Epidural sieve: A blessing in disguise!

A 34-year-old female, G2P1L1, presented at 40 weeks' gestation in active labour and requested for epidural analgesia. She had a previous normal vaginal delivery and was a well-controlled gestational diabetic. General and systemic examinations were normal. Hemoglobin was 11.4 g/dl.

The patient was positioned laterally and using midline approach at L3--L4 interspace, the epidural space was located with loss of resistance to air at 5.5 cm from skin. The catheter was fixed at 9.5 cm. Test dose 3 ml 2% lignocaine with adrenaline was given. Sensory blockade up to T8 was achieved, and analgesia was maintained with infusion ropivacaine 0.15% at 10 ml/h. Post- procedure vitals were stable, foetal heart rate was 153/min, and labour was augmented with oxytocin infusion. An hour later, she complained of mild left sided abdominal discomfort, and a bolus of 3 ml 0.15% ropivacaine was administered.

Three hours later the patient experienced continuous left sided abdominal pain unrelated to contractions and prolonged foetal bradycardia for 3 min on Cardiotocography. The maternal haemodynamics were stable. A per vaginum examination showed a fully dilated cervix with the vertex at station minus 2. On reexamining the patient in the operating room there was persistent foetal bradycardia with no changes in vaginal examination, necessitating a category 1 lower segment caesarean section. Preoperatively the vitals were normal. Standard monitors were attached. The patient was co-loaded with 500 ml crystalloid, O2 was started at 4 L/min and a wedge was placed under the right buttock. Epidural anaesthesia was augmented with 10 ml 2% lignocaine with adrenaline after negative aspiration for CSF and blood. An additional bolus of 5 ml 2% lignocaine with adrenaline was given to achieve a sensory level of T4 and surgery was commenced. About 200 ml of clear fluid was noted in the peritoneal cavity and the lower uterine segment appeared oedematous and congested. On opening the uterovesical fold, fresh blood and clots were noticed between myometrial layers and they were evacuated. The lower segment of the uterus was opened, and the baby was delivered. The APGAR score was 5/10 and the baby required bag and mask resuscitation. After placental delivery, a tear was observed on the right lateral aspect of the lower segment extending inferolaterally to the cervix and upper vagina. It was repaired in two layers. Few episodes of hypotension due to a blood loss of 1700 ml were managed with boluses of ephedrine and 500 ml colloid. The maximum allowable blood loss was approximately 2,400 ml, hence blood was not transfused intraoperatively. The postoperative hemoglobin was 8.3 g/dl.

The overall incidence of uterine rupture is about 0.07% but it leads to adverse maternal and foetal outcomes.[1] The risk of uterine rupture increases with multiparity, uterine instrumentation, trauma, post-surgical scarring, foetal macrosomia, and use of uterotonics.[23] Incomplete ruptures leave the peritoneum intact, whereas uterine contents spill into the peritoneal cavity in frank rupture.[4] Our patient had an incomplete rupture.

Initial nonspecific signs delay diagnosis. Foetal bradycardia, variable decelerations are the most common presentations (70%). Maternal signs include hypotension (5-10%), bleeding per vaginum. (3-5%), uterine atony, and rarely abdominal pain unrelated to contractions.[3] The initial abdominal discomfort post-procedure was a nonspecific sign, treated with bolus without further evaluation. Persistent late decelerations served as ominous signs requiring immediate attention without much thought about the ongoing abdominal pain.

Chestnut suggested that epidural analgesia improved specificity of abdominal pain as a symptom of uterine rupture.[5] Crawford described the epidural sieve wherein appreciation of physiological pain is prevented but pathological pain is transmitted.[6] Pain of placental abruption and uterine rupture are examples. Gradation of effectiveness of blocking impulse transmission occurs when axons are subject to local anaesthetic, thus increasing intensity or frequency of stimuli can overcome established block in certain situations.[6]

The concentrations used for labour analgesia are slightly higher than minimal blocking concentration resulting in axonal blockade providing analgesia. Any stimulus greater than physiological pain can cause impulse conduction through the blocked axonal segment leading to perception.[6]

Rashique et al. reported that addition of opioids to local anaesthetic abolished the sieve delaying diagnosis.[7] Similar findings occurred with a large epidural bolus of local anaesthetic.[8]

Inadequate dosage, tachyphylaxis, faulty technique, missed segment, catheter dislodgement/migration are differentials.[9] To achieve analgesia doses are increased or boluses given instead of evaluating the cause of pain. Sudden change in character of pain, persistence, and increased drug requirement often indicate pathological pain.

Camus et al. recommended usage of lowest effective local anaesthetic dose, minimizing opiods, and accounting for cumulative effects of boluses for early recognition of uterine rupture under epidural analgesia.[9]

The existing epidural catheter was used for anaesthesia as the monitored foetal heart rate remained above 100/min, maternal haemodynamics were stable, faster action of lignocaine with adrenaline as compared with other local anaesthetics and to avoid complications of general anaesthesia.

Frequent requirement of top-ups due to breakthrough pain in a previously effective epidural should be monitored vigilantly and evaluated for a cause that could be more serious than a failed block. Awareness of obstetric complications by the anaesthetist can prompt early diagnosis. As rightly said pain is the fifth vital sign that should not be ignored!

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Conflicts of interest

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