Extreme hypernatraemia is rare in adults. Due to the fact that rapid correction of hypernatraemia may result in neurological complications, a gradual reduction of sodium concentration is generally advised. However, it is difficult in patients with extreme hypernatraemia, severe metabolic acidosis and renal failure. We describe a patient with extreme hypernatraemia (serum Na+ 202 mEq/l), severe metabolic acidosis ( 7.6 mEq/l) and renal failure who was successfully treated with continuous venovenous haemofiltration (CVVH) with a portion of commercial CVVH replacement fluid and additional sodium bicarbonate. We believe this is the first case report of such a novel treatment and may apply to other patients who suffer from extreme hypernatraemia, severe metabolic acidosis and renal failure.
A 69-year-old woman presented at our emergency room with progressive deterioration of consciousness for 4 days. Her past history included hypertension, chronic renal failure with serum creatinine of 3.7 mg/dl 1 month before admission, ischaemic stroke with left hemiplegia, and status post-craniotomy after stroke. Her consciousness was clear after the cerebral vascular accident but she depended on others for daily activity. She ate less and became more and more lethargic over the 4 days before admission.
On arrival at the emergency department, her conscious status was E2M4V2. Vital signs revealed a blood pressure of 137/71 mmHg, heart rate of 62 b.p.m. and respiratory rate of 18 breaths/min. The initial laboratory data showed blood urea nitrogen (BUN) 114.7 mg/dl; creatinine 8.69 mg/dl; serum sodium 202.4 mEq/l; glucose 91 mg/dl; potassium 4.6 mEq/l; and blood osmolality 455 mosml/kg. Under the impression of acute exacerbation of chronic renal failure, extreme hypernatraemia, 5% dextrose water was given at a rate of 120 ml/h. The serum sodium level decreased from 202.4 to 188.5 mEq/l (13.9 mEq/l) in the first 24 h. However, the serum sodium concentration in the next 24 h decreased only 2.5 mEq/l because of infusion of high volume sodium bicarbonate for correction of metabolic acidosis. The patient became more and more dyspnoeic, and the arterial blood gas at 60 h after admission revealed pH 7.34, 9.1 mEq/l, PaO2 241 mmHg (O2 mask 10 l/min) and PaCO2 17 mmHg. BUN was 134.7 mg/dl. Creatinine was 7.96 mg/dl. Chest X-ray revealed cardiomegaly and pulmonary oedema. She was therefore intubated and dialysis was arranged for further fluid and electrolyte management. The serum sodium concentration increased to 190.5 mEq/l after infusion of 7% NaHCO3 for metabolic acidosis.
For the purpose of gradual correction of the sodium concentration, CVVH was the chosen mode of dialysis for this patient. We used an AK 10 blood pump (Gambro, Lund, Sweden) and a Hemofilter 6S membrane (Gambro, Hechingen, Germany) through a 12,12-Fr dual lumen catheter (Arrow, Erding, Germany), which was placed in a femoral vein. The blood flow rate was 200 ml/min during the dialysis procedure. Commercial CVVH replacement fluid solution A and CVVH replacement fluid solution B (Taiwan Biotech Co., Ltd, Taoyung, Taiwan) were mixed with a flow rate of 800 ml/h. The sodium concentration of the mixture is 142.3 mEq/l. The net ultrafiltration rate was adjusted according to her volume status. The serum sodium level dropped unexpectedly from 190.5 to 174.8 mEq/l in 6 h after starting CVVH. As her sodium reduction rate was above the target of 12 mEq/h, the sodium concentration of the replacement fluid was then adjusted by adding 7% NaHCO3. We added 1.45 ml of 7% NaHCO3 to 1 liter of commercial replacement fluid mixture for each 1 mEq/l elevation of sodium concentration. By this method, the replacement fluid was adjusted every 6 h with a 3 mEq/l targeted reduction of sodium concentration. As the serum sodium concentration was 174.8 mEq/l, the replacement fluid sodium concentration was set at 172 mEq/l. The serum sodium concentration then decreased gradually to 151.8 mEq/l by 54 h after commencement of CVVH. CVVH was changed to intermittent haemodialysis afterwards. The patient's consciousness improved to E4M5-6Vt on the 6th day after admission. She was extubated on the 8th hospitalization day and was transferred to a general ward for further care.
Hypernatreamia is a common problem associated with high mortality and morbidity [1]. Managing extreme hypernatraemia is challenging. Though well-controlled studies to ascertain the optimal treatment of chronic hypernatraemia do not exist, gradual correction of hypernatraemia with a rate of no more than 12 mEq/l/h was suggested [1,2]. Free water hydration is the most commonly used method for hypernatraemia. However, fluid overload might develop in patients with heart failure and renal failure, as occurred in our patient. Since conventional haemodialysis and peritoneal dialysis cannot fulfill the requirement for gradual reduction of serum sodium concentration, we chose continuous renal replacement therapy. Moss et al. reported the first case of hypernatraemia (serum Na+ 189 mEq/l) corrected by continuous arteriovenous haemodiafiltration in 1990 [3]. The patient died of diffuse alveolar damage and cardiogenic shock. Jen-Jar Lin et al. used continuous venovenous haemodialysis to correct hypernatraemia (serum Na+ 180 mEq/l), hyperglycaemia and other electrolyte imbalance in a 12-year-old female patient [4]. They used custom-made dialysate with adjustment of dialysate electrolyte every 6 h and controlled the serum sodium level in 4 days. The patient survived without neurological sequelae after the critical episode. Custom-made dialysate and replacement fluid were not available in our hospital. So we chose CVVH, which needs only replacement fluid but no dialysate. The adjustment of sodium concentration was by adding 3% NaCl to the replacement fluid. The concentration of other electrolytes did not change much with 7% NaHCO3. For example, to elevate [Na+] from 142.3 to 190 mEq/l requires 69.2 ml of 7% NaHCO3 in 1 liter of fluid. The reduction of [K+], [Ca+], [Mg2+] and [Cl] is only 6.4%, which is insignificant clinically.
We present an unusual case with extreme hypernatraemia, severe metabolic acidosis and renal failure treated with CVVH and a special formula consisted of addition of 7% NaHCO3 to commercial solution. The patient's conscious status returned to her baseline status, suggesting a successful outcome of our treatment.
Conflict of interest statement. None declared.
1 Division of Nephrology Department of Internal Medicine China Medical University Hospital2 Division of Nephrology Department of Internal Medicine National Taiwan University Hospital Taiwan Email: cch{at}www.cmuh.org.tw
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