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Year 3 TCDs > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is the definition of acute kidney injury?

A

It is a clinical syndrome characterised by a rapid reduction in renal excretory function due to several different causes:

  1. Pre-renal (85% - reduced renal perfusion)
  2. Renal (10%)
  3. Post-renal (5% - obstruction)
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2
Q

What are the common causes of AKI?

A

Pre-Renal (85%) = reduced renal perfusion

  • Dehydration
  • Sepsis
  • Hypotension
  • Shock
  • Hepatomegaly syndrome
  • Severe heart failure
  • Intra-abdominal hypertension/compartment syndrome

Renal (10%)

  • NSAIDs
  • ACE inhibitors
  • ARBs
  • Gentamicin
  • GN/Vasculitis
  • Contrast
  • Interstitial nephritis
  • Myeloma
  • Rhabdomyolysis (death of muscle tissue)

Post-Renal (5%) = obstruction

  • Prostate enlargement
  • Renal stones
  • Pelvic cancer
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3
Q

What are the key points in a history and examination to cover with reference to a patient with AKI?

A
  1. AKI RISK FACTORS:
    - Age > 65
    - History of AKI
    - CKD
    - Symptoms/history or urological obstruction/conditions that may lead to obstruction
    - Chronic conditions (HF, liver disease, diabetes)
    - Neurological/cognitive impairment or disability (may limit fluid intake)
    - Sepsis
    - Hypovolemia
    - Oliguria
    - Nephrotoxic drug use within the last week (i.e. NSAIDs, ACE, ARBs, diuretics)
    - Exposure to iodinated contrast agents within past week
  2. POTENTIAL CAUSES FOR AKI:
    - Reduced fluid intake
    - Increased fluid losses
    - Urinary tract symptoms
    - Recent drug ingestion
    - Sepsis
  3. SYSTEMIC CLINICAL FEATURES:
    - Fever
    - Rash
    - Joint pain
  4. CLINICAL EXAMINATION SHOULD INCLUDE:
    - General (rash, uveitis, joint swelling)
    - Assessment of volume status (drowsy/yawning/thirsty, core temperature, CRP, HR, BP, JVP)
    - Signs of renovascular disease (audible abdo bruits, impalpable peripheral pulses)
    - Abdo exam (palpable bladder)
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4
Q

What investigations would you perform in a patient with AKI and why?

Patient has AKI 3 and is confused, has 1 week history of diarrhoea

A
  1. Chest x-ray -> look for pulmonary oedema or pneumonia
  2. Urine dipstick -> look for dipstick blood + protein’
  3. Urine culture -> look for urine infection
  4. Renal tract US -> look for obstructed kidneys (hydronephrosis), kidney size
  5. Stool culture -> pathogens causing diarrhoea
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5
Q

What is the importance of a urine dipstick in AKI?

A

> 3+ proteinuria = intrinsic renal disease

If blood + protein positive = glomerulonephritis

Positive for blood + no RBC = myoglobin

Send urine PCR/MSU if dipstick positive
If negative likely excludes intrinsic renal disease

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6
Q

Name 4 complications of AKI that if not resolved requires dialysis

A
  1. Hyperkalemia
  2. Pulmonary oedema
  3. Metabolic acidosis
  4. Uraemic encephalopathy (confusion, myoclonic jerks, seizures, coma) OR uraemic pericarditis (inflammation of pericardial sac)
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7
Q

What do kidneys do?

A
  1. Reduce salt + water in the body
  2. Remove waste from the blood into the urine
  3. Regulate BP
  4. Create erythropoietin to control production of RBCs
  5. Activate vitamin D
  6. Remove drugs from the body
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8
Q

How many nephrons are damaged with a decrease in GFR?

A

50%

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9
Q

What is the natural history of AKI?

