Aortic Dissection: A case report

Karthikeyan B1, Moosa Kunhi2, Srinivasan. T M3

1Consultant, Cardiothoracic Surgery, Kauvery Hospital, Radial Road, Chennai

2 Senior Consultant, Cardiothoracic Surgery, Kauvery, Hospital Radial Road, Chennai

3Clinical Lead, Cardiac Anaesthesia, Kauvery Hospital, Radial Road, Chennai

Background

Aortic dissection, a critical cardiovascular emergency, characterised by an intimal tear in the ascending aorta, often extending distally. The intimal tear results in separation of the aortic wall layers, specifically the intima and media, leading to the creation of a false lumen within the aorta. Without urgent surgical intervention, catastrophic complications such as haemorrhage, neurological injury and malperfusion are not uncommon. Despite advances in diagnostic imaging and treatment modalities, aortic dissection continues to pose significant challenges in clinical management [1].

This article presents a case report of aortic dissection with catastrophic post-surgical results despite timely intervention highlighting the complexities of perioperative management, potential complications and implications for clinical practice.

Case Presentation

A 36-year-old gentleman presented to our emergency department with six-hour history of excruciating chest pain radiating to his back. The pain started following sudden exertion when trying to hold a heavy falling object. His significant past history include previous mitral valve replacement with a mechanical bileaflet valve at the age of 27 in a different institution for myxomatous mitral valve disease and has been on acenocoumarol since then. He presented again nine months earlier with palpitation and was diagnosed to have grade II paravalvular leak for which he underwent paravalvular device closure with a AVP II device. At the time of procedure, his aortic root was dilated measuring 50mm at the sinus of Valsalva level with moderate aortic regurgitation. His significant other past history includes extrapulmonary tuberculosis and surgery for a suspected club foot when he was a child. He is not a known hypertensive and a lifetime non-smoker.

At the time of presentation here, he was clearly in distress and his blood pressure was over 180/100mmhg measured in both arms. He had no symptoms and signs of any malperfusion related complications. Transthoracic echocardiogram demonstrated a flap in ascending aorta associated with dilated aortic root, moderate to severe aortic regurgitation, and his ejection fraction was normal. His echo did not demonstrate any significant pericardial effusion.

Given the clinical suspicion for an acute aortic syndrome, an urgent computed tomography angiogram of the chest and abdomen was urgently performed, confirming a type A aortic dissection extending from the aortic root  to the level of the infrarenal segment of aorta. His aortic root was measuring 55mm at the sinus level. Origin of brachiocephalic trunk/left common carotid artery (common origin), left subclavian artery, celiac axis and superior mesenteric artery were from the false lumen.

His blood pressure was aggressively brought down. His blood investigations revealed a INR of 3.8. Hence Vitamin K and two units of fresh frozen plasma was transfused.

Fig (1): 3D reconstruction of Pre-op CT Aorta showing Bovine arch with type A aortic dissection extending into abdominal aorta.

Fig (2a): Intraoperative image showing intimal tear at the aortic root, tricuspid aortic valve and amplatzer device in the mitral position. Fig (2b). Bentall Procedure with 23mm St Jude composite graft.

Management

Following optimisation, the patient was taken to the operating room. Due risk of the procedure was clearly explained to the patient and family especially the high risk of mortality and morbidity in his case due to the redo nature of the procedure, preexisting mitral valve prosthesis and his previous paravalvular leak device. High risk of bleeding was also explained due to his elevated INR.

After induction with general anaesthesia, we proceeded with left femoral artery cannulation and a redo sternotomy was performed. Dense adhesions were encountered. after full heparinisation, cardiopulmonary bypass established through femoral artery and right atrial cannulation. Suture line from his previous surgery was noted on the aorta. Heart arrested through direct ostial del-nido cardioplegia. Patient was cooled to 24 degrees Celsius. Extensive dissection noted in his aortic root proximally extending up to the both coronary ostia. His distal aorta was healthy and normal sized. No reentry tears or compression of true lumen noted in the distal aorta. Aortic valve leaflets were tricuspid and non coapting causing the regurgitation. We proceeded with Bentall’s surgery. Transected distal part of ascending aorta false lumen obliterated using PTFE felt. Aortic root replaced with 23mm St Jude Composite graft with classic Bentall type reimplantation of the coronary ostia. Patient was rewarmed and came off cardiopulmonary bypass smoothly with minimal inotropic supports. Patient had diffuse bleeding from all his suture site. Despite blood products and use of topical haemostatic agents, bleeding was persistent. Hence it was decided to pack the chest and close the skin over 3 drains. Patient was transferred to cardiac surgical ICU with stable hemodynamics and blood products were continued postoperatively.  On Day 2, Patient was taken back to theatre for relook and pack removal. On exploration, all bleeding had settled. Hence packs removed, antibiotic wash given and sternum closed in routine fashion. Throughout the procedure patient maintained good hemodynamics requiring only minimal inotropes.

