Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Frontal Sinusitis Sinusitis affects approximately .5-5% of individuals suffering from viral upper respiratory tract infections. The exact percentage of persons developing frontal sinusitis is not known although roughly 3-6% of children with pansinusitis will have frontal disease. Anatomically the frontal sinus is a pyramidal shaped structure with vertical and horizontal segments in the frontal bone. It borders the anterior cranial fossa and the roof of the orbit. The supratrochlear artery provides an inflow of blood while the dural, diploic, supraorbital, and ophthalmic veins drain the frontal sinus mucosa. Supraorbital and supratrochlear branches of the fifth cranial nerve supply sensation. The lining of all of the paranasal sinuses is pseudostratified ciliated columnar epithelium continuous with the posterior two-thirds of the nose. The anterior wall of the frontal sinus is cancellous bone while the floor is a laminar plate without a marrow cavity. Fifty-five percent of frontal sinuses drain directly into the frontal recess, 30% above the ethmoid infundibulum, 15% into the infundibulum, and 1% above the ethmoid bulla. The frontal sinus, not present at birth, develops from either the frontal recess or from anterior ethmoidal cells. It is radiographically visible by seven years of age and reaches full size by adulthood. The etiology of frontal sinusitis stems from blockage of the nasofrontal duct ostium. Mechanical obstruction and local mucosal edema lead to symptoms of frontal headache, fever, rhinorrhea and cough. Progression to chronic disease should be suspected with evidence of trauma near the sinus ostia, long standing inflammation of sinus mucosa, persistent headache or sinus opacification on radiographs. Acute sinusitis in adults has been tied to non-typable H. influenza, S. pneumonia, S. pyogenes, alpha hemolytic streptococcus, and neisseria. S. pneumonia, B. catarrhalis, and H. influenza account for acute disease in children. Organisms associated with chronic sinusitis are the same in adults and children and include chronic respiratory anaerobes (streptococcus, bacteroides, veillonella), along with H. influenza, S. viridans, and an occasional staphylococcal species. Surface cultures of nasal mucosa do not correlate with sinus aspirates for bacterial identification. Radiological work-up of frontal sinus disease should be guided by clinical suspicion. Caldwell and Water's views provide the best plain film evidence of opacification, mucosal thickening,and air/fluid levels. Computed tomography can be used to assess intracranial and bony involvement. Magnetic resonance imaging and A-mode ultrasound are of limited use in this disease. Medical treatment consists of analgesics, topical decongestants, and antibiotics. Persistent frontal pain, periorbital edema, and forehead edema indicate disease progression mandating surgical intervention. Removal of intranasal foreign bodies, crushing the middle turbinate, and septoplasty focus on alleviating mechanical nasal obstruction. Trephination should be done in the floor of the sinus to avoid contamination of the cancellous bone with bacteria predisposing to future osteomyelitis. A drain placed through the trephine allows extrusion of sinus contents and can be used to irrigate with antibiotic solutions. External approaches by Reidel, Killian, Lothrop, and Lynch have been abandoned in most cases due to the cosmetic deformities they produce. The Sewall-Boyden procedure of trephination, external ethmoidectomy, and nasofrontal duct reconstruction has been proposed with recurrence of sinusitis in 14% of patients. The osteoplastic flap with frontal sinus obliteration using abdominal fat is considered the definitive procedure of choice for treating chronic frontal sinusitis. Recently, however, endoscopic enlargement ot the frontal sinus ostium has gained attention. Removal of agar nasi cells and entrance through the floor of the frontal sinus with silastic stenting provides drainage without disfiguring skin incisions. Endoscopic frontal sinus approaches have not gained wide popularity in the pediatric population. More study with attention to long term follow-up is needed before endoscopic therapies can become preferred methods of treatment. Complications of frontal sinusitis include recurrent sinusitis, mucocele, pyocele, orbital sequelae, and intracranial spread of infection. Mucoceles develop from inadequately removed sinus mucosa in a poorly drained space. They expand locally and erode bone due to the secretion of high levels of PGE-2. Pyoceles form when mucoceles become secondarily infected. Orbital complications include optic neuritis, cellulitis, subperiosteal abscess formation, and intraorbital abscess. Intracranial spread of infection leads to meningitis, subdural empyema, brain abscess, and cavernous sinus thrombosis. The consortium of frontal osteomyelitis and subperiosteal abscess have been termed Pott's Puffy Tumor. Signs and symptoms include a soft and fluctuant forehead mass, headache, photophobia and fever. The patient presented in this grand rounds had these findings and illustrated the need for aggressive operative treatment and consultation by the neurosurgical service. The initial trephination did not drain the abscess because the pus had tracked in the cancellous meshwork of the frontal bone and was not localized to the frontal sinus. Violation of the posterior table of bone in the sinus mandated removal of involved bone and inspection of the dura. This patient also received six weeks of intravenous antibiotics and will have close long term follow-up. In summary, frontal sinusitis is a very serious condition requiring aggressive medical management with a low index of suspicion for the development of complications requiring surgical intervention. Intracranial complications often require evaluation by the neurosurgical service with a combined surgical approach to remove infected tissues. The length of antibiotic therapy is dictated by the seriousness of disease. Long term follow-up is mandatory. Case Presentation A 15-year-old white male referred with left frontal headaches and a soft mass over his left forehead. The pain started two months prior to presentation after a contact lens caused left eye irritation with orbital swelling. He had received courses of Keflex and Cefotetan prior to admission. He denied nasal obstruction, rhinorrhea, fever, head trauma, and could not relate the onset of pain to swimming. His physical exam revealed full function in all cranial nerves, mild left upper eyelid edema, and a three centimeter swelling over the left eyebrow. His left turbinate was pale, edematous and refractory to treatment with neosynephrine drops. A CT scan of the head revealed left ethmoid and frontal opacification with left maxillary mucosal thickening. Also noted was a left frontal mass consistent with a subperiostial abscess. A frontal trephination did not relieve the mass on his forehead necessitating frontal sinus obliteration and removal of osteomyelitic cranial bone. He will have a complete six week course of intravenous antibiotics with close follow-up in Nacogdoches. 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