CHAPTER 49 DUODENAL INJURIES
Duodenal injuries are uncommon, but not so rare as to preclude a comprehensive understanding of treatment strategies by general surgeons. A 6-year statewide review in Pennsylvania documented a 0.2% incidence of blunt duodenal injury (206 of 103,864 trauma registry entries), and only 30 of these patients had full-thickness duodenal injuries.1 Blunt duodenal injuries are the result of a direct blow to the epigastria, which in adults is usually from a steering wheel injury in an unrestrained driver, and in children is the result of a direct blow from a bicycle handlebar, fist, or similar mechanism. Penetrating wounds are more common causes of duodenal injury, with about 75% of patients in published reports sustaining penetrating trauma.2 This figure may primarily be a reflection of the experience of urban trauma centers where penetrating mechanism are more prevalent, and of academic centers that publish their results. Penetrating duodenal wounds are usually rapidly diagnosed as part of a laparotomy and evaluation of the tract of the offending agent. But blunt duodenal injuries are often more insidious in their presentation, making the initial diagnosis difficult. Despite this well-known observation, delays in the diagnosis of duodenal trauma continue to plague trauma surgeons and seriously compromise patient care.3
DETERMINANTS OF OUTCOME
Directly attributable duodenal mortality ranges from 2%–5%, and is the result of the common complications of wound dehiscence, sepsis, and multiple organ failure.4–11 Associated causes of mortality in patients with a duodenal injury can be garnered from large series of duodenal injuries reported during the late 20th century. These reports demonstrated an average mortality in patients with a duodenal injury of 18%, but with great individual report variability, ranging from 6%–29%.6,12–14 Morbidity rates after duodenal injury range from 30%–63%, although only about a third of these are directly related to the duodenal injury itself.6,9,12 Reasons for this variability in morbidity and mortality statistics include the mechanism of injury, associated injuries, and time to initial diagnosis. For example, Ivatury and colleagues’ review of 100 consecutive penetrating duodenal injuries documented a 25% mortality rate,6 compared with mortality rates of 12%–14% in patients with blunt injury mechanisms.3,9
Early death from a duodenal injury, particularly with penetrating wounds, is caused by exsanguination from associated vascular, liver, or spleen injuries.15,16 The proximity of the duodenum to other vital structures makes isolated injuries uncommon, but not unheard of. While exsanguinating hemorrhage and associated injuries are responsible for early deaths, infection and multiple-system organ failure are responsible for most late deaths. Up to one-third of patients who survive the first 48 hours develop a complication related to the duodenal injury. Anastomotic breakdown, fistula, intra-abdominal abscess, pneumonia, septicemia, and organ failure are the common complications. Late deaths in patients with a duodenal injury typically occur 1–2 weeks or more after the injury, with about one-third of the late deaths attributable to the injury itself.9,12
The time from injury to definitive treatment is also an important factor in the development of late complications and subsequent mortality. Roman and colleagues17 identified 10 patients in whom the diagnosis of duodenal injury was delayed over 24 hours; 4 of the 10 died, and 3 of the 10 had duodenal fistulas. In a true trauma classic report, Lucas and Ledgerwood18 demonstrated the remarkable importance (and frequency) of a delay in diagnosis of duodenal injury. In their report, a delay in diagnosis of more than 12 hours occurred in 53% of their patients, and a delay of more than 24 hours in 28%; mortality was 40% among the patients in whom the diagnosis was delayed greater than 24 hours, as opposed to 11% in those undergoing surgery within 24 hours. Snyder and coworkers9 confirmed these observations, noting that of the four patients with blunt duodenal trauma in their series in whom the diagnosis was delayed, two died and the other two developed duodenal fistula. Cuddington and associates3 also noted that 100% of the deaths directly attributable to duodenal injury occurred in patients in whom there was a delay in diagnosing such injury.
The implication of these observations is that the first priority in managing duodenal trauma should be control of hemorrhage. The next priority is limiting bacterial contamination from colon or other bowel injury to prevent late infections. A clear identification of the extent of the duodenal injury should follow as the next priority, with an emphasis on determining the status of the pancreas as well, as this affects definitive treatment plans.13,19
ANATOMY AND PHYSIOLOGY
The duodenum is the first portion of the small intestine, beginning just to the right of the spine at the level of the first lumbar vertebra and extending from the pyloric ring to the duodenojejunal flexure, commonly known as the ligament of Treitz. The duodenum is named from the Latin word duodeni, which means “twelve each,” because it is in total 25 to 30 cm, or about 12 fingerbreadths, in length. For convenience of description, the duodenum is arbitrarily divided into four divisions, differentiated by the alteration in direction of the organ.20 The superior or first portion of the duodenum passes backward and upward toward the neck of the gallbladder, and most of this portion is intraperitoneal. The descending (vertical) or second portion forms an acute angle with the first portion and descends 7–8 cm. It contains the bile and pancreatic duct openings. This portion (and the remainder of the duodenum) is entirely retroperitoneal; this is the segment mobilized by a Kocher maneuver. The transverse or third portion of the duodenum runs 12 cm horizontally to the left in front of the ureter, inferior vena cava, lumbar column, and aorta, and ends at just at the left edge of the third lumbar vertebra. The superior mesenteric artery runs downward over the anterior surface of the third portion of the duodenum. The ascending or fourth portion of the duodenum runs upward and slightly to the left for only a short distance (2–3 cm) alongside the spine to the duodenal suspensory ligament of Treitz.
