Original Article

Acute subdural hematoma after aortic surgery: A retrospective comparative study

Asian Cardiovascular & Thoracic Annals 2015, Vol. 23(1) 24–30 ß The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492314531138 aan.sagepub.com

Hiroaki Osada1, Akira Marui2, Shiro Tanaka3, Katsuaki Meshii1, Motoaki Ohnaka1 and Hiroyuki Nakajima1

Abstract Background: Acute subdural hematoma is uncommon following open-heart surgery, but may result in increased mortality and morbidity. Methods: A retrospective analysis was performed involving all patients who underwent thoracic aortic surgery from January 2009 to February 2013. There were 53 patients who had thoracic aortic repair with open distal anastomosis and required selective cerebral perfusion with or without retrograde cerebral perfusion. We evaluated the incidence of postoperative acute subdural hematoma. The patients were divided into two groups: a subdural hematoma group who had symptomatic subdural hematoma postoperatively, and a non-subdural hematoma group who had no subdural hematoma. The variables were compared between the 2 groups. Results: Eight (15.1%) patients had a transient symptomatic subdural hematoma; none required surgical evacuation of the hematoma. There were significant differences between the two groups in terms mean and maximum retrograde cerebral perfusion flow, and the volume of intraoperative platelet transfusion. Multivariate analysis revealed that a significant risk factor for acute subdural hematoma following thoracic aortic surgery was the amount of intraoperative platelet transfusion (odds ratio ¼ 0.9, 95% confidence interval: 0.81–0.98, p ¼ 0.015). Conclusions: This retrospective study demonstrated that the subdural hematoma group received fewer units of platelets, thus it appears to be important to give platelets appropriately. Strict flow regulation or avoidance of retrograde cerebral perfusion is suggested.

Keywords Aortic aneurysm, thoracic, Hematoma, subdural, acute, Platelet transfusion, Postoperative complications

study was to evaluate the incidence and risk factors of acute SDH in these operations.

Introduction Acute subdural hematoma (SDH) is characterized by an acute hemorrhagic collection in the subdural space. The most common etiology of SDH is head trauma.1,2 Acute SDH following open-heart surgery is relatively rare,3,4 but it may result in increased mortality and morbidity perioperatively. Because much emphasis has historically been placed on hypoperfusion by cardiopulmonary bypass (CPB) or microembolism as etiologies of neurological dysfunction after open-heart surgery, few studies on postoperative acute SDH have been reported, especially in thoracic aortic surgery. Because in recent years, we have experienced some acute SDH after thoracic aortic repair, the aim of this

1 Department of Cardiovascular Surgery, Mitsubishi Kyoto Hospital, Kyoto, Japan 2 Department of Cardiovascular Surgery/Translational Research Center, Kyoto University Hospital, Kyoto, Japan 3 Translational Research Center, Kyoto University Hospital, Kyoto, Japan

Corresponding author: Hiroaki Osada, MD, Department of Cardiovascular Surgery, Mitsubishi Kyoto Hospital, 1 Katsuragoshomachi, Nisikyo-ku, Kyoto 615-8087, Japan. Email: [email protected]

