Anaesth Intensive Care 2011; 39: 65-68

Effect of intravenous ondansetron on sensory and motor

block after spinal anaesthesia with hyperbaric bupivacaine
T.SAMRA*, I.BALA, K.CHOPRA, S. PODDER
Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India

SUMMARY
Ondansetron is a potent antiemetic and a competitive antagonist at serotonin receptors, which are also involved
in modulation of pain. This study was designed to assess the effect of systemic ondansetron on sensory and
motor block after subarachnoid anaesthesia with hyperbaric bupivacaine. Sixty patients undergoing transurethral
resection of bladder tumours were randomly assigned to one of two groups. Group 1 received 2 ml (4 mg) of
ondansetron whereas patients in group 2 received 2 ml of normal saline 15 minutes prior to administration of
subarachnoid block with 2.5 ml of hyperbaric bupivacaine 0.5%. Time to attain peak sensory block (P=0.27),
time to two segment regression (P=0.19) and time to regression to the S2 dermatome (P=0.84) did not
significantly differ between the two groups. No differences in regression of sensory block were noted at any time.
The mean duration of motor block also did not differ (P=0.44), with similar regression of block at all time intervals
except at 90 minutes.
We concluded that intravenous ondansetron does not affect the intensity or duration of sensory and motor block
after spinal anaesthesia with hyperbaric bupivacaine.
Key Words: ondansetron, duration, spinal anaesthesia, bupivacaine

Ondansetron is a potent, selective and competitive

antagonist at serotonin (5-HT3) receptors1. Identical
receptors, located presynaptically on primary sensory
fibres in the dorsal horn of the spinal cord, are
involved in pain modulation2,3. Pretreatment with
ondansetron and granisetron enhances regression of
sensory block after intrathecal administration of 5%
hyperbaric lignocaine4 and hyperbaric bupivacaine5
respectively. In contrast, pretreatment with high dose
ondansetron has no effect on the duration of motor
and sensory block after subarachnoid anaesthesia
with ropivacaine6.
Antiemetics such as ondansetron are often
administered in the perioperative period7, so a
possible interaction with local anaesthetic agents,
including the effect on intensity and duration of
spinal block, needs to be clarified. We conducted
this study with the objective of assessing whether
intravenous ondansetron affected the duration of
sensory and motor block. Secondary outcomes were
the time to peak sensory block and regression of
sensory and motor block.
* M.B., B.S., M.D. (Anaesthesia), Senior Resident.
M.B., B.S., M.D. (Anaesthesia), Professor.
M.Sc., Statistician.
M.D. (Anaesthesia), Associate Professor.
Address for correspondence: Dr T. Samra, C II/77, Moti Bagh 1, New
Delhi 110021, India. Email: drtanvirsamra@yahoo.in
Accepted for publication on August 4, 2010.
Anaesthesia and Intensive Care, Vol. 39, No. 1, January 2011

METHODS
This was a randomised, double-blind clinical trial in
which 60 patients undergoing transurethral resection
of bladder tumours under spinal anaesthesia were
included (30 per group). The study was approved by
the hospital ethics committee and written informed
consent obtained from all patients. Randomisation
was done by means of a random number chart.
Patients were allocated into groups by means of
sealed envelopes containing the randomly determined
treatment assignment. Envelopes were labelled
with a subject number and opened in numerical
order in the operating theatre. Patients in group 1
(ondansteron) received 4 mg (2 ml) of ondansetron
whereas patients in group 2 (control) received
placebo (2 ml of normal saline) 15 minutes prior to
subarachnoid block with 2.5 ml of 0.5% hyperbaric
bupivacaine. Two investigators were involved in
the study conduct. The drug solutions were made
by one investigator, who did not have subsequent
involvement in data collection. All assessments in
the study were performed by the second investigator
who was blinded to the contents of the study syringe.
Exclusion criteria were patients with a history of
back surgery, uncontrolled hypertension, a nervous
system disorder, intake of analgesics (e.g. paracetamol, nonsteroidal anti-inflammatory drugs with
or without opioids), alpha2-agonists, calcium channel
blockers, patients with known hypersensitivity to

