TURP Syndrome PDF
TURP Syndrome PDF
TURP Syndrome PDF
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Hypertension
TURP Syndrome Bradycardia
Risk Factors
1. Open Prostatic Sinuses Irrigation
2. High Irrigation Pressure Absorption
< 3. Lengthy Resection
+ Cardiovascular
4. Hypotonic lrrigants >I-
Solute
I
+: /1
b Hyponatremia LHypodsmolity Pulmonary *Respiratory -+ Death
Edema , Failure
l-+ I t
0 Clinical Intervention
Figure 1. The variety of mechanisms and pathways that lead to transurethral resection of the prostate (TURF’) syndrome. The triggering
event is the entry of irrigation solution into the intravascular compartment (A), which increases intravascular volume (B) with its sequelae
and decreases (C) and/or increases (D) solute concentration. The figure shows the complex interactions that need to be considered when the
TURP syndrome unfolds. IV = intravenous.
Table 1. Signs and Symptoms Attributed to Transurethral Resection of the Prostate Syndrome by Major Physiologic
System and Increasing Severity
pressure (CVP). After 30 to 35 minutes, when the rate (45). Bleeding and red blood cell destruction are ad-
of irrigant absorption slowed, flow from the plasma to ditional sources of volume and oxygen-carrying ca-
the interstitium increased to an average of 75 mL/min pacity losses. The hemoglobinemia that follows such
and CVP decreased. Three patients then became sud- hemolysis, coupled with hypotension, can cause acute
denly hypotensive (systolic blood pressure ~80 mm renal failure and death (18,37,46).
Hg), two of whom became hypotensive again after the
procedure. Three other patients suddenly became hy- Osmotically Active Solutes
potensive within the first postoperative hour. Such
fluctuating intravascular fluid volume may explain Glycine, sorbitol, and mannitol are electrically non-
the intraoperative hypervolemia and hypertension fol- conducting, but osmotically active, solutes that are
lowed by postoperative hypovolemia and severe added to irrigation fluids to decrease the risk of mas-
hypotension. sive intravascular hemolysis. Their use in irrigation
Sympathetic blockade induced by regional anesthe- solutions has reduced the occurrence of significant
sia may compound TURF syndrome. Intraoperative hemolysis and death by more than 50% (46).
endotoxemia can occur in up to 45% of patients with Although distilled water may still be used by some
negative preoperative urine cultures despite routine clinicians (17,18,24,36), the irrigation solutions most
antibiotic prophylaxis (44). often used now range in calculated osmolality from
Absorption of distilled water during TURF’ can 178 mOsm/kg water for 3% sorbitol to 200 mOsm/kg
cause acute hypoosmolality with massive hemolysis for 1.5% glycine solutions or to isotonic sorbitol or
440 REVIEW ARTICLE GRAVENSTEIN ANESTH ANALG
TRANSURETHRAL RESECTION OF THE PROSTATE (TURF) SYNDROME 1997;84:438-46
Table 2. Surgical Features of Transurethral Resection of Table 3. Factors That, Alone or in Combination, Can
the Prostate by Patient Age Affect the Central Nervous System During Transurethral
Resection of the Prostrate
Average Maximum
Substrate
Patient age (yr) (17,18,24) 63-73 >90
Resection time (h) Cl.2 3.5 Drugs Solute Hypoxia
(17,18,23,24)
Resected mass (g) 22-24 110 Benzodiazepine Hyperammonemia Congestive heart
(17,18,24,25) failure
Absorbed volume (L) 1 8.8 Local anesthetic Hyperglycinemia High spinal
(2627) anesthesia
Absorption rate (mL/min) 10-30 200 Narcotic Hypoglycinemia Myocardial infarction
(27-29) Hyponatremia Pulmonary edema
Blood loss (L) (26,30,31) 0.176-0.534 3 Hypoosmolality Sepsis
Stroke
‘I Numbers I,, parentheses are reference numbers.
HYPERTROPHIC PROSTATE NORMAL PROSTATE reduce the time that a large number of prostatic si-
nuses are open and thus capable of absorbing fluid
(14,371 (Figure 2).
