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19. Irving SP: Spontaneous regression of a dentigerous cyst in a middle-aged adult. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 57:604, 1984 20. Liu B, Yu S-F, Li T-J: Multinucleated giant cells in various forms of giant cell containing lesions of the jaws express features of osteoclasts. J Oral Pathol Med 32:367, 2003 21. Itonaga I, Hussein I, Kudo O, et al: Cellular mechanisms of osteoclast formation and lacunar resorption in giant cell granuloma of the jaw. J Oral Pathol Med 32:224, 2003

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22. Trombelli L, Farina R, Marzola A, Bozzi L, Liljenberg B, Lindhe J: Modeling and remodeling of human extraction sockets. J Clin Periodontol 35:630, 2008 23. Chiba I, Teb BG, Iizuka T, et al: Conversion of a traumatic bone cyst into central giant cell granuloma: Implications for pathogenesisA case report. J Oral Maxillofac Surg 60:222, 2002 24. Kaban LB, Troulis MJ, Ebb D, August M, Hornicek FJ, Dodson TB: Antiangiogenic therapy with interferon alpha for giant cell lesions of the jaws. J Oral Maxillofac Surg 60:1103, 2002
J Oral Maxillofac Surg 67:1547-1551, 2009

Massive Hemorrhage During Oral and Maxillofacial Surgery: Ligation of the External Carotid Artery or Embolization?
Gary F. Bouloux, MD, DDS, MDSc, FRACDS(OMS),* and Vincent J. Perciaccante, DDS
Major hemorrhage during maxillofacial surgery is an uncommon but potentially life-threatening problem. The surgical procedures most readily associated with acute hemorrhage typically involve orthognathic surgery oncology, pathology, and the temporomandibular joint. When acute hemorrhage is encountered, the surgeon must remain calm, temporarily arrest the bleeding, and ultimately denitively control the hemorrhage. Although ligation of the offending artery, vein, or vascular malformation is clearly the treatment of choice, identifying the offending vessel and gaining adequate access to it are often difcult or impossible to perform. In these situations, although temporary arrest of the bleeding is usually possible with packing and pressure, denitive control of the bleeding has historically been achieved with either ligation of the external carotid artery (ECA) or selective embolization. The choice is often determined more by the availability of a skilled interventional radiologist procient in angiography and embolization and the ability of the surgeon to perform ligation of the ECA. When both modalities are available, the choice can be more problematic. Considerable controversy still exists as to which modality is the most efcacious and least morbid. Ligation of the ECA comprises a rather heterogeneous group of procedures. Whereas all involve ligation of the proximal portion of the ECA immediately distal to the bifurcation, a variable number of the branches of the ECA may also be ligated. Ligation of several branches of the ECA reduces collateral blood ow and hence contributes signicantly to the arrest of bleeding. This necessitates a more superior dissection to the level of the digastric muscle and the hypoglossal nerve. Selective embolization of bleeding vessels requires catheterization of the femoral artery, angiography to identify the bleeding vessel, and deposition of a thrombogenic agent. The latter may include a variety of substances including polymethyl methacrylate, polyvinyl alcohol, cyanoacrylate, gelatin, silicone, cotton, metal coils, and autologous blood and muscle. Embolization may not be possible if the bleeding vessel is excessively tortuous, small, or in vasospasm. Embolization usually provides the opportunity to arrest bleeding much closer to the site of vessel injury than does ligation. The clinical importance of this, however, is a source of debate and controversy. The following 3 cases illustrate the application of both ECA ligation and selective embolization.

*Chief, Grady Memorial Hospital, and Assistant Professor, Department of Oral and Maxillofacial Surgery, Emory University School of Medicine, Atlanta, GA. Clinical Assistant Professor, Department of Oral and Maxillofacial Surgery, Emory University School of Medicine, Atlanta, GA; and Private Practice, Fayetteville, GA. Address correspondence and reprint requests to Dr Bouloux: Department of Oral and Maxillofacial Surgery, Emory University School of Medicine, 1365B Clifton Rd NE, Suite 2300, Atlanta, GA 30322; e-mail: gbouloux@hotmail.com
2009 American Association of Oral and Maxillofacial Surgeons

