Exploration des troubles acido-basiques Approche …€¦ · Exploration des troubles...

Exploration des troubles acido-basiques

Approche du modèle de Stewart . . . .

Max GUILLOTRéanimation MédicaleHôpital de Hautepierre

O

OHHO

H3C

Lactates

Troubles Acido-Basiques

Production quotidienne d’acides :CO2 + H20 ➜ HCO3- + H+


Production quotidienne d’acides

Systêmes tampons :

HCO3-/CO2 (systême ouvert)Phosphore/Phosphate (systême fermé)Albumine/Albuminate (systême fermé)...



Systêmes tampons

Equation d’Henderson - Hasselbach

pH = pKa + log (Base/Acide)



Systêmes tampons

Equation d’Henderson - Hasselbach

pH = 6,10 + log (HCO3-/CO2)

Diagramme de Davenport

pH

HCO3-

7,40

24

pH

HCO3-

7,40

24


PaCO2 : 60 mmHg

40 mmHg

20 mmHg

pH

HCO3-

7,40

24

Acidose métabolique

40 mmHg

pH

HCO3-

7,40

24


20 mmHg

pH

HCO3-

7,40

24

Troubles mixtes

40 mmHg

Simple ou Mixte ?

Evaluer la compensation

Troubles métaboliques

Degré de réponse

Délai Limites

Acidose( ⬇ HCO3-)

▲PaCO2 =

1,3 x ▲HCO3-12 à 24 heures

PaCO2 =10 mmHg

Alcalose( ⬆ HCO3-)

▲PaCO2 =


PaCO2 = 55 mmHg

d’après C. Ichai. Désordres Métaboliques et Réanimation. Springer. 2010

Simple ou Mixte ?


Troubles respiratoires

Degré de réponse

Délai Limites

Acidose aiguë( ⬆ PaCO2)

▲PaCO2 =

0,1 x ▲HCO3-5 à 10

minutesHCO3- =30 mmHg

Acidose chronique( ⬆ PaCO2)

▲PaCO2 =


HCO3- = 45 mmHg


Simple ou Mixte ?


Troubles respiratoires

Degré de réponse

Délai Limites

Alcalose aiguë( ⬇ PaCO2)

▲PaCO2 =

0,2 x ▲HCO3-5 à 10

minutesHCO3- =18 mmHg

Alcalose chronique( ⬇ PaCO2)

▲PaCO2 =


HCO3- = 14 mmHg


Simple ou Mixte ?


amount of strong acid or base required tochange the SID to a new equilibrium pointwhere pH ! 7.40 and PCO2 ! 40 mm Hg.This relationship between SBE and SID isnot surprising. The term SID refers to theabsolute difference between completely (ornear completely) dissociated cations andanions. According to the principle of elec-trical neutrality, this difference is balancedby the weak acids and CO2 such that SIDcan be defined either in terms of strongions or in terms of the weak acids and CO2offsetting it. Of note, the SID defined interms of weak acids and CO2, which wassubsequently termed the effective SID (22),is identical to the buffer base term coinedby Singer and Hastings more than half acentury ago (8). Thus, changes in SBE alsorepresent changes in SID (19–21).

Metabolic Acidosis. Clearly, given theresults shown in Table 2, if intubationand mechanical ventilation have not al-ready performed on clinical grounds,they should be accomplished without de-lay. However, additional analysis of thedata in Table 2 is required. The next ap-propriate step is to examine the corrected

anion gap (AGc) or, better yet, the strongion gap (SIG). The time-honored aniongap (AG) is insufficient, as the exampleshould clearly illustrate. In the columnlabeled time 1, the AG is 15 mEq/L (or 11mEq/L if K" is ignored), a value that isclearly within the normal range, and yetthe plasma lactate concentration isgrossly abnormal. How can this be? Theanswer is that the “normal range” for theAG only applies when the conditions arenormal. Critically ill patients hardly everhave a normal AG.

The AG is calculated, or rather esti-mated, from the differences between theroutinely measured concentrations of se-rum cations (Na" and K") and anions(Cl# and HCO3

#) (23). Normally, this dif-ference or “gap” is made up by two com-ponents. The major component is theionic portion of the weak acids (A#)—essentially the charge contributed by al-bumin and, to a lesser extent, by phos-phate. The minor component is made upof strong ions, such as sulfate and lactate,whose net contributions are normally $2mEq/L. However, there are also unmea-

sured (by the AG) cations, such as Ca2"

and Mg2", and these tend to offset theeffects of sulfate and lactate except wheneither is abnormally increased. Plasmaproteins other than albumin can be ei-ther positively or negatively charged butin the aggregate tend to be neutral (22)except in rare cases of abnormal parapro-teins, such as in multiple myeloma. Inpractice, the AG is calculated as follows:AG ! (Na" " K") # (Cl# " HCO3

#).Because of its low and narrow extra-

cellular concentration, K" is often omit-ted from the calculation. However, thistoo is insufficient for the critically ill.Patients in the intensive care unit mayhave serum K" concentrations rangingfrom 2 to 6 mEq/L, sometimes evenhigher. To assume that a 4-mEq/L rangecan be ignored is the same as assumingthat a 4-mEq/L concentration of unmea-sured anion can be ignored. As will beillustrated, such an assumption is haz-ardous. Respective normal values for theAG, with relatively wide ranges reportedby most laboratories, are 12 % 4 (if K" isconsidered) and 8 % 6 mEq/L (if K" isnot considered). What is considered thenormal AG has decreased in recent yearsfollowing the introduction of more accu-rate methods for measuring Cl# concen-tration (24, 25).

Many authors have raised doubtsabout the diagnostic value of the AG incertain situations (26, 27). The primaryproblem with the AG is its reliance on theuse of a so-called normal range producedby albumin and to a lesser extent phos-phate as discussed previously. These con-stituents may be grossly abnormal in pa-tients with critical illness, leading to achange in what is considered the normalrange for these patients. Moreover, be-cause these anions are not strong anions,their charge will be altered by changes inpH. This has prompted some authors toadjust the normal range for the AG by thepatient’s albumin and phosphate concen-tration. Each 1 g/dL albumin has acharge of 2.8 mEq/L at pH 7.4 (2.3 mEq/Lat 7.0 and 3.0 mEq/L at 7.6), and each 1mg/dL phosphate has a charge of 0.59mEq/L at pH 7.4 (0.55 mEq/L at 7.0 and0.61 mEq/L at 7.6). Thus, the AG must becorrected (or zeroed) to yield the AGc (5).

AGc ! ([Na " K] # [Cl " HCO3])

# (2[Albumin in g/dL)

" 0.5[Phosphate in mg/dL])

# Lactate [4]

Table 3. Acid-base patterns observed in humans

Disorder HCO3#, mEq/L PCO2, mm Hg SBE, mEq/L

Metabolic acidosis $22 ! (1.5 & HCO3#) " 8 $#5

Metabolic alkalosis '26 ! (0.7 & HCO3#) " 21 '"5

! 40 " (0.6 & SBE)Acute respiratory

acidosis! ([PCO2 # 40]/10) " 24 '45 ! 0

Chronic respiratoryacidosis

! ([PCO2 # 40]/3) " 24 '45 ! 0.4 & (PCO2 # 40)

Acute respiratoryalkalosis

! 24 # ([40 # PCO2]/5) $35 ! 0

Chronic respiratoryalkalosis

! 24 # ([40 # PCO2]/2) $35 ! 0.4 & (PCO2 # 40)

SBE, standard base excess.Reproduced with permission from Kellum (5).

Figure 1. Results of a computer simulation of in vivo CO2 titration curves for human plasma using thetraditional Van Slyke equation. In these simulations, CO2 is altered and the resulting pH and standardbase excess are plotted. The various curves are produced using different concentrations of total weakacids (ATOT) from normal (17.2) to 25% of normal. Also shown is the titration curve using theATOT-corrected standard base excess (SBEc). Reproduced with permission from Kellum (21).

2632 Crit Care Med 2007 Vol. 35, No. 11

Kellum. Crit Care Med. 2007

Intérêt du Base Exces (BE) ?

Détecter un trouble métabolique en cas de trouble ventilatoire

Quantité d’acides ou de bases fortes pour normaliser le pH un sang oxygéné, maintenu à température 37°C en présence d’une PCO2 à 40 mm Hg

Simple ou Mixte ?

Intérêt du Base Exces (BE) ?

Détecter un trouble métabolique en cas de trouble ventilatoire

Quantité d’acides ou de bases fortes pour normaliser le pH un sang oxygéné, maintenu à température 37°C en présence d’une PCO2 à 40 mm Hg

Mauvaise prise en compte des tampons faibles

Simple ou Mixte ?

pH

HCO3-

7,40

24

Troubles complexes

pH

HCO3-

7,40

24


PaCO2 : 60 mmHg

40 mmHg

20 mmHg

Acidose Métabolique

Alcalose Métabolique

Cas clinique n° 1

Cas clinique n°1

Patiente, 56 ans, admise pour coma

Retrouvée au sol, Glasgow 6,

Pas de témoin, de médicament, d’alcool, de CO

Pas signe de localisation

Phases d’agitation

Examen Cardio-Pneumo : sp

ATCD ?

Cas clinique n°1

Transférée en réa : VS sous O2 MHC

Examen neuro inchangé

Scanner cérébral : pas de lésion

EEG : tracé altéré, pas de crise

ATCD ?

