Perioperative AKI

By the end of this chapter you should be able to:

• Explain why perioperative AKI is multifactorial — a summation of multiple hits rather than a single insult.
• Describe the specific mechanisms of cardiac-surgery-associated AKI, from bypass inflammation to haemolysis and microemboli.
• Identify the patient at high preoperative risk and use risk scores and biomarkers appropriately.
• Recognise intraoperative hypotension as a modifiable driver of postoperative AKI.
• Diagnose abdominal compartment syndrome as a reversible surgical cause of AKI and treat it by decompression.
• Prevent perioperative AKI across the preoperative, intraoperative, and postoperative phases.
• Reject the interventions that do not work — remote ischaemic preconditioning, statins for prevention, N-acetylcysteine — in favour of the care bundle.
• Manage the trauma-specific drivers: haemorrhagic shock, crush injury, massive transfusion, and the tense abdomen.

• Perioperative AKI is common and underrecognised, and even small creatinine rises after surgery predict higher mortality and later CKD.
• It is multifactorial: ischaemia-reperfusion, hypotension, inflammation, nephrotoxins, haemolysis, and congestion summate as multiple hits.
• Cardiac-surgery-associated AKI is the archetype, affecting roughly a fifth to a third of patients and driven by bypass-specific mechanisms.
• Cardiopulmonary bypass injures the kidney through non-pulsatile flow, a systemic inflammatory response, haemodilution, hypothermia, microemboli, and haemolysis releasing free haemoglobin.
• Intraoperative hypotension — a mean arterial pressure below about 65 mmHg, and its duration — is strongly and modifiably linked to postoperative AKI.
• Abdominal compartment syndrome is a reversible surgical cause: raised intra-abdominal pressure narrows the renal perfusion gradient, and decompression restores function.
• Preoperative risk rises with CKD, diabetes, age, heart failure, anaemia, and the type and urgency of surgery; scores and cell-cycle-arrest biomarkers refine it.
• Preoperative prevention: optimise volume, treat anaemia, minimise or hold nephrotoxins, and delay elective surgery after contrast.
• Intraoperative prevention: maintain perfusion and avoid hypotension, use goal-directed haemodynamic therapy and balanced fluids, and limit bypass time.
• Postoperative prevention: apply the KDIGO care bundle, avoid nephrotoxins, de-resuscitate fluid overload, and measure intra-abdominal pressure when at risk.
• A biomarker-guided KDIGO bundle reduces moderate-to-severe AKI after cardiac surgery — the best evidence that disciplined prevention works.
• Remote ischaemic preconditioning, perioperative statins, N-acetylcysteine, fenoldopam, and natriuretic peptides do not prevent perioperative AKI.
• Trauma AKI comes from haemorrhagic shock, crush rhabdomyolysis, massive transfusion, and abdominal compartment syndrome; early haemorrhage control and tranexamic acid matter.
• Do not withhold a genuinely indicated trauma contrast scan for fear of contrast nephropathy.

Perioperative acute kidney injury is rarely caused by one thing. A patient comes to surgery with a kidney already softened by age, diabetes, or CKD, then meets a sequence of insults — a period of hypotension, a bypass run, a transfusion, a nephrotoxic antibiotic, a rising abdomen — each of which alone might be tolerated, but which together tip the kidney into injury. The clinical task is to recognise the at-risk patient, minimise each modifiable hit, and find the one cause — the tense abdomen — that is surgically reversible.

AKI as a summation of hits

The organising idea of this chapter is summation. Perioperative AKI is the cumulative result of several injuries layered on a baseline vulnerability, which is why no single preventive measure fixes it and why the strongest strategy is to reduce every modifiable hit at once. It is common — and consequential out of proportion to its apparent mildness: even a small postoperative creatinine rise predicts higher mortality, longer stay, and progression to CKD. Treating a 0.3 mg/dL rise after surgery as trivial is the first error; it is a marker of a kidney that took damage.

The cardiac-surgery archetype

Cardiac surgery on cardiopulmonary bypass is the most studied perioperative AKI, affecting roughly a fifth to a third of patients, and it displays the multiple-hit model in full. Bypass delivers non-pulsatile flow at a controlled pressure that can fall below the kidney's autoregulatory needs; it triggers a systemic inflammatory response through contact activation; it haemodilutes and cools the patient; and manipulation of an atheromatous aorta showers microemboli into the renal circulation. On top of this, the shear of the bypass circuit haemolyses red cells, releasing free haemoglobin that injures the tubule as a pigment, exactly as in Chapter 8. Add the preoperative contrast angiogram, the perioperative antibiotics, and the low-output state that can follow a difficult operation, and the cardiac-surgery kidney faces a stack of insults. Understanding the stack is what lets you shorten bypass time, limit haemodilution, and treat each component.

Intraoperative hypotension: the modifiable hit

Of all the hits, intraoperative hypotension is the most modifiable and the most clearly causal. Both the depth and the duration matter: time spent with a mean arterial pressure below roughly 65 mmHg is associated with postoperative AKI in a dose-dependent way across cardiac and non-cardiac surgery. This makes the anaesthetic management of blood pressure a renal-protective act. Goal-directed haemodynamic therapy — titrating fluids and vasopressors to flow-based targets rather than guessing — reduces AKI, and the simple discipline of not tolerating prolonged intraoperative hypotension is among the few perioperative interventions with a clear mechanism and supporting data.

