Walter L. Biffl
Injuries to the pancreas and duodenum present a significant challenge, for a number of reasons. First, while the deep, central position of the pancreas and duodenum afford the organs some degree of protection, their retroperitoneal location confounds the clinical detection of injury. Second, the infrequency of these injuries has resulted in a lack of significant management experience among practicing trauma surgeons. Third, anatomic and physiologic factors contribute to a disturbingly high incidence of complications following injury; morbidity is exacerbated by delays in diagnosis and treatment. Consequently, trauma to the pancreas and duodenum is associated with relatively poor outcomes that have not improved significantly, despite advances in trauma and critical care management (see Tables 32-1 and 32-2).1–16
TABLE 32-1 Duodenal Trauma: Mortality by Mechanism of Injury in Large Series (>100 Patients)
TABLE 32-2 Pancreatic Trauma: Mortality by Mechanism of Injury in Large Series (>100 Patients)
Most early descriptions of duodenal and pancreatic injuries are isolated autopsy observations. The first acknowledged literature report of pancreatic trauma was published by Travers in 1827. By 1903, von Mikulicz-Radeck reported only 45 cases in the literature.17 Of note, 72% of operated patients survived, a success rate that rivals modern-day results. Many of the recommendations suggested in that early series still hold true today: thorough abdominal exploration, hemostasis, and drainage. 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. Although much sentinel work in trauma was done during the Vietnam War, virtually no reports of pancreatic or duodenal injuries are available except for a single report of two cases of pancreaticoduodenectomy.18
The first successful surgical repair of a duodenal rupture was published by Herczel in 1896. In 1904, Summers19 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 Giuseppi20 from 10 London hospitals. There were 29 patients with duodenal injuries, all of whom died. In fact, the authors cited only one known survivor of duodenal trauma to that point in time. Cave, in a World War II experience, recorded 118 cases of duodenal injuries with a mortality of 57%, which is still the single largest military series of duodenal injuries.21
Recent Historical Trends
Pancreatic and duodenal trauma remain uncommon, and no single institution has extensive experience. Trauma centers such as Ben Taub, Grady Memorial, UT-Southwestern, L.A. County, Detroit Receiving, Memphis, and Denver General Hospital saw only 10–20 duodenal and 10–20 pancreatic injuries per year in the 1960s–1980s.1–3,5,7–10,12,22,23 Recent series document incidences of 0.2–0.3% for duodenal injuries and 0.004–0.6% for pancreatic injuries.7,15,24,25 Duodenal or pancreatic injuries are found in 3–6% of patients undergoing laparotomy for trauma.7,26 The risk of pancreatic or duodenal injury is much higher in penetrating compared with blunt trauma, as suggested by the data in Tables 32-1 and 32-2.1–16,27 However, the most recent series have documented a reversal of this trend, consistent with decreasing urban violence over the past 15 years. The Harborview Hospital experience is comprised of 71% blunt trauma patients,15 and a recent survey of Level I Trauma Centers in New England found that 91% of pancreaticoduodenal injuries were caused by blunt trauma.16
The anatomic location of the pancreatic-duodenal axis, and its proximity to other vital structures, makes isolated injuries distinctly uncommon (Figs. 32-1 and 32-2). In virtually every large series, over 90% of pancreatic and duodenal injuries are associated with injuries to other organs.1–3,5–9,12,13,27 The common associated injuries and their frequencies are listed in Tables 32-3 and 32-4. On average, there are 2.5–4.6 associated injuries with each pancreatic or duodenal injury.7,27 Not surprisingly, complication rates are higher when there are associated injuries, and the mortality rate increases progressively with each associated injury.16 Notably, the combination of pancreatic and duodenal injuries doubles the mortality rate compared with that of either injury alone (Table 32-5).
