AKI Flashcards

1
Q

AKI definition

A

Syndrome arising from a rapid drop in GFR (over hours/days) that is characterised by retention of waste products of metabolism + disordered electrolyte, acid-base and fluid balance

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2
Q

AKI criteria

A

Serum creatinine rises by >26umol/L within 48 hours
Serum creatinine rises by >150% within last 7 days
Urine output <0.5ml/kg/hr for >6 consecutive hours

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3
Q

AKI Stage 1

A

Rise in creatinine >26umol/L or 150-200% above baseline

Urine <0.5ml/kg/h for >6hrs

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4
Q

AKI Stage 2

A

Creatinine 200-300% above baseline

Urine <0.5ml/kg/hr >12hrs

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5
Q

AK Stage 3

A

Creatinine>300% above baseline or creatinine >354umol/L with acute rise of >45umol/L or on RRT
Urine <0.3ml/kg/hr for >24hr, or anuric for 12hr

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6
Q

Pre-renal AKI

A

Decrease in renal blood flow leads to reduction in GFR
Potentially reversible by restoration of renal perfusion
Kidneys remain structurally normal

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7
Q

Pre-renal AKI causes

A
Due to a decrease in effective circulating volume
- haemorrhage
- volume depleted
- low CO
- sepsis
- congestive heart failure
- cirrhosis
- hepato-renal syndrome
Due to arterial stenosis/occlusion
- Renal artery stenosis
- NSAIDs
-ACEIs/ACRBs
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8
Q

Renal AKI

A

Damage to renal parenchyma that causes decrease in renal function

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9
Q

Renal AKI Causes

A

Acute tubular necrosis
Vascular
Acute glomerulonephritis
Acute interstitial nephritis

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10
Q

Renal AKI- Acute tubular necrosis causes

A

Ischaemic (prolonged renal hypoperfusion –> ATN)- e.g. untreated pre-AKI
Nephrotoxic:
- Haemo/myoglobinuria (due to rhabdomyolysis)
- Myeloma casts
- Intratubular crystals (tumour lysis syndrome –> urate crystals)
-Nephrotoxic drugs (aminoglycosides, cisplatin, atorvastatin, ethylene glycol)
-Radiocontrast agents

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11
Q

Renal AKI- Vascular causes

A

Vasculitis
Thrombotic microangiopathies
Hypertensive emergency

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12
Q

Renal AKI- acute glomerulonephritis

A

Inflammation and damage of glomerular membrane

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13
Q

Renal AKI- acute interstitial nephritis

A

Allergic reaction where interstitium of kidney becomes inflamed
Usually due to NSAIDs or antibiotics (methicillin, penicillin, cephalexin), PPIs

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14
Q

Post-renal AKI

A

Any cause of increased backpressure on the kidneys can reduce tubular function
Obstruction can occur at any level along the urinary tract
AKI will only occur if both kidneys obstructed (will occur always if only have 1 kidney)

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15
Q

Post-renal AKI causes

A

Bladder outflow obstruction- BPH, tumours

Bilateral ureteric obstruction- tumour, stones, stricture

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16
Q

AKI presentation

A

Raised urea
Raised creatinine
Decreased urine output (<400ml/day)
Volume depletion (low JVP, postural drop)= pre-renal causes of AKI
Volume overload (pulmonary oedema)= renal causes of AKI
Hyperkalaemia (–>cardiac arrhythmias)
Non-specifically sick, deteriorating patient

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17
Q

Uraemia symptoms

A
Nausea
Vomiting
Fatigue
Anorexia
Weight loss
Muscle cramps
Pruritis
Mental status change
Visual disturbances
Increased thirst
Hyperventilation
Uraemic frost
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18
Q

