J Oral Maxillofac 48:770-773,






3. Rivard JC, Lebowitz, PW: Bradycardia after alfentanylsuccinylcholine. (Case report). Anesth Analg 67907, 1988 4. Glenski JA, Friesen RH, Lane GA, et al: Low-dose sufentanil as a supplement to halothane/N,O anaesthesia in infants and children. Can J Anaesth 35:379, 1988 5. Schemling WT, Kampine JP, Warltier DC: Negative chronotropic actions of sufentanil and vecuronium in chronically instrumented dogs pretreated with propranolol and/or diltiazem. Anesth Analg 69:4, 1989 6. Starr NJ, Sethna DH, Estafanous FG: Bradycardia and asystole following rapid administration of sufentanil with vecuronium. Anesthesioloav 64:521. 1986 7. Savarese JJ, Lowenstein E: The&me of ‘the game: No anesthesia by cookbook (editorial). Anesthesiology 62:703, 1985 8. Maryniak JK, Bishop VA: Sinus arrest after alfentanyl. Br J Anaesth 59:390, 1987 9. Sherman EP, Lebowitz PW, Street WC: Bradycardia following sufentanil-succinylcholine. Anesthesiology 66:106, 1987


To the Editor:-We read with interest the recent case report by Drs Ragno, Marcoot, and Taylor in the October issue of JOMS.’ While we agree with the authors’ analysis of the problem and their recommendations for treatment, we were surprised that they failed to mention the use of sufentanil and its pharmacologic actions.2-9 We feel the use of the drug may have contributed to the severity of the response (asystole), and offer here evidence from the literature to support that argument. (We realize that the dose of sufentanil reported in the article is probably a typographical error, that is “40 mg” is really meant to read “40 micrograms”). The use of narcotics as sole or primary anesthetic agents has found its niche in cardiac anesthesia, but the lessons learned from narcotic induction apply in any circumstance in which moderate to high doses of narcotics are used.2 Induction with sufentanil and vecuronium is associated with a higher incidence of bradycardia and hypotension requiring pharmacologic intervention.’ It is not uncommon to see bradycardia in children (who are known to have higher resting vagal tone) during induction with narcotics with doses similar to that reported in the article.4 Vagal tone is augmented by narcotics through their action on the sympathetic nervous system (inhibition) and the locus ceruleus in the brain stem (potentiation). It is well known that any vagotonic stimulus (laryngoscopy, ocular pressure or rotation of the globe, cold water on the face) or drugs such as beta blockers, calcium channel blockers, and succinylcholine will augment the action of narcotics, particularly the more potent drugs sufentanil and alfentanyLz-’ In summary, we agree with the diagnosis and recommended steps to avoid and treat the trigeminovagal reflex, but feel that some mention should be made of the potentiation of the response by sufentil, and suggest that this response, though rare, is more likely to be seen if the anesthetist is using moderate to high doses of potent narcotics, as in this case.


The author replies:-Drs Altom and Wright point out the possible effect of sufentanil in potentiating the severity of the response of the trigeminal-vagal reflex. Narcotics may indeed produce bradycardia and could potentially cause potentiation of vagal effects. In the case at hand, the patient had been receiving sufentanil via an IV drop (rate, 40 micrograms per hour) for 1 hour without any bradycardiac episodes before the asystolic event. We thus felt potentiation of the reflex by sufentanil, while possible, was probably not a significant factor, and thus discussion was omitted. We appreciate the comments presented and agree one should be aware of possible potentiation of this reflex by narcotics. MAJ JAMESR. RAGNO JR Fort Stewart, Georgia MAXILLOMANDIBULAR




To the Editor:-We appreciate the support and comments of Dr Robert Riley’s discussion in the December issue following our article on obstructive sleep apnea. His research and leadership in the surgical treatment of sleep apnea are well known and frequently quoted. As surgical treatment for obstructive sleep apnea becomes more commonly performed, I hope a full understanding of the disease and surgical expectations are well established. Although the experience at Stanford University is positive, these data need to be substantiated by other centers. Our article certainly does that. In addition, certain standards of care and follow-up need to be recognized. In this regard, Dr Riley suggests that our patients were objectively studied by polysomnography at 1 week and 6 weeks following surgery. This is not true nor is it stated in the article. No patients were studied 1 week postoperatively. We feel that patients are often so sick that waiting 6 months to be studied, as indicated by Dr Riley, may have serious consequences if no other intervention is undertaken. Although no patients in our study have gotten worse after maxillomandibular advancement, there is always the possibility; therefore waiting 6 months may not be advisable or safe. When comparing our 6-week or 6-month postoperative stud-


