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Audio-Digest FoundationGeneral Surgery


Volume 55, Issue 07
April 7, 2008

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LUNG AND AORTIC INJURIES

SURGICAL OPTIONS IN THE MANAGEMENT OF LUNG INJURIES —Robert C. Mackersie, MD, Professor, Department of Surgery, University of California, San Francisco, School of Medicine, and Director, Trauma Service, San Francisco General Hospital
Background: most operative lung injuries not blunt; occasionally, blunt injury becomes penetrating; 20% to 40% of penetrating lung injuries require resection; general indications for related thoracotomy—majority (94%-96%) of all thoracic trauma will not require thoracotomy to control hemorrhage or other problems; hemorrhage >1500 mL; persistent or recurrent shock (attributable to thoracic injury); persistent chest tube output; refractory (massive) hemothorax; massive endobronchial bleeding; major air embolism—results from communication between bronchi and pulmonary vessels; air and blood do not mix; air in pulmonary vein causes cardiac arrest and embolism; endobronchial bleeding, in and of itself, harmful; air trapped in lung parenchyma and exits via pulmonary vein; can cause coronary and cerebral embolism and airlock in left ventricle, leading to instant death; relatively uncommon; endobronchial bleeding—more common; blood trapped in lung; exits via adjacent bronchus; alveolar flooding damaging to lung parenchyma; albumin component in whole blood strong inhibitor of surfactant producing alveolar collapse; albumin also chemoattractant and precursor to acute respiratory distress syndrome (ARDS); important to perform serial x-rays to assess which patients may benefit from early operation
Initial steps: tracheal intubation—usually no time for double-lumen tubes (in general, not worth doing); if massive endobranchial hemorrhage present, particularly on left side, perform directed right mainstem intubation; bronchial blockers one of less complicated interventions; delaying thoracotomy to control hemorrhage often mistake; thoracotomy— resuscitative; unless patients present in near-arrest, they should be transported to operating room (OR) for optimal conditions; positioning—keep options open; most patients have combined thoracoabdominal injuries; anterolateral thoracotomy and laparotomy if necessary; beware of “down lung syndrome” (use of single-lumen tubes, full posterolateral thoracotomy with patient up, and if excessive endobronchial hemorrhage present, bleeding can drop down into “good” lung; this causes injury to unaffected lung, which produces severe intraoperative hypoxia and postoperative problems); prevented if hilar control of hemorrhage initiated as soon as possible; full posterolateral thoracotomy acceptable if injuries clearly isolated; anterolateral thoracotomy has advantage of allowing entrance into abdomen if necessary; identify bleeding site—necessary once in chest (not always lung); look for tamponade first (easiest to treat); major vascular injuries potential bleeding source; hilar control—done manually or through hilar “twist” (requires cutting inferior pulmonary ligament); clamps dangerous in this area
Surgical options: simple oversew—do not oversew deep tracts (causes trapping of air and blood in contained space); stapled or sutured tractotomy and oversew (more commonly used treatment for more serious lung injuries); nonanatomic wedge resection; lobectomy and pneumonectomy reserved for unique cases; less resection and greater preservation of lung parenchyma better for patient; use with caution to avoid trapping of air and blood; incorporate entire suture line; most bleeding self-limited; newer tissue adhesives and glues used; wedge resection—feasible in periphery of lungs; reinforce suture line carefully; avoid lung sequestrum (nonperfused or nonventilated portion of lung that collapses); tractotomy—most commonly performed procedure for major and more central lung injuries (gunshot wound classic model); prevent mixing of blood and air to gain control of hemorrhage and bronchial leak (necessary to open tract); easiest way to open tract to use gastrointestinal anastomosis (GIA) staplers and open up thinnest portion of lung possible, paying attention to anatomy; be sensitive to parenchymal thickness; good hilar control allows time to control bleeding and air-blood interface; simple oversew augmented with tissue adhesives (eg, fibrin glue, glutaraldehyde compounds) to close lung and reattach pleural visceral attachment; some patients develop ARDS-type syndrome, with relatively high peak airway pressures; this can wreak havoc on tenuous stapled suture line with large bronchopleural fistulas (forestalled by oversewing stapled suture lines with running suture); avoid lung sequestrum; anatomic resections—lobectomies and pneumonectomies; reserved for more destructive injuries; avoid if possible; data suggest outcomes equivalent with anatomic or nonanatomic pulmonary resections; may be necessary to perform intrapericardial proximal vascular control
Factors related to outcome: age; associated injuries; shock; transfusion requirements; associated comorbidities; degree of endobronchial hemorrhage; nonventilated lung or nonperfused lung (sequestrum) created sometimes by surgical tractotomy (can develop infection); with infection, reoperation problematic
