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Elisabeth Fandrich


524 K,C,T

Autonomic Dysreflexia

Autonomic dysreflexia is a condition that is potentially life-threatening. The

autonomic nervous system overreacts to excessive stimulation of the nerves below
the level of the spinal cord injury. Normally, when the autonomic nervous system
response is activated, the mediating parasympathetic nervous system response is
triggered. In the case of the patient with a spinal cord injury, the parasympathetic
nervous system response is blocked at the site of the injury.

Severe hypertension occurs as a result of the vasoconstriction elicited by the

autonomic nervous system response. This severe hypertension can lead to seizures
or even a stroke if it is not controlled and reversed as soon as possible.

The body itself will try to counteract the hypertensive state by vasodilation. This
will only occur above the location of the spinal cord injury. The result of this is that
the lower body has a blood pressure that is very high, and the upper body has a
lower blood pressure. The vagus nerve is stimulated by the high blood pressure
which triggers bradycardia. Rather than stimulating vasodilation like it normally
would, the signal never reaches the vessels lower than the site of the injury.

Autonomic dysreflexia can be triggered by any strong nerve stimuli below the site of
injury, but the most common causes are as follows: bladder distention, constipation,
renal calculi, ejaculation, uterine contractions, skin rash, pressure sores,
thrombophlebitis, enemas, exposure to hot/cold stimuli, gastric ulcers,or

When a patient exhibits signs of autonomic dysreflexia, a quick assessment must be

done, catheters must be inspected for kinks, bladder distention, constipation, etc.
The stimulus that has triggered the autonomic dysreflexia must be discontinued

Manifestations of autonomic dysreflexia are paroxysmal hypertension (no known

reason), pounding headache, blurred vision, bradycardia, diaphoretic above site of
spinal cord injury, piloerection, nasal congestion, nausea, and papillary dilation.

Treatment for autonomic dysreflexia is to remove the causative stimulus, and

administer medications to lower blood pressure.

524, K, C, T is a 45 year old man who has a longstanding history of paraplegia (the
result of a motorcycle accident as a teenager). He was in the transitional care unit
(TCU) for the treatment of a leg ulceration (MRSA and cellulitis) . Over the course of
the day, he reported back pain with increased muscle spasms. His blood pressure
increased, IV labetalol was administered with initial improvement then overall
worsening of symptoms. His suprapubic catheter was flushed and found to have
been kinked. The catheter was replaced and had good urine output. His blood
pressure did not improve. He became tachycardic and diaphoretic. He was
transferred to the ICU where his condition was stabilized then transferred to the
acute care floor.

Lab values were overall normal with the exceptions of decreased RBC (4.49 chronic
infection), decreased Hgb (12.1 may be false low caused by antibiotics), increased
RDW (18.4 may be result of dietary insufficiencies), A:G ratio decreased (0.7
prolonged immobilization), increased C-Reactive Protein (1.8 chronic infection).

His blood pressure was still higher than normal at 0800 on 10/08/08 (178/62), but
he was otherwise asymptomatic. Additional hypertension medications were
prescribed in an attempt to prevent another episode of autonomic dysreflexia.


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