Acute limb ischemia

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Acute Limb Ischemia:

Acute Limb Ischemia LCDR Kevin Casey, MC, USN July 28, 2011

Acute Limb Ischemia (ALI):

Acute Limb Ischemia (ALI) Sudden occlusion of an artery, commonly due to acute thrombosis, embolic event, or trauma. It often will happen when thrombosis occurs on a pre-existing atheroma (so-called ‘acute on chronic disease’). Incidence is 14/100,000 (12% of operations performed in the average vascular unit). Arm ischemia accounts for 1/5 of all extremity ischemia cases and has a better prognosis than does LE ischemia Iatrogenesis is becoming a more common cause of ALI secondary to increased number of endovascular interventions

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Thrombosis : greater risk of limb loss; Embolism : greater risk of death 2/3 of pts will require immediate amputation in absence of intervention Overall life expectancy for pts with LE ALI is similar to many cancers: 17-44% are alive at 5 years

Clinical differentiation between thrombosis & embolism:

Embolism: Obvious cardiac source No hx of claudication Normal pulses in contralateral limb Few collaterals Angiogram : minimal atherosclerosis Clinical differentiation between thrombosis & embolism Thrombosis: No obvious cardiac source History of claudication Decreased pulses in contralateral limb Well developed collaterals Angiogram : diffuse atherosclerosis

Diagnostic Criteria: Six P’s:

Diagnostic Criteria: Six P’s

Diagnostic Criteria: Six P’s:

Diagnostic Criteria: Six P’s Pain: usually first symptom May be acute as in trauma or embolus; often with thrombosis the pain is insidious but becomes unrelenting Pain is usually present throughout the entire limb, compared with CLI in which it is most commonly described over the forefoot

Diagnostic Criteria: Six P’s:

Diagnostic Criteria: Six P’s Pain: Paresthesia : sign of progressive ischemia The myelinated fibers of proprioception and light sensation are lost early in acute ischemia Larger sensory nerves (temperature, pain, pressure) are maintained unless prolonged ischemic time ensues.

Diagnostic Criteria: Six P’s:

Diagnostic Criteria: Six P’s Pain: Paresthesia : Paralysis: true paralysis rarely occurs; more often motor deficit/weakness begins to occur and is an ominous sign Absent dorsi - and plantar flexion indicate loss of extensor and flexor muscles of lower leg After 8 hours of absolute ischemia skeletal muscle becomes rigid, contracted, and unsalvageble

Diagnostic Criteria: Six P’s:

Diagnostic Criteria: Six P’s Pain: Paresthesia : Paralysis: Pallor: Indicates major obstruction to the leg Initial pallor may be followed by a gradual improvement secondary to collateral filling In the absence of collateral circulation, the limb will become waxy and marble white

Diagnostic Criteria: Six P’s:

Diagnostic Criteria: Six P’s Pain: Paresthesia : Paralysis: Pallor: Pulselessness : Absolute prerequisite of acute ischemia; comparison to the other limb vital The importance of an accurate and thorough pulse examination cannot be overemphasized Pt with pulses should lead the clinician to look for other sources of pain

Diagnostic Criteria: Six P’s:

Diagnostic Criteria: Six P’s Pain: Paresthesia : Paralysis: Pallor: Pulselessness : Poikilothermia : “cold limb”, again comparison to the contralateral limb very important

SVS Criteria for Limb Viability:

SVS Criteria for Limb Viability Class I: Not immediately threatened; no sensory or motor loss, audible arterial and venous signals/pulses Class IIa : Marginally threatened; salvageable, needs urgent treatment; min/no sensory loss; no motor deficit; +/- audible arterial, audible venous signal Class IIb : Immediately threatened; warrants urgent intervention; +++ sensory loss, possible rest pain; mild muscle weakness; usually inaudible signals, audible venous signal Class III: Irreversible; major tissue loss and permanent nerve damage probable; profound sensory and motor deficits (possible paralysis); inaudible arterial and venous systems


Management Heparin!!! Should be a reflex reaction Prevents clot propagation and distal thrombosis Aggressive resuscitation should be undertaken as these pts tend to be old, malnourished and dehydrated; often should be placed in ICU CBC, CMP, Coags , CEs, CXR, EKG Invasive monitoring: a-line, CVP, foley Despite various charts and other discussions, the remainder of the algorithm is not quite as easy.


