peripheral vascular disease
Download
Skip this Video
Download Presentation
Peripheral Vascular Disease

Loading in 2 Seconds...

play fullscreen
1 / 78

Peripheral Vascular Disease - PowerPoint PPT Presentation


  • 599 Views
  • Uploaded on

Peripheral Vascular Disease. Arterial/Venous: Acute/Chronic. Peripheral Vascular Disease. A term used to describe a group of diseases that involve pathophysiological changes in the “peripheral” arteries (i.e., excluding the coronary arteries) or veins resulting in blood flow disturbances.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about ' Peripheral Vascular Disease' - dougal


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
peripheral vascular disease

Peripheral Vascular Disease

Arterial/Venous: Acute/Chronic

peripheral vascular disease1
Peripheral Vascular Disease
  • A term used to describe a group of diseases that involve pathophysiological changes in the “peripheral”arteries (i.e., excluding the coronary arteries) or veins resulting in blood flow disturbances.
lymphatic disorders also considered a form of pvd
Lymphatic disorders (also considered a form of PVD)

Lymphatic system (ducts and nodes)

  • plays a role in filtering foreign particles
  • provides the only means by which interstitial proteins can return to the venous system (if blocked, obstructed [or *removed], edema may develop with risk of infection)
raynaud s disease
Raynaud’s Disease
  • characterized by bilateral intermittent arteriolar vasoconstriction/vasospasm in the hands and feet, often precipitated by emotional factors, cold, tobacco, causing color (white to blue to red) and temperature changes as well as burning pain in affected digits
  • is usually associated with underlying systemic disease (e.g., autoimmune disorders)
  • unlike other acute arterial disorders Raynaud’s is, with proper management (e.g., avoidance of triggers), essentially benign and self-limiting
management
Management
  • Thought to be vasospasm resulting from an exaggerated response to SNS stimulation
  • calcium channel blockers (i.e. nifedipine (Adalat), diltiazem *Cardizem) may be used)
  • Prevention
    • avoid/manage stress
    • avoid exposure to cold/cold H20
    • avoid nicotine, caffeine, drugs that elicit a vasoconstrictive effect
    • safety precautions
acute arterial insufficiency acute arterial occlusion
Acute Arterial Insufficiency(Acute Arterial Occlusion)
  • usually involves complete blockage, is of sudden onset, and constitutes an emergency situation (muscle necrosis within 2-3 hours)
  • etiologies include:
    • arterial compression
    • thrombosis/embolism
    • arterial injury/damage
  • Risk factors
    • nonmodifiable; modifiable

Risk factors:

Age

Gender (male)

Family history

Modifiable risk factors:

Hypertension

Diabetes

Hyperlipidemia

Smoking

Obesity

thrombosis
Thrombosis
  • The formation of a blood clot within a blood vessel
  • Can occur in the arterial or venous systems
  • Leads to obstruction of a blood vessel in the circulatory system
  • Can lead to ischemia and infarction, and even death
  • Can also lead to embolism
    • Clot within a vessel breaks free and travels through body (“embolizes”)
    • Thromboembolism is combination of a thrombosis and embolus
why does this happen
Why does this happen?
  • Hemostasis
    • Formation of blood clot formation at the site of vessel injury
    • Carefully regulated system
      • Involves platelets and coagulation factors
    • Lack of coagulation factors  bleeding
    • Overactive coagulation cascade  thrombosis
arterial thrombosis
Arterial thrombosis

(ie. ischemic limb)

what are the features of an acute ischemic limb

Fixed mottling & cyanosis

What are the features of an acute ischemic limb?

