Venous Thromboembolism (VTE)

Formation of thrombus along with inflammation of a vein

1.Superficial Vein Thrombosis (SVT)
2.Deep Vein Thrombosis (DVT)

Signs & Symptoms

click to edit

-If SVC involvement = arms, neck, back, face involved
-If IVC involvement = bilateral swelling and cyanosis
-systemic temperature >100.4 F
-unilateral leg edema
-pain
-tenderness with palplation
-dilated superficial veins
-sense of fullness in thigh or calf
-paresthesias
-warm skin
-erythema

Health Promotion

Community
-Avoid oral contraceptives
-Drink adequate fluids to avoid dehydration
-Exercise legs during long periods of bedrest or sitting.
Inpatient Setting
-Patient education
-Leg exercises
-Early ambulation
-Adequate hydration
-Graduated compression stockings
-Intermittent pneumatic compression, such as sequential compression devices (SCDs)
-Venous plexus foot pump

Complications

DRUGS
✅
3 main types
⭐1. Anticoagulants
⭐2.Thrombin inhibitors direct/indirect
⭐3. Factor Xa inhibitors**


Anticoagulants

Factor Xa inhbitors: Subq/PO These cause rapid anticoagulation
Routine ✏ coagulation tests NOT req'd.
Used ⭐ for VTE prophylaxis & treatment, surgical 6hrs prior to surgery
May ⚠ cause thrombocytopenia
If excess bleeding give factor VIIa
No antidote
Rivaroxaban ( XARELTO)- oral used for VTE prevention
Fondanaprinux (ARIXTRA)
VTE prophylaxis- if pt in hospital and not bleeding : GIVE low dose UH,LMWH or fondaparinux
Some pts required VT prophylaxis only while in hospital – if orthopedic surgery – 35 day spost surgery cont.

Anticoagulants: DO
Prevent VTE prophylaxis
Prevent new clot formation or spread & emboli
They ⚠ DONOT dissolve a clot!clot lysis done by intrinsic fibrinolytic system

Vitamin K antagonist (VKA)> such as: warfarin- takes 2-3days to show effect...Then more time to achieve effect. Therefore, IV UH or LMWH and warfarin is reqd for 5 days
✏ Monitor INR (other way of reporting PT ) have vit K avail (Kcentra)


Thrombin inhibitors- direct/indirect


INDIRECT
2 major kinds UH/LMHW
1.(UH) Unfractioned heparin admin as IV cont infusion or SubQ
Brand: (Hep-Lock, Liquaemin, Calciparine)
IV heparin: monitor ✏ aPTT.Have antidote avail protamine sulfate to reverse excess bleeding if needed
Caution: ⚠ Serious S.E. is HIT- immune reaction to (pt develops antibodies for heparin in blood ) Reduction in platelets results STOP 🚩 Heparin. Give non-heparin anticoagulant. Other SE osteoporosis
2.LMWH- Better choice- longer half-life, predictable response, less bleeding complications or SE. ❤ Does not require continuous level monitoring and dose adjustment. Protamine sulfate- neutralizes effect. 🖊 Do not expel air bubble on admin.
Low molecular weight heparin (LMWH) brands
*Enoxaparin (LOVENOX)
Tinzaparin (INNOHEP)
Daltaparin (FRAGMIN)
Nadroparin(FRAXIPARINE)

1.Pulmonary Embolism

2.Post-Thrombotic Syndrome (PTS)

-results from chronic venous hypertension caused by valvular destruction from inflammation and scarring, stiff noncompliant vein walls, persisten venous obstruction

S&S - pain, heaviness, aching, swelling, cramps, itching, tingling, persistent edema, increase pigmentation, ecxema, secondary variscosities, lipodermatosclerosis, venous ulcerations

Begins 2 years after VTE
Risks - leg symptoms 1 month after VTE, recurrent VTE, obesity, older age, female

  1. Phlegmasia cerulea dolens

may develop in pts with advance stages of cancer, resulting from severe VTE with near-total venous flow occlusion

-massive swelling, deep pain, intense cyanosis of extremtity
-can lead to gangrene, amputation

Thrombin Inhibitors *DIRECT
Given IV or SubQ- Used in pt’s with HIT that need anticoagulants.
Measure ✏ ACT/aPTT for therapeutic effect 1) lepidurin(REFLAN)
2) bivalirudin (ANGIOMAX)
3) desidurin(IPRIVASK)
no ❌ antidote
Synthetic forms: IV/subQ
1)argatroban (ACOVA)
2)Dabigatran (PRADAXA)
Measure ✏ aPTT
Used mainly for VTE prevention and in joint repl surgery or A-fib stroke prevention
used in pt with risk for HIT .
NO ❌ antidote

ANTICOAGULANTS FOR: VTE

LMWH,UH such as:
Rivaroxaban ( XARELTO)
Fondaparinux (ARIXTRA
Oral VKA started and continues for 3 months
INR ✏ goal : 2-3

THROMBOLYTIC THERAPY – for VTE prophylaxis
If pt has a thrombus already: thrombolytic drug Given via catheter (drugs urokinase, Tpa)-DISSOLVES CLOT

Diagnostic Studies ✅

click to edit

Blood Laboratory Studies: -ACT, aPTT, INR, bleeding time, Hgb, Hct, platelet count: alteration if patient has underlying blood dyscrasias (ex. polycythemia)
-D-dimer: Elevated results suggest VTE >250mcg/L
-Fibrin monomer complex: forms when concentraiton of thrombin exceeds antithrombin. Normal <6.1mg/L

Noninvasive Venous Studies:
-Venous Compression ultrasound: Veins fail to collapse with application of external pressure.
-Duplex ultrasound: veins examinated for respirator variation, compressibility, and intraluminal filling defects

Invasive Venous Studies:
-Computed tomography venography: uses spiral CT to evaluate veins in pelvis, thighs, and calves after injection of venous phase contrast material
-Magnetic resonance venography: can be done with or without contrast. Highly accurate for pelvic and proximal veins.
-Contrast venography (phlebogram): X-ray determination of location and extent of clot using contrast media to outline filling defects.

Collaborative Care: ❤

click to edit

Prevention and Prophylaxis:
-Patients on bedrest: change position q2h
-Flex and extend feet, knees, and hips q2-4h
-Ambulate at least 4-6 times per day as tolerated
-Elastic compression stockings: worn properly and consistently
-Sequential compression devices: Not worn when patient has active VTE

Surgical Therapy:
-Venous thrombectomy: removal of thrombus through incision in the vein. (anticoagulant therapy recommended after surgery)
-Vena cava interruption devices (ex. Greenfield, Vena Tech,TrapEase filters): inserted percutaneously through the right femoral or right internal jugular veins. Permits filtration of clots without interruption of blood flow.
*Over time, venous congestion can occur from buildup of trapped clots.

Drug Therapy

incidence
-highest incidence in patients who have undergone hip surgery, total knee replacement or open prostate surgery

Etiology
Table 38-8 Lewis pg 848
1) Venous Stasis
2) Damage of endothelium
3) Hypercoagulabiltiy

Pathophysiology
localized platelet aggregration and fibrin entrab RBCs, WBCs, platelets


thrombus enlarges-increased number of blood cells and fibrin collect behind it


eventually blocks lumen of vein


if thrombus does not detach-undergoes lysis or becomes firmly organized


may detach and become embolus