ANNALS OF SURGERY Vol. 227, No. 6, 861-869 © 1998 Lippincott-Raven Publishers

Diagnosis and Initial Management of Blunt Pancreatic Trauma Guidelines From a Multiinstitutional Review

Edward L. Bradley 111, MD,* Peter R. Young, Jr., MD,t Michael C. Chang, MD,t James E. Allen, MD,* Christopher C. Baker, MD,t Wayne Meredith, MD,t Larry Reed, MD,§ and Michael Thomason, MDII

From the State University ofNew York at Buffalo, Buffalo, New York;* Bowman Gray School of Medicine, Winston-Salem, North Carolina;t University ofNorth Carolina School of Medicine, Chapel Hill, North Carolina;t Duke University School of Medicine, Durham, North Carolina;§ and Carolinas Medical Center, Charlotte, North Carolinall

Objective Patients requiring delayed surgical intervention after an un- The authors' objective was to resolve the current controver- successful period of observation demonstrated notably sies surrounding the diagnosis and management of blunt higher -specific mortality and morbidity rates, pancreatic trauma (BPT). principally because of the incidence of unrecognized inju- ries to the MPD. Although detection of MPD by Summary Background Data computed tomography was no better than flipping a coin, The diagnosis of BPT is notiously difficult: serum amylase has endoscopic pancreatography was accurate in each of the been claimed to be neith sensitsve nor specific, and recent anec- five cases in which it was used. dotal reports have suggested a role for computed tomography. The therapy of BPT has been controversial, with some suggesting selec- tive obsevation and others advocating immediate exploration to prevent a delay-induced escalation in morbidity and death. Conclusions The principal cause of pancreas-specific morbidity after BPT Methods is to the MPD. Parenchymal pancreatic injuries not in- The authors conducted a retrospective chart review of docu- volving the ductal system rarely result in pancreas-specific mented BPT from six institutions, using a standardized binary morbidity or death. Delay in recognizing MPD injury leads to data form composed of 187 items and 237 data fields. increased mortality and morbidity rates. CT is unreliable in diagnosing MPD injury and should not be used to guide ther- Results apy. Initial selection of patients with isolated BPT for observa- A significant correlation between pancreas-specific morbid- tion or surgery can be based on the determination of MPD ity and injury to the main (MPD) was noted. integrity.

Although more than 170 years have passed since the first particular, serum amylase has been claimed to be neither description of a pancreatic injury from ,l prob- sensitive nor specific for pancreatic trauma,2 and anecdotes lems in diagnosis and management remain. The diagnosis of of complete pancreatic transection defying clinical recogni- a blunt pancreatic injury can be difficult. Physical signs may tion for many days have been described.35 be absent, and laboratory findings are often nonspecific. In Even when the diagnosis of blunt pancreatic injury is suspected, opinions differ regarding the optimal form of management. Based on the successful nonoperative man- Presented at the 109th Annual Meeting of the Southern Surgical Associa- agement of other solid injuries, various workers have tion, November 30 to December 3, 1997, the Homestead, Hot Springs, recommended nonoperative therapy for the management of Virginia. blunt pancreatic trauma (BPT), abandoning this conserva- Address reprint requests to Edward L. Bradley III, MD, Chief of Surgery, Buffalo General Hospital, 100 High St., Buffalo, NY 14203. tive course only in patients developing or clinical Accepted for publication December 1997. deterioration.3,6-8 In direct opposition to this selective ap- 861 862 Bradley and Others Ann. Surg. - June 1998

proach, others have advocated prompt operative interven- pancreatic trauma was graded according to the system of tion in patients with suspected pancreatic injury to prevent Booth and Flint18: grade I (contusion), grade II (laceration the well-recognized delay-induced escalation in morbidity <50% not involving the main pancreatic duct [MPD]), and mortality rates.49-11 grade III (MPD injury), and grade IV (extensive crush Because the prevalence of pancreatic injuries is low (only injury involving the MPD). The magnitude of systemic 1 of 250,000 hospital admissions),'2"3 few surgeons or injury was quantified by the Injury Severity Score.19 Pan- institutions can accumulate the breadth of experience nec- creas-specific mortality (PSM) and pancreas-specific com- essary to address these persisting clinical questions. Adding plications (PSC) were defined as those solely attributable to to the uncertainty, previous reports of BPT have been re- the pancreatic injury. stricted to operative- or autopsy-proved cases,3'4 14-17 Statistical analysis of the collected data was performed thereby not only minimizing the clinical problem of diag- using the Stratified Program for Social Sciences (SPSS) nosis but also introducing a severity bias into recommen- package. Univariate nonparametric tests of