Glinical Aspects of Diseases of the Nose, Sinuses, and Face 159 «The drug must not damage the ciliary action, the mucosa, or the superficial film of secretions. ‘+ The pH of the drug should be around 7.0, and its osmotic pressure should be between 0.5 and double isotonic; hypertonic solutions dry out the nasal mucosa. ‘© Locally applied drugs should not have general- ized effects, and should be neither antigenic nor carcinogenic. Groups of drugs. Vasoactive substances—e.g., epi nephrine, or imidazoline derivatives such as naph- azoline and xylometazoline—cause the mucosa to shrink due to vasoconstriction. Uncritical persistent Use involves a risk of habituation, leading to rhinitis medicamentosa and resistant mucosal swelling, failure of the autonomic vascular regulation, and organic mucosal damage. Local or systemic decon- gestants of any type should therefore be used for a brief period only—i.e,, fora maximum of 1-2 weeks ata time. ed Note: In infants and small children, there is a risk of acute intoxication due to the use of nose drops. Special preparations should therefore be used for children. Antibiotics: The prerequisites for antibiotic treat- ment are a correct diagnosis, a clear indication for antibioticuse, and selection of the most appropriate antibiotic and duration of treatment. Swabs and cultures, white blood counts, erythrocyte sedimen- tation rate (ESR), C-reactive protein (CRP) assay, and in certain cases procalcitonin values are impor- tant for diagnosis and assessment of the course. Usually, several antibiotics are equally suitable. ‘The final choice depends on the severity of the disease, the patient's immune status, age, allergies, impairment of liver or kidney function, the activity spectrum of the antibiotic, potential undesired re- actions, and price. Specific information on the most common pathogens and recommended antibiotics is dis- cussed under the headings for the individual clin- ical entities. Corticosteroids: These are a double-edged sword. Although they have strong antiallergic and antiin- flammatory effects on the upper airways, they also elicit inflammation at other sites, especially in the gastrointestinal tract. Modern topical corticoste- roids—e.g., mometasone, fluticasone, of triamcino- lone—have marked anti-inflammatory and antial- lergic effects on the nasal mucosa, but very low biological availability. Because they are absorbed only to a very slight extent, they appear in minimal concentrations in serum, thus avoiding side effects and allowing long-term administration. Treatmentis usually empirical at first. Ideally, itshould be reconsidered after reexamining the patient 48-72 hours later in the light of results for cultures, resistance testing or blood cultures, and should then be continued with the most suitable drug. If possible, anarrow-spectrum antibiotic is preferable to a broad-spectrum one Mild bacterial rhinitis in an immunologically competent patient does not require antibiotic therapy. Oral corticosteroids should be given in single, decreasing (tapered) doses in the morning over a period of up to 3 weeks. Secretolytic agents: In Germany, standardized Myrtol has been shown to be effective in acute sinusitis and acute bronchitis. It has various effects on inflamed mucosa in the nose and paranasal si- nuses. It alkalizes the acidic mucosal environment and has secretolytic, secretomotoric, and antimi- crobial effects. Standardized Myrtol may be given for mild bacterial infections or can be used to sup- plement an antibiotic. Antihistamines, leukotriene antagonists, cro- mons: See pp. 150, 168. = Acute and Chronic Rhinosinusitis The European Position Paper on Rhinosinusitis and Nasal Polyps (2005) recommends use of the term “rhinosinusi- tis'—firstly because every infection of the nose involves the mucosa ofthe paranasal sinuses, which reacts in various ‘ways and at various intensities, and secondly because the ‘reat majority of acute and chronic inflammations of the paranasal sinuses are rhinogenous. This section is based on the following interna- tional consensus statements and position papers, and as far as possible on evidence-based criteria: + European Position Paper on Rhinosinusitis and Nasal Polyps (2005, 2007). * The World Health Organization (WHO) guide- lines on Allergic Rhinitis and its Impact on ‘Asthma (ARIA) (2001).160 __2 Nose, Nasal Sinuses, and Face Fig. 2.44 The anterior ethmoidal labyrinth isthe etiologic center for acute, recurrent, and chronic inflammations of the maxillary and frontal sinuses. The mucosal disease