Acute Kidney Injury Flashcards

1
Q

Define acute Kidney injury

A

Acute kidney injury is a syndrome of decreased renal function, it is measured by serum creatine or urine output over hours-days.

  • rise in creatine of >26umol/L within 48 hours
  • rise in creatine > 1.5 x baseline within 7 days
  • urine output <0.5mL/kg/h for >6 consecutive hours
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2
Q

What factors make up acute kidney injury (RIFLE)

A

RIFLE

  • Risk of renal dysfunction;
  • Injury to the kidney
  • Failure of kidney function,
  • Loss of kidney function
  • End-stage kidney disease
  • 3 levels of dysfunction
  • 2 outcomes
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3
Q

How many stages does acute kidney injury have

A

3

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4
Q

Who came up with the stages of acute kidney injury

A

The acute kidney injury network

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5
Q

Define stage 1, 2 and 3 of acute kidney injury (RIFLE)

A

Stage 1
• Rise in serum creatinine of ≥ 26 μmol/L within 48 hours or
• 1.5-1.9 x increase in serum creatinine known or presumed to have occurred within in the last 7 days or
• 6 -12 hours oliguria (urine output < 0.5ml/kg/hour)

Stage 2

  • Serum creatine = 2-2.9 x baseline
  • Urine output <0.5ml/kg/hour for >12 hours

Stage 3

  • Serum creatine = >353.6umol/L or > 3 x baseline or having renal replacement therapy
  • Urine output = anuria for >12 hours
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6
Q

What is the minimum GFR rate for solute removal

A

• 6 hours oliguria (urine output < 0.5ml/kg/hour) - minimum GFR for solute removal

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7
Q

Who gets AKI

A
  • Elderly
  • CKD (eGFR < 60 ml/min/1.73 m2)
  • Cardiac failure
  • Liver disease
  • Diabetes
  • Vascular disease
  • Potentially nephrotoxic medications - NSAID, ACE inhibitors
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8
Q

What things can cause an AKI

A

STOP

  • Sepsis and hypo perfusion
  • Toxicity (drugs and contrast)
  • Obstruction - ureters, prostate or beyond bladder
  • Parenchymal disease -disease of the kidneys itself
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9
Q

How do you prevent AKI

A

4Ms
Monitoring: observations (BP, pulse), fluid input/output charts, blood tests

Maintain circulation: well hydrated, adequately resuscitation, oxygenation

Minimise renal insults: reducing nephrotoxic medications, iodinated contrast if CT scan, hospital acquired infections

Manage acute illnesses appropriately

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10
Q

How do you manage AKI

A

Fluids

Monitoring

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11
Q

How do you assess volume status in fluid management of AKI

A

Most important thing to do is to assess volume status
- Do this by doing the Blood pressure lying or staining, measure heart rate, JVP, capillary refill, conscious level, lactate and weight ( important in patients with dialysis and using fluid)

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12
Q

What should you do if the patient is hypovalaemic in fluid management of AKI

A

If hypovolaemic renal perfusion will improve with volume replacement
• give bolus fluids (250 – 500 mls) with regular review until volume replete
- give further boluses of 250-500mL crystalloid with clinical review after each
• If you have given ≥ 2 L Stop + remains hypoperfused consider further circulatory support e.g. something to increase CO such as isotonic compounds or something to cause vasoconstriction

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13
Q

What happens if you give too much fluid in fluid management of AKI

A

• Too much fluid is harmful (pulmonary oedema, delayed recovery)

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14
Q

once there euvolaemic and passing urine what should you do - fluid management of AKI

A

• If euvolaemic + passing urine give maintenance fluids (estimated daily output + 500 ml)

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15
Q

Which type of fluid should you give in fluid management of AKI

A
  • Isotonic crystalloid fluids - E.G. plasmalyte, Hartmann’s) - these contain potassium (5mmol/L) - if your giving a low concentration of potassium to someone who has a high concentration of potassium you reduce the plasma potassium but risk of hypokalaemia is low yet you are increasing there whole body potassium if they are not passing urine
  1. 9% saline
    - safe
    - can worsen metabolic acidosis if large volumes are infused rapidly
    - as the chloride can cause a hypercholermic acidosis

Colloids

  • high molecular weight states
  • dextran can worsen AKI
  • therefore they are not used anymore
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16
Q

What is the downside of using isotonic fluids for AKI fluid management

A

these contain potassium (5mmol/L) - if your giving a low concentration of potassium to someone who has a high concentration of potassium you reduce the plasma potassium but risk of hypokalaemia is low yet you are increasing there whole body potassium if they are not passing urine

