AKI Flashcards
AKI definition
Syndrome arising from a rapid drop in GFR (over hours/days) that is characterised by retention of waste products of metabolism + disordered electrolyte, acid-base and fluid balance
AKI criteria
Serum creatinine rises by >26umol/L within 48 hours
Serum creatinine rises by >150% within last 7 days
Urine output <0.5ml/kg/hr for >6 consecutive hours
AKI Stage 1
Rise in creatinine >26umol/L or 150-200% above baseline
Urine <0.5ml/kg/h for >6hrs
AKI Stage 2
Creatinine 200-300% above baseline
Urine <0.5ml/kg/hr >12hrs
AK Stage 3
Creatinine>300% above baseline or creatinine >354umol/L with acute rise of >45umol/L or on RRT
Urine <0.3ml/kg/hr for >24hr, or anuric for 12hr
Pre-renal AKI
Decrease in renal blood flow leads to reduction in GFR
Potentially reversible by restoration of renal perfusion
Kidneys remain structurally normal
Pre-renal AKI causes
Due to a decrease in effective circulating volume - haemorrhage - volume depleted - low CO - sepsis - congestive heart failure - cirrhosis - hepato-renal syndrome Due to arterial stenosis/occlusion - Renal artery stenosis - NSAIDs -ACEIs/ACRBs
Renal AKI
Damage to renal parenchyma that causes decrease in renal function
Renal AKI Causes
Acute tubular necrosis
Vascular
Acute glomerulonephritis
Acute interstitial nephritis
Renal AKI- Acute tubular necrosis causes
Ischaemic (prolonged renal hypoperfusion –> ATN)- e.g. untreated pre-AKI
Nephrotoxic:
- Haemo/myoglobinuria (due to rhabdomyolysis)
- Myeloma casts
- Intratubular crystals (tumour lysis syndrome –> urate crystals)
-Nephrotoxic drugs (aminoglycosides, cisplatin, atorvastatin, ethylene glycol)
-Radiocontrast agents
Renal AKI- Vascular causes
Vasculitis
Thrombotic microangiopathies
Hypertensive emergency
Renal AKI- acute glomerulonephritis
Inflammation and damage of glomerular membrane
Renal AKI- acute interstitial nephritis
Allergic reaction where interstitium of kidney becomes inflamed
Usually due to NSAIDs or antibiotics (methicillin, penicillin, cephalexin), PPIs
Post-renal AKI
Any cause of increased backpressure on the kidneys can reduce tubular function
Obstruction can occur at any level along the urinary tract
AKI will only occur if both kidneys obstructed (will occur always if only have 1 kidney)
Post-renal AKI causes
Bladder outflow obstruction- BPH, tumours
Bilateral ureteric obstruction- tumour, stones, stricture
AKI presentation
Raised urea
Raised creatinine
Decreased urine output (<400ml/day)
Volume depletion (low JVP, postural drop)= pre-renal causes of AKI
Volume overload (pulmonary oedema)= renal causes of AKI
Hyperkalaemia (–>cardiac arrhythmias)
Non-specifically sick, deteriorating patient
Uraemia symptoms
Nausea Vomiting Fatigue Anorexia Weight loss Muscle cramps Pruritis Mental status change Visual disturbances Increased thirst Hyperventilation Uraemic frost
Uraemic induced platelet dysfunction
Ecchymosis (bleeding under skin)
GI bleeds
increased bleeding tendency
Uraemic encephalopathy
Headaches
Confusion
Coma
Uraemic pericarditis
Chest pain
Malaise
Pericardial friction rub
AKI Hyperkalaemia- symptoms
Muscle weakness Lethargy Nausea Vomiting Palpitations
AKI Hyperkalaemia- ECG changes
Tented T waves PR prolongation Loss of P wave Prolonged QRS complex ST elevation Sine wave --> VF, BBB, MI
AKI Hyperkalaemia- treatment
IV calcium gluconate (cardioprotective) Insulin + dextrose IV salbutamol Calcium resonium K+ wasting diuretics
AKI Pulmonary oedema
Occurs due to failure of salt + water excretion
AKI pulmonary oedema- symptoms
Tachypnoea Tachycardia Cool + clammy Respiratory crackles Wheeze
AKI pulmonary oedema- investigations
Low SaO2
PaO2<8kPa
Alveolar shadowing on CXR
AKI pulmonary oedema- treatment
Oxygen (aim for SaO2>95%) Pain relief High dose diuretics (bolus of furosemide) Vasodilators (nitrates) Dialysis CPAP
AKI- metabolic acidosis
Associated with raised anion gap metabolic acidosis due to accumulation of sulphates and phosphates, and impaired reabsorption of bicarbonate
Degree of acidosis is modest and doesn’t usually require treatment as will resolve when renal function restored
pH<7.1 is indication for dialysis
AKI- uraemic encephalopathy
Syndrome occurs when GFR drops (often below 15) and leads to urea accumulation
Symptoms- confusion, severe pruritic, agitation, seizure, nausea, vomiting
Treatment- dialysis
Prerenal AKI treatment
Improve renal perfusion- saline, blood transfusion, albumin
Do not put urinary catheter
Do not give diuretics (doesn’t improve renal function)
