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Acute limb ischemia

ALI is most dreaded emergency presentation of peripheral arterial disease.
Definition, presentation, grading, clinical presentation, diagnostic imaging, and management of acute limb ischemia.

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Acute limb ischemia

  1. 1. ACUTE LIMB ISCHEMIA
  2. 2. DEFINITION “Acute limb ischemia is Sudden decrease in limb perfusion that threatens limb viability (within 2 weeks of the onset of symptoms) and requires urgent evaluation and management.”
  3. 3. Introduction ■ Acute limb ischemia (ALI) is one of the most treatable and potentially devastating presentations of Peripheral Artery Disease (PAD) ■ Critical limb ischemia (CLI) is defined as limb pain that occurs at rest or impending limb loss caused by severe compromise of blood flow to the extremity. ■ Chronic ischemia induces the development of collateral blood vessels and results in skin changes secondary to progressive ischemia.
  4. 4. Burden of Acute Limb Ischemia ■ Acute limb ischemia is a surgical emergency with significant morbidity and mortality. ■ The incidence of ALI is 9–16 cases per 100,000 persons per year for the lower extremity and around 1–3 cases per 100,000 persons per year for the upper extremity. ■ Most published series report a 10% to 30% amputation rate ■ The short-term mortality is 15% to 20% (3-year). ■ This is a time-sensitive condition, and the diagnosis is primarily clinical.
  5. 5. Pathophysiology ■ Insufficient oxygenated blood to meet the metabolic demand of the tissues. ■ Ischemia → shift aerobic to anaerobic metabolism → lactate production. → depletion of ATP → leakage of extracellular calcium into muscle cells → cell death. ■ Severity Depends on – degree of obstruction – Site of occlusion, – Presence of collaterals – Affected tissues – systemic perfusion, such as cardiac output and peripheral vascular resistance
  6. 6. Pathophysiology ■ The tissues most sensitive to ischemia are – peripheral nerves, (irreversible damage after 6 hours) – skin, – subcutaneous tissues, – skeletal muscle (up to 10 hrs)
  7. 7. Pathophysiology : Reperfusion injury ■ Ischemic tissue → free radicals → trigger peroxidation of membrane lipids → increased capillary permeability and filtration → swelling → compartment syndrome. ■ Inflammation → leukocyte-activated platelet aggregation and complement system activation → occlusion of the reperfused vessels (no-reflow phenomenon) ■ Byproducts of cell death are released into the systemic circulation and include potassium, phosphate, myoglobin, creatine kinase, and thromboplastin. – and can lead to rhabdomyolysis, cardiac dysrhythmia, multiorgan failure, disseminated intravascular coagulation, and death.
  8. 8. Etiology The etiology of lower extremity ALI is traditionally either ■ embolism, ■ in situ thrombosis with preexisting peripheral arterial disease (PAD), ■ graft/stent thrombosis , ■ trauma, or ■ peripheral aneurysm with embolism or thrombosis .