66

T.Samra, I.Bala et al

local anaesthetic or with another contraindication to

spinal anaesthesia. All patients were fasted for eight
hours for solid food and no premedication was given.
In the operating theatre an intravenous infusion
was maintained with sodium chloride 0.9% at
8 ml/kg/hour. Electrocardiogram, non-invasive
blood pressure and a pulse oximeter were attached.
Lumbar puncture was performed with the patient
in the lateral decubitus position using a 26 gauge
Quincke needle at the L2-L3 or L3-L4 intervertebral space in the midline. The time at which the
intrathecal injection was made was considered to
be time zero. Patients were placed in the lithotomy
position once the sensory block had reached its
highest level.
Sensory block was determined using a 22 gauge
blunted needle in the midline, and dermatome levels
were tested every two minutes after intrathecal
injection until the level stabilised for four consecutive
intervals. The highest dermatomal level of sensory
block and the time to reach this level were noted.
Motor block was assessed at the time of peak sensory
level using a modified Bromage scale8 (MBS) scored
as 0=no block, 1=able to bend knee, 2=able to
dorsiflex the foot and 3=complete motor block.
Subsequently the level of sensory and motor block
was assessed every 10 minutes throughout the
intraoperative and postoperative period and time
to two segment regression was noted. Heart rate
and non-invasive blood pressure were noted every
three minutes in the first 15 minutes after spinal
anaesthesia and then every five minutes until
the end of surgery. Patients requiring additional
analgesics or general anaesthesia for completion of
surgery were excluded from the study.
The duration of motor block was considered the
time taken for MBS to return to zero and the duration
of sensory block was considered the time until the
block had regressed to the S2 dermatome. Adverse
effects such as shivering, nausea, vomiting, headache
and abdominal discomfort were noted.
Sample size estimation was done to detect a
difference of 25% in the duration of block between
the two groups, with power of 0.8 and alpha error
of 0.05, based on hospital data revealing that the
duration of block with intrathecal bupivacaine was
150 to 180 minutes with standard deviation 20 to
25% of this mean duration. P <0.05 was considered
statistically significant. Students t-test was used
to analyse demographic and haemodynamic data.
Inter-group differences in the levels of sensory block
and the degree of motor block were tested with the
Mann-Whitney U test. The incidence of adverse
effects was compared with chi-square tests.

RESULTS
There were no patients excluded from the study.
Groups were comparable with respect to demographic
data (Table 1). Mean (SD) surgical duration was
58.219.6 minutes in group 1 and 65.78.6 minutes
in group 2 (P=not significant [NS]).
The mean (SD) duration of sensory block was 171.7
12.6 minutes in group 1 and 172.313.6 minutes in
group 2 (P=NS). The mean (SD) duration of motor
block was 13213.5 minutes and 133.313.5 minutes
in groups 1 and 2 respectively (P=NS).
The time to peak sensory block was 12.1
1.3 minutes in group 1 and 12.51.6 minutes in
group 2 (P=NS). The median peak cephalad spread
of sensory block was T6 in both groups (range T4
to T8). Time to two segment regression was 66.0
9.7 minutes in group 1 and 62.710.1 in group 2
(P=NS). Level of sensory block expressed as
dermatomes (median and range), in groups 1 and 2
after 10 minutes, is shown in Table 2. No significant
difference was found between the groups in
regression of sensory block up to a maximum
Table 1
Patient characteristics
Group 1
(ondansetron),
n=30

Group 2
(control),
n=30

P value

Age (y)*

5712.5

5712.2

0.55

Weight (kg)*

627.3

63.57.1

0.79

Height (cm)*

1655.9

1647.0

0.72

Gender ratio (M:F)

25:5

23:7

0.52

ASA status (I:II)

18:12

20:10

0.60

M=male, F=female, ASA=American Society of Anesthesiologists

physical status classification. * Values are mean (SD).
Table 2
Level of sensory block
Time
(min)

Group 1
(ondansetron), n=30

Group 2 (control),
n=30

P value

20

T6 (T4-T8)

T6 (T4-T8)

0.95

40

T6 (T4-T9)

T6 (T4-T9)

0.63

60

T7 (T4-T10)

T8 (T4-T10)

0.06

80

T8 (T5-T10)

T9 (T6-T11)

0.29

100

T10 (T6-T12)

T10 (T6-T12)

0.09

120

T11 (T7-L1)

T11 (T6-L1)

0.18

140

L1 (T8-L3)

T12 (T8-L4)

0.87

160

L3 (T11-S2)

L1 (T8-S2)

0.36

180

S2 (L1-S2)

S2 (T11-S2)

0.15

200

S2 (L1-S2)

S2 (L1-S2)

0.16

Values are median (range). No significant differences between

groups 1 (ondansetron) and 2 (control).
Anaesthesia and Intensive Care, Vol. 39, No. 1, January 2011

Ondansetron and sensory and motor block with hyperbaric bupivacaine

Dermatomes (T6-S2)

T6 dermatome

T7 dermatome
G-1 (Ondansetron)
T8 dermatome
T9 dermatome
T10 dermatome
T11 dermatome
T12 dermatome
L1 dermatome

67

G-2 ( Control)

L3 dermatome
L4 dermatome
L5 dermatome
S2 dermatome

10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180 190 200

Time (minutes)
Figure 1: Regression of sensory block. Regression at each time point shown by median dermatome in group 1
(G-1 ondansetron) and group 2 (G-2 control). No significant differences between the groups.

