372 DUODENAL INJURIESrelated to almost half the deaths in this series. In fact, delays 6. Sinha R, Sharma N, Joshi M: Laparoscopic repair of small bowel perfora-exceeding as little as 8 hours resulted in increased morbidity and tion. J Soc Laparoendosc Surg 9:399–402, 2005.mortality. 7. Maull KI, Reath DB: Impact of early recognition on outcome in nonpen- Mortality after penetrating injury is most commonly related to etrating wounds of the small bowel. South Med J 77:1075–1077, 1984. 8. Brasel KJ, Olsen CJ, Stafford RE, Johnson TJ: Incidence and signiﬁcanceinjury to other intraperitoneal and/or retroperitoneal injuries.22 of free ﬂuid on abdominal computed tomographic scan in blunt trauma. J Trauma 44:889–892, 1998. 9. Malhotra AK, Fabian TC, Katsis SB, et al: Blunt bowel and mesenteric CONCLUSIONS injuries: the role of screening computed tomography. J Trauma 48: 991–1000, 2000.Small bowel injuries may follow blunt or penetrating trauma. The 10. Allen TL, Mueller MT, Bonk T, et al: Computed tomographic scanningmajor concern in the patient who sustains blunt small bowel injury without oral contrast solution for blunt bowel and mesenteric injuries inis recognizing the presence of the injury. In patients with associated abdominal trauma. J Trauma 56:314–322, 2004.injuries requiring operation or in those sustaining gunshot wounds, 11. Gonzalez RP, Ickler J, Gachassin P: Complementary roles of diagnostic peritoneal lavage and computed tomography in the evaluation of bluntsmall bowel injuries are promptly discoverable. The trend toward abdominal trauma. J Trauma 51:1128–1136, 2001.CT-based nonoperative management and the inaccuracy of early 12. Mitsuhide K, Junichi S, Atsushi N et al: Computed tomography scanningpostinjury CT places patients with isolated blunt small bowel injury and selective laparoscopy in the diagnosis of blunt small bowel injury: aat risk of delayed diagnosis and increased morbidity and mortality. prospective study. J Trauma 58:696–703, 2005.The importance of injury mechanism and physical ﬁndings is often 13. Brownstein MR, Bunting T, Meyer AA, Fakhry SM: Diagnosis and man-overlooked. Patients who are neurologically intact will demonstrate agement of blunt small bowel injury: a survey of the membership of theabdominal tenderness; many will have peritoneal ﬁndings at presen- American Association for the Surgery of Trauma. J Trauma 48:402–407,tation. The presence of a seat-belt contusion should elevate concern. 2000.Injuries that can be repaired by lateral enterorrhaphy rarely cause 14. Kaban G, Somani RA, Carter J: Delayed presentation of small bowel injury after blunt abdominal trauma. J Trauma 56:1144–1145, 2004.postoperative complications, which are more commonly related to 15. Hackam DJ, Ali J, Jastaniah SS: Effects of other intra-abdominal injuriesassociated injuries after both blunt and penetrating trauma. Surgical on the diagnosis, management and outcome of small bowel injuries.judgment is required to ensure early diagnosis and appropriate op- J Trauma 49:606–610, 2000.erative management. 16. Fakhry SM, Brownstein M, Watts DD, et al: Relatively short diagnostic delays (Ͻ8 hours) produce morbidity and mortality in blunt small bowelREFERENCES injury: an analysis of time of operative intervention in 198 patients from a multicenter experience. J Trauma 48:408–415, 2000. 1. Nance ML, Peden GW, Shapiro MB, et al: Solid viscus injury predicts 17. Fang JF, Chen RJ, Lin BC, et al: Small bowel perforation: is urgent surgery major hollow viscus injury in blunt abdominal trauma. J Trauma 43: necessary? J Trauma 47:515–520, 1999. 618–623, 1997. 18. Bensard DD, Beaver B, Besner GE, Cooney DR: Small bowel injury in 2. Velitchkov NG, Losanoff JE, Kjossev KT, et al: Delayed small bowel injury children after blunt abdominal trauma: is diagnostic delay important? as a result of penetrating extraperitoneal high-velocity ballistic trauma to J Trauma 41:476–483, 1996. the abdomen. J Trauma 48:169–170, 2000. 19. Neugebauer H, Wallenboeck E, Hungerford M: Seventy cases of injury of 3. Fakhry SM, Watts DD, Luchette FA: Current diagnostic approaches lack the small intestine caused by blunt abdominal trauma: a retrospective sensitivity in the diagnosis of perforated small bowel injury: analysis from study from 1970 to 1994. J Trauma 46:116–121, 1999. 275,557 trauma admissions form the EAST multi-institutional HVI trial. 20. Maull KI: Stomach, small bowel and mesentery injury. In Dudley H, J Trauma 54:295–306, 2003. Carter D, Russell RC, editors: Operative Surgery. London, Butterworths, 4. Shaftan GW: Indications for operation in abdominal trauma. Am J Surg 1989, pp. 401–413. 99:657–664, 1960. 21. Kirkpatrick AW, Baxter KA, Simons RK, et al: Intra-abdominal complica- 5. Chiu WC, Shanmuganathan K, Mirvis SE, Scalea TM: Determining the tions after surgical repair of small bowel injuries: an international review. need for laparotomy in penetrating torso trauma: a prospective study J Trauma 55:399–406, 2003. using triple-contrast enhanced abdominopelvic computed tomography. 22. Stevens SL, Maull KI: Small bowel injuries. Surg Clin North Am 70: J Trauma 51:860–869, 2001. 541–560, 1990.DUODENAL INJURIES in published reports sustaining penetrating trauma.2 This ﬁgure may primarily be a reﬂection of the experience of urban trauma centersGregory J. Jurkovich where penetrating mechanism are more prevalent, and of academic centers that publish their results. Penetrating duodenal wounds are usu- ally rapidly diagnosed as part of a laparotomy and evaluation of the tract of the offending agent. But blunt duodenal injuries are often mored insidious in their presentation, making the initial diagnosis difﬁcult. uodenal injuries are uncommon, but not so rare as to preclude a Despite this well-known observation, delays in the diagnosis of duode- comprehensive understanding of treatment strategies by general nal trauma continue to plague trauma surgeons and seriously compro-surgeons. A 6-year statewide review in Pennsylvania documented a mise patient care.30.2% incidence of blunt duodenal injury (206 of 103,864 trauma regis-try entries), and only 30 of these patients had full-thickness duodenalinjuries.1 Blunt duodenal injuries are the result of a direct blow to the DETERMINANTS OF OUTCOMEepigastria, which in adults is usually from a steering wheel injury in anunrestrained driver, and in children is the result of a direct blow from a Directly attributable duodenal mortality ranges from 2%–5%, andbicycle handlebar, ﬁst, or similar mechanism. Penetrating wounds are is the result of the common complications of wound dehiscence,more common causes of duodenal injury, with about 75% of patients sepsis, and multiple organ failure.4–11 Associated causes of mortality
