TRATAMENTO CLÍNICO DE TRAUMA CRANIOENCEFÁLICO EM GRAXAIM-DO-CAMPO (Lycalopex gymnocercus)

Autores

DOI:

https://doi.org/10.22456/1679-9216.136228

Palavras-chave:

Animais selvagens, Atropelamento, Lesão encefálica, TCE

Resumo

Background: The pampas fox (Lycalopex gymnocercus) is a wild canid that occurs in the state of Rio Grande do Sul, Brazil. Environmental changes have brought this animal into proximity with urbanized areas. Therefore, one of the greatest threats to the species is being run over, which is considered the main cause of traumatic brain injury (TBI). Data on the treatment of brain injuries in veterinary medicine, especially in wild animals, is still insufficient, so the guidelines applied here are based on human medicine and small animal medicine. The purpose of this paper is to report the clinical treatment used in a case of TBI in a pampas fox (L. gymnocercus).

Case: A 2.5 kg juvenile male pampas fox (L. gymnocercus) was admitted to a Wildlife Rehabilitation Center in Rio Grande do Sul. The patient presented with opisthotonos, in a stupor and a score of 10 on the Glasgow Coma Scale. The animal received clinical treatment, isotonic fluid therapy (lactated Ringer’s solution 50ml/kg/day), and later, hyperosmolar therapy (hypertonic 3%, 4ml/kg and mannitol 1g/kg), analgesia (dipyrone 25mg/kg and meloxicam 0.1mg/kg) and antibiotic therapy (sulfamethoxazole with trimethoprim 20mg/kg). Clinical follow-up included blood pressure monitoring and complementary tests such as radiography, ultrasound, blood count and biochemistry. The animal exhibited fractures of the parietal bone, microcytic hypochromic anemia and an increase in the enzymes ALT, AST and CK. Dexamethasone (0.15mg/kg) was introduced on the eighth day of treatment. This was followed by physiotherapy sessions aimed at encouraging the patient to remain in a standing position. After 55 days, the animal was returned to the wild.

Discussion: The Glasgow Coma Scale is used in order to standardize the assessment of the depth and duration of unconsciousness and coma in small animals with TBI, based on a similar table to the one used for humans. Motor activity, brainstem reflexes and levels of consciousness are assessed, generating a score. In this case, the patient scored 10, with a prognosis ranging from poor to guarded. After the occurrence of TBI, edema and hemorrhage add volume to the intracranial space, contributing to na increase in intracranial pressure (ICP). The purpose of TBI treatment is to maintain cerebral blood flow and prevent increases in ICP. To this end, 3% hypertonic fluid therapy was administered, which acts by extracting fluid from the intraparenchymal space into the vascular space, reducing intracranial oedema. By the third day of treatment, the patient had already overcome opisthotonus, but was unable to maintain a standing posture, so the 3% hypertonic solution was replaced by mannitol, which is an osmotic, hyperosmolar diuretic and also acts as a free radical eliminator, helping to improve the stability of the neuronal membrane and further inhibiting the development of cytotoxic edema. Dexamethasone was applied eight days after the animal’s arrival. The use of glucocorticoids is recommended as an adjuvant treatment in patients that do not respond adequately to the use of mannitol and that are not hyperglycemic. Their use can be beneficial in stabilizing plasma membranes in the CNS, increasing energy supply to CNS tissues, reducing edema, promoting diuresis, reducing the formation of free radicals in the CNS, and reducing the formation of cerebrospinal fluid (CSF). With the end of the drug treatment, the patient was able to remain in sternal decubitus, but still had difficulty standing and walking normally. Physiotherapy sessions were started, such as passive range of movement and stretching of the pelvic limbs, assisted support and exercises to stimulate proprioception by gently brushing the patient’s foot pads, which contributed to its improvement and consequently its return to nature.

Downloads

Não há dados estatísticos.

Referências

Adeodato A.G., Pedro Neto O. & Rabelo R.C. 2005. Traumatismo crânio-encefálico. In: Rabelo R.C. & Crowe D.T. Fundamentos da Terapêutica Intensiva Veterinária em Pequenos Animais. Rio de Janeiro: L.F. Livros, pp.329-350.

Aguiar E.S.V. 2011. Trauma cranioencefálico. In: Emergências decorrentes do trauma em pequenos animais. Porto Alegre: Editora da UFRGS, pp.223-239.

