Lawrence N. Diebel
Injuries to the stomach and small bowel are common in penetrating abdominal trauma.
The incidence of gastrointestinal injury following gunshot wounds that penetrate the peritoneal cavity is over 80%. Thus, exploratory laparotomy is warranted on virtually all gunshot wounds that penetrate the peritoneal cavity. The incidence of hollow viscus injury (HVI) secondary to stab wounds that have penetrated the peritoneal cavity is much less, which in most series is about 30%. Thus, a selective approach to operative exploration has been advocated following stab wounds.
Blunt injuries to the stomach and small bowel are much less common than penetrating injury, but collectively compromise the third most common type of blunt abdominal injury. The increasing use of computed tomography (CT) for diagnostic evaluation of the patient with blunt abdominal trauma and selective nonoperative management of solid organ injuries have contributed to some of the difficulties and controversies in the management of HVIs following blunt trauma. In contradistinction to some of the diagnostic difficulties with stomach and small bowel injuries, operative repair of stomach and small bowel injuries is relatively straightforward. The key to the successful management of stomach and small bowel injuries is prompt recognition and treatment, thus decreasing the likelihood of abdominal septic complications and subsequent late death.
Intestinal injuries were reported early in the medical literature (see Chapter 1). Small bowel perforation from blunt trauma was first recognized by Aristotle.1 Hippocrates was the first to report intestinal perforation from penetrating abdominal trauma. In 1275, Guillaume de Salicet described the successful suture repair of a tangential intestinal wound. Reports of attempted surgical repair of gastric and intestinal wounds appeared in the literature with heightened interest and controversy during the American Civil War, the Spanish-American War, the Russo-Japanese War, and other military conflicts. However, the dismal results of surgical intervention lead to abandonment of laparotomy even with obvious intestinal injury during these military campaigns.2
By the late 19th century, improved surgical techniques led to renewed interest in laparotomy and repair of penetrating abdominal injuries. Theodore Kocher was the first surgeon to report successful repair of a gunshot wound of the stomach. Although still controversial, in 1901 President William McKinley, shot in the abdomen by an assassin, underwent expeditious transport and surgical repair of several gastric wounds. However, a wound to the pancreas was overlooked, and McKinley died 8 days later.
A laparotomy for intestinal perforation at the start of World War I carried a mortality rate of 75–80%, almost equal to the mortality rate of nonoperative management. However, in the later part of World War I, operative management was recognized as the preferred management for penetrating abdominal trauma.
In World War II, prompt evacuation, improvements in anesthesia, and better understanding and treatment of shock led to mortality rates of 13.9% for jejunal or ileal injuries and 36.3% if multiple injuries were present.3 Further improvements in mortality were noted during the Korean War and Vietnam conflicts. Lessons learned by military surgeons were quickly adopted by surgeons in civilian centers. However, the sheer volume of trauma in several major trauma centers dictated that patients with abdominal stab wounds be treated expectantly and operations performed on the basis of physical signs of peritonitis or hemodynamic instability. Based on this experience, it became obvious that stab wounds and/or low velocity gunshot wounds did not share the same risk as wounds from military weapons. Thus, selective management became a formal policy at larger experienced centers and soon included GSW that appeared tangential, or involved posterior, flank, or thoracoabdominal locations.
Patients with gastrointestinal injuries under these circumstances may benefit from a staged operative approach for abdominal injuries. Simple repairs or temporizing measures aimed at controlling ongoing peritoneal contamination by gastrointestinal injuries are performed at the initial operation. Definitive repair for more complex gastrointestinal injuries is undertaken at a later operation after hemodynamic stabilization.
Nonetheless, prompt recognition and repair of injuries are responsible for the low morbidity and mortality from isolated gastric and small bowel injuries. Associated injuries contribute significantly to morbidity and mortality in patients with gastric and small bowel injuries.
ANATOMY AND PHYSIOLOGY
The stomach generally occupies the left upper quadrant of the abdomen. The nondistended stomach, especially in a supine individual, is located largely in the intrathoracic abdomen where it is offered some protection by the lower chest wall. The position of the stomach can be quite variable and in the erect individual may extend into the lower abdomen, particularly when distended with food or liquid. The stomach is fixed on its lesser curvature by the gastrohepatic ligament, cephalad by the gastrophrenic ligament, and distally by the retroperitoneal duodenum. The greater curvature of the stomach is loosely bound to the transverse colon via the greater omentum and to the spleen by the gastrosplenic ligament. The stomach enjoys a rich blood supply from the left and right gastric arteries, the left and right gastroepiploic arteries, and the short gastric arteries (Fig. 31-1). Venous drainage follows the arterial supply to the stomach for the most part.
FIGURE 31-1 Blood supply to the stomach. An anomalous left hepatic artery can arise as a branch of the left gastric artery. This should be looked for when doing gastric resections. (Reproduced with permission from Agur AMR, Dalley AF, eds. Grant’s Atlas of Anatomy. 11th ed. Copyright Lippincott Williams & Wilkins; 2004.)
The normal stomach is relatively free of bacteria and other microorganisms because of the low intraluminal pH.4 However, up to 103 organisms/mL, including lactobacilli, aerobic streptococci, and even Candida, may be isolated. Low gastric acidity due to H2-receptor blockade or now proton pump inhibitors leads to increased bacterial concentrations in the stomach and proximal gastrointestinal tract, increasing the risk of peritoneal contamination with gastric perforation. Retained food in the stomach may also increase the risk of infection following gastric perforation. Factors include acid neutralization and increased luminal bacteria in the postabsorptive state as well as serving as an adjuvant in the event of peritoneal contamination.
The small bowel distal to the ligament of Trietz is approximately 5–6 m in length in the adult. Protected anteriorly only by the abdominal wall musculature and occupying most of the true abdominal cavity, the small intestine is anatomically vulnerable to injury.
The small intestine is suspended from the posterior abdominal wall by its mesentery, the base of which extends from the duodenal jejunal flexure, superior to inferior and left to right to the level of the right sacroiliac joint. The arterial supply to the small bowel is provided by the superior mesentery artery (SMA), which emerges from under the pancreas and then courses anterior to the uncinate process of the pancreas to enter the root of the mesentery. The blood supply to the small bowel comes from the left side of the SMA via intestinal arteries (Fig. 31-2). The jejunal and ileal branches vary in number and supply all but the terminal part of the ileum. This is supplied by branches from the ileocolic artery. Numerous intestinal arcades form within the mesentery to assure excellent collateral blood supply to the small intestine. Venous return from the small intestine follows the arterial supply: the superior mesenteric vein joins the inferior mesenteric vein and splenic vein to form the portal vein.
FIGURE 31-2 Blood supply to the small bowel. Multiple branches to the jejunum and ileum originate directly from the superior mesenteric artery. The distal ileum is supplied via the ileocolic artery. (Reproduced with permission from Agur AMR, Dalley AF, eds. Grant’s Atlas of Anatomy. 11th ed. Copyright Lippincott Williams & Wilkins; 2004.)
Although no clear distinction exists, the first 40% or so of the bowel is jejunum and the remainder is the ileum (Fig. 31-3). The jejunum has a larger diameter, more circular folds, and larger villi, but less lymphoid tissue than the ileum. The mesentery of the jejunum contains only a single arcade, whereas more than two or three sets of vascular arcades are present in the ileum. Mesenteric fat is also more prominent in the ileum than in the jejunum. The proximal jejunum is the primary site of carbohydrate, protein, and water-soluble vitamin absorption. Fat absorption occurs over a larger length of small bowel. The ileum is the primary site of carrier-mediated bile salt and vitamin B12 absorption. Loose intercellular junctions contribute to significantly greater water and sodium fluxes in the jejunum than in the ileum. Tighter intercellular junctions and active transport of sodium chloride allow for significant fluid reabsorption and concentration of luminal content in the ileum (and colon). However, distinctions between jejunum and ileum are of clinical importance only if a significant length of bowel is resected. The ileocecal valve is thought to act as a “break” to the delivery of small bowel content into the cecum. It may also be a barrier for reflux of colonic content into the small bowel. However, ileal peristalsis probably is the main factor in those functions.
FIGURE 31-3 (A and B) The jejunum and ileum can be distinguished from one another by differences in luminal diameter, number of arterial arcades, and the presence or absence of fat encroaching on the gut wall. (Reproduced with permission from Agur AMR, Dalley AF, eds. Grant’s Atlas of Anatomy. 11th ed. Copyright Lippincott Williams & Wilkins; 2004.)
The luminal content of the proximal small bowel is of neutral pH and is relatively sterile, containing few bacteria. Most studies of the small bowel microflora have demonstrated increasing bacterial counts with distance away from the pylorus.5 The proximal small bowel flora resembles the gastric flora. The jejunum and proximal ileum contain gram-positive and gram-negative organisms at 104–105 cfu/mL. The bacterial concentration in the distal ileum rises to 105–108 in the ileum. There is also a higher number of anaerobic species in the ileum. This increase in bacterial load in the ileum is thought to contribute to an increased risk of infection with full-thickness injury in the distal small bowel versus the proximal small bowel.
