Critical limb ischemia. povd . dr mnr

POVD PAD CRITICAL LIMB ISCHEMIA

1. CRITICAL LIMB ISCHEMIA Surgical clinics of North America volume 87 number5 August 2013 DR MUHAMMED MUNEER M MS GENERAL SURGERY SGMC & RF TRIVANDRUM KERALA

2. Critical limb ischemia PAOD /PAD/PVD- refers to obstruction or deterioration of arteries other than those supplying the heart and with in the brain` Critical limb ischemia refers to the clinical state of advanced arterial occlusive disease , placing an extremity at risk for gangrene and limb loss. CLI is a progressive evolution & clinical manifestation of PAD. Clinically , critical limb ischemia is defined by specified hemodynamic findings in conjunction with either of the following 1- ischemic rest pain 2- lower extremity ulceration with hemodynamic findings incompatible with wound healing

3. Introduction CLI – has 2 broad clinical subcategories that are vital to differentiate 1- acute limb ischemia 2- chronic limb ischemia

4. Pictures:

5. Acute limb ischemia Refers to the acute arterial thrombosis of a extremity, resulting in an abrupt cessation of flow to the extremity. Surgical emergency mandating urgent extremity revascularization to avoid need for amputation. The potential source of acute limb ischemia are arterial embolus, in situ arterial thrombosis in the setting of advanced chronic arterial occlusive disease and major arterial trauma

6. Chronic arterial occlusive disease Chronic arterial occlusive disease with critical limb ischemia is the condition of progressive atherosclerosis, creating a state of extremity hypoperfusion with insufficient tissue oxygenation. Need prompt treatment Not an emergency state Need imaging ,patient risk stratification, and planning of revasculariation

7. Ethiology for c/ cAOD > 95% of c/c lower limb arterial occlusive disease is secondary to atherosclerotic stenosis or occlusions Others includes Prior embolization Popliteal artery aneurysm cystic disease Thromboangitis obliterans (Burgers disease) Fibromuscular dysplasia Aortic coarctation , takayasu arteritis Endofibrosis of the external iliac artery Persistant sciatic artery Radiation injury

8. PAD- epidemiology PAD is a disease of aging Disease prevalence -10% in individual aged 65 > 30% in octagenarieans >30 % as concomitant PAD with new or established – CAD CVA Equal prevalence among genders Presence of PAD or low ABI(<0.9),associate with twofold increase in total mortality

9. contd PAD PAD is an under recognized condition Classical clinical presentation-lower extremity claudication Historically claudication defined using ROSE questionare 1)pain involving one or both calves 2)provoked by excertion 3)not present at rest 4)prompt patient to stop excertion 5)must abate with in 10 min of rest 6)no abatement in leg pain during continued excertion

10. Clinical classification of PAD : fontaine and Rutherford system

11. Contd PAD <10% of patient present with typical claudication symptoms Majority are asymptomatic(40%) or present with atypical leg pain(50% Minority with a/c or limb threatening condition Critical limb ischemia 1-3%) Acute limb ischemia <1% Diagnosis of PAD-missed in 85-90%when relying on clinical history

12. PATHOPHYSIOLOGY

13. CAUSES Atherosclerosis Arterial thromboembolism/ cardioembolism Degenerative d/s ( Marfan,Ehlers-Danlos syn ) Dysplastic (fibromuscular dysplasia) Vasculitis (large-giant cell artertis , medium- polyarteritis nodosa,small -rheumatoid arthritis,SLE )) Buerger disease Inherited thrombophilias Entrapment syndromes

14. SCREENING Patient considered at high risk for PAD People <50yr with DM & additional atherosclerotic risk People >50ys with DM &/ or smoking history Anyone >65 yrs With known vascular disease in other arterial systems (coronary ,carotid, renal ) Those with reduced or abnormal pulse on physical xmn Those with symptoms of PAD

15. ABI S imple ,inexpensive ,& noninvasive test ABI is considered as 5 th vital sign ABI is ratio of highest ankle(DP and PTA) systolic blood pressure & the highest arm (brachial) systolic blood pressure SBP is 8-15% higher in the lower extremities  ABI is greater than one Normal ABI 1- 1.4 >1.4 or 1.4 s/o non compressible vessels 0.7 - 0.9 mild 0.4 – 0.7 moderate < 0.4 severe 0.9- 1 borderline reduced category – subclinical disease

16. Clinical correlation of different levels of ABI ABI PRESENTATION 1.11+/- 0.10 NORMAL O.59 +/-0.15 INTERMITENT CLAUDICATION 0.26 +/- 0.13 ISCHEMIC REST PAIN 0.05+/- 0.08 TISSSUE LOSS

17. ABI ABI Clinical Correlation >0.9 Normal Limb 0.5-0.9 Intermittent Claudication <0.4 Rest Pain <0.15 Gangrene CAUTION: Patient’s with Diabetes + Renal Failure: T hey have calcified arterial walls which can falsely elevate their ABI.

