Case 13- AKI and Sepsis Flashcards

1
Q

Pre renal AKI causes

A

Dehydration
Sepsis
Hypotension
Shock
Severe heart failure

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2
Q

Renal AKI causes

A

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

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3
Q

Post renal AKI causes

A

Prostate enlargement eg. BPH
Renal stones
Pelvis cancer

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4
Q

Investigations for suspected AKI

A

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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5
Q

Medication that causes neutropenia

A

Clozapine
Methotrexate
Carbimazole
Quinine (malaria)
Rituximab

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6
Q

Hyperkalaemia causes

A

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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7
Q

Hyperkalaemia Sx

A

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

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8
Q

Investigations for suspected sepsis

A

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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9
Q

Emergency management of hyperkalaemia

A

Insulin and dextrose
Calcium gluconate (stabilise cardiac muscle cells)

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10
Q

Dialysis indications in AKI

A

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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11
Q

Management of an AKI

A

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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12
Q

Pre renal AKI/uraemia

A

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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13
Q

Intrinsic AKI osmolarity/uraemia (ATN)

A

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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14
Q

Complications of an AKI

A

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

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15
Q

Sepsis Sx

A

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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16
Q

Sepsis differentials

A

MI
PE
Hyperthyroidism

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17
Q

Management of sepsis

A

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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18
Q

Neutropenic sepsis

A

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

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19
Q

ATN

A

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

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20
Q

Causes of ATN

A

Ischaemia- shock, sepsis, dehydration

Direct toxin damage- contrast dye, gentamicin, NSAID

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21
Q

Management of ATN

A

Same as AKI

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22
Q

ATN Investigations

A

Urinalysis- muddy brown casts or renal tubular epithelial cells in the urine

23
Q

Potassium requirement when prescribing fluids

A

1 mmol/kg/day

24
Q

Proteinuria and urine dip

A

Protein rules out a pre or post AKI cause (must be a renal cause)

25
Q

Glucose requirement when prescribing fluids

A

50-100g/day irrespective of weigh

26
Q

3 things to remember that cause intrinsic AKI

A

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)

27
Q

Hyperkalaemia- stabilisation of the cardiac membrane

A

IV calcium gluconate

28
Q

Hyperkalaemia- shift potassium to intra cellular fluid

A

Insulin/dextrose infusion
Nebulised salbutamol

29
Q

Hyperkalaemia- removal of potassium from body

A

Calcium resonium (rectal ie. enema)
Loop diuretics
Dialysis

30
Q

AKI definition

A

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

31
Q

AKI stage 1

A

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

32
Q

AKI stage 2

A

Increase in creatinine 2-2.9x baseline (7 days)
Reduction in urine output to 0.5ml/kg/hour for 12 hours

33
Q

AKI stage 3

A

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

34
Q

AKI referral to nephrology criteria

A

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

35
Q

Haemolytic uraemic syndrome Sx

A

AKI
Haemolytic anaemia
Thrombocytopenia

36
Q

Causes of HUS

A

Primary- complement dysregulation

Secondary
Shiva toxin producing E. coli
Pneumococcal infection
HIV
SLE, drugs, cancer

37
Q

Investigations for HUS

A

Urinalysis
FBC, blood film, UE
Stool culture- OCR for shiva toxin

38
Q

Management of HUS

A

Supportive- fluids, dialysis etc.
No role for ABX
Eculuzumab (C5 inhibitor monoclonal antibody) has greater evidence than plasma exchange

39
Q

Staging of hyperkalaemia

A

Mild 5.5-5.9
Moderate 6.0-6.4
Severe 6.5+

40
Q

When to initiate emergency management of hyperkalaemia

A

Severe hyperkalaemia (6.5+) or ECG changes

41
Q

Further management of hyperkalameia after initial pharmacotherapy management

A

Stop exacerbating drugs eg ACE-I
Treat underlying cause
Lower total body potassium eg. Calcium resonium, loop diuretics, dialysis if needed

42
Q

Features of hypokalaemia

A

Muscle weakness, hypotonia

43
Q

Hypokalaemia and ECG changes

A

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

44
Q

Features of rhabdomyolysis

A

AKI with disproportionately raised creatinine
Elevated CK (10,000)
Myoglobinuria
Hypocalcaemia
Elevated phosphate
Hyperkalaemia
Metabolic acidosis

45
Q

Causes of rhabdomyolysis

A

Seizure
Collapse and subsequent time on floor
Ecstasy
Crush injury
Statins (esp. if with clarithromycin)

46
Q

Management

A

IV fluids
Urinary alkinisation

47
Q

Sterile pyuria

A

White cells in urine without presence of bacteria

48
Q

Causes of sterile pyuria

A

Partially treated UTI
Chlamydia infection (urethritis)
Renal stones
Appendicitis
Bladder/renal cancer
APKD

49
Q

Hyaline casts

A

Tamm horsfall protein
Normal urine, after exercise, during fever, loop diuretics use

50
Q

Red cell casts

A

Nephritic syndrome

51
Q

Rhabdomyolysis and AKI

A

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))

52
Q

Drugs to stop in an AKI

A

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

53
Q

AKI and pulmonary oedema

A

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.