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The Pivotal Role of Transesophageal Echocardiography in the Management of Traumatic Thoracic Aortic Rupture With Associated Intra-abdominal Hemorrhage
corrected with an FI02 of 60 percent administered by face mask (Ventimask). He was started on a regimen of mechanical ventilation with a positive end-expiratory pressure of 8 cm H20 . Seventy-two hours after the initiation of ventilatory support , the patient had normal arterial gas values and regression of pulmonary infiltrates, but remained in coma needing ventilatory support. A study of complement levels showed a decrease of total hemolytic activity , CHlOo 28 HU (>70 HU) with decrease of Cis inhibitor (Cllnh), 8.9 mg/dl (15 to 33 mg/dl), and C4 fraction, 6 mg/dl (20 to 50 mg/dl) , The C3 and Clq fractions were normal (Fig 2). Alpha2-macroglobulin was about 97 mgjdl (220 to 400 mg/dl), Treatment with tranexamic acid (500 mg three times a day) and danazol (200 mg three times a day) was started. Ventilatory weaning was complicated with seizures. On the tenth day, an EEG suggested cortical brain damage, and carbamazepine (200 mg three times a day) therapy was added. Spontaneous ventilation was achieved 45 days after hospital admission with no major neurologic damage. The Cl Inh was still low (10.3 mg/dl), The total complement hemolytic activity and fractions were normal (Fig 2). Alpha-j-macroglobulln was also normal (210 mgjdl). Treatment with tranexamic acid (500 mg three times a day) and danazol (200 mg three times a day) was maintained. Three months after hospital discharge, the patient remained without symptoms, but maintained low levels of Cl Inh, 10.8 mg/dl,
Inh, may be predominantly involved. A decrease of £xTmacroglobulin was also found during the acute episode of angioedema (Fig 2) as we had previously observed in other cases of HA, and could be related to the kinin pathway acttvatton." Gastric contents aspiration could also explain the development of ARDS in this patient and the alterations observed in the complement system profile, especially the decrease of total hemolytic activity observed in this patient. I •S However, the persistence of low levels of CI Inh, 3 months after hospital discharge, is consistent with the diagnose of HA . A neurologic insult due to hypoxemic brain insult can explain the difficulty in weaning the patient, and his development of seizures. As far as we know, the association between HA and ARDS has not been described yet. We believe that CIs inhibitor deficiency may contribute to ARDS establishment through mechanical obstruction and kinin or complement uncontrolled activation, but gastric contents aspiration and hypoxemic brain insult could also be implicated in the ARDS seen in this patient. REFERENCES
DISCUSSION
Adult respiratory distress syndrome is a common presentation of several entities. Among them it is frequently associated with sepsis, multiple trauma, and severely burned patients. 1 Less frequently, ARDS follows upper airway obstruction, and has been related to the accumulation of liquid in the extracapillary space as a result of the hemodynamic conditions created by negative intrapleural pressure transmitted to the lung interstitium.f The mechanisms that result in releasing inflammatory mediators and chemotactic factors of inflammatory cells with alveolar endothelium and pavement damage are unknown. In this patient, the upper airways obstruction is closely related to ARDS. However, other factors must explain why the patient developed ARDS that lasted several days despite rapid tracheostomy. Edema of the glottis is an example of mechanical upper airway obstruction that can lead to ARDS . The CIs Inh is a protease inhibitor of various biologic systems with contact actlvatlon.P It participates in the regulation of complement activation, and it also plays a role in the kinin, fibrinolytic, and coagulation systems.' The kinin activation and anaphylotoxin formation with vasodilatation and chemiotactism of inflammatory cells may also be involved in the inflammatory component of ARDS. The complement system profile observed in this patient, with low levels of C4 and CI Inh is typical of hereditary angioedema (HA).3 Independently of its etiology, complement system activation has been described in ARDS. In the first 48 h, this activation occurs predominantly through the alternate pathway.V' Accordingly, the complement activation indicator most frequently found in patients with ARDS is the decrease of C3 levels, and C3a and C5a for mation.P In our patient, a classic pathway consumption, due to CI
