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Urinary system > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

List the functions of the kidneys

A
  • Body fluid homeostasis – urine production
  • Regulation of vascular tone – controls BP
  • Excretory function – physiological waste e.g. urea, creatinine, drugs
  • Electrolyte homeostasis -Na, K, Cl, Ca, Phos
  • Acid-base balance –H+ and bicarbonate
  • Endocrine function – production of erythropoietin; vitamin D metabolism and activation; renin
  • Drug metabolism and disposal
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2
Q

What % of hospital admission patients develop AKI?

A

1 in 7 (some say 1 in 5)

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3
Q

Describe the traditional definition of AKI

A

• Rapid loss of glomerular filtration and tubular function over hours to days
• Retention of urea/creatinine
– Failure of homeostasis; even small increases in C are dangerous

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4
Q

What are some problems with the traditional definition of AKI?

A

– Lack of standardisation
– Absolute creatinine, changes in creatinine, urine output, need for dialysis
– Creatinine is insensitive and a late marker
– RRT hard endpoint but very late marker
– Wide spectrum of renal injury

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5
Q

Describe the current definition of AKI

A

• Increase in SCreatinine
– By ≥ 26.5 μmol/l (0.3 mg/dl ) within 48 hours; or
– To ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or

• Urine volume <0.5 ml/kg/h for 6 hours

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6
Q

Describe some immediately dangerous consequences of AKI

A

Acidosis – can cause cardiac arrest

Electrolyte imbalance - Hyperkalaemia can cause cardiac arrest

Intoxication - e.g. opiates can cause respiratory (and then cardiac) arrest

Overload - overload with fluid and pulmonary oedema can cause cardiac arrest

Uraemic complications

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7
Q

What are the 3 classes of aetiology for AKI?

A
  • Pre-renal - Blood flow to kidney
  • Renal (intrinsic) - Damage to renal parenchyma
  • Post-renal - Obstruction to urine exit
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8
Q

List some pre-renal causes of AKI

A

Reduce effective circulation volume
– Volume depletion (haemorrhage/dehydration) - D&V
– Hypotension / shock – Sepsis is a major contributor in up to 50% cases of AKI
– Congestive cardiac failure / Liver failure

Arterial occlusion

Vasomotor
– NSAIDs/ACE inhibitors

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9
Q

List some intrinsic renal causes of AKI

A

Acute tubular necrosis (ATN) - Ischaemic

Toxin-related
–	Drugs (aminoglycosides / amphotericin / NSAID)
–	Radiocontrast
–	Rhabdomyolysis (Haem pigments
–	Snake venom / Heavy metals - Pb, Hg
–	Mushrooms etc

Acute interstitial nephritis (many causes including drugs (PPIs))

Acute Glomerulonephritis

Myeloma

Intra renal vascular obstruction
– Vasculitis
– Thrombotic microangiopathy

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10
Q

What type of cause is myeloma?

A

intrinsic renal

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11
Q

List some post-renal causes of AKI

A

Obstruction
– Intraluminal (calculus, clot, sloughed papilla)
– Intramural – within wall (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
– Extramural – outside urinary system, compression (RPF, malignancy)

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12
Q

Why is the kidney susceptible to hypoperfusion?

A

Intrarenal heterogeneity of:
o Blood supply
o Oxygenation
o Metabolic demand
The cortex is richly perfused, whereas the medulla receives around 10-15% of renal blood flow
Medulla is hypoxic, yet metabolically active

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13
Q

Describe the course of acute ischaemic renal injury

A

Initiation
• Exposure to toxic/ischaemic insult
• Renal parenchymal injury evolving
• AKI potentially preventable

Maintenance
• Established parenchymal injury
• Usually maximally oliguric now
• Typical duration 1-2 weeks (up to several months)

Recovery
• Gradual increase in urine output
• Fall in serum creatinine (may lag behind diuresis)

If GFR recovers quicker than tubule resorptive capacity, excessive diuresis may result (eg post-obstructive natriuresis)

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14
Q

List an iatrogenic cause of AKI

A

Radiocontrast nephropathy (RCN)

  • AKI following administration of iodinated contrast agent for imaging purposes
  • Common contributor to hospital acquired AKI
  • Usually transient renal dysfunction resolving after 72h
  • May lead to permanent loss of function
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15
Q

List some risk factors for radiocontrast nephropathy

A
  • Diabetes mellitus
  • Renovascular disease
  • Impaired renal function
  • Paraprotein
  • High volume of radiocontrast
  • All of the above
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16
Q

What are the clinical features of myeloma

A 
o	Anaemia
o	Back pain
o	Weight loss
o	Fractures
o	Infections
o	Cord compression
o	Markedly elevated ESR
o	Hypercalcaemia
17
Q

How is multiple myeloma diagnosed?

