IR in Renovascular Hypertension

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IR in Renovascular Hypertension

7 May, 11:30 AM

[Music] good evening everyone i am dr tandi and i welcome you all on the behalf of netflix uh today we are gathered here for a very interesting session by iria kerala and to introduce the speaker we have talked to zunim all for the same uh dr zuniman uh handing it over to you welcome to the academy session uh of this evening uh i am introducing dr manish kumar yeah who is the consultant interventional radiologist in king's uh toranto he is uh he did as a dn um mbbs and we have one he completed his mbbs at mrd environmental college uh under the able uh guidance of combating chilean and of the bangladesh uh he completed in 2013 afterwards by 2014 till date he has joined caroline institute of medical sciences trevantan he is the chief international radiologist here in my colleague and [Music] heading the division of intervention radiology about the start of uh fellowship also here in international radiology uh he is completely certified by the european board of international radiology last year 2081 he is a very hard-working uh consultant and even though he is in my department we hardly see each other because he's always we seen [Music] okay [Music] also for the introduction uh good evening everyone uh today we will be discussing about renal vascular hypertension we will try to understand the the pathophysiology the principles of management and what role does the intervention radiology play in the management of these cases so basically why we are talking about renal vascular hypertension is uh first of all kidney is a major organ in our body which is required to not only help in excretion of byproducts of lot of metabolic activity but it also maintains the acid-base balance required for the electrolyte balance and also the fluid volume it control controls the fluid volume uh in our body so uh there are a variety of mechanisms in play as far as kidneys is concerned so one of those effect of one of those uh disturbances is uh renal vascular hypertension uh it is actually um adrenal vascular hypertension is one of the most renal mediated hypertension hypertension has a lot of causes including the essential hypertension and secondary hypertension and one of the types of hypertension is the renal mediated hypertension again renal there are a lot of causes in that one of them is renal artery stenosis this talk will be focused on renal natural stenosis and its mediated hypertension essentially it comprises of around one to five percent of all hypertensions why we are talking about this is important to identify and treat it because this is one of the causes of hypertension which are reversible and once we reverse the hypertension we can help to protect a lot of organs from the effect of this hypertension be it heartbeat eyes kidneys itself and a variety of organs can be protected by just by treating these kind of hypertension so um so looking at the diagnosis um patients with one of the criterias to diagnose renal vascular hypertension is actually to demonstrate the the hypertension reversibility after revascularization so um most of the time we work on uh on understanding that probably this is a renal mediated hypertension or renal vascular hypertension and as we progress towards revascularization and after revasculation we see the reversal of this hypertension that is the true or diagnostic criteria to say that it was indeed renovated hypertension so essentially the diagnosis includes involvement of uh renal angiotensin and renin mechanism and reverse stability these are the two essential criterias to diagnose it as a renal vascular hypertension but there are other groups as well which are not included in the diagnosis of renal vascular hypertension such as uh rain laundry stenosis but it may not benefit from a revascularization such as a very shrunken or small kidney again they don't come in the purview of renal vascular hypertension then there are um essential hypertensions which may have some amount of grain larger strosses which may not be hemodynamically significant again these do not compromise come in the purview of this particular diagnosis so question arises when do we suspect renal vascular hypertension um criteria wise acute onset when suddenly a sudden onset of hypertension in somebody who is young less than 30 years of age our primary diagnosis in these patients will be fibromuscular dysplasia then abrupt onset of hypertension after 50 years of age that's where we are looking at atherosclerotic renal artery stenosis then presentation with accelerated or malignant hypertension the sudden increase in hypertension or which is very difficult to control hypertension this can be due to renal hypertension and more importantly more what we see more often in the chronic phases is refractory hypertension when the hypertension is not getting controlled with more and it requires more than three drugs and still it remains uncontrolled then uh the second we looked at the hypertension related criteria and the second important factor is renal dysfunction is when we see unexplained hysodemia rising creatinine or bond especially in angular age group we suspect atherosclerotic greenhouse genesis if we if there is a renal dysfunction which is induced by a inhibitors again we will understand how the a centimeters play a role in reducing this function and as well as in treatment so if introduction of ace inhibitors produces the rise in create again it's an indication towards that probably we are dealing with adrenal vascular hypertension unilateral small cavity if there is a discrepancy in size between the two kidneys or more than one and half or two centimeter that's where we suspect that one of the ate is having rheumatoid stenosis and another factor is unexplained hypokalemia this is one of the criterias to