NS2P2 Peripheral Vascular Disease: Part 2 Venous

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NS2P2 Peripheral Vascular Disease: Part 2 Venous
2015-05-14 03:18:29
Heart Cardiac NS2 NSP2 Michelle Vascular

( Module 2.4 NS 2 part II)
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  1. **Venous Vascular Disorders
    • => Acute Venous Disease
    • Superficial vein thrombosis (SVT)
    • Venous Thromboembolism (VTE): Deep vein thrombosis (DVT) & Pulmonary embolus (PE)

    • => Chronic Venous Disease
    • Varicose veins
    • Chronic venous insufficiency (CVI)
    • Venous stasis ulcers
  2. **Venous Thrombosis
    Formation of thrombus in association with inflammation of a vein

    Can occur in superficial or deep veins (illiac and femoral-greatest concern--can break off and go straight to longs)

    • => Three important etiological factors (Virchow’s Triad):
    • Venous stasis
    • Endothelial damage
    • Hypercoagulability
  3. **Virchow’s Triad: Venous Stasis (first Factor)
    Unidirectional flow of blood is impeded : pooling of blood, usually in lower extremities

    Occurs when venous valves are dysfunctional or extremities are inactive (bed-[rest. Calf muscle pumps blood back to heart. Plane flights for long increases risk)

    • => Venous stasis allows for
    • More time for blood to clot since it's just sitting there
    • Increased blood viscosity: Dehydration will worsen thisSmall clots not “washed” away (which occurs with motion, but no motion means they'll just get bigger

    • => Who’s at risk?
    • Pregnant: hypercoagubility and pospartum bed rest and inactivity. "Milk Leg" because they'd have swollen leg three days within post-partum
  4. **Virchow’s Triad: Endothelial damage (second factor)
    The smooth delicate inner lining of muscles get injured (from smoking, htn)

    Endothelial injury attracts platelets and stimulates the intrinsic clotting pathway

    • => Caused by:
    • Accidental and surgical trauma
    • Fractures and burns
    • IV therapy--irritating to the veins (especially high-dose antibiotics, potassium, chemo agents)
    • Recreational IV drug use
    • Diabetes, vasculitis, sepsis
  5. **Virchow’s Triad: Hypercoagulability of the blood
    Blood is predisposed to clot; imbalance of clotting factors

    Can be due to inherited or acquired factors

    Factor V disease: a mutation of one of the clotting factors in the blood called factor V. This mutation can increase your chance of developing abnormal blood clots (thrombophilia), usually in your veins. Most people with factor V Leiden never develop abnormal clots.

    Other issues: thalassemia

    • => Occurs in many hematological disorders
    • Severe anemias
    • Polycythemia: too viscous due to too many RBCs
    • Various malignancies: cancer=Hypercoagulble: makes plts stickier.Clotting disorders

    • => Other causes include
    • Systemic infections
    • Dehydration
    • Smoking
    • Estrogen-based oral contraceptives and HRT
    • women over 35 who smoke and take contraceptives are at high risk
  6. **How many risk factors?73 y/o obese male with colon cancer who is one day s/p hemicolectomy. He has a PICC line and his last chemotherapy treatment was several weeks ago
    • -Venous stasis: age, immob, obesity
    • -Endothelial damage: surgery, PICC line, chemo

    -Hypercoag: cancer
  7. **How many risk factors?Athlete in 30s had recent foot surgery that required casting and that developed a hematoma. Took an airplane across country. Collapsed from a PE shortly after flight.
    -Venous Stasis: long flight, surgery, immob, casting (decreased circ), dehydration
  8. **Venous Thrombosis & Clinical Manifestations
    -Normal blood flow through a vein: valves stop backflow

    -Early development of a thrombus: : sitting and not going anywhere. If it breaks off--> Pulmonary embolism D:

    • => Clinical Manifestations
    • Vary according to:
    • Size
    • Location of thrombus
    • Adequacy of collateral circulation
  9. **Superficial Vein Thrombosis (SVT): Risks & Manifestations
    • => Risk Factors
    • Upper extremities- IV therapy and IV drug use
    • Lower extremities- varicose veins

