Amy D. Wyrzykowski and David V. Feliciano
A number of new approaches to the management of patients with major truncal or extremity trauma have evolved over the past 20 years. These include the following: minimizing time at the scene of trauma and in the emergency department; the presence of in-house attending surgeons, particularly in centers with a significant percentage of penetrating trauma; minimizing admission laboratory testing; initiating resuscitation in the operating room for patients with severe hypotension, cardiac arrest, or external hemorrhage; and early operative control of hemorrhage. All of these are now accepted as major factors in decreasing morbidity and mortality.1–4 Another major change has been the recognition that conservative operative techniques and shortened operative times, even when all organ repairs have not been completed, will increase survival in civilian and military patients with cervical, truncal, or extremity injuries and intraoperative “metabolic failure.”5–22 Finally, it has been recognized that standard closure of a thoracotomy or the midline abdominal incision is impossible to achieve in many severely injured patients, is too time-consuming in others, and may cause an abdominal compartment syndrome in the postoperative period after a laparotomy.23–33
This chapter will describe the techniques used during “damage control” operations (as named by Rotondo et al.);7 prevention and sequelae of primary or secondary abdominal compartment syndrome; the alternate techniques for closure of a thoracic, abdominal, or extremity incision in patients with major trauma;34–43 care of the patient in the surgical intensive care unit (SICU) after a damage control operation; the approach to reoperation; and late repair of incisional hernias when the abdomen has been left open at a reoperation.41,44–47
DAMAGE CONTROL OPERATIONS
Damage control operations are performed in injured patients with profound hemorrhagic shock and preoperative or intraoperative metabolic sequelae that are known to adversely affect survival. The widely accepted three stages of damage control are:
1. Limited operation for control of hemorrhage and contamination. Includes control of hemorrhage from the heart or lung; conservative management of injuries to solid organs; resection of major injuries to the gastrointestinal tract without reanastomosis; control of hemorrhage from major arteries and veins in the neck, trunk, or extremities; packing of organs or spaces should a coagulopathy occur; and use of an alternate coverage or closure of a cervical incision, thoracotomy, laparotomy, or site of exploration of an extremity.
2. Resuscitation in the SICU. Includes vigorous rewarming of the hypothermic patient; restoration of a normal cardiovascular state by the infusion of blood, blood products, and fluids and the use of inotropic and related drugs; correction of residual coagulopathy after hypothermia is reversed; and supportive care to minimize the magnitude of acute lung injury (ALI) and acute kidney injury (AKI).
3. Reoperation. Includes completion of definitive repairs, search for missed injuries, and formal closure of the incision, if possible.
Clinical Recognition of Patients Likely to Need Damage Control Operations
Reports to the hospital from prehospital providers or a rapid evaluation in the emergency department by experienced members of the trauma team are the mechanisms used to select patients for abbreviated resuscitation and immediate operation with damage control techniques in the operating room.
Unless an emergency department thoracotomy is indicated, patients in this small subset (Table 38-1) should stop in the emergency department only long enough to obtain control of the airway, decompress an obvious pneumothorax, draw blood for type and cross match, and apply an identification bracelet. These patients should then be transported immediately to the operating room. Patients arriving by air with hypotension or mangled extremities should bypass the emergency room entirely and be taken directly to the operating room from the helipad.
TABLE 38-1 Patients Likely to Need Damage Control Operations
Intraoperative Indications to Perform Damage Control Operations
The primary indication to modify the conduct of an operation for major trauma to the neck, chest, abdomen, or an extremity is unresolved metabolic failure despite control of hemorrhage by suture, resection, or packing. Metabolic failure is characterized by severe hypothermia despite warming maneuvers initiated in the emergency department and continuing in the operating room, persistent acidemia despite vigorous resuscitation and control of hemorrhage, and a coagulopathy (nonmechanical bleeding) not amenable to operative control.48–58Patients are more likely to die from their intraoperative metabolic failure than they are from the failure to complete organ repairs.5–9,12–14,51–58Most have been massively transfused and have a mortality of 20–50%.7,12–14,52,59–63
Hypothermia continues to be a common problem in victims of major trauma. In one older series, 66% of severely injured patients with an Injury Severity Score (ISS) greater than or equal to 25 admitted to a level I trauma center were hypothermic (<36°C [96.8°F] on an esophageal temperature probe), including 23% who were severely hypothermic (<34°C [93.2°F]).64 Another older review documented that 57% of 74 trauma patients admitted directly to the operating room from the emergency department developed hypothermia (<36°C [96.8°F]) between the time of injury and the time they were moved out of the operating room.65
There are many causes of hypothermia in victims of major trauma. Hypovolemic shock in the preoperative period adversely affects oxygen delivery and leads to decreases in oxygen consumption and, therefore, diminished production of heat.66–68 Should the patient be intoxicated at the time of injury, vasodilatation will further compromise the ability to retain heat. The trauma team itself may be responsible for accelerating the loss of heat from a victim in shock. Undressing the patient in a cool resuscitation room, failing to cover the patient’s head with a turban and the trunk and extremities with warm blankets or the Bair Hugger patient warming system (Augustine Medical, Inc, Eden Prairie, Minnesota) during resuscitation, and infusion of unheated crystalloids and packed red blood cells (PRBCs) are all sources of heat loss in the emergency department. Paralyzing the patient, which prevents shivering, and administering anesthetic agents, which prevent vasoconstriction; failing to cover areas of the body not undergoing operation; opening one or more body cavities in a cold operating room; and irrigating body cavities with unheated crystalloid solutions all further exacerbate heat loss during a thoracotomy or laparotomy. These multiple sources of heat loss cannot be adequately compensated for by increasing heat production in the patient in shock. The resuscitation and surgical teams are responsible for preventing or reversing hypothermia using the techniques listed in Table 38-2.48
TABLE 38-2 Maneuvers to Prevent or Reverse Hypothermia During Damage Control Operations
The effect of hypothermia on mortality in severely injured patients is no longer controversial except for one study. In one large retrospective review, mortality among euthermic and hypothermic trauma patients was not significantly different when patients in both groups were stratified by physiologic and anatomic indicators of injury severity.69 This is in marked contrast to the review of iliac vascular injuries by Cushman et al. who noted that the risk of dying was nearly four times greater when the patient’s initial body temperature in the operating room was less than 34°C (93.2°F).70 If the patient’s last body temperature in the operating room was less than 35°C (95.0°F), the risk of death was nearly 41 times greater than it was for patients with a body temperature greater than 35°C.
While hypothermia is helpful in certain elective operative procedures and has been used for cerebral protection in patients with injury to the brain, it has well-known adverse effects on the cardiovascular, respiratory, renal, gastrointestinal, endocrine, central nervous, and coagulation systems (see Chapter 49).48,71,72 Both terminal cardiac dysfunction and irreversible nonmechanical bleeding have been noted in many injured hypothermic patients dying in the postoperative period after a trauma operative procedure. It would appear logical, therefore, to practice damage control and rapidly complete any trauma operation in which the patient’s initial body temperature is less than 34–35°C (93.2–95.0°F) or the temperature decreases below this level at any time during the operation.27,30,73 This is particularly true in patients undergoing thoracotomy or laparotomy because hypothermia will not be correctable until the chest or abdomen is closed.
Prolonged hypovolemic shock produces a state of persistent metabolic acidosis in the patient with major trauma. This leads to a “circular” phenomenon in which secondary decreases in cardiac output, hypotension, and an increased susceptibility to ventricular arrhythmias may be irreversible, despite adequate volume replacement.8,49,50,55,58,74–76 Also, severe acidosis may cause the uncoupling of β-adrenergic receptors, with a secondary decrease in the patient’s response to endogenous and exogenous catecholamines.77 While acidosis by itself is an unusual reason to terminate a laparotomy being performed for trauma, it often accompanies hypothermia and a coagulopathy.49,50,51,53,55 A persistent metabolic acidosis is a manifestation of anaerobic metabolism occurring during hypoperfusion. Markers of this phenomenon in the injured patient that should initiate damage control operations are listed in Table 38-3.49,70,75,76,78
TABLE 38-3 Intraoperative Indications to Perform Damage Control Operations49,69,74,75,77
Nonmechanical bleeding has been common during emergency trauma thoracotomies, laparotomies, or operative procedures in patients with exsanguination from an injury to an extremity in the past. With current massive transfusion protocols using a goal of 1 U PRBCs:1 U fresh frozen plasma:1 platelet pack, coagulopathies resulting in irreversible bleeding have become a less significant cause of mortality in the immediate postoperative period and have led to improved survival in massively transfused patients.63,79,80 It is now recognized that the historic replacement of volume losses with large amounts of crystalloid solutions and cold PRBCs leads to clotting abnormalities secondary to dilution, deficiency of clotting factors, and hypothermia.8,50,58,59,81–83 Hypothermia has a well-known adverse effect on enzymes associated with the coagulation cascade and on the function of platelets.7,12,13,59,81–83 In addition to a decrease in the incidence of coagulopathies, the implementation of improved transfusion ratios has been associated with reductions in multiorgan failure, fewer infectious complications, and a decreased incidence of the abdominal compartment syndrome.84 Improved transfusion ratios have been associated with decreased mortality in injured civilians, also.85–88
The role of recombinant activated factor VII (Novoseven, Novo Nordisk A/S, Bagsvaerd, Denmark) in the management of a life-threatening coagulopathy remains controversial. While the administration of rFVIIa appears to be safe in the trauma population and has not been associated with an increased risk of severe thrombotic events,89–91 it is extremely costly and the benefits remain unclear. Whereas early studies had promising results including decreased transfusion requirements and decreased 30-day mortality,91,92 more recent work has not found an improvement in outcome.93 When a coagulopathy does result, surgical attempts to control such nonmechanical bleeding, especially from the liver and retroperitoneum, are usually unsuccessful. In the major trauma patient who develops a coagulopathy characterized by an international normalized ratio (INR) or partial thromboplastin time 50% greater than normal during any major operative procedure after major sources of hemorrhage have been controlled, damage control would include the techniques to be described (see Table 38-3).
Operative Techniques in Thoracic Trauma
Exsanguinating hemorrhage from the lung is most rapidly controlled by the application of a DeBakey aortic clamp to the hilum or by twisting the hilum to kink the major vessels in the emergency department or operating room (see Chapter 25).94 When the site of blood loss has been a stab wound deep into the pulmonary parenchyma or a gunshot wound completely through a lobe, the technique of pulmonotomy(sometimes called nonneurosurgical “tractotomy”) is used.95–97 Pulmonotomy refers to the division of pulmonary parenchyma between noncrushing vascular clamps or by using a linear stapling and cutting device to expose injured parenchymal vessels. After selective ligation of these, the pulmonary parenchyma is closed in the usual fashion using a continuous 0 or 2-0 absorbable suture, with reinforcement material added to the staple line, if possible. When the divided lung is edematous, it may not be possible to fully close the pulmonotomy.
Other than compression with a finger, the quickest way to control hemorrhage from a small wound or rupture of a ventricle in the emergency department or operating room is to apply 6-mm-wide skin staples (Auto Suture 35 W, United States Surgical Corporation, Norwalk, Connecticut) (see Chapter 26).98,99 Formal cardiac repair with Teflon pledgets may then be accomplished over the staples or as they are sequentially removed in the operating room.
Larger wounds or ruptures of a ventricle in patients surviving by virtue of tamponade may be controlled by the insertion of a Foley balloon catheter into the hole.100,101 With the balloon inflated and traction applied to the catheter, Teflon-pledgeted sutures can then be passed through the ventricle from side to side over the balloon. The thin wall of the right ventricle puts the inflated balloon at significant risk of puncture as each suture is placed. Pushing the catheter and balloon into the ventricle with each bite of the suture will avoid this complication, although blood loss may be significant.
With a longitudinal perforation or significant rupture of a ventricle, the time-honored technique of inflow occlusion is useful in avoiding cardiopulmonary bypass.102 Curved aortic or angled vascular clamps are first applied to the superior and inferior vena cavae. As the heartbeat slows, horizontal mattress sutures are inserted rapidly on either side of the defect and then crossed to control hemorrhage. A continuous suture is placed to close the defect, and, before it is tied down, air is vented out of the elevated ventricle by releasing the clamps on the cavae.
Operative Techniques in Abdominal Trauma
The liver has a blood supply of 1,500 mL/min and is the major site of synthesis of all the coagulation factors except factor VIII (see Chapter 29). Therefore, appropriate operative management of a major hepatic injury is a key component of a successful damage control laparotomy.