The tense abdomen: a reversible cause

Abdominal compartment syndrome deserves its own emphasis because it is the perioperative AKI you can actually reverse with a knife. Sustained intra-abdominal pressure — from bowel oedema, packing, ascites, or massive resuscitation — above roughly 20 mmHg, with new organ dysfunction, compresses the renal veins and parenchyma, raising renal venous pressure and narrowing the perfusion gradient until GFR collapses. Oliguria is often the first sign. The diagnosis is made by measuring bladder pressure, and the treatment, when medical decompression fails, is decompressive laparotomy, after which renal function characteristically recovers. Missing it means watching a reversible AKI progress; finding it means a definitive intervention. In any oliguric postoperative or trauma patient with a tense abdomen, measure the pressure.

Trauma: shock, crush, transfusion, and the abdomen

Trauma AKI overlaps the surgical picture but has its own drivers. Haemorrhagic shock produces the pre-renal-to-ATN injury of Chapter 2, so early haemorrhage control and balanced resuscitation — with tranexamic acid given early to reduce bleeding deaths — protect the kidney. Crush injury releases myoglobin, causing the pigment nephropathy whose detailed management belongs to Chapter 12 but whose mainstay is early, generous fluid. Massive transfusion brings its own hazards — citrate-related hypocalcaemia, hyperkalaemia, and the metabolic disturbance of stored blood — that must be monitored and corrected. And the trauma abdomen is a classic site for compartment syndrome. One reassurance threads through: the contrast of a trauma pan-scan is almost always justified by the diagnostic stakes, and should not be withheld for fear of contrast nephropathy, as Chapter 8 argued.

Prevention across three phases

Because established perioperative ATN is treated supportively like all ATN, prevention is the real therapy, and it spans three phases. Before surgery: identify the high-risk patient, optimise volume, treat anaemia, minimise or hold nephrotoxins — NSAIDs avoided, and renin-angiotensin blockers commonly held to reduce intraoperative hypotension — and delay elective surgery after a contrast load. During surgery: maintain perfusion and refuse to tolerate prolonged hypotension, use goal-directed haemodynamics and balanced fluids, and keep bypass time short. After surgery: apply the KDIGO care bundle to every high-risk kidney, avoid nephrotoxins, de-resuscitate accumulated fluid, and measure intra-abdominal pressure when the abdomen is at risk. The one positive trial to anchor on is the biomarker-guided KDIGO bundle, which reduced moderate-to-severe AKI after cardiac surgery — proof that the unglamorous bundle, applied with discipline, is what protects the kidney.

What does not work

Perioperative nephrology has a long list of attractive interventions that failed, and knowing them prevents wasted effort and harm. Remote ischaemic preconditioning — brief limb ischaemia to precondition the kidney — was a beautiful idea that large trials did not support, despite a positive signal in one biomarker-selected study. Statins started for the operation do not prevent cardiac-surgery AKI and may even worsen it. N-acetylcysteine, fenoldopam, dopamine, and natriuretic peptides have all failed for prevention, just as they failed for established ATN. The discipline this evidence demands is the same as in the sepsis chapter: resist the plausible, active-feeling intervention, and spend the effort on the bundle that works.

Table 11.1 — Sources of perioperative and trauma AKI

Table 11.2 — Cardiac-surgery-associated AKI: the hits

Table 11.3 — Preoperative risk and prediction

Table 11.4 — Prevention across the three phases

Table 11.5 — Perioperative prevention: what does NOT work

Table 11.6 — Trauma-specific causes and responses

Clinical Reasoning

One triad per mechanism the narrative exposed: the physiology, why it matters, and the bedside move.

Safety & Evidence

Panel A — Red flags

Panel B — Never do

Pitfall 1 — Hunting for one cause

Pitfall 2 — Missing the tense abdomen

Pitfall 3 — Dismissing the small rise

Pitfall 4 — Unproven prophylaxis

Pitfall 5 — Tolerating intraoperative hypotension

Graded statements (by evidence type)

Patient Decisions

Natural-frequency estimates for orientation, pooled from trials and cohorts; they vary with surgery type, urgency, and baseline function. They convey the size of the perioperative decisions, expressed per 100 comparable patients.

Apply & Test

Paste-ready notes. Tick the boxes that apply and delete the rest; make the modifiable hits and the abdominal-pressure check explicit.

Template 1 — Perioperative AKI risk and prevention plan

• Procedure ___ ; urgency ___ ; baseline eGFR ___ ; risk factors: ☐ CKD ☐ diabetes ☐ age ☐ heart failure ☐ anaemia.
• Preoperative: ☐ volume optimised ☐ anaemia treated ☐ nephrotoxins held ☐ elective surgery delayed after contrast.
• Intraoperative plan: ☐ avoid MAP < 65 ☐ goal-directed haemodynamics ☐ balanced fluids ☐ limit bypass time.
• Risk score / biomarker: ___ .
• NOT used (no benefit): ☐ remote ischaemic preconditioning ☐ perioperative statin ☐ N-acetylcysteine.
• Postoperative high-risk bundle planned: ☐ yes.

Template 2 — Postoperative / trauma AKI review

• AKI stage ___ ; modifiable hits identified: ☐ intraoperative hypotension ☐ bypass ☐ transfusion ☐ nephrotoxins ☐ contrast ☐ haemolysis.
• Abdomen: ☐ soft ☐ tense — bladder pressure ___ mmHg; abdominal compartment syndrome ☐ no ☐ yes → decompress.
• Trauma measures: ☐ haemorrhage controlled ☐ tranexamic acid (early) ☐ crush → fluids ☐ transfusion electrolytes monitored.
• KDIGO bundle applied: ☐ nephrotoxins stopped ☐ perfusion optimised ☐ monitoring ☐ no hyperglycaemia ☐ contrast avoided.
• Fluid state: ☐ adequate ☐ overloaded → de-resuscitate.
• RRT indication: ☐ none (supportive) ☐ present → Chapters 13–14.