Acute arterial embolism without collateral circulation compensation will result in acute limb ischemic signs: Pulselessness, Pain, Pallor, Paresthesia and Paralysis, the “5 P’s”. The “5P” signs. The appearance of these phenomena and their degree are related to the degree of ischemia.
Weakness or loss of arterial pulsation:
Occurs in the artery distal to the embolized arterial segment. Sometimes a conductive pulsation may be palpable in the artery distal to the embolization due to the impact of the blood flow. If embolization is incomplete, a weakened distal arterial beat may be palpable. In addition, arterial embolization will cause pressure pain in the affected artery, which usually occurs proximal to the ischemic changes in the limb. Using an ultrasound Doppler stethoscope or flow recorder, the inability to hear normal arterial sounds or the absence of arterial waveforms is a more reliable method of examination.
Pain :
After an arterial embolism, most patients have acute onset of severe pain in the limb. The pain starts at the embolization site and gradually extends to the distal limb of the embolization. The site of pain may be displaced, with severe abdominal pain when the dislodged embolus rides across the bifurcation of the abdominal aorta, or femoral pain when the embolus is flushed by blood flow to the femoral artery. The affected limb is painful to the touch, and active or passive movement of the limb can cause pain, thus putting it in a braked state.
Pallor and decreased skin temperature:
The skin is waxy and pale due to impaired blood supply distal to the embolized artery. If there is still a small amount of blood in the subcutaneous venous plexus, there are bruises of varying sizes on the pale skin base. The superficial veins are deflated due to reduced blood flow. Skin temperature changes are related to the site of arterial embolism. When the bifurcated segment of the abdominal aorta is embolized, the skin temperature of the buttocks and bilateral lower extremities decreases; when the iliac artery is embolized, the skin temperature of the ipsilateral thigh decreases, while that of the common femoral artery decreases below the mid-thigh in embolism; when the N artery is embolized, the skin temperature of the mid-calf and its distal side decreases. In embolism of the subclavian and axillary arteries, the symptoms involve the entire upper extremity; in embolism of the brachial artery, the symptoms involve the forearm; in embolism of a single branch of the ulnar radial artery or the anterior and posterior tibial arteries, the symptoms are limited and mild because of the abundant collateral circulation.
Skin temperature changes can be detected in several ways as follows.
1.The examiner touches the affected limb with the dorsal side of the middle knuckle of the middle index finger and moves it from the proximal to the distal side, and can perceive the plane where the skin temperature of the affected limb decreases.
2.Comparing the skin temperature of the same plane of both limbs by the same method, the skin temperature of the affected limb can be found to be lower than that of the non-embolized limb.
3.Use the skin thermometer to compare the measurement of bilateral limbs, the degree and plane of skin temperature decrease can be measured.
Sensory and motor impairment.
When there is already ischemic damage to peripheral nerves, the distal limb can have a skin sensory loss area, and its proximal end has a hyperalgesia area and a skin sensory sensitivity area. When the embolism is long, there is ischemic necrosis of peripheral nerve damage and muscle tissue, it can cause symptoms such as finger and toe movement disorder, hand and foot prolapse.
The examiner can detect the skin sensory disorder of the affected limb by touching the skin of the affected limb with the hand or by the simple method of needling. Passive movement of the fingers or toes of the affected limb can clarify the presence or absence of deep sensory loss.
Tissue necrosis.
Once an arterial embolism is of long duration, irreversible tissue ischemic necrosis will eventually occur. In addition to the dry necrosis of the fingers or toes caused by the embolism of the terminal artery, when the main artery is blocked, the tissue necrosis is widespread, the limb is cold, dark purple in color and reticular bruising; the skin is blistered and contains bloody exudate; the tissue is thickened and hardened. At this time, there are obvious systemic symptoms: depression, high fever, chills, accelerated heart rate, and even lower blood pressure and other toxic symptoms.
Once the main artery is completely blocked, the distal tissues are in acute ischemic state, and there is no sufficient side branch compensation. Therefore, if left untreated, the survival of the limb is bound to be endangered.
Non-surgical treatment.
Non-surgical treatment is an effective adjunct to surgical treatment. It is mainly applied to small arterial embolism, such as embolism of the distal ulnar or radial artery in the upper extremity, and embolism of the distal tibial and peroneal trunk arteries in the lower extremity, which usually have better side branches to maintain blood supply. For the systemic condition is serious, or has been in a dying state, not emphasized text may endure surgery, or the affected limb has appeared obvious signs of tissue necrosis, surgery has been impossible to save the limb and other cases, only non-surgical treatment can be used.
1, general treatment: reduce the activity of the affected limb. Pay attention to the warmth of the affected limb, preferably with constant temperature in the room, prohibit hot compresses (even if the temperature is not high, it is easy to cause burns and aggravate tissue metabolism), prohibit cold compresses, so as to avoid vasoconstriction of the affected limb and reduced arterial blood flow. And pay attention to the observation of vital signs, maintain the water-electrolyte acid-base balance, and symptomatic treatment can be given when the pain is severe.
