Thoracoabdominal aortic aneurysm

Thoracoabdominal aortic aneurysm

Patient (1) - 69 PMH: 2013 - MVP, aortic root replacement with biological valve (Perimount) and subtotal aortic arch replacement Analysis for oppressive chest complaints reveals large thoracoabdominal aortic aneurysm

Underlying disease? Marfan Ehlers-Danlos Turner s syndrome Polycystic kidney disease Loeys-Dietz syndrome Syphilis / arteritis Traumatic injury

Risk factors for rupture? In total 80% will rupture (10-20% 5-year survival) Higher age and COPD increase rupture risk For aneurysm > 6 cm annual rupture risk 7% For aneurysm > 7 cm 43% will rupture Incidence CAD < 30% in contrast to AAA (> 70%)

Indications for repair Rupture All symptomatic aneurysms regardless of size should be repaired (pain/pressure) However in 95% no heralding symptoms Acute dissection with malperfusion/ other life-threatening complication Symptomatic aneurysm (pain or compression other organs) Enlargement 1 cm/year Absolute size > 6.5 cm or > 6.0 cm with connective tissue disorder

Repair strategies Cardiovascular risk factors Open Endovascular Hybrid Spirometry - most open repairs require single lung ventilation Pre-existing renal function (AKI most important risk factor for early postoperative mortality) CTA with 3-D reconstruction Preoperative workup

Modified Crawford classification Extent I Extent II Extent III Extent IV Extent V

Patient (2) Rapidly progressive TAAA 7.9 cm No underlying other disease (degenerative) Extent II Open repair

Patient (3) Preoperative ICU admission (28/11) Arterial line (right radial artery) Pulmonary artery catheter (PAP 29/13, CI 3.8) ELD (10 cm H2O)

Is CSF drainage useful? CSF drainage No CSF drainage 24 23,7 18 % 12 6 0 12 9,3 7,3 4 4,3 SC damage 30-D mortality In-hospital mortality RCT s N = 3 Cinà CS. J Vasc Surg 2004;40:36-44

Risk factors for paraplegia Overall mortality 10% Previous EVAR/TEVAR Preoperative hypotension Intraoperative hypotension Open distal anastomoses Postoperative complications in 200 patients Paraplegia 17 (8.5%) Cerebral infarction 5 (2.5%) Perioperative MI 1 (0.5%) Pneumonia 5 (2.5%) Atelectasis 19 (9.5%) AKI 5 (2.5%) Acute hepatic failure 3 (1.5%) Bowel ischemia 7 (3.5%) Gastrointestinal bleeding 1 (0.5%) Chylothorax 4 (2%) Vocal cord paralysis (left) 16 (8%) Phrenic nerve paralysis 1 (0.5%) Reoperation surgical bleeding 3 (1.5%) Wongkornrat W. Asian Cardiovasc Thorac Ann 2014

Intraoperative monitoring Insertion of double lumen endotracheal tube Central access with PA catheter for HD monitoring Arterial monitoring of upper and lower extremities with aortic clamping and left heart bypass Lumbar CSF drain in Extent I and II repair (IT pressure < 10 mmhg) - continue for 3-5 days Monitoring of SSEP/MEP with Extent II repair and hypothermic circulatory arrest

Circulatory support LHB with decompression of the proximal circulation in conjunction with distal perfusion through left atrial drainage via the left inferior pulmonary vein and arterial inflow distal to the aortic clamp site usually the iliac system Alternative is partial CP bypass by femoral vein canulation (advanced to RA) and same arterial inflow (includes membrane oxygenation) Circulatory arrest if proximal clamp is impossible with same canulation with total body retrograde perfusion

Additional measures to prevent ischemic injury Permissive or active systemic hypothermia (32 0 C) Cold selective renal perfusion (4 0 C) Reattachment of segmental arteries Sequential aortic clamping Selective visceral perfusion

Extent I Extent II Extent III Extent IV Extent V

Operative procedure 29/11 10.02-15.36 (24 mm Hemabridge from left SA until aortic bifurcation with left-left bypass, CSF drainage, sequential aortic clamping, selective renal perfusion and IC artery reimplantation) left thoracophrenolaparotomy (retroperitoneal approach) - 4 tempi Period 1 - clamp distal LSA and T6 - E to E anastomosis native aorta and prosthesis Period 2 - clamp proximal prosthesis and T12 - reimplantation IC 10 (L/R) Period 3 - clamp distal reimplanted IC10 and infrarenal - reimplantation renal arteries and AMS/TC (single island) Period 4 - clamp infrarenal and above bifurcation - E to E anastomosis native aorta

Left-left bypass LUPV and LFA Stage 1 Stage 2 Stage 3 Stage 4

Postoperative course ICU return 29/11:16.00 Stable hemodynamics (CI 3 l/min/m2, PAP 35/20, MAP > 85-90 mmhg) Paroxysmal AF (rate control - spontaneous SR) Sedation immediate stop - no SC damage Extubation 30/11: 08.00

Postoperative course Stable renal function (creatinine 47 - adequate diuresis) Restart oral intake 30/11 Removal ELD 02/12 Discharge home 12/12

