Loss of consciousness following spinal anaesthesia for Caesarean section

Y. K. Chan*, R. Gopinathan and R. Rajendram

Department of Anaesthesiology, Faculty of Medicine, University of Malaya Medical Centre, 50603 Kuala Lumpur, Malaysia

Accepted for publication: April 14, 2000


    Abstract
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
A healthy parturient under spinal anaesthesia for Caesarean section lost consciousness for an hour, 20 min after the intrathecal injection of 2 ml of 0.5% heavy bupivacaine. The patient was haemodynamically stable before losing consciousness. The differential diagnosis is discussed.

Br J Anaesth 2000; 85: 474–6

Keywords: anaesthesia, depth; anaesthetic techniques, subarachnoid; anaesthesia, obstetric


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Spinal anaesthesia is increasingly used for Caesarean section1 as it is remarkably safe and effective.2 Its safety3 lies in the fact that parturients are conscious throughout anaesthesia and are not exposed to the hazards of intubation. Patients can lose consciousness in the presence of a total spinal block,4 usually characterized by severe hypotension.5 However, loss of consciousness with this technique in a haemodynamically stable patient is unusual. We report a parturient who lost consciousness 20 min after a successful spinal anaesthetic block.


    Case report
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
The parturient, a 25 yr old, 160 cm, 55 kg normotensive primigravida with mild polyhydramnios, required an elective Caesarean section for delivery of a baby with bilateral pleural effusions of unknown cause. She had no other medical condition of note; in particular, she had no psychiatric history. Plasma electrolytes were normal before surgery. Sodium citrate and oral ranitidine were given in the ward before delivery; no other drugs were administered and the patient was not on any medication. Immediately before spinal blockade, Unasyn 1.5 g (subactam 500 mg and ampicillin 1000 mg) diluted in sterile water was administered as an intravenous infusion. For spinal block, a 26 G Atraucan (B Braun) spinal needle was used at L3/4 in the midline with the patient in the sitting position. Cerebrospinal fluid flowed from the needle after a single attempt and 2 ml of 0.5% heavy bupivacaine was injected after initial aspiration. The patient was then placed horizontally with a left lateral tilt and a single pillow to support the head. A T4 level of block was obtained by 5 min and the Bromage score before surgery was zero. Before delivery of the baby, the parturient’s arterial pressure was measured every 5 min with a Dinamap. This averaged around 110/60 mm Hg with one transient episode of hypotension (90/50 mm Hg) about 5 min after the spinal injection, which improved with the administration of ephedrine 5 mg. The heart rate averaged 80–100 beats min–1. Three litres of oxygen were administered by nasal prongs; oxygen saturation was 99–100%. Hartmann’s solution (500 ml) was given as a preload and a second 500 ml was commenced before the baby was delivered. During this period the patient was alert and communicating with the anaesthetist. No other drugs were administered for 15 min before delivery of the baby.

At the time of delivery, 20 min after administration of the intrathecal drug, the patient suddenly stopped communicating, as if going off to sleep. She was not responding to verbal commands or to deep pain. There was no frothing, and no uprolling of the eyeballs. The incident was not preceded by nausea and vomiting. There were no complaints of chest pain, inability to breathe or weakness of the upper limbs immediately before loss of consciousness. There was a transient period of apnoea with a dramatic drop in oxygen saturation to around 75%. The patient’s lungs were ventilated with a face mask for 1 min on the circle system after which spontaneous ventilation resumed. No bronchospasm or urticaria was noted. The anaesthetist tried to intubate the patient at this stage but was unsuccessful as the patient had a very strong gag reflex. A decision was made not to give additional drugs to sedate or paralyse the patient as it was noted that she was able to protect her airway. Both of her pupils were about 3 mm wide and reactive to light. Throughout this period of loss of consciousness, arterial pressure averaged around 100/55 mm Hg and the pulse rate was about 80 min–1. Ten minutes into the incident the patient was responding to deep pain with non-purposeful movements of the upper limbs. Gradually the movements on deep pain became more purposeful but there was still no verbal response. One hour after the onset of the incident, the patient opened her eyes to commands and had slurred speech when she attempted to talk. Muscle power in the upper limbs at this stage was grade 4 and her sensory level was at T2 bilaterally. The blood sugar concentration was 3.9 mmol litre–1. One and a half hours after the onset of the loss of consciousness, the patient was fully alert and her upper limb muscle power was grade 5 with a sensory level at T5. When questioned about her loss of consciousness, she said that she had felt extremely sleepy, had gone to sleep and was unable to recall the event. Four hours after loss of consciousness, the spinal block had totally worn off, with grade 5 muscle power in all four limbs. The patient was discharged back to the ward where the anaesthetist visited her for the next few days. The baby died because of severe heart failure, with a single atrium, single ventricle and pulmonary atresia, 2 h after delivery.

Twenty-four hours after spinal injection, the patient complained of giddiness and a postural frontal headache which gradually worsened. CT scan results were normal and an EEG showed no abnormal foci. An epidural blood patch relieved the headache immediately. The patient was discharged 1 week after the incident with no further complaints.


