Acute Kidney Injury Flashcards
what are the functions of the kidneys?
homeostasis of:
- body fluids (urine production)
- electrolytes (Na, K,Cl, Ca, P)
- acid-base (H+, bicarbonate)
regulation of:
- vascular tone (blood pressure)
- excretory function (drugs, urea, creatinine)
- endocrine function (erythropoietin, vitamin D, renin)
what is the traditional definition of AKI?
- increase in serum creatinine
- decrease of urine ouput
What are the stages in the development of AKI?
- Normal
- Increased risk
- Damage
- Decreased GFR
- Kidney failure
- Death
What are stages of AKI defined by?
Creatinine and urine output (GFR)
What is the incidence of AKI?
- 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)
What are the immediately dangerous consequences of AKI?
- Acidosis
- Electrolyte imbalance
- Intoxication TOXINS
- Overload
- Uraemic complications
What are the possible outcomes of AKI?
Short term (in hospital)
- Death
- Dialysis
- Length of stay
Intermediate/Long term (Post discharge)
- Death
- CKD
- Dialysis
- CKD related CV events
When is it too late in AKI?
Once creatinine reaches 400
What are the 3 classes of causes of AKI?
- Pre-renal (blood flow to the kidney)
- Renal (intrinsic) (damage to renal parenchyma)
- Post-renal (obstruction to urine exit)
What are the pre-renal causes of AKI?
Reduction in effective circulating volume
- Sepsis
- Hypovolaemia
- Hepatorenal syndrome
- Cardiac failure
- Hypotension
Arterial occlusion
Vasomotor
-NSAIDs/ACEI
What are the renal (intrinsic) causes of AKI?
- Acute tubular necrosis (ischaemia)
- Toxin related
- Acute interstitial nephritis
- Acute Glomerulonephritis
- Myeloma
- Intra-renal vascular obstruction (vasculitis and thrombotic microangiopathy)
What are the post-renal causes of AKI?
Obstruction
- Intraluminal (calculus, clot, sloughed papilla)
- Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
- Extramural (RPF, malignancy)
What is the most common cause of AKI?
Poor perfusion leading to established tubule damage
What can sustained failure of circulation to the kidneys result in?
Acute tubular necrosis
What can exacerbate acute tubular necrosis?
Toxic injury
Why is the kidney susceptible to hypoperfusion?
- 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
What does the kidney have the potential to do after AKI?
Regenerate
Describe the course of acute ischaemic renal injury and recovery.
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)
When may excessive diuresis result during the recovery of AKI?
If GFR recovers quicker than tubule resorptive capacity, excessive diuresis may result (eg post-obstructive natriuresis
What is radiocontrast nephropathy?
AKI following administration of iodinated contrast agent
What is a common contributor to hospital acquired AKI?
Radiocontrast nephropathy
How does radiocontrast nephropathy usually present?
-Usually transient renal dysfunction, resolving after 72h but may lead to permanent loss of function
What are the risk factors for RCN?
- Diabetes mellitus
- Renovascular disease
- Impaired renal function
- Paraprotein
- High volume of radiocontrast
What is the 2nd most common haematological malignancy?
Myeloma
What is the pathological process in myeloma?
A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
Who is myeloma common in?
The elderly
What are the clinical features of myeloma?
- Anaemia
- Back pain
- Weight loss
- Fractures
- Infections
- Cord compression
- Markedly elevated ESR
- Hypercalcaemia
How is myeloma diagnosed?
- Bone marrow aspirate - >10% clonal plasma cells
- Serum paraprotein ± immunoparesis
- Urinary Bence-Jones protein (BJP)
- Skeletal survey - lytic lesions
What can cause renal failure in myeloma?
- Cast nephropathy - ‘myeloma kidney’
- Light chain nephropathy
- Amyloidosis
- Hypercalcaemia
- Hyperuricaemia
Give examples of causes of AKI.
- Cardiac failure
- Haemorrhage
- Sepsis
- Vomiting diarrhoea
- Glomerulonephritis
- Vasculitis
- Radiocontrast
- Myeloma
- Rhadomyolysis
- Drugs (NSAIDs, Gentamicin)
- Stones
- Prostate disease
- Tumours
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
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.,
What is important to explore on examination of AKI?
- Vital signs (BP, pulse etc.,)
- Volume status
- Systemic illness (rash, joints, eyes etc.,)
- Obstruction
What blood tests should be carried out for AKI?
- FBC
- U+Es, bicarb, LFTs, bone
- Clotting
- Blood gas
- ANCA, Ig, C3 C4 dsDNA
What urine tests should be carried out for AKI?
- Urine dip (?blood, ?protein)
- Urine PCR or ACR
- Urine Bence Jones Protein
What radiological test may carried out in the diagnosis of AKI?
US
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
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
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
What are the 5 Rs for IV prescribing?
- Resuscitation
- Routine maintenance
- Replacement
- Redistribution
- Reassessment
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?
How can precipitants be removed?
- Stop drugs that are causing
- Treat sepsis
- Diagnose GN/other interstitial disease and give specific therapy
How can progression of AKI be prevented?
- Support BP
- Reduce further insults i.e. do not give IV radiocontrast unless absolutely necessary
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
What rhythms of cardiac arrest can hyperkalaemia result in?
- Asystole
- Ventricular fibrillation
- PEA with bizarre, wide complex rhythm
What is the treatment for hyperkalaemia?
Stabilise (myocardium)
-Calcium Gluconate
Shift (K+ intracellularly)
- Salbutamol
- Insulin-Dextrose
Remove
- Diuresis
- Dialysis
- Anion exchange resins
Give examples of antidotes to toxins.
- Naloxone for morphine (and other opiates)
- Digiband for Digoxin
What are the main indications for dialysis?
- Decreased bicarb
- Increased potassium
- Pulmonary oedema
- Pericarditis
How is haemodialysis carried out?
- Solute removal by diffusion
- Intermittent therapy – each session lasting 3-5 hours
How is haemofiltration carried out?
- Solute removal by convection
- Larger pore size
- Continuous therapy
What are the advantages of haemodialysis?
- Rapid solute removal
- Rapid volume removal
- Rapid correction of electrolyte disturbances
- Efficient treatment for hypercatabolic patient
What are the disadvantages of haemodialysis?
- Haemodynamic instability
- Concern if dialysis associated with hypotension, may prolong AKI
- Fluid removal only during short treatment time
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
What are the disadvantages of CRRT?
- Need for continuous anticoagulation
- May delay weaning/mobilisation
- May not have adequate clearance in hypercatabolic PATIENT
