Abstract
A 53-year-old man was involved in a road traffic accident. He was driving the car and was wearing a seat belt. This is the radiograph obtained in casualty (Figure 15.1a). What does it show?
This is a plain lateral radiograph of the cervical spine that shows anterior translation of the C6 vertebra on C7. This translation is more than 25% so this is likely a bifacet dislocation. The inferior facets of C6 can be seen to lie anterior to the superior facets of C7. This is a bifacet dislocation. The C7/T1 border is not clearly seen and therefore this is an inadequate radiograph.
Structured oral examination question 1
Bifacet dislocation
EXAMINER: A 53-year-old man was involved in a road traffic accident. He was driving the car and was wearing a seat belt. This is the radiograph obtained in casualty (Figure 15.1a). What does it show?
CANDIDATE: This is a plain lateral radiograph of the cervical spine that shows anterior translation of the C6 vertebra on C7. This translation is more than 25% so this is likely a bifacet dislocation. The inferior facets of C6 can be seen to lie anterior to the superior facets of C7. This is a bifacet dislocation. The C7/T1 border is not clearly seen and therefore this is an inadequate radiograph. Further imaging is required, and a CT would be my choice in this patient. There is no obvious anterior soft-tissue swelling or any associated fractures of the facets, laminae or spinous processes.
EXAMINER: Assume there is no injury at C7/T1. How will you manage this patient?
CANDIDATE: I will manage this patient according to ATLS guidelines. I will perform a primary survey to identify and treat immediately life-threatening injuries, carrying out any emergency treatment and stabilization of the patient as required.
I would then proceed with a secondary survey to identify and treat potentially life-threatening injuries; spinal assessment is part of this. The aim is to protect the cord and maintain cord perfusion. I would ensure adequate fluid resuscitation, supplementary oxygen and catheterize the patient. I am mindful that 10% of patients have a fracture elsewhere so maintaining the patient supine on a spinal board with triple spine immobilization (rigid collar, sandbag, tape) and log-rolling is required. The incidence of neurological deficit with a bifacet dislocation is 50% so a full neurological assessment is required. I would want to assess for any neurological injury and obtain an ASIA grading. Given the mechanism of injury and the injury identified I would obtain a trauma CT series (head, cervical spine, thoracic/lumbar spine, chest, abdomen and pelvis) to exclude any associated injuries (Figure 15.1b) [1].
I would want to make an early referral to the local spinal injuries unit for transfer of the patient for more specialized surgical management of this injury.
COMMENT: This is a highly unstable injury resulting from hyperflexion of the cervical spine with a high risk of associated spinal cord damage. The patient may present with spinal shock including bradycardia and hypotension unresponsive to fluid resuscitation. This is due to loss of vasomotor sympathetic tone. Candidates should be able to safely deal with the initial management of this injury in casualty and get past the initial questions. This will allow them to then move on to discuss more definitive management of the injury (score 6). If a candidate is doing very well (score 7–8) they may discuss the more controversial areas of management (i.e. MRI versus no MRI prior to reduction (score 7) with evidence (score 8)). If a candidate is struggling with A&E management (score 4–5) they may not get past the initial management of the patient in the A&E department.1
EXAMINER: Assume the patient is being managed in an appropriate spinal injuries unit.
CANDIDATE: I will then need to reduce and stabilize the spine.
EXAMINER: How will you reduce the dislocation?
CANDIDATE: The dislocation can be reduced closed with traction or open with an anterior surgical approach.
EXAMINER: Well of course all options apply, what would you do?
CANDIDATE: I would take the patient immediately to theatre and apply halo traction. I would add 5 kg weight initially and increase steadily in 2 kg increments, observing carefully the neurological function and the reduction of the spine using an image intensifier. Once the vertebral bodies and facet joints have been realigned traction can be reduced and a collar applied (Figure 15.1d –h) [2].
CANDIDATE: This is controversial [3]. In an awake cooperative patient this is not required. The potential risk is displacing a disc fragment into the canal causing catastrophic deficit. This would be identifiable in an awake cooperative patient and can be addressed with immediate anterior decompression and stabilization. An existing deficit will not have the potential to improve until the spine is realigned and an MRI delays this.
EXAMINER: Are you telling me you would never get an MRI first?
