acute kidney injury Flashcards

1
Q

what does AKI stand for?

A

acute kidney injury

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2
Q

what is the definition of acute kidney injury?

A

increase in serum creatinine:

  • by 26.5umol/L or more within 48 hours or
  • to >1.5x baseline, which is known or presumed to have occurred within the prior 7 days or
  • urine volume <0.5ml/kg/h for 6 hours
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3
Q

how many stages of acute kidney injury are there?

A

3

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4
Q

what does the immediately dangerous consequences of AKI depend on?

A

causes

  • acidosis
  • electrolyte imbalance
  • intoxication toxins
  • overload
  • uraemic complications
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5
Q

what can the causes of AKI be classified into?

A

pre-renal

intrinsic (renal)

post-renal

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6
Q

what are the normal functions of the kidneys?

A
  • body fluid homeostasis
  • electrolyte homeostasis
  • acid/base homeostasis
  • regulation of vascular tone
  • excretory function
  • endocrine function
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7
Q

what are possible bad short term and intermediate/long term complications of AKI?

A

short term (in hospital): death, dialysis, length of stay

intermediate/long term (post-discharge): death, CKD, dialysis, CKD related CV elements

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8
Q

how does mortality change with the stage of AKI?

A

mortality increases with stage

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9
Q

What does renal hypoperfusion cause

A

Ischemia of renal parenchyma → prolonged ischemia → intrinsic damage → Acute tubular necrosis (ATN)

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10
Q

what are pre-renal causes of AKI?

A

Renal hypoperfusion:

cardiac failure( reduced CO)

haemorrhage (hypovolaemia)

sepsis (systemic vasodilatation)

vomiting and diarrhoea

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11
Q

How are causes of intrinsic renal causes of AKI categorised?

A

Location of pathology:

  • Vasculature
  • Glomerular
  • Tubulointerstitial
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12
Q

what are renal causes of AKI?

A
  • Vasculature
    • Large vessel disease:
      • Atherosclerosis (Renal artery stenosis)
      • Thromboembolic disease (renal artery thrombosis)
      • Dissections (aortic)
    • Small vessel disease
      • Vasculitidies
      • Thromboembolic disease
      • Microangioplastic haemolytic anaemias
      • Malignant hypertension
  • Glomerular
    • Primary (no systemic disease association)
      • glomerulonephritis
    • Secondary (systemic disease association)
  • Tubulointerstitial

radiocontrast

myeloma

rhabdomyolysis

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13
Q

what are post renal causes of AKI?

A

Caused by obstructions:

tumours

prostate disease

stones

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14
Q

how is AKI prevented?

A

by identifying patients who are at risk

(presence of risk event or risk factor)

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15
Q

what are examples of AKI risk events?

A

sepsis (pneumonia, cellulitis, UTI)

toxins (x-ray contrast, NSAIDs, gentamicin, herbal medicine)

hypotension

hypovolaemia (haemorrhage, vomiting, diarrhoea)

major surgery

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16
Q

what are some risk factors for AKI?

A
  • age > 75
  • previous AKI
  • ♡ failure
  • liver disease
  • chronic kidney disease
  • DM
  • vascular disease
  • cognitive impairment
17
Q

What is the protocol when identifying patients at risk of AKI?

A

In presence of risk event or factor consider:

  • treat sepsis if present
  • avoid toxins
  • optimise BP and volume status
  • prevent harm
18
Q

Much of AKI is avoidable, how can it be prevented?

A
  • Avoid dehydration
  • Avoid nephrotoxic drugs
  • Review clinical status in those at risk and act on findings
19
Q

What are medicine “sick day rules”?

A

When you have vomiting or diarrhoea (unless only minor) or fever, sweats and shaking you stop taking certain medications

Restart medications when well (24-48 hours after eating and drinking normally)

20
Q

When should medicines be restarted after “sick day” rules?

A
  • Restart medications when are well (after 24-48 hours of eating and drinking normally)
21
Q

What are exampls of medications that should be stopped on “sick days”?

A
  • ACE inhibitors
  • ARBs
  • NSAIDs
  • Diuretics
  • Metformin
22
Q

What investigations should be done for AKI?

A
  • Renal function
  • Urine dipstick
  • FBC
  • USS
  • Blood gas
  • Specific blood tests if indicated
23
Q

What parts of the history are important for AKI?

24
Q

What parts of the examination are important for AKI?

25
What does RRT stand for?
Renal replacement therapy
26
What are potential indications for renal replacement therapy (RRT)?
* Dependant on cause to an extend of at least in the first few hours * Acidosis * Electrolyte imbalance * Intoxication toxins * Overload * Uraemic complications
27
What electrolyte imbalance can occur in AKI that can have serious consequences?
Hyperkalaemia
28
What are ECG changes present in hyperkalaemia?
* Peaked T waves (usually earliest sign of hyperkalaemia) * P wave widens and flattens * PR segment lengthens * P waves eventually disappear * Prolonged QRS interval with bizarre QRS morphology * High-grade AV block with slow junctional and ventricular escape rhythms * Any kind of conduction block (bundle branch blocks, fascicular blocks) * Sinus bradycardia or slow AF * Development of sine wave appearance * Can cause cardiac arrest * Asystole * Ventricular fibrillation * PEA with bizarre, wide complex rhythm
29
What is usually the earliest sign of hyperkalaemia?
Peaked T-waves
30
What is the treatment of hyperkalaemia?
* Stabilise (myocardium) * Calcium gluconate * Shift (K+ intracellularly) * Salbutamol * Insulin-dextrose * Remove * Diuresis * Dialysis * Anion exchange resins
31
What medicine can be used to stabilise the myocardium in hyperkalaemia?
Calcium gluconate
32
What medication can be used to shift K intracellular in hyperkalaemia?
* Salbutamol * Insulin-dextrose
33
What can be done to remove K from the body in hyperkalaemia?
* Diuresis * Dialysis * Anion exchange resins
34
What kind of cardiac arrest can hyperkalaemia cause?
* Can cause cardiac arrest * Asystole * Ventricular fibrillation * PEA with bizarre, wide complex rhythm
35
How does the T wave change in hyperkalaemia?
Peaked T waves
36
How does the P wave change in hyperkalaemia?
Widens and flattens at first Eventually completely disapears
37
How does the PR segment change in hyperkalaemia?
Lengthens
38
How does the QRS complex change in hyperkalaemia?