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Cardiology System. Part IV| Acute arterial occlusion of the lower limbs and its effects on driving.

Arterial obstruction is acute in 95% of cases, and is the peripheral manifestation of a pre-existing systemic disease caused by atherosclerosis, cardiopathy or diabetes.

Pain is the main symptoms, and the sudden onset of arterial occlusion and seriousness of the resulting ischemia determine the characteristics of the pain.

Embolisms can be of cardiac origin, in an arterial aneurysm, non-aneurysmatic aterosclerotic lesions, etc.

Thrombosis associated with aterosclerotic or aneurysmatic obstruction, desiccant aneurysm, arteritis, cystic disease of the popliteal artery, trapped popliteal artery, compartimental syndrome, haematological disease with hypercoagulability, tumours and certain drugs such as ergotamine, barbiturates, heroin, etc.

In excess of 75% of acute arterial obstructions of the lower limbs presenting at the accident and emergency department are found between the terminal aorta and popliteal space. Twenty per cent of these present multiple embolisms.

Symptoms.

Characteristic symptoms are pain, pallor, paralysis, parenthesis and low temperature with an absence of pulses.

The later pain is more distal and caused ischemia in the affected areas, especially in muscle mass. If the ischemia persists, it will eventually evolve into a thrombosis of the venal system.

The peripheral nerves are those most sensitive to the ischemia, which is why the condition leads to diminished or absence of distal surface sensitivity.

When there is paralysis, anaesthesia and muscle rigidity, this indicates the onset of necrosis, which will develop into gangrene within a matter of a few hours.

En cases of acute thrombosis, there is usually a history of intermittent claudation. Highly developed collateral circulation can mean the degree of ischemia and pain can be mild, as the obstruction there are other routes around the obstruction.

Treatment.

An emergency arterial embolectomy of the affected limb can prevent the expected development of the process.

When the episode is of thrombotic origin, the extent of the damage and the quality of the arteries must be quickly ascertained to be able to programme reconstructive surgery or the thromboendarterectomy.

In patients with very severe or prolonged ischemia, oedema is produced by the revascularisation, which perpetuates the ischemia because of the added compartimental syndrome, and requires, in many instances, a fasciotomy.

The myoglobin liberated by the lysis of the muscle reaches the kidney, in some cases leading to acute renal failure, a risk that increases with revascularisation.

When gangrene develops, the affected part of the limb will require amputation according to the location of the ischemia.

Differential diagnosis of deep vein thrombosis (DVT).

In the first stage of the DVT, superficial venous distension is observed, along with cyanosis, distal pulse and increased volume of the affected limb.

Massive deep vein thrombosis develops into phlegmasia cerulea dolens because of the progressive ischemia secondary to the increase in venal pressure, with serious oedema, associated arterial spasm and thrombosis of the distal bed. Half of these cases evolve into necrosis.

These episodes require heparin therapy, fibrinolytics and in certain cases the performance of a thrombectomy and fasciotomy to try and vascularise the limb.

Patients with intermittent claudation that does not interfere with driving should be warned that if any new symptoms appear that affect the limbs, such as pain, cold, pallor, paresthesia or difficulties with moving, they should not drive and should immediately be examined by a doctor to rule out the possibility of acute thrombosis.

If the diagnosis of acute arterial obstruction is confirmed, the patient must not drive until the limb has recovered from the ischemic episode without sequelae, and muscular function is adequate to satisfy the demands of driving.

A specialist will inform the patient about his recovery, and at what time he is capable of driving again.

An anticoagulated patient should be warned of the increased risk of suffering haemorrhages even in the case of a small collision, and should be told to drive with extreme caution.

Although the patient may feel completely better, he must not drive if there is a risk he will suffer a further ischemic episode, for example when an emboligenic focus persists.

Once the source of the embolism has been eliminated, the patient will be able to drive if the medical report permits it.

Multiple embolisms mean the focus of origin must be located to indicate the best possible treatment, associated in some cases with an embolectomy.

Haematological diseases with hypercoagulation should be treated and driving is not advised while the risk of thrombosis remains. The haematologist will report when the patient is correctly controlled and may drive.

The medications related to episodes of thrombosis will be withdrawn or changed for others without these risks.

Gangrene means the affected part of the body will need to be amputated.

Common post-operative care of all amputations is designed to provide a resting period for the tissues through the use of ferula, compression of injured tissues, exercise and postural changes to prevent contractures; in addition to rehabilitation to finally fit a prosthesis that is compatible with the needs and abilities of the patient, including driving.

A person who has a lower limb amputated will require a prolonged period of adaptation, which will involve learning to walk with crutches until he may safely walk with a permanent prosthesis.

Driving is an activity that will come after this process, and will require the appropriate adaptations to be made to the vehicle.

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