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17
Q

What is the downside of using 0.9% saline for AKI fluid management

A
  • can worsen metabolic acidosis if large volumes are infused rapidly
  • as the chloride can cause a hypercholermic acidosis
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18
Q

What is the downside of using colloids for AKI fluid management

A
  • high molecular weight states
  • dextran can worsen AKI
  • therefore they are not used anymore
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19
Q

How do you monitor AKI

A
  • Consider urinary catheter + hourly input/output
  • U&Es, bone profile, venous bicarbonate ≥ daily whilst creatinine rising
  • Blood gases + lactate if septic/hypoperfused
  • Daily weights
  • Regular fluid assessment
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20
Q

How do you investigate AKI

A
  • Urinalysis - urine microscopy
  • urine dip = protein creatine ratio
    • Ultrasound scan ≤ 24 hours (≤ 6 hours if pyonephrosis (sepsis) suspected)
    • Inflammatory markers, CK, Liver Function Tests (LFTs)
    • If platelets low blood film/LDH/reticulocyte count (HUS/TTP/accelerated HTN with MAHA
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21
Q

What further should you investigate AKI

A
  • Consider serum protein electrophoresis/free light chains + urine Bence Jones protein
  • If blood and protein +++ on dip or acute glomerulonephritis suspected:
  • HIV, HCV IgG, Hep B surface antigen (also if going to be filtered/dialysed)
  • ANCAs
  • Anti-GBM
  • Complements (C3, C4)
  • Rheumatoid factor
  • ANA/ENAs (dsDNA)
22
Q

How should you support recovery from AKI

A

• Treat sepsis
• Maintain perfusion - make sure they are hydrated
• Stop NSAIDs, ACE, ARB, metformin, potassium-sparing diuretics, adjust drug doses (Renal Drug Database/Renal Drug Handbook)
• If hypotensive = stop antihypertensives, if underfilled = diuretics
- try to minimise iodinated contrast = if a scan is required they should get contrast but make sure they are well perfused and try to minimise it

23
Q

Name some nephrotic drugs

A
NSAIDs
ACE
ARB
metformin
potassium-sparing diuretics
24
Q

Name the complications of acute kidney injury

A
Hyperkalemia 
Pulmonary oedema 
Acidosis 
severe uraemia 
insufficient urine output
25
Q

What does an ECG of hyperkaelmia look like

A
  • small or absent p waves
  • tented T waves
    progresses
  • sine wave
  • increase PR interval
  • widened QRS complex
  • Sinusoidal rhtyhm
  • MI
26
Q

How do you manage hyperkalemia

A
  • If the ECG changes you should give calcium gluconate - 10mls and 10% over 10 minutes

• If K > 6.5 mmol/L or ECG changes insulin dextrose
(effective for lowering the potassium for about ≤ 4 hrs) - 10 units in 50mls of 50% dextrose
- Monitor for blood glucose for hypoglycaemia

• If bicarbonate < 22 mmol/L + not overloaded give 1.26% bicarbonate IV 500 ml 1-4 hrs (N.B. hypocalcaemia)

  • this will rise the pH and lower the level of potassium
  • calcium binds to albumin when pH goes up so can lead to hypocalcamia

To remove potassium from the body

  • calcium resonium
  • loop diuretics
  • renal replacement therapy
27
Q

What is the only thing that can lower whole body potassium

A

• Lowering whole body potassium ultimately requires recovery of function or renal replacement therapy (haemodialysis or filtration)

28
Q

How is pulmonary oedema caused by AKI

A
  • fluid overload due to salt and water infusion

- goes into the lung

29
Q

How do you manage fluid overload in AKI

A
  • oxygen supplementation if required
  • fluid restriction - consider oral and IV volumes
  • diuretics = only in symptomatic fluid overload
  • renal replacement therapy
30
Q

What does an X ray of pulmonary odeam look like

A
  • Backwing pulmonary oedema
  • pleural effusion
  • starts in the central
  • Kerley B lines
  • cardiomegaly
31
Q

what is the only way to fully resolve pulmonary oedema

A

• Resolution will require recovery of renal function or RRT

32
Q

How do you manage acidosis in AKI

A

• Ensure acidosis renal in origin (raised anion gap, gases, lactate, ketones etc.)

