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ANESTHÉSIE DE LINSUFFISANT RÉNAL CHRONIQUE Laurent Jacob Hôpital Saint-Louis, PARIS.

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Présentation au sujet: "ANESTHÉSIE DE LINSUFFISANT RÉNAL CHRONIQUE Laurent Jacob Hôpital Saint-Louis, PARIS."— Transcription de la présentation:

1 ANESTHÉSIE DE LINSUFFISANT RÉNAL CHRONIQUE Laurent Jacob Hôpital Saint-Louis, PARIS

2 IRC - Aspects Démographiques J ACOBS 2003, Actualité Necker Patients en Dialyse 4> Transplantations rénales par an Patients sur liste dattente Transplantés suivis 4# IRC

3 IRC, Epidémiologie 3Incidence : 6500 Nouveaux cas / an % / an 3Age moyen 358 ans /Homme; 359 ans/ Femmes 3 20 % > 75 ans 3 Incidence x 6 > 60 ans et x 7 > 75 Ans 3Incidence : 6500 Nouveaux cas / an % / an 3Age moyen 358 ans /Homme; 359 ans/ Femmes 3 20 % > 75 ans 3 Incidence x 6 > 60 ans et x 7 > 75 Ans 3Prévalence cas en 1995, en % / An 3USA, Population > 15 Ans non Diabétique 3Cl créat< 60 ml/mn = 13% 3Cl Créat < 30 ml = 0,26% 3Budget > 8 Milliards FF/An 3 > 1 % Budget Assurance Maladie 3Prévalence cas en 1995, en % / An 3USA, Population > 15 Ans non Diabétique 3Cl créat< 60 ml/mn = 13% 3Cl Créat < 30 ml = 0,26% 3Budget > 8 Milliards FF/An 3 > 1 % Budget Assurance Maladie

4 IRC -Etiologie uEnfants: 3Malformation urinaires 3SHU Maladie H é r é ditaire uAdultes : N é phropathies Glom é rulaires Diab è tes (> 50 % USA; >20% Europe) N é phropathies Vasculaires 3Polykystose uEnfants: 3Malformation urinaires 3SHU Maladie H é r é ditaire uAdultes : N é phropathies Glom é rulaires Diab è tes (> 50 % USA; >20% Europe) N é phropathies Vasculaires 3Polykystose uFemmes 2 fois moins fr é quente / hommes 2 fois moins fr é quente / hommes Py é lon é phrites Chroniques. Py é lon é phrites Chroniques. N é phrites Interstitielles. N é phrites Interstitielles. N é phropathies Toxiques N é phropathies Toxiques uFemmes 2 fois moins fr é quente / hommes 2 fois moins fr é quente / hommes Py é lon é phrites Chroniques. Py é lon é phrites Chroniques. N é phrites Interstitielles. N é phrites Interstitielles. N é phropathies Toxiques N é phropathies Toxiques

5 IRC ET RISQUE D IRA POST OPÉRATOIRE à 1 Millions personnes DFG < 60 ml /mn à 1 Millions personnes DFG < 60 ml /mn - Probl è me du d é pistage des formes mineures -Cr é atinin é mie insuffisante -Cockcroft, MDRD - R é duction n é phroniques -Fragilit é / Deshydratation - Je û n - diur é tiques -Vuln é rabilit é / Isch é mie, toxiques, sepsis - N é phropathies peu ou pas symptomatiques HTA et n é phroangioscl é rose St é nose de l art è re r é nale N é phropathie glom é rulaire DIABETE +++, risque des antidiab é tiques oraux TABAC : RR d IRC x 3

6 1-Identifier lIRC et protéger la fonction rénale résiduelle 2-Evaluer le retentissement physiologique de lIRCT 3 Prévoir le retentissement Pharmacologique

7 CR É ATININE PLASMATIQUE [Créatininémie] = Taux de production Taux délimination Muscle Rein ( µm/min) (100 ml/min) (100 µm/ml)

8 Relation Créatininémie et DFG 1 Ucr x Vu 1 Ucr x Vu DFG = X [Gcr] = Pcr Pcr Pcr Pcr 3Production de Créatinine: Créatine et phosphocréatine du muscle 3Alimentation Protéines cuites, Créatine 3Masse musculaire 3Technique de Dosage Jaffé Chromogènes 3Insuffisance Rénale Sécrétion Tubulaire UcrxVu= DFGxPcr + TScr, = +35ml Sécrétion Tubulaire UcrxVu= DFGxPcr + TScr, = +35ml Métabolisme Intestinal Métabolisme Intestinal 3Interférence dosage Acidocétose (Acéto Acétate) Acidocétose (Acéto Acétate) Hyperbilirubinémie Hyperbilirubinémie

