The Journal of Craniofacial Surgery
Brief Clinical Studies
Volume 26, Number 4, June 2015
TABLE 1. Patient Characteristics Age, y
Sex
Defect Size, cm2
Defect Location
Defect Etiology
Expander Volume, mL
Expander Shape
Complication
21 22 25 20
Male Male Female Male
25 96 63 72
Face Head Face Face
Nevus Lymphatic malformation Vascular malformation Scar
100 250 250 250
Rectangular Rectangular Rectangular Rectangular
Minimal exposition None None None
1 2 3 4
replacement. Minimum flap motion yields less flap area loss and results in less scar tissue. The simpler the flap, the best the resulting scar. In the Alagoz technique, the final suture line can be linear or crescentic. In selected cases, round expanders can be used and central defect can be closed with a purse string suture. The limitations for this technique can be the absence of skin to expand at the site of the defect and the anatomic obstacles. FIGURE 1. Schematic placement of the expander under the defect and tissue gain correlation with the markings around the defect.
When the expander is classically placed under the healthy tissue next to the defect, the final flap size developed should theoretically be at least twice the defect size for a successful reconstruction. Thus, half of the flap can be used for the coverage of the defect and the other half for the donor site.2,3 In the classic approach, total expanded surface area required for reconstruction should be better estimated as the sum of the defect and donor-site areas as well as 20% to 30% more. This additional area is necessary owing to the loss in rotation or advancement as well as dog-ear and tissue retraction.10 However, the burden of the final incision scars or the shortage in the expected actual gain of the expanded flap can be handled by a smart donor-site selection. The Alagoz technique offers to place the expander right under the desired final reconstruction site, namely, under the defect as far as the anatomic structures allow. Thus, the defect is resurfaced with the most convenient contiguous tissue. In this technique, tissue gain similar in size to the defect is sufficient for reconstruction. After removing the defect located at the top of the expander, encircling flap can easily cover the defect. Because expanded donor area simultaneously contains the defect site, in contrast to the classic concept, there is no need for larger donor-site expansion to cover both donor and defect area separately. Rotation or transposition of the flap is usually not necessary. Reconstruction can be accomplished with less flap
REFERENCES 1. Manders EK, Schenden MJ, Furrey JA, et al. Soft-tissue expansion: concepts and complications. Plast Reconstr Surg 1984;74:493–507 2. Radovan C. Tissue expansion in soft-tissue reconstruction. Plast Reconstr Surg 1984;74:482–492 3. Neumann CG. The expansion of an area of skin by progressive distention of a subcutaneous balloon; use of the method for securing skin for subtotal reconstruction of the ear. Plast Reconstr Surg 1957;19:124–130 4. Duits EH, Molenaar J, van Rappard JH. The modeling of skin expanders. Plast Reconstr Surg 1989;83:362–367 5. Morgan RF, Edgerton MT. Tissue expansion in reconstructive hand surgery: case report. J Hand Surg Am 1985;10:754–757 6. van Rappard JH, Molenaar J, van Doorn K, et al. Surface-area increase in tissue expansion. Plast Reconstr Surg 1988;82:833–839 7. Zide BM, Karp NS. Maximizing gain from rectangular tissue expanders. Plast Reconstr Surg 1992;90:500–504 8. Bauer BS, Margulis A. The expanded transposition flap: shifting paradigms based on experience gained from two decades of pediatric tissue expansion. Plast Reconstr Surg 2004;114:98–106 9. Antonyshyn O, Gruss JS, Zuker R, et al. Tissue expansion in head and neck reconstruction. Plast Reconstr Surg 1988;82:58–68 10. Bhandari PS. Mathematical calculations in a spherical tissue expander. Ann Plast Surg 2009;62:200–204
Peripheral Facial Nerve Paralysis Triggered by Alveolar Osteitis Melek Ramoglu, DDS, PhD, Mehmet Demirkol, DDS, PhD, Mutan Hamdi Aras, DDS, PhD, and Bilal Ege, DDS, PhDy
FIGURE 2. Upper row, Scar view before expansion. Middle row, Scar view during the expansion and partial exposure of the expander. Lower row, Final scar after the expansion.
