Acute Kidney Injury Flashcards
(110 cards)
1
Q
Function of kidneys
A
Body fluid homeostasis - urine production Regulation of vascular tone - BP Excretory function - urea - creatinine - drugs Electrolyte homeostasis - Na, K, Cl, Ca, P Acid base homeostasis - H+ - bicarbonate Endocrine function - Erythropoietin - Vit D metabolism - Renin
2
Q
Traditional definition of acute renal failure
A
Rapid loss of glomerular filtration and tubular function over hours to days
3
Q
What does retention or urea/creatinine show?
A
Failure of homeostasis
4
Q
What is urea and creatinine excreted by?
A
The kidneys
5
Q
What can small rises in creatinine cause?
A
Increased odds of death
6
Q
Definition of acute kidney injury
A
Increase in serum creatinine
- By >26.5 umol/l (0.3mg/dl) within 48 hours OR
- to 1.5x baseline, which is known or presumed to have occurred within the prior 6 days
Urine volume <0.5ml/kg/h for 6 hours
7
Q
Stages of AKI
A
AKI 1
AKI 2
AKI 3
8
Q
What is AKI 1?
A
Serum creatinine - 1.5-1.9x baseline OR - 26.5 umol/l increase Urine output - < 0.5ml/kg/h for 6-12 hours
9
Q
What is AKI 2?
A
Serum creatinine
- 2.0-2.9 x baseline
Urine output
- <0.5 ml/kg/h for >12 hours
10
Q
What is AKI 3?
A
Serum creatinine - 3x baseline OR - Increase to >354 umol/l (and above) OR - initiation of RRT Urine output - < 0.3ml/kg/h > 24 hours OR - Anuria for > 12 hours
11
Q
Stages of AKI
A
Antecedents - normal - increased risk Intermediate stage - Damage AKI - Decreased GFR - kidney failure Outcomes - death - complications
12
Q
What are the stages of AKI defined as?
A
Creatinine
Urine output
13
Q
How many hospital admissions are complicated by AKI?
A
1 in 7
14
Q
What are the immediately dangerous consequences of AKI?
A
AEIOU A - acidosis E - Electrolyte imbalance I - Intoxication TOXINS O - overload U - uraemic complications
15
Q
Mortality of dialysis requiring-AKI in hospital
A
45-75%
16
Q
Mortality of non dialysis AKI stages
A
AKIN 1 - 8%
AKIN 2 - 25%
AKIN 3 - 33%
17
Q
What is the blood values where you would act on AKI?
A
Rise in serum creatinine >50% baseline
Baseline creatinine of 80umol/L
Rises to 120umol/L (may still be in normal range)
Significant kidney injury
18
Q
Pathological causes of AKI
A
Pre renal - blood flow to kidney
Renal (intrinsic) - damage to renal parenchyma
Post renal - obstruction to urine exit
19
Q
Causes of intrinsic AKI
A
Acute tubular injury - prolonged pre renal AKI - rhabdomyosis - haemoglobuineria - nephrotoxins (Iodinated contrast, NSAIDs, gentamicin) snake venom, heavy metals Mushrooms Acute tubular necrosis (ATN) Tubulointestinal injury Acute Glomerulonephritis Myeloma Vasculitis - Lupus - ANCA associated Thrombotic microangiopathy
20
Q
Causes of pre renal AKI
A
Sepsis Hypovolaemia - haemorrhage - burns - vomiting/diarrhoea - diuretics Hepatorenal syndrome Cardiac failure Liver failure Hypotension - medications
21
Q
Causes of post renal AKI
A
Kidney stones Clot Sloughed papilla Prostatic hypertrophy Tumours Ureteric stricture Retroperitoneal / radiation fibrosis RPF
22
Q
Commonest cause of AKI
A
Poor perfusion leading to established tubular damage
23
Q
Pathology of pre renal AKI
A
Failure of the circulation (loss of volume and/or pressure) to provide sufficient plasma flow to maintain blood chemistry and fluid balance
24
Q
Outcomes of pre renal AKI
A
If promptly treated, can resolve
If sustained, may lead to acute tubular necrosis
25
Why are the kidneys susceptible to hypoperfusion?
