3000 – Week 9
Peripheral artery disease
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Thickening of arterial walls, resulting in in a narrowing of arteries
•
Aortoiliac, femoral, popliteal, tibial, peroneal
•
Associated with CAD
•
800,000 Canadians are impacted by CAD
•
Risk increased with age
•
Symptoms at 50-70y
•
atherosclerosis causing thickening, narrowing the arteries
•
Seen in the bigger vessels – aortoiliac, femoral...
•
Starts to develop younger but symptoms become more prominent in older age
•
With diabetes, the lower structures are impacted
Etiology and pathophysiology
•
Leading cause: _atherosclerosis_
•
Thickening of intima & media layers
•
Inflammation and endothelial injury contribute
•
Symptoms when artery is _60-75_% occluded
•
Risk factors:
•
•
Smoking, diabetes, uncontrolled hypertension, hyperlipidemia
•
Others: age, family history, hyperuricemia, obesity, sedentary lifestyle,
stress, hyperhomocysteinemia
atherosclerosis
•
Fatty deposits in vessel walls
•
Fatty streak
•
•
Pro-inflammatory markers (like cytokines)
•
Start of coagulation cascade – coagulation markers
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Fatty streak turns into plaque, clots form on plaque
•
Starts to develop at a young age. Don't see signs until the vessels are
significantly occluded
Prevention
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Lifestyle – diet (reduce saturated fats, increase fiber, reduce LDL cholesterol
and increase HDL), exercise
•
Diabetes impacts vessel walls with hyperglycemia – development of plaques
sticking to the sugary vessels or the lumen of hyperglycemic vessels, causing
plaque and clotting
•
Hyperhomocysteinemia – amino acid used to build up proteins
Clinical manifestations
•
Dependent on site, extent of obstruction, availability of collateral circulation
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Intermittent claudication – “leg attack” (about 10% of patients)
•
Aortoiliac – glutes/thighs
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Femoral &/or popliteal – calf
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Appearance and integrity of limb
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Paresthesia
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Unaware of of extent of lower body injury
•
Pallor
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Pain at rest
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Thickened toenails
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Collateral circulation
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Obstruction or not enough blood flow from a vessel, requiring creation of
new vessels to bypass the obstruction. Feeds the parts not getting enough
blood and oxygen
•
Often seen in lower vessels
•
•
•
•
Feet at more risk because they are more distal and they have smaller vessels
Paresthesia
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Reduced blood flow to nerves for normal sensation – tingling, numbness
•
Risk for injury (pressure injuries, poor fitting shoes) and infection
Thickened toenails
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Happen when toes aren't getting enough flow
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Thick and yellow
•
Can be better seen in patients with darker skin tone (not as easy to see other
symptoms)
Sometimes elevating the limb prevents blood flow to the feet
Critical lower limb ischemia
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Diagnosed with 2+ weeks of chronic ischemic rest pain
•
PAD often develops slowly
•
•
Prolonged ischemia of skin & muscle à atrophy
Decreased arterial blood flow can cause delayed wound healing
•
Arterial ulcers, didiculty healing
•
Infection, necrosis, gangrene
•
Serious complications!
•
Blood flow so compromised that the tissue/limb (lower) begins to die (become
ischemic)
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Ischemia can spread - develop into necrosis and spread proximally
•
Necrosis --> infection which can then spread easily through the bloodstream
Diagnosis
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Doppler ultrasound with duplex
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Manual doppler does not replace palpation of a pulse!
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Segmental BP
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Ankle-Brachial Index
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CT angiography
Prevention
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DM & atherosclerosis (CAD, PAD) = ↑ risk of CV event
•
Risk factor modification
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Aggressive mgmt. of LDL
•
Lifestyle modification
•
Smoking cessation
•
Optimal BP control
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Optimal glycemic control
•
Reduce sodium intake
•
DASH diet
•
Pharmacologic interventions
•
Exercise – slow & progressive
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Formal & supervised
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At-home: walking
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Conservative
Treatment
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Protect from trauma
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Decrease pain
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Prevent infection
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Promote perfusion
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Revascularization
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Surgical, endovascular
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Percutaneous transluminal angioplasty + stent
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Arthrectomy
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Endarterectomy
Treatment: peripheral artery bypass graft
•
Most common
•
Graft with autogenous or synthetic
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Creates a bypass around the lesion
Nursing interventions
•
Assess history and risk factors
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Health history; DM
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tobacco use, exposure to second hand smoke
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Hypertension, hyperlipidemia, hypertriglyceridemia
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Hyperuricemia, impaired renal function
•
Obesity, sedentary lifestyle
•
increased CRP, homocysteine
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family history
•
stress
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Assess for clinical manifestations
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System assessments
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Cardio: PP – palp vs doppler, temp/cap refill, bruits
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Neuro: decreased O2 delivery to brain?
