AKI Flashcards
Define AKI
A sudden decline in renal function (GFR) significant enough to produce uraemia, and also often oliguria – a urine output of <400ml/day.
It normally occurs over hours/days or week
- often reversible. Diagnosis is usually based on serum urea and/or creatinine levels.
Severe Acute Kidney Injury is defined as a creatinine level of >500umol/L
Appropriate investigations of AKI and what should results be?
Urine dipstick
Urine microscopy – look particularly for the presence of red cell casts and red cells.
Blood tests – U+E’s (particularly Cr and K+, FBC, free haemoglobin and myoglobin.
Kidney function is monitored through urine output analysis and creatinine clearance monitoring – creatinine clearance monitoring is the ideal, i.e. it is a more precise indication of GFR than serum urea monitoring alone!
Check if the patient is on any nephrotoxic drugs.
What are the defining criteria of AKI?
- Increase in serum urea > 26 μmol/L within 48 hrs
- Increase in serum creatinine to > 1.5 times baseline within preceding 7 days
- Urine volume < 0.5 ml/kg/hr for 6 hours
Broadly speaking what how can the causes of AKI be classified?
Pre-renal
Renal
Post-renal
Aetiology of AKI
• Usually occurs in context of catastrophic illness
o Hypotension, sepsis, orthopaedic surgery
o Common in critical illness
o 45% are ATN
o 21% are pre-renal
• 48% are hospital acquired
Describe what causes a pre-renal AKI
Inadequate perfusion of kidneys
- Hypovolaemia due to diuretics (renal loss), NSAIDS, ACEi, diarrhoea, DKA, vomiting (dehydration - extrarenal loss)
- Systemic vasodilation due to sepsis
- Decreased CO due to HF/MI
- Intrarenal vasoconstriction (cardiorenal syndrome)
Describe what causes a renal AKI
Intrinsic kidney damage
eg. acute tubular necrosis, glomerulonephritis, small vessel vasculitis/thrombosed renal artery
Describe what causes a post-renal AKI
Obstruction of urine flow
Most commonly stones, clots, blocked catheters, malignancies (bladder, prostate etc), fibrosis
Which type of AKI is most common in hospital?
Pre-renal
RF for AKI
- Advanced age*
- Underlying renal disease* eg CKD
- Malignant hypertension
- DM*
- Sodium retaining states
- Radiocontrast
- Nephrotoxin* exposure: NSAIDs, chemotherapy, aminoglycosides
- Trauma, haemorrhage
- Sepsis*
- Surgery
- Cardiac arrest
- Fluid loss
Epidemiology of AKI
Greater incidence in ICU (20-50%) – mainly caused by sepsis
Presenting symptoms of AKI
• Symptoms of uraemia o Nausea, vomiting, anorexia, confusion • Features of underlying disease o Pre-renal Hypovolaemia: thirst, dizziness, vomiting, confusion o Intrinsic Glomerular: nephritic syndrome (haematuria, proteinuria, hypertension) Tubular: hypovolaemia o Post-renal Flank pain, haematuria Urgency, frequency and hesitancy • Oliguria/anuria - decreased urine output • Complications o Salt and water retention Orthopnoea Pulmonary oedema
Presenting symptoms of acute interstitial nephritis
Oliguria + triad (of drug side effect): rash, fever, eosinophilia +/- painful joints
Signs of AKI
Asterixis
Signs of pre-renal AKI
AF
Hypotension + tachycardia, dry mucous membranes
CCF -> JVP, ascites
Signs of intrinsic AKI
Butterfly rash (SLE?)
Nephrotic syndrome -> pulmonary + peripheral oedema, raised JVP
Vascular obstruction -> petechiae/purpura/bruising + pallor + tiredness
Signs of post-renal AKI
Costovertebral angle tenderness
Prostatic hypertrophy
Bladder enlargement
What investigations would you do for AKI
Urinalysis Bloods Renal US AXR CXR ECG Venous blood gas
What might you find in urinalysis indicative of AKI
o RBCS, WBCs, cellular casts, proteinuria, bacteria, nitrites, leucocyte esterase, glucose, urine osmolality
What might you find in bloods indicative of AKI
In a metabolic profile: Acutely elevated serum creatinine Hyperkalaemia Metabolic acidosis o Serum urea:creatinine ratio >20:1 = pre-renal
FBC
Anaemia, thrombocytopenia -> intrinsic AKI
Infection -> pre-renal + intrinsic AKI
Blood film - could look for schistocytes = small vessel disease = intrinsic AKI
Serology
Auto-antibodies – Anti-GBM, ANA (SLE), anti-streptolysin-O
Immunoglobulins - IgA
Protein electrophoresis (multiple myeloma)
What might you see on renal US?
o Dilated renal calyces (hydronephrosis) – post renal
What might you see on AXR
renal stones
What might you see on CXR
Pulmonary oedema
Cardiomegaly
What might you see on ECG
Severe hyperkalaemia
Peaked T waves
Widened QRS
Increased PR interval
What might you see on venous blood gas
metabolic acidosis
Management of pre-renal AKI
o Volume expansion +/- blood transfusion
o Vasopressor
o Treat infection
Management of renal AKI
o Treat underlying condition
o Stop nephrotoxic agents
o Treat infection
Management of post-renal AKI
o Bladder catheterisation
o Relief of obstruction above bladder neck
What things should you monitor in all AKI patients?
Creatinine K+ Na+ Phos Ca glucose
What do you give to a patient who’s volume overloaded
Loop diuretic
What do you give to a patient who is hyperkalaemic and why?
Calcium gluconate - reduces ventricular fibrillation
Insulin and glucose - insulin drives K+ into cells via the sodium potassium ATP pump
Salbutamol nebuliser
In what cases would you use renal replacement therapy?
- Hyperphosphataemia - asymptomatic
- Uraemia -> affects all systems -> buzzword = pericarditis, pruritis, skin colour changes, peripheral weakness (loads of others, refer to 1st page)
- Volume overload -> HTN, pulmonary oedema, peripheral oedema
- Hyperkalaemia -> muscle weakness, tingling/numbness, n&v, chest pain, palpitations, arrhythmias
- Metabolic acidosis -> tachypnoea
- CKD
- ESRD (end stage renal failure)
Prognosis of AKI
• Recovery depends on cause, severity and duration
o Increased mortality
• 6% of ICU patients need RRT
• Irreversible in >5%
