AKI And CKD Flashcards

(58 cards)

1
Q

Define AKI

A

A syndrome of decreased renal function, measured by serum creatinine or urine output, occuring over hours-days

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2
Q

How can AKI be staged?

A

According to highest creatine rise of longest period /severity of oliguria

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3
Q

How can AKI be defined?

A

Rise in serum creatinine >26 micromol/L within 48 hours

Rise in creatinine 1.5 times baseline within 7 days

Urine output <0.5mL/kg/H for >6 consecutive hours

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4
Q

Name some risk factors for developing AKI

A

Pre-existing CKD

Age

Male

Comorbidities - DM, CVS disease, malignancy, chronic liver disease, complex surgery

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5
Q

Name 7 causes for AKI

A
Sepsis 
Major surgery
Cardiogenic shock 
Other hypovolaemia
Drugs 
Hepatorenal syndrome 
Obstruction
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6
Q

How can AKIs be divided?

A

According to the

  • pre renal - decreased perfusion to the kidney
  • renal - intrinsic renal disease
  • post renal disease - obstruction to urine
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7
Q

Name 4 causes of pre-renal AKI pathology

A

Decreased vascular volume = haemorrhage, burns, D&V, pancreatitis

Decreased cardiac output = cardiogenic shock, MI

Systemic vasodilation = sepsis, drugs

Renal vasoconstriction = NSAIDs, ACEi, ARB, hepatorenal Syndrome

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8
Q

Name 3 causes of renal AKIs

A

Glomerular = glomerulonephritis, acute tubular necrosis (prolonged renal hypoperfusion causing intrinsic renal damage)

Interstitial = drug reaction, infection, infiltration

Vessels = vasculitis, DIC

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9
Q

Name two causes of post renal AKIs

A

Within renal tract - stone, renal tract malignancy, stricture, clot

Extrinsic compression - pelvic malignancy, prostatic hypertrophy, retro-peritoneal fibrosis

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10
Q

Name 3 life threatening complications from AKI

A

NEWS scoring - refer critical care

Pulmonary oedema - may require dialysis

Urgent K+

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11
Q

How would you treat hypovolaemia in AKI?

A

Bolus fluid 250-500ml, until volume replete

If 2L given without response - seek expert help

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12
Q

What needs to be monitored during AKI?

A

Fluid balance - consider catheter and hourly urine output

K+ - check response to treatment and at least daily creatinine until it falls

Observations - every 4 hours

Lactate - if signs of sepsis

Daily creatinine until decrease (lags 24 hours behind clinical response)

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13
Q

What investigations can be done for AKI?

A

Urine dipstick (pre-catheter) and quantification of proteinuria. Proteinuria and haematuria may suggest intrinsic renal disease

USS within 24 hours - unless obvious cause or AKI improving

Check liver function - (hepatorenal)

Check platelets - if low, requires blood film to check for haemolysis

Investigate intrinsic renal disease if indicated - immunoglobulins, paraprotein, complement, autoantibodies (ANCA, anti-GBM)

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14
Q

What do small kidneys <9cm on USS suggest?

What do asymmetric kidneys on USS suggest?

A

CKD

Asymmetry - renal Vascular disease

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15
Q

What is the management for AKI?

A

Treat sepsis

Stop nephrotoxic medication - NSAIDs, ACEi, ARBs, aminoglycosides

Stop drugs that increase complications e.g. diuretics (esp. K+ sparing) ,metformin, antihypertensives

Check drug dosages appropriate for renal impairment

Consider gastroprotection - H2/PPI and nutritional support

Avoid radiological contrast

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16
Q

What drugs may increase AKI complications?

A

Diuretics - especially K+ sparing

Metformin

Antihypertensives

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17
Q

What is the generic treatment for a pre-renal AKI?

A

Correct volume depletion and/or treat renal perfusion via circulatory/Cardiac Support, treat any underlying sepsis

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18
Q

What is the generic treatment for a renal AKI?

A

Refer for likely biopsy and specialist treatment of intrinsic renal disease

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19
Q

What is the generic treatment for a post-renal AKI?

A

Catheter, nephrostomy or urological investigation

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20
Q

What are the symptoms of hypovolaemia?

A

Decrease BP

Reduced urine output

Non-visible JVP

Poor tissue turgor

Increase pulse

Daily weight loss

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21
Q

What are the symptoms of fluid overload?

A

High BP

Increased JVP

Lung crepitations

Peripheral oedema

Gallop rhythm

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22
Q

What may be late signs of hypovolaemia?

