Delayed neuromonitoring alarm after scoliosis correction in Lenke type 4 adolescent idiopathic scoliosis

A 12-year-old girl underwent surgery for Lenke type 4 adolescent idiopathic scoliosis. After scoliosis correction, the transcranial motor-evoked potential (Tc-MEP) showed no alarm. However, the Tc-MEP amplitude had declined ~10 min after correction, with a normal blood pressure (BP) and body temperature and without any technical monitoring errors. Therefore, we suspected indirect spinal cord ischaemia because of the delayed true-positive Tc-MEP alarm. All the strong corrections made loss of Tc-MEP and all the correction releases made recovers of waveform. Finally, a weak correction was performed, and the Tc-MEP amplitude was recovered. Because transient spinal cord ischaemia due to correction of triple curves may cause a delayed monitoring alarm, the monitoring team should frequently check Tc-MEP after these manoeuvres. This patient had no neurological deficits and was considered to be a rescue case.

Can scoliosis lead to spinal cord ischaemia? Early diagnosis and rehabilitation: A paradigmatic case report and literature review

INTRODUCTION: Scoliosis is frequently associated with pain and radiculopathy, but it is not considered a possible cause of acute spinal cord injury (SCI). Here we present a case report in which scoliosis was apparently linked to spinal cord ischaemia. CASE PRESENTATION: A 20-year-old woman with conservatively treated severe scoliosis presented with acute spinal cord infarction, which occurred during a spinal flexion while she was tidying up the bed. Other causes of SCI were excluded. Early rehabilitation was started and the patient progressively regained motor and sensory functions, with an AIS reduction from A to C. Bowel and bladder disorders persisted and were autonomously managed with a trans-anal irrigation device and intermittent catheterisation after voluntary micturition. DISCUSSION: Early detection and management of spinal curvature disorders are essential in preventing long-term complications of scoliosis. Although the aetiology of spinal cord ischaemia in severe scoliosis should be better clarified, this rare case report suggests that scoliosis might be involved in its pathogenesis. Thus, we recommend early diagnosis of spinal curvature disorders and adequate rehabilitative treatment in order to prevent potential subsequent neurological complications.

Chronic type B aortic dissection complicated by repetitive spinal cord ischaemia

Chronic type B aortic dissection complicated by repetitive transient spinal cord ischaemia is rare. Reduced blood flow in the segmental arteries supplying the radicular arteries in the false lumen is the main cause of this pathology. Individual variations in spinal cord circulation are difficult to identify; therefore, the mechanisms of spinal cord ischaemia are poorly understood. We encountered a patient with chronic type B aortic dissection experiencing repetitive spinal cord ischaemia that finally led to spinal cord infarction. The patient recovered, except for mild monoparesis of the right leg. With the growth of the dissected aorta, we planned for surgical treatment to restore the blood supply in the spinal cord. The patient underwent thoraco-abdominal aortic repair using deep hypothermia, and favourable neurological results were achieved.

Near real-time bedside detection of spinal cord ischaemia during aortic repair by microdialysis of the cerebrospinal fluid

OBJECTIVES Spinal cord ischaemia (SCI) remains the most devastating complication after thoraco-abdominal aortic aneurysm (TAAA) repair. Its early detection is crucial if therapeutic interventions are to be successful. Cerebrospinal fluid (CSF) is readily available and accessible to microdialysis (MD) capable of detecting metabolites involved in SCI [i.e. lactate, pyruvate, the lactate/pyruvate ratio (LPR), glucose and glycerol] in real time. Our aim was to evaluate the feasibility of CSF MD for the real-time detection of SCI metabolites. METHODS In a combined experimental and translational approach, CSF MD was evaluated (i) in an established experimental large animal model of SCI with 2 arms: (a) after aortic cross-clamping (AXC, N = 4), simulating open TAAA repair and (b) after total segmental artery sacrifice (Th4–L5, N = 8) simulating thoracic endovascular aortic repair. The CSF was analysed utilizing MD every 15 min. Additionally, CSF was collected hourly from 6 patients undergoing open TAAA repair in a high-volume aortic reference centre and analysed using CSF MD. RESULTS In the experimental AXC group, CSF lactate increased 3-fold after 10 min and 10-fold after 60 min of SCI. Analogously, the LPR increased 5-fold by the end of the main AXC period. Average glucose levels demonstrated a 1.5-fold increase at the end of the first (preconditioning) AXC period (0.60±0.14 vs 0.97±0.32 mmol/l); however, they decreased below (to 1/3 of) baseline levels (0.60±0.14 vs 0.19±0.13 mmol/l) by the end of the experiment (after simulated distal arrest). In the experimental segmental artery sacrifice group, lactate levels doubled and the LPR increased 3.3-fold within 30 min and continued to increase steadily almost 5-fold 180 min after total segmental artery sacrifice (P < 0.05). In patients undergoing TAAA repair, lactate similarly increased 5-fold during ischaemia, reaching a maximum at 6 h postoperatively. In 2 patients with intraoperative SCI, indicated by a decrease in the motor evoked potential of >50%, the LPR increased by 200%. CONCLUSIONS CSF is widely available during and after TAAA repair, and CSF MD is feasible for detection of early anaerobic metabolites of SCI. CSF MD is a promising new tool combining bedside availability and real-time capacity to potentially enable rapid detection of imminent SCI, thereby maximizing chances to prevent permanent paraplegia in patients with TAAA.