1102
UNILATERAL
J Oral Maxillofac 48:1102-1104.
PHARYNGEAL
PLEXUS
INJURY
Surg
1990
Unilateral Pharyngeal Plexus Injury Following Use of an Oropharyngeal Pack During Third-Molar Surgery ROBERT W. MERMER,DDS,*
DAVID ZWILLENBERG, MD,t ANDREW MARON, DDS,$ AND CHARLES B. BRILL, MD§
Weakness of the palate and pharynx due to trauma to the lower cranial nerves or pharyngeal plexus can be secondary to penetrating wounds of the neck, basal skull fractures,’ or local surgical procedures.‘*3 We report a case of transient unilateral pharyngeal plexus injury following third-molar extraction under general anesthesia with nasotracheal intubation in which oropharyngeal packing was used. Report of a Case A 31-year-old healthy white woman graduate student underwent elective surgical removal of all four third molars under general nasotracheal anesthesia. Premedications included fentanyl, glycopyrrolate, and midazolam. Genereal anesthesia, lasting 2 hours, was induced with sodium thiopental and vecuronium, and maintained with nitrous oxide, isoflurane, and oxygen. Nasotracheal intubation was accomplished through the right nares in one pass using a no. 6.5 cuffed tube. Marcaine (Cook-Waite Laboratories, New York, NY), OS%, (40.5 mg) containing 1:200,000 epinephrine (0.040 mg) was used for bilateral mandibular, greater palatine, and posterior superior alveolar nerve blocks. After suctioning the pharynx, a moistened oropharyngeal pack was placed. Dexamethasone and clindamycin were given intraoperatively. The surgery was uneventful except that a nondisplaced linear fracture of the alveolar lingual plate occurred associated with removal of the mandibular right third molar. There was no excessive retraction, bleeding, or suction-
* Assistant Professor, Residency Program Director, Department of Oral and Maxillofacial Surgery, Hahnemann University, Philadelphia. t Clinical Associate Professor, Department of Otorhinolaryngology, Thomas Jefferson University Hospital, Philadelphia. $ Third Year Resident, Department of Oral and Maxillofacial Surgery, Hahnemann University, Philadelphia. 5 Clinical Professor, Pediatric and Neurology Department, Thomas Jefferson University Hospital. Philadelphia. Address correspondence &d reprint requests to Dr Mermer: Department of Oral and Maxillofacial Surgery, Hahnemann University, Broad and Vine Sts, Philadelphia, PA 19102-1192. 0 1990 American geons 0276-2193/90/461
Association O-001 6$3.00/O
of Oral and Maxillofacial
Sur-
ing. The patient was extubated immediately postoperatively and had normal vital signs. Immediately following the procedure, the patient was aware of right-sided soreness in the throat, hoarseness, and nasal speech with air escape. That evening, she had nasal regurgitation of liquids on the right side, difficulty swallowing, and fear of choking. Her speech was nasal and weak, but normal in rate. There was weakness of coughing, whistling, and shouting. The letters “B” and “K” were poorly articulated. There were no other symptoms of cranial nerve, brainstem, cerebellar, or cerebral dysfunction. One week following the procedure, a superficial eschar and minor submucosal hemorrhage were noted on the right side of the nasopharynx. Indirect laryngoscopy showed normal vocal cord motion and no signs of trauma. Positive neurologic findings included palatal drooping, with absent elevation of the right side of the soft palate and deviation of the uvula to the left with respiration, phonation, and gagging. The right wall of the pharynx sagged medially and moved to the left at the beginning of phonation. There was decreased sensation to touch on the right side of the soft palate. tonsil, and posterior third of the tongue. Taste and general sensation on the anterior two thirds of the tongue were normal. The gag reflex could be elicited from both sides of the pharynx. The results of the remainder of the neurological examination were normal. The clinical impression was palatal and pharyngeal dysfunction due to trauma to the pharyngeal plexus. Three weeks postoperatively, her nasality of speech, swallowing difficulty, palatal elevation, and pharyngeal movement were improved. A speech pathologist was used for therapy and exercises to aid in recovery. Intraoral sensation. speech, swallowing, and pharyngeal motion were normal by 2 months postoperatively. There was minimal right-sided palatal weakness 3 months after surgery.
