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Author: Admin | 2025-04-28
Out a pelvic mass causing bilateral ureteral obstruction should be reserved for those with obvious hydronephrosis on POCUS but little or no post-void residualA common pitfall is to attribute AKI to obstructive nephrolithiasis; unless the patient has a solitary kidney, nephrolithiasis rarely causes AKI; look for other causes of AKI insteadPrerenal AKIPrerenal AKI, caused by decreased renal perfusion, is the most common cause of all AKIs (90%) [7]. Prerenal causes occur in the setting of recent volume losses, such as hemorrhage, gastrointestinal or urinary fluid losses, sepsis, and recent postoperative courses during which the patient was hypotensive.Common causes of pre-renal AKI include:Volume depletion (renal losses – ie. Diuretics, and extra-renal losses – GI losses, third spacing, hemorrhage)Shock of any etiologyCardiorenal syndromeAdditional pre-renal causes of AKI to consider include:Hepatorenal syndromeAbdominal compartment syndromeHypertensive emergencyThrombotic thrombocytopenic purpura & hemolytic uremic syndromeFluid of choice in AKIOur experts recommend Ringers Lactate (RL) as the fluid of choice as it has relatively neutral effect on acid-base status and may reduce the risk of further AKI compared to Normal Saline. Consider 1L bolus up front followed by 150mL/hr and aim for a urine output of ≥50mL/hr (≥200mL/hr in rhabdomyolysis).Bicarb should be considered in patients with uremic acidosis based on the BICAR-ICU trial but probably best reserved for the ICU.Intrinsic renal AKIIntrinsic renal AKI is caused by direct injury to the kidney parenchyma. Intrarenal causes of AKI are usually considered only after pre-renal and post-renal causes have been ruled out. The “can’t miss” diagnosis for emergency physicians in a patient with AKI is nephritic syndrome. Thus it is important to get a urine dip to look for protein and blood in all patients with AKI.Nephritic syndrome presents as: acutely elevated Cr with hypertension, hematuria, proteinuria and no obvious pre-renal or post-renal cause.Other important causes of renal AKI to consider in the ED include:Nephrotoxic medications (ACEi, NSAIDs, Gentamicin etc.)Acute Tubular Necrosis (ATN) (rhabdomyolysis, hemolysis, tumor lysis syndrome)Renal thrombosisOther lab test to differentiate pre-renal vs. renal AKI:Other than ordering a urine dip to assess for intrinsic renal cause of AKI, there little role for measuring BUN in the ED. BUN:Cr ratio is not reliable at distinguishing pre-renal from renal causes [2]. Similarly, there is a limited role for urine electrolytes in the ED except in suspected of hepatorenal syndrome.Pearl: Nephritic syndrome presents with acutely elevated Cr, hypertension, hematuria, proteinuria and no obvious pre-renal or post-renal cause.Post-renal AKIPost-renal AKI is caused urologic obstruction to urine flow. It’s important to measure a post-void residual in all patients with an AKI. The most common causes are BPH and urethral catheter obstruction.Imaging to rule out an obstructive cause should not be performed in every patient with AKI NYD. Imaging should be considered in patients with obvious bilateral hydronephrosis on POCUS but little or no post void residual. These patients warrant further imaging as they might have a rare post-renal bilateral ureteric obstruction cause of AKI such as obstructive metastatic cancer, lymphoma or a kidney stone with a solitary kidney.Pitfall: A common pitfall is to
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