Management For a viable limb, the options include: Thromboembolectomy for pt with signs or sxs of acute embolism (acute presentation, normal contralateral limb, suspected source) This is unlikely to treat a stenosed artery or thrombosed graft In such cases, treatment options lean toward a surgical bypass vs. thrombolysis vs. observation CTA vs. angio can be helpful; duplex also an invaluable tool


Management For threatened limb, intervention is more urgent: There is debate upon whether preoperative imaging wastes valuable time In pts without muscle loss, there is value to an on-table angio so as to perform thrombolysis if warranted Otherwise, LE bypass may need to be undertaken


Management Pts with irreversible ischemia: Complete neuro deficit, tense muscles, and a mottled limb from capillary breakdown warrant amputation Attempts at revascularization usually prove futile and risk renal and cardiac toxicity from reperfusion syndrome Overall prognosis very poor

Compartment Syndrome:

Compartment Syndrome Increased pressure within a fascial compartment compromises the circulation and function of the tissues within that space. Skeletal muscle can tolerate ischemia for periods of up to 6 hours Reperfusion syndrome occurs secondary to diffuse hyperemic flow to the entire extremity Increased microvascular permeability promotes local edema and intra- fascial HTN  venous obstruction This leads to the development of superoxide and hydroxyl free radicals, acidosis, hyperkalemia , ARF, arrhythmias, respiratory distress

Compartment Syndrome:

Compartment Syndrome Low threshold to perform fasciotomy : You will never be criticized for performing an unnecessary fasciotomy but you will regret not performing one when warranted Extremity compartment pressures >30 mandate opening up all compartments Pulse exam not a reliable indicator Treat reperfusion injury: aggressive hydration, alkalinize the urine (minimize toxic myoglobin )

Case Report:

Case Report Pt is an 74 yo male who presented to the ER c/o 1+ days of RLE pain (9/10) over his foot and lower leg. Pain began rather suddenly, although he couldn’t tell exactly when, but describes the pain as deep and constant. Pain progressively worsened and kept him awake at night until he came into the ER. Pt has a hx of claudication , R>L, at about 3-4 blocks, but has never seen a physician for it before


H&P Past Medical History HTN HLP COPD on home O 2 BPH Past Sx History denies


H&P Medications Multiple inhalers Pepcid Social Hx: 50+ pk-yr tobacco hx; quit 3 years ago; drinks 3-4 beers/day, denies drug use :lives with wife; former rancher ROS: noncontributory

Physical Exam:

Physical Exam Vital signs: AFVSS AAO, pleasant man in mild distress RRR, NSR LCTAB Abd: soft Ext: RLE: palp fem, pop; no DP/PT signals foot cool; strength 4/5 limited by pain; able to move toes; sensation intact LLE: examination wnl with good pulses

Hospital Course:

Hospital Course Labs WNL Pt started on Heparin GTT CTA ordered



Operative Plan:

Operative Plan Pt taken to the OR the following AM for a RLE femoral and popliteal artery dissection An on-table RLE angiogram was initially performed to aid in surgical planning

Operative Plan:

Operative Plan R fem and R BK-pop/TP trunk dissected Following angiogram, Fogarty balloon (#3) passed down both the PT and peroneal arteries with retrieval of some fresh thrombus and back bleeding from both vessels; tPA administered Repeat angiogram showed improved runoff, more in the peroneal than the PT

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Peroneal artery Posterior tibial artery

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Harvested B LE GSVs using U/S guidance Performed E-S femoral and TP trunk anastomoses with rSVG; vein ends anastomosed in a spatulated end-end fashion with 6’0 prolene Pt had dopplerable peroneal and PT arteries on completion Partial reversal with protamine Completion angiogram performed

Post-op course:

Post-op course Pt had a palpable PT leaving the OR Returned to RR intubated , HD stable Had been partially reversed in the OR secondary to bleeding No major post-op complications; prolonged course secondary to conditioning and eventually pt d/ c’d to SNF.

