AKI, CKD and dialysis Flashcards

1
Q

Define AKI

A

Acute kidney injury is the short term decline in renal function, measured by either a rise in creatinine from baseline OR a decline in urine output

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2
Q

Describe the epidemiology of AKI

A

VERY common in hospital eg. 10-20%

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3
Q

Describe the aetiology of AKI

A

3 main groups of causes:

  1. Pre-renal (most common): hypovolaemia eg. sepsis, decreased renal blood flow eg. drugs, RAS, hypotension
  2. Renal (3rd most common): ATN, TIN, etc
  3. Post-renal (2nd most common): stones, neoplasms, BPH
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4
Q

Describe the presentation of AKI

A

Usually detected in patients with other illness

  • Fatigue, malaise
  • Uraemia: confusion, CP, pruritis
  • Palpitations
  • SOB
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5
Q

Describe the investigations for AKI

A

Detecting AKI: U+Es
Cause of AKI:
-Urine dip + MCS
-Bloods: FBC, CRP, LFTs, VBG + culture (if indicated)
-USS
-> if nothing on above to suggest pre/post renal cause, refer to renal + antibodies, consider biopsy

+ monitoring: ECG, CXR

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6
Q

Describe the signs of AKI on examination

A
  • Fluid status exam: may be dry (hypovolaemic) or overloaded (HF)
  • Confusion
  • Pericardial friction rub
  • Signs of causative illness eg. vasculitic rash, arthritis
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7
Q

Describe the general management of AKI (not specifics)

A

A to E approach

  • Gain IV access, take bloods
  • ECG and cardiac monitor if available

STOP:

  • Sepsis 6 if indicated
  • Stop nephroToxic drugs (NSAIDs, ACEi/ARBs, aminoglycosides)
  • Optimise BP/hypovolaemia: fluid resus + fluid balance chart
  • Prevent harm: find + treat cause
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8
Q

Describe the management of hyperkalaemia

A
  1. Continuous cardiac monitor (after ECG)
  2. Start Ca gluconate 10ml 10%
  3. Start insulin + dextrose infusion- 10 units Actrapid and 50mls of 50% dextrose STAT + measure BM
  4. Nebulised salbutamol 10-20mg
  5. Repeat ECG and bloods
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9
Q

Which fluids should you use for resus in AKI?

A

Best is balanced crystalloid (Hartmanns, Ringers lactate) unless hyperkalaemia/rhabdo

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10
Q

What are the ECG changes in hyperkalaemia?

A

Tented T waves
Flattened p waves
Broad QRS

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11
Q

What are the indications for emergency dialysis?

A
Refractory pulmonary oedema
Resistent hyperkalaemia 
Refractory metabolic acidosis
Uraemic pericarditis
Uraemic encephalopathy
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12
Q

At what level of hyperkalaemia should you commence treatment?

A

Mild (5.5-6): look for and treat underlying cause
Mod (6.0-6.4): ECG and insulin dextrose +/- Ca gluconate + monitor if ECG changes present
Sev (>6.5): ECG, cardiac monitor, Ca gluconate, insulin dextrose

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13
Q

Describe the management of acidosis in AKI

A

Seek expert advice
pH <7.2 is indication for sodium bicarb
*If serum bicarb <16, no fluid overload present

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14
Q

Describe the management of pulmonary oedema in AKI

A
A to E approach 
Sit upright
Start high flow O2 eg. 15L via non-rebreath mask
IV GTN 
Consider IV furosemide with senior input
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15
Q

Describe the causes of ATN

A

Ischaemia eg. from hypovolaemia
Contrast
Toxins
Drugs: aminoglycosides

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16
Q

Describe the causes of TIN

A
Immune-mediated injury due to drugs commonly:
Rifampicin
Sulfa drugs
Pee pills (diuretics)
Pain relief (NSAIDs)
Penicillin
PPIs
Phenytoin
17
Q

Name the indications for renal biopsy

A
  • Renal AKI
  • CKD with no clear aetiology
  • Haematuria ?cause
  • Nephrotic syndrome in adults/ non-steroid sensitive in children
18
Q

Define CKD

A

Chronic kidney disease is a chronic impairment in kidney function present for 3+ months, characterised by a decline in GFR, proteinuria or haematuria

19
Q

Describe the staging of CKD

A
Staged in 2 ways
eGFR (G)
1: 90-120
2: 60-89
3a: 45-59
3b: 30-44
4: 15-29
5: <15

ACR (A)

1: <3
2: 3-30
3: >30

20
Q

Describe the epidemiology of CKD

A

Quite common!
Increases with age
Increasing incidence with time
Black > white people

21
Q

Describe the aetiology of CKD

A

Most commonly:

  • DM
  • Hypertension
  • Glomerular nephrotic and nephritic syndromes
  • PKD
22
Q

Describe the consequences of CKD in relation

to the function of the kidneys

A
  • Sodium and fluid imbalance
  • Electrolyte abnormalities (K, phos)
  • Waste buildup: azotaemia and increased serum creatinine
  • Endocrine abnormalities: renal osteodystrophy, anaemia
23
Q

Describe the presentation of CKD

A

Often asymptomatic, detected incidentally
Non-specific: fatigue, malaise, nausea, anorexia
Pruritis
SOB, swelling
Palpitations

24
Q

Describe the signs of CKD on examination

A

May have none

  • Pedal oedema
  • Pallor
  • Signs of causative disease eg. diabetic retinopathy, HTN
25
Q

Describe the investigations for CKD

A

Urine: dipstick, MCS, ACR
Bloods: FBC, U+Es and other electrolytes, LFTs, VBG, serology, lipids, HbA1c
USS
*Biopsy if unclear aetiology

26
Q

Describe the management of CKD

A

Conservative:

  • Lifestyle: exercise, diet (low salt, low K, fluid restriction)
  • Vitamin supplementation (activated D3, Ca)

Medical:

  • Treat cause: DM, immunosuppressants, anti-HTN
  • Reduce CVS RFs: statins for all, BP + glycaemic control
  • EPO injections
  • Diuretics if overloaded
  • RRT: HD or PD when G5/uraemic

Surgical:
-Transplant: for GFR <20

27
Q

Describe the prognosis of CKD

A

Most patients will die of CVD before reaching ESRD

28
Q

Describe the types of RRT

A

Haemofiltration: used in ITU, acute RRT
Haemodialysis: long-term RRT, done in clinic/rarely home, requires AV fistula or long-term Tesio line
Peritoneal dialysis: long-term RRT, done at home daily, requires inserted catheter

29
Q

Describe the pros and cons of the different methods of dialysis

A

HD:
+ less frequent, done by professional
- have to attend clinic 3x/wk for 4 hours, hard to travel

PD:
+ convenient at home, can travel, can do overnight
- uncomfortable, higher risk of infection, self managed

30
Q

Name some common nephrotoxic drugs/drugs to stop in AKI

A
NSAIDs
ACEis/ARBs
Contrast
Metformin
Chemotherapy drugs
ABx: Aminoglycosides, sulfonamides, penicillins
Allopurinol 
Methotrexate (post-renal AKI)
31
Q

Which drugs raise serum potassium?

A

Spironolactone
Thiazides
ACEis + ARBs
NSAIDs