There is ample historical evidence that an emergency hepatic resection performed by a general or trauma surgeon with little experience in a similar elective procedure will result in a mortality rate of 20–44%.103–108 This excessive mortality is certainly related to the magnitude of the hepatic injury, but also to the belated decision to resect at the same time that the aforementioned metabolic failure occurs in many patients. For this reason, more limited techniques of hemostasis should be applied when a hepatic injury is present and damage control is to be performed.109,110
Indirect control of hepatic hemorrhage may be accomplished by extensive compressive hepatorrhaphy, using a continuous suture or interrupted vertical mattress sutures of absorbable material. While this technique is used much less frequently than it was in the past, it is appropriate for a damage control operation.
Damage control techniques in which the sources of hepatic hemorrhage are approached directly include hepatotomy with selective vascular ligation, resectional debridement with selective vascular ligation, and rapid resectional debridement.109 Both former techniques are performed with a vascular clamp on the porta hepatis (Pringle maneuver), and experience with the finger fracture technique should allow for early control of hemorrhage.109–111 When a coagulopathy is already present, hepatotomy or resectional debridement is not appropriate if the surgeon has only modest experience with hepatic trauma. After the Pringle maneuver is performed, rapid resectional debridement is initiated by applying a large Kelly clamp or vascular clamp just outside of a lateral area of partial avulsion (i.e., hepatic segments VI, VII on the right or II, III on the left) or by applying two clamps around the contused sides of a central laceration. The tissue within the clamps is then rapidly debrided, and an O-chromic tie can then be placed around the clamp and all the enclosed tissue ligated en bloc. An alternate technique is to use deep horizontal mattress sutures on either side of the debrided laceration and fill the space between with a viable omental pack (Fig. 38-1).
FIGURE 38-1 Technique of rapid resectional debridement using large vascular clamps, horizontal mattress sutures, and omental pack. (Reproduced with permission from Feliciano DV, Pachter HL. Hepatic trauma revisited. Curr Probl Surg. 1989;26:453. © Elsevier.)
Damage control techniques in which compression or tamponade rather than a suture or metal clip is used to control hepatic hemorrhage include balloon catheter tamponade, absorbable mesh tamponade, and perihepatic packing. Balloon catheter tamponade using a Foley or Fogarty balloon catheter or an inflated Penrose drain over a red rubber catheter is most useful to control hemorrhage from a deep lobar stab or missile track.101,112,113 Inflation of the balloon is performed at different levels of the track until hemorrhage is controlled. Removal of the balloon catheter is performed at a reoperation when the patient’s metabolic failure has been corrected. Alternatively, an absorbable mesh may be used to create a tamponade effect. Absorbable mesh can be used to reapproximate a disrupted lobe with viable fragments that are still attached to the hilum or to replace a disrupted Glisson’s capsule after rupture of a subcapsular hematoma and may be an excellent alternative to major hepatic resection.114,115 For the former, the technique involves mobilization of the injured lobe and circumferential wrapping with a mesh sewn to itself at various locations. Although it may be time-consuming in the patient with a severe coagulopathy, it does avoid the need for reoperation. The insertion of dry laparotomy pads as perihepatic packs continues to be necessary in less than 10% of patients undergoing operative repair of hepatic injuries. Primary indications, in addition to the onset of metabolic failure, include the need to transfer the patient to a center with more experienced hepatic surgeons, a desire to avoid opening a large subcapsular hematoma, and the presence of bilobar injuries.57,116–118 The insertion of perihepatic packs mandates a reoperation and remains one of the classical indications for use of the alternate closures of the midline incision to be described. When placing perihepatic packs, one should be mindful of the possible need for hepatic angiography as an adjunct to laparotomy. If the radiopaque markers of the laparotomy pads are not strategically placed away from the hilum, they may obscure the visualization required for successful angiography.
Operative venovenous bypass of the liver, postoperative venous stenting, and postoperative arterial embolization are all adjuncts to the standard damage control techniques described earlier. All have been applied successfully in selected patients in recent years.119–124
With American Association for the Surgery of Trauma (AAST) Organ Injury Scale (OIS) grade III, IV, or V injuries, splenectomy remains the safest choice when damage control is necessary (see Chapter 30).125,126 Should an AAST OIS grade I or II injury be present, rapid mobilization and direct suture may be faster than splenectomy and will avoid the creation of a denuded retroperitoneal area in the patient with a coagulopathy (Fig. 38-2). With rupture of the capsule, a topical agent such as microfibrillar collagen (Avitene, Bard, Murray Hill, New Jersey) or fibrin glue is applied to the parenchyma under an absorbable mesh. If the condition of the patient does not permit the time needed to suture absorbable mesh as a replacement capsule, a mesh sheet is compressed against the parenchyma with a laparotomy pad pack.
FIGURE 38-2 Rapid two-suture splenorrhaphy is faster than splenectomy for patients with AAST grade I or II injuries. (Reproduced with permission from Feliciano DV, Spjut-Patrinely V, Burch JM, et al. Splenorrhaphy: the alternative. Ann Surg. 1990;211:569.)
Near transections of the duodenum are stapled shut, while an associated injury to the head of the pancreas is packed (see Chapters 31–33). At the reoperation after metabolic failure has been corrected, duodenal continuity can be restored with an end-to-end anastomosis. A pyloric exclusion with polypropylene suture (Fig. 38-3) and an antecolic gastrojejunostomy (Fig. 38-4) are added in selected patients with severe duodenal contusion, narrowing after a suture repair, or a combined complex pancreatoduodenal injury.127,128
FIGURE 38-3 (A and B) Pyloric exclusion is performed through a dependent gastrotomy and completed with no. 1 polypropylene suture. (Reproduced with permission from Baylor College of Medicine.)
FIGURE 38-4 An antecolic gastrojejunostomy is added to the pyloric exclusion to allow for oral intake before the pyloric exclusion opens. (Reproduced with permission from Baylor College of Medicine.)
In the patient with a limited number of enterotomies or colotomies from a penetrating wound, a rapid one-layer, full-thickness closure using a continuous suture of 3-0 or 4-0 polypropylene material is appropriate. Multiple large perforations within a short segment of the small bowel or colon are treated with segmental resection, using metallic clips for mesenteric hemostasis and staples to transect the bowel. In the unstable patient, neither an end-to-end anastomosis nor the maturation of a colostomy is performed until the reoperation in 12–72 hours.129 With shotgun wounds and multiple partial and full-thickness perforations of the jejunum, a jejunectomy may be appropriate as all of its absorptive capabilities are duplicated by the ileum.
Parenchymal defects not involving the duct are either ignored at the damage control procedure or filled with omentum held in place by a tacking suture (see Chapter 32). The insertion of a closed-suction drain is delayed until the reoperation. Ductal transections to the left of the mesenteric vessels that do not involve the splenic vessels are packed or drained, with the distal pancreatectomy and splenectomy once again delayed until the reoperation (Fig. 38-5). Major parenchymal or ductal injuries in the head or neck of the pancreas are also packed or drained, once hemorrhage from the gland or underlying mesenteric–portal vessels is controlled. Pancreatoduodenectomy or reconstruction after a pancreatoduodenectomy caused by the original injury is obviously delayed until the reoperation.129
FIGURE 38-5 Distal pancreatectomy with splenectomy may be completed at the reoperation rather than at the damage control laparotomy. (Reprinted with permission from Cushman JG, Feliciano DV. Contemporary management of pancreatic trauma. In: Maull KI, Cleveland HC, Feliciano DV, et al., eds. Advances in Trauma and Critical Care. Vol. 10. St. Louis: Mosby; 1995:309–336. © Elsevier.)
In any patient with multiple upper abdominal visceral and vascular injuries, a significant injury to the celiac axis or one of its branches is treated with ligation (see Chapter 34). An injury to the renal artery is also best treated with ligation and nephrectomy in the presence of a palpably normal contralateral kidney and multiple associated injuries, although the nephrectomy can be delayed until the reoperation. The use of a large intraluminal shunt (thoracostomy tube) is a theoretical consideration when there has been segmental loss of either the suprarenal or infrarenal aorta in a patient with profound shock; most experienced trauma surgeons, however, would choose to rapidly insert a 12-, 14-, or 16-mm woven Dacron, albumin-coated Dacron, or polytetrafluoroethylene (PTFE) interposition graft and accept an operative procedure that would be 20–25 minutes longer. The superior mesenteric artery or common or external iliac artery is smaller in young trauma patients, and an intraluminal Argyle, Javid, or Pruitt-Inahara shunt may be rapidly inserted under proximal and distal ties to avoid the need for ligation or emergency interposition grafting.17,130 Should arterial ligation be chosen rather than repair or shunting for a significant injury to the common or external iliac artery, a rapid ipsilateral two-skin incision, four-compartment below-knee fasciotomy may prevent myonecrosis with its associated renal and septic problems should the patient survive to undergo an early (within 6 hours) extra-anatomic revascularization procedure.126
When life-threatening arterial hemorrhage from either a blunt pelvic fracture or a penetrating wound occurs in the deep pelvis and cannot be controlled by packing, several innovative approaches have been used in the past. The first is to insert a Fogarty balloon catheter into the internal iliac artery beyond a proximal tie on the side of the hemorrhage. Advancement of the balloon and sequential inflation is performed until the hemorrhage ceases.131 The catheter may then be folded on itself, the excess cut off, and a ligature applied to maintain inflation of the balloon.100,101,131 The other option is for the surgical team to inject a slurry of autologous clot, two cans of microfibrillar collagen (Avitene, MedChem Products, Inc, Woburn, Massachusetts), one packet of bovine topical thrombin (Armour Pharmaceutical Co, Kankakee, Illinois), and 1 g calcium chloride into the distal internal iliac artery beyond a proximal ligature.132
Ligation is the treatment of choice whenever there is a significant injury to the common or external iliac vein, infrarenal inferior vena cava, superior mesenteric vein, or portal vein in a patient with profound shock (see Chapter 34).133–137 After ligation of the infrarenal inferior vena cava, bilateral four-compartment below-knee fasciotomies should be performed immediately if the pressure in the anterior compartment of the leg is greater than 25–35 mm Hg, depending on the patient’s hemodynamic status. Bilateral thigh fasciotomies will likely be necessary, as well, within the first 48 hours after ligation. When there are large defects in the sacrum or pelvic sidewall involving numerous pelvic veins or in the paravertebral area, a number of innovative approaches are available to rapidly control hemorrhage. Included among these are packing the missile track with several vaginal packs (to allow for postoperative pelvic or paravertebral arteriography), inserting fibrin glue, or placing a Foley catheter with a 30-mL balloon inflated at the site of hemorrhage as previously described. Placing packs outside the blast cavity in the deep pelvis or paravertebral area often fails to control hemorrhage in the patient who develops a coagulopathy. Bleeding from presacral veins can be controlled by inserting sterile tacks directly into the visible defect or by suturing a free piece of omentum into an obvious area of perforation.
When severe shock, hypothermia, acidosis, and massive transfusion have led to a coagulopathy and diffuse nonmechanical bleeding, the insertion of intra-abdominal packing for tamponade is appropriate.57,116–118,138–140 Diffuse intra-abdominal packing has been found to be particularly useful when a coagulopathy occurs and extensive retroperitoneal or pelvic dissection has been necessary during a laparotomy for a trauma. Dry, folded laparotomy pads much as described for perihepatic packing are preferred followed by an alternate form of incisional closure. In general, a relaparotomy is performed to remove the packs, irrigate out old blood and clot, and rule out injuries missed at the original damage control laparotomy.