•
MSK: sensation, movement of limbs
Nursing interventions: post operative
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Monitoring
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Q15min, then q1h
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Pain management
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Monitor perfusion and bleeding
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Avoid knee flexion
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Ambulate POD #1
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Avoid sitting with legs down
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May use graduate compression stockings
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Monitor for infection
•
Avoid sitting with legs down
•
•
•
Blood pooling, edema, poor return to heart
Monitoring vitals
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Just manipulated blood vessels
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Risk of bleeding (drop in BP, increased HR, etc.)
Be cautious with positioning - flexion
Venous thrombosis
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Thrombus formation
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Associated with inflammation of vein
•
Most common vein disorder
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Superficial or deep
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Venous thromboembolism – VTE
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Spectrum of DVT to PE
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Can reduce blood return to the heart. Blood in the veins decreases and can pool,
clot
Etiology: Virchow’s triad
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•
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Venous Stasis
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Dysfunction values, inactive muscles
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Obesity, CHF, afib, pregnancy, long inactive periods
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Slowing, poor blood return to heart
•
If valves don’t work well, blood can stay in the valves for an abnormally long
time
Endothelial damage
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Direct – surgery, trauma, intravascular cannulation
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Indirect – chemotherapy, vasculitis, diabetes, sepsis,
hyperhomocysteinemia
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Stimulates platelet activation & initiates coagulation cascade
•
Can disrupt vessel's ability to function normally
•
IV causes vessel disruption
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Vesicant drugs – drugs that are hard on vessels (like chemotherapy or
vancomycin which has an abnormal pH that can be hard on vessel walls)
Hypercoagulability of blood
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Blood more likely to clot
•
Many disorders and medications predispose hypercoagulable state
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Smoking
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Some autoimmune diseases, pregnancy, smoking
•
Recruitment of clotting factors throughout the body, leading to development
of clots
Pathophysiology
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Localized platelet aggregation & fibrin entrap RBCs, WBCs and platelets à create
thrombus
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Frequently formed on valves as venous stasis often occurs here
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As the clot increases, more blood cells collect and create a tail that occludes the
vein lumen
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If a thrombus partially occludes a lumen, it is often covered by endothelium and the
thrombotic process is stopped
•
if the thrombus does not become attached, it will be lysed OR it becomes organized
and adherent to vessel wall in 5-7 days
•
•
Organized thrombi can detach and cause emboli
•
Turbulent blood flow is a factor in this detachment – can move through
venous circulation to heart and lodge in pulmonary vasculature: PE
Thrombus tail
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Flaps around with turbulent blood flow
•
Can break od easily and become an embolism, travel to other parts of the
body
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Endothelium can engulf the thrombus. When that doesn't happen, the tail moves
with turbulent blood flow, breaks od, embolism
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More turbulent blood flow can be caused by plaque build-up, damage to the walls
(like an IV catheter), where vessels split (blood becomes more turbulent where it's
trying to split), sugar in hyperglycemic patients
Superficial vein thrombosis
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Palpable, firm, cord-like superficial vein
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Area may be tender, warm, rubor
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Possible:
•
Mild fever, mild leukocytosis
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Edema (rare)
•
Common cause: ___IV cannulation___
•
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Small vein, caustic med, IV longer than 48h
Risk factors:
•
Increased age, pregnancy, obesity, malignancy, estrogen treatment, recent
sclerotherapy, long distance travel, chronic venous insudiciency, history of
VTE, SVT
Interprofessional care: superficial venous thrombosis
•
Ultrasound to confirm diagnosis (and rule out DVT)
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If IV-related:
