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Management of Gastric Injuries
Abdominal Trauma
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Management of Gastric Injuries
Rodney Durham, MD*
Early gastric surgery was primarily concerned with the management of gastric trauma. In the sixteenth century, Schenck described a Bohemian hunting accident that resulted in a spear wound to the abdomen. The patient survived but developed a gastric fistula. 2 In 1825, William Beaumont17 reported the case of Alexis St. Martin, a young Canadian who sustained a shotgun wound to the chest and abdomen. This wound also resulted in the formation of a gastric fistula. The patient survived and provided the clinical stimulation for Beaumont's pioneering observations on gastric physiology. In 1767, Nolleston Fils32 reported the first successful repair of a gastric injury. He irrigated and sutured a saber wound to the stomach, and the patient survived. The first successful repair of a gunshot wound to the stomach, which is attributed to Theodore Kocher, was not recorded until the late nineteenth century. 30 In contrast to penetrating injuries, the occurrence of blunt gastric trauma was not recognized until the present century. Piacastelli4 is credited with describing the first case of blunt gastric rupture in 1922. Since this time, approximately 75 cases have been reported in the literature. At present, gastric injuries are estimated to occur in 7 to 20% of cases of penetrating abdominal trauma. 2, 27, 35 Blunt gastric trauma is rare and is estimated to occur in 0.4 to 1. 7% of blunt abdominal injuries. I, 3, 9, 10, 36, 39, 40, 45, 49
ANATOMY The stomach, located in the intrathoracic portion of the abdomen, is well protected from injury by the overlying rib cage. It is loosely suspended in the abdomen by the gastrohepatic ligament superiorly, the gastrocolic ligament inferiorly, and by its attachment to the spleen laterally. In addition
*Assistant Professor of Surgery,
Department of Surgery, Division of General SurgeryfTrauma, St. Louis University Medical Center, St. Louis, Missouri
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to these attachments, it is relatively fixed at the gastroesophageal junction and the retroperitoneal duodenum. The gastric wall consists of an external serosal layer followed by three layers of smooth muscle-an outer longitudinal layer, a middle circular layer, and an inner oblique layer. A strong submucosal layer is followed by a mucosal layer with a rich capillary network. This network is supplied by arterioles, which originate in the submucosa. The thickness and strength of the stomach wall are factors that contribute to the rarity of blunt gastric rupture. The stomach is supplied by four major nutrient arteries with extensive collateral circulation between the vascular beds. The left gastric artery most commonly arises from the celiac axis and usually splits into anterior and posterior trunks before it reaches the stomach. Branches from the left gastric artery supply the distal esophagus and the cardiac portion of the stomach. In a small number of patients, the left gastric artery may arise from the aorta or from a common gastrosplenic trunk. 44 The right gastric artery is generally smaller than the left gastric artery and most commonly originates from the common hepatic artery. It anastomoses with the left gastric circulation along the lesser curvature. The left gastroepiploic artery is a collateral of the splenic artery and supplies the greater curvature. It reaches the stomach about halfWay up the greater curvature and supplies the stomach distal to this point. It anastomoses with the right gastroepiploic in about 75% of cases. 44 The more proximal portion of the greater curvature is supplied by the short gastric vessels, which originate from the gastroepiploic artery as well as from the splenic artery. The right gastroepiploic artery arises from the gastroduodenal artery and supplies the pyloric area and the distal greater curvature. It is generally larger than the left gastroepiploic artery. In addition to supplying the stomach, the gastroepiploic arcade also provides the blood supply to the omentum. 6 Venous drainage from the lesser curvature is via the coronary vein to the portal vein. On the greater curvature, drainage is via the short gastric vessels and right and left gastroepiploic veins to the splenic vein. 48 Because of the extensive collateralization of the gastric blood supply, three of the four major arteries may be disrupted without causing necrosis of the gastric wall. 38 This allows repair of most gastric injuries without fear of devascularizing a portion of the gastric wall. On the other hand, gastric injuries may bleed extensively, and care must be taken to obtain adequate hemostasis when repairing these wounds.
BACTERIOLOGY Gastric flora are pH dependent. 31 pH values below 4 are bactericidal, and the bacterial flora of the fasting stomach are sparse. Total bacterial counts are generally less than 103 organisms/ml and are derived from the oral flora. These organisms include streptococci, lactobacilli, micrococci! staphylococci, veillonella, and oral bacteroides. 21 As long as gastric pH decreases below 4 for 1 or 2 hours each day, no bacterial colonization of
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the stomach occurs. If gastric pH remains above 4 continuously, the stomach becomes colonized with salivary flora. At pH values above 5, fecal organisms may also colonize the stomach. 20 , 24 During meals, salivary flora are ingested. Neutralization of gastric pH by food allows bacterial counts to rise as high as 106 organisms/ml. 24 Predominant organisms include Streptococcus viridans, Bacteroides melaninogenicus and asaccharolyticus, staphylococci, and Neisseria. Gastric emptying and a return to more acidic pH generally clear these organisms from the stomach in about 60 minutes. 16 These high gastric bacterial counts after meals have important implications for trauma patients, in whom injuries often occur when the stomach is full. This is particularly true of blunt gastric rupture, in which extensive contamination of the peritoneal cavity leads to intra-abdominal abscesses in up to 50% of patients. 3 Although extensive peritoneal contamination and intra-abdominal abscesses are rare in penetrating trauma, bacterial contamination can occur. Stone42 reported positive peritoneal cultures for aerobic organisms in 47% of penetrating gastric injuries. Cultures for anaerobic organisms were positive in about 20% of these patients. MECHANISM OF INJURY Extensive tissue damage from penetrating injuries in civilian practice does not usually occur unless the wounding agent is a high-velocity rifle or a shotgun fired at close range. Most penetrating injuries in civilian settings are due to knife wounds or low-velocity firearms, which do not create significant blast or cavitation effects. The primary mechanism of injury with these weapons is a crushing of the tissue in the bullet path. The amount of tissue damaged may be increased by tumbling of the bullet within the tissue or by the use of hollow-tipped bullets, which deform on impact. 18 Stab wounds generally create a straight tract through the tissue, injuring adjacent organs. In contrast, bullets may take an erratic path. Missiles traveling through tissues of different densities may change course at tissue interfaces, or may be deflected off bone. Because civilian gastric trauma is due to low-velocity weapons or knife wounds, most injuries are simple perforations that result in minimal tissue destruction with little peritoneal contamination. Blunt gastric injuries most commonly occur after motor-vehicle or motor-pedestrian accidents. 3, 9, 11,40,49 However, injuries have also been reported after cardiopulmonary resuscitation, falls, and direct violence, particularly involving child abuse. A number of different mechanisms of injury have been postulated. Yajk0 49 stated that the most common mechanism of injury was a sudden increase in intraluminal pressure resulting from a direct blow to a full stomach. With this mechanism of injury, rupture of the stomach is most frequent along the anterior surface of the stomach or the greater curvature. 3 However, injuries may occur at any point along the stomach wall. Animal studies have demonstrated that with increases in intraluminal pressure, the seromuscular layer is disrupted first, followed by the mucosa and the submucosa. 41 In clinical practice, seromuscular tears of the stomach occur more frequently than rupture, but they are seldom of
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clinical significance. Overdistension of the stomach with increased intraluminal pressure appears to be the mechanism involved in gastric rupture following cardiopulmonary resuscitation. Ventilation of these patients with a face mask can result in gastric distension. Forceful compression of the chest and upper abdomen can then result in gastric rupture. 14, 47 A second mechanism of injury is compression of the stomach against the vertebral column. This may be the mechanism involved in partial and complete transection of the stomach. Only two such cases have been reported in the literature to date. 28, 39 Shearing of the stomach wall at points of fixation may occur with rapid deceleration. Because the stomach is relatively mobile, these injuries are rare and tend to occur at the gastroesophageal junction, at the pylorus, or at sites of perigastric adhesions. Despite the rich blood supply of the stomach, a few cases of gastric necrosis following blunt abdominal trauma have been documented. Garfinkle 19 reported one case of ischemic gastric necrosis along the greater curvature that he attributed to avulsion of the gastroepiploic vessels.
