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Indian Pediatr 2009;46: 577-583 |
|
Free Water Excess is Not the Main Cause for
Hyponatremia in Critically Ill Children Receiving Conventional
Maintenance Fluids |
S Singhi and M Jayashree
From the Department of Pediatrics, Advanced Pediatrics
Centre, Postgraduate Institute of Medical Education and Research,
Chandigarh, India.
Correspondence to: Dr Sunit Singhi, Professor and Head,
Department of Pediatrics and Incharge, Pediatric Emergency and Intensive
Care Units, Advanced Pediatrics Centre, PGIMER, Chandigarh 160 012, India.
Email: [email protected]
Manuscript received: February 26, 2008;
Initial review: April 7, 2008;
Accepted: August 28, 2008.
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Abstract
Objective: To examine occurrence of hyponatremia
in critically ill children receiving conventional maintenance fluids
(0.18% saline in 5% dextrose) and its relationship with electrolyte free
water (EFW), sodium intake and natriuresis.
Design: Prospective observational study.
Setting: Pediatric Intensive Care Unit of a
tertiary care teaching hospital.
Subjects: Thirty eight patients, 3 months-12
years, consecutively admitted to PICU over 30 days. Main outcome measure
was occurrence of hyponatremia (serum sodium
£130 mEq/L). Serum and urinary
sodium, and osmolality were measured, and type and volume of intravenous
fluids and total urine output were recorded 12 hourly. Daily intake of
sodium and EFW, urinary sodium excretion and net balance of fluid and
sodium were estimated from above. Data of hyponatremic and non-hyponatremic
patients was compared using ANOVA, Mann-Whitney U, and Chi-square tests.
Results: Fourteen episodes of hyponatremia were
recorded in 12 patients over 397 patient days (3.5 episodes/100 patient
days). Their mean (SD) serum sodium dropped from 139 (9.3) at admission
to 128 (1.0) mEq/L, over a median interval of 3.5 days (range 1-15
days). Net fluid and sodium balance in hyponatremic patients did not
differ significantly from non-hyponatremic patients. Within the
hyponatremic group, sodium intake, urinary sodium and sodium balance
were similar before and after the occurrence of hyponatremia, while
total fluid (P=0.009) and EFW intake (P=0.001) were lower in the days
preceding hyponatremia.
Conclusions: Fluid and sodium balance, magnitude
of natriuresis and EFW intake alone did not explain occurrence of
hyponatremia in critically ill children; contribution of other
mechanisms needs to be studied.
Keywords: Electrolyte free water, Fluid therapy, Hyponatremia,
Maintenance fluids, Sodium balance.
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H yponatremia
is the most common electrolyte disorder in hospitalized critically ill
patients(1,2). This could result from a deficit of sodium or a surplus of
water(3). Most often it has been attributed to free water excess resulting
from impaired free water excretion that is caused by an inappropriate
release of antidiuretic hormone in response to various non-osmotic
stimuli(4). Use of conventional "hypotonic" maintenance fluid (0.18%
saline in 5% dextrose) has been alleged to aggravate this free water
excess in sick children in whom the excretion of hypotonic urine is
impaired(5,6).
Intracellular fluid (ICF) volume is inversely related
to the serum sodium; therefore, hyponatremia may aggravate the risk of
cerebral edema and herniation(3,7,8). The reported morbidity and mortality
associated with hospital-acquired hyponatremia have given momentum to
calls for increasing the tonicity of the parenteral maintenance
solution(5,6,9). Some authors on the contrary feel that simple restriction
of fluids rather than isotonic saline would tackle the problem better, by
improving the secondary desalination that results from over expansion of
the intravascular space(10,11). The debate on the issue continues(10-12).
With this background, we have examined the relationship
of hyponatremia with free water intake, sodium intake and natriuresis in
critically ill children receiving conventional maintenance fluids (0.18%
saline in 5% dextrose). Our hypothesis was that occurrence of hyponatremia
is not fully explained by electrolyte free water (EFW) intake, that occurs
with conventional maintenance fluids and natriuresis, that occurs in sick
children. In our previous studies, hyponatremia was seen in sick children
attending pediatric emergency service even before they had received
intravenous fluids(13) and it got corrected in patients with pneumonia(14)
and meningitis(15) while receiving 0.18% saline in 5% dextrose as
maintenance fluids, with improvement in primary disease.
