multiple electrolyte and metabolic emergencies in a...
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Case ReportMultiple Electrolyte and MetabolicEmergencies in a Single Patient
Caprice Cadacio,1 Phuong-Thu Pham,2 Ruchika Bhasin,1
Anita Kamarzarian,1 and Phuong-Chi Pham1
1Olive View-UCLA Medical Center, 14445 Olive View Drive, 2B-182, Sylmar, CA 91342, USA2Ronald Reagan UCLA Medical Center, 200 Medical Plaza, Los Angeles, CA 90095, USA
Correspondence should be addressed to Phuong-Chi Pham; [email protected]
Received 12 December 2016; Accepted 12 January 2017; Published 31 January 2017
Academic Editor: Yoshihide Fujigaki
Copyright © 2017 Caprice Cadacio et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.
While some electrolyte disturbances are immediately life-threatening and must be emergently treated, others may be delayedwithout immediate adverse consequences. We discuss a patient with alcoholism and diabetes mellitus type 2 who presentedwith volume depletion and multiple life-threatening electrolyte and metabolic derangements including severe hyponatremia(serum sodium concentration [SNa] 107mEq/L), hypophosphatemia (“undetectable,” <1.0mg/dL), and hypokalemia (2.2mEq/L),moderate diabetic ketoacidosis ([DKA], pH 7.21, serum anion gap [SAG] 37) and hypocalcemia (ionized calcium 4.0mg/dL), mildhypomagnesemia (1.6mg/dL), and electrocardiogram with prolonged QTc. Following two liters of normal saline and associatedincrease in SNa by 4mEq/L and serum osmolality by 2.4mosm/Kg, renal service was consulted. We were challenged withminimizing the correction of SNa (or effective serum osmolality) to avoid the osmotic demyelinating syndrome while replacingvolume, potassium, phosphorus, calcium, and magnesium and concurrently treating DKA. Our management plan was furthercomplicated by an episode of significant aquaresis. A stepwise approach was strategized to prioritize and correct all disturbanceswith considerations that the treatment of one condition could affect or directly worsen another.The current case demonstrates thata thorough understanding of electrolyte physiology is required in managing complex electrolyte disturbances to avoid disastrousoutcomes.
1. Introduction
Managing various electrolyte and metabolic disturbances isgenerally a simple task for nephrologist. However, in complexcases, one must be vigilant of potentially life-threateninginteractions among multiple simultaneous treatment plansand cautiously formulate a comprehensive treatment algo-rithm to prevent disastrous outcomes.
2. Case Report
Clinical History. A 33-year old male with known alcoholabuse and diabetes mellitus type 2 presented with a two-day history of nausea, vomiting, watery diarrhea, and lightheadedness. Patient denied fevers and chills but endorsedmild midepigastric dull pain and poor oral intake.
Physical Exam. Temperature was 37.2∘C, blood pressure114/85mmHg, heart rate 109 beats per minute, respiratoryrate 22 per minute, and oxygen saturation 98%. Patient wasacutely ill-appearing, slow in verbal responses, alert andoriented, and free of stigmata of advanced liver disease. Oralmucosa was dry. Heart exam was notable for tachycardia.Lungs were clear bilaterally. Abdomen had hypoactive bowelsounds and mild midepigastric tenderness without guardingor rebound. Extremities were significant for a few ecchy-moses. Neurological exam was nonfocal.
Initial Laboratory Data. Serum chemistries at presentationand hospital course are presented in Table 1. Most notableabnormalities included serum sodium (SNa) 107mEq/L,potassium (SK) 2.8mEq/L, total CO
212mEq/L, glucose
331mg/dL, and anion gap (SAG) 37mEq/L. Others were
HindawiCase Reports in NephrologyVolume 2017, Article ID 4521319, 6 pageshttps://doi.org/10.1155/2017/4521319
2 Case Reports in Nephrology
Table1:Clinicaldata.
