Management of ischemic complications after subarachnoid hemorrhage THORALF M. SUNDT, Ja., M.D. Cerebrovascular Clinical Research Center and the Department of Neurologic Surgery, Mayo Clinic and Mayo Foundation, Rochester, Minnesota

The author reviews a form of management for patients deteriorating preoperatively or postoperatively from apparent ischemia attributed to progressive vasospasm after a subarachnoid hemorrhage. The clinical picture and relative frequency of this complication are considered in relationship to the status (grade) of the patient, location of the aneurysm, and ultimate neurological recovery. Experience suggests that the drug regimen reported is useful when instituted early after the onset of symptoms and is safe with proper monitoring techniques. The data do not justify early operative intervention after a subarachnoid hemorrhage, operation when there is angiographic evidence of severe spasm, or expectation of a dramatic effect in patients with a profound deficit or a fixed deficit several hours old. KEY WORDS aneurysm 9 infarction lidocaine hydrochloride 9 vasospasm 9

XPERIENCE gained with the use of isoproterenol and lidocaine hydrochloride in the treatment of cerebral ischemia attributed to progressive vasospasm after a subarachnoid hemorrhage (SAH) is now sufficient for a final report. In order to facilitate an evaluation of these agents and place in proper perspective the incidence of this complication, only the cases treated on one surgical service in the period during which this method of management evolved ( J a n u a r y 1970 to December 1973) are tabulated. The rationale for this form of therapy and the pharmacology of the drugs/,7 the levels of critical cerebral blood f l o w / a n d the ischemic tolerance of neural tissue 8 have been considered previously.

E

4]8

9 isoproterenol

M a t e r i a l and M e t h o d s

Selection o f Patients

This study includes 159 patients with an acute S A H or with a mass lesion effect from an aneurysm without recent SAH. They were all operated on by the author (148 cases) or by a chief resident with the author serving as first assistant (11 cases). The operating microscope was used in all cases. Patients were graded according to the classification of Botterell, et al. 1 In patients with an acute S A H the operation usually was performed between 7 and 10 days after the hemorrhage. The 35 patients with ischemic symptoms are summarized in Table 1 according to their preoperative grade and the location of the J. Neurosurg. / Volume 43 / October, 1975

Management of ischemic complications after SAH TABLE

1

lidocaine hydrochloride (Xylocaine) were administered intravenously by the technique and Distribution of all surgical patients and of patients in the dosages previously reported/However, with ischemic symptoms by grade attd location o/symptomatic aneurysm* as experience increased, it became apparent that some patients would not respond to 0.8 Preop. Aneurysm Location mg of isoproterenol in 150 ml of 5% glucose Grade ICA ACA MCA BAS PICA and water given at a rate of 15 to 20 microdrops/min. In these patients, the 1 2/39 3/I 1 3/8 0/6 0/3 amount of isoproterenol was increased to 1.2 2 6/17 1/10 2/5 0/3 0/2 3 4,/12 8/13 2/10 0/4 0/0 rag. All patients had constant cardiac 4 1/4 1/6 0/4 2/2 0/0 monitoring and, if premature ventricular contotal 13/72 13/40 7/27 2/15 0/5 tractions (PVC) occurred or the pulse rate ex* Shown as number of patients treated/all patients. ceeded 120/min, the concentration or rate of ICA =internal carotid artery; ACA= anterior com- administration of the isoproterenol was municating artery; MCA=middle cerebral artery; decreased. The lidocaine solution (2 gm in BAS= basilar artery; PICA= posterior inferior cere- 500 ml of 5% glucose and 0.25% saline with bral artery. 20 mEq of potassium chloride) was given at a constant rate of 20 microdrops/min but the rate was increased occasionally if premature symptomatic aneurysm. We repaired 55 contractions were noted. aneurysms in this group of 35 patients. ThirWe used the following therapeutic teen aneurysms, nine of the internal carotid guidelines: artery (ICA), two of the anterior com1. Treatment must be instituted early in municating artery (ACA), and two basilar, order to limit the region of infarction; a presented as mass lesions with or without a delay of several hours will result in history of a previous subarachnoid hemorirreversible regions of infarction. rhage; none of these patients developed symp2. During administration of the drugs, the toms of vasospasm. patient must be observed carefully with continuous cardiac monitoring by General Patient Care means of reliable equipment; inexpenPhenobarbital for sedation and codeine for sive units display apparent PVC's when analgesia were the major medications used the patient is merely touched. preoperatively on all 159 patients. Hypoten3. The blood volume must be adequate to sive agents were not used except in unusual withstand dilatation of the peripheral instances when the peripheral blood pressure vascular bed. Cerebral perfusion is was very high. Dexamethasone was seldom pressure-dependent as well as volumeused preoperatively or postoperatively. Fluids dependent in patients with this synwere moderately restricted before and after drome/ and these agents will decrease operation, and close attention was given to the peripheral blood pressure if blood electrolyte balance.' Later in the series, volume is marginal. epsilon-aminocaproic acid (EACA) was often 4. The dosage of isoproterenol must be used. Blood volume and circulating red cell adequate; if improvement is not noted mass were carefully monitored and kept within 1 to 2 hours the concentration adequate postoperatively in all patients. and rate of administration of the drug Drug therapy was instituted preoperatively should be increased consistent with the in patients in whom there was evidence of a patient's cardiac tolerance. progressing focal deficit with or without a decreasing level of consciousness. Treatment Summary of Cases was given postoperatively for similar inThe following case history is an example of dications but with one important restriction, the use of drug therapy in these cases. namely, it was reserved for patients who awoke initially essentially unchanged from Case Report their preoperative state, but whose condition subsequently deteriorated. This 56-year-old woman with an aneurysm Drug Regimen. Isoproterenol (Isuprel) and of the right internal carotid artery underwent

