Original Article
European Journal of Trauma and Emergency Surgery
Disproportionate Acidosis After Traumatic Bladder Rupture: A Case-Control Study Subhash Reddy1, John A. Carr2
Abstract Background: Traumatic bladder injury is rare and often missed on initial evaluation. We sought to identify early markers of bladder injury with a high sensitivity. Methods: A retrospective review from 1999 to 2008. Results: There were 28 patients diagnosed with traumatic bladder injury. The most common mechanism was car accidents with pelvic fractures. 93% (26) of the patients presented with significant metabolic acidosis, without evidence of hemorrhagic shock. For intra- and extraperitioneal bladder ruptures, the mean hemoglobin level on arrival was 12.4 + 2.0 (range 9.0–16.0) and 11.4 + 1.9 (range 8.2–14.7). The average pH on arrival for intraperitoneal ruptures was 7.22 + 0.16 (range 6.86–7.37) and for extraperitoneal ruptures, 7.22 + 0.16 (range 6.85–7.37). The pH improved in all patients with intraperitoneal rupture after surgical repair, up to a mean of 7.27 + 0.11 (range 7.06–7.36, p = 0.5) within 12 h. Extraperitoneal ruptures recovered more quickly with a pH after catheter drainage of 7.34 + 0.04 (range 7.27–7.37, p = 0.1) within 12 h. The ISS for intraperitoneal and extraperitoneal ruptures were similar, 30 + 12 (range 13–57) and 32 + 13 (range 13–57, p = 0.7). A cohort of trauma patients, matched by ISS, age, and pelvic fracture, but without bladder rupture, was used for comparison. Their mean ISS was 30 + 10 (range 14–57). The average pH for this group on arrival was 7.33 + 0.11 (range 7.16–7.42), and 47% of these patients had a normal pH. There was a significant difference between the pH on arrival in the ruptured compared to the nonruptured cohort (intraperitoneal pH 7.22, p = 0.008, extraperitoneal pH 7.22, p = 0.02). Three patients died (mortality 10.7%).
Conclusions: Disproportionate acidosis in the trauma patient is a sensitive indicator of bladder injury, especially with a pelvic fracture or hematuria. Fully resuscitated patients with persistent acidosis and an appropriate mechanism should be evaluated for bladder injury. Key Words Bladder rupture Æ Bladder injury Æ Pelvic fracture Æ Acidosis Eur J Trauma Emerg Surg 2010;36:361–8 DOI 10.1007/s00068-009-9133-x
Introduction Traumatic bladder rupture was historically diagnosed by the previously well-known triad of gross hematuria, pelvic fracture, and an appropriate biochemical profile, with elevated blood urea nitrogen (BUN) and creatinine [1, 2]. This has fallen out of general knowledge due to the widespread use of screening computed tomography (CT) to evaluate every blunt abdominal trauma patient. While retrograde cystography remains the gold standard, with sensitivity and specificity rates of 95–100 and 100%, respectively, CT scanning has supplanted cystography due to rapid availability and ease of performance [3, 4]. In many trauma centers, retrograde CT cystography has replaced the conventional retrograde cystogram due to equally high sensitivity and specificity rates [3]. However, the overall sensitivity of CT when it is used to diagnose traumatic bladder injury ranges
1
Department of Surgery, Michigan State University, Lansing, MI, 48912, USA, 2 Division of Trauma Surgery, Flint, MI, 48503, USA. Presented at the 56th Annual Meeting of the Michigan Chapter of the American College of Surgeons, Shanty Creek Resort, Bellaire, MI. Received: July 13, 2009; revision accepted: September 17, 2009; Published Online: November 21, 2009
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widely, from 60 to 100%, with poor results in classifying both intraperitoneal (80% accuracy) and extraperitoneal (55% accuracy) [3–7]. This is because a standard CT scan of the abdomen and pelvis performed with intravenous contrast to evaluate a trauma patient does not include the necessary retrograde filling of the bladder with 300 cc of contrast to fully distend and evaluate the bladder. This can result in ‘‘missed’’ injuries or delays in diagnosis, especially since 6–19% of patients with bladder rupture will not have gross hematuria (although all have microscopic hematuria) [7, 8]. Furthermore, trauma patients with multiple other injuries and a suspected bladder rupture may actually have a retrograde cystogram performed less than half the time [7]. This is understandable when considering that a significant percentage of these patients will require emergency neurosurgical or orthopedic procedures that take precedent, or will have a CT finding of free fluid in the abdomen that leads to an emergency laparotomy. Regardless, the retrograde cystogram or CT cystogram is not a commonly performed procedure in the emergency setting unless the patient presents with gross hematuria. Moreover, gross hematuria alone is not indicative of a traumatic bladder rupture, since other injuries also cause this, including renal injury. However, the combination of a pelvic fracture and gross hematuria should greatly increase suspicion [9]. Interestingly, in the context of isolated traumatic pelvic fractures with urologic injury of any type, 23% were initially missed, with a delay in diagnosis of 19 h for intraperitoneal bladder ruptures and 6.7 days for extraperitoneal ruptures [10]. Thus, traumatic bladder rupture is not a straightforward diagnosis in the multi-injured patient. Our personal experience has been that the BUN and creatinine were not dramatically elevated initially so as to raise suspicion of a bladder injury. However, our anecdotal experience has been that all of these patients are profoundly acidotic due to reabsorption of excreted hydrogen ions in the urine. We decided to perform a retrospective study of our experience with traumatic bladder rupture and determine if the presence of significant acidosis after resuscitation could be used as a sensitive indicator of the diagnosis prior to imaging, and as a red flag that may signal the need for a retrograde CT cystogram.
