Anaesthesiology Intensive Therapy

2018, vol. 50, no 2, 103–109

ISSN 1642–5758
10.5603/AIT.a2018.0010
ORIGINAL AND CLINICAL ARTICLES www.ait.viamedica.pl

Hyperbaric oxygen therapy for spinal cord ischaemia after

complex aortic repair — a retrospective review
Matteo Parotto1, Maral Ouzounian2, Ludwik Fedorko1, George Oreopoulos3, Thomas Lindsay3,
Rita Katznelson4

1Department of Anaesthesia and Pain Management, Toronto General Hospital/University Health Network,

Toronto, Ontario, Canada

2Division of Cardiac Surgery, Peter Munk Cardiac Centre, University Health Network and Department

of Surgery, University of Toronto, Toronto, Ontario, Canada

3Division of Vascular Surgery, Toronto General Hospital, Toronto, Ontario, Canada
4Hyperbaric Medicine Unit, Department of Anaesthesia and Pain Management, Toronto General Hospital,

Toronto, Ontario, Canada

Abstract
Background: Complex aortic repair (CAR) carries high rates of debilitating postoperative complications, including
spinal cord injury. The rate of spinal cord deficits post-CAR is approximately 10%, with permanent paraplegia in 2.9%
and paraparesis in 2.4% of patients. Treatment options are limited. Rescue therapies include optimization of spinal
cord perfusion and oxygen delivery by mean arterial pressure augmentation (> 90 mm Hg), cerebrospinal fluid drain-
age, and preservation of adequate haemoglobin concentration (> 100 g L-1). Hyperbaric oxygen therapy (HBOT) has
been described in several case reports as part of the multimodal treatment for spinal cord ischemia.
HBOT has been used in our centre as adjunct rescue treatment for patients with spinal cord injury post-CAR that were
refractory to traditional medical management, and we aimed to retrospectively review these cases.
Methods: After Research Ethics Board approval, we performed a retrospective review of all post-CAR patients who
developed spinal cord injury with severe motor deficit and were treated with HBOT at our institution since 2013.
Results: Seven patients with spinal cord injury after CAR were treated with HBOT in addition to traditional rescue
therapies. Five patients showed varying degrees of recovery, with two displaying full recovery. One developed oxygen-
induced seizure, medically treated. No other HBOT-related complications were noted.
Conclusions: Our retrospective study shows a potential benefit of hyperbaric oxygen therapy on neurological out-
come in patients who developed spinal cord injury after CAR. Prospective research is needed to understand the role,
efficacy, benefits and risks of HBOT in this setting.

Anaesthesiology Intensive Therapy 2018, vol. 50, no 2, 103–109

Key words: spinal cord ischaemia, hyperbaric oxygen therapy, aortic aneurysm

Distal Arch and Thoracoabdominal aortic aneurysms A recently published retrospective data collection of
(TAAA) represent an extremely challenging clinical entity [1]. a large cohort of patients who underwent CAR for TAAA at
Affected patients risk life-threatening rupture without a single institution reported a rate of spinal cord deficits of
surgical intervention. Complex aortic repair (CAR) for 9.6%, with permanent paraplegia in 2.9%, and permanent
this pathology carries substantial risk, including a risk of paraparesis in 2.4% of the patients [2]. This could appear
death or, in those who survive, life-altering complications as an immediate intraoperative or perioperative event or
such as stroke, paraplegia, and renal failure necessitating as a delayed finding, materialising up to several days after
dialysis [2]. surgery. Permanent neurological deficit is a major cause