DIAGNOSIS AND INITIAL MANAGEMENT Initial management of these patients addresses life-threatening injuries. Once the airway, ventilation, and circulation have been assessed, patients should undergo resuscitation and then evaluation for an abdominal injury. A nasogastric tube is placed during the resuscitation phase that serves both diagnostic and therapeutic functions. The return of gross blood on nasogastric aspirate is suggestive of an upper gastrointestinal injury. Hematemesis or bright red blood per nasogastric tube was present in 45% of gunshot wounds and 37% of stab wounds in a series of patients with gastric injuries treated at Parkland Memorial Hospital. The nasogastric tube serves a therapeutic function by decompressing the stomach. Aerophagia is frequent in the trauma patient and, along with gastric ileus produced by intraabdominal injury, can lead to Significant gastric dilatation that may not be decompressed by the gastric injury. This in turn can result in respiratory distress, vomiting, pulmonary aspiration, and, in some cases, shock. 7 These complications may be avoided by early gastric decompression. The diagnosis of gastric injury due to gunshot wounds to the abdomen is usually made at celiotomy. Mandatory exploration is performed for all gunshot wounds and results in the discovery of significant injuries in 95% of patients in whom peritoneal penetration has occurred. 30 In contrast, patients with stab wounds to the abdomen have a lower incidence of significant intra-abdominal injury and may be managed selectively in the absence of a clear indication for exploration, such as peritonitis or shock. 43 Stable patients with stab wounds to the anterior abdominal wall undergo local exploration of the wound. If penetration of the peritoneum has occurred, peritoneal lavage is performed. Patients with positive lavages are explored, whereas patients with negative lavages are observed for 24 hours. In those patients with hematemesis or gross blood per nasogastric tube in conjunction with a stab wound in the vicinity of the stomach, lavage is not
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required, and the patient should be explored. Finally, in dealing with stab wounds to the stomach, it should be noted that the full stomach can expand into the lower quadrants of the abdomen. MUfl,34 reported a young man who sustained a stab wound to the right lower quadrant. Bright red blood was found on nasogastric aspiration, and peritoneal lavage revealed 40,000 red blood cells. The patient was explored for persistent gastric hemorrhage and was found to have a through-and-through wound to the greater curvature of the stomach. Fifty to eighty per cent of patients with blunt gastric rupture present with signs of peritoneal irritation or shock. 9 About 60% of these patients give a history of recent ingestion of a meal. 40 Free intraperitoneal air is not a constant finding .. Brunsting,3 in a review of the literature, found free air to be reported in 16 to 66% of patients. In patients with equivocal exams, peritoneal lavage is usually positive for blood or gastric contents. 3 Ilematemesis is often present in those lesions that involve the gastric mucosa. Contrast studies or computed tomography (CT) are rarely needed, but may occasionally be performed in patients without obvious signs of injury. Once a decision has been made to explore the patient, perioperative antibiotics are given and should provide coverage for both aerobic and anaerobic organisms. Antibiotic coverage is continued for 12 to 24 hours after operation. 13. 25 OPERATIVE MANAGEMENT The abdomen is opened through a midline incision, which allows rapid access to the entire peritoneal cavity. Control of hemorrhage is the first priority, followed by containment of enteric spill. Gastric injuries are rarely life-threatening, and management of other intra-abdominal injuries takes precedence. Bleeding and enteric spill from gastric injuries are temporarily controlled by figure-of-eight sutures or Babcock forceps placed across the wound. Once hemorrhage and enteric spill are controlled, careful exploration of the abdomen is indicated to identify all injuries. Both blunt and penetrating gastric trauma are commonly associated with injuries to adjacent organs. The injuries most commonly associated with penetrating trauma in the Parkland series were to the liver, diaphragm, and colon. Blunt trauma is associated with splenic, thoracic, orthopedic, and hepatic injuries. 3 When exploring the abdomen, the entire stomach should be examined carefully. Penetrating injuries usually create paired wounds, and the stomach should be examined for both entrance and exit wounds. Wounds are most likely to be missed in four areas: (1) the gastroesophageal junction, (2) the greater curvature at the omental and splenic attachments, (3) the lesser curvature at the gastrohepatic ligament, and (4) the posterior wall of the stomach. Adequate exposure of the gastroesophageal junction may require takedown of the triangular ligament of the liver. Division of one or more of the short gastric vessels may be necessary to expose the superior aspect of the greater curvature, whereas inferiorly, the omental attachments may
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have to be divided. Exposure of the lesser curvature may require takedown of the gastrohepatic ligament. Care should be taken during this dissection not to injure the vagal nerves. The posterior wall of the stomach can be examined through the lesser sac by dividing the gastrocolic omentum distal to the gastroepiploic vessels or by dividing the avascular junction of the omentum with the transverse colon. Most blunt and penetrating injuries of the stomach can be managed by debridement and simple closure. Partial or complete transections of the stomach and devascularizing injuries are rare but may require resection. Of 243 penetrating gastric injuries treated at Parkland Memorial Hospital over an 8-year period, 98% underwent simple repair and 2% required resection. Repair of the stomach is usually accomplished with a two-layer inverting closure. After repair, gastric wounds reach 75% of the tensile strength of the normal stomach over 21 days. Mter this period, no further gain in tensile strength is seen. 23 The inner layer of the gastric repair is performed with a continuous absorbable suture to obtain hemostasis of the gastric wall, and the outer layer is performed with an interrupted, nonabsorbable suture. Absorbable suture such as chromic retains only 37% of its tensile strength after 1 week of exposure to an acidic environment. Both polyglycolic acid and polyglycolide-Iactide copolymer retain 90% of their tensile strength after 1 week of exposure to a pH of 3, and they are better choices than chromic for the inner layer of the repair.5 An alternative absorbable suture is polydioxanone (PDS). In an animal study of pyloric patency after a pyloric exclusion procedure, PDS was found to maintain closure of the pylorus for an average of 4 weeks after the procedure, versus 2 weeks for polyglycolic acid. This finding was attributed to a slower rate of hydrolysis of PDS when exposed to the acidic environment of the stomach. 15 An outer layer of nonabsorbable suture material adds security to the repair. Among nonabsorbable sutures, polypropylene, monofilament nylon, and Dacron retained almost 100% of their original tensile strength at 4 weeks when exposed to an acidic pH; silk, on the other hand, retained 72% of its tensile strength. 5 Care should be taken not to narrow the gastric lumen when repairing wounds in the area of the gastroesophageal junction or the pylorus. Consideration may be given to performing a pyloroplasty in wounds involving the pylorus. A gastric drainage procedure should also be performed for injuries along the lesser curvature when damage to the vagal nerves has occurred. Repairs in other areas of the stomach are rarely difficult because of the mobility of the stomach and its rich blood supply. These injuries generally heal rapidly and without complication. Drainage of these wounds is not indicated. Before closure of the abdomen, the peritoneal cavity should be irrigated to remove gross contamination. This is particularly applicable to blunt injuries, in which contamination may be extensive. If concomitant diaphragmatic injuries are present with gross contamination of the pleural cavity, the pleural cavity should also be lavaged to remove both gastric contents and residual blood, which is a rich culture medium. These injuries usually
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require the placement of a chest tube, and lavage of the pleural cavity may be carried out through the chest tube or through the diaphragmatic defect. Mter operation, gastric decompression is essential to avoid distension of the stomach and tension on the gastric repair. Nasogastric suction is maintained until bowel function returns.