Outcome Open TAAA repair (N) 30-D survival (%) AKI (%) Spinal cord ischemia (%) Crawford 1993 1509 92 9.0 15.5 Coselli 2007 2286 95 5.6 3.8 Safi 2005 355 93 2.1 1.3 Frederick JR. Ann Cardiothorac Surg 2012;1:277-285

CBF manipulation

Tight regulation important Nutrient & oxygen supply Limited capacity for substrate storage High metabolic rate

Principal regulators Cerebral metabolism PaCO2 Mean arterial pressure (MAP) Autonomic nervous system

Metabolic regulation PaCO2 PaO2 (< 50 mmhg) 1-3% /mm CO2 3-6% /mm CO2 Appears to be regulated by CaO2 Highly influenced by PaCO2 >> with PaCO2 and << with PaCO2 CBF different for ICA and VA during PaCO2 and PaO2

ph or PaCO2? ph Pial arteries ph N PaCO2 N ph or PaCO2 N ph N PaCO2 N ph ph ph N PaCO2 N ph PaCO2

Hypoxia Direct vascular mechanisms ph Adenosine? NO? PaO2 Neuron Astrocyte Neurovascular unit

Autoregulation - old and new Old New Slope 0.21 Slope 0.81 Buffering capacity against hypertension is certainly better

Autoregulation Regulation (change in resistance) probably takes places in all cerebral vessels but larger arteries of the brain play a prominent role. This may also be true for the carotid and vertebral arteries Important interaction with PaCO2

Autonomic regulation Cerebrovasculature is extensively innervated by adrenergic and cholinergic fibers arranged in three layers of nerve plexi Sympathetic nervous system (by vasoconstriction) has an important effect on cerebral autoregulation Role of parasympathetic nervous system unclear

If regulation is intact (metabolic, autoregulation and autonomic nervous system, it will be very difficult to manipulate cerebral blood flow

60 P < 0.05 P < 0.05 MCA MFV (cm/sec) 55 50 45 40 110 P < 0.05 P < 0.05 P < 0.05 MAP (mmhg) 100 90 80 70 2,5 P < 0.05 CVR (mmhg/(cm/s)) 2 1,5 1 Baseline Low NE High NE High NE + PE High NE + PE (late) PE Kimmerly DS. Clin Physiol Funct Imaging 2003;23:314-319

Healthy volunteers Ephedrine Dobutamine Dopexamine Dobutamine MAP 25% Before After Before After Before After Ephedrine MAP 25% MAP (mmhg) 86 ± 9 104 ± 9 89 ± 9 106 ± 8 89 ± 11 90 ± 9 Dopexamine CI 25% CI (l/min) NA NA NA NA 2.2 ± 0.3 2.8 ± 0.3 MCAFV (cm/s) 57 ± 18 56 ± 13 52 ± 11 56 ± 13 59 ± 5 62 ± 7 Moppett IK. BJA 2004;92:39-44

3.6 ± 2.9% / mmhg PaCO2 Bisschops LLA. Crit Care Med 2010;38:1542-1547

Cerebral blood flow 80 100 60 75 75 MFV ACM (cm/sec) 40 56 34 SjbO2 (%) 50 55 20 25 0 T = 0 T = 3 T = 6 T = 9 T = 12 T = 18 T = 24 T = 48 Time after admission to ICU (hrs) 0 T = 0 T = 3 T = 6 T = 9 T = 12 T = 18 T = 24 T = 48 Time after admission to ICU CBF during hypothermia < normothermia without evidence of inadequate oxygen supply = normothermia = hypothermia Buunk G. Intensive Care Med 1996;22:1191-1196 Bisschops LLA. Crit Care Med 2010;38:1542-1547

Sepsis 70 60 Before *** After 90 MFV ACM (cm/s) 50 40 30 20 MFV ACM (cm/s) 80 70 10 0 Dobutamine PGI2 60 Dob 0 Dob 2 Dob 4 Dob 6 Dob 8 Dob 10 Dob 0 N = 10 Septic encephalopathy MFV ACM correlated with CI but not MAP Berré J. J Crit Care 1994;9:1-6 N = 14 - Septic encephalopathy MFV ACM correlated beter with CI than MAP CEO2 decreased from 46 ± 3% to 36 ± 4% Berré J. Crit Care Med 1997;25:392-398

Sepsis 120 21 patients with severe sepsis 90 MFV ACM (cm/s) 60 30 NE 7 [2-70] μg/min NE 20 [8-110] μg/min 14 patients had impaired CA defined as a CAI outside 0-2 ( MAP%/ CVR%) Patients with a PaCO2 > 40 mmhg all had impaired CA 0 MAP 65 ± 6 MAP 95 ± 13 Taccone FS. Neurocrit Care 2010;12:35-42

Conclusions Under normal circumstances CBF manipulation with inotropic agents / vasopressors is ineffective CBF regulation under normal circumstances is extremely complex and incompletely understood Under pathological circumstances metabolic regulation of CBF appears to be effective in most circumstances but CA apparently not

Questions Group 1: How can we measure cerebral autoregulation in daily practice? Group 2. What is the evidence that increasing MAP with NE increases CBF in patients with SAH and delayed ischemia?

Questions Group 3: Is cerebral autoregulation intact in comatose patients after a cardiac arrest? Group 4: Design a RCT investigating whether increasing CBF in comatose patients after cardiac arrest would be beneficial