Newsletter, 2003 Vol. 9. Issue 4

CORTICOSTEROIDS, NEUROLOGICAL DISEASE AND COLONC PERFORATION

A 5.25 kg, 5 year old male (neutered) Dachshund-mix presented to the Veterinary Surgical Referral Center for hindlimb paralysis on 8/26/03. He had presented to the referring veterinarian 3 days earlier for lethargy, "not acting like himself, and difficulty using the left rear leg. He had a serum chemistry profile and CBC done, with all results normal. Deramaxx and Glycoflex were prescribed. On 8/25 he was rechecked and was losing hindlimb motor control. He was given SoluDeltaCortef i.v. 100 mg initially as a bolus and again 5 hours later. He was sent for a surgical consult the next day.

On presentation here, there was hindlimb paralysis with no voluntary motor movement to the rear limbs. Reflexes were UMN in nature and deep pain sensation was intact. After initial evaluation and consultation with the owner, he was admitted for a myelogram and possible surgical decompression of a suspected thoracolumbar disc herniation. Preoperatively, he was given 12 mg Dexasone SP i.v. The myelogram showed a lesion at the level of T12-13, compatible with a ruptured disc. The dog was taken to surgery where a left sided hemilaminectomy was done to decompress his spinal cord. A ruptured disc was identified and removed. Postoperatively, he was placed on a continuous drip of intravenous fluids with the addition of SoluDeltaCortef at a rate of 1mg/lb/hr for 24 hours. He was hospitalized for 2 days then returned to the referring veterinarian's office on 8/28/03. On 9/2/03 the dog began vomiting acutely that afternoon. Later that night he was brought in to the local emergency clinic, dead on arrival. A necropsy was subsequently done at OSU and a perforating ulcer found in the colon wall, just caudal to the cecum.

Colonic perforation is a rare, but well described complication that seems to be compounded by the combined use of corticosteroids and concurrent neurologic disease. It is uniformly fatal. In the case above, the prior use of a non-steroidal anti-inflammatory drug (Deramaxx) may have contributed to the colonic perforation.

In reviewing the literature, the following findings are reported by Toombs, et. al.

1) nonambulatory neurosurgical patients treated with dexamethasone, especially males, appear to be at the greatest risk for development of colonic perforation; 2) colonic perforation is preceded or attended by variable nonspecific signs -most frequently depression, anorexia, and emesis; 3) the complication is associated with a 100% mortality and clinical signs precede death by an average of 24 hours; 4) antemortem diagnosis and treatment of the complication are difficult and appear to have no effect in reducing mortality; and 5) a prophylactic approach to gastrointestinal complications is warranted in high-risk patients - (a) use prednisone instead of dexamethasone; (b) limit treatment with corticosteroids to as short a time as possible; (c) avoid successive or concurrent use of multiple drugs with known ulcerogenic potential; (d) correct fecal retention problems before surgery; (e) avoid enemas during the first week after surgery; and (f) manage urine retention by continuous bladder decompression (closed urine drainage system) rather than repeated manual expression of the bladder.

This case is presented as a cautionary example of a fatal complication associated with treatment of a herniated disc. Dexamethasone was used in this instance as there was a manufacturer's back order on SoluMedrol, our preferred drug in acute spinal injury. The use of Deramaxx may or may not have been a contributing factor. Prolonged use of steroids in spinal cord injury should be avoided, especially dexamethasone.