significance dations for therapy. The current report is the product of a were used, including the Pearson correlation coefficient, the multiinstitutional study designed to increase the population chi square test, and the Mann-Whitney test. Multivariate of patients with BPT to address these vexing issues in analysis was also carried out using logistic regression to diagnosis and initial management. identify independently significant variables. Statistical sig- nificance was set at p < 0.05. PATIENTS AND METHODS This study resulted from a collaborative initiative be- RESULTS tween the Department of Surgery of the State University of New York at Buffalo and the North Carolina State Trauma Demographics Registry. Participating institutions from the Registry in- The 101 patients with documented BPT included 61 male cluded the Bowman Gray School of Medicine, Carolinas patients and 40 female patients with an average age of Medical Center, Duke University School of Medicine, and 27.9 ± 19.8 years (range, 2 to 95 years). The average Injury the of North University Carolina School of Medicine. Severity Score was 18.9 ± 14.1. The overall mortality rate Charts from each of the institutions with ICD-9-CM codes was 18.1% (18 of 101), including 2 patients who died in the for pancreatic injuries resulting from blunt abdominal emergency department shortly after arrival; however, only 5 trauma to (863.81 863.84; 863.91 to 863.94) were consid- of the deaths (27.7%) could be attributed solely to the ered for review. Chart review was standardized using a pancreatic injury. Pancreatic injury resulted from motor specifically designed binary data form composed of 187 vehicle accidents in 53 of the 101 patients 25 items (52.4%), of with 237 data fields. Included in these data fields were whom were restrained by seat belts. Nonvehicular accidents demographic information, injury mechanisms, history and were responsible for 31 injuries and violence for 17. Injury physical vital findings, sign information, admission and to the pancreas was solitary in 42 cases (41.5%) and com- subsequent laboratory values, imaging studies, and hospital bined with 87 other organ injuries in the remaining 59 course information, including surgical findings where avail- patients (1.4 organ injuries/patient) (Table 1). able. There were 51 grade I injuries, 18 grade II, 30 grade III, To evaluate recent innovations in diagnosis and therapy, and 2 grade IV. The frequency of MPD was, therefore, only patients seen from 1988 to 1996 were entered into the 31.7% (32/101). Contusions and pancreatic lacerations not One hundred six study. patients meeting these criteria were involving the duct accounted for most of identified the pancreatic from the participating institutions during this injuries in this series (68.3%; 69 of 101). 9-year period. Chart review failed to support the hospital- assigned diagnosis of BPT in 5 patients, leaving 101 cases for analysis. Clinical Findings Documentation of the existence of a pancreatic injury in 76 of these patients was by direct observation at surgery (73 Abdominal pain was noted in 78.5% of cases; when cases) or autopsy (3 cases). Computed tomographic (CT) present, it was most often either diffuse (38%) or epigastric findings constituted evidence for pancreatic trauma in 22 (23.6%). Bowel sounds were present at initial contact in additional patients. Tomographic criteria included unequiv- 45.5% of patients. Abdominal tenderness existed in 79.5% ocal pancreatic swelling, with or without evidence of of cases and was most often diffuse (45%). Rebound ten- peripancreatic fluid or parenchymal disruption. In the re- derness was unusual, present initially in only 9.9% of cases. maining three cases, a clinical diagnosis of pancreatic Abdominal wall ecchymoses were present in 34.6%, most trauma was made from a typical history of steering wheel commonly over the epigastrium. Neither these nor other trauma to the upper associated with abdominal individual clinical findings could be correlated with the tenderness and marked hyperamylasemia. grade of pancreatic injury or with the subsequent develop- To stratify the severity of pancreatic injuries for analysis, ment of morbidity or death (p > 0.05). Vol. 227 * No. 6 Blunt Pancreatic Trauma 863

predicted a ductal injury that was not present). Moreover, of Table 1. ASSOCIATED ORGAN INJURIES the 32 cases with operatively proved ductal injuries, CT was Number done in 22. Ductal injury was correctly predicted in only 9 of these 22 patients, resulting in a 42.9% sensitivity for the Number of patients in study 101 prediction of ductal injury by CT. Because true negatives Number with isolated pancreatic were not evaluated in this study, specificity cannot be cal- injury 42 Number with injury to the pancreas culated from these data. and one other organ 31 Endoscopic pancreatography was performed in five pa- Number with injury to the pancreas tients, correctly demonstrating an MPD injury in all five. In and two or more organs 28 four cases, the finding of a ductal injury by pancreatography Specific organ injuries led to abandonment of conservative management and to Spleen 34 26 urgent surgical exploration. In the fifth case, endoscopic 6 pancreatography was done on the operating table when Kidney 6 surgical exploration raised the possibility of an MPD injury. Colon 5 In this patient, the proposed surgical management was al- Stomach 2 tered as a result of the demonstrated ductal disruption. Gallbladder 2 Jejunum 2 Aorta 2 Management Inferior mesenteric vein 1 Ileum 1 Patients were initially separated into two groups based on Total 85 intent to treat: immediate operation (IO; 57 patients) and nonoperative observation (OBS; 42 cases). Pancreatic pro- cedures in the 57 IO patients included drainage alone (24), Laboratory Values distal pancreatectomy (17), exploration without drainage (11), pyloric exclusion (3), and other (2). Pancreas specific Initial serum amylase values were elevated in 73.4% of complications developed in 17 of the 48 (35.4%) at-risk IO the patients. The incidence of hyperamylasemia increased to patients and were as follows: (9), pancre- 89.1% when serial determinations were done. The average atic (5), traumatic (2), and initial value for serum amylase was 176.6 ± 376.4 Somogyi (1). units. Although the average initial hemoglobin level of Of the 42 OBS patients initially managed nonoperatively, 10.2 ± 5.1 g and hematocrit value of 31.3 ± 13.6 were each only 22 (52.3%) successfully completed the nonoperative significantly lower than an age-matched population (p < course. Only 1 of these 22 successfully managed patients 0.01), these findings were not specific for pancreatic injury. had a ductal injury. In contrast, 20 of the 42 OBS patients Moreover, none of the other routine laboratory tests (SMA (47.7%) required delayed operative intervention (DO), and 18, white blood count, and differential) reliably identified 12 of these 20 patients exhibited ductal injuries. Reasons either the existence or grade of a pancreatic injury (p > offered for DO were CT demonstration of duct disruption 0.05). The urinary amylase value was normal in 12 of the 14 (7), clinical deterioration (6), demonstration of MPD injury cases tested (85.7%). Although the serum lipase level was by pancreatography (4), and diagnostic peritoneal lavage elevated (>300 units) in 9 of the 11 cases tested (81.8%), positive for blood (3). the serum amylase level was also increased in each of these Statistical analysis demonstrated marked differences be- 9 patients. tween TO, OBS, and DO patients (Table 2). Of the 187 variables tested, only 8 were found to be significantly dif- Imaging Studies ferent among the three treatment groups. 10 patients were significantly older and had more abdominal pain, fewer Abdominal CT was done in 54 of the 99 surviving pa- bowel sounds, and a higher Injury Severity Score. Isolated tients (54.5%). In 37 of these 54 patients, the presence and pancreatic injury was more common in OBS patients, but severity of the pancreatic injury were verified by surgery or the injury rarely involved the MPD. Both the 10 and DO autopsy. Although pancreatic injury was correctly predicted groups had a significantly higher incidence of MPD injury. by CT in 25 of these 37 proved cases (true positives), CT The increase in pancreas specific mortality in DO patients was falsely positive in 2 patients and falsely negative in 10 approached statistical significance (0.074 vs. TO and 0.062 cases. Accordingly, the overall sensitivity for CT in cor- vs. OBS), as did PSC (0.084 vs. OBS). Of the 11 PSCs in 42 rectly predicting the existence of an unspecified pancreatic OBS patients, 9 (81.8%) occurred in DO cases. injury was 71.4%. Of the 25 proved true positives, however, Most importantly, a significant correlation was found the CT-predicted grade of pancreatic injury was precise in between MPD injury and the subsequent development of only 16: 6 were underestimated (including 3 with MPD PSCs (p = 0.040). Although many variables were signifi- injury not predicted by CT) and 3 were overestimated (CT cantly correlated with PSCs (Table 3), only seven were 864 Bradley and Others Ann. Surg. * June 1998

Table 2. SIGNIFICANT VARIABLES BETWEEN THE TREATMENT GROUPS* Immediate Observation Delayed Surgery Variable Surgery (IS) (OBS) (DS)

Abdominal hemorrhage 0.035vs. DS Abdominal pain 0.019vs. DS 0.038vs. OBS Age 0.002vs. OBS Associated organ injury 0.001 vs. DS Decreased bowel sounds 0.01 2vs. OBS Isolated pancreatic injury 0.004 vs.DS Injury Severity Score 0.001 vs. OBS Main pancreatic duct injury 0.008vs. OBS 0.001 vs.OBS

