Intra-operative determinants of postoperative AKI
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A presentation by Peter Noordzij at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine. All available content from SSAI2017: https://scanfoam.org/ssai2017/ Delivered in collaboration between scanFOAM, SSAI & SFAI.
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Intra-operative determinants of postoperative AKI
- 1. Intra-operative determinants of postoperative AKI Peter Noordzij MD PhD
- 2. | DISCLOSURE I have no financial relationships with any commercial interest related to the content of this presentation
- 3. | DUTCH FACTS 650,000 1.9% 7-47% 18-46% Noordzij et al. Anesthesiology 2010, Bihorac et al Ann Surg 2009 surgical procedures 30-day mortality AKI (7-47%) AKI related mortality
- 5. | RISK STRATIFICATION FOR AKI High risk surgery Ischemic heart disease Congestive heart failure Cerebrovascular disease Insulin therapy for diabetes Creatinine >2.0 mg/dL (177 umol/L) Revised cardiac risk index
- 6. | RISK STRATIFICATION FOR AKI Diabetes Hypertension Proteinuria Serum creatinine fluctuations Older age CKD Meersch et al. Anesth Analg 2017
- 7. | Mooney et al. Anesthesiology 2013 STUDIE DESIGN Meta-analysis POPULATION 49 studies TYPE OF SURGERY Mainly cardiac and vascular surgery (44 studies) TEST eGFR STUDY PERIOD 30 days, long term ENDPOINTS Mortality, MACE, AKI RISK STRATIFICATION eGFR <60 3 fold risk of 30-day death 3 fold risk of 30-day AKI 1.6 fold risk of long term death 1.5 fold risk of long term MACE
- 9. | PERIOPERATIVE KIDNEY INJURY Transfusion managementInflammation Drugs Fluid management Anemia Type of surgery Haemodynamics Patient characteristics
- 10. | ANEMIA AND AKI Walsh et al. Anesth Analg 2013 STUDIE DESIGN Observational cohort study POPULATION 27,381 patients TYPE OF SURGERY Major noncardiac surgery INTERVENTION None STUDY PERIOD 7 days ENDPOINT AKI 7.5 mmol/l 2.0 g/dl = 1.2 mmol/l
- 11. | CONCLUSIONS ANEMIA Preoperative anemia is common and a risk factor for AKI Δ Hb > 2 mmol/l occurs often and further identifies patients at risk for AKI Actual cause of AKI is most likely a combination of renal ischemia and inflammation
- 12. | FLUID MANAGEMENT AND AKI AKI compartment syndrome Venous congestion ▼ oxygenation Fluid overload + inflammation
- 13. | GDT AND RENAL OUTCOME Pearse et al. JAMA 2014 STUDIE DESIGN Randomised controlled trial POPULATION 734 patients TYPE OF SURGERY Major abdominal surgery INTERVENTION CO guided HD therapy until 6h post surgery STUDY PERIOD 30 days ENDPOINT Composite of mortality and complications
- 14. | GDT AND RENAL OUTCOME Schmid et al. Crit Care 2016 STUDIE DESIGN Randomised controlled trial POPULATION 180 patients TYPE OF SURGERY Major abdominal surgery INTERVENTION GDT with PiCCO STUDY PERIOD 30 days ENDPOINT Change in creatinine, complications, mortality Δ creat 18 ± 39 vs 16 ± 42 umol/l Δ eGFR -12 ± 24 vs -10 ± 24 umol/l Small difference in dobutamine use Dialysis 5 vs 5% Hospital mortality 5 vs 4% Risk factors for AKI are: hypotension (MAP <70), hypovolemia (GEDI <640), use of colloids (HES)
- 15. | TYPE OF FLUID STUDIE DESIGN Randomised controlled trial POPULATION 2,278 ICU patients TYPE OF SURGERY Cardiac and noncardiac surgery INTERVENTION None STUDY PERIOD 90 days ENDPOINT AKI, mortality
- 16. | CONCLUSIONS FLUID MANAGEMENT Fluid overload and risk of impaired renal perfusion and oxygenation GDT does not attenuate the risk of AKI Balanced crystalloid solutions do not prevent AKI compared with 0.9% NaCl in surgical ICU patients Colloids should be avoided in patients at risk of AKI
- 17. | RENAL HYPOPERFUSION LOW BLOOD PRESSURE I/R INJURY
- 18. | HYPOTENSION AND AKI Sun et al. Anesthesiology 2015 STUDIE DESIGN Retrospective cohort study POPULATION 5,127 patients TYPE OF SURGERY Noncardiac surgery INTERVENTION None STUDY PERIOD 48 hours ENDPOINT AKI for MAP 55, 60, 65mmHg
- 19. | HYPOTENSION AND AKI Rettig et al. Eur J Anesthesiology 2017 STUDIE DESIGN Observational cohort study POPULATION 202 patients TYPE OF SURGERY Major abdominal surgery INTERVENTION None STUDY PERIOD 7 days ENDPOINT eGFR on day 1, 3, 7
