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Right to left intrapulmonary shunt with portosystemic shunt|Portosystemic shunt|7|Male
Right to left intrapulmonary shunt with portosystemic shunt|Portosystemic shunt|7|Male
2016abernethyabnormalAtriumcannulatedchestcomplicationscongenitalconnectingdemonstratedemonstrateddevelopeddrainingechoencephalopathyFistulaflowhepaticintrahepaticleftlivermediatorsminimallynormalocclusionoxidepatientpatientspediatricpelvisperformedperipheralportalportosystemicpulmonarysheathshortnessshuntshuntingSIRsplenicstablesyndromesystemictoleratetransplantationtypeultrasoundunremarkablevascularvasoactiveveinveinsvenogramvenous
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
anticoagulantanticoagulationcatheterchapterclotcoumadindefensesdirectedheparininpatientintermediatelovenoxNonepatientpatientsplasminogenprocessriskrotationalstreptokinasesystemicsystemicallythrombectomythrombolysisthrombustpa
Chronic Thromboembolic Pulmonary Hypertension | Management of Patients with Acute & Chronic PE
Chronic Thromboembolic Pulmonary Hypertension | Management of Patients with Acute & Chronic PE
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Why is the Capnography Reading Abnormal- Physiology | Respiratory Compromise: Use of Capnography During Procedural Sedation
Why is the Capnography Reading Abnormal- Physiology | Respiratory Compromise: Use of Capnography During Procedural Sedation
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Pathophysiology | Pulmonary Emoblism Interactive Lecture
Pathophysiology | Pulmonary Emoblism Interactive Lecture
arteriesballoonbloodblowchaptercircuitcoronaryfibershypokinetichypotensionintramuralischemicleftmassivePathophysiologypressurepulmonaryresistancesystemicvasculatureventricleventricular
CTEPH Studies | Management of Patients with Acute & Chronic PE
CTEPH Studies | Management of Patients with Acute & Chronic PE
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Case- May Thurner Syndrome | Pelvic Congestion Syndrome
Case- May Thurner Syndrome | Pelvic Congestion Syndrome
arterycatheterizecausingchapterclassiccliniccommoncommon iliaccompressioncongestionendovascularevidenceextremitygonadalhugeiliaciliac veinimagingincompetenceincompetentMay Thurner Syndromeobstructionoccludedpelvicpressuresecondarystentsymptomstreatmentsvalvularvaricositiesvaricosityveinveinsvenavenous
TIPS: Techniques- Stent Grafts | TIPS & DIPS: State of the Art
TIPS: Techniques- Stent Grafts | TIPS & DIPS: State of the Art
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Treatment Options- Carotid Endarterectomy (CEA) | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- Carotid Endarterectomy (CEA) | Carotid Interventions: CAE, CAS, & TCAR
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Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
angiographyangioplastyarterybleedbloodcalcifiedcarotidchapterclaviclecommondebrisdevicedistalembolicembolizationexposurefemoralflowimageincisioninstitutionlabeledpatientprocedureprofileproximalreversalreversesheathstenosisstentstentingstepwisesurgicalsuturedsystemultimatelyveinvenousvessel
Ideal Stent Placement | TIPS & DIPS: State of the Art
Ideal Stent Placement | TIPS & DIPS: State of the Art
anastomosiscentimeterchaptercoveredcurveDialysisflowgraftgraftshemodynamichepatichepatic veinhyperplasiaintimalnarrowingniceoccludesocclusionportalshuntshuntssmoothstentstentsstraighttipsveinveinsvenousvibe
General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
acuityalertanticoagulantanticoagulationbiopsybleedingcardiacchapterchartdysfunctionhematologicalhistoryhypertensivelivermedicationsNonepatientpatientsplavixprocedureprovidersradiologistsriskstablestentthrombocytopenia
TIPS: Techniques- CO2 Venography | TIPS & DIPS: State of the Art
TIPS: Techniques- CO2 Venography | TIPS & DIPS: State of the Art
balloonboluscapsulecatheterchaptercirculationconnectioncontrastcorrelationdiedifferencedistalfattyhepatichepatic veinimageimaginginjectleaklearningocclusionportalrefluxsegmentsteptrappingveinveinsvenogramvisualizewedgewedged
PV Access | TIPS & DIPS: State of the Art
PV Access | TIPS & DIPS: State of the Art
accessaccessedangulationanterioranteriorlyballoonchaptercirrhosisglidehepatichepatic veinliverneedlepasspintoportalposteriorprolapsesagittalsheathshrinkagestenttractveinvenouswire
Indirect Angiography | Interventional Oncology
Indirect Angiography | Interventional Oncology
ablateablationablativeaneurysmangioangiographybeamBrachytherapycandidateschapterdefinitivelyembolizationentirehccindirectintentinterdisciplinaryischemiclesionographypatientportalresectionsbrtsurgicaltherapyvein
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
angiogramangioplastyarteryballoonballooningbandschaptercomplicationscontrastflowHorizonimageimagesluminalNoneocclusionocclusionspatientsproximallypulmonaryradiationrecanstenosisthrombustreatedultrasoundwebs
Endovascular AVF creation | Twitter Case Files SIR 2019
Endovascular AVF creation | Twitter Case Files SIR 2019
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Complications & Pitfalls | TIPS & DIPS: State of the Art
Complications & Pitfalls | TIPS & DIPS: State of the Art
accessarteryballoonbranchchapterclinicallydeepdefectgramhepaticimagesliverneedleocclusiveperfusionportaportalsegmentalsegmentsstentthrombosestipstracttypicalveinvenous
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
bleedingcatheterchaptermilligramNonepatientpatientsperiodriskslowersystemictargetedthrombolysistpaversus
Algorithm for Treatment | Pelvic Congestion Syndrome
Algorithm for Treatment | Pelvic Congestion Syndrome
balloonbloodcatheterizechaptercoilscontrastgonadalnesterocclusionpelvicrecurrencerefluxsclerosissymptomstreatttlevaricosevaricositiesveinveinsvenavenogramvenous
Treatment Case 2 | Pelvic Congestion Syndrome
Treatment Case 2 | Pelvic Congestion Syndrome
chapterembolizationgonadaliliacinternalocclusionvaricositiesveinveinsvenavenous
Pre-procedure Assessment | Procedural Sedation: An Education Review
Pre-procedure Assessment | Procedural Sedation: An Education Review
abnormalitiesadverseairwayanesthesiaanesthesiologistapneaauscultationcervicalchaptercomorbiditiescopddiseaseedemaejectionfractionhabitushemodynamicallylitersmedicationsneckneurologicNonepatientpatientsphysiologicproceduralpulmonaryrenalsedationsleepslidesspinestatus
Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
angiogramangiographyarterialarteriesarterycapillarycatheterchapterclassificationcurativediseasedistalflushlobesmanagementmedicationNonepatientpatientspressureproximalpulmonarysegmentalsheathstenosissurgeonsurgicalthrombustreatedtypevesselswebswedge
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
abnormalangioangioplastyarteryAsahiaspectBARDBoston Scientificcatheterchaptercommoncommon femoralcontralateralcritical limb ischemiacrossCROSSER CTO recanalization catheterCSICTO wiresdevicediseasedoppleressentiallyfemoralflowglidewiregramhawk oneHawkoneheeliliacimagingkneelateralleftluminalMedtronicmicromonophasicmultimultiphasicocclusionocclusionsoriginpatientsplaqueposteriorproximalpulserecanalizationrestoredtandemtibialtypicallyViance crossing catheterVictory™ Guidewirewaveformswirewireswoundwounds
UFE and Adenomyosis | Uterine Artery Embolization The Good, The Bad, The Ugly
UFE and Adenomyosis | Uterine Artery Embolization The Good, The Bad, The Ugly
accessadenomyosisarteryaxisbifurcationcardiaccathetercatheterschaptercharacteristiccomplicationsdiameterdimeembolizationfemoralfibroidfibroidshematomahydrophiliclabsNonepatientspracticeradialsheathulnaruterine
The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
adventitiaangiogramaortaarteryaspiratedbloodcatheterschapterclotdysfunctionFistulafrontalhemorrhagehypotensionhypoxiaintracraniallobelungPE in right main Pulmonary Arteryperfusionpertpigtailpressorspulmonarypulmonary arteryresectionselectivesheathspinsystolictachycardicthrombustpatranscranialtumorventricle
Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
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Registry and Data | Management of Patients with Acute & Chronic PE
Registry and Data | Management of Patients with Acute & Chronic PE
arterycathetercatheter directedchaptercomplicationsdirectedechoheparinimprovementintermediateinterventionalmassiveNonepatientpatientsperfectpressurepulmonarypulmonary arteryratioreductionregistryriskseattlestrainstudiesstudysystolicthrombolysistpaunfractionated
Stent Graft Deployment | TIPS & DIPS: State of the Art
Stent Graft Deployment | TIPS & DIPS: State of the Art
balloonballooningbarebasicallybifurcationcapturedchaptercirculationcorddeepdeployentryidealplasticportalportionpullsheathstentstentstipsveinveinsvenous
Ablative Radioembolization | Interventional Oncology
Ablative Radioembolization | Interventional Oncology
adjacentadministerarterialbladecancerchaptercompletedosedosesentiregreyinvadinglesionliverlobelobectomynecrosispathologicpatientportalremnantresectionresponsesegmentsurgeontinytreattumorvein
The Disease Process | TIPS & DIPS: State of the Art
The Disease Process | TIPS & DIPS: State of the Art
ascitesbasicallybloodchaptercirculationcirrhosisconnectionsdipsesophagealextrahepaticgastricHypertensionlivermesenteryorganperineumpleuralportalportosystemicpressurerenalshuntshuntsslidesspleenstepsurgicaltampathoraxtipstransplanttransplantationvalvesvaricesvein
Transcript

Okay. So this is a generally healthy 7-year old male with no significant

past medical/surgical history and with normal birth and development. He had a very vague history of "liver shunt" that was never followed up. And he was noted to be very hypoxic, having shortness of breath

while playing Tee Ball. His physical examination was unremarkable and he demonstrated normal growth and development. The concerns were seasonal and there was exercise induced asthma. He was placed on several medications. But he failed to show any improvement.

On follow-up appointment, the patient was noted to be very hypoxic, starting at 87% standing and 83% with minimal exhaustion. Chest 2 view was done at an outside institution so the image is not available unfortunately, but it demonstrated increased peripheral

interstitial markings. So with continued shortness of breath and no response to medication, high-resolution CT was recommended. And at the same time, ECHO was performed to rule out a pulmonary right-to-left

shunt. CT of the chest without contrast was negative and the ECHO demonstrated in intact arterial and ventricular septum. However, there was a positive bubble test were demonstrated a early filling of the left atrium only after 3 cardiac cycles diagnostic of right-to-left intrapulmonary shunt. With this positive ECHO result

and a vague history of a liver shunt, there was increasing concern for portopulmonary syndrome. So a CT of the chest, abdomen, and pelvis was performed. So the CT of the chest did not demonstrate any pulmonary AVM's, however it demonstrated an enlarged main pulmonary trunk as you

can see. The arteriole phase of the CTA of the athena pelvis did not demonstrate an early venous filling of the portal vasculature which would suggest arteriovenous fistula. However on the portal phase, I want you guys to focus right here, following

the right atrium cordially, you can see a large vascular structure, coursing through the liver, and connecting to the portal system. [BLANK_AUDIO] And splitting up, right here. And now the coronal reformat gives you the same thing,

gonna focus right here. Here is a large vascular system, structure connecting the portal to the systemic. To summarize, there was a portal systemic shunt in the branch

of the left portal vein extending through the liver, connecting to the dilated vascular structure which was then emptying into the hepatic vein and the inferior vena cava. Hepatic veins were isodense to portal vein suggestive of shunting. And the liver and spleen were fortunately unremarkable

otherwise. To confront the CT findings, a limited abdominal ultrasound was performed. And this demonstrated a largely focally ectatic left portal vein, which had internal turbulent venous flow and connecting to the left hepatic vein and finally draining into the IVC. His labs were fortunately unremarkable and his ammonia was within

normal limits for the patients weight and age. So the diagnosis was a congenital intrahepatic portosystemic shunt. So this is an abnormal intrahepatic connection between the branches of the portal vein and the hepatic vein. So normally, people would develop a sinusoids. The vitalline veins would develop a sinusoids. And as you see

right here, these would be the vitelline veins and these would develop sinusiods in a normal liver. And connected a sinus venosus. But in our patient, there was a lack of sinusoid formation resulting in a in a direct shunt.

So there're different types of congenital Portosystemic Shunt. Type 1 is the No Intrapathic portal flow which should be (congenital absence of portal vein or type I Abernethy malformation). So you can see the Splenic and the SMV directly draining into the IVC in type I A. Type I B, you will see the Splenic and the SMV coming together endangering into the IVC. Type II is a partial shunt with preserved hepatic portal flow (t

ype II Abernethy malformation). So you can see the splenic and SMV coming together forming the portal vein and going in through the liver and there is an extra hepatic shunt from the portal to the IVC as you see right there. And our patient was presenting with 2A which is a Fistula arising from the left portal vein and it can also be a right portal vein going to the systemic.

The other two are more rare. And IIb is a Fistula from the main portal vein. IIc is a mesenteric, gastric, splenic vein fistula to the systemic circulation. Portopulmonary syndrome at the exact mechanism is not really well known but its thought to be a combination of upregulation of nitric oxide and inability for the liver to metabolize vasoactive mediators.

So this is the normal alveolus. This is the abnormal alveolus receiving all the vasoactive mediators and nitric oxide. This will result in V/Q mismatch, diffusion limitation and shunting through the AVMs. These patients will often times present with cyanosis,

clubbing, polycythemia and impaired exercise, tolerance from hypoxemia. And serious complications include systemic embolizations, pulmonary hemorrhage or cerebral abscesses. So this was an unusual case of congenital intrahepatic portosystemic shunt where the patient presented with isolated

portopulmonary syndrome without clinical evidence of hepatic encephalopathy which is most commonly the presenting symptom. Although CTA of the chest did not a demonstrate a pulmonary AVM, ECHO findings were diagnostic. And the AVM's were most likely due to the shunt which was shunting the vasoactive mediators and the nitric oxide to the lungs directly. Despite the presence of a large shunt, the patients hepatic function

determined by LFs were well preserved. So the patient was soon admitted under transplant and I was consulted for possible minimally evasive intervention. So we could just be cowboys and just go and close this thing but there are a lot of questions that were not answered yet.