TABLE 32-3 Associated Injuries in 1,234 Cases of Duodenal Trauma
TABLE 32-4 Associated Injuries in 1,086 Cases of Pancreatic Trauma
TABLE 32-5 Combined Pancreaticoduodenal Trauma: Mortality by Mechanism of Injury in Large Series (>100 Patients)
A survey of several large series over the past three decades demonstrates that stab victims do better than gunshot victims; however, there is a consistent mortality rate of 16–17% for both pancreatic and duodenal injuries, whether blunt or penetrating (Tables 32-1 and 32-2). This reported rate has not changed significantly over time, but there appears to be a trend toward lower mortality rates. Current experience, with the routine use of sensitive diagnostic modalities, identifies more low-grade injuries that may have previously escaped detection. In the series from Seattle15 and New England,16 for example, three quarters of the patients had grade I or II injuries (see Grading). This could explain decreased overall morbidity and mortality rates.
Three quarters of patients who die from a pancreatic or duodenal injury do so within the first 48 hours, from exsanguinating hemorrhage in the setting of multiple associated injuries or from devastating neurologic injury (Table 32-6). Thus, predictors of survival include age, overall injury severity, indices of shock, and severe brain injury, rather than pancreatic or duodenal injury grade.7,15,26 Late deaths in cases of pancreatic and duodenal trauma are most often ascribed to sepsis and multiple organ failure, 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.15,16 Among those patients with a delay in the initial diagnosis of pancreaticoduodenal injury, morbidity and mortality rates are considerably higher.15,16
TABLE 32-6 Timing of Death Following Pancreatic or Duodenal Trauma
ANATOMY AND PHYSIOLOGY
The duodenum and pancreas are intimately associated with many vital structures in a deep and narrow region (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 or first, descending or second, transverse or third, and ascending or fourth portion. 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 the first portion of the duodenum and the most distal part of the fourth portion of the duodenum. 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.
FIGURE 32-1 Anatomic relation of the pancreas and duodenum, emphasizing the proximity of major associated structures. (A) Relation to adjacent organs. (B) Important vascular structures in close proximity to the pancreas and duodenum.
FIGURE 32-2 Drawing showing the incidence of injuries to nearby organs and vessels in patients with duodenal wounds. (Reproduced with permission from Morton JR, Jordan GL Jr: Traumatic duodenal injuries: Review of 131 cases. J Trauma 8:127, 1968.)
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 and 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. A part of the head, the uncinate process, extends to the left behind the SAM 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. There are numerous collateral vessels throughout the pancreas that protects it from ischemia, but also contributes to vigorous bleeding following injury. The second portion of the duodenum has a unique blood supply that originates from both the gastroduodenal artery and the inferior pancreatoduodenal 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. Because the pancreatoduodenal vessels are located on the surface of the head of the pancreas, portions may be resected without causing necrosis of the second portion of the duodenum. If all of the pancreatoduodenal vessels are injured by trauma, a pancreatoduodenectomy will be necessary. The body and tail of the pancreas receive collateral circulation from the SMA and splenic artery. 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 pancreatic and CBDs. The CBD descends from above to 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. R 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 approximately 10% of the gland remaining after resection may maintain normal hormonal balance. Both duct and acinar cells of the pancreas secrete between 500 and 800 mL/day 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.28 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 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 juncture of the 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. But in many cases, the integrity of the pancreatic duct remains in question. In these situations, it is crucial to assess the status of the main pancreatic duct (see below).
Diagnosis of blunt injuries in hemodynamically stable patients is more challenging. A common mechanism in both duodenal and pancreatic injuries is blunt force to the epigastrium. 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. Leukocytosis, unexplained metabolic acidosis, or fever may herald an occult injury. The utility of serum amylase—and more recently, lipase—assays has been debated. In 1943, Naffziger and colleagues suggested that amylase was of diagnostic value in the evaluation of patients with blunt abdominal trauma.29 Unfortunately, subsequent reports highlighted the poor sensitivity and specificity of the test. Bouwman et al.29 evaluated isoenzymes of amylase, with the same disappointing conclusion. Takishima et al.30 found that if the amylase level was measured more than 3 hours after trauma, it was most likely to reflect pancreatic injury. In sum, amylase levels should not be relied upon to either diagnose or exclude pancreatic injury. In a patient with persistent epigastric pain after blunt abdominal trauma, hyperamylasemia should prompt further diagnostic evaluation. On the other hand, a normal value in that setting may not be sufficient to avoid further work-up.