Methods We performed a retrospective review of our prospectively collected trauma registry at Hurley Medical
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Center, a Level 1 trauma center in central Michigan. The review included all trauma patients with bladder rupture or perforations from 1999 to 2008. Inclusion criteria were blunt traumatic injury to the abdomen or penetrating injury with bladder rupture. Patients with renal or ureteral injuries, iatrogenic injuries, and preexisting renal disease were excluded. Patients were divided into two groups: intraperitoneal bladder perforation (IBP) and extraperitoneal bladder perforation (EBP). The two groups were compared with regard to age, sex, mechanism of injury, hemodynamic parameters at presentation, diagnostic modalities, electrolytes, arterial blood gas (ABG) profiles at various intervals, time of actual intervention (surgical or catheter drainage), and discharge status. Within each of these two groups, the electrolyte profile, BUN, creatinine, and the ABG profiles from time of presentation until 48 hours after actual intervention were collected and compared. We used our trauma registry to accrue a similar cohort of trauma patients for comparison who were matched by three criteria: injury severity score (ISS), age, and the presence of a pelvic fracture without bladder injury. We surveyed our database of over 1,050 patients with similar mechanisms of injury and found 45 matching patients. Of these 45, only 17 of them had a blood gas analysis performed on arrival, and these data were used for the comparison. In addition, the pH and base deficits were compared between all groups. Base deficit was plotted in addition to pH, since the pH could be low secondary to respiratory insufficiency with retained CO2. To ensure accuracy, the logarithmic conversion of the pH into hydrogen ion concentration was also used for statistical analysis. If bladder injury was diagnosed after the patient left the emergency room (ER), it was defined as a delay in diagnosis. The pH, base deficit, BUN, creatinine, and potassium were graphed from the time of arrival to 48 h later to show the trends. If a patient lacked a specific time data point, the other data points were used to extrapolate the curve. Not every patient’s data were charted to avoid overcrowding the graph; rather, a random sample of the data was plotted to show a representative trend. This study was approved by the Institutional Review Board of Hurley Medical Center prior to its initiation. Since the data was found to be normally distributed, we used a two-tailed Student’s t test with equal variance for statistical analysis. All values are expressed as the mean ± standard deviation (SD), and a p value of less than 0.05 was considered significant.
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Reddy S, Carr JA. Disproportionate Acidosis After Traumatic Bladder Rupture
Categorical data were compared using v2 with or without Yate’s correction or Fisher’s exact test.
Results From 1999 to 2008, there were 28 patients diagnosed with traumatic bladder rupture. Fifteen were men and 13 were women. There were 13 intraperitoneal ruptures, 13 extraperitoneal ruptures, and two patients had combined intra- and extraperitoneal ruptures. Twentyfive of the patients (89%) were in automobile accidents and had concomitant pelvic fractures. A single patient, who also had a pelvic fracture, was crushed against a brick wall for a total association between bladder injury and pelvic fracture of 93%. Only two patients did not have associated pelvic fractures: one had a gun shot wound and one patient had a tree fall across his abdomen. None of the patients had a medical history of renal disease. The diagnosis was suspected on the initial CT scan in 21 (75%) and confirmed by retrograde cystography. The diagnosis was initially missed and detected later in five patients (18%). The single patient who was shot and the one patient involved in a car accident who was unstable were diagnosed in the operating room at the Figure 1. Trends of the blood urea nitrogen levels after intraperitoneal rupture.
time of laparotomy. All patients with intraperitoneal ruptures, the two patients with intra- and extraperitoneal ruptures, and one large extraperitoneal rupture were all repaired surgically with a two-layered closure. The remaining extraperitoneal tears were treated with catheter drainage only. The serum BUN and creatinine on arrival were not abnormally high so as to alert the clinician to possible bladder rupture. This was true for both the intra- and extraperitoneal ruptures. The mean BUN/creatinine for intra- and extraperitoneal ruptures, respectively, on presentation were 17 ± 7 (range 8–36)/1.4 ± 0.5 (range 0.6–2.2) and 15 ± 5 (range 7–23)/1.4 ± 0.6 (range 0.8–2.9). After surgical repair of the intraperitoneal ruptures, both the BUN and creatinine significantly decreased to a mean of 10 ± 4 (p = 0.05) and 0.9 ± 0.2 (p = 0.007) within 12 h. However, with extraperitoneal ruptures, there was no significant change noted (BUN 15 ± 7, p = 0.9 and creatinine 1.1 ± 0.5, p = 0.4) within 12 h after catheter drainage was initiated. See Figures 1, 2, 3, 4. Similarly, the serum potassium was not abnormal on presentation and did not change significantly after intervention. The mean level on arrival for intra- and extraperitoneal ruptures was 3.8 ± 0.5 (range 2.4–4.8)
Intraperitoneal- BUN
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Hours From Injury Figure 2. Trends of the blood urea nitrogen levels after extraperitoneal rupture.
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Figure 3. Trends of the creatinine levels after intraperitoneal rupture.
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and 4.2 ± 0.9 (range 3.3–6.0). After repair or catheter drainage, the mean levels within 12 h were 4.3 ± 0.9 (p = 0.1) and 4.5 ± 1.1 (p = 0.6) and did not change significantly thereafter. In contrast, 93% (26) of the patients presented with significant metabolic acidosis, without evidence of hemorrhagic shock. Granted, the pelvic fractures did cause various degrees of hematoma formation within the endopelvic fascia, but initial hemoglobin levels and repeat levels after hydration did not fully account for the initial acidosis in the majority of patients. For intra- and extraperitoneal bladder ruptures, the mean Figure 5. Trends of the hemoglobin levels after intraperitoneal rupture.