The arterial blood supply of the duodenum is derived from the pancreaticoduodenal artery. The superior branch comes off the hepatic artery, and the inferior branch from the superior mesenteric artery. These two arteries run in a groove between the descending (second) and transverse (third) portions of the duodenum and the head of the pancreas, with well-developed collateralization via a continuous marginal artery. The venous drainage parallels the arterial supply, with the posterosuperior arcade draining into the portal vein and the anteroinferior arcade draining into the gastrocolic trunk.21
DIAGNOSTIC ADJUVANTS
The radiologic signs of duodenal injury on the initial plain abdominal or upright chest radiograph are often quite subtle, with mild spine scoliosis or obliteration of the right psoas muscle being occasionally all that suggests a retroperitoneal duodenal injury. The presence of air in the retroperitoneum is a clear sign of duodenal injury, but this is often difficult to distinguish from the overlying transverse colon. Computed tomography (CT) at the current time is the best method of early diagnosis of a duodenal injury, but it is not infallible. In a 1997 report describing a 6-year statewide experience with duodenal injuries, Ballard et al.1 reported that of 30 documented blunt duodenal injuries, the initial CT scan missed 27%. The (CT) scan must be performed with both oral and intravenous contrast (Figure 1). The exam must be interpreted with great suspicion for injury, and uncertainty in interpretation is adequate justification for 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 prospectively (preoperatively) interpreted as suggestive for bowel injury, which increased to 88% (15 of 17 injuries) when evaluated retrospectively.23 These investigators emphasized that using CT for the diagnosis of blunt bowel rupture requires careful inspection and technique to detect the often-subtle findings.
A more cumbersome alternative to CT is upper gastrointestinal series with water-soluble contrast medium followed by barium if the initial exam is negative. Some have advocated this study if the initial CT is difficult to interpret, but I would argue that subtle findings on CT are adequate justification for operative exploration. In a series of 96 patients with CT findings suspicious for duodenal injury, the sensitivity of a subsequent duodenography was 54% with a specificity of 98%.24 For those injuries requiring operative repair, the sensitivity was only 25%, with a 25% false-negative rate. Allen et al.25 demonstrated that 83% of the patients with a delay in the diagnosis of blunt duodenal injury had subtle CT findings, including pneumoperitoneum, unexplained fluid, and unusual bowel morphology that were dismissed. These authors emphasized the point that subtle findings of duodenal injury on abdominal CT should mandate laparotomy.
Diagnostic peritoneal lavage (DPL) is unreliable in detecting isolated duodenal and other retroperitoneal injuries. Nevertheless, DPL is often helpful because approximately 40% of patients with a duodenal injury have associated intra-abdominal injuries that will result in a positive peritoneal lavage. The findings of amylase or bile in the lavage effluent are more specific indicators of possible duodenal injury. Serum amylase levels are nondiagnostic as well, but if elevated additional investigation (CT or celiotomy) for the possibility of pancreatic or duodenal injury is warranted. At celiotomy, the presence of any central upper abdominal retroperitoneal hematoma, bile staining, or air mandates visualization and a thorough examination of the duodenum. Asensio and colleagues26 have published the technical details of exposing the entire duodenum and pancreas.
TREATMENT
Treatment principles are governed by the severity of duodenal injury and the likelihood of postrepair complications. Approximately 70% of duodenal wounds can be safely repaired primarily, and the remaining 30% are “severe” injuries that require more complex procedures. Snyder and colleagues9 are credited with cataloging the factors that determine whether a duodenal wound can be primarily repaired. In their review of 247 patients treated for duodenal trauma, they reported an overall duodenal fistula rate of 7% and a mortality rate of 10.5% in the 228 patients surviving for greater than 72 hours. These investigators felt that five of the factors listed in Table 1 most significantly correlate with the severity of duodenal injury and subsequent morbidity and mortality. A more recent addition, as noted in the table, is the presence of a pancreatic injury, a significant predictor of late morbidity and mortality. Each of these factors, either individually or in combination, has been used to develop a variety of duodenal injury classification systems. Snyder and colleagues9 demonstrated that patients with “mild” duodenal trauma had 0% mortality and 2% duodenal fistula rate, as compared with 6% mortality and 10% fistula rate among those with severe duodenal injuries. In general, patients with a “mild” duodenal injury and no pancreatic injury can be primarily repaired. Patients with more severe duodenal injuries may require more complex treatment strategies. A useful algorithm approach to the management of duodenal injuries is provided in Figure 2.27