spreads radially from the ethmoid to the large sinuses, olfactory rim, and inferior turbinate. Inflammation may spread to the orbit through the lamina papyracea, ‘+ International Conference on Sinus Disease: Ter- minology, Staging, Therapy (Princeton, 2003). ‘+ Recommendations of the European Academy of Allergology and Clinical Immunology (EAACI). ‘* The European Rhinology Society (ERS) EP30S document (2007), ‘+ The European Position Paper on Rhinosinusitis and Nasal Polyps (EP30S), published by the European Rhinologic Society (ERS) (2007). Pathogens and Antibiotics (Initial Empirical Therapy) Acute rhinosinusitis: Pathogens include Streptococ- cus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, Streptococcus pyogenes, and anaerobic bacteria. Antibiotics: ami- nopenicillin with or without a B-lactamase inhibi- tor; second- and third-generation cephalosporins, macrolides, and quinolones. In severe disease, in- travenous administration, otherwise orally. Chronic rhinosinusitis: Pathogens: Staphylococ- ‘cus aureus, Streptococcus pneumoniae, Haemophilus influenzae, Pseudomonas, anaerobic bacteria, fungi; beware of mixed infections. Antibiotics: aminope- nicillin with or without a B-lactamase inhibitor; ‘macrolides, quinolones, second- and third-genera- tion cephalosporins, and clindamycin. In severe dis- ease, intravenous administration. Acute Rhinosinusitis ‘Acute and intermittent rhinosinusitis is defined as sudden onset of two or more of the following symp- toms: blockage/congestion, discharge, anterior/post- nasal drip, facial pain/pressure, reduction/loss of smell for up to 12 weeks, Ethmoidal Sinusitis The anterior ethmoid bone is the morphologic con- nection between the nose and the maxillary and frontal sinuses, Both paranasal sinuses drain through the anterior ethmoid to the nose (Figs. 2.44, 2.45), Viral, bacterial, or allergic infections of the nasal mucosa or nasopharynx spread immedi- ately to the ethmoidal sinus. Mucosal swelling, edema, and subsequently hyperplasia lead to ob- struction of the drainage routes (ethmoidal infun- dibulum, frontal recess), backup of secretions, and infection of the frontal and maxillary sinuses. Clinical Features. Impaired nasal breathing, hypos- ‘mia or anosmia, sensation of pressure between the eye and nose, subfebrile temperatures, acute in- flammation; depending on severity, a feeling of pressure and pain in frontal and maxillary sinuses (Figs. 2.46, 2.47a,b). Diagnosis. Routine otorhinolaryngology examina- tion; inspection (attention to edema of the upper eyelid); palpation of the medial angle of the eye, exclusion of diplopia; nasal endoscopy (critical): mucosal edema, track of pus in the middle nasal meatus; swabs for culture and resistance testing. Diagnostic imaging: Paranasal sinuses (occipito- ‘mental andjor occipitonasal projections), coronal CT in case of recurrent exacerbations or chronic sinusitis and always before surgery.Glinical Aspects of Diseases of the Nose, Sinuses, and Face 161 Fig. 2.45 Schematic illustration of typical cell formations | ‘causing recurrent sinusitis. a, Cell formations in the medial ‘orbital wal, with a large ethmoidal bulla and orbitoethmoid cells (Haller cells); b, pneumatized sections of the middle turbinate; «, the uncinate process, which varies in size, length, and point of insertion; d, deviated nasal septum. Olfactometry, allergy tests (prick test, RAST) in chronic and recurrent forms. Differential diagnosis. Charlin neuralgia, cluster headaches. Complications. Especially in children, rapid spread to the orbital cavity (due to thinness of the lamina apyracea) and development of orbital complica- tions (see p. 186). Treatment. Acute ethmoidal sinusitis: Decongestant nose drops, high tamponades, decongestion and aspiration of the middle nasal meatus. Application of infrared light or microwave or short-wave ther- apy, secretolytic agents; administration of antibiot- ics in case of failure of conservative therapy or Fig.2.46 Schematicillutration of ethmoidal sinusitis. Chit dren are at particular risk for orbital complications, due to the thinness of the lamina papyracea, (ilustration courtesy of A. Muecke, Berlin, Germany.) purulent infection (see maxillary sinusitis). Possibly oral corticosteroids, or medialization of the medial turbinate. In some countries, supplementing anti- biotics with simple antral lavage in severe acute purulent sinusitis has been found to be often effec- tive. Surgery is indicated for recurrent sinusitis with involvement of the maxillary and/or frontal sinuses, orbital, or