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Urology Renal Function

Jerome OHara, M.D.

Cleveland, Ohio

Objectives:
1)
2)
3)

Experience an overview of renal anatomy and physiology

Understand the effects of mannitol on renal function
Differentiate among new surgical TURP techniques and how they impact anesthetic
management and patient outcomes
Renal Anatomy and Physiology

Renal Anatomy
The kidneys and ureters are located in the retroperitoneal space at the level of the L2 vertebral body. Renal
anatomy is divided into the renal cortex, medulla, and renal pelvis, which drain urine into the ureter. Renal pain
sensation is conducted to spinal cord segments T10L1 by sympathetic fibers. Sympathetic innervation is
provided by preganglionic fibers from T8L1 while the vagus nerve provides parasympathetic innervation to
the kidney.
The nephron, the microscopic functional unit of the kidney, serves secretory and regulatory functions.
Each nephron consists of:
Glomerulus a capillary network responsible for filtration of the blood. Its blood supply comes from
the afferent arteriole and is drained into the efferent arteriole. Changes in the tone of these vessels
determine the glomerular filtration rate (GFR) and formation of the ultrafiltrate. In order for a molecule
to cross from plasma to the tubular fluid it must pass in succession through the fenestrated capillary
endothelium, the glomerular basement membrane, and the epithelial slit diaphragm. The process is
dependent on molecular size and charge.
Bowmans capsule - the initial segment of the renal tubular system that envelops the glomerulus
and receives ultrafiltrate.
Proximal convoluted tubule (PCT) a tubule in which the majority of the ultrafiltrate and
solutes are reabsorbed back into the circulation. The transport of almost all substances (glucose, amino
acids, phosphate, lactate, etc) is coupled with a sodium transporter system. The most important proteinbased active transport system is the sodium-potassium-adenosine triphosphatase (Na-K-ATPase)
system. In the PCT about 65% of filtered sodium is actively reabsorbed followed by passive absorption
of water.
Loop of Henle - divided into thin and thick portions. The thick portion is relatively impermeable to
water and contains very active metabolic cells (mTAL) which are prone to ischemic injury during
periods of renal hypoperfusion.
Distal convoluted tubule (DCT) and collecting duct ADH and aldosterone regulate the
reabsorption of water and ion exchange in this portion of the nephron.

Juxtaglomerular apparatus plays an important role in autoregulation of renal blood flow (RBF)
and GFR. Renin is released from the macula densa when chloride ion delivery to the juxtaglomerular
apparatus decreases. Renin activates formation of angiotensin and angiotensin II, which in turn
increase RBF and GFR (by changing the tone of afferent and efferent arterioles) and release of
aldosterone.
Vasa recta originate from the efferent arteriole of juxtamedullary nephrons and descend deep into
the medulla to parallel the loops of Henle. They then return in a cortical direction with the loops to join
other peritubular capillaries, which empty into cortical veins. They play the key role in the counter
current exchange system.

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There are two types of nephrons:

Cortical, constituting the majority of the nephrons, are located entirely in the renal cortex, and have an
abundant blood supply.
Juxtamedullary: Their glomerulus and PCT are located in the renal cortex; the loop of Henle descends deep
into the renal medulla. These nephrons are responsible for maintenance of high osmolarity (countercurrent
exchange) of the renal medulla and play a key role in the kidneys ability to concentrate the urine. Their blood
supply is very precarious, receiving only 5% of total RBF and extracting 80% of oxygen compared to 20% in
the cortex. Metabolically very active mTAL cells are prone to ischemic injury during renal hypoperfusion due
to the ratio of high oxygen consumption to supply.
Renal Physiology
The kidneys play a crucial role in the maintenance of extracellular volume and composition constant as well as
in the excretion of waste substances. Large amounts of fluid and solutes are filtered from the blood, waste
products are excreted in the form of urine, and necessary components are reabsorbed into the circulation.
Kidneys receive about 20% of systemic cardiac output, resulting in 180 liters/day of glomerular ultrafiltrate.
More than 99% of ultrafiltrate is reabsorbed into systemic circulation; the result is 1 to 2 liters of urine
production daily.
Filtration
GFR is a measure of glomerular function expressed as milliliters of filtrate/minute. GFR can be thought of as
the product of the tendency of the glomerular membrane to facilitate filtration (i.e. glomerular permeability and
surface area) and the pressure inside the glomerular capillary, which forces fluid through the filter.
GFR depends on the following factors:
The ultrafiltration constant (Kf) is directly related to glomerular capillary permeability and glomerular
surface area; it is relatively constant.
Glomerular filtration pressure depends on capillary pressure (PGC) and glomerular oncotic pressure
(GC). PGC is directly related to renal artery pressure, but is heavily influenced by arteriolar tone at
points upstream (afferent) and downstream (efferent) from the glomerulus. An increase in afferent
arteriolar tone causes filtration pressure and GFR to fall. Increase in efferent arteriolar tone tends to
increase filtration pressure and GFR. The GC is directly dependent on plasma oncotic pressure.
Autoregulation of Renal Blood Flow and Glomerular Filtration Rate
To preserve GFR, in healthy subjects a relatively constant RBF over the wide range of systemic blood pressure of
MAP 50 to 150 mmHg is maintained. However, in patients with hypertension the range of MAP when RBF is
constant shifts to the higher MAP range. Renal autoregulation is accomplished by local feedback signals that
modulate glomerular arteriolar tone.
Autoregulation is believed to occur by means of two mechanisms:
Myogenic mechanism: An increase in arterial pressure causes the afferent arteriolar wall to stretch
and then through reflex to constrict, whereas a decrease in arterial pressure causes arteriolar dilatation.
Tubuloglomerular feedback: It is achieved by the juxtaglomerular apparatus. If RBF falls, a
concomitant decrease in GFR results and signals the afferent arteriole to dilate. Glomerular flow and
pressure will then increase in an attempt to restore GFR to previous levels. A decrease in GFR triggers
release of renin, which results in formation of angiotensin II. In response to angiotensin II efferent
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arteriolar constriction occurs to increase glomerular pressure, which in turn increases GFR.
Simultaneous afferent arteriolar dilatation and efferent arteriolar constriction allow glomerular flow
and filtration to increase.
Reabsorption of Sodium and Water