    • => Clinical Manifestations
    • the veins feels Palpable, firm subcutaneous cord-like vein (like scar tissue, phlebitis)
    • Area surrounding the vein may be tender to touch, reddened, and warm
    • Mild systemic temperature
    • Edema of extremity may or may not occur
  10. **Collaborative Care: SVT
    • DC/Change site of IV Elevation and HEAT of affected extremity
    • NSAIDS (?)
    • I&D (if there's an infectious agent or abscess), antibiotics w/ infectious SVT
    • Anticoagulation w/ SVT of greater saphenous vein (hep or coum)
    • Anti-embolism stockings or sleeves, exercise, risk factor modification upon discharge SCD's
  11. **Deep Vein Thrombosis
    Can occur after surgery; if it occurs--might not reimburse b/c never should have happened.

    Estimated 1-2 cases of VTE per 1000 people yearly

    60-100K people die yearly from VTE Highest risk: surgical and orthopedic patients > 40 (they don't wanna get out bed post op, risk factors for clotting)

    VTE prophylaxis is a core measure for hospitalized patients ½ will have long term complications

    1/3 will have a recurrence within 10 years

    • => Risk Factors
    • Age > 40
    • Obesity
    • Recent surgery or injury
    • Use of estrogen-containing medications
    • Pregnancy and postpartum period
    • Personal or family history of blood clots
    • Active cancer or recent treatment
    • Smoking
    • Limited mobility (cast, etc)
    • Varicose veinsProlonged travel
  12. **DVT: Clinical Manifestations
    • May be asymptomatic
    • S/S are nonspecific

    • => May present with
    • Unilateral leg edema, erythema "red warm unilateral extremities"
    • Lower extremity pain
    • Low grade temperature
    • Tenderness to palpation
    • Homan’s sign-positive. No longer considered definitive.
  13. **DVT Prevention
    • => Lifestyle changes
    • Smoking cessation
    • Avoidance of obesity and physical inactivity (long periods of sitting/standing; avoid crossing legs)
    • Measures to promote venous return

    => Early and frequent mobilization: Ambulation day of surgery or POD #1

    • => TED hose-Thrombo-Embolic Deterrent/SCDs-Sequential Compression Device (shouldn't be loose)
    • -address all three of virchow's triad:
    • -compression: prevents stasis and decreease venous distension--> decrease venous endothelial damage
    • -increased blood velocity enhances natural fibrolysis; breaking down and washing away those small clots.

    => Prophylactic anticoagulant therapy: lovenox
  14. **DVT: Acute Management
    Continuous IV UH (unfractionated Heparin) therapy or SQ UH/LMWH therapy followed by oral anticoagulation (like coumadin)

    -lovenox preferred (hep is 3x day) and better on kidneys..

    - coumadin takes longer for blood levels to reach therapeutic levels

    Bed rest with extremity elevated

    Assessment of affected area q shift

    Anticoagulation precautions

    Pain relief

    Patient education; monitor for bleeding, avoid unecssary IV sticks, no IM, soft tooth brush, electric shaving, avoid falls, brain bleed?

    -lab monitoring for hep (ptt Q6)
  15. **Unfractionated Heparin

    Indirect thrombin inhibitor; BODY BREAKS DOWN CLOT, NOT THE MEDICATION

    poorly absorbed through GI tract so IV and SubQ

    Affects both the intrinsic and common clotting pathways

    Used for prophylaxis or treatment of DVT

    • Doses:
    • -Prophylactic dose is 5000 units SQ every 8-12 hrs
    • -Treatment dose based on PTT resultsAvailable SQ and IV only

    Antidote available: PROTAMINE SULFATE 1 mg usually (IV push)

