Article, Radiology

Left brachiocephalic vein perforation: computed tomographic features and treatment considerations

Brief Report

Left brachiocephalic vein perforation: computed tomographic features and treatment considerations

Sheung-Fat Ko MDa,?, Shu-Hang Ng MDa, Fu-Ming Fang MDa, Yung-Liang Wan MDa, Ming-Jang Hsieh MDb, Po-Ping Liu MDc, Chia-Te Kung MDd, Ber-Ming Liu MDd

aDepartment of Radiology, College of Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center,

Chang Gung University, Kaohsiung 833, Taiwan

bDepartment of Cardiovascular and Thoracic Surgery, College of Medicine,

Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University, Kaohsiung 833, Taiwan

cDepartment of Traumatology, College of Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center,

Chang Gung University, Kaohsiung 833, Taiwan

dDepartment of Emergency Medicine, College of Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University, Kaohsiung 833, Taiwan

Received 22 May 2007; revised 11 June 2007; accepted 13 June 2007

Abstract

Objective: To report the clinical and computed tomographic findings of 5 cases of left brachiocephalic vein perforation (LBCVP).

Methods: The clinical and imaging features of 5 patients with LBCVP (1 woman, 4 men; mean age, 57.6 years) encountered over the last 2 decades were reviewed.

Results: Etiologies included left jugular central catheter penetration in 2 patients, blunt trauma in 2, and idiopathic in 1. All patients manifested acute chest pain with a widened mediastinum on chest radiographs. Characteristic computed tomographic features included a cord-like hematoma along the course of the left brachiocephalic vein associated with a left upper anterior mediastinal hematoma (AMH). Three clinically stable patients with AMH smaller than 5 cm convalesced after conservative treatment and 2 clinically unstable patients with AMH bigger than 7 cm recovered well after surgery. Conclusions: Computed tomography is helpful in diagnosing LBCVP. Under close surveillance, patients with stable LBCVP with AMH smaller than 5 cm may be managed conservatively. However, emergency surgery is warranted if there are any signs of instability.

(C) 2007

Introduction

* Corresponding author.

E-mail addresses: [email protected], [email protected] (S.-F. Ko).

Percutaneous Central venous catheter placement for administration of drugs or parenteral nutrition, monitoring of central venous or Pulmonary arterial pressure, and short- term dialysis is more and more common in medical practice. However, owing to the angulation between the left internal

0735-6757/$ – see front matter (C) 2007 doi:10.1016/j.ajem.2007.06.013

Case No.

Age/sex

Clinical features

Blood pressure/ hemoglobin

CT Findings

Treatment

Follow-up

1

2

3

4

5

60 y/F

53 y/M

57 y/M

60 y/M

58 y/M

Acute sharp chest pain after left jugular central catheter insertion Acute sharp chest pain after left jugular central catheter insertion

Sharp chest pain after MVA

Sharp chest pain after MVA

Acute sharp chest pain

100/76 mm Hg/

9.3 g%

110/70 mm Hg/

9.8 g%

106/65 mm Hg/

9.1 g%

86/48 mm Hg/

7.6 g%

98/66 mm Hg/

8.7 g%

Cord-like hematoma along LBCV, left AMH (5 x 2 cm) with

lower AM extension

Cord-like hematoma along LBCV, left AMH (4 x 2 cm) with

lower AM extension

Cord-like hematoma encasing LBCV with subtle contrast agent leakage, left AMH (5 x 3 cm) with

lower AM extension

Cord-like hematoma along LBCV,

left AMH (10 x 8 cm) with fluid-fluid level and lower AM extension

Cord-like hematoma along LBCV, left AMH (7 x 5 cm) with

lower AM extension,

aortic arch saccular aneurysm (5 x 3 cm)

Medical

Medical

Medical

Left BCV ligation

Venoplasty

1 y, A

3 y, A

6Y, A

10 y, A

14 y, A

A indicates alive; AM, anterior mediastinal, M, male; F, female; MVA, motor-vehicle accident.

jugular and left brachiocephalic vein (LBCV), an inadver- tently torqued catheter over this angulation may lead to catastrophic Vascular injury [1-3]. blunt chest trauma may injure intrathoracic vessels and usually affects the aorta, arch vessels, and small mediastinal veins [4-9]. Left brachiocephalic vein perforation (LBCVP) caused by chest trauma is rare [9]. Spontaneous brachiocephalic vein rupture is extremely unusual, and, to our knowledge, only 1 case of simultaneous rupture of the subclavian artery and brachio- cephalic vein, in a 25-year-old man with Ehlers-Danlos syndrome, has been documented [10]. The objective of this study was to present our experience of 5 unusual cases of LBCVP with an emphasis on computed tomographic features and treatment implications.

