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 Table of Contents  
Year : 2021  |  Volume : 8  |  Issue : 5  |  Page : 249-251

Hyponatremic encephalopathy: An uncommon presentation associated with dengue shock syndrome: Two case reports

Consultant Pediatrician, Seven Hills Hospital, Mumbai, Maharashtra, India

Date of Submission22-Jun-2021
Date of Decision28-Aug-2021
Date of Acceptance04-Sep-2021
Date of Web Publication28-Sep-2021

Correspondence Address:
Dr. Hasmukh Chapsi Gala
Kalpataru Towers, D-191, Off Akurli Road, Kandivali East, Mumbai- 400 101, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcc.jpcc_37_21

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Hyponatremia of mild-to-moderate degree is commonly seen in dengue infection. Severe hyponatremia with encephalopathy in dengue infection is rarely seen. Two cases of dengue shock syndrome presented with severe hyponatremia and hyponatremic encephalopathy. Following correction of hyponatremia, sensorium normalized in both cases. Serum sodium levels should be checked and monitored in patients of dengue fever, especially with altered sensorium, as early recognition and management of such hyponatremia can prevent serious morbidity and even mortality.

Keywords: Dengue shock syndrome, hyponatremic encephalopathy, severe hyponatremia

How to cite this article:
Gala HC. Hyponatremic encephalopathy: An uncommon presentation associated with dengue shock syndrome: Two case reports. J Pediatr Crit Care 2021;8:249-51

How to cite this URL:
Gala HC. Hyponatremic encephalopathy: An uncommon presentation associated with dengue shock syndrome: Two case reports. J Pediatr Crit Care [serial online] 2021 [cited 2021 Oct 16];8:249-51. Available from: http://www.jpcc.org.in/text.asp?2021/8/5/249/326861

  Introduction Top

Mild-to-moderate degree of hyponatremia is commonly seen in association with dengue fever (DF).[1],[2],[3],[4] However, severe hyponatremia with encephalopathy as a presenting feature in dengue infection is rare. The cause and management of severe hyponatremia and associated encephalopathy in two cases of dengue shock syndrome (DSS) are discussed. Serum sodium levels should be checked and closely monitored in cases of DF, including DSS.

  Case Reports Top

Case 1

A 10-months-old male infant was admitted with the fever of 104.8 F of 1-day duration and two episodes of vomiting. Routine blood tests suggested viral fever and the patient was started on maintenance intravenous (IV) fluid. Fever subsided on the 2nd day of admission. On the 3rd day, the patient was found to be drowsy but arousable with Glasgow coma scale (GCS) score of 11/15. He also had signs of poor perfusion in the form of tachycardia with heart rates (HR) 150/min, tachypnea with the respiratory rate (RR) 50/min, NIBP-70/40 mmHg, weakly felt peripheral pulses, and cold peripheries.

Blood investigations showed hemoconcentration and thrombocytopenia: Complete blood cell (CBC)-hemoglobin (Hb)-16 g/dl (baseline-11 g/dl), packed cell volume, (PCV)-44 (baseline-33), platelet count-24,000/cmm (baseline-normal), CRP was 0.04 mg/L, Serum sodium was 120 meq/L, Serum potassium was 4.2 meq/L and SGPT was 69 IU/L. X-ray chest showed right-sided lamellar pleural effusion and haziness of the right lung field. Dengue NS-1 antigen was positive. Diagnosis of DSS with hyponatremic encephalopathy was made and the baby was admitted to the pediatric intensive care unit (PICU) for further management.

Normal saline bolus 20 ml/kg was given twice and 5 ml/kg 3% saline was given. 0.45% DNS drip as maintenance fluid and 0.9% NS drip @ 3 ml/kg/h for correction of hypovolemia and hyponatremia was started as per dengue hemorrhagic fever (DHF) management protocol. After 24 h, hematocrit dropped to 33, systemic perfusion improved and serum sodium level also improved to 133 meq/L. Platelet count dropped to 8,000/cmm. Sensorium improved to GCS score 15/15. One unit of platelet concentrate (random donor platelet concentrate) was transfused. Repeat platelet count done on the 5th day was 19,000/cmm. General condition and platelet count improved over the next 3 days and the patient was discharged after 8 days of hospital stay.

