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What is aortic aneurysm?
- Weakened, bulging area of vessel wall
- Results from atherosclerosis which weakens media
- Incidence is 5-7% over age of 60
- Risk factors: smoking, diabetes, HTN, hyperlipidemia
- Diagnosing: Sonogram (screening), CT more accurate to determine length and diameter
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Clinical manifestations of aortic aneurysm
- Often asymptomatic
- Found on sonogram or CT
- May note pulsatile mass on exam
- Thrombi and plaque can embolize to lower extremities causing blue toe syndrome
- Rupture is usually fatal
- Posterior rupture may be tamponaded
- Leads to retroperitoneal bleed
- Grey turner's sign
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Treatment of aortic aneurysm
- Small aneurysm: less than 4cm may be watched; control of BP; risk factor modification
- Repair indicated for > 5-6cm unless not a surgical candidate (e.g. terminal illness, unlikely to survive surgery)
- Endovascular repair: synthetic graft threaded into aneurysm via femoral artery; much less invasive; risk of leakage
- Open repair: aorta cross-clamped for 30-45minutes; diseased segment removed and synthetic graft is sutured in; risk for ischemia below cross-clamped area (kidney damage, SCI, due to interruption of blood flow)
- Open repair is more definitive, but has severe surgical mortality
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Post-op nursing care of aneurysm repair
- SICU post-op (pt will be intubated, will likely have CVP monitor, A-line, NG tube, multiple IVs, foley, tele)
- Thoracic aneurysm will have thoracotomy (chest tubes)
- Maintain BP (if BP too high, graft can rupture; if too low, thrombosis can occur)
- Pain control
- Monitor renal function (Cr, BUN, hourly urine output, electrolytes, CVP)
- Monitor for infection (WBCs, fever, wound drainage, IV sites, foley, graft infection is serious complication)
- Monitor GI function (bowel sounds, distention)
- Monitor neuro status (especially peripheral neuro, make sure no damage below level of cross-clamping; LOC)
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Why is monitoring urine output critical?
Cardiac output and renal perfusion
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Aortic aneurysm repair discharge teaching
- No lifting for 4-6 weeks
- Monitor for infection (fever, inflammation at site, drainage, redness)
- Antibiotic prophylaxis
- Risk factor modification
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What is aortic dissection?
- Tear in the intima
- Allows blood to enter between intima and media (false lumen)
- May impede blood flow to brain, spinal cord, kidneys, and extremities
- Rupture is usually fatal
- Risk factors: Marfan's syndrome (connective tissue disorder), chronic HTN (incr stress on arteries), elderly
- Dx: Chest x-ray shows widened mediastinum, CT
- Tx: Lower BP with nitroprusside or beta blocker, plan for surgical repair
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Clinical manifestations of aortic dissection
- Sudden severe chest pain described as tearing radiating to back and shoulders
- Significantly different BP and pulses between extremities (uneven perfusion between limbs)
- Neurological compromise
- Aortic valve insufficiency
- Cardiac tamponade
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Aortic dissection nursing care
- Critical care monitoring (a-line, tele)
- Titrate med to BP (Esmolol beta blocker; adjust drips to keep BP within parameters)
- On-going assessment (peripheral pulses, neuro status, heart and lung sounds)
- Pain management (continue to assess and admin analgesics based on assessment and orders)
- Psychological support
- Prepare patient for surgery (consent signed, pre-op meds, NPO)
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What is peripheral arterial disease?
- Severe atherosclerosis occludes blood flow to extremities
- Results in ischemia of muscle and nerve tissue
- Risk factors: smoking, diabetes, HTN, hyperlipidemia
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Clinical manifestations of peripheral arterial disease
- Intermittent claudication (pain during exertion from anaerobic metabolism and lactic acid build-up; resolves with rest; one of first symptoms)
- Neuropathy (especially in diabetics; nerve damage from chronic ischemia resulting in numbness, tingling, burning pain)
- Diminished or absent pulses
- Trophic changes (skin is thin, pale, shiny; no hair growth; fungus in toenails)
- Arterial ulcers (minor trauma may lead to difficult to heal ulcers because perfusion is so poor; teach pt to check feet daily especially if have neuropathy)
- Gangrene (may necessitate amputation)
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Diagnosing peripheral arterial disease
- Arterial duplex: non-invasive sonogram to determine degree of arterial flow and location of blockages
- Ankle-Brachial Index (ABI)
- Angiography: invasive study, dye is injected and x-rays are taken; definitive study of degree and location of stenosis; done if surgery is planned (stent or bypass); NPO, consent, dye allergies, no Metformin for 48 hours
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What is the Ankle-Brachial Index?
