Acute Kidney Injury Flashcards
Definition of Acute kidney injury
Decline of renal excretory function over hours or days (RAPID)…recognized by the rise in serum urea and creatinine and leading to a failure to maintain fluid, electrolyte and acid-base homeostasis.
reversible
RIFLE criteria
Any one of:
Risk
- rise in creatinine >26umol/L in 48 hours or rise in creatinine >1.5 x baseline (best figure in 3/12)
- urine output <0.5ml/kg/h for >6 consequetive hours
Injury
- SCr increased by 2 x baseline
- Urine output <0.5ml/kg/hr for >12 consecutive hours
Failure
- Scr 3x baselines
- Urine outpu <0.3ml/kg/hr or anuria for 12 hours
Loss
- Persistent ARF = complete loss of kidney function >4 weeks
end stage kidney disease
- end stage kidney disease >3 months
AKIN Criteria for diagnosis of AKI
- time course - rapid (
- reduction in kidney function:
- rise in serum creatinine (absolute increase of >0.3mg/dl or percentage of >50%)
- reduction in urine out[ut (,0.5ml/kg.hr for >6 hours)
Symptoms of acute renal failure
Oliguria/anuria -little or no passage of urine
Nausea and vomitting - increased urea and other toxins
fitting
confusion
fever- sepsis?
Swollen ankes/SOB- oedema
Signs
hypertension
pallor
swollen bladder- chronic urinary retention/ obstruction
dehydration
fluid overload - raised JVP, pulmonary oedema, peripheral oedema
Pericardial rub
metabolic acidosis
potasssium - muscle weakness and cardiac instability
Risk factors for developing AKI
- Age >75
- chronic kidney disease
- cardiac faiilure
- PVD
- CLD
- diabetes
- drugs (newly started)
- sepsis
- poor fluid intake/ increased losses
- history of urinary symptoms
Classification of Acute Renal failure
- Pre-renal- circulatory failure
- Renal- the cells of the kidney
- Post-renal- Urinary tract obstruction
Pre-renal causes of AKI
Anything that impairs renal perfusion
- hypotension
- hypovolaemia (burns, diarrhoea, haemorrhage)
- hypoperfusion
- hypoxia
Intra-renal causes of AKI
Acute tubular necrosis (Toxic or ischaemic)
Vascular causes (Large vessel occulsion, hypertension, scleroderma)
Glomerulonephritis
Interstitual nephritis (drugs, infection related)
Vasculitis (good pastures, wegeners, churg-strauss
Haematological (myeloma, haemolytic uraemic syndrome)
other causes (rhabdomyolysis)
Acute tubular necrosis - 80%
Obstructive - 10%
Glomerulonephritis (primary & secondary) - 3%
Acute tubulointerstitial nephritis- 2%
Vasculitis - 1.5%
Atheroembolic - 1%
Other - 2.5%
Post -renal causes of AKI
Anything between the renal pelvis and urethral meatus which obstructs flow of urine
- Calculi
- tumours (ureter, bladderm prostate, cervix, ovarian, can be extrinsic)
- lymph nodes (compression)
- protstate
Note Males = prostate
females = gynae tumours
all causes of acute renal failure
Patients cant VOID RIGHT
- Vasculitis
- obstruction
- infection
- drugs (acute tubular necrosis)
- renal artery stenosis
- interstitial nephropath
- glomerular nephropathy
- hypovolaemia
- thromboemolism
Differential diagnosis
Must exclude pre-renal and obstruction first
Then think of intrinsic AKI
- ATN (toxic or ischaemic) - 80%
- Obstruction - 10%
- Glomerulonephritis (primary/secondary)-3%
Breakdown of renal causes:
- Glomeruli (vascultitis)–>glomerulonephritis, drugs (gentamicin)
- Tubules ->tublo-interstitial nephritis, rhabdomyolysis
Acute tubular necrosis
Ischaemic damage due to renal hypoperfusion (hypotension, sepsis, toxins often all three)
- reversible in time but time taken varies (may need dialysis until recovery occurs)
- some never recover and some have chronic renal impairment
Toxins that cause ATN
Exogenous:
- drugs (NSAIDs, gentamicin, ACEI), contrast, posions
Endogenous:
- Myoglobin, haemoglobin, Immunoglobulins (myeloma),, calcium, urate
NSAID and ACEi effect on an unwell patients kidneys
NSAIDS
As MAP falls
PGs dilate afferent arteriole to increase flow (protect renal perfusin)
If patient on NSAIDs they cant make prostaglandins and so inadequate renal perfusion
ACEi
Normally angiotensin II contracts the efferent arteriorle, patients on ACE I cant contract efferent arteriole to maintain pressure
Investigations
Monitoring
- BP
- urine dip (haematuria, proteinuria)
- ECG (hyperkalaemia)
- ABG (acidosis, respiratory failure)
- FBC
- U &E (urea and creatinine)
- CRP/ESR
Identify the cause
- Blood culutre (infection/sepss)
- US KUB (stones)
- Myleoma screen (bence-jones proteins)
- renal screen (ANA, ANCA, anti-BM))
- dopppler renal USS and/ or angiography
- CXR (pneumonia)
- CT KUB (stones)
- Renal biopsy (tumour)
AKI management
- Assesent - renal effects of all drugs taken
- ABCDE approach, and as part of C
- asses fluid volume status - check BP, JVP, skin turgour, capillary refill, urine output (catheterize)
- Check an urgent K+ on a venous blood specimen and an ECG to check for life threatening hyperkalaemia
- History - risk factors, co-morbidites, previous renal disease, recent fluid intake and losses, new drugs, systemic features (rash, joint pain, fever)
- Examination - full systemic examination. Specific features- palpable bladder, palpable kidnes, abdominal/pelvic masses, renal bruits, rashes
- Bedside tests - dip the urine
- Blood tests
- imaging - ALWAYS RULE OUT OBSTRUCTION
- Acute or chronic- see card
- Refer to a nephrologist if needed
Is the injury acute or chronic?
