Deep Vein Thrombosis (DVT)

Deep Vein Thrombosis (DVT)

• DVT involves the formation of a thrombus alongside vein inflammation.
• Superficial vein thrombosis features a thrombus in superficial veins, typically in the extremities.
• Deep vein thrombosis involves a thrombus in a deep vein, usually in the iliac or femoral veins.
• Venous thromboembolism occurs when a DVT detaches, moves to the pulmonary artery, and causes a pulmonary embolus.

Etiology of DVT - Virchow's Triad

• Venous stasis can be caused by dysfunctional valves, inactivity of extremity muscles, obesity, pregnancy, post-operative states, and immobility.
• Damage to the endothelium can be direct via fracture, surgery, or trauma, or indirect via chemotherapy or diabetes.
• Hypercoagulability of the blood can be caused by hematologic disorders, anemias, malignancies, or clotting/protein deficiencies.

Risk Factors for DVT

• Risk factors include pregnancy, oral contraceptives, post-menopausal therapy (SERMS), hormone replacement therapy, post-chemotherapy/hysterectomy, and tobacco use.

Pathophysiology of DVT

• Platelet aggregation and fibrin entrap red blood cells (RBCs), white blood cells (WBCs), and platelets, forming a thrombus.
• A thrombus enlarges as more cells adhere.
• An Embolus results if a thrombus detaches which may lead to a pulmonary embolus.

DVT: Clinical Manifestations

• Clinical manifestations include unilateral leg edema, extremity pain, fullness in the calf/thigh, erythema and warmth.
• A positive Homan's sign can be an indicator, involving pain with dorsiflexion of the foot.

DVT Complications

• A major complication of DVT is pulmonary embolism (PE), where thrombi block the pulmonary arteries.
• Emboli are mobile clots which lodge in narrow parts of the circulatory system.
• Pulmonary embolism has a 30% mortality rate.
• Pulmonary embolism can result from other causes, including atrial fibrillation and upper extremity DVT.

PE: Clinical Manifestations

• Clinical manifestations include dyspnea, chest pain, hemoptysis, cough, pleuritic chest pain, and crackles on auscultation of lungs.

Hemostasis

• Hemostasis is the general term for any process that stops bleeding.
• Coagulation is hemostasis that occurs due to physiologic clotting of blood.
• The process has a complex relationship between substances promoting clot formation and those inhibiting coagulation or dissolving formed clots.

Coagulation System

• The coagulation system follows a "Cascade" effect.
• Each activated factor acts as a catalyst that amplifies the next reaction.
• The end result is fibrin, a clot-forming substance.
• The system involves the intrinsic and extrinsic pathways.

Coagulation Modifier Drugs

• Anticoagulants, given orally or parenterally, inhibit the action or formation of clotting factors and prevent clot formation.
• Antiplatelet drugs interfere with platelet function, inhibit platelet aggregation, and prevent platelet plugs.
• Thrombolytic/Fibrinolytic drugs break down existing clots.
• Other modifiers include direct thrombin inhibitors and direct inhibitors of Factor XA.

Parenteral Anticoagulants (Heparin)

• Heparin prevents clotting by activating antithrombin, inhibiting thrombin, and working on different points of the clotting cascade.
• It is used prophylactically to prevent clot formation (thrombus) and emboli (dislodged clot).
• Heparin is used in emergency conditions requiring prompt therapy (Stroke, DVT, PE) and disseminated intravascular coagulation.
• Also used preventatively for stroke, MI, DVT, and PE.
• Adverse reactions of Heparin include hemorrhage, heparin-induced thrombocytopenia, hypersensitivity reactions, and toxicity.
• Heparin is administered subcutaneously (SQ) or intravenously (IV).

Parenteral Anticoagulants (Heparin) Nursing Administration

• For intravenous heparin, obtain baseline vitals and labs (CBC, PLT, HCT).
• Obtain APTT (Activated Partial Thromboplastin Time) every 4-6 hours until stable levels, maintaining a therapeutic APTT of 1.5-2.5 times normal.
• Read label, double-check dose with a second nurse, and administer Heparin through an infusion pump only.
• Protamine Sulfate is the antidote for Heparin.
• For subcutaneous heparin, use a 25-28 gauge needle of 1/2-5/8 inches.
• Injections should be placed in the abdomen at least 2 inches away from the umbilicus.
• Aspiration is not required, and gentle pressure should be applied to the injection site for 1-2 minutes, rotating sites.

Parenteral Anticoagulants: enoxaparin (Lovenox)

• Enoxaparin is a low molecular weight heparin (LMWH) that primarily acts on coagulation factor Xa, limiting thrombin generation needed for fibrin production.
• Used to prevent DVT in post-op patients, prevent complications from certain types of MI, and to treat DVT/PE.
• Route of administration is subcutaneous (SQ) only.
• Adverse effects include hemorrhage, neurologic damage from hematoma formation in those receiving spinal or epidural anesthesia, and thrombocytopenia.
• Administered with pre-filled syringes without expelling the air bubble, injecting in the abdomen (without aspiration), rotating sites, and monitoring for bleeding.
• Antidote is Protamine Sulfate.