suspect renal artery stenosis because the kidney compensate for the other kidney the normal compensate for the hyper stenotic kidney and produces hypokalemia so that is one of the criterias and most of the time this hypokalemia get reversed after we treat the hypertension other findings which may prompt a diagnosis of renal artery stenosis is abnormal associated with hypertension uh which is acute in onset i mean um the high potential starts and within few weeks we see retinopathy that means that probably we are dealing with the renal vascular cause presence of other vascular diseases like in carotid coronary or vertical system again suggest towards renal vascular hypertension then one of the presentations may be with a flash pulmonary edema or a congestive heart failure uh either the first episode or the second episode happening in spite of based medical therapy is again makes one thing of you know hypertension so these are the criterias which are listed as per the standard of practice recommendation to suspect secondary hypertension most of these three are covered in these is um flash pulmonary edema uh presence of renal dysfunction and hypertension which is uncontrolled these are the most important um conditions where we have to look for android and in majority of these cases repeat them and it can result in reversal so looking at the causes of renal vascular hypertension uh the most common causes are atherosclerosis and fibromuscular dysplasia these two are the most common causes of renal hypertension and this is what we essentially see in our day-to-day practice is uh lethal fiber muscular dysplasia other causes are there but they are rare uh another important cause is the diabetes syndrome on the rear but we do see some cases which can present with renal vascular hypertension so understanding a bit of pathophysiology what happens and how it affects the whole casket uh probably this chart is the clue to understanding why these changes happen and um what is the role of uh ace inhibitors or um angiotensin medications so basically what happens is whenever there is a renal arteriosis here we are talking about the unilateral legal artery stenosis whenever there is a renal artery genosis the pressure of the blood reaching the nephrons in that particular kidney and drops down so there is efferent arterial receives blood which is low in pressure so there are baroreceptors situated in the this juxtaposed cells which sense that there is a low in decrease in the pressure so once that happens they tend to signal to increase running situation and then down the line as blood as the urine passes through the distal convoluted tubule there are sodium receptors in the macular densa which picks up that there is a low sodium concentrate partly because of low pressure from the apparent arteriole this again sends signals to increase remnant production so renin uh basically is an enzyme which converts angiotensin to an angiotensin ocean to an angiotensin one so the liver produces the angiotensin and the rhythm is produced by the kidneys which helps in converting this to angiotensin one and then angiotensin one is converted to angiotensin two which is the active metabolite by the help of angiotensin converting enzymes which is secreted by the lungs and then this is the active mutable through which the whole system uh intervenes and this acts on the adrenals to produce increased aldosterone at the same time this works on the blood vessels to produce vasoconstriction and inducing hypertension by direct effect of vasoconstriction and by this effect by increasing aldosterone levels again acting on the kidney and this time it is a normal kidney which responds to this increase in aldosterone thereby increasing sodium retention so the sodium is retained inside the body and which also results in water retention so uh so there is actually hypervalenia which happens and that's how the patient presents with flash pulmonary edema and that is one of the reasons of hypertension uh flash pulmonary edema and uh to some extent because of african arterial vasoconstriction the egfr goes down uh and the filtration goes down and that's how the renal function comes down and the acetaminophen so this mechanism explains why there is hypertension why this pulmonary edema and why there is decrease in the adrenal function so moving on to atherosclerotic disease so um as we know atherosclerotic is seen more commonly in older patients it comprises of around 70 to 80 percent of renal artery stenosis what is seen in clinical practice uh what is typical about atherosclerotic disease is we see disease in the very proximal uh in fact approximately one third of the regional arteries that's what will be involved and sometimes it may be a iotic plaque which may be overhanging or the renal origin reducing the renal stenosis sometimes rheostem producing the narrowing in the renal artery so uh the implications of that is that whenever we stand with atherosclerotic disease we always try to cover the uh iotic origin so we we have to get the stem to project a little bit into the abdominal iodide when we are dealing with such disease so as i said there are two variants one is a eccentric block in the proximal renal artery and the other block is the plaque in the iota which powers the renal ocean it can sometimes extend into the inside the renal artery um the second most common cause is fibromuscular dysplasia which comprises 15 to 20 percent of all greenhouse gases so essentially fmd as well as atherosclerosis they together make up around 85 to 90 percent of vascular hypertension so these are the two most important among the fmp the most common type which we see in practice is the medial fibroplasia which amounts to around 70 percent the other types are very medial intimate medial hyperplasia and administration and periodic fibroblasts what is typical about medial fibroplasia is uh most of