Class 03-Introduction to Clotting/Perfusion

Phlegmasia cerulean dolens

(swollen, blue, painful leg)—rare—complication of a severe lower extremity VTEs. It involves the major leg veins, causing near-total occlusion of venous outflow. Patients typically have sudden, massive swelling; deep pain; and intense cyanosis of the extremity. If untreated, the venous obstruction causes arterial occlusion and gangrene, requiring amputation.

Low-Molecular-Weight Heparins (LMWH [e.g., enoxaparin and dalteparin])

- LMWH inactivates the Xa factor. - LMWHs produce more stable responses at recommended doses. As a result, frequent laboratory monitoring of aPTT is not required. - LMWHs are administered subcutaneously once or twice a day, depending on the drug or drug regimen, and they are available in prefilled syringes with attached needles. - These agents are most commonly prescribed to prevent DVT and acute PE after orthopedic or abdominal surgery. Hip and knee replacement anticoagulant therapy often includes enoxaparin, and abdominal surgery includes dalteparin. - The half-life of LMWHs is two to four times longer than that of heparin. - Patients should be instructed not to take antiplatelet drugs such as aspirin while taking LMWHs or heparin. Antidote If bleeding occurs, protamine sulfate is the anticoagulant antagonist used. The dosage is 1 mg of protamine sulfate for every 100 units of unfractionated heparin or LMWH given to be neutralized. Contraindications The LMWHs are contraindicated for patients with strokes, peptic ulcers, and blood anomalies. These drugs should not be given to patients having eye, brain, or spinal surgery.

Intrinsic vs. Extrinsic

1. Intrinsic pathway Activated by trauma inside a blood vessel Ionized Ca+ needed to activate Factors XII(7), VIII(8), IX(9) & XI(11) are involved Slow to form 15-20 sec. to initiate Lab test used to measure Activated Partial Thromboplastin Time (aPTT) 2. Extrinsic pathway Activated by damaged external surfaces Ionized Ca+ and Tissue Factor needed to activate Factor VII (7) is involved Fast to form 2-6 minutes to initiate Lab test used to measure Prothrombin Time (PT)

Virchow's Triad

1. Venous Stasis: occurs when the valves are dysfunctional or the muscles of the extremities are inactive. Venous statis occurs most often in people who are obese or pregnant, have chronic HF or atrial fibrillation, have been traveling on long trips without regular exercise, have a prolonged surgical procedure, or are immobile for long periods (e.g. spinal cord injury, fractured hip, limb paralysis). • Advanced age • Atrial fibrillation • Bed rest • Chronic heart failure • Fractured leg or hip • Long trips without adequate exercise • Obesity • Orthopedic surgery (especially hip or lower extremity) 2. Endothelial damage: Damage to the endothelium of the vein may be caused by direct or indirect injury. Damaged endothelium stimulates platelet activation and starts the coagulation cascade. This predisposes the patient to thrombus development. · Abdominal and pelvic surgery (e.g., gynecologic, urologic surgery) · Caustic or hypertonic IV drugs · Pelvis, hip, or leg fractures · History of VTE · Indwelling, peripherally inserted central vein catheter · IV drug abuse · Trauma 3. Hypercoagulability of blood: Blood hypercoagulability occurs in many disorders. These include: • Antiphospholipid antibody syndrome • Antithrombin III deficiency • Cancer (especially breast, brain, hepatic, pancreatic, GI) • Dehydration or malnutrition • Elevated (clotting) factor VIII or lipoprotein (a) • Erythropoiesis-stimulating drugs (e.g., epoetin alfa [Procrit]) • High altitudes • Hormone therapy • High homocysteine levels • Nephrotic syndrome • Oral contraceptives, especially in women older than 35 years who use tobacco • Polycythemia vera The patient a/r for developing VTE usually has predisposing condition the these 3 disorders listed above

chest x-ray

Abnormal finding (atelectasis [collapsed lung] or plural effusion [fluid in the plural space]) may be seen on a chest x-ray.

Hemophilia

An X-linked recessive disorder in which blood fails to clot properly, leading to excessive bleeding if injured.