e292
Abstract: Peripheral facial nerve paralysis is the most common cranial nerve disorder; it is determined by the branches of the seventh cranial nerve and results in a characteristic facial distortion that is determined in part by the nerve branches involved. Peripheral facial nerve paralysis during dental treatment is very rare; when it does occur, it can be associated with the injection of local anesthetic, prolonged attempts to remove a mandibular third molar, and subsequent infection. Our article presents the case of a patient admitted with unilateral peripheral facial nerve paralysis occurring simultaneously with alveolar osteitis. #
2015 Mutaz B. Habal, MD
Copyright © 2015 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
The Journal of Craniofacial Surgery
Volume 26, Number 4, June 2015
Brief Clinical Studies
Key Words: Facial paralysis, alveolar osteitis, tooth extractions
A
22-year-old female patient was referred to our clinic complaining of pain from an extracted upper-left molar 4 days previously. Her medical history was unremarkable. She denied any history of trauma, surgery, or viral infection such as herpes zoster infection, as well as previous experience of facial weakness. After clinical and radiographic examinations, the patient’s condition was diagnosed as alveolar osteitis (Figs. 1A, B),1–3 and the extraction socket was routinely irrigated with saline (0.9% isotonic sodium chloride solution). Twenty-four hours after irrigation, the patient returned to our clinic with a feeling of heaviness on the left side of her face; she was unable to laugh or close her left eye. When the patient was examined again, we observed a loss of control of the left facial muscles, asymmetric laughing, whistling, and ability of the left eye with little effort (Figs. 2A, B). 1,2,4– 6 The patient did not report any preceding pain behind the ear, deafness, or hyperacusis in the detailed anamnesis. There was no swelling or pain during palpation of the buccal surface of extraction socket. The patient’s condition was diagnosed as probable peripheral facial nerve paralysis (PFNP) related to alveolar osteitis, identified as grade 4 (moderately severe dysfunction) according to the HouseBrackmann scoring system, which involved obvious weakness and disfiguring asymmetry, normal symmetry and tone at rest, and incomplete eye closure.1 Initially, we started treatment with a prescription of oral antibiotics (amoxicillin, 875 mg þ clavulanic acid, 125 mg, 2 times daily) and 40 mg daily of methylprednisolone, reducing the dose during 10 days. However, after the medical treatment, the patient was lost to follow-up. The most common cause of PFNP in relation to dental interventions is the injection of local anesthetic in the form of an inferior alveolar nerve block for the extraction of mandibular third molars.2– 4 This immediate paralysis, which is likely caused either by anesthetizing the aberrant facial nerve trunk in the retromandibular space or the facial nerve within the parotid fascia, is temporary. In such iatrogenic cases, the facial nerve can be temporarily blocked, but the anesthetic effect in the injected area disappears within hours.5 Other possible dental-related causes to consider include a prolonged attempt to extract a mandibular third molar and infection after surgery as well as facial weakness after intraoral surgery under local anesthesia.3,6 The symptom reported most frequently by patients with facial paralysis before the specific findings of facial weakness arise is a feeling of pain behind the ear (mastoid region). In some cases, pain located in the jaws can be evaluated as a prodromal symptom of facial paralysis. Especially during the prodromal stage of facial From the Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Gaziantep University, Gaziantep, Turkey; and yDepartment of Oral and Maxillofacial Surgery, Faculty of Dentistry, Adiyaman University, Adiyaman, Turkey. Received July 31, 2014. Accepted for publication January 20, 2015. Address correspondence reprint requests to Mehmet Demirkol, DDS, PhD, Department of Oral Maxillofacial Surgery, Faculty of Dentistry, Gaziantep University, Gaziantep, Turkey, 27310, Gaziantep, Turkey; E-mail: [email protected] This study was presented as an oral presentation of the 19th Congress of the Balkan Stomatological Society (BaSS) in Belgrade, April 24-27, 2014. Copyright # 2015 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000001596
#
2015 Mutaz B. Habal, MD
FIGURE 1. A, Intraoral view of the patient. B, Panoramic radiography of the patient.
