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Medicine - Renal > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

What is acute kidney injury?

A

Rapid deterioration in a patient’s renal function over hours or days

  • >50% rise in serum creatinine from baseline within last 7 days
  • Increase in serum creatinine by >26.5mmol/l within 48 hours
  • Urine output <0.5ml/kg/hour for >6 hours
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2
Q

How many stages of AKI are there?

A

3

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3
Q

How can the causes of AKI be divided?

A
  • Pre-renal
  • Renal
  • Post-renal
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4
Q

What is the four most common causes of AKI?

A
  • Sepsis
  • Hypoperfusion - hypovolaemia, hypotension
  • Medications
  • Obstruction
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5
Q

Name 3 pre-renal causes of AKI.

A

decreased vascular volume - dehydration, haemorrhage, burns

decreased cardiac output - cardiogenic shock, MI

systemic vasodilation - sepsis

renal vasoconstriction - NSAIDs, ACEi, ARB

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6
Q

Name 3 renal causes of AKI.

A

Glomerular - glomerulonephritis

Interstitial - nephrotoxic drug e.g. gentamicin, infiltration e.g. myeloma

Vessels - vasculitis

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7
Q

Name 3 post-renal causes of AKI.

A

Luminal - stone, stricture

Intra-mural - renal tract malignancy

Extra-mural - pelvic malignancy, BPH

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8
Q

What initial investigations would you consider in someone with AKI?

A
  • C - ECG for hyperkalaemic changes, Urgent ABG for K+, Bloods - FBC (infection? haemorrhage? low platelets - HUS?), U&Es (monitor progression of AKI), CRP (infection?), bone profile, LFTs (hepatorenal), bicarbonate
  • E - Urine dipstick - UTI? if haematuria + proteinuria - glomerulonephritis? vasculitis?
  • USS KUB
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9
Q

Risk of AKI = baseline risk x acute illness risk

Who is at increased risk of AKI at baseline?

A
  • Chronic Kidney Disease - eGFR <60 ml/min/1.73 m2
  • and/or history of proteinuria
  • Age >75 years
  • Heart failure
  • Liver disease
  • Cardiovascular disease (previous MI, stroke, PVD)
  • Diabetes mellitus
  • Recent use of nephrotoxins, e.g. NSAIDs, ACEi, ARB, gentamicin, iodinated contrast
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10
Q

Risk of AKI = Baseline risk x acute illness risk

How is acute illness risk increased?

A
  • Hypotension (Consider relative hypotension in people with a history of hypertension as this will result in renal hypoperfusion)
  • Sepsis
  • High Early Warning Score
  • Hypovolaemia
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11
Q

How can AKI be prevented?

A
  • Identify patients at risk at baseline
  • Optimise volume status
  • Treat sepsis promptly
  • Avoid nephrotoxins
  • Review medications e.g. adjust drug doses, withhold antihypertensives if hypotensive
  • Reduce risk of contrast-induced AKI by being aware of the indications for using contrast
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12
Q

Who is at a high risk of contrast-induced AKI?

A

acutely ill, with AKI/CKD, sepsis and hypovolaemia

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13
Q

The definition of AKI using creatinine requires comparing with a previous value when the patient was well. How do you diagnose AKI when you do not have a normal value of creatinine for the patient?

A

If a baseline serum creatinine value is not available within 3 months and AKI is suspected:

  • repeat serum creatinine within 24 hours
  • a baseline serum creatinine value can be estimated from the nadir serum creatinine value if patient recovers from AKI
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14
Q

What clues can you get from the history to indicate sepsis is the cause of AKI?

A
  • Fever
  • Productive cough
  • Vomiting and diarrhoea
  • Dysuria
  • Urinary catheter in situ
  • Immunosuppression - can predispose and prevent rise in WCC, masking the sepsis
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15
Q

What clues can you get from the history to suggest hypoperfusion as the cause of AKI?

A
  • Vomiting and/or diarrhoea
  • Haemorrhage
  • Cardiac failure acute e.g. recent MI, or chronic
  • Diuretics (over diuresis)
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16
Q

Name 5 medications that may contribute in causing an AKI (and therefore should be stopped if someone has AKI).

A
  • NSAIDs - reduces renal blood flow and nephrotoxic
  • ACEi - reduces renal blood flow
  • ARB - reduces renal blood flow
  • Gentamicin and Vancomycin - high levels of aminoglycosides are nephrotoxic
  • Iodinated contrast agents
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17
Q

What clues from the history would suggest obstruction as a cause for the AKI?

