ENFERMEDAD DE BUERGER FISIOPATOLOGIA PDF

Tromboangeitis obliterante (Buerger). ➢ Otras Vasculitis cicatrice con el tratamiento médico habitual. El 59% de pacientes con enfermedad coronaria. El concepto “tiempo es cerebro” expresa que el tratamiento del ictus debe ser enfermedad o la esperanza en que los síntomas se resuelvan de forma Blaser T, Hofmann K, Buerger T, Effenberger O, Wallesch C, Goertler M: Risk of. Conocer, igualmente, las enfermedades linfáticas que afectan las extremidades, los factores que las condicionan, su clínica, complicaciones y tratamiento. 6.

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It is the sudden blockage of an artery by material formed in a remote location and has migrated through the bloodstream to enfermedqd occlusion occurs. It is the most common cause of acute ischemia. The proportion of arterial embolization is 2: The average age is between 70 and 80 years. The arterial embolus is usually a result of heart disease, proximal arterial injury or a complication of a cardiac or vascular surgical procedure.

Presently they are usually located at the bifurcations. If we exclude the brain strokes, the distribution would be:. Four phenomena can occur in a sequential embolism: 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 sudden interruption of irrigation in an area will impact clinically depending on the balance between supply and demand of blood, sensitivity of these burger 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.

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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.

Finally, the muscle freezes and becomes necrotic. It is at this moment when the skin also usually presents irreversible damage.

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 buergre and its intensity is related to the degree of collateral flow and time of evolution.

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.

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The end result is a restoration process of spontaneous pulse and no ischemia. Residual symptoms are intermittent claudication, ischemic neuropathy severe Wolkmann contracture, and pain and coldness changes skin with areas of superficial skin gangrene.

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. Patient’s death can occur within fiiopatologia hours with a result of visceral embolism or heart failure. 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. 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: This also allows us to detect the level of arterial obstruction by the embolus.

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. 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. 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.

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

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To achieve this it is necessary the immediate administration of a bolus dose intravenous heparin anticoagulant Na 1 mgr per kg body weight. 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.

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.

It is necessary to protect the ischemic limb of decubitus ulcers, especially in heel and malleoli. Until the embolism is settled definitively analgesics should be administered to mitigate the discomfort of patients. 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.

Vasculitis – Síntomas y causas – Mayo Clinic

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.

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: Our channel of videos released on Youtube.

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Presentaciones Vascular | Residentes de Cirugía, Universidad de Chile | Hospital del Salvador

Photo shows in our Issuu channel. Keep updated with our new RSS feed news. Skip to content Home About us Embolia 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. Preguntas y Respuestas al Doctor 3. El tratamiento que le han indicado el el protocolo correcto. En junio otra tvp en el mismo sitio,en noviembre despues de resonancias y eco el diagnostico de la Fosiopatologia.

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