Mechanism of Injury/Pathophysiology
Blunt injuries to the stomach and small bowel are infrequently encountered. Injuries include contusions, intramural hematomas, lacerations, full-thickness perforations, and mesenteric avulsions. In the East Association for the Surgery of Trauma (EAST) multi-institutional study, HVI was noted in only 1.2% of over 225,000 admissions during the 2-year study period.6 Most HVIs in this study were hematomas and several tears. Perforated small bowel injury accounted for less than 0.1% of blunt trauma admissions. Full-thickness perforations of the small bowel (unspecified site) and jejunum/ileum each accounted for 20–25% of all full-thickness HVIs. Gastric perforations following blunt trauma are rare and accounted for only 2.1% of the total HVI in the EAST study.
Most gastric injuries are related to pedestrian motor vehicle or high-speed motor vehicle crashes. The stomach is thick walled and relatively resistant to a blunt injury. However, when full after a recent meal, trauma to the left side of the body or inappropriate use of seat belts may contribute to rupture. Blunt gastric injuries include lacerations and full-thickness perforations, which most frequently involve the anterior gastric wall.7,8 Peritoneal signs and blood nasogastric tube aspirate are usually present and lead to early surgical intervention. Associated injuries are often severe because of the degree of force necessary to produce a gastric blowout.9 Associated injuries include liver, spleen, and pancreas, as well as injuries to the chest and head. Associated injuries are the main reason for the higher mortality rates for patients with blunt gastric rupture versus other HVIs.10–12
Small bowel perforation secondary to blunt abdominal trauma is uncommon, but thought to be increasing in incidence. Motor vehicle crashes are the most important mechanism for blunt intestinal trauma, followed by falls and bicycle accidents. Localized blows to the abdominal wall may also cause HVI. Mechanisms postulated for injury to the intestine to occur include: (1) crushing of bowel against the spine, (2) sheering of the bowel from its mesentery of a fixed point by sudden deceleration, and (3) bursting of a “pseudo-closed” loop of bowel owing to sudden increase in intraluminal pressure. More recently Cripps and Cooper have demonstrated experimentally the potential for small intestinal injury in high-velocity, low-momentum impacts that do not greatly compress the abdominal cavity.13 Earlier series had described proximal jejunum and distal ileum as sites more prone to injury due to their relative immobility. More recent reports have not shown this to be the case, as mid-jejunal perforations have been increasingly reported.
Although the use of seat belts alone or in combination with air bags is effective in reducing fatalities, there may be an increase in injuries associated with both proper and improper use of these devices. Garret and Brownstein first referred to the seat belt mark as ecchymoses across the abdominal wall that corresponds to the lap belt14 (Fig. 31-4). With the advent of the three-point restraint system, injuries may also involve the neck and chest. The “seat belt syndrome” now refers to intestinal injuries associated with lumbar fractures and abdominal or chest wall ecchymoses.14 Injury to other organs may occur and include the stomach and colon.
FIGURE 31-4 Patients with blunt intestinal injury sometimes have ecchymoses of the abdominal wall caused by restraint devices. The findings may be relatively subtle (A) or more severe (B). The presence of such ecchymoses does not always signify underlying blunt intestinal injury. By the same token, many patients with blunt intestinal injury do not have abdominal wall ecchymoses. The patient in (A) had a grade II injury while a grade IV injury (C) occurred in patient (B).
Anderson et al. reported a 4.38-fold increase in risk of small bowel injuries with lap/shoulder restraint use and a more than 10-fold increase in risk with lap belts alone, compared with no restraint use.15Chandler et al. reported 112 patients involved in motor vehicle crashes.16 Sixty percent of patients were wearing a seat belt, and the remainder were unrestrained. There was no difference in the overall incidence of abdominal injury between belted and unbelted patients (15% vs. 10%, respectively). However, the incidence of small bowel perforation was significantly increased in patients with a seat belt versus no belt (6% vs. 2.2%, respectively). The presence of a seat belt sign (SBS) was associated with an even greater likelihood of abdominal injuries and small bowel perforation (64% and 21%, respectively).
More recently in the EAST multi-institutional study, the SBS was associated with a 4.7-fold increase in relative risk of small bowel perforation in patients following motor vehicle crashes.17 The second highest relative risk of small bowel perforation was the use of a seat belt without evidence of an abdominal seat belt mark (2.4-fold increase in relative risk). Small bowel injuries noted with the use of seat belt use include small bowel transections (usually in the proximal jejunum) as a manifestation of a deceleration injury, sheering or crushing injuries usually involving the terminal ileum and associated mesentery, and (blowout) perforations on the antimesenteric aspect of the bowel. This latter injury is felt to be due to an acute sudden increase in intraluminal pressure in a functionally closed loop of bowel. It is believed that when air bags are deployed in combination with a properly placed seat belt, there is a decrease in the incidence of abdominal injuries.
Children with an “SBS” may also have a higher rate of gastrointestinal injury. Sokolove et al. demonstrated that children with an SBS had a significantly greater risk of intra-abdominal injury, including gastrointestinal and pancreatic injuries.18 However, the increased risk of injury was only apparent in patients with abdominal pain or tenderness. In a study by Chidester et al., the SBS only had a sensitivity of 25% and a specificity of 85% for abdominal injury.19Similar to the study by Sokolove, the presence of SBS with abdominal tenderness was more predictive of abdominal injury.
The association of a Chance-type fracture of the lumbar spine as a predictor of HVI is variably reported in the literature (Fig. 31-5). Anderson et al. reported 62.5% of 16 patients with Chance-type fractures had HVIs.15 Nine perforations occurred in the small bowel, and the remainder were in the colon. However, in the EAST multi-institutional trial with small bowel perforations there was no difference in incidence of Chance-type fracture in perforating or nonperforating small bowel injury patient groups versus patients without small bowel injury.17 The incidence of bowel perforations was quite low in all groups, and ranged between 2% and 3% of patients.
FIGURE 31-5 Some injuries to the lumbar spine are commonly caused by seat belts, and are frequently accompanied by associated blunt intestinal injury. Transversely oriented fractures through bone (A) are also sometimes known as Chance fractures. The mechanism of injury responsible for such fractures can cause soft-tissue disruption and dislocation in the same orientation as seen with Chance fracture (B).
In about 20% of patients with blunt intestinal perforations no other injuries are present. Other patients have significant extra-abdominal injuries with blunt injury as their sole intra-abdominal injury. Approximately 25% of patients with blunt intestinal injury have more than one injury requiring surgical intervention.20–22 Thus, in patients undergoing laparotomy for blunt intestinal rupture a complete evaluation for other injuries and a thorough laparotomy are mandated.
On rare occasions, patients may return to the hospital several days or weeks after blunt abdominal trauma with signs and symptoms of bowel obstruction. Contrast-enhanced CT of the abdomen performed at this time usually shows a thickened bowel loop, and narrowing of the lumen. This finding is due to intestinal stenosis resulting from mesenteric vascular injury. The stenosis is felt to be due to infarction resulting from the mesenteric injury rather then a direct injury to the intestine.23
Penetrating injuries to the stomach and small intestine are often more obvious. The anatomic location and space occupied by these organs make them the prime target following injury due to knives, gunshot wounds, shotgun wounds, and other piercing instruments. Of those with peritoneal penetration only 30% of patients with knife wounds have significant injuries requiring operation, whereas over 80% of patients who suffer gunshot wounds have injuries requiring surgical repair. Thus, most institutions employ selective observation of patients with knife wounds even with peritoneal penetration. The decision for operation is based on clinical signs of peritonitis. Many institutions apply a selective approach to shotgun wounds.24 For non-close-range shotgun wounds, operative intervention is based on the range of the blast and pellet distribution as well as an estimate of the number of pellets penetrating the peritoneal cavity. Patients with shrapnel wounds to the abdominal region may also be managed selectively, depending on findings from the physical exam and imaging studies.25
Blast injuries to the GI tract are the result of a “multidimensional injury” as four separate mechanisms may play a role.26 The primary blast injury results from an overpressure wave induced by the blast itself. Although primary blast injuries to the GI tract more commonly occur in the colon, the small bowel may also be affected. Exposure to extreme blast overpressure (which is invariably fatal) results in immediate lacerations of the bowel.
Nonfatal blast exposure may result in multiple contusions or intramural hematomas, which may evolve to full-thickness injury. The initial injury involves the mucosa–submucosa of the bowel wall; the presence of serosal injury is evidence of a transmural lesion at high risk of perforation. Because of the nature of this injury, there may be delay of 1–2 days, and rarely up to 14 days, before clinical symptoms occur. The overall incidence of bowel perforation is low (0.1–1.2%) but is increased with explosive amount, or when the victim is close to the center of the explosion or in an enclosed area.
