perioperative Acute kidney I presentation

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1. Perioperative Acute kidney injury Presenter : Dr Viral T rivedi 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

5. 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

6. 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

7. 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

8. Etiology o f perioperative acute kidney injury Pre renal

9. Intrinsic

10. Postrenal

11. 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

12. 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

13. 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

14. 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

15. 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 .

16. 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

17. Biomarkers

18. 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.

19. 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.

20. 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

21. 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).

22. 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

23. 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

24. 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

25. 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.

26. Thank you