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Met 3b > AKI > Flashcards

AKI Flashcards

1
Q

AKI definition

A

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

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2
Q

AKI criteria

A

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

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3
Q

AKI Stage 1

A

Rise in creatinine >26umol/L or 150-200% above baseline

Urine <0.5ml/kg/h for >6hrs

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4
Q

AKI Stage 2

A

Creatinine 200-300% above baseline

Urine <0.5ml/kg/hr >12hrs

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5
Q

AK Stage 3

A

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

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6
Q

Pre-renal AKI

A

Decrease in renal blood flow leads to reduction in GFR
Potentially reversible by restoration of renal perfusion
Kidneys remain structurally normal

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7
Q

Pre-renal AKI causes

A 
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
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8
Q

Renal AKI

A

Damage to renal parenchyma that causes decrease in renal function

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9
Q

Renal AKI Causes

A

Acute tubular necrosis
Vascular
Acute glomerulonephritis
Acute interstitial nephritis

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10
Q

Renal AKI- Acute tubular necrosis causes

A

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

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11
Q

Renal AKI- Vascular causes

A

Vasculitis
Thrombotic microangiopathies
Hypertensive emergency

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12
Q

Renal AKI- acute glomerulonephritis

A

Inflammation and damage of glomerular membrane

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13
Q

Renal AKI- acute interstitial nephritis

A

Allergic reaction where interstitium of kidney becomes inflamed
Usually due to NSAIDs or antibiotics (methicillin, penicillin, cephalexin), PPIs

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14
Q

Post-renal AKI

A

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)

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15
Q

Post-renal AKI causes

A

Bladder outflow obstruction- BPH, tumours

Bilateral ureteric obstruction- tumour, stones, stricture

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16
Q

AKI presentation

A

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

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17
Q

Uraemia symptoms

A 
Nausea
Vomiting
Fatigue
Anorexia
Weight loss
Muscle cramps
Pruritis
Mental status change
Visual disturbances
Increased thirst
Hyperventilation
Uraemic frost
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18
Q

Uraemic induced platelet dysfunction

A

Ecchymosis (bleeding under skin)
GI bleeds
increased bleeding tendency

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19
Q

Uraemic encephalopathy

A

Headaches
Confusion
Coma

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20
Q

Uraemic pericarditis

A

Chest pain
Malaise
Pericardial friction rub

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21
Q

AKI Hyperkalaemia- symptoms

A 
Muscle weakness
Lethargy
Nausea
Vomiting
Palpitations
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22
Q

AKI Hyperkalaemia- ECG changes

A 
Tented T waves
PR prolongation
Loss of P wave
Prolonged QRS complex
ST elevation
Sine wave 
--> VF, BBB, MI
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23
Q

AKI Hyperkalaemia- treatment

A 
IV calcium gluconate (cardioprotective)
Insulin + dextrose
IV salbutamol
Calcium resonium
K+ wasting diuretics
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24
Q

AKI Pulmonary oedema

A

Occurs due to failure of salt + water excretion

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25
AKI pulmonary oedema- symptoms
``` Tachypnoea Tachycardia Cool + clammy Respiratory crackles Wheeze ```
26
AKI pulmonary oedema- investigations
Low SaO2 PaO2<8kPa Alveolar shadowing on CXR
27
AKI pulmonary oedema- treatment
``` Oxygen (aim for SaO2>95%) Pain relief High dose diuretics (bolus of furosemide) Vasodilators (nitrates) Dialysis CPAP ```
28
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
29
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
30
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
31
Renal AKI treatment
``` GN= immunosuppression IBE= antibiotics AIN= stop offering medication + corticosteroids ATN= self-correcting but may take a while (up to 6 wks) ```
32
Post-renal AKI treatment
Obtain drainage of urine - bladder or below= urinary catheter - above bladder= anterograde (nephrostomy) or retrograde drainage (JJ stent)
33
Hyperkalaemia treatment
``` IV calcium gluconate Insulin + dextrose Salbutamol (IV or nebuliser) Calcium resonium Dialysis ```
34
Pulmonary oedema treatment
``` High dose diuretics Pain relief Vasodilators (IV GTN) Dialysis CPAP ```
35
Uraemic encephalopathy treatment
Dialysis
36
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
37
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
38
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
39
Haemodialysis- intermittent
``` Faster correction of electrolyte imbalances Fewer bleeding complications Lower cost More haemodynamic instability Less control of fluid balance ```
40
Haemodialysis- continuous
More haemodynamic stability Lower risk of fluid balance shift problems (cerebral oedema) Slower correction of electrolyte imbalances
41
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)
42
Haemodiafiltration
Combined HD + HF get the best of both modalities
43
Hypovolaemic signs
``` Dry mucous membrane Reduced tissue tugor Low JVP Postural hypotension Drop in body weight Low urine output ```
44
Hypervolaemic sign
Oedema Raised JVP Pulmonary oedema Increased body weight
45
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
46
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
47
Blood products
Appropriate in pre-renal AKI due to loss of circulating BV due to haemorrhage
48
Urinalysis
Exclude UTI | Significant protein --> consider nephrotic/nephritic syndrome (measure PCR or ACR)
49
Microscopy Casts- Hyaline cast
Normal
50
Microscopy casts- lipid cast
High urinary protein nephrotic syndrome
51
Microscopy Casts- Muddy brown cast
ATN
52
Microscopy Casts- Pigment cast
Haemo/myoglobinuria
53
Microscopy Casts- Crystals
Tumour lysis syndrome
54
Microscopy Casts- Red cell cats
GN
55
Microscopy Casts- White cell casts
Infection Acute interstitial nephritis Post-strep acute GN
56
Microscopy Casts- Bacterial casts
Infection
57
Microscopy Casts- eosinophil cast
Acute interstitial nephritis
58
Microscopy- haematuria alone
Post-renal AKI Vasculitis Trauma
59
Blood tests- Low Hb
Haemolysis | GI bleed
60
Blood tests- raised WCC
Infection
61
Blood tests- Abnormal LFTs
Hepatorenal syndrome
62
Blood tests- high urea:creatinine ratio
pre-renal AKI (sign of dehydration)
63
Blood tests- raised ESR
any inflammatory condition
64
Blood tests- blood culture
sepsis
65
Blood tests- creatine kinase
rhabdomyolysis
66
Blood tests- urate
tumour lysis syndrome
67
Blood tests- lactate
tissue hypoperfusion
68
Blood tests- hypercalcaemia
Myeloma | sarcoidosis
69
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
70
Ultrasound
Hydronephrosis (accumulation of urine in kidney) that indicates obstruction in urinary tract
71
CXR
pulmonary oedema

Met 3b (21 decks)

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