Methods
This was a prospective observational study conducted in
the Pediatric Intensive Care Unit (PICU) of a multi-specialty teaching and
regional referral hospital in North India from mid March 2004 to mid April
2004, after approval from the Institute’s Ethics Committee. All patients
admitted to the PICU during this period were enrolled consecutively into
the study except those who had a PICU stay <24 hours.
Demographic details, weight, diagnosis, PRISM scores
and indication for PICU admission were recorded. Nutritional status was
assessed as percentage weight for age, using NCHS standards and IAP
Classification(16). Serum sodium (Dimension Clinical Chemistry Analyzer,
Dade Behring, USA) and osmolality (Model 3300, Advanced Instuments,
Norwood, USA) were measured 12 hourly. Urine was collected every 12 hours
and sodium concentration estimated from an aliquot from total collection.
Sodium levels were measured using ion selective electrodes.
Volume and type of intravenous and oral fluids given to
patients and total urine output were recorded. Intake of fluids (mL/kg/day),
sodium (mEq/kg/day) and electrolyte free water (EFW) (mL/kg/day), urine
output (mL/kg/day), and urinary sodium excretion (mEq/kg/day) were derived
from above data. Net daily balance of fluid and sodium were estimated from
24-hour fluid and sodium intake, urine output and urinary sodium
excretion. The EFW input was calculated using the tonicity and the volume
of the fluid infused(12). For example, for every litre of 0.18% saline in
5% dextrose that was infused, only one-fifth i.e, 200 mL is
isotonic to plasma and the rest 800 mL is EFW.
Data analysis: Any record of serum sodium
£130
mEq/L was counted as one episode of hyponatremia. If more than one
consecutive serum sodium levels were
£130
mEq/L, before it got corrected, it was counted as one episode.
Hyponatremia was corrected as per standard protocol if patient was
symptomatic or if the level was <125 mEq/L(17). The influence of EFW
intake on serum sodium was analyzed using the initial measured sodium and
total body water (which was estimated as 60% of body weight)(6). To
examine relationship of hyponatremia with free-water intake, sodium intake
and natriuresis, the data of hyponatremic patients on all the days
preceding the episode of hyponatremia was compared with the data of all
the days following the occurrence of hyponatremia. Additionally, the data
of hyponatremic patients on all the days preceding hyponatremia was also
compared with that of the normonatremic children (serum sodium >130 mEq/L).
Descriptive statistics (frequency, median, mean and SD) were used for data
presentation. For comparisons across the three groups, ANOVA was used for
parametric data and Mann Whitney- U test for non-parametric data.
Categorical data were compared using the Chi Square test.
Results
Thirty-eight patients, aged 2 months to 13 years, with
a median PRISM score of 13 (range 4-20) were included in the study. They
comprised 397 patient- days. 29 children had malnutrition (weight for age
<80% of expected); 20% (6/29) of them had severe malnutrition (weight for
age <60% of expected).
Fourteen episodes (3.5 episodes/100 patient days) of
hyponatremia were recorded. One patient was hyponatremic at admission to
PICU, while 13 episodes occurred in 11 patients during the ICU stay; 2
patients had 2 episodes each. The mean (SD) serum sodium in these patients
had dropped from 139 (9.6) mEql/L (range 131-154 mEq/L) to 128 (1.0) mEq/L
(range 127-129 mEq/L). The median time from admission to occurrence of
hyponatremia was 3.5 days (range 1-15 days). The median serum and urine
osmolality at the time of detection of hyponatremia were 276 (260-329)
mOsm/kg and 340 (180-649) mOsm/kg, respectively. The salient
characteristics of patients who had hyponatremia compared with those
having normal serum sodium are depicted in Table I.