Biologie

Cas clinique n°1

Biologie :

pH : 7,56 PaO2 186 mmHg PaCO2 55 mmHgHCO3- 30 mmol/L Lactates 0,8 mmol/L

Cas clinique n°1

Biologie :


1 - Hypothèses diagnostiques ?

2 - Démarche diagnostique ?


Première phase : Instauration

2 mécanismes :

H+ + HCO3-



2 mécanismes :

H+ + HCO3-Pertes de H+

DigestivesRénalesIntracellulaireAnesth-Réa



2 mécanismes :

H+ + HCO3-

Charge

DeshydratationPertes de H+



Deuxième phase : Entretien

H+ + HCO3-

Charge

Deshydratation

Excrétion Rénale ?

Pertes de H+



Deuxième phase : Entretien

H+ + HCO3-

Charge

Deshydratation

Excrétion Rénale ⬇:Réabsorption⬆

Sécrétion ⬇

Pertes de H+



Mécanismes de l’entretien :

Hypovolémie - Hyperladostéronisme

Réabsorption de Na+



Hypovolémie - Hyperladostéronisme

Réabsorption de Na+ + HCO3-



Hypochlorémie ➜ Hypochlorurie




Cl-H+ HCO3-ATP +

Cl-

Cellules A

Urin

esSang




H+HCO3- +

Cl-

Cellules B

Urin

esSang



Hypokaliémie



Hypokaliémie

Cl-H+ HCO3-ATP +

Cl-

Cellules A

Urin

esSang



Hypokaliémie

Cl-H+ HCO3-ATP +

Cl-

Cellules A

K+

H+ATPU

rines

Sang


Démarche diagnostique

Cause de l’instauration ?

Augmentation de HCO3-Perte d’acides

Mécanismes d’entretien ?

HypovolémieHypochlorémieHypokaliémie



Contexte :

Prise de diurétiquesVomissementsDiarrhées - Adénome villeuxApports de BicarbonatesBPCO sous ventilation mécanique



Pas de contexte :

Evaluation du volume extracellulaire :



Pas de contexte :

Evaluation du volume extracellulaire :

Deshydratation : Diurétiques, Vomissements, Diarrhées

Pas de déshydratation :Hyperminéralocorticisme Ir



Comment évaluer le volume extra-cellulaire ?




Natriurése ?




Natriurése ?

NON!car :augmentée en cas de vomissementsaugmentée en cas de diurétiquesaugmentée en cas d’alcalose métabolique




Chlorurie ?

< 25 meq/L en cas de déshydratation

sauf si diurétiques ou hypokaliémie...




Chlorurie : < 25 meq/L > 40 meq/L

Vomissement Hyperminéralocorticisme Ir

Diurétiques (tardifs) Diurétiques (précoces)

Diarrhées Charge en HCO3-

Hypercapnie corrigée Hypokaliémie

Mucoviscidose Bartter et Gitelman

⬇Apports en Cl-

Cas clinique n°1

Biologie :


Iono urinaire : Chlore élevé

1 - Hypothèses diagnostiques ?

Diurétiques

Cas clinique n°1

Biologie :


Prise en charge ?

Traitement/Arrêt du facteur déclenchantTraitement du facteur d’entretien

Cas clinique n°2

Cas clinique n°2

Patient, 38 ans, inconscient à domicileDépressif, Tabac 15 PA, OH 50 g/j

A l’arrivée du SAMU : Glasgow à 3

Pas de signe de localisation

Cardio-Pneumo : sp

Pas de médicament, d’alcool, de CO

IOT puis transfert en réa

Cas clinique n°2

Pendant le transfert :

ACR sur TV : 10 minutes de MCE et 3 CEE

ECG : tachycardie sinusale

Cas clinique n°2

A l’arrivée en réanimation :

Examen inchangé

Scanner cérébral : sp

HypoTA : perfusion de Noradrénaline

Cas clinique n°2

Biologie :

GDS : pH 6,95 PaO2 85 mmHg PaCO2 34 mmHg HCO3- 9 mmol/L

Cas clinique n°2

Biologie :

GDS : pH 6,95 PaO2 85 mmHg PaCO2 34 mmHg HCO3- 9 mmol/L

Acidose métabolique : Cause ?

Cas clinique n°2

Biologie :

GDS : pH 6,95 PaO2 85 mmHg PaCO2 34 mmHg HCO3- 9 mmol/L Lactates 1,5 mmol/L

Cas clinique n°2

Biologie :


Acidose métabolique : Cause ?

Cas clinique n°2

Biologie :


Iono : Na+ 142 mmol/L K+ 4,5 mmol/L Cl- 102 mmol/L

Cas clinique n°2

Biologie :



Trou anionique : (Na+ + K+) - (Cl- + HCO3-)

Cas clinique n°2

Biologie :



Trou anionique : (142 + 4,5) - (9+102) : 36,5 mmol/L

Acidose métabolique à trou anionique augmenté


Na+

C+

Cl-

A-

Electro-neutralité

HCO3-

K+


Na+

C+

Cl-

A-

HCO3-

Trou Anionique Norme = 16 mmol/lK+


Na+

K+

C+

Cl-

AlbuminatePhosphate

UA-

A-

Trou Anionique Norme = 16 mmol/l

HCO3-


Na+

C+

Cl-

A-

Trou Anionique = 16 mmol/l

Avec TA normal :

HCO3-

K+


Na+

C+

Cl-

A-


Avec TA normal :Fuite de HCO3-

Charge acide

HCO3-

K+


Na+

C+

Cl-

A-


Avec TA normal :Fuite de HCO3-Diarrhée hauteFistule biliaireAcidose tubulaire

Charge acideInsuffisance rénale aiguëHyperchlorémieInsuffisance Surrénale Aiguë

HCO3-

K+


Na+

C+

Cl-

HCO3-

A-

Trou Anionique > 16 mmol/l

Avec TA augmenté :

K+


Na+

C+

Cl-

HCO3-

A-


Avec TA augmenté :

AlbuminatePhosphate

HCO3-

K+ UA-


Na+

C+

Cl-

HCO3-

A-


Avec TA augmenté :

HyperlactatémieAcidocétoseInsuffisance rénaleIntoxications

Albuminate

UA-

Phosphate

HCO3-

K+

Cas clinique n°2

Biologie :


Iono : Na+ 142 mmol/L K+ 4,5 mmol/L Cl- 102 mmol/L, Urée 3,5 mmol/L Créat 70 µmol/LGlycémie 5,8 mmol/L

Cas clinique n°2

Biologie :



Cause : Intoxication (Méthanol / Ethylène-G)

Cas clinique n°2

Biologie :



Cause : Intoxication Isopropanolol (0,75g/L)

Cas clinique n°3

Cas clinique n°3

Patient admis en réanimation

Choc septique à point de départ pulmonaire

Biologie :

GDS : pH 7,31 PaO2 72 mmHg PaCO2 32 mmHgHCO3- 14 mmol/L

Acidose métabolique : Démarche diagnostique ?

Cas clinique n°3



Biologie :

GDS : pH 7,31 PaO2 72 mmHg PaCO2 32 mmHgHCO3- 14 mmol/L


Trou anionique : 14,5 mmol/L

Cas clinique n°3



Biologie :

GDS : pH 7,31 PaO2 72 mmHg PaCO2 32 mmHgHCO3- 14 mmol/L Lactates 10 mmol/L


Trou anionique : 14,5 mmol/L

Cas clinique n°3



Biologie :


Iono : Na+ 137 mmol/L K+ 4,2 mmol/L Cl- 113 mmol/L Albumine 16 g/L

Cas clinique n°3



Biologie :



Trou anionique corrigé : TA + 0,25 x (40-Alb)

Cas clinique n°3



Biologie :



Trou anionique corrigé : 14,5 + 0,25 x (40-16)

Cas clinique n°3



Biologie :



Trou anionique corrigé : 20,5 mmol/L

Quel soluté ?

Anesthésie pour Tx Rénale :

Hydratation per operatoire - 2 solutés possibles

NaCl 0,9% :

Na+ : 153 mmol/LCl- : 153 mmol/LK+ : 0 mmol/L

Ringer Lactate :

Na+ : 130 mmol/LCl- : 111 mmol/LLactate : 28 mmol/LK+ : 4 mmol/LCa2+ : 1,5 mmol/L

Modèle de Stewart

Modèle classique de description des TAB :

- ne repose que sur le tampon HCO3- / CO2

- les variables HCO3- et CO2 sont dépendantes

- limité dans les situations complexes

- repose sur une définition d’un acide

La recherche scientifique...