p values were determined by Mann-Whitney U test and confirmed by chi square analysis. confirmed by multivariate analysis. Not surprisingly, the third of these admissions for pancreatic injuries occur as a development of a pancreatic fistula was strongly correlated result of blunt trauma.3 When the universe of patients suf- with an MPD injury and was independently correlated with fering blunt is considered, however, the peripancreatic abscess. Peripancreatic were the incidence of pancreatic injury increases to 1 % to principal cause of PSM, required more reoperations, and 2%.3 11,14,20 Despite the hope that the use of seat belts resulted in a significant delay in hospital discharge. Pseudo- would decrease the incidence of BPT,'5 there is no evidence cysts were negatively correlated with the presence of other that this has occurred. organ injuries. The mortality rate for BPT has not appreciably changed during the past 20 years despite revolutionary changes in DISCUSSION general patient management. In earlier reports, the global Pancreatic injuries are uncommon, with a reported prev- mortality rate for BPT ranged from 16% to 20%,3,4,9,1 1 not alence of 0.4 per 100,000 hospital admissions.12,13 Only a appreciably different from the overall 17.8% mortality rate

Table 3. SIGNIFICANT VARIABLES INFLUENCING PANCREAS-SPECIFIC MORBIDITY AND MORTALITY Variable Abscess Fistula Pseudocyst Death

Abdominal ecchymosis 0.019 0.031 Abdominal pain 0.001 Abscess 0.001 t Age 0.001 Albumin 0.001 Amylase 0.001 0.002 0.013(-) Associated organ injury 0.030 0.046 0.009(-)t Creatinine 0.014 Calcium 0.001 Chloride 0.002 Days (surgery to discharge) 0.001 t 0.016 0.002 Glucose 0.025(-) 0.041 Grade pancreatic injury 0.023(-) 0.044(-) Hemoglobin 0.003 Injury severity score 0.001 Lipase 0.001 LDH 0.046 Main pancreatic duct injury 0.01 8t Pancreas-specific mortality 0.003t Rebound tenderness 0.001 0.001 Reoperation required 0.005t 0.025 0.038

- - inverse correlation; LDH = lactic dehydrogenase. p values were derived from univariate chi square analysis. t Significant variable remaining after multivariate logistic regression. Vol. 227 * No. 6 Blunt Pancreatic Trauma 885 observed in this study. Despite popular misconceptions, cidents,3""5 history is not helpful and physical findings are mortality rates for BPT approximate those for penetrating usually nonspecific. pancreatic injury. The overall mortality rate in this series of Diagnostic peritoneal lavage has not proved to be useful blunt pancreatic injuries was not significantly less than the in diagnosing a significant injury to the pancreas. Several 19% mortality rate observed in penetrating pancreatic trau- cases of complete transection of the pancreas have been ma.17 As noted by previous investigators, ,20,21 the princi- described with normal lavage findings.4'26 Failure of lavage pal cause of early death after BPIT is related to the presence to recognize pancreatic injury has been attributed to the of associated injuries, particularly vascular injuries; late anatomic liabilities of the retroperitoneal location and lim- death arises largely from pancreatic complications. Of the ited access of lavage fluid to the lesser sac. 18 deaths in the current series, only 5 were attributed to Serum amylase has been claimed to be neither sensitive pancreatic causes; 4 of these 5 deaths occurred in the IO nor specific in the diagnosis of pancreatic injury.2 This group. opinion seems to have been based primarily on anecdotal Similarly, the frequency of PSCs (abscess, fistula, observations that serum amylase was normal in a few pa- pseudocyst, necrosis) has also been largely unchanged dur- tients with complete transection of the gland9" 6 and that ing this same period. PSCs occurred in 28 of 83 at-risk amylase has often been elevated in patients with blunt In a col- patients (33.7%) in this series versus 30% of the at-risk abdominal trauma who recovered spontaneously.2 literature including more than 400 cases in an earlier study.23 The observation that both mor- lective review of the cases, we found that the initial serum amylase level was tality and morbidity rates from BPT have not kept pace with elevated in 82% of patients with documented pancreatic innovations in supportive care suggests that we have either after blunt 3,4,11,21,27-2 arrived at an irreducible number of complications, or that a injuries trauma. '' 129 Moreover, Tak- presence of hyperamy- fundamental change in approach to these lesions is needed. ishima et al.30 observed that the lasemia after blunt pancreatic trauma is time-dependent: an It has become increasingly clear that the principal cause elevated serum amylase level was present in all their pa- of PSC and PSM is the presence of an injury to the pancre- tients when the specimen was drawn >3 hours after injury. atic ductal system. In 1971, Bach and Frey9 first proposed In the current study, the serum amylase level at presentation that pancreatic duct disruption was responsible for PSM and was elevated in 73.4% of 79 patients but increased to 89.1% PSC. Although a similar opinion has been subsequently when serial determinations were done. Others have also 122-25 et '7 were the first to voiced by others,' Heitsch al. noted that the prevalence of hyperamylasemia in patients demonstrate a statistically significant increase in the mor- with blunt pancreatic injury increases when serial amylase tality rate when BPT was associated with ductal disruption. determinations are done.9"6 Because hyperamylasemia has Although the current study also demonstrates a significant been observed in more than 75% of patients with blunt