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Diploma in Anaesthesia > Acute Renal Failure and the Effects of Anaesthesia on Renal Function > Flashcards

Acute Renal Failure and the Effects of Anaesthesia on Renal Function Flashcards

1
Q

Suggest a definition for acute renal failure

A

Acute renal failure is a sudden (within 1 - 7 days) and persistent (>24 hours) decrease in renal function leading to the accumulation of nitrogenous and non-nitrogenous waste products.

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2
Q

What prompted the establishment of the RIFLE criteria in 2004

A

There are more than 30 definitions of acute renal failure. Most relate to absolute or relative changes in serum creatinine.

A lack of consensus in definitions has made comparisons of studies in the literature difficult

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3
Q

What does RIFLE stand for

A 
Risk
Injury
Failure
Loss
ESKD
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4
Q

What is the RIFLE criteria used for

A

The RIFLE criteria allow for AKI to be objectively and uniformly defined.

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5
Q

Describe the RIFLE criteria

A

Risk:
SCr x 1.5 or GFR >25 % | UO < 0.5ml/kg/hr x 6h

Injury:
SCr x 2 or GFR >50% | UO < 0.5ml/kg/hr x 12h

Failure:
SCr ≥ 354 umol/L or acute rise ≥ 44umol/L or
SCr x 3/GFR >75% | UO< 0.3 ml/kg/hr x 24h / anuria x 12h

Loss:
ARF > 1/12

ESKD
ARF > 3/12

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6
Q

Classify Acute Kidney Injury

A

Classifying changes have to occur within 48 hours

Stage 1
Baseline SCr x 1.5 to 2.0
UO < 0.5 ml/kg/hr x 6 - 12 h

Stage 2
Baseline SCr x 2 - 3
UO < 0.5 ml/kg/hr x > 12 h

Stage 3
Baseline SCr > x 3 or SCr ≥ 354 umol/L with acute Increase of 44 umol/L
UO < 0.3 ml/kg/hr x 24 hours or anuria x 12 hours

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7
Q

What is the Cockcroft Gault equation

A

Estimated GFR = 1.22(140-age) x weight (kg) x SCr

x 0.85 if female

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8
Q

How is body surface area calculated from weight and height

A

Mosteller formula

= √[(cm x kg)/3600]
= xxx m^2

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9
Q

What is the normal range for GFR adjusted for body surface area?

A

100 - 130 ml/min/1.73m^2

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10
Q

What is urea?

A

by-product of protein metabolism

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11
Q

What are the effects of urea retention

A
  1. Increased oxidative stress
  2. Altered regulation of K+ and H20 regulation (altered Na/K/Cl co-transport function)
  3. Altered immune function
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12
Q

Why can’t urea be used to calculate GFR

A

Urea rises as GFR falls but the relationship is NON-LINEAR

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13
Q

What increases the rate of urea production

A
  1. High protein intake
  2. ‘Protein meal’ from an upper GI bleed
  3. Critical illness (sepsis/burns/trauma)
  4. Drug therapy: tetracyclines and corticosteroids
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14
Q

What reduces plasma urea levels (even if GFR is reduced)

A
  1. Chronic liver disease

2. Low protein intake

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15
Q

Why is there is disproportionate increase in urea in states of acute volume depletion

A

Compensatory mechanisms (RAAS) lead to enhanced reabsorption of Na and H2O in the PCT. Re-absorption of urea in the PCT is simultaneously enhanced leading to a disproportionate increase in urea versus creatinine

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16
Q

What % of urea is passively reabsorbed in the PCT

A

40 - 50% of urea filtered

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17
Q

What is creatine phosphate

A

Creatine phosphate is a rapidly mobilizable potential store for high energy phosphate bonds in myosites and neurones.

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18
Q

What is creatinine, how is it produced and excreted

A

Creatinine is an amino acid product of creatine phosphate metabolism.

Released into plasma at a relatively constant rate (c.f. urea)
Filtered freely at glomerulus
Neither reabsorbed nor metabolized by the kidney

19
Q

What % of kidney function should be lost before a rise in serum creatinine is observed

A

> 50%

20
Q

Why does serum creatinine not rise until approximately 50% of kidney function is lost

A

10 - 40% of creatinine clearance occurs by tubular secretion. As GFR falls secretion may increase preventing an immediate rise in creatinine subsequent to declining GFR

21
Q

Which drugs impair creatinine secretion causing a transient reversible increase in serum creatinine

A

Trimethoprim

Cimetidine

22
Q

What factors affect creatinine production

A 
Age (less)
Sex (male more)
Dietary intake (more protein more Cr)
Muscle mass (more mass more Cr)
Disease (rhabdomyolysis)
23
Q

Does serum creatinine depict real time changes in GFR with acute reductions in kidney function

A

NO - Time is required for accumulation to occur prior to detection of abnormal raised levels - this results in a delayed diagnosis of AKI

24
Q

What are the limitations of urine output as a gauge of kidney function

A

UO lacks sensitivity and specificity for acute kidney injury. Even patients with severe AKI, characterized by a marked raise in SCr, can maintain normal or raised urine output.

