Prevention and

Management AKI
in ICU

dedi atila
 Introduction
1. Acute kidney injury (AKI) is a common complication in critically
ill patients and is associated with high morbidity and mortality
2. Acute kidney injury complicates 5–7% of acute care hospital
admissions and up to 30% of admissions to the ICU
3. Several studies had already demonstrated that even small
increases in serum creatinine were associated with a poorer
prognosis
4. Considering acute kidney disease as an independent risk
factor of mortality
Etiologies of
AKI
 Potential outcomes
following episode of
Acute Kidney Injury

Prevention Management
Harty J. Prevention and Management of Acute Kidney Injury. Ulster Med J 2014;83(3):149-157
Primary prevention
Patients at
risk
 Primary prevention
AKI prevention measures in critical patients

Management of acute illness

Measures to improve renal perfusion

Diuretics
AKI prevention measures in critical patients
Management of acute
illness
 Sepsis stands out as the main cause of acute kidney
dysfunction, with an incidence of 15---20%.
 Non-septic AKI, it has a higher mortality rate, a longer stay
in the ICU, but a better rate of renal recovery
 Hypovolemia and hypotension tend to trigger AKI
 Acute heart failure (HF) is also associated with a higher risk
of AKI and a worse prognosis
AKI prevention measures in critical patients
Management of acute
illness
 Traditionally, secondary renal hypoperfusion has been
attributed to a low cardiac output
 Treat and avoid situations that might decompensate the HF
 Administration of inotropic intravenous agents
 Loop diuretics would be the pharmacological treatment of
choice for the control of water overload
 Identifying risk factors, improving cardiac function and
preventing acute decompensation
AKI prevention measures in critical patients
Measures to improve renal
perfusion
 Under normal conditions the kidneys receive 25% of total
blood flow
 But they are extremely sensitive to decreases in blood flow
with a rapid deterioration of renal function
 adequate glomerular filtration rate (GFR)
 maintain an adequate mean arterial pressure (MAP)
 volume expansion
 Inotropik
 vasopressor
AKI prevention measures in critical patients
Diuretics

 Loop diretic
 Mannitol
 Primary prevention
Specific measures
 Nephrotoxicity by drugs

 AKI due to intra-tubular deposits

 Contrast-associated acute kidney injury

 Perioperative AKI

 AKI in liver failure

 Specific measures
Nephrotoxicity by drugs

Dependent modifiable risk factors:

Duration of treatment, daily/total
accumulated dose and pharmacodynamic
and pharmacokinetic interactions.
The associations of drugs also constitute
a frequent risk, such as triple therapy
drugs

Mas-Font S et al. Prevention of acute kidney injury in Intensive

Care Units. Med Intensiva. 2017;41(2):116---126
 Specific measures
Nephrotoxicity by drugs

Mas-Font S et al. Prevention of acute kidney injury in Intensive

Care Units. Med Intensiva. 2017;41(2):116---126
 Specific measures
AKI due to intra-tubular deposits

 Rhabdomyolysis
 Treatment of the underlying etiology is the first measure
 Intensive fluid replacement
 Electrolytic corrections
 Specific measures
Contrast-associated acute kidney
injury

Figure 1 Recommendations for CA-AKI prevention.

Mas-Font S et al. Prevention of acute kidney injury in Intensive Care Units.
Med Intensiva. 2017;41(2):116---126
 Specific measures
Perioperative AKI
● Perioperative oliguria is, commonly, secondary to salt and water retention
in response to tissue damage, pain and moderate degrees of hypovolemia
and hypotension
● Heart surgery has the highest risk
● The main causes of AKI include ischemia, hypoxia, inflammation and
nephrotoxicity
● The role of intraoperative hypotension has been related, finding an
increase in risk when mean blood pressure was <60 mmHg during >20 min
and <55 mmHg during >10 min.
● Remote ischemic preconditioning (RIPC) has proven cardiac and kidney
protection with halogenated anesthetics
 Specific measures
AKI in liver failure

• Splanchnic vasodilatation that is

triggered by portal hypertension
• Nephrotoxic drugs and NSAIDs should
be avoided
• Early antiviral treatment
• Water overload should be prevented
• Hepatorenal syndrome (HRS) can be
efficiently prevented through the
administration of albumin
 Secondary prevention
 Early detection of the disease is the most important secondary prevention
 Once an AKI diagnosis has been established, the patient should be reassessed
from an angle more focused on renal function:
1. History: antecedents, nephrotoxic agents, renal insults, etc
2. Renal evaluation:
a. Urine analysis
b. Ultrasound in those cases in which the cause of AKI has not been
identified
c. Estimation of creatinine clearance by measuring urinary creatinine over a
time interval (2, 6, 12 or 24 h).
3. Hemodynamic evaluation
 Management of AKI

Fluid volume expansion

● If clinical assessment points toward intravascular volume deficit,
optimization of the hemodynamic status and correction of any volume
deficit should have a salutary effect on kidney function and help to
minimize further extension of the kidney injury
● Albumin vs. Saline
● Hydroxyethylstarch vs. Saline
 Management of AKI

Vasopressors
● use of vasopressors in conjunction with fluids in patients with
vasomotor shock with, or at risk for, AKI.
● In septic shock with AKI norepinephrine is the vasopressor of choice
with target mean arterial pressure of 65–70 mmHg.
● patient with chronic hypertension, a higher target mean arterial
pressure of 80 – 85 mmHg is recommended
 Management of AKI

Diuretics
● not using diuretics to treat AKI, except in the management of volume
overload.
● Furosemide may, however, be useful in achieving fluid balance to
facilitate mechanical ventilation according to the lung-protective
ventilation strategy in hemodynamically stable patients with acute
lung injury
 Management of AKI

Renal replacement therapy

● decision to start RRT is based most often on clinical features of
volume overload and serum biochemical abnormalities
● based on patient’s clinical context and be individualized
● continuous vs. intermittent RRT
● timing of RRT, early vs. late
 Management of AKI

Glycemic control and nutritional support

● Insulin therapy targeting plasma glucose 110–149 mg/dl (6.1–8.3
mmol/l).
● total energy intake of 20–30 kcal/kg/d in patients with any stage of
AKI.
● avoid restriction of protein intake with the aim of preventing or
delaying initiation of RRT
● administering 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients
without need for dialysis (2D), 1.0–1.5 g/kg/d in patients with AKI on
RRT (2D), and up to a maximum of 1.7 g/kg/d in patients on
continuous renal replacement therapy (CRRT) and in hypercatabolic
 Conclusion
 Since no effective treatment for AKI is available, all efforts are aimed at prevention and early
detection of the disorder in order to establish secondary preventive measures to impede AKI
progression.
 In critical patients, the most frequent causes are sepsis and situations that result in renal
hypoperfusion; preventive measures are therefore directed at securing hydration and correct
hemodynamics through fluid perfusion and the use of inotropic or vasoactive drugs,
according to the underlying disease condition.
 A number of situations could lead to AKI, related to the administration of nephrotoxic drugs,
intra-tubular deposits, the administration of iodinated contrast media, liver failure and major
surgery (mainly heart surgery). In these cases, in addition to hydration, there are other
specific preventive measures adapted to each condition.
 The key elements in any AKI management strategy are optimization of hemodynamics,
correction of fluid and electrolyte imbalances, discontinuation of nephrotoxic drugs, dose
adjustment of administered medications and avoidance of contrast media.