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Anaesthesiol Intensive Ther 2018, vol. 50, no 2, 103–109

of morbidity and leads to decreased long-term survival of tor deficit and were treated with HBOT at our institution since
patients with CAR [3, 4]. 2013. HBOT was applied at 2.4–2.8 ATA (Table 1) once or twice
The causes leading to spinal cord injury in aortic repairs daily until complete neurological recovery or symptoms pla-
include infarction of the spinal cord from direct interruption teau. The patients were treated in a multiplace hyperbaric
of the cord blood supply or a critical collateral, systemic hy- chamber (Fink engineering PTY LTD, rectangular Hyperbaric
poperfusion, atheromatous embolic infarction, or spontane- System, Australia) that can accommodate two critically ill in-
ous thrombosis of an atherosclerotic radicular artery, and tubated ventilated patients at once. The chamber is equipped
ischemia-reperfusion injury that progresses to infarction [4–7]. with a ventilator (IPER Hyperbaric Ventilator, Siaretron 1000,
The rescue therapies in spinal cord injury post CAR in- Italy), monitor (CARESCAPE B650, GE Medical Systems, World-
clude optimization of spinal cord perfusion and oxygen wide) and infusion pumps (CAREFUSION Alaris PC infusion
delivery by the following: mean arterial pressure (MAP) pumps, Guardrails, BD, Worldwide) that are compatible with
augmentation (typically > 90 mm Hg), cerebrospinal fluid a hyperbaric environment. During hyperbaric oxygen therapy,
(CSF) pressure decrease by spinal cerebrospinal fluid (CSF) patients were managed by two attendants inside the chamber,
drainage and preservation of adequate haemoglobin con- namely a respiratory therapist and hyperbaric technologist.
centration (typically > 100 g L-1) [6]. The management of patient sedation (if needed), haemody-
Hyperbaric oxygen therapy (HBOT) is a medical treat- namic parameters and CSF drainage was not different from
ment based on an intermittent inhalation of 100% oxygen in intensive care unit management. Two additional hyperbaric
a hyperbaric chamber at a pressure higher than one absolute technologists, namely a controller and an assistant controller,
atmosphere (ATA, 1 ATA = 760 mm Hg, normal atmospheric operated the chamber outside. A hyperbaric physician, trained
pressure at sea level). It is currently used in clinical practice in in cardiac anaesthesia and intensive care medicine, and an
a number of urgent and elective indications. HBOT is a safe, intensive care nurse, were present in the unit supervising the
non-invasive intervention, and the only absolute contraindi- patient from outside of the chamber. The hyperbaric physician
cation is a non-treated pneumothorax. Physiological effects was ready to enter the chamber if necessary.
of HBOT are based on a marked increase in the amount of Patient characteristics including age, gender and comor-
dissolved oxygen carried by the blood. High plasma oxygen bidities were recorded. Baseline and postoperative labs were
concentration enhances the rate and distance of oxygen also recorded, along with pertinent surgical data and post-
diffusion into ischaemic areas with compromised circula- operative data that include duration of cardiopulmonary
tion. Long-lasting consequences of HBOT are related to the bypass, blood transfusions, haemodynamic and respiratory
stimulating effect of supra-physiological oxygen concentra- data, timing of spinal cord deficits and rescue therapies,
tions on a variety of biochemical processes. HBOT activates HBOT treatment and outcome.
oxidant-antioxidant mechanisms with nitric oxide playing
a key role [8] and such stimulates secretion of growth fac- RESULTS
tors, vascular endothelia growth factor, hypoxia-inducible A total of seven patients (6 males, 1 female) with spinal
factor-1, and stem cells. By activating signal transduction cord injury after CAR were treated with HBOT when tradi-
cascades HBOT modifies inflammatory response and im- tional rescue therapies (MAP augmentation, Hb > 100 g L-1
proves ischaemic-reperfusion injury [9]. and/or CSF drainage) had failed. A summary of relevant
Therefore, HBOT has the potential for several positive data and treatment details is described in Table 1. The onset
effects in spinal cord deficits after CAR, such as correction of of spinal cord injury varied from intraoperative to 7 days
tissue hypoxia, modulation of ischaemia-reperfusion injury postoperatively. The time from the onset of spinal cord
and reduction of inflammatory oedema. Case reports have injury signs/symptoms to the institution of HBOT ranged
previously described HBOT use in this setting [10]. from 8 hours to 30 hours.
We report a retrospective review of a single centre ex- Two patients died from perioperative complications
perience with the use of HBOT as an adjuvant treatment for (1 developed multiple organ failure related to sepsis, 1 had
acute spinal cord deficit after CAR. an extensive myocardial infarction that led to cardiac ar-
rest). Five patients showed varying degrees of neurological
METHODS recovery, with two patients displaying complete recovery.
Institutional Research Ethics Board approval was ob- One patient developed oxygen induced seizures (1 episode
tained. The requirement for written informed consent was of 1 minute duration) while receiving HBOT treatment; the
waived by the ethics committee, given the retrospective seizures resolved after intravenous midazolam (2 mg) admin-
analysis nature of our study. We performed a retrospective istration. No other HBOT-related complications were noted.
review of the clinical details and outcomes of all post-CAR A brief description of each individual case is provided
patients that developed spinal cord injury with severe mo- in supplemental results sections.