18. Other modalities Pulse volume recording Continuous wave Doppler usg Duplex usg MRI CT Angiography & contrast angiography

19. Risk factors Smoking – Most powerful risk factor Potent risk factor for develop of PAD (2-6 fold) than CAD Effect on endothelial funcn , alter vascular tone, promt inflamn , and erythrocytosis , which alter rheologic properties of blood Worse disease specific outcome n increased bypass graft failure

20. Diabetes mellitus Potent risk factor (2 fold increase) 1% increase in HbA1c 30 % increase in PAD 5 fold increase in incidence of amputations Smoker have PAD above knee ,DM pts – PAD below knee DM Promots PAD By- (1) hyperglycemia , hyper insulinemia , free fatty acid production- impaired NO production n endothelial dysfunction. (2)- hyperglycemia oxidative stress n platelet aggregation which alter the rheologic properties ofblood

21. Hypertension Claudication increase by 2fold in men n 4fold in women 50% of pt with PAD having HTN

22. Hyperlipidemia Low HDL Elevated total cholesterol Elevated low density lipoprotein 10%rise in risk in pt with 10mg/dl rise total cholesterol

23. Non traditional risk factors assoc with progression of PAD Elevated homocysteine - 2 fold increase in vascular disease C reactive protein Interleukin 6 (IL-6) (strongest n independent predictor) Intercellular adhesion molecule.

24. Medical managment Comprehensive life style modefication Targeted BMI 25 kg/m2 Reduction of dietary total n saturated fat Daily aerobic exercise Tobacco cessation- Nicotine replacement therapy- chewing gum, trance dermal patch, nasal spray,inhalers , and tablets Bupropion ( aminoketone antidepresent ) Varenicline ( chantix ) ( alpha 4 beta2 nicotinic acetylecholine receptor partial agonist)

25. DM Significant reduction in microvascular complications (retinopathy, neuropathy , nephropathy) with tight glycemic control (HbA1c <7 %) but not with macrovascular complications American Diabetes assoc recommends Annual evaluation of presence of PAD in all pt with DM Pt with DM > 50 yr a screening ABI should be done, rpt every 5 yrs All pts with DM n PAD should b evaluate for peripheral neuropathy , should receive foot care to prevent ischemic complications n limblosss

26. Blood pressure Both micro n macro complic reduced by tight blood pressure control By reduction of 10mmHg syst BP mortality n DM complications are reduced by 12%, lower limb extremity amputation are reduced by 16 % Goal in DM – Non DM- < 140/90mmHg DM and /or with ckd - < 130/80 mmHg Drug recommeded - ACEI Beta blocker worsen symptoms of claudication

27. Guidline recommented medical interventions for reducing cvs risk and improving symptoms in patients with PAD CLINICAL CATEGORY GUIDELINE RECOMMENDED INTERVENTIONS Reduce CV risk and rates smoking cessation counsel +pharmacotherapy ( vareniciline , bupropion , nicotine replacement ) antiplatelet therapy aspirin or clopidogrel in symptomatic PAD for reduction of cardiovascular events( clopidogrel is an alternate to aspirin) ANTIHYPERTENSIVE THERAPY BP < 140 /90 AND < 130/80 IN DM AND /OR CKD PTS LIPID LOWERING AGENTS Treat LDL to a goal <100 mg/dl or < 70 mg/dl in patients at high vascular risk ( eg ; multisystem atherosclerotic disease) Diabetes treatment Optimize glycemic control –HbA1c<7%, annual evaluation for the presence of PAD and peripheral neuropathy ,screening ABI for all patients with DM >50 yrs of age and regular preventive foot care Improve PAD symptoms and quality of life Exercise therapy and cilastozol Supervised exercise therapy for at least 30-40mts min in 3 times weekly for at least 12 wk , to improve claudication symptoms and increase walking distance in patient with out heart failure

