Chapter 32: Duodenum and Pancreas

Injuries to the pancreas and duodenum present a significant challenge, for a number of reasons. First, while their deep, central position affords the organs some degree of protection, their retroperitoneal location compromises the clinical detection of injury. This can lead to delays in diagnosis and treatment, which may result in morbidity and mortality.^{1,2,3,4,5,6,7} Second, even when managed promptly, anatomic and physiologic factors contribute to a disturbingly high incidence of complications. Third, the infrequency of these injuries has resulted in a lack of significant management experience—both of the primary injuries as well as the complications—among practicing trauma surgeons. Consequently, trauma to the pancreas and duodenum is associated with relatively poor outcomes that have not improved significantly over the past few decades, despite advances in trauma and critical care management (Tables 32-1 and 32-2).^{1,3,6,8,9,10,11,12,13,14,15,16,17,18,19}

Most early descriptions of duodenal and pancreatic injuries were isolated autopsy observations. The first known literature report of pancreatic trauma was published by Travers in 1827. By 1903, von Mikulicz-Radeck reported only 45 cases in the literature.²⁰ Of note, 72% of operated patients survived, a success rate that rivals modern-day results. Many of the recommendations from that early series still hold true today: thorough abdominal exploration, hemostasis, and drainage. Although military experience has shaped much of contemporary trauma management, a paucity of reports of injuries to the pancreas have emanated from wartime experiences. The first series of five patients from the American Civil War included one survivor, and a similar experience was described after World War I. World War II annals include 62 cases of pancreatic trauma, but only nine were reported from the Korean War. Virtually no reports of pancreatic or duodenal injuries are available from the Vietnam War experience except for two cases of pancreaticoduodenectomy.

The first account of successful surgical repair of a duodenal rupture was published by Herczel in 1896. In 1904, Summers²¹ cautioned about the difficulty in diagnosis of a retroperitoneal perforation of the duodenum from a gunshot wound, and may have been the first to describe the potential application of the pyloric exclusion procedure. The earliest reported series of traumatic duodenal ruptures was that of Berry and Giuseppi²² from 10 London hospitals. The authors described 29 patients with duodenal injuries, all of whom died; further, the authors cited only one known survivor of duodenal trauma to that point in time. From World War II, Cave²³ recorded 118 cases of duodenal injuries with a mortality of 56%, which is still the single largest military series of duodenal injuries.

Recent Historical Trends

Pancreaticoduodenal trauma remains uncommon, and few single institutions have extensive experience. Busy trauma centers such as Ben Taub, Grady Memorial, UT-Southwestern, L.A. County, Detroit Receiving, UT-Memphis, and Denver General Hospital reported just 10–20 duodenal and 10–20 pancreatic injuries per year in the 1960s–1980s.^{1,8,9,11,13,14,15,16,18,24,25} All of the patients in those series were diagnosed at laparotomy. In contrast, contemporary practice involves liberal imaging with high-resolution computed tomographic (CT) scanning, and as a result many occult low-grade injuries are identified. A recent analysis of the US Nationwide Inpatient Sample from 1998 to 2009 found that the incidence of pancreaticoduodenal injuries increased by 8% over the time period.²⁶ While the grade of injury was not documented, only 20% of patients underwent “pancreas-specific” surgical procedures. In the recent collective experience of trauma centers in New England, over 80% of pancreaticoduodenal injuries were grade I or II, and over 40% were managed nonoperatively.²⁷ Yet despite the increased detection of pancreaticoduodenal injuries, the total number is still low: 230 total patients in the 11-year experience of 11 New England trauma centers,²⁷ and only 2268 per year across the United States.²⁶ The current incidence of duodenal injuries is 0.2–0.3% of trauma admissions, and of pancreatic injuries is 0.004–0.6%.^6,13,28,29 From 2010 through 2014 at Denver Health Medical Center (DHMC), there were, on average, just 17 pancreatic or duodenal injuries per year (unpublished data). The incidence of pancreatic or duodenal injuries at DHMC was 2% following penetrating and 0.6% following blunt trauma. Duodenal and pancreatic injuries each occurred with a frequency of 1.2% following penetrating trauma; in contrast, blunt pancreatic injuries (0.5%) were more than twice as common as blunt duodenal injuries (0.2%). Whereas reports from the 1970s through 1990s^{1,3,6,8,9,10,11,12,13,14,15,16,17,18,19} contained a majority of penetrating trauma victims (see Tables 32-1 and 32-2), that trend has reversed due to decreasing urban violence over the past 20 years and liberal blunt trauma imaging. For example, the recent DHMC patient experience as described above (unpublished data) consists of 64% blunt trauma victims, and the Harborview Hospital experience is comprised of 71% blunt trauma patients.⁶ In the US Nationwide Inpatient Sample in 2009, only 25% of pancreaticoduodenal injuries were due to gunshot or stab wounds.²⁶

A survey of several large series over the last three decades of the 20th century demonstrates that gunshot victims have more than double the mortality rate compared with stab wound victims (see Tables 32-1 and 32-2).^{1,3,6,8,9,10,11,12,13,14,15,16,17,18,19} On the other hand, the overall mortality rate among penetrating and blunt trauma patients with pancreaticoduodenal injuries was the same, between 16% and 18%. Contemporary series with greater numbers of low-grade injuries report lower overall mortality, but it is still significant (ie, 12%).^26,27 Of note, the occurrence of combined pancreatic and duodenal injuries is associated with nearly double the mortality rate compared with that of either injury alone (Table 32-3).^{1,11,13,15,16,27}

It is important to recognize that the mortality is not typically attributed to the pancreaticoduodenal injury but rather to associated injuries and in particular major vascular injuries. The anatomic location of the pancreaticoduodenal axis, and its proximity to other vital structures, makes isolated injuries distinctly uncommon (Figs. 32-1 and 32-2). In virtually every large series, more than 90% of pancreatic and duodenal injuries are associated with injuries to other organs.^{1,8,9,11,12,13,14,15,18,19,30} On average, there are 2.5–4.6 associated injuries with each pancreatic or duodenal injury.^13,30 The common associated injuries and their frequencies are listed in Tables 32-4 and 32-5. Not surprisingly, complication rates are higher when there are associated injuries, and the mortality rate increases progressively with each associated injury.³¹ Collective analysis of 11 large trials reveals that 304 (68%) of 447 deaths occurred within the first 12–48 hours and were attributed to hemorrhagic shock or massive traumatic brain injury (Table 32-6).^{2,3,6,10,11,12,13,14,16,19,32,33} Moreover, the overall mortality attributed to the pancreatic or duodenal injuries is consistently fewer than 2%.

