presence of polycythaemia, polyarthritis and Buerger’s
disease and may also herald the
Axillary
vein thrombosis