Acute Kidney Injury Flashcards
Define Acute Kidney Injury
- Clinical syndrome
- Decline in renal excretory function over hours/days (<3/12)
- Resulting in failure to maintain homeostasis of:
- Fluid
- Electrolyte
- Acid-base
What is the KDIGO criteria for AKI Stage I?
Any of:
- Serum creatinine 1.5-1.9x baseline
- Serum creatinine increase of ≥0.3 mg/dl within 48h
- Urine output <0.5 ml/kg/hr for 6-12h
What is the KDIGO criteria for AKI Stage II?
Either:
- Serum creatinine 2.0-2.9x baseline
- Urine output <0.5 ml/kg/h for ≥12h
What is the KDIGO criteria for Stage 3 AKI?
Any of:
- Serum creatinine 3x of baseline
- Serum creatinine increase of ≥4.0 mg/dl
- Initiation of renal replacement therapy
- Urine output <0.3 ml/kg/hr for ≥24h
- Anuria ≥12h
Classify the aetiology of acute kidney injury
- Pre-renal (commonest)
- Intrinsic renal: includes pre- or post-renal causes damaging renal cells
- Post-renal
List five causes of pre-renal AKI
- Hypovolaemia:
- Dehydration
- Haemorrhage
- DaV; third space losses; renal losses
- Burns
- Reduced CO: cardiac failure; liver failure; sepsis
- Renal artery stenosis
- NSAIDs; Coxibs; ACEi; loop diuretics
Explain how NSAIDs and Coxibs cause AKI
- Both inhibit COX enzymes needed for prostaglandin (PG) synthesis
- PG is a vasodilator which can act on the afferent arteriole
- Inhibition causes afferent vasoconstriction and renal hypoperfusion
List five causes of intrinsic renal AKI
- Tubular:
- Acute tubular necrosis (80-90%)
- Acute interstitial nephritis (rare): 4-7d after starting abx
- Rhabdomyolysis: CK >10,000
- Multiple myeloma
- Nephrotoxins: abx; contrast; chemotherapy
- Sepsis
- Glomerular: glomerulonephritis; SLE; haemolytic-uraemic syndrome
- Vasculitis; renal artery stenosis; thrombosis; dissection
Explain the pathophysiology of acute tubular necrosis
Almost any cause of pre-renal AKI if prolonged to the point at which renal autoregulation fails, will lead to ischaemic ATN
- Sustained hypoperfusion of renal tubules ➔ tubular cell death
- Nephrotoxins causing direct injury and tubular cell death
What is haemolytic uraemic syndrome?
Commonest cause of AKI in children
Toxins associated with E. coli O157:H7
Triad of:
- Microangiopathic haemolytic anaemia: Coomb’s -ve
- Thrombocytopenia
- AKI
Supportive treatment
List four causes of post-renal AKI
- Ureteric: bilateral renal stones, retroperitoneal fibrosis, GU tumours
- Bladder: acute urinary retention, blocked catheter
- Urethral: prostate enlargement, renal stones
Give five risk factors for AKI
- Aged 65+
- Hx of AKI
- CKD Stage 3+ (eGFR <60)
- Symptoms or Hx of urological obstruction
- Chronic conditions: heart failure; liver disease; diabetes
- Neurological or cognitive impairment
- Sepsis
- Oliguria
- Nephrotoxic drugs or contrast agents within 1/52
- Immunocompromised; cancer therapy; toxins
Provide three complications of AKI
- Hyperkalaemia
- Hyponatraemia
- Hypermagnesaemia; hyperphosphataemia
- Hypocalcaemia
- Metabolic acidosis
- Volume overload: peripheral and pulmonary oedema
- Uraemia
- CKD and ESRD
Name three clinical features of suspected AKI
- NaV; diarrhoea; evidence of dehydration
- Reduced urine output; changes in urine colour
- Confusion; fatigue; drowsiness
List three signs seen in AKI
- HTN
- Dehydration: prolonged CRT; tachycardia; postural hypotension
- Sepsis: eg. fever; respiratory signs; indwelling urinary catheter
- Urinary retention: enlarged bladder or prostate
- Fluid overload: raised JVP, peripheral and pulmonary oedema
How can the risk of AKI be reduced?
- Early identification
- Avoid pre- and peri-operative hypovolaemia
- Continuous monitoring of fluid status during IV fluids
- Avoid nephrotoxins where possible: NSAIDs, aminoglycosides, contrast
- NaCl 0.9% for 12h pre- and post-contrast
- Prompt treatment of suspected sepsis
Request three investigations for suspected AKI
- U+Es
- Urinalysis
- USS KUB
- FBC; LFTs; bone profile; CRP; glucose
- Clotting screen
- Blood cultures
- ECG
- CXR
- Medication review
Outline the management of AKI
AKI Care Bundle
- Monitor: 4hrly EWS; hourly urine output; fluid balance; daily weight
- Routine U+Es; bone profile; VBG
- Identify and treat reversible causes
- Optimise fluid balance using IVI; consider catheterisation
- Medication review
- Referral for RRT and nephrology where appropriate
What are the indications for renal replacement therapy for AKI?
- Hyperkalaemia unresponsive to medical treatment
- Fluid overload unresponsive to medical treatment
- Persistent or worsening metabolic acidosis
- Uraemic symptoms: Intractable vomiting; confusion; twitching
- Evidence of pericardial effusion
Outline the emergency treatment of hyperkalaemia
10ml of 10% calcium gluconate IV: cardioprotective IV insulin actrapid + dextrose Dialysis if persistent hyperkalaemia
What ECG changes are seen with hyperkalaemia?
Tall tented T waves Small/absent p waves Increased PR interval Widened QRS Sine wave pattern Asystole
List three clinical features of uraemia
- Anorexia; intractable NaV
- Uraemic polyneuropathy; restless legs
- Pruritus
- Pericarditis
- Encephalopathy
- Intellectual clouding; drowsiness
- Seizures
- Coma
- Haemorrhage: abnormal platelet adhesion
- ‘Uraemic frost’: acummulation in skin
Define contrast nephropathy
- 25% increase in creatinine
- Within 2 days of IV administration of contrast media
How is contrast nephropathy best prevented?
IV 0.9% sodium chloride for 12h pre- and post-op
What follow-up monitoring should be done after an episode of AKI?
Monitor for development or progression of CKD for at least 2-3 years after AKI
