There might be no safe ventilation. Much too often, all there is for us to measure at the bedside are nothing but global indicators of stress/strain, more or less refined. Heterogeneity at the alveolar level-inhomogeneities or stress raisers - render global parameters less useful than previously predicted. In fact, Mead had already stated it through his work on stress distribution at the alveolar level.
ECMO (VA ECMO) might be regarded as one other way of decatecholaminization (M.Singer). Stop stressing the already stressed heart. Unfortunately, fem-fem VA ECMO still needs inotropic support to lessen the LV distension. Levosimendan and IABP combined could help decrease the catecholamine usage in this context.
Edelman-derived quantification of dyselectrolytemias.
Equation-based monitoring of hyponatremia therapy with a focus on safely and predictably increasing sodium as per guideline advice using a strategy involving desmopressin administration in severe hyponatremias, especially those patients at risk of becoming overcorrectors. Explanation of risk factors responsible for overshooting when correcting hyponatremia. Adrogue-Madias, Barsoum, Nguyen-Kurtz equations are explained and proven to be of help at least conceptually when attempting to have a desmopressin-guided therapy in hyponatremia. All recommendations are done in accordance with European and American guidelines published in 2013 and 2014.
Buying time in situations of extreme hemodynamic instability by partially reversing acidemia with a controlled strategy involving bicarbonate, calcium and hyperventilation.
Minimizing CO2 buildup as well as resulting hypocalcemia after alkalinization improves hemodynamics in a rat-derived french study.
Math modelled approach to gas-exchange monitoring Cosmin Balan
mathematical modelled approach to gas exchange monitoring.
overview of one parameter models and description of Sapsford and Kjaergaard's two parameter models.computer algorithm in assessing gas exchange at the bedside in a MIGET fashion. prediction of hypoxemia and full description of gas exchange through models that fit perfectly to patient data.
we are teleologically cardioprotected. we are already cardioprotected. nature has given us everything we need to be unbreakable.we just have to push the right buttons.
please, pay heed to the turtles! they know best!
Paradigms have been shifting.
Flow-centered ideas, ventriculo-arterial coupling and redistributions between compartments with different time constants.
There might be no safe ventilation. Much too often, all there is for us to measure at the bedside are nothing but global indicators of stress/strain, more or less refined. Heterogeneity at the alveolar level-inhomogeneities or stress raisers - render global parameters less useful than previously predicted. In fact, Mead had already stated it through his work on stress distribution at the alveolar level.
ECMO (VA ECMO) might be regarded as one other way of decatecholaminization (M.Singer). Stop stressing the already stressed heart. Unfortunately, fem-fem VA ECMO still needs inotropic support to lessen the LV distension. Levosimendan and IABP combined could help decrease the catecholamine usage in this context.
Edelman-derived quantification of dyselectrolytemias.
Equation-based monitoring of hyponatremia therapy with a focus on safely and predictably increasing sodium as per guideline advice using a strategy involving desmopressin administration in severe hyponatremias, especially those patients at risk of becoming overcorrectors. Explanation of risk factors responsible for overshooting when correcting hyponatremia. Adrogue-Madias, Barsoum, Nguyen-Kurtz equations are explained and proven to be of help at least conceptually when attempting to have a desmopressin-guided therapy in hyponatremia. All recommendations are done in accordance with European and American guidelines published in 2013 and 2014.
Buying time in situations of extreme hemodynamic instability by partially reversing acidemia with a controlled strategy involving bicarbonate, calcium and hyperventilation.
Minimizing CO2 buildup as well as resulting hypocalcemia after alkalinization improves hemodynamics in a rat-derived french study.
Math modelled approach to gas-exchange monitoring Cosmin Balan
mathematical modelled approach to gas exchange monitoring.
overview of one parameter models and description of Sapsford and Kjaergaard's two parameter models.computer algorithm in assessing gas exchange at the bedside in a MIGET fashion. prediction of hypoxemia and full description of gas exchange through models that fit perfectly to patient data.
we are teleologically cardioprotected. we are already cardioprotected. nature has given us everything we need to be unbreakable.we just have to push the right buttons.
please, pay heed to the turtles! they know best!
Paradigms have been shifting.
Flow-centered ideas, ventriculo-arterial coupling and redistributions between compartments with different time constants.
TTP-HUS
Thrombotic microangiopathy is marker for TTP/HUS as well as for DIC/DIC-like (secondary thrombotic microangiopathy-TMA), this giving us a first overlapping area.
ADAMTS 13 (ADAMTS 13 Ab/ADAMTS 13 relative or absolute deficiency) - a recent marker for TTP, regulatory complement factors flaws (CFH, MCP-CD46, IF and CD46 Ab, CFH Ab as well)-pathogenetic elements in D- HUS, increased PAI 1-recently proved for TTP, all of this are nowadays valid pathogenetic lego bricks in that wall we call secondary TMA, this giving us our second overlapping area.
Plasma exchange, grade IA recommendation for “true” TTP, has been gaining a place in the last decade in the supportive basket for secondary TMA(e.g., sepsis ), this giving us a third overlapping area.
At least three overlapping areas and the lack of certain particular cases (malignant hypertension, HCT related TMA, D+ HUS early years) deliver us a syndrome (TMA) likely to be highly responsive to plasma exchange and, in certain situations, to tailored corticotherapy, monoclonal CD20 Ab, C5 Ab.
