Final_Renal Flashcards
Kidneys are responsible for
- water conservation
- electrolyte homeostasis
- acid-base balance
- several neurohumoral/ hormonal functions
AKI- types
- prerenal (azotemia)
- renal (kidney itself)
- post-renal (outflow obstruction)
AKI- tx
● No specific tx
● Management aims to limit further injury in sepsis:
○ Treat underlying cause
○ MAP>65mmHg
○ Fluid resuscitation (LR)
○ Vasopressor therapy (Norepi in sepsis = safe for kidneys)
○ Activated C-Protein
○ Steroid replacement (for adrenal insufficiency)
○ Dialysis - mainstay for severe AKI
AKI - anesthesia management
- Rx dosing adjustments: decrease dose, increase interval
- same as tx of AKI
- only life saving surgery for pts with AKI
CKD - what is it?
Kidney damage with GFR <60 mL/min/1.73m for 3 mos or more
CKD - progression
● Stage I
○ GFR decreases→ increases in BUN + Creat
○ Non-linear process - i.e. Creatinine can be normal while 50% dec. GFR
● Stage II
○ Hyperkalemia
○ Body compensates - ↑ blood flow to collecting tubules to get rid of K+
● Stage III
○ Homeostasis and regulation of extracellular fluid compartment volume
■ System starts to become overwhelmed
■ Biggest increase in damage over last ~ decade
CKD complications
- uremic syndrome
- renal osteodystrophy
- anemia
- uremic bleeding
- neuro changes
- CV changes (HTN, HL, silent MI, uremic pericarditis)
CKD management
● Aggressive tx of underlying cause
● Pharmacologic therapy (delay dx progression, prevent further complications)
● Preparation for RRT (access, AV fistula–> peritoneal HD, iHD, RRT)
● Manage BP
● Dietary interventions
● Epo for anemia at all stages of CKD
● Lifestyle modifications
CKD - anesthesia management (pre-op, induction)
Preop: LABS (chem), coagulopathies, anemia; HD regimen
Induction:
-Induction drugs?
■ Most safe to use
■ Thiopental=Dose ↓
(d/t ↑ volume of distribution, ↓ protein binding)
- response
HOTN almost immediately after: be prepared=pressors
-Is succinylcholine safe to use?
K+ released from Sux not exaggerated in CKD=safe to use
*Attenuated SNS activity impairs compensatory vasoconstriction ○ Exaggerated (HD) response to: ■ blood volume ■ PPV ■ body position changes
○ ACEs/ARBS → more HOTN intraop esp if haven’t followed guidelines for pre-op use of Rx
CKD - anesthesia management (maintenance)
Maintenance:
- Balanced anesthesia
(VA + muscle relaxants + opioids = equal mix) - What about sevoflurane?
○ Fluoride Toxicity + Compound A accumulation
○ Do providers use Sevo? Yes in real world (higher flows)
● What about volatile agents?
○ Safe - but could use cause precipitous drop in BP d/t decreased SVR
○ Know which VAs drop SVR more than others
● What about TIVA? ✔ Fine
● What about muscle relaxants?
○ Slowed excretion of Roc/Vec
○ Cisatracurium: No change
● What about neostigmine?
○ MOA prolonged
○ Not a problem if reversing
● What about opioids?
○ morphine/meperidine depends on renal clearance
○ Morphine metabolite may accumulate & cause post-op respiratory depression
○ Careful use of longer acting opioids → make sure breathing well post-op
nephrolithiasis
Kidney Stone
Biggest causative factor of nephrolithiasis
Calcium Oxylate
Struvite
Magnesium ammonium phosphate (often formed from infxn process: UTI)
Biggest growth in which kidney failure over 2014-2017?
Stage 3: GFR 30-59
TURP syndrome is due to
IV fluid volume shifts + plasma solute effects caused by absorption of irrigation solution