COMPLICATIONS Overall morbidity and mortality in patients with penetrating injuries to the abdomen involving the stomach are 27% and 14%, respectively. In the Parkland experience, the majority of these complications and deaths are due to associated injuries and not to the gastric injury. Complications directly related to the gastric injury occur in about 6% of patients; deaths occur in 0.4% of patients. The overall mortality rate with blunt gastric injury has been reported to be between 0 and 66%, with most series reporting about a 50% mortality in adults and 20% in children. I, 3, 9, 36, 40, 49 Early mortality in these patients is directly related to the severity of the associated injuries. Complication rates of 50 to 75% have been reported in those patients who survive. Unlike penetrating trauma, many of these complications are directly related to the gastric injury. These complications in both penetrating and blunt trauma include intra-abdominal abscess, disruption of the gastric repair, fistula formation, empyema, missed injuries, hemorrhage, and obstruction. Intra-abdominal abscesses following penetrating gastric trauma are infrequent. Unlike blunt gastric trauma, extensive contamination of the peritoneal cavity is rare with penetrating injuries in civilian practice. Contamination, when it occurs, is usually successfully managed with lavage and perioperative antibiotics. In the Parkland series of the 243 patients who survived their initial injuries, only two patients developed intraabdominal infections secondary to the gastric injury. Both of these infections were related to disruption of the gastric repair. One of these breakdowns probably occurred after inadequate debridement of the gastric wall following a shotgun blast and resulted in an intra-abdominal abscess and the death of the patient. The second breakdown resulted in an abscess that drained spontaneously via a sump drain that had been placed for an associated pancreatic injury. The resultant gastrocutaneous fistula closed with conservative management. The reason for the breakdown of the gastric repair was not clear, but it may have been due to a technical complication. Blunt gastric trauma results in a high percentage of intra-abdominal abscesses. Brunsting,3 in his review of the literature, found an overall abscess rate of 52%, whereas gastrocutaneous fistulas occurred in 16% of patients who survived the initial operation. Most abscesses in blunt trauma were not related to breakdown of the gastric repair. Siemens40 attributed the high abscess rates in these patients to the extensive contamination of the peritoneal cavity that occurs with rupture of the full stomach. Rupture results in contamination of the peritoneal cavity, not only with food particles but also with significant numbers of oral flora that are found in the stomach in concentrations of up to 106 organisms/ml after meals. 16. 24 These abscesses
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occurred despite the use of peritoneal lavage and perioperative antibiotics. Although these measures are important, they may not prevent the development of intra-abdominal abscesses. These patients should be followed closely in the postoperative period. Adjunctive tests, such as CT of the abdomen and contrast studies of the upper gastrointestinal tract, should be considered in patients presenting a septic pictllre. Aggressive drainage of intra-abdominal sources of sepsis should then be undertaken. Concomitant penetrating injuries to the diaphragm and stomach can result in significant contamination of the pleural cavity by gastric contents. Coselli8 reported 53 patients with traumatic hemothorax or pneumothorax who were initially treated with tube thoracostomy and subsequently developed empyemas. This group of patients represented 1.3% of the total number of thoracic injuries treated with chest-tube drainage during this period. The majority of these injuries were due to penetrating trauma. Over 50% of the patients who developed empyemas had combined thoracic and abdominal injuries, with the most frequent abdominal injuries being to the stomach and the liver. Organisms cultured from these infections were predominantly enteric pathogens. Villalba46 reviewed 27 patients who developed empyemas after penetrating trauma to the chest. These patients represented 1.3% of all patients with penetrating chest trauma over a 5-year period. Diaphragmatic injuries, particularly if they were unrecognized at laparotomy, were cited as a risk factor for developing empyema. Associated intra-abdominal injuries most commonly involved the spleen, stomach, and liver. Eighty-one patients with penetrating gastric injuries treated at Parkland Memorial Hospital had combined gastric and diaphragmatic injuries. Ten patients (12.5%) developed empyemas. In these patients, the stomach was the only hollow viscus injured in the abdomen. All of these patients were initially treated with tube thoracostomy. One patient, with extensive contamination, underwent irrigation of the pleural cavity through the diaphragmatic defect. Seven patients subsequently required thoracotomies for drainage of their empyemas, whereas three patients had thin fluid empyemas and were treated by repeat tube thoracostomy. The predominant organisms responsible for these empyemas were Streptococcus species, anaerobes, and staphylococci-all of which are found in oral flora and contaminate the stomach immediately following a meal. The incidence of empyemas following penetrating thoracic trauma is 1 to 4%.8.12,22,29,33,46 The 12.5% incidence of empyemas in patients with concomitant gastric and diaphragmatic injuries is more than three times that reported with penetrating thoracic trauma alone. It has been recommended that in injuries with gross contamination of the pleural cavity, the chest should be lavaged through a separate thoracic incision. 30 Irrigation of the chest through the diaphragmatic defect or through a chest tube is a less morbid procedure and will usually accomplish the same ends. In either event, both gross contamination and residual blood should be removed from the chest cavity, as retained hemothorax represents a good culture medium and has been associated with an increased incidence of empyema.8, 22, 33, 46 Missed injuries are uncommon after blunt gastric trauma, but may
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occur with penetrating trauma if the stomach is not carefully examined. In the Parkland experience, gunshot wounds resulted in multiple injuries in 89% of cases. Stab wounds resulted in a 47% incidence of multiple gastric wounds. Overall, 72% of penetrating injuries produced more than one gastric wound. Wounds to the stomach should not be assumed to be a single tangential wound until the entire stomach is examined. One patient in the above series had a missed injury to the posterior wall of the stomach and to the pancreas when the lesser sac was inadequately explored. A similar injury from a gunshot wound to the stomach and pancreas led to the death of President McKinley in 1901. Careful examination of the stomach, as described under the section on operative management, should avoid this complication. Hemorrhage is a well-documented complication after gastric surgery. The most frequent site of hemorrhage is from the spleen or short gastric vessels, which may be injured when the stomach is mobilized. Bleeding from the gastric suture line may also occur and is reported in 2% of gastrointestinal anastomoses done under elective circumstances. 26 Persistent bleeding from the nasogastric tube requires prompt re-exploration. The complication is best avoided by utilizing a two-layer closure of the gastric wall with an inner running hemostatic stitch and an outer seromuscular layer. Obstruction is a relatively infrequent complication after repair of gastric injuries. the stomach wall is usually easily mobilized to close even large defects without tension or compromise of the gastric lumen. However, closure of gastric wounds in the area of the gastroesophageal junction or the pylorus may present problems. Wounds at the gastroesophageal junction are complex and may require resection and esophagogastrostomy to avoid obstruction of the lumen. Wounds at the pylorus may be amenable to the use of a pyloroplasty or, on rare occasions, may require resection and Billroth II reconstruction. In addition to stenosis at the site of repair, perigastric adhesions have also been reported as a cause of post-traumatic gastric obstruction. 37 Overall, stenosis and obstruction have been found in approximately 2% of elective gastrointestinal anastomoses 26 and in less than 0.5% of penetrating injuries in the Parkland series. SUMMARY The stomach, located in the intrathoracic portion of the abdomen, is well protected from injury. It has a thick wall that is easily mobilized and a rich blood supply that ensures rapid healing of wounds. Although the gastric contents may be contaminated by oral flora immediately after meals, in the resting state, the stomach has few, if any, endogenous organisms. All of these factors make morbidity and mortality associated with penetrating injuries low. In contrast, blunt injuries often cause extensive contamination of the peritoneal cavity with resultant high morbidity and mortality. REFERENCES 1. Asch MJ, Coran AG, Johnston PW: Gastric perforation secondary to blunt trauma in children. J Trauma 15:187-189, 1975
