Duodenum and Pancreas

Walter L. Biffl

INTRODUCTION

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)

HISTORY

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.

Diagnosis

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%.³⁶ 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, CT should be repeated.

FIGURE 32-4

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