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FIGURE 10.6. Placement of trocars for laparoscopic splenectomy.
technique in identifying accessory spleens. Approximately
10% of patients are said to have accessory spleens, but the
figure is probably higher in patients who have previously
sustained splenic injury.
Partial Splenectomy
Subtotal splenectomy has been used in recent years in
order to salvage at least some splenic function. The main
indications are hypersplenism or traumatic injury in
children that requires splenectomy. In hypersplenism,
approximately 80% of the spleen is resected. All patients
undergoing a partial splenectomy should receive the same
immunization as patients undergoing total splenectomy.
The technique of partial splenectomy requires excellent exposure and full mobilization of the spleen. Arrangement of the splenic vessels at the hilum is inspected. The
splenic artery usually divides into three main branches
before entering the spleen: a superior branch supplying
20% to 25% of the spleen, a large central branch supplying 60% to 70%, and a small inferior branch supplying
10% to 20%. In elective partial splenectomy, the inferior
portion of the spleen is usually easier to preserve. Next, the
splenic veins are carefully dissected. The vessels to that
portion of the spleen to be resected are ligated and divided.
The devascularized region then turns dark purple. The
spleen is transected either with electrocautery or a carefully performed finger-fracture technique. The cut edge of
spleen is sutured with overlapping horizontal mattress
sutures of 1-0 absorbable material over Teflon® pledgets
(Du Pont,
TM
Wilmington, DE), using long straight needles
(Figure 10.7).
Incidental Intraoperative Injury of
the Spleen
The spleen may be inadvertently injured in a number of
upper abdominal operations, especially gastric, hiatal
hernia, and left colon operations. Inadvertent injury to the
spleen is more common in patients who have had previous abdominal surgery because of adhesions to the splenic
capsule. In these circumstances, splenic injury may be
avoided by early division of adhesions to the spleen before
retraction is applied. Another cause of operative trauma to
the spleen is the use of deep and unprotected retractors
and vigorous application of retraction. The most common
injury is a linear capsular tear or avulsion of a small
piece of spleen. Massive injury or injury extending to the
hilum is infrequent. Bleeding from capsular tears can
frequently be managed without splenectomy, provided
the bleeding can be controlled. Successful techniques
include:
1. Temporary firm packing.
2. Application of hemostatic agents in combination with
packing, including thrombin-impregnated Gelfoam®
(Pharmacia Upjohn, Peapack, NJ) and Avitene®microfibrillar collagen (Davol Inc., Cranston, RI).
M anagement of Clinical D isorders ..................................................................................................... 329
TABLE 10.4. Complications of Splenectomy
Hematologic changes
Thrombocytosis
Leukocytosis
Atelectasis
Injury to surrounding structures
Gastric perforation
Colonic injury
Pancreatic fistula
Postoperative hemorrhage
Subphrenic abscess
Postsplenectomy sepsis
Increased incidence of pneumonia, septicemia, meningitis
Overwhelming postsplenectomy sepsis of
䊏
0.8% in adults
䊏
Higher in children
Pulmonary Complications
FIGURE 10.7. Technique for partial splenectomy.
3. Splenorrhaphy, which requires ligation of individual
vessels and approximation of the splenic capsule with
1-0 absorbable sutures tied over Teflon® pledgets
(Figure 10.8).
Postsplenectomy Course
and Complications
Complications that may occur following splenectomy are
summarized in Table 10.4.
Hematologic Changes
Leukocytosis and increased platelet counts are seen in
most patients following splenectomy. The changes develop
within 24 to 48 h and may last for weeks or months.
Peripheral blood shows typical Howell–Jolly bodies.
Left lower lobe atelectasis may sometimes develop
postsplenectomy.
Subphrenic Hematoma
Subphrenic hematoma presents with left upper quadrant
pain, nausea, and sometimes fever. Abdominal ultrasound
or CT scan establishes the diagnosis. Treatment with
percutaneous catheter drainage is effective.
