vascular Flashcards
what is an aneurysm
focal dilation/increase in arterial diameter of an artery, generally beyond 50%
fusiform–> bulges out on all sides
saccular–> bulges at one site on one side–> generally more dangerous
where do aneurysms occur?
infrarenal aorta is the most common
other aortic sites–> suprarenal, thoracic, abdominal
peripheral sites–> commonly femoral or popliteal
who should be screened for a AAA
all first degree relatives of AAA patients if above 50
all mean over 65 should have a screening U/S, especially if have risk factors like HTN
—> this is not done in canada because of funding
who should have their AAA treated?
those at risk of rupture (over or equal to 5.5 cm in diameter)
how do AAAs present?
rupture is almost always fatal–> sudden severe abdo pain and CV collapse
can also be asymptomatic on exam when not ruptures
focal dilation of AA with a major risk of rupture and bleeding
what do you expect to find on the physical exam of someone with a AAA
upper abdo pulsatile mass, non tender, pulsatility beside it too
assess presence and estimate size (transverse diameter)
what investigations should be done for a AAA
U/S
CT from arch to groin if needed
what causes aneurysms
age is a significant risk factor
CV disease–> impacted by smoking, atherosclerosis, hypercholesterolemia, family history
males get them more often
what determines the risk of rupture for a AAA
size related mostly
we fix large aneurysms and leave small ones with monitoring
asymptomatic indications are generalyl for greater than 5-5.5 cm in transverse diameter
surgery for smaller aneurysms does not seem to provide additional survival benefit
indications for aortic aneurysm repair
- rupture is most important reason–> most urgent and serious symptom
- emboli and thrombosis (microemboli and thrombotic debris can be thrown into smaller vessels, causing ischemia)
- pain or tenderness
- mass effect
what is the classic triad of ruptured AAA symptoms
abdo pain
pulsatile mass
hypotension
ddx for ruptured AAA
pancreatitis perforated viscus ischemic bowel renal colic MI with abdo pain pneumonia
what are the two main ways aortic aneurysms are repaired
- open repair
2. endovascular stent graft repair (more common)–> metal stent framework with fabric sent through the femoral artery
how do you perform an open aortic aneurysm repair
open repair with graft replacement sewn into inside of vessel (dont even have to remove aortic husk)
risks are less than 5% mortality
how do you manage a ruptured AAA
- urgent transfer to tertiary center with retroperitoneal containment
- poor prognosis–> 50/50 of those who make it to hospital
- ABCs
- -volume resuscitation–> at least two large bore IVs with crystalloid, blood, cross match
- -limit resus to BP max of about 100-110 (HTN may pop it) and clinical indications until you have definitive control
- -normal BP in ruptured aneurysm is not a cause for complacency - endovascular repair with aortic balloon occlusion
how do popliteal aneurysms present
non painful, non tender pulsatile mass behind knee
femoral mass on CT and filated popliteal artery
common complications of popliteal aneurysm
typically cause microemboli–> blue foot, extremely painful infarction of the toes
knee keeps flexing and extending, squeezing the aneurysm which fragments emboli into the feet
may have limb or tissue loss
what is the indication to treat a popliteal aneurysm
just its presence alone–> because of high risk for embolism
bypass or stent graft
what are the main complications of visceral aneurysms
rupture/hemorrhage
what are the indications for visceral aneurysm repair
greater than 2cm because of risk of rupture
not true in young women–> pregnancy weakens arterial walls and can cause rupture so all visceral aneurysms are treated in young women
ddx for TIA/stroke
TIA (stroke if weakness beyond 24 hours)
seizure
migraine
hemorrhagic stroke (transient as edema subsides)
tumour
define TIA
transient focal loss of neurological function–> usually diagnosed based on history, usually due to ischemic events
can be anywhere between the heart and head–> great vessels, carotid bifurcation, lacunae, small vessels
carotids are common site of origin
list the causes of stroke
- intracranial hemorrhage
- TIA
- cardiogenic embolus–> afib, MI (causes thrombogenic surfaces in the heart), valvular heart disease
- small vessel occlusion in the head
- non vascular pathology (ie tumour)
what investigations should be done in stroke patients
CT
vascular imaging/angiogram
maybe cardiac imaging
how should you manage a TIA/stroke patient
- treat right away and investigate for a cause right away–> risk of further stroke is highest immediately following TIA or initial minor stroke –> hard to predict what the next event will be
- immediately people get ASPIRIN when come in the door (antiplatelet to prevent furhter emboli) or CLOPIDOGREL
- statin drugs immediately to lower lipids and stabilize plaque
- some BP control indicated but want to avoid excessive BP lowering (may extend ischemia)
- anticoagulation with heparin NOT normally indicated if its an ischemic stroke
- thrombolysis–> tPA only if the patient is seen in the first 3 hours, if there is still deficit present, if the CT is negative for intracranial hemorrhage and there are no contraindications