Discussion The pharyngeal plexus, which supplies sensory and motor branches to the soft palate and pharynx,4
lies in the retropharyngeal space between the superior and middle constrictor muscles anteriorly and the longus capitus and coli muscles, prevertebral fascia, and bodies of the second and third cervical vertebrae posteriorly. It is made up of sensory fi-
1103
MERMER ET AL
bers to the glossopharyngeal (IX) and vagus (XI nerves, motor branches from X and the spinal accessory (XI) nerves, and fibers from the sympathetic chain,5*6 all acting to coordinate speech and swallowing. Dysfunction of the pharyngeal plexus may be caused by nervous system lesions at various sites, including supranuclear, brain stem, peripheral nerve, and neuromuscular junction (Table I). The findings of sensory loss over the right side of the pharynx, soft palate, and posterior third of the tongue, and weakness of the right side of the pharynx and soft palate, indicated dysfunction of branches of the right IX, X, and Xl nerves. The lack of laryngeal, sternocleidomastoid, and trapezius weakness excluded injury to the main trunks of the X and XI. The presence of the gag reflex elicited from the right side of the pharynx indicated a partial lesion with a good prognosis. Normal facial sensation, movement, taste, and hearing, and the absence of diplopia, vertigo, nystagmus, tongue weakness, or bilateral involvement, excluded diffuse cranial nerve involvement. The absence of somnolence, ataxia, and spasticity excluded a brain stem lesion. Even brief intubation can cause laryngotracheal edema, resulting in transient sore throat and dysphonia.’ The patient had no evidence of laryngeal trauma on examination, I week postoperatively. The association of the patient’s immediate postprocedure localized neurological symptoms with prolonged recovery, nasotracheal intubation, oropharyngeal packing, and right-sided nasopharyngeal eschar and hemorrhage, all point to trauma to the right pharyngeal plexus as the cause of the dysfunction. The pharynx and pharyngeal plexus were probably compressed between the packing and endotracheal tube in front, and the bodies of the second and third cervical vertebrae behind, causing ischemia of the nerves. Oral surgery patients undergoing general anesthesia may be susceptible to this type of nerve injury because of neck extension and stretching due to decreased muscle tone, especially with the use of muscle relaxants, and the loss of protective perceptive power (inability to complain of pain).8 The prolonged recovery time, greater than 3 months, indicates that the axons of the nerves were injured, but that the nerve sheaths remained intact (axonotmesis).8 Healing, in this situation, occurs by axonal regeneration, at the rate of approximately 1 mm/d, after a variable latent period. Although other cranial nerve palsies (oculomotor, facial, and hypoglossal), as well as trigeminal nerve sensory deficits, have been reported following third-molar extraction,‘-” pharyngeal plexus in-
Table 1, Neurological Causes of Palatal and Pharyngeal Dysfunction
Supranuclear Pseudobulbar palsy Parkinsonism Gilles de la Tourette syndrome Brain stem Neoplasms Intrinsic brain stem Infectious Polio Syphilis Tuberculosis Rabies Genetic Spinal muscular atrophy Infantile Juvenile Progressive bulbar paralysis Malformations Arnold-Chiari Syringobulbia Amyotrophic lateral sclerosis Multiple sclerosis Vascular Hemorrhage Thromboembolic Cranial nerve, pharyngeal plexus Trauma Basal skull fracture Penetrating neck wounds Surgery Neuro Posterior fossa Jugular foramen ENT Pharyngectomy Parotid. deep lobe Vascular Carotid artery Oral Pharyngeal packing lntubation Neoplasms Head and neck carcinoma Glomus jugulare tumor Primary nerve tumors Lymphoma Metastatic Vascular Carotid artery aneurysm Jugular vein thrombosis Peripheral neuropathy Infectious Cervical adenitis Retropharyngeal abscess Herpes zoster Meningitis Diphtheria Guillain-Barre syndrome Malformations Skull base Cervical spine Neuromuscular junction Botulism
