Anesth Analg 2003;97:1536-1538
© 2003 International Anesthesia Research Society
GENERAL ARTICLES
Transurethral Resection Syndrome After Bladder Perforation
Ihab Dorotta, MD*,
Ayman Basali, MD*,
Michael Ritchey, MD*,
Jerome F. O’Hara, Jr., MD*, and
Juraj Sprung, MD PhD
Departments of Anesthesiology, *Cleveland Clinic Foundation, Cleveland, Ohio; and
Mayo Clinic, Rochester, Minnesota
Address correspondence to Juraj Sprung, MD, PhD, Department of Anesthesiology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. Address e-mail to sprung.juraj{at}mayo.edu
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Abstract
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IMPLICATIONS: Transurethral bladder tumor resection may be complicated by bladder perforation with intraabdominal extravasation of irrigant. This complication ("TURBT syndrome") may be associated with water and electrolyte disturbance, which differs from that associated with "TURP syndrome."
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Introduction
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The use of irrigating solutions is essential for distension of mucosal surfaces and visualization of the surgical field during both transurethral resection of prostate (TURP) and transurethral resection of bladder tumors (TURBT) (1). Whereas TURP resection may be associated with excessive intravascular absorption of irrigating fluid resulting in hypervolemia, hypertension, and hyponatremia ("TURP syndrome"), such complications are infrequent during TURBT surgery. Bladder perforation associated with intraperitoneal extravasation of irrigant fluid during TURBT surgery may rarely evolve in specific hydroelectrolyte imbalance (2,3), which has different dynamics, time course, and therapeutic approach compared with the "TURP syndrome" (3,4). We describe four patients who developed "TURBT syndrome" and discuss issues relevant to pathophysiology, diagnosis, and treatment of this rare condition.
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Case Reports
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Case 1
A 72-yr-old man underwent TURBT resection by using a 1.5% glycine as the bladder irrigant. On awakening from a 90-min general anesthesia, the patient’s abdomen was distended, his breathing was labored, he was confused, and complained of severe abdominal pain. The arterial blood pressure decreased to 90/40 mm Hg. A cystogram revealed intraperitoneal extravasation of fluid through the perforation on the posterior bladder wall. An immediate exploratory laparotomy resulted in evacuation of 4 L of irrigating fluid from the abdomen. His intraoperative serum sodium was 127 mEq/L, and the urine output remained small despite fluid administration (3.7 L intraoperatively) and the 2 20-mg IV doses of furosemide. Systolic blood pressure decreased to <100 mm Hg requiring further crystalloid administration (1.5 L) and repeated phenylephrine boluses. The first postoperative serum sodium was 121 mEq/L, and the patient was confused and unable to follow commands. In the recovery room, treatment included 2.5 L of 0.9% saline infusion followed by 20 mg of furosemide IV. His confusion resolved by postoperative day one, at which time the serum sodium was 132 mEq/L. Serum creatinine postoperatively increased to 1.4 mEq/L, but subsequently normalized.
Case 2
A 68-yr-old woman underwent bladder biopsy under spinal anesthesia. Sterile water was used to provide bladder distention. Approximately 15 min into the surgery, she complained of sudden shoulder and chest pain and her abdomen became distended. Endoscopic inspection of the bladder revealed a perforation of the anterior dome of the bladder. An exploratory laparotomy under general anesthesia was performed and several liters of irrigant were drained from the peritoneal cavity. Her lowest serum sodium was 123 mEq/L, but gradually increased with infusion of 2.0 L of normal saline, as well as 3% hypertonic saline (1.0 L) over the 12 h, and furosemide (40 mg) IV. The following day her creatinine increased to 3.0 mEq/L, and by the third postoperative day it was 1.1 mEq/L.
Case 3
An 81-yr-old woman underwent TURBT resection under general anesthesia. Preoperative creatinine was 0.7 mEq/L, and hematocrit 44%. Sterile water was used as the bladder irrigant. After the first hour of surgery, her abdomen revealed distension but an intraoperative cystogram did not demonstrate bladder perforation. The patient was transferred to the recovery room sedated with her trachea intubated. Soon after arrival her blood pressure decreased to 90/50 mm Hg and the urine was noted to be "cherry red." The hematocrit decreased to 33%, although she received only 1.0 L of normal saline, and the estimated blood loss was "minimal." Urine was tested positive for free hemoglobin. Her serum sodium was 112 mEq/L, and she was acidotic (base deficit 16 mEq/L, pHa 7.14). Her hematocrit further decreased to 24% requiring blood transfusion. The urine output remained small and serum sodium continued to decrease despite administration of 4.0 L of 0.9 normal saline, 1.0 L of 3% hypertonic saline, and 200 mg of furosemide over 9 h. Nine hours after completion of surgery, the patient had a seizure and the serum sodium was 106 mEq/L. At that time, a repeat cystogram revealed a posterior wall bladder perforation with intraperitoneal fluid accumulation. Exploratory laparotomy resulted in removal of 2.0 L of intraperitoneally accumulated fluid. The perforation was repaired and both suprapubic tube and bilateral ureteral stents were placed. Her serum sodium continued to slowly increase over the next 3 days (see Fig. 1). The postoperative course was complicated by renal failure (creatinine of 6.9 mEq/L) and she was discharged home after a 24-day hospitalization requiring permanent hemodialysis.
