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SAM Module B Urinary system > AKI > Flashcards

AKI Flashcards

1
Q

What can cause decreased renal perfusion and therefore AKI?

A 
Shock (hypovolaemic, distributive)
NSAIDs, ACE inhibitor 
Decreased cardiac output:
Congestive heart failure
Dysrhythmia
Tamponade
Cardiac arrest
Deep anaesthesia (eg, extensive surgery) (H)
Severe trauma
Severe hyperthermia or hypothermia
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2
Q

What are the main groups of things that can cause AKI?

A 
Decreased renal perfusion
Prolonged urinary tract obstruction
Increased renal vascular resistance
Systemic inflammatory response syndrome
Renal hypertension
Vascular
Severe hypoxia
Drug and toxin associated
Infectious
Neoplasia
Immune-mediated
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3
Q

What can cause increased renal vascular resistance?

A

Hyperviscosity/polycythemia

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4
Q

What can cause renal hypertension?

A

Malignant hypertension

Hypertension

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5
Q

What can cause SIRS?

A

Sepsis
Multiple organ dysfunction
Pancreatitis

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6
Q

What vascular issues can cause AKI?

A 
Renal vessel thrombosis
Coagulopathy
Disseminated intravascular coagulation
Vasculitis
Hepatorenal syndrome
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7
Q

What can cause severe hypoxia?

A

Submersion injury
Severe pneumonia
Failure of fresh gas flow during anaesthesia

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8
Q

What are the main infectious causes of AKI?

A 
Primary
Pyelonephritis
Leptospirosis
Borreliosis (Lyme nephritis)
Secondary
Feline infectious peritonitis
Babesiosis
Leishmaniosis
Bacterial endocarditis
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9
Q

What are the main neoplastic causes of AKI?

A

Tumour lysis syndrome (H)
Lymphosarcoma (lymphoma)
Nephroblastoma

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10
Q

What are the main immune-mediated causes of AKI?

A 
Transfusion reaction (H)
Systemic lupus erythematosus
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11
Q

Which patients are most likely to get hospital acquired AKI?

A 
Older animals, those with cardiac disease or pre-existing chronic kidney disease (CKD) and patients with a low urine output
CLose creatinine measurements in these patients is important
Should also closely monitor animals with disease processes resulting in haemoglobinaemia (eg, haemolysis) or myoglobinaemia (eg, extensive muscle injury) 
Hypoalbuminaemia (decreased COP)
Dehydration
Increased blood viscosity
Systemic hypertension
Acidosis
Fever
Radiocontrast media
Hyponatraemia
Burns
Multiple myeloma
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12
Q

What are the main causes of acute on chronic dz?

A

glomerulonephritis, ureteral obstruction, chronic interstitial nephritis with acute tubular necrosis, chronic recurrent pyelonephritis, partial ureteral obstruction with pyelonephritis and obstructive calcium oxalate nephrolithiasis

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13
Q

How does S.G help work out renal v pre-renal component of azotaemia?

A

A USG of between 1.008 and 1.015 would be expected if they have renal. A USG greater than 1.015 suggests a pre-renal component to elevations in creatinine from baseline.

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14
Q

What may prevent using S.G to define an azotaemia?

A

hypoadrenocorticism and hypercalcaemia, prevent an appropriate urine concentration despite the kidneys otherwise functioning adequately.
glucosuria and colloid fluid therapy can lead to increased USG, preventing the identification of a renal azotaemia.

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15
Q

What are the characteristics of FF in the abdomen with uroabdomen?

A

Fluid obtained by abdominocentesis has elevated concentrations of potassium, urea and creatinine compared with serum concentrations

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16
Q

Which antimicrobials can cause AKI?

A 
Aminoglycosides
Cephalosporins
Penicillins
Sulfonamides
Quinolones
Tetracyclines
Vancomycin
Carbapenems
Polymyxin B
Rifampin
TMPS
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17
Q

What whole groups of drugs can cause AKI?

A

NSAIDs
ACE inhibitors
Diuretics

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18
Q

Which chemotheraputic agents can cause AKI?

A

Cisplatin
Carboplatin
Doxorubicin
Methotrexate

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19
Q

What antifungal drug can cause AKI?

A

Amphotericin B

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20
Q

What calcium antagonists can cause AKI?

A

Bisphosphonates

Galium nitrate

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21
Q

What miscellanious toxins can cause AKI?

A 
Lillies
Grapes, raisins and sultanas
Vitamin D intoxication (psoriasis cream or rodenticide)
Vitamin D3 analogue
Cortinarius mushrooms
Snake envemonation
Bee sting
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22
Q

What heavy metals can cause AKI?