2
3 4
5 6
Petty TL. Acute respiratory distress syndrome (ARDS) . Dis Mon Jan 1990; 9-58 Timby J, Reed C, Zeilender S, Glauser FL. 'Mechanical' causes of pulmonary edema. Chest 1990; 98:973-79 Kaplan AP. Urticaria and angioedema. In: Kaplan AP, ed. Allergy. New York: Churchill-Livingstone, 1985; 439-71 Zilow G, Sturm JA, Rother U, Kirsch6nk M. Complement activation and the prognostic value of C3a in patients at risk of adult respiratory distress syndrome. Clin Exp Immunol 1990; 79:151-57 RobbinsRA, RussWD, RasmussenJK, Clayton MM. Activation of the complement system in the adult respiratory distresssyndrome . Am Rev Respir Dis 1987; 135:651-58 Torresda Costa], Delgado L, Correia 0, MartinesT, Rodrigues M, Azevedo M. Contact system inhibitors in angioedema. Schweiz Med Wochenschr 1991; 121(40/115):27
The Pivotal Role of Transesophageal Echocardiography in the Management of Traumatic Thoracic Aortic Rupture With Associated Intra-abdominal Hemorrhage* Collin E. M. Brathwaite, M.D. , F.C.C.P.; Jonathan M . Cilley, M.D., F.C.C.P.; William H. O'Connor, M.D .; Steven E. Ross, M.D., F.C.C,P.; and Richard L . Weiss , M.D., F.C.C.P. -From the Departments of Surgery (Drs. Brathwaite , Cilley, and Ross) and Medicine (Drs. O'Connor and Weiss), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School at Camden/Cooper Hospital-University Medical Center, Camden, NJ. Reprint requests: Dr . Brathwaite, 3 Cooper Piau, Suite 411, Camden, NJ 08103 CHEST /105/6/ JUNE. 1994
1899
Rupture of the thoracic aorta after blunt trauma, particularly when associated with multiple injuries, presents a major problem of resuscitation and management. Transesophageal color Doppler echocardiography (TEE) during laparotomy played a major role in confirming the diagnosis of thoracic aortic rupture in a patient. (Chest 1994; 105:1899-1901) TEE=transesophageal echocardiography
T
ra umatic rupture of the thoracic aorta continues to be a significant cause of morbidity a nd mortality . It is estimated that more than 80 percent of pati ents die before hospital admission.' Even in areas of rapid transport and sophisticated prehospital care, up to 30 percent of patients will exsanguinate during resuscitation.f The management of this injury is particularly more vexing when there is associated intra-abdominal hemorrhage. The appropriate sequence of angiography, laparotom y, and thoracotomy remains controversial.? Recently, interest has grown in th e newly developed method of transesophageal color Doppler echocardiography (TEE) for the diagnosis of various form s of chest trauma.v" In the following case report, we found TEE to playa pivotal role in establishing the diagnosis of aortic rupture and facilitating the timing of various surgical procedures. CASE REPORT
A 48-year-old woman was tran sported by helicopter to Cooper Hospita l/University Medical Center after being the dr iver in a motor vehicle crash . The pati ent was hypotensive in the field and hospital ad mission systolic blood pressure was 70 mm Hg . Chest radiograph demonstrated a widened mediastinum (Fig 1). A di agnostic peritoneal lavage revealed intraperitoneal bleeding and , thus. the patient underwent emergency laparotomy. A ruptured spleen and mesent eric laceration with devitalized proximal ileum were identified. Splen ectomy and segmental small bowel resection with primary anastomosis wer e performed. Because of the widened medi astinum noted on admiss ion. TEE was performed sim ultaneously with laparotomy.
