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    7 views9 pages

    Prepladder Arterial 1

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    sandhu27152715

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    © All Rights Reserved
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    Dl ARTERIAL DISEASES PART-1 Anatomy e097 * The abdominal aorta gives visceral branches, including the renalartery, and continuesas the infrarenal sorta. ‘+ The abdominal aorta then bifarcates into two common iliac arteries, right and left. The common iliac artery then divides into internal ilinc artery and extemal iliac artery. * Below the inguinal HESHth,, the,,cxisrnal i continues down as the commonfemoral artery, + The common femoral artery further divides into the deep femoral artery and superficial femoral artery. The superficial femoral artery continues down as the popliteal artery. The popliteal artery further divides into the anterior tibial amtery and a tibioperoneal trunk. The Tibioperoneal trunk further divides into the posterior tibial artery and the peroneal artery. While the anterior tibial art inves downas the dorsal pedis artery. © artery » vestigations (for workup of a patient with PAD) 000206 | Werequiretwg sets of investigations: © Physiological testing & evaluation of hemodynamic parameters ‘©. Imaging (required for evaluation of arterial anatomy) + Physiological testing: © Doppler Ultrasound: > Doppler works on the principle of Doppler shift or the Doppler effect (change in frequency of a wave, when reflected by amovingobject). ~> InDoppler,a continuous wave signal is transmitted by a probe, which is keptin the artery and the receiver in the probe is going to pick up the reflected beam. There is a change in the frequency of the reflected beam as compared to the trmsmitted beam because of the moving RBCs. - Doppler effect ~ Normal blood flow is a triphasic blood flow. Three phases: a, Sharpsystolic upstroke/ sharp systolic forward flow b.Reversal of flow in early diastole/ early diastolic flow reversal . Late diastolic flow/ low amplitude slow flow in the tediastole = Thezeroflowbasclincisbeingcrossed. = When there is obstruction, the blood flow becomes, abnormal: a. It ean be scen as a biphasic flow. In biphasic, these phases can be seen: * Sharp systolic upstroke/ sharp systolic forward flow * Reversal of flow inthe diastole is presentas well. * But in biphasic flow, there is absence of late diastolic flow. * Zero flow baseline is being crossed. ~ When there is severe obstruction, beyond that, the ppatiem which you gets the monophasic pattern. In monophasic flow, only systolic forward flow is seen, Early diastolic flow reversal and late diastolic flow arenotseen. ¢. The zero-flow basclineisnot beingcrossed. aro ow Zero ow b any blasts AL) © Hemodynamic parameters: They can provide a useful quantitative assessment in patients of peripheral artery disease, Parametersare: HaemodynamicParameters ‘ABI (Ankle Brachial Index) ‘Segmental pressures Absolutedigit pressure /toe systolic pressure Tocbrachial index ‘Transcutmeous oxygen saturation/ Pressure Palse volume recordings © ABI (Ankle Brachial Index/ Ankle Brachial, Index): = apie —__Hishersytolic pressure at the ankle Higher systolic pressure in he branchial artery “+ It is measured with a hand-held Doppler probe. The patient lies in supine, and we place a cuff over the alle. And along with that we place the hmnd-beld probe over the posterior tibial antery (PTA) and the dorsalis pedis arty (DPA). Retum offlow or return of signal over these arteries indicates the systolic blood pressure + We also measure the systolic blood pressure in the brachial arteries (both arms), “+ We measure systolic pressure in PTA as wall as DPA, s0 whichever pressure is higher that will betaken as numertar to calculate the ABI. Along with that between both the arms (brachial arteries), whichever systolic pressure is higher will be taken as a denominator, + Forexample, if the patient has symptoms in the right