CRITICAL ILLNESS AND INTENSIVE CARE II
Acute kidney injury
in surgical patients
Muhammad Imran
Nigel S Kanagasundaram
Abstract
Acute kidney injury (AKI) is a common and dangerous complication of
surgical admission with even mild degrees of renal dysfunction being
associated with reduced survival. Unfortunately, as confirmed by the
UK’s National Confidential Enquiry into Patient Outcome and Death (NCE-
POD), its recognition is often delayed and management frequently sub-
optimal. A failure to recognize relevant risk factors may expose surgical
patients, unnecessarily, to an increased likelihood of developing AKI. In
this review article, we present a structured approach to prevention, diag-
nosis and initial management that should provide a framework for the
clinical care of all patients either at risk of, or suffering with, AKI.
Keywords Acute kidney injury; creatinine; morbidity; mortality; neph-
rotoxic medications; renal replacement therapy; urine output
Introduction
Acute kidney injury (AKI), formerly known as acute renal failure,
is common, affecting around 7% of hospital in-patients1 and up
to 25% of those receiving critical care.2 It is also dangerous, with
even mild disease associated with worse survival.3 Mortality
rates increase sharply as AKI worsens4 and may exceed 50% in
septic, multi-organ failure.5 Evidence also suggests that patients
are not dying simply with AKI, but because of it.6
Survivors often fail to recover renal function7 and significant
numbers need long-term dialysis.8 Long-term survival, itself may
be reduced especially in those with persisting renal dysfunction.8
AKI also carries a significant economic impact; severe disease
often requires expensive interventions such as dialysis or critical
care, but even modest AKI may increase hospital costs.9
The management of AKI is often seen as challenging because
of its perceived complexity. Ample evidence exists, though, that
even the basics of care are often neglected.10,11 The most recent
confirmation has come from the UK’s National Confidential
Enquiry into Patient Outcome and Death (NCEPOD)11 which
found systematic failings in the recognition and management of
AKI and its complications, and frequent omission of fluid
balance, fluid administration and regular blood monitoring.
NCEPOD found that shortcomings in practice were worst in those
Muhammad Imran MBBS MRCP(UK) MRCP Renal Medicine (UK) PGCertClinEduc is
a Locum Consultant Nephrologist at Newcastle upon Tyne Hospitals
NHS Foundation Trust, UK. Conflicts of interest: none declared.
Nigel S Kanagasundaram MB ChB FRCP MD is Honorary Clinical Senior
Lecturer at the Institute of Cellular Medicine, Newcastle University, UK;
and Consultant Nephrologist at Newcastle upon Tyne Hospitals NHS
Foundation Trust, UK. Conflicts of interest: none declared.
SURGERY 30:10
who developed AKI during their hospital stay rather than those
admitted with it,11 suggesting a slackening of surveillance for this
common complication of hospitalization.
Bearing in mind the diffidence with which practitioners view
AKI and evidence of clear shortcomings in practice, this article
provides a structured approach for its prevention, assessment
and management in a hospital setting.
Risk factors and prevention
Up to 30% of AKI may be preventable through early recognition
and simple management of patient risk factors.10 Common risk
factors include increasing age and pre-existing chronic kidney
disease (CKD)12 (Table 1). Certain drugs may be directly nephro-
toxic: examples include aminoglycoside antibiotics, such as
gentamicin, non-steroidal anti-inflammatory drugs (NSAIDs),
chemotherapeutic agents, such as cisplatin, and radio-contrast
media. Other drugs, such as angiotensin-converting enzyme
(ACE) inhibitors, are not directly nephrotoxic but reduce the
glomerular filtration rate through their mechanism of action.
When weighing the balance of risk versus benefit for the initiation
or continuation of these drugs in the individual patient, consider
the presence of other risk factors for AKI and the availability of non-
nephrotoxic alternatives. A wide variety of drugs may cause an
acute allergic interstitial nephritis (see ‘intrinsic AKI’, below). As
these reactions are idiosyncratic, they cannot necessarily be pre-
vented but should be borne in mind as a potential aetiology for AKI.
Patients with one or more risk factors for AKI should undergo
more frequent (daily) biochemical monitoring and regular clin-
ical review of fluid balance, volume status and medications.
Maintaining vigilance for the risk factors for AKI allows
preventative intervention. For instance:

the elderly diabetic may require temporary omission of an
ACE inhibitor around the time of major surgery

the immediate postoperative patient with pre-existing CKD
should avoid NSAID analgesia

the avoidance of iodinated radio-contrast-enhanced
examination in a septic, perioperative patient when alter-
native radiological modalities are available.
Fluid management
Appropriate fluid management can mitigate the risk of AKI. A
decision on whether fluid is required for ‘maintenance’ (routine
requirements) or ‘replacement’ (correction of abnormal losses)
will guide the choice of fluid and electrolyte.
Colloid resuscitation with high-molecular-weight hydroxyl
ethyl starch solutions may increase the risk of AKI in those with
severe sepsis.12
So-called ‘normal saline’ (sodium chloride 0.9%) puts the patient
at risk of sodium overload and hyperchloraemic metabolic acidosis
if used injudiciously (2 litres will provide 308 mmol of sodium, at
least three times the usual daily requirement). Structured guidance
on optimal fluid prescribing, including the use of the more balanced
solutions, lactated Ringer’s and Hartmann’s, is given elsewhere.13
Contrast nephropathy prophylaxis
Consider this if other risk factors for AKI, in particular pre-
existing CKD, are present. If the investigation cannot be
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 CRITICAL ILLNESS AND INTENSIVE CARE II

(Table 2). A previous iteration, using the RIFLE criteria,24 is still

12 evident in much contemporary literature and practice.
Common risk factors for acute kidney injury
C Chronic kidney disease (CKD, eGFR <60 ml/min/1.73 m2) Aetiology and categorization
C Age >75
C Sepsis AKI has a wide range of causes but can be broadly categorized as
C Cardiac failure shown in Figure 1.
C Liver disease
C Diabetes mellitus
Pre-renal azotaemia
C Drugs affecting renal function
This is an appropriate response to reduced renal perfusion, by
C Hypovolaemia
which the kidneys attempt to retain sodium and water and, as
C Atherosclerotic peripheral vascular disease
a result, renal excretory capacity is impaired. Importantly, no
renal cellular injury has occurred (hence ‘azotaemia’ e the
eGFR, estimated glomerular filtration rate. accumulation of uraemic waste products rather than ‘injury’).
Table 3 details the usual causes.
Table 1
Intrinsic AKI
avoided, specific prophylactic measures that should be consid- This is caused by tubulo-interstitial, glomerular or micro-vascular
ered include: cellular injury. Most intrinsic AKI is tubular in aetiology and

omission of ‘higher risk’ drugs on the day of investigation usually takes the form of acute tubular necrosis (ATN). ATN may
until renal function is stable

omission of metformin for 48 hours from the day of
investigation12 Acute Kidney Injury Network (AKIN) diagnostic and

selection of alternative contrast agent: low osmolar agents staging system for AKI23
carry a lower risk than high osmolar agents12 and iso-
osmolar agents may carry a lower risk than low osmolar Diagnosis of AKI
agents in pre-existing CKD14 The diagnosis is made when one of the following criteria is met:

