Renal II Flashcards
1
Q
How does anesthesia affect renal function?
A
- Neuraxial
- T4-T10 sympathectomy decreases release of catechols, renin, and vasopressin
- maintain RBF and GFR with fluid boluses
- T4-T10 sympathectomy decreases release of catechols, renin, and vasopressin
- Surgical stress response- usually canges in RBF, not the actual anesthetic agent, esp in major surgery, CPB, hypovolemia, or aortic cross clamping
- Pharmacology- most agents decrease GFR and UOP but it is resolved w/emergence
- d/t CV depression
- prehydrate and attenuate against stress response
- renal autoreg and hormonal function usually maintained
- IA- can be renal protective
- nephrotoxic concern with free Fl- in older agents (negligible in Iso)
- Ventilation- increased pressure on IVC, pulmonary arterial, and renal venous pressures caused by high PIP and PEEP can decrease RBF, GFR, and UOP
2
Q
General info about chronic kidney disease:
What is it?
When is HD required?
What is most common cause?
A
- CKD is the decrease in the number of functioning nephrons
- 30% of nml nephrons can eliminate the full load of waste products, but will become overloaded and overworked
- blood flow to the functioning flomerulus increases 50-100%
- wastes accumulate in the ECF
- tubular solutes arent reabsorbed, act as an osmotic diuretic
- HD required when Cr >3 or GFR <30
- Most common cause: DM
- second: HTN
3
Q
What are the physiologic effects of CKD?
(10)
A
- generalized edema
- high levels of nitrogens (Cr, urea, uric acid), phenols, sulfates, phos, K
- osteomalacia and secondary hyperparathyroidism
- VitD must be converted to allow Ca++ absorption from intestines
- accumulation of phos causes decreased Ca++ levels and increased PTH secretion causing bone resorption
- Prurities- cause unknown
- anemia (Hgb 5-8)- decreased EPO production (compensated)
- Coagulopathies- decreased circulating vWF
- increased risk for GI bleed
- tx with desmopressin, EPO, cryo, or estrogen therapy
- altered electrolyte balance
- systemic HTN- d/t volume expansion and RAAS activation
- goal: <130/85 usually w/ ACEI or ARBs
- CNS abnormalities
- infections- most common cause of death
4
Q
What is considered an AKI?
What increases the mortality rate?
A
- AKI
- increased Cr by >0.5
- 50% decrease in Cr clearance
- may be oliguric or nonoliguric
- High mortality rate (50-80%) if:
- HD is required
- Multiple organ dysfunction occurs
- hypotension occurs
- respiratory failure ensures
- **No elective surgery, if emergency procedure, keep MAP > 65
5
Q
What patients are at high risk of an AKI post-anesthesia?
A
- pre-op renal disease (#1)
- CHF or CAD
- intra-op cardiac events (inadequate BP or CO)
- sepsis or emergency surgery, trauma, MODS
- elderly
- ESLD
- hypovolemia
- nephrotoxic exposure
- CPB
- aortic cross clamping
- liver/kidney transplant
- nephrectomy
6
Q
What are the different categories of AKI?
A
-
Prerenal- d/t decreased blood supply to kidneys
- CHF
- low CO/BP
- low blood volume
-
Intrarenal- d/t severe ischemia, nephrotoxic exposure, parenchymal disease
- TALOH is esp vulnerable- necrosis occurs, releasing debris into tubules and blocking
- Acute glomerulonephritis d/t infection (strep)
- antibodies develop that are insoluble and get trapped in glomerulus and inflammatory process damages kidney
-
Post renal- d/t obstructionof urinary collecting system by renal calculi, etc
- if cause is found w/in a few hours, normal function can be restored
7
Q
What are the physiologic effects of AKI?
A
- retention of water, waste procucts, and electrolytes in the blood and ECF
- HTN, CHF, pulmonary edema
- diluted RBCs–> Hct 20-30%
- GI bleed- anorexia, nausea, ileus
- hyperkalemia/metabolic acidosis (can be fatal)
- neurologic changes
- uremia induced immune suppression leading to infection
8
Q
How can AKI be prevented and treated?
