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What is it= Also known as hypertensive autonomic crisis, it is a condition associated with autonomic dysregulation following a spinal cord injury at or above T6 level
- Hypertensive crisis in the setting of noxious stimuli
- Defined as systolic BP at least 25 mmHg or more above baseline (at least 150mHg or more)
Etiology and Epidemiology
- SCI (SCI= spinal cord injury) at or above T6 level
- Develops in over half of SCI patients meeting the above criteria
- 92% of SCI patients meeting the above criteria will develop autonomic dysreflexia within the first year following injury; the higher the injury and/or the more complete the injury, the more severe and frequent the episodes will be
Pathophysiology
- Review of some autonomic anatomy; VIEW IMAGE BELOW
- Following spinal cord injury, you no longer receive sympathetic input regulation from higher order centers. Spinal reflex circuits control sympathetic activity at all levels at and below the spinal cord lesion
- In the acute period following injury, patients may experience a “neurogenic shock” state characterized by hypotension, bradycardia (loss of higher order sympathetic stimulation)
- After time, there is hypersensitivity in preganglionic sympathetic neurons due to reorganized circuits and loss of descending modulatory stimulus to these spinal reflex circuits
- When there is a noxious stimuli, there is unchecked reflexic sympathetic overactivity below the lesion... leads to diffuse peripberal and splanchnic vasoconstriction--> increased BP
- In a patient without a spinal cord injury, parasympathetic response corrects increased sympathetic tone in a balanced manner... increase in BP--> stimulation of baroreceptors in the carotid sinus/aortic arch--> slowed heart rate and vasodilation via inhibition of sympathetic preganglionic neurons
- In a spinal cord injury patient, the parasympathetic response is blocked from traveling below the spinal injury... no stimulation from modulatory pathways from the medullary vasomotor center can travel down the spinal cord to inhibit sympathetic preganglionic neurons... The Effect= persistent vasoconstriction of circulation below the SCI
- HOWEVER parasympathetic response is still able to travel to pathways ABOVE the spinal cord lesion, leading to parasympathetic effects above the SCI (vasodilation, flushing, lacrimation, diaphoresis, nasal congestion, bradycardia, hypotension… etc)
TRIGGERS:
(source: https://pn.bmj.com/content/21/6/532)
- MOST COMMON STIMULUS OF AD= DISTENTION OF HOLLOW ORGANS
-bladder distention in 85% of cases... fecal impaction/constipation second
- The 6 B’s : Bladder, Bowel, Back passage, Boils, Bones, Babies
- pressure ulcers/ injuries, infections (including UTI, skin infections, etc) , sexual intercourse, medical procedures/ labor in an pregnant patient
Presentation
( Source: https://www.ncbi.nlm.nih.gov/books/NBK482434/)
- the presenting complaint is commonly a severe headache
- HYPERTENSION
- Above the level of the SCI: profuse diaphoresis, flushing, piloerection, pupillary constriction, nasal congestion, bradycardia
- Below the level of the SCI: cool, pale skin
Management
- FIRST STEP IS TO CHECK THE BLADDER!!! 85% of autonomic dysreflexia is due to bladder distention!!!
- If Bladder is normal or if you manage bladder distention and BP is still high, check for fecal impaction
- If bladder and bowel are normal, assess for a noxious triggering stimulus in a systematic fashion
- If a trigger cannot be identified or if blood pressure does not improve below 150 mmHg systolic, employ emergency antihypertensive medications
- nitroglycerine 2% paste on the skin above the level of the spinal cord injury
- others= nifedipine, po nitrates, captopril, clonidine
- PEARL: WHY DON’T WE GIVE THEM MEDICATION FIRST???
- If we remove the noxious trigger, we should get quick relief... if we attempt maneuvers to lower the BP before removing the noxious trigger, we will have to deal with rebound hypotension
Prevention = intermittent self cath frequently throughout the day, proper bowel management, appropriate prophylaxis for decubitus ulcers and periodic inspection of skin
SOURCES:
Allen KJ, Leslie SW. Autonomic Dysreflexia. [Updated 2022 Feb 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482434/
Bycroft J, Shergill IS, Choong EAL, et al Autonomic dysreflexia: a medical emergency Postgraduate Medical Journal 2005;81:232-235. Available from: https://pmj.bmj.com/content/81/954/232
Eldahan, Khalid C. and Rabchevsky, Alexander G., "Autonomic Dysreflexia After Spinal Cord Injury: Systemic Pathophysiology and Methods of Management" (2018). Physiology Faculty Publications. 136. https://uknowledge.uky.edu/physiology_facpub/136
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