volumen, auch schlecht für die niere? - ake-nutrition.at · fallbeispiel # 1 • 83 jährige...
TRANSCRIPT
M. Joannidis
Internistische Intensiv- und Notfallmedizin
Universitätsklinik für Innere Medizin I
Volumen, auch schlecht für die Niere?
Fallbeispiel # 1
• 83 jährige Patientin, Hypertonie, Z.n. Apoplex mit Gangunsicherheit als Residuum, Globalherzinsuffizienz
• vor 3 Tagen gestürzt, RQW am re US mit großem Hämatom, seitdem wenig gegessen und getrunken
• Prämedikation: – Lasix 40 mg
– Aldactone 50 mg
– Renitec 10 mg
Fallbeispiel # 1
• 83 jährige Patientin, Hypertonie, Z.n. Apoplex mit Gangunsicherheit als Residuum, Globalherzinsuffizienz
• vor 3 Tagen gestürzt, RQW am re US mit großem Hämatom, seitdem wenig gegessen und getrunken
• Prämedikation:
• Lasix 40 mg, Aldactone 50 mg, Renitec 10 mg
• Aufnahmestatus:
• P 75, RR 106/50, reduzierter AZ, verwirrt,
• Zunge trocken, Lunge frei, HT o.B.
• US -Ödeme bds
• Bei Anlage eines Harnkatheters 100 ml Harn entleert, nach einer Stunde 20 ml
• US Niere: unauffällig, keine Hydronephrose
Labor (Patientin #1)
Astrup (venös):
– pH 7.36
– pCO2 38.9 mm Hg
– pO2 42.7 mm Hg
– HCO3- 22.2 mmol/l
• Serum: – K+ 7.4 mmol/l
– Na+ 126 mmol/l
– Cl- 91 mmol/l
– Ca 2.3 mmol/l
– P 1.2 mmol/l
– Glucose 116 mg/dl
– Kreatinin 2.47 mmol/l
– Harnstoff 112.6 mmol/l
– Hb 9.5 g/dl
– Protein 6.7 mg/dl
Labor (Patientin #1)
Astrup (venös):
– pH 7.36
– pCO2 38.9 mm Hg
– pO2 42.7 mm Hg
– HCO3- 22.2 mmol/l
• Serum: – K+ 7.4 mmol/l
– Na+ 126 mmol/l
– Cl- 91 mmol/l
– Ca 2.3 mmol/l
– P 1.2 mmol/l
– Glucose 116 mg/dl
– Kreatinin 2.47 mmol/l
– Harnstoff 112.6 mmol/l
– Hb 9.5 g/dl
– Protein 6.7 mg/dl
Serum Kreatinin vor 7 Monaten = 1,05 mg/dl
-> AKI Stadium 2 (2-fach< Anstieg < 3-fach)
UO= 20 ml/h seit 1 h
Cecconi, M. et al. Intensive Care Med (2015) 41:1529–1537
Fluid challenges in intensive care:
the FENICE study A global inception cohort study
Diagnose der
Akuten Nierenschädigung (AKI)
AKI Serum Kreatinin Harnausscheidung
Stadium 1 ≥1,5 bis <2,0-facher Anstieg innerhalb von 7d*
oder
Anstieg um >0,3 mg/dl innerhalb von 48 h
<0,5 ml/kg/h für 6-12 h
Stadium 2 ≥2,0 bis <3,0-facher Anstieg innerhalb von 7d* <0,5 ml/kg/h für ≥12 h
Stadium 3
≥3,0-facher Anstieg innerhalb von 7d*
oder
Anstieg* um >0,5 mg/dl (bei SCr >4 mg/dl)
oder
Beginn einer Nierenersatztherapie
<0,3 ml/kg/h für ≥24 h
oder
Anurie für ≥12 h
*Anstiege werden auf bekannten (Vorbefunde
innerhalb von 3 -12 Monaten)
oder
auf errechneten Referenzwert bezogen (MDRD-
Formel, falls keine Vorgeschichte von chronischer
Niereninsuffizienz besteht)
Kidney Int 2012, Suppl. 2012, 2: 1-138 www.KDIGO.org
Surgical Insult, Pain, Trauma,
Haemodynamic Instability
ADH RAAS SNS
OLIGURIA
Pathological
Reversible Irreversible
AKI
Mechanisms of Oliguria
Physiological
Lehner G et al, Nephron 2016
Die häufigsten Ursachen für AKI
• Hypovolämie
• Herzinsuffizienz
• Sepsis
• Medikamentenassoziierte AKI
(Nephrotoxine, NSAR, ACE Hemmer…)
Merkregel -> 4 H´s:
Hypovolämie, Herzinsuffizienz, Hyperinflammation, Hypermedikation
Himmelfarb, J. et al. Clin J Am Soc Nephrol 2008;3:962-967
Conceptual model for development and
clinical course of acute kidney injury
Himmelfarb, J. et al. Clin J Am Soc Nephrol 2008;3:962-967
