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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2021  |  Volume : 32  |  Issue : 5  |  Page : 1431-1440
Management of severe hypernatremic dehydration and acute kidney injury in children in a critical care nephrology and dialysis unit

Department of Pediatric Nephrology, Bangladesh Institute of Child Health and Dhaka Shishu (Children) Hospital, Sher e Bangla Nagar, Dhaka, Bangladesh

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Date of Web Publication4-May-2022


Our study aimed to manage the children presented with severe hypernatremic dehydration and acute kidney injury (AKI) an updated fluid management protocol was used to find out the rate of decline of serum sodium per day and their outcome. This is a prospective interventional study was conducted from November 2015 up to October 2016 in the Critical Care Nephrology and Dialysis Unit of Dhaka Shishu (Children) Hospital, Bangladesh. A total of 45 children with hypernatremia and AKI were evaluated. Patients were treated by the calculated amount of dextrose in normal saline mixed with various dilutions of 3% NaCl with a difference of serum to infusate sodium concentration around 10 mEq/L as per the American Academy of Pediatrics - 2005. Intermittent peritoneal dialysis was done when in the failure stage of AKI or when serum sodium (Na+) >180 mEq/L. Depending on the outcome samples were divided into survival and death groups. Data were processed by software STATA 13 and analysis was done by one-way ANOVA, Tukey test, Chi-square test, F-test, and Student’s t-test. Age ranged from one month to 6½ years and 91% were infants. Total 64% of patients were in the failure stage of AKI and majority were in the death group, 31% in injury and 4.4% patient in the risk stage. Out of 45 cases, 30 (67%) had severe hypernatremia. Significant reduction of serum Na+ was found and the rate of decline between days was optimum (8.4 mmol/L/day). Overall 60% survived with normal renal functions and 40% died. The calculated amount of dextrose in normal saline mixed with various dilutions of 3% NaCl is safe in severe hypernatremic dehydration with AKI.

How to cite this article:
Shireen A, Tahmina F, Farhana Y, Umme T, Sukriti B, Hossain MK. Management of severe hypernatremic dehydration and acute kidney injury in children in a critical care nephrology and dialysis unit. Saudi J Kidney Dis Transpl 2021;32:1431-40

How to cite this URL:
Shireen A, Tahmina F, Farhana Y, Umme T, Sukriti B, Hossain MK. Management of severe hypernatremic dehydration and acute kidney injury in children in a critical care nephrology and dialysis unit. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 May 25];32:1431-40. Available from: https://www.sjkdt.org/text.asp?2021/32/5/1431/344764

   Introduction Top

Severe hypernatremia when associated with acute kidney injury (AKI), results in increased mortality and long-term morbidity. Management of severe hypernatremic dehydration is very crucial when associated with AKI. Renal excretion of sodium is largely impaired in critically ill patients, particularly in patients with AKI. Sodium overload effect in patients with AKI is expected to be even more striking. Recently, a group also retrospectively noted that correcting this abnormality ultimately resulted in better survival.[1] There is a chance of developing life-threatening complications during intravenous (IV) correction of hypernatremia due to too rapid or too slow correction.[2],[3] It is still unclear how to calculate total daily fluid requirement and what might be the ideal fluid of choice in severe hypernatremic dehydration. Very often infants and children with severe hypernatremia [serum sodium (Na+) >170 mmo/L] with dehydration are being managed with quarter strength (Na+ = 37mmol/L) or half-strength (Na+ = 77 mmol/L) dextrose in normal saline and frequently presented with neurological complications due to sudden drop in body fluid tonicity. When serum N+ is >170 mmol/ L, then correction of dehydration with an infusate containing 37 mmol/L or 77mmol/L, even normal saline with154 mEq/L Na+ is too hypotonic compared to patients serum Na+. American Academy of Pediatrics 2005 has given a protocol for correction of hypernatremic dehydration by using calculated amount of sodium chloride (NaCl) infusion prepared by adding various dilutions of 3% NaCl with dextrose in normal saline with a difference of serum to infusate Na+ concentration around 10 mEq/L, which provides optimum correction of hypernatremia and dehydration.[4] Critically ill adult patients with traumatic injuries and hypernatremia (serum Na+ >150 mEq/L) were treated with ¼ strength normal saline. It was found to be effective for decreasing serum sodium concentration, but evidence for minor hemolysis warrants further research to establish its safety before recommending its routine use.[5]