- Ratio of ankle SBP (post tibial artery) to highest brachial SBP
- BP in legs should be higher than BP in arms
- Normally 0.9 to 1.3
- 0.5 to 0.9 indicates mild to moderate disease
- Less than 0.5 indicates severe disease
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Treatment of peripheral arterial disease
- Risk factor modification (smoking cessation, control of BP, lipids, diabetes)
- Exercise (slightly beyond point of claudication to try to get cells to utilize O2 and develop collateral circulation)
- Medications (stains, anti-platelets)
- Pentoxipfylline (Trental): older med; makes red cells a little more slippery so can get into tighter spaces; better able to deliver O2 to tissue; anti-platelet characteristics
- Cilostizol (Pletal): newer med; inhibits platelet aggregation and promotes vasodilation; can worsen heart failure
- Angioplasty with stent placement
- Bypass surgery
- Amputation
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Patient education
- Smoking cessation
- Inspect feet daily (don't cut own toenails)
- Protect feet from injury
- Podiatry referral
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Arterial bypass surgery post-op nursing care
- Monitor surgical site (bleeding, signs of infection)
- Monitor peripheral neurovascular status distal to site, "6 P's": pallor, pain, paralysis, parasthesia (tingling, numbness), pulselessness, poikilothermia (one extremity is colder than the other)
- Pain management
- Promote mobility (early ambulation to promote blood flow thru graft)
- Discharge teaching (medications and side effects, foot care, monitor incision, need for exercise, monitor changes in perfusion, color changes)
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Vein function
- Low pressure, high volume system
- Valves prevent back flow of blood against gravity
- Muscle activity compresses vessel and pushes blood back towards heart
- Thrombophlebitis (inflammation and thrombosis of vein)
- Relies on valves, muscle activity, and changes in thoracic pressure to push blood back up to heart
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Virchow's Triad
- Venous stasis (immobility)
- Endothelial damage
- HypercoagulabilityFactors predisposing to thrombophlebitis (elderly, immobility, CHF, atrial fib, bedrest, CVA, varicose veins, pregnancy, orthopedic surgery)
- IVs, trauma, previous clot, leg fracture
- Smoking, dehydration, malignancy, oral contraceptives, hormone replacement therapy, coagulation defects, sepsis
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What is superficial thrombophlebitis?
- Palpable cordlike vein
- Upper extremity usually at IV site; lower extremity usually trauma to varicose vein
- Clinical manifestations: tenderness, erythema, low grade fever
- No embolization risk
- Tx: remove IV, analgesics (aspirin), elevate extremity, warm moist heat
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Deep vein thrombosis (DVT)
- High risk of embolization
- Effects 5% of surgical patients
- Clinical manifestations: unilateral edema, pain, erythema, low grade fever, +/- Homan's sign
- Complications: pulmonary embolism (SOB, pleuritic chest pain, hypoxia, tachycardia), chronic vein insufficiency, arterial compromise due to severe edema (rare)
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DVT prevention
- Mobilization (get post-op and post partum patients out of bed ASAP)
- Ankle pumps (promote venous return back to heart)
- TEDs (compression hose encourage venous return; important that they are properly fitted without wrinkles)
- Sequential Compression Devices (SCDs)
- Anticoagulation (low molecular weight heparin is becoming tx of choice for DVT prevention in orthopedic and trauma patients; fewer bleeding complications; no need to titrate)
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DVT diagnosis and treatment
- Venous doppler (non-invasive; usually sufficient to make dx)
- Anticoagulation with Heparin and Warfarin (initiate both because Warfarin takes 3-5 days to become therapeutic)
- INR goal of 2.0 to 3.0
- Admission for IV unfractionated heparin or outpatient treatment with low molecular weight heparin
- Heparin drip APTT 1.5 to 2.5 x control; monitor for HIT and bleeding; Must teach patient or family LMWH subq injection technique
- Continue Warfarin 3 to 6 months after resolution
- TEDs when ambulating
- Recurrent DVT requires life long anticoagulation
- Inferior Vena Cava filter for high risk of embolization or recurrent DVT (IVC filter placed in interventional radiology; catches clots)
- Catheter-Directed Thrombolysis (CDT)
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Bleeding complications
- Monitor CBC, coagulation studies (PTT & PT/INR; look for new anemia; platelet counts)
- Assess for bruising, mental status change, hematuria, GI bleed, epistaxisis (observe for indication of hemorrhage or excessive anticoagulation)
- Protamine sulfate: antidote to heparin
- Vitamin K: antidote to coumadin
- Fresh frozen plasma (for acute hemorrhage; contains multiple activated clotting factors)
- Monitor PTT when on heparin; heparin can cause heparin induced thrombocytopenia
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Warfarin (Coumadin) teaching
- Observe for bleeding (report to health care provider or ER if severe)
- PT/INR (routine lab monitoring)
- Missed dose (don't double up unless instructed to)
- Avoid OTC, especially aspirin and NSAIDs
- Multiple drug interactions
- Avoid excessive intake or fluctuations in intake of Vitamin K rich foods
- Avoid trauma (use soft toothbrush, electric razor; no contact sports)
- Medic-alert bracelet
- Direct pressure to stop bleeding
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What is a pulmonary embolism?