FI(;rIlE I. Chest radiograph showing widened mediastinum . 1900
A 5.0-MHz biplan e TEE probe was inserted into the esophagus and a standard examinat ion of the heart and great vessels was performed. The cardiac chambers and valvular structures wer e normal in size and function . In evaluating the thoracic aorta, a medial rupture of this structure was noted with a contained pseudoaneurysm just distal to but not involving the origin of the left subclavi an artery (Fig 2). There was color flow signal entering the conta ined rupture site in a pulsatile manner . The proximal-distal extent of the hematoma around the thoracic aorta was identified dearly. The pseudoaneurysrn extended above and adjacent to the aortic arch. A small left pleural effusion was noted as well. After completion of the laparotomy, the patient was positioned and underwent left posterolateral thoracotom y. A320 0 disrupt ion of the aorta with a 3-cm pseudoaneurysm was found and repaired with a 20-mm low-porosit y woven Dacron interposition graft. during a cross-damp per iod of 22 min. The aorti c repair was followed by repair of several orthopedic injuries; then the pat ient was transferred to the trauma intensive care unit. A follow-up TEE was performed the first day postoperatively and revealed no significant ventricular dysfunction and excellent graft function ing. After a brief period of ventil atory support. the patient's condition gradually improved and she was subsequently discharged from the hospital on the 22nd postoperative da y. DISCt:SSIO~
The rapid and successful treatment of patients with combined traumatic rupture of the thoracic aorta and ongoing intra-abdominal hemorrhage requires judicious application of d iagnostic procedures, as well as appropriate timing of therapeutic interventions. In reporting a retrospective review of 57 multiply injured patients with thoracic aortic rupture, Lee and colleagues" recommend laparotomy for patients in unst able conditions with a positive diagnostic peritoneal lavage and suspected aortic injury . If the patient's condition stabilizes after laparotomy, this should be followed by aortography and then thoracotomy . Although aortography is con sidered the gold standard for confirming thoracic aortic rupture, and computed tomography may play a role in initial evaluation, both investigations require transporting an often mechanically ventilated, unstable pati ent within the hospital, thus involving inevitable delays.
FIGI'H E 2. Transesophageal echocardiography demonstrating aortic rupture, AO=dl'scend ing thoracic aorta; PsA= pseudoaneurysm extendi ng from the medial portion of the aorta with color flow Doppler signal indicating to and from blood flow,
PivotalRole of TEE in Management of TraumaticThoracic Aortic Rupture (Brathwaite at at)
Transesophageal echocardiography was pivotal in this case since it was rapidly performed simultaneously with laparotomy. Undue delay and transportation of this patient were avoided . Though others have reported the use of TEE to diagnose aortic injury ,6.i this has usually been complemented by aortography. In one other report, Galvin et all! reported the use of bedside TEE in the intensive care unit prior to thoracotom y without aortography for aortic transection. That patient also underwent laparotomy for intraabdominal bleeding prior to thoracotomy ; however, he ultimately died . The authors of the current report believe that the intraoperative use of TEE during laparotomy in that patient may have prevented dela y in laparotomy. Though we are not yet ready to abandon aortography for TEE in diagnosing aortic rupture, TEE clearlv has a role in those patients with multiple injuries who require laparotomy. If the study unequivocally demonstrates a lesion confined to the descending aorta, then one should proceed without aortograph y. With increasing expertise and technological advancement, TEE may become the definitive diagnostic test for traumatic thoracic aortic rupture. R EFERE:'\ CES
2
3
4
5
6
7
8
et aJ.Traumatic disruptions of the thoracic aorta: treatment and outcome. Surgery 1990; 108:864-70 Cowley RA. Turney SZ. Hankins JR. Rodriguez A. Altar S. Shankar BS. Rupture of thoracic aorta caused by blunt trauma: a 15-year experience. j Thorac Cardiovasc Surg 1990; 100: 652-61 Lee RB. Stahlman CC. Sharp KW. Tr eatment pnormes IIIl-'atient s with tra umatic rupture of the thoracic aorta. Am Surg 1992; 58:37-4.'3 Shipiro M], Yanofsky SO. Trapp j . Durham RM. Labovitz A. Sear [E, et al. Cardiovascular evaluation in blunt thoracic trauma using transesophageal echoc ardiography (TEE) . j Traum a 1991; 31:835-40 Brathwaite CEM. Weiss RL. Baldino WA. Hoganson N. Ross SE. Multichamber gunshot wounds of the heart : the utility of transesophageal echocardiography. Che st 1992; 101:287-88 Coarin j P, Le Bret F. Riou B. jacqueus Yves. Viars P. Early diagnosis of traumatic thoracic aortic rupture by transesophageal echocardiography. Chest 1993; 103:618-19 Brooks SW. Cmolik BL. Young jc. Townsend RN. Daimond DL. Transesophageal echocardiographic exam ination of a palient with traumatic aortic transection from blunl chest trauma: a case report. j Trauma 1991; 31:841-45 Calvin IF. Black IW. Lee CL . Horton DA. Transesophageal echocard iograph y in acute aortic transection. Ann Tho rac Surg 1991; 51:310-11
DelRossi AJ. Madden CD . Cilley JH. Spence RK. Alexander JB.
