Hyperbaric oxygen therapy in the treatment of post cardiac surgical strokes--a case series and review of the literature.
This paper reviews a series of 12 patients with post-cardiac surgical stroke in one centre between 1993 and 2006 who were treated with hyperbaric oxygen therapy (HBOT) and examines the rationale behind the use of HBOT in this condition.
Between 1993 and 2006, 12 patients with postcardiac surgical stroke were treated with hyperbaric oxygen in the Christchurch Hospital hyperbaric facility. Data were collected from a retrospective review of the hospital medical and hyperbaric unit records. The main outcome measures were survival, neurological outcome and the type of discharge facility to which the patients were sent. Follow-up information was obtained from the medical records and telephone contact with the patients where possible.
A 55-year-old man undergoing an aortic valve replacement (AVR) had spontaneous return of cardiac activity following release of the aortic clamp and before air could be evacuated from the left ventricle. Blanching was noted over the distribution of the right temporal artery and the heart then fibrillated. Defibrillation was eventually achieved and postoperatively he remained with a diminished Glasgow Coma Score of 11/15 and also had a dense left hemiplegia. He was transferred to the Christchurch Hospital hyperbaric facility the following day for HBOT.
After the first treatment which consisted of a Royal Navy treatment table 62 (RN62), he had some improvement in his left-sided weakness but it was also apparent that he had some right-sided weakness. He was able to be extubated at this stage and went on to have three further daily 18:60:30 treatments during which time he continued to improve.
When assessed one week later prior to his referral back to his home team, he had made a complete neurological recovery.
A 72-year-old woman underwent an AVR with no apparent intraoperative problems. However, postoperatively she failed to regain consciousness and had a left-sided hemiparesis. A computed tomography (CT) scan demonstrated a 'watershed' pattern infarction of the right middle and posterior cerebral artery territories. She was kept intubated and transferred one day postoperatively to Christchurch Hospital for HBOT. The first treatment was a table RN62 and was followed up with four daily 18:60:30 treatments. She was extubated after the second treatment and by the end of the treatment course, was fully conscious and with minimal left-sided weakness. This had completely resolved when assessed two weeks later.
A 53-year-old woman with mixed mitral valve disease and moderate aortic prosthetic incompetence from an AVR 20 years previously, underwent a mitral valve replacement (MVR) and closure of a fistula between the left atrium and aorta. The procedure was complicated by puncture of the carotid artery when cannulation of the right internal jugular vein was attempted. The day following surgery, she had failed to regain consciousness, had extensor posturing in her limbs and diminished left-sided motor responses. She underwent one RN62 treatment 20 hours following surgery with no apparent improvement in her responses. A CT scan showed an extensive right middle cerebral artery territory infarction with 8 mm of midline shift as well as infarctions in the cerebellar and pontine regions. Echocardiography excluded any left ventricular thrombus. A few hours after her HBOT she developed an enlarged unresponsive right pupil accompanied by a hypertensive response which failed to respond to intracranial pressure control measures and she died later that day.
A 53-year-old man had a MVR and annuloplasty with no apparent intraoperative problems. However, postoperatively it was clear that he had a dense left hemiplegia. A RN62 treatment was commenced within four hours of the end of surgery, followed by two daily Royal Navy table 61 (RN61) treatments. A CT scan showed a single area of oedema or infarction of the watershed territories of the right middle and anterior cerebral arteries, which at the time led to the suggestion that air embolism was not likely to be the cause. As he had not demonstrated any dramatic improvement by day three, no further HBOT was undertaken. At surgical follow-up at six weeks, he had made a complete neurological recovery.
A 63-year-old woman had an uneventful AVR. Upon wakening she had an obvious left-sided hemiparesis affecting her arm to a greater extent than her leg. She was not referred to the hyperbaric service until her second postoperative day with no change in her condition at that time. She underwent a RN61 HBOT and this was repeated the following day. This was associated with significant improvement in her symptoms. She went on to complete six further daily treatments each of 14:90:30 and at the end of this treatment course she had minimal weakness in her left shoulder and elbow only.
