jhautonomic dysfunction
TRANSCRIPT
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AutonomicDysfunction
PACU Presentation
Jesse Hill June 2011
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The Case
}Mr. S is a 44 y/o male hx of T5 paraplegia
secondary to MVA 6 years ago wh
opresents for sacral decubitus ulcer incisionand debridement
}No other significant pmhx
}No medications/allergies
}Normal preoperative vitals
} BP 105/60 HR 72 RR 16 Sp02 100%
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Case Continued
} Uncomplicated GA ² 2 hour case
} 2mg Versed/250 mcg Fentanyl intra-op} 1500mL crystalloid/Minimal EBL/No foley
} Patient appears comfortable
} Initial PACU vitals normal
} BP 130/90 HR 72 RR 16 SpO2 99%
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Case Continued
} 40 minutes after arrival in PACU, patient
complains of poundingh
eadach
e,sweating, and nasal congestion
}No recent meds given
} Vitals BP 180/110, HR 41, RR 16, SpO2 100%
}
Wh
at is going on«.
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Differential Diagnosis} Common
} Pain} Emergence agitation} Hypercarbia} Hypo xia
} Less Common} Bladder distention} Volume overload} Shivering} Hypothermia} Medication reaction
} Rare} Serotonin syndrome} Malignanthyperthermia} Subarachnoid hemorr hage} Etc, etc, etc
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Autonomic Dysrefle xia
} Syndrome of e xcessive, uncontrolledsympathetic output that can occur in
patients with spinal cord injuries} Frequency varies widely depending on
level and severity of injury, but can be ashigh as 40-70%
}
Increasing frequency with
h
igh
er level ofinjury
} T6 or higher
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Pathophysiology
} Mediated by spinal refle xes that remain intact
despite the cord injury
} Noxious stimulus below level of cord injury
produces afferent impulse that generatessympathetic response which causes
vasoconstriction below the spinal cord lesion
}
AroundT6 ² splanc
hnic vascular bed is involvedwhich provides the mass of blood vessels
necessary to elevate systemic blood pressure
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Pathophysiology
} Because of the spinal cord injury,descending central inhibitory pathways
that modulate the sympathetic responseare blocked
} Lack of homeostasis
} Parasympathetic vasodilation above the
lesion (headache, flushing, sweating) andbradycardia
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Pathophysiology
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Common Triggers
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Consequences
}Medical emergency
}
Life-threatening hypertension} SAH, Seizures, Retinal hemorr hage
} Dysr hythmias
} Pulmonary edema
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Treatment
} Sit patient up with legs hanging down
}
Loosen tight fitting/constrictive clothing} Perform bladder catheterization or flush
indwelling catheter
} Pharmacological treatment
}
Consider manual bowel disimpaction} Search for other causes
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Pharmacology
} Rapid onset, short duration drugs
}
NTG
5-25
mcg IV or 1 inch
Nitropaste} Nitroprusside 5 mcg IV
} Phentolamine 5-10mg IV
} Nifedipine IR 10mg PO
} Labetolol/Esmolol/Diltiazem/Hydralazine ²
possibly limited by HR/onset/duration
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Back to the case
} Prompt recognition of signs and symptomsof autonomic dysrefle xia by PACU staff
} Patient catheterized and 700mL of urineevacuated
} Prompt resolution of hemodynamic
disturbances
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References
}Miller·s Anesthesia, 7th edition. Ch. 12
}
Blackmer, J. Reh
ab Medicine: AutonomicDysrefle xia. CMAJ. Oct 2003
}Autonomic Dysrefle xia: A MedicalEmergency. Postgraduate Medical
Journal. April 2005 81(954)