Subphrenic Abscess
Although subphrenic abscess is frequently due to secondary infection of blood or fluid collection, it is important to rule out injury to either the stomach or the splenic
flexure of the colon as an underlying cause. Gastric
and colonic injury are ruled out with upper and lower
gastrointestinal studies with barium or Gastrografin
(Figure 10.9). The abscess is usually readily drained
percutaneously.
FIGURE 10.8. Repair of spleen rupture using splenorraphy and pledgets.
330 ............................................................................................................................................... Spleen
A
B
FIGURE 10.9. Subphrenic abscess can be demonstrated with contrast and ultrasound studies. (A)
Upright radiograph of the abdomen in a patient with previous liver trauma due to a bullet wound
demonstrates an air–fluid level typical of a subphrenic abscess (arrows). (B) Ultrasonography demonstrates the subphrenic fluid collection (F), bordered by the diaphragm (arrows) and by the liver (L).
(Courtesy of Henry I. Goldberg, MD.)
M anagement of Clinical D isorders ..................................................................................................... 331
Gastric Perforation
Gastric perforation is a rare complication probably occurring from inadvertent inclusion of the gastric wall in a ligature, although direct inadvertent injury is also possible.
The clinical course is sepsis, often accompanied by respiratory failure. A Gastrografin study can show the leak from
the gastric fundus. Reoperation is nearly always necessary
to close the gastric perforation and adequately drain the
left subphrenic space.
Colonic Injury
Injury to the splenic flexure usually presents as subphrenic
abscess. Percutaneous drainage results in evacuation of
purulent and fecal material. If sepsis is rapidly controlled
and peritonitis is not present, conservative management
may be possible so that a controlled fecal fistula develops.
The fistula closes with time. On the other hand, if sepsis
is not controlled, and particularly if signs of peritoneal
irritation are present, reoperation will be necessary. The
options then are to resect the splenic flexure and perform
primary anastomosis or to create a diverting colostomy.
Adequate antibiotic coverage is essential.
Injury to the Pancreas
The proximity of the tail of the pancreas to the splenic
hilum has been emphasized. Typically, injury to the pancreas occurs during ligation and division of the splenic
artery and vein at the hilum. The usual presentation is persistent fluid from the drainage tube. The fluid tends to be
slightly cloudy but clear. The amylase content of the fluid
should be measured and will be found to be high, indicating that a pancreatic fistula has developed.
Pancreatic fistulas are typically self-limited and close
within 1 to 3 weeks on a regimen of no oral intake and
administration of the longacting somatostatin analog
octreotide (50–100mg q8h subcutaneously). Rarely will
pancreatic fistula fail to heal. Operative management may
be necessary to accomplish distal pancreatectomy or a
Roux-en-Y pancreaticojejunostomy.
Postsplenectomy Sepsis
Singer reported that deaths from sepsis in splenectomized
patients are 200 times as frequent as in the general population.
4
Furthermore, the incidence of pneumonia, septicemia, and meningitis is 166 times greater in patients
who have undergone splenectomy for trauma.
4
This
finding is the basis for vaccination for pneumococcus, H.
influenza, and meningococcus presplenectomy or immediately after surgery. Overwhelming postsplenectomy
infection occurs in 0.3% of children and 0.1% of adults
with a mortality rate of 1% to 7%.
5
This complication
occurs within 2 years of splenectomy in two-thirds of
cases.
6
The increased susceptibility to infection following
splenectomy is probably due to: (1) decreased clearance of
bacteria from the blood; (2) reduced phagocytosis; (3)
reduced formation of IgM; and (4) decreased production
of opsonins, which contributes to reduced phagocytosis.
Children, especially those less than 2 years old, are particularly susceptible. Preventive measures include: (1) vaccination as described above, (2) prophylactic penicillin
administration in all children under 2 years of age, (3) a
prescription to all adults for penicillin or other antibiotic,
and (4) education about the symptoms of sepsis, so that
they can start treatment if necessary before they go to the
hospital.
REFERENCES
1. Schwartz SI, Shires GT, Spencer FC, eds. Principles of Surgery.
6th ed. New York: McGraw Hill; 1994:1440.
2. Schwartz SI. Splenectomy for hemorrhagic disorders. In: Hiatt
JR, Phillips EH, Morgenstern L, eds. Surgical Diseases of the
Spleen. New York: Springer-Verlag; 1996.
3. Sheldon GF, Croom RD III, Meyer AA. The spleen. In: Sabiston
DC Jr, ed. Textbook of Surgery: The Biological Basis of Modern
Surgical Practice. Philadelphia: WB Saunders; 1997:1207–1208.
4. Singer DB. Postsplenectomy sepsis. In: Perspectives in Pediatric
Pathology. Vol 1. Chicago: Year Book Medical; 1973:285–331.
5. Styrt B. Infection associated with asplenia: risks, mechanisms,
and prevention. Am J Med 1990;88:33N–42N.
6. Cullingford GL, Watkins DN, Watts AD, et al. Severe late postsplenectomy infection. Br J Surg 1991;78:716–721.
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Adekile AD, Owunwanne A, Al-Za’abi K, et al. Temporal sequence
of splenic dysfunction in sickle cell disease. Am J Hematol
2002;69:23–27.
Alonso Cohen MA, Galera MJ, Ruiz M, et al. Splenic abscess. Wor ld
J Surg 1990;14:513–517.
Badura RA, Oliveira O, Palhano MJ, et al. Spontaneous rupture of
the spleen as presenting event in infectious mononucleosis.
Scand J Infect Dis 2001;33:872–874.
Bohnsack JF, Brown EJ. The role of the spleen in resistance to infec-
tion. Annu Rev Med 1986;37:49–59.
Brodsky J, Abcar A, Styler M. Splenectomy for non-Hodgkin’s lym-
phoma. Am J Clin Oncol 1996;19:558–561.
Bynum B. The spleen. Lancet 2002;359:1624.
Cusack JC Jr, Seymour JF, Lerner S, et al. Role of splenectomy in
chronic lymphocytic leukemia. J Am Coll Surg 1997;185:
237–243.
Delaitre B, Pitre J. Laparoscopic splenectomy versus open splenec-
tomy: a comparative study. Hepatogastroenterology 1997;44:
45–49.
George JN, Woolf SH, Raskob GE, et al. Idiopathic thrombocy-
topenic purpura: a practice guideline developed by explicit
methods for the American Society of Hematology. Blood 1996;
88:3–40.
Glasgow RE, Yee LF, Mulvihill SJ. Laparoscopic splenectomy. The
emerging standard. Surg Endosc 1997;11:108–112.
332 ............................................................................................................................................... Spleen
Herneth AM, Pokieser P, Philipp MO, et al. Role of Doppler sonog-
raphy in the evaluation of accessory spleens after splenectomy.
J Ultrasound Med 2001;20:1347–1351.
Horowitz J, Smith JL, Weber TK, et al. Postoperative complications
after splenectomy for hematologic malignancies. Ann Surg
1996;223:290–296.
Katkhouda N, Hurwitz MB, Rivera RT, et al. Laparoscopic splenec-
tomy: outcome and efficacy in 103 consecutive patients. Ann
Surg 1998;228:568–578.
Lipshy KA, Shaffer DJ, Denning DA. An institutional review of the
management of splenic trauma. Contemp Surg 1996;48:330.
Moore EE, Cogbill TH, Jurkovich GH, et al. Organ injury scaling:
spleen and liver (1994 revision). J Trauma 1995;38:323–324.
Morgenstern, L. A History of splenectomy. In: Hiatt JR, Phillips EH,
Morgenstern L, eds. Surgical Diseases of the Spleen.New York:
Springer-Verlag, 1996.
Prevention of pneumococcal disease: recommendations of the Advi-
sory Committee on Immunization Practices (ACIP). MMWR
1997 Apr 4;46(RR-8):1–24.
Schwab CW. Selection of nonoperative management candidates.