A 74-year-old man underwent a Bentall's procedure with no obvious problems. His recovery was complicated by a left hemiplegia, which became apparent upon wakening. He was referred to the hyperbaric service and underwent an extended RN62 which was initiated four hours following the end of his surgery. Following this treatment he had some return of function in his hand and foot. Over the next four days he received daily table 18:60:30 treatments, during which time he made steady improvement. By the end of the treatment course he was able to walk unassisted and had minimal weakness in his left arm and leg.
A 69-year-old woman had an off-pump coronary artery bypass procedure. However, during the procedure a tear occurred in the ascending aorta, necessitating a repair on cardiopulmonary bypass. When assessed postoperatively while still intubated, she had no movement in either leg or in her right arm. Her level of consciousness remained diminished. She was transferred to the hyperbaric unit and underwent a RN62 HBOT. Following this treatment she had an improved level of consciousness and was moving her left arm and leg. The following day she had a 18:60:30 treatment and was then able to be extubated. There was some return of function in her right arm and leg, however no further HBOT was offered as she was known to have bilateral carotid artery stenosis and an ischaemic cerebrovascular accident was thought the more likely diagnosis. However, she continued to improve such that by the time she left hospital she was largely independent and walking with a gutter frame.
A 77-year-old man had an AVR and mitral valve repair which appeared to go uneventfully. He was slow to wake postoperatively and once able to be assessed, he had an obvious left hemiparesis. He was kept intubated and transferred for HBOT. Ten hours after the end of his surgery he was commenced on a RN62. The next day there was no significant change in his condition and no further HBOT was offered. A CT scan showed a "low density lesion in the right fronto-parietal region consistent with ischaemia and low density white matter change consistent with small vessel disease". However, his symptoms continued to improve such that he was able to leave hospital one week following his surgery with normal power in his left arm and minimal weakness in the leg.
One day following this 65-year-old man's uneventful MVR and closure of a patent foramen ovale, he remained confused and with left-sided weakness and neglect. He underwent a RN62 HBOT some 24 hours following his surgery. The following day he had one further 14:90:30. Following his treatment course he demonstrated some improvement and by the time he was seen for his six-week surgical follow-up, his symptoms and signs had completely resolved.
A 77-year-old woman had a combined AVR and coronary artery bypass procedure. At surgery some intravascular air was noted at the time of regrafting one of the vessels. Postoperatively she was slow to wake and had a dense left hemiplegia. The following morning she was extubated but required reintubation due to a marginal airway and raised arterial carbon dioxide. She was then transferred for HBOT which commenced 24 hours following her surgery. A RN62 was followed by
extubation and then three daily 18:60:30 HBOT.
However, the last treatment was abandoned after 30 minutes due to claustrophobia and agitation. She was much improved by the end of the treatment course. Her limbs were of normal strength but there was mild facial asymmetry and mild short-term memory deficit.
A 79-year-old woman was slow to wake following an uneventful AVR and coronary artery bypass procedure. She appeared agitated and had a dense left hemiplegia. Preoperative carotid ultrasound had excluded any carotid disease and, despite the absence of any intraoperative concerns, she was offered HBOT. Some 18 hours following her surgery she underwent a RN62 HBOT while still intubated. The following day she had one further 18:60:30 HBOT. At this stage, there had been no obvious response and no further HBOT was offered. She was then extubated and her postoperative course was further complicated by a chest infection and congestive heart failure.
By the time she was transferred to another hospital for rehabilitation she had made a complete recovery from her hemiplegia. However, she was then transferred back to the cardiological team after another two weeks with cardiogenic shock, to which she succumbed.