Predictors of survival include age, overall injury severity, indices of shock, and severe brain injury—but interestingly, not pancreatic or duodenal injury grade.^6,13,34 Late deaths in cases of pancreatic and duodenal trauma are most often ascribed to sepsis and multiple organ failure (MOF), often provoked by complications related to the original pancreatic or duodenal injury. This underscores the importance of early and prompt diagnosis. One quarter to one half of patients who survive initial operation can be expected to develop a complication.^6,27 Among those patients with a delay in the initial diagnosis of pancreaticoduodenal injury, morbidity and mortality rates are considerably higher.^{1,2,3,4,5,6,7}

The duodenum and pancreas are intimately associated with many vital structures in a deep and narrow region (see Figs. 32-1 and 32-2). The name duodenum is derived from duodenum digitorum (“space of 12 digits”), from the Latin duodeni (“12 each”)—so named by Greek physician Herophilus for its length, approximately 12 finger-breadths. It extends about 30 cm, from the pyloric ring to the ligament of Treitz. Classically the duodenum is divided into four portions: superior (first, or D1), descending (second, or D2), transverse (third, or D3), and ascending (fourth, or D4). The first portion of the duodenum extends from the pylorus to the common bile duct (CBD) and gastroduodenal artery. The second portion extends from that point to the ampulla of Vater. The third portion extends from the ampulla of Vater to the superior mesenteric artery (SMA) and vein (SMV), which emerge from posterior to the pancreas and descend anteriorly over the duodenum. The fourth portion extends from the SMA and SMV to the point where the duodenum emerges from the retroperitoneum to join the jejunum, just to the left of the second lumbar vertebra, at the ligament of Treitz. Thus, the duodenum is almost entirely a retroperitoneal structure, with the exception of the anterior half circumference of D1 and the most distal part of D4. The first portion, distal region of the third portion, and the fourth portion of the duodenum lie directly over the vertebral column. The psoas muscles, aorta, inferior vena cava, and right kidney complete the posterior boundaries of the duodenum. The liver and gallbladder overlie the first and second portions of the duodenum anteriorly; the second and third are bounded by the hepatic flexure and right transverse colon, and the fourth portion lies beneath the transverse colon, mesocolon, and stomach. The head of the pancreas is intimately associated within the C loop, or second portion.

The pancreas is divided into the head, contained within the duodenal C-loop; the neck, which is the narrowest portion and overlies the SMA and SMV; the body, which is rather triangular in cross section and which extends to the left across the vertebral column; and the tail, which extends into the splenic hilum. In blunt force trauma, the vertebral column may act as a fulcrum over which the pancreas may be transected. The root of the transverse mesocolon crosses the head anteriorly. Posteriorly, the head is separated from the body by the pancreatic incisure, where the superior mesenteric vessels lie. The uncinate process, a part of the head, extends to the left behind the SMA and SMV. The body of the pancreas extends laterally. The base of the transverse mesocolon is attached at the anterior margin, and is covered with peritoneum and forms the posterior wall of the omental bursa. The inferior surface of the pancreas is covered with peritoneum from the posterior mesocolon. The body of the pancreas rests on the aorta. The tail of the pancreas lies in front of the left kidney, in intimate proximity to the splenic flexure of the colon, often abutting the spleen via the lienorenal ligament. The splenic artery runs along the upper border of the gland, often crossing in front of the tail. The splenic vein lies in a groove behind the body and tail, usually on the inferior edge of the pancreas.

The blood supply of the pancreas and duodenum comes from the gastroduodenal, SMA, and splenic arteries. A network of vessels throughout the pancreas protects it from ischemia, but also contributes to vigorous bleeding following injury. The blood supply to the body and tail arises from the SMA and splenic arteries. The second portion of the duodenum has a unique blood supply that originates from both the gastroduodenal artery and the inferior pancreaticoduodenal artery, a branch of the SMA. Both of these vessels divide into anterior and posterior branches that are located on the edge of the head of the pancreas and anastomose with each other anteriorly and posteriorly. The second portion of the duodenum receives radial branches from these vessels that comprise its only blood supply. Consequently, if all of the pancreaticoduodenal vessels are injured by trauma, a pancreaticoduodenectomy will be necessary. The third portion of the duodenum receives its blood supply from the notoriously short mesentery of the SMA.

Although the arterial and venous supply as described is relatively constant, variations do exist and should be kept in mind during surgical exploration in this region. Origin of the common hepatic artery (5%) and a replaced right hepatic artery (15–20%) from the SMA are among the most frequent anomalous findings. In other instances, the right hepatic may arise from the aorta, gastroduodenal, or even left hepatic artery. In 4% of the population, the entire common or proper hepatic artery is aberrant, arising from the SMA, aorta, or left gastric artery. In addition, if the bifurcation of the proper hepatic artery is low, the right hepatic may lie in front of the CBD or cross in front of it as well as the cystic duct.

Surgeons dealing with injuries to the duodenum and pancreas should be particularly well versed with the anatomic positions of the CBD and pancreatic duct. The CBD descends from above to pass behind the first part of the duodenum, continuing downward on the posterior surface of the head of the pancreas where it is overlapped by lobules of pancreas obscuring its identification. In this region, the CBD curves to the right and joins with the main pancreatic duct of Wirsung prior to entering the posteromedial wall of the second part of the duodenum as the ampulla of Vater. The main pancreatic duct usually traverses the entire length of the gland and is located posteriorly slightly above a line halfway between the superior and inferior edges of the pancreas. The accessory duct of Santorini typically branches out from the main duct near the neck and empties separately into the duodenum about 2.5 cm proximal to the duodenal papilla. The CBD and main pancreatic duct may rarely enter the duodenum through separate openings. This is important to recognize when attempting cholangiopancreatography via the gallbladder or CBD.