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hemoglobin level on arrival was 12.4 ± 2.0 (range 9.0– 16.0) and 11.4 ± 1.9 (range 8.2–14.7). After hydration and resuscitation, the levels were 11.7 ± 2.0 (range 8.0– 14.2, p = 0.3) and 10.5 ± 1.9 (range 7.1–13.8, p = 0.3). The hemoglobin levels did not fluctuate significantly after repair (see Figures 5, 6). The average pH on arrival for intraperitoneal ruptures was 7.22 ± 0.16 (range 6.86–7.37). For extraperitoneal ruptures, the mean value was exactly the same at 7.22 ± 0.16 (range 6.85–7.37). The pH improved in all patients with intraperitoneal rupture after surgical repair, up to a mean of 7.27 ± 0.11 (range 7.06–7.36, p = 0.5)
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Figure 6. Trends of the hemoglobin levels after extraperitoneal rupture.
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within 12 h. Mean values at 12–24, 24–36, and 36–48 h after surgery were 7.33 ± 0.09 (p = 0.2), 7.40 ± 0.07 (p = 0.004), and 7.40 ± 0.04 (p = 0.005). Patients with extraperitoneal ruptures recovered more quickly, with a mean value after catheter drainage of 7.34 ± 0.04 (range 7.27–7.37, p = 0.1) within 12 h. Mean values at 12–24, 24–36, and 36–48 h after catheter drainage were 7.38 ± 0.06 (p = 0.05), 7.39 ± 0.06 (p = 0.02), and 7.43 ± 0.05 (p = 0.006). As the graphs show (Figures 7, 8), fluid resuscitation prior to intervention did improve the pH initially in most (but not all) patients. However, it was not Figure 7. Trends of the pH after intraperitoneal rupture.
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until after the intervention, surgery or catheter drainage, that the pH normalized. To ensure accuracy, the pH values underwent logarithmic conversion to hydrogen ion concentration and the statistical analysis was repeated. The results remained statistically valid. After repair of intraperitoneal ruptures, the mean hydrogen ion concentration in the patients’ sera decreased to 5.6·10–8 ± 1.6·10–8 (p = 0.5) within 12 h. Mean values at 12–24, 24–36, and 36–48 h after surgery were 4.7·10–8 ± 1.0·10–8 (p = 0.2), 4.0·10–8 ± 6.8·10–9 (p = 0.02), and 4.0·10–8 ± 3.4·10–9
Intraperitoneal- pH 750
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Hours From Injury Figure 8. Trends of the pH after extraperitoneal rupture.
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(p = 0.03). After drainage of extraperitoneal ruptures, the mean hydrogen ion concentration decreased to 4.6·10–8 ± 4.7·10–9 (p = 0.2) within 12 h. Mean values at 12–24, 24–36, and 36–48 h after surgery were 4.2·10–8 ± 5.6·10–9 (p = 0.1), 4.1·10–8 ± 6.1·10–9 (p = 0.05), and 3.7·10–8 ± 4.8·10–9 (p = 0.04). The base deficit trends mirrored the pH as expected for both groups. On arrival, the base deficit for intra- and extraperitoneal ruptures was –10 ± 5 (range –4 to –20) and –9 ± 7 (range –1 to –24). Within 12 h after surgery, the mean base deficit for intraperitoneal ruptures was –9 ± 5 (p = 0.8). The extraperitoneal ruptures recovered more quickly, with the mean base deficit within 12 h improving to –5 ± 3 (p = 0.2). The mean values for the intraperitoneal ruptures at 24–36 and 36–48 h after surgery were –1 (p = 0.001) and 1 (p = 0.003). For the extraperitoneal injuries, the mean values at 24–36 and 36–48 h were –3 (p = 0.02) and –1 (p = 0.02). See figures 9 and 10. The ISS for intraperitoneal and extraperitoneal ruptures were the same on average, 30 ± 12 (range 13– 57) and 32 ± 13 (range 13–57, p = 0.7), respectively. A similar cohort of trauma patients, matched by type of pelvic fracture, ISS and age, but without bladder rupFigure 9. Trends of the base deficits after intraperitoneal rupture.
Base Def
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ture, were then used for comparison. Their mean ISS was 30 ± 10 (range 14–57). The mean pH for this group on arrival was 7.33 ± 0.11 (range 7.16–7.42), and 47% of these patients had a normal pH on arrival (normal range 7.35–7.45). There was a statistically significant difference between the pH on arrival in the bladder rupture patients, both intraperitoneal and extraperitoneal, compared to the nonruptured cohort (intraperitoneal pH 7.22, p = 0.008, extraperitoneal pH 7.22, p = 0.02, Figure 11). ROC analysis for pH is shown in Figure 12. At a pH below 7.31, the sensitivity to detect bladder rupture is 78% and the specificity is 59%. Three patients died (mortality 10.7%) within the 30-day postoperative or postaccident period from multisystem organ failure. Five patients were discharged home and the remaining twenty patients were sent to rehabilitation centers.
Discussion Any laboratory textbook will cite an average urine pH range of 4.5 to 8.0. However, within this wide range, most urine samples will have an acidic pH of around 6.0 [11]. Thus, it is easy to understand how a large
Intraperitoneal- Base Deficit Patient 1 Patient 2 Patient 3 Patient 4 Patient 5 Patient 6 Patient 7
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7.5 7.45 7.4 7.35 7.3 7.25 7.2 7.15 7.1 7.05 7
7.33 (+/- 0.11)
7.22 (+/- 0.05) 7.22 (+/- 0.05)
Arrival
Control (n=17)
IP
EP
Figure 11. Difference in arrival pH between patients with bladder rupture and controls.
