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Acta Neurochir (Wien)(1995) 135.

179-185 :Acta
N+ochirurgica
9 Springer-Verlag 1995
Printed in Austria

The Haemodynamic Effect of Transcranial Doppler-Guided High-Dose


Nimodipine Treatment in Established Vasospasm after
Subarachnoid Haemorrhage

S. C. Zygmunt and T. J. Delgado-Zygmunt

Department of Neurosurgery, University Hospital of Northern Sweden, Ume~, Sweden

Summary the ability of the calcium channel antagonist nimodi-


Eleven patients (7 females) with aneurysmal subarachnoid hae- pine, to prevent the ischaemic consequences of vaso-
morrhage (SAH) and transcranial Doppler (TCD) signs of vaso- spasm and to improve clinical outcome [4, 7, 26, 32,
spasm during prophylactic intravenous nimodipine treatment 34, 36-38, 41]. Nimodipine has also been used for
(2 mg/h) were treated with TCD-guided high-dose (4 mg/h) intra-
treatment in patients with established vasospasm [11,
venous nimodipine. The patients were followed clinically and with
serial TCD investigations. Increasing nimodipine to high-dose 26]. Despite the improvement in clinical outcome
treatment led to a reduction of the abnormally elevated mean flow with nimodipine, there are only a few reports demon-
velocities (FV) in all patients. There was also a reversal of clinical strating a reduction or reversal of angiographic vaso-
signs of delayed ischaemia. In one patient, repeated computer tomo- spasm with nimodipine treatment [6, 8]. Most studies
graphic (CT) investigationsrevealed a reversal of ischaemic changes.
have relied on clinical or computer tomographic (CT)
Reduction of nimodipine from 4 to 2 mg/hr resulted in a return to
abnormally elevated mean FV as well as a return of clinical signs of signs of ischaemic brain damage as indicators in the
cerebral ischaemia. The outcome was favourable in 82% of the evaluation of the effectiveness of treatment, perhaps
patients and there was no mortality or vegetative survival. No because of the risk of morbidity and mortality with
patient deteriorated clinically due to vasospasm during treatment angiography [33, 35].
with high-dose nimodipine. The individual effect of nimodipine As a result of the transcranial Dopper (TCD) ultra-
treatment can be monitored by the use of serial TCD investigations.
TCD-guided high-dose nimodipine treatment appears to be an sonographic technique, a non-invasive tool for evalu-
effective treatment in SAH patients developing vasospasm despite ation of vasospasm has become available [1, 2, 18,
prophylactic standard dose treatment. The data give support for a 19, 22, 31, 42, 45]. TCD studies in patients treated
direct vascular effect of nimodipine on cerebral vasospasm. with intravenous nimodipine have demonstrated an
Keywords: Subarachnoid haemorrhage; vasospasm; nimodi- overall reduction in the severity of TCD vasospasm
pine; transcranial Doppler. and a reduced incidence of delayed cerebral ischae-
mia [15, 16, 23, 43, 44].
Introduction In clinical trials using intravenous nimodipine, the
Since the proposal by Robertson in 1949 that the standard dosage has been 2 - 3 mg/h although admin-
delayed ischaemic complications following aneurysm istration of dosages up to 4 mg/h has been used in
rupture might be secondary to vasospasm [39], vari- individual cases [44]. It has been suggested that an
ous therapeutic protocols have been designed. H o w - increased nimodipine dosage could reduce the sever-
ever, delayed cerebral ischaemia associated with ity of vasospasm [23].
vasospasm is still an important cause of morbidity The aim of this study was to evaluate if TCD could
and mortality following aneurysmal subarachnoid be used to monitor the individual haemodynamic
haemorrhage (SAH) [3, 13, 17, 28, 29, 40]. effect of standard versus high-dose nimodipine in
During the last decade, a range of controlled clini- patients developing vasospasm in spite of prophylac-
cal trials as well as open studies have demonstrated tic standard dose nimodipine treatment.
180 S. C. Zygmunt and T. J. Delgado-Zygmunt: Transcranial Doppler-Guided Nimodipine Treatment in Vasospasm