So we had to know how developed are the hepatic veins? How developed is the peripheral portal system in the rest of the liver? What is the pre-procedural direction and quantity of flow to the right liver lobe? Will be the change that portal pressures following occlusion and

will the patient be able to tolerate this. So we decided to obtain answers to this questions by performing a temporary occlusion of this shunt intraoperatively with a balloon. The back up plan was to consider liver transplantation if the patient was unable to tolerate it and if the hepatic veins and the intrahepatic portal system was poorly developed.

So this is the initial hepatic venogram, and in this pediatric patient, we chose the left IJ for stable intravascular sheath position in a 9-fr Pinnacle was placed. The right and middle hepatic veins were cannulated and a hepatic venogram was performed.

A free and wedge hepatic venogram demonstrated well developed right and middle hepatic veins. The shunt was then cannulated through the left hepatic vein with a coaxial 7-Fr, double angle 45 cm sheath for stability. Through this shunt, a 5-Fr

glide Cobra catheter was finally advanced into the main portal vein and a direct portovenogram was performed. And this demonstrated a small but patent right branch of the portal vein with hepatopetal flow and well developed intrahepatic portal branches were documented. We then performed occlusion

portogram by inflating a properly sized balloon in the shunt for 20 minutes. So, before the occlusion, we saw the gradient was 1 and after the occlusion for 20 minutes the gradient rose to 9. So the change was only eight, so decided to proceed with the shunt

occlusion. The shunt was closed with two 2nd generation 16 millimeter Amplatzer plugs, and the final venogram demonstrated a total occlusion of the shunt. He was admitted to PICU for post op monitoring. He was initially

on 2LNC but was weaned pretty quickly and saturating at 93 with ambulation without any problem. He was then downgraded to floor pretty quickly. And repeat ultrasound demonstrated complete occlusion of the previously demonstrated shunt with no residual shunting.

He had stable HGB and LFTs and he was discharged on post procedure day two in a stable condition. In the most recent follow up, we performed an ultrasound. There's no left portal veins in the region of the left portal vein. So, this is what we saw before,

left portal vein left hepatic vein, IVC, and now we see the implantser. Oh sorry. And in the critical note, he's doing well, he's in the 3rd grade now and he's enjoying playing baseball, and he has no shortness of breathe and he's thriving. And his lungs remain stable and notably his pneumonial level has actually gone down.

[BLANK_AUDIO] So to summarize, congenital intrahepatic portosystemic shunt is a very very congenital anomaly that can result in hepatic encephalopathy from increased ammenomia. Other complications include heart failure and fatty degeneration of the liver from luck of nutrition to the hepatic cells due to

reduced inflow. Portopulmonary syndrome is an uncommon complication resulting from congenital intrahepatic portosystemic shunt, is believed to be due to increased NO and vasoactive medators being shunt to the lungs. Congenital intrahepatic portosystemic shunt, can be differentiated from Abernethy malformation by the presence of an intrahepatic shunt versus an extrahepatic

from the portosystem to the systemic circulation. Our patient presented with a clinically symptomatic portopulmonary syndrome alone. And he had no signs of liver dysfunction and demonstrated sufficient blood supply to the liver parenchyma to proceed with the occlusion. And patient demonstrated almost immediate improvement in symptoms

and continues to be asymptomatic. Orthotopic liver transplantation may not be necessary to correct portopulmonary syndrome. And early occlusion of the shunt can serve as a minimally invasive option from IRs, for pediatric

patients who demonstrate noncirrhotic intrahepatic vascular abnormalities with early reversible pulmonary vasodilatation. Thank you for your

PE the first one of course is

anticoagulation so heparin and bridging the patient to coumadin or now aid a direct oral anticoagulant is really the mainstay of treatment most patients again 55 percent of patients with PE have low risk PE all of those patients

should be on according to the chest guidelines three months of anticoagulation so they're gonna get heparin as an inpatient if they even need it and they're gonna get sent home on lovenox bridge to coumadin or they're

gonna get the one of the new drugs like Xarelto or Eliquis but here's all the other things that we do so these patients that are in the intermediate high risk so I'm gonna try to keep saying those terms to try to kind of put

that in everyone's brain because I think the massive and sub massive PE is what everyone used to talk about but we want to keep up with our colleagues in cardiology who are using the correct terminology we're gonna say high risk

and an intermediate but in those patients - intermediate high risk or Matt or the high risk PE patients we're gonna be treating them with systemic thrombolysis catheter directed thrombolysis ultrasound assisted

thrombolysis and maybe some real lytic and elected me or thrombectomy there's other techniques that we can use for one-time removal of clot like rotational and electa me suction thrombus fragmentation and then of course

surgical mblaq t'me so when anticoagulation is not enough so I like to show this slide because it shows the difference between anticoagulation and thrombolysis they are very different and sometimes I think everybody in this room

understands the difference but I think our referring providers don't and so when we when we get consulted and we recommend anticoagulation they're like yeah TPA well that's not the right thing so anticoagulation stops the clotting

process so when you start a patient on a heparin drip they should theoretically no longer before new thrombus on that thrombus so when you have thrombus in a vessel you get a cannon you get a snowball effect more

and more thrombus is gonna want to form heparin stops that TPA however for thrombolysis actually reverses the clouding process so that tissue plasminogen activator or streptokinase or uro kindness will actually dissolve

clot so there you're stopping new clot forming versus actually dissolving clot anticoagulation allows for natural thrombolysis so your body has its own TPA and so when you put a patient on heparin you're allowing your natural

body defenses to work you're giving it more time TPA accelerates that process so you give TPA either systemically or through a catheter you're really speeding up that process anticoagulation on its own has a

lower bleeding risk you're putting a patient on heparin or Combe it in it's it is less but it is still real thrombolysis however is a very very high bleeding risk patients when I when I consult a patient for thrombolysis I

tell them that we are about to do give them the absolute strongest blood clot thinning agent or an reversal agent which is the TPA and we're gonna just run it through your veins for hours and hours

um and that sort of gives them an idea of what we're doing anticoagulation in and of itself is really not invasive you just give it through an IV or even a pill thrombolysis however is given definitely through an IV through

systemic means and a large volume there thereafter or catheter directed so again

after after years in these patients so I'm gonna kind of change gears here from acute PE to chronic PE and this is actually something that I'm very interested in is actually what happens

in these patients so chronic thromboembolic pulmonary hypertension or CTF which I'm going to say for the rest of the talk because that's a lot easier is really what happens in some patients whose pee never really goes away another

term you may hear is post PE syndrome but that's the same thing essentially so post PE syndrome or CTF occurs in about 3 to 5 percent of patients with acute PE and it's a it's higher in patients with recurrent PE so if patients have some

sort of blood clotting disorder where they keep getting a clot they may get CTF we have no idea as to who is gonna be the patient who's gonna get it so we don't know right now who the patients

are and that's sort of a focus in the cardiology and IR and hematology and sort of worlds to figure out who's gonna get post PE syndrome it's one of the leading causes of pulmonary hypertension and it's really under diagnosed because

patients just don't know so patient has a PE they go through the system they go they get discharged they're alive and well and then they just never recover they're still fatigued they're just really never able to get back to their

life they think it's you know that they have this chronic bronchitis again or common or frequent pneumonia it turns out that they have post PE syndrome or CTF and it's never been diagnosed so CTF has this very complex algorithm and it

involves a lot of different teams but a patient who has PE and clinical suspicion what actually has this walk-test so they walk down a hall which is a known length and it sees how far they can get on a sir

of time and that's the six-minute walk this these patients if they have a positive six-minute walk test which requires no intervention really they go on and have a VQ scan or VQ scan with some other sort of imaging if they's

find if these tests come back with findings suggestive of CTF then they get a pulmonary angiogram in a right heart catheterization for every patient because then you have to make a decision as to what you're gonna do

surgical treatment medical treatment or now an interventional treatment so this is a VQ scan I'm a board-certified radiologist and I am NOT an expert at reading these anymore but what you what you want to look at is that if there are

areas that look abnormal that don't match so in a VQ report you're looking for areas of mismatch which means that ventilate that the that ventilation is happening but there's no perfusion so we're looking for VQ deficiencies this

has a very high sensitivity for PE but not a good specificity it's a lot less radiation exposure than CT but as we all know in a patient who has a VQ scan for a qpe we're really not sure if it's real or not but in chronic PE a VQ is a gold

standard actually at least in the initial diagnosis after that you get a

is my cap nog Rafi reading actually I want to back up a little bit here do I want to back up no I don't I don't want to back up so um let's look at the first

question why is my cap nog Rafi reading abnormal so let's first talk about physiology so a question I get a lot of times is sue the patient comes down for a procedure to the floor I put a sample line set on

them I plug them into the monitor and I'm getting a value of 28 29 30 why are my values abnormal anyone ever see this is anyone still awake okay so there's a few reasons the patients that we are dealing with generally aren't

healthy right I mean sometimes I go to work and I get chest pain I'm like can I just be in an ambulatory gallbladder room today because the patients that are coming from down to IR are sick what their physiology is sick too so we have

Krebs cycle we take oxygen in right it circulates to ourselves it participates in aerobic metabolism we get the byproducts of heat and energy and we get carbon dioxide as a by-product carbon dioxide really diffuse about diffuses

into our blood travels to the lungs and gets exhaled where we measure it so let's talk metabolism really quickly so if someone has a fever if their metabolism is ramped up you think they're gonna be producing more carbon

dioxide yes let's say they're a little hypothermic maybe they're gonna be producing a little bit less you see it for sure in the car patients who are cardiac arrest that are cool to status post cardiac

arrest right those values go way down normal physiology normal physiologic response somebody comes down and they're mildly hypoxic they've got pneumonia or some sort of VQ mismatch and they're hyperventilating to UM debeso

compensate for their hypoxia do you think there's co2 values gonna be a little lower at baseline yeah so these are the patients that you're seeing right so we have reasons that patients could be hyper cap neck like metabolism

right somebody who's in pain someone who's developing a fever early stages of sepsis they may actually have a little bit of a higher value somebody who's sedated or hypoventilating may have a higher value and when we talk about

perfusion is the blood moving round and round is that circulating co2 coming back to the core do we have increased cardiac output with continuous constant ventilation and certainly we can we're gonna look at equipment issues next and

the same goes true more probably in your cases of the hypocapnia patient so someone who is not fully exhaling someone who's in bronchospasm or a COPD or you're not getting that nice square waveform you're only getting some of the

mixed gas ventilation that they're exhaling rights and the conducting airway is mixing with the alveolar gases someone's a little hypothermic someone who's been NPO for 24 hours right it's the opposite of carb-loading right so

you kind of throw them into a little bit of like acidosis you know they're kind of not burning carbs for fuel are they gonna be producing as much carbon dioxide not so much right so when you're coming so when

patients come down to you and you put them on the monitor consider these things so ventilation perfusion gradients so we have what we call our VQ matches and our body is designed beautifully right so when everything is

working great it works great so the way we ventilate all of our lungs owns is very closely matched to the perfusion of all of our lungs ohms so by me standing up here I'd like to think I'm pretty healthy if you did a blood gas and you

put me on one of those filter line sets right now you would hopefully see a gradient that's very small the normal gradient between a PA co2 on a blood gas so the level of carbon dioxide on a blood gas in the arterial blood and what

you see when I fully exhale into the monitor should be between two and five millimeters so these are your patients come down healthy physiology you put them on and you get a value of like 32 then you

could assume that if they were healthy two to five millimeters okay their blood gas would probably like 35 for POC to everyone follow now does any of our patients read the physiology tech books textbooks no they typically don't so

when you have patients come down they may have shunt right so they may have we have our little airway here a and B you're out like picture them as lungs and lung a is blocked so we have no ventilation going to lung a but blood is

still chugging through right so blood is still going through the pulmonary circuit so we're gonna have Patapsco a dia depending on the size of the shunt is this the end of the world are we gonna cancel the case no but just being

aware of the patient's physiology would explain to you why I put this patient on this and I'm getting a value of 30 you follow and it's not the end of the world you document 30 and you monitor for trends as you're going along with your

sedation same thing goes through with dead space dead spaces were ventilating but we have an area of the lung that is not being perfused pulmonary emboli other circulations some medications hypovolemia shocky patients same thing

the VQ mismatch not the end of the world it's part of the patient's physiology maybe part of the reason why they're down there just being aware of these things though so the technology works right our equipment works if just amazed

it's picking up something that we don't connect all the dots on physiologically that sometimes confuses us a little bit so I hope that clears up part of it so when we're monitoring capnography certainly ventilation is what we think

of first and it's important co2 being expired by the lungs that's what we're looking for but if we back up and look at the physiology of carbon dioxide production in the body we are also inferring that

it's being metabolized and being created from Krebs cycle and aerobic metabolism and that we have perfusion occurring okay I'm sure if some of us have seen in our you know nursing careers patients who are kind of peri-arrest and

the capnography kind of drops off it's like a poor man's swan you're watching cardiac output drop in real time because carbon carbon dioxide is not being delivered to the lungs so when we're looking at our patients when

they first come down we first want to establish a baseline value we want to put on a monitor have a patient take some nice deep breaths full ventilations not just one but a few you want to you know have them take a few and look at

their other vital signs their mental baseline status and we're gonna look for trends in their carbon dioxide value so if someone starts off at twenty nine I don't care that they're not 35 to 45 which is textbook normal this person may

not have the stimulus to breathe if I let too much co2 accumulate so we're really looking for the trends okay now somebody will say well how much of you know how much should we look for 10 to 20 percent change from your baseline is

somewhere where you want to start paying attention to what's going on okay maybe like titrating your sedation or just being a little bit more cautious with how much more sedation but again it's more important to look at the trend

value behavior of your carbon dioxide than it is the absolute numbers themselves so first you having a problem let's consider the patient's physiology

okay pathophysiology right ventricular the right ventricle is everything when it comes to the pathophysiology of this disease I'm gonna lead you through this because I think it's interesting and important I'm gonna go to this side this

time be fair to both sides of the room so when you have a PE that increases your pulmonary vascular resistance normally the pulmonary vasculature is a very low resistance circuit but when you start putting clots in it it's restive