A 67-year-old woman had a MVR and tricuspid valve repair during which a "rush of air" was noted from the aortic root needle. Postoperatively she had a diminished level of consciousness with a dense left hemiplegia and left-sided neglect. She was kept intubated to facilitate HBOT. Some 12 hours following her surgery she received a RN62 treatment followed by two further daily treatments, one RN61 and one 18:60:30. Her level of consciousness had improved after the second treatment such that she was able to be extubated but there was minimal improvement in her hemiplegia. A CT scan on day two following her surgery showed extensive areas of oedema and infarction throughout the right cerebral hemisphere, consistent with a watershed type of infarction plus some focal areas of haemorrhagic transformation.
At follow-up she had improved to some degree but had residual left-sided hemiparesis such that she could only walk with the aid of a stick.
There were five males and seven females in the series with an average age of 67 years (range 53 to 79 years). All patients had undergone an open-heart procedure with 11 of the 12 receiving a valve replacement and the 12th a coronary artery bypass graft complicated by a tear to the ascending aorta, which required repair. In only four of the 12 cases was there any clinical suspicion of an air embolism event at the time of surgery.
The most common presentation was delayed or incomplete recovery in the intensive care unit plus focal neurological signs of a stroke, which in all cases affected the patient's left side.
The average delay between surgery and the first HBOT was approximately 18 hours (range 4 to 48 hours). This delay was due to the inherent difficulties of making the diagnosis in a patient recovering from anaesthesia or an initial failure to consider the diagnosis. As well, three patients were transferred from another centre.
The HBOT was carried out in the Christchurch Hospital multiplace hyperbaric facility with trained staff in attendance. The first HBOT was preceded in all cases by bilateral myringotomies performed by an ear, nose and throat surgeon to prevent aural barotrauma. The mean number of HBOTs per patient was three (range one to three). The initial HBOT was usually a RN62 (lasting a total of 4.75 hours, initially at a pressure of 2.8 ATA and then reduced to 1.9 ATA), which is the standard treatment used for the initial presentation of cerebral arterial gas embolism (CAGE) related to self-contained underwater breathing apparatus (SCUBA) diving accidents. Patients who presented later than 24 hours usually received a shorter initial treatment, such as a RN61 (similar profile to RN62 but for only 2.25 hours). Follow-up treatments were usually treatment table 18:60:30 or 18:90:30 (60 or 90 minutes respectively at 2.8 ATA, followed by a 30 minute decompression). The choice of treatment table was usually a pragmatic one to fit in with the availability of staff and the clinical state of the patient. Treatment courses were stopped once the patient recovered or died or when no further improvement was seen after two sequential treatments.
The HBOT was generally well tolerated with no complication in any of the patients attributable to HBOT. In one patient, the final treatment was abandoned after 30 minutes of the scheduled 90 minutes because of agitation due to claustrophobia.
By the end of the HBOT course there was a partial or complete resolution of neurological symptoms and signs in eight of the 12 patients. Three patients demonstrated minimal neurological improvement and one further patient who received a single HBOT died a rapid neurological death.
At follow-up, five of the remaining 11 patients had fully recovered and four had minimal residual symptoms. One patient remained hemiplegic but mobile and one patient had made a full neurological recovery but died a cardiological death one month following her surgery. In total, nine of the 10 surviving patients were able to return to their home or previous level of care.
Risk factors for post-cardiac surgical strokes
A number of studies have identified risk factors for the development of post-cardiac surgical strokes (2,3,5-8). Patient factors include age, hypertension, diabetes and history of a previous stroke. As well, there is some evidence that coronary artery bypass procedures performed without cardiopulmonary bypass are associated with a lower incidence of strokes (9-12) or new cerebral ischaemic lesions on magnetic resonance imaging (MRI) scanning (13), compared with those procedures performed 'on pump'. Although the long-term benefits are less apparent, it is also clear that 'open' procedures such as valve replacements where the left ventricle is opened are associated with an increased risk compared to coronary artery bypass procedures (2,4,6,7). This has implications when considering the pathophysiology of strokes in this context.
Theroretical mechanisms for the development of postcardiac surgical strokes
Several mechanisms have been proposed to explain the development of postoperative strokes in the setting of cardiac surgery. These are:
1. Solid particulate matter from the bypass circuit or atheromatous plaque fragments dislodged from the aorta during cross-clamping.
