Acute Kidney Injury Alerts A CrossSectional Comparison with the Clinical

Diagnosis

PICO

AKI Pathophysiology
Sudden decrease in kidney function and GFR caused
by:
Poor perfusion / reduction of blood flow to kidney
Toxins (medications, chemo, recreational drugs)
Tubular Ischemia
Infections
Obstruction of urine flow
Damage to glomeruli, interstitial tissue or tubules

AKI Risk Factors

Any

reduction in kidney function

Hypotensive shock / dehydration
Urine retention
All nephrotoxic medication
High blood pressure
Heart failure
Kidney disease
Liver diseases
Diabetes

AKI
Manifestations
Typically asymptomatic or
symptoms are masked by
primary disease process

Decreased Urine Output

Sleep disturbances
Weight loss
Anorexia
fatigue

Etiology Health acquired

4% of hospital admissions
20% of critical care
admissions

Types of Acute Kidney Injury

Prerenal Acute Kidney Injury
Any condition Decreasing blood flow to the kidneys and leading to

ischemia in the nephrons, such as:

Shock
Heart Failure
Pulmonary embolism
Anaphylaxis
Sepsis
Pericardial Tamponade

Types of Acute Kidney Injury

Intrarenal (Intrinsic) Acute Kidney Injury
Actual physical, chemical, hypoxic, or immunologic damage directly to the kidney
tissue, such as:

Acute interstitial nephritis

Exposure to nephrotoxins
Acute glomerular nephritis
Vasculitis
Acute tubular necrosis
Renal artery or vein stenosis
Renal artery or vein thrombosis

Types of Acute Kidney Injury

Post Renal Acute Kidney Injury
Obstruction of the urine collecting system such as:
Ureter, bladder, or urethral cancer
Kidney, ureter, or bladders stones
Bladder atony
Prostatic hyperplasia or cancer
Urethral stricture
Cervical cancer

Clinical Manifestations of AKI

Typically asymptomatic or symptoms are
masked by primary disease process
Decreased Urine Output
Sleep disturbances
Weight loss
Anorexia
fatigue

Treatment of AKI
Treatment for AKI involves identifying the illness or injury that originally
damaged your kidneys.
IV fluids such as Furosemide to promote renal perfusion
Low dose renal dose Dopamine to enhance perfusion
Insulin to treat Hyperkalemia (monitor for s/s of hypoglycemia)
Calcium Channel Blockers to improve GFR
Diet Therapy - proteins to replace proteins lost
0.6g/kg
If on dialysis 1-1.5g/kg
Renal Replacement Therapy (RRT):
Hemodialysis
Peritoneal Dialysis

AKI Outcomes
Complete restoration of kidney function if caught early
and perfusion restored
Renal failure
Permanent renal failure - 5-10%
Death 20% of all cases
30% of all cases that are referred to nephrology
50% if dialysis is required

Population
4464 patients in a regional population who developed
significant renal impairment over a 6 month period
Mixture of AKI, CKD, and unknown impairment

Renal Failure
Acute Kidney Injury

Chronic Kidney
Disease

Less than a week onset

Years before symptomatic

<50% of nephrons

90-95% of nephrons involved

Good prognosis if caught

Permanent and gradual loss of kidney function

High mortality rate if missed

Common in community

Most common kidney problem in acute settings

AKI
Complicates 1/7 hospital admissions
43% of admitted patients did not have AKI recognized
until kidney function was permanently compromised
22% of recognized AKI received inappropriate treatment
17% of recognized AKI had avoidable complications

Intervention
Acute Kidney Injury alert algorithm that
automatically detects RIFLE criteria upon lab
values being entered into system

Diagnosing AKI
Algorithm

Traditional

Algorithm scans medical records for changes in BUN, Creatinine

and Urine output

Unexplainable decrease in urine noted

HCP notified of decrease

When diagnostic changes meet criteria, HCP is alerted by

algorithm of clinically significant changes in lab values

HCP treats & assesses / requests lab values to collaborate

decrease in kidney function

RIFLE Criteria
Risk, Injury, Failure, Loss, End-Stage Kidney Disease
**normal refer to lab value WDL or, in CKD, normal for pt

RIFLE
Classification

Creatinine Level

GFR

Urine Output

Risk

1.5 x normal

25% less than

normal

<0.5 mL/kg q6h

Injury

2.5 x normal

50% less than

normal

<0.5 mL/kg q12h

Failure

3 x normal

50% less than

normal

<0.5 mL/kg q24h

Loss

Complete loss of
function > 4
weeks

End Stage Kidney

Disease

Complete loss of
function > 3
months

n/a

n/a

Require renal
replacement
therapy
Require renal
replacement
therapy

Diet/Nutrition

Encourage patients with kidney injury or disease to follow fluid

and dietary restrictions regarding sodium, potassium, and protein.
Choose low potassium foods such as: apples, cabbage, green
beans, grapes and strawberries. Examples of high potassium
foods include bananas, oranges, potatoes, spinach and tomatoes.
Avoid products with added salt such as: frozen dinners, canned
soups, fast food, salty snack foods, canned vegetables and
processed meats and cheeses.
Limit phosphorus intake. Phosphorus is found in milk, cheese,
dried beans, nuts and peanut butter.