Diagnosis of myocarditis and use of diuretics were significantly more
frequent in hyponatremic patients. The proportion of malnourished patients
in both the groups were similar (10 out of 12 vs 19 out of 26, P=0.9).
TABLE I
Characteristics of Patients with Hyponatremia and Normonatremia
Characteristics |
Hyponatremia (n=12) |
Normonatremia (n=26) |
P
value |
Age
(years) |
5.5 (3.6)a |
4.2 (4.0)a |
0.41* |
Male:Female |
1.4:1 |
2.3:1 |
|
PRISM
score |
13.5 (4-20)b |
9 (5-20)b |
0.46† |
Weight
for age, % of expected |
75.2 (12.3)a |
78.7 (14.9)a |
0.45* |
Mechanical ventilation, n (%) |
6 (50) |
13 (50) |
0.72 |
Use of
diuretics, n (%) |
4 (33) |
1 (4) |
0.047 |
Diagnosis, n (%) |
|
|
|
Pneumonia |
4 (33.3) |
2 (7.6) |
0.12 |
Myocarditis with cardiogenic shock |
4 (33.3) |
– |
0.01 |
Pyogenic meningitis |
3 (25) |
3 (11.5) |
0.29 |
Congenital heart disease |
– |
4 (15.4) |
|
Pericardial effusion |
– |
1 (3.8) |
|
Others |
1 (8.3) |
14c (53.8) |
|
Serum
osmolality, mOsm/ Kg |
276 (260-329)b |
280 (262-310)b |
0.17† |
* P by Students’ t test, †P by Mann Whitney U test; amean (SD), bmedian (range);
cincludes acute gastroenteritis (n=3), acute leukemia with febrile neutropenia (n=2),
acute laryngotracheobronchitis (n=2) and nephrotic syndrome with septic shock (n=2)
acute leukemia with acute gastroenteritis, tetanus, snake envenomation, diphtheria and
acute liver failure (n=1 each).
|
Relationship of EFW intake and fall of serum sodium
The median (5th-95th centile) EFW intake among the
hyponatremic patients before occurrence of hyponatremia was 70.7
(21.1-105.0) mL/kg/day. The correlation between EFW intake and the fall in
serum sodium was not significant (Pearson’s correlation r = –0.574; P=0.083).
Only 4 patients had received an EFW volume that could explain fall in
their serum sodium (Fig. 1). The hyponatremic patients
(before and after occurrence of hyponatremia) and the non-hyponatremic
patients had similar fluid and sodium balance and sodium excretion (Table
II). Within the hyponatremic group, in the days preceding
hyponatremia compared to the days following hyponatremia, the median
(5th-95th centile) sodium intake and excretion were not significantly
different but total fluids and EFW intake and urine output mL/kg/day was
signi- ficantly lower (Table II). Total fluid intake
and EFW intake in pre-hyponatremic phase was also significantly lower than
that in patients without hyponatremia.
|
Fig. 1 Relationship between electrolyte
free water (EFW) intake and fall in serum sodium. The line indicates
expected fall in serum sodium for the given EFW intake. Each dot
represents data of one patient and shows observed fall in serum
sodium with respect to their EFW intake. The correlation between EFW
intake and the fall in serum sodium was not significant (Pearson’s
correlation r=–0.574; P=0.083). |
TABLE II
Fluid and Sodium Balance in Patients with Hyponatremia, Before and After Occurrence of
Hyponatremia,Compared to Patients Without Hyponatremia
|
Preceding
hyponatremia
(A) |
Following
hyponatremia
(B) |
No
hyponatremia
(C) |
P
value
|
Urine
output |
48.4 |
70.1 |
62.8 |
0.005 |
(mL/kg/day) |
(15.6–91.7) |
(31.3–128.8) |
(54.9–153) |
A vs B
=0.002 |
Total
fluid intake |
91.0 |
106 |
98.6 |
0.009
|
(mL/kg/day) |
(35–130) |
(57–151) |
(55.4–151) |
A vs B =0.016 |
|
A vs C =0.007 |
Fluid
balance |
32.5 |
40 |
44.7 |
0.076 |
(mL/kg/day)
|
(1.2–85.3) |
(5.0–90.0) |
(3.4–96) |
|
Electrolyte free water |
70.7 |
91.7 |
83.2 |
<0.0001 |
(mL/kg/day) |
(21.1–105.0) |
(52.3–135.2) |
(42.4–108.7) |
A vs B =0.002 |
|
A vs C =0.000 |
B vs C =0.031 |
Sodium
intake |
2.4 |
