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Ann Thorac Surg 2011;92:1510-1512. doi:10.1016/j.athoracsur.2011.03.125
© 2011 The Society of Thoracic Surgeons

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Case Reports

Repair of Lacerated Intrapericardial Inferior Vena Cava After Cardiac Massage

Ichiro Kashima, MD*, Yoshihiko Mochizuki, MD, Masahiko Okamoto, MD

Department of Cardiovascular Surgery, Ashikaga Red Cross Hospital, Ashikaga, Tochigi, Japan

Accepted for publication March 25, 2011.

* Address correspondence to Dr Kashima, Department of Cardiovascular Surgery, Ashikaga Red Cross Hospital, 3-2100, Honjyo, Ashikaga, Tochigi, 326-0808 Japan (Email: i.kashima{at}ashikaga.jrc.or.jp).


    Abstract
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We successfully undertook surgical treatment of intrapericardial laceration of the inferior vena cava caused by external cardiac massage in a patient with acute coronary syndrome. Injury to the inferior vena cava without blunt trauma is very rare, and diagnostic imaging does not show it clearly, making it difficult to diagnose. Rapid and accurate judgment and management are necessary, because the mortality due to this injury is very high.


    Introduction
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Blunt trauma resulting in injury to the inferior vena cava (IVC) is rare but serious, and leads to critically hemodynamic instability with high mortality [1, 2]. It is difficult to diagnose, because diagnostic imaging techniques, such as computed tomography (CT), usually only show indirect signs [1]. As a result this injury seldom comes to mind, especially in patients who have successfully been resuscitated from a life-threatening disease. We report a case of surgical repair of intrapericardial laceration of the IVC caused by external cardiac massage in a patient with acute coronary syndrome.

A 71-year-old man became unconscious and fell at home. During transport by ambulance his pulse ceased to be detectable, and he received cardiac massage by the emergency and rescue team. On arrival in the hospital, his heartbeat recovered and he regained consciousness. An echocardiogram and CT scan revealed pericardial effusion, but showed no sign of aortic dissection or IVC injury (Fig 1). His electrical cardiogram did not show typical ischemic change, but it was speculated that he had acute coronary syndrome, because there was a slight elevation of creatine phosphokinase and creatine phosphokinase-MB levels. An emergency coronary arteriogram revealed total occlusion at the basal portion of the right coronary. The patient's hemodynamics became unstable, with pericardial fluid augmentation, according to echocardiogram, and he was transported to our institution with a primary diagnosis of cardiac tamponade due to oozing rupture of infarcted tissue. On arrival in the emergency room of our hospital, he was alert, oriented, and complained of dyspnea. His blood pressure was 88/65 mm Hg, with a pulse rate of 92 beats per minute, and a respiratory rate of 18 per minute. Laboratory findings included a white blood cell count of 14,700 per mL, hemoglobin at 12.1 g/dL, creatine at 1.06 mg/dL, creatine phosphokinase of 621 IU/L, creatine phosphokinase-MB (M = muscle type; B = brain type) of 75 IU/L, and a positive result of cardiac troponin assay. An echocardiogram confirmed cardiac tamponade with near-circumferential pericardial fluid exceeding 20 mm.


Figure 1
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Fig 1. Computed tomographic scan of the arterial phase at the primary hospital shows intrapericardial effusion and physiologic reflux in the inferior vena cava, without any sign of extravasation (arrow).

 
The patient was immediately taken to the operating room where a median sternotomy was performed. When the intrapericardial hematoma was removed after the pericardiotomy, there was rapid egress of dark unclotted blood from the dorsal side. There was no oozing from the surface of the infarcted myocardium, but a lacerated injury of the IVC was identified at the cava-atrium junction. Cardiopulmonary bypass was appropriate because it was not possible to control the hemorrhage by direct application of pressure by the surgeon's finger, and therefore the hemodynamics were unstable. On closer inspection, three laceration injuries were confirmed in the IVC (Fig 2). The lacerated foramens were repaired with pledgeted 4-0 polypropylene sutures. Coronary revascularization was not performed, because rescue was the priority of this surgery. After the operation, the man recovered uneventfully. After 14 days he was moved to a psychiatric ward for management of his alcohol dependence.