World J Surg 2001;25:1389–1392.
Schwartz SI. Role of splenectomy in hematologic disorders. World J
Surg 1996;20:1156–1159.
Taylor MA, Kaplan HS, Nelsen TS. Staging laparotomy with
splenectomy for Hodgkin’s disease: the Stanford experience.
World J Surg 1985;9:449–460.
Tsiotos G, Schlinkert RT. Laparoscopic splenectomy for im-
mune thrombocytopenic purpura. Arch Surg 1997;132:642–
646.
Uranus S, Pfeifer J. Nonoperative treatment of blunt splenic injury.
World J Surg 2001;25:1405–1407.
S elected R eadings............................................................................................................................... 333
334 ...........................................................................................................................................................
Abdominal trauma occurs as a result of either
acceleration–deceleration injuries or missile injuries.
ACCELERATION–DECELERATION INJURY
Most blunt abdominal trauma, whether caused by motor
vehicle accidents, falls, or direct blow to the abdomen, is
due to acceleration–deceleration injury. When the body is
suddenly accelerated or halted, intra-abdominal organs,
which are either filled with fluids or tethered, can undergo
shearing or avulsion. Such injuries can cause tearing of
the mesentery and hemorrhage, as well as fracture of the
spleen and avulsion of the renal pedicle.
MISSILE INJURY
Several types of missile injury are possible: low velocity,
high velocity, and bullet wounds.
11
Abdominal Trauma
MECHANISMS OF INJURY
Most civilian bullet wounds are low velocity. Missiles
fired from handguns have a velocity in the range of 600 to
1100 ft/sec.
1
Typically, wounds from low-velocity missiles
are restricted to the path of the bullet. It must be remembered, however, that the bullet may be deflected within the
abdomen, and the path may not be direct from the entry
to the exit wound. High-velocity missiles typically have a
small entrance wound and a large exit wound, and they
cause extensive damage to the tissue in their path. The
damage caused by shotguns depends on whether they are
fired at short or long range.
Short-range injuries cause massive soft tissue destruction. Long-range shotgun injuries are multiple, lowvelocity pellet injuries. They cause widespread penetration
but do not generally cause severe injury unless the missile
directly hits an organ or blood vessel.
Abdominal trauma is a major cause of death. Nearly 40% of deaths from abdominal trauma
are due to blunt trauma caused primarily by motor vehicle accidents. In these circumstances,
abdominal trauma is often associated with head, chest, and extremity injury. Delay in
diagnosis and treatment is a major contributing factor to mortality, which is often due
to hemorrhage, sepsis, and multiple organ failure. Penetrating abdominal trauma, whether
due to handguns or knives, is a significant problem associated with the use of alcohol and
drugs. These injuries affect individuals in the most productive part of their lives. Organized
trauma systems, including prehospital care, transport, and trauma centers, have improved
the care of the injured patient. But much remains to be done to prevent trauma and improve
legislation and the socioeconomic factors that contribute to the trauma environment.
This chapter focuses primarily on injuries of the gastrointestinal tract and only mentions
injuries of the genitourinary system and the great vessels in the retroperitoneum.
E valuation of A bdominal Trauma........................................................................................................ 335
The reader is referred for full discussion to the excellent
literature that exists on trauma. This chapter only briefly
recapitulates the principles. The ABCDE mnemonic
recommended by the American College of Surgeons
Advanced Trauma Life Support (ATLS) is indispensable
to prioritize the initial management of the traumatized
patient. It recommends investigating the extent of injury
in this sequence: airway, breathing, circulation, disability,
and environment (Table 11.1).