- 20. | CONCLUSIONS HYPOTENSION Episodes of hypotension may lead to AKI and should be kept as short as possible Optimal perfusion pressure cannot be specified and depends on autoregulatory range (premorbid conditions) For now, MAP >55 mmHg seems relatively safe Which vasopressor is most effective is unknown
- 21. | INTERVENTIONS TO PREVENT AKI? ? ? X DEXMED STATINS BICARBONATE
- 22. | OVERALL CONCLUSIONS (I) AKI is a major cause for in-hospital mortality AKI may lead to late-stage CKD and cardiovascular events eGFR is more accurate than creatinine in risk stratification Treatment options are limited
- 23. | OVERALL CONCLUSIONS (II) Identify the high risk patient Treat pre-operative anemia Minimize Hb drops Prevent fluid overload Reduce I/R injury by treating hypotensive episodes
Editor's Notes
- Good afternoon, my name is Peter Noordzij and I work as an anesthetist and ICU physician in a large referral hospital for cardiac and abdominal surgery in The Netherlands. This presentation will be about determinants of acute kidney injury during the surgical period.
- I have no disclosures related to this topic
- Each year in The Netherlands approximately 3% of the population is undergoing a major surgerical procedure. With an overall postoperative mortality just below 2%. Acute kidney injury after surgery is common (30-40% of all AKIs) and occurs in more than 7% of patients undergoing major surgery. Depending on risk factors, such as type of surgery, the incidence of AKI ranges from 7 to 48%. Mortality after AKI depends on the severity of the disease. The slide displays the current AKI stages and diagnosing criteria. The mildest form of AKI (stage I) is characterised by either an absolute creatinine increas within 48 hours, of a relative increases wihin 7 days or a lack of urine production for 6-12 hours. AKI related mortality 18% risk class, 46% failure class according to RIFLE criteria AKI most common in cardiac, CPB, pre-ex CKD, gastric bypass AKI in 1% of patients with a normal preop kidney function
- The majority of patients who suffer an episode of AKI will recover. And laboratory values will suggest complete or near complete recovery of renal function. This makes it easy to underestimat ethe effect of AKI, but the truth is that a significant portion of post-AKI survivors will develop CKD. CKD is a risk factor future AKI, with further deterioration of renal function. CKD is associated with higher risk of major adverse cardiac events (MACEs) such as MI, stroke, and heart failure. Progression of CKD as a result of critical reduction of renal mass that leads to compensatory glomerular hypertrophy and increased glomerular pressures culminating in glomerulonefrosis.
- Renal disease is a marker of cardiac risk in many settings, including surgery. To determine such risk models often use creatinine to identify patients with moderate to severe renal dysfunction. However, estimated GFR provides a more accurate indication of renal function than serum creatinine. Simple formulae, which combine basic demographic information with serum creatinine levels to estimate GFR can be used for risk stratification. The CKD-EPI formula is most accurate. (provides a more precise estimate of GFR at higher levels). In healthy persons MDRD is not specific enough. Albuminuria results when increased permeability allows filtration of protein across the glomerular membrane, and it is thought to reflect the generalized vascular endothelial dysfunction (Steno hypothesis) [9] or systemic inflammation involving the glomerulus
- AKI is a serious surgical complication with high hospitalization related death rates and long-term consequences. Risk stratification for AKI must include proper detection of CKD that may not be reflected by a significant decrease in eGFR. History of diabetes, hypertension, proteinuria, high serum creatinine nonlinearity, African-American race, and older age should at least be considered as important risk factors for AKI and further progression to CKD.
- In a meta-analysis published in … the aim was to clarify the strength and consistency of the relationship between eGFR and adverse outcomes after any type of surgery. This figure shows relative risk of all-cause mortality within 30 days of surgery in selected subgroups of patients with baseline estimated glomerular filtration rate (eGFR) &lt;60 ml・min・1.73 m−2 Estimated glomerular filtration rate less than 60 is associated with a three fold increased risk of mortality. With a strong non linear increase in mortality at lower preop eGFR rates MDRD = Modified Diet in Renal Disease Study.
- Besides pre-operative renal impairment there are several other patiënt and surgical risk factors for AKI. Such as comorbidities, type of surgery and anesthesia related factors (hypotension, transfusion ans use of nephrotoxic agents).
- Several patient characteristics and surgical risk factors predispose for AKI. However, many of them cannot be influenced by anesthesia management. For example undergoing cardiac surgery with CPB associated systemic inflammation. Luckily there are several risk factors we can influence. For example by reducing prolonged periods of hypotension or preventing fluid overload and anemia. The rest of his presentation will discuss the anesthesia management of these modifiable AKI risk factors. Intraoperative: I/R injury, hypotension, inflammtion, CPB (off pump in favor of AKI), abdominal compartment syndrome (low urine output during surgery is not predictive of AKI, but fluid overload + edema is)
- In a large, single-center study of xxx patients Walsh and colleagues investigated the relationship between perioperative Hb levels and AKI. This slide shows low pre-operative hemoglobin concentrations are an important risk factor for AKI. Almost 30% of patients had a preoperative Hb below 7.5 mmol/l and a decrease in Hb of 1 mmo/l doubled the risk of AKI. Similarly, postoperative decrements in hemoglobin were independently associated with AKI. (reduce the oxygen-carrying capacity of blood) Larger decrements in hemoglobin may represent bleeding, hypotension, blood transfusions and extensive surgery with greater systemic inflammation. In either case, the measured decrement in hemoglobin is an easily quantified risk factor for AKI Results: Hb &lt;7.5 = 29% Daling &gt;4.0 g/L = 32% AKI = 7.4%
- Major surgery is associated with inflammation. Inflammation leads to endothelial dysfunction and tissue edema. If we overload the patient with fluids, tissue edema increases with an increased risk of AKI. Reasons are: renal compartment syndrome, venous congestion and renal hypoxia. The kidneys are enclosed in a fascia. Renal volume expansion may lead to raised tissue pressure and, in severe cases, RCS. Also, fluid administration may decrease oxygen delivery due to hemodilution. AND lead to increased sodium filtration, reabsorptive work and oxygen consumption will increase Hypotension and impaired CO reduce RBF and cause AKI. However, AKI is commonly seen despite restoration of CO and mean arterial pressure. In septic patients, increased central venous pressure (CVP) have been associated with AKI progression (In 137 septic patients, CVP but not CO or MAP was independently associated with new or persistent AKI). (Finally, stressed tubular cells consume more than twice the amount of oxygen than the healthy kidney to reabsorb the same amount of sodium)
- As no specific AKI-treatment exists, hemodynamic support including fluid management remains the cornerstone of treatment of patients at risk of AKI. Administration of intravenous fluids, used to maintain renal blood flow (RBF), renal tissue oxygenation and glomerular filtration rate (GFR). Two recent RCTs assessed the impact of GDT on renal outcomes following major noncardiac surgery. The largest study randomized 734 patients undergoing major abdominal surgery to a CO-guided algorithm (GDT group) during and 6 h following surgery or to usual care. During the intervention period, the administered volumes were similar in the two groups (median 4190 ml in the GDT group vs. 4024 ml in the usual care group). AKI, which was defined as a doubling of serum creatinine or sustained oliguria less than 0.5 ml/kg/h for 12 h, occurred in 17 (approximately 5%) patients in each group. Although this trial was negative, In an additional updated meta-analysis, the inclusion of the OPTIMISE results further strengthened the overall conclusion that GDT of some type is probably beneficial for high-risk patients and has few documented adverse effects.
