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Renal medicine > AKI > Flashcards

AKI Flashcards

1
Q

Define AKI

A

It is defined as a rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine, and leading to a failure to maintain fluid, electrolyte and acid–base homeostasis.

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2
Q

What is the pathophysiology of AKI?

A

There are many causes of AKI and it is frequently multifactorial. It is helpful to classify it into three subtypes:
• ‘pre-renal’, when perfusion to the kidney is reduced
• ‘renal’, when the primary insult affects the kidney itself
• ‘post-renal’, when there is obstruction to urine flow at any point from the tubule to the urethra (Fig. 15.18).

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3
Q

List some pre-renal causes of AKI

A

In pre-renal AKI, a reduction in perfusion reduces GFR
Impaired perfusion:
•Hypovolaemia (decrease in circulating volume e.g. dehydration, haemorrhage)
•Hypotension (decrease vascular resistance e.g. sepsis, pancreatitis)
•Heart failure (poor perfusion and cardiac output)
•Reduced local perfusion of kidneys (e.g. dissecting aneurysm, renal emboli)

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4
Q

List some renal causes of AKI

renal parenchymal disorders (injury to glomerulus, tubule or vessels)

A

Multiple myeloma

Infectious causes (Malaria, Legionnaires’ disease, Leptospirosis)

Vascular causes 
•	Vasculitides
•	Haemolytic uraemic syndrome 
•	Thrombcytic thrombocytopenic purpura 
•	Disseminated intravascular coagulation 
•	Malignant hypertension 
•	Scleroderma
  • Interstitial causes - Interstitial nephritis (usually caused by drugs e.g. NSAIDs, abx)
  • Glomerular causes - Glomerulonephritis
  • Tubular causes - Acute tubular necrosis
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5
Q

List some post renal causes of AKI

A 
Ureter 
•	Abdominal/pelvic mass compressing 
•	Complication of pelvic surgery 
•	Bilateral calculi  
•	Retroperitoneal fibrosis 
Bladder
•	Neuropathic bladder 
•	Anticholinergic or sympathomimetric drugs 
•	Bladder stones or tumour 
•	Uterovaginal prolapse 
Urethra
•	BPH, prostate cancer
•	Blocker catheter, trauma
•	Urethral stricture 
•	Infection e.g. Herpes (cos painful)
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6
Q

What features of a history might be suggestive of a pre-renal AKI?

A

Volume depletion (vomiting, diarrhoea, burns, haemorrhage)
Drugs (diuretics, ACE inhibitors, ARBs, NSAIDs, calcineurin inhibitors, iodinated contrast)
Liver disease
Cardiac failure

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7
Q

What might a patient tell you in the history that might be suggestive of a renal AKI? [particularly linked to ATN]

A

Prolonged pre-renal state
Sepsis
Toxic ATN: drugs (aminoglycosides, cisplatin, tenofovir, methotrexate, iodinated contrast)
Other (rhabdomyolysis, snake bite, Amanita mushrooms)

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8
Q

What might you see on examination of a patient with pre-renal aki?

A

Low BP (including postural drop) Tachycardia
Weight decrease
Dry mucous membranes and increased skin turgor
JVP not visible even when lying down

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9
Q

What are the complications of an AKI and what should you do to avoid these?

A

• Hyperkalaemia
• Pulmonary oedema
•Uraemia—may require dialysis if severe or complications, eg encephalopathy,
pericarditis, contact renal team. Otherwise symptomatic management.
• Acidaemia—may require dialysis, consider sodium bicarbonate orally or IV if in
HDU/ICU setting, discuss with nephrology before initiating.

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10
Q

What are the functions of the kidney?

A 
Blood
Electrolytes (Na, K, Cl-)
Acid-base balance [pH/H+/HCO3-]
Volume 
Hb

BP: RAAS (Na ions)

Hormonal control
EPO
Vit. D hydroxylation
Local prostaglandins circulation in kidney
Renin
Prolactin-hyperprolactinaemia
insulin

Removal of toxins and waste:urea

Urine production

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11
Q

Based on the list of functions, what are the possible implications of kidney failure?

A 
Hyperkalaemia
Metabolic acidosis
Anaemia: EPO fails
In CKD: increased renin leads of increased BP (N.B. increased bp also causes renal failure)
hypocalcaemia
hyperphosphatemia
tertiary hyperparathyroidism
drugs-Abx reduced dose as some are cleared by the kidney
Oliguric--> anuric which is 5ml/hr
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12
Q

Generally speaking, how is AKI recognised?