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Figure 1. Perioperative serum sodium in our four patients. Nadir of hyponatremia is slow (between 2 and 9 h) and has a protracted course.
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Case 4
A 77-yr-old man underwent TURBT resection under spinal anesthesia and with glycine 1.5% solutions as the bladder irrigant. At the conclusion of the surgery, the patient began to complain of shoulder discomfort, which evolved into sharp anterior left chest wall pain on arrival to the recovery room. Examination revealed abdominal distention and serum sodium of 118 mEq/L. The patient remained alert and oriented. Serial electrocardiogram and cardiac enzymes (troponin T) excluded a myocardial event. While in the recovery room, his systolic blood pressure decreased to 90 mm Hg, but promptly increased with fluid administration. Cystogram confirmed bladder perforation with retroperitoneal extravasation. The patient received continuous infusion of normal saline (159 mL/h), 1.0 L of 3% hypertonic saline at a rate of 100 mL/h, and 90 mg of furosemide. His serum sodium increased to 127 mEq/L on the first postoperative day. Preoperative and postoperative creatinine values remained within the normal limits.
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Discussion
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The use of irrigating fluids as a distending media during endoscopic procedures has evolved over the years from the use of distilled water to a variety of other nonconducting osmotically active solutions (5). Direct intravascular absorption of these fluids, such as may occur during TURP surgery, may induce acute hypervolemia, hypertension, dilutional hyponatremia, hypo-osmolality (6), and hemolysis (when distilled water is used such as in our patient 3). A combination of high hydrostatic pressure and hypo-osmolality causes fluids to shift from the intravascular space to interstitial (pulmonary edema) and intracellular (brain edema) compartments ("TURP syndrome"). In contrast to "TURP syndrome," severe water and electrolyte imbalance has been rarely reported during resectoscopic bladder surgery (7,8).
We describe four patients who developed severe water and electrolyte imbalance after either intraperitoneal or retroperitoneal extravasation of irrigating solution during TURBT surgery. In contrast to the faster onset of "TURP syndrome," the water and electrolyte imbalance after bladder perforation is typically slower (3,7,9,10). It takes between one (1,3,11) and six hours (9) for serum sodium to reach its nadir, and this may be related to both the amount of extravasated volumes and site of extravasation (intraperitoneal versus retroperitoneal). In our patients, hyponatremia reached its nadir between two and nine hours despite all the treatments (Fig. 1).
A very different fluid and solute dynamic occurs during "TURBT syndrome" (3,11) compared with the "TURP syndrome." Peritoneum is a biologic membrane and the net effects of fluids and solute shifts between the capillary blood and the intraperitoneal fluid depends on both the amount and composition of intraperitoneally extravasated fluid. An intraabdominal infusion of distilled water grossly reduces serum osmolarity, increases hematocrit (hemoconcentration), and decreases glomerular filtration rate (11). Because liquid distending media are electrolyte-free, serum sodium tends to equilibrate with intraperitoneal or retroperitoneal extravasate, leading in its net movement extravascularly (1,3,11). Because the sodium from intravascular space is "dialyzed" to intraperitoneal fluid, hyponatremia may reflect its net deficit more so than during the "TURP syndrome" (where hyponatremia is attributed to dilution). Hyponatremia during "TURBT syndrome" may lead to the net water flux along osmotic gradient out of the intravascular space and hypovolemia, hypotension, oliguria, acute renal impairment, and metabolic acidosis typically ensue (1,3,5,10–13). Furthermore, solutes in the irrigant, such as glycine and sorbitol, equilibrate with total body water and move intracellularly to be rapidly metabolized (7). The net effect may be further decreased in both plasma osmolarity and intravascular volume. At the same time, serum potassium remains relatively unchanged (1,11). This may be attributed to the large intracellular potassium load which promptly equilibrates the loss of extracellular potassium, especially in the presence of acidosis, and when 1.5% glycine is used, to the hyperkalemic effect of glycine transport into the cells (14).