A

o Bone marrow aspirate - >10% clonal plasma cells
o Serum paraprotein ± immunoparesis
o Urinary Bence-Jones protein (BJP)
o Skeletal survey - lytic lesions

18
Q

List some causes of AKI

A
  • Cardiac failure
  • Haemorrhage
  • Sepsis
  • Vomiting and diarrhea
  • Tumours
  • Prostate disease
  • Stones
  • Drugs e.g. NSAIDs, gentamicin
  • Rhabdomyolysis
  • Myeloma
  • Radiocontrasts
  • Vasculitis
  • Glomerulonephritis
19
Q

How can AKI be prevented?

A

o Avoid dehydration
o Avoid nephrotoxic drugs
o Review clinical status in those at risk + act on findings
o ? hold medication e.g. beta blockers, ACE inhibitors
o ? Give fluids
o Treat sepsis – major risk of developing AKI

20
Q

Describe briefly the management of AKI

A
  • Remove / treat cause if possible
  • Make safe!
  • Pre-renal – do they need fluid? BP support
  • Renal (intrinsic) - can you remove precipitant?
  • Post-renal – do they need a catheter?
21
Q

What acronym is used for management of AKI?

A

STOP-AKI

Sepsis
Toxins
Optimise BP
Prevent harm

22
Q

Describe supportive management of AKI

A 
Fluid balance
–	Volume resuscitation if volume deplete
–	Fluid restriction if volume overload
–	Optimise blood pressure
–	Give fluid /vasopressors
–	Stop ACE inhibitors / anti-hypertensives

Stop nephrotoxic drugs
– NSAIDs
– Aminoglycosides

23
Q

What are the 5 R’s for IV prescribing of fluids?

A 
Resuscitate
Routine maintenance
Replacement
Redistribution
Review/reassessment
24
Q

Describe the ECG changes in hyperkalaemia as it increases in severity

A
  • Peaked T waves (usually the earliest sign of hyperkalaemia)
  • P wave widens and flattens (can be small and indiscernible) – represents loss of atrial contraction
  • 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 a sine wave appearance (a pre-terminal rhythm)
  • Asystole – flatline ECG
  • Ventricular fibrillation
  • PEA with bizarre, wide complex rhythm
25
Q

How is hyperkalaemia treated?

A

Stabilise the myocardium
– Calcium Gluconate

Shift the K+ intracellularly
– Salbutamol
– Insulin-Dextrose

Remove any excess potassium
– Diuresis – urinate out potassium
– Dialysis – may be needed if kidneys are functioning well
– Anion exchange resins

26
Q

What is used to stabilise the myocardium in hyperkalaemia?

A

Calcium Gluconate

27
Q

What is used to shift K+ intracellularly in hyperkalaemia?

A

– Salbutamol

– Insulin-Dextrose

28
Q

How can excess K+ be removed in hyperkalaemia?

A

Diuresis – urinate out potassium

Dialysis – may be needed if kidneys are functioning well

Anion exchange resins

29
Q

What antidote is available for digoxin?

A

Digibind

30
Q

What antidote is available for morphine?

A

Naloxone

31
Q

Describe haemodialysis and haemofiltration

A

Haemodialysis (HD)
– Solute removal by diffusion
– Intermittent therapy – each session lasting 3-5 hours

Haemofiltration/CRRT – used in ITU
– Solute removal by convection
– Larger pore size
– Continuous therapy

32
Q

What are the advantages and disadvantages of haemodialysis?

A

Advantages of HD
o Rapid solute removal
o Rapid volume removal
o Rapid correction of electrolyte disturbances
o Efficient treatment for hypercatabolic patient

Disadvantages of HD
o Haemodynamic instability
o Concern if dialysis associated with hypotension, may prolong AKI
o Fluid removal only during short treatment time

33
Q

What are the advantages and disadvantages of haemofiltration/continuous renal replacement therapy?

A

Advantages of CRRT
o Slow volume removal associated with greater haemodynamic stability
o Absence of fluctuation in volume and solute control over time
o Greater control over volume status

Disadvantages of CRRT
o Need for continuous anticoagulation
o May delay weaning/mobilisation
o May not have adequate clearance in hypercatabolic patient

Urinary system (22 decks)

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