Partially digested chyle from the stomach and the proteolytic and lipolytic secretions of the biliary tract and pancreas mix in the duodenum. The powerful digestive enzymes commonly found in this location include lipase, trypsin, amylase, elastase, and peptidases. Approximately 10 L of fluid from the stomach, bile duct, and pancreas passes through the duodenum in a day. Under normal conditions, the small intestine absorbs more than 80% of this fluid, but following injury, this high volume and enzymatically charged flow accounts for the disastrous consequences of a lateral duodenal fistula and associated derangements in water and electrolyte homeostasis.

The duodenum has several key roles in vitamin and mineral absorption as well as food processing. Vitamin B₁₂ malabsorption may result from extensive duodenal resection. The protein is hydrolyzed by pancreatic enzymes in the duodenum to allow free cobalamin (B₁₂) to bind to gastric parietal cell-derived intrinsic factor.

The duodenum is the main site for transcellular transport of calcium. A key step in transport is mediated by calbindin, a calcium binding protein produced by enterocytes. Regulation of calbindin synthesis appears to be the main mechanism facilitating vitamin D regulated calcium absorption.

The pancreas consists of both endocrine and exocrine cells. The endocrine cells are distributed throughout the substance of the gland, and the α-, β-, and δ-islet cells produce glucagon, insulin, and gastrin, respectively. The secretion of insulin and glucagon are responsive to blood glucose levels. Islet cell concentration is thought to be greater in the tail than the body and head of the gland, although it is generally held that normal hormonal balance may be maintained as long as approximately 10% of the gland remains after resection. Both duct and acinar cells of the pancreas secrete between 500 and 800 mL/d of clear, alkaline, isosmotic fluid. In addition, the acinar cells produce amylase, proteases, and lipases. Pancreatic amylase is secreted in its active form and serves to hydrolyze starch and glycogen to glucose, maltose, maltotriose, and dextrins. Proteolytic enzymes produced by these cells include trypsinogen, which is converted to trypsin in the duodenal mucosa by enterokinase. Pancreatic lipase is secreted in an active form and hydrolyzes triglycerides to monoglycerides and fatty acids. The acinar and duct cells also secrete the water and electrolytes found in pancreatic juice.

Bicarbonate secretion is directly related to the rate of pancreatic secretion; chloride secretion varies inversely with bicarbonate secretion so that the sum total of both remains constant. The hormone secretin, released from the duodenal mucosa, is the major stimulant for bicarbonate secretion, and serves to buffer the acidic fluid entering the duodenum from the stomach. Both endocrine and exocrine pancreatic functions are interdependent. Somatostatin, pancreatic polypeptides, and glucagons are all believed to have a role in inhibition of exocrine secretion. When pancreatic exocrine function is reduced to less than 10%, diarrhea and steatorrhea develop.

The approach to patients with abdominal trauma begins with an initial evaluation as described in the American College of Surgeons Advanced Trauma Life Support (ATLS) course.³⁵ Many pancreatic and duodenal injuries are the result of penetrating trauma, and the injury is usually discovered during exploratory laparotomy. The hemodynamically unstable patient requires little preoperative evaluation other than expeditious transport to the operating room. Prior to exploring patients with gunshot wounds, plain x-rays of the chest, abdomen, and pelvis should be obtained if possible; information regarding potential trajectory and involvement of more than one body cavity is invaluable. Blood typing is performed in anticipation of potential transfusion, and antibiotics are administered. It is critical that thorough exploration and examination of the pancreas and duodenum are performed during trauma laparotomy, particularly when there is retroperitoneal hematoma, bile staining, fat necrosis, or edema in the supramesocolic region.

Intraoperative evaluation of the duodenum and head of the pancreas begins with full mobilization achieved by the Kocher maneuver to the midline with coincident mobilization and medial rotation of the hepatic flexure of the colon. This provides exposure of the anterior and posterior surfaces of the second and third portions of the duodenum as well as the head and uncinate process of the pancreas. The distal CBD and third portion of the duodenum are exposed by dissection of the overlying peritoneal attachments and fascia. By detaching the hepatic flexure of the colon from the second portion of the duodenum, evaluation of potential injury to the mesenteric vessels may be assessed. Full medial rotation of the right colon, cecum, and terminal ileum will allow complete evaluation of associated hepatic or vascular injuries in the right upper and middle abdomen. Incision in the right side of the root of the transverse colon will allow reflection of the small bowel superiorly for further exposure of the third part of the duodenum. The body and tail of the pancreas are examined by division of the gastrocolic ligament and reflection of the stomach cephalad. Insertion of a curved retractor in the lesser sac allows full inspection of the anterior surface of the pancreas from the head to tail and from superior to inferior surfaces. In cases of active hemorrhage in the region of the neck of the pancreas suspected to originate from the superior mesenteric or portal vein behind the pancreas, the pancreas should be divided without hesitation. A stapling device will allow for rapid exposure of the injured vessel and hemorrhage control of the pancreas. Further exposure of the posterior surface of the pancreas is accomplished by division of the retroperitoneal attachments along the inferior border of the pancreas and retraction of the pancreas cephalad. Additional mobilization of the spleen and reflection of the spleen and tail of the pancreas from the left to the midline is a useful technique for further evaluation of the remaining areas of the pancreas. Most injuries sustained in penetrating trauma will be discovered with direct exploration. In many cases, the integrity of the main pancreatic duct remains in question. The importance of specific intraoperative assessment of the duct is in evolution (see below).

The clinical diagnosis of blunt pancreaticoduodenal injuries can be more challenging. A common mechanism in both duodenal and pancreatic injuries is blunt force to the epigastrium. Handlebar injuries are a common mechanism in children; in those under 4 years of age, nonaccidental trauma is the most common mechanism.³⁶ Patients may have persistent abdominal pain and tenderness, but these findings may be elusive in the presence of intoxication, shock, brain injury, and severe associated injuries. Diagnostic peritoneal lavage is not considered reliable for evaluation of the retroperitoneum, so it plays a limited role in diagnosing pancreaticoduodenal trauma.³⁷ Leukocytosis, unexplained metabolic acidosis, or fever may herald an occult injury but they may not be present until later as inflammation and the systemic inflammatory response worsen. The utility of serum amylase—and more recently, lipase—assays has been debated, as the sensitivity and specificity of the tests are poor. Takishima et al³⁸ found that if the amylase level was measured more than 3 hours after trauma, it was most likely to reflect pancreatic injury. But it is important to recognize that enzyme levels should not be relied upon to either diagnose or exclude pancreatic injury. In a patient with persistent epigastric pain after blunt abdominal trauma, further diagnostic evaluation is warranted and the amylase or lipase levels should not necessarily influence decision making. On the other hand, in the patient without a reliable clinical examination, it is reasonable to pursue imaging if enzymes levels are elevated.

