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Urology > AKI (Londono) > Flashcards

AKI (Londono) Flashcards

1
Q

Objectives

A
  1. understand the basic pathophysiological causes of renal injury
  2. become familiar with the staging systems of AKI and their application
  3. recognize the differences in clinical presentation and lab findings between AKI and CKD
  4. learn management strategies for animals with AKI
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2
Q

AKI definition

A
  • inc in serum Cr by >/= 0.3 mg/dL OR
  • inc in serum Cr by >/= 1.5 times baseline OR
  • Urine production < 0.5 ml/kg/hr (6 hours)
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3
Q

pathophys AKI

A
  1. Initiation =>
  2. Extension =>
  3. Maintenance =>
  4. Recovery
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4
Q

Recognition AKI

Cr measurement

A
  1. principal biomarker of AKI
  2. will inc once > 75% of renal function is lost
  3. delayed recognition of novel biomarkers
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5
Q

Recognition AKI

Urine output

A
  • normal: 20-50 ml/kg/day or 1-2 ml/kg/hr
  • oliguria < 1.0 ml/kg/hr
  • anuria < 0.1 ml/kg/hr
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6
Q

Other indications for recognizing AKI

A
  • Urea Nitrogen (BUN)
  • Complete history
  • thorough physical examination
    • pre/post renal
  • clearance studies
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7
Q

Staging AKI

Rifle (Humans)

A
  • Risk
    • inc Cr 1.5-2 times baseline or
    • urine output of < 0.5 ml/kg/hr for > 6 hours
  • Injury
    • inc Cr 2-3 times baseline (loss of 50% GFR) or
    • urine otput < 0.5 ml/kg/hr for more than 12 hours
  • Failure
    • inc Cr > 3 times baseline (loss of 75% of GFR) or
    • inc in Cr greater than 4 mg/dL
    • urine output < 0.3 ml/kg/hr for > 24 hours or anuria for > 12 hrs
  • Loss of function
    • persistent renal failure (need dialysis) for > 4 weeks
  • End-stage renal dz
    • persistent renal failure (need dialysis) for more than 3 months
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8
Q

IRIS staging

(veterinary)

A
  • Grade I: < 1.6 mg/dl
  • Grade II: 1.7-2.5 mg/dl
  • Grade III: 2.6-5.0 mg/dl
  • Grade IV: 5.1-10.0 mg/dl
  • Grade V: 10.0 mg/dl

*subgrades of each category into non oliguric (NO) or oliguric (O) or requiring renal replacement therapy (RRT)

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9
Q

AKI

Common presenting complaints

A
  • non-specific clinical signs
  • gastrointestinal signs common
  • PU/PD may be reported by owners
  • secondary to critical illness (burns)
    • can develop AKI in the hospital
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10
Q

AKI Clinical presentation

PE

A
  • Dehydration
    • dry MM, skin tent, sunken eyes
  • hypovolemia
    • weakness, tachycardia, faint pulses
  • arrhythmias
    • bradyardia with severe K+ elevation
  • abdominal pain
  • large +/- painful kidneys
  • normal body condition or overweight
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11
Q

Clinical presentation AKI

HX

A
  • Acute onset of clinical signs (hours to days)
  • previously healthy
  • exposure to toxins
  • travel history/environment
  • frequent visits to the litter box
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12
Q

Etiology

causes of renal AKI

A
  1. Glomerular disease
    • GN, thrombosis
  2. Tubular injury
    • ischemia, toxins
  3. interstitial nephritis
  4. vascular disease
    • vasculitis, thrombosis
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13
Q

Etiology: Pre-renal AKI

A
  • Renal autoregulation
    • pre-glomerular vasodilation
      • prostaglandins: affected by NSAIDS
    • post-glomerular vasoconstriction
      • angiotensin II: affected by ace inhibitors

*questions on clinics!!!!

