Case 13- AKI and Sepsis Flashcards
Pre renal AKI causes
Dehydration
Sepsis
Hypotension
Shock
Severe heart failure
Renal AKI causes
NSAIDS, ACEI, ARBS
Gentamicin, amoxicillin
Glomerulonephritis
Interstitial nephritis
ATN
Contrast agent
Myeloma
Rhabdomyolysis
Post renal AKI causes
Prostate enlargement eg. BPH
Renal stones
Pelvis cancer
Investigations for suspected AKI
Urine output chart, observations, urinalysis and culture
Bloods- FBC, UE, LFT, CRP, blood cultures, VBG (lactate, oxygen)
CXR- infection (sepsis can cause the AKI)
ECG- if hyperkalaemia present
Renal tract USS
(Renal biopsy- unlikely)
Myeloma and nephritic screen
Medication that causes neutropenia
Clozapine
Methotrexate
Carbimazole
Quinine (malaria)
Rituximab
Hyperkalaemia causes
AKI, CKD, rhabdomyolysis, adrenal insufficiency, aldosterone antagonists, ACE-I, NSAIDS, DKA, Addison’s disease, burns, heparin
NB- thiazide diuretics cause hypokalaemia
Hyperkalaemia Sx
Tachycardia, irregular pulse, chest pain, weakness,palpitations, light headed ness
Investigations for suspected sepsis
Urine output chart, observations
ECG and Urinalysis, culture and sensitivities (MSU), sputum culture if applicable
Bloods- FBC UE LFT ABG (lactate) CRP Coagulation profile
CXR
Lumbar puncture- if meningitis
NB- get to HDU!! Involve seniors and preform QSOFA
NB- sepsis 6
Emergency management of hyperkalaemia
Insulin and dextrose
Calcium gluconate (stabilise cardiac muscle cells)
Dialysis indications in AKI
AEIOU (refractory)
Acidosis
Electrolyte abnormalities eg. Hyperkalaemia, hyponatraemia, hypercalcaemia (EXG changes)
Intoxicants- methanol, lithium, salicylate
Overload- acute pulmonary oedema
Uraemia- urea >60, ureamic pericarditis, encephalopathy
NB- CKD: dialysis required when eGFR below 15
Management of an AKI
Treat underlying cause (depends on pre, renal, or post)
Stop nephrotoxic drugs eg. NSAID ACE-I
Monitor and correct pH, fluid balance and electrolytes
Insert a catheter
Involve the renal team (may require dialysis)
Pre renal AKI/uraemia
Concentrated urine as the tubules are still working
High osmolality (500+)
Low NA (<20)
Good response to fluid
Raised urea:creatinine (100+)
Normal or bland sediment
Fractional sodium excretion (<1%)
NB- kidneys hold onto sodium to preserve volume (that’s why sodium is low)
Intrinsic AKI osmolarity/uraemia (ATN)
Tubules not working so dilute urine
Low osmolality (<350)
High urine NA (40+)
Poor response to fluid
Normal urea:creatinine
Muddy brow casts
Fractional sodium excretion (>1%)
Complications of an AKI
Hyperkalaemia
Fluid overload eg. Heart failure and pulmonary oedema
Metabolic acidosis
Uraemia can cause encephalopathy and pericarditis
Sepsis Sx
Tachypnoea, high or low temp, tachycardia, altered mental status (acute), low sats, hypotension, oliguria, poor cap refill, mottled skin, cyanosis, malaise, lethargy, nausea, vomiting
Sepsis differentials
MI
PE
Hyperthyroidism
Management of sepsis
Sepsis 6
Measure lactate, urine output, take 2 blood cultures from separate sites
Give oxygen (above 94), IV fluids, IV broad spectrum antibiotics
Neutropenic sepsis
Sepsis in a patient with a low neutrophil count of less than 1x10 (9)
ATN
Damage and necrosis to the epithelial cells of the renal tubules (most common cause of AKI)
Causes of ATN
Ischaemia- shock, sepsis, dehydration
Direct toxin damage- contrast dye, gentamicin, NSAID
Management of ATN
Same as AKI
ATN Investigations
Urinalysis- muddy brown casts or renal tubular epithelial cells in the urine
Potassium requirement when prescribing fluids
1 mmol/kg/day
Proteinuria and urine dip
Protein rules out a pre or post AKI cause (must be a renal cause)
Glucose requirement when prescribing fluids
50-100g/day irrespective of weigh
3 things to remember that cause intrinsic AKI
