Ann Thorac Surg 2006;81:1485-1487
© 2006 The Society of Thoracic Surgeons
Case report
Traumatic Hemoptysis Treated With Recombinant Human Factor VIIa
James V. O'Connor, MD
a
,
*
,
Deborah M. Stein, MD
b
,
Richard P. Dutton, MD
c
,
Thomas M. Scalea, MD
d
a Department of Thoracic and Vascular Surgery, R. Adams Cowley Shock Trauma Center, Baltimore, Maryland
b Department of Trauma and Critical Care, R. Adams Cowley Shock Trauma Center, Baltimore, Maryland
c Department of Anesthesiology, R. Adams Cowley Shock Trauma Center, Baltimore, Maryland
d Program in Trauma Department, R Adams Cowley Shock Trauma Center, Baltimore, Maryland
Accepted for publication March 8, 2005.
* Address correspondence to Dr O'Connor, Thoracic and Vascular Surgery, R Adams Cowley Shock Trauma Center, University of Maryland School of Medicine, 22 S Greene St, Baltimore, MD 21201 (Email: joconnor{at}umm.edu).
| Dr Dutton discloses that he has a financial relationship with Novo Nordisk.
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Abstract
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Blunt thoracic trauma resulting in massive hemoptysis is rare. Although there are several indications for the administration of recombinant factor VIIa, we are unaware of a report of its utilization in the treatment of hemoptysis following chest trauma. We report a case of the successful use of factor VIIa in the treatment of life-threatening hemoptysis secondary to blunt force thoracic injury and traumatic coagulopathy.
Although chest trauma is common, life-threatening hemoptysis as its result is distinctively uncommon. In the acutely injured patient, a combination of hemorrhage, transfusion, acidosis, and hypothermia may result in coagulopathy with ensuing hemoptysis. Recombinant factor VIIa (factor VIIa Novo 7 [Novo Nordisk, Bagsvaerd, Denmark]) has been used "off label" for the treatment of life-threatening hemorrhages in trauma patients as well as those with nontraumatic causes.
A 21-year-old woman who was an unrestrained passenger in a motor vehicle accident was ejected during a collision. On admission, she was alert, complaining of abdominal pain and shortness of breath. Vital signs included a systolic blood pressure of 80 mm Hg, a pulse rate of 130 beats per minute, and a respiratory rate of 28 beats per minute with distress. On examination, the abdomen was tender and distended and there were diminished bilateral breath sounds. Resuscitation included endotracheal intubation and volume administration. Plain roentgenograms demonstrated a lateral compression type II fracture and portable supine chest roentgenogram revealed bilateral pneumothoraces (Fig 1). Pertinent initial laboratory data included a hematocrit of 27%, a platelet count of 67,000, an international normalized ratio of 0.9, a partial thromboplastin time (PTT) of 52 seconds. An arterial blood gas on 0.4 PI
2 was a pH of 7.39, PC
2 was 39 mm Hg, PO
2 was 266 mm Hg, HCO
3 was 23 mmol/L, the base excess was –1.5 mmol/L, and SAO
2 was 100%. Bilateral tube thoracostomies were performed with minimal serosanguineous output and no air leak. Focused ultrasound examination for trauma demonstrated free peritoneal fluid and an exploratory laparotomy was performed.
A grade III liver laceration and intraperitoneal bladder rupture were repaired. There was a non-expanding pelvic hematoma. Precipitous, significant hemoptysis occurred, requiring continuous endotracheal tube suctioning. The oxygen saturation dropped to 76% without air leak or bleeding from either chest tube. Flexible bronchoscopy demonstrated diffuse bilateral hemorrhage. An intraoperative chest roentgenogram was performed (Fig 2). The arterial blood gas was 7.11, PCO
2 was 53 mm Hg, PO
2 was 66 mm Hg, HCO
3 was 16 mmol/L, the base excess was –14, and saturation was 87%. The international normalized ratio was 2.2, the PTT was 71 seconds, and the platelet count was 135,000. Abdominal bleeding was controlled, but hemoptysis continued despite administration of 18 units of packed red blood cells, 14 units of fresh frozen plasma, and platelets. Human factor VIIa was administered as a single dose of 6 mg (100 mcg/kg) with near instantaneous cessation of bleeding. Damage control laparotomy was expeditiously completed. Laboratory data after factor VIIa infusion demonstrated an international normalized ratio of 0.5 and a PTT of 32 seconds. An arterial blood gas on 1.0 PIO
2 pH was 7.34, PCO
2 was 40 mm Hg, PO
2 was 312 mm Hg, HCO
3 was 21 mmol/L, and the base excess of – was 4.1 with 100% saturation.