Table 1 Summary of clinical and CT features of 5 patients with left brachiocephalic vein perforation

Methods

From July 1986 through March 2007, of approximately

1.3 million ED visits (approximately 60000-65000 visits each year), a total of 5 cases of LBCVP were found after a Retrospective investigation of the hospital database. The medical records of these patients were reviewed for clinical presentation, known prior diseases, pertinent laboratory data, and outcomes. All patients had chest radiographs for evaluation. The chest radiographs of 2 patients were obtained after central venous catheter removal, whereas the radio- graphs of the other 3 patients were taken within 15 minutes after arrival at the ED. Three patients had noncontrast computed tomography (CT; patients 1, 2, and 4 in Table 1)

and 2 patients (patients 3 and 5 in Table 1) had both noncontrast and contrast CT for analysis. Three patients

underwent conservative treatment after the diagnosis was established based on the clinical and CT findings, and a follow-up CT was performed 1 month after discharge. A 3-month follow-up CT was also performed for patient 3. The remaining 2 patients underwent emergency surgery.

Results

The clinical and CT findings of the patients are summarized in Table 1.

Clinical findings

The patients included 1 woman and 4 men (age range, 53-60 years; mean, 57.6 years). None had prior history of vascular or connective tissue disease, but patients 1 and 5 had a history of hypertension for more than 10 years. Patient 1 was a 60-year-old woman with dyspnea and was referred to our ED by a community hospital owing to acute sharp chest pain after a central catheter was inserted via the left jugular vein. Patient 2 was admitted for lumbar spine surgery but experienced sharp chest pain after a central catheter was inserted via the left jugular vein. Because of chest pain and poor venous return, the catheters were subsequently removed. Patients 3 and 4 presented with chest pain 1 to 2 hours after blunt chest trauma in motor vehicle accidents. Patient 5 presented with acute sharp chest pain without radiation to the back and there was no operation history or recent trauma. This patient was a retired soldier and had a history of blunt chest and abdominal trauma due to an explosive injury, in which he recovered after conservative

Fig. 2 Case 3. A, noncontrast CT revealing a cord-like hyperdense hematoma (small white arrows) along the course of the LBCV and a left upper AMH (big white arrow). B, Computed tomography revealing subtle extravasation (open arrows) of the contrast agent from the LBCV that is encased by a cord-like hematoma.

treatment, 10 years before this admission. All patients experienced a decline in both blood pressure and Hemoglobin levels. Otherwise, physical and laboratory examination results were unremarkable.

Imaging features

On chest radiographs, a widened mediastinum (Fig. 1A) was demonstrated in all 5 patients but there was no pneumomediastinum. For patients 1 and 2, noncontrast CT

Fig. 1 Case 1. A, Chest radiograph revealing widening of the mediastinum. B, Noncontrast CT revealing a cord-like hyperdense hematoma (small black and white arrows) along the anterior border of the LBCV (open arrows) and a left upper AMH (big white arrow). C, Computed tomography showing a left AMH (big white arrow) and caudal extension of the hematoma (small black and white arrows) into the lower anterior mediastinal fat.

surgical findings, Treatment outcome, a”>Fig. 3 Case 4. A, Noncontrast CT revealing a large left upper AMH (big white arrows) with intralesional fluid-fluid level (open arrows) and a cord-like hyperdense hematoma (small white arrows) along the course of the LBCV. B, Computed tomography revealing caudal extension of the hematoma (black and white arrows) anterior to the parietal pericardium.

