**2. Background summary of the literature**

## **2.1 Intraoperative cerebral embolism and brain dysfunction**

Whilst clinical stroke is relatively infrequent in cardiac surgery (1-3%) (Calafiore, Di Mauro et al. 2002; Douglas and Spaniol 2009; Rosenberger, Shernan et al. 2008; Shroyer, Coombs et al. 2003), such events can be properly viewed as major cerebral injury. Subclinical brain injury on the other hand is not often clinically apparent but may be detected by subtle neurocognitive testing and this is frequently present (20-60%) (Hammon, Stump et al. 1997; Mahanna, Blumenthal et al. 1996; Zamvar, Williams et al. 2002). MRI studies post cardiac surgery similarly highlight a far higher frequency of cerebral embolic events then the clinical assessment of neurological status would suggest (Deslauriers, Saunders et al. 1996; Djaiani, Fedorko et al. 2004; Vanninen, Aikia et al. 1998). Brain injury may be caused by other factors related to cardiopulmonary bypass, systemic inflammatory response syndrome, tissue oedema, air embolism, post-operative hypotension, anaesthetic agents used, ischaemia and reperfusion injury, or alternative causes of embolism. Nevertheless, the *predominant cause* of embolic brain injury reflects surgical manipulation of the atheromatous aorta and thus offers the greatest prospect for changing outcome.

Epiaortic Ultrasound Assessment of the Thoracic Aorta in Cardiac Surgery 37

patients) is assuming that the presence of important aortic atheroma is predictable. Indeed the unpredictability of the presence, location and severity of aortic atheroma is the most powerful argument in favor of routine comprehensive ultrasound examination of the entire thoracic aorta being performed. Specifically, the absence of atheroma seen in the descending aorta or proximal aorta by TOE does *not always predict* the absence of clinically important atheroma in the distal ascending aorta or proximal arch (the TOE "blind spot") (Royse,

We described six zones for the thoracic aorta; three in the ascending aorta, two in the aortic arch and the descending aorta. TOE typically images zones 1-2 and 5-6 well; and epiaortic echocardiography images zones 1-4 well. For reference, most aortic cannulations and clamping occurs in zones 3-4; proximal aortic graft anastomoses in zone 2 and aortic incision for valve replacements in zone 1. An intra-aortic balloon pump will be deployed in zone 6. Within these zones, the site of the atheroma is further subcategorised into cross sectional

We found that the prevalence of atheroma increased with distance from the aortic root. There was a marked increase in frequency and severity distal to the aortic arch. Increasing age resulted in greater prevalence. Considering moderate or severe atheroma in zones 1-4, the prevalence was 29% in patients aged 70-79, and 34% in those aged more than 80 years

A variety of definitions have been published, but most commonly this simple classification is used, Table 1 (Royse, Royse et al. 1998). The greater the severity of atheroma, the greater the likelihood that manipulation will result in embolism; excepting that most believe embolism is unlikely to arise from "mild" atheroma. In clinical practice the term "clinically

The morphology of the atheromatous plaque may further predict the likelihood of embolism. Without good data, it would seem intuitive that a soft friable, frond-like atheromatous plaque is more likely to break free and embolise, than a flat, fibrous plaque.

The detection of aortic atheroma does not directly lead to the avoidance of atheroma dislodgement and embolism. The actual avoidance of dislodgement requires a change to the surgical strategy. Thus the detection of atheroma is the important first step, and allows a

quadrants of the aorta - anterior, posterior, left or right lateral.

important atheroma" generally refers to moderate or severe atheroma.

Nil Intimal thickening < 2 mm Mild Intimal thickening 2 – 4 mm Moderate Flat intimal thickening > 4 mm Severe Complex intimal thickening > 4 mm or any mobile atheroma

Grade Criteria

**3. Strategies to avoid aortic atheroma dislogement** 

**2.5 Assessment of aortic atheroma severity** 

Table 1. Classification of atheroma grade

Royse et al. 1998).

(Royse and Royse 2006).