Glomerulonephritis (many specific causes- displaying nephritic and nephrotic syndromes)
ATN- most common cause of AKI, due to ischaemia or nephrotoxins
AIN- drug-induced AKI (hypersensitivity reaction)
Hyperkalaemia- stabilisation of the cardiac membrane
IV calcium gluconate
Hyperkalaemia- shift potassium to intra cellular fluid
Insulin/dextrose infusion
Nebulised salbutamol
Hyperkalaemia- removal of potassium from body
Calcium resonium (rectal ie. enema)
Loop diuretics
Dialysis
AKI definition
Urine output of less than 0.5ml/kg/hour for 6 hours (8 paeds)
Rise in creatinine of 26 or more in 48 hours
>50% rise in creatinine over 7 days
Paeds or young adults- 25% fall in eGFR in 7 days
AKI stage 1
Increase in creatinine to 1.5-1.9x baseline (7 days)
Increase in creatinine 26.5 (48 hours)
Reduction in urine output to 0.5ml/kg/hour for 6 hours
AKI stage 2
Increase in creatinine 2-2.9x baseline (7 days)
Reduction in urine output to 0.5ml/kg/hour for 12 hours
AKI stage 3
Increase in creatinine 3x baseline (7 days)
Increase in creatinine to 353.6 (48 hours)
Reduction in urine output to 0.3ml/kg/hour for 24 hours or the commencement of RRT
AKI referral to nephrology criteria
Renal transplant
No known cause
Vasculitis/glomerulonephritis/ myeoloma/tubulointerstitial nephritis
Inadequate response to treatment
Complications of an AKI
Stage 3 AKI
CKD stage 4 or 5
Qualify for RRT
Haemolytic uraemic syndrome Sx
AKI
Haemolytic anaemia
Thrombocytopenia
Causes of HUS
Primary- complement dysregulation
Secondary
Shiva toxin producing E. coli
Pneumococcal infection
HIV
SLE, drugs, cancer
Investigations for HUS
Urinalysis
FBC, blood film, UE
Stool culture- OCR for shiva toxin
Management of HUS
Supportive- fluids, dialysis etc.
No role for ABX
Eculuzumab (C5 inhibitor monoclonal antibody) has greater evidence than plasma exchange
Staging of hyperkalaemia
Mild 5.5-5.9
Moderate 6.0-6.4
Severe 6.5+
When to initiate emergency management of hyperkalaemia
Severe hyperkalaemia (6.5+) or ECG changes
Further management of hyperkalameia after initial pharmacotherapy management
Stop exacerbating drugs eg ACE-I
Treat underlying cause
Lower total body potassium eg. Calcium resonium, loop diuretics, dialysis if needed
Features of hypokalaemia
Muscle weakness, hypotonia
Hypokalaemia and ECG changes
U waves
Small or absent T waves
Prolonged PR interval
ST depression
NB-In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT
Features of rhabdomyolysis
AKI with disproportionately raised creatinine
Elevated CK (10,000)
Myoglobinuria
Hypocalcaemia
Elevated phosphate
Hyperkalaemia
Metabolic acidosis
Causes of rhabdomyolysis
Seizure
Collapse and subsequent time on floor
Ecstasy
Crush injury
Statins (esp. if with clarithromycin)
Management
IV fluids
Urinary alkinisation
Sterile pyuria
White cells in urine without presence of bacteria
Causes of sterile pyuria
Partially treated UTI
Chlamydia infection (urethritis)
Renal stones
Appendicitis
Bladder/renal cancer
APKD
Hyaline casts
Tamm horsfall protein
Normal urine, after exercise, during fever, loop diuretics use
Red cell casts
Nephritic syndrome
Rhabdomyolysis and AKI
Rhabdomyolysis would give a CK of >10,000 (if CK is raised but not this high, and the patient has been on the floor, think of dehydration as a cause of their AKI (unable to drink for many hours))
Drugs to stop in an AKI
DAMN AKI
Diuretics
Aminoglycosides (eg. gent, neo and strep) and ACE inhibitors
Metformin
NSAIDs (except cardioprotective aspirin eg. 75mg)
NB- you would however use diuretics in AKI due to fluid overload
AKI and pulmonary oedema
Start with IV furosemide
If medical management has failed to resolve the fluid
overload, then haemodialysis is indicated in order to lower the pulmonary arterial pressure and prevent further overload.
