Year : 2013  |  Volume : 16  |  Issue : 2  |  Page : 83--85

Acute aortic dissection: Pitfalls in the diagnosis

Praveen Kumar Neema 
 Additional Professor Anaesthesiology,SCTIMST, Trivandrum, India

Correspondence Address:
Praveen Kumar Neema
B-9, NFH, Sree Chitra Residential Complex, Poonthi Road, Kumarapuram, Trivandrum - 695 011

How to cite this article:
Neema PK. Acute aortic dissection: Pitfalls in the diagnosis.Ann Card Anaesth 2013;16:83-85

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Neema PK. Acute aortic dissection: Pitfalls in the diagnosis. Ann Card Anaesth [serial online] 2013 [cited 2019 Oct 13 ];16:83-85
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The first documented report of fatal aortic dissection was described by Frank Nicholls in 1760; the patient was George II, the King of England. [1] Until the first part of the 20 th century, aortic dissection was exclusively postmortem diagnosis. [2] On 7 July 1954, DeBakey et al., performed the first successful surgical resection of a dissecting thoracic aortic aneurysm. [3] Interestingly, DeBakey himself underwent and survived open surgical repair of 'Type-A' aortic dissection at the age of 97 year. [4]

Forty percent patients suffering acute aortic dissection (AAD) die immediately before reaching any health-care center and the survivors carry an added mortality of '1%/h'. [2] This high mortality is mainly associated with 'Type-A' AAD (acute dissection involving the ascending aorta). This extraordinary high mortality dictates that the 'Type-A' AAD must be diagnosed as early as possible and managed aggressively. The clinical features suggestive of AAD include severe pain, often described as ripping or tearing; however, patients may describe the pain as sharp or stabbing, and fluctuating, not experienced before, and usually, in a patient not known to have angina. Pain is accompanied by anxiety, tachycardia and hypertension. The pain of 'Type-A' AAD is mid-sternal and known to migrate with the progress of dissection. The dissection can spread in an anterograde or retrograde fashion often involving side branches causing malperfusion syndromes, or aortic insufficiency or rupture resulting in pericardial tamponade. [5] Pain in the back or abdomen may herald dissection of the descending aorta. Patients having associated aortic valve regurgitation or coronary involvement are acutely unstable hemodynamically due to myocardial ischemia and dysfunction; similarly, patients having rupture are also severely compromised due to pericardial tamponade and blood loss. The other important clinical features depend on the extent of dissection and the involvement of major branch vessels resulting in malperfusion ischemia of various organ systems. The risk of death is increased in patients who present with involvement of coronary arteries causing acute myocardial ischemia/infarction, or malperfusion of the brain or develop complications of pericardial tamponade. [6],[7],[8],[9],[10] Other predictors of increased in-hospital death include age ≥ 70 years, hypotension, kidney failure, and pulse deficits. [11] The most common causes of death are aortic rupture, stroke, visceral ischemia, cardiac tamponade, and circulatory failure.

In general, based on clinical presentation, two groups of patients can be identified -hemodynamically stable or unstable. This distinction, hemodynamically stable or unstable, is most important since the further management for both groups is distinctly different. The unstable patients are prepared for urgent surgical intervention while the patient is simultaneously stabilized and investigated. Initially the patient is screened at the bedside by echocardiographic techniques such as transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) with color Doppler interrogation; here, it should be noted that the echocardiographic examination may miss abdominal segments. Conversely, multi-detector-computed tomography (MD-CT) technology allows rapid acquisition of thinly collimated images of the entire aorta during arterial transit of contrast bolus; and 64-, 256-slice CT scanners can image coronary arteries and large and medium-sized vessels of both the chest and the abdomen and have replaced invasive diagnostic angiography. However, CT scan requires patient transport to the diagnostic suite and stable hemodynamic conditions. The aims of imaging are confirmation of clinical suspicion, classification of dissection, localization of tears, and assessment of both the extent of dissection, and the presence or absence of pericardial, mediastinal, or pleural hemorrhage, aortic regurgitation and pericardial tamponade. In the acutely unstable patients, the surgical intervention continues while anesthesiologist acquires definitive information by TEE imaging.