Serum
chem
istry
Admission
Afte
r2Lno
rmal
salin
e(renalservice
was
consulted)
12to
14ho
urs
after
admission
8ho
ursa
fterinsulin
administratio
n(30to
32ho
ursa
ftera
dmission)
Disc
harge(12
days
after
admission)
Totalamou
ntreplaced
durin
gho
spita
lization
Electro
lyteconcentrations
offlu
idsa
dministered
Sodium
(mEq
/L)
107
111
113
117132
2literso
fnormalsalin
eatpresentatio
n154m
Eq/L
Potassium
(mEq
/L)
2.8
2.2
2.9to
3.2
2.7
4.5
480m
EqKC
l100m
Eq/L
TotalC
O2
(mEq
/L)
1211
614
25Corrected
with
insulin
Serum
aniongap
(mEq
/L)
3731
3019
10Corrected
with
insulin
—
Glucose
(mg/dL
)331
248
250
108
217
Corrected
with
insulin
—
Phosph
orus
(mg/dL
)Not
done
<1.0
<1.0
<1.0
5.5
240m
molKP
O4
15mmolmixed
in200m
Lno
rmalsalin
eorfreew
ater
asneeded
toachieve
sodium
correctio
ngoal
Totalcalcium
(mg/dL
)7.2
6.9
6.8
6.8
8.4
4gcalcium
glucon
ate
(9.3mmol)
10%solutio
nIonizedcalcium
(mg/dL
)[no
rmal
4.6–
5.4]
4.1
Not
done
4.0
Not
done
Not
done
Magnesiu
m(m
g/dL
)1.6
Not
done
3.1
Not
done
1.78g
4gmixed
in250m
Lno
rmalsalin
e
Case Reports in Nephrology 3
mild transaminitis, mildly elevated lipase, and hemoglobin12 g/dL.
Renal service was consulted following the increase inSNa from 107 to 111mEq/L over one hour (effective serumosmolality [Sosm] increase of 2.4mosm/Kg) with the admin-istration of two liters of normal saline.
Additional Investigations. Renal service requested STATserum phosphorus and magnesium which resulted as<1mg/dL and 1.6mg/dL, respectively. Other findings weremoderate serum ketones, lactic acid 1mmol/L, and Sosm255mosm/Kg (serum osmolality gap 6mosm/Kg).
Venous Blood Gas at Six Hours following Presentation toEmergency Department (ED). pH was 7.40, pCO
217mmHg,
and HCO310mEq/L (SAG 31mEq/L), and at thirteen hours,
pH was 7.21, pCO214mmHg, and HCO
36mEq/L (SAG
30mEq/L). Urine studies show osmolality 450mosm/Kg,sodium 25mEq/L, and potassium 25mEq/L.
Diagnoses. Diagnoses included volume depletion, diabeticketoacidosis (DKA) (with initial concurrent metabolic andrespiratory alkaloses), severe hyponatremia, hypokalemia,hypophosphatemia, mild to moderate hypocalcemia, andmild hypomagnesemia.
Clinical Follow-Up. Patient received emergent potassiumchloride (KCl) infusion via a central line (200mL/hr of100mEq/L KCl solution [total 480mEq KCl]) and potas-siumphosphate (KPO
4) (total 240mmol),magnesium sulfate
(total 8 g), and calcium gluconate (total 4 g) via peripherallines. Oral thiamine and folate were given daily. All netfluid and effective solutes (sodium and potassium) wereclosely monitored. Calculations were performed (based onCurbsideConsultant.com) every six hours to readjust all fluidrates as needed to ensure a goal sodium correction rate of4–6mEq/L/24 hours. Treatment of DKA was intentionallydelayed until SK reached 2.9mEq/L to avoid insulin-drivenintracellular potassium uptake, exacerbation of hypokalemia,and precipitation of life-threatening arrhythmias.Onhospitalday 3, patient developed significant aquaresis with approx-imated free water clearance of 230 to 300mL/hr (urineoutput of 3140mL over 8 hour; urine studies: osmolality186mosm/Kg, sodium 13mEq/L and potassium 16mEq/L;SNa 122mEq/L). Twomicrograms of desmopressin (DDAVP)and two liters of electrolyte-free water were given intra-venously to slow urine output and prevent rapid overcorrec-tion of SNa, respectively. Over the first four hospital days, SNacorrected at an average of 5mEq/L/day. Additionally, patientalso underwent upper gastroendoscopy for gastrointestinalbleed and nausea which revealed diffuse gastritis, presumedto be induced by his chronic alcohol consumption.His nausearesolved with proton pump inhibitor and supportive care.
