Injury, Int. J. Care Injured 46 (2015) 1860–1864
Contents lists available at ScienceDirect
Injury journal homepage: www.elsevier.com/locate/injury
Case Report
Successful balloon dilatation for postoperative caval stenosis caused by primary venorrhaphy for traumatic retro-hepatic caval injury in a three-year-old child: Report of a case Daisuke Masui a,*, Yasushi Iinuma a, Yutaka Hirayama a, Kohju Nitta a, Hisataka Iida a, Tetsuya Otani b, Naoyuki Yokoyama b, Seiichi Sato c, Fujito Numano c, Minoru Yagi d a
Department of Pediatric Surgery, Niigata City General Hospital, Japan Department of Digestive Surgery, Niigata City General Hospital, Japan c Department of Pediatrics, Niigata City General Hospital, Japan d Department of Pediatric Surgery, Kurume University School of Medicene, Niigata City General Hospital, Shumoku 463-7, Chuo-ku, Niigata City 950-1197, Japan b
A R T I C L E I N F O
A B S T R A C T
Article history: Accepted 13 March 2015
Inferior vena cava injuries are highly lethal. We experienced a case of retrohepatic inferior vena cava injury as a result of blunt trauma in a three-year-old female. Because the site of bleeding of the IVC was identified, we repaired it with running sutures. An attempt at primary repair resulted in postoperative narrowing of the vena cava. There was pressure gradient of the right atrium and inferior vena cava, and collateral circulation developed. Since it was also found that the haemodynamics was unstable, the child underwent another intervention before the stenosis of the IVC was fixed. To the best of our knowledge, there have been no previous reports of therapeutic radiological intervention for stenosis that developed after treatment of a traumatic IVC injury. The IVC in the present case recovered enough patency so that the collateral venous flow could be decreased after balloon dilatation angioplasty. ß 2015 Elsevier Ltd. All rights reserved.
Keywords: Paediatric Inferior vena cava injury Blunt trauma Balloon dilatation
Introduction Inferior vena cava (IVC) injuries caused by blunt trauma are rare, however, they are usually associated with high mortality, especially in children. The optimal management of patients with IVC injuries requires rapid transportation to tertiary trauma centres, aggressive fluid resuscitation, and prompt surgical repair. The prehospital mortality rate for IVC injuries is as high as 36% [1]. For patients that reach the hospital alive, the overall mortality rates range from 20% to 57% [1]. The repair of IVC injuries itself can also carry significant morbidity and mortality, and the deaths are reported to be commonly caused by intraoperative exsanguination. The survival rates for patients with IVC injuries obviously depend on the location of the injury. Infra-renal caval injury is associated with a
* Corresponding author at: Department of Pediatric Surgery, Kurume University School of Medicine, Asahi-Machi 67, Kurume, Fukuoka 830-0011, Japan. Tel.: +81 942 31 7631; fax: +81 942 31 7705. E-mail address: [email protected] (D. Masui). http://dx.doi.org/10.1016/j.injury.2015.03.032 0020–1383/ß 2015 Elsevier Ltd. All rights reserved.
