Acute Arterial Occlusion

Etiology

The most common cause of acute limb ischemia is in situ thrombotic occlusion. It is more common in the lower extremities, and the initiating event is a preexisting history of peripheral artery disease (PAD). Thrombotic occlusions can occur in an upper and lower extremities segment but most commonly affect the superficial femoral artery. Patients with a preexisting PAD history tend to have the well-established development of collateral vessels, creating variability in symptoms and severity. Other causes include embolic occlusion from the left heart, aorta, and iliac vessels and penetrating or blunt trauma.[5]

Epidemiology

Published studies regarding the true incidence of acute limb ischemia are lacking. However, in a prospective population-based study in Oxford, England, over a 10-year time frame, the incidence of critical limb ischemia was determined to be 22 per 100,000 per year. Acute limb ischemia affects older men and women equally, with a median age of 75. Risk factors include age, smoking, diabetes, obesity, sedentary lifestyle, family history of vascular disease, high cholesterol, and high blood pressure. Non-traumatic ischemia of the lower extremities is more common than the upper extremities and is more likely to result in limb loss. Atherosclerosis affects around 10% of the Western population over 65 years. With the number of older people expected to increase by 22% by 2040, atherosclerosis will become a huge financial concern in medicine. The estimated PAD prevalence in the general US population was 4.3%, which means in 2000, around 5 million people in the US had PAD. That number rises with age; therefore, the increasing older population means more people are affected by PAD.[6]

Pathophysiology

In situ thrombosis most commonly affects the femoral or popliteal arteries, while emboli most widely lodge in aortic, iliac, femoral, and popliteal bifurcations. Once arterial blood flow is impeded, under-perfused tissues switch to anaerobic metabolism, producing lactate, causing acidosis and increasing free radicals (see Image. One Hundred Percent Proximal Circumflex Artery Occlusion, TIMI flow 0). Prolonged and untreated, this state will cause the hypoxic muscle to run out of its ATP stores. This is followed by impaired calcium/sodium pump and sodium/potassium-ATPase functioning, leading to intracellular calcium leakage into the myocytes. Increasing free calcium negatively interacts with the muscle's myosin, actin, and proteases and eventually causes muscle fiber necrosis. In addition, intracellular potassium, phosphate, creatine kinase, and myoglobin are released into the systemic circulation due to the necrotic muscle.

Under resting circumstances, normal blood flow to peripheral muscle groups averages around 300 to 400 mL/min.[7] Once a person starts exercising, blood flow increases in active muscle groups as much as 10-fold due to the rise in compensatory vasodilation and cardiac output at the tissue level. This leads to an increase in oxygen demand. When exercise stops, blood flow returns to baseline within minutes. An atherosclerotic blood vessel leads to stenosis, which can cause occlusion at some point. In atherosclerosis, each stenotic segment reduces the pressure on the head experienced by peripheral muscle groups. Subsequently, at rest, the blood pressure at the ankle is lower than that measured in a healthy individual. This reduction in blood pressure becomes more significant once physical activity starts, leading to a greatly diminished distal blood pressure. Homocysteine is also an underlying factor that causes atherosclerosis, which leads to occlusion and ischemia.[8]

History and Physical

The classic presentation of acute arterial occlusion involves the "6 Ps": pallor, pain, paresthesia, paralysis, pulselessness, and poikilothermia.[9] These clinical manifestations can occur anywhere distal to the occlusion. Most patients initially present with pain, pallor, pulselessness, and poikilothermia. Pain is often localized and less severe when the limb is dependent. As the ischemia prolongs, paresthesia replaces pain, and the final stages of injury cause paralysis. Patients with embolic occlusion tend to have an abrupt onset with more severe symptoms, as collateralization of the vasculature has not occurred at this point. It is essential to realize that symptoms can develop for hours to days and present as new or recurring. Low kidney function has been linked with the development of arterial occlusive disease. A study conducted in Japan found advanced chronic kidney disease to be an independent risk factor.[10]