Postpneumonectomy problems: massive transfusion and blood; increased sensitivity to pulmonary edema; endobronchial bleeding; right heart failure; ventilator-induced lung injury (worse with one lung); several studies show dismal outcome; National Trauma Database Study showed that independent of factors (eg, shock, massive transfusion, comorbidities), simply removing lung detrimental to patient and independent predictor of mortality; sparing parenchymal resection (to extent possible) helps with outcome
AORTIC DISSECTION John M. Marek, MD, Associate Professor, Division of Vascular Surgery, Department of Surgery, University of New Mexico Health Sciences Center, Albuquerque
Incidence: most frequent catastrophic aortic disorder; estimated 2 to 3 times more frequent than ruptured abdominal aortic aneurysms; medical management of type B dissections associated with 30-day mortality of 12%; most deaths with type A or B dissections due to rupture of aorta; most patients >40 yr of age at presentation; in older population, estimated incidence 5-times greater in men than women (equal in younger population); 50% of dissections in younger women occur during pregnancy (usually during third trimester or labor), possibly associated with preeclampsia or hypertension; higher incidence in patients with connective tissue disorders (eg, Marfan’s syndrome); also in bicuspid aortic valve and aortic coarctation; cocaine use, especially in younger patients; iatrogenic procedures (eg, cardiac catheterization)
Natural history: estimated 10% to 15% of patients die suddenly in first 15 min in type A dissection; with no intervention, estimated mortality rate, 1% to 2%/hr; 50% of patients alive at 48 hr; 10% survival rate at 3 mo; without intervention, type A dissections have 1-mo survival rate, with emergency surgery gold standard; in type B, with medical management, 70% survival at 1 mo not unusual; type I basically type A dissection; type II mostly type B dissection; even with operative interventions, not actually curing patients of dissection
Classifications: Stanford—type A, any involvement of ascending aorta (biggest prognostic indicator for acute management of patients); DeBakey—types I, II, IIIa, and IIIb; type I involves ascending aorta down to iliac bifurcation; type II involves only ascending aorta; type IIIa involves descending aorta to inguinal ligament; in type IIIb, involvement all way down to distal aorta; most occur in ascending aorta (proximal two-thirds or type A dissection); only 20% type B dissections; in aortic arch (neither classic type A nor type B), 10%; abdominal dissections fairly infrequent; initial entry point occurs within first 9 cm from aortic valve (takeoff of left subclavian artery) in most dissections
Pathogenesis: complex; inciting event rupture of intima, whereby blood gets into subintimal plane, and dissection occurs in medial layers; one postulated explanation that degeneration of medial fibers decreases cohesiveness of aortic layers; previously, term cystic medial necrosis used to describe pathologic entity of aortic dissection; medial degeneration more extensive as patients get older, and with higher incidence of hypertension, connective tissue disorders, and bicuspid aortic valve
Clinical presentation: acute (<2-wk duration) or chronic; patients with type A dissection typically younger, with less hypertensive history; in type B dissections, 70% to 80% of patients have hypertension (less frequent in type A); higher incidence of congenital defects in type A dissections; initial presentation varied; ranges from hypovolemic shock due to rupture, to cardiogenic shock from tamponade; aortic regurgitation common in type A dissection; most patients initially present with hypertension; International Registry of Acute Aortic Dissection (IRAD) involves 11 countries and 22 centers of excellence in aortic dissection management; pain—sudden onset classic presentation (highly associated with aortic rupture); usually sharp; classic ripping or tearing pain in 51% of patients; mostly in chest; whether pain in anterior chest or back related to location of dissection; in type A dissections, anterior chest pain typical; in aortic arch dissections, anterior chest or back pain typical; in dissections that extend to descending aorta or type B dissections, interscapular pain or abdominal pain seen; abdominal pain present in 30% of patients (possibly due to dissection extending distally); index of suspicion varies with type of pain at presentation; most physicians suspect aortic dissection with chest and back pain (less suspected if presentation typical anterior chest pain); only 8% of physicians suspect aortic dissection if presentation abdominal pain; pain lasts from hours to days initially; if pain lasts longer, or if pain-free interval present with return of chest pain, may indicate progression of dissection or impending rupture (ominous sign); 25% of patients present with hypovolemic or cardiogenic shock; pulse differential—relatively common; in upper extremities, normal right arm pulse with diminished left arm pulse associated with propagation of dissection and occlusion of left subclavian artery; in lower extremity, present in 15% to 20% of patients presenting with acute lower extremity ischemia; if renal arteries involved with branched vessel occlusion, patient may have oliguria or anuria; cardiac murmur in 25% of patients (due to aortic regurgitation frequently seen in proximal type A dissections); 20% to 30% present with stroke, paraplegia, syncope, or Horner syndrome; aortic regurgitation frequently present in type A dissections and second most common cause of death (most common cause aortic rupture); cardiac tamponade or acute pericardial effusion ominous sign that patient needs emergency surgery after diagnosis (or diagnosis made in OR with transesophageal echocardiography); low coronary perfusion with type A dissection not infrequent because of involvement of cusp of coronary arteries; >8% of emergency department (ED) visits for chest pain; majority due to myocardial infarctions (MIs); missed diagnosis of aortic dissection (ie, confusing with MI) potentially catastrophic, especially if patient given thrombolytics or if delay in diagnosis of type A dissection; initial suspicion of aortic dissection usually not good in these patients (as low as 15% suspected by physicians); 20% of diagnoses made at autopsy
