REFRESHER
COURSE
OUTLINE
Jean-Louis Vincent MD PhD
Tissue hypoxia is one of the most important factors in the pathogenesis of multiple organ failure and the ability to measure and monitor tissue perfusion effectively is, therefore, important in the ongoing assessment and management of the critically patient. It is increasingly realised that systemic measures of oxygenation may represent inadequate monitors of regional perfusion and.the search continues to identify the most reliable methods of assessing local tissue oxygenation, to complement global parameters. To be considered practical, such techniques must be widely available at relatively low cost, minimally invasive, and easy to use.
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Monitoring tissue perfusion mental studies have shown that a decrease in oxygen delivery below a critical value is accompanied by a rise in lactate concentration. I Clinical studies also show that pathological oxygen uptake/supply dependency is associated with raised lactate. 2 Studies have also confirmed that blood lactate concentrations correlate well with outcome from circulatory failure. 3,4 The use of sequential measurements of lactate is of more importance than an isolated level in assessing tissue oxygenation and this can be easily achieved by the use of automated analys e r s . 5,6
Limitations Mixed venous oxygen saturation (SVO2 Mixed venous oxygen saturation is a useful indicator of the relationship between oxygen uptake and supply but is not a direct measure of tissue oxygenation. An alteration in tissue oxygen extraction capabilities in certain conditions such as sepsis, trauma, and prolonged surgery can limit the increase in oxygen uptake which would normally occur, and the interpretation of S~O2 in such circumstances may become difficult. Measurement of SVO2 is moderately invasive, involving the use of a pulmonary artery catheter. Measurements may be intermittent, by taking samples of mixed venous blood from the pulmonary artery, or continuous, using modified catheters equipped with fibreoptic fibres. A normal value is about 70% in the critically ill patient. Measurement of S~O2 is an essential part of the haemodynamic monitoring of critically ill patients but other more specific indicators of tissue perfusion give valuable additional information.
Blood lactate concentrations represent a good measure of tissue perfusion but they have several important limitations. First, the lactate level at any time is a balance between its production and elimination. Clearance occurs primarily in the liver and liver failure could cause abnormally high levels. Patients with stable cirrhosis seem to maintain relatively normal concentrations but, nevertheless, the presence of liver disease can magnify levels raised because of circulatory failure and delay their return to normal once resuscitation is complete. Second, blood lactate concentrations are raised not only in hypoxia associated with acute circulatory failure but also in certain cellular metabolic defects and during seizures (Table I). Fortunately, except for seizures, these other conditions are relatively rare and all are fairly easily recognized. Third, in animal studies, increased lactate production may occur in the presence of endotoxin, even in the absence of tissue hypoxia.7
Blood lactate concentrations Lactate is a substance produced as a result of glucose metabolism, the end result of which is the production of pyruvate. This can, in turn, be metabolized by way of three pathways. Tissue hypoxia results in anaerobic metabolism, leading to increased lactate production by reduction of pyruvate with nicotinamide adenine dinucleotide mediated by lactate dehydrogenase.
Summary Despite these drawbacks, blood lactate concentrations can provide a valuable guide to tissue hypoxia and levels >1.5 to 2 mEq-L -l should alert the clinician to the possibility of reduced tissue oxygenation. However, they are a fairly general guide of global tissue hypoxia and the possibilities of a more local measure of tissue hypoxia are interesting.
Advantages A major advantage of this form of monitoring is the ease of measurement involving a simple blood sample. The normal concentration is around 1 mEq. L -l. ExperiC A N J A N A E S T H 1996 / 4 3 : 5 / pp R55-R57
From the Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Belgium.
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CANADIAN J O U R N A L OF ANAESTHESIA
TABLEI Causesof lacticacidosis TypeA Imbalancebetweenoxygensupplyand demand - circulatoryshock - cardiacarrest - severeanaemia - severehypoxaemia - seizures,intense shivering,exhaustingexercise Type B Cellular metabolic defect -
phenformin intoxication
- alcohol intoxication - t h i a m i n e o r biotin d e f i c i e n c y -
neoplastic diseases
- f r u c t o s e o r sorbitol i n f u s i o n -
inborn metabolic errors
- decompensated diabetes
Gastric intramucosal pH (pHi)
The measurement of pHi was first devised in 19818 but its use as a monitor in critically ill patients was not seriously considered until five years later. It has been postulated that gut ischaemia may increase bacterial translocation, thus stimulating the cascade of inflammatory mediators leading ultimately to multiple organ failure. The selective reduction in blood flow to the coeliac, mesenteric and hepatic circulations in low cardiac output states makes the potential of a local measure of gut tissue perfusion valuable as an early warning signal.