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2. Blaisdell FW, Trunkey DD (eds): Trauma management. In Abdominal Trauma. New York, Thieme-Stratton, 1982, pp 77-86 3. Brunsting LA, Morton JH: Gastric rupture from blunt abdominal trauma. J Trauma 27:887-891, 1987 4. Case MES, Nanduri R: Laceration of the stomach by blunt trauma in a child: A case of child abuse. J Forensic Sci 28:496-501, 1983 5. Chu CC, Moncrief G: An in vitro evaluation of the stability of mechanical properties of surgical suture materials in various pH conditions. Ann Surg 198:223-228, 1983 6. Clemente CD: Anatomy: A Regional Atlas of the Human Body. Philadelphia, Lea & Febiger, 1975 7. Cogbill TH, Bintz M, Johnson JA, et al: Acute gastric dilatation after trauma. J Trauma 27:1113-1117, 1987 8. Coselli JS, Mattox KL, Beall AC: Reevaluation of early evacuation of clotted hemothorax. Am J Surg 148:786-790, 1984 9. Courcy PA, Soderstrom C, Brotman S: Gastric rupture from blunt trauma: A plea for minimal diagnostics and early surgery. Am Surg 50:424-427, 1984 10. Cox EF: Blunt abdominal trauma: A five-year analysis of870 patients requiring celiotomy. Ann Surg 199:467-474, 1984 11. Dajee H, MacDonald AC: Gastric rupture due to seat belt injury. Br J Surg 69:436-437, 1982 12. Daly RC, Mucha P, Pairolero PC, et al: The risk of percutaneous chest tube thoracostomy for blunt thoracic trauma. Ann Emerg Med 14:865-870, 1985 13. Dellinger EP, Wertz MJ, Lennard ES, et al: Efficacy of short-course antibiotic prophylaxis after penetrating intestinal injury. Arch Surg 121:23-30, 1986 14. Demos, NJ, Poticha SM: Gastric rupture occurring during external cardiac resuscitation. Surgery 55:364-366, 1964 15. DeSantis M, Devereux DF, Thompson D: Pyloric exclusion. Am Surg 53:711-714, 1987 16. Drasar BS, Shiner M, McLeod GM: Studies on the intestinal flora. Gastroenterology 56:71-79, 1969 17. Earle AS (ed): Surgery in America, 2nd ed. New York, Praeger Publishers, 1983, pp 117127 18. Fackler ML: Wound ballistics: A review of common misconceptions. JAMA 259:27302736, 1988 19. Garfinkle SE, Matolo NM: Gastric necrosis from blunt abdominal trauma. J Trauma 16:406-407, 1976 20. Garvey BM, McCambley JA, Tuxen DV: Effects of gastric alkalization on bacterial colonization in critically ill patients. Crit Care Med 17:211-216, 1989 21. Gorbach SL: Intestinal microflora. Gastroenterology 60:1110-1129, 1971 22. Graham JM, Mattox KL, Beall AC: Penetrating trauma of the lung. J Trauma 19:665669,1979 . 23. Hastings JC, Van Winkle W, Barker E, et al: Effect of suture material on healing wounds of the stomach and colon. Surg Gynecol Obstet 140:701-707, 1975 24. Hill M: Normal and pathological microbial flora of the upper gastrOintestinal tract. Scand J Gastroenterol Suppl111:1-5, 1985 25. Hofstetter SR, Pachter HL, Bailey AA, et al: A prospective comparison of two regimens of prophylactic antibiotics in abdominal trauma: Cefoxitin versus triple drugs. J Trauma 200:561-566, 1984 26. Jex RK, van Heerden JA, Wolff BG, et al: Gastrointestinal anastoIl)oses: Factors affecting early complications. Ann Surg 206:138-141, 1987 27. Jones RC, ThaI ER, Johnson NA, et al: Evaluation of antibiotic therapy follOwing penetrating abdominal trauma. Ann Surg 201:576-585, 1985 28. Leddy JE, Frew EMS: Complete transection of the body of the stomach resulting from blunt trauma. Can J Surg 20:264-266, 1977 29. MandaI AK, Montano J, Thadepalli H: Prophylactic antibiotics and no antibiotics compared in penetrating chest trauma. J Trauma 25:639-643, 1985 30. Mattox KL, Moore EE, Feliciano DV: Trauma. Norwalk, CT, Appleton & Lange, 1988, pp 411, 459-472 31. McNulty CAM, Wise R: Gastric microflora. Br Med J 291:367-368, 1985 32. Meade RH: An introduction to the history of general surgery. Philadelphia, WB Saunders, 1968, p 197
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33. Millikan JS, Moore EE, Steiner E, et al: Complications of tube thoracostomy for acute trauma. Am J Surg 140:738-741, 1980 34. Murr P, Moore EE, Dunn EL, et al: Stabbed stuffed-stomach syndrome. N Engl J Med 300:625, 1979 35. Nance FC, Cobin I: Surgical judgment in the management of stab wounds to the abdomen: A retrospective and prospective analysis based on a study of 600 stabbed patients. Ann Surg 170:569, 1969 36. Richardson G, Schiller WR, Shuck J: Gastric rupture from blunt trauma. Rocky Mtn Med J 76:309-310, 1979 37. Schwartz GE, Sclafani SJA: Post-traumatic gastric stenosis due to perigastric adhesions. Radiology 154:14, 1985 38. Schwartz SI, Shires GT, Spencer FC: Principles of Surgery, 5th ed. New York, McGrawHill Book Co., 1989, pp 1157-1158 39. Semel L, Frittelli G: Gastric rupture from blunt abdominal trauma. NY State J Med 81:938, 1981 40. Siemens RA, Fulton RL: Gastric rupture as a result of blunt trauma. Am Surg 43:229, 1977 41. Silbergleit A, Beras EM: Neonatal gastric rupture. Minn Med 49:65, 1966 42. Stone HH, Kolb LD, Geheber CE: Incidence and significance of intraperitoneal anaerobic bacteria. Ann Surg 181:705, 1975 43. ThaI ER: Peritoneal lavage: Reliability of RBC count in patients with stab wounds to the chest and abdomen. Arch Surg 119:579-584, 1984 44. Vandamme JPJ, Bonte J: The blood supply of the stomach. Acta Anat 131:89-96, 1988 45. Vassy LE, Klecker RL, Koch E, et al: Traumatic gastric perforation in children from blunt trauma. J Trauma 15:184, 1975 46. Villalba M, Lucas CE, Ledgerwood AM, et al: The etiology of post-traumatic empyema and the role of decortication. J Trauma 19:414, 1979 47. Vinen JD, Gaudry PL: Case reports: Pneumoperitoneum complicating cardiopulmonary resuscitation. Anaesth Intensive Care 14:193, 1986 48. Woodburne RT: Essentials of Human Anatomy, 7th ed. New York, Oxford University Press, 1983, pp 402-405 49. Yajko RD, Seydel F, Trimble C: Rupture of the stomach from blunt abdominal trauma. J Trauma 15:177-183, 1975
Address reprint requests to Rodney Durham, MD Department of Surgery St. Louis University Medical Center 3635 Vista Avenue at Grand Boulevard PO Box 15250 St. Louis, MO 63110-0250
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Management of Gastric Injuries
Rodney Durham, MD*
Early gastric surgery was primarily concerned with the management of gastric trauma. In the sixteenth century, Schenck described a Bohemian hunting accident that resulted in a spear wound to the abdomen. The patient survived but developed a gastric fistula. 2 In 1825, William Beaumont17 reported the case of Alexis St. Martin, a young Canadian who sustained a shotgun wound to the chest and abdomen. This wound also resulted in the formation of a gastric fistula. The patient survived and provided the clinical stimulation for Beaumont's pioneering observations on gastric physiology. In 1767, Nolleston Fils32 reported the first successful repair of a gastric injury. He irrigated and sutured a saber wound to the stomach, and the patient survived. The first successful repair of a gunshot wound to the stomach, which is attributed to Theodore Kocher, was not recorded until the late nineteenth century. 30 In contrast to penetrating injuries, the occurrence of blunt gastric trauma was not recognized until the present century. Piacastelli4 is credited with describing the first case of blunt gastric rupture in 1922. Since this time, approximately 75 cases have been reported in the literature. At present, gastric injuries are estimated to occur in 7 to 20% of cases of penetrating abdominal trauma. 2, 27, 35 Blunt gastric trauma is rare and is estimated to occur in 0.4 to 1. 7% of blunt abdominal injuries. I, 3, 9, 10, 36, 39, 40, 45, 49