0278-2391/09/6707-0032$36.00/0 doi:10.1016/j.joms.2009.03.014

1548

MASSIVE HEMORRHAGE DURING SURGERY lope was perforated posteriorly and the bleeding vessel retracted beyond the periosteal envelope. Concern for injury to the facial nerve limited thorough exploration of the area. The wound was packed, the corticotomies were completed, and the sagittal split was accomplished, which permitted greater access to the area of bleeding. Through the sagittal split, the area of bleeding was difcult to identify, although an area was identied and clipped with mediumsized Hemoclips (Teleex Medical, Research Triangle Park, NC). The bleeding stopped at this point, and the contralateral sagittal split was completed. While the patient was being wired into intermaxillary xation, bleeding again resumed on the right side. The only way the bleeding could be stopped was by use of direct pressure. A decision to ligate the ECA was then made. A vertical incision was made in the skin of the right neck, and dissection was carried along the anterior border of the sternocleidomastoid muscle, which was reected laterally. The common carotid artery, internal jugular vein, and vagus nerve were identied. The ECA was ligated at its origin with No. 2 silk, as was the superior thyroid artery. Dissection proceeded superiorly along the ECA with ligation of the next 2 proximal branches, most likely the ascending pharyngeal and lingual arteries. Doppler examination showed cessation of ow in the ECA. Intraoral hemorrhage ceased immediately with completion of the ligation. Total blood loss was 3,500 mL, requiring 12 L of crystalloid, 4 U of whole blood, 1 U of fresh-frozen plasma, and 1 L of albumin. The patients recovery was uneventful. CASE 3 A 17-year-old male patient with a vascular malformation of the left face and chronically infected third molar teeth required the removal of all third molar teeth. A computed tomography scan with contrast was performed. An enhancing soft tissue mass was present along the left lateral and anterior maxilla measuring 3 2 cm. Inferiorly, the mass extended to the soft tissue of the left cheek overlying the mandible. Multiple enhancing vessels were seen that extended into the pterygomasseteric space. The largest enhancing channel, likely a draining vein, measured approximately 1.6 cm in diameter. Enlargement of the masseter, medial, and lateral pterygoid muscles was noted, and a 1-cm phlebolith was present within the masseter muscle at the level of the mid ramus. Draining vessels extended posteriorly to the skull base in the region of the left internal jugular vein, superiorly about the pterygoid plexus of veins at the level of the pterygopalatine fossa, and superiorly to the left inferior-lateral orbit, where additional, abnormally distended vessels and probable abnormal soft tissue were present. This mass of vessels and soft tissue occupied a space measuring approximately 2 1.5 cm in the inferior, lateral, and posterior orbit. On the day of surgery, the patient was rst taken to the interventional radiology department, and an arteriogram was obtained for the purpose of evaluating the lesion. The lesion was noted to be low ow with late venous lling. No embolization was deemed necessary; however, the femoral catheter sheath was left in place. The patient was taken to the operating room for surgical removal of 4 impacted, infected third molars. Upon incision into normal-appearing tissue in the left maxilla, for access to the upper left third molar, bleeding was noted to be extensive from the soft tissue. The wound was packed. Multiple attempts were made to stem the bleeding by use of electrocautery, packing, and suturing. Packing maintained hemostasis; however, as soon as the packing was removed,

