3: aortic and peripheral vascular disease Flashcards
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)
risk factors for aortic dissection
hypertension 67%
collagen disorders (marfan’s 1/3 develop dissection)
pregnancy (half under 40 y/o)
congenital heart defects
aortic dissection pathophysiology
medial degeneration (loss of smooth mm. and elastic fibers) repeated flexion of aorta hydrodynamic stress on intima
*not aneurysmal!!
DeBakey classifications of aortic dissection
type I - asc/arch/desc
type II - ascending only
type IIIa - descending, above diaphragm
type IIIb - descending, below diaphragm
aortic dissection presentation
tearing, ripping, knife-like pain
migrating pain (radiates to back)
vasovagal symtoms
neuro deficits, syncope in some
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)
diagnostic tests ordered in aortic dissection
labs
EKG
imaging - CXR
-echo/TEE!
CT scan
aortographytreatment for type A aortic dissections
surgical repair
- resect original tear
- graft blood to true lumen
- operative mortality 7%
treatment for type B aortic dissections
medical management
-BP control (B blockers, 15-20% mortality)
surgical management if:
- increasing pain
- HTN
- major branch occlusion
epidemiology of abdominal aortic aneurysm (AAA)
degenerative process of aging (nonspecific)
65-70 y/o
risk factors for AAA
age more than 65
PAD
FH
other arterial aneurysms
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)
presentation of unruptured AAA
abdominal pain, back or flank pain
gradual onset/vague/dull quality (colicky)
presentation of ruptured AAA
pain
hypotension
pulsatile abdominal mass
AAA physical exam
HALLMARK: pulsatile, expansile abdominal mass***
abdominal bruits
pulses often maintained
early findings of thromboembolic events suggest proximal source (blue toes)
AAA diagnostic testing
stable: duplex screening
acute symptoms: bedside DUS to conform to surgery
-presence of AAA
-free fluid in abdomen
asymptomatic management of AAA
serial DUS until >4.0 or symptoms
patient education
symptomatic management of AAA
surgical repair
- endovascular
- open techniques
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
atherosclerosis risk factors
cigarettes
diabetes
hypercholesterolemia
HTN
presentations of PAD
- thromboembolic
- symptoms of claudication
- “my leg fell off”
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