Blood supply
Oxygenation
Metabolic demand
26
Perfusion of kidneys
Cortex richly perfused
| Medulla receives around 10-15% of renal blood flow
27
Does the kidney have the potential to regenerate following an acute kidney injury?
Yes
28
Pathology of initiation of AKI
Exposure to toxic/ischaemic insult
Renal parenchymal injury evolving
AKI potentially preventable
29
Pathology of maintenance of AKI
Established parenchymal injury
Usually maximally oliguric now
Typical duration 1 - 2 weeks (up to several months)
30
Pathology of recovery of AKI
Gradual increase in urine output
Fall in serum creatinine (may lag behind diuresis)
If GFR recovers quicker than tubule resorptive capacity, excess diuresis may result (e.g. post obstructive natriuresis)
31
What is radiocontrast nephropathy (RCN)?
AKI following administration of iodinated contrast agent
32
Presentation of RCN
Transient renal dysfunction
| Resolving after 72 hours
33
What may RCN lead to?
Permanent loss of function
34
Risk factors for RCN
```
DM
Renovascular disease
Impaired renal function
Paraprotein
High volume of radiocontrast
```
35
What is myeloma?
A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
36
Who is myeloma common in?
Elderly
37
Presentation of myeloma
```
Anaemia
Back pain
Weight loss
Fractures
Infections
Cord compression
Marked elevated ESR
Hypercalcaemia
```
38
Investigations of myeloma
Bone marrow aspirate > 10% clonal plasma cells
Serum paraprotein +/- immunoparesis
Urinary Bence-Jones Protein (BJP)
Skeletal survery - lytic lesions
39
Pathology of renal failure in myeloma
```
Cast nephropathy 'myeloma kidney'
Light chain nephropathy
Amyloidosis
Hypercalcaemia
Hyperuricaemia
```
40
Investigations of AKI
```
Fluid status
Drugs
Insults
Renal failure
Urine dipstick
FBC
USS
Blood gas
Renal biopsy
Renal USS
```
41
What is better than treatment for AKI?
Prevention
42
At risk events for AKI occuring
Sepsis (e.g. pneumonia, cellulitis, UTI etc)
Toxins (e.g. X ray contrast, NSAIDs, gentamicin, herbal remidies)
Hypotension
Hypovolaemia
Major surgery
43
Causes of hypovolaemia
Haemorrhage
Vomiting
Diarrhoea
44
Risk factors for AKI
```
Age > 75
Previous AKI
Heart failure
Liver disease
Chronic kidney disease
DM
Vascular disease
Cognitive impairment
```
45
What is done to identify patients at risk of AKI?
In the presence of a risk event and one or more risk factors, consider activating the below STOP AKI Prevention care bundle
- STOP
- S = sepsis (if suspected screen and treat promptly - SEPSIS 6)
- T = Toxins - avoid (e.g. gentamicin, NSAIDs, iodinated contrast)
- O = optimise BP and volume status - avoid/correct hypovolaemia, review BP meds
- P = prevent harm - daily U and Es, fluid balance and medication review
46
Examples of nephrotoxic drugs
Gentamicin
NSAIDs
Iodinated contrast
Aminoglycosides
47
How should you optimise BP and volume status?
Consider IV fluids if hypovolaemic;
- resus fluids 250-500mls IV crystalloid ? bolus over 15 mins and review response
Withhold Antihypertensives
Withhold Diuretics
48
How is fluid balance monitored?
Input
Output
Daily weights
49
Treatment of AKI
```
Remove/treat cause if possible
If pre renal
- Fluid
- BP support
Renal
- remove participant
Post renal
- catheter
Treat sepsis
Stop/avoid potential nephrotoxins
Optimise BP
- fluids
- withhold antihypertensive drugs
Treatment of complications
```
50
What are the 5Rs from IV prescribing?
