BCC4: Plunkett on Thoracic Aortic Dissection

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Budding cardiothoracic intensivists will enjoy this talk by Brian Plunkett on thoracic aortic dissection given at Bedside Critical Care Conference 4. For the audio access and similar talks, head over …

Budding cardiothoracic intensivists will enjoy this talk by Brian Plunkett on thoracic aortic dissection given at Bedside Critical Care Conference 4. For the audio access and similar talks, head over to intensivecarenetwork.com

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  • So an interesting topic for a number of reasons.
    I was a little surprised to see that Teik Oh only has 20 lines on Aortic dissection.
    It is common: 3 x incidence of ruptured abdominal aneurysm
    It is highly lethal: 90% of type A’s and 30% or type B’s
    We can make a big difference to outcomes with good clinical acuity, rapid diagnosis and prompt medical management
  • So this is not how the patient feels
    This is how the surgical registrar feels asking for an ICU bed for the ‘usually really well’ octogenarian presenting with an acute dissection. But there is some cause for hope – the population is aging, ICUs are expanding, admission criteria seem to be softening, and as struggling surgeons we might get more work.
  • All jokes aside this is high morbidity and resource taxing stuff, and we all have an obligation to both be realistic about outcomes and resource constraints.
  • When I said it kills, I wasn’t joking – this is from a few weeks ago.
    1min intervals at the top.
    Gone in 60seconds! – about 20seconds actually.
    This is free rupture into the left chest, and you can see the futility of the near immediate CPR with an empty heart.
    Similarly I’ve had people become hemiplegic while I’m consenting then, or die while being check in at the front of theatre.
    Must expedite medical management and (if appropriate) transfer to surgical repair quickly
  • So here is a little primer on aortic dissection, before I try and walk you through some of the surgery. I don’t think you need to know a whole lot about the surgery, but you need to be able to understand the op report.
    So Aortic Dissection: blood leaves the combination of a primary aortic wall disease and a hypertensive or hypervolaemic patient precipitates an intimal tear through which blood propagates along the weak medial layer producing a false channel. The forces are high and the destruction is impressive. Multiple re-entry tears are often present in the descending aorta. Most entry tears are in ascending aorta (60%), 10% in arch, rest in descending
    - this disease is not your friend, it is hear to hurt you!
  • So as I said you really need an elevated blood pressure or blood volume and in most cases a concurrent disease of the aortic wall:
    But if your like me, this all doesn’t really help. It’s nice hen someone comes in with rendering chest & back pain an says their Marfanoid, with a nappointment in a week to get their ascending aorta repaired – but it’s not that fair
  • SO this is what you see intraoperatively.
    Left: Angry looking ascending Ao with blood swirling around in adventitia.
    Care decompressing pericardium, handling – rupture
    Right, now circulatory arrested and opened aorta to see clot in false lumen, and the tear through to the true lumen.
  • May shear off or extend into branch arteries – here the flap is seen in the SMA with the red arrow and further down there is no flow in the vessel with white arrow – that’s bad right! We can also see a renal branch infarction.
  • This CT demonstrates a couple of things –
    There is nearly always a mediastinal haematoma with a dissection. If you see artifact on CT, and there is a mediastinal haematoma, don’t dismiss it. In this case it is compressing the Right PA – therefore pressurised!.
    This thin adventitial layer on the false lumen can rupture, note the blood in the left chest.
  • There are two other entities related to aortic dissection collectively called Acute aortic syndromes
    – not to be outdone by cardiologists creating acute coronary syndromes, we created our own acute syndrome
    Penetrating atherosclerotic ulcer: may rupture in over 40%.
    Acute intramural haematoma: may rupture in up to 35% of patients
    - these from penetrating ulcers or rupture of the vasovasorum in the aortic wall – no entry tear!
    The syndromes in ascending are usually treated with emergent / urgent operation, and frequent repeat imaging and endovascular / surgical treatment in the descending aorta.
  • Classification: 2 types: DeBakey and Stanford.
    Just learn Stanford – simple, and differentiates on management as well.
    Stanford A – a operation (doesn’t matter how far it goes around),
    Stanford B – boring medical management. ‘We really nail our aid memoirs in surgery!’
    There is a little controversy over isolated arch involvement. In most centres it is classified and managed as for Type A. If it is just watched, the patient must have early repeat imaging (within 12-24hrs, and become pain free with medical therapy.
    2/3’s are Type A’s
  • Clinical features:
    ‘Tearing’ or ‘ripping’ pain –
    Ascending – retrosternal or neck,
    Descending interscapular,
    can migrate as dissection extends, persistent (doesn’t go away),
    other symptoms from branch malperfusion
    (stroke, paraplegia, anuria, mesenteric ischaemic symptoms, ischaemic limbs,
    Dyspnoea from acute aortic regurgitation & heart failure, and /or evolving tamponade
    About 10% are silient – syncope, hypotension, neuro deficit (older, steroids, marfans)