TAB


Théorie de BronstedAH ➜ A- + H+ Henderson - Hasselbach

TAB


Théorie de BronstedAH ➜ A- + H+ Henderson - Hasselbach

Théorie d’ArrhéniusModèle de Stewart

TAB

Modèle de Stewart

Electro-neutralité

∑A- ∑C+=

Modèle de Stewart

Equilibre de Dissociation de l’Eau

H2O H+ HO-+

Modèle de Stewart

Dissociation de l’eau et Electroneutralité

H+ HO-=

Modèle de Stewart

L’ajout d’un anion rompt l’électroneutralité

H+ HO-= A-

Modèle de Stewart

Les anions se comportent comme des acides

H+ HO-= A-

Modèle de Stewart

L’ajout d’un cation rompt l’électroneutralité

H+ HO-=C+

Modèle de Stewart

Les cations se comportent comme des bases

H+ HO-=C+

Modèle de Stewart

Théorie d’Arrhénius :Electroneutralité

Dissociation de l’eau

H+ HO-=∑C+ ∑A-

Modèle de Stewart

Augmentation des cations = Alcalose

H+ HO-=∑C+ ∑A-

Modèle de Stewart

H+ HO-=∑C+ ∑A-

Augmentation des Anions = Acidose

Modèle de Stewart

Electro-neutralité

∑A-∑C+

Modèle de Stewart

Electro-neutralité

∑A-

Na+

K+

Mg2+

Ca2+

Modèle de Stewart

Electro-neutralité

Na+

K+

Mg2+

Ca2+

Cl-

HCO3-

Albuminate-

Phosphate-

XA-

Modèle de Stewart

Electro-neutralité

Na+

K+

Mg2+

Ca2+

Cl-

HCO3-

Albuminate-

Phosphate-

Cations et anions dont la charge ne dépend pas du pH

Lactates-

Electro-neutralité

SIDapp : 40 meq/l

Modèle de Stewart

Na+

K+

Mg2+

Ca2+

Cl-

Strong Ion DifferenceSIDapp : SID apparant

Cations et anions dont la charge ne dépend pas du pH :

Ions forts

Lactates-

Electro-neutralité

SIDapp : 40 meq/l

Modèle de Stewart

Na+

K+

Mg2+

Ca2+

Cl-

Lactates-

Le SID est une des variables qui régule le pH

Electro-neutralité

SIDeff : 40 meq/l

Modèle de Stewart

Le SID est une des variables qui régule le pH

Na+

K+

Cl-

HCO3-

Albuminate-

Phosphate-

Mg2+

Ca2+SIDeff : SID effectif

XA-

Modèle de Stewart

SID apparent = (Na+ + K+ + Ca2+ + Mg2+) - (Cl- + Lactates-)

SID effectif = HCO3- + Albuminate- + Phosphate-

Albuminate- = (0,123 x pH - 0,631) x Albumine (g/l)

Phosphate- = (0,309 x pH - 0,469) x Phosphore (mmol/l)

SIDapp = SIDeff = 40 +/- 2 meq/l

Modèle de Stewart

Métabolique Respiratoire

pH HCO3- PaCO2

Acidose ➘ ➘ ➚

Alcalose ➚ ➚ ➘

Approche Classique

Modèle de Stewart

Approche Moderne

Métabolique Respiratoire

SID Atot PaCO2

Acidose ➘ ➚ ➚

Alcalose ➚ ➘ ➘

Modèle de Stewart

Patient admis pour choc septique sur pneumonie

Biologie :

pH : 7,40 PaCO2 : 39 mmHg HCO3- : 24 mmol/l

Na+ 140 mmol/l Cl- : 104 mmol/l K+ : 4,3 mmol/l

Approche classique ?

Modèle de Stewart


Biologie :



Approche classique ?

Pas de trouble acido-basique

Modèle de Stewart


Biologie :



Ca2+ : 1,8 mmol/l Mg2+ : 1 mmol/l Lactates : 4,9

Phosphore : 0,9 mmol/l Albumine 16 g/l

SIDeff = SIDapp = 35 meq/L ➜ Acidose métabolique

Albumine 16 g/L ➜ Alcalose métabolique

Quel Soluté ?

NaCl 0,9% :

Na+ : 153 mmol/LCl- : 153 mmol/LK+ : 0 mmol/L

Ringer Lactate :

Na+ : 130 mmol/LCl- : 111 mmol/LLactate : 28 mmol/LK+ : 4 mmol/LCa2+ : 1,5 mmol/L

Quel Soluté ?

NaCl 0,9% : Ringer Lactate :(Figs. 1, A and B). All five patients in the NS groupwith serum potassium concentrations larger than 6mEq/L were treated for hyperkalemia. The serumpotassium concentrations of the patients treated forhyperkalemia were 6.2 mEq/L, 6.6 mEq/L, 7.1mEq/L, 7.2 mEq/L, and 7.7 mEq/L.

Patients randomized to receive NS exhibited moremetabolic acidosis during surgery than patients whowere randomized to receive LR (Table 2). Eight (31%)patients in the NS group received sodium bicarbonatefor the treatment of metabolic acidosis in comparisonto no patients in the LR group (P ! 0.004). Within-group analysis of the NS group revealed that mean "sd lowest intraoperative blood pH in the patients whowere treated for metabolic acidosis was 7.20 " 0.09versus 7.28 " 0.06 in patients who were not treated formetabolic acidosis (P ! 0.01). The mean " sd lowestintraoperative blood pH in the LR group was 7.33 "0.07. Serum chloride concentration at the end of sur-gery was 111 " 4 mEq/L in the NS group versus 106" 4 in the LR group (P # 0.0001).

Of note, cumulative postoperative urine output waslarger (Fig. 2A) and postoperative serum creatininewas lower (Fig. 2B) in patients in the NS group whoreceived treatment for acidosis compared with patientswho received no treatment for acidosis. The serum chlo-ride concentration in patients who received bicarbonatewas 113 " 4 mEq/L versus 110 " 4 mEq/L in patientswho did not receive bicarbonate (P ! 0.1).

Urine flow rate (range) in the first 4 h after revas-cularization of the donor kidney was 400 " 370 (130–1050) mL/h in patients treated for hyperkalemia and370 " 410 (0–1520) mL/h in NS-treated patients withno hyperkalemia (P ! 0.9). One patient received treat-ment for both hyperkalemia and metabolic acidosis.One patient in the NS group who received a transfu-sion of packed red blood cells was treated for hyper-kalemia, and no patients who received blood transfu-sions were treated for metabolic acidosis.

DiscussionThis is the first study that has compared the effects ofNS and LR as IV fluid therapy in kidney transplant

recipients. There was no significant difference be-tween groups in the primary outcome measure of theserum creatinine on POD 3. The study was terminatedbecause of concerns for patient safety. However, ourresults strongly suggest that the administration oflarge volumes of LR to patients undergoing kidneytransplantation is safe and that LR may be superior toNS for IV fluid therapy in this setting. These resultshave important implications for patient managementbecause more than 10,000 kidney transplants are per-formed annually in the United States, with manythousands more conducted world wide each year (15).

Table 2. Postoperative Renal Function

NS (n ! 26) LR (n ! 25)

4-h urine output, L 1.6 " 1.6 2.1 " 1.524-h creatinine clearance, mL/min 81 " 41 94 " 30Postoperative Day 3 serum creatinine, mg/dL 2.3 " 1.8 2.1 " 1.71-wk serum creatinine, mg/dL 1.9 " 1.2 1.6 " 1.36-mo serum creatinine, mg/dL 1.5 " 0.6 1.5 " 0.4Patients requiring dialysis, No. (%) 2 (8) 1 (4)

Data are mean " sd unless otherwise stated.NS ! 0.9% NaCl (normal saline) group; LR ! lactated Ringer’s solution group.

Figure 1. Perioperative potassium concentrations in (A) LR- and (B)NS-treated patients. NS ! 0.9% NaCl; LR ! lactated Ringer’s solution

ANESTH ANALG O’MALLEY ET AL. 15212005;100:1518–24 0.9% NACL OR LACTATED RINGER’S SOLUTION DURING KIDNEY TRANSPLANT

(Figs. 1, A and B). All five patients in the NS groupwith serum potassium concentrations larger than 6mEq/L were treated for hyperkalemia. The serumpotassium concentrations of the patients treated forhyperkalemia were 6.2 mEq/L, 6.6 mEq/L, 7.1mEq/L, 7.2 mEq/L, and 7.7 mEq/L.

Patients randomized to receive NS exhibited moremetabolic acidosis during surgery than patients whowere randomized to receive LR (Table 2). Eight (31%)patients in the NS group received sodium bicarbonatefor the treatment of metabolic acidosis in comparisonto no patients in the LR group (P ! 0.004). Within-group analysis of the NS group revealed that mean "sd lowest intraoperative blood pH in the patients whowere treated for metabolic acidosis was 7.20 " 0.09versus 7.28 " 0.06 in patients who were not treated formetabolic acidosis (P ! 0.01). The mean " sd lowestintraoperative blood pH in the LR group was 7.33 "0.07. Serum chloride concentration at the end of sur-gery was 111 " 4 mEq/L in the NS group versus 106" 4 in the LR group (P # 0.0001).

Of note, cumulative postoperative urine output waslarger (Fig. 2A) and postoperative serum creatininewas lower (Fig. 2B) in patients in the NS group whoreceived treatment for acidosis compared with patientswho received no treatment for acidosis. The serum chlo-ride concentration in patients who received bicarbonatewas 113 " 4 mEq/L versus 110 " 4 mEq/L in patientswho did not receive bicarbonate (P ! 0.1).

Urine flow rate (range) in the first 4 h after revas-cularization of the donor kidney was 400 " 370 (130–1050) mL/h in patients treated for hyperkalemia and370 " 410 (0–1520) mL/h in NS-treated patients withno hyperkalemia (P ! 0.9). One patient received treat-ment for both hyperkalemia and metabolic acidosis.One patient in the NS group who received a transfu-sion of packed red blood cells was treated for hyper-kalemia, and no patients who received blood transfu-sions were treated for metabolic acidosis.

