AKI Flashcards
What can cause decreased renal perfusion and therefore AKI?
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
What are the main groups of things that can cause AKI?
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
What can cause increased renal vascular resistance?
Hyperviscosity/polycythemia
What can cause renal hypertension?
Malignant hypertension
Hypertension
What can cause SIRS?
Sepsis
Multiple organ dysfunction
Pancreatitis
What vascular issues can cause AKI?
Renal vessel thrombosis Coagulopathy Disseminated intravascular coagulation Vasculitis Hepatorenal syndrome
What can cause severe hypoxia?
Submersion injury
Severe pneumonia
Failure of fresh gas flow during anaesthesia
What are the main infectious causes of AKI?
Primary Pyelonephritis Leptospirosis Borreliosis (Lyme nephritis) Secondary Feline infectious peritonitis Babesiosis Leishmaniosis Bacterial endocarditis
What are the main neoplastic causes of AKI?
Tumour lysis syndrome (H)
Lymphosarcoma (lymphoma)
Nephroblastoma
What are the main immune-mediated causes of AKI?
Transfusion reaction (H) Systemic lupus erythematosus
Which patients are most likely to get hospital acquired AKI?
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
What are the main causes of acute on chronic dz?
glomerulonephritis, ureteral obstruction, chronic interstitial nephritis with acute tubular necrosis, chronic recurrent pyelonephritis, partial ureteral obstruction with pyelonephritis and obstructive calcium oxalate nephrolithiasis
How does S.G help work out renal v pre-renal component of azotaemia?
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.
What may prevent using S.G to define an azotaemia?
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.
What are the characteristics of FF in the abdomen with uroabdomen?
Fluid obtained by abdominocentesis has elevated concentrations of potassium, urea and creatinine compared with serum concentrations
Which antimicrobials can cause AKI?
Aminoglycosides Cephalosporins Penicillins Sulfonamides Quinolones Tetracyclines Vancomycin Carbapenems Polymyxin B Rifampin TMPS
What whole groups of drugs can cause AKI?
NSAIDs
ACE inhibitors
Diuretics
Which chemotheraputic agents can cause AKI?
Cisplatin
Carboplatin
Doxorubicin
Methotrexate
What antifungal drug can cause AKI?
Amphotericin B
What calcium antagonists can cause AKI?
Bisphosphonates
Galium nitrate
What miscellanious toxins can cause AKI?
Lillies Grapes, raisins and sultanas Vitamin D intoxication (psoriasis cream or rodenticide) Vitamin D3 analogue Cortinarius mushrooms Snake envemonation Bee sting
What heavy metals can cause AKI?
Mercury Lead Bismuth salts Copper Nickel Silver Gold Chromium Arsenic
What are the non-acute kidney disease causes of azotaemia?
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
What electrolyte disturbances can be seen?
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
What would be seen on blood gas analysis?
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.
What may be seen on sediment exam?
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
What would glucosuria without hyperglycaemia suggest?
Glucosuria without systemic hyperglycaemia may also be noted, which is strongly suggestive of renal injury to the proximal tubule
If you suspect lepto but titres on MAT are low, what should be done?
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
What tests should be considered if the patient has been abroad?
Ehrlichia canis, Borrelia burgdorferi, Rickettsia rickettsii (Rocky Mountain spotted fever) and Leishmania species
What is the antidote to ethylene glycol toxicity?
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
How do you treat suspect lepto cases?
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.
What are the s/e of using ethanol?
severe respiratory depression, coma, hypothermia, metabolic acidosis, serum hyperosmolality and diuresis
What are the signs of fluid overload?
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
How does frusemide work?
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
How does mannitol work?
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
How do you treat hyperkalaemia?
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
How do you treat hypernatraemia?
Often due to polyuric phase of AKI
If persists over 48 hours should be corrected very slowly to prevent cerebral oedema
What are some secondary causes of hypertension?
AKI, chronic kidney disease, hyperadrenocorticism, diabetes mellitus, phaeochromocytoma, hyperthyroidism obesity
How do you get patients off IVFT?
Once eating, drinking, azotaemia stable or resolved, taper fluids by 25% each day and ensure are stable
How many AKI animals are hypertensive
80%
Which animals may benefit from renal replacement therapy?
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
What renal replacement therapy options are there?
peritoneal dialysis (PD), intermittent haemodialysis (IHD) and continuous renal replacement therapy (CRRT)
What is the difference between acute renal failure and acute renal injury?
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
WHat is AKI?
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
Outline the four stages in AKI
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
How can you categorise the two types of AKI?
Community acquired
Hospital acquired
What is the antidote for NSAID toxicity?
misoprostol, for at least 3 days
How much fluid should be given to an AKI patient
Just enough to restore perfusion.
Agressive ‘flushing’ is not effective
Get an acurate weight twice daily
Once you have rehydrated an AKI patient and their urine output is less than 2ml/kg/hr, what should you do?
Re-assess hydration and BP.
Give 3-5% of bodyweight in fluid, re-assess
INI, place urinary catheter and start treatment
What are the main treatments for anuria/ oliguria?
- 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 - 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
What medications aside from diuretics may be needed in AKI patients?
•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
What are the prognostic factors for AKI in cats?
•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
What are the prognostic factors for AKI in dogs?
>900 azotaemia Anuria Anaemia Hypocalcaemia Azotaemia that worsens despite IVFT Lepto has a better prognosis ethylene glycol = grave once azotaemic
What is the general mortality in AKI in pets?
approx 50%
Compare uraemic ulceration in AKI and CKD
Typically abscent at the start of AKI, often present in CKD
