1 / 45

Acute Renal Failure : The Response to Severe Injury and Hypovolemic Shock

TRAUMA-ICU NURSING EDUCATIONAL SERIES. Acute Renal Failure : The Response to Severe Injury and Hypovolemic Shock. Bradley J. Phillips, M.D. Critical Care Medicine Boston Medical Center Boston University School of Medicine. Renal Function and Failure. Overview Renal Physiology

Audrey
Download Presentation

Acute Renal Failure : The Response to Severe Injury and Hypovolemic Shock

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. TRAUMA-ICU NURSING EDUCATIONAL SERIES Acute Renal Failure:The Response to Severe Injury and Hypovolemic Shock Bradley J. Phillips, M.D. Critical Care Medicine Boston Medical Center Boston University School of Medicine

  2. Renal Function and Failure • Overview • Renal Physiology • Trauma and Renal Function • Initial management of Oliguria • Acute Renal Failure • Key Management Issues

  3. Glomerular Architecture

  4. Physiology in Normal State • Renal blood flow (RBF) • 20-25% cardiac output • distribution • 85% outer cortical • 15% inner cortex outer medulla • <1% inner medulla

  5. Physiology in Normal State • Glomerular filtration • 20% of plasma filtered as cell-free and protein-free • normal GFR 125 ml/min • calculate • most accurate - insulin • completely filtered/neither secreted or absorbed • good estimation - creatinine • (Cr Urine / Cr Plasma) x urine (ml/min)

  6. Proximal Convoluted Tubule 60-80% reabsoprtion of H2O, Na, Cl, K, HCO3 100% glucose/amino acids Distal Convoluted Tubule 20% reabsoprtion of H2O Renin/Aldosterone Effect Loops of Henle 20% of H2O (descending) 25% Na, Cl, K Large amounts HCO3, Mg, Cl Secretion of H ions Active Na Reabsorption Collecting Ducts reabsoprtion of H2O, ADH effect Glomerular Component Functions

  7. Renal Physiology after Trauma • Class I Hemorrhage (10-15%) • autoregulation maintains GFR • Class II Hemorrhage (15-30%) • exceeds autoregulation • vasoconstriction at afferent & efferent • GFR decreases by 50-60% • Class III Hemorrhage (30-40%) • GFR decreases to less than 20% resuscitation relieves vasocontriction over hours to days, afferent then efferent arterioles

  8. Oliguria after Trauma • Rapid replenishment of the circulatory volume and cardiac output • at least 3-4 L for every 1 L of blood loss • Factors • general anesthetic • loss of renal autoregulation • loss of systemic vasoconstriction

  9. Key Management Issue IV Fluid Resuscitation

  10. Renal Function and Trauma • Postresuscitative oliguria • even if MAP and CO restored • persistant for several hours secondary to renal arteriole vasoconstriction • shifting of fluid from plasma to interstitial space secondary to depletion during hypotension/hypovolemia • Postresuscitative polyuria • usually transient • not excessive (< 250 cc for 30-45 mins, < 3 hrs) • “wash out” effect of inner medulla • use other parameters ( ie HR, base deficit)

  11. Postoperative Fluid Sequestration • Obligatory extravascular sequestration • Phase II (Lucas, Resuscitation of the Injured Patient: Three Phases of Resuscitation, Surg Clin North Am, 1977) • Last 12-36 hours • Clinical signs • tachycardia • reduced pulse pressure • oliguria • weight gain • some respiratory insufficiency • Hormoral effect - ADH, aldosterone

  12. Fluid Mobilization Phase • Phase III - mobilization and diuresis • Water added to plasma faster than excreted • “Postresuscitation Hypertension” • Renal blood flow still remains decreased • Caution with diuretics • role in post elective surgery in elderly patient with CHF • avoid in trauma patients • can precipitate oliguria/renal dysfunction

  13. Mechanical Ventilation and Fluid Therapy • Reduce renal blood flow • even if zero PEEP • PEEP reduces RBF more • additional fluid may be required to maintain UOP

  14. Acid-Base Balance • Hemorrhagic shock • increased lactate acidosis • metabolic acidosis persistent after intravascular volume repleted (hours) • cell metabolism • impaired renal excretion of acids • Renal acid excretion • absorb Na/HCO3, excrete PO, NH3 • normal excrete 70-80 mEq /day • can excrete 4-5x normal with severe acidosis • depends on GFR and RBF

  15. Renal Response to Sepsis • Hyperdynamic state • increased CO, increased RBF, decreased SVR, expanded ECF volume, increased UOP • “inappropriate polyuria” • vasodilators of sepsis • “wash out” effect • Hypodynamic state • later stages of severe sepsis • decreased CO, increased SVR, decreased GFR and RBF

