13. Acute Kidney Injury (AKI) Flashcards
Give me a brief overview of the function of a kidney
They make urine, regulate salt and water (make 3-4 pints a day)
remove waste products from blood into. urine
Produce hormones that regulate BP and also create erythropoietin to control the production of RBC
They activate vitamin D to keep bones healthy
They clean your blood and remove many drugs that some people take for their condition
What two criteria make up the staging of AKI
serum creatinine (SCr) urine output
what is the criteria for stage 1 AKI
SCr increase more than 26 micrnmol/L within 48 hours or increase between 1.5-1.9x reference value
urine output less than 0.5ml/kg/hour for more than 6 consecutive hours
what is the criteria for stage 2 AKI
increase between 2-2.9 x reference SCr
urine output less than 0.5ml/kg/hour for more than 12 hours
what is the criteria for stage 3 AKI
increase more than 3X reference range of SCr or increased greater than 354 micro mols/L or commenced on renal replacement therapy (RRT)
Urine output less than 0.3ml/kg/hr for more than 24 hours or anuria for 12 hours
In someone with suspected AKI what checklist is used to improve the care of someone with AKI
think SALFORD
What is think SALFORD
an institue AKI care bundle that is used in all patients with 26mmol/L or 1.5X rise in creatinine or oliguria (less than 0.5ml/kg/hr) for 6 hours
what does think SALFORD stand for
Sepsis and other causes - treat
ACE/ARB and NSAIDS suspend/review drugs
Labs (repeat creatinine within 24hours) & Leaflets (for the patient)
Fluid assessment and response (history and examination, initiate fluid chart, measure daily weights- if hypovolaemic give bolus IV 250mls and reassess)
Obstruction (USS within 24 hours for AKI 3)
Renal/critical care referral
Dip the urine and record it
Name some symptoms and signs of AKI
nausea and vomitting, or diarrhoea, evidence of dehydration
reduced urine output or changes in urine colour
confusion, fatigue and drowsiness
An acute illness with any of the risk factors (see other questions)
What is the NICE criteria for AKI
- Rise in creatinine of ≥ 25 micromol/L in 48 hours
- Rise in creatinine of ≥ 50% in 7 days
- Urine output of < 0.5ml/kg/hour for > 6 hours – this is termed oliguria
What is oliguria
Urine output of < 0.5ml/kg/hour for > 6 hours
Name the various risk factors that would predispose a patient to developing AKI injury
chronic kidney disease
other organ failure/chronic diseases (heart failure, diabetes, liver disease)
Older age (above 65 years)
History of AKI
cognitive impairment
nephrotoxic medications such as NSAIDS, ACE inhibitors, ahminoglycosides, ARB, diuretics within the past week
Use of a contrast medium such as during CT scan
hypovolaemia
oliguria
sepsis
name some nephrotoxic medications
NSAIDS and ACE inhibitors, aminoglycosides, ARBs, diuretics
Whenever someone asks you the cause of renal impairment what can you split it into
pre-renal, renal and post-renal causes
what is the most common cause of AKI
pre-renal
renal
post-renal
pre-renal
why does pre-renal pathology cause AKI
it is due to inadequate blood supply to the kidneys which reduces the filtration of blood
name some pre-renal causes of AKI
Dehydration
hypotension (shock)
Heart failure
Hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis
Sepsis
hepatorenal syndrome (to do with liver cirrhosis)
Name some renal causes of AKI
this is where there is an intrinsic disease in the kidney -glomerulonephritis - Interstitial nephritis - Acute tubular necrosis Rhabdomyolysis
How is post renal AKI caused
by obstruction to the outflow of urine from the kidney, causing a back pressure into the kidney and reduced kidney function aka “obstructive uropathy”
name some post-renal causes of AKI
kidney stones
masses scubas cancer. in the abdo or pelvis
ureter strictures
enlarged prostate or prostate cancer - benign prostatic hyperplasia
the first step to treating an AKI is to correct the underlying cause, how could you do this
fluid rehydration with IV fluids in pre-renal AKI
stop nephrotoxic medications such as NSAIDs and antihypertensives that reduce filtration pressure
relieve obstruction in a posit-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate
what are the main complications with AKI
hyperkalaemia
fluid overload, heart failure and pulmonary oedema
metabolic acidosis
Ureamia (high urea) can lead to encephalopathy or pericarditis
From the list below name the drugs that are usually safe to continue in AKI Paracetamol warfarin statins aspirin (at a cardio protective dose of 75mg OD) Clopidogrel Beta-blockers NSAIDS (except if aspirin at cardiac dose eg 75mg OD) ahminoglycosides ACE inhibitors ARB diuretics metformin lithium digoxin
Paracetamol warfarin statins aspirin (at a cardio protective dose of 75mg OD) Clopidogrel Beta-blockers
From the list below name the drugs that should be stopped in AKI as it may worsen renal function Paracetamol warfarin statins aspirin (at a cardio protective dose of 75mg OD) Clopidogrel Beta-blockers NSAIDS (except if aspirin at cardiac dose eg 75mg OD) ahminoglycosides ACE inhibitors ARB diuretics metformin lithium digoxin
NSAIDS (except if aspirin at cardiac dose eg 75mg OD) ahminoglycosides ACE inhibitors ARB diuretics