J. Neurosurg. / Volume 43 / October, 1975

419

4~

o

41 M 36 F

14 15

MCA

MCA ACA

MCA

ICA

ICA

ICA

MCA

ICA

1CA

ICA

ICA

ACA

MCA

2 1

1

2

2

1

2

2

2

2

1

2

1

1

1

Grade

5 9

15

8

11 (2)

9

7

8

9 (2)

5

9

10 (2)

14

31

6

Preop. Interval (days)t

dysphasia stupor; aphasia; hemiplegia

upper monoplegia upper monoplegia

stupor; disorientation

hemiplegia

hemiplegia

hemiplegia

confusion; stupor; dysphasia

dysphasia

dysphasia

hemiplegia

mild dysphasia

mild dysphasia

decorticate

Deficit at Time of Rx

2

Time, Onset Deficit to Rx (hrs)

stupor; confused; disoriented; rt leg coma

Deficit at Time of Rx

poor

good poor

good

poor good

poor

good

excellent

indeterminate

excellent

good good

poor

excellent

Response to Rx

poor

poor poor

excellent

death poor

poor

excellent

good

poor

excellent

excellent excellent

poor

excellent

Ultimate Neurological Recovery Comment

sudden onset of deficit after EACA instituted preop

later shunted; minimal improvement; partial self-care; mentation poor died after dismissal to nursing home immediate postop, hemiparesis; spasm; good improvement but occlusion of MCA at site of repair 11 days postop has returned to normal activities; normal personality; minor difficulty in memory, continues to improve self-care; unable to work needs nursing care

emergency op. after sudden onset hemiplegia; no hematoma found; severe spasm; Rx begun during op. "red angry" brain; temporal lobe hematoma; retained homonymous hemianopsia with macular sparing initial early recovery from op. but later deteriorated; required nursing care "red angry" brain; cerebration normal but blind as result of subhyloid hemorrhage from SAH minor speech impairment persisted

--

had ventricular drainage; evaluation of response to agents difficult

Rx begun immediately postop

* ACA = anterior communicating artery; BAS = basilar artery; ICA = internal carotid artery; MCA = middle cerebral artery. t Time from last subaraehnoid hemorrhage to operation; number in parenthesis shows number of multiple bleeds.