levels have also been shown to correlate with increased mortality in intensive care unit patients.ll,12 Limitations The measurement of pHi is based on two assumptions: first, that the PCO2 in the saline is the same as that in the tissues and second, that the arterial blood bicarbonate concentration is the same as that in the gastric mucosa. It also has its limitations. Technically, the measurement process is time consuming and requires considerable care. A time lapse of 30 to 90 min is required after instilling the saline in the balloon before measurements can be taken, to allow for equilibration of gases and pHi. Monitoring must therefore, be intermittent. Several factors can potentially influence pHi levels including CO2 generating antacids, enteral nutrition and changes in gastric acid secretion. It has been suggested that ranitidine should be administered to patients undergoing pHi measurement to limit this last effect. 13 The calculation of pHi using arterial bicarbonate concentrations makes it partially dependent on systemic acid-base balance. Therefore, pHi represents a valuable tool for local assessment of impaired tissue perfusion. Further study needs to be done to define a normal value but the majority of studies are currently using 7.35 or 7.32 as a lower normal limit. Technical difficulties and the time lapse required between measurements have led to the suggestion of another, simpler measure, that of regional PCO2. Regional PCO2 (PrCO2)
Advantages Basically, this minimally invasive technique involves passing a nasogastric tube with a CO2 permeable balloon at its tip into the gastric lumen. The balloon is filled with saline, the CO2 allowed to equilibrate with that in the mucosa, and the saline then aspirated for PCO2 analysis. The pHi is then calculated using the Henderson-Hasselbach formula:
pHi
= C.(HCO3-/PCO2)
where C is a constant value, HCO3- the bicarbonate concentrate in arterial blood and the PCO2 the tension in the balloon. A normal pHi indicates that the stomach, and hence the splanchnic circulation, is adequately oxygenated, whilst a low pHi suggests inadequate splanchnic oxygenation. Studies confh'm the ability of pHi to detect intestinal mucosal ischaemia 9 and its correlation with other measures of tissue hypoxia such as blood lactate. It is a more sensitive indicator and is able to detect ischaemia in patients who appear by other global haemodynamic measurements to be adequately oxygenatedJ ~ Low pHi
The equilibrium of mucosal and intraluminal PCO 2 has been well documented experimentally 14 and this property of CO2 diffusion can be employed to simplify the measure of pHi. If the balloon at the tip of the nasogastric tube is insufflated with air, the PCO2 measured in this will reflect the gastric PrCO2. This will be influenced by PaCO2 and blood gas measurements still need to be taken. An alternative would be to measure, simultaneously with the PrCO2, the PCO2 of the expired air (end-tidal CO2 or PETCO2) and to calculate the difference (PrCO2 - PETCO2). 15 This measurement avoids the technical problems and calculations associated with pHi measurement, obtains a value independent of systemic bicarbonate concentration and can be an almost continuous monitor of tissue perfusion (Table II). Combination
monitoring
Each monitoring technique has its positive and negative aspects. Rather than spending time arguing the benefits of any one indicator, the most effective and reliable assessment of tissue perfusion will be achieved by using a combination of several methods. This approach is sup-
Vincent: MONITORING TISSUE PERFUSION
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TABLE II Reasonswhy PrCO2 measurement is preferable to pHi 1 Regional tonometry relies on the theory that large increases in PCO2 occur during ischaemia. 2 Experimentally, the vent-arterial differences in PCO2 reflect the differences in tissue hypoxia at least as well as the arterio-venous differences in pH. 3 The systemic bicarbonate concentration does not necessarily correspond to the local level. 4 The systemic bicarbonate level is influenced by factors other than tissue ischaemia (in particular, renal failure). 5 The handling of saline solutions represents a frequent source of error. 6 Certain blood gas analysers are not suited for the analysis of saline solutions and need specific calibration. 7 Intermittent pHi calculations do not give accurate information on events occurring between two successive measurements. 8 pHi calculations are complex, requiring specialized charts or even computer programs. 9 Regional PCO2 can be measured at the bedside, possibly combined with PaCt2 or end-expiratory CO2 measurement.
ported by Friedman et al. who found that a combination of pHi with lactate concentration may help to predict outcome from severe sepsis? 6 It is important to remember that the results obtained from technical measurements can never replace basic patient evaluation and must only be viewed as a complement to regular clinical assessment.