Goals of Nutritional Support in

AKI

Prevent protein-energy wasting

Preserve lean body mass and nutritional status
Avoid further metabolic derangements
Avoid complications
Improve wound healing
Support immune function
Minimize inflammation
Improve antioxidant activity and endothelial function
Reduce mortality

Comparison
Clinical diagnosis from an experienced
nephrologist with automated AKI detection
using the RIFLE criteria.

 All patients in cohort had chart, lab values for year previous
and medical history assessed by nephrologist.

 Due to reliance on creatinine and GFR levels the success of

algorithm was dependent on the frequency of blood test
ordered by HCP
Etiology of AKI was immaterial to test allowing for diagnosis in
atypical disease processes

Outcome
Using stage one alerts provided sensitive and
timely diagnosis with a success rate ranging from
86.4% to 95.5% depending on the floor that the
patient was staying on.

AKI diagnosis
Overall 90.5% of patients with AKI were detected via automated
algorithm
RIFLE AKI patients not detected were identified using
retrospective creatinine analysis which suggests that lack of
baseline data adversely affected early detection.
Normal is 0.6-1.2.
My last 5 years of lab work has my creatinine between 0.84 and 0.91. A 1.5
increase for my highest value would be 1.35. Without medical history (because
why would I even mention former kidney function tests if Im in the hospital for,
say, an allergic reaction?) it would not flag me until 1.8

AKI diagnosis

Algorithm using retrospective analysis of creatinine

identified:
96.4% of AKI with more diagnoses of mild AKI being identified.
Misdiagnosed more patients with CKD without AKI as having AKI

AKI Overdiagnosed in
Patients with CKD
Removing criteria that kept CKD patients from alerting
staff also delayed diagnosis and treatment for 67% of
patients who had mild AKI

What are some causes of post renal kidney injury?

Select all that apply.

1. Bladder Cancer
2. Dehydration
3. Calculi
4. Tubular necrosis
5. Bladder neck obstruction.

Answer:
1. Bladder Cancer
3. Calculi
5. Bladder neck obstruction.

A client with acute kidney injury has a serum

potassium level of 6.0 The nurse should plan which
action as a priority?
A) check sodium level
B) place client on a cardiac monitor
C) encourage increased vegetables in the diet
D) allow an extra 500mL of fluid intake to dilute the
electrolyte concentration.

ANSWER: B-cardiac monitor.

Rationale: the client with hyperkalemia is at risk of developing cardiac dysrhythmias and cardiac arrest. Because
of this the client should be placed on a cardiac monitor. Fluid intake is not increased because it contributes to fluid
overload and would not affect the serum potassium level significantly.

A client has developed acute kidney injury

(AKI) as a complication of
glomerulonephritis. The nurse should assess
the client for which expected manifestation
of AKI?
A) Hypertension
B) Decreased cardiac output
C) Bradycardia
D) Decreased central venous pressure.

ANSWER: A-Hypertension.
Rationale: AKI caused by glomerulonephritis is classified as intrinsic or intrarenal failure. This form of AKI commonly manifests with hypertension,
tachycardia, oliguria, lethargy, edema, and other signs of fluid overload. AKI from prerenal causes is characterized by decreased blood pressure or a
recent history of the same, tachycardia, and decreased cardiac output and central venous pressure. Bradycardia is not part of the clinical picture for any
form of renal failure.

The nurse is caring for a client with acute

kidney injury (AKI). When performing an
assessment, the nurse would expect to note
which breathing pattern?
A) Apnea
B) Kussmauls
C) Decreased respirations
D) Cheyne-Stokes respirations.

Answer: B Kussmauls.
Rationale: Clinical manifestations associated with AKI occur as a result of metabolic acidosis. The nurse would
expect to note Kussmaul's respirations as a result of the metabolic acidosis because the bodily response is to
exhale excess carbon dioxide. The breathing patterns noted in options 1, 3, and 4 are not characteristic of AKI.

References not in APA format

Journal article: http://

journals.plos.org/plosone/article?id=10.1371/journal.pone.01
31909
7th edition Iggy text 1538-1545
Wikipedia, naturally https://
en.wikipedia.org/wiki/Acute_kidney_injury
http://www.mayoclinic.org/diseases-conditions/kidney-failure
/basics/lifestyle-home-remedies/con-200224029
http://ckj.oxfordjournals.org/content/3/1/1/T1.expansion.html
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2596697 /