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 Table 1. Patients’ data and treatment details from the retrospective review of all patients who developed spinal cord injury post CAR and underwent HBOT at our centre
Patient Age Gender CAR repair Onset of Spinal Details of Spinal Cord Injury Type of HBOT Number of HBOT Outcome
Cord Injury treatment treatments
signs/symptoms

1 51 Male Open repair of distal arch and POD # 1 Intraoperative bleeding from 2.4 ATA 11 Full recovery of motor and bowel
descending thoracic aneurism repair epidural venous plexus with left- function, partial recovery of sensory
sided numbness/weakness, bladder function, persistent bladder dysfunction
and bowel dysfunction
2 62 Male Open repair of extent II TAAA POD # 0 Loss of intraoperative motor-evoked 2.4 ATA 4 Full recovery
potentials
3 67 Male Urgent open repair of ruptured POD # 1 Complete paraplegia 2.4 ATA 4 Deceased (multiple organ failure)
aneurysm

4 53 Male Urgent open repair of extent I TAAA POD # 7 Left leg weakness 2.8 ATA for 2 treatments, 9 Full recovery
for symptomatic chronic dissection 2.4 ATA for 7 treatments

5 41 Male Open repair of TAAA from left POD # 1 Complete paraplegia 2.8 ATA for 5 treatments, 11 Walking with assistance, normal bladder
subclavian to infrarenal aorta 2.0 ATA for 6 treatments and bowel function
6 72 Female 2 stage endovascular repair of TAAA POD # 1 Right leg weakness 2.0 ATA 1 Deceased (myocardial infarction on
(stage II) POD # 2)
7 62 Male Open repair of TAAA in previous POD # 2 Decreased leg strength and 2.4 ATA 2 Leg strength and sensation improved,
thoracic endovascular aortic repair sensation, bowel and bladder able to stand and walk short distances;
(TEVAR), and bilateral common iliac dysfunction bladder dysfunction persists, bowel
arteries aneurysm repair dysfunction resolved
CAR: complex aortic repair; TAAA: thoraco-abdominal aortic aneurysm; HBOT: hyperbaric oxygen therapy; POD: post-operative day; ATA: absolute atmosphere

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Anaesthesiol Intensive Ther 2018, vol. 50, no 2, 103–109