The active, energy-dependent reabsorption of sodium begins almost immediately as ultrafiltrate enters the PCT.
Here ~65% of sodium is reabsorbed. Cells of the mTAL are metabolically active in their role of reabsorbing sodium
and chloride. Sodium pumps in the DCT and collecting duct are unique in that they are under the control of
aldosterone.
Reabsorption of water is a passive, osmotically driven process tied to sodium and other solute reabsorption
occuring mainly in the PCT. Approximately 20% of the ultrafiltrate flows into the DCT and collecting duct. Here
water reabsorption is controlled by the antidiuretic hormone (ADH) which is secreted by the pituitary gland.
Production of concentrated urine depends on the degree of water permeability of the DCT and collecting duct in
response to physiologic needs. ADH causes renal cortical vasoconstriction when released in large amounts, such as
during the physiologic stress response to trauma, surgery, or other critical illness. This induces a shift of RBF to the
hypoxia-prone renal medulla.
Renin-Angiotensin-Aldosterone System
Renin-angiotensin activity plays an important role in regulating RBF and GFR. Renin that is released by the macula
densa may be triggered by hypotension, decreased tubular fluid chloride ion concentration, or sympathetic
stimulation. It enhances angiotensin II production, which induces renal efferent arteriolar vasoconstriction and
afferent arteriole vasodilatation. Angiotensin II also promotes ADH release from the posterior pituitary, sodium
reabsorption, and aldosterone release by the adrenal medulla. Aldosterone, in turn, stimulates the DCT and
collecting duct to actively reabsorb sodium (and water) which results in intravascular volume expansion.
Sympathetic nervous system stimulation may also directly cause release of aldosterone. During stress the above
mechanisms are activated, leading to renal cortical vasoconstriction, a shift in RBF to salt-and-waterconserving
juxtamedullary nephrons, a decrease in GFR, and salt and water retention.
The sympathetic nervous system responds to stress by releasing epinephrine and norepinephrine, both of
which have profound effects on renal physiology. The action of norepinephrine is similar to that of angiotensin II: It
shifts the blood flow from the cortex to the renal medulla; and increases reabsorption of sodium and water, resulting
in decreased urine output. It also activates the renin-angiotensin-aldosterone axis as well as the release of ADH
from the pituitary gland. Moderate stimulation of the sympathetic system does not decrease GFR; however, a more
intense stress response may induce a decrease in RBF and GFR by causing afferent arteriolar constriction. If this
extreme condition is not reversed, ischemic damage to the kidney may result, and acute renal failure (ARF) may
manifest clinically. Activation of the renin-angiotensin-aldosterone axis is very important for the preservation of
intravascular volume, and it provides vital organ perfusion during stress.
The posterior pituitary releases ADH in response to an increase in either extracellular sodium concentration
or extracellular osmolality. The arterial baroreceptors are activated when hypovolemia leads to a decrease in blood
pressure, whereas atrial receptors are stimulated by a decline in atrial filling pressure. Both of these circulatory
reflex systems stimulate release of ADH from the pituitary and cause retention of water by the kidney in an effort to
return the intravascular volume toward normal.
The description above is derived from several sections (here quoted verbatim) of the chapter, The renal system
and anesthesia for urologic surgery, by OHara JF Jr., Cywinski JB, and Monk TG, in: Barash PG, ed. Clinical
Anesthesia. Philadelphia: Lippincott Williams & Wilkins, 2005. (Used by permission, pending)

