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01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
01 Graciano   Acute Renal Failure In The Intensive Care Unit
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01 Graciano Acute Renal Failure In The Intensive Care Unit

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  • 1. Acute Renal Failure in the Intensive Care Unit Ana Lia Graciano, MD Pediatric Critical Care The University of North Carolina-Chapel Hill
  • 2. Basic Renal Physiology
  • 3.
    • nephron
    • the functional unit of the kidney
    • capable of forming urine
    • has two major components:
      • glomerulus
      • tubule:
        • proximal
        • loop of Henle
        • distal
        • collecting
  • 4. renal parenchyma cortex medulla nephrons cortical juxtamedullary structural organization
  • 5.
    • renal blood supply:
      • the kidneys receive 20% of the cardiac output
      • vascular supply:
            • renal arteries
            • interlobar arteries
            • arcuate arteries
            • interlobular arteries
            • afferent arterioles
            • glomerular capillaries
            • efferent arterioles
            • peritubular capillaries
  • 6. C: cortex OS : outer stripe IS : inner stripe IM : inner medulla Afferent Arteriole Efferent Arteriole Vasa Recta IM
    • there are two capillary beds arranged in series
    • the efferent arteriole helps to regulate the hydrostatic pressures in both sets of capillaries
    renal circulation C OM
  • 7.
    • steps in urine formation
    • filtration (glomerular function)
    • reabsorption and secretion (tubular function)
    • 98% of the ultrafiltrate is reabsorbed
    • tubular reabsorption is quantitatively more important than tubular secretion in the formation of urine, but secretion determines the amount of K+ and H+ ions that are excreted
  • 8. glomerular filtration rate (GFR)
    • GFR depends on the interplay between hydrostatic and oncotic pressures within the nephron
    • hydrostatic pressure is usually higher in the glomerulus than within the tubule, forcing filtrate out of the capillary bed into the tubule
    • oncotic pressure is generated by non-filtered proteins: it helps to retain fluid in the intravascular space
    • GFR : Kf * (hydrostatic pressure - oncotic pressure)
    • Normal GFR : 100 ml/min/1.72m 2
    • *Kf filtration coefficient in the glomerulus
  • 9. Adjusting the resistances of the afferent and efferent arterioles, the kidneys can regulate both the hydrostatic pressures in the glomerular and peritubular capillaries, changing the rate of glomerular filtration and/or tubular reabsorption in response to homeostatic demands.
  • 10. determinants of Glomerular Filtration Rate (GFR) Glomerular hydrostatic pressure Glomerular colloidosmotic pressure Bowman’s capsule pressure net filtration pressure: hydrostatic + colloid osmotic pressure
  • 11. determinants of renal blood flow (RBF)
    • RBF=
    • renal artery pressure - renal vein pressure
    • total renal vasculature resistance
  • 12. autoregulation a feedback mechanism that keeps renal blood flow (RBF) and glomerular filtration rate (GFR) constant despite changes in arterial blood pressure.
  • 13.
    • autoregulation of GFR
    • as renal blood flow increases, GFR increases, leading to an increase in NaCl delivery to the macula densa.
    • a feedback loop through the macula densa to the juxtaglomerular cells of the afferent arteriole results in increased vascular tone, decreased renal blood flow and a decrease in GFR.
    • NaCl to the macula densa then decreases leading to relaxation of the afferent arteriole (increasing glomerular hydrostatic pressure) and increases renin release from juxtaglomerular cells of afferent and efferent arterioles
    • renin increases angiotensin I, then converted to angiotensin II which constrict efferent arteriole increasing hydrostatic pressure returning GFR to normal
  • 14. afferent arteriolar resistance - + Proximal tubule NaCl reabsorption Macula densa feedback mechanism for autoregulation afferent arteriolar resistance arterial pressure Glomerular hydrostatic pressure GFR macula densa NaCl renin angiotensin II efferent arteriolar resistance
  • 15. Tubular Function
    • proximal tubule
      • 70% of Na is reabsorbed in the proximal tubule
  • 16. Tubular Function
    • loop of Henle
        • 20 % of Na, Cl and K reabsorbed
        • urine concentration and dilution occurs in the loop of Henle through an osmotic gradient provided by the countercurrent mechanism (vasa recta)
        • urine flow rate is regulated by NaCl, prostaglandins, adenosine and urine volume presented to the macula densa
  • 17.
    • distal tubule
      • secretes K and bicarbonate
      • proximal segment of distal tubule is impermeable to water (urine dilution)
      • distal segment (cortical collecting tubule): K and bicarbonate secretion
    Tubular Function
  • 18.
    • collecting duct
      • regulates final urine concentration
      • aldosterone receptors regulate Na uptake and K excretion
      • ADH increases water reabsorption. In the absence of ADH, the collecting duct is impermeable to water
    Tubular Function
  • 19. major sites of solute and water movement across the nephron
  • 20. Acute Renal Failure (ARF)
  • 21. acute renal failure: definition ARF is an abrupt decline in glomerular and tubular function, resulting in the failure of the kidneys to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis.
  • 22.
      • Azotemia is a consistent feature of acute renal failure (ARF), oliguria is not.
      • anuria ::: urine output < 0.5 ml/kg/h
  • 23. acute renal failure: pathophysiology Increase in NaCl delivered to macula densa. Damage to proximal tubule cells increases NaCl delivery to distal nephron,. This causes disruption of feedback mechanism. Obstruction of tubular lumen. Casts (necrosis of tubular cells and sloughed basement membrane) clog the lumen. This will increase the tubular pressure and then GFR will fall. Backleak of fluid through the tubular basement membrane.
