FA3 Urinary > Lecture 8 > Flashcards

Lecture 8 Flashcards

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1
Q

What is the most common cause of fluid overload in AKI patients?

A

failure to decrease fluid rate in the face of decreased urine production

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2
Q

What are the characteristics of weight gain in AKI patients?

A

-5 to 10% weight gain is clinically significant
-want to confirm euhydration and evaluate fluid input/urine output in patients gaining weight

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3
Q

What are the clinical signs of mild to moderate fluid overload?

A

-chemosis (swollen, fluid-filled conjunctiva)
-serous nasal discharge
-regurgitation

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4
Q

What are the clinical signs of severe fluid overload?

A

-cavitary effusion
-marked edema
-tachypnea
-intra-abdominal hypertension
-organ failure

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5
Q

What are the effects of increased interstitial pressure and renal edema?

A

-increased venous pressure
-increased renal vascular resistance
-increased extrinsic pressure
-increased tubular pressure
-decreased ultrafiltration gradient

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6
Q

What is effect of renal edema on the cellular level?

A

-more space between capillaries and cells
-decreased oxygen diffusion/delivery to renal cells

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7
Q

Why is it best to avoid diuresis therapy in AKI patients?

A

many forms of AKI are volume unresponsive; better to avoid potential fluid overload

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8
Q

Why is it difficult to predict what the kidneys will do with fluids in AKI patients?

A

-complicated relationships between renal blood flow, GFR, and pressure gradients
-hormone activation; RAAS, ADH
-abnormal microcirculation

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9
Q

What are the goals of fluid therapy in AKI patients?

A

-achieve and maintain euvolemia and euhydration
-rapidly restore adequate tissue perfusion
-correct hypovolemia within 1 to 2 hours; dehydration within 6 hours

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10
Q

What is the approach with traditional fluid therapy?

A

-maintain near maximal stroke volume
-consider dehydration, maintenance, and ongoing losses

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11
Q

What are the components of R.O.S.E. fluid therapy?

A

-resuscitation
-optimization
-stabilization
-evacuation (de-escalation)

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12
Q

What are the characteristics of resuscitation in ROSE therapy?

A

-life-saving measures
-correct shock within 30 min. to 2 hours
-10 mL/kg over 15 minutes; up to 3 boluses

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13
Q

What are the characteristics of optimization in ROSE therapy?

A

-optimize and maintain tissue perfusion
-compensate for shock over hours to a few days
-monitor heart rate, blood pressure, and urine output
-can do a fluid challenge of 5 mL/kg over 20 minutes

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14
Q

What are the characteristics of stabilization in ROSE therapy?

A

-steady state/maintenance
-zero or negative fluid balance
-ensure euhydration; correct dehydration and overhydration
-replace losses and account for nutrition and medications

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15
Q

What is the insensible loss rate for fluids?

A

22 mL/kg/day

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16
Q

What are the characteristics of evacuation in ROSE therapy?

A

-organ recovery
-mobilize accumulated fluid
-occurs over days to weeks
-want to decrease fluid dose by 10-20% every 12 hours
-monitor for dehydration

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17
Q

What are the goals surrounding oliguria and anuria?

A

-rapid identification
-early intervention
-convert within 6 to 8 hours

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18
Q

What are the urine production rates for normal euhydrated patients, oliguric patients, and anuric patients?

A

-normal: 2 to 5 mL/kg/hour
-oliguric: less than 1 mL/kg/hour
-anuric: no urine production

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19
Q

What are the first things to assess in oliguric or anuric patients?

A

-hydration status
-blood pressure
-patency of urinary catheter

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20
Q

What is the management for euhydrated, oliguric/anuric patients?

A

-stop IV fluids
-start furosemide

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21
Q

How does furosemide work?

A

-prevents reabsorption of sodium
-improves distal tubular flow
-does NOT improve GFR or outcome

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22
Q

What are the benefits of using furosemide?

A

-increases urine production to manage fluid overload and consequent hypertension
-facilitates potassium clearance
-increases intratubular flow to facilitate removal of luminal debris and obstructions

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23
Q

How is furosemide given to oliguric/anuric patients?

A

-start with test bolus of 1 to 1.5 mg/kg IV
-response to bolus should be seen within 30 minutes to 1 hr
-if positive response, start patient on CRI of 0.5 to 1 mg/kg/hour

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24
Q

Which treatments are no longer recommended for oliguric/anuric patients?

