The document discusses perioperative acute kidney injury (AKI) as a significant complication associated with major surgery, leading to increased morbidity and mortality. It outlines the definitions, pathophysiology, risk factors, and management strategies for preventing AKI, emphasizing the complexity of its etiology and the importance of careful perioperative management. Key recommendations include monitoring hemodynamic parameters, optimizing preoperative conditions, and judicious use of fluids and vasopressors.

1. Perioperative Acute kidney injury
Presenter : Dr Viral Trivedi
Moderator : Dr Saurabh sir
No. Of slides: 30

2. Introduction
• AKI is a common complication of patients undergoing major surgery and is associated
with both short-term morbidity and mortality and longer-term adverse outcomes,
including the development of CKD
• AKI has been as‐sociated with a higher incidence of many adverse outcomes, including a
longer hospital length of stay, intensive care unit (ICU) admission, the need for prolonged
mechanical ventilation.
• Acute kidney injury is not an uncommon disorder and is associated with considerable
morbidity and mortality
• The incidence of AKI is reported to be between 22 and 57% in critical care patients.

3. • Perioperative AKI is a leading cause of morbidity and mortality. It is associated with
increased risk of sepsis, anaemia, coagulopathy, and mechanical ventilation
• A study investigating patients after general surgery reported an eight-fold increase in
mortality in patients with perioperative AKI, whereas a more recent large-scale study of
patients undergoing intra-abdominal surgery found that non-AKI patients had a 30 day
mortality of 1.9%, compared with 31% in patients with AKI.

4. Definition
• Most definitions use urine output and sCr as markers of renal function because they are
unique to the kidney and easily measured
• It is characterized by rapid decline in the glomerular filtration rate (GFR) and the
accumulation of nitrogenous waste products (blood urea nitrogen [BUN] and creatinine
• AKI is also a serious perioperative complication for patients undergoing major surgery
• AKI defined as any of the following:
- Increase in serum creatinine by 0.3 mg/dl or more within 48 hrs
- Increase in serum creatinine to 1.5 times baseline
- Urine output less than 0.5 ml/kg/hr for 6 hours

6. • Postoperative AKI defined as KDIGO criteria for AKI are met within 7 days of an
operative intervention
• Although postoperative AKI is often low grade (stage 1–2), with relatively modest
absolute changes in serum creatinine, these changes can represent quite large reductions
in the GFR in healthy individuals, suggesting AKI is often identified late, when
significant damage may have occurred

7. Pathophysiology
• Prerenal, intrinsic renal, and postrenal sources
• In the perioperative setting, patients may be at increased risk for prerenal AKI, either
attributable to volume depletion or to exacerbation of associated chronic prerenal
physiologic conditions, such as congestive heart failure, which may be exacerbated by
volume overload.
• Intraoperatively, hypotension due to vasodilation and negative inotropy/chronotropy from
anesthetic agents may lead to prerenal physiology.
• Depending on the nature of the surgical procedure, the patient may also be at increased
risk of postrenal aki attributable to obstruction of the ureters, bladder, or urethra

8. • The causes of postoperative AKI are often complex, multifactorial, and rarely represent a
single underlying pathophysiology
• Major pathologic processes involved in the development of postoperative AKI, which
may be considered as preoperative, intraoper‐ ative, or postoperative in nature.
• Depending on the complex interaction of these processes, damage may occur with or
without loss of function, but the implicated factors remain the same
• Postoperative AKI often has a multifactorial etiology mediated by common injury
pathways that affect the kidney microcirculation, oxygen (O ) demand, and inflammation.
In most cases, a combination of preoperative risk factors, intraoperative events, and
postoperative events leads to the development of AKI

10. Etiology of perioperative acute kidney injury
Pre renal

11. Intrinsic

12. Postrenal

14. Preoperative Factors
• Include patient characteristics such as sex, obesity, and older age, and known kidney
dysfunction, hypertension, diabetes, and other comorbidities
• baseline serum creatinine should be acquired before surgery
• Antihypertensives, particularly angiotensin-converting enzyme inhibitors (ACEis) and an‐
giotensin II receptor blockers (ARBs) are routinely held in the 24 hours before surgical
proce‐ dures due to the higher risk of intraoperative hypotension associated with their
ongoing use
• withholding these agents in the perioperative period may be effective at reducing
postoperative AKI incidence

15. Intraoperative Factors
• Cardiac and vascular surgery may cause kidney injury through a myriad of different
mechanisms
• where a combination of hemodynamic, mechanical, inflammatory, and other mechanisms
are implicated
• Many of these relate to, or are complicated by, cardiopulmonary bypass

16. • Intra-abdominal surgery is associated with raised intra-abdominal pressure that is
mediated through several mechanisms,
• Raised intra-abdominal pressure represents a higher risk for the development of
postoperative AKI
• This occurs via venous congestion, an increase in intrarenal pressure, and a reduction in
kidney perfusion, which impairs glomerular and tubular function
• At intra-abdominal pressure >15 mm Hg, oliguria and subsequent anuria is witnessed,
with a corresponding rise in serum urea and creatinine.
• These changes appear to be potentially reversible if intra-abdom‐ inal hypertension is
recognized and reversed in a timely manner

17. • Anesthetic approaches may also influence the risk of postoperative AKI. Maintenance of
euvolemia and intraoperative hemodynamic stability are key features in minimizing
development of postoperative AKI.
• Historically, some halogenated anaesthetics are considered nephrotoxic, such as
methoxyflurane, which is no longer in routine use
• Use of sevoflurane associated with increased plasma fluoride concentrations and with
production of a haloalkene called ‘compound A’
• Regarding the choice of anaesthetic technique, most reports concern the beneficial effects
of inhaled anaesthetics and propofol to attenuate AKI in experimental studies; however,
such an effect has not been shown in humans

18. • A study on healthy volunteers found that the sympathetic block caused by epidural
anaesthesia did not change renal blood flow significantly
• A meta-analysis found the incidence of AKI to be lower for neuraxial anaesthesia when
compared with general anaesthesia.

19. Postoperative Factors
• Postoperative factors include hypovolemia, decreased cardiac output, mechanical
ventilation, and exposure to potentially nephrotoxic drugs.
• Therefore, consideration before the routine use of potential nephrotoxins (including
NSAIDS; certain antibiotics, particularly aminoglycosides; and loop diuretics) should be
given with consideration to their cumulative effect

20. Biomarkers

21. Perioperative management
Identification of patients at risk of developing acute kidney injury
• The first step in preventing and treating AKI is to identify patients at risk.
• Extremes of age, co-morbidities, anaemia, potential hypovolaemia, use of contrast dye,
use of nephrotoxic drugs, and emergency or high-risk surgery should all alert the
anaesthetist to the possibility of perioperative AKI.
• Some of these risk factors can be optimized before surgery.

22. Haemodynamic goals
• The main haemodynamic goal in the perioperative patient is to prevent tissue
hypoperfusion and thus organ hypoxia.
• Direct monitoring of tissue hypoxia is not readily feasible in the clinical setting. Thus,
indirect measures, such as MAP, heart rate variability, and lactate concentrations, are
usually used.
• In the ICU setting, MAP >60–65 mm Hg (>75 mm Hg in patients with chronic
hypertension) is recommended to prevent AKI.
• It was found that duration of MAP <55 mmhg was independently correlated with AKI
• The risk of AKI was increased when MAP was <60 mmhg for > 20 min or <50 mmhg for
>10 min.

23. Choice of fluid solution
• Perioperative fluid therapy is aimed to maintain intravascular volume and allow tissue
perfusion.
• Normal saline (0.9%) or balanced solutions (ringer’s lactate, plasma-lyte, etc.). Colloid
solutions include synthetic hydroxyethyl starches (hes), gelatins, and albumin.
• Crystalloid solutions contain different mixtures of electrolytes. Saline contains only nacl,
unlike balanced crystalloids, which are more similar to plasma content.
• The association of colloid solutions with aki is controversial. Several recent studies report
an increase in incidence of AKI and renal replacement therapy in critically ill patients
infused with HES rather than crystalloids

24. Intraoperative fluid management and urine output
• A common practice to maintain effective blood volume and thus kidney perfusion is i.v.
hydration.
• Correcting hypovolaemia is an essential perioperative haemodynamic goal, and
appropriate hydration is considered important for the avoidance of AKI.
• Infusion of crystalloids during anaesthesia shows reduced clearance and slower
distribution such that intraoperative oliguria may not reflect fluid status or predict future
AKI
• Recommendation to maintain urine output of at least 0.5 ml kg−1 h−1 should be
considered.
• Urine output in anaesthetized patients may not be an adequate indicator of fluid balance
and is not predictive of postoperative AKI in elective surgeries (non-vascular, noncardiac,
and non-transplant).

25. Use of diuretics
• Loop diuretics and mannitol are commonly used during surgery in an attempt to prevent
AKI or treat oliguria and anuria based on experimental studies reporting renoprotective
properties of diuretics. This practice has not been shown to be benefiial.1
• On the contrary, use of diuretics can be harmful because these agents can cause prerenal
damage and nephrotoxicity.
• Diuretics are not recommended except to treat volume overload

26. Anaemia and use of blood products
• Low haemoglobin concentration reduces the oxygen-carrying capacity of the blood
• A large observational study involving non-cardiac surgery patients found preoperative
anaemia and early postoperative decrements of haemoglobin to be associated with AKI
• Perioperative anaemia and perioperative PRBC transfusions are risk factors for AKI in
cardiac surgery,140–143 such that every unit of transfused blood increases the incidence
of cardiac surgery-associated AKI by 10–20%
• It is therefore advisable to optimize patients’ preoperative haemoglobin status

27. Use of vasopressors
• The role of vasopressors in preventing AKI is not entirely clear. The benefit of
vasopressor use in the setting of AKI is maintenance of renal perfusion pressure within
autoregulatory limits
• Norepinephrine constricts renal arterioles and reduces renal blood flow (but not
GFR).Nonetheless, it is commonly used and is considered safe and effective
• Epinephrine has a prominent α-adrenoreceptor-mediated effect in the kidney.
Epinephrine is more rarely used, mainly because of its potential to cause tachycardia,
lactataemia, and hyperglycaemia.
• Phenylephrine is a potent vasoconstrictor, but with a profound α-adrenergic activity that
causes vasoconstriction.
• The current KDIGO guidelines state that the evidence so far does not support the use of
one vasoactive agent over another

29. Conclusion
• Perioperative AKI continues to be a feared consequence of surgery. It is associated with
both short- and long-term deleterious effects
• The complexity of perioperative AKI pathophysiology involves the combined roles of
ischaemia and inflammation as causes of AKI.
• Specific co-morbidities, surgeries, and interventions increase the risk of AKI, such as
cardiac or transplant surgery and use of contrast dye
• Urine output does not predict postoperative AKI.
• Careful selection and use of i.v. fluids and vasopressors and appropriate blood
management are important to prevent perioperative AKI.

30. Thank you