spinal cord injury and anesthesia – Flashcards
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What cause spinal cord injury?
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Trauma #1 cause Other causes: Tumors Congenital disease Degenerative disease (SC and vertebral column) Multiple Sclerosis (most frequent cause of atraumatic SCI)
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What is the extent of paralysis if C4 is injured?
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quadriplegia
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What is the extent of paralysis if C6 is injured?
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quadriplegia
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What is the extent of paralysis if T6 is injured?
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paraplegia
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What is the extent of paralysis if L1 is injured?
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paraplegia
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__ most common sight of injury
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C7
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Transections above __-__ are incompatible with survival
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C2-C4
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___ -___ keeps the diaphragm alive!
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C3-C5
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The 6 "P"s of sipnal cord injury
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Paralysis Pain Position Paresthesia Ptosis Priapism (presence indicates SNS is involved)
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Pathophysiology of Acute Spinal Cord Injury
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Flaccid paralysis Total absence of sensation below the level of the injury Loss of thermoregulation (poikilothermic) Loss of reflexes below the level of transection Hypotension secondary to loss of sympathetic nervous system activity Diminished SVR Bradycardia secondary to loss of cardiac accelerators T1-T4
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Spinal Shock
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Triad due to relative sympathectomy: Hypotension Bradycardia Hypothermia Lasts for days to 3 weeks following injury
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Lasts for days to 3 weeks following injury
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Alveolar hypoventilation Inability to clear bronchial secretion PE HUGE ASPIRATION RISK
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Spinal Shock Sympathectomy
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Massive vasodilation Poikilothermic Unopposed vagal stimulation ↓ HR ↓SVR ↓ Venous return ↓ CO
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Diagnosis of Acute Spinal Cord Injury
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CT MRI X-Ray AP lateral Regardless of type of injury, the entire cervical spine including T1 MUST be evaluated If it is unclear, all suspected cervical spine injuries MUST be treated as unstable
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Treatment of SCI
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Immediate immobilization of neck Halo-thoracic device (most effective) Hard neck collars (25% limit of neck flexion/extension) Soft neck collars (not effective) Hemodynamic support to maintain MAP/CPP (fluid, pressors, invasive monitoring) Steroid therapy (based on institution policy) OG/NGT
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Acute Spinal Cord Injury Airway Management
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Manual in-line stabilization during direct laryngoscopy RSI for oral ETT placement Awake fiberoptic if airway is clear and patient able to cooperate (coughing and thrashing patient could worsen SCI) Approved blind technique - Fastrack LMA/light wand Awake surgical airway LAST RESORT
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Acute Spinal Cord Injury Anesthetic Management
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Fluid replacement Large bore IV/Central line/Aline/PA line? Support BP - Vassopressors Mechanical ventilation Poikiolthermic - temp control Caution with nitrous - possible pnuemo Avoid hypoxemia Positioning is paramount
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Induction for SCI
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1.Induction Avoid Sux Unlikely to cause an increase in K in the immediate post-transection period BUT...(>24 hrs do not give sux due to hyperkalemia) Severe fasciculation's may worsen C-spine instability Roc for RSI Etomidate (hemodynamic stability) Ketamine *contraindicated in head injury
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Maintenancefor Acute SCI
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Maintenance All IA are ok Avoid Nitrous Pancuronium (hemodynamic stability-counteract loss of SNS activity)
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Emergence for acute SCI
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Emergence Plan on keeping patient intubated and sedated
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Pathophysiology ofChronic Spinal Chord Injury
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Spinal reflexes gradually return Over activity of SNS results in muscle spasm Orthostatic hypotension Tracheal suctioning causes bradycardia ACTH deficiency C3-C5 lesions- denervated diaphragm Below C5 - normal TV, decreased ERV Treatment of spacticity: baclofen, baclofen subarachnoid pump, dorsal rhizotomy, myelotomy, spinal cord stimulator
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Spinal Cord InjuryAutonomic Hyperreflexia
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Following spinal shock spinal cord reflexes return Hallmark Signs: systemic HTN and reflex bradycardia Vasodilation above the level of the spinal cord transection Seen in 85% of pts with transection above T5-7 Unlikely below T10 Initiated by cutaneous or visceral stimulation below the level of the transection (ie bladder distention, surgery)
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Autonomic Hyperreflexia Pathophysiology
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Medical emergency Unopposed reflex sympathetic activity Normally sympathetic activity is modulated from supraspinal centers. With a transected cord, inhibitory cord impulses can not travel below transection. Splanchnic nerves are responsible. Above T5 isolates the splanchnic outflow tract.
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S/S of Autonomic Hyperreflexia
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Severe HTN Pulmonary edema Bradycardia/arrthymia CV collapse Cerebral hemmorhage Seizures Death
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Autonomic HyperreflexiaTriggers
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Hot/cold stimulation Bladder /bowel distention Foley placement Child birth Cutaneous stimulation (surgery)
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Chronic Spinal Cord Injury Anesthetic Management
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PREVENTION of Autonomic Hyperreflexia Consider neuraxial anesthesia (spinal preferred) Difficult to assess the height of a sensory block below transection Consider A-line pre-induction Have short acting vasodilators readily available (Nifedipine prophylaxis/nitroprusside) Central acting antihypertensives (eg. clonidine) are ineffective
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Chronic Spinal Cord InjuryPre-op Assessment
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Labs, Chem 10 Renal function - renal failure secondary to chornic UTIs Skin assessment - decubiti often present (positioning) DVT - possibly on heparin, IVC filter pathologic fractures Depression - SSRIs, TCA Chronic pain - narcotics, NSAIDs, muscle relaxants Baclofen therapy - if withdrawn can cause seizures
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Induction for Chronic Spinal Cord Injury
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Induction : premed with benzos (spasticity) GETA-muscle relaxation required for skeletal muscle spasm due to surgical stim IV induction agents all acceptable *consider avoiding ketamine (possible hypertension) Esmolol/Nitroprusside available NDMRs primary choice AVOID SUX- upregulation hyperkalemia
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Maintenance for Chronic Spinal Cord Injury
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V.A better than N20/narcotic for prevention/treatment of AH
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Emergence for Chronic Spinal Cord Injury
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. Emergence Smooth, controlled, fully reversed May be difficult to extubate (where is the lesion?) AH can first occur post-op when the anesthetic drugs wear off