REMEMBER THE 6 P’S:

  • PAIN
  • PALLOR
  • PULSELESNESS
  • PERISHING COLD (POIKILOTHERMIA)
  • PARASTHESIAS
  • PARALYSIS

excruciating pain

color pale or cyanotic

may be pulseless

skin cool to touch

loss of sensation/ position sense

loss of movement

chronic arterial insufficiency peripheral arterial disease
Chronic Arterial Insufficiency(Peripheral Arterial Disease)
  • primarily caused by atherosclerosis,disrupting the balance between arterial oxygen supply and demand
  • risk factors same as for CAD, with diabetes, HTN, and smoking as particularly high risk factors(see Table 40-3 Collaborative Care: Peripheral Arterial Disease
peripheral arterial disease
Peripheral Arterial Disease
  • Thickening of artery walls
  • Progressive narrowing of the arteries of the upper and lower extremities
  • resulting in  tissue perfusion and ischemia in the area distal to the obstruction
  • may be acute or chronic
risk factors
Risk Factors
  • Typical Patient:
  • Smoker (2.5-3x)
  • Diabetic (3-4x)
  • Hypertension
  • Hx of Hypercholesterolemia/AF/IHD/CVA
slide14

Patients at risk — Based in part upon the above observations, the 2005 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on PAD, which were produced in collaboration with major vascular medicine, vascular surgery, and interventional radiology societies, identified the following groups at risk for lower extremity PAD

  • Risk Factors:
  • Atherosclerosis (same as RF’s for CAD and CVD)
  • Smoking (2.5-3x)
  • Diabetes 3-4x
  • Hypertension, increased age >50, male and family history
  • RARE: homocysteinuria
peripheral arterial disease1
Peripheral Arterial Disease
  • one limb is usually affected more than the other, therefore always compare bilaterally
  • lower limbs more susceptible than the upper limbs
  • most common locations for stenosis are the aortoiliac bifurcation and the femoral bifurcation
  • nearly half of the clients with arterial PVD have associated CAD
clinical manifestations
Clinical Manifestations
  • intermittent claudication (pain in calf, thigh, or buttock depending on the location of the blockage)
  • rest pain in forefoot especially at night (advanced disease)
  •  capillary refill
  • elevational pallor
  • dependent rubor
  • “pins & needles” sensation (paresthesia, due to ischemia)
  • affected limb cool to touch
peripheral arterial disease2
Peripheral Arterial Disease
  • weakened or diminished pulses
  • chronic trophic changes
    • thin, shiny, dry or scaling skin with hair loss
    • thick, yellow, & brittle toenails
    • muscle atrophy
  • ulceration (*arterial), gangrene possible
  • bruit
  • Erectile dysfunction (e.g., aortoiliac disease)
  • *please note the differing characteristics of arterial and venous ulceration in course text (Table 40-2)
slide20

ULCER

  • associated with claudication + signs of ischaemia
  • occur on dorsum of foot + anterior skin
  • ↓ pulses, cold to touch, hairless skin
  • Painful, punched out edge
diagnosis
Diagnosis
  • history (symptoms & presence of risk factors)
  • physical exam (signs)
  • doppler assessment of peripheral pulses
  • ankle/brachial index [ABI] (normal is ~1)
    • see p. 1015
  • treadmill (exercise testing)
  • angiography (necessary before any surgery)
slide23

ABI Clinical Correlation

  • >0.9
  • Normal Limb
  • 0.5-0.9
  • Intermittent Claudication
  • <0.4
  • Rest Pain
  • <0.15
  • Gangrene (BP higher in ankle than arm)
slide25

Take the highest measurement in both limbs

  • low ABI is also predictive of an increased risk of all-cause and cardiovascular mortality and of the development of coronary artery calcification
  • 95% sensitive in detecting angiogram positive disease and around 99% specific in identifying supposedly healthy subjects
goals of management
Goals of management
  • reduce progression of the disease
  • promote arterial blood flow
  • promote vasodilation
  • prevent vascular compression
  • pain relief
  • attain/maintain tissue integrity
  • promote adherence
management1
Management
  • risk reduction/reduce disease progression
    • smoking cessation
    • weight reduction
    • exercise (e.g., walking), unless contraindicated
    • reduction of blood lipid levels
      • diet (e.g., cholesterol, saturated fats and TFAs, fiber) and, in some cases, pharmacologic intervention (e.g., antilipidemeic drugs)
    • blood glucose and blood pressure control
    • antiplatelet meds
slide28

