The Egyptian Journal of Internal Medicine

CASE REPORT
Year
: 2015  |  Volume : 27  |  Issue : 3  |  Page : 121--122

Treating double-digit hyponatremia: walking a tight rope


Manjunath Kulkarni1, Prashanth Kadri1, Raghavendra Bakki Sannegowda2, Maria Bethsaida1, Nikhil D'Souza1,  
1 Department of Nephrology, Father Muller Medical College, Kankanady, Mangalore, Karnataka, India
2 Department of Neurology, Father Muller Medical College, Kankanady, Mangalore, Karnataka, India

Correspondence Address:
Manjunath Kulkarni
Department of Nephrology, Father Muller Medical College, Kankanady, Mangalore, Karnataka
India

Abstract

We report the case of a diabetic patient who presented with severe hyponatremia (serum sodium concentration of 88 mEq/l) caused by hypovolemia and thiazide diuretic use. His serum sodium levels were gradually corrected using a combination of isotonic and hypotonic fluids based on urine output and rate of rise in sodium levels. The patient had complete recovery without any evidence of osmotic demyelination.



How to cite this article:
Kulkarni M, Kadri P, Sannegowda RB, Bethsaida M, D'Souza N. Treating double-digit hyponatremia: walking a tight rope.Egypt J Intern Med 2015;27:121-122


How to cite this URL:
Kulkarni M, Kadri P, Sannegowda RB, Bethsaida M, D'Souza N. Treating double-digit hyponatremia: walking a tight rope. Egypt J Intern Med [serial online] 2015 [cited 2020 Oct 23 ];27:121-122
Available from: http://www.esim.eg.net/text.asp?2015/27/3/121/164644


Full Text

 Introduction



Hyponatremia is most common electrolyte abnormality encountered in clinical practice. Untreated severe hyponatremia may cause coma, seizures, and brain damage. Rapid correction is associated with risk of osmotic demyelination. We report the case of a patient with severe hyponatremia, whose serum sodium levels were successfully corrected.

Case presentation

A 44-year-old male presented with 1 week history of vomiting and 2 days history of dysarthria and unsteady gait. His medical history included diabetes and hypertension. His serum creatinine evaluated a month prior admission was 3.7 mg/dl. The patient was on glibenclamide and was recently started on a combination of telmisartan, amlodipine, and hydrochlorthiazide.

On examination, his blood pressure was 110/80 mmHg. There was no edema. Neurological examination revealed signs of cerebellar involvement.

Laboratory reports showed the following: hemoglobin, 11 g/dl; blood urea, 78 mg/dl; serum creatinine, 4.46 mg/dl; plasma glucose, 314 mg/dl; serum sodium, 88 mEq/l (serum sodium corrected for glucose was 93 mEq/l); serum potassium, 3.22 mEq/l; serum chloride, 49.5 mEq/l; serum bicarbonate, 18.7 mEq/l; serum albumin, 3.5 g/dl; serum uric acid, 5.97 mg/dl; serum thyroid-stimulating hormone, 0.417 μIU/ml; and serum cortisol, 1203 nmol/l. Urinalysis revealed urine protein 3+ and absence of red blood cell and pus cells. Urine electrolyte evaluation revealed the following: urine sodium, 19 mEq/l; urine potassium, 27.74 mEq/l; and urine chloride, 21.4 mEq/l. Serum osmolarity was 207 mEq/l. Urine osmolarity was 239 mEq/l. Ultrasound examination of the kidneys was normal. Computed tomography of the brain did not show any abnormality.

