Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management
Background: Primary hypoadrenocorticism is a rare condition resulting from immune-mediated destruction of the adrenal cortices. It can also occur due to necrosis, neoplasms, infarctions, and granulomas. The clinical and laboratory changes are due to deficient secretion of glucocorticoids and mineral...
| Autores: | , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2021 |
| País: | Brasil |
| Institución: | Universidade Federal do Rio Grande do Sul (UFRGS) |
| Repositorio: | Repositório Institucional da UFRGS |
| Idioma: | inglés |
| OAI Identifier: | oai:www.lume.ufrgs.br:10183/231314 |
| Acceso en línea: | http://hdl.handle.net/10183/231314 |
| Access Level: | acceso abierto |
| Palabra clave: | Hipoadrenocorticismo primário Hiponatremia Mielinólise central da ponte Imageamento por ressonância magnética Cães Terminologia Addison Syndrome Hyponatremia Osmotic myelinolysis Magnetic resonance imaging |
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oai:www.lume.ufrgs.br:10183/231314 |
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BR |
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Brasil |
| title |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management |
| spellingShingle |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management Pöppl, Alan Gomes Hipoadrenocorticismo primário Hiponatremia Mielinólise central da ponte Imageamento por ressonância magnética Cães Terminologia Addison Syndrome Hyponatremia Osmotic myelinolysis Magnetic resonance imaging |
| title_short |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management |
| title_full |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management |
| title_fullStr |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management |
| title_full_unstemmed |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management |
| title_sort |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management |
| author |
Pöppl, Alan Gomes |
| author_facet |
Pöppl, Alan Gomes Pires, Érico Haas Barbieri, Claudia Ruga Colomé, Lucas Marques |
| author_role |
author |
| author2 |
Pires, Érico Haas Barbieri, Claudia Ruga Colomé, Lucas Marques |
| author2_role |
author author author |
| topic |
Hipoadrenocorticismo primário Hiponatremia Mielinólise central da ponte Imageamento por ressonância magnética Cães Terminologia Addison Syndrome Hyponatremia Osmotic myelinolysis Magnetic resonance imaging |
| topic_facet |
Hipoadrenocorticismo primário Hiponatremia Mielinólise central da ponte Imageamento por ressonância magnética Cães Terminologia Addison Syndrome Hyponatremia Osmotic myelinolysis Magnetic resonance imaging |
| description |
Background: Primary hypoadrenocorticism is a rare condition resulting from immune-mediated destruction of the adrenal cortices. It can also occur due to necrosis, neoplasms, infarctions, and granulomas. The clinical and laboratory changes are due to deficient secretion of glucocorticoids and mineralocorticoids, which leads to electrolyte disorders associated with hyponatremia and hyperkalemia. These disorders can cause hypotension, hypovolemia and shock, putting a patient’s life at risk if inadequate hydroelectrolytic supplementation and hormone replacement is provided. Nevertheless, rapid sodium chloride supplementation is contraindicated due to the risk of central pontine myelinolysis induction. The present study aims to describe a thalamic osmotic demyelination syndrome after management of a primary hypoadrenocorticism crisis in a 2-year-old, female West White Highland Terrier. Case: The patient had a presumptive diagnosis of hypoadrenocorticism already receiving oral prednisolone and gastrointestinal protectants in the last 2 days. After prednisolone dose reduction the dog presented a severe primary hypoadrenocorticism crisis treated with intravenous sodium chloride 0.9% solution along with supportive therapy. Four days after being discharged from the hospital, the patient showed severe neurological impairment and went back to the clinic where a neurological examination revealed mental depression, drowsiness, ambulatory tetraparesis and proprioceptive deficit of the 4 limbs, postural deficits, and cranial nerves with decreased response. Due to these clinical signs, a magnetic resonance imaging was performed. It showed 2 intra-axial circular lesions, symmetrically distributed in both thalamus sides, with approximately 0.8 cm in diameter each without any other anatomical changes on magnetic resonance imaging. The images were compatible with metabolic lesions, suggesting demyelination. Furthermore, liquor analysis did not show relevant abnormalities, except for a slight increase in density and pH at the upper limit of the reference range. After treatment, the patient had a good neurological evolution secondary to standard primary hypoadrenocorticism treatment, without sequelae. Discussion: In the present case report, primary hypoadrenocorticism gastrointestinal signs seemed to be triggered by a food indiscretion episode, not responsive to the symptomatic therapies employed. The patient´s breed and age (young West White Highland Terrier bitch) is in accordance with the demographic profile of patients affected by the disease, where young females are frequently more affected. Regarding the probable thalamic osmotic demyelination syndrome documented in this case, is important to notice that myelinolysis or demyelination is an exceedingly rare noninflammatory neurological disorder, initially called central pontine myelinolysis, which can occur after rapid correction of hyponatremia. It has already been observed in dogs after correction of hyponatremia of different origins, including hypoadrenocorticism and parasitic gastrointestinal disorders. Currently, the terms “osmotic myelinolysis” or “osmotic demyelination syndrome” are considered more suitable when compared to the term “central pontine myelinolysis” since it has been demonstrated in dogs and humans the occurrence of demyelination secondary to the rapid correction of hyponatremia in distinct regions of the central nervous system including pons, basal nuclei, striatum, thalamus, cortex, hypoppocampus, and cerebelum. The present case report emphasizes the difficulties for hormonal confirmation of primary hypoadrenocorticism in a patient already on corticosteroid treatment, as well as proposes that the current term osmotic demyelination syndrome replace the term “central pontine myelinolysis” in veterinary literature related to the management of hypoadrenocorticism crisis. |