Report of Cases
CASE 1 A 43-year-old woman with bilateral temporomandibular joint bony ankylosis was scheduled to undergo a 2-stage surgical procedure. Stage I involved bilateral gap arthroplasties and coronoidectomies, whereas stage II would involve insertion of bilateral custom temporomandibular joint prostheses 6 weeks later. During stage I surgery, a standard preauricular incision was made and the bony ankylosis well exposed. Channel retractors were placed anteriorly and posteriorly adjacent to the proposed area of bony resection. A No. 701 ssure bur was used to perform the superior ostectomy. During removal of the most medial bone, a signicant arterial bleed was encountered. Temporary control was obtained with gauze and lap sponges. Pressure was maintained for 15 minutes, after which the gauze and sponges were removed with immediate resumption of profuse bleeding. Direct access to the bleeding vessel was not possible at this point. A decision was then made to ligate the ECA. A retromandibular incision was made extending inferiorly along the anterior border of the sternocleidomastoid muscle. Dissection proceeded with identication of the common carotid artery, internal carotid artery (ICA), and ECA as well as the vagus nerve. Superiorly, the hypoglossal nerve was visualized. The ECA was then ligated with silk sutures immediately after the bifurcation. Ligation of the superior thyroid, ascending pharyngeal, and lingual arteries was also performed to reduce collateral ow. Upon completion of this, the gauze and sponges were removed from the preauricular wound with immediate and profuse return of bleeding that did not appear to have been reduced. Accordingly, the wound was repacked with immediate cessation of bleeding. A decision was then made to perform gap arthroplasty and coronoidectomy on the contralateral side, which was completed without complication. Attention was then directed back to the side of the bleeding. A second ostectomy was rapidly performed 20 mm inferior to the rst. This was performed with gauze packed as best as possible superiorly to minimize ongoing bleeding from the rst ostectomy site. Osteotomes were then inserted into both ostectomy sites and twisted. This separated the bone at both locations, allowing for immediate delivery of the 20-mm section of bone. Profuse hemorrhage was encountered from the medial aspect. The source of the bleeding was identied as the middle meningeal artery, which was ligated inferiorly and superiorly immediately before entrance into the foramen spinosum and the middle cranial fossa. All bleeding ceased immediately. Total blood loss was 2,000 mL. The remainder of the procedure was then completed without difculty. Throughout the procedure, vital signs remained stable and a total of 3 U of packed red blood cells, 1 L of Hespan (Braun Inc, Bethlehem, PA), and 4 L of crystalloid were transfused. The postoperative course was uneventful. CASE 2 A 17-year-old healthy female patient with mandibular hyperplasia and retrogenia was taken to the operating room for bilateral sagittal split osteotomy setback and sliding advancement genioplasty. After completion of the medial corticotomy on the right side, attention was directed to the lateral cortex. At this time, excessive hemorrhage was seen coming from the medial dissection. Repeated attempts were made to identify the source of the bleeding, but these were not successful. It is believed that the periosteal enve-

BOULOUX AND PERCIACCANTE signicant bleeding resumed. The patient was taken back to the interventional radiology department, where embolization of the left internal maxillary artery, the left ascending pharyngeal artery, and the left facial artery was performed with polyvinyl alcohol particles ranging from 355 to 500 m in size. Embolization was continued until there was cessation of ow within these vessels. Removal of the packing resulted in continued profuse bleeding. A decision was then made to ligate the ECA. This was performed in the manner as described in case 2. At the completion of this, bleeding was noted to be reduced but continued to be problematic. Attention was directed back into the oral cavity, and the wound was again addressed locally by use of packing. The wound was packed with absorbable collagen hemostat material and oversewn with silk. Hemostasis was obtained. The remainder of the procedure was aborted. Total blood loss was estimated to be 2,000 mL and required 5 L of crystalloid. No blood products were transfused. The postoperative course was uneventful.

1549 tic modality inherently less predictable in this situation. The rich collateral blood supply involving the ECA is the most likely reason for continued blood loss despite ECA ligation. This was the most likely explanation for the continued blood loss in case 1. Collateral pathways involving the contralateral ECA, ipsilateral ICA via the ophthalmic artery, contralateral ICA via the circle of Willis, ipsilateral subclavian artery via the costocervical and thyrocervical trunks, and ipsilateral vertebral artery have been shown.4,5 Increased intracerebral blood ow has also been observed after increasing ECA blood ow with endarterectomy, presumably indicating the presence of ECA/ICA collaterals.6,7 Increased ICA perfusion has also been documented with ECA ligation, presumably a result of increasing ICA perfusion pressure.8 In reference to ECA ligation, direct ligation of the internal maxillary artery via a transantral approach has been advocated for persistent bleeding from this artery.9 Though technically difcult to perform, this allows access to the middle third of the artery. However, serious complications have been reported resulting from the procedure itself, including superior orbital ssure syndrome and apex orbital syndrome.10,11 The effect of ligation of the ECA on maxillary artery hemorrhage has been investigated in baboons.12 Ligation of the proximal ECA reduced blood ow by 73%. The additional ligation of the superior thyroid, ascending pharyngeal, lingual, and facial arteries reduced hemorrhage by 85%. When the posterior auricular artery was also ligated, hemorrhage decreased by a total of 99%. The same benecial effect of multiple ligations has been shown in the dog model.13 Nien-Teh14 reported success with ligation of the ECA and its proximal branches in 3 patients with severe hemorrhage from the initial part of the internal maxillary artery. Successful arrest of hemorrhage with ligation of the ECA and a variable number of branches has also been reported for post-tonsillectomy hemorrhage.15,16 Despite the proposed advantages of ligation of ECA branches, successful arrest of hemorrhage with ligation of the ECA alone has been reported with large high-ow arteriovenous malformations,17 epistaxis,18 and congenital hemangiopericytoma19 and before composite resections for oral carcinoma.20 Successful arrest of epistaxis has also been reported with ligation of both the ECA and anterior ethmoidal artery.21 The method of ECA ligation described within many studies is not always clear in terms of which, if any, additional branches were ligated. In many instances ligation of the ECA was distal to the superior thyroid artery,15,20,21 whereas in others it also included ligation of the anterior ethmoidal artery.18,21 The variation in surgical technique makes direct comparisons challenging. Complications related to ECA ligation and its