In the original series from Grady Memorial Hospital reported by Stone et al.,138 17 trauma patients with intraoperative coagulopathies underwent damage control laparotomy including the insertion of diffuse packing with laparotomy pads. Reexploration was performed at 15–69 hours in 12 surviving patients, and 11 survived removal of the packs and definitive laparotomy.138
Operative Techniques with Vascular Trauma in an Extremity
Damage control operations on an extremity are appropriate when exsanguination has caused intraoperative metabolic failure (shotgun wound of femoral triangle); when multisystem injuries have occurred and an emergent craniotomy, thoracotomy, or laparotomy needs to be performed in addition to the vascular repair of the extremity (occlusion of superficial femoral artery from a femur fracture); or when the instability of an open fracture precludes formal repair of the associated vascular injury (mangled extremity) (see Chapter 41).141
After rapid control of hemorrhage, an intraluminal Argyle or Javid shunt is inserted into the debrided ends of the injured femoral or popliteal artery and tied in place to preserve distal flow as the patient is resuscitated in the intensive care unit.17 The Pruitt-Inahara shunt may be used also and has inflatable balloons on either end so that tying the shunt in place is not necessary. This shunt has a T-port, which allows for the infusion of heparin, a vasodilator such as papaverine, or for arteriography in the postoperative period. A recent 10-year review of the use of 101 intravascular shunts at a single center found that shunts have a thrombosis rate of 5% and a limb/patient survival rate of 73% supporting their use in damage control procedures.17 In spite of their utility, the use of shunts nationwide is very limited.142
While ligation of major venous injuries in the extremities has been well tolerated in many stable patients,143,144 patients undergoing damage control operations often have severe sequelae.141 Among these are a compartment syndrome below the level of ligation in the lower extremity and excessive hemorrhage from soft tissue injuries and fasciotomy sites. Even if a compartment syndrome does not occur immediately, reperfusion injury as the patient undergoes resuscitation in the intensive care unit will often cause the syndrome to develop. For these reasons, venous outflow after segmental resection of an injured femoral or popliteal vein should be restored with a temporary intraluminal shunt as part of a damage control operation. Short segments of thoracostomy tubes (size 24–28 French) are used as shunts for the popliteal, superficial femoral, or common femoral veins. After removal of the shunt at a reoperation, an externally supported PTFE graft is used for segmental replacement.145
When vascular control has been difficult to obtain with combined femoral or popliteal arterial and venous injuries, there may be some delay before the intraluminal shunts are inserted. In such a situation or when ligation of the femoral or popliteal vein has been necessary to prevent exsanguination, additional time should be spent to complete an ipsilateral four-compartment below-knee fasciotomy as part of the damage control operation. With two attending surgeons or senior residents performing these procedures, they can be completed within 20 minutes. The additional time involved prevents myonecrosis in the early postoperative period and allows the critical care team to focus on respiratory, cardiac, and renal resuscitation.
INDICATIONS FOR ALTERNATE CLOSURES OF INCISIONS
Intraoperative Metabolic Failure
In the previously described patients with hypothermia (temperature <35°C [95.0°F]), persistent acidemia , and/or the onset of an intraoperative coagulopathy, a damage control operation should be terminated with an alternate closure of the incision.
One of the fundamental principles of the damage control operation is that a reoperation will be necessary to complete repairs and resections, perform anastomoses, look for missed injuries, change thoracostomy tubes, insert drains, and attempt closure of the incision. There are also techniques utilized at first operations for trauma, whether damage control was necessary or not, that mandate an early reoperation. Patients in whom the following techniques are used will also benefit from alternate forms of closure of the thoracic or abdominal incision:
• Insertion of perihepatic packing
• Insertion of intra-abdominal packing
• Planned second-look operation
Examples of patients who may require an early second-look procedure after laparotomy for abdominal trauma include those with primary repair of the renal or superior mesenteric artery and those with ligation of the superior mesenteric or portal vein. In the former group, repair of a small vasoconstricted artery in a hypotensive patient often leaves the surgeon with concern about an early postoperative thrombosis.137,146 Early reoperation allows for visual inspection of the end organ after the patient has become hemodynamically stable. With major venous injuries, the dusky and congested appearance of the bowel after major splanchnic venous ligation during the initial operation often prompts concerns about secondary infarction of the involved intestine.134–136 Planned reoperation is worthwhile in such patients, particularly if the base deficit does not correct in the first 8–12 hours after the ligation was performed.
Closure of the Incision Cannot Be Performed or Will Cause an Abdominal Compartment Syndrome
Edema and distention of the midgut have been commonly noted in the past during prolonged laparotomies for trauma in which patients in shock have been treated with the old paradigm of massive crystalloid resuscitation in addition to blood. Presumably, these changes are related to cellular edema from metabolic failure of the sodium pump in the cell membrane, a “capillary leak” phenomenon with secondary interstitial edema related to the release of vasoactive substances, reperfusion injury, the development of an ileus, or some combination of these.23,24,147–150 The volume of the midgut may increase significantly and, if perihepatic or intra-abdominal packs have been inserted as well, make formal fascial closure of the midline abdominal incision time-consuming and extraordinarily difficult. Should fascial closure be completed successfully, the increased volume and secondary increase in pressure (normal: 0 to subatmospheric) in the abdominal cavity may have severe adverse systemic effects, manifesting as the abdominal compartment syndrome.23–33
ABDOMINAL COMPARTMENT SYNDROME
The abdominal compartment syndrome refers to new organ dysfunction/failure (especially decreased blood flow to the body wall and abdominal organs and secondary pressure effects on the respiratory, cardiovascular, and central nervous systems) when the intra-abdominal pressure (IAP) is sustained at greater than 20 mm Hg level.23,24,151 While occasionally discussed in the literature since the 1800s, it is only in the past 25 years that the diagnosis has been made on a regular basis in patients on a variety of surgical and medical services.25–33,151,152
The current subtypes of the abdominal compartment syndrome are defined as follows:151
1. Primary—acute or subacute intra-abdominal hypertension from an abdominal cause;
2. Secondary—subacute or chronic intra-abdominal hypertension from an extra-abdominal cause;153 and
3. Recurrent—redevelopment of the abdominal compartment syndrome following treatment of a primary or secondary type.
Measurement of Intra-Abdominal Pressure
Direct measurement of IAP is accomplished by inserting an intraperitoneal catheter attached to a manometer or transducer.154 In the clinical setting, indirect measurement is possible through a catheter inserted into the urinary bladder,155,156 stomach,157 or inferior vena cava.158 The ease and accuracy of measuring IAP at the level of the symphysis pubis through a saline column (25 mL) previously injected into an empty bladder and connected to a pressure transducer or manometer is well known and remains the technique of choice.155,156 The validity of the bladder pressure as a measure of IAP has been well documented.159 A technique for the continuous measurement of IAP via the urinary bladder has also been described utilizing the irrigation port of a three-way Foley catheter; this technique may theoretically allow for a more timely identification of elevated IAP.160,161
The World Society of the Abdominal Compartment Syndrome (WSACS) defines IAP as being measured at end expiration in the relaxed patient in a supine position.151 This pressure is normally less than 10 mm Hg, while intra-abdominal hypertension is defined as a pressure greater than 12 mm Hg.
Clinical Manifestations of Intra-Abdominal Hypertension
A comprehensive discussion of all the effects of intra-abdominal hypertension causing an abdominal compartment syndrome is beyond the scope of this chapter, and the reader is referred to published clinical and laboratory reviews and studies (Table 38-4).24–33,151,152,162–189
TABLE 38-4 Clinical and Laboratory Manifestations of Increased Intra-Abdominal Pressure162–189
The group at Denver Health Medical Center first proposed a grading system for the abdominal compartment syndrome in 1996.24 This grading system was slightly modified in a subsequent publication and is presented along with recommendations for management based on an indirect measurement of IAP in Table 38-5.190 These recommendations were based on a study of 145 acutely injured patients (ISS >15) undergoing laparotomy, 21 of whom developed an abdominal compartment syndrome (Table 38-6). Of interest, this study validates an IAP of 25 mm Hg as an indicator to decompress the abdominal compartment syndrome.
TABLE 38-5 Grading of the Abdominal Compartment Syndrome
TABLE 38-6 Percentage of Patients with Respective Organ Dysfunction Per Grade of Abdominal Compartment Syndrome
WSACS has subsequently defined the categories of intra-abdominal hypertension as follows:151 (1) grade I—IAP 12–15 mm Hg; (2) grade II—IAP 16–20 mm Hg; (3) grade III—IAP 21–25 mm Hg; (4) grade IV—IAP greater than 25 mm Hg. Using this classification system and the data in the older Denver paper, two thirds of patients now classified as grade IV would be expected to have the following: (1) a peak airway pressure greater than 45 cm H2O; (2) a systemic vascular resistance greater than 1,000 dynes. sec/cm5; and (3) a urine output less than 0.5 mL/(kg h).24,151
Abdominal Perfusion Pressure
In one report, abdominal perfusion pressure defined as mean arterial pressure minus IAP was compared with IAP, arterial pH, base deficit, arterial lactate, and urinary output as an end point of resuscitation and as a predictor of survival.191 The authors found that an abdominal perfusion pressure of 50 mm Hg was a potential end point for resuscitation in the patient with an elevated IAP. Also, the abdominal perfusion pressure was statistically superior to the other end points listed in predicting survival for patients with intra-abdominal hypertension and the abdominal compartment syndrome.
Secondary Abdominal and Extremity Compartment Syndromes
There is now widespread recognition that the abdominal compartment syndrome can occur in the absence of intra-abdominal injuries.28,30,31,33 This “secondary” abdominal compartment syndrome is thought to be due to an ischemia and reperfusion injury in the gastrointestinal tract as well as a capillary leak syndrome from abdominal viscera.28,30 All patients who have developed this syndrome present with severe injuries, sepsis, or burns >41% and usually >70% total body surface area. Massive resuscitation has been necessary in all patients reported to date (mean of L of crystalloid and U of PRBCs in one report).30 Of interest, the diagnosis of a secondary abdominal compartment syndrome has been made from 3 hours to 9 days after injury.28,30,31 The mortality in four reports has been 65.5% (19/29).28,30,31
Another related concern in the patient undergoing a massive resuscitation is the development of a secondary extremity compartment syndrome (SECS). Similar to secondary ACS, SECS is associated with extremely high morbidity and mortality (70%).192 Serial measurement of creatine phosphokinase (CPK) and urine myoglobin may be appropriate in high-risk patients as a screening tool. Any individual with persistently rising CPKs or the unexplained development of myoglobinuria may benefit from measurement of extremity compartment pressures and fasciotomies as appropriate.
Prevention and Management of the Abdominal Compartment Syndrome
The abdominal compartment syndrome is prevented by leaving the midline celiotomy incision open in high-risk patients. Because the syndrome can have a delayed presentation after trauma and resuscitation or develop even though there are no abdominal injuries (secondary abdominal compartment syndrome), there are still critically injured or ill patients who will require treatment. Innovative approaches to avoiding a return to the operating room for abdominal decompression have included laparoscopic decompression or the insertion of either an angiocatheter or a peritoneal dialysis catheter to remove intraperitoneal fluid.193,194 Another interesting approach used successfully in a laboratory model has been the application of a continuous negative abdominal pressure (CNAP) device.189,195
OPERATIVE TECHNIQUES FOR THE OPEN ABDOMEN
Management of the open abdomen can be divided into two phases. In the acute phase, the goal is to provide some variant of temporary coverage to allow the patient to be taken from the operating room to the intensive care unit for additional resuscitation and stabilization with the intent on returning to the operating room when normal physiology has been restored. In the second phase, which follows reoperation, the issue is the management of the abdominal wound and techniques range from delayed fascial closure to planned ventral hernia.
Towel Clip or Suture Closure of the Skin
The simplest and most rapidly performed technique for temporary closure of a thoracic, abdominal, or groin incision in the unstable trauma or septic patient is towel clip or suture closure of only the skin.23Depending on the length of the incision, up to 25–30 standard towel clips may be necessary to complete closure of the wound during a 2-minute period. In order to prevent manipulation of the towel clips and minimize secondary contamination of the chest, abdomen, or groin through the spaces between the towel clips, a large adherent plastic drape is placed over the towel clips and Jackson-Pratt drains are placed lateral to the incision in the operating room prior to transfer to the intensive care unit. When suture closure of only the skin is chosen, 2-0 nylon or thicker suture material is used, depending on the tension of the closure. These skin-closure-only techniques are used much less frequently than they were in the past as increases in postoperative IAP have led to the abdominal compartment syndrome in a significant number of patients.
