Nuffield Department of Anaesthetics, John Radcliffe Hospital, Headington, Oxford OX3 9DU, UK
* Corresponding author. E-mail: mark.stoneham{at}nda.ox.ac.uk
Accepted for publication December 23, 2004.
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Abstract |
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Keywords: anaesthetic techniques, regional, cervical plexus block ; drugs, oxygen ; surgery, carotid endarterectomy
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Introduction |
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Pharmacological augmentation of arterial pressure can reverse neurological deficits that develop following carotid cross-clamping during awake carotid surgery.4 The mechanism postulated to explain this effect is an increase in driving pressure across the Circle of Willis from the vertebral and contra-lateral internal carotid arteries. In this case report, this intervention failed to reverse the neurological changes in two patients undergoing awake CEA. However, increasing the inspired oxygen concentration did reverse the neurological deficit, allowing surgery to conclude successfully.
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Case reports |
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On this occasion, her unpremedicated arterial pressure, recorded on the ward and in the anaesthetic room, was approximately 160/85 (mean 115 mm Hg). Perioperative monitoring consisted of: 5 lead ECG; invasive arterial pressure; arterial blood gases; oxygen saturation; and end-tidal respiratory gases estimated from within a standard variable-performance medium concentration (MC) oxygen facemask. No other cerebral monitoring technique was used. The patient was fully conscious, without sedation, throughout the procedure.
Vascular access, placement of deep and superficial cervical plexus blocks, surgical incision, and dissection proceeded uneventfully. Analysis of a sample of arterial blood, taken with the patient breathing oxygen 2 litre min1 via an MC mask revealed that the arterial partial pressure of oxygen () was 16 kPa, and the arterial partial pressure of carbon dioxide (
) was 5.1 kPa. As the MC mask is known to deliver 0.250.3%
, this
is consistent with the patient having no or negligible pulmonary shunt fraction.5
The patient's neurological status was unchanged following a period of 2 min trial cross-clamping. The surgeons therefore proceeded to eversion carotid endarterectomy rather than the standard surgical technique.6 However, 10 min after carotid cross-clamping, the patient became slightly confused, following which there was a gradual loss of consciousness until, 3 min after carotid incision, the patient was aphasic and unconscious, responding to painful stimuli with grimacing only.
This is an unusual time for presentation of a neurological deficit. Commonly this happens either immediately following carotid cross-clamping or later, when it is often associated with relative hypotension.7 However, at this stage, the patient's arterial invasive arterial pressure was 175/90 mm Hg, with sinus rhythm, rate 52 and oximetric oxygen saturation () reading 100%. With a ventilatory frequency (measured from the end-tidal carbon dioxide monitoring) of 13 to 15, the end-tidal oxygen concentration varied from 2840% (estimated from within the MC mask).
With an unresponsive patient, available options were limited. Whilst the surgeons prepared to insert an internal carotid artery shunt (considered by some surgeons to be more difficult using the inversion endarterectomy technique8), pharmacological augmentation of arterial pressure was considered and rejected as arterial pressure was already elevated. Instead, conversion to general anaesthesia was planned.
The MC mask was exchanged for an oro-nasal anaesthetic facemask administering oxygen 100%, 6 litre min1 via a circle breathing system. The plan was pre-oxygenation with oxygen 100%, intubation with a laryngeal mask airway, followed by spontaneous ventilation until the end of the procedure using a propofol infusion to maintain anaesthesia. However, after only 1 min of pre-oxygenation, the patient became more responsive. Over the next 3 min, her conscious level improved such that she became orientated in space and time, with normal speech and contra-lateral motor power. Although the dynamic change in was not recorded, assuming no change in V/Q shunt and an
of 1.0, the
may be estimated to be above 80 kPa.9
Eversion endarterectomy was completed successfully without further neurological problems with a total cross-clamp time of 28 min. Her postoperative course was uneventful. She was discharged home on the second postoperative day.
A male patient of 78 yr with a 70% stenosis of the left ICA presented for left CEA under regional anaesthesia following a dysphasic stroke 6 months earlier. Anaesthetic and surgical techniques were as described for the previous case. Oxygen 2 litre min1 was administered via an MC mask. The patient became confused and dysphasic 5 or 6 min after carotid cross-clamping. Cautious incremental administration of metaraminol (total dose 2 mg) elevated his arterial pressure to 185/85 without change in the neurological status. However, administration of oxygen 100% from a circle breathing system via an anaesthetic facemask reversed the neurological deficit completely. The MC mask was replaced, whereupon the patient became restless, anxious, and frightened over 2 or 3 min. These feelings disappeared once oxygen 100% was administered again. The operation thereafter proceeded uneventfully.
