Control of Bleeding During Tooth Removal - Part 2
By Dr. Philip Banghart
Occasionally, patients will return to the dentist with bleeding after adequate intraoperative (primary) hemostasis has been achieved. The reason for the post-operative (secondary) bleeding is often secondary to trauma precipitated by the patient continuing to spit blood from the mouth instead of effectively applying pressure with a gauze sponge. Often times, a patient will continue to repeatedly change the gauze after surgery, which in effect disrupts the clot formation each time the gauze is removed from the extraction site. Paradoxically, repeated replacement of gauze can perpetuate bleeding because the clot ends up "on the gauze" after each subsequent removal. Simply inform the patient that oozing of blood and blood-tinged saliva is normal for up to 12 - 24 hours after extraction and to avoid frequent unnecessary removal and changing of the gauze.
Nevertheless, the dentist must have a planned systematic protocol to control persistent post-surgical bleeding. The patient should be positioned in the dental chair, and all blood and saliva evacuated with suction. Good lighting is imperative to determine the precise source of bleeding. If generalized oozing is encountered, the bleeding site can be covered with a folded, damp 2 x 2 or 4 x 4 inch gauze held in place with firm pressure for 5 minutes. This measure will control most bleeding.
If this measure is unsuccessful, local anesthesia should be administered so that the socket can be treated more aggressively. Block techniques are recommended instead of infiltration. Infiltrations with epinephrine solutions may result in artificial or temporary control of bleeding. Recurrent bleeding may occur after the epinephrine dissipates.
Once local anesthesia has been achieved, the dentist should gently curette and debride the extraction site and suction out the old blood clot. The initial goal is to determine whether the bleeding is coming from soft tissue or bone. After careful flap retraction, the periosteum should be inspected to ascertain if the excessive bleeding is secondary to diffuse oozing or specific arterial bleeding. Bone should be inspected for nutrient canal bleeding versus diffuse bleeding. The same measures as discussed in Part I, Control of Bleeding During Tooth Removal, should be applied to manage the hemorrhaging. These measures include removal of granulation tissue and smoothing sharp bony edges. Soft tissue bleeders should be controlled with vessel clamping followed by ligation or vessel cauterization if direct pressure fails. If nutrient canals in bone are the source of bleeding, burnishing the surrounding bone, applying bone wax or cautery will typically control the hemorhaging. Once the persistent bleeding is controlled a hemostatic agent is typically positioned in the extraction socket. An absorbable gelatin sponge (Gelfoam) soaked in thrombin is usually quite effective. A collagen plug (Collaplug) or oxidized cellulose (Surgicel) can also be utilized.
Avoiding An Epidemic
by Ali Alijanian, D.D.S.
As strange as it may sound, we in the dental community may be facing a potentially serious epidemic that stems from a side effect associated with the drugs used in the treatment of cancer patients. These are the IV biphosphonates pamidronate (Aredia; Novartis Pharmeceuticals, East Hanover, NJ) and zolendronate (Zometa; Novartis Pharmeceuticals) that are being used in the treatment of cancer patients with bone metastasis or the treatment of hypercalcemic states. These drugs have been implicated in the condition that is known as biphosphonate induced osteonecrosis. There are a number of published reports implicating these drugs in the avascular necrosis of the jaws.(1,2,3) There are various clinical entities that may be similar in presentation such as osteomyelitis and radiation induced osteoradionecrosis. I would like to describe each of these individually and explain why these drugs have been implicated in a condition that seems similar, but is different. We must take this condition seriously, otherwise we may inflict a great deal of harm on to our patients.
When you are faced with a patient with exposed painful non-healing bone the following conditions must be ruled out:
Osteomyelitis of the jaws may come in various forms that I will not go into in detail. However, it is important to understand that this is an infectious process. By definition it is the inflammation of the marrow space and there is a clear etiology associated with it such as an infected tooth or a sequestrum, i.e. a foreign body. The symptoms are consistent with pain, drainage, parasthesia, and possible swelling. The treatment is removal of the source, sequestrotomy, and long-term antibiotic therapy.
Radiation induced osteoradionecrosis is a result of hypoxia, hypocellular, and hypovascular bone induced by high levels of radiation therapy. These patients may develop exposed necrotic bone or delayed healing with bone exposure after the removal of a tooth or with any trauma resulting in bone exposure. The treatment is local debridment and in severe conditions the effected bone must be sectioned down to bleeding margins. The best course of treatment is preoperative antibiotic therapy with atraumatic extractions and in some conditions HBO therapy if applicable.