CANDIDATE: If it were a unifacet dislocation with only nerve root injury I would organize an MRI first as there is no urgent requirement to reduce the dislocation. If the patient were obtunded or uncooperative and not able to cooperate with serial examinations during reduction manoeuvres I would organize an MRI scan first [4]. I would also do so if they were neurologically intact (Figure 15.1c).
EXAMINER: How would you stabilize this injury?
CANDIDATE: An anterior cervical discectomy and fusion (ACDF). This can be done with a cage and plate or tricortical iliac crest graft (harvested with a small sagittal saw) and a plate. I would prefer the latter as autograft will more reliably achieve fusion. These injuries may also require instrumented stabilization posteriorly depending on the degree of soft-tissue injury and instability. This can be done as a delayed procedure or at the same time. ACDF with plating gives the injury a degree of stability before a patient is turned prone and the cord should not be in danger.
EXAMINER: What would you do if closed reduction failed?
CANDIDATE: If a closed reduction fails, an anterior or posterior approach should be performed to reduce the locked facet dislocation. This is usually via a posterior approach.
Key Points
Cervical disc herniation can occur with facet dislocations. When reduction occurs the disc herniation can be displaced posteriorly into the spinal canal, causing catastrophic deficit. This is rare. An MRI scan can be performed as follows:
1. Before reduction.
a. Advantage – allows identification of disc herniation, which then provides an argument for proceeding with open discectomy rather than closed reduction.
b. Disadvantage – delays treatment which in the presence of neurological deficit might adversely affect outcome as cord is compressed for longer.
2. After reduction.
a. Advantage – allows identification of disc herniation that might dictate surgical approach, e.g. herniation behind vertebral body may require corpectomy.
b. Disadvantage – time-consuming and often these herniations are not clinically significant so should not affect treatment which is ACDF.
3. Not performed.
a. Advantage – facilitates more rapid reduction by avoiding delay. Studies suggest that closed reduction can be safely performed, provided that serial neurological examination is possible during this procedure. Studies report the incidence of herniated disc material is higher after successful closed reduction than before but without increase in neurological injury, i.e. is not clinically relevant.
b. Disadvantage – very small risk of worsening deficit by displacing disc herniation.
It is generally accepted that an MRI scan should be performed before reduction if the patient is neurologically intact and in the patient that is obtunded or non-cooperative. In an awake cooperative patient with deficit this has little chance of improving until cord compression is alleviated by reduction and the incidence of disc herniation is higher after closed reduction, but the incidence of neurological deficit is not, i.e. these herniations don’t appear to be clinically significant.
Figure 15.1a Lateral radiograph demonstrating C6 on C7 facet dislocation.
Figure 15.1b C6 7 facet dislocation parasagittal CT.
Figure 15.1c Parasagittal MRI stir of C6 on C7 facet dislocation.
Figure 15.1d–h Image intensification views of closed reduction of C6 on C7 facet dislocation.
References
Structured oral examination question 2
Incomplete cord injury
EXAMINER: A 75-year-old female presents with abnormal neurological findings having fallen onto her face. What does the MRI scan show (Figure 15.2a)?
CANDIDATE: The MRI scan (sagittal T2 sequence) demonstrates multilevel central canal narrowing most notable at C4/5 and C5/6. The narrowing is due to a combination of anterior disc/osteophyte complex and posterior ligamentum flavum infolding. At C4/5 where the narrowing appears severe (but requires axial cuts for proper assessment) there is focal high signal change in the cord, which is either myelomalacia (spinal cord damage due to compression) or oedema (due to the acute injury).
EXAMINER: What pattern of injury do you expect?
CANDIDATE: It is likely that the pattern of injury is one of central cord syndrome. It is the most common incomplete spinal cord injury. The history is characteristic, often an elderly person with a hyperextension injury. The pathophysiology is one of anterior osteophytes and posterior infolded ligamentum flavum compressing the cord. There is a pre-existing cervical degenerative disc disease that may well have been asymptomatic. There may be forehead/facial bruising.
EXAMINER: What do you think the clinical features will be?
CANDIDATE: There will be weakness affecting the upper and lower limbs. The upper limbs are affected to a greater extent, with the motor deficit especially apparent in the hand.
EXAMINER: What is the pathophysiology of the condition?
