1. Anesthesia for Autonomic Hyperreflexia: Case Presentation & Review
Mark Todd Wright, SRNA
AVANA Conference 2013
OHSU Nurse Anesthesia Program

2. Disclosures $10,000 from AVANA
As you know all AVANA speakers receive $10,000.

3. Case Presentation

4. 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.

5. 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)

6. 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

7. AH Case Presentation Medical History
AH during previous anesthetic
HTN-resolved
Pertinent Surgical and anesthesia hx when arrives.

8. 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

9. 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.

10. 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

11. 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.]

12. AH Case Presentation: Maintenance, Emergence, & Postop
VSS throughout case. No incidence of AH

13. 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

14. 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.

15. 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

16. 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

17. 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.

18. 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

19. 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

20. 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

21. 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.

22. 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: