Acute kidney injury (AKI) is common after surgery and associated with increased mortality and long-term renal dysfunction. Major surgery can lead to AKI through hypotension, blood loss, inflammation, and use of nephrotoxic substances. Identifying at-risk patients preoperatively and maintaining adequate perfusion and cardiac output intraoperatively through fluid management and treatment of hypotension may help prevent postoperative AKI. Ongoing studies aim to determine optimal fluid strategies, but current evidence suggests avoiding starch and maintaining hemodynamic targets with balanced fluids and vasopressors.
2. Importance
Acute kidney injury (AKI) is common after surgery
It is associated with increased mortality and long-term renal
dysfunction
Perhaps there is room for improvement, preoperatively,
intraoperatively and in the postoperative period
4. How dangerous?
•“At 10-year follow-up, adjusted cardiovascular-specific mortality
estimates were 6%, 11%, 12%, 19%, and 27% for patients with no
kidney disease, AKI with no CKD, CKD with no AKI, AKI with CKD, and
ESRD, respectively (P < 0.001).”
•Registry study (single center) of >50 000 patients
Ann Surg. 2016 Dec;264(6):987-996.
•”In eight studies that reported the short-term mortality, relative risk of
death in the presence of post-operative AKI was 12.6 fold (95% CI,
6.8-23.4).”
•Systematic review (in total n=82,514; 19 studies)
Intensive care medicine. 2016;42(4):521-30.
5. Pathophysiology (major surgery->AKI), simplified
•Major surgery involves large shifts in volume
•Hypotension is common (and perhaps underappreciated*)
•Blood loss
•Intraperitoneal insults can compromise renal blood flow
•Inflammation-surgical trauma
•Other adverse events like massive blood loss-transfusion, severe
hypotension, bacterial leakage, hypoxia etc
6. Pathophysiology (major surgery->AKI), simplified (2)
•Use of harmful substances for the kidney such as contrast media,
nephrotoxic antibiotics, and NSAIDs
•Preop:
•Advanced age
•Comorbidities (common+predispose to a greater risk of AKI)
•Diabetes
•Chronic kidney disease (CKD)
•Heart failure
•Demographic shifts: complex surgery is now performed in older and
more chronically ill patients, increasing the number of patients at risk
7. Prevention of postoperative AKI [preop]
•Identify patients at risk
•Advanced age
•CKD
•Multiple comorbidities
•Surgery during critical illness
•Surgery with an ongoing infection
•Planned surgery will compromise renal blood flow?
•Act
•Surgical approach in high risk patients (no data but endovascular
aortic repair>open AAA surgery with renal flow occlusion?)
•Correct anemia
8. Prevention of postoperative AKI [intraop]
•Identify patients at risk
•Advanced age
•CKD
•Multiple comorbidities
•Surgery during critical illness
•Surgery with an ongoing infection
•Planned surgery will compromise renal blood flow?
•Act
•Extreme vigilance with regards to hypotension – use patients own
baseline*
•Avoid hypovolemia
•Adequate (so, so easy to write) cardiac output
•Avoid (if possible) starch, contrast, aminoglycosides, NSAIDs
•Beware of hypervolemia!
•Transfusions when necessary
•Intraoperative oliguria – not always a trigger for volume!
•Diuretics in hypervolemia *if* positive response
9. *Hypotension and AKI
• Univariate analysis
– Sex
– Comorbity
– BP medication
– Preop creatinine
– Intraop hypotension
– Postop fluid balance
EJA 2017, In Press
10. *Hypotension and AKI
Risk factor OR
(unadjusted)
(95% CI)
OR (adjusteda)
(95% CI)
OR (adjustedb)
(95% CI)
Hypotensive event*
(>40-≤50%) vs ≤40%
1.56 (0.98-
2.48)
1.61 (0.99-2.62) 1.48 (0.90-2.44)
Hypotensive event*
(>50%) vs ≤ 40%
2.38 (1.30-
4.36)
2.27 (1.20-4.30) 2.02 (1.05-3.89)
EJA 2017, In Press
*Decrease in systolic blood pressure in percent relative to baseline for >5 min.
aAdjusted for the covariates: gender (male), ASA>2, treated hypertension,
pre-operative creatinine >90µmol/L and fluid balance in quartiles.
b Adjusted for the covariates mentioned above and blood loss in quartiles.
•Multivariable analysis
11. Goal directed prevention of postoperative AKI [intraop]
•The OPTIMISE trial (major GI surgery) found a cardiac output-guided
fluid and vasopressor treatment algorithm to lead to fewer
postoperative complications (such as ischemic insults, respiratory
failure, and AKI), but no postop mortality reduction
JAMA 2014; 311: 2181–2190
•RCT of transpulmonary thermodilution to guide goal-directed therapy
neither found the intervention to increase the rate of achieved
hemodynamic targets (!) nor (unsurprisingly) to reduce the
postoperative increase in creatinine
•But same study - intraoperative hypotension and hypovolemia:
the most important risk factors for postoperative AKI
Crit Care 2016; 20:50
12. Fluids peri- and postoperatively
•OPTIMISE: total amount of iv fluids did not differ between the
treatment arms, ~4000 ml, but the intervention group received more
colloids of any type….even starch…
•Ok, so avoid starch (6S, CHEST etc)
•Balanced solutions>0.9% sodium chloride? (SPLIT trial, but more
data needed)
•RELIEF: restrictive vs liberal fluid therapy in major abdominal surgery
•Randomized 3000 patients and one endpoint is AKI assessed by
creatinine [to be published in 2018]
•Peri/postoperative oliguria – a trigger for fluids? Sometimes yes, more
often nope, nein, nichts, nihil, nej.
Goren O, Matot I. Perioperative acute kidney injury. Br J Anaesth 2015;
115(Suppl 2):ii3–ii14
13. Perioperative AKI: conclusions
•Varying definitions for AKI have distorted comparability of studies
•Around one-fifth of patients undergoing major noncardiac surgery
develop an increase in creatinine or oliguria or both
•AKI increases risk for postop adverse outcomes including death
•Recognizing high-risk patients preoperatively: important!
•Prompt treatment of intraoperative hypotension and
hypoperfusion
•Avoiding nephrotoxins
•The large multicenter RCT of restrictive vs liberal fluid
management in major abdominal surgery (RELIEF) will aid in how
to optimize perioperative fluid management