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Patients and methods A retrospective analysis was performed involving all patients who underwent thoracic aortic surgery including the ascending aorta and aortic arch at Mitsubishi Kyoto Hospital, Kyoto, Japan, from January 2009 to February 2013. There were 53 patients (27 men, 26 women; mean age 68.0  10.8 years; age range 42–87 years) who underwent thoracic aortic surgery with open distal anastomosis and required selective cerebral perfusion (SCP) with or without retrograde cerebral perfusion (RCP). Only one patient had a history of Marfan syndrome. We evaluated the incidence of postoperative SDH, patient histories, perioperative laboratory test results, and CPB data from all 53 patients’ records. The diagnosis of acute SDH was based on brain computed tomography (CT) findings and confirmed by a radiologist and physical examination by a neurologist. The patients were divided into two groups: the SDH group had symptomatic SDH postoperatively, and the non-SDH group had neurologically asymptomatic or no SDH detected by brain CT. We compared several perioperative variables between the two groups. A median sternotomy, moderate hypothermia, circulatory arrest, and SCP were performed in all cases. At the time of surgery, moderately hypothermic CPB with arterial (39 direct ascending aorta, 3 left ventricle apex, 5 axillary only, 3 femoral only, 3 combined axillary and right femoral) and bicaval venous cannulation was initiated, and core cooling was begun. At 25 C, the CPB flow was discontinued. During this period of systemic circulatory arrest, only a short duration of RCP from the superior vena cava cannula was started in 36 (67.9%) cases, increasing the flow to 20–30 mm Hg of central venous pressure to avoid air or debris from coming into the arch vessels. We routinely used this, but in some cases, especially when the superior vena cava cannula contained air, we could not apply RCP. After the SCP cannula was inserted into the arch vessels (brachiocephalic artery, left common carotid artery, left subclavian artery), RCP was discontinued. Total SCP flow was maintained at approximately 500 mLmin1. For total arch replacement, a straight graft (elephant trunk) was inserted into the proximal descending aorta and anastomosed with 4/0 polypropylene sutures. The proximal elephant trunk was then pulled and anastomosed to the branched graft. After restarting the systemic circulation, the arch vessels were reconstructed. Finally, the proximal side of the branched graft was anastomosed to the native aorta, usually just above the sinotubular junction. For ascending aorta replacement, one branched graft was anastomosed just below the brachiocephalic artery, and systemic circulation was restarted. The proximal aorta was then reconstructed. Without regard to the preoperative platelet count, we routinely prepared 20–30 units of platelets for

transfusion, but the amount depended on the surgeon’s choice. All patients were transfused intraoperatively. Perioperative baseline patient data were selected as variables as well as factors that might influence perioperative brain injury and hemostasis. All continuous variables are expressed as mean  standard deviation. Differences in baseline characteristics between the two groups (with and without acute SDH) were examined by analysis of variance, Fisher’s exact test, or the unpaired Student’s t test. Logistic regression models were used to identify the risk factors for SDH. Odds ratios, 95% confidence intervals, and p values are reported. Confounding factors in the logistic regression included age, age >75 years, sex, body surface area, diagnosis of acute aortic dissection, emergency surgery, prior hypertension, hyperlipidemia, diabetes, stroke, carotid artery disease, peripheral arterial disease, atrial fibrillation, chronic obstructive pulmonary disease, chronic kidney disease (defined as estimated glomerular filtration rate 75 years Male sex Body surface area Diagnosis of acute aortic dissection Emergency surgery Hypertension Hyperlipidemia Diabetes Prior stroke Chronic kidney disease Hemoglobin Platelet count Total arch replacement Operation time CPB time Aortic crossclamp time Circulatory arrest time Minimum body temperature Pre-CPB systemic blood pressure Pre-CPB central venous pressure Pre-CPB ACT Post-CPB ACT SCP duration Max SCP flow Mean SCP flow RCP duration Max RCP flow Mean RCP flow Blood loss Red blood cell transfusion Fresh frozen plasma transfusion Platelet transfusion

1.025 (0.955–1.116) 1.329 (0.245–6.215) 0.957 (0.203–4.502) 1.239 (0.039–38.69) 0.292 (0.039–1.423) 0.318 (0.043–1.555) 2.844 (0.441–55.881) 1.855 (0.337–8.886) 2.000 (0.092–18.403) 2.000 (0.092–18.403) 1.649 (0.302–7.83) 1.039 (0.709–1.569) 1.117 (0.991–1.276) 2.4 (0.491–17.603) 0.996 (0.988–1.003) 1.000 (0.988–1.012) 1.004 (0.99–1.018) 1.026 (0.995–1.062) 0.834 (0.546–1.279) 0.968 (0.912–1.018) 0.981 (0.760–1.208) 0.998 (0.991–1.001) 1.006 (0.984–1.026) 1.011 (0.998–1.026) 1.001 (0.994–1.007) 1.005 (0.996–1.014) 1.000 (0.996–1.002) 1.004 (1.001–1.008) 1.006 (1.001–1.013) 0.998 (0.994–1.001) 0.920 (0.78–1.054) 0.776 (0.559–1.012) 0.915 (0.839–0.987)

0.508 0.724 0.954 0.901 0.132 0.163 0.302 0.454 0.590 0.590 0.540 0.845 0.069 0.291 0.313 0.997 0.503 0.099 0.393 0.223 0.867 0.152 0.570 0.087 0.691 0.277 0.961 0.016 0.02 0.352 0.253 0.061 0.022

Odds ratio (95%CI)

p value

1.004 (0.996–1.013) 1.001 (0.988–1.014)

0.280 0.860

0.9 (0.808–0.98)

0.015

ACT: activated clotting time; CI: confidence interval; CPB: cardiopulmonary bypass; Max: maximum; RCP: retrograde cerebral perfusion; SCP: selective cerebral perfusion.