5
6
7
8
9
10
11
Conclusion The detection of altered tissue perfusion and hence reduced oxygenation is predictive of mortality. Therefore a reliable technique, available for use at the bedside of every critically ill patient, is required to enable early accurate identification o f inadequate oxygenation. A combination of systemic and regional measures is likely to give the most reliable assessment of a patient's condition, and continuous or at least regularly repeated measurements, in addition to clinical evaluation, are necessary to give an accurate picture, enabling appropriate treatment to be instituted and its effects monitored.
12
13
14
15
References 1 Cain SM, Adams RP. Appearance of excess lactate in anesthetized dogs during anemic and hypoxic hypoxia. Am J Physiol 1965; 209: 604-8. 2 Bakker J, Vincent JL. The oxygen supply dependency phenomenon is associated with increased blood lactate levels. J Crit Care 1991; 6: 152-9. 3 Henning R J, Weil MH, Weiner F. Blood lactate as a prognostic indicator of survival in patients with acute myocardial infarction. Circ Shock 1982; 9: 307-15. 4 Bakker J, Coffernils M, Leon M, Gris P, Vincent JL.
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Blood lactate levels are superior to oxygen-derived variables in predicting outcome in human septic shock. Chest 1991; 99: 956--62. Vincent JL, Dufaye P, Berre J, Leeman M, Degaute JP, Kahn RJ. Serial lactate determinations during circulatory shock. Crit Care Med 1983; 11: 449-51. Bakker J, Gris P, Coffernils M, Kahn R J, Vincent JL. Serial blood lactate levels can predict the development of multiple organ failure following septic shock. Am J Surg 1996 (in press). Zhang H, Vincent JL. Oxygen extraction is altered by endotoxin during tamponade-induced stagnant hypoxia in the dog. Circ Shock 1993; 40: 168-76. Fiddian-Green RG, Pittenger G, Whitehouse WM Jr. Back-diffusion of CO2 and its influence on the intramural pH in gastric intestines of rats. J Surg Res 1982; 33: 3%48. Fiddian-Green RG, McGough E, Pittenger G, Rothman E. Predictive value of intramural pH and other risk factors for massive bleeding from stress ulceration. Gastroenterology 1983; 85: 613-20. Fiddian-Green RG. Studies in splanchnic ischemia and multiple organ failure. In: Marston A, Buckley GB, Fiddian-Green R, Haglund U (Eds.). Splanchnic Ischemia and Multiple Organ Failure. London, Melbourne, Auckland: E. Arnold, 1989; 349--63. Gys T, Hubens A, Neels H, Lauwers LF, Peeters R. Prognostic value of gastric intramucosal pH in surgical intensive care patients. Crit Care Med 1988; 16: 1222-4. Doglio GR, Pusajo JF, Egurrola MA, et al. Gastric mucosal pH as a prognostic index of mortality in critically ill patients. Crit Care Med 1991; 19: 1037-40. Heard SO, Helsmoortel CM, Kent JC, Shahnarian A, Fink MP. Gastric tonometry in healthy volunteers: effect of ranitidine on calculated intramural pH. Crit Care Med 1991; 19: 271-4. Cunningham JA, Cousar CD, Jaffin JH, Harmon JW. Extraluminal and intraluminal PCO2 levels in the ischemic intestines of rabbits. Curr Surg 1987; 44: 229-32. Cr~teur J, Vincent J L Tonomttrie gastrique: signification et interprttation des rtsultats. In: Socitt6 de Rtanimation de Langue Fran~aise (Ed.). Rtanimation-Urgences. Paris: Arnette, 1996: 253-63. Friedman G, Berlot G, Kahn R J, Vincent JL. Combined measurements of blood lactate concentrations and gastric intramucosal pH in patients with severe sepsis. Crit Care Med 1995; 23:1184-93.