Plain x-rays are of limited use in the diagnosis of blunt pancreatic or duodenal injuries. The focused abdominal sonography for trauma (FAST) is accurate in identifying hemoperitoneum, and is thus a useful tool to direct prompt transfer of unstable patients to the operating room, or to select stable patients for further evaluation. However, FAST does not evaluate the retroperitoneum reliably. Contrast-enhanced ultrasound has been reported to detect some pancreatic injuries.³⁹ However, its accuracy has not been studied prospectively and its role remains poorly defined. While plain x-ray or fluoroscopic duodenography was employed in the past for diagnosis in equivocal cases, it has been supplanted by computed tomography (CT) scanning.⁴⁰

In the stable patient with suspicion of intraabdominal injury, CT scanning is the primary diagnostic modality; multidetector row CT (MDCT) provides superior imaging.⁴¹ Contrast extravasation from the duodenum is an obvious sign of perforation, but most CT scans for trauma are performed without enteric contrast. Other signs include periduodenal fluid or air. More subtle findings, such as edema, hematoma, or thickening of the bowel wall; surrounding fluid, hematoma, or fat stranding in the retroperitoneum; or intramural gas, should raise suspicion of duodenal injury (Fig. 32-3). It is critical to differentiate perforation from contusion or duodenal wall hematoma, as the former generally mandates laparotomy while the latter is typically managed nonoperatively (see below). Equivocal CT studies may call for repeat CT scanning with contrast in the duodenum. If there is any question, the most conservative approach is operative exploration to definitive diagnose or exclude injury, as delay in diagnosis is associated with morbidity.⁴

The CT findings of pancreatic injury may be subtle, particularly when the imaging is performed within 12 hours of injury (Fig. 32-4).⁴² Specific signs of injury include fractures or lacerations of the pancreas (Fig. 32-5); active hemorrhage from the gland or blood between the pancreas and splenic vein; and edema or hematoma of the parenchyma.^41,42,43 Nonspecific findings include peripancreatic blood or fat stranding.⁴³ Contusions may escape detection. The reported sensitivity and specificity of CT for pancreatic injuries is in the 80% range, but these data were based on earlier-generation scanners.^41,42 More recent data suggest that MDCT, with imaging timed during the portal venous phase, could achieve 100% accuracy of not only pancreatic but pancreatic duct injuries.⁴⁴ However, a multicenter study of the American Association for the Surgery of Trauma (AAST)⁴⁵ looked at the accuracy of 16- and 64-detector row MDCT for detecting pancreatic injury in general, and pancreatic ductal injury specifically. Although specificity was better than 90%, the sensitivity of MDCT for pancreatic or pancreatic ductal injury was only 47–60%. Dreizin and colleagues⁴⁶ describe pitfalls associated with interpretation of whole-body CT (eg, information overload, suboptimal sensitivity and specificity of various findings) and offer diagnostic pearls for radiologists. They discuss advances such as near-isotropic datasets with 3D postprocessing techniques, but acknowledge that data in the trauma setting are lacking. Ultimately, the accuracy of CT is dependent on not just the technology, but also the technique, the timing after injury, and the skills of the interpreting clinician. In the face of a normal initial CT, if a pancreatic injury is clinically suspected, repeat CT should be considered. If a pancreatic laceration is clearly demonstrated on CT scanning, operative management is generally indicated in the setting of extensive pancreatic fluid, severe abdominal pain or tenderness, severe systemic inflammatory response syndrome, or CT findings suspicious for hollow visceral injury.

The integrity of the main pancreatic duct is the most important determinant of prognosis, as most major morbidity is related to ductal disruption.^3,5,6 Consequently, management is largely dependent on the status of the duct. As noted, CT scanning—even with MDCT—is currently not 100% reliable for identifying ductal disruption. Evaluation of the duct can be accomplished in stable patients via endoscopic retrograde cholangiopancreatography (ERCP)^47,48 or magnetic resonance cholangiopancreatography (MRCP).⁴⁹ Delineation of ductal anatomy during MRCP may be further enhanced by the administration of secretin, which increases pancreatic exocrine output and distends the pancreatic duct.⁵⁰ Both ERCP and MRCP are dependent on the availability of the resource, which is not universal even in high-level trauma centers. Advantages of MRCP include its noninvasiveness and the ability to visualize not only the duct, but the pancreatic parenchyma and remainder of the abdomen.⁴² On the other hand, ERCP offers the advantage of therapeutic interventions (eg, stent placement, drainage of fluid collections, drain placement).^47,48 Currently there are few series reporting the accuracy of MRCP, and it has not been prospectively compared with ERCP in the trauma setting. However, it is considered an appropriate next step in evaluating a pancreatic duct whose integrity is questioned after CT scanning. An algorithm summarizing the diagnostic evaluation is presented in Fig. 32-6.

Patients who are unstable, or who have pancreatic injury first diagnosed in the operating room, require intraoperative assessment of pancreatic ductal integrity. Although intraoperative ERCP is an option, it may be difficult to orchestrate rapidly, and the requisite bowel insufflation can interfere with abdominal closure. In the past, surgeon-performed pancreatography was recommended.⁵¹ The standard approach is to clamp the common hepatic duct and infuse contrast into the gallbladder for cholangiopancreatography (Fig. 32-7). Alternative techniques include performing a duodenotomy and cannulating the ampulla of Vater for cholangiopancreatography, or transecting the tail of the pancreas and cannulating the distal duct. The latter techniques have had inconsistent results; hence, opening the duodenum or transecting the pancreas to perform these evaluations appears ill-advised. Moreover, these maneuvers may be unnecessary. A simplified management guideline based on intraoperative clinical assessment of the duct has proven useful in reducing pancreas-related morbidity and mortality (see below).^3,32 The indicators of ductal injury, as originally described by Heitsch and colleagues,⁵² include direct visualization of ductal injury, complete transection of the gland, laceration of more than 50% of the gland, central perforation, and severe maceration.^3,32 In indeterminate cases, probability of ductal injury is based on the wound location and the operating surgeon’s assessment of high versus low probability.