28. Improve PAD symptoms and quality of life Exercise therapy and cilastozol Supervised exercise therapy for at least 30-40mts min in 3 times weekly for at least 12 wk , to improve claudication symptoms and increase walking distance in patient with out heart failure

29. Acute limb ischemia treatment steps 1- Confirm diagnosis ( physical xmn n arterial imaging) 2- Initiate anticoagulation (heparin warfarin thrombin inhibitors, factor Xa inhibitor, aspirin, clopidogrel ) 3- Perform revascularization 4- Monitor post procedure for compartment syndrome n rabdomyolysis 5- Evaluate patient for potential embolic source n continue therapeutic anticoagulation

30. Diagnosis of acute ischemia Clinical hallmark of ALI is acute onset of pain in cojunction with absent pulses in the affected extremty Severity vary depending on etiology –( arterial embolism vs insitu thrombosis in a setting of c/c AOD)

31. What are the features of an acute ischemic limb? REMEMBER THE 6 P’S: PAIN PALLOR PULSELESNESS PERISHING COLD (POIKILOTHERMIA) PARASTHESIAS PARALYSIS Fixed mottling & cyanosis

32. Arterial embolism Insitu thrombosis WORSENING chronic OAD ABRUPT ONSET OF SEVER PAIN ACUTE THROMBSIS DUE TO – PLAQUE RUPTURE OR THROMBOSIS PPT BY CRITICAL LOW VELOCITY PATIENT LACK COLLATERALS AROUND THE FLUSH OCCLUTION VAGUE LIMB PAIN SEVERITY DEPENT ON COLLATERAL ARTERIAL FLOW COMPLETE BLOCK OF ARTERIAL FLOW COOL LIMB, PULSELESS FOOT, BOUNDING “ WATER HAMMER PULSE “ PULSES PROXIMAL TO & ABSENT PULSE DISTALLY DEPENDENT RUBOR INSTED OF PALLOR DISTAL PART IS COLD TO TOUCH NEUROLOGIC ABNORMALITY AFTER 3-4 HR (SENSORY) FOLLOWED BY MOTOR LOSS. PALE LIMB POOR CAPILLARY REFILL C/L LIMB WILL B NORMAL REVASCULARISATION WITH IN 6 HRSIS CRITICAL C/L PULSE \ DOPPLER WILL B ABNL ( ATEROSCLEROSIS AFFECT BOTH LIMB)

33. INVASTIGATIONS Emergency arterial imaging is needed for any pts with limp pain n absent pulse Duplex usg - rapid can performed bed side, 100% sensitivity evaluating aorto -iliac inflow & tibial arterial out flow vessels may b sub optimal  normal is triphasic  biphasic  monophasic  absent

34. CT angiography- rapid availability high quality imaging- which allows precise planning of revascularisation Provide imaging of entire arterial tree from aortic inflow to digital level CTA requires 150ml of iodinated contrast CI in pts with kidney injury (GFR < 40) Aggressive hydration prior to proceedure Post procedure – Sodium bicarbonate is recommended for CTA or invasive angio Invasive diagnostic angiogram- Has an advantage of smultaneous percutaneous revascularisation with both mechanical thrombectomy and thrombolytic therapy

35. CT Angiography Digital Subtraction Angiography Value of angiography Localizes the obstruction Visualize the arterial tree & distal run-off Can diagnose an embolus: Sharp cutoff, reversed meniscus or clot silhouette

36. MR Angiogram Limited role in acute limb ischemia Xmn take 45-60 mts Less often available Poor arterial imaging than 64 slice CT ECHO cardiogram and aortic imaging is mandatory to investigate the proximal source of embolus.

37. Treatment of acute limb ischemia Consider revascularisation after global pt evaluation ,ambulatory status, relative quality of life, surgery risk A 30 day amputation risk is 15%- should discussed with pt n family Goal of revascularisation At least one tibial artery patent with angiographic conformation of out flow to the foot In Upper limb- outflow to the hand via radial or ulnar artery (ideally both) with filling of palmar arch is the treatment goal If no CI to anticoagulation- give IV heparin bolus 100U /kg followed by IV infusion 15U/kg with a goal of Partial Thromboplastin (PTT) time of 60-80

38. Treatment options for acute limb ischemia

39. Option 1 Endovascular percutaneous thrombectomy and thrombolysis Arterial access –proximal to the arterial occlusion, MC C/L retrograde CFA access Guide wire and catheter crossing thru the thrombus burden If needed brachial artery access may b used (if thrombus at bifurcation Followed by catheter sheath is inserted->angiography performed -> a hydrophilic glide wire with 4 Fr catheter is inserted to cross thrombus, which pass as distally as possible Angiojet catheter for percutaneous mechanical thrombectomy pass over guide wire