60th
Annual International Scientific Assembly October 30 November 3, 1994 New Orleans For more information call 800 343-ACCP
A M E R I C AN C O LLEG E OF CHE ST P H Y S IC I A N S
CHEST/105/6/ JUNE. 1994
1901
Inh, may be predominantly involved. A decrease of £xTmacroglobulin was also found during the acute episode of angioedema (Fig 2) as we had previously observed in other cases of HA, and could be related to the kinin pathway acttvatton." Gastric contents aspiration could also explain the development of ARDS in this patient and the alterations observed in the complement system profile, especially the decrease of total hemolytic activity observed in this patient. I •S However, the persistence of low levels of CI Inh, 3 months after hospital discharge, is consistent with the diagnose of HA . A neurologic insult due to hypoxemic brain insult can explain the difficulty in weaning the patient, and his development of seizures. As far as we know, the association between HA and ARDS has not been described yet. We believe that CIs inhibitor deficiency may contribute to ARDS establishment through mechanical obstruction and kinin or complement uncontrolled activation, but gastric contents aspiration and hypoxemic brain insult could also be implicated in the ARDS seen in this patient. REFERENCES
DISCUSSION
Adult respiratory distress syndrome is a common presentation of several entities. Among them it is frequently associated with sepsis, multiple trauma, and severely burned patients. 1 Less frequently, ARDS follows upper airway obstruction, and has been related to the accumulation of liquid in the extracapillary space as a result of the hemodynamic conditions created by negative intrapleural pressure transmitted to the lung interstitium.f The mechanisms that result in releasing inflammatory mediators and chemotactic factors of inflammatory cells with alveolar endothelium and pavement damage are unknown. In this patient, the upper airways obstruction is closely related to ARDS. However, other factors must explain why the patient developed ARDS that lasted several days despite rapid tracheostomy. Edema of the glottis is an example of mechanical upper airway obstruction that can lead to ARDS . The CIs Inh is a protease inhibitor of various biologic systems with contact actlvatlon.P It participates in the regulation of complement activation, and it also plays a role in the kinin, fibrinolytic, and coagulation systems.' The kinin activation and anaphylotoxin formation with vasodilatation and chemiotactism of inflammatory cells may also be involved in the inflammatory component of ARDS. The complement system profile observed in this patient, with low levels of C4 and CI Inh is typical of hereditary angioedema (HA).3 Independently of its etiology, complement system activation has been described in ARDS. In the first 48 h, this activation occurs predominantly through the alternate pathway.V' Accordingly, the complement activation indicator most frequently found in patients with ARDS is the decrease of C3 levels, and C3a and C5a for mation.P In our patient, a classic pathway consumption, due to CI
2
3 4
5 6
Petty TL. Acute respiratory distress syndrome (ARDS) . Dis Mon Jan 1990; 9-58 Timby J, Reed C, Zeilender S, Glauser FL. 'Mechanical' causes of pulmonary edema. Chest 1990; 98:973-79 Kaplan AP. Urticaria and angioedema. In: Kaplan AP, ed. Allergy. New York: Churchill-Livingstone, 1985; 439-71 Zilow G, Sturm JA, Rother U, Kirsch6nk M. Complement activation and the prognostic value of C3a in patients at risk of adult respiratory distress syndrome. Clin Exp Immunol 1990; 79:151-57 RobbinsRA, RussWD, RasmussenJK, Clayton MM. Activation of the complement system in the adult respiratory distresssyndrome . Am Rev Respir Dis 1987; 135:651-58 Torresda Costa], Delgado L, Correia 0, MartinesT, Rodrigues M, Azevedo M. Contact system inhibitors in angioedema. Schweiz Med Wochenschr 1991; 121(40/115):27
The Pivotal Role of Transesophageal Echocardiography in the Management of Traumatic Thoracic Aortic Rupture With Associated Intra-abdominal Hemorrhage* Collin E. M. Brathwaite, M.D. , F.C.C.P.; Jonathan M . Cilley, M.D., F.C.C.P.; William H. O'Connor, M.D .; Steven E. Ross, M.D., F.C.C,P.; and Richard L . Weiss , M.D., F.C.C.P. -From the Departments of Surgery (Drs. Brathwaite , Cilley, and Ross) and Medicine (Drs. O'Connor and Weiss), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School at Camden/Cooper Hospital-University Medical Center, Camden, NJ. Reprint requests: Dr . Brathwaite, 3 Cooper Piau, Suite 411, Camden, NJ 08103 CHEST /105/6/ JUNE. 1994