9 FG et clairance de la cr é atinine Shemesh O Kidney Int 1985; 28:

10 DFG & Cr é atinine plasmatique Cl CR 99% Cl CR 99% DFG DFG Créat P 100% Créat P 100% Cl CR 69% Cl CR 69% DFG DFG Créat P 75% Créat P 75% Cl CR 99% Cl CR 99% DFG DFG Créat P 100% Créat P 100% Cl CR 69% Cl CR 69% DFG DFG Créat P 75% Créat P 75% DFG =1/Pcréat x [K]

11 Effet de lâge sur le rein u Masse Rénal g à 20 ans g à 80 ans 3 Sclérose glomérulaire si HTA u DSR 310% /Décades 3RPF 600ml 300ml à 80 ans 3Débit Cortical >> Médullaire 3 Résistance Afférentes & efférentes 3 Vasodilatation, Autorégulation 3 Fraction de filtration u DFG 31 ml /an > 30 ans 3>> si HTA & Diabètes 3 Masse musculaire // Créatininémie stable

12 Cl Créat (ml/mn) = [140-âge(ans)]X Poids (Kg) X F Créatinine( µmol/l) F = 1,04 chez lhomme et 1,23 chez la femme Femme,75 ans, 52 Kg, Créat 100 µmol/l, Cl Créat = 35 ml/mn Homme, 25 ans, 100 Kg, Créat = 100 µmol/l; Cl Créat = 140 ml/mn Formule de Cockcroft et Grault Validé chez le volontaire sain en situation stable Validé chez le volontaire sain en situation stable Surestimation DFG Surestimation DFG - Obèse - Œdème - Dysfonction rénale évolutive

13 DÉBIT FILTRATION GLOMÉRULAIRE MESURÉ ET ESTIMÉ Levey AS Annals Intern Med 1999; 130(6); Cl. créatinine CockroftMDRD

14 Filtration glomérulaire et Cystatine-C 0,5 0,8 1,0 1,2 1,5 1,8 2,0 2,2 2,5 2,83,0 Cystatine-C, mg/l Débit de filtration glomérulaire, ml/min DFG mesuré, ml/min DFG estimé, ml/min DFG = / CysC 1/O.75 n = 208 patients Grubb AO Adv Clin Chem. 2000;35:63-99

15 Kidney International, Vol 65(2004),pp Factors influencing serum cystatine C levels other than renal function and the impact on renal function measurement E RIC L. K NIGHT, J ACOBIEN C. V ERHAVE, D ONNA S PIEGELMAN, H ANS L. H ILLEGE, D ICK D E Z EEUW, G ARY C. C URHAN, and P AUL E. D E J ONG Channing Laboratory, Renal Division, Brigham and Womens Hospital, Harvard Medical School, Boston, Massachusetts ; Renal Unit, Department of Medecine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts ; Department of Epidemiology and JH, Harvard School of Public Health, Boston, Massachusetts ; and Division of Neprology, Department of Internal Medecine, Department of Cardiology, Department of Clinical Pharmacology, University Medical Center Groningen,Groningen, The Netherlands …/… Conclusion. Serum cystatin C appears to be influenced by factors other than renal function alone. In addition we found no evidence that multivariate serum cystatin C-based estimates of renal function are superior to multivariate serum creatinine-based estimates Kidney International, Vol 65(2004),pp Factors influencing serum cystatine C levels other than renal function and the impact on renal function measurement E RIC L. K NIGHT, J ACOBIEN C. V ERHAVE, D ONNA S PIEGELMAN, H ANS L. H ILLEGE, D ICK D E Z EEUW, G ARY C. C URHAN, and P AUL E. D E J ONG Channing Laboratory, Renal Division, Brigham and Womens Hospital, Harvard Medical School, Boston, Massachusetts ; Renal Unit, Department of Medecine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts ; Department of Epidemiology and JH, Harvard School of Public Health, Boston, Massachusetts ; and Division of Neprology, Department of Internal Medecine, Department of Cardiology, Department of Clinical Pharmacology, University Medical Center Groningen,Groningen, The Netherlands …/… Conclusion. Serum cystatin C appears to be influenced by factors other than renal function alone. In addition we found no evidence that multivariate serum cystatin C-based estimates of renal function are superior to multivariate serum creatinine-based estimates