Antiplatelets (e.g, Asprin [ASA])

Antiplatelets are used to prevent thrombosis in the arteries by suppressing platelet aggregation. Antiplatelet drug therapy is mainly for prophylactic use in (1) prevention of MI or stroke for patients with a family history of these, (2) prevention of repeat MI or stroke, and (3) prevention of stroke for patients having transient ischemic attacks (TIAs). Long-term, low-dose aspirin therapy has been found to be both an effective and inexpensive treatment for suppressing platelet aggregation. Aspirin inhibits cyclooxygenase (COX), an enzyme needed by platelets to synthesize thromboxane A2 (TxA2). For patients with a family history of stroke or MI, the recommended aspirin dose is 50 to 325 mg/day for stroke prophylaxis and 75 to 162 mg/day for MI prophylaxis. Aspirin has prolonged antiplatelet activity, it should be discontinued at least 7 days before surgery.

Venous Thromboembolism or Deep Vein Thrombosis (DVT): Diagnostic testing

Blood laboratory studies · ACT, aPTT, INR, bleeding time, Hgb, Hct, PLT count - Altered if patient has underlying blood dyscrasia (e.g., increased Hgb and Hct in patient with polycythemia) · D-dimer (a test to let you know that there is a clot going on) - Fragment of fibrin formed from fibrin degradation and clot lysis. High results suggest VTE. Normal results: <250 ng/mL (<250mcg/L) · Fibrin monomer complex - Forms when concentration of thrombin exceeds that of antithrombin. Presence is evidence of thrombus formation and suggest VTE. Normal result: 6.1 mg/L

duplex ultrasound

Combination of compression ultrasound with spectral and color flow Doppler. Veins examined for compressibility and intraluminal filling defects to help determine location and extent of thrombus (most widely used test to diagnose VTE).

Pulmonary Embolism (PE)

Embolus derives from the Greek word meaning "plug" or "stopper" A Pulmonary Embolism (PE) is a blockage of one or more pulmonary arteries by thrombus (blood clot attached to the interior wall of an artery or vein), fat or air embolus, or tumor tissue. The PE obstructs alveolar perfusion (chokes of the oxygenation to the lung tissue, resulting in necrosis. The lower lobes of the lung are most often affected. Most PE's arise from deep vein thrombosis (DVTs) in the deep veins of the legs. Venous thromboembolism (VTE) is the preferred term to describe the spectrum of pathologic conditions from DVT to PE. *DVT and VTE are used interchangeably and refer to the same thing. A saddle embolus refers to a large thrombus lodged at an arterial bifurcation.

Venous compression ultrasound

Evaluation of deep femoral, popliteal, and posterior tibial veins Normal finding: Veins collapse with application of external pressure. Abnormal finding: Veins do not collapse with application of external pressure. Failure to collapse suggests a thrombus.

Ventilation-perfusion (V/Q) scan

Has 2 parts (it is most accurate when both parts are done) - Part I: Perfusion scanning involves IV injection of a radioisotope. A scanning device images the pulmonary circulation - Part II: Ventilation scanning involves inhalation of a radioactive gas, such as xenon. Scanning reflects the distribution of gas through the lungs.

Diagnostic Studies for PE

Important but not diagnostic: These diagnostic studies are important to rule out MI. Arterial blood gases (paO2 levels may be low r/t inadequate oxygenation, pH is often normal unless Resp. acidosis develops) Electrocardiogram: used to rule out cardiac issues Troponin levels: used to rule out an MI) B-type natriureticpeptide (BPN): Used to rule out HF

Thrombocytes (Platelets [PLT])

Initiate clotting process, plug opening in the capillary wall, and play a role in clot shrinkage and retraction Stem cells transform into a megakaryocyte (immature PLTs) which fragments into PLTs. · Partially regulated by thrombopoietin (TPO) (hormone that triggers bone marrow to produce PLTs)

Heparin

Is a natural substance in the liver that prevents clot formation. The primary use of heparin is to prevent venous thrombosis, which can lead to PE or stroke. It does this by combining with antithrombin III (which accelerates the anticoagulant cascade of reactions that prevents thrombosis formation). By inhibiting the action of thrombin, conversion of fibrinogen to fibrin does not occur, and the formation of a fibrin clot is prevented. Administered - Heparin is poorly absorbed through the gastrointestinal (GI) mucosa, and much is destroyed by heparinase, a liver enzyme. Because heparin is poorly absorbed orally, it is given subcutaneously or by IV. It can be administered as an IV bolus or in IV fluid for continuous infusion. Lab Test's - Partial thromboplastin time (PTT) and activated partial thromboplastin time (aPTT) are laboratory tests used to detect deficiencies of certain clotting factors, and these tests are used to monitor heparin therapy. Every 6 hours. Antidote Protamine sulfate can be an anticoagulant, but in the presence of heparin, it is an antagonist that reverses the action of heparin. Before discontinuing heparin, oral therapy with warfarin therapy is begun.