Discussion
Hemorrhage after Le Fort I osteotomy has previously been reported with the maxillary artery or greater palatine artery as the most likely source.1 Management of the bleeding involved packing, ligation of the internal maxillary artery, or ligation of the ECA. Of the 15 cases reported, 3 were treated with ECA ligation, with successful arrest of bleeding in 2. Hemorrhage during mandibular osteotomies has also been reported with the maxillary artery or retromandibular vein as the most likely source.2 Twenty-one cases were reported, with 5 patients having ECA ligation; of these 5 patients, 4 had successful arrest of bleeding. Hemorrhage after temporomandibular joint surgery has also been reported.3 The offending vessels cited included the supercial temporal, maxillary, and middle meningeal arteries. The former is relatively easy to manage and is not usually problematic. The management of acute hemorrhage can be difcult. Although ligation of the offending blood vessel is the treatment of choice, access is often limited or impossible. In these situations a decision to perform ECA ligation or angiography and embolization is often made. Ligation of the ECA is a relatively simple procedure that can be performed in 30 minutes. The morbidity with this procedure is minimal. The efcacy in terms of arresting ongoing blood loss is less certain. Several authors report excellent control of bleeding with this procedure, particularly when it is combined with ligation of several branches of the ECA. However, some authors have found continued arterial bleeding despite ECA ligation and have therefore questioned the value of this procedure. This was the situation in case 1. Although continued bleeding was also encountered after ligation of the ECA in case 3, the nature of the vascular malformation and the multiple large venous tributaries makes this therapeu-

1550 branches are generally conspicuous by their absence. Hemiparesis, facial paresthesia, facial pain, gait disturbance, and diplopia were all reported by 1 author, although many patients within that series had transantral ligation of the internal maxillary artery, and complications were not listed according to the individual procedure.18 Failure to arrest bleeding in case 1 despite ligation of the ECA and several proximal branches may be the result of several factors. The blood supply to the area of the temporomandibular joint is complex and involves not only the ipsilateral ECA but also the contralateral ECA (via collaterals), the ICA (via intracerebral collaterals to the middle and accessory meningeal arteries and the ophthalmic artery), and potentially, the vertebral arteries (via intracerebral collaterals). The more distal the vessel, the more likely that additional vessels will contribute to perfusion. The location of the bleeding medial to the temporomandibular joint (but distal relative to the ECA) is such that ligation of the ECA, or even the maxillary artery itself, may not arrest the bleeding. The successful use of ECA ligation in case 2 illustrates the potential benet of this procedure when bleeding is more proximal. Although the actual vessel responsible in this case is unclear, the internal maxillary artery would be the most likely source, given the arterial nature of the bleed and the location. The ligation of the proximal ECA together with the rst 3 branches (superior thyroid, ascending pharyngeal, and lingual arteries) clearly eliminated the bleeding despite collateral supply to the internal maxillary artery. The more proximal location of the bleeding may have favored the good response to ligation that was seen because fewer collateral vessels can inuence perfusion. Angiography with therapeutic arterial embolization has been available for almost 50 years. It has gained wide application in the management of acute hemorrhage. The most important advantage of embolization over ligation is that it is highly selective and can potentially be placed at a site that is inaccessible to surgery. When the hemodynamic effects of embolization were compared with those of ligation in the rabbit model, the former was shown to eliminate collateral blood supply whereas ligation failed to reduce collateral blood supply.22 This is a result of being able to access the vessel closer to the area of interest and hence reduce or eliminate the collateral vessels that would otherwise contribute to the perfusion. Successful embolization for hemorrhage has been reported for epistaxis,23 epistaxis after Le Fort I osteotomy,24-26 temporomandibular joint surgery,27 pseudoaneurysm after trauma,28,29 and vascular lesions30 and after tonsillectomy.31 Only one embolization failure was noted that subsequently required ECA ligation, but this was in a patient with a large high-

