OR2.7-8 | Axial Skeleton Injuries — Graded Quiz

Correct. With CT-angiography demonstrating active arterial haemorrhage from the superior gluteal artery after external stabilisation has failed to restore haemodynamics, selective transcatheter embolisation is the definitive and least invasive haemostatic intervention.

The superior gluteal artery is the most commonly injured artery in unstable pelvic fractures. When external stabilisation (binder) and resuscitation fail to correct haemodynamic instability, and CT-angiography demonstrates arterial bleeding, selective angioembolisation is the definitive intervention.

Identified arterial haemorrhage after failed external stabilisation is best controlled by selective angioembolisation — the most targeted and definitive approach. Laparotomy with packing is reserved when IR is unavailable.

Correct. Blood at the urethral meatus, scrotal/perineal haematoma, or high-riding prostate are all contraindications to urethral catheterisation. A retrograde urethrogram must be performed first to define the injury before any catheter is passed.

Blood at the urethral meatus is a contraindication to urethral catheterisation; a retrograde urethrogram should be performed first to exclude urethral injury. If urethral injury is confirmed, suprapubic catheterisation is required.

Blood at the urethral meatus signals possible urethral disruption — forcing a catheter risks converting a partial tear into a complete rupture. A retrograde urethrogram must come first.

Correct. High cervical cord injury eliminates sympathetic outflow (T1–L2), causing peripheral vasodilation (hypotension) and loss of cardiac sympathetic acceleration, leaving unchecked vagal (parasympathetic) activity — producing bradycardia. This is neurogenic shock.

Neurogenic shock results from a complete cervical cord injury above T6 disrupting sympathetic outflow (T1–L2). Loss of sympathetic tone causes vasodilation (hypotension) and unopposed vagal action causes bradycardia — distinguishing it from haemorrhagic shock which produces tachycardia.

The classic tetrad of neurogenic shock is hypotension + bradycardia + flaccid paralysis + warm skin. Haemorrhagic shock produces tachycardia, not bradycardia. This clinical picture is pathognomonic of neurogenic shock from a high cervical injury.

Correct. Autonomic dysreflexia is a clinical emergency. Sitting the patient upright uses orthostatic pooling to lower blood pressure; removing the stimulus (unkinking the catheter to relieve bladder distension) breaks the sympathetic reflex. These are the immediate first steps before any pharmacotherapy.

Autonomic dysreflexia is a life-threatening complication of spinal cord injury above T6. It is triggered by a noxious stimulus below the level of injury (most commonly bladder distension or kinking of catheter) causing uncontrolled sympathetic discharge. The first step is to sit the patient up (lowers BP by orthostatic redistribution) and immediately remove the triggering stimulus (unkink/change the catheter).

This is autonomic dysreflexia — identify and remove the trigger (bladder distension from kinked catheter) first and sit the patient upright. Antihypertensives are second-line if removing the trigger does not resolve the crisis.

Correct. The sciatic nerve exits the pelvis through the greater sciatic foramen below the piriformis. A sacral fracture in the sacral ala region or posterior column of the acetabulum can compress or stretch the sciatic nerve at this exit point.

Sacral fractures in lateral compression injuries can injure sacral nerve roots (S1–S4) as they exit through sacral foramina, or injure the sciatic nerve at its exit through the greater sciatic notch. S1 root injury causes weak plantarflexion and diminished ankle jerk; lower sacral root (S3–S4) injury causes bladder/bowel dysfunction.

The sciatic nerve passes through the greater sciatic foramen and is the neural structure most at direct risk from sacral fractures near the sciatic notch.

Correct. This is an unstable burst fracture (posterior ligamentous complex disrupted) with significant canal compromise and evolving neurological deficit. Urgent surgical decompression and instrumented stabilisation is the standard of care to prevent further neurological deterioration and allow early rehabilitation.

An L1 burst fracture with neurological deficit, posterior ligamentous complex disruption (indicating instability), and significant canal compromise warrants urgent surgical decompression (laminectomy/corpectomy) with posterior stabilisation. The 12-hour window represents a viable early surgery interval that may halt progression and potentially improve neurological recovery.

Posterior ligamentous complex disruption makes this fracture mechanically unstable; conservative management is insufficient. With neurological deficit and significant canal compromise, surgical decompression with stabilisation is indicated.

Correct. The pelvic spring test must be performed only once. Instability is confirmed; repeating the test risks dislodging a stabilising haematoma and dramatically worsening haemorrhage. A pelvic binder should be applied immediately and CT imaging obtained.

The manual pelvic spring test should be performed only ONCE during the primary/secondary survey. Repeated testing can displace clot, increase haemorrhage, and worsen haemodynamic instability. Once instability is confirmed clinically, imaging (X-ray, CT) takes over and no further manipulation is performed until definitive intervention.

Rule: pelvic spring test = once only. Repeating it risks catastrophic haemorrhage from clot disruption. Apply the binder and image the pelvis — do not re-examine manually.

Correct. Pathological spinal fractures from metastatic disease require full-spine MRI (to detect multilevel involvement), oncological staging, and MDT review to determine whether radiation, surgery, cement augmentation (vertebroplasty), or systemic therapy is most appropriate.

Pathological fractures from metastatic disease require specific investigations to assess spinal instability and degree of cord threat: MRI of the entire spine (multilevel disease is common) and urgent oncology/neurosurgical review. Anti-resorptive therapy (bisphosphonate/denosumab) and steroids for cord oedema if needed are also part of management.

Not all pathological fractures need surgery; the decision requires full-spine MRI to assess extent of disease and instability, and MDT review to integrate oncological and spinal management goals.

Correct. The immediate treatment for orthostatic hypotension during tilt-table mobilisation is to return the patient to supine, which rapidly redistributes blood centrally and restores cerebral perfusion pressure.

Orthostatic hypotension is common during early mobilisation after cervical cord injury due to loss of sympathetic vascular tone. The immediate response is to lower the head of the table/tilt back towards supine to redistribute blood centrally, and not to administer vasopressors as first-line in this context.

The first action is always positional: return to supine. Preventive measures (abdominal binder, compression stockings) are applied before the next tilt session; vasopressors and IV fluids are reserved for refractory cases.

Correct. The sciatic nerve lies posterior to the hip joint and is stretched or compressed by the posteriorly displaced femoral head in posterior dislocation/posterior wall acetabular fractures. Foot drop (peroneal division injury) is the classic neurological deficit.

Posterior hip dislocation and posterior wall acetabular fractures are caused by axial loading through a flexed knee and hip (dashboard injury). The sciatic nerve — particularly its peroneal division — is at greatest risk (incidence ~10–15%) due to its course posterior to the hip joint. It manifests as foot drop.

The sciatic nerve (especially its peroneal division) is the nerve at greatest risk in posterior hip dislocation and posterior wall acetabular fractures. Foot drop and altered sensation over the dorsum of the foot are the hallmarks.