DiscussionThis is the first study that has compared the effects ofNS and LR as IV fluid therapy in kidney transplant

recipients. There was no significant difference be-tween groups in the primary outcome measure of theserum creatinine on POD 3. The study was terminatedbecause of concerns for patient safety. However, ourresults strongly suggest that the administration oflarge volumes of LR to patients undergoing kidneytransplantation is safe and that LR may be superior toNS for IV fluid therapy in this setting. These resultshave important implications for patient managementbecause more than 10,000 kidney transplants are per-formed annually in the United States, with manythousands more conducted world wide each year (15).

Table 2. Postoperative Renal Function

NS (n ! 26) LR (n ! 25)

4-h urine output, L 1.6 " 1.6 2.1 " 1.524-h creatinine clearance, mL/min 81 " 41 94 " 30Postoperative Day 3 serum creatinine, mg/dL 2.3 " 1.8 2.1 " 1.71-wk serum creatinine, mg/dL 1.9 " 1.2 1.6 " 1.36-mo serum creatinine, mg/dL 1.5 " 0.6 1.5 " 0.4Patients requiring dialysis, No. (%) 2 (8) 1 (4)

Data are mean " sd unless otherwise stated.NS ! 0.9% NaCl (normal saline) group; LR ! lactated Ringer’s solution group.

Figure 1. Perioperative potassium concentrations in (A) LR- and (B)NS-treated patients. NS ! 0.9% NaCl; LR ! lactated Ringer’s solution


determine the safety of the administration of LR topatients undergoing kidney transplantation throughsecondary end-points, including the serum potassiumconcentration and acid-base balance.

MethodsThe study was approved by the IRB of the ColumbiaPresbyterian Hospital of the New York PresbyterianHospital. After written, informed consent was ob-tained, eligible patients undergoing kidney transplan-tation were randomized in a prospective, double-blindfashion to receive either NS (Table 1) or LR (Table 1)for intraoperative fluid replacement during surgeryfor kidney transplantation. Randomization wasachieved by computer generation of random numberlists, in blocks of four, and a closed envelope tech-nique. Separate randomization lists were compiled forthe two surgeons who performed all kidney trans-plant operations. Exclusion criteria were age !18 yrold, a religious or ethical prohibition from the receiptof blood or blood products, or serum potassium level"5.5 mEq/L before surgery.

General anesthesia was induced with a combinationof IV midazolam (2–5 mg), fentanyl (1–3 !g/kg), andpropofol (1–3 mg/kg). Anesthesia was maintained us-ing isoflurane in air/oxygen and fentanyl, with mus-cle relaxation achieved using IV intermediate-actingnondepolarizing neuromuscular blockers. Standardmonitoring, according to the recommendations of theAmerican Society of Anesthesiologists, was used. It is

routine at our institution to insert a radial arterialcannula after the induction of anesthesia for monitor-ing of systemic arterial blood pressure and for bloodsampling during surgery. Additional monitoring (e.g.,central venous pressure monitoring) was at the discre-tion of the physician caring for the patient.

For living donor transplantation, the left kidney wasprocured from living donors via a laparoscopic ap-proach unless otherwise indicated. The donor kidneywas flushed with ice cold LR before transfer to theoperating room for implantation into the recipient.Kidneys harvested from cadaveric donors were pre-served with either Euro-Collins or University of Wis-consin solution for the duration of transfer to ourcenter. The donor kidney was implanted in the rightor left retroperitoneal space of the recipient with vas-cular anastomoses to the right or left external or inter-nal iliac artery and vein. A dopamine infusion wascommenced at 2 !g · kg#1 · min#1 (this infusion wasdiscontinued on arrival to the postanesthesia careunit). Ureteroneocystostomy was performed by theestablished Leadbetter-Politano (13) or Lich-Gregoirtechnique (14).

Preoperative and postoperative immunosuppres-sive therapy was administered according to institu-tional guidelines. Briefly, all patients received tripletherapy comprising tapering-dose steroids, a cal-cineurin inhibitor, and either mycophenolate mofetilor sirolimus. The clinician caring for the patient deter-mined the precise combination and dose ofmedications.

Table 1. Demographic and Perioperative Variables

NS (n $ 26) LR (n $ 25) P-value

Age, y 44 % 13 44 % 11 nsSex, No. (%) men 17 (65) 15 (60) nsWeight, kg 72 % 14 75 % 18 nsLiving donor, No. (%) 25 (96) 23 (92) nsPatients requiring preoperative hemodialysis, No. (%) 18 (69) 13 (52) nsVolume of study fluid, L 6.1 % 1.2 5.6 % 1.4 nsOperating room time, h 5.6 % 1.1 5.6 % 1.3 nsWarm ischemia time, min 34 % 13 34 % 9 nsPatients receiving intraoperative dopamine, No. (%) 23 (85) 20 (80) nsBlood loss, mL 309 % 162 310 % 190 nsPatients transfused, No. (%) 3 (11) 2 (8) nsBaseline serum creatinine, mg/dL 7.0 % 2.7 8.0 % 2.6 nsBaseline serum potassium, mEq/L 4.2 % 0.7 4.5 % 0.5 nsPeak intraoperative serum potassium, mEq/L 5.1 % 1.1 5.1 % 0.6 nsEnd of surgery serum potassium, mEq/L 4.5 % 0.8 4.6 % 0.6 nsBaseline pH 7.39 % 0.05 7.36 % 0.08 nsLowest intraoperative pH 7.26 % 0.08 7.33 % 0.07 0.001End of surgery pH 7.28 % 0.07 7.37 % 0.07 !0.0001End of surgery serum chloride, mEq/L 111 % 4 106 % 4 !0.0001Baseline serum bicarbonate, mEq/L 22 % 5 22 % 6 nsLowest intraoperative serum bicarbonate, mEq/L 16 % 3 19 % 4 0.004End of surgery serum bicarbonate, mEq/L 18 % 3 21 % 4 0.007

Data are mean % sd unless otherwise stated.NS $ 0.9% NaCl (normal saline) group; LR $ lactated Ringer’s solution group.


0‘Maley et al. Anest Analg. 2005

Modèle de Stewart

Meilleure description de l’équilibre acido-basique ?

Prend en compte :

- les troubles ioniques : natrémie, chlorémie

- les tampons : albumine

Patients : état de choc, dénutrition, inflammation, remplissage vasculaire abondant

Modèle de StewartORIGINAL ARTICLE

Comparison of lactated Ringer’s solution and 0.9% saline inthe treatment of rhabdomyolysis induced by doxylamineintoxicationYoung Soon Cho, Hoon Lim, Seung Ho Kim. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

See end of article forauthors’ affiliations. . . . . . . . . . . . . . . . . . . . . . . .

Correspondence to:Dr Y S Cho, Department ofEmergency Medicine,Soonchunhyang UniversityBucheon Hospital, 1174,Jung-dong, Wonmi-gu,Bucheon-si, Gyeonggi-do420-020, Republic of Korea;[email protected]

Accepted 5 December 2006. . . . . . . . . . . . . . . . . . . . . . . .

Emerg Med J 2007;24:276–280. doi: 10.1136/emj.2006.043265

Objective: To compare the effectiveness and side effects of lactated Ringer’s solution (LR) and 0.9% saline(NS) in the treatment of rhabdomyolysis induced by doxylamine intoxication.Methods: In this 15-month-long prospective randomised single-blind study, after excluding 8 patients among97 doxylamine-intoxicated patients, 28 (31%) patients were found to have developed rhabdomyolysis andwere randomly allocated to NS group (n = 15) or LR group (n = 13).Results: After 12 h of aggressive hydration (400 ml/h), urine/serum pH was found to be significantly higherin the LR group, and serum Na+/Cl2 levels to be significantly higher in the NS group. There were nosignificant differences in serum K+ level and in the time taken for creatine kinase normalisation. The amount ofsodium bicarbonate administered and the frequency administration of diuretics was significantly higher in theNS group. Unlike the NS group, the LR group needed little supplemental sodium bicarbonate and did notdevelop metabolic acidosis.Conclusion: LR is more useful than NS in the treatment of rhabdomyolysis induced by doxylamineintoxication.

Doxylamine succinate is an antihistamine commonly usedas an over-the-counter drug to relieve insomnia, and hasan anticholinergic effect. In Korea, in urban emergency

departments doxylamine overdose accounts for 25% of visitsdue to drug overdose.1 This drug is relatively safe, but is knownto induce rhabdomyolysis.

Rhabdomyolysis induced by doxylamine overdose was firstreported in 1983,2 and Koppel et al3 described complicationsincluding rhabdomyolysis in 1987. It has been reported that theincidence of rhabdomyolysis induced by doxylamine overdosewas 5–57%, and that rhabdomyolysis can progress to acuterenal failure. Hence, early detection and treatment of rhabdo-myolysis is necessary to minimise kidney damage.4–6

Treatment of rhabdomyolysis induced by doxylamine over-dose is by aggressive hydration and urine alkalisation.Aggressive hydration with intravenous crystalloids such as0.9% saline (NS) or lactated Ringer’s solution (LR) at a rate of300–500 ml/h in an adult is essential. To date, it has beenbelieved that there is no difference in effectiveness between NSand LR.7 8

The development of renal failure in patients with rhabdo-myolysis has been linked to renal tubular damage from thetoxicity of myoglobin and haemoglobin decomposition pro-ducts. At urine pH (5.6, myoglobin dissociates into ferrihe-mate and globin. As ferrihemate has been demonstrated to bedirectly nephrotoxic, urine alkalisation is necessary to minimisekidney damage.9

Some investigators have reported that compared with LR,large amount of NS intravenous infusions could inducehyperchloraemic metabolic acidosis, and theorised that aggres-sive hydration with NS might actually induce urine acidifica-tion rather than alkalisation.10–12

We conducted an investigation to compare the effectivenessand side effects of LR and NS as intravenous hydratingcrystalloid solutions in the treatment of rhabdomyolysisinduced by doxylamine intoxication.

