Flashcards in AKI Deck (10):
Rapid (days to weeks) impairment in kidney function= retention of products in blood that are normally secreted eg nitrogenous.
ECF volume, acid-base and electrolyte metabolism dysregulation.
Raised serum creatinine (1.5x or more from baseline in 7 days) and urea. Low urine output (under 0.5ml/kg/h for 6 hrs).
Commonly ischaemia, sepsis, nephrotoxins, prostatic disease.
-Pre renal (60%) GFR reduction- renal hypoperfusion eg hypotension, stenosis, CHF, anaphylaxis, valve disease, tampnade, cirrhosis, sepsis. ACEi and NSAIDs.
No cell damage so tries to restore BV by aldosterone and ADH. Responds to fluid resus.
-Intrinsic renal- acute tubular necrosis(ATN). Glomerular damage autoimmune acute glomerulonephritis, drugs (AB, NSAID, PPI), infection. Interstitial damage eg drugs, lymphoma, infection pyelonephritis, tumour lysis syndrome following chemo. Vascular eg vasculitis, HTN, thrombus or emboli, large vessel occlusion. Acute tubule interstitial nephritis.
-Post renal (10%)- UT obstruction so back pressure eg prostate, fibrosis, stones, tumour, extrinsic compression, blood clot, TB stricture, AAA, ureter ligation.
To cause AKI stones must be in all kidneys, neck of bladder or urethra.
RFs- age, CKI, HF, PVD, DM, drugs and chemo, sepsis, poor fluid intake or increased loss, history of urinary symptoms.
-Top 4 causes most common to least common STOP-
Sepsis as low BP, pre renal.
Toxins eg furosemide.
Obstruction usually prostate or retention, post renal.
Altered fluid intake and loss
Systemic features eg rash, joint pain, fever.
Productive cough and haemoptysis.
GU and GI symptoms.
Obstruction- Anuria, loin or suporapubic pain, previous renal stones or prostate problems.
Palpable bladder or kidneys, pelvic mass, DRE
Abdo or pelvic masses.
Positive dip or culture.
volume depleted-cool peripheries, tachyc, hypotension, low JVP, reduced skin turgor.
Volume overload- gallop, raised JVP, pulmonary oedema, peripheral oedema.
Sepsis- pyrexia, vasodilation, bounding pulse, rapid capillary refill, hypotension.
Stop nephrotoxic drugs eg NSAIDs, ACEi.
Monitor obs, UE, fluid balance.
Treat fluid balance eg electrolytes, diuretics, vasodilators as appropriate.
Treat underlying cause eg fluids, AB, catheter, stent, tumour tx.
Dialysis if refractory fluid overload (pulmonary oedema), persistent hyperK, metabolic acidosis, uraemia symptoms (pericarditis, LOC, intractable N+V), encephalopathy, pericarditis, OD.
Full bloods including VBG for pH. Especially look for hyperK, hypoNa, hypoCa, hyperP. Casts in glomerulonephritis.
Urine dip- blood+ protein (present in glomerulonephritis, not pre renal or ATN), leucocytes. Urine culture if indicated.
US renal tract
Maybe renal biopsy
Acute tubular necrosis
Damaged cells cant reabsorb salt and water OR expell excess water.
Causes- Ischaemia, nephrotixins (Mb, urate, bilirubin, drugs, endotoxin, XR contrast, sepsis. Often 2 or more.
Aggressive fluid resus risks fluid overload.
Lot AKI due to ATN potentially reversible if caught in time.
Monitor at risk
Detect early and ID cause
-RFs- age, CKD, HD, liver disease, DM, CA, neuro impairment, previous AKI, dehydration, loss volume, sepsis, critical illness, burns, trauma, cardiac surgery, nephrotoxins, radio iodinated contrast.
Usually recover 2-3 weeks if no superimposed insults.
Quite high mortality.
Can progress to CKI.