A

-mannitol
-dopamine
-fenoldopam

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25
What are the end-points for furosemide treatment in AKI patients?
-non-oliguric -adequate fluid mobilization; 3 to 4 ml/kg/h -eliminate excess fluid over 24 to 72 hours -match ins and outs once euhydrated
26
What are the indications for renal replacement therapy?
-AKI refractory to medical management -life-threatening electrolyte abnormalities -life-threatening acid-base -persistent oligoanuria -fluid overload -exposure to dialyzable toxins
27
What are the types of renal replacement therapy?
-peritoneal -intermittent -continuous
28
What are the characteristics of hospitalization times for AKI?
-typically around a week for severe AKI -depends on renal function improvement, comorbidities, and complications
29
What are the take home points regarding AKI grade and recovery?
-grade does not correlate with potential to recover -recovery phase can take months -lack of improvement within first few days of treatment does not correlate with inability to recover
30
What is the prognosis for acute-on-chronic AKI presentation?
-short term survival around 60% -long-term survival relatively poor
31
What are the specific causes of AKI?
-leptospirosis -antifreeze -medications -grapes/raisins (dogs) -lilies (cats) -jerky treats
32
What are the traditional approaches to acute toxicities?
-emesis -charcoal -gastric lavage -fluid diuresis -intralipid therapy
33
What is the general prognosis for toxin-induced AKI?
-better prognosis with early, aggressive intervention -poorer prognosis with delayed intervention or signs of AKI
34
What are the possible causes of medication-associated AKI?
-antimicrobials: aminoglycosides -antifungals: amphotericin B -chemo: cisplatin -radiograph contrast agents -ACE-inhibitors and angiotensin-receptor blockers -NSAIDs
35
What are the characteristics of NSAID toxicity?
-most common toxin -dose-dependent and drug dependent
36
Why is fluid diuresis not helpful in cases of acute NSAID toxicity?
-NSAIDs are highly protein bound -increased fluids does not equate to increased albumin passing through glomerulus
37
What are the possible treatments for NSAID toxicosis?
-lipid emulsions -therapeutic plasma exchange for acute overdose
38
What are the characteristics of ethylene glycol?
-sweet taste -low lethal dose -rapidly absorbed in GI tract -crosses BBB
39
What are the signs of ethylene glycol toxicity that manifest within 1 to 4 hours?
-lethargy -vomiting -ataxia -PUPD
40
How long does it take for ethylene glycol to metabolize into toxic metabolites?
3 to 4 hours
41
What are the characteristics of ethylene glycol toxic metabolites?
*glycolic and glycooxylic acid: -severe metabolic acidosis *oxalic acid: -binds with calcium -precipitates in renal tubules
42
What are the characteristics of calcium oxylate monohydrate crystals?
-picket fence appearance -frequently seen with ethylene glycol toxicity -not 100% sensitive; can have EG toxicity without crystal formation
43
What are the key lab findings in ethylene glycol toxicity?
-increased serum osmolality and anion gap -metabolic acidosis -calcium oxylate monohydrate cylindruria
44
How is ethylene glycol toxicity diagnosed?
-history -clinical signs -lab findings -rapid cage-side tests to detect EG molecule
45
What is the specific treatment for ethylene glycol toxicity?
prevent metabolism of EG by using ethanol or fomepizole to target alcohol dehydrogenase enzyme
46
How long does it take for all of the parent ethylene glycol compound to metabolize?
24 hours
47
What are the pros and cons of ethanol as a treatment for ethylene glycol?
pros: -cheap cons: -CNS and resp. depression -metabolic acidosis -hyperosmolarity
48
What are the pros and cons of fomepizole as a treatment for ethylene glycol?
pros: -effective in dogs and cats -no drunken side effects cons: -expensive -limited availability
49
What are the pros and cons of renal replacement therapy as a treatment for ethylene glycol?
pros: -can remove both EG and toxic metabolites cons: -expensive -limited availability
50
What is the prognosis for ethylene glycol toxicity?
-best prognosis with early, aggressive intervention -guarded to grave prognosis if azotemic or oligoanuric
51
What are the characteristics of lily intoxication in cats?
-toxic dose and compound unknown -all parts considered toxic; flowers most toxic -peace and calla lilies do NOT fall into this category
52
What are the clinical signs of lily toxicity in cats?
-initial transient GI signs; ptyalism and vomiting -apparent clinical recovery -anorexia -lethargy -PUPD -abdominal pain -possible neuro. signs
53
What are the histopath. findings in lily toxicity?
-acute tubular necrosis -interstitial edema -intact basement membrane
54
What are the urinalysis findings in lily toxicity?
-isosthenuria -renal glucosuria -tubular proteinuria -cylindruria
55
What are the characteristics of lily toxicity treatment?
-need early, aggressive treatment within 6 hours -decontamination involves emesis, activated charcoal, and bathing cat -IV fluid diuresis -delayed treatment/AKI development may require dialysis -no antidote
56
What is the prognosis for lily toxicity?
-recovery likely with early/aggressive treatment, only GI, and no AKI -guarded prognosis with delayed intervention or signs of AKI
57
What are the characteristics of grape/raisin toxicity in dogs?
-toxic compound is tartaric acid -not all dogs equally effected -not dose-dependent
58
What are the clinical signs of grape/raisin toxicity?
-GI signs within 24 hours; nausea, vomiting -anorexia -vomiting -diarrhea -abdominal pain -neuro. signs (reversible)
59
What are the histopath findings in grape/raisin toxicity?
-acute tubular necrosis -intact basement membrane
60
What are the urinalysis findings in grape/raisin toxicity?
-isosthenuria -possible renal glucosuria -tubular proteinuria -cylindruria
61
What is the treatment for grape/raisin toxicity?
-need early, aggressive treatment -decontamination involves emesis and activated charcoal -IV fluid diuresis -delayed treatment/AKI development may require dialysis -no antidote
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