Kasr Alaini hospital 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
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
Sites of Emboli Emboli lodge at the site of bifurcation of the Artery. Femoral 36% Aorto-iliac 22% Popliteal 15% Upper limb 14% Visceral 7% Others 6% (1303 cases from two US hospitals)
Pathophysiology Occlusion of artery: Propagation of thrombus: proximally till origin of a branch and distally up-to entry of collateral.
(a) Hypertrophy of collaterals, re-canalisation of thrombus, chronic ischemia OR (b) Propagation of thrombus, occlusion of branches and collaterals, Cellular ischemia, leakage of proteins and fluid from capillary bed. Pathophysiology Increase in hydrodynamic pressure in extra- vascular space venous flow obstruction, aggravates ischemia. Edema of cells lead to narrowing of lumen of small vessels : No reflow phenomenon Cellular death-Release of toxic products :free radicals etc. Reperfusion Injury Lactic acid, K+, Myoglobin etc . accumulate and are suddenly released in circulation: cardiac arrhythmias (cardiodepressor factors), sudden death, renal failure Active oxygen metabolites : Superoxide (O2-) and hydroxyl (OH-) radicals. 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 Ps 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 Ps 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 Ps 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 Ps 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 Ps 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 Ps Pain: Paresthesia: Paralysis: Pallor: Pulselessness: Poikilothermia: cold limb, again comparison to the contralateral limb very important
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
Factors affecting outcome Presence or absence of collaterals. Occlusion of a diseased/ normal artery. Occlusion of native artery/ graft. Duration of ischemia Co- morbidities. Site of occlusion
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 Routine lab. Investigations. Invasive monitoring: a-line, CVP, foley Despite various charts and other discussions, the remainder of the algorithm is not quite as easy.
Treatment. Conservative alone Thromboembolectomy Thrombolysis alone Thrombolysis followed by surgery Percutaneous mechanical thrombectomy (PMT) Primary amputation Secondary amputation
Treatment. 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 Treatment. 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 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 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) Fasciotomy : Methods
Fasciotomy : Methods Wound debridement Thrombolysis (I&IIa) Primarily useful in thrombotic occlusions Advantages: - Requires small puncture for per cutaneous technique - Unmasks lesion responsible for occlusive event which can be tackled by surgery / endovascular therapy.
Thrombolysis Disadvantages: Prolonged treatment time. Repeated angiograms for follow-up. Not suitable for embolic ischemia. Generally fails if ischemia is of more than 72- 96 hrs. Not to be used in severely ischemic limbs (IIb&III)
Thrombolytic agents Streptokinase - less costly - higher incidence of allergic reactions and bleeding complications. Urokinase- 4000 IU/min X 4hrs followed by 2000 IU/min rt-PA -Alteplase-0.9mg/kg < 90mg,10%bolus.
Contraindications (thrombolysis) Absolute- Active internal bleeding Recent(<2 Mo) CVA Intracranial pathology Relative Recent(<10 d) surgery Left heart thrombus Active peptic ulcer Recent major trauma Uncontrolled HT Percut Mech Thrombectomy Aspiration Catheters : Fragmentation of clot by high-speed motor or by Venturi effect along with clot trapping bags or expanding catheters.
Micro fragmentation only: Mechanical fragmentation of thrombus.
Devices: Angiojet, Trellis etc.
No convincing proof of efficacy! Take home message Acute arterial occlusion is associated with high morbidity and mortality. There is no absolute time limit for revascularization, it is the physiologic & clinical assessment of the limb that dictates most appropriate form of therapy. Be aware of compartment pressures. Amputation of the limb doesn't mean treatment failure as it can be life saving.