Vascular Disorders Flashcards
Definition of a TIA
Brief neurological deficity that completely resolves within 24 hours
Risk of another TIA if a patient with a TIA is not treated?
40% of another attack within 2 years
Work up for a patient w/hx of TIA
Physical exam for carotid bruits, focal neurologic deficit, heart disease, echo if murmur is present and duplex u/s of carotid vessels.
Carotid endarterectomy/stenting vs. aspirin in stroke prevention
3x more effective in preventing strokes over a 2 year period.
Indications for carotid endarterectomy/stenting?
Ipsilateral neurological symptoms (amaurosis fugax, TIA, stroke w/recovery) AND > 70% internal carotid stenosis. Asymptomatic carotid bruit AND > 70% internal carotid stenosis.
What are risks of carotid endarterectomy?
1-3% risk of stroke (most common cause immediate post-op is inappropriate smothing of the resected portion of the artery and emboli), hypoglossal nerve injury, vagus nerve injury and marginal branch of facial nerve injury.
What are the branches of the internal carotid artery?
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What are the steps of a carotid endarterectomy?
Get a-line to carefully monitor pts BP, EEG to monitor neurologic function if under general anesthesia. 1) Incision along SCM 2) Dissect to carotid sheath 3) Protect vagus, isolate carotid artery and avoid carotid body 4) Expose ICA to level of hypoglossal nerve 5) Heparin and clamp vessel 6) Open vessel and dissect out plaque 7) Close artery w/ or w/o patch
Follow up for patients post-carotid endarterectomy
Recurrent carotid narrowing over 5 years has 13% incidence. TIA from opposite artery may still occur and pt should take aspirin, control lipids, exercise, quit smoking and exercise to decrease further atherosclerotic disease.
What are the branches of the external carotid artery.
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Amaurosis fugax
The opthalmic artery is the first branch off the carotid. This is when an emboli travels through the opthalamic artery to the retina causing transient monocular blindness or hazy vision like a shade being pulled over the eye. Fundoscopic exam may show a bright shiny spot at the retinal artery (Hollenhorst plaque).
Location of speech center in right handed patients
Left temporal lobe
Stroke work up and tx
If the patient’s TIA does not resolve within 24 hours, you can still do a carotid duplex u/s, but endarterectomy/stent is not necessary immediately. The patient should be observed for improvement and stabilization of neurologic status and then endarterectomy/stent can be considered as early as 2-4 weeks later.
Common findings in patients with acute arterial occlusions
6 P’s: Pain, paresthesias, pallor, pulselessness, poikelothermia, paralysis.
Time limit for revascularization of an acute arterial thrombus in the limbs
Less than 6 hours
Tx for patient presenting with acute arterial thrombus of < 6 hours
Immediate heparin, then ballon catheter embolectomy with a Fogarty catheter as the procedure of choice. This involves 1st entering the vessel distal to the embolus and 2nd extracting the most proximal embolus 1st. More distal thrombi can be cleaned out at the same time.
What are the most common sites of arterial emboli?
10-15% in aortic saddle, 15-20% in common iliac, 40-45% in common femoral, 15% in popliteal, 5-10% in upper extremity, 5-10% in viscera or kidney and 10-15% in carotid.
Characteristics of a threatened limb, how can you treat such a limb?
Slow to intact cap refill, mild muscle weakness, mild sensory loss, inaudible arterial pulses and audible venous pulses w/doppler. Limb can be salvaged if treated promptly.
Characteristics of a limb with irreversible ischemia
Absent cap refill (marbling), profound paralysis (rigor), profound sensory loss, inaudible arterial and venous pulses on doppler.
What are the most common sources of arterial emboli
Cardiac accounts for 75%, with 50-60% due to a-fib and 20-25% due to acute MI. Aneurysm or atherosclerotic plaques from the aorta account for 10-15%. Other causes include aortic dissection and femoral artery puncture sites that disloged tunica intima and created an embolus.
What condition commonly arises after revascularization of an acutely ischemic limb?