1.6 |
2.3 |
0.028
|
(mEq/kg/day) |
(0.2–11.9) |
(0.2–9.1) |
(0.2–7.4) |
B vs C
=0.017 |
Urinary
sodium |
2.8 |
5.3 |
5.8 |
0.4 |
(mEq/kg/day) |
(1.5–20.1) |
(1.3–21) |
(1.0–15.4) |
|
Sodium
balance |
1.2 |
0.20 |
0.45 |
0.3 |
(mEq/kg/day) |
(–13.2–11.7) |
(–15.2–4.9) |
(–13.2–7.9) |
|
Values show median (5th–95th centile). |
Although the use of diuretics were more frequent in
hyponatremic patients, urine output, and sodium and fluid balance was not
significantly different in the patients who received diuretics and who did
not. In fact, total fluid, EFW intake and sodium excretion were lower in
patients who received diuretics (Table III). Possibly
the patients in diuretic group were those who needed an improvement in
their urine output because of their underlying conditions and diuretics
were used to normalize urine output.
TABLE III
Fluid and Sodium Balance of Patients with Hyponatremia with Respect to Use of Diuretics
|
Diuretics used |
Diuretics not
used |
P value |
Intake (mL/kg/day)
|
95.0 (31-199) |
105.0 (38-183) |
0.05 |
Urine
output (mL/kg/day) |
54.3 (15.4-166) |
60.9 (14.5-112.5) |
0.1 |
Fluid
balance (mL/kg/day) |
31.6 (–20.5-179.0) |
41.4 (3.2-316) |
0.2 |
Electrolyte free water intake (mL/kg/day) |
66.8 (13.9-176) |
89.7 (24.2-135.2) |
0.008 |
Sodium
intake (mEq/kg/day) |
2.0 (0.23-16) |
1.7 (0.08-14.4) |
0.08 |
Sodium
excretion (mEq/kg/day) |
3.5 (0.57-24.2) |
7.2 (1.9-20.1) |
0.005* |
Sodium
balance (mEq/kg/day) |
0.90 (–33.9-11.7) |
0.12 (–16.6-14.4) |
0.1 |
Values represent median (5th -95th
Centile); *Mann-Whitney U test. |
There were 8 deaths in the study population; 2 in
hyponatremic and 6 in those having serum sodium >130 mEq/L group (P=0.65).
None of the deaths were directly attributable to hyponatremia.
Discussion
The incidence of hyponatremia in study population was
3.5 episodes/100 patient days. The difference in incidence compared to
that reported previously by other authors is probably related to the lower
cut off values taken for definition of hypo- natremia ( £130
mEq/L in our study versus
£136
mEq/L in other studies)(5,6). Cut off of
£130
mEq/L was used by us because in a previous study we found it to be
associated with significant increase in mortality in sick children
attending pediatric emergencies(13).
We found that though the hyponatremic children were
hypo-osmolar with a net positive fluid balance, the magnitude of the
positive fluid balance, sodium balance and natriuresis in the days
preceding hyponatremia in these patients was similar to that of post
hyponatremic phase and those having serum sodium >130 mEq/L group. Over
expansion of intravascular space and dilutional hyponatremia usually
results from either an increased EFW intake or an impaired water
excretion(5). In our patients, the magnitude of EFW intake alone could not
explain the fall in serum sodium in all the patients. In fact the EFW
intake and fluid balance was lower in the hyponatremic group compared to
the normo-natremic group. Our observations are in contrast to the findings
reported by Hoorn, et al.(6) and Moritz, et al.(9). The
former, in their retrospective study on hospital-acquired hyponatremia,
demonstrated that intake of EFW in the form of hypotonic infusions was a
major cause for fall in serum sodium. These authors felt that though SIADH
was a part and parcel of critical illness, hyponatremia occurred only in
the setting of an associated increased water intake(6). This hypothesis
was supported by the latter group, which demonstrated that administration
of hypotonic fluids was the main contributor to hospital-acquired
hyponatremia(9).