Sensitivity - 78% at pH 7.31, 100% at pH 7.27 Specificity - 59% at pH 7.31, 100% at pH 7.13 pH 100
Sensitivity
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60
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100-Specificity Figure 12. ROC analysis.
amount of urine pouring into the abdominal cavity could quickly induce a profound metabolic acidosis. Hydrogen ions in the urine are quickly absorbed across the peritoneum, with a mean transit time of only 20 min [12]. This would allow the trauma patient to become significantly acidotic within the time it takes to transport the patient from the accident scene to the hospital. As mentioned in our results, almost all of these patients were significantly acidotic on arrival. When comparing the group with bladder rupture to our matched ISS cohort with pelvic fractures but without bladder rupture, we found a statistically significant difference, with a much more profound acidosis occurring in the group with bladder rupture despite similar fracture patterns, age, ISS, and hemoglobin levels. It would be easy to argue that the majority of trauma patients with a high ISS would be acidotic on presentation secondary to a combination of blood loss and shock; however, as our results show, those
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with bladder rupture had a much more significant acidosis on arrival than their counterparts without bladder injury, and the majority of patients were not anemic on arrival. The finding of a significant acidosis with a normal hemoglobin level should become a red flag for bladder rupture when evaluating a trauma patient, especially if the acidosis persists after resuscitation. While a few of the patients in this series did have an initial mild improvement in their acidosis after fluid resuscitation, most did not, and their pH did not normalize until after surgery or catheter drainage. This is the first study to document this finding, which should allow an earlier radiological investigation of the bladder on arrival. It also has implications for trauma centers that accept a large number of patients in transfer, as a persistent acidosis will herald a missed bladder injury. As with most traumatic injuries in the abdominal cavity, having a high index of suspicion is initially necessary to pursue the appropriate diagnostic evaluation, and we feel that a disproportionate acidosis is a highly sensitive marker of bladder injury. As previous studies have shown, signs and symptoms of bladder injury may be very difficult to discern or absent in the multi-injured trauma patient, and relying on the CT scan for diagnosis is an unreliable approach, especially if delayed cuts through the bladder are not routinely performed [13, 14]. In addition, the patient will not initially complain of an inability to urinate, abdominal distension will not occur immediately, and, as mentioned previously, hematuria may be absent. There were five patients (18%) in the current study in which the diagnosis was missed in the emergency department, despite having a CT scan of the pelvis. This was due to a combination of factors, including insufficient (or no) contrast in the bladder during the scan, neurological and respiratory issues requiring urgent intervention, initial mild hematuria that was felt to be improving, and, for lack of a better explanation, the chaotic environment of the emergency department. Interestingly, the BUN, creatinine, and potassium levels were not helpful in identifying the diagnosis. There have been several manuscripts that have described patients with bladder rupture consistently having elevated serum BUN and creatinine levels, and it is true that this will occur eventually if the injury is not treated expeditiously [15, 16]. However, in sophisticated trauma systems, we consider a ‘‘missed injury’’ to be any that are not diagnosed in the trauma bay; therefore, not enough time will elapse for the BUN and creatinine to sufficiently rise in the blood
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stream for these parameters to be helpful. However, as shown by our results, hydrogen ions will rapidly move across the peritoneum and produce an acidosis that is significant and obvious within the time frame of the first or secondary survey, and long before the patient leaves the emergency department. This study is limited by its retrospective nature and the fact that only 17 of the 45 patients in the matched cohort had blood gas analysis performed on arrival. This creates a selection bias since laboratory data were not available on all of the patients with a pelvic fracture and without bladder rupture. In conclusion, disproportionate acidosis in the trauma patient is a sensitive indicator of bladder injury, especially in any patient with a pelvic fracture or hematuria. Fully resuscitated patients with persistent acidosis and an appropriate mechanism should be evaluated for bladder injury.
Conflict of interest statement The authors declare that there is no actual or potential conflict of interest in relation to this article.
References 1.
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4.
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Shah PM, Kim K, Ramirez-Schon G, Reynolds BM. Elevated blood urea nitrogen: an aid to the diagnosis of intraperitoneal rupture of the bladder. J Urol 1979;122:741–3. Heyns CF, Rimington PD. Intraperitoneal rupture of the bladder causing the biochemical features of renal failure. Br J Urol 1987;60:217–22. Quagliano PV, Delair SM, Malhotra AK. Diagnosis of blunt bladder injury: a prospective comparative study of computed tomography cystography and conventional retrograde cystography. J Trauma 2006;61:410–22. Haas CA, Brown SL, Spirnak JP. Limitations of routine spiral computed tomography in the evaluation of bladder trauma. J Urol 1999;162:51–2. Deck AJ, Shaves S, Talner L, Porter JR. Current experience with computed tomographic cystography and blunt trauma. World J Surg 2001;25:1592–6.
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Deck AJ, Shaves S, Talner L, Porter JR. Computerized tomography cystography for the diagnosis of traumatic bladder rupture. J Urol 2000;164:43–6. 7. Hsieh CH, Chen RJ, Fang JF, Lin BC, Hsu YP, Kao JL, Kao YC, Yu PC, Kang SC. Diagnosis and management of bladder injury by trauma surgeons. Am J Surg 2002;184:143–7. 8. Rehm CG, Mure AJ, O’Malley KF, Ross SE. Blunt traumatic bladder rupture: the role of retrograde cystogram. Ann Emerg Med 1991;20:845–7. 9. Morey AF, Iverson AJ, Swan A, Harmon WJ, Spore SS, Bhayani S, Brandes SB. Bladder rupture after blunt trauma: guidelines for diagnostic imaging. J Trauma 2001;51:683–6. 10. Ziran BH, Chamberlin E, Shuler FD, Shah M. Delays and difficulties in the diagnosis of lower urologic injuries in the context of pelvic fractures. J Trauma 2005;58:533–7. 11. Guyton AC, Hall JE, eds. Textbook of medical physiology, 11th edn. Philadelphia: Saunders, 2005. 12. Waniewski J. Transit time, residence time, and the rate of approach to steady state for solute transport during peritoneal dialysis. Ann Biomed Eng 2008;36:1735–43. 13. Corriere JN Jr, Sandler CM. Diagnosis and management of bladder injuries. Urol Clin North Am 2006;33:67–71. 14. Miller PR, Croce MA, Bee TK, Malhotra AK, Fabian TC. Associated injuries in blunt solid organ trauma: implications for missed injury in nonoperative management. J Trauma 2002;53:238–42. 15. Mokoena T, Naidu AG. Diagnostic difficulties in patients with a ruptured bladder. Br J Surg 1995;82:69–70. 16. Sullivan MJ, Lackner LH, Banowsky LH. Intraperitoneal extravasation of urine. BUN-serum creatinine disproportion. JAMA 1972;221:491–2.