Compartment syndrome due to acute muscular edema.
Pressures in compartment syndrome that lead to irreversible ischemic injury of muscles and nerves
20-40 mmHg
How do you manage a patient with compartment syndrome?
4 compartment fasciotomy should be performed with high degree of clinical suspicion. Needle and pressure-measuring device can be done to check pressures if suspicion is not as high before performing fasciotomy. Fasciotomy is the closed w/split thickness skin graft
Long-term management of a patient recovering from compartment syndrome after 4 compartment fasciotomy
PT to maintain full ROM. Chronic warfarin anticoagulation to prevent further arterial emboli. Echo, angio, CT etc should be used to dx source of emboli once the patient has recovered.
A patient presents with intermittent claudication. If he has an arterial occlusion in his lower extremity, where will it most likely be found?
Superficial femoral artery in the adductor hiatus is the most common location of occlusive disease in the lower extremity.
What is the noninvasive workup for a patient complaining of intermittent claudication?
ABI and Doppler to detect stenotic areas and locate the level of the occlusion. Normal ABI is 0.9-1.1. In mild claudication, ABI is 0.6-0.8 and indicates single level disease. Severe claudicationi ABI is < 0.5 and indicates multilevel disease. An ABI < 0.3 is typically indicative of rest pain or tissue loss.
What is the measured BP in patients with advanced diabetes when checking ABIs?
Typically as high as the cuff is inflated, this is because their vessels have become calcified from atherosclerotic disease and are now non-compressible.
How do you interpret triphasic, diphasic vs. monophasic Doppler waveforms?
Triphasic = good vessels with phase of rapid systolic flow, reversal flow due to elastic recoil and finally a diastolic outflow phase. Diphasic = loss of the reverse flow, indicating decreased elasticity of the vessels due to atherosclerosis, can also be normal. Monophasic = severe disease with no changes.
Most common way claudication is managed?
Non-operatively with lifestyle modification (exercise, smoking cessation, lipid-lowering drugs, diet and weight loss). With this approach 1/3 get better, 1/3 stay the same and 1/3 get worse. Revascularization surgery is really only done in patients without critical limb ischemia when the claudication is an impairment to their activities of daily living. Note that you should not order an arteriogram unless you are actually planning for surgery due to the inherent risks of the test.
What is Leriche syndrome
Claudication, impotence and pulselessness indicating aortoiliac occlusive disease.
When is it appropriate to operate on a patient with claudication?
Aortoiliace occlusive disease, impairment of ADLs, pt is otherwise healthy, ulceration in a patient w/insufficient blood supply to heal it and rest pain.
How can you predict the likelihood of an ischemic foot lesion to heal?
Ankle SBP > 65 in non-diabetics and > 90 in diabetics = likely will heal. Ankle SBP 55-65 in non-diabetics and 80-90 in diabetics = probable. Ankle SBP < 55 in non-diabetics and < 80 in diabetics = unlikely.
Next step once you decide that a patient needs revascularization surgery for claudication/limb ischemia.
Arteriogram to assess the different levels of occlusion. This will tell you if the patient has inflow disease (iliac occlusive disease) or outflow disease (single or multiple occlusions in the superficial femora, popliteal and distal arteries).
A patient has occlusion of the superficial femoral and politeal arteries with distal reconstitution. What revascularization procedure will you do?
Fem-pop bypass. Distally you whould give preference to reconstitution with the femoral, anterior or posterior tibial arteries. Peroneal artery should only be used if the tibials are occluded.
What fem-pop bypass grafts tay patent for the longest period of time?
Above the knee (saphenous or PTFE), below-knee (saphenous way better than PTFE) and infrapopliteal (saphenous way better than PTFE)
F/u after revascularization surgery for claudications
Duplex u/s graft examination for stenosis, aspirin, lipid-lowering agents and education about foot care if needed. Note that these patients have atherosclerotic disease and are most likely to die from CAD.
What are the procedures you can do for a patient with common iliac occlusion?
