Quantitative approach in dysnatremias

Quantitative Approach in Dysnatremias
- a complementary tool for the busy intensivist -
13th November 2015

Assigning a context
 Define the determinants(“independent” variables) of plasma water sodium
 Define the physiological basis of sodium-related transport(e.g. Layton’s math-models of urine
concentrating mechanism, mammalian transporters, Gibbs-Donnan equilibrium,
intercompartmental dynamics-Hahn’s fluid distribution kinetics)
 Describe the generation of dysnatremias in terms of plasma water sodium determinants
 Classification, etiology and pathophysiology of dysnatremias
 Incidence, short and long-term prognosis of dysnatremias
 Clinical/pathological frame and implications of dysnatremias
 Diagnosis (differential) of dysnatremias (e.g. the never ending debate about CSW(Maesaka’s
RSW) vs SIADH – Stern’s salt “wanting” syndromes)
 Describe cell-volume related physiology and its clinical implications
 Build a quantitative-based framework to treat/prevent dysnatremias
 Devise new monitoring frameworks(e.g. trending the urinary uric fractional excretion
according to Maesaka’s algorithm to better delineate between SIADH-RSW)

Narrowing the context to hyponatremia
 Define the rules, pitfalls, risk factors inherent to hyponatremia correction
 Describe classical ill-derived equations to prevent/amend overcorrection and/or
perform/guide correction
 Provide a quantitative, physiologically – derived, still perfectible equation(“master equation”
or maybe just “intractable abracadabra” J Appl Physiol 101: 692–694, 2006) for understanding
plasma water sodium determinants
 Describe the shortcomings of equation-based ways to manage hyponatremias
 Describe a case naturally resembling a beaker - meant to be the ideal patient to be dealt with
when using an equation-based management
 Provide a solution whereby at least severely hyponatremic patients at high risk of
overcorrection-related complications might benefit from being artificially, temporarily
transformed into human beakers

You just cannot escape this anymore

Diagnosis, Evaluation, and Treatment of Hyponatremia: Expert Panel Recommendations-2013
Joseph G. Verbalis, Steven R. Goldsmith, Arthur Greenberg, Cynthia Korzelius, Robert W. Schrier, Richard H. Sterns, Christopher J. Thompson. The American Journal of Medicine (2013) 126, S1-
S42
Clinical practice guideline on diagnosis and treatment of hyponatraemia – 2014
Goce Spasovski, Raymond Vanholder, Bruno Allolio, Djillali Annane, Steve Ball, Daniel Bichet, Guy Decaux, Wiebke Fenske, Ewout Hoorn, Carole Ichai, Michael Joannidis, Alain Soupart, Robert
Zietse, Maria Haller, Sabine van der Veer, Wim Van Biesen and Evi Nagler on behalf of the Hyponatraemia Guideline Development Group. European Journal of Endocrinology (2014) 170, G1–
G47; Intensive Care Med. 2014 Mar;40(3):320-31; Nephrol Dial Transplant. 2014 Apr;29 Suppl 2:i1-i39
 most common disorder of electrolytes occurring in
15%-30% of acutely or chronically hospitalized
patients – Madias et al; Am J Med. 2006; 119:S30-
S35
 severe hyponatremia(serum [Naþ] <125 mmol/L)
more than doubled the risk of in-hospital mortality
(RR 2.10; P <.001) in an ICU with a overall mortality
rate of 37.7% - Bennani et al; Rev Med Interne.
2003;24:224-229
 Dissenting results as to whether chronic
hyponatremia is just a marker of the underlying
disease severity or is itself a risk factor - Chawla,
Sterns et al; Clin J Am Soc Nephrol. 2011
May;6(5):960-5
 Overall, chronic hyponatremia, not in the least
inconsequential, indirectly is proven to be a cause
of increased morbidity and mortality - Kinsella et
al; Clin J Am Soc Nephrol. 2010;5:275-280
 Classification according to biochemical and clinical
severity
 In terms of overall severity and therapeutic
management, the clinical picture will override the
biochemical one
 Defining target /aim and limit concepts
 Always aiming for the smallest increase needed to
effect a clinical improvement
 Low treshold for searching other explanations in
view of the low specificity of hyponatremia
associated symptoms
 Focus on defining acute versus chronic given the
risks related to brain volume autoregulation
 Low treshold for positing chronic instead of acute
with less than severe symptoms
 Greatly limiting the aim for acute hyponatremia-4
to 6 mmol/l/first 6h
 Setting a common aim of 4-6mmol/l /24h for acute
and chronic states but with a different time-scale
 Setting a limit at 8-10mmol/l/24h
 Describe high risk ODS patients
 Describe management for preventing ODS
R
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L
E
S

