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Surgery > vascular > Flashcards

vascular Flashcards

1
Q

what is an aneurysm

A

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

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2
Q

where do aneurysms occur?

A

infrarenal aorta is the most common

other aortic sites–> suprarenal, thoracic, abdominal

peripheral sites–> commonly femoral or popliteal

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3
Q

who should be screened for a AAA

A

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

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4
Q

who should have their AAA treated?

A

those at risk of rupture (over or equal to 5.5 cm in diameter)

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5
Q

how do AAAs present?

A

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

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6
Q

what do you expect to find on the physical exam of someone with a AAA

A

upper abdo pulsatile mass, non tender, pulsatility beside it too

assess presence and estimate size (transverse diameter)

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7
Q

what investigations should be done for a AAA

A

U/S

CT from arch to groin if needed

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8
Q

what causes aneurysms

A

age is a significant risk factor

CV disease–> impacted by smoking, atherosclerosis, hypercholesterolemia, family history

males get them more often

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9
Q

what determines the risk of rupture for a AAA

A

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

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10
Q

indications for aortic aneurysm repair

A
  1. rupture is most important reason–> most urgent and serious symptom
  2. emboli and thrombosis (microemboli and thrombotic debris can be thrown into smaller vessels, causing ischemia)
  3. pain or tenderness
  4. mass effect
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11
Q

what is the classic triad of ruptured AAA symptoms

A

abdo pain

pulsatile mass

hypotension

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12
Q

ddx for ruptured AAA

A 
pancreatitis
perforated viscus
ischemic bowel
renal colic
MI with abdo pain
pneumonia
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13
Q

what are the two main ways aortic aneurysms are repaired

A
  1. open repair

2. endovascular stent graft repair (more common)–> metal stent framework with fabric sent through the femoral artery

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14
Q

how do you perform an open aortic aneurysm repair

A

open repair with graft replacement sewn into inside of vessel (dont even have to remove aortic husk)

risks are less than 5% mortality

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15
Q

how do you manage a ruptured AAA

A
  1. urgent transfer to tertiary center with retroperitoneal containment
  2. poor prognosis–> 50/50 of those who make it to hospital
  3. 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
  4. endovascular repair with aortic balloon occlusion
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16
Q

how do popliteal aneurysms present

A

non painful, non tender pulsatile mass behind knee

femoral mass on CT and filated popliteal artery

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17
Q

common complications of popliteal aneurysm

A

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

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18
Q

what is the indication to treat a popliteal aneurysm

A

just its presence alone–> because of high risk for embolism

bypass or stent graft

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19
Q

what are the main complications of visceral aneurysms

A

rupture/hemorrhage

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20
Q

what are the indications for visceral aneurysm repair

A

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

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21
Q

ddx for TIA/stroke

A

TIA (stroke if weakness beyond 24 hours)

seizure

migraine

hemorrhagic stroke (transient as edema subsides)

tumour

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22
Q

define TIA

A

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

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23
Q

list the causes of stroke

A
  1. intracranial hemorrhage
  2. TIA
  3. cardiogenic embolus–> afib, MI (causes thrombogenic surfaces in the heart), valvular heart disease
  4. small vessel occlusion in the head
  5. non vascular pathology (ie tumour)
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24
Q

what investigations should be done in stroke patients

A

CT

vascular imaging/angiogram

maybe cardiac imaging

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25
Q

how should you manage a TIA/stroke patient

A
  1. 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
  2. immediately people get ASPIRIN when come in the door (antiplatelet to prevent furhter emboli) or CLOPIDOGREL
  3. statin drugs immediately to lower lipids and stabilize plaque
  4. some BP control indicated but want to avoid excessive BP lowering (may extend ischemia)
  5. anticoagulation with heparin NOT normally indicated if its an ischemic stroke
  6. 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
  7. intracranial clot suction if visualized in a tertiary location
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26
Q

what is the most common location of a TIA or stroke etiology

A

extracranial carotid artery

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27
Q

how do you perform carotid enderarterectomy

A

open artery

extract intimal layer and its debris

partch artery

leave artery with smooth intraluminal surface

small but serious surgery

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28
Q

what are the risks associated with carotid enderarterectomy surgery

A

1-2% risk of stroke associated with surgery but without surgery and only medical therapy, the risk of stroke is usually much higher

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29
Q

indications for carotid enderarterectomy

A

simple and stenosis based

  1. in symptomatic carotid stenosis–> greater than 50% stenosis following TIA or minor stroke ipsilateral to the carotid stenosis lesion with recovery
  2. 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
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30
Q

what are the long term outcomes of stroke patients

A

about 25% recover
about 25% die
about 25% have some form of permanent disability

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31
Q

what is the initial management of MVA leg trauma

A
  1. ABCs–stabilize BP
  2. DE
  3. xray etc…
32
Q

how do embolism and thrombosis differ with regard to the following characteristic:
onset

A

embolism–sudden

thrombosis–less dramatic

33
Q

how do embolism and thrombosis differ with regard to the following characteristic:
prior claudication

