INTRODUCTION
Spinal cord reperfusion injury following a cervical laminectomy is rare. To date there have been only a few reported cases. We report a patient with cervical spondylotic myelopathy who developed quadriplegia and respiratory failure requiring mechanical ventilation after cervical laminectomy.
CASE STUDY
A 67-year-old man presented with a 5-month history of neck pain and discomfort extending into the upper part of the chest particularly on the left side. He denied any limb weakness. He was investigated for a cardiac cause for his pain but the cardiac examination was normal. He was otherwise well.
Examination revealed a fit man. He had a degree of neck muscle spasm and some restriction of neck movement mainly on extension. There was no tenderness. The reflexes, power and sensation (including joint position sense and stereognosis and graphaesthesia) as well as gait were all normal.
Cervical spine X-rays demonstrated degenerative changes involving C3 to C7 with a retrolisthesis Grade 1 at C3–4 and C4–5. MRI of the spine showed an unexpected severe segmental spinal stenosis involving the segments from the lower border of C2 to the upper border of C7. There was marked reduction in the AP diameter of the spinal canal, such that the cervical cord was compressed at all the above segments but maximum at C3–4, C4–5 and C5–6 levels. There was no signal abnormality within the cord itself (Grade 0). Increased signal intensity of the spinal cord is divided into 3 grades based on sagittal T2-weighted MR images as follows: Grade 0, none; Grade 1, light (obscure); and Grade 2, intense (bright).
It was concluded that severe secondary spinal stenosis had arisen as a result of multi-segment degenerative spondylosis with the patient experiencing pain without major weakness. The Nurick Grade was 0 (no root or cord symptoms). The option of extensive laminectomy with possibility of further anterior surgery aimed at stabilising the cervical spine was offered in view of the severity of the stenosis but the patient refused any intervention.
Nine months later, he presented complaining of neck pain associated with numbness and clumsiness of both hands. On examination, he had hyperreflexia in the lower limbs, Grade 3/5 handgrip with agraphesthesia and astereognosia. His gait had become stiff. The Nurick grade was now 3 (mild gait abnormality – does not prevent employment).
MRI of the cervical spine (Figure 1) on this occasion revealed multiple level spinal cord compression with intramedullary T2-high intensity abnormality (Grade 1) at C7–T1 levels.
Pre-operative MRI – Sagittal STIR image demonstrates the spinal stenosis due to the disc disease at multiple consecutive levels. There is high signal intensity (Grade 1) within the cord
In view of the progression of the disease, he agreed to undergo surgical management. The patient was stable during the procedure and there was no surgical or anaesthestic adverse event (specifically no intraoperative hypotension).
Decompression surgery was performed using a posterior approach with a C2–C7 laminectomy. The immediate postoperative course was uneventful with satisfactory resolution of symptoms and ambulation, handgrip improved to grade 4/5 power.
Four days after surgery, he developed sudden flaccid quadriplegia and difficulty breathing. This was associated with a drop in Glasgow coma score (GCS) to 3/15 but reactive pupils. The wound was opened in the intensive care unit. There was no epidural hematoma but the thecal sac was tense on palpation, suggesting significant cord swelling.
Urgent MRI of the cervical spine showed more extensive high-signal intensity of the cervical cord with cord expansion extending to the medulla on T2-weighted images (Grade 2) (Figure 2). Brain MRI demonstrated bilateral high intensity signal on T2 with restricted diffusion involving the Globi Pallidi consistent with ischemia (see Figure 3A and B). The patient was connected to mechanical ventilation and he received intravenous dexamethasone. The patient died 4 weeks later.
DISCUSSION
Surgical treatment of cervical spondylotic myelopathy consists mainly of one of three options: anterior approach, posterior approach and combined anterior-posterior approach. In our patient, expansive C2–C7 laminectomy was performed with clinical deterioration within 4 days of the surgery. Epidural hematoma was ruled out by emergency re-opening of the surgical wound. The thecal sac was found tense, suggestive of significant cord swelling. When postoperative paraplegia or tetraplegia develops, the deficit in most patients is on recovery from anaesthesia.(1) There is a group of patients who have normal neurological function in the immediate postoperative period and deteriorate a few days later (delayed onset neurological deficit). This suggests that the damage may be related to the reperfusion of the spinal cord after decompression.(1)
In our patient, the deficit occurred 4 days post-surgery after clinical improvement suggesting non-mechanical trauma as the cause. The deterioration may be explained by spinal cord reperfusion injury following decompression of a chronic lesion.(1–3) Non-mechanical (in the absence of iatrogenic mechanical injury to the cord) spinal cord injury following a cervical laminectomy is a rare occurrence. There are only few reported cases.(1–4) Most authors have reported C5 palsy following posterior cervical surgery. Reperfusion induced microcirculatory impairment can occur at any level following surgical decompression for a chronic compressive lesion.(4) Reperfusion injury to the ischemic brain and thoracic spinal cord is well described, but uncommon in the cervical spinal cord. The mechanism may, however, be identical with oxygen free radicals contained in the reflow blood and lipid peroxidation.(1,2) Antwi et al. hypothesised ischemic cord due to small artery occlusion.(4)
The MRI revealed spinal cord enlargement with abnormal expansion of the T2 high-signal intensity lesion extending above the level of surgery up to medulla and bilateral basal ganglia. These MRI findings are compatible with the reperfusion injury hypothesis.(5) Seichi reported 6.1% of postoperative abnormal expansion of T2 hyperintensity of which 43 % were asymptomatic.(5) The increased T2 signal of the spinal cord in our patient concurs with findings in a previous report.(5) The T2 high-intensity signal on postoperative MRI (“white cord”) may be due to congestion from rapid reperfusion of the spinal cord following decompression. Aggravation of myelopathy by intramedullary lesion of unknown cause after surgery is reported in few cases.(2–5) This intramedullary lesion may be attributable to the reperfusion mechanism rather than to iatrogenic spinal cord injury.(2–4) Vinodh described a case where the MRI showed T2 hyperintensity extending to lower brain stem.(6) To our knowledge, there have not been previous reports of spinal cord swelling and intramedullary lesion extending to the medulla and bilateral basal ganglia as observed in our patient.
Most of the reported patients had pre-operative T2 changes.(3) Early diagnosis and avoidance of delayed surgical decompression may be crucial in preventing spinal cord reperfusion injury.(2) Prophylactic neuroprotective drugs such as free radical scavengers and calcium channel blockers might reduce the incidence of spinal cord reperfusion injury.(3,5) Cerebrospinal fluid drainage has been found of benefit by some authors.(1,2) Others have tried high dose steroids.(3)
CONCLUSION
The risk of spinal cord reperfusion injury, though rare, should not be ignored. The presence of pre-operative T2 changes must increase awareness of this risk. Surgeons should be aware of this rare condition and it should be discussed with patient when obtaining informed consent.(2,6) Our case highlights the importance of postoperative imaging of other areas not involved in a surgical procedure especially after deterioration following decompressive cervical spinal surgery.