S42
six a day makes sense for safety; so six in six hours for severe sx’s and stop
Sterns RH, Hix JK, Silver S. Treating profound hyponatremia: a strategy for controlled correction. Am J Kidney Dis. 2010;56:774-779
R
U
L
E
S
R
U
L
E
S
 Adrogue HJ, Madias NE. The challenge of hyponatremia. J Am Soc
Nephrol. 2012
 Arampatzis S, Frauchiger B, Fiedler GM, et al. Characteristics,
symptoms, and outcome of severe dysnatremias present on hospital
admission. Am J Med. 2012

S42
S
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E
A
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D
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 Hypokalemia#Hyperkalemia
 Alcoholism
 Malnutrition
 Contextual SIADH
 Hypoxemia
 Low solutes(e.g.beerpotomania)#urea
 Corticoid deficiency-after substitution
 Hypothyroidism-after substitution
 Serum sodium<105mmol/l
 Advanced liver disease
►acute water diuresis(EFWC) is most often responsible for overcorrection◄
Mohmand et al,Clin J Am Soc Nephrol 2: 1110–1117, 2007

Reasons behind large positive EFWC
- contextual SIADH or non-osmotic induced ADH secretion-
 Undiagnosed hypovolemia is the most common feature of
overcorrectors
 Unpredictable time-dependent stimulation due to thiazide,
SSRI ►
 Stress,pain, exercise - related but in this case without
consequences due to the acute nature
 Hypothiroidism induced ADH-secretion(indirectly-low EABV)
 Glucorticoid deficiency induced ADH suppression failure
sAntidepressants
SSRIs
Tricyclic
MAOI
Venlafaxine
Anticonvulsants
Carbamazepine
Sodium valproate
Lamotrigine
Antipsychotics
Phenothiazides
Butyrophenones
Anticancer drugs
Vinca alkaloids
Platinum compounds
Ifosfamide
Melphalan
Cyclophosphamide
Methotrexate
Pentostatin
Antidiabetic drugs
Chlorpropamide
Tolbutamine
Miscellaneous
Opiates
MDMA (XTC)
Levamisole
Interferon
NSAIDs
Clofibrate
Nicotine
Amiodarone
Proton pump
inhibitors
Vasopressin
analogues
Desmopressin
Oxytocin
Terlipressin
Vasopressin

Urea as a protector and therapeutic strategy
- lessons from the elasmobranchs -
 Sharks are osmoconformers
 Have a low adaptability to outer osmolarity variation but still much higher than
predicted (high urea, high K)
 Urea has been proven to be a true antioxidant - Novel cardiac protective e€ffects of
urea: from shark to rat, Wang et al, Br. J. Pharmac., 1999
 Urea is known to act as a cryoprotector in amphibians - Cryoprotection by urea in
terrestrially hibernating frog, Constazo, J Exp Biol 2005; Urea loading enhances
freezing survival and postfreeze recovery in a terrestrially hibernating frog,
Constazo J Exp Biol 2008
400mOsm
1000mOsm/kg
Na
280 m0sm
K
7-14 m0sm

- icu beginnings -
EFWC = Vu × (𝟏 −
𝑼 𝑵𝑨 + 𝑼 𝑲
𝑷 𝑵𝑨
))
Vu =
𝒔𝒐𝒍𝒖𝒕𝒆 𝒆𝒙𝒄𝒓𝒆𝒕𝒊𝒐𝒏
𝑼𝒐𝒔𝒎
 Decaux, Soupart; Nephrol Dial Transplant (2007)
22: 1856–1863
 Decaux, Soupart, Critical Care 2010
 Decaux, Soupart; Nephron. 1993;63(4):468-70
 Decaux, Musch; Clin J Am Soc Nephrol 3: 1175–
1184, 2008.
 Soupart, Decaux; Clin J Am Soc Nephrol 7: 742–
747, 2012
 Reeth, Decaux; Clinical Science (1989) 77,35 1-
355
 Soupart, Decaux; Nephrol Dial Transplant (2007)
22: 1856–1863
 Decaux, J.L.Vincent; Annals of Intensive Care
2012
 Decaux, Soupart, Kidney International (2015) 87,
323–331; Urea minimizes brain complications
following rapid correction of chronic
hyponatremia compared with vasopressin
antagonist or hypertonic saline
‘Only a pathetic oaf would suggest anything so ludicrous. Putting back into the
body the final waste product of protein metabolism could only be deleterious!’
1950 (from Rocque, Neurosurgery 2012; 70: 1049–1054)