Jowerlimb, then wehave tocaloulte Right ABI Higher of the right ankle systolic pressures (posterior) tibial or dorsalis . pode ~ Right ABI" $iicher ann systolic pressures (eft or right arms) Higher of the left ankle systolic press (esti il dna is LERABI~ Ti cher am eyetlic prassures Octo ee + Normal ABI valve-0.9 101.3 ~ ABI < 0.9 ~ indicates that there is some degree of ischemia (bemodynamically significant occlusion or obstruction) and it is ako a risk factor for patients developing some CVS events (higherrisk). + For every 0.1 decrease in ABI below 09, increasesthe relative riskof CVS eventy/ CVS disease by 10%. ~ Gradually decreasing ABI - indicates the imminent Aimbloss, If ABI is <0.4 ~ indicates critical fimb threatening ischemia (CLT). Patients who have ABI of <0.5, have 2 times greater risk of undergoingamputation as compared to patien's who have ABI of>0.5. + False elevation: If ABI >1.4, can be du to diabetes ‘mellitus (ulceration or gangrene or amputation of the Istand 2nd toe), CCRD, heavy calcifications leading to incompressible arteries. (digital vessels are usually not susceptible to calcification, and bence they canbe ‘usedfor ABI) + In these patients, we can measure absolute digit pressure (toe systolic pressure), and after that we can measure Toe Brachial Index (TBI). ~ Toe Brachial Index < 0.7 indicates ischemia. Normal ‘TBI is morethan 0.7. Toe systolic pressure of less than ‘50 mm Hg also indicates ischemia. So, if the ABI is falsely elevated, you have to rely om the toe brachial index (TBD. Sometimes patients have symptoms such as clandications but because of good collaterals, resting ABIisnormal. In these patients we go for postexercise ABL In post exercise ABI, we tell the patient to do the ‘treadmill exercise tllthe symptoms appear. Inpatients who have the arterial occlusion, because of exercise induced vasodilatation, there will be a drop in pressure stenoticarea, ~ In these patients, postexercise, if ABI falls by > 0.2 or ‘more than 20% of the resting ABI, itis suggestive of arterialocctusion. If in these patients, post exercise, ankle systolic pressure falls by more than 20 mm Hg, that is also indicative ofarteril occlusion. ~ Failure of ABI to retum to pre-exercise levels in 3 minutesis again suggestive ofarterialocclusion, ‘Segmental Limb Pressures: They can haveanimportant sein tellingus aboutthe level of occhision. ~ inthis, we canjitieiuipls cls together or oneby ‘one down the loWeFlithb Positions of the cuffs: one in the upper thigh, one inthe lower thigh, inthe calf and over the ankle. > Systolic pressure in a particular segment is indicated by return of signal or the retum of flow below the cuff. Systolic pressure at cach level is expressed as the ratio, tohighestsystolicpressure intheupperlimb. > High thigh pressure -itis usually 20mm Hg more than thebrachial pressure > Low thigh pressure-itisusually equivalent o brachial pressure. = Subsequent pressure at any level should not fall by > 10mmHg. levels is more than 20, it indicates occlusion at that particular evel. + So, segmental limb pressure is giving us the idea that occlusion is present, and also the probable level of occhasion. A = © PulseVolume Recordings: —+ When there is a non-compressible vessel because of calcifications, we can use segmental plahysmography for detecting the mderlying ererial occlusion. We again pat cuffs at mokkiple levels to detect the change in blood volume and flow. They can produce the pulse volume recordings when attached with a plethysmograph. + On pulse volume recordings, if there is absence of ‘brisk upstroke of pulse or rounded peak of the wave or dissppearance of dicroticnotch- they areindicativeof proximal obstrection/ proximal disease. © Transcutaneous Oxygen Saturation/ Pressure: Again, ‘usefalin patients who have non compressible vessels This local pressure of Oxygen reflects the vascularization of the skin. ~ Transcutancous Oxygen level of less than 30 is indicative of Critical Limb Threatening Ischemia (am. Imaging: © DuplexUSG: + Itisa