revealed a cord-like hyperdense hematoma along the anterior border of the LBCV, the presence of left upper anterior mediastinal hematoma (AMH), and caudal extension of the hematomas into the lower anterior mediastinum anterior to the parietal pericardium (Fig. 1B and C). For patient 3, in addition to a left AMH, contrast CT revealed subtle leakage of the contrast agent from the LBCV, which was encased by a perivenous cord-like hematoma (Fig. 2). For patient 4, noncontrast CT clearly depicted a cord-like hematoma along the course of the LBCV, a large left AMH with intralesional fluid-fluid level, which was suggestive of active bleeding, and caudal extension of the hematoma into the lower anterior mediastinum (Fig. 3A and B). For patient 5, besides a characteristic cord-like hematoma, there was also a left AMH with caudal extension of the

hematoma (Fig. 4A and B) and a saccular aortic aneurysm with mural thrombus.

Surgical findings, treatment outcome, and follow-up

Patients 1, 2, and 3 were hemodynamically stable and were treated conservatively. Complete resolution of the cord-like perivenous hematoma and AMH in patients 1 and

2 was demonstrated on the 1-month follow-up CT. For patient 3, total regression of the lesions was shown on the 3-month follow-up CT. Patients 4 and 5 underwent emergency surgery owing to rapidly deteriorating hemody- namic status under the initial impressions of AMH with

Fig. 4 Case 5. A, Contrast CT showing a cord-like hematoma (small black and white arrows) along the course of the LBCV and a left AMH (large arrow). Note the saccular aortic arch aneurysm (open arrow). B, Computed tomography revealing caudal extension of the hematoma (arrows) anterior to the parietal pericardium.

active bleeding and suspected rupture of aortic aneurysm, respectively. For patient 4, a large AMH due to a 2-cm laceration in the anterior wall of the LBCV at the left parasternal level was found during surgery, and the LBCV beyond the laceration was collapsed and partially encased by some perivenous Blood clots. The lacerated part was ligated. For patient 5, the surgeons found an AMH due to a 1-cm laceration in the anterior wall of the LBCV at the left parasternal level and the LBCV beyond the laceration was encased by a perivenous hematoma. The laceration was managed with venoplasty. In addition, an aortic aneurysm was noted but there was no evidence of aneurysmal rupture. histopathologic examination of the brachiocephalic vein wall specimens showed no underlying vascular lesions. All patients recovered without recurrence of LBCV lesions during follow-up (range, 1-14 years; mean, 5.6 years).

Discussion

Acute chest pain is a commonly encountered problem in the ED. It may occur in a variety of disease processes involving the cardiovascular system, respiratory system, gastrointestinal tract, and/or musculoskeletal system. A thorough history and physical examination are the first steps in evaluating such patients [5,6,11]. Among our cases, a pertinent clinical history of acute chest patient after catheter insertion via the left jugular vein was highly suggestive of catheter-induced vascular injury in patients 1 and 2. Patients 3 and 4 were victims of motor vehicle accidents, and thoracic injury with traumatic aortic rupture was initially suspected. For patient 5, acute aortic syndrome or coronary arterial disease was probable in this elderly man with a long history of hypertension.

Chest radiography has traditionally been the primary screening method for chest pain [5,11]. For patients 1 and 2, a widened mediastinum on the chest radiographs was suggestive of vascular complications, probably involving the LBCV, due to advertent central catheter penetration. Further confirmation and assessment of the site of catheter- induced venous or arterial injury, and lesion extent are important for treatment decision making [1-5]. For patients 3, 4, and 5, a widened mediastinum was evocative of traumatic aortic rupture in patients 3 and 4, and acute aortic lesion in patient 5. However, improper radiographic technique, multiple injuries, and/or altered mental status of the patient may lead to a false-positive finding [5,12,13]. In addition, patients with paraspinal hemorrhage, paramediast- inal lung contusion, a tortuous aorta, or mediastinal lipomatosis may also exhibit a widened mediastinum [6,7,12,13]. Immediate thoracic angiography based solely on abnormality found on a chest radiograph may reveal only 10% to 20% of cases that actually have aortic injury, whereas a substantial number of such Angiographic examinations

eventually turn out to be normal [12,14]. As in our cases, the LBCV lesion could hardly be disclosed, even if emergency thoracic arteriograms had been performed.