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Monitorage de la perfusion tlssulalre L'hypoxie tissulaire repr6sente un 616ment important dans la pathog6n6se de la d6faillance multivisc6rale. L'habilet6 ~t mesurer efficacement et ~ monitorer la perfusion tissulaire est donc importante pour l'6valuation et le traitement du malade en phase critique. Il devient de plus en plus 6vident que les mesures de l'oxyg6nation syst6mique monitorisent pauvrement la perfusion r6gionale. C'est ce qui explique la recherche actuelle de nouvelles m&hodes d'6valuation de l'oxyg6nation tissulaire plus fiables qui compl6teront les param6tres globaux. Pour que ces techniques soient applicables, elles doivent ~rre couramment r~pandues, accessibles ~t un coot relativement modique, peu effractives et faciles /~ utiliser. La saturation du sang veineux m~l~ (SV02) La saturation du sang veineux m~16 constitue un param~tre de la relation entre l'utilisation et l'apport en oxyg~ne mais elle ne mesure pas directement l'oxygtnation tissulaire. Certaines conditions comme le sepsis, les traumatismes et la chirurgie prolongte, l'alttration de la capacit6 d'extraire l'oxyg~ne tissulaire peuvent limiter son utilisation courante, car dans ces conditions, l'interprttation de la SVO2 s'avtrera difficile. La mesure de la SvO2 est peu effractive mais ntcessite tout de m~me l'insertion d'un cathtter de S~van-Ganz. Elle est intermittente si on prtl~ve destchantillons du sang veineux m816 de l'arttre pulmonaire, ou continue, si on utilise un cathtter de Swan-Ganz modifi6 muni de fibres optiques. Pour le patient en phase critique, la valeur normale se situe ~ 70% environ. La mesure de la SVO2 constitue une 616ment important du monitorage htmodynamique en phase critique mais il existe des indicateurs plus sptcifiques de la perfusion fissulaire. Ceux-ci peuvent nous fournir des renseignements suppltmentaires de grande valeur. La concentration de lactate Le lactate est le rtsultat du mttabolisme glucidique dont l'aboutissement final est le pyruvate. A son tour, la dtgradation du pyruvate emprunte une de trois voies mttaboliques. L'hypoxie tissulaire induit le mttabolisme anatrobique avec augmentation de la production de lactate par rtduction du pyruvate par la nicotinamide adtnine dinucltotide avec mtdiation par la d6shydrogtnase lactique. CAN J A N A E S T H 1996 I 4 3 : 5 / pp R58-R60
CONFI~RENCE
D'ACTUALISATION
Jean-Louis Vincent MD PhD
Avantages Un avantage majeur de ce type de monitorage est sa simplicit6 car il ne ntcessite qu'un seul prtltvement sanguin. La concentration normale se situe ~ environ 1 mEq.L-L Des 6tudes en laboratoire ont montr6 qu'une diminution de l'apport en oxyg~ne en dessous d'une valeur critique s'accompagne d'une augmentation du lactate plasmatique. I Des 6tudes cliniques ont aussi montr6 que la dtpendance pathologique de la relation consommation/transport en oxyg~ne est associte ~ une augmentation du lactate. 2 D'autres 6tudes ont aussi conf'u'm6 que la concentration de lactate est en corrtlation avec le pronostic de la dtfaillance circulatoire.3,4 Pour 6valuer l'oxygtnation tissulaire, des mesures stquentielles du lactate plasmatique sont prtftrable ~ la mesure d'un 6chantillon isolte et ceci, ne peut 8tre rtalis6 qu'avec des analyseurs automatists. 5,6 Limites MSme si elle exprime une mesure valable de la perfusion tissulaire, la concentration du lactate plasmatique a aussi ses limites. D'abord, le niveau de lactate dtpeint l'tquilibre entre sa production et son 61imination. De plus, sa clearance est surtout htpatique de sorte que l'insuffisance htpatique entra~nera des concentrations anormalement 61ev~es. Les cirrhotiques stabilists semblent capables de maintenir des concentrations relativement normales; ntanmoins en prtsence d'une pathologie htpatique, la dtfaillance circulatoire peut faire augmenter le lactate h des niveaux encore plus 61evts et retarder leur retour h la normale une fois la rtanimation complttte. Deuxi~mement, les concentrations de lactate augmentent non seulement pendant l'hypoxie associte une dtfaillance circulatoire aigu~ mais aussi au cours de certaines anomalies mttaboliques cellulaires et pendant les crises convulsives (Tableau I). Heureusement h l'exception des crises convulsives, ces autres conditions sont relativement rares et peuvent ~tre diagnostiqutes facilement. Troisi~mement, au cours d'ttudes animales, il a 6t6 montr6 qu'ne endotoxine peuvait augmenter la production de lactate m~me en absence d'hypoxie tissulaire. 7 Rdsumd Malgr6 ces inconvtnients, la concentration du lactate procure un indice valable de l'hypoxie tissulaire. Des