A

There are 4 possible processes:

  1. Full recovery
  2. AKI -> CKD (AKI that persists for more than a few months)
  3. Acute on chronic kidney disease
  4. AKI -> ESRD (end stage renal disease; requiring dialysis or transplant)
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10
Q

Define the staging of AKI

A

Stage 1:
1.5-1.9x baseline Creatinine OR ≥ 26umol/L increase
<0.5ml/kg/hr for 6-12h

Stage 2:
2-2.9x baseline increase in Creatinine
<0.5ml/kg/hr for ≥12h

Stage 3:
>3x baseline increase in Creatinine OR ≥354umol/L increase OR initiation of RRT OR if under 18y, eGFR < 35ml/min
<0.3ml/kg/hr for ≥24h OR anuria for ≥12h

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11
Q

What do you do if you suspect AKI?

A

Think “SALFORD”!

  1. Sepsis + other causes - treat!
  2. ACE/ARB + NSAIDs - suspend/review
  3. Labs - repeat creatinine within 24h
  4. Fluid assessment + response (daily weights if hypovolemic give bonus IV 250ml + reassess)
  5. Obstruction - USS should be performed within 24h in non-resolving AKI 3 of unknown cause
  6. Renal/critical care referral - non-resolving AKI 3, possible intrinsic disease requiring specialist tx, CKD 4-5, renal transplant, severe AKI complications
  7. Dip urine
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12
Q

Name 4 causes of fluid overload and dehydration

A

Overload:

  • Iatrogenic (too much IV fluid)
  • Cardiac failure
  • Renal failure
  • Increased ADH secretion

Dehydration:

  • Diabetes
  • Diarrhoea + vomiting
  • Fever
  • Drugs (i.e. diuretics)
  • Insufficient replacement fluid
  • Hemorrhage
  • Sepsis
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13
Q

What bloods will be elevated in AKI?

A

Urea&raquo_space; creatinine
Albumin
Hematocrit (Hct)

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14
Q

What needs to be reviewed in a patient with altered hydration status?

A
  1. Fluid balance chart
  2. Observations chart
  3. Drug kardex
  4. Bloods
  5. Chest x-ray
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15
Q

Outline what you’re looking for in a hydration status examination

A

End of Bed:

  • Body habituate, breathlessness, oedema
  • IV lines, NGT, NBM (nil by mouth), food/drink (“into patient”)
  • Catheter, vomit bowel, drains, Tomas (“out of patient”)

Hands:
- Warm, CRT, skin turgor, pulse, lying/standing BP (significant difference > 20mmHg)

Neck:
- Carotid, JVP

Head:
- Temperature, sunken eyes, dry mouth

Chest:
- Parasternal heave (RH dilatation), displaced apex beat (LH dilatation), 3rd heart sound (HF)

Back/Legs:

  • Lung bases (crackles - LHF)
  • Sacral/pedal oedema (RHF)

Extras:

  • Review charts, suggest daily weights
  • Bloods (LFTs, FBC)
  • Chest x-ray
  • Specific gravity of urine (for dehydration)
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16
Q

What is the management of underloaded or fluid overloaded patients?

A

Underloaded/dehydrated:
- IV fluids (250-500ml Hartmann’s or 0.9% NaCl)

Overloaded:

  • Nitrates
  • Diuretics
  • CPAP
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17
Q

What changes are seen in ECG in hyperkalemia?

A
  1. Peaked T waves (tented)
  2. Small/indiscernible P waves
  3. Broad QRS complexes
  4. Slurring of QRS into ST component
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18
Q

What causes acute tubular necrosis? Histology? Treatment?

A

Usually a result of a combination of factors which have caused renal ischemia + toxicity (i.e. hypotension, dehydration, sepsis, associated nephrotoxic drugs)

The histology shows laughing of the renal tubular epithelium causing dilation and obstruction of tubules and some mild leukocyte infiltration

Treatment is supportive + withdrawal of nephrotoxic agents + treatment of associated sepsis.

Usually there’s recovery after 2-3 weeks (max 6wks). 50% mortality b/c of associated illness. Only a very small proportion of people are left with CKD.

