Acute Kidney Injury Flashcards
1
Q
What are the functions of the kidneys?
A
- Body fluid homeostasis
- Regulation of vascular tone
- Excretory function
- Electrolyte homeostasis
- Acid-base homeostasis
- Endocrine function (erythropoietin, vitamin D)
2
Q
What is the traditional definition of AKI?
A
- Rapid loss of glomerular filtration and tubular function over hours to days
- Retention of urea/creatinine
- Oliguric / non-oliguric
- Potentially recoverable
3
Q
What classification system is used in AKI?
A
RIFLE
4
Q
What system is currently used to stage AKI?
A
KDIGO
5
Q
What are the stages in the development of AKI?
A
- Normal
- Increased risk
- Damage
- Decreased GFR
- Kidney failure
- Death
6
Q
What are stages of AKI defined by?
A
Creatinine and urine output (GFR)
7
Q
What is the incidence of AKI?
A
- 1 in 7 (some say 1 in 5) hospital admissions complicated by AKI
- Hospital admissions 1 in 5 to 7
- ITU admissions (more than half)
- In the Community (uncommon 1.5% per y)
8
Q
What are the immediately dangerous consequences of AKI?
A
- Acidosis
- Electrolyte imbalance
- Intoxication TOXINS
- Overload
- Uraemic complications
9
Q
What are the possible outcomes of AKI?
A
Short term (in hospital)
- Death
- Dialysis
- Length of stay
Intermediate/Long term (Post discharge)
- Death
- CKD
- Dialysis
- CKD related CV events
10
Q
When is it too late in AKI?
A
Once creatinine reaches 400
11
Q
What are the 3 classes of causes of AKI?
A
- Pre-renal (blood flow to the kidney)
- Renal (intrinsic) (damage to renal parenchyma)
- Post-renal (obstruction to urine exit)
12
Q
What are the pre-renal causes of AKI?
A
Reduction in effective circulating volume
- Sepsis
- Hypovolaemia
- Hepatorenal syndrome
- Cardiac failure
- Hypotension
Arterial occlusion
Vasomotor
-NSAIDs/ACEI
13
Q
What are the renal (intrinsic) causes of AKI?
A
- Acute tubular necrosis (ischaemia)
- Toxin related
- Acute interstitial nephritis
- Acute Glomerulonephritis
- Myeloma
- Intra-renal vascular obstruction (vasculitis and thrombotic microangiopathy)
14
Q
What are the post-renal causes of AKI?
A
Obstruction
- Intraluminal (calculus, clot, sloughed papilla)
- Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
- Extramural (RPF, malignancy)
15
Q
What is the most common cause of AKI?
A
Poor perfusion leading to established tubule damage
16
Q
What can sustained failure of circulation to the kidneys result in?
A
Acute tubular necrosis
17
Q
What can exacerbate acute tubular necrosis?
A
Toxic injury
18
Q
Why is the kidney susceptible to hypoperfusion?
A
- Intrarenal heterogeneity of blood supply, oxygenation and metabolic demand
- The cortex is richly perfused, whereas the medulla receives around 10-15% of renal blood flow
- Medulla hypoxic, yet metabolically active
19
Q
What does the kidney have the potential to do after AKI?
A
Regenerate
20
Q
Describe the course of acute ischaemic renal injury and recovery.
A
Initiation
- Exposure to toxic/ischaemic insult
- Renal parenchymal injury evolving
- AKI potentially preventable
Maintenance
- Established parenchymal injury
- Usually maximally oliguric now
- Typical duration 1-2 weeks (up to several months)
Recovery
- Gradual increase in urine output
- Fall in serum creatinine (may lag behind diuresis)
21
Q
When may excessive diuresis result during the recovery of AKI?
A
If GFR recovers quicker than tubule resorptive capacity, excessive diuresis may result (eg post-obstructive natriuresis
22
Q
What is radiocontrast nephropathy?
A
AKI following administration of iodinated contrast agent
23
Q
What is a common contributor to hospital acquired AKI?
A
Radiocontrast nephropathy
24
Q
How does radiocontrast nephropathy usually present?
A
-Usually transient renal dysfunction, resolving after 72h but may lead to permanent loss of function
25
What are the risk factors for RCN?
- Diabetes mellitus
- Renovascular disease
- Impaired renal function
- Paraprotein
- High volume of radiocontrast
26
What is the 2nd most common haematological malignancy?
Myeloma
27
What is the pathological process in myeloma?
A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
28
Who is myeloma common in?
The elderly
29
What are the clinical features of myeloma?
- Anaemia
- Back pain
- Weight loss
- Fractures
- Infections
- Cord compression
- Markedly elevated ESR
- Hypercalcaemia
30
How is myeloma diagnosed?
- Bone marrow aspirate - >10% clonal plasma cells
- Serum paraprotein ± immunoparesis
- Urinary Bence-Jones protein (BJP)
- Skeletal survey - lytic lesions
31
What can cause renal failure in myeloma?
- Cast nephropathy - ‘myeloma kidney’
- Light chain nephropathy
- Amyloidosis
- Hypercalcaemia
- Hyperuricaemia
32
Give examples of causes of AKI.
