Adjunctive hyperbaric oxygen therapy for spinal cord ischemia after complex aortic repair.

OBJECTIVE: Spinal cord ischemia (SCI) with paraplegia or paraparesis is a devastating complication of complex aortic repair (CAR). Treatment includes cerebrospinal fluid drainage, maintenance of hemoglobin concentration (>10 g/L), and elevating mean arterial blood pressure. Animal and human case series have reported improvements in SCI outcomes with hyperbaric oxygen therapy (HBOT). We reviewed our center's experience with HBOT as a rescue treatment for spinal cord ischemia post-CAR in addition to standard treatment. METHODS: A retrospective review of the University Health Network's Hyperbaric Medicine Unit treatment database identified HBOT sessions for patients with SCI post-CAR between January 2013 and June 2021. Mean estimates of overall motor function scores were determined for postoperative, pre-HBOT, post-HBOT (within 4 hours of the final HBOT session), and at the final assessment (last available in-hospital evaluation) using a linear mixed model. A subgroup analysis compared the mean estimates of overall motor function scores between improvement and non-improvement groups at given timepoints. Improvement of motor function was defined as either a ≥2 point increase in overall muscle function score in patients with paraparesis or an upward change in motor deficit categorization (para/monoplegia, paraparesis, and no deficit). Subgroup analysis was performed by stratifying by improvement or non-improvement of motor function from pre-HBOT to final evaluation. RESULTS: Thirty patients were treated for SCI. Pre-HBOT, the motor deficit categorization was 10 paraplegia, three monoplegia, 16 paraparesis, and one unable to assess. At the final assessment, 14 patients demonstrated variable degrees of motor function improvement; eight patients demonstrated full motor function recovery. Seven of the 10 patients with paraplegia remained paraplegic despite HBOT. The estimated mean of overall muscle function score for pre-HBOT was 16.6 ± 2.9 (95% confidence interval [CI], 10.9-22.3) and for final assessment was 23.4 ± 2.9 (95% CI, 17.7-29.1). The estimated mean difference between pre-HBOT and final assessment overall muscle function score was 6.7 ± 3.1 (95% CI, 0.6-16.1). The estimated mean difference of the overall muscle function score between pre-HBOT and final assessment for the improved group was 16.6 ± 3.5 (95% CI, 7.5-25.7) vs -4.9 ± 4.2 (95% CI, -16.0 to 6.2) for the non-improved group. CONCLUSIONS: HBOT, in addition to standard treatment, may potentially improve recovery in spinal cord function following SCI post-CAR. However, the potential benefits of HBOT are not equally distributed among subgroups.

A Case Report of Thoracic Endovascular Aneurysm Repair under Local Anesthesia with Resolution of Acute Onset Lower Extremity Paraplegia from an Acute Complicated Type B Aortic Dissection.

Spinal cord ischemia (SCI) is a rare presenting symptom of acute complicated type B aortic dissection, occurring in approximately 3% of patients . We present a case report of a patient with this presentation who had observed resolution of his paraplegia symptoms immediately after placement of a thoracic stent graft under local anesthesia. The temporal association between true lumen flow restoration and paraplegia resolution intraoperatively is a novel finding. We feel that this case report may provide support for recognized cord perfusion theory , as well as contribute to the understanding of the time frame associated with SCI and reversibility of paraplegia.

Hyperbaric oxygen therapy for spinal cord ischaemia after complex aortic repair - a retrospective review.

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 drainage, 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 outcome 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.

Reversal of Spinal Cord Ischemia Following Endovascular Thoracic Aortic Aneurysm Repair With Hyperbaric Oxygen and Therapeutic Hypothermia.

BACKGROUND: Neurological adverse events with spinal cord ischemia (SCI) remain one of the most feared complications in patients undergoing thoracic endovascular aortic repair (TEVAR). These patients can develop irreversible paraplegia with lifelong consequences with physical and psychological agony. CASE PRESENTATION: We herein present a patient who developed SCI with bilateral lower leg paraplegia on the third postoperative day following TEVAR. Spinal catheter was inserted for spinal fluid drainage. A hyperbaric oxygen therapy was initiated for 90 minutes for 2 days, which was followed by therapeutic hypothermia for 24 hours with a target temperature of 33°C. The patient exhibited significant neurological recovery following these treatments, and he ultimately regained full neurological function without spinal deficit. DISCUSSION: This represents the first reported case of full neurological recovery of a patient who developed complete SCI following TEVAR procedure. The neurological recovery was due in part to immediate therapeutic hypothermia and hyperbaric oxygen therapy which reversed the spinal ischemia.