40. Thrombus treated with both tissue plasminogen activator (TPA) bolus of 5mg and mechanical spray /suctioning with catheter 0.035-inch glide wire n 6Fr thrombectomy catheter or 0.018-inch and 3 Fr catheter is used Residual thrombus treated with continuous TPA drip of 0.05 to 0.1U/kg per hour +/- heparin drip too Fibrinogen level ,PTT, INR ratio check every 6 hrs Goal PTT is 30 to 50 sec If underlying AOD is identified treat with angioplasty

41. Anticoagulants and antiplatelets like heparin warfarin thrombin inhibitors factorXa inhibitors aspirin clopidogrel – prevents thrombus formation TPA directly induces lysis of a fibrin based clot. Patient which are not candidate for thrombolytic therapy should undergo emergent surgical revascularisation.

42. CI of thrombolytic therapy CVA with in 3 months IC tumor or other pathology Intrathoracic ,abdominal pelvic or thoracic surgery with in 3 weeks Major trauma within 3 weeks Sever HTN (SBP > 180mmHg) that cannot controlled with medication Cirrhosis with coagulation abnormality Pt who r not a candidate for thrombolytic therapy need urgent revascularisation

43. Option 2 open surgical thrombectomy with as- needed adjuctive revascularisation or thrombolytic therapy

44. Acute arterial embolus Surgical embolectomy Exposure site based on anatomic location and extent of thrombus burden BK popliteal artery cut down with retrograde n anterograde fogarty balloon thrombectomy for lower extremity embolus CFA cutdown Brachial artery cut down at antecubital level just above bifurcation After sx muscle fascia never closed bcoz of risk of compartment syndrome

45. Fr 5 – iliac n sub clavian artery Fr 4- femoral popliteal brachial Fr 3- tibial radial ulnar All proceedure should b followed by completion angiography If thrombectomy is unsuccessful at tibial artery level intraarterial distal thrombolytic therapy can b performed (5mg TPA Injected directly to the thrombosed vessel  10 mts later secondary angio performed )

46. Surgical Treatment in a setting of c/c arterial occlusion Treatment is challenging than acute embolus Difficult to make out in angio or CTA which vessel s blocked recently or blocked for months These patients have subtle pain, chronic occlusion become symptomatic due to acute event and reached a critical treshold of tissue ischemia Option include – thrombectomy ,bypass, endartrectomy , thrombolytic therapy, angioplaty , and stending Thrombectomy -> post thrombectomy agiography -> +/- bypass, +/- angioplasty

47. Percutaneous vs open sx revascu in A/C ischemia Treat all pts with a/c limb ischemia (with out CI of TPA) with percutaneous mechanical thrombectomy +/- continued percut Thrombolytic drip 90% of a/c thrombus are able to removewith in mts

48. Monitoring and treatment of post revascularization compartment syndrome and rabdomyolysis Compartment syndrome Reperfusion edema in confined space result in venouse compression, worsening edema , & ultimately neurological ischemia. Risk high in those lacking collateral vessels (embolus pts ,trauma) Pt with prolonged ischemia before revascularisation Anterior and lateral compartments are MC first symptomatic distribution Presents with peroneal nerve distribution sensory deficit on dorsum of the foot Pain with passive extension of muscle – most reliable findings Any suspicion – do 4 –compartment fasciotomy or measure the comp. Pressure Pressure > 30mmHg need fasciotomy to avoid permanent neurologic injury

49. Rabdomyolysis Pt with prolonged A/c limb ischemia , >6 hrs are at risk of acute tubular necrosis due to recirculation of necrotic muscle break down pdt myoglobin Oliguria and discoloured urine (pink or red ) Diagnosis Urine myoglobin level Microscopy neg for RBC Uine dip + ve for blood Treatment IV hydration , diuresis by mannitol , alkalinasation of urin by IV soda bicarb

50. Critical limb ischemia secondary to chronic arterial occlusive disease Definition & epidemiology Clinically defined by specified hemodynamic finding in conjunction with either of following Ischemic rest pain Lower extremity ulceration with hemodynamic finding incompatible with wound healing