Vincent:
TABLEAU I
Les causes de l ' a c i d o s e lactique
Type A Dts&tuilibre entre r a p p o r t et la d e m a n d e en o x y g ~ n e - c h o c circulatoire - art& cardiaque
- antmie grave - hypoxtmie grave - crises convulsives,frissonnementintense, exercice violent
Type B A n o m a l i e s du m t t a b o l i q u e cellulaire - intoxication it la p h e n f o r m i n e - intoxication/t I'alcool - d~ficience en thiamine ou biotine - perfusion de fructose ou sorbitol - erreurs i n n t e s m t t a b o l i q u e s - diab~te non c o m p e n s 6
Le pH gastrique intramuqueux
adtquatement oxygtnte; par contre, un pHi abaiss6 sugg~re une insuffisance de l'oxygtnation splanchnique. Des 6tudes confirment la capacit6 du pHi 9 ~ dtceler l'ischtmie de la muqueuse intestinale et sa corrtlation avec d'autres mesures d'hypoxie tissulaire comme le lactate sanguin. I1 ~'agit d'un indice plus sensible et capable de dttecter l'ischtmie chez des patients qui semblent bien oxygtnts si on se fie h d'autres mesures htmodynamiques globales. 1~ Les baisses de pHi sont aussi en corrtlation avec l'augmentation de la mortalit6 chez les patients hospitalists en unit6 de soins intensifs.ll, 12
Limites
niveaux plus 61evts que 1,5 ~ 2 m E q . L -~ devraient orienter le clinicien vers une baisse de l'oxygtnation tissulaire. Cependant, comme il s'agit d'un indice pluttt gtntral de la perfusion tissulaire globale les possibilitts qu'offre une mesure de l'hypoxie tissulaire plus locale doivent attirer notre attention. (pHi)
La mesure du phi a 6t6 introduite en 19818 mais son utilisation comme moniteur du patient en phase critique n'a 6t6 s6rieusement envisag6 que cinq ans plus tard. On a postul6 que l'isch6mie intestinale pouvait augmenter la translocation bact6rienne et ainsi stimuler la cascade des m6diateurs inflammatoires et provoquer ultimement une d6faillance multivisc6rale. Dans les 6tats de bas d6bits cardiaques, la r6duction s61ective du d6bit sanguin aux circulations coeliaque, m6sent6rique et h6patique confirme le potentiel de l'efficacit6 de la mesure de la perfusion tissulaire intestinale comme signal d'alerte prtcoce.
Avantages Cette technique est tr~s peu effractive et ntcessite l'introduction dans la lumi~re gastrique d'un tube nasal posstdant ~ son extrtmit6 un ballonnet permtable au CO2. Le ballonnet est rempli de solut6 physiologique, on laisse le CO2 s'tquilibrer avec celui de la muqueuse et le solut6 physiologique est alors aspir6 pour l'analyse de la PCO 2. Le p H e s t alors calcul6 avec l'tquation de Henderson-Hasselbach: pHi
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M O N I T O R A G E DE LA P E R F U S 1 O N T I S S U L A I R E
= C.(HCO3-/PCO2)
o~ C est une constante, HCO 3- la concentration art~rielle de bicarbonate e t P C O 2 le niveau final mesur6 dans le ballon. Un pHi normal indique que l'estomac et, par constquent, la circulation splanchnique est
La mesure du phi repose sur deux suppositions: premi~rement, que la PCO 2 du solut6 physiologique est la m~me que celle des tissus, et deuxi~mement, que la concentration du bicarbonate arttriel est la m~me que la celle de la muqueuse gastrique. Cette m&hode a aussi ses limites. Techniquement, elle consomme du temps et ntcessite beaucoup de minutie. Un intervalle de 30 ~ 90 minutes est requis apr~s l'instillation du solut6 physiologique dans le ballonnet et pour permettre au gaz et au pH de s'tquilibrer avant qu'on puisse prendre la mesure. Le monitorage ne peut donc ~tre qu'intermittent. Plusieurs facteurs peuvent influencer les niveaux du pHi dont les antiacides qui lib~rent du CO2, l'alimentation parenttrale et les variations de la stcrttion d'acide gastrique. On a suggtr6 d'administrer de la ranitidine aux patients chez qui on mesure le pHi pour limiter ce dernier effet) 3 L'utilisation de la concentration de bicarbonate arttriel pour le calcul du pHi rend le rtsultat partiellement.dtpendant de l'tquilibre acido-basique systtmique. Le pHi reprtsente donc un outil valable pour 6valuer la dtficience de la perfusion tissulaire. I1 faudra rtaliser d'autres 6tudes pour d6finir une valeur normale mais la majorit6 des 6tudes actuelles mentionnent 7,35 ou 7,32 comme limite inftrieure de la normale. Les difficultts techniques et l'intervalle de temps requis entre les mesures a permis de croire qu'une mesure plus simple serait prtftrable, celle du PCO2 rtgional. Le PCO 2 r~gional (PrC02)