Duodenum

Treatment and decision making is best reviewed in light of injury severity. The classification system most commonly used for injury stratification is the AAST Organ Injury Scale (OIS) (Tables 32-7 and 32-8).⁵³ Injuries are graded on a I–V scale in ascending order of severity. Of note, this scale adds associated pancreatic injury as a major morbidity cofactor in duodenal injury.

Grades I and II

Duodenal intramural hematomas are more common in children than adults and may be identified at the time of exploration, or may be detected on CT scanning (Fig. 32-8). If duodenal hematoma is discovered at initial operative exploration, the duodenum must be thoroughly mobilized and examined to rule out perforation. Hematomas can range from serosal staining to obstructing masses. Whether or not to open and evacuate the hematoma is debated: almost all hematomas resolve in this setting, and opening of the duodenum risks conversion of a closed to open injury. A selective approach is favored by many. Small hematomas with minimal luminal compromise are managed expectantly, with initial nasogastric suction and advancement of oral diet as tolerated. Distal feeding jejunostomy is placed for enteral nutritional support in the setting of luminal compromise up to 50%, or severe associated injuries. Incision and clot evacuation is reserved for larger hematomas with mass effect and luminal compromise more than 50%. Following evacuation of the hematoma and meticulous hemostasis, the incision is closed with single-layer running absorbable closure.

For those without indications for laparotomy, expectant management is appropriate. Treatment generally consists of IV hydration, parenteral nutrition, and nasogastric tube suction. Nearly all duodenal hematomas will resolve spontaneously within 2–3 weeks, but the clinical course may be marked by progressive gastric outlet obstruction with or without bilious emesis. Obstruction can develop as fluid is sequestered into a hyperosmotic hematoma. For patients who continue to manifest complete obstruction after 10–14 days, repeat CT scan should be done to reevaluate the obstructive process, and operative management should be considered.^54,55 Operative approaches for evacuation of the hematoma include open or laparoscopic drainage procedures.⁵⁶

Most duodenal lacerations occur as a result of penetrating trauma (see Table 32-1). Simple duodenal lacerations with minimal tissue destruction often result from either stab wounds or small caliber gunshot wounds. The vast majority can be safely repaired primarily with a meticulous single layer closure if adequate blood supply is ensured.¹² Duodenotomies can be repaired with running or interrupted sutures; a monofilament repair is preferred. Repair in the direction in which the injury is formed is generally recommended. Although earlier reports advocated transverse repair of select longitudinal injuries to minimize luminal compromise, current use of single layer monofilament closure has eliminated this concern in most cases.⁵⁷ Avoidance of tension is paramount. In rare situations of laceration to the pancreatic side of the duodenum, mobilization may not be possible for repair. In such situations, an antimesenteric duodenotomy may be performed, with repair of the injury from the inside.

Grade III

Some grade III lacerations may be repaired by simple duodenorrhaphy, as long as a tension-free repair may be achieved. In those that are judged too extensive for primary repair after mobilization and debridement, other options must be considered. If a segment is removed and the ends can be mobilized without tension, end-to-end duodenoduodenostomy may be performed. Such a repair is rarely feasible in the second portion of the duodenum due to the intimate attachments to the pancreas and thus difficulty with mobilization. In this area, careful identification of the ampulla of Vater is essential to avoid injury at the time of repair. Injuries to the second portion of the duodenum distal to the ampulla can be repaired with division of the duodenum and end-to-end duodenojejunostomy using a Roux-en-y limb of jejunum passed through the transverse mesocolon to the proximal duodenum. In these situations, the distal duodenal stump is oversewn and a jejunojejunostomy is created for intestinal continuity (Fig. 32-9). In the setting of extensive tissue loss but without the need for resection, the duodenum may be similarly reconstructed with a Roux-en-y duodenojejunostomy. Although jejunal mucosal patches and interposition grafts based on a vascular pedicle of the jejunal mesentery have been described, they are rarely used.⁵⁵ Repair of injuries to the third and fourth portion of the duodenum may be compromised by the short mesentery, with limited ability to mobilize the bowel. If it appears the blood supply is compromised, resection and primary duodenojejunostomy is recommended. An intriguing potential alternative to create a tension-free repair while avoiding extensive anatomic reconstruction is to apply a patch graft, analogous to patch angioplasty techniques employed in vascular surgery. Encouraging results have been reported from preclinical studies with nonabsorbable materials such as expanded polytetrafluoroethylene⁵⁸ as well as bioprosthetic materials⁵⁹; further controlled study is warranted.

“Protecting” the Duodenal Repair

When confronted with a patient with a tenuous duodenal repair or an intermediate grade duodenal injury and associated pancreatic injury, the pyloric exclusion procedure as described by Vaughan et al⁸ has been promoted (Fig. 32-10). This procedure is simpler than the original “diverticulization” technique described by Berne et al,⁶⁰ as it does not require gastric antrectomy, vagotomy, biliary T-tube drainage, or tube duodenostomy. In the pyloric exclusion procedure, the duodenal injury is repaired primarily and is “protected” by gastric diversion. To accomplish this, a gastrotomy is created along the greater curve of the stomach adjacent to the pylorus; the pylorus is oversewn from the inside; and a gastrojejunostomy is created with a loop of jejunum. A long jejunal limb should be created to prevent reflux of enteric contents to the duodenum. If a fistula develops, it is a functional end duodenal fistula, which is usually easier to manage than a higher output lateral fistula. A feeding jejunostomy is employed in this setting to ensure a route for enteral nutrition.⁶¹ Some authors additionally advocate a retrograde tube passed into the duodenum for decompression.⁹ The patient will often tolerate an oral diet after 10–14 days. The incidence of marginal ulceration may be reduced by the performance of vagotomy; however, significant bleeding is an infrequent (3%) complication.^8,62 Furthermore, the pylorus has been documented to reopen within 3–7 weeks in over 90% of patients. Thus, routine vagotomy is not justified.^8,62