combination ofB mode USG + Doppler. B mode USG provides us with the vessel images and Doppler ‘ives us the waveforms. That means the duplex USG provides us with both the anatomical as well as Physiological details. + Lots of color coding is used, which can givea detailed visualization of the blood flow (change in direction, velocity, and turbulence). > By using Duplex scan, peak systolic velocity + end diastolic velocity canbe calculated. > IF the ratio of peak systolic velocity within stenosis to peak velocity of normal proximal segment is more than 2 —+ that indicates more than 50% occlusion of thevessel. somosvoa => 10 can bo 8d good €s txiomraphy (experienced Soo ems + In case the pressure gradient between 2 subsequent" = Aortoiliac segment - difficult to visualize Because of bowelgasses, obesity, + Duplex = umble t0 evaluate the recently implanted PTFE or polyester grafis. (Because they will contain air and that will ntallow thesonographic beam{o pass) + Heavily calcified vessels also decrease the usefulness ofthe Duplex in determining theseverity of stenosis. If the Duplex sean is giving inadequate visualization or inadequate quantification of arterial diseases, and we're planning an intervention; then we need to go for ‘additional imaging. + When planning an intervention (revascolarization procedure, endoscopic procedure or surgical procedure), ‘we need some addtional imaging to delineste thenature of oochision disease or to delineate the length of ‘occlusivedisease better. > For this purpose, the gold standard investigation is, ‘Conventional Angiography. ~ Conventional angiography has the benefit that we can simultaneously establish a diagnosis as well as give ‘endovasculartreatment. > Currently conventional angiography is used mainly for therapeutic purposes rather than diagnostic purposes. — Access - Common Femoral Antery (contralsteral ‘common femoral artery). “> Seldinger Technique + Angiography is done using contrast medium, so it can cause contrast nephropathy. So to prevent that we shoulduse owerioniclond/isoosmolarcontrast. + Prerequisite before the angiography - for patients who are on Metformin + ACE inhibitors, these drugs have to be stopped at least 48 hours before and after the procedure. Because these drugs can cause a lot of metabolic complications associated with the contrast. > Digital Subtraction Angiography is a type of ‘conventional angiography in which images are igitized; and background bone and soft tissue shadows are removed which gives a better or more clear delineation of the vascular anatomy. 1 especially useful in multilevel disease, when contrast can't reach the distal arteries where it supplements i visualizing the arterial anatomy. + DSA provides more dynamicinformation. ~ Complications ofangiography: ~ Bleeding-whichcan leadto groinhematoma. = Pscudomeurysm ~ Thrombosis ~ Arterial dissection = AsV fistula Contrastmedisted side effects (contrast allargy). © CT Anglography: 4 Provides excellent anstomical delineation to plan revascularization procedurs, + Beneficial: Aortoiline segment can bevisualized. > Maltidetector CT - henes, increase the speed and volume of coverage. + Single bolus of contrast passes through entire arterial system, > It provides 3D reconstrction + Muhiplanar formatting which isnot passible with conventional angiography. ~ There's depiction ofthe entire vessel wall which helps differentiate thrombus from califications. > Buthsavy cakifications + stents can cause artifacts. > Disadvantages: ~ Itdoes not provide physiological denis, — Exposes the patient to ionizing contrast-\. an leadtocontrast nephropathy. ~ Ih is not useful br ititd popliteal visualization such asfortibialorfootvessels. © MRAnglography: ~+ Contrast MRA with gadolinium- has a very high sensitivity and specificity- to sce the severity of the stenosisand to sec the lengthofthestenasis. + Superiority in identifying distal target vessels! infra popliteal vessels as compared toCT Angiography. ~ Patients with DM (Heavy calcifications seen