27 beans acute renal-failure

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27 beans acute renal-failure

  1. 1. Bad Beans Acute Renal Failure
  2. 2. 3 AM <ul><li>“ Mr. Henle hasn’t peed all night long!” </li></ul><ul><li>How is UO measured? By shift or by hour? Foley or urinating on own? Has the patient been sleeping? </li></ul><ul><li>What is the trend over last 2-3 hours vs. last 24 hours? </li></ul><ul><ul><li>Oliguria = <400ml/24 hrs or <20ml/hr </li></ul></ul><ul><ul><li>Anuria = <50ml/24 hrs </li></ul></ul><ul><li>Recent surgery? </li></ul><ul><li>Other symptoms or changes in vital signs? </li></ul>
  3. 3. Nursing orders <ul><li>While on way to see patient have nurse: </li></ul><ul><ul><li>Flush catheter if patient has one </li></ul></ul><ul><ul><li>Obtain orthostatic blood pressures to help establish fluid status </li></ul></ul>
  4. 4. Physical exam <ul><li>Subjective: Dysuria, nausea, weakness, and fatigue </li></ul><ul><li>Tachycardia and/or a drop in HR >15 bpm or drop in SBP >15mmHg with orthostatics could indicate dehydration </li></ul><ul><li>Decreased mental status = decreased perfusion </li></ul><ul><li>Rales = fluid overload, CHF </li></ul><ul><li>Abdominal pain and distension = obstruction, UTI </li></ul><ul><li>Itching = azotemia </li></ul>
  5. 5. Labs <ul><li>UA: </li></ul><ul><ul><li>High specific gravity = dehydration </li></ul></ul><ul><ul><li>RBCs = UTI, urolithiasis </li></ul></ul><ul><ul><li>WBCs, bacteria = UTI </li></ul></ul><ul><ul><li>Casts: RBC (glomerulonephritis), WBC (pyelonephritis), and epithelial cells and granular casts (ischemic damage) </li></ul></ul><ul><li>Electrolytes to assess for metabolic d/o </li></ul><ul><li>Urine Na, Creatinine </li></ul><ul><ul><li>FENa = (UNa x Pcr)/(PNa x Ucr) </li></ul></ul><ul><ul><li><1% = prerenal; >1% = renal </li></ul></ul><ul><li>ECG to look for peaked T waves, indicates hyperkalemia </li></ul>
  6. 6. Etiology: Overview <ul><li>Prerenal azotemia: most common cause of ARF (30-60% of all cases). Can lead to ATN </li></ul><ul><ul><li>Rapidly reversible </li></ul></ul><ul><ul><li>Causes: hypoperfusion, NSAIDs, and ACE inhibitors. </li></ul></ul><ul><li>Postrenal azotemia: (1-10% of hospital ARF), bladder outlet or ureteral obstruction </li></ul><ul><li>Intrinsic renal disease: most commonly presents as acute tubular necrosis (ATN) and acute interstitial nephritis (AIN). </li></ul><ul><ul><li>ATN is caused by ischemia, toxins, and glomerulonephritis. </li></ul></ul><ul><ul><li>AIN is primarily caused by nephrotoxic drugs. </li></ul></ul><ul><li>Elderly more susceptible to ARF (3.5 X more common); Creatinine clearance dependent on age </li></ul>
  7. 7. Prerenal <ul><li>Potentially reversible </li></ul><ul><li>Volume depletion: </li></ul><ul><ul><li>Surgical: Hemorrhage, shock </li></ul></ul><ul><ul><li>Gastrointestinal (GI) losses: Vomiting, diarrhea, fistulas </li></ul></ul><ul><ul><li>Renal: Over-diuresis, salt-wasting disorders </li></ul></ul>
  8. 8. Prerenal <ul><li>Decrease in cardiac output: </li></ul><ul><ul><li>Acute disorders: Myocardial infarction, arrhythmias, malignant hypertension, tamponade, endocarditis </li></ul></ul><ul><ul><li>Chronic disorders: Valvular diseases, chronic cardiomyopathy (ischemic heart disease hypertensive heart disease) </li></ul></ul><ul><li>Redistribution of extracellular fluid </li></ul><ul><ul><li>Hypoalbuminemic states: Nephritic syndrome, advanced liver disease, malnutrition </li></ul></ul><ul><ul><li>Physical cause: Peritonitis, burns, crush </li></ul></ul><ul><ul><li>Peripheral vasodilation: Sepsis, antihypertensive agents </li></ul></ul><ul><ul><li>Renal artery stenosis (bilateral) </li></ul></ul>