Case 2

Six years 9 months old boy was referred to our hospital with history of 2 episodes of convulsions and altered sensorium following convulsion. There was also history of fever, headache, and vomiting for 5 days before admission. Details of treatment received before admission, including fluids were not known. Dengue NS-1 antigen test was positive whereas peripheral smear for malarial parasite and Widal test were negative. On admission, HR was 140/min, RR-44/min, blood pressure (BP)-80/40 mmHg, peripheral pulses were feeble, central pulses well felt, capillary refill time of 4 s. Clinical examination on admission revealed altered sensorium with GCS score of 10/15 with intermittent tonic posturing.

CBC showed Hb-15.9 g/dl; PCV-43, suggestive of hemoconcentration; WBC-21,200/cmm; Platelet count-17,000/cmm and serum sodium was very low at 114 mmol/l. Serum potassium level was 3.9 mmol/l. Blood sugar on admission was 330 mg/dl and it gradually normalized. Computed tomography Brain was normal and cerebrospinal fluid study could not be done due to poor hemodynamic condition and thrombocytopenia. PT and APTT were deranged. Repeat tests for malaria including rapid malarial antigen tests were negative. Two-dimensional echo was normal except for mild pericardial effusion. Diagnosis of DSS with hyponatremic encephalopathy was made and the patient was admitted to the PICU.

He was started on IV Ceftriaxone and IV acyclovir. He received random donor platelet transfusions following which platelet count improved to 73,000/cmm. Correction of hyponatremia was done initially with 3% saline and then 0.9% saline was used with the aim of slow correction of severe hyponatremia over the next 48–72 h. Isotonic saline @ 5 ml/kg/h was started for intravascular fluid deficit correction along with 0.9% DNS as a maintenance fluid. He also needed inotropic support for poor systemic perfusion. He received packed red blood cells on the 2nd day of admission in view of low hemoglobin (8.2 g/dl). He required mechanical ventilation on the 2nd day. SGPT on admission was 437 U/l, which increased to 2450 U/l on the next day. Gradually, his hemodynamics improved with normalization of BP and perfusion and decrease in hematocrit to 30 within 12 h of starting the above treatment.

Serum sodium level improved to 126 mmol/l on the 2nd day and to 137 mmol/l on the 3rd day of hospitalization. His sensorium became completely normal by the 3rd day of hospitalization. He was discharged after 12 days of hospital stay.

  Discussion Top

DF and DSS is a mosquito-borne illness caused by the dengue virus and it is a common infectious disease affecting millions of people in tropical countries. Neurological manifestations in dengue infection are not uncommon. In one large study of 1493 children with dengue infection by Pancharoen C. et al., 80 (5.4%) children had neurological manifestations.[5] Neurological manifestations in dengue are caused by the direct neurotropic effect of the virus (encephalitis, myelitis), secondary to systemic complications (encephalopathy) or postinfectious immune-mediated, for example, acute demyelinating encephalomyelitis (ADEM), Guillain-Barre syndrome (GBS).[6]

Hyponatremia is commonly seen in DF and DSS, but most of the time it is mild.[1],[2],[3],[4] Hyponatremia seen in dengue infection could be due to salt depletion, excess water from increased metabolism, decreased renal excretion, transient inappropriate antidiuretic hormone secretion, the influx of sodium into cells as a result of dysfunction of the sodium-potassium pump, and the loss of sodium in the urine from acute tubular necrosis.[1],[7] In both the above cases, there was hemoconcentration suggesting the presence of third spacing and hypovolemia. Hyponatremia in both cases was due to third spacing and increase in total body fluid as a result of DSS. In addition, the hypotonic maintenance fluid that was given for the first 2 days in the first case, also contributed to the severe hyponatremia. Details of type of fluid received before admission was not known in the second case. Severe hyponatremia could explain the convulsion and altered sensorium in the second case. In both cases sensorium normalized following normalization of serum sodium, suggesting hyponatremia as a cause of encephalopathy, although poor systemic perfusion could have contributed to the encephalopathy.