Diagnostic tests: electrocardiography—frequently abnormal; ST changes not infrequent but nonspecific; usually initial screening test; chest x-ray—initial screening test for patient with chest pain; usual tests include computed tomography (CT), magnetic resonance imaging (MRI), echocardiography, and rarely, angiography (formerly gold standard; presently used for intervention, not for diagnosis); MRI—gold standard for diagnosis; 100% sensitivity and specificity; good at locating proximal ascending aortic dissection and extent of dissection; problem of availability in ED; cannot be performed in patients with metallic implants; CT angiography—most frequently utilized study for diagnosis; not as sensitive or specific, due to difficulty in visualizing ascending aorta; requires intravenous (IV) contrast load; retrograde dissection into aortic arch—worst prognosis; most patients require intervention, due to higher mortality within first year; treated with endoluminal graft; transesophageal echocardiography—more accurate than transthoracic echocardiography; safe; quick; performed at bedside or in ED; sensitive; able to quantify aortic regurgitation, pericardial effusion, and left ventricular dysfunction; investigator-dependent (limitation); in some centers, used during endoluminal graft placement to ensure occlusion of false lumen; less effective for evaluating aortic arch (trachea blocks view); angiography—invasive and time-consuming
Medical management: IV β-blockers; unless patient hypotensive, key in initial medical management; if not effective, start nitroprusside; starting with nitroprusside before β-blocker propagates dissection; labetalol good alternative; lifelong β-blocker therapy necessary, regardless of other procedures peformed; if dissection has uncomplicated course, transition to oral therapy possible
Indications for surgery: include all type A dissections, unless prohibitive operative risks present; in type B dissections, classic indications include rupture, large left pleural hemothorax, visceral ischemia, continued pain, and uncontrolled hypertension (impending rupture); operative mortality high; if patient stable with no malperfusion syndrome, mortality rates close to 10% to 12% (higher if patient in shock or with malperfusion syndrome); patients impaired with bypass, circulatory arrest, and retrograde cerebral perfusion; aortic valve replacement if necessary; for type B dissections, classic open surgery also carries high mortality rates (14%-16% in perioperative period); of great concern in open surgery and endografting, depending on how much of thoracic aorta replaced or covered, incidence of paraplegia (permanent in 20%-30%); branched vessel involvement in >40% (no intervention necessary if in subclavian artery; necessary in carotid, visceral, and renal arteries); number of patients present with acute lower extremity ischemia, more commonly on left side, due to nature of how dissection propagates; for endoluminal approaches to branched vessel occlusions, determine whether significant compression of true lumen present (treat first)
Endoluminal grafts: Gore TAG device approved by Food and Drug Administration (FDA) in March 2005 for descending thoracoabdominal aneurysms; intravascular ultrasonography while performing procedures critical because necessary to be in true lumen throughout course of procedure; complications from endoluminal grafts mostly related to access; for chronic type B dissections, most patients survive initial hospital stay with medical management; however, some patients continue to expand aorta and at risk for rupture; according to data, 1-yr survivability after type B dissection, 50% to 90%; close follow- up mandatory; aorta dilated to 5.5 to 6.5 cm threshold for action to prevent rupture; most patients die of rupture in follow-up; 20% to 40% of patients eventually develop aneurysmal degeneration requiring surgery; 25% of thoracoabdominal aneurysms due to chronic dissections; if not treated within 1 yr, most patients die from rupture; at 5 yr, only 20% alive; patency of false lumen—thought that patients whose false lumen thrombosed initially have better outcome; patent false lumen predictor of dissection-related death; if initial diameter of aorta during hospitalization >45 mm with patent false lumen, at 1, 5, and 10 yr, most patients have dilation of aorta; if diameter smaller initially, with occluded false lumen, most patients have fairly benign course; study—looked at false lumen patency; those with partial thrombosis of false lumen had worst outcome at 1 yr; theory that mean arterial pressures in partially thrombosed false lumen higher; INvestigation of STEnt grafts in patients with type B Aortic Dissection (INSTEAD) trial—not yet published; 136 participants with uncomplicated type B dissections; no deaths in medical management arm; 11% required stent grafts due to significant dilation of aorta; 10% incidence of deaths at 1 yr in stent graft arm; early intervention with stent grafting may be unwarranted for patients with uncomplicated type B dissection (just close follow-up)

