CASE PRESENTATION: A 40-year-old woman presented with general weakness,
hypokalemia, and
metabolic acidosis. The patient was treated with oral and intravenous
potassium chloride, along with intravenous
sodium bicarbonate. Although her
bicarbonate deficit was 365 mEq, we treated her with an overdose of intravenous
sodium bicarbonate, 480 mEq for 24 hours, due to the severity of her acidemia and her altered mental status. The next day, she developed
hypernatremia with serum
sodium levels rising from 142.8 mEq/L to 172.8 mEq/L. Six days after developing
hypernatremia, she exhibited tetraparesis,
drooling, difficulty swallowing, and
dysarthria, and a brain MRI revealed high signal intensity in the central pons with sparing of the peripheral portion, suggesting CPM. We diagnosed her with CPM associated with the rapid development of
hypernatremia after intravenous
sodium bicarbonate therapy and treated her with
plasma exchange. After two consecutive
plasma exchange sessions, her
neurologic symptoms were markedly improved except for mild
diplopia. After the
plasma exchange sessions, we examined the patient to determine the reason for her symptoms upon presentation to the hospital. She had normal anion gap
metabolic acidosis, low blood
bicarbonate levels, a urine pH of 6.5, and a calyceal stone in her left kidney. We performed a
sodium bicarbonate loading test and diagnosed
distal renal tubular acidosis (RTA). We also found that she had Sjögren's syndrome after a positive screen for anti-Lo, anti-Ra, and after the results of Schirmer's test and a lower lip biopsy. She was discharged and treated as an outpatient with oral
sodium bicarbonate and
potassium chloride.
CONCLUSION: