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Intracranial Injuries
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CT scanning, performed on all patients with a significant closed head injury (GCS score <14), identifies and quantitates intracranial lesions. Patients with intracranial hemorrhage, including epidural hematoma, subdural hematoma, subarachnoid hemorrhage, intracerebral hematoma or contusion, and diffuse axonal injury, are admitted to the SICU. In patients with abnormal findings on CT scans and GCS scores of ≤8, intracranial pressure (ICP) should be monitored using fiber-optic intraparenchymal devices or intraventricular catheters.29 Although an ICP of 10 mm Hg is believed to be the upper limit of normal, therapy generally is not initiated until ICP is >20 mm Hg.29 Indications for operative intervention to remove space-occupying hematomas are based on the clot volume, amount of midline shift, location of the clot, GCS score, and ICP.29 A shift of >5 mm typically is considered an indication for evacuation, but this is not an absolute rule. Smaller hematomas that are in treacherous locations, such as the posterior fossa, may require drainage due to brain stem compression or impending herniation. Removal of small hematomas may also improve ICP and cerebral perfusion in patients with elevated ICP that is refractory to medical therapy. Patients with diffuse cerebral edema resulting in excessive ICP may require a decompressive craniectomy, although a recent AAST multicenter trial questions the benefits.67,68 Patients with open or depressed skull fractures, with or without sinus involvement, may require operative intervention. Penetrating injuries to the head require operative intervention for hemorrhage control, evacuation of blood, skull fracture fixation, or débridement.
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General surgeons in communities without emergency neurosurgical coverage should have a working knowledge of burr hole placement in the event that emergent evacuation is required for a life-threatening epidural hematoma (Fig. 7-51).69 The typical clinical course of an epidural hematoma is an initial loss of consciousness, a lucid interval, and recurrent loss of consciousness with an ipsilateral fixed and dilated pupil. While decompression of subdural hematomas may be delayed, epidural hematomas require evacuation within 70 minutes.68 The final stages of this sequence are caused by blood accumulation that forces the temporal lobe medially, with resultant compression of the third cranial nerve and eventually the brain stem. The burr hole is made on the side of the dilated pupil to decompress the intracranial space. After stabilization, the patient is transferred to a facility with neurosurgical capability for formal craniotomy.
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In addition to operative intervention, postinjury care directed at limiting secondary injury to the brain is critical. The goal of resuscitation and management in patients with head injuries is to avoid hypotension (SBP of <100 mm Hg) and hypoxia (partial pressure of arterial oxygen of <60 or arterial oxygen saturation of <90).29 Attention, therefore, is focused on maintaining cerebral perfusion rather than merely lowering ICP. Resuscitation efforts aim for a euvolemic state and an SBP of >100 mm Hg. Cerebral perfusion pressure (CPP) is equal to the mean arterial pressure minus the ICP, with a target range of >50 mm Hg.29 CPP can be increased by either lowering ICP or raising mean arterial pressure. Sedation, osmotic diuresis, paralysis, ventricular drainage, and barbiturate coma are used in sequence, with coma induction being the last resort. The partial pressure of carbon dioxide (Pco2) should be maintained in a normal range (35–40 mm Hg), but for temporary management of acute intracranial hypertension, inducing cerebral vasoconstriction by hyperventilation to a Pco2 of <30 mm Hg is occasionally warranted. Moderate hypothermia (32°–33°C [89.6°–91.4°F]) has been proposed to improve neurologic outcomes when maintained for at least 48 hours, but studies to date have not validated this concept.29,70,71 Patients with intracranial hemorrhage should be monitored for postinjury seizures, and prophylactic anticonvulsant therapy (e.g., phenytoin [dilantin]) is indicated for 7 days after injury. 29,72
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Maxillofacial Injuries
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Maxillofacial injuries are common with multisystem trauma and require coordinated management by the trauma surgeon and the specialists in otolaryngology, plastic surgery, ophthalmology, and oral and maxillofacial surgery. Delay in addressing these systems that control vision, hearing, smelling, breathing, eating, and phonation may produce dysfunction and disfigurement with serious psychological impact. The maxillofacial complex is divided into three regions; the upper face containing the frontal sinus and brain, the midface containing the orbits, nose, and zygomaticomaxillary complex, and the lower face containing the mandible. High-impact kinetic energy is required to fracture the frontal sinus, orbital rims, and mandible, whereas low-impact forces will injure the nasal bones and zygoma.
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The most common scenario, which at times may be life-threatening, is bleeding from facial fractures.73 Temporizing measures include nasal packing, Foley catheter tamponade of posterior nasal bleeding, and oropharyngeal packing. Prompt angioembolization will halt exsanguinating hemorrhage. Fractures of tooth-bearing bone are considered open fractures and require antibiotic therapy and semiurgent repair to preserve the airway as well as the functional integrity of the occlusion (bite) and the aesthetics of the face. Orbital fractures may compromise vision, produce muscle injury causing diplopia, or change orbital volume to produce a sunken appearance to the orbit. Nose and nasoethmoidal fractures should be assessed carefully to identify damage to the lacrimal drainage system or to the cribriform plate producing cerebrospinal fluid rhinorrhea. After initial stabilization, a systematic physical examination of the head and neck should be performed that also includes cranial nerve examination and three-dimensional CT scanning of the maxillofacial complex (Fig. 7-52).
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Treatment of injuries to the cervical spine is based on the level of injury, the stability of the spine, the presence of subluxation, the extent of angulation, the level of neurologic deficit, and the overall condition of the patient. In general, physician-supervised axial traction, via cervical tongs or the more commonly used halo vest, is used to reduce subluxations and stabilize the injury. Immobilization of injuries also is achieved with spinal orthoses (braces), particularly in those with associated thoracolumbar injuries. Surgical fusion typically is performed in patients with neurologic deficit, those with angulation of >11 degrees or translation of >3.5 mm, and those who remain unstable after halo placement. Indications for immediate operative intervention are deterioration in neurologic function and fractures or dislocations with incomplete deficit. Historically, methylprednisolone was administered to patients with acute spinal cord injury after blunt injury, with clinical data suggesting a small benefit to initiating a 24-hour infusion if started within 3 hours and a 48-hour infusion if started 3 to 8 hours.74 Current guidelines, however, no longer recommend steroids for acute injuries.75 The role and timing of operative surgical decompression after acute spinal cord injury is debated. However, evidence supports urgent decompression of bilateral locked facets in patients with incomplete tetraplegia or with neurologic deterioration. Urgent decompression in acute cervical spinal cord injury is safe. Performing surgery within 24 hours may decrease length of stay and complications.76 Complete injuries of the spinal cord remain essentially untreatable. Yet, approximately 3% of patients who present with flaccid quadriplegia have concussive injuries, and these patients represent the very few who seem to have miraculous recoveries.
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Cervical vascular injuries due to either blunt or penetrating trauma can result in devastating neurologic sequelae or exsanguination. Penetrating injuries to the carotid artery and internal jugular vein usually are obvious on operative neck exploration. The principles of vascular repair techniques (discussed previously) apply to carotid injuries, and options for repair include end-to-end primary repair (often possible with mobilization of the common carotid), graft interposition, and transposition procedures. All carotid injuries should be repaired except in patients who present in coma with a delay in transport. Prompt revascularization of the internal carotid artery, using a temporary Pruitt-Inahara shunt, should be considered in patients arriving in profound shock. Otherwise, carotid shunting should be done selectively as in elective carotid endarterectomy but the patient should be systemically anticoagulated. Currently, we administer heparin with an ACT target of 250 sec. Tangential wounds of the internal jugular vein should be repaired by lateral venorrhaphy, but extensive wounds are efficiently addressed by ligation. However, it is not advisable to ligate both jugular veins due to potential intracranial hypertension. Vertebral artery injuries due to penetrating trauma are difficult to control operatively because of the artery’s protected location within the foramen transversarium. Although exposure from an anterior approach can be accomplished by removing the anterior elements of the bony canal and the tough fascia covering the artery between the elements, typically the most efficacious control of such injuries is angioembolization. Fogarty catheter balloon occlusion, however, is useful for controlling acute bleeding if encountered during neck exploration.
