Acute Limb Ischemia: Pearls and Pitfalls

Featured on #FOAMED REVIEW 35TH EDITION – Thank you to Michael Macias from emCurious (@EMedCurious) for the shout out!

Authors: Daniel Purcell, MD, Matthew Salzberg, MD, and Vincent Kan, MD (UMass EM Residency) // Edited by: Alex Koyfman, MD (@EMHighAK) and Manpreet Singh, MD (@MPrizzleER)

OVERVIEW

Acute limb ischemia (ALI) is characterized by a sudden decrease in limb perfusion that cannot only threaten limb viability, but can potentially lead to loss of life if not recognized and treated promptly [1].  Suggestive symptoms may include:

  • New or worsening claudication
  • Altered sensation
  • Muscle weakness/paralysis
  • Distorted external appearance
  • Impaired temperature regulation
  • Ischemic pain at rest

The most common cause of ALI occurs secondary to generalized, chronic atherosclerosis, eventually contributing to thrombosis of an occluded vessel, but embolic sources, trauma, and vascular manipulation can precipitate acute pathology.

The nature of acute arterial occlusion depends upon the time course of vessel occlusion, the location of the affected vessel(s), and the ability to recruit collateral channels in an attempt to bypass the occlusion. A detailed history and physical examination is critical in determining these limb/life-threatening emergency situations, as a multitude of patient presentations can also mimic an ischemic extremity.  Treatment depends upon the clinical presentation and associated degree of ischemia. Extensive tissue necrosis can develop by approximately 6 hours with complete arterial occlusion, thus attempts to preserve the limb should be initiated with administration of immediate anti-coagulation therapy and early vascular consultation.

It is important for emergency physician to recognize and act quickly in patients with potential ALI, given the potential complications with untreated limb hypoperfusion

PATHOPHYSIOLOGY

The development of limb ischemia occurs secondary to a decrease/cessation of perfusion to skin, muscle and nerves distal to the occluded segment, with an accompanying decrease in production and function of metabolically functional tissue.

Acute versus chronic limb ischemia differs with respect to the time frame of development, with the presenting complaints considered acute if it develops within two weeks of symptom onset. The difference is critical with respect to the amount of collateral circulation development that has developed prior to the onset of worsening symptoms. Chronic circumstances generally demonstrate a large network of collateral vessels that are somewhat protective, providing native vessels that can bypass the occluded segment. With acute occlusions, there are no alternative routes of perfusion available, thus urgent recognition and timely revascularization provide the only hope to preserve limb viability.

TABLE 1. Differentiation of Embolus and Thrombosis

Table1

Potential etiologies of acute limb ischemia caused by embolic disease most commonly arise from such sources as an impaired or damaged myocardium, diseased arterial structure or thrombosis at the site of an atherosclerotic plaque and/or vessel bifurcation (turbulent flow). Risk factors for such events include:

  • Atrial fibrillation
  • Recent/previous MI with impaired LV function
  • Diseased/prosthetic valves
  • Large vessel aneurysmal disease (Aortic aneurysm, femoral/popliteal aneurysm)
  • Prior lower extremity revascularization procedure (angioplasty/stent, bypass graft)
  • Risk factors for aortic dissection, neurologic disease (transverse myelitis)
  • Direct arterial trauma
  • Generalized arteriosclerosis
  • Deep vein thrombosis (paradoxical embolism)

 

APPROACH TO PATIENT WITH ACUTE LIMB ISCHEMIA

HISTORY

Obtaining a detailed summary of the events leading to presentation is of critical importance, including onset, duration, location, intensity of symptoms, any previous history of claudication or associated vascular procedures including vascular repair and arterial bypass.

Past medical history such as cardiomyopathy, congestive heart failure, renal failure, hypertension, diabetes, malignancy, hypercoagulable states, and/or tobacco use can affect overall morbidity and mortality.

Suspect embolus when the patient can communicate exact time of onset, has a known embolic source (i.e. atrial fibrillation), no prior history of claudication and/or a normal appearance/examination of the opposite limb.

