Keywords
hypercapnia - spinal cord anatomy - spinal cord blood flow
Introduction
Perioperative central cord syndrome (CCS) is described in the anesthesia literature
in scattered case reports following emergent intubations or prolonged cervical extension
for surgical positioning in patients with pre-existing cervical stenosis.[1]
[2]
[3] Presentation is classically one of “man in a barrel,” weakness primarily affecting
upper extremities, sometimes with lower extremity involvement. Our post-anesthesia
care unit (PACU) recently encountered a patient in whom CCS was caused by a cervical
epidural hematoma following cervical spine surgery, presenting initially as respiratory
depression, which we found no prior reports of. Rapid interpretation of physical exam
was the key to the patient's emergent management. We present her presentation as well
as her pathophysiology in a message of vigilance to the anesthesiologist. The patient
provided written Health Insurance Portability and Accountability Act authorization
for publication.
Case Report
An otherwise healthy 46-year-old woman with a history of cervical stenosis arrived
in our institution's PACU for recovery following an uneventful C3 to 5 anterior cervical
discectomy and fusion (ACDF) with C4 corpectomy. Recovery began unremarkably, and
she was alert, conversant, and moving all extremities appropriately. Preparations
were being made for transfer to the ward when she reported neck pain and received
intravenous fentanyl and hydromorphone.
Shortly thereafter, the supervising anesthesiologist was summoned to evaluate shortness
of breath. He found the patient dyspneic with shallow respirations and difficulty
moving her hands. She appeared somnolent but remained arousable, which improved with
naloxone administration and gentle, passive ventilatory assistance via a Jackson Rees
circuit and supplemental oxygen. Once more alert, the patient was able to clench her
eyes and jaw with good strength. She mouthed words in response to questions appropriately
though her voice grew increasingly weak and inaudible. The patient's subsequent neurologic
exam then deteriorated rapidly to full paralysis of the upper extremities followed
by weakness in the lower extremities and eventual quadriplegia—all while awake and aware!
As preparations were made for re-intubation, an arterial line was placed for hemodynamic
management in the setting of a suspected spinal cord pathology. The patient winced
with radial artery cannulation but was unable to flinch her arms in recoil. She was
induced and intubated for respiratory failure uneventfully via video laryngoscopy
and was taken sedated for emergent imaging which showed a fluid collection in the
anterior epidural space spanning from C1 to C6 ([Fig. 1]). The patient's vital signs were notable for significant systolic hypertension which
resolved with ventilatory support and mechanical ventilation and were thus attributed
to hypercapnia.
Fig. 1 Representative slices of the patient's emergent CT, demonstrating a fluid collection
in the anterior epidural space (indicated by white arrows). Artifact from newly placed surgical hardware limit the visibility of the lesion.
An image of the lesion from the “bone window” is included.
The patient was taken to the operating room for emergent exploration of her surgical
site under neuromonitoring. Mean arterial pressure was maintained above 85 mm Hg as
surgeons evacuated a cervical epidural hematoma and achieved hemostasis of local venous
bleeding. Motor evoked potentials, initially absent in all extremities, gradually
returned in the legs and, then, arms. Her initial surgery was ultimately converted
to a C2 to 5 ACDF with additional corpectomy at C3, and the patient made a full neurologic
recovery with the exception of urinary retention at the time of discharge.
Discussion
This patient's presentation is one of CCS with life-threatening respiratory depression,
paraplegia of upper extremities followed by quadriplegia with sparing of cranial nerves
as well as pain sensation in affected limbs. Had rapid recognition and supportive
measures not been immediately available, this patients outcome may have been devastating.
One can imagine how terrifying her experience must have been as she was essentially
physiologically decapitated. Reviewing basic spinal cord anatomy and physiology aids
in understanding this woman's presentation.
We interpret the rapid onset (and resolution) of the patient's syndrome as suggestive
of an obstructive vascular etiology,[4] as explained below. The spinal cord is perfused by paired posterior spinal arteries
and a single anterior spinal artery. Venous blood exits the spinal cord via small,
penetrating intramedullary venules which merge into anterior and posterior spinal
veins running longitudinally along the cord's surface. The anterior medial spinal
vein drains venous blood from the center of the cord and thus impedance of its drainage
can specifically result in central spinal cord ischemia via edematous inhibition of
blood flow. Epidural space compression may further impair spinal cord blood flow via
the obstruction of the epidural venous plexus, which receives venous blood from radicular
veins exiting neuroforamen after draining the aforementioned surface veins.[4]
[5]
We suspect that this patient's expansive cervical anterior epidural hematoma obstructed
drainage of the anterior medial spinal vein and epidural venous plexus, resulting
in edematous impedance to blood flow within the central spinal cord ([Fig. 2]). Within her affected C3 to 5 levels, the resulting distribution of ischemia compromised
centrally located ventral gray nuclei as well as exiting ventral nerve roots, resulting
initially in a lower motor neuron-type diaphragmatic paralysis. Ensuing hypercapneic
respiratory failure, likely compounded by opioid administration, superimposed carbon
dioxide narcosis. This explains her initial depressed level of consciousness improved
by naloxone and ventilator support.
Fig. 2 Artist's rendition of this patient's cervical spinal cord lesion. Pertinent spinal
cord tracts and structures appear labeled with their somatotopic organization indicated
(C, cervical; T, thoracic; L, lumbar; S, sacral). The area in red represents the cord
lesion from focal ischemic injury, presumably following the obstruction of the depicted
spinal venous system. Note that the affected area includes ventral gray nuclei and
projections to the phrenic nerve, producing the patient's presenting respiratory depression
from a central motor lesion. The involvement of the cervical corticospinal tracts
with spinothalamic tract sparing explains the subsequent “man in the barrel” motor
paralysis classic to a central cord syndrome, which preceded her ultimate quadriplegia.
As the area of ischemia expanded outward, loss of the descending upper motor neurons
(UMNs) of the corticospinal tracts resulted in sequential UMN-type paralysis of the
upper and, then, lower limbs according to the somatotopic arrangement of the tracts
(medially located cervical neurons and laterally located sacral neurons). Hematoma
evacuation alleviated venous compression, normalizing cord perfusion, and neurological
function was restored. Sparing of laterally located, ascending sensory neurons of
the spinothalamic tracts explains our patient's preserved perception of pain (with
arterial cannulation) and distinguishes her syndrome from either a complete cord transection
or an anterior spinal artery syndrome in both of which the spinothalamic tracts are
compromised. The patient's presentation with bilateral deficits distinguishes her
case from a Brown-Sequard (cord hemitransection) syndrome.[1]
[6]
This patient's mechanism of injury is distinct from the classical description by Schneider
in 1954 of guillotine-like axial compression of the cervical spinal cord by inward
tenting of dorsal ligamentum flavum during cervical hyperextension—the cause of CCS
within the trauma literature.[1]
[7]
[8]
[9]
[10] Fortunately, our patient's presentation occurred while still in a closely monitored
PACU. The rapidity of onset coupled with the patient's inability to speak or call
for help would have very possibly led to a fatal outcome. We urge anesthesiologists
to consider CCS as part of their differential for respiratory depression in patients
having undergone cervical spine surgery.