Postoperatively the patient was taken to the intensive care unit. A chest roentgenogram was obtained on postoperative day 1 as shown in Figure 3. Extubation was accomplished on postoperative day 2. The intensive care unit course was protracted because additional abdominal and urologic procedures were required. After a 3-week hospital course, the patient was discharged to a rehabilitation facility without the need for supplemental oxygen.
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Comment
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Significant hemoptysis in the trauma patient may result from alveolar injury with small vessel involvement, airway injury, or coagulopathy. Small vessel and alveolar damage are common in the setting of blunt thoracic trauma, but rarely significant enough to cause hemoptysis or warrant intervention. However, in the presence of coagulopathy, these injuries can cause hemorrhage resulting in compromised oxygenation, ventilation, or hemodynamics.
Bronchoscopy is the diagnostic modality of choice. Treatment options for hemoptysis vary depending on cause and degree of hemorrhage. Hemoptysis may require endotracheal intubation for airway protection, possibly with a double-lumen endotracheal tube and initiation of hemodynamic support. Discreet vessel injury can often be treated with angiographic embolization or bronchoscopic control [1]. Diffuse small vessel injury, often secondary to pulmonary contusion, generally requires supportive care. Therapeutic bronchoscopy may be needed to adequately clear the airway of blood or clots. Massive hemoptysis with hemodynamic and respiratory compromise is relatively rare and may require rigid bronchoscopy, double-lumen endotracheal tube, or bronchial blockers and angiography.
When traumatic coagulopathy occurs, treatment algorithms must include rapid replacement of clotting factors, the prevention of hypothermia, and acidosis. Recombinant factor VIIa is now being used to reverse coagulopathy and control exsanguinating hemorrhage [2, 3]. First developed for use in hemophiliacs with allo-antibiotics against factor VIII and IX, factor VIIa is now being used on an "off label" basis in hemorrhaging non-hemophiliacs. The mechanism of action of factor VIIa is through the binding of tissue factor and subsequent activation of platelets at sites of vessel entry. Although no prospective data are available to validate the efficiency of factor VIIa in trauma patients, many published case reports and series describe its successful use in the acutely bleeding patient [4, 5]. Several reports have focused on the successful use of recombinant factor VIIa to control diffuse pulmonary hemorrhage in non-injured patients [6–8].
In our patient, after control of the intraabdominal bleeding, hemoptysis became manifest secondary to the development of coagulopathy. The use of recombinant factor VIIa was an effective treatment allowing rapid control of diffuse hemorrhage and reversal of respiratory compromise. Although there are no prospective data supporting the use of factor VIIa in this patient population, this anecdotal report adds to the growing body of literature supporting the use of factor VIIa in the acutely hemorrhaging non-hemophiliac patient.
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References
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- Corder R. Hemoptysis Emerg Med Clin North Am 2003;21:421-435.[Medline]
- Dutton RP, McCunn M, Hyder M, et al. Factor Vlla for correction of traumatic coagulopathy J Trauma 2004;57(4):709-719.[Medline]
- Martinowitz U, Kenet G, Lubetski A, et al. Possible role of recombinant activated factor Vll (rFVll1a) in the control of hemorrhage associated with massive trauma Can J Anesth 2002;49:S15-S20.[Medline]
- Laffan M, O'Connell NM, Perry DJ, et al. Analysis and results of the recombinant factor VIIa extended-use registry Blood Coagul Fibrinolysis 2003;14:S35-S38.
- Eikelboom JW, Bird R, Blythe D, et al. Recombinant activated factor VII for the treatment of life-threatening hemorrhage Blood Coagul Fibrinolysis 2003;14:713-717.[Medline]
- Pastores SM, Papadopoulos E, Voight L, Halpern NA. Diffuse alveolar hemorrhage after allogeneic hematopoietic stem cell transplantationtreatment with recombinant factor VIIa. Chest 2003;124:2400-2403.[Abstract/Free Full Text]
- Leibovitch L, Kenet G, Mazor K, et al. Recombinant activated factor VII for life-threatening pulmonary hemorrhage after pediatric cardiac surgery Pediatr Crit Care Med 2003;4:444-446.[Medline]
- Henke D, Falk RJ, Gabriel DA. Successful treatment of diffuse alveolar hemorrhage with activated factor VII Ann Intern Med 2004;140:493-494.[Free Full Text]
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Successful Use of Recombinant Activated Coagulation Factor VII in a Patient with Massive Hemoptysis From a Penetrating Thoracic Injury
Ann. Thorac. Surg.,
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