Adisorn Lumpaopong et al. had retrospectively reviewed 73 children with DF and 77 children with DHF and found that the prevalence of hyponatremia in children with DF was 61% and DHF was 72%.[2] Most hyponatremic patients had mild hyponatremia, only 3% had moderate hyponatremia whereas none of the patients had severe hyponatremia.

Jutarat Mekmullica et al. had evaluated serum and urine sodium levels in 49 children with dengue and compared it with 44 nondengue patients.[1] They found that the mean sodium level was significantly lower in dengue patients as compared to the nondengue patients (P < 0.0001).

Hyponatremia was 9.7 times more common in dengue patients. Among dengue patients mean serum sodium level was significantly lower in shock patients compared to nonshock patients (P = 0.003). They also found that urine sodium level of ≤20 meq/l, suggesting intravascular volume depletion, was 8.1 times more common in dengue patients as compared to nondengue patients. R. Joshi et al. reported in their study of 57 dengue patients that 23 patients had hyponatremia and 3 of these had severe hyponatremia associated with encephalopathy.[8]

Akshay et al., in their study of 99 cases admitted in their PICU (age 1 month–18 years) found that 33, 12 and 18 patients had mild (130–135 meq/l), moderate (120–130 meq/l), and severe (<120 meq/l) hyponatremia, respectively.[3] They also found that moderate and severe hyponatremia is associated with an increased risk of bleeding manifestations and central nervous system (CNS) complications. Among CNS complications, most patients had encephalopathy, where as some had GBS, ADEM, and hypokalemic paralysis.

Vinay et al. in their study of 202 dengue patients (age >18 years) found that mild (125–135 meq/l), moderate, and (120–125 meq/l) severe hyponatremia (<120 meq/l) was present in 54%, 2.5% and 3% of patients respectively.[4] They concluded that mild hyponatremia and mild hypokalemia were common among the patients of DF where as moderate and severe hyponatremia and hypokalemia were more common among DHF and DSS.

Regular serum sodium level monitoring in patients of DF, especially with altered sensorium may help in early recognition and management of hyponatremia to prevent serious morbidity and even mortality.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Mekmullica J, Suwanphatra A, Thienpaitoon H, Chansongsakul T, Cherdkiatkul T, Pancharoen C, et al. Serum and urine sodium levels in dengue patients. Southeast Asian J Trop Med Public Health 2005;36:197-9.  Back to cited text no. 1
Lumpaopong A, Kaewplang P, Watanaveeradej V, Thirakhupt P, Chamnanvanakij S, Srisuwan K, et al. Electrolyte disturbances and abnormal urine analysis in children with dengue infection. Southeast Asian J Trop Med Public Health 2010;41:72-6.  Back to cited text no. 2
Reddy AA, Reddy TP, Pranam GM, Pranam U, Manjunathe GA. Serum sodium as a prognostic marker in dengue fever cases admitted to PICU in Navodaya hospital, Raichur, India. Int J Contemp Pediatr 2017;4:222-5.  Back to cited text no. 3
Vinay GK, Virendra CP, Amit B, Rahul P. Study of electrolyte disturbances in dengue infected patients. Int J Contemporary Med Res 2019;6:B5-B8.  Back to cited text no. 4
Pancharoen C, Thisyakorn U. Neurological manifestations in dengue patients. Southeast Asian J Trop Med Public Health 2001;32:341-5.  Back to cited text no. 5
Murthy JM. Neurological complication of dengue infection. Neurol India 2010;58:581-4.  Back to cited text no. 6
[PUBMED]  [Full text]  
Miller AS, Wonnacott AC, McBride JW. Dengue induced syndrome of inappropriate secretion of anti-diuretic hormone. J Clinic Case Rep 2012;2:109.  Back to cited text no. 7
Joshi R, Baid V. Profile of dengue patients admitted to a tertiary care hospital in Mumbai. Turk J Pediatr 2011;53:626-31.  Back to cited text no. 8


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