16 %50%0% DFG Max DFG Base NOTION DE RÉSERVE DE FILTRATION GLOMÉRULAIRE R. Bellomo Int Care Med 2004 DFG ml/mn

17 ÉVALUATION PRÉOPÉRATOIRE

18 IRC & PATHOLOGIE CARDIOVASCULAIRE 3HTA 3Hypertrophie du VG 3Insuffisance coronaire Art é rioscl é rose Dysfontion VG Dyslipid é mie Fistules art é rioveineusesMauvaise adaptation An é mie conditions de Charge 3Dysautonomie Surcharge hydrosod é e 3HTA 3Hypertrophie du VG 3Insuffisance coronaire Art é rioscl é rose Dysfontion VG Dyslipid é mie Fistules art é rioveineusesMauvaise adaptation An é mie conditions de Charge 3Dysautonomie Surcharge hydrosod é e

19 Renal Transplantation, Cardiovascular Mortality Raine, Nephrol dial transplant 1996 Transplanted Pts Hemodialysis Total CV= 36% Total CV = 58%

20 IRC Retentissement h é matologique 3Carence en EPO H é molyse, H é morragies digestives Occultes 3Carence en Fer, Folates Vit B6 & B12 An é mie non r é g é n é rative Hb <6g/100ml Hct< 30% Transfusion = sensibilisation Substitution syst é matique en EPO (SC>>IV) + FER Hb = g /100ml 3Carence en EPO H é molyse, H é morragies digestives Occultes 3Carence en Fer, Folates Vit B6 & B12 An é mie non r é g é n é rative Hb <6g/100ml Hct< 30% Transfusion = sensibilisation Substitution syst é matique en EPO (SC>>IV) + FER Hb = g /100ml

21 IRC &TENDANCE HÉMORRAGIQUE uDysfonction plaquettaire Adh é sivit é & Agr é gation Adh é sivit é & Agr é gation Alt é ration Facteur VW Alt é ration Facteur VW D é ficit Facteur 3 Plaquettaire TEMPS DE D é ficit Facteur 3 Plaquettaire TEMPS DE u Thromboxane A 2 SAIGNEMENT u Prostacycline u L-Arg-NO D é ficit en ADP ATP & s é rotonine D é ficit en ADP ATP & s é rotonine Alt é ration fonctionnelle des r é cepteurs GpIIb-IIIa Alt é ration fonctionnelle des r é cepteurs GpIIb-IIIa uDysfonction plaquettaire Adh é sivit é & Agr é gation Adh é sivit é & Agr é gation Alt é ration Facteur VW Alt é ration Facteur VW D é ficit Facteur 3 Plaquettaire TEMPS DE D é ficit Facteur 3 Plaquettaire TEMPS DE u Thromboxane A 2 SAIGNEMENT u Prostacycline u L-Arg-NO D é ficit en ADP ATP & s é rotonine D é ficit en ADP ATP & s é rotonine Alt é ration fonctionnelle des r é cepteurs GpIIb-IIIa Alt é ration fonctionnelle des r é cepteurs GpIIb-IIIa

22 Background Bleeding is recognized as a major complication in chronic ur é mia (Morgani, 1764) Bleeding is recognized as a major complication in chronic ur é mia (Morgani, 1764) çDialysis reduced the incidences of these complications çGastric and mucosal bleeding çIncreased blood loss with surgical procedure çCorrelation with Skin Bleedind Time lenghtening çRecent publication pointed out hypercoagulability related to endothelial alteration, chronic inflammation,oxydative stress and decreased fibrinolytic efficiency leading to a vasculopathic state (Morris, J Nephrol 2000)

23 Pathophysiologic Mechanisms Implicated in the Uremic bleedind Diathesis A Weigert, Am J Med Sci Defect in platelet function and metabolism çAbnormal aggregability çDecreased thromboxane A2 production çAbnormal Ca mobilisation çIncreased intracellular AMPc and GMPc 3Defect of Vascular endothelial /smooth muscle Cell metabolism çIncresed PGI2 and NO release 3Defect of platelet-vessel wall interaction çDecreased platelet adhesion and vWF activity 3Anemia