central complications. Chronic ethmoidal sinusitis: Topical corticoste- roids, antibiotics. Surgery is indicated if conserva~ tive therapy has failed, for recurrent sinusitis (max- illary and/or frontal), for nasal and paranasal poly- posis, for chronic sinusitis with or without bron- chial asthma, or for suspected tumor. The surgical techniques depend on endoscopic and CT findings: infundibulotomy; anterior or complete ethmoidec- tomy, possibly with supraturbinate fenestration of162 2 Nose, Nasal Sinuses, and Face the maxillary cavity or enlargement of the frontal recess; pansinus operation. Maxillary Sinusitis Acute or chronic bacterial, fungal, or allergic rhi- nogenous, or (more rarely) odontogenic inflamma- tion. The vast majority of cases originate at the lateral nasal wall and the anterior ethmoid. The maxillary and frontal sinuses are functionally downstream from the ethmoid. Symptoms of acute maxillary sinusitis. These in- clude acute pain in the central and ipsilateral parts of the face, hyperesthesia of the facial skin, but occasionally only a sensation of pressure or fullness. Sensitivity to tapping over the check, ipsilateral swelling of the turbinates, and a stream of pus in the middle meatus and on the floor of the nose are other findings (Figs. 2.48, 2.49). Odontogenic sinusitis: Pathogens are Streptococ- cus intermedius and Streptococcus constellatus, often mixed with anaerobes (e.g., Fusobacteria, Peptostreptococcus, ot Prevotella). Symptoms of chronic maxillary sinusitis. Pain is often slight, and there may be only a sensation of pressure. Symptoms also include headache that in- creases on bending head forward, swollen cheeks, palpebral edema, chronicnasal obstruction, mucoid or purulent secretion, painful trigeminal nerve exit, Fig.2.47a,b aAS-yearold boy with palpebral edema as 8 sign of incipient orbital complications. b The axial CTshows eth- moid sinusitis and neuralgia in the distribution of the infraorbital nerve, disorders of smell including cacosmia, nasal fetor, chronic rhinitis, and hypertrophic turbinates, streams of secretion, and possibly polyps. Diagnosis. Case history, routine otorhinolaryngol- ogy examination, inspection, palpation (cheek, fa- cial wall of maxillary sinus), nasal endoscopy, ex- amination for pain on bending head forward and of nerve exits, pain on tapping, percussion of the teeth, dental status, Sonography: A-mode ultrasound reveals partial or total echo at the back wall of the maxillary sinus. Radiography: Plain radiography shows partial or total clouding, or an air-fluid level in the maxillary sinus. CT is appropriate in severe cases, in chronic sinusitis, when complications are present, and if surgery is indicated. Allergy testing: Prick test, RAST, intranasal prov- ocation, Treatment of acute rhinogenous sinusitis. Conser- vative, Nasal detumescence by use of decongestant nose drops, heat application (infrared light at a distance of 30 cm from the face and nose) or deep heat (short wave), steam inhalation with chamo- mile or volatile oils. Herbal secretolytic agents (e.g., standardized Myrtol, which has bacteriostatic, mucolytic, secre-Clinical Aspects of Diseases of the Nose, Sinuses, and Face 163 tomotoric, and deodorizing effects); analgesics (paracetamol, ibuprofen). Note: Acetylsalicylic acid (ASA, aspirin) must be used ‘with caution, due to the high rate of ASA intolerance among sinusitis patients. Antibiotics: The first choice is an aminopenicillin in ‘combination with a B-lactamase inhibitor, or a sec- ond- or third-generation cephalosporin. Alterna- tives are macrolides, ketolides, or third- or fourth- generation fluoroquinolones, as indicated by resis- tance testing. Lavage or drainage of the maxillary sinus is in- dicated in persistent empyema (swabs should be taken first). In patients with allergies, a third-generation antihistamine (see p. 151), steroids (topical or oral), or hyposensitization are indicated, In suspected Aspergillus infection, a search should be made for a foreign body (overstuffed root canal; endoscopy of the maxillary sinus). For Aspergillus sinusitis, see p. 182. Treatment of acute odontogenic sinusitis. Inpatients with odontogenic sinusitis, the first-line treatment is dental repair, root canal treatment, or extraction. Antibiotics: The first choice is penicillin (phenoxymethyl penicilin, aminopenicilin plus a Bactamase inhibitor); ater- natives (after resistance testing) are metronidazole, incosa- imide, cephalosporins, or macrolides; reserve antibiotics are carbapenems (imipenem, meropenem). Surgical