A

Decreased BP

Skin turgor

Capillary refill time

DONT wait for these signs!

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23
Q

What is the 4 stage process to fluid resuscitation?

A
  1. Give 500ml crystalloid over 15mins
  2. Reassess fluid state. Get expert help if unsure or if patient remains shocked
  3. Further boluses of 250-500ml crystalloid with clinical review after each
  4. Stop when euvolaemic or seek expert help when 2L given

Crystalloid solution = normally 0.9% saline

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24
Q

What may 0.9% saline solution cause?

A

Hyperchoraemic acidosis

Contains increased chloride and is non-buffered

25
Name a balanced/buffered crystalloid When does caution need to be given if using this solution?
Hartman’s Because they are balanced they are often used preferentially However, they contain 4-5mmol/L of K+ so caution if hyperkalaemia and oligio/anuria
26
When is a colloid bolus used?
Blood component should be used in resuscitation due to haemorrhage
27
How do you manage hypervolaemia (fluid overload)?
Oxygen supplementation if required Fluid restriction - consider oral and IV volumes. Give antibiotics in minimal fluid and consider concentrated nutritional preparations Diuretics - only in symptomatic fluid overload. They are ineffective and potentially harmful if used to treat oliguria without fluid overload Renal replacement therapy
28
When are diuretics used to treat hypervolaemia?
Only if patient is symptomatic with fluid overload They are ineffective and potentially harmful if used to treat oliguria without fluid overload
29
How do you treat acidosis?
Treat the underlying cause which will stop acid production
30
What are the ECG changes seen in hyperkalaemia?
Tall tented T waves Increased PR interval Small or absent P waves Widened QRS complex
31
What is the 4 stage process for treating hyperkalaemia? K+ >6.5mmol/L or with any ECG changes
1. 10ml of 10% Calcium chloride - cardioprotective but does not treat K+ level 2. IV insulin and dextrose - stimulates intracellular uptake of K+. Monitor hourly for hypoglycaemia 3. Salbutamol - causes intracellular K+ shift but high doses are required and tachycardia can limit use 4. Definitive treatment requires K+ removal. If underlying pathology cannot be corrected renal replacement may be indicated
32
What are the 4 possible indications for renal replacement therapy in AKI? What does it aim to do?
Fluid overload unresponsive to medical treatment Severe/prolonged acidosis Recurrent/persistent hyperkalaemia despite medical treatment Uraemia e.g. pericarditis, encephalopathy Aim = provide organ support and prevent complications, rather than waiting for them to occur
33
What are the possible complications for renal replacement therapy in AKI?
Risk of dialysis catheter insertion and maintenance Procedural hypotension Bleeding due to the requirement for Anticoagulation Altered nutrition Altered drug clearance
34
Define CKD
Abnormal kidney structure or function present for >3months, with implications for health
35
What 3 ways can CKD be classified?
GFR category table Presence of albuminuria as a marker of kidney damage Cause of kidney disease
36
What is the GFR for category 1,2,3a,3b,4,5?
``` 1 = GFR >90 2 = 60-89 (only CKD if evidence of kidney damage) 3a = 45-59 mild - moderate 3b = 30-44 moderate - severe 4 = 15-29 - severe 5 = <15 = kidney failure ```
37
What are the three most common causes of CKD?
Diabetes Glomerulonephritis Increased BP/renovascular disease
38
What does decreased GFR and albuminruria increase the risk of?
Mortality CVS mortality Progressive kidney disease and kidney failure AKI
39
What are the three things to clarify in a patient with suspected CKD?
Does the patient really have CKD? - does eGFR reflect true GFR? Is it corrected for ethnicity and drugs? Requires evidence of chronicity >3months Possible causes - previous UTI? PMH of DM, increased BP, IHD? Drug history and when meds were started? Family history? Rule out malignancy? Current state - patients may have symptoms of CKD if GFR <30. Symptoms of fluid overload e.g. SOB, peripheral oedema, nausea, vomiting, restless legs, weakness, pruitis, bone pain
40
What symptoms will a person with GFR <30 show?
Fluid overload - SOB, peripheral oedema Anorexia Nausea/vomiting Restless legs Fatigue Weakness Pruitis Bone pain Amenorrhoea Impotence
41
What signs may you seen on examination of the face in a person with CKD?
Anaemia Xanthelasma Yellow tinge (uraemia) Jaundice (hepatorenal) Gum hypertrophy (ciclosporin) Cushingoid (steroids) Periorbital oedema (nephrotic syndrome)
