© I985S . Karçcr AG. Basel 0 0 14-3022/85/024.3-014552.75/0 Eur. Neurol. 24: 145-148 (1985) Spontaneous Cerebellar Hemorrhage after Coronary Artery Bypass Surgery Douglas /•.. Andersona, José Billerb, Ronald R. Sehreiberc •' Division of Neurosurgery (Department of Surgery). b Department of Neurology.c Division of Cardiology (Department of Internal Medicine). Loyola University Medical Center, Maywood, 111., USA Key Words. Cerebellar hemorrhage • Coronary artery bypass surgery • Cranial computerized tomography Introduction Spontaneous parenchymatous brain hem­ orrhage accounts for approximately 10% of all strokes in the United States [10], and con­ tinues to be associated with a high morbidity and mortality rate [11]. Cerebellar hemor­ rhage itself represents about 10% of all spon­ taneous intracerebral hemorrhages, and may produce a life-threatening syndrome. The early clinical picture of a hemorrhage into the cerebellum is characterized by headaches. dizziness, vertigo, nausea, vomiting, and in­ ability to stand or walk [3]. In the vast major­ ity of instances, operative intervention is necessary for survival and optimal outcome [4-8]. Cranial computerized tomography (CT) demonstrates accurately the localization and dimensions of the hemorrhage as well as the degree of vcntriculomcgaly and associ­ ated brain edema [9]. Cerebellar hemorrhage is most commonly secondary to arterial hy­ pertension. but may occur with vascular mal­ formation. neoplasms, trauma, bleeding dis- Downloaded by: Karolinska Institutet, University Library 130.237.122.245 - 2/4/2019 2:48:16 PM Abstract. A patient had a spontaneous intracercbellar hemorrhage following coronary artery bypass surgery. His clinical course, characterized by headaches, gait ataxia, and then signs of brain stent compression, is emphasized. Following diagnosis by cranial computerized tomography, successful surgical decompression by suboccipital craniotomy was performed. Reports of neurologic complications, especially intracranial hemorrhage, following coronary artery bypass surgery, arc reviewed. Possible pathophysiologic mechanisms for these prob­ lems, and the diagnosis and treatment of this previously undcscribcd complication of coro­ nary artery bypass surgery are discussed. 146 Anderson/Biller/Schrciber orders, vasculitis or extravasation into a hemorrhagic infarction. This report describes the unusual, and to our knowledge, pre­ viously unreported occurrence of a cerebellar hemorrhage in the immediate postoperative period following coronary artery bypass sur­ gery. Case Report In February 1983, a 54-year-old normotensive, diabetic male underwent aortocoronary vein graft by­ pass to the diagonal branch of the left anterior de­ scending, diagonal, obtuse marginal, ramus and right coronary arteries. Pump time was 1 h and 40 min and cross clamp time was 70 min. Patient’s chest tubes. Swan Ganz catheter, arterial line and Foley catheter were all discontinued at appropriate intervals. 3 days postoperativcly, he noticed a mild to moderate bifrontal and occipital headache. The headache progressed, and approximately 10 days postoperativcly he devel­ oped nausea and vomiting. In addition, he noted a tendency to veer towards the right side on walking and had a single episode of binocular horizontal diplopia. A neurological consultation was then immediately re­ quested. He had no prior history of headaches, trauma or focal neurological disturbances. Medication in­ cluded digoxin, propranolol (Indcral), aspirin, di­ pyridamole (Persantin) and tolbutamide (Orinase). During the examination, he was awake, oriented to place, person, time and situation, and had two 15second episodes of 40 bcats/min bradycardia. Other­ wise his vital signs were normal. He responded to questions slowly with slight hoarseness but no dysar­ thria. He had bilateral horizontal nystagmus with the fast component in the direction of gaze. There was a minimal right pronator drift with slight right-sided terminal dysmetria and appendicular ataxia. Funduscopy was normal. The remainder of the neurological examination was unremarkable. Routine studies of blood yielded normal results. Emergency uninfused CT demonstrated a right cerebellar hemorrhage (fig. 1) with displacement of the fourth ventricle and mild to moderate temporal horn enlargement (fig. 2). Emer­ gency neurosurgical consultation was requested. After pretreatment with mannitol (Osmitrol 20%), steroids (Decadron), and hyperventilation, a suboccipital cra­ niotomy in the sitting position was performed. A corticotomy was made in the right cerebellar hemisphere just lateral to the midline. This immediately revealed approximately 30 mm of acute and subacute blood clot which was resected. The clot was found to have shifted vermian structures significantly across the midline to the left. The wound was irrigated and closed in the usual fashion. Postoperative course was uncomplicated. Pathologic examination disclosed no evidence of tumor or arteriovenous malformation. Follow-up examination 12 months after surgery showed a completely normal neurologic examina­ tion. Downloaded by: Karolinska Institutet, University Library 130.237.122.245 - 2/4/2019 2:48:16 PM Fig. 1. CT of the posterior fossa demonstrating a high-density lesion in the posterior aspect of the