MASSIVE HEMORRHAGE DURING SURGERY

ow arteriovenous malformation.17 Complications after embolization are uncommon but include hemorrhage and hematoma formation at the point of catheter insertion, infection, dissecting aneurysm, cerebrovascular accident, cranial nerve injury and facial paralysis, skin and mucosal necrosis, and death.32 Many of these complications are thought to be due to migration of embolic material to intracerebral locations via the many collateral vessels of the ECA. The facial nerve is particularly at risk within the petrous bone, deriving a portion of its blood supply from the petrosal branch of the middle meningeal artery, the caroticotympanic branch of the ICA, and the stylomastoid branch of the occipital artery. The involvement of the trigeminal nerve may be the result of obstruction of the accessory meningeal artery, which supplies a portion of the trigeminal nerve and ganglion. Failure of embolization to prevent or arrest hemorrhage is rare but has been reported in patients with hemorrhage due to vascular malformations.17,32 Embolization was not attempted in either case 1 or case 2. In case 1 ECA ligation, though unsuccessful, eliminated embolization as a potential treatment. In case 2 successful ECA ligation eliminated the need for any additional procedure. It is noteworthy that when one chooses to perform embolization as the initial treatment, the possibility of subsequent ECA ligation still exists, should the need arise. The decision of how to manage severe acute hemorrhage is inuenced by many factors. The bleeding vessel should be the primary site to arrest the hemorrhage, but this is frequently impossible as a result of access. When this is the case, a decision to perform ECA ligation or embolization must be made. If only one of these modalities is available, then clearly, there is no decision to be made. ECA ligation is relatively simple to perform, can be performed relatively quickly, and has few complications, but the efcacy of this procedure in arresting hemorrhage is probably less than that of embolization. However, embolization requires a skilled interventional radiologist, requires more procedural time, and is associated with a greater number of complications. The results of embolization, however, are more predictable, and it should be the initial treatment of choice for the management of severe acute maxillofacial hemorrhage when local measures and/or direct ligation of the bleeding vessel is not possible.

References
1. Lanigan DT, West RA: Management of postoperative hemorrhage following Le Fort I maxillary osteotomy. J Oral Maxillofac Surg 42:367, 1984 2. Lanigan DT, Hey J, West R: Hemorrhage following mandibular osteotomies: A report of 21 cases. J Oral Maxillofac Surg 49: 713, 1991