The patients who are hemodynamically stable are thoroughly examined and investigated. In the setting of suspected aortic dissection; biomarkers such as troponin, D-dimers and electrocardiogram (ECG) changes may be used strategically in combination with swift imaging for definitive diagnosis. [12],[13],[14],[15],[15] The absence of both D-dimer elevation and ECG changes is considered specific to rule out AAD. D-dimers when elevated above 500 mg/L appear to correlate with the extent and severity of AAD, but fail to distinguish AAD from pulmonary embolism. For stable patients, any imaging modality will work depending on the availability and expertise. If available, the imaging is done in the following order - 1 TEE with color Doppler flow; 2 MD-CT with computed tomography angiography (CTA) or magnetic resonance imaging with MRA 3D reconstruction. Angiography is rarely required now. TEE imaging in addition to suprasternal TTE has a near-perfect sensitivity and specificity for 'Type-A' AAD; [16] however, TEE, has a blind spot at the proximal arch due to bronchial air. Color Doppler can demonstrate proximal dissection, entry sites and false lumen flow in real time. Arguably, in a hemodynamically stable patient, it is almost always possible to arrive at a definitive diagnosis.

In this issue of Annals of Cardiac Anesthesia, Baloria et al, [17] in an article "Aortic dissection: To be or not to be?" describes false diagnosis of AAD resulting in a patient undergoing sternotomy. The diagnosis was made on CTA. It is important to examine the factors that lead to sternotomy so that such repetition can be avoided in the future. Because of the high mortality associated with 'Type-A' AAD, the diagnosis of aortic dissection itself puts the care givers under tremendous pressure. However, as described earlier, it is very important to identify patients who have no option but to go for urgent surgical intervention and the ones who can be appropriately investigated. In the patient described by Baloria et al., the AAD was not found in the operating room by the attending echo-cardiographer during TEE examination. The diagnosis of AAD was based on CTA. The dissection seen in the image ([Figure 1] shown on page 127) is posteriorly placed whereas dissection flap is usually located in right anterior region that alone should have raised suspicion of false diagnosis. Moreover, the CT image shown in the article, apparently, is a non-gated one which is prone for pulsation artefacts. Perhaps, the artefacts in the ascending aorta could have been overcome if the CT aortogram was done with a cardiac gating. The gated CTA, possibly, would have shown contrast difference between true and false lumen in presence of AAD or no difference in false and true lumen if AAD was absent. The authors have not described detailed preoperative work-up while the patient was prepared for surgical intervention. Therefore, no comments can be made about ECG findings, D-Dimer levels, presence or absence of blood in the pleura; myocardial ischaemia/infarction, aortic incompetence, pericardial tamponade, kidney failure, pulse deficits and malperfusion of the brain. However, the patient was hemodynamically stable for at least 12 hours after the suspected diagnosis of 'Type-A' AAD which clearly indicate possibility of false diagnosis of 'Type-A' AAD. Further, during TEE examination after induction of anesthesia, the aortic root was found intact and the aortic valve function was normal. However, there was massive pericardial effusion and the drained pericardial fluid was serous. At this stage, it was clear that the diagnosis of AAD is inconsistent with the findings and the operating team should have abandoned the surgical intervention and the patient should have been investigated further by other imaging modalities and unnecessary sternotomy could have been avoided. Perhaps, peer-pressure and the inherent nature of the anesthesiologists and the fear of adverse outcome in case of wrong diagnosis would have prevented the anesthesiologist from asserting. It is important to realize that intraoperative TEE in majority centers are performed by anesthesiologists and their experience of TEE may easily surpass that of cardiologists. Moreover, TEE imaging has near perfect sensitivity and specificity in diagnosis of AAD. A scientific approach, sound knowledge and effective communication of the attending anesthesiologist are the key factors that can prevent unnecessary surgical intervention. The present day anesthesiologist has to understand that they are perioperative diagnosticians and they are a vital part of the decision making process; hence, they need to act so as and when required.


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