1.Ragno JR Jr, Marcoot RM, Taylor SE: Asystole during Le Fort I osteotomy. J Oral Maxillofac Surg 47:1082, 1989 2. Bovill JG, Sebel PS, Stanley TH: Opioid analgesics in anesthesia: With special reference to their use in cardiovascular anesthesia. Anesthesiology 61:731, 1984





ies, no evidence exists that apnea improves or worsens; therefore, our patients underwent postoperative studies at 6 weeks. In addition, most of our patients underwent surgery because they did not respond to, or refused to wear, nasal CPAP. Therefore, 6 months of nasal CPAP while awaiting surgery is unreasonable. Pressures necessary to correct apnea prior to surgery often change postoperatively and, therefore, it is not in the patient’s best interest to continue nasal CPAP without reevaluation. The article stated that multiple sites of upper airway obstruction may contribute to the overall syndrome, and therefore, all of our patients were studied the same way as Dr Riley’s group, by physical examination, cephalometric analysis, and fiberoptic pharyngoscopy. Finally, the discussion claimed that we failed to include the patients’ weight as part of their objective analysis. This is not true, and weight loss was carefully studied. As stated in the article, weight loss occurred in all cases and the difference between the failure group and the successful group was insignificant. The point is that weight loss was not responsible for our successful results. In conclusion, I appreciate the research, development, and support of Drs Riley and Powell in the area of surgical treatment for obstructive sleep apnea. I hope many other members of our specialty become actively involved with research in this area. PETER D. WAITE, MPH, DDS, MD VIRGIL WOOTEN, MD Birmingham, Alabama ALLOGENEIC BONE OR HYDROXYLAPATITE FOR THE SINUS LIFT PROCEDURE? To the Editor:-This letter concerns the discussion by Dr Thomas Golec of the article by Jensen et al entitled “Reconstruction of the Severely Resorbed Maxilla With Bone Grafting and Osseointegrated Implants: A Preliminary Report” (J Oral Maxillofac Surg 4833, 1990). Reconstruction of the severely resorbed maxilla is best accomplished by placing a preformed iliac graft with immediate implant placement. ‘*’ This is the best way to get retention of the graft as well as integration of implants. With this technique 5-year survival of implants has been reported at above 90% in some centers. The key to successful retention of an implant in this setting is that it engages native bone, which in some cases is essentially absent. I have described the site selection for the highly resorbed jaw (class D site) as having less than 3 mm of bone available so that an implant can not mechanically engage the site. Autogenous grafting of a jaw area is required in these cases before an implant can be placed.3 In my experience, implants that are lost early are not integrated because of the lack of this initial mechanical stabilization into native bone. To overcome this difficulty, Dr Golec advises using hydroxylapatite in the sinus and as an onlay augmentation material to provide additional mechanical, though minimal osseointegrative, support to the subsequently placed implant.4 Indeed, the implant longevity and success may be in proportion to the osseointegrating capacity of the native bone and to a very limited extent to osseo-conducted bone in the areas of the hydroxylapatite implant. It has been my experience that an HA particulate implant is

never totally ossified, but has fibrous encapsulation present throughout much of the implant. Biopsies of sinus grafts have shown this as well.’ When the HA graft is placed into the sinus fist and surgical implantation is done later, should perforation of the sinus occur any nonintegrated HA could support a chronic infection that may not be possible to clear without secondary surgical intervention. This could also lead to loss of implants that are placed. When matured HA grafts are drilled into, especially in the mandible, HA particles generate increased heat in the drilling procedure and this can impair primary osseous repair. This is much less likely in the maxilla, but should be a consideration. I would recommend, therefore, in the elderly where an iliac bone graft is proscribed that a sinus lift or nasal mucosal lift be used with allograft augmentation and immediate placement of implants. This has proven highly successful over the past 2 years that I have used the technique. I do not attempt immediate placement of implants if there is not at least 3 mm of bone available to engage the implant. All trephine biopsies done (6 months after implant and sinus graft placement) under these conditions have shown formation of bone in the sinus. Implants have consistently integrated. Up to 15 mm of bone has been formed in the first molar area and has been confirmed histologically. Augmented sinus bone has proven to be clinically denser than adjacent bone at the biopsy stage. This technique appears to me to have several advantages over the ceramic implants as well as the iliac bone grafts where implant placement is delayed for a few months after grafting. The allograft solution should not be overlooked for the class C implant sites (3-7 mm vertical bone). It has been much more predictable than with the use of the ceramic in my hands and may be a preferred technique from a biological standpoint. OLE T. JENSEN, DDS, MS Denver, Colorado

References 1. Breine U, Branemark PI: Reconstruction of alveolar ,jaw bone. Stand J Plast Reconstr Surg 14:23, 1980 2. Branemark PI: Personal communication, April 1988 3. Jensen OT: Site classification for the osseointegrated implant. J Prosthet Dent 61:228, 1989 4. Smiler DG, Holmes RE: Sinus lit procedure using porous HA: A preiiminary report. J Oral Implants 13:42, 1986 5. Kirsch A: Personal communication, October 1989 REDISCOVERY OF THE TEMPORALIS MUSCLE. FLAP FOR ANKYLOSIS To the Editor:-1 read with interest the article by Pogrel and Kaban, “The Role of a Temporalis Fascia and Muscle Flap in Temporomandibular Joint Surgery” (J Oral Maxillofac Surg 48: 14, 1990). I commend the authors on their article and partially on their review of the literature. J.B. Murphy in Chicago, as far as I have been able to determine, and as they noted in their bibliography, was the first to use the temporal muscle for correction of a temporomandibular joint ankylosis. The procedure, however, fell into oblivion until it was repopularized by Dr Paul Tessier, who showed a movie of this operation at an Educational Foundation meeting of the American Society of Plastic and Reconstructive Surgeons in Dal-

Maxillomandibular advancement surgery for obstructive sleep apnea.

J Oral Maxillofac 48:770-773, Surg 1990 POSSIBLE POTENTIATION OF TRIGEMINAL-VAGAL 3. Rivard JC, Lebowitz, PW: Bradycardia after alfentanylsuccin...
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