A

AKI is usually recognized by a falling urine output and rising serum urea and creatinine, or both

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13
Q

What can cause a reduced conc of urea?

A

Low protein intake
Liver failure
Sodium valproate treatment

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14
Q

What can cause an increased conc. of urea?

A

Corticosteroid treatment
Tetracycline treatment
Gastrointestinal bleeding

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15
Q

What can cause an increased in creatinine?

A

High muscle mass
Red meat ingestion
Muscle damage (rhabdomyolysis)
Decreased tubular secretion (e.g. therapy with cimetidine or trimethoprim)

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16
Q

What causes a reduction in creatinine?

A

Low muscle mass

17
Q

CASE ONE: Mrs Chowdhury is a 68 year old woman who is recovering from surgery. You have been bleeped and told she has not passed urine in in her catheter bag for the last 6 hours. What could you ask the nurse to do while they wait for your arrival?

A
  • Have the fluid chart ready to show trend – gradual decrease? Suddenly stopped?
  • If it suddenly stopped it might be blocked. Have they tried flushing it?
  • Observations to know how unwell she is and prioritise.
18
Q

The nurse tells you the output has been decreasing gradually, and that she already ensured that the catheter isn’t blocked. Observations: Heart rate 100bpm, Resp rate 12/min, temp 36.8, Blood pressure 115/65, O2 sats 97%.
Does she need review?

A
  • Yes because Normal is 0.5ml/kg/hr
  • Reduced urine output (oliguria) = <30mL/hour. Anuria- complete absence of urine output.
  • Oliguria may be the first and only sign of impending acute renal failure
  • If left untreated complications include: hyperkalaemia, metabolic acidosis, pulmonary oedema
19
Q

You arrive on the ward and find Mrs Chowdhury fast asleep and with normal obs apart from her anuria.
What clues in the notes might help establish the cause of the poor urine output?

A
  • Fluid balance chart (intake? Positive balance? Restrictions?)- should be 3 L in and more if febrile.
  • In (oral, IVI, NG) Out (urine, fluid faeces, NG, vomit, stoma, drain, wounds) Daily weights?
  • Surgical notes (type of surgery- pelvic? Bladder? Laparotomy or long surgery= dehydration, blood loss)
  • Drug chart (nephrotoxic drugs- NSAIDs, gentamicin, vancomycin, ACEi, diuretics, IV contrast)
  • Bloods- Hb and Renal function (50% increase in baseline creatinine =AKI)
  • PMH (HTN, DM, cardiac disease, HF)
20
Q

After taking a history you suspect that Mrs Chowdhury has reduced urine output due to hypovolaemia. Outline how you plan to assess her hydration status to support your suspicion.

A

General inspection:
• Age (elderly/very young= at risk) and elderly generally more likely CKD and CCF)
• Shortness of breath (may indicate pulmonary oedema)
• Scars/dressings indicating recent surgery
• Visible oedema (indicating fluid overload)
• Colour (pallor may indicate hypovolaemia secondary to blood loss)

Hands
• Any oedema? or peripheral stigmata of relevant diseases e.g. leukonychia- ?nephrotic syndrome
• Assess peripheral temperature – cool peripheries may indicate hypovolaemia
• Palpate the radial pulse – tachycardia may indicate hypovolaemia
• Check capillary refill time (normal <2 seconds) – prolonged in hypovolaemia

Arms:
• Lying/standing BP: drop of 20mmHg systolic on standing= postural hypotension = hypovolaemia.
• Assess skin turgor: decreased skin turgor in dehydration (unreliable in elderly)

  • Face: Mouth: dry mucous membranes – dehydration
  • Eyes: Sunken eyes- dehydration. Conjunctival pallor- underlying renal/cardiac disease or haemorrhage)

• Neck: If JVP > 3cm you need to consider fluid overload

  • Chest: >RR- ?pulmonary oedema secondary to fluid overload. Central capillary refill.
  • Heart sounds: S3 gallop rhythm may be heard in fluid overload.
  • Auscultate the lungs – bilateral coarse crackles may indicate pulmonary oedema
  • Abdomen: ?distended abdomen ?shifting dullness to differentiate ascites from other causes of distension
  • Legs: Check for pedal oedema and level – associated with fluid overload

Ref: CCE2/2019 Workshops : Clinical approach to renal disease

21
Q

Can you think of any patients that are at increased risk of developing AKI?

