akut kidney injury
DESCRIPTION
gagal ginjal akutTRANSCRIPT
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ACUTE KIDNEY INJURY (AKI)
Do We Know What We Mean?
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Definition of AKI
• There are more than 35 definitions of AKI (formerly acute renal failure) in literature!
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Definition of AKI
• RIFLE classification• AKIN classification
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Definition ok AKI based on RIFLE criteria “Acute Dialysis Quality Initiative (ADQI 2005)”
Increase in SCr Urine output
Risk of renal injury
Injury to the kidney
Failure of kidney function
1,5 x baseline0.3 mg/dl increase2 X baseline
3 X baseline OR> 0.5 mg/dl increase if SCr >=4 mg/dl
< 0.5 ml/kg/hr for > 6 h
< 0.5 ml/kg/hr for >12h
Anuria for >12 h
Loss of kidney functionEnd-stage disease
Persistent renal failure for > 4 weeksPersistent renal failure for > 3 months
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Definition of Acute Kidney Injury (AKI) based on “Acute Kidney Injury Network (AKIN 2007)”
Stage Increase in Serum Creatinine
Urine Output
1 1.5-2 times baseline OR 0.3 mg/dl increase from baseline
<0.5 ml/kg/h for >6 h
2 2-3 times baseline <0.5 ml/kg/h for >12 h3 3 times baseline OR
0.5 mg/dl increase if baseline>4mg/dlORAny RRT given
<0.3 ml/kg/h for >24 hOR Anuria for >12 h
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Risk Factor
• Age > 75 yrs• Drugs (ACEi, diuretics, NSAIDS)• Chronic kidney disease (eGFR < 60 ml/mnt)• Hypovolemia/Sepsis• Diabetes
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AKI: causes• attempt 3 groups categorise
• sepsis/hypovolemia 70%• drug related, acute GN 20%• obstruction 10%
PRE-RENALINTRA RENALPOST-RENAL
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TYPES OF AKIA. Pre renal
B. Post renal
C. Intra renal
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Major Disease Categories Causing AKI
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Disease Category IncidencePrerenal azotemia caused by acute renal hypoperfusion
55-60%
Intrinsic renal azotemia caused by acute diseases of renal parenchyma: -Large renal vessels dis. -Small renal vessels and glomerular dis. -Acute tubular necrosis (ATN) (ischemic and toxic) -Tubulo-interestitial dis. -Intratubular obstruction
35-40%
*>90%*
Postrenal azotemia caused by acute obstruction of the urinary tract
<5%
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Prerenal Azotemia
• Intravascular volume depletionbleeding, GI loss, Renal loss, Skin loss, Third space loss (skin burns)
• Decreased cardiac outputchronic heart failure (CHF)
• Renal vasoconstrictionLiver Disease, Sepsis, Hypercalcemia
• Pharmacologic impairment of autoregulation and GFR in specific settingsACEi in bilateral renal artery stenosis, nonsteroidal anti-inflammatory drugs (NSAIDs) in any renal hypoperfusion setting
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Intrinsic Renal Azotemia• Large Renal Vessel Disease
Thrombo-embolic disease• Renal Microvasculature and Glomerular Disease
Inflammatory: glomerulonephritis, allograft rejectionVasospastic: malignant hypertension, scleroderma crisis, pre-eclampsia, contrastHematologic: Hemolytic-Uremic Syndrome (HUS) & Thrombocytopenic Purpura (TTP), Disseminated intravascular coagulation
• ATNIschemicToxic
• Tubulo-interestitial DiseaseAcute Interestitial Nephritis (AIN), Acute cellular allograft rejection, viral (HIV, BK virus), infiltration (sarcoid)
• Intratubular Obstructionmyoglobin, hemoglobin, myeloma light chains, uric acid, tumor lysis, drugs (indinavir, acyclovir, foscarnet, oxalate in ethylene glycol toxicity)
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Postrenal azotemia
• Stones;• Blood clots;• Papillary necrotic tissue;• Urethral disease;
anatomic: posterior valvefunctional: anticholinergics, L-DOPA
• Prostate disease;• Bladder disease;
anatomic: cancer, schistosomiasisfunctional: neurogenic bladder.
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AKIStages
• Onset – 1-3 days with ^ BUN and creatinine and possible decreased urinary output (UOP);
• Oliguric – UOP < 400/d, ^BUN, Crest, Phos, K, may last up to 14 d
• Diuretic – UOP ^ to as much as 4000 mL/d but no waste products, at end of this stage may begin to see improvement
• Recovery – things go back to normal may take 3 months to 12 months
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Initial diagnostic tools in AKI• History and Physical exam• Detailed review of the chart, drugs administered,
procedures done, hemodynamics during the procedures.
• Urinalysis protein, blood, crystals, infection
• Urine microscopy casts, cells (eosinophils)
• Urine electrolytes• Renal imaging
Ultrasound, Mag-3 scan, Retrograde Pyelogram• Markers of CKD
iPTH, size<9cm, anemia, high phosphate, low bicarb• Renal biopsy
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AKI
• Subjective symptoms–Nausea–Loss of appetite;–Headache;–Lethargy;–Tingling in extremities.