mortality rate of 25%, whereas injuries between the renal veins and the hepatic veins are associated with a mortality rate of 41–55% [2]. The death rate surpasses 80% at the level of the hepatic veins or the supra-hepatic vena cava [2]. It is generally accepted that children do not tolerate these severe conditions as well as adults, therefore, the paediatric case reports describing the recovery from these lethal injuries have been limited. We herein present the case of a three-year-old female with a retro-hepatic IVC (RH-IVC) injury caused by blunt trauma, who had survived this lethal injury by undergoing primary venorrhaphy. In this case, the repaired IVC developed postoperative stenosis. The postoperative balloon dilatation angioplasty after IVC repair is also described. Case report A three-year-old, previously healthy female, was transferred to a referring institution after suffering direct abdominal compression by the family car which her mother was slowly backing in her residential parking area. The patient was temporarily unresponsive
D. Masui et al. / Injury, Int. J. Care Injured 46 (2015) 1860–1864
after this accident, and her mother initiated basic life support immediately. On presentation to the emergency department, the presence of severe liver injury was suspected. She was transferred to our hospital 2 h after the accident. At presentation to our emergency department, the patient was severely ill and her vital signs were unstable. She showed tachypnea, a pulse of 190 beats/min, peripheral coldness, and a prolonged capillary refilling time (more than 3 s). Her blood pressure could not be measured. The physical examinations revealed severe abdominal distension, tenderness and muscle guarding. Laboratory findings revealed severe anaemia (red blood cells 2.39 106 mL, Hb 7.3 g/dl), elevated aspartate aminotransferase at 515 IU/L and alanine aminotransferase at 398 IU/L. Severe metabolic acidosis (pH 7.219, BE 9.0 mEq/L, HCO3 16.7 mEq/L) and coagulopathy (31% prothrombin time) were also observed. Contrast enhanced computed tomography (CT) demonstrated massive haemorrhage in the abdominal cavity, and poor contrast enhancement with contrast extravasation from the branch of the right hepatic artery in the entire part of the right posterior hepatic lobe (Fig. 1). A collapsed IVC was also observed at the level of retrohepatic region. These findings were suspected to have resulted from the presence of an AAST (American Associations for the Surgery of Trauma) grade IV–V liver injury, and immediate laparotomy via an upper abdominal transverse skin incision was initially performed. Although a damage control surgery was scheduled, the presence of juxta-hepatic venous injuries had not been observed until the exposure of abdominal cavity was obtained. Massive haemorrhage was encountered following laparotomy and the right posterior hepatic lobe proved to be almost completely disrupted from the residual liver. This disrupted segment showed discoloration, with a complete tear of both the right posterior hepatic artery and the portal vein (Fig. 2). Therefore, resectional debridement of the segment was selected. However, continuous massive bleeding from the RH-IVC was encountered, immediately after mobilization of right posterior hepatic lobe. Two approximately 1 cm-long RH-IVC tears were then noted to be present in addition to the liver disruption. Fortunately, digital pressure could provide immediate vascular control, and subsequently, intestinal Kelly clamps were placed at both the proximal and distal extents of the tears. After this procedure, good temporary vascular control could be obtained, and complete hemostasis was obtained by using running sutures of 4-0
Fig. 1. A computed tomography scan showed massive haemorrhage in the abdominal cavity and poor contrast enhancement, with contrast extravasation from the branch of the right hepatic artery in the entire regions of the right posterior hepatic lobe.
1861
Fig. 2. The right posterior hepatic segment was already dissected and discoloured dark red.
polypropylene for the RH-IVC tears. After the establishment of hemostasis, resectional debridement for the posterior right hepatic lobe was performed. The total amount of intraoperative haemorrhage was 3550 ml. A total of 1400 ml of packed red cells, 1000 ml of fresh frozen plasma and 200 ml of platelet-rich plasma were transfused during surgery. After surgery, the patient received meticulous cardiopulmonary support in the ICU, and her vital signs could be maintained. On the first postoperative day, oliguria and severe abrupt oedema of both lower extremities and the lower trunk emerged. An ultrasound examination demonstrated the inevitable stenosis of the RH-IVC, and this oedema was considered to have resulted from the primary repair for the RH-IVC. After the administration of a diuretic agent, the oliguria and oedema gradually resolved over 2 days. Contrast enhanced CT on the 22nd postoperative day also demonstrated stenosis of the RH-IVC and the dilatation of the azygos and hemiazygos vein. Although the formation of a thrombus was not confirmed at that time, the administration of low dose aspirin (75 mg/day) was initiated to decrease the probability of future thromboembolism. After that, the postoperative course was uneventful, and the patient was discharged on the 25th postoperative day. After discharge, she occasionally complained of hot flashes at the lower trunk following bathing. Furthermore, she developed distinct venous dilatation of her abdominal surface and minor bruising which also caused the skin to become red. These changes were suspected to have resulted from the development of collateral drainage veins following the stenosis of the RH-IVC. To estimate the degree of the stenosis and the development of collateral veins, an IVC venogram (IVC-gram) was performed in 9 months after the surgery. The IVC-gram at the level just distal to the stenosis demonstrated the patency of the IVC. The minimum diameter of RH-IVC stenosis proved to be only 2 mm (Fig. 3). However, another IVC-gram at the level distal to the bilateral renal veins revealed that most of the injected contrast material finally drained to both
1862
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Fig. 3. The angiogram showed that the area with the most extensive stenosis was 2 mm in diameter (indicated with arrows). Fig. 4. An angiogram showed the presence of multiple venous collaterals to the azygos/hemiazygos vein at the height of the renal vein.