ANATOMY The stomach, located in the intrathoracic portion of the abdomen, is well protected from injury by the overlying rib cage. It is loosely suspended in the abdomen by the gastrohepatic ligament superiorly, the gastrocolic ligament inferiorly, and by its attachment to the spleen laterally. In addition
*Assistant Professor of Surgery,
Department of Surgery, Division of General SurgeryfTrauma, St. Louis University Medical Center, St. Louis, Missouri
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to these attachments, it is relatively fixed at the gastroesophageal junction and the retroperitoneal duodenum. The gastric wall consists of an external serosal layer followed by three layers of smooth muscle-an outer longitudinal layer, a middle circular layer, and an inner oblique layer. A strong submucosal layer is followed by a mucosal layer with a rich capillary network. This network is supplied by arterioles, which originate in the submucosa. The thickness and strength of the stomach wall are factors that contribute to the rarity of blunt gastric rupture. The stomach is supplied by four major nutrient arteries with extensive collateral circulation between the vascular beds. The left gastric artery most commonly arises from the celiac axis and usually splits into anterior and posterior trunks before it reaches the stomach. Branches from the left gastric artery supply the distal esophagus and the cardiac portion of the stomach. In a small number of patients, the left gastric artery may arise from the aorta or from a common gastrosplenic trunk. 44 The right gastric artery is generally smaller than the left gastric artery and most commonly originates from the common hepatic artery. It anastomoses with the left gastric circulation along the lesser curvature. The left gastroepiploic artery is a collateral of the splenic artery and supplies the greater curvature. It reaches the stomach about halfWay up the greater curvature and supplies the stomach distal to this point. It anastomoses with the right gastroepiploic in about 75% of cases. 44 The more proximal portion of the greater curvature is supplied by the short gastric vessels, which originate from the gastroepiploic artery as well as from the splenic artery. The right gastroepiploic artery arises from the gastroduodenal artery and supplies the pyloric area and the distal greater curvature. It is generally larger than the left gastroepiploic artery. In addition to supplying the stomach, the gastroepiploic arcade also provides the blood supply to the omentum. 6 Venous drainage from the lesser curvature is via the coronary vein to the portal vein. On the greater curvature, drainage is via the short gastric vessels and right and left gastroepiploic veins to the splenic vein. 48 Because of the extensive collateralization of the gastric blood supply, three of the four major arteries may be disrupted without causing necrosis of the gastric wall. 38 This allows repair of most gastric injuries without fear of devascularizing a portion of the gastric wall. On the other hand, gastric injuries may bleed extensively, and care must be taken to obtain adequate hemostasis when repairing these wounds.
BACTERIOLOGY Gastric flora are pH dependent. 31 pH values below 4 are bactericidal, and the bacterial flora of the fasting stomach are sparse. Total bacterial counts are generally less than 103 organisms/ml and are derived from the oral flora. These organisms include streptococci, lactobacilli, micrococci! staphylococci, veillonella, and oral bacteroides. 21 As long as gastric pH decreases below 4 for 1 or 2 hours each day, no bacterial colonization of
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the stomach occurs. If gastric pH remains above 4 continuously, the stomach becomes colonized with salivary flora. At pH values above 5, fecal organisms may also colonize the stomach. 20 , 24 During meals, salivary flora are ingested. Neutralization of gastric pH by food allows bacterial counts to rise as high as 106 organisms/ml. 24 Predominant organisms include Streptococcus viridans, Bacteroides melaninogenicus and asaccharolyticus, staphylococci, and Neisseria. Gastric emptying and a return to more acidic pH generally clear these organisms from the stomach in about 60 minutes. 16 These high gastric bacterial counts after meals have important implications for trauma patients, in whom injuries often occur when the stomach is full. This is particularly true of blunt gastric rupture, in which extensive contamination of the peritoneal cavity leads to intra-abdominal abscesses in up to 50% of patients. 3 Although extensive peritoneal contamination and intra-abdominal abscesses are rare in penetrating trauma, bacterial contamination can occur. Stone42 reported positive peritoneal cultures for aerobic organisms in 47% of penetrating gastric injuries. Cultures for anaerobic organisms were positive in about 20% of these patients. MECHANISM OF INJURY Extensive tissue damage from penetrating injuries in civilian practice does not usually occur unless the wounding agent is a high-velocity rifle or a shotgun fired at close range. Most penetrating injuries in civilian settings are due to knife wounds or low-velocity firearms, which do not create significant blast or cavitation effects. The primary mechanism of injury with these weapons is a crushing of the tissue in the bullet path. The amount of tissue damaged may be increased by tumbling of the bullet within the tissue or by the use of hollow-tipped bullets, which deform on impact. 18 Stab wounds generally create a straight tract through the tissue, injuring adjacent organs. In contrast, bullets may take an erratic path. Missiles traveling through tissues of different densities may change course at tissue interfaces, or may be deflected off bone. Because civilian gastric trauma is due to low-velocity weapons or knife wounds, most injuries are simple perforations that result in minimal tissue destruction with little peritoneal contamination. Blunt gastric injuries most commonly occur after motor-vehicle or motor-pedestrian accidents. 3, 9, 11,40,49 However, injuries have also been reported after cardiopulmonary resuscitation, falls, and direct violence, particularly involving child abuse. A number of different mechanisms of injury have been postulated. Yajk0 49 stated that the most common mechanism of injury was a sudden increase in intraluminal pressure resulting from a direct blow to a full stomach. With this mechanism of injury, rupture of the stomach is most frequent along the anterior surface of the stomach or the greater curvature. 3 However, injuries may occur at any point along the stomach wall. Animal studies have demonstrated that with increases in intraluminal pressure, the seromuscular layer is disrupted first, followed by the mucosa and the submucosa. 41 In clinical practice, seromuscular tears of the stomach occur more frequently than rupture, but they are seldom of
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clinical significance. Overdistension of the stomach with increased intraluminal pressure appears to be the mechanism involved in gastric rupture following cardiopulmonary resuscitation. Ventilation of these patients with a face mask can result in gastric distension. Forceful compression of the chest and upper abdomen can then result in gastric rupture. 14, 47 A second mechanism of injury is compression of the stomach against the vertebral column. This may be the mechanism involved in partial and complete transection of the stomach. Only two such cases have been reported in the literature to date. 28, 39 Shearing of the stomach wall at points of fixation may occur with rapid deceleration. Because the stomach is relatively mobile, these injuries are rare and tend to occur at the gastroesophageal junction, at the pylorus, or at sites of perigastric adhesions. Despite the rich blood supply of the stomach, a few cases of gastric necrosis following blunt abdominal trauma have been documented. Garfinkle 19 reported one case of ischemic gastric necrosis along the greater curvature that he attributed to avulsion of the gastroepiploic vessels.