2. A decrease in cerebral perfusion pressure during the perioperative period.
3. Gaseous emboli which enter the arterial circulation from the bypass circuit or while the cardiac chambers are open to the atmosphere.
Attempts have been made to relate the CT or MRI appearances of the lesion to the presumed mechanism of injury (2,4). For instance, solid particulate emboli are likely to cause a single cerebral artery territory infarction. A decrease in cerebral perfusion pressure is more likely to affect the watershed territory between adjacent vessels, and gaseous emboli should give multiple lesions affecting more than one vessel territory.
However, in the case of apparent single lesions, multiple lesions are often identified with more detailed or repeat examinations (2,6). In the case of watershed infarcts, a combination of multiple gaseous emboli and low perfusion pressure is more likely to result in injury than either factor in isolation8. Thus the scan appearances of a patient with a post-cardiac surgical neurological insult are non-specific and do not exclude CAGE as a cause.
Furthermore, studies specifically looking at the causes of stroke in this context found that the majority were due to emboli (2,4). One such study (14) used a locally developed classification system to identify the aetiology of post-cardiac surgical strokes and identified 388 such patients. They concluded that emboli accounted for 62% of cases with an additional 19% being due to multiple aetiology or hypoperfusion and 13% having an unknown aetiology. In addition, a study looking at new postoperative lesions on MRI scans found that the majority were ischaemic injuries caused by intraoperative emboli (15).
Interestingly, all the patients in this current series had left-sided symptoms with two patients also having right-sided weakness. This is not surprising given the anatomy of the aortic arch which would favour air passing preferentially up the right carotid artery with a resultant right hemispheric lesion and left hemiparetic symptoms and signs. This propensity to left-sided symptomatology has been reported previously (16).
Doppler studies undertaken during cardiac heart valve procedures demonstrate echogenic particles during all such operations (17). Their numbers peak at certain points of the procedure, such as aortic cross-clamping and unclamping and when the heart starts to eject. The incidence of postoperative neurological deficit has been shown to correlate with the intraoperative echo count (2,7,18). It is likely therefore, that embolic phenomena are a major contributor to these lesions.
What cannot be discerned either radiologically or from the echo count of conventional transcranial Doppler is the nature of the emboli: that is, whether they represent gas bubbles or solid particulate matter, but air emboli are thought to be likely in the majority of cases (6,19).
The mechanisms of injury by gaseous emboli include:
* obstruction to blood flow if the air bubble is large enough to occupy several generations of branching arterioles, such that the net surface tension pressure acting on the column exceeds the cerebral perfusion pressure (20);
* endothelial damage from the passage of bubbles and an inflammatory response which initiates a sequence of events characterised by endothelial swelling and increased vascular resistance, leucocyte and platelet adherence and damage to the blood-brain barrier leading to cerebral oedema and neuronal apoptosis.
Although air can be detected in all patients undergoing cardiopulmonary bypass, the vast majority do not develop neurological deficits. With the exception of those rare cases where there are technical problems associated with bypass, the major risk of significant air embolism is during procedures in which the left ventricle or aorta are opened, such as valve replacement surgery. All of the patients in this series had undergone such procedures and indeed, the decision to treat with HBOT or not was to a large extent determined by the nature of the operation the patient had received.
Iatrogenic CAGE, its diagnosis and the role of neuro-imaging
Air or gas may enter the circulation during many invasive medical and surgical interventions (21-23). Air entering the venous system usually causes pulmonary symptoms, as the air bubbles embolise to the lungs. HBOT is not indicated for venous air embolism. However, a large volume of air in the venous system may overwhelm the filtering mechanism of the lungs and thereby traverse across to the arterial circulation. As well, approximately 30% of the population have a potentially patent foramen ovale which allows right-to-left shunting of air bubbles. Air or other gases in the arterial circulation from these mechanisms or directly into the pulmonary veins or systemic arteries may embolise to the central nervous system and cause symptoms such as confusion, decreased level of consciousness, coma, seizures and focal neurological changes.