PTA if single, short-segment iliac stenosis. Aortobifemoral bypass if bilateral loss of femoral pulses. If patient has poor risk factors for a transabdominal approach, an axillofemoral bypass graft may be considered. If the other femoral artery were patent, a femorofemoral bypass can be performed.
Who gets PTA vs. bypass graft for lower extremity occlusive disease?
If the patient is expected to live > 2 years and has a viable autologous graft, they should get bypass because long-term success rates are better.
What part of the aortobifemoral bypass graft surgery has the greatest cardiovascular risk?
Aside from high risk during anesthesia induction, hemorrhage or stress, clamping the aorta increases the afterload on the heart (anticipate this by giving afterload reducing agents before clamping) and unclamping the aorta has risk of bleeding from the graft, hypotension from sudden decrease in afterload and subsequent increase in CO. In addition to this, the LE static blood becomes acidotic and hyperkalemic, which can adversely affect cardiac function/rhythm with unclamping.
A patient comes out of an operation for LE revascularization and has a painul cyanotic big toe that was not present prior to the procedure. What happened? What can you do to help this”
Trash foot from atheroembolization of fibrin, platelets or dislodged atherosclerotic debris after unclamping that blocked the small pedal or digital ateries. You can’t really help this guy because small pedal or digital vessals are inaccessible to embolectomy catheters. If he has patent tibial vessels and palpable pedal pulses significant healing commonly occurs. You can try to help with heparinization or antiplatelet therapy, but thrombolytic therapy is contraindicated in the post-surgical period.
What is the likelihood of cardiac risk in major vascular reconstruction?
MI, arrhythmia or heart failure occur perioperatively in 10% of patients. Cardiac mortality is 2-3%
Preoperative evaluation of patients preparing for major vascular reconstruction surgery?
Labs to check cardiac, pulmonary and renal status. Carotid duplex u/s and cardiac stress test +/- catheterization because 70% of perioperative and late fatalities are due to cardiac events.
Prior to vascular surgery, who gets coronary angiography, who gets to go straight to surgery and who gets dipyridamole-thallium scintigraphy (DT scan)
Coronary angiography = Mod to severe angina, CHF w/exertion, LVEF < 20% (< 30% is good predictor of CHF, but not MI). Straight to surgery = asymptomatic and active lifestyle, stable angina w/vigorous lifestyle, age > 80. DT scan = hx of MI, moderate angina, mild angina w/sedentary lifestyle.
What is dipyridamole-thallium scintigraphy?
Dipyridamole inhibits adenosine uptake into the heart and pharmacologically stresses the myocardium. Thallium is a tagged radionucleotide that shows areas of poor perfusion when the heart is stressed by dipyridamole. It has a good negative predictive value (96-99%) but poor positive predictive value (1-20%). If positive, next test should be a coronary angio.
How long should vascular surgery be delayed if a patient had an MI 2 weeks ago?
At least 3 months
Eagle’s criteria
Risk for perioperative cardiac morbidity: Age > 70, DM, Angina, Ventricular arrhythmia requiring tx, Q waves on pre-op ECG and DTS redistribution. 0 risk factors = 3% risk of MI. 1-2 risk factors = 15% risk of MI and patients need DTS +/- cardiac cath. > 3 risk factors = 50% risk of MI, and patients need coronary angio.
What other aneurisms should you check for on CT or u/s in a patient with a AAA? What if the patient has a popliteal aneurism?
Iliofemoral and popliteal. Note that 50% of patients with popliteal aneurisms have AAA and 50-75% of popliteal aneurisms are bilateral.
Guidelines for repairing a stable patient with AAA?
5.5 cm or larger in greatest diameter w/ life expectancy > 2 years. 4-5cm is debatable beause they grow at an average rate of 4mm/year.
Post-op problems to look out for in patients who undergo repair of AAA?
Major fluid shifts w/mobilization of 3rd spaced fluids on day 3. If fluids are not restricted or diuretics utilized the patients can develop pulmonary edema. Pts should also be monitored for arrhythmias from electrolyte abnormalities and MI from aortic clamping/unclamping. Incidence of erectile dysfunction is high after this procedure due to dissection of hypogastric circulation or autonomic nerves near the IMA…in this case the patient should see a urologist.
