Back to Dr. Davidson's Home Page Back to Table of Contents CHAPTER 3 The Nose Epistaxis Sinusitis Acute Sinusitis Chronic Sinusitis History Endoscopic Sinus Surgery Allergic Rhinitis Vasomotor Rhinitis Nasal Obstruction Rhinorrhea Smell Loss

The nose and paranasal sinuses are the cause of many major and minor ailments. Their anatomy and function are poorly understood by most. The nose and sinuses can be involved in congenital abnormalities, tumors, infections, trauma, and metabolic disease. EPISTAXIS The bloody nose is a common emergency problem. The majority are spontaneous, with no identifiable cause, although many are traumatic. Causes such as hemophilia, other coagulopathies, leukemia, hereditary hemorrhagic telangiectasia or intranasal neoplasms must be considered. As usual, a complete history is taken. Use of aspirin, NSAIDs, or sodium warfarin or (coumadin) or Plavix? other anticoagulant ingestion should be ascertained. Children and many adults often cause bleeding by nose picking. A pubertal male may have an angiofibroma. A person with a long history of smoking should be examined for an intranasal or paranasal sinus epidermoid cancer. Patients may require a laboratory examination. The complete blood cell count evaluates the hematocrit and signs of leukemia. Prothrombin time, partial thromboplastin time/INR, platelet count, and Ivy bleeding time or other platelet function evaluate coagulation. The majority of nosebleeds occur anteriorly from the nasal septum and cease spontaneously. If the nose is actively bleeding, the origin can often be seen by visual examination with a headlight, nasal speculum, and nasal suction. An actively bleeding nose is treated as follows: A cotton pledget moistened in 4% cocaine is placed against the nasal septum. Cocaine is a good anesthetic and a potent vasoconstrictor ¼ % Neo-Synephrine or lidocaine with adrenalin is the next best, albeit inferior, option. If a definite bleeding site is identified, it may be cauterized with a silver nitrate stick. Cauterization of both sides of the nasal septum should not be done because of the risk of creating a septal perforation. Once the bleeding is controlled, it is wise to reduce the airflow through the nose for 5 days by placing a small piece of cotton in the nose. The cotton is saturated with petrolatum or other ointment and the patient can change it daily or twice daily. Recurrent or uncontrollable nosebleeds should be treated by trained personnel, commonly with an anterior nasal pack. Most emergency department physicians are skilled at this, but if not, a head and neck surgeon should be consulted. Posterior nosebleeds are usually arterial and are often profuse. A head and neck surgeon should be called immediately, and for serious bleeding, 2 to 4 units of blood should be ordered. Posterior nosebleeds are controlled by obstructing the posterior nasal choana with a Foley balloon or a 4" x 4" gauze packing in the nasopharynx. The anterior naris is occluded with an anterior nasal pack, and the bleeding is thereby tamponaded. This is called an anterior-posterior pack. All patients with posterior nosebleeds and anterior – posterior nasal packing are admitted to the hospital and should be under the care of a head and neck surgeon. Some physicians use anterior-posterior packs for 5 days, others for 3 days, and some recommend surgical arterial ligation or endoscopic nasal procedures. These are options for the patients and the surgeons. Figure 3.1 is an algorithm for the diagnosis and treatment of epistaxis. Supplementary information is available in the Ambulatory Healthcare Pathways and for patients in the bloody nose section of Geriatric Otolaryngology. Case Study: Epistaxis A 42-year-old steel worker presented to the emergency department with a profusely bleeding nose. Pressure to the outside of the nose temporarily stopped the bleeding. The bleeding had begun spontaneously 15 minutes earlier. The patient denied trauma, but had taken two aspirin that morning for a backache. His blood pressure was 160/90. The patient asked for a cigarette, but before he could reach for one, he vomited bright red blood. The nose began bleeding again. Blood was drawn for complete blood cell count, prothrombin time, partial thromboplastin time/INR, platelet count, and typing and cross matching for 4 U. Lactated Ringer's was started using an IV catheter. Bleeding was from the left side of the nose. A No.18 Foley catheter was passed through the nose, inflated with 20 ml water, and pulled back against the posterior nasal choana. Blood now poured out anteriorly. An anterior nasal pack was inserted using 1-inch plain gauze moistened with povidone-iodine ointment. This controlled the bleeding. Mask oxygen therapy was begun. The patient's blood pressure was 180/95 and the pulse 120. Administration of 25 mg