A
  • Hx of kidney stones
  • Prostatic symptoms - BPH (poor flow, hesitancy, terminal dribble) or malignancy (recent weight loss, bone pain)
  • Known single kidney - obstruction of one ureter will cause AKI
  • Pelvic malignancy
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18
Q

What features in the history suggest Vasculitis as a cause of AKI

A
  • Constitutional symptoms (although fever and weight loss are non-specific they are features of vasculitis)
  • Joint pain
  • Rashes - purpuric
  • Nasal stuffiness
  • Haemoptysis
  • Uveitis
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19
Q

What features may suggest myeloma as the cause of AKI?

A

CRAB

  • Hypercalcaemia
  • Renal failure
  • Anaemia
  • Back pain
20
Q

What feature in the history may suggest rhabdomyolysis as a cause of AKI?

A

Falls/immobility

21
Q

A patient is diagnosed with AKI. What are you specifically looking for on examination to suggest a pre-renal cause of AKI?

A
  • Volume status examination
  • Evidence of sepsis, e.g. fever, respiratory signs, surgical site, red swollen joints, cellulitis, indwelling urinary catheters, cannulae
  • Evidence of haemorrhage, e.g. haematemesis, melaena
22
Q

A patient is diagnosed with AKI. What would you look for on examination to suggest an intrinsic renal cause for the AKI.

A
  • Volume status examination
  • Rash (vasculitis, interstitial nephritis)
  • Red eye (vasculitis)
  • Red swollen joints (vasculitis)
  • Swollen limb (rhabdomyolysis)
23
Q

A patient is diagnosed with AKI. What would you look for on examination to suggest a post-renal cause of the AKI?

A
  • Tense ascites (intra-abdominal hypertension)
  • Palpable bladder
  • Large prostate
24
Q

Name 5 ways you can assess fluid status.

A
  • Capillary refill (<3 s)
  • Pulse rate (tachycardia may be masked by beta
  • blockers)
  • Blood pressure (lying and standing if patient able to
  • stand safely)
  • Skin turgor (over clavicle)
  • Jugular venous pressure
  • Oedema (peripheral and pulmonary)
  • Fluid balance charts
  • Daily weights (trends in body weight are a sensitive
  • indicator of volume status)
25
Q

What are the complications of AKI? Name 5

A
  • Hyperkalaemia (potassium > 6.0 mmol/L)
  • Acidosis
  • Acute confusion (uraemic encephalopathy)
  • Pulmonary oedema
  • Pericarditis (pericardial friction rub)
26
Q

You have done the routine initial investigations for a patient with AKI, they have all come back as normal. The patient is immobile, has back pain and has a rash. What further tests would you now consider?

Tests you have already done - urine dip, FBC, U&Es, LFTs, bone profile, bicarbonate, CRP

A
  • Cultures - blood, urine, wound - sepsis?
  • USS KUB - obstruction?
  • Creatine kinase - rhabdomyolysis?
  • Myeloma screen - serum and urine electropheresis, serum free light chains
  • Vaculitis screen - ANCA
27
Q

Why is it important to identify and manage AKI early?

A

Treatment is initially supportive but ultimately dependent upon the underlying cause. It is important to reduce both the severity and duration of AKI as this predicts progression to chronic kidney disease (CKD).

28
Q

How would approach the assessment of a patient with AKI?

A

A-E approach

29
Q

The bloods have come back for an unwell patient. You review the bloods and notice a Stage 2 AKI. You assess the patient using an A-E approach. They appear dehydrated. Their blood pressure is 94/50. What are your next steps?

A

500ml 0.9% Sodium Chloride over 15 mins

30
Q

The bloods have come back for an unwell patient. You review the bloods and notice a Stage 2 AKI. You assess the patient using an A-E approach. They appear dehydrated. Their blood pressure is 94/50. You give them a fluid bolus. They have no clinical response and no signs of fluid overload. What are your next steps?

A

Repeat fluid bolus and ALERT SENIOR

31
Q

The bloods have come back for an unwell patient. You review the bloods and notice a Stage 2 AKI. You assess the patient using an A-E approach. They appear dehydrated. Their blood pressure is 94/50. You give them a fluid bolus and they respond to this with an increase in their blood pressure. You discuss further fluid therapy with a senior member in your team. What further steps should you take?

A
  • Identify cause of AKI - if sepsis prompt treatment
  • Avoid nephrotoxins - aminoglycosides, NSAIDs
  • Adjust dose of renally excreted drugs - LMWH, opioids, penicillin, digoxin
  • Nutrition - seek dietician support
32
Q

When should you refer a patient with AKI to the renal team?

