Acute arteriosclerosis of the extremities

More than 80 years ago, the only treatment for acute anaemia in the extremities was amputation. Since 1911, after the first successful embolization of blood clots, there appeared to be many different treatment methods. The revolution in the treatment of acute anaemia in the limbs occurred after the introduction of heparin (1914), the technique of taking embolized blood clots using sond Fogarty (1963) and the technique of re-circulating blood vessels with emergency surgery.

This is an emergency internal - surgical vascular surgery, requiring prompt hospitalization, rapid diagnosis and emergency treatment. However, the current mortality rate is still about 20-25%, and the likelihood of the patient being discharged from the hospital with both legs intact is only about 70% of cases.

Called acute anaemia in the limbs when anaemia plays a prognostic role for the survival of the limbs if there is no emergency intervention for several hours (before 6 hours).

There are three main groups of causes that cause acute anaemia in the limbs, which are from embolism, acute thromboembolism and artery trauma.

Vascular embolism

An embolism is caused by a blood clot moving from elsewhere due to an embolism. The blood clot can be either alone or in combination with calcifications, atheroma or other septic organs, and the location of the clot originating either in the heart or in the artery.

Heart disease causes embolism

This is the most common cause of peripheral embolism (90% of cases). Common classical causes are:

Paroxysmal arrhythmia (atrial fibrillation is the leading cause).

The movement of blood clots in the left atrium is enlarged and stagnant (mitral valve disease, heart failure, left atrial disease).

Myocardial Infarction: Thrombosis in the heart wall, left ventricular aneurysm.

Valvular Causes: calcified thromboembolism in calcified aortic stenosis, infectious embolism in Osler's disease, and especially in the case of patients with an artificial heart valve.

Other rare causes: Ventricular aneurysm, non-obstructive cardiomyopathy, mitral valve prolapse, left atrial mucous tumour ...

Arterial disease causes embolism

10% of embolism cases. May be due to:

Ulcerative atheroma: These plaques are then overlaid by a blood clot, and the movement of the clot can cause an embolism. The most common is atherosclerosis from the aorta in the lower renal segment causing embolism in the lower extremities.

Aneurysms: The second most common cause of arterial embolism. The embolism comes from a thrombus that forms inside the bulge. Abdominal aortic aneurysm and aneurysms are the most common.

Other less common agents: Inflammatory aneurysms (Takayasu), inverse embolism from venous thrombosis, heparin-induced thrombocytopenia.

Acute thromboembolism

Acute occlusion of the artery atherosclerosis

This is the most common cause of thromboembolism. There are several different mechanisms for acute thromboembolism:

A thrombus forms on an ulcerated plaque and blocks the lumen of the artery.

The thrombus is organized and merged into the vessel wall, it is epithelialized and narrows the lumen. When there is a decrease in systemic blood flow, it often causes blockage of the lumen and is the most common mechanism.

A hematoma under the plaque is also a cause of embolism.

Thrombosis in aneurysms

Acute thromboembolism is the most common complication of an aneurysm of the limb of any cause. Thrombosis usually occurs after several episodes of embolism in the arteries of the leg (which often have no clinical manifestations) and it destroys the vascular bed downstream.

Other causes of acute thromboembolism

Non-atherosclerotic artery disease: Buerger's disease, Takayasu's disease, inflammatory periarticular nodular disease.

Aortic dissection of type I or III according to De Barkey.

Mechanical presses:

Artery syndrome does not escape.

Peripheral cysts of the artery.

Tumours adjacent to blood vessels (bone shoots in the limbs).

Haematological causes: Often favours the formation of blood clots, especially in the narrowed and pathological arteries.

Hypercoagulable states: Multiple red blood cells, thrombocytosis, scattered lupus erythematosus, cancer.

Congenital impairment of coagulation factors - haemostasis (antithrombine III, protein C, protein S, abnormality of the fibrinogen system, abnormal platelet aggregation).

Drug-induced agents: Progestifs, barbiturates injected into the artery, substances causing venous fibrosis, drugs ...).

Arterial injury

Arterial wounds, artery crashes, or physician-induced artery damage (catheter puncture) can all cause acute embolism.

In organizational compression injuries, prolonged garnet or burial (burial syndrome) can also cause acute embolism.

The reasons are not clear

Sometimes no cause is found. Acute embolism then poses a problem in treatment, especially to avoid relapse.

Pathophysiology

Factors that increase the decrease in blood flow below the embolism site.

Blood pressure: Shock or decreased arterial blood pressure may be the only decompensating factors in chronic obstructive artery disease. Maintains blood pressure to facilitate perfusion of collateral circulation.

Collective circulation: Compensates for the consequences of acute embolism in a few hours.

Lower arterial bed: Vary for each patient.