The diagnosis of CAGE is usually situational, whereby an acute change in the neurological status of the patient is seen in the context of a procedure where air embolism could have occurred (21). Other clinical signs that may be seen include mydriasis, air in the retinal arteries and marbling or irregular pallor of the skin or mucous membranes.
Most centres report CT or MRI scanning as less than helpful, except in individual cases where other pathologies such as haemorrhage are being excluded (23-27). Thus there are no definitive signs or investigations and CT scans may confirm but do not exclude CAGE as the diagnosis and may lead to excessive delays in treatment (23).
Our case series reinforces the suggestion (25,28) that, as with other high risk procedures, postcardiac surgical patients who are slow to regain consciousness and have evidence of focal neurological signs in the absence of other known potential causes, should be considered as having a diagnosis of CAGE.
Conventional treatment of intraoperative air embolism
Avoidance of embolic injury involves attention to surgical technique such as avoidance of cross-clamping atheromatous regions of the aorta and meticulous de-airing. When embolisation has been observed, treatment has generally included:
* patient positioning (supine),
* evacuation of air,
* 100% oxygen,
* retrograde perfusion,
* optimisation of cerebral blood flow,
* supportive measures such as positive pressure ventilation and vasopressors, and
* some centres advocate moderate hypothermia and/or steroids but the latter is certainly not recommended.
Ongoing supportive care includes control of seizure activity and consideration of the use of a lignocaine infusion for 48 hours postoperatively. This has been shown in a prospective randomised clinical trial to have a neuro-protective effect during cardiac surgery (20). None of the patients in this current series had received lignocaine but its use would be considered in future cases. Other neuroprotective agents such as beta blockers and aspirin have also been effective in animal models. Of interest is that all of these agents have anti-inflammatory effects (29,30).
Hyperbaric oxygen therapy
HBOT is the intermittent use of a partial pressure of oxygen above atmospheric pressure for the treatment of disease. There are a number of recognised indications including CAGE associated with compressed air diving accidents. Experimental studies and extensive clinical experience over many years from civil engineering operations, military and sports diving has established HBOT as the definitive treatment for this condition. The beneficial effects of HBOT in CAGE are:
* reduction in bubble size as a function of the pressure (Boyle's law) (21,31),
* increased rate of bubble resolution by enhancing the nitrogen diffusion gradient (31,32),
* increased oxygen delivery to ischaemic tissues (25),
* a reduction in intracranial pressure due to vasoconstriction (21),
* decreased cerebral oedema (25), and
* decreased leucocyte activation and adhesion to damaged endothelium, which limits the inflammatory response and reperfusion injury (33-35).
HBOT and iatrogenic CAGE
In common with the pathophysiology of CAGE related to compressed air diving, CAGE due to invasive medical procedures and surgery should logically also be treated with HBOT. Iatrogenic CAGE is a rare complication of many invasive procedures that are undertaken in many different medical disciplines (36). It is for this reason that the potentially beneficial role of HBOT in iatrogenic CAGE is unlikely to ever be subjected to a prospective randomised clinical trial. The precise incidence is unknown and likely underestimated, as the symptoms may be transient, non-specific or simply undiagnosed. The recognition and treatment of iatrogenic CAGE has lagged far behind medical knowledge (37).
HBOT is the only specific therapeutic modality designed to enhance the dissolution of bubbles in the intravascular space (32) and it can be argued that prospective randomised studies are not required to demonstrate simple physical principles. Air bubbles can remain in the intravascular space for more than 48 hours after embolism (38), with larger bubbles (which are more likely to be symptomatic) taking the longest time to resolve (19). There exists a considerable body of human case reports, case series and animal studies starting with Bert in 1868, showing that HBOT improves survival and functional brain recovery, and on this basis, HBOT is considered the standard of care for definite cases of iatrogenic CAGE (22,26,39,40).
