The International Registry of Acute Aortic Dissection (IRAD) data revealed that 4.6% of AAAD patients presented with cerebrovascular accidents and 2.9% of those patients presented with coma . Another report also suggested that neurological dysfunction was observed in 20.3% of patients with AAAD . A complicated stroke has a strong impact on morbidity and is associated with higher rates of postoperative complications and a significantly longer hospital stay . Pacini et al. suggested that dissection of supra-aortic branches was an independent predictor of postoperative cerebral morbidities with an estimated odds ratio of 2.18 . Such cerebrovascular events are a severe problem that need to be solved in order to improve the prognosis of patients with AAAD. In this case, the preoperative image examination revealed that the false lumen in the right common carotid artery was thrombosed and the right middle cerebral artery was occluded because of static cerebral malperfusion due to AAAD.
Incidence of neurologic events during CPB has been found in 2.8% of patients . Surgical repair for AAAD requires CPB and full heparinization, frequently with concurrent deep hypothermia and circulatory arrest. This can lead to hemorrhagic conversion, which results in worsening of neurological outcomes. Reperfusion injuries also occur in the cerebral ischemic regions. In the present case, the initial diagnosis was isolated extensive cerebral infarction without a diagnosis of AAAD. It developed into hemorrhagic infarction with brain edema, and emergent decompressive craniectomy was performed without hesitation. After the definitive diagnosis of acute extensive cerebral infarction due to critical cerebral malperfusion of AAAD, there was no choice over strict blood pressure control and brain protection therapy, given the problem of brain hemorrhage and edema caused by emergent aortic repair.
Our concern was that, while being on standby for elective surgery, emergent or urgent surgery might be required in the setting of rupture or progression of dissection, which would result in more severe cerebral dysfunction. Strict blood pressure control is necessary to prevent rupture and progression of the dissection. In the present case, we attempted to reduce the possibility of lethal aortic events by using strict therapies for hypertension and brain edema for 9 weeks. Since the diameter of the ascending aorta was 62 mm and sufficient recovery of her neurological conditions had been recognized, elective aortic repair was finally decided upon.
Patients with severe brain injury and edema usually require emergent surgical intervention; decompressive craniectomy is the procedure of choice to release intracranial pressure and open the brain cavity for further surgical treatment . There is growing evidence supporting the efficacy of decompressive craniectomy, including the reduction of intracranial pressure and prevention of brain edema . The defective dura area may be left open or sealed with artificial dura substitutes. In addition, during prolonged CPB with deep hypothermia, brain edema theoretically worsens . As far as we investigated, regarding brain herniation during and after aortic repairs, several case reports described that decompressive craniectomy is required after aortic repair for AAAD [9,10,11], whereas there are few reports of aortic repair after decompressive craniectomy for critical cerebral infarction secondary to AAAD. There is a case report of delayed repair of AAAD 4 months after closing craniotomy . Aortic repair with craniectomy left open, as in the present case, is extremely rare. Regarding brain protection for critical cerebral malperfusion due to AAAD, prompt ligation of the right common carotid artery to prevent brain edema and bleeding during open aortic repair was recommended as a useful option . In contrast, Okita et al. recommended direct right common carotid artery cannulation for patients with cerebral malperfusion . Definitive treatment for AAAD patients with severe cerebral malperfusion has not yet been established.
In the aortic repair, the core temperature was set to a bladder temperature below 25 °C (lower than the usual 28 °C) for more meticulous brain protection. In addition, the SCP perfusion temperature was also lower (20 °C) than the usual temperature of 23 °C. For such a high-risk case, limited hemiarch replacement was performed to reduce the cerebral ischemic time because the primary entry was located at the lesser curve of the proximal arch. Fortunately, the patient did not have a new neurological disorder, although an increased amount of cerebrospinal fluid in the cranial space was recognized on the postoperative CT scan. Owing to CPB and SCP with deep hypothermia, preoperative open decompression craniectomy with a compliant artificial dura seemed to be effective in releasing the intracranial pressure. Moreover, continuous monitoring of bilateral rSO2 by NIRS was also useful for real-time monitoring of cerebral perfusion during the ICU stay as well as the stay in the operating room.