Very little is known regarding the management of severe hypernatremic dehydration when associated with AKI in children. Hence, our aim was to assess the safety of updated fluid management protocol with various dilutions of 3% NaCl saline and intermittent peritoneal dialysis (IPD) in children with severe hyper-natremic dehydration and AKI. This study was also intended to determine the rate of decline of serum sodium per day and to find out the immediate outcome of the study cases in critical care nephrology and dialysis unit of a tertiary care teaching hospital.

   Subjects and Methods Top

A prospective interventional study was conducted for 12 months (from November 2015 up to October 2016) in the Critical Care Nephrology and Dialysis Unit of Dhaka Shishu (Children) Hospital, Bangladesh.

Inclusion criteria

Children of both sexes, aged between one month and 6½ years, who were presented with hypernatremic dehydration and AKI were included. Written informed consent was taken from the parent or legal guardian.

Study procedure

A total of 45 children with hypernatremia and AKI were evaluated. AKI staging was done by pediatric RIFLE criteria [Table 1].
Table 1: Pediatric RIFLE criteria of acute kidney injury staging.[6]

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Hypernatremia was classified into mild, moderate, and severe with serum sodium 150–155 mEq/L, >155–170 mEq/L, >170 mEq/L, respectively. The Winter season was considered between November and February. The use of concentrated oral rehydration salt (ORS) was considered when ORS was prepared by the small volume of water <500 mL. All patients were treated by IPD with 2.5% glucose-containing fluid initially to avoid rapid drop of tonicity. The indications for IPD were serum creatinine raised three-fold from the baseline or urine output <0.3 mL/kg/h for 24 h or anuria for 12 hs, serum Na+ 180 mmol/L with evidence of symptomatic hypernatremia like encephalopathy, intractable severe metabolic acidosis, pulmonary edema due to volume overload, severe symptomatic hyperkalemia (serum K+ >7 mEq/L) and when there was no response to supportive treatment. Fluid adjustment was done according to serum Na+ level. The aim was to reduce the serum Na+ no more than 10 mmol/L over the next 24 h. In general, recommendations for treating hypernatremic dehydration consist of an emergency phase (restoration of vascular volume with 10–20 mL/kg of isotonic IV fluid such as dextrose in normal saline with 154 mEq/L of sodium) followed by a rehydration phase (the sum of the free water deficit and maintenance fluid requirements administered evenly over 48 h in moderate hypernatremia and 72 h in severe hypernatremia. Along with the calculated amount of free water deficit, maintenance fluid and ongoing losses (10 mL/kg) were added. By using the following formula we have calculated daily fluid and sodium requirements. FWD= 4 mL × wt. in kg × (observed-desired serum Na+) (when serum Na+ >170 mmol/L, we used 3 instead of 4). The maintenance fluid requirements - as the patient had impaired renal function or large amounts of ongoing losses, “insensible + losses” were used rather than the traditional maintenance IV fluid rate. Severe hypernatremia with dehydration were managed with infusion of IV fluid with a difference of sodium level 10 mEq/L from the patients serum Na [e.g. when serum Na+ = 185 mEq/L, infusate Na was maintained at (185–10=) 175 mEq/L].