Computed tomography has been reported to be useful in evaluating traumatic and nonTraumatic causes of a widened mediastinum [1,4,5,7,11,12]. In the present study, CT was useful for confirming the presence of mediastinal hematoma in all of our cases. However, mediastinal hematomas may not necessarily be associated with aortic rupture. Nonaortic sources include mediastinal small veins; arch or thoracic cage vessels; fractures of the sternum, ribs, and spine; and, rarely, as in our cases, injury to the LBCV [1,7-9,12]. Wicky et al [1] reviewed the clinical and imaging features of 11 cases of severe vascular complica- tions after central venous catheter misplacement. Among them, 3 had LBCVP due to misplacement of a dialysis catheter through the left jugular vein. From an anatomical viewpoint, central catheter insertion via the left internal jugular vein is a potential site of perforation due to the sharp angulation (106? +- 9?) of the LBCV as it drapes over the aorta or arch vessels. A central catheter inadvertently torqued at this angulation may make direct contact with the vessel wall and even cause perforation [2,15]. Computed tomography allows definitive diagnosis when the distal tip of the catheter has coursed outside the vascular structures. Furthermore, other findings, such as pneumothorax, hemopericardium, and even life-threatening arterial injury, can be demonstrated [1]. Three-dimensional CT demonstra- tion of a case of LBCVP by a pacemaker lead with its tip positioned in between the mediastinal pleura and the parietal pericardium has recently been described [3]. In patients 1 and 2, CT was performed after the catheter was removed and the exact perforation site, presumably at the sharp angulation of the LBCV as it drapes over the aorta, could not be demonstrated. Nevertheless, CT clearly depicted the medial spread of hemorrhage via the anterior wall of the LBCV, accumulation of blood at the angulation site forming a left AMH, and subsequent caudal extension of the hematoma into the mediastinal fat anterior to the parietal pericardium.

For a widened mediastinum caused by trauma, a negative chest CT offers an approximately 100% negative predictive rate of aortic injury [4,5,12]. In contrast, using hemomediastinum as the sole CT criterion for predicting aortic injury, the positive predictive value varies from 50% to 90% for small traumatic pseudoaneurysms that may be overlooked and mediastinal hemorrhage that may be the result of leakage from a small artery or vein [4,12]. In our series, CT did not show any abnormal density around the aorta or the major arteries but it depicted a cord-like perivenous hematoma along the course of the LBCV, a left upper AMH and caudal extension of the hematoma into the lower anterior mediastinal fat in front of the parietal pericardium. Computed tomography demonstration of subtle leakage of contrast agent from the LBCV further added weight to the diagnosis of patient 3. For patient 4,

consistent with the rapid deterioration in hemodynamic status, the presence of a large left AMH with fluid-fluid level was highly suggestive of active bleeding. For patient

5 with clinical presentations mimicking acute aortic syndrome, the direct or immediate cause of LBCVP could not definitively be identified. There was no history of thoracic surgery, recent trauma, or underlying connective tissue disease. However, in this retired soldier, we postulate that prior explosive injury with blunt chest trauma might plausibly induce vascular insult, which might be a predisposing factor of LBCVP.

Surgical intervention for large mediastinal hematomas is recommended in patients with rapid clinical deterioration that may be unexpectedly fatal [1,4-8,12,13]. Patients 1, 2, and 3 had a stable clinical status and AMH of less than 5 cm in size, and they were successfully managed with conservative treatment. However, close surveillance is important in such patients and surgery is warranted if there are any signs of hemodynamic instability. The other

2 patients had rapid clinical deterioration and AMH of greater than 7 cm in size, as measured on CT. Such CT findings, especially for patient 4 with fluid-fluid level within the AMH, might be suggestive of large vascular damage and, thus, spontaneous regression is arduous. Fortunately, both patients underwent emergency surgery and recovered well.

In summary, this case series highlights that CT is helpful in diagnosing LBCVP with characteristic features including a cord-like hematoma along the course of the LBCV associated with a left upper AMH and variable degrees of caudal anterior mediastinal extension of the hematoma. Under close surveillance, stable patients with LBCVP and AMH b5 cm in size may be managed conservatively. However, emergency surgery is warranted if there are any signs of instability.

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