  9. 9. Postrenal <ul><li>1-10% of all cases </li></ul><ul><li>Ureteral obstruction: Bilateral or in a solitary kidney (calculi, neoplasm, clot, retroperitoneal fibrosis, iatrogenic) </li></ul><ul><li>Urethral obstruction: Prostatic hypertrophy, prostate cancer, prostatitis, clot, calculus, neoplasm, foreign object </li></ul><ul><li>Venous occlusion: Bilateral or a solitary kidney (renal vein thrombosis, neoplasm) </li></ul>
  10. 10. Renal/Intrinsic <ul><li>Glomerular and small vessel disease: </li></ul><ul><ul><li>Rapidly progressive glomerulonephritis (RPGN) </li></ul></ul><ul><ul><li>subacute bacterial endocarditis </li></ul></ul><ul><ul><li>proliferative glomerulonephritis </li></ul></ul><ul><ul><li>Vasculitides </li></ul></ul><ul><ul><li>progressive systemic sclerosis </li></ul></ul><ul><ul><li>malignant hypertension </li></ul></ul><ul><ul><li>HUS </li></ul></ul><ul><ul><li>Cryoglobulinaemia </li></ul></ul><ul><ul><li>Eclampsia </li></ul></ul><ul><ul><li>disseminated intravascular coagulation </li></ul></ul><ul><li>Interstitial nephritis: Drug induced, infection, sarcoid, infiltrative </li></ul><ul><li>Tubular lesions: Post-ischemic, drugs pigment, light chain, hypercalcemia </li></ul>
  11. 11. Diagnosis: Procedures <ul><li>Cystoscopy with retrograde pyelogram: evaluates for obstruction and upper tract tumors/malformations </li></ul><ul><li>Renal biopsy (for severe ARF of unknown cause): </li></ul><ul><ul><li>Indicated with nephrotic syndrome, hematuria, or glomerular disease </li></ul></ul><ul><li>Renal ultrasonography: kidney size </li></ul><ul><ul><li>Small kidneys = reflect chronic renal disease. </li></ul></ul><ul><ul><li>Hydronephrosis = obstructive nephropathy. </li></ul></ul>
  12. 12. Risk factors <ul><li>Advanced age </li></ul><ul><li>Comorbid conditions (heart failure, liver or kidney failure, diabetes) </li></ul><ul><li>Contrast exposure (dehydrated, diabetic) </li></ul><ul><li>Nephrotoxic medications (aminoglycosides, NSAIDs, angiotensin converting enzyme inhibitors) </li></ul><ul><li>Volume depletion (especially in diabetes) </li></ul><ul><li>Rhabdomyolysis; surgery (cardiac surgery) </li></ul>
  13. 13. Management: General <ul><li>Discontinue/re-dose nephrotoxic drugs </li></ul><ul><li>Foley catheterization for accurate output </li></ul><ul><li>Daily weight, monitor BP, labs </li></ul><ul><li>Diet </li></ul><ul><ul><li>Eliminate potassium if serum level increased </li></ul></ul><ul><ul><li>Oral and IV amino acids </li></ul></ul><ul><ul><li>Provide nutrition with increased carbohydrates to decrease catabolism. T otal caloric intake of 35 to 50 kcal/kg/day should be maintained with most calories provided by carbohydrates (100 g/day). </li></ul></ul><ul><li>Correct easy bleeding with DDAVP, estrogen, and cryoprecipitate </li></ul><ul><li>Prednisone in acute interstitial nephritis may help </li></ul><ul><li>Mannitol - alkaline diuresis in rhabdomyolysis </li></ul>