This patient was started on insulin, normal saline infusion, and potassium infusion. Serial monitoring of serum sodium was carried out. The rate at which fluids were administered was altered on the basis of urine output and serum sodium levels. On successive days, serum sodium elevated to 96, 105, 115, 119, 125, 127, 128, and 131 [Figure 1]. During the period of rapid rise in serum sodium, hypotonic fluids were used to prevent further rise.{Figure 1}

The patient gradually improved, and by the second day of treatment the patient became fully conscious and was neurologically normal. MRI of the brain was taken 1 week later and did not show any evidence of osmotic demyelination.{Figure 1}

 Discussion



This patient presented with severe symptomatic hyponatremia. Hyponatremia in this case was multifactorial in origin. Thiazide diuretic use, vomiting, and probably osmotic diuresis because of hyperglycemia contributed to hyponatremia. Serum sodium corrected for glucose was 93 mEq/l. Reports were also suggestive of high anion gap acidosis and uncontrolled diabetes mellitus. The patient also had acute kidney injury on chronic kidney disease. Acute kidney injury was secondary to volume depletion.

Risk factors for rapid correction in this case were hypovolemia and thiazide diuretic use.

There was definitive indication for prompt correction of serum sodium levels. Apart from management of hyperglycemia with insulin, this patient was started on normal saline infusion. Serial monitoring of serum sodium levels and hourly urine output monitoring was carried out. During the first 48 h, the rise in serum sodium was well within the recommended maximum. The urine output was stable during this period, probably because of correction of coexistent hypovolemia and hyperglycemia.

During the third day of treatment, this patient experienced emergence of diuresis and for a brief period of time serum sodium levels did go up beyond the desirable correction levels. This was managed with infusion of hypotonic fluids to prevent further rise in serum sodium levels. Desmopressin was not used in this case because of coexisting renal failure. After 72 h, this patient had a stable urine output and a gradual increase in serum sodium levels.

This case demonstrates that gradual correction of serum sodium requires a close watch on serum sodium levels to monitor the rate of correction and urine output. The emergence of water diuresis is an early warning sign for overcorrection. Prediction equations are not very reliable in clinical practice. One study found that, in 40% of cases, emergence of water diuresis was responsible for overcorrection [1]. If overcorrection of serum sodium is seen during treatment, hypotonic fluids may be used to prevent further rise, or to relower the sodium levels [2]. Other strategies would be to use desmopressin or a combination of hypotonic fluids and desmopressin. In one instance, authors have used a combination of 3% saline and desmopressin as a strategy to treat severe hyponatremia [3].

Cases of double-digit hyponatremia (serum sodium <100 mEq/l) are relatively rare in the literature [3-7].

Only few such cases have been successfully corrected with good outcomes [3-6].

Double-digit hyponatremia is rare and treatment should be carefully monitored as it is fraught with risk of overcorrection and osmotic demyelination. Using hourly urine output monitoring and monitoring serum sodium levels closely can guide the rate of fluid administration. Hypotonic fluids should be used at the earliest sign of overcorrection.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Mohmand HK, Issa D, Ahmad Z, Cappuccio JD, Kouides RW, Sterns RH. Hypertonic saline for hyponatremia: risk of inadvertent overcorrection. Clin J Am Soc Nephrol 2007; 2:1110-1117.
2Soupart A, Ngassa M, Decaux G. Therapeutic relowering of the serum sodium in a patient after excessive correction of hyponatremia. Clin Nephrol 1999; 51:383-386.
3Sterns RH, Hix JK, Silver S. Treating profound hyponatremia: a strategy for controlled correction. Am J Kidney Dis 2010; 56:774-779.
4Iioshi M, Sakuragi T, Higa K, Hamada T. Severe hyponatremia during transurethral resection of prostate. Masui 2005; 54:414-417.
5Walker GV, Peterson MC. Survival in a patient with severe paraneoplastic hyponatremia: a case report. Cases J 2008; 1:248.
6Croxson M, Lucas J, Bagg W. Diluting delirium. N Z Med J 2005; 118:U1661.
7Hayashi T, Ishida Y, Miyashita T, Kiyokawa H, Kimura A, Kondo T. Fatal water intoxication in a schizophrenic patient - an autopsy case. J Clin Forensic Med 2005; 12:157-159.