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Remove IV
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If related to IV med/solution: warm compresses, elevate, oral NSAIDs
(systemic anticoagulation NOT indicated)
•
If lower extremity, or in greater saphenous or near saphenofemoral junction – LMWH
or unfractionated heparin, then warfarin
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Wear compression socks/bandages, mild exercise (walking)
Deep vein thrombosis: clinical manidestations
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Unilateral edema
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Tenderness with palpation
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Dilated superficial veins
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Sensation of fullness in leg
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Paresthesia
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Warm skin
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Fever
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Homans sign (positive)
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Flex foot à pain in deep calf; also reproducible with squeeze
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Conflicting opinions for its use à ?thrombus to break od
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Not palpable
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In arm (brachial vein) caused by PICC line
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Leg feels "heavy" - fullness
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Squeezing can cause thrombus to break od
Thrombosis
T – trauma
H – Hormones, OCP’s
R – road tradic accidents
O – operations
M – malignancy
B – blood disorders; polycythemia
O – orthopedic surgery/old age
S – serious illness
I – immobilization
S – splenectomy
DVT Complications
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Post-thrombotic syndrome
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20-50% of people with VTE, even with adequate anticoagulation
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From chronic venous hypertension from vein wall and valve damage (acute
inflammation) à vein valve damage, outflow obstruction (blood to heart)
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Symptoms: pain, heaviness, swelling, cramps, pruritis, paresthesia,
“bursting” pain with exercise, venous claudication
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Signs: persistent edema, hyperpigmentation, eczema, secondary
varicosities, lipodermatosclerosis
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Advanced stages: venous ulcers
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Symptoms usually within 2y of VTE
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PE
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Phlegmasia cerulea dolens (rare!)
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Venous ulcers are often darker, larger in size – from lack of good blood return to the
heart, blood starts to pool
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Limb becomes dark, purple – from blood pooling
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Phlegmasia cerulea dolens
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When toes get swollen, cool, edematous and become bright blue in colour
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Pooling isolated to the toes
Interprofessional care
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Prevention and prophylaxis is key!
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•
•
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All hospitals in Canada should have thromboprophylaxis policy (adults)
Early ambulation
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Bedrest – turn and reposition q2h; passive and active lower extremity ROM
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If ambulating – up for meals, ambulated 4-6x/day
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Educate patient and family!
Graduated stockings
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Increase blood flow velocity, prevent vessel dilation, improve valve function,
and stimulate endothelial fibrinolytic activity
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No wrinkles!
•
Must be worn properly
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Preventative only (do not wear if VTE)
Sequential Compression Devices
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Inflatable, wrapped around legs
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Apply external pressure
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Must be worn continuously at rest
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Can be used with other measures (anticoagulation, stockings)
Pharmacologic care
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•
Goals
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Prevent clot formation (prophylaxis)
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If clot known, prevent new development, prevent spread, prevent
embolization
3 major drug classes
•
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Vitamin K antagonists
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Long term use
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Requires INR monitoring; med must be taken at the same time each
day
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Dietary considerations: minimize foods with Vitamin K
Thrombin inhibitors
•
•
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Indirect