Gong its its resistance goes up it's kind of analogous to the left an electrical circuit what does that do to the right ventricle well it increases the after load on that right ventricle so what that does is it causes the right

ventricle to blow up like a balloon now by Laplace's law if you take a balloon and you blow it up the intramural pressure is higher in the balloon so if you can imagine that thin walled balloon if you took the pressure at each point

inside of the balloon because it still got a finite thickness the pressure is higher than if it's decompressed now the problem with that is that how does the right ventricle get blood it gets blood from the coronary arteries but if the

pressure inside the ventricle is higher than the pressure differential is less and what what what is Flo rely upon it relies upon a difference in pressure from point A to point B so if that starts to equalize your blood flow to

the right ventricle decreases okay that's why the right ventricle gets ischemic now when the right ventricle becomes ischemic it can't squeeze as hard so it gets hypokinetic when it dilates it also does

not seem to squeeze out as well because the muscle fibers aren't overlapping as well okay so both of those things lead to both so that the right ventricle is now not squeezing is hard and it's not getting blood forward to the left

ventricle so that results in LV preload reduction though LV is not seeing as much blood on top of that when the right ventricle dilates it starts impinging on the left ventricle so now the left ventricular cavity is smaller and it can

accept less blood your output is only as good as your input okay so that's where you start developing systemic hypotension because your left ventricle can't pump out as much blood what happens when your left ventricle can't

pump out as much blood you don't get as much blood into your coronary arteries you don't get as much blood into your coronary arteries you're not getting as much blood into your right ventricle this is the vicious cycle that leads to

right ventricular failure and the progressive death that you see with massive PE now if you were to draw a line like that everything above the line is sub massive PE everything below the line is massive PE okay this is a big

experiment I did we were trying to create sub massive PE we created a massive PE this used to be mostly the L the left-sided chambers and all of a sudden became the right-sided chambers to me this drove home how much the right

side can blow out and dilate that's the only point of this picture I hope I didn't cross you out okay so let's talk

that was one example so these are there have a lot of potential complications reperfusion pulmonary edema is a very very big potential complication so you could get through the case patient does

great you open up multiple pulmonary arteries and then they start coughing up blood and then they end up started drowning in their own blood and the ICU so we do not want to push that and the initial papers that you can see down

below on that table they had a very high almost 10% in some cases pulmonary edema requiring treatment requiring patients being put on CPAP or being intubated and that is because they treated too much at one time

and so now as this when this first started in the early 2000s the operators were treating multiple segments at multiple times at one time and they were using large balloons and we figured out that that was what was killing patients

and so we changed our treatment so this is the first study that was ever performed for this it was performed by dr. Feinstein I believe this was published in circulation it was done in Harvard at MGH they had 18 patients with

36 month follow-up they all improved in their ability to walk as well as their lifestyle but many of them 11 out of 18 patients had reperfusion injury so this was the first paper and at that time it became the last paper because so many

patients did poorly but here's what they're sort of what they did and the ones that did okay they you could see that they had an improvement in the New York Heart Association classification again that just means they can walk

further they're not less short of breath and that they could walk further in 6 minutes which is again our sort of first test outcomes over time whence this has become increased so you can see that study was in 2001 and then

it kind of went away for a long time and it came back in 2012 in Japan where the most operators are there they've treated up to 255 procedures now since this slide was made we're up to a thousand in Japan and those patients are doing very

well but you'll notice that they have multiple procedures so again you don't try to one-and-done these patients they come back four to six times we've treated a couple patients where I work and we've treated that was patients four

times already and so they do much better but it's a slow slow and steady treatment so I want to wrap up with saying that the IR team is very critical to patients who are getting treated for PE we're involved in the diagnosis as

the radiology team acute and chronic PE it's very important to know as I've shown you in some of the examples and some of the images which when it's acute and versus chronic doing thrombolysis on a patient with chronic PE is useless all

you're doing is putting them at a risk you're not going to be able to break up that clot it's very important to have inter and multidisciplinary approach to patient care so interdisciplinary meaning everybody in this room nurses

technologists and physicians working together to take care of that patient that's on your table right now and multi-disciplinary because you have to work with cardiology vascular medicine the ICU teams and the

referring providers whether it's neurosurgery vascular surgery whomever it is who's Evers patient gets a PE you have to work together and it's very important again to have collaborative care in these patients if we're doing a

procedure and somebody notices that the patient is desaturating that's very very important when you're working in the pulmonary arteries if somebody notices that the patient's groin is bleeding you have to speak up so it's very important

that everybody is working together which is really what we need to do for these patients so there's my references and there's my kid so thank you guys very much hopefully this was helpful I'd be

now other causes this is a little bit different different scenario here but it's not always just as simple as all

there's leaky valves in the gonadal vein that are causing these symptoms this is 38 year old Lafleur extremity swelling presented to our vein clinic has evolved our varicosities once you start to discuss other symptoms she does have

pelvic pain happiness so we're concerned about about pelvic congestion and I'll mention here that if I hear someone with exactly the classic symptoms I won't necessarily get a CT scan or an MRI because again that'll give me secondary

evidence and it won't tell me whether the veins are actually incompetent or not and so you know I have a discussion with the patient and if they are deathly afraid of having a procedure and don't want to have a catheter that goes

through the heart to evaluate veins then we get cross-sectional imaging and we'll look for secondary evidence if we have the secondary evidence then sometimes those patients feel more comfortable going through a procedure some patients

on the other hand will say well if it's not really gonna tell me whether the veins incompetent or not why don't we just do the vena Graham and we'll get the the definite answer whether there's incompetence or not and you'll be able

to treat it at the same time so in this case we did get imaging she wanted to take a look and it was you know shame on me because it's it's a good thing we did because this is not the typical case for pelvic venous congestion what we found

is evidence of mather nur and so mather nur is compression of the left common iliac vein by the right common iliac artery and what that can do is cause back up of pressure you'll see her huge verax here and here for you guys

huge verax in that same spot and so this lady has symptoms of pelvic venous congestion but it's not because of valvular incompetence it's because of venous outflow obstruction so Mather 'nor like I mentioned is compression of

that left common iliac vein from the right common iliac artery as shown here and if you remember on the cartoon slide for pelvic congestion I'm showing a dilated gonna delve a non the left here but in this case we have obstruction of

the common iliac vein that's causing back up of pressure the blood wants to sort of decompress itself or flow elsewhere and so it backed up into the internal iliac veins and are causing her symptoms along with her of all of our

varicosities and just a slide describing everything i just said so i don't think we have to reiterate that the treatments could you go back one on that I think I did skip over that treatments from a thern er really are also endovascular

it's really basically treating that that compression portion and decompressing the the pelvic system and so here's our vena Graham you can see that huge verax down at the bottom and an occluded iliac vein so classic Mather nur but causing

that pelvic varicosity and the pelvic congestion see huge pelvic laterals in pelvic varicosities once we were able to catheterize through and stent you see no more varicosity because it doesn't have to flow that way it flows through the

way that that it was intended through the iliac vein once it's open she came back to clinic a week later significant improvement in symptoms did not treat any of the gonadal veins this was just a venous obstruction causing the increased

pressure and symptoms of pelvic vein congestion how good how good are we at

craft is basically the only FDA approved stain crafts and I'll show you a

different way of doing it as well besides the Viator especially in countries where the Viator does not does not exist okay the Viator stand sits in the liver just like just like in my hand here the bare

portion is on the portal venous circulation the covered portion is basically on the hepatic vein part of the circulation okay the bare portion is chain-linked and is very flexible that's why kind of cut can crimp like that okay

they're both self expanding the bare portion is self expanding held by the sheath only the covered portion is held by a court okay so they're both self expanding but they're constraints by two different two different two different

methods one's a sheath constraint and one is a is a cord constraint okay these are the measurements the bare portion theoretically allows portal flow to pass if you're in a branch so it doesn't cost from boses of the portal vein branch in

the covered portion is important to cover the parental tract the youth that you've created in the past you had a lot of billary leaks into the tips if it's a bear stance bile is from by genic so it causes thromboses bile also instigates a

lot of reactionary tissue such as pseudo intimal hyperplasia that actually causes the narrowings of the of these tips if you causing bear stance the coverage stance prevents the bile leaks from actually leaking into into the shunt

itself okay and that's why it has a higher patency rate okay ideally this is how it's it's a portal vein and hepatic vein you'll hear people say proximal and distal you'll he'll hear radiologists especially diagnostic

radiologist referring to proximal and distal proximal and distal some people refer to the portal venous and is proximal some people refer to the paddock venous and is proximal and vice versa okay and it

gets confusing nobody knows well what's proximal okay the people that say portal venous and is proximal there they're talking about its proximal to flow so it's basically the first thing that flow hits people that

call the paddock venous and proximal they're talking relatives of the body more central is proximal more peripheral is distal okay so they're using these the same terminology is very confusing so the best thing to use and I we tell

that to radiologists who tell that to IRS is to talk a portal venous and hepatic venous end you don't talk proximal distal everybody knows where the portal venous end is and where everybody knows where the peregrinus end

is and there's no confusion strictly speaking which is the correct one which is proximal for us as IRS tax nurses proximal is always to flow proximal is always anticipate to flow so the correct thing is actually proximal

is the portal venous ends remember P proximal P portal okay proximal is where the expected flow is coming in that's actually the correct one but just to leave e8 the confusion portal venous and hepatic venous end okay there's a new

stents which is the controlled expansion stents it's in my opinion it feels exactly like the old stance the only difference between it is that it's constrained still has the same twenty to twenty millimeter or two centimeter bare

portion chain-linked it still has that four to eight centimeter covered portion but it's constrained in the middle okay and has the same gold ring to actually market the to the to a bare portion and the cover portion self expanding portion

and is constrained down to eight millimeters you can dilate it to eight and nine and ten initially there was a constant there was a misconception that it was like a string like a purse string that you break and jumps from eight

and no this is actually truly a controlled where if you put a nine-millimeter balloon it will dilate to nine only eight balloon little dialect to eight only the only the only key thing is that the atmospheres has to

be ten millimeters at least okay so it has to be a high pressure balloon has to be at least 10 min 10 10 atmospheres okay so when you're passing that that balloon over make sure that it's that that it that at least it's burst is 10

millimeters or or EXA or more on a 10 mil on on 10 atmospheres okay next thing is when you're making a needle pass you got your target now with a co2 you got the portal vein you've got your stank craft and you know how it works okay how

do you make your needle pass okay and how do you know if your needle has hit the portal vein or not there are two schools to do this okay one school is to make a needle pass and aspirate as you pull back and when you get blood back

you basically inject contrast okay before you do all that when you make your needle pass you push saline and especially if you do if you're using a large system so there are several kits out there there is the cook kits that's

a color pinto needle that's a large gauge 14 gauge needle there is the new gore kits which is also 14 gauge needle it's a big system these large systems you need to push out that poor plug that's kind of like a biopsy you have to

push it out with saline first and then as you pull back aspirate okay the other system is a ratio cheetah or a Rocha cheetah it's actually pronounced rasa schita and that's a very small system that there won't be a core that you have

to push out okay so anyway if you're using a large system like a coop into a needle which is the cook system or the gore system you push that plug out and then there are two schools school two aspirates you get blood back you inject

contrast if you're in the hepatic in in the portal vein you basically access it with a wire the other school is to do a ptc style you actually puff contrasts as you pull back you do not ask for H saline you actually puff

contrasts as you pull back okay the latter puffing contrasts as you pull back is the minority I would say less than two percent of operators are gonna puff okay ninety-eight percent of operators at

least are gonna actually aspirate and not puff okay I'm actually in the minority I'm in the 2% and there are advantages and disadvantages like I promised you two different ways and advantages and disadvantage to each to

each one the advantages of puffing contrasts even if you missed the portal vein after a while you actually get contrast around the portal vein and you actually have a visual of the portal vein that's the advantage so when you're

actually injecting contrast and you're missing it you get contrast around the portal vein it actually goes around the portal and you actually see the portal vein and it takes training sometimes this one's easy

okay I'll show you some more difficult ones but this is a beautiful pussy typical portal vein okay in addition to that oh go back in do you see that you see that hole in the middle there see that signal signal you watch that

because you're gonna see it again and again that's usually a posterior portal vein posterior right portal vein heading heading away from you okay that's usually a good target and I'll show you that again here's a little

little bit less obvious to the untrained eye but this is actually where the portal vein sits right there okay so sometimes it needs training right just actually see where the portal vein is and once you've stained the portal vein

then you have a real-time image of where the portal vein is you can actually go go after it and it reduces your needle passes disadvantages of using contrast and puffing away is that it creates a mess okay if you make multiple passes

you and you miss on the multiple passes then you start creating a mess and even with your DSA you can't even see the portal you can't see the portal vein because you've got this great mess another disadvantage of using contrast

is that you have to stomach what you're gonna see okay you make a needle pass and you don't inject contrast you have no proof of where you've been but if you're making a needle pass and you're

injecting contrast you and everybody else is gonna see where you've been that's usually not a good thing sometimes you will see bowel you see gold bladder you'll see arteries you'll see veins you'll see all sorts of stuff

that nobody wants to see and you don't want to document okay so that's another disadvantage so I recommend especially young physicians especially young physicians in places that are not used to this especially young physicians that

are new to hospitals and they're gonna they're gonna make multiple passes not to do this was they're gonna be very they'll be criticized a lot by their texts and by the institution by their colleagues as to what have you done you

know big mass artery you've hit artery but the guys and gals that are just aspirating and not injecting they're actually not documenting what they're going through but they're going through the same stuff okay

okay next up this I think this video yep

it's obviously either done with general

anesthesia or perhaps a regional block at our institution is generally done with general anesthesia we have a really combined vascular well developed combined vascular practice we work closely with our surgeons as well as

you know those who are involved in the vascular interventional space as far as the ir docs and and in this setting they would do generally general anesthetic and a longitudinal neck incision so you've got that and the need for that to