correlation between MPD and PSM and PSC, it goes one abdominal trauma and proved pancreatic injury, hyperamy- step further in noting that isolated pancreatic contusions and lasemia should at least be considered a sign of probable minor (nonductal) lacerations rarely result in morbidity or pancreatic injury in the setting of blunt abdominal trauma. death. However, because we also found that hyperamylasemia was A second important cause of increased morbidity from as likely to occur after pancreatic contusion as after ductal BPT can be traced to delay in establishing the diagnosis of laceration, the presence of hyperamylasemia per se cannot pancreatic duct injury. Several groups have suggested that a be used to determine the grade of pancreatic injury or to delay in recognition of a pancreatic duct injury for as little dictate a particular therapeutic approach. Accordingly, we as 24 hours can adversely influence the PSC rate.4" 0 Al- propose that the finding of an elevated serum amylase value though we found a strong trend in the frequency of PSCs in after blunt trauma mandates additional inquiry regarding the patients requiring delayed surgical intervention versus con- nature of the injury to the pancreas. tinued observation (45% vs. 9.1%), this observation did not Despite initial promise, CT has not emerged as a clini- reach statistical significance. Much of this delay can be cally reliable method for either recognition or grading of a attributed to the fact that the diagnosis of pancreatic duct pancreatic injury. Udekwu et al.3' found that the overall injury remains a clinical problem. Because prompt surgical accuracy of dynamic CT for diagnosing pancreatic trauma is intervention is usually undertaken in patients with penetrat- the lowest of all the abdominal organs. Others have found ing injuries or multiple organ involvement, delay in diag- the CT to be "normal" in up to 40% of patients with an nosis of a pancreatic duct injury most commonly occurs in operatively proven pancreatic injury.'3'32'33 Furthermore, patients with blunt abdominal trauma isolated to the pan- because both false-negative and false-positive predictions of creas. Isolated pancreatic trauma occurred in 41.6% of our ductal injury are common,4'34 CT predictions of ductal patients, an incidence higher than previous reports of injury cannot be relied on in an individual patient. We found 3 3,11 33%." that the sensitivity of CT in diagnosing all grades of pan- Aside from a heightened level of clinical suspicion gen- creatic injury was acceptable (71.4%), but its accuracy in erated by the high frequency of pancreatic injuries associ- detecting major ductal injury (grade III or IV) was worse ated with steering wheel compression during vehicular ac- than flipping a coin. Whether this undistinguished record 866 Bradley and Others Ann. Surg. * June 1998 will improve with more frequent use of helical CT scanning survivors were observed in 13 cases of pancreatic trauma or with recently described specialized signs (e.g., the finding treated nonoperatively. Subsequent surgeons have estab- of fluid between the splenic vein and the posterior surface of lished the value of wide anatomic exposure, duodenal mo- the pancreas35) remains to be determined. bilization to rule out duodenal perforation, exploration of Because morbidity and mortality rates for isolated pan- pancreatic hematomas, 9 resection of distal injuries rather creatic trauma are significantly correlated with the presence than drainage,'7 and drainage of proximal injuries rather of a pancreatic duct injury, detection of a duct injury in such than resection.' In a 1990 randomized prospective study patients assumes a pivotal role in initial management. Fur- controlled for severity of injury, Fabian et al.43 demon- thermore, because we and others410 have found that delay strated convincingly that closed suction drainage results in a in recognizing a pancreatic duct injury increases morbidity statistically significant decrease in pancreatic infections ver- and mortality rates, investigation of the ductal system sus sump suction. should be undertaken earlier in the course of possible pan- The value of adjunctive therapies to these surgical prin- creatic injuries. Finally, demonstration of ductal integrity ciples remains uncertain. In a retrospective comparison of 7 becomes even more important in patients with blunt abdom- patients given prophylactic octreotide, Amirata et al.44 inal trauma associated with hyperamylasemia who are being noted fewer complications than in 21 patients not receiving considered for nonoperative management. the agent. However, Nwariaku et al.45 were unable to dem- In 1978, Belohlavek et al.36 performed endoscopic retro- onstrate any significant difference in the incidence of pan- grade pancreatography in two patients with suspected pan- creatic complications between 21 patients given octreotide creatic injuries. Since then, several anecdotal reports have and 55 not given octreotide, when the severity of pancreatic attested to the clinical value of endoscopic pancreatography