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Blunt injury to the carotid or vertebral arteries may cause dissection, thrombosis, or pseudoaneurysm, typically in the surgically inaccessible distal internal carotid (Fig. 7-53).77 Early recognition and management of these injuries is paramount, because patients treated with antithrombotics have a stroke rate of <1% compared with stroke rates of 20% in untreated patients. Because treatment must be instituted during the latent period between injury and onset of neurologic sequelae, diagnostic imaging is performed based on identified risk factors (Fig. 7-54).78 After identification of an injury, antithrombotics are administered if the patient does not have contraindications (intracranial hemorrhage, falling hemoglobin level with solid organ injury or pelvic fracture). Heparin, started without a loading dose at 15 units/kg per hour, is titrated to achieve a PTT between 40 and 50 seconds or antiplatelet agents are initiated (aspirin 325 mg/d or clopidogrel 75 mg/d). The types of antithrombotic treatment appear equivalent in published studies to date, and the duration of treatment is empirically recommended to be 6 months.79,80 The role of carotid stenting for grade III internal carotid artery injuries remain controversial. Thrombosis of the internal jugular veins caused by blunt trauma can occur unilaterally or bilaterally and is often discovered incidentally, because most patients are asymptomatic. Bilateral thrombosis can aggravate cerebral edema in patients with serious head injuries; stent placement should be considered in such patients if ICP remains elevated.
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Subclinical fractures of the larynx and trachea may manifest as cervical emphysema. Fractures documented by CT scan are usually repaired. Common injuries include thyroid cartilage fractures, rupture of the thyroepiglottic ligament, disruption of the arytenoids or vocal cord tears, and cricoid fractures. After débridement of devitalized tissue, tracheal injuries are repaired end-to-end using a single layer of interrupted absorbable sutures. Associated injuries of the esophagus are common in penetrating injuries due to its close proximity. After débridement and repair, vascularized tissue is interposed between the repaired esophagus and trachea, and a closed suction drain is placed. The sternocleidomastoid muscle or strap muscles are useful for interposition and help prevent postoperative fistulas.
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The most common injuries from both blunt and penetrating thoracic trauma are hemothorax and pneumothorax. More than 85% of patients can be definitively treated with a chest tube. The indications for thoracotomy include significant initial or ongoing hemorrhage from the tube thoracostomy and specific imaging-identified diagnoses (Table 7-10). One caveat concerns the patient who presents after a delay. Even when the initial chest tube output is 1.5 L, if the output ceases and the lung is re-expanded, the patient may be managed nonoperatively if hemodynamically stable.
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Over 90% of thoracic great vessel injuries are due to penetrating trauma, although blunt injury to the innominate, subclavian, or descending aorta may cause a pseudoaneurysm or frank rupture.40,81,82 Simple lacerations of the ascending or transverse aortic arch can be repaired with lateral aortorrhaphy. Repair of posterior injuries, or those requiring interposition grafting of the arch, require full cardiopulmonary bypass, and repair of complex injuries may require circulatory arrest. Innominate artery injuries are repaired using the bypass exclusion technique,82 which avoids the need for cardiopulmonary bypass. Bypass grafting from the proximal aorta to the distal innominate with a prosthetic tube graft is performed before the postinjury hematoma is entered. The PTFE graft is anastomosed end to side from the proximal undamaged aorta and anastomosed end-to-end to the innominate artery (Fig. 7-55). The origin of the innominate is then oversewn at its base to exclude the pseudoaneurysm or other injury. Subclavian artery injuries can be repaired using lateral arteriorrhaphy or PTFE graft interposition; due to its multiple branches and tethering of the artery, end-to-end anastomosis is not advocated if there is a significant segmental loss.
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Descending thoracic aortic injuries may require urgent if not emergent intervention. However, operative intervention for intracranial or intra-abdominal hemorrhage or unstable pelvic fractures takes precedence. To prevent aortic rupture, pharmacologic therapy with a selective β1 antagonist, esmolol, should be instituted in the trauma bay, with a target SBP of <100 mm Hg and heart rate of <100/min.36,83 Endovascular stenting is now the mainstay of treatment, but open operative reconstruction is warranted, or necessary, in select patients.84,85 Endovascular techniques are particularly appropriate in patients who cannot tolerate single lung ventilation, patients >60- years-old who are at risk for cardiac decompensation with aortic clamping, or patients with uncontrolled intracranial hypertension. While endograft sizing has improved, the major question is long-term outcome in younger patients. Open repair of the descending aorta is accomplished using partial left heart bypass.86 With the patient in a right lateral decubitus position, the patient’s hips and legs are rotated 45 degrees toward the supine position to gain access to the left groin for common femoral artery cannulation. Using a left posterolateral thoracotomy, the fourth rib is transected to expose the aortic arch and left pulmonary hilum. Partial left heart bypass is performed by cannulating the superior pulmonary vein with return through the left common femoral artery (Fig. 7-56). A centrifugal pump is used to provide flow rates of 2.5 to 4 L/min to maintain a distal perfusion pressure of >65 mm Hg. This prevents ischemic injury of the spinal cord as well as the splanchnic bed, and reduces left ventricular afterload.36 Heparinization is not required, a significant benefit in patients with multiple injuries, particularly in those with intracranial hemorrhage. Unless contraindicated, however, low-dose heparin (100 units/kg) typically is administered to a target ACT of 250 sec to prevent thromboembolic events. Once bypass is initiated, vascular clamps are applied on the aorta between the left common carotid and left subclavian arteries, on the left subclavian, and on the aorta distal to the injury. In most patients a short PTFE graft (usually 18 mm in diameter) is placed using a running 3-0 polypropylene suture. However, primary arterial repair should be done when possible. Air and thrombus are flushed from the aortic graft before the final suture is tied, and the occluding vascular clamps are removed. The patient is then weaned from the centrifugal pump, the cannulas are removed, and primary repair of the cannulated vessels is performed. Removal of air or potential clot in the pulmonary vein is important during decannulation to avoid left heart emboli to the systemic circulation.
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Blunt and penetrating cardiac injuries have widely differing presentations and therefore disparate treatments. Survivable penetrating cardiac injuries consist of wounds that can be repaired operatively; most are stab wounds. Before repair of the injury is attempted, hemorrhage should be controlled; injuries to the atria can be clamped with a Satinsky vascular clamp, whereas digital pressure is used to occlude the majority of ventricular wounds. Foley catheter occlusion of larger stellate lesions may be effective, but even minimal traction may enlarge the original injury. Temporary control of hemorrhage, and at times definitive repair, may be accomplished with skin staples for left ventricular lacerations; the myocardial edges of the laceration must coapt in diastole for stapling to be technically feasible. Definitive repair of cardiac injuries is performed with either running 3-0 polypropylene suture or interrupted, pledgeted 2-0 polypropylene suture (Fig. 7-57).87 Use of pledgets may be particularly important in the right ventricle to prevent sutures from pulling through the thinner myocardium. Injuries adjacent to coronary arteries should be repaired using horizontal mattress sutures, because use of running sutures results in coronary occlusion and distal infarction. Gunshot wounds may result in stellate lesions or contused, extremely friable myocardium adjacent to the wound. When the edges of such complex wounds cannot be fully approximated and hence the repair is not hemostatic, the authors have used surgical adhesive (BioGlue) to achieve hemostasis.88 Occasionally, interior structures of the heart may be damaged. Intraoperative auscultation or postoperative hemodynamic assessment usually identifies such injuries.89 Echocardiography (ECHO) can diagnose the injury and quantitate its effect on cardiac output. Immediate repair of valvular damage or septal defects rarely is necessary and would require cardiopulmonary bypass, but structural intracardiac lesions may progress and, thus, patients must have a follow-up ECHO.