FIGURE 2. A, Facial appearance of the patient showing failure to close the eye with effort on the affected side. B, Facial appearance of the patient showing inability to move the left corner of the mouth and smile.
paralysis, the only existing symptom may be odontalgia, which may increase the difficulty of making a diagnosis for physicians who are not familiar with this clinical picture.6 In this report, the patient reported no pain in the mastoid region. The present case lacked any apparent swelling and infectious event around the extraction socket that set this process into action. Thus, the causative factor leading to PFNP differs from other published case reports in the literature.5,7,8 Peripheral facial nerve paralysis was thought to be triggered by alveolar osteitis. Although the exact mechanism remains unclear, the most likely explanation for this may be that an existing infection that was previously restricted to the alveolar socket spread posteriorly and superiorly into the buccal or masticatory regions. The terminal branches of the facial nerve, and especially the buccal and zygomatic branches, which are likely aberrant and located near the extraction socket, could be potentially seeded with an infectious agent.6 To the best of our knowledge, this report is the first clinical condition that thought to implicate alveolar osteitis as a precipitating factor. As our case represented incomplete facial paralysis, we started with low-dose corticosteroid treatment. A shortcoming in this case report is that we could not follow the patient to determine how much the paralysis had improved. In clinical practice, it should be kept in mind that postoperative infection, even if it is minimal, may play a direct or indirect role in terminal branches of facial nerve motor neuropathy, such as presented in our case. Thus, more careful postoperative follow-up should be carried out.
REFERENCES 1. Kang TS, Vrabec JT, Giddings N, et al. Facial nerve grading systems (1985-2002): beyond the House-Brackmann scale. Otol Neurotol 2002;23:767–771 2. Shuaib A, Lee MA. Recurrent peripheral facial nerve palsy after dental procedures. Oral Surg Oral Med Oral Pathol 1990;70:738–740 3. Cousin GC. Facial nerve palsy following intra-oral surgery performed with local anesthesia. J R Coll Surg Edinb 2000;45:330–333 4. Miles PG. Facial palsy in the dental surgery. Case report and review. Aust Dent J 1992;37:262–265 5. Ling KC. Peripheral facial nerve paralysis after local dental anesthesia. Oral Surg Oral Med Oral Pathol 1985;60:23–24 6. Tolstunov L, Belaga GA. Bell’s palsy and dental infection: a case report and possible etiology. J Oral Maxillofac Surg 2010;68:1173–1178 7. Vasconcelos BC, Bessa-Nogueira RV, Maurette PE, et al. Facial nerve paralysis after impacted lower third molar surgery: a literature review and case report. Med Oral Pathol Oral Cir Bucal 2006;11:175–178 8. Burke RH, Adams JL. Immediate cranial nerve paralysis during removal of a mandibular third molar. Oral Surg Oral Med Oral Pathol 1987;63:172–174
e293
Copyright © 2015 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
Brief Clinical Studies
Volume 26, Number 4, June 2015
TABLE 1. Patient Characteristics Age, y
Sex
Defect Size, cm2
Defect Location
Defect Etiology
Expander Volume, mL
Expander Shape
Complication
21 22 25 20
Male Male Female Male
25 96 63 72
Face Head Face Face
Nevus Lymphatic malformation Vascular malformation Scar
100 250 250 250
Rectangular Rectangular Rectangular Rectangular
Minimal exposition None None None
1 2 3 4
replacement. Minimum flap motion yields less flap area loss and results in less scar tissue. The simpler the flap, the best the resulting scar. In the Alagoz technique, the final suture line can be linear or crescentic. In selected cases, round expanders can be used and central defect can be closed with a purse string suture. The limitations for this technique can be the absence of skin to expand at the site of the defect and the anatomic obstacles. FIGURE 1. Schematic placement of the expander under the defect and tissue gain correlation with the markings around the defect.