right cerebellar hemisphere. Fig. 2. A slightly higher CT scan showing the superior aspect of the lesion in figure 1, distortion and right to left displacement of brain stem structures, and evidence of ventricular (temporal horn) enlarge­ ment. Spontaneous Cerebellar Hemorrhage after Coronary Artery Bypass Surgery Most instances of neurological dysfunc­ tion after open heart surgery result from a combination of predisposing and operative factors. Cerebral complications have been at­ tributed to macroembolization of air or par­ ticulate matter, microembolization of air, fat, platelet-fibrin aggregates, foreign particles or antifoaming agents. Other causes of brain damage relate to inadequate cerebral perfu­ sion in patients predisposed by prior cerebro­ vascular disease, prolonged cardiopulmonary bypass, or low perfusion pressures due to inadequate capillary bed perfusion [1-12]. The pathologic entities usually described in­ clude focal or multifocal infarcts, emboli lodged in small cerebral vessels, cerebral edema and intracranial hemorrhage [5-7], usually petechial, pcrvascular or focal in the subarachnoid space. Intracranial hemorrhage has been described by Humphreys et al. [5] to occur in children who had repair of congeni­ tal heart defects. Hungxict al. [6] reported 20 cases of intracranial hemorrhage following open heart surgery. In their series, almost all patients were under the age of 15, and symp­ toms appeared within 24 h of surgery. Addi­ tionally, 85% of the hemorrhages occurred in the epidural or subdural space. In only 2 cases was the hemorrhage in the brain sub­ stance or the subarachnoid space. The author found at surgery, tearing of the superior sagit­ tal sinus in 3 cases, bleeding from parasagittal veins in 1 case, and dural vessel oozing in 2 cases. Additionally, autopsies in 4 cases re­ vealed subarachnoid hemorrhage in 2 cases, diffuse petechial hemorrhage in 1, and intra­ cerebral hematoma with intraventricular ex­ tension in 1. Intraoperative anticoagulation, hypertonic perfusion, excessive diuresis, and venous and/or arterial hypertension during or after perfusion were postulated as poten­ tial pathogenetic mechanisms by the authors. In our patient, no history of hypertension could be elicited prior to, during or after cor­ onary vein graft bypass surgery, ‘pump time’ was not prolonged and no coagulation abnor­ malities were detected prior, during, or after surgery. Symptoms progressed somewhat slowly initially. Later, however, there was progression of neurologic signs compatible with brain stem compression, emphasizing the often unpredictable course of some cere­ bellar hemorrhages. The pathogenesis of cer­ ebellar or other intracranial hemorrhages af­ ter open heart surgery is unclear, but un­ doubtedly is multifactorial and dependent on the combined effects of anticoagulation, ve­ nous or arterial hypertension and periopera­ tive embolism. References 1 Aguilar, M.J.; Gerbodc, F.; Hill, J.D.: Neuropathological complications of cardiac surgery. J. thorac. cardiovasc. Surg. 61: 676-685 (1971). 2 Bricrlcy, J.B.: Ncuropathological findings in pa­ tients dying after open heart surgery. Thorax 18: 291-304 (1963). 3 Caplan, L.R.: Intracerebral hemorrhage; in Tyler, Dawson, Current neurology, vol. 2, chapter 12, pp. 185-205 (Houghton Mifflin, Boston 1979). 4 Fisher. C.M.; Picard, E.H.; Polak, A.; Dalai. P.; Ojemann, R.G.: Acute hypertensive cerebellar hemorrhage: diagnosis and surgical treatment. J. nerv. ment. Dis. 140: 38-57 (1965). 5 Humphreys, R.P.; Hoffman. H.J.; Mustard. W.T.; Truslcr, G.A.: Cerebral hemorrhage following heart surgery. J. Neurosurg. 43: 671-675 (1975). 6 Hungxi, S.; Xiaogin, H.; Kongsoon. L.; Jiaquians, G.; Letien, X.: Intracranial hemorrhage and hema­ toma following open heart surgery; in Becker. Psychopathological and neurological dysfunctions fol­ lowing often heart surgery, pp. 293-299 (Springer. Berlin 1982). Downloaded by: Karolinska Institutet, University Library 130.237.122.245 - 2/4/2019 2:48:16 PM Discussion 147 7 Krous, H.F.; TenckhofT, L.; Gould, N.S.; Stamm, S.J.: Subdural hematoma following open heart operations. Ann. thor. Surg. 19: 269-276 (1975). 8 LaBaugc. R.; Boukobza, M.; Zinszher, J.; Blard. J.M.; Pages, M.; Salvanig, P.: Hématomes spon­ tanés du cervelet. Revue neurol. 139: 193-204 (1983). 9 Little, J.R.; Tubman, D.E.; Ethier, R.: Cerebellar hemorrhage in adults. J. Neurosurg. 48: 575-579 (1978). 10 Mohr, J.P.; Caplan, L.R.; Melski, J.W.; Goldstein, R.J.; Duncan, G.W.; Kistler, J.P.; Pessin, M.S.; Bleich, H.L.: The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 28: 754-762 (1978). 11 Ojcmann, R.G.; Mohr, M.P.: Hypertensive brain hemorrhage; in Keener, Clinical neurosurgery, vol. 23, chapter 17, pp. 220-244 (1976). Anderson/Biller/Schreiber 12 Thomassen, R.W.; Howbert, J.P.; Winn, D.F., Jr.; Thompsen, S.W.: The occurrence and character­ ization of emboli associated with the use of a sili­ con antifoaming agent. J. thorac. cardiovasc. Surg. 41: 611-622 (1961). Received: May 11, 1984 Accepted: July 11, 1984 Douglas E. Anderson, MD, Division of Neurological Service, Loyola University, Stritch School of Medicine, 2160 S. First Avenue, Maywood, IL 60153 (USA) Downloaded by: Karolinska Institutet, University Library 130.237.122.245 - 2/4/2019 2:48:16 PM 148