AAA mortality rate when ruptured
50% die before reaching a hospital, 80% die perioperatively. If the patient survives post-op complications inclued acute renal failure, MI and multiorgan system failure from hypovolemic shock.
Risk of AAA rupture by size
< 5cm = 4% yearly, 20% 5 years. 5-7 cm = 7% yearly, 33% 5 years. > 7cm = 19% yearly, 95% 5 years.
1st step when a patient comes to the ED with a ruptured AAA
Get them straight to the OR to clamp that aorta ASAP then fluid resuscitate during repair. Increased volume/BP can convert a contained rupture to a free intraperitoneal rupture and result in rapid death.
Why are patients with ruptured AAA at 2-3% risk of ischemic colitis (brown/bloody diarrhea, abdominal pain, ileus, distention, sepsis or peritonitis)?
The rectosigmoid segment is at risk for ischemia because of IMA interruption from the aneurism + compromised collateral flow from the SMA and hypogagstric arteries.
How do you diagnose and treat ischemic colitis
Sigmoidoscopy shows edematous, hemorrhagic or necrotic mucosa. Tx w/bowel rest, hydration, blood products if needed, GI decompression, abx, repeat endoscopy and colectomy for portions w/full-thickness involvement (mortality rate of 50%).
A patient with repair of a ruptured AAA survives and comes back for follow up 1 year later with fever and inflammation where the femoral incision was. What are common causes of this condition? How do you dx it? How do you tx it?
Vascular graft infection can arise months to years post-op and is typically due to normal skin flora S. epidermidis (evades immune system w/glycocalyx slime) or S. aureus at the implantation site. Dx with CT. Tx with graft removal, infected tissue debridement, revascularization by extra-anatomic bypass and long-term abx.
A patient presents 1 year after having a ruptured AAA repaired complaining of an upper GI bleed. What absolutely needs to be at the top of your differential? How do you dx it? How do you tx it?
Aortoenteric fistula. Erosion of the graft into the 3rd or 4th part of the duodenum. Dx w/CT or angio, even if bleeding has resolved because pts typically present with a small sentinal bleed followed by massive bleed 1-2 days later. Tx w/graft removal, GI tract repair and extra-anatomic bypass. Note that mortality/limb loss approaches 50% with this.
Clinical presentation and management of chronic mesenteric ischemia? Dx and Tx?
Presents as post-prandial abdominal pain, usually w/o heme in stool. Dx w/arteriogram and tx w/revascularization or stenting.
How can you diagnose aortic dissection?
Transesophageal echocardiography, CT, angiogram or MRI, depending on the urgency of the situation.
What are the different types of aortic dissections
Type I = false lumen involves ascending aorta, arch and descending aorta. Type II = ascending only. Type III = descending only, distal to subclavian. Types I and II are stanford A dissections and type III is a stanford B dissection.
How do you treat a patient with an aortic dissection?
Managment is typically medical with control of hypertension using beta blockers. The exception to this rule are dissections that involve the ascending aorta, these need to be repaired surgically (types I and II, type A).
What is the most reliable sign/symptom in your H&P of a patient with suspect DVT? What signs/symptoms are non-specific?
H&P is only accurate 50% in patients with DVT because 50% of patients have occult (silent) DVT. The most reliable clinical sign of DVT is new onset unilateral leg swelling measured > 3cm compared to the other leg. Homans’ sign, a palpable cord and thigh/calf tenderness are non-specific.
Test used to diagnose DVT
Duplex u/s has a sensitivity and specificity > 90%.