The infusate fluid was prepared by adding various amounts of the 3% NaCl in 5% dextrose in normal saline [Pediatrics in Review 2005;26(4):148-50].[4] To prepare this fluid we used (the amount of 3% normal saline that was added to 1 L of normal saline to make an IV solution that has the desired concentration of sodium was calculated from the) following equation: [1000 × (desired Na+-154)/(500-desired Na+] = mL of 3% normal saline. During IV correction the patients were kept under close observation in critical care set up and IV fluid was administered either via infusion or syringe pump. Only four patients developed convulsion during fluid therapy due to rapid lowering of serum sodium and was managed with IV 3% NaCl 4 mL per kg immediately. Metabolic acidosis, hypokalemia, and hypocalcemia were corrected as required. Glucose was added to IV fluid to avoid over correction. We assessed vitals, hydration status, neurological status, and urine output routinely. Random blood sugar, serum creatinine, serum calcium, arterial blood gas for pH and serum HCO[3] levels were also measured periodically. Serum electrolytes were monitored 4–6 hourly to avoid too slow or rapid correction. Oral feeding was started when the patient’s general condition became stable and able to swallow. Then, IV fluid was gradually discontinued.

   Statistical Analysis Top

All the findings with etiology and outcome of AKI and hypernatremia were noted in the data collection sheet and analyzed accordingly. Depending on the outcome patients were divided into two groups, survived and death. Data were processed by using software STATA 13 (StataCorp. 2013. Stata Statistical Software: Release 13. College Station, TX: StataCorp LP.) Data were analyzed by oneway ANOVA, Tukey test, Chi-square test, F test and Student’s t-test, P <0.05 was considered significant.

   Results Top

A total of 45 patients were admitted with hypernatremia and AKI during the study period. Age ranged from one month to 6½ years, 41 (91%) were under one year and four were older than one year. Among the 45 study children, 31 were male (M) and 14 were female (F), M:F = 2.2:1. The overall 27 (60%) survived with normal renal functions and 18 (40%) died.

Majority (36%) of mothers were illiterate and 33% had primary level of education [Figure 1].
Figure 1: Maternal educational status of the study children.

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The major clinical presentations were diarrhea (89%) and convulsion (69%), followed by vomiting, severe dehydration, oliguria, anuria, and fever [Figure 2].
Figure 2: Presenting complaint of the study children.

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Out of 45 cases, 30 (67%) had severe hypernatremia, among them 16 survived with normal kidney functions and 14 expired. Moderate degree of hypernatremia was found in 15 children and 11 of them survived and four expired [Figure 3].
Figure 3: Severity of hypernatremia (n=45).

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About 64% (n=29) patients were in the failure stage of AKI, 31% (n=14) in injury and two patients (4.4%) in the risk stage. Majority of death (n=13) was found in the failure stage [Figure 4].
Figure 4: Acute kidney injury staging (n=45).

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Out of 27 survived children [Figure 5], 16 were with severe hypernatremia with severe dehydration and they were managed with IPD and calculated amount of 3% NaCl mixed with dextrose in normal saline. The rate of decline of serum sodium between days shows significant reduction (P = 0.000, F test). The rate of decline of mean serum sodium per day in survived group after correction with calculated amount of IV fluid was 8.4 mEq/L [Table 2].
Figure 5: Rate of decline of mean serum sodium between days- in survived group of severe hypernatremia with severe dehydration (n=16).

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Table 2: Daily average rate of decline of serum sodium (N=16).

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The average rate of decline of serum Na+ per day was 8.4 mmol/L. Significant rate of decline was found on day 1 versus day 2 and day 2 versus day 3. Although the rate of decline was not significant on day 3 versus day 4, day 4 versus day 5 and day 5 versus day 6, but the rate of decline was satisfactory [Figure 6].
Figure 6: Day-wise reduction of serum sodium level in survived group (N= 16).