When the extent of edema and distention of the thorax or the presence of multiple intra-abdominal packs prevents towel clip or suture closure of the skin of the abdominal incision, the insertion of a silo to cover the exposed viscera is performed (Fig. 38-6). Complete coverage of the open abdomen using a polyvinyl plastic silo was first performed by Oswaldo Borraez G. at the San Juan de Dios Hospital in Bogota, Colombia, in March 1984. As the technique of complete silo coverage has become more acceptable since that time, a variety of materials and techniques have been used. When only a small- or moderate-sized silo is needed, an adherent plastic wound drape (Steri-Drape, 3M Healthcare, St. Paul, Minnesota) is applied to the skin edges around the open abdomen. In patients with significant distention of the midgut or peritoneal contents secondary to packs, the soft plastic drape will not be adequate to maintain the midgut within the confines of the abdominal incision. A readily available stronger silo is a 2.5-L plastic bag of irrigating solution used by the urology service (Fig. 38-7).196 A large silo of this material is constructed by cutting three seams of the bag open, and then gas autoclaving the large rectangular piece that results. This silo is sewn to the skin edges of the abdominal wound with 2-0 nylon or polypropylene suture. Another strong silo is Silastic sheeting (Dow Corning Corp, Midland, Michigan), but this is considerably more expensive than the bag of irrigating solution.197 Even the “fish” available in every operating room has been used as a temporary silo.198 Some groups have used gradual reduction in the size of the silo, much as has been described in the pediatric surgical literature for neonates with an omphalocele or gastroschisis.199 In patients with significant distension of the midgut after removal of the temporary silo at a first reoperation, application of a vacuum-assisted closure (VAC) device (Kinetic Concepts, Inc, San Antonio, Texas) is now commonly performed (see below).
FIGURE 38-6 Esmarch bandage silo closure of bilateral anterolateral thoracotomy in patient with six missile perforations in the heart and inferior vena cava.
FIGURE 38-7 Plastic irrigating bag sewn to the skin edges of the abdominal wound makes an excellent silo.
In patients with significant hepatic injuries requiring perihepatic packs, a combination of closures may be appropriate. In such a patient, it is sometimes desirable to have a “tight” closure of the upper abdomen to maintain tamponade of the injured liver. Partial fascial closure limited to the upper abdomen or partial towel clip closure of the same area may be used in conjunction with a silo placed over the lower abdomen. This arrangement maintains a tamponade effect on the injured liver while allowing ample room for expansion of the midgut to avert the development of an abdominal compartment syndrome.
Vacuum-Assisted Wound Closure
A number of early reports described excellent results with “homegrown” vacuum pack coverage of the open abdomen.200,201 On a cellular level, studies have shown that the application of micromechanical forces created by the negative suction promotes cell division, angiogenesis, and the local elaboration of growth factors all without increasing apoptosis.202,203 Practically speaking, applying suction to the open wound over the midgut allows for the rapid removal of peritoneal fluid and collapses spaces between the viscera. As both of these results will make the contents of the abdominal cavity smaller, there is a greater chance of formal aponeurotic closure of the midline incision. In the report by Barker et al.,38 216 vacuum packs were placed in 112 patients. While 22 patients (19.6%) died before abdominal closure was attempted, 62 (55.4%) went on to formal closure of the incision. The overall mortality rate in this large series was 25.9%.
As previously mentioned, the Kinetic Concepts, Inc VAC system has been utilized in many centers.39 A nonadherent occlusive plastic barrier (Steri-Drape, 3M Healthcare) with small perforations placed in it is covered by an appropriately sized polyurethane foam sponge that is part of the VAC system. The suction tubing that is part of the system is attached, and the entire system is covered with an airtight occlusive drape. KCI has recently introduced an updated product, ABThera, which theoretically provides improved negative pressure distribution throughout the abdominal cavity. In the report by Garner et al.,39 13 of 14 injured patients in whom the original system was used underwent formal closure of the midline incision before discharge. Clinical studies on the ABThera are currently lacking. Also new to the market is the ABRA Abdominal Wall Closure System available from Canica (Ontario, Canada). This product integrates a silicone traction component with a skin fixation component. The combination is used to provide gentle elastic traction on the tissues theoretically preventing loss of abdominal domain and facilitating primary wound closure. As with the ABThera, clinical studies are still needed on this device.
This older technique using nylon cloth material over the midgut has been used at Detroit Receiving Hospital for over 35 years.36,204 The cloth is covered with “generous” gauze packs, while several widely spaced retention sutures are placed through the abdominal wall above the packs. Every effort is made to keep the midgut below the aponeurotic edges.
As midgut edema resolves, the patient is returned to the operating room for removal of the gauze and gradual tightening of the retention sutures until the linea alba can be closed. In the report by Bender et al., 15 of 17 patients surviving longer than 24 hours had successful closure of the midline incision using the technique described.204 There were no enterocutaneous fistulae or incisional hernias in the 14 long-term survivors. A number of related approaches have been described in the literature as well.41,42
INTENSIVE CARE BEFORE REOPERATION
Following the control of surgical bleeding, patients are brought to the intensive care unit for ongoing resuscitation. The immediate goals are to both provide adequate oxygenation and reverse the effects of inadequate tissue perfusion and resultant metabolic failure. The lethal triad of hypothermia, coagulopathy, and acidosis must be aggressively rectified if the patient is to survive.
All of the previously described warming maneuvers used in the emergency department and operating room—increased ambient temperature, external rewarming using a Bair Hugger or similar device, warming lights, and warmed fluid and blood products—are implemented in the intensive care unit, also. For refractory cases of hypothermia, Gentilello et al.205 have described the use of a continuous arteriovenous rewarming (CAVR) device. In the patient with a systolic blood pressure greater than 80 mm Hg, femoral arterial and venous catheters are connected through the heating mechanism of a standard countercurrent fluid warmer. The patient’s own blood pressure drives the blood through heparin-bonded tubing; therefore, use of this system is limited in hypotensive patients. In a mixed group of 34 hypothermic patients (<35°C [95.0°F]) with trauma, major operations, or near drowning, 16 patients treated with CAVR had resolution of their hypothermia in 39 minutes versus 3.23 hours in the group of 18 treated with the conventional methods described above. Inability to correct a patient’s hypothermia after a damage control operation is a marker of inadequate resuscitation or irreversible shock.70
The multifactorial coagulopathy still seen in some trauma patients must be aggressively managed, as well. Postoperatively, patients undergoing damage control procedures should have serial coagulation parameters monitored including routine measurement of fibrinogen levels to assess the need for cryoprecipitate in addition to fresh frozen plasma and PRBCs. Several parameters may be utilized to assess the adequacy of a resuscitation, with acidosis being one of the most common. It is generally accepted that resuscitation is not complete until the patient’s oxygen debt is repaid; simple restoration of normal vital signs is not adequate as a patient may simply be in “compensated” shock while continuing to have occult hypoperfusion and ongoing tissue damage.206 Extensive studies have been performed to determine the parameters that best define the end point of resuscitation. These end points can be divided into two broad categories, global and regional. In addition to acid–base status, parameters for monitoring global resuscitation include oxygen delivery, mixed venous saturation, right ventricular end-diastolic volume, left ventricular stroke work index, and others.206 From a regional perspective, gastric tonometry and intramucosal pH have been used to assess gastric perfusion. Additionally, both spectroscopy and electrodes have been applied to measure tissue pO2, pCO2, and pH in muscle and subcutaneous tissue to assess peripheral perfusion.206,207 While these techniques may all provide data that can be used to predict outcome, none has been proven to be a superior marker of the end point of resuscitation.208 Still, it is recommended that one of these end points be monitored in addition to the standard clinical parameters to assess the adequacy of resuscitation.209
Failure to attain the desired end points of resuscitation during the ICU phase of damage control may reflect continuing hemorrhage.57,210 An early return to the operating room is a difficult decision because the hypothermia-related coagulopathy is often not resolved. Therefore, the surgeon must decide whether mechanical or surgical hemorrhage is occurring versus diffuse oozing from a coagulopathy in which an early reoperation may not be indicated. Morris et al.211 have suggested several indicators for an emergent return to the operating room based on continuing hemorrhage after a damage control laparotomy (Table 38-7).211
TABLE 38-7 Indications for Emergent Return to the Operating Room After a Damage Control Laparotomy
Another obvious indication for an early reoperation is the development of the previously described abdominal compartment syndrome. A progressive increase in inspiratory pressures on the ventilator coupled with oliguria and a “tight” abdomen mandates a rapid measurement of IAP through the bladder catheter.155,156 Reoperation is necessary when the clinical signs are accompanied by an IAP greater than 25 mm Hg, as previously described.24,190 Morris et al.57,211 and many others have noted that sudden release of the abdominal compartment syndrome at the time of reoperation may lead to a reperfusion phenomenon and a cardiac arrest. For this reason, Morris has recommended that volume loading with 2 L of a solution composed of 0.45% normal saline, 50 g mannitol/L, and 100 mEq sodium bicarbonate/L be performed before release of the abdominal wall.
When postoperative bleeding is not a concern, a return to the operating room is based on reversal of metabolic failure and normalizing of cardiovascular, pulmonary, and coagulation parameters as suggested by Morris et al. (Table 38-8).211 In a review of patients with perihepatic packs inserted to control hemorrhage, relaparotomy was performed at a mean time of 3.7 days from the original damage control operation.116 The timing of reoperation, however, may be more critical than has previously been thought, as it may act as a “trigger” for sensitized leukocytes circulating during post-traumatic inflammation (“second hit phenomenon”). As multiple-organ failure may result, the timing of reoperation may turn out to be one of the more critical factors in determining survival after a damage control operation.212–215Another factor to consider is that the presence of intra-abdominal packs alone results in peritoneal endotoxin and accumulation of inflammatory mediators even when cultures are sterile.216
TABLE 38-8 Guidelines for Elective Return to the Operating Room After a Damage Control Laparotomy
A patient who is normotensive, without a coagulopathy, and is in the diuretic phase of recovery after resuscitation from shock is an ideal candidate for reoperation. While this usually takes place within 48–72 hours of the damage control laparotomy, it may be delayed in patients with massive distention of the midgut so that a further diuresis may occur.
If towel clips were used to close the abdominal wall at the damage control laparotomy, five of every six are removed at the first stage of reoperation. The remainder are then elevated off the abdominal wall by placing them on a sponge stick as scrubbing and painting of the abdominal wall are performed. After the surgical team has placed sterile towels around the wound, the final towel clips are removed. This technique prevents evisceration during the period of skin preparation.
Once the towel clips, skin sutures, or silos have been removed, clots and packs are evacuated manually and with the suction device. A complete examination of all abdominal contents is performed to detect any injuries missed at the damage control laparotomy.23 Resections, anastomoses of the bowel, and maturation of colostomies are rapidly performed in the hemodynamically stable patient. Prior to closure, the abdominal cavity is vigorously irrigated with saline solution containing antibiotics. This solution is left in the abdominal cavity during the 3–5 minutes that it takes for the surgical team to change gloves and place towels around the wound. The irrigating solution is then aspirated from the abdominal cavity, and drains are inserted as indicated. The linea alba is closed with permanent suture, while the subcutaneous tissue and skin are packed open.
Techniques for the Management of the Open Abdomen at Reoperation
Repeat Application of a Silo
When a VAC device is not available, a Steri-Drape or plastic silo may be reapplied at the reoperation in the distended patient as it protects the midgut, prevents evaporation, and allows for visual confirmation that the midgut is decreasing in size during the diuretic phase of recovery.43
Vacuum-Assisted Fascial Closure
Any of the vacuum dressing techniques discussed in Section “Operative Techniques for the Open Abdomen” can also be initiated following resuscitation at the reoperation.39,217–219 Cothren et al.217 reported a 100% fascial closure rate using vacuum-assisted sequential fascial reapproximation. At the time of initial operation, a silo was applied. Following stabilization of the patient, they used a variant of the technique described by Miller et al.219—placing a nonadherent dressing over the viscera and under the fascia, using fascial sutures to provide moderate tension, placing a superficial sponge layer, and then placing the wound to suction. They returned patients to the operating room every 2 days for replacement of the sponges and gradual fascial closure. Other authors have reported excellent results with vacuum devices reporting closure rates ranging from 71.9% to 92% and few complications, also.39,218,219 At the present time, this appears to be the preferred technique for management of the open abdomen.
Zippers, Slide Fasteners, Velcro Analogue
Originally described by Leguit in 1982,201 the zipper closure of the abdominal wall was popularized by Stone et al.220 in the United States in their open treatment of patients with pancreatic abscesses. Either a conventional zipper is sutured to the skin or fascia with a continuous suture of 0 or 2-0 nylon or polypropylene or a commercial zipper with adhesive side pieces is applied to the skin edges. The major advantage of using the skin is that it preserves the fascia for formal wound closure at an appropriate time.