Secondary blast injuries are caused by projectiles from the explosion that cause perforating injury to the victim. Tertiary blast injuries are the result of the generation of “blast winds” that propel the victim into rigid objects causing blunt injury. Quaternary injuries are the result of fire and heat generated by the explosion. Most injuries seen clinically are due to secondary or tertiary blast effects. Patients with penetrating torso injury or involving >4 body areas are at high risk for intraperitoneal injury.26 Patients with abdominal trauma after terror-related blast injury have a higher incidence of bowel injury (71.4%) and a lower incidence of solid organ injury (33%).26 Shrapnel is the leading cause of abdominal trauma in this setting.27 In the presence of peritoneal signs, the decision to perform surgery is easily made. Because bowel perforation may be delayed, careful observation is critical, even with negative initial image studies or diagnostic peritoneal lavage (DPL) results.
An accurate history of the traumatic event can help determine the potential for intra-abdominal injuries. In patients with a knife wound of the left thoracoabdominal region, diaphragmatic and gastric injuries are a primary concern. The small bowel is at risk of perforation following virtually any penetrating injury that violates the peritoneum. Evisceration of abdominal contents after abdominal stab wound is associated with significant intra-abdominal organ injury in 75% of patients even with no overt clinical signs that would mandate laparotomy. Certain patterns of blunt abdominal injury should alert the clinician as to the probability of gastric and small bowel perforations. Thus, a low threshold for laparotomy is appropriate in this setting. These include the use of seat belts, handle bar injury, and blows to the abdomen such as being kicked by a horse or other large animal. At the very minimum, individuals with an SBS should be admitted and observed with serial abdominal exams.
The incidence of small bowel injury in patients diagnosed with solid organ injuries by CT is variable. Nance et al. in a review of 3,089 patients with solid organ injury from the Pennsylvania Trauma Systems Foundation found 296 patients who had an HVI (9.6%).22 The frequency of HVI increased with the number of solid organs injured: 7.3% with one solid organ injury, 15.4% with two solid organ injuries, and 34.4% with three solid organs injured. More recently, Miller et al. reviewed the Memphis experience with nonoperative management of 803 hemodynamically stable patients with blunt liver or spleen injuries.21 Overall, the incidence of associated intra-abdominal injury was higher in the patients with liver injury at 5% as compared with 1.7% of patients with isolated splenic injury. Bowel injury was discovered in 11% of liver injury patients and no patients with isolated splenic injury. It is believed that the blunt force capable of producing liver injuries or multiple solid organs places the small bowel at increased risk for perforation and should arouse clinical suspicion for bowel injury.
Patients with penetrating gastric injuries usually present with significant peritoneal signs due to the peritoneal irritation from the intraperitoneal leakage of the low pH content of the stomach. Bloody nasogastric aspirate or free air demonstrated on an upright chest x-ray may be indicative of gastric injury but is neither completely sensitive nor specific for the presence of gastric injury.
In patients with obvious peritoneal penetration clinical findings following penetrating trauma to the small intestine may be minimal at first. This is because the luminal content of the small bowel has an almost neutral pH and is relatively sterile. Intestinal spill may also be relatively small, limiting the initial inflammatory response.
In the East multi-institutional trial of blunt small bowel injury, 1.2% of 227,972 blunt trauma admits were found to have a hollow viscous injury.17 A total of 72.5% of patients with perforating small bowel injury had abdominal tenderness; however, only 33.5% had peritoneal signs. Nonetheless, a careful physical exam by an experienced surgeon may discern the likelihood of intestinal perforation. In patients with an SBS on the abdominal wall, tenderness or guarding away from the seat belt should heighten the concern for the possibility of perforated small bowel injuries. Perforations of the stomach and small bowel are recognized by signs of peritoneal irritation: tenderness with guarding and rebound. Sensitivity of clinical examination to identify patients in need of operation exceeds 95% for stab wounds and gunshot wounds. In other studies, clinical examination of the abdomen has been shown to be unreliable in approximately 50% of blunt abdominal trauma patients.17 Significant limitations include patients with head injury and altered level of consciousness, intoxication due to drugs or alcohol, and spinal cord injury. The variable effect of hemoperitoneum from associated solid organ injuries and the presence of distracting injuries (e.g., pelvic fracture) in the multi-injured patients may also limit the clinical reliability of the findings on physical exam.
Laboratory studies including hematocrit, WBC, and serum amylase are not useful in the initial evaluation of patients with gastric and small intestinal injuries.17 In patients managed nonoperatively with solid organ injury or in patients with penetrating injuries undergoing serial clinical exams, unexplained tachycardia, hypotension, leucocytosis, an increase in serum amylase, or the development of a metabolic acidosis should arouse suspicion of a missed HVI.
A variety of diagnostic tests have been used to further evaluate the abdomen following blunt and penetrating injuries (see Chapters 15 and 16). DPL is very sensitive in detecting intraperitoneal injury but is now infrequently used. The most common peritoneal lavage finding with bowel injuries is gross blood.28 However, this may be due to associated solid organ or mesenteric injuries.
Peritoneal lavage with blood cell count has been used to diagnose HVI. However, Jacobs et al. found that a lavage white blood cell count >500/mm3 as the sole positive lavage criterion is a nonspecific indicator of intestinal perforation.29 It was suggested that sequential determinations of DPL and WBC may be useful in the diagnosis of intestinal perforation. Repeat lavage, diagnostic laparoscopy, or limited laparotomy in the patient already in the operating room for repair of other injuries may be prudent.
DPL amylase and alkaline phosphatase levels may also be useful in identifying HVIs. Jaffin et al. found an alkaline phosphate level >10 IU in the DPL effluent to have a specificity of 99.8% and a sensitivity of 94.7% in detecting small bowel and colonic injury.30 McAnena et al. used lavage amylase >20 IU/L and lavage alkaline phosphatase levels ≥3 IU/L as predictors of HVIs following blunt penetrating trauma.31 These values had a sensitivity of 54%, specificity of 48%, and a positive predictive value of 88% for significant abdominal injury.
The ability of DPL to detect hollow viscus perforation in the presence of hemoperitoneum secondary to solid organ injury may be improved by adjusting the positive criteria for WBC. Otomo et al. proposed a “positive” WBC criterion of WBC ≥ RBC/150 when peritoneal lavage was positive for hemoperitoneum.32 These criteria had a sensitivity of 96.6% and a specificity of 99.4% for intestinal injury when performed more than 3 hours after injury. Fang et al. used a “cell count ratio” in diagnosing hollow viscus perforation.33 The cell count ratio was defined as the ratio between white blood cell count and red blood cell count in the lavage fluid divided by the ratio of the same parameters in the peripheral blood. A cell count ratio of ≥1 predicted hollow viscus perforation with a specificity of 97% and a sensitivity of 100% when performed before 1.5 and 5 hours from the time of injury. The “lag time” between intestinal perforation and peritoneal white cell response was felt to account for the reliability of the “corrected” peritoneal lavage white blood cell counts calculated in these later two studies to detect hollow viscus perforations.
The Focused Assessment by Sonography for Trauma (FAST) has been a widely used test in the initial evaluation of suspected abdominal trauma. This is not as sensitive as DPL or CT in detecting stomach or small bowel injuries. This is most likely because of the relative inability of the FAST exam to pick up small amounts of free fluid typically found with isolated hollow viscus perforations. Rozycki et al. reported on 1,540 patients (1,227 with blunt injuries, 313 with penetrating injuries) who had FAST examinations performed as part of their initial assessment following injury.34 The sensitivity and specificity for detecting hemoperitoneum were 83.7% and 99.7%, respectively. However, there were 16 blunt abdominal trauma patients with false-negative ultrasound results. Three of these patients were subsequently found to have significant small bowel injuries. As an isolated finding, an additional patient had small bowel perforation and a ruptured bladder. Bowel injuries have been also missed by FAST examinations in patients with pelvic ring fractures. Detection of actual bowel injuries by FAST is unreliable.
CT scan is the most commonly used diagnostic modality in evaluating the abdomen in hemodynamically stable blunt trauma victims. It is occasionally used in evaluating hemodynamically stable patients with penetrating injuries particularly to the back and flank areas.
It is apparent that when blunt small bowel perforation is present, abdominal CT is usually abnormal.35–38 A number of CT findings are indicative or more often arouse suspicion for significant bowel and mesenteric blunt injuries. CT findings specific of bowel perforation include extraluminal oral contrast and discontinuity of hollow viscus wall. However, as oral contrast extravasation is noted in less than 10% of documented cases of small bowel perforation, it is not advocated for routine care at most centers (Fig. 31-6). CT findings suggestive of bowel injury include pneumoperitoneum, gas bubbles close to the bowel wall, thickened (>4–5 mm) bowel wall, bowel wall hematoma, and intraperitoneal free fluid without solid organ injury. Active contrast extravasation is a specific sign of mesenteric laceration, and mesenteric hematoma or fluid collection in the mesenteric folds is a CT finding suggestive of mesenteric injury (Fig. 31-7).
FIGURE 31-6 This CT was obtained a few hours after injury. The findings were highly suspicious of oral contrast extravasation (arrows). The patient was found to have rupture of the small intestine at surgery.