Management of a patient with LE DVT or PE
70-100 U/kg heparin IV bolus initially. Maintenance infusion 15-25 U/kg for 4-6 days. Maintain PTT at 1.5-2x normal, check PTT 6 hours after initial dose (heparin t1/2 = 90 min), q8 for 1st 24 hours, then qd thereafter. Bed rest for 1st 24-48 hours and continued duplex u/s as heparin has anti-inflammatory properties that reduce the pain associated w/DVT. After 5-7 days, the patient can be started on Warfarin (Coumadin) and kept on it for 4-6 months with an INR of 2-3 (1.3-1.5x normal PT).
How do heparin, warfarin, plavix and aspirin work?
Heparin: activates ATIII. Warfarin: inhibits vitamin K epoxide. Plavix: inhibits platelet activation at ADP receptor. Aspirin: inhibits TxA2 > PGI2.
What are major problems associated with heparin therapy?
Hemorrhage and HIT due to anti-heparin abs binding to and activating platelets
How long should you keep a patient on heparin after starting them on warfarin for long term DVT prophylaxis?
Several days. Warfarin inhibits synthesis of clotting factors II, VII, IX and X along with protein C and protein S. Early on proteins C/S are inhibited more and induce a hypercoaguable state anywhere from 1-10 days and heparin will help prevent clots during this time.
How can you limit post-thrombotic syndrome after patients suffer from a DVT?
Supportive stockings and ulcer care. Note that if the patient has arterial occlusive disease, the supportive stockings will be counterproductive due to arterial compression.
Long-term morbidities of DVT
Recurrence and post-thrombotic syndrome. Post-thrombotic syndrome is due to venous valve insufficiency resulting in venous HTN, chronic edema, skin ulceration around ankles and claudication.
High risk for DVT
Elderly, previous PE/DVT, long surgery, pelvic/ortho surgery, surgery for cancer, procoagulant state (polycythemia vera), hyperviscous (multiple myeloma) and hx of MI, CHF or COPD.
Moderate risk for DVT
Age > 40, 2-3 hour surgery, abdominal/thoracic surgery, obesity and smoking.
Low risk for DVT
Healthy, < age 40, short surgery or bleeding disorder (chronic renal or liver failure)
Precautions to take for patients at risk for DVT
Trendelenberg position (knees and feet higher than right atrium), early ambulation, low-dose heparin (5,000 IU q8-12hrs until patient is ambulatory, coag studies are not necessary) and SCDs.
Work up of a patient with suspected PE
Good H&P, ECG (to r/o MI), ABGs (most common finding is low PCO2 due to hyperventilation), CXR (r/o PTX, atelectasis and pneumonia). If these tests don’t really show anything, you can do a CTPA, which is the gold standard for PE.
How does a V/Q scan work? How does it predict the likelihood of PE?
Radioactive xenon gas is inhaled and lungs are assessed for for ventilation on CXR. Radioactive technecium is injection and lungas are assessed for perfusion on CXR. Impaired regional alveolar ventilation results in vasconstriction and a perfusion deficit on the scan. If the ventilation scan is normal in an area with segmental perfusion deficit, the deficit is very likely to be due to mechanical obstruction (PE), rather than physiologic (90% specific).
What are long-term complications seen in patients with PE?
Most return to baseline after 1 month, exceptions to this include the elderly and those with pre-existing cardiopulmonary disease.
What makes interpretation of V/Q scans difficult?
Pre-existing lung disease like COPD, bronchitis and restrictive lung disease, especially if there is no prior CXR to compare against.
What type of PE do V/Q scans suck at picking up?
Saddle emboli. This is because they do not yet affect the smaller pulmary arteries and perfusion deficits will not be prominent. This is one reason why we use CTPA.
When would you consider placement of a Greenfield infrarenal IVC filter?
Heparin failure to prevent PE and complications with heparin
Phlegmasia cerulea dolens
Acute interruption of venous outflow resulting in inflammation, cyanosis and pain in the affected limb that can progress to sensorimotor loss and venous gangrene.
Tx of phlegmasia cerulea dolens
Anticoagulation and limb elevation come 1st. Then proceed to confirming the diagnosis with duplex u/s, CT or contrast venography. Most conditions resolve with this treatment, venous thrombectomy is rarely indicated.
