acute kidney injury (3)

7/27/2019 Acute Kidney Injury (3)

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NUR CHAYATI

Dept. Gawat Darurat

PSIK FKIK UMY


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Old term: acute renal failure (ARF)

Traditionally defined as the abrupt decrease of

renal function sufficient to result in retention of

nitrogenous waste products, as well as loss ofregulation of extracellular volume and electrolytes

While consensus historically exists in this

definition, none exists regarding the quantificationof this decline in function to fully denote as ARF


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Anatomi ginjal

BEAN SHAPE

RETROPERITO

NEALLOWER THAN

THE LEFT

NEPHRON AS

UNIT

FUNCTIONAL

20-25% CO

1200 ml/mnt


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NEPHRONA.aFFEREN

A.eFFEREN


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Kidney function

Regulation of body fluid

Regulation of electrolyte balance

Regulation of acid base balance

Regulation of blood pressure

Excretion of nitrogenous waste product

Regulation of erytropoiesis

Metabolism of vitamin D

Synthesis of prostaglandin


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Kosinski (2009), acute renal failure is asudden decline in both glomerular andtubular function, resulting in the failure of thekidneys to excrete nitrogen and waste

products with a corresponding failure tomaintain fluid, electrolyte and acid-basebalance

ARF may be associated with decreasedurinary output of less than 30 ml/h.


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ARF: the sudden decline in GFR, resulting in

retention of nitrogenous waste products

(azotemia). Usually accompanied by oliguria

(uop < 400mL/24 hr)non oliguric (>

400mL/24hr)


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AKI

Decrease in renal function not limited to ARF,but broad clinical syndrome encompassingvarious etiologies: including specific kidney

disease (ex acute interstitial nephritis, acuteglomerular, and vasculitic renal diseases),non specific conditions (ischemia, toxic

injury), and extrarenal pathology.


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AKI

An abrupt (within 48hr) reduction in kidney function

currently defined as an absolute increase in serum

creatinine of either >0.3 mg/dL or a percentage

increase of >50% or a reduction in urin out put(documented as oliguria of 6hr)


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Definition and classification/staging system for acute

kidney injury (AKI)AKI stage Creatinine criteria Urine output criteria

AKI stage I Increase of serum creatinine by

0.3 mg/dl ( 26.4 mol/L)

or

increase to 150% 200% from baseline < 0.5 ml/kg/hour for > 6 hours

-------------------------------------------------------------------------------------------------------------------

AKI stage II Increase of serum creatinine to

> 200% 300% from baseline < 0.5 ml/kg/hour for > 12 hours

-------------------------------------------------------------------------------------------------------------------

AKI stage III increase of serum creatinine to

> 300% from baseline < 0.3 ml/kg/hour for > 24 hoursor or anuria for 12 hours

serum creatinine 4.0 mg/dl

354 mol/L) after a rise of at least 44 mol/L

ortreatment with renal replacement therapy


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Epidemiology

Prevalence 1% all patients admitted to hospital

10-30% patients admitted to ICU

Etiology

Hemodynamic 30% Parenchymal 65%

Acute tubular necrosis 55%

Acute glomerulonephritis 5%

Vasculopathy 3% Acute interstitial nephritis 2%

Obstruction 5%


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Mortality

Dialysis requiring 40-90%

Increased mortality even in patients not requiring dialysis

25% increase in creatinine associated with a

mortality rate of 31% compared with 8% for matched

patients without renal failure


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Etiology of Acute Renal FailurePRE RENAL

1. VOLUME DEPLETION1) Hemorrhage

2) Trauma

3) Surgery

4) Diarrhea

5) Vomitting

6) Diuretics

7) Osmotic diuresis

8) Diabetes incipidus

9) Burns

10) Hipoalbuminemia

2. VASODILATION

11) Sepsis

12) Anaphylaxis

13) Medication

(antihipertensive)

14) Anasthesia

3. IMPAIRED CARDIAC

PERFORMANCE

15) Heart failure

16) IMA

17) Cardiogenic shock

18) Pulmonary embolism19) Pulmonary

hypertension

4. MISCELLANEOUS

Renal

vasoconstriction

Hypercalcemia

Norepinephrine

NSAIDs

GFR


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Conditions that Lead to Intra-renal Acute Renal Failure

1. GLOMERULAR,

VASCULAR/

HEMATOLOGICAL

PROBLEM

Glomerulonephritis

(post streptococcal)