    Side effects- HIT and bleeding

    normal PTT: 25-35; we shoot for 1.5-2.5x baseline for therapeutic (so 45-75)
  16. **Heparin Therapy SQ
    • Administer deep SQ
    • Use ½ or 5/8 inch needle, 25 or 27 gauge
    • Pinch up the skin, inject at 90 degree angle
    • Administer at least 2 inches away from umbilicus
    • Do not aspirate or massageRotate sites
  17. **Heparin Therapy IV
    Always infuse heparin on an infusion pump (NEVER with gravity)

    loading dose to get drug up to therapeutic level (IV push)

    Standard concentration is 50 units/ml: 25,000 units/500 ml D5W

    Hospital policy- 2 RNs to check dosage

    Keep the pump locked

    Loading dose and then continuous infusion

    • => Changes in rate usually made by RN based on lab results (standing order)
    • PTT usually obtained q6
    • Infusion may be temporarily halted, decreased, or increased based on results
  18. **Heparin-Induced Thrombocytopenia (HIT): TYPE 2
    Two types: Type 1: asymptomatic that resolves after stopping heparin (more autoimmune)

    HIT (Type II) is an immune response to heparin therapy

    Develops 5-14 days after initiation of heparin therapy

    • =>Characterized by
    • Thrombocytopenia: sudden decrease iin plts
    • Hypercoagulability:Thrombosis

    =>Diagnosed by presence of heparin antibodies; so the body is just developing an immune response to heparin. Suspect if Platelets is <100 or drop of 30-50% from baselinne while on therapy-DVT, PE, skin lesions

    • ==Pathophysiology of HIT==
    • Heparin forms complex with platelet factor PF4
    • IgG antibodies are produced and bind w/ complex

    • =>Immunocomplex binds to platelet surface causing
    • Platelet activation and aggregation
    • Further PF4 release
    • Increased platelet activation and further stimulation of coagulation cascade

    • =>Risk factors
    • IV use (hep)
    • Longer duration of use
    • more common in UFH>LMWH
    • Surgical patient
    • Female

    • =>Signs/ Symptoms
    • Acute systemic reaction after IV bolus: fever chills dyspnea flushing
    • Skin lesions at injection sites: blistering and superficial necrosis, Limb tissue ischemia
    • S/S acute thromboembolism
    • Skin Necrosis and HIT
    • No acute bleeding like in thrombocytopenia, not common
    • Notify provider immediately
    • Discontinue all sources of heparin even flushes
    • Start patient on alternative anticoagulant: Argatroban (Acova) IV drip
    • Warfarin may be started once platelets are stabilized Heparin contraindicated for future use
  19. **Enoxaparin (Lovenox)
    • =>LMWH: Advantages
    • Greater bio-availability
    • More predictable response and longer half life than heparin
    • Less risk of HIT
    • Does not require routine coagulation monitoring and dose adjustment
    • Home therapy
    • =>Disadvantages Cost

    • =>LMWH Administration
    • Prophylaxis: usually 30-40 mg SQ QD or BID
    • Max safe dose is 1mg/kg BID or 1.5mg/kg daily; Adjusted for renal patients (30 mg, not usual 40)
    • Administration techniques same as heparin; Preferred site?
    • Monitor plts
    • rotate sites!
    • =>Adverse reactions
    • Epidural/spinal hematomas
    • Bleeding
    • HIT
  20. **Vitamin K Antagonists: Warfarin (Coumadin)
    widely used anticoagulant

    Inhibits activation of vitamin-K dependent coagulation factors (II, VII, IX, X)Affects the extrinsic pathway

    Available PO only Takes several days to achieve therapeutic effect thus other anticoagulant used to bridge for >4 days (lovenox to coumadin bridge)

    Monitored w/ daily INR until target value reached and adjust dose. Requires ongoing monitoring.Target INR: 2-3. Can be higher in mechanical heart valves (3-4). Greater than 4. HOLD--contraindicated for bleeding

    Antidote available
  21. **Warfarin Therapy
    Starting dose often 5 mg PO QD (same time every day); usually given in evening so they can check INR in morning (takes that long to affect the blood)