- Blockage of pulmonary artery or main branches by thrombi, fat, or air (usually thrombus)
- Sources: thrombi from deep veins in legs or right atrium, fat from long bone fractures, air from open central line
- Pulmonary infarction is rare (due to bronchial circulation)
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Clinical manifestations of a PE
- Dyspnea, tachycardia, tachypnea, hypoxia (caused by ventilation/perfusion mismatch)
- Anxiety (caused by hypoxia)
- Pleuritic chest pain (worse with cough, deep breath)
- Cough, hemoptysis (pleural irritation)
- HPN, Shock (impaired cardiac output due to inadequate return to left ventricle)
- Pulmonary HTN (results from recurrent PEs)
- Sudden collapse and death (if severe; due to lack of cardiac output)
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Diagnosing PE
- Spiral CT (test of choice; minimally invasive, good specificity and sensitivity)
- V/Q scan (Nuclear med; injection and inhalation of radioisotope tracer; looks for ventilation perfusion mismatch; reports probabilities; either high or low probability; not 100% confirmation)
- D-Dimer (blood test looks for fibrin degradation products; if normal, low probability of PE; positive test indicates there is a clot somewhere)
- Venous doppler (looks for source; confirms diagnosis if in doubt)
- Pulmonary angiography (definitive; invasive)
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Treatment of PE
- Hospitalization
- Heparin drip (titrate heparin to APTT; target: 1.5 to 2.5)
- O2 to maintain sats
- Morphine for pain
- Monitor ABGs, coags, vitals, EKG, cardiopulmonary status
- Possible IVC filter
- Emergent embolectomy low survival rate
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APTT calculation
- 1.5 to 2.5 x control
- Example1: Patient - 80, control - 28 (range 42-70); patient APTT is too high
- Example2: Patient - 49, control - 28; patient APTT is within range
- Example3: Patient - 30, control - 28; patient APTT is too low
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What are varicose veins?
- Large, dilated subcutaneous veins
- Familial, usually result from valvular incompetence
- Risk factors: obesity, pregnancy, DVT, excessive standing
- Symptoms: ache after prolonged standing, edema
- Conservative treatment: avoid prolonged sitting or standing; avoid constrictive clothing; walking to promote venous return; support/compression stockings
- Invasive treatment: sclerotherapy or vein stripping
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What is venous insufficiency?
- Incompetent valves in deep veins; inadequate venous return
- Results in increased hydrostatic pressure, interstitial edema, leak of RBCs
- Causes edema, staining of skin (from hemoglobin in interstitial tissue), dermatitis
- Compression: patients often require high grade medical compression stockings to control edema
- Leg elevation above heart level
- Low sodium diet to decrease edema
- Skin care to treat dermatitis, prevent breakdown, cellulitis
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What are venous stasis ulcers?
- Painful, weeping ulcers with irregular borders
- Etiology: severe venous insufficiency
- Often above medial malleolus
- Must have compression to heal
- Ensure adequate arterial circulation prior to applying high levels of compression (ABI to ensure adequate arterial flow, ABI < 0.8 contraindication to high grade compression)
- Slow healing
- Maintain moist wound bed but absorb excess drainage
- Observe for cellulitis
- May require grafting
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