A
- Fluid resuscitation
- no data supporting colloids vs crystalloids
- mannitol may be helpful in transplants w/approp fluid bolus
- N-acetylcysteine + IVF may be protective agains contrast dye
- Vasopressors
- increased SBP to decrease renal SNS and RAAS and increase plasma hydrostatic pressure in glomerulus to increase GFR
- NE used in septic pts improves GFR and UOP
- dopamine/loop diuretics not supported
- Drug dosing
- use pharmacy guidelines– helpful to know CRcl/GFR
- reduce doses of drugs cleared unchanged by the kidneys and GFR <50
- consider the Vd
- protein binding is altered
- acidic drugs = less binding
- basic drugs = more binding
9
Q
Anesthetic drugs in the pt with an AKI:
propofol, ketamine, etomidate
midaz
precedex
morphine
meperidine
hydromorphone
fentanyl, alfent, sufent, remi
long acting NMB
roc/vec
cisatra, atracurium
succ
A
- TPL- highly protein bound, high free fraction with AKI
- prop, ket, etomi- no major change
- midaz- active metab 60-80% renally cleared; avoid repeat dosing
- precedex- highly PB, longer sedation with AKI
- morphine- avoid repeat dosing d/t potent, highly PB metabolite
- meperidine- avoid d/t metabolite
- hydromorphone- accumulation of active metab, avoid repeat dosing
- fent, sufent, alf- all good choices
- long acting NMB- avoid
- roc/vec- single dose ok, but prolonged effect possible
- cisatra, atracurium- normal dosing
- succ- check K first
10
Q
What drugs are nephrotoxic?
When would you want to avoid them especially?
A
- aminoglycosides
- radiocontrast dyes
- cyclosporin
- amphotericin B
- Especially avoid if given with NSAIDs, DM, shock, or hypovolemia
11
Q
What tests can be used to measure GFR?
A
- GFR- best b/c it parallels nephron function
- BUN (5-10) - >50 = decreased GFR
- varies inversely with GFR
- depends on urea production (metab of ammonium in the liver)
- can be altered by:
- high protein diet
- GI bleed
- dehydration
- Creatinine (0.5-1)
- varies inversely from GFR (2x increase in Cr = 50% decrease in GFR)
- specific indicator b/c it is freely filtered and not reabsorbed
- depends on muscle mass, physical activity, and protein intake and catabolism
- Creatinine clearance (110-150, <25 = moderate disease)
- most reliable estimate of GFR
- men have higher levels d/t muscle mass
- elderly lower d/t decreased muscle mass; an elevated CrCl is more concerning
12
Q
What tests are done to test tubular function?
A
- Urine specific gravity (1.003-1.030)
- Urine Osm (38-1400)
- Urine Na
13
Q
What are the goals for the HD patient?
A
- avoid infection and CV events
- 25% of annual mortality rate for all dialysis pts
- perserve vascular access
- avoid IV in non-dominant arm and upper arm
- AV fistula usually cephalic vain anastomosed to radial artery
- emergency access = double lumen dialysis catheter inserted into the jugular or femoral vein
14
Q
What are the different types of dialysis?
A
- Hemodialysis (most common)
- circulation through extracorporeal circuit that filters waste products into dialysstae
- purified blood is pumped from the dialyzer into the AV fistula
- Peritoneal dialysis
- peritoneum acts as a blood filter
- catheter inserted into abdomen and dialysate is pumped into abdominal cavity; waste products move from blood into dialysate solution
- after 6-24 hours, waste filled dialysate is drained from abdomen and replaced with clean dialysate
15
Q
What are the side effects of dialysis?
A
- hypotension- tx with decreased ultrafiltration rate or NS bolus
- hypersensitivity
- hypokalemia- b/c most K is in the ICF after dialysis, equilibration post-dialysis takes time
- cramps, HA, N/V
- anemia
- infection