  16. Key Management Issue IV Fluid Resuscitation PEARL: Check Urine Na. If less than 10 meq/L…???

  17. Acute Renal Failure • Mortality in posttrauma = 50- 60% • acute oliguric > 90% • contrast nonoliguric < 20%

  18. Terminology • ARF - sudden, severe deterioration • rule of thumb - Cr increasing > 1.0 mg/dL/day • Acute tubular necrosis (ATN) - form of ARF • Oliguria: UOP less than 400 ml/d • 500 mOsm daily solute concentrated to 1200 mOsm/kg • Anuria: UOP less than 50 ml/d • Nonoliguric renal failure • progressive azotemia despite UOP > 400 ml/d • High-output renal failure • acute renal insufficiency with UOP > 4 L/d

  19. Acute Renal Failure • Etiology • severe and prolonged hypotension • severe sepsis • massive blood transfusions • compartment syndrome • myoglobinuria/hemoglobinuria • radiocontrast • aortic cross clamping (> 30 minutes) • drug-induced • postinfectious glomerulonephritis • Contributing factors • age • pre-existing renal vascular disease • pre-existing renal insufficiency

  20. Myoglobinuria/hemoglobinuria • Muscle necrosis or RBC destruction • Hypotension significant increase risk of ATN • can occur even if renal perfusion well maintained • Skeletal muscle (per kg of tissue) • 40-45 meg K • 730 ml of H2O • 23 mmol of PO4 • 4 g myoglobin ( takes 100-150 mg/dL to discolor urine) • Severe crush injury/muscle ischemia causes hyperkalemia, hyperphosphotemia,azotemia, hypocalemia, DIC, hypotension, and myoglobinuria

  21. Predictors of ARF ? • Vivino G. Antonelli M. Moro ML. Cottini F. Conti G. Bufi M. Cannata F. Gasparetto A. Risk factors for acute renal failure in trauma patients.Intensive Care Medicine. 24(8):808-14, 1998 Aug • prospective, consecutive 153 trauma patients • CPK > 10,000, PEEP > 6, hemoperitoneum • Loun B. Astles R. Copeland KR. Sedor FA. Adaptation of a quantitative immunoassay for urine myoglobin. Predictor in detecting renal dysfunction.American Journal of Clinical Pathology. 105(4):479-86, 1996 Apr. • urine assay for myoglobinuria • levels > 20,000 mcg/L

  22. Key Management Issue Administer IV Fluid Resuscitation and Maintain UOP > 100 cc/hr

  23. Rhabdomyolysis • Treatment • volume, volume, volume!!! • shock and rhabdomyolysis = renal failure • maintain UOP > 100 - 200 cc/hr • ? role or sodium bicarbonate • precipitation of myoglobin urine pH < 5.6 • check urine pH • consider if UOP marginal or severe hyperkalemia • mannitol (avoid lasix if possible) • volume expander, mild diuretic, free radical scavenger • follow CPK levels (most sensitive)

  24. Drug-Induced ARF • Pathogenesis depends on drug • Predisposing factors • volume depletion • age • pre-existing renal disease • prolonged therapy • other nephrotoxic agents

  25. Drug-Induced ARF • Antibiotics • aminoglycosides (most publicized) • however use of cephalosporins and clindamycin potentate nephrotoxicity • amphotericin B • vancomycin • PCN can cause hypersensitivity nephritis • Limit nephrotoxicity • low trough • ? once a day dosing (proven to limit ototoxicity) • avoid NSAIDS • avoid combination of nephrotoxic antibiotics • avoid hypotension

  26. Radiocontrast-Induced Nephropathy • Incidence as high as 13% • Mechanisms • direct toxicity • renal ischemia (vasoconstriction) • intratubular obstruction • immunologic abnormality • Clinical • serum Cr elevation within 24 hours • serum Cr peak day 3-5 • renal function normally returns by 10 days • hemodialysis seldom needed

  27. Key Management Issue Administer IV Fluid Resuscitation Only IV fluid hydration has been shown to reduce incidence of IV contrast nephropathy (not lasix or dopamine) Should maintain UOP 12 hours before and 24 hours post procedure

  28. Classification of ARF • Prerenal azotemia • inadequate renal perfusion • characterized by low urine Na/high urine Cr • Postrenal azotemia • complete obstruction bilateral ureteral or lower urinary tact • Acute tubular interstitial nephritis • usual drug-induced • signs of hypersensitivity (check urine eosinophils) • renal biopsy

  29. ARF - Clinical Changes • Increase serum Cr (> 1 to 1.5 mg/dL/d) • directly related to decreased GFR • Increase BUN (exceeds > 25 mg/dL/d) • related to decreased GFR and reabsorption • Hyponatremia • intake fluids > UOP (particularly hypotonic solutions) • increased endogenous water • increased loss of urine sodium