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 allow 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. Recently, contrast-enhanced ultrasound has been reported to detect some pancreatic injuries.31 However, its role is poorly defined at this time. Diagnostic peritoneal lavage is not considered reliable for evaluation of the retroperitoneum, so it plays a limited role in diagnosing pancreaticoduodenal trauma.
In the stable patient with suspicion of intraabdominal injury, computed tomography (CT) scanning is the primary diagnostic modality. Signs of duodenal perforation include free air and contrast extravasation. 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 wall hematoma, as the former mandates laparotomy but the latter may be managed nonoperatively. Duodenography has been employed to help clarify the presence of perforation; however, its sensitivity is poor (54%) and thus it should not be considered an adjunct to CT.32 There are no specific data about the sensitivity and specificity of multidetector CT (MDCT), but accumulating experience suggests superior imaging with proper protocols.33 Equivocal studies may require 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.34
FIGURE 32-3 Computed tomography (CT) finding of retroperitoneal duodenal perforation. CT scan shows poor definition of the structures in the region of the head of the pancreas (curved arrow) and diminished enhancement of the head compared to the body. A collection of extraluminal, retroperitoneal gas (straight arrow) lies immediately posterior to the second portion of the duodenum (d), consistent with a duodenal perforation. This patient is also depicted in Fig. 32-4. (Reproduced with permission from Smith DR, Stanley RJ, Rue LW III: Delayed diagnosis of pancreatic transection after blunt abdominal trauma. J Trauma 40:1009, 1996.)
The CT findings of pancreatic injury may be subtle, particularly when the imaging is performed within 12 hours of injury (Fig. 32-4). 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.33 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.33,35 It is believed that MDCT will improve on this. However, a recent American Association for the Surgery of Trauma (AAST) multicenter study looked at the accuracy of 16- and 64-detector row CT for detecting pancreatic injury in general, and pancreatic ductal injury specifically. Although specificity was better than 90%, the sensitivity of MDCT for either injury was only 47–60%.36Ultimately, 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, CT should be repeated.
FIGURE 32-4 Computed tomography scan of pancreas, demonstrating subtle early signs of injury, including irregularity of the neck of the pancreas (arrow), peripancreatic fluid, and intrahepatic hematoma (H). (Reproduced with permission from Smith DR, Stanley RJ, Rue LW III: Delayed diagnosis of pancreatic transection after blunt abdominal trauma. J Trauma 40:1009, 1996.)
FIGURE 32-5 CT scan of pancreas, demonstrating midbody transection from a direct epigastric blow.
The integrity of the main pancreatic duct is the most important determinant of prognosis, as most major morbidity is related to ductal disruption. Consequently, management is dependent on the status of the duct. As noted, CT scanning—even with MDCT—is not reliable for identifying ductal disruption. Evaluation of the duct can be accomplished in stable patients via endoscopic retrograde cholangiopancreatography (ERCP).37,38 This technique is particularly valuable in the trauma patient in whom there may be subtle changes on CT, and chemical evidence of pancreatitis but without overt clinical findings mandating laparotomy. In such cases, observation may be justified if a duct disruption can be excluded. An alternative technique that may be useful in a stable patient is magnetic resonance cholangiopancreatography (MRCP).39 Advantages of MRCP include its noninvasiveness and the ability to visualize not only the duct, but the pancreatic parenchyma and remainder of the abdomen.35Delineation of ductal anatomy may be further enhanced by the administration of secretin, which increases pancreatic exocrine output and distends the pancreatic duct.40 Currently there are few series reporting the accuracy of MRCP, and it has not been prospectively compared with ERCP. However, it is considered an appropriate next step in evaluating a pancreatic duct whose integrity is questioned after CT scanning.