- intracranial clot suction if visualized in a tertiary location
what is the most common location of a TIA or stroke etiology
extracranial carotid artery
how do you perform carotid enderarterectomy
open artery
extract intimal layer and its debris
partch artery
leave artery with smooth intraluminal surface
small but serious surgery
what are the risks associated with carotid enderarterectomy surgery
1-2% risk of stroke associated with surgery but without surgery and only medical therapy, the risk of stroke is usually much higher
indications for carotid enderarterectomy
simple and stenosis based
- in symptomatic carotid stenosis–> greater than 50% stenosis following TIA or minor stroke ipsilateral to the carotid stenosis lesion with recovery
- in asymptomatic stenosis–> 80% occlusion in low surgical risk patients found accidentally on imaging but havent had a TIA–> still benefits from enderarterectomy as not all strokes are preceeded by a TIA or a TIA isnt recognized
what are the long term outcomes of stroke patients
about 25% recover
about 25% die
about 25% have some form of permanent disability
what is the initial management of MVA leg trauma
- ABCs–stabilize BP
- DE
- xray etc…
how do embolism and thrombosis differ with regard to the following characteristic:
onset
embolism–sudden
thrombosis–less dramatic
how do embolism and thrombosis differ with regard to the following characteristic:
prior claudication
embolism–rare
thrombosis–common
how do embolism and thrombosis differ with regard to the following characteristic:
source (afib/AAA)
embolism–yes
thrombosis–no
how do embolism and thrombosis differ with regard to the following characteristic:
arrhythmia
embolism–common
thrombosis–possible
how do embolism and thrombosis differ with regard to the following characteristic:
other leg
embolism–usually normal
thrombosis–usually abnormal
how do embolism and thrombosis differ with regard to the following characteristic:
angiogram
embolism–sharp cutoff
thrombosis–diffuse disease
what are the 6 Ps of limb ischemia
Paralysis–most important; if you have paralysis you have 6 hours to revacsularize before necrosis begins
Pain
Pallor
Poikilothermia
Pulselessness
Paresthesia
what is the simple treatment of fracture
reduce the fracture quickly before muscle spasm sets it
if ischemia persists, need to call for help (as an MSI)
what is compartment syndrome
reperfusion of the revascularized limb–leads to disruption of cellular membranes, swelling and pressure in the muscular compartments, then pain and numbness
you need to do a surgical FASCIOTOMY down to the muscle to relieve the muscle of swelling (medial and lateral incision down to the muscle bellies)
what are causes of acute arterial ischemia
thrombosis
EMBOLUS
dissection
how do you manage a patient with peripheral ischemia due to a cardiac embolus
HEPARIN is of vital important (unfractionated) in acute ischemic conditions
can do CT/angio now because is fast enough that it doesnt unnecessarily delay surgery
surgery should be done ASAP especially if paralysis present
what are the 4 stages of progression of peripheral vascular disease
stage 1–non specific symptoms
stage 2–intermittent claudication; benign, and doesnt necessarily require intervention
stage 3–rest pain; especially in people who smoke/have diabetes; skin can break pen and cause holes or wounds or sores, especially over bony prominences, that can lead to gangrene
stage 4–ulceration, gangrene
ddx of claudication
- neurogenic claudication
- -immediate pain upon standing or sitting, usually predictable during exercise that doesnt go away right after stopping exercise - arthritis
- -this typically is pain in joints - excessive lactic acidosis from over activity or inadequate training
- rare causes
- -myositis
- -cellulitis
define claudication
leg pain during walking
most claudicants should be managed with risk factor modification initially (while still benign)
only 1% of patients progress to limb loss
what is the most useful exam for those with claudication
measurement of resting and exercise ankle pressures–>
ankle-brachial index measured at the pedal pulse
an A-B index of above 1 or equal to 1 is considered normal
what is the number one risk factor for claudication and PVD
smoking
treatment for claudication
NO SMOKING
exercise primarily by walking until the pain occurs, but then push yourself (isnt harmful to muscles) and over time this will help collateral vessels
walk twice daily or join a club for team behavioural modification
meds–>most target CVD because there is so much overlap
- -statins
- -antiplatelets (ASA or plavix)
- -other medical condition treatments (for DM, HTN etc)
how do you manage diabetic foot
multidisciplinary (vascular, podiatry, endo etc)
swab for C and S, broad spectrum abx, management of infection and possible sepsis etc
wound care and surgical debridement and specialized dressings
xray to look for bone infection or gas gangrene (requires urgent surgery
ABI index with or without imaging to assess ischemia stage
revascularize and debride or amputate as needed
remove pressure (special shoes etc)
how does critical limb ischemia present
- rest pain
- ischemic ulcer (toe or heel)
- gangrene (toe or heel)
management of critical limb ischemia
- high risk for amputation (20% per year)
