Acute kidney injury
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This document discusses acute kidney injury (AKI), also known as acute renal failure. It defines AKI as an abrupt loss of kidney function occurring within 7 days, characterized by an increase in serum creatinine and potentially leading to complications affecting other organ systems. The document outlines causes, risk factors, stages, diagnosis, and management of AKI, including identifying and treating the underlying cause, avoiding nephrotoxic substances, optimizing renal hemodynamics, treating complications, and considering renal replacement therapy such as hemodialysis if needed.
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Acute kidney injury
- 1. Acute kidney injury Yousaf khan Lecturer Renal dialysis IPMS- KMU
- 2. Acute kidney injury Acute renal failure (ARF) Abrupt loss of Kidney function that develops within 7 days. Increase in serum creatinine AKI may lead to a number of complications, metabolic acidosis high potassium levels Uremia changes in body fluid balance Effects on other organ systems including death People who have experienced AKI may have an increased risk of chronic kidney disease in the future.
- 3. Diagnostic Approach Time of onset – prior serum creatinine Careful review of history and physical exam ◦ Comorbidities ◦ Medications ◦ Current illness (vomiting, diarrhea, blood loss, etc) ◦ BP, volume status, skin lesions, flank/abdominal signs
- 4. Signs and symptoms Accumulation of urea and other nitrogen- containing substances in the bloodstream lead to Fatigue loss of appetite Headache Nausea Vomiting Marked increases in the potassium level can lead to irregularities in the heartbeat, which can be severe and life-threatening Fluid balance is frequently affected, though blood pressure can be high, low or normal
- 5. Stages of acute injury
- 6. Consistent Risk Factors Age Hypovolemia Hypotension Sepsis CKD Hepatic dysfunction Cardiac dysfunction DM Exposure to nephrotoxins
- 7. Differential Diagnosis of AKI Pre-renal Renal Post-renal
- 8. Prerenal Decrease effective blood flow to the kidney low blood volume low blood pressure heart failure liver cirrhosis renal artery stenosis renal vein thrombosis Renal ischaemia can result in depression of GFR inadequate cardiac output
- 9. Intrinsic Glomerular ◦ Rapidly progressive GN, post-strep GN, Interstitial nephritis ◦ Infection-related, inlammation, drug-induced, infiltrative (lymphoma, leukemia, sarcoidosis) Tubular Lesions ◦ Post-ishemia, nephrotoxic (drugs, contrast, anesthetics, heavy metals), pigment nephropathy, light chain, hypercalcemia
- 10. Postrenal Bladder flow obstruction ◦ Urethral, bladder neck (BPH), neurogenic bladder Ureteral obstruction (bilateral or single kidney) ◦ Stones, clots, tumours, papillary necrosis, retroperitoneal fibrosis, surgical ligation
- 11. Urine Output and AKI Anuric ◦ < 100 cc / 24 hrs Oliguric ◦ < 300 cc / 24 hrs Non-olguric ◦ Normal urine output, but inadequate clearance ◦ GFR 2 ml/min will produce ~3L of urine/day if there is no tubular reabsorption
- 12. Diagnosis Clinical history Urea and creatinine Urine sediment analysis renal ultrasound renal biopsy Indications for renal biopsy in the setting of AKI include Unexplained AKI, in a patient with two non- obstructed normal sized kidneys AKI in the presence of the nephritic syndrome Systemic disease associated with AKI Renal transplant dysfunction
- 13. Principles of AKI Management Identify AKI Avoid further nephrotoxic injury Optimize renal hemodynamics Treat complications ◦ Fluid balance, electrolytes, uremia Nutritional support Renal Support (RRT) Monitoring after AKI
- 14. Treatment Identification and treatment of the underlying cause. (1) to prevent cardiovascular collapse and death (2) to call for specialist advice. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.
- 15. Specific therapies In prerenal AKI without fluid overload administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid. Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion. Intrinsic AKI require specific therapies. If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.
- 16. Renal replacement therapy Renal replacement therapy such as with Hemodialysis Peritoneal dialysis CRRT
- 17. Thank you