prophylactic volume expansion:
C serum creatinine rises by 26 mmol/litre from the baseline value
 sodium chloride 0.9% at 1 ml/kg/hour for 12 hours pre- within 48 hours or
and post-procedure12 or
C serum creatinine rises 1.5-fold from the baseline value which
 isotonic sodium bicarbonate at 3 ml/kg/hour for 1 hour pre- is known or presumed to have occurred within 1 week or
procedure and 1 ml/kg/hour for 6 hours post-procedure.15
C urine output is <0.5 ml/kg/hour for >6 consecutive hours
Assess volume status carefully before, during and after these If the patient does not have a baseline serum creatinine value
regimens to prevent fluid overload. within 1 week of their admission or presentation use a reference
Monitor renal function for up to 72 hours post-procedure in high- serum creatinine value within 3 months (acceptable up to 1 year).19
risk patients (i.e. those in whom prophylaxis has been considered).
If a reference serum creatinine value is not available within 3
There is no clear evidence supporting the routine use of
months (acceptable up to 1 year) and AKI is suspected then repeat
N-acetylcysteine in contrast nephropathy prophylaxis.12
serum creatinine within 24 hours.
Rhabdomyolysis A reference serum creatinine value can be estimated from the nadir
Rhabdomyolysis often has a surgical cause such as trauma, serum creatinine value if patient recovers from AKI.
compartment syndrome or vascular insufficiency. Myoglobin, Severity of AKI
filtered through the glomeruli, can cause intra-tubular cast forma- After diagnosis, the maximum stage reached over a given time
tion and also dissociates to release tubulo-toxic free iron in more period, using either serum creatinine or urine output criteria, is
acid urine. The risk of AKI is low if peak serum creatine kinase is less used to grade the severity of that episode of AKI.
than 10,000 U/litre,16e19 but those with greater muscle damage
may benefit from an early diuresis20 and urinary alkalinization.21 Stage Serum creatinine criteria Urine output criteria
One regimen involves sodium chloride 0.9% at 10e15 ml/kg/
1 Increase in serum creatinine <0.5 ml/kg/hour
hour to achieve urinary flow rates over 100 ml/hour, with the
of 26 mmol/litre or increase for >6 hours
cautious addition of sodium bicarbonate 1.4% to maintain urinary
to 150e200% from baseline
pH over 6.5.22 Look out for fluid overload and exacerbation of
2 Increase in serum creatinine <0.5 ml/kg/hour
hypocalcaemia by alkalinization. Once AKI is established and
to >200e300% from baseline for >12 hours
progressing, further fluid therapy should be continued only very
3 Increase in serum creatinine <0.3 ml/kg/hour
cautiously.
to >300% from baseline or for 24 hours or anuria
increase in serum creatinine to for 12 hours
Defining AKI
354 mmol/litre or the requirement
Definitions in the literature cover a wide range of disease severity, for renal replacement therapy
but an international consensus is developing following introduction
of the Acute Kidney Injury Network (AKIN) staging system23 Table 2

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 CRITICAL ILLNESS AND INTENSIVE CARE II

Urinalysis is usually but not always normal in tubular disease.