    Dose adjusted until target INR reached

    SE: bleeding

    • =>Drug response depends on
    • Genetic factors
    • Liver function
    • Medication use
    • Vitamin K intake

    diet education: keep K STABLE. spinach is okay, stable from day to day
  22. **Other Anticoagulant Options
    • =>Direct Factor II (thrombin) inhibitors
    • Dabigatran (Pradaxa)- prophylaxis with a. fib
    • Argatroban (Acova)- alternative for HIT --most common
    • Monitor w/ PTT
    • No antidote for bleeding
    • Decrease dose in inefficient renal fuction

    • =>Factor X inhibitors
    • Apixiban- prophylaxis with a. fib
    • Rivaroxaban (Xarelto)- VTE prophylaxis and treatment--newest PO

    • Fondaparinux (Arixtra)- VTE prophylaxis and treatment subQ. Not too commonNo routine monitoring; can check assays (coagualtion)
    • Recombinant factor VII-a may be useful for bleeding (?)Antidote currently being studied
  23. **DVT: Additional Treatment Options
    =>Thrombolytic Therapy: Catheter-directed thrombolytics (put in cath to where clot with TPA)pts musst be medically stable

    =>Venous thrombectomy: go in and take out thrombus

    =>Vena Cava Interruption DeviceInferior Vena Cava (IVC) filter--little umbrella deployed into vena cava vein to catch future clots. Eventually replaced because they do get clogged up. Filter device “umbrella”
  24. ** Pulmonary Embolus (PE)
    DVT that travels to lungs

    Blockage of an artery of the lungs (clot travels yhrough IVC to R side of heart -> logged in pulmonary artery so areas of lungs not getting perfusion. Caues aveolar dead space in lung. VQ mismatch!)

    "Feeling of doom" prior to PE, and lots of anxiety.

    • Most common cause: lower extremity DVT
    • Less common causes include air or fat emboli, septic emboli (clot of infectious material), tumors, parasites
    • Common cause of death in hospitalized patients
    • Second most common cause of sudden death-
    • -10% die within the first hour
    • --Only symptom in 25% of patients

    10-30% die within one month of diagnosis

    can come from R side of heart, upper ext and pelvic pain

    reoccurence common in ppl that have these complications

    =>Pulmonary Circulation

    • => Clinical Manifestations
    • Anxiety, feeling of doom
    • Sudden respiratory distress, dyspnea (can be progressive) or hematological collapse: weak pulse, pallor and HTN
    • Tachypnea
    • Tachycardia
    • Cough
    • Pleuritic chest pain: pain with deep breaths
    • Hemoptysis: cough blood
    • Crackles
    • Fever

    Sudden change in mental status
  25. ** PE: Diagnostics & Collaborative Care
    •  Diagnostic Studies
    • Spiral (helical) CT with contrast
    • Pulmonary angiogram
    • Ventilation Perfusion (V/Q) Lung scan
    • Plasma D-dimer

    • =>Additional diagnostics
    • Venous Ultrasound
    • ABGs
    • CXR
    • EKG

    • **PE: Collaborative Care
    • Supportive measures
    • Bed rest in semi-Fowler’s position
    • Pain relief
    • Anticoagulation therapy
    • Thrombolytic therapy
    • =>Surgical intervention
    • Embolectomy
    • IVC Filter insertion
  26. **Varicose Veins (Varicosities)
    Dilated or tortuous subcutaneous veins frequently found in saphenous system; lower extremities. testicular varices.

    found with Incompetent venous valves (does'nt keep blood flow from going back so increase in venous distension

    • => Risk factors
    • Females Previous DVTChronic cough Prolonged standingConstipation ObesityAge Pregnancy
  27. **Varicose Veins & Collaborative Care
    • Most common symptom:Heavy, achy feeling or pain after prolonged standing, Relieved by walking/elevation
    • Swelling
    • Nocturnal leg cramps
    • SVT most common complication
    • Diagnosed by appearance/ ultrasound