- In a more recent second RCT … patients undergoing abdominal surgery underwent fluid optimalisation using picco (CI &gt;2.5, MAP &gt;70 (GEDI = global end diastolic index)). Also in this study no differences in HD parameters were found between groups, which is probably the result of performing the trial itself.
- Besides the amount of intravenous fluid administration, type of fluid can be a major determinant of AKI. Evidence suggests that chloride-rich solutions may cause harm. In some recent observational studies, infusion of chloride rich-solutions was associated with a higher occurrence rate of AKI and need for RRT than infusion of balanced solutions. Additional experimental studies suggest that chloride-rich solutions decrease RBF and GFR via tubule-glomerular feedback-activation. RCT 2278 eligible ICU patients were enrolled. Incidence of AKI 9-10%. Among patients receiving crystalloid fluid therapy in the ICU, use of a buffered crystalloid compared with saline did not reduce the risk of AKI. Figure: Day 0 is the day of enrollment. The baseline creatinine was defined as lowest serum creatinine in 6 months prior to intensive care unit admission. The prestudy fluid therapy creatinine was defined as the most recent measurement of serum creatinine taken in the 24 hours prior to the commencement of study fluid. Serum creatinine values are approximated by a log-normal distribution so results are presented as geometric means. The error bars indicate 95%CIs.
- Hypotension is most prevalent during the intraoperative period and may be an important determinant of postoperative AKI. Kidneys maintain glomerular filtration through activation of the sympathetic nervous system (ADH, Angiotensin II), but persistent hypoperfusion leads to ischemia due to vasoconstriction. The minimum magnitude and duration of hypotension needed to trigger harm is unclear. This compensatory effect is dependent of autoregulation, which is impaired in patients with chronic renal impairment. A historical animal study demonstrated a MAP of 50 to 60 mmHg to be the lower limit of autoregulation of renal blood flow
- AKIN criteria 50% relative or 0,3 In a retrospective study of 5,127 patients undergoing noncardiac surgery, an increased risk of postoperative acute kidney injury (defined as more than 50% or 0.3 mg/dl increase in serum creatinine concentration) was found when intraoperative mean arterial pressure was less than 60 mmHg for more than 20 min and less than 55 mmHg for more than 10 min mg/dl increase. In a sensitivity analysis, the association between MAP &lt; 55 and renal dysfunction was lost for AKI stage I, but remained present or longer duration of hypotension indifferent subgroups.
- An association between hypotension and change in eGFR could not be observed in a recent study performed by our group. Routine perioperative creatinine measurements were performed in 202 patients undergoing abdominal surgery. instead of measurement on indication. Endpoint was change in eGFR as eGFR represents renal function better than creatinine. This slide shows the association for each minute spend below absolute and relative MAP tresholds and the relationship with change in postoperative eGFR. In MV analysis non of the intraoperativ ehypotension definitions were associated with change in eGFR. It seems that in daily practice anesthesia teams are able to minimize the influence of hypotension due to adequate HD management. Also, Dicohotomising continues variables increases the risk of a type I error, continuous variable increases statistical power Possibly underpowered? May be used as a basis for sample size calculations
- Dexmed to prevent AKI appears promising but data remain unsufficient to make a clear recommendation Statins are associated with reduced risk of AKI in cohort studies, but RCTs are lacking Urinary alkalization is not beneficial in preventing AKI
- eGFR is a more accurate measure of renal function than creatinine and enables milder degrees of renal dysfunction to be detected.
- Treatment options are limited. Risk assessment and prevention are important