Acute Kidney Injury (AKI)
Dr Svitlana Zhelezna
Clinical Teaching Fellow
UHCW NHS Trust
svitlana.zhelezna@uhcw.nhs.uk
2013/2014 academic year
Objectives:
Recognise AKI
 Investigate and decide on: pre-renal,
renal and post renal causes
 Recognise and manage hypovolemia
 Manage hyperkalemia
 Indications for emergency dialysis
and heamofiltration

Definition of AKI

Rise in serum creatinine >50% from
baseline

Or

Urine output <0.5ml/kg/hr for 6 hours
Effects of Acute Kidney Injury:
Raised Urea, Creatinine and Uric Acid:
- Confusion
- Drowsiness
Failure to Excrete Normal Acidic Products:
- Metabolic Acidosis
- Respiratory Hyperventilation
Electrolyte Imbalances (Hyperkalaemia):
- Dysrhythmias
Urea (2.5-7.5 mmols/L)
Other causes for raised urea:
 High protein intake.
 Increased tissue breakdown (i.e febrile
illness, crush injuries).
 Dehydration.
 Steroid or Tetracycline Administration.
 Absorption of Blood from G.I. Tract.
Creatinine (60 -125 mmols/L)

is a by product of normal muscle metabolism

is excreted in urine primarily as a result of
glomerular filtration

more reliable indicator of renal function and of a
glomerular filtration than Urea.
RIFLE Classification
Acute Tubular
Necrosis
Renal tubular cell injury
after a toxic or ischaemic
insult results in:
 sloughing of tubular debris and cells into the
tubular lumen with eventual obstruction of the
tubular flow,
 increased intra-tubular pressure and back leak
of glomerular filtate out of the tubule and into
the interstitium and renal venous blood
Three Phases of AKI:

Phase 1: Oliguric Phase.
Usually lasts 10-14 days but may last from several
hours to several weeks.

Phase 2: Poliuric Phase.
Occurs 2 to 6 weeks after the onset.

Phase 3: Recovery Phase.
May last 3 to12 months.
AKI Outcomes:




Renal function loss – i.e. persistent loss of
renal function lasting > 4 weeks
End Stage Kidney Disease – i.e. GFR <
15ml/min for > 3 months
Other associated complications – e.g. sepsis,
bleeding, respiratory failure etc.
Increased Mortality
How to approach a
patient?
What to look for when clerking ?
Ask about:
 family history of renal disease
 exactly when the presenting symptoms
started, and which came first
 joint pains, or rash, or nose bleed, or ear
trouble (vasculitis)
 backache or bone pains (myeloma and other
malignancy)
 drugs taken (NSAID, ACEI ect.)
Volume Status/Dehydration:







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Skin Turgor
Mucus Membranes
JVP
Pulse rate and volume
Blood Pressure (check postural BP)
Peripheral perfusion –capillary refill
Chest sounds
Peripheral Oedema
Urine output
Investigations:





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U&E’s, FBC, LFTs, ABG
Urine Dip/MSU if indicated
ECG
CXR
CRP if indicated
Blood cultures if indicated
Principles of Treatment:





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Check Medication! Stop all nephrotoxic if you can
(ACEI, diuretics, NSAIDS), Check that the dosages of
those remaining /commencing are correct in renal failure
(Enoxaparin, some antibiotics)
Treat lifethreatening hyperkalaemia first
Correct hypovolaemia/hypoperfusion – restore
pressure
Exclude obstruction ASAP (Imaging)
Treat the underlying cause
Consider Renal replacement therapy if no response
Case 1
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66 y.o. man presents to A&E at 10am
PC: increasing SOB for 7/7, coughing up phlegm and
having fever.
PMH: DM, HTN
DH: metformin, aspirin, ramipril, atenolol and simvastatin.
O/E: pale, sweaty, BP 85/50, HR 115, Sats 92% on air, RR
25, T 38.3, coarse crackles on the right side of his chest.
CXR - RLL pneumonia.
Blood results: Na 130, K 4.5, Urea 14.3, Creat 189
The nurse asks you to assess the patient at 2 pm as he
hasn't passed urine since admission.
What would be your management?
Initiate management:




Reassess the patient including volume
status, vitals, check the catheter if in place
CHECK CURRENT MEDICATIONS!
Investigations: ABG, Urine dip
Treatment: fluid resuscitation, call for senior
help
Fluid balance
(adults, resting state, mL per day)
Totaling: in/out ~2500 ml/day
Maintenance fluids:
WEIGHT
For the first 10 Kg
For the next 10-20 Kg
For each Kg above 20
RATE
100 mL/kg/24hrs
Add 50 mL/kg/24hrs
Add 20 mL/kg/24hrs
or
or
or
4 mL/kg/hr
+2 mL/kg/hr
+1 mL/kg/hr
So, the maintenance fluid requirements for a 25-kg child is:
1000 + 500 + 100 = 1600 (mL/24hrs)
or 40 + 20 + 5 = 65 (mL/hr)
So, the maintenance fluid requirements for a 70-kg adult is
1000 + 500 + 1200 = 2700 (mL/24hrs)
Or 40 + 20 + 50 = 110 (mL/hr)
Fluid requirements in illness:
Pre-existing Normal Deficits:

(missing maintenance) is
estimated by multiplying the
normal maintenance volume
by the length of the fasting
period:
Estimated Abnormal Fluid Losses:



For 70-kg man fasting for 8 hours this
amount is
(40 + 20 + 50) mL/h x 8 hrs = 880 mL.
In reality, this deficit will be somewhat
less as a result of renal conservation
Known losses: bleeding,
vomiting, excessive diuresis or
diarrhoea…
Occult losses due to fluid
sequestration in body cavities
or traumatized tissues
(obstructed bowels, ascites,
intramuscular haematoma …);
Increased insensible losses
due to hyperventilation, fever
and sweating
(an extra 500 ml/day is required for every
degree Celcius above 37, ~20 ml/hr);
Fluid requirements in illness
Maintenance requirements for an adult
Na - 50-100 mmol/day
K - 40-80 mmol/day
In 1.5-2.5 Iitres of water by the oral, enteral or
parenteral route (or a combination of routes).
Additional amounts should only be given to
correct deficit or continuing losses
Contents of common crystalloids in
mmol/L
Na
K
Ca
Cl
HCO3 Osm
Plasma
140
4
2.3
100
26
285-295
Na Cl 0.9%
Dextrose 5%
Dex.Saline
Hartmann’s
154
0
30
131
0
0
0
5
0
0
0
0
308
252
255
278
5.0
4.0
4.0
6.5
Ringer’s
147
4
0
154
0
0
0
0
2
111
Lactate 29
2.2
156
Lactate 28
0
0
0
0
0
302
6.9
150
1000
300
2000
8.0
8.0
Na Bicarb 1.2% 150
Na Bicarb 8.4% 1000
0
0
pH
7.4
Fluid requirements in illness
Excessive losses from gastric aspiration/vomiting
crystalloid solution with K supplement.
↓Cl - 0.9% NaCl + K (sufficient amount) and care not
to produce sodium overload.
↓Na (excessive diuretic exposure) - Hartmann's
Diarrhoea, ileostomy, small bowel fistula, ileus,
obstruction - volume for volume with Hartmann's
.
What is Hyperkalaemia?
Level of potassium above 5.5 mmol/l in venous
blood
ECG changes (peaked T waves and
broadening of QRS complex) are important
but may NOT be seen even if potassium
level is life threatening
May cause sudden death or progressive
bradycardia and death
ECG Changes:
Causes of Hyperkalaemia:



AKI/Renal failure
Sepsis with acute kidney injury
Drugs (spironolactone, ACE
inhibitors, amiloride and OTHERS)
Treatment:
K+ >6.0
mmol/l
Calcium resonium 15G qds PO in water,
recheck K+ after 2 hours
K+ >6.5
mmol/l
Above plus: Refer to a nephrologist,
Dextrose-insulin (10U actrapid insulin in 50ml 50%
dextrose, intravenously, over 5 minutes, check BM every
30min for 2 hours
K+ >7.0
mmol/l
Above plus: URGENT REFERRAL
Neb Salbutamol 5mg and repeat in 2 hours
IV Sodium Bicarbonate 500ml 1.26% over 30 mins OR
If central line in situ:
IV Sodium Bicarbonate 50ml 8.4% over 5 mins
(not in pulmonary oedema)
IV Calcium Gluconate 10ml 10%
Recheck K+ and BM in 2 and 4 hours
Acute Renal Failure →
Emergency Haemodialysis:





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K+ > 7mmol/L, resistant to medical therapy
Pulmonary oedema refractory to medical
therapy
Metabolic pH < 7.2 or base excess < -10
Other possible indications include:
Uraemic pericarditis
Uraemic encephalopathy
Renal Replacement Therapy
Dialysis:
 No clear proven advantage
for either in treatment of
renal failure
 Theoretical advantage of
clearance of middle
molecules
Haemofiltration:
 No need to transfer patient
to renal unit
 Can be continuous
 Improved haemodynamic
stability
 Permits vasopressers and
other drug therapies
including TPN
 Reduced risk of
disequilibrium syndrome
When to call nephrology?
Any known dialysis patient admitted
 Any known renal transplant patient
admitted

Any case of AKI where cause is not clear
 Worsening AKI
 Emergency dialysis indications
 Suspect glomerulonephritis

Summary:

worry if




Patient has not passed urine or very little
U&E creatinine is going up, check dynamics
Patient is dehydrated plus cardiovascular
compromised (past MI, CCF)
remember


Normal creatinine does not mean patient is not
developing AKI
Call early for senior or specialist help
Thank you!
Any questions?