There is one important difference in the pathophysiology of iatrogenic CAGE ompared to that associated with diving accidents. SCUBA divers who suffer CAGE will also have accumulated a nitrogen load in their tissues because of breathing air at increased ambient pressure for the duration of their dive. The significance of this is that the HBOT treatment regimen used to treat divers is designed to offload this tissue nitrogen load. The initial HBOT treatment for divers with CAGE usually exceeds four to five hours duration. In theory, a much shorter treatment schedule for iatrogenic CAGE may be all that is required and many of the case reports and series had successful outcomes with shorter HBOT treatment schedules. Many different HBOT regimens have been used (31,41-44) and further studies of the appropriate HBOT treatment regimen would be of benefit.
The natural history of CAGE post-cardiac surgery without HBOT
A study dating back over 40 years found an approximate mortality of 90% for untreated iatrogenic CAGE. This was reduced to 33% with conventional supportive treatment (45,46). Specifically in the context of adverse neurological outcomes following cardiac surgery, two large studies have looked prospectively at this group. Salazar et al4 reported on 5971 consecutive patients and found a 3.6% incidence of stroke in the first nine postoperative days, most of whom presented on the first day. The incidence was higher in valve replacement patients versus coronary artery bypass patients. The occurrence of stroke was associated with an increased intensive care and hospital length of stay, increased hospital mortality (19% vs 4%), an increased chance of discharge to long-term rehabilitation or nursing-care environment and reduced long-term survival.
Roach et al (1) looked at 2108 cardiac patients of whom 6.1% had adverse cerebral outcomes, most of which were strokes. These were also associated with increased length of stay, mortality and likelihood of discharge to long-term care facilities.
Thus mortality and morbidity remains excessive in post-cardiac surgical strokes and the most likely aetiology is iatrogenic CAGE.
What is the evidence that HBOT improves outcome in iatrogenic CAGE?
Retrospective studies and case series
A study of nine patients (47) with haemodialysis-associated CAGE who received conventional treatment demonstrated little improvement. Once HBOT was instituted there was dramatic improvement within 10 minutes in seven of the patients and with resolution in the other two patients following an extended HBOT treatment regimen.
Another series of 30 patients (48) found near or complete resolution of symptoms following HBOT in 24 of the patients while only two died. A retrospective study of all iatrogenic CAGE patients admitted to a unit in Marseille between 1980 and 199940 divided their group of 86 patients into venous causes of CAGE (63 patients) and arterial causes (23 patients). Outcomes were described as total recovery in 50 (58%) of patients, longterm neurological sequelae in 29 (34%) cases and mortality in seven (8%) cases. In the larger venous group, treatment with HBOT was clearly associated with better outcomes if given early rather than delayed.
Another study of 16 patients (21) also found improved outcomes with HBOT, especially if given within six hours of injury.
In a case series of patients who had an in-hospital ischaemic stroke within four hours of a procedure with a high risk of CAGE (37), six patients who received HBOT were compared with a historical group of 15 patients who did not. The mortality in the HBOT group was zero compared to 13% in the controls and neurological outcomes were much more favourable in that all patients not receiving HBOT were discharged into long-term care, while the HBOT group were independent at home.
Specifically in CAGE during cardiac surgery, a review of the experience of the facility at the Israeli Naval Medical Institute between 1985 and 199822 identified 17 patients referred, all of whom were treated with HBOT. Full recovery occurred in eight patients but six were left with a severe deficit and three died (18% mortality). In this group, the diagnosis of CAGE was made by the surgical team who then initiated conventional treatment before deciding whether to refer for HBOT or not. Referral was therefore often relatively late and they also found a significant association between treatment delay and outcome in this series.
There is a sound theoretical basis and reasonable clinical experience to support the use of adjunctive HBOT in post cardiac surgery strokes to improve clinical outcomes. There are no prospective data to support such a claim.
What harm could treating with HBOT do?
The potential side-effects or complications of HBOT are well recognised and include the following:
* The difficulty of managing a complicated postoperative patient in an HBU environment.