ABDOMINAL INJURIES 373in patients with a duodenal injury can be garnered from large series portion (and the remainder of the duodenum) is entirely retroperi-of duodenal injuries reported during the late 20th century. These toneal; this is the segment mobilized by a Kocher maneuver. Thereports demonstrated an average mortality in patients with a duo- transverse or third portion of the duodenum runs 12 cm horizontallydenal injury of 18%, but with great individual report variability, to the left in front of the ureter, inferior vena cava, lumbar column,ranging from 6%–29%.6,12–14 Morbidity rates after duodenal injury and aorta, and ends at just at the left edge of the third lumbar verte-range from 30%–63%, although only about a third of these are di- bra. The superior mesenteric artery runs downward over the anteriorrectly related to the duodenal injury itself.6,9,12 Reasons for this vari- surface of the third portion of the duodenum. The ascending orability in morbidity and mortality statistics include the mechanism fourth portion of the duodenum runs upward and slightly to the leftof injury, associated injuries, and time to initial diagnosis. For ex- for only a short distance (2–3 cm) alongside the spine to the duode-ample, Ivatury and colleagues’ review of 100 consecutive penetrat- nal suspensory ligament of Treitz.ing duodenal injuries documented a 25% mortality rate,6 compared The arterial blood supply of the duodenum is derived from thewith mortality rates of 12%–14% in patients with blunt injury pancreaticoduodenal artery. The superior branch comes off the he-mechanisms.3,9 patic artery, and the inferior branch from the superior mesenteric Early death from a duodenal injury, particularly with penetrating artery. These two arteries run in a groove between the descendingwounds, is caused by exsanguination from associated vascular, liver, (second) and transverse (third) portions of the duodenum and theor spleen injuries.15,16 The proximity of the duodenum to other vital head of the pancreas, with well-developed collateralization via a con-structures makes isolated injuries uncommon, but not unheard of. tinuous marginal artery. The venous drainage parallels the arterialWhile exsanguinating hemorrhage and associated injuries are re- supply, with the posterosuperior arcade draining into the portal veinsponsible for early deaths, infection and multiple-system organ fail- and the anteroinferior arcade draining into the gastrocolic trunk.21ure are responsible for most late deaths. Up to one-third of patients The duodenal mucosa resembles that of the remainder of thewho survive the ﬁrst 48 hours develop a complication related to the small bowel, with the characteristic histologic feature of the submu-duodenal injury. Anastomotic breakdown, ﬁstula, intra-abdominal cosal Brunner’s glands in the most proximal (ﬁrst) portion. The vis-abscess, pneumonia, septicemia, and organ failure are the common cous, mucoid, alkaline secretion of these glands probably affordscomplications. Late deaths in patients with a duodenal injury typi- some protection to the duodenum from gastric acid and serves tocally occur 1–2 weeks or more after the injury, with about one-third begin neutralization of this acid. The mixing of pancreatic and bileof the late deaths attributable to the injury itself.9,12 juices with the gastric efﬂux also normally occurs in the duodenum. The time from injury to deﬁnitive treatment is also an important The duodenum sees an average of 2500 ml gastric juice, 1000 ml offactor in the development of late complications and subsequent bile, 800–1000 ml of pancreatic juices, and 800 ml of saliva, for amortality. Roman and colleagues17 identiﬁed 10 patients in whom total of about 5 liters of combined ﬂow through the duodenum perthe diagnosis of duodenal injury was delayed over 24 hours; 4 of the day. Such massive ﬂow volumes make it clear that duodenal integrity10 died, and 3 of the 10 had duodenal ﬁstulas. In a true trauma clas- is crucial, and help to explain why duodenal ﬁstulae can be such asic report, Lucas and Ledgerwood18 demonstrated the remarkable difﬁcult complication of injury to this organ.importance (and frequency) of a delay in diagnosis of duodenal in-jury. In their report, a delay in diagnosis of more than 12 hours oc-curred in 53% of their patients, and a delay of more than 24 hours in DIAGNOSTIC ADJUVANTS28%; mortality was 40% among the patients in whom the diagnosiswas delayed greater than 24 hours, as opposed to 11% in those un- The radiologic signs of duodenal injury on the initial plain abdomi-dergoing surgery within 24 hours. Snyder and coworkers9 conﬁrmed nal or upright chest radiograph are often quite subtle, with mildthese observations, noting that of the four patients with blunt duo- spine scoliosis or obliteration of the right psoas muscle being occa-denal trauma in their series in whom the diagnosis was delayed, two sionally all that suggests a retroperitoneal duodenal injury. The pres-died and the other two developed duodenal ﬁstula. Cuddington and ence of air in the retroperitoneum is a clear sign of duodenal injury,associates3 also noted that 100% of the deaths directly attributable to but this is often difﬁcult to distinguish from the overlying transverseduodenal injury occurred in patients in whom there was a delay in colon. Computed tomography (CT) at the current time is the bestdiagnosing such injury. method of early diagnosis of a duodenal injury, but it is not infallible. The implication of these observations is that the ﬁrst priority in In a 1997 report describing a 6-year statewide experience withmanaging duodenal trauma should be control of hemorrhage. The duodenal injuries, Ballard et al.1 reported that of 30 documentednext priority is limiting bacterial contamination from colon or other blunt duodenal injuries, the initial CT scan