METHODSThis randomised mono-blind study was conducted on patientswho visited the emergency departments of two tertiary teachinghospitals located in Seoul, Korea, after intentional doxylamineoverdose, from January 2005 to May 2006. We excludedpatients who had ingested other additional drugs, or who hada history of renal, muscular, central nervous system andischaemic heart disease from the study. The initial history andphysical examination included sex, age, medical history, timefrom drug ingestion to hospital arrival, amount of doxylamineingested and associated symptoms. Then general detoxificationmeasures—for example, activated charcoal administration andgastric lavage—if indicated, were performed. The initial bloodsamples were sent to the laboratory for blood urea nitrogen,creatine, serum electrolyte (sodium, potassium and chloride),creatine kinase (CK), pH and myoglobin analysis. Urine wascollected for pH and myoglobin analysis. The serum CK,electrolyte and urine pH were measured every 12 h thereafter.

We randomly allocated patients into the NS or LR group bypicking one plastic piece from a box containing 5 pieces labelledas NS and another 5 pieces labelled as LR. This was done by anurse who was not directly involved in patient care. Afterobtaining written, informed consent, patients in the LR groupreceived lactated Ringer’s solution and those in the NS groupreceived 0.9% saline at the rate of 120 ml/h. Only theinvestigators, not the patients, knew which crystalloid wasinfused.

We defined rhabdomyolysis as serum CK .1000 IU/l. Whenrhabdomyolysis was diagnosed from the serum CK result,aggressive NS or LR infusion at the rate of 400 ml/h wasstarted. When urine pH .6.5 was not achieved after 12 haggressive hydration, bicarbonate was administered (fig 1). Theremaining patients who did not develop rhabdomyolysis or

Abbreviations: CK, creatine kinase; LR, lactated Ringer’s solution; NS,0.9% saline

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GENERAL ARTICLES

A Randomized, Double-Blind Comparison of LactatedRinger’s Solution and 0.9% NaCl DuringRenal TransplantationCatherine M. N. O’Malley, FFARCSI*, Robert J. Frumento, MPH*, Mark A. Hardy, MD†,Alan I. Benvenisty, MD†, Tricia E. Brentjens, MD*, John S. Mercer, MD,and Elliott Bennett-Guerrero, MD*

Departments of *Anesthesiology and †Surgery, Columbia University, College of Physicians & Surgeons, New York

Normal saline (NS; 0.9% NaCl) is administered duringkidney transplantation to avoid the risk of hyperkale-mia associated with potassium-containing fluids. Re-cent evidence suggests that NS may be associated withadverse effects that are not seen with balanced-salt flu-ids, e.g., lactated Ringer’s solution (LR). We hypothe-sized that NS is detrimental to renal function in kidneytransplant recipients. Adults undergoing kidney trans-plantation were enrolled in a prospective, randomized,double-blind clinical trial of NS versus LR for intraop-erative IV fluid therapy. The primary outcome measurewas creatinine concentration on postoperative Day 3.The study was terminated for safety reasons after in-terim analysis of data from 51 patients. Forty-eight pa-tients underwent living donor kidney transplants, and

three patients underwent cadaveric donor transplants.Twenty-six patients received NS, and 25 patients re-ceived LR. There was no difference between groups inthe primary outcome measure. Five (19%) patients inthe NS group versus zero (0%) patients in the LR grouphad potassium concentrations !6 mEq/L and weretreated for hyperkalemia (P " 0.05). Eight (31%) pa-tients in the NS group versus zero (0%) patients inthe LR group were treated for metabolic acidosis(P " 0.004). NS did not adversely affect renal function.LR was associated with less hyperkalemia and acidosiscompared with NS. LR may be a safe choice for IV fluidtherapy in patients undergoing kidney transplantation.

(Anesth Analg 2005;100:1518–24)

N ormal saline (NS) or potassium-free fluids arerecommended for IV fluid therapy during kid-ney transplantation (1–4). A survey of U.S. kid-

ney transplant centers revealed that NS and NS-basedsolutions are the preferred IV fluids for administrationduring kidney transplant surgery (5).

What is the basis for the use of NS in patients withrenal failure, in particular in kidney transplant recip-ients? Theoretically, the administration of large vol-umes of potassium-containing fluids such as lactatedRinger’s solution (LR) might cause hyperkalemia inpatients with chronic renal failure and end-stage renaldisease (ESRD). This concern was the most frequentlycited reason for the use of NS during kidney trans-plantation in a one survey (5).

Evidence suggests that balanced salt-based solu-tions such as LR may offer clinical benefits over NSand NS-based solutions. Although controversial, theadministration of large volumes of NS is associatedwith the development of hyperchloremic metabolicacidosis (6–9), which may theoretically cause hyper-kalemia through an extracellular shift of potassiumions (10). Infusion of NS has also been associated witheffects such as subjective mental changes and abdom-inal discomfort in healthy volunteers (8). The use ofbalanced salt-based solutions in elderly surgical pa-tients may be associated with better splanchnic perfu-sion than NS-based solutions (9). Intriguing differ-ences in indices of renal function have also beensuggested in studies of patients treated with NS-basedand balanced salt-based solutions (7,8,11,12).

Therefore, in view of these data and the predomi-nant use of NS in kidney transplant recipients, wedesigned a randomized, blinded clinical trial to ex-plore the effects of NS administration on graft functionas reflected by the serum creatinine concentration onpostoperative day (POD) 3. In addition, we aimed to

Presented, in part, at the Annual Meeting of the American Societyof Anesthesiologists, October 14, 2003, San Francisco, CA.

Accepted for publication November 2, 2004.Address correspondence and reprint requests to Catherine M.N.

O’Malley, FFARCSI, Department of Anesthesia, St. James’s Hospi-tal, Dublin 8, Ireland. Address e-mail to [email protected].

DOI: 10.1213/01.ANE.0000150939.28904.81

©2005 by the International Anesthesia Research Society1518 Anesth Analg 2005;100:1518–24 0003-2999/05

Normal Saline Versus Lactated Ringer’s Solution forIntraoperative Fluid Management in Patients UndergoingAbdominal Aortic Aneurysm Repair: An Outcome StudyJonathan H. Waters, MD, Alexandru Gottlieb, MD, Peter Schoenwald, MD,Marc J. Popovich, MD, Juraj Sprung, MD, PhD, and David R. Nelson, MS

Department of General Anesthesiology, Cleveland Clinic Foundation, Cleveland, Ohio

Metabolic acidosis and changes in serum osmolarity areconsequences of 0.9% normal saline (NS) solution ad-ministration. We sought to determine if these physio-logic changes influence patient outcome. Patients un-dergoing aortic reconstructive surgery were enrolledand were randomly assigned to receive lactated Ring-er’s (LR) solution (n ! 33) or NS (n ! 33) in a double-blinded fashion. Anesthetic and fluid managementwere standardized. Multiple measures of outcomewere monitored. The NS patients developed a hyper-chloremic acidosis and received more bicarbonate ther-apy (30 " 62 mL in the NS group versus 4 " 16 mL in theLR group; mean " sd), which was given if the base def-icit was greater than #5 mEq/L. The NS patients alsoreceived a larger volume of platelet transfusion (478 "302 mL in the NS group versus 223 " 24 mL in the LR

group; mean " sd). When all blood products weresummed, the NS group received significantly moreblood products (P ! 0.02). There were no differences induration of mechanical ventilation, intensive care unitstay, hospital stay, and incidence of complications.When NS was used as the primary intraoperative solu-tion, significantly more acidosis was seen on comple-tion of surgery. This acidosis resulted in no apparentchange in outcome but required larger amounts of bi-carbonate to achieve predetermined measurements ofbase deficit and was associated with the use of largeramounts of blood products. These changes should beconsidered when choosing fluids for surgical proce-dures involving extensive blood loss and requiring ex-tensive fluid administration.

(Anesth Analg 2001;93:817–22)

R ecent reports have investigated the impact ofnormal saline infusion on acid-base balance (1–4). These reports describe the development of

metabolic hyperchloremic acidosis after the adminis-tration of 0.9% (“normal”) saline (NS) containing so-lutions. In this study, we hypothesized that NS wouldbe associated with hyperchloremic metabolic acidosisand attempted to determine whether the acidosis af-fected hospital outcome. This outcome was evaluatedby assessing the incidence of complications, bloodproduct use, ventilator time, intensive care unit (ICU)stay, and hospital stay.

A single study has been published evaluating out-come differences in patients resuscitated with NS ver-sus lactated Ringer’s (LR) solution (5). This study of

Vietnam War casualties found no difference in sur-vival between resuscitation fluids in a patient popu-lation composed of young, previously healthy sol-diers, a population very different from the populationroutinely cared for in most hospitals today. Importantchanges in perioperative management have occurredsince the Vietnam War; subtle outcome differencesmay not have been recognized in a study of this earlierera. These differences may currently be important.