the azygos and hemiazygos veins via many lumbar veins leading to the left renal vein (Fig. 4). The pressure gradient between the distal and proximal levels to the stenosis was 4 mmHg. Although the formation of a thrombus was not detected, and the future risk of complications caused by these venous haemodynamic changes were unclear, the necessity of performing balloon dilatation angioplasty for the stenosis was debated among the attending physicians in order to prevent the possibility of late complications caused by a constant large amount of collateral venous flow. In consequence, balloon dilatation angioplasty for the stenosis was performed 10 months after the surgery. Right femoral venous access was obtained percutaneously with a 6-Fr sheath. An IVC-gram showed that the narrowest region of the IVC was 2.1 mm in diameter. We selected a Conquest balloon catheter (Bard Peripheral Vascular Inc, Tempe, AZ) to expand this lesion. Following the IVC-gram, and after guide insertion, balloon catheters with a diameter 6 mm and 8 mm (each 40 mm in length) were inserted into the IVC through the narrowest region, and were used to dilate this region (Fig. 5). We had initially performed dilatation with the 6 mm catheter at 8 atm-pressure. However, a waist was observed in the balloon, which suggested that the narrowest region could not be dilated at this pressure. After raising the balloon pressure to 12 atm, the waist portion of the balloon disappeared. Subsequently, the dilatation at 12 atm for 30 s was repeated three times. However, after this procedure, the IVC-gram still demonstrated mild stenosis of the IVC, so the catheter with a diameter 8 mm was inserted. The waist portion of the balloon disappeared at 8, 12, and 14 atm balloon pressure, respectively. The 14 atm-pressure was considered to be the maximum pressure that could be safely used
to expand the narrowest region of the IVC, therefore, the dilatation at 14 atm for 30 s was repeated three times. After these serial dilatations, the IVC-gram still demonstrated slight stenosis of the IVC, but the main venous flow and good patency of the IVC was recovered, and the blood flow to collateral veins was also reduced (Fig. 6). During this procedure, there were no complications, and balloon dilatation angioplasty for the stenosis after IVC repair was successfully accomplished. After balloon dilatation, the hot flashes following bathing, the venous dilatation of the abdominal surface and the skin colour change immediately disappeared. She has recovered a normal quality of life, and receives regular follow-up by the referring institution. Discussion To obtain vascular control for an IVC injury, various traditional procedures, such as damage control surgery (i.e. perihepatic gauze or sponge packing and delayed surgery), primary venorraphy and the ligation of the IVC have been reported [1–4]. Recently, endovascular repair or percutaneous balloon catheter occlusion have also been reported [5,6]. Anatomically, the primary repair of the IVC after obtaining total hepatic vascular isolation is the most desirable treatment, however, the management strategies are limited, especially in the emergency setting in children. There have been only a few reports that have described paediatric patients who survived this lethal condition in the literature, and these patients had received immediate primary venorraphy, ligation or damage
D. Masui et al. / Injury, Int. J. Care Injured 46 (2015) 1860–1864
Fig. 5. Dilatation was performed using balloons with diameters of 6 mm and 8 mm (indicated with an arrow).
control surgery. We believe that the present case is the youngest patient who has survived this lethal condition [7 9]. In this case, only the right posterior hepatic segment was disrupted. We speculate that this was the result of the localized shearing forces applied to this segment, which caused the tears of the corresponding site of the RH-IVC. Therefore, the exposed area of the RH-IVC was limited, and the sites of the tears may have been compressed by the disrupted liver segment for a while before laparotomy. Fortunately, the application of digital pressure could provide immediate vascular control, and subsequently primary venorraphy based on the intestinal allis clamps method was possible, as described by Henry et al. [10] The disrupted right posterior hepatic segment was almost completely devoid of perfusion, so resectional debridement was unavoidable. The primary venorraphy of the IVC caused post-operative stenosis. In cases of supra-renal ligation of the IVC, It is well known that the collaterals develop primarily through the left renal vein and its retroperitoneal tributaries [9]. The same haemodynamic changes were also observed in this case, and are considered to have been unavoidable. The documentation of postoperative complications related to the IVC repair is usually based on clinical examinations. Among the reported complications, Timberlake et al. [11] indicated that oedema of the lower extremities and trunk occurred in the early postoperative period in 35% of the patients, but that it was transient and improved with time. Other studies have documented thrombosis and pulmonary embolism rates of 7–10% and 5–7%, respectively, after primary venorrhaphy. Furthermore, transient
1863
Fig. 6. The main venous flow and good patency of the IVC was recovered.