71 F

21

41 F

20

,o

37 F 38 F

18 19

.~

58 F

17

63 F

16

~"

Age, Sex

Case No.

3

Treatment response in Grade 3 and Grade 4 patients with isehemia from vasospasm

TABLE

;~

,-t

6"

""

O

""

0

O ~-

0xl

T. M. Sundt, Jr. operation 9 days after her SAH. The aneurysm arose from the intracavernous portion of the carotid artery, and the surgical dissection necessitated the removal of the anterior clinoid process and the lateral wall of the cavernous sinus. The patient awoke with no neurological deficit except a third nerve palsy on the side of surgery; she was fully alert and oriented. Five hours later, there was sudden onset of a profound left hemiplegia, forced deviation to the right, homonymous hemianopsia, and denial of the left side. It was thought that the patient probably had suffered an acute internal carotid occlusion at the site of aneurysm repair. However, angiograms demonstrated no abnormality at the repair site, but did reveal severe spasm of the entire middle cerebral artery and its major branches. A combination drip of isoproterenol and lidocaine hydrochloride was instituted and was tolerated without cardiac abnormalities. Within 4 hours she had regained proximal movement in the left leg and her level of consciousness was improved. Good use of the left leg and proximal function of the left arm were noted within 8 hours. Over the following 5 days, her condition improved daily and the drug regimen was gradually tapered off. Proximal weakness, primarily in abduction in the left arm, along with minimal parietal sensory abnormalities represented the major findings by the seventh postoperative day. The patient was discharged from the hospital on the tenth postoperative day. When she was seen for follow-up examination 1 year later, she was entirely normal with no restriction in activities.

Postoperative angiographic confirmation of an increased degree of spasm was obtained only if the diagnosis was in doubt (six cases). The final clinical results of the entire group of patients operated on, with and without full drug treatment, are summarized in Table 5. The criteria for classification of results were as follows: excellent, normal life with no significant deficit; good, significant deficit, such as a homonymous hemianopsia, but gainful employment possible; poor, a major deficit, so that gainful employment is not possible; and death in 3 months. The presence of a number of variables in patients suffering from S A H makes a statistical analysis of the relationship of vasospasm to the location of the aneurysm difficult. However, it appears from Table 1 that in patients in Grades l to 3, this complication is more common with aneurysms arising from the anterior circulation than with those which arise from the posterior circulation. There were 101 female patients and 58 male patients in the series. None of the 13 patients operated on for a mass lesion effect from an aneurysm without a recent SAH developed symptoms of spasm. Of the group of 146 patients with an acute SAH, 35 (24 females, 11 males) or 24%, developed ischemic symptoms preoperatively or postoperatively attributed to progressive vasospasm and representing a major or potentially major complication. Therapy was instituted in all these patients, but had to be discontinued or decreased to homeopathic concentrations in five patients (Table 4), leaving 30 who were treated with "effective" dosages (0.6 to 0.8 mg isoproterenol/150 ml). Results of Drug Therapy Treatment results are summarized in Tables 2 and 3 tabulate details of 30 cases Tables 2 and 3. Response to treatment was treated with isoproterenol and lidocaine graded as follows: excellent (10 cases), hydrochloride, according to the preoperative definite improvement in symptoms noted grade of the patient. In general, treatment within 2 hours from the time treatment was was instituted preoperatively in Grade 3 and 4 started; good (12 cases), apparent arrest in patients and postoperatively in Grade 1 and 2 the progression of symptoms with a gradual patients. Five patients could not tolerate the improvement over a period of several days drugs, and these cases are summarized in thereafter; and poor (6 cases), no visible Table 4. change in the predicted temporal profile of Angiographic evidence of spasm was pres- the syndrome. Two cases were considered inent in all Grade 3 and 4 patients managed determinate, meaning an arrest in the with these agents. Angiographic evidence of progression of symptoms but with no imspasm prior to operation in Grade 1 and 2 provement in neurological symptoms during patients was usually present but was not the course of treatment. In general, the exsevere except in Cases 6, 13, and 14 (Table 2). cellent responses occurred in Grade 1 or 2 422