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19
Q

What are the 3 phases of ATN?

A
  1. Oligouric Phase
    - Kidneys produce less than 500ml of urine/day. Patients in this phase are vulnerable to fluid overload + electrolyte imbalance especially potassium. Creatinine levels usually rise quite rapidly during this phase
  2. Maintenance Phase
    - The patient is no longer oligouric and this increased urinary output helps maintain fluid + electrolyte balance. Creatinine levels are usually stable or rise very slowly
  3. Polyuric Recovery Phase
    - Kidneys produce large quantities of dilute urine, so large that patients can become hypovolemic and unwell. Number of causes for this phase but one explanation is that the distal tubules and collecting ducts recover last and in particular their aquaporin channels. These damaged aquaporin channels don’t allow water to be reabsorbed and thus high quantities of dilute urine are produced. Patients are also susceptible to electrolyte loss (i.e. hypokalemia) in this phase. Creatinine levels fall swiftly.
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20
Q

What is creatinine a marker of?

A

Glomerular filtration + levels rise in the blood when the kidney is damaged

GFR is proportional to 1/Creatinine

** Creatinine is the favoured marker of pre-renal failure compared to urea

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21
Q

What is the difference between urea and creatinine?

A

Urea:
- Derived from proteins, amino acids, ammonia
- Liver converts ammonia -> urea
- Urea excreted via kidneys or the GI tract
..Kidney tubules re-absorb some urea back into blood
..Rumen + colon = site where urea recycling can occur

Creatinine:

  • Muscle breakdown product (not muscle breakdown marker tho - that’s creatine kinase - CK)
  • Freely filtered into urine from kidney
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22
Q

What ions are absorbed at different portions in the nephron?

A

PCT (65% of absorption happens here)
- NA+, amino acids, glucose, H20 absorbed

Loop of Henle

  1. Descending Limb
    - NO ions are reabsorbed, just H20 via passive transport
  2. Ascending Limb
    - NA+, Cl-, K+ absorbed but NO H2O via active transport

DCT:
- NA+, Cl- absorbed

Collecting Tubule:
- Urea reabsorbed to maintain osmolarity in medulla to drive H2O reabsorption in the Loop of Henle (urea recycling)

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23
Q

What is countercurrent multiplication?

A

Describing what occurs in the descending + ascending limb of the Loop of Henle

H2O is absorbed passively from descending limb b/c increased reabsorption of ions making surroundings very “salty” in medulla

24
Q

What does RAAS do and where is it released from?

A

RAAS controls the BP from the juxtaglomerular apparatus

RAAS prevents ischemia + maintains renal blood flow

  • Increased NA+ and H2O reabsorption
  • Protects nephron by vasoconstricting efferent renal arteriolar to maintain GFR
25
Q

What is the definition of sepsis?

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection

26
Q

How is sepsis treated?

A
  1. Early administration of antibiotics
  2. Vasopressors (1-6h after onset; norepinephrine/epinephrine/vasopressin)
  3. Fluids (colloids/crystalloids)
  4. Urinary catheter
  5. Lung protective ventilation
  6. Enteral feeding
  7. Insulin therapy
27
Q

What investigations should be done for someone with suspected sepsis and 1+ high risk criteria?

A

Carry out a venous blood test for the following:

  • Blood gas including glucose + lactate measurement
  • Blood culture
  • Full blood count
  • CRP
  • Urea + electrolytes
  • A clotting screen
28
Q

What immediate treatment should be given in someone with sepsis?

A
  1. Broad spectrum antibiotic at the maximum recommended dose (within 1h of identifying that they meet any high risk criteria in an acute hospital setting)
  2. IV fluid bolus without delay (within 1h of identifying that they meet any high risk criteria in an acute hospital setting)
29
Q

Why is lactate measured in sepsis?