CVP line rarely needed
Aim is to reverse cause of AKI- e.g. treat heart failure
Renal AKI treatment
GN= immunosuppression IBE= antibiotics AIN= stop offering medication + corticosteroids ATN= self-correcting but may take a while (up to 6 wks)
Post-renal AKI treatment
Obtain drainage of urine
- bladder or below= urinary catheter
- above bladder= anterograde (nephrostomy) or retrograde drainage (JJ stent)
Hyperkalaemia treatment
IV calcium gluconate Insulin + dextrose Salbutamol (IV or nebuliser) Calcium resonium Dialysis
Pulmonary oedema treatment
High dose diuretics Pain relief Vasodilators (IV GTN) Dialysis CPAP
Uraemic encephalopathy treatment
Dialysis
Diuretic phase during AKI recovery
Recovery from AKI can result in polyuric state with large vol urine production
Assess signs of hypovolaemia + hypernatraemia that may mean IV fluid resuscitation needed
Indications in AKI for RRT
Hyperkalaemia >6.5mmol/L
Vol overload (pulmonary oedema, hypervolaemic vol status)
Acidosis pH<7.1
Critically unwell patients
Uraemic complications (pericarditis, encephalopathy)
Diuretic resistant cardiac failure
Poison or toxin removal (lithium, ethylene glycol)
Hyperthermia
Haemodialysis
Solute clearance by diffusion across a semi-permeable membrane
Pores allow small molecules through but prevent passage of larger weight molecules
Allows products such as bicarb to be replaced
Diffusion rate maximised by counter-current exchange mechanism
Haemodialysis- intermittent
Faster correction of electrolyte imbalances Fewer bleeding complications Lower cost More haemodynamic instability Less control of fluid balance
Haemodialysis- continuous
More haemodynamic stability
Lower risk of fluid balance shift problems (cerebral oedema)
Slower correction of electrolyte imbalances
Haemofiltration
Solute clearance by convection
Can remove large molecular weight molecules
Continuously delivered
Large vols need to be filtered to attain adequate solute clearance
More suitable for a patient on ITU who couldn’t handle a drop in BP
In haemofiltration, fluid shifts are less pronounced and it is performed continuously (slow clearance) while a
patient is in renal failure
Also referred to as continuous arteriovenous haemofiltration (CAVH)
Haemodiafiltration
Combined HD + HF get the best of both modalities
Hypovolaemic signs
Dry mucous membrane Reduced tissue tugor Low JVP Postural hypotension Drop in body weight Low urine output
Hypervolaemic sign
Oedema
Raised JVP
Pulmonary oedema
Increased body weight
Crystalloids
Saline can result in hyperchloraemic metabolic acidosis
UK guidelines recommend use of balanced crystalloids over saline in AKI
Sodium bicarb may be useful in acidotic volume-depleted patients
Colloids
Contain osmotically active ingredients that remain in intravascular compartment and pull in extravascular water
Starch containing solutions thought to worsen AKI
AVOID COLLOIDS IN AKI
Blood products
Appropriate in pre-renal AKI due to loss of circulating BV due to haemorrhage
Urinalysis
Exclude UTI
Significant protein –> consider nephrotic/nephritic syndrome (measure PCR or ACR)
Microscopy Casts- Hyaline cast
Normal
Microscopy casts- lipid cast
High urinary protein nephrotic syndrome
Microscopy Casts- Muddy brown cast
ATN
Microscopy Casts- Pigment cast
Haemo/myoglobinuria
Microscopy Casts- Crystals
Tumour lysis syndrome
Microscopy Casts- Red cell cats
GN
Microscopy Casts- White cell casts
Infection
Acute interstitial nephritis
Post-strep acute GN
Microscopy Casts- Bacterial casts
Infection
Microscopy Casts- eosinophil cast
Acute interstitial nephritis
Microscopy- haematuria alone
Post-renal AKI
Vasculitis
Trauma
Blood tests- Low Hb
Haemolysis
GI bleed
Blood tests- raised WCC
Infection
Blood tests- Abnormal LFTs
Hepatorenal syndrome
Blood tests- high urea:creatinine ratio
pre-renal AKI (sign of dehydration)
Blood tests- raised ESR
any inflammatory condition
Blood tests- blood culture
sepsis
Blood tests- creatine kinase
rhabdomyolysis
Blood tests- urate
tumour lysis syndrome
Blood tests- lactate
tissue hypoperfusion
Blood tests- hypercalcaemia
Myeloma
sarcoidosis
Blood tests- Immunological testing
Anti-nuclear antibodies- SLE
Anti-neutrophil cytoplasmic antibodies- small vessel vasculitis
Anti GBM antibodies- Anti GBM disease
Anti streptolysin O titres- post-streptococcal GN
Immunoglobulins- multiple myeloma
Antiphospholipia antibodies- antiphospholipid syndrome
Ultrasound
Hydronephrosis (accumulation of urine in kidney) that indicates obstruction in urinary tract
CXR
pulmonary oedema