When the expander is classically placed under the healthy tissue next to the defect, the final flap size developed should theoretically be at least twice the defect size for a successful reconstruction. Thus, half of the flap can be used for the coverage of the defect and the other half for the donor site.2,3 In the classic approach, total expanded surface area required for reconstruction should be better estimated as the sum of the defect and donor-site areas as well as 20% to 30% more. This additional area is necessary owing to the loss in rotation or advancement as well as dog-ear and tissue retraction.10 However, the burden of the final incision scars or the shortage in the expected actual gain of the expanded flap can be handled by a smart donor-site selection. The Alagoz technique offers to place the expander right under the desired final reconstruction site, namely, under the defect as far as the anatomic structures allow. Thus, the defect is resurfaced with the most convenient contiguous tissue. In this technique, tissue gain similar in size to the defect is sufficient for reconstruction. After removing the defect located at the top of the expander, encircling flap can easily cover the defect. Because expanded donor area simultaneously contains the defect site, in contrast to the classic concept, there is no need for larger donor-site expansion to cover both donor and defect area separately. Rotation or transposition of the flap is usually not necessary. Reconstruction can be accomplished with less flap
REFERENCES 1. Manders EK, Schenden MJ, Furrey JA, et al. Soft-tissue expansion: concepts and complications. Plast Reconstr Surg 1984;74:493–507 2. Radovan C. Tissue expansion in soft-tissue reconstruction. Plast Reconstr Surg 1984;74:482–492 3. Neumann CG. The expansion of an area of skin by progressive distention of a subcutaneous balloon; use of the method for securing skin for subtotal reconstruction of the ear. Plast Reconstr Surg 1957;19:124–130 4. Duits EH, Molenaar J, van Rappard JH. The modeling of skin expanders. Plast Reconstr Surg 1989;83:362–367 5. Morgan RF, Edgerton MT. Tissue expansion in reconstructive hand surgery: case report. J Hand Surg Am 1985;10:754–757 6. van Rappard JH, Molenaar J, van Doorn K, et al. Surface-area increase in tissue expansion. Plast Reconstr Surg 1988;82:833–839 7. Zide BM, Karp NS. Maximizing gain from rectangular tissue expanders. Plast Reconstr Surg 1992;90:500–504 8. Bauer BS, Margulis A. The expanded transposition flap: shifting paradigms based on experience gained from two decades of pediatric tissue expansion. Plast Reconstr Surg 2004;114:98–106 9. Antonyshyn O, Gruss JS, Zuker R, et al. Tissue expansion in head and neck reconstruction. Plast Reconstr Surg 1988;82:58–68 10. Bhandari PS. Mathematical calculations in a spherical tissue expander. Ann Plast Surg 2009;62:200–204
Peripheral Facial Nerve Paralysis Triggered by Alveolar Osteitis Melek Ramoglu, DDS, PhD, Mehmet Demirkol, DDS, PhD, Mutan Hamdi Aras, DDS, PhD, and Bilal Ege, DDS, PhDy
FIGURE 2. Upper row, Scar view before expansion. Middle row, Scar view during the expansion and partial exposure of the expander. Lower row, Final scar after the expansion.
e292
Abstract: Peripheral facial nerve paralysis is the most common cranial nerve disorder; it is determined by the branches of the seventh cranial nerve and results in a characteristic facial distortion that is determined in part by the nerve branches involved. Peripheral facial nerve paralysis during dental treatment is very rare; when it does occur, it can be associated with the injection of local anesthetic, prolonged attempts to remove a mandibular third molar, and subsequent infection. Our article presents the case of a patient admitted with unilateral peripheral facial nerve paralysis occurring simultaneously with alveolar osteitis. #
2015 Mutaz B. Habal, MD
Copyright © 2015 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
The Journal of Craniofacial Surgery
Volume 26, Number 4, June 2015
Brief Clinical Studies
Key Words: Facial paralysis, alveolar osteitis, tooth extractions
A
22-year-old female patient was referred to our clinic complaining of pain from an extracted upper-left molar 4 days previously. Her medical history was unremarkable. She denied any history of trauma, surgery, or viral infection such as herpes zoster infection, as well as previous experience of facial weakness. After clinical and radiographic examinations, the patient’s condition was diagnosed as alveolar osteitis (Figs. 1A, B),1–3 and the extraction socket was routinely irrigated with saline (0.9% isotonic sodium chloride solution). Twenty-four hours after irrigation, the patient returned to our clinic with a feeling of heaviness on the left side of her face; she was unable to laugh or close her left eye. When the patient was examined again, we observed a loss of control of the left facial muscles, asymmetric laughing, whistling, and ability of the left eye with little effort (Figs. 2A, B). 