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AKI• Objective symptoms
– Oliguric phase –• vomiting • disorientation, • edema, • ^K+ • decrease Na • ^ BUN and creatinine• Acidosis metabolic
(kusmaul breathing)• uremic
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• CHF and pulmonary edema
• hypertension caused by
hypovolemia, anorexia • sudden drop in UOP• convulsions, coma• changes in bowels
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AKI• Objective systoms
– Diuretic phase• Increased UOP (4 L/day)• Gradual decline in BUN and creatinine• Hypokalemia• Hyponatriuemia• Tachycardia
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AKI• Diagnostic tests
– History &Physical examenation – BUN, creatinine, sodium, potassium. pH,
bicarb. Hgb and Hct– Urine studies– Ultrasound of kidneys– Kidneys, ureters, and bladder (KUB)– Abdomen and renal CT– Retrograde pyelogram
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ACUTE KIDNEY INJURY NURSING CARE PLANS
NURSING PROIRITY• Reestablish or maintain fluid
and electrolyte balance.• Prevent complications.
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AKI DIAGNOSING AND INTERVENTING
1) Risk for Imbalance electrolyte2) Excess Fluid Volume3) Risk for Decreased Cardiac Output4) Risk for Imbalanced Nutrition5) Risk for Infection6) Risk for Deficient Fluid Volume
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AKI NURSING INTERVENTION
1) Risk for Imbalance electrolyte; hyperkalemia Obtain specimens for laboratory
analysis of potasium Avoid false report of hyperkalemia Verify all high pottasium level Monitor cause of hyperkalemeia Monitor neurological, cardiac,
gastrointestinal manifestasi of hyperkalemia
Administer electrolyte binding and electrolyte exreting resin (e.g sodium polystyrene sulfonate (kayexalate) as prescribed is appropriate
Administer prescribed medication to shift potasium into the cell (e.g 50% dextrose and insulin, sodium bicarbonate, calcium chloride, and calcium gluconate), as appropriate
Maintain potasium restriction (e.g banana, orange juice, avocadro, and caffein)
Avoid pottasium-sparing diuretics Monitor fluid status Monitor renal funtion Prepare for dyalysis
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AKI NURSING INTERVENTION
2). Excess Fluid Volume• Accurately record intake and
output (I&O)• Monitor urine specific gravity• Weigh daily at same time of day,
on same scale, with same equipment and clothing
• Assess skin, face, dependent areas for edema.
• Monitor heart rate (HR), BP, and JVD/CVP
• Auscultate lung and heart sounds
• Assess level of consciousness. Investigate changes in mentaltion, presence of restlessness
• Monitor diagnostic studies. E.g: BUN, Cr, serum sodium, Hb, Hct,
• Administer medications as indicated. Furosemid
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AKI NURSING INTERVENTION
3). Risk for Decreased Cardiac Output• Monitor BP and HR• Observe ECG for changes in
rhythm. • Auscultate heart sounds.• Assess color of skin, mucous
membranes, and nail beds• Monitor for GI bleeding• Maintain bed rest
• Monitor laboratory studies; K, Ca, Mg
• Administer mediactions as indicated.(Inotropic agents: digoxin (Lanoxin)
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AKI NURSING INTERVENTION
4). Nutrition: imbalanced, risk for less than body requirements• Assess and document dietary intake• Provide frequent, small feedings• Give patient/SO a list of permitted
foods or fluids and encourage involvement in menu choices
• Offer frequent mouth care or rinse with diluted acetic acid solution. Give gums, hard candy, breath mints between meals
• Weigh daily• Monitor laboratory studies: BUN,
albumin, transferrin, sodium, and potassium
• Consult with dietitian support team• Provide high-calorie, low to
moderate protein diet. 1 gr/d in oliguric phase, and high protein at diuresis phase
• Maintain proper electrolyte balance by strictly monitoring levels
• Administer medications as indicated; iron, vit D, Vit B, Vit C, calcium carbonate also antiemetic (Compazine or tigan)
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AKI NURSING INTERVENTION
5). Risk for Infection• Promote good hand washing by
patient and staff• Avoid invasive procedures;
catheterization• Provide routine catheter care• Encourage deep breathing,
coughing, frequent position changes
• Asses skin integrity• Vital sign• Monitor labstudies; WBC
• Obtain specimen for culture and sensitivity and administer appropriate antibiotics as indicated
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AKI NURSING INTERVENTION
6). Risk for Deficient Fluid Volume• Measure I&O accurately. Weigh
daily • Provide allowed fluids
throughout 24-hr period.• Monitor BP and HR• Note signs and symptoms of
dehydration: dry mucous membranes, thirst, sensorium, peripheral vasoconstriction
• Control environmental temperature; limit bed linens as indicated
• Monitor lab sudies
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DIALYSIS SUPPORTING
– Hemodialysis• Yugular, subclavian approach• Femoral approach
– Hemofiltration – Peritoneal dialysis– Continous renal replacement therapy (CRRT)
• Can be done continuously• Does not require dialysate
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