promote arterial blood flow

    • keep lower extremities below the level of the heart (e.g., reverse trendelenburg position)
    • encourage, or assist with, walking or graded isometric exercise to increase collateral circulation (*if not contraindicated)
    • avoid prolonged standing or sitting in one position
    • pharmacologic therapy
      • Inhibit platelet aggregation
slide29

promote vasodilation and prevent vascular compression

    • apply external warmth (e.g., socks, warm bath, or warm drink), promoting tissue perfusion
      • NEVER APPLY DIRECT HEAT AS IT MAY CAUSE A BURN
    • prevent exposure to cold and chilling
    • avoid crossing legs/constrictive clothing and accessories
    • smoking cessation
    • minimize stressful situations
slide30

pain relief

    • analgesics (opioids)
  • maintain tissue integrity
    • prevent infection/injury/trauma
    • meticulous foot care
    • well-balanced diet that includes adequate protein
    • attain and maintain ideal weight
  • Promote self care
    • patient/client education
surgical radiological management
Surgical/Radiological Management
  • Management depends on the etiology and may include:
    • embolectomy
    • revascularization
    • anticoagulation
    • fibrinolytic agents
    • amputation
  • Prevention best
    • know those at risk and monitor them closely
slide32

percutaneous transluminal angioplasty (PTA) with stent insertion (e.g., isolated lesion)

  • endarterectomy (e.g., carotid artery)
  • thrombolytic therapy (acute emboli/arterial graft occlusion)
  • arterial bypass (vascular) grafting (e.g., femoral-popliteal graft using saphenous vein)
  • followed by anticoagulation/antiplatelets
  • amputation (in presence of gangrene)
venous disorders
Venous Disorders
  • Acute Venous Disorders
    • superficial thrombophlebitis
    • thrombophlebitis/deep vein thrombosis (DVT)/PE
  • Chronic Venous Disorders
    • varicose veins
    • chronic venous insufficiency
venous thromboembolism
Venous thromboembolism

Deep vein thrombosis

Pulmonary embolism

venous thromboembolism1
Venous thromboembolism
  • Deep venous thrombosis
    • Blood clot in the proximal veins of the leg
    • Less commonly in the arms
    • Symptoms include:
        • Pain (never massage)
        • Swelling (calf circumference)
        • Redness
        • Warmth
        • PE could be first manifestation!
        • Above affecting one limb (unilateral)! Most common in lower extremities
slide38

most common in the lower extremities

  • 50% may be asymptomatic
  • unilateral swelling distal to the site (elevated venous pressure from venous pooling pushes fluid into interstitial spaces creating edema) *[may need to measure circumference]
  • *pain on dorsiflexion (Homan’s sign) is present in less than 1/3 and is no longer considered a valid sign for DVT
  • tenderness to palpation of calf (never massage!)
  • redness or warmth of the leg
  • dilated (prominent) veins
  • low-grade fever
  • unfortunately, pulmonary embolism may be the first clinical manifestation for some
venous thromboembolism2
Venous thromboembolism
  • Pulmonary embolism
      • Blood clot (from DVT) breaks off
      • Travels to lung
      • Can lead to infarct
      • Symptoms:
          • Chest pain
          • Shortness of breath
          • Lightheadedness (low BP)
          • Syncope
          • Hemoptysis
      • Can be life threatening!
pulmonary embolism
Pulmonary embolism
  • Untreated PE
    • Mortality rate of ~30%1
    • Most die within hours of diagnosis
  • Treated PE
    • Prospective NEJM study looked at 399 patients with newly diagnosed PE
    • 94% received conventional treatment
    • Only 2.5% (10 patients) died of PE
  • Treatment of PE is life-saving!
venous thromboembolism3
Venous thromboembolism
  • Incidence estimated at 1-2 in 1000
  • Known predisposing conditions – Virchow’s triad:

Venous stasis

Alterations affect the balance between bleeding and clotting

Vessel wall injury

Hypercoagulability

slide43

Venous stasis: immobility or absence of calf muscle pump, paralysis, stroke, anesthesia, immobility due to bedrest, prolonged travel, obesity, pregnancy, restrictive clothing, reduced blood flow, CHF, shock, vasodilation

  • Hypercoagulability: abrupt withdrawal from anticoagulants, accompanies some malignant neoplasms (especially visceral and ovarian tumors), dehydration, blood dyscrasias (e.g., polycythemia vera), sepsis, use of oral contraceptives (especially in combination with smoking), HRT
  • Vessel wall injury: physical/traumatic or chemical irritation to the vein (e.g., IV insertion/ IV medications & solutions), fractures and dislocations (e.g., hip), severe blows to an area, diseases of the vein, abdominal, pelvic, hip, or knee surgery
venous thromboembolism4
Venous thromboembolism
  • Risk factors:
    • Recent surgery (OR:25 (10-50)
    • Immobility
    • Trauma
    • Hormones (OCP’s, HRT)
    • Pregnancy
    • Previous DVT/PE
    • Family history
    • Cancer
    • Be aware of a “perfect storm”

Thromboprophylaxis is effective, and every inpatient should be risk-stratified….this includes nurses asking the questions!!!!

slide45

previous DVT (must identify high risk situations and initiate prophylaxis, for example, LMWH)

  • thrombus formation is usually attributed to two or more factors of Virchow’s triad: venous stasis hypercoagulability injury to the venous wall
superficial thrombophlebitis
Superficial Thrombophlebitis
  • clot formation obstructing venous flow in the superficial veins
  • may be iatrogenic: IV catheters or the instillation of caustic chemicals (potent drugs like antibiotics), contrast media, TPN
  • best to prevent (e.g., central line usage, revisit the standard nursing care for a client receiving IV therapy!)
  • What do you do?

Iatrogenic: caused by medical treatment

Remove IV, elevate hand, warm, moist heat, NSAIDs, sometimes anticoagulants

medical management
Medical Management
  • anticoagulation (prevent clot formation or clot extension)
    • unfractionated heparin IV (continuous drip or intermittent infusion) or SC
    • low-molecular weight heparin (LMWH)
    • warfarin [Coumadin]
  • thrombolytic therapy
treatment of dvt pe
Treatment of DVT/PE
  • Goals of treatment:
    • Short term:
      • Prevent the extension of thrombus and embolization of DVT
      • Reduce mortality for PE by reducing recurrent events
      • Relief of symptoms
    • Long term:
      • Prevent recurrent events
treatment of vte
Treatment of VTE

General Principles

  • Parenteral heparin for minimum 5 days
  • Initiate oral anticoagulants (ie. warfarin) on day 1
  • May stop heparin once INR >2.0 for 24 to 48h
  • Consider outpatient therapy
    • No comorbidities requiring hospitalization
    • No hypoxia or chest pain
    • Need careful follow-up
heparin vs lmwh
Heparin vs LMWH

Heparin (unfractionated)

LMWH

SQ, once daily or BID

No need for routine monitoring (predictable pharmacokinetics)

More expensive

Useful

Outpatient therapy

Poor venous access

  • Needs IV admin
  • Needs aPTT testing using nomogram
  • Inexpensive
  • Useful
    • High risk for bleeding or requiring surgery
    • Renal failure
  • Antidote (protamine sulfate)
slide51

Unfractionated heparin:

  • anticoagulation effect achieved by preventing the activation of clotting factor IX and by inhibiting the action of thrombin in forming fibrin threads, drug of choice in thromboembolic disease, 4-hour half-life and, in the event of bleeding, is stopped immediately
  • contraindicated in bleeding disorders or in disorders that increase the risk of bleeding, (e.g., severe hypertension, recent neurosurgery, active GI ulcer, cerebrovascular hemorrhage, and overt bleeding from the GI, GU, or respiratory tract)
slide52

stopped once warfarin is therapeutic, dose based on weight, considered therapeutic when the aPTT is 1.5 – 2.5 times the control (normal), IV pump required for continuous infusion