missed 27%. The (CT)bowel injury to prevent late infections. A clear identiﬁcation of the scan must be performed with both oral and intravenous contrastextent of the duodenal injury should follow as the next priority, with (Figure 1). The exam must be interpreted with great suspicion foran emphasis on determining the status of the pancreas as well, as this injury, and uncertainty in interpretation is adequate justiﬁcation foraffects deﬁnitive treatment plans.13,19 operative exploration. False-negative exams are known to occur.22 In one careful study of the accuracy of CT in diagnosing duodenal and other small bowel injuries, only 59% (10 of 17) scans were prospec- ANATOMY AND PHYSIOLOGY tively (preoperatively) interpreted as suggestive for bowel injury, which increased to 88% (15 of 17 injuries) when evaluated retrospec-The duodenum is the ﬁrst portion of the small intestine, beginning tively.23 These investigators emphasized that using CT for the diagno-just to the right of the spine at the level of the ﬁrst lumbar vertebra sis of blunt bowel rupture requires careful inspection and techniqueand extending from the pyloric ring to the duodenojejunal ﬂexure, to detect the often-subtle ﬁndings.commonly known as the ligament of Treitz. The duodenum is named A more cumbersome alternative to CT is upper gastrointestinalfrom the Latin word duodeni, which means “twelve each,” because it series with water-soluble contrast medium followed by barium if theis in total 25 to 30 cm, or about 12 ﬁngerbreadths, in length. For initial exam is negative. Some have advocated this study if the initialconvenience of description, the duodenum is arbitrarily divided into CT is difﬁcult to interpret, but I would argue that subtle ﬁndings onfour divisions, differentiated by the alteration in direction of the CT are adequate justiﬁcation for operative exploration. In a series oforgan.20 The superior or ﬁrst portion of the duodenum passes back- 96 patients with CT ﬁndings suspicious for duodenal injury, theward and upward toward the neck of the gallbladder, and most sensitivity of a subsequent duodenography was 54% with a speciﬁc-of this portion is intraperitoneal. The descending (vertical) or second ity of 98%.24 For those injuries requiring operative repair, the sensi-portion forms an acute angle with the ﬁrst portion and descends tivity was only 25%, with a 25% false-negative rate. Allen et al.257–8 cm. It contains the bile and pancreatic duct openings. This demonstrated that 83% of the patients with a delay in the diagnosis
374 DUODENAL INJURIESA B Figure 1 Duodenal perforation. Nineteen-year-old female dropped a 185-lb barbell on abdomen, presented to emergency department 4 hours later with mild abdominal pain and nausea. Afebrile, hemodynamics stable, persistent epigastric tenderness without peritoneal signs, WCC 16 K, amylase 114. Arrow points to nonluminal air in the retroperitoneum and free extravasation of contrast.of blunt duodenal injury had subtle CT ﬁndings, including pneumo- Table 1: Determinants of Duodenal Injury Severityperitoneum, unexplained ﬂuid, and unusual bowel morphologythat were dismissed. These authors emphasized the point that subtle Mild Severeﬁndings of duodenal injury on abdominal CT should mandate Determinants of Injury Severitylaparotomy. Diagnostic peritoneal lavage (DPL) is unreliable in detecting iso- Agent Stab Blunt or missilelated duodenal and other retroperitoneal injuries. Nevertheless, DPL Size Ͻ75% wall Ն75% wallis often helpful because approximately 40% of patients with a duo- Duodenal site 3, 4 1, 2denal injury have associated intra-abdominal injuries that will resultin a positive peritoneal lavage. The ﬁndings of amylase or bile in the Injury-repair Ͻ24 Ն24lavage efﬂuent are more speciﬁc indicators of possible duodenal in- interval (hr)jury. Serum amylase levels are nondiagnostic as well, but if elevated Adjacent injury No CBD CBDadditional investigation (CT or celiotomy) for the possibility of pan- No pancreatic injury Pancreatic injurycreatic or duodenal injury is warranted. At celiotomy, the presence of Outcomeany central upper abdominal retroperitoneal hematoma, bile stain-ing, or air mandates visualization and a thorough examination of the Mortality (%) 6% 16%duodenum. Asensio and colleagues26 have published the technical Duodenal 6% 14%details of exposing the entire duodenum and pancreas. morbidity (%) CBD, Common bile duct. TREATMENTTreatment principles are governed by the severity of duodenal injuryand the likelihood of postrepair complications. Approximately 70% rithm approach to the management of duodenal injuries is providedof duodenal wounds can be safely repaired primarily, and the re- in Figure 2.27 A classiﬁcation system for all organ injuries has beenmaining 30% are “severe” injuries that require more complex proce- developed by the American Association for the Surgery of Traumadures. Snyder and colleagues9 are credited with cataloging the factors (AAST) and is known as the Organ Injury Scale (OIS).28 This classi-that determine whether a duodenal wound can be primarily repaired. ﬁcation for duodenal wounds is listed in Table 2, with duodenalIn their review of 247 patients treated for duodenal trauma, they re- injuries graded from I to V, minor to major injury. In a review ofported an overall duodenal ﬁstula rate of 7% and a mortality rate of 164 duodenal trauma patients managed at eight trauma centers and10.5% in the 228 patients surviving for greater than 72 hours. These to whom the AAST/OIS classiﬁcation scheme was applied, there wereinvestigators felt that ﬁve of the factors listed in Table 1 most signiﬁ- 38 class I, 70 class II, 48 class III, four class IV, and four class V inju-cantly correlate with the severity of duodenal injury and subsequent ries. Primary repair alone was performed in 71% (117) of all cases.4morbidity and mortality. A more recent addition, as noted in the Primary duodenal repair was performed in 90 of 108 patients withtable, is the presence of a pancreatic injury, a signiﬁcant predictor of class I or II injuries. More complex duodenal treatment strategies,late morbidity and mortality. Each of these factors, either individu- including pyloric exclusion, duodenoduodenostomy, duodenojeju-ally or in combination, has been used to develop a