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Patients with blunt cardiac injury typically present with persistent tachycardia or conduction disturbances, but occasionally present with tamponade due to atrial or right ventricular rupture. There are no pathognomonic ECG findings, and cardiac enzyme levels do not correlate with the risk of cardiac complications.23 Therefore, patients for whom there is high clinical suspicion of cardiac contusion and who are hemodynamically stable should be monitored for dysrhythmias for 24 hours by telemetry. Patients with hemodynamic instability should undergo ECHO to evaluate for wall motion abnormalities, pericardial fluid, valvular dysfunction, chordae rupture, or diminished ejection fraction. If such findings are noted or if vasoactive agents are required, cardiac function can be continuously monitored using a pulmonary artery catheter and serial SICU transthoracic or transesophageal ECHO.
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Trachea, Bronchi, and Lung Parenchyma
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Less than 1% of all injured patients sustain intrathoracic tracheobronchial injuries, and only a small number require operative intervention. Although penetrating injuries may occur throughout the tracheobronchial system, blunt injuries most commonly occur within 2.5 cm of the carina. For patients with a massive air leak requiring emergent exploration, initial control of the injury to provide effective ventilation is obtained by passing an endotracheal tube either beyond the injury or into the contralateral mainstem bronchus. Principles of repair are similar to those for repair of cervical tracheal injuries. Devitalized tissue is débrided, and primary end-to-end anastomosis with 3-0 PDS suture is performed. Dissection should be limited to the area of injury to prevent disruption of surrounding bronchial vasculature and ensuing ischemia and stricture. Suture lines should be encircled with vascularized tissue, either pericardium, intercostal muscle, or pleura. Expectant management is employed for bronchial injuries that are less than one-third the circumference of the airway and have no evidence of a persistent major air leak.11,12 In patients with peripheral bronchial injuries, indicated by persistent air leaks from the chest tube and documented by endoscopy, bronchoscopically directed fibrin glue sealing may be useful.
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The majority of pulmonary parenchymal injuries are suspected based upon identification of a pneumothorax; the vast majority is managed by tube thoracostomy. Identified parenchymal injuries encountered during thoracic exploration for a massive hemothorax are managed without resection as much as possible. Peripheral lacerations with persistent bleeding can be managed with stapled wedge resection using a stapler. For central injuries, the current treatment is pulmonary tractotomy, which permits selective ligation of individual bronchioles and bleeders, prevents the development of an intraparenchymal hematoma or air embolism, and reduces the need for formal lobar resection (see Fig. 7-49).90,91 A stapling device, preferably the longest stapler available, is inserted directly into the injury track and positioned along the thinnest section of overlying parenchyma. The injury track is thus filleted open, which allows direct access to the bleeding vessels and leaking bronchi. The majority of injuries are definitively managed with selective ligation, and the defect is left open. Occasionally, tractotomy reveals a more proximal vascular injury that must be treated with formal lobectomy. Injuries severe enough to mandate pneumonectomy usually are fatal because of right heart decompensation.92
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One parenchymal injury that may be discovered during thoracic imaging is a posttraumatic pulmonary pseudocyst, colloquially termed a pneumatocele.93 Traumatic pneumatoceles typically follow a benign clinical course and are treated with aggressive pain management, pulmonary toilet, and serial chest radiography to monitor for resolution of the lesion. If the patient has persistent fever or leukocytosis, however, chest CT is done to evaluate for an evolving abscess, because pneumatoceles may become infected. CT-guided catheter drainage may be required in such cases, because 25% of patients do not respond to antibiotic therapy alone. Surgery, ranging from partial resection to anatomic lobectomy, is indicated for unresolving complex pneumatoceles or infected lesions refractory to antibiotic therapy and drainage.
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The most common complication after thoracic injury is development of an empyema. Management is based on CT diagnostic criteria.94 Percutaneous drainage is indicated for a single loculation without appreciable rind. While fibrinolytics are often used for empyema there is a paucity of data to support their use. Early decortication via video-assisted thoracic surgery should be done promptly in patients with multiple loculations or a pleural rind of >1 cm.95 Antibiotic treatment is based on definitive culture results, but presumptive antibiotics should cover MRSA in the SICU.
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Due to the proximity of the structures, esophageal injuries often occur with tracheobronchial injuries, particularly in cases of penetrating trauma. Operative options are based on the extent and location of esophageal injury. With sufficient mobilization, a primary single-layer end-to-end anastomosis may be performed after appropriate débridement. As with cervical repairs, if there are two suture lines in close approximation (trachea or bronchi and esophagus) interposition of a vascularized pedicle is warranted to prevent fistula formation. Perforations at the gastroesophageal junction may be treated with repair and Nissan fundoplication or, for destructive injuries, segmental resection and gastric pull-up. With large destructive injuries or delayed presentation of injuries, esophageal exclusion with wide drainage, diverting loop esophagostomy, and placement of a gastrostomy tube should be considered.
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Chest Wall and Diaphragm
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Virtually all chest wall injuries, consisting of rib fractures and laceration of intercostal vessels, are treated nonoperatively with pain control, pulmonary toilet or ventilatory management, and drainage of the pleural space as indicated. Early institution of effective pain control is essential. The authors advocate pre-emptive rib blocks with 0.25% bupivacaine hydrochloride (Marcaine) in the trauma bay, followed by thoracic wall pain catheters.96 Epidural anesthesia is reserved for multiple segmental fractures. Persistent hemorrhage from a chest tube after blunt trauma most often is due to injured intercostal arteries; for unusual persistent bleeding (see Table 7-10), thoracotomy with direct ligation or angioembolization may be required to arrest hemorrhage. In cases of extensive flail chest segments or markedly displaced rib fractures, open reduction and internal fixation of the fracture with plates may be warranted. The current role of operative rib fixation remains controversial. Chest wall defects, particularly those seen with open pneumothorax, are repaired using local approximation of tissues or tissue transfer for coverage. Scapular and sternal fractures rarely require operative intervention but are markers for significant thoracoabdominal force during injury; significant displacement may benefit from sternal plating (Fig. 7-58). Careful examination and imaging should exclude associated injuries, including blunt cardiac injury and descending aortic tears. On the other hand, clavicle fractures often are isolated injuries and should be managed with pain control and immobilization. The exception is posterior dislocation of the clavicular head, which may injure the subclavian vessels.
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Blunt diaphragmatic injuries usually result in a linear tear, and most injuries are large, whereas penetrating injuries are variable in size and location depending on the agent of injury. Regardless of the etiology, acute injuries are usually repaired through an abdominal approach to manage potential associated intraperitoneal visceral injury. After delineation of the injury, the chest should be evacuated of all blood and particulate matter, and thoracostomy tube placed if not previously done. Allis clamps are used to approximate the diaphragmatic edges, and the defect is closed with a running No. 1 polypropylene suture. Occasionally, large avulsions or shotgun wounds with extensive tissue loss will require polypropylene or biologic mesh to bridge the defect. Alternatively, transposition of the diaphragm cephalad one to two intercostal spaces may allow repair without undue tension.61
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Liver and Extrahepatic Biliary Tract
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The liver’s large size makes it the organ most susceptible to blunt trauma, and it is frequently involved in upper torso penetrating wounds. Nonoperative management of solid organ injuries is pursued in hemodynamically stable patients who do not have overt peritonitis or other indications for laparotomy. Patients with > grade II injuries should be admitted to the SICU with frequent hemodynamic monitoring, determination of hemoglobin, and abdominal examination. The only absolute contraindication to nonoperative management is hemodynamic instability. Factors such as high injury grade, large hemoperitoneum, contrast extravasation, or pseudoaneurysms may predict complications or failure of nonoperative management. Angioembolization and endoscopic retrograde cholangiopancreatography (ERCP) are useful adjuncts that can improve the success rate of nonoperative management.97,98 The indication for angiography to control hepatic hemorrhage is transfusion of 4 units of RBCs in 6 hours or 6 units of RBCs in 24 hours without hemodynamic instability.