3. Discussion
The current case was challenged by multiple concurrentproblems including the need for continuing volume sup-port and substantial administration of both KCl and KPO
4
without rapidly correcting hyponatremia, optimization of
all treatable osmotic demyelinating syndrome (ODS) risks,correction of DKA to prevent respiratory decompensationwithout worsening the life-threatening hypokalemia, andintermittent infusions of magnesium sulfate and calciumgluconate while anticipating and managing any significantaquaresis without derailing the planned SNa correction rate.The algorithm for the comprehensivemanagement of currentpatient is summarized in Figure 1.
Hypokalemia was the most life-threatening and one offirst abnormalities to be treated emergently. Etiologies likelyincluded poor dietary intake, renal wasting given recent vom-iting and poorly controlled diabetes, and diarrhea. Imme-diate life-saving interventions included KCl infusion via acentral line along with instructions to avoid alkalinizationor administration of insulin or glucose-containing fluids, thelatter because of endogenous insulin secretion, and to preventintracellular K+-shift and worsening hypokalemia.
While aggressive potassium administration was critical,SNa level had to be closely monitored because potassiumeffectively increases SNa. Serum sodium concentration hasbeen shown to be directly proportional to the sum of totalexchangeable Na+ and K+ content [1]. Mechanisms wherebyK+ administration can raise SNa include the following [2]:
(1) intracellular K+-uptake induces an equivalent extra-cellular Na+-movement and hence increased SNa,
(2) parallel K+-Cl- intracellular uptake leads to increasedintracellular osmolality which leads to intracellularfree water shift and lower extracellular free watervolume and hence increased SNa, or
(3) intracellular K+-uptake induces an equivalent extra-cellular H+-movement to maintain electrical neutral-ity. While H+ can bind to the extracellular buffersystem and not perturb extracellular osmolality, theintracellular K+-gained increases intracellular osmo-lality and hence intracellular free water shift. Thelower extracellular free water volume increases extra-cellular SNa.
Given the direct effect of K+ on SNa, both sources of potas-sium, KCl and KPO
4, were accounted for in all calculations
for expected changes in SNa. Further sodium administra-tion was withheld because potassium supplement alonewas determined to be sufficient to correct hyponatremia.Failure to recognize this fact and unwarranted infusion ofsodium-containing solutions could have easily led to rapidhyponatremia overcorrection.
Hypophosphatemiamay be a risk factor for ODS [3]. Ourroutine hyponatremia treatment protocol requested a STATlevel, which was likely life-saving. Patient’s severe hypophos-phatemia could arise from poor oral intake, renal wasting,hypomagnesemia-induced skeletal resistance to parathyroidhormone (PTH 161 pg/mL, 1,25 (OH)
2vitaminD 146 pg/mL),
and possibly some degree of intracellular uptake associatedwith primary respiratory alkalosis at presentation [4]. Thelatter could induce intracellular alkalemia and associatedincreased glycolysis and intracellular uptake of phosphorusfor ATP production [5]. Phosphorus replacement was given
4 Case Reports in Nephrology
Initial presentation
Renal consult andmanagement
SeverehypophosphatemiaReplace
potassium as
Immediatecentral lineplacement
Normal serum potassium, phosphorus, sodium, and magnesium levels
Determine rate of correction goal based on ODS risksCheck serummagnesium,phosphorus
Resolution of diabetic ketoacidosis
Mildhypomagnesemia
Replacemagnesium as
Moderate diabeticketoacidosis
Severehypokalemia hyponatremia hypovolemia
Normocalcemia
Immediate intervention
Indirect therapy; indirect outcome Direct therapy; direct outcome
Immediate life-threatening conditions Nonimmediate life-threatening, but serious conditions
Diabeticketoacidosis with
increasingrespiratory
distress
Other supportive measures
Outcome per both direct and indirect therapies
Hold insulin,alkalinization, andglucose-containing
fluidadministration
Monitor urineoutput, sodium,and potassium;administer freewater & DDAVPand adjust KCl infusion rate as
needed
Administer insulinand glucose
support cautiouslyonce hypokalemia
becomes lesssevere
Continue to replace potassium
needed; monitor for appropriaterise in serum sodium and
accordingly adjust infusion rates
Moderate hypokalemia
Mild to moderatehypocalcemia
Euvolemia
Replacecalcium as
calciumgluconate
Replacephosphorus as
Supplementthiamine as
clinicallyindicated
ED bolus 2liters of
normal saline
(KCl and KPO4)
KPO4
and phosphorus (KPO4) as
∗∗Marked∗Severe
MgSO4
Figure 1: Algorithm for the treatment ofmultiple concurrent life-threatening disturbances. ∗For hyponatremia, correction resulted frombothpotassium infusion (indirect therapy) and fine adjustment with intermittent free water infusion and single administration of desmopressin(direct therapy) to achieve rate of correction goal during an episode of aquaresis. ∗∗For volume depletion, patient received two liters ofnormal saline on presentation to the emergency department (direct therapy) and continuous KCl infusion at 200mL/hour (indirect therapy,i.e., themain purpose for KCl infusion, was potassium replacement, but patient benefited from the infusion asmaintenance intravenous fluid)over the following 2 to 3 days while his oral intake was poor. ODS: osmotic demyelination syndrome; ED: emergency department; DDAVP:desmopressin.