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Heparin-induced thrombocytopenia is a risk; requires CBC
monitoring
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Heparin: IV/SC (frequent aPTT monitoring with IV), LMWH: SC
(less monitoring needed)
Direct
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Bind directly to thrombin, no plasma protein or platelet
interactions
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continuous IV infusion, SC, or oral (depending on med)
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No antidote
Factor Xa inhibitors
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Produce rapid anticoagulation
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Used for VTE treatment and prophylaxis
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No coagulation monitoring needed
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Factor VIIa as “antidote”
Nursing interventions: HIT
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HIT = Heparin-induced thrombocytopenia
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Clotting and bleeding cascade simultaneously
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The diagnosis of HIT is based on three criteria: 1) The patient is receiving or has had
recent exposure to UFH or LMWH. 2) At least one clinical feature of the syndrome is
present (significant fall in platelet count, new venous and/or arterial thrombosis). 3)
There is laboratory evidence of HIT antibodies
1. Check lab values for target therapeutic levels; inform MD/NP if outside target
2. Evaluate lower extremity for ecchymosis/hematoma development if intermittent
compression is being used
3. Check platelets for signs of HIT
4. Monitor for bleeding (urine, stool), emesis, sputum, epistaxis & bleeding gingivae,
excessive menstrual bleeding
5. Inspect skin frequently, especially under splints, etc. for signs of bleeding, oozing or
visible bleeding from trauma or surgical incision
6. Fall risk assessment and prevention
Anticoagulation Therapy for VTE Prophylaxis
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Initial treatment:
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LMWH, unfractioned heparin, or fondaparinux,
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Overlap with warfarin, for at least five days or until the INR is 2.0 or higher for
24 hours
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Patients with one or more comorbidities, complex medical issues, or a very large
VTE are hospitalized for treatment
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They usually receive IV unfractioned heparin
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Depending on the extent of the clot, pt’s can be managed safely and edectively as
outpatients
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Pt’s taking anticoagulants should avoid taking ASA (aspirin), NSAID’s, fish oil
supplements, garlic supplements, certain antibiotics and ginkgo biloba (herb)
Thrombolytic treatment for VTE
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Given via catheter
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Directly dissolves clot with thrombolytic drug
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Can reduce symptoms and improve venous flow
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May reduce valvular reflux and decrease Post Thrombotic Syndrome
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Post-thrombotic syndrome (PTS) is a venous stress disorder that develops from
long-term edects from a previous deep venous thrombosis (DVT). The morbidity
associated with PTS may be significant and patients can present with edema,
chronic pain, swelling, skin changes, and heaviness of the adected limb
Surgical therapy
•
Mechanical thrombectomy
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VC interruption devices (IVC filter)
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Venous congestion
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Used with PE, proximal leg VTE with bleeding
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Placed in body through catheter through femoral vessels, fed into IVC,
catches emboli/travelling clots before they go into the heart
•
Can become clogged with clots, needs to be replaced
Nursing management of VTE
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Assess for risk factors (subjective data)
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Prolonged rest/immobility, medications, surgery, IV cannulation, central
venous catheter pregnancy, heart failure, coagulation disorders
•
•
Physical assessment (objective data)
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General: ____Fever, anxiety, pain_____
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Integumentary: increased size of limb, shiny, warm, erythematous, tender
•
Cardiovascular: warmth & distention in superficial veins, edema, cyanosis of
extremities (neck & back if superior VC involved)
Lab results
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Leukocytosis, abnormal coagulation, increased hematocrit, increased RBC,
d-dimer positive
Nursing considerations
•
Minimize venipuncture
•
Use small gauge needle for venipuncture and apply manual pressure to
venipuncture sites for at least 10 minutes (longer if needed)
•
Avoid IM injections
•
•
Risk of bleeding is greater:
•
•
increased risk of bleeding
Patient on LMWH or unfractionated heparin with gastro-duodenal ulcer, prior
bleeding history, thrombocytopenia, hepatic or renal failure
Assess patients for mental status changes
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especially in older patients (cerebral bleeding