Postoperative Course

However, in the postoperative period, the patient’s clinical course was marked by a cascade of neurological complications. On day 1 following sternal closure, patient developed seizures. Neurologist reviewed the patient was initially loaded with levetiracetam. Despite that, patient had ongoing seizures which was suggestive of status epilepticus whenever we tried to wean propofol. Hence he was started on multiple anti-epileptics including phenytoin and sodium valproate. CT Brain showed multifocal infarcts in bilateral frontoparietal and left temporal deep grey caudate nucleus with suspicious brainstem hypodensities in right pons. EEG showed bilateral cerebral dysfunction. Propofol was increased as per neurologist advice to achieve burst suppression pattern. Repeat CT did not show any progress of disease or features of cerebral oedema.

Patient family counselled regarding the need for long term care including MRI brain to assess the prognosis, followed by the need for early tracheostomy and possibly PEG insertion to maintain nutrition and long term physiotherapy care [2].

However, the family was not very keen to pursue any active treatment for logistic reasons and transferred the patient to their local hospital for further palliative care.

Discussion

Aortic dissections remains a significantly underdiagnosed and underreported condition in India[3]. Importantly, this patient had a history of  myxomatous mitral valve disease, indicative of an underlying connective tissue disorder. Additionally, the patient underwent another cardiac procedure nine months prior at which time a dilated aortic root was documented, yet no further surveillance was pursued. Given the well-documented association between connective tissue disorder, valvular pathology and aortic aneurysm formation, a high degree of clinical vigilance and proactive surveillance could have potentially identified the progression of aortic disease before dissection occurred. [4], [5]

Current guidelines (American College of Cardiology (ACC), American Heart Association (AHA), and European Society of Cardiology (ESC) emphasize regular aortic imaging in patients with known connective tissue disorders or aortic dilation[6]. Current guidelines recommends annual imaging for aortic diameters > 4cm in the presence of connective tissue disorder and more frequent (every 6 months) when aortic diameter is > 4.5cm or rapid growth (>0.5cm/year) [7] even in the absence of formal diagnosis if the patient has previous valvular heart disease [8]. In this case, serial imaging could have provided early signs of impending dissection, allowing for elective surgical intervention before a life-threatening rupture occurred.

Stroke is a devastating yet well documented complication following surgical repair of Type A aortic dissection contributing to significant postoperative mortality and morbidity[9]. The incidence of post-surgical stroke in these patients ranges from 10% to 30%, with both ischemic and haemorrhagic mechanisms implicated. Several factors contribute to the increased risk of stroke. Preoperative malperfusion involving compromised cerebral blood flow due to dissection involving the brachiocephalic or carotid arteries, age, prolonged circulatory arrest, and the presence of atherosclerosis are all associated with higher stroke rates. Additionally, intraoperative factors such as hypotension, embolic events related to aortic manipulation and cannulation, as well as postoperative complications like hypotension and coagulopathy, can further exacerbate the risk. The prolonged hypotension can lead to global cerebral ischemia resulting in watershed infarcts and diffuse brain injury.

Early identification of patients at high risk of postoperative stroke is crucial for optimising perioperative management. Preoperative imaging such as CT angiography can help assess the extent of carotid or vertebral artery involvement Intraoperative monitoring with near-infrared spectroscopy(NIRS) or transcranial doppler can aid in real time detection of cerebral hypoperfusion or embolic events, allowing for immediate corrective measures.

Postoperatively, strict blood pressure control, maintenance of cerebral perfusion and close neurological monitoring are essential in mitigating further ischemic injury.  In this case, the development of stroke may have been influenced by a combination of preoperative factors, intraoperative challenges and postoperative complications such as hypotension, preexisting carotid involvement, prolonged cardiopulmonary bypass and possible embolization during aortic reconstruction.

Conclusion

This case underscores the intricate challenges in managing patients with complex aortic pathologies, especially in the context of prior cardiac interventions. The occurrence of a Type A aortic dissection in a patient with previously documented aortic dilation and underlying mitral valve disease emphasizes the importance of diligent aortic surveillance protocols, particularly in the presence of predisposing factors such as connective tissue disorders. Furthermore, this case highlights the ongoing challenges in preventing and managing postoperative stroke in Aortic dissection patients. Future research should focus on refining risk stratification strategies, optimizing intraoperative neuroprotection techniques, and developing targeted postoperative management protocols to improve outcomes in this high-risk patient population.

References

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