Acute Kidney Injury

• 1.Hailemariam Bekele Hayelom Michael Acute Kidney Injury

2. Objectives Define Acute Kidney Injury (AKI) Understand pathophysiologic mechanisms in AKI Review the diagnostic approach to AKI Identify the syndromes of AKI Identify strategies to prevent AKI Review the roles of supportive care and renal replacement therapy and pearls in the therapy and management of AKI 3. Out line Introduction Anatomy of kidney Epidemiology Diagnosis clinical features investigation Management Complications 4. Introduction: Acute Kidney Injury Acute kidney injury (AKI) has now replaced the term acute renal failure A universal definition and staging system has been proposed to allow earlier detection and management of AKI 5. Definition: acute kidney injury is a syndrome characterized by: Sudden decline in GFR (hours to days ) Retention of nitrogenous wastes Disturbance in extracellular fluid volume and Disturbance in electrolyte and acid base homeostasis 6. The loss of kidney function is most easily detected by measurement of the serum creatinine Serum creatinine is used to estimate the glomerular filtration rate (GFR). Serum creatinine does not accurately reflect the GFR Recognizing the need for a uniform definition for ARF, the ADQI group proposed a consensus graded definition, called the RIFLE criteria 7. RIFLE Criteria The RIFLE criteria consists of three graded levels of injury (Risk, Injury, and Failure) Based upon either the magnitude of elevation in serum creatinine or urine output, Two outcome measures (Loss and End-stage renal disease The RIFLE strata are as follows 8. RIFLE Strata The 2nd International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group 9. Azotemia: an abnormal increase in concentration of urea and other nitrogenous substances in the blood plasma Uremia: the complex of symptoms due to severe persisting renal failure that can be relieved by improving clearance Oliguria: UOP 1% indicates ATN 45. Fractional excretion of Na+: is ratio of urine-to- plasma Na ratio to urine-to-plasma creatinine expressed as a percentage [ (UNa/PNa)/(Ucr/Pcr )X 100]. Value below 1% suggest prerenal failure , and values above 1% suggest ATN Serum K+ and other electrolytes 46. 3. Radiography/imaging Ultrasonography: helps to see the presence of two kidneys, for evaluating kidney size and shape, and for detecting hydronephrosis or hydroureter. It also helps to see renal calculi, and renal vein thrombosis. Retrograde pyelography: is done when obstructive uropathy is suspected 47. Complications of AKI Intravascular overload: may be recognized by weight gain , hypertension ,elevated central venous pressure ( raise JVP) , Pulmonary edema Electrolyte disturbance Hyperkalemia: (serum K+ >5.5 mEq/L): decreased renal excretion combined with tissue necrosis or hemolysis. Hyponatremia : ( serum Na+ concentration < 135 mEq/L ): excessive water intake in the face of excretory failure 48. Hyperphosphatemia : ( serum Phosphate concentration of > 5.5 mg /dl ) failure of excretion or tissue necrosis Hypocalcemia : ( serum Ca++ < 8.5 mg/dl ) results from decreased Active Vit-D , hyperposhphatemia , or hypoalbuminemia Hypercalcemia: (serum Ca++ > 10.5 mg /dl) may occur during the recovery phase following rhabdomyolysis induced acute renal failure. 49. Metabolic acidosis :( arterial blood PH < 7.35 ) is associated with sepsis or severe heart failure Hyperuricemia: due to decreased uric acid excretion Bleeding tendency : may occur due to platelet dysfunction and coagulopathy associated with sepsis Seizure: may occur related to uremia 50. Management of AKI 1. Prevention: Because there are no specific therapies for ischemic or nephrotoxic AKI, Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients, such as the elderly and those with preexisting renal insufficiency. 51. Indeed, aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma, burns, or cholera prevention is of paramount importance. 52. The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR; for example, reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment 53. Preliminary measures Exclusion of reversible causes: Obstruction should be relived , infection should be treated Correction of prerenal factors: intravascular volume and cardiac performance should be optimized 54. Maintenance of urine output: Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form. High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses 55. Specific Therapies: To date, there are no specific therapies for established intrinsic renal ARF due to ischemia or nephrotoxicity. Management of these disorders should focus on elimination of the causative hemodynamic abnormality or toxin, avoidance of additional insults, and prevention and treatment of complications. Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology. 56. Prerenal ARF: The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid. Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells, whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (e.g., burns, pancreatitis). 57. Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic. Hypotonic solutions (e.g., 0.45% saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses, although isotonic saline may be more appropriate in severe cases 58. Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids. Serum potassium and acid-base status should be monitored carefully. 59. Postrenal ARF: Management of postrenal ARF requires close collaboration between nephrologist, urologist, and radiologist. Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter, which provides temporary relief while the obstructing lesion, is identified and treated definitively. Similarly, ureteric obstruction may be treated initially by percutaneous catheterization of the dilated renal pelvis or ureter. 60. 4. Supportive Measures: (Conservative therapy ) Dietary management: Generally, sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcal/kg lean body weight. In some patients, severe catabolism occurs and protein supplementation to achieve 1.25 gm of protein /kg body weight is required to maintain nitrogen balance. Restricting dietary protein to approximately 0.6 g/kg per day of protein of high biologic value (i.e., rich in essential amino acids) may be recommended in sever azotemia. 61. Fluid and electrolyte management : Following correction of hypovolemia, total oral and intravenous fluid administration should be equal to daily sensible losses (via urine, stool, and NG tune o surgical drainage ) plus estimated insensible ( i.e. , respiratory and derma ) losses which usually equals 400 500 ml/day. Strict input output monitoring is important. 62. Hypervolemia: can usually be managed by restriction of salt and water intake and diuretics. Metabolic acidosis: is not treated unless serum bicarbonate concentration falls below 15 mmol/L or arterial pH falls below 7.2. More severe acidosis is corrected by oral or intravenous sodium bicarbonate. 63. Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levels. Patients are monitored for complications of bicarbonate administration such as hypervolemia, metabolic alkalosis, hypocalcemia, and hypokalemia. From a practical point of view, most patients requiring sodium bicarbonate need emergency dialysis within days. 64. Hyperkalemia: cardiac and neurologic complications may occur if serum K+ level is > 6.5 mEq/L o Restrict dietary K+ intake o Give calcium gluconate 10 ml of 10% solution over 5 minutes o Glucose solution 50 ml of 50 % glucose plus Insulin 10 units IV o Give potassium binding ion exchange resin o Dialysis: it medial therapy fails or the patient is very toxic 65. Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate, which reduce gastrointestinal absorption of phosphate. Hypocalcemia does not usually require treatment. 66. Anemia: may necessitate blood transfusion if severe or if recovery is delayed. GI bleeding: Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard than H2 antagonists, or proton pump inhibitors. Meticulous care of intravenous cannulae, bladder catheters, and other invasive devices is mandatory to avoid infections 67. Dialysis Indications and Modalities of Dialysis: - Dialysis replaces renal function until regeneration and repair restore renal function. Hemodialysis and peritoneal dialysis appear equally effective for management of ARF. Absolute indications for dialysis include: Symptoms or signs of the uremic syndrome Refractory hypervolemia Sever hyperkalemia Metabolic acidosis. 68. Clinical course and prognosis Stages: acute renal failure due to ATN typically occurs in three stages: Azotemic , Diuretic , and recovery phases. The initial azotemic stage can be either oliguric or non oliguric type. Morbidity and mortality: are affected by the presence of oliguria o GI bleeding, septicemia, metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients. 69. The mortality rate for oliguric patients is 50 % where as that of nonoliguric patients is only 26 % 70. Prognosis: The mortality rate among patients with ARF approximates 50. It should be stressed, however, that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs. E.g. the mortality of ATN is 60 % when it results from surgery or trauma, 30 % when it occurs as a complication of medical illnesses, and 10-15 % when pregnancy is involved. 71. Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN. In agreement with this interpretation, mortality rates vary greatly depending on the cause of ARF: ~15% in obstetric patients, ~30% in toxin-related ARF, and ~60% following trauma or major surgery. 72. Oliguria (3 mg/dl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness. Mortality rates are higher in older debilitated patients and in those with multiple organ failure 73. Patients with no complicating factors who survive an episode of acute renal failure have a 90 % chance of complete recovery of kidney function.