Clinica Vascular Zurbano, Varices, Tratamientos Laser, Masaje Linfatico, Cirugia Vascular, Tratamiento del Linfedema, Tratamiento Aneurisma

It is the sudden blockage of an artery by material formed in a remote location and has migrated through the bloodstream to where occlusion occurs. It is the most common cause of acute ischemia.

DEFINITION

It is the sudden blockage of an artery by material formed in a remote location and has migrated through the bloodstream to where occlusion occurs. It is the most common cause of acute ischemia.

The proportion of arterial embolization is 2:1 in favor of females. The average age is between 70 and 80 years.

ETIOLOGY

The arterial embolus is usually a result of heart disease, proximal arterial injury or a complication of a cardiac or vascular surgical procedure.

- The most common source of the embolus is in the left heart and produced by: rheumatic valve disease (15-30%), myocardial infarction and its sequels (10%) and myocardium sclerosis associated with abnormal heart rhythm (atrial fibrillation - 70 -- 85%). Less often involve vascular tumors (myxomas), endocarditis, cardiac surgery (3-6% of ACVA postoperative embolic origin) ... etc. In general, 50-60% of patients who suffer a stroke was or had been the previous days in atrial fibrillation.

- The existence of arterial aneurysms (aorta, subclavian, popliteal ...) or extensive athermanous plaques leads to the formation of organized thrombi that may occasionally embole distally.

- Other sources of emboli are rare so-called "paradoxical" venous thrombosis secondary to migrate to a heart with abnormal communication between right and left chambers,  also, it is rare stroke of foreign bodies (bullets, fragments of catheters, prostheses ...) , hydatid, tumor cells, ... etc..

- In 2-3% of the emboli an apparent cause of the embolism can be found.

LOCATION

The most common destination of emboli is the brain (60%), lower limbs (30%), upper limbs (6%) and visceral arteries (4%). Presently they are usually located at the bifurcations. If we exclude the brain strokes, the distribution would be:

- Upper Extremity 14%

- Visceral 7%

- Aortoiliac 22%

- Femoral 36%

- Popliteal 15%

- Other 6%

In 10% of the cases, strokes are multiple and 15% of patients are re-embolized.

PATHOPHYSIOLOGY

Four phenomena can occur in a sequential embolism: mechanical arterial occlusion, vasospasm distal side branches, secondary thrombosis and morphologic alterations of the arterial wall.

The ischemic territory will be greater the larger the occluded arterial segment, but the more proximal occlusion is the greater the chances of compensation for collateral arterial circulation.

Reflex arterial spasm secondary to stroke affects not only the occluded vessel but the proximal side.

The post-embolic blood stasis is followed by a secondary thrombosis; it can affect the entire arterial tree distal microcirculatory level and, thus worsening prognosis (there is a clear relationship between the thrombus extension and development of gangrene secondary). The secondary thrombus develops in contiguity of the impact zone of the embolus in 63% of the time and distance or discontinuously by 37%.

The presence of a thrombus secondary  embolus and trigger a cascade of inflammatory mechanisms at the arterial wall: polyarthritis with infiltration of inflammatory cells, decreased microcirculation, red cell entrapment, thrombosis of the vasa vasorum, the average edema and hemorrhage intramural arterial wall.

The blood stasis can trigger venous thrombosis up to 25% of the cases.

The sudden interruption of irrigation in an area will impact clinically depending on the balance between supply and demand of blood, sensitivity of these tissues against hypoxia and local changes and the triggering cell.

The peripheral nerves are most sensitive to hypoxia and after 6 hours irreversible damage may occur.

The skin and subcutaneous tissue are very resistant to ischemia and irreversible damage may occur at times only after several days of evolution. (Mottled skin, bullae and necrosis).

Muscle tolerance to ischemia is due to their low metabolic rate at rest, their glycogen stores and its initial capacity of anaerobic glycolysis. The persistence of ischemia produces mystical destruction and release of CPK, LDH, SGOT, K, free radicals and myoglobin in the urine. Finally, the muscle freezes and becomes necrotic. It is at this moment when the skin also usually presents irreversible damage.

CLINIC

The classic presentation is a picture of acute onset of pain, pallor, coldness, numbness and paralysis.

The nature and character of pain is variable. The initial pain appears to be due to the impact of the plunger on the arterial wall and its sudden strain, while the delayed pain is caused by ischemia and muscle tissue.

Paresthesia, paralysis, pallor and coldness are subsequent to pain and its intensity is related to the degree of collateral flow and time of evolution.

DEGREES OF ISCHEMIA OF ORIGIN EMBOLISM

1. - Moderate ischemia with atypical course. After the initial hours the pain is mitigated, the color and temperature return to normal, functional impotence disappears and pulses can be normalized. These cases appear to be due to a partial embolic occlusion strong initial vasospasm and absence of secondary thrombosis, or a small embolus in areas with important pathways of collateral circulation. The end result is a restoration process of spontaneous pulse and no ischemia.

2. - Advanced Ischemia with risk of gangrene and incomplete recovery from ischemia. Residual symptoms are intermittent claudication, ischemic neuropathy severe Wolkmann contracture, and pain and coldness changes skin with areas of superficial skin gangrene.