25
Q

How should urine output be used clinically to assess kidney function

A

Trends of urine output over a period of time are useful clinical barometer of GFR

26
Q

What limits the use of UO as a gauge of kidney function during the intra-operative period?

A

Increased ADH release in response to surgical stress reduces intra-operative urine output. However, if the UO reduction persists, alternate explanations must be sought

27
Q

Case: An otherwise fit 57-year-old Caucasian male underwent a difficult elective open abdominal aortic aneurysm repair 12 hours ago with a prolonged aortic cross clamp time. He has passed no urine postoperatively, his preoperative creatinine was 122 μmol/L and is 136 μmol/L postoperatively.

Select one option from the answers below.

Possible answers:
A.	At risk 	 
B.	Renal injury 	 
C.	Renal failure 	
D.	Unable to classify
A

C - Renal Failure

His urine output places him in the failure group.

The change in creatinine level is below that required to suggest failure, but this is due to the short time interval resulting in a lack of significant accumulation.

28
Q

Classify the causes of pre-renal failure

A
  1. Reduced absolute circulating volume
    - haemorrhage
    - dehydration
    - redistribution (third space fluid loss)
  2. Reduced effective circulating volume
    - Heart failure
    - Decompensated liver cirrhosis
  3. Arterial occlusion or stenosis of renal artery or raised intra-abdominal pressure
  4. Reduced CO
    - Myocardial ischaemia
    - Tamponade
  5. Drugs
    - ACEi
    - NSAIDS
29
Q

Describe the different biochemical urinary measurements in pre-renal and renal failure

A

Urinary Na (mmol/L)

  • Pre-renal: <20
  • Renal: >40

FeNa

  • Pre-renal: <1%
  • Renal: >1%

Urinary Osmolarity (mosm/L)

  • Pre-renal: >500
  • Renal: <350

Urine/plasma urea

  • Pre-renal: >8
  • Renal: < 3

Urine microscopy
- Pre-renal: Hylaine or fine granular casts
- Renal: Coarse granular muddy brown and mixed cellular casts
(- vasculitis/GN - dysmorphic RBCs or RBC casts)

Specific gravity

  • Pre-renal: High - 1,020
  • Renal: Fixed 1,010 - 1,020
30
Q

Classify the causes of intra-renal failure

A

Endogenous toxins

  • Rhabdomyolysis (myoglobinuria)
  • Haemolysis (haemoglobinuria)
  • Myeloma
  • Intratubular crystals (uric acid/oxalate)

Exogenous toxins

  • Aminoglycosides
  • Radiocontrast
  • Cisplatin

Vascular

  • Malignant hypertension
  • Vasculitis
  • Acute Glomerulonephritis

Ischaemia/Sepsis

Drugs

  • Antibiotics (penicillins, cephalosporins, quinolones)
  • NSAIDS
  • Diuretics (thiazides, furosemide)
  • Allopurinol
  • Phenytoin
  • Rifampicin
31
Q

How do NSAIDS cause pre-renal failure

A

Prostaglandins (PGs) with best-defined renal functions are PGE2 and prostacyclin (PGI2). These vasodilatory PGs increase renal blood flow and glomerular filtration rate under conditions associated with decreased actual or effective circulating volume, resulting in greater tubular flow and secretion of potassium.

NSAIDS inhibit COX enzyme which inhibits the production of PGE2 and PGI2 locally in the kidney leading to a loss of the protective vasodilatory effects

32
Q

Describe the problems encountered with ARF

A
  1. Volume overload and pulmonary oedema
  2. Electrolyte imbalance (K+)
  3. Metabolic acidosis
  4. Uraemia - e.g. pericarditis
  5. Altered drug handling
    - Reduced excretion and potential accumulation
    - Acidosis/Uraemia displace protein bound drugs
33
Q

What are the ECG findings in hyperkalaemia

A

Flat P
Widened QRS
Peaked T
Progressing toward sine wave pattern

Non-specific repolarization abnormalities
Bradycardia
AV block
Cardiac arrest: PEA/Asystole/VF

34
Q

What is the treatment of severe hyperkalaemia?