Although there are no prospective studies to prove the benefit of either diverticulization or pyloric exclusion, several reports from the 1970s and 1980s suggested that the introduction of the pyloric exclusion procedure was associated with a reduction in duodenal leak/fistula and its incumbent morbidity and mortality.^{8,12,24,62,63} On the other hand, recent series have questioned the necessity of this adjunct, pointing out that most injuries may be managed safely and successfully by primary repair.^{55,64,65,66,67,68} It should be noted that these recent publications are retrospective reviews of patients whose injuries were severe enough that the trauma surgeon felt a pyloric exclusion was necessary—that is, there is selection bias. Regardless, it is clear that (1) the vast majority of injuries are appropriately managed by repair or resection, without gastric diversion; and (2) morbidity and mortality related to duodenal injuries has decreased in the last two decades. This is likely due in part to contemporary application of damage control principles, allowing duodenal repair under better physiologic conditions.⁶⁹ Ultimately, the surgeon must exercise his or her judgment based on the patient’s overall condition and that of the duodenal tissue, and associated injuries. This author generally favors pyloric exclusion in patients with grade III duodenal injuries and associated grade III-IV pancreatic injuries, or grade IV duodenal injuries not requiring resection. If the procedure is employed, the method of closure is an important consideration. If the pylorus opens too early, the benefit of diversion is lost. In animal studies, pyloric patency was re-established within 2 weeks with polyglycolic acid sutures, while polydioxanone (PDS) held for 4–5 weeks. Of note, pyloric closure with polypropylene did not reopen in one of four animals by 6 weeks.⁷⁰ Further, Martin and colleagues⁶² reported one patient with an intact polypropylene closure at 53 days. In a rat study, external closure with polypropylene was associated with the lowest rate of pyloric patency at 21 days (57%).⁷¹ Reopening of the pylorus after stapled exclusion has not been well-documented. Thus, in order to close the pylorus for an adequate interval, while anticipating reopening within 6 weeks, PDS appears to be optimal. The use of periduodenal drains is debated, and there is no level I evidence supporting either routine use or nonuse. In general, drains are unnecessary after repair of grade I or II, or straightforward grade III injuries, unless there is an associated pancreatic injury (see below). Drains should be placed in any case in which repair is felt to be tenuous enough that a “protective” maneuver such as pyloric exclusion is employed. The advantage is that in case of leak, there will be a controlled fistula. If a drain is to be utilized, a closed suction drain is preferred over other types of drains.⁷²

Grades IV and V

These injuries involve major disruption or devascularization of the second portion of the duodenum with avulsion of the ampulla of Vater or distal CBD (grade IV) or massive disruption of the pancreaticoduodenal complex (grade V). In general, these injuries are caused by blunt trauma or large caliber/high-velocity gunshot wounds, and are associated with other significant injuries. In the face of significant hemorrhage, acidosis, hypothermia, and coagulopathy, a damage control approach is indicated. This entails hemostasis, debridement, and drainage, with subsequent definitive operative management after physiologic derangements are corrected.⁶⁹ If the patient with a grade V injury survives and is brought back for reconstructive surgery, complex repairs and/or resections are generally necessary. If the duodenum can be repaired utilizing reconstructive techniques as described above, then the bile duct may be reimplanted into the duodenum or a Roux-en-Y hepaticojejunostomy created. If the duodenum cannot be repaired, and/or the pancreatic head is destroyed, a pancreaticoduodenectomy is necessary (see discussion below regarding grade V pancreas injuries).⁵⁵

Pancreas

The AAST OIS for pancreatic injury reflects the fact that the major determinant of morbidity following pancreatic trauma is the integrity of the main pancreatic duct (Table 32-9 and Fig. 32-11).⁵³

Grades I and II

With liberal application of sensitive MDCT imaging, many low-grade injuries are diagnosed in patients who have no other indications for laparotomy. Nonoperative management (NOM) is currently recommended for low-grade injuries.⁷³ This has been practiced for the past two decades in children, with good results.^74,75 There is not a great deal of literature in adults, but the approach appears safe. Duchesne et al²⁹ suggest that patients with apparent grade I or II injuries could be managed nonoperatively if ductal disruption is excluded by MRCP or ERCP. Of 35 patients managed in this way, 5 (14%) failed—three with pancreatic abscess, and 2 with missed bowel injuries. In the multicenter trial of New England trauma centers,²⁷ Forty-nine patients with grade I or II pancreatic injuries and another 17 with combined pancreatic and duodenal injuries (both grade I or II) were managed nonoperatively. Four (6%) failed; three had pancreatic drainage at laparotomy, and it is not clear that any of them had prolonged LOS or morbidity related to the pancreatic injury. The recurring themes in the reports of nonoperative management are that (a) it is safe to manage patients with grade I and grade II injuries nonoperatively; (b) it is important to exclude main pancreatic ductal disruption (ie, grade III injury); and (c) main ductal disruptions may be best managed operatively, to avoid pancreatic duct-related complications (see below).

When grade I and grade II injuries are discovered intraoperatively, the vast majority can be treated with no more than surgical hemostasis and drainage.^{3,6,14,19,25,32} Even capsular tears that are not bleeding are not repaired and may be simply drained with closed suction drainage. Drainage is employed liberally as many minor appearing injuries will drain for several days. Unnecessary attempts at repair of lacerations without evidence of ductal disruption can result in late pseudocyst formation, whereas the vast majority of controlled, minor pancreatic fistulae are self-limited and easily managed with soft closed suction drains. The drains are usually removed within a few days, as long as the amylase concentration in the drain is less than that of serum. If amylase levels are elevated, drainage is continued until there is no further evidence of pancreatic leak. Prolonged gastric ileus is common with even minor pancreatic injuries, so distal enteral access with jejunostomy should be considered in such cases. As the composition of most standard tube feeding increases the pancreatic effluent volume and amylase concentration, lower fat and higher pH (4.5) elemental diets are less stimulating to the pancreas.⁷⁶

Grade III

Differentiating grade II from grade III injuries can be challenging, as described above. The nonsurgical diagnosis often requires MRCP or ERCP. In contrast to grade I and II injuries, NOM of grade III injuries is controversial.⁷³ Several reports have addressed this in pediatric patients. Wood and colleagues⁷⁷ reported that after operative management of grade II–IV injuries, the rate of pancreatic complications was significantly lower than after NOM; length of stay and readmission rates were lower although differences were not statistically significant. In larger single- and multi-institutional series, patients with grade III or higher injuries managed nonoperatively have longer LOS, higher overall morbidity rates, higher rates of pseudocyst formation, and longer time to a regular diet.^78,79,80 At this time, data on NOM in adults are sparse.

