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Systems: Urinary AB > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What are the functions of the kidneys?

A
  • Body fluid homeostasis
  • Regulation of vascular tone
  • Excretory function
  • Electrolyte homeostasis
  • Acid-base homeostasis
  • Endocrine function (erythropoietin, vitamin D)
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2
Q

What is the traditional definition of AKI?

A
  • Rapid loss of glomerular filtration and tubular function over hours to days
  • Retention of urea/creatinine
  • Oliguric / non-oliguric
  • Potentially recoverable
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3
Q

What classification system is used in AKI?

A

RIFLE

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4
Q

What system is currently used to stage AKI?

A

KDIGO

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5
Q

What are the stages in the development of AKI?

A
  • Normal
  • Increased risk
  • Damage
  • Decreased GFR
  • Kidney failure
  • Death
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6
Q

What are stages of AKI defined by?

A

Creatinine and urine output (GFR)

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7
Q

What is the incidence of AKI?

A
  • 1 in 7 (some say 1 in 5) hospital admissions complicated by AKI
  • Hospital admissions 1 in 5 to 7
  • ITU admissions (more than half)
  • In the Community (uncommon 1.5% per y)
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8
Q

What are the immediately dangerous consequences of AKI?

A
  • Acidosis
  • Electrolyte imbalance
  • Intoxication TOXINS
  • Overload
  • Uraemic complications
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9
Q

What are the possible outcomes of AKI?

A

Short term (in hospital)

  • Death
  • Dialysis
  • Length of stay

Intermediate/Long term (Post discharge)

  • Death
  • CKD
  • Dialysis
  • CKD related CV events
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10
Q

When is it too late in AKI?

A

Once creatinine reaches 400

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11
Q

What are the 3 classes of causes of AKI?

A
  • Pre-renal (blood flow to the kidney)
  • Renal (intrinsic) (damage to renal parenchyma)
  • Post-renal (obstruction to urine exit)
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12
Q

What are the pre-renal causes of AKI?

A

Reduction in effective circulating volume

  • Sepsis
  • Hypovolaemia
  • Hepatorenal syndrome
  • Cardiac failure
  • Hypotension

Arterial occlusion

Vasomotor
-NSAIDs/ACEI

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13
Q

What are the renal (intrinsic) causes of AKI?

A
  • Acute tubular necrosis (ischaemia)
  • Toxin related
  • Acute interstitial nephritis
  • Acute Glomerulonephritis
  • Myeloma
  • Intra-renal vascular obstruction (vasculitis and thrombotic microangiopathy)
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14
Q

What are the post-renal causes of AKI?

A

Obstruction

  • Intraluminal (calculus, clot, sloughed papilla)
  • Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
  • Extramural (RPF, malignancy)
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15
Q

What is the most common cause of AKI?

A

Poor perfusion leading to established tubule damage

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16
Q

What can sustained failure of circulation to the kidneys result in?

A

Acute tubular necrosis

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17
Q

What can exacerbate acute tubular necrosis?

A

Toxic injury

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18
Q

Why is the kidney susceptible to hypoperfusion?

A
  • Intrarenal heterogeneity of blood supply, oxygenation and metabolic demand
  • The cortex is richly perfused, whereas the medulla receives around 10-15% of renal blood flow
  • Medulla hypoxic, yet metabolically active
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19
Q

What does the kidney have the potential to do after AKI?

A

Regenerate

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20
Q

Describe the course of acute ischaemic renal injury and recovery.

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)
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21
Q

When may excessive diuresis result during the recovery of AKI?

A

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

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22
Q

What is radiocontrast nephropathy?

A

AKI following administration of iodinated contrast agent

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23
Q

What is a common contributor to hospital acquired AKI?

A

Radiocontrast nephropathy

24
Q

How does radiocontrast nephropathy usually present?

A

-Usually transient renal dysfunction, resolving after 72h but may lead to permanent loss of function

25
Q

What are the risk factors for RCN?

A
  • Diabetes mellitus
  • Renovascular disease
  • Impaired renal function
  • Paraprotein
  • High volume of radiocontrast
26
Q

What is the 2nd most common haematological malignancy?

A

Myeloma

27
Q

What is the pathological process in myeloma?

A

A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains

28
Q

Who is myeloma common in?

A

The elderly

29
Q

What are the clinical features of myeloma?

A
  • Anaemia
  • Back pain
  • Weight loss
  • Fractures
  • Infections
  • Cord compression
  • Markedly elevated ESR
  • Hypercalcaemia
30
Q

How is myeloma diagnosed?

A
  • Bone marrow aspirate - >10% clonal plasma cells
  • Serum paraprotein ± immunoparesis
  • Urinary Bence-Jones protein (BJP)
  • Skeletal survey - lytic lesions
31
Q

What can cause renal failure in myeloma?

A
  • Cast nephropathy - ‘myeloma kidney’
  • Light chain nephropathy
  • Amyloidosis
  • Hypercalcaemia
  • Hyperuricaemia
32
Q

Give examples of causes of AKI.