heal ultimately dissect out the internal carotid the external carotid common carotid and get vessel loops and good control over each of those and then once you have all of that you hyper NIH's the patient systemically not unlike what we

do in the angio suite and then they make a nice longer-term longitudinal incision on the carotid you spot scissors to cut those up and they actually find that plaque you can see that plaque that's shown there it's you know actually

pretty impressive if you've seen it and let's want to show an illustrative picture there ultimately that's open that's removed you don't get the entirety of the plaque inside the vessel but they get as much as they can and

then they kind of pull and yank and that's one of the pitfalls of this procedure I think ultimately is you don't get all of it you get a lot more than you realize is they're on on angiography but you don't get all of it

and whatever is left sometimes can be sometimes worse off and then ultimately you close the wound reverse the heparin and closed closed it overall and hope that they don't have an issue with wound healing don't have an issue with a

general anesthetic and don't have a stroke in the interim while they've clamped and controlled the vessel above and below so here's a case example from our institution in the past year this is a critical asymptomatic left internal

carotid artery stenosis pretty stenotic it almost looks like it's vocally occluded you can see that doesn't look very long it's in the proximal internal carotid artery you can see actually the proximal external carotid artery which

is that kind of fat vessel anteriorly also looks stenotic and so it's going to be addressed as well and this is how they treated it this is the exposure in this particular patient big incision extractors place and you can see vessel

loops up along the internal and external carotid arteries distally along some early branches of the external carotid artery off to the side and then down below in the common core artery and ultimately you get good vessel control

you clamp before you make the incision ultimately take out a plaque that looks like this look how extensive that plaque is compared to what you saw in the CT scan so it's not it's generally much more

impressive what's inside the vessel than what you appreciate on imaging but it's the focal stenosis that's the issue so ultimately if yet if the patient was a candidate stenting then you just place a stent

across that and he stabilized this plaque that's been removed and essentially plasti to that within the stent so it doesn't allow any thrombus to break off of this plaque and embolize up to the brain that's the issue of raw

it's the flow through there becomes much more turbulent as the narrowing occurs with this blockage and it's that turbulent flow that causes clot or even a small amount of clot to lodge up distally within the intrical in

terrestrial vasculature so that's the issue here at all if you don't take all that plaque out that's fine as long as you can improve the turbulent blood flow with this stent but this is not without risk so you take that plaque out which

looks pretty bad but there are some complications right so major minor stroke in death an asset which is a trial that's frequently quoted this is really this trial that was looking at medical therapy versus carotid surgery

five point eight percent of patients had some type of stroke major minor so that's not insignificant you get all that plaque out but if you know one in twenty you get a significant stroke then that's not so bad I'm not so good right

so but even if they don't get a stroke they might get a nerve palsy they might get a hematoma they may get a wound infection or even a cardiovascular event so nothing happens in the carotid but the heart has an issue because the

blockages that we have in the carotid are happening in the legs are happening in the coronary so those patients go through a stress event the general anesthetic the surgery incision whatever and then recovery from that I actually

put some stress on the whole body overall and they may get an mi so that's always an issue as well so can we do something less invasive this is actually a listing of the trials the talk is going to be available to you guys so I'm

not going to go through each of this but this is comparing medical therapy which I started with and surgery and comparing the two options per treatment and showing that in certain symptomatic patients if they have significant

stenosis which is deemed greater than 70% you may be better off treating them with surgery or stenting than with best medical therapy and as we've gotten better and better with being more aggressive with best medical therapy

this is moving a little bit but here's the criteria for treatment and so you have that available to you but really is

quick I did want to mention t-carr briefly and try to get you guys closer to back on time this is a hybrid procedure this is combining the surgical procedure we talked about first and carotid stenting it takes combined

carotid exposure at the base of the clavicle or just above the clavicle and reverses blood flow just like we talked about but tastes slightly different technique or approach to doing this and then you put the stent in from a drug

carotid access here's the components of the device right up by the neck there is where the incision is made just above the clavicle and you have this sheet that's about eight French in size that only goes in about us to 2 cm or 1 and a

half cm overall into the vessel and then that sheath is sutured to the the chest wall and then it's got a side arm that goes what's labeled number six here is this flow reversal urn enroute neuroprotection kit it reverses the

blood flow and then you get a femoral sheath in the vein right in the common femoral vein and you reverse the blood flow so this is a case a picture from our institution up on the right is the patient's neck and that's the carotid

exposure and the initial sheath is in place so the sidearm of that sheath is the enroute protection system which is going up up at the top of the image there we're gonna back bleed that let that sidearm of that sheath continue to

bleed up to the very top and then connect that to the common femoral venous sheet that we have in place there's a stepwise of that and then ultimately what we see at the end of the procedure is that filter inside that

little canister can be interrogated after and you can see the debris this is in the box D here on the bottom left the debris that we captured during the flow reversal and this is a what we call a passive and then active flow reversal

system so once the system is in place the direct exposure carotid sheath in place the flow controller and AV shunt in place you see the direction of blood flow so now all that blood flow in that common carotid artery is going reverse

direction and so when you place a sheath or wire and and ultimately through that sheath up by the carotid artery there's no risk for distal embolization because everything is flowing in Reverse here's a couple

case examples ferns from our institution this is a patient who had a symptomatic critical greater than 90% stenosis has tandems to nose he's so one proximal at the origin and one a little bit more distal we you can see the little

retractors down at the base of the image there in the sheath that's essentially the extent of the sheath from the bottom of that image into the vessel only about a cm or two post angioplasty instant patient tolerated that quite well here's

another 71 year-old asymptomatic patient greater than 90% stenosis pretty calcified lesion a little more extensive than maybe with the CT shows there's the angiography and then ultimately a post stent placement using the embolic

protection device and overall the trials have shown good good safety met profile overall compared to carotid surgery so it's a minimum minimal exposure not nearly as large the risk of stroke is less because you're not mucking around

up there you're using the best of a low profile system with flow reversal albeit with a mini surgical exposure overall we've actually have an abstract or post trip this year's meeting this is just a snapshot of that you can check it out

this is our one year experience we've had comparable low complication rates overall in our experience so in summary

stamp placement we talked a little bit about it I'm gonna talk to you a little

bit more about it and ideal stance is a straight stance that has a nice smooth curve with a portal vein and a nice smooth curve with a bad igneous end well you don't want is it is a tips that T's the sealing of the hepatic vein okay

that closes it okay and if there's a problem in the future it's very difficult to select okay or impossible to select okay you want it nice and smooth with a patek vein and IVC so you can actually get into it and it actually

has a nice hemodynamic outflow the same thing with the portal thing what you don't want is slamming at the floor of the portal vein and teeing that that floor where where it actually portly occludes your shunts okay or gives you a

hard time selecting the portal vein once you're in the tips in any future tips revisions okay other things you need it nice and straight so you do not want long curves new or torqued or kinks in your tips you

a nice aggressive decompressive tips that is nice and straight and opens up the tips shunt okay we talked a little bit you don't want it you don't want to tee the kind of the ceiling of the of the hepatic vein another problem that we

found out you want that tips stance to extend to the hepatic vein IVC Junction you do not want it to fall short of the paddock vein IVC Junction much okay much is usually a centimeter or centimeter and a half is it is acceptable

the problem with hepatic veins and this is the same pathology as the good old graft dialysis grafts what is the common sites of dialysis graft narrowing at the venous anastomosis why for this reason it's the same pathogenesis veins whether

it's in your arm for analysis whether it's in your liver or anywhere are designed for low flow low turbidity flow of the blood okay if you subject a vein of any type to high turbot high velocity flow it reacts by thickening its walls

it reacts by new intimal hyperplasia so if you put a big shunt which increases volume and increased flow turbidity in that area in that appear again the hepatic vein reacts by causing new into our plays you actually get a narrowing

of the Phatak vein right distal to the to the to the Patek venous end of the shunt so you need to take it all the way to the Big C to the IVC okay how much time do I have half an hour huh 17 minutes okay

Viator stents is one way let's say you don't have a variety or stent many countries you don't have a virus then what's an alternative do a barre covered stem combination you put a wall stent and then put a covered stance on the

inside okay so put a wall stent a good old-fashioned you know oldie but a goodie is is a 1094 okay you just put a ten nine four Wahl cent which is the go to walls down so I go to stand for tips before Viator

and then put a cover sentence inside whatever it is it's a could be a fluency it could be a could be a vibe on and and do that so that's another alternative for tips we talked about an ace tips as a central straight tips and it's not out

and fishing out in the periphery okay this is an occlusion with a wall stance this is why we use think this is why now we use stent grafts this is complete occlusion of the tips we're injecting contrast this is not the coral vein this

is actually the Billy retreat visit ptc okay that's a big Billy leaked into the into the tips okay and that's why we use covered stance I'm gonna move forward on this in early and early and experienced

guys do so when we do our screening phone calls and our pre screens before

the actual procedure there's a few factors that we look at for the patients with blood pressure the patient needs to be vitally stable before we do a procedure there may be a slightly increased risk of bleeding for kidney

biopsy if patients are hypertensive although it hasn't been noted to be statistically significant in the literature so we are always aware of patients being hypertensive we do want them to be taking their medications the

day of the procedure we also do a full medication reconciliation with the patient making sure that we're checking on any anti platelets anticoagulant medications and we have a list of our hold times that we use for a reference

we already discussed for those of you who are at this session this morning the issue of liver disease is it stable liver disease they may have adequate he stasis even though their INR is not within the normal range and so we

recommend a stable INR of less than 2.5 for those patients and in our practice a lot of the providers are going away from correcting the INR s for our patients we also screen for hematological disorders do they have some known condition that

makes them more likely to bleed or conversely more likely to clot and that may factor into whether or not anticoagulation can be held do they have a current diagnosis of cancer are they going to be getting one of those

angiogenesis inhibitors might they have thrombocytopenia and we just do a brief review of the patient's chart before we call them to kind of look for those diagnoses do they have a history of bleeding especially if they have no one

platelet dysfunction you know a known history of bleeding can be a reliable predictor of bleeding risk for some patients and do they have a cardiac or a neurological history as we learned this morning patients that have recently had

a cardiac stent placed we can't just say yeah stop your plavix hold off 5 days it'll be fine that could be a very serious risk to the patient did they recently have a stroke have they had a PE why are they on their anticoagulation

if they're on it so we really need to be aware of the whole patient and having that pre-screening phone call with them can allow our nurses to figure out a lot of these problems and then alert the radiologists and try and troubleshoot

before the patient walks in the door and says yeah I took my warfarin this morning I'm all ready for my liver biopsy the radiologists don't like that much in it you know it's really a bad thing for our high volume area to have

that happen and this is just another chart of our oh did I get mixed up here you guys are gonna fire me from running this clicker there we go so the whole times are again based on the half-life and the mechanism of action and this is

pretty similar to what you saw in the the presentation earlier today and specifically that imbruvica that's something that we alert the radiologists who they have a discussion with the patient decide is this something that we

want to continue with and I will say that in our practice with the volume and the the level of acuity of our patients I think that a lot of our providers are fairly comfortable with a certain level of risk because that's just who our

patient population is you know we have a very large hospital two large hospitals and very sick patients so that's something that we you know some of them are more comfortable than others but it's a risk-benefit thing that they have

to decide on themselves with the patient obviously all right so here are our

technically step by step of how tips are done okay and and the ideal tips with

every step of this procedure I'm gonna show you two ways of doing it okay and the advantages and disadvantages of the two ways in every step okay so first of all the primary thing is to get into the portal vein and how do you visualize the

portal vein okay so one way is to do co2 Vinogradova nog Rafi to hit the portal vein me with experience no I don't need co2 venography to hit the portal vein but I still do it in an in a teaching institution because I have texture that

are learning nurses they're learning and physicians are learning so I actually do the imaging for them so they actually can get the general idea of what we're doing this is our target this is where we're coming off and that's it but in an

experience hands is it necessary absolutely not okay so co2 photography very helpful for in teaching and teaching institutions so everybody and the whole team can actually know exactly what our target is so not essential like

like we discuss and there are two methods of doing this and in a funny way I'm gonna show you that's actually the same method but one is a micro of the other one okay so two ways one way is then wedge a catheter that's the old way

kind of more traditional way than let's not call it always more traditional way of doing a co2 port and the other one is using a balloon of balloon occlusion castra and this is wedging it with a four French five French catheter you

take it all the way to where the catheter is larger than the hepatic vein and now you've wedged it okay and this is kind of a mag up you see that that's a little that's a little wedge okay you wedge you inject contrast the contrast

just sits there it's wedged it's trapped okay and then this is with a balloon to your left is a balloon full of air to the right full of contrast and you basically trapped it again you fill contrast and consciousness it's there

what's the difference between this image and this image no difference the only difference is size that's all it's the same idea you're just trapping a segment of the liver the difference is this is a very

small segment and this is a larger segment okay so essentially it's actually the same technique one is just well technically when it comes to your side all one needs a four or five French calf the other one needs a balloon

occlusion caster okay same image so then you inject co2 the key thing here if you're the type of physician where you put contrasts you have a balloon sitting or a wedge and you have to count contrast there okay

rookie mistake is that they leave the contrast and then they hit the co2 okay what is that you've lost the advantage of the co2 in the beginning of your bolus is actually contrast okay so you need to bleed out the contrast and

replace it completely co2 so your entire bolus okay is co2 and not and not and not the and not the contrast okay that defeats the purpose why is co2 advantageous over contrast contrast is a thick fluid co2 is gas is viscous it's

volatile it actually can squeeze through tight spaces as it's a gas and that's what we want we want to squeeze that co2 which is a contrast through the sinusoids reflux it back into the portal circulation so we're trapping it and

we're trying to push co2 squeezing it through the sinusoids refluxing it back into the portal circulation so you can actually visualize the portal circulation okay and all and the disadvantage of a wedge is what you see

here if you're a wedge and you're immediately sub capsular and you slam you slam that co2 aggressively what you will get is an explosion you get a rip of those of the hepatic capsule scroll the glisten capsule and then you've got

a leak and if the patient is quite low is a quite low path they can actually die from this believe it or not they will die from this and not die from the needle passes okay so that's kind of co2 and that's kind of

a little a little passive air into the perineum nice imaging not a good outcome so one way to avoid this is to still wedge but wedge away from the hepatic capsule so you're out in the periphery in the paddock veins but you're deep

inside the liver you're not you're not right underneath the capsule so that's one way of doing it the other another way is to actually use a balloon okay so this is this is just another wedge here okay and you actually use a balloon I'm

just showing you a correlation with a balloon it's a little safer because you're a little distance away from from the hepatic capsule I'm just showing you a more and more image of the same thing co2 with correlation after you access

since it's a beautiful correlation with with the portal vein venogram okay there are problems with wedges and with balloons is that sometimes you get a gas you know a co2 leak you're wedged but there's hepatic veins at vadik vein

connections and all you see is a fatty veins you can't force reflux the co2 into the portal circulation so that's one problem okay so what do you do with that you change the sights just change a different different branch okay try to

avoid that connection between the badeck veins and it back veins go somewhere else where there is no connection where you can actually make a true hip wedge and force that co2 into the portal circulation okay another way this is

just a draw a drawing out whether it alone or a catheter you get that you get the escape from the Patek vein to fatty vein is to go distal go beyond that connection so if you can go distal go distal if you can't go distal then

change your branch try to find a place where there is no hepatic vein tip a degree engine attraction preferably but not necessarily not the same branches connected to because that usually goes both ways but not always sometimes

you're lucky and if that connection is kind of like a one-way valve one way street and it's not a two-way street but that's just sheer luck okay this is an example hepatic vein to about a vein connection and what we did was basically

switch to another place another vein and we actually get the portal venogram here okay next up sting crafts Viator's thank

so this shows you this shows you how so this typically you've accessed the portal vein now and you're in next up you basically pass the wire down this just gives you a little depiction of

what you're what you're what you're doing here this think of this is a sagittal and Deliver okay hepatic vein and portal vein it's the sagittal and what you're trying to do is

and if you're in the right hepatic vein you need to pass your needle anteriorly to hit the right portal vein okay and the right portal vein is usually anterior and interfere to the Patek vein okay so you pass your wire you're you