  9. 9. Changes in the pattern of etiology
  10. 10. EMBOLISM: mechanisms ■ Atherosclerotic heart disease – Coronary heart disease – Acute myocardial infarction – Arrhythmia ■ Valvular heart disease – Rheumatic – Degenerative – Congenital – Bacterial – Prosthetic ■ Artery to artery – Aneurysm – Atherosclerotic plaque ■ Idiopathic (5-10%) ■ Iatrogenic ■ Paradoxical embolus ■ Trauma ■ Other – Air – Amniotic fluid – Fat – Tumor – Chemicals – Drugs Cardiac causes → 80-90%
  11. 11. THROMBOSIS: mechanisms ■ Atherosclerosis ■ Low-flow states – Congestive heart failure – Hypovolemia – Hypotension ■ Hypercoagulable states ■ Vascular grafts – Progression of disease – Intimal hyperplasia – Mechanical ■ Arterial plaque rupture ■ Trauma ■ Aortic/arterial dissection ■ HIV arteriopathy ■ Arteritis with thrombosis ■ Popliteal adventitial cyst with thrombosis ■ Popliteal entrapment with thrombosis ■ Vasospasm with thrombosis (e.g., ergotism, cocaine) ■ External compression ■ Iatrogenic – catheter induced
  12. 12. Embolism versus Thrombosis Embolism Thrombosis Sources Frequently detected Not specified Onset Sudden Acute Site Normal vessels On stenosis, calcified Previous history a known embolic source, such as cardiac arrhythmias Symptoms of chronic ischemia Findings Normal pulses in uneffected limb Evidence of peripheral arterial disease Multiplicity Multiple sites Single site Angiography multiple occlusions, no collaterals Diffuse atherosclerosis Collaterals present The timing of presentation depends on the severity of ischemia, which is linked to the etiology. Patients with embolism, trauma, and popliteal aneurysms present early (hours), compared to those with in situ thrombosis presenting later (days)
  13. 13. Nonatherosclerotic causes ■ arterial trauma, ■ vasospasm, drugs(cocaine, vasopressors) ■ low flow states: eg cardiogenic shock/sepsis ■ vasculitis, ■ hypercoagulable states, ■ aortic dissection, - should be strongly considered in patients with unilateral or bilateral iliac occlusion. ■ external arterial compression, such as with popliteal cyst, popliteal artery entrapment syndrome. – should be considered in younger patients with absent atherosclerotic risk factors. ■ Iatrogenic; arterial catheterization
  14. 14. Clinical features of acute ischemia Pain : symptom PALLOR POIKILOTHERMIA PULSELESS PARASTHESIA PARALYSIS Either constant or elicited by passive movement of the involved extremity. Embolic occlusions are usually very sudden and of great intensity, such that patients often present within a few hours of onset.
  15. 15. Clinical features of acute ischemia Pain : symptom PALLOR POIKILOTHERMIA PULSELESS PARASTHESIA PARALYSIS COLOR Early: Pale Later: Cyanosed → Mottling → fixed mottling & cyanosis Pallor An area of fixed cyanosis surrounded by reversible mottling Empty veins: compare with normal limb
  16. 16. The limb is cold sudden loss of previously palpable pulse implies embolic cause. compare with the other side Slow capillary refilling of the skin after finger pressure Bounding water hammer pulses proximal to occlusion Clinical features of acute ischemia Pain : symptom PALLOR POIKILOTHERMIA PULSELESS PARASTHESIA PARALYSIS
  17. 17. Loss of sensory function Numbness will progress to anesthesia Progress of Sensory loss Light touch Vibration sense Proprioreception Deep pain Pressure sense Clinical features of acute ischemia Pain : symptom PALLOR POIKILOTHERMIA PULSELESS PARASTHESIA PARALYSIS
  18. 18. Loss of motor function: Indicates advanced limb threatening ischemia fine movement affected first Late irreversible ischemia: Muscle turgidity Intrinsic foot muscles are affected first, followed by the leg muscles Detecting early muscle weakness is difficult because toes movements are produced mainly by leg muscles Clinical features of acute ischemia Pain : symptom PALLOR POIKILOTHERMIA PULSELESS PARASTHESIA PARALYSIS
  19. 19. other clinical features ■ Signs- ■ Limb blood pressure (<50mm hg) ■ Edema does not occur, however, with acute arterial occlusion unless diagnosis is delayed and swelling begins to develop
  20. 20. Differential diagnosis ■ low cardiac output (especially when superimposed on chronic lower extremity PAD) ■ acute deep vein thrombosis (DVT), (especially when associated with features of phlegmasia cerulea dolens) ■ Chronic peripheral neuropathy (diabetic neuropathy), or ■ acute compressive peripheral neuropathy (compartment syndrome) ■ Potential causes of nonischemic limb pain include acute gout, spontaneous venous hemorrhage, or traumatic soft tissue injury.
  21. 21. Stages of acute limb ischemia
  22. 22. Class III (irreversible) Class II (salvageable)
  23. 23. Diagnosis and Management ■ Diagnosis of ALI is primarily clinical. ■ In patients with suspected ALI, initial clinical evaluation should rapidly assess limb viability and potential for salvage and does not require imaging ■ The severity of the ischemia, according to the classification presented above, will dictate the extent of diagnostic tests performed for systemic risk factor assessment.
