Atypical presentation of subdural block resulting in Horner’s syndrome and loss of consciousness

Abstract

Horner’s syndrome is a rare side effect for patients receiving epidural anaesthesia. Studies described Horner’s syndrome due to cephalic spread of injected anaesthetics, a high spinal anaesthesia, or a sign of an inadvertent subdural block. A 31-year-old woman (Gravida 1 Para 0) at 40 weeks and 2 days had a caesarean section secondary to second stage arrest. Fourteen minutes after she received the lidocaine bolus, she became unresponsive with nystagmus, unequal pupils and no pupillary reflex. Head CT and MRI showed no intracranial haemorrhage and 2 hours later, she had spontaneous resolution of neurological symptoms with no further sequelae. Although Horner’s syndrome is a benign, transient process, clinicians should be mindful regarding epidural catheter placement causing subdural blocks resulting in spontaneous, reversible neurological deficits.

Background

Horner’s syndrome is a rare side effect for patients receiving epidural anaesthesia with an incidence of about 0.5%–0.82%.^{1 2} The rate of occurrence increases to as high 4% when patients receive bolus of anaesthetic medication prior to caesarean section.¹ Symptoms of Horner’s syndrome include ptosis, miosis, anhidrosis, facial congestion and enophthalmos.³ Cephalic spread of injected anaesthetics, high spinal anaesthesia or an inadvertent subdural block have resulted in Horner’s syndrome.^{1 4} There is no clear guideline in the management of Horner’s syndrome following epidural placement as some authors indicate that Horner’s syndrome is a benign and transient process requiring no further treatment.^{1 3} However, if a subdural block is suspected, then neuraxial analgesia should be discontinued with close monitoring of the patient. Patients may present with cardiovascular collapse resulting in hypotension, bradycardia, and hypoxia.^1–3

With written and verbal consent, we present an atypical presentation of a patient with suspected Horner’s syndrome and loss of consciousness due to a suspected inadvertent subdural block.

Case presentation

A 31-year-old woman (gravida 1, para 0) at 40 weeks and 2 days was admitted to labour and delivery for an elective induction of labour. She had received an epidural 16 hours prior to delivery during her induction. Of note, the anaesthesiologist had reported a light pink/red tinged aspirate from the epidural catheter during placement; but the patient had reported adequate anaesthesia. She progressed to fully dilated and pushed for over 2 hours in different positions with no fetal descent. At this time, second stage arrest of labour was diagnosed, and delivery by caesarean section was recommended to the patient. The patient was given a bolus of 16 mL 2% lidocaine with epinephrine.

During the caesarean section, 0.2 mg of intramuscular methergine was given for uterine atony 1 min after placental delivery. Estimated blood loss was 800cc. Two minutes later (14 min after the patient received the lidocaine bolus), she had a loss of consciousness. She was unresponsive to sternal rub and jaw was clenched. She had nystagmus, subjective left ptosis (constricted pupil) with no active pupillary reflex to light stimulus. Her oxygen saturation briefly decreased to 90% to room air and returned to 98%–99% after jaw thrust performed by the anaesthesiologist. Magnesium sulfate was started for treatment of a suspected eclamptic seizure. Vitals were stable with blood pressures being 120–130 s/60–70 s mm Hg and heart rates 100–120 s bpm during this time.

Investigations

A code stroke was called, and the patient was taken for an emergency head CT scan without contrast, which demonstrated no haemorrhage or ischaemia. Gas was noted within the cavernous sinus (figure 1). While the patient was having her CT performed, she regained consciousness (alert, oriented and able to follow commands) with no neurological deficit other than persistent constriction of left pupil. Due to the emergent situation, an objective assessment with an MRD1 was not performed to measure her constricted pupil. Her symptoms resolved before the neurologist was able to objectively assess the patient’s physical findings. The patient was unresponsive for a total of 25 min. An MRI of the head was performed, and the findings continued to show subarachnoid air in the prepontine cistern as well as the left Cerebellopontine (CP) angle cistern (figure 2).

Figure 1.

Head CT without contrast depicting air bubbles in the cavernous sinus and no intracranial haemorrhage.

Figure 2.

MRI of head showed subarachnoid air in the prepontine cistern as well as the left Cerebellopontine (CP) angle cistern.

Treatment

She was immediately transferred to the intensive care unit for further monitoring. Approximately 2 hours after lidocaine bolus, the patient was re-evaluated, and it was noted that she had spontaneous resolution of any neurological deficits including physical findings (left ptosis). The patient was alert and lucid. She indicated that she had no recollection of the events during the caesarean section and felt as though she had just ‘awaken from sleep’. On further questioning, the patient denied sudden headache, tinnitus or metallic taste prior to losing consciousness. A video electroencephalography was within normal limits with no signs of seizure activity. A repeat head CT was performed 2 days later showing complete resolution of the air bubble. The epidural catheter was removed on post-operative day 1.