Another option for septic or trauma patients reported by Teichmann et al.,221 Wittmann et al.,222 and Aprahamian et al.223 is the Wittmann Patch (Starsurgical, Burlington, Wisconsin). In this system two sheets of Velcro-like biocompatible material are sewn to the aponeurotic edges of the midline incision. Closure is accomplished by the adherence between the overlapping Velcro-like sheets. As edema of the midgut resolves, excess patch material is trimmed, and the fascial edges can be pulled closer together. The major advantages of this system are in the ease of access for reoperations and the tension on the aponeurotic edges that prevents the usual lateral retraction. Tieu et al.224 reported an 82% closure rate using the Wittmann Patch in a mixed population of trauma and critically ill surgery patients. In a study by Weinberg et al.,225 delayed primary fascial closure was achieved in 78% of trauma patients treated with the Wittmann Patch. A “modified Wittmann” technique was described by Fantus et al.226 who placed a nonadherent layer, such as the previously mentioned sterile x-ray cassette cover, under the abdominal wall and over the viscera to decrease the formation of adhesions that can form between the two hindering delayed fascial closure. They achieved good closure rates, also.
For the trauma patient with marked distention of the midgut, a PTFE body wall patch is strong and watertight and creates a smooth layer of granulation tissue that can be covered with a split-thickness skin graft when the prosthesis is removed. Unfortunately, this prosthesis is quite expensive, and similar results have been obtained with less expensive absorbable meshes as previously described.
Numerous clinicians have described short-term success with closure of the abdominal wall with Marlex mesh in the presence of extensive fasciitis or intra-abdominal sepsis.227–230 Healing of the wound over the mesh has been reported in many patients, even in those in whom grossly purulent material surrounds the mesh.231 Numerous long-term complications, however, are common. In the report by Voyles et al.229 describing the use of Marlex (Bard) mesh in 31 acute abdominal wall defects, 9 wounds were closed by split-thickness grafts over granulated mesh. In each instance, extrusion of the mesh and/or enteric fistulae developed. Nine other wounds healed by secondary intention, and six of these developed extrusion of the mesh or enteric fistulae. Stone et al.228 reported on the use of Marlex mesh in 23 patients with acute full-thickness loss of the abdominal wall from trauma or sepsis and noted that the mesh eventually had to be removed in all but 2 patients. They also commented that “Marlex has twice the incidence of postoperative wound sepsis, almost six times as many associated bowel fistulas, and less than one third as many successful skin graft takes for cover” compared with Prolene mesh.
These data strongly suggest that a permanent rigid prosthesis such as Marlex or Prolene mesh should not be inserted in abdominal wall defects in the presence of extensive contamination from a perforated gastrointestinal tract secondary to trauma, acute intra-abdominal sepsis, or necrotizing infection in the abdominal wall.232 The risk of secondary infection and damage to the underlying bowel as the prosthesis develops “wrinkles” from contraction of the wound has now been documented on numerous occasions.
Synthetic meshes such as polyglactin (Vicryl) and polyglycolic acid (Dexon) have been available to the surgeon for the past 30 years. They have been used primarily for renorrhaphy, splenorrhaphy, and hepatorrhaphy in abdominal trauma and for closure of the pelvic floor after abdominoperineal resection of the rectum. In laboratory studies using absorbable meshes to repair defects in the abdominal wall, bursting strength has been comparable to that of permanent meshes for the first 8 weeks after insertion.233–235 Unfortunately, as the mesh is absorbed, hernias or decreased bursting strength at the site of the mesh develop by 10–12 weeks after insertion.233,235
The primary clinical use of absorbable meshes as an alternate form of coverage of the open abdomen on the trauma service has been in patients with marked distention of the midgut at the time of removal of a plastic silo or VAC device.236 It has been used in patients with open abdomens from septic processes in the abdominal wall or in the abdominal cavity, also.230,231 Fabian et al.45 have described four stages in the use of absorbable mesh to cover an open abdomen. These include the following: (a) coverage of the midgut; (b) removal of the mesh after granulation tissue has formed at 2–3 weeks (Fig. 38-8); (c) split-thickness skin grafting of granulation tissue or abdominal skin and subcutaneous flap closure over the granulation tissue several days later (Fig. 38-9); and (d) definitive reconstruction in 6–12 months.
FIGURE 38-8 Remains of double-layer absorbable mesh coverage of open abdomen on the day a split-thickness skin graft is to be applied. Patient sustained quadriplegia, rupture of the descending thoracic aorta, and a secondary abdominal compartment syndrome after being struck by a motor vehicle.
FIGURE 38-9 A meshed split-thickness skin graft has been applied to the granulated abdomen of the same patient as in Fig. 38-8.
One practical point in using absorbable mesh is that the Dexon variant has wider interstices that allow for drainage of intra-abdominal fluid.75 Another is to use fine mesh gauze packing above the absorbable mesh. The gauze packing will aid in keeping the small bowel below the level of the fascia of the abdominal wall, much as has been described by Bender et al.204 with their technique. This prevents the gradual dilation of the bowel and thinning of its wall as is commonly seen in patients in whom the abdomen has been left open and should significantly lower the incidence of enterocutaneous fistulas in such patients.
In summary, absorbable meshes avoid the major problems associated with permanent meshes (see above). When placed loosely over the midgut, they allow for distention and prevent abdominal compartment syndrome. Also, erosion into the bowel or infection of the mesh secondary to contamination from trauma or a septic process in the abdomen or abdominal wall is less likely. They help prevent evisceration when gauze packing is placed above the mesh, are soft and pliable, allow for drainage of contaminated abdominal fluid through the mesh, and permit the ingrowth of granulation tissue.34,35,45,236 An incisional hernia occurs in all patients in whom the mesh is allowed to granulate, and repair is deferred until the patient has fully recovered from the original traumatic or septic event.
WHAT HAPPENS TO PATIENTS WHEN A VACUUM-ASSISTED CLOSURE IS NOT USED?
Tremblay et al.40 reported on a 4-year experience with 181 patients with an open abdomen who were managed with techniques other than VAC—silos, skin only or towel clip closure, open packing, and modified visceral packing. The morbidity in the series was high as 14% of patients developed enterocutaneous fistulas, 5% suffered wound dehiscence, and almost half of the patients in the series were left with large incisional hernias at the time of discharge. The results in this series do not compare favorably with the closure rates and complications associated with the use of the VACs (see above). It appears, then, that some method of vacuum-assisted technique should be applied in the majority of patients.
LATE CLOSURE OF THE INCISIONAL HERNIA
Only 10–20% of patients undergoing use of a VAC device are left with an incisional hernia after damage control procedures. When a hernia does result, either following an attempted closure or as the planned result following the use of absorbable mesh, it is appropriate to delay closure for 6–12 months. Any stomas should also be taken down in the same delayed fashion. This interval allows the patient to improve his or her nutritional status, fully recover from the original injuries, and complete the formation of adhesions and scars in the abdominal cavity and body wall. When assessing the patient with a massive ventral hernia preoperatively, one must carefully examine the abdominal skin graft. If the physician can pull the graft up and off of the underlying small bowel, that is, if the patient passes the “pinch test,” the timing is supposedly right for repair.45 In truth, dense adhesions between the underside of the skin graft and the underlying small bowel are present in over half of the patients. Additionally, one must determine if adequate skin will be available to cover the viscera and prosthetic, if used, once the skin graft to the abdomen has been excised. If it appears that skin will be lacking, lateral tissue expanders should be placed under the skin 2–3 months prior to undertaking reconstruction of the abdominal wall. Should scarring of the abdominal wall or the presence of a colostomy prevent the use of a tissue expander on one side of the abdominal wall, a tensor fascia lata myocutaneous flap may have to be elevated off the ipsilateral thigh, and then tacked back in place several weeks before reconstruction of the abdominal wall. Finally, there are patients in whom the extent of evisceration under the old skin graft brings the anterior and posterior abdominal walls into close proximity resulting in a loss of domain of the abdominal cavity. Such patients will usually require the insertion of large prosthetic patches to cover the hernia defect as well an extensive amount of skin to cover the patch.
It is the policy of the senior author of this chapter to perform the takedown of end colostomies and restoration of gastrointestinal continuity before any reconstruction of the abdominal wall. As a first stage, the old skin graft is detached from the abdominal wall for 180° of its 360° attachment. For a left-sided colostomy, the best exposure for the takedown of the end colostomy and colon reanastomosis would result from detaching the skin graft from the 12- to 6-o’clock positions. The detached skin graft is folded back, adhesions are divided, the rectal or left colon pouch is mobilized, and the anastomosis is performed. The reflected skin graft is then returned to its original position and the abdominal viscera are covered by tacking the edge of the skin graft back down. The abdominal wall reconstruction is then performed at a later date.
In selected patients, the narrow midline defect that remains after excision of the skin graft over the midgut can be readily closed with a continuous or interrupted suture technique using no. 1 polypropylene material.46 When it is not possible to close secondary to excessive tension on linea alba, the components separation technique of closure is used. The skin and fat are elevated off the underlying fascia through the midline incision or using a lateral laparoscopic approach until the flaps extend to several centimeters lateral to the rectus sheath. The external oblique aponeurosis is then divided lateral to the rectus muscle bilaterally from the lower thoracic wall to just above the inguinal ligament. Each relaxing incision usually creates an additional 4–5 cm of width to the abdominal wall and often allows for closure of the midline. This is, actually, the “second step” of the components separation technique first described by Ramirez et al.44 If this does not allow the linea alba to be reapproximated, the posterior rectus sheath is divided to complete the standard components separation. When there is extensive scarring of the remnant edge of the linea alba on either side of the midline, excision of the scar back to viable rectus muscle is necessary. When a greater release is needed, the modified technique described by Fabian et al.45 can be used. After the rectus abdominis muscle is separated from the posterior rectus sheath, the internal oblique component of the anterior rectus sheath is divided from the epigastrium to the arcuate line. The final stage involves suturing the anterior rectus sheaths in the midline, as well as approximating the medial border of the posterior rectus sheath to the lateral border of the previously divided anterior rectus sheath. Using the technique described in nine patients, one patient developed a wound infection and a recurrent incisional hernia. More recently, bioprosthetics such as AlloDerm (Life Cell Corporation, Branchburg, New Jersey) are being utilized to enhance abdominal wall reconstruction and decrease the recurrence rate.237 The AlloDerm can be used as layered overlay patch or an underlay patch or both to help alleviate the tension on the midline fascial closure and reduce recurrence of the hernia. Buinewicz and Rosen238 achieved a recurrence rate of only 5% using the AlloDerm. Employing both an AlloDerm overlay and underlay, Kolker et al.239 had no recurrent hernias with a mean follow-up of 16 months.
If the midline can still not be reapproximated, a prosthetic patch should be used. In the presence of complete omental coverage over the midgut, a polypropylene or Marlex mesh can be utilized. In the absence of omentum, a PTFE body wall patch is appropriate.23 If a colostomy is being taken down (as previously noted, this is not recommended by the authors) or there is other contamination during the procedure, a bioactive mesh may be preferable. Multiple options are currently available and the reader is referred to the available studies.237–239 The single greatest problem has been either persistent or recurrent incisional hernias when a bioprosthesis is used to bridge a significant gap in the abdominal wall.
1. Krausz MM, Bar-Ziv M, Rabinovici R, et al. “Scoop and run” or stabilize hemorrhagic shock with normal saline or small-volume hypertonic saline? J Trauma. 1992;33:6.
2. Hoyt DB, Shackford SR, McGill T, et al. The impact of in-house surgeons and operating room resuscitation on outcome of traumatic injuries. Arch Surg. 1989;124:906.
3. Frankel HL, Rozycki GS, Ochsner MG, et al. Minimizing admission laboratory testing in trauma patients: use of a microanalyzer. J Trauma. 1994;37:728.
4. Rhodes M, Brader A, Lucke J, et al. Direct transport to the operating room for resuscitation of trauma patients. J Trauma. 1989;29:907.
5. Feliciano DV, Burch JM, Spjut-Patrinely V, et al. Abdominal gunshot wounds. An urban trauma center’s experience with 300 consecutive patients. Ann Surg. 1988;208:362.
6. Nicholas JM, Rix EP, Easley KA, et al. Changing patterns in the management of penetrating abdominal trauma: the more things change, the more they stay the same. J Trauma. 2003;55:1095–1108.
7. Rotondo MF, Schwab CW, McGonigal MD, et al. “Damage control”: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35:375.
8. Moore EE, Burch JM, Franciose RJ, et al. Staged physiologic restoration and damage control surgery. World J Surg. 1998;22:1184.