FIGURE 31-7 This CT was done shortly after injury. Multiple abnormalities are noted including thickened bowel and free fluid (arrows). However, a large amount of free air is the most notable finding. At operation a mid-jejunal perforation was found.
Malhatra et al. reviewed the Presley Regional Trauma Center experience with screening helical CT evaluation of blunt bowel and mesenteric injuries.38 One hundred of 8,112 scans were suspicious of blunt bowel/mesenteric injuries. There were 53 patients with bowel/mesentery injuries (true positive) and 47 without (false positive). The most common finding in both true-positive and false-positive groups was unexplained intraperitoneal fluid present in 74% and 79% of scans, respectively. Pneumoperitoneum and bowel wall thickening were much more common in true-positive scans. Multiple findings suspicious for bowel/mesenteric injury were seen in 57% of the true-positive scans but in only 17% of false-positive scans. The overall sensitivity and specificity of CT for bowel/mesenteric injury were 88.3% and 99.4%, respectively. The positive and negative predictor values were 53.0% and 99.9%, respectively.
In the EAST study, free fluid without solid organ injury had a 38.4% incidence of perforating small bowel injury.17 Even with the use of multidetector CT scans, free intraperitoneal fluid is the most common finding of blunt infected or mesenteric injury.36,39 It is important to semiquantify free fluid to help distinguish significance. Minimal fluid is defined as fluid in one anatomic region, and large amount of fluid is defined as fluid in multiple areas.40 Patients with minimal fluid can be followed by clinical exam or repeat CT imaging. Patients with larger amounts of fluid may be best served by DPL, diagnostic laparoscopy, or operative exploration. Of note, 12.2% of patients diagnosed with small bowel perforations in the EAST trial had a completely normal CT.17 Thus, if associated injuries do not mandate admission, a short period of observation may still be warranted, particularly if there is abdominal tenderness or the drug and/or alcohol screen is positive.41
In the initial report, Velmahos and colleagues demonstrated the safety of selective nonoperative management in over 1,800 patients with abdominal GSW.42 During observation, 80 of 792 patients selected for nonoperative management developed symptoms and underwent laparotomy, which was therapeutic in 57. In a follow-up study on 100 patients with nontangential abdominal GSW, the sensitivity and specificity of CT scanning were 70.5% and 90%, respectively.42 The two false-negative scans involved HVIs, which were repaired without complication. The most sensitive indicator for laparotomy for HVI from penetrating trauma is extension of the wound track, to or near a hollow viscus43 (Fig. 31-8). Therefore, oral or rectal contrast may not be necessary when used to evaluate patients with penetrating abdominal injuries.44 A recent meta-analysis by Goodman et al. demonstrated CT scanning in hemodynamically stable patients who had high (>90%) specificity, negative predictive value, accuracy, and slight lower positive predictive value.45
FIGURE 31-8 A single contact CT in a patient with tangential GSN shows the missile tract in close proximity to bowel with air around bowel loops.
Diagnostic laparoscopy is occasionally helpful in avoiding laparotomy in hemodynamically stable patients with penetrating thoracoabdominal trauma.46 Indications include penetrating left thoracoabdominal trauma with suspected diaphragmatic injuries. On some occasions small diaphragmatic tears and even gastric perforations may be repaired using laparoscopic techniques. Penetrating injuries to the anterior right thoracoabdominal area and tangential gunshot wounds to the abdomen may also be evaluated laparoscopically. Indications for diagnostic laparoscopy are less certain for patients with blunt intestinal trauma. A major limitation cited with diagnostic laparoscopy is in the relative inability to detect hollow viscus perforations. Earlier reports demonstrate an excessively high rate of missed injuries.46 Kawahara et al. recently demonstrated their experience in 75 hemodynamically stable patients with suspected abdominal injuries.47 Importantly, no small bowel injuries were missed, and unnecessary laparotomy was avoided in 73%. The reported accuracy was 98.66% with 97.61% sensitivity and 100% specificity. Obviously, advanced laparoscopic training is required, especially if therapeutic laparoscopy is attempted. Expertise in advanced laparoscopic surgical techniques is undoubtedly helpful in reliably excluding bowel injuries. A 30° angle laparoscope is used for abdominal exploration. Proper selection of sites for port placement is paramount for effective laparoscopic evaluation for bowel injury. Earlier recommendations include placement of the laparoscope through a 10-mm port 4 cm above the umbilicus, a second port in the suprapubic region, and a third port in a paramedian position at the level of the umbilicus on the side opposite the abdominal entrance wound. Currently, a supraumbilical port and two pararectus sites at the level of the umbilicus are advocated.47 After inspection for blood or bile, the bowel is examined from the ligament of Treitz to the ileocecal valve using atraumatic bowel graspers, and inspection of both sides of the bowel is required in sequential 10-cm segments. In patients found to have intestinal perforation, it is safest to convert to a laparotomy to properly address the bowel injury, as well as any additional injuries found on formal exploration.
After the initial evaluation and resuscitation of the injured patient, patients with suspected or recognized injury to the stomach or small bowel should undergo immediate operation. Under most circumstances the abdomen should be explored through a midline incision. Paraxyphoid extension is useful in the exposure of upper stomach or esophageal wounds. In patients with large traumatic abdominal wall defects (e.g., close-range shotgun wounds), the abdominal wall defect may be used for access to the peritoneal cavity. Usually, debridement with further surgical extension of the abdominal wall defect is necessary. Occasionally, stable patients with large defects and eviscerated bowel or omentum due to stab wounds may be explored through a surgical extension of the abdominal wall defect.
After the initial control of significant hemorrhage, contamination from the GI tract is then addressed. In patients with ongoing hemorrhage temporized by packing, gastric and bowel perforations should then be rapidly controlled. Hemostasis and control of gastrointestinal spill is best obtained with a running Vicryl or Dexon suture closure of the perforation. This is particularly effective if there is significant bleeding from the lacerated stomach/intestine or adjacent mesentery. Alternatively, atraumatic clamps may be used to control spillage from the bowel. All injuries identified are then repaired as the next step.
It is useful to grade stomach and small intestinal injuries according to their severity (Tables 31-1 and 31-2). In the patient who is hemodynamically stable, definitive repair of these injuries is relatively straightforward and based on their severity grade.
TABLE 31-1 Stomach Injury
TABLE 31-2 Small Bowel Injury Scale
Mobilization of the stomach is essential for detection of gastric injuries. Exposure is generally easier if the stomach is decompressed first by a properly placed nasogastric tube. A bloody nasogastric return should arouse suspicion for a gastric injury. Certain areas of the stomach are more difficult to assess: the gastroesophageal junction, high in the gastric fundus, the lesser curvature, and the posterior wall. Division of the left triangular ligament and mobilization of the lateral segment of the left lobe are helpful in exposing the gastroesophageal junction. A Bookwalter or Omni-Tract self-retaining retractor can greatly facilitate this exposure. In the hemodynamically stable patient, the reverse Trendelberg position can aid in exposure of this area and allow better visualization of associated diaphragmatic injuries.
If the gastrohepatic ligament is divided, care must be taken to avoid injury to the vagus nerve or its branches or the occasional anomalous left hepatic artery. To visualize high in the gastric fundus, the short gastric vessels should be divided and ligated. Overzealous traction in this area may cause a tear of these vessels or of the splenic capsule leading to troublesome bleeding. The posterior wall of the stomach may be inspected by opening the avascular portion of the gastrocolic ligament along the greater curvature of the stomach. This may be extended up to the short gastric vessels to visualize areas high in the fundus if necessary. It is better to enter this space in the upper or mid portion of the greater curvature of the stomach to avoid making a rent in the transverse mesocolon and possibly causing injury to middle colic artery.
When an anterior hole in the stomach is found, a diligent search for a second hole must be undertaken. This is usually relatively straightforward. However, there are several areas that can hide injuries and should be carefully inspected. These include the greater and lesser curvature of the stomach, the proximal posterior gastric wall, and fundus as well as the posterior cardia. If a suspicion still exists after the search for a second hole comes up empty, a useful diagnostic adjunct is to have the anesthesiologist insufflate the stomach with air through the nasogastric tube. With the stomach submerged in saline, a telltale leakage of bubbles localizes any missed injury. Rarely, it may be necessary to enlarge the known injury so as to inspect the stomach from the inside in search of another injury to the stomach. A tangential wound to the stomach and bowel can occur but this is a diagnosis of exclusion.
Gastric injuries thus identified are treated according to their severity (Table 31-1). Most intramural hematomas (grades I and II) are repaired with interrupted 3-0 silk seromuscular sutures after evacuation of the hematoma and hemostasis are obtained. Small grade I and II perforations can be closed primarily in one or two layers. Because the stomach is quite vascular and often bleeds profusely, we prefer a two-layer closure after hemostasis is achieved. A running locked absorbable suture should be used for the inner layer, and interrupted seromuscular sutures of 3.0 or 4.0 silk should be used for the outer layer.
