Acute Kidney Injury Flashcards
1
Q
What is it?
A
significant deterioration in renal function over hrs or days, clinically manifesting as an abrupt and sustained rise in serum urea and creatinine
2
Q
What are the causes
A
- Pre-renal: hypovolaemia, sepsis, CCF, cirrhosis, renal artery stenosis, NSAIDs, ACEi
- Intrinsic: ATN due to ischaemia or nephrotoxins, aminoglycosides, amphotericin B, tetracyclines, contrast, uric acid crystals, haemoglobinuria (rhabdomyolysis) or myeloma, vasculitis, malignant HTN, cholesterol, HUS, TTP, GN, interstitial nephritis
- Post-renal: obstruction
3
Q
When should chronic renal failure be suspected over AKI?
A
Hx of comorbidity (DM, HTN)
Long duration of sx
Prev abnormal bloods
Small kidney (<9cm) on US w increased ethogenicity
4
Q
what would make u suspect that the cause of AKI is obstruction?
A
- single functioning kidney
- Hx of renal stones, BPH or prev. surgery
- palpable bladder
- complete anuria
- renal US showing dilatation of pelvis + calyces
5
Q
what tests would u do in suspected AKI
A
- Bloods - U+E, FBC, LFT, clotting, CPR/ESR, creatinine, ABG, cultures, hepatitis serology
- Serum Igs, complement levels, autoabs
- Urine - dipstick, microscopy, MC + S, chemistry
- CXR - pulm oedema,
- ECG - signs of hyperkalaemia
- Renal US
6
Q
What is the immediate management of AKI?
A
- identify and correct pre-renal and post renal factors
- Urgent US scan, check for palpable bladder
- find and rx exacerbating factors e.g. sepsis
- stop nephrotoxic drugs
7
Q
What are the possible problems u would look out for in AKI and what signs would point to them?
A
- Vasculitis - epistaxis, haematuria, rash, raised ESR/CRP, autoabs
- Low intravascular volume - reduced turgor and UO, invisible JVP
- Fluid overload - gallop rhythm, raised JVP + BP, lung creps, peripheral oedema
8
Q
What are the potential complications of AKI? how would.u treat them?
A
- hypercalcaemia - IV calcium gluconate 10% 10ml, IV insulin + glucose, salbutamol 5mg nebs, calcium resonium, haemodialysis if anuric
- bleeding (impaired haemostats due to raised urea, made worse by precipitating cause) - give PPIs or H2 antagonists, if active bleeding: FFP + platelets
- Pulmonary oedema - sit up, high flow O2, IV morphine, (+IV metoclopramide), furosemide, CPAP, venesection (if in extremis)