Occlusive arterial embolism to an otherwise normal arterial bed will nearly universally result in the abrupt onset of severe pain in the affected extremity. These patients lack collateral vessels around the flush occlusion, making the affected limb completely devoid of any arterial flow. The physical exam findings in this state are the presence of bounding “water hammer” pulses proximal to the occlusion and absent pulses distal to the occlusion. The distal extremity will be cool to touch and after 3–4 h may have neurological abnormalities (sensory loss followed by motor loss). The limb is pale with poor capillary refill. The contralateral limb in this situation will typically have normal pulses, unless the patient has underlying peripheral artery occlusive disease (PAD). Revascularization within 6 h is critical to avoid limb loss. Sources of arterial embolism are:

In situ arterial thrombosis secondary to worsening chronic occlusive disease may present in a more indolent fashion. These patients experience acute primary vessel thrombosis due to either plaque rupture and secondary in situ arterial thrombosis or due to a critically low velocity flow state resulting in intra-arterial thrombosis. While the primary symptom will be limb pain, the acuity may be vaguer than patients with embolism. Physical exam findings will still be a cool, pulseless foot, often with dependent rubor instead of pallor. The contralateral pulse and Doppler exam is typically abnormal as atherosclerosis affects both limbs. The severity of pain symptoms is inversely proportional to the quality of collateral arterial flow around the occlusion.

ALI affects sensory nerves first. Therefore, loss of sensation is one of the earliest signs of ischemia. Motor nerves are affected next, and muscle weakness should be a clue to more severe disease and/or longer duration of ischemia. The skin and muscle tissue are affected last, making muscle tenderness a very late finding. In early acute ischemia, the skin distal to the affected artery will appear very pale. This can progress to a dusky blue color as capillary venodilation occurs. The skin will appear non-blanching, as the associated vessels are empty. As ischemia progresses capillary disruption occurs, leading to extravasation of blood and mottled appearance. There will be no blush with digital pressure at this point. Once ischemia has reached this stage, the skin is nonviable, and revascularization bears a significant risk of compartment syndrome and acute renal failure. Occasionally, if ALI is secondary to thrombosis, collaterals can develop over the following 6–8 h and a more normal skin color will return.

In patients with ALI secondary to peripheral arterial occlusive disease , the chief complaint may be ischemic rest pain, whereas the patient previously only had claudication. This pain may be worse when the patient is lying flat or with the affected limb elevated. Pain may be alleviated by placing the limb in a dependent position, thus allowing gravity to supplement arterial flow to the limb. Diabetic patients may not complain of pain if they have a coexisting peripheral neuropathy. This subset of patients may instead present with ischemic or gangrenous ulceration.

A complete history is essential in patients presenting with new onset ischemia, as many factors can influence the diagnosis and treatment course. Pain is most often the first symptom and chief complaint in patients with ALI. The severity of symptoms is a clue to the severity of ischemia as well as to the underlying cause; symptoms may range from claudication to severe disabling pain. Severe acute ischemia is typically an easy diagnosis, as patients present with extreme pain as well as loss of strength and sensation. Less severe ischemia can present more subtly and is often confused with musculoskeletal pain or sciatica. Duration of symptoms is a critical element of history. With severe acute ischemia, irreversible muscle necrosis can occur in 6–8 h if untreated. Onset and distribution of symptoms, prior episodes of pain, and previous functional status of the affected limb are also important components of the history. Sensory loss, followed by muscle weakness, and pain are signs of progressive severe ischemia. The history should be conducted in an attempt to determine the cause of ischemia. Therefore, it is important to ask carefully about associated factors, including cardiac disease/events (myocardial infarction, atrial fibrillation, valvular disease), hypercoagulable pathology (history of previous blood clots or malignancy), and peripheral vascular disease (rest pain, nonhealing ulcers, claudication). The history of previous vascular procedures should be ascertained. Comorbidities such as diabetes mellitus, hyperlipidemia, and hypertension are often present. Tobacco use and family history are also important contributions to the history. It is important to bear in mind that patients may have risk factors for both embolic and thrombotic disease processes; the presence of atherosclerosis cannot rule out an embolic source of ALI. Patients with acute chronic thrombus often have a history of previous intermittent claudication in either leg.

Examination of the affected limb will define the severity of ischemia. The “rule of Ps ”—pain, pulse deficit, pallor, poikilothermia, paresthesias, and paralysis—is a guiding tool.

Pain is often the primary complaint and can be chronic to severe. It is important to document the severity, localization, and progression of pain symptoms. Patients with ALI often have diffuse pain throughout the affected limb. Muscle weakness and tenderness, especially in the calf, is an ominous finding. In severe cases, pain can be replaced with paresthesia as sensory nerves become ischemic.

The vascular supply can be roughly approximated by the color of the skin. Pallor is seen in the early stages of ischemia, which then progresses to cyanosis. Sluggish capillary refill is a sign that at least some degree of distal flow is present and that runoff vessels may be patent. The skin may appear mottled at this point. A severely pale limb is a late finding that indicates total ischemia. Figure 5.1 represents an acutely ischemic limb before and after revascularization .

The limb will be cool to the touch as a result of loss of distal flow. This temperature change is secondary to vasoconstriction and plays a role in the propagation of the ischemic cascade. Coolness is usually present one level below the occluded artery and should be documented at presentation to help determine progression.

Neurologic findings will also help guide classification of ischemia. Loss of sensation is a relatively early sign; be sure to test specifically for loss of fine touch and proprioception, as these small fibers is the most susceptible to ischemic changes. The first dorsal web space of the foot is often the first area to become affected.

Paralysis is an indication of limb threatening ischemia. It is important to determine the extent of paralysis; loss of dorsiflexion and plantar flexion points to a more proximal level of occlusion than paralysis of the toes only. There is a reduced chance of functional limb salvage once motor function is severely diminished, highlighting the importance of immediate revascularization in patients with an acutely painful, cold limb.

Pulse examination can help determine the level of the occlusion. Typically pulses are present one arterial level above the occlusion; however, early clot can sometimes transduce a weak pulse. Palpable normal pulses in the contralateral limb point toward embolism as the cause of ALI. Bounding water hammer pulses may also present proximal to the level of occlusion after acute embolism, with weakened or absent pulses distally. Pedal arterial signals may be absent or reduced with bedside Doppler exam. The presence of normal triphasic Doppler signals at the pedal level largely excludes the diagnosis of ALI. Soft monophasic signals may be associated with patent distal vessels but proximal occlusion. Absent Doppler signal at the ankle is a poor prognostic sign; arteries may be patent with negligible flow or may be completely occluded. In patients with severe late ischemia, ankles will be impossible to Doppler secondary not only to lack of flow, but also to tenderness. Ankle pressures of 30–50 are expected in less severe ALI, and ABI of 0.3 is diagnostic of critical ischemia. The Doppler can also be used to measure flow in the extremity veins. Lack of venous signal in the popliteal fossa indicates popliteal venous occlusion, which is a poor prognostic sign.