Transient Thalamic Changes on MRI in a Child With Hypernatremia Dawn S. Hartfield, MD*, John A. Loewy, MD ² , and Jerome Y. Yager, MD* Severe hypernatremia has been associated with a wide variety of central nervous system lesions. Neurologic sequelae are the usual outcome in those cases in which a lesion has been documented neuroradiologically. The authors report a 7-month-old male with severe hyper- natremia who developed obtundation after correction of the electrolyte imbalance. Magnetic resonance im- aging revealed bilateral thalamic signal changes that resolved on follow-up study, in accordance with com- plete clinical recovery. To the authors’ knowledge, bilateral thalamic signal changes are previously unre- ported findings associated with hypernatremia. Perti- nent literature and the clinical course of the authors’ patient are the basis for questioning currently recom- mended guidelines for the rate of correction of hyper- natremia. © 1999 by Elsevier Science Inc. All rights reserved. Hartfield DS, Loewy JA, Yager JY. Transient thalmic changes on magnetic resonance imaging in a child with hypernatremia. Pediatr Neurol 1999;20:60-62. Introduction Severe hypernatremia has been associated with a wide variety of central nervous system lesions, the pathogenesis of which may differ depending on the chronicity of the illness and rapidity of treatment [1-6]. Neurologic se- quelae are the usual outcome in those cases in which a lesion has been documented neuroradiologically. The authors report a 7-month-old male with severe hypernatre- mia secondary to dehydration who, on magnetic resonance imaging (MRI) had bilateral thalamic signal changes that had resolved on the follow-up study. To the authors’ knowledge, bilateral thalamic signal changes are previ- ously unreported findings associated with hypernatremia. Pertinent literature and the clinical course of the authors’ patient are the basis for questioning currently recom- mended guidelines for the rate of correction of hypernatre- mia. Case Report The authors’ patient presented as a healthy 7-month-old aboriginal male with a 4-day history of vomiting and diarrhea. Despite being treated as an outpatient using oral rehydration with a balanced electrolyte solution, he continued to be febrile and vomit, and he developed anuria, prompting evaluation and admission to the Royal University Hospital, Saskatoon, Saskatchewan. Physical examination on arrival at the Emergency Department found the child to be lethargic and 10% dehydrated. His rectal temperature was 39.3°C, heart rate and respiratory rate were 169 beats and 56 breaths per minute, respectively, blood pressure was 106/64 mm Hg, and oxygen saturation was 98% by pulse oximetry. General physical examination was normal, revealing no focus of infection. Neurologically the child was lethargic, had spontaneous movements of all four limbs, with no evidence of a focal deficit, and responded appropriately to pain. Laboratory investigations revealed severe hypernatremia (Fig 1), with a serum sodium of 197 mmol/L. His serum creatinine was 80 mmol/L and urea 10.9 mmol/L, consistent with dehydration. He was also anemic (hemo- globin 86 g/dL), but had a normal white blood cell count and cerebro- spinal fluid examination. He was fluid resuscitated with isotonic saline and then transferred to a pediatric intensive care unit for further treatment. The hypernatremia was treated with peritoneal dialysis for 5 days. By the sixth day after admission, his serum sodium had declined to 144 mmol/L. Despite correction of the severe hypernatremia, on day 6 he deteriorated and became obtunded, responding only to deep painful stimuli with limb extension. He required intubation for airway protection. Examination was unremarkable for focal neurologic signs. Funduscopic examination was normal. An electroencephalogram (EEG) revealed diffuse slowing with no seizure activity. A computed tomography scan was normal. Gradually the child began to improve, demonstrating spontaneous movement by day 10 and appropriate withdrawal to painful stimuli by day 12. His serum sodium at that time was 135 mmol/L. MRI was performed on day 13 and demonstrated symmetric attenuation of both thalami on T 1 -weighted images (Fig 2A). On T 2 -weighted images the thalami were hyperintense, with slight inhomogeneity (Fig 2B). In addition, the thalami appeared symmetrically lobulated and bulky com- pared with normal. EEG performed at that time revealed increased activity compared with the previous EEG but no epileptiform discharges. On day 18 the child had an improved level of consciousness and a normal From the Departments of *Pediatrics and ² Radiology; University of Saskatchewan; College of Medicine; Saskatoon, Saskatchewan, Canada. Communications should be addressed to: Dr. Yager; Department of Pediatrics; Royal University Hospital; 103 Hospital Drive, Room 3717; Saskatoon, Saskatchewan S7N 0W8, Canada. Received February 26, 1998; accepted June 29, 1998. 60 PEDIATRIC NEUROLOGY Vol. 20 No. 1 © 1999 by Elsevier Science Inc. All rights reserved. PII S0887-8994(98)00092-7 ● 0887-8994/99/$20.00