24 PLATELET DEFECT D. Mezzano, Thrombosis and Hemostasis 1996 ç 48 CRF patients (Creat Cl < 20 ml/mn) vs 12 Control volunters Plasma Creat 968 µ mol/l Plasma Creat 968 µ mol/l µ mol/l BT< 9,5 mn µ mol/l BT > 9,5 mn ç BT > 9,5 mn 52% Patients ç Platelet count: /mm 3

25 PLATELET DEFECT D. Mezzano, Thrombosis and Hemostasis 1996 Platelet aggregation% p < 0,001 p < 0,001 p < 0,001 Platelet content p < 0,001 Plasma vWF/FVIII complex

26 PLATELET DEFECT D. Mezzano, Thrombosis and Hemostasis 1996 Increased Thrombine Activation & Fibrinolysis markers in CRF Patients ç Plasma Prothrombin Fragment ç Thrombin-AntiThrombin Complexes ç Fibrinogen ç Factor VII:C ç Total fibrinogen degradation products (PDF)

27 CRF & Increased Bleedind Tendency Cryopr é cipitates: Janson N Engl J Med 1980 BT Min

28 CRF & Increased Bleedind Tendency 3Desmopressine (DDAVP) 0,3 µg/Kg; Manucci N Engl J Med 1983 BT Min

29 CRF & Increased Bleedind Tendency 4Role of Conjugated Estrogens M.Livio; N Engl J Med 1986 BT min

30 Effect of EPO Therapy on Bleeding time in CRF Patients G. Vigano ; Am J Kidney Dis 1991 PCV % BT min R = 0.89 P < 0,001

31 CRF & Increased Bleedind Tendency HEMATOCRIT > 30% HEMATOCRIT < 30% RBC enhanced platelet adhesion & aggregation by ADP release and PGI 2 inactivation RBC enhanced platelet adhesion & aggregation by ADP release and PGI 2 inactivation

32 Effect of rHuEPO Therapy on Uremia Bleeding in CRF Patients 3rHuEPO improve Hemostasis in uremic patient äDecreases BT within 1 Week äCorrection of hematocrit (2 weeks) äImprovement in Platelet aggregation (ADP, Collagen, Epinephrine, Ristocetin) äPlasma and intra platelet Serotonin contents äNo significant modification in coagulation factors or vWF Ag & Ristocetin& FVIIIc äGpIIb/IIIa Dysfunction & number not corrected + J Malyszko, Thrombosis research W Tang, Am J Nephrol 1998

33 Role of Dialysable Factors ç Plasma from CRF induces control Platelet defect ç Correction of bleeding tendency after CAPD > Hemodialysis No correlation was found between plasma Ur é a, Ph é nol, Phenol Acid and BT in CRF patients No correlation was found between plasma Ur é a, Ph é nol, Phenol Acid and BT in CRF patients ç Role of Guanidino succinic acid accumulation with NO production Increase

34 Uremic bleeding Effect of Dialysis J. H. STEWART and P.A. CASTALDI, QJM patients, 20 Dialysis (11CAPD- 9 HD) 4Clinical bleeding corrected at Day 1 4BT >20 min 19/20 measurements ç Unchanged in 6 patients ç Decreased in 13 Patients ç Normalized in 6 Patients

35 Uremic bleeding Effect of Dialysis 4G. Remuzzi & M Livio, Nephron 1978 ç Bleedind and BT only partially corrected by dialysis 4J-P Arendt Proc EDTA 1981 ç CAPD > HD 4M.Assouad, Am J Nephrol 1998 ç Hypercoagulability (Abnormal fibrinolysis) during CAPD 4J Malyszko Peritoneal Dialysis Int 2001 ç CAPD patients higher degree of hypercoagulation than HD patients

36 Uremic bleeding & L Arg-NO Pathway M. Noris & G. Remuzzi; Blood 1999 çL-NMMA BT in Uremic and volounters çNO Inhalation BT in ARDS Patients ç NO in exhaled air plasma NO X in CRF Pts ç NO Synthase and NO Production by Estrogens BT by Estrogens by LNMMA BT by Estrogens by LNMMA çRole of TNF and IL 1 in NO Synthase activation (Dialysis/LPS) çRole of Guadinido Succinic Acid AGS induced Vd L-NMMA AGS induced Vd L-NMMA AGS induced NOx L-NMMA AGS induced NOx L-NMMA