defects in the renal function were also reported, but normalization of the renal function occurred by 1 month after the injury. Thus, many of the post-operative complications after IVC repair have been reported to be relatively uncommon, and severe complications related to this surgery have been limited, even if the vessel is narrow [1,3,8,12,13]. However, we focused on the presence of a pressure gradient between the levels distal and proximal to the stenosis. In this case, the inferior venous pressure distal to the stenosis was 4 mmHg higher than that proximal to the stenosis, which was considered to mean that the venous flow from the bilateral renal veins to the IVC was constantly subjected to outflow block pressure. We speculated that this constant condition might cause complications in the future. Furthermore, this patient underwent IVC repair when she was only three years old, therefore, the true risk of long-term complications is still unclear. We were especially concerned about the potential that a physiological increase in intra-abdominal pressure (i.e. in case of a future pregnancy) might adversely affect her health due to the large amount of collateral venous flow. Therefore, in consideration of the patient’s youth, we believed that radical correction of the haemodynamic changes to restore a more normal condition was necessary, and we proceeded with balloon dilatation angioplasty for the stenosis 10 months after the surgery, in addition to the administration of low dose aspirin as an anticoagulant. Several reports of therapeutic radiological intervention in cases of Budd–Chiari syndrome have been documented [14,15].
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However, to the best of our knowledge the application of balloon dilatation angioplasty for stenosis after IVC repair in trauma patients has not been reported previously. The balloon dilatation angioplasty was safely performed, and the IVC subsequently recovered enough patency that there was also a decrease in the collateral venous flow, with only slight residual stenosis. The efficacy of this procedure has been clinically confirmed, and a second balloon dilation has not been necessary. However, meticulous follow-up will be needed regarding the patency of the IVC and the possible need for second balloon dilatation angioplasty. The indications for, timing of and choice of balloon dilatation angioplasty for treating stenosis after IVC repair in trauma patients are still unclear. Even without our group of consulting physicians, there was much controversy regarding the indications for this procedure based on the patient’s postoperative condition. Therefore, further studies and the accumulation of other cases will be needed to estimate the significance and the necessity of our management. Conflicts of interest The authors declare that there are no conflicts of interest. Acknowledgement The authors thank Brian Quinn, Japan Medical Communication, for his critical reading of the manuscript.
References [1] Ochsner JL, Crawford ES, De Bakey ME. Injuries of the vena cava caused by external trauma. Surgery 1961;49:397–405. [2] Ivy ME, Possenti P, Atweh N, Sawyer M, Bryant G, Caushaj P. Ligation of the suprarenal vena cava after a gunshot wound. J Trauma 1998;45:630–2. [3] Klein SR, Baumgartner FJ, Bongard FS. Contemporary management strategy for major inferior vena caval injuries. J Trauma 1994;37:35–41. [4] Losty PD, Okoye BO, Walter DP, Turnock RR, Lloyd DA. Management of blunt liver trauma in children. Br J Surg 1997;84:1006–8. [5] Castelli P, Caronno R, Piffaretti G, Tozzi M. Emergency endovascular repair for traumatic injury of the inferior vena cava. Eur J Cardiothorac Surg 2005;28:906–8. [6] Bui TD, Mills JL. Control of inferior vena cava injury using percutaneous balloon catheter occlusion. Vasc Endovasc Surg 2009;43:490–3. [7] Schmidt B, Schimpl G, Hollwarth ME. Blunt liver trauma in children. Pediatr Surg Int 2004;20:846–50. [8] Decou JM, Abrams RS, Gauderer MW. Seat-belt transection of the pararenal vena cava in a 5-year-old child: survival with caval