A
  • AKI stage 3 (SCr ≥3 × baseline value)
  • Persistent oliguria and/or rising serum creatinine despite supportive therapy
  • Complications refractory to medical treatment:
    • Hyperkalaemia (K+> 6.0 mmol/L)
    • Pulmonary oedema
    • Acidosis (pH <7.15)
    • Uraemic encephalopathy
    • Uraemic pericarditis
33
Q

One of the complications of AKI is hyperkalaemia. What are the signs of this on an ECG?

A
  • May be normal even in life-threatening hyperkalaemia
  • Peaked T waves
  • Prolonged PR interval and eventual loss of P wave • QRS widening
  • AV dissociation
  • Ventricular fibrillation or tachycardia
34
Q

When should you initiate immediate hyperkalaemia treatment?

A

K+ >6.5mmol/L

OR

ECG changes

35
Q

A patient with AKI develops hyperkalaemia. You treat hyperkalaemia with calcium gluconate, insulin and dextrose and salbutamol back to back nebulisers and have alerted a senior. The patients potassium still remains high. What are the next steps?

A

Urgent referral to nephrology

It must be remembered that unless the cause of the AKI is treated, the measures described are only temporary. The potassium will need to be monitored closely until recovery of sufficient kidney function to excrete potassium or renal replacement therapy is commenced.

36
Q

A patient with AKI has peaked T waves and prolonged PR interval on ECG. What are your next steps?

A
  • IV 10ml 10% calcium gluconate over 2-5 mins - rapidly stabilises myocardium
  • 10 UNITS ActRapid added to 50ml of 50% dextrose indused IV over 20 minutes - increases cellular potassium uptake
  • Medication review - stop drugs that contain potassium or interfere with renal excretion of potassium e.g. ACEi, ARB, beta blockers, potassium sparing diuretics
37
Q

What are the first signs of recovery from AKI?

A

an increase in urine output if the patient was oliguric

and/or

a reduction in the rise in the daily serum creatinine followed by a plateau in its value prior to a fall

38
Q

Why are some patients polyuric following AKI?

A

Recovery from AKI can result in a polyuric state in some patients with the production of large urine volumes until the capacity of the renal tubule to concentrate urine returns. There must therefore be careful attention to the patient’s volume status and fluid requirements.

39
Q

How should you manage discharge and follow-up after AKI?

A
  • Kidney function should be checked prior to discharge. Patients will require long-term follow up if there is evidence of chronic kidney disease (CKD). Refer patients to nephrology left with an estimated glomerular filtration rate (eGFR) <30 mL/min/1.73m2
  • Medications should be reviewed prior to discharge with a plan to reintroduce medications that may have been held during the acute illness, e.g. antihypertensives, diuretics at an appropriate time. This may require an early follow up with the GP.
  • Patients should be informed as to why they developed AKI and their risk factors. They should be told that this means they have a risk of developing CKD/or that they have developed CKD
40
Q

You are writing a discharge letter for a patient who developed AKI in hospital. What should be included regarding the AKI?

A
  • Severity of AKI
  • Cause of AKI
  • Risk factors for AKI
  • Discharge kidney function
  • Advice on whether medications need to be reviewed or reintroduced
41
Q

What should be monitored in a patient with AKI?

A
  • Fluid balance - fluid balance chart (consider catheterisation), regular clinical assessment of fluid status
  • K+ - check response to treatment and at least daily until creatinine falls
  • Observations - minimum every 4 hours
  • Lactate if signs of sepsis
  • Daily creatinine until this falls (lags approx 24 hours behind clinical response)
42
Q

You have given fluids to a septic patient with AKI. On clinical assessment, they have bibasal crackles and pitting oedema in their lower legs. What are your next steps.

A
  • A-E assessment
  • B - Oxygen supplementation if required
  • C - Fluid restriction - consider oral and iv volumes. Give antibiotics in minimal fluid and consider concentrated nutritional support preparations.
  • To treat the pulmonary oedema, consider CPAP and IV furosemide
  • Refer to nephrology for renal replacement therapy if refractory to treatment
43
Q

Once you have identified the cause of AKI, how would you broadly manage pre-renal, intrinsic and post-renal causes?

A
  • pre-renal - correct volume depletion and/or perfusion
  • renal - renal biopsy
  • post-renal - urinary catheter if below or nephrostomy drain if above bladder - refer to urology
44
Q

Interpret the following urinalysis results in a patient with AKI.

  • No blood or protein
  • Blood & protein
  • Blood
A
  • No blood or protein – pre-renal
  • Blood & protein – renal
  • Blood - post renal
45
Q

A patient with AKI has had urinalysis. Results show blood and protein. What are your next steps?

A

send urine for MSU & ACR (albumin:creatinine ratio) Consider renal screen if deteriorating renal function

If suspected intrinsic disease refer to Nephrologist

Medicine - Renal (1 decks)

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