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Postoperative paraplegia refers to new onset neurological deficit which occurs as a result of damage/insult to the spinal cord below T1 whereas quadriplegia/tetraplegia with or without respiratory dysfunction will occur when the insult is above the first thoracic vertebra. Usually it affects the cervical spinal nerves resulting in complete paralysis of both arms and legs. In addition to the arms and legs being paralyzed, the chest and abdominal muscles will be affected resulting in weakened breathing (paradoxical respiration) and the inability to properly cough and clear the secretions from the chest.
Anterior cord syndrome is when the damage is in the front of the spinal cord, so a patient can have loss of motor power, decreased sensations to pain, temperature and touch below their level of injury. Pressure and joint sensations can be preserved. It is possible for some patients with this injury to later recover some movement if motor recovery is evident days after the initial injury.
Posterior cord syndrome is when the damage is in the posterior aspect of the spinal cord. This type of injury may leave a patient with good muscular power, and temperature and pain sensations; however, they may have problems in coordinating movement of their limbs.
Paraplegia is one of the major mortifying complications. Occasional case reports of midcervical quadriplegia in the postoperative period after posterior fossa procedures performed in the sitting position have been reported in the literature. Hitselberger and House mentioned five unreported cases of midcervical quadriplegia after cerebellopontine angle neuroma resection performed in the sitting position. Acute focal pressure on the spinal cord, along with the flexion of the neck, was the postulated mechanism. Matjasko and colleagues reported a case of quadriparesis due to sitting position in a patient with severe cervical stenosis.
Wilder highlighted the fact that acute flexion of the neck in a patient under general anesthesia in the sitting position may cause stretching of the cord at the level of fifth cervical vertebra due to which regional cord perfusion is compromised, especially if intraoperative hypotension occurs.
According to a previous report, quadriplegia can also be a major complication of lumbar spinal surgery. Several possible mechanisms have been held responsible for cervical spinal cord damage.
First, neuromuscular blocking drugs cause a decrease in the tone in the cervical musculature during general anesthesia so that already present spondylitic bars may cause compression of the spinal cord. Haisa and Kondo demonstrated slight intervertebral disk bulge which occurred during surgery because of acute neck flexion that led to compression and cord stretching, leading to myelomalacia.
Second, blood flow may be impaired in the upper spinal cord as a result of prone position with hyperflexion. Wilder suggested that flexion of the cervical spine during general anesthesia may produce enough spinal cord stretching to alter the autoregulation by mechanically affecting the spinal cord vessels.
When the neck position is changed from neutral position to full flexion, the entire cervical cord is elongated by 10% of its initial length as compared to the neutral position. Hence the longitudinal arteries are stretched and constricted with this elongation.
Anatomically, the cervical spinal cord receives its major share of blood from the longitudinal trunks (anterior and posterior spinal arteries), supplied by radicular branches of vertebral arteries. Turnbull et al. demonstrated that the cervical cord receives zero to eight radicular arteries.
Because of the very critical sources of blood supply to the spinal cord, any pathology that interferes with the arterial supply can cause ischemia, infarction, or both. The vertical extensity of spinal cord infarction depends upon the limit of vascular occlusion and collateralization.
Though spinal arteries are least susceptible to atherosclerosis, but multiple aortic atheromas may occasionally be the cause of infarction or ischemia. Various other possible sources of infarction are emboli originating from disk substance, infection, or stasis of blood because of extreme neck rotation or hyperflexion in the prone position.
The vertebral body in its anterior most and lateral extents receive nutritional vessels termed anterior central arteries, sourcing from the anterior branches of paired vertebral arteries at the same or adjacent level. In contrast to the bony territory of the spinal cord, the radicular arteries which are the major sources of blood to the cervical spinal cord originate eccentrically and unilaterally form the paired vertebral arteries, passing through the root sheath of dura mater along with the nerve roots to the cervical cord with increasing obliquity from the cranial to caudal end, and contribute to blood supplying the longitudinal arterial trunk of the spinal cord. Therefore, the levels of cord ischemia are not the same as the levels of the vertebral column.
Few case reports also describe the use of oxidized cellulose (Surgicel) as a hemostat in spine surgeries which may swell up and cause spinal cord compression resulting in paraplegia. Oxidized cellulose is used commonly in many surgical fields as a hemostat. However, its tendency to swell up once placed causes increase in the compression risk of the cord in closed or bone walled spaces.
Complete cessation of motor activity and loss of sensation either immediately postoperatively or can be delayed up to as long as 48 h postsurgery may be considered as an ongoing complication of spine surgery. This may be associated with urinary or bowel incontinence and areflexia in the involved myotomes.
Inactivity due to paraplegia and quadriplegia can cause multiple problems:
Pressure sores
Spastic limbs
Pneumonia
Urinary tract infection
Osteoporosis
Chronic pain
Paraplegic and quadriplegic patients may also become depressed because of:
Social isolation
Lack of emotional support
Increased dependence on others
During surgery, when the spine is subjected to corrective forces, while the spinal canal is invaded surgically, or when a bony resection is to be performed, the cord is always at risk of injury. The incidence of paraplegia after scoliosis surgery in the absence of spinal cord monitoring has been reported to be between 3.7% and 6.9% but can be reduced to 0.5% by intraoperative monitoring (IOM). The American Academy of Neurology published guidelines on IOM stating that “extensive evidence favours the use of monitoring as a safe and efficacious tool in clinical situations where there is a significant risk to the nervous system, provided we appreciate its limitations.” It is now considered mandatory to do spinal cord monitoring for these procedures.
IOM ideally detects abnormalities in the function of spinal cord early in order that the surgeon is alarmed and can take appropriate steps to correct them before irreversible damage occurs. The time, between a change in the electrophysiological recordings after overdistraction, and the onset of irreversible damage, however, is in the order of only 5–6 min in animal studies.
A motor deficit is functionally more damaging to the patient than a sensory deficit. It is important to consider while evaluating the advantages of these methods of monitoring, few of which will assess motor tracts, and few will assess the sensory tracts of the cord.
As the anesthetic technique can have multitude effects on the ability to monitor spinal cord function accurately, the knowledge of intraoperative spinal cord monitoring is essential to the anesthetist. There are four main methods of IOM: the Stagnara wake-up test, ankle clonus test, somatosensory-evoked potentials (SSEPs), and motor-evoked potentials (MEPs).
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