Suspect chronic if small kidneys
When to refer to a nephrologist?
- assess the patient, correct -pre and post renal factors. treat urgent problems
- always refer:
- hyperkalaemia in an oligoanuric patient, hyperkalaemia or fluid overload unresponsibe to medical rx,
- urea >40 mmol/l +/- signs of uraemia such as pericarditis
- patients with suspected glomerulonephritis (blood and protein on urinalysis) or systemic disease
- Consider refereal
- no obvious reversible ause,
- creatine >300 or rising >50 umol/L per day
- what they want to know-
- history and time course
- U& e results
*
Serological abnormalities in AKI
- fluid balance - patient can be either hypovolaemic or fluid overloaded
- acid base balance- usually a metabolic acidosis
- electrolyte abnormalities - most commonly and immediately worrying - hyperkalaemic
- haematological - anaemia
Management of fluid balance
- fluid resucitation
- generally ringers-lactate and harttmans solutions should be avoided as K+
- IV furosemide
Acidosis treatment
generally the correction of the underlying cause by fluid resusciation should be enough to resolve a metabolic acidosis (If raised potassium and HCO3
However if pH is very low (
- Give give bicarbonate supplementation - Iv NaBicarb 1.26%
- risks of IV alkali therapy- hypernatramiea, excess |CO2 and metabolic alkalosis, however, mean that if possible, when the normal management procedures are not effective, dialysis should be preferred
Potassium management
- *K<6=** abnormal but no immediate concern
- *K6-6.4**=risk of arrhythmia (VT) - need treatment esp if ECG changes
- *K>6.5-** MEDICAL EMERGENCY
Treatment
Potassium >6.0 mmol/L
- Calcium Resonium- reduces absorption from the gut - 15g PO
Potassium >6.5 mmol/L
- Insulin - dextrose (50ml 50% dextrose with 10 units of actrapid insulin, IV over 5 mins) dextrose = moves potassium into cells, must watch blood suga
- Calcium resonium 15g PO
- Calcium gluconate to stabalise cardiac membrane
ECG changes in hyperkalaemia
- TALL TENTED T WAVES
- Absent or small p waves
- increased PR interval
- widened QRS complex
- sine wave pattern
Mangement of haemtological abnormalities
- in the case of severe anaemia correction usually requires transfusion of blood products
Pulmonary oedema management
- sit up and give high flow O2
- venous vasoldilator eg diamorphine 2.5mg
- IV diuretic (furosemide)
- if no response urgent haemodilaysis or haemofiltration is needed
- consider CPAP
Immediate treatment of AKI
General measures
- Airway and breathing
- Ciculation-shock-restore renal perfusion: Hyperkalaemia, Pulmonary oedema
- Stop nephrotoxic drugs - eg NSAIDS, ACEI, Gentamicin, amphotericin. Stop metformin if creatining is >150mmol/l
- Monitoring- consider transfer to ICU/HDU
- check pulse, BP, JVP and urine output hourly
- daily U&E
- daily fluid balance chart and daily weight
- nutrition - vital in critically unwell patientL aim for normal calorie intake
- Exclude obstruction & consider renal causes (pre-renal cause sufficient to account for ARF?)
treat the underlying cause
- Pre-renal: correct volume depletion with appropriate fluids, treat sepsis with Antibiotics, inoptropic support if signs of shock
- Post-renal - catheterize and consider CT of renal tract and urologiy referal if obstruction likely
- Intrinsic renal - refer ealy to nephrology if concern over tuulointerstitial or glomerular pathology
Manage complication
- Hyperkalameia
- pulmonary oedema
- uraemia- may require dialysis
AKI outcomes
- Dialysed for AKI- mortality 20-30% (ofen in ITU)
- 85% return to baseline kidney function
- 10% are left with some renal impairment
- 5% do not recover kidney function i.e. need long term dialysis or transplant
Absolute indications for dialysis
- severe refractory hyperkalaemia
- Hyperkalaemia (persistent >7 mmol/L)
- metabolic acidosis (if PH <7.2, bicrabonate <12)
- pulmonary oedema (refractory)
- pericarditis
- symptomatic uraemia - encephalopathy
Recovery from ATN
- Often a polyuric phase for 48-72hr
- May be up to 6l urine/day
- Often subsequent low K, Ca, Mg as ‘low quality urine
- Tubules fail to concentrate urine
Prevention of AKI - Sick day rules
30% of cases are preventable
reviewing drugs:
- withhold/avoid:
- diuretics, aceI, antihypertensives if BP low (do not stop B-Blockers acutely, consider decreased dose)
- metformin if creatiinng rising (risk of lactic acidosis)
- NSAIDs,
- nephrotoxic Abx (gentamicin, nitrofurantoin)
- use with caution
- opiates
- contrast
- acutely unwell patients have multiple contrast scanes - important cause of AKI