Lipodermotosclerosis

Lipodermatosclerosis. Skin on lower leg becomes scarred, and the leg becomes tapered like an "inverted bottle." Hallmark signs are leathery skin, brown discoloration, changes in pigmentation, and circumferential or near circumferential scarring and shrinking of the extremity.

Pathophysiology of a blood clot

Localized PLT aggregation and fibrin entrap RBCs, WBCs and more PLTs to form a thrombus A frequent site of thrombus formation is the valve cusps of veins, where venous stasis occurs. If partial occlusion of vein endothelial cells cover thrombus and stop the thrombotic process. Thrombus becomes adherent and organized within 5 to 7 days. If breaks free the embolus flow through venous circulation to heart and lodges in pulmonary circulation becoming a pulmonary embolus.

Superficial Vein Thrombosis

May have palpable, firm subcutaneous cordlike vein Surrounding are may be itchy, tender to the touch, reddened and warm Mild temperature elevation and leukocytosis may be present Extremity edema may or may not be present Lower extremity superficial vein thrombosis often involves 1 or more varicose veins Interprofessional Care Diagnosis—Duplex ultrasound or doppler ultrasound (clot 5 cm or larger) Lower leg—Sub Q—Fondaparinux (Atrixa) reduces symptoms and prevents extension and recurrence with less risk of major bleeding problems. Thrombus less than 5cm not near the saphenofemoral junction—may be treated with only NSAIDs for symptoms. Teaching Wearing of graduated compression stockings or bandages Apply warm compresses Elevate the limb above level of the heart Apply topical NSAIDs Perform mild exercise (e.g. walking)

Clinical management: Invasive and non invasive Procedures for clotting problems

Phlebotomy 1. Removal of blood; can be useful in patients with SCA, Polycythemia. Thrombectomy 2. Removal of a thrombus from a vessel Filters 3. Placement of filter in vessel Nutrition 1. Consider the vitamin K (vitamin used to clot) content of food Positioning (Do the "V" and "A" trick Mike taught us [A=legs down V=legs elevated]) 2. Elevation of extremity (venous thrombosis) 3. Dependent position (arterial thrombus)

Interprofessional Care

Prevention—the key! Sequential compression devices Early ambulation Prophylactic anticoagulation Goals of treatment Reduce and Prevent further thrombi Prevent further embolization to pulmonary system Provide cardiopulmonary support Supportive care variable O2àmechanical ventilation Pulmonary toilet Fluids, diuretics, analgesics

Post-Thrombotic Syndrome

Results from chronic inflammation and chronic venous hypertension. Chronic venous hypertension is caused by vein wall and vein valve damage (from acute inflammation and thrombus reorganization) , venous valve reflux, and persistent venous (outflow) obstruction. Symptoms: pain, aching, fatigue, heaviness, sensation of swelling, cramps, pruritus, tingling paresthesia, bursting pain with exercise, and venous claudication. Clinical signs: persistent edema, spider veins, venous dilation, redness, cyanosis, increased pigmentation, eczema, pain during compression, atrophie blanche (white scar tissue) and lipodermatosclerosis.

Nursing management for clots

Semi—Fowler's position—first thing you should do—helps facilitate breathing Oxygen therapy Frequent assessments IV access Monitor Laboratory results Emotional support and reassurance Patient Teaching Regarding long-term anticoagulant therapy Measures to prevent DVT Importance of follow-up exams

systemic vs local

Systemic: Problem extends to entire body; is usually the result of a significant hematological event. (e.g., SCA, Polycythemia, lack of clotting factors) Localized: Problem is localized; is usually a problem in a vein or an artery, either injury to a vessel or a clot within a vessel.