- middle ear
* Oxygen toxicity
In a well-managed hyperbaric facility these potential problems have a very low incidence and generally with no long-term consequences.
Given the difficulty in making a definite diagnosis of CAGE as the cause of a particular cerebral insult following cardiac surgery, it is important to consider the potential effect on outcome of HBOT given to a patient who has a stroke due to non-CAGE related pathology. A recent systematic review (49) addressed the use of HBOT in the acute presentation of ischaemic strokes. The reviewer cautioned that the theoretical benefits of HBOT of increased oxygen delivery, reduced cerebral oedema and the inhibition of leucocyte activation must be considered alongside the potential toxicity of increased oxygen free-radical species generated in a high oxygen dose environment. A detailed analysis of the data identified three pilot studies (42-44) with reasonably robust methodology totalling 106 patients, and found no convincing evidence that HBOT improved outcome when applied during the acute presentation of ischaemic strokes. However, this conclusion has been questioned by one of the Cochrane reviewers as there was a wide range of oxygen doses across these studies and significant delays in the application of the HBOT in many cases. A recent preliminary single-blinded controlled trial (50) compared 18 patients with lacunar infarcts and periventricular hypodensity on CT scan, treated with daily HBOT for 10 days, with a control group of eight patients who received sham HBOT. Neurological outcomes were improved in the HBOT group at six months follow-up compared to the control group. Overall there is no clear signal as to whether HBOT in the context of non-CAGE stroke is beneficial or harmful.
* Iatrogenic CAGE is a rare complication of invasive medical procedures across many medical disciplines. Clinical experience suggests that HBOT confers improved outcomes for patients. Strokes following cardiac surgery remain a serious problem for patients and healthcare providers alike. It is likely that iatrogenic CAGE is an important factor in the pathogenesis of this condition.
* There is a sound theoretical basis for advocating the use of HBOT in post-cardiac surgical strokes, which is supported by a number of case series. These series reported improved outcomes. We have presented a series of 12 such patients treated in one centre, of whom 10 had a good neurological outcome.
* Prospective studies are lacking. Whether prospective studies on humans can ever be justified in this condition is debatable. It is disappointing that while many authors recognise that iatrogenic CAGE from any cause is relatively uncommon and under-recognised, despite basic physiological principles they advocate only general supportive measures until the efficacy of treatment with HBOT is proven (16,51).
* With the present state of knowledge, HBOT remains the definitive treatment for strokes associated with cardiac bypass surgery. Indeed it is the only therapeutic option apart from general supportive measures and is a treatment modality associated with minimal morbidity. However, prospective studies would be useful in establishing the optimum therapeutic regimen and perhaps the length of delay before HBOT is no longer of benefit.
* As a treatment modality, HBOT is low risk in a properly managed hyperbaric facility. However, as with all such clinical dilemmas, the risks of transferring potentially unstable postoperative patients must be weighed against the potential benefits in each individual case. We would propose that any patient known to have suffered an intraoperative air embolism, and/or is slow to recover from a cardiac bypass procedure and who demonstrates focal neurological signs should be considered for hyperbaric oxygen therapy.
Accepted for publication on July 6, 2009.
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Address for correspondence: Dr A. J. Gibson, Department Intensive Care Medicine, Christchurch Hospital, Private Bag, Christchurch, New Zealand.
A. J. GIBSON *, F. M. DAVIS [dagger]
Hyperbaric Medicine Unit, Christchurch Hospital, Christchurch, New Zealand
* M.B., Ch.B., F.A.N.Z.C.A., F.J.F.I.C.M., Medical Officer, Hyperbaric Medicine Unit and Specialist, Department of Intensive Care Medicine.
[dagger] M.A., F.R.C.A., F.A.N.Z.C.A., M.D., Medical Director.
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|Author:||Gibson, A.J.; Davis, F.M.|
|Publication:||Anaesthesia and Intensive Care|
|Date:||Jan 1, 2010|
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