1104
NECROTIZING
Table 1. Neurological Causes of Palatal and Pharyngeal Dysfunction (Cont’d) Myasthenia gravis Myasthenic-myopathic Muscle Dystrophy Oculopharyngeal Myotonic lnflammatory Poly/dermatomyositis
syndrome (Lambert-Easton)
jury is not mentioned in texts as a complication of general anesthesia.‘,12 Superficial injury from packs and large, cuffed endotracheal tubes has been cited as the major cause of post-oral surgery sore throat, but neurologic dysfunction has not been reported.13 References 1. DeJong RN: The Neurologic Examination York, Harper & Row. 1970
(3rd ed). New
2. Weiss K, Kramar R, Fit? P: Cranial and cervical nerve in-
J Oral Marillofac
SOFT-TISSUE
INFECTIONS
Local complications of carotid artery_ surgery. J I_ Cardiovasc Surg 28: 171, 1987 3. Sataloff RT, Myers DL, Kremer FB: Management of cranial nerve injury following surgery of the skull base. Otolaryngot Clin North Am 17577, 1984 4. Broomhead IW: The nerve supply to the nerves of the soft palate. Br .I Plastic Sure 4:l. 1951 5. Kerr AG, Groves J: Sco&Brown’s Otolaryngology, Basic Sciences, vol 1 (5th ed). London, Butterworths, 1987 6. English GM: Otolaryngology, vol 3. Philadelphia, PA, Lippincott, 1984 7. Hedden M, Eroz CJ, Donnelly WH, et al: Laryngotrachael damage after prolonged use of ortracheal tubes in adults. JAMA 207:203, 1969 8. Orkin FK, Cooperman LH: Complications in anesthesiology. Philadelphia, PA, Lippincott, 1983 9. Burke RH. Adams JL: Immediate cranial nerve uaralvsis during removal of a mandibular third molar. &al !&u-g Oral Med Oral Path01 63: 172, 1987 10. Stankiewicz JA. Pazevic JP: Hvoonlossal nerve nalsv after tooth extraction. J Oral Maxiliofic Surg 46: 148, 1988 11. Robinson PP: Observation on the recovery of sensation following inferior alveolar nerve injuries. Br J Oral Maxillofat Surg 26: 177, 1988 12. Allen GD: Dental Anesthesia & Analgesia (Local & General) (3rd ed). Baltimore, MD, Williams & Wilkins, 1984 13. Fine J, Kaltman S, Bianco M: Prevention of sore throat after nasotracheal intubation. J Oral Maxillofac Surg 46946, 1988 14. Sexton J, Dohlman L: Benefits of the pharyngeal pack. J Oral Maxillofac Surg 47:891, 1989 juries:
Surg
48:1104-1108,1990
Necrotizing
Soft-Tissue Infections Dental Origin
of
DAN M. FLISS, MD,* FERIT TOVI, MD,t AND HOWARD J. ZIRKIN, MD$.
Complications of dental infections are usually confined to the adjacent soft tissues. Sometimes when fascial spaces are involved, however, deep cervical abscesses may develop that can lead to mediastinitis. Septic thrombophlebitis originating from
Received from Soroka University Hospital, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. * Lecturer, Department of Otolaryngology. t Associate Professor, Department of Otolaryngology. $ Senior Lecturer, Pathological Institute. Address correspondence and reprint requests to Dr Fliss: Department of Otolaryngology, Soroka Medical Center, PO Box 151, Beer-Sheva 84101, Israel. 0 1990 American
Association
geons 0278-21931901481 O-001 7$3.00/O
of Oral and Maxillofacial
Sur-
a primary dental infection occasionally results in orbital or intracranial complications. Another uncommon, but life-threatening complication of dental infection is necrotizing soft-tissue infection (NSTI). This fulminant and devastating entity has been reported to develop initially in the cervical fascia, but as the infectious necrotizing process spreads, soft-tissue components below and above the affected fascia also may become involved. Late diagnosis has been associated with increased morbidity and high mortality rates. Among the 15 cases of NSTI treated in the Otolaryngology, Head and Neck Department of the Soroka Medical Center during the last 10 years, 3 cases were of dental origin. This article reports our experience with this unusual and aggressive condition.