Conceptual model for development and
clinical course of acute kidney injury
Fluid Accumulation has
consequences: HAGIE
Hospital acquired generalised interstitial edema
Lyons W. Crit Care Med 2000
Lyons W. J Trauma 2002
Minimised by –
Fluid “restriction” and colloid
resuscitation to appropriate
haemodynamic targets
Surviving Sepsis Campaign 2012
MANAGEMENT OF SEVERE SEPSIS
Initial Resuscitation (grade 1A):
a) CVP 8–12 mm Hg
b) MAP ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d) Superior vena cava oxygenation saturation (Scvo2) 70%
or mixed venous oxygen saturation (Svo2) 65%
SCC 2012, Dellinger R etal , Crit Care Med 2013
Fluid resuscitation in septic shock: A positive fluid
balance and elevated central venous pressure are
associated with increased mortality
Boyd, John H et al Critical Care Medicine. 39(2):259-265, February 2011.
Fluid Balance CVP
12 hours:
Fluid balance +4,9 L
Fluid balance +8,2 L
4 days:
Fluid balance +13,0 L
Fluid balance +20,1 L
Fluid resuscitation in septic shock: A positive fluid
balance and elevated central venous pressure are
associated with increased mortality
Boyd, John H et al Critical Care Medicine. 39(2):259-265, February 2011.
12-hr fluid balance: Survivors vs. nonsurvivors within CVP groups
Einflußfaktoren auf die GFR
Prowle JR et al., Nat Rev Nephrol 2010; 6: 107-15
Massive
Tubulusschwellung
Interstitielles Ödem,
erhöhter ZVD
Erhöhter intrabdomineller
Druck
Firth JD et al. Lancet 1988, i: 1121
Effects of increasing venous pressure on GFR, sodium
excretion, and fractional sodium excretion in kidneys perfused
with a constant arterial pressure
Raised Venous Pressure : A Direct Cause of
Renal Sodium Retention and Edema
Association between systemic hemodynamics and septic acute
kidney injury in critically ill patients:
a retrospective observational study
Legrand et al. Critical Care 2013, 17:R278
Statistical model of nonparametric logistic
regression showing the relationship
between mean central venous pressure
during the first 24 hours after admission
and the probability of new or persistent
acute kidney injury.
Note the plateau for the incidence of acute
kidney injury (AKI) when the lower limit of
central venous pressure (CVP) was between 8
and 12 mmHg. Over this limit, the rise in CVP
was associated with a sharp increase in new
or persistent AKI incidence.
Intraabdominal Hypertension/
Abdominal Compartment Syndrome (ACS)
Maerz and Kaplan, Critical Care Medicine 2008
Intra Abdominal Hypertension and
Abdominal Compartment Syndrome
Pre-disposing Factors Common Etiological Factors
Dalfino K et al, Intensive Care Medicine 2008
Oliguria
azotemia
Pathophysiology of CRS Type 1
Renal hypoperfusion
Reduced oxygen delivery
Necrosis / apoptosis
Decreased GFR
Resistance to ANP/BNP
BIOMARKERS
KIM-1
Cystatin-C
N-GAL
Creatinine
Hemodynamically mediated damage
Immune mediated damage
Humorally mediated damage
Humoral
signalling Cytokine
secretion
Exogenous factors
Contrast media
ACE inhibitors
Diuretics
Acute
Kidney
Injury
Caspase
activation
Apoptosis
Caspase
activation
Apoptosis
Decreased
perfusion
Acute decompensation
Ischemic insult
Coronary angiography
Cardiac surgery
Decreased CO Increased
venous
pressure
Toxicity
Vascocostriction.