in DM - calcified crue! disease) - Duplex USG and CT Angiography are not veryreliable -MRA has ability to separa out the contrast from vessdl cakifications. “> Majority of peripheral arterial stents are compatible with the MRA, although they may cause downgrading ofthe irtages. + Nitinol stents cause minimal anfscts with MRA. > Disadvantages: ~ Patients with implants such 2s pacemakers cannot undergoMRA. ~ Gadolinium induced Nephrogenic systemic fibrosis inpatients with GFR <30 mi‘min, ArterialOcelusion onsen + Acute occlusion: Sudden occlusion - sudden cutoff of the blood supply. ‘+ Chronic occlusion: Gradual occlusion of the vessel. It gives time forthe formation of the collaterals. Andthese collaterals Provide alternate route for passage of blood, Hence, symptoms are gradual and start getting severe only when the Iumen is critically narrowed, and the collaterals will not be able tomeet the demand. AA AX + Riskfactors: (© Age: Usually more commonly seenafter SO years of age. © Smoking o DM © Hypertension 0. Hyperlipidemia © Gender: More commonly seen in makes © Sedentary lifestyle © Causes: © Atherosclerosis -Mostcommon caus ofarteratocctasion “+ Peripheral artery disease is peripheral manifestation of systemic atherosclerosis. © Nonatherosclerotic vasculopathies) causes: > Buergers disease -Thromboangitis obliterans > Arteritis: ~ PAN arteritis medusae > Wagner's granulomatosis > Behcetdisease > Cystic adventitial disease — Pseudoxanthomaclasticum ‘+ Comparison between Buerger’ disease and atherosclerosis: Age/ Cause 50 years decades of life). Plaque formation ‘Thrombus formation ‘More common in male Males and females are equally affected Gender Predisposition Smoking (Main factor) Combination of rmulipl risk factors - Hypertension, diabetes, hyperlipidemia, smoking, te. Predominantly involves only the lower limbs. Site Lower limbs are more ‘commonly involved than upper limbs. Involvement Arteries, veins as well Mainly involves as nerves arteries. Commonly associated Can also lead to with migrangpy seo" OR ay aU Superficial syndrome ‘Tarombophlebitis and Raynavd’s Phenomenon Vessclsize Small to Medium Medium to Large Progression Distal toproximal Proximal to distal In Buerger' disease there can be segmental involvement with presence of skip lesion + Chronic Arterial Occlusion: one very important symptom! pain which patient with chronic arterial occlusion have is ‘Claudication (commonly called as Intermittent claudication/ ‘Vasculogenic claudication) ‘+ Intermittentclavdicationisacramplikepainin _scles- when there is ischemia, there is decreased blwu supply ‘which can lead to increased anacrobic metabolism leading to sccumblation of metabolites that lead to pain, + Interminent claudication comes after exercise’ walking (it does not come at the Ist step of the exercise). The distance ‘which the patient coversafter which the pain occurs is called the “clandicationdistance.” © Claudication distance remains constant on day to day basis, but as the disease progresses, the claudication distance decreases. Itwill also decrease in case the patient is walking. uphill andthe patientis walking witha weight. ‘* Claudication gets relieved when the patient stops walking There is no need for a change of body position for intermintentelawdication to got relieved. + Interminent claudication usually gets relieved quickly in less than Sminutes. + The muscle which gets affected with intermittent claudication depends on the level of occlusion. It is one muscle group below the levelofocclision (Clavdication in buttocks, thighs and calves Gilatera!). Femoral and distal pulses absent in both limbs. Bruit over aontiliac region Impotence (Leriche) ‘+ Unilateral claudication in the thigh and calf and sometimes the buttock + Brut over the iliac region Unilateral absence of femoral and distal pokes Femoropopliteal Crt Eyed rhe) Artery Obstruction Unilateral claudication in the calf (most common) Femoral pulses palpable with absent unilateral distal pulses Most common site of ocehusion is