treatment is indicated when conserva~ tive treatment fails (e.g., in chronic rhinosinusitis with or without bronchial asthma, fungal infec- tions, recurrent empyema, or polyposis). Treatment of chronic maxillary sinusitis. Antibiot- ics are used as described above. Surgical treatment: Infundibulotomy, anterior or complete ethmoidectomy with supraturbinate fen- estration of the maxillary sinus, if necessary with intracavitary repair (removal of polyps, cysts, or fungal concrements). Frontal Sinusitis This is an acute or chronic rhinogenous infection of the frontal sinus involving viral, bacterial, or allergic inflammation and obstruction of the anterior eth- moid (frontal recess). The spectrum of pathogens is, Fig. 2.48 A track of pus along the lateral nasal walla typical finding in purulent maxillary sinusitis. " * © Fig. 2.49 Mucosal edema in both maxillary sinuses, visual- ized on a plain film, described above. It may also occur in the form of diving sinusitis or barosinusitis. Usually, anatomic variations that impede ventilation and drainage of the frontal sinus are present (e.g, high septal devi- ation, pneumatization variations of the ethmoid air cells; see p. 161). Clinical Features. These include severe pain in the forehead, sensitivity of the forehead to pressure or164 2 Nose, Nasal Sinuses, and Face Gheeraeat Pritt Fig. 2.50a, ba Empyema of both frontal sinuses. Occlusion of the anterior ethmoid by hyperplastic, edem- atous mucosa, tapping, tender sites of exit of the supraorbital nerve, and tracks of secretions or pus on the ante- rior part of the middle meatus. The mucosa of the middle meatus is often glazed, swollen, and red (Fig. 2.50a,b). Complications. Orbital complications (see p. 186), osteomyelitis of the frontal bone with abscess for- mation (Pott pufly tumor), meningitis, epidural ab- scess, brain abscess, thrombosis of the sagittal si- ‘nus, mucocele. Diagnosis. Routine otorhinolaryngology examina- tion; inspection: edema of forehead and eyelids, conjunctivitis; palpation: floor of frontal sinus pain- ful, exit of the first trigeminal nerve (supraorbital branch), tender pain on bending the head forward. Nasal endoscopy: Edema, pus and mucoid pus in idle nasal_meatus; inflammatory redness. ‘Swabs: culture, resistogram. Radiography of the paranasal sinuses shows mucosal hyperplasia or empyema. Further diagnostic measures: Coronal CT in case of recurrent exacerbations or preoperatively. Laboratory investigations: CRP, white blood count, ESR. Allergy tests: Prick tests, RAST. Depending on the clinical findings, an ophthal- mologist or neurologist should be consulted (Ium- bar puncture if meningitis is suspected). Treatment. Decongestion and aspiration of the middle nasal meatus. Application of infrared heat or deep heat by microwave or short wave, endo- scopically guided placement of high tamponade in the middle nasal meatus—e.g, using a sponge soaked with tetracaine and epinephrine. “High fil- lings” in the middle meatus. Antibiotics: Start empirically, then assess effec- tiveness after 3 days; if necessary, adjustment ac- cording to the resistogram (see maxillary sinusitis, p.162). If empyema is present, the frontal sinus is drained with endoscopic surgery; in the age of endoscopic microsurgery, puncture using the Kiimmel and Beck method has become less impor- tant (see p. 140). Surgical intervention: Indications are recurrent or chronic exacerbations or orbital or central com- plications (e.g, subperiosteal abscess, orbital phlegmon, meningitis, epidural abscess, brain ab-linical Aspects of Diseases of the Nose, Sinuses, and Face 165 scess, sinus thrombosis, failure of conservative therapy, osteomyelitis, mucocele). The principles of endonasal and external surgery of the frontal sinus are explained on pp. 171, 177. Sphenoid Sinusitis ‘Acute, chronic, rarely allergic inflammation of one or both sphenoid sinuses, usually due to morpho- logic or inflammatory obstruction of the ostium. Drainage of the sphenoidal cavity proceeds via the sphenoethmoidal recess, rather than through the anterior ethmoid to the nose as in the maxillary and frontal sinuses (Fig. 2.51a, b). Pathogenesis. This disorder may develop independently, ‘and alone, or in association with other forms of sinusitis (pansinusitis). Acute and chronic sinusitis in ventilated pa- tients (usually in intensive-care units) starts with sphenoid sinusitis, due to the patient’s constantly supine position. For the pathogen spectrum, see page 160. Clinical Features. Signs of infection are largely lack- ing; overall, the