ANNALS OF SURGERY Vol. 171 April 1970 No. 4 Neurological Complications of Carotid Artery Surgery JAi s E. BLAiN, M.D., RiciLuA D. CHAPMAN, M.D., EDWIN J. WYLIE, M.D., F.A.C.S. From the Department of Surgery, University of California School of Medicine, San Francisco, California POSTOPERATIVE stroke is the most fre- rological deficit or acute progression of an quent and most disastrous complication of old deficit occurred after 55 (9%) of these cerebrovascular reconstructive surgery. Pa- operations. In most instances postoperative tients who undergo operation on the ca- neurological deficits, when viewed retro- rotid arteries are particularly vulnerable. spectively, resulted from an unwise deci- Since prevention of stroke is the primary sion to operate or an error in surgical man- objective of most carotid artery operations, agement. In three additional patients the technics to prevent it at the time of opera- postoperative deficit was merely a gradual tion are of paramount importance. Post- progression of a preoperative deficit and operative neurological deficits in our pa- was not related to the operation. A tabula- tients who had carotid operations were re- tion of the severity of the deficits and the viewed to determine causes and to assess ultimate neurological status of the patients the value of methods designed to prevent is shown in Table 1. Visual disturbances, these deficits. dysphagia, and monoparesis are examples Six hundred thirteen endarterectomies of deficits classified as mild. Under moder- for occlusive or ulcerating lesions at the ate deficits we included hemiparesis. Se- carotid bifurcation were performed in 488 vere deficit was applied to complete uni- patients between October, 1958 and June, lateral paralysis (hemiplegia) with or 1969. Staged bilateral operations were per- without changes in the level of conscious- formed in 125 of the patients. A new neu- ness. All deaths were caused by brain Submitted for publication July 14, 1969. damage. 459 BLAND, CHAPMAN AND WYLIE Annals of Surgery 460 April 1970 TABLE 1. Comparison of Initial and Ultimate Status in Patients with Neurological Deficits Follouing Carotid Endarterectomy Ultimate Status on Follow-up Initial Status after Onset of Complication No Change Improved Recovered Mild deficit 10 1 9 Moderate deficit 22 6 8 8 Severe deficit 8 1 4 3 Death 18 (31%) Totals 58 7 (12%) 13 (22%) 20 (35%) When modifications were made in selec- Stroke before Beginning of Operation operative tion of operative candidates and One patient developed hemiplegia co- anesthetic technics, the total stroke and incident with a severe hypotensive response was from 11 per cent morbidity decreased to preoperative medication. He had a his- in the first two thirds of the series to 4.6 tory of recurrent transient attacks of cere- per cent in last third. In the last 100 the bral ischemia. Arteriography showed se- on were carotid operations patients who vere unilateral internal carotid stenosis. He at free of neurological deficits the begin- was hemiplegic on arrival in the operating operation a postoperative ning of the room 30 minutes after he was given pre- one patient. stroke occurred in only Since medication which lowered blood pressure report 51 submission of this additional to 90/60. Hemiplegia lessened when nor- on 37 patients carotid endarterectomies mal blood pressure was restored but per- in have been performed this category. sisted in mild degree after an uneventful None of these patients developed a post- carotid endarterectomy performed under operative neurological deficit. general anesthesia. Five months after op- onset In most patients the time of of the eration neurological function was normal. postoperative neurological deficit gave a reliable clue as to its cause. Further infor- Stroke during Operation mation was provided by postoperative ar- Twenty-six patients developed hemi- teriography or surgical exploration when- plegia or hemiparesis during operation. In ever feasible. Autopsies were performed in 17 the operations were performed under 17 of 18 patients whose strokes progressed local anesthesia and the onset could be re- to death. In the 18th patient the cause of lated to the stage of the operation. death was established during surgical ex- Stroke appeared before clamp occlusion ploration pre-mortem. of the common carotid artery in five pa- tients. In one it coincided with a sudden In 51 patients the causes of postopera- drop in blood pressure. In the other four tive stroke, identified with reasonable cer- the neurological deficit appearing during were acute blood pressure tainty, changes, mobilization of the carotid bulb was cerebral embolization, cerebral ischemia thought to be caused by cerebral emboli- during carotid clamping, local carotid zation: all four had ulcerated lesions, reti- thrombosis, and progression of pre-existing nal emboli were observed in two, and in cerebral infarction. These etiological fac- a third the diagnosis of embolization was tors are conveniently described in relation confirmed by autopsy. to the period in the surgical