DISCUSSION models of spinal cord injury. It is postulated that by increas-

We present a retrospective case series describing the ing oxygen delivery to the ischaemic spinal cord, HBOT
beneficial effect of HBOT in spinal cord injury after CAR. reduces hypoxia and hypoxia-induced apoptosis, corrects
To our knowledge, this is the first series described in the acidosis and improves microcirculation, limits axonal death
literature. The patients included in this retrospective re- and promotes axonal regeneration. All these effects result
view presented different degrees of spinal cord injury and in better clinical recovery of compromised neurological
showed improvement in neurological function after HBOT, function. The time and number of administered HBOTs, as
when traditional rescue therapies (MAP augmentation, Hb well as its combination with other therapeutic interventions,
> 100 g L-1 and/or CSF drainage) had failed. No major HBOT could significantly affect post injury outcomes.
complications were observed, with 1 patient experiencing Animal studies have revealed that early HBOT admin-
a single seizure episode that promptly responded to medi- istration attenuates the death of motor neurons in rabbits
cal management. with spinal cord ischaemia. Single HBOT applied 30 minutes
It is important to notice that our retrospective case series after the ischaemic insult has a better neuro-protective ef-
has several limitations, including the relatively low number fect than HBOT administered 3 hours post injury. However,
of patients, the heterogeneity of HBOT (frequency, duration, repeated HBOTs can significantly expand the therapeutic
ATA) utilized and the variable outcomes observed. window for HBOT application. In a rat model of spinal cord
However, a growing body of evidence is emerging indi- injury, animals treated with serial HBOTs started 6 hours post
cating that hyperbaric oxygen therapy, alone or in combina- injury showed better neurological recovery in comparison
tion with other therapeutic modalities, may have positive to animals who received a single HBOT early (30 min or 3
effects in different types of spinal cord injury. hours post-injury). The authors concluded that serial HBOTs
Wajima et al. [11] reported successful treatment of acute have beneficial effects, even hours after the injury, and are
epidural haematoma at L3-L5 level after epidural steroid superior to single hyperbaric oxygen exposure. This observa-
injection. The patient was treated with HBOT immediately tion was confirmed by another report where rats with acute
after developing paraplegia and experienced complete spinal cord lesion were treated 30 minutes or 24 hours after
neurological recovery without surgical intervention after injury for 10 days with hourly HBOTs at 2.0 ATA. Both groups
5 daily HBOTs. Kohshi et al. [12] described the conservative demonstrated better functional recovery in comparison to
treatment of spinal epidural abscess causing spinal cord control (non-treated) group. There was no clinical difference
compression at the C1-C4 level. The addition of HBOT to the in neurological examination at one and two weeks post-
antibiotic therapy caused a dramatic improvement in the injury between the group that had started HBOTs 30 minutes
neurological symptoms with complete neurological recov- after the insult and the group that started treatments with
ery. Combination of HBOT, thrombolysis and hypothermia a 24 hour delay. The combined administration of HBOT with
prevented permanent neurological injury and paralysis in hypothermia caused higher activity of antioxidant enzymes
an oncological patient with acute spinal cord ischaemia due in the injured spinal cord tissue than HBOT or hypothermia
to vertebral artery occlusion [13]. alone. It was also more effective than methylprednisolone
Several case reports have demonstrated the therapeutic treatment [16]. The addition of HBOT to stem cell transplan-
effect of HBOT in patients with early and delayed spinal tation had a synergistic effect on axon regeneration and
cord ischaemia after CAR [10, 14, 15]. Puttaswami et al. [10] functional recovery in rats with spinal cord injury [17].
described complete resolution of postoperative paraplegia The molecular mechanisms of HBOT in spinal cord in-
after treatment with HBOT in a patient who underwent jury include effects on apoptosis, hypoxia-inducible factor
resection of type II thoraco-abdominal aneurysm. Another (HIF)-1alpha and neurotrophic growth factors, as well as
case report of paraplegia after emergent repair of type modification of local inflammatory response in the injured
A aortic dissection showed that HBOT led to significant tissue. Rats with compression spinal cord injury treated with
neurological improvement after a lack of response for 3 HBOT immediately after the insult had smaller spinal cord
days of combined management with cerebrospinal fluid infarction, less apoptosis, decreased spinal cord production
drainage, steroids and mannitol [14]. Morishito et al. [15] of interleukin-1beta and tumour necrosis factor-alpha, lower
described urgent HBOT in a case of delayed paraplegia that expression of HIF-1alpha and higher production of interleu-
developed 15 days after axillo-bifemoral bypass for acute kin-10 and vasculo-endothelial and glial cell line-derived
Type B aortic dissection. The patient recovered with no neurotrophic growth factors in comparison with untreated
residual neurological compromise after being treated with controls [18–20]. These findings correlated with the better
hyperbaric oxygen for 2 days. motor function scores in the HBOT treated animals [18, 19].
The mechanisms of the beneficial effects of HBOT in The iNOS mRNA-iNOS-NO signalling pathway could also be
spinal cord injury after CAR have been studied in animal involved in HBOT induced neuro-protection [21].