Stage 6: Fibrinolytic system (breaks down clots)

The fibrinolytic system is initiated when Plasminogen is activated into Plasmin. Thrombin (Plasminogen activators) is one of the substances that can promote fibrinolysis by activating the conversion of Plasminogen to Plasmin. Plasmin once activated attacks either fibrin or fibrinogen by splitting the molecules into smaller elements known as fibrin degradation products.

· Magnetic resonance venography

Uses MRI with specialized software to evaluate blood flow through veins. Can be done with or without contrast. Highly accurate for pelvic and proximal veins. Less accurate for calf veins. Can distinguish acute and chronic thrombus

Computed tomography venography (CTV)

Uses spiral CT to evaluate veins in the pelvis, thighs, and calves after injection of contrast material. May be done simultaneously with CT angiography of pulmonary vessels for patients being evaluated for VTE.

Surgical and Interventional Radiology Therapies

Venous Thrombectomy - involves the removal of a clot through a vein incision. Anticoagulant therapy is used after venous thrombectomy. Vena cava interruption devices (e.g., Greenfield, Vena Tech, TrapEase filters) - can be placed percutaneously through the right femoral or right internal jugular veins. The filter device is opened, and the spokes penetrate the vessel walls. The filters act as a "sieve-type" device, allowing filtration of clots without interruption of blood flow. Complications after the insertion are rare but include air embolism, improper placement, migration of the filter, and perforation of the vena cava with retroperitoneal bleeding. Over time, clots can clog the filter and completely block the vena cava, requiring filter removal and replacement. A filter device is recommended with acute PE or proximal VTE of the leg in patients with active bleeding or if anticoagulant therapy is contraindicated or ineffective.

Venous Thrombosis

Venous Thrombosis: Involves formation of thrombus (blood clot) associated with inflammation in the vein. This is the most common disorder of the veins. We classify is as either superficial vein thrombosis or deep vein thrombosis (DVT) Superficial Thrombosis (ST): - Defined: as the formation of a thrombus in a superficial vein. Location: superficial vein (usually greater or lesser saphenous vein) - Considered the lesser of the two types. However about 25% of patients with STs may also have a DVT or PE at the time of diagnosis. Deep Vein Thrombosis (DVT) or Venous Thromboembolism (VTE) - Defined: involves a thrombus in a deep vein - Location: deep vein (usually iliac and/or femoral veins) - *DVT and VTE are used interchangeably; however VTE is the preferred terminology.

Oral anticoagulants (e.g. Warfarin)

Warfarin is an oral anticoagulant used mainly to prevent thromboembolic conditions such as thrombophlebitis, PE, and embolism formation caused by atrial fibrillation, which can lead to stroke. It does this by inhibiting hepatic synthesis of vitamin K, thus affecting the clotting factors II, VII, IX, and X. Lab test's Oral anticoagulants prolong clotting time and are monitored by the prothrombin time (PT [a laboratory test that measures the time it takes blood to clot in the presence of certain clotting factors, which warfarin affects]). This laboratory test is usually performed immediately before administering the next drug dose until the therapeutic level has been reached. Today, the international normalized ratio (INR) is the laboratory test most frequently used to report PT results. Patients on warfarin therapy are maintained at an INR of 2 to 3. The desired INR for patients who have a mechanical heart valve or recurrent systemic embolism is 2.5 to 3.5, but the desired level could be as high as 4.5. Monitoring INR at regular intervals is required for the duration of drug therapy. Warfarin has a long half-life and very long duration. Laboratory testing of PT or INR should be scheduled at recommended intervals. Side Effects and Adverse Reactions Bleeding (hemorrhage) is the major adverse effect of warfarin. Patients should be monitored closely for signs of bleeding such as petechiae, ecchymosis, GI bleeding, ocular hemorrhage, and hematuria. Drug Interactions Because warfarin is highly protein bound, it is affected by drug interactions. Aspirin, nonsteroidal antiinflammatory drugs (NSAIDs), other types of antiinflammatory drugs, sulfonamides, phenytoin, cimetidine, allopurinol, and oral hypoglycemic drugs for diabetes can displace warfarin from the protein-bound site and can cause more free-circulating anticoagulant. Numerous other drugs also increase the action of warfarin, and bleeding is likely to occur. Acetaminophen should be used instead of aspirin by patients taking warfarin. Antidote The antidote for warfarin overdose is vitamin K, but it takes 24 to 48 hours to be effective. If excessive vitamin K is given, it may take warfarin 1 to 2 weeks before it can be effective again. For acute bleeding, fresh frozen plasma is indicated.