These reports had challenged the conventional practice
of use of hypotonic maintenance fluids and suggested that these be
replaced by isotonic saline(6,9,18). This, however, could not be accepted
universally because of contrasting concerns. First concern is the ongoing
natriuresis, which may negate the effect of this intervention(19,20).
Giving intravenous isotonic saline solutions to acutely ill children leads
to more sodium excretion than water(6,11,19). The other is the risk of
sodium overload and hypernatremia in presence of isotonic fluids in
children due to their minimal excretory capacity of sodium(21,22).
Impaired excretion of free water, as a result of SIADH
secondary to various osmotic and non-osmotic stimuli is a common event in
critically ill children(23). Excessive ADH production may cause secondary
increase in net urinary sodium loss (desalination), which is attributed to
suppression of aldosterone caused by SIADH mediated water retention and
over expansion of the intravascular space(24). Hence, hyponatremia
in the setting of SIADH is primarily dilutional while secondary
natriuresis sustains the hyponatremia. Though the findings in our
hyponatremic group could be explained on the basis of SIADH, this does not
explain why those having serum sodium >130 mEq/L group with similar fluid
and sodium balance did not become hyponatremic. This, therefore, points to
contribution from an alternative mechanism, other than water retention,
increased water input or excessive natriuresis.
Hyponatremia could occur due to redistribution of
sodium without an actual loss. An intracellular shift of sodium chloride
and water has been shown in an experimental model of early septic
shock(25). A combination of intracellular shift of sodium and dilution of
extracellular spaces due to water retention in this model resulted in
hyponatremia and hypoosmolarity(26). Increase in RBC sodium coinciding
with hyponatremia in sick septicemic children further substantiates this
mechanism of translocation(27).’Sick cell hypothesis’ may be other
mechanism for hyponatremia; in critically ill patients; intracellular
solutes may leak out of the cell due to increased membrane permeability
causing redistribution hyponatremia, with an increased osmolar gap(28,29).
Indeed, ‘osmolar gap’ hyponatremia has been postulated as a mechanism in
more than 50% of hyponatremic episodes in adult ICU patients(28,29). Since
we did not find enough evidence to suggest significant EFW excess or
natriuresis to explain the fall in sodium, we postulate that translocation
and redistribution could have been a possible mechanism in our patients.
This may also possibly explain the normal or high osmolality in some of
our patients in the absence of hyperglycemia or mannitol therapy. This
argument is further supported by our previous observations on pneumonia
and meningitis patients(14,15); hyponat-remia that was present at
admission in these patients corrected itself over 3-5 days concomitant
with recovery from illness while the patients were receiving 0.18% saline
in 5% dextrose as maintenance fluid.
There are some limitations in this study. The study
sample was small, which may have limited the significance of differences
in hyponatremic and non-hyponatremic group with respect to EFW intake and
sodium excretion. The cut off value of hyponatremia was
£130
mEq/L, in contrast to
£135 mmol/L, which might have
influenced the incidence of hyponatremia in our study.
To conclude, our findings do not support the contention
that use of conventional hypotonic maintenance fluids is the main cause of
hyponatremia in critically ill children. Whether an alternative mechanism
such as translocation and/or redistribution of sodium contributes to
hyponatremia in sick children needs further investigation.
Contributors: SS was involved with the study
planning, design and writing of the manuscript. JM was involved with the
data analysis and writing of the manuscript.
Funding: None.
Competing interest: None stated.
What is Already Known?
• Hyponatremia in hospitalized critically ill
patients is attributed to free water excess resulting from impaired
free water excretion and use of conventional maintenance fluids.
What this Study Adds?
• It does not support the contention that use of conventional
maintenance fluid (0.18% saline in 5% dextrose) is the main cause of
hyponatremia in such patients. |
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