1,2,4– 6 The patient did not report any preceding pain behind the ear, deafness, or hyperacusis in the detailed anamnesis. There was no swelling or pain during palpation of the buccal surface of extraction socket. The patient’s condition was diagnosed as probable peripheral facial nerve paralysis (PFNP) related to alveolar osteitis, identified as grade 4 (moderately severe dysfunction) according to the HouseBrackmann scoring system, which involved obvious weakness and disfiguring asymmetry, normal symmetry and tone at rest, and incomplete eye closure.1 Initially, we started treatment with a prescription of oral antibiotics (amoxicillin, 875 mg þ clavulanic acid, 125 mg, 2 times daily) and 40 mg daily of methylprednisolone, reducing the dose during 10 days. However, after the medical treatment, the patient was lost to follow-up. The most common cause of PFNP in relation to dental interventions is the injection of local anesthetic in the form of an inferior alveolar nerve block for the extraction of mandibular third molars.2– 4 This immediate paralysis, which is likely caused either by anesthetizing the aberrant facial nerve trunk in the retromandibular space or the facial nerve within the parotid fascia, is temporary. In such iatrogenic cases, the facial nerve can be temporarily blocked, but the anesthetic effect in the injected area disappears within hours.5 Other possible dental-related causes to consider include a prolonged attempt to extract a mandibular third molar and infection after surgery as well as facial weakness after intraoral surgery under local anesthesia.3,6 The symptom reported most frequently by patients with facial paralysis before the specific findings of facial weakness arise is a feeling of pain behind the ear (mastoid region). In some cases, pain located in the jaws can be evaluated as a prodromal symptom of facial paralysis. Especially during the prodromal stage of facial From the Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Gaziantep University, Gaziantep, Turkey; and yDepartment of Oral and Maxillofacial Surgery, Faculty of Dentistry, Adiyaman University, Adiyaman, Turkey. Received July 31, 2014. Accepted for publication January 20, 2015. Address correspondence reprint requests to Mehmet Demirkol, DDS, PhD, Department of Oral Maxillofacial Surgery, Faculty of Dentistry, Gaziantep University, Gaziantep, Turkey, 27310, Gaziantep, Turkey; E-mail: [email protected] This study was presented as an oral presentation of the 19th Congress of the Balkan Stomatological Society (BaSS) in Belgrade, April 24-27, 2014. Copyright # 2015 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000001596
#
2015 Mutaz B. Habal, MD
FIGURE 1. A, Intraoral view of the patient. B, Panoramic radiography of the patient.
FIGURE 2. A, Facial appearance of the patient showing failure to close the eye with effort on the affected side. B, Facial appearance of the patient showing inability to move the left corner of the mouth and smile.
paralysis, the only existing symptom may be odontalgia, which may increase the difficulty of making a diagnosis for physicians who are not familiar with this clinical picture.6 In this report, the patient reported no pain in the mastoid region. The present case lacked any apparent swelling and infectious event around the extraction socket that set this process into action. Thus, the causative factor leading to PFNP differs from other published case reports in the literature.5,7,8 Peripheral facial nerve paralysis was thought to be triggered by alveolar osteitis. Although the exact mechanism remains unclear, the most likely explanation for this may be that an existing infection that was previously restricted to the alveolar socket spread posteriorly and superiorly into the buccal or masticatory regions. The terminal branches of the facial nerve, and especially the buccal and zygomatic branches, which are likely aberrant and located near the extraction socket, could be potentially seeded with an infectious agent.6 To the best of our knowledge, this report is the first clinical condition that thought to implicate alveolar osteitis as a precipitating factor. As our case represented incomplete facial paralysis, we started with low-dose corticosteroid treatment. A shortcoming in this case report is that we could not follow the patient to determine how much the paralysis had improved. In clinical practice, it should be kept in mind that postoperative infection, even if it is minimal, may play a direct or indirect role in terminal branches of facial nerve motor neuropathy, such as presented in our case. Thus, more careful postoperative follow-up should be carried out.
REFERENCES 1. Kang TS, Vrabec JT, Giddings N, et al. Facial nerve grading systems (1985-2002): beyond the House-Brackmann scale. Otol Neurotol 2002;23:767–771 2. Shuaib A, Lee MA. Recurrent peripheral facial nerve palsy after dental procedures. Oral Surg Oral Med Oral Pathol 1990;70:738–740 3. Cousin GC. Facial nerve palsy following intra-oral surgery performed with local anesthesia. J R Coll Surg Edinb 2000;45:330–333 4. Miles PG. Facial palsy in the dental surgery. Case report and review. Aust Dent J 1992;37:262–265 5. Ling KC. Peripheral facial nerve paralysis after local dental anesthesia. Oral Surg Oral Med Oral Pathol 1985;60:23–24 6. Tolstunov L, Belaga GA. Bell’s palsy and dental infection: a case report and possible etiology. J Oral Maxillofac Surg 2010;68:1173–1178 7. Vasconcelos BC, Bessa-Nogueira RV, Maurette PE, et al. Facial nerve paralysis after impacted lower third molar surgery: a literature review and case report. Med Oral Pathol Oral Cir Bucal 2006;11:175–178 8. Burke RH, Adams JL. Immediate cranial nerve paralysis during removal of a mandibular third molar. Oral Surg Oral Med Oral Pathol 1987;63:172–174
e293
Copyright © 2015 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