3. - Severe ischemia, which is the most common type. Its evolution is towards the emergence of gangrene a few days of onset of symptoms. The multiple embolizations, the extension of secondary thrombosis and poor general condition (heart disease) are factors that negatively influence the development of stroke.

4. - Very severe ischemia resulting from arterial occlusion with great impact and affected ischemic tissue and neurological early. Patient's death can occur within 24 hours with a result of visceral embolism or heart failure.

EXPLORATION

On inspection we will appreciate paleness and bloodless distal venous layer.

On palpation cold is felt, dry skin and lack of sweating. The pressure on fingers and muscle mass can be painful. The "princeps" signs are the absence of pulses immediately below the location of the embolus, occasionally also above if secondary thrombus has spread proximally.

If we try to mobilize the patient's limb we can appreciate the existence of muscle paralysis (loss of function) with inability to move the distal tip and reflexes have also been reduced. The duration and intensity of the latter are important prognostic factors.

FURTHER EXPLORATIONS

The ECG may show signs of recent or older myocardial infarction, atrial fibrillation, and auricle-ventricular heart failure.

The chest X-ray may not discover any findings, though often an increase in cardiac silhouette with occasional spills lungs. In cases where embolism originating from a thoracic aortic aneurysm or abdominal calcifications and we can see bulges in the wall of this vessel in simple Rx of the chest or abdomen. These findings must be confirmed by TACs.

The blood tests are not significant, only in big strokes and very late leukocytosis can occur, acidosis and elevated discrete CPK, LDH and K.

The AngioTAC, The angioRNM or arteriography may be useful techniques to confirm the stroke, its location and its extension or establish a differential diagnosis with other diseases such as acute arterial thrombosis. There is no pathognomonic sign of stroke in these imaging techniques; however, a healthy artery tree with a sudden interruption of blood flow by an image of rounded outline and with little collateral circulation may arouse suspicion of distal embolism.

Doppler echocardiography as a complementary technique allows us to confirm or rule out possible cardiac etiologies: mitral stenosis, atrial thrombi, ventricular aneurysms, post-infarction, dyskinesia in the heart wall, and subclavian aneurysm, abdominal aorta, iliac, popliteal, ... etc. This also allows us to detect the level of arterial obstruction by the embolus.

DIFFERENTIAL DIAGNOSIS

Acute arterial thrombosis. Clinically very similar to a stroke, but patients with this condition often have a history of intermittent claudication, not associated with heart rhythm disturbances in the contralateral limb often lacking a pulse and vascular imaging techniques draw attention to signs of atheroma chronic.

Aortic dissection. It sometimes debuts as an acute ischemia of a limb, but is part of a picture of hypertensive crisis and chest pain or back pain. Occasionally a murmur is heard of aortic insufficiency or pulse difference can be seen between the upper extremities, diagnosed by angiography, angioRNM, AngioTAC or transesophageal echocardiography.

Fegmasia cerulea dolens. It is produced by massive iliofemoral vein thrombosis. It is characterized by marked cyanosis to the root of the limb, present or somewhat diminished pulses, edema of the entire limb pitting on palpation and no loss of function of the foot.

Syndrome under flow. It is caused by hypovolemia and low cardiac output. Sepsis, myocardial infarction, pulmonary embolism, dehydration or acute abdomen can trigger them.

Neurological disorders. We must make the differential diagnosis and pathology term-aortic embolism compression at the lumbar level as both charts display symptoms of sudden onset of weakness and loss of sensation in both limbs.

PRE-SURGERY TREATMENT

It must have a multipronged approach:

- Protection of the distal arterial layer versus secondary thrombosis. To achieve this it is necessary the immediate administration of a bolus dose intravenous heparin anticoagulant Na (1 mgr per kg body weight).

- Protection and visceral muscle. In cases of severe ischemia it may be beneficial the administration of hypertonic solutions of MANITOL for it appears to decrease the cell swelling and promote osmotic diuresis (diuresis and alkalinization of urine may prevent renal complications arising from myoglobinuria).

- Protection heart. The cell membrane integrity is altered by ischemia and release of potassium occurs. It should be corrected by volume replacement, insulin and glucose and, in exceptional cases, it is necessary the administration of calcium ion resin-or dialysis. Lactic acid production can also alter cardiac function and is necessary the administration of bicarbonate to correct acidosis.

- Skin protection. It is necessary to protect the ischemic limb of decubitus ulcers, especially in heel and malleoli.

- Protection of pain. Until the embolism is settled definitively analgesics should be administered to mitigate the discomfort of patients.

SURGICAL TREATMENT

The treatment of choice is surgical embolectomy. Whenever possible it should be done under local anesthesia or loco-regional. Be monitored electrocardiographically to the patient, he will be given oxygen through nasal cannula and venous forearm catch. If necessary sedative medication is added.

The embolectomy involves inserting, through an artery, a catheter with an inflatable balloon at the tip. You must enter the catheter traversing the thrombus secondary embolus at all its length, then the balloon is inflated and the catheter is dragged along with the clot.

EVOLUCION POST-QUIRURGICA

The, embolectomy resolves the acute ischemia but not its cause. It is important therefore to maintain anticoagulation in the post-surgical period because re-embolization possibilities are: with anticoagulation 10%and without anticoagulation 30% only in the first month after surgery.

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