RAA activation, Na + H2O
retention, vasoconstriction
BNP
Sympathetic Activation
Hormonal factors
Monocyte
Activation Endothelial
activation
Natriuresis
Acute
Heart
Disease
or
Procedures
ADQI Acute Dialysis Quality Initiative Consensus Group ADQI
More in AHF
Ähnliche Situation in der Sepsis unter
“Fluid Resuscitation”?
Restricting volumes of resuscitation fluid in adults with septic shock
after initial management:
the CLASSIC randomised, parallel-group, multicentre feasibility trial
P.B. Hjortrup et al , Intensive Care Med 2016
DOI 10.1007/s00134-016-4500-7
Fluid restriction group:
isotonic crystalloid (saline or Ringer’s
solutions) fluid boluses of 250–500 mL
in the case of severe hypoperfusion
defined as either
1. Plasma lactate of > 4 mmol/L,
2. MAP below 50 mmHg in spite of the
infusion of norepinephrine,
3. mottling beyond the edge of the
kneecap (mottling score greater
than 2)
4. oliguria, but only in the first 2 h after
randomisation (< 0.1 mL/kg IBW in
the last hour).
151 adult patients with septic shock
Standard group:
Fluids as long as circulation improves
Restricting volumes of resuscitation fluid in adults with septic shock
after initial management:
the CLASSIC randomised, parallel-group, multicentre feasibility trial
P.B. Hjortrup et al , Intensive Care Med 2016 DOI 10.1007/s00134-016-4500-7
Fluid Management in ALI Fluid and Catheter Treatment Trial(FACTT)
ARDS Clinical Network Trial, NEJM 2006
Fluid balance / week
Conserv. Strategy (n=503): Liberal Strategy (n=498):
-136 (+ 491) ml + 6992 (+502) ml
Pat. on RRT: conservative 10% liberal 14% (p=0.06)
Furosemide Doses and Changes in Serum
Creatinine During the FACTT Trial
ARDS Clinical Network Trial, NEJM 2006
Furosemide Dose
Grams M E et al. CJASN 2011;6:966-973
AKI ?
Biomarker?
Serum Creatinine
Diuretics for control of hypervolemia may improve
outcome.......?
Chawla LS et al, Crit Care 2013, 17:R207
Development and standardization of a furosemide
stress test to predict the
severity of acute kidney injury
Urinary Output response to 1.0-1.5 mg/kg furosemide in patients with AKI stage I or II
Sensitivity 84%
Sensitivity 87%
Welches
Flüssigkeitsmanagement?
Kristalloide? Kolloide?
theoretisch ~3-facher
Volumeneffekt ….
aber
fraglicher klinischer
Benefit
Are Colloids Better Than Crystalloids for Fluid
Resuscitation in Critically Ill Patients?
B. Hohertz et al, Annals of Emergency Medicine, Volume 65, no. 4 : April 2015
Perel P, Roberts I, Ker K., Colloids versus crystalloids for fluid resuscitation
in critically ill patients. Cochrane Database Syst Rev. 2013;(2):CD000567.
Osmotic Nephrosis: Acute Kidney Injury With Accumulation of Proximal
Tubular Lysosomes Due to Administration of Exogenous Solutes
Dickenmann M et al, Am J Kidney Dis 2008, 51:491-503
HES
Gelatine
Mannit
Dextrane
The Cochrane Library 2013, Jul 23;7
RESULTS: This review included 42 studies (11,399 patients)…..
…RIFLE-I (injury) outcome with a RR of AKI of 1.22 (95% CI 1.08 to 1.37; 8338
patients)….
…significant increase in the need for RRT in the HES treated individuals compared to
individuals treated with other fluid therapies (RR 1.31, 95% CI 1.16 to 1.49; 19 studies,
9857 patients). ..
….Overall, methodological quality of the studies was good 9857 patients)
AUTHORS' CONCLUSIONS: The current evidence suggests that all HES products
increase the risk in AKI and RRT in all patient populations and a safe volume of any HES
solution has yet to be determined. In most clinical situations it is likely that these risks
outweigh any benefits, and alternate volume replacement therapies should be used in
place of HES products.
Hydroxyethyl starch (HES) versus other fluid therapies:
effects on kidney function.
