AKI Flashcards

1
Q

What is AKI?

A

AKI is a syndrome of decreased renal function measured by serum creatinine or urine output, occurring over a period of hours/days

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2
Q

What staging system is used for AKI?

A

Staging System:
Kidney Disease improving global outcomes score
Stage 1 - Creatinine >26.5umol/l or 1.5x baseline. Urine output <0.5ml/kg/hour for 6 hours
Stage 2 - Creatinine 2-3x baseline. Urine output <0.5ml/kg/hour for 12 hours
Stage 3 - Creatinine > 353.6umol/or >3x baseline or on renal replacement therapy. Urine output <0.3ml/kg/hr for 24 hours or anuria for 12 hours

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3
Q

What are the causes of AKI?

A

Causes
Pre-Renal:
Fluid Loss - (Diarrhoea and Vomiting, Haemorrhage)
Reduced cardiac output - Shock, MI
Systemic Vasodilation - Sepsis, Drugs
Renal Vasoconstriction – Renovascular Disease, NSAIDS, ACE inhibitors, ARB, Hepatorenal syndrome

Renal:
Glomerular - Glomerulonephritis, Rhabdomyolysis/Tumour lysis Syndrome
Tubulo Interstitial Nephritis - ATN (Can be as a result of Pre-Renal Ischaemia, Nephrotoxic Drugs, Infection or crystal deposit)
Vascular - Vasculitis, DIC

Post Renal:
Within Renal Tract - Renal Stone, Renal Tract Malignancy, Clot, Stricture
Extrinsic – Pelvic/Prostate/Cervical/Ureteral Malignancy, Benign Prostatic hypertrophy

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4
Q

What will you find in a history taking of AKI?

A

Symptoms:
Often Asymptomatic
Low urine output
Nausea and Vomiting
Dehydration – Dizziness, confusion, lethargy
Abdominal/Back pain
Dyspnoea/PND/Orthopnoea - Pulmonary oedema due to Reduced Na excretion
Uraemia - Confusion, itching, Uraemic tinge (yellowish skin, Pericarditis
Nephrotic syndrome - proteinuria, hypoalbuminemia and oedema
Nephritic syndrome - haematuria, proteinuria and hypertension, Red blood cell casts
Fever, Rash, Eosinophilia - Think intrinsic renal disease

Risk Factors:
Pre-existing renal disease/CKD
Elderly 
Male - Think prostate problems 
Diabetes
CVS disease
Malignancy
Liver disease
Recent Surgery
Hypertension
Peripheral Vascular Disease – Very strong link with renal artery disease 

Specific Questions to ask: Try to work out if its pre, intrinsic or post renal
Pre-Renal – History of D&V, Bleeds, Hospital admission (improper fluids). Are they thirsty, have they been peeing. Are they light headed on standing)? Any signs of infection? Use of ACEi or NSAIDS
Intrinsic Renal - Oedema and/or HTN, ask about newly prescribed medications (including recreational and over the counter) or use of contrast imaging. If initially pre-renal, ischaemic can cause it to progress to intrinsic renal (ATN). Any recent trauma (that could cause rhabdomyolysis). Any recent infection (That could cause post infective glomerulonephritis) Recent travel (tropical infection e.g. Malaria)
Post renal - Ask about prostate problems (urgency, frequency, or hesitancy). History of renal stones, any flank pain or blood in urine.
Nephrotic Syndrome – Minimal Change GN (Children), Focal Segmental GN (Adults), Membranous GN, Diabetes, Amyloidosis, SLE
Nephritic Syndrome – IGA nephropathy, Post streptococcal, Vasculitis, SLE, Goodpasture’s, Alport’s

Differentials:
CKD – Long duration of symptoms, Nocturia, not acutely ill, anaemia, electrolyte abnormalities (Calcium low and phosphate high), Small kidney on US

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5
Q

What will you find on examination of AKI?

A

Examination findings:
End of the bed:
Need to assess fluid status – Dehydrated think pre-renal, fluid overload think intrinsic renal disease
Mental state reduced - uraemia
Look for rashes that may indicate vasculitic conditions like SLE that have affected the kidney
Hands:
BP - Low in pre-renal, high in intrinsic renal disease
Uraemic flap
Chest:
Pericardial rub or signs of pericarditis in uraemia
Abdomen:
Palpable Bladder/Distended abdomen - Indicates post renal cause
Pelvic/Abdominal palpable mass- may be a post obstructive malignity
Renal bruit - Renovascular disease

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6
Q

What investigations will you order in AKI?