  • nomogram used for dose adjustment (as well as frequency of blood work) based on coagulation parameters (e.g., aPTT)
  • LMWH:
  • Introduced in the 1980’s
  • Produced by chemically changing unfractionated heparin
  • Results in smaller molecules
  • Different properties than heparin
clotting cascade very simplified don t memorize keep learning it
Clotting Cascade (very simplified)(don’t memorize, keep learning it!)

aPTT

heparin

PT/

INR

warfarin

slide54

The coagulation cascade has two pathways which lead to fibrin formation. These are the contact activation pathway (also known as the intrinsic pathway), and the tissue factor pathway (also known as the extrinsic pathway). It was previously thought that the coagulation cascade consisted of two pathways of equal importance joined to a common pathway. It is now known that the primary pathway for the initiation of blood coagulation is the tissue factor pathway. The aPTT (Activated Partial Thromboplastin Time [APTT]) in contrast to the PT, measures the activity of the intrinsic and common pathways of coagulation.

slide55

The division of the clotting cascade into the intrinsic, extrinsic and common pathways. The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. INR, the result (in seconds) for a prothrombin time performed on a normal individual will vary according to the type of analytical system employed, INR = (patient PT/mean normal PT)ISI... International Sensitivity Index (ISI)

low molecular weight heparin lmwh
Low molecular weight heparin (LMWH)

Pros

Cons

More expensive

Patients may not like injections

Pharmacokinetics unclear is not known in certain patients (i.e. pregnancy, obesity, renal impairment)

Can’t reverse it with antidote (protamine)

  • More predictable anticoagulant response
  • Do not require lab monitoring
  • Long half-life (4-6 hours) – once daily or BID admin
  • Lower affinity for platelet factor 4, so less HIT
  • Less bleeding complications
  • Can be done at home
warfarin therapy
Warfarin therapy
  • Start with 5 to 10 mg dose, lower dose in frail or elderly patients initially
  • Check INR q 1-2 days during initial week
  • Once heparin stopped, check INR 2-3 times per week initially and aim to keep INR 2.0-3.0, this is the Target
  • Once dose stable, INR checked once weekly to monthly
  • Vitamin K antidote (po or SQ, sometimes IV)
slide58

inhibits hepatic synthesis of vitamin K-dependent clotting factors

  • therapeutic effect delayed for 3-5 days (long half- life, therefore narrow therapeutic index), therefore administered in conjunction with heparin until desired anticoagulant effect achieved
  • therapeutic effect determined by the PT (desired value of 1.5-2 times normal) & International Normalization Ratio (INR) (desired is between 2 & 3)
duration of warfarin therapy
Duration of Warfarin Therapy

Reversible Cause 3 months

Idiopathic

  • First episode Minimum 6 months
  • Second episode long term
patient and family teaching
Patient and family teaching
  • What do tell your patient so they will understand?
  • What education would they need to prevent complications?
  • New anticoagulants (i.e. direct thrombin inhibitors)
slide61

Warfarin: Oral blood thinner, For DVT/PE, goal is to prevent new clots and to prevent enlargement of existing clot, Does not break down clot, but allows for body to break down clot itself.

  • Takes about 5 days to work, Needs monitoring (INR), initially frequently (every 2 days), but as levels stabilize can be less frequent, Needs overlap with heparin initially
  • Major side effect is bleeding, No contact sports, no mountain biking, use helmets, If head injury, see doctor immediately, Tell doctor if procedure or surgery planned, Do not take ASA, NSAIDS,etc
  • Do not use in pregnancy (use birth control), teratogenic, Can be affected by other meds (antibiotics), Can be affected by diet (keep diet stable – no excess in greens, no nee to avoid completely, but don’t increase consumption dramatically)
other treatments
Other treatments
  • IVC filters
    • placed IVC, prevent large emboli, used if contraindications to blood thinners
    • complications
  • Thrombolytic therapy
    • lysis of clot, considered if risk of limb loss
    • complications
  • Thrombectomy
    • Using catheters or surgery, used in severe cases if thrombolysis unsuccessful, must foloow strict protocol
slide63