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The mean serum sodium level [Figure 7] at the time of admission was 173.84 mEq/L versus 180.16 mEq/L in survived and death Groups, respectively. The mean serum Na+ at the time of discharge was 140.35 mEq/L in survived patients, and at the time of death, it was 167.75 mEq/L. Significant reduction of serum sodium was found in survived group after treatment (P = 0.000, Student’s t-test).
Figure 7: Mean level of serum sodium before and after treatment in the survived and death groups.

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After IPD there was satisfactory decline of mean serum creatinine level in the survived group (P = 000, t-test) [Figure 8]. All patients were discharged with normal urinary output.
Figure 8: Mean level of serum creatinine before and after treatment in the survived group (n=27).

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We compared [Table 3] the above variables to explore the factors responsible for severe hypernatremia. In 58% (n=26) of cases, the cause of hypernatremia was intake of concentrated ORS. About 78% occurrence was found in winter season with an odds ratio of 1.45. Most of the patients had diarrhea (89%) and vomiting (56%). The risk of severe hypernatremia is more commonly associated with the winter season, diarrhea, and vomiting, although the factors are not statistically significant.
Table 3: Factors associated with risk of severe hypernatremia.

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Most (91%) cases were under one year of age and 40% (n=18) of them died. Although statistically not significant, increased mortality in this series was found with failure stage of AKI (n=13), severe hypernatremia (14), intake of concentrated ORS (n=11), convulsion (n=17), severe dehydration (n=13) [Table 4].
Table 4: Risk factors associated with death.

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   Discussion Top

Children with severe dehydration and severe hypernatremia were treated with replacement of free water deficit with the infusion of calculated amount of IV fluid with a difference of sodium level 10 mmol/L from the patients’ serum. Maintenance fluid and on-going losses were adjusted as well. Four infants developed convulsion during the initial period of correction which was managed with 3% NaCl IV immediately. Besides that, no significant complication was found. Satisfactory rate of decline of serum Na+ had been found. Along with fluid management, dialysis was also needed when serum sodium value exceeded 180 mmol/L. It was known that the rate of correction of serum Na+ >0.5 mEq/L/h was associated with neurological complications. A recent study reported that hypernatremia correction is independently associated with survival, with the effect being greater with faster correction rates up to 12 mEq/L per day during the 48 h after intensive care unit (ICU) admission.[7] A largest cohort study in critically ill adults with hypernatremia showed that rapid correction of both admission and hospital-acquired hypernatremia occurred in a third of patients, and that rapid correction >0.5 mEq/L/h or >12 mEq/L/day was not associated with in-hospital mortality or cerebral edema. Hence, the fear of rapid correction of hypernatremia may be over stated and clinicians should consider correcting the serum sodium level with free-water administration to shorten the length of stay in this vulnerable patient population.[8] It is important for the clinician to understand how to determine the correct fluid and electrolyte solutions to meet the child’s maintenance, deficit, and ongoing losses. This fluid management needs critical care setup with close monitoring to avoid complications. In this study, significant improvement in serum Na+ and serum creatinine in the survived group had been found when compared to the worst outcome in the death group. It can be explained in this way that the majority of death groups were with severe hypernatremia (67%), most (64%) of them were in the advance stage of AKI, higher rate of convulsion (69%), use of concentrated ORS (58%), state of severe dehydration (69%), the higher number of cases (n=38) under one year of age . Although these factors are not statistically significant, the combined effect of these might accelerate death in this group.

This study suggests that young infants are more prone to hypernatremia because they depend on caregivers for their feeding and water requirements. Diarrhea and vomiting are still the major causes of hypernatremia.[9],[10] It also stresses that illiteracy and ignorance are the most important cause of improper mixing of ORS in this series. Several studies showed that less important care is given for hydration in winter than in summer. Faulty thoughts of giving less water during winter to avoid cough and cold is another reason behind it. Consumption of appropriately prepared ORS in rotavirus-caused diarrhea may still result in a hyperosmolar condition. Children become excessively thirsty, which often results in caregivers’ frequently administering ORS to quench thirst and ultimately leads to severe and extreme hypernatremia.[11]