SDH following open-heart surgery in 1975. They noted that possible mechanisms include tearing of the bridging veins, which results from a fluid shift to the brain, and a bleeding tendency induced by heparin. On the other hand, Osaka and colleagues9 suggested that a possible mechanism of acute SDH is cerebral dehydration and volume change induced by massive urine excretion. Once bleeding occurs, the hematoma may enlarge rapidly secondary to a bleeding tendency following postoperative consumption coagulopathy.

They also stated that predisposing factors for acute SDH are female sex and advanced age. Whether the mechanism of SDH in thoracic aortic surgery is identical to that in general open-heart surgery with CPB has not been determined. Thoracic aortic surgery often requires a special procedure for brain protection, such as hypothermic CPB, SCP, and RCP. We used only a short duration of RCP from the beginning of systemic circulatory arrest until SCP was started, to prevent thromboembolism with debris or air from arch vessels.

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To maintain an RCP pressure of 20 to 30 mm Hg, the RCP flow volume may need to be increased. This may injure bridging veins. For brain protection during thoracic aortic surgery, SCP and RCP are widely accepted procedures. RCP was first introduced in 1990.13,14 Some studies have shown that even intermittent pressure augmentedRCP, intermittently elevating the central venous pressure up to 45 mm Hg, has advantages for patients with severely impaired brain circulation.15,16 However, Okita and colleagues17 reported that the prevalence of transient brain dysfunction was significantly higher in RCP than in SCP. Based on a recent Japanese comparative study of antegrade and retrograde cerebral perfusion using the Japan Adult Cardiovascular Surgery Database, transient neurological dysfunction occurs more often in RCP (5.8% of 499 RCP cases).18 However, they did not discuss flow volume or pressure of antegrade or retrograde cerebral perfusion. The results of our study indicate that the transient neurological dysfunction which they addressed, may have been induced by acute SDH. In our analysis, higher RCP flow volume index may be one of the causes of acute SDH after thoracic aortic surgery (cut-off values were 360 and 198 mLmin1m2 for maximum and mean RCP flow volume index, respectively). We should have maintained a lower RCP flow volume index to maintain backflow from the arch vessels when establishing SCP, or not performed RCP, using only SCP for brain protection and prevention of SDH. Further investigation with a prospective study may be needed. On the other hand, postoperative over-anticoagulation has been suggested as a cause of SDH. Thoracic aortic surgery is often complicated by massive bleeding associated with coagulopathy. Although there were no significant differences between the two groups in preoperative warfarin or aspirin administration or preand post-CPB activated clotting time, the SDH group received a significantly lower platelet transfusion volume. Appropriate platelet transfusion might avoid SDH. The higher preoperative platelet count group may have received a smaller platelet transfusion. Although there was no clear relationship between the SDH site and symptoms, all patients in the SDH group fortunately had small hemorrhages, did not require surgical evacuation, and improved without any further intervention. Some patients who undergo concomitant coronary artery bypass grafting and valve surgery will need postoperative antiplatelet or anticoagulant administration. Although the symptoms are transient, a decreased incidence of acute SDH is preferable. Few reports on thoracic aortic surgery discuss whether the use of RCP influences acute SDH. This study shows that even a short duration RCP may

cause SDH, suggesting the use of strict RCP flow regulation or even avoidance of RCP. Furthermore, our study indicates that it is important to give platelets appropriately. Funding This research received no specific grant from any funding agency in the public, commerical, or not-for-profit sectors.

