Department of Anaesthesiology, Faculty of Medicine, University of Malaya Medical Centre, 50603 Kuala Lumpur, Malaysia
Accepted for publication: April 14, 2000
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Abstract |
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Br J Anaesth 2000; 85: 4746
Keywords: anaesthesia, depth; anaesthetic techniques, subarachnoid; anaesthesia, obstetric
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Introduction |
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Case report |
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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 patients 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 min1. 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 litre1. 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.
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Discussion |
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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.
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Footnotes |
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References |
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