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Gawat Darurat PSIK FKIK UMY

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 of regulation of extracellular volume and electrolytes
While consensus historically exists in this definition, none exists regarding the quantification of this decline in function to fully denote as ARF

Anatomi ginjal


20-25% CO 1200 ml/mnt



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

Kosinski (2009), acute renal failure is a sudden decline in both glomerular and tubular function, resulting in the failure of the kidneys to excrete nitrogen and waste products with a corresponding failure to maintain fluid, electrolyte and acid-base balance ARF may be associated with decreased urinary output of less than 30 ml/h.

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)

Decrease in renal function not limited to ARF, but broad clinical syndrome encompassing various etiologies: including specific kidney disease (ex acute interstitial nephritis, acute glomerular, and vasculitic renal diseases), non specific conditions (ischemia, toxic injury), and extrarenal pathology.

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 <0.5 ml/kg/hr for >6hr)

Definition and classification/staging system for acute kidney injury (AKI)

AKI stage AKI stage I Creatinine criteria Increase of serum creatinine by Urine output criteria

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 or serum creatinine 4.0 mg/dl 354 mol/L) after a rise of at least 44 mol/L or treatment with renal replacement therapy < 0.3 ml/kg/hour for > 24 hours or anuria for 12 hours


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%

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

Etiology of Acute Renal Failure

1. VOLUME DEPLETION 1) 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 embolism 19) Pulmonary hypertension 4. MISCELLANEOUS Renal vasoconstriction Hypercalcemia Norepinephrine NSAIDs


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 pre renal azotemia Hypotension from any cause Hypovolemia from any cause Medication Radiocontrast DM Advanced age Transfussion reacting causing hemoglobinuria

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)


Antimicrobial agents Aminoglycosides Amphotericin B Acyclovir Foscarnet Pentamidine

Radiocontrast agents Miscellaneous Allopurinol, cimetidine, dilantin

Chemotherapy drugs: Cisplatin, 5-FU, mitomycin C, streptozocin Antiviral: Acyclovir, indinavir, Ritonavir, Adenovir

Radiocontrast-Induced Acute Renal Failure

Induces renal vasoconstriction and direct cytotoxicity via oxygen free radical formation Risk factors: Renal insufficiency Advanced age Hypotension

- Diabetes - > 125 ml contrast

Usually non-oliguric ARF; irreversible ARF rare

Contrast Induced Nephropathy

Assess CIN risk
eGFR <30 Hospital admission, Nephrology consult, Dialysis planning, renal protection eGFR 30-59 Discontinue NSAIDs, IV volume expansion, Intra-arterial: isoosmolar, Intravenous: iso-osmolar or low osmolar contrast; limit contrast volume 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

Conditions that Lead to Post-renal Acute Renal Failure

1.BPH 2. Blood clots 3. Renal stones or crystals 4. Tumors 5. Post operative edema 6. Drugs Tricyclic antidepressants Ganglionic blocking agents 7. Foley cathether obstruction 8. Ligation of ureter during surgery

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 urine 5) Review urinary indices


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

3 phases of the disease process


From the occurrence of the precipitating event to the beginning 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 is well established - GFR 5-10 mL/mnt - Last 8-14 days 1-11 months - Anuric Condition oliguric (uop > 400 mL/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????

Nursing care plan

Physical Exam.
Skin new rashes.
Petechiae Malar rash


Rub Gallop

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.

BUN/Creatinine ratio.
> 20:1 suggest prerenal or obstruction. Can be elevated by anything leading to increased urea production/absorption.
GI bleed TPN Steroids Drugs Tigecycline.

Creatinine in anephric state typically only rises 1mg/dl/day.

If greater should be concerned for rhabdomyolysis Serum Cr. Dipengaruhi oleh massa otot tiap individu

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

Nursing Dx
4. Anxiety r.t diagnosis, treatmen plan, prognosis, and unfamiliar environment 5. Deficient knowledge r.t disease process and theraeutic regimen

Its for your home work

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, systems thinking, response to diversity, facilitator of learning, and clinical inquiry.

- low in protein and sodium and - high in fats and carbohydrates to prevent the protein 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 the gastrointestinal tract is not functional.

Provision of emotional support and teaching

Acute renal failure is often very sudden and unexpected for both the patient and the family members. Thorough patient teaching about nutritional needs, fluid restrictions, medications, and the role of dialysis is essential in providing emotional support patients and family members.

1. Renal 1. The primary effect of ARF is a decrease in urinary 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 loses its ability to remove waste products. 3. metabolic acidosis, hypercalemia, hyponatremia, hyperphosphatemia, hypocalcemia, and hypermagnesemia.

3. Cardiovascular - In general, the fluid volume overload experienced in ARF may lead to hypertension, pulmonary edema, peripheral edema, and arrhythmias. - The kidneys fail to excrete excess potassium which may lead to the following: muscle weakness, neuromuscular irritability, bradycardia, heart block, asystole, or other arrhythmias (Campbell, 2003).

4. Respiratory

Dyspnea may result from the decrease in oxygenation either from associated anemia or from fluid volume overload and pulmonary edema associated with ARF.
Auscultation of lung field may reveal crackles.

5. Hematologic Anemic secondary to the impaired RBC production, hemolysis, bleeding, hemodilution, and decrease RBC survival.

Damaged kidneys produce less erythropoietin to stimulate RBC production and the damaged red blood cells are not replaced.
The decrease in hemoglobin leads to insufficient oxygenation manifested by dyspnea.

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.

Diagnostic Tools
Conventional Biomarkers
1. urine output 2. creatinin 3. urea.

New Biomarkers

Cystatin C, Interlukin 18 (IL 18), Neutrophil Gelatinas-Associated Lipocalin (NGAL), and Kidney injury Molecule (KIM-1).

Diagnostic Imaging

1. X rays, 2. computed tomography scan (CT), 3. magnetic resonance imaging (MRI), ultrasound, 4. arteriogram, 5. renal biopsy.

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)*

1. KDIGO Clinical prctice guideline for acute kidney injury. 2012. 2 (1). df/KDIGO%20AKI%20Guideline.pdf 2. So Yoon Jang, S.Y. Renal Fellow. UNC Kidney Center At the Courtesy of Dr. Hladik and Dr. Derebail. 3. Sole, Klein & Moseley. 2009. Introduction to Critical care Nursing. Fifth Edition. Saunders. Elsevier. 4. Stroud, B. 2013. Acute Renal Failure.