STILE Trial:

STILE Trial The STILE was an older randomized prospective trial that evaluated sx vs chemical thrombolysis for nonembolic acute limb ischemia in native vein or grafts A follow-up evaluation of the 237 pts (subgroup) who had native artery occlusion of less than six months (by sxs); majority (95%) had dz in either the iliac or femoropopliteal arterial beds (by angiogram) Pts were assigned to one of three groups: surgery, thrombolysis for 12 hours, or thrombolysis for 36 hours.

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2/3 male; mean age was 66 yo At 1-year, there was no SD between overall mortality rates b/t the sx vs thrombolysis groups. However, major amputation and continued ischemic sxs were significantly higher in the thrombolysis groups. DM was a predictor of amputation and morbidity in both groups. Time from onset of sxs was also an independent predictor of amputation and overall morbidity . Weaver F, Comerota A, Marston, et al. Surgical revascularization vs thrombolysis for nonembolic lower extremity natvie artery occlusions: results of a prospectve randomized trial. J Vasc Surg 1996;24:513-23.

Case Report #2:

Case Report #2 Pt is a 57 yo male who presented to clinic c/o a several day history of RUE paresthesia and “feeling cold” Sxs began while playing tennis and noticed that his hand became weak and he had trouble gripping his racquet Since then pt has had repeated similar sxs , mostly with exertion. Denies any previous hx in the past.


H&P PMHx: Spherocytosis, s/p splenectomy HTN HLP PSHx: As stated Spine surgery


H&P Medications Lipitor Benicar SocHx Denies any tobacco or drug history; social EtOH

Physical Examination:

Physical Examination AFVSS AAO CV: RRR Pulm : LCTAB GI: NTND Ext: RUE: R brachial 2+, radial 1+, ulnar biphasic; RUE cooler c/w contralateral UE; motor, sensory intact RUE U/S: WBI 0.92; proximal ulnar occlusion with monophasic waveforms; distal radial occlusion with multiphasic waveform

Interventional Suite:

Interventional Suite Day 2: Following 24 hours thrombolysis Angiogram Angioplasty axillary artery (8 x 40 Fox) Angiojet mechanical thrombolysis ulnar and interosseous arteries Chemical thrombolysis

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Pt d/ c’d home on anticoagulation Physical examination improved; hand warm Pt returned two weeks later for ligation of the circumflex humeral artery aneurysm. Did well and returned to athletics at 6 months.

Axillary branch artery :

Axillary branch artery Arteries arising from the axillary and SCA are prone to injury secondary to repetitive movements Pitchers, volleyball players, tennis players PCHA and ACHA often arise from the same trunk; the former is larger and enters the quadrilateral space enclosed by the axillary n. humerus, and triceps m. Most common sequelae are distal embolization and often ipsilateral pain/paresthesia Distinctly different from axillary artery injuries/trauma

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Dalman RL, Olcott C. Upper extremity revascularization proximal to the wrist. Ann Vasc Surg 1997;11:643-50.

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Treatment Dissolve distal emboli via preoperative thrombolysis Remove embolic source, ie resection of the aneurysm Reekers JA, den Hartog B, Kuyper C, et al. Traumatic aneurysm of the posterior circumflex humeral artery: A volleyball player’s disease? JIVR 1993;4:405-8. Kee ST, Dake MD, Wolfe-Johnson, et al. Ischemia of the throwing hand in major league baseball pitchers: Embolic occlusion from aneurysms of axillary artery branches. JVIR 1995;6:679-82.