Anesthesia for Urologic Surgery Flashcards
how much cardiac output do the kidneys receive?
20-25%
nephron location
outer cortex
inner medulla
three processes of kidney that contribute to homeostasis
- filtration
- reabsorption
- excretion (tubular)
normal GFR
125 mL/min
normal urine specific gravity
1.000-1.025
increased GFR
- caused by increased renal blood flow
- dilation of afferent
- constriction of efferent
decreased GFR
- caused by decreased renal blood flow
- constriction of afferent
- dilation of efferent
renal hormones include…
- aldosterone
- antidiuretic hormone
- angiotensin
- atrial naturetic factor
- vitamin D
- prostaglandins
anesthetic drugs effect on renal function
- depress normal renal function
- renal blood flow may decrease by 30-40%
- impairment of autoregulation
general anesthesia associated with decrease in…
- renal blood flow
- GFR
- urinary flow
- electrolyte secretion
spinal and epidural
- all the same as general anesthesia
- magnitude of change parallels the degree of sympathetic block and blood pressure depression
volatile anesthetic effects on kidneys
- all cause mild increase in renal vascular resistance
- compensatory mechanism in response to decreases in cardiac output and SVR
- historically, methoxyflurane caused high fluoride ion concentrations and nephrotoxicity
prevention of effects of volatiles on kidneys
- preop hydration
- decreased concentrations of volatiles
- maintenance of blood pressure
- all attenuate reductions in renal blood flow and GFR
sevoflurane and the kidneys
- not associated with nephrotoxocity even though it has been associated with high fluoride levels
- degraded by absorbents to form compound A (vinyl ether)
- potential exists for compound A nephrotoxocity
what can the CRNA do to decrease risk of compound A nephrotoxicity?
- high gas flows (1 L/min FGF for 2 MAC hours)
- decrease gas concentration
- use of carbon dioxide absorbents
isoflurane and desflurane
-not associated with nephrotoxicity
fluoride ion toxicity
- fluoride interferes with active transport of sodium and chloride in the loop of Henle
- potent vasoconstrictor
- potent inhibitor of many enzyme systems (ADH)
- causes nephrotoxicity thorugh proximal tubular swelling and necrosis - related to dosage, duration, and peak fluoride concentrations
S/S fluoride ion nephrotoxicity
- polyuria
- hypernatremia
- serum hyperosmolality
- elevated BUN and Cr
- decreased Cr clearance
acute kidney injury
- renal functional or structural abnormality that occurs within 48 hours
- increase in Cr 0.3 mg/dL or 50% increase
- UOP < 0.5 mL/kg/hr x6 hours
AKI risk increased by what?
- hypovolemia
- electrolyte imbalance
- contrast dye
prerenal AKI
- hypoperfusion of kidneys without parenchymal damage
- ex = hemorrhage, N/V/D, diuretics, sepsis, shock, CHF, NE, NSAIDs, ACE-I
intrinsic AKI
- result of damage to renal tissue
- ex = tubular injury d/t hypoperfusion, myoglobin, chemo, infection, lymphoma, toxemia of pregnancy, vasculitis
postrenal AKI
- due to urinary tract obstruction
- ex = renal calculi, peritoneal mass, prostate/bladder urethra tumor, fibrosis, hematoma, strictures
risk factors for AKI
- aging (>50 years of age)
- preop renal dysfunction
- comorbidities - cardiac failure, hepatic failure, DM, HTN
- surgical procedures
- emergency of high risk procedures
surgical procedures that put patient at increased risk for AKI
- cardiac bypass
- aortic cross clamp
- arteriography
- intra-aortic balloon pump
emergency or high risk procedures that put patient at risk for AKI
- ruptured AAA
- ischemic time
- large volume of blood transfused
AKI preoperative treatment
- fluid deficit replacement with balanced salt solution (to minimize ADH and RAAS)
- attenuation of surgical stress (neuraxial, opioids)
- patient monitoring considerations - art line, TEE, CVP, foley catheter
AKI Perioperative treatment
- fluid replacement
- improve CO
- normalize SVR
- diuretic use to prevent oliguria NOT recommended
- early treatment of prerenal causes (10% mortality)
- post renal – good prognosis with early identification
- intrarenal AKI = most difficult to treat
prevention/management of AKI
- most common cause = prolonged hypoperfusion
- prophylaxis reduced mortality more than dialysis
- duration and magnitude of insult determines severity of AKI
treatment of AKI
- administer volume (NS) to euvolemia
- improve cardiac output by afterload reduction
- normalize systemic vascular resistance
- key strategy = minimize magnitude and duration of renal ischemia
chronic kidney disease (CKD)
- renal function decreases 10% per decade
- CKD exists when GFR is less than 60 mL/min/1.73 m2 for three months
- s/s not apparent until less than 40% of normal functioning nephrons remain
- 95% loss of renal function = uremia, CHF, volume overload
CV effects of CKD
- HTN and CHF
- 90% volume dependent
- 10% secondary to increased renin
- pericardial effusion
- ischemic heart disease most common cause of death
- pericarditis seen in patients with severe anemia
respiratory effects of CKD
respiratory depression secondary to delayed clearance
neurologic effects of CKD
- fatigue and weakness are early complaints
- autonomic neuropathy
disequilibrium syndrome
- rapid increase in brain intracellular volume –> increased sodium
- seizure, stupor, coma
hematologic effects of CKD
- normochromic, normocytic anemia - decrease in EPO, reduction in RBC life d/t dialysis, blood loss from frequent sampling
- prolonged bleeding - decrease plt function, DDAVP increases factor 8
GI effects of CKD
dialysis patients at greater risk for GI bleed, due to inflammation and mucosal changes
infection effects of CKD
- protein malnutrition
- neutrophil, monocyte and macrophage changes
- leading cause of death in dialysis dependent patients