A

embolism–rare

thrombosis–common

34
Q

how do embolism and thrombosis differ with regard to the following characteristic:
source (afib/AAA)

A

embolism–yes

thrombosis–no

35
Q

how do embolism and thrombosis differ with regard to the following characteristic:
arrhythmia

A

embolism–common

thrombosis–possible

36
Q

how do embolism and thrombosis differ with regard to the following characteristic:
other leg

A

embolism–usually normal

thrombosis–usually abnormal

37
Q

how do embolism and thrombosis differ with regard to the following characteristic:
angiogram

A

embolism–sharp cutoff

thrombosis–diffuse disease

38
Q

what are the 6 Ps of limb ischemia

A

Paralysis–most important; if you have paralysis you have 6 hours to revacsularize before necrosis begins

Pain

Pallor

Poikilothermia

Pulselessness

Paresthesia

39
Q

what is the simple treatment of fracture

A

reduce the fracture quickly before muscle spasm sets it

if ischemia persists, need to call for help (as an MSI)

40
Q

what is compartment syndrome

A

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)

41
Q

what are causes of acute arterial ischemia

A

thrombosis

EMBOLUS

dissection

42
Q

how do you manage a patient with peripheral ischemia due to a cardiac embolus

A

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

43
Q

what are the 4 stages of progression of peripheral vascular disease

A

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

44
Q

ddx of claudication

A
  1. neurogenic claudication
    - -immediate pain upon standing or sitting, usually predictable during exercise that doesnt go away right after stopping exercise
  2. arthritis
    - -this typically is pain in joints
  3. excessive lactic acidosis from over activity or inadequate training
  4. rare causes
    - -myositis
    - -cellulitis
45
Q

define claudication

A

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

46
Q

what is the most useful exam for those with claudication

A

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

47
Q

what is the number one risk factor for claudication and PVD

A

smoking

48
Q

treatment for claudication

A

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)
49
Q

how do you manage diabetic foot

A

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)

50
Q

how does critical limb ischemia present

A
  1. rest pain
  2. ischemic ulcer (toe or heel)
  3. gangrene (toe or heel)
51
Q

management of critical limb ischemia

A
  1. high risk for amputation (20% per year)
  2. need referral
  3. imaging and revascularization (endovascular approach or open/surgical approach)
52
Q

what is the rate of DVT in north america

A

1/1000

increases with age

53
Q

what is virchows triad

A

etiology of DVT–

  1. stasis
  2. hypercoagulability
  3. vessel wall damage
54
Q

symptoms of DVT

A

may have minimal sx

pain
swelling
erythema

clinical diagnosis is thus unreliable

55
Q

what test is usually used to diagnose DVT

A

U/S–90% accuracy

56
Q

risk factors for DVT

A 
immobility
obesity
malignancy
pregnancy
CHF
age
hypercoagulable state
trauma/surgery
previous DVT
57
Q

investigations for DVT

A 
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
58
Q

treatment for DVT

A

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

59
Q

what are the wells criteria for PE

A

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

60
Q

list complications of DVT

A
  1. PE–up to 50%
  2. venous valvular incompetence–up to 100% (late)
  3. recurrent thrombosis–most common early but continues long term, up to 10%
  4. post phlebetic syndrome–months to many years, 50% but greater with follow up exceeding 5 years
  5. paradoxial embolus–imemdiate, low frequency
61
Q

how do you classify DVT

A

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

62
Q

how is fem-pop DVT best managed

A

mostly recanalizes, with last post phlebetic syndrome due to valvular reflux….. best managed by anticoagulation

63
Q

how is iliofemoral DVT best managed

A

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

64
Q

what might be helpful in patients with high risk of DVT who are taking a long plane ride

A

single dose of LMWH

65
Q

in which patients is an IVC filter indicated

A

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

66
Q

list the types of chronic venous disease

A

varicose veins

ededma

skin changes

venous ulcers

67
Q

what is the CEAP classification for chronic venous disease

A

C0–no signs

C1–telangiectasia

C2–varicose veins

C3–peripheral edema

C4–skin pigmentation and lipodermatosclerosis

C5–healed ulcer

C6–active venous ulcer

68
Q

symptoms of varicose veins

A

pain with standing, specifically in the veins

heaviness

increased warmth (from blood)

itchiness (blood and histamine)

leg cramps (etiology unsure)

usually NOT foot pain

69
Q

causes of varicose veins

A

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

70
Q

pathophysiology of varicose veins

A

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

71
Q

treatment/management of varicose veins

A

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

72
Q

how do you treat non-truncal varicosities

A

phlebotomy (can be outpatient with micropunctures)

sclerotherapy (foam or liquid)

compression stockings

73
Q

list complications of chronic venous disease

A

thrombosis

bleedings

dermatitis

ulcers

74
Q

describe how thrombosis can result from chronic venous disease and how it can present

A

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

75
Q

how should you manage ulcers caused by chronic venous disease

A

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

Surgery (20 decks)

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