case_images: PMC9114638_01
case_images: Trend of serum sodium concentrations, urine sodium concentrations, and urine osmolality along with the interventions taken in Case 1 who presented with traumatic brain injury and later diagnosed with SIADH. The urine biochemistry was performed on urinary spot samples. The urine sodium concentrations were persistently raised >=130 mmol/L throughout the hospital stay except on day 21.
case_images: fmed-09-897940-g0001.jpg
case_images: PMC9114638_01_fmed-09-897940-g0001.jpg
case_images: F1
case_images: Urine sodium concentration was persistently high even after saline infusion drip was discontinued (Figure 1). Despite strict fluid restriction, his serum sodium continued to downtrend to 121 mmol/L (Figure 1).
case_images: PMC9114638_02
case_images: Trend of serum sodium concentrations, urine sodium concentrations, and urine osmolality with the interventions taken in Case 2 with recurrent SIADH. The current SIADH episode illustrated here was caused by dyspepsia from gastritis. His urine sodium concentration was elevated at 187 mmol/L initially and reduced as his hyponatremia due to SIADH improved. The urine biochemistry was performed on urinary spot samples.
case_images: fmed-09-897940-g0002.jpg
case_images: PMC9114638_02_fmed-09-897940-g0002.jpg
case_images: F2
case_images: This was associated with a rise in serum sodium level, a fall in urine sodium levels, and a rise in urine output, indicative of free water excretion (day 4 admission [D4], Figure 2), which led the serum sodium levels to rise rapidly from 115 mmol/L to 124 mmol/L in 24 h (D5, Figure 2). The ensuing rise in sodium was appropriate and corresponded with a gradual fall in urine sodium and osmolality levels (Figure 2).