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3. Vallerand WP, Dolwick MF: Complications of temporomandibular joint surgery. Oral Maxillofac Surg Clin North Am 2:481, 1990 4. Takeuchi Y, Numata T, Konno A, et al: Hemodynamic changes in the head and neck after ligation of the unilateral carotid arteries: A study using color Doppler imaging. Ann Otol Rhinol Laryngol 103:41, 1994 5. Robbins JP, Fitz-Hugh GS, Craddock WD: Arterial collateralization after common carotid ligation. Ann Otol Rhinol Laryngol 82:257, 1973 6. Connolly JE, Stemmer EA: Endarterectomy of the external carotid artery: Its importance in the surgical management of the extra cranial cerebrovascular occlusive disease. Arch Surg 106: 799, 1973 7. Machleder HI, Barker WF: External carotid artery shunting during carotid endarterectomy: Evidence for feasibility. Arch Surg 108:785, 1974 8. Abraham J, Shetty G, Chandy J: Preliminary observation on the hemodynamics of the internal carotid artery following bilateral external carotid ligation in the monkey. J Neurosurg 35:192, 1971 9. McDonald TJ, Pearson BW: Follow-up on maxillary artery ligation for epistaxis. Arch Otolaryngol 106:635, 1980 10. Beall J, Scholl P, Jafek B: Total ophthalmoplegia after internal maxillary artery ligation. Arch Otolaryngol 111:696, 1985 11. Johnson LP, Parkin JL: Blindness and total ophthalmoplegia. A complication of transantral ligation of the internal maxillary artery for epistaxis. Arch Otolaryngol 102:501, 1976 12. Rosenberg I, Austin JC, Wright PG, et al: The effect of experimental ligation of the external carotid artery and its major branches on hemorrhage from the maxillary artery. Int J Oral Surg 11:251, 1982 13. Nien-Teh Y: Effect of multiple ligations of the external carotid artery and its branches on blood ow in the internal maxillary artery in dogs. J Oral Maxillofac Surg 52:849, 1994 14. Nien-Teh Y: Hemorrhage of the initial part of the internal maxillary artery treated by multiple ligations: Report of four cases. J Oral Maxillofac Surg 52:1066, 1994 15. Hofman R, Zeebregts CJ, Dikkers FG: Fulminate post-tonsillectomy hemorrhage caused by aberrant course of the external carotid artery. J Laryngol Otol 119:655, 2005 16. Windfuhr JP: Excessive post-tonsillectomy hemorrhage requiring ligature of the external carotid artery. Auris Nasus Larynx 29:159, 2002 17. Fathi M, Mana A, Ghenaati H, et al: Large arteriovenous highow mandibular, malformation with exsanguinating dental socket hemorrhage: A case report. J Craniomaxillofac Surg 25:228, 1997

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18. Cooke ET: An evaluation and clinical study of severe epistaxis treated by arterial ligation. J Laryngol Otol 99:745, 1985 19. Fanning NF, Kahn A, Corbally MT: External carotid artery ligation for life threatening hemorrhage in exsanguinating orbital facial congenital hemangiopericytoma. J Pediatr Surg 32: 1252, 1997 20. Martis C: Case for ligation of the external carotid artery in composite operations for oral carcinoma. Int J Oral Surg 7:95, 1978 21. Hassard AD, Kirkpatrick DA, Wong FS: Ligation of the external carotid and anterior ethmoidal arteries for severe or unusual epistaxis resulting from facial fractures. Can J Surg 29:447, 1986 22. Okada S, Ohta Y, Suwa F, et al: Experimental ligation versus embolization of the external carotid artery: A comparative hemodynamics study. J Osaka Dent Univ 30:23, 1996 23. De Vries N, Versluis RJ, Valk J, et al: Facial nerve paralysis following embolization for severe epistaxis: Case report and review of the literature. J Laryngol Otol 100:207, 1986 24. Solomons NB, Blumgart R: Severe late onset epistaxis following Le Fort I osteotomy: Angiographic localization and embolization. J Laryngol Otol 102:260, 1988 25. Lustbader DP, Schwartz MH, Zito J, et al: The use of percutaneous transcatheter embolization to control postoperative bleeding following Le Fort I osteotomy. J Oral Maxillofac Surg 49:426, 1991 26. Hemmig SB, Johnson RS, Ferraro N: Management of a ruptured pseudoaneurysm of the sphenopalatine artery following a Le Fort I osteotomy. J Oral Maxillofac Surg 45:533, 1987 27. Peoples JR, Herbosa EG, Dion J: Management of internal maxillary artery hemorrhage from temporomandibular joint via selective embolization. J Oral Maxillofac Surg 46:1005, 1988 28. Zachariades N, Rallis G, Papademetriou G, et al: Embolization for the treatment of pseudoaneurysm and transection of facial vessels. Oral Surg Oral Med Oral Pathol 92:491, 2001 29. DOrta JA, Shatney CH: Post-traumatic pseudoaneurysm of the internal maxillary artery. J Trauma 22:161, 1982 30. Zhao-ju Z, Yun-tang W, Guang-xi S, et al: Clinical application of angiography of oral and maxillofacial hemangiomas: Clinical analysis of seventy cases. Oral Surg Oral Med Oral Pathol 55:437, 1983 31. Levy EI, Horowitz MB, Cahill AM: Lingual artery embolization for severe and uncontrolled postoperative tonsillar bleeding. Ear Nose Throat J 80:208, 2001 32. Frame JW, Putnam G, Wake MJ, et al: Therapeutic arterial embolization of vascular lesions in the maxillofacial region. Br J Oral Maxillofac Surg 25:181, 1987