the patients will be essentially woman they'll be in the younger age group less than 30 years of age 25 to 50 is the typical age group which we see it's rare in children's and um what distinguishes it from atherosclerotic by location-wise is involves the distal two-third of the renal artery in major branches that means the proximal third is um uh involved by the atherosclerosis and the distal two-thirds is by fmd it can also affect other sites like carotid vertebral mesenteric anemia um mind you um most of the fmp is not a systemic disease they are mostly local disease so hence um they do not tend to need any systemic therapy and most of time interventions are curative so what happens in the median fiber plates is basically this is a cross section of the uh arterial wall so uh there is a loss of the internal elastic lamina this blue line which you are seeing that is lost and there are collagen bands which replace the muscle so there is collagen deposition in the smooth muscle layer and these are non-elastic bands which produces the stenosis so these collagen bands and the loss of elastic lamina produces the stenosis and then there is a postgenetic dilatation so uh which together form a string of lead appearance as you can see here so the narrowings are caused by the collagen bands and the dilatations are actually osteonautic dilatation followed by another band and then dilatation so this this is a very overworked form of medial fibroplasia this is the most common variant called bcp in clinical practice then coming to the second most common is the perimeter fibroblast again woman 15 to 30 years of age this compromises of around 50 to 20 percent of fmd of all fmd this produces tight stenosis because of the collagen deposition in outer border of the media that's why the name is perimeter fibroblasia so outer part of the tunica media this is a unica media the outer border it produces collagen deposition producing perimeter fibroblasts so as the name suggests it's a perimeter so around the medial layer you get a collagen deposition and that produces the steam losses uh intimal fibrous glacier as the name suggests these are more involvement of internal elastic lamina so um more uh collagen deposition occurs in the internal elastic lamina has the name intimal fibroblasia so just before the ending just under the intimal layer will be this uh internal elastic membrane which is again involved with a collagen deposition which is more circumferential and results in intimal fiber placement this is a small percentage around five percent of all ifmts and most common in males children and young adults than females so this is one family which is more common in males than demons then medial hyperplasia it is quite rare uh this is because as the name suggests medial layer tunica media there is excessive proliferation of the smooth muscle which results in narrowing the last one is advantageous by the artillery fibroblasia this is less than one percent of all the fmds it produces focal or tubular stenosis and this is characterized by dense fibrous tissue around the artery so most of the time it will be advantageous or around the artery where the fibroplasty happens and there is collagen deposition causing the disease so coming on to radiological evaluation what are the imaging modalities available to us so broadly they are grouped into two types one is an anatomical depiction of the stenosis and second is the functional depiction or hemodynamic effect of the stenosis so to demonstrate the anatomical the catheter dsa is considered the gold standard and all the other anatomical methods are compared with the result with respect to dsa another uh important diagnostic evaluation is the ct andrography and mr angiography the color doppler plays a very important role in screening patients for renal muscular hypertension as well as it has an important role in follow-up whether to see for recurrences then uh functional imaging is basically angiotensin converting and sometimes inhibition centigraphy is a nuclear medicine medicine test which can be done uh then mr angiography in terms of dynamic mr sequences and the fast gradient sequences they they have the ability to capture how much is contrast enhancement and differential contrast enhancement of one kp with respect to another which again gives a very important functional information with respect to renal function and it comes in the functional imaging doppler ultrasound in terms of various parameters it gives us more objective quantification of function between the two kidneys then another test which is very rarely used is serum or renal vein training measurements this is a measurement of activation of our mechanism which indicates towards renal vascular hypertension i've heard about ace inhibition reynolds integrity graphic probably may be a question for dmv itself um basically it has a sensitivity of 80 percent and specificity of 100 we can see is highly specific it is positive if it is positive indicates that definite component of adrenal vascular hypertension and it definitely reversal of the chemos is shows improvement it is a functional test uh the most common indications today is uh intermediate clinical suspicion the current recommendation for which tests to employ indicates that if the suspicion is low we need not do any test if the suspicion is intermediate uh usually uh this particular base in innovation raymond's into graph is used if the suspicion is high and directly go for a anatomical detection and go for treatment another places where there is a role of this particular test is whether the renal artery stenosis is functionally significant or not as we see is like measuring ffr in coronary this is kind of ffr for renal is is how much is the reversibility of of treating the string larger stenosis so what the data shows is around 90 to 98 percent improvement in blood pressure if these patients