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Anesthesia for Autonomic Hyperreflexia: Case Presentation & Review
Mark Todd Wright, SRNA AVANA Conference 2013 OHSU Nurse Anesthesia Program
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Disclosures $10,000 from AVANA
As you know all AVANA speakers receive $10,000.
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Case Presentation
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Autonomic Hyperreflexia
Recently, I was assigned the anesthetic care of a patient with a SPI and Hx of AH. 6 yrs ago he initiated anti-HTNs therapy, had a subsequent bout of orthostatic hypotn, and suffered a fall a flight of stairs; transecting his spinal C5-C7. AH has anesthetic implications that warrant review for even the most experienced of anesthesia providers since it is a potentially life threatening hypertensive complication that occurs in greater that 85% of pt with SPI above T6.
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AH Case Presentation 63 y/o M, scheduled for a sigmoid colectomy w/ colostomy. NKA BMI 29.3 / 98 Kg Tobacco: 20 pk/yr (quit 2007)
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AH Case Presentation Active Problems
Quadriplegia—C5-C7 transection X6 yrs Chronic pain Oxycodone 5 mg 1-2 tabs q 4 hrs Venlafaxine 75 mg daily Mild RAD—Duoneb prn (rare use) HTN resolved after smoking cessation & accident
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AH Case Presentation Medical History
AH during previous anesthetic HTN-resolved Pertinent Surgical and anesthesia hx when arrives.
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AH Case Presentation Labs & Diagnostics
12-lead EKG: NSR (01/2013) BMP: WNL Hgb: 11.1 Hct: 36.0 Plt: 157 INR 1.2 HR: 63 BP: 123/73 RR: 16 SpO2: 98% T: 36.6˚C
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AH Case Presentation Airway/ROS
Auscultation: RRR CTA Airway ROM: (-) Dentition: (-) Neck: (-) T→D: (-) ULBT: grade I Mouth: > 3 cm MP: 2 Anatomy palp: easy The preop eval showed sensory loss below T4 & motor loss below C7. No CV or pulm complications. Anemia. BLE contractures. Straight cath. Anesthesia hx of AH.
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AH Case Presentation Spinal & Induction
L3-L4 (+CSF) Midazolam 1 mg IV Bupi 12 mg + Epi wash 500 mL LR co-load Induction Lidocaine 60 mg Fentanyl 100 mcg Propofol 120 mg Rocuronium 50 mg Standard monitoring was applied. SAB was placed at the L3-L4 interspace in the L lateral decub position w/ slight reverse Trendelenburg. Sensory was maintained at T4 (nipple line). VSS throughout, slight drop in bp and hr
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AH Case Presentation: Maintenance, Emergence, & Postop
Sevoflurane 1-1.5% BIS 40-50 Fentanyl prn Nipride gtt (readily available) VSS throughout case. No incidence of AH. [Add additional information once arrives.]
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AH Case Presentation: Maintenance, Emergence, & Postop
VSS throughout case. No incidence of AH
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Autonomic Hyperreflexia/Dysreflexia
Episodic & potentially life-threatening HTN that develops in pts w/ spinal cord lesion at or above T6. Occurs > 85% Caused by noxious, visceral, or nociceptive stimuli below spinal lesion SBP ↑ > mmHg SBP increase of greater than is considered a dysreflexic episode. I have read case studies and other literature that reported AH below T6 to as low as t10 journals
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VA & Spinal Cord Injury (SCI)
250,000 Americans w/ serious SCI 42,000 SCI Veterans/heroes 26,000 (2008) 13,000 specialty care (2008) VA is on of 20 professional organizations in the Consortium for Spinal Cord Medicine—develops guidelines to improve care in all americans VA provides coordinated lifelong care for veterans of all ages: emergency care, medical and surgical surgical stabilization, surgical care, and specialty sustaining care.