The most widely used indicator of volume gain is
serum sodium dilution (14,31) or breath-alcohol level
when ethanol is used as a tracer in the irrigation
solution (1,30,49). Other methods follow volumetric
fluid balance (14,38,49), CVP trend (441, plasma elec-
PROSTATIC
SINUSES
ATERAL
OBE
trolyte concentrations (e.g., magnesium and calcium)
(501, irrigation solutes [glycine (31), sorbitol (3311,
transthoracic impedance change (51), and the patient’s
weight gain (52).
COMPRESSED PROSTATE I No method guarantees that TURP syndrome will be
PROSTATIC
URETHRA avoided (36). Before reflexively treating TURP syndrome
with hypertonic saline, hypervolemia with near-normal
Figure 2. Anatomy of hypertrophic prostrate. The hypertrophic osmolality must be excluded (39,531.Symptomatic car-
gland represents glandular and leiomyomatous hyperplasia of the diovascular or pulmonary compromise requires aggres-
submucosal glands and the smooth muscle of the prostatic urethra, sive intervention. After adequate pulmonary gas ex-
which pushes the normal prostatic tissue to create a “surgical cap-
sule.” (Reproduced with permission from Wong KC, Liu W-S: An- change and hemostasisare established, administration of
esthesia for urologic surgery. In: Stoelting RK, Barash PG, Gallagher blood, the positive inotropic agents calcium and mag-
TJ, eds. Advances in anesthesia. Vo13. Chicago: Year Book Medical, nesium (50), or diuretics or augmentation of intra-
1986:379). vascular volume may be needed.
death (54). The incidence of serum sodium concentra- mannitol, while maintaining the low sodium concen-
tion less than 125 mmol/L after TURP may reach 15% tration, returned field responses to near control levels.
(15) with a mortality of 40% when hyponatremia is The increased field response, therefore, results from a
symptomatic (headache, nausea, vomiting) (53,55). Di- decreased osmolality, and not a decreased sodium
lutional hyponatremia may be aggravated by electro- concentration, which is consistent with predictions
lyte losses into accumulations of infused but extrava- based on the Nernst equation (61).
sated nonelectrolyte fluid (43). The Nernst equation predicts that the decrease in
Hyponatremia is common, and serum sodium con- extracellular sodium concentration that accompanies
centration decreases of 6 to 54 mmol/L have an inci- the hypoosmolality seen with TURP only minimally
dence ranging from 7% to 26% (34,39). Decreases from alters neuronal excitability. Replacing a Na+ value of
a normal preoperative level to 113 and 104 mmol/L 140 mmol/L with 100 mmol/L in the Nernst equation
after just 15 minutes of resection with isotonic irrig- increases the calculated transmembrane resting poten-
ants have been reported (9,ll). tial of -60 mV by 9 mV. Thus, theoretically, serum
Even markedly hyponatremic patients may show no sodium concentration should not substantially con-
signs of water intoxication (31,39). Neither a decrease tribute to neuronal excitability independent of serum
in serum sodium concentration from 34 to 54 mmol/L osmolality, even when these changes are of the mag-
without TURP syndrome nor a significant change in nitude typically associated with severe TURP
serum osmolality has been reported (39). When 3% syndrome.
mannitol irrigation was used on one TURP patient, The brain reacts to a sustained hypoosmotic stress
serum sodium concentration decreased from 133 to within seconds to minutes, with intracellular de-
99 mmol/L (56). Osmolality was measured postoper- creases in Na+, K+, Cl-, and in so-called “idiogenic
atively at 290 mOsm/kg but was calculated at osmoles,” which act to decrease intracellular osmola-
239 mOsm/kg. This difference was attributed to the lity and prevent swelling (61). However, with acute
osmotic effect of mannitol not accounted for by the osmotic change (within hours or even minutes), such
calculation. Although severe hyponatremia has been compensatory mechanisms may not work fast enough
associated with hemolysis and renal failure (36), car- (61). Cerebral edema caused by acute hypoosmolality
can increase intracranial pressure, which results in
diovascular and electrocardiogram changes (11,35,50),
bradycardia and hypertension by the Cushing reflex
respiratory compromise (11,57), seizure (35,58,59),
(62). Furthermore, cerebral edema is not caused by
coma (11,58), and death (11,34,35,57,58), other hy-
decreased serum colloid oncotic pressure, but by de-
ponatremic patients did well. Hyponatremia may not
creased osmolality (63).
be the sole or even the primary cause of the neurolog-
Only a few studies correlate a patient’s fate after
ical manifestations of TURP syndrome.