are treated who come positive with this particular test what are the limitations um it is limited if there is a renal efficiency so it works when the kitties are good good functioning and it works best when there is a unilateral with this test if there is a bilateral disease better to do a pre and post inhibition scintigraphy if if the suspicion is reasonably high and we are looking at human lateral disease probably just a host inhibition scintigraphy is enough to save time what are the agents which are used uh technician 93 uh mercaptoestyle triglycerine that is also known as mac3 this is the most common agent which is used another agent is iodine 131 uh then another common uh agent which is used is dtpa that is technician acetic acid which is commonly used so mc3 and ddpa are most commonly used agents for capital precipitography so basically what happens is we know normally the different arterioles bring blood into the glomeruli where the urine is secreted and the egfr happens and then the ethereum takes the blood away from the kidney and return it to the circulation so when there is a renal artery you know since it kind of produces less blood coming to the apparent arteriole and then we understood the mechanism angiotensin and angiotensinogen 2 which produces basal constriction of the apparent arteriole so this phasor constriction maintains the ejfr so it does not mask it kind of masks the renal disfunction because of this particular mechanism what the capital trailer is innovation does is uh blocks the con so there is no way of construction so if there is no as a construction the perfectly escapes from the renal system which has effect on the gfr and the decrease in the gfr so what we pick up is um after introducing introduction of this innovator the decays in egfr is that's what we are looking for so basically uh patient should be office individuals for a week and the study comprises of these pre and post ac innovation studies and single phase study can also be done more commonly in unilateral so basically this patient this is the posterior image so this is the right uh this is the left and this is the right side as you can see uh this is uh post inhibition patient has already received capillary after the injection and we can all already see there is decreased uptake in the affected kidney and then in the daylight scan i'm not sure if we can appreciate there is retention of radio pharmaceutical in partic in the left kidney radio tracer in the left kidney and the right kidney has already started expanding this again represented graphically yes this is a normal right kidney at the cortical phase it shows rapid rise and then rapid fall as the radio depressor is washed off whereas affected killing is shows a lesser peak compared to the normal side and then it is kind of flat use off it does not show that peak and then falling down it shows kind of vladimir again this is a renal perfusion scan the same radio tracer this is the iot bracing which acts as a control especially in cases of bilateral renal artery stenosis this is the right side which shows a continuous higher peak and then maintain this is a left side which shows a much slower peak indicating towards large numbers so many times the pre pre capital test it may be normal so once we introduce capital we see this differential function of both the kidneys and that gives us the clue towards the renal vascular production what is the role of doppler the doppler is less expensive non-invasive extremely good screening tool and it is widely used all all over the world for screening of linovascular hypertension the limitations are obviously the operator dependent and then technical problems of body habits bowel gas and inability image small accessory arteries one word of caution in doppler assessment is if we don't see uh uh if we don't see the main arteries on our doctor probably the evaluation is incomplete and we should suggest towards another examination or move on to another cross-sectional imaging uh just by looking at the kidneys we may not be or a segmental or between lotteries we may not be able to confirm whether there is renal vascular hypertension or not so evaluation of the renal austrian is very very essential on a good doppler study mr angiography again in the past it was uh most relied on face contrast and i am a flight time manager that we choose to show a signal drop out because of the turbulence just prior to the site but they had a lot of problems in terms of overestimating the stenosis and the slow flow may also be picked up as absence of signal but then what things changed about this particular modality was um gadolinium enhanced uh 3d sequences which came these are much more faster sequences and they give extremely good images which are very very uh similar to dsa images it has increased the sensitivity to 97 in sensitive specificity to 92 percent this is in comparison with catheter angiography and as i said the dynamic studies can also give us a lot of functional changes as in this image you can see apart from the stenosis we also look at the enhancement pattern you see this kp is much less enhancing than this particular so obviously this stenosis has to be much more um significant compared to this particular stenosis so that kind of functional information we are talking about speaking geography we know it has excellent special resolution and um and it demonstrates beautifully these images and within advent of multi-slice and if you aromatic detector cities and then moving on to dual energy seed it has actually changed the picture and it gives us information even in heavily calcified iota where you can subtract the classification and get the true block which is underlying those calculations it has a high sensitivity of 94 to sensitivity of 87 percent then uh volume render techniques again a very good depiction but all these things do not replace your looking