9. Ferrada R, Birolini D. New concepts in the management of patients with penetrating abdominal wounds. Surg Clin North Am. 1999;79: 1331.
10. Eiseman B, Moore EE, Meldrum DR, et al. Feasibility of damage control surgery in the management of military combat casualties. Arch Surg. 2000;135:1323.
11. Holcomb JB, Helling TS, Hirshberg A. Military, civilian, and rural application of the damage control philosophy. Mil Med. 2001;166:490.
12. Shapiro MB, Jenkins DH, Schwab CW, et al. Damage control: collective review. J Trauma. 2000;49:969.
13. Johnson JW, Gracias VH, Schwab CW, et al. Evolution in damage control for exsanguinating penetrating abdominal injury. J Trauma. 2001;51:261.
14. Hoey BA, Schwab CW. Damage control surgery. Scand J Surg. 2002; 91:92.
15. Firoozmand E, Velmahos GC. Extending damage-control principles to the neck. J Trauma. 2000;48:541.
16. Vargo DJ, Battistella FD. Abbreviated thoracotomy and temporary chest closure: an application of damage control after thoracic trauma. Arch Surg. 2001;136:21.
17. Subramanian A, Vercruysse G, Dente C, et al. A decade’s experience with temporary intravascular shunts at a civilian level I trauma center. J Trauma. 2008;65:316.
18. Granchi T, Schmittling Z, Vasquez J, et al. Prolonged use of intraluminal arterial shunts without systemic anticoagulation. Am J Surg. 2000; 180:493.
19. Scalea TM, Boswell SA, Scott JD, et al. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: damage control orthopaedics. J Trauma. 2000;48:613.
20. Pape HC, Hildebrand F, Pertschy S, et al. Changes in the management of femoral shaft fractures in polytrauma patients: from early total care to damage control orthopedic surgery. J Trauma. 2002;53:452.
21. Pape HC, Giannoudis P, Krettek C. The timing of fracture treatment in polytrauma patients: relevance of damage control orthopedic surgery. Am J Surg. 2002;183:622.
22. Kos X, Fanchamps JM, Trotteur G, et al. Radiologic damage control: evaluation of a combined CT and angiography suite with a pivoting table. Cardiovasc Intervent Radiol. 1999;22:124.
23. Feliciano DV, Burch JM. Towel clips, silos, and heroic forms of wound closure. In: Maull KI, Cleveland HC, Feliciano DV, et al., eds. Advances in Trauma and Critical Care. Vol. 6. Chicago: Year Book; 1991:231.
24. Burch JM, Moore EE, Moore FA, et al. The abdominal compartment syndrome. Surg Clin North Am. 1996;76:88.
25. Saggi BH, Sugerman HJ, Ivatury RR, et al. Abdominal compartment syndrome. J Trauma. 1998;45:597.
26. Ertel W, Oberholzer A, Platz A, et al. Incidence and clinical pattern of the abdominal compartment syndrome after “damage-control” laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med. 2000;28:1747.
27. Offner PJ, de Souza AL, Moore EE, et al. Avoidance of abdominal compartment syndrome in damage-control laparotomy after trauma. Arch Surg. 2001;136:676.
28. Biffl WL, Moore EE, Burch JM, et al. Secondary abdominal compartment syndrome is a highly lethal event. Am J Surg. 2001;182:645.
29. Raeburn CD, Moore EE, Biffl WL, et al. The abdominal compartment syndrome is a morbid complication of postinjury damage control surgery. Am J Surg. 2001;182:542.
30. Maxwell RA, Fabian TC, Croce MA, et al. Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock. J Trauma. 1999;47:995.
31. Kopelman T, Harris C, Miller R, et al. Abdominal compartment syndrome in patients with isolated extraperitoneal injuries. J Trauma. 2000;49:744.
32. Mayberry JC, Goldman RK, Mullins RJ, et al. Surveyed opinion of American trauma surgeons on the prevention of the abdominal compartment syndrome. J Trauma. 1999;47:509.
33. Ivy ME, Atweh NA, Palmer J, et al. Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma. 2000; 49:387.
34. Dayton MT, Buchele BA, Shirazi SS, et al. Use of an absorbable mesh to repair contaminated abdominal wall defects. Arch Surg. 1986;121:954.
35. Mayberry JC, Mullins RJ, Crass RA, Trunkey DD. Prevention of abdominal compartment syndrome by absorbable mesh prosthesis closure. Arch Surg. 1997;132:957.
36. Saxe JM, Ledgerwood AM, Lucas CE. Management of the difficult abdominal closure. Surg Clin North Am. 1993;73:243.
37. Lyle WG, Gibbs M, Howdieshell TR. The tensor fascia lata free flap in staged abdominal wall reconstruction after traumatic evisceration. J Trauma. 1999;46:519.
38. Barker DE, Kaufman HJ, Smith LA, et al. Vacuum pack technique of temporary abdominal closure: a 7-year experience with 112 patients. J Trauma. 2000;48:201.
39. Garner GB, Ware DN, Cocanour CS, et al. Vacuum-assisted wound closure provides early fascial reapproximation in trauma patients with open abdomens. Am J Surg. 2001;182:630.
40. Tremblay LN, Feliciano DV, Schmidt J, et al. Skin only or silo closure in the critically ill patient with an open abdomen. Am J Surg. 2001; 182:670.
41. Paran H, Mayo A, Afanasiev A, et al. Staged primary closure of the abdominal wall in patients with abdominal compartment syndrome. J Trauma. 2001;51:1204.
42. Koniaris LG, Hendrickson RJ, Drugas G, et al. Dynamic retention. A technique for closure of the complex abdomen in critically ill patients. Arch Surg. 2001;136:1359.
43. Howdieshell TR, Yeh KA, Hawkins ML, et al. Temporary abdominal wall closure in trauma patients: indications, technique, and results. World J Surg. 1995;19:154.
44. Ramirez OM, Ruas E, Dellon AL. “Components separation” method for closure of abdominal-wall defects: an anatomic and clinical study. Plast Reconstr Surg. 1990;86:519.
45. Fabian TC, Croce MA, Pritchard E, et al. Planned ventral hernia. Staged management for acute abdominal wall defects. Ann Surg. 1994;219:643.
46. Sleeman D, Sosa JL, Gonzalez A, et al. Reclosure of the open abdomen. J Am Coll Surg. 1995;180:200.
47. Livingston DH, Sharma PK, Glantz AI. Tissue expanders for abdominal wall reconstruction following severe trauma: technical note and case reports. J Trauma. 1992;32:82.
48. Gentilello LM. Temperature-associated injuries and syndromes. In: Mattox KL, Feliciano DV, Moore EE, eds. Trauma. 4th ed. New York: McGraw-Hill; 2000:1153–1162.
49. Tremblay LN, Feliciano DV, Rozycki GS. Assessment of initial base deficit as a predictor of outcome: mechanism of injury does make a difference. Am Surg. 2002;68:689.
50. Ferrara A, MacArthur JD, Wright HK, et al. Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion. Am J Surg. 1990;160:515.
51. Krishna G, Sleigh JW, Rahman H. Physiological predictors of death in exsanguinating trauma patients undergoing conventional trauma surgery. Aust N Z J Surg. 1998;68:826.
52. Cinat ME, Wallace WC, Nastanski F, et al. Improved survival following massive transfusion in patients who have undergone trauma. Arch Surg. 1999;134:964.
53. Eddy VA, Morris JA Jr, Cullinane DC. Hypothermia, coagulopathy, and acidosis. Surg Clin North Am. 2000;80:845.
54. Asensio JA, McDuffie L, Petrone P, et al. Reliable variables in the exsanguinated patient which indicate damage control and predict outcome. Am J Surg. 2001;182:743.
55. Ku J, Brasel KJ, Baker CC, Rutherford EJ. Triangle of death: hypothermia, acidosis, and coagulopathy. New Horizons. 1999;7:61.
56. Burch JM, Ortiz V, Richardson RJ, et al. Abbreviated laparotomy and planned reoperation for critically injured patients. Ann Surg. 1992; 215:476.
57. Morris JA Jr, Eddy VA, Binman TA, et al. The staged celiotomy for trauma. Issues in unpacking and reconstruction. Ann Surg. 1993; 217:576.
58. Moore EE. Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg. 1996;172:415.
59. Phillips TF, Soulier G, Wilson RF. Outcome of massive transfusion exceeding two blood volumes in trauma and emergency surgery. J Trauma. 1987;27:903.
60. Wudel JH, Morris JA Jr, Yates K, et al. Massive transfusion: outcome in blunt trauma patients. J Trauma. 1991;31:1.
61. Kivioja A, Myllynen P, Rokkanen P. Survival after massive transfusions exceeding four blood volumes in patients with blunt injuries. Am Surg. 1991;57:398.
62. Hakala P, Lindahl J, Alberty A, et al. Massive transfusion exceeding 150 U of packed red cells during the first 15 hours after injury. J Trauma. 1998;44:410.
63. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma. 2007;63:805–813.
64. Jurkovich GJ, Greiser WB, Luterman A, et al. Hypothermia in trauma victims: an ominous predictor of survival. J Trauma. 1987;27:1019.
65. Gregory JS, Francbaum L, Townsend MC, et al. Incidence and timing of hypothermia in trauma patients undergoing operations. J Trauma. 1991; 31:795.
66. Chaudry CH. Cellular mechanisms in shock and ischemia and their correction. Am J Physiol. 1983;245:R117.
67. Weg JG. Oxygen transport in adult respiratory distress syndrome and other acute circulatory problems: relationship of oxygen delivery and oxygen consumption. Crit Care Med. 1991;19:650.
68. Durham CM, Siegel JH, Weireter LJ, et al. Oxygen debt and metabolic academia as quantitative predictors of mortality and the severity of the ischemic insult in hemorrhagic shock. Crit Care Med. 1999;19:231.
69. Steinemann S, Shackford SR, Davis JW. Implications of admission hypothermia in trauma patients. J Trauma. 1990;30:200.
70. Cushman JG, Feliciano DV, Renz BM, et al. Iliac vascular injury: operative physiology related to outcome. J Trauma. 1997;42:1033.
71. King RC, Kron IL, Kanithanon RC, et al. Hypothermic circulatory arrest does not increase the risk of ascending thoracic aortic aneurysm resection. Ann Surg. 1998;227:702.
72. Clifton GL, Allen S, Barrodale P, et al. A phase II study of moderate hypothermia in severe brain injury. J Neurotrauma. 1993;10:263.
73. Rutherford EJ, Fusco MA, Nunn CR, et al. Hypothermia in critically ill trauma patients. Injury. 1998;29:605.
74. Yudkin J, Cohen RD, Slack B. The haemodynamic effects of metabolic acidosis in the rat. Clin Sci. 1976;50:177.
75. Brasel KJ, Ku J, Baker CC, Rutherford EJ. Damage control in the critically ill and injured patient. New Horizons. 1999;7:73.
76. Davis JW, Kaups KL. Base deficit in the elderly: a marker of severe injury and death. J Trauma. 1998;45:873.
77. Davies AO. Rapid desensitization and uncoupling of human beta-adrenergic receptors in an in vitro model of lactic acidosis. J Clin Endocrinol Metab. 1984;59:398.
78. Abramson D, Scalea TM, Hitchcock R, et al. Lactate clearance and survival following injury. J Trauma. 1993;35:584.
79. Kauvar DS, Lefering R, Wade CE. Impact of hemorrhage on trauma outcome: an overview of epidemiology, clinical presentations, and therapeutic considerations. J Trauma. 2006;60:S3–S11.
80. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg. 2008;248:447–458.
81. Reed RL, Johnston TD, Hudson JD, Fischer RP. The disparity between hypothermic coagulopathy and clotting studies. J Trauma. 1992; 33:465.
82. Watts DD, Trask A, Soeken K, et al. Hypothermic coagulopathy in trauma: effect of varying levels of hypothermia on enzyme speed, platelet function, and fibrinolytic activity. J Trauma. 1998;44:846.
83. Cosgriff N, Moore EE, Sauaia A, et al. Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidoses revisited. J Trauma. 1997;42:857.
84. Cotton BA, Au BK, Nunez TC, et al. Predefined massive transfusion protocols are associated with a reduction in organ failure and postinjury complications. J Trauma. 2009;66:41–49.
85. Sperry JL, Ochoa JB, Gunn SR, et al. An FFP:PRBC transfusion ratio >1:1.5 is associated with a lower risk of mortality after massive transfusion. J Trauma. 2008;65:987–993.