TURP with both serum sodium concentration and os-
molality (14,39,46). In a series of 72 patients under-
Hypoosmolality going TURP, serum sodium concentration decreased
by 10 to 54 mmol/L in 19 (26%), while osmolality
The crucial physiological derangement of CNS func- changed in only two (3%) (39). The two patients who
tion is not hyponatremia peuse, but acute hypoosmo- had both hyponatremia (serum sodium concentration
lality. This is to be expected because the blood-brain decreases of 27 and 30 mmol/L) and hypoosmolality
barrier, with an effective pore size of 8 A, is essentially (serum osmolality of 260 and 256 mmol/L) developed
impermeable to sodium but freely permeable to water pulmonary edema and encephalopathy. The five pa-
(60). In rabbits, signs of water intoxication induced by tients in this series with the largest decreases in serum
administration of vasopressin and 2.5% glucose solu- sodium concentration (by 34 to 54 mmol/L) had no
tion were reversed by administration of osmotically changes in serum osmolality and no signs of TURP
active agents such as urea and mannitol without cor- syndrome.
recting the serum sodium concentration (61). Treatment of Hyponatremia and Hypoosmolality. Pre-
One method of determining the independent neu- cautions can be taken to avoid severe hyponatremia
rophysiological effects of serum sodium concentration and hypoosmolality. Diuretics have been implicated
and osmolality has been to measure field potentials in the rapid onset of hyponatremia (64). When used
from prepared brain slices. Field potentials can be routinely or to treat hypervolemia after TURP, they
triggered or arise spontaneously and represent the may worsen hyponatremia and hypoosmolality and,
voltage generated by the synchronous discharge of thus, lead to TURP syndrome. Furosemide and bumet-
many neurons aligned in parallel. anide act within minutes on the ascending loop of
Hypotonic saline (Nat of 123 mmol/L and a tonic- Henle where they inhibit chloride uptake, which
ity of 245 mOsm/kg) as a brain slice superfusate in- causes urinary sodium loss and promote salt-wasting
creased the amplitude of field potentials in rat hip- after TURP (41,50). Mannitol also causes sodium
pocampal slices. Correcting the osmolality with losses during the first 12 hours after TURP but does
442 REVIEW ARTICLE GRAVENSTEIN ANESTH ANALG
TRANSURETHRAL RESECTION OF THE PROSTATE (TURF) SYNDROME 1997;84:438-46
not lower serum level during the first three to five correction of acute asymptomatic hyponatremia or
postoperative hours (65). hypoosmolality may be clinically indistinguishable
A patient’s serum sodium concentration and osmo- from correction of chronic hyponatremia and
lality may continue to decrease for some time after the hypoosmolality.
procedure because much irrigant is slowly absorbed The presence of symptoms has been described as
from the perivesicular and retroperitoneal spaces (26). the single most important factor determining morbid-
The TURP syndrome can start 4 to 24 hours later ity and mortality from hyponatremia (55). The safest
(12,14,27,54) with coma, blindness, grand ma1 sei- treatment of hyponatremia and hypoosmolality may
zures, and hemiplegia (14,54). Problems may be fore- be symptomatic (74). Instituting therapy in the ab-
stalled by using loop and other salt-wasting diuretics sence of symptoms risks too rapid a correction be-
with a concomitant infusion of saline-even in the cause the correction rate is difficult to control (59).