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Mannitol and Renal Function

The renal effect of mannitol has been attributed to its osmotic action, expansion of extracellular fluid volume,
increased medullary blood flow, and a greater "washout" of solutes and hence diuresis.
Stahl WM. Effect of mannitol on the kidney: changes in intrarenal hemodynamics. N Engl J Med
1965; 272:381-6.
Mannitol as a renal preservation therapy for prophylaxis or treatment of ARF remains controversial. In a recent
study, Redfors and colleagues summarized the effect and current clinical status of the use of mannitol in renal
therapy. It is presented in part below:
Mannitol is a diuretic agent which has been used in the perioperative setting in the belief that it exerts
renoprotective properties. It is freely filterable in the glomeruli and due to its limited reabsorption it creates an
osmotic force in the tubuli, sufficient to inhibit the reabsorption of fluids and solutes along the nephron. It has been
shown in renal transplant patients, that mannitol given to a hydrated recipient just before renal artery cross-clamp
removal, reduces the incidence of ARF after cadaveric kidney transplantation. However, several small
randomised controlled trials have found no reduction in the incidence of ARF with mannitol over hydration in a
variety of conditions including cardiac surgery, traumatic rhabdomyolysis and vascular and biliary tract surgery. On
the contrary, it has been suggested that high doses of mannitol may even cause ARF.
Most animal studies have shown that mannitol increases RBF by renal vasodilation both during normotensive and
hypotensive conditions. It has been suggested that the mannitol-induced renal vasodilatory response to experimental
renal ischaemia is mediated directly by increased synthesis of prostacyclin, or indirectly by augmenting plasma
levels of ANP due to plasma volume expansion.
Reports on the effects of mannitol on GFR are conflicting. Animal data have shown that mannitol decreases,
increases or has no effect on GFR. In normal volunteers, mannitol does not seem to affect GFR. However,
experimental data have shown that in hypoperfused kidneys, mannitol infusion tends to restore
GFR towards normal levels both when given prior to and after the hypotension has been induced. [Flores and
colleagues, in J Clin Invest 1972; 51:118-126] suggested that mannitol maintains GFR in renal ischaemia primarily
by an osmotic effect to reduce vascular endothelial cell swelling. Another mechanism could be that mannitol
prevents/decreases ischaemia-induced swelling of tubular cells which might obstruct tubular lumen. Mannitol might,
in this situation, open up collapsed tubular segments which will increase tubular flow and restore GFR.
Redfors B, Swrd K, Sellgren J, Ricksten SE. Effects of mannitol alone and mannitol plus
furosemide on renal oxygen consumption, blood flow and glomerular filtration after cardiac
surgery. Intensive Care Med 2009; 35:115-22.
As previously mentioned, mannitol has the potential to precipitate renal dysfunction. Dickenmann and colleagues
reviewed the topic of osmotic nephrosis. The findings are presented in part below.
Osmotic nephrosis describes a morphological pattern with vacuolization and swelling of the renal proximal tubular
cells. The term refers to a nonspecific histopathologic finding rather than defining a specific entity. Osmotic
nephrosis can be induced by many different compounds, such as sucrose, hydroxyethyl starch, dextrans, and contrast
media.
In the 1960s, studies in rats, rabbits, and dogs showed osmotic nephrosis of the proximal tubules after treatment
with mannitol. The degree of vacuolization was related to the amount of infused mannitol. Furosemide had a
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synergistic role in the development of osmotic nephrosis when both agents were used together. Simultaneous
cyclosporine and mannitol infusions in rats led to massive vacuolization of proximal tubular epithelia, but when
each substance was infused alone in the same dose, it did not induce histological changes. This finding, later also
observed in humans, emphasizes the importance of concomitant nephrotoxic factors in the development of osmotic
nephrosis. The infusion rate of mannitol, total applied dose, and resulting osmolal gap (difference between measured
plasma osmolality and calculated plasma osmolality) have an important role in the pathogenesis of osmotic
nephrosis. Such conditions as advanced age and preexisting kidney failure, in which the maximal rate of renal
excretion is decreased, are predisposing factors. Based on reviewed studies the following conclusions concerning
the risk of mannitol-induced osmotic nephrosis were drawn: (1) acute kidney injury in patients with normal baseline
kidney function usually develops when the total mannitol dose exceeds 1,100 g; (2) in patients with preexisting
kidney disease, much smaller doses (~300 g) can precipitate kidney failure; (3) daily mannitol doses greater than
200 g resulting in an osmolal gap greater than 60 mOsm/kg are likely to cause acute kidney injury; and (4)
preexisting impaired kidney function, comedication with furosemide, and kidney transplantation (including therapy
with cyclosporine) are independent risk factors. Treatment with hemodialysis in patients with established
mannitol-induced osmotic nephrosis leads to accelerated removal of mannitol from the extracellular space and may
shorten the recovery time from acute kidney injury.

Dickenmann M, Oettl T, Mihatsch MJ. Osmotic nephrosis: acute kidney injury with accumulation of
proximal tubular lysosomes due to administration of exogenous solutes . Am J Kidney Dis 2008; 51:491503. Review.
PMID: 18295066 [PubMed indexed for MEDLINE]

A recent acute kidney injury review evaluating clinical evidence of renal preservation therapies found that mannitol
was unlikely to be beneficial.
Kellum JA, Unruh ML, Murugan R. Acute kidney injury. Clin Evid (online) March 28, 2011.
PMID: 21443811 [PubMed in process], as of May 27, 2011.
The following is a 2011 description of mannitol indications and description of renal effects. Source:
www.rxlist.com/mannitol_iv-drug.htm Copyright 2011 by RxList Inc. Accessed May 27, 2011
Mannitol
(mannitol) Injection, Solution
DRUG DESCRIPTION
Mannitol I.V. (Mannitol Injection, USP) is a sterile, nonpyrogenic solution of mannitol in water for injection
available in concentrations of 5%, 10%, 15%, 20% for administration by intravenous infusion only.