UNILATERAL
J Oral Maxillofac 48:1102-1104.
PHARYNGEAL
PLEXUS
INJURY
Surg
1990
Unilateral Pharyngeal Plexus Injury Following Use of an Oropharyngeal Pack During Third-Molar Surgery ROBERT W. MERMER,DDS,*
DAVID ZWILLENBERG, MD,t ANDREW MARON, DDS,$ AND CHARLES B. BRILL, MD§
Weakness of the palate and pharynx due to trauma to the lower cranial nerves or pharyngeal plexus can be secondary to penetrating wounds of the neck, basal skull fractures,’ or local surgical procedures.‘*3 We report a case of transient unilateral pharyngeal plexus injury following third-molar extraction under general anesthesia with nasotracheal intubation in which oropharyngeal packing was used. Report of a Case A 31-year-old healthy white woman graduate student underwent elective surgical removal of all four third molars under general nasotracheal anesthesia. Premedications included fentanyl, glycopyrrolate, and midazolam. Genereal anesthesia, lasting 2 hours, was induced with sodium thiopental and vecuronium, and maintained with nitrous oxide, isoflurane, and oxygen. Nasotracheal intubation was accomplished through the right nares in one pass using a no. 6.5 cuffed tube. Marcaine (Cook-Waite Laboratories, New York, NY), OS%, (40.5 mg) containing 1:200,000 epinephrine (0.040 mg) was used for bilateral mandibular, greater palatine, and posterior superior alveolar nerve blocks. After suctioning the pharynx, a moistened oropharyngeal pack was placed. Dexamethasone and clindamycin were given intraoperatively. The surgery was uneventful except that a nondisplaced linear fracture of the alveolar lingual plate occurred associated with removal of the mandibular right third molar. There was no excessive retraction, bleeding, or suction-
* Assistant Professor, Residency Program Director, Department of Oral and Maxillofacial Surgery, Hahnemann University, Philadelphia. t Clinical Associate Professor, Department of Otorhinolaryngology, Thomas Jefferson University Hospital, Philadelphia. $ Third Year Resident, Department of Oral and Maxillofacial Surgery, Hahnemann University, Philadelphia. 5 Clinical Professor, Pediatric and Neurology Department, Thomas Jefferson University Hospital. Philadelphia. Address correspondence &d reprint requests to Dr Mermer: Department of Oral and Maxillofacial Surgery, Hahnemann University, Broad and Vine Sts, Philadelphia, PA 19102-1192. 0 1990 American geons 0276-2193/90/461
Association O-001 6$3.00/O
of Oral and Maxillofacial
Sur-
ing. The patient was extubated immediately postoperatively and had normal vital signs. Immediately following the procedure, the patient was aware of right-sided soreness in the throat, hoarseness, and nasal speech with air escape. That evening, she had nasal regurgitation of liquids on the right side, difficulty swallowing, and fear of choking. Her speech was nasal and weak, but normal in rate. There was weakness of coughing, whistling, and shouting. The letters “B” and “K” were poorly articulated. There were no other symptoms of cranial nerve, brainstem, cerebellar, or cerebral dysfunction. One week following the procedure, a superficial eschar and minor submucosal hemorrhage were noted on the right side of the nasopharynx. Indirect laryngoscopy showed normal vocal cord motion and no signs of trauma. Positive neurologic findings included palatal drooping, with absent elevation of the right side of the soft palate and deviation of the uvula to the left with respiration, phonation, and gagging. The right wall of the pharynx sagged medially and moved to the left at the beginning of phonation. There was decreased sensation to touch on the right side of the soft palate. tonsil, and posterior third of the tongue. Taste and general sensation on the anterior two thirds of the tongue were normal. The gag reflex could be elicited from both sides of the pharynx. The results of the remainder of the neurological examination were normal. The clinical impression was palatal and pharyngeal dysfunction due to trauma to the pharyngeal plexus. Three weeks postoperatively, her nasality of speech, swallowing difficulty, palatal elevation, and pharyngeal movement were improved. A speech pathologist was used for therapy and exercises to aid in recovery. Intraoral sensation. speech, swallowing, and pharyngeal motion were normal by 2 months postoperatively. There was minimal right-sided palatal weakness 3 months after surgery.
