progressive enlargement leading to rupture and fatal hemorrhage - majority die before getting to hospital - average growth rate 0.2-0.5 cm/y - most ruptures more than 5 cm (but may rupture earlier)

- thromboembolic - symptoms of claudication - "my leg fell off"

3: aortic and peripheral vascular disease Flashcards by Katie Hutchins

give me some epidemiology facts about aortic dissection

5-10/1million
most lethal condition
males 2-3x more
50-70 y/o (except collagen shit, congenital shit, pregnancy, coarctation, turner syndrome, trauma)

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risk factors for aortic dissection

hypertension 67%
collagen disorders (marfan’s 1/3 develop dissection)
pregnancy (half under 40 y/o)
congenital heart defects

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aortic dissection pathophysiology

medial degeneration (loss of smooth mm. and elastic fibers) 
repeated flexion of aorta 
hydrodynamic stress on intima

*not aneurysmal!!

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DeBakey classifications of aortic dissection

type I - asc/arch/desc
type II - ascending only
type IIIa - descending, above diaphragm
type IIIb - descending, below diaphragm

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aortic dissection presentation

tearing, ripping, knife-like pain
migrating pain (radiates to back)
vasovagal symtoms
neuro deficits, syncope in some

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aortic dissection physical exam

general - apprehensive, sense of impending doom
tachycardia
cool clammy skin
BP disconnect (central vs. peripheral)
murmur - suggesting aortic regurgitation
signs of tamponade (friction rub, JVD, pulsus paradoxus, muffled heart tones)

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diagnostic tests ordered in aortic dissection

labs 
EKG 
imaging - CXR 
              -echo/TEE! 
CT scan 
aortography

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treatment for type A aortic dissections

surgical repair

resect original tear
graft blood to true lumen
operative mortality 7%

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treatment for type B aortic dissections

medical management
-BP control (B blockers, 15-20% mortality)

surgical management if:

increasing pain
HTN
major branch occlusion

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epidemiology of abdominal aortic aneurysm (AAA)

degenerative process of aging (nonspecific)

65-70 y/o

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risk factors for AAA

age more than 65
PAD
FH
other arterial aneurysms

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AAA natural history

progressive enlargement leading to rupture and fatal hemorrhage

majority die before getting to hospital
average growth rate 0.2-0.5 cm/y
most ruptures more than 5 cm (but may rupture earlier)

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presentation of unruptured AAA

abdominal pain, back or flank pain

gradual onset/vague/dull quality (colicky)

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presentation of ruptured AAA

pain
hypotension
pulsatile abdominal mass

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AAA physical exam

HALLMARK: pulsatile, expansile abdominal mass***
abdominal bruits
pulses often maintained
early findings of thromboembolic events suggest proximal source (blue toes)

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AAA diagnostic testing

stable: duplex screening
acute symptoms: bedside DUS to conform to surgery
-presence of AAA
-free fluid in abdomen

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asymptomatic management of AAA

serial DUS until >4.0 or symptoms

patient education

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symptomatic management of AAA

surgical repair

endovascular
open techniques

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PAD/atherosclerosis pathophysiology

large/medium arteries
basic lesion - fibrofatty plaque + raised lesion w/i intima
progression - plaques increase in size and thickness
ultimately compromise arterial flow

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atherosclerosis risk factors

cigarettes
diabetes
hypercholesterolemia
HTN

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presentations of PAD

thromboembolic
symptoms of claudication
“my leg fell off”

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describe arterial insufficiency

symptoms worsen with ambulation
elevation worsens
weak/absent pulses
compression worsens
lack of oxygenated blood to tissues

describe venous insufficiency

symptoms improve with ambulation
elevation helps
normal pulses
compression helps
excess of deoxygenated blood pooling in tissues

diagnostic work up for arterial insufficiency

segmental arterial pressure study

cuff arms + 3 or 4 on limbs
couple DUS with actual BP measurement
compares limbs
identifies level of lesion

ABI

less than 0.7 significant disease
less than 0.5 rest pain is common

angiogram
-allows for surgical planning (open vs. endovascular)

emergent surgical management of PAD

- acute thrombosis - plaque disruption, thrombophilia - intractable rest pain due to ischemia - gangrenous limbs

expectant management of PAD

claudication mild symtpoms - anti-platelet therapy - compression therapy - follow symptoms and restudy if symptoms worsen - encourage cessation of smoking

does PAD or venous insufficiency affect more people?

venous insufficiency

complication of venous insufficiency

stasis ulcers

what is the 3rd most common cause of death among hospitalized patients?

fatal PE

what symptoms do patients who survive DVT +/- PE get?

chronic pain and swelling

which gender gets venous insufficiency more?

females to males 3:1

musculovenous pump: what happens to blood during muscle relaxation?

blood is drawn inward through perforating veins superficial veins act as collecting system

describe the superficial venous system

vessels relatively more fragile values are less well developed lack of structural support from superficial tissue

physical findings in venous insufficiency

venulectasia/telangiectasia combined tributary and small vessel disease hyperpigmentation (chronic venous pressure - hemosiderin) eczematoid dermatitis atrophie blanche corona phlebectatica stasis dermatitis lipodermatosclerosis (sclerosing panniculitis) superficial thrombophlebitis stasis ulceration recurrent stasis ulcer

what is eczematoid dermatitis?

inflammation typically adjacent to a bulbous tributary

what is atrophie blanche?

inflammation and scarring leading to plaques of skin without pigment

what is corona phlebectatica?

red flare around a lesion that is a pre-cursor to stasis ulceration

what is stasis dermatitis?

heavy inflammatory changes in a gaiter area bilaterally in a patient with bilateral saphenous vein reflux - pre ulcerous condition

what is lipodermatosclerosis/sclerosing panniculitis?

painful inflammatory lesions that are firm and contracted - pre ulcerous

what is superficial thrombophlebitis?

firm palpable cords over superficial varices overlying inflammation common to see seasonal patterns

what is stasis ulceration?

end stage venous disease representing true urgency for control of venous condition

primary causes of varicose veins

hereditary hormonal pregnancy gravity

secondary causes of varicose veins

obesity trauma gravity occupations requiring prolonged sitting or standing

what are varicose veins a problem?

they can lead to complications from chronic venous HTN, similar to other chronic diseases that go unchecked

symptoms of varicose veins

pain heaviness intensification cramping

complications of varicose veins

``` superficial phlebitis (SVT) DVT venous stasis dermatitis/ulceration bleeding chronic pain syndrome ```

when is venous evaluation indicated?

presence of advanced disease quality of life impairment unexplained leg pain +/- swelling

ways to evaluate veins

hand held doppler (fairly high false (+); intersaphenous v.) detailed venous mapping

what treatment options are best?

depends, but generally speaking, lesser invasive therapies offer less pain and less down-time

what is thrombophilia

imbalance b/w clot formation and dissolution virchow's triad: injury, stasis, inherited/acquired changes

when do you consider thrombophilia?

``` young patient with VTE recurrent idiopathic thrombosis unusual site of thrombosis family history of VTE/multiple miscarriages heparin resistance warfarin induced skin necrosis ```

causes of thrombophilia: hereditary, loss of fxn

antithrombin deficiency | protein C and S deficiency

causes of thrombophilia: hereditary, gain of fxn

APC/factor V leiden mutation prothrombin gene mutation factor elevations hyperhomocysteinemia

causes of thrombophilia: acquired

anti-PLA syndrome HIT malignancy