Patients who are unstable, or who have pancreatic injury first diagnosed in the operating room, may require intraoperative pancreatography to assess the duct. Although intraoperative ERCP is an option, it may be difficult to mobilize a gastroenterology team rapidly, and the requisite bowel insufflation can interfere with abdominal closure. Alternatively, pancreatography may be performed by the surgeon.41 The simplest approach is to clamp the common hepatic duct and infuse contrast into the gallbladder for cholangiopancreatography (Fig. 32-6). If imaging is inadequate, a duodenotomy is then performed for identification and cannulation of the ampulla of Vater. A blunt-tipped probe can be passed, which may confirm the diagnosis of ductal disruption. If not, pancreatography is performed with 2–3 mL of water soluble contrast material under very low pressure with fluoroscopic imaging (Fig. 32-7). Some have recommended intraoperative pancreatography via transecting the tail of the pancreas and cannulation of the distal duct (Fig. 32-8). This technique has had inconsistent results; hence, transecting the pancreas to perform these evaluations appears ill-advised.
FIGURE 32-6 Intraoperative cholangiopancreatogram obtained via the gallbladder. Complete pancreatogram is obtained, depicting proximal pancreatic duct injury and extravasation of contrast.
FIGURE 32-7 Intraoperative cholangiogram obtained via duodenotomy and direct cannulation of the ampulla. Overly forceful injection resulted in contrast extravasation into the pancreatic head. Also note a distal pancreatic duct injury with contrast extravasation near the laparotomy pad marker.
FIGURE 32-8 Intraoperative proximal pancreatogram obtained via an injured mid-body pancreatic duct. Normal residual proximal duct is confirmed prior to performing distal pancreatectomy.
Decision Making and Treatment Options
Treatment and decision making is perhaps best reviewed in light of injury severity. The classification system most commonly used for injury stratification is the AAST Organ Injury Scale (OIS) (Table 32-7and Fig. 32-9).42 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.
TABLE 32-7 AAST Duodenum Organ Injury Scale
FIGURE 32-9 Algorithm I. Algorithm for duodenum injury.
Grades I and II
Duodenal intramural hematomas may be identified at the time of exploration, but are more often detected on CT scanning (Fig. 32-10). The clinical course is marked by progressive gastric outlet obstruction with or without bilious emesis. The lesion is more common in children, and there is a high frequency of nonaccidental trauma.43 Obstruction develops as fluid is sequestered into a hyperosmotic hematoma. If there are no other indications for laparotomy, treatment generally consists of IV hydration, parenteral nutrition, and nasogastric tube suction.44 Most duodenal hematomas will resolve spontaneously within 3 weeks. For patients who continue to manifest complete obstruction after 7–10 days, repeat CT scan should be done to reevaluate the obstructive process, and operative management should be considered.45Operative approaches for evacuation of the hematoma include open or laparoscopic drainage procedures. At exploration, the pancreas and duodenum must be thoroughly mobilized and examined. Duodenal stricture or occult perforation or unsuspected injury to the head of the pancreas should be sought. Injuries can range from serosal staining to obstructing masses. Treatment is somewhat controversial. Opening of the hematoma at the time of initial operation is condoned by some authors, who favor tube decompression of the stomach and distal tube jejunostomy for postoperative enteral nutrition while the hematoma resolves. With patience, almost all hematomas resolve in this setting, and opening of the duodenum risks conversion of a closed to open injury. Our group favors a selective approach. We treat small hematomas with minimal luminal compromise with nasogastric suction and distal feeding tube jejunostomy, reserving incision and evacuation for larger hematomas with mass effect and luminal compromise (>50%). In such situations, we perform meticulous hemostasis with closure of duodenum with running absorbable closure.
FIGURE 32-10 Diagnosing duodenal hematoma in a 30-year-old male. (A) Upper gastrointestinal radiograph showing narrowing of the second and third portions of the duodenum. (B) Computed tomography scan in the same patient, showing a giant hematoma of the transverse portion of the duodenum.