Vasculitis

Malignant

hypertension

SLE

DIC

Hemolytic uremic

syndrome Scleroderma

Hypertension og

pregnancy

Thrombosis

a/v.renalis

2. TUBULAR PROBLEM

(ACUTE TUBULAR

NECROSIS/ ACUTE

INTERSTITIAL

NEPHRITIS)

Ischemia

Causes of prerenal azotemia

Hypotension from

any cause

Hypovolemia from

any cause

Medication Radiocontrast

DM

Advanced age

Transfussion

reacting causing

hemoglobinuria


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Common Nephrotoxic Medications

NSAIDS ACE inhibitors

Angiotensin receptor blockers

Antibiotics

Penicillins methacillin

Ampicillin, amoxacillin, carbenacillin, oxacillin

Cephalosporins

Quinolones (ciprofloxacin)

Anti-tuberculous medications (rifampin, INH, ethambutol)

Sulfonamides (TMP-SMX, furosemide, thiazides)


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COMMON NEPHROTOXIC AGENTS

Antimicrobial agents

Aminoglycosides

Amphotericin B

Acyclovir

Foscarnet Pentamidine

Chemotherapy drugs: Cisplatin, 5-FU, mitomycin C,

streptozocin

Antiviral: Acyclovir, indinavir, Ritonavir, Adenovir

Radiocontrast agents

Miscellaneous

Allopurinol, cimetidine,

dilantin


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Radiocontrast-Induced

Acute Renal Failure

Induces renal vasoconstriction and direct cytotoxicity via

oxygen free radical formation

Risk factors:

Renal insufficiency - Diabetes

Advanced age - > 125 ml contrast

Hypotension

Usually non-oliguric ARF; irreversible ARF rare


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Contrast Induced Nephropathy

Assess CIN risk eGFR 60, Discontinue metformin

Optimal Volume Status

Low-osmolality contrast media

Evaluate Creatinine 24 72hr after contrast exposure

Adequate IV volume expansion with isotonic crystalloid for 3 12hr before

the procedure and continue for 6 24hr afterward. Oral fluid data is

insufficient No adjunctive medical or mechanical treatment has been proved to be

efficacious

Prophylactic hemodialysis and hemofiltration not validated


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Conditions that Lead to Post-renal Acute Renal Failure

1.BPH

2. Blood clots

3. Renal stones or crystals

4. Tumors

5. Post operative edema6. Drugs

Tricyclic antidepressants

Ganglionic blocking agents

7. Foley cathether obstruction

8. Ligation of ureter duringsurgery

5 K St i E l ti A t R l


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5 Key Steps in Evaluating Acute Renal

Failure

1) Obtain a thorough history and physical;

review the chart in detail

2) Do everything you can to accurately assess

volume status

3) Always order a renal ultrasound

4) Look at the urine5) Review urinary indices


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Symptoms:

Fever, rash, joint pains, myalgias

Concern for SLE, vasculitis, acute interstitial nephritis.

Dyspnea heart failure. Hemoptysis

Preceding bloody diarrhea

Preceding pharyngitis post-Strep, post-infectious


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3 phases of the disease process

INITIATION

(ONSET) PHASE

MAINTENANCE

(OLIGURIC/ANURIC) PHASE

RECOVERY

(DIURETIC )PHASE

From the occurrence of the

precipitating event to thebeginning of the change in

urine output.

1. Several hours-2 days

2. Normal renal process

begin to deteriorate

3. INTRINSIC RENAL

DAMAGE IS NOT YET

ESTABLISHED

Potentially reversible

- Intrinsic renal damage iswell established

- GFR 5-10 mL/mnt

- Last 8-14 days 1-11

months

- Anuric Condition

oliguric (uop > 400mL/mnt)

- Complication:

hyperkalemia, infection

- Renal tissue recovers and

repairs itself (4-6 months)

- Gradual increase in uop

& improvement in

laboratory value

- Diuresis happen caused

of:

1. salt and water

accumulation in ECF

2. osmotic diuresis from

retained waste

product

3. Diuretic agents

DANGER????


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Nursing care plan


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Assessment

Physical Exam.

Skin new rashes.

Petechiae

Malar rash

Eye

Papilledema

Cardio

Rub

Gallop


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Assessing volume status.

Is the patient intravascularly volume depleted?

Neck veins JVP

Peripheral edema or lack of.

Orthostatic vitals.

Pt. may be edematous (low albumin) or have

significant right sided heart disease.


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BUN/Creatinine ratio. > 20:1 suggest prerenal or obstruction.