    Will be asked about diastolic murmur, ECG changes, BP and pulse differentials, pain, pericardial / pleural effusion, AR
  • Diagnosis:
    CXR wide mediastinum, is the classic, but may see pleural eff, double aortic shadow, loss of aortic knuckle etc.
    ECG, ST depression is common, ST elevation rare – hence thrombolytics ok in elevation in absence of ischaemic leg or stroke, often have no specfiic changes – therefore it is not surprising the people get antiplatelets and clexane
    TTE has a role to detect root flap, acute AR, tamponade, but TOE much greater sensitivity (but not a first line). Aortography once the gold standard now has essentially no role.
    CTA is where we want to go, diagnosis, extent, malperfusions, complications.
    MRI is only for diagnostic delemmas, or where CTA contraindicated or CTA & TOE equivocal and very suspicious - ideally patient stabilised.
    Legends amongst bosses of sternotomies for Type A dissections with normal looking aorta and magical resolution of dissection on periop TOE.
    CT examples – unusually a visible entry tear in ascending
  • Medical therapy:
    B-blockers to decrease dP/dT, which is essentially the rate of rise of the arterial pressure impulse and the driven impulse extending the dissection, the inotopy of the heart if you like. This is the cornerstone of medical therapy – B-blockers decrease the rate of rise, and by decreasing the rate, you decrease the frequency.
    Nitroprusside, more titrateable and potent than GTN, but in isolation causes cardiac response of increased dP/dT, so must B-block first – can’t use B-blockers – test dose esmolol, or use diltiazem for a weaker effect. Transition over time to oral agents. Terrible case with potentiation in type B can intubate, and use more potent opioid agents (Remifentanyl) if can’t use or control with B-blockers.
    Care with AR – tachycardia is likely compensatory, and B-blockade may precipitate collapse
  • Type B
    80% survival to 1 year. Need close follow up for risk of dissection progression or aneurysm formation.
    Complications that dictate immediate operation (interposition graft reapproximating the layers, distal anastomosis): haemothorax / rupture, persistent pain not relieved with antihypertensive therapy, threatened limb ischaemia, paraparesis (if paraplegic – not an indication for operation, completed), renal failure,
  • So this is what we hope to achieve (spoken like a true surgeon - of course we also want the patient to recover and go home!)
    Principles:
    Replace ascending aorta,
    replace or repair aortic
    Replace arch if site of tear or significantly aneurysmal.
  • The real trick is in reconstituting the layers distally, that may be very friable and a bit like wet tissue paper
    Most use a buttress, in this case the adventitia rolled in, but more commonly teflon, or bovine or autologus pericardium
    Now sewing the aorta is why they bleed. Contrary to popular belief, it isnot always because the surgeons didn’t put enough sutures in.
    It si also why sometimes they do not want to take them back – because they can’t fix it surgically
  • A. supracommissural – STJ up to innominate
    B. Hemiarch, undermines the arch
    C. Total arch, with or without Correl patch, individual anatmosis, or as in D a trificated debranching graft.
    E. Frozen elephant trunk, - traditional elephant trunk, now antegrade deployed distal stents
    Now if your going to operate on the central circulation, you need to be on bypass and for the arch on circulatory arrest
    Process: establish CPB, cool down (with a vent), when very cold establish DHCA, and do the distal anastomosis, come back on bypass either through fem or a side arm on the graft, and do the proximal / root while rewarming. At 18 degrees you have around 30min to get the distal completed before you enter the territory of irrevecable cerebral injury
  • TO prolong that protected interval surgeons employ one of three strategies
    Retrograde CP (unusual now)
    Direct antegrade (left)
    Axillary antegrade (right)
  • Root:
    Usually want to do the minimum to render a competent aortic valve and get them off the table (they don’t usually start well!)
    If the root architecture is destroyed, degenerated, or bicuspid then it is excised and one of three approaches taken
    Usually people proceed to tried & true Bentall’s procedure
    Can do a valve sparing repair (Yacoub or David procedure) unusual as time consuming.
    Often times simply resuspending the commissures and reconstituting the root with glue, sutures is enough
  • This is very morbid stuff, and by the very nature of the dissection, cooling and rewarming, as well as the technical aspects of the surgery takes along time
    Patient exposed to extracoporeal circuit for a long time, large amount of inflammatory and coagulation system activation
  • With the advent of hybrid operating theatres, one thing we may see more of is
    Debranching the arch, and stenting right across the whole arch
    Outcomes have not been overwhelming thus far, and it exposes the patient to the complications of stents: leaks etc but may be coming in the future
  • Finally Type B interventions
    When complicated these can be managed by open surgery, but usually when aneurysmal, and that is out of the remit for this talk.
    Otherwise, they are usually managed with a limited deployment of a covered stent graft to close the intimal tear
    Paraplegia is a constant concern due to the variable intercostal supply to the spinal arteries, and so caution is taken
    Self expanders. 15-20% mortality in a complex group
     