Outcome and follow-up

The patient was downgraded to the postpartum floors. During that time, she remained stable without any further episodes of unconsciousness or neurological deficits including unilateral ptosis. The patient was seen for her 6-week postpartum follow-up and continued to remain stable with no more instances of unresponsiveness, memory loss or ocular abnormalities. Her follow-up with neurology was benign and required no additional workup.

Discussion

Horner’s syndrome caused by lumbar anaesthesia is a rare but benign and transient condition that does not typically require extensive workup.³ Physiological effects of pregnancy are theorised to increase epidural pressure, due to the narrowing of the epidural space in obstetric patients, for which uterine contractions also contribute to cephalic spread of the anaesthetic agent and disrupt the oculosympathetic pathway.^{1 3} Patient positioning is also a factor in cephalic spread as patients are typically placed with a left lateral tilt during a caesarean section. Anaesthetic medication is usually lipophilic and tends to concentrate on the ‘lower side’. These gravitational forces tend to favour the ipsilateral (left) side during a caesarean section, which is why Horner’s syndrome is often unilateral.^{3 4} Timing of symptoms related to Horner’s syndrome occur on average between 10 and 25 min after a bolus with resolution of symptoms occurring after about 215 min later.^{3 4}

Dural puncture may be unrecognised until a large bolus of local anaesthesia is injected into the epidural catheter. This causes a rupture of the fragile subarachnoid membrane and potentially allows a high level of anaesthetic medication to enter the intrathecal space resulting in loss of consciousness, apnoea and cranial nerve involvement.^{2 4 5} Subdural block may be difficult to diagnose due to varying symptoms and findings. In addition, onset of symptoms is typically 15–20 min and last for about 2 hours.⁵ Although relatively benign, Horner’s syndrome may precede a high sympathetic block resulting in a cardiovascular collapse.³

Our patient did not experience any cardiac instability including maternal hypotension, bradycardia or a decline in respiratory drive during her episode. The authors theorise that hypotension may have been prevented due to rapid increase in cardiac output from physiological autotransfusion proceeding placental delivery and injection of intramuscular methylergometrine (methergine). Although the patient became unresponsive, she was without apnoea and was still able to breath on her own 14 min after the anaesthetic loading dose. Karaca et al reported that their patient experienced bilateral pupillary dilation in addition to loss of consciousness and apnoea in their case report resulting from an accidental subdural block.⁵ On the contrary, our patient developed Horner’s like symptoms with unilateral left sided pupillary constriction, with eventual complete resolution of all neurological deficits. Given the patient’s timing of symptoms from the lidocaine bolus, it is likely that her symptoms were caused by an unrecognised mild subdural block leading to a loss of consciousness in combination with Horner’s syndrome.

There was initial concern that the patient had suffered a reversible cerebral vasoconstriction syndrome (RCVS) caused by injection of intramuscular methergine. Ishibashi et al describes RCVS as cerebral vasoconstriction with acute severe headache.⁶ However, our patient did not show signs of hypertensive emergency and no symptoms of an acute headache prior to losing consciousness. She also regained consciousness about 40 min after the start of the caesarean section, which is not congruent with the expected half-life of methergine (120 min).⁶

Other potential causes, though less likely, may have been due to the occurrence of pneumocephalus, which is the introduction of intrathecal air into the cerebrospinal fluid (CSF) during epidural placement or redosing. If the dura is inadvertently punctured, air may be injected into the subarachnoid space and CSF via the loss of resistance technique.^{7 8} Patients do not typically present symptoms but are associated with severe headaches immediately after epidural placement. Given that the patient had received her epidural 16 hours prior to her caesarean section, pneumocephalus is an unlikely aetiology for her symptoms. Although, the CT and MRI demonstrated air bubbles in the subarachnoid space, this is an incidental finding.

Loss of consciousness has been reported with potential transient damage to cranial nerves including cranial nerve palsies from pneumocephalus. However, the air bubbles usually dissolve within 24 hours with no neurological sequalae.⁹

Of the countless epidurals performed every year, obstetricians should be aware of the potential neurological causes of placement of epidural during labour as well as for caesarean section. Although Horner’s syndrome on its own is a benign, transient process, clinicians should be mindful regarding epidural catheter placement that may lead to subdural blocks can be associated with spontaneous, reversible neurological deficits.

Patient’s perspective.

I am thankful for the medical team for helping me. Unfortunately, I have no recollection or memory as to what had happened. I’m surprised at everything that happened. I just felt like I had gone to sleep and woke up.

It’s been over a month and a half since the incident and I feel well. I haven’t had any more episodes like before and am following up with the neurologist.

Learning points.

• Subdural blocks can present atypically resulting in both Horner’s syndrome and loss of consciousness in obstetric patients.

• Subdural blocks can result in spontaneously reversible neurological events.

• Clinicians should be aware of the effects of epidural and subdural blocks, especially during a caesarean section.

Ethics statements

Patient consent for publication

Obtained.