IVC: Bleeding, Venous thrombosis at insertion site, Filter migration or misplacement, Perforation of IVC, IVC obstruction due to filter thrombosis

nursing management of dvt
Nursing Management of DVT
  • promote venous return
    • elevation of the affected extremity when on bedrest, early ambulation as tolerated, elastic compression stockings applied before ambulating, calf pumping exercises
    • ongoing assessment of pain, peripheral pulses, skin color/temperature, and edema (measure calf circumference daily)
  • relieve discomfort
    • warm moist packs, mild analgesic
slide65

monitor for and manage the complications of anticoagulant therapy

    • monitor aPTT, PT, INR, platelet count (risk of heparin induced thrombocytopenia), Hgb, PCV (Hct.), monitor for signs of bleeding anywhere in the body, institute safety precautions
    • monitor for drug-drug (e.g., ASA), drug-food (e.g., foods high in Vit K), drug-natural/herbal product (e.g., ginseng) interactions that potentiate or decrease the effects of oral anticoagulants
varicose veins
Varicose Veins
  • Permanently distended superficial veins due to loss of valvular competence
  • common sites: greater and lesser saphenous veins in the leg, perforator veins in the ankle, and lower trunk
  • faulty valves elevate venous pressure, causing distension and tortuosity
slide68

Primary varicose veins (without involvement of the deep veins) often result from a familial or congenital predisposition that leads to loss of elasticity of the vein wall

  • Secondary varicosities (involving the deep veins) often occur due to trauma, obstruction, DVT, or inflammation causing damage to the valves as well as pregnancy
  • more common in women & may also be more common in those whose occupation requires prolonged standing (e.g., nurses!)
slide69

symptoms may include a mild aching, a feeling of heaviness, muscle fatigue, itchiness, swelling, muscle cramps, especially at night

  • may also show signs of chronic venous insufficiency (such as edema, pain, pigmentation, and ulceration) with increasing risk for injury and infection
management2
Management
  • Prevention
    • avoid activities that cause venous stasis
      • restrictive clothing, crossing legs, sitting/standing for long periods, pressure on popliteal area
    • frequently change position
    • leg elevation when tired
    • calf pumping exercises/walking
    • elastic compression stockings (may be knee-hi or thigh-high)
    • weight reduction if overweight
surgical management
Surgical Management
  • Sclerotherapy (i.e hypertonic saline injected)
  • vein ligation and stripping

WARNING, especially at the end!

http://www.youtube.com/watch?v=jy3hNgVvNJs

chronic venous insufficiency
Chronic Venous Insufficiency
  • also known as postphlebitic syndrome
  • follows most severe cases of DVT within 5-10 yrs
  • 50% develop chronic induration and stasis dermatitis
  • 20% suffer from venous stasis ulcers*
  • marked by chronically swollen limbs; thick, coarse, brownish skin around the gaiter area, venous stasis ulceration; and itchy, scaly skin*
management3
Management
  • institute measures to increase venous return and decrease venous pressure
    • see interventions for prevention of varicose veins
    • compression stocking
    • careful skin care
  • avoid injury
venous stasis ulcers
Venous stasis ulcers
  • Reflects the end stage of chronic venous insufficiency whereby prolonged venous pressure prevents nutrient blood flow, depriving cells of needed oxygen, glucose, and other substances and therefore breakdown in the form of ulcers
slide76

appear as superficial, with a beefy red to yellow fibrinous granulation tissue, with irregular borders, often exudative, located in the area of the medial or lateral malleolus/anterior tibial area and accompanied by moderate to severe edema

management4
Management
  • prevent/treat infection (“cellulitis”)
  • debridement to promote healing (*remember to protect new tissue)
  • hydrocolloid dressings
  • stimulated healing (a form of skin grafting along with compression)
  • promoting adequate nutrition for healing (high in protein, Vitamins C & A, iron, zinc)
ad