meperidine hydrochloride IV over 2 minutes caused a rapid fall in blood pressure to 110/60 with a pulse of 140. Rapid infusion of 500 ml of Ringer's lactate brought the pressure up to 130/80 with a pulse of 100. The hematocrit was 35, but a repeat hematocrit after the first liter of fluid was given was 25. Two units of blood were given. The patient was admitted to the head and neck surgery service. The same afternoon a 12-year-old boy entered the emergency department soaked with blood. He had been watching television and suddenly began bleeding profusely from the nose. Just as suddenly, the bleeding stopped. History was not helpful, except that the boy's voice had become slightly hypo nasal (such as occurs with a stuffy nose) over the past month. Examination was normal except that the soft palate seemed full. A head and neck surgery consultation was requested. Examination of the nasopharynx revealed a large, pulsating mass. A tentative diagnosis of angiofibroma was made, and the patient was admitted to the hospital the following morning for diagnostic angiography. Figure 3.1. Algorithm for the diagnosis and treatment of epistaxis. SINUSITIS Sinusitis is an incredibly common patient complaint affecting upwards of 30-40 millions of Americans annually, contributing to a multi-billion dollar pharmaceutical industry and millions of patient visits on an annual basis. The thinking and understanding around sinusitis is changing and this section very much reflects this change. The paranasal sinuses are a collection of air containing pockets in the frontal, ethmoid, sphenoid and maxillary bones. There are multiple theories as to reasons for their existence. Some opine that the sinuses lighten the mass of the facial skeleton. As the total volume of the paranasal sinuses is arguably less than 25cc on a side, the total volume of bone cannot exceed more than 50 cubic centimeters. The total weight saved should not be more than a couple hundred grams and I seriously doubt made any difference in man’s evolutionary survival. The other theory for the existence of paranasal sinuses is that it somehow alters man’s voice. I also have trouble with this theory for the majority of speech is oral, not nasal. Patients who have had sinus operations, thereby altering the anatomy of the paranasal sinuses seem to have no change in their vocal quality. The bottom line is that we have paranasal sinuses and for the moment their only value lies in maintaining a business for the pharmaceutical and medical industries. Acute Sinusitis Acute sinusitis presents in one of two classic fashions. The first is on the tail of an acute upper respiratory tract infection (URI). Rhinitis in the form of an acute upper URI, on the average, afflicts every American twice a year. Virtually everyone suffering from an upper URI initially develops a clear nasal discharge emanating both from the nose and the paranasal sinuses. This invariably develops into a bacterial super infection, manifest clinically as a green or yellow mucopurulent nasal discharge. During the upper URI, many patients have signs and symptoms of paranasal sinus disease. These include pressure, pain, nasal congestion, purulent rhinorrhea, both anterior and posterior, presenting as a postnasal drip. Physical examination reveals tenderness over the afflicted sinuses, easily evoked for maxillary and frontal sinus disease, not easily evoked for ethmoid or sphenoid sinus disease. The nose will sometimes show a mucopurulent discharge particularly if the patient is resolving an URI. An oropharyngeal exam will show inflammation in the posterior pharyngeal wall typically seen in the two lateral gutters, evidence of the posterior nasal mucopurulent drainage. To a large degree, the diagnosis of sinusitis in a slow resolving URI, is a clinical diagnosis. The bacteria involved are similar to those seen in acute otitis media. The mainstay of medical therapy is an antibiotic. My own preference is to begin with first line antibiotic therapy and only advance to second and third line antibiotics if the initial treatment fails. There are many that begin with more powerful antibiotics. This may seem wise for the individual but it shows ignorance for world health. This practice increases bacterial opportunity to develop resistance to second and third line antibiotics and increases the cost of healthcare. It adversely affects the individual, for it increases the chance that they will develop allergy to antibiotics, which may be required later in life for some other life threatening illness. Therefore, I typically begin with amoxicillin. If the patient fails to improve over 3-4 days or worsens over the ensuing 24-36 hours, one can move up to a second generation antibiotic. This can be the addition of clavulanic acid in the form of Augmentin® or a number of available