ligation. J Pediatr Surg 1999;34:1074–6. [9] Gazzaniga AB, Colodny AH. Long-term survival after acute ligation of the vena cava above the renal veins. Ann Surg 1972;175:563–8. [10] Henry SM, Duncan AO, Scalea TM. Intestinal allis clamps as temporary vascular control for major retroperitoneal venous injury. J Trauma 2001;51:170–2. [11] Timberlake GA, Kerstein MD. Venous injury: to repair or ligate, the dilemma revisited. Am Surg 1995;61:139–45. [12] Carr JA, Kralovich KA, Patton JH, Horst HM. Primary venorrhaphy for traumatic inferior vena cava injuries. Am Surg 2001;67:207–13. [13] Burch JM, Feliciano DV, Mattox KL, Edelman M. Injuries of the inferior vena cava. Am J Surg 1988;156:548–52. [14] Meng Q-Y, Sun N-F, Wang J-X, Wang R-H, Liu Z-X. Endovascular treatment of Budd–Chiari syndrome. Chin Med J 2011;124:3289–92. [15] Nagral A, Hasija RP, Marar S, Nabi F. Budd–Chiari syndrome in children: experience with therapeutic radiological intervention. J Pediatr Gastroenterol Nutr 2010;50:74–8.
Contents lists available at ScienceDirect
Injury journal homepage: www.elsevier.com/locate/injury
Case Report
Successful balloon dilatation for postoperative caval stenosis caused by primary venorrhaphy for traumatic retro-hepatic caval injury in a three-year-old child: Report of a case Daisuke Masui a,*, Yasushi Iinuma a, Yutaka Hirayama a, Kohju Nitta a, Hisataka Iida a, Tetsuya Otani b, Naoyuki Yokoyama b, Seiichi Sato c, Fujito Numano c, Minoru Yagi d a
Department of Pediatric Surgery, Niigata City General Hospital, Japan Department of Digestive Surgery, Niigata City General Hospital, Japan c Department of Pediatrics, Niigata City General Hospital, Japan d Department of Pediatric Surgery, Kurume University School of Medicene, Niigata City General Hospital, Shumoku 463-7, Chuo-ku, Niigata City 950-1197, Japan b
A R T I C L E I N F O
A B S T R A C T
Article history: Accepted 13 March 2015
Inferior vena cava injuries are highly lethal. We experienced a case of retrohepatic inferior vena cava injury as a result of blunt trauma in a three-year-old female. Because the site of bleeding of the IVC was identified, we repaired it with running sutures. An attempt at primary repair resulted in postoperative narrowing of the vena cava. There was pressure gradient of the right atrium and inferior vena cava, and collateral circulation developed. Since it was also found that the haemodynamics was unstable, the child underwent another intervention before the stenosis of the IVC was fixed. To the best of our knowledge, there have been no previous reports of therapeutic radiological intervention for stenosis that developed after treatment of a traumatic IVC injury. The IVC in the present case recovered enough patency so that the collateral venous flow could be decreased after balloon dilatation angioplasty. ß 2015 Elsevier Ltd. All rights reserved.
Keywords: Paediatric Inferior vena cava injury Blunt trauma Balloon dilatation
Introduction Inferior vena cava (IVC) injuries caused by blunt trauma are rare, however, they are usually associated with high mortality, especially in children. The optimal management of patients with IVC injuries requires rapid transportation to tertiary trauma centres, aggressive fluid resuscitation, and prompt surgical repair. The prehospital mortality rate for IVC injuries is as high as 36% [1]. For patients that reach the hospital alive, the overall mortality rates range from 20% to 57% [1]. The repair of IVC injuries itself can also carry significant morbidity and mortality, and the deaths are reported to be commonly caused by intraoperative exsanguination. The survival rates for patients with IVC injuries obviously depend on the location of the injury. Infra-renal caval injury is associated with a
* Corresponding author at: Department of Pediatric Surgery, Kurume University School of Medicine, Asahi-Machi 67, Kurume, Fukuoka 830-0011, Japan. Tel.: +81 942 31 7631; fax: +81 942 31 7705. E-mail address: [email protected] (D. Masui). http://dx.doi.org/10.1016/j.injury.2015.03.032 0020–1383/ß 2015 Elsevier Ltd. All rights reserved.