  24. 24. Management: initial work-up ■ Routine blood studies should be performed before heparin is administered. – CBC: elevated platelet in thrombotic disease – Creatinine kinase: predictive of major amputation. – Hypercoagulable state and Homocysteine: prothrombin time, partial thromboplastin time, thrombin time, lupus anticoagulant, anti-cardiolipin antibody, activated protein C resistance, factor V Leiden – Renal function test: elevated in DM,HTN. No contrast study if deranged – Lipid profile: hyperlipidemia – FBS and HbA1c – ESR: elevated in collagen vascular disease – CRP: marker of worsening PVD ■ A plain chest x-ray and electrocardiogram should be obtained from every patient. ■ Echocardiogram: In suspected embolism, as soon as time allows.
  25. 25. Management: Early heparinisation ■ early heparinization is remains one of the mainstays in the treatment of ALI. – immediate full-dose heparinization can result in symptomatic improvement in some patients, either from the anticoagulation effects of heparin or volume expansion – prevents proximal and/or distal thrombus propagation and preserves the microcirculation – IV unfractionated heparin 80-150 U/kg bolus, followed by infusion of 18 U/kg/hour – aPTT ratio 2-2.5 – If the patient has a known history of HIT or an anti-thrombin III deficiency, alternative agents, such as direct thrombin inhibitors (lepirudin or argatroban), can be used.
  26. 26. Management ■ Adequate analgesia ■ IV fluid resuscitication ■ Oxygen delivered by face mask ■ Correction of underlying electrolyte imbalances and systemic anticoagulation should proceed concomitantly. ■ Aspirin initiated. ■ Limb placed in dependent position and kept warm
  27. 27. Emergent imaging Include: ■ Duplex ultrasound, ■ CTA, ■ MRA and ■ invasive angiogram
  28. 28. Duplex Ultrasonography ■ First-Level Noninvasive Diagnostic test ■ Low cost ■ In experienced hands may offer quality data as high as coming from the angiography ■ Thromboemboli: anechoic in the acute phase and gradually increasing in echogenicity in a later phase. (possible to hypothesize the onset of the disease) ■ Also assess vessel wall status
  29. 29. Duplex Ultrasonography Duplex ultrasound findings at different limb levels: ( a ) Doppler spectral analysis above the acute occlusion (“stump” signal). ( b ) The vessel profile is irregular, some calcifications appear as hyperechoic thickening of the vessel wall, and hypoechoic material is present intraluminally at the level of thrombotic occlusion. ( c ) Downstream to the occlusion a monophasic flowmetry (reduced PSV and significant systolic phase prolongation) with low resistance patterns may be appreciated.
  30. 30. CT Angiography ■ accurate analysis of the location, extent, and grading of steno-obstructive disease ■ Still uses ionizing radiation and iodinated contrast agent. ■ Limitation: “blooming artifact,” which affects the evaluation of the lumen of diffusely calcified vessels and pronounced in small caliber vessels particular below-the-knee vessels. absence of flow in the right common iliac artery (white arrow)
  31. 31. MR Angiography ■ Better for distal small and pedal vessels as compared to CT angiography ■ Higher cost, large number of artifacts. ■ More time consuming than CT. ■ Gadolinium worsens CKD patients and precipitates nephrogenic systemic fibrosis
  32. 32. Angiography ■ Invasive ■ Used to be gold standard test for road mapping before surgery ■ Replaced by CTA and MRA ■ On table arteriography has an established place intraoperatively as a guide for extension of the procedure to ensure complete clearance of the arterial tree and distal patency and for the evaluation of immediate results after surgical treatment. ■ Safer in recent years due to fine 3-4 F catheters
  33. 33. Complication of arteriography ■ Hematoma ■ Occlusion ■ Pseudoaneurysm ■ A-V fistulas ■ Catheter induced complications – Arterial dissection – Subintimal injection ■ Contrast reactions
  34. 34. Management of ALI ■ Main target: Rapid restoration of arterial flow with least risk to patient ■ For viable limbs (Category I ALI), revascularization should be performed an on urgent basis (within 6–24 hours). ■ For marginally or immediately threatened limbs (Category IIa and IIb ALI), revascularization should be performed emergently (within 6 hours). ■ For nonsalvageable limb (Category III), Amputation should be performed as the first procedure.