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In the 15% of patients for whom emergent laparotomy is mandated, the primary goal is to arrest hemorrhage. Initial control of hemorrhage is best accomplished using perihepatic packing and manual compression. With extensive injuries and major hemorrhage a Pringle maneuver should be done immediately. Intermittent release of the Pringle is helpful to attenuate hepatic cellular loss. In either case, the edges of the liver laceration should be opposed for local pressure control of bleeding. Hemorrhage from most major hepatic injuries can be controlled with effective perihepatic packing. The right costal margin is elevated, and the pads are strategically placed over and around the bleeding site (see Fig. 7-36). Additional pads should be placed between the liver, diaphragm, and anterior chest wall until the bleeding has been controlled. Sometimes 10 to 15 pads may be required to control the hemorrhage from an extensive right lobar injury. Packing of injuries of the left lobe is not as effective, because there is insufficient abdominal and thoracic wall anterior to the left lobe to provide adequate compression with the abdomen open. Fortunately, hemorrhage from the left lobe usually can be controlled by mobilizing the lobe and compressing it between the surgeon’s hands. If the patient has persistent bleeding despite packing, injuries to the hepatic artery, portal vein, and retrohepatic vasculature should be considered. A Pringle maneuver can help delineate the source of hemorrhage. In fact, hemorrhage from hepatic artery and portal vein injuries will halt with the application of a vascular clamp across the portal triad; whereas, bleeding from the hepatic veins and retrohepatic vena cava will continue.
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Injuries of the portal triad vasculature should be addressed immediately. In general, ligation from the celiac axis to the level of the common hepatic artery at the gastroduodenal arterial branch is tolerated due to the extensive collaterals, but the proper hepatic artery should be repaired. The right or left hepatic artery, or in urgent situations the portal vein, may be selectively ligated; occasionally, lobar necrosis will necessitate delayed anatomic resection. If the right hepatic artery is ligated, cholecystectomy also should be performed. If the vascular injury is a stab wound with clean transection of the vessels, primary end-to-end repair is done. If the injury is destructive, temporary shunting should be performed followed by interposition reversed saphenous vein graft (RSVG). Blunt avulsions of the portal structures are particularly problematic if located at the hepatic plate, flush with the liver; hemorrhage control at the liver can be attempted with directed packing or Fogarty catheters. If the avulsion is more proximal, at the superior border of the pancreatic body or even retropancreatic, the pancreas must be transected to gain access for hemorrhage control and repair.
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If massive venous hemorrhage is seen from behind the liver despite use of the Pringle maneuver, the patient likely has a hepatic vein or retrohepatic vena cava injury. If bleeding can be controlled with perihepatic packing, the packing should be left undisturbed and the patient observed in the SICU. Placement of a hepatic vein stent by interventional radiology may be considered. If bleeding continues despite repeated attempts at packing, then direct repair, with or without hepatic vascular isolation, should be attempted. Three techniques have been used to accomplish hepatic vascular isolation: (a) direct repair with suprahepatic and infrahepatic clamping of the vena cava and stapled assisted parenchymal resection;99 (b) temporary shunting of the retrohepatic vena cava; and (c) venovenous bypass (Fig. 7-59).100
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Numerous methods for the definitive control of hepatic parenchymal hemorrhage have been developed. Minor lacerations may be controlled with manual compression applied directly to the injury site. Topical hemostatic techniques include the use of an electrocautery (with the device set at 100 watts), argon beam coagulator, microcrystalline collagen, thrombin-soaked gelatin foam sponge, fibrin glue, and BioGlue. Suturing of the hepatic parenchyma with a blunt tipped 0 chromic suture (e.g., a “liver suture”) can be an effective hemostatic technique. A running suture is used to approximate the edges of shallow lacerations, whereas deeper lacerations are approximated using interrupted horizontal mattress sutures placed parallel to the edge of the laceration. When the suture is tied, tension is adequate when visible hemorrhage ceases or the liver blanches around the suture. Caution must be used to prevent hepatic necrosis. This technique of placing large liver sutures controls bleeding through reapproximation of the liver laceration rather than direct ligation of bleeding vessels. Aggressive finger fracture to identify bleeding vessels followed by individual clip or suture ligation was advocated previously but currently has a limited role in hemostasis. Hepatic lobar arterial ligation may be appropriate for patients with recalcitrant arterial hemorrhage from deep within the liver and is a reasonable alternative to a deep hepatotomy, particularly in unstable patients. Omentum can be used to fill large defects in the liver. The tongue of omentum not only obliterates potential dead space with viable tissue but also provides an excellent source of macrophages. Additionally, the omentum can provide buttressing support for parenchymal sutures.
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Translumbar penetrating injuries are particularly challenging, because the extent of the injury cannot be fully visualized. As discussed later in “Damage Control Surgery,” options include intraparenchymal tamponade with a Foley catheter or balloon occlusion (see Fig. 7-48).101 If tamponade is successful with either modality, the balloon is left inflated for 24 to 48 hours followed by sequential deflation and removal at a second laparotomy. Hepatotomy with ligation of individual bleeders occasionally may be required; however, division of the overlying viable hepatic tissue may cause considerable blood loss in the coagulopathic patient. Finally, angioembolization is an effective adjunct in any of these scenarios and should be considered early in the course of treatment.
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Several centers have reported patients with devastating hepatic injuries or necrosis of the entire liver who have undergone successful hepatic transplantation.102 Clearly this is dramatic therapy, and the patient must have all other injuries delineated, particularly those of the central nervous system, and have an excellent chance of survival excluding the hepatic injury. Because donor availability will limit such procedures, hepatic transplantation for trauma will continue to be performed only in extraordinary circumstances.
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Cholecystectomy is performed for injuries of the gallbladder and after operative ligation of the right hepatic artery. Injuries of the extrahepatic bile ducts are a challenge due to their small size and thin walls. Because of the proximity of other portal structures and the vena cava, associated vascular injuries are common. These factors may preclude primary repair. Small lacerations with no accompanying loss or devitalization of adjacent tissue can be treated by the insertion of a T tube through the wound or by lateral suturing using 6-0 monofilament absorbable suture. Virtually all transections and any injury associated with significant tissue loss will require a Roux-en-Y choledochojejunostomy.103 The anastomosis is performed using a single-layer interrupted technique with 5-0 monofilament absorbable suture. To reduce anastomotic tension, the jejunum should be sutured to the areolar tissue of the hepatic pedicle or porta hepatis. Injuries of the hepatic ducts are almost impossible to satisfactorily repair under emergent circumstances. One approach is to intubate the duct for external drainage and attempt a repair when the patient recovers or attempt stenting via ERC. Alternatively, the duct can be ligated if the opposite lobe is normal and uninjured.
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Patients undergoing perihepatic packing for extensive liver injuries typically are returned to the OR for pack removal 24 hours after initial injury. Earlier exploration may be indicated in patients with evidence of ongoing hemorrhage. Signs of rebleeding are usually conspicuous, and include a falling hemoglobin, accumulation of blood clots under the temporary abdominal closure device, and bloody output from drains; the magnitude of hemorrhage is reflected in ongoing hemodynamic instability and metabolic monitoring. Postoperative hemorrhage should be re-evaluated in the OR once the patient’s coagulopathy is corrected. Alternatively, angioembolization is appropriate for complex injuries. Patients with hepatic ischemia due to prolonged intraoperative use of the Pringle maneuver have an expected elevation but subsequent resolution of transaminase levels, whereas patients requiring hepatic artery ligation may have frank hepatic necrosis. Although febrile patients should be evaluated for infectious complications, patients with complex hepatic injuries typically have intermittent “liver fever” for the first 5 days after injury.
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Aside from hemorrhage and hepatic necrosis, additional complications after significant hepatic trauma include bilomas, arterial pseudoaneurysms, and biliary fistulas (Fig. 7-60). Bilomas are loculated collections of bile, which may or may not be infected. If infected, they should be treated like an abscess via percutaneous drainage. Although small, sterile bilomas eventually will be reabsorbed, larger fluid collections should be drained. Biliary ascites, due to the disruption of a major bile duct, often requires reoperation and wide drainage. Primary repair of the injured intrahepatic duct is unlikely to be successful. Resectional débridement is indicated for the removal of peripheral portions of nonviable hepatic parenchyma.