Categorization of acute renal dysfunction Rapidly progressive glomerulonephritis (RPGN) gives rise to the
nephritic syndrome, characterized by haematuria, proteinuria, and
Acute renal dysfunction AKI with oedema and hypertension. Causes include anti-glomerular
basement membrane (anti-GBM) antibody disease (Goodpasture’s
syndrome if lung haemorrhage co-exists e the target antigen is also
found on the alveolar basement membrane), lupus nephritis, post-
Pre-renal Intrinsic acute Post-renal acute infectious GN and small vessel vasculitis (Wegener’s gran-
azotaemia kidney injury kidney injury
ulomatosis, microscopic polyangiitis). Urinalysis, by definition, is
always abnormal. Some of these patients may be admitted to
surgical wards (for example with haematuria or loin pain). Vigi-
lance and rapid referral to the renal team is of paramount impor-
Tubulointerstitial Glomerular Vascular tance as these conditions are potentially treatable.
Renal biopsy may be avoided in post-infectious GN if there is
a typical clinical course of a group A, b-haemolytic streptococcal
Figure 1
pharyngitis or impetigo (cultures, raised anti-streptolysin O titre),
a latent period of about 10 or 21 days, respectively, and low
serum complement.
be caused by ischaemia, sepsis or, less commonly, nephrotoxins, Renal biopsy is usually required for the diagnosis of other
such as aminoglycoside antibiotics, NSAIDs, radio-contrast media causes of RPGN. All will show inflammatory crescents in at least
(which also cause renal vasoconstriction), myoglobin or cisplatin. some sampled glomeruli but are distinguished by the pattern of
Less common causes of tubulo-interstitial disease include immune staining, with linear deposition of immunoglobulin G
acute allergic interstitial nephritis (e.g. secondary to diuretics, (IgG) along the basement membranes in anti-GBM disease, ‘full
NSAIDs, penicillins and proton pump inhibitors) and cast house’ immune complex deposition in lupus nephritis, and no
nephropathy (due to multiple myeloma, characterized by (‘pauci-immune’) staining in small vessel vasculitis. The detec-
monoclonal immunoglobulins and Bence Jones proteinuria). tion of serum auto-antibodies (anti-GBM antibodies, anti-nuclear
antibodies, anti-neutrophil cytoplasmic antibodies (ANCA))
helps corroborate the histology and the broader clinical picture if
there are extra-renal manifestations. ANCA will tend to stain in
Causes of pre-renal azotaemia a cytoplasmic pattern (cANCA) in Wegener’s granulomatosis and
in a peri-nuclear (p-ANCA) pattern in microscopic polyangiitis.
Cause Examples
Enzyme-linked immunoassays for anti-proteinase-3 and anti-
Decreased effective myeloperoxidase antibodies (corresponding to c- and p-ANCA,
intravascular volume respectively) are now available and carry greater specificity. If
C Total body volume depletion RPGN is a serious diagnostic consideration, it is vital that
Haemorrhage immunology results are obtained urgently and there is a rapid
Gastrointestinal loss Vomiting, diarrhoea referral for a renal opinion.
Renal losses e diuretics, Micro-vascular causes of intrinsic AKI include cholesterol
salt-losing nephropathy emboli syndrome, haemolyticeuraemic syndrome, malignant
Skin loss Burns, sweating hypertension and scleroderma.
C Volume redistribution
Third spacing of fluid Peritonitis, ascites, acute Post-renal (obstructive) AKI
pancreatitis, hypoalbuminaemia Consider this in anyone with AKI as rapid relief of obstruction
Increased vascular capacity Sepsis, anaphylaxis can limit renal damage and quickly restore organ function. It is
Hepato-renal failure diagnosed by the presence of hydronephrosis and/or hydroureter
on renal tract imaging e usually ultrasound. Post-renal AKI may
Decreased cardiac output
be a particular risk in certain surgical scenarios such as renal
Heart failure, valvular heart
stone disease, other structural disease of the renal tract (e.g.
disease, pericarditis,
neoplasms) and its treatment, and retroperitoneal and pelvic
tamponade
diseases and their treatments. Acute urinary retention may occur
Renal vascular disease Chronic ischaemia or acute
as a result of a blocked urethral catheter, a reduction in detrusor
embolism
contractility and bladder sensation caused by opiates or anti-
Drugs cholinergic medication or over-distension in a patient with pre-
NSAIDs existing problems with detrusor contractility.
ACE inhibitors
Ciclosporin Pre-renal azotaemia and ischaemic ATN e a clinical
Amphotericin continuum
In the patient with pre-renal azotaemia, if renal perfusion cannot
Table 3 quickly be restored (e.g. through volume replacement or