1899
Rupture of the thoracic aorta after blunt trauma, particularly when associated with multiple injuries, presents a major problem of resuscitation and management. Transesophageal color Doppler echocardiography (TEE) during laparotomy played a major role in confirming the diagnosis of thoracic aortic rupture in a patient. (Chest 1994; 105:1899-1901) TEE=transesophageal echocardiography
T
ra umatic rupture of the thoracic aorta continues to be a significant cause of morbidity a nd mortality . It is estimated that more than 80 percent of pati ents die before hospital admission.' Even in areas of rapid transport and sophisticated prehospital care, up to 30 percent of patients will exsanguinate during resuscitation.f The management of this injury is particularly more vexing when there is associated intra-abdominal hemorrhage. The appropriate sequence of angiography, laparotom y, and thoracotomy remains controversial.? Recently, interest has grown in th e newly developed method of transesophageal color Doppler echocardiography (TEE) for the diagnosis of various form s of chest trauma.v" In the following case report, we found TEE to playa pivotal role in establishing the diagnosis of aortic rupture and facilitating the timing of various surgical procedures. CASE REPORT
A 48-year-old woman was tran sported by helicopter to Cooper Hospita l/University Medical Center after being the dr iver in a motor vehicle crash . The pati ent was hypotensive in the field and hospital ad mission systolic blood pressure was 70 mm Hg . Chest radiograph demonstrated a widened mediastinum (Fig 1). A di agnostic peritoneal lavage revealed intraperitoneal bleeding and , thus. the patient underwent emergency laparotomy. A ruptured spleen and mesent eric laceration with devitalized proximal ileum were identified. Splen ectomy and segmental small bowel resection with primary anastomosis wer e performed. Because of the widened medi astinum noted on admiss ion. TEE was performed sim ultaneously with laparotomy.
FI(;rIlE I. Chest radiograph showing widened mediastinum . 1900
A 5.0-MHz biplan e TEE probe was inserted into the esophagus and a standard examinat ion of the heart and great vessels was performed. The cardiac chambers and valvular structures wer e normal in size and function . In evaluating the thoracic aorta, a medial rupture of this structure was noted with a contained pseudoaneurysm just distal to but not involving the origin of the left subclavi an artery (Fig 2). There was color flow signal entering the conta ined rupture site in a pulsatile manner . The proximal-distal extent of the hematoma around the thoracic aorta was identified dearly. The pseudoaneurysrn extended above and adjacent to the aortic arch. A small left pleural effusion was noted as well. After completion of the laparotomy, the patient was positioned and underwent left posterolateral thoracotom y. A320 0 disrupt ion of the aorta with a 3-cm pseudoaneurysm was found and repaired with a 20-mm low-porosit y woven Dacron interposition graft. during a cross-damp per iod of 22 min. The aorti c repair was followed by repair of several orthopedic injuries; then the pat ient was transferred to the trauma intensive care unit. A follow-up TEE was performed the first day postoperatively and revealed no significant ventricular dysfunction and excellent graft function ing. After a brief period of ventil atory support. the patient's condition gradually improved and she was subsequently discharged from the hospital on the 22nd postoperative da y. DISCt:SSIO~
The rapid and successful treatment of patients with combined traumatic rupture of the thoracic aorta and ongoing intra-abdominal hemorrhage requires judicious application of d iagnostic procedures, as well as appropriate timing of therapeutic interventions. In reporting a retrospective review of 57 multiply injured patients with thoracic aortic rupture, Lee and colleagues" recommend laparotomy for patients in unst able conditions with a positive diagnostic peritoneal lavage and suspected aortic injury . If the patient's condition stabilizes after laparotomy, this should be followed by aortography and then thoracotomy . Although aortography is con sidered the gold standard for confirming thoracic aortic rupture, and computed tomography may play a role in initial evaluation, both investigations require transporting an often mechanically ventilated, unstable pati ent within the hospital, thus involving inevitable delays.