at the raw data that means the cross-sectional imaging that gives us the best information about the ct and geography and the limitations we all are aware of use of contrast and increase ionizing radiation which prohibit uh use of this technique especially in presence of criminal dysfunction where one would feel the bias towards the mr angiography so this is a vrt and this is a myth or demonstrates a very good bird's eye view of the stenosis and brt gives us a three dimensional picture and you can turn it all around and look at the noses from all types of angles you want to see intraortel angiography is still the code standard it's not the first line because it's more invasive but once you confirm your diagnosis by uh some form of anatomical or functional imaging then that's when intra arterial angiography comes into typically uh all angiographies use seldinger technique use of contrast media is either iodinated or carbon dioxide this has again changed the picture in a renal base function where even with significantly the range renal this function can go ahead with angiography again in patients who are sensitivity sensitive to iodinated contrast gadolinium plays an important role important thing to note about is if this is a two dimensional imaging modality so uh you need to take multiple projections so to be sure that um there is a stenosis if we if we don't see in one projection it doesn't it's not there so we need to take multiple projections to be sure that we are not missing onto something uh this is acr guidelines on on what to choose for you know vascular hypertension so basically they haven't divided into three three variants this particular variant is when there is a high suspicion so as we discussed when the suspicion is high then only we need to investigate further if the suspicion is low we need not investigate and if the suspicion is medium probably we should look at a more functional assessment of the renewable vascular hypertension so in high suspicion cases with the wrong normal renal function mr and ct angiography both have the same score so you can either choose between mr and cd the doppler is scored at six and nuclear medicine again so these are the first imaging modality which has to be chosen if we look at the variant two where there is stimulus and function definitely the mr and doctor scores much above the city and geography where the city and geography is much less indicated so typically what we do is uh [Music] use make use of more ultrasound and mr angiography where if the ultrasound is pretty sure of either stenosis or no renal artery stenosis then we stop with that and um if there is no renal artist gnosis we probably take adrenal vascular hypertension out of picture and then if there is a stenosis we go ahead and treat it the problem comes in when there is an adequate quality of the scan in in terms of not able to visualize the iota and the origin of the alien arteries that's when we should suggest towards moving on to a cross-sectional imaging with mr or ct and then which is considered as a black and white imaging value if there if there is a suspicion then we go ahead and treat it [Music] so what are the treatment options for uh real artist analysis one is medical uh second is um percutaneous translument renal angioplasty and third surgery so medical in terms of there was a lot of uh trials which came with uh renewable stenosis and intervention which proved that actually um a lot of screened renal artist noses were being treated by angioplasty which did not show any significant significant benefit to the patient protecting organs or controlling the hypertension that opens the debate for whether they should be managed medically and that's what the current recommendation is for angioplasty there are three strong indications which we spoke about previously one is the hypernation which is uncontrolled with three medications or more and a presence of renal dysfunction and third being flash pulmonary uh all the other variants are probably given a trial of medical management and then if it doesn't work then go for revascularization so what type of medical therapy we are looking at is is basically we have to indicate the um the effect of uh renin in terms of either we can use rename incubators or we can use ace inhibitors which inhibits the conversion of angiotensin one to two or you can block the angiotensin receptors so all these comes in the same group where we block this uh pathway of rendering angiotensin system then another as we said as we talked about there's a lot of fluid retention so diabetics have to be a part of a medical therapy where we increase sodium excretion by using diuretics and control hypertension as well as fluid balance then we also look at calcium channel blockers specifically this dihydropyridine class which can be used uh should be used as first line medical therapy one word of caution is rash inhibitors should not be used if there is a suspicion of violently doing large stenosis because they they produce rapid rise in renal function and they can actually produce a very low blood pressure they can actually crash the blood pressure so if there is a parallel stenosis and they they need to be they should not be used if there is a united unilateral stenosis and um you can have a good control over the blood volume that's when slowly this needs to be introduced so uh the what we do in angioplasty for atherosclerosis and fmd is slightly different in atherosclerosis we work on fracturing diarrhoma as in any other paper vascular disease or coronary artery disease which is a atherosclerotic nature we produce a controlled layer of the indium manda media here lies the word control where we are trying to achieve a control tear if it goes uncontrolled that's where the complication starts and then our dilatation of adventitia whereas in fmd we are working at fracturing of the bands or the