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Pseudoaneurysms and biliary fistulas are rare complications in patients with hepatic injuries. Because hemorrhage from hepatic injuries often is treated without isolating individual bleeding vessels, arterial pseudoaneurysms may develop, with the potential for rupture. Rupture into a bile duct results in hemobilia, which is characterized by intermittent episodes of right upper quadrant pain, upper GI hemorrhage, and jaundice. If the aneurysm ruptures into a portal vein, portal venous hypertension with bleeding esophageal varices may occur. Either scenario is best managed with hepatic arteriography and embolization. Biliovenous fistulas, causing jaundice due to rapid increases in serum bilirubin levels, should be treated with ERCP and sphincterotomy. Rarely, a biliary fistulous communication will form with intrathoracic structures in patients with associated diaphragm injuries, resulting in a bronchobiliary or pleurobiliary fistula. Due to the pressure differential between the biliary tract (positive) and the pleural cavity (negative), the majority require operative closure. Occasionally, endoscopic sphincterotomy with stent placement will be required to address the pressure differential, and the pleurobiliary fistula will close spontaneously.
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Until the 1970s, splenectomy was considered mandatory for all splenic injuries. Recognition of the immune function of the spleen refocused efforts on operative splenic salvage in the 1980s.104,105 After demonstrated success in pediatric patients, however, nonoperative management has become the preferred means of splenic salvage. The identification of contrast extravasation as a risk factor for failure of nonoperative management led to liberal use of angioembolization. The role of selective angioembolization (SAE) in splenic salvage remains controversial with some groups advocated pre-emptive SAE.106 It is clear, however, that up to 20% of patients with splenic trauma warrant early splenectomy and that failure of nonoperative management often represents inappropriate patient selection.107,108 Unlike hepatic injuries, which usually rebleed within 48 hours, delayed hemorrhage or rupture of the spleen can occur up to weeks after injury. Indications for early intervention include initiation of blood transfusion within the first 12 hours and hemodynamic instability.
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Splenic injuries are managed operatively by splenectomy, partial splenectomy, or splenic repair (splenorrhaphy), based on the extent of the injury and the physiologic condition of the patient. Splenectomy is indicated for hilar injuries, pulverized splenic parenchyma, or any >grade II injury in a patient with coagulopathy or multiple injuries. The authors use autotransplantation of splenic implants (Fig. 7-61) to achieve partial immunocompetence in younger patients who do not have an associated enteric injury. Drains are not used. Partial splenectomy can be employed in patients in whom only the superior or inferior pole has been injured. Hemorrhage from the raw splenic edge is controlled with horizontal mattress sutures, with gentle compression of the parenchyma (Fig. 7-62). As with hepatic injuries, splenorrhaphy hemostasis is achieved by topical methods (electrocautery; argon beam coagulation; application of thrombin-soaked gelatin foam sponges, fibrin glue, or BioGlue), envelopment of the injured spleen in absorbable mesh, and pledgeted suture repair.
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After splenectomy or splenorrhaphy, postoperative hemorrhage may be due to loosening of a tie around the splenic vessels, an improperly ligated or unrecognized short gastric artery, or recurrent bleeding from the spleen if splenic repair was used. An immediate postsplenectomy increase in platelets and WBCs is normal; however, beyond postoperative day 5, a WBC count above 15,000/mm3 and a platelet/WBC ratio of <20 are strongly associated with sepsis and should prompt a thorough search for underlying infection.109 A common infectious complication after splenectomy is a subphrenic abscess, which should be managed with percutaneous drainage. Additional sources of morbidity include a concurrent but unrecognized iatrogenic injury to the pancreatic tail during rapid splenectomy resulting in pancreatic ascites or fistula, and a gastric perforation during short gastric ligation. Enthusiasm for splenic salvage was driven by the rare, but often fatal, complication of overwhelming postsplenectomy sepsis. Overwhelming postsplenectomy sepsis is caused by encapsulated bacteria, Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis, which are resistant to antimicrobial treatment. In patients undergoing splenectomy, prophylaxis against these bacteria is provided via vaccines administered optimally at 14 days.110
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Stomach and Small Intestine
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Little controversy exists regarding the repair of injuries to the stomach or small bowel because of a rich blood supply. Gastric wounds can be oversewn with a running single-layer suture line or closed with a stapler. If a single-layer closure is chosen, full-thickness bites should be taken to ensure hemostasis from the well-vascularized gastric wall. The most commonly missed gastric injury is the posterior wound of a totally penetrating injury. Injuries also can be overlooked if the wound is located within the mesentery of the lesser curvature or high in the posterior fundus. To delineate a questionable injury, the stomach can be digitally occluded at the pylorus while methylene blue-colored saline is instilled via a nasogastric tube. Alternatively, air can be introduced via the NG tube with the abdomen filled with saline. Partial gastrectomy may be required for destructive injuries, with resections of the distal antrum or pylorus reconstructed using a Billroth procedure. Patients with injuries that damage both Latarjet nerves or vagi should undergo a drainage procedure (see Chap. 26). Small intestine injuries can be repaired using a transverse running 3-0 PDS suture if the injury is less than one- third the circumference of the bowel. Destructive injuries or multiple penetrating injuries occurring close together are treated with segmental resection followed by end-to-end anastomosis using a continuous, single-layer 3-0 polypropylene suture.111 Mesenteric injuries may result in an ischemic segment of intestine, which mandates resection.
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Following repair of GI tract injuries, there is an obligatory postoperative ileus. Return of bowel function is indicated by a decrease in gastrostomy or nasogastric tube output. The topic of nutrition is well covered in other chapters, but a few issues warrant mention. Multiple studies have confirmed the importance of early total enteral nutrition (TEN) in the trauma population, particularly its impact in reducing septic complications.112 The route of enteral feedings (stomach vs. small bowel) tends to be less important, because gut tolerance appears equivalent unless there is upper GI tract pathology. Although early enteral nutrition is the goal, evidence of bowel function should be apparent before advancing to goal tube feedings. Overzealous jejunal feeding can lead to small bowel necrosis in the patient recovering from profound shock. Patients undergoing monitoring for nonoperative management of grade II or higher solid organ injuries should receive nothing by mouth for at least 48 hours in case they require an operation. Although there is general reluctance to initiate TEN in patients with an open abdomen, a recent multicenter trial demonstrates TEN in the postinjury open abdomen is feasible.113 For those patients without a bowel injury, TEN was associated with higher fascial closure rates, decreased complications, and decreased mortality. TEN in patients with bowel injuries does not appear to alter fascial closure rates, complications, or mortality; hence EN appears to be neither advantageous nor detrimental in these patients. Prospective randomized controlled trials are warranted to further clarify the role of EN in this subgroup. Once resuscitation is complete, initiation of TEN, even at trophic levels (20 mL/h), should be considered in all injured patients with an open abdomen.
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Duodenum and Pancreas
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The spectrum of injuries to the duodenum includes hematomas, perforation (blunt blow-outs, lacerations from stab wounds, or blast injury from gunshot wounds), and combined pancreaticoduodenal injuries. The majority of duodenal hematomas are managed nonoperatively with nasogastric suction and parenteral nutrition. Patients with suspected associated perforation, suggested by clinical deterioration or imaging with retroperitoneal free air or contrast extravasation, should undergo operative exploration. A marked drop in nasogastric tube output heralds resolution of the hematoma, which typically occurs within 2 weeks; repeat imaging to confirm these clinical findings is optional. If the patient shows no clinical or radiographic improvement within 3 weeks, operative evaluation is warranted.
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Small duodenal perforations or lacerations should be treated by primary repair using a running single-layer suture of 3-0 monofilament. The wound should be closed in a direction that results in the largest residual lumen. Challenges arise when there is a substantial loss of duodenal tissue. Extensive injuries of the first portion of the duodenum (proximal to the duct of Santorini) can be repaired by débridement and end-to-end anastomosis because of the mobility and rich blood supply of the distal gastric atrium and pylorus. In contrast, the second portion is tethered to the head of the pancreas by its blood supply and the ducts of Wirsung and Santorini; therefore, no more than 1 cm of duodenum can be mobilized away from the pancreas, and this does not effectively alleviate tension on the suture line. Moreover, suture repair using an end-to-end anastomosis in the second portion often results in an unacceptably narrow lumen. Therefore, defects in the second portion of the duodenum should be patched with a vascularized jejunal graft. Duodenal injuries with tissue loss distal to the papilla of Vater and proximal to the superior mesenteric vessels are best treated by Roux-en-Y duodenojejunostomy with the distal portion of the duodenum oversewn (Fig. 7-63). In particular, injuries in the distal third and fourth portions of the duodenum (behind the mesenteric vessels) should be resected, and a duodenojejunostomy performed on the left side of the superior mesenteric vessels.