injury was controlled. We can shed no light on this issue in the recognition of pancreatic duct injuries.37 Of because of the small number of patients in our series re- particular interest were two patients with CT diagnoses of ceiving octreotide, nor can we comment on the claim that "complete disruption" of the pancreas but normal pancre- the number of pancreatic complications can be reduced by atograms. Both patients were managed nonoperatively with the use of fibrin glue.46 Finally, although the routine use of uncomplicated recovery.3438 Barkin et al.,40 in a small cholecystostomy has been advocated in patients undergoing prospective study of the value of endoscopic pancreatogra- exploration for blunt pancreatic injury,14 the physiologic phy in suspected BPT, found pancreatography to be both rationale is unclear, and adjunctive biliary drainage has few sensitive and specific in all five of their patients. Their current advocates. conclusion is supported by the current study, in which a More recently, several workers have questioned a pro- ductal injury was established in each of our five patients grammatic surgical approach toward all pancreatic injuries. undergoing endoscopic pancreatography. Extrapolation of successful nonoperative management of Moreover, the demonstration of ductal disruption in our hepatic and splenic injuries to BPT has been advocated, cases led to a shift from nonoperative treatment to operative principally by pediatric surgeons.6'7'47 Others prefer a more management in four patients. In the fifth case, on-table selective clinical approach, basing the necessity for explo- pancreatography was requested by the operating surgeon to ration on abdominal findings and the overall clinical pic- demonstrate a suspected leak in the head of the gland, and ture.3'8 15 19,27 However, as we and others4"0"'l have shown, resulted in a change in surgical approach. Rupture of the any delay in recognizing an MPD injury results in an pancreatic duct can occur in the face of an intact pancreatic escalation of mortality and morbidity rates. surface.9 Others have also found on-table pancreatography On the basis of our findings, it is reasonable to conclude to be useful,24'41 not only in the diagnosis of ductal injury that nonoperative therapy will be largely successful in pa- but also in eliminating the morbidity associated with duo- tients with hyperamylasemia and isolated pancreatic paren- denotomy or distal pancreatectomy to provide access to the chymal injuries that do not involve the ductal system ductal system for pancreatography. Although it appears that (grades I and II). In contrast, grade III and IV injuries, endoscopic pancreatography is an underused and valuable which involve the MPD, carry the highest risks of PSM and adjunct in the diagnosis and management of suspected BPT, PSCs, risks that increase even further with delay. Accord- it is not universally available, often most notably during the ingly, the optimal approach to patient selection for nonop- early morning hours when trauma is prevalent. Neverthe- erative management of isolated blunt pancreatic injuries less, it seems clear that endoscopic pancreatography de- should be based on demonstration of ductal integrity. We serves wider application in patients with hyperamylasemia propose that endoscopic pancreatography be done in pa- after blunt abdominal trauma, particularly in patients being tients with blunt abdominal trauma in whom there is reason considered for nonoperative management. Detection of duc- to suspect an isolated pancreatic injury, such as hyperamy- tal integrity by magnetic resonance pancreatography is an lasemia or an enlarged pancreas demonstrated on CT. Ob- intriguing possibility that requires further study. servation can be continued in patients with an intact ductal In 1903, Mikulicz42 reported the superiority of operative system, whereas prompt surgical intervention is required for management of pancreatic injuries by demonstrating sur- those with demonstrated MPD disruption. If nonoperative vival in 7 of 11 patients undergoing resection, whereas no management has been selected, however, the frequency of Vol. 227. No. 6 Blunt Pancreatic Trauma 867 duodenal disruption associated with pancreatic trauma man- 9. Bach RD, Frey CF. Diagnosis and treatment of pancreatic trauma. dates that a Gastrografin study be done to rule out a coex- Am J Surg 1971; 121:20-29. isting duodenal perforation. 10. Lucas CE. Diagnosis and treatment of pancreatic and duodenal injury. Surg Clin North Am 1977; 57:49-65. Although magnetic resonance pancreatography also of- 11. Jones RC. Management of pancreatic trauma. Am J Surg 1985; 150: fers the potential for determination of MPD integrity, lim- 698-704. ited experience prevents meaningful evaluation. 