NEET your needle and when if you're missing the portal vein usually what's happening is that you're scooping behind it okay your posterior to it and sometimes you'll find the operators will actually increase the curve in the

needle so they can actually reach anterior anterior and actually hit the portal vein because usually usually if you if you know you're in the right place that the right hepatic vein not in the middle of petting vain and

you're missing the portal vein you need to reach anterior more so they put a little extra curve in the kelp into needle to actually catch that right portal vein okay with liver cirrhosis you get shrinking shrinkage of the liver

size the liver decreases the portal vein starts moving more anterior and more superior and closer to that paddock vein okay and it becomes more and more difficult to actually hit it so the smaller the liver the harder the liver

the smaller the space and you've got a thick mat piece of metal okay it's very difficult to hit that okay it becomes more and more challenging with with smaller levels to hit to hit the portal vein especially centrally okay this is

an access kit a new access kit by Gore it's basically the similar to the similar to the Cal Pinto needle it's a little longer with a little bit increase angulation compared to the traditional ring kits or the Cole Pinto needle but

once accessed you pass a wire okay into the portal circulation there are two ways of doing this okay there's a traditional old-school way that's my way is that to use a Benson wire okay the youngsters the Millennials are using

glide wires okay so if you're dealing with a millennial physician they're usually going for the glide okay if you're dealing with them with an older you know guy or gal they're using usually using a Benson wire okay the

advantage of the Benson wire is that has a floppy tip it actually you just push it in and hits the wall it prolapses into the main portal vein right away as you can see just prolapse and portal vein if you're using a glide where

you're catching all sorts of things you'll have small branches you don't know where you're going your V's even sometimes dissecting outside of the portal vein they're second-guessing themselves all the time but actually the

good way with a little bit of more different skillset is that you use use actual good old fashioned Benson wire actually goes in prolapses right away into the ends of the main into the main portal vein rarely would I actually use

light or switch to a glare that's usually if I'm coming in in a small in a small branch or an orchid angle where I have to use a glide right to try to get around the angle because I don't have enough room for a Benson to actually hit

the wall and prolapse is very really really tight space so tights Bates funny angles I'll switch to a glide where if it's a straight forward a Benson as very is very straight forward okay try to get the sheath as much into the portal vein

over the over the needle over the wire as possible and then you balloon your tract okay through the sheath okay some people will balloon with a six millimeter boom some people will balloon with an eight millimeter blue eye

balloon with an eight four okay at night and I make sure it's a four so that I actually use the balloon as the measurements for this four centimeters actually you I actually use the balloon to measure my to measure my Viator's

stance okay with the balloon there there'll be two waists there's a portal venous entry site and the Ematic venous entry site so you actually gauge that and take a picture of it so you actually see how long your tract is where's your

hepatic venous access who has your portal venous axis actually gives you a lot of anatomy here been engaging in actually putting where your Viator stent is okay usually high pressure balloon I use it and ate some people will use a

six or even a seven millimeter balloon

to talk about is indirect angiography this is kind of a neat trick to suggest to your intervention list as a problem solver we were asked to ablate this lesion and it looked kind of funny this patient had a resection for HCC they

thought this was a recurrence so we bring the comb beam CT and we do an angio and it doesn't enhance so this is an image here of indirect port ography so what you can do is an SMA run and see at which point along the

run do you pacify the portal vein and you just set up your cone beam CT for that time so you just repeat your injection and now your pacifying the entire portal vein even though you haven't selected it and what to show

well this was a portal aneurysm after resection with a little bit of clot in it the patient went on some aspirin and it resolved in three months so back to our first patient what do you do for someone who has HCC that's invading the

heart this patient underwent 2y 90s bland embolization microwave ablation chemotherapy and SBRT and he's an eight-year survivor so it's one of those things where certainly with the correct patient selection you can find the right

things to do for someone I think that usually our best results come from our interdisciplinary consensus in terms of trying to use the unique advantages that individual therapies have and IO is just one of those but this is an important

lesson to our whole group that you know a lot of times you get your best results when you use things like a team approach so in summary there are applications to IO prior to surgery to make people surgical candidates there are definitive

treatments ie your cancer will be treated definitively with curative intent a lot of times we can save when people have tried cure intent and weren't able to and obviously to palliate folks to try to buy them time

and quality of life thermal ablation is safe and effective for small lesions but it's limited by the adjacent anatomy y9t is not an ischemic therapy it's an ablative therapy you're putting small ablative radioactive particles within

the lesion and just using the blood supply as a conduit for your brachytherapy and you can use this as a new admin application to make people safer surgical candidates when you apply to the entire ride a panic globe

thanks everyone appreciate it [Applause] [Music]

talk here with something that's new on the horizon believe it or not it was actually on the horizon 20 years ago and then it went away because there were a lot of patients that were treated with a

lot of complications and it's making a resurgence and this is balloon pulmonary angioplasty or BPA for short so this is an intervention which may be feasible in non-operative candidates so I mentioned to the Jamison classification earlier

type 1 and type 2 disease should be treated with surgery again it should be treated is curative but patients with type 2 and a half or 3 disease can be treated with balloon pulmonary angioplasty in the right in the right

frame which means that a surgeon has said I cannot operate on this a medical doctor has said boy they're not going to get better with their medicine let's try something else well this is that something else and that's what involves

everyone in this room so this is these are usually staged interventions with potentially high radiation and contrast dose if you think about it it's like Venis recan and a pulmonary AVM all-in-one so it's a potentially a long

complex procedure with a lot of contrast and a lot of radiation but it can provide a lot of benefit to these patients I'm going to talk about the comp potential complications at the end which is one reason why not

everyone should do these all the time so this is a pulmonary angiogram from the literature when you're injecting a selective pulmonary artery you can see that this patient has multiple stenosis there's no real good flow there the

vessels look shriveled up like I mentioned to you before you can get a balloon across it and balloon the areas and then you can see afterwards so the image a on the left is before an image D is afterwards believe it or not this are

in the most experienced hands because the most experienced hands are for palm the BP AR in Japan they do hundreds of cases of these a year at each hospital I've personally only done five so but this is a something that I'm very

interested in and you can see how how much benefit it has for that patient another way you can see these are the webs and the bands that I mentioned to you earlier so what's interesting is that if you look on the first set of

images on the top and the images on the bottom those are the same patients it's the same view before top rows before and the bottom rows after balloon pulmonary angioplasty so the first image is a pulmonary angiogram where if you kind of

see this there's there's some area areas of haziness those are the webs and bands the image on the the middle is the blown-up views and you can see those areas and then the image on the right is intravascular ultrasound which I use

every day in my practice it's a catheter with an ultrasound on it and when you look at it on the top image image see you can see a lot of thrombus you're actually not seeing flow and on image F on the bottom you're seeing red which is

the blood flow so these patients can actually improve the luminal diameter bye-bye ballooning them you can treat occlusions again image on the left shows you a pulmonary artery with a basically an occlusion proximally and then after

you reek analyze it and balloon it you can see that they can get much more

so this is our MGH page we started it about a year ago check it out if you guys like it some pretty good cases we mostly post cases some policy stuff industry and changing things it's not purely cases but certainly take a look if you like it give us a follow so what

I have today is I have two cases that I picked and you know for all the thousands of cases that all these huge academic medical centers do I tried to pick a couple that might be a little interesting and that aren't being done

in all the different centers across the institution so I'll start off with the first which is an endovascular AVF creation so what's nice about this is that you know what we see so far from this is that the length of stay impact

has been certainly reduced in certainly the maturation times and the Rhian turn re intervention rates have been reduced so I'll go through this and normally wouldn't go step by step for a few things but I think you know not all

institutions are doing this yet I think that you will I do think this is going to be a shift for a lot of the dialysis patients and everybody who works anion knows what a huge impact it is the ESRD patients is just astronomical the

numbers of them it's just continuing to rise so procedural steps the first step is you're going to access the brachial vein advance the guide Y down to the ulna insert a six French sheath and perform a vena Graham and the rationale

for that of course is to make sure you don't have any issues centrally some centers do that in advance some centers don't I will mention also that the ultrasound mapping is absolutely critical to make sure that

you get the right patient you start off by seeing them in the outpatient clinic and then you're going to go and have them have vascular ultrasound to make sure you have a good candidate so the next is you're gonna access the brachial

artery same thing advance your guide wire down to the ulna from there you're gonna insert the venous side now this is one of two approved vendors that will allow you to do an endovascular creation this was a wave link it's a to stick

system and it requires two catheters which is why you see the next step is pretty much repeated but just flipping it to the arterial side so from there there's a magnetic zone it actually has like a little canoe so it's got a

backing of a ceramic sort of a space there if you can think of sort of the older or atherectomy cut home catheters that had that little carro canoe you would actually take the debris out it's very

look into that and I'll show you that in a couple of images once you align that you're gonna sort of engage the little electrode this is an RF ablation RF created type fistula so it creates a little slit between the Adri and the

vein and what happens is is that you know of course don't forget you have to ground the patient just like any RF once you get the magnets and you get the electrode alignment you're going to engage the device for two seconds and

the fistula is created and then from there a lot of centers are actually going in there embolize in one of the brachial veins and this is basically to sum some of that stuff obviously to the superficial system for draining I have

read that there are a few places that actually go back back in through the newly-created fistula like even at the time of the procedure with the 4 millimeter balloon and just sort of open that up I'm not sure that that's 100%

necessary but I'm sure all these fine people on the panel could help us with that so here you see and I skipped all the entry steps but here you can see the Venus in the arterial catheter you know in position here and there's that little

canoe thing pointed out by the arrow that I had talked about and you use fluoro to sort of align these two things when you first start doing these cases take your time the first one was over an hour and a half for us now obviously

it's about a third at that time this is the little electrode this is when it's advanced and pretty much ready to engage can you play the video for me so this is quick so what happens is you suppress the

device the electrode actually advances and as it advances towards the veena side what happens is is that it actually just creates this fistula through the RF sort of energy from there you're gonna do a post vena graph in here you can see

after we did an initial post intagram there was enough sort of flow between the PIAT brachial so we decided to embolize one and this patient was our first patient and is doing very well so far this is done on I'm gonna say just

because you know to dr. brains point I don't want to get on the hook for certain dates and patient identification but this was done in mid-march so we saw them two weeks out and we're gonna see them again another couple weeks so just

there's a couple of trials that you can read into one is the neat one is the flex trial I think the technical success is really promising at 96% the maturation days you can see there's a massive massive comparison where they

could be ready to be dialyzed in 60 days and this could be a game-changer for many patients the six-month patency rate is what I've seen in most of the reports it's around 98% compared to about 50% with the surgical place and then you can

see that this about 3.5 interactions or re interventions that are required in about 0.5 at a year's time out from this so it's really making a big difference for these patients and I think this is what we do in i/o we continue advanced

things innovate and obviously look to do things in a more timely cost-effective minimally invasive way at the beginning when these new procedures come out the devices themselves might be at a higher price point but we'll see how that goes

moving forward as more and more vendors get into the space so the second case

people were thinking about the covered

portion actually actually would be occlusive in that paddock veins a lot of people are concerned about that this could be kind of like a but carry you're gonna actually occlude flow in the paddy vein caused thromboses that didn't pan

out at least clinically okay it didn't pan out and that's another advantage of actually accessing very close to the paddock vein IVC junction that's where the biggest vein is so you don't get a lot of occlusive problems okay but

usually clinically it does not pan out so the bigger the hepatic vein the more likely you have a lot of room around your your graft you won't be occlusive to the paddock vein that's more important for for transplants than other

than others I told you it's rare this is actually a very rare case of such that where you actually have a segmental segmental kind of but carry after a tips okay and you know this is actually from a form of venous outflow from the ematic

vein this is a perfusion defect typical it's a wedge right typical perfusion defect in the liver that's how you death so you know this is vascular this is a perfusion problem but you've got hepatic artery readout artery the red arrows

running into the segments and you have portal vein running into the segments so what's the problem it's actually a paddock vein occlusion okay by the stents subclinical no no clinical complaints you let it be

in the patients usually recover okay treat the patients and not the images okay on the other side if you put their tips too deep sometimes you actually get thromboses of the portal vein branch

again you get a call from hepatology you've got portal vein thrombosis is the patient doing okay yes treat the patient and not the images they usually resolve this it's not not a big problem another technical problem