DIAGNOSIS AND INITIAL MANAGEMENT Initial management of these patients addresses life-threatening injuries. Once the airway, ventilation, and circulation have been assessed, patients should undergo resuscitation and then evaluation for an abdominal injury. A nasogastric tube is placed during the resuscitation phase that serves both diagnostic and therapeutic functions. The return of gross blood on nasogastric aspirate is suggestive of an upper gastrointestinal injury. Hematemesis or bright red blood per nasogastric tube was present in 45% of gunshot wounds and 37% of stab wounds in a series of patients with gastric injuries treated at Parkland Memorial Hospital. The nasogastric tube serves a therapeutic function by decompressing the stomach. Aerophagia is frequent in the trauma patient and, along with gastric ileus produced by intraabdominal injury, can lead to Significant gastric dilatation that may not be decompressed by the gastric injury. This in turn can result in respiratory distress, vomiting, pulmonary aspiration, and, in some cases, shock. 7 These complications may be avoided by early gastric decompression. The diagnosis of gastric injury due to gunshot wounds to the abdomen is usually made at celiotomy. Mandatory exploration is performed for all gunshot wounds and results in the discovery of significant injuries in 95% of patients in whom peritoneal penetration has occurred. 30 In contrast, patients with stab wounds to the abdomen have a lower incidence of significant intra-abdominal injury and may be managed selectively in the absence of a clear indication for exploration, such as peritonitis or shock. 43 Stable patients with stab wounds to the anterior abdominal wall undergo local exploration of the wound. If penetration of the peritoneum has occurred, peritoneal lavage is performed. Patients with positive lavages are explored, whereas patients with negative lavages are observed for 24 hours. In those patients with hematemesis or gross blood per nasogastric tube in conjunction with a stab wound in the vicinity of the stomach, lavage is not
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required, and the patient should be explored. Finally, in dealing with stab wounds to the stomach, it should be noted that the full stomach can expand into the lower quadrants of the abdomen. MUfl,34 reported a young man who sustained a stab wound to the right lower quadrant. Bright red blood was found on nasogastric aspiration, and peritoneal lavage revealed 40,000 red blood cells. The patient was explored for persistent gastric hemorrhage and was found to have a through-and-through wound to the greater curvature of the stomach. Fifty to eighty per cent of patients with blunt gastric rupture present with signs of peritoneal irritation or shock. 9 About 60% of these patients give a history of recent ingestion of a meal. 40 Free intraperitoneal air is not a constant finding .. Brunsting,3 in a review of the literature, found free air to be reported in 16 to 66% of patients. In patients with equivocal exams, peritoneal lavage is usually positive for blood or gastric contents. 3 Ilematemesis is often present in those lesions that involve the gastric mucosa. Contrast studies or computed tomography (CT) are rarely needed, but may occasionally be performed in patients without obvious signs of injury. Once a decision has been made to explore the patient, perioperative antibiotics are given and should provide coverage for both aerobic and anaerobic organisms. Antibiotic coverage is continued for 12 to 24 hours after operation. 13. 25 OPERATIVE MANAGEMENT The abdomen is opened through a midline incision, which allows rapid access to the entire peritoneal cavity. Control of hemorrhage is the first priority, followed by containment of enteric spill. Gastric injuries are rarely life-threatening, and management of other intra-abdominal injuries takes precedence. Bleeding and enteric spill from gastric injuries are temporarily controlled by figure-of-eight sutures or Babcock forceps placed across the wound. Once hemorrhage and enteric spill are controlled, careful exploration of the abdomen is indicated to identify all injuries. Both blunt and penetrating gastric trauma are commonly associated with injuries to adjacent organs. The injuries most commonly associated with penetrating trauma in the Parkland series were to the liver, diaphragm, and colon. Blunt trauma is associated with splenic, thoracic, orthopedic, and hepatic injuries. 3 When exploring the abdomen, the entire stomach should be examined carefully. Penetrating injuries usually create paired wounds, and the stomach should be examined for both entrance and exit wounds. Wounds are most likely to be missed in four areas: (1) the gastroesophageal junction, (2) the greater curvature at the omental and splenic attachments, (3) the lesser curvature at the gastrohepatic ligament, and (4) the posterior wall of the stomach. Adequate exposure of the gastroesophageal junction may require takedown of the triangular ligament of the liver. Division of one or more of the short gastric vessels may be necessary to expose the superior aspect of the greater curvature, whereas inferiorly, the omental attachments may
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have to be divided. Exposure of the lesser curvature may require takedown of the gastrohepatic ligament. Care should be taken during this dissection not to injure the vagal nerves. The posterior wall of the stomach can be examined through the lesser sac by dividing the gastrocolic omentum distal to the gastroepiploic vessels or by dividing the avascular junction of the omentum with the transverse colon. Most blunt and penetrating injuries of the stomach can be managed by debridement and simple closure. Partial or complete transections of the stomach and devascularizing injuries are rare but may require resection. Of 243 penetrating gastric injuries treated at Parkland Memorial Hospital over an 8-year period, 98% underwent simple repair and 2% required resection. Repair of the stomach is usually accomplished with a two-layer inverting closure. After repair, gastric wounds reach 75% of the tensile strength of the normal stomach over 21 days. Mter this period, no further gain in tensile strength is seen. 23 The inner layer of the gastric repair is performed with a continuous absorbable suture to obtain hemostasis of the gastric wall, and the outer layer is performed with an interrupted, nonabsorbable suture. Absorbable suture such as chromic retains only 37% of its tensile strength after 1 week of exposure to an acidic environment. Both polyglycolic acid and polyglycolide-Iactide copolymer retain 90% of their tensile strength after 1 week of exposure to a pH of 3, and they are better choices than chromic for the inner layer of the repair.5 An alternative absorbable suture is polydioxanone (PDS). In an animal study of pyloric patency after a pyloric exclusion procedure, PDS was found to maintain closure of the pylorus for an average of 4 weeks after the procedure, versus 2 weeks for polyglycolic acid. This finding was attributed to a slower rate of hydrolysis of PDS when exposed to the acidic environment of the stomach. 15 An outer layer of nonabsorbable suture material adds security to the repair. Among nonabsorbable sutures, polypropylene, monofilament nylon, and Dacron retained almost 100% of their original tensile strength at 4 weeks when exposed to an acidic pH; silk, on the other hand, retained 72% of its tensile strength. 5 Care should be taken not to narrow the gastric lumen when repairing wounds in the area of the gastroesophageal junction or the pylorus. Consideration may be given to performing a pyloroplasty in wounds involving the pylorus. A gastric drainage procedure should also be performed for injuries along the lesser curvature when damage to the vagal nerves has occurred. Repairs in other areas of the stomach are rarely difficult because of the mobility of the stomach and its rich blood supply. These injuries generally heal rapidly and without complication. Drainage of these wounds is not indicated. Before closure of the abdomen, the peritoneal cavity should be irrigated to remove gross contamination. This is particularly applicable to blunt injuries, in which contamination may be extensive. If concomitant diaphragmatic injuries are present with gross contamination of the pleural cavity, the pleural cavity should also be lavaged to remove both gastric contents and residual blood, which is a rich culture medium. These injuries usually
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require the placement of a chest tube, and lavage of the pleural cavity may be carried out through the chest tube or through the diaphragmatic defect. Mter operation, gastric decompression is essential to avoid distension of the stomach and tension on the gastric repair. Nasogastric suction is maintained until bowel function returns.