Routine care and patient teaching
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Avoid straining to have a BM
•
Apply stocking devices properly, and as ordered (must be fitted)
•
Protect the skin (moisturize) & use paper tape after venipuncture
•
Avoid disruption of established clots (do not rub or massage the area)
•
Avoid restraints if possible
•
Pt should not forcefully blow their nose
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Avoid restrictive clothing
•
Electric razor only
•
Soft tooth brush or mouth swabs
•
Reposition and provide care in a gentle manner
Ambulatory and home care
Focus on modification of VTE risk factors
•
Compression stockings
•
Pt cannot be measured for “every-day” compression stockings until the
edema has resolved
•
Wear for 2 years post VTE
•
monitoring and following through with lab checks and values
•
Take meds as prescribed
•
knowing when to follow up (signs and symptoms of concern)
•
Encourage smoking cessation, stop using birth control or hormone replacement,
avoid sitting or standing in a motionless, leg dependent position
•
If patients are planning to travel, LMWH may be recommended before hand
Pulmonary embolism
•
Blockage of pulmonary artery by thrombus, fat, air, tumor, infective vegetation,
amniotic fluid
•
thrombus material that travels through the venous circulation to the heart and into
the narrowing blood vessels until it blocks alveolar perfusion
•
Most arise as DVT in legs
•
Also: R heart (afib), upper extremities (pacing wires, central line), pelvic veins
(birth or surgery)
•
Lethal PEs from femoral or iliac veins
•
30% mortality
•
Decreases to 6-8% mortality with treatment
Risk factors
•
Immobility or reduced mobility
•
Surgery within the past 3 months
•
Hx of DVT
•
Malignancy
•
Obesity
•
Oral contraceptives and hormone therapy
•
Cigarette smoking
•
Prolonged air travel
•
Heart failure
•
Pregnancy
•
Clotting disorders
Signs and symptoms
•
“Classic” triad – occurs in about 20% of patients:
•
_dyspnea_______
•
Hemoptysis (coughing up blood)
•
___chest pain___
•
Slow or sudden onset
•
Mild-moderate hypoxemia is common
•
Cough, pleuritic chest pain, crackles, fever, louder pulmonic heart sound, altered
mental status
•
May have ECG changes
Clinical manifestations
•
•
Large emboli
•
Abrupt hypotension, pallor, fever, dyspnea, hypoxemia, possible chest pain
•
ECG changes (tachycardia, RV strain)
•
Mortality with symptoms ~10%
Medium emboli
•
•
Pleuritic chest pain, dyspnea, slight fever, productive cough with bloodstreaked sputum, pleural friction rub, tachycardia
Small emboli
•
Often undetectable UNLESS underlying heart disease – causes severe
cardiac compromise
Complications
•
•
Pulmonary infarction when:
•
Occlusion of a medium or large vessel (>2cm diameter)
•
Insudicient collateral blood flow from bronchial circulation
•
Pre-existing lung disease
Many small emboli cause a decrease in capillary bed and pulmonary hypertension
•
About 50% of pulmonary bed involved
•
Impacted gas exchange, hypoxia
Diagnostics: spiral CT
•
CT with contrast
•
Contrast is required to view the vlood vessels
•
Pt must have IV access to give the dye
•
If pt cannot have contrast, a ventilation-perfusion (VQ) scan is done
Diagnostics: VQ Scan
•
Two components
•
Most accurate when both are performed
•
Perfusion scanning involves IV injection of a radioisotope. A scanning device
images the pulmonary circulation
•
Ventilation scanning involves inhalation of radioactive gas. Scanning then
reflects the distribution of gas through the lung
Other diagnostics
•
D-dimer
•
Pulmonary angiography
•
ABG
•
CXR
•
ECG changes
Interprofessional care
•
•
Prevent PEs
•
Early ambulation post-op
•
Prophylactic anticoagulant in hospital
Treat as soon as PE expected
•
Prevent further growth or multiplication of thrombi
•
Prevent thrombus from entering pulmonary vasculature
•
Provide cardiopulmonary support if needed
•
Turn and reposition, DB&C, spirometry
•
Oxygen if needed
•
Intubate if needed
•
Shock: vasopressors, IV fluids
•
Treat pain
Pharmacologic therapy
•
•
•
Fibrinolytic drugs
•
Tissue Plasminogen activator (tPA) or alteplase (Activase)
•
dissolves the PE AND the source of the thrombus in the pelvis or deep leg
veins
•
Given when pt with a PE is hemodynamically unstable, and has R ventricular
dysfunction
•
Treatment should begin immediately
•
Pt should receive properly managed anticoagulant therapy to prevent further
emboli
Heparin
•
prevents future clots but does not dissolve existing clots; need to identify
what has caused clots to decide the future plan of care
•
Pt’s need to be closely monitored (aPPT levels)
Warfarin
•
Taken for 3- 6 months
Surgical treatment: embolectomy
•
Required if the patient does not respond to conservative therapy, embolectomy,
may be required
•
Rare procedure
•
•
50% mortality rate!
If a patient has this procedure, a vena cava filter is also placed
Nursing considerations
•
Prevention
•
•
•
•
The same as VTE
Acute interventions
•
bed rest, semi fowler’s position (to facilitate breathing)
•
IV access
•
Know the adverse edects of the medication used to treat the PE & monitor
closely
•
Oxygen as needed
•
Carefully monitor VS, cardiac dysrhythmias, Sp02, ABG’s, and lung sounds
•
Lab results (INR & aPPT)
•
Assess for complications of anticoagulation therapy & PE’s
•
Assess fall risk
•
Assess and treat pain and anxiety, (can experience a “sense of doom”)
Home care
•
Recognizing any comorbidities (if any exist), and their thrombo-embolic
disease
•
Teaching regarding long term anticoagulant therapy & the importance of
attending follow up appointments
Emotional support
•
Patient and family