Acute Kidney Injury (AKI) Flashcards

1
Q

Define Acute Kidney Injury (AKI)

A
  • Rapid decline in renal function
  • ↓ GFR
  • ↑ Creatinine
  • ↓ Urine output (<5ml/kg/hr)
  • Inability to maintain fluid, electrolyte and acid base balance
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2
Q

What are the 3 causes of AKIs?

A
  • Pre-renal: Impaired renal perfusion
  • Renal: Direct injury to renal parenchyma
  • Post-renal: Obstruction to urinary flow
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3
Q

What are the Pre-renal causes of AKI?

A
  • Hypovolaemia (e.g. dehydration (D&V), burns)
  • Haemorrhage
  • Sepsis
  • Third space losses
  • Heart failure/cardiogenic shock
  • Renal artery stenosis
  • Renal artery thrombosis
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4
Q

What are the Renal causes of AKI?

A
  • Acute tubular necrosis (45-70% of AKI)
    - Toxic: drugs, rhabdomyolysis, myeloma
    - Ischaemic
  • Acute interstitial nephritis
    - Drugs
    - Infection
  • Glomerulonephritis
  • Nephrotoxins
  • Vascular
    - Vasculitis
    - HUS/TPP
    - Thrombosis
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5
Q

What are the Post-renal causes of AKI?

A
  • Retroperitoneal fibrosis
  • Lymphoma
  • Tumour
  • Benign prostatic hyperplasia (BPH)
  • Strictures
    - Post-surgical
    - Post-infection
  • Urinary tract calculi
  • Pyelonephritis
  • Urinary retention
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6
Q

What are the Risk Factors for AKI?

A
  • Diabetes Mellitus
  • Age >75yrs
  • Peripheral Vascular Disease (PVD)
  • Hypertension
  • Heart Failure
  • Nephrotoxins e.g. radiocontrast, gentamicin, NSAIDs
  • Trauma
  • Surgery
  • Connective Tissue Disease e.g. SLE
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7
Q

What is the Epidemiology of AKI?

A

13-22% of hospitalised patients

Elderly

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8
Q

What are the Presenting Symptoms of AKI?

A
  • Nausea, Vomiting, Oliguria/Anuria, Confusion and other
  • Pre-renal: dizziniess, thirst
  • Renal: haematuria, fever, flank pain
  • Post-renal: haematuria, flank pain, urgency, frequency, hesitancy
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9
Q

What are the Signs of AKI on examination?

A
  • Hypertension
  • Distended bladder
  • Pre-renal: dehydration, postural hypotension
  • Fluid Overload e.g. in HF, cirrhosis, nephrotic syndrome
    - raised JVP
    - pulmonary/peripheral oedema
  • Pallow
  • Rash
  • Bruising (vascular disease)
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10
Q

What are the investigations on Bloods for AKI?

A

U&Es

  • Increased Urea
  • Increased Creatinine
  • Increased K+
  • Metabolic Acidosis
  • Creatine Kinase (rhabdomyolysis)

FBC

  • Anaemia (CKD, blood loss)
  • Increased WBC (infection)

Immunology

  • Serum immunoglobins and protein electrophoresis (multiple myeloma)
  • SLE = ANA, anti-dsDNA (high), complement (low)
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11
Q

What are the investigations of Urine for AKI?

A
  • Osmolality (high in pre-renal failure)
  • Output (low)
  • Urinalysis
    - RBCs, WBCs
    - Cellular casts
    - Proteinuria (e.g. Bence-Jones Proteins)
    - Bacteriuria (infection)
    - Nitrates
    - Myoglobin (rhabdomyolysis)
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12
Q

What are the Investigations for AKI?

A
  • Bloods
  • Urine
  • Renal Screen e.g. ANA (associated with SLE), ANCA, anti-GBM, HIV, Hepatitis serology, complement
  • Bladder Catheterisation (diagnostic + therapeutic)
  • Renal Ultrasound (post-renal obstructive causes, small kidneys in CKD, RAS)
  • Renal biopsy (renal cause)
  • CXR (fluid overload)
  • ECG (hyperkalaemia)
  • AXR (renal stones)
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13
Q

What is the Management plan for AKIs?

A

•Treat the cause
•FOUR main components to management:
oProtect patient from hyperkalaemia (calcium gluconate)
oOptimise fluid balance
oStop nephrotoxic drugs
oConsider for dialysis
•Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
•Identify and treat infection •Urgent relief of urinary tract obstruction
•Refer to nephrology if intrinsic renal disease is suspected
•Renal Replacement Therapy (RRT) considered if:
oHyperkalaemiarefractory to medical management
oPulmonary oedema refractory to medical management
oSevere metabolic acidaemia
oUraemic complications

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14
Q

How do you manage/assess fluid status?

A

Assess hydration and fluid balance:

  • pulse, BP, JVP, CVP
  • skin turgor
  • pulmonary/peripheral oedema
  • fluid (input/output) and weight charts
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15
Q

How do you manage the Complications of AKIs?

A
  • Metabolic acidosis (if pH < 7.2): 50-100ml bicarbonate
  • Hyperkalaemia (ECG changes, K+ >7mmol/L):
    - 10ml of 10% Calcium gluconate IV (cardioprotective)
    - 50ml of 50% dextrose
    - 5U insulin
    - Nebulised salbutamol
    - PO/PR calcium resonium (reduced bowel absorption)
  • Pulmonary oedema
    - O2 – consider CPAP or BiPAP
    - IV GTN
    - IV furosemide
    - IV diamorphine (respiratory depression relieves anxiety and breathlessness)

Other complications: Uraemia, bleeding

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16
Q

What is necessary for Pre-Renal AKI management?

A
  • Volume expansion with normal saline or RBC transfusion
  • Inotropes if persistent hypotension
  • Diuretics if volume overload
17
Q

What is the Management of Post-renal AKIs?

A
  • Bladder Catheterisation

- Relieve obstruction (e.g. stricture with stenting, calculi)

18
Q

Outline the Prognosis of patients with AKI

A
  • Inpatient mortality varries depending on cause and comorbidities
  • Indications of poor prognosis: age, multiple organ failure, oliguria, hypotension, CKD
  • Patients who develops AKI are at risk of developing CKD