A

Lactate accumulates in the blood as a result of anaerobic respiration, which is a pathological physiological response to lack of oxygen reaching the tissues. Raised lactate levels are a marker of poor tissue perfusion, or shock, and will result in organ damage and can lead to multi-organ failure. The body’s defence mechanism tries to maintain oxygen to vital organs so often skin, kidneys and gut are affected first. Cerebral blood flow is prioritised so confusion is often a late sign. Eventually if untreated, the patient will have a cardiac arrest.

If this patient’s lactate level is >4mmol/l they are at very high risk of circulatory collapse + cardiac arrest, so need to be referred to ITU for consideration of invasive circulatory support (inotropes)

30
Q

Why are U&Es measured in sepsis?

A

The kidneys are often affected early in sepsis, and because of low blood flow in renal medulla, they are particularly sensitive to ischemic damage. This is why in a patient presenting with AKI it’s very important to look out for and rule out sepsis.

31
Q

Why is clotting measured in sepsis?

A

In severe sepsis there is dysregulation of coagulation system and several recent studies have suggested treatments focusing on these pathways may improve sepsis outcomes. It’s also a marker of severity of sepsis.

32
Q

What does CRP measure?

A

CRP is produced by the liver in response to inflammation. It’s therefore also called an acute phase protein.

It was first identified in patients with pneumococcal pneumonia. It’s production is also stimulated by other bacterial infections (excluding TB) but not by viral infections or malaria.

It’s important to remember it’s not a specific marker of infection but its levels can become significantly increased due to trauma, surgery, or any other cause of inflammation including autoimmune conditions. On the other hand, steroids suppress its production and steroid dose reduction can lead to increase in CRP.

CRP should be used only in conjunction with the clinical situation as a nonspecific marker of inflammation.

33
Q

What fluid would you prescribe for a patient with sepsis?

A

Immediate fluid resuscitation = 500ml bolus of crystalloid fluid (i.e. Hartmann’s, 0.9% NaCl) over less than 15min

Reassess BP immediately after

Can have up to 2L of fluid as blouses to see if BP responds before referring to ICU for invasive circulatory support

34
Q

What is the daily requirements for maintenance fluids?

A

Normal daily fluid and electrolyte requirements:

  1. 25-30ml/kg/day water
  2. 1mmol/kg/day Na+, K+, Cl-
  3. 50-100g/day glucose (i.e. glucose 5% contains 5g/100ml)

Nasogastric fluids or enteral feeding is preferred when maintenance is needed for more than 3 days

35
Q

What is the requirement for replacement fluids?

A
  1. Measure existing fluid/electrolyte deficits or excesses:
    - dehydration
    - fluid overload
    - hyperkalemia/hypokalemia
  2. Ongoing abnormal fluid or electrolyte losses:
    - Vomiting + NG tube loss
    - biliary drainage loss
    - high/low volume ileal stoma loss
    - diarrhea/excess colostomy loss
    - ongoing blood loss
    - sweating/fever/dehydration
    - pancreatic/jejunal fistula/stoma loss
    - urinary loss (i.e. post-AKI, polyuria)
  3. Redistribution + other complex issues:
    - gross oedema
    - severe sepsis
    - hypernatremia/hyponatremia
    - renal, l;over, cardiac impairment
    - post-operative fluid retention and redistribution
    - malnourished and reseeding issues

Prescribe by adding to or subtracting from routine maintenance, adjusting for all other sources of fluid and electrolytes

Monitor and reassess fluid and biochemical status

36
Q

What is the difference between osmolality, osmolarity, and tonicity?

A

Osmolality: osm/kg of solvent

Osmolarity: osm/L of solution

Tonicity: Relative osmolality between 2 fluid compartments

37
Q

Why are crystalloids more commonly used over colloids?

A

Colloids are larger molecules that cannot easily pass through semipermeable membranes.

  • Prolonged volume expansion
  • Possible anaphylactic reaction
  • Starches increase risk of AKI and bleeding in surgical patients
38
Q

What groups need to be specially considered before giving fluids?

