Kernicterus in an Adult Dog
AbstractBackground: Kernicterus or bilirubin encephalopathy is a condition rarely observed in animal characterized by a yellowish discoloration of the central nervous system. It is a potentially fatal condition due to bilirubin neurotoxic effects caused by the increase of non-conjugated bilirubin pigment, which passes blood brain barrier and has been attributed to an imbalance between albumin and bilirubin levels. Intracellular bilirubin is toxic for cells and can cause decrease in protein synthesis, specially albumin, depression of cell respiration and cellular death. This paper describes kernicterus in a 2-year-old Great Dane female dog.
Case: Clinically, the animal showed apathy, lethargy, weight loss and jaundice, which progressed to vomiting and neurological signs characterized by loss of consciousness and eventually coma. Blood parameters were within normal range, except for high levels of alanine aminotransferase (523 U/L), suggesting a liver lesion. The animal was submitted to euthanasia due to the poor prognosis, and at post-mortem examination it showed dehydration and severe jaundice, especially oral, vaginal and ocular mucosas, subcutaneous tissue and blood vessels intima surface. The liver had an accentuated lobular pattern, and the stomach mucosa was reddened. Multiple petechiae were observed in the epicardium, as well as icterus in the blood vessels of the heart. Furthermore, the brain and cerebellum cortex, thalamic region and nuclei region of brainstem
showed extensive icteric areas. Microscopically, the liver presented a mononuclear portal hepatitis, centrilobular necrosis and presence of yellowish pigments. The brain had neuronal necrosis, mild vacuolization of the white matter, perineuronal edema and Alzheimer type II astrocytes, while cerebellum showed Purkinje cells necrosis. Hepatic cooper measurement was within range values, and direct imunofluorescence for the detection of Leptospira sp. was negative.
Discussion: Kernicterus pathogenesis has been extensively studied, as the condition is commonly seen in neonatal humans. Diagnosis is based on gross and microscopic lesions in brain, which are consistent with bilirubin encephalopathy caused by the necrosis and degeneration of neurons. This condition is related to cases of intense hyperbilirubinemia, which exceeds
the albumin binding capacity and, therefore, the excess of unconjugated bilirubin that can pass through the blood brain barrier. Liver disease causes deficient production of protein, especially albumin, decreasing the potential binding capacity to bilirubin, and consequently causing hyperbilirubinemia. In this case, the previously detected hepatic lesion suggested by liver enzymes increased, probably led to protein production dysfunction, causing hypoalbuminemia and hyperbilirubinemia. Unfortunately, albumin and bilirubin seric levels could not be measured. Decrease in albumin production along with the excess of unconjugated bilirubin caused the jaundice, and in cases like this one described, the blood brain barrier
is compromised and the kernicterus occurs. Unconjugated bilirubin has negative effect in the glutamate uptake causing extracellular accumulation of it, which is consequently neurotoxic, causing necrosis and degeneration leading to a characteristic encephalopathy in animals with kernicterus. In this report, it was not possible to determine the primary hepatic disease, however this caused clinical neurotoxic disease, known as bilirubin encephalopathy.
Keywords: kernicterus, icterus, dog.
Ahlfors C. & Herbsman O. 2003. Unbound bilirubin in a term newborn with kernicterus. Pediatrics. 111: 1110-1112.
Dennery P.A., Seidman D.S. & Stevenson D.K. 2001. Neonatal hyperbilirubinemia. The New England Journal of Medicine. 344: 581-590.
Govaert P., Lequin M., Swarte R., Robben S., De Coo R., Weisglas-kuperus N., De Rijke Y., Sinaasappel M. & Barkovich J. 2003. Change in globus pallidus with (pre) term kernicterus. Pediatrics. 112: 1256-1263.
Hanko E., Hansen T.W., ALmaas R, Lindstad J. & Rootwelt T. 2005. Bilirubin induces apoptosis and necrosis in human NT2-N neurons. Pediatric Research. 57: 179-184.
Kumar V., Abbas A.K. & Fausto N. 2005. Robbins and Cotran Pathologic Basis of Disease.7th edn. Philadelphia: Elsevier Saunders, 1525p.
Loynachan A.T., Williams N.M. & Freestone J.F. 2007. Kernicterus in neonatal foal. Journal of Veterinary Diagnostic Investigation. 19: 209-212.
Ribeiro A.J.V., Batigália V.A., Kronka F.C. & Rodriguez A.L.A.A.S. 2004. Kernicterus: relato de caso – breve revisão de literatura. Arquivos de Ciências da Saúde. 11: 55-58.
Rubin E. & Killeen A.A. 2005. Doenças Genéticas e do Desenvolvimento. In: Rubin E., Gorstein F., Rubin R., Schwarting R. & Strayer D. Rubin Patologia: Bases Clínicopatológicas da Medicina. 4.ed. Rio de Janeiro: Guanabara Koogan, pp.223-286.
Sangster C.R., Stevenson C.K., Kidney B.A., Montgomery D.L. & Allen A.L. 2007. Kernicterus in an adult dog. Veterinary Pathology. 44: 383-385.
How to Cite
This journal provides open access to all of its content on the principle that making research freely available to the public supports a greater global exchange of knowledge. Such access is associated with increased readership and increased citation of an author's work. For more information on this approach, see the Public Knowledge Project and Directory of Open Access Journals.
We define open access journals as journals that use a funding model that does not charge readers or their institutions for access. From the BOAI definition of "open access" we take the right of users to "read, download, copy, distribute, print, search, or link to the full texts of these articles" as mandatory for a journal to be included in the directory.
La Red y Portal Iberoamericano de Revistas Científicas de Veterinaria de Libre Acceso reúne a las principales publicaciones científicas editadas en España, Portugal, Latino América y otros países del ámbito latino