emergently to avoid respiratory and cardiac arrest amongother potential serious complications.
Volume depletion is typically managed with normal saline(NS), but not in current case. Patient received predomi-nantly K+-containing fluids (200mL/hour of 100mEq/L KClsolution and 25 to 50mL/hour of KPO
4solution [15mmol
KPO4mixed in 200mL of either normal saline or sterile
water as indicated by SNa]). Since K+ is an effective solute,either K+ or Na+-containing solutions that are relatively iso-tonic to patient’s effective osmolality will effectively expandintravascular volume. With the exception of two liters of NSgiven in the ED, patient's total body volume was repletedand maintained with the infusion of K+-containing fluidsintended for potassium and phosphorus repletion. Failure torecognize the volume expansion capacity of relatively isotonicKCl-containing fluid and unwarranted infusion of NS forthe sole purpose of volume support would have complicatedthe treatment of hyponatremia. Additionally, high volumeinfusions of multiple fluids would have led to excess urinaryloss of ketone bodies necessary for bicarbonate productionwith insulin administration [6].
Hypocalcemia was likely due to poor nutrition, mal-absorption, and hypomagnesemia-induced hypoparathy-roidism [7, 8]. Given prolonged QTc, patient received lowdose calcium gluconate intravenously following the initiationof KPO
4administration to avoid any potential calcium-
induced worsening of severe hypophosphatemia via calciumphosphate precipitation.
Diabetic ketoacidosis was potentially life-threatening, butnot the most serious derangement. Insulin administrationwas intentionally delayed to avoidworsening of hypokalemia.
Patient’s respiratory status, however, was closely monitored.Once SK reached 2.9mEq/L, insulin was cautiously givento avoid respiratory failure as patient exerted high work ofbreathing to compensate for the metabolic acidosis. Within12 hours of insulin administration, SAG, likely all reflectingketone bodies, decreased from 30mEq/L to 19mEq/L witha parallel increase in total CO
2from 6 to 14mEq/L. The
rapid inverse change in SAG and total CO2demonstrates
perfectly how sufficient fluid resuscitation, not excessive fluidadministration with resultant urinary loss of serum ketonebodies, can allow for preservation of serum ketone bodies,where rapid hepatic conversion to bicarbonate occurs withinsulin administration [6]. Patient’s respiratory status alsoimproved significantly with correction of metabolic acidosis.
Hyponatremiawas likely multifactorial and includes con-tinuing free water intake in the presence of enhanced secre-tion of antidiuretic hormone (ADH) with volume depletionand/or inappropriate ADH secretion in the setting of nau-sea, “beer potomania,” and small degree of hyperglycemia-induced extracellular free water shift. The major goal inhyponatremia correction is ODS prevention. This requiresboth setting an appropriate correction goal and recognizingand optimizing any concurrent factors that could potentiatethe risk of developing ODS [3, 9]. The correction goalwas determined to be 4 to a maximum of 6mEq/L/daybecause of patient’s ODS risks including severe hypona-tremia, hypokalemia, alcoholism, hypophosphatemia, hypo-magnesemia, glucose intolerance, and presumed thiaminedeficiency [3, 9]. Routine assessment of reversible ODS riskfactors is warranted because electrolytes such as phosphorusand magnesium are not routinely measured at many institu-tions, including our own (Table 2).