mortality rate of 25%, whereas injuries between the renal veins and the hepatic veins are associated with a mortality rate of 41–55% [2]. The death rate surpasses 80% at the level of the hepatic veins or the supra-hepatic vena cava [2]. It is generally accepted that children do not tolerate these severe conditions as well as adults, therefore, the paediatric case reports describing the recovery from these lethal injuries have been limited. We herein present the case of a three-year-old female with a retro-hepatic IVC (RH-IVC) injury caused by blunt trauma, who had survived this lethal injury by undergoing primary venorrhaphy. In this case, the repaired IVC developed postoperative stenosis. The postoperative balloon dilatation angioplasty after IVC repair is also described. Case report A three-year-old, previously healthy female, was transferred to a referring institution after suffering direct abdominal compression by the family car which her mother was slowly backing in her residential parking area. The patient was temporarily unresponsive
D. Masui et al. / Injury, Int. J. Care Injured 46 (2015) 1860–1864
after this accident, and her mother initiated basic life support immediately. On presentation to the emergency department, the presence of severe liver injury was suspected. She was transferred to our hospital 2 h after the accident. At presentation to our emergency department, the patient was severely ill and her vital signs were unstable. She showed tachypnea, a pulse of 190 beats/min, peripheral coldness, and a prolonged capillary refilling time (more than 3 s). Her blood pressure could not be measured. The physical examinations revealed severe abdominal distension, tenderness and muscle guarding. Laboratory findings revealed severe anaemia (red blood cells 2.39 106 mL, Hb 7.3 g/dl), elevated aspartate aminotransferase at 515 IU/L and alanine aminotransferase at 398 IU/L. Severe metabolic acidosis (pH 7.219, BE 9.0 mEq/L, HCO3 16.7 mEq/L) and coagulopathy (31% prothrombin time) were also observed. Contrast enhanced computed tomography (CT) demonstrated massive haemorrhage in the abdominal cavity, and poor contrast enhancement with contrast extravasation from the branch of the right hepatic artery in the entire part of the right posterior hepatic lobe (Fig. 1). A collapsed IVC was also observed at the level of retrohepatic region. These findings were suspected to have resulted from the presence of an AAST (American Associations for the Surgery of Trauma) grade IV–V liver injury, and immediate laparotomy via an upper abdominal transverse skin incision was initially performed. Although a damage control surgery was scheduled, the presence of juxta-hepatic venous injuries had not been observed until the exposure of abdominal cavity was obtained. Massive haemorrhage was encountered following laparotomy and the right posterior hepatic lobe proved to be almost completely disrupted from the residual liver. This disrupted segment showed discoloration, with a complete tear of both the right posterior hepatic artery and the portal vein (Fig. 2). Therefore, resectional debridement of the segment was selected. However, continuous massive bleeding from the RH-IVC was encountered, immediately after mobilization of right posterior hepatic lobe. Two approximately 1 cm-long RH-IVC tears were then noted to be present in addition to the liver disruption. Fortunately, digital pressure could provide immediate vascular control, and subsequently, intestinal Kelly clamps were placed at both the proximal and distal extents of the tears. After this procedure, good temporary vascular control could be obtained, and complete hemostasis was obtained by using running sutures of 4-0
Fig. 1. A computed tomography scan showed massive haemorrhage in the abdominal cavity and poor contrast enhancement, with contrast extravasation from the branch of the right hepatic artery in the entire regions of the right posterior hepatic lobe.