  35. 35. Management of ALI ■ The revascularization strategy can range from catheter-directed thrombolysis to surgical thromboembolectomy. ■ The technique that will provide the most rapid restoration of arterial flow with the least risk to the patient should be selected. ■ Prolonged duration of ischemia (> 6-8 hrs.) is the most common factor in patients requiring amputation for treatment of ALI.
  36. 36. Intervention options ■ Endovascular therapies – Thrombolytics – Mechanical ■ Surgical intervention – Thrombo-embolectomy with Fogarty balloon catheter – Bypass surgery – Intra-operative thrombolysis (hybrid) – amputation
  37. 37. Intra-arterial thrombolysis ■ Catheter passed into occluded vessel, left embedded in clot and thrombolytic agent infused over 24 to 48 hrs. ■ The method abandoned if no progression of dissolution of clot with time (>24 hours) ■ Thrombolytic agents: tPA, alteplase, reteplase & tenecteplase. ■ Patients with profound ischemia who may not tolerate such a prolonged procedure are not candidates for catheter-directed thrombolysis. ■ Percutaneous endovascular thrombolysis options are more effective in patients with – viable or marginally threatened limb and recent occlusion (<2 weeks), – Arterial thrombosis, – thrombosis of synthetic grafts, and stent thrombosis
  38. 38. Catheter directed thrombolysis Pros: ■ Direct delivery of drug into existing thrombus ■ Reduces thrombolytic drug dosages ■ Lyses clot in both large and small vessels ■ Lower reperfusion syndrome than embolectomy ■ Done via percutaneous approach with local anaesthesia Cons: takes >24 hours to be effective, Risk of major bleeding (6-9%),
  39. 39. Contraindications to thrombolytic therapy Absolute contraindications ■ Established cerebrovascular events (including transient ischemic attack) within last 2 months ■ Active bleeding diathesis ■ Recent (<10 days) gastrointestinal bleeding ■ Neurosurgery (intracranial or spinal) within last 3 months ■ Intracranial trauma within last 3 months ■ Intracranial malignancy or metastasis
  40. 40. Contraindications to thrombolytic therapy Relative major contraindications ■ Cardiopulmonary resuscitation within last 10 days ■ Major nonvascular surgery or trauma within last 10 days ■ Uncontrolled hypertension (>180 mmHg systolic or >110 mmHg diastolic) ■ Puncture of noncompressible vessel ■ Recent eye surgery Minor contraindications • Hepatic failure, particularly with coagulopathy • Bacterial endocarditis • Pregnancy • Diabetic hemorrhagic retinopathy
  41. 41. Mechanical thrombectomy Percutaneous mechanical thrombectomy (PMT) with mechanical pulse spray/ suctioning with catheter as adjunctive therapy to thrombolysis (Angiojet catheter) ■ Pros: – Disrupts the thrombus- allows better penetration of the clot by a thrombolytic agent – Reduces thrombolytic dosing – Reduces therapy time- increasingly being used in class IIb – Done via percutaneous approach with local anaesthesia – Less vessel injury ■ Cons: – Can be used only large vessel – Expensive device
  42. 42. Mechanical thrombectomy
  43. 43. SURGICAL THROMBOEMBOLECTOMY ■ Local or general anesthesia ■ The artery (usually the larger proximal), exposed and held in slings and longitudinal or transverse incision given ■ Fogarty balloon catheter introduced past the occlusion, inflated and withdrawn with the clot. ■ Good back-bleeding and antegrade bleeding suggest that the entire clot has been removed. ■ Completion angiography to ascertain adequacy.
