Autonomic dysreflexia

Two to four months post-injury the person with cervical spinal cord injury may suddenly experience a flushing in the face and complain of severe headache. The blood pressure increases from 100/60 to 240/120 mmHg. When looking for triggering factors, the staff might find an obstruction of the urinary outlet. When urine passes again the blood pressure returns to normal. This reaction, the so-called autonomic dysreflexia reaction, is seen in cord-injured people with a lesion level above T6. The clinical reaction is not an all-or-none reaction but graded; in mild cases the person just feels a small chill. Investigations have shown that the reaction is caused by a severe vasoconstriction below lesion level in skin, muscular (Karlsson et al., 1998) and renal vascular beds (Gao et al., 2002). Presumably also the splanchnic/gastrointestinal vascular bed is involved. The reaction is mediated by the sympathetic nervous system as shown by a profound increase in noradrenalin spillover below lesion level (Karlsson et al., 1998; Gao et al., 2002). The peripheral afferent stimulation of the sympathetic neurons may be asymptomatic and much more frequent than previously known. Continuous measurement of noradrenalin in blood samples collected every 30 min in 24 h revealed several peaks even in subjects who were asymptomatic (Karlsson et al., 1997b).

The reaction is triggered by distension of hollow organs below lesion level such as the urinary bladder, the gall bladder, the renal pelvis and ureters or the gastrointestinal system. A bone fracture below lesion level may also give rise to the reaction. When the triggering factor is withdrawn, the blood pressure returns to normal. However, if the cord-injured person or the treating staff is unfamiliar with the reaction, there is a serious risk of complications as intracranial hemorrhage or cerebral infarction. In our clinical practice there have been two cases in the last 2 years. The first was a woman in her 50s who sustained a C4-C5 level spinal cord injury and tetraplegia a few years ago. She was discharged to home and some months later became severely constipated and developed an auto-nomic dysreflexia reaction. She was treated at a local hospital where there was inadequate knowledge of autonomic dysreflexia. The blood pressure stayed very high and the patient developed a cerebral infarction. Another case was seen recently. A person with cervical spinal cord injury who had been injured for more than 30 years was treated for a serious infection. He developed an abscess in the abdomen and suffered from a prolonged episode of dysreflexia. During this period we measured his cerebral blood flow and found signs of decreased perfusion in parts of the brain, indicating vasoconstriction. We speculated that this vasoconstriction might have been an autoregulatory response of the cerebral vessels in the presence of greatly increased systemic arterial pressure.

The autonomic dysreflexia reaction has other side effects and can influence metabolism. Regional investigation of adipose tissue metabolism above and below lesion level showed an increase in glycerol release — activation of lipolysis — during induced dysreflexia, that is, during sympathetic activation below lesion level (Karlsson et al., 1998). Whether this is of importance for the insulin resistance sometimes seen after spinal cord injury (Karlsson, 1999) is not known.

Another associated risk with the autonomic dysreflexia reaction is the vasoconstriction in the renal vascular bed (Gao et al., 2002). This sympathetic activation below lesion level might contribute to the development of renal failure. Previously, many tetraplegic patients used bladder tapping to condom drainage as a method of bladder emptying. Bladder tapping is known to induce auto-nomic dysreflexia every time it is performed. The introduction of intermittent catheterization may thus have the advantage of maintaining renal function both by the intermittent total emptying of the bladder, with markedly lower risk of urinary tract infections, and by the absence of triggering factors for renal vasoconstriction.

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