Address for Correspondence John Alfred Carr, MD, FACS Division of Trauma Surgery 7 West Hurley Medical Center One Hurley Plaza Flint MI 48503 USA Phone (+1-810) 257-9355, Fax 762-6341 e-mail: [email protected]
Eur J Trauma Emerg Surg 2010 Æ No. 4
European Journal of Trauma and Emergency Surgery
Disproportionate Acidosis After Traumatic Bladder Rupture: A Case-Control Study Subhash Reddy1, John A. Carr2
Abstract Background: Traumatic bladder injury is rare and often missed on initial evaluation. We sought to identify early markers of bladder injury with a high sensitivity. Methods: A retrospective review from 1999 to 2008. Results: There were 28 patients diagnosed with traumatic bladder injury. The most common mechanism was car accidents with pelvic fractures. 93% (26) of the patients presented with significant metabolic acidosis, without evidence of hemorrhagic shock. For intra- and extraperitioneal bladder ruptures, the mean hemoglobin level on arrival was 12.4 + 2.0 (range 9.0–16.0) and 11.4 + 1.9 (range 8.2–14.7). The average pH on arrival for intraperitoneal ruptures was 7.22 + 0.16 (range 6.86–7.37) and for extraperitoneal ruptures, 7.22 + 0.16 (range 6.85–7.37). The pH improved in all patients with intraperitoneal rupture after surgical repair, up to a mean of 7.27 + 0.11 (range 7.06–7.36, p = 0.5) within 12 h. Extraperitoneal ruptures recovered more quickly with a pH after catheter drainage of 7.34 + 0.04 (range 7.27–7.37, p = 0.1) within 12 h. The ISS for intraperitoneal and extraperitoneal ruptures were similar, 30 + 12 (range 13–57) and 32 + 13 (range 13–57, p = 0.7). A cohort of trauma patients, matched by ISS, age, and pelvic fracture, but without bladder rupture, was used for comparison. Their mean ISS was 30 + 10 (range 14–57). The average pH for this group on arrival was 7.33 + 0.11 (range 7.16–7.42), and 47% of these patients had a normal pH. There was a significant difference between the pH on arrival in the ruptured compared to the nonruptured cohort (intraperitoneal pH 7.22, p = 0.008, extraperitoneal pH 7.22, p = 0.02). Three patients died (mortality 10.7%).
Conclusions: Disproportionate acidosis in the trauma patient is a sensitive indicator of bladder injury, especially with a pelvic fracture or hematuria. Fully resuscitated patients with persistent acidosis and an appropriate mechanism should be evaluated for bladder injury. Key Words Bladder rupture Æ Bladder injury Æ Pelvic fracture Æ Acidosis Eur J Trauma Emerg Surg 2010;36:361–8 DOI 10.1007/s00068-009-9133-x
Introduction Traumatic bladder rupture was historically diagnosed by the previously well-known triad of gross hematuria, pelvic fracture, and an appropriate biochemical profile, with elevated blood urea nitrogen (BUN) and creatinine [1, 2]. This has fallen out of general knowledge due to the widespread use of screening computed tomography (CT) to evaluate every blunt abdominal trauma patient. While retrograde cystography remains the gold standard, with sensitivity and specificity rates of 95–100 and 100%, respectively, CT scanning has supplanted cystography due to rapid availability and ease of performance [3, 4]. In many trauma centers, retrograde CT cystography has replaced the conventional retrograde cystogram due to equally high sensitivity and specificity rates [3]. However, the overall sensitivity of CT when it is used to diagnose traumatic bladder injury ranges
1
Department of Surgery, Michigan State University, Lansing, MI, 48912, USA, 2 Division of Trauma Surgery, Flint, MI, 48503, USA. Presented at the 56th Annual Meeting of the Michigan Chapter of the American College of Surgeons, Shanty Creek Resort, Bellaire, MI. Received: July 13, 2009; revision accepted: September 17, 2009; Published Online: November 21, 2009
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widely, from 60 to 100%, with poor results in classifying both intraperitoneal (80% accuracy) and extraperitoneal (55% accuracy) [3–7]. This is because a standard CT scan of the abdomen and pelvis performed with intravenous contrast to evaluate a trauma patient does not include the necessary retrograde filling of the bladder with 300 cc of contrast to fully distend and evaluate the bladder. This can result in ‘‘missed’’ injuries or delays in diagnosis, especially since 6–19% of patients with bladder rupture will not have gross hematuria (although all have microscopic hematuria) [7, 8]. Furthermore, trauma patients with multiple other injuries and a suspected bladder rupture may actually have a retrograde cystogram performed less than half the time [7]. This is understandable when considering that a significant percentage of these patients will require emergency neurosurgical or orthopedic procedures that take precedent, or will have a CT finding of free fluid in the abdomen that leads to an emergency laparotomy. Regardless, the retrograde cystogram or CT cystogram is not a commonly performed procedure in the emergency setting unless the patient presents with gross hematuria. Moreover, gross hematuria alone is not indicative of a traumatic bladder rupture, since other injuries also cause this, including renal injury. However, the combination of a pelvic fracture and gross hematuria should greatly increase suspicion [9]. Interestingly, in the context of isolated traumatic pelvic fractures with urologic injury of any type, 23% were initially missed, with a delay in diagnosis of 19 h for intraperitoneal bladder ruptures and 6.7 days for extraperitoneal ruptures [10]. Thus, traumatic bladder rupture is not a straightforward diagnosis in the multi-injured patient. Our personal experience has been that the BUN and creatinine were not dramatically elevated initially so as to raise suspicion of a bladder injury. However, our anecdotal experience has been that all of these patients are profoundly acidotic due to reabsorption of excreted hydrogen ions in the urine. We decided to perform a retrospective study of our experience with traumatic bladder rupture and determine if the presence of significant acidosis after resuscitation could be used as a sensitive indicator of the diagnosis prior to imaging, and as a red flag that may signal the need for a retrograde CT cystogram.