I'm gonna focus mostly on technical for you guys this is a but key area okay and the but carry especially in the acute stage the liver is not like a cirrhotic liver is big liver is actually engorged okay so it's very large usually

your needle is too short to even reach the portal vein okay that's a big problem okay because your access needle is too short for a very large engorged the portal vein so this is as deep as it

goes do I have a see that that do you see that needle tip that's as deep as the needle tip goes okay the portal vein is a good distance away okay luckily this is a co2 porta gram luckily I'm actually in a small branch right

there I just hit it on you know and on this is not the there's not a needle tract this is just luckily hitting it a little branch and on so I'm actually accessing the portal vein and I can do a co2 porta gram here okay

typical inexperienced person would say you know this looks good I'm lucky I'm in a branch but it's a nice smooth curve I'll just pass a wire down and I'll balloon it and I'll put a stent in it's a nice curve and you know so it's my

lucky day I don't need to extend my needle or get a bigger longer needle to reach the portal vein here's the problem with this and this is exactly what this is exactly what this is they pass a wire and it looks beautiful just put a stent

and go home okay here's the problem this is actually the small branch access sites this is actually where you really need to access world vane but your needle is not long enough okay

what we found out is that if you are in a small in a small portal vein no matter how much you balloon it it will come down again and it will be narrow so believe it or not if you go sideways in a portal vein and rip it open with a

balloon it will stay open but if you go down of small portal vein and balloon it open it will always contract down okay so you cannot do a tips simply by ballooning and putting a stent in in this case okay what we do is we actually

denude the vein itself we actually rip it off okay and make it a raw parenchyma and we do that with a Tortola device we literally rip off the paddock the paddock portal sorry the portal vein endothelium and media and adventitia rip

it off make it completely raw as if it's an access as if it's a liver brain coma which is which it is now and then we then we balloon dilates okay rip it off denude it angioplasty it's okay and then put the stent and see that aggression

despite all that aggression of ripping it off it still has an hour kind of an hourglass shape to the to the tips okay that little constraint there that's the hepatic venous access sites this is the parenchymal tract to see nice and open

with a balloon but the but the actual vein that we've been through despite our aggression in actually ripping it off it's still narrowed down but this is as good as it gets okay

a little bit more systemic versus catheter directed thrombolysis so once you've decided that a patient needs TPA what are the differences here well if

you give patients systemic TPA you're gonna give them a much more rapid delivery this is for those patients who have high-risk PE they're the ones who are coding for those patients you give them 200 milligrams of IV usually you

get 50 first and then another 150 over a very short time period they have a very high risk of bleeding as a result of that a catheter is much slower you're gonna infuse one milligram maybe which is what I think most people do

over several hours maybe a few maybe a day so it's slower targeted versus non targeted well catheter is much more targeted you're gonna give Pete you're gonna give the TPA right into the

pulmonary arteries that's the whole point in our in our thought process as a result you give a lot less drug so when you give a patient based off of some of the trials 24 milligrams of TPA over a 24-hour period that's a lot less than

200 milligrams in a 10 minute period and then the bleeding risk is very different for these patients catheter based treatments have a high bleeding risk but it's possibly lower than the initial bleeding risk of patients getting

systemic TPA so I wanted to go through a

typical symptoms if you want to hit the play on this I think this is one we've probably already seen but it's it's the the algorithm that I go through for treatment so we do my renal vena Graham

there we go it's classic definitely has reflux and so next I will selectively catheterize the gonadal vein and here you see very large pelvic varicosities and so my standard is to actually treat the varicose veins with a sclerostin

much like I would sclerosis a varicose vein in the leg and there's a few reasons that I do that and so here's how I do it I'll put an occlusion blown up you see the picture on the left of the screen has an occlusion balloon it's the

same occlusion balloon we use for a tips procedure and I'll temporarily block the gonadal vein and fill up the system or the varicosities with contrast so that I get a sense for the volume of sclerosis and I would use then the picture on the

right is a venogram after I've injected the sclerostin so I've evaluated the volume and then I've replaced all that contrast by forcing it through the system to drain out the pelvic veins and filling the varicosities with

soldier column I do that because I believe and there's no data to prove it that it helps prevent superficial phlebitis in those varicosities so if we're just gonna block off the gonna dull vein then we have stagnant blood in

all the pelvic varicosities and stating that blood wants to clot and when blood clots on its own it'll stretch and expand the vein and cause pain and so in my own personal experience that has created a little bit worse post

procedural symptoms for patients compared to the patients that I use so TRADOC all to actually treat the varicosities so that's what I start out with and then since I'm kind of an old-fashioned guy I still go with the

coils and so I coiled the whole going a ttle vein and you can use sort of whatever you want you know that's the simplest thing for me are using nester coiours coils and and fill it up some people use the long detachable shaping

coils kind of an expensive way to do it if it saves you radiation then then that's that's one of the reasons to do it but the point is in in the venous system you have to be able to and I show this slide because you can see a

collateral vein or at least a branch there a confluence point that we've coiled off too if you do not treat the entire length there's a there's a lot higher chance for recurrence and veins have a way to find their way around if

they can communicate back up then patient gets recurrent symptoms and that can happen in about ten percent of cases so in order to prevent that you treat the whole gun out of vein and that's sort of why I think some people like to

use liquid sclerosis because then they will be able to sort of profuse all those branch points that would have a chance for recurrence case number two

you see again renal Dena Graham you can see a hint of the gonad of Ain selective

vena Graham again showing us the large gonadal vein and that's my post so charcoal with the occlusion balloon and then treat I showed the cartoon slide before that we look at all four of those territories so I always start with the

left but then I'm gonna look at the right gonadal vein as well as the internal iliac veins on both sides in this case the right go Natalie was normal as were the internal iliac veins so not seeing any varicosities

normal venous outflow so this patient it was only treated with a left gonadal vein embolization

includes an interview of the patient abnormalities of major organ systems like cardiac status do they have a reduced ejection fraction do they have coronary artery disease I want to know

if they have an EF of 10% because if they become hemodynamically unstable and I want to give them fluids I'm not going to bolus a patient with a very low ejection fraction with two liters of fluid you're gonna cause

pulmonary edema and you're going to worsen the situation renal status is huge a lot of our patients are renal e impaired and that can affect the way that they clear the sedation medications that we're giving pulmonary status do

they have COPD asthma or sleep apnea sleep apnea is major in procedural sedation neurologic status do they have a history of seizures endocrine status hyper or hypo metabolism of medications can occur if they have a thyroid

disorder we want to know about adverse experiences with sedation in the past do they have a history of a difficult airway for us at NYU if they have been already been identified as a difficult airway that automatically means we're

doing the procedure with anesthesia current medications potential drug interactions is very important we'll go over that a few slides drug allergies and herbal supplements that they're taking tobacco alcohol or

substance use and frequent or repeated exposure to sedation agents is just going to increase their tolerance of the medications physical exam vital signs auscultation of heart and lungs and then their airway assessment sorry excuse me

do they have any Strider snoring or sleep apnea advanced RA they're gonna have a hard time tilting their neck back if they have cervical spine disease or they have rheumatoid arthritis chromosomal abnormalities like

trisomy 21 patients with Down syndrome can have an enlarged tongue that can impair your ability to manually ventilate them if respiratory depression wants to occur body habitus if they have significant obesity especially of the

head and neck areas and head and neck limited neck extension short neck decreased ornamental distance which is basically just looking at how far back they can tilt their head any neck mass and then again cervical spine disease or

trauma do they have a c-spine collar are they on c-spine precautions that's not a patient we're going to be able to manipulate their airway and then mouth opening we do use Mallampati and I'll review

that in a couple of slides so the AFC classification is a categorization of the patient's physiologic status that can be helpful in predicting operative risk it is recommended by the AFA that if a patient is an Asaf or that that

should prompt an evaluation by an anesthesiologist I will tell you at NYU we will still get procedural sedation to some patients who are in Asaf or but we like to identify it ahead of time because if they have significant

comorbidities that will potentially increase their likely hurt likelihood of having an adverse outcome we then have a lower threshold for activating a rapid response or a code if something was to happen if we got concerned about

something so the airway assessment is

criteria for CTF means that the patient has a mean pulmonary arterial pressure which we measure intraoperatively exceeding 25 millimeters mercury at rest with the mean pulmonary capillary wedge pressure less than 15 so I'm not a

cardiologist but what that means to me is a mean capillary pulmonary wedge pressure less than 15 means that their left heart is not failing so if you have a capillary wedge pressure higher than 15 that means your left heart is not

working correctly and you can't blame it on the CTF so you can't blame it on the right side if the left side isn't working other things that matter are the abnormal pulmonary vascular resistance and having a systolic pulmonary artery

pressure greater than 40 so what I want to show you and highlight is the law the lost art of pulmonary angiography which i think is now sort of again a lost art some places do a lot of it and some places don't do very much but diagnostic

pulmonary angiography is actually the gold standard in the planning of either surgery or medical management for patients with CTF we do we do these on almost all of our patients with CTF to make that decision with the surgeons and

the cardiologists so the utility is very it's very useful you're able to measure our pressure you're able to decide whether we're the where the thrombus exists in this image here in patients with disease in the

blue and yellow outlined areas those are the patients who can have the operation the operation is curative it's not just medication that you have to take for the rest of your life you can actually remove that chronic clot it's much like

a femoral endarterectomy that are done for patients with peripheral arterial disease although it's a lot more complicated because they have to crack your chest open what's important is getting very very

good high-quality pulmonary angiogram xand so we do we used to do about we do about a hundred of these a year where I trained or actually where I work now and you get very magda up views and you're gonna show all of the vessels and so

these are the views that we use at our institution they happen to be the pipette criteria so it's the same thing you used to do for acute PE you put a flush catheter in the main pulmonary arteries when you're looking at the

upper lobes and when you're looking at the lower lobes you want to push the catheter further into the pulmonary arteries and inject usually what I do is a two to three second injection so that you can stack the images very well and

show all of them in one view this allows your surgeon to make a decision easily as to whether they can operate or they can't operate on this and then I use a higher frame rate usually because these patients are wide awake we when we do

this case we give our patients twenty five mics of fentanyl one time and that's it just to help get the sheath in I usually do this with a seven French sheath and then use a flush cap pulmonary artery catheter many of which

are currently off the market but when we do this we just give them that twenty five Mike's because they have to hold their breath and I usually go up to a high frame rate in the first run and then adjust based off of how well that

patient is holding their breath this really takes a team effort from our nursing technologists and the and the physicians in the room to make sure that this patient does a good job because it's gonna change their management so

there are a lot of different types of angiographic findings on one of these pulmonary angiogram they're really really interesting pulmonary angiogram zin these patients and they're sometimes not at all subtle so you're looking for

a pruning of distal vessels if we start in the top left where you're just not seeing the Brent normal branch pattern you look for stenosis so we're not usually used to looking at stenosis and the pulmonary arteries but this is

actually what you're looking for in CTF you're looking for webs or bands so you'll usually see little areas where you just doesn't look like there's great opacification there's little areas that there's not good at pacification those

are little webs inside the vessel believe it or not looks like a cobweb that grew inside there from that thrombus and then you're looking for areas of complete occlusion that there's just no vessels there those are all

vessels that can be treated in patients with CTF so this is the Jameson classification before we talk about the sort of the interventional management the surgical management is again the curative and dr. Jameson is the head

surgeon at University of California in San Diego which is the largest Palm CTF program in the in the world and he's done I think over 3 500 of these operations I think he's retired at this point but they named the classification

after him and so type 1 is proximal disease so it involves the main pulmonary arteries these are the ideal patients who can get the best benefit from this in their life type 2 is the next best

it's segmental proximal just type 3 is distal segmental and then type 4 is just a mess of sort of all of it but you can't really get a good surgical plane so type 1 and 2 are treated with pulmonary thromboembolism

towards balloon pulmonary angioplasty or BPA and type 4 are generally treated with medication so PT II or pulmonary

so just a compliment what we everybody's talked about I think a great introduction for diagnosing PID the imaging techniques to evaluate it some of the Loney I want to talk about some of the above knee interventions no disclosures when it sort of jumped into

a little bit there's a 58 year old male who has a focal non-healing where the right heel now interestingly we when he was referred to me he was referred to for me for a woman that they kept emphasizing at the anterior end going

down the medial aspect of the heel so when I literally looked at that that was really a venous stasis wound so he has a mixed wound and everybody was jumping on that wound but his hour till wound was this this right heel rudra category-five

his risk factors again we talked about diabetes being a large one that in tandem with smoking I think are the biggest risk factors that I see most patient patients with wounds having just as we talked about earlier we I started

with a non-invasive you can see on the left side this is the abnormal side the I'm sorry the right leg is the abnormal the left leg is the normal side so you can see the triphasic waveforms the multiphasic waveforms on the left the

monophasic waveforms immediately at the right I don't typically do a lot of cross-sectional imaging I think a lot of information can be obtained just from the non-invasive just from this the first thing going through my head is he

has some sort of inflow disease with it that's iliac or common I'll typically follow within our child duplex to really localize the disease and carry out my treatment I think a quick comment on a little bit of clinicals so these

waveforms will correlate with your your Honourable pencil Doppler so one thing I always emphasize with our staff is when they do do those audible physical exams don't tell me whether there's simply a Doppler waveform or a Doppler pulse I

don't really care if there's not that means their leg would fall off what I care about is if monophasic was at least multiphasic that actually tells me a lot it tells me a lot afterwards if we gain back that multiphase the city but again

looking at this a couple of things I can tell he has disease high on the right says points we can either go PITA we can go antegrade with no contralateral in this case I'll be since he has hide he's used to the right go contralateral to

the left comment come on over so here's the angio I know NGOs are difficult Aaron when there's no background so just for reference I provided some of the anatomy so this is the right you know groin area

right femur so the right common from artery and SFA you have a downward down to the knee so here's the pop so if we look at this he has Multi multi multiple areas of disease I would say that patients that have above knee disease

that have wounds either have to level disease meaning you have iliac and fem-pop or they at least have to have to heal disease typically one level disease will really be clot against again another emphasis a lot of these patients

since they're not very mobile they're not very ambulatory this these patients often come with first a wound or rest pain so is this is a patient was that example anyway so what we see again is the multifocal occlusions asta knows

he's common femoral origin a common femoral artery sfa origin proximal segment we have a occlusion at the distal sfa so about right here past the air-duct iratus plus another occlusion at the mid pop to talk about just again

the tandem disease baloney he also has a posterior tibial occlusion we talked about the fact that angio some concept so even if I treat all of this above I have to go after that posterior tibial to get to that heel wound and complement

the perineal so ways to reach analyze you know the the biggest obstacle here is on to the the occlusions i want to mention some of the devices out there I'm not trying to get in detail but just to make it reader where you know there's

the baiance catheter from atronics essentially like a little metal drill it wobbles and tries to find the path of least resistance to get through the occlusion the cross or device from bard is a device that is essentially or what