Uraemic induced platelet dysfunction

A

Ecchymosis (bleeding under skin)
GI bleeds
increased bleeding tendency

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19
Q

Uraemic encephalopathy

A

Headaches
Confusion
Coma

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20
Q

Uraemic pericarditis

A

Chest pain
Malaise
Pericardial friction rub

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21
Q

AKI Hyperkalaemia- symptoms

A
Muscle weakness
Lethargy
Nausea
Vomiting
Palpitations
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22
Q

AKI Hyperkalaemia- ECG changes

A
Tented T waves
PR prolongation
Loss of P wave
Prolonged QRS complex
ST elevation
Sine wave 
--> VF, BBB, MI
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23
Q

AKI Hyperkalaemia- treatment

A
IV calcium gluconate (cardioprotective)
Insulin + dextrose
IV salbutamol
Calcium resonium
K+ wasting diuretics
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24
Q

AKI Pulmonary oedema

A

Occurs due to failure of salt + water excretion

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25
Q

AKI pulmonary oedema- symptoms

A
Tachypnoea
Tachycardia
Cool + clammy
Respiratory crackles
Wheeze
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26
Q

AKI pulmonary oedema- investigations

A

Low SaO2
PaO2<8kPa
Alveolar shadowing on CXR

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27
Q

AKI pulmonary oedema- treatment

A
Oxygen (aim for SaO2>95%)
Pain relief
High dose diuretics (bolus of furosemide)
Vasodilators (nitrates)
Dialysis 
CPAP
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28
Q

AKI- metabolic acidosis

A

Associated with raised anion gap metabolic acidosis due to accumulation of sulphates and phosphates, and impaired reabsorption of bicarbonate
Degree of acidosis is modest and doesn’t usually require treatment as will resolve when renal function restored
pH<7.1 is indication for dialysis

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29
Q

AKI- uraemic encephalopathy

A

Syndrome occurs when GFR drops (often below 15) and leads to urea accumulation
Symptoms- confusion, severe pruritic, agitation, seizure, nausea, vomiting
Treatment- dialysis

30
Q

Prerenal AKI treatment

A

Improve renal perfusion- saline, blood transfusion, albumin
Do not put urinary catheter
Do not give diuretics (doesn’t improve renal function)
CVP line rarely needed
Aim is to reverse cause of AKI- e.g. treat heart failure

31
Q

Renal AKI treatment

A
GN= immunosuppression
IBE= antibiotics
AIN= stop offering medication + corticosteroids
ATN= self-correcting but may take a while (up to 6 wks)
32
Q

Post-renal AKI treatment

A

Obtain drainage of urine

  • bladder or below= urinary catheter
  • above bladder= anterograde (nephrostomy) or retrograde drainage (JJ stent)
33
Q

Hyperkalaemia treatment

A
IV calcium gluconate
Insulin + dextrose
Salbutamol (IV or nebuliser)
Calcium resonium
Dialysis
34
Q

Pulmonary oedema treatment

A
High dose diuretics
Pain relief
Vasodilators (IV GTN)
Dialysis
CPAP
35
Q

Uraemic encephalopathy treatment

A

Dialysis

36
Q

Diuretic phase during AKI recovery

A

Recovery from AKI can result in polyuric state with large vol urine production
Assess signs of hypovolaemia + hypernatraemia that may mean IV fluid resuscitation needed

37
Q

Indications in AKI for RRT

A

Hyperkalaemia >6.5mmol/L
Vol overload (pulmonary oedema, hypervolaemic vol status)
Acidosis pH<7.1
Critically unwell patients
Uraemic complications (pericarditis, encephalopathy)
Diuretic resistant cardiac failure
Poison or toxin removal (lithium, ethylene glycol)
Hyperthermia

38
Q

Haemodialysis

A

Solute clearance by diffusion across a semi-permeable membrane
Pores allow small molecules through but prevent passage of larger weight molecules
Allows products such as bicarb to be replaced
Diffusion rate maximised by counter-current exchange mechanism

39
Q

Haemodialysis- intermittent

A
Faster correction of electrolyte imbalances
Fewer bleeding complications
Lower cost
More haemodynamic instability
Less control of fluid balance
40
Q

