Do patients with high paraplegia need anesthesia?

Let me ask a question first: a 25-year-old pregnant woman, 35W pregnancy expectant, a C5-6 cervical spine fracture due to a car accident at 26 weeks of gestation, loss of sensation and movement below the T2 plane after the operation, planning to have a cesarean section, as the chief anesthesiologist, you will What kind of anesthesia to choose? At first glance, the operation plane is already in an "anaesthetized" state, and there will be no pain when the operation is performed directly, and there is no need for the intervention of an anesthesiologist.
However, when such patients are actually operated under no anesthesia, unexplained high malignancy often occurs Blood pressure without pain.

In fact, this is the occurrence of autonomic dysflexia (AD), or hyperactivity (AH).

[Definition] Autonomic dysflexia (AD) refers to a group of clinical syndromes characterized by a sudden increase in blood pressure caused by spinal cord injury at the T6 spinal cord or above.

[Epidemiology] AD mostly occurs 2-6 months after spinal cord injury, the incidence is 30%-85%; the incidence of cervical spinal cord injury is about 60%, and the incidence of thoracic spinal cord injury is about 20%.

[Possible mechanism] (1) The spinal cord at the far side of the injury plane is still active is a prerequisite for AD.

Under normal circumstances, all visceral vascular reflexes are integrated at the level of the spinal cord to maintain the relative stability of blood pressure; after spinal cord injury, the stimulation below the injury level, through the hypogastric nerve (sympathetic) and pelvic nerve (parasympathetic), from the spinal cord The dorsolateral afferent upwards, but it is blocked at the injury site, and excites the interneurons, and then synapses with the sympathetic preganglionic neurons, causing reflex excitement of the sympathetic nerve efferent fibers, stimulating the damage below the injury level The blood vessels of the internal organs and limbs constrict, causing blood pressure to rise.

Among them, the excitement of the greater splanchnic nerve (from the T5-9 spinal cord segment) can cause a dramatic increase in blood pressure to play an important role.
Therefore, the possibility of AD with spinal cord injury above T6 is significantly higher and more intense.The visceral nerves release a large amount of adrenaline, causing the abdominal, pelvic organs, and lower limb skin and muscle vascular beds to contract violently, leading to a sudden increase in blood pressure, stimulating the carotid sinus and aortic sinus baroreceptors, and regulating the blood pressure through the brainstem.
The vagus nerve reflexively emits inhibitory impulses.

However, the inhibitory impulse cannot be transmitted down to the area below the injury plane, and only causes the vasodilation response in the area above the injury plane, which is manifested as head and face congestion, flushing, sweating, and nasal blockage.

(2) After spinal cord injury, the morphology and excitability of sympathetic preganglionic fibers will change, such as the increase of synaptic density; in addition, the increase of receptor sensitivity or receptor density of peripheral blood vessels will aggravate the occurrence of AD.

[Inducing factors and clinical symptoms] Stimulation below the injury level may be induced, especially noxious irritation.

Such as bladder dilation, catheterization, pregnancy, childbirth, surgery, constipation, etc.

Sympathetic excitement below the injury level, vagal excitement above the injury level; increased blood pressure, slower pulse, sweating, chills, chills, anxiety, nausea, urination, and transients above the injury level.
Blurred vision, metallic taste in the mouth, dizziness, dizziness, convulsions, and cerebral hemorrhage.

[Diagnosis] The diagnostic criteria suggested by Karlsson: (1) Increase in systolic blood pressure is greater than 20% of the original normal value, or increase by 30-40mmHg; (2) At least one of the following 5 items: sweating, chills, headache, facial congestion, Chills.

[Prevention and Treatment] Since the onset of AD generally has incentives, removing the incentives can effectively prevent the onset of AD.

Once it occurs, immediately increase the perfusion of the lower limbs with the head-up and the feet-low.
The first choice is calcium ion antagonists (such as nifedipine) and nitrates (such as isosorbide dinitrate).
Sodium nitroprusside can be used to relax the visceral contracted blood vessels immediately during the operation.

"Anaesthesia-like" illusion Many times, high spinal cord injury gives anesthesiologists an illusion of "anaesthesia", which is no different from spinal anesthesia.

However, when you think about it carefully, it is completely different.
During spinal anesthesia, local anesthetics gradually act on the spinal cord through the cerebrospinal fluid from bottom to top to produce anesthesia with a blocking plane.
All spinal nerves below the plane are blocked and will not be excited for a short time; Spinal cord injury is mostly the injury of 1-2 spinal cord segments.
It is still active below the plane and can be excited, but it cannot accept the excitement from the high center.
And this kind of "anaesthesia" is not reliable, and it may cause serious problems in many cases.
Complications.

Therefore, going back to the initial case, cesarean section for such patients with high paraplegia must be anesthetized.
The purpose of anesthesia is not simply painless.
In such patients, AD should be avoided as much as possible.
Obviously, the waist Anesthesia is the best choice; at the same time, it is more important to avoid various factors that may induce AD ​​before anesthesia, such as catheterization, constipation, and severe postural changes.

Bits of knowledge will be shared with you, and I hope to gain from you.

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Focus on the neglected side effects of adrenaline