Discussion The pharyngeal plexus, which supplies sensory and motor branches to the soft palate and pharynx,4
lies in the retropharyngeal space between the superior and middle constrictor muscles anteriorly and the longus capitus and coli muscles, prevertebral fascia, and bodies of the second and third cervical vertebrae posteriorly. It is made up of sensory fi-
1103
MERMER ET AL
bers to the glossopharyngeal (IX) and vagus (XI nerves, motor branches from X and the spinal accessory (XI) nerves, and fibers from the sympathetic chain,5*6 all acting to coordinate speech and swallowing. Dysfunction of the pharyngeal plexus may be caused by nervous system lesions at various sites, including supranuclear, brain stem, peripheral nerve, and neuromuscular junction (Table I). The findings of sensory loss over the right side of the pharynx, soft palate, and posterior third of the tongue, and weakness of the right side of the pharynx and soft palate, indicated dysfunction of branches of the right IX, X, and Xl nerves. The lack of laryngeal, sternocleidomastoid, and trapezius weakness excluded injury to the main trunks of the X and XI. The presence of the gag reflex elicited from the right side of the pharynx indicated a partial lesion with a good prognosis. Normal facial sensation, movement, taste, and hearing, and the absence of diplopia, vertigo, nystagmus, tongue weakness, or bilateral involvement, excluded diffuse cranial nerve involvement. The absence of somnolence, ataxia, and spasticity excluded a brain stem lesion. Even brief intubation can cause laryngotracheal edema, resulting in transient sore throat and dysphonia.’ The patient had no evidence of laryngeal trauma on examination, I week postoperatively. The association of the patient’s immediate postprocedure localized neurological symptoms with prolonged recovery, nasotracheal intubation, oropharyngeal packing, and right-sided nasopharyngeal eschar and hemorrhage, all point to trauma to the right pharyngeal plexus as the cause of the dysfunction. The pharynx and pharyngeal plexus were probably compressed between the packing and endotracheal tube in front, and the bodies of the second and third cervical vertebrae behind, causing ischemia of the nerves. Oral surgery patients undergoing general anesthesia may be susceptible to this type of nerve injury because of neck extension and stretching due to decreased muscle tone, especially with the use of muscle relaxants, and the loss of protective perceptive power (inability to complain of pain).8 The prolonged recovery time, greater than 3 months, indicates that the axons of the nerves were injured, but that the nerve sheaths remained intact (axonotmesis).8 Healing, in this situation, occurs by axonal regeneration, at the rate of approximately 1 mm/d, after a variable latent period. Although other cranial nerve palsies (oculomotor, facial, and hypoglossal), as well as trigeminal nerve sensory deficits, have been reported following third-molar extraction,‘-” pharyngeal plexus in-
Table 1, Neurological Causes of Palatal and Pharyngeal Dysfunction
Supranuclear Pseudobulbar palsy Parkinsonism Gilles de la Tourette syndrome Brain stem Neoplasms Intrinsic brain stem Infectious Polio Syphilis Tuberculosis Rabies Genetic Spinal muscular atrophy Infantile Juvenile Progressive bulbar paralysis Malformations Arnold-Chiari Syringobulbia Amyotrophic lateral sclerosis Multiple sclerosis Vascular Hemorrhage Thromboembolic Cranial nerve, pharyngeal plexus Trauma Basal skull fracture Penetrating neck wounds Surgery Neuro Posterior fossa Jugular foramen ENT Pharyngectomy Parotid. deep lobe Vascular Carotid artery Oral Pharyngeal packing lntubation Neoplasms Head and neck carcinoma Glomus jugulare tumor Primary nerve tumors Lymphoma Metastatic Vascular Carotid artery aneurysm Jugular vein thrombosis Peripheral neuropathy Infectious Cervical adenitis Retropharyngeal abscess Herpes zoster Meningitis Diphtheria Guillain-Barre syndrome Malformations Skull base Cervical spine Neuromuscular junction Botulism