· Contrast venography (phlebogram)

X-ray determination of location and extent of clot using contrast media to outline filling defects. Identifies the presence of collateral circulation. Once the gold standard, but now rarely done

Thrombocytopenia

a condition in which there is an abnormally small number of platelets circulating in the blood

Atrial Fibrillation (A-Fib)

an irregular and often very fast heart rate originating from abnormal conduction in the atria Atrial Fibrillation (causes clots because of the stagnant blood in the atrium)

Hemostasis

describes the arrest of bleeding. This process is important in minimizing blood loss when various body structures are injured. 1. Vascular injury and subendothelial exposure - When a blood vessel is injured, an immediate local vasoconstrictive response occurs. Vasoconstriction reduces the leakage of blood from the vessel by restricting the vessel size and pressing the endothelial surfaces together. The latter reaction enhances vessel wall stickiness and keeps the vessel closed after vasoconstriction subsides. Vascular spasm may last for 20 to 30 minutes. This allows time for the body to activate the platelet response and plasma clotting factors. The platelet response and plasma clotting factors are triggered by endothelial injury and the release of substances such as thromboxane A2 (TXA2). Platelets begin to fill endothelial gaps. 2. Adhesion - The loss of endothelial cells exposes adhesive glycoproteins, such as collagen and von Willebrand factor (vWF), to which more platelets adhere. The stickiness is termed adhesiveness. The formation of clumps is termed aggregation or agglutination. 3. Activation - The interaction described previously causes the platelets to undergo an activation process. This leads to changes in platelet shape. The platelets then can bind adhesive proteins, including fibrinogen and vWF. Release of various platelet granules (including adenosine phosphate [ADP]) recruits and activates other platelets, clotting factors, and growth factors. 4. Aggregation - Platelet aggregation is stimulated by TXA2 and ADP, which induce fibrinogen receptors on the platelet. The formation of a visible fibrin clot on the platelet plug is the conclusion of a complex series of reactions involving different clotting (coagulation) factors. Plasma proteins circulate in inactive forms until stimulated to start clotting through 1 of 2 pathways, intrinsic or extrinsic. Regardless of how we begin to clot, coagulation ultimately follows the same final common pathway of the clotting cascade. 5. Platelet plug formation - The final blood clot is a meshwork of protein strands that stabilizes the platelet plug and traps other cells, such as RBCs, phagocytes, and microorganisms. 6. Clot retraction and dissolution Fibrinolysis, a process resulting in the dissolution of the fibrin clot. The fibrinolytic system starts when plasminogen is activated by substances such as tissue plasminogen activator (t-PA) and urokinase-like plasminogen activator (u-PA) to plasmin. The plasmin attacks either fibrin or fibrinogen by splitting the molecules into smaller elements known as fibrin split products (FSPs) or fibrin degradation products (FDPs). *Thrombin is the most powerful enzyme in the coagulation process. It is 1 of the substances that can activate the conversion of plasminogen to plasmin, thereby promoting fibrinolysis. Excessive fibrinolysis predisposes the patient to bleeding. In this situation, bleeding results from the destruction of fibrin in platelet plugs or from the anticoagulation effects of increased FSPs. Increased FSPs lead to impaired platelet aggregation, reduced prothrombin, and an inability to stabilize fibrin.

Polycythemia

increased number of erythrocytes and hemoglobin in the blood

D-dimer

is a lab test that measures the amount of cross-linked fibrin fragments. These fragments are the result of clot degradation and are rarely found in healthy people. The disadvantage of D-dimer testing is that it is neither specific (many other conditions cause elevation) nor sensitive (because up to 50% of patients with a small PE have normal results.

Spiral (helical) CT scan (also known as CT angiography or CTA)

is the most common test to diagnose PE. The scanner continuously rotates around the patient while obtaining views or (slices) of the pulmonary vasculature. It then is reconstructed by the program to view a 3D reconstruction of the patients lungs to view the PE. ***This test requires an IV injection of contrast media*** in order to view the pulmonary blood vessels. So, you must check to see if the patient is allergic to the contrast dye before performing this test.

Clotting

refers to a physiological process in which blood is converted from a liquid to a semisolid gel.