I call is a frakking device they're examples they'll take a little peppermint they'll sort of tap away don't roll the hole peppermint so it's like a fracking device essentially it's a water jet

that's pulse hammering and then but but to be honest I think the most effective method is traditional wire work sorry about that there are multiple you know you're probably aware of just CTO wires multi weighted different gramm wires 12

gram 20 gram 30 gram wires I tend to start low and go high so I'll start with the 12 gram uses supporting micro catheter like a cxi micro catheter a trailblazer and a B cross so to look at here the sheath I've placed a sheet that

goes into the SFA I'm attacking the two occlusions first the what I used is the micro catheter about an 1/8 micro catheter when the supporting my catheters started with a trailblazer down into the crossing the first

occlusion here the first NGO just shows up confirmed that I'm still luminal right I want to state luminal once I've crossed that first I've now gone and attacked the second occlusion across that occlusion so once I've cross that

up confirm that I'm luminal and then the second question is what do you want to do with that there's gonna be a lot of discussions on whether you want Stan's direct me that can be hold hold on debate but I think a couple of things we

can agree we're crossing their courageous we're at the pop if we can minimize standing that region that be beneficial so for after ectomy couple of flavors there's the hawk device which

essentially has a little cutter asymmetrical cutter that allows you to actually shave that plaque and collect that plaque out there's also a horrible out there device that from CSI the dime back it's used to sort of really sort of

like a plaque modifier and softened down that plaque art so in this case I've used this the hawk device the hawk has a little bit of a of a bend in the proximal aspect of the catheter that lets you bias the the device to shape

the plaque so here what I've done you there you can see the the the the the teeth itself so you can tell we're lateral muta Liz or right or left is but it's very hard to see did some what's AP and posterior so usually

what I do is I hop left and right I turned the I about 45 degrees and now to hawk AP posterior I'm again just talking left to right so I can always see where the the the the AP ended so I can always tell without the the teeth

are angioplasty and then here once I'm done Joan nice caliber restored flow restored then we attacked the the common for most enosis and sfa stenosis again having that device be able to to an to direct

that device allows me to avoid sensing at the common femoral the the plaque is resolved from the common femoral I then turn it and then attack the the plaque on the lateral aspect again angioplasty restore flow into the common firm on the

proximal SFA so that was the there's the plaque that you can actually obtain from that Hawk so you're physically removing that that plaque so so that's you know that's the the restoration that flow just just you know I did attack the

posterior tibial I can cross that area I use the diamond back for that balloon did open it up second case is a woman

patients may be asking you is like what about adenomyosis and I've been hearing something about that which is not exactly fibroids right it's a different entity though the symptoms could be kind of the same and for the years and years

and years we wouldn't have any options for patients who had adenomyosis in fact the only option for patients with adenomyosis is surgery but adenomyosis can coexist with fibroids and sometimes patient presents with adenomyosis alone

so we've had some studies now that have looked at that and although the data is not as robust and not as awesome as for patients with fibroids we do provide a performing bolas Asian for those patients with particles that are little

smaller than what we would use for fibroids with results as you're seen there before now the only other new thing that's on the market and it's not so new to you guys that are probably doing radial in femorals anyway working

in cardiac labs and IR labs it's actually what we call the trophy if you go back one slide for me mr. a the person and press play then we will be able to see that radial access I do not work for Merritt they don't give me a

dime I just thought that this was a good video is there volume on that at all if not I can just talk about it and really what it says is that if you need to a radial UFE or have radial axis for a uterine embolization patients just love

it more they and especially like patients that are already just intimidated they don't want you going near their groins at all they actually could just lay on the table we don't have to put up we don't put a Foley in

they just get a radial access the same way that you would just be starting in a line except we have special types of radial catheters and and sheaves to do that and I don't offer a radial access to

patients who are too tall for our catheters or if they've had multiple prior radial access and don't have an intact ulnar artery to complete their hand but it's much like any of that femoral access that you would normally

see they make special hydrophilic sheaths now they're called from this particular company slender technology where the inner diameter of the sheath essentially the sheath is the same like five French on the outside but they have

cored out the inside so it's a bigger diameter so it's a five six so on the outside it's a five but it will take a six French in the inner inner lumen and you know my practice we do more than 80% of all our arterial punctures with a

radial access and everybody here comes dr. Sean Deroche Nia who is the leading author of that paper for SI R and one of my esteemed partners so most patients are able to get up and walk out if you are go from a radial access the access

is actually closed with just a radial band and the complications of having a hematoma or having the patient's bleed out those just all go away but radial axis have their own complications so I'm not here to say that it is not that but

in our practice we found it to be safe and effective our patients want it and it's become like a practice differentiator so if you're working in a practice that don't do radial you EFI's right now you should mention it because

if you're in a population where the other providers are only doing femoral then you will automatically get the patients that only want that so here's a patient that had a radial access you can see a catheter that is coming from the

aorta while you can't see that it's not up and over the bifurcation but maybe you do can see that and there's a catheter in the uterine artery with the characteristic

shape of the uterine artery and the characteristic curlicue vessels of of the fibroid and on the left you can see the Imogen for beforehand and the Imogen on the right of post embolization where there is stagnant flow in the main

uterine not main uterine artery in the horizontal portion of the uterine artery for greater than five cardiac beads and again there's there's no reason that you have to know that level of detail except that you're scrubbing in but if you're

in the audience you're looking at this you're like dr. Newsome I see an air bubble there as well then I'd say good because because I do see it too so you can see the preimage and you can see the post image for pre and post embolization

these these procedures can be quick these procedures are very very rewarding and and I love to do it

let me show you a case of massive PE

this launched our pert pert PE response team 30 year-old man transcranial resection of a pituitary tumor post-op seizures intracranial frontal lobe hemorrhage okay so after his brain surgery developed a frontal lobe

hemorrhage and of course few days after that developed hypotension and hypoxia and was found to have a PE and this is what the PE look like so I'll go back to this one that's clot in the IVC right there and

that's clot in the right main pulmonary artery on this side clot in the IVC clot in the right main pulmonary artery systolic blood pressure was around 90 millimeters of mercury for about an hour he was getting more altered tachycardic

he was in the 120s at this point we realized he was not going the right direction for some reason the surgeon didn't want to touch him still to this day not sure why but that was the case he was brought to the ir suite and I had

a great Mickey attending who came with him and decided to start him on pressors and basically treat him like an ICU patient while I was trying to get rid of his thrombus so it came from the neck because I was conscious of this clot in

the IVC and I didn't want to dislodge it as I took my catheters past it and you see the Selective pulmonary and on selective pulmonary angiogram here and there's some profusion to the left lung and basically none to the right lung

take a sheath out to the right side and do an injection that you see all this cast of thrombus you really see no pulmonary perfusion here you can understand why at this point this man is not doing well what I did at this point

was give a little bit of TPA took a pigtail started trying to spin it through aspirated a little bit wasn't getting anywhere he was actually getting worse I was starting to feel very very nervous I had remembered for my AV

fistula work that there was this thing called the cleaner I don't have any stake in the company but I said you know I don't have a lot to lose here and I thought maybe this would be better than me trying to spin a pigtail through

the clock so the important thing about the cleaners it does not go over a wire so you have to take the sheet out then take out the wire then put the cleaner through that sheath and withdraw the sheath

you can't bareback it especially in the pulmonary circulation the case reports are poking through the pulmonary artery and causing massive hemorrhage and the pulmonary artery does not have an adventitia which is the outer layer just

a little bit thinner than your average artery okay so activated it deployed it and you started to get better and this is what it looked like at the end now this bonus question does somebody see anything on this this picture here that

made me very happy on this side this picture here that made me feel like hey we're getting somewhere I'm sorry the aorta the aorta you start to see the aorta exactly and that that was something I was not seen before the

point being that even though this doesn't look that good in terms of your final image the fact that you see filling in the aorta and mine it might have been some of the stuff I had done earlier I can't I can't pinpoint which

of the interventions actually worked but that's what I'm looking for I'm looking for aortic blood flow because now I've got a hole in that in that clot that's getting blood flow to the left ventricle which starts to reverse that RV

dysfunction that we were concerned about make sure I'm okay with time so we'll

of these issues filters are generally still use or were used up until a few years ago or five years ago almost exclusively and then between five years and a decade ago there was this new concept of proximal protection or flow

reversal that came about and so this is the scenario where you don't actually cross the lesion but you place a couple balloons one in the external carotid artery one in the common carotid artery and you stop any blood flow that's going

through the internal carotid artery overall so if there's no blood flowing up there then when you cross the lesion without any blood flow there's nothing nowhere for it to go the debris that that is and then you can angioplasty and

or stent and then ultimately place your stent and then get out and then aspirate all of that column of stagnant blood before you deflate the balloons and take your device out so step-by-step I'll walk through this a couple times because

it's a little confusing at least it was for me the first time I was doing this but common carotid artery clamping just like they do in surgery right I showed you the pictures of the surgical into our directa me they do the vessel loops

around the common carotid approximately the eca and the ICA and then actually of clamping each of those sites before they open up the vessel and then they in a sequential organized reproducible manner uncle Dee clamp or unclamp each of those

sites in the reverse order similar to this balloon this is an endovascular clamping if you will so you place this common carotid balloon that's that bottom circle there you inflate you you have that clamping that occurs right

so what happens then is that you've taken off the antegrade blood flow in that common carotid artery on that side you have retrograde blood flow that's coming through from the controller circulation and you have reverse blood

flow from the ECA the external carotid artery from the contralateral side that can retrograde fill the distal common carotid stump and go up the ica ultimately then you can suspend the antegrade blood flow up the common

carotid artery as I said and then you clamp or balloon occlude the external carotid artery so now if you include the external carotid artery that second circle now you have this dark red column of blood up the distal common carotid

artery all the way up the internal carotid artery up until you get the Circle of Willis Circle of Willis allows cross filling a blood on the contralateral side so the patient doesn't undergo stroke because they've

got an intact circulation and they're able to tolerate this for a period of time now you can generally do these with patients awake and assess their ability to tolerate this if they don't tolerate this because of incomplete circle or

incomplete circulation intracranial injury really well then you can you can actually condition the patient to tolerate this or do this fairly quickly because once the balloons are inflated you can move fairly quickly and be done

or do this in stepwise fashion if you do this in combination with two balloons up you have this cessation of blood flow in in the internal carotid artery you do your angioplasty or stenting and post angioplasty if need be and then you

aspirate your your sheath that whole stagnant column of blood you aspirate that with 320 CC syringes so all that blood that's in there and you can check out what you see in the filter but after that point you've taken all that blood

that was sitting there stagnant and then you deflate the balloons you deflate them in stepwise order so this is what happens you get your o 35 stiff wire up into the external carotid artery once it's in the external cart or you do not

want to engage with the lesion itself you take your diagnostic catheter up into the external carotid artery once you're up there you take your stiff wire right so an amp lats wire placed somewhere in the distal external carotid

artery once that's in there you get your sheath in place and then you get your moment devices a nine French device overall and it has to come up and place this with two markers the proximal or sorry that distal markers in the

proximal external carotid artery that's what this picture shows here the proximal markers in the common carotid artery so there's nothing that's touched that lesion so far in any of the images that I've shown and then that's the moma

device that's one of these particular devices that does proximal protection and and from there you inflate the balloon in the external carotid artery you do a little angiographic test to make sure that there's no branch

proximal branch vessels of the external carotid artery that are filling that balloon is inflated now in this picture once you've done that you can inflate the common carotid artery once you've done that now you can take an O on four

wire of your choice cross the lesion because there's no blood flow going so even if you liberated plaque or debris it's not going to go anywhere it's just gonna sit there stagnant and then with that cross do angioplasty this is what

it looks like in real life you have a balloon approximately you have a balloon distally contrast has been injected it's just sitting there stagnant because there's nowhere for it to go okay once the balloons are inflated you've

temporarily suspends this suspended any blood flow within this vasculature and then as long as you confirm that there's no blood flow then you go ahead and proceed with the intervention you can actually check pressures we do a lot of

pressure side sheath pressure measurements the first part of this is what the aortic pressure and common carotid artery pressures are from our sheath then we've inflated our balloons and the fact that there's even any

waveform is actually representative of the back pressure we're getting and there's actually no more antegrade flow in the common carotid artery once you've put this in position then you can stent this once the stent is in place and you

think you like everything you can post dilated and then once you've post dilated then you deflate your balloon right so you deflate your all this debris that's shown in this third picture is sitting there stagnant

you deflate the external carotid artery balloon first and then your common carotid artery and prior to deflating either the balloons you've aspirated the blood flow 320 CC syringes as I said we filter the contents of the third syringe

to see if there's any debris if there's debris and that third filter and that third syringe that we actually continue to ask for eight more until we have a clean syringe but there's no filter debris out because

that might tell us that there's a lot of debris in this particular column of blood because we don't want to liberate any of that so when do you not want to use this well what if the disease that you're dealing with extends past the

common carotid past the internal carotid into the common carotid this device has to pass through that lesion before it gets into the external carotid artery so this isn't a good device for that or if that eca is occluded so you can't park

that kampf balloon that distal balloon to balloon sheath distally into the external carotid artery so that might not be good either if the patient can't tolerate it as I mentioned that's something that we assess for and you

