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Abstract

Case Description—A 7-month-old male Siberian Husky affected by lower motor neuron tetraparesis was anesthetized for electrodiagnostic testing and collection of muscle and nerve biopsy specimens.

Clinical Findings—Preanesthetic physical examination revealed a high rectal temperature, and serum biochemical analysis revealed high muscle and liver enzyme activities. The dog was anesthetized twice. The dog was anesthetized with isoflurane and developed moderate hypercarbia and mild hyperthermia. Injectable anesthetic agents were used to anesthetize the dog the second time, during which the dog developed severe malignant hyperthermia. A genetic test performed after anesthesia did not reveal a mutation of the RYR1 gene, the gene that mediates calcium-release channels in skeletal muscle. On the basis of clinical features, and because other neuromuscular disorders were ruled out, a genetic channelopathy involving the skeletal muscle ion channels was suspected.

Treatment and Outcome—The dog was disconnected from the breathing system, and active cooling of the body was performed with ice packs applied to the body surface and alcohol applied to the foot pads. Cold crystalloid solutions were administered IV. Intermittent positive-pressure ventilation with 100% oxygen was performed to decrease end-tidal partial pressure of carbon dioxide. Because dantrolene was not available, acepromazine was administered to facilitate a decrease in body temperature. The dog recovered from malignant hyperthermia and was discharged to the owner after 13 days of hospitalization.

Clinical Relevance—Dogs affected by genetic muscle disorders should be considered at risk for perianesthetic malignant hyperthermia, even in the absence of an RYR1 gene mutation.

Abstract

Objective—To determine whether the composition of electrolyte pastes formulated for oral administration influences voluntary water intake (WI) by horses recovering from furosemide-induced dehydration.

Animals—6 horses.

Procedure—Voluntary WI, body weight, and blood and urine constituents were measured before and after induction of dehydration by furosemide administration and overnight withholding of water; these same variables also were measured during a 36-hour rehydration period. Each horse was evaluated 4 times with random application of 4 treatments (electrolyte pastes) that provided 0.5 g of KCl/kg of body weight, 0.5 g of NaCl/kg, 0.25 g of NaCl and 0.25 g of KCl/kg, or no electrolytes (control treatment). Electrolyte pastes were administered 3 times (4, 8, and 12 hours after start of the rehydration period).

Results—Administration of all electrolyte pastes resulted in significantly greater voluntarily WI, compared with the control treatment, and was accompanied by significantly greater recovery of body weight when NaCl was a component of the paste. Administration of NaCl and NaCl-KCl pastes tended to produce a state of transient hyperhydration; however, electrolyte administration also resulted in significantly greater urine production and electrolyte excretion during the final 24 hours of the rehydration period. Adverse effects of oral administration of hypertonic electrolyte pastes were not observed.

Conclusion and Clinical Relevance—Oral administration of electrolyte pastes to dehydrated horses increases voluntary WI and improves rehydration during the rehydration period. Rehydration is more rapid and complete when NaCl is a component of the electrolyte paste. (Am J Vet Res 2002;63:19–27)