cephalosporins or a second-generation macrolide. If second line therapy fails to provide relief then I assume that Pseudomonas is the infectious organism and move to a quinolone such as ciprofloxacin. For those who are allergic to penicillins, the erythomycins offer a reasonable alternative. The second-generation macrolide causes far gastric discomfort. Ancillary therapies are basically symptomatic. Decongestants such as pseudoephedrine decrease nasal secretion and pressure. Humidification achieved with steam, nose drops or hypertonic saline nasal irrigation provides symptomatic relief and theoretically helps wash away purulent secretion. For those with allergic rhinitis one can argue that nasal steroids decrease inflammation, decrease the allergic rhinitis and enhance drainage and resolution. One can also argue that as a steroid they suppress the normal immune defense system and should therefore be discontinued. No scientific data is available to answer this question. Topical decongestants such as neosynephrine and oxymetazoline may provide some short-term symptomatic relief and often help some individuals sleep during a viral or bacterial respiratory tract infection. There are unfortunately too many people whose nasal patency is compromised and who will become addicted to the topical decongestants. These individuals become addicted secondary to the tachyphylaxis reaction, namely the rebound swelling. This is a condition called rhinitis medicamentosa and is a condition, I believe suffered by millions of Americans. For this reason I rarely recommend topical decongestants. However if a patient is used to taking these and wants to take them for several days, I voice little objection. Antihistamines have been recommended by the pharmaceutical industry. They may provide some symptomatic relief. They unfortunately impair ciliary function and thicken the nasal secretion. These are contraindicated in the management of acute sinusitis. I therefore never prescribe any form of antihistamine -- those who use them are welcome to continue. Two special circumstances need to be kept in mind. Acute frontal and acute sphenoid sinusitis have potential to spread rapidly into the neurocranium. Hence those with acute frontal sinusitis and those suspected of acute sphenoid sinusitis are recommended for immediate sinus CT scan. If acute frontal or acute sphenoid sinusitis is found the patient is placed on intravenous antibiotics and if after 24 hours improvement is not evident they are evaluated for immediate endoscopic sinus surgery drainage procedures. The other classic case of acute sinusitis is the individual with allergic rhinitis. Typically the allergic rhinitis worsens during the allergic season. Because one or another of the sinus ostia is obstructed, infection ensues and the patient develops acute sinusitis. This infection is exactly the same as that seen at the tail end of an URI. The evaluation and management are identical. Chronic Sinusitis The thinking regarding chronic sinusitis has evolved rapidly in the past quarter century. We use to view sinusitis as a bacterial disease and research was focused on identifying the bacteria and prescribing the best antibiotic. Chronic sinusitis is not a bacterial disease, it is an illness caused by dysfunction of the mucociliary transport system and by osteal obstruction, either anatomic or inflammatory. Yes, when the ostium is obstructed and the mucociliary transport system is impaired, bacteria do grow. Yes, the symptomology of sinusitis is caused by bacterial growth, yes, antibiotic therapy reduces the symptoms, but the focus of one’s attention must be on the ostia and the mucociliary transport system. History The history of the recognition of the mucociliary transport system is interesting. A German physician in the late 1950’s named Professor Walter Messerklinger became interested in the mucociliary transport system. He persuaded the diener at the local medical school to provide him the decapitated heads of those recently deceased. He would transport the head to his laboratory and then would examine the interior of the nose and paranasal sinuses with state-of-the-art, German made, incredibly clear, glass rod telescopes or endoscopes. It turned out that blood was a good marker and it also turned out that the cilia continued to function for approximately 48 hours after death. Using the little bit of blood that was present in the nose, he would watch the movement of the blood and therefore the ciliary transport system. He found that the cilia carried the blood or any other material trapped in the overlying mucus towards the natural sinus ostium. This was true for maxillary, frontal, sphenoid and ethmoid sinuses. Secretions would be carried to the ostium and from there into the nose and from the nasal cavity posteriorly, to the nasal