Large (grade III) injuries near the greater curvature can be closed by the same technique or by the use of a GIA stapler. Care must be taken to avoid stenosis in the gastroesophageal and pyloric area. A pyloric wound may be converted to a pyloroplasty to avoid possible stenosis in this area. Extensive wounds (grade IV) may be so destructive that either a proximal or a distal gastrectomy is required. Reconstruction with either a Billroth I or a Billroth II anastomosis is dictated by the presence or absence of an associated duodenal injury. In rare cases, a total gastrectomy and a Roux-en-Y esophagojejunostomy is necessary for severe injuries (grade V).
If a diaphragm injury occurs in association with a gastric perforation, contamination of pleural cavity with gastric contents can be problematic. Under most circumstances it is sufficient to clear the pleural space through the diaphragmatic rent following closure of the gastric perforation. It may be necessary to enlarge the diaphragmatic injury to achieve complete evacuation of the pleural contamination. The powered irrigation system used in laparoscopic surgery may be an ideal method to clear the pleural cavity prior to chest tube insertion and closure of the diaphragm. The pleural contamination may be so severe, particularly if operation is delayed, that on rare occasions, a separate thoracotomy to provide adequate drainage of the pleural space is necessary. Thoracoscopic evacuation of the gastric contamination of the pleural space followed by chest tube placement is another option.
Small Bowel Injuries
Examination of the small intestine for injury is achieved by evisceration of the small bowel to the right and careful inspection of its entire length. The small bowel is examined loop by loop; no injuries are definitively repaired until the entire bowel is inspected. The decision to resect versus repair bowel is made only after careful assessment of the proximity of bowel perforations and the adequacy of the blood supply to the bowel in question. Mesenteric hematomas adjacent to the bowel wall following penetrating injury should be carefully opened and the mesenteric aspect of the bowel inspected for injury. Other small nonexpanding mesenteric hematomas should be reassessed at intervals throughout the operative procedure to assure their stability.
If significant bleeding from the mesentery is encountered, it should be controlled directly by either placement of clamps on the ends of the bleeding vessels followed by suture ligature or the accurate placement of sutures in a figure eight fashion. Mesenteric defects are closed later. Bleeding at the root of the mesentery requires extra caution in obtaining hemostasis because of the concern for compromising the blood supply to the bowel. Exposure and repair of proximal jejunal injuries may be facilitated by taking down the ligament of Trietz. The inferior mesenteric vein is at risk with injuries in this area. Occasionally division of this vein is necessary for exposure and repair of bowel injuries near the ligament of Trietz. Treatment of small bowel injury depends on its grade (Table 31-2). Obvious serosal tears should be closed with interrupted silk seromuscular sutures. Small serosal tears may be left alone if one is certain as to the depth of the intestinal wound. A grade I intramural hematoma can be safely inverted with 3-0 or 4-0 silk seromuscular sutures.
Full-thickness small bowel perforations including less than 50% of the circumference (grade II) are repaired by careful debridement and primary closure (Fig. 31-9). The preferred method is to use a two-layer closure with a continuous Vicryl or Dexon suture for the inner layer and interrupted silk sutures for the outer layer. Alternatively, a single-layer closure with a running or interrupted suture can be used. A transverse closure is preferable because it assures the widest luminal opening. A transverse closure without tension may not always be possible, however, particularly with long lacerations along the antimesenteric border of bowel. A longitudinal single-layer closure may be preferable in this instance. Adjacent through-and-through wounds of the bowel are joined transversely using electrocautery and closed as a single defect. Multiple grade II injuries can usually be closed individually. Small bowel resection for multiple perforations is not recommended unless resection and anastomosis would take less time than closing the perforations individually and the amount of bowel sacrificed is minimal. An additional concern is the tendency to compromise the bowel lumen with closure of multiple perforations in a short segment.
FIGURE 31-9 Treatment of grade I and II small bowel injuries. Grade I injuries are treated by inversion with seromuscular sutures. Grade II injuries are treated by careful debridement and primary closure. Either a one- or two-layer closure may be used. Adjacent through-and-through perforations are treated as a single defect by dividing the bridge of tissue separating them with electrocautery. (Reproduced with permission from Carrico CJ, Thal ER, Weigelt JA, eds. Operative Trauma Management: An Atlas. Norwalk, CT: Appleton & Lange; 1998. Copyright The McGraw-Hill Companies, Inc.)
Concerns about the mesenteric circulation and residual luminal diameter dictate the treatment of grade III and IV injuries. Injuries to more than 50% of the small bowel circumference should usually be resected because of the high likelihood of luminal narrowing with primary closure (Fig. 31-10). However, grade III wounds that are oriented transversely or in the relative large proximal to mid jejunum may be primarily repaired provided that an adequate lumen (at least 30% of the circumference) is maintained.
FIGURE 31-10 Grade III small bowel injuries are usually treated by resection and anastomoses. Proximal small bowel injuries or transversely oriented wounds may on occasion be primarily repaired. (Reproduced with permission from Carrico C, Thal ER, Weigelt JA, eds. Operative Trauma Management. 1st ed. Copyright McGraw-Hill Inc; 1998.)
Complete transection of the bowel (grade IV) is treated by resection of the injured bowel and its adjacent blood supply followed by anastomosis (Fig. 31-11). Grade V injuries involve small bowel transections with segmental tissue loss or segmental devascularization and require resection with anastomosis (Fig. 31-12).
FIGURE 31-11 Treatment of grade IV small bowel injuries requires resection of the injured bowel and its adjacent blood supply. Anastomosis may be performed using either suture or stapling techniques.
FIGURE 31-12 Isolated mesenteric injury: Mesenteric injuries can be caused by both blunt and penetrating mechanisms. If the blood supply is disrupted enough to lead to questions about the viability of a short segment of small intestine, that segment should be resected.
There remains some controversy as to the safety of stapled versus handsewn anastomoses for traumatic bowel injuries.48–52 Most of the available data are from retrospective studies with only one prospective study (Table 31-3). There are no controlled clinical trials comparing techniques for intestinal anastomosis following trauma. However, it is now the general consensus that the complication rate is similar for stapled and handsewn anastomoses.
TABLE 31-3 Small Bowel Injury: Handsewn versus Stapled Anastomoses
A handsewn anastomosis is the tried and true method to reestablish GI continuity. Techniques include a single- or two-layered anastomosis. Burch et al. conducted a prospective randomized study comparing a single-layer anastomosis with 3-0 polypropylene versus a two-layer anastomosis with running absorbable suture for the inner layer and 3-0 silk Lembert for the outer layer.53 One hundred and twenty-five patients were enrolled in the study of which only 31 were trauma patients. No differences in anastomotic leaks or intra-abdominal abscess between the two groups were noted. If a stapled anastomosis is performed, care should be taken if the enterotomy created for the GIA stapler is closed with a TA stapling device. The GIA staple line should be offset approximately 5 mm to avoid intersecting staple lines and potential tissue ischemia when using the TA stapler to close this defect. Regardless of the technique used, intestinal anastomotic healing is dependent on a good blood supply, a tension-free suture or staple line, an adequate lumen, a watertight closure, and no distal obstruction. The most appropriate factor in selecting the timing and technique of bowel anastomoses remains sound surgical judgment.
There are several important tenants regarding intestinal anastomoses in the trauma setting. First, the surgeon should rely on techniques that he or she is most experienced with. Second, it may be preferable to hand sew, rather than staple, markedly thickened or edematous bowel. A staple line reinforcement with bioresorbable materials is another option. Third, certain circumstances make any anastomosis at risk for complications. These include shock with massive fluid and blood administration, associated pancreatic injury, and the development of an abdominal compartment syndrome.51,54
Patients who incur significant bleeding during laparotomy may develop progressive acidosis, hypothermia, and coagulopathy. A damage control laparotomy should be considered and have bleeding controlled or temporized by packing and undergo further resuscitation before definitive repairs are performed. Only GI tract injuries that require simple repair should be definitively treated. More severe bowel injuries may be controlled by stapling of the bowel proximally and distally with resection of the injured part of the bowel. Anastomosis is performed in the operating room 24–48 hours later when the patient has been stabilized.55 If patients are returned to the operating room after more than 72 hours, great morbidity (abscess rate) and mortality have been reported.56
Bowel resection with anastomosis does not appear to place the anastomosis at risk of breakdown in the patient with an open abdomen if abdominal closure is achieved “early.”53,55 Two-hundred and four patients with enteric injuries and postinjury open abdomen were entered into the 2010 Western Trauma Association multi-institutional trial.57 Colonic anastomosis, particularly involving the left colon, had a greater leak rate than small bowel anastomosis. The leak risk was also higher in patients postinjury with ongoing hypoperfusion (indexed by 12-hour heart rate and base deficit). In particular, there was a four times greater likelihood of developing a leak if abdominal closure was not achieved until 7 days postinjury versus day 5 (3% vs. 12%). Protection of the bowel anastomosis with omental covering, gentle handling of the bowel on reoperation, and early facial closure are advised to prevent intestinal fistula formation.54,56 Anastomosis at a larger stage is facilitated by a decrease in bowel edema that may be significantly less at this time. Additionally, it allows reevaluation of bowel of questionable viability.