A
  1. OMIGABCDE
  2. Discontinue cause if possible
  3. ECG findings: Give calcium chloride 10% 10ml over 10 min (Or calcium gluconate10 ml - repeated x3 if required)
  4. K+ shift: 50ml 50% dex with 10U actrapid then 10% Dex follow up infusion monitor hgt
  5. Salbutamol 10 -20 mg neb
  6. Fluid overloaded: NaHCO3- 8.4 % 50 - 100 mls
    Fluid depleted - start with isotonic NaHCO# after calculating HCO3- deficit
  7. Increase K+ excretion (Kayexelate vs furosemide)
35
Q

What are indications for early Renal Replacement Therapy

A
  1. Hyperkalaemia with ECG changes
  2. Severe pulmonary edema
  3. Uraemic pericarditis resulting in obstructive shock
36
Q

What are the relative indications for RRT

A 
Oliguria - UO < 200 ml in 12 h
Anuria - UO < 50 ml in 12 h
Hyperkalaemia > 6.5 mmol/L
Severe acidaemia pH < 7.0
Azotaemia: Urea > 30 mmol/L
Uraemic complications: 
- encephalopathy
- pericarditis
- neuropathy
Hyperthermia
Drug overdose with dialysable toxin
37
Q

What should be considered prior to taking a patient who has recently had RRT to theatre

A
  1. ? anticoagulant used on filter and platelet count
  2. ? volume status (fluid removed during RRT)
  3. ? vascular access (fistulae C/I unless life threatening issue)
  4. Ineffective RRT possible: check and Rx UE and CMP before anaesthesia
38
Q

What different anticoagulants can be used on the haemodialysis filter

A
  1. Heparin
    - Most common agent used
    - T1/2 heparin is 90 minutes
    - check aPTT
    - check platelets (consumed on filter)
    - Caution: neuraxial blockade
  2. None
    - If systemically anticoagulated
    - OR if at risk of bleeding
    - Can reduce filter time as clot more likely and full dose RRT may not be achieved
  3. Prostacyclin (epoprostenol)
    - Direct inhibition of platelet aggregation
    - T1/2 = 2 minutes
    - Used if heparin contra-indicated or in combination with heparin in a prothrombotic patient
  4. Citrate
    - Chelates calcium and prevents clotting
    - Calcium has to be replaced in the blood returning to the patient
    - Check Ca levels
39
Q

Describe pharmacalogical alterations in patients at risk of or with ARF

A
  1. Induction agents - limit dose to avoid hypotension
  2. NMB
    - SUX - consider possible K + rise (use Roc for RSI)
    - Atracurium ideal (Hofmann degradation)
    - Vecuronium and mivacurium ok (minimal renal excretion)
  3. Volatile agents: Avoid Sevoflurane
  4. Analgaesia:
    - Avoid large repeated doses morphine/pethidine.
    - Avoid NSAIDS
  5. Antibiotic prophylxis
    - Dose adjustment
    - Avoid aminoglycosides
  6. Anticoagulants
    - LMWH - needs dose adjustment
40
Q

Why should sevoflurane be avoided in ultra-low flow circuits?

A

Undergoes temperature-dependent degradation by baralyme and soda lime –> formal a special haloalkene = compound A.

Compound A is metabolized to nephrotoxins which can result in kidney damage (theoretical risk)

No demonstrated increase in risk of ARF with sevoflurane in millions of anaesthetics worldwide

41
Q

Describe the SNS response to hypovolaemia and the local role of prostaglandins in the kidney

A

SNS –> VC autoregulation to maintain filtration pressure

PGI2 is released locally to cause local vasodilatation and partially oppose the VC

NSAIDS –> unopposed vasoconstriction and may cause further deterioration in renal function

42
Q

Why are morphine and pethidine less suitable in patients with renal failure.

Which opioids are preferred in ARF

A

Morphine-6-glucoronide (active metabolite or morphine) –> excessive prolonged opioid effects/side effects

Norpethidine (metabolite of pethidine) –> pro-convulsant –> accumulates in renal failure

Fentanyl and alfentanil –> use as normal but remember that they have context specific half life if used as infusions

Fentanyl PCA instead of morphine PCA

43
Q

What happens to the renal blood flow autoregulatory range in hypertension

A

it shifts to the right and is narrower meaning that at MAP that achieve adequate renal blood flow in normotensive patients may generate insufficient renal blood flow in hypertensive patients as the autoregulatory range has narrowed and shifted

(Draw Graph relative renal blood flow to MAP)

44
Q

What should be considered with regard to neuraxial blockade in patients with ARF

A

Consider that sympathetic blockade may extend above renal sympathetic fibres –> loss of normal autoregulatory mechanisms to maintain renal perfusion

Caution is also required with the timing of the pre- and postoperative dialysis due to the potential use of anticoagulation

Diploma in Anaesthesia (73 decks)

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