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Mannitol IV Indications & Dosage

INDICATIONS
Mannitol I.V. (Mannitol Injection, USP) is indicated for the following purposes in adults and pediatric
patients.
Therapeutic Use
1. Promotion of diuresis in the prevention or treatment of the oliguric phase of acute renal failure before
irreversible renal failure becomes established
2. Reduction of intracranial pressure and brain mass.
3. Reduction of high intraocular pressure when the pressure cannot be lowered by other means.
4. Promotion of urinary excretion of toxic materials.
Diagnostic Use
Measurement of glomerular filtration rate.
DOSAGE AND ADMINISTRATION
The usual adult dosage ranges from 50 to 200 g in a 24-hour period, but in most instances an adequate
response will be achieved at a dosage of approximately 100 g/24 hours. The rate of administration is
usually adjusted to maintain a urine flow of at least 30 to 50 mL/hr. The total dose should be adjusted
according to the clinical response and adverse events.
Prevention of Acute Renal Failure (Oliguria): When used during cardiovascular or other types of
surgery, 50 to 100 g of mannitol may be given.
Treatment of Oliguria: The usual dose to promote diuresis in oliguric patients: Adults, 300 to 400
mg/kg of body weight (21 to 28 g for a 70 kg patient) or up to 100 g of solution, given as a single dose
(often in conjunction with furosemide); pediatric patients, 0.25 to 2 g/kg body weight over a period of 2 to
6 hours. Doses should not be repeated in patients with persistent oliguria.
Measurement of Glomerular Filtration Rate (GFR): 100 mL of a 20% solution (20 g) should be
diluted with 180 mL of sodium chloride injection (normal saline) or 200 mL of a 10% solution (20 g) should
be diluted with 80 mL of sodium chloride injection (normal saline). The resulting 280 mL of 7.2% solution
is infused at a rate of 20 mL per minute. The urine is collected by catheter for a specific period of time and
analyzed for mannitol excreted in mg per minute. A blood sample is drawn at the start and at the end of
the time period and the concentration of mannitol determined in mg/mL of plasma. GFR is the number of
mL of plasma that must have been filtered to account for the amount excreted per minute in the urine.
Normal clearance rates are approximately 125 mL/minute for men; 116 mL/minute for women.

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Mannitol IV W arnings
WARNINGS INCLUDE
1. The obligatory diuretic response following rapid infusion of 25% mannitol may further aggravate
pre-existing hemoconcentration. Excessive loss of water and electrolytes may lead to serious
imbalances. Serum sodium and potassium should be carefully monitored during mannitol
administration.
2. If urine output continues to decline during mannitol infusion, the patient's clinical status should be
closely reviewed and mannitol infusion suspended if necessary. Accumulation of mannitol may
result in overexpansion of the extracellular fluid which may intensify existing or latent congestive
heart failure.
3. Excessive loss of water and electrolytes may lead to serious imbalances. With continued
administration of mannitol, loss of water in excess of electrolytes can cause hypernatremia.
Electrolyte measurements, including sodium and potassium are therefore of vital importance in
monitoring the infusion of mannitol.
4. Osmotic nephrosis, a reversible vacuolization of the tubules of no known clinical significance, may
proceed to severe irreversible nephrosis, so that the renal function must be closely monitored
during mannitol infusion.