Approximately 75% of duodenal lacerations occur as a result of penetrating trauma (Table 32-1). Exploratory laparotomy is performed via a midline incision. As described previously, standard trauma principles are employed for control of hemorrhage and enteric leaks. Exposure of the pancreas and duodenum is initiated with performance of the Kocher maneuver, which allows for evaluation of the head of the pancreas as well as the C-loop. 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. After evaluation of the head of the pancreas, the neck, body, and tail are examined by opening the gastrocolic omentum from the left to the right. Adhesions to the stomach are taken down and the inferior border of the pancreas is visualized by incising the anterior reflection of the transverse mesocolon. Any evidence of blood, bile, or air in the retroperitoneum requires thorough exploration. Simple duodenal lacerations with limited injury or 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.6 Duodenotomies can be repaired with running or interrupted sutures; a monofilament repair is preferred. Avoidance of tension is paramount. 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.46 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.
Some grade III lacerations may be repaired by simple duodenorrhaphy. Snyder et al.3 identified severity factors that were associated with morbidity and mortality, and often preclude primary duodenorrhaphy; blunt trauma or gunshot wound; involvement of >75% of the duodenal wall; injury in D1 or D2; an interval from injury to repair >24 hours; and CBD injury. 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. In these situations, the distal duodenal stump is oversewn and a distal jejunojejunostomy is created for intestinal continuity (Fig. 32-11). 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. Repair of injuries to the third and fourth portion of the duodenum may be compromised by the short mesentery, causing difficulty in mobilization and leading to ischemia. Resection and duodenoduodenal anastomosis in this setting is associated with a high rate of fistula formation. This is another role for resection and duodenojejunostomy.
FIGURE 32-11 Roux-en-Y duodenojejunostomy is used to treat duodenal injuries between the papilla of Vater and superior mesenteric vessel when tissue loss precludes primary repair. (Reproduced with permission from Brunicardi FC et al. Schwartz’s Principles of Surgery, 8th ed. McGraw-Hill, Inc., 2005. Fig. 6-52, p. 168. © The McGraw-Hill Companies, Inc.)
When confronted with a patient with an intermediate grade duodenal injury and associated pancreatic injury, the pyloric exclusion procedure as described by Vaughan et al.1 has been preferred (Fig. 32-12). This procedure is simpler than the original “diverticulization” technique described by Berne et al.47 The duodenal injury is repaired 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 with nonabsorbable monofilament suture; and a gastrojejunostomy is created with a loop of jejunum. A long jejunal limb should be used 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 needle catheter jejunostomy is employed in this setting to ensure a route for enteral nutrition, and we have found this to be a safer method than standard jejunostomy.48,49 Even in the setting of an end fistula, the patient will often tolerate an oral diet after 10–14 days. The pylorus usually opens within 6–12 weeks; therefore, vagotomy is not usually performed. This procedure may also be employed as a protective adjunct for a tenuous duodenal repair. Other techniques that have been described include omental patch or jejunal patch with a loop of jejunum, although such procedures are unproven. As an alternative to pyloric exclusion and gastric diversion, Stone and Fabian2 advocated routine lateral tube duodenostomy or retrograde jejunostomy for decompression. However, this is no longer practiced. An interesting potential technique is bioprosthetic repair of complex duodenal defects. Primarily studied in preclinical models to date, there is a potential advantage of providing a durable repair more expediently.50
FIGURE 32-12 (A) Pyloric exclusion is used to treat combined injuries of the duodenum and the head of the pancreas, as well as isolated duodenal injuries when the duodenal repair is less than optimal. (B) The pylorus is oversewn through a gastrotomy. The gastrotomy will subsequently be used to create a gastrojejunostomy. (C) These authors frequently employ needle-catheter jejunostomy tube feedings for these patients. (Reproduced with permission from Brunicardi FC, et al. Schwartz’s Principles of Surgery, 8th ed. McGraw-Hill, Inc., 2005. Fig. 6-53, p. 169. © The McGraw-Hill Companies, Inc.)
