Spinal cord injury • R2 吳佩諭 • 2003/1/16
Pathophysiology of spinal cord injury • Primary injury: hemarrhage, and perhaps vasospasm, immediate reduction of blood flow • Secondary injury: infarction of spinal cord with permanent loss of function • Methylprednisolone 30 mg/kg followed by infusion 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 injuries
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 stomach • Nasal intubation not be performed when having suspected basal skull fracture or facial fracture involving the sinuses.
Emergency intubation in an unconscious or uncooperative patient— • Oral intubation under general anesthesia with 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 response to stimuli below the level of lesion. • These stimuli include distention of viscera (bladder, 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 aggravated 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