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Commonly used drugs in obstetric anaesthesia

Created: 7/8/2006
Updated: 12/3/2007

Prevention of gastric aspiration


Metoclopramide is a benzamide dopamine antagonist.

It is mainly used in obstetrics as a prokinetic agent. The gastrointestinal smooth muscle stimulatory effects are related to its ability to antagonize the inhibitory neurotransmitter, dopamine; to augment acetylcholine release and sensitize the muscarinic receptors of the gastrointestinal smooth muscle; and to coordinate gastric-pyloric-small intestinal motor function. The lower oesophageal sphincter tone is increased by about 17 mmHg.

Metoclopramide exerts its antiemetic effects through dopamine (D2) receptor antagonism at the medullary chemoreceptor trigger zone. However many studies have shown it to be no more effective than placebo.

Dose: 10 mg by mouth, IM or IV, 8 hourly

It is well absorbed from the gut but oral bioavailability varies significantly as a result of variable first-pass metabolism.

Side effects: Metoclopramide crosses the blood-brain barrier and may cause acute dystonic reactions and other extrapyramidal effects up to 72 hours after administration. These occur more commonly in young females and can be treated with procyclidine. Rarely it may precipitate the neuroleptic malignant syndrome.


Ranitidine is a specific and competitive histamine H2-receptor antagonist at parietal cells. Gastric pH is raised and the volume of secretions reduced.

Dose: By mouth 150 mg at the onset of labour and then 6 hourly thereafter. Alternatively you can administer 50 mg intramuscular or by slow intravenous injection, 45-60 minutes before induction of anaesthesia. Rapid IV administration may produce cardiac arrhythmias.

The oral bioavailability is 50% and 50% of an administered dose is excreted unchanged in the urine, so dosing may need to be adjusted in the presence of renal impairment.

Sodium citrate  (Na3C6H5O7)

Sodium citrate is an antacid used as prophylaxis against aspiration pneumonitis before a rapid sequence induction.

30 ml of a .3 molar solution should be given less than 10 minutes before the start of surgery due to its limited duration of action.

Pulmonary aspiration of particulate antacid (e.g. magnesium trisilicate) is associated with a higher risk of aspiration pneumonitis than a nonparticulate antacid, such as sodium citrate.

The efficacy of sodium citrate depends on gastric volume and acidity. A total of 30 ml of sodium citrate neutralises 255 ml of hydrochloric acid with a pH of 1.0. The effective duration of action of sodium citrate is variable and depends on the rate of gastric emptying, i.e. the pH will remain above 3.0 for a longer period if gastric emptying is delayed.

Obstetric Anaesthesia: Principles and Practice by D.H. Chestnut



Nitrous oxide mixed 50:50 with oxygen is a ubiquitous method of obstetric analgesia with maintenance of consciousness. It may also be used in the setting of minor procedures in the trauma department where transient analgesia is required. It is most often administered via a demand valve for self administration. A safety feature is that the mother controls administration.
Click here for more information on Entonox

Pethidine (Meperidine)

Pethidine is a weakly basic phenylpiperidine derivative, related to fentanyl and sufentanil. It is a synthetic opioid

Dose: 1 mg/kg up to 150 mg intramuscularly. Absorption via the intramuscular route may be variable. The duration of action is 120-150 minutes.

Pethidine may produce serious interaction if administered with monoamine oxidase inhibitors (MAOI)

The UK National Birthday Trust (NBT) survey reported that only 16% of women who received pethidine rated it as helpful but 25% rated it as unhelpful. Midwives rated pethidine much higher.

Effects on the parturient:
Confusion, loss of control, sedation and hypoxia. The combination of Entonox and pethidine tends to exacerbate maternal desaturation. Pethidine decreases gastric emptying by at least 5 hours in 70% of women and increases gastric volumes during labour.

Effects on the foetus and neonate:
Pethidine is principally bound to a1-acid glycoprotein and its high lipid solubility enables significant amounts to cross the placenta and reach the foetus. The highest foetal concentrations are observed 2–3 hours after intramuscular administration. Pethidine becomes trapped in the foetus because, as a weak base, pethidine is more ionized in the acidic environment of the foetal circulation. This effect is exaggerated in a distressed acidotic foetus. The less lipid-soluble metabolite norpethidine also accumulates in the foetus. The half-life of norpethidine in the neonate is about 62 hours, causing prolonged sedation and respiratory depression. It also has proconvulsant properties.