Methods We performed a retrospective review of our prospectively collected trauma registry at Hurley Medical
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Center, a Level 1 trauma center in central Michigan. The review included all trauma patients with bladder rupture or perforations from 1999 to 2008. Inclusion criteria were blunt traumatic injury to the abdomen or penetrating injury with bladder rupture. Patients with renal or ureteral injuries, iatrogenic injuries, and preexisting renal disease were excluded. Patients were divided into two groups: intraperitoneal bladder perforation (IBP) and extraperitoneal bladder perforation (EBP). The two groups were compared with regard to age, sex, mechanism of injury, hemodynamic parameters at presentation, diagnostic modalities, electrolytes, arterial blood gas (ABG) profiles at various intervals, time of actual intervention (surgical or catheter drainage), and discharge status. Within each of these two groups, the electrolyte profile, BUN, creatinine, and the ABG profiles from time of presentation until 48 hours after actual intervention were collected and compared. We used our trauma registry to accrue a similar cohort of trauma patients for comparison who were matched by three criteria: injury severity score (ISS), age, and the presence of a pelvic fracture without bladder injury. We surveyed our database of over 1,050 patients with similar mechanisms of injury and found 45 matching patients. Of these 45, only 17 of them had a blood gas analysis performed on arrival, and these data were used for the comparison. In addition, the pH and base deficits were compared between all groups. Base deficit was plotted in addition to pH, since the pH could be low secondary to respiratory insufficiency with retained CO2. To ensure accuracy, the logarithmic conversion of the pH into hydrogen ion concentration was also used for statistical analysis. If bladder injury was diagnosed after the patient left the emergency room (ER), it was defined as a delay in diagnosis. The pH, base deficit, BUN, creatinine, and potassium were graphed from the time of arrival to 48 h later to show the trends. If a patient lacked a specific time data point, the other data points were used to extrapolate the curve. Not every patient’s data were charted to avoid overcrowding the graph; rather, a random sample of the data was plotted to show a representative trend. This study was approved by the Institutional Review Board of Hurley Medical Center prior to its initiation. Since the data was found to be normally distributed, we used a two-tailed Student’s t test with equal variance for statistical analysis. All values are expressed as the mean ± standard deviation (SD), and a p value of less than 0.05 was considered significant.
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Categorical data were compared using v2 with or without Yate’s correction or Fisher’s exact test.
Results From 1999 to 2008, there were 28 patients diagnosed with traumatic bladder rupture. Fifteen were men and 13 were women. There were 13 intraperitoneal ruptures, 13 extraperitoneal ruptures, and two patients had combined intra- and extraperitoneal ruptures. Twentyfive of the patients (89%) were in automobile accidents and had concomitant pelvic fractures. A single patient, who also had a pelvic fracture, was crushed against a brick wall for a total association between bladder injury and pelvic fracture of 93%. Only two patients did not have associated pelvic fractures: one had a gun shot wound and one patient had a tree fall across his abdomen. None of the patients had a medical history of renal disease. The diagnosis was suspected on the initial CT scan in 21 (75%) and confirmed by retrograde cystography. The diagnosis was initially missed and detected later in five patients (18%). The single patient who was shot and the one patient involved in a car accident who was unstable were diagnosed in the operating room at the Figure 1. Trends of the blood urea nitrogen levels after intraperitoneal rupture.
time of laparotomy. All patients with intraperitoneal ruptures, the two patients with intra- and extraperitoneal ruptures, and one large extraperitoneal rupture were all repaired surgically with a two-layered closure. The remaining extraperitoneal tears were treated with catheter drainage only. The serum BUN and creatinine on arrival were not abnormally high so as to alert the clinician to possible bladder rupture. This was true for both the intra- and extraperitoneal ruptures. The mean BUN/creatinine for intra- and extraperitoneal ruptures, respectively, on presentation were 17 ± 7 (range 8–36)/1.4 ± 0.5 (range 0.6–2.2) and 15 ± 5 (range 7–23)/1.4 ± 0.6 (range 0.8–2.9). After surgical repair of the intraperitoneal ruptures, both the BUN and creatinine significantly decreased to a mean of 10 ± 4 (p = 0.05) and 0.9 ± 0.2 (p = 0.007) within 12 h. However, with extraperitoneal ruptures, there was no significant change noted (BUN 15 ± 7, p = 0.9 and creatinine 1.1 ± 0.5, p = 0.4) within 12 h after catheter drainage was initiated. See Figures 1, 2, 3, 4. Similarly, the serum potassium was not abnormal on presentation and did not change significantly after intervention. The mean level on arrival for intra- and extraperitoneal ruptures was 3.8 ± 0.5 (range 2.4–4.8)
Intraperitoneal- BUN
30.0
Patient 1 Patient 2 Patient 3 Patient 4 Patient 5 Patient 6 Patient 7 Patient 8
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24-36
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Hours From Injury Figure 2. Trends of the blood urea nitrogen levels after extraperitoneal rupture.