- context-sensitive osmolar effectiveness -
σ=0.5
σ=0.5
Sterns et al,Kidney International (2015) 87, 268–270

A tribute to the forerunners of urea treatment
1892
Friedrich W., Magy.orv.Arch.1:400-415,1892
Manucher J. Javid, MD.
1925
Crawford, Arch Intern Med (Chic).
1925;36(4):530541
Heart failure-
diuretic
The 1950’s
Manucher and Settlage
See review - Neurosurgery 70:1049–1054, 2012
ICP
management
1960s-
1970s
1980-
Guy Decaux, Alain Soupart
Belgium, Erasme
hNa+
management

 Know the cause, the subtype(e.g.pseudohyponatremia, hyperosmolar hypertonic
hyponatremia, RSW vs SIADH) or the probable course after having begun
correction(underlying hypovolemia )
 Frequently monitoring(plasma as well as urine Na, K; urine flow, total balance; even hourly
basis) with a limited possibilty for now to have a quasicontinuous urinary flow and electrolyte
monitoring(K.I.N.G. system, Italy-Milan, P.Caironi)
 Judicious use of equation based-forecasting(Adrogue-Madias, Barsoum-Levine, EFWC-
approach or the tonic balance approach, sodium deficit formula)
 Targeting normal-high potassium(4.5-5.5 mmol/l)
 Use urea in selected cases(e.g. euvolemic hyponatremia-SIADH)
 Avoid vaptans for chronic hyponatremia management
 Prompt counteraction of overcorrection(D5W, half normal saline, oral water input,
desmopressin) +/- CS►
Classical approach to minimize the risk of
overcorrection
Soichi Oya et al,Neurology November
27, 2001 vol. 57 no. 10 1931

Equation-driven correction of hNa+
𝑵𝒂 𝒅𝒆𝒇 = (𝑵𝒂 𝒂𝒄𝒕 − 𝑵𝒂𝒊𝒅 𝒆𝒂𝒍) × 𝑻𝑩𝑾
𝑵𝒂 𝟐=
𝑽𝒐𝒍𝒊𝒏𝒇×(𝑵𝒂𝒊𝒏𝒇+𝑲𝒊𝒏𝒇) + 𝑻𝑩𝑾×𝑵𝒂 𝟏
𝑻𝑩𝑾+𝑽𝒐𝒍𝒊𝒏𝒇
𝑵𝒂 𝟐=
𝑽𝒐𝒍𝒊𝒏𝒑𝒖𝒕× 𝑵𝒂𝒊𝒏𝒑𝒖𝒕+𝑲𝒊𝒏 𝒑𝒖𝒕 −𝑽𝒐𝒍 𝒐𝒖𝒕× 𝑵𝒂 𝒐𝒖𝒕+𝑲𝒐𝒖𝒕 + 𝑻𝑩𝑾×𝑵𝒂 𝟏
𝑻𝑩𝑾+∆𝑽𝒐𝒍
𝑵𝒂 𝟐 =
𝑵𝒂 𝟏 × 𝑻𝑩𝑾
𝑻𝑩𝑾 − 𝑬𝑭𝑾𝑪
Halperin’s tonicity balance – reply to EFWC
approach. Undistinguishable from BL.
Sodium deficit formula
Adrogue-Madias
Barsoum-Levine
Electrolyte free water formula
EFWC = Vu × (𝟏 −
𝑼 𝑵𝑨 +
𝑼 𝑲
𝑷 𝑵𝑨
)
Simplicity should have been the ultimate sophistication
+
Na1 =
𝑵𝒂 𝒆+𝑲𝒆
𝑻𝑩𝑾 𝟏
Na2 =
𝑵𝒂 𝒆+𝑲𝒆+∆(𝑵𝒂+𝑲)
𝑻𝑩𝑾 𝟏+∆𝑻𝑩𝑾
Na2 =
(𝑵𝒂 𝟏×𝑻𝑩𝑾 𝟏)+∆(𝑵𝒂+𝑲)
𝑻𝑩𝑾 𝟏+∆𝑻𝑩𝑾
 The orange equations are all derived from the blue one
 The blue equation is itself a marked oversymplification of
another one which we’ll deal with later(Edelman-derived by
Nguyen and Kurtz)
 Orange SDF psupp. that ∆TBW=0 – TBWsensibility is actually high
and does not suit as a model for 99.9% of all path. states
 Orange AM does not take into account anything but the
infusate. If output is large, then it would be futile to use it.
 Orange BL seems identical to the blue one. Indeed it is if you
discard e.g. metabolic water. Output refers to urine, drains,
vomiting etc. whilst input refers to iv, oral.
 The numerator Nae+Ke stands for total exchangeable sodium
and potassium which by definition (1958) is the sum of total
osmotically active as well as inactive sodium and potassium.
This sheds doubt on the blue equation(and therefore on all the
other) as Na(osm. active) cannot be the result of smth inactive.
 Orange EFWC psupp. that the kidney is the single most
important determinant of Nap. What if there is no urine output?
 Tzamaloukas et al, J Am Heart Assoc. 2013.
 Lindner et al, Nephrol Dial Transplant (2008) 23: 3501–3508
 Nguyen, Kurtz, Clin Exp Nephrol (2004) 8:12–16
 Nguyen, Kurtz, Clin Exp Nephrol (2005) 9:1–4
 Barsoum, Levine, Nephrol Dial Transplant (2002) 17:1176-1180
 Adrogue, Madias, J Am Soc Nephrol 23: 1140–1148, 2012
 Halperin et al, Crit Care Clin 18 (2002) 249 – 272
 Halperin et al, ICM Volume 27, Issue5/May 2001