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14
Q

Renal blood flow to the kidneys is limited when systolic blood flow

A
  • drops below 70
    • at this point auto-regulatory mechanisms are not as effective
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15
Q

Causes of low blood pressure

A
  • blood loss/hypovolemia
  • anesthetic protocols
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16
Q

Etiology: post-renal

A
  • Obstructive dz
    • urolithiasis (i.e. ureteroliths in cats)
    • Neoplasia
    • Prostatic disease
    • FLUTD
  • Uroabdomen
17
Q

Etiology: Renal

4 intrinsic causes

A
  1. Glomerular dz
    • inflammation of glomerular membrane => can cause obstruction
    • will lose protein, have low albumin
  2. Renal tubular injury
    1. Toxins: ethylene glycol, lilies, grapes/raisins
    2. Nephrotoxic drugs: antibiotics (aminoglycosides), NSAIDS, radiocontrast agents
    3. Metabolic dz: hypercalcemia
    4. Endogenous substances: myoglobin, hemoglobin
  3. Interstitial nephritis (usually do to infectious dz)
    1. Pyelonephritis
    2. leptospirosis
    3. granulomatous dz
    4. neoplasia (lymphoma)
  4. Vascular dz
    1. vasculitis: systemic inflammation (sepsis, trauma, pancreatitis)
    2. thromboembolism: cushings, IMHA
18
Q

AKI biochem

A
  • azotemia (BUN and Creatinine)
    • may be disporportionate in GI hemorrhage or severe dehydration
  • Electrolyte derangements
    • hyperphosphatemia and hyperkalemia
      • due to decreased renal excretion
  • Elevations in liver enzymes
    • leptospirosis
  • Elevated CK values
    • rhabdomyolysis
  • Low Albumin
    • GN, SIRS (systemic inflammatory response syndrome), or sepsis
19
Q

AKI: blood gas

A
  • mild to severe metabolic acidosis
    • dec renal reabsorption bicarb
    • dec excretion of organic/inorganic acids
  • Elevated Anion gap ( > 25 dogs; > 30 cats)
    • consistent with EG intox
    • anion gap: (Na+ + K+) - (HCO3 + Cl-)
    • ionized hypocalcemia may be observed
20
Q

AKI: Hematology

A
  • hematocrit can be normal or elevated
    • non-regenerative anemai in CKD
    • severe GI hemorrhage may also cause anemia (low TS)
  • Leukocytosis
    • mild in cases of sterile inflamatin or stress leukogram
    • severe, left-shifted (infectious etiologies)
    • leukopenia should raise concern for sepsis
  • Thrombocytopenia
    • leptospirosis
    • thromboembolic dz
21
Q

AKI: Urinalysis

A
  • Hallmark signs is azotemia with inappropriately concentrated urine
    • Dogs < 1.035
    • Cats < 1.040
    • Isosthenuria common in AKI (1.008-1.012)
  • Glucosuria with tubular damage
    • not specific, consider ddx for tubular damage
  • proteinuria/pigmenturia
    • markers for inflammation
    • could be from a GI dz
    • evaluate other parts of Urinary system
  • pyuria and bacteruria
    • suspect pyelonephritis
  • granular casts with tubular damage
    • non-specific
  • Calcium oxalate monohydrate crystals
    • ethylene glycol poisoning
22
Q

AKI: Microbio

A
  • always perform urine aerobic culture
  • positive culture
    • may indicate pyelonephritis
  • negative culture
    • doesn’t rule out pyelonephritis
  • blood cultures in sepsis before antibiotics
  • abdominal effusion culture in cases of uroabdomen
23
Q

AKI: Serology

A
  • Leptospirosis
    • common in dogs, not cats
    • titers: detect antibodies against infection OR recent vaccination
    • may be negative during acute phase
    • always perform convalescent titers (2-4 weeks post)
    • Lepto PCR in urine or blood or both
      • looks for DNA of LIVE organisms
      • before antibiotics
  • Other infectious organisms
    • RMSF (rockky mountain spotted fever)
    • Ehrlichia
    • babesia
    • leishmania (Europe)
24
Q

AKI: Imaging

A
  • Abdominal rads
    • assess renal shape and size
    • radiopaque uroliths (size limitation)
    • Heavy metal intoxication
  • Ultrasonography
    • most sensitive modality for parenchymal/structural changes
    • detection of small ureteroliths
    • neoplastic disease (kidney, bladder, ureter)
25
Q

AKI: Blood Pressure

A
  • Several limitations in veterinary patients
  • Diagnostic work up:
    • hypotension (pre-renal causes of AKI)
    • hypertension (end-organ damage)
  • Monitoring
    • should be performed at least twice daily
      • endogenous epi and norepi in sick patients inc BP
    • Hypertension and blood pressure control common in AKI
26
Q

Persistent hypertension

A
  • Affect GFR and cause AKI
27
Q

AKI: Urine output

A
  • measure output when possible
    • urinary catheterization
      • most accurate
      • inc risk of infection
      • inc patient discomfort
    • collect voided urine
      • at ever walk or measure pee pads
    • monitor body weight
      • cheap, non-invasive and reliable
      • before and after walk
28
Q