variety of duode- nostomy, or pancreatoduodenectomy, were employed in 26 ofnal injury classiﬁcation systems. Snyder and colleagues9 demon- 56 (46%) patients with class III to V injuries, or 29% of the totalstrated that patients with “mild” duodenal trauma had 0% mortality population.and 2% duodenal ﬁstula rate, as compared with 6% mortality and Primary repair is usually the simplest, fastest, and most appropri-10% ﬁstula rate among those with severe duodenal injuries. In gen- ate way to manage duodenal injuries.29 Primary repair is appropriateeral, patients with a “mild” duodenal injury and no pancreatic injury for complete transection of the duodenum if there is little tissue loss,can be primarily repaired. Patients with more severe duodenal inju- if the ampulla is not involved, and if the mucosal edges can be de-ries may require more complex treatment strategies. A useful algo- brided and closed without tension. The repair is done as with any
ABDOMINAL INJURIES 375 F Detected at Evacuation of laparotomy hematoma Hematoma G A NG suction Detected non- TPN History and physical examination operatively Observation Abdominal trauma H Grade I/II simple Suture closure Pyloric exclusion laceration E J Duodenal Inspection at Primary repair or Injury laparotomy Proximal to antrectomy ampulla Gastojejunostomy I Stump closure Grade III laceration Primary repair or B Distal to Labs Roux-en-Y ampulla Abdominal x-ray C duodenojejunostomy Contrast studies D K Complex biliary reconstruction Grade IV/V laceration or destruction Pancreatico- duodenectomy Figure 2 Algorithm for the management of duodenal injuries. (From Jurkovich G: Duodenal injury. In McIntyre R, Van Stiegmann G, Eiseman B, editors: Surgical Decision Making, 5th ed. Philadelphia, Elsevier, 2004, pp. 512–513.)Table 2: AAST-OIS Grading of Duodenal InjurySeverityGrade Type DescriptionI Hematoma Single portion of duodenum Laceration Partial thicknessII Hematoma More than one portion Laceration Ͻ50% circumferenceIII Laceration 50%–75% D2 50%–100% D1, D3, D4IV Laceration Ն75% D2 Involves ampulla or distal CBDV Laceration Massive disruption of duodeno- pancreatic complex Devascularization Figure 3 Extensive disruptions of the duodenum may be treated by resection with end-to-end Roux-en-Y duodenojejunostomy. (FromAAST-OIS, American Association for the Surgery of Trauma Organ Injury Asensio J, Feliciano D, Britt L, Kerstein M: Management of duodenal injuries.Severity scoring system. Curr Probl Surg 11, 1993, p. 1064, ﬁgure 9.)Modiﬁed from American Association for the Surgery of Trauma (AAST).small bowel repair. I prefer a two-layer closure, but a watertight, ing a duodenal wound. In this report of 60 patients with penetratingserosa-approximating single layer repair is equally acceptable. How- duodenal injuries, there was a 64% incidence of abdominal sepsisever, if adequate mobilization for a tension-free repair is impossible, and a 27% death rate in 11 patients with duodenal gunshot wounds,or if the injury is very near the ampulla and mobilization risks com- compared with a 7% abdominal sepsis and 0% mortality inmon bile duct injury, a Roux-en-Y jejunal limb anastomosis to the 30 patients who had either primary repair of Roux-en-Y anastomoticproximal duodenal injury with oversewing of the distal duodenal repair of similar injuries. In 17 patients from that same series withinjury is the most reasonable option (Figure 3). Mucosal jejunal duodenal stab wounds, the complication rate was also higher if thepatch repair as depicted in Figure 4 is rarely, if ever, used, and was not “sucker patch” repair of a duodenal wound was used. It is usuallyused in any patient in the most recent multicenter trial in which only preferable to fully debride the wound and transect the duodenum,ﬁve patients (3%) had duodenoduodenostomy or duodenojejunos- mobilize the edges, and perform a direct end-to-end duodeno–tomy repairs.4 While historically utilized, a 1985 report by Ivatury duodeno anastomosis. Because the duodenal mesentery is short, thiset al.30 demonstrates why this is generally a poor solution to manag- is usually readily accomplished. Pancreatoduodenectomy is only
376 DUODENAL INJURIES required for duodenal injuries if there is uncontrollable pancreatic hemorrhage or combined duodenal and distal common bile duct or pancreatic duct injury. Most often this represents the completion of a debridement initiated by the injury forces. Several techniques may help protect a tenuous duodenal repair. Buttressing the repair with omentum (my preference) or a “serosal patch” from a loop of jejunum seems logical, although the beneﬁt of such techniques is unproven.6,31 Diversion of gastric contents is an- other option, most commonly accomplished by the Vaughan/Jordan pyloric exclusion technique.32 Probably ﬁrst described by Summers in 1904 as an adjunct to treatment of duodenal wounds,33 pyloric exclu- sion is a less disruptive procedure than true duodenal “diverticuliza- tion” advocated by Berne and Donovan and colleagues34,35 (Figure 5). Duodenal “diverticulization” employs primary closure of the duodenal wound, antrectomy, vagotomy, end-to-side gastrojeju- nostomy, T-tube common bile duct drainage, and lateral tube duo-Figure 4 Injuries in which loss of duodenal wall has occurred that denostomy. The concept is to completely divert both gastric andcannot be repaired, primarily without severe narrowing of the lumen, biliary contents away from the duodenal injury, provide enteralmay be repaired by use of a serosal patch technique. The serosa of a nutrition via the gastrojejunostomy, and convert a potential un-loop of jejunum is sutured to the edges of the duodenal defect. controlled lateral duodenal ﬁstula to a controlled ﬁstula. A lessExperimental studies have demonstrated that the serosa exposed to formidable and less destructive alternative is the “pyloric exclu-the duodenal lumen rapidly undergoes complete mucosal sion,” which does not employ antrectomy, biliary diversion, orresurfacing. (From Asensio J, Feliciano D, Britt L, Kerstein M: Management vagotomy32,34,36,37 (Figure 6). This procedure is performed throughof duodenal injuries. Curr Probl Surg 11, 1993, p. 1060, ﬁgure 6.) a gastrotomy and consists of grasping the pylorus with a Babcock clamp and suturing closed the pylorus