A
  • Cardiac failure
  • Haemorrhage
  • Sepsis
  • Vomiting diarrhoea
  • Glomerulonephritis
  • Vasculitis
  • Radiocontrast
  • Myeloma
  • Rhadomyolysis
  • Drugs (NSAIDs, Gentamicin)
  • Stones
  • Prostate disease
  • Tumours
33
Q

What investigations should be carried out for AKI?

A
  • History
  • Examination
  • Drugs
  • insults
  • Renal function etc
  • Urine dipstick
  • FBC
  • USS
  • Blood gas
  • Fancy blood tests for specifics if indicated
  • Renal biopsy for histology
34
Q

What is important to explore when taking a history of AKI?

A
  • Past medical history / systemic diseases (new rash, nose bleeds, sore eyes, joint pains)
  • Family history / social
  • Drug exposure (what / when)
  • Pre/post renal factors
  • Uraemic symptoms
  • Timing of symptoms – shortness of breath / urine output / vomiting etc.,
35
Q

What is important to explore on examination of AKI?

A
  • Vital signs (BP, pulse etc.,)
  • Volume status
  • Systemic illness (rash, joints, eyes etc.,)
  • Obstruction
36
Q

What blood tests should be carried out for AKI?

A
  • FBC
  • U+Es, bicarb, LFTs, bone
  • Clotting
  • Blood gas
  • ANCA, Ig, C3 C4 dsDNA
37
Q

What urine tests should be carried out for AKI?

A
  • Urine dip (?blood, ?protein)
  • Urine PCR or ACR
  • Urine Bence Jones Protein
38
Q

What radiological test may carried out in the diagnosis of AKI?

A

US

39
Q

How is AKI prevented in hospitals?

A
  • Avoid dehydration
  • Avoid nephrotoxic drugs
  • Review clinical status in those at risk… and act on findings.
  • ? Hold medication
  • ? Give fluids
  • Treat sepsis
40
Q

What is the STOP AKI prevention care bundle?

A
  • Sepsis: if suspected screen and treat promptly
  • Toxins: avoid
  • Optimise: BP and volume status (avoid/correct hypovolaemia)
  • Prevent: harm
41
Q

What supportive management is there for 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
42
Q

What are the 5 Rs for IV prescribing?

A
  • Resuscitation
  • Routine maintenance
  • Replacement
  • Redistribution
  • Reassessment
43
Q

What questions should you ask yourself when managing a patient with AKI?

A
  • Do they need fluid
  • Can you remove the precipitant?
  • Can you stop it getting worse?
  • Do they need a catheter?
  • How to make them safe?
44
Q

How can precipitants be removed?

A
  • Stop drugs that are causing
  • Treat sepsis
  • Diagnose GN/other interstitial disease and give specific therapy
45
Q

How can progression of AKI be prevented?

A
  • Support BP

- Reduce further insults i.e. do not give IV radiocontrast unless absolutely necessary

46
Q

What ECG changes occur in hyperkalaemia?

A
  • Peaked T waves
  • Tall tented T waves
  • 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 a sine wave appearance (a pre-terminal rhythm)
  • Cardiac arrest
47
Q

What rhythms of cardiac arrest can hyperkalaemia result in?

A
  • Asystole
  • Ventricular fibrillation
  • PEA with bizarre, wide complex rhythm
48
Q

What is the treatment for hyperkalaemia?

A

Stabilise (myocardium)
-Calcium Gluconate

Shift (K+ intracellularly)

  • Salbutamol
  • Insulin-Dextrose

Remove

  • Diuresis
  • Dialysis
  • Anion exchange resins
49
Q

Give examples of antidotes to toxins.

A
  • Naloxone for morphine (and other opiates)

- Digiband for Digoxin

50
Q

What are the main indications for dialysis?

A
  • Decreased bicarb
  • Increased potassium
  • Pulmonary oedema
  • Pericarditis
51
Q

How is haemodialysis carried out?

A
  • Solute removal by diffusion

- Intermittent therapy – each session lasting 3-5 hours

52
Q

How is haemofiltration carried out?

A
  • Solute removal by convection
  • Larger pore size
  • Continuous therapy
53
Q

What are the advantages of haemodialysis?

A
  • Rapid solute removal
  • Rapid volume removal
  • Rapid correction of electrolyte disturbances
  • Efficient treatment for hypercatabolic patient
54
Q

What are the disadvantages of haemodialysis?

A
  • Haemodynamic instability
  • Concern if dialysis associated with hypotension, may prolong AKI
  • Fluid removal only during short treatment time
55
Q

What are the advantages of CRRT?

A
  • Slow volume removal associated with greater haemodynamic stability
  • Absence of fluctuation in volume and solute control over time
  • Greater control over volume status
56
Q

What are the disadvantages of CRRT?

A
  • Need for continuous anticoagulation
  • May delay weaning/mobilisation
  • May not have adequate clearance in hypercatabolic PATIENT

Systems: Urinary AB (26 decks)

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