Hyperbaric oxygenation in fluid microembolism.

Because clinicians require objectively demonstrable neurological deficits to confirm a diagnosis, the recognition of embolic events in the nervous system is generally restricted to the effects of ischemic necrosis produced by arterial occlusion. However, magnetic resonance imaging (MRI) has shown that lesser degrees of damage associated with small emboli are common, especially in the mid brain, and are usually clinically silent. They are frequently associated with atheromatous embolism in the elderly, but microembolic debris, such as fat, is common in the systemic venous return of healthy people and generally trapped in the microcirculation of the lung being removed by phagocytosis. However, pulmonary filtration may fail and microemboli may also pass through an atrial septal defect in so-called 'paradoxical' embolism. Studies of bubbles formed on decompression in diving have demonstrated the importance of pulmonary filtration in the protection of the nervous system and that filtration is size dependant, as small bubbles may escape entrapment. Fluid and even small solid emboli, arresting in or passing through the cerebral circulation, do not cause infarction, but disturb the blood-brain barrier inducing what has been termed the 'perivenous syndrome'. The nutrition of areas of the white matter of both the cerebral medulla and the spinal cord depends on long draining veins which have been shown to have surrounding capillary free zones. Because of the high oxygen extraction in the microcirculation of the gray matter of the central nervous system, the venous blood has low oxygen content. When this is reduced further by embolic events, tissue oxygenation may fall to critically low levels, leading to blood-brain barrier dysfunction, inflammation, demyelination and eventually, axonal damage. These are the hallmarks of the early lesions of multiple sclerosis where MR spectroscopy has also shown the presence of lactic acid. Significant elevation of the venous oxygen tension requires oxygen to be provided under hyperbaric conditions. Arterial tension is typically increased ten-fold breathing oxygen at 2 atmospheres absolute (ATA), but this results in only a 1.5-fold increase in the cerebral venous oxygen tension. The treatment of decompression sickness, and both animal and clinical studies, have confirmed the value of oxygen provided under hyperbaric conditions in the restoration and preservation of neurological function in the 'perivenous' syndrome.

[Preface and comments: Protection of the brain and the spinal cord].

Basic and clinical investigations have been performed, focusing on the mechanism of ischemic brain and spinal cord injuries, and preventive measures against ischemic insults such as drug therapy, hypothermia, maintenace of blood flow to brain and spinal cord, preconditioning, and no use of high dose fentanyl. In this special issue, five experts have provided new relevant information concerning brain and spinal cord protection. Further research in brain and spinal cord protection will contribute to better understanding of ischemic central nervous system injuries and to the establishment of novel therapies for protection of central nervous system.

Adenovirus-mediated glial cell line-derived neurotrophic factor gene delivery reduces motor neuron injury after transient spinal cord ischemia in rabbits.

OBJECTIVE: Glial cell line-derived neurotrophic factor (GDNF) has protective effects on various injuries involving the central and peripheral nervous systems in vitro and vivo. However, the possible protective effect of GDNF on spinal cord ischemia and the exact mechanism involved in the ameliorative effect of GDNF on ischemic spinal cord injuries are not fully understood. Therefore, we investigated the possible protective effect of the adenovirus-mediated GDNF gene delivery on transient spinal cord ischemia in rabbits. METHODS: The adenoviral vector (lacZ gene as a control or GDNF gene contained) was injected directly into the lumbar spinal cord via a needle inserted into the dorsal spine 2 days before the animal was subjected to 15 minutes of spinal cord ischemia induced by infrarenal aortic occlusion. In situ terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL staining) was performed, and temporal profiles of the GDNF and caspase-3 (caspase-3 is the marker of apoptotic change) immunoreactivity were investigated. RESULTS: In the control rabbit, the majority of motor neurons showed selective cell death at 7 days of reperfusion. Immunocytochemistry showed that in situ TUNEL staining was selectively detected at 2 days of reperfusion in motor neuron nuclei. GDNF and caspase-3 were selectively induced in the motor neuron cells at 8 hours of reperfusion. In the GDNF-treated group, a large population of motor neuron cells was still surviving at 7 days after having been subjected to 15 minutes of ischemia. Unlike the control group, the GDNF-treated group expressed GDNF persistently. Induction of TUNEL staining and immunoreactivity for caspase-3 were greatly reduced by the GDNF treatment. CONCLUSION: These results suggest that the reduction in motor neuron death by GDNF was greatly associated with a reduction in DNA fragmentation and apoptotic signals of the caspase-3 cascade; they further suggest a great potential for gene therapy for paraplegic patients in the future.