Mannitol IV Clinical Pharmacology

CLINICAL PHARMACOLOGY
When administered intravenously mannitol is confined to the extracellular space, only slightly metabolized
and rapidly excreted by the kidney. Approximately 80% of a 100 g dose appears in the urine in 3 hours.
The drug is freely filtered by the glomeruli with less than 10% tubular reabsorption; it is not secreted by
tubular cells. Mannitol induces diuresis by elevating the osmolarity of the glomerular filtrate and thereby
hindering tubular reabsorption of water. Excretion of sodium and chloride is also enhanced.
New Surgical TURP Techniques
Introduction
In males presenting with symptomatic benign prostatic hypertrophy (BPH) the surgeons goal is to resect as much
prostatic tissue as possible while preserving the prostatic capsule. Complications occur when surgical resection of
the rich plexus of prostatic veins is opened. This creates a conduit for bleeding and for absorption of bladder
irrigating fluid when under pressure.As a result, bipolar electrode resection and prostate lasers are replacing
monopolar TURP as alternative surgical techniques for BPH resection.
Monopolar TURP
The conventional gold standard for TURP was the monopolar electrode resectoscope. With the monopolar
electrode, layers of prostatic tissue are resected with a cutting current transmitted through a single-limb electrode
which exits the patient by way of a grounding pad. A non-electrolyte bladder-irrigating solution is required to avoid
dispersion of the electrical current as well as tissue damage at the site of prostatic resection. TURP syndrome is a
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potentially serious complication which can occur when a nonelectrolyte, hypoosmolar bladder-irrigating solution is
used. The severity of the complication depends on the amount of the intravascular bladder-irrigating solution that is
absorbed via prostatic veins opened during resection.
TURP Complications
Complications caused by TURP include dilutional hyponatremia, glycine toxicity, ammonia toxicity,
bacteremia, anemia, hypothermia, bladder perforation, bleeding, and coagulopathy. Factors related to the volume of
irrigating fluid absorption include the duration of resection and the height of the irrigating solution bag above the
patient. The ideal irrigation fluid for monopolar TURP would be isotonic, nonhemolytic, nontoxic, nonelectrolytic,
nonmetabolized, visually non-distorting, rapidly excreted, and inexpensive. However, since there is no ideal
bladder-irrigating fluid for monopolar TURP surgery, 1.5% glycine is used instead, as the standard solution. A
review of the pathophysiology and management of TURP syndrome in monopolar TURP reported that TURP
syndrome may present clinically as early as 15 minutes after resection begins or up to 24 hours postoperatively, with
intravascular rates reaching 200 ml/min of the bladder-irrigating flud [1].
Bipolar TURP
Bipolar TURP electrode technology incorporates a continuous loop electrode to resect prostatic tissue of
BPH. This surgical tool is designed to contain the inflow and outflow of current via the resectoscope for prostatic
tissue resection. By being completely self-contained within the bipolar unit, the current is prevented from passing
through the patient. The advantage of this system is that for the bladder-irrigating solution, an electrolyte-containing
solution such as normal saline can be used. Although intravascular absorption of normal saline can occur via
resected prostatic veins opened during prostatic resection, hypoosmolality and hyponatremia associated with TURP
syndrome are prevented. Nevertheless, the risk of volume overload as a consequence of the bladder-irrigating
solution can still occur with the bipolar TURP technique.
In a review of 16 studies conducted over a 10-year period, Issa compared the safety properties of
monopolar and bipolar TURP [2]. He found a statistically significant decrease in overall complication rate,
transfusion rate, and TURP syndrome with bipolar TURP. A randomized outcome study by Chen and colleagues, in
which monopolar and bipolar TURP were compared, found that bipolar TURP was associated with significantly less
fluid absorption, less change in serum sodium and in hemoglobin, and comparable urologic efficacy in prostate
symptom scores and maximum urinary flows [3]. Two meta-analytic studies comparing monopolar and bipolar
TURP also reported favorable outcomes in the bipolar TURP groups [4,5].
Laser TURP
Laser TURP techniques produce a thin coagulation treatment zone (17 mm) during prostatic tissue
resection [6].This prevents excessive bleeding and intravascular absorption of bladder-irrigating fluid. In contrast to
monopolar and bipolar TURP techniques, which open prostatic veins, the thin coagulation treatment zone seals
them. As a result, bleeding and absorption of bladder irrigating fluid are minimized. Laser TURP is accordingly
advocated for use in anti-coagulated patients. Laser TURP can, however, require several hours, depending on the
size of the prostatic gland that is to be resected. Initially, sterile water was used as the bladder-irrigating fluid with
laser TURP, without significant hyponatremia occurring [7].Glycine as the bladder irrigating fluid is also acceptable.
Significant absorption of the bladder-irrigating fluid during laser TURP does not normally occur. At present, normal
saline is generally recommended as the bladder irrigating solution during laser TURP. Of interest is our clinical
experience, which suggests that deactivation of an automatic implantable cardioversion device is not routinely
needed during laser TURP.
In their review of the anesthetic implications of newer laser TURP techniques, Hanson and colleagues [8]
found that there was minimal absorption of bladder-irrigating fluid; that the techniques could be performed on anticoagulated patients; and that the techniques carried a lower risk of TURP syndrome. These findings placed less
emphasis on regional as the "preferred anesthetic technique". Geavlete and colleagues [9] reported in a prospective
randomized trial that in contrast to monopolar TURP, laser TURP demonstrated significantly decreased operative
times, a shorter catherization period, shorter hospital stay and fewer complications. A meta-analysis comparing laser
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and monopolar TURP reported less clot retention and incidence of TURP syndrome, comparable postoperative
bleeding and a higher re-operation rate in the first year postoperatively [5,9].
Overall mortality from TURP has steadily decreased: by 2.5% (in 1962), 1.3% (in 1974), 0.23% (in 1989),
and 0.10% (in 2003) [10].
References
1.