Rapid control of the airway by early intubation is indicated if the patient: (1) is comatose or semicomatose; (2)
is apneic or cyanosed; (3) has sustained major injury of
the head, face, or neck; (4) has sustained chest trauma; or
(5) is profoundly hypotensive. Abdominal trauma is often
associated with thoracic injury, and tension pneumothorax should be ruled out. Signs of tension pneumothorax
are: (1) hypotension; (2) distended neck veins; (3) inadequate ventilation, cyanosis, absence of breath sounds in
one chest cavity; and (4) shift of the mediastinum and
trachea to the opposite side. A chest tube must be inserted
immediately.
Two large-bore intravenous lines are required when the
patient is hemodynamically unstable. Volume resuscitation begins with the rapid administration of crystalloids.
A urinary catheter is needed to monitor urine output, and
a decision must be made whether monitoring of central
venous or pulmonary artery pressure is required. Colloid
resuscitation with albumin, plasma, or blood will be
needed if hypotension is not reversed with the rapid infusion of 1 to 2 L of crystalloids. The goal of volume resuscitation is to restore tissue perfusion as judged by adequate
urine output (50 ml/h), systolic pressure (>100 mm Hg),
pulse rate (<100/min), central venous pressure
(>6 mm Hg), and pulmonary artery pressure (>8mmHg).
Inability to restore hemodynamic stability with rapid fluid
administration usually indicates serious internal bleeding
in the chest, the abdomen, or the soft tissues of the
extremity.
GENERAL PRINCIPLES OF MANAGEMENT
TABLE 11.1. Initial Management of Trauma: ATLS*
Recommendations
A: Airway (establish patent airway)
B: Breathing (ensure both lungs are ventilated)
C: Circulation (restore circulating blood volume; control external
bleeding by compression)
D: Disability (assess neurologic deficit; look for C-spine fracture)
E: Environment (expose patient completely to assess entire
body)
* Advanced Trauma Life Support System recommended by American College
of Surgeons.
EVALUATION OF ABDOMINAL TRAUMA
THE UNCONSCIOUS PATIENT
If the patient with multiple trauma is unconscious, it
should be assumed that intraabdominal injury is present
until specifically excluded. The quickest way to determine
this is with diagnostic peritoneal lavage (DPL) after emptying the patient’s bladder with a catheter. The open technique is preferred. A small infraumbilical incision is made
and carried down to the peritoneum, which is then
grasped with forceps and opened under direct vision. A
lavage catheter is inserted. If no blood is immediately
encountered, 1L of saline is instilled into the peritoneal
cavity and then withdrawn. The peritoneal tap is positive
if: (1) gross blood is present; (2) more than 100,000 red
blood cells/mL are present; and/or (3) bile, fecal matter, or
bacteria are present.
If the unconscious patient with multiple trauma is
hemodynamically stable, particularly if injury to a solid
abdominal organ is suspected, abdominal CT examination
may be preferable because liver or splenic fractures can be
visualized.
THE CONSCIOUS PATIENT
The clinician is aided by the knowledge of symptoms
and signs when the patient is lucid. The patient may
complain of abdominal pain and/or may clearly demonstrate peritoneal irritation. A rapid increase in abdominal
girth usually indicates severe intraabdominal bleeding.
The absence of peritoneal signs, however, does not exclude
the possibility of intraabdominal injury. Such patients, if
hemodynamically stable, can be followed by repeated
abdominal examination. If, however, the patient requires
operative treatment for injury of other systems (head,
extremity), peritoneal dialysis should be performed before
surgery.
Abdominal injury may be associated with the use of
motor vehicle seat belts. The most specific abdominal
injury associated with seat belts is Chance’s fracture: fracture of an upper lumbar vertebra, usually L-1, associated
with rupture of the small intestine, usually the jejunum
(Figure 11.1). But abdominal seat belt injuries may include
lacerations of the colon, small bowel, liver, and spleen.
A
FIGURE 11.1. Chance’s fracture. (A) Frontal view of the lumbar vertebrae in a patient with a seat belt
injury shows lateral displacement of the pedicles (arrow), indicating fracture. (B) Lateral view of the
lumbar spine in the same patient shows the compression fracture of the L-3 vertebral body (arrow).