Understanding Nae+Ke
- 1958 -
 98 patients were studied with “maximum heterogeneity in clinical and
metabolic status to to assure that any correlations between body composition
and serum electrolyte concentrations would have general validity”
 Isotope administration Na34 and K42
 D2O administration
 Regression equations obtained by least squares method
 Equilibrium time is never straightforward-main issue

Edelman’s results
- 1958 -
 Nap is a reflection of the ratio between the sum of monovalent cations (Na and K) and
TBW – the slope is ~1
 The y-intercept (Na for a ratio=0) “probably is a measure of the quantity of osmotically
inactive exchangeable sodium and potassium per unit of body water.”

Edelman revisited
Nguyen, Kurtz
What do the slope and the y-
intercept stand for in terms
of physiological significance?
Comprehensive
mathematical description of
factors determining Nap
Appreciation of the fact that
the slope as well as the y-
intercept might be variable
in certain disease states
Multiple equations derived
to serve particular issues e.g.
definition of an isonatric
urine
 Still perfectible in
terms of
mathematical
manipulation of
physiological
parameters
 Disease states
might be
characterized by
activation of
inactive pools or
vice versa(resistant
Na-HTN) # Nguyen
et al. J Appl Physiol
102: 445–447,
2007.
While there is still uncertainty regarding the 95% conf.interval of the slope and
y-intercept, the Nguyen&Kurtz formula “is worth one’s salt” (J Appl Physiol
100: 1105–1106, 2006;) as it highlights all Na-determinants.
Ring, Troels, J Appl
Physiol 101: 692–
694, 2006
INTRACTABLE
ABRACADABRA
Denmark, Aalborg
Dorrington, J Appl
Physiol 104: 569,
2008
PROOF or SPOOF
UK, Oxford
www.soapoperadigest.com
“The truth is in the spoof”
Napw =
𝑮
𝜣
×
𝑻𝑩𝑾
-
𝑮
𝜣
×
𝑵𝒂 𝟎𝒔𝒎 𝒊𝒏𝒂𝒄𝒕𝒊𝒗𝒆+𝑲 𝒐𝒔𝒎 𝒊𝒏𝒂𝒄𝒕𝒊𝒗𝒆
𝑻𝑩𝑾
−
𝑶𝒔𝒎𝑰𝑪𝑭+𝑶𝒔𝒎𝑬𝑪𝑭
𝑻𝑩𝑾
+ 𝑲𝒑𝒘 +
𝑶𝒔𝒎𝒐𝒍 𝒑𝒘
𝑽 𝒑𝒘
Napw = 𝟏. 𝟏𝟏 ×
𝑻𝑩𝑾
- 25.6