Extraperitoneal- BUN
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Figure 3. Trends of the creatinine levels after intraperitoneal rupture.
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Creat
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Hours From Injury Figure 4. Trends of the creatinine levels after extraperitoneal rupture.
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and 4.2 ± 0.9 (range 3.3–6.0). After repair or catheter drainage, the mean levels within 12 h were 4.3 ± 0.9 (p = 0.1) and 4.5 ± 1.1 (p = 0.6) and did not change significantly thereafter. In contrast, 93% (26) of the patients presented with significant metabolic acidosis, without evidence of hemorrhagic shock. Granted, the pelvic fractures did cause various degrees of hematoma formation within the endopelvic fascia, but initial hemoglobin levels and repeat levels after hydration did not fully account for the initial acidosis in the majority of patients. For intra- and extraperitoneal bladder ruptures, the mean Figure 5. Trends of the hemoglobin levels after intraperitoneal rupture.
Hgb
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hemoglobin level on arrival was 12.4 ± 2.0 (range 9.0– 16.0) and 11.4 ± 1.9 (range 8.2–14.7). After hydration and resuscitation, the levels were 11.7 ± 2.0 (range 8.0– 14.2, p = 0.3) and 10.5 ± 1.9 (range 7.1–13.8, p = 0.3). The hemoglobin levels did not fluctuate significantly after repair (see Figures 5, 6). The average pH on arrival for intraperitoneal ruptures was 7.22 ± 0.16 (range 6.86–7.37). For extraperitoneal ruptures, the mean value was exactly the same at 7.22 ± 0.16 (range 6.85–7.37). The pH improved in all patients with intraperitoneal rupture after surgical repair, up to a mean of 7.27 ± 0.11 (range 7.06–7.36, p = 0.5)
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Figure 6. Trends of the hemoglobin levels after extraperitoneal rupture.
Extraperitoneal- Hemoglobin
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within 12 h. Mean values at 12–24, 24–36, and 36–48 h after surgery were 7.33 ± 0.09 (p = 0.2), 7.40 ± 0.07 (p = 0.004), and 7.40 ± 0.04 (p = 0.005). Patients with extraperitoneal ruptures recovered more quickly, with a mean value after catheter drainage of 7.34 ± 0.04 (range 7.27–7.37, p = 0.1) within 12 h. Mean values at 12–24, 24–36, and 36–48 h after catheter drainage were 7.38 ± 0.06 (p = 0.05), 7.39 ± 0.06 (p = 0.02), and 7.43 ± 0.05 (p = 0.006). As the graphs show (Figures 7, 8), fluid resuscitation prior to intervention did improve the pH initially in most (but not all) patients. However, it was not Figure 7. Trends of the pH after intraperitoneal rupture.
0-12
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24-36
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until after the intervention, surgery or catheter drainage, that the pH normalized. To ensure accuracy, the pH values underwent logarithmic conversion to hydrogen ion concentration and the statistical analysis was repeated. The results remained statistically valid. After repair of intraperitoneal ruptures, the mean hydrogen ion concentration in the patients’ sera decreased to 5.6·10–8 ± 1.6·10–8 (p = 0.5) within 12 h. Mean values at 12–24, 24–36, and 36–48 h after surgery were 4.7·10–8 ± 1.0·10–8 (p = 0.2), 4.0·10–8 ± 6.8·10–9 (p = 0.02), and 4.0·10–8 ± 3.4·10–9
Intraperitoneal- pH 750
pH
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700 690 Arrival
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Hours From Injury Figure 8. Trends of the pH after extraperitoneal rupture.
Extraperitoneal- pH 750
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(p = 0.03). After drainage of extraperitoneal ruptures, the mean hydrogen ion concentration decreased to 4.6·10–8 ± 4.7·10–9 (p = 0.2) within 12 h. Mean values at 12–24, 24–36, and 36–48 h after surgery were 4.2·10–8 ± 5.6·10–9 (p = 0.1), 4.1·10–8 ± 6.1·10–9 (p = 0.05), and 3.7·10–8 ± 4.8·10–9 (p = 0.04). The base deficit trends mirrored the pH as expected for both groups. On arrival, the base deficit for intra- and extraperitoneal ruptures was –10 ± 5 (range –4 to –20) and –9 ± 7 (range –1 to –24). Within 12 h after surgery, the mean base deficit for intraperitoneal ruptures was –9 ± 5 (p = 0.8). The extraperitoneal ruptures recovered more quickly, with the mean base deficit within 12 h improving to –5 ± 3 (p = 0.2). The mean values for the intraperitoneal ruptures at 24–36 and 36–48 h after surgery were –1 (p = 0.001) and 1 (p = 0.003). For the extraperitoneal injuries, the mean values at 24–36 and 36–48 h were –3 (p = 0.02) and –1 (p = 0.02). See figures 9 and 10. The ISS for intraperitoneal and extraperitoneal ruptures were the same on average, 30 ± 12 (range 13– 57) and 32 ± 13 (range 13–57, p = 0.7), respectively. A similar cohort of trauma patients, matched by type of pelvic fracture, ISS and age, but without bladder rupFigure 9. Trends of the base deficits after intraperitoneal rupture.