Conflict of interest statement None declared

References 1. Osborn AG. Acute Subdural Hematoma. In: Osborn AG, Hedlund GL, Blaser SI, Illner A, Slzman KL, Harnsberger HR (eds) Diagnostic Imaging Brain. Vol 2, 1st ed. Salt Lake City: Amirsys Inc, 2004, pp. 14–17. 2. Victor M and Ropper A. Craniocerebral trauma. In: Victor M, Ropper A (eds) Adams and Victor’s Principles of Neurology, 7th ed. New York: McGrawHill, 2001, p. 925. 3. Kasahara S, Sakai A, Isomatsa Y, Akishima S, Nie N and Oosawa M. Subdural hematoma complicated after open heart surgery: a case report of two cases with successful treatment. Kyobu Geka 1994; 47: 732–735. 4. Maruyama M, Kuriyama Y, Sawada T, et al. Subdural hematoma following cardiovascular surgery. Jpn J Stroke 1987;9:408–14. Available at: http://www.readbag.com/ icr-heart-journal-content-2007-jul-pdfs-aoyagi-3434. Accessed March 18, 2014. 5. Maxeiner H and Wolff M. Pure subdural hematomas: a postmortem analysis of their form and bleeding points. Neurosurgery 2002; 50: 503–508. 6. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas [Review]. Neurosurgery 2006; 58: S16–S24. 7. Salazar JD, Wityk RJ, Grega MA, et al. Stroke after cardiac surgery: short- and long-term outcomes. Ann Thorac Surg 2001; 72: 1192–1201. 8. Nakajima M, Tsuchiya K, Kanemaru K, et al. Subdural hemorrhagic injury after open heart surgery. Ann Thorac Surg 2003; 76: 614–615. 9. Osaka M, Konishi T and Koishizawa T. Bilateral subdural hematoma following aortic root and subtotal aortic arch replacement. Gen Thorac Cardiovasc Surg 2009; 57: 33–36. 10. Oka K, Kamota T, Satou M, et al. Subdural hematoma following cardiac surgery. Kyobu Geka 2008; 61: 868–872. 11. Aoyagi S, Kosuga T, Fukunaga S, Tayama E and Ueda T. Subdural hematoma after open-heart surgery. J Heart Valve Dis 2007; 16: 450–453. 12. Krous HF, Tenckhoff L, Gould NS, et al. Subdural hematoma following open-heart operations. Ann Thorac Surg 1975; 19: 269–276. 13. Ueda Y, Okita Y, Aomi S, Koyanagi H and Takamoto S. Retrograde cerebral perfusion for aortic arch surgery: analysis of risk factors. Ann Thorac Surg 1999; 67: 1879–1882.

Downloaded from aan.sagepub.com at UNIV OF PITTSBURGH on June 2, 2015

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14. Ueda Y, Miki S, Kusuhara K, Okita Y, Tahata T and Yamanaka K. Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion. J Cardiovasc Surg (Torino) 1990; 31: 553–558. 15. Kawata M, Sekino M, Takamoto S, et al. Retrograde cerebral perfusion with intermittent pressure augmentation provides adequate neuroprotection: diffusion- and perfusion-weighted magnetic resonance imaging study in an experimental canine model. J Thorac Cardiovasc Surg 2006; 132: 933–940. 16. Kubota H, Takamoto S, Yoshino H, et al. Clinical application of intermittent pressure-augmented retrograde cerebral perfusion. Ann Thorac Surg 2010; 90: 1340–1343.

17. Okita Y, Minatoya K, Tagusari O, Ando M, Nagatsuka K and Kitamura S. Prospective comparative study of brain protection in total aortic arch replacement: deep hypothermic circulatory arrest with retrograde cerebral perfusion or selective cerebral perfusion. Ann Thorac Surg 2001; 72: 72–79. 18. Usui A, Miyata H, Ueda Y, Motomura N and Takamoto S. Risk-adjusted and case-matched comparative study between antegrade and retrograde cerebral perfusion during aortic arch surgery: based on the Japan Adult Cardiovascular Surgery Database: the Japan Cardiovascular Surgery Database Organization. Gen Thorac Cardiovasc Surg 2012; 60: 132–139.

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Acute subdural hematoma after aortic surgery: a retrospective comparative study.

Acute subdural hematoma is uncommon following open-heart surgery, but may result in increased mortality and morbidity...
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