To answer the primary hypothesis of this study,patients undergoing aortic surgery were used to as-sess the potential impact of these fluids. This popula-tion of patients was considered to be particularly vul-nerable to any detrimental effects of these fluids.These patients possess a number of characteristics thatcould amplify any differences. For example, these pa-tients receive large volumes of crystalloid fluids and inour institution, all patients undergoing these proce-dures are taken to the ICU intubated, all patientsreceive a general anesthetic with epidural opioids forpostoperative pain management, and all have invasivemonitoring. Because of the nature of the operativeprocedure and the severity of coexisting disease, they

Supported, in part, by a grant sponsored by the I. H. Page Centerfor Health Outcomes Research.

Accepted for publication May 23, 2001.Address correspondence and reprint requests to Jonathan H.

Waters, MD, Department of General Anesthesiology, ClevelandClinic Foundation, 9500 Euclid Ave., E31, Cleveland, OH 44195.Address e-mail to [email protected].

©2001 by the International Anesthesia Research Society0003-2999/01 Anesth Analg 2001;93:817–22 817

The Effect of Intravenous Lactated Ringer’s Solution Versus0.9% Sodium Chloride Solution on Serum Osmolality inHuman VolunteersE. Lynne Williams, FRCA, Kathy L. Hildebrand, BN, Shelley A. McCormick, MSN, andM. Jay Bedel, BSN

Anesthesiology Department, Allegheny University Hospitals, Allegheny General Hospital, Pittsburgh, Pennsylvania

Animal studies have shown that large volumes of IVlactated Ringer’s solution (LR) decrease serum osmola-lity, thereby increasing cerebral water. These studieshave led to recommendations to limit LR to avoid cere-bral edema in neurosurgical patients. Eighteen healthyhuman volunteers aged 20–48 yr received 50 mL/kgLR over 1 h on one occasion and 0.9% sodium chloride(NS) on another. Venous samples were taken at base-line (T1), at infusion end (T2), and 1 h after T2 (T3). Timeuntil first urination was noted. With LR, serum osmola-lity decreased by 4 ! 3 mOsm/kg from T1 to T2 andincreased insignificantly with NS. At T3, osmolality re-turned almost to baseline in the LR group. Blood pHincreased from T1 to T2 with LR by 0.04 ! 0.04 anddecreased with NS by 0.04 ! 0.04. These pH changes

persisted at T3. Subjective mental changes occurredonly with NS. Abdominal discomfort was more com-mon with NS. Time until first urination was longer withNS (106 ! 11 min) than with LR (75 ! 10 min) (P "0.001). In healthy humans, an infusion of large volumesof LR, but not NS, transiently decreased serum osmola-lity, whereas acidosis associated with NS persisted andurinary output was slower with NS. Implications:

Large volumes of lactated Ringer’s solution adminis-tered to healthy humans produced small transientchanges in serum osmolality. Large volumes of sodiumchloride did not change osmolality but resulted inlower pH.

(Anesth Analg 1999;88:999–1003)

L actated Ringer’s solution (LR) and 0.9% sodiumchloride solution (NS) are commonly used as IVfluids. The osmolarity of LR is 273 mOsm/L. In

dilute physiological solutions, the values of osmolalityand osmolarity are interchangeable (1). However,when measured by the depression of freezing point,the osmolality of LR is 254 mOsm/kg (2,3). This dis-crepancy is due to the incomplete ionization of thesolutes in LR. However, the measured osmolality ofNS (mOsm/kg), which is more completely ionized, issimilar to the calculated osmolarity of 308 mOsm/L.Thus, the osmolality of LR is lower than, and that ofNS is equal to or higher than, the osmolality of normalserum (285–295 mOsm/kg) (4). In animal studies ofisovolemic hemodilution with large volumes of IV LR,the serum osmolality decreased (1,2,5–9). Because theblood-brain barrier (BBB) allows the passage of wateralong osmotic gradients (10), serum osmolality is a

determinant of brain water content, so that low serumosmolality may contribute to cerebral edema (5–7,11,12). Based on these data, it has been recom-mended that IV LR be administered cautiously toneurosurgical patients (6,13).

Studies demonstrating changes in osmolality asso-ciated with the administration of large volumes of IVLR and NS have been performed only in animals(1,2,6,7). We undertook the current investigation inhealthy human volunteers to determine whether largevolumes of IV LR or NS would result in changes ofserum osmolality.

MethodsThe protocol was approved by our institutional re-view board. Twenty healthy human volunteers aged20–48 yr were enrolled in the study. After givingwritten, informed consent, each volunteer was ran-domly assigned to one of two groups using sealedenvelopes. The investigations were performed beforenoon. There was no restriction on oral intake beforethe IV infusions, and each subject urinated and was

Accepted for publication January 28, 1999.Address correspondence to E. Lynne Williams, MB, BS, FRCA,

Department of Anesthesiology, Allegheny University Hospitals, Al-legheny General, 320 E. North Ave., Pittsburgh, PA 15212. Addresse-mail to [email protected].


Lactated Ringer’s is Superior to Normal Saline in theResuscitation of Uncontrolled Hemorrhagic ShockS. Rob Todd, MD, Darren Malinoski, MD, Patrick J. Muller, BS, and Martin A. Schreiber, MD

Background: Normal saline (NS) andlactated Ringer’s solution (LR) continueto be used interchangeably for the resus-citation of hemorrhagic shock in some in-stitutions. We hypothesized that, asidefrom hyperchloremic acidosis, NS resusci-tation would be similar to that of LR in aswine model of uncontrolled hemorrhage.

Methods: Twenty swine weighing amean of 37 kg underwent invasive lineplacement, midline celiotomy, and sple-nectomy. After a 15-minute stabilizationperiod, we recorded a baseline mean arte-rial pressure (MAP) and created a gradeV liver injury. The animals bled freely for30 minutes after which we measuredblood loss. We blindly randomized theswine to receive NS (10 animals) versusLR (10 animals) to achieve and maintain

the baseline MAP for 90 minutes postin-jury. Laboratory values were obtained atbaseline and upon completion of the2-hour study period.

Results: Initial blood loss was 25mL/kg in the NS group and 22 mL/kg inthe LR group (p ! 0.54). Animals re-quired 256.3 " 145.4 mL/kg of fluid in theNS group as compared with 125.7 " 67.3mL/kg in the LR group (p ! 0.04). Theurine output was higher in the NS group(46.6 " 39.5 mL/kg versus 18.9 " 12.9mL/kg, p ! 0.04). Upon study completion,the NS group had a significant hyperchlo-remia (119 " 1.9 mEq/L versus 105 " 2.9mEq/L, p < 0.01) with acidosis (7.28 "0.12 versus 7.45 " 0.06, p < 0.01) in com-parison to the LR group. In addition,resuscitation with NS resulted in signifi-

cantly lower fibrinogen levels (99 " 21mg/dL versus 123 " 20 mg/dL, p ! 0.02).The serum lactate was 4.7 " 2.2 in the LRgroup and 1.7 " 1.7 in the NS swine (p <0.01) at the end of the study.

Conclusions: Resuscitation of uncon-trolled hemorrhagic shock with NS requiressignificantly greater volume and is associ-ated with greater urine output, hyperchlor-emic acidosis, and dilutional coagulopathyas compared with LR. Resuscitation withLR results in an elevation of the lactatelevel that is not associated with acidosis.Lactated Ringer’s solution is superior toNS for the resuscitation of uncontrolledhemorrhagic shock in swine.

Key Words: Hemorrhagic shock, lac-tated Ringer’s, normal saline, resuscita-tion, trauma.

J Trauma. 2007;62:636–639.

Hemorrhage remains a major cause of early death aftertrauma.1 Primary treatment measures include definitivecontrol of the hemorrhage and volume resuscitation.

The optimal resuscitation regimen (specifically the type offluid) is currently unknown, and normal saline (NS) andlactated Ringer’s solution (LR) are often used interchange-ably for the resuscitation of hemorrhagic shock. The purposeof this study was to analyze the effects of NS and LR on theresuscitation of uncontrolled hemorrhagic shock in a swinemodel. We hypothesized that, aside from hyperchloremicacidosis in the NS group, the effects of NS versus LR resus-citation would be similar in this model.

MATERIALS AND METHODSThis was a prospective randomized, controlled trial.

Twenty Yorkshire crossbred pigs underwent a 16-hour pre-operative fast (except for water ad libitum). We preanesthe-tized the swine with an intramuscular injection of 8 mg/kgTelazol (Fort Dodge Animal Health, Fort Dodge, IA). Theywere then intubated with a 7.0-mm or 7.5-mm oral endotra-cheal tube and placed on mechanical ventilation. Anesthesiawas maintained using 2% isoflurane in 100% oxygen. Anesophageal thermometer and gastric tube were inserted.

Animal temperature was controlled utilizing externalwarming devices. Once the swine were anesthetized, weperformed left cervical cutdowns and inserted polyethylenecatheters into the common carotid artery and the externaljugular vein. The arterial catheter was used for continuousmonitoring and blood sampling. Mean arterial pressure(MAP), systolic blood pressure (SBP), diastolic blood pres-sure (DBP), and heart rate (HR) were continuously recordedand averaged every 10 seconds using a digital data collectionsystem with a blood pressure analyzer (DigiMed, Louisville,KY). The venous line was used for administration of theresuscitation fluids.