symptoms are vague. The patient may report pain or a feeling of pressure within the skull, radiating to the occiput or the temple. Deep pain in the eyes is also possible. Nasal respiration is usually not obstructed, Secretions usually drain into the nasopharynx, causing postnasal drip and coughing. There is a stream of pus on the posterior wall of the pharynx or in the superior meatus. Anatomy. Several nerves run along the lateral wall of the sphenoid sinus—e.., the optic, abducent, and maxillary nerves. The posterior ethmoidal air cells may invade the body of the sphenoid in a cranial direction, interfering with pneumatization; they may project above the ethmoidal cav- ity. f they achieve a typical pyramidal configuration (i.e. with the tip pointing dorsally) with prominence of the optic nerve, they are termed Onodi cells (posterior sphenoethmot dal air cells). Complications. Orbital complications, spread of in- flammation to the optic nerve, visual impairment, paralysis of the abducent nerve; central complica- tions: meningitis, brain abscess, thrombosis of the cavernous sinus; osteomyelit \gnosis. Routine otorhinolaryngology examina- tion, nasal endoscopy, swabs of free pus for culture and resistance testing, coronal CT. Fig. 2.51a, b Sphenoid si- rusitis, caused by occlusion of the sphenoidal ostium by a polyp. If diagnosis of the pathogen is equivocal, espe- cially before surgery, vascularization has to be studied (e. g,, by magnetic resonance angiography or angiography). Consultation with an ophthalmol- ogist and a neurologist, and a radioisotope bone scan, are indicated if osteomyelitis is suspected. Allergy tests: prick test, RAST. Differential diagnosis. Mucocele, benign or malig- nant tumors, fungal disease, pituitary tumor, men- ingioma of the sphenoid wing. ‘Treatment. Conservative: Localized decongestion and aspiration of the sphenoid, tamponade of the sphenoethmoidal recess with a pointed swab con- taining, e.g, tetracaine/epinephrine; antibiotics (see pp. 159, 160); antiinflammatory agents; in ap- propriate cases, antiallergic therapy (see p. 150); oral steroids. Surgery: Indications are failure of conservative treatment and incipient or overt complications. Principle of the operation: The method of choice is endoscopic or microscopic transnasal (via the sphenoethmoidal recess) or transethmoidal en- largement of the ethmoidal cavity ostium, or trep-166 2 Nose, Nasal Sinuses, and Face Fig. 2.52a-c Endoscopic pansinus surgery. a The preoperative CT, showing polypoid mucosa inallof the paranasal sinuses. bb The preoperative endoscopic view, showing polyposis of the nose and paranasal sinuses. anation of the anterior wall. Alternatively, a trans- septal or transmaxillary route can be used. For sur- gery of complications or tumors (see pp. 226, 288), midfacial degloving or lateral rhinotomy may be required. Pansinusitis Rhinogenous inflammation of all paranasal sinuses on one or (more commonly) both sides, caused by viruses, bacteria, or allergenic agents. The symp- toms are those of disease of the various sinuses combined, and may be bilateral. he Note: In patients with diffuse mucosal edema or hyper- plasia of all the paranasal sinuses, one should always ‘check for acetylsalicylic acid intolerance and asthma. Diagnosis. See Ethmoidal Sinusitis, above. ‘Treatment. Conservative, in the acute phase. Top- ical steroids, depending on findings; oral cortico- steroids; antibiotics. Surgery, when there is a chronic course and in severe symptoms. Ethmoidectomy with supratur- binate fenestration of the maxillary sinus, enlarge- ment of the frontal recess, andjor removal of the floor of the frontal sinus (Draf I-IIl), or pansinus operation (Fig. 2.52a-c). « Endoscopic view of the cleared, spacious ethmoid, show- ing an open, epitheliaized window to the maxillary and sphenoid sinuses (0° lens) Chronic Rhinosinusitis CChronic rhinosinusits is one of the most common health problems, witha serious impact on lower airway disease and ‘overall health, The condition is diagnosed when symptoms persist for more than 12 weeks. Whereas acute sinusitis is an inflammatory rhinogenous process caused by obstruction of ventilation and drainage of the paranasal sinuses located functionally downstream from the ethmoid, in chronic rhinosinusitis the postulated cause involves gradual obstruction of the ostiomeatal complex by ‘edema, induration, hyperplasia, and polyposis of the mur The role of anatomic blockage in the origin of chronic thinosinusitis is controversial. The spectrum of pathogens