Intravenous buscopan for analgesia following laparoscopic sterilisation


C. M. Wilson , Department of Anaesthesia, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK


Following reports that tubal smooth muscle spasm may contribute to pelvic pain following laparoscopic sterilisation, we studied the effect of buscopan (an anticholinergic agent used to relieve smooth muscle spasm) on 45 patients undergoing general anaesthesia for day-case laparoscopic sterilisation. Patients were randomly allocated to receive either buscopan 20 mg or saline placebo after induction of anaesthesia. There were no significant differences in pain scores or postoperative analgesic requirements between the two groups. We conclude that intravenous buscopan confers no benefit in day-case laparoscopic sterilisation.

Pain following laparoscopic sterilisation can be severe and difficult to treat, particularly in the first few hours postoperatively [1, 2]. This may necessitate the administration of opioids, with an associated increase in nausea, sedation and unplanned hospital admission in day-case patients. It is suggested that the initial severe pain seen with occlusion of the fallopian tubes may be secondary to smooth muscle spasm and can be reduced using anticholinergic agents [2, 3]. Buscopan, an anticholinergic drug, is used to relieve smooth muscle spasm of the urogenital, biliary and gastrointestinal tracts during radiological procedures [4[5]–6]. It has a rapid onset of action when given intravenously, but is poorly absorbed orally and, because of minimal transfer across the blood–brain barrier, has no central sedative side-effects making it suitable for use in day-case anaesthesia.


We studied 46 patients, undergoing day-case laparoscopic sterilisation using Filshie clips. All were ASA 1 or 2, aged 27–40 years and weighed less than 100 kg. This was a randomised, controlled, double-blind trial, with Regional Ethics Committee approval and written informed consent given by all participants. Patients were not studied if they were allergic to buscopan, NSAIDs or were unsuitable for a laryngeal mask airway. All patients were premedicated with rectal diclofenac 100 mg. Routine monitoring (ECG, noninvasive blood pressure, oximetry) was instituted before standardised coinduction with midazolam 2 mg, fentanyl 100 μg and droperidol 0.625 mg, followed by a sleep dose of propofol (up to 2.5−1). A laryngeal mask airway was then inserted and anaesthesia maintained with 66% nitrous oxide and 0–2% enflurane in oxygen, breathed spontaneously. Patients were randomly allocated to receive either buscopan 20 mg or 0.9% saline 2 ml following induction. Postoperative pain was treated on patient request with codydramol (dihydrocodeine/paracetamol) two tablets orally, or morphine 10 mg intramuscularly, and nausea or vomiting with prochlorperazine 12.5 mg intramuscularly.

Study data were collected by the recovery ward nurses who were blinded to patient group. Pain and sedation scores, presence of nausea or vomiting, and any analgesic or anti-emetic drugs required were recorded on admission to recovery, and at 1, 2 and 3 h postoperatively. Pain was scored on a 10-cm visual analogue scale, ranging from 0 = no pain to 10 = worst pain imaginable. Sedation was scored on a four-point scale: unrousable; sleepy; agitated; awake and calm.

Data were analysed using the Mann–Whitney U-test for VAS pain scores, and the Chi-squared test for categorical data, with p < 0.05 and a two-point difference in pain scores between the groups taken as being significant. For a power of 0.8 a sample size of 23 was required for each group. We recruited 46 patients but excluded one as no data were recorded postoperatively.


The main findings of the study are shown in Table 1 and Fig. 1. There were no statistically significant differences in pain scores, analgesic requirements, sedation, or nausea and vomiting between the two groups. Overall, 69% of patients required postoperative analgesia, 33% received codydramol alone, 20% received morphine alone and 16% received both. The incidence of nausea was 36% in the buscopan group and 25% in the placebo group, with the majority of the anti-emetic given along with morphine in the first hour. Only one patient vomited.

Table 1.  Postoperative analgesia and anti-emetic requirements, incidence of nausea (number of patients for each group) and sedation scores (median, interquartile range) Thumbnail image of
Figure 1.

Pain scores (median, interquartile range) for each study period.


In this study we were unable to demonstrate any benefit from buscopan 20 mg given intravenously over 0.9% saline control in reducing pain scores in the first 3 h following laparoscopic sterilisation.