The animals underwent a midline celiotomy, suprapubicFoley catheter placement, and splenectomy. Splenectomiesare performed in swine hemorrhage models because of thespleen’s distensibility and the resultant variation in amountsof sequestered blood. The spleen was weighed and LR was

Submitted for publication July 2, 2004.Accepted for publication August 9, 2006.Copyright © 2007 by Lippincott Williams & Wilkins, Inc.From the Methodist Hospital (S.R.T.), Houston, TX; University of

California (D.M.), Irvine, California; and the Oregon Health & ScienceUniversity (B.J.M., M.A.S.), Portland, OR.

Supported by US Army Medical Research and Materiel Command(DAMD17-01-1-0693).

Presented at the 26th Annual Conference on Shock, Phoenix, Arizona,June 7–10, 2003.

Address for reprints: S. Rob Todd, MD, Department of Surgery, TheMethodist Hospital, 6550 Fannin Street, SM1661A, Houston, TX 77030;email: [email protected].

DOI: 10.1097/TA.0b013e31802ee521

The Journal of TRAUMA! Injury, Infection, and Critical Care

636 March 2007

CARDIOVASCULAR ANESTHESIA SOCIETY OF CARDIOVASCULAR ANESTHESIOLOGISTSSECTION EDITORKENNETH J. TUMAN

The Effects of Balanced Versus Saline-Based Hetastarch andCrystalloid Solutions on Acid-Base and Electrolyte Statusand Gastric Mucosal Perfusion in Elderly Surgical Patients

Nicholas J. Wilkes, FRCA, Rex Woolf, FRCA, Marjorie Mutch, RGN, Susan V. Mallett, FRCA,Tim Peachey, FRCA, Robert Stephens, MBChB, and Michael G. Mythen, MD

Centre for Anaesthesia, Royal Free and University College Medical School, London, United Kingdom

The IV administration of sodium chloride solutions mayproduce a metabolic acidosis and gastrointestinal dys-function. We designed this trial to determine whether, inelderly surgical patients, crystalloid and colloid solutionswith a more physiologically balanced electrolyte formula-tion, such as Hartmann’s solution and Hextend®, can pro-vide a superior metabolic environment and improved in-dices of organ perfusion when compared with saline-based fluids. Forty-seven elderly patients undergoingmajor surgery were randomly allocated to one of twostudy groups. Patients in the Balanced Fluid group re-ceived an intraoperative fluid regimen that consisted ofHartmann’s solution and 6% hetastarch in balanced elec-trolyte and glucose injection (Hextend). Patients in the Sa-line group were given 0.9% sodium chloride solution and6% hetastarch in 0.9% sodium chloride solution (Hes-pan®). Biochemical indices and acid-base balance weredetermined. Gastric tonometry was used as a reflection of

splanchnic perfusion. Postoperative chloride levels dem-onstrated a larger increase in the Saline group than theBalanced Fluid group (9.8 vs 3.3 mmol/L, P ! 0.0001).Postoperative standard base excess showed a larger de-cline in the Saline group than the Balanced Fluid group("5.5 vs "0.9 mmol/L, P ! 0.0001). Two-thirds of pa-tients in the Saline group, but none in the Balanced Fluidgroup, developed postoperative hyperchloremic meta-bolic acidosis (P ! 0.0001). Gastric tonometry indicated alarger increase in the CO2 gap during surgery in the Salinegroup compared with the Balanced Fluid group (1.7 vs 0.9kPa, P ! 0.0394). In this study, the use of balanced crystal-loid and colloid solutions in elderly surgical patients pre-vented the development of hyperchloremic metabolicacidosis and resulted in improved gastric mucosal perfu-sion when compared with saline-based solutions.

(Anesth Analg 2001;93:811–6)

E lderly patients have a diminished ability to re-spond to the hemodynamic and metabolic de-mands of anesthesia and surgery (1). Inappropri-

ate IV fluid management seems to be one of thegreatest problems associated with poor outcome inelderly surgical patients (2). Perioperative intravascu-lar volume optimization, guided by gastric tonometryor transesophageal Doppler ultrasonography, mayimprove outcome after major surgery (3,4). There is,

however, little consensus as to the preferred choice ofIV fluid. Crystalloid solutions satisfy basic fluid re-quirements and compensate for insensible losses dur-ing open surgical procedures. Colloid solutions main-tain the circulating blood volume when used asplasma volume expanders. Sodium chloride 0.9% so-lution is often administered because it is isotonic withplasma and is initially distributed in the extracellularcompartment. Its nonphysiologic levels of chloride,however, have been linked to the development of ametabolic acidosis and the possible impairment ofsplanchnic perfusion, as judged by reduced urine flowand abdominal discomfort in healthy volunteers (5).The relevance of this type of metabolic acidosis topatients is unclear (6,7). Our trial was designed tocompare balanced crystalloid and colloid solutionswith sodium chloride-based solutions in relation topostoperative biochemical status, acid-base balance,and clinically available indices of splanchnic and pe-ripheral perfusion in elderly surgical patients.

Supported by unrestricted grants from Abbott Laboratories andBioTime Inc., Berkeley, CA.

Presented in part at the World Congress of Anesthesiologists,Montreal, June 5–9, 2000, and at the annual meeting of the AmericanSociety of Anesthesiologists, San Francisco, CA, October 14–18,2000.

Accepted for publication April 16, 2001.Address correspondence to Nicholas J. Wilkes, Department of An-

aesthesia, Royal Free Hospital, Pond Street, London NW3 2QG, UnitedKingdom. Address e-mail to [email protected].


The Effect of Different Crystalloid Solutions on Acid-BaseBalance and Early Kidney Function AfterKidney Transplantation

Necmiye Hadimioglu, MD*

Iman Saadawy, MD†

Tayyup Saglam, MD*

Zeki Ertug, MD*

Ayhan Dinckan, MD‡

BACKGROUND: This study aimed to quantify changes in acid-base balance, potassiumand lactate levels as a function of administration of different crystalloid solutionsduring kidney transplantation, and to determine the ideal fluid for such patients.METHODS: In this double-blind study, patients were randomized to three groups(n ! 30 each) to receive either normal saline, lactated Ringer’s, or Plasmalyte, all at20–30 mL ! kg"1 ! h"1. Arterial blood analyses were performed before induction ofanesthesia, and at 30-min intervals during surgery, and total IV fluids recorded.Urine volume, serum creatinine and BUN, and creatinine clearance were recordedon postoperative days 1, 2, 3, and 7.RESULTS: There was a statistically significant decrease in pH (7.44 # 0.50 vs 7.36 #0.05), base excess (0.4 # 3.1 vs –4.3 # 2.1), and a significant increase in serumchloride (104 # 2 vs 125 # 3 mM/L) in patients receiving saline during surgery.Lactate levels increased significantly in patients who received Ringer’s lactate(0.48 # 0.29 vs 1.95 # 0.48). No significant changes in acid-base measures or lactatelevels occurred in patients who received Plasmalyte. Potassium levels were notsignificantly changed in any group.CONCLUSIONS: All three crystalloid solutions can be safely used during uncompli-cated, short-duration renal transplants; however, the best metabolic profile ismaintained in patients who receive Plasmalyte.(Anesth Analg 2008;107:264–9)

Patients undergoing renal transplantation are sub-ject to a wide variety of intraoperative complicationsincluding hemodynamic instability, acid-base andelectrolyte disturbances because of impaired renalfunction, and co-morbid diseases.1 Maintenance ofintravascular volume during kidney transplantation iscrucial to ensure optimal graft perfusion and function.2

Crystalloids alone are usually sufficient to maintainvolume during kidney transplantation, carry no infec-tious risk, and have no specific nephrotoxic effects.3–5

Previous studies have shown that metabolic acido-sis is a complication of normal saline infusion becauseof its high chloride content. Ringer’s lactate containspotassium and can potentially aggravate hyperkale-mia in patients with impaired renal function.6 Despitewidespread use of Plasmalyte for patients with renalcompromise, Plasmalyte has not specifically been

compared with other crystalloids in patients undergo-ing kidney transplantation. For this reason, we de-signed a study comparing metabolic profile and renalfunction in renal transplant patients managed withsaline, Ringer’s lactate, or Plasmalyte.

METHODSFollowing approval of the Hospital Ethics Commit-

tee, written informed consent was obtained from allpatients. This prospective, randomized, double-blindstudy was conducted on 90 patients, aged 18–65 yr,ASA III and IV scheduled for living-related kidneytransplantation. Exclusion criteria were severe cardio-vascular disease, liver dysfunction, cadaveric kidneytransplantation, diabetes, and serum potassium level$5.5 mM/L.

A computer randomization program was used forpatient group assignments. Patients received 0.9%normal saline, Ringer’s lactate, or Plasmalyte with 30patients in each group. The study solutions wereprepared in unlabeled bags by the hospital pharmacy.Patients and clinicians were blinded to group assign-ments. Salt make-up the study solutions is shown inTable 1.

Before induction of anesthesia, an 18-G IV catheterand 20-G arterial artery cannula were inserted underlocal anesthesia. After preoxygenation, general anes-thesia was induced using IV thiopental (3–5 mg/kg),

From the *Department of Anesthesia, Faculty of Medicine,Akdeniz University, Antalya, Turkey; †Department of Anesthesia,Faculty of Medicine, Cairo University, Egypt; and ‡Department ofGeneral Surgery, Akdeniz University, Antalya, Turkey.