The osteonecrosis that occurs as a side effect of the drugs, has been dubbed biphosphonate-induced osteonecrosis. These drugs are used to treat hypercalcemia in some malignancies or in reducing osteolysis in bone metastasis.(4) They do this by inhibiting osteoclastic activity, (5) which is one of the cornerstones for bone remodeling. Therefore the bone in these patients does not have this capability and it functions as dead bone for a lack of a better word. This is why we must take every action to avoid bone exposure of any kind since the normal bone physiology that results in bone remodeling (repair) has been interrupted. Furthermore, these patients cannot stop taking these medications since there life depends on it. Even if they stopped taking them the effects will not reverse for a very long time.
Biphosphonates such as etidronate (Didronel; Proctor & Gamble, Mason, OH), residronate (Actonel; Proctor & Gamble), and tiludronate (Skelid; Sanofi Weinthrop (Sanofi-Sythe Labo Inc), New York, NY) are in common usage today and do not cause bone necrosis. However, these drugs are non-nitrogen containing biphosphonates and are rapidly metabolized. Pamidronate (Aredia) and Zoledronate (Zometa) are nitrogen containing biphosphonates, and are much more potent and are not metabolized. (6) Therefore, they accumulate in bone and have an ongoing affect that results in bone necrosis after surgical insult.
Since the bone is unable to repair itself, these patients are refractory to any treatment and the best line of action is avoiding such complications by not performing any surgical procedures. In the event a tooth needs to be removed, the best course of action is a coronectomy and root canal therapy, even if it turns out to be a simple extraction. With edentulous patients soft tissue liners can be used to avoid any bone exposure.
If a complication should arise, then the best treatment is no further surgical intervention and the following recommendations may be followed: long term or intermittent penicillin therapy, 0.12% chlorhexidine rinse, and periodic minor debridement of soft textured sequestrating bone and wound irrigation. (1) According to the preliminary reports aggressive therapy leads to more problems.
Taking note on the issue raised in this article can save you from facing a serious complication in your practice. Therefore, it is essential to obtain relevant history on patients that have had chemotherapy and make sure that they have not been administered these medications. We must avoid any type of surgery that will result in bone exposure at all cost in patients that have been exposed to these medications. If there is no other option available then the patient must be informed about the risks and complications involved and be prepared for the long term care that he or she may have to receive.
1. Marx RE. Pamidronate (Aredia) and Zoledronate (Zometa) induced avascular necrosis of the Jaws: a growing epidemic. J Oral Maxillofac Surg 2003 Sep; 61(9): 1115-7
2. Bagan JV, Murillo J, Jimenez Y, Poveda R. Avascular jaw osteonecrosis in association with cancer chemotherapy: series of 10 cases. J Oral Pathol Med. 2005 Feb; 34 (2):120-3
3. Ruggiero SL, Mehrotra B, Rosenburg TJ, Engroff SL. Osteonecrosis of the jaws associated with the use of bisphosphonates: a review of 63 cases. J Oral Maxillofac Surg. 2004 May;62(5):527-34
4. Hughes DE, MacDonald BR, Russell RG. et al. Inhibition of osteoclast like cell formation by biphosphonates in long term cultures of human bone marrow. J Clin Invest 83 (1989), p. 1930.
5. Sato M and Grasser W. Effects of Biphosphonates on isolated cat osteoclast as examined by reflected light microscopy. J Bone Miner Res 5 (1990), p.31.
6. Tenenbaum HC, Shelemay A, Girard B. et al., Biphosphonates and periodontics: potential application for regulation of bone mass in the periodontium and other therapeutic diagnosis uses. J Periodontol 73 (2002), p 813
If you received this e-mail in error and would like to be removed from our database, call Dr. Gilbert at 909.982.8888
The content of this OMS OPN is presented in summary form, is general in nature, and is provided for informational purposes only. The content is not intended to be relied on for medical or dental diagnosis or treatment, nor are the contents to be considered either as medical or dental advice. No representation or warranty of any kind, either express or implied, have been made as to the completeness, accuracy or reliability of the information provided. The publisher, authors and others involved with OMS OPN do not assume any liability for the contents of any material provided and use of any information is solely at your own risk.