51. Atherosclerosis is major etiology (95 %) 90 % of symptomatic PAD have some degree of CAD and> 60 % is having severe CAD Prevalence of PAD after age 70 is 14.5 % prevalence: >55 years is 10%–25% 70%–80% of affected individuals are asymptomatic PVD pt’s = 4X more likely to die within 10 years than pt’s without the disease. Prognosis at 1 yr in patient’s with Critical Limb Ischemia (rest pain): Alive with two limbs — 50% Amputation — 25% Cardiovascular mortality 25%

52. symptoms Ischemic rest pain at the foot when pt laying flat or elevate the limb Loss of gravity’s supplemental efffect on arterial flow to foot creates a “tipping point “ at which tissue in the foot become ischemic Pain relieved with lowering of extremity DN in DM may not have rest pain bcoz of c/c sensory loss Ulcers r primarily ischemic

53. Diagnosis Absent pedal pulses , dependent rubor of foot Absent calf hair & pedal hair Cool sensation, ulceration Non invasive doppler with ankle and digital pressure -100% sensitivity Arterial calcification in pt with DM & renal failure- ( falsely elevated ABI) Doppler wave form & digital pressure are still reliable in calcification Hemodynamic criteria for critical limb ischemia- ABI < 0.4 AND TOE PRESSRE < 30mm Hg

54. Arterial duplex scan to asscess infrainguinal stenosis Invasive angiogram (DSA), CTA MRA

55. Treatment goals Medical therapy Revascularisation goal Recommended for ambulatory patients with critical limb ischemia General guiding principle- 1-Endovascular therapy- stenosis at arterial level , short segment occlusion in illiac or SFA 2-SURGICAL BYPASS- long segment occlusion 3- Surgical endarterectomy – occlusion or high grade stenosis at CFA bifacation level

56. Endovascular therapy 1- obtain arterial access & perform angiography 2- pass a guidewire beyond areas of stenosis or occlusion 3-Confirm that the guide wire in lumen of distal arterial line 4-Perform angioplasty, stent placement ( if residual stenosis or if presence of dissection) or arterectomy over guide wire 5- Confirm success of results with completion angiography

57. 1-2 % pts have risk of complications at access site Bleeding ( refractory case after reversal with tense hematoma on skin or transfusion requirement >4U of PRBC need surgical arterial repair) Pseudoaneurysm ( > 2cm size can b managed by sono guided thrombin injection 1000U in 3ml NS) Arterial dissection (managed by surgical endarterectomy )

58. Open surgery therapy Surgical bypass long segment occlusive disease A native vein or prosthetic material is used for bypassing the obstruction Bypass proceedure is classified to Anatomic , eg-femoropopliteal bypass Extra anatomic- femorofemoro crossover graft, iliofemoral crossover graft, axillobifemoral graft. Aorto iliac reconstruction with prosthetic Dacron (woven & knitted) or PTFE ( polytetra fluroethylene ) conduit Infrainguinal long segment arterial occlusion autogenous venous conduit is used ( I/L GSV > C/L GSV > upper limb Cephalic and basilic veins ) Human umbilical vein ( glutaraldehyde –tanned, dacron supported )

59. Some Bypass Options:

60. complications Open sx have fairly high mortality Wound complication ( 20 %) Persistent edema (20 %) in 1 yr Graft thrombosis 10 % Major amputations 10 % Graft infection 1-2 %

61. Hybrid surgical therapy Combination of endovascular and open surgery For pt with critical limb ischemia with short segment lesion in one anatomic distribution and more advanced in another segment sugery vs Endo vascular Endovascular is having decreased morbidity Surgical rx have more durability of reconstruction ( 5 yr patency is > 75 %) For endo vascular 2 yr primary patency is 28 %, secondary patency with percut re intervention is >80% Limb salvage rate is same for both

62. Post vascularization surveillance Serial arterial duplex and ABI with digital pressures Duplex scan at 1, 3, 6, and 12 months and every 6 months Angioplasty and stent site restenosis Lower extremity bypass are at risk of neo- intimal hyperplasia-induced stenosis A velocity ratio of 3:1 b/w stenosed area and prox normal arterial seg s/o >50% stenosis

63. Non reconstructable tibial occlusive disease and critical limb ischemia Pt benefit from intermittent pneumatic compression treatment at calf level Last measure for attempt to salvage before amputation in patients with critical limb ischemia Research on going— Angiogenesis via stem cell and growthfactor implantation in calf as well as bone marrow stimulation with granulocyte colony stimulating factor Thanks``