Case Reports in Nephrology 5
Table2:Teaching
pointsbo
x.
Generalteaching
points
Com
mentspertinenttocurrentcase
Treatm
ento
fone
electrolyteor
metabolicabno
rmality
cancritically
worsen
another.In
apatient
with
multip
ledistu
rbances,ac
omprehensiv
emanagem
entp
lan
mustp
rioritizethe
mosttoleastlife-th
reateningdistu
rbance
andtre
ataccordingly.
Additio
nally,con
siderationmustb
emadefor
allp
ossib
letre
atmentinteractio
ns,
particularlywhenthetreatmento
falesscriticalproblem
canexacerbatea
life-threateningcond
ition
(i)Hypokalem
iaandhypo
phosph
atem
iawerethe
twomostlife-th
reatening
cond
ition
sincurrentp
atient.Since
thetreatmento
fdiabetic
ketoacidosis(D
KA)
with
insulin
with
orwith
outg
lucose
supp
ortcou
ldhave
exacerbatedthes
evere
hypo
kalemiaandprecipitatecardiaca
rrest,such
treatmentw
asintentionally
delay
ed.A
ggressivep
otassiu
mreplacem
entw
ithbo
thKC
land
KPO4to
achievea
saferserum
potassium
levelw
asdo
nePR
IORto
thetreatmento
fDKA
Comprehensiv
eprotocolfor
them
anagem
ento
fhypon
atremia:
(i)Determineo
smoticdemyelin
ationris
ks(O
DS)
andapprop
riaterateof
correctio
n(ii)A
ssessa
ndtre
atallcorrectableODSris
ks(hypokalem
ia,hypom
agnesemia,
hypo
phosph
atem
ia,alteredglucosem
etabolism
,and
clinicaln
eedforthiam
ine)
(iii)Und
ersta
ndthatpo
tassium
canincrease
serum
sodium
exactly
asifthes
ame
amou
ntof
sodium
isbeingadministered
(iv)M
onito
rurin
eoutpu
tand
itscontento
fsod
ium
andpo
tassium
fora
nypo
ssible
aquaretic
phase
(i)Whilehypo
natre
miawas
beingcorrectedwith
KCland
KPO4infusio
ns,the
immediateplan
tomon
itora
ndcorrectfactors[hypop
hosphatemiaand
hypo
magnesemia]a
ssociatedwith
high
ODSris
ksledto
thep
rompt
recogn
ition
ofsevere
andlife-threateninghypo
phosph
atem
ia(ii)Inadditio
nto
thec
orrectionof
concurrent
electrolytedistu
rbances,thiamine
supp
lementatio
nshou
ldbe
considered
inpatie
ntsw
ithmalnu
trition
oralcoho
lism
asthiamined
eficiency
hasb
eenim
plicated
inincreasin
gther
iskforO
DS
(iii)Cu
rrentp
atient’sserum
sodium
concentrationim
proved
asplannedwith
only
potassium-con
tainingflu
ids
(iv)A
ggressivem
onito
ringof
both
urineo
utpu
tand
contento
feffectivee
lectrolytes
(sod
ium
andpo
tassium)a
llowsfor
prom
ptinterventio
nandthus
preventio
nof
rapidover
correctio
nof
hypo
natre
mia
KClisa
seffectivea
sNaC
lsolutionas
avolum
eexp
andera
ndmay
bepreferredor
even
requ
iredwhenpo
tassium
iscritically
deficient
(i)Th
esub
stitutio
nof
KClfor
NaC
lsolutionforv
olum
eexp
ansio
ncanon
lybe
givenin
caseso
fsevereh
ypokalem
ia.Th
eratea
ndconcentrationof
theK
Clsolutio
nMUST
beadjuste
dto
assure
asafer
ateo
fincreaseinserum
sodium
(ii)N
otethata
maxim
umof
20mEq
ofKC
lmay
becontinuo
uslyinfusedperh
our
throug
hac
entralveno
uscatheter
Respira
tory
hyperventilationandmetabolicacidosisassociated
with
diabetic
ketoacidosisalon
emay
beeasilyandprom
ptlyreversed
with
thea
dministratio
nof
insulin
.Persis
tent
abno
rmalities
shou
ldthus
prom
ptan
evaluatio
nforo
ther
underly
ingetiologies
(i)Fo
llowingthea
dministratio
nof
insulin
,our
patie
nt’srespira
tory
statusimproved
from
arespiratory
rateup
tomid-30’s
breathsp
erminuted
ownto
mid-20’s
with
in24
hours
(ii)S
imilarly
,patient’sserum
totalC
O2im
proved
from
6to
14mEq
/Lwith
in8ho
urs
(iii)Note,ho
wever,close
mon
itorin
gof
potassium
mustb
edon
efollowinginsulin
andglucoses
uppo
rttherapy.With
theinitia
tionof
insulin
therapy,patie
nt’sserum
potassium
decreasedfro
mah
ighof
3.2m
Eq/L
to2.7m
Eq/L
with
in7ho
urs
6 Case Reports in Nephrology
In terms of actual hyponatremia correction, the infu-sion of potassium-containing solutions alone was sufficient.Patient’s SNa improved daily at expected rates from thepredominant infusions of KCl and KPO
4solutions (Table 1).