  • 24.
    • acute renal failure: clinical setting in the PICU
      • postoperative states (especially cardiac surgery)
      • shock states
      • trauma, burn or crush injuries
      • nephrotoxic drugs
      • neonatal asphyxia
  • 25.
    • acute renal failure: common clinical features
      • azotemia
      • hypervolemia
      • electrolytes abnormalities:
      •  K+  phosphate
      •  Na+  calcium
      • metabolic acidosis
      • hypertension
      • oliguria - anuria
  • 26.
    • acute renal failure: classification
    • Prerenal (hypoperfusion)
    • Renal (intrinsic)
    • Postrenal (obstructive)
  • 27. prerenal
    • decreased perfusion without cellular injury
    • renal tubular and glomerular functions are intact
    • reversible if underlying cause is corrected
  • 28. prerenal
    • common etiologies:
      • dehydration
      • hypovolemia
      • hemodynamic factors that can compromise renal perfusion (CHF, shock)
    • Sustained prerenal azotemia is the main factor that predisposes patients to ischemia- induced acute tubular necrosis (ATN)
  • 29. Prerenal azotemia and ischemic tubular necrosis represent a continuum. Azotemia progresses to necrosis when blood flow is sufficiently compromised to result in the death of tubular cells. Most cases of ischemic ARF are reversible if the underlying cause is corrected.
  • 30. postrenal
    • obstruction of urinary tract
    • important to rule out quickly :
      • potential for recovery of renal function is often inversely related to the duration of the obstruction
  • 31. renal
    • classified according primary site of injury:
      • tubular
      • interstitium
      • vessels
      • glomerulus
  • 32. acute renal failure: diagnosis
    • History and Physical examination
    • Blood tests : CBC, BUN/creatinine, electrolytes, uric acid, PT/PTT, CK
    • Urine analysis
    • Renal Indices
    • Renal ultrasound (useful for obstructive forms)
    • Doppler (to assess renal blood flow)
    • Nuclear Medicine Scans
      • DMSA: anatomy
      • DTPA and MAG3: renal function, urinary
      • excretion and upper tract outflow
  • 33. renal indices
    • Reabsorption of water and sodium:
      • - intact in pre-renal failure
      • - impaired in tubulo-interstitial disease and ATN
    • Since urinary indices depend on urine sodium concentration, they should be interpreted cautiously if the patient has received diuretic therapy
  • 34. renal indices Renal Failure Index (RFI) RFI: urine [Na] urine creatinine / serum creatinine
  • 35. renal indices Fractional Excretion of Na (FENa) FENa: [ urine Na/serum Na] x 100 % [urine creatinine/serum creatinine]
  • 36.
    • prerenal azotemia:
      • Urine sediment : hyaline and fine granular casts
      • Urinary to plasma creatinine ratio : high
      • Urinary Na : low
      • FENa : low
      • Increased urine output in response to hydration
  • 37.
    • renal azotemia:
      • Urine sediment: brown granular casts and tubular epithelial cells
      • Urinary to plasma creatinine ratio : low
      • Urinary Na: high
      • FENa: high
  • 38. urine and serum laboratory values
  • 39. acute renal failure: prevention
    • recognize patients at risk (postoperative states, cardiac surgery, septic shock)
    • prevent progression from prerenal to renal
    • preserve renal perfusion
      • isovolemia, cardiac output, normal blood pressure
      • avoid nephrotoxins (aminoglycosides, NSAIDS, amphotericin)
  • 40.
    • hemoglobinuria + myoglobinuria
    • hemoglobinuria:
    • transfusion reactions, HUS, ECMO
    • myoglobinuria:
    • crush injuries, rhabdomyolisis
    • urine (+) blood but (-) red blood cells
    •  CPK  K+
    • treatment
    • aggressive hydration + urine alkalinization
    • mannitol / furosemide
  • 41. acute renal failure: management
    • treat the underlying disease
    • strictly monitor intake and output (weight, urine output, insensible losses, IVF)
    • monitor serum electrolytes
    • adjust medication dosages according to GFR
    • avoid highly nephrotoxic drugs
    • attempt to convert oliguric to non-oliguric renal failure (furosemide x 3)
  • 42. acute renal failure: fluid therapy
    • If patient is fluid overloaded
        • fluid restriction (insensible losses)
        • attempt furosemide 1-2 mg/kg
        • Renal replacement therapy (see later)
    • If patient is dehydrated:
        • restore intravascular volume first
        • then treat as euvolemic (below)
    • If patient is euvolemic:
        • restrict to insensible losses (30-35 ml/100kcal/24 hours) + other losses (urine, chest tubes, etc)
  • 43. sodium
    • most patients have dilutional hyponatremia which should be treated with fluid restriction
    • severe hyponatremia (Na< 125 mEq/L) or hypernatremia (Na> 150 mEq/L): dialysis or hemofiltration
  • 44. potassium
    • Oliguric renal failure is often complicated by hyperkalemia, increasing the risk in cardiac arrhythmias
    • Treatment of hyperkalemia:
      • sodium bicarbonate (1-2 mEq/kg)
      • insulin + hypertonic dextrose: 1 unit of insulin/4 g glucose
      • sodium polystyrene (Kayexalate): 1 gm/kg . Can be repeated qh. (Hypernatremia and hypertension are potential complications)
      • dialysis
  • 45. nutrition
    • provide adequate caloric intake
    • limit protein intake to control increases in BUN
    • minimize potassium and phosphorus intake
    • limit fluid intake
    If adequate caloric intake can not be achieved due to fluid limitations, some form of dialysis should be considered

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