  44. 44. Fogarty balloon embolectomy catheter
  45. 45. SURGICAL THROMBOEMBOLECTOMY ■ Pros: – Rapid revascularization – Transfemoral approach can be done via local anaesthesia – Adjunct by intraoperative thrombolysis ■ Cons: – Risk of Vessel injury – Reperfusion injury chances more and thus, compartment syndrome
  46. 46. Intra-operative Thrombolysis Operative Thromboembolectomy Complete/ Near complete thrombus extraction Incomplete thrombus extraction with small volume residual thrombus Extensive residual thrombus, Multivessel distal occlusion Bolus thrombolytic agent into arterial segment during arterial occlusion Bolus during arterial occlusion(+repeat dose) Or 20-30 min infusion High dose isolated limb perfusion (Manual infusion or partial bypass with pump oxygenator)
  47. 47. Intra-operative Thrombolysis ■ Pros: – Adjunct to surgical thromboembolectomy- clear residual thrombus in small arteries and arteriole – Minimal risk of bleeding ■ Cons: – Maybe inadequate in some patients with extensive distal and small vessel thrombosis
  48. 48. Arterial bypass surgery ■ Use in patient that – failed other procedures- last resort! – Severe tissue injury – Associated Peripheral vascular disease ■ Main treatment for thrombosed popliteal artery aneurysm ■ High surgical risk ■ Rarely used for ALI
  49. 49. Amputation Performed as the first (index) procedure in ■ A non-salvageable (Class III limb) ■ Low potential of limb salvage ■ Risk of reperfusion syndrome
  50. 50. Complications of arterial revascularization ■ Reperfusion syndrome – Hypotension – Hyperkalemia – Myoglobinuria – Renal failure ■ Compartment syndrome ■ Ischemic neuropathy ■ Muscle necrosis ■ Recurrent thrombosis ■ Lower leg swelling
  51. 51. Reperfusion syndrome ■ Directly relates to severity and extent of ischemia ■ The myoglobin from damaged muscle precipitates in kidney tubules and causes acute tubular necrosis. ■ Alkalinization of urine increases the solubility of myoglobin, thus preventing it from crystallizing in the tubules. ■ In addition to alkalinization, therapy consists of forced saline diuresis and removal of the source of dead muscle that is releasing the myoglobin.
  52. 52. Compartment syndrome ■ every reperfused patient is monitored for this complication. ■ occurs after prolonged ischemia is followed by reperfusion. ■ Capillary leak → fluid in interstitial space in fascial compartment → ■ Clinical signs: – excessive pain in the compartment – pain on passive stretching of the compartment, and – sensory loss due to nerve compression
  53. 53. compartment syndrome ■ The most commonly affected compartment is the anterior compartment in the leg → Numbness in the 1st web space between is diagnostic due to compression of the deep peroneal nerve. ■ Compartment pressure is measured by inserting an arterial line into the compartment. ■ pressures greater than 20 mmHg are an indication for fasciotomy
  54. 54. Fascial compartments of the lower leg Anterior Compartment Lateral Compartment Superficial Posterior Compartment Deep Posterior Compartment Muscles Tibialis anterior Extensor digitorum longus Peroneus tertius Extensor hallucis longus Extensor digitorum brevis Extensor hallucis brevis Peroneus longus Peroneus brevis Gastrocnemius Plantaris Soleus Tibialis posterior Flexor digitorum longus Flexor hallucis longus Artery Anterior tibial artery Anterior and posterior tibial branches of the popliteal artery Posterior tibial artery Peroneal artery Nerve Deep peroneal nerve Superficial peroneal nerve Tibial nerve
  55. 55. Fasciotomy ■ the medial incision, long openings are then made in the fascia of the superficial and deep posterior compartments. ■ Through the lateral incision, the anterior and peroneal compartments are opened. ■ Both skin and fascial incisions should be of adequate length to ensure full compartment decompression.
  56. 56. References ■ Schwartz’s Principles of Surgery, 10th edition ■ Critical Limb Ischemia: Acute and Chronic, (Robert S. Dieter • Raymond A. Dieter, Jr Raymond A. Dieter, III • Aravinda Nanjundappa), Springer, 2017 ■ Acute Limb Ischemia: An Emergency Medicine Approach (Jamie R. Santistevan, MD), Emerg Med Clin N Am - (2017), Elsevier Inc. ■ 2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity Peripheral Artery Disease: Executive Summary
  57. 57. THANK YOU

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