Lethal peracute rhabdomyolysis associated with stress and general anesthesia in three dystrophin-deficient cats

Citation
F. Gaschen et al., Lethal peracute rhabdomyolysis associated with stress and general anesthesia in three dystrophin-deficient cats, VET PATH, 35(2), 1998, pp. 117-123
Citations number
32
Categorie Soggetti
Veterinary Medicine/Animal Health","Medical Research Diagnosis & Treatment
Journal title
VETERINARY PATHOLOGY
ISSN journal
03009858 → ACNP
Volume
35
Issue
2
Year of publication
1998
Pages
117 - 123
Database
ISI
SICI code
0300-9858(199803)35:2<117:LPRAWS>2.0.ZU;2-2
Abstract
Three cats affected with dystrophin deficiency and hypertrophic muscular dy strophy developed peracute rhabdomyolysis with a fatal outcome. Two cats we re anesthetized with isoflurane for routine procedures and did not recover properly from the anesthetic procedure. One cat was manually restrained for an echographic examination and started staggering after a short struggle; its condition worsened, and it died. Blood chemistry findings included seve re hyperkalemia, hyperphosphatemia, hypocalcemia, massive increases in crea tine kinase, aspartate aminotransferase, and alanine aminotransferase conce ntrations, and high ion gap metabolic acidosis. Light microscopic evaluatio n of skeletal muscle revealed severe acute rhabdomyolysis with marked exten sive necrosis of large groups of fibers and endomysial edema. These lesions were observed in many skeletal muscles but particularly in the masseter an d supraspinatus muscles and in the diaphragm. Typical changes associated wi th dystrophin deficiency in cats were also noted. Histochemical analysis re vealed that the dystrophin deficiency was associated with a decrease in the percentage of type 1 myofibers in all three cats. This change was marked i n the 20-month-old cat and milder in the younger cats (6.5 and 8.5 months o f age). Percentages of type 2A fibers were markedly decreased and percentag es of type 2X fibers were markedly increased in the younger cats. Rhabdomyo lysis has been reported in dystrophinopathic humans but not in other animal models of dystrophin deficiency. An increased sensitivity of the dystrophi n-deficient sarcolemmal membrane to volatile anesthetic agents, stress, or intense muscular activity is suspected.