86. Dente CJ, Shaz BH, Nicholas JM, et al. Early predictors of massive transfusion in patients sustaining torso gunshot wounds in a civilian level I trauma center. J Trauma. 2010;68:298–304.
87. Gunter OL Jr, Au BK, Isbell JM, et al. Optimizing outcomes in damage control resuscitation: identifying blood product ratios associated with improved survival. J Trauma. 2008;65:527–534.
88. Teixeira PGR, Inaba K, Shulman I, et al. Impact of plasma transfusion in massively transfused trauma patients. J Trauma. 2009;66:693–697.
89. Harrison TD, Laskosky D, Jazaeri O, et al. “Low-dose” recombinant activated factor VII results in less blood and blood product use in traumatic hemorrhage. J Trauma. 2005;59:150–154.
90. Martinowitz U, Kenet G, Segal E, et al. Recombinant activated factor VII for adjunctive hemorrhage control in trauma. J Trauma. 2001;51: 431–439.
91. Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel, randomized, placebo-controlled, double-blind clinical trials. J Trauma. 2005;59:8–18.
92. Spinella PC, Perkins JG, McLaughlin DF, et al. The effect of recombinant activated factor VII on mortality in combat-related casualties with severe trauma and massive transfusion. J Trauma. 2008;64:286–294.
93. Hauser CJ, Boffard K, Dutton R, et al. Results of the CONTROL trial: efficacy and safety of recombinant activated factor VII in the management of refractory traumatic hemorrhage. J Trauma. 2010;69:489–500.
94. Feliciano DV, Mattox KL. Indications, technique, and pitfalls of emergency center thoracotomy. Surg Rounds. 1981;4:32.
95. Wall MJ Jr, Hirshberg A, Mattox KL. Pulmonary tractotomy with selective vascular ligation for penetrating injuries to the lung. Am J Surg. 1994;168:655.
96. Asensio JA, Demetriades D, Berne JD, et al. Stapled pulmonary tractotomy: a rapid way to control hemorrhage in penetrating pulmonary injuries. J Am Coll Surg. 1997;185:486.
97. Wall MJ Jr, Villavicencio RT, Miller CC, et al. Pulmonary tractotomy as an abbreviated thoracotomy technique. J Trauma. 1998;45:1015.
98. Macho JR, Markison RE, Schecter WP. Cardiac stapling in the management of penetrating injuries of the heart: rapid control of hemorrhage and decreased risk of personal contamination. J Trauma. 1993;34:711.
99. Bowman MR, King RM. Comparison of staples and sutures for cardiorrhaphy in traumatic puncture wounds of the heart. J Emerg Med. 1996;14:615.
100. Feliciano DV, Burch JM, Mattox KL, et al. Balloon catheter tamponade in cardiovascular wounds. Am J Surg. 1990;160:583.
101. Ball CG, Wyrzykowski AD, Nicholas JM, et al. A decade’s experience with balloon catheter tamponade for the emergency control of hemorrhage. J Trauma. 2011;70:330–333.
102. Trinkle JK, Toon RS, Franz JL, et al. Affairs of the wounded heart: penetrating cardiac wounds. J Trauma. 1979;19:467.
103. McClelland R, Shires T, Poulos E. Hepatic resection for massive trauma. J Trauma. 1964;4:282.
104. Aronsen KF, Bengmark S, Dahlgren S, et al. Liver resection in the treatment of blunt injuries to the liver. Surgery. 1968;63:236.
105. Foster JH, Lawler MR Jr, Welborn MB Jr, et al. Recent experience with major hepatic resection. Ann Surg. 1968;167:651.
106. Payne WD, Terz JJ, Lawrence W Jr. Major hepatic resection for trauma. Ann Surg. 1969;170:929.
107. Donovan AJ, Michaelian MJ, Yellin AE. Anatomical hepatic lobectomy in trauma to the liver. Surgery. 1973;73:833.
108. Lim RD Jr, Giuliano AE, Trunkey DD. Postoperative treatment of patients after liver resection for trauma. Arch Surg. 1977;112:429.
109. Feliciano DV, Pachter HL. Hepatic trauma revisited. Curr Probl Surg. 1989;26:453.
110. Pachter HL, Spencer FC, Hofstetter SR, et al. Significant trends in the treatment of hepatic trauma. Experience with 411 injuries. Ann Surg. 1992;215:492.
111. Pachter HL, Feliciano DV. Complex hepatic injuries. Surg Clin North Am. 1996;76:763.
112. Poggetti RS, Moore EE, Moore FA, et al. Balloon tamponade for bilobar transfixing hepatic gunshot wounds. J Trauma. 1992;33:694.
113. Thomas SV, Dulchavsky SA, Diebel LN. Balloon tamponade for liver injuries: case report. J Trauma. 1993;34:448.
114. Stevens SL, Maull KI, Enderson BL, et al. Total mesh wrapping for parenchymal liver injuries—a combined experimental and clinical study. J Trauma. 1991;31:1103.
115. Jacobson LE, Kirton OC, Gomez GA. The use of an absorbable mesh wrap in the management of major liver injuries. Surgery. 1992;111:455.
116. Feliciano DV, Mattox KL, Burch JM, et al. Packing for control of hepatic hemorrhage. J Trauma. 1986;26:738.
117. Saifi J, Fortune JB, Graca L, et al. Benefits of intra-abdominal pack placement for the management of nonmechanical hemorrhage. Arch Surg. 1990;125:119.
118. Sharp KW, Locicero RJ. Abdominal packing for surgically uncontrollable hemorrhage. Ann Surg. 1992;215:467.
119. Horwitz JR, Black T, Lally KP, et al. Venovenous bypass as an adjunct for the management of a retrohepatic venous injury in a child. J Trauma. 1995;39:584.
120. Baumgartner F, Scudamore C, Nair C, et al. Venovenous bypass for major hepatic and caval trauma. J Trauma. 1995;39:671.
121. Rogers FB, Reese J, Shackford SR, et al. The use of venovenous bypass and total vascular isolation of the liver in the surgical management of juxtahepatic venous injuries in blunt hepatic trauma. J Trauma. 1997; 43:530.
122. Denton JR, Moore EE, Coldwell DM. Multimodality treatment for grade V hepatic injuries: perihepatic packing, arterial embolization, and venous stenting. J Trauma. 1997;42:964.
123. Biffl WL, Moore EE, Franciose RJ. Venovenous bypass and hepatic vascular isolation as adjuncts in the repair of destructive wounds to the retrohepatic inferior vena cava. J Trauma. 1998;45:410.
124. Asensio JA, Roldan G, Petrone P, et al. Operative management and outcomes in 103 complex hepatic injuries AAST-OIS grades IV and V trauma. Surgeons still need to operate, but angioembolization helps. J Trauma. 2003;54:647–653.
125. Moore EE, Cogbill TH, Jurkovich GJ, et al. Organ injury scaling: spleen and liver [1994 revision]. J Trauma. 1995;38:323.
126. Feliciano DV, Spjut-Patrinely V, Burch JM, et al. Splenorrhaphy. The alternative. Ann Surg. 1990;211:569.
127. Martin TD, Feliciano DV, Mattox KL, et al. Severe duodenal injuries. Treatment with pyloric exclusion and gastrojejunostomy. Arch Surg. 1983;118:631.
128. Feliciano DV, Martin TD, Cruse PA, et al. Management of combined pancreatoduodenal injuries. Ann Surg. 1987;205:673.
129. Carrillo C, Folger RJ, Shaftan GW. Delayed gastrointestinal reconstruction following massive abdominal trauma. J Trauma. 1993; 34:233.
130. Reilly PM, Rotondo MF, Carpenter JP, et al. Temporary vascular continuity during damage control: intraluminal shunting for proximal superior mesenteric artery injury. J Trauma. 1995;39:757.
131. Sheldon GF, Winestock DP. Hemorrhage from open pelvic fracture controlled intraoperatively with balloon catheter. J Trauma. 1978; 18:68.
132. Saueracker AJ, McCroskey BL, Moore EE, et al. Intraoperative hypogastric artery embolization for life-threatening pelvic hemorrhage: a preliminary report. J Trauma. 1987;27:1127.
133. Burch JM, Feliciano DV, Mattox KL, et al. Injuries of the inferior vena cava. Am J Surg. 1988;156:548.
134. Pachter HL, Drager S, Godfrey N, et al. Traumatic injuries of the portal vein. The role of acute ligation. Ann Surg. 1979;189:383.
135. Stone HH, Fabian TC, Turkleson ML. Wounds of the portal venous system. World J Surg. 1982;6:335.
136. Donahue TK, Strauch GO. Ligation as definitive management of injury to the superior mesenteric vein. J Trauma. 1988;28:541.
137. Feliciano DV, Burch JM, Graham JM. Abdominal vascular injury. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. Stamford, CT: Appleton & Lange; 1996:615.
138. Stone HH, Strom PR, Mullins RJ. Management of the major coagulopathy with onset during laparotomy. Ann Surg. 1983;197:532.
139. Rumley TO. Improved packing technique in the control of diffuse hemorrhage of the abdomen. Surg Gynecol Obstet. 1983;156:82.
140. Talbert S, Trooskin SZ, Scalea T, et al. Packing and re-exploration for patients with nonhepatic injuries. J Trauma. 1992;33:121.
141. Feliciano DV. Evaluation and treatment of vascular injuries. In: Browner BD, Jupiter JB, Levine AM, Trafton PG, Krettek C, eds. Skeletal Trauma. Basic science, management, and reconstruction. Philadelphia: Saunders; 2009:323.
142. Ball CG, Kirkpatrick AW, Rajani RR, et al. Temporary intravascular shunts: when are we really using them according to the NTDB? Am Surg. 2009;75:605–607.
143. Mullins RJ, Lucas CE, Ledgerwood AM. The natural history following venous ligation for civilian injuries. J Trauma. 1980;20:737.
144. Timberlake GA, O’Connell RC, Kerstein MD. Venous injury: to repair or ligate, the dilemma. J Vasc Surg. 1986;4:553.
145. Feliciano DV, Herskowitz K, O’Gorman RB, et al. Management of vascular injuries in the lower extremities. J Trauma. 1988;28:319.
146. Accola KD, Feliciano DV, Mattox KL, et al. Management of injuries to the superior mesenteric artery. J Trauma. 1986;26:313.
147. Trunkey DD, Illner H, Wagner IY, et al. The effect of hemorrhagic shock on intracellular muscle action potentials in the primate. Surgery. 1973;74:241.
148. Bock JC, Barker BC, Clinton AG, et al. Post-traumatic changes in, and effect of colloid osmotic pressure on the distribution of body water. Ann Surg. 1989;210:395.
149. Doty DB, Hufnagel HV, Moseley RV. The distribution of body fluids following hemorrhage and resuscitation in combat casualties. Surg Gynecol Obstet. 1970;130:453.
150. McCord JM. Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med. 1985;321:159.
151. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. I. Definitions. Intensive Care Med. 2006;32:1722.
152. Ball CG, Kirkpatrick AW. Intra-abdominal hypertension and the abdominal compartment syndrome. Scand J Surg. 2004;99:197.
153. Kirkpatrick AW, Balogh Z, Ball CG, et al. The secondary abdominal compartment syndrome: iatrogenic or unavoidable? J Am Coll Surg. 2006;202:668.
154. Emerson H. Intra-abdominal pressures. Arch Intern Med. 1911;7:754.
155. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration. Ann Surg. 1984;199:28.
156. Iberti TJ, Kelly KM, Gentili DR, et al. A simple technique to accurately determine intra-abdominal pressure. Crit Care Med. 1987;15:1141.
157. Sugrue M, Buist MD, Lee A, et al. Intra-abdominal pressure measurement using a modified nasogastric tube: description and validation of a new technique. Intensive Care Med. 1994;20:588.
158. Lacey SR, Bruce J, Brooks SP, et al. The relative merits of various methods of indirect measurement of intra-abdominal pressure as a guide to closure of abdominal wall defects. J Pediatr Surg. 1987; 22:1207.
159. Fusco MA, Martin RS, Chang MC. Estimation of intra-abdominal pressure by bladder pressure measurement: validity and methodology. J Trauma. 2001;50:297–302.
160. Balogh Z, Jones F, D’Amours S, et al. Continuous intra-abdominal pressure measurement techniques. Am J Surg. 2004;188:679–684.