A
  • Children
  • Pregnant women
  • Renal/hepatic failure
  • Burns
  • Toxicity
  • Diabetes
  • Traumatic brain injury
39
Q

How is fluid prescribed in kids?

A

Use saline for resus
Use saline + 5% glucose for replacement/maintenance

First 10kg = 100ml/kg
Second 10kg = 50ml/kg
Remainder = 20ml/kg

40
Q

What is the most common cause of AKI?

A

Pre-renal disease (or acute tubular necrosis)

Commonest pre-renal cause = true V depletion due to GI (diarrhea/vomiting), renal (diuretics), or 3rd space fluid + electrolyte losses + hemorrhage

Heart failure + liver cirrhosis also can cause pre-renal AKI even in the presence of peripheral oedema

Although early recognition and intervention can lead to complete resolution of pre-renal AKI, prolonged ischemia may lead to prolonged or worsening renal impairment due to acute tubular necrosis.

41
Q

Name 5 factors that can contribute to AKI

A
  1. Hypotension
  2. NSAIDs
  3. Renal stones
  4. Dehydration
  5. Sepsis
42
Q

Name 5 risk factors for AKI

A
  • Age
  • Diabetes
  • NSAIDs
  • Blood pressure
  • History of AKI
43
Q

Of the following medications, which would you stop in AKI?

Ramipril (ACE-i)
Doxycycline (antibiotic)
Diclofenac (NSAID)
Metformin (biguadine)
Losartan (ARB)
A

Stop ramipril, diclofenac, metformin, and losartan

44
Q

What group of drugs have NICE said that if started in the last week is recognised as a risk factor for AKI?

A

ARB
ACE inhibitors
NSAIDs

45
Q

From the list below, which of the following do not require dose review in patients with AKI?

Paracetamol
Morphine
Vancomycin
Insulin
Gentamicin
Senna
A

Paracetamol + Senna do not need review

46
Q

Which patients with AKI need discussion with the renal team?

A
  1. All patients with a renal transplant
  2. All patients with an AKI 3
  3. All AKI patients with blood + protein on urine dipstick
  4. All patients with no known cause of AKI and have deteriorating renal function
47
Q

Name complications of AKI that require renal replacement therapy

A
  1. Refractory hyperkalemia which doesn’t respond to medical management
  2. Refractory pulmonary oedema which doesn’t respond to medical management
  3. Severe acidosis which doesn’t respond to medical management
  4. Uraemic encephalopathy/coma
48
Q

Name 2 medications that can cause hyponatremia

A
  1. Omeprazole
  2. Furosemide
    - inhibits Na+ transport in the renal medulla
49
Q

Prescribe a vitamin D replacement for a patient with severe renal impairment

A

Alafcalcidol, 50 nanograms, PO

50
Q

How long do you have to give antibiotics for someone with suspected sepsis?

A

1h

51
Q

What is the imaging used for suspected abdominal-originating sepsis

A
  • US

- Contrast CT

52
Q

What are the bloods for sepsis?

A
  • FBC
  • Blood gas including glucose + lactate
  • Blood culture
  • CRP
  • U&E
  • Clotting screen
53
Q

What is the normal amount of electrolytes one should be having/day?

A

1mmol/kg/day for sodium, potassium, and cholride

50-100g/day of glucose (i.e. glucose 5% = 5g in 100ml)

54
Q

What is the typical resuscitations fluids, maintenance fluids, and replacement fluids given?

A

Resuscitation: 0.9% NaCl 500ml over 15min

Maintenance: 0.18% NaCl with 4% glucose + 15mmol KCl 500ml over 6º

Replacement: 0.9% NaCl 500ml over 2º then 4º then 6º

55
Q

What is the treatment for ATN with worsening AKI and oliguria < 30ml/hr?

A

Treatment is supportive while waiting for kidneys to recover

STOP fluids but encourage oral intake with oliguria

Year 3 TCDs (24 decks)

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