Additionally, as per our routine hyponatremia managementprotocol, monitoring of urine output, sodium, and potassiumwas done at regular intervals. Patient indeed developeda significant aquaretic phase when electrolyte-free waterand DDAVP were promptly given to divert hyponatremiaovercorrection. Significant aquaresis during the treatment ofhyponatremia may occur in multiple clinical settings andgenerally stems from the rapid cessation of ADH secretionfollowing the correction of underlying stimuli that inducedADH secretion like correction of volume depletion, nausea,pain, among others [10]. In current case, the aquaretic phasewas likely due to the correction of volume depletion andnausea.
Hypomagnesemia was likely due to poor oral intake,gastrointestinal malabsorption, and possibly urinary lossassociated with diabetes mellitus [11]. Patient was monitoredclosely for hypomagnesemia and treated as needed.
Thiamine was also supplemented given history of alco-holism to minimize ODS risk [4].
Respiratory and metabolic alkalosis on presentation werelikely due to pain/anxiety and volume depletion, respectively.Both conditions resolved with comprehensive supportivecare.
4. Conclusions
Wepresent a complex case involvingmultiple life-threateningelectrolyte and metabolic disturbances which demonstratesthe critical need for prioritization for the treatment of eachabnormality and considerations for all interactions amongmultiple concurrent treatment plans.
Aggressive potassium replacement prior to the adminis-tration of insulin for the DKA is vital to prevent worsening oflife-threatening hypokalemia.
Both sodium and potassium are equivalent effectivesolutes. Hyponatremia can be corrected with the predomi-nant infusion of potassium. Similarly, volume expansion withrelatively isotonic KCl solution is as effective as NaCl incurrent case of severe hypokalemia.
The treatment of hyponatremia must incorporate correc-tion rate, monitoring, and treatment of all factors (potassium,phosphorus, magnesium, glucose, and thiamine) associatedwith increased ODS risks. Additionally, during the treatmentof hyponatremia, transient aquaresis may arise for variousreasons and must be anticipated and immediately treated toavoid rapid overcorrection [11].
Insulin effectively converts ketone bodies to bicarbonateif the former have not been lost in the urine with excessivefluid administration.
Despite multiple life-threatening electrolyte and meta-bolic disturbances, patient was discharged within twelve daysin good condition and continued to do well at one monthfollow-up.
Teaching points are summarized in Table 2.
Competing Interests
The authors declare that they have no competing interests.
References
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[8] R. K. Rude, S. B. Oldham, and F. R. Singer, “Functionalhypoparathyroidism and parathyroid hormone end−organresistance in human magnesium deficiency,” ClinicalEndocrinology, vol. 5, no. 3, pp. 209–224, 1976.
[9] J. G. Verbalis, S. R. Goldsmith, A. Greenberg et al., “Diagnosis,evaluation, and treatment of hyponatremia: expert panel rec-ommendations,”TheAmerican Journal of Medicine, vol. 126, no.10, supplement 1, pp. S1–S42, 2013.
[10] P. C. Pham, P. V. Chen, and P. T. Pham, “Overcorrection ofhyponatremia: where do we go wrong?” American Journal ofKidney Diseases, vol. 36, no. 2, article no. E12, 2000.
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Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014
Research and TreatmentAIDS
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Gastroenterology Research and Practice
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Evidence-Based Complementary and Alternative Medicine
Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com