  14. 14. Management: Prerenal <ul><li>Goal is to restore BP and intravascular volume </li></ul><ul><li>Fluid deficit: </li></ul><ul><ul><li>Fluid bolus with 500ml, recheck fluid status, repeat. </li></ul></ul><ul><ul><li>Monitor vital signs and electrolytes </li></ul></ul><ul><li>Normal or increased fluid status: </li></ul><ul><ul><li>CHF: monitor O2 status. Lasix 20-80mg IV. </li></ul></ul><ul><ul><li>Monitor diuresis, potassium status, daily weight </li></ul></ul>
  15. 15. Management: Postrenal <ul><li>Place foley, note residual. If >400ml and discomfort is relieved, leave catheter in place. </li></ul><ul><li>If foley in place, flus with 20-30ml saline </li></ul><ul><li>Consider stones or mass obstruction </li></ul><ul><li>Daily weights, strict I/O </li></ul>
  16. 16. Management: Renal <ul><li>Hyperkalemia: </li></ul><ul><ul><li>Continuous cardiac monitoring </li></ul></ul><ul><ul><li>Kayexalate 15 to 30g in 50-100ml 20% sorbitol PO q 3-4 hours or in 200ml 20% sorbitol PR q 4 hours </li></ul></ul><ul><ul><li>Dialysis for failed kidneys: can remove 30-60 mEq/hr </li></ul></ul><ul><li>Contrast dye: </li></ul><ul><ul><li>Creatinine peaks within 72 hours with slow recovery over 7 to 14 days with appropriate therapy. </li></ul></ul><ul><li>Aminoglycosides: </li></ul><ul><ul><li>higher risk: elderly, volume depletion, >5 days, large doses, preexisting liver disease, and preexisting renal insufficiency. </li></ul></ul><ul><ul><li>Correct preexisting volume depletion and monitor drug levels </li></ul></ul>
  17. 17. Management: Renal <ul><li>Acidosis: </li></ul><ul><ul><li>Treat as determined by cause of acidosis </li></ul></ul><ul><ul><li>Watch for co-existing hyperkalemia </li></ul></ul><ul><ul><li>Control is aided by restriction of dietary protein </li></ul></ul><ul><li>Consider dialysis: </li></ul><ul><ul><li>Fluid overload unresponsive to diuretics </li></ul></ul><ul><ul><li>Hyperkalemia with K+ >6 to 8 </li></ul></ul><ul><ul><li>Metabolic acidosis pH <7.20 </li></ul></ul><ul><ul><li>BUN >35mmol/L with mental status changes, pericarditis or seizure </li></ul></ul>
  18. 18. Complications <ul><li>Death (50%) </li></ul><ul><li>Sepsis infection (leading cause of mortality) </li></ul><ul><li>Once ARF stabilizes, fluid replacement should be equal to insensible losses (500 mL/day) plus urinary or other drainage losses to avoid hypervolemia </li></ul><ul><li>Hypertension exacerbated by fluid overload: Use antihypertensives that do not decrease renal blood flow (non-dihydropyridine calcium channel blockers, cardioselective beta-blockers, and central acting agents). </li></ul><ul><li>Anemia is common, caused by increased red blood cell (RBC) loss and decreased RBC production. </li></ul><ul><li>Platelet dysfunction may occur secondary to the uremia and present as gastrointestinal (GI) bleeding. </li></ul>
  19. 19. Special Cases <ul><li>Elderly: </li></ul><ul><ul><li>Elderly more susceptible to ARF (3.5 X more common) </li></ul></ul><ul><ul><li>Creatinine clearance dependent on age </li></ul></ul><ul><ul><li>Evolution to acute tubular necrosis more common </li></ul></ul><ul><li>Pregnancy: </li></ul><ul><ul><li>Infected uterus (e.g., Clostridium welchii clostridium perfringens) </li></ul></ul><ul><ul><li>Toxemia and related obstetric complications. </li></ul></ul><ul><ul><li>Pregnant patients only group with a sharp drop in ARF mortality (1.7%) </li></ul></ul><ul><li>Pediatric: Congenital anomalies (e.g., nurethral valves, etc) </li></ul>

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