Mutter TC, Ruth CA, Dart AB.
Albumin
• Albumin verbessert Diurese bzw. Flüssigkeitsbilanz
(Sepsis, Herzchirurgie – HLM)
• Keinerlei Signal für Nierenschädigung in der Sepsis
(ALBIOS)
• Albumin reduziert AKI bei
Leberzirrhose/Standardtherapie bei hepato-renalem
Syndrom
Dubois M-J et al, Critical Care Medicine. 34(10):2536-2540, October 2006
Caironi P et al, N Engl J Med 2014;370:1412-21
Lee EH et al, Anesthesiology 2016 Feb 18 epub.
Caironi P et al, N Engl J Med 2014;370:1412-21.
Wiedermann CJ et al, Gastroenterol Res Pract. 2015;2015:912839
Crystalloid fluid therapy:
is the balance tipping towards
balanced solutions?
Young P & Joannidis M, Intensive Care Med. 2014 Dec;40(12):1966
Normal saline can induce metabolic acidosis and renal hypoperfusion!
Effect of a Buffered Crystalloid Solution vs Saline on Acute
Kidney Injury Among Patients in the Intensive Care Unit
The SPLIT Randomized Clinical Trial
Young P et al, JAMA. 2015 Oct 27;314(16):1701-10
Only 77 patients with sepsis
~1,7 L fluids (median) in 48h administered
Schädigung der Niere durch
Infusionslösungen?
“Chloridreiche”
Lösungen
(0.9% NaCl)?
potentiell
schädlich
Künstliche
Kolloide:
HES/Gelatine (?)
schädlich
“Balancierte”
Lösungen
Albumin
Kristalloide? Kolloide?
…also, für die Niere gesprochen:
• Volumengabe, gut bei Hypovolämie
– Kristalloide als Mittel der ersten Wahl
– Biologische Kolloide>synthetischen Kolloide
– Kein HES!
• Volumengabe, sinnlos bei Euvolämie
– Man kann die GFR nicht anschupfen….!
• Volumengabe, schädlich für die Niere bei
Hypervolämie
– Diuretika helfen!
– Frühzeitig an Vasopressoren, ggf. Inotropika denken!
Danke für Ihre Aufmerksamkeit! [email protected]
49. Gemeinsame Jahrestagung der ÖGIAIN und DGIIN 7-10. Juni 2017 , Congress Innsbruck
Personalisierte Intensivmedizin im Zeitalter der Standardisierung
Beispiel #2
53 jährige Patientin,
Vorstellung in der Notaufnahme wegen zunehmender Atemnot , Fieber,
Schüttelfrost, Husten, verminderte Harnausscheidung seit 2 Tagen
Vorerkrankungen: DM II, schwere art. Hypertonie
Prämed: Metformin, Labetalol, Irbesartan
SP: RR 83/50, Puls 102, adipös, SO2 90% unter RL, AF 26
Beinödeme bds., Herz o.B.
Lunge: Deutliche Stauungs-RGs beidseits
• Serum:
– Kreatinin 3,02 mg/dl
– Harnstoff 75,2 mg/dl
– Glucose 277 mg/dl
– CRP 37,8 mg/dl
– Leuko 21,000/µl
– Hb 10.6 g/dl
Beispiel #2
53 jährige Patientin,
Vorstellung in der Notaufnahme wegen zunehmender Atemnot , Fieber, Schüttelfrost, Husten,
verminderte Harnausscheidung seit 2 Tagen
DM II, schwere art. Hypertonie
Prämed: Metformin, Labetalol, Irbesatan
SP: RR 83/50, Puls 102, adipös, SO2 90% unter RL, AF 26
Beinödeme bds., Herz o.B.
Lunge: Deutliche Stauungs-RGs beidseits
• Harn:
– Leuko 25
– Nitrit positiv
– pH 6
– Protein 750
– Ery 150
Labor
Blutgase (arteriell)
– pH 7,47
– pCO2 25,3 mm Hg
– pO2 58 mm Hg
– HCO3- 21,3 mmol/l
– BE -4,7
– Laktat 49 mg/dl (<19,8) ~5,5 mmol/l
Welche Therapie?
1. Diuretika (a real dose!!)
2. HES
3. Albumin
4. Albumin + Kristalloide
5. Vasopressoren + Kristalloide
6. Vasopressoren
Welche Therapie?