Signs and symptoms of large intraperitoneal fluid extravasation during TURBT may be detected earlier under regional anesthesia (see our case 2) and the symptoms include abdominal distension along with discomfort, shoulder pain, nausea, confusion, blurred vision, and/or chest pain (1,3). Furthermore, by using an irrigant containing a trace amount of ethanol (1%), the absorption can be measured by the ethanol expired-breath test with a pocketsize breath analyzer (15). Finally, crude monitoring modalities are recording of irrigant entering and exiting the patients’ bladder, and repeat abdominal palpation for signs of distension during surgery. All our patients had a grossly distended abdomen by the end of surgery.
The most important step in managing these patients is early recognition of bladder perforation and prevention of large fluid extravasation. The most complicated clinical course occurs when there is a delay in recognition of the problem (our case 3). Initial medical treatment may involve volume expansion, because extracellular fluid extravasation is associated with hypovolemia. Maintenance of adequate intravascular volume may prevent severe consequences on renal perfusion; three of our patients developed renal impairment; one of them remained dialysis-dependent. Definitive treatment for large intraperitoneal fluid accumulation is prompt surgical drainage of the pooled fluid (3). Diuretics may be an alternative to surgical drainage, but their use should be reserved for milder cases and only after normovolemia is restored (10). A significant number of these patients may fail to diurese spontaneously (13), a situation encountered in our patients. Using diuretics before intravascular volume is adequately replenished may be deleterious for the kidney function. Finally, medical treatment of symptoms caused by hyponatremia involves using normal saline or slow infusion of hypertonic saline in conjunction with diuretics.
We described hydroelectrolyte imbalance during TURBT surgery associated with intraperitoneal or extraperitoneal fluid accumulation. This clinical picture may resemble "TURP syndrome" but management is different because severe hyponatremia in these patients is associated with intravascular fluid deficit which may lead to renal impairment.
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References
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- Olsson J, Hahn RG. Simulated intraperitoneal absorption of irrigating fluid. Acta Obstet Gynecol Scand 1995; 74: 707–13.[ISI][Medline]
- Uchida T, Ao T, Ikeda S, et al. Clinical statistics of the bladder tumor: transurethral resection cases. Hinyokika Kiyo 1990; 36: 1033–8.[Medline]
- Montesinos Baillo A, Banus Gassol JM, Palou Redorta J, et al. Physiopathology and surgical treatment of extravasated peritoneal fluid after transurethral resection. Eur Urol 1984; 10: 183–6.[ISI][Medline]
- Bach A, Jurs G, Krier C, Fleischer F. TUR syndrome as a late postoperative complication: case report. Anasth Intensivther Notfallmed 1988; 23: 214–6.[Medline]
- Hahn RG. Irrigating fluids in endoscopic surgery. Br J Urol 1997; 79: 669–80.[ISI][Medline]
- Marx GF, Orkin LR. Complications associated with transurethral surgery. Anesthesiology 1962; 23: 802–13.[ISI][Medline]
- Hahn RG. Transurethral resection syndrome after transurethral resection of bladder tumours. Can J Anaesth 1995; 42: 69–72.[Abstract/Free Full Text]
- Ekengren J, Conner P, Lindholm M, Hahn RG. Fluid absorption during transurethral bladder surgery. Scand J Urol Nephrol 1995; 29: 519–20.[ISI][Medline]
- Weber S, Acuff JH, Mazloomdoost M, Kirimli BI. Transurethral prostatectomy complicated by intraperitoneal extravasation of irrigating fluid. Can J Anaesth 1987; 34: 193–5.[Abstract/Free Full Text]
- Hahn RG. Transurethral resection syndrome from extravascular absorption of irrigating fluid. Scand J Urol Nephrol 1993; 27: 387–94.[ISI][Medline]
- Mahoney SA, Forsythe WE III, Persky L. Intraperitoneal extravasation of irrigant solutions. J Urol 1965; 94: 276–81.[ISI][Medline]
- Marmar JL, Allen SD. The transurethral resection reaction secondary to intraperitoneal extravasation of irrigating solution. J Urol 1970; 104: 457–8.[ISI][Medline]
- Olsson J, Nilsson A, Hahn RG. Symptoms of the transurethral resection syndrome using glycine as the irrigant. J Urol 1995; 154: 123–8.[ISI][Medline]
- Hahn RG. Hyperkalemia from nonelectrolyte solutions. Anesthesiology 1993; 78: 794–5.[ISI][Medline]
- Hahn RG, Olsson J. Ethanol monitoring of the transurethral resection syndrome. J Clin Anesth 1996; 8: 652–5.[ISI][Medline]
Accepted for publication June 19, 2003.
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Abstract
Introduction