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Supplemental Results Section Case 3

67-year-old male.
Case 1: Surgical intervention: Emergent open repair of ruptured
51-year-old male. abdominal aortic aneurysm, right femoral artery embolec-
Surgical intervention: 3rd time redo left thoracotomy tomy
and repair of distal arch and proximal descending thoracic CSF drainage: instituted post-operatively, approximately
aneurysm with 22 mm Gelweave graft from left common 11 hours after onset of spinal cord injury signs/symptoms.
carotid artery to T7, left subclavian artery bypass with 8 mm The patient was deeply sedated for severe hypoxemia and
graft. Circulatory arrest time: 21 min. Intraoperative course was difficult to assess neurologically. MRI of spinal cord was
complicated by bleeding from epidural venous plexus and performed to confirm the diagnosis of spinal cord ischaemia
trivial CSF leak, resolved with gentle packing, Gelfoam (Phar- prior to CSF drain insertion.
macia and Upjohn Company, Kalamazoo, Michigan, USA), Spinal cord deficits: paraplegia.
Surgicel (Ethicon, Sommerville, NJ, USA) and Evicel (Ethicon, Onset of spinal cord injury signs/symptoms: observed
Sommerville, NJ, USA). approximately 21 hours after the end of surgery, on post-
CSF drainage: Not inserted operative day (POD) #1.
Spinal cord deficits: severe weakness in left leg, mild Initiation of HBOT treatment: on POD #2, approximately
weakness in right leg, bilateral sensory dysfunction in both 24 hours after observation of spinal cord injury.
legs, bowel incontinence, urinary retention. Number of HBOT treatments: 4, at 2.4 ATA.
Onset of spinal cord injury signs/symptoms: observed Outcome: deceased due to multi-organ failure. No evi-
approximately 12 hours after the end of surgery, on post- dence of recovery of paraplegia after HBOT treatment.
operative day (POD) #1.
Initiation of HBOT treatment: approximately 11 hours Case 4
after onset of spinal cord injury signs/symptoms. 53-year-old male.
Number of HBOT treatments: 11, at 2.4 ATA. Surgical intervention: Repair of extent IV TAAA with 26
Outcome: full motor recovery, partial sensory recovery, mm Gelweave graft (VASCUTEK, TERUMO, Inchinnan, Scot-
intact bowel function, persistent urinary retention requiring land, UK), repair of left common femoral artery. Previous
intermittent catheterization. thoracic endovascular aortic repair (TEVAR) from left sub-
clavian to distal descending thoracic aorta for type B aor-
Case 2 tic dissection. No patent intercostal arteries to re-implant.
62-year-old male. Celiac, superior mesenteric artery, and right renal arteries
Surgical intervention: Repair of extent II TAAA with 28 re-implanted as a Carrel patch. Left renal artery re-implanted
mm Coselli branched Gelweave graft. Reimplantation of as a button.
celiac, superior mesenteric artery, left and right renal arter- CSF drainage: instituted pre-operatively; removed on
ies with individual bypass grafts. Bifurcated distal aorto-iliac POD #5, given lack of symptoms or signs of spinal cord
repair replacing left and right common iliac arteries to their injury; re-instituted on POD #7, approximately 4 hours after
bifurcation. No patent intercostal arteries to re-implant. Use onset of spinal cord injury signs/symptoms.
of left heart bypass. Spinal cord deficits: left leg weakness.
CSF drainage: instituted pre-operatively. Onset of spinal cord injury signs/symptoms: observed
Spinal cord deficits: intraoperative loss of somato-sensory on POD #7.
evoked potentials (SSEP) and motor evoked potentials (MEP) Initiation of HBOT treatment: on POD #8, approximately
to the legs, with recovery of SSEP but not MEP before the 24 hours after onset of spinal cord injury signs/symptoms.
end of surgery. On awakening from anaesthesia, after the Number of HBOT treatments: 9; 2 treatments at 2.8 ATA,
end of surgery, no movement of left leg, severe weakness 7 treatments at 2.4 ATA.
of right leg. Outcome: full recovery of motor function after the last
Onset of spinal cord injury signs/symptoms: intraopera- HBOT treatment.
tively (approximately 8 hours prior to the end of surgery).
Initiation of HBOT treatment: immediately after the end Case 5
of surgery (direct transfer from the operating room to the 41-year-old male.
HBOT unit). Surgical intervention: Repair of extent II TAAA with 28
Number of HBOT treatments: 4, at 2.4 ATA. mm Coselli branched Gelweave graft (VASCUTEK, TERUMO,
Outcome: full motor recovery by POD #2. Inchinnan, Scotland, UK) using left heart bypass. T10-T11