Accepted date for publication March 3, 2008.Address correspondence and reprint requests to Necmiye Had-

imioglu, MD, Department of Anesthesiology, Faculty of Medicine,Akdeniz University, Antalya, Turkey. Address e-mail to [email protected].

Copyright © 2008 International Anesthesia Research SocietyDOI: 10.1213/ane.0b013e3181732d64

Vol. 107, No. 1, July 2008264

Modèle de Stewart

Gregor LindnerChristoph SchwarzHeidelinde GrussingNikolaus KneidingerAndreas FazekasGeorg-Christian Funk

Rising serum sodium levels are associatedwith a concurrent development of metabolicalkalosis in critically ill patients

Received: 7 September 2012Accepted: 11 October 2012

! Springer-Verlag Berlin Heidelberg andESICM 2012

G. Lindner ())Department of Emergency Medicine,Inselspital University Hospital Bern,Freiburgstrasse, 3010 Bern, Switzerlande-mail: [email protected].: ?41-78-6852782

C. SchwarzDepartment of Nephrology, MedicalUniversity of Graz, Graz, Austria

H. GrussingDepartment of Anesthesiology, GeneralIntensive Care Medicine and PainManagement, Medical University ofVienna, Vienna, Austria

N. KneidingerDepartment of Respiratory Medicine,University of Munich, Munich, Germany

A. Fazekas ! G.-C. FunkDepartment of Respiratory and Critical CareMedicine, Otto Wagner Hospital,Vienna, Austria

A. Fazekas ! G.-C. FunkLudwig Boltzmann Institute for COPD andRespiratory Epidemiology, Vienna, Austria

Abstract Purpose: Changes inelectrolyte homeostasis are importantcauses of acid–base disorders. Whilethe effects of chloride are well stud-ied, only little is known of thepotential contributions of sodium tometabolic acid–base state. Thus, weinvestigated the effects of intensivecare unit (ICU)-acquired hypernatre-mia on acid–base state.Methods: We included critically illpatients who developed hypernatre-mia, defined as a serum sodiumconcentration exceeding 149 mmol/L, after ICU admission in this retro-spective study. Data on electrolyteand acid–base state in all includedpatients were gathered in order toanalyze the effects of hypernatremiaon metabolic acid–base state by useof the physical–chemical approach.Results: A total of 51 patients wereincluded in the study. The time ofrising serum sodium and hypernatre-mia was accompanied by metabolic

alkalosis. A transient increase in totalbase excess (standard base excessfrom 0.1 to 5.5 mmol/L) paralleled bya transient increase in the base excessdue to sodium (base excess sodiumfrom 0.7 to 4.1 mmol/L) could beobserved. The other determinants ofmetabolic acid–base state remainedstable. The increase in base excesswas accompanied by a slight increasein overall pH (from 7.392 to 7.429,standard base excess from 0.1 to5.5 mmol/L). Conclusions: Hyper-natremia is accompanied bymetabolic alkalosis and an increase inpH. Given the high prevalence ofhypernatremia, especially in criticallyill patients, hypernatremic alkalosisshould be part of the differentialdiagnosis of metabolic acid–basedisorders.

Keywords Acid–base !Stewart’s approach ! Hypernatremia !Critically ill

Introduction

Hypernatremia is defined as a serum sodium concentrationexceeding 145 mmol/L [1]. Usually, the development ofthirst protects us against the development of hypernatremia,which is always associated with hyperosmolality [2]. Thus,

individuals with a disturbed sensation of thirst, unconsciouspeople, or those with no access to free water are prone todevelop hypernatremia [1]. Consequently, hypernatremia ismainly a problem in persons living in nursing homes orcritically ill patients who are mechanically ventilated andwhose fluid intake is managed by the physician [3, 4].

Intensive Care MedDOI 10.1007/s00134-012-2753-3 ORIGINAL

PRELIMINARYCOMMUNICATION

Association Between a Chloride-Liberalvs Chloride-Restrictive Intravenous FluidAdministration Strategy and Kidney Injuryin Critically Ill AdultsNor’azim Mohd Yunos, MDRinaldo Bellomo, MD, FCICMColin Hegarty, BScDavid Story, MDLisa Ho, MClinPharmMichael Bailey, PhD

THE ADMINISTRATION OF INTRA-venous chloride is ubiquitousin critical care medicine.1,2 Inaddition, many of the fluids

used for hydration and resuscitationcontain supraphysiological concentra-tions of chloride,3-5 which induce or ex-acerbate hyperchloremia and meta-bolic acidosis,6,7 may cause renalvasoconstriction and decreased glo-merular filtration rate (GFR),8-10 pro-long time to first micturition,11 and de-crease urine output in major surgery.12

Recently, in a double-blind random-ized controlled trial, 2 L of saline de-creased cortical perfusion in humanstudy participants compared withPlasma-Lyte.13 These effects of chlo-ride on the kidney are of potential con-cern because acute kidney injury (AKI)is associated with high mortality14 andmay require treatment with costly andinvasive renal replacement therapy(RRT).15,16

Given the high risk of AKI in criti-cally ill patients and the experimental as-sociation between chloride administra-tion and decreased renal function, wehypothesized that a chloride-restric-tive intravenous fluids strategy in criti-cally ill patients might be associated with

For editorial comment see p 1583.

Author Affiliations: Johor Bahru Clinical School,Monash University Sunway Campus, Malaysia (Dr Yu-nos); Departments of Intensive Care (Dr Bellomo),Laboratory Medicine (Mr Hegarty), Anaesthesia (DrStory), and Pharmacy (Ms Ho), Austin Hospital, Mel-bourne, Australia; and Australia and New Zealand

Intensive Care Research Centre, Department of Epi-demiology and Preventive Medicine, Monash Univer-sity, Melbourne, Australia (Drs Bellomo and Bailey).Corresponding Author: Rinaldo Bellomo, MD, FCICM,Austin Health, Heidelberg, Victoria 3084, Australia([email protected]).

Context Administration of traditional chloride-liberal intravenous fluids may precipi-tate acute kidney injury (AKI).

Objective To assess the association of a chloride-restrictive (vs chloride-liberal) in-travenous fluid strategy with AKI in critically ill patients.

Design, Setting, and Patients Prospective, open-label, sequential period pilot studyof 760 patients admitted consecutively to the intensive care unit (ICU) during the con-trol period (February 18 to August 17, 2008) compared with 773 patients admittedconsecutively during the intervention period (February 18 to August 17, 2009) at auniversity-affiliated hospital in Melbourne, Australia.

Interventions During the control period, patients received standard intravenous flu-ids. After a 6-month phase-out period (August 18, 2008, to February 17, 2009), anyuse of chloride-rich intravenous fluids (0.9% saline, 4% succinylated gelatin solution,or 4% albumin solution) was restricted to attending specialist approval only duringthe intervention period; patients instead received a lactated solution (Hartmann so-lution), a balanced solution (Plasma-Lyte 148), and chloride-poor 20% albumin.

Main Outcome Measures The primary outcomes included increase from baselineto peak creatinine level in the ICU and incidence of AKI according to the risk, injury,failure, loss, end-stage (RIFLE) classification. Secondary post hoc analysis outcomesincluded the need for renal replacement therapy (RRT), length of stay in ICU and hos-pital, and survival.

Results Chloride administration decreased by 144 504 mmol (from 694 to 496 mmol/patient) from the control period to the intervention period. Comparing the control pe-riod with the intervention period, the mean serum creatinine level increase while inthe ICU was 22.6 µmol/L (95% CI, 17.5-27.7 µmol/L) vs 14.8 µmol/L (95% CI, 9.8-19.9 µmol/L) (P=.03), the incidence of injury and failure class of RIFLE-defined AKIwas 14% (95% CI, 11%-16%; n=105) vs 8.4% (95% CI, 6.4%-10%; n=65) (P!.001),and the use of RRT was 10% (95% CI, 8.1%-12%; n=78) vs 6.3% (95% CI, 4.6%-8.1%; n=49) (P=.005). After adjustment for covariates, this association remained forincidence of injury and failure class of RIFLE-defined AKI (odds ratio, 0.52 [95% CI,0.37-0.75]; P!.001) and use of RRT (odds ratio, 0.52 [95% CI, 0.33-0.81]; P=.004).There were no differences in hospital mortality, hospital or ICU length of stay, or needfor RRT after hospital discharge.

Conclusion The implementation of a chloride-restrictive strategy in a tertiary ICUwas associated with a significant decrease in the incidence of AKI and use of RRT.

Trial Registration clinicaltrials.gov Identifier: NCT00885404JAMA. 2012;308(15):1566-1572 www.jama.com

1566 JAMA, October 17, 2012—Vol 308, No. 15 ©2012 American Medical Association. All rights reserved.

Downloaded From: http://jama.jamanetwork.com/ by a Université de Strasbourg User on 01/30/2013








































Approche classique :

GDS, Na+, K+, Cl-, Albumine

Urines : pH, Iono Urinaire, Osmolarité urinaire

Permet d’explorer la majorité des situations


Approche de Stewart :

GDS, Na+, K+, Cl-, Ca2+, Mg2+, Albumine, Phosphore

Lactates

Urines : pH, Iono Urinaire, Osmolarité urinaire

Permettra d’explorer toutes les situations cliniques ?


reamed-htp.org

Exploration des troubles acido-basiques Approche …€¦ · Exploration des troubles...

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