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 CRITICAL ILLNESS AND INTENSIVE CARE II
vasopressor therapy), tubular cell injury will develop resulting in
overt, ischaemic ATN. At this stage, restoration of renal perfu-
sion will not quickly restore renal excretory capacity e tubular
recovery will occur in its own time provided further renal insults
are avoided. About 75% of all acute renal dysfunction can be
attributed to the combination of pre-renal azotaemia and acute
tubular necrosis.25
Initial assessment
History
Consider any history suggesting sepsis, volume depletion (e.g.
vomiting, diarrhoea, thirst) or pre-existing CKD (there may be
biochemical evidence in hospital or primary care). Review all
prescribed and non-prescribed medication. Enquire into any
urinary symptoms or any suggestion of a less common diagnosis
(fevers, rashes, arthralgias, haemoptysis, weight loss, uveitis,
etc).
Clinical examination
The most important aspects are assessment of volume status and
reagent strip urinalysis.
In intravascular volume depletion, blood pressure (BP) may
be low or relatively low (compared to pre-morbid readings).
There may be a postural BP drop (>20 mmHg systolic and/or
>10 mmHg diastolic suggests volume depletion in the absence of
other causes; if the patient cannot stand, look for a lyingesitting
deficit). The jugular venous pressure (JVP) may be reduced
(reclining the patient can reveal the top of the waveform).
Reduced skin turgor, dry mucous membranes and reduced
capillary refill are soft signs but can contribute to the overall
picture.
In volume overload, the JVP will be elevated. There may be
a third heart sound and evidence of pulmonary or peripheral
oedema. Peripheral oedema can still occur with intravascular
volume depletion, though, so should be seen in the context of
other indicators of volume status.
Perform urinalysis in all who are not completely anuric, if at
all possible before urethral catheterization. Urine culture will
differentiate infection from other causes of haematuria and
Clinical features suggesting a rare diagnosis
Clinical feature
Fever, arthralgias, rashes
Haemoptysis
Haemolysis, thrombocytopaenia
Hypercalcaemia, hyperuricaemia, bone pain, lytic lesions
Recent vascular intervention þ/ livedo reticularis,
hypocomplementaemia
Raised serum creatinine, creatine kinase >10,000 U/litre,
prolonged severe immobility, crush injuries
Table 4
SURGERY 30:10
proteinuria (e.g. tumour, catheter trauma, stones or infarc-
tion), but urine microscopy is required to detect the red cell
casts that will identify haematuria of glomerular origin due to
an RPGN.
A distended urinary bladder can indicate lower tract
obstruction. There may be a vasculitic or allergic rash or uveitis,
suggesting a less common cause.
Investigations
Check serum biochemistry (including venous bicarbonate), full
blood count and inflammatory markers. Urine should be cultured
and careful microscopy of a fresh specimen performed if hae-
maturia and proteinuria are present. Perform a renal ultrasound
if obstruction cannot be confidently excluded. However, hydro-
nephrosis may be absent if another cause for oliguria (e.g. ATN)
co-exists or in the very early phases of obstruction, when the
pelvi-calyceal system is relatively non-compliant e the ultra-
sound should be repeated, some days later, if there is a high
index of suspicion. To investigate intrinsic renal disease,
a myeloma screen should be considered and, in the presence of
haematuria and proteinuria, anti-nuclear antibodies, anti-
neutrophil cytoplasmic antibodies (ANCA), anti-GBM anti-
bodies and serum complement.
The five questions a clinician needs to ask in their initial
assessment are:
Is this really AKI?
If previous measurements of renal function are not available,
frequent (e.g. 12-hourly) monitoring of serum creatinine may
reveal a rapid rise effectively excluding chronic disease. However,
pre-renal azotaemia may show a ‘wandering baseline’ and ATN
on the cusp of recovery may require a longer period of monitoring.
Is this pre-renal azotaemia?
Are there risk factors for reduced renal perfusion? The thera-
peutic response to restoration of renal perfusion can be diag-
nostic; failure of renal function to improve after this suggests
either progression to overt acute tubular necrosis or an alterna-
tive aetiology.
Possible diagnoses
Small vessel vasculitis (e.g. Wegener’s granulomatosis,
microscopic polyangiitis), systemic lupus erythematosus,
anti-glomerular basement
membrane antibody disease
Small vessel vasculitis, anti-glomerular basement
membrane antibody disease
Haemolytic e uraemic syndrome
Multiple myeloma
Cholesterol emboli syndrome
Rhabdomyolysis
539 Ó 2012 Elsevier Ltd. All rights reserved.
 CRITICAL ILLNESS AND INTENSIVE CARE II

Is post-renal AKI a possibility? Initial management

This should be considered in all cases, especially if there is
a history of lower urinary tract symptoms, renal stones, pelvic or
retroperitoneal surgery or possible pelvic or retroperitoneal
malignancy.
If this is intrinsic AKI, is this ATN?
Diagnosis is usually on clinical grounds based on the presence of
precipitating causes. Recovery usually occurs after 7e21 days,
but may be more prolonged if the renal insult is severe or
subsequent insults are sustained.
If this is not ATN, is there a less common diagnosis?
Consider if there is no obvious precipitating insult, if renal
recovery is unusually delayed, or other features (e.g. abnormal
urinalysis) are suggestive (Table 4).
The five questions a clinician needs to ask in their initial
management are:
Have I treated the underlying cause?
Initial steps include treatment of sepsis, withdrawal of neph-
rotoxins and restoration of renal perfusion through
fluid resuscitation or vasopressor therapy. Fluid resuscitation
should be performed with care e small volume boluses (e.g. 250
ml of crystalloid or colloid) with close monitoring of response to
minimize the risk of iatrogenic fluid overload.
Central venous pressure monitoring should not be seen as
a substitute for careful and regular clinical assessment and
should be needed only when fluid therapy is otherwise difficult
to manage.