Andrade Neto J.P. 2015. Trauma cranioencefálico. In: Jericó M.M., Andrade Neto J.P. & Kogika M.M. (Eds). Tratado de Medicina Interna de Cães e Gatos. 2.ed. Rio de Janeiro: Roca, pp.2107-2113.

Dewey C.W. & Fletcher D.J. 2016. Head-Trauma Management. In: Dewey C.W. & Costa R.C. (Eds). Practical Guide to Canine and Feline Neurology. 3rd edn. Hoboken: Wiley-Blackwell, pp.237-248.

Heller H.B. 2018. Increased Intracranial Pressure Following Traumatic Brain Injury in Small Animal Patients. Advances in Small Animal Medicine and Surgery. 31(4): 1-2. DOI: https://doi.org/10.1016/j.asams.2018.04.001

Kaneko J.J., Harvey J.W. & Bruss M.L. 2008. Apêndice VII. In: Clinical biochemistry of domestic animals. 6th edn. San Diego: Academic press, pp.889-895.

Kasper C.B., Trinca C.S., Sanfelice D., Mazim F.D. & Trigo T.C. 2014. Os Carnívoros. In: Gonçalves G.L., Quintela F.M. & Freitas T.R.O. (Eds). Mamíferos do Rio Grande do Sul. Porto Alegre: Pacartes, pp.174-175.

McCourt M.R. & Rizzi T.E. 2022. Hematology of Dogs. In: Brooks M.M., Harr K.E., Seelig D.M., Wardrop K.J. & Weiss D.J. (Eds). Schalm’s Veterinary Hematology. 7th edn. Hoboken: Blackwell, pp.2774-2815.

Millis D.F.D.L. & Adamson C. 2008. Novas modalidades terapêuticas na reabilitação veterinária. In: Taylor R., Marcellin-Little D.J., Millis D.L. & Levine D. (Eds). Reabilitação e Fisioterapia na Prática de Pequenos Animais. São Paulo: Roca, pp.95-117.

Papich M.G. 2012. Manual Saunders de Terapia Veterinária: Pequenos e Grandes Animais. 3.ed. Rio de Janeiro: Elsevier, pp.677-678.

Sen Y., Baser M. I., Kurt B.K. & Bumin A. 2021. Novel ultrasonographic imaging technique in cat and dog intensive care patients: A-FAST3. Ankara Üniversitesi Veteriner Fakültesi Dergisi. 68(3): 311-320. DOI 10.33988/auvfd.909936 DOI: https://doi.org/10.33988/auvfd.909936

Stockham S.L. & Scott M.A. 2011. Enzimas. Fundamentos de Patologia Clínica Veterinária. Rio de Janeiro: Guanabara Koogan, pp.533-561.

Syring R.S., Otto C.M. & Drobatz K.J. 2001. Hyperglycemia in dogs and cats with head trauma: 122 cases (1997–1999). Journal of the American Veterinary Medical Association. 218(7): 1124-1129. DOI 10.2460/javma.2001.218.1124. DOI: https://doi.org/10.2460/javma.2001.218.1124

Tavares W. 2014. Drogas Antifólicas, Sulfonamidas, Sulfonas e Diaminopirimidinas. In: Antibióticos e Quimioterápicos para o Clínico. 3.ed. São Paulo: Editora Atheneu, pp.349-350.

Weber M.M., Roman C. & Cáceres N.C. 2013. Carnívoros continentais. In: Mamíferos do Rio Grande do Sul. Santa Maria: UFSM, pp.364-365.

Arquivos adicionais

Publicado

2024-06-18

Como Citar

Thurow Schulz, Érica, Aranha da Costa, E., Ramos, M. C., Santos Beanes, A., Chagas dos Passos, M., da Costa da Silva, L. C., … França, R. T. (2024). TRATAMENTO CLÍNICO DE TRAUMA CRANIOENCEFÁLICO EM GRAXAIM-DO-CAMPO (Lycalopex gymnocercus). Acta Scientiae Veterinariae, 52. https://doi.org/10.22456/1679-9216.136228

Edição

Seção

Case Report

Artigos Semelhantes

1 2 3 4 5 6 7 8 9 10 > >> 

Você também pode iniciar uma pesquisa avançada por similaridade para este artigo.