Edelman revisited
Nguyen, Kurtz
“The truth is in the spoof”
Napw =
𝑮
𝜣
×
𝑻𝑩𝑾
-
𝑮
𝜣
×
𝑻𝑩𝑾
−
𝑻𝑩𝑾
+ 𝑲𝒑𝒘 +
𝑽 𝒑𝒘
Napw = 𝟏. 𝟏𝟏 ×
𝑻𝑩𝑾
- 25.6
 G=correction factor as dictated
by Gibbs-Donnan equilibrium
(1.04)
 Θ=average osmotic coeffiecient
of osmotic salts(0.93)
 Nae, Ke=total exchangeable
cations(osm. Active + inactive)
 Osm = osmoles non Na, non K
 Pw=plasma water
 ICF=intracellular fluid
 ECF=extracellular fluid
(PW+ISF)
Nap = 𝟏. 𝟎𝟑 ×
𝑻𝑩𝑾
- 23.8Plasma has 93% water

𝑮
𝜣

𝑻𝑩𝑾

𝑻𝑩𝑾

𝑶𝒔𝒎 𝑰𝑪𝑭+𝑶𝒔𝒎𝑬𝑪𝑭
𝑻𝑩𝑾
 𝑲 𝒑𝒘

𝑽 𝒑𝒘
 Increase
 Increase
 Decrease
 Increase
 Decrease
 decrease▲
 With all parameters left
unchanged except for
𝑻𝑩𝑾
,
increasing this one will
translate into cation
inactivation and thereby a
plasma sodium decrease
 OsmECF + OsmICF (Ca2+,Mg2+ ,
organic cations, glucose etc)=
OsmISF + OsmPW + OsmICF OsmPW
will oppose the other two but
mass balance will eventually
favor a direct proportionality :
Napw versus
𝑶𝒔𝒎 𝑰𝑪𝑭+𝑶𝒔𝒎 𝑬𝑪𝑭
𝑻𝑩𝑾

Unforseen theoretical implications
Defining the role of albumin infusion
in cirrhosis-associated hyponatremia
Nguyen, Am J Physiol Gastrointest Liver Physiol
307: G229–G232, 2014
 “we have demonstrated for the first time that
changes in the [Alb] can directly lead to changes in
the [Na] due to the effect of Gibbs-Donnan
equilibrium. Our findings demonstrated that, for
each 1 g/dl increase in the plasma [Alb], plasma [Na]
is expected to increase by 1 mmol/l due to the Gibbs-
Donnan effect”

Unforseen clinical implications
“Fluid overconsumption or retention of a moderate fluid overload is the
‘easiest’ way to induce EAH. Loss of the electrolytes sodium and potassium
can be significant over time and in hot weather, and should be considered in
post-event rehydration. The most effective treatment of hyponatraemia
associated to exercise would be to induce excretion of EFW”

More than eleven equations
Nguyen et al, Kidney International, Vol. 68
(2005), pp. 1982–1993
just keep in mind that people cannot be beakers1

Numerators as well as denominators
- how to assess them both simultaneously -
+100
mmol
NaCl
1M
cation challenge test
Assess carefully any other ∆V and
∆E over the next 10-15 minutes
Adrogue and Madias, J Am Soc Nephrol 23:
1140–1148, 2012
Draw blood test, measure Nap1
Draw blood test, measure Nap2
Solve the 2
unknowns
Solve for (Nae+Ke) and TBW1
Use the values for further predictionsjust keep in mind that people cannot be beakers2
HOW MUCH?
Nap2 = 𝟏. 𝟎𝟑 ×
𝑵𝒂 𝒆+𝑲𝒆+𝟏𝟎𝟎
𝑻𝑩𝑾 𝟐+𝟎.𝟏
- 23.8
Nap1 = 𝟏. 𝟎𝟑 ×
𝑻𝑩𝑾 𝟏
- 23.8