A 
Mercury
Lead
Bismuth salts
Copper
Nickel
Silver
Gold
Chromium
Arsenic
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23
Q

What are the non-acute kidney disease causes of azotaemia?

A

Pre-renal
Dehydration
Loop diuretic use (furosemide)
Hypoadrenocorticism

Post-renal
Urinary tract trauma
Bladder rupture
Urethral trauma
Ureteral trauma

Urinary tract obstruction
Urolithiasis
Neoplasia
Iatrogenic

Chronic kidney disease

24
Q

What electrolyte disturbances can be seen?

A

High K if blockage (above 6 can start to see CV signs)
Low K if polydipsic (start to see severe effects below 2.5)
High or low Na
Can get low Ca in ethylene glycol tox

25
Q

What would be seen on blood gas analysis?

A

Patients with AKI often suffer from severe metabolic acidosis due to decreased renal excretion of acid. A pH of less than 7.1 is critical as this can lead to significant cardiovascular depression and damage to enzymatic pathways.

26
Q

What may be seen on sediment exam?

A

Monohydrate calcium oxalate crystals are compatible with ethylene glycol toxicity. Urine sediment may also contain evidence of acute tubular injury with fine or coarse granular casts

27
Q

What would glucosuria without hyperglycaemia suggest?

A

Glucosuria without systemic hyperglycaemia may also be noted, which is strongly suggestive of renal injury to the proximal tubule

28
Q

If you suspect lepto but titres on MAT are low, what should be done?

A

If lower titres are present, but suspicion is strong, a second MAT should be performed within two to four weeks. An increasing level would be suggestive of active infection

29
Q

What tests should be considered if the patient has been abroad?

A

Ehrlichia canis, Borrelia burgdorferi, Rickettsia rickettsii (Rocky Mountain spotted fever) and Leishmania species

30
Q

What is the antidote to ethylene glycol toxicity?

A

inhibition of alcohol dehydrogenase with the use of ethanol or 4-methylprazole (4-MP) in dogs with ethylene glycol toxicity is most effective within six to eight hours of ingestion, cats 4

31
Q

How do you treat suspect lepto cases?

A

Dogs that do not have evidence of another cause of AKI should be treated with antibiotics that target Leptospira species while diagnostic results are pending. Intravenous ampicillin or amoxicillin are commonly used initially to reduce multiplication, shedding and transmission of the organism. Oral tetracyclines, such as doxycycline, or fluoroquinolones are then used for elimination of the carrier state.

32
Q

What are the s/e of using ethanol?

A

severe respiratory depression, coma, hypothermia, metabolic acidosis, serum hyperosmolality and diuresis

33
Q

What are the signs of fluid overload?

A 
Peripheral oedema – particularly easy to note   as swelling around the hock, Achilles tendons and intermandibular space
Exophthalmos
Serous nasal discharge
Ascites or pleural fluid
Tachypnoea/dyspnoea
Pulmonary crackles and oedema
34
Q

How does frusemide work?

A

inhibiting the sodium-potassium-chloride (Na+-K+-2Cl−) cotransporter located on the apical membrane of the renal tubular cells of the thick ascending limb of the loop of Henle
Likely only helpfull for its diuretic effects

35
Q

How does mannitol work?

A

elevates plasma osmolality resulting in expansion of the intravascular volume.
osmotic diuretic as it is filtered freely through the glomeruli and is not reabsorbed by the renal tubules.
been shown to cause significant natriuresis by either direct or indirect stimulation of atrial natriuretic peptide release or inhibition of sodium and water reabsorption in the collecting ducts of the nephron, resulting in further diuresis.
Other proposed benefits of mannitol include renal arteriole dilation, decreased vascular resistance and blood viscosity, and scavenging of oxygen free radicals.
Cannot be excreted by anuric kidneys so contraindicated in volume overloaded patients

36
Q

How do you treat hyperkalaemia?

A

Potassium-free or potassium-deficient isotonic crystalloid fluid such as Lactated Ringer’s or Hartmann’s
Discontinue all potassium supplementation
10 per cent calcium gluconate intravenously over five to 10 minutes with electrocardiogram monitoring for (worsening of) bradycardia
0.25 to 0.55 IU/kg regular insulin with 2 g of 50 per cent glucose per unit of insulin intravenously (subsequent evaluations of serum glucose and potassium concentrations are indicated to avoid hypoglycaemia and evaluate the effects of therapy)
2.5 to 5 per cent glucose infusion intravenously; monitor blood glucose periodically
If hyperglycaemia occurs with persistence of hyperkalaemia, repeat a low dose of regular insulin
If normoglycaemic and normokalaemic, glucose infusion can be discontinued
1 to 2 mEq/kg sodium biocarbonate intravenously
1 to 4 mg/kg furosemide intravenously
If severe hyperkalaemia persists with the above treatments, consider renal replacement therapy in those with potentially reversible disease and committed owners

37
Q

How do you treat hypernatraemia?

