AKI Study Guide - Lecture notes acute kidney injury PDF

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acute kidney injury lecture
dr. krakorian...

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AKI Study Guide I.

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Objectives a. Define AKI b. Describe epidemiology of AKI c. Identify leading causes of AKI d. Addess the important biochemical markers and feature of the H&P patients with AKI e. Recommend appropriate therapeutic management and monitoring of patients with AKI Background a. Definition i. Abrupt, sustained decline in renal function and decreased GFR ii. Kidneys cannot 1. Excrete nitrogenous waste 2. Concentrate urine 3. Regular fluid and electrolyte balance 4. Maintain acid-base homeostasis b. AKI vs CKD i. AKI 1. Sudden decline 2. Duration 1-4 weeks 3. Reversible a. Takes 1-3 months for full recovery 4. Nephron function regenerates 5. Good prognosis 6. 50% mortality in high risk patients ii. CKD 1. Slow progressive decline 2. Occurs over months/years 3. Irreversible 4. Nephron function doesn’tregenerate 5. Poor prognosis when end-stage kidney disease develops c. Epidemiology i. Overall incidence rate 1. 5-7% of hospitalized patients in general wards 2. 90% filtered by kidneys 4. Regular 0.6- 1.3 mg/dL ii. Elevated BUN in AKI 1. Nitrogenous waste product 2. Influences: diet, exercise, drugs, GI bleed 3. 50% filtered by kidneys 4. Regular 8-20mg/dL iii. Remember: 1. Estimated creatinine clearance (eClCr) and estimated GFR (eGFR) 4mg/dL b. Urine Output Criteria i. 0.3mg/dL or increased >1.5-2x baseline b. Urinary Output i. 6 hours 2. Stage 2 a. Criteria i. Increased SCr > 2-3x baseline b. Urinary Output i. 12 hours 3. Stage 3 a. Criteria i. Increased SCr to >3x from baseline ii. SCr >4mg/dL with an acute rise of at least 0.5mg/dL b. Urinary Output i. 400mL/da 7. Avoid volume overload and pulmonary edema 8. Problems a. Fluid replacement not always successful b. May need to add vasopressor (NE, EPI) in persistently hypotensive patients ii. Pre-renal AKI with Hypervolemia – volume overload 1. Signs/symptoms a. Pulmonary edema 2. Treatment a. IV loop diuretic i. Furosemide (Lasix) ii. Titrate dose to effectiveness b. Match urine losses with IV fluid replacement c. High dose may be needed in severe AKI and worsening HF 3. Monitor input/output, BP, HR, electrolytes, weight, heating (ototoxicity) 4. Goal: non-oligouria 5. Diuretic resistence a. Identify patients at risk i. Persistently decreased GFR ii. Markedly reduced diuretic response (edema) b. Management i. Maintain look diuretic

ii. iii. iv. v.

Dosing strategies to overcome resistance Increase dose, BID, convert PO to IV Sequential Nephron Blockade Add on thiazide diuretic to loop diuretic = combination therapy

iii. Hyperkalemia 1. Acute Hyperkalemia a. >5.5 mEq/L with EKG changes b. Step 1: STAT calcium gluconate or calcium chloride IV – 1 gm i. MOA: antagonizes K effect on heart c. Step 2: Concurrently treat with i. Insulin Lispro 10u IV + Dextrose 50% 50mL OR Sodium bicarbonate 50 mEq IV 1. MOA: redistributes extracellular K  intracellular ii. Sodium polystyrene sulfonate (kayexalate) 30-45gm PR or PO 1. MOA: rids K from body d. Step 3: Renal replacement therapy (RRT) such as hemodialysis in persistent hyperkalemia i. MOA: rids K from body 2. Chronic Hyperkalemia a. Background i. Kayexalate PO or PR, multiple da dosing, side effects ii. Black box warning—rare, intestinal necrosis of the colon 1. Usually when used with sorbitol b. Patiromer (Veltassa)—FDA approved i. Nonabsorbed cation exchange polymer ii. Binds K+ in exchange for Ca2+ in the distal colon iii. Once daily dosing, doesn’t taste bad iv. Space other drugs within 6 hours c. Sodium Zirconium Cyclosilicate (ZS-9)—Investigational new drug (not FDA approved) i. Cation exchanger with high K+ selectivity ii. Dissolves in water, tasteless iv. Metabolic Acidosis 1. Sodium bicarbonate 50 mEq IV (may repeat PRN) a. Limitations: large sodium load 2. Hemofiltration of hemodynamic instability (ICU)