involved in chronic rhinosinusiis differs from that in acute sinusitis. There has been 2 change in the way in which bacterial infection is assessed. In addition to biomechanical and bacteria factors, other pathomechanismsforinflamma- tion of the nasal and sinonasal mucosa are now being con- sidered. In the mucosa and secretions of patients with increased numbers of neutrophilic granulocytes are found, as well as eosinophils, mast cell, basophils, and mononuclear cells (T lymphocytes, CD8* suppressor cells, cytotoxic T cells, and CD4' T-helper cells). Raised concentrations of histamines and leukotrienes and prostaglandin D have been found in the nasal secretions of patients with chronic hinosinustis chronic rhinosinusitis, Chronic Hyperplastic Rhinosinusitis with Nasal Polyps Eosinophils and fungi are considered to be of par- ticular importance in chronic hyperplastic rhinosi- nusitis with nasal polyps. The granules of eosino-Glinical Aspects of Diseases of the Nose, Sinuses, and Face 167 philic granulocytes contain cytotoxic proteins, which ate released when degranulation occurs: e0- sinophil cationic protein (ECP), major basis protein (MBP), eosinophil peroxidase (EPO), and eosino- phil-derived neurotoxin (EDN). It has been sug- gested that eosinophils migrate from the epithe- lium into the mucus, where they dock onto T cells. When they degranulate within the supraepithelial mucus blanket, they release their cytotoxic cyto- kines, in particular MBP, which docks onto fungal elements to form so-called “horseshoes.” This leads to a toxic-inflammatory reaction on the surface epithelium, paving the way for secondary invasion by bacteria, infection, and eventually chronic rhi- nosinusitis. The most common fungi involved are Alternaria, Penicillium, Candida, and Aspergillus. The term “eosinophilic fungal rhinosinusitis” has been proposed for rhinosinusitis induced by fungi. Immune and Tissue-Specific Reactions In contrast to the biomechanical and infectious pathome- cchanism involved in acute sinusitis, immune and tissue-spe- | Combined topieal GS, srextment Fig. 2.57 Decision algorithm for the treatment of polypo- sis nasi (adapted fom C. Bachert, Allrgologie 200412 484-94), Polypectomy: So-called blind polypectomy is no longer Indicated. The method of choice is functional endoscopic, surgery of the ethmoid (ethmoidectomy) and the paranasal sinuses. Microdebriders have the advantage of allowing effi- ent and atraumatic surgery with litte bleeding, preventing postoperative adhesions (Fig. 2.58a, b). Churg-Strauss Syndrome The Churg-Strauss syndrome is a necrotizing vasculitis cas- sically characterized by hypereosinophilia and bronchial asthma, al Features. Otorhinolaryngology manifestations include sinusitis intially, and later asthma, Diagnosis. Required diagnostic criteria are asthma, eos nophilia, sinusitis, pulmonary infiltrate, histologic proof of vasculitis, and mononeuritis muttiplex. Treatment. Corticosteroids alone or with cyclophospha- mide andjor plasma exchange. Prognosis. Favorable in the long term. Rhinosinusitis and HIV Rhinosinusitis is very common in HIV patients. Na~ sal obstruction may be due to rhinosinusitis, al- lergy, neoplasm or adenoid hypertrophy. Clinical Features. Kaposi sarcoma or lymphoma present with nasal obstruction, epistaxis, and rhi- northea. Adenoid hypertrophy in adults raises a concern regarding HIV. Pathogenesis. Acute sinusitis pathogens are similar to those in normal patients. Stophylococcus, Pseudomonas, anaerobes, and fungi are found in chronic rhinosinusits in HIV patients. Diagnosis. Swabs from the middle nasal meatus, and determination of the current viral load. Treatment. CD4 counts > 200/mm?: amoxicillin plus clavulanic acid, systemic decongestants, guai- fenesin 1200 mg b.i.d. for 3 weeks; topical decon- gestant spray for 1 week, CD4 counts < 200/mm?: add coverage for Staphylococcus, Pseudomonas, and anaerobes—e. g., with ciprofloxacin plus clindamy- cin; severe infections require hospitalization, intra- venous antibiotics, and endoscopic drainage; in se- lected patients with HIV, endoscopic sinus surgery is effective, although less so than in immunologi- cally competent patients. im Rhinogenous Headache ‘The quality of rhinogenous headache depends on the underlying cause. Sinus inflammation is char- acterized by a dull, nagging, position-dependent headache that is associated with a sensation of pressure over the affected sinus (Fig. 2.59). Head- ache is a late symptom of tumors of the nose and paranasal sinuses. Adenoid cystic carcinoma grows