| publishDate |
2021 |
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article |
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publishedVersion |
| url |
http://hdl.handle.net/10183/231314 |
| language |
eng |
| eu_rights_str_mv |
openAccess |
| institution |
UFRGS |
| collection |
Repositório Institucional da UFRGS |
| reponame_str |
Repositório Institucional da UFRGS |
| instname_str |
Universidade Federal do Rio Grande do Sul (UFRGS) |
| bitstream_url_str_mv |
http://www.lume.ufrgs.br/bitstream/10183/231314/2/001132035.pdf.txt http://www.lume.ufrgs.br/bitstream/10183/231314/1/001132035.pdf |
| spelling |
Osmotic demyelination syndrome after primary hypoadrenocorticism crisis management Pöppl, Alan Gomes Pires, Érico Haas Barbieri, Claudia Ruga Colomé, Lucas Marques Hipoadrenocorticismo primário Hiponatremia Mielinólise central da ponte Imageamento por ressonância magnética Cães Terminologia Addison Syndrome Hyponatremia Osmotic myelinolysis Magnetic resonance imaging Background: Primary hypoadrenocorticism is a rare condition resulting from immune-mediated destruction of the adrenal cortices. It can also occur due to necrosis, neoplasms, infarctions, and granulomas. The clinical and laboratory changes are due to deficient secretion of glucocorticoids and mineralocorticoids, which leads to electrolyte disorders associated with hyponatremia and hyperkalemia. These disorders can cause hypotension, hypovolemia and shock, putting a patient’s life at risk if inadequate hydroelectrolytic supplementation and hormone replacement is provided. Nevertheless, rapid sodium chloride supplementation is contraindicated due to the risk of central pontine myelinolysis induction. The present study aims to describe a thalamic osmotic demyelination syndrome after management of a primary hypoadrenocorticism crisis in a 2-year-old, female West White Highland Terrier. Case: The patient had a presumptive diagnosis of hypoadrenocorticism already receiving oral prednisolone and gastrointestinal protectants in the last 2 days. After prednisolone dose reduction the dog presented a severe primary hypoadrenocorticism crisis treated with intravenous sodium chloride 0.9% solution along with supportive therapy. Four days after being discharged from the hospital, the patient showed severe neurological impairment and went back to the clinic where a neurological examination revealed mental depression, drowsiness, ambulatory tetraparesis and proprioceptive deficit of the 4 limbs, postural deficits, and cranial nerves with decreased response. Due to these clinical signs, a magnetic resonance imaging was performed. It showed 2 intra-axial circular lesions, symmetrically distributed in both thalamus sides, with approximately 0.8 cm in diameter each without any other anatomical changes on magnetic resonance imaging. The images were compatible with metabolic lesions, suggesting demyelination. Furthermore, liquor analysis did not show relevant abnormalities, except for a slight increase in density and pH at the upper limit of the reference range. After treatment, the patient had a good neurological evolution secondary to standard primary hypoadrenocorticism treatment, without sequelae. Discussion: In the present case report, primary hypoadrenocorticism gastrointestinal signs seemed to be triggered by a food indiscretion episode, not responsive to the symptomatic therapies employed. The patient´s breed and age (young West White Highland Terrier bitch) is in accordance with the demographic profile of patients affected by the disease, where young females are frequently more affected. Regarding the probable thalamic osmotic demyelination syndrome documented in this case, is important to notice that myelinolysis or demyelination is an exceedingly rare noninflammatory neurological disorder, initially called central pontine myelinolysis, which can occur after rapid correction of hyponatremia. It has already been observed in dogs after correction of hyponatremia of different origins, including hypoadrenocorticism and parasitic gastrointestinal disorders. Currently, the terms “osmotic myelinolysis” or “osmotic demyelination syndrome” are considered more suitable when compared to the term “central pontine myelinolysis” since it has been demonstrated in dogs and humans the occurrence of demyelination secondary to the rapid correction of hyponatremia in distinct regions of the central nervous system including pons, basal nuclei, striatum, thalamus, cortex, hypoppocampus, and cerebelum. The present case report emphasizes the difficulties for hormonal confirmation of primary hypoadrenocorticism in a patient already on corticosteroid treatment, as well as proposes that the current term osmotic demyelination syndrome replace the term “central pontine myelinolysis” in veterinary literature related to the management of hypoadrenocorticism crisis. 1678-0345 http://hdl.handle.net/10183/231314 001132035 |
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1878427871644483585 |
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2021 |
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Barbieri, Claudia Ruga Colomé, Lucas Marques Pires, Érico Haas Pöppl, Alan Gomes |
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6,9303427 |