2.Anticoagulation therapy: prevent secondary thrombosis in the embolized artery, the development of atrial thrombosis, and the formation of venous thrombosis. Heparin, or low molecular weight heparin, is commonly used in the acute phase, and the prothrombin time is monitored and generally controlled within 20s, and hypertension is controlled to avoid serious complications such as cerebral hemorrhage. In the chronic phase, a bicoumarin derivative such as warfarin is used to maintain treatment for 3-6 months and monitor the prothrombin time.
The main complication of anticoagulation therapy is bleeding, commonly subcutaneous bruising, wound bleeding or hematoma, bleeding from the gastrointestinal or urinary tract, or even cerebral hemorrhage. Heparin can be counteracted by fisetin, generally 1mg of fisetin against 1mg of heparin. Heparin has a short half-life in the body, and the longer the interval after heparin injection, the smaller the dose of fisetin required. If bleeding continues, fresh blood or plasma and prothrombinogen complex complex can be transfused. For those who apply anticoagulation with bicoumarins derivatives, vitamin K 10-50mg can be injected intramuscularly or intravenously.
3. Thrombolytic therapy: The key to success or failure is early medication. Within 3 days after the onset of the disease, the drug is effective. 6-7 days after the onset of the disease, the thrombus is mechanized and the thrombolytic therapy is ineffective. Within 3 days of onset, urokinase 250,000 U/time, 2 times/d, can be injected into peripheral veins. It can also be injected directly into the blood vessel proximal to the embolized artery or thrombolysed by catheter.
Before and after thrombolytic therapy, patients should be informed of any contraindications to thrombolytic therapy. If bleeding or hematoma at the injection site, nasal bleeding or gastrointestinal bleeding is found, the drug should be stopped immediately, and fresh blood or fibrinogen should be transfused, and fibrinolytic inhibitors should be applied if necessary.
4, dispel aggregation treatment: inhibit platelet adhesion and aggregation, commonly used drugs include enteric aspirin, dipyridamole, dextran 4 anhydride 40, epoprostenol (prostacyclin), compound salvia, etc.. They can be used alone or in combination with two drugs (e.g. dextran 4 anhydride 40 with compound salvia, etc.). The bleeding effect of antiplatelet therapy is rare, and when anticoagulation or thrombolytic therapy is contraindicated, antiplatelet therapy can be used as appropriate. The platelet count, clotting time and thromboelastography can be monitored to determine the number and function of platelets in the body.
5, vasodilator therapy: directly or indirectly act on peripheral blood vessels to increase blood flow. Vasodilators are more effective in treating vasospastic diseases than ischemic diseases caused by structural changes in the blood vessel wall. Recently, many new vasodilating drugs such as prostaglandin E1 and prostacyclin have been used clinically and have achieved certain efficacy. Sympathetic nerve block or epidural anesthesia can also be used to release arterial spasm and promote the establishment of collateral circulation.
6, other: hyperbaric chamber to increase the partial pressure of blood oxygen and oxygen saturation, to improve limb ischemia to a certain extent.
Surgical treatment.
1.Embolysis.
After 6-8h arterial embolism, the muscle tissue is not yet necrotic, the embolus is not yet adhered to the intima, and the endothelial cells are not seriously damaged, so it is the best time for surgical embolization. Even if the disease has been longer, and the limb has 1 or several toes (fingers) on the verge of necrosis, but there is no obvious mass necrosis, if the embolization can restore the main artery and blood flow, it should still be operated to reduce the purpose of amputation.
There are 2 methods of embolization.
Forgarty balloon catheter embolization: The surgical route depends on the site of embolization. Forgarty balloon catheter embolization avoids direct exposure of the embolized artery, reduces surgical trauma and shortens operative time, and can be performed through the catheter to the proximal and distal arteries of the embolism. The procedure can be performed under local anesthesia or nerve block anesthesia, which is undoubtedly beneficial for patients with severe systemic conditions.
Arteriotomy for embolization: Care should be taken to first free and block the distal artery to prevent the embolus from migrating distally during the procedure. Then free the proximal artery of embolism and block the proximal blood flow before cutting the artery to remove the embolism.
2, amputation: when the limb has clear tissue necrosis, in order to prevent the serious consequences of toxemia, according to the extent of necrosis, should choose different planes of amputation.
Postoperative treatment.
After embolization, monitoring and treatment of cardiovascular disease and systemic condition should not be neglected. For those who have embolism for a long time, postoperative anticoagulation therapy is appropriate to prevent thrombus formation. In the early postoperative period, the distal artery pulsation may still be weak, and generally a strong pulsation can be restored after 2 to 3 days. If the arterial pulsation is delayed and there are signs of insufficient blood supply to the distal tissues, further examination should be performed to clarify whether there is distal arterial occlusion, which should be actively treated. When the limb swells sharply after embolectomy, it indicates the existence of fascial septal syndrome and requires timely decompression by fascial septotomy. After arterial flow reconstruction, the clinical manifestation of post-ischemic reperfusion injury occurs, which is one of the causes of death after embolization, mostly occurs in those with longer time of main artery embolization, and a large amount of toxic products enter the circulation after embolization causing metabolic changes, manifested as acidosis, hyperkalemia and renal failure. Properly managed. Renal failure, maintaining water and electrolyte balance, may still save life.