Figure 2
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Fig 2. The operative schema shows three laceration injuries of approximately 1 cm in the right, left, and back side of the inferior vena cava at its junction with the right atrium.

 

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A tear of the inferior vena cava at its junction with the right atrium after external cardiac massage has been reported after autopsy, [3] but we did not find any literature regarding the surgical repair for it. In general, diagnosis of blunt caval injury is troublesome, and CT scans only show indirect or subtle signs of caval injury such as peri-caval effusion or a filling defect in the IVC, apart from one case report diagnosed by CT of an intrapericardial blunt rupture of the IVC [1, 4]. In our case, enhanced CT scanning took place only at the arterial phase in the primary hospital. The CT image of the venous phase might show direct signs of extravasation of intrapericardial IVC.

According to the literature, blunt injury to the intrapericardial IVC can be caused in a variety of ways. These include rapid acceleration–deceleration movements, because the heart is displaced anteroposteriorly against the IVC, fixed by the diaphragm [5, 6]. This is not uncommon in motor vehicle crashes, but in the present case the cause was powerful external cardiac massage.

A median sternotomy must be performed for appropriate exposure of the injury to the intrapericardial IVC for surgical management. If the hemorrhaging is uncontrollable by direct pressure, clamping the IVC or continuous suction of the bleeding is appropriate by using an atrial caval active shunt or by cardiac pulmonary bypass to permit repair by stitching. In the present case, compression of the cava-atrial junction after the primary closure was not seen on the operative transesophageal echocardiographic image. It is important to ascertain that there is no significant gradient across the repair. When stenosis is involved, a patch repair is a good option to avoid venous congestion below the diaphragm. Soon after the onset, it is difficult to make and confirm the diagnosis, because of the relatively stable hemodynamics and unclear indications from diagnostic imaging. Consequently, this injury seldom comes to mind as a cause of the symptoms, especially in patients who have successfully been resuscitated and do not have traumatic injury. However, the mortality of blunt traumas of an IVC is a sobering 50% to 100% [1, 7]; therefore, rapid and accurate judgment and remedy are necessary in these cases.

In conclusion, it is important to take injury of the intrapericardial IVC into consideration, even if there is no obvious sign of extravasation in diagnostic imaging whenever severe pericardial effusion occurs after external cardiac massage.


    References
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  1. Netto FA, Tien H, Hamilton P, et al. Diagnosis and outcome of blunt caval injuries in the modern trauma center J Trauma 2006;61:1053-1057.[Medline]
  2. Fey GL, Deren MM, Wesolek JH. Intrapericardial caval injury due to blunt trauma Conn Med 1999;63:259-260.[Medline]
  3. Jude JR, Kouwenhoven WB, Knickerbocker GG. Cardiac arrest JAMA 1961;178:1063-1070.[Medline]
  4. Chaumoitre K, Zappa M, Portier F, Panuel M. Rupture of the right atrium-superior vena cava junction from blunt thoracic trauma: helical CT diagnosis AJR 1997;169:1753.[Medline]
  5. Park CS, Wesselhoeft Jr CW. Blunt traumatic laceration of the suprahepatic inferior vena cava presenting as abdominal pain and shock in child: a case report J Trauma 1995;38:68-69.[Medline]
  6. Parmley LF, Manion TW, Mattingly WC. Nonpenetrating traumatic injury of the heart Circulation 1958;18:371-396.[Abstract/Free Full Text]
  7. Huerta S, Dolich MO, Cohen AJ. Blunt trauma to the intrapericardial inferior vena cava: a case report and review of the literature Injury Extra 2005;36:337-340.




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