While ERCP has an established role in managing complications of pancreatic injuries (see below), its role in primarily managing grade III injuries is unclear. Some authors suggest that stenting in the acute phase may allow NOM.^48,49,81 However, there are no prospective data comparing this with surgical treatment. At this time, it is probably advisable only for selected patients with minimal duct disruption. As noted above, verification of ductal injury may require ERCP. To help refine decision making, Takishima et al⁸² proposed a classification of pancreatic ductal injuries based on pancreatography. They suggested that class 1 (normal ducts) and 2a (branch injuries without extraparenchymal extravasation) injuries could be managed nonoperatively, while class 2b (branch injuries with leak into the retroperitoneum), 3a (main duct injuries in the body or tail), and 3b (main duct injuries in the head) injuries require surgical drainage.

In patients undergoing emergent laparotomy without the benefit of preoperative imaging, assessment of pancreatic ductal integrity is pivotal to decision making. As described above, a simplified management guideline based on intraoperative clinical assessment of the duct has largely obviated the need for intraoperative ERCP or surgeon-performed pancreatography.^3,32 Indicators of ductal injury include direct visualization of ductal injury, complete transection of the gland, laceration of more than 50% of the gland, central perforation, and severe maceration.^3,32,52 In indeterminate cases, probability of ductal injury is based on the wound location and the operating surgeon’s assessment of high versus low probability. If the surgeon’s assessment is low probability, closed suction drainage is recommended. If there is clear indication of high suspicion of ductal injury, the management is based on the location of the injury. Injuries to the head should be drained, while injuries to the body and tail are treated by distal pancreatectomy.^3,32,37,73 In the vast majority of patients, distal resection should leave no concern for later pancreatic endocrine or exocrine function.³⁷ If there is any concern for injury to the proximal duct (grade IV), a proximal pancreatogram can be performed through the end of the transected duct; such situations are rarely encountered. The pancreas is divided at the injury location, and the proximal stump is closed. The optimal method of closure is debated. Roux-en-y pancreaticojejunostomy is rarely employed and does not appear to be justified. The primary options are sutured and stapled closures. A recent meta-analysis reported that a stapled closure was superior to sutured closure.⁸³ The addition of direct suture closure of the ductal orifice was not superior to stapled closure alone. Of note, this meta-analysis was dominated by observational studies. In the largest prospective randomized trial performed to date, pancreatic fistula rate was 28% following hand-sewn closure and 32% following stapled closure; this difference was not statistically significant.⁸⁴ The preference of many surgeons is to perform a stapled resection using a TA-type stapler with 4.8 mm staples, which generally avoids excessively crushing the gland. In young trauma patients, the pancreatic duct is small but can usually be identified; individual ligation of the duct is again a matter of preference.²⁵ In the hemodynamically stable patient, the distal pancreatectomy can generally be performed without splenectomy.^37,85 While the risk of overwhelming postsplenectomy sepsis is very low in the trauma population, the ability of the host to combat encapsulated organisms may be compromised and so it is considered a worthwhile exercise. Efforts should be made to establish enteral access at the time of initial laparotomy in virtually all patients with grades III–V injuries.

Grade IV

Trauma to the pancreatic head and neck represents the most challenging of pancreatic injuries. If ductal status cannot be determined, wide external drainage and postoperative ERCP evaluation of the duct is recommended; stenting is reasonable if there is ductal disruption.^3,32,73 In the setting of major disruption at the pancreatic neck, careful assessment of the remaining pancreatic tissue and consideration of future function should be weighed when contemplating an extended distal pancreatectomy. Roux-en-y pancreaticojejunostomy to the distal pancreatic fragment has been recommended to preserve functioning pancreatic tissue, as resection of greater than 85–90% has been felt to be associated with a significant risk of pancreatic insufficiency.⁸⁶ However, as Yellin et al⁸⁶ pointed out, it has been demonstrated that 95% pancreatectomy can be performed without creating a diabetic individual. For destructive injuries of the pancreatic head without associated duodenal injury the surgeon should consider the duodenum-preserving pancreatic head resection (Beger procedure).⁸⁷ Current trends emphasize the effectiveness of closed suction drainage alone even for extensive proximal gland injuries. It is important to remember that hemorrhage control and drainage can allow planning of the optimal reconstructive option, including enlisting a surgeon with appropriate expertise.

Grade V

Pancreaticoduodenectomy is rarely performed for trauma, and a recent analysis of data from the National Trauma Data Bank suggests it was performed for inappropriate indications in as many as 21% of cases.⁸⁸ Indications for the procedure include massive unreconstructable injury to the head of the pancreas, including the intrapancreatic bile duct and proximal main pancreatic duct; and avulsion of the ampulla of Vater from the duodenum with destruction of the second portion of the duodenum. As described above, these injuries are usually encountered with the patient in poor physiologic condition, so the principles of damage control apply (see above). A recent large series from Seattle emphasized that this procedure should be done in a staged manner, after initial damage control, to optimize the patient’s physiologic status.⁸⁹ In addition to improved physiologic status, there are tissue changes that facilitate reconstruction, such as dilation of the biliary and pancreatic ducts.⁹⁰ Delcore and colleagues⁹¹ previously suggested that pancreaticogastrostomy reconstruction is preferable to pancreaticojejunostomy in these circumstances, for physiologic as well as anatomic reasons. A recent meta-analysis supports a lower rate of pancreatic as well as biliary fistulae when pancreaticogastrostomy is performed.⁹²

Complications of Pancreatic and Duodenal Trauma

Two-thirds of deaths associated with pancreatic and duodenal injuries occur in the first 48 hours (Table 32-6). The other deaths are generally due to late sepsis and multiple organ failure, often attributable at least in part to complications of the pancreatic or duodenal injury and/or repair. The morbidity related to duodenal injuries varies with the grade, ranging from 7 to 55%.^12,13,27,28 The morbidity related to pancreatic injuries is consistently higher, ranging from 24 to 52%.^3,6,27,37 Patients with combined pancreaticoduodenal injuries have morbidity rates between 50% and 87%.^88,89 The risk of complications can be predicted by the AAST injury grade, associated injuries, combined pancreaticoduodenal injuries, hypothermia, and packing without drainage during initial damage control laparotomy.

