Síguenos en Twitter     Síguenos en Facebook     Síguenos en YouTube     Siguenos en Linkedin     Correo Salutsantjoan     Gmail     Dropbox     Instagram     Google Drive     StumbleUpon     StumbleUpon     StumbleUpon     StumbleUpon     StumbleUpon     StumbleUpon     StumbleUpon


My photo
FACP. Colegio de médicos de Tarragona Nº 4305520 / fgcapriles@gmail.com




Wednesday, May 13, 2015

Insuficiencia renal aguda


emDocs - May 13, 2015 - Authors: Subhanir Sunil Chitnis and Karma Warren
Editor: Alex Koyfman and Manpreet Singh
Acute kidney injury (AKI) is a sudden, potentially reversible, kidney dysfunction with partial or complete loss of glomerular filtration resulting in electrolyte and fluid abnormalities as well as retention of nitrogenous waste products [1]. In contrast, Chronic Kidney Disease (CKD) describes loss of kidney function for at least three months [2]. While a decrease in Glomerular Filtration Rate (GFR) is used to categorize CKD, an increase in serum creatinine or decrease in urine output is used to characterize AKI. The most recent definition of AKI is provided by the Kidney Disease: Improving Global Outcomes (KDIGO) group which reconciled the 2004 RIFLE criteria and the follow-up AKIN update. [2,3]
Accordingly, acute kidney injury is defined by any of the following:
  • Increase in serum creatinine by ≥0.3 mg/dL within 48 hours; or
  • Increase in serum creatinine by ≥1.5 times baseline within seven days; or
  • Urine volume <0.5 mL/kg/h for six hours
ED Management
Patients meeting the KDIGO definition for AKI typically require admission to the hospital (if etiology is identified/addressed and close follow-up established then reliable patients can be discharged – shared decision-making). Since there are various causes of AKI, simultaneous attempts should be made to treat the direct and indirect causes of AKI. As such, for all pre-renal causes of AKI, IV fluid resuscitation should not be delayed. Similarly, patients with rhabdomyolysis should receive aggressive fluid resuscitation to avoid new or worsening AKI. Likewise, relieving obstruction in post-renal AKI should be done without delay. Patient’s may require suprapubic catheterization if urethral catheterization fails. For more proximal obstruction,nephrostomy tube may be required until the obstruction is relieved. Patients with prolonged obstruction can havepostobstructive diuresis and should be admitted if they have persistent diuresis of about 250 mL/hr or more for two hours.Eliminate any nephrotoxic substances, including any medications and treatments that can worsen AKI. Patients with fluid overload may demonstrate hypoxia and require positive pressure ventilation. Consider dialysis for severe acidosis, electrolyte abnormalities, ingestion of toxins like ASA, methanol, lithium and ethylene glycol, volume overload and uremia with pericarditis, encephalopathy, or BUN > 100."