The effects of pethidine can be reversed by an intramuscular dose of naloxone. Naloxone should not be given to the neonate of an opioid-dependent parturient.

Local anaesthetics

Click here for more information on Local Anaesthetic Pharmacology.


Lidocaine is a common local anaesthetic and has Class 1b anti-arrhythmic properties. It is an amide-type local anaesthetic and was developed in 1943

It is 70% protein bound to a1-acid glycoprotein. Lidocaine has a more rapid onset of action and longer duration of action than ester-type local anaesthetics such as procaine. It is approximately 90% metabolized in the liver by N-dealkylation (cytochrome CYP1A2 and CYP3A4) to the pharmacologically active metabolites monoethylglycinexylidide and glycinexylidide.

The elimination half-life of lidocaine is approximately 1.5–2 hours in most patients. This may be prolonged in patients with hepatic impairment or congestive heart failure.

Lidocaine 2% may be used to top-up and epidural. 20 ml is often combined with adrenaline 1 ml of 1:200 000 and an opiate. After a test dose, 5-8 ml may be given every 2-3 minutes.

Lidocaine is more likely than bupivacaine, prilocaine or procaine to induce transient neurological symptoms (TNS) when used for spinal anaesthesia. These symptoms have been described as pain and dysesthesia in the buttock, thighs or calves, occurring after the recovery from spinal anaesthesia, usually within 24 hr and resolving within 72 hr


Bupivacaine is an amide local anaesthetic.

It is a clear, colourless solution prepared as a 0.25 and 0.5% (with or without adrenaline 1:200 000). For subarachnoid block, a 0.5% (heavy) solution containing 80 mg/ml glucose (specific gravity 1.026), is available.

The toxic dose of bupivacaine is 2 mg/kg (with or without adrenaline). It is one of the more cardiotoxic local anaesthetics.

Bupivacaine may be administered by infiltration, intrathecally and epidurally. It is commonly used for epidural infusions (with or without an opioid) for labour and post-operatively.

Because of the pKa of 8.1, the onset of action is intermediate or slow. Bupivacaine is the most highly protein-bound (95%) amide local anaesthetic which is the reason for its long duration of action. It is metabolised in the liver by N-dealkylation to pipecolylxylidine and pipecolic acid.


Ropivacaine is an amide local anaesthetic produced in three concentrations (2, 7.5 and 10 mg/ml). It is unique in that membrane separation synthesis yields an enantiomerically homogeneous solution that is more than 99% pure S-(-) isomer.

Ropivacaine is highly plasma protein binding (94%) and the lipid solubility lies somewhere between that of lidocaine and bupivacaine. The duration of action and onset time are similar to those of bupivacaine. The analgesic potency of ropivacaine is 0.60 (0.47-0.75) relative to bupivacaine. Claims for reduced motor block must be considered with differences in analgesic potency in mind.

Studies have demonstrated that Ropivacaine less neuro- and cardiotoxic than bupivacaine.

Ropivacaine is extensively metabolised by the cytochrome P450 system in the liver to 3 and 4-hydroxy-ropivacaine, both of which have some local anaesthetic activity.


Levobupivacaine is the S(-) enantiomer of bupivacaine.

It is prepared as a sterile, colourless solution (pH 4.0-6.5) containing levobupivacaine hydrochloride equivalent to 2.5 mg/mL, 5.0 mg/mL, and 7.5 mg/mL of levobupivacaine.

The pKa of 8.1 for levobupivacaine is the same as that of bupivacaine. Protein binding is more than 97%, mainly to a1-acid glycoprotein.

It is extensively metabolized with no unchanged levobupivacaine detected in urine or faeces. In vitro studies using showed that cytochromes CYP3A4 and CYP1A2 mediate the metabolism of levobupivacaine to desbutyl levobupivacaine and 3-hydroxy levobupivacaine, respectively. The 3-hydroxy levobupivacaine appears to undergo further transformation to glucuronide and sulphate conjugates.

Animal and human studies have shown levobupivacaine to be less neuro- and cardiotoxic than racemic bupivacaine. The maximum dose of levobupivacaine has yet to be decided, although caution would suggest that be the same as that recommended for bupivacaine at 2 mg/kg.

Further reading:

Click here for more information on Toxicity from Local Anaesthetic Drugs.

