Spinal cord injury

R2 吳佩諭 2003/1/16

Pathophysiology of spinal cord injury Primary injury: hemarrhage, and perhaps vas

ospasm, immediate reduction of blood flow Secondary injury: infarction of spinal cord with

permanent loss of function Methylprednisolone 30 mg/kg followed by infu

sion of 5.4 mg/kg for the next 23 hr

Cardiovascular system

Sudden increase in BP, bradycardia and dysrhythmias

Followed within minutes by hypotension with total loss of neuronal conduction and flaccid paralysis

Lesions above T5 are associated with severe bradycardia and hypotension.

Spinal shock may last from hours to weeks, with return of reflex activity below the level of lesion.

Respiratory system

Reduction in FRC, FVC, paradoxical breathing

Severe hypoventilation with hypoxemia and hypercapnia

Atelectasis and pneumonia

GI system– Paralytic ileus

GU system– AUR– Recurrent UTI with renal dysfunction

Temperature regulation– Poikilothermic in high cervical cord lesions

Associated injuries– Head injuries in cervical cord lesions– Chest contusion, rib or pelvic fractures in TL spine injuri

es

Anesthetist’s role

Acute phase– Initial resuscitation at ER, typically airway

management– For acute decompression of spinal cord– For surgical treatment of associated injuries

Intermediate phase– For stabilization of spinal column– For associated injuries

Chronic phase

Acute phase- airway management in patients suspected of having cervical injuries

Elective intubation in an awake patient without hypoxia or hypercapnia--– Obtain necessary x-rays– Awake fiberoptic intubation, either oral or nasal– Not do translaryngeal nerve block in pts with full st

omach– Nasal intubation not be performed when having su

spected basal skull fracture or facial fracture involving the sinuses.

Emergency intubation in an unconscious or uncooperative patient—– Oral intubation under general anesthesia w

ith rapid-sequence technique using MILT(manual in-line traction)

– Fluid resuscitation

Maintenance of anesthesia

Goal: maintain adequate spinal cord perfusion, which is dependent on systemic perfusion

Because of cardiovascular lability, all drugs should be givenslowly by titration

Normocapnia or mild hypocapnia is recommanded.

Monitoring- in acutely quadriplegic pts A-line and PA catheter are advised. Hypotension should be treated with fluid and inotropic agents rather than direct vasoconstrictors.

Hyperglycemia- Emergence

Intermediate / chronic phase

(1)autonomic hyperreflexia (2)spinal cord monitoring

– SSEP: iv infusion of narcotic supplemented with low-dose inhaled anesthetic or with nitrous oxide

– MEP: electrical or magnetic stimulation of motor cortex

– Wake-up test

(3)use of induced hypotension

Autonomic hyperreflexia

Occurs after recovery from spinal shock 75-85% of pt with lesions above T6 Widespread reflex sympathetic discharge in r

esponse to stimuli below the level of lesion. These stimuli include distention of viscera (bl

adder, bowel), cutaneous stimulation, uterine contractionslower extremity surgery.

Autonomic hyperreflexia

Below the lesion, the signs are pallor, pilomotor erection, intense muscle contraction, and increasd spasticity.

Above the lesion there is flushing, mucous and conjunctival congestion, intense sweating, mydriasis and lid retraction.

Symptoms include severe headache, shortness of breath, blurred vision, anxiety, agitation, chest pain, and nausea.

Severe hypertension, cardiac changes

Obstetric anesthesia and analgesia in chronic SCI women Medical complications in SCI women aggrava

ted by pregnancy: Pulmonary Pathologic fracture Thromboembolic phenomena Hypotension AH

Case 1– paraplegic for 10 yrs following compression fracture of T-spine and cord injury at T5

Case 2– quadriparetic for 7 yrs, anterior cord syndrome at C6-7 level, with history of AH

Case 3– paraplegic for 21 yrs, complete cord lesion at T11-12