A
  • Age more than 75 years
  • Chronic kidney disease
  • Previous AKI
  • Diabetes mellitus
  • Heart failure
  • Vascular disease
  • Liver disease
  • Cognitive impairment
22
Q

AKI Risk Events

A
  • Sepsis e.g. Pneumonia, cellulitis, UTI etc
  • Burns
  • Toxins e.g. NSAIDs, Gentamicin, diuretics, ACE inhibitors, contrast media, ARBs
  • Hypotension e.g. relative to baseline BP
  • Hypovolaemia e.g. haemorrhage, vomiting, diarrhoea
  • Major Surgery (planned or emergency) – bleeding, drainage, third space fluid losses
23
Q

How might the approach to prescribing in a patient with AKI differ?

A
  • Eliminate the potential cause/risk/contributory factor for AKI
  • Avoid inappropriate combinations of medications in the context of AKI
  • Ensure that doses of prescribed medication are appropriate for the patient’s level of renal function
  • Ensure that all medicines prescribed are clinically appropriate.
  • Monitor blood levels of drugs wherever possible
  • Keep course of treatment as short as possible
  • Discuss treatment with pharmacist/microbiologist
  • https://renaldrugdatabase.com/
24
Q

What are some causes of hypovolaemia?

A
  • Dehydration
  • Reduced intake (nil by mouth, confusion)
  • Gut losses (vomiting, nasogastric tube losses, diarrhoea)
  • Renal losses (diuretics, hyperglycaemia)
  • Burns, sweating
  • Haemorrhage
  • Third space losses (pancreatitis, peritonitis, bowel obstruction)
  • Systemic vasodilatation (septic shock, cirrhosis)
  • Cardiac failure or shock (myocardial infarction, arrhythmias, cardiomyopathy, tamponade)
25
Q

How may patients with renal disease present?

A 
Renal pain and dysuria
Oliguria and polyuria
AKI
Proteinuria and nephrotic syndrome
Haematuria
CKD
!SILENCE!-so we do U&amp;Es before surgery and other major interventions
26
Q

What is the KDIGO staging of AKI?

A

Stage 1:
Increase >26μmol/L in 48h OR increase > 1.5 x baseline

<0.5mL/kg/h for >6 consecutive hours

Stage 2
Increase 2-2/9 x baseline
<0.5mL/kg/h for >12h

Stage 3
Increase >3 ≈ baseline OR >354 μmol/L OR commenced on RRT irrespective of stage

<0.3mL/kg/h for >24h or anuria for 12h

27
Q

How do you manage hyperkalaemia

A 
 10mL of 10% calcium gluconate IV via a big vein over 2min, repeated as neces-
sary until ECG improves. This is cardioprotective but does not affect K+ level.
 Intravenous insulin + glucose:  Insulin stimulates intracellular uptake
of K+, lowering serum K+ by 1–2mmol/L over ~60min.
 Salbutamol nebulizers work in the same way as insulin/glucose but high doses
are required (10–20mg) and tachycardia can limit use.
 If venous bicarbonate low (ie patient is acidotic) giving IV sodium bicarbonate
(eg 50mL of 8.4% NaHCO3 as an infusion or bolus into a big vein) can help to
drive K+ into cells, though the effect is unpredictable.
28
Q

How do you manage pulmonary oedema?

A
  • Sit up and give high-flow O2
  • Venous vasodilator, eg diamorphine 2.5mg IV (+antiemetic, eg cyclizine 50mg IV).
  • Furosemide 80–250mg IV either as IVI over 1h or boluses titrated to response (larger doses are needed in renal failure).
  • If no response, urgent haemodialysis or haemofiltration is needed.
  • Consider continuous positive airway pressure ventilation (CPAP). • IV nitrates also have a role
29
Q

How do you treat the underlying cause of an intrinsic renal AKI?

A

Refer EARLY to nephrology if concern over tubulointerstitial or glomerular pathology, any signs of systemic disease, multi-organ involvement (eg pulmonary-renal, hepatorenal syndromes) or indications for dialysis

Renal medicine (4 decks)

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