want to have someone who's got some experience with this is a case that it takes a quite a bit of kind of movement and coordination with with the physician technologists or and co-operators that

study that was done was the perfect registry so all these studies have some name perfect the PE stands for pulmonary

embolism I don't know what the rest means but it's a registry of a hundred and one consecutive patients so these are patients that had what they termed at that time massive PE as well as sub massive PE it was seven sites and they

took all their data over three years so basically they said if you treated a patient with PE let us know send us all their info we're gonna put it in this one paper the therapy was all over the place for so patients with sub massive

or intermediate high risk PE they got catheter directed thrombolysis usually over 12 to 24 hours but again it was not specific it was whatever they did we want to know about it put it in one and sort of reported patients with

massive PE which are very different from those patients with intermediate high risk PE got mechanical fragmentation with some low-dose TPA and this was left open to whatever you were doing at your institution and then they looked at how

patients did overall and they looked at only survival to hospital discharge so they just want to know if patients like made it through that hospitalization overall they found that most patients were treated successfully so they didn't

die on the on the table and that they were able to get through there were six deaths for four mostly from the massive PE group and two from the sub massive and eighty nine point one percent had reduction in RV strain so that's one of

the risk factors or that's one of the goals endpoints that we look in in every study is RV strain did we improve their RV strain pre and post intervention and that can be measured either under an echo or on a CT scan one thing that we

don't know is by reducing that RV strain did we actually improve their life their quality of life or their overall survival and that's one some of the other studies mentioned 84% of these patients are almost 85 had a reduction

in their pulmonary artery pressure so as interventional radiologists and I believe interventional cardiologists also when we start our case we measure the pulmonary artery pressure we're really measuring the strain on the heart

as a result of the high pulmonary artery pressure so at the end of the case we want to know if we didn't even better and I always talk with our trainees and our team about the fact that once you do one of these cases you're really only

looking at the pressure you're not necessarily looking at what the picture looks like because sometimes the picture doesn't look very very good at the end of a PE lysis but the patients are doing much better one thing that's important

to notice is that there was a thirteen point one percent who had complications had complications that's a large number of patients so when you give patients thrombolysis they can have complications and many of them require blood

transfusions or have large hematomas or pseudo aneurysms and things that require further intervention the ultima study is another study this is a study looking at patients receiving unfractionated heparin so patients got just heparin and

other patients got Kathryn directive thrombolysis so this is the standard of care which is heparin versus TP a from a catheter this was a small group of patients only 59 patients and they were all patients who had acute PE with

an r v lv ratio greater than one so that's sort of night now the new standard the RVL v ratio should be less than one and that's basically just looking on a CT scanner and echo how big the RV is the left ventricle pumps all

the blood to the main to your body so that is much stronger than the than the right and it has a much larger size in on average and this is one of the methods that we use in all studies so what they looked at over time here is

these patients and how there are VL v ratio changed after they either received TPA or whether they got just the standard of care which is heparin and you'll see that there is an improvement in the patients who had a catheter

directed thrombolysis and overall they had better a change in their RV LV ratio so that's sort of the marker that we we have been using but again it still doesn't tell us do these patients live longer do they have better quality life

afterwards this Seattle to study is another study that was performed and this is actually a sort of a changing game-changing study at least for a catheter directed thrombolysis in the beginning this was a

industry-sponsored study it's May it was sponsored by the the makers of eCos catheters but it was what was nice about this study is that it was very well defined everyone had to do the same thing so if you're trying to study if

something works or not it's got to be consistent in this group they had massive patients and sub massive but they all had an RV LV ratio greater than 0.9 on CT every patient got unfractionated heparin or or lovenox low

molecular weight heparin and then they all received 24 milligrams of TPA that's the study everybody got the same thing and what you see here on this on the right is that the patients who had T who had catheter directed thrombolysis all

had a reduction in their RV LV ratio they all had a reduction in their mean systolic mean or systolic pulmonary artery pressure and they all had a reduction improvement in their Mead modified Miller index which is actually

a score of how much clot there is in the pulmonary arteries so that suggests that there's an improvement at least in the short term and these patients had reduced bleeding 13% vs. 10% is reduced it's not still

not great but these patients all got TPA so this is a summary slide from chest to in the chest guidelines in 2015 looking at the three studies I just mentioned to you so perfect Seattle - and Altima and it's basically again

showing you that there has been improvement in patients right ventricular strain as well as the patients mean systolic PA pressures but I will tell you even with this data we still don't know what the right answer

is because we don't know how this affects patients in the long term and how they're gonna do in their overall life so back to our patient to move on

okay stent graft deployments once you've ballooned you basically pass the sheath over the balloon all the way down to the portal circulation the reason for that

is the Viator stance has a bare portion that's captured by the sheath so your sheath has to be deep into the portal circulation so when you unsheath it it opens up and then you pull back so it snags on your portal venous entry so

it's a feel thing and a visual at the same time for the operator okay so your sheath has to be deep in the portal circulation so that dilates put your sheath all the way down this is a run just to make it look pretty for you guys

and then you basically deploy the Viator stent via tourists and like I said has a bear portion that's captured by the plastic here and that plastic sheath basically transfers the capture of the bare

portion from plastic to your entry or access sheath okay as a ring to it and put it in has a feel to it that ring has to be right there it's very common for people starting off to deploy it inside the sheath up so it's a kind of a feel

thing to actually make sure that it's actually in there snug with it with the sheath okay then you push the stents all the way into the sheath now the bare portion is captured by the sheath you remove the plastic it's over over and

done with and then you pass pass your your stent all the way down to the portal vein and then unsheath it like a wall stents let it open pull everything back till it snags on the portal venous entry sites and then unsheathed the rest

of it which is the covered portion and that stays constrained by the cord and then you pull then you pull the cord keep key portion here is this is the ideal tips and ideal ace tips is a tips from the portal vein bifurcation to the

a patek vein IVC junction okay that's an ace tips it's usually a straight tips it's the straightest tips you'll see it runs parallel to the caiva okay rookies will be doing tips down out in the

periphery and Deliver okay they'll be fishing for small portal veins out of his small hepatic veins and at the end their tips is gonna be like a big seat like a big C loop okay it'll be a longer tips with more stance and it won't be an

aggressive decompressive tips okay but an ace tips is a more aggressive central tips straights it comes from the portal vein bifurcation to the paddock vein IVC Junction that's kind of like an ace tips

okay unsheath it and then and you and then you pull the cord to basically deploy it and this is kind of a reenactments the Styrofoam cup is the portal vein the sheath is in there now over the wire there's no wire in the in

the reenactments and then you unsheath the bear portion so it opens up okay and then you pull everything back till it catches on the portal vein okay you move the sheath all the way back and

then you pull the cord you see the cord right there you pull the cord and it basically opens up the covered portion okay and it opens up from the portal venous end so it actually capped catches it right away catches that portal venous

entry sites there's no slippage and so basically rips open tip to hub okay and that's kind of your final product and then you go in and and then you go in and balloon okay so here it is ballooning put the sheath

over the balloon sheath is deep into the portal circulation you put the tips in your unsheath to cut the the the bare portion let it flower open you pull everything back to like snags you unsheath the rest of the stunt and then

you pull the cord okay and then you dilate with 8 or 10 or whatever so this is visit with the debilitation and that's kind of your final product ideal

them so my particular area of interest is a blade of radium ization and what we'd like to do is to break the liver

down into a bunch of little tiny perfused volumes off of a single vascular pedicle or what we call angio zones and those are those allow us to segment out if you only have small volume disease for example like here in

segment three why do I have to treat the entire left to paddock low I can actually treat just that small portion just like it what it tastes only now I'm administering y9t but since it's expendable liver I

can administer doses that are way higher orders of magnitudes higher than what I could if our infusing into the liver just on its own so here's an example of that if you look at this lesion in the right of panic lobe you'll see these

little lines over them what we want to achieve is around a 205 GRA threshold for these lesions that's the red line everything that's south of red in terms of color orange Holly to blue is not cold enough to kill tumor so if we

administer a dose of a tea grade to the lobe we get this coverage which is to be a partial response if I administer 150 grey suddenly that red line gets larger what happens when you administer 400 grey now you've officially covered the

entire lesion and so you're going to lose the adjacent liver at those kind of doses and as well - what what the real question then is not sort of how much dose you give it's you give what you need to to ablate the tumor in its

entirety and you see what the patient's left with if someone's left with anatomically a lot of remnant liver because of how you've segmented out that lesion then go ahead and dose extremely high and that's essentially what we've

seen in pathologic results it's one of the highest things of high school pathological crosa rates you can achieve with a trans arterial therapy it's highly competitive with thermal ablation in the correctly selected bleezin

so this is an example of what it looks like when you segment out a little lesion like this and this patient ultimately went to resection and this was a complete pathologic necrosis but as you can see even it was a cirrhotic

patient we chose a very small volume of liver that we felt the patient would tolerate so that's a blade of vernalization let's take a look at what looks like in real time so we have a little capsular lesion we felt that

ablating this patient who was a potential transplant candidate we felt we can probably with a blade of radium realization so you go in and this is the comb beam CT that looks at a complete enhancement of the lesion within the NGO

zone this is what the MAA looks like when we administer it you can see how it tends to cluster within the tumor but you can see what the adverse territory is the liver adjacent to it this is what the engine room looks like how highly

selective it is the day of and this is what the wine ID actually looks like is the wine 90 doing its job and you can see how conformal it is there's no risk whatsoever to the liver that's adjacent outside of that field of

a maximum of around 11 millimeters and this is a patient at one month with a complete imaging response and this patient never developed a recurrent to the site and what's actually sole mode of treatment for this person's liver

cancer this is how you get complete pathologic response if you look at those little tiny grey dots in there those are actually the spheres within tiny little vessels within the tumor sometimes they go even to the portal branch but you can

see how they're not clustered uniformly but when you make them super hot that allows them to give range where otherwise they would be fine a little bit short so this also applies to the whole lobe this was a patient that had a

very unusual presentation of colon cancer that was invading the portal II we weren't sure what to do with this patient no one was because a very rare occurrence so we said well we would like

to resect him but there's not enough liver and we're not sure if this person's gonna survive because we've never seen portal cancer invading the portal vein so we said let's treat it with the radiation lobectomy and what's

cool here is if you look at the the arteries even though the tumor is invading the portal vein it's bringing arterial supply along with it like a vagabond and that's the conduit that allows us to treat these patients so

when we saw that we felt this patient we good candidate for irradiation lobectomy which is applying an ablative dose of y9t to the entire low not just a small segment in patients where otherwise cannot because of the anatomy the tumor

or if you're trying to shrink that lobe to get that person ready for surgery why because if you look at the size of the lobe on the left from this first image and compare it here you can see how much larger it got what happens is that part

that the surgeon ultimately tens on resecting in volutes over time and becomes completely vitalized and turns into scar tissue so we know that if a surgeon goes in afterwards to cut it out it's going to not result in liver

failure and that level of security allows people to have sir who otherwise wouldn't this patient is not going to have metastatic disease because we followed their blood level markers let me see how low they are and

is going to have enough liver remnant so the patient went to resection and this is the pathologic specimen and this was also a complete pathologic necrosis so I

so these are a lot of slides most limited you know I'm talking I'm talking to you guys I'm talking showing you a lot of technical stuff you know and a lot of slides and I'm gonna talk mostly technical of you know how tips and dips are done kind of a step by step so even

the title it's kind of a workshop step by step of how basically you do you do tips and dips and what and and what are they so in general when you have when you have this is basically kind of out flow spleen spleen dumps blood into the

portal vein the mesentery dumps blood into the portal vein portal vein goes into liver liver does its thing and then dumps the blood into the eppadi veins to the right atrium okay for that because the liver is connected with the spleen

and the guts in series unlike any other organ basically the liver has to be a low-resistance organ because the portal circulation is low-pressure look the liver has to be a low-resistance organ with liver disease especially liver

cirrhosis you actually get increased resistance and in the liver with that disease and you get basically a backup of the blood flow in the portal circulation and increases the pressure in the portal circulation that's kind of

the genesis of or the pathogenesis of portal hypertension backing up circulation the spleen and in the guts then you get ascites and hydra thorax that's kind of think of it as weeping of fluid into the pleural space and into

the and into the perineum part of it is oncotic part of is osmotic basically think of it nutritional and pressure driven causes at the same time we all have potential portosystemic connections in other words they're there but they're

not connected or they're not opened up in plumbing they hold them bleed valves or pressure valves when the pressure is high and you know they start weeping or leaking you know in your in your basements we have the same thing

we have so many portosystemic connections there are about 55 named ones there are innumerable ones that are actually that are actually not named the common ones that we know are because of because of bleeding is esophageal

varices that's the connection usually between the left gastric vein and the azekah can be hazardous system you can also get gastric varices and that's usually connecting between a spleen and the left renal vein through a gas renal

shunts you can get also all sorts of connections even down in the internal hemorrhoids we get actually portal hypertension hemorrhoids and bleeding and so many numerous other shunts that we just don't have time to cut to cover

it to cover all these so the general to the general thought of treating all these complications of portal hypertension is to decompress the system to reduce the pressure and that's along the lines of years and decades of

surgery shunts that were placed and now tips ism largely replaced all these surgical shunts with the exception of Vancouver and Tampa okay that they still do some surgical actually a lot of surgical shunts most most other places

in North America converge to a tip to a tip shunt the the advantage of the tips of over surgical shunts is the usual what we hear is minimally invasive it you know it's a quick recovery less morbidity and mortality areason for

white tips has beaten the surgical shunts is the transplant era all these surgical shunts are actually extrahepatic so when you go for a transplants and liver hits the buckets they actually have to go and shut down

these shunts wherever they created them steena renal portal cable in the tips it goes out with a liver in the bucket so there's no complication of transplantation that's the real advantage of tips over surgical shunts

and that's why it's become very very prevalent in in in North America with a transplant error when approaching gastric varices just briefly another way is a BRT Oh which is to go basically into the left renal vein go up the shunt

and specifically screw rows the stomach and that's not the that's not this kind of subject of our of our discussion here I'm gonna talk to you

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