Case 13- AKI and Sepsis Flashcards by pio monaghan

Pre renal AKI causes

Dehydration
Sepsis
Hypotension
Shock
Severe heart failure

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Renal AKI causes

NSAIDS, ACEI, ARBS
Gentamicin, amoxicillin
Glomerulonephritis
Interstitial nephritis
ATN
Contrast agent
Myeloma
Rhabdomyolysis

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Post renal AKI causes

Prostate enlargement eg. BPH
Renal stones
Pelvis cancer

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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

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Medication that causes neutropenia

Clozapine
Methotrexate
Carbimazole
Quinine (malaria)
Rituximab

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Hyperkalaemia causes

AKI, CKD, rhabdomyolysis, adrenal insufficiency, aldosterone antagonists, ACE-I, NSAIDS, DKA, Addison’s disease, burns, heparin

NB- thiazide diuretics cause hypokalaemia

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Hyperkalaemia Sx

Tachycardia, irregular pulse, chest pain, weakness,palpitations, light headed ness

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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

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Emergency management of hyperkalaemia

Insulin and dextrose
Calcium gluconate (stabilise cardiac muscle cells)

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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

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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)

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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)

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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%)

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Complications of an AKI

Hyperkalaemia
Fluid overload eg. Heart failure and pulmonary oedema
Metabolic acidosis
Uraemia can cause encephalopathy and pericarditis

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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

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Sepsis differentials

MI
PE
Hyperthyroidism

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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

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Neutropenic sepsis

Sepsis in a patient with a low neutrophil count of less than 1x10 (9)

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ATN

Damage and necrosis to the epithelial cells of the renal tubules (most common cause of AKI)

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Causes of ATN

Ischaemia- shock, sepsis, dehydration

Direct toxin damage- contrast dye, gentamicin, NSAID

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Management of ATN

Same as AKI

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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.