presence of near normal serum sodium concentra- Therefore, osmolality should be monitored and cor-
tion-during the first 12 postoperative hours (41,65). rected aggressively only until symptoms substantially
Pretreatment with hypertonic saline may decrease resolve; then correction should be continued slowly
the degree of dilutional hyponatremia (66). This ap- (Na+ correction + 1.5 mmol . L-l * h-i).
proach may decrease the incidence of TURP syndrome
caused by hypoosmolality, but likely will exacerbate Hyperammonemia
the incidence and severity of the syndrome’s hyper-
volemia manifestations. Because the serum sodium The portal bed and kidneys can metabolize glycine
concentration need not reflect serum osmolality that gains intravascular access. The primary pathway
(35,39,56), serum sodium concentration should be re- used by the liver and kidneys is oxidative deamina-
ported together with osmolality when the irrigant so- tion (75), which leads to the formation of two poten-
lution contains osmotically active solutes (such as gly- tially toxic metabolites: glyoxylic acid and ammonia
tine, mannitol, or sorbitol). If osmolality is near (76). The brain also contains a glycine cleavage en-
normal, no intervention to correct sodium is recom- zyme system that splits glycine into carbon dioxide, a
mended for asymptomatic patients, even in the face of one-carbon fragment, and ammonia (77).
reduced serum sodium concentration. It seems clear that an increase of serum ammonia
The most feared complication of correcting hypona- during TURP is the result of glycine absorption be-
tremia is central pontine myelinolysis (CPM). Because cause patients undergoing retropubic resections with-
demyelination can occur in extrapontine areas, the out glycine do not develop hyperammonemia (78).
disease is also referred to as “osmotic demyelination The alteration of CNS function caused by hyperam-
syndrome” (67). Although CPM is most often seen in monemia may be a factor in perioperative manage-
women [probably due to sex differences in cellular ion ment, however, the role of hyperammonemia in TURP
pump capacity (55)], it has been reported after rapid as syndrome remains unclear.
well as slow correction of serum sodium concentration In the treatment of hyperammonemia, the methods
in TURP patients (59,68). for limiting the increase of plasma ammonia concen-
When treatment is instituted too slowly for symp- tration when glycine irrigants are used include
tomatic hyponatremia (~0.7 mmol . L-l * h-l) L-arginine, which acts in the liver by preventing he-
(57,68), it has been associated with a higher morbid- patic release of ammonia and accelerating ammonia
ity and mortality than has rapid correction conversion to urea. The time necessary to deplete en-
(21.0 mm01 * L-’ * h-i) (64). Many reports (58,59, dogenous arginine stores may be as little as 12 hours,
69-71) suggesting that a 1.5- to 2.0-mmol * L-i * h-i which approximates preoperative fast time (79). Pro-
correction rate is safe have failed to consider changes phylactic administration of intravenous L-arginine
in osmolality. Several investigators have suggested markedly moderated the increase in blood ammonia
that osmotic stressis probably greater when correcting concentration in fasting patients receiving intravenous
chronic compared with acute hyponatremia (72,73). glycine. Infusion of L-arginine with or at the conclu-
Extracellular changes in blood osmolality equili- sion of glycine administration prevented further in-
brate within minutes across the blood-brain barrier creases in blood ammonia concentration and acceler-
and brain cell membranes (61). Hypoosmotic stress ated its return to normal (79). Doses between 4 g
affects intracellular ion and amino acid concentrations (20 mmol) infused over three minutes and 38 g
(72,73). There is up-regulation of the processes for the (180 mmol) infused over 120 minutes have been rec-
export of organic osmolytes from the cell and down- ommended (79). No toxicity was noted with either
regulation of the synthesis of amino acids in response of these regimens. The purchase cost of L-arginine
to hypoosmotic stress (61). Once induced by hypoos- is approximately $85 per 300-mL bottle of a
molality, it is not known how fast the elimination of preservative-free 10% L-arginine solution with a cal-
these amino acids can be reversed by the correction of culated osmolality of 950 mOsm/kg water (R-GENE
the hypoosmolality. If the reversal is slow, the rapid lo@; Kabivitrum, Franklin, OH).
ANESTH ANALG REVIEW ARTICLE GRAVENSTEIN 443
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