Non-dialytic management of complications of acute kidney injury

Hyperkalaemia Treat as an emergency in the presence of ECG changes or if serum Kþ 6.5 mmol/litre or higher. Patients
should undergo cardiac monitoring.
C Cardio-protection
 Give either 10 ml of 10% calcium gluconate, or 5 ml of 10% calcium chloride solution over 2e5 minutes,
intravenously, with constant cardiac monitoring. Reversal of ECG changes occurs within 1 minute and lasts
for up to 1 hour. The dose can be repeated at 5-minute intervals if ECG changes persist, up to a maximum
of four doses.
C Increase cellular Kþ uptake
 Give 10 units of a short-acting insulin (e.g. actrapid) in 50 ml of 50% glucose via a large bore cannula
(the glucose is highly irritant) over 10 minutes. Onset of action occurs within 10e20 minutes, peaks at
30e60 minutes and lasts for 4e6 hours. This can be repeated every 4 hours. Capillary blood glucose
should be monitored for 6 hours after administration in case of hypoglycaemia.
 Give 200e500 ml of 1.26% or 1.4% sodium bicarbonate intravenously over 15e60 minutes. This should
only be used if venous bicarbonate is <16 mmol/litre with no evidence of volume overload. Ionized calcium
falls with rapid correction and can trigger tetany, seizures and cardiac instability. Correct low ionized
calcium via different intravenous route due to incompatibility of bicarbonate and calcium solutions.
 in peri-arrest/cardiac arrest, use 50 ml 8.4% or 50e100 ml 4.2% sodium bicarbonate, intravenously,
for rapid onset.
N.B. b2-adrenergic agonists work via a similar mechanism to insulin (increased uptake via membrane
Naþ/Kþ ATPase), but the high doses needed (e.g. 20 mg of nebulized salbutamol) can be unpleasant
and precipitate arrhythmias.
N.B. the above measures temporarily reduce serum potassium, but do not reduce total body potassium;
management of hyperkalaemia must include this or hyperkalaemia is likely to recur rapidly.
C Reduce total body potassium
 Intravenous furosemide: doses of 40e80 mg or higher can be used.
 If the hyperkalaemic patient is oligo-anuric then likely to require renal replacement therapy.
N.B. cation exchange resins (e.g. calcium resonium) have no role in the acute management of hyperkalaemia.
Pulmonary oedema High-flow oxygen and, if available, continuous positive airway pressure ventilation.
Intravenous furosemide: doses of 40e80 mg or higher can be used but should not delay more definitive
management with renal support if unsuccessful. It has no role in ‘treating’ or preventing AKI, per se.
Intravenous nitrates: may be a useful holding measure but should not delay definitive management with
renal support if this is required.
Severe metabolic See above for use of sodium bicarbonate.
acidosis (pH <7.2)