CANDIDATE: The cord is usually injured as a result of posterior pinching by a buckled ligamentum flavum or from anterior compression by osteophytes. There is usually cord contusion with stasis of axoplasmic flow and/or Wallerian degeneration of the corticospinal tracts. The original description of the condition was based on post-mortem studies that demonstrated a destructive haematomyelia, but more frequently this is absent, and the injury caused by oedema alone.2 If haemorrhage is present this has been correlated with a worse injury and limited neurologic recovery.
EXAMINER: How will you manage this person?
CANDIDATE: Initial management of such an injury in the emergency department would include a full ATLS work-up. I would want to take a full history and perform a thorough clinical examination including a full neurological examination and document my findings in the notes. The spine should be fully immobilized, systolic blood pressure maintained, a urinary catheter passed, and careful fluid resuscitation undertaken. A digital rectal exam should be performed and an American Spinal Injury Association (ASIA) score should be obtained.
It is also important to perform serial neurological examinations especially to check for any deterioration in function, as this is a strong indication to consider surgical decompression.
CANDIDATE: Administration of methylprednisolone for the treatment of acute spinal cord injury (SCI) is no longer recommended. I am not sure of the specifics of the literature, but there is very little hard evidence to support the clinical benefit of steroids in the management of acute SCI, but plenty of evidence documenting their harmful side effects.
EXAMINER: What about prognosis?
CANDIDATE: Central cord syndrome has a good prognosis although full functional recovery is not likely. It is usual to see significant early neurological recovery. In the absence of spinal instability, I would manage this condition non-operatively. The typical recovery sequence begins with the lower limbs, followed by bladder and bowel function, the proximal muscles of the upper extremity and finally the hands are the last to recover function. Typically, the patient is ambulatory at final follow-up. If there is a plateau in recovery with MRI-proven cord compression, or if there are signs of instability, surgical decompression and stabilization should be considered [1].
EXAMINER: What surgical approach would you use?
CANDIDATE: The optimal surgical approach is a matter of debate. As a general rule, the ideal surgical approach should target the site of predominant compression of the spinal cord: anterior, posterior, or combined. Usually, if the compression is restricted to one or two levels, the anterior approach is preferred; if more than two levels are involved, the posterior approach may be more advantageous.
EXAMINER: Are you aware of any other incomplete cord syndromes?
CANDIDATE: Anterior cord syndrome affects the anterior two-thirds of the spinal cord via anterior spinal artery lesions. It is a vascular phenomenon. It causes profound motor weakness due to involvement of the corticospinal tracts. Proprioception and vibratory sense (both carried in the dorsal, unaffected, columns) are preserved. This condition has the worst prognosis.
Brown–Sequard syndrome is a hemi-section of the spinal cord, seen with a penetrating trauma. There is ipsilateral loss of motor function, proprioception and vibratory sense; there is contralateral loss of pain and temperature sensation.
COMMENT: If a candidate is progressing well with the viva, they may be asked to draw out the spinal cord tracts and spend more time discussing anterior cord and Brown–Sequard syndromes.
Key Points
Central cord syndrome has a reasonable prognosis. Historically, non-surgical treatment was advocated for CCS.
Early surgery is indicated if there is instability from a co-existing fracture that requires stabilization [2]. In this situation it would be reasonable to describe the case as neurological deficit as a result of a fracture, which is therefore by definition unstable, and perform early stabilization. If the cause of the CCS is a large central disc protrusion, early surgery is supported.
The Surgical Timing in Acute Spinal Cord Injury Study (STACIS) suggests decompressive surgery should be performed within 24 hours if there is a neurological deficit or 12 hours if the neurological deficit is deteriorating [3].
Figure 15.2a T2 sagittal MRI scan, cervical spine. C5–7 hyperintense signal.
Figure 15.2b Cross-section of spinal cord.
References
Structured oral examination question 3
Thoracolumbar burst fractures
EXAMINER: What does this X-ray (Figures 15.3a and 15.3b) show?
CANDIDATE: There is a fracture of the T12 vertebral body (it is reasonable to say a vertebral body at the thoracolumbar junction but L5/S1 not visible so exact level difficult to be sure) with greater than 50% loss of the vertebral body height. There is retropulsion of the posterosuperior corner of the vertebral body. On the AP view there is widening of the interpedicular distance. This is a burst fracture. It does not involve the inferior end plate, so it is an incomplete burst fracture.