Although there are no randomized prospective studies to prove the benefit of any type of gastric diversion and drainage in severe injuries, several reports do support the use of pyloric exclusion and gastrojejunostomy in selected cases, and particularly for intermediate- to high-grade duodenal injuries combined with pancreatic injuries.6,22,51,52 On the other hand, recent series have called the necessity of this adjunct into question, suggesting that patients may be managed safely with primary repair.53,54 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.
Grades IV and V
These injuries involve massive 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.55
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 32-8 and Fig. 32-13).42
TABLE 32-8 AAST Pancreas Organ Injury Scale
FIGURE 32-13 Algorithm II. Algorithm for pancreatic trauma.
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. Recognizing that most of the related morbidity is due to ductal disruption, nonoperative management has been suggested for low-grade injuries. This has been more widely practiced in children, with good results.56 There is not a great deal of literature in adults, but the approach appears safe. Duchesne et al.25 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,16 69 (41%) of 170 patients with pancreatic or combined pancraticoduodenal injuries were managed nonoperatively, with 7 (10%) failing. 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; and (c) main ductal disruptions may be best managed operatively, to avoid pancreatic duct-related complications (see below). More data are needed in this area.
When grade I and grade II injuries are discovered intraoperatively, the vast majority can be treated with no more than surgical hemostasis and drainage.15,57 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 needle catheter 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 and are particularly well suited for use in needle catheter jejunostomies.58
Distal transection or parenchymal injury with main pancreatic duct disruption generally requires surgical management in order to prevent pancreatic ascites or major fistula. Most ductal injuries can be identified either by preoperative studies in the stable patient or intraoperatively, as previously described. The anatomic division between the head and body of the pancreas is the neck, where the SMA and SMV pass behind the pancreas. This anatomic division will provide an estimated 50% of pancreatic tissue. Management decisions are based upon the anatomic location of the parenchymal and duct injury (i.e., proximal vs. distal). Ductal injuries at or distal to the neck are treated definitively with distal pancreatectomy.14,59 In the vast majority of patients, distal resection should leave no concern for later pancreatic endocrine or exocrine function.60 If there is any concern for injury to the duct proximally in this setting (grade IV), a proximal pancreatogram can be performed through the end of the transected duct. In our experience, 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 pancreati-cojejunosotmy does not appear to be justified. Alternatively, the parenchyma can be closed with nonabsorbable mattress sutures placed in a full-thickness noncrushing technique. The preference of many surgeons, however, is to perform a stapled resection using a TA-type stapler with 4.8-mm staples, which generally avoids excessively crushing the gland.61 In young trauma patients, the pancreatic duct is small but can usually be identified; it should be individually ligated at the time of pancreatic division.23 In the hemodynamically stable patient, the distal pancreatectomy can often be performed without splenectomy.14,59 Efforts should be made to establish enteral access at the time of initial celiotomy in virtually all patients with grades III–V injuries to avoid the use of parenteral nutrition, with its attendant risks and complications.62
Verification of ductal injury will require laparotomy in most cases. To further refine decision making, Takishima et al.63 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; 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. Although Takishima and colleagues did not address it, there have been several reports describing therapeutic applications of ERCP for acute trauma. Theoretically, performing sphincterotomy and/or placing stents would promote healing and eliminate leakage from traumatically disrupted ducts, just as is done for other disorders.64,65 Although this seems an attractive minimally invasive alternative, results have been mixed. It has not been a panacea, and still is associated with complications. A prospective randomized clinical trial would help in determining the role of therapeutic ERCP in the management of acute pancreatic trauma. At this time, it is probably advisable only for select patients with minimal duct disruption.