In this study, we did not find a statistical link between the factors like young age of occurrence, the severity of hypernatremia, the severity of AKI, convulsion, use of concentrated ORS and mortality. The small cohort size also probably explains why the relationship between hypernatremia and death did not reach statistical significance. Previous studies also had similar conclusion.[12],[13],[14],[15] Acute watery diarrhea with severe dehydration was found as an important cause of AKI in Bangladesh. Poor socioeconomic status, lack of food hygiene, poor hand washing before meal, lack of health education and public awareness are responsible for this in our country.[14]

The mortality in AKI in children has been reported to vary widely from 16% to 43.8%.[9],[13],[14],[15],[16] The incidence of acute renal failure in a hospital study done in Thailand showed 0.5–9.9 cases per 100 pediatric patients with a mortality rate of 41.5%.[17] In the present study, mortality rate was 40%, which is comparable to previous studies. Neurological symptoms are frequent in hypernatremia caused by the hyperosmolar effect of hypernatremia itself and due to rapid correction with hypotonic fluid[1],[4],[9],[11] and we reported that 69% of patients had convulsion at admission. Most of them were initially managed with IV fluid in the local hospital, so the neurological complications in this series may be due to both cellular dehydration and cerebral edema. We did not perform magnetic resonance imaging (MRI) of the brain in all cases due to financial reasons, but few of the MRI scans had shown cortical atrophy and few had shown mild changes. During follow up normal developmental milestones were noticed in patients with mild changes, but gross motor dysfunction was found in those with diffuse cortical atrophy. As hypernatremia is a common and largely preventable complication of intensive care, it is recommended that the intensivists should be very careful to provide adequate sodium and water balance for them. The rate of correction is critical and must be adjusted to the rapidity of development of hypernatremia.[18] Hypernatremia acquired in the ICU occurring in eight out of every 100 patients admitted, with a high associated mortality of one in three. As moderate elevation of sodium is also associated with high mortality rates, focusing on early detection and treatment in this group may be worthwhile. Preventing hypernatremia appears to be an appropriate goal in clinical practice.[19]

   Conclusion Top

Infants are the common victims of hypernatremia. Management of severe hypernatremic dehydration with AKI by IPD and calculated amount of 3% NaCl with various dilutions of IV fluid containing sodium concentration around 10 mEql/L lower than patient’s serum is safe and results in optimum reduction. Intake of concentrated ORS and winter seasonal occurrence of diarrhea are the most important causes of hypernatremia in infancy. Patients with hypernatremia when present with convulsion in an advanced stage of AKI, results in the worst outcome.

   Limitations Top

This is a small sampled, single-center study. Long-term neurological outcomes of study subjects were not shown as MRI was not performed in all cases due to financial constraint but the patients were assessed during follow up for one year. We did not compare the rate of decline of serum Na with only fluid management versus fluid management plus IPD. Therefore, a large multicenter observational study with neurological imaging and long-term follow-up is required.

   Acknowledgment Top

The authors would like to thank all the nurses and dialysis technicians of Critical Care Nephrology and Dialysis Unit of Dhaka Shishu (Children) Hospital for their sincere and special attention and continuous support during the management of these study children.

Conflict of interest: None declared.