with absorbable size 0 poly- glycolic acid or polyglactin, or Maxon® (polyglyconate) or PDS® (polydioxanone) suture and construction of loop gastrojejunos- A tomy. This diverts gastric ﬂow away from the duodenum for sev- B eral weeks while the duodenal and pancreatic injuries heal. The pylorus eventually opens (2 weeks to 2 months) and the gastroje- junostomy functionally closes. Fang and colleagues38 at Chang- Gung Memorial Hospital in Taiwan have described a technical method of a controlled release of the pyloric exclusion knot and thereby timing the opening of the pyloric occlusion. Marginal ul- ceration at the site of gastrojejunostomy has been reported in 5%–33% of patients, prompting some to add truncal vagotomy to the procedure.14,32,36,38 Most surgeons do not add a truncal vagot- omy to pyloric exclusion, however, because nearly all of the pyloric closures open within a few weeks, regardless of the type of suture material used, and the occasional marginal ulcer can be medically managed in the interim. The data supports the use of pyloric ex- clusion and gastrojejunostomy in “severe” duodenal injuries7,14 or in cases of delayed diagnosis,36 although no prospective, random- ized trial has proven the true beneﬁt of gastric diversion. In addi-Figure 5 (A) Berne diverticulization and (B) pyloric tion, the added operating time and the extra anastomosis suggestexclusion. (From Jurkovich GJ: Duodenum and pancreas. In Moore EE, a good deal of selectivity should be applied to its use.Feliciano DV, Mattox K, editors: Trauma, 5th ed. New York, McGraw-Hill, Mortality directly related to the duodenal injury is the result2004, p. 717.) of duodenal dehiscence, uncontrolled sepsis, and subsequent C A B Figure 6 Pyloric exclusion technique.
ABDOMINAL INJURIES 377multiple-system organ failure. Knowledge of the lethal natureof duodenal dehiscence and duodenal ﬁstula certainly tempts theoperating surgeon to add pyloric exclusion, anastomosis buttress-ing, and duodenostomy to the repair of class III or IV duodenalinjuries. As noted previously, concomitant pancreatic injury shouldalso be included as a high-risk confounder that might warrantpyloric exclusion added to the duodenal repair. In one report of40 patients with penetrating duodenal injuries, there were 14 pa-tients with combined duodenal and pancreatic wounds. Fivepatients with this combination of injuries had primary duodenalrepair alone, and two incurred duodenal leaks. Three of the pa-tients with combined injuries had pyloric exclusion as a treatmentadjunct, and none had duodenal leaks.39 An alternative or addition to gastric diversion is duodenaldecompression via retrograde jejunostomy. Stone and Fabian10reported a ﬁstula rate of less than 0.5% (1 in 237 patients) in avariety of duodenal injuries all treated by retrograde jejunostomytube drainage, in contrast to a 19.3% incidence of duodenal com-plications when decompression was not used. Retrograde duode-nodenal drainage is preferred to lateral duodenostomy. Directdrainage with a tube through the suture line results in a high de-hiscence or ﬁstula rate of 23%. Hasson and colleagues40 reviewed Athe literature up to 1984 on penetrating duodenal trauma andtube duodenostomy, evaluating eight retrospective series and over550 patients. They reported overall mortality of 19.4% and a ﬁs-tula rate of 11.8% without decompression, compared with 9%mortality and 2.3% ﬁstula rate with decompression. They too con-cluded that tube drainage should be performed either via stomachor retrograde jejunostomy, as these methods had a lower ﬁstularate and less overall mortality than lateral tube duodenostomy.Nonetheless, as is the case of pyloric exclusion for gastric diver-sion, there has been no prospective, randomized analysis of theefﬁcacy of tube duodenal drainage techniques, and not all sur-geons support use of decompression techniques. In very massive injuries of the proximal duodenum and head ofthe pancreas, destruction of the ampulla and proximal pancreaticduct or distal common bile duct may preclude reconstruction. Inaddition, because the duodenum and the head of the pancreas havea common arterial supply, it is essentially impossible to entirelyresect one without making the other ischemic. In this situation, apancreatoduodenectomy is required. Between 1961 and 1994, 184Whipple procedures were reported for trauma, with 26 operativedeaths (14%) and 39 delayed deaths, for a 64% overall survival rate.41With appropriate selection criteria, pancreatoduodenectomy for in-jury can be performed with similar morbidity and mortality as de-scribed in resections done for cancer.42–44 DUODENAL HEMATOMADuodenal hematoma is generally considered an injury of childhoodplay or child abuse, but can occur in adults as well. In one report,50% of the cases of duodenal hematoma in children resulted fromchild abuse.45 Remarkably, the duodenum is the fourth most com-monly injured intra-abdominal organ after blunt abdominal trauma, Boccurring in 2%–10% of children.46 Nearly one-third of the patients Figure 7 Duodenal hematoma. The two images are sequential.present with obstruction of insidious onset at least 48 hours after (A) Initial showing near total duodenal obstruction. (B) Portraysinjury, presumably the result of ﬂuid shift into the hyperosmotic contrast passage into the jejunum. The hematoma has inﬁltrated theduodenal hematoma. Duodenal hematoma in general represents a wall, producing fold thickening, loop narrowing, and displacement.nonsurgical injury, in that the best results are obtained with conser- The mesentery is also involved, and there is a pronouncedvative or nonsurgical management.47 It can be diagnosed either by hematoma component nearly occluding the ﬁrst jejunal loop. Thiscontrast-enhanced CT scan or upper gastrointestinal (UGI) study case shows the characteristic involvement of the duodenum as it(Figure 7). The initial water-soluble contrast (meglumine diatri- traverses the spine, sparing, but obstructing, the proximal duodenalzoate) exam should be followed by barium to provide the greater (1 and 2) segments.detail needed to detect the so-called “coiled spring” or “stacked coin”sign. Although characteristic of intramural duodenal hematoma, thisﬁnding is present in only approximately one-quarter of patients withhematoma.
