acute kidney injury (aki)

Acute Kidney Injury (AKI)

Dr Svitlana ZheleznaClinical Teaching Fellow

UHCW NHS Trustsvitlana.zhelezna@uhcw.nhs.uk

2013/2014 academic year

Objectives:

Recognise AKIInvestigate 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:

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:

U&E’s, FBC, LFTs, ABG Urine Dip/MSU if indicated ECG CXR CRP if indicated Blood cultures if indicated

Principles of Treatment:

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 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 RATEFor the first 10 Kg 100 mL/kg/24hrs or 4 mL/kg/hrFor the next 10-20 Kg Add 50 mL/kg/24hrs or +2 mL/kg/hr For each Kg above 20 Add 20 mL/kg/24hrs or +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 is1000 + 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:

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

Estimated Abnormal Fluid Losses:

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 pH

Plasma 140 4 2.3 100 26 285-295 7.4

Na Cl 0.9% 154 0 0 154 0 308 5.0Dextrose 5% 0 0 0 0 0 252 4.0Dex.Saline30 0 0 0 0 255 4.0Hartmann’s 131 5 2 111 0 278

6.5 Lactate 29

Ringer’s 147 4 2.2 156 0 302 6.9Lactate 28

Na Bicarb 1.2% 150 0 0 0 150 300 8.0Na Bicarb 8.4% 1000 0 0 0 1000 2000 8.0

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 hoursIV 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:

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 admittedAny known renal transplant patient

admitted

Any case of AKI where cause is not clearWorsening AKIEmergency dialysis indicationsSuspect 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?