PHYSICAL EXAMINATION

Careful examination is necessary to detect signs of ischemia. Initial evaluation should include:

  • External appearance/temperature of the skin
  • Peripheral pulses in affected and contralateral limbs
  • Neuromotor evaluation for sensation and muscle strength

The 6 Ps (paresthesia, pain, pallor, pulselessness, poikilothermia, paralysis) comprise the classic presentation of acute occlusion in patients without underlying occlusive vascular disease. In contrast, signs of chronic insufficiency can be delineated through examination of hair, skin changes, atrophy of skin and subcutaneous tissues, and muscle.  Physical exam findings of ALI may include loss of pulses, cool and pale or mottled skin, evidence of ischemic ulcers, and/or gangrene. Deoxygenation of stagnated blood and surrounding pallor secondary to vasoconstriction may also be demonstrated by mottling/marbling. Vascular evaluation should include palpation/auscultation of Doppler pulses, which allows for determination of perfusion pressure via the ankle-brachial index (ABI) ratio. Adequate perfusion pressure is maintained when the ratio exceeds 0.9.

Figure 2: Ankle-Brachial Index

ABI

Embolic sources generally have “bounding pulses” initially based upon transmitted pulses through fresh clot. Thrombotic sources usually demonstrate less sharp demarcation based upon collateral circulation maintaining some perfusion distal to the blockage.

DIFFERENTIAL DIAGNOSIS:

Differential for Acute Limb Ischemia include

  • Direct arterial trauma
  • Vasospasm
  • Extrinsic compression (i.e. Compartment syndrome, Thoracic Outlet syndrome)
  • “Blue toe” syndrome => emboli lodge in distal end arteries causing acutely cyanotic extremities; generally have proximal source contributing to showering of emboli (Note: Will still have pulses!)
  • Diseased arterial structures (aortic dissection, PE) / low flow states (CHF, hypovolemia) can lead to decreased systemic perfusion
  • Acute neurologic syndromes (intracranial event, transverse myelitis) that lead to decreased perfusion
  • Deep Venous Thrombosis
  • Vasculitis (i.e. Buerger’s disease, Takayasu’s disease)
  • Non-arterial etiology: musculoskeletal trauma, radiculopathy (spinal stenosis, acute disc herniation), spontaneous hemorrhage (hemarthrosis)
  • Chronic limb ischemia

 

TREATMENT:

The degree of intervention depends upon the clinical presentation and associated degree of ischemia. Initial treatment for any suspected ischemic extremity should consist of immediate administration of weight-based IV Heparin bolus (80 units/kg) and associated continuous IV infusion (18 units/kg/hr) barring any contraindications [6].  Vascular surgery should be consulted immediately for further recommendations, in addition to prompt examination.

Pre-operative labs should be drawn, including CBC, BMP with focus on renal function and potassium levels, Coagulation studies, and Type and Screen. Creatinine Kinase may be drawn to evaluate potential rhabdomyolysis but ultimately will likely not change management. Obtain an EKG and Chest X-ray and any other potential pre-operative information, and optimize any pre-existing medical conditions for surgical intervention, if necessary.

Careful IV hydration is recommended, as often patients with acute ischemia can be relatively volume depleted. Acute renal failure related to myoglobinuria after revascularization and/or IV contrast from potential radiologic studies may also be reduced by adequate hydration.  The extremity should be placed in a dependent position to maximize perfusion and have any constricting clothing/bandages removed while maintaining the limb at a warm temperature. Overall goals include maintaining systemic blood pressure (especially in patients with known low flow states), administering adequate IV analgesia, and supplemental oxygen as needed.

Generally, there is early symptomatic improvement with Heparin therapy, but its positive effects are of unclear origin. It may be attributable to its anticoagulation effects, its simple volume expansion, and/or a combination of both effects. Its use also helps prevent proximal and/or distal propagation of clot in the occluded vessel, as well as helps preserve or improve microcirculation.

If vascular surgery chooses not to treat the Acute Limb Ischemia with operative management and to treat medically, a goal activated partial thromboplastin time of 60 to 100 seconds, or an INR of 2.0 to 3.0, should be targeted with the above-mentioned heparin regimen. If this route is chosen, continuous monitoring of worsening clinical symptomatology must be strictly implemented to guard against unsuspecting worsening.