12. Nilsson E, Norrby S, Skullman S, Sjodahl R. Pancreatic trauma in a In addition to a short-term increase in morbidity and defined population. Acta Chir Scand 1986; 152:647-665. mortality rates in patients with an unrecognized ductal in- 13. Akhrass R, Kim K, Brandt C. Computed tomography. An unreliable and indicator of pancreatic trauma. Am Surg 1996; 62:647-651. jury delayed surgical intervention, the long-term mor- 14. Wilson RF, Tagett JP, Pucelik JP, Walt AJ. Pancreatic trauma. bidity rate associated with failure to recognize the presence J Trauma 1967; 7:643-651. of a pancreatic duct injury has also been described. Fibrous 15. Walters RL, Gaspard DJ, Germann TD. Traumatic pancreatitis. Am J stricture formation at the site of a pancreatic duct injury can Surg 1966; 111:364-368. result in delayed progressive occlusion of the duct with 16. Jones RC. Management of pancreatic trauma. Ann Surg 1978; 187: upstream dilatation, consequent abdominal pain, and recur- 555-564. 17. Heitsch RC, Knutson CO, Fulton RL, Jones CE. Delineation of critical rent pancreatitis.48-50 Because this "upstream pancreatitis" factors in the treatment of pancreatic trauma. Surgery 1976; 80:523- may occur months to years after the original injury, the 529. diagnosis is often not considered. When diagnosed by pan- 18. Booth FV, Flint LM. Pancreatoduodenal trauma. In Border J, ed. Blunt creatography, posttraumatic duct obstructions are readily multiple trauma. New York: Marcel Dekker; 1990:497-509. managed by decompression or resection of the gland. 19. Baker SP, O'Neill B, Haddon W, et al. The injury severity score. A To improve results in BPIT, we conclude that a funda- method for describing patients with multiple injuries and evaluating emergency care. J Trauma 1974; 14:187-196. mental change in our approach to patients with blunt ab- 20. Davis JJ, Cohn I, Nance FC. Diagnosis and treatment of blunt abdom- dominal trauma and suspected pancreatic injury is neces- inal trauma. Ann Surg 1976; 183:672-678. sary. The development of hyperamylasemia in this setting 21. Cogbill TH, Moore EE, Feliciano DV, et al. Conservative management strongly suggests a pancreatic injury and should serve as an of duodenal trauma. A multicenter perspective. J Trauma 1990; 30: indicator for determination of the integrity of the pancreatic 1469-1475. ductal If no reason 22. Smego D, Richardson J, Flint L. Determinants of outcome in pancre- system. other for exploration exists, atic trauma. J Trauma 1985; 25:771-776. patients can be assigned to continued observation when the 23. Carr ND, Cairns SJ, Lees WR, Russell RCG. Late complications of duct is intact or to urgent surgery when the ductal system pancreatic trauma. Br J Surg 1989; 76:1244-1246. has been breached. 24. Gougeon FW, Legros G, Archambault A, Bessette G, Bastien E. Pancreatic trauma. A new diagnostic approach. Am J Surg 1976; 132:400-402. Acknowledgments 25. Clements RH, Reisser JR. Urgent endoscopic retrograde pancreatog- raphy in the stable trauma patient. Am Surg 1996; 62:446-448. The authors thank Robert Rutledge, MD, the University of North Caro- 26. Thal AP, Wilson RF. A pattern of severe blunt trauma to the region of lina at Chapel Hill, for his assistance in the early stages of planning for this the pancreas. Surg Gynecol Obstet 1964; 119:773-778. study, and to Sharon Rhyne, RN, hospital consultant, North Carolina 27. Yellin AE, Vecchione TR, Donovan AJ. Distal pancreatectomy for Department of Human Resources, for advice and access to the North pancreatic trauma. Am J Surg 1972; 124:135-142. Carolina Trauma Registry database. The authors also thank Saira Hasnain, 28. Berne CJ, Donovan AJ, White EJ, Yellin AE. 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37. Bozymski EM, Orlando RC, Holt JW. Traumatic disruption of the Secondly, Octreotide has been demonstrated to reduce the risk pancreatic duct demonstrated by ERCP. J Trauma 1981; 21:244-245. of complications after elective pancreatic surgery, most notably for 38. Stone A, Sugawa C, Lucas C, Hayward S, Nakamura R. The role of distal pancreatectomies and enucleations. Could you give us your endoscopic retrograde pancreatography in blunt abdominal trauma. approach to the use of octreotide in the trauma setting, and do you Am Surg 1990; 56:715-720. think it has any role? 39. Hall RI, Lavelle MI, Venables CW. Use of ERCP to identify the site of traumatic injuries of the main pancreatic duct in children. Br J Surg Thirdly, I am worried about the widespread application of ERCP 1986; 73:411-412. because of the very real entity of ERCP-induced pancreatitis which 40. Barkin JS, Ferstenberg RM, Panullo W, Manten HD, Davis RC Jr. can be severe and lethal. Are you concerned about the widespread Endoscopic retrograde cholangiopancreatography in pancreatic possibility of use and possible deleterious effect? And do you have trauma. Gastrointest Endosc 1988; 34:102-105. any recommendations for prophylaxis, as there are some sugges- 41. Blind PJ, Mellbring G, Hjertkvist M, Sandzen B. Diagnosis of trau- tions that there may be some drugs to prophylax against ERCP matic pancreatic duct rupture by on-table endoscopic retrograde pan- pancreatitis? creatography. Pancreas 1994; 9:387-389. And, lastly, Ed, in the manuscript I was unclear how the ERCP 42. von Mikulicz-Radecki J. Surgery of the pancreas. Ann Surg 1903; results really influence the outcome? That is, what was actually 38:1-29. 