Base Def
3.0 0.0
ture, were then used for comparison. Their mean ISS was 30 ± 10 (range 14–57). The mean pH for this group on arrival was 7.33 ± 0.11 (range 7.16–7.42), and 47% of these patients had a normal pH on arrival (normal range 7.35–7.45). There was a statistically significant difference between the pH on arrival in the bladder rupture patients, both intraperitoneal and extraperitoneal, compared to the nonruptured cohort (intraperitoneal pH 7.22, p = 0.008, extraperitoneal pH 7.22, p = 0.02, Figure 11). ROC analysis for pH is shown in Figure 12. At a pH below 7.31, the sensitivity to detect bladder rupture is 78% and the specificity is 59%. Three patients died (mortality 10.7%) within the 30-day postoperative or postaccident period from multisystem organ failure. Five patients were discharged home and the remaining twenty patients were sent to rehabilitation centers.
Discussion Any laboratory textbook will cite an average urine pH range of 4.5 to 8.0. However, within this wide range, most urine samples will have an acidic pH of around 6.0 [11]. Thus, it is easy to understand how a large
Intraperitoneal- Base Deficit Patient 1 Patient 2 Patient 3 Patient 4 Patient 5 Patient 6 Patient 7
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Hours From Injury Figure 10. Trends of the base deficits after extraperitoneal rupture.
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7.5 7.45 7.4 7.35 7.3 7.25 7.2 7.15 7.1 7.05 7
7.33 (+/- 0.11)
7.22 (+/- 0.05) 7.22 (+/- 0.05)
Arrival
Control (n=17)
IP
EP
Figure 11. Difference in arrival pH between patients with bladder rupture and controls.
Sensitivity - 78% at pH 7.31, 100% at pH 7.27 Specificity - 59% at pH 7.31, 100% at pH 7.13 pH 100
Sensitivity
80
60
40
20
0 0
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100-Specificity Figure 12. ROC analysis.
amount of urine pouring into the abdominal cavity could quickly induce a profound metabolic acidosis. Hydrogen ions in the urine are quickly absorbed across the peritoneum, with a mean transit time of only 20 min [12]. This would allow the trauma patient to become significantly acidotic within the time it takes to transport the patient from the accident scene to the hospital. As mentioned in our results, almost all of these patients were significantly acidotic on arrival. When comparing the group with bladder rupture to our matched ISS cohort with pelvic fractures but without bladder rupture, we found a statistically significant difference, with a much more profound acidosis occurring in the group with bladder rupture despite similar fracture patterns, age, ISS, and hemoglobin levels. It would be easy to argue that the majority of trauma patients with a high ISS would be acidotic on presentation secondary to a combination of blood loss and shock; however, as our results show, those
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with bladder rupture had a much more significant acidosis on arrival than their counterparts without bladder injury, and the majority of patients were not anemic on arrival. The finding of a significant acidosis with a normal hemoglobin level should become a red flag for bladder rupture when evaluating a trauma patient, especially if the acidosis persists after resuscitation. While a few of the patients in this series did have an initial mild improvement in their acidosis after fluid resuscitation, most did not, and their pH did not normalize until after surgery or catheter drainage. This is the first study to document this finding, which should allow an earlier radiological investigation of the bladder on arrival. It also has implications for trauma centers that accept a large number of patients in transfer, as a persistent acidosis will herald a missed bladder injury. As with most traumatic injuries in the abdominal cavity, having a high index of suspicion is initially necessary to pursue the appropriate diagnostic evaluation, and we feel that a disproportionate acidosis is a highly sensitive marker of bladder injury. As previous studies have shown, signs and symptoms of bladder injury may be very difficult to discern or absent in the multi-injured trauma patient, and relying on the CT scan for diagnosis is an unreliable approach, especially if delayed cuts through the bladder are not routinely performed [13, 14]. In addition, the patient will not initially complain of an inability to urinate, abdominal distension will not occur immediately, and, as mentioned previously, hematuria may be absent. There were five patients (18%) in the current study in which the diagnosis was missed in the emergency department, despite having a CT scan of the pelvis. This was due to a combination of factors, including insufficient (or no) contrast in the bladder during the scan, neurological and respiratory issues requiring urgent intervention, initial mild hematuria that was felt to be improving, and, for lack of a better explanation, the chaotic environment of the emergency department. Interestingly, the BUN, creatinine, and potassium levels were not helpful in identifying the diagnosis. There have been several manuscripts that have described patients with bladder rupture consistently having elevated serum BUN and creatinine levels, and it is true that this will occur eventually if the injury is not treated expeditiously [15, 16]. However, in sophisticated trauma systems, we consider a ‘‘missed injury’’ to be any that are not diagnosed in the trauma bay; therefore, not enough time will elapse for the BUN and creatinine to sufficiently rise in the blood
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stream for these parameters to be helpful. However, as shown by our results, hydrogen ions will rapidly move across the peritoneum and produce an acidosis that is significant and obvious within the time frame of the first or secondary survey, and long before the patient leaves the emergency department. This study is limited by its retrospective nature and the fact that only 17 of the 45 patients in the matched cohort had blood gas analysis performed on arrival. This creates a selection bias since laboratory data were not available on all of the patients with a pelvic fracture and without bladder rupture. In conclusion, disproportionate acidosis in the trauma patient is a sensitive indicator of bladder injury, especially in any patient with a pelvic fracture or hematuria. Fully resuscitated patients with persistent acidosis and an appropriate mechanism should be evaluated for bladder injury.
Conflict of interest statement The authors declare that there is no actual or potential conflict of interest in relation to this article.
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Address for Correspondence John Alfred Carr, MD, FACS Division of Trauma Surgery 7 West Hurley Medical Center One Hurley Plaza Flint MI 48503 USA Phone (+1-810) 257-9355, Fax 762-6341 e-mail: [email protected]
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