  • make sure your not missing something
  • look for a raised anion gap acidosis
  • Sodium bicarbonate reserved for correction of hyperkalaemia - bicarbonate can crate carbon dioxide therefore you have to make sure that you have adequate ventilation for the patient
  • pH < 7.15 should go to critical care referral if appropriate
  • May be an indication for RRT
33
Q

What requires dialysis

A
Hyperkalemia 
Pulmonary oedema 
Acidosis 
severe uraemia 
insufficient urine output
34
Q

When should you refer to the renal time

A
  • AKI not responding to treatment
  • Complications – hyperkalaemia, acidosis, fluid overload
  • Stage 3 AKI
  • AKI with difficult fluid balance
  • AKI due to intrinsic renal disease
  • AKI with hypertension
35
Q

How many patient deaths are associated with acute kidney injury

A
  • about 100,000

- 1/3rd were thought to be preventable - dehydration

36
Q

what are the commonest causes of AKI

A
  1. sepsis
  2. Major surgery
  3. Cardiogenic shock
  4. other hypovolaemia
  5. drugs
  6. Hepatorenal syndrome
  7. Obstruction
37
Q

What are the three sites in which acute kidney injury occurs

A
  • Pre-renal = decrease perfusion to the kidney
  • Renal = intrinsic renal disease
  • Post-renal = obstruction to urine
38
Q

What is the pathology of pre renal acute kidney injury

A
  • decrease in vascular volume = due to haemorrhage, burns, pancreatitis
  • decrease cardiac output = Cardiogenic shock and MI
  • systemic vasodilation = sepsis and drugs
  • Renal Vasoconstriction = NSAIDs, ACE-i, ARB, hepatorenal syndrome
39
Q

What is the pathology of renal acute kidney injury

A
  • Glomerular damage = glomerulonephritis, ATN
  • Interstitial damage = drug reaction, infection, infiltration
  • Vessels damage = vasculitis, HUS, TTP, DIC
40
Q

What is the pathology of post-renal acute kidney injury

A
  • Within renal tract = stone, renal tract malignancy, stricture, clot
  • Extrinsic compression = pelvic malignancy, prostatic hypertrophy, retro-peritoneal fibrosis
41
Q

What is the management of AKI

A

Pre-renal

  • Give IV fluids
  • Bolus fluids 250-500mls crystalloids over 15mins with regular review
  • Give further boluses of 250-500mls crystalloid
  • Stop with euvolemic or 2L given and seek expert help

Renal

  • Biopsy
  • Refer to renal team if intrinsic renal disease

Post renal
- Catheter, nephrostomy or urological intervention

42
Q

Name 3 pathological consequences of AKI

A
  • hyperkalaemia
  • fluid overload
  • uraemia
43
Q

What are the signs of hypovolaemia

A
  • decrease in blood pressure
  • decrease in urine volume
  • non visible JVP
  • poor tissue turgor
  • increase in pulse
  • daily weight loss
44
Q

What are the signs of fluid overload

A
  • increase in blood pressure
  • increase in JVP
  • lung crepitations
  • peripheral oedeem
  • gallop rhythm
45
Q

In what situations are colloids given for acute kidney injury

A
  • hepatorenal syndrome
  • septic shock
    Under specialist advice
46
Q

What are the indications of renal replacement therapy

A
  • fluid overload and unresponsive to medical treatment
  • severe/prolonged acidosis
  • recurrent/persistent hyperkalaemia despite medical treatment
  • uraemia e.g. pericarditis, encephalopathy
47
Q

Name differential diagnosis for AKI

A

Decrease serum urea

  • low protein intake
  • liver failure
  • sodium valproate treatment

Increased serum urea

  • corticosteroid treatment
  • tetracycline treatment
  • gastrointestinal bleeding

Decreased creatine
- low muscle mass

Increased creatine

  • high muscle mass
  • red meat ingestion
  • muscle damage
  • decreased tubular secretion
48
Q

Why do you do urinalysis and urine microscopy in acute kidney injury

A
  • Look for red cell clasts - these are indicative of glomerulonephritis
  • tested for haemoglobin and myoglobin
  • urine protein: creatine ratio is helpful if parenchymal disease is possible
49
Q

in AKI how long does it take creatine to rise in the plasma

A
  • takes 48 -72 hours
50
Q

what can you measure in plasma instead of creatine that is indicated of AKI

A
  • urinary and plasma biomarkers such as kidney injury molecule 1, neutrophil gelatinise associated lipocalin rise within a few hours of AKI
51
Q

What are the symptoms and signs of an AKI

A
  • Reduced urine output
  • Pulmonary and peripheral oedema
  • Arrhythmias – secondary due to changes in potassium and acid-base balance
  • Features of uraemia
52
Q

How do you tell the difference between dehydration and AKI

A

urea is proportionally higher than the rise in creatinine in dehydration