Lecture 14 - Acute Kidney Injury Flashcards
What was the traditional definition of acute renal failure?
Rapid loss of glomerular filtration and tubular function over hours to days
(leading to retention of urea/creatinine and oliguria)
What is the current definition of acute renal failure based off of?
KDIGO
Define acute renal failure by the KDIGO definition
Increase in serum creatinine by >=26.5micromol/l (0.3mg/dl) within 48 hours or >=1.5x baseline which is known/presumed to have occurred within the last 7 days
Urine volume <0.5ml/kg/h for 6 hours
Define AKI stage 1
Serum creatinine:
- 1.5-1.9x baseline OR >=26.5 micromol/l increase
Urine output:
- <0.5ml/kg/h for 6-12h
Define AKI stage 2
Serum creatinine:
- 2-2.9x baseline
Urine output:
- <0.5ml/kg/h for 12h or more
Define AKI stage 3
Serum creatinine:
- 3x baseline OR >=354 micromol/l increase OR initiation of RRT
Urine output:
- <0.3ml/kg/h for 24h or more or anuria for 12h or more
1 in ____ hospital admissions are complicated by AKI
7
What are the immediately dangerous consequences of AKI?
AEIOU Acidosis Electrolyte imbalance Intoxication (TOXINS) Overload Uraemic omplications
Death and dialysis
What are the 3 types of AKI?
Pre-renal
Renal/intrinsic
Post-renal
What are pre-renal causes of AKI due to problems with?
Problems with blood flow to the kidneys
What are renal causes of AKI due to?
Damage to the renal parenchyma
What are post-renal causes of AKI due to?
Obstruction to urine exit –> backing up and affecting normal kidney function
What are pre-renal causes of AKI?
Sepsis Hypovolaemia (e.g. haemorrhage, burns, vomiting, diarrhoea, diuretics) Hepatorenal syndrome Cardiac failure Hypotension, e.g. due to meds Arterial occlusion Vasomotor - e.g. NSAIDs/ACEi
What are intrinsic causes of AKI?
Acute tubular necrosis
Acute interstitial nephritis (many causes incl. drugs, e.g. PPIs)
GN
Myeloma
Intrarenal vascular obstruction (vasculitis, thrombotic micoangiopathy)
Toxin related - drugs (aminoglycosides, radiocontrast, rhabdomyolysis, snake venom, mushrooms etc.)
What are causes of post-renal AKI?
Intraluminal - kidney stones, clots, sloughed papilla
Intramural - malignancy, ureteric stricutre, radiation fibrosis, BPH
Extramural -retroperitoneal fibrosis, malignancy
What is the most common cause of AKI?
Pre-renal (e.g. hypotension/hypovolaemia) –> insufficient plasma flow, if treated promptly can resolve, if not can lead to acute tubular necrosis
(which is exacerbated by toxic drugs)
Why are the kidneys particularly susceptible to hypoperfusion?
Highly metabolic with all the activity
What are the three phases of ATN?
Initiation
Maintenance
Recovery
What is involved in the initiation phase of ATN?
Exposure to toxic/ischaemic insult
Renal parenchymal injury evolving
But reversible
What is involved in the maintenance phase of ATN?
Established parenchymal injury
Maximally oliguric
Lasts 1-2 weeks
What is involved in the recovery phase of ATN?
Gradual increase in urine output
Fall in serum creatinine
If in ATN the gFR recovers quicker than the tubule resorptive capacity what may occur?
Excessive diuresis (post-obstructive natriuresis)
What is radiocontrast nephropathy?
AKI follow administration of iodinated contrast agent
How does radiocontrast nephropathy tend to present?
As transient renal dysfunction usually resolving after 72h
May lead to permanent loss of function
What are risk factors for radiocontrast nephropathy?
DM Renovascular disease Impaired renal function Paraprotein High volume of radiocontrast
What can cause renal failure in myeloma?
Cast nephropathy - myeloma kidney Light chain nephropathy Amyloidosis Hypercalcaemia Hyperuricaemia
What things should you ask in your history of someone with suspected AKI?
Drugs they're on Insults - e.g. D+V in last 10 days? Pre/post-renal factors Uraemic symptoms Timing of symptoms - SoB, UO, vomiting Systemic diseases - e.g. rashes/nose bleeds, sore joints, eye pain
What investigations should you do for someone in AKI?
UE, Bicarb, LFTs, bone Clotting Urine dipstick FBC - anaemia? USS Blood gas ?ANCA/Ig/C3 C4 dsDNA ?renal biopsy
What are AKI risk events?
Sepsis
Toxins (e.g. contrast, aminoglycosides, ACEi, ARBs, diuretics use in last week)
Hypotension
Hypovolaemia (e.g. haemorrhage, diarrhoea)
Major surgery
What are AKI risk factors?