Gravenstein D. Transurethral resection of the prostate (TURP) syndrome: a review of the

pathophysiology and management. Anesth Analg. 1997; 84(2):438-46. Review.

2.

Issa MM. Technological advances in transurethral resection of the prostate: bipolar

versus monopolar TURP. J Endourol. 2008; 22(8):1587-95.

3.

Chen Q, Zhang L, Fan QL, Zhou J, Peng YB, Wang Z. Bipolar transurethral resection in
saline vs traditional monopolar resection of the prostate: results of a randomized trial
with a 2-year follow-up.BJU Int. 2010; 106(9):1339-43.

4.

Mamoulakis C, Ubbink DT, de la Rosette JJ. Bipolar versus monopolar transurethral

resection of the prostate: a systematic review and meta-analysis of randomized controlled
trials. Eur Urol. 2009; 56(5):798-809.

5.

Burke N. Whelan JP, Goeree L, Hopkins RB, Campbell K, Goeree R, Tarride JE. Systematic review and
meta-analysis of transurethral resection of the prostate versus minimally invasive procedures for the
treatment of benign prostatic obstruction. Urology. 2010; 75(5):1015-22. Review.

6.

Wosnitzer MS, Rutman MP. KTP/LBO laser vaporization of the prostate. Urol Clin North Am. 2009;
36(4):471-83.

7.

Malek RS, Kuntzman RS, Barrett DM. High power potassium-titanyl-phosphate laser vaporization
prostatectomy. J Urol. 2000; 163(6):1730-3.

8.

Hanson RA, Zornow MH, Conlin MJ, Brambrink AM. Laser resection of the prostate:
implications for anesthesia. Anesth Analg. 2007; 105(2):475-9.

9.

Geavlete B, Multescu R, Dragutescu M, Jecu M, Georgescu D, Deavelete P. Transurethral resection (TUR)

in saline plasma vaporization of the prostate vs standard TUR of the prostate: the better choice in benign
prostatic hyperplasia? BJU Int. 2010; 106(11):1695-9.

10.

Reich O, Gratzke C, Bachmann A, Seitz M, Schlenker B, Hermanek P, Lack N, Stief CG.

Morbidity, mortality and early outcome of transurethral resection of the prostate: a prospective multicenter
evaluation of 10,654 patients. Urology Section of the Bavarian Working Group for Quality Assurance. J
Urol. 2008; 180(1):246-9.

Conclusion
This session of urology/renal function provided an overview of renal anatomy and physiology. A discussion of the
effects of mannitol on renal function suggest that low-dose mannitol infusion acts as a renal vasodilator whereas
high-dose mannitol can cause ARF. Mannitol-induced ARF responds to hemodialysis therapy. Newer surgical

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techniques such as bipolar and laser TURP have been developed to minimize the incidence of TURP syndrome.
These newer techniques are replacing monopolar TURP.

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Disclosure
This speaker has indicated that he or she has no significant financial relationship with the
manufacturer of a commercial product or provider of a commercial service that may be
discussed in this presentation.