37 Uremic bleeding & L Arg-NO Pathway M. Noris & G. Remuzzi; Blood 1999 AGS -log[M] % Relax Rat Aorta AGS + L-NMMA AGS Platelet NO Platelet NO Endothelial NO Endothelial NO Platelet GMPc p<0,01 p<0,01 p<0,01

38 ABNORMAL PROSTANOIDES SYNTHESIS in CRF A. Weigert, Am J Med Sci 1998 Decreased Vasoconstriction Defect in Platelet Adhesion, Activation & Aggregation Arachidonic acid Endoperoxyde PLATELET ENDOTHELIAL CELL TxA 2 TxA 2 PGI 2 PGI 2 AMPc AMPc GMPc GMPc NO NO Cyclooxygenase

39 Conclusion 3Hemostatic defect in uremia is a complexe phenomenon ç Accumulation of dialysable compound ç Anemia ç Defect of platelet-vessel wall interaction ç Increased PGI 2 and NO release ç Decreased Thromboxane A 2 production 4RHuEPO, Hemodialysis, DDAVP, Cryoprecipitates & Estrogens 4Hypercoagulation : Inflamation, Oxydative stress, initial pathology, Hemodialysis

40 IRC & RETENTISSEMENT MÉTABOLIQUE 3Hyponatrémie 3Hémodialyse 3Hyperkaliémie 3G30% + Insuline 3CO 3 HNa 3CaCl 2 3Hémodialyse (Pré & Post opératoire) 3Acidose métabolic

41 É VALUATION PR É OP É RATOIRE É valuation Cardiovasculaire 3Traitements 3Echocardiographie 3Monitoring Strat é gie de r é veil É valuation Hematologique 3Besoins Transfusionnels Risque h é morragique 3FAV Dialyse post op é ratoire É valuation Cardiovasculaire 3Traitements 3Echocardiographie 3Monitoring Strat é gie de r é veil É valuation Hematologique 3Besoins Transfusionnels Risque h é morragique 3FAV Dialyse post op é ratoire

42 IRCT- EFFETS PHARMACOLOGIQUES 3Acidose & Hypoalbuminémie 3Hémodilution & hyperhydratation 3Augmentation du volume de distribution *Augmentation Forme libre, non-ionisée =ACTIVE *Accumulation * Posologie initiale * Réinjections * Interval entre les injections + Diminution de lélimination des agents hydrosolubles ou de leurs métabolites. 3Acidose & Hypoalbuminémie 3Hémodilution & hyperhydratation 3Augmentation du volume de distribution *Augmentation Forme libre, non-ionisée =ACTIVE *Accumulation * Posologie initiale * Réinjections * Interval entre les injections + Diminution de lélimination des agents hydrosolubles ou de leurs métabolites.

43 IRCT& Morphine M. Chauvin, Anesth é siology 1987 M. Chauvin, Anesth é siology % é limination r é nale inchang é e 10 % é limination r é nale inchang é e Diminution de la clearance des m é tabolites hydrosolubles (M3G & M6G) Diminution de la clearance des m é tabolites hydrosolubles (M3G & M6G) D é tectables dans le plasma> 36h (vs 36h (vs < 12h Contrôle) *Majoration du risque de dépression respiratoire M. Chauvin, Anesth é siology 1987 M. Chauvin, Anesth é siology % é limination r é nale inchang é e 10 % é limination r é nale inchang é e Diminution de la clearance des m é tabolites hydrosolubles (M3G & M6G) Diminution de la clearance des m é tabolites hydrosolubles (M3G & M6G) D é tectables dans le plasma> 36h (vs 36h (vs < 12h Contrôle) *Majoration du risque de dépression respiratoire

44 IRCT & Morphine G. D Honneur Anesthesiology Morphine per-os 30 mg G. D Honneur Anesthesiology Morphine per-os 30 mg ng/ml Morphine M6G M3G

45 IRC & MORPHINIQUES 3Alfentanyl ; Chauvin, Anesth Analg Sufentanyl : Fymann, Can J Anesth 1988 *Pas de modifications Pharmacodynamiques 3Alfentanyl ; Chauvin, Anesth Analg Sufentanyl : Fymann, Can J Anesth 1988 *Pas de modifications Pharmacodynamiques