- Cardiac failure
- Haemorrhage
- Sepsis
- Vomiting diarrhoea
- Glomerulonephritis
- Vasculitis
- Radiocontrast
- Myeloma
- Rhadomyolysis
- Drugs (NSAIDs, Gentamicin)
- Stones
- Prostate disease
- Tumours
33
What investigations should be carried out for AKI?
- History
- Examination
- Drugs
- insults
- Renal function etc
- Urine dipstick
- FBC
- USS
- Blood gas
- Fancy blood tests for specifics if indicated
- Renal biopsy for histology
34
What is important to explore when taking a history of AKI?
- Past medical history / systemic diseases (new rash, nose bleeds, sore eyes, joint pains)
- Family history / social
- Drug exposure (what / when)
- Pre/post renal factors
- Uraemic symptoms
- Timing of symptoms – shortness of breath / urine output / vomiting etc.,
35
What is important to explore on examination of AKI?
- Vital signs (BP, pulse etc.,)
- Volume status
- Systemic illness (rash, joints, eyes etc.,)
- Obstruction
36
What blood tests should be carried out for AKI?
- FBC
- U+Es, bicarb, LFTs, bone
- Clotting
- Blood gas
- ANCA, Ig, C3 C4 dsDNA
37
What urine tests should be carried out for AKI?
- Urine dip (?blood, ?protein)
- Urine PCR or ACR
- Urine Bence Jones Protein
38
What radiological test may carried out in the diagnosis of AKI?
US
39
How is AKI prevented in hospitals?
- Avoid dehydration
- Avoid nephrotoxic drugs
- Review clinical status in those at risk… and act on findings.
- ? Hold medication
- ? Give fluids
- Treat sepsis
40
What is the STOP AKI prevention care bundle?
- Sepsis: if suspected screen and treat promptly
- Toxins: avoid
- Optimise: BP and volume status (avoid/correct hypovolaemia)
- Prevent: harm
41
What supportive management is there for AKI?
Fluid balance
- Volume resuscitation if volume deplete
- Fluid restriction if volume overload
Optimise blood pressure
- Give fluid /vasopressors
- Stop ACE inhibitors / anti-hypertensives
Stop nephrotoxic drugs
- NSAIDs
- Aminoglycosides
42
What are the 5 Rs for IV prescribing?
- Resuscitation
- Routine maintenance
- Replacement
- Redistribution
- Reassessment
43
What questions should you ask yourself when managing a patient with AKI?
- Do they need fluid
- Can you remove the precipitant?
- Can you stop it getting worse?
- Do they need a catheter?
- How to make them safe?
44
How can precipitants be removed?
- Stop drugs that are causing
- Treat sepsis
- Diagnose GN/other interstitial disease and give specific therapy
45
How can progression of AKI be prevented?
- Support BP
| - Reduce further insults i.e. do not give IV radiocontrast unless absolutely necessary
46
What ECG changes occur in hyperkalaemia?
- Peaked T waves
- Tall tented T waves
- P wave widens and flattens
- PR segment lengthens
- P waves eventually disappear
- Prolonged QRS interval with bizarre QRS morphology
- High-grade AV block with slow junctional and ventricular escape rhythms
- Any kind of conduction block (bundle branch blocks, fascicular blocks)
- Sinus bradycardia or slow AF
- Development of a sine wave appearance (a pre-terminal rhythm)
- Cardiac arrest
47
What rhythms of cardiac arrest can hyperkalaemia result in?
- Asystole
- Ventricular fibrillation
- PEA with bizarre, wide complex rhythm
48
What is the treatment for hyperkalaemia?
Stabilise (myocardium)
-Calcium Gluconate
Shift (K+ intracellularly)
- Salbutamol
- Insulin-Dextrose
Remove
- Diuresis
- Dialysis
- Anion exchange resins
49
Give examples of antidotes to toxins.
- Naloxone for morphine (and other opiates)
| - Digiband for Digoxin
50
What are the main indications for dialysis?
- Decreased bicarb
- Increased potassium
- Pulmonary oedema
- Pericarditis
51
How is haemodialysis carried out?
- Solute removal by diffusion
| - Intermittent therapy – each session lasting 3-5 hours
52
How is haemofiltration carried out?
- Solute removal by convection
- Larger pore size
- Continuous therapy
53
What are the advantages of haemodialysis?
- Rapid solute removal
- Rapid volume removal
- Rapid correction of electrolyte disturbances
- Efficient treatment for hypercatabolic patient
54
What are the disadvantages of haemodialysis?
- Haemodynamic instability
- Concern if dialysis associated with hypotension, may prolong AKI
- Fluid removal only during short treatment time
55
What are the advantages of CRRT?
- Slow volume removal associated with greater haemodynamic stability
- Absence of fluctuation in volume and solute control over time
- Greater control over volume status
56
What are the disadvantages of CRRT?
- Need for continuous anticoagulation
- May delay weaning/mobilisation
- May not have adequate clearance in hypercatabolic PATIENT