Hemorrhage

Exsanguination is the most common cause of early death associated with pancreatic and duodenal injuries. Early application of damage control maneuvers is therefore necessary for successful management. Damage control techniques such as packing of hemorrhage and stapling or drainage of intestinal leaks will allow for deferred debridement and reconstruction. Correction of coagulopathy and hypothermia, and optimization of oxygen delivery may be lifesaving, followed by definitive operative treatment upon return to the operating room.^69,89,93

Recurrent (Secondary) Hemorrhage

Postoperative hemorrhage is a common concern after laparotomy for pancreatic and duodenal injuries, especially given the extent of associated injuries, which can be a source of bleeding. Approximately 10% of patients after pancreatic and duodenal trauma will sustain some degree of hemorrhage. Transfusion therapy should be guided by evaluation of the patient’s hemodynamic and coagulation status with attention to oxygen delivery. As in a patient presenting with initial trauma, it is important to resuscitate the patient with efforts to correct associated acidosis, coagulopathy, and hypothermia prior to embarking on a reexploration.⁶⁹ In a stable patient with recurrent hemorrhage, angiography may identify the bleeding point for treatment with embolization. Other causes of postoperative hemorrhage late in the treatment course include progressive pancreatic necrosis or intra-abdominal infection/abscess. Serial CT scan evaluation of pancreatic necrosis with aspiration and culture will predict the need for subsequent invasive radiological intervention and drainage. Many patients can be spared complicated and difficult reoperation with these techniques. Hemorrhagic pancreatitis is a rare complication, which may be indistinguishable from postoperative hemorrhage, and has a reported 75% mortality.^14,16

Pancreatic Fistula

Pancreatic fistula is a significant complication, with an incidence in current series of 11–37%.^3,6 In a multicenter review of distal pancreatectomy for trauma, the postoperative fistula rate was 14%; 89% closed within 8 weeks.³⁷ A recent review of posttraumatic biliary and pancreatic fistulae calculated that a pancreatic fistula was responsible for 27 additional hospital days and $191,000 in additional costs.⁹⁴A pancreatic fistula may be diagnosed in a patient with a measurable drain output with an amylase level greater than three times the serum level, on or after postoperative day 3.⁹⁵ A “benign” pancreatic fistula is defined as output less than 200 mL/d, and most will resolve spontaneously if adequate drainage without obstruction is established.⁹⁴ High output lateral fistulae (>700 mL/d) are rare. They are severe management challenges, and many will require long periods of drainage, nutritional support, or late surgical intervention.⁹⁴ Early ERCP with sphincterotomy and/or stenting may accelerate resolution, but more data are needed to clarify its role.⁸¹ Stoma therapists can offer creative solutions for skin protection in these patients. Given the frequency of this complication, liberal enteral access is advised at the time of initial surgery (see above). In the 1990s there was some enthusiasm for the somatostatin analogue octreotide in decreasing the volume of fistula drainage in patients with prolonged high-output fistulae; however, current meta-analysis of randomized trials does not demonstrate any benefit in fistula closure rates.⁹⁶ A somatostatin analogue with a longer half-life and broader binding profile than octreotide was recently found to decrease the rate of clinically significant postoperative pancreatic fistula, leak, or abscess following pancreatic surgery.⁹⁷ Future investigation in trauma is warranted.

Duodenal Fistula and Stricture

Duodenal fistula generally results from failure of surgical repair due to suture line dehiscence, sometimes with distal duodenal obstruction from stricture. Patients with duodenal obstruction in the postoperative period should be evaluated with CT scan to rule out extrinsic compression from associated phlegmon or abscess. Avoidance of tension at the time of duodenal repair is essential to avoid subsequent stricture formation. With careful attention to these principles, duodenal stricture is rare. The incidence of duodenal fistula is generally less than 5%.³⁷ However, it is still recommended to consider protecting the surgical repair with pyloric exclusion in high-risk injuries. If a fistula develops, the diversion results in a less morbid end versus lateral fistula, and if a duodenal stricture or obstruction occurs, drainage is protected via the gastroenterostomy. Most such fistulae heal within several weeks. Once again, it is advisable to establish enteral access at the time of initial repair in high-risk injuries.

Abdominal Abscess

Abscess formation should be considered in patients who develop sepsis after pancreatic or duodenal injury. The best predictors of postoperative abscesses are inadequate debridement or drainage during the initial operative management. Reexploration in this setting carries significant morbidity and mortality and should be avoided whenever possible. Image-guided drainage is preferable, and often is required more than once. Control of infections is important top avoid progression to multiple organ failure.

Pancreatic Pseudocyst and Pancreatitis

Early pseudocyst formation may be indistinguishable from abscess; percutaneous aspiration may be helpful from both a diagnostic and therapeutic standpoint. Delayed pseudocysts may be managed surgically or endoscopically. In the setting of a pseudocyst, ERCP may be employed to evaluate the continuity of the pancreatic duct. If the duct is intact, percutaneous drainage will often resolve the problem. Endoscopic stenting has been described, but there is a paucity of data on late outcomes.⁸¹ Occasionally, pseudocyst formation is the presenting symptom of missed blunt pancreatic trauma.

Transient hyperamylasemia is common in patients after laparotomy for pancreatic trauma; true acute pancreatitis with clinical abdominal pain is much less frequent. A CT scan should be performed to rule out associated abscess, pseudocyst, or other complications. If the diagnosis is confirmed, treatment includes nasogastric suction, bowel rest, and nutritional support. Elemental enteral formulas appear to be tolerated well and should be provided. Most cases will resolve spontaneously. Chronic pancreatitis has been reported after pancreatic trauma; its treatment would follow the same principles as chronic pancreatitis due to other causes.⁹⁸

Pancreatic Insufficiency

This is a concern when resecting more than 80% of the pancreas, for grade IV or V injuries (see above). With careful attention to injury patterns as described, both exocrine and endocrine insufficiency should be rare after pancreatic trauma. In the trauma setting, it may be assumed that any resection distal to the mesenteric vessels will preserve adequate pancreas for normal function.³⁷