Acute Kidney Injury **** Flashcards
What is it?
What 2 things are used to QUICKLY measure the function of the kidneys ACUTELY?
Decreased renal function
Serum creatinine and urine output
Criteria:
Over what creatinine, conc is classed as AKI?
How many times over the baseline would creatinine rise in a wk to be classed as AKI?
Under how many ml’s/kg/hr over a 6 hr consecutive period is classed as AKI?
What staging system is used?
How many stages are there?
> 26 μ/mmol/L
1.5x
<0.5 ml/kg/hr over 6 hrs or 8 hrs for kids - IF YOU ACTUALLY CALCULATE THIS, THE URINE PRODUCTION HAS TO BE TINY
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KDIGO stages
3
KDIGO stages:
Creatinine and urine output are used.
Stages 1:
- How many times over the baseline is creatinine?
- How many hours is there urine output <0.5 ml/kg/hr?
Stage 2:
- How many times over the baseline is creatinine?
- How many hours is there urine output <0.5 ml/kg/hr?
Stage 3:
- How many times over the baseline is creatinine?
- How many hours is there urine output <0.3 ml/kg/hr?
x1.5
6 hrs
x2
12 hrs
x3
24 hrs
Name the types of AKI
What 4 renal functions would you be worried about?
Prerenal
Renal
Postrenal
Excretion of waste products
EPO production
Vit D metabolism
Homeostasis
Prerenal AKI:
Renal hypoperfusion:
- This causes prerenal azotaemia. What does azotaemia?
- What will prolonged hypoperfusion lead to?
Causes:
VOLUME DEPLETION:
- What will cause reduced blood volume? - 3
- How do burns cause hypoperfusion?
LOW CARDIAC OUTPUT:
- What will cause reduced cardiac output? - 3
DISTRIBUTIVE:
- How does pancreatitis cause hypoperfusion?
- What are some other distributive causes?
VASOCONSTRICTORS:
- How do NSAIDs cause hypoperfusion?
- How do ACEi and ARBs cause hypoperfusion?
When burn size exceeds 20% TBSA, heat injury releases cytokines, inflammatory mediators that increase capillary leak, and severe hypoproteinemia ensues. This causes intravascular volume shifts with resultant interstitial edema formation, vascular volume depletion and electrolyte imbalance.
Accumulation of uraemic waste
Acute tubular necrosis ---- D&V prolonged Haemorrhage GI bleed
MI
Massive PE
Tamponade
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This is caused by release of cytokines and other pro inflammatory mediators. These further cause vasodilatation, intravascular volume depletion, and end organ hypoperfusion.
Shock (e.g. sepsis)
Anaphylaxis
They constrict afferent arterioles
They dilate efferent arterioles (more than afferent)
Renal (Intrinsic) AKI:
Tubero-interstitial disease:
- What does ATN and AIN stand for?
- What is inflammation of the glomeruli called?
Microangiopathy (microvascular):
- Haemolytic uremic syndrome - what is it and how does it lead to this?
- TTP - A rare blood disorder, where blood clots form in small blood vessels throughout the body. The clots can limit or block the flow of oxygen-rich blood to the body’s organs, such as the brain, kidneys, and heart. What does TTP stand for?
- DIC - how does it lead to AKI?
Acute tubular necrosis-caused by long term hypoperfusion
Acute interstitial nephritis - a renal lesion that typically causes a decline in renal function and is characterized by an inflammatory infiltrate in the kidney interstitium
A condition that affects the blood and blood vessels. It results in the destruction of blood platelets and anaemia and kidney failure due to damage to the very small blood vessels of the kidneys.
Thrombotic Thrombocytopenia Purpura
A condition in which blood clots form throughout the body, blocking small blood vessels.
HUS, TTP and DIC are similar in presentation but the underlying mechanism is different!!!
Postrenal AKI:
What is the pathophysiology?
List some causes? - 6
Obstruction within the renal tract or extrinsic compression
Stones Catheter Strictures Prostatism UTI Cancers
S+S:
What are some signs of fluid overload?
What are some uraemic symptoms?
Polyuric (aka diuretic) phase - what is it?
Pulmonary oedema (+/- orthopnoea and paroxysmal nocturnal dyspnoea) Peripheral oedema
Fatigue
N&V
Confusion
The kidneys try to heal and urine output increases, but tubule scarring and damage occur.
(1) Management:
Are there life-threatening complications:
- What is done for a high NEWS score?
- What is done for pulmonary oedema?
- What is classed as hyperkalemia and how is it managed?
- Why does hyperkalaemia happen?
NEWS- high - critical care referral
Dialysis
Hyperkalaemia - >6.4 mmol/l - VBG and ECG for changes
When kidneys fail they can no longer remove excess potassium, so the level builds up in the body.
(2) Management - Monitoring:
How is fluid balance monitored?
Why is potassium checked?
How often are obs done?
What is used as a sign of sepsis?
What is measured daily to look at the clinical response?
A urinary catheter and hourly urine output
Monitoring response to Rx - alongside creatinine
4 hourly
Lactate
Creatinine
(3) Management - Investigations:
Urinalysis:
- What does haematuria and proteinuria suggest?
- What does pyuria suggest? - 2
- What can be done to look for what type of intrinsic disease is present?
Intrinsic disease (e.g. glomerulonephritis)
Stones
UTI
Tumour
Trauma
UTI
AIN - it is an inflammatory condition
Microscopy
(3) Management - Investigations:
Bloods:
- FBC - what may raised WBC to suggest? - 2
- FBC - what do low platelets suggest? - 2
- What blood test is done primarily to check renal function?
- Why are LFT’s done here if the patient has liver disease?
- Why is coag done? - 1
- Why is creatine kinase (CK) done?
- An ABG is done to look for metabolic acidosis. Why does this happen?
Infection - UTI
AIN - it is an inflammatory condition
U&E
To look for possible hepatorenal syndrome - a cause of hypoperfusion
DIC
Rhabdomyolysis - When muscle is damaged, a protein called myoglobin is released into the bloodstream. It is then filtered out of the body by the kidneys. Myoglobin breaks down into substances that can damage kidney cells.
The kidneys do this by removing acid from the body through urine. Metabolic acidosis is caused by a build-up of too many acids in the blood. This happens when your kidneys are unable to adequately remove the acid from your blood.
(3) Management - Investigations:
Imaging:
- First-line imaging for kidneys?
- What do you expect the kidneys to look like in someone with CKD?
- What does asymmetry suggest?
- Why may an ECG be done?
- Why may a CXR be done?
Distinguishing from CKD;
- What results from GFR monitoring suggests AKI?
- What additional symptom do people with CKD have?
USS
Small kidneys (<9cm)
Renal vascular disease
Hyperkalaemic changes
Rising GFR suggests AKI
Nocturia
(4) Management - Support:
You can stop all nephrotoxic drugs - give a few examples of these?
You can stop drugs that increase the risk of complications such as…..?
Why is metformin and digoxin dangerous in AKI?
NSAIDs
ACEi
ARBs
Diuretics (especially K sparing)
Metformin
Antihypertensives
Both metformin and digoxin are dangerous in AKI as due to the reduced renal function, they are not excreted by the kidneys as efficiently hence can build up and lead to toxicity.
Metformin toxicity can lead to lactic acidosis.
(5) Actual Management:
Pre-renal Rx?
Renal Rx?
Post-renal Rx - think about no being able to get rid of urine?
Correct volume depletion or increase renal perfusion via cardiac support
Stop causative drugs - need specialist Rx
Catherine
Nephrostomy - think of Glady’s at the care home
Urological intervention