Lipid emulsion to treat overdose of local anaesthetic; Anaesthesia; Volume 61 Page 107 - February 2006

Successful resuscitation of a patient with ropivacaine-induced asystole after axillary plexus block using lipid infusion; Anaesthesia Volume 61 Page 800 - August 2006

Drugs which contract the uterus

The routine prophylactic administration of an uterotonic agent is an integral part of active management of the third stage of labour, helping to prevent postpartum haemorrhage (PPH). The two most widely used uterotonic agents are: ergometrine-oxytocin (Syntometrine ®) (a combination of oxytocin 5 international units (iu) and ergometrine 0.5 mg) and oxytocin (Syntocinon ®).


Oxytocin in a nonapeptide that is synthesized in hypothalamic neurons and transported down axons of the posterior pituitary for secretion into blood. Its effects are numerous, the most important of which is uterine contraction.  Synthetic oxytocin (Syntocinon®) is free vasopressin and extraneous animal protein.

The induction and acceleration of labour
Missed and incomplete abortion
Post-partum haemorrhage (atonic uterus)

After delivery; 5 units by slow intravenous injection
For infusions, please refer to your departmental protocol
Induction of labour, see NICE guidelines

Side effects:
Hypotension and reflex tachycardia. It may prolong the Q-T interval and cause T-wave flattening. Antidiuretic effects in high doses.


Ergometrine is an amine ergot alkaloid that stimulates contractions of uterine and vascular smooth muscle.  Like other ergot alkaloids, ergometrine produces arterial vasoconstriction by stimulation of alpha-adrenergic and serotonin receptors and inhibition of endothelial-derived relaxation factor release.

Ergometrine may be administered by IM or IV injection at a dose of 0.2 – 0.5 mg. However, because the risk of severe adverse effects is increased with IV use of ergometrine, its use via this route is recommended only for emergencies such as excessive uterine bleeding or any other life-threatening situation

Side effects:
Hypertension, diarrhoea, nausea and vomiting.
Dizziness, hallucinations, vertigo and tinnitus have also been reported.

Ergometrine is contraindicated in eclampsia, preeclampsia or a history of hypertension and in patients with peripheral vascular disease or heart disease. It is also contraindicated if there is any suspicion of retained placenta.

A recent Cochrane review concluded:
The use of ergometrine-oxytocin as part of the routine active management of the third stage of labour appears to be associated with a small but statistically significant reduction in the risk of PPH when compared to oxytocin for blood loss of 500 ml or more. No statistically significant difference was observed between the groups for blood loss of 1000 ml or more. A statistically significant difference was observed in the presence of maternal side-effects, including elevation of diastolic blood pressure, vomiting and nausea, associated with ergometrine-oxytocin use compared to oxytocin use. Thus, the advantage of a reduction in the risk of PPH, between 500 and 1000 ml blood loss, needs to be weighed against the adverse side-effects associated with the use of ergometrine-oxytocin.

Carboprost (Haemabate)

Carboprost (Haemabate) is a prostaglandin (PGF2a) and potentiates the uterotonic effect of oxytocin.  It is used to treat postpartum haemorrhage due to uterine atony in patients unresponsive to ergometrine and oxytocin.

Carboprost  250mcg by deep i.m. injection. Direct intramyometrial injection of Carboprost has a faster onset of action. This dose may be repeated but after at least 15 minutes in severe cases. The total dose should not exceed 2 mg (8 doses).

Prostaglandin F2a may cause bronchospasm, therefore use cautiously in asthmatics.

History of glaucoma or raised intra-ocular pressure, uterine scars; excessive dosage may cause uterine rupture


Misoprostol is a synthetic prostaglandin E1 (PGE1) analogue. used to treat postpartum haemorrhage due to uterine atony in patients unresponsive to ergometrine and oxytocin.

Misoprostol 400 – 800 mcg (2-4 x 200 mcg tablets). The sublingual, oral, rectal and intrauterine routes have all been used successfully.

Nausea, vomiting, diarrhoea, abdominal pain, dyspepsia, flatulence, rashes and dizziness.

Drugs which relax the uterus

On rare occasions emergency tocolysis (uterine relaxation) may be required.
E.g. Fetal distress with a tonic uterus, uterine inversion, and occasionally for a manual removal of retained placenta.

For emergency tocolysis during surgery the only drugs that are sufficiently rapid and safe include:
Inhalational anaesthetic agents

Other classes of drugs that are used in a non-urgent setting (preterm labour) include:
NSAIDs (e.g. Indomethacin)
Calcium channel blockers (e.g. Nifedipine)
Magnesium sulphate
Beta-2 agonists (e.g. Ritrodrine)

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