Material and Methods Transcranial Doppler


The material consists of 11 SAH patients (7 females) develop- TCD measurements of the systolic, diastolic and the mean flow
ing TCD signs of vasospasm during prophylactic nimodipine treat- velocities (FV) in the supraclinoid portion of the internal carotid
ment. The patients were admitted to the Department of Neurosur- artery (ICA), MCA and the proximal segment of the anterior cere-
gery, University Hospital of Northern Sweden, Ume~ between bral artery (A1) on both sides were performed using EME TC2-
November 1991 and June 1993. All patients had subarachnoid hae- 64B (EME, Oberlingen, Germany). Mean FV values above
morrhage (SAH) after rupture of an anterior circulation cerebral 80 cm/sec were considered pathological. An elevation of the mean
aneurysm. The mean age was 46 (24-58) years. Four patients had FV in the MCA and/or ICA above 120 cm/sec was used as a criter-
hypertension and one borderline hypertension. Seven patients were ion for vasospasm while in the ACA, values above 100 cm/sec
admitted within 48 hours of the SAH, the othe~ four were admitted were used [1, 22, 42, 46].
on day 3, 5, 13 and 14, respectively (day of SAH defined as day 0).
The clinical status on admission was classified according to Hunt
and Hess (H & H) [25]; four patients were in grade II, four were in Nimodipine Treatment
grade III and three in grade V (Table 1). Five of the patients were All patients were initially treated with a prophylactic standard
operated on early (<72 h), one subacutely (day 4) and five were dose (2 rag/h) of nimodipine (Nimotop| Bayer AG) intravenous-
operated on late (>8 days) (for classification see Ohman and Heis- ly and followed clinically and with the use of TCD. Upon develop-
kaner [34]). The aneurysms were ligated using standard microsur- ment of TCD signs of vasospasm despite standard dose treatment,
gical technique. None of the patients were treated with antifibrino- the dosage was increased to 4 mg/h "high dose". Daily bilateral
lytic agents or hypertensive/hypervolaemic therapy. TCD measurements were performed and the haemodynamic effect
of nimodipine treatment on cerebral vasospasm was studied. The
Radiographic Assessment high-dose treatment was administered for 24 hours in all patients.
All patients were investigated using CT scanning and angiogra- After this, the TCD investigation was repeated whereafter the dose
phy. The distribution of blood on the CT scans was graded accord- was reduced to 2 mg/h. TCD measurements after another 24 hours
ing to the criteria of Fisher et al. [12]. Four patients were in gra- revealed a return to abnormally elevated values in all patients
de II, two in grade III and five in grade IV (Table 1). CT scanning resulting in re-introduction of high-dose treatment. The nimodipine
was repeated if clinical deterioration occurred. dose was subsequently decreased under TCD control. Standard
Four vessel angiography was performed in ten patients. One laboratory tests including electrolyte evaluation, liver tests and
patient had two vessel angiography performed because of technical urine analyses were performed before the initiation of treatment, at
problems during the investigation. Four patients had multiple aneu- least twice a week during treatment and following termination of
rysms. The location of the ruptured aneurysm was as follows: in the treatment.
five patients the anterior communicating artery (ACoA), in four the
middle cerebral artery (MCA) and in two the posterior communi-
Assessment of Outcome
cating (PCoA). Five of the patients had signs of vasospasm on the
initial angiography (Table 1). Follow-up angiography was per- The outcome at six months after the SAH was assessed using
formed in three of these patients. Glasgow Outcome Scale (GOS) [27].

Table 1. Clinical Data

Case Age Sex Clinical ~ CT b Ruptured Multiple Angiographic FVm~c DID d GOS e
no. (yrs) grade aneurysm aneurysm vasospasm (cm]sec)

1 56 M V IV ACoA - + 126 (ACA) - severe disability


2 46 F III IV ACoA - - 160 (MCA) + good recovery
3 58 F V IV ACoA - - 200 (MCA) - severe disability
4 47 F II IV MCA + + 156 (MCA) - good recovery
5 51 M II II MCA - + 128 (MCA) - moderate
disability
6 41 F III IV MCA + + 142 (MCA) good recovery
7 57 F III II ACoA + + 196 (MCA) + good recovery
8 33 M II II ACoA - - 164 (ICA) + good recovery
9 24 F II III PCoA - - 140 (ICA) + good recovery
10 50 M V II MCA + - 138 (ICA) + good recovery
11 46 F III III PCoA - - 172 (ICA) + good recovery

a Admission grade according to Hunt and Hess (1968).


b Grading according to Fisher et al. (1980).
~ Maximal mean flow velocity on TCD.
a Delayed ischaemic deficits prior to high-dose nimodipine treatment.
Glasgow outcome scale [26].

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