
Diazepam as a Treatment for Metronidazole Toxicosis in Dogs: A Retrospective Study of 21 Cases
Author(s) -
Evans Jason,
Levesque Donald,
Knowles Kim,
Longshore Randy,
Plummer Scott
Publication year - 2003
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/j.1939-1676.2003.tb02452.x
Subject(s) - diazepam , metronidazole , medicine , discontinuation , anesthesia , bolus (digestion) , antibiotics , microbiology and biotechnology , biology
The currently recommended treatment for metronidazole toxicosis is drug discontinuation and supportive therapy. Reported recovery times are 1–2 weeks. The records of 21 dogs with metronidazole toxicosis were retrospectively analyzed to determine whether diazepam improved recovery. The dosage and duration of metronidazole therapy and the response and recovery times of 13 dogs treated with diazepam were compared to those of 8 dogs receiving only supportive care. Response time was defined as the time to resolution of the debilitating clinical signs. Recovery time was the time to resolution of all residual clinical signs. The average dosage and duration of metronidazole administration for the diazepam‐treated and untreated groups were 60.3 mg/kg/d for 44.9 days and 65.1 mg/kg/d for 37.25 days. The protocol for diazepam administration consisted of an initial IV bolus and then diazepam PO q8h for 3 days. The average dosage of both the IV and PO diazepam was 0.43 mg/kg. The average response time for the diazepam‐treated dogs was 13.4 hours compared to 4.25 days for the untreated group. Recovery time also was markedly shorter for the diazepam‐treated dogs (38.8 hours) compared to the untreated group (11 days). Results of this study showed that dogs with metronidazole toxicosis recover faster when treated with diazepam. Although the mechanism of metronidazole toxicosis or how diazepam exerts its favorable effect is not known, it is likely related to modulation of the ‐y‐aminobutyric acid (GABA) receptor within the cerebellar and vestibular systems.