43. Fabian TC, Kudsk KA, Croce MA, et al. Superiority of closed suction done based upon those five positive ERCP's that would have been drainage for pancreatic trauma. A randomized, prospective study. Ann done differently had the patients not had those studies? Surg 1990; 211:724-730. Overall, I think it's a very nice manuscript, and I applaud the 44. Amirata E, Livingston DH, Elcavage J. Octreotide decreases pancreatic work. [Applause] complications after pancreatic trauma. Am J Surg 1994; 168:345-347. 45. Nwariaku FE, Terracina A, Mileski WJ, Minei JP, Carrico CJ. Is DR. HENRY L. LAWS (Birmingham, Alabama): I would like to octreotide beneficial following pancreatic injury? Am J Surg 1995; make one brief comment. A couple of my colleagues, Dr. Randy 170:582-585. Reizer and Ron Clements, actually have advocated, after having 46. Kram HB, Clark SR, Ocampo HP, Yamaguchi MA, Shoemaker WC. some experience with it, the use of ERCP to make this diagnosis. Fibrin glue sealing of pancreatic injuries, resections and anastomoses. I'd like Dr. Bradley to try to clarify for us, if he could, when Am J Surg 1991; 161:479-481. would an and how would 47. Bass J, DiLorenzo M, Desjardins JG, Grignon A, Quimet A. Blunt exactly you get ERCP, immediately you pancreatic injuries in children. The role of percutaneous external embark on that after the injury? Have you seen hematomas in the drainage in the treatment of pancreatic . J Pediatr Surg lesser sac, either operatively or on the CT that might or might not 1988; 23:721-724. help you? 48. Bradley EL III. Chronic obstructive pancreatitis as a delayed compli- And, frankly, at the time of operation, how good are we at cation of pancreatic trauma. Hepatobil Surg 1991; 5:49-60. detecting whether the duct is injured or not? 49. Taxier M, Sivak MV Jr, Cooperman AM, Sullivan BH Jr. Endoscopic retrograde pancreatography in the evaluation of trauma to the pan- DR. BASIL A. PRuIrr, JR. (San Antonio, Texas): Thank you, Dr. creas. Surg Gynecol Obstet 1980; 150:65-68. Laws. I am sure Dr. Bradley knows better, but it is not right for 50. Gholson CF, Sittig K, Favrot D, McDonald JC. Chronic abdominal him to claim that .6 is somehow different when statistically that is pain as the initial manifestation of pancreatic injury due to remote insignificant, and that's like waiting by the "no sweating" sign, Ed. blunt trauma of the abdomen. South Med J 1994; 87:902-904. Thank you.

DR. JAMES A. O'NEILL, JR. (Nashville, Tennessee): Thank you Discussion very much, Dr. Laws. I rise to ask a question and in one way, also to speak in rebuttal. DR. CHARLES J. YEO (Baltimore, Maryland): I congratulate Dr. Dr. Bradley's excellent manuscript addressed an uncommon Bradley and his coauthors, and I commend the manuscript to you; problem, but one that can lead to significant morbidity. And he it's a well-written manuscript. It contains a lot of information that made some reference to the way pediatric surgeons approach this Dr. Bradley didn't have time to present today, and it's nicely particular problem. I thought it might be useful to clarify a couple structured. of those points. In summary, this represents a review of 101 patients at five I think that the state of the art with regard to the treatment of institutions over 9 years, so you are looking on the average of 2 to pancreas injury in young subjects relates to the patterns of injury 3 patients per institution per year. So we are dealing with an which are ordinarily encountered. And, basically, while you can uncommon but complicated, potentially life-threatening entity. see all four grades, of course, grade IV, ordinarily is, in fact, Overall, clinical findings did not correlate with the grade of almost universally, associated with injuries to other organs that pancreatic injury or complications, and CT had a low sensitivity, lead the surgeon to operation and to intervene when the pancreas only 71%. And only 43% sensitivity for actually finding main is injured as well. pancreatic ductal injury. Of note, ERCP was used in only five The other forms of injury really are basically two. One is patients, so that's 5% of this cohort, and it has been proposed as contusion and the other is pancreatic transection at the vertebral possibly needing wider application. column, which involves main pancreatic duct injury. And it is I have four questions for Dr. Bradley and his group. exceedingly rare to see main pancreatic duct injury in small First, you have alluded to the fact that better imaging studies subjects without transection of the pancreas, in our experience. may diminish your enthusiasm for ERCP, most notably, MRCP Now the way we have tended to approach this -and I think this and some of the new ultra-fast magnetic resonance imaging stud- is fairly universal -is that if there are continuing signs of ies. Do you have any information regarding MRCP and its ability peritonitis and continuing hyperamylasemia, then one is led to to visualize these ductal injuries? either operate or to obtain imaging studies. Virtually always today