webs which are formed if you remember the pathophysiology there is collagen deposition and in the in the layers of the artery so we are trying to fracture those bands uh in family so uh these are the three indications most uh that's what we will we have talked about this before then um in atherosclerosis the technical success is 80 percent we see this is much higher in in terms of fmdp benefit is 70 to 80 percent um reduction blood pressure especially unique distances so there are around 20 to 30 percent or almost one third of the patient who do not experience a blood pressure drop so that brings us to the previous argument of whether um is there any benefit of renal revascularization and that's where all the three modern indications for renal angioplasty have come into so um we today when we do this angioplasty we are not only looking at uh blood pressure control we are also looking at um saving the kidneys uh prevent any renal deterioration in further course of time or at least slow down that progression and the third is the endorphin damage or from the hypertension they're trying to protect the kidneys the heart uh the retina the vision and the breakage so in preparation what we do is typically uh both fmd and atherosclerotic group they are started on dual energy let's they have to be started on statins especially for atherosclerotic which stabilizes the block um then if there is a renal dysfunction we keep general protection hydration because these are already hyper volumic state so hydration is a tricky business in renovascular hypertension you can use soda by [Music] and then take up these patients so um this is one of the difficult cases we had today probably we would do it differently so this patient he was a 70 year old he was on three or four medications with hypertension not controlled he had no renal dysfunction at that point but uncontrolled hypertension was an indication and we can see here this was a very tight stenosis in the proximal one-third of the renal artery and the age group and presence of coronary artery disease indicates towards what we're dealing with as atherosclerotic moreover his uh elaiax and iota was extremely torturous you can make out from uh the way this caterpillar is sitting so um this was a difficult case it was tried elsewhere as well but it came to us and then we decided to use a triaxial technique what typically we do is use a short shape which remains in the but here what we did differently is use a longer sheet which goes all the way up toyota so it gives us some support for the guiding to sit against even then you can see the guiding is just floating there it's not not even close to the osteo uh that was this challenge and then we go ahead wire the artery dilate the relation so that we can take the stand again getting the stand there is a challenge because the guiding is not really at the osteum and a very big issue of stability of the guiding layer and somehow we managed to put the stand the stand should protrude a millimeter into the yoda and then luckily we could get a decent result uh probably today i i would do this case differently by going through the radial artery once we are through the radiant probably to make our life much more easier and today most of most people who are doing legal are slowly adapting towards radium use of radio to go ahead with these this is a transplant renal lateral stenosis which is not atherosclerotic you can see attachments it's there then once the genomes is confirmed go with balloon angioplasty with a stent then you can see very good perfusion and flow there so what are the complications which can come the complication rates are higher 10 to 13 compared to fmd group so that's again it brings us to the same argument whether um in atherosclerosis it should be done or not um the complications include thrombosis dissection or rupture we discuss we are trying to achieve a current rupture of the block if it goes uncontrolled it results in a dissection and rupture then embolization these um these block fragments can hybalize into the kidney producing renal dysfunction these are associated complications like mi or a stroke which may happen because of the inherent disease which is atherosclerotic itself then renal insufficiency because of multiple causes because they are already renal borderline patients elderly patients and then effect of embolism of these plaques pseudonyms and hematomas and access site how different uh is fmp ptca is basically it has a much more higher success rate ninety percent success rate clinical benefit is seventy to ninety percent and they do not recover so this is something which is worth breathing uh probably we should treat probably every fmd because they present younger they they have higher benefit and we see they have much less complications then they do not recur compared to atherosclerosis which uh fades takes away the benefit of angioplasty from these patients so this is the good group which which should be treated uh fmd is not a systemic disease so hence they do not tend to recover this is a typical how the fmp will look like is astronautic segments uh not involving the austrian and beyond so this was an angiogram you can see the stenosis you somehow get over wire across important thing is to try to get it through the lumen and then we do the standard get the balloon dilated and this is the end result uh we need not achieve a prediction perfect result because the the flow uh cylinder is actually um the square of the radius that means if we increase the radius by four times we are increasing the volume flow by 16 times so we need not uh try and get a picture perfectly resolved even a decent result is good enough and this is what we got and this lady was treated around five years back and uh she still follows up but she is completely normal her blood pressure is normal and she is off medication so fmd is one group where