A previous study from this hospital showed that glycopyrrolate 0.3 mg is effective in reducing postoperative pain after sterilisation [3], so our lack of success with buscopan is disappointing. Buscopan is a cholinergic, muscarinic antagonist which acts predominantly on intramural parasympathetic ganglia of abdominal and pelvic smooth muscle. As a quaternary ammonium ion it has poor blood–brain barrier penetration, and whilst of proven efficacy in relieving smooth muscle spasm when given intravenously [4], it is poorly absorbed from the gut.

Buscopan has a rapid onset of action, with effects lasting for 20–30 min [7]. The manufacturers recommend a repeat dose after 30 min to 1 h if necessary. In our study the procedures usually lasted around 15–20 min (not formally measured) so it is possible that the clinical effects of the buscopan were already wearing off, and that we should have continued with a repeat dose of buscopan as our first-line analgesic treatment rather than opioids. It is also possible that the midazolam and droperidol (both drugs known to produce smooth muscle relaxation [8]) prevented a further demonstrable reduction in fallopian tube spasm and therefore pain scores between the two groups. However, as the pain scores recorded on our patients are similar to those obtained in other studies where these drugs were not used this seems unlikely [1[2]–3, 9, 10]. Excessive sedation from droperidol, preventing an adequate assessment of pain, has also been suggested as a reason for our failure to demonstrate any analgesic effect with buscopan in the first hour. We used a relatively low dose of droperidol (0.625 mg) which is unlikely to have prevented any significant differences in pain scores from becoming apparent.

Pain following diagnostic laparoscopy may be due to the surgical incisions and peritoneal irritation from CO2 insufflation or blood tracking up to the diaphragm [11], and may last for several days [1, 9]. Measures such as local anaesthetic wound infiltration or rectus sheath block and careful removal of CO2 from the abdominal cavity reduce pain significantly immediately postoperatively [10]. Simple oral analgesia is usually sufficient for subsequent pain management [2].

Pain due to laparoscopic sterilisation is greater than after laparoscopy alone, though tends to be of shorter duration, with no significant difference in pain scores between the two procedures by the time of arrival home [1, 12]. The initial more severe pain with sterilisation must therefore be secondary to the clips or rings placed on the fallopian tubes, probably owing to tubal ischaemia or smooth muscle spasm [2], rings inducing more pain than clips [13]. The fallopian tubes have no demonstrable somatic nerve supply, and are innervated solely by autonomic nerves via the mesosalpinx [10].

There have been a number of studies investigating methods of pain relief after laparoscopic sterilisation. Maximal removal of CO2 from the peritoneal cavity reduces pain, but positioning the patient head down in recovery has little effect [13]. Surgically applied local anaesthetic gives the most consistent improvement in pain scores when compared to controls, with the duration of analgesia dependent on the route of administration. Bilateral mesosalpinx block with 0.5% bupivacaine was the most successful method, with per-cervical bupivacaine, topical lignocaine gel applied to the clips and intraperitoneal instillation of bupivacaine solution also reducing postoperative pain [9, 10, 14, 15].

Studies investigating the use of nonsteroidal analgesics in laparoscopic sterilisation have shown varying success. Higher dose (550 mg) naproxen reduced pain scores but pre-operative rectal indomethacin 200 mg, intramuscular diclofenac 75 mg and intravenous ketorolac 60 mg failed to significantly relieve pain when compared to controls [2, 12, 16, 17]. While some of these findings may be due partly to inadequate dose of drug, or insufficient power of the study, the most likely reason for failure to provide adequate analgesia must be the limited strength of the nonsteroidal anti-inflammatory agents. This seems especially likely given that intramuscular codeine has also proved to be inadequate after laparoscopic sterilisation when compared to laparoscopy alone [1]. In another study from this hospital, glycopyrrolate 0.3 mg given at induction of anaesthesia produced a significant reduction in initial pain scores and opioid requirements following laparoscopic sterilisation. Conditions and patients in this study were comparable to ours, and glycopyrrolate is a similar drug to buscopan in that it has no central nervous system effects. We can offer no explanation for the discrepancy in our results.

We conclude that buscopan 20 mg intravenously does not reduce pain scores following laparoscopic sterilisation. Other studies suggest that, while some reduction in postoperative pain may be achieved by the use of local anaesthetics, nonsteroidal anti-inflammatory drugs or antispasmodic agents individually, a multimodal approach to analgesia following laparoscopic sterilisation may be required to produce a consistent reduction in pain scores sufficient to allow early mobilisation and discharge without the use of strong opioid analgesics.