Age >=65 Previous AKI Heart failure Liver disease CKD DM Vascular disease Cognitive impairment
In the presence of a risk event and 1+ risk factors for AKI what should you consider activating?
STOP AKI Bundle - Sepsis - treat if suspected Toxins - avoid Optimise BP + volume status Prevent harm - daily UE, fluid balance, med review
What is the basic principle of treating AKI?
Removing the cause
What are the 5 questions you should ask yourself whilst treating someone with an AKI?
Do they need fluid? Can you remove the precipitant? Can you stop it getting worse? Do they need a catheter? How to make it safe?
What is involved in maintaining someone’s fluid balance whilst they are in AKI?
Volume resus if deplete, fluid restriction if overload Optimise BP (give fluid/vasopressors, stop ACEi/antiHTNs)
What drugs should be stopped in AKI?
Nephrotoxic drugs, e.g. NSAIDs/gentamicin
What is resuscitation fluid?
IV fluids to urgently restore circulation with hypovolaemia
What is routine maintenance fluid for?
IV fluids for those who cannot take orally/enterally to meet maintenance requirements
What is replacement fluid for?
Those not requiring urgent IV resus but do not additional to maintenance to correct existing deficit, e.g. diarrhoea
What do NICE recommend for maintenance fluids in adults?
25-30ml/kg/day water and 1mmol/kg/day of K, Na and Cl, 50-100g/day glucose
What specific point should you remember about Hartmann’s fluid?
Contains K - do not give in hyperkalaemia
If large volumes of 0.9% saline are given what is there a risk of?
Hypercholraemic metabolic acidosis
What may be involved in removing the precipitant in AKI?
Stop causative drugs
Treating sepsis
Diagnose GN/other interstitial disease + give therapy
What can you do to stop AKI getting worse?
Support BP (vasopressors, stop anti-HTNs) Reduce further insults, e.g. try to avoid IV radiocontrast
What ECG changes do you see in hyperkalaemia?
Peaked T waves usually the earliest sign Tall tented T waves P wave widens and flattens PR segment lengthens P waves eventually disappear Prolonged QRS High grade AV block with slow junctional and ventricular escape rhythms Any conduction block Sinus brady/slow AF Sine wave (pre-terminal) VF --> cardiac arrest
How do you treat hyperkalaemia?
Stabilise myocardium - IV calcium gluconate
Shift K intracellularly - salbutamol, insulin-dextrose
Remove - diuresis, dialysis, anion exchange resins
What are indications for dialysis in AKI?
Low bicarb, high lactate or pCO2
High K, high or low Na, high Ca, high uric acid, high phosphate or mg
To remove toxins, e.g. aspirin, theophylline, lithium, ethylene glycol, methanol, metformin
Overload, e..g pulmonary oedema
Pericarditis due to uraemia
What are the signs and symptoms of AKI?
Reduce UO
Pulmonary/peripheral oedema
Arrhythmias (2ndary to K and acid base balance)
Features of uraemia (e.g. pericarditis, encephalopathy)
What electrolytes are looked at in a U and E?
Na
K
Urea
Creatinine
How does NICE recommend making a diagnosis of AKI?
In line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
a rise in serum creatinine of 26 micromol/litre or greater within 48 hours OR
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days OR
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than OR
>=25% fall in eGFR in children/young adults in 7 days
Which AKI patients should have imaging?
If no identifiable cause for deterioration or risk of urinary tract obstruction they should have a renal USS within 24h of assessment
List some drugs which are usually safe to continue in AKI
Paracetamol Warfarin Statins Aspirin (75mg) Clopidogrel Betablockers
List some drugs which should be stopped in AKI as they may worsen renal function
NSAIDs Aminoglycosides ACEi ARBs Diuretics
List some drugs which may have to be stopped in AKI not because they worse AKI but because there is an increased risk of toxicity
Lithium
Digoxin
Metformin
Name 3 ways by which K can be removed from the body in hyperkalaemia?
Dialysis
Loop diuretics
Calcium resonium (oral/enema)
Which part of the kidney is particularly susceptible for renal tubular hypoxia and why?
Medulla as it is already a relatively hypoxic environment
Post-operative renal failure is more likely to occur in which patients?
Elderly, with PVD, high BMI, COPD, on vasopressors or nephrotoxic meds and undergo emergency surgery
When should you refer to a nephrologist in AKI?
If any of the following apply:
- renal transplant
- ITU patient with unknown AKI cause
- vasculitis/GN/tubulointerstitial nephritis/myeloma
- AKI with no known cause
- Inadequate response to treatment
- complication of AKI
- stage 3 AKI
- CKD stage 4 or 5
- quality for renal replacement hyperkalaemia/metabolic acidosis/complications of uraemia/fluid overload
What are the different investigation results you should see in pre-renal uraemia vs acute tubular necrosis?
Kidneys hold on to sodium in pre-renal uraemia to try to preserve volume
