CODES
ICD9
- 356.9 Unspecified hereditary and idiopathic peripheral neuropathy
- 782.0 Disturbance of skin sensation
ICD10
- G62.9 Polyneuropathy, unspecified
- R20.0 Anesthesia of skin
- R20.2 Paresthesia of skin
PERIPHERAL VASCULAR DISEASE
Sally A. Santen
•
Samantha R. Hauff
BASICS
DESCRIPTION
- Obstruction of ≥1 of the peripheral arteries secondary to embolism or thrombus
- Caused by atherosclerosis or embolus
- Patients with PAD may also have coronary artery and cerebrovascular disease.
- Epidemiology:
- Risks factors (selected):
- Age
- Smoking
- Diabetes
- Hyperlipidemia
- HTN
- Associated with morbidity and mortality from other forms of atherosclerosis (coronary artery disease, stroke)
- Complications:
- Aneurysm
- Thrombosis
- Ulceration
- Limb loss
- Chronic arterial insufficiency (CAI):
- Progressive obstructing atherosclerotic disease causing subacute ischemia and pain (claudication)
- 10% develop critical leg ischemia.
- Acute arterial insufficiency (AAI):
- Caused by arterial thrombosis (50%) or embolism
- Causes acute limb ischemia with signs and symptoms of the 6 Ps (below)
- Atheroembolism:
- Caused by rupture or partial disruption of an atherosclerotic plaque (aorta, femoral, iliac)
- Gives rise to cholesterol emboli that shower and obstruct arteriolar networks
- May be precipitated by invasive arterial procedures such as cardiac catheterization
ETIOLOGY
- Obstruction by atherosclerotic plaques (CAI)
- Arterial thrombosis
- Arterial emboli:
- Cardiac emboli from dysrhythmias, valvular heart disease, or cardiomyopathy (80%)
- Aneurysms
- Infection
- Tumor
- Vasculitis or foreign body
- Thrombosis of plaques from pre-existing CAI
- Atheroembolism
DIAGNOSIS
SIGNS AND SYMPTOMS
History
- CAI:
- Claudication:
- Aching pain in the calves (femoropopliteal occlusion) or buttocks and thighs (aortoiliac region)
- Occurs with activity and slowly relieved by rest or dependent positioning
- Classic claudication presents in about 1/2 of patients with PVD.
- Severe disease presents with limb pain at rest:
- Usually starting in the foot
- Rapidly progressive claudication or ulceration
- AAI:
- Extremity pain:
- Sudden onset
- Gradual increase in severity
- Starts distally and moves proximally over time
- Decrease in intensity once ischemic sensory loss occurs
- Atheroembolism:
- Complaint of cold and painful fingers or toes
- Small atherosclerotic emboli may affect both extremities.
- Usually related to recent arteriography, vascular or cardiac surgery
- Multiorgan involvement is common (renal, mesentery, skin, others)
Physical-Exam
ALERT
Sudden onset of pain and pallor in extremity is limb and life threatening.
- CAI:
- Absent or decreased peripheral pulses
- Delayed capillary refill with cool skin
- Increased venous filling time
- Bruits
- Pallor and dependent rubor of the leg
- Muscle and skin atrophy
- Thickened nails and loss of dorsal hair
- Ulcerations (especially toes or heels) or gangrene with severe disease
- AAI:
- 6 Ps:
- Pain (1st, sometimes only symptom)
- Pallor
- Pulselessness
- Poikilothermic
- Paresthesias (late finding)
- Paralysis (late finding)
- Identification of a source of a possible embolic process is crucial (atrial fibrillation, cardiomegaly).
- Atheroembolism:
- Ischemic and painful digits
- “Blue toe syndrome”
- Livedo reticularis
ESSENTIAL WORKUP
- CAI:
- Ankle–brachial index (ankle systolic BP divided by higher arm systolic BP)
- Bedside test to determine whether CAI is present (see NEJM video reference)
- Ratio of <0.9 is abnormal and <0.4--5 indicates severe disease.
- Calcific arteries (diabetes) can have false negative ABI or elevated ABI (>1.3).
- AAI:
- Physical diagnosis using the 6 Ps
- Those with acute-on-chronic arterial insufficiency tolerate limb ischemia better than those without CAI, due to well-developed collateral circulation.
- Atheroembolism:
- Clinical diagnosis: Affected areas painful, tender, and may be either dusky or necrotic
- Workup may investigate source of emboli with duplex US, CT angiogram, EKG.