    Discussion
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A non-sedated parturient given an intrathecal local anaesthetic injection should never lose consciousness. In this particular parturient, there was no history of epilepsy or diabetes to cause loss of consciousness. A blood sugar concentration of 3.9 mmol litre–1 is at the low end of the normal range but was not low enough to account for the loss of consciousness. The normal EEG indicated that the event could not be explained by an epileptic seizure. A CT scan done when the patient developed a headache 24 h after the incident was normal. This indicated that there was no space-occupying lesion intracranially to account for the loss of consciousness during the Caesarean section. As magnetic resonance imaging (MRI) is superior to CT scanning for evaluating most suspected central nervous system pathology,6 we should, in retrospect, have subjected the patient to MRI instead. Only 2 ml of 0.5% bupivacine was given intrathecally and the patient was subsequently placed horizontally, so the signs could not be attributed to a total spinal block. The patient did not develop significant hypotension, respiratory depression or pupillary dilation to warrant a diagnosis of total spinal block.4 5 The anaesthetist was certain that the loss of consciousness could not be attributed to any intravenous sedative drugs being given inadvertently, as no drugs were administered for 15 min before delivery of the baby. It was unlikely that the patient had an amniotic fluid embolism,7 although the event occurred at the time of delivery of the baby. She was stable cardiovascularly and at no time was there any coagulopathy. The event was also unlikely to be the result of a pulmonary embolism,8 as the patient had a normal cardiac rhythm. There was no cardiovascular compromise at the time of the event and no residual neurological deficit after regaining consciousness. However, echocardiography was not attempted. Air embolism occurring at the time of delivery can also be responsible for the loss of consciousness. For loss of consciousness to have occurred, air must have reached the left side of the heart through a patent foramen ovale. This was not ruled out by echocardiography, but air embolism is unlikely as there were no complaints of dyspnoea or chest pain,9 nor was there residual neurological deficit beyond the period of loss of consciousness. The patient described by Davis, Glover and Maycock,10 with cerebral arterial air embolism, not only had a prolonged recovery from general anaesthesia but had a neurological deficit for several days despite hyperbaric oxygen therapy.

Skowronski and Rigg11 and Philip and Walter12 described loss of consciousness in patients following the administration of epidural anaesthesia for labour. In both these parturients, the loss of consciousness had occurred, as in our patient, in the presence of remarkable haemodynamic stability. These were described as total spinal anaesthesia. These complications were probably the result of subdural spread. The signs that alerted the anaesthetists to the cranial extension in these case reports were difficulty in breathing,11 arm weakness12 and dysarthria.12 These signs developed slowly with time and the anaesthetists involved were able to detect them. In our case, the loss of consciousness after 20 min of relatively uneventful spinal blockade was the first sign of a possible cranial extension. The loss of consciousness precluded detailed sensory and motor testing in the head, but the gradual and progressive return of function indicated that it could have been compatible with anaesthetic blockade that receded with time. Although we do not have radiological evidence to prove that this incident was caused by subdural blockade, we believe that the clinical events that occurred in our patient are in keeping with this suggestion.5 13 These include relatively stable arterial pressure, slow onset of symptoms after 20 min and complete recovery after almost 2 h. The absence of sympathetic blockade14 15 is consistent with subdural blockade.

The parturient could have lost consciousness as a psychogenic response to distress felt at the time of the Caesarean section, knowing that her newborn was critically ill and not expected to survive the neonatal period. Hysteria cannot be excluded from the differential diagnosis since measurements taken during the incident were normal except for a transient episode of hypoxia and the 1 h loss of consciousness. Normal antenatal and postnatal mental health makes this diagnosis improbable.

In summary, we have described loss of consciousness in a parturient who had a successful spinal block. The loss of consciousness occurred in the presence of remarkable haemodynamic stability. Despite investigations, we were unable to determine the cause. We can only speculate that a subdural block complicating the spinal block may have accounted for this most unusual event.


    Footnotes
 
* Corresponding author Back


    References
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
1 Brown GW, Russell IF. A survey of anaesthesia for Caesarean section. Int J Obstet Anesth 1995; 4: 214–8

2 Moore DC. Spinal (subarachnoid) block; a review of 11574 cases. J Am Med Assoc 1966; 195: 907–12[Medline]

3 Report on confidential enquiries into maternal deaths in the United Kingdom 1988–1990. London, HMSO, 1994.

4 Gillies IDS, Morgan M. Accidental total spinal analgesia with bupivacaine. Anaesthesia 1973; 28: 441–5[ISI][Medline]

5 Collier C. Total spinal or massive subdural block? Anaesth Intens Care 1982; 10: 92–3[Medline]

6 Quint DJ. Indications for emergent MRI of the central nervous system. J Am Med Assoc 2000; 283: 853–5[Free Full Text]

7 Clark SL. New concepts of amniotic fluid embolism: a review. Obstet Gynecol Surv 1990; 45: 360–8

8 Dehring DJ, Arens JF. Pulmonary thromboembolism: Disease recognition and patient management. Anesthesiology 1990; 73: 146–64[ISI][Medline]

9 Malinow AM, Naulty JS, Hunt CO, Datta S, Ostheimer G. Precordial ultrasonic monitoring during Cesarean delivery. Anesthesiology 1987; 66: 816–9[ISI][Medline]

10 Davis FM, Glover PW, Maycock E. Hyperbaric oxygen for cerebral arterial air embolism occuring Caesarean section. Anaesth Intens Care 1990; 18: 403–5[ISI][Medline]

11 Skowronski GA, Rigg JRA. Total spinal block complicating epidural analgesia in labour. Anaesth Intens Care 1981; 9: 274–6[ISI][Medline]

12 Philip JH, Walter UB. Total spinal anesthesia late in the course of obstetric bupivacaine epidural block. Anesthesiology 1976; 44: 340–1[ISI][Medline]

13 Reynolds F, Speedy HM. The subdural space: the third place to go astray. Anaesthesia 1990; 45: 120–3[ISI][Medline]

14 Pearson RMG. A rare complication of extradural analgesia. Anaesthesia 1984; 39: 460–3[ISI][Medline]

15 Stevens RA, Stanton-Hicks MD. Subdural injection of local anesthetic: a complication of epidural anesthesia. Anesthesiology 1985; 63: 325–6





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