(Courtesy of Vincent McCormick, MD.)
B
MANAGEMENT OF SPECIFIC INTRAABDOMINAL ORGAN INJURIES
GASTRIC INJURY
TABLE 11.2. Management of Duodenal Injury
Injury Surgical treatment
Gastric injuries may be caused by blunt trauma but are more
often due to penetrating injury, either by bullet or knife
wounds. Penetrating wounds are often associated with injury
to the diaphragm or colon. Gastric perforations are easily
treated by debridement and two-layer closure. Both the ante-
Duodenal hematoma (Grade I) Conservative (NG suction and
TPN)
Duodenojejunostomy if no
resolution of obstruction
in 2–3 weeks
rior and posterior walls of the stomach must be inspected.
Associated diaphragmatic injuries significantly raise the
likelihood of postoperative empyema of the left chest.
DUODENAL INJURY
Duodenal injuries may result from either blunt or penetrating trauma and may vary in their severity. Table 11.2
provides a useful scale of duodenal trauma. Generally,
Retroperitoneal rupture
Grade II Primary repair and closed
drainage
Grade III Primary repair, pylorus
exclusion, tube decompression of duodenum
Major disruption (Grade IV) Primary repair, pyloric
exclusion, or pancreaticoduodenectomy
severe injury (Grades IV and V) is seen in bullet wound
trauma. Two important types of duodenal injury seen in
blunt trauma are intramural hematoma and retroperitoneal rupture.
Massive disruption (Grade V) Pancreaticoduodenectomy
Abbreviations: NG suction, nasogastric suction; TPN, total parenteral
nutrition.
336 ............................................................................................................................ Abdominal T rauma
Duodenal Hematoma (Grade I)
Duodenal hematoma is an uncommon injury caused by
blunt trauma. It occurs more frequently in children than
in adults; the mechanism is often blunt injury to the upper
abdomen caused by a fall on the handlebar of a bicycle.
The trauma may be trivial and symptoms may not occur
for 8 to 12h.
Clinical Presentation
The presenting symptom is persistent vomiting and inability to eat or drink. Abdominal pain is uncommon.
Duodenal hematoma typically occurs distal to the entrance of the common bile duct, and the vomitus is typically bilious. Abdominal examination may show bruising
in the upper abdomen but is otherwise negative. A nasogastric tube should be inserted.
Diagnosis
Diagnosis can be established either by upper gastrointestinal examination with a water-soluble contrast medium or
abdominal CT scan (Figure 11.2). If an upper GI examination is done, complete obstruction is seen, usually
between the second and third parts of the duodenum.
Characteristically, the contrast medium ends in obstruction that has a “spring-coil” appearance. No contrast
medium, however, leaks out of the duodenum. The hematocrit and white blood count are usually normal. Rarely,
associated trauma to the head of the pancreas may cause
elevation of the serum amylase.
Management
In the past, acute obstruction of the duodenum from
intramural hematoma was an indication for urgent
surgery. Most patients now, however, are given time to
resolve their obstruction.
Initial conservative management is instituted with
nasogastric suction, correction of fluid and electrolytes,
and total parenteral nutrition. Institution of acid reduction therapy with an H
-receptor antagonist or proton-
2
pump inhibitor significantly decreases nasogastric suction.
Gastrografin swallow is repeated within 10 to 15 days. If
obstruction has resolved, nasogastric suction is discontinued; oral fluids are then started slowly and advanced to
a solid food diet as tolerated. If obstruction has not
resolved completely, further conservative management for
another week is appropriate.
Surgical treatment is indicated if the obstruction fails
to resolve within approximately 3 weeks. No attempt
should be made to evacuate the intramural hematoma.
Instead, the site of obstruction should be bypassed. The
bypass procedure of choice is side-to-side duodenojejunostomy (Figure 11.3). Gastrojejunostomy should be
avoided whenever possible because: (1) it bypasses
the pylorus and can lead to the dumping syndrome,
and (2) late occurrence of anastomotic ulcer is a possible
complication.