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Optimal management of pancreatic trauma is determined by where the parenchymal damage is located and whether the intrapancreatic common bile duct and main pancreatic duct remain intact. Patients with pancreatic contusions (defined as injuries that leave the ductal system intact) can be treated nonoperatively or with closed suction drainage if undergoing laparotomy for other indications. Patients with proximal pancreatic injuries, defined as those that lie to the right of the superior mesenteric vessels, are also managed with closed suction drainage,114 In contrast, distal pancreatic injuries are managed based upon ductal integrity. Pancreatic duct disruption can be identified through direct exploration of the parenchymal laceration, operative pancreatography, ERCP, or magnetic resonance cholangiopancreatography. Patients with distal ductal disruption undergo distal pancreatectomy, preferably with splenic preservation.
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Injuries to the pancreatic head add an additional element of complexity because the intrapancreatic portion of the common bile duct traverses this area and often converges with the pancreatic duct. In contrast to diagnosis of pancreatic duct injuries, identification of intrapancreatic common bile duct disruption is relatively simple. The first method is to squeeze the gallbladder and look for bile leaking from the pancreatic wound. Otherwise, cholangiography, optimally via the cystic duct, is diagnostic. Definitive treatment of this injury entails division of the common bile duct superior to the first portion of the duodenum, with ligation of the distal duct and reconstruction with a Roux-en-Y choledochojejunostomy. For injuries to the head of the pancreas that involve the main pancreatic duct but not the intrapancreatic bile duct, there are few options. Distal pancreatectomy alone is rarely indicated due to the extended resection of normal gland and the resultant risk of pancreatic insufficiency. Central pancreatectomy preserves the common bile duct, and mobilization of the pancreatic body permits drainage into a Roux-en-Y pancreaticojejunostomy (Fig. 7-64). Although this approach avoids a pancreaticoduodenectomy (Whipple procedure), the complexity may make the pancreaticoduodenectomy more appropriate in patients with multiple injuries. Some injuries of the pancreatic head do not involve either the pancreatic or common bile duct; if no clear ductal injury is present, drains are placed. Rarely, patients sustain destructive injuries to the head of the pancreas or combined pancreaticoduodenal injuries that require pancreaticoduodenectomy. Examples of such injuries include transection of both the intrapancreatic bile duct and the main pancreatic duct in the head of the pancreas, avulsion of the papilla of Vater from the duodenum, and destruction of the entire second portion of the duodenum. In these cases of extensive injuries, damage control principles are often employed.
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In contrast to proximal injuries, pancreatic resection continues to be advocated for major ductal disruption in the more distal pancreas. Several options exist for treating injuries of the pancreatic body and tail. In stable patients, spleen-preserving distal pancreatectomy should be performed. An alternative, which preserves both the spleen and distal transected end of the pancreas, is either a Roux-en-Y pancreaticojejunostomy or pancreaticogastrostomy. If the patient is physiologically compromised, distal pancreatectomy with splenectomy is the preferred approach. Regardless of the choice of definitive procedure, the pancreatic duct in the proximal edge of transected pancreas should be individually ligated or occluded with a TA stapler. Application of fibrin glue over the stump may be advantageous.
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Pyloric exclusion often is used to divert the GI stream after high-risk, complex duodenal repairs (Fig. 7-65).115 If the duodenal repair breaks down, the resultant fistula is an end fistula, which is easier to manage and more likely to close than a lateral fistula. To perform a pyloric exclusion, first a gastrostomy is made on the greater curvature near the pylorus. The pylorus is then grasped with a Babcock clamp, via the gastrostomy, and oversewn with an O polypropylene suture. A gastrojejunostomy restores GI tract continuity. Vagotomy is not necessary because a risk of marginal ulceration has not been documented. Perhaps surprisingly, the sutures maintain diversion for only 3 to 4 weeks. Alternatively, the most durable pyloric closure is a double external staple line across the pylorus using a TA stapler.
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Complications should be expected after major pancreaticoduodenal injuries. Delayed hemorrhage is rare but may occur with pancreatic necrosis or abdominal infection; this usually can be managed by angioembolization. If closed suction drains have been inserted for major pancreatic trauma, these should remain in place until the patient is tolerating an oral diet or enteral nutrition. Pancreatic fistula is diagnosed after postoperative day 5 in patients with drain output of >30 mL/d and a drain amylase level three times the serum value. Pancreatic fistula develops in over 20% of patients with combined injuries and should be managed similar to fistulas after elective surgery (see Chap. 33). Similarly, a duodenal fistula, presumptively an end fistula if a pyloric exclusion has been done, will typically heal in 6 to 8 weeks with adequate drainage and control of intra-abdominal sepsis. Pancreatic pseudocysts in patients managed nonoperatively suggest a missed injury, and ERCP should be done to evaluate the integrity of the pancreatic duct. Late pseudocysts may be a complication of operative management and are treated much like those in patients with pancreatitis (see Chap. 33). Intra-abdominal abscesses are common and routinely managed with percutaneous drainage.
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Currently, three methods for treating colonic injuries are used: primary repair, end colostomy, and primary repair with diverting ileostomy. Primary repairs include lateral suture repair or resection of the damaged segment with reconstruction by ileocolostomy or colocolostomy. All suturing and anastomoses are performed using a running single-layer technique (Fig. 7-66).111 The advantage of definitive treatment must be balanced against the possibility of anastomotic leakage if suture lines are created under suboptimal conditions. Alternatively, although use of an end colostomy requires a second operation, an unprotected suture line with the potential for breakdown is avoided. Numerous large retrospective and several prospective studies have now clearly demonstrated that primary repair is safe and effective in virtually all patients with penetrating wounds.116 Colostomy is still appropriate in a few patients, but the current dilemma is how to select which patients should undergo the procedure. Currently, the overall physiologic status of the patient, rather than local factors, directs decision making. Patients with devastating left colon injuries requiring damage control are clearly candidates for temporary colostomy. Diverting ileostomy with colocolostomy, however, is used for most other high-risk patients.
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Rectal injuries are similar to colonic injuries with respect to the ecology of the luminal contents, overall structure, and blood supply of the wall, but access to extraperitoneal injuries is limited due to the surrounding bony pelvis. Therefore, indirect treatment with intestinal diversion usually is required. The current options are loop ileostomy and sigmoid loop colostomy. These are preferred because they are quick and easy to perform, and provide essentially total fecal diversion. For sigmoid colostomy, technical elements include: (a) adequate mobilization of the sigmoid colon so that the loop will rest on the abdominal wall without tension, (b) maintenance of the spur of the colostomy (the common wall of the proximal and distal limbs after maturation) above the level of the skin with a one-half-inch nylon rod or similar device, (c) longitudinal incision in the tenia coli, and (d) immediate maturation in the OR (Fig. 7-67). If the injury is accessible (e.g., in the posterior intraperitoneal portion of the rectum), repair of the injury should also be attempted. However, it is not necessary to explore the extraperitoneal rectum to repair a distal perforation. If the rectal injury is extensive, another option is to divide the rectum at the level of the injury, oversew or staple the distal rectal pouch if possible, and create an end colostomy (Hartmann’s procedure). Extensive injuries may warrant presacral drainage with Penrose drains placed along Waldeyer’s fascia via a perianal incision (see Fig. 7-67). In rare instances in which destructive injuries are present, an abdominoperineal resection may be necessary to avert lethal pelvic sepsis.