COMPLICATIONS Overall morbidity and mortality in patients with penetrating injuries to the abdomen involving the stomach are 27% and 14%, respectively. In the Parkland experience, the majority of these complications and deaths are due to associated injuries and not to the gastric injury. Complications directly related to the gastric injury occur in about 6% of patients; deaths occur in 0.4% of patients. The overall mortality rate with blunt gastric injury has been reported to be between 0 and 66%, with most series reporting about a 50% mortality in adults and 20% in children. I, 3, 9, 36, 40, 49 Early mortality in these patients is directly related to the severity of the associated injuries. Complication rates of 50 to 75% have been reported in those patients who survive. Unlike penetrating trauma, many of these complications are directly related to the gastric injury. These complications in both penetrating and blunt trauma include intra-abdominal abscess, disruption of the gastric repair, fistula formation, empyema, missed injuries, hemorrhage, and obstruction. Intra-abdominal abscesses following penetrating gastric trauma are infrequent. Unlike blunt gastric trauma, extensive contamination of the peritoneal cavity is rare with penetrating injuries in civilian practice. Contamination, when it occurs, is usually successfully managed with lavage and perioperative antibiotics. In the Parkland series of the 243 patients who survived their initial injuries, only two patients developed intraabdominal infections secondary to the gastric injury. Both of these infections were related to disruption of the gastric repair. One of these breakdowns probably occurred after inadequate debridement of the gastric wall following a shotgun blast and resulted in an intra-abdominal abscess and the death of the patient. The second breakdown resulted in an abscess that drained spontaneously via a sump drain that had been placed for an associated pancreatic injury. The resultant gastrocutaneous fistula closed with conservative management. The reason for the breakdown of the gastric repair was not clear, but it may have been due to a technical complication. Blunt gastric trauma results in a high percentage of intra-abdominal abscesses. Brunsting,3 in his review of the literature, found an overall abscess rate of 52%, whereas gastrocutaneous fistulas occurred in 16% of patients who survived the initial operation. Most abscesses in blunt trauma were not related to breakdown of the gastric repair. Siemens40 attributed the high abscess rates in these patients to the extensive contamination of the peritoneal cavity that occurs with rupture of the full stomach. Rupture results in contamination of the peritoneal cavity, not only with food particles but also with significant numbers of oral flora that are found in the stomach in concentrations of up to 106 organisms/ml after meals. 16. 24 These abscesses
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occurred despite the use of peritoneal lavage and perioperative antibiotics. Although these measures are important, they may not prevent the development of intra-abdominal abscesses. These patients should be followed closely in the postoperative period. Adjunctive tests, such as CT of the abdomen and contrast studies of the upper gastrointestinal tract, should be considered in patients presenting a septic pictllre. Aggressive drainage of intra-abdominal sources of sepsis should then be undertaken. Concomitant penetrating injuries to the diaphragm and stomach can result in significant contamination of the pleural cavity by gastric contents. Coselli8 reported 53 patients with traumatic hemothorax or pneumothorax who were initially treated with tube thoracostomy and subsequently developed empyemas. This group of patients represented 1.3% of the total number of thoracic injuries treated with chest-tube drainage during this period. The majority of these injuries were due to penetrating trauma. Over 50% of the patients who developed empyemas had combined thoracic and abdominal injuries, with the most frequent abdominal injuries being to the stomach and the liver. Organisms cultured from these infections were predominantly enteric pathogens. Villalba46 reviewed 27 patients who developed empyemas after penetrating trauma to the chest. These patients represented 1.3% of all patients with penetrating chest trauma over a 5-year period. Diaphragmatic injuries, particularly if they were unrecognized at laparotomy, were cited as a risk factor for developing empyema. Associated intra-abdominal injuries most commonly involved the spleen, stomach, and liver. Eighty-one patients with penetrating gastric injuries treated at Parkland Memorial Hospital had combined gastric and diaphragmatic injuries. Ten patients (12.5%) developed empyemas. In these patients, the stomach was the only hollow viscus injured in the abdomen. All of these patients were initially treated with tube thoracostomy. One patient, with extensive contamination, underwent irrigation of the pleural cavity through the diaphragmatic defect. Seven patients subsequently required thoracotomies for drainage of their empyemas, whereas three patients had thin fluid empyemas and were treated by repeat tube thoracostomy. The predominant organisms responsible for these empyemas were Streptococcus species, anaerobes, and staphylococci-all of which are found in oral flora and contaminate the stomach immediately following a meal. The incidence of empyemas following penetrating thoracic trauma is 1 to 4%.8.12,22,29,33,46 The 12.5% incidence of empyemas in patients with concomitant gastric and diaphragmatic injuries is more than three times that reported with penetrating thoracic trauma alone. It has been recommended that in injuries with gross contamination of the pleural cavity, the chest should be lavaged through a separate thoracic incision. 30 Irrigation of the chest through the diaphragmatic defect or through a chest tube is a less morbid procedure and will usually accomplish the same ends. In either event, both gross contamination and residual blood should be removed from the chest cavity, as retained hemothorax represents a good culture medium and has been associated with an increased incidence of empyema.8, 22, 33, 46 Missed injuries are uncommon after blunt gastric trauma, but may
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occur with penetrating trauma if the stomach is not carefully examined. In the Parkland experience, gunshot wounds resulted in multiple injuries in 89% of cases. Stab wounds resulted in a 47% incidence of multiple gastric wounds. Overall, 72% of penetrating injuries produced more than one gastric wound. Wounds to the stomach should not be assumed to be a single tangential wound until the entire stomach is examined. One patient in the above series had a missed injury to the posterior wall of the stomach and to the pancreas when the lesser sac was inadequately explored. A similar injury from a gunshot wound to the stomach and pancreas led to the death of President McKinley in 1901. Careful examination of the stomach, as described under the section on operative management, should avoid this complication. Hemorrhage is a well-documented complication after gastric surgery. The most frequent site of hemorrhage is from the spleen or short gastric vessels, which may be injured when the stomach is mobilized. Bleeding from the gastric suture line may also occur and is reported in 2% of gastrointestinal anastomoses done under elective circumstances. 