378 DUODENAL INJURIES Although the initial treatment is nonoperative, associated injuries 12. Shorr R, Greaney G, Donovan A: Injuries of the duodenum. Am J Surgshould be excluded, particularly pancreatic injury. Desai et al.46 re- 154(7):93–98, 1987.ported that 42% of pediatric patients with a duodenal injury (perfora- 13. Jurkovich GJ, Bulger E: Duodenum and pancreas. In Moore EE,tion or hematoma) had a concomitant pancreatic injury, and Jewett Feliciano DV, Mattox K, editors: Trauma, 5th ed. New York, McGraw-Hill, 2004, pp. 709–733.et al.47 found a 20% incidence of pancreatic injury in patients with a 14. Martin T, Feliciano D, Mattox K, Jordon G: Severe duodenal injuries:duodenal hematoma. Continuous nasogastric suction should be em- treatment with pyloric exclusion and gastrojejunostomy. Arch Surg 118:ployed and total parenteral nutrition begun. The patient should be 631–635, 1983.re-evaluated with UGI contrast studies at 5–7-day intervals if signs of 15. Heitsch R, Knutson C, Fulton R, et al: Delineation of critical factors in theobstruction do not spontaneously abate. Ultrasound has also been treatment of pancreatic trauma. Surgery 80(4):523–529, 1976.used to follow a resolving duodenal hematoma.48 Percutaneous drain- 16. Sukul K, Lont H, Johannes E: Management of pancreatic injuries. Hepa-age of an unresolving duodenal hematoma has been reported,49,50 but togastroenterology 39:447–450, 1992.operative exploration and evacuation of the hematoma is usually rec- 17. Roman E, Silva Y, Lucas C: Management of blunt duodenal injury. Surgommended after 2 weeks of conservative therapy to rule out stricture, Gynecol Obstet 132:7–14, 1971. 18. Lucas C, Ledgerwood A: Factors inﬂuencing outcome after blunt duode-duodenal perforation, or injury to the head of the pancreas as factors nal injury. J Trauma 15(10):839–846, 1975.that might be contributing to the obstruction.51 One review of six cases 19. Smego DR, Richardson JD, Flint LM: Determinants of outcome in pan-of duodenal and jejunal hematomas resulting from blunt trauma dem- creatic trauma. J Trauma 25(8):771–776, 1985.onstrated resolution with nonoperative management in ﬁve of the six 20. Anatomy and physiology of the duodenum. In Shackelford R, Zuidemapatients, with an average hospital stay of 16 days (range, 10–23 days), G, editors: Surgery of the Alimentary Tract. Philadelphia, WB Saunders,and total parenteral nutrition of 9 days (range, 4–16 days). The sixth 1981, pp. 38–45.case had evidence of complete bowel obstruction on UGI series, which 21. Edwards E, Malone P, MacArthur J: Operative Anatomy of Abdomen andfailed to resolve after 18 days of conservative management. Laparot- Pelvis. Philadelphia, Lea & Febiger, 1975.omy revealed jejunal and colonic strictures with ﬁbrosis, which were 22. Sherck J, Oakes D: Intestinal injuries missed by computed tomography. J Trauma 30(1):1–5, 1990.successfully resected.52 Another report included 19 cases of duodenal 23. Mirvis S, Gens D, Shanmuganathan K: Rupture of the bowel afterhematoma in children, 17 (89%) managed nonoperatively and blunt abdominal trauma: diagnosis with CT. Am J Roentgenol 159(6):2 patients in operative incision and drainage occurred within the ﬁrst 1217–1221, 1992.24 hours and never attempted nonoperative management.46 Nasogas- 24. Timaran CH, Daley BJ, Enderson BL: Role of duodenography intric decompression and total parenteral nutrition were employed for the diagnosis of blunt duodenal injuries. J Trauma 51(4):648–651,an average of 9.3 (±7.7) days (range, 2–29 days), with an average hos- 2001.pital stay of 16.4 (±17.8) days (range, 2–37 days). 25. Allen G, Moore F, Cox CJ, Mehall J, Duke J: Delayed diagnosis of blunt If a duodenal hematoma is incidentally found at celiotomy, a duodenal injury: an avoidable complication. J Am Coll Surg 187:393–399,thorough inspection must ensue to exclude perforation. This will 1998. 