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AH Pathophysiology Review
Stimulus below transection. Activation of preganglionic sympathetic nerves Vasoconstriction HTN Stimulation of carotid sinus = bradycardia Reflexive cutaneous vasodilation Stimulus > afferent transmission of impulses to spinal cord proper/parenchyma > impulses increase SNS activity over the splanchnic outflow tract > normal outflow modulation of inhibitory impulses does not occur > vasoconstriction below spinal cord transection > systemic hypertension and stimulation of the carotid sinus > reflex bradycardia > HTN & bradycardia are the hallmarks of AH > also a reflexive cutaneous vasodilation above lesion
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AH Clinical Presentation
Awake: C/o HA, blurred vision, nasal stuffiness Anesthetized: Hallmarks: HTN & Bradycardia Piloerection & flushing (above) Untreated: Loss of consciousness Seizures Cardiac dysrhythmias Cerebral, retinal, or subarachnoid hemorrhage ↑ afterload → LV failure & pulm edema Untreated, precipitate to cerebral, retinal, subarchnoid hemorrhage Loss of consciousness, szs & cardiac dysrhythmias
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Autonomic Hyperreflexia
Recently, I was assigned the anesthetic care of a patient with a SPI and Hx of AH. 6 yrs ago he initiated anti-HTNs therapy, had a subsequent bout of orthostatic hypotn, and suffered a fall a flight of stairs; transecting his spinal C7. AH has anesthetic implications that warrant review for even the most experienced of anesthesia providers since it is a potentially life threatening hypertensive complication that occurs in greater that 85% of pt with SPI above T6.
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AH Anesthetic Implications Pre-op
HEENT—↓ ROM & mouthing opening CV—↓ BP, orthostatic hypoTN Pulm—↓ lung volumes, cough reflex, atelectasis GI—atonicity, full stomach? Renal—UTI, chronic FC CNS—bowel & bladder dysfunction, chronic & central pain Low resting BP d/t diminution of SNS activity below lesion Nifedipine is the most commonly used primary agent for management of AH Attention to CV, pulm function, volume status & airway
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AH Anesthetic Implications Treatment
Nifedipine or prazosin prophylaxis STOP the stimulus (if possible) Neuraxial block & GA SAB > EA &/or GA > N2O + opioid Vasodilators SNP, Nicardipine BB for tachyarrhythmias NOTE: centrally acting hypotensive agents are not effective (clonidine) Direct vasodilators (SNP), ganglionic blockers (trimethaphan), alpha antagonists (phentolamine). Intrasphincteric anal block for anorectal procedures EA for laboring women
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AH Anesthetic Implications Clinical Pearls
NDNMB prn SCh & profound hyperK+ Common triggers: Irritation of urinary bladder, colon, & labor Waning of anesthesia (post-op) Literature is lacking for definitive treatment Low BP d/t diminution of SNS activity below lesion Nifedipine is the most commonly used primary agent for management of AH
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References Fleisher LA, Roizen MF. Essence of Anesthesia Practice. 3rd ed. Philadelphia/Elsevier. 2011; 10. Hines RL, Marshall KE eds. Stoelting’s Anesthesia and Co-Existing Disease. 5th ed. Philadelphia: Churchill Livingstone/Elsevier; 2008. Lagarto, F., Pina, P.. Autonomic Dysreflexia - a clinical case: 4AP Eur J Anaesthesiol. 2012;29:75. Cited in: Your Full Text at Accessed April 02, 2013. Groothuis, Jan, Rongen, Gerard, Deinum, Jaap, et al. Sympathetic Nonadrenergic Transmission Contributes to Autonomic Dysreflexia in Spinal Cord-Injured Individuals. Hypertension. 2010;55(3): doi: /HYPERTENSIONAHA Stevens, Robert, Bhardwaj, Anish, Kirsch, Jeffrey, Mirski, Marek. Critical Care and Perioperative Management in Traumatic Spinal Cord Injury. J Neurosurg Anesthesiol. 2003;15(3): Cited in: Your Full Text at Accessed April 02, 2013.
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References BROECKER, B., HRANOWSKY, N., HACKLER, R.. Low Spinal Anesthesia for the Prevention of Autonomic Dysreflexia in the Spinal Cord Injury Patient. Surv. anesthesiol ;24(3):184. Cited in: Your Full Text at Accessed April 02, 2013. Spinal Cord Injury Fact Sheet for Veterans:
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