Extensive destruction of the small bowel or its mesentery (grade V) necessitates resection and anastomosis. Treatment of isolated mesenteric injuries without bowel perforation is dependent on the viability of the bowel. Resection is required for devascularized bowel. If the involved bowel segment is short and there is doubt about the viability of the bowel, resection should be performed.
Proximal injuries to the mesenteric blood vessels may result in large segments of questionable bowel viability. Clinical judgment about bowel viability has under the best circumstances only a 65% predictive value. Adjunctive techniques to access bowel viability such as intravenous fluorescein and bowel inspection using a Wood’s lamp, Doppler flow studies, and bowel surface oximetry may be useful. However, it is usually wiser to terminate the procedure, provide temporary abdominal closure, and perform a second-look procedure in 24 hours after the patient is rewarmed and perfusion deficits corrected before deciding to perform an extensive bowel resection. Performing resection at this later time may allow preservation of bowel that was of questionable viability at the first operation. With massive bowel resections, it is important to note the location and length of the segment of the resected bowel. The most critical measurement is the length of the remaining small bowel. Preserving as much of the ileum as clinically possible and the ileocecal value, if feasible, may obviate the complications related to extensive bowel resections.
The postoperative care of patients with gastric and small bowel injuries is usually relatively straightforward. Complications when they do arise are more often related to associated injuries or to delays in the operative management of the stomach and bowel injuries. Antibiotics are limited to a 24-hour course, usually of a single agent such as cefoxitin or ampicillin–sulbactam.58 However, appropriate dosing may be problematic in patients undergoing massive volume resuscitation with crystalloid and blood products.
The advisability of routine nasogastric decompression following procedures involving an intestinal anastomosis is still controversial, despite prospective randomized controlled trials finding no advantage to this practice. A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy was conducted by Cheatham et al. on 3,964 patients from 26 published trials.59 Routine nasogastric decompression was not supported by this meta-analysis of the literature. However, these studies did not involve trauma patients. The potential impact of other clinically important variables including the presence of multiple associated injuries, hemorrhagic shock, and postresuscitation bowel edema as well as an impaired sensorium from head injuries or drugs and alcohol may make nasogastric decompression the more prudent choice. It is our practice to continue nasogastric decompression, which was initiated during the initial resuscitation, until ileus resolves. It is also advisable to have a properly functioning nasogastric tube in place to decompress the proximal GI tract following a damage control laparotomy and planned reestablishment of gastrointestinal tract continuity. In patients in whom a jejunostomy is placed at laparotomy it is also useful to decompress the stomach and monitor gastric outputs as jejunal enteral feeds are initiated. Jejunal feeding may increase gastric output significantly that may lead to pulmonary aspiration in these patients.60
In uncomplicated cases involving stomach or small bowel injuries there is no evidence to support routine nutritional support of patients who were well nourished pre-injury. On the other hand, in critically ill or injured patients it is prudent to start nutritional support early before hypermetabolism or sepsis intervenes.61 Available clinical evidence suggests that moderately to severely injured patients should have enteral feedings started between 24 and 48 hours postinjury. Those with more severe injuries are more likely to have intolerance to enteral feedings.
There is convincing evidence in the literature that patients with blunt and penetrating injuries sustain fewer septic complications when fed enterally as opposed to parenterally.62 However, total parenteral nutrition should be started by day 7 in severely injured patients who do not tolerate enteral feeding or fail to tolerate at least 50% of their goal rate of enteral feedings. There are conflicting data on the effects of enteral feeding on hepatosplenic circulation and metabolic demands.63,64 It is safest to start short enteral feedings at the end of active shock resuscitation. It appears that starting enteral feedings up to 36 hours postinjury and at a “trophic infusion rate” (15 mL/h) for up to 4 days is effective in decreasing pneumonia rates without untoward effects on the ICU course of patients with severe blunt abdominal trauma.65 There does not appear to be a clear advantage to postpyloric enteral feeding versus gastric feeding in trauma patients. Thus, with few exceptions (severe closed head injury, or severe pancreatic duodenal injury) surgical feeding jejunostomy (with the exception of a needle catheter jejunostomy) should not be routinely performed at the initial laparotomy. Further, bowel edema may make this simple procedure a far greater challenge than necessary. If patients do not tolerate intragastric feeds, it is far simpler to place a nasojejunal tube endoscopically at a later time.
Immunomodulating (IMD) enteral formulas are enriched with glutamine, alone or in combination with arginine, nucleotides, and lipids, with high levels of omega-3 fatty acids.66 Other supplements include antioxidants and trace elements, including selenium. A meta-analysis conducted by Marik and Zaloga of 20 studies included 7 studies in trauma patients.67 They concluded that IMDs supplemented with arginine, with or without additional glutamine or omega-3 fats, did not appear to offer an advantage over standard enteral formulas in ICU, trauma, and burn patients (, ). It is likely these IMDs may offer benefit only in the most severely injured patients when given early with adequate protein calorie support.66
There is some concern for initiating enteral feeds in the early (less than 24–48 hours) postinjury period. It is well known that gastrointestinal motility is adversely impaired following abdominal surgery. Bowel perforation requiring repair or resection and anastomosis is another confounding variable. A systemic review and meta-analysis evaluated early (within 24 hours of intestinal surgery) versus traditional management in patients following gastrointestinal surgery.68 Thirteen trials with a total of 1,173 patients were included in this analysis. Mortality was reduced with early postoperative feedings; however, the mechanism was not clear. Although early postoperative feeding increased vomiting, no obvious advantage in keeping patients NPO following gastrointestinal surgery could be demonstrated. Postoperative ileus (POI), an inevitable consequence of any laparotomy, may hamper not only attempts at enteral feeding but also the timely recovery of the patient. There are multiple pathogenic mechanisms responsible for POI.69 Neural reflexes seem to be the most important, compounded by inflammatory mediators and the administration of opioids for pain control. Conventional treatments of POI include nasogastric suction, early ambulation, implementation of early enteral feeding, and the use of prokinetic drugs. Although nasogastric decompression and early ambulation are time-honored therapies for POI, neither method has ever been scientifically proven to speed the resolution of POI. Early enteral feeding most likely only has a modest effect on the resolution of POI, even though it is usually tolerated following injury. Enteral feeding tolerance is best achieved using a standardized protocol for initiating feeds and criteria for advancing the rate of infusion.70
Pharmacologic agents have been employed to improve enteral feeding tolerance and to relieve POI. The most commonly used agents include metoclopramide and erythromycin. Metoclopramide is a dopamine D2 receptor agonist, as well as a 5-HT3 receptor antagonist and a 5-HT4 receptor agonist. Its actions include increases in gastric motility, but only a modest effect on small bowel motility. Erythromycin stimulates GI motility by acting on motilin receptors located primarily in the proximal GI tract. A systemic evidence review by Booth et al. in 2002 concluded that these promotility agents improve gastric emptying and improve tolerance of enteral feedings.71 There was no effect on other important outcomes. Long-term use of erythromycin is limited by its antibacterial action and tachyphylaxis. The Cochranereview of systemic prokinetic pharmacologic treatment of POI following abdominal surgery in adults was reported in 2008.72 Thirty-nine randomized control trials were reviewed with a total of 4,615 patients. There were major flaws in most of the studies reviewed. There was insufficient evidence to recommend metoclopramide or erythromycin or other agents, except alvimopan, a peripheral μ-opioid receptor antagonist for POI. However, methodological concerns were raised concerning some of the studies supporting the effectiveness of alvimopan. As several mechanisms have been casually related to the development of POI, a multimodality approach for the management of POI would seem to be the most prudent.
Complications directly related to gastric and small injuries include intra-abdominal septic complications and anastomotic disruption. An intra-abdominal septic complication most often presents as an intra-abdominal abscess. Anastomotic failures may present as peritonitis and/or the development of an external fistula. Infectious complications following gastric injury are most common following blunt trauma and if there is an associated colon injury. In these patients, ongoing fever and leukocytosis should mandate diagnostic imaging of both the chest and abdomen to look for foci of infection to drain.
The most important etiologic factor relating stomach or small bowel injuries to intra-abdominal abscess formation is delayed recognition and surgical treatment.11,12
Diagnosis of blunt intestinal injury is especially problematic in the pediatric trauma population and may contribute to delays in operative treatments. Canty et al. suggested a delay of up to 24 hours after blunt intestinal trauma did not increase mortality or morbidity.73 A delay in definitive repair over 24 hours was directly associated with increased morbidity but not mortality. Additionally, a multi-institutional retrospective study of 214 patients failed to demonstrate a correlation between time to surgery, complication rate, and hospital length of stay.74 The authors recommended serial examination rather than repeat abdominal CT to diagnose children with blunt intestinal injury after initial nondiagnostic imaging studies.