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Complications related to colorectal injuries include intra-abdominal abscess, fecal fistula, wound infection, and stomal complications. Intra-abdominal abscesses occur in approximately 10% of patients, and most are managed with percutaneous drainage. Fistulas occur in 1% to 3% of patients and usually present as an abscess or wound infection with subsequent continuous drainage of fecal output; the majority will heal spontaneously with routine care (see Chap. 29). Stomal complications (necrosis, stenosis, obstruction, and prolapse) occur in 5% of patients and may require either immediate or delayed reoperation. Stomal necrosis should be carefully monitored, because spread beyond the mucosa may result in septic complications, including necrotizing fasciitis of the abdominal wall. Penetrating injuries that involve both the rectum and adjacent bony structures are prone to development of osteomyelitis. Bone biopsy is performed for diagnosis and bacteriologic analysis, and treatment entails long-term IV antibiotic therapy and occasionally débridement.
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Abdominal and Pelvic Vasculature
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Injury to the major arteries and veins in the abdomen can be a technical challenge.117,118,119,120,121 Although penetrating trauma indiscriminately affects all blood vessels, blunt trauma most commonly involves renal vasculature and occasionally the abdominal aorta. Patients with a penetrating aortic wound who survive to reach the OR frequently have a contained hematoma within the retroperitoneum. Due to lack of mobility of the abdominal aorta, few injuries are amenable to primary repair. Small lateral perforations may be controlled with 4-0 polypropylene suture or a PTFE patch, but end-to-end interposition grafting with a PTFE tube graft is the most common repair. Blunt injuries are typically extensive intimal tears of the infrarenal aorta and are exposed via a direct approach; most require an interposition graft. To avoid future vascular-enteric fistulas, the vascular suture lines should be covered with omentum.
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Penetrating wounds to the superior mesenteric artery (SMA) are typically encountered upon exploration for a gunshot wound, with “black bowel” and associated supramesocolic hematoma being pathognomonic. Blunt avulsions of the SMA are rare but should be considered in patients with a seat belt sign who have midepigastric pain or tenderness and associated hypotension. For injuries of the SMA, temporary damage control with a Pruitt-Inahara shunt can prevent extensive bowel necrosis; additionally, temporary shunting allows control of visceral contamination before placement of a PTFE graft. For definitive repair, end-to-end interposition RSVG from the proximal SMA to the SMA past the point of injury can be performed if there is no associated pancreatic injury. Alternatively, if the patient has an associated pancreatic injury, the graft should be tunneled from the distal aorta beneath the duodenum to the distal SMA. For proximal SMV injuries, digital compression for hemorrhage control is followed by attempted venorrhaphy; ligation is an option in a life-threatening situation, but the resultant bowel edema requires aggressive fluid resuscitation. Temporary abdominal closure and a second-look operation to evaluate bowel viability should be done.
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Transpelvic gunshot wounds or blunt injuries with associated pelvic fractures are the most common scenarios in patients with iliac artery injuries. As with abdominal vascular injuries, a Pruitt-Inahara shunt can be used for temporary shunting of the vessel for damage control. Definitive interposition grafting with excision of the injured segment is appropriate (see “Vascular Repair Techniques”). Careful monitoring for distal embolic events and reperfusion injury necessitating fasciotomy is imperative.
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In general, outcome after pelvic vascular injuries is related to (a) the technical success of the vascular reconstruction and (b) associated soft tissue and nerve injuries. Vascular repairs rarely fail after the first 12 hours, whereas, soft tissue infection is a limb threat for several weeks. Following aortic interposition grafting, the patient’s SBP should not exceed 120 mm Hg for at least the first 72 hours postoperatively. Patients requiring ligation of an inferior vena cava injury often develop marked bilateral lower extremity edema. To limit the associated morbidity the patient’s legs should be wrapped with elastic bandages from the toes to the hips and elevated at a 45- to 60-degree angle. For superior mesenteric vein injuries, either ligation or thrombosis after venorrhaphy results in marked bowel edema; fluid resuscitation should be aggressive and abdominal pressure monitoring routine in these patients. Prosthetic graft infections are rare complications, but prevention of bacteremia is imperative67; administration of antibiotics perioperatively and treatment of secondary infections is indicated. Long-term arterial graft complications such as stenosis or pseudoaneurysms are uncommon, and routine graft surveillance rarely is performed. Consequently, long-term administration of antiplatelet agents or antithrombotics is not routine.
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When undergoing laparotomy for trauma, the best policy is to explore all penetrating wounds to the kidneys.122 Parenchymal renal injuries are treated with hemostatic and reconstructive techniques similar to those used for injuries of the liver and spleen: topical methods (electrocautery; argon beam coagulation; application of thrombin-soaked gelatin foam sponge, fibrin glue, or BioGlue) and pledgeted suture repair. Two caveats are recognized, however: The collecting system should be closed separately, and the renal capsule should be preserved to close over the repair of the collecting system (Fig. 7-68). Renal vascular injuries are common after penetrating trauma and may be deceptively tamponaded, which results in delayed hemorrhage. Arterial reconstruction using graft interposition should be attempted for renal preservation. For destructive parenchymal or irreparable renovascular injuries, nephrectomy may be the only option; a normal contralateral kidney must be palpated, because unilateral renal agenesis occurs in 0.1% of patients.
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Over 90% of blunt renal injuries are treated nonoperatively. Hematuria typically resolves within a few days with bed rest, although rarely bleeding is so persistent that bladder irrigation to dispel blood clots is warranted. Persistent gross hematuria may require embolization, whereas urinomas can be drained percutaneously. Operative intervention after blunt trauma is limited to renovascular injuries and destructive parenchymal injuries that result in hypotension. The renal arteries and veins are uniquely susceptible to traction injury caused by blunt trauma. As the artery is stretched, the inelastic intima and media may rupture, which causes thrombus formation and resultant stenosis or occlusion. The success rate for renal artery repair approaches 0%, but an attempt is reasonable if the injury is <5 hours old or if the patient has a solitary kidney or bilateral injuries.123 Image-guided endostent placement is now employed for many of these injuries recognized by CT scanning. Reconstruction after blunt renal injuries may be difficult, however, because the injury is typically at the level of the aorta. If repair is not possible within this time frame, leaving the kidney in situ does not necessarily lead to hypertension or abscess formation. The renal vein may be torn or completely avulsed from the vena cava due to blunt trauma. Typically, the large hematoma causes hypotension, which leads to operative intervention. During laparotomy for blunt trauma, expanding or pulsatile perinephric hematomas should be explored. If necessary, emergent vascular control can be obtained by placing a curved vascular clamp across the hilum from an inferior approach. Techniques of repair and hemostasis are similar to those described earlier.
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Injuries to the ureters are uncommon but may occur in patients with pelvic fractures and penetrating trauma. An injury may not be identified until a complication (i.e., a urinoma) becomes apparent. If an injury is suspected during operative exploration but is not clearly identified, methylene blue or indigo carmine is administered IV with observation for extravasation. Injuries are repaired using 5-0 absorbable monofilament, and mobilization of the kidney may reduce tension on the anastomosis. Distal ureteral injuries can be treated by reimplantation facilitated with a psoas hitch and/or Boari flap. In damage control circumstances, the ureter can be ligated on both sides of the injury and a nephrostomy tube placed.
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Bladder injuries are subdivided into those with intraperitoneal extravasation and those with extraperitoneal extravasation. Ruptures or lacerations of the intraperitoneal bladder are operatively closed with a running, single-layer, 3-0 absorbable monofilament suture. Laparoscopic repair is becoming common in patients not requiring laparotomy for other injuries. Extraperitoneal ruptures are treated nonoperatively with bladder decompression for 2 weeks. Urethral injuries are managed by bridging the defect with a Foley catheter, with or without direct suture repair. Strictures are not uncommon but can be managed electively.
