ACUTE RENAL FAILURE S. Kache, MD, P. Trinkus, MD

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1 ACUTE RENAL FAILURE S. Kache, MD, P. Trinkus, MD Definition Acute Renal failure is a rapid decline (hours, days, weeks) in glomerular and tubular functions with loss of the ability to maintain fluid and electrolyte homeostasis and to excrete organic solutes including drugs and metabolites manifesting as: Rising BUN and creatinine Alteration in electrolyte concentrations: Na, K, Ca, PO4, CO2, H + Edema and intravascular volume excess Oliguria, polyuria, or normal urine output may be present Etiologic Classification Pre-Renal Azotemia: Altered hemodynamics from either: o True hypovolemia blood loss or dehydration from gastroenteritis, DI, salt wasting states, Addisonian crisis o Effective hypovolemia sepsis, anaphylaxis, drug induced vasodilation, low cardiac output, nephrosis, protein loosing enteropathy Renal ischemia from: o Intra-renal redistribution stress, anesthesia, surgery, vasoconstrictors o Vascular compromise renal vein thrombosis, bilateral arterial thrombosis, aortic cross clamp Intra-renal Azotemia: Pre-renal etiologies noted above can lead to acute tubular necrosis (ATN) Additional causes vasculitis (polyarteritis nodosa, Lupus, Wegener s granulomatosis), microangiopathic states (hemolytic uremic syndrome, DIC, TTP), glomerulonephritis (acute post streptococcal and others). Tubulointerstitial nephritis drugs, infection, or infiltrative process (sarcoid, malignancy) Nephrotoxins myoglobin, red cell membranes, uric acid, phosphate, drugs, radiocontrast material, epinephrine, aoglycosides, NSAIDS quite common in PICU Post- renal (obstructive) renal failure: Posterior urethral valves most common Urethral strictures, bladder obstruction from clots (hemorrhagic cystitis), ureteral stones, extrinsic compression Intra-peritoneal collecting system rupture (inadvertent surgical injury) leads to resorption azotemia. Clinical Presentation The signs and symptoms of acute renal failure may be non-specific. Dysuria, altered urine volume and urine discoloration may point to the renal system but most serious complications relate to other organ system dysfunction. Physical exam may reveal Acute Renal Failure 1

2 altered vital signs with low or high blood pressure, tachycardia, tachypnea, somnolence, rales, retractions, a gallop rhythm, edema, or loss of skin turgor, poor perfusion and diished pulses depending on the underlying etiology of the renal failure. DIAGNOSTIC STUDIES: Summary Table of studies by condition in children PRERENAL AZOTEMIA ACUTE TUBULAR NECROSIS RHABDO-MYOLYSIS, IV HEMOLYSIS GLOMERULO- NEPHRITIS HEMOLYTIC UREMIC SYNDROME Urine flow Oliguria Variable, (severity) Variable, (severity) Usually oliguria Usually oliguria to anuria Urinalysis Minor changes Granular casts and Pigmenturia Red cell casts, hematuria, Hematuria, RBC casts, proteinuria pigment proteinuria Urine > 400 mosm < 350 mosm < 350 mosm > 400 mosm Variable (V) osmolality Spec Gravity > < < > V Urine Na < 10* > 30 < 30 < 10 V FENa < 1%* > 2% > 2% < 1% V Blood work BUN rises > creatinine CPK elevated Specific to cause of GMN Thrombotic microangiopathy, hemolytic anemia, low platelets * In neonates urine Na < 40 and FENa < 2% suggest a prerenal etiology FENa: Calculation of the fractional excretion of sodium (FENa) estimates the relative clearance of sodium and creatinine. In pre-renal azotemia more than 99% of filtered sodium is reabsorbed. If the FENa is elevated intrinsic renal injury has occurred. Technique: urine and serum Na and Creat are measured on simultaneously obtained specimens. FENa = (Urine Na/Urine creat)/ (Plasma Na/ Plasma creat) X 100. [Rearranging: U/P Na X P/U Cr X 100 = FENa] Imaging Ultrasound is indicated urgently in any new onset renal failure patient to identify obstructive and congenital abnormalities. Nuclear studies are generally not urgently indicated. A variety of tracers are available that may be useful in identifying scarring (DMSA) or in assessing function (MAG3, DTPA). Intravenous pyelography is also generally not indicated in the assessment of ARF. Complications requiring PICU admission include: Fluid overload: hypertension or heart failure with pulmonary edema Pericarditis: with effusion and tamponade Uremic or hypertensive encephalopathy with coma, intracranial hemorrhage and/or seizures Hyperkalemia can lead to arrhythmias which can be fatal Poor platelet function from uremia can lead to GI bleeding 2