26 Persistent bleeding from the nasogastric tube requires prompt re-exploration. The complication is best avoided by utilizing a two-layer closure of the gastric wall with an inner running hemostatic stitch and an outer seromuscular layer. Obstruction is a relatively infrequent complication after repair of gastric injuries. the stomach wall is usually easily mobilized to close even large defects without tension or compromise of the gastric lumen. However, closure of gastric wounds in the area of the gastroesophageal junction or the pylorus may present problems. Wounds at the gastroesophageal junction are complex and may require resection and esophagogastrostomy to avoid obstruction of the lumen. Wounds at the pylorus may be amenable to the use of a pyloroplasty or, on rare occasions, may require resection and Billroth II reconstruction. In addition to stenosis at the site of repair, perigastric adhesions have also been reported as a cause of post-traumatic gastric obstruction. 37 Overall, stenosis and obstruction have been found in approximately 2% of elective gastrointestinal anastomoses 26 and in less than 0.5% of penetrating injuries in the Parkland series. SUMMARY The stomach, located in the intrathoracic portion of the abdomen, is well protected from injury. It has a thick wall that is easily mobilized and a rich blood supply that ensures rapid healing of wounds. Although the gastric contents may be contaminated by oral flora immediately after meals, in the resting state, the stomach has few, if any, endogenous organisms. All of these factors make morbidity and mortality associated with penetrating injuries low. In contrast, blunt injuries often cause extensive contamination of the peritoneal cavity with resultant high morbidity and mortality. REFERENCES 1. Asch MJ, Coran AG, Johnston PW: Gastric perforation secondary to blunt trauma in children. J Trauma 15:187-189, 1975
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2. Blaisdell FW, Trunkey DD (eds): Trauma management. In Abdominal Trauma. New York, Thieme-Stratton, 1982, pp 77-86 3. Brunsting LA, Morton JH: Gastric rupture from blunt abdominal trauma. J Trauma 27:887-891, 1987 4. Case MES, Nanduri R: Laceration of the stomach by blunt trauma in a child: A case of child abuse. J Forensic Sci 28:496-501, 1983 5. Chu CC, Moncrief G: An in vitro evaluation of the stability of mechanical properties of surgical suture materials in various pH conditions. Ann Surg 198:223-228, 1983 6. Clemente CD: Anatomy: A Regional Atlas of the Human Body. Philadelphia, Lea & Febiger, 1975 7. Cogbill TH, Bintz M, Johnson JA, et al: Acute gastric dilatation after trauma. J Trauma 27:1113-1117, 1987 8. Coselli JS, Mattox KL, Beall AC: Reevaluation of early evacuation of clotted hemothorax. Am J Surg 148:786-790, 1984 9. Courcy PA, Soderstrom C, Brotman S: Gastric rupture from blunt trauma: A plea for minimal diagnostics and early surgery. Am Surg 50:424-427, 1984 10. Cox EF: Blunt abdominal trauma: A five-year analysis of870 patients requiring celiotomy. Ann Surg 199:467-474, 1984 11. Dajee H, MacDonald AC: Gastric rupture due to seat belt injury. Br J Surg 69:436-437, 1982 12. Daly RC, Mucha P, Pairolero PC, et al: The risk of percutaneous chest tube thoracostomy for blunt thoracic trauma. Ann Emerg Med 14:865-870, 1985 13. Dellinger EP, Wertz MJ, Lennard ES, et al: Efficacy of short-course antibiotic prophylaxis after penetrating intestinal injury. Arch Surg 121:23-30, 1986 14. Demos, NJ, Poticha SM: Gastric rupture occurring during external cardiac resuscitation. Surgery 55:364-366, 1964 15. DeSantis M, Devereux DF, Thompson D: Pyloric exclusion. Am Surg 53:711-714, 1987 16. Drasar BS, Shiner M, McLeod GM: Studies on the intestinal flora. Gastroenterology 56:71-79, 1969 17. Earle AS (ed): Surgery in America, 2nd ed. New York, Praeger Publishers, 1983, pp 117127 18. Fackler ML: Wound ballistics: A review of common misconceptions. JAMA 259:27302736, 1988 19. Garfinkle SE, Matolo NM: Gastric necrosis from blunt abdominal trauma. J Trauma 16:406-407, 1976 20. Garvey BM, McCambley JA, Tuxen DV: Effects of gastric alkalization on bacterial colonization in critically ill patients. Crit Care Med 17:211-216, 1989 21. Gorbach SL: Intestinal microflora. Gastroenterology 60:1110-1129, 1971 22. Graham JM, Mattox KL, Beall AC: Penetrating trauma of the lung. J Trauma 19:665669,1979 . 23. Hastings JC, Van Winkle W, Barker E, et al: Effect of suture material on healing wounds of the stomach and colon. Surg Gynecol Obstet 140:701-707, 1975 24. Hill M: Normal and pathological microbial flora of the upper gastrOintestinal tract. Scand J Gastroenterol Suppl111:1-5, 1985 25. Hofstetter SR, Pachter HL, Bailey AA, et al: A prospective comparison of two regimens of prophylactic antibiotics in abdominal trauma: Cefoxitin versus triple drugs. J Trauma 200:561-566, 1984 26. Jex RK, van Heerden JA, Wolff BG, et al: Gastrointestinal anastoIl)oses: Factors affecting early complications. Ann Surg 206:138-141, 1987 27. Jones RC, ThaI ER, Johnson NA, et al: Evaluation of antibiotic therapy follOwing penetrating abdominal trauma. Ann Surg 201:576-585, 1985 28. Leddy JE, Frew EMS: Complete transection of the body of the stomach resulting from blunt trauma. Can J Surg 20:264-266, 1977 29. MandaI AK, Montano J, Thadepalli H: Prophylactic antibiotics and no antibiotics compared in penetrating chest trauma. J Trauma 25:639-643, 1985 30. Mattox KL, Moore EE, Feliciano DV: Trauma. Norwalk, CT, Appleton & Lange, 1988, pp 411, 459-472 31. McNulty CAM, Wise R: Gastric microflora. Br Med J 291:367-368, 1985 32. Meade RH: An introduction to the history of general surgery. Philadelphia, WB Saunders, 1968, p 197
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33. Millikan JS, Moore EE, Steiner E, et al: Complications of tube thoracostomy for acute trauma. Am J Surg 140:738-741, 1980 34. Murr P, Moore EE, Dunn EL, et al: Stabbed stuffed-stomach syndrome. N Engl J Med 300:625, 1979 35. Nance FC, Cobin I: Surgical judgment in the management of stab wounds to the abdomen: A retrospective and prospective analysis based on a study of 600 stabbed patients. Ann Surg 170:569, 1969 36. Richardson G, Schiller WR, Shuck J: Gastric rupture from blunt trauma. Rocky Mtn Med J 76:309-310, 1979 37. Schwartz GE, Sclafani SJA: Post-traumatic gastric stenosis due to perigastric adhesions. Radiology 154:14, 1985 38. Schwartz SI, Shires GT, Spencer FC: Principles of Surgery, 5th ed. New York, McGrawHill Book Co., 1989, pp 1157-1158 39. Semel L, Frittelli G: Gastric rupture from blunt abdominal trauma. NY State J Med 81:938, 1981 40. Siemens RA, Fulton RL: Gastric rupture as a result of blunt trauma. Am Surg 43:229, 1977 41. Silbergleit A, Beras EM: Neonatal gastric rupture. Minn Med 49:65, 1966 42. Stone HH, Kolb LD, Geheber CE: Incidence and significance of intraperitoneal anaerobic bacteria. Ann Surg 181:705, 1975 43. ThaI ER: Peritoneal lavage: Reliability of RBC count in patients with stab wounds to the chest and abdomen. Arch Surg 119:579-584, 1984 44. Vandamme JPJ, Bonte J: The blood supply of the stomach. Acta Anat 131:89-96, 1988 45. Vassy LE, Klecker RL, Koch E, et al: Traumatic gastric perforation in children from blunt trauma. J Trauma 15:184, 1975 46. Villalba M, Lucas CE, Ledgerwood AM, et al: The etiology of post-traumatic empyema and the role of decortication. J Trauma 19:414, 1979 47. Vinen JD, Gaudry PL: Case reports: Pneumoperitoneum complicating cardiopulmonary resuscitation. Anaesth Intensive Care 14:193, 1986 48. Woodburne RT: Essentials of Human Anatomy, 7th ed. New York, Oxford University Press, 1983, pp 402-405 49. Yajko RD, Seydel F, Trimble C: Rupture of the stomach from blunt abdominal trauma. J Trauma 15:177-183, 1975
Address reprint requests to Rodney Durham, MD Department of Surgery St. Louis University Medical Center 3635 Vista Avenue at Grand Boulevard PO Box 15250 St. Louis, MO 63110-0250