1. Diuretika (a real dose!!)
2. HES
3. Albumin
4. Albumin + Kristalloide
5. Vasopressoren + Kristalloide
6. Vasopressoren
Verlauf
0
20
40
60
80
100
120
140
160
Aufnahme 8h 20h 32h
0
0,5
1
1,5
2
2,5
3
3,5
MAP
Stundenharn
S-Kreatinin
Arterenol
+Imipenem 3*1g
Preservation and optimization of renal function:
Strategies of maintaining renal perfusion in the ICU
• Volume Resuscitation/Challenge – depending on response ->
CI/MAP increase mandatory (!)
– CVP > 5-8 mm Hg (< 12 mm Hg)
– MAP > 65-75 mm Hg ( 85 mm Hg chronic hypertension, < 95 mm Hg)
– ScvO2 > 70% , lactate < 4mmol/l
• Early Resuscitation -> after stabilization, apply conservative fluid
regimen (even by giving high dose diuretics)
– Monitor IAP (in risk patients)
– Avoid artificial colloids, especially HES in sepsis
– Albumin may be an alternative in certain conditions (sepsis)
– Preferably use balanced solution (?)
• Vasopressors: NE , combined with vasopresssin (refractory shock)
• Inotropes:
– Levosimendan for acute heart failure/septic myocardial depression (?)
Optimierung der Nierenperfusion
• Volumenstatus (Flüssigkeit)
• Vasopressoren (Nordrenalin>Vasopressin)
• Inotropika
High versus Low Blood-Pressure Target in
Patients with Septic Shock
Asfar P et al., N Engl J Med 2014;370:1583-1593
Multicenter, open-label trial, patients with
septic shock were treated to maintain a mean
arterial pressure target of either 80 to 85 mm
Hg or 65 to 70 mm Hg.
Levosimendan for Prevention of Acute Kidney Injury After
Cardiac Surgery:
A Meta-analysis of Randomized Controlled Trials
Zhou C et al, AJKD, Volume 67, Issue 3, 2016, 408–416
Levosimendan (Levo) reduced the incidence of acute kidney injury
-> Levosimendan (Levo) reduced the need for renal replacement therapy
(odds ratio [OR], 0.43; P = 0.002).
Effects of levosimendan on systemic and regional
hemodynamics in septic myocardial depression
Morelli A et al, Intensive Care Med. 2005
-> Improvement of microcirculation (sublingual)!
Morelli A et al, Crit Care 2010
N=15/15, LEV < 55%, levosimendan 0.2 µg/kg/min, dobutamine 5 µg/kg/min
Therapie des AKI • Schock -> Schocktherapie
• Hypovolämie – Volumensubstitution: Kristalloide – bilanzierte Lösungen (z.B. Elomel, Ringer-
Laktat), isotones Kochsalz bei Hyponatriämie
• Sepsis – Volumen (>1000 ml Kristalloide, 30 ml/kg über 4-6h),
– Vasopressoren (z.B. Arterenol 5mg/50ml Perfusor starten mit 0.5-1,ml/h
– Dosierung nach MAP (> 65 mmHg) , bei vorbestehender chronischer Hypertonie höher (> 80 mm Hg)
– Rasche Antibiotikagabe
• Reduziertes effektiv zirkulierendes Volumen: – Herzinsuffizienz
• pos. inotrope Substanzen (Levosimendan 12 mg /24h>Dobutamin, )
– Leberzirrhose
• Vasopressinanaloga (z.B. Terlipressin max 6 x 2 mg)
• Albumin (200 ml/20%)
• Parazenthese beim abdominellem Kompartment-Syndrom (IAP > 20 mm Hg)
• Medikamentös induziertes AKI – Absetzen der Prämedikation
Zusätzliche iatrogene Nierenschädigung, soweit möglich, vermeiden:
Aminoglykoside, Vancomycin, Teicoplanin, Amphothericin B
NSAR, ACE Hemmer, Metformin absetzen
0,9% NaCl < 1000 ml -1500ml !
-> alternativ „balancierte“ Elektrolytlösungen geben
künstlichen Kolloide vor allem HES
(jodhaltige i. v. Röntgenkontrastmittel)
Achtung!