26. Asensio JA, Demetriades D, Berne JD, et al: A uniﬁed approach to therequire an extended Kocher maneuver, which usually successfully surgical exposure of pancreatic and duodenal injuries. Am J Surgdrains the subserosal hematoma. It is unclear whether the serosa of 174(1):54–60, 1997.the duodenum should intentionally be incised along its extent to 27. Jurkovich G: Duodenal injury. In McIntyre R, Van Stiegmann G,“evacuate” the hematoma, or whether this in fact increases the likeli- Eiseman B, editors: Surgical Decision Making, 5th ed. Philadelphia, Else-hood of converting a partial duodenal wall tear into a complete vier, 2004, pp. 512–513.perforation. Unless my index of suspicion is very high for a full- 28. Moore E, Cogbill T, Malangoni M, et al: Organ injury scaling II: pancreas,thickness duodenal wall injury, I generally do not open a duodenal duodenum, small bowel, colon, and rectum. J Trauma 30(11):1427–1429,hematoma found incidentally, although I do inspect it carefully. A 1990.feeding jejunostomy should be placed, because an extended period of 29. Asensio J, Feliciano D, Britt L, Kerstein M: Management of duodenal in- juries. Curr Probl Surg 11:1021–1100, 1993.gastric decompression will likely be required. 30. Ivatury R, Gaudino J, Ascer E, Nallathambi M, Ramirez-Schon G, Stahl W: Treatment of penetrating duodenal injuries: primary repair vs. repairREFERENCES with decompressive enterostomy/serosal patch. J Trauma 25(4):337–341, 1985. 1. Ballard RB, Badellino MM, Eynon CA, Spott MA, Staz CF, Buckman RF Jr: 31. McInnis W, Aust J, Cruz A, et al: Traumatic injuries of the duodenum: a Blunt duodenal rupture: a 6-year statewide experience. J Trauma 43(2): comparison of primary closure and the jejunal patch. J Trauma 15: 229–232discussion 33, 1997. 847–858, 1975. 2. Asensio J, Feliciano D, Britt L, Kerstein M: Management of duodenal in- 32. Vaughan G, Grazier O, Graham D, et al: The use of pyloric exclusion in juries. Curr Probl Surg 11:1021, 1993. the management of severe duodenal injuries. Am J Surg 134:785–790, 3. Cuddington G, Rusnak C, Cameron R, Carter J: Management of duode- 1977. nal injuries. Can J Surg 33(1):41–44, 1990. 33. Summers JJ: The treatment of posterior perforations of the ﬁxed portions 4. Cogbill T, Moore E, Feliciano D, et al: Conservative management of duode- of the duodenum. Ann Surg 39:727, 1904. nal trauma: a multicenter perspective. J Trauma 30(22):1469–1475, 1990. 34. Berne C, Donovan A, White E, et al: Duodenal “diverticulization” for 5. Flint L, McCoy M, Richardson J, Polk H: Duodenal injury: analysis of com- duodenal and pancreatic injury. Am J Surg 127:503–505, 1974. mon misconceptions in diagnosis and treatment. Ann Surg 191(6):697–702, 35. Donovan A, Hagen W, Berne D: Traumatic perforations of the duode- 1980. num. Am J Surg 111:341–350, 1966. 6. Ivatury R, Nallathambi M, Gaudino J, Rohman M, Stahl W: Penetrating 36. Buck JR, Sorensen VJ, Fath JJ, Horst HM, Obeid FN: Severe pancreatico- duodenal injuries: an analysis of 100 consecutive cases. Ann Surg duodenal injuries: the effectiveness of pyloric exclusion with vagotomy. 202(2):154–158, 1985. Am Surg 58(9):557–560discussion 561, 1992. 7. Kashuk J, Moore E, Cogbill T: Management of the intermediate severity 37. Cogbill T, Moore E, Kashuk J: Changing trends in the management of duodenal injury. Surgery 92:758–764, 1982. pancreatic trauma. Arch Surg 117:722–728, 1982. 8. Levison M, Petersen S, Sheldon G: Duodenal trauma: experience of a 38. Fang JF, Chen RJ, Lin BC: Controlled reopen suture technique for pyloric trauma center. J Trauma 24(6):475–480, 1984. exclusion. J Trauma 45(3):593–596, 1998. 9. Snyder W, Weigelt J, Watkins W, Bietz D: The surgical management of 39. McKenney MG, Nir I, Levi DM, Martin L: Evaluation of minor penetrat- duodenal trauma. Arch Surg 115:422–429, 1980. ing duodenal injuries. Am Surg 62(11):952–955, 1996.10. Stone H, Fabian T: Management of duodenal wounds. J Trauma 19(5): 40. Hasson J, Stern D, Moss G: Penetrating duodenal trauma. J Trauma 334–339, 1979. 24(6):471–474, 1984.11. Vasquez JC, Coimbra R, Hoyt DB, Fortlage D: Management of penetrat- 41. Delcore R, Stauffer J, Thomas J, Pierce G: The role of pancreatogastros- ing pancreatic trauma: an 11-year experience of a level-1 trauma center. tomy following pancreatoduodenectomy for trauma. J Trauma 37(3): Injury 32(10):753–759, 2001. 395–400, 1994.