Retroperitoneal Rupture of the Duodenum
(Grades II and III)
Retroperitoneal rupture of the duodenum most commonly results from steering wheel injury in motor vehicle
FIGURE 11.2. Duodenal hematoma. The CT scan of a patient after a motorcycle injury demonstrates a
large duodenal hematoma (arrow) occupying the space between the head of the pancreas (P), the
gallbladder (G), and the kidney (K). (Courtesy of Henry I. Goldberg, MD.)
M anagement of Specific I ntraabdominal Organ I njuries.................................................................... 337
FIGURE 11.3. Side-to-side duodenojejunostomy.
accidents. The mechanism of injury is violent compression
of the duodenum against the vertebra—particularly when
the duodenum is closed at both ends—by the contracted
pylorus proximally and by closure of the duodenojejunal
flexure distally by the ligament of Treitz. The site of
rupture is typically between the second and third portions
of the duodenum, with extravasation of intestinal contents
into the retroperitoneum.
Clinical Presentation
Because the duodenal rupture is retroperitoneal, peritoneal signs take time to develop. As a result, diagnosis is
often delayed for 24 to 48h, increasing morbidity and
mortality. Hence, in any severe injury of the upper
abdomen, the possibility of retroperitoneal duodenal
rupture must be considered. The symptoms are upper
abdominal and thoracolumbar back pain. Fever and tachycardia are present and, with time, signs of peritonitis. If
not treated emergently, full-blown peritonitis and septic
shock ensue.
Diagnosis
Diagnosis is confirmed with radiologic studies. Plain films
of the abdomen may show free retroperitoneal air, either
alveolar in appearance or outlining retroperitoneal organs
such as the kidney (Figure 11.4). Free air in the abdominal cavity is very rare. A picture of ileus may be present.
Gastrografin upper GI studies or abdominal CT scan
shows duodenal rupture and extravasation of dye into the
retroperitoneum. CT scan is preferable because it facilitates diagnosis of any associated pancreatic injury.
Management
Fluid resuscitation and nasogastric suction should be
instituted. Broad-spectrum antibiotics should be given
intravenously and laparotomy performed as soon as the
diagnosis is established. A midline incision is used to open
and carefully explore the abdomen for associated injuries.
The duodenum is best exposed by the Cattell maneuver,
which consists of incising the lateral peritoneum and
reflecting the right and transverse colon to the left (Figure
11.5). The Kocher maneuver can then be performed and
the rupture will become apparent, usually between the
second and third portions of the duodenum. The required
surgical treatment depends on duration of injury and
extent of damage to the duodenal wall. When treatment is
undertaken early and the tear is simple, the edges of the
perforation can be debrided and the duodenum closed in
two layers. The peritoneum is then thoroughly irrigated
with saline, and the abdomen is closed after instituting
closed-suction drainage of the periduodenal area using a
large-bore sump drain.
When duodenal injury is more complex (Grade III)
or treatment delayed, postoperative complications must
be anticipated. Usually, the edges of the defect can be
debrided and duodenal closure accomplished without
compromising the duodenal lumen. Jejunal serosal patch
may be used for further protection. If this is not possible,
the duodenal defect may be managed by creating a sideto-side duodenojejunostomy. In either case, not only must
adequate closed-drainage of the retroperitoneum be established, but tube gastrostomy and feeding jejunostomy
should also be constructed in anticipation of protracted
postoperative course and/or duodenal leak. On occasion,
intraluminal decompression of the duodenum may be
advisable and is accomplished by threading a catheter into
the duodenum through a jejunostomy and bringing the
catheter out through a stab wound in the left upper quadrant. If the duodenal repair is such that the surgeon has
serious concern about dehiscence, the judicious procedure
is pyloric exclusion, in which the pylorus is stapled closed
and gastrojejunostomy performed (Figure 11.6). In addition, tube decompression of the duodenum should be
performed.
338 ............................................................................................................................ Abdominal T rauma
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