Fang et al. retrospectively reviewed 111 consecutive blunt trauma patients with bowel injuries from a single institution.75 Delays in surgery for more than 24 hours did not significantly increase the mortality compared with when operations were performed within 4 hours of injury. However, intestinal-related complications including sepsis, wound infection, anastomotic failures, and intra-abdominal abscess formation increased dramatically.
Fakhry et al. published a multicenter experience in 198 patients with blunt small bowel injuries.76 There were 21 deaths (10.6% of total) with 9 of these deaths attributable to delay in operation for small bowel injury. In patients in whom small bowel injury was the major injury, the incidence of mortality increased with time to operative intervention. Mortality rates were 2% if the patient was operated on within 8 hours, 9.1% if operated on between 8 and 16 hours, 16.7% if operated on between 16 and 24 hours, and 30.8% if operated on more than 24 hours after injury . The incidence of bowel-related complications, especially intra-abdominal abscess formation, also increased significantly with time to operative intervention. Based on the available literature it seems advisable to determine the need for operation within 8 hours of injury and anticipate complications should operative intervention occur at a later time.
Bleeding complications after gastric or small bowel trauma may present as bleeding into the peritoneal cavity or into the bowel lumen. Bleeding from the short gastric vessels or from a torn splenic capsule is a common iatrogenic source of bleeding in this area. Bleeding from the mesentery or lesser curvature of the stomach may not be apparent intraoperatively in the hypotensive patient. This may only become clinically apparent when the patient normalizes his or her blood pressure; continued bleeding postoperatively then manifests as hypotension and a falling hematocrit.77 After the patient is resuscitated, it is necessary to reoperate. Suture line bleeding can be troublesome and may manifest as bloody nasogastric secretions. Endoscopic hemostatic techniques may be carefully employed in this setting, particularly if the bleeding is from the stomach.
Anastomotic leak following repair of gastric and small bowel injury can lead to significant morbidity and mortality. The definition of anastomotic leak is variable in both emergency and elective gastrointestinal reviews on the topic.78These studies suggest, however, that an anastomotic leak occurs much later than previously thought. Anastomotic failure may present as a contained leak, diffuse peritonitis, or a gastrocutaneous or enterocutaneous fistula (ECF). Risk factors for breakdown of intestinal repair include resection and anastomosis rather than repair, massive perioperative blood and fluid administration, associated pancreatic injuries, and the development of the abdominal compartment syndrome. In patients with enteric injuries and managed with open abdomen technique, failure to obtain fascial closure after postinjury day 5 was found to increase leak rate in the Western Trauma Association multi-institutional study.57,79 Additional factors include evidence for ongoing hypoperfusion and the use of vasopressors during the initial resuscitation and in the early postinjury ICU management.
CT is the best diagnostic imaging study to identify anastomotic leaks that are not clinically obvious. Therapeutic options include medical care only if there is a tiny radiographically evident but clinically insignificant leak. Reoperation is necessary with primary repair and drainage for a small leak discovered early postoperatively if there is minimal peritonitis in the otherwise stable patient. Percutaneous drainage is useful for a symptomatic leak presenting in a delayed fashion as an intra-abdominal abscess. If there is complete disruption of an anastomosis with widespread peritoneal contamination, it is advisable to consider a proximal diverting enterostomy.
Anastomotic leaks diagnosed in the immediate postoperative period may be surgically approached as the relevant tissue planes are amenable to surgical dissection. After 10 or 14 days, the inflammatory process makes dissection of bowel extremely difficult. In this case proximal diversion and/or controlled external drainage of the leak may be safer.
An ECF is a dreaded complication following trauma laparotomy and may be the result of an anastomotic leak, missed injury, or complications with an open abdomen following a damage control laparotomy. An ECF developing with an open abdomen is referred to as an enteroatmospheric fistula (EAF) and is probably the most common type of ECF encountered by trauma surgeons.80,81 An EAF may result from anastomotic breakdown or de novo from exposed bowel in the open abdomen. Factors associated with the development of an EAF include deserolization and iatrogenic injury to the bowel in an open abdomen and dense granulation tissue with adhesion of bowel loops to the fascial rim or adjacent bowel loops.80 Excessive force on the bowel from coughing or even movement by the patient in this setting can lead to shearing of the bowel and bowel disruption. It is advisable to protect the bowel to avoid this complication. Measures include keeping omentum and/or nonadherent dressing materials over exposed bowel, gentle dressing changes by experienced caregivers, and aggressive attempts to obtain abdominal fascial closure as “early as possible.” Vacuum packs, vacuum-assisted wound management, and progressive closure with abdominal retention sutures are useful techniques to facilitate “early” fascial closure. Absorbable mesh materials and human acellular dermal materials (HADM) or other non-cross-linked biological materials may also be used to facilitate early abdominal closure.56 However, prolonged use of vacuum-assisted closure (VAC) of abdominal wounds and absorbable mesh materials may also contribute to the development of an EAF.80
A single institution review of the development of an ECF in the era of open abdomen management was published by Fischer et al.82 The overall incidence of ECF following trauma laparotomy was 1.9%. Patients with open abdomen had a higher ECF incidence (8% vs. 0.5%) and a lower rate of spontaneous closure (37% vs. 43%). The development of an ECF initiates the requirement for a prolonged ICU and hospital length of stay as well as the need for a team of dedicated and experienced nurses, wound care therapists, and surgeons.
There are three phases in the management of an ECF.80 Phase 1 is the recognition of the fistula and patient stabilization. Initial clinical priorities include fluid and electrolyte imbalance, control of sepsis, nutrition, and wound care. The patient may present with enteric content coming from the wound or indolent sepsis and a leak eventually identified by imaging studies. External loss of intestinal fluids rich in electrolytes, minerals, and protein leads to fluid and electrolyte imbalances as well as eventual malnutrition.
Identification of the fistula site and/or measurement of the electrolyte composition of the fistula effluent are sometimes helpful for fluid replacement (Table 31-4). However, in most cases, normal saline with 10–20 mEq of potassium is a suitable fluid to use for the initial intravenous fluid replacement. Patients with ECF may also develop significant calcium, magnesium, and phosphate deficits that should be corrected.
TABLE 31-4 Composition and Volume of Gastrointestinal Secretions
Fistulas are classified as high output (>500 mL per day), moderate output (200–500 mL per day), or low output (<200 mL per day). This may be important to classify fistulas in this manner as it may allow anticipation of the method for nutritional support, and may be useful in predicting the likelihood of spontaneous closure and mortality.80
Control of sepsis may include image-guided or surgical drainage of intra-abdominal abscesses identified by CT. Empiric antibiotic should be started in septic patients and modified after relevant culture data are obtained. The presence of an ECF without clinical signs of sepsis does not warrant antibiotic therapy.
The provision of adequate nutritional support is critical in the stabilization phase. Total parental nutrition has long been recognized to be an important factor in the management of ECF. These patients are usually hypercatabolic and generally require 25–32 cal/kg per day in total calories with a calorie to nitrogen ratio of 150:1 and a protein intake of at least 1.5 g/kg per day. Attempts at enteral nutritional support may aggravate fluid and electrolyte imbalances in the early phase of ECF management.
Adjuncts to control fistula drainage include nasogastric drainage, and acid suppression with H2-receptor antagonists or protein pump inhibitors. Fistula output can be reduced with somatostatin and octreotide. These agents reduce GI secretions and prolong transit times, thereby simplifying management of fistula output. However, no evidence exists that these agents increase spontaneous closure rates. Administration of somatostatin and its analog octreotide has been shown to have an inconsistent effect on fistula output and time to fistula closure. Furthermore, the use of these agents does not increase the rate of nonoperative closure of fistulas.83 If used, fistula output should be monitored before and after a trial with the use of these agents to determine efficacy.
Protecting the integrity of the skin surrounding the fistulas will improve the quality of the surrounding tissues and decrease infectious complications. Low-output fistulas are usually managed with conventional measures. High-output fistulas or fistula(s) in the patient with an open abdomen may benefit by the use of the VAC system. These may be applied over the entire wound with the fistula or as a VAC dressing with openings for stoma pouches of the fistula openings.84,85 The main benefit of the use of the VAC system for ECF appears to be improved wound care before definitive surgery (Fig. 31-13).
FIGURE 31-13 Fistula VAC: the use of a VAC sponge is a valuable method for management of enteroatmospheric fistula. The VAC sponge is applied with polyurethane drape and negative pressure. The ostomy bag is adherent to the VAC drape collecting the enteric contents. (Reproduced with permission from Goverman J, Yelon JA, Platz JJ, Singson RC, Turcinovic M. The ‘fistula VAC,’ a technique for management of enterocutaneous fistulae arising within the open abdomen: report of 5 cases. J Trauma. 2006;60(2):428–431. Copyright © Wolters Kluwer Health.)