the saphenofemoral artery nd hence the most common site of claudication is the calf, Femoral and popliteal pulses palpable ‘Ankle pulses absent lavdication in calf and foot Cee) (ene et) (ieee) © Boyd's Classification: ‘© Grade: Patient continues towalk, and the pain subsides. ‘© GradeII: Patient continves to walk with the effort, but the pain docsn' subside, (© Grade III: Patient stops walking and takes rest since the painissosevere. © GradeIV:Restpain Diferentiation between different types of pain (other causes ofpain): ReferTable 12.1 * Aortoiliae Disease: © Type I: focal disease and involving the distal aorta and proximal common iliac. © Type Il: Diffuse aortoiliac disease above the inguinal ligament © Type III: Multilevel disease involving the aortoiliac segment as wellasinfrainguinalarteries. Tet et oem CLT1 (Critical Limb Threatening Ischemia) + CTLIisa new terminology according to the Global Vascular Guidelines. The oldterminology usedto be CTI. * Patient is said to have CTLI if there is objective documentation of peripheral artery disease with any of thethree: ‘© Ischemic Rest Pain with its confirmatory hemodynanuc parameters © Tissueloss © Gangrene afthefoot RestPaln: + Ihisapain occurring even at rest. tmainly occurs when there isanserobic metabolism even atest ‘+ Restpainisscen more commonlyin foot- forefoot. + Itismore commen iasmoker> diabetics. ‘+ Its ahvays more commonly seen at night, Because at night the patent willie down, effect of gravity will go and because ofthat rest painwillbe more at + Rest pain occurs more on elevation of limb and decresscs when the paticathangshis limb. + Confinmatory hemodynamic parameters forthe estpain: (©. Ankle Brachial Index (ABI)is<04. © Ankle Systolic Pressure is<50, © Toe Systolic Pressuris<30. (© Transcutancoms Oxygen Pressercis<30. ‘Tissve Loss/ Ulceration ‘+ Definition: For defined tissue Joss, or that tise loss is ‘occurring because of CLTI: the tse losshas tobe for more tan 2 weeks, with objective evidence of PAD’ ‘occlusion which severe enough o impede the bloo ‘+ Sites:Berween oes, dorsum of foot, over the shin, owe. yt oftheleg. © Characteristics: © Painful (© Pinched outedges (© Granulationtissus—pale (© Scrroudingskin-pakeandcold (©. Absence of distal pulses present. + Symptoms and signs of neuropathic uler versus ischemic ker os oT f Painfol Painles ‘Normal pulses Absent pubes Regular margins, typically Inegularmayin punched-ovt sppearmce (Often oested onplantsr Commonly located ssrfice of foot(Presue ghbrous mains ‘bearing areas) Presence of eases CCalluses absent or infrequent Loss of sensation reflexes, Variable sensory findings sd vibration Increased blood flow Decreased blood flow (arteriovenous shunting) Sei ee ies Cold foot Uargrese + Mainly occorsinthedist partofibe lowerlim. ‘= Dry gangrene: Macroscopic death of tissues with desiccation. Occurs because of gradual decrease in blood, flow. Hence the line of demarcation is more developad or developscaly. 1+ Wet gangrene: Macroscopic deathoftissuss with putrefscton. Occurs because of DM or secondsry 10 infection. Line of not well developed ‘© Gangrene is blackish in color because of degradation of nd deposition of FeSulphide, © Weveto lock for signs of peripheral ischemia: oss of bait, Jess of abeutneous fat brinle als, muscleatrophy. (© Sunset siga: sign of chronic arterial occhision. On clevationof the ib, there willbe presence of pallor and {guttering ofthe veins. There willbe rubor or redness on ‘making the limb dependent. © Capillary filing ime willbe prolonged. © Peripheral pulses ay be absent/fecbl. O1dCassifcation: a PIE Birrehe oreeiti rs Fontalne lassifcatlon Rutherford classification ‘Stage Clinkal Grade Category Clinical 1 Asymptomatic 00 Asymptamasic. Ms Mikdclautication 1 1 Mild claudication My Modertetosevere 12 Moderate to claudication Sevetb anos lace 13 Severe claudication MM Ischemicrestpain 4 Ischemic rest pain 1V Ulersinor = LS Minor tissue spangrene Toss Drawbacks: ‘+ Donotincludewoundcharacteristics. ‘+ Do pot consider