1861
Fig. 2. The right posterior hepatic segment was already dissected and discoloured dark red.
polypropylene for the RH-IVC tears. After the establishment of hemostasis, resectional debridement for the posterior right hepatic lobe was performed. The total amount of intraoperative haemorrhage was 3550 ml. A total of 1400 ml of packed red cells, 1000 ml of fresh frozen plasma and 200 ml of platelet-rich plasma were transfused during surgery. After surgery, the patient received meticulous cardiopulmonary support in the ICU, and her vital signs could be maintained. On the first postoperative day, oliguria and severe abrupt oedema of both lower extremities and the lower trunk emerged. An ultrasound examination demonstrated the inevitable stenosis of the RH-IVC, and this oedema was considered to have resulted from the primary repair for the RH-IVC. After the administration of a diuretic agent, the oliguria and oedema gradually resolved over 2 days. Contrast enhanced CT on the 22nd postoperative day also demonstrated stenosis of the RH-IVC and the dilatation of the azygos and hemiazygos vein. Although the formation of a thrombus was not confirmed at that time, the administration of low dose aspirin (75 mg/day) was initiated to decrease the probability of future thromboembolism. After that, the postoperative course was uneventful, and the patient was discharged on the 25th postoperative day. After discharge, she occasionally complained of hot flashes at the lower trunk following bathing. Furthermore, she developed distinct venous dilatation of her abdominal surface and minor bruising which also caused the skin to become red. These changes were suspected to have resulted from the development of collateral drainage veins following the stenosis of the RH-IVC. To estimate the degree of the stenosis and the development of collateral veins, an IVC venogram (IVC-gram) was performed in 9 months after the surgery. The IVC-gram at the level just distal to the stenosis demonstrated the patency of the IVC. The minimum diameter of RH-IVC stenosis proved to be only 2 mm (Fig. 3). However, another IVC-gram at the level distal to the bilateral renal veins revealed that most of the injected contrast material finally drained to both
1862
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Fig. 3. The angiogram showed that the area with the most extensive stenosis was 2 mm in diameter (indicated with arrows). Fig. 4. An angiogram showed the presence of multiple venous collaterals to the azygos/hemiazygos vein at the height of the renal vein.
the azygos and hemiazygos veins via many lumbar veins leading to the left renal vein (Fig. 4). The pressure gradient between the distal and proximal levels to the stenosis was 4 mmHg. Although the formation of a thrombus was not detected, and the future risk of complications caused by these venous haemodynamic changes were unclear, the necessity of performing balloon dilatation angioplasty for the stenosis was debated among the attending physicians in order to prevent the possibility of late complications caused by a constant large amount of collateral venous flow. In consequence, balloon dilatation angioplasty for the stenosis was performed 10 months after the surgery. Right femoral venous access was obtained percutaneously with a 6-Fr sheath. An IVC-gram showed that the narrowest region of the IVC was 2.1 mm in diameter. We selected a Conquest balloon catheter (Bard Peripheral Vascular Inc, Tempe, AZ) to expand this lesion. Following the IVC-gram, and after guide insertion, balloon catheters with a diameter 6 mm and 8 mm (each 40 mm in length) were inserted into the IVC through the narrowest region, and were used to dilate this region (Fig. 5). We had initially performed dilatation with the 6 mm catheter at 8 atm-pressure. However, a waist was observed in the balloon, which suggested that the narrowest region could not be dilated at this pressure. After raising the balloon pressure to 12 atm, the waist portion of the balloon disappeared. Subsequently, the dilatation at 12 atm for 30 s was repeated three times. However, after this procedure, the IVC-gram still demonstrated mild stenosis of the IVC, so the catheter with a diameter 8 mm was inserted. The waist portion of the balloon disappeared at 8, 12, and 14 atm balloon pressure, respectively. The 14 atm-pressure was considered to be the maximum pressure that could be safely used
to expand the narrowest region of the IVC, therefore, the dilatation at 14 atm for 30 s was repeated three times. After these serial dilatations, the IVC-gram still demonstrated slight stenosis of the IVC, but the main venous flow and good patency of the IVC was recovered, and the blood flow to collateral veins was also reduced (Fig. 6). During this procedure, there were no complications, and balloon dilatation angioplasty for the stenosis after IVC repair was successfully accomplished. After balloon dilatation, the hot flashes following bathing, the venous dilatation of the abdominal surface and the skin colour change immediately disappeared. She has recovered a normal quality of life, and receives regular follow-up by the referring institution. Discussion To obtain vascular control for an IVC injury, various traditional procedures, such as damage control surgery (i.e. perihepatic gauze or sponge packing and delayed surgery), primary venorraphy and the ligation of the IVC have been reported [1–4]. Recently, endovascular repair or percutaneous balloon catheter occlusion have also been reported [5,6]. Anatomically, the primary repair of the IVC after obtaining total hepatic vascular isolation is the most desirable treatment, however, the management strategies are limited, especially in the emergency setting in children. There have been only a few reports that have described paediatric patients who survived this lethal condition in the literature, and these patients had received immediate primary venorraphy, ligation or damage
D. Masui et al. / Injury, Int. J. Care Injured 46 (2015) 1860–1864
Fig. 5. Dilatation was performed using balloons with diameters of 6 mm and 8 mm (indicated with an arrow).