Pathophysiological consequences

Consequences in place

If anaemia is prolonged, it will cause cell necrosis. Lack of oxygen in the muscle will dilate capillaries, causing oedema of the interstitial organization and increasing interstitial pressure, hindering and stagnating venous circulation, increasing oedema; At the same time, due to anaerobic metabolism (capillary dilating acid metabolites), it creates a vicious pathology cycle.

Increased interstitial pressure (creating a chamber compression syndrome that interferes with capillary circulation).

Systemic consequences

Due to rhabdomyolysis, it increases enzymes in muscle structure, Potassium ... and causes many systemic complications:

 Volumetric shock (due to drainage to the extracellular matrix).

Metabolic disturbances (hyperkalaemia, metabolic acidosis, hyperuricemia, myoglobinuria, myoglobinuria, an increase in blood creatinine, hypercalcemia, hyperphosphatemia and sometimes causing sporadic thrombosis (CIVD).

Renal impairment: Mechanisms can be combined: Reduced flow (shock), myoglobin deposition in the renal tubules, direct toxicity to the renal tubules (acid environment).

 Bacterial infections: Often bacteria develop in necrotic muscle tissue, in muscle tissue after opening the corneal weight.

Diagnosis of acute anaemia in the extremities

Diagnosis is mainly based on clinical practice and must have an attitude of early and correct management.

Diagnosis is easy when in its typical form, symptoms include:

Pain.

Chi is pale.

Loss of pulse.

Reduction or loss of sensation.

Decreased movement or paralysis.

Chi cold.

Venous circulation is slow or absent, venous circulation is flat.

However, sometimes clinical is incomplete, but on physical examination and objective comparison we can see that cold limbs, peripheral vessels are lost.

Severe degrees of limb anaemia:

Level I: Anaemia causes incomplete sensory and motor impairment (arterial pressure at the distal end of the Doppler upper limb <40 mmHg).

Level II: Total loss of sensation and movement.

Level III: Muscle mass pain when touching, spasticity of muscle mass in the limbs due to anaemia.

Level IV: Skin lesions, limb necrosis.

Subclinical (vascular Doppler, echocardiography, angiography, hematological bilan) should be considered and should not delay treatment.

Diagnosis of the lesion

The site of embolism can be derived from the initial site of pain, from the site of vascular loss and the limitation of limb anaemia.

In clinical practice, acute lower limb embolism may experience:

Aortic-pelvic occlusion: Patient is in shock, cardiovascular collapse, anaemia of both lower extremities spreading to the navel, motor paralysis - early feeling of lower extremities (in about 1 hour), bilateral thigh vessels not palpable.

Thigh-crooked artery obstruction: Characterized by distant anaemia (lower legs, feet), still catchable thigh vessels, not captured atrophy.

Pelvic-thigh artery occlusion: Anaemia in the lower leg and can spread to the thigh, thigh vessels cannot catch.

Diagnose the cause

In the case of artery trauma: Usually easily diagnosed.

Out of the trauma context:

Diagnose embolism or thrombosis based on history, onset of illness, sudden onset of symptoms, limb physical examination and comparison.

Table: Distinguishing causes of embolism and acute arterial thrombosis.

The principles of treatment

Treat as soon as possible when identifying acute anaemia in the limbs. The main treatment steps include:

Avoid spreading the blood clot

Heparin anticoagulant therapy: Heparin is used as soon as the diagnosis is confirmed. Heparin 5,000 UI dose administered intravenously at the beginning of treatment, followed by a dose of about 500 UI / kg / day continuously infused via an electric pump and adjusted dose according to TCA.

Low molecular weight heparin is not indicated in this case.

Removing blood clot causing embolism

Mainly by surgery.

Remove the embolism with the sonde Fogarty.

Bridging blood vessels in case of acute thrombosis causes embolism on pathological arteries.

Using drugs to dissolve blood clots through arteries or in combination with techniques to remove blood clots.

Open the fascia when there is cavity compression.

Amputation of the limb when irreversible anaemia, or when vascular restorative therapy fails, or when there are life-threatening systemic disorders (reperfusion syndrome causes renal failure, disorder metabolism).

Pain relief

Can be used in combination with vasopressors.

Protect limbs with anaemia

Take care of the limb with anaemia until circulation is restored. Need to warm, avoid rubbing, avoid using tape on the anaemic skin.

Treatment of pathological processes that facilitate anaemia

Shock treatment reduces volume, reduces cardiac flow.

Preventing the consequences of acute anaemia

Mainly prevention of the metabolic consequences and reperfusion syndrome.

Treatment of metabolic acidosis (Bicarbonates)

Treatment of hyperkalaemia (Kayexalate, Glucagon, dialysis, limb wash).

Treatment of acute renal failure.

Redefine the cause

It is necessary to distinguish 4 groups.

An embolism on a healthy artery.

Thrombosis on the pathological artery.

Thrombosis on a healthy artery.

Emboli on the pathological artery.