Table 5

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 CRITICAL ILLNESS AND INTENSIVE CARE II
Do not rely on the use of urine output as an end-point for
resuscitation as oliguria is a predictable and transient response to
the hormonal changes occurring in the first 12e24 hours after
surgery/trauma.13 Evidence of hypovolaemia should remain the
primary drive for further fluid therapy.12
Is renal perfusion being maintained?
Loss of vascular auto-regulation in the injured kidney allows
fluctuating systemic perfusion to be transmitted directly
through to the nephron. Careful maintenance of renal perfusion
optimizes the chances of renal recovery regardless of the cause
of AKI.
Am I performing appropriate monitoring?
Perform at least daily volume assessment using inputeoutput
charting, clinical examination and daily weights. Physiological
severity scoring should supplement bedside observation and
inform the need to escalate care. Biochemistry (including
calcium, phosphate and venous bicarbonate), haematology and
inflammatory markers should be checked at least daily.
Look out for sepsis e one of the leading causes of death in AKI.6
Monitor dietary intake as AKI patients are at particular risk of
malnutrition.
Am I successfully preventing or managing any
complications?
Review medication and adjust dosages according to renal func-
tion and renal replacement therapy (RRT) modality as a failure to
do so is a significant cause of morbidity.26
Prevention of sepsis should include strict application of local
infection control practices and pressure area care. Minimize the
Indications for starting renal replacement therapy12
Biochemical indications
Refractory hyperkalaemia of 6.5 mmol/litre or higher
Serum urea >27 mmol/litre
Refractory metabolic acidosis with pH <7.15
Refractory electrolyte abnormalities: hyponatraemia, hyper-
natraemia or hypercalcaemia
Tumour lysis syndrome with hyperuricaemia and
hyperphosphataemia
Urea cycle defects, and organic acidurias resulting in hyper-
ammonaemia, methylmalonic acidaemia
Clinical indications
Urine output <0.3 ml/kg for 24 hours or absolute anuria for 12 hours
AKI with multiple organ failure
Refractory volume overload
End organ involvement: pericarditis, encephalopathy, neuropathy,
myopathy, uraemic bleeding
Creation of intravascular space for plasma and other blood
product infusions and nutrition
Severe poisoning or drug overdose
Severe hypothermia or hyperthermia
Table 6
SURGERY 30:10
risk of catheter-associated infection by removing redundant
urinary or vascular catheters, and changing older central and
peripheral vascular access according to local guidelines.
Investigate and manage promptly any evolving inflammatory
response.
In more severe AKI, supplementary nutrition will have to take
into account any associated hypercatabolism, the potential loss of
nutrients through continuous RRT and any electrolyte or volume
disturbances; in these circumstances, specialist dietetic input is
recommended.
Other complications associated with AKI include hyper-
kalaemia, pulmonary oedema and acidosis. Their treatment is
summarized in Table 5.
Should I contact the renal unit?
Patients with severe AKI (stage 3) or those with indications for
RRT (Table 6) should receive critical care or renal care e the
discriminating factor being the level of non-renal organ support
that is required. Current best practice now includes not only
absolute indications to commence renal support (e.g. uraemic
pericarditis) but also the need to anticipate complications before
initiating therapy.12
Early contact is needed if a rare diagnosis is possible as this
may be treatable.
Finally, if optimal management of renal perfusion pressures
and vigorous treatment of the precipitating cause fails to halt
progressive AKI, seek renal advice; although a rare diagnosis
may have been missed, ATN itself can take weeks to resolve.
Subsequent management
The need for renal biopsy
This should be considered:

when pre- and post-renal factors and ATN cannot be
confidently diagnosed

if there is any suspicion of RPGN

if apparent ATN is unusually prolonged; there may be an
alternative aetiology or superimposed insult (e.g. an
antibiotic-related allergic interstitial nephritis).
Renal replacement therapy
Discussion of modality, technology, prescription and delivery are
beyond the scope of this article although details are given,
elsewhere.27
Post-discharge
Patients who have persistent renal impairment but who do not
require RRT after hospital discharge should be managed
according to local chronic kidney disease guidelines as they have
a high risk of mortality and a risk of progressing to end-stage
renal disease.7,8
Conclusions
AKI is a common and dangerous complication of hospital
admission, management of which is frequently sub-optimal.
Where preventative strategies fail, early recognition and a struc-
tured approach to diagnosis and management can ensure that
patients with AKI receive timely and appropriate care, in the
most appropriate clinical setting. A
541 Ó 2012 Elsevier Ltd. All rights reserved.
 CRITICAL ILLNESS AND INTENSIVE CARE II
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Practice points
C The term ‘acute renal failure’ has now been replaced by ‘acute
kidney injury (AKI)’ to reflect the spectrum of disease severity
C AKI is a dangerous condition with increasing severity reducing
the chances of survival
C Even mild AKI carries an increased risk of mortality
C A consensus definition for AKI has now emerged, enhancing
prospects for comparative research and clinical audit
C Long-term outcomes in survivors of AKI may not be benign,
with significant numbers being left with residual renal
dysfunction. This, in turn, increases long-term mortality and
the risks of progression to end-stage renal disease
C Surgical patients are at risk from hypovolaemia and other
causes of reduced effective circulating volume, inappropriate
drug prescribing and sepsis
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