Haemodialysis- continuous

A

More haemodynamic stability
Lower risk of fluid balance shift problems (cerebral oedema)
Slower correction of electrolyte imbalances

41
Q

Haemofiltration

A

Solute clearance by convection
Can remove large molecular weight molecules
Continuously delivered
Large vols need to be filtered to attain adequate solute clearance
More suitable for a patient on ITU who couldn’t handle a drop in BP
In haemofiltration, fluid shifts are less pronounced and it is performed continuously (slow clearance) while a
patient is in renal failure
Also referred to as continuous arteriovenous haemofiltration (CAVH)

42
Q

Haemodiafiltration

A

Combined HD + HF get the best of both modalities

43
Q

Hypovolaemic signs

A
Dry mucous membrane
Reduced tissue tugor
Low JVP
Postural hypotension
Drop in body weight
Low urine output
44
Q

Hypervolaemic sign

A

Oedema
Raised JVP
Pulmonary oedema
Increased body weight

45
Q

Crystalloids

A

Saline can result in hyperchloraemic metabolic acidosis
UK guidelines recommend use of balanced crystalloids over saline in AKI
Sodium bicarb may be useful in acidotic volume-depleted patients

46
Q

Colloids

A

Contain osmotically active ingredients that remain in intravascular compartment and pull in extravascular water
Starch containing solutions thought to worsen AKI
AVOID COLLOIDS IN AKI

47
Q

Blood products

A

Appropriate in pre-renal AKI due to loss of circulating BV due to haemorrhage

48
Q

Urinalysis

A

Exclude UTI

Significant protein –> consider nephrotic/nephritic syndrome (measure PCR or ACR)

49
Q

Microscopy Casts- Hyaline cast

A

Normal

50
Q

Microscopy casts- lipid cast

A

High urinary protein nephrotic syndrome

51
Q

Microscopy Casts- Muddy brown cast

A

ATN

52
Q

Microscopy Casts- Pigment cast

A

Haemo/myoglobinuria

53
Q

Microscopy Casts- Crystals

A

Tumour lysis syndrome

54
Q

Microscopy Casts- Red cell cats

A

GN

55
Q

Microscopy Casts- White cell casts

A

Infection
Acute interstitial nephritis
Post-strep acute GN

56
Q

Microscopy Casts- Bacterial casts

A

Infection

57
Q

Microscopy Casts- eosinophil cast

A

Acute interstitial nephritis

58
Q

Microscopy- haematuria alone

A

Post-renal AKI
Vasculitis
Trauma

59
Q

Blood tests- Low Hb

A

Haemolysis

GI bleed

60
Q

Blood tests- raised WCC

A

Infection

61
Q

Blood tests- Abnormal LFTs

A

Hepatorenal syndrome

62
Q

Blood tests- high urea:creatinine ratio

A

pre-renal AKI (sign of dehydration)

63
Q

Blood tests- raised ESR

A

any inflammatory condition

64
Q

Blood tests- blood culture

A

sepsis

65
Q

Blood tests- creatine kinase

A

rhabdomyolysis

66
Q

Blood tests- urate

A

tumour lysis syndrome

67
Q

Blood tests- lactate

A

tissue hypoperfusion

68
Q

Blood tests- hypercalcaemia

A

Myeloma

sarcoidosis

69
Q

Blood tests- Immunological testing

A

Anti-nuclear antibodies- SLE
Anti-neutrophil cytoplasmic antibodies- small vessel vasculitis
Anti GBM antibodies- Anti GBM disease
Anti streptolysin O titres- post-streptococcal GN
Immunoglobulins- multiple myeloma
Antiphospholipia antibodies- antiphospholipid syndrome

70
Q

Ultrasound

A

Hydronephrosis (accumulation of urine in kidney) that indicates obstruction in urinary tract

71
Q

CXR

A

pulmonary oedema