- need referral
- imaging and revascularization (endovascular approach or open/surgical approach)
what is the rate of DVT in north america
1/1000
increases with age
what is virchows triad
etiology of DVT–
- stasis
- hypercoagulability
- vessel wall damage
symptoms of DVT
may have minimal sx
pain
swelling
erythema
clinical diagnosis is thus unreliable
what test is usually used to diagnose DVT
U/S–90% accuracy
risk factors for DVT
immobility obesity malignancy pregnancy CHF age hypercoagulable state trauma/surgery previous DVT
investigations for DVT
blood work including: INR PTT platelets Hbg Hct
coagulation workup to assess for thrombophilia protein C and S antithrombin III factor V leiden lupus antocoagulant
treatment for DVT
anticoagulation, initially with UNFRACTIONATED HEPARIN or LMW heparin then oral therapy with coumadin for 3-6 months
side effects: bleeding, HIT, osteoporosis
coumadin can cause bleeding, skin necrosis and teratogenicity
can also use compressive treament (i.e elastic stockings) of the legs
what are the wells criteria for PE
symptoms of DVT
no alternative better diagnosis
tachy with pulse above 100
immobilization more than 3 days or surgery in previous 4 weeks
prior history of DVT or PE
presence of hemoptysis
presence of malignancy
list complications of DVT
- PE–up to 50%
- venous valvular incompetence–up to 100% (late)
- recurrent thrombosis–most common early but continues long term, up to 10%
- post phlebetic syndrome–months to many years, 50% but greater with follow up exceeding 5 years
- paradoxial embolus–imemdiate, low frequency
how do you classify DVT
based on location in leg
class I–> isolated to calf; low incidence of post thrombotic or post phlebitis syndrome
class II–> popliteal area
from the level of the common femoral vein (Class III) and up, there are fewer collaterals and less valves
how is fem-pop DVT best managed
mostly recanalizes, with last post phlebetic syndrome due to valvular reflux….. best managed by anticoagulation
how is iliofemoral DVT best managed
few valves
has little recanalization and postphlebetic syndrome occurs immediately due to obstruction from venous thrombosis—best managed by thrombolysis with or without stent if iliac vein is narrowed
what might be helpful in patients with high risk of DVT who are taking a long plane ride
single dose of LMWH
in which patients is an IVC filter indicated
in patients with DVT and PE that are recurrent on anticoagulation or are contraindicated with anticoagulants (they are inserted to catch potential pulmonary emboli)
prevents potentially fatal PE but does not treat the DVT
as soon as the patient can be anticoagulated, they should be
give symptomatic leg treatment with compression stockings
list the types of chronic venous disease
varicose veins
ededma
skin changes
venous ulcers
what is the CEAP classification for chronic venous disease
C0–no signs
C1–telangiectasia
C2–varicose veins
C3–peripheral edema
C4–skin pigmentation and lipodermatosclerosis
C5–healed ulcer
C6–active venous ulcer
symptoms of varicose veins
pain with standing, specifically in the veins
heaviness
increased warmth (from blood)
itchiness (blood and histamine)
leg cramps (etiology unsure)
usually NOT foot pain
causes of varicose veins
valvular incompetence
more common in women
family history, age, ethnicity (more in latinos), pregnancy, obesity, prior deep vein clot all increase the risk and incidence
pathophysiology of varicose veins
reflux in saphenous vein causes venous hypertension in superficial veins of the leg
normal valve function in deep veins and perforating veins (though they can be involved)
venous recirculation and congestion in lower leg
treatment/management of varicose veins
thorough diagnosis followed up by U/S to ID the highest level of competence and where the problem starts, then treat in a top-down way
remove truncal reflux first–in the greater or lesser saphenous veins, then address the residual reflux in smaller branches
surgery (ligation or stripping of saphenous veins)–> removal of saphenous vein
endothermal treatment (destruction of the vein by lasers or radiofrequency)
foam sclerotherapy
compression stockings
how do you treat non-truncal varicosities
phlebotomy (can be outpatient with micropunctures)
sclerotherapy (foam or liquid)
compression stockings
list complications of chronic venous disease
thrombosis
bleedings
dermatitis
ulcers
describe how thrombosis can result from chronic venous disease and how it can present
superficial thrombosis is usually related to the size of the varicosities initiated by stasis or trauma
presents acutely with pain, heat, erythema, and rarely embolize to PE
treat with symptomatic relief, but watch for propagation to saphenofemoral junction
assess with U/S and again if pain continues or migrates to saphenofemoral junction–treatt with ICE not with warm compresses
abx NOT helpful
consider LMWH for large thromboses resistant to conservative treatment
how should you manage ulcers caused by chronic venous disease
rule out arterial ischemia
dont culture unless significant pain, pus or drainage
use specialized dressings (Profore) that are very tight (only if ABI above 7) and then stockings after ulcer heals and refer to vascular specialist for long term management of reflux in the veins