CANDIDATE: I will be honest, I don’t know.
COMMENT: Under physiological load the spine is sufficiently stable to prevent significant pain, neurological deficit and progressive deformity.
EXAMINER: So, is this fracture stable?
CANDIDATE: At the thoracolumbar junction a fracture with this much loss of height is likely to become progressively kyphotic, so no, it is not stable.
EXAMINER: What is your management?
CANDIDATE: I would manage the patient according to ATLS principles. This will ensure optimal cord perfusion. This combined with maintenance of neutral spinal alignment aims to prevent secondary injury. There may be other treatment priorities identified, e.g. concurrent abdominal trauma. The initial aim is to prevent secondary injury by protecting (neutral spinal alignment) and perfusing (appropriate resuscitation) the cord.
A full neurological examination is undertaken, and the presence of sacral sparing documented (which is suggestive of a better prognosis). The neurological examination is repeated (frequently if a deficit is identified) in order to ascertain whether there is a progressive neurological deficit.
EXAMINER: Do you mean neurogenic shock?
CANDIDATE: Neurogenic shock is a loss of sympathetic tone. It is a vascular phenomenon. Typically, the patient will be hypotensive but bradycardic. It is important to exclude other causes of hypotension, however (10–15% of patients with spinal injuries have visceral injuries), before attributing hypotension to neurogenic shock.
EXAMINER: So, is this likely here?
CANDIDATE: The majority of sympathetic innervation has come off the cord before T12, so no. Spinal shock is possible. This is a neurological phenomenon. It is a temporary loss of spinal cord function and reflex activity below the level of the injury. It is typically characterized by diaphragmatic breathing (if cervical/high thoracic), paralysis, absent reflexes, erection, urinary retention and an absent bulbocavernosus reflex.
EXAMINER: What is the importance of spinal shock and how do you know when it’s over?
CANDIDATE: The importance of spinal shock is that one cannot evaluate the neurologic deficit until the spinal shock phase has resolved. Resolution is determined by the return of the bulbocavernosus reflex – squeezing the glans penis elicits an anal sphincter contraction. It can also be performed by tugging the catheter, which is the best way to perform the assessment in a female.
EXAMINER: Is there any further imaging you would obtain?
EXAMINER: You have just told me the fracture is unstable, we are going to treat it as an unstable injury, so is a CT really needed, are you not just using up limited NHS resources?
COMMENT: This is testing higher-order judgement and the appropriate reasoning for use of musculoskeletal imaging.3 The ICB place a lot of importance on these types of questions as they deal with the real-life world of NHS clinical practice rather than just reading facts from a book for an exam.
CANDIDATE: The majority of orthopaedic units would request a CT scan. Kyphotic and translation injuries can be visualized on sagittal and coronal reconstructions. The scan would demonstrate any degree of canal compromise. Vertebral body height, disc spaces, interpedicular distances and interspinous process intervals can be seen and compared between injured and the non-injured levels.
EXAMINER: Would an MRI not be better?
CANDIDATE: CT scans have a limited role in demonstrating associated soft-tissue injuries. An MRI scan is better at picking up disc herniations, epidural or subdural haematomas, ligamentous injuries and spinal cord parenchymal injury.
MRI and CT are complimentary imaging modalities that provide different information. In the absence of neurological deficit, it is usual to request a CT. I would request an MRI in addition if there is neurological deficit.
EXAMINER: So how would you manage this fracture?
CANDIDATE: The fracture is unstable. I would advocate posterior stabilization with pedicle screws and rods [1]. The fracture can be reduced using the principle of ligamentotaxis.
Key Points
Protecting the cord and perfusing the cord to prevent secondary injury are paramount. Lumbar burst fractures (L3–L5) without neurological deficit are usually treated conservatively. Lumbar burst fractures with neurological deficit are by definition unstable (see definition of stability above) and are treated surgically.
There is no general consensus on how to treat neurologically intact thoracolumbar burst fractures (T10–L2), which can be treated with extension orthoses or with surgery [2]. In the long term some progression of deformity and back pain is expected in neurologically intact patients despite adequate bracing; therefore, follow-up radiographs should be obtained at regular intervals to assess the angle of kyphosis and vertebra height loss.
Figure 15.3a and 15.3b AP and lateral radiograph burst thoracolumbar fracture.