Do they work?
 66 patients, 681 patient-days(194 hypernatraemic)
 Excellent output-input balance
 Day-per-day change in plasma sodium concentration
 Results are definitely not to be expanded to hyponatremic patients as per author’s conclusions

 all four formulae were inaccurate in the clinical setting for different reasons
 although there is a good correlation between the predicted and actual changes for the whole group, the formulae were
unable to predict changes in the serum sodium level in the individual patient and thus are not without risk in practice
 the analysis of major pathophysiological mechanisms (extrarenal and renal losses of electrolyte-free water, volume
status, etc) that contributes to hypernatraemia was more important for therapy guidance than all the proposed formulae
(see Halperin, Crit Care Clin 2002; 18:249–272)
just keep in mind that people cannot be beakers3

Some think they do
EFWC = Vu × (𝟏 −
𝑼 𝑵𝑨 + 𝑼 𝑲
𝑷 𝑵𝑨
))
↑EFWC

Are they really spoof or intractable abracadabra?
Napw =
𝑮
𝜣
×
𝑻𝑩𝑾
-
𝑮
𝜣
×
𝑻𝑩𝑾
−
𝑻𝑩𝑾
+ 𝑲𝒑𝒘 +
𝑽 𝒑𝒘
𝑵𝒂 𝟐=
𝑵𝒂 𝟐=
𝑽𝒐𝒍𝒊𝒏𝒑𝒖𝒕× 𝑵𝒂𝒊𝒏𝒑𝒖𝒕+𝑲𝒊𝒏𝒑 𝒖𝒕 −𝑽𝒐𝒍 𝒐𝒖𝒕× 𝑵𝒂 𝒐𝒖𝒕+𝑲𝒐𝒖𝒕 + 𝑻𝑩𝑾×𝑵𝒂 𝟏
►acute water diuresis (EFWC) is most often responsible for overcorrection◄
Mohmand et al, Clin J Am Soc Nephrol 2: 1110–1117, 2007
Spasovski et al, European Journal of Endocrinology (2014) 170, G1–G47
Verbalis et al, The American Journal of Medicine (2013) 126, S1-S42
just keep in mind that people cannot be
beakers
4

People actually can be turned into human
beakers.
 Sterns, Kidney International
(2009) 76, 587 – 589
 Kengne, Kidney International
(2009) 76, 614–621
Predictable,
constant UO
and Uosm.
Overcorrection of hNa+ is a medical emergency
- lessons learned from rats -

Human Beakers
Desmopressin 2-4mcg/6h
𝑵𝒂 𝟐=
𝑵𝒂 𝟐=
𝑽𝒐𝒍𝒊𝒏𝒑𝒖𝒕× 𝑵𝒂𝒊𝒏𝒑𝒖𝒕+𝑲𝒊𝒏𝒑 𝒖𝒕 −𝑽𝒐𝒍 𝒐𝒖𝒕× 𝑵𝒂 𝒐𝒖𝒕+𝑲𝒐𝒖𝒕 + 𝑻𝑩𝑾×𝑵𝒂 𝟏
Preemtively or as a rescue therapy
Rochester General Hospital, Professor Richard Sterns
Control UO and UOsm

Clin J Am Soc Nephrol 3: 331-336, 2008

Am J Kidney Dis. 61(4):571-578. 2013

 Frequent monitoring of UO, Nap, urinary electrolytes
 Use of 3% and less often higher than that
 Use of desmopressin 1-4mcg/6-8h preemtively
 Treat overcorrection as a medical EMERGENCY
 Eventually use D5W or 0.45 saline
 Use the 6 rule as an aim and limit the increase to 8-10mmol/24h
 Have a low treshold to declare at risk of ODS
 Have a low treshold to search for other explanations related to supposedly hyponatremia-
symptoms especially in case of moderate-mild hNa (biochemically)
 Search for causes of “contextual SIADH”
 May use an equation based management as long as frequent monitoring and clinical
judgement + physiological reasoning are not curtailed
 Avoid using vaptans – unpredictable behavior
 Potassium will increase Nap as per Edelman equation – fatal case review see Berl et al,
American Journal of Kidney Diseases, Vol 55, No 4 (April), 2010: pp 742-748
 In case of overcorrection you may use CS but primordial is reversing the Na increase
Controlled hyponatremia correction
- Sterns’ management -
 Sterns, Clin J Am Soc Nephrol 3: 331-336, 2008
 Sterns, Kidney International (2009) 76, 587 – 589
 Kengne, Kidney International (2009) 76, 614–621
 Sterns, Am J Kidney Dis 56:774-779. 2010
S42

People actually can be turned into human
beakers.

Quantitative approach in dysnatremias

Quantitative approach in dysnatremias

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