In the setting of such an acute life and limb-threatening event, it is always important to ensure that the overall medical condition of the patient is well considered, and to treat any underlying medical complications that may co-exist.

Figure 3: Algorithm for the Diagnosis and Treatment of Acute Limb Ischemia

Graph
OUTCOME/PROGNOSIS:

Following thrombolytic therapy or revascularization, reperfusion injury of the affected limb and associated systemic injury can occur. This is a condition whereby large numbers of highly reactive oxygen radicals, associated inflammatory mediators and catabolic byproducts are generated. This chain of events ultimately damages surrounding endothelial cells, leading to heightened tissue permeability, which causes dramatic swelling, increased compartmental pressures, decreased muscle function secondary to ischemia and potential systemic collapse. This can ultimately lead to arrhythmias, renal failure, and cause systemic acid-base abnormalities that can impair cardiopulmonary and renal function (hyperkalemia, acidosis, ATN). Likewise, prophylactic fasciotomies may be performed in anticipation of these potential consequences.

Despite great advances in care and heightened diagnostic recognition, ALI is still associated with rates of limb loss as high as 30 percent and associated in-hospital mortality rates as high as 20 percent. Likewise, approximately 15-20% patients die within one year after presentation, usually from medical illnesses that led to their presentation. Cardiopulmonary complications account for the majority of the deaths, only underscoring the severity of diminished baseline medical condition of these patients.

KEY POINTS:

  • Acute limb ischemia is a sudden decrease in limb perfusion that can potentially threaten limb viability. Suspect acute limb ischemia as a cause for pain and/or neurologic/vascular deficit in the appropriate setting.
  • Irreversible tissue necrosis can occur in as little as six hours from symptom onset
  • Assessment of limb appearance, temperature, pulses, sensation, and strength should be implemented to determine whether the limb is viable, threatened, or irreversibly damaged.
  • Patients who have acute cessation of blood flow with decreased sensation or motor function need immediate anti-thrombotic therapy +/- revascularization to avoid amputation.
  • Implement anti-coagulation (Heparin) therapy and obtain immediate vascular consult in patients with suspected ALI as long as there are no contraindications.
  • Think of possible causes of ALI where anticoagulation may be contraindicated (aortic dissection, compartment syndrome, vasculitis, vasospasm)
  • Mobilize resources to diagnose and treat ALI
  • Time is limb, and choose life over limb if patient unexpectedly decompensates
  • Despite advances in therapy, morbidity and mortality remain high, thus early diagnosis and prompt implementation of therapy is essential to heighten chances of limb salvage
  • It is associated with long-term disability, and potentially loss of life if not recognized and treated promptly.

FOAMed Resources:

References / Further Reading:

  1. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg 2007; 45 Suppl S:S5.
  2. Kasijaran, K. & Ouriel, K. “Current Options in the Diagnosis and Management of Acute Limb Ischemia Prog Cardiovasc Nurs. 2002;17(1)
  3. Rochester Trial Ouriel et al, J Vasc Surg 1194;19:1021-1030.
  4. STILE Study (Surgery versus Thrombolysis for Ischemia of the Lower Extremity) Ann Surg. 1994;220:251-266.
  5. TOPAS Trial (Thrombolysis or Peripheral Arterial Surgery) Ouriel et al. NEJM,1998;338:1105-1111.
  6. Rutherford RB. Rutherford’s Vascular Surgery. W.B. Saunders Company; 2010;162:2528.
  7. Acute Limb Ischemia N Engl J Med 2012;366:2198-206

Figures:

Chart embolus vs thrombus: Callum, K. &Bradbury, A.;”Acute Limb Ischemia.” BMJ. 4/8/2000 320 (7240): 991.

  • Available at: http://www.bpac.org/BPJ/2014/April/ankle-brachial.aspx. Accessed January 4, 2015.

Acute Limb Ischemia N Engl J Med 2012;366:2198-206

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