3 Specific metabolic disturbances: hyponatremia, hypocalcemia, hyperphosphatemia, and acidosis Treatment When a patient is admitted to the ICU with renal failure, unless emergent RRT is required, the following treatments should be attempted. Fluid resuscitation: assure adequate pre-renal perfusion; consider CVC placement with CVP monitoring Adequate Blood pressure: consider inotropes Diuretics: consider single large dose loop diuretic or Mannitol Fluid Management Assure adequate renal perfusion. o Dehydrated patients should be adequately fluid resuscitated. o Consider 25% albu to maintain oncotic pressure; gm/kg can be infused over several hours for serum albu < gm/dl. o Low blood pressure and poor cardiac output should be treated with inotropes and / or vasopressors. Fluid overloaded patients have no mandatory fluid intake. Provide sufficient glucose to prevent hypoglycemia. o Fluid replacement is calculated based on insensible losses plus urine output and other measurable losses. o Insensible losses are estimated as 300 ml/m 2 and given as dextrose in water. Electrolytes Hyperkalemia: note of the treatments listed below, only lasix and kayexalate decrease total body K +. All other treatments cause intra-cellular shift of the K +. EMERGENCY MANAGEMENT OF HYPERKALEMIA Agent Onset Dose Comments/Complications Calcium Chloride Immediate mg/kg Sodium Bicarbonate Hyperventilation Immediate Myocardial membrane stabilization 1 2 meq/kg Potassium shift intra-cellular Manual hyperventilation in intubated patients Glucose and Insulin Glucose 1 gm/kg Insulin 0.1 unit/kg ß- agonist 30. Standard inhalation dosing by nebulizer Lasix Hyperventilation induces alkalosis leading to intra-cellular shift of K + Potassium shifts intra-cellular; risk of hypo- or hyper- glycemia Limited pediatric data 1 2 mg/ kg Wastes K via kidneys; only effective if patient with some urine output Kayexalate 2 6 hours 1 gm/kg PO or PR in sorbitol Hypernatremia, fluid loss (sorbitol) Acute Renal Failure 3

4 Symptomatic Hyponatremia: o Manifests as irritability, stupor, seizures, and coma. o 3% NaCl solution: 0.51 meq Na per ml, 6 to 12 ml/kg is needed. 3 5 ml/kg given rapidly for symptom resolution 3 5 ml/kg adistered over 2 hours Calcium: Treat symptomatic hypocalcemia with: o Calcium gluconate 60 mg/kg by slow IV push o Calcium chloride 20 mg/kg by slow IV push Phosphate: Attempt to control hyperphosphatemia with oral calcium salts, e.g. calcium carbonate; if possible otherwise dialysis is necessary. Renal Replacement Therapy - RRT (Dialysis) Absolute Indications: o Uremic pericarditis o Uremic encephalopathy o ~ Absolute BUN level > mg/dL o Refractory volume overload with pulmonary edema or hypertension o Severe electrolyte abnormalities: K, Na, Ca or PO4 derangement o Intractable acidosis Relative indications: o Rapidity of disease progression o Often required in tissue injury syndromes or tumor lysis syndrome with hyperkalemia and hyperphosphatemia failing conservative measures o Neonatal hyperammonemia from urea cycle disorder or other inborn error of metabolism Comparison of various modes of RRT Comparative Strengths of Dialysis Techniques Therapeutic Concern PD HD CVVH (D) Fluid removal Toxin removal (+) Requires stable Hemodynamics K+ removal Anticoagulation required Hypotension a risk (+) Causes Disequilibrium syndrome (PD = peritoneal dialysis, HD = acute hemodialysis, CVVH = continuous veno-venous hemofiltration) 4

5 o CCVH is the RRT of choice in the ICU setting, since it is well tolerated by patients with hemodynamic instability and removes fluid gently. o Hemodialysis is required for emergent hyperkalemia, hyperammonemia, fluid overload, or toxin removal, patients require. o PD is usually not considered in ICU patients. Specific Disease Entities: Hemolytic Uremic Syndrome (HUS) occurs both in diarrheal and non-diarrheal (atypical) forms. It is the most common cause of acute renal failure in healthy children. Typical HUS is usually Shiga (vero) toxin associated and presents with sudden onset of pallor, mild jaundice and petechiae in association with bloody diarrhea and, sometimes, shock. These patients require PICU care in the severe forms when shock or encephalopathy is present or dialysis is required. Tissue injury syndromes are seen in the setting of newly presenting tumors or crush injuries with rhabdomyolysis. In acute tumor lysis massive uric acid, potassium and phosphate release occur on initiation of chemotherapy. In rhabdomyolysis, release of intracellular electrolytes and myoglobin lead to renal failure. Aggressive hydration and alkalinization of the urine can prevent acute renal failure. o A bicarbonate infusion at meq/kg/ hr should be initiated. o Urine ph should be checked every 4-6 hours. Anticipate the need for dialysis if K > 7 or rising rapidly, PO4 > 10, or the uric acid > Hepatorenal syndrome is renal failure associated with liver failure (cirrhosis and ascites) when no other cause of renal disease is identified. Common precipitants are GI bleeding, dehydration (diuresis, paracentesis), and nephrotoxic drugs. Intense renal vasoconstriction is present and the renal diagnostic indices are identical to those of prerenal azotemia. Specific management issues include cautious fluid resuscitation and avoidance of precipitants. Liver transplantation is curative with a brisk urine flow often occurring in the OR. Acute Renal Failure 5