A

Often due to polyuric phase of AKI

If persists over 48 hours should be corrected very slowly to prevent cerebral oedema

38
Q

What are some secondary causes of hypertension?

A 
AKI, 
chronic kidney disease, 
hyperadrenocorticism, 
diabetes mellitus, 
phaeochromocytoma, 
hyperthyroidism
obesity
39
Q

How do you get patients off IVFT?

A

Once eating, drinking, azotaemia stable or resolved, taper fluids by 25% each day and ensure are stable

40
Q

How many AKI animals are hypertensive

A

80%

41
Q

Which animals may benefit from renal replacement therapy?

A

RRT is indicated in severe cases of AKI in which renal function is expected to be, at least partially, reversible. Animals that are anuric, refractory to fluid therapy or severely uraemic with life-threatening electrolyte abnormalities benefit most from RRT

42
Q

What renal replacement therapy options are there?

A

peritoneal dialysis (PD), intermittent haemodialysis (IHD) and continuous renal replacement therapy (CRRT)

43
Q

What is the difference between acute renal failure and acute renal injury?

A

ARF‐ “a rapid loss of nephron function leading to retention of nitrogenous wastes”
AKI – “a spectrum of disease associated with a sudden onset of renal parenchymal injury

44
Q

WHat is AKI?

A

An abrupt drop in kidney function
• results in abnormal GFR, tubular function and urine production
• a sudden inability to maintain fluid, acid‐base, and electrolyte balance
• it may result in azotaemia

45
Q

Outline the four stages in AKI

A

Initiation phase - damage starts
Extension phase - ischaemia, hypoxia, inflammatory response ongoing cellular injury, cell death.
Maintenance phase - stabilisation of GFR, typically see azotaemia, uraemia,urine production is variable
Recovery phase - azotaemia improves and the tubules undergo repair can be marked polyuria during this stage

46
Q

How can you categorise the two types of AKI?

A

Community acquired

Hospital acquired

47
Q

What is the antidote for NSAID toxicity?

A

misoprostol, for at least 3 days

48
Q

How much fluid should be given to an AKI patient

A

Just enough to restore perfusion.
Agressive ‘flushing’ is not effective
Get an acurate weight twice daily

49
Q

Once you have rehydrated an AKI patient and their urine output is less than 2ml/kg/hr, what should you do?

A

Re-assess hydration and BP.
Give 3-5% of bodyweight in fluid, re-assess
INI, place urinary catheter and start treatment

50
Q

What are the main treatments for anuria/ oliguria?

A
  1. Furosemide
    • increases urine output but does not improve GFR or outcome
    • Allows you to carry on with IVFT
    • initial bolus of 1‐2mg/kg IV followed by a CRI of 0.5‐1mg/kg/h
  2. Mannitol
    • 20% mannitol can be given‐ 0 5. ‐1 /k g g over 20 mins
    • Can repeat it q 4‐6h, or give a CRI
    • Avoid more than 2‐4 g/kg/d
51
Q

What medications aside from diuretics may be needed in AKI patients?

A

•Vomiting - H2 antagonists, PPIs
maropitant, metoclopramide or ondansetron

•Hypertension
exacerbated by overhydration overhydration
reduce ivft, give diuretics. If persistent‐ can use antihypertensives but most are oral
Nitroprusside
Hydralazine
Amlodipine
ACEi are associated with worsening of renal function in humans

  • Nutrition - AKI is a highly catabolic disease
  • Pancreatitis and/or lung injury seem to be common in acute uraemia
52
Q

What are the prognostic factors for AKI in cats?

A 
•Hyperkalaemia
•low albumin
•decreased bicarbonate at presentation
•degree of azotaemia and changes in calcium or phosphate did NOT predict survival
ethylene glycol = grave once azotaemic
53
Q

What are the prognostic factors for AKI in dogs?

A 
>900 azotaemia
Anuria
Anaemia
Hypocalcaemia
Azotaemia that worsens despite IVFT
Lepto has a better prognosis
ethylene glycol = grave once azotaemic
54
Q

What is the general mortality in AKI in pets?

A

approx 50%

55
Q

Compare uraemic ulceration in AKI and CKD

A

Typically abscent at the start of AKI, often present in CKD

SAM Module B Urinary system (13 decks)

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