  30. ARF - Clinical Changes • Hyperkalemia • reduced excretion from decreased GFR • impaired renal tubules secretion • faster if muscle protein breakdown due to ischemia or injury • Metabolic acidosis • accelerated protein catabolism • decreased excretion of acid load • Other electrolytes • hyperPO4, hyperMg • hypoCa

  31. Differential Diagnosis • Postrenal azotemia • rule out urinary tract obstruction • Prerenal azotemia • hypovolemia • cardiac failure

  32. Hypovolemia • Renal response to decreased blood flow • normal - conserve H20 and Na • ARF - impaired ability to concentrate/conserve • Differentiation of Pre-renal vs ARF • renal failure index • fractional excretion of sodium RFI = Urine Cr / Plasma Cr < 1.0 prerenal azotemia FE = (U Na/P Na) / (U Cr/P Cr) x 100 < 1.0 prerenal azotemia SIMULATANEOUS SPOT PLASMA & URINE SAMPLES

  33. Urinalysis • Prerenal azotemia • unremarkable • Obstructive uropathy • unremarkable • Glomerular disease • heavy proteinuria • sterile pyuria • mild microhematuria • casts (granular/WBC) • ? eosinophils

  34. Key Management Issue Fluid Challenge!!!!! • RULE OUT HYPOVOLEMIA • 1. test response to fluid challenge • at least 500 to 1,000 cc (15-30 minutes) • 2. consider CVP or pulmonary artery monitoring

  35. Treatment of ARF • Diuretics • after hypovolemia ruled out • if given soon after onset of oliguria may convert to non-oliguric renal dysfunction (better prognosis) • types • mannitol • osmotic diuretic decrease proximal Na reabsorption • dose: 25 g IV bolus • lasix • inhibits active Na transport in loop of Henle • dose: 20-40 mg IV initial, then double every 30 minutes if no response (max dose 500 mg) • dopamine (low dose, 1-3 ug/kg/min) • effects partially due to inhibition of ADH

  36. Sodium and Water Balance • Fluid restriction is important treatment of ARF • careful to maintain perfusion • problem sometimes with initial hemodialysis • Fluid requirements • GI and renal loss plus 500 cc • accurate daily weights and I/O’s

  37. Metabolic Acidosis • Hypercatabolic generation of acid loads • Produces anion gap • Best treated with reducing catabolism or hemodialysis, not sodium bicarbonate

  38. Hemodialysis • Indications • refractory pulmonary edema • hyperkalemic crisis • uremic complications • severe metabolic acidosis A E I O U Y Acidosis Electrolyte disturbance Intoxication Overload Uremia Why not

  39. Hemodialysis • Ultrafiltration • indicated in hemodynamically unstable patients • continuous venovenous (CV VH) or arteriovenous(CAVH) • filtrate removal of 500-800 ml/hr • require often some heparinization • Hemodialysis • rapid correction of uremia, fluid overload, electrolyte disturbances, and acidosis • “prophylactic” dialysis probably beneficial • added benefit by providing for adequate calories and protein

  40. ARF - Special Consideration/Complication • Adjustment of medications • Coagulopathy • platelet dysfunction in aggregation • treatment with DDAVP (0.3 ug/kg) • low antithrombin III levels • microvascular thrombosis • Hyperkalemia • increased with blood transfusions, acidosis, and hyperosmolemia (ie treatment with diuretics) • usual treatment (glucose + insulin, calcium IV) • avoid kayexelate (Na exchange for K)

  41. ARF - Special Consideration/Complication • Anemia • reduced EPO levels • contributing factors include GI blood loss and hemodialysis (ie hemolysis) • treatment with recombinant EPO/Fe replacement • Stress gastritis • more than 20% of ARF patients • treatment • AlOH antacids (also treats hyperphosphotemia) • H2 blockers

  42. ARF - Special Consideration/Complication • Pericarditis (uremia) • with or without pleuritis • presence of chest pain or friction rub • some with fever with or without leukocytosis • treatment with hemodialysis • Nutritional support • problems • insulin resistance • negligible free water and urea clearance • ? high energy requirement

  43. ARF - Special Consideration/Complication • Nutritional support • treatment • minimize free water • do not restrict protein if needed unless unable to clear with hemodialysis

  44. Outcomes of ARF • Oliguric ARF • expect return of renal function in 3 weeks • if enter diuretic phase, likelihood of survival greatly increased • older patients progress to chronic renal failure much more often • Non-oliguric ARF • increasing secondary earlier and aggressive fluid resuscitation and conversion with diuretics • easier to manage than oliguric • only few require dialysis • much lower mortality

  45. Questions ?

More Related