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AUTONOMiC DYSREFLEXiA

Autonomic dysreflexia (AD) is dysfunction of the auto­nomic nervous system after SCI at or above T6. As a result of noxious stimuli below the level of injury, there is increased sympathetic activity leading to vasocon­striction below the level of injury and hypertension.

The central nervous system response is vasodilatation above

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Shea Classification of Pressure Ulcers

bgcolor=white>Red area or ulcer of epidermis or into epidermis
GRADE DESCRIPTION
1
2 Full dermis thickness to subcutaneous fat
3 Fascia and muscle exposed
4 Bone visible
5 Large cavity through a small sinus
Source: Adapted from Bergman SB, Yarkony GM, Stiens SA. Spinal cord injury rehabilitation: Medical Complications. Arch Phys Med Rehabil. 1997;78:553.

National Pressure Ulcer Advisory Panel Classification

GRADE DESCRIPTION
I Nonblanchable erythema
II Partial skin loss of epidermis, dermis
III Full-thickness skin loss
IV Damage through fascia, muscle, or bone
Source: Adapted from Yarkony GM. Pressure ulcers: Classification and overview. In: Betz RR, Mulcahey MJ. eds. The Child with a Spinal Cord Injury. Rosemont, IL: American Academy of Orthopedic Surgeons, 1996.

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the level of injury, with increased vagal tone and bra­dycardia.

Symptoms of AD include pounding headache, sweating above the level of the lesion, red splotches on the face and neck, and nasal congestion. Bradycardia may be present. Inciting factors are bladder and bowel distention and rapid change in position from sitting to supine. Urinary tract infection, renal or bladder stones, and suppository or enema insertion may also be incit­ing factors. AD can present as an acute emergency, more commonly in older adults than in children, who are better able to withstand extreme hypertension.

Treatment of AD consists of relief of inciting factors. The child is immediately placed in the sitting position, and the bladder is emptied. The child should be exam­ined for other potential noxious stimuli, such as tight clothing or pressure sores. Most episodes of AD resolve with these treatments. If a rectal examination must be done, this may exacerbate the AD and should be done with the use of local anesthetic on the glove. If AD per­sists, nifedipine should be administered sublingually. An older treatment is nitroglycerine paste, which can be wiped off the skin, terminating its action once the hypertension resolves. Prevention of AD consists of effective bowel and bladder management programs.

Wheelchair tetraplegic athletes have been known to induce AD (“boosting”) to improve their ath­letic performance. Performance is improved by the increased sympathetic tone, shunting blood away from the viscera, thus improving cardiac output. AD can be induced by maintaining a full bladder or using a noxious stimulus (eg, a tack) below the level of injury. Boosting is dangerous, and thus is banned in wheel­chair athletics.

Hypercalcemia

As discussed previously, hypercalcemia is most likely to occur in adolescent boys in the first two to three months after SCI. Serum calcium should be routinely followed throughout the rehabilitation inpatient course, and treatment with fluids, furosemide, and calcitonin, as described previously, should be instituted.

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Source: Alexander M.A., Matthews D.J.. Pediatric Rehabilitation: Principles and Practice. 4 th. åd. — New York: Demos Medical Publishing,2010. — 540 ð.. 2010
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