we will be able to take these patients off medication atherosclerotic on the other hand they may not be completely off medication we may be able to reduce the medications to some extent but they will never be of medications or very rarely the of medications but fmd there is a very good chance that they can be off medications uh complications in this area is very less compared to if you see the atherosclerotic group mainly focus on dissection thrombosis and regulatory rupture um if if any of these happens we are forced to stand otherwise fmd is a no stand disease with just angioplasty and leave it and get fantastic results um the indications for stem is one of these otherwise we don't stand so how do we follow up with them is we do blood pressure charting because we tend to see the blood pressure coming down especially in fmd group and the creating improving inspired receiving some contrast and then we try to taper off the antihypertensive dual antiplatelet should be given for at least six weeks that's when the block healing and the endothelialization of the strength happens after that in atherosclerotic group uh they will be on lifelong aspirin and statins after three months when the healing is completed and the lesions have stabilized and then we do follow up with the top three six and twelve months if they're doing good with the blood pressure surgery is in today's world is uh this although it's quite effective but it has a higher complication rate that's where the surgery is not their favorite treatment option in today's world basically what are the options is auto renal or other arterial bypasses giving lateral nephrectomy especially if the kidney is very small small and artectomy if the plaque is very vocal and then athletic to me i i just said it has high technical rate but uh and a very low reaction rate of less than 10 percent again the clinical benefit is 60 to 90 percent complication rates is 31 in today's world it is probably very high uh to have somebody you have a 31 complication rates with this kind of surgery and a pretty high mortality rate as well or three to twenty percent so um the complication rates and the mortality rates that's what puts surgery down and brings angioplasty as a frontline treatment for revascularization so uh basically how we go about is as i said in the beginning of my talk is unless we improve the blood pressure we do not know for sure that it is renal vascular hypertension so we basically we screen this test and then we do a biochemical and assessment with the doppler or mri geography then if they are they are a candidate for intervention they go for catheter and geography if it is atherosclerotic we do angioplasty plus denting if it is fibromuscular dysplasia we just do angioplasty we don't bring trouble and we need to salvage the vessel and if that leads to cure or improvement of blood pressure then we are sure that we are dealing with renal vascular hypertension if it does not then probably we are dealing with the primary hypertension with some renal vascular disease not adrenal vascular hypertension thank you it was a really wonderful talk and elaborating the geology path of physiology the various diagnostic modalities and the role of intervention for uh i think for the graduates in diagnostic and directional radiology it will be a very useful talk i am just checking on the comment box whether there is any doubts or any questions hi dr manish thank you good evening yeah this time yeah as dr suny moon said you touched almost all points in with regards to hypertension starting from anatomy pathology physiology and then imaging modalities and also treatment and for the students now for the residents always uh you one should when asked for the example one should write the treatment side also at least some aspects not because radiology is supposed to know the treatment once you know the treatment actually you can actually give some suggestions to the physician in what way actually the investigation is to be tailored so like that one is supposed to know also during first year exams no the treatment will be asked for each and everything so in exam also this is one of the as far as the renal muscular hypertension is concerned this is one of the favorite questions that can be asked in the exam as long question so both as far as the exams are concerned and also a practical side so because the as a radiologist you can do interventions uh and also a lot of investigations with regards to rhinos hypertension the photos one more thing you can add if you want like in the series of investigations now one thing what will be the finding in uh intravenous urogram so that if you want you can add like small sized smooth kidney so they can be asked i mean that can be rooted anyway well said um well prepared well said and also uh to the point and i am sure that this would be highly useful for the residents who have read the session thank you very much dr manish [Music] uh office banners uh when comedy madam couldn't join today uh whenever sir is here the image sensor and the resume server was there i thank all of them for uh uh continuing with those academic sessions meticulously and providing this platform uh thanks big steam actually it was a little confusing in the beginning to use my metrics but it was okay and this is the first time we are using both writing initially we had a session on uh netflix alone uh there was no technical glitches depend on snoopy and uh again i thank manish for such a wonderful and informative talk thank you


IRIA Kerala brings you an interesting session on diagnosing and managing renovascular hypertension. Dr. Manish will be talking about its presentation, workup, indications for intervention, and post-intervention management. Join us live for this amazing session on Interventional Radiology in Renovascular Hypertension.


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