Suggested Reading

Estrera AL et al: Update on outcomes of acute type B aortic dissection. Ann Thorac Surg 83:S842, 2007; Gómez- Caro A et al: Role of conservative medical management of tracheobronchial injuries. J Trauma 61:1426, 2006; Hansen MS et al: Frequency of and inappropriate treatment of misdiagnosis of acute aortic dissection. Am J Cardiol 99:852, 2007; Hatzaras IS et al: Role of exertion or emotion as inciting events for acute aortic dissection. Am J Cardiol 100:1470, 2007; Huh J et al: Surgical management of traumatic pulmonary injury. Am J Surg 186:620, 2003; Karmy- Jones R et al: Descending thoracic aortic dissections. Surg Clin North Am 87:1047, 2007; Kawanishi Y et al: Three cases of newly developed paraplegia after repairing type A acute aortic dissection. Ann Thorac Surg 84:1738, 2007; Khaladj N et al: Should a patient with acute aortic dissection type A go to the intensive care unit or operating room? Ann Thorac Surg 84:1069; author reply 1069, 2007; Lee CH et al: Type A aortic dissection: a hidden and lethal cause for failed thrombolytic treatment in acute myocardial infarction. Heart 93:825, 2007; Odero A et al: Endovascular treatment of acute type B dissection and Kommerell's diverticulum. Ann Thorac Surg 84:1736, 2007; Pape LA et al: Aortic diameter >or = 5.5 cm is not a good predictor of type A aortic dissection: observations from the International Registry of Acute Aortic Dissection (IRAD). Circulation 116:1120, 2007; Schoder M et al: Endovascular repair of acute type B aortic dissection: long-term follow-up of true and false lumen diameter changes. Ann Thorac Surg 83:1059, 2007; Sorokin VA et al: Combined open and endovascular repair of acute type A aortic dissection. Ann Thorac Surg 83:666, 2007; Tarver K et al: Extensive aortic dissection presenting as acute inferior myocardial infarction. Heart 93:1225, 2007; Tsai TT et al: Partial thrombosis of the false lumen in patients with acute type B aortic dissection. N Engl J Med 357:349, 2007; Wong B: Partial thrombosis of the false lumen in aortic dissection. N Engl J Med 357:1868; author reply 1868, 2007.

Educational Objectives

The goal of this program is to improve the surgical management of lung injuries and aortic dissection. After hearing and assimilating this program, the clinician will be better able to:
1. Recognize the indications for thoracotomy due to lung injuries.
2. Differentiate, and determine the most appropriate, surgical options for lung injuries.
3. Review the Stanford and DeBakey classifications of aortic dissection.
4. Distinguish between type A and type B aortic dissections, based on pain characteristics.
5. Review the indications for surgery in aortic dissection.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the faculty and planning committee reported nothing to disclose.

Acknowledgements

Dr. Mackersie was recorded at the Detroit Trauma Symposium, held November 8-9, 2007, in Detroit, MI, and sponsored by the DMC Detroit Receiving Hospital and Wayne State University School of Medicine. Dr. Marek was recorded at Current Concepts in General Surgery and Trauma Update, held September 5-7, 2007, in Albuquerque, NM, and sponsored by the University of New Mexico Health Sciences Center, Department of Surgery, and Office of Continuing Medical Education. The Audio-Digest Foundation thanks Drs. Mackersie and Marek and the sponsors for their cooperation in the production of this program.

Reproduction of this summary in whole or in part in any form or medium without express written permission is prohibited.

If, after reviewing this written summary, you would like to hear the contents and/or earn CME/CE credit:

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