```
Resuscitation
Routine maintenance
Replacement
Redistribution
Reassessment
```
51
When would patients need replacement fluids?
If dont need urgent IV resuscitation but do need IV additional to maintenance to correct existing deficit or ongoing abnormal External losses e.g. diarrhoea, fever
52
When would patients need redistribution fluids?
When the patients have abnormal internal fluid redistribution or abnormal fluid handling, particularly with sepsis, or major illness, cardiac, liver or renal disease e.g. tissue oedema, GI tract/thoracic/peritoneal collection
53
How many ml from water are usually on the intake in health?
2500ml
| 25-35ml/kg/day
54
How much output of water is normal? How is water excreted from the body?
```
Urine
Insensible
- skin
- lungs
- faeces
```
55
How much Na and K are taken in on average?
1mmol/kg/day both
56
What is the only electrolytes dextrose contains?
Glucose
| variable K
57
What is the only electrolytes NaCl / glucose solution contains?
Na
Variable K
Cl
Glucose
58
What electrolytes does Hartmanns contain?
```
Na
K
Cl
Ca
Bicarb precursor (lactate)
```
59
What electrolytes does plasma contain?
```
Na
K
Cl
Ca
Bicarb
Glucose
```
60
What electrolytes does plasma lyte contain?
Na
K
Cl
Bicarb precursor (acetate and gluconate)
61
ECG changes in hyperkalaemia
```
Peaked T waves
- tall tented T waves
P wave widens and flattens
PR segment lengthens
P waves eventually disappear
Prolonged QRS interval
High grade AV block with slow junctional and ventricular escape rhythms
Sinus bradycardia or slow AF
Development of a sine wave appearance (a pre terminal rhythm)
Cardiac arrest
Asystole
VF
```
62
Treatment of hyperkalaemia
```
Stabilise myocardium
- calcium gluconate
Shift (K+ intracellularly)
- salbutamol
- insulin-dextrose
Remove
- diuresis
- dialysis
- anion exchange resins
```
63
Treatment of morphine toxicity
Naloxone
64
Treatment of digoxin toxicity
Digibind
65
Indication for dialysis in AKI
```
Acidosis
- Decreased HCO3
- Increased lactate
- increased pCO2
Electrolytes
- Increased K
- Increased or decreased Na
- Increased Ca
- Increased uric acid
- Increased PO4-
- Increased Mg2+
Intoxication
- aspirin
- theophylline
- lithium
- ethylene glycol
- methanol
- metformin
Overload
- nutrition
- pulmonary oedema
- HTN
Uraemia
- altered mental status
- Pericarditis
- unexplained bleeding
```
66
Solute removal in haemodialysis vs hemofiltration
Haemodialysis
- removal by diffusion
Haemofiltration
- removed by convection
67
What type of therapy is haemodyalsis?
Intermittent
| Each session lasting 3 - 5 hours
68
What type of therapy is haemofitration?
Continous
69
When is haemofiltration used?
In an ITU setting usually to treat AKI but can be used in multiple organ dysfunction or sepsis
70
Advantages of haemodialysis
Rapid solute removal
Rapid volume removal
Rapid correction of electrolyte disturbances
Efficient treatment for hypercatabolic patient
71
Disadvantages for haemodialysis
Haemodynamic instability
Concern if dialysis associated with hypotension, may prolong AKI
Fluid removal only during short treatment time
72
Advantages of continuous therapy
Slow volume removal associated with greater haemodynamic stability
Absence of fluctuation in volume and solute control over time
Greater control over volume status
73
Disadvantages of continuous renal replacement therapy
Need for continuous anticoagulation
May delay weaning/mobilisation
May not have adequate clearance in hypercatabolic patient
74
What is the staging system for AKI called?
AKIN staging system
75
How many stages are there in AKI?
3
76
What is the pneumonic to remember immediate problems of AKI?
AEIOU
77
What are the long term problems caused by AKI?
Secondary problems / infections
- pneumonia
- sepsis
- MI
78
What is the most common type of cause of AKI?