management Cerebral ischemia secondary to clamp when the neurological deficit appeared. occlusion of the common carotid artery Volume 171 NEUROLOGICAL COMPLICATIONS OF CAROTID ARTERY SURGERY Number 4 461 was the presumptive cause of stroke in 21 covered from their neurological deficits patients, 11 of whom underwent the entire within one week. operation under local anesthesia. Although Two patients who developed stroke had all 11 patients had tolerated 3-minute pe- acute hypertension soon after operation. riods of trial occlusion, a deficit followed One of these patients described at least 15 a longer period of operative occlusion. Two transient monoparetic attacks in the week patients had shown intolerance to trial oc- before operation but had no neurological clusion under local anesthesia and the op- deficit at the time of operation. Endarterec- eration was completed under general anes- tomy removed an ulcerated stenotic ca- thesia with adjunctive hypothermia (30 rotid lesion. The second patient had re- C). The remaining eight patients were op- sidual hemiparesis from a stroke one year erated upon under general anesthesia from previously, caused by occlusion of the op- the beginning but without additional cere- posite carotid artery. In both patients the bral blood flow support. In the ten patients postoperative stroke occurred after the in whom operation was begun or con- onset of severe hypertension within 6 cluded under general anesthesia the neuro- hours after operation. Both patients died; logical deficit was apparent on return of autopsy showed massive intracranial hem- consciousness. Postoperative patency of the orrhages and patency of the surgically operated carotid artery was proven early treated carotid arteries. in the series in 11 patients by either arteri- Occlusion of the surgically treated ca- ography or surgical exploration. Since we rotid artery caused postoperative stroke in later refrained from both arteriography and ten patients. In eight of these neurological re-operation in patients with acute stroke, deficits appeared within the first 24 hours. intolerance to operative clamp occlusion in The longest interval between operation ten patients is assumed but not proven to and arterial occlusion was 12 days. Pre- be the cause of the strokes. It may be sig- operative occlusion or severe stenosis of nificant that 16 of the 21 patients (75%) the opposite internal carotid artery was had severe stenosis or occlusion of the op- present in eight of the ten patients. Five posite carotid arteries although the fre- patients died as a result of stroke and in quency of contralateral carotid disease in each case autopsy showed a distal intimal the entire series was only 47 per cent. flap. Stroke progressed to death in only one of Revascularization of a recently infarcted the 21 patients in this group and 11 recov- area of the brain was believed to be the ered fully from their deficits. cause of postoperative stroke in five pa- tients. Four of the patients had developed Postoperative Stroke hemiparesis from internal carotid artery Thirty-one patients developed neuro- occlusion within 3 days before operation. logical deficits or had sudden progression The neurological deficit was unchanged or of a previous deficit during the postopera- lessened for the first few hours after opera- tive period. A plausible explanation for the tion but then rapidly increased and pro- deficit was evident in 19. gressed to coma and death. Massive hem- Airway obstruction and coincident hypo- orrhage into infarcted brain and patency tension were followed by hemiparesis in of the operated carotid artery were demon- two patients in whom signs of stroke first strated at autopsy. The fifth patient had appeared in the recovery room. One of had monoparesis and aphasia for 3 days these patients had an old occlusion of the but recovered completely 4 weeks before opposite carotid artery. Both patients re- operation. Although the intracranial arteries BLAND, CHAPMAN AND WYLIE Annals of Surgery 462 April 1970 appeared normal on preoperative arterio- occlusion of the left middle cerebral ar- grams, the operative finding of a severely tery. In the first patient the occluded artery stenotic ulcerated carotid lesion suggested could not be reopened and in the second, that the original stroke was caused by cere- staged operations to remove stenotic ul- bral infarction from an embolus to a cerated lesions in both internal carotid ar- branch of the middle cerebral artery. This teries failed to alter the steadily deteriorat- patient recovered from postoperative stroke ing course. and its cause was not determined. In eight patients the cause of the post- Discussion operative stroke is unknown. The average A review of the causes of postoperative interval between operation and the onset stroke identifies four critical areas: selec- of the deficit was 7 hours in five patients tion of patients, methods of anesthesia, and 3 days in four patients. One patient surgical technic, and postoperative man- died. Autopsy, limited by the family's re- agement.