AKI VS CKD

A
  • AKI
    • acute onset CS
    • normal BC or overweight
    • large/painful kidneys
    • normal HCT/hemoconcentration
    • hyperkalemia
  • CKD
    • hx of PU/PD, weight loss or absent CS
    • poor body cond
    • small/irregular kidneys
    • non-regenerative anemia
    • normal K or hypokalemia
29
Q

Management principles

A
  1. Identify and correct pre-renal and post-renal factors
  2. Antibiotics
  3. Identify and treat acute compliations
    • hyperkalemia
    • metabolic acidosis
  4. Review other drugs
  5. Accurately monitor fluid balance and daily body weight
  6. Optimize nutritional support
  7. Management of GI signs
  8. Renal replacement therapies
30
Q

Indentifying pre-renal factors

A
  • fluid therapy should rapidly correct hydration deficits and ongoing losses
    • use fluids with low Cl concentrations
  • hypovolemic and hypotensive animals should receive shock doses of IV fluids
    • something about risk of fluid overload and heart disease
  • Goal directed therapy and improved markers of perfusion
    • lactate is a marker of perfusion
31
Q

Fluids:

Cl rich

Hetestarch

A
  • Chloride rich soluntions
    • may elevate mean serum creatinine level
    • inc incidence of AKI
    • inc need for renal replacement therapy
  • Hetestarch
    • assoc with in-hospital mortality
    • inc need for renal replacement therapy
32
Q
  1. Identify post-renal factors
A
  • Cats commonly suffer from calcium oxalate uroliths
  • study showing sx outcomes better than Med manag outcomes
    • urethral stints…
  • Urinary obstruction
    • rapidly establish urinary tract patency
  • Post obstructive diuresis
    • keep up with urine output, post-renal may become pre-renal
  • watch K+ levels
33
Q
  1. Antibiotics
A
  • Collect urine and blood samples first
  • start antibiotic therapy and continue until infectious causes of AKI have been ruled out
    • unasyn: broad spectrum
    • lepto: doxy
  • adjust antibiotic therapy based on sensitivity results

*culture may take 48 hours

34
Q
  1. Identify and treat acute complications
A
  • Medical management
    • Aimed to provide window for kidney to recover
    • not used when severe CS present
    • narrow window for kidney recovery (hours to days)
    • patients can die from uremia despite potential for recovery
  • Hyperkalemia
    • mech: dec renal excretion and metabolic acidosis
    • conseq: cardiac arrhythmias, tremors
    • prevalence: highly variable
    • tx: shift intracell bicarb, glucose, insulin
  • Acidosis
    • corrected with med manag
    • rarely is main indication for dialysis
    • bicarb: be careful, something about crossing blood brain barrier
35
Q
  1. Review other drugs
A
  • Discontinue all potential nephrotoxic agents
    • aminoglycoside antibiotics
    • NSAIDS
    • Sedation protocols
  • Radiocontrast agent concerns
  • FLUIDS are therapeutic agents
    • review, adjust frequently
36
Q
  1. Accurately monitor fluid balance and daily body weight
A
  • goal: convert oliguric animals to non-oliguric
  • avoid volume overload at all costs
  • clinically, anuric animals may be more likely to be fluid overloaded
    • kidney capsule can also get edematous
  • common reason for therapeutic failure
  • weigh frequently
  • fluid over load
    • more than a 10% inc in body weight from baseline
37
Q
  1. Optimize nutritional support
A
  • improved survival
  • Goal
    • preserve lean body mass
    • avoid further metabolic complications
    • support immune system
    • improve GI tract function
  • Feeding tubes should be part of a therapeutic plan
  • Do not force feed renal diets
    • creates aversion
  • Phosphate binder therapy with each meal
38
Q
  1. Initialize dialysis before uremic complications emerge
A
  • Severe hyperkalemia
  • severe fluid overload
    • with concurrent low urine production
  • severe acid base disturbance
  • severe or progressive azotemia
  • oliguria/anuria
  • uncontrolled CS
  • re-surgical conditioning
39
Q
  1. Management of GI signs
A
  • Uremic Gastritis
    • secondary to decreased Gastrin elimination
  • anti-emetics
    • cerenia
    • ondansetron (non-dyalized)
    • metaclopramide (prokinetic)
  • decreased acid reduction
    • H2-blockers
    • proton pump inhibitors
    • sulcralfate

Urology (15 decks)

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