Pre renal AKI
79
What kind of obstruction of pre renal AKI is needed to cause an AKI?
Bilateral OR
| Unilateral with something else e.g. sepsis
80
Why in prevention of AKI are anti-hypertensives withholded?
Hypotension can cause an AKI
81
What medicines should be stopped on sick days? Give examples of "sick days"
ACEIs, ARBs, NSAIDs, Diuretics, Metformin
| Sick days = vomiting, diarhrhoea, vomiting, fever, sweats, shakes
82
What happens in the body when you are unwell?
Stimulate RAAS -> conserve salt and water
| Stimulate sympathetic system
83
Can metformin cause an AKI?
No, but it can cause lactic acidosis if unwell for another reason e.g. sepsis
84
Most patients with AKI will have a degree of what?
Hypovolaemia
85
What does ATN stand for?
Acute tubular necrosis
86
How can AKI cause ATN?
Insult to the kidneys so severe that they develop necrosis of the tubules
87
What is trimethoprim bad to use in?
CKD
88
What can trimethoprim cause in CKD?
Hyperkalaemia
Increased creatinine
Does not reduce GFR but inhibits the tubular secretion of creatinine and effects the K channels as well
89
Indications for RRT in AKI
Refractory AEIOU
90
What are the uraemic complications?
Uraemic encephalopathy
| Uraemic pericarditis
91
In hyperkalaemia, what can help stabilise the myocardium and how? Then what can be done once the K > 6.5?
Calcium gluconate 10mls/10% / calcium chloride
Does not lower the K but stops an MI
Then have to push potassium back into the cells by
- nebulised salbutamol 2.5-5mg
- insulin dextrose IV 6 - 10 units in 50mls/50% dextrose over 30 mins
92
What do nebulised salbutamol and insulin dextrose IV do?
Lower K+
93
Why should you not give diuretics in AKI? (unless in fluid overload)
Can worsen AKI
94
When having insulin dextrose, what should be done for a few hours after?
Monitor blood glucose
95
What group of patients are more likely to be hyperkalaemic and why?
DM patients
| Not as much insulin
96
What is renal papillary necrosis?
Coagulative necrosis of the renal papillae
97
Causes of renal papillary necrosis
```
Severe acute pyelonephritis
Diabetic nephropathy
Obstructive nephropathy
Analgesic nephropathy (NSAIDs)
Sickle cell anaemia
```
98
Presentation of renal papillary necrosis
Visible haematuria
Loin pain
Proteinuria
99
What investigation is required in the investigation of all patients presenting with an AKI of unknown etiology?
Renal USS
100
What is a sign of acute interstitial nephritis? What is it often due to?
Eosinophilic casts
| Often due to a drug reaction
101
Pathology of rhabdomyolysis
The toxicity of myoglobin on the tubular cells directly causes damage and necrosis of the cells - so causing tubular cell necrosis
102
What does a raised anion gap suggest?
Increased production or reduced excretion of fixed / organic acids
103
Examples of things causing raised anion gap acidosis
Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (DKA)
Drugs / Toxins (salicylates, methanol, ethylene glycol)
104
What is a metabolic acidosis with a normal anion gap due to?
Loss of bicarbonate or accumulation of H+ ions
105
Causes of metabolic acidosis with normal anion gap
Renal tubular acidosis
Diarrhoea
Addisons disease
Pancreatic fistula
106
What would indicate a AKI caused by dehydration?
A urea that is proportionally higher than the rise in creatinine
107
What should be considered in a young female patient who develops AKI after initiation of an ACEI?
Fibromuscular dysplasia
108
Causes of renal vascular disease
```
Renal artery stenosis secondary to atherosclerosis (90%)
Fibromuscular dysplasia (10%)
```
109
What % of patients with fibromuscular dysplasia are female?
90%
110
Presentation of fibromuscular dysplasia
HTN
CKD or acute renal failure e.g. 2ndry to ACEI initiation
'Flash' Pulmonary oedema