The second phase involves anatomic definition of the fistula. CT and/or fistulogram help define the anatomic details and any associated pathology that guide further interventions. Nutrition is continued by the parenteral route with attempts at the use of the enteral route. It is likely that at least 4 ft of functioning small bowel between the ligament of Treitz and the fistula is necessary for significant absorption of even low-residue formulas. However, recent reports have advocated that the provision of at least some of the caloric requirement should be by the enteral route. This may be helpful for “trophic” effects of enteral feedings on the intestine and, if tolerated, allow easier management in the outpatient setting. In patients with diversion of the proximal small bowel as an ostomy, reinfusion of the succus entericus into the distal GI tract may be helpful as well.86
Spontaneous closure of ECFs in patients provided adequate nutritional support and free of sepsis usually occurs within 4–6 weeks. Unfortunately spontaneous closure occurs only in about 30% of trauma patients.82 Definitive surgery (phase 3) in a patient with a persistent ECF is usually delayed 4–6 months following the initial operation. Failure to obtain spontaneous closure should not be a primary factor in the timing of operative intervention. But rather nutritional and wound status, as well as the overall clinical condition, of the patient should be optimal before embarking on an often long and difficult surgical procedure. The procedure should include complete lysis of adhesions to eliminate the possibility of distal obstruction as a contributing factor for the failure of spontaneous closure. Options include resection and reanastomoses of the involved bowel segments or oversewing or wedge resection of the fistula. Recurrence of an ECF is related to the method of surgical closure. In a study by Lynch et al., oversewing or wedge resection of the ECF was associated with 36% recurrence rate, while resection with reanastomoses had a 16% recurrence rate.87 After resection of the fistula and reestablishment of GI continuity, attention is then directed to closure of the abdominal wound. Closure with autologous tissue, often requiring a compound separation technique, is optimal.88 The use of HADM or a non-cross-linked biological material is a second option if closure with autologous tissue is not practical89 (Fig. 31-14). Absorbable mesh closure and acceptance of a later incisional hernia is another viable option. The use of other prosthetic materials, including cross-linked biological materials, is ill-advised due to concerns for the breakdown of intestinal anastomotic repair or the development of a de novo intestinal fistula.90,91
FIGURE 31-14 An enterocutaneous fistula that fails to close spontaneously should be managed operatively when the nutritional and wound statuses are optional (A). Closure with non-cross-linked biological materials may be used when autologous tissue is not available (B).
Small bowel obstruction (SBO) is a well-known complication following abdominal operation. Patients with nontherapeutic laparotomies for trauma had a 2.4% incidence of SBO in a report by Renz and Feliciano.92 The rate is higher if operative repair is required and may be up to 7.4% in patients with penetrating abdominal trauma and 10.8% in patients with small or large bowel injuries.93 However, trauma laparotomy does not appear to have added risk versus that reported following elective colorectal and general surgery on the development of early SBO and need for operative management.
CT imaging has superior sensitivity and specificity, compared with plain radiographs for making the diagnosis of mechanical SBO.94 The identification of a transition zone and “small bowel feces sign” on CT make the diagnosis of mechanical SBO more certain.94,95 However, the presence of radiographic transition zones does not increase the likelihood of need for operative intervention.96 CT findings suggestive of bowel ischemia include decreased bowel wall enhancement, mucal thickening, congestion of mesenteric veins, or ischemia. However, these findings could not discriminate between patients with strangulated and those with nonstrangulated SBO in a report by Rocha et al.94
The absence of these findings may be helpful in deciding on a course of conservative management for at least 10–14 days following initial laparotomy. Various clinicoradiological scores have been proposed to predict the risk for strangulated SBO.96,97 Fortunately, early postoperative SBO often resolves spontaneously. Thus, it may be initially treated expectantly with only a small risk of bowel strangulation.98
In patients reoperated for postoperative bowel obstruction or in patients who later require elective reestablishment of GI continuity, it may be prudent to attempt to minimize adhesion formation. A hyaluronic acid and carboxymethylcelloluse (HA/CMC) bioresorbable membrane (S) is the most common antiadhesive barrier used in general surgery. It is applied to potentially adhesiogenic tissues before closure of the abdomen. It adheres to moist tissue surfaces and is cleared from the body within 28 days of implantation. Initial clinical studies were promising. A multicenter trial by Fazio et al. compared HA/CMC application with no treatment in 1,701 patients who underwent intestinal resections.99 Although the overall bowel obstruction rate was unchanged, there was a significant reduction in the number of patients requiring reoperation for bowel obstruction.
A more recent Cochrane systemic review of intraperitoneal agents for preventing adhesions and adhesive intestinal obstruction included six randomized trials involving the use of HA/CMC.100 Although the use of HA/CMC reduced the incidence of adhesions, there was no reduction of intestinal obstruction needing surgical intervention.
Resection of significant amounts of small bowel may lead to problems with malabsorption. In general, jejunal resections are better tolerated than ileal resections. Removal of significant portions of the jejunum may lead to lactose intolerance; however, this is usually self-limited. Resection of the distal ileum often leads to vitamin B12 deficiency as well as bile salt deficiencies, and subsequent fat malabsorption. Ileal resection also removes the “ileal breaking mechanism” that may cause decreased transit time throughout the gut. This may result in profuse diarrhea and significant fluid and electrolyte imbalances. The ileocecal valve also has an important role as it acts to decrease the volume of stool by slowing intestinal transit time.
The short bowel syndrome may result from traumatic injury to the intestine and/or its blood supply. In a series of 196 adult patients evaluated at a single institution over 23 years, 8% of short bowel syndrome cases were secondary to traumatic injury.101 Eighty percent of trauma-related short bowel syndrome was due to mesenteric injuries. Clinical manifestations include malabsorption, diarrhea, steatorrhea, fluid and electrolyte disturbances, and malnutrition. Late complications include cholelithiasis and renal oxalate stones. Although resection of up to 100 cm of ileum causes diarrhea, short bowel syndrome is fully manifest when the remaining jejunum and ileum is less than 200 cm in length. Plasma citrulline may be a useful biomarker to index small bowel enterocyte mass.102
Physiologic adaptation of patients with short bowel syndrome follows three phases.103 The acute phase occurs during the immediate postoperative weeks and may last 1–3 months. This phase is marked by poor absorption of almost all macronutrients and micronutrients. Ostomies, if present, may have outputs exceeding 5 L per day during the first few days. Aggressive intravenous fluid and electrolyte replacement is necessary to prevent life-threatening dehydration and electrolyte imbalances. Gastric hypersecretion is frequent in this phase and may be treated with proton pump inhibitors. Loperamide, codeine, or diphenoxylate, or even tincture of opium, is used to slow gastric and intestinal transit to control diarrhea. Careful monitoring of fluid and electrolytes, particularly potassium, magnesium, and calcium, is critical. Fluid needs can be monitored by urinary and fistula output, as well as by urinary sodium and osmolarity. The primary route of nutrition is parenteral; however, enteral feeding should be slowly initiated later in this phase.103
Adaptation occurs during the subacute phase and enhances bowel absorption. This adaptive process in humans occurs over a period of months to 1–2 years and is due to dilation of the remaining bowel coupled with improved cell transport function and prolonged intestinal transit time. Intestinal adaptation may be mediated by growth factors and nutrients including human growth hormone (HGH), insulin-like growth factor, epidermal growth factor, transforming growth factor α, and glucagen-like peptide 2 (GLP-2).104 Nutrients including glutamine and fatty acids may also act as growth factors in intestinal adaptation. The maintenance phase is characterized by achievement of maximal absorptive capacity. The goal of this phase is to achieve nutritional and metabolic homeostasis by primarily oral feeding.
Enteral feeding to provide intraluminal nutrients to maintain gut mass is necessary for the adaptation response to occur. Thus, enteral nutrition remains the primary therapy in maximizing luminal nutrient absorption in the intestinal remnant. In a recent study the use of growth hormone, glutamine, and nutrients to facilitate bowel adaptation led to a significant reduction in the number of TPN-dependent adults with short bowel syndrome.105–107 The addition of GLP-2 may have a synergistic effect with HGH, glutamine, and optimal dietary management.
A number of surgical techniques have been used in an attempt to slow transit time and/or increase functional bowel length. Most of these techniques have met with limited success and risk further bowel loss.108 Restoring the colonic remnant to the GI tract may be helpful as the colon takes on an absorptive function by deriving energy from short-chain fatty acids and prolonging transit time, particularly if the ileocecal valve is intact. However, at least 3 ft of small intestine is required to prevent diarrhea and perianal complications. Surgical lengthening with the Bianchi procedure or serial transverse enteroplasty (STEP) may improve efficacy of enteral nutrition and reverse complications of TPN. The STEP is technically easier to perform than the Bianchi procedure. Both have been shown to improve absorption of nutrients by increasing the function of the remnant small bowel.108
Intestinal transplantation is reserved as a last alternative for patients unable to compensate and adapt following intestinal resection. It may also be offered to patients who require TPN to maintain body mass and have limited or no remaining venous access for parenteral nutrition, or parenteral nutrition–related liver disease. Trauma patients seem to have equivalent long-term survival rates as compared with nontrauma patients following intestinal transplantation.109 A multidisciplinary approach to the treatment of intestinal failure due to short bowel syndrome appears to be the best outcome for these patients.110
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