   References Top

Besen BA, Gobatto AL, Melro LM, Maciel AT, Park M. Fluid and electrolyte overload in critically ill patients: An overview. World J Crit Care Med 2015;4:116-29.  Back to cited text no. 1
Bataille S, Baralla C, Torro D, et al. Under correction of hypernatremia is frequent and associated with mortality. BMC Nephrol 2014; 15:37.  Back to cited text no. 2
Foulkes DM. Fluids and Electrolytes. The Harriet Lane Hand Book. 16th ed. The John Hopkins Hospital, The United States Mosby; 2002.  Back to cited text no. 3
Schwaderer AL, Schwartz GJ. Treating hypernatremic dehydration. Pediatr Rev 2005;26: 148-50.  Back to cited text no. 4
Dickerson RN, Maish GO 3rd, Weinberg JA, Croce MA, Minard G, Brown RO. Safety and efficacy of intravenous hypotonic 0.225% sodium chloride infusion for the treatment of hypernatremia in critically ill patients. Nutr Clin Pract 2013;28:400-8.  Back to cited text no. 5
Akcan-Arikan A, Zappitelli M, Loftis LL, Washburn KK, Jefferson LS, Goldstein SL. Modified RIFLE criteria in critically ill children with acute kidney injury. Kidney Int 2007;71:1028-35.  Back to cited text no. 6
Darmon M, Pichon M, Schwebel C, et al. Influence of early dysnatremia correction on survival of critically ill patients. Shock 2014;41:394-9.  Back to cited text no. 7
Chauhan K, Pattharanitima P, Patel N, et al. Rate of correction of hypernatremia and health outcomes in critically ill patients. Clin J Am Soc Nephrol 2019;14:656-63.  Back to cited text no. 8
Gennari FJ. Hypo-hypernatraemia: Disorders of water balance. Oxford Textbook Of Clinical Nephrology. 2nd ed. England Oxford University Press; 1998.  Back to cited text no. 9
Androgue HJ, Madias NE. Hypernatremia. N Engl J Med 2000;342:1493-9.  Back to cited text no. 10
Das SK, Afroze F, Ahmed T, et al. Extreme hypernatremic dehydration due to potential sodium intoxication: Consequences and management for an infant with diarrhea at an urban intensive care unit in Bangladesh: A case report. J Med Case Rep 2015;9:124.  Back to cited text no. 11
Finberg L, Harrison HE. Hypernatremia in infants; an evaluation of the clinical and biochemical findings accompanying this state. Pediatrics 1955;16:1-14.  Back to cited text no. 12
Bruck E, Abal G, Aceto T Jr. Pathogenesis and pathophysiology of hypertonic dehydration with diarrhea. A clinical study of 59 infants with observations of respiratory and renal water metabolism. Am J Dis Child 1968;115: 122-44.  Back to cited text no. 13
Afroz S, Simi MA, Sharmim S, et al. Aetilogy and outcome of acute kidney failure in Bangladeshi children-Dhaka medical college hospital experience. J Dhaka Med Coll 2016; 24:86-91.  Back to cited text no. 14
Afroz S, Ferdaus T, Sharmin T, Hossain N. Aetilogy and outcome of hypernatremia in post diarrhoeal acute kidney injury in children – An experience in Dhaka medical college hospital. North Int Med Coll J 2017;8:225-7.  Back to cited text no. 15
Bailey D, Phan V, Litalien C, et al. Risk factors of acute renal failure in critically ill children: A prospective descriptive epidemiological study. Pediatr Crit Care Med 2007;8: 29-35.  Back to cited text no. 16
Vachvanichsanong P, Dissaneewate P, Lim A, McNeil E. Childhood acute renal failure: 22-year experience in a university hospital in southern Thailand. Pediatrics 2006;118:e786-91.  Back to cited text no. 17
Lindner G, Funk GC. Hypernatremia in critically ill patients. J Crit Care 2013;28: 20.e11-20.  Back to cited text no. 18
O’Donoghue SD, Dulhunty JM, Bandeshe HK, Senthuran S, Gowardman JR. Acquired hypernatraemia is an independent predictor of mortality in critically ill patients. Anaesthesia 2009;64:514-20.  Back to cited text no. 19

Correspondence Address:
Afroz Shireen
Department of Pediatric Nephrology, Bangladesh Institute of Child Health and Dhaka Shishu (Children) Hospital, Sher e Bangla Nagar, Dhaka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.344764

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]

  [Table 1], [Table 2], [Table 3], [Table 4]


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