161. Zengerink I, McBeth PB, Zygun DA, et al. Validation and experience with a simple continuous intra-abdominal pressure measurement technique in a multidisciplinary medical/surgical critical care unit. J Trauma. 2008; 64:1159.
162. Mutoh T, Lamm WJ, Embree LJ. Volume infusion produces abdominal distension, lung compression, and chest wall stiffening in pigs. J Appl Physiol. 1992;72:575.
163. Diebel L, Saxe J, Dulchavsky S. Effect of intra-abdominal pressure on abdominal wall blood flow. Am Surg. 1992;58:573.
164. Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intra-abdominal pressure on mesenteric arterial and intestinal mucosal blood flow. J Trauma. 1992;33:45.
165. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. J Trauma. 1997;43:852.
166. Chang MC, Miller PR, D’Agostino R, Meredith JW. Effects of abdominal decompression on cardiopulmonary function and visceral perfusion in patients with intra-abdominal hypertension. J Trauma. 1998;44:441.
167. Ivatury RR, Porter JM, Simon RJ, et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma. 1998;44:1016.
168. Friedlander MH, Simon RJ, Ivatury R, et al. Effect of hemorrhage on superior mesenteric artery flow during increased intra-abdominal pressures. J Trauma. 1998;45:433.
169. Diebel LN, Wilson RF, Dulchavsky SA, et al. Effect of increased intra-abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma. 1992;33:279.
170. Nakatani T, Sakamoto Y, Kaneko I, et al. Effects of intra-abdominal hypertension on hepatic energy metabolism in a rabbit model. J Trauma. 1998;44:446.
171. Shenasky JG, Gillenwater JY. The renal hemodynamic and functional effects of external counterpressure. Surg Gynecol Obstet. 1972; 134:253.
172. Harman PK, Kron IL, McLachlan HD, et al. Elevated intra-abdominal pressure and renal function. Ann Surg. 1982;196:594.
173. Richards WO, Scovill W, Shin B, et al. Acute renal failure associated with increased intra-abdominal pressure. Ann Surg. 1983;197:183.
174. Cullen DJ, Coyle JP, Teplich R, et al. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med. 1989;17:118.
175. Sugrue M, Jones F, Janjua KJ, et al. Temporary abdominal closure: a prospective evaluation of its effects on renal and respiratory physiology. J Trauma. 1998;45:914.
176. Bloomfield GL, Blocher CR, Fakhry IF, et al. Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels. J Trauma. 1997;42:997.
177. Doty JM, Saggi BH, Blocher CR, et al. Effects of increased renal parenchymal pressure on renal function. J Trauma. 2000;48:874.
178. Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion. J Trauma. 1995;39:1071.
179. Obeid F, Saba A, Fath J, et al. Increases in intra-abdominal pressure affect pulmonary compliance. Arch Surg. 1995;130:544.
180. Simon RJ, Friedlander MH, Ivatury RR, et al. Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma. 1997;42:398.
181. Richardson JD, Trinkle JK. Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res. 1976;20:411.
182. Diamant M, Benumof JL, Saidman LJ. Hemodynamics of increased intra-abdominal pressure: interaction with hypovolemia and halothane anesthesia. Anesthesiology. 1978;48:23.
183. Kashtan J, Green JF, Parsons EQ, et al. Hemodynamic effect of increased abdominal pressure. J Surg Res. 1981;30:249.
184. Barnes GE, Laine GA, Giam PY, et al. Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol. 1985; 248:208.
185. Robotham JL, Wise RA, Bromberger-Barnea B. Effects of changes in abdominal pressure on left ventricular performance and regional blood flow. Crit Care Med. 1985;13:803.
186. Bloomfield GL, Dalton JM, Sugerman HJ, et al. Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma. 1995;39:1168.
187. Bloomfield GL, Ridings PC, Blocher CR, et al. Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion. J Trauma. 1996;41:936.
188. Bloomfield GL, Ridings PC, Blocher CR, et al. A proposed relationship between increased intra-abdominal, intrathoracic, and intracranial pressure. Crit Care Med. 1997;25:496.
189. Saggi BH, Sugerman HJ, Bloomfield GL, et al. Nonsurgical abdominal decompression reverses intracranial hypertension in a model of acute abdominal compartment syndrome. Surg Forum. 1997;48:544.
190. Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997;174:667.
191. Cheatham ML, White MW, Sagraves SG, et al. Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49:621.
192. Tremblay LN, Feliciano DV, Rozycki GS. Secondary extremity compartment syndrome. J Trauma. 2001;53:833–837.
193. Corcos AC, Sherman HF. Percutaneous treatment of secondary abdominal compartment syndrome. J Trauma. 2001;51:1062.
194. Chen RJ, Fang JF, Lin BC, et al. Laparoscopic decompression of abdominal compartment syndrome after blunt hepatic trauma. Surg Endosc. 2000;14:966.
195. Bloomfield G, Saggi B, Blocher C, et al. Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension. J Trauma. 1999;46:1009.
196. Fernandez L, Norwood S, Roettger R, Wilkins HE III. Temporary intravenous bag silo closure in severe abdominal trauma. J Trauma. 1996;41:258.
197. DiGiacomo JC, Kustrup JF Jr. Alternatives in temporary abdominal closures. Arch Surg. 1994;129:884.
198. Rowlands BJ, Flynn TC, Fischer RP. Temporary abdominal wound closure with a silastic “chimney.” Contemp Surg. 1984;24:17.
199. Schuster SR. A new method for the staged repair of large omphaloceles. Surg Gynecol Obstet. 1967;125:837.
200. Sherck J, Seiver A, Shatney C, et al. Covering the “open abdomen”: a better technique. Am Surg. 1998;64:854.
201. Leguit P Jr. Zip-closure of the abdomen. Neth J Surg. 1982;34:41.
202. Saxena V, Hwang CW, Huang S, et al. Vacuum-assisted closure: microdeformations of wounds and cell proliferation. Plast Reconstr Surg. 2004;114:1086–1096.
203. McNulty AK, Schmidt M, Feeley BS, Kieswetter K. Effects of negative pressure wound therapy on fibroblast viability, chemotactic signaling, and proliferation in a provisional wound (fibrin) matrix. Wound Repair Regen. 2007;15:838–846.
204. Bender JS, Bailey CE, Saxe JM, et al. The technique of visceral packing: recommended management of difficult fascial closure in trauma patients. J Trauma. 1994;36:182.
205. Gentilello LM, Cobean RA, Offner PJ, et al. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. J Trauma. 1992;32:316.
206. Tisherman SA, Barie P, Bokhari F, et al. Clinical practice guideline: endpoints of resuscitation. J Trauma. 2004;57:898–912.
207. Crookes BA, Cohn SM, Bloch S, et al. Can near-infrared spectroscopy identify the severity of shock in trauma patients? J Trauma. 2005;58: 806–816.
208. Moore FA, Haenel JB, Moore EE, et al. Incommensurate oxygen consumption in response to maximal oxygen availability predicts post-injury multiple organ failure. J Trauma. 1992;33:58.
209. Durham RM, Neunaber K, Mazuski JE, et al. The use of oxygen consumption and delivery as endpoints for resuscitation in critically ill patients. J Trauma. 1996;41:32.
210. Hirshberg A, Wall MJ Jr, Mattox KL. Planned reoperation for trauma: a two year experience with 124 consecutive patients. J Trauma. 1994;37:365.
211. Morris JA Jr, Eddy VA, Rutherford EJ. The trauma celiotomy: the evolving concepts of damage control. Curr Probl Surg. 1996;33:611.
212. Botha AJ, Moore FA, Moore EE, et al. Postinjury neutrophil priming and activation: a vulnerable window. Surgery. 1995;118:358.
213. Botha AJ, Moore FA, Moore EE, et al. Early neutrophil sequestration after injury: a pathogenic mechanism for multiple organ failure. J Trauma. 1995;39:411.
214. Partrick DA, Moore FA, Moore EE. Neutrophil priming and activation in the pathogenesis of postinjury multiple organ failure. New Horizons. 1996;4:194.
215. Waydhas C, Nast-Kolb D, Trupka A, et al. Posttraumatic inflammatory response, secondary operations, and late multiple organ failure. J Trauma. 1996;41:624.
216. Adams JM, Hauser CJ, Livingston DH, et al. The immunomodulatory effects of damage control abdominal packing on local and systemic neutrophil activity. J Trauma. 2001;41:792.
217. Cothren CC, Moore EE, Johnson JL, et al. One hundred percent fascial approximation with sequential abdominal closure of the abdomen. Am J Surg. 2006;192:238–242.
218. Stone PA, Hass SM, Flaherty SK, DeLuca JA, et al. Vacuum-assisted fascial closure for patients with abdominal trauma. J Trauma. 2004; 57:1082–1086.
219. Miller PR, Meredith JW, Johnson JC, et al. Prospective evaluation of vacuum-assisted fascial closure after open abdomen. Ann Surg. 2004;239:608–616.
220. Stone HH, Strom PR, Mullins RJ. Pancreatic abscess management by subtotal resection and packing. World J Surg. 1984;8:341.
221. Teichmann W, Wittmann DH, Andreone PA. Scheduled reoperations (etappenlavage) for diffuse peritonitis. Arch Surg. 1986;121:147.
222. Wittmann DH, Aprahamian C, Bergstein JM. Etappenlavage: advanced diffuse peritonitis managed by planned multiple laparotomies utilizing zippers, slide fastener, and Velcro analogue for temporary abdominal closure. World J Surg. 1990;14:218.
223. Aprahamian C, Wittmann DH, Bergstein JM, et al. Temporary abdominal closure (TAC) for planned relaparotomy (etappenlavage) in trauma. J Trauma. 1990;30:719.
224. Tieu BH, Cho SD, Leum N, et al. The use of the Wittmann patch facilitates a high rate of fascial closure in severely injured trauma patients and critically ill emergency surgery patients. J Trauma. 2008;65:865–879.
225. Weinberg JA, George RL, Griffin RL, et al. Closing the open abdomen: improved success with Wittmann patch staged abdominal closure. J Trauma. 2008;65:345–348.
226. Fantus RJ, Mellett MM, Kirby JP. Use of controlled fascial tension and an adhesion preventing barrier to achieve delayed primary fascial closure in patients managed with an open abdomen. Am J Surg. 2006;192:243–247.
227. Gilsdorf RB, Shea MM. Repair of massive septic abdominal wall defects with Marlex mesh. Am J Surg. 1975;130:634.
228. Stone HH, Fabian TC, Turkleson ML, et al. Management of acute full thickness losses of the abdominal wall. Ann Surg. 1981;193:612.
229. Voyles CR, Richardson JD, Bland KI, et al. Emergency abdominal wall reconstruction with polypropylene mesh: short-term benefits versus long-term complications. Ann Surg. 1981;194:219.
230. Wouters DB, Krom RA, Slooff MJ, et al. The use of Marlex mesh in patients with generalized peritonitis and multiple organ system failure. Surg Gynecol Obstet. 1983;156:609.
231. Usher FC, Ochsner J, Tuttle LLD. Use of Marlex mesh in the repair of incisional hernias. Am J Surg. 1958;24:969.
232. Jones JW, Jurkovich GJ. Polypropylene mesh closure of infected abdominal wounds. Am J Surg. 1989;55:73.
233. Lamb JP, Vitale T, Kaminski DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery. 1983;93:643.
234. Jenkins SD, Klamer TW, Parteka JJ. A comparison of prosthetic materials used to repair abdominal wall defects. Surgery. 1983;94:392.
235. Tyrell J, Silberman H, Chandrasoma P, et al. Absorbable versus permanent mesh in abdominal operations. Surg Gynecol Obstet. 1989;168:227.
236. Smith PC, Tweddell JS, Bessey PQ. Alternative approaches to abdominal wound closure in severely injured patients with massive visceral edema. J Trauma. 1992;32:16.
237. Gupta A, Zahriya K, Mullens PL, et al. Ventral herniorrhaphy: experience with two different biosynthetic mesh materials, Surgisis and Alloderm. Hernia. 2006;10:419–425.
238. Buinewicz B, Rosen B. Acellular cadaveric dermis (Alloderm): a new alternative for abdominal hernia repair. Ann Plast Surg. 2004;52: 188–194.
239. Kolker AR, Brown DJ, Redstone JS, et al. Multilayer reconstruction of abdominal wall defects with acellular dermal allograft (Alloderm) and component separation. Ann Plast Surg. 2005;55:36–42.