Today we discussed an approach to a patient with an ischemic limb. This may be subdivided into acute vs. chronic ischemia, as these present and are managed differently.
Chronic peripheral arterial disease
Occurs in patients with vascular risk factors; almost always accompanied by CAD and cerebrovascular disease
Usually affects 3 distinct areas:
Aortoiliac-weak/absent femoral pulse (and popliteal, DP)
Femoropopliteal- weak/absent popliteal pulse (and DP)
Peroneotibial - weak/absent dorsalis pedis
Symptoms: Claudication, arterial ulcers and their complications (usually on toes, heel)
Signs:
-Skin, hair, nail changes- definitely should look, but not very helpful when looked at from EBM standpoint
Wounds/sores/ulcers- very specific; classically punched-out ulcer without surrounding venous stasis changes
-Temperature: asymmetrically cool foot is not sensitive, but is quite specific for PAD
-Pulses: absent femoral pulse is highly specific, not sensitive. Any absence of femoral, popliteal, DP is sensitive (i.e. if there is no pulse abnormality at all, negative LR is 0.3). Presence of any pulse abnormality is reasonably specific (positive LR is 15)
-Bruits: Presence is specific, absence is not helpful (i.e. not very sensitive)
-Special tests:
Cap refill: should do, but not very helpful from EBM standpoint
Pallor on elevation, dependent rubor: Sensitive for femoropopliteal disease, not very specific.
Venous refill time (find a prominent foot vein, elevate the leg to at least 45 degrees for one minute then sit patient up and measure the time it takes for the vein to rise above the skin surface again)- over 20s is very specific, but not sensitive.
Investigations: Ankle-brachial index
1.3: non-compressible, calcified arteries
1.0-1.3: normal
0.4-0.9: moderate obstruction, often with claudication
less than 0.4: advanced ischemia
Others: Arterial dopplers, angiogram (CTA, conventional angiogram)
Therapy:
Non-pharmacologic: exercise, smoking cessationPharmacologic: evidence for clopidogrel from CAPRIE trial; soft evidence for pentoxifylline
Aortoiliac-weak/absent femoral pulse (and popliteal, DP)
Femoropopliteal- weak/absent popliteal pulse (and DP)
Peroneotibial - weak/absent dorsalis pedis
Symptoms: Claudication, arterial ulcers and their complications (usually on toes, heel)
Signs:
-Skin, hair, nail changes- definitely should look, but not very helpful when looked at from EBM standpoint
Wounds/sores/ulcers- very specific; classically punched-out ulcer without surrounding venous stasis changes
-Temperature: asymmetrically cool foot is not sensitive, but is quite specific for PAD
-Pulses: absent femoral pulse is highly specific, not sensitive. Any absence of femoral, popliteal, DP is sensitive (i.e. if there is no pulse abnormality at all, negative LR is 0.3). Presence of any pulse abnormality is reasonably specific (positive LR is 15)
-Bruits: Presence is specific, absence is not helpful (i.e. not very sensitive)
-Special tests:
Cap refill: should do, but not very helpful from EBM standpoint
Pallor on elevation, dependent rubor: Sensitive for femoropopliteal disease, not very specific.
Venous refill time (find a prominent foot vein, elevate the leg to at least 45 degrees for one minute then sit patient up and measure the time it takes for the vein to rise above the skin surface again)- over 20s is very specific, but not sensitive.
Investigations: Ankle-brachial index
1.3: non-compressible, calcified arteries
1.0-1.3: normal
0.4-0.9: moderate obstruction, often with claudication
less than 0.4: advanced ischemia
Others: Arterial dopplers, angiogram (CTA, conventional angiogram)
Therapy:
Non-pharmacologic: exercise, smoking cessationPharmacologic: evidence for clopidogrel from CAPRIE trial; soft evidence for pentoxifylline
Surgical: Stenting, revascularization
Acute limb ischemia:
Acute onset of P's: pain (esp. resting), pallor, pulselessness, parasthesia, paralysis.
Etiology- thrombotic vs. embolic.
If thrombotic, usually progression of atherosclerotic disease to critical point. Other possibilites include primary arterial disease (i.e. large vessel vasculitis), spontaneous arterial clot event (e.g. antiphospholipid antibody syndrome, myeloproliferative disorders, Bechet's, possibly hyperhomocysteinemia, others)
If embolic, cardioembolic is common- A-fib, akinetic LV
Therapy: Anticoagulation and urgent surgical intervention- open or endovascular.
Links:
Acute limb ischemia:
Acute onset of P's: pain (esp. resting), pallor, pulselessness, parasthesia, paralysis.
Etiology- thrombotic vs. embolic.
If thrombotic, usually progression of atherosclerotic disease to critical point. Other possibilites include primary arterial disease (i.e. large vessel vasculitis), spontaneous arterial clot event (e.g. antiphospholipid antibody syndrome, myeloproliferative disorders, Bechet's, possibly hyperhomocysteinemia, others)
If embolic, cardioembolic is common- A-fib, akinetic LV
Therapy: Anticoagulation and urgent surgical intervention- open or endovascular.
Links:
Click here for JAMA: Does the Clinical Examination Predict Lower Extremity Peripheral Arterial Disease?
Click here for Archives of Internal Medicine: Physical examination and chronic lower-extremity ischemia: a critical review
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