Modified bromage score

3.5
3

3 (3-2) 3 (3-2) 3 (3-2) 3 (3-2)

G-1 (Ondansetron)

2.5

G-2 (Control)

2 (3-1)*

2
1.5

1 (2-0) 1 (1-0)

1
0.5
0

00

10

30

50

70
90
110
Time (minutes)

130

150

Figure 2: Intensity of motor block. Values are median (range) of

modified Bromage scale score 0 to 3 in group 1 (G-1 ondansetron)
and group 2 (G-2 control). *P <0.05 only at 90 minutes.

assessment time of 200 minutes after intrathecal

injection (Figure 1).
The intensity of motor block, expressed as a
MBS, is depicted in Figure 2. The MBS at the time
of peak sensory block was the same in both the
groups (median 3, range 2 to 3) and was clinically
satisfactory. A significant difference between groups
in regression of motor block was found only at one
time interval, at 90 minutes.
No adverse effect related to either intrathecal
drug or intravenous ondansetron was reported. The
intraoperative and postoperative haemodynamic
parameters did not significantly differ between the
groups. Six patients in group 1 and seven in group 2
experienced shivering (P=NS).
DISCUSSION
In this study intravenous ondansetron, given
before subarachnoid injection of bupivacaine, had
Anaesthesia and Intensive Care, Vol. 39, No. 1, January 2011

no effect on the duration of either sensory or motor

block, nor on the time to peak sensory block, the
intensity of sensory or motor block or the regression
of sensory and motor block.
Our results agree with those of Paraskeva et al6
who found that pretreatment with ondansetron the
night before surgery and prior to spinal anaesthesia
with ropivacaine had no effect on sensory block.
Ropivacaine is a similar local anaesthetic to
bupivacaine but less potent9. In contrast, Fassoulaki
et al4 demonstrated that systemic ondansetron
enhanced regression of sensory block after spinal
lignocaine. In their study the sensory block was
assessed for 30 minutes only and the maximal
dermatomal spread and total duration of block
were not recorded. Due to its short duration of
action and high incidence of transient neurological
symptoms10, hyperbaric lignocaine is no longer
recommended for subarachnoid block.
Mowafi et al5 demonstrated faster recovery
of sensory block after intravenous granisetron,
given prior to subarachnoid block with hyperbaric
bupivacaine. Granisetron is a more potent and
selective
5-HT3
receptor
antagonist11
than
ondansetron. It is metabolised primarily by
cytochrome P-450(CYP)3A isozyme12 whereas
ondansetron is metabolised via a number of CYP450
enzymes13. Variability in the pharmacokinetics
of granisetron in comparison to ondansetron is
explained by the heterogeneity in CYP3A activity.
Ondansetron is non-selective and acts on a range
of receptor subtypes (5-HT1A-D, 5-HT2A-C, 5-HT3,
5-HT4), all of which are expressed in central and
peripheral neurones14. Serotonin exerts both an
inhibitory and excitatory influence on pain processing

T.Samra, I.Bala et al

68

via these receptors15,16. These factors may account

for the difference in results between our study using
ondansetron and the study using granisetron.
Our research methodology differed from the
previous studies in that data on regression of motor
and sensory block were collected more frequently.
It also differed in that pretreatment with the 5-HT3
antagonist occurred only once prior to spinal
anaesthesia, omitting an additional dose the night
before surgery. In addition, we gave 4 mg whereas
Paraskeva et al6 administered 8 mg of ondansetron.
One potential limitation of our study was in the
method used to test sensory block. Assessment
of loss and return of the pinprick sensation was
performed using a 22 gauge blunt needle but pinprick
intensity varies with each measurement and stimulus
variability may cause variability in response. Also,
significant variability is present in the evaluation of
sensory block, even for the same stimulus intensity
in different patients. Measurements in the intraoperative period were done with the patient in
the lithotomy position whereas postoperative
assessments were with the patient supine, which
might have affected regression of sensory block.
In conclusion, intravenous ondansetron does not
affect the onset, intensity, regression or duration of
spinal block produced by hyperbaric bupivacaine and
can be used for prophylaxis and treatment of nausea
and vomiting during regional anaesthesia without an
effect on block characteristics.
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