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Female Reproductive Tract
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Gynecologic injuries are rare. Occasionally the vaginal wall will be lacerated by a bone fragment from a pelvic fracture. Although repair is not mandated, it should be performed if physiologically feasible. More important, however, is recognition of the open fracture, need for possible drainage, and potential for pelvic sepsis. Penetrating injuries to the vagina, uterus, fallopian tubes, and ovaries are also uncommon, and routine hemostatic techniques are used. Repair of a transected fallopian tube can be attempted but probably is unjustified, because a suboptimal repair will increase the risk of tubal pregnancy. Transection at the injury site with proximal ligation and distal salpingectomy is a more prudent approach.
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Pelvic Fracture Hemorrhage Control
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Patients with pelvic fractures who are hemodynamically unstable are a diagnostic and therapeutic challenge for the trauma team. These injuries often occur in conjunction with other life-threatening injuries, and there is no universal agreement among clinicians on management. Current management algorithms in the United States incorporate variable time frames for bony stabilization and fixation, as well as hemorrhage control by preperitoneal pelvic packing and/or angioembolization. Early institution of a multidisciplinary approach with the involvement of trauma surgeons, orthopedic surgeons, interventional radiologists, the director of the blood bank, and anesthesiologists is imperative due to high associated mortality rates (Fig. 7-69).
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Evaluation in the ED focuses on identification of injuries mandating operative intervention (e.g., massive hemothorax, ruptured spleen) and injuries related to pelvic fracture that alter management (e.g., injuries to the iliac artery). Immediate temporary stabilization with sheeting of the pelvis or application of commercially available compression devices should be performed. In high risk patients, (e.g. autopedestrian accident) with profound shock, this should be done before radiographic confirmation. If the patient’s primary source of bleeding is the fracture-related hematoma, several options exist for hemorrhage control. Because 85% of bleeding due to pelvic fractures is venous or bony in origin the authors advocate immediate external fixation and preperitoneal pelvic packing.124,125 Anterior external fixation decreases pelvic volume, which promotes tamponade of venous bleeding and prevents secondary hemorrhage from the shifting of bony elements. Pelvic packing, in which six laparotomy pads (four in children) are placed directly into the paravesical space through a small suprapubic incision, provides tamponade for the bleeding (Fig. 7-70). Pelvic packing also eliminates the often difficult decision by the trauma surgeon: OR vs. interventional radiology? All patients can be rapidly transported to the OR and packing can be accomplished in under 30 minutes. In the authors’ experience, this results in hemodynamic stability and abrupt cessation of the need for ongoing blood transfusion in the majority of cases.125 Patients also can undergo additional procedures such as laparotomy, thoracotomy, external fixation of extremity fractures, open fracture débridement, or craniotomy. Currently, angiography is reserved for patients with evidence of ongoing pelvic bleeding after admission to the SICU (>4 units of RBCs in the first 12 postoperative hours after the coagulopathy is corrected). Patients undergo standard posttrauma resuscitative SICU care, and the pelvic packs are removed within 48 hours, a time frame chosen empirically based on the authors’ experience with liver packing. The authors elect to repack the patient’s pelvis if there is persistent oozing and perform serial washouts of the preperitoneal space if it appears infected.
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Another clinical challenge is the open pelvic fracture. In many instances the wounds are located in the perineum, and the risk of pelvic sepsis and osteomyelitis is high. To reduce the risk of infection, performance of a diverting sigmoid colostomy is recommended. The pelvic wound is manually débrided and then irrigated daily with a high-pressure pulsatile irrigation system until granulation tissue covers the wound. The wound is then left to heal by secondary intention with a wound vacuum-assisted wound closure (VAC) device.
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Extremity Vascular Injuries, Fractures, and Compartment Syndromes
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Patients with injured extremities often require a multidisciplinary approach with involvement of trauma, orthopedic, and plastic surgeons to address vascular injuries, fractures, soft tissue injuries, and compartment syndromes. Immediate stabilization of fractures or unstable joints is done in the ED using Hare traction, knee immobilizers, or plaster splints. In patients with open fractures the wound should be covered with povidoneiodine (Betadine)-soaked gauze and antibiotics administered. Options for fracture fixation include external fixation or open reduction and internal fixation with plates or intramedullary nails. Vascular injuries, either isolated or in combination with fractures, require emergent repair. Common combined injuries include clavicle/first rib fractures and subclavian artery injuries, dislocated shoulder/proximal humeral fractures and axillary artery injuries, supracondylar fractures/elbow dislocations and brachial artery injuries, femur fracture and superficial femoral artery injuries, and knee dislocation and popliteal vessel injuries. On-table angiography in the OR facilitates rapid intervention and is warranted in patients with evidence of limb threat at ED arrival. Arterial access for on-table lower extremity angiography can be obtained percutaneously at the femoral vessels with a standard arterial catheter, via femoral vessel exposure and direct cannulation, or with superficial femoral artery (SFA) exposure just above the medial knee. Controversy exists regarding which should be done first, fracture fixation or arterial repair. The authors prefer placement of temporary intravascular shunts first with arterial occlusions to minimize ischemia during fracture treatment, with definitive vascular repair following. Rarely, immediate amputation may be considered due to the severity of orthopedic and neurovascular injuries. This is particularly true if primary nerve transection is present in addition to fracture and arterial injury.126 Collaborative decision making by the trauma, orthopedic, and plastic/reconstructive team is essential.
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Operative intervention for vascular injuries should follow standard principles of repair (see “Vascular Repair Techniques”). For subclavian or axillary artery repairs, 6-mm PTFE graft and RSVG are used. Because associated injuries of the brachial plexus are common, a thorough neurologic examination of the extremity is mandated before operative intervention. Operative approach for a brachial artery injury is via a medial upper extremity longitudinal incision; proximal control may be obtained at the axillary artery, and an S-shaped extension through the antecubital fossa provides access to the distal brachial artery. The injured vessel segment is excised, and an end-to-end interposition RSVG graft is performed. Upper extremity fasciotomy is rarely required unless the patient manifests preoperative neurologic changes or diminished pulse upon revascularization, or the time to operative intervention is extended. For SFA injuries, external fixation of the femur typically is performed, followed by end-to-end RSVG of the injured SFA segment. Close monitoring for calf compartment syndrome is mandatory. Preferred access to the popliteal space for an acute injury is the medial one-incision approach with detachment of the semitendinosus, semimembranosus, and gracilis muscles (Fig. 7-71). Another option is a medial approach with two incisions using a longer RSVG, but this requires interval ligation of the popliteal artery and geniculate branches. Rarely, with open wounds a straight posterior approach with an S-shaped incision can be used. If the patient has an associated popliteal vein injury, this should be repaired first with a PTFE interposition graft while the artery is shunted. For an isolated popliteal artery injury, RSVG is performed with an end-to-end anastomosis. Compartment syndrome is common, and presumptive four-compartment fasciotomies are warranted in patients with combined arterial and venous injury. Once the vessel is repaired and restoration of arterial flow documented, completion angiography should be done in the OR if there is no palpable distal pulse. Vasoparalysis with verapamil, nitroglycerin, and papaverine may be used to treat vasoconstriction (Table 7-11).
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Compartment syndromes, which can occur anywhere in the extremities, involve an acute increase in pressure inside a closed space, which impairs blood flow to the structures within. Causes of compartment syndrome include arterial hemorrhage into a compartment, venous ligation or thrombosis, crush injuries, and reperfusion injury. In conscious patients, pain is the prominent symptom, and active or passive motion of muscles in the involved compartment increases the pain. Paresthesias may also be described. In the lower extremity, numbness between the first and second toes is the hallmark of early compartment syndrome in the exquisitely sensitive anterior compartment and its enveloped deep peroneal nerve. Progression to paralysis can occur, and loss of pulses is a late sign. In comatose or obtunded patients, the diagnosis is more difficult to secure. In patients with a compatible history and a tense extremity, compartment pressures should be measured with a hand-held Stryker device. Fasciotomy is indicated in patients with a gradient of <35 mm Hg (gradient = diastolic pressure – compartment pressure), ischemic periods of >6 hours, or combined arterial and venous injuries. The lower extremity is most frequently involved, and compartment release is performed using a two-incision, four-compartment fasciotomy (Fig. 7-72). Of note, the soleus muscle must be detached from the tibia to decompress the deep flexor compartment.
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