Vascular Occlusive Syndromes of the Upper Extremity Medication
- Author: Bradon J Wilhelmi, MD; Chief Editor: Harris Gellman, MD more...
Upon surgical repair of traumatic vascular injury and before the release of vascular clamps to allow return of blood perfusion, systemic heparin (3000-5000 U) is administered.
Postoperatively, only aspirin (325 mg/day PO) administration is recommended unless intraoperative anastomosis complications are confronted. If such complications do occur, postoperative therapeutic heparin infusion is continued (titrated to keep activated partial thromboplastin time [aPTT] in the range of 50-80 s). Dipyridamole is an appropriate alternative to aspirin and has a similar platelet mode of action.
After iatrogenic vascular injuries, acute thrombolytic therapy has been advocated as first-line therapy, especially for cases involving embolic showering to distal nutrient microvessels. Thrombolytic medication options include either tissue plasminogen activator (t-PA), 100 mg IV over 2 hours, or streptokinase, 1.5 million U IV over 1 hour. However, thrombolytic therapy is contraindicated in the presence of a pseudoaneurysm, in which case surgical intervention is preferred.
Hypothenar hammer syndrome, which presents with pain in the region of the hook of hamate along with paresthesia and decreased temperatures in the ring and little fingers, follows disruption of the internal elastic lamina. The condition results in aneurysmal dilatation and mural thrombosis of the ulnar artery in the Guyon canal.
Diagnosis is made on the basis of history, a positive result on an Allen test, and, in a minority of cases (10%), a pulsatile mass. Doppler ultrasound or angiography of the upper extremity will confirm the diagnosis. Treatment involves thrombolytic agents (t-PA, 100 mg IV over 2 hours, or streptokinase, 1.5 million U IV over 1 hour) acutely and, if this treatment is unsuccessful, surgery. In fact, most cases of hypothenar hammer syndrome are diagnosed at a time when successful thrombolysis is no longer possible.
Vaso-occlusive disease of the terminal vessels may arise from proximal showering of emboli from either vascular or cardiac thrombi. Treatment consists of immediate anticoagulation with heparin (3000-5000 U IV bolus followed by titrated infusion to keep aPTT in the range of 50-80 s) followed by 3 months of warfarin PO therapy (titrated to keep prothrombin time [PT] in the range of 2-3 s).
Thrombolytic therapy can be attempted if anticoagulation does not improve symptoms acutely (t-PA, 100 mg IV over 2 hours, or streptokinase, 1.5 million U IV over 1 hour). Embolectomy can be attempted if emboli are embedded in vessels proximal to the superficial arch and anticoagulant therapy has proven ineffective.
Initial treatment of both Raynaud disease and Raynaud phenomenon involves inhibition of vasospasms, thus improving microvascular flow and maximizing capillary perfusion. Treatment initially consists of smoking cessation, biofeedback therapies (temperature control), and calcium channel blockers. Calcium channel blockers include diltiazem, 60 mg PO every 12 hours, or verapamil, 150 mg PO at bedtime.
Prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation. Used for treatment and prevention of deep vein thrombosis (DVT), pulmonary embolism (PE), unstable angina, atrial fibrillation with emboli formation, and acute arterial occlusion.
Acts with antithrombin III to inactivate thrombin and inhibit thromboplastin formation.
Interferes with hepatic synthesis of vitamin K–dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.
Tailor dose to maintain an INR in the range of 2-3.
Used for acute myocardial infarction (AMI), pulmonary emboli (PE), and acute ischemic stroke.
t-PA and fibrin-specific agent with brief half-life of 5 min. Initiates local fibrinolysis by binding to fibrin in the thrombus. Used in management of AMI, acute ischemic stroke, and PE.
Adjunctive therapy with IV heparin necessary to maintain patency of arteries recanalized by t-PA, especially during first 24-48 h.
Streptokinase (Kabikinase, Streptase)
Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins. Increase in fibrinolytic activity that degrades fibrinogen levels for 24-36 h takes place with intravenous infusion of streptokinase.
Used for angina, prevention of reinfarction, hypertension, atrial fibrillation or flutter, and paroxysmal atrial tachycardia (PAT).
During depolarization, inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.
Calcium channel blockers also inhibit movement of calcium ions across cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
Calcium channel blocker. Only the nondihydropyridines are effective for rate control. During depolarization, inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.
Used for prophylaxis and treatment of PE and DVT, and AF with embolization, as well as other postoperative indications.
To complement usual warfarin therapy. Platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity leading to increased cyclic-3', 5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.
Used to manage mild pain, headache, fever, and inflammation, as well as for prevention of emboli and myocardial infarction (MI).
Benefits adults. Inhibits prostaglandin synthesis preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis.
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