the presence of severity of infection in the ‘wound. ‘New Classification: WIFICIassification~ Society of Vascular Sugeons Advantages: (0 It ca predict the amputation risk in the patients with peripheralartery disease. (© Along with that it may also predict the likelihood of © Limb Staging: Very important recent advancement in benefit the patient will receive for the revascularization ‘management of PAD. When you've a patient with peripheral procedure. artery disease, especially with chronic limb ischemia - ‘+ Three parameters includedin this classification: ‘you've todo limb staging. © Wound © schemia © Infection 1 + Every parameter we givea grade of0-3.So,every parameter, is getting 4 grades. Based on this, wecan stage the limb from T-IV.As thestage increases, theriskof amputationat I-year TIT increases. (Analogous to TNM staging ofthe cancer) v W: Wound (Clinical Category) ‘SVS grades for rest pain and wounds/issue loss (ul.» and gangrene): 0 (Ischemic rest pain, ischemia grade 3; no ulcer), 1 (mild), 2 (moderate), 3 (severe) rns ay 0 Nouker No gangrene Clinical description ischemic rest pain (requires typical symptoms + ischemia grade 3); no wound 1 Small, shallow ulser(s) on distal leg or foot, no exposed bone, unless No gangrene limited to distal phalanx Clinical description: minor tissue loss, Salvageable with simple. xmputstion (I oF? digits) or skin coverage. Deeper ulcer with exposed bone, joi Sr-tendgn, generally not Gangrenous changes limited to digits involving the heel shallow heel WEEE "Without calcancal involvement Clinical description: major tissue loss salvageable with multiple digital mputations or standard TMA skin digits ital 3 Extensive, deep ulcer involving forefoot and/or midfoot, deep, full Extensive gangrene involving forefoot and or thickness bee! uleer calcaneal involvement ‘midfoot, full thickness beel necrosis calcancal Clinica! description: extensive tissue loss salvageable only with a involvement ‘complex foot reconstruction or nontraditional TMA (Chopartor Lisfranc), flap coverage or complex wound management needed for large soft I: Ischemia Hemodynamics/perfusion Measure TP or TePO, if ABI incompressible (>1.3) 'SVS grades 0(none), | (mild),2 (moderate), and 3 (severe) SS ne 0 >100 mm Hg 60 mm Hg 1 05079 70-100 mm Hg 40-59 mm Hg 2 04.059 50-70 mm Hg 30-39 mm Hg 3 039 <50 mm Hg. <30mmHg |: Foot Infection S grades 0 (none), 1 (mild), 2 (moderate), and 3 severe limb and/or life-threatening VS adaptation of Infectious Diseases Society of America (IDSA) and International Working Group on the Diabetic Foot WGDF) perfusion, extent/size, depthitissue loss, infection, sensation (PEDIS) classifications of diabetic foot infection. Tere) Mn oe th) aa | Io symptoms or signs of infection 0 afection present, as defined by the presence of at least two of the following items Local swelling or induration Erythema >0.5 to 2 cm around the uleer Local tendemess or pain Local warmth Purulent discharge (thick, opaque to white, or sanguincous secretion) ee eee focal infection involving only the skin and the subcutanco. _uc (without svolvement of deeper tissue and without systemic signs as described below) 1 Mild xclude other causes of an inflammatory response of the skin (¢.g., trauma, gout, acute ‘harcot neuroosteoarthropathy, fracture, thrombosis, venous statis) ‘cal infection (as described above) with erythema >2cm, or involving structures ceper than skin and subcutaneous tissues (¢.g., abscess, osteomyelitis, septic arthritis, 1sciitis) and No systemic inflammatory response signs (as described below) ocal infection (as described above) with the signs of SIRS, as manifested by two or 2 Moderate 1ore of the following © Temperature >38°C of 36°C ¢ Heart rate >90 beats/min * Respiratory rate >20 breaths/min or PaCO, <32 mm Hg ¢ Wh “od cell count >12000 or <4000 cufmm or 10% immature (band) for 3 Severe Dead Dot) pet (ett Oe Nature Cramps Location ‘Most commonly calf Velief ‘Stop walking. Relief in

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