Renal (FINAL EXAM) Flashcards
(159 cards)
1
Q
The kidneys play a vital and varied role in ___.
A
regulating the volume and composition of body fluids, eliminating toxins, and elaborating hormones (e.g. renin, erythropoietin, the active form of vitamin D).
2
Q
Factors related to operative procedures and to anesthetic management frequently have a significant impact on kidney physiology and function and may lead to _____.
A
perioperative fluid overload, hypovolemia, and acute kidney injury, which are major causes of perioperative morbidity, mortality, extended hospital length of stay, and increased costs.
3
Q
Each kidney is made up of approximately 1 million functional units called ___.
A
nephrons.
4
Q
A nephron consists of a ___.
A
renal corpuscle and a tortuous tubule
5
Q
The renal corpuscle is a ____.
A
proximal structure composed of a glomerulus and a Bowman capsule
Here, ultrafiltrate of blood is formed, which flows through the nephron’s tubules
6
Q
Nephrons are classified as _____.
A
cortical or juxtamedullary, and the renal corpuscles of all nephrons are in the renal cortex
7
Q
The major anatomical and functional divisions of the nephron are the _____.
A
proximal convoluted tubule, the loop of Henle, the distal renal tubule, the collecting tubule, and the juxtaglomerular apparatus
8
Q
Throughout the nephron, ultrafiltrate’s volume and composition are modified by ____.
A
both reabsorption and secretion of solutes, and the collected final product is eliminated as urine.
9
Q
Filtration definition
A
Movement of water and solutes across glomerular capillaries
10
Q
Reabsorption definition
A
The removal of water and solutes from the filtrate in tubular lumen
11
Q
Secretion definition
A
Transport of solutes from the peritubular fluid into the tubular fluid
12
Q
Excretion definition
A
The removal of water and solutes from the body via urination
13
Q
Each renal corpuscle contains a____
A
glomerulus, which is composed of tufts of capillaries that jut into Bowman’s capsule, providing a large surface area for blood filtration.
14
Q
The glomerular endothelial cells are separated from the epithelial cells of Bowman’s capsule by _____.
A
only by their fused basement membranes.
15
Q
The glomerular and epithelial cells provide____.
A
an effective filtration barrier to cells and large molecular weight substances.
This barrier has a negative charge, favoring the filtration of cations over anions.
16
Q
Mesangial cells are located____.
A
between the basement membrane and epithelial cells near adjacent capillaries.
17
Q
What do mesangial cells do?
A
These contractile cells regulate glomerular blood flow and exhibit phagocytic activity.
Mesangial cells contract, reducing glomerular filtration, in response to angiotensin II, vasopressin, norepinephrine, thromboxane A2, leukotrienes, prostaglandin F2
Mesangial cells relax, increasing glomerular filtration, in response to atrial natriuretic peptide (ANP), prostaglandin E2, and dopaminergic agonists
18
Q
Glomerular hydrostatic pressure is opposed by ____.
A
both glomerular colloid oncotic pressure and Bowman capsule pressure.
19
Q
What are important in determining glomerular filtration pressure?
A
Afferent and efferent arteriolar tone are both important in determining glomerular filtration pressure: filtration pressure is directly proportional to efferent arteriolar tone but inversely proportional to afferent tone.
20
Q
Approximately ____% of plasma is normally filtered into the Bowman capsule as blood passes through the glomerulus.
A
20%
21
Q
What are the different pressures inside the nephron?
A
Net filtration pressure = 10 mmHg
Gomerular hydrostatic pressure = 60 mmHg
Bowman’s capsule pressure = 18 mmHg
Glomerular oncotic pressure = 32 mmHg
22
Q
Of the ultrafiltrate formed in Bowman’s capsule, how much is normally reabsorbed in the proximal renal tubule?
A
about 70%
23
Q
The major function of the proximal tubule is ____
A
Na+ reabsorption
24
Q
Sodium is actively transported out of the proximal tubule by____.
A
membrane bound Na+/K+ATPase
The resulting low intracellular concentration of Na+ allows passive movement of Na+ down its gradient from tubular fluid into the tubular epithelial cells
Sodium reabsorption is coupled with the reabsorption of other solutes and the secretion of H+. Phosphate, glucose, and amino acids are also reabsorbed here
25
What is the Loop of Henle responsible for?
The loop of Henle (descending and ascending portions) are responsible for maintaining a hypertonic medullary interstitial
26
The thin descending segment of the loop of Henle descends from ___.
the renal cortex into the renal medulla, turns back upon itself, and then rises back up toward the cortex as the ascending portion
27
The countercurrent multiplier mechanism
This mechanism is dependent on differential permeability and transport characteristics between the descending and ascending limbs
The descending limb and the thin ascending limb are permeable to water, Na+, Cl, and urea.
The thick ascending limb is impermeable to water and urea and actively reabsorbs Na+ and Cl– and therefore can generate an osmotic gradient
28
The distal tubule receives hypotonic fluid from _____ and is normally responsible for ___.
The distal tubule receives hypotonic fluid from the loop of Henle and is normally responsible for only minor modifications of tubular fluid
29
The distal nephron has very tight junctions between tubular epithelial cells and is relatively impermeable to _____.
water and sodium
30
Sodium reabsorption in the distal tubule normally accounts for only about how much of the filtered sodium load?
5%
31
energy on the capillary vs luminal side of the distal tubule
As in other parts of the nephron, the energy is derived from Na+–K+ATPase activity on the capillary side, but on the luminal side, Na+ is reabsorbed by an Na+–Cl carrier
32
Where is the major site of parathyroid hormone and vitamin D mediated calcium reabsorption?
The distal tubule
33
The latter portion of the distal tubule is referred to as ___.
the connecting segment and participates in aldosterone mediated Na+ reabsorption.
34
The collecting tubule can be divided into ____.
cortical and medullary portions, and together they normally account for the reabsorption of 5% to 7% of the filtered sodium load.
35
Cortical Collecting Duct of the nephron consists of what two cell types?
(1) **principal cells** that primarily secrete potassium and participate in aldosterone stimulated Na+ reabsorption
(2) **intercalated cells** that are responsible for acid–base regulation. Because principal cells reabsorb Na+ via an electrogenic pump, either Cl must also be reabsorbed, or K+ must be secreted to maintain electroneutrality. Increased intracellular [K+] favors K+ secretion.
36
Aldosterone enhances what kind of activity in the cortical collecting duct of the nephron?
Aldosterone enhances Na+–K+ATPase activity in this part of the nephron by increasing the number of open K+ and Na+ channels in the luminal membrane. Aldosterone also enhances the H+ secreting ATPase on the luminal border of I cells.
37
Intercalated cells additionally have a ___ pump.
luminal K+–H+ ATPase pump, which reabsorbs K+ and secretes H+, and are also capable of secreting bicarbonate ion in response to large alkaline loads.
38
What occurs in the cortical collecting tubule?
Secretion of hydrogen ions and reabsorption of bicarbonate and potassium in the cortical collecting tubule.
39
The medullary collecting tubule joins ____.
collecting tubules from other nephrons to form a single ureter in each kidney
40
ADH’s site of action = ____
the medullary collecting duct, which stimulates the expression of aquaporin 2
41
Dehydration increases ____.
vasopressin secretion, which increases the membrane’s permeability to water. As a result, water is drawn out of the collecting tubule fluid produces concentrated urine (up to 1400 mOsm/L)
42
adequate hydration suppresses _____
vasopressin secretion, allowing fluid in the collecting tubules to pass through the medulla relatively unchanged and remain hypotonic (100–200 mOsm/L).
43
Which part of the nephron is responsible for acidifying urine?
Medullary collecting duct, the hydrogen ions secreted are excreted in the form of phosphates and ammonium ions
44
Juxtaglomerular apparatus
This small organ within each nephron consists of a specialized segment of the afferent arteriole, containing juxtaglomerular cells within its wall, and the end of the thick, ascending cortical segment of the loop of Henle, the macula densa.
45
What do juxtaglomerular cells synthesize?
the enzyme renin and are innervated by the sympathetic nervous system.
46
Release of renin depends on ____
β1 adrenergic sympathetic stimulation, changes in afferent arteriolar wall pressure, and changes in chloride flow past the macula densa.
47
Discuss the steps that happen to renin in the juxtaglomerular apparatus.
Renin released into the bloodstream converts angiotensinogen, from the liver, to angiotensin I.
Angiotensin I is converted by angiotensin converting enzyme (ACE) from the lungs to form angiotensin II.
Angiotensin II plays a major role in blood pressure regulation and aldosterone secretion.
Proximal renal tubular cells have ACE and angiotensin II receptors.
Angiotensin II enhances sodium reabsorption in proximal tubules.
Extrarenal production of renin and angiotensin II also takes place in the vascular endothelium, the adrenal glands, and the brain.
48
The kidneys receive how much of total cardiac output?
25%
49
Renal blood flow percentages
Approximately 80% of RBF normally goes to cortical nephrons, and only 10% to 15% goes to juxtamedullary nephrons.
The renal cortex extracts relatively little oxygen
In contrast, the renal medulla maintains high metabolic activity and is relatively vulnerable to ischemia
50
Renal blood flow percentages
Approximately 80% of RBF normally goes to cortical nephrons, and only 10% to 15% goes to juxtamedullary nephrons.
The renal cortex extracts relatively little oxygen
In contrast, the renal medulla maintains high metabolic activity and is relatively vulnerable to ischemia
51
the glomerular capillaries, which favor filtration, peritubular capillaries are primarily _____.
“reabsorptive”
52
Clearance
is used to measure RBF and GFR
The renal clearance of a substance is defined as the volume of blood that is completely cleared of that substance per unit of time
53
RPF AND RBF
Renal plasma flow (RPF) is measured by p-aminohippurate (PAH) clearance
RPF is 660 mL/min
RBF is 1200 mL/min
54
GFR
**the volume of fluid filtered from the glomerular capillaries into the Bowman capsule per unit time**
Women: 95 mL/min
Men: 120 mL/min
normally 20% of RPF
Less accurate than measuring inulin clearance, but a more practical measurement
Creatinine is a product of phosphocreatine breakdown in muscle.
GFR is dependent on the relative tones of both the afferent and efferent arterioles
55
Save this card for if he wants us to memorize the formulas for GFR, RBF etc.
leave blank or delete
56
What control mechanisms regulate RBF?
Regulation of RBF includes 1) intrinsic autoregulation, 2) tubuloglomerular feedback, 3) hormonal regulation, and 4) neuronal regulation
57
Intrinsic regulation
Autoregulation of RBF occurs between MAP of 80-180 mmHg and is afferent glomerular arterioles responding to blood pressure changes
58
Tubuloglomerular feedback
* Increased tubular flow (secondary to increased GFR) results in GFR reduction
* Decreased tubular flow (secondary to decreased GFR results in increased GFR
* A change in GFR prompts macula densa and mesangial cells to alter afferent arteriolar tone through the release of calcium, renin, and adenosine
59
Hormonal Regulation
* Decreases in afferent glomerular arteriolar pressure, increases in sympathetic nervous system activity, and decreases in distal tubule sodium load stimulate renin release, resulting in angiotensin II release, which causes arterial vasoconstriction
* Atrial natriuretic peptide (ANP) helps regulate blood pressure and expanded extracellular fluid volume by promoting vasodilation and renal excretion of sodium and water.
60
A1 receptor activation = _____
increases Na reabsorption in the PCT
61
A2 receptor activation = _____
decreases Na reabsorption and promotes water excretion
62
D1 receptor activation =____
dilates afferent and efferent arteriole
63
D2 receptor activation on presynaptic postganglionic sympathetic neurons =_____
can also vasodilate arterioles through inhibition of NE secretion
64
Reversible decreases in RBF, GFR, urinary flow, and sodium excretion occur during _____.
both neuraxial and general anesthesia.
Such changes are usually less pronounced during neuraxial anesthesia.
Most of these changes are indirect and are mediated by autonomic and hormonal responses to surgery and anesthesia.
65
AKI is less likely to occur when ____.
an adequate intravascular volume and normal blood pressure are maintained.
66
Do volatiles cause AKI?
There is no evidence that currently utilized vapor anesthetic agents cause AKI in humans. However, compound A, a breakdown product of sevoflurane, produces renal toxicity when sevoflurane is administered with reduced fresh gas flow rates to laboratory animals.
67
Risk Index For Postop AKI
The risk index identifies preoperative predictors of AKI following general surgery
Risk Factor
* Age ≥ 56 y
* Male sex
* Active congestive heart failure
* Ascites
* Hypertension
* Emergency surgery
* Intraperitoneal surgery
* Renal insufficiency—mild or moderate
* Diabetes mellitus—oral or insulin therapy
Risk Index classification is based on the number of risk factors present: class I (0–2 risk factors), class II (3 risk factors), class III (4 risk factors), class IV (5 risk factors), class V (≥6 risk factors)
68
Pneumoperitoneum produced during laparoscopy creates ____.
**an abdominal compartment syndrome like state**
The increase in intraabdominal pressure often produces oliguria or anuria that is proportional to insufflation pressure
Mechanisms include vena cava and renal vein compression; kidney parenchymal compression; decreased cardiac output; and increases in plasma levels of renin, aldosterone, and ADH
Abdominal compartment syndrome can also be produced by several comorbid problems, with similar adverse impact on kidney function via the same mechanisms
69
CV effects of anesthesia and how it contributes to AKI
Depending on the dose, most IV and inhalational anesthetics and neuraxial anesthetics can decrease systemic blood pressure
Decrease in blood pressure (below limits of autoregulation) can reduce RBF, GFR, urinary flow and sodium excretion
**The effects can be reversed by administering pressor agents and intravenous fluids**
70
Neuroendocrine effects of anesthesia that contribute to AKI
Increased stress response (r/t anxiety, pain, surgical stimulation) resulting in SNS stimulation and hormone secretion (e.g. catecholamines, renin, angiotensin II, etc.)
71
How do volatile anesthetics risk AKI?
Halothane, isoflurane, sevoflurane, and desflurane decrease renal vascular resistance
72
_____ may prevent catecholamine induced redistribution of RBF.
Alpha adrenergic antagonists
73
______ may impair renal response to dopamine
Dopamine antagonists (e.g. metoclopramide, haldol, etc.)
74
____ prevent synthesis of vasodilatory prostaglandins
NSAIDS (e.g. ketorolac)
75
____ block protective effects of angiotensin II
ACEI
76
Radiocontrast agents cause ____
AKI
May be mitigated by IV fluids and pretreatment with N-acetylcysteine (600 mg orally every 12 h in four doses beginning prior to contrast administration) due to free radical scavenging or sulfhydryl donor–reducing properties
77
Fenoldopam, mannitol, loop diuretics, and low dose dopamine infusion _____.
do not help maintain renal function or confer protection against AKI
78
MANNITOL
(Class, MOA, Use, Route, Dose)
**Class**: Osmotic diuretic
**Mechanism of Action**: Increases osmolarity of plasma drawing in fluid from ICF & ECF and into the vasculature; mannitol is filtered at the glomerulus but not reabsorbed which draws fluids & electrolytes (Na, Cl, bicarb) into urine which causes an incrase in UOP
Mannitol activates the intrarenal synthesis of vasodilating prostaglandins and may be a free radical scavenger
**Clinical Use**: Acute reduction of intracranial pressure and cerebral edema, evaluation of acute oliguria, and although not evidence based, some clinicians may administer as prophylaxis against AKI
**Route**: IV
**Dosing (IV): 0.25-1 g/kg over 30-60 mins **
79
MANNITOL
(Distribution, Metabolism, Eliimination, Considerations)
**Distribution**
Onset: 15 minutes
DOA: 3 – 6 hours
**Metabolism**
Not metabolized
**Elimination**
Renally excreted (100% unchanged)
**Considerations**
Risk for hypovolemia, electrolyte abnormalities, pulmonary edema
High dose mannitol can be nephrotoxic
80
FUROSEMIDE
(Class, MOA, Use, Route, Dose)
**Class** Loop diuretics (e.g. bumetanide, torsemide, ethacrynic acid)
**Mechanism of Action**: Inhibits reabsorption of Na+–K+–2Cl in the thick ascending loop of Henle. Sodium reabsorption at that site requires that all four sites on the Na+–K+–2Cl luminal carrier protein be occupied. Loop diuretics compete with Cl for its binding site on the carrier protein. The large amounts of Na+ and Cl presented to the distal nephron overwhelm its limited reabsorptive capability.
**Clinical Use**: Treatment for hypertension (particularly when thiazides are ineffective), peripheral and pulmonary edema, evaluation of acute oliguria, treatment of hypercalcemia and correction of hyponatremia
**Route**: IV, PO
**Dosing (IV)**: Start with 5 mg and titrate up as needed (5 – 100 mg)
81
FUROSEMIDE
(Distribution, Metabolism, Eliimination, Considerations)
**Distribution**: Onset: 5 minutes
DOA: 2 hours
**Metabolism**: Hepatically metabolized
**Elimination**: Renally excreted
**Considerations**
Increased delivery of Na+ to the distal and collecting tubules increases K+ and H+ secretion at those sites and thus produces hypokalemia and metabolic
Urinary calcium and magnesium loss promoted by loop diuretics may result in hypocalcemia or hypomagnesemia, or both.
Hypercalciuria can promote urolithiasis
Reversible and irreversible hearing loss has been reported with loop diuretics, especially furosemide and ethacrynic acid
82
Hydrochlorothiazide
(Class, MOA, Use, Route, Dose)
**Class**: Thiazide diuretic (e.g. chlorthalidone, quinethazone, metolazone)
**Mechanism of Action**: They compete for the Cl- site on the luminal Na-Cl carrier protein and inhibit reabsorption of Na & Cl in the distal tubule.
augment Ca2+ reabsorption in the distal tubule.
**Clinical Use**: Treatment for hypertension (first line treatment), edematous disorders, hypercalcuria, nephrogenic diabetes insipidus,
**Route**: PO
**Dosing: 25 – 100 mg PO/day**
83
Hydrochlorothiazide
(Distribution, Metabolism, Eliimination, Considerations)
**Distribution**
Onset: 2 hours
DOA: 6 hours
**Metabolism**: Not metabolized
**Elimination**: Renally excreted (100% unchanged)
**Considerations**
Risk for hypovolemia, electrolyte abnormalities, pulmonary edema
Potentiates neuromuscular blockade
84
Potassium Sparing Diuretics
These are weak diuretic agents and characteristically do not increase potassium excretion
85
Aldosterone antagonists
(e.g. spironolactone) are direct antagonists of aldosterone receptors at the collecting tubule
These agents can result in hyperkalemia or kidney disease in those receiving β blockers or ACE inhibitors
Metabolic acidosis may also be seen
86
Noncompetitive potassium-sparing diuretics
(e.g triamterene)
Inhibit Na+ reabsorption and K+ secretion by decreasing the number of open sodium channels in the luminal membrane of collecting tubules and are not dependent upon aldosterone activity
87
Carbonic Anhydrase Inhibitors
Carbonic anhydrase inhibitors ( e.g. acetazolamide) interfere with Na+ reabsorption and H+ secretion in proximal tubules.
Used for metabolic acidosis in edematous patients, reduction of intraocular pressure and prophylaxis against altitude sickness
88
_______ is the most accurate method available for clinically assessing GFR.
Creatinine clearance measurement
Measurements are usually performed over 24 h or 2h
89
Creatinine Clearance values depending on different kidney disease stages
Normal = 100-120
Decreased kidney reserve = 60-100
Mild kidney impairment = 40-60
Moderate kidney insufficiency = 25-40
Kidney failure = <25
End-stage kidney disease = <10
90
What can be overestimated in late stage renal disease?
GFR can be overestimated in late-stage renal disease, and thus, when evaluating kidney function, it is important to look for other signs, including hypertension, proteinuria, or abnormalities in urine sediment
91
What is Creatinine?
Creatine is a product of muscle metabolism
Creatinine production - Men: 20 mg/kg/day, Women:15 mg/kg/day
Normal creatine – Men: 0.8 – 1.3 mg/dL; Women: 0.6 to 1 mg/dL
Creatine is filtered but not reabsorbed
92
Thus, serum creatine is directly related to _____ and inversely related to _______.
Thus, serum creatine is directly related to body muscle mass and inversely related to glomerular filtration
93
What is more reliable in the ambulatory patient than the critically ill?
GFR
94
BUN:Creatinine ratios greater than 15:1 are seen in _____.
volume depletion and in edematous disorders associated with decreased tubular flow (eg, congestive heart failure, cirrhosis), as well as in obstructive uropathies
95
Low renal tubular flow rates enhance urea reabsorption but do not affect ______.
creatinine excretion
This can be caused by decreased kidney perfusion or obstruction of the urinary tract.
96
Urinalyisis versus microscopic analysis
**Urinalysis**
Urinalysis typically includes pH; specific gravity; detection and quantification of glucose, protein, and bilirubin content; and microscopic analysis
**Microscopic analysis**
Red cells may be indicative of bleeding due to tumor, stones, infection, coagulopathy, or trauma (commonly, urinary catheterization)
White cells and bacteria are generally associated with infection
Disease processes at the level of the nephron produce tubular casts
Crystals may be indicative of abnormalities in oxalic acid, uric acid, or cystine metabolism.
97
SLIDE 32 (pros and cons of different tests, find out if we need to memorize, if so that is stupid)
98
Altered kidney function and the effects of anesthetic agents (general info)
In the presence of kidney impairment, dosage modifications may be required to prevent accumulation of the drug or its active metabolites
Moreover, the systemic effects of AKI can potentiate the pharmacological actions of many of these agents. This may be the result of decreased protein binding of the drug, greater brain penetration due to some breach of the blood–brain barrier, or a synergistic effect with the toxins retained in kidney failure.
99
IV induction agents (and their impact from renal failure)
Propofol and etomidate - minimally impaired by kidney function
Ketamine – minimally impaired by kidney function however norketamine is dependent on renal excretion and accumulate with ESRD
**Barbiturates** – increased effects likely related to increase free circulating barbiturate (d/t decreased protein binding)
**Benzodiazepines **– increased effects likely related to increase free circulating benzodiazepines
**Diazepam and midazolam** have active metabolites that are excreted in the urine
100
Opiods- impact from renal disease
Most opioids used in anesthetics practice are inactivated by the liver, some of these metabolites are then excreted in urine (e.g. morphine, meperidine).
Morphine-6-glucuronide accumulation can respiratory depression
Normeperidine accumulation may promote seizure activity
Remifentanil is unaffected by kidney function due to rapid ester hydrolysis in blood
Opioid agonists-antagonists (e.g. butorphanol, nalbuphine, and buprenorphine) are unaffected by kidney disease
101
How are anticholinergics impacted by renal failure?
Atropine and glycopyrrolate is generally safe but there is the potential for accumulation with repeat doses
Scopolamine may have increased CNS effects related to decrease renal function
102
How are volatile agents impacted by renal failure?
VA agents are ideal for patients with kidney disease as they are not dependent on the kidneys for elimination
There is a potential for accelerated induction and emergence in severely anemic patients (hgb <5 g/dL) with chronic kidney disease
Some clinicians may avoid sevoflurane (and avoid < 2L/min gas flow) for lengthy procedures
Also, some clinicians may avoid nitrous oxide (or air) to maintain FiO2 of >50% in severely anemic patients (< 7 g/dL) with ESRD to increase arterial oxygen content
103
How are reversal agents impacted by renal failure?
Most antimuscarinics are renally excreted and thus recurarization due to inadequate DOA is unlikely
The sugammadex-muscle relaxant complex may persist for several days in the protein with kidney disease and is not recommend with low creatine clearance (<30 mL/min) or renal replacement therapy
104
How are muscle relaxants impacted by renal failure?
Succinylcholine can be used in patients with kidney disease in the absence of hyperkalemia.
decreased plasma cholinesterase has been reported after dialysis, although prolonged blockade is rarely seen
Cisatracurium and atracurium are degraded by plasma ester hydrolysis and nonenzymatic Hofmann elimination and are considered NMBA of choice in patients with kidney failure.
Vecuronium elimination is primarily hepatic but ~20% is eliminated in urine, thus blockade may be modestly prolonged with larger doses
Rocuronium primarily undergoes hepatic elimination but may have a prolonged DOA
**A large portion of curare and pancuronium undergo renal elimination.**
105
Drugs with potential for
significant accumulation
with ESRD
106
Acute Kidney Failure
This syndrome is a rapid deterioration in kidney function that results in the retention of nitrogenous waste products (azotemia). These substances, many of which behave as toxins, are byproducts of protein and amino acid metabolism. Impaired kidney metabolic activity may contribute to widespread organ dysfunction
107
Kidney failure can be classified as ______.
prerenal, renal, and postrenal, depending on its cause(s), and the initial therapeutic approach varies accordingly.
Prerenal kidney failure results from an acute decrease in renal perfusion; intrinsic kidney failure is usually due to underlying kidney disease, kidney ischemia, or nephrotoxins; and postrenal failure is the result of urinary collecting system obstruction or disruption.
Both prerenal and postrenal forms of kidney failure are readily reversible in their initial stages, but with time both progress to intrinsic kidney failure.
108
Most adult patients with kidney failure first develop ____.
oliguria.
109
The course of prerenal and postrenal kidney failure is dependent upon _____.
promptness in diagnosis and correction of the causal condition. Diagnostic ultrasound, including point of care ultrasound, is increasingly used to rapidly and noninvasively evaluate possible obstructive uropathy.
110
Management priorities in patient with AKI
* Search for and correct prerenal and postrenal causes
* Review medications and patient administered substances and stop any potential nephrotoxins
* Administer medications in doses appropriate for their clearance
* Optimize cardiac output and renal blood flow
* Monitor fluid intake and output; measure body weight daily
* Search for and treat acute complications (hyperkalemia, hyponatremia, acidosis, hyperphosphatemia, pulmonary edema)
* Search for and aggressively treat infections and sepsis
* Provide early nutritional support
* Provide expert supportive care (management of catheter and skin care; pressure sore and deep venous thromboembolic prophylaxis; psychological support)
111
The most common causes of chronic kidney disease (CKD) are _____.
hypertensive nephrosclerosis, diabetic nephropathy, chronic glomerulonephritis, and polycystic kidney disease.
112
Symptoms of CKD
113
GFR 25 mL/min =
symptoms of chronic kidney disease begin to appear
114
GFR 10 mL/min =
patient is dependent upon RRT (e.g. hemodialysis, hemofiltration, or peritoneal dialysis)
115
Metabolic Consequences of Renal Failure
**Metabolic**
Hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperuricemia, and hypoalbuminemia, typically develop in patients with kidney failure.
* Hyperkalemia is a potentially lethal consequence of kidney failure
* Hypermagnesemia is generally mild unless magnesium intake is increased
* Hypocalcemia is secondary to resistance to parathyroid hormone, decreased intestinal calcium absorption secondary to decreased kidney synthesis of 1,25 dihydroxycholecalciferol, and hyperphosphatemia associated calcium deposition into bone.
Water and sodium retention can result in worsening hyponatremia and extracellular fluid overload, respectively. Failure to excrete nonvolatile acids produces an increased anion gap metabolic acidosis
116
Oxygen-Hemoglobin Dissociation Curve
117
Hematologic Consequences of Renal Failure
**Hematologic
Red Blood Cells**
* Anemia is nearly always present when the creatinine clearance is below 30 mL/min.
* Hemoglobin concentrations are generally 6 to 8 g/dL due to decreased erythropoietin production, red cell production, and red cell survival
* Shifts to the right on oxygen dissociation curve
Increased levels of 2,3 diphosphoglycerate develops in response to the decrease in blood oxygen carrying capacity
* The metabolic acidosis associated with CKD
**Platelets and White Blood Cells**
* Both platelet and white cell function are impaired in patients with kidney failure.
* This is manifested as a prolonged bleeding time and increased susceptibility to infections, respectively
118
Cardiovascular consequences of renal failure
* Cardiac output increases to maintain oxygen delivery due to decreased blood oxygen carrying capacity
* Hypertension due to sodium retention and abnormalities in the renin–angiotensin system
* Left ventricular hypertrophy
* Extracellular fluid overload from sodium retention increases risk for congestive heart failure and pulmonary edema
* Arrhythmias related to metabolic abnormalities and to the deposition of calcium in the conduction system
* Peripheral vascular and coronary artery atherosclerotic disease is common
* Uremic pericarditis may develop
* Hypovolemia may also occur secondary to excessive fluid removal during dialysis
119
Pulm, Endocrine, GI, Neuro consequences of renal failure
**Pulmonary**: Patients with renal disease may be dependent on increased minute ventilation to compensate for metabolic acidosis.
**Endocrine**: Type 2 diabetes is one of the most common causes of chronic kidney disease
Secondary hyperparathyroidism can produce metabolic bone disease and fractures
**Gastrointestinal**: Increased risk for peptic ulcers and GI hemorrhage
Autonomic neuropathy can cause delayed gastric emptying
**Neurologic**: Asterixis, lethargy, confusion, seizures, and coma are manifestations of uremic encephalopathy, and symptoms usually correlate with the degree of azotemia.
Autonomic and peripheral neuropathies are common
120
Pre-Op Considerations for renal failure patient
**Optimal perioperative management is dependent upon RRT**
Assess for signs of fluid overload or post dialysis hypovolemia
It can be helpful to assess current weights, as well as pre and post dialysis weight
Hemodialysis is more effective than peritoneal dialysis; Continuous renal replacement therapy is used for hemodynamically unstable patients
**History and physical**
Thorough pulmonary and cardiac assessment
Electrocardiogram – assess for signs of hyperkalemia or hypocalcemia, ischemia, conduction block, and ventricular hypertrophy
Echocardiography - assess cardiac function, ventricular hypertrophy, wall motion abnormalities, and pericardial fluid.
ABG – help evaluate oxygenation, ventilation, hemoglobin level, and acid-base status
Bleeding time and coagulation studies (especially when considering neuraxial anesthesia)
Serum electrolyte, BUN, and creatinine measurements to assess the adequacy of dialysis
**Premedication**
Careful titration of benzodiazepines
Consider aspiration prophylaxis
Continue hypertensive agents until the time of surgery
121
Intra-Op Monitoring and Induction concerns for patient with renal failure
**Monitoring**
Because of the risk of thrombosis, blood pressure should not be measured by a cuff on an arm with an arteriovenous fistula
**Induction**
Patients with nausea, vomiting, or GI bleeding should undergo RSI and intubation
Induction doses should be decreased for critically ill patients or those hypovolemic s/p dialysis
Propofol, 1 to 2 mg/kg, or etomidate, 0.2 to 0.4 mg/kg, is often used. An opioid, βblocker (esmolol), or lidocaine may be used to blunt the hypertensive response to airway instrumentation and intubation. Succinylcholine, 1.5 mg/kg, can be used to facilitate endotracheal intubation in the absence of hyperkalemia. Rocuronium (1 mg/kg), vecuronium (0.1 mg/kg), cisatracurium (0.15 mg/kg), or propofol–lidocaine induction without a relaxant may be considered for intubation in patients with hyperkalemia.
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Anesthesia Maintenance for pts with renal failure
The ideal anesthetic maintenance technique should control hypertension with minimal deleterious effect on cardiac output
Volatile anesthetics, propofol, fentanyl, sufentanil, alfentanil, and remifentanil are satisfactory maintenance agents. Meperidine should be avoided because of the accumulation of its metabolite normeperidine. Morphine may be used, but prolongation of its effects may occur.
Controlled ventilation should be considered for patients with kidney failure under general anesthesia
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Fluid Replacement for pts with renal failure
Superficial procedures only warrant replacement of insensible fluid losses only
In situations requiring significant fluid volume for maintenance or resuscitation, isotonic crystalloids, colloids, or both may be used.
Balanced crystalloids are preferred to chloride rich crystalloids because of the deleterious effects of hyperchloremia on kidney function
**However, 0.9% saline is preferable to balanced crystalloids in patients with alkalosis and hypochloremia.
Lactated Ringer’s solution should be avoided in hyperkalemic patients when large fluid volumes are required because it contains potassium 4 mEq/L.**
Blood that is lost should be replaced with colloid or packed red blood cells as clinically indicated
An allogeneic blood transfusion may decrease the likelihood of kidney rejection following transplantation because of associated immunosuppression.
Hydroxyethyl starch has been associated with an increased risk of AKI and death when administered to critically ill patients or those with preexisting impaired kidney function or when used for volume resuscitation
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Cystoscopy
Cystoscopy is a very common urological procedure, the indications for which include hematuria, recurrent urinary infections, renal calculi, and urinary obstruction
Bladder biopsies, retrograde pyelograms, transurethral resection of bladder tumors, extraction or laser lithotripsy of kidney stones, and placement or manipulation of ureteral catheters (stents) are also commonly performed through the cystoscope
Anesthetic management often requires regional or general anesthesia
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Lithotomy Position
After supine, lithotomy is the most common position for patient undergoing urologic and gynecologic procedures
Two people should move the leg up and down in lithotomy position
Legs supports should be padded where they touch the patient’s leg
When arms are tucked, confirm fingers do not get caught between the lower section of the table
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Lumbar sacral plexus nerve injuries
that occur with the lithotomy position
Common peroneal nerve (resulting in loss of dorsiflexion) r/t lateral knee rests against the strap support
Saphenous nerve injury r/t numbness along the medial calf.
Obturator and femoral nerve injury r/t excessive flexion of the thigh against the groin
Sciatic nerve injury r/t extreme flexion at the thigh
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Physiologic changes in lithotomy position
Decrease FRC (amplified by steep Trendelenburg)
Increase in preload when legs go up and decrease in preload when legs come down
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Anesthetic technique for cystoscopy
General anesthesia (ETT and LMA) and Regional Anesthesia (Spinal and Epidural) are suitable options
General Anesthesia
Due to the short duration of the procedure, depending on the patient’s characteristics and need for NMBA, an LMA is often utilized
Regional Anesthesia
Again, due to the short duration of the procedure, a spinal is preferred over an epidural
A T10 sensory level is used for cystoscopies
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Transurethral resection of the prostate (TURP)
* Benign prostatic hyperplasia (BPH) frequently leads to bladder outlet obstruction and may require surgical intervention
* Indications for transurethral resection of the prostate (TURP) include bladder outlet obstruction due to BPH, bladder calculi, recurrent episodes of urinary retention, urinary tract infections, and hematuria.
TURP requires regional or general anesthesia.
* Despite advanced age and prevalence of significant comorbidity, perioperative mortality and medical morbidity for this procedure are both less than 1%
* A blood type and screen is adequate although prostatic bleeding can be difficult to control through the cystoscope.
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Surgical complication of TURP
**Most common**
Clot retention
Failure to void
Uncontrolled acute hematuria
Urinary tract infection
Chronic hematuria
**Less common**
TURP syndrome
Bladder perforation
Hypothermia
Sepsis
Disseminated intravascular coagulation
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TURP SYNDROME
TURP is conventionally performed by passing a monopolar electrical loop through a special cystoscope (resectoscope).
With continuous irrigation and direct visualization, prostatic tissue is resected by applying a cutting current to the loop.
The absorption of large amounts of fluid (2 L or more) results in a constellation of symptoms and signs commonly referred to as TURP syndrome
The manifestations are primarily those of circulatory fluid overload, water intoxication, and, occasionally, toxicity from the solute in the irrigating fluid
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Manifestations of TURP syndrome
Hyponatremia (symptoms develop at < 120 mEq/L)
Hypoosmolality
Fluid overload
Congestive heart failure
Pulmonary edema
Hypotension
Hemolysis
Solute toxicity
Hyperglycinemia (glycine) – r/t circulatory depression and CNS toxicity
Hyperammonemia (glycine) – r/t CNS toxicity
Hyperglycemia (sorbitol)
Intravascular volume expansion (mannitol)
*glycine may be related to transient blindness
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Treatment of TURP Syndrome
The absorbed water must be eliminated, and hypoxemia and hypoperfusion must be treated
Patients can be managed with fluid restriction and intravenous furosemide
Symptomatic hyponatremia resulting in seizures or coma should be treated with hypertonic saline (3%-5%)
Seizure activity can be terminated with small doses of midazolam (2–4 mg)
Endotracheal intubation may be considered to prevent aspiration until the patient’s mental status normalizes.
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New advances in the prevention of TURP Syndrome
Recently, additional procedural methods for the treatment of BPH have included bipolar TURP, laser and radiofrequency ablation, photodynamic and thermal therapy, and cryotherapy, and these evolutionary changes in TURP technique have markedly reduced the incidence and severity of TURP syndrome
Low voltage bipolar TURP allows the use of isotonic saline irrigation fluid, thus avoiding TURP syndrome
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What causes hypothermia with a TURP?
Large volumes of irrigating fluids at room temperature can be a major source of heat loss in patients.
Irrigating solutions should be warmed to body temperature prior to use to prevent hypothermia
Postoperative shivering associated with hypothermia may dislodge clots and promote postoperative bleeding
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How does a bladder perforation occur with a TURP?
Related to the resectoscope going through the bladder wall or from overdistention of the bladder with irrigation fluid
Signs and symptoms
Surgical colleagues may report poor retention of irrigating solution
Awake patients will typically report nausea, diaphoresis, and retropubic or lower abdominal pain
In an anesthetized patient, larger perforations may present with hypotension or hypertension, and vagal mediated bradycardia
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How does coagulopathy occur with a TURP?
Coagulopathy may be suspected from diffuse, uncontrollable bleeding but must be defined with laboratory tests
DIC may result from the intraoperative release of thromboplastins from prostate tissue
DIC Treatment may include heparin, clotting factors, platelets, and hematology consult
Primary fibrinolysis should be treated with Amicar or tranexamic acid
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How does septicemia occur with a TURP?
The prostate is often colonized with bacteria, which can enter the blood stream via opened venous sinuses
Prophylactic antibiotic therapy (most commonly gentamicin, levofloxacin, or cefazolin) is usually administered prior to TURP.
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Blood loss with a TURP
averages approximately 3 to 5 mL/min of resection (usually 200–300 mL total) and is rarely life threatening.
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Lithotripsy
The treatment of kidney stones has evolved from primarily open surgical procedures to less invasive or entirely noninvasive techniques
Cystoscopic procedures, including flexible ureteroscopy with stone extraction, stent placement, and intracorporeal lithotripsy (laser or electrohydraulic), along with medical expulsive therapy (MET), have become first line therapy
Extracorporeal shock wave lithotripsy (ESWL) is used primarily for 4 mm to 2 cm intrarenal stones, and percutaneous and laparoscopic nephrolithotomy is used for larger or impacted stones
During ESWL, ureteral stents are often placed, and repetitive high energy shocks (sound waves) are generated and focused on the stone, causing it to fragment
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Pre-Op Considerations for an ESWL
Patients with a history of cardiac arrhythmias and those with a pacemaker or implantable cardioverter defibrillator (ICD) may be at greater risk for arrhythmias during ESWL
The shock waves are usually timed to occur 20 ms after the R wave to correspond with the ventricular refractory period
Shock waves can damage the internal components of implanted cardiac devices
The manufacturer should be contacted as to the best method for managing the device (eg, reprogramming or applying a magnet)
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Effects of immersion with ESWL
With older electrohydraulic units, the patient is placed in a heated water bath, which conducts the shock waves to the patient. Modern lithotripters generate shock waves either electromagnetically or from piezoelectric crystals
Regarding the latter, immersion into a heated water bath (36–37°C) initially results in vasodilation that can transiently lead to hypotension
Arterial blood pressure, however, subsequently rises as venous blood is redistributed centrally due to the hydrostatic pressure of water on the legs and abdomen
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Anesthesia for a Lithotripsy
Pain during lithotripsy is from the dissipation of a small amount of energy as shock waves enter the body through the skin
The pain is localized to the skin and is proportionate to the shock wave intensity
Older immersion baths us high energy shock waves
Newer lithotripsy units use low energy shock waves
**Regional Anesthesia**
Continuous epidural anesthesia is commonly used during ESWL with older water bath lithotripters
When using the loss of resistance technique for placement of the epidural catheter, saline should be used instead of air during epidural catheter insertion as air in the epidural space can dissipate shock waves and may promote injury to neural tissue
Spinal anesthesia can also be used but offers less control over the sensory level and an uncertain duration of surgery
Disadvantages of regional anesthesia or sedation include the inability to control diaphragmatic movement (excessive diaphragmatic excursion can move the stone out of the wave focus and may prolong the procedure) and bradycardia (this will prolong the procedure when shock waves are coupled to the ECG).
Glycopyrrolate may be administered to accelerate the ESWL procedure
**General Anesthesia**
GETA allows control of diaphragmatic excursion during lithotripsy using older water bath lithotriptors
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Surgery for Urologic Malignancies
Improved survival rates for patients with urological cancer following radical surgical resections have resulted in an increase in the number of procedures performed for prostatic, bladder, testicular, and kidney cancer
The desire for accelerated, less complicated recovery with smaller, less painful incisions has prompted the development of laparoscopic pelvic and abdominal operations, including radical prostatectomy, cystectomy, pelvic lymph node dissection, nephrectomy, and adrenalectomy.
Robot assisted technology is increasingly being applied to these procedures
**Positioning**
Many urological procedures are carried out with the patient in a hyperextended supine position to facilitate exposure of the pelvis during pelvic lymph node dissection, retropubic prostatectomy, or cystectomy
The operating room table is also tilted head down to make the operative field horizontal
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Prostate CA
Adenocarcinoma of the prostate is the most common nonskin cancer in men and is second only to lung cancer as the most common cause of cancer deaths in men older than 55 years.
Approximately one in six men will be diagnosed with prostate cancer in their lifetime.
Patients with prostate cancer may present to the operating room for 1) open radical retropubic prostatectomy with lymph node dissection, and 2) robot assisted laparoscopic radical prostatectomy with pelvic lymph node dissection
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Radical Retropubic Prostatectomy
Open radical retropubic prostatectomy is usually performed through a lower midline abdominal incision.
The prostate is removed with the seminal vesicles, ejaculatory ducts, and part of the bladder neck.
Following prostatectomy, the remaining bladder neck is anastomosed directly to the urethra over an indwelling urinary catheter
Anesthetic considerations include risk for blood loss (depending on the prostate size, duration of procedure, and surgeon), +/- arterial line, +/- central line, enhanced recovery approach (consider using ketorolac and acetaminophen); in the setting of a continuous epidural anesthetic, a T6 level is needed; administration over indigo carmen (may cause hypo or hypertension)
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Robot Assisted Laparoscopic Radical Prostatectomy
Most radical prostatectomies are performed laparoscopically, and nearly all laparoscopic prostatectomies in the United States are performed with robot assistance
Compared to an open technique, robot assisted laparoscopic radical prostatectomies are a longer procedure but with less blood loss and fewer blood transfusions, lower postoperative pain scores and lower opioid requirements, less postoperative nausea and vomiting, and shorter hospital length of stay
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Anesthesia for Robot Assisted Laparoscopic Radical Prostatectomy
Steep Trendelenburg may contribute to head and neck edema and increase intraocular pressure
Complications include airway edema, post extubation respiratory distress, postoperative visual loss involving ischemic optic neuropathy or retinal detachment, and brachial plexus injury
Enhanced recovery approach may be considered (+/- ketorolac and/or acetaminophen)
Continuous epidural anesthesia is less common d/t low post-op pain scores and discharge within 24 hours
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Bladder Cancer
Bladder cancer occurs at an average patient age of 65 years with a 3:1 male to female ratio.
Transitional cell carcinoma of the bladder is second to prostate adenocarcinoma as the most common malignancy of the male genitourinary tract.
The association of cigarette smoking with bladder carcinoma results in coexistent coronary artery and chronic obstructive pulmonary disease in many of these patients.
There may be underlying kidney disease related to age or urinary tract obstruction.
Staging includes cystoscopy and imaging. Intravesical chemotherapy is used for superficial tumors, and transurethral resection of bladder tumors (TURBT) is carried out via cystoscopy for low grade, noninvasive bladder tumors. Some patients may receive preoperative radiation to shrink the tumor before radical cystectomy.
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Transurethral bladder resection (TURBT)
Laterally located tumors may be proximal to the obturator nerve
In the setting of a spinal anesthetic or general anesthesia without NMBA, use of the cautery resectoscope may result in stimulation of the obturator nerve and adduction of the legs
Thus, most TURBT procedure are done with GETA and NMBA
TURBT is rarely associated with the absorption of significant amounts of irrigating solution
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Radical Cystectomy
All anterior pelvic organs are removed
Women: bladder, uterus, cervix, ovaries, and part of the anterior vaginal vault
Men: bladder, prostate, and seminal vesicles
Radical cystectomy is associated with the greatest risk of perioperative morbidity and mortality of all major urological procedures
improvements in neoadjuvant chemotherapy and enhanced recovery after surgery programs have resulted in progressively lower rates of perioperative morbidity and mortality as well as higher rates of 1and 5 year survival
When compared with open radical cystectomy, robot assisted radical cystectomy is associated with reduced perioperative complications, less blood loss and transfusion, and shorter hospital length of stay
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Anesthetic Considerations for a Radical Cystectomy
GETA with NMBA, +/- continuous epidural or transversus abdominus plane block
Risk for blood loss (blood transfusions common)
+/- controlled hypotension, although this may increase risk for AKI
Monitoring: 2 large bore IVs, +/- arterial line, urinary output (although urinary tract is disrupted early on in procedure)
Urinary diversion (ie, implanting the ureters into a segment of bowel) is usually performed immediately following radical cystectomy
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Testicular cancer and treatment
The initial treatment for all tumors is radical (inguinal) orchiectomy, and subsequent management (e.g. surveillance, radiotherapy, chemotherapy) depends on tumor histology
When chemotherapeutic agents are used, specific organ toxicity may be encountered, such as impaired kidney function following cisplatin, neuropathy following vincristine, and pulmonary fibrosis following bleomycin
Patients with history of bleomycin use are at increased risk for oxygen toxicity and fluid overlaod
Use low inspired oxygen (while maintaining spO2 > 90%) and PEEP between 5-10 mmHg
**Radical Orchiectomy**
Performed with regional or general anesthesia
Anesthetic management may be complicated by reflex bradycardia from traction on the spermatic cord
**Retroperitoneal Lymph Node Dissection**
Retraction of the inferior vena cava during surgery often results in transient arterial hypotension
Postoperative pain associated with open RPLND incisions is severe, and continuous epidural analgesia, intrathecal morphine or hydromorphone, or TAP block should be considered
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Renal Cancer
Tumors confined to the kidney may be treated by open or laparoscopic partial or total nephrectomy or by percutaneous cryoablation or radiofrequency ablation
The tumor may extend into the renal vein, inferior vena cava, and right atrium
Staging includes CT or MRI scans and an arteriogram
Preoperative arterial embolization may shrink the tumor mass and reduce operative blood loss
Preoperative evaluation of the patient with renal carcinoma should focus on tumor staging, kidney function, the presence of coexisting systemic diseases, and anesthetic management needs dictated by the scope of anticipated surgical resection.
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Percutaneous Cryoablation or Radiofrequency Ablation
Small kidney tumors without metastasis are commonly ablated by interventional radiologists using percutaneous cryoprobes or radiofrequency probes with ultrasonography or CT guidance
Often performed with GETA and NMBA on an outpatient basis (~ 3-hour procedure)
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Radical Nephrectomy
Hand assisted laparoscopic technique is often utilized for partial or total nephrectomy associated with a smaller tumor mass.
The kidney, adrenal gland, and perinephric fat are removed
Often performed with GETA +/- continuous epidural
Risk for significant blood loss, two large bore IVs, +/- arterial line, consider TEE probe with vena cava involvement
Subcostal, flank, or midline incisions for open nephrectomy are extremely painful, and epidural analgesia is very useful
Postpone bolusing epidural risk of significant operative blood loss has passed
157
Radical Nephrectomy with Excision of Tumor Thrombus
A thoracoabdominal approach allows the use of cardiopulmonary bypass when necessary
Cardiopulmonary bypass may be used when the tumor cannot be pulled back from the right atrium into the cava and is often kept on immediate standby for cases involving extensive tumor thrombus
Central venous catheterization should be performed cautiously to prevent dislodgement and embolization of tumor thrombus extending into the right atrium
Heparinization and hypothermia will exacerbate the already significant risk for blood loss
Tumor embolization may be heralded by sudden supraventricular arrhythmias, arterial desaturation, and profound systemic hypotension. TEE is critical in this situation
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Kidney Transplant
Transplantation is carried out by placing the donor kidney retroperitoneally in the iliac fossa and anastomosing the renal vessels to the iliac vessels and the ureter to the bladder
**Pharmacology**
* Heparin is administered prior to clamping of iliac vessels
* Mannitol is administered to promote osmotic diuresis following renal reperfusion
* Immunosuppression agents are administered perioperatively (eg corticosteroids, cyclosporine, antithymocyte globulin)
* Cisatricurium is the muscle relaxant of choice
**Hyperkalemia** has been reported after release of the vascular clamp, potentially related to the potassium rich preservative solution
Donor kidney washout of the preservative solution with ice cold lactated Ringer’s solution just prior to the vascular anastomosis may help
Serum electrolyte concentrations (particularly potassium) should be monitored closely after completion of the anastomosis
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Make a card for blood flow through the kidney (per Josh)
Blood enters the kidney through the renal artery - afferent arteriole - glomerulus - efferent arteriole - peritubular capillaries - renal vein - exits the kidney.
