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ODP071 A Fit of Hypophosphatemia

BACKGROUND: Hypophosphatemia is a commonly encountered electrolyte disturbance that is seen in association with a broad range of disorders. Severe hypophosphatemia can be life threatening and is known to cause seizures. Clinical case: A 65 year old female was found down at home by emergency medical...

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Detalles Bibliográficos
Autores principales: Naha, Sowjanya, Salam, Waqar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9624803/
http://dx.doi.org/10.1210/jendso/bvac150.318
Descripción
Sumario:BACKGROUND: Hypophosphatemia is a commonly encountered electrolyte disturbance that is seen in association with a broad range of disorders. Severe hypophosphatemia can be life threatening and is known to cause seizures. Clinical case: A 65 year old female was found down at home by emergency medical services. She was noted to be frothing and had irregular breathing. She was still confused when she was brought to the emergency department but had no focal neurological deficits on examination. Her mentation subsequently improved without intervention. Her past history was notable for a left parafalcine meningioma which was resected in 2019. Her vital signs were stable at presentation. Laboratory evaluation showed critically low phosphate (0.6 mg/dL, n: 2.5-4.5 mg/dL); other electrolytes including sodium, potassium, calcium and magnesium levels were all normal. Additional work up showed slightly elevated parathyroid hormone level (86.8 pg/mL, n: 15-65 pg/mL), borderline low vitamin D (29.5 ng/mL, n: 30-80 ng/mL) and elevated lactate (2.9 mmol/L, n: 0.5-2.2 mmol/L). The patient was immediately treated with 45 mmol of IV sodium phosphate. Repeat serum phosphate showed rapid normalization and the patient was ultimately discharged without any phosphate supplements. Repeat serum phosphate three months later was normal. CONCLUSION: Although severe hypophosphatemia is known to precipitate seizures, seizure activity itself can induce transient hypophosphatemia. In fact, hypophosphatemia has been proposed as a means to diagnose convulsive seizures and distinguish them from syncopal episodes. Transcellular shift has been proposed as a mechanism to explain this phenomenon. In this case, we believe the patient developed seizures as a sequela of brain surgery and that hypophosphatemia developed as an epiphenomenon. Rapid resolution of hypophosphatemia after cessation of seizures and absence of a credible alternative cause should alert physicians to the possibility of this effect. Presentation: No date and time listed