DIAGNOSIS TESTS & NTERPRETATION
Lab
- CBC and platelets
- Electrolytes, BUN, creatinine, glucose
- Coagulation studies
- Creatine phosphokinase to evaluate for ischemia.
- Special tests for suspected etiologies:
- Hold blood for hypercoagulable studies
- Sedimentation rate, CRP for vasculitis
- Blood cultures for endocarditis
Imaging
- Doppler US:
- Visualizes both venous and arterial systems
- Identifies level of arterial occlusion, as well as thrombosis and aneurysm
- Sensitivity and specificity >80–90% for occlusion of vessels proximal to the popliteal vessels
- Plethysmography/segmental pressure measurements:
- Uses measurements of the volume and character of blood flow to detect areas of CAI
- Less widely available than US, therefore requires an experienced technician
- Approximates US in sensitivity and specificity
- Angiography:
- Determines details about the anatomy, including the level of occlusion, stenosis, and collateral flow
- Useful where the diagnosis of AAI is uncertain or before emergent bypass grafting
- Advantage is intervention (atherectomy, angioplasty, or intraluminal thrombolytics) can be done at the time of diagnosis.
- CT angiogram:
- CT is useful for diagnosis of occlusive aortic disease or dissection.
- Rapidly available and reliable
- Many centers have moved to CT angiogram as the 1st-line diagnostic tool. The decision for operative or angiographic intervention is based on the CT angiogram.
- Requires contrast, therefore may not be 1st line for patients with renal insufficiency
- MRI:
- Sensitive for evaluation of CAI and dissection
- Disadvantages are that MRI is time consuming and expensive.
DIFFERENTIAL DIAGNOSIS
- Acute thrombosis or emboli
- Arterial dissection
- Deep venous thrombosis
- Venous insufficiency
- Compartment syndrome
- Buerger disease
- Spinal stenosis
- Neuropathy
- Bursitis
- Arthritis
- Reflex sympathetic dystrophy
TREATMENT
PRE HOSPITAL
- Maintain hemodynamic stability with fluids.
- Apply cardiac monitor.
- Place the ischemic limb at rest and in a dependent position.
- Provide oxygen if low oxygen saturation or pulmonary symptoms.
INITIAL STABILIZATION/THERAPY
- IV fluid bolus for hypotension
- EKG, monitor, pulse oximetry
- Supplemental oxygen
- Pain control
- Avoid temperature extremes
ED TREATMENT/PROCEDURES
- CAI:
- Antiplatelet therapy with 75 or 325 mg of aspirin or clopidogrel (75 mg/day) may be used as 1st-line treatment. Dual therapy has not been shown to improve outcomes, although may be indicated in other forms of atherosclerosis.
- Other approved drugs include: Cilostazol 100 mg BID, dipyridamole 200 mg BID, pentoxifylline 400 mg TID
- Revascularization depending on the severity and location of obstruction:
- Balloon angioplasty
- Atherectomy
- Bypass grafting
- Risk-factor modification:
- Tobacco cessation
- Aggressive management of hyperlipidemia, HTN, diabetes
- Exercise therapy
- AAI:
- Limit further clot propagation with IV heparin.
- Do not anticoagulate patients suspected of having an aortic dissection or symptomatic aneurysm.
- Emergent consultation with vascular surgery or interventional radiology:
- To determine which diagnostic study is best to make the diagnosis
- To begin arrangements for possible operative therapy or other intervention
- Options for operative therapy include thrombectomy, embolectomy, angioplasty, regional arterial thrombolysis, bypass grafting.
- Blood flow to the affected limb must be re-established within 4–6 hr after onset of ischemic symptoms.
- Complications of AAI include:
- Compartment syndrome
- Irreversible ischemia requiring amputation
- Rhabdomyolysis, renal failure
- Electrolyte disturbances
- Atheroembolism:
- Treat conservatively if a limited amount of tissue is involved and renal function is not significantly compromised.
- No clear therapy for the ischemic digits besides supportive wound care and analgesia
- Some studies have tried corticosteroids to decrease inflammation, statins to stabilize plaque, aspirin, or dipyridamole
- Amputation for irreversibly necrotic toes
- Vascular surgeon referral within 12–24 hr of ED visit
- Prevent further embolic events by a thorough investigation and correction of the source of atheroemboli.