A

Bedside:
Urine dipstick – Leucocytes and Nitrates (Infection), Blood and Protein (Glomerulonephritis), Blood (Renal Stones), Protein (Other intrinsic renal disease)
ECG - If K+ high to look for arrhythmia
Blood/Urine Culture if suspecting infection
Urine osmolarity - Raised in pre-renal, Reduced in intrinsic renal, Normal in post renal
Full set of observations
Capillary glucose – Ruling out diabetic kidney disease

Bloods:
LFT’s - Looking for hepatorenal syndrome and ruling out other cause of oedema
U&E - Showing the urea: creatinine ratio (>20 indicates pre-renal) and looking for hyperkalaemia, also gives creatine for AKI staging
ABG - Looking for raised lactate (Sepsis, Severe Shock, Acidosis)
FBC - Anaemia can indicate underlying renal disease, WCC raised in sepsis
Serum Calcium – Raised calcium increases risk of renal stones
Clotting – Protein loss in nephrotic syndrome can cause deranged clotting, or to look for DIC

Imaging:
Remember you cannot give radiological contrast in renal failure
USS - Within 24 hours, small kidney suggests CKD, Asymmetry suggests renal vascular disease, enlarged suggest post renal obstruction
CXR to look for pulmonary oedema or cardiomegaly (Rules out heart failure as cause of oedema)

Special Tests: If intrinsic renal disease indicated
Renal Biopsy
Urine Microscopy – Muddy Brown Casts (ATN)
Renal Immunoglobulins and autoantibodies
Paraprotein
24 hour urinary protein - ?3.5g/day is nephrotic syndomre
Complement protein – Low in SLE or Acute Infectious Glomerulonephritis

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7
Q

What is the management of AKI?

A

Resuscitation:
A-E approach
Get IV Access/Give O2 to maintain sats of 94+ /Attach 12 lead ECG
Attach catheter and monitor urine output
May need to use 250ml fluid bolus as could cause overload. Examine patient for fluid overload each bolus. Saline should be fine
Assessment with AMPLE history and brief examination
Get help - If NEWS score high, consider referral to ITU, or refer to renal team for dialysis if needed (see below)
Frequent Observations – Hourly Observations, Daily U&E’s, Fluid Input/output chart and weight monitoring
Stop these drugs in AKI – NSAIDS, Aminoglycosides, Ace inhibitors, ARB’s, Diuretics

Medical:
Supportive Treatment - Treat any infection with antibiotics, , stop nephrotoxic drugs (NSAIDS, ACEi, ARB, Aminoglycosides) and adjust other drug doses for renal failure. Give a PPI for gastric protection and offer nutritional support if needed.

Treat complications – Hyperkalaemia (10% calcium gluconate 10ml IV over 5 minutes followed by 10 units rapid insulin with 50% glucose 50ml IV over 30 minutes and salbutamol 2.5mg nebulisers), Pulmonary Oedema (High Flow O2 and Furosemide), Uraemia (Renal Replacement Therapy). All patients with complications will need to be referred for renal replacement therapy once initial management has been started

Pre-Renal - Correct volume depletion or renal hypo-perfusion with fluids and cardiac support. If hypervolaemic then fluid restrict, give O2, give diuretics and refer for renal replacement therapy if needed.

Renal - Refer to renal team for biopsy and further management. Tubulo Interstitial nephritis and Glomerulonephritis may require steroids. Unless ATN suspected, then supportive treatment. If treated for ATN then there will be am oliguric phase is followed by a polyureic phase within about 7 days.

Post Renal - Catheter, Nephrostomy (stick a tube directly into the bladder that pokes out the skin) or Urological intervention based on the location of the obstruction

Indication for dialysis: 
AKI not responding to treatment
Any complications of AKI - K+, acidosis, fluid overload that not improving with initial therapy
Stage 3 AKI
AKI due to intrinsic renal disease
AKI with hypertension
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