Rapid Correction of Severe Hyponatremia After Computed Tomography With Intravenous Contrast

Abstract

To the Editor: Overly rapid correction of hyponatremia is a major concern in severely hyponatremic patients because of the potential development of osmotic demyelination. Numerous factors can contribute to overly rapid correction of hyponatremia (Table 1).1Pham P-CT Pham P-MT Miller J et al.Treatment of chronic hyponatremia.Proc UCLA Healthcare. Fall 2002; 6: 32-36Google Scholar We report a case in which a patient developed osmotic diuresis after contrast dye injection that rapidly self-corrected the severe hyponatremia.TABLE 1Potential Causes of Overly Rapid Correction of HyponatremiaAdapted from Proceedings of UCLA HealthCare,1Pham P-CT Pham P-MT Miller J et al.Treatment of chronic hyponatremia.Proc UCLA Healthcare. Fall 2002; 6: 32-36Google Scholar with permission. Unawareness of the recommended rate of correction for hyponatremiaMiscalculationsUnrecognized sources of sodium Exogenous Sodium administration at another site before transfer to the current unitAddition of excess salt to patient's diet by patient's family or facility staff membersEndogenous Potassium supplementation with resultant extracellular sodium shiftExcess free water loss Water deprivation in primary polydipsiaWithdrawal of thiazide diuretics during treatment of hyponatremiaGlucocorticoid replacement in a cortisol-deficient patientRecovery from acute respiratory failureExcessive gastrointestinal, pulmonary, or skin hypotonic fluid lossSevere hyponatremia with subsequent cerebral edema and pituitary infarctionNonelectrolyte osmotic diuresis: urea, glucose, mannitol, contrast dye, total parenteral nutritionIntracellular free water shift SeizuresRhabdomyolysisCorrection of hyperglycemiaPotassium supplementation Open table in a new tab Report of a Case. A 59-year-old woman with diabetes mellitus and hypertension presented with a 1-week history of slow mentation, fatigue, nausea, vomiting, abdominal pain, and subjective left hemiparesthesia. A dietary history revealed that she routinely ate only fruits and cereals and drank only water. Her medications included hydrochlorothiazide, fosinopril, atenolol, metformin, and aspirin. Physical examination revealed dry oral mucosa, slow mentation, and generalized sluggish deep tendon reflexes. On initial evaluation, the serum sodium concentration was 115 mEq/L, and urinary studies revealed an osmolality of 526 mosm/kg, a sodium level of 130 mEq/L, and a chloride level of less than 10 mEq/L. The patient was given two 500-mL boluses of normal saline during the first 12 hours of hospitalization. In the interim, she underwentcomputed tomography of the head and abdomen with intravenous contrast (iohexol). Despite correction of the hypovolemia, the patient had no improvement in her symptoms or serum sodium concentration during the first 24 hours. However, approximately 24 to 26 hours after presentation, she developed progressive polyuria (up to 150-175 mL/h). During the polyuric phase, the urine osmolality ranged from 217 to 393 mosm/kg. During the subsequent few hours, the patient's mentation noticeably improved in association with a spontaneous rapid increase in serum sodium concentration (8 mEq/L over 6 hours). In fact, hypotonic saline had to be administered to halt the rapid self-correction of the hyponatremia. Given the patient's history of poor dietary nutrition, use of hydrochlorothiazide, and current pain and vomiting, we suspected that the hyponatremia resulted from ongoing water intake concurrent with the patient's inability to excrete free water maximally because of a reduced dietary solute load and syndrome of inappropriate secretion of antidiuretic hormone-induced enhanced free water reabsorption.2Fichman MP Vorherr H Kleeman CR Telfer N Diuretic-induced hyponatremia.Ann Intern Med. 1971; 75: 853-863Crossref PubMed Scopus (239) Google Scholar, 3Thaler SM Teitelbaum I Berl T “Beer potomania” in non-beer drinkers: effect of low dietary solute intake.Am J Kidney Dis. 1998; 31: 1028-1031Abstract Full Text Full Text PDF PubMed Scopus (89) Google Scholar Despite saline infusion, the patient's serum sodium concentration remained at 115 mEq/L 12 to 18 hours after presentation, presumably a reflection of the sustained syndrome of inappropriate secretion of antidiuretic hormone caused by her nausea and pain. However, by 24 hours after presentation, the patient had a rapid increase in urinary output as well as serum sodium concentration despite the discontinuation of all intravenous fluids at least 6 hours previously. At that point, the patient possibly had adequate volume reexpansion, reduced proximal tubular reabsorption of salt and water, and resultant increased distal delivery for excretion. In addition, the control of nausea and pain and the volume reexpansion may have inhibited antidiuretic hormone secretion sufficiently to result in the aquaretic phase. However, subsequent urinary electrolyte studies revealed high osmolality (217-393 mosm/kg) relative to serum osmolality (240-264 mosm/kg), which suggested that she had osmotic diuresis, not aquaresis. Further analysis of her urine by ultraviolet spectrophotometry revealed that the predominant source of the urine osmolality during the polyuric phase was the contrast dye iohexol. The findings in this case are important because computed tomography with intravenous contrast is performed routinely for the evaluation of nonspecific complaints in severely hyponatremic patients.