ABDOMINAL INJURIES 37942. Heimansohn DA, Canal DF, McCarthy MC, Yaw PB, Madura JA, Broadie 48. Megremis S, Segkos N, Andrianaki A, et al: Sonographic diagnosis and TA: The role of pancreaticoduodenectomy in the management of traumatic monitoring of an obstructing duodenal hematoma after blunt trauma: injuries to the pancreas and duodenum. Am Surg 56(8):511–514, 1990. correlation with computed tomographic and surgical ﬁndings. J Ultra-43. McKone T, Bursch L, Scholten D: Pancreaticoduodenectomy for trauma: sound Med 23(12):1679–1683, 2004. a life saving procedure. Am Surg 54(6):361–364, 1988. 49. Gullotto C, Paulson EK: CT-guided percutaneous drainage of a duodenal44. Oreskovich M, Carrico C: Pancreaticoduodenectomy for trauma: a viable hematoma. Am J Roentgenol 184(1):231–233, 2005. option? Am J Surg 147(5):618–623, 1984. 50. Kortbeek JB, Brown M, Steed B: Percutaneous drainage of a duodenal45. Wooley M, Mahour G, Sloan T: Duodenal hematoma in infancy and haematoma. Injury 28(5–6):419–420, 1997. childhood. Am J Surg 136:8–14, 1978. 51. Touloukian R: Protocol for the nonoperative treatment of obstructing46. Desai KM, Dorward IG, Minkes RK, Dillon PA: Blunt duodenal inju- intramural duodenal hematoma. Am J Surg 145:330–335, 1983. ries in children. J Trauma 54(4):640–645, discussion 645–646, 2003. 52. Czyrko C, Weltz C, Markowitz R, O’Neill J: Blunt abdominal trauma47. Jewett TJ, Caldarola V, Karp M, Allen J, Cooney D: Intramural hematoma resulting in intestinal obstruction: when to operate? J Trauma 30(12): of the duodenum. Arch Surg 123(1):54–58, 1988. 1567–1571, 1990.PANCREATIC INJURIES spleen. The splenic artery and vein can be found along the superior border of the pancreas. The superior mesenteric artery and vein re-Louis J. Magnotti and Martin A. Croce side just behind the neck of the pancreas and are enclosed posteriorly by the uncinate process. This process can be absent or can almost completely encircle the superior mesenteric artery and vein. The head of the pancreas is suspended from the liver by the hepa- toduodenal ligament and is ﬁrmly ﬁxed to the medial aspect of thet he pancreas is relatively protected deep within the conﬁnes of the retroperitoneum. As such, injuries to the pancreas areuncommon, but not rare, and can present a diagnostic dilemma. In second and third portions of the duodenum. A line extending from the portal vein superiorly to the superior mesenteric vein inferiorly marks the division between the head and the neck of the gland. The neck of the pancreas measures approximately 1.5–2 cm in length andfact, despite advances in modern trauma care, there remains signiﬁ- lies at the level of the ﬁrst lumbar vertebra. It overlies the superiorcant morbidity and mortality, with mortality rates ranging from mesenteric vessels and is ﬁxed between them and the celiac trunk9%–34%.1 Frequent complications are also common following pan- superiorly. The body of the pancreas is technically deﬁned as thatcreatic injuries, occurring in 30%–60% of patients. The high compli- portion of the pancreas that lies to the left of the superior mesentericcation rate associated with these injuries is primarily secondary to vessels. There is no true anatomic division between the body and thediagnostic delays and missed injuries. When identiﬁed early, the tail, nor is there any imaginary dividing line as in the case of the headtreatment of most pancreatic injuries is straightforward. It is the and neck.delayed recognition and/or treatment of these injuries that can result The main pancreatic duct of Wirsung originates in the tail of thein devastating outcomes. pancreas and typically traverses the entire length of the gland and There are few well-documented historical accounts about the joins the common bile duct before emptying into the duodenum.management of pancreatic injuries. The ﬁrst documented case of Throughout its course in the tail and body, the duct lies midway be-pancreatic trauma was an autopsy report from St. Thomas Hospital tween the superior and inferior margins and slightly more posterior.in London in 1827 in which a patient struck by the wheel of a stage- The accessory duct of Santorini usually branches out from the pan-coach suffered a complete pancreatic body transection.2 Over the creatic duct in the neck of the pancreas and empties separately intonext several decades, reports of pancreatic injuries were scattered. In the duodenum. A signiﬁcant number of anatomic variants exist and1903, after extensive review of the literature, only 45 cases of pancre- must be recognized: (1) in 60% of individuals, the ducts open sepa-atic trauma, 21 resulting from penetrating injuries and 24 from blunt rately into the duodenum; (2) in 30%, the duct of Wirsung carriestrauma could be identiﬁed.3 The occurrence of complications fol- the entire glandular secretion and the duct of Santorini ends blindly;lowing pancreatic injury was also noted early. In 1905, Korte4 re- and (3) in 10%, the duct of Santorini carries the entire secretion ofported a case of an isolated pancreatic transection with resultant the gland and the duct of Wirsung is either small or absent. In allpancreatic ﬁstula. The ﬁstula closed spontaneously and the patient cases, the ducts lie anterior to the major pancreatic vessels.survived. The arterial and venous blood supply of the pancreas is relatively The following chapter attempts to clarify the anatomic and constant. The arterial blood supply of the pancreas originates fromphysiologic basis for the concerns over injuries to the pancreas as well both the celiac trunk and the superior mesenteric artery. The bloodas elucidate speciﬁc diagnostic and therapeutic interventions after supply to the head of the pancreas appears to be the greatest, with lesstraumatic injuries to the pancreas. ﬂow to the body and tail and the least to the neck. The veins, like the arteries, are found posterior to the ducts, lie superﬁcial to the arter- ies, and parallel the arteries for the most part throughout their ANATOMY course. The venous drainage of the pancreas is to the portal, splenic, and superior mesenteric vein.A complete understanding of pancreatic relational anatomy is es-sential for providing appropriate treatment and understanding thepotential for associated injuries. The pancreas is about 15–20 cm in PHYSIOLOGYlength, 3.1 cm wide, and 1–1.5 cm thick. The average mass is 90 g(ranging from 40 to 180 g).5 The inferior vena cava, aorta, left kidney, The pancreas is a compound tubuloalveolar gland with both endo-both renal veins, and right renal artery lie posterior to the pancreas. crine (insulin, glucagon, somatostatin) and exocrine (digestive en-The head of the pancreas is nestled in the duodenal sweep, with the zyme precursors, bicarbonate) function. The endocrine cells arebody crossing the spine and the tail resting within the hilum of the separated histologically into nests of cells known as the islets of