Evaluation

Initial evaluation of acute arterial occlusion begins with a physical exam. A detailed physical examination should assess for changes in temperature along the affected extremity. A comparison should always be made with the unaffected side. A complete bilateral pulse exam should be conducted with manual palpation, and an arterial Doppler exam should be included when the deficient pulse is noted.[11] Muscle strength and sensation testing should also be assessed. When occlusion has been identified, confirmatory testing with a CT angiogram is generally conducted as it is quicker and more readily available.[12] However, the time required to order, perform and interpret imaging must be balanced against the urgency for treatment to preserve life and limb. Since most episodes of acute limb ischemia present to the emergency department, an immediate vascular surgery consult must be initiated. The severity of ischemia can be further assessed with the physical exam, utilizing the Rutherford classification of acute limb ischemia. Finding the cause of occlusion is also essential. For example, a patient with a history of atrial fibrillation with abrupt initial symptoms is more likely to have an embolic occlusion than a patient with a history of PAD and claudication more prone to having a thrombotic source.[13]

Treatment / Management

Cases of limb-threatening ischemia require emergent vascular surgery consult. The surgical approach is directed at the reperfusion of the affected extremity. This can be accomplished by surgical bypass, endarterectomy, or embolectomy. Results are variable and will ultimately depend on the duration of the ischemia and the extent of occlusion. Catheter-directed thrombolysis by an interventional radiologist is becoming more common and is reserved for patients with a salvageable limb (Rutherford class II, IIa, and IIb). Patients presenting with profound paralysis and absent pain with inaudible arterial and venous pulses are considered to have irreversible damage and will require amputation. Surgical treatment options are typically reserved for more severe cases or where nonsurgical management fails. These options include the following:

• Open bypass surgery
• Endovascular therapy, such as stenting, balloon angioplasty, or atherectomy

Whereas open surgery was a popular treatment option 2 decades ago, endovascular therapy for PAD has become increasingly popular since then.[14] While the patient waits for surgical or interventional radiology assessment, initial therapy should include fluid resuscitation, pain control, and administration of unfractionated heparin to minimize thrombus propagation. The general goal of anticoagulation is to increase partial thromboplastin by a factor of 2.0 to 2.5 above baseline. Management after revascularization requires close and frequent observation. Prolonged ischemia of greater than 4 hours increases the risk of compartment syndrome and must be monitored with hourly neurovascular checks.[15][16][17]

Differential Diagnosis

Acute arterial occlusion can present in a variety of ways and can mimic several underlying pathological processes. Whenever a patient presents with pain and other relevant features of arterial ischemia, the following differentials should be considered:

• Arterial embolus
• Acute arterial thrombosis
• Aortic dissection
• Chronic exertional compartment syndrome
• Chronic venous insufficiency
• Degenerative disk disease
• Osteoarthritis
• Spinal stenosis
• Thromboangiitis obliterans
• Varicose vein surgery

Staging

The Society for Vascular Surgery has created a classification of an acutely ischemic limb:

• Class I: Non-threatened extremity; elective revascularization may or may not be necessary
• Class II: Threatened extremity; immediate revascularization is indicated to prevent tissue loss
• Class III: Ischemia has progressed to infarction, and salvage of the extremity is not possible

Prognosis

A study conducted on a group of patients with arterial occlusive disease reported that two-thirds of the patients required surgery at the beginning of their hospitalization for ongoing severe ischemia. While the mortality due to acute thrombosis was lower, the risk of major amputation was found to be 35%. They concluded that vascular reconstruction should not be delayed in acute arterial ischemia secondary to thrombosis.[18]

Complications

The following is a list of complications that patients can develop as a result of acute arterial occlusion:

• Compartment syndrome[19]
• Amputation
• Necrosis and gangrene
• Bleeding
• Stroke
• Myocardial infarction
• Death