3. Hemodialyze via temporary dialysis catheter 4. Monitor: Na, K, total CO2, vital signs g. Dialysis i. Indications for Dialysis 1. A—acidosis 2. E—electrolyte disturbances (usually kyperkalemia) 3. I—intoxications (lithium or ethylene) 4. O—overload (volume overload) 5. U—uremia (BUN > 100) h. ATN i. Long standing pre-renal ischemia ATN ii. Urinalysis: granular, muddy brown casts 1. Non-oligouria = better outcome iii. Aminoglycoside- Induced ATN 1. Dose-related 2. Drug monitorying: associated with high tobra levels >2 3. Signs: toxicity appears 5-10 days after therapy begins a. Usually non-oligouric (urine output >400mL/da) b. Increased BUN, SCr c. Decreased Mg2+, K+ d. Urine may show muddy brown casts 4. Predisposed by hypotension, concurrent nephrotoxins and liver disease 5. Treatment: discontinue aminoglycoside a. Supportive care b. Recovery within 304 weeks iv. Drug induced ATN management 1. IV fluit to maintain brisk diuresis 2. Correct electrolyte abnormalities 3. Control BP 4. Discontinue cause and all potentially nephrotoxic drugs 5. Minimize further insults to kidney i. Antibiotic induced AIN i. Not dose related ii. Beta lactam antibiotics 1. Penicillins, cephalosporins 2. Onset of AIN a. 3-5 days on second exposure to drug b. 2-3 weeks after first exposure 3. Signs a. Maculopapular rash, fever, oliguria, arthralgias (joint pain) b. Absence of signs doesn’t rule out AIN 4. Urinalysis: WBCs, WBC casts, RBCs, RBC casts, eosinophils

5. Blood: increased BUN, SCr, eosinophils 6. Discontinue causative agent and document Rx in PMR a. Do not try again j. Contrast Dye ATN- Risk Factors i. AKI begins 24-48 hours of imagine with contrast dye ii. Signs/symptoms may appear in 48 hours iii. High risk factors 1. Age, diabetes, underlying renal insufficiency, drugs a. Diuretics, metformin, ACE inhibitors, ARBs, NSAIDs 2. Stop drugs ~24 hours before and after contrast administration a. For metformin: stop 24 hours before and 48 hours after iv. Prevention k. Rhabdomyolysis i. Cause: overexertion 1. Drugs—statins, cocaine, EtOH ii. Signs/symptoms 1. First clues: myalgia, severe muscle weakness, dark coca cola colored urine iii. Labs 1. Urinalysis: brown debris, muddy brown granular casts, myoglobin 2. BUN:SCr ration 5:1 3. Urine: Na > mEq/L 4. FeNa >2% 5. CK >15,000 IU/mL with elevated CK-MM (muscle) 6. Increasing CK number = increased severity iv. Causes 1. Hyperkalemia (most life-treatening) 2. Hyperphosphatemia, hypocalcemia 3. Hyperuricemia >40mg/dL from muscle damage v. Treatment 1. Remove cause 2. Mild to severe AKI = dialysis 3. IV hydrastion to maintain diuresis and rid body of myoglobin 4. Treat underlying cause (esp of hyperkalemia) 5. Must treat immediately a. Prognosis good if treated quickly...