42
What signs may you seen on examination of the periphery in a person with CKD?
Peripheral oedema Vasculitic rash Signs of peripheral vascular disease or neuropathy AV fistula Signs of immunosuppression - bruising from steroids, skin malignancy Uraemia flap/encephalopathy
43
What investigation can you do for suspected CKD?
Blood test - U&Es, Hb, Urine dipstick - microscopy, culture, stain Imaging Histology - consider renal biopsy in progressive disease, nephrotic syndrome, systemic disease, AKI without recovery
44
What renal monitoring should be completed in a CKD patient?
GFR and albumin at least annually according to risk High risk = monitor every 6 months Small fluctuations are common but a drop in eGFR stage >25%
45
What are the risk factors for CKD decline?
DM Increased BP Metabolic disturbance Volume depletion Infections NSAIDs Smoking All CKD has increased superimposed risk of AKI and needs monitoring and prompt treatment during intercurrent illness
46
What 5 things does management of CKD require?
1. Appropriate referral to nephrology 2. Treatment to slow renal disease progression 3. Treatment of renal complications of CKD 4. Treatment of other complications of CKD 5. Preparation for renal replacement therapy e.g. dialysis/transplant
47
What treatment can be offered to slow renal disease progression?
BP - target 140/90mmHg. If DM or albumin:Creatinine ratio >70 then BP aim 130/80mmHg RAAS antagonist - do not combine RAAS antagonist due to risk of hyperkalaemia and hypotension. Check K+ and renal function, prior to and within 1-2weeks of starting treatment/changing dose Glycaemic contra - target HbA1c of 7% unless risk of hypoglycaemia, comorbidity or limited life expectancy Lifestyle - exercise, healthy weight, smoking cessation, reduce salt intake
48
Why should RAAS antagonists not be combined when using them to slow renal disease progression? What should be checked prior to starting RAAS antagonist? Name two RAAS antagonists.
Due to risk of hyperkalaemia and hypotension. Check K+ and renal function, prior to and within 1-2weeks of starting treatment/changing dose ACEi or ARB
49
Name some renal complications of CKD
Anaemia Acidosis Oedema Bone-mineral Disorders Restless legs/cramps
50
When should sodium bicarbonate supplements be considered in CKD? When should caution be given?
Patients with eGFR <30 and low serum bicarbonate Used to treat acidosis Patients with hypertension and fluid overload due to sodium component
51
How do you treat oedema caused by CKD?
Restrict fluid and sodium intake High loop diuretics may be needed Can combine loop and thiazide diuretics to have powerful effect
52
How is anaemia as a result of CKD treated?
Investigate and treat deficiencies - iron, folate, B12 Iron therapy may need to be given IV Consider treatment with erythropoietin stimulating agent like ‘Epo’ if Hb <110g/L and likely to benefit in terms of function and quality of life
53
What bone mineral disorders occur as a complication of CKD? How are they treated?
Increased serum phosphate and reduced hydroxylation of vitamin D by the kidney Treat phosphate >1.5mmol/L with dietary restriction and phosphate binders Give vitamin D supplements if deficient If increased PTH persists/increases treat with activated vit D analogue
54
What needs to be excluded with symptoms of restless legs/cramps as a result of CKD?
Exclude iron deficiency as possible exacerbating factor Give sleep hygiene advice Treatment for severe cases - gabapentin/ pregabalin/ dopamine agonists is off licence
55
What treatment may be given for CVS complications of CKD?
Antiplatelets (low dose aspirin)- for those CKD patients at risk of atherosclerosis unless bleeding risk outweighs benefit Atorvastatin 20mg for primary and secondary prevention of CVS disease GFR< 60 nay affect troponin and BNP values - interpret results carefully
56
When should planning for renal replacement therapy for CKD begin?
Progressive CKD where the risk of renal failure is 10-20% within a year. Referral to nephrology less than 1 year before RRT is required is considered a late referral
57
What should you check prior to prescribing in renal failure?
How administration of the drug should be altered due to decreased GFR - determined largely to the extent to which the drug is renally excreted Significant for aminoglycosides, penicillins, cephalosporins, heparin, lithium, opiates, and digoxin Loading doses should not be changed
58
Name some drugs with renal excretion
``` Aminoglycosides Penicillins Cephalosporins Heparin Lithium Opiates Digoxin ```