46 CURARES 3Curares dépolarisants 3RD Miller Anesthesiology Hyperkaliémie transitoire et modérée, = 0,7 mmol/l 3Intubation estomac plein 3Curares dépolarisants 3RD Miller Anesthesiology Hyperkaliémie transitoire et modérée, = 0,7 mmol/l 3Intubation estomac plein

47 Bromure de Pancuronium D Hollander Acta Anaesth Scand Allongement majeur de T1/2 > 500 min Risque de curarisation prolong é e majeure D Hollander Acta Anaesth Scand Allongement majeur de T1/2 > 500 min Risque de curarisation prolong é e majeure

48 Atracurium & Vécuronium uRD Miller Anesthesiology 1984 Dur é e d action (1/3 Pavulon) R é cup é ration rapide (1/2 Pavulon) Accumulation des m é tabolites du V é curonium apr è s administration prolong é e (3-desacetyl Vecuronium) V Segredo Anesthesiology 1990 uRD Miller Anesthesiology 1984 Dur é e d action (1/3 Pavulon) R é cup é ration rapide (1/2 Pavulon) Accumulation des m é tabolites du V é curonium apr è s administration prolong é e (3-desacetyl Vecuronium) V Segredo Anesthesiology 1990

49 Cisatracurium & CRF Clairance T 1/2 ã Eastwood, BJA 1995 ONSET RECOV 25% RECOV 90% ã Boyd, BJA 1996

50 CRF & Nondepolarizing neuromuscular blocking Agent 3Esmeron, Scenohradzsky, Anesthesiology Mivacurium, Phillips BJA Pipecuronium, Caldwell, Anesthesiology Doxacurium, Cook, Anesth Analg 1992 * Interindividual variability * Prolonged effect * Importance of monitoring 3Esmeron, Scenohradzsky, Anesthesiology Mivacurium, Phillips BJA Pipecuronium, Caldwell, Anesthesiology Doxacurium, Cook, Anesth Analg 1992 * Interindividual variability * Prolonged effect * Importance of monitoring

51 Midazolam 3Diminution fixation protéique 88 vs 96 % 3Métabolisme Hépatique 3Élimination rénale inchangée 2% 3Vinick Anesthesiology Augmentation fraction libre 3,9 % 6,5 % 3Diminution délai daction 3Augmentation durée daction 3Accumulation de métabolites hydrosolubles actifs: -hydroxy Midazolam (Bauer Lancet 1995) 3Diminution fixation protéique 88 vs 96 % 3Métabolisme Hépatique 3Élimination rénale inchangée 2% 3Vinick Anesthesiology Augmentation fraction libre 3,9 % 6,5 % 3Diminution délai daction 3Augmentation durée daction 3Accumulation de métabolites hydrosolubles actifs: -hydroxy Midazolam (Bauer Lancet 1995)

52 Propofol 3Kirvela, BJA Hepatic & extra hepatic metabolisme 3Proteine binding 98 % 3T1/2 unchanged 3Vasodilation and MAP decrease majoration 3Kirvela, BJA Hepatic & extra hepatic metabolisme 3Proteine binding 98 % 3T1/2 unchanged 3Vasodilation and MAP decrease majoration

53 SEVOFLURANE & Renal Function E.J. Finck, Anesthesiology 1994 Fluor µmol/l MAX URINARY OSMOLALITY MAX URINARY OSMOLALITY

54 Conclusion çSituation de plus en plus fréquentes ; démographie en expansion çDétection de la réduction de parenchyme rénal fonctionnel : Créatinine marqueur insuffisant çPrévention = Assurance Qualité? ã Dépistage sujet à risque ã Eviction agents néphrotoxiques ã Hyperhydratation ã Médicaments ??? çAnesthésie IRC : Terrain & Pharmacologie

55 HYPERKALIÉMIE

56 HYPERKALIÉMIE TRAITEMENT DURGENCE Traitement ActionDose DélaiDurée Gluconate Antagonisme 10-20ml 1-3 mn 30mn de Calcium 10%de membrane CO 3 HNaTransfert50-100ml5-10mn2 H G10%-InsulineTransfert1000ml30 mn4-6 H ± 10 U. DiurétiquesExcrétionVariable EERExcrétionLong?