From the list below name the drugs that may have to be stoped in AKI as increased risk of toxicity (but does usually worsen the AKI itself) Paracetamol warfarin statins aspirin (at a cardio protective dose of 75mg OD) Clopidogrel Beta-blockers NSAIDS (except if aspirin at cardiac dose eg 75mg OD) ahminoglycosides ACE inhibitors ARB diuretics metformin lithium digoxin
metformin
lithium
digoxin
Hyperkalaemia needs prompt treatment to avoid arrhythmias which could be life threatening;
which drug is used to stabilise the cardiac membrane
IV calcium glconate
Hyperkalaemia needs prompt treatment to avoid arrhythmias which could be life threatening;
which drugs are used to shift potassium from extracellular to intracellular fluid compartments
combined insulin/dextrose infusion
nebulised salbutamol
Hyperkalaemia needs prompt treatment to avoid arrhythmias which could be life threatening;
which drugs can be used to remove potassium from the body
calcium resonium (orally or enema)
Loop diuretics
Dialysis
Hydration status examination:
name some causes of fluid overload
o Iatrogenic: whereby medical intervention/treatment has caused it ie too much fluids
o Cardiac failure
o Renal failure
o Increased ADH secretion
Hydration status examination:
name some causes whereby your fluid output will be increased
Diabetes
Diarrhoea and vomiting
Fever (excessive sweating)
Drugs (anti diuretics)
Hydration status examination:
name some broad causes of dehydration
decreased input of fluids increased output of fluids insufficient replacement of fluids during surgery Haemorrhage Sepsis
Hydration status examination:
before going to the patient what things can you look at (ie test results or charts)
fluid balance abs chart meds bloods CXR
Hydration status examination:
what things can you comment on from the end of the bed
• What’s going into them
o IV lines, NGT, NBM, food or drink
• what’s going out
o Catheter, vomit bowels, drains, stomas
Hydration status examination:
what can you comment on in the hands, arms and neck
Hands
Hands
• Warm, CRT, skin turgor
Arms
• Pulse (weak, increased in dehydration and overload)
• Lying/standing BP (more than 20 mmHg difference is significant)
Neck
• Carotid pulse (character- weak/thready)
• JVP (more than 4cm is significant and could this be overload)
Hydration status examination:
what can you comment on in the face, chest and back/legs
Chest • Parasternal heave (RH dilatation) • Displaced apex beat (LH dilatation) • 3rd heart sound (heart failure) Back/legs • Lung bases (crackles- LVF) • Sacral or ankle odema (RVF)
Hydration status examination:
how could you finish off this exam
- Review charts and bloods
- Daily weights
- Repeat bloods
- CXR to look for pulmonary odema
What ECG changes occur in a patient with hyperkalaemia
- There are usually no P waves- but regular rhythm
- Wide QRS complex (more than 3 small squares) with similar to, but no recognisable pattern of LBBB
- Peaked T waves
what happens if high levels of potassium are not treated
will go on to develop VF and have a cardiac arrest
An ECG for hyperkalaemia is often mistaken for what other clinical abnormality
LBBB
What drug is used to stabilise the myocardium in hyperkalemia
calcium glutinate
which drugs are used to shift potassium back into the cells in hyperkalaemia
short acting insulin in dextrose
nebulised salbutamol
How is hypokalaemia treated
- Correct any other underlying electrolyte abnormalities such as hypomagnesaemia
- Administer potassium chloride in NaCl at a maximum rate of 20mmol/hour
in a patient with an AKI what could their ABG classically look like
partially compensated metabolic acidosis with low PH, low bicarbonate and compensatory low CO2
Urine dipstick:
what does proteinuria 3+ indicate and on the flip side if it is negative what can you exclude
intrinsic renal disease
Urine dipstick:
if there is blood and protein then what should you consider
glomerulonephritis
Urine dipstick:
if dipstick is positive for blood but no RBC when what should you consider
myoglobin
An AKI with negative urinalysis usually indicates what kind of AKI cause
pre-renal
renal
post renal
pre-renal
Dialysis is considered for patients with kidney injury if. what kind of complications cannot be resolved
hyperkalaemia
pulmonary oedema
metabolic acidosis
uraemia encephalopathy (confusion, myoclonic jerks, seizures, coma) or uraemia pericarditis
Why is the kidney susceptible to ischemic damage and necrosis
in order to have counter current multiplication mechanise in the renal tubules you need low and sluggish blood flow, especially in the renal medulla
what is the protective mechanism that the kidney has which tries to prevent ischemia and maintain renal blood flow
the RAAS system (renin-angiotensin-aldosterone) mechanism
where is the RAAS mechanism located
juxtaglomerular apparatus of the kidney
how does the RAAS system work
it increases the overall effective circulation by increasing reabsorption of salt (Na) and water
also protects the nephron locally by vasoconstriction of efferent renal arteriole to maintain GFR
Which drugs all prevent the protective RAASm mechanism making tubular ischemia and necrosis more likely
ACE-I, ARB and NSAIDS
What are the 3 phases of acute tubular necrosis (ATN)
oliguric phase
maintenance phase
polyuric recovery phase