J. Neurosurg. / Volume 43 / October, 1975

Management of ischemic complications after SAH TABLE 4 Summary o/ cases of five patients unable to tolerate isoproterenol-lidocahw drip*

Preop. Case Age, Aneurysm Interval Grade No. Sex Location (days)f

Reason Drugs Terminated

F-1

65 F

ICA

4

arrhythmias

death

F-2

52 F

ACA

3

tachycardia; hypertension

poor

F-3

50 F

ICA

9

2

PVC

excellent

F-4

41 M

ACA

12

1

seizures

excellent

F-5

36 M

ACA

10

3

arrhythmias

good

8 5 & 10

Ultimate Neurological Recovery

Comment initial trial without adequate lidocaine coverage or monitoring apparent initial drug response after shunt; good improvement; subsequent gradual mental deterioration persistent cardiac focus before and after Rx; mild dysphasia gradually cleared discontinued because of question of seizures from lidocaine; however, has required anticonvulsant drugs postop; drug given for lower monoparesis that gradually cleared without deficit

* ACA= anterior communicating artery; ICA= internal carotid artery; PVC~ premature ventricular contraction. t From last subarachnoid hemorrhage to operation.

patients with a less profound deficit and without a major alteration in the level of consciousness.

Discussion Some degree of vasospasm is undoubtedly present in all patients who are categorized immediately in Grade 3 or 4 by a severe bleed. However, the presence of other complicating components of the bleed (hematoma, cerebral edema, communicating hydrocephalus, and major vessel occlusion) makes an appraisal of the role of spasm in these cases most uncertain. It is therefore necessary to examine the pattern of the conversion of a Grade 1 or 2 patient to a Grade 3 or 4. The distinguishing feature of the ischemic syndrome which is attributed to progressive vasospasm preoperatively or postoperatively is the temporal profile of the neurological deficit with s y m p t o m s of both regional and general flow alterations, the former manifested by a focal deficit and the latter by an alteration in the level of consciousness. Characteristically, the evolution of the deficit is slow, in comparison to acute deficits seen from embolic occlusions, and begins with a relatively minor deficit, such as a minimal J. Neurosurg. / Volume 43 / October, 1975

dysphasia or weakness of an extremity, that culminates over a period of hours or in some cases days, in stupor with a major focal deficit or, if severe enough, in c o m a or death. Rarely, the evolution is more rapid, occurring over a period of minutes; the diagnosis is uncertain in such instances and m u s t be reconfirmed with angiography to exclude a mass lesion or a major vessel occlusion. Preoperatively, this syndrome is seen most frequently in patients who have complaints suggestive of a severe degree of meningeal TABLE 5 Distribution of a l l surgical patients and patients treated fully for ischemic symptoms by grade and final clinical result*

Preop. Grade 1 2 3 4 total

Final Clinical Result Excellent Good Poor Death 7/63 6/32 6/15 0/2 19/112

0/3 1/1

0/0 0/2

0/1 2/15

2/8 7/20

1/10

5/10

0/1 1/2 0/4 1/5 2/12

* Excludes patients in whom therapy was discontinued. Results shown as number of patients treated/ all patients. 423

T. M. Sundt, Jr. irritation indicated by severe neck stiffness with headache, irritability, and a high fever. It is seemingly more severe in young hypertensive women. Angiographic confirmation is most likely to be obtained if angiography is performed between the fifth and seventh days after the bleed. On occasion it may be difficult to distinguish this syndrome from a rebleed. The absence of an ictus consisting of a sudden recurrent headache with or without the loss of consciousness suggests spasm, but doubt may exist and a recurrent bleed can be the source of increased spasm. Postoperatively, the syndrome is most likely to appear in patients in whom a "red, angry, swollen brain" is encountered at operation 2 and particularly if this is associated with a considerable amount of clotted blood around the vessels from which the aneurysm arose. Operation in the presence of severe angiographic spasm or evidence of marked meningeal irritation is hazardous. If the operation can be delayed for at least 10 days after the bleed, it can be performed with relative safety with respect to spasm. A diagnosis of spasm m the postoperative period must be reserved for patients who awaken from anesthesia unchanged from their preoperative state and subsequently deteriorate. Patients who awaken from anesthesia with a neurological deficit not present prior to induction of anesthesia must be considered to have sustained their deficit from surgical trauma, a critical vessel occlusion (such as the anterior choroidal artery), a period of hypotension, or a subcortical clot associated with stiff brain retraction. Not infrequently, major angiographic evidence of spasm is present without clinical symptoms. It is probable that the decrease in flow in such patients has not yet reached the critical perfusion value. 7 These patients are vulnerable to neurological deterioration that can be precipitated by hypotension. It has been the author's experience that such patients often deteriorate within 2 or 3 days subsequent to angiography (but not related thereto) and there is then good correlation between the angiographic and clinical pictures. Our only attempt to operate in the presence of severe angiographic spasm, documented the day prior to operation, resulted in death (Case 6 in Table 2). 424