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 Matteo Parotto et al., Hyperbaric oxygen therapy for spinal cord ischaemia

intercostal artery bypass with 10mm Dacron graft due to Initiation of HBOT treatment: on POD#1, approximately
intraoperative loss of MEP and SSEP signals, with full intraop- 8 hours after onset of spinal cord injury signs/symptoms.
erative recovery of evoked potentials. Aorto-left subclavian Number of HBOT treatments: 1, at 2.0 ATA.
artery bypass with 8mm graft (near occlusion of previous Outcome: deceased on POD #2 following cardiac arrest
left subclavian artery graft). Two previous sternotomies: in the setting of massive acute myocardial infarction. Unable
(1) repair ascending aorta for type A dissection; (2) redo to assess spinal cord deficits post HBOT treatments due to
sternotomy + valve-sparing root + total arch repair for an- clinical deterioration with need for sedation and mechani-
eurysmal degeneration. cal ventilation.
CSF drainage: instituted pre-operatively.
Spinal cord deficits: paraplegia. Case 7
Onset of spinal cord injury signs/symptoms: Observed on 62-year-old male.
POD #2, approximately 32 hours after the end of surgery. Surgical intervention: open repair of extent IV TAAA with previ-
Initiation of HBOT treatment: POD #2, approximately 4 ous TEVAR from left subclavian artery to distal descending tho-
hours after the onset of spinal cord injury signs/symptoms. racic aorta, and repair of bilateral common iliac artery aneurysms.
Number of HBOT treatments: 11; 5 treatments at 2.8 ATA, CSF drainage: instituted pre-operatively.
6 treatments at 2.0 ATA. Spinal cord deficits: bilateral severe leg weakness, with
Outcome: moderate weakness in hip flexors and knee altered sensation, bowel and bladder dysfunction.
extensors bilaterally, mild weakness in right ankle dorsiflex- Onset of spinal cord injury signs/symptoms: POD #2, ap-
ors, long toe extensor and ankle plantar extensor. Normal proximately 30 hours after the end of surgery.
bladder and bowel function. Fully independent on activities Initiation of HBOT treatment: POD #2, approximately 16
of daily living and working full-time. hours after onset of spinal cord injury signs/symptoms.
Number of HBOT treatments: 2, at 2.4 ATA.
Case 6 Outcome: full sensory and motor recovery in right leg
72-year-old female. with exception of mild weakness on ankle dorsiflexors and
Surgical intervention: endovascular repair of extent II long toe extensors; mild weakness in left leg hip flexors, knee
TAAA with 4-vessel fenestrated graft. extensors, ankle plantar flexors, and moderate weakness in
CSF drainage: instituted pre-operatively. ankle dorsiflexors and long toe extensors; persistent left foot
Spinal cord deficits: right leg weakness. paraesthesia; walking without assistance; indwelling foley
Onset of spinal cord injury signs/symptoms: observed on catheter for persistent bladder dysfunction; full recovery
POD#1, approximately 24 hours after the end of surgery. of bowel function.

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