Acute Kidney Injury Flashcards
1
Q
COMMS: Normal kidney function
A
Normal kidney function
- Filter waste products in blood and carry to urine to be passed out
- Help control BP - control amount of water passing in and out of blood and control hormones that alter BP
- Produce hormone - erythropoetin - that controls production of red blood cells from bone marrow
- Regulate levels of fluid in body
- Regulate levels of salt and other chemicals
2
Q
COMMS: AKI
A
- Sudden injury to kidney
- Can no longer perform normal functions
- Fluid salts and chemicals in blood can rise or fall as no longer regulated
- This imbalance can affect other organs
3
Q
RISK FACTORS: AKI
A
- Age >75 yrs
- Chronic kidney disease
- Cardiac failure
- Peripheral vascular disease
- Chornic liver disease
- Diabetes
- Sepsis
- Poor fluid intake
- Hx urinary symptoms
- Drugs
- NSAIDs
- ACEi/AR2B
- Aminoglycosides - GENTAMICIN
- Diuretics
4
Q
AETIOLOGY: AKI
A
Pre-renal (ischaemia of kidney as poor blood flow)
- Hypotension
- Renal artery stenosis (+/- ACEi)
Intrinsic Renal
- Tubular - Acute tubular necrosis (often due to nephrotoxins/contrast)
- Glomerular - SLE, HSP, drugs, infections
- Interstitial - lymphoma, infection, tumour lysis syndrome
- Vascular - vasculitis, malignant HTN, thrombus, HUS/TTP
Post-Renal (urinary tract obstruction)
- Stones/clots
- Malignancy
5
Q
What pathology happens when kidneys stop working?
A
- Oliguria (reduced urine output) = <0.5ml/kg/hr
- Fluid overload
- Rise in serum molecules which kidney normally excretes
- CREATININE = high
- POTASSIUM = high
- UREA = high
6
Q
CLINICAL FEATURES: AKI
A
- Asymptomatic (initially)
- Urine ouput = Low
- Pulmonary and peripheral oedema
- Arrhythmias (2nd to K+/acid-base changes)
- Uraemia features
- Fatigue
- Weakness
- Itching
- Loss of appetite
- CNS disturbances
7
Q
INITIAL ASSESSMENT: AKI
A
- Circulation (ABCDE)
- Volume status - BP, JVP, skin turgor, Cap refill, urine output (catheter)
- K+ check on venous bood and ECG (hyperkalaemia)
- Hx
- Co-morbidity check: renal disease, recent fluid intake/loss, new drugs
- Examination:
- Palpable bladder, palpabale kidneys (polycystic disease), abdo masses, renal bruits
- Urine dip
- Infection = leucocytes + nitrates
- Glomerular disease = blood + protein
- Urine microscopy
- Casts, crystals, cells
- Infection culture
8
Q
INVESTIGATIONS: AKI
A
Bloods
- Serum creatinine = > 26 micromol/litre w/i 48 hours
- Serum creatinine = > 50% from baseline in last 7 days
- Urine output = <0.5ml/kg/hour for >6h
- Imaging*
- Renal US if obstruction suspected
9
Q
MANAGEMENT: AKI
A
Supportive
- Careful fluid balance
- Stop any exacerbating drugs
- Treat hyperkalaemia promptly
- Specialist referral if:
- Unknown cause
- Severe
- Urinary obstruction
- Renal replacement therapy (haemodialysis) if severe
10
Q
Which drugs are usually stopped in AKI?
A
- NSAIDs
- Aminoglycosides e.g. gentamicin
- ACEi
- AR2Bs
- Diuretics
11
Q
What are the main indications for dialysis in AKI?
A
- Severe pulmonary oedema
- Persistent hyperkalaemia
- Severe metabolic acidosis
- Uraemic complications (e.g. encephalopathy/pericarditis)
- Drug overdose (BLAST)
- Barbiturates
- Lithium
- Alcohol
- Salicylates
- Theophylline