Oral Anticoagulants: warfarin sodium (Coumadin)

• Warfarin antagonizes Vitamin K, preventing the synthesis of additional coagulation factors.
• It is used for treatment of DVT, prevention of clots in those with AFIB and prosthetic valves, and prevention of transient ischemic attacks (TIA), PE, and DVT.
• Route of administration is oral only.
• Monitored by prothrombin time (PT) and international normalized ratio (INR), with PT-INR being the monitored value.
• Vitamin K is the antidote.
• Requires long-term outpatient therapy.
• Therapy dosages can vary; for example, 5mg PO daily on Monday, Wednesday, Friday, and Sunday, and 2.5mg PO daily on Tuesday, Thursday, and Saturday.

Warfarin Sodium: Nursing Implications

• Warfarin therapy should begin while the patient is still on heparin until PT-INR levels indicate adequate anticoagulation.
• The full therapeutic effect takes several days.
• PT-INR should be monitored regularly with follow-up appointments.
• The therapeutic PT-INR should be 2-3 times the normal value.
• Herbal products can lead to increased bleeding when interacted with, including capsicum pepper, garlic, ginger, ginkgo, St. John's wort, and feverfew.

Direct Thrombin Inhibitors: dabigatran (Pradaxa)

• Dabigatran acts directly by inhibiting thrombin, preventing thrombus development.
• It is used to prevent stroke or embolism in patients with afib not caused by valvular heart disease.
• Route of administration is oral (should not be crushed); can be taken with or without food; discontinue other anticoagulants when starting dabigatran.
• Adverse effects include bleeding and GI discomfort.

Direct Inhibitor of Factor XA: rivaroxaban (Xarelto)

• Rivaroxaban acts through anticoagulation by inhibiting Factor Xa.
• It is used to prevent DVT and PE in clients undergoing total hip or knee/arthroplasty.
• Administer tablets orally once a day, with or without food at the same time every day.
• Monitor Hgb, HCT, and liver and kidney function during treatment.
• Adverse effects include bleeding and elevated liver enzymes.

Anticoagulants: Patient Education

• Patient education should include the importance of regular lab testing, signs of abnormal bleeding, measures to prevent bruising/bleeding/tissue injury, and wearing a medical alert bracelet.
• Patients should avoid foods high in vitamin K and consult the physician before taking other meds or over-the-counter products, including herbals.

Antiplatelet Drugs

• Antiplatelet drugs prevent platelet adhesion, reduce the risk of fatal and nonfatal strokes, and address acute unstable angina and MI.
• Adverse effects include bleeding.
• Aspirin is cardio-protective, available in PO and suppository forms, and comes in 81mg or 325mg dosages.
• Clopidogrel (Plavix) is often used in patients with stents and is taken at 75mg PO daily.
• Antiplatelet/glycoprotein inhibitors like eptifibatide (Integrilin) are usually administered in the ICU or cardiac cath lab.
• Adverse effects of eptifibatide medications include bleeding, hypotension, and bradycardia.

Thrombolytic Drugs/Fibrinolytics

• Thrombolytic drugs break down or lyse pre-formed clots and are also known as "Clot busters".
• Indications include DVT, pulmonary embolus, and occlusion of shunts or catheters.
• They are used in the treatment of acute MI, which requires initiation within 6 hours of symptom onset, and for acute ischemic stroke, with must be initiated within 3 hours of onset.
• Examples include anistreplase (Eminase), alteplase (t-PA, Activase), reteplase (Retavase), and tenecteplase (TNKase).

Thrombolytic Drugs/Fibrinolytics: Mechanism of Action

• These function to activate the fibrinolytic system and break down any clots inside blood vessels quickly.
• Activate plasminogen and convert it to plasmin, which can digest fibrin.
• The drugs reestablish blood flow to the affected area, such as to the lungs via the pulmonary artery and the heart muscle via the coronary arteries, preventing tissue destruction.
• Adverse effects include bleeding (internal, intracranial, superficial) and other effects, such as nausea and vomiting, hypotension, anaphylactic reactions, and cardiac dysrhythmias.

Thrombolytic Drugs: Nursing Implications

• Nursing implications include following strict manufacturer's guidelines for preparation and administration, monitoring the IV site for bleeding/redness/pain, and monitoring for bleeding from gums, mucous membranes, nose, and injection sites.
• Signs of internal bleeding (decreased BP restlessness increased pulse) should be observed, as well as monitoring for changes in mental status.

Coagulation Modifier Drugs: Nursing Implications

• Monitor for therapeutic effects and for signs of excessive bleeding.
• Signs of excessive bleeding include bleeding of gums while brushing teeth, unexplained nosebleeds, heavier menstrual bleeding, bloody or dark stools, bloody urine or sputum, abdominal pain and vomiting blood.