Guytonian approach to shock - mean systemic filling pressure centeredCosmin Balan
In a world of binary decision there remains little room for applied maths and physiology. Or maybe not...
Parkin's approach brings out a forgotten tool-the volume state. Although reductionistic as well as Guyton's entire view, it might be a better language for us, for clinicians and for all those lost in translation when they've stumbled across loose binary decisions such as SVV,PPV,SPV etc.
Mean systemic filling pressure has been resurrected.
Parkin, Maas, Pinsky and Geerts have come a long way from Versprille.
TTP-HUS
Thrombotic microangiopathy is marker for TTP/HUS as well as for DIC/DIC-like (secondary thrombotic microangiopathy-TMA), this giving us a first overlapping area.
ADAMTS 13 (ADAMTS 13 Ab/ADAMTS 13 relative or absolute deficiency) - a recent marker for TTP, regulatory complement factors flaws (CFH, MCP-CD46, IF and CD46 Ab, CFH Ab as well)-pathogenetic elements in D- HUS, increased PAI 1-recently proved for TTP, all of this are nowadays valid pathogenetic lego bricks in that wall we call secondary TMA, this giving us our second overlapping area.
Plasma exchange, grade IA recommendation for “true” TTP, has been gaining a place in the last decade in the supportive basket for secondary TMA(e.g., sepsis ), this giving us a third overlapping area.
At least three overlapping areas and the lack of certain particular cases (malignant hypertension, HCT related TMA, D+ HUS early years) deliver us a syndrome (TMA) likely to be highly responsive to plasma exchange and, in certain situations, to tailored corticotherapy, monoclonal CD20 Ab, C5 Ab.
Guytonian approach to shock - mean systemic filling pressure centeredCosmin Balan
In a world of binary decision there remains little room for applied maths and physiology. Or maybe not...
Parkin's approach brings out a forgotten tool-the volume state. Although reductionistic as well as Guyton's entire view, it might be a better language for us, for clinicians and for all those lost in translation when they've stumbled across loose binary decisions such as SVV,PPV,SPV etc.
Mean systemic filling pressure has been resurrected.
Parkin, Maas, Pinsky and Geerts have come a long way from Versprille.
3. PATOGENEZA
Studii pe animale
Second hit injury
Context clinic
Context interventional
Dose dependent
Agent dependent
Cumulativ
Non linear
Marker si inductor de
prognostic negativ
mecanisme descrise in special in
studii cu compusi “vechi”-generatie I
CIN vs CAN
care este impactul real uman?
concluzii contradictorii si
nerepetabile intre studii
4. Probleme…
Un diagnostic de excludere chiar acolo unde este mai putin probabil
sa il excluzi (ex. angio-ateroembolie).
Definitie heterogena cu impact heterogen asupra concluziilor de
prognostic si preventie.
Efect nociv prezent teoretic (generatia I) dar neclar dpdv practic
(generatiile noi).
Greu de cuantificat patogenetic (uman) cel putin din cauza
comorbiditatilor asociate; dovezi indirecte; lot martor - ?
CIN este inlocuit cu CAN din cauza acestor neajunsuri.
Cat de real este CIN/CAN ?
http://ccforum.com/content/16/2/R67
6. DEFINITIA CREEAZA INCIDENTA
3 intervale de timp
3 valori cut-off de Cr
9 definitii
Lakhal, Ehrmann
J Crit Care 2011
AKIN reflecta cel mai bine prognosticul pe termen scurt si lung.
13. Calculator imperfect
Contextul interventional-arterial vs
venos(cut off ClCr diferit – 60 vs 45)
Tipul de agent (generatie 1,2 sau 3)
Intervalul de repetare
Asociere de nefrotoxine(ex. AG)
Ce risc calculeaza?
CI-AKI AKI
APASA
Daca ai net
18. PREVENTIE
ANTIOXIDANTI
REPLETIE VOLEMICA
VASODILATATORI RENALI
HEMODIAFILTRARE
MODIFICAREA FACTORILOR DE RISC ATUNCI CAND E POSIBIL.
19. VOLUM
NS 1-1.5ml/kg/h pentru 6h inainte si dupa contrast
Bicarbonat izoosmolar 3ml/kg/h cu o ora inainte si
1ml/kg/h pentru 6 ore dupa SC( efect antioxidant –
ROS dependent de pH prin r. Haber-Weiss)
20. NACC
600-1200 mg oral de 2 ori pe zi cu o zi inainte si in
ziua adm. SC
Administrarea iv. este descurajata
21. Hemodiafiltrare
Imediat dupa adm. SC o poate inlatura dar nu
previne CIN/CAN
Nu este recomandata profilactic de cei mai multi
autori
Rol profilactic la CKD 5(ClCr< 15ml/min/1.73m2)
22. Nu au rol, cel putin in prezent
Fenoldopam
Dopamine
Bloc.can Ca
Furosemide
Manitol
PG.
Ac. ascorbic
ANP
ATP
L arginina
IECA
Nebivolol
Aminofilina
Statine
25. Concluzii
Este un diagnostic de excludere
Patogeneza ce implica toxicitate directa si VC
Incidenta dependenta de agent,context clinic si
interventional
Epidemiologie neclara si extrem de heterogena
Greu de separat de comorbiditati
ASIGURAREA
VOLEMIEI
Preventia implica repletie volemica, +/- NACC si
influentarea cator mai multi factori de risc(ex. cantitatea
de SC, agentul, raport risc/beneficiu).