Can be elevated by anything leading to increased ureaproduction/absorption.

GI bleed TPN

Steroids

Drugs Tigecycline.

Creatinine in anephric state typically only rises1mg/dl/day. If greater should be concerned for rhabdomyolysis

Serum Cr. Dipengaruhi oleh massa otot tiap individu


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Nursing Dx

1. Excess fluid volume related to sodium and

water retention and excess intake

2. Risk for infection r.t depressed immune

response secondary to uremia and impaired

skin integrity

3. Imbalanced nutrition: less than body

requirements related to uremia, altered oral

mucous membranes, and dietary restriction


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Nursing Dx

4. Anxiety r.t diagnosis, treatmen plan,

prognosis, and unfamiliar environment

5. Deficient knowledge r.t disease process and

theraeutic regimen


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NOC, NIC

Its for your home work


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Nurse competencies

AACN Synergy Model. The eight nursing

competencies of the Synergy Model are as

follows: clinical judgment, advocacy and moral

agency, caring practice, collaboration, systemsthinking, response to diversity, facilitator of

learning, and clinical inquiry.


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Nutrition

- low in protein and sodium and

- high in fats and carbohydrates to prevent theprotein burden on the patients kidneys

(Campbell, 2003).- Fluids are generally restricted to the amount

of the patients urine output plus 500 to 700

ml.- Parental nutrition is recommended if thegastrointestinal tract is not functional.

i i f i l d


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Provision of emotional support and

teaching

Acute renal failure is often very sudden andunexpected for both the patient and the family

members.Thorough patient teaching about nutritionalneeds, fluid restrictions, medications, and therole of dialysis is essential in providing

emotional support patients and familymembers.


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Complication

1. Renal

1. The primary effect of ARF is a decrease inurinary output that leads to fluid retention and

edema.2. The decrease in filtration leads to BUN and

creatinin build up in the blood as the kidney losesits ability to remove waste products.

3. metabolic acidosis, hypercalemia, hyponatremia,hyperphosphatemia, hypocalcemia, andhypermagnesemia.


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3. Cardiovascular

- In general, the fluid volume overload experienced inARF may lead to hypertension, pulmonary edema,

peripheral edema, and arrhythmias.

- The kidneys fail to excrete excess potassium which maylead to the following: muscle weakness, neuromuscular

irritability, bradycardia, heart block, asystole, or otherarrhythmias (Campbell, 2003).


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4. Respiratory

Dyspnea may result from the decrease in

oxygenation either from associated

anemia or from fluid volume overload andpulmonary edema associated with ARF.

Auscultation of lung field may revealcrackles.


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5. Hematologic

Anemic secondary to the impaired RBC production,hemolysis, bleeding, hemodilution, and decreaseRBC survival.

Damaged kidneys produce less erythropoietin tostimulate RBC production and the damaged redblood cells are not replaced.

The decrease in hemoglobin leads to insufficientoxygenation manifested by dyspnea.


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6. Gastrointestinal

Uremia may cause nausea, vomiting, anorexia,

gastric ulcers and colitis which places the

patient at risk for GI bleeding.

The increase in urea may also cause the

patients breath to smell like foul urine.


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Diagnostic Tools

Conventional Biomarkers

1. urine output

2. creatinin

3. urea.


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New Biomarkers

Cystatin C,

Interlukin 18 (IL 18),

Neutrophil Gelatinas-Associated Lipocalin

(NGAL), and

Kidney injury Molecule (KIM-1).


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Diagnostic Imaging

1. X rays,

2. computed tomography scan (CT),

3. magnetic resonance imaging (MRI),

ultrasound,

4. arteriogram,

5. renal biopsy.


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Evidence Based Practice

Contrast induced nephropathyHow is this

happen? What should the nurses do?

Canadian Association of Radiologist

(Consensus Guidelines for The Prevention of

Contrast Induced Nephropathy)*


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Refferences

1. KDIGO Clinical prctice guideline for acute kidneyinjury. 2012. 2 (1).http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf

2. So Yoon Jang, S.Y. Renal Fellow. UNC Kidney Center Atthe Courtesy of Dr. Hladik and Dr. Derebail.

3. Sole, Klein & Moseley. 2009. Introduction to Criticalcare Nursing. Fifth Edition. Saunders. Elsevier.

4. Stroud, B. 2013. Acute Renal Failure.

http://rnjournal.com/journal-of-nursing/acute-renal-failure
http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdfhttp://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdfhttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdfhttp://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf

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