1104
NECROTIZING
Table 1. Neurological Causes of Palatal and Pharyngeal Dysfunction (Cont’d) Myasthenia gravis Myasthenic-myopathic Muscle Dystrophy Oculopharyngeal Myotonic lnflammatory Poly/dermatomyositis
syndrome (Lambert-Easton)
jury is not mentioned in texts as a complication of general anesthesia.‘,12 Superficial injury from packs and large, cuffed endotracheal tubes has been cited as the major cause of post-oral surgery sore throat, but neurologic dysfunction has not been reported.13 References 1. DeJong RN: The Neurologic Examination York, Harper & Row. 1970
(3rd ed). New
2. Weiss K, Kramar R, Fit? P: Cranial and cervical nerve in-
J Oral Marillofac
SOFT-TISSUE
INFECTIONS
Local complications of carotid artery_ surgery. J I_ Cardiovasc Surg 28: 171, 1987 3. Sataloff RT, Myers DL, Kremer FB: Management of cranial nerve injury following surgery of the skull base. Otolaryngot Clin North Am 17577, 1984 4. Broomhead IW: The nerve supply to the nerves of the soft palate. Br .I Plastic Sure 4:l. 1951 5. Kerr AG, Groves J: Sco&Brown’s Otolaryngology, Basic Sciences, vol 1 (5th ed). London, Butterworths, 1987 6. English GM: Otolaryngology, vol 3. Philadelphia, PA, Lippincott, 1984 7. Hedden M, Eroz CJ, Donnelly WH, et al: Laryngotrachael damage after prolonged use of ortracheal tubes in adults. JAMA 207:203, 1969 8. Orkin FK, Cooperman LH: Complications in anesthesiology. Philadelphia, PA, Lippincott, 1983 9. Burke RH. Adams JL: Immediate cranial nerve uaralvsis during removal of a mandibular third molar. &al !&u-g Oral Med Oral Path01 63: 172, 1987 10. Stankiewicz JA. Pazevic JP: Hvoonlossal nerve nalsv after tooth extraction. J Oral Maxiliofic Surg 46: 148, 1988 11. Robinson PP: Observation on the recovery of sensation following inferior alveolar nerve injuries. Br J Oral Maxillofat Surg 26: 177, 1988 12. Allen GD: Dental Anesthesia & Analgesia (Local & General) (3rd ed). Baltimore, MD, Williams & Wilkins, 1984 13. Fine J, Kaltman S, Bianco M: Prevention of sore throat after nasotracheal intubation. J Oral Maxillofac Surg 46946, 1988 14. Sexton J, Dohlman L: Benefits of the pharyngeal pack. J Oral Maxillofac Surg 47:891, 1989 juries:
Surg
48:1104-1108,1990
Necrotizing
Soft-Tissue Infections Dental Origin
of
DAN M. FLISS, MD,* FERIT TOVI, MD,t AND HOWARD J. ZIRKIN, MD$.
Complications of dental infections are usually confined to the adjacent soft tissues. Sometimes when fascial spaces are involved, however, deep cervical abscesses may develop that can lead to mediastinitis. Septic thrombophlebitis originating from
Received from Soroka University Hospital, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. * Lecturer, Department of Otolaryngology. t Associate Professor, Department of Otolaryngology. $ Senior Lecturer, Pathological Institute. Address correspondence and reprint requests to Dr Fliss: Department of Otolaryngology, Soroka Medical Center, PO Box 151, Beer-Sheva 84101, Israel. 0 1990 American
Association
geons 0278-21931901481 O-001 7$3.00/O
of Oral and Maxillofacial
Sur-
a primary dental infection occasionally results in orbital or intracranial complications. Another uncommon, but life-threatening complication of dental infection is necrotizing soft-tissue infection (NSTI). This fulminant and devastating entity has been reported to develop initially in the cervical fascia, but as the infectious necrotizing process spreads, soft-tissue components below and above the affected fascia also may become involved. Late diagnosis has been associated with increased morbidity and high mortality rates. Among the 15 cases of NSTI treated in the Otolaryngology, Head and Neck Department of the Soroka Medical Center during the last 10 years, 3 cases were of dental origin. This article reports our experience with this unusual and aggressive condition.