FIGI'H E 2. Transesophageal echocardiography demonstrating aortic rupture, AO=dl'scend ing thoracic aorta; PsA= pseudoaneurysm extendi ng from the medial portion of the aorta with color flow Doppler signal indicating to and from blood flow,
PivotalRole of TEE in Management of TraumaticThoracic Aortic Rupture (Brathwaite at at)
Transesophageal echocardiography was pivotal in this case since it was rapidly performed simultaneously with laparotomy. Undue delay and transportation of this patient were avoided . Though others have reported the use of TEE to diagnose aortic injury ,6.i this has usually been complemented by aortography. In one other report, Galvin et all! reported the use of bedside TEE in the intensive care unit prior to thoracotom y without aortography for aortic transection. That patient also underwent laparotomy for intraabdominal bleeding prior to thoracotomy ; however, he ultimately died . The authors of the current report believe that the intraoperative use of TEE during laparotomy in that patient may have prevented dela y in laparotomy. Though we are not yet ready to abandon aortography for TEE in diagnosing aortic rupture, TEE clearlv has a role in those patients with multiple injuries who require laparotomy. If the study unequivocally demonstrates a lesion confined to the descending aorta, then one should proceed without aortograph y. With increasing expertise and technological advancement, TEE may become the definitive diagnostic test for traumatic thoracic aortic rupture. R EFERE:'\ CES
2
3
4
5
6
7
8
et aJ.Traumatic disruptions of the thoracic aorta: treatment and outcome. Surgery 1990; 108:864-70 Cowley RA. Turney SZ. Hankins JR. Rodriguez A. Altar S. Shankar BS. Rupture of thoracic aorta caused by blunt trauma: a 15-year experience. j Thorac Cardiovasc Surg 1990; 100: 652-61 Lee RB. Stahlman CC. Sharp KW. Tr eatment pnormes IIIl-'atient s with tra umatic rupture of the thoracic aorta. Am Surg 1992; 58:37-4.'3 Shipiro M], Yanofsky SO. Trapp j . Durham RM. Labovitz A. Sear [E, et al. Cardiovascular evaluation in blunt thoracic trauma using transesophageal echoc ardiography (TEE) . j Traum a 1991; 31:835-40 Brathwaite CEM. Weiss RL. Baldino WA. Hoganson N. Ross SE. Multichamber gunshot wounds of the heart : the utility of transesophageal echocardiography. Che st 1992; 101:287-88 Coarin j P, Le Bret F. Riou B. jacqueus Yves. Viars P. Early diagnosis of traumatic thoracic aortic rupture by transesophageal echocardiography. Chest 1993; 103:618-19 Brooks SW. Cmolik BL. Young jc. Townsend RN. Daimond DL. Transesophageal echocardiographic exam ination of a palient with traumatic aortic transection from blunl chest trauma: a case report. j Trauma 1991; 31:841-45 Calvin IF. Black IW. Lee CL . Horton DA. Transesophageal echocard iograph y in acute aortic transection. Ann Tho rac Surg 1991; 51:310-11
DelRossi AJ. Madden CD . Cilley JH. Spence RK. Alexander JB.
60th
Annual International Scientific Assembly October 30 November 3, 1994 New Orleans For more information call 800 343-ACCP
A M E R I C AN C O LLEG E OF CHE ST P H Y S IC I A N S
CHEST/105/6/ JUNE. 1994
1901