Heilbrun has recently documented, by immediate postoperative angiograms, the early onset of vasospasm. 3 He recommended presymptomatic treatment in such cases, and this deserves consideration in the future when a form of treatment has withstood the critical appraisal of many investigators. Many complications in aneurysm surgery are not the result of spasm, and the use of these medications can only be evaluated in properly selected cases. The development of a Korsakoff syndrome, occasionally the result of spasm, is usually secondary to surgical trauma in the septal and preseptal areas? Three patients had this syndrome; in one it preceded the operation. It was transient in one and permanent in two. Spasm was not considered a major factor in these patients; all three had ACA aneurysms. Although most deaths in this series occurred in patients considered to be Grade 3 or 4 preoperatively, the grave condition of the patient was not always the cause of death. Deaths resulted from recurrent bleeding immediately prior to induction of anesthesia or during induction of anesthesia (two cases), major vessel occlusion (one case), poor aneurysmal repair with recurrent hemorrhage (two cases), and uncontrollable bleeding during repair of an aneurysm (one case).

References 1. Botterell EH, Lougheed WM, Scott JW, et al: Hypothermia, and interruption of carotid, or carotid and vertebral circulation, in surgical management of intracranial aneurysms. J Neurosurg 13:1-42, 1956 2. Drake CG: Personal communication, January, 1972 3. Heilbrun MP: The relationship of neurological status and the angiographical evidenceof spasm to prognosis in patients with ruptured intracranial saccular aneurysms. Stroke 4: 973-979, 1973 4. Ransohoff J, Goodgold A, Benjamin MV: Preoperative management of patients with ruptured intracranial aneurysms. J Neurosurg 36:525-530, 1972 5. Scoville WB: Psychosurgery and other lesions of the brain affecting human behavior, in Hitchcock E, Laitinen L, Vaernet K (eds): Psychosurgery. Springfield, Ill, Charles C Thomas, 1972, pp 5-21 6. Smigiel MR Jr, Sundt TM Jr: The comparative effectiveness of alpha-blockade and betastimulation in modifying experimental basilar J. Neurosurg. / Volume 43 / October, 1975

Management of ischemic complications after SAH arterial spasm. J Neurosurg 41:300-305, 1974 7. Sundt TM Jr, Onofrio BM, Merideth J: Treatment of cerebral vasospasm from subarachnoid hemorrhage with isoproterenol and lidocaine hydrochloride. J Neurosurg 38:557-560, 1973 8. Sundt TM Jr, Sharbrough FW, Anderson RE, et ai: Cerebral blood flow measurements and electroencephalograms during carotid endarterectomy. J Neurosurg 41:310-320, 1974

J. Neurosurg. / Volume 43 / October, 1975

This investigation was supported in part by Research Grant NS 6663 from the National Institutes of Health, Public Health Service. Address reprint requests to: Thoralf M. Sundt, Jr., M.D., Cerebrovascular Clinical Research Center and the Department of Neurologic Surgery, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901.

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Management of ischemic complications after subarachnoid hemorrhage.

The author reviews a form of management for patients deteriorating preoperatively or postoperatively from apparent ischemia attributed to progressive ...
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