Cavernous sinus thrombosis complicating odontogenic parapharyngeal space neck abscess: A case report and discussion D. P. FELDMAN, BA, N. A. PICERNO, BS, MD, and E. S. PORUBSKY, MD, Carmel, Indiana
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69-year-old black male was transferred from a community health center for further evaluation and treatment of a bilateral proptosis with ophthalmoplegia. The patient’s family reported that he was started on penicillin 500 mg 4 times a day 6 days earlier for a dental abscess. The patient was brought to the hospital several days later complaining of weakness, diplopia, diaphoresis, and lethargy. Computed tomography at the time of initial admission revealed no intracranial abnormalities, however, a right hypodense parapharyngeal mass was noted. This mass exhibited compression of the adjacent airway and appeared to have extension into the carotid space. Because of the progressive mental status changes and deteriorating airway, the patient was taken to the operating room, intubated, and examined under anesthesia. Attempts at aspiration of the abscess were unsuccessful, and the patient was transferred to our institution. Physical examination at the time of arrival revealed an intubated patient who was able to follow verbal commands. Head examination illustrated bilateral proptosis, severe chemosis, complete ophthalmoplegia, and pupils equal but nonreactive. Facial swelling and periorbital cellulitis were present bilaterally. Corneal reflex was absent. The right neck was tender to palpation and edematous. Cranial nerves VII through XII were intact. A respiratory examination found a bilateral air entry with wheezing. Cardiovascular, gastrointestinal, genitourinary, and extremity findings were noncontributory. The only significant laboratory data were an elevated white count of 15.6 with 78 polymorpho-nuclear cells and 11 bands. The initial choice of antibiotics included ampicillin sulbactam 3g 4 times a day and clindamycin 900 mg 3 times a day, both given intravenously. The CT scan revealed a right parapharyngeal abscess and a bilateral cavernous sinus thrombosis with progression of the inflammation since the CT scan at the other hospital 48 hours earlier. Consultation with neu-
From the Medical College of Georgia, School of Medicine (Dr Feldman) and the Department of Otolaryngology (Drs Picerno and Porubsky). Reprint requests: Nicolette A Picerno, MD, 11546 Spring Way Dr, Carmel, IN 46033; e-mail:
[email protected] Otolaryngol Head Neck Surg 2000;123:744-5. Copyright © 2000 by the American Academy of Otolaryngology– Head and Neck Surgery Foundation, Inc. 0194-5998/2000/$12.00 + 0 23/4/110964 doi:10.1067/mhn.2000.110964 744
rology and ophthalmology physicians resulted in anticoagulation therapy with heparin to elevate the partial thermboplastin time. Timolol 0.5% eye drops were administered twice a day. The following day, the patient underwent a tracheotomy, incision and drainage of the parapharyngeal abscess, and extraction of the right third molar. A large volume of purulent drainage was removed from the abscess with dissection made to the styloid process. The wound was irrigated with saline solution and 2 large bore drains were inserted. Postoperatively the patient did well. The infectious disease department was consulted. They recommended nafcillin, ceftriaxone, and metronidazole for coverage of the diphtheroid and Pseudomonas grown in the wound cultures. These organisms were also cultured from the eyes. The patient began to improve by postoperative day 3. He was weaned off the ventilator and transferred to the floor on postoperative day 7. Mental status and vision also steadily improved. Antibiotics were continued for a total of 17 days. Heparin was converted to warfarin, and the patient was discharged to a rehabilitation facility on day 21. At his 6 month follow-up, the patient had completely recuperated and had no residual cranial nerve deficits. DISCUSSION In our review of the literature over the past 40 years, we were able to discover only 1 case in which a mandibular dental infection indirectly caused thrombosis of the cavernous sinus.1 Mazzeo cited that mandibular infections may gain access to the carotid sheath via the parapharyngeal space or by
Fig 1. Preoperative view of orbital cellulitis, proptosis, chemosis, and ophthalmoplegia.
Otolaryngology– Head and Neck Surgery Volume 123 Number 6
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entering the pterygoid plexus directly from the alveolar ridge2; infection can thereby spread directly to the dural sinuses. The literature is full of numerous cases in which maxillary dental abscesses were the nidus to the ailment. Postoperative complications are more common and potentially more serious after extraction of maxillary molars, which correlates with the increased number of studies found in the literature.3 Our case was further complicated by a parapharyngeal abscess, which led to a more precipitous decline in the patient’s health before admission to the hospital. The patient presented to our hospital with the classical signs of a cavernous sinus thrombosis: bilateral proptosis, chemosis, sluggish pupils, palsy of cranial nerves III, IV, and VI, and a lack of a corneal reflex. Literature4 has stated that the advancement of unilateral to bilateral proptosis of the eyes is pathognomonic to the above diagnosis. The lack of extraocular movements is to be expected since cranial nerves III, IV, VI, V1, and V2 run either within or against the cavernous sinus; inflammation of this area would compress the nerves, creating the above physical symptoms. Our patient was immediately transferred to the critical care unit where the infectious disease department assisted with the initial choice of broad spectrum antibiotics. The chosen antibiotics then included nafcillin, ceftriaxone, and metronidazole when cultures taken from the parapharyngeal abscess led to the isolation of diphtheroid and pseudomonad species; the nafcillin was instituted since between half to two thirds of cases involving cavernous sinus thrombosis involve Staphylo-
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coccus aureus.5 Standard procedure was initiated to anticoagulate the patient with heparin to degrade and prevent the progression of the thrombosis. The most common cause of cavernous sinus thrombosis is infection of the sphenoid and ethmoid sinuses; otitis media is the second most common cause, with maxillary dental infection accounting for only 10% of the dural infections.4 This case was unique in that not only was the nidus of infection from an unusual location, the parapharyngeal space via the mandibular tooth, but the patient regained complete function without deficit after treatment and rehabilitation. The preantibiotic days had mortality rates for thrombosis of the cavernous sinus in the range of 100%.5 Morbidity and mortality still remain elevated today, with 20% to 34% of patients still dying with treatment. More than 50% of those who recover do so with permanent deficits, including blindness, nerve palsy, coma, or neurologic abnormalities. REFERENCES: 1. Ogundiya D, Keith D, Mirowski J. Cavernous sinus thrombosis and blindness as complications of an odontogenic infection. Oral Maxillofac Surg 1989;47:1317-21. 2. Mazzeo V. Cavernous sinus thrombosis. J Oral Med 1974;29:536. 3. Dever C, Sazima H, Schaberg S. Life threatening infection after extraction of third molars. J Am Dent Assoc 1980;101:649-50. 4. Ahmmed A, Camilleri A, Small M. Cavernous sinus thrombosis following manipulation of fractured nasal bones. J Laryngol Otol 1996;110:69-71. 5. Kriss T, Kriss V, Warf B. Cavernous sinus thrombophlebitis: case report. Neurosurgery 1996;39:2.
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