Diagnostic des troubles acidobasiques mixtes et complexes

Diagnostic des troubles acidobasiques mixtes et complexes

Ils se définissent comme la coexistence de deux, voire trois TAB. Leur diagnostic est important en raison de leur fréquence chez les patients hospitalisés [26, 44-46], de leur gravité potentielle du fait de l’addition de leurs effets sur le pH.Par ailleurs, leur analyse fournit une aide précieuse au diagnostic étiologique et conditionne certaines

thérapeutiques. Ils doivent être évoqués systématiquement devant une pathologie qui prédispose à ce type de troubles (choc septique, arrêt cardiorespiratoire, BPCO et traitements diurétiques...) ou des données de laboratoire « discordantes » après validation de la gazométrie, c’est-à-dire :

• une nette divergence entre les valeurs mesurées (m) et les valeurs prévisibles (p) pour les réponses à un trouble simple ;

• lors de troubles aigus, quelle que soit la valeur du pH si les valeurs mesurées dépassent les capacités de compensation : HCO3 – c < 15 mmol l–1 signe toujours une acidose métabolique ; HCO3 – c > 32 mmol l–1 signe toujours une alcalose métabolique ; PaCO2 > 50 mmHg signe toujours une acidose respiratoire ;

• l’association d’un pH normal avec des valeurs de HCO3 – et de

PaCO2 anormales car les mécanismes compensateurs ne normalisent jamais totalement le pH ;

• en présence d’une acidose métabolique : D TA ou D Cl– > D HCO3 – évoque une alcalose métabolique associée.

En pratique, il faut, en premier lieu, déterminer le trouble prévalent. L’histoire et le contexte cliniques sont les premiers éléments d’orientation. Ils seront confirmés par l’interprétation classique de la gazométrie : si le pH est acide, le trouble prévalent est une acidose et inversement. La deuxième étape consiste à comparer les valeurs mesurées, données par le laboratoire, avec les valeurs prévisibles, ce qui permet d’identifier le trouble associé. La coexistence de deux troubles métaboliques allant en sens inverse est mise en évidence en comparant l’amplitude des variations du bicarbonate (D HCO3 – ) à celles du chlore (D Cl– ) et/ou du TA (D TA) (Tableau 8).

Conclusion

De nombreux concepts physiologiques et physiopathologiques qui semblaient acquis sont largement remis en question et ouvrent de nouveaux horizons diagnostiques et thérapeutiques pour les TAB. L’approche actuelle de la régulation du pH intègre une coopération interorganes foie/muscle/rein. Le foie et le muscle éliminent du NH4

+ en consommant du bicarbonate pour le premier et en l’économisant pour le second ; le rein n’est finalement qu’un simple effecteur permettant l’élimination des ions H+ fournis par le couple foie/muscle.

Longtemps considérée comme délétère, l’acidose peut avoir des effets différents selon son contexte d’apparition. Ainsi, lorsque la cellule a un métabolisme énergétique normal,

l’acidose extracellulaire « subie » par la cellule reste probablement un trouble délétère. À l’inverse, si l’acidose est la « conséquence » d’une faillite énergétique cellulaire, de nombreux arguments portent à croire que l’acidose est un mécanisme de défense ou même de protection pour la cellule visant à limiter temporairement son dysfonctionnement métabolique. L’alcalose est, en revanche, souvent délétère du fait de ses effets arythmogènes et de la baisse du débit sanguin cérébral qu’elle induit.

L’approche classique d’Henderson-Hasselbalch permet le plus souvent le diagnostic des TAB. Néanmoins, le concept de Stewart permet, chez des patients complexes, de réajuster certains diagnostics qui semblent incompréhensibles par la simple approche classique.

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