    • =>Collaborative Care
    • Lifestyle Changeslong term compression treatments: wearing tedhose every day
    • =>Sclerotherapy Injection of sclerosing agent into target vein
    • Noninvasive, outpatient procedure
    • =>Laser or Pulsed Light Therapy
    • Vein sclerosis due to heat
    • Multiple treatments required
    • Costly

    • =>Surgical ligation or endovenous ablation
    • High recurrence rate
  28. **Ligation and Stripping of Varicose Veins Surgery Video
    General anesthesiatwo cutes: near groin and kneeClamp varicose vein, cut it at two ends, pass wire through vein and pulled out "stripping"
  29. **Chronic Venous Insufficiency (CVI)
    • Chronic, inadequate venous return, often seen in elderly
    • Occurs secondarily to previous VTE, varicose veins, incompetent valves
    • Predisposes patient to venous stasis ulcers

    • =>Pathophysiology: CVI
    • Incompetent Valves-- diseased vein valve
    • Increased hydrostatic pressure in veins leading to Edema and RBC destruction (brownish discoloration-hemosiderin)
    • Fibrosclerotic remodeling (thick, hard skin)
    • Finally--Ulceration.

    • => Clinical Manifestations
    • Leathery, brawny skin
    • Prolonged edema
    • Stasis dermatitis
    • Chronic, achy, dependent pain

    • =>Venous stasis ulcers
    • Very painful
    • Located above malleolus
    • Weeping wound

    => can occur with Cellulitis andcause secondary lymphedema
  30. **CVI: Collaborative Care
    • =>Compression is Essential
    • Custom-fitted graduated compression stockings
    • Elastic tubular bandages
    • SCDs
    • Velcro Wraps
    • Unna Boot
    • Multi-layer bandages (meticulus skin care!!)

    • =>Moist wound environment dressings
    • Hydrogels, hydrocolloids if areas of necrosis
    • Calcium alginates for bleeding, heavy exudate
    • Collagen dressings w/ epithelialization

    • =>Nutritional support
    • High in protein, Vitamin C, zinc

    • =>Treatment of infection
    • Wound culture
    • Topical or systemic antibiotics

    • =>Debridement of exudates and fibrous tissue
    • Skin grafting with severe wounds
    • Hydrogel
    • Calcium Alginate dressing
    • Maggot Therapy: biochem debriedment to clean up dead tissue.
    • medihoney: ointment, bacteriocidal

    • => Long-term care:
    • Education
    • Leg and foot careCompression hoseNutritionExerciseElevation at rest
  31. **Nursing Diagnoses: VTE and CVI
    Acute pain r/t venous congestion and impaired venous return

    Risk for impaired skin integrity r/t altered tissue perfusion

    Impaired skin/tissue integrity

    Ineffective tissue perfusion r/t venous insufficiency

    Risk for injury r/t alteration in blood clotting

    Ineffective health maintenance r/t lack of knowledge about prevention/management
  32. **Differentiating characteristics of PAD and CVI
    • =>Arterial
    • Skin color: dependent rubor or elevation pallor
    • Temperature is cool
    • No edema
    • Pulses decreased or absent
    • Hair loss on feet, lgs and toes
    • Nails thickened and brittle
    • Cap refill >3sec.
    • Pain: intermittent claudication or rest pain, ulcer may or may not be painful

    • =>Venous
    • Skin color: bronze
    • Temperature is warm
    • Lower leg edema
    • Pulses present but difficult to palpate
    • Hair absent or present
    • Nails are normal or thickened
    • Cap refill <3sec.
    • Pain: dull ache or heaviness in calf or thigh, ulcer is very painful
  33. **Differentiating Characteristics of Arterial and Venous Ulcers
    • => Arterial ulcers
    • Location-pressure points over bony prominences
    • Margins- round smooth, looks “punched out
    • ”Skin characteristics: Texture is thin, shiny, friable, dry

    • =>Venous ulcers
    • Location-near medial malleolus
    • Margins- irregular shapes
    • Skin characteristics: Texture is thick, indurated, w/ brownish discoloration