control surgery. We believe that the present case is the youngest patient who has survived this lethal condition [7 9]. In this case, only the right posterior hepatic segment was disrupted. We speculate that this was the result of the localized shearing forces applied to this segment, which caused the tears of the corresponding site of the RH-IVC. Therefore, the exposed area of the RH-IVC was limited, and the sites of the tears may have been compressed by the disrupted liver segment for a while before laparotomy. Fortunately, the application of digital pressure could provide immediate vascular control, and subsequently primary venorraphy based on the intestinal allis clamps method was possible, as described by Henry et al. [10] The disrupted right posterior hepatic segment was almost completely devoid of perfusion, so resectional debridement was unavoidable. The primary venorraphy of the IVC caused post-operative stenosis. In cases of supra-renal ligation of the IVC, It is well known that the collaterals develop primarily through the left renal vein and its retroperitoneal tributaries [9]. The same haemodynamic changes were also observed in this case, and are considered to have been unavoidable. The documentation of postoperative complications related to the IVC repair is usually based on clinical examinations. Among the reported complications, Timberlake et al. [11] indicated that oedema of the lower extremities and trunk occurred in the early postoperative period in 35% of the patients, but that it was transient and improved with time. Other studies have documented thrombosis and pulmonary embolism rates of 7–10% and 5–7%, respectively, after primary venorrhaphy. Furthermore, transient
1863
Fig. 6. The main venous flow and good patency of the IVC was recovered.
defects in the renal function were also reported, but normalization of the renal function occurred by 1 month after the injury. Thus, many of the post-operative complications after IVC repair have been reported to be relatively uncommon, and severe complications related to this surgery have been limited, even if the vessel is narrow [1,3,8,12,13]. However, we focused on the presence of a pressure gradient between the levels distal and proximal to the stenosis. In this case, the inferior venous pressure distal to the stenosis was 4 mmHg higher than that proximal to the stenosis, which was considered to mean that the venous flow from the bilateral renal veins to the IVC was constantly subjected to outflow block pressure. We speculated that this constant condition might cause complications in the future. Furthermore, this patient underwent IVC repair when she was only three years old, therefore, the true risk of long-term complications is still unclear. We were especially concerned about the potential that a physiological increase in intra-abdominal pressure (i.e. in case of a future pregnancy) might adversely affect her health due to the large amount of collateral venous flow. Therefore, in consideration of the patient’s youth, we believed that radical correction of the haemodynamic changes to restore a more normal condition was necessary, and we proceeded with balloon dilatation angioplasty for the stenosis 10 months after the surgery, in addition to the administration of low dose aspirin as an anticoagulant. Several reports of therapeutic radiological intervention in cases of Budd–Chiari syndrome have been documented [14,15].
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However, to the best of our knowledge the application of balloon dilatation angioplasty for stenosis after IVC repair in trauma patients has not been reported previously. The balloon dilatation angioplasty was safely performed, and the IVC subsequently recovered enough patency that there was also a decrease in the collateral venous flow, with only slight residual stenosis. The efficacy of this procedure has been clinically confirmed, and a second balloon dilation has not been necessary. However, meticulous follow-up will be needed regarding the patency of the IVC and the possible need for second balloon dilatation angioplasty. The indications for, timing of and choice of balloon dilatation angioplasty for treating stenosis after IVC repair in trauma patients are still unclear. Even without our group of consulting physicians, there was much controversy regarding the indications for this procedure based on the patient’s postoperative condition. Therefore, further studies and the accumulation of other cases will be needed to estimate the significance and the necessity of our management. Conflicts of interest The authors declare that there are no conflicts of interest. Acknowledgement The authors thank Brian Quinn, Japan Medical Communication, for his critical reading of the manuscript.
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