L'tquilibre entre la PCO 2 de la muqueuse et celle de la lumi~re gastrique a 6t6 bien documentte en laboratoire. 14 La capacit6 de diffusion du CO 2 peut servir/~ simplifier, la mesure du pHi. Si le ballonnet situ6 ~ l'extrtmit6 du tube nasogastrique est gonfl~ avec de l'air, la mesure de la PCO2 du ballonnet refl6tera la PrCO2 gastrique. Comme celle-ci subit l'influence de la PaCt2, il est 6vident que l'analyse des gaz arttriels sera requise. Toutefois, on peut aussi mesurer simultan6ment avec la
R60 TABLEAU II
CANADIAN JOURNAL OF ANAESTHESIA Pourquoi la mesure du PrCO2 est prtf&able au pHi
1 La tonomttrie r~gionale s'appuie sur la thtode scion laquelle d'importantes augmentations de CO 2 surviennent pendant I'ischtmie tissulaire. 2 En laboratoire, les difftrences veino-arttrielles de PCO2 refl~tent les difftrences d'hypoxie tissulaire au moins aussi bien que les diff&ences arttdo-veineuses de pH. 3 La concentration systtmique de bicarbonate ne correspond pas ntcessairement ~ la concentration locale. 4 La concentration systtmique de bicarbonate est influenc~ par des facteurs autres que l'isch~mie tissulaire (en particulier par l'insuflisance rtnale. 5 La manipulation du solut6 physiologique procure une source d'erreurs fr~quentes. 6 Certains analyseurs de gaz sanguins ne sont pas adaptts ~ la mesure des solutions physiologiques et n~cessitent une calibration sptcifique. 7 Les calculs intermittents du pHi ne fournissent pas de renseignements precis sur ee qui se passe entre deux pr~l~vements successifs. 8 Les calculs du pHi sont complexes, ntcessitent des tables Sl~Ciales ou des programmes d'ordinateur 9 La PCO2 r~gionale peut se mesurer au lit du malade, et si possible en association avecla PaCO2 ou la PE'rCO2.
PrCO2, la PCO2 de l'air expir6 (la CO2 ttlt-expiratoire ou PE'rCO2, et calculer la difftrence (PrCO2 PETCO2)). 15 Cette fagon de mesurer nous permet de contourner les difficultts techniques et les calculs associts avec la mesure du pHi, procure une valeur indtpendante du bicarbonate systtmique et constitue un monitorage quasi continu de la perfusion tissulaire (Tableau II).
Le monitorage combin6 Chaque technique de monitorage a ses aspects positifs et ntgatifs. Pour 6viter de perdre son temps ~ discuter les avantages d'un indicateur sur un autre, il est bon de mentionner que la perfusion tissulaire est 6valute plus efficacement et avec plus de prtcision si associe plusieurs mtthodes ensemble. Cette approche est proposte par Friedman et al. qui ont trouv6 que la combinaison des mesures du pH et de la concentration de lactate permet de prtdire le pronostic du sepsis grave. 16 I1 est cependant important de rappeler que les rtsultats obtenus ~ partir de mesures de laboratoire ne remplaceront jamais l'tvaluation de base et ne doivent ~tre considtrts que comme un compltment ~ l'tvaluation clinique rtguli~re. Conclusion La dttection des alttrations de la perfusion tissulaire et, par constquent, de la baisse de l'oxyg6nation est pronostique de la mortalitt. Une technique fiable et r6alisable au lit du patient en phase critique est requise pour l'identification prtcoce et prtcise de l'insuffisance de l'oxyg~nation tissulaire afin d'intervenir pour limiter
les complications substquentes. La combinaison de la mesure systtmique avec la mesure rtgionale est capable de procurer une 6valuation plus fiable de la condition du patient; des mesures continues ou au moins rtptttes rtguli~rement sont ntcessaires en plus de l'tvaluation clinique pour fournir une image prtcise de l'ttat du patient et permettre l'institution d'un traitement appropal6 ainsi que le monitorage de ses effets.
Rtftrences (Voir page R57)