Trauma to the pancreatic head and neck represents the most challenging of pancreatic injuries. Careful assessment of the remaining pancreatic tissue and consideration of future function should be weighed when contemplating an extended distal pancreatectomy. Prior to embarking on such a procedure, one must carefully assess the status of the pancreatic duct and CBD (see above). 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. Resection of greater than 85–90% is associated with a significant risk of pancreatic insufficiency.66 In the rare situation where resection will result in less than 20% of intact pancreatic tissue, the pancreas should be divided, the proximal segment closed, and the distal portion preserved with drainage into a Roux-en-Y pancreaticojejunostomy.60 Current trends emphasize the effectiveness of closed suction drainage alone even for extensive proximal gland injuries.14,67However, the effectiveness of this technique with major ductal injury remains to be established.
Although rarely warranted, recent experience indicates that for devastating injury to the head of the pancreas, pancreaticoduodenectomy can be performed with acute outcomes similar to the elective setting.68–70 Indications for this procedure include massive pancreatic or retropancreatic hemorrhage; 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). As Seamons et al.71 recently reinforced the concept of pancreatic resection during damage control is ill-advised. Once the patient’s condition improves, the reconstruction is performed. In addition to improved physiologic status, there are tissue changes that facilitate reconstruction.72 Pancreatogastrostomy reconstruction may be preferable to pancreaticojejunostomy in these circumstances, for physiologic as well as anatomic reasons.69
Combined Pancreatic and Duodenal Injuries
Combined pancreatic and duodenal injuries are quite common given their intimate anatomic relationship: 30% of duodenal and 16% of pancreatic injuries are combined (Tables 32-3 and 32-4). Such injuries are more common following penetrating trauma. The presence of both injuries significantly increases the complication rates, with morbidity and mortality from combined pancreatoduodenal injury twice that observed from either injury alone (Table 32-5). Grades I–II duodenal lacerations with limited surrounding tissue damage, in combination with grades I–II pancreatic injuries, can be treated with primary duodenal repair and drainage. With higher grade duodenal or pancreatic injuries, the risk of duodenal suture line dehiscence is increased and pyloric exclusion should be considered. Grades IV–V injuries are discussed above. The basic principles of management include adequate debridement and drainage, duodenal diversion, and nutritional support.73–75
Complications of Pancreatic and Duodenal Trauma
Three quarters 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%.6,7,16,24 The morbidity related to pancreatic injuries is consistently higher, ranging from 24 to 52%.14–16,59,67 Patients with combined pancreatoduodenal injuries have morbidity rates in the 21–36% range.16,75 The risk of complications can be predicted by the AAST injury grade, associated injuries, combined pancreatoduodenal injuries, hypothermia, and packing without drainage during initial damage control laparotomy.7,15,42,71
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 life-saving, followed by definitive operative treatment upon return to the operating room.71 In our experience, this can usually be accomplished within 24–36 hours.55
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.76 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.55 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.8,10
Pancreatic fistula is a significant complication, with an incidence in current series of 11–37%.14,15,67 A pancreatic fistula may be diagnosed in a patient with a measurable drain output with an amylase level greater than three times the serum level.77 A “benign” pancreatic fistula is defined as output less than 200 mL/day, and most will resolve spontaneously if adequate drainage without obstruction is established.78 High output lateral fistulae (greater than 700 mL/day) are rare. They are severe management challenges, and many will require long periods of drainage, nutritional support, or late surgical intervention.78 Early ERCP with sphincterotomy and/or stenting may accelerate resolution, but more data are needed to clarify its role.64 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). The somatostatin analogue octreotide has shown some promise in treating patients with prolonged high-output fistulae.79 It has been shown to decrease the volume of fistulae drainage, but does not decrease the duration of the fistulae or increase the rate of spontaneous closure. There is a paucity of controlled data in trauma, but results have not supported routine use.80 In a multicenter review of distal pancreatectomy for trauma, the postoperative fistula rate was 14%; 89% closed within 8 weeks.59 Persistent pancreatic fistulae may require surgical treatment if not resolving. Of note, 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.78
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%.59 However, it is still recommended to protect 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 heal within several weeks. Once again, it is advisable to establish enteral access at the time of initial repair in high-risk injuries.
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.81 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.64 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 probably 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 employed with avoidance of total parenteral nutrition (TPN) and its associated complications. 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.82
This is a concern when resecting >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.59
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