Autonomic Dysreflexia with Triggering Stimulus

Case: A 33-year old male with AD symptoms

A 33-year-old male with a history of a C6 complete SCI as a result of a motor vehicle accident 10 years ago have been on self CIC 6 to 8 times a day with approximate volumes in the 200mls. Pharmacotherapy with oxybutynin 15 mg and terazosin 1 mg at night were initiated. He does have some urinary leakage between catheterizations. Of note, when his bladder is very full, the patient states that he sometimes has difficulty getting a catheter into his urethra. Over the past few weeks, it has been getting somewhat worse. His blood pressures at times have gone up to 180mmHg systolic.
Very recently, he had difficulty with AD and was seen in a local ER and was treated. He did have a renal ultrasound, which did show some grade 2 left caliectasis.  Subsequent urodynamic evaluation demonstrated progression of his bladder dysfunction. His bladder capacity is smaller. His bladder compliance is worse. He has high-pressure DSD associated with dysreflexia at a volume of approximately 60 mL.

There is no option here, this patient needs an augmentation cystoplasty on an urgent basis. This is a dangerous bladder associated with DSD high pressures and AD, the latter is very dangerous.

Comments and Lessons: The autonomic dysreflexia (AD) is a real danger and could result in cardiovascular or cerebrovascular disease. Most patients with high spinal lesions have some autonomic instability usually AD, a paroxysmal event where uncontrolled unmodulated discharge of the sympathetic cell mass in the intermediolateral area of the cord is generated by a sensory input. Most commonly this is a bladder related, either an overfilled bladder, or one that is reflexly contractile with high pressure DSD. Even in normal persons an over-distended bladder results in slight changes in pulse pressure, and local well controlled sympathetic responses directed at the bladder and perivesical ganglia. These responses facilitate urine storage reflexes. In spinal man, where the lesion is at or above T5, a massive sympathetic over response to sensory input can result. This massive response indicates that sympathetic responses to afferent bladder and rectal input are normally controlled and moderated by brain stem centers. AD results when there are enough sympathetic neuronal cells free from brainstem influences. This does not occur in patients with lower lesions.  Treatment is directed at the inciting cause. Patients with AD in the afternoon while in their wheel chairs are usually suffering from a full bladder. Adjustment of intermittent catheterization will obviate the problem. In quadraplegics patients treated with a sphincterotomy and condom catheter drainage, AD may occur during the day or at night when urine outputs are very high. In the latter cases the ideal sphincterotomy is a total bilateral one such that the resulting detrusor leak point pressure is very low (5 cms or less). That allows Crede voiding when the patient is in his or her chair, and prevent rapid overfilling of the bladder at night.

Where high pressure reflex contractility with DSD is the cause of the AD? Immediate treatment with an alpha blocking agent, for example, minipress (prazosin) 2 mg po TID, or Chlorpromazine 12 to 25 mg BID to QID will blunt the dysreflexic response. This provides some time for adjustment of bladder medication or surgery to increase bladder capacity. Patients with known AD who must undergo sphincterotomy, can be pre treated with chlopromazine 25 mg IM TID. Chronic use of these agents can cause postural hypotension in a population with grossly impaired righting reflexes related to their spinal cord injury. The effects of the agents mentioned above are gradually cumulative and with time decreased dosage is quite possible.

There is another kind of dysreflexia which fortunately is rather rare, and not usually severe in character, but in some circumstances it can be lethal. This involves a parasympathetic over-response to some visceral afferent stimulus as for example gastric distention, or rectal distention. There is increased vagal tone, blood pressure and pulse drop, and patients are poorly or non responsive. Generally this is mistaken for a cardiac event or urosepsis. Treatment is with atropine IV. Most patients with high lesion have some degree of this syndrome, which is usually unrecognized.

Please also refer to this.

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