57 Gluconate de Ca ++ P.Action Potentiel Seuil Potentiel de repos HYPERKALIÉMIE HYPERKALIÉMIE- ELECTROPHYSIOLOGIE

58 IRC - Aspects Démographiques uP Jungers, N é phrol Dial Transplant 1996 Cr é at >200 µ mol 260 /10 6 H Cr é at > 500 µ mol 79 / 10 6 H 344% RRT within 12 month uF. Valderiabano N é phrol Dial Transplant EDTA Report - France data Pts with RRT Kidney transplantation uP Jungers, N é phrol Dial Transplant 1996 Cr é at >200 µ mol 260 /10 6 H Cr é at > 500 µ mol 79 / 10 6 H 344% RRT within 12 month uF. Valderiabano N é phrol Dial Transplant EDTA Report - France data Pts with RRT Kidney transplantation Age %

59 INTERPRÉTATION DE LA CRÉATININÉMIE

60 Estimation du débit de filtration glomérulaire GFR a = 170 x Creat x age x if female X 1.18 if black X BUN X albumin GFR b = x Creat x age x if female X 1.21 if black a. Levey AS Annals Intern Med 1999; 130(6); b. Levey AS J Am Soc Nephrol 2000; 11: 155a Formules de Levey Modification Diet in Renal Disease Limite Inférieure: 75 ml/mn/1,73m 2 Limite Inférieure: 75 ml/mn/1,73m 2

61 UREMIC BLEEDIND PATHOGENESIS

62 PLATELET DYSFUNCTION çNormal Platelet count çReduced Platelet Adhesion, Activation and Aggregation çMultifactorial mechanisms

63 Mannucci, P. M. N Engl J Med 2004;351:

64 Pathophysiologic Mechanisms Implicated in the Uremic bleedind Diathesis A Weigert, Am J Med Sci Defect in platelet function and metabolism çAbnormal aggregability çDecreased thromboxane A2 production çAbnormal Ca mobilisation çIncreased intracellular AMPc and GMPc 3Defect of Vascular endothelial /smooth muscle Cell metabolism çIncresed PGI2 and NO release 3Defect of platelet-vessel wall interaction çDecreased platelet adhesion and vWF activity 3Anemia

65 UREMIC BLEEDING: Platelet and Vessel wall interaction defect Platelet thrombus Stabilisation Thrombine, CD40 GpIIb/IIIa Endothelial injury Matrix, Collagen exposition vWF Platelet GpIb Platelet GpIb Collagen R Platelet Adhesion Platelet Activation Platelet release ADPSerotonine TBXA 2 -Thrombin -Thrombin Phospholipase C activation Cytosolic Ca ++ increase AMP C decrease Platelet modification GPIIb/IIIa Activation Plasma vWF & Fibrinogen linckage Hämostaseologie 2004

66 UREMIC BLEEDIND Role of Rheologic factors

67 CRF Hematologic consequenses 3EPO deficiency 3Hemolysis 3Iron, Folates Vit B6 & B12 deficit 3Occult Digestive Haemorrhage Non regenerative Anemia Hb <6g/100ml Hct< 30% Blood transfusion = sensitization 3EPO deficiency 3Hemolysis 3Iron, Folates Vit B6 & B12 deficit 3Occult Digestive Haemorrhage Non regenerative Anemia Hb <6g/100ml Hct< 30% Blood transfusion = sensitization

68 Uremic bleeding & L Arg-NO Pathway Putrescine L-Ornithine L-Ornithine L-Arginine L-Arginine L-Arginosuccinate L-Citrulline Fumarate H2OH2OH2OH2O NH2 C = O NH2Urea GuanidinoSuccinic GuanidinoSuccinicAcid Ac Aspartic Estrogens, Dexamethasone CRF

69 IRC & TRAITEMENT DU RISQUE HÉMORRAGIQUE *Hémodialyse *Anémie : correction HCT>30% *Desmopressine (0,3µg/kg) IV or SC *oestrogènes conjugués *Hémodialyse *Anémie : correction HCT>30% *Desmopressine (0,3µg/kg) IV or SC *oestrogènes conjugués

70 HÉMORRAGIQUE IRC & TENDANCE HÉMORRAGIQUE TS Min TS Min Hct % Hct %

71 IRC & TENDANCE HÉMORRAGIQUE HEMATOCRITE > 30% HEMATOCRITE < 30%

72 IRC & TENDANCE H É MORRAGIQUE Cryopr é cipitates: Janson N Engl J Med 1980 TS Min

73 IRC & TENDANCE H É MORRAGIQUE 3Desmopressine (DDAVP) 0,3 µg/Kg; Manucci N Engl J Med 1983 BT Min


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