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Discussion |
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To explain the first of these, it is relevant to calculate the oxygen content of the blood at the time the patient first lost consciousness. Before carotid cross-clamping, the patient was breathing oxygen at 2 litre min1 via an MC mask.10 Her measured from arterial blood gas analysis, was 16 kPa. With a measured preoperative haemoglobin concentration of 135 g litre1, the oxygen content of the blood (
) is calculated simply as follows5:
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Substituting the figures for this case results in a calculated oxygen content of 186 ml litre1. It is reasonable to assume that, although it was not directly measured during the period of cerebral hypoxia, increasing the from 30 to 100% would increase the
to approximately 80 kPa. Thus, using the same equation (1), the oxygen content of the blood would have increased to: (0.228x80)+(1.35x135x1)=200.5 ml litre1, an increase of 14.5 ml litre1 (8%). The question is whether this increase in oxygen content could account for the dramatic improvement in neurological condition?
The steps by which decreases from air to the mitochondria are known as the oxygen cascade.5 Included are factors such as: dilution of inspired oxygen by water vapour and carbon dioxide in the alveoli; the alveolar/arterial
difference; haemoglobin carriage of oxygen; the haemoglobinoxygen dissociation curve; oxygen consumption; and oxygen diffusion through tissues. Thus, the
within the mitochondria may be as low as 0.5 kPa, although there is considerable variation between different areas of the brain.12
Eventually, under hypoxic conditions, oxygen tension reaches the critical , below which oxidative cellular phosphorylation fails. This is the start of the neurotoxic cascade,13 which ultimately, ends in cell death. In isolated mitochondria, the critical
is below 0.13 kPa,14 although as a result of the barrier to oxygen diffusion presented by the proteinaceous nature of cytoplasm, this is more likely to be 0.51.3 kPa in intact cells.15
An increase of 8% in blood oxygen content would presumably raise mitochondrial by a similar amount. This could be enough to take it above the critical level so that oxidative phosphorylation in ischaemic cerebral neurones could restart. Of course, this hypothesis is, with current technology, impossible to prove.
varies immensely in tissues and within cells. Factors include distance from capillary supply, diffusion through cellular and extracellular substrates and the oxygen partial pressure gradients. Little is known of precise neurocellular oxygen dynamics but inherently it would appear obvious that a significant increase in the gradient could rescue a cell from a critical oxygenation state to one which allows oxidative processes to occur normally. Indeed, one could even speculate that the time it took for the neurological deficit to develop (more than 5 min in both cases) indicates that the pre-event mitochondrial
must have been very close to the critical level.
Shift of the haemoglobinoxygen dissociation curve may also have been advantageous in this case. Two separate factors may contribute here. First local tissue ischaemia causes anaerobic metabolism, leading to a local increase in [H+]. This decreases pH and shifts the oxygen dissociation curve to the right, thereby helping to unload oxygen to the tissues. At low values, the oxygen dissociation curve is steep, and large amounts of oxygen are liberated per unit drop in
. Secondly, if we assume the
increased from 16 to 80 kPa, alveolar ventilation may decrease, leading to a rise in
. Eventually, ventilation may decrease by 10%, leading to an increase of up to 0.5 kPa in
. This will also tend to right-shift the oxygen dissociation curve, helping to unload oxygen to the tissues.16
Of course, the duration of ischaemia is also critical here. For cerebral tissues, irreversible hypoxia may result after just a few minutes of ischaemia. In this case, the duration of the neurological deficit was itself only 1 or 2 min.
This phenomenon could be investigated by looking at the influence of oxygen 100% on the of blood in the internal carotid artery above the carotid cross-clamp, and on jugular venous
. It would be interesting to know what the decrement in distal carotid
associated with detectable neurological deficit is. Near infrared spectroscopy has previously been used to monitor cerebral oxygenation during carotid endarterectomy17 18 and angiography,19 but the technique is global and does not offer the sensitivity that is required to elucidate oxygen status changes in the most oxygen-sensitive brain areas.20
The management of patients developing neurological deficit during awake carotid endarterectomy is controversial. The options available depend on the experience of the anaesthetist, the conscious level of the patient, and the degree of neurological deficit. There is one major decision to makewhether to attempt to reverse the neurological deficit or to convert to general anaesthesia, which is the fall-back option. This must obviously be considered a priority if the patient's airway is compromised because of reduced conscious level or seizure activity. However, there have been previous descriptions of pharmacological intervention to reverse the neurological deficit, in particular elevation of arterial pressure.4 The mechanism hypothesized to explain this is via an increase in perfusion pressure across the Circle of Willis. Exponents of general anaesthesia for carotid surgery have also described deliberate hypertension to 25% above baseline as a preventative measure to maintain cerebral perfusion.21
Given that the aim of any such intervention is to increase the of blood in the ipsilateral cerebral cortex, then increasing the oxygen content of the blood to as high a level as possible may be considered as an additional intervention to be tried. For patients undergoing carotid endarterectomywhich is a preventative, not curative, operationto suffer a perioperative stroke is a disaster. The administration of supplementary oxygen is another therapeutic possibility, which may be added to the list of options when cerebral ischaemia occurs. At the very least it may buy time in terms of the integrity of the cortical neurones.
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