    Inaddition: Direct stents to obstructed branch arteries, percutaneous balloon fenestration, stenting across distal re-entry tear if true lumen threatened, - tailored approaches by specialist groups,
    One approach to these complicated patient is early endovascular mamangement to resucitate the patient and malperfused organs with a delayed definitive surgical approach once patient recovered.
  • -> that is surgical coronary revascularization with and without the use of the cardiopulmonary bypass machine…
    So my goal from the outset was to give you an insight into the technical challenges and potential advantages of the OPCAB approach to coronary revascularisation, demonstrate that not all OPCAB is created equal, and explain the limitations of the literature to date. To finish Ed has kindly given us a preview of some soon to be published local data that seems to support the premise that in expert hands anaortic OPCAB can offer significant advantages.
  • -> that is surgical coronary revascularization with and without the use of the cardiopulmonary bypass machine…

Transcript

  • 1. Brian Plunkett Advanced Trainee in Cardiothoracic Surgery Dept Cardiothoracic Surgery, RNSH Aortic Dissection Bedside Critical Care, Cairns, 2013
  • 2. Pathogenesis Entry tears: Asc Ao 60%, Arch 10%, Descending 30% Intimal tear, propagates in medial layer antegrade (90%)
  • 3. Pathogenesis: Risk Factors A: age, atherosclerosis, aneurysm B: bicuspid aortic valve (fibrillin def.) blood pressure (hypertension) C: connective tissue disorder Marfan’s, Ehlers-Danlos, Lewy Deitz D: degenerative cystic medial degeneration E: trauma, iatrogenic, surgery, pregnancy 2-3 / 100,000 age 60-70 M:F >2:1
  • 4. Pathogenesis
  • 5. Pathogenesis
  • 6. Pathogenesis
  • 7. Pathogenesis: Acute Aortic Syndrome Penetrating atherosclerotic ulcer & acute intramural haematoma
  • 8. Classification
  • 9. Presentation Pain – ‘ripping’, ‘tearing’ - may radiate to back Symptoms of organ malperfusion - MI, stroke, mesenteric ischaemia Dyspnoea -AR, tamponade, haemothorax Hypo or hypertension, BP differential AR murmur Absent distal pulses
  • 10. Diagnosis 60% 95% 98%99%
  • 11. Management - Medical Medical & drug history, clinical exam: document neurology and pulses Normalise the blood pressure (care with AR) Defer intubation until theatre if possible Opioids, invasive monitoring Pray they haven’t given aspirin, clopidogrel, clexane
  • 12. Type A Essentially all patients considered (age, met’s) Resect primary tear, stabilize aortic wall End organ protection, correct malperfusion Prevent life threatening rupture, tamponade, AR, coronary dissection Type B Reserved for ‘complicated’ cases Rupture or impending rupture (pain, eff.) Threatened or evident malperfusion Sometimes controversial Surgery
  • 13. Surgery
  • 14. Surgery
  • 15. Approaches to the Ascending Aorta
  • 16. Cerebral perfusion strategies
  • 17. Approaches to the Aortic Root Bentall’s David & Yacoub
  • 18. De-branching and replacing ascending aorta
  • 19. De-branching and stenting the arch
  • 20. Stenting Type B dissections 10% 30 day medical mortality, 25% with surgery, paraplegia 15%+
  • 21. Key points Goals • early diagnosis, initiate therapy before confirmation • atypical NSTEMI – think AoD before anticoagulation • early path to definitive therapy • the right operation for the right patient Pitfalls • misdiagnosis: MI, stroke, ischaemic limb embolism • delayed care • failure to control, or adequately control HR & BP