Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • Some patients developed osmotic demyelination disease ODS

    2019-05-07

    Some patients developed osmotic demyelination disease (ODS) after rapid correction of hyponatremia. Predisposing factors to development of ODS were syndrome of inappropriate antidiuretic hormone, alcoholism, liver cirrhosis, liver transplantation, renal failure, burns, malnutrition, or neoplasm. Other associated diagnoses include electrolyte imbalances (hypophosphatemia, hypokalemia, and hyponatremia), renal failure, dialysis, hepatitis, hyperemesis (hyperemesis gravidarum, anorexia nervosa or bulimia, and pharmacologic side effects), diabetes mellitus, leukemia, lymphoma, Wilson disease, sudden disruption of desmopressin treatment in diabetes insipidus patient, and pituitary surgery, a situation where SIADH may be a transient and resolved suddenly. One research conducted in the intensive care unit found that the most common associated factor was hypokalemia which is defined as serum potassium level of ≦ 1.5 mEq/L (41%), followed by chronic alcoholism, prolonged diuretic therapy, and postoperative fluid therapy (each about 30% of the cases). Our patient was admitted with mild dehydration and multiple electrolyte disorders, especially severe hyponatremia mainly due to malnutrition, resulting from preexisting xerostomia with severe stomatitis after radiation therapy. This posed a serious threat to various complications of electrolyte imbalances and risk of too rapid correction of serum sodium level, consequently CPM developed in our patient. Other possible contributors of hyponatremia, including syndrome of inappropriate antidiuretic hormone (SIADH), secretion as paraneoplastic syndrome of nasopharyngeal tumor or CCRT related SIADH should be ruled out. However, the effort to properly diagnose SIADH requiring measurement of urine, ampk inhibitor osmolality and urine sodium at a minimum was lacking in this case. The full diagnostic criteria should also include normal thyroid and adrenal functions. There is one case report which is the first report of pathological confirmation of the SIADH in nasopharyngeal carcinoma by molecular and immunologic studies. It shows that ectopic secretion of vasopressin by the primary NPC tumor appears to be the mechanism of paraneoplastic syndrome. One author proposed that SIADH following chemoradiotherapy for squamous cell carcinoma of head and neck might be produced by the release of vasopressin after rapid tumor cells lysis due to cytotoxic agents. Wenig and Heller offered different pathophysiologic explanation, where six cases of SIADH received radical neck dissection for cervical metastasis of head and neck cancer, with 5 of them also receiving radiotherapy. They suggested that SIADH resulted indirectly from increased intracranial pressure due to impaired venous return. Our patient experienced hyponatremia one week after her first regimen of induction chemotherapy without malnutrition status at that time. We highly suspect both episodes of hyponatremia in this patient were possibly due to SIADH following chemotherapy, although no laboratory support of SIADH was made. There are reports of therapeutic interventions to prevent ODS after rapid correction of hyponatremia: reinduction of hyponatremia, administration of myo-inositol, urea, or minocycline (by inhibiting the activation of microglia). Isolated case reports suggest the role of steroids, plasmapharesis, and imidazolepyridine tartrate in treatment of CPM. Aggresive supportive therapy should be provided for managing complications of neurological deficit resulting from CPM. Anyhow, prevention is better than cure. Verifying the chronicity of hyponatremia (acute defined as a duration of <48 h while chronic defined as a duration of ≥48 h) is much more crucial than severity of hyponatremia before initiating sodium correction as to avoid the rapidity of sodium rise which may end up with osmotic demyelinating syndrome. Among the published recommendations, there was no consensus about the optimal treatment for symptomatic hyponatremia. However, blood sodium rise not exceeding 8–12 mmol/L/day is considered safe and widely accepted. Hence, frequent monitoring of serum sodium is needed to ensure a graded correction of hyponatremia.