pharynx, wherein the living they would have been swallowed. The most junior faculty person in the department, Dr. Heinz Stammberger, was assigned the task of carrying the camera and assisting Professor Messerklinger throughout his experiments. While at first, he was disappointed and unenthusiastic, he slowly but surely began to realize that Professor Messerklinger’s understanding of the mucociliary transport system was the key to sinus surgery. Prior to this time operations such as Caldwell-Luc procedures and nasal antral windows attempted to treat sinus disease either by ablative operations, or by establishing drainage holes in what was felt to be dependent positions. Based on this new understanding and the availability of the endoscope, endoscopic sinus surgery evolved. The Europeans, not realizing the importance of this operation, did very little with it. It then came to the United States where its importance was recognized and it’s practice spread rapidly. Today, several hundred thousand endoscopic sinus surgeries are performed annually in the United States. It is the gold standard in surgical management of chronic sinusitis. What we have learned from all this, is that chronic sinusitis is an illness of the mucociliary transport system and of ostial obstruction. The bacterial infection is nothing more than a consequence of the stagnate paranasal sinus secretions. The usual history, evaluation and treatment of chronic rhinosinusitis are described in consultation for sinusitis. At risk of repeating myself the following was the discussion in the 2nd Edition of the Clinical Manual of Otolaryngology. It is kept for it provides insight into the bacteriology and some of the conventional thinking and approach to sinus disease. While it is true that I almost never order a standard radiograph to evaluate the paranasal sinuses, there are some who think that the standard radiographs provide useful information. It is my strong opinion that they do not, but they do provide some anatomic understanding of the nose and paranasal sinuses. It is interesting that surgeons now operate viewing the interior of the human body with endoscopes, visualizing and imaging that anatomy preoperatively and intraoperatively with axial, coronal and sagittal imaging technology. While this has greatly improved our diagnostic and therapeutic abilities, it leaves today’s medical student with little personal experience of open operative anatomy. Perhaps the conventional radiographs and some of the traditional descriptions will fill part of that void. Consultation: Sinusitis A 26-year-old college student presented with left facial pain. She had had a cold that persisted for 10 days. One day before examination, she began to notice pain and pressure over her left cheek. She went to her dentist who took an X ray and told her she had a sinus infection. He referred her for treatment. History was unremarkable. The patient's temperature was 101°F. The nose was clear, but mucopurulent material was dripping from the nasopharynx. Percussion over the left maxillary sinus elicited tenderness. The patient had a classic left maxillary sinusitis. This was treated with penicillin and a saline nasal douche. The patient was instructed to return if her symptoms did not disappear in 3 to 4 days or if they recurred. The diagnosis of sinusitis is made entirely on the clinical presentation. Table 3.1 lists the normal pathogens isolated from acute sinusitis. Treatment is a prescription for 7 to 10 days of antibiotics. Amoxicillin is excellent for gram-positive cocci and anaerobic coverage, but lacks coverage for resistant species of H. influenza. Amoxicillin with clavulanic acid may be a better drug for this reason. Macrolides remain the drug of choice for those who are penicillin sensitive. Second generation macrolides have fewer side effects and are therefore preferred by patients. Table 3.1 Organisms from Maxillary Sinus Disease* Streptococcus pneumoniae Hemophilus influenzae Viruses Moraxella catarrhalis Group A Streptococcus Staphylococcus aureus Gram-negative bacilli      Proteus      Klebsiella      Escherichia coli Pseudomonas aeruginosa Anaerobes      Peptostreptococcus      Bacteroides *The organisms at the top of the list are most common in acute paranasal sinus disease, those at the bottom are more common in chronic paranasal sinus disease. Those individuals who do not improve will normally return 2 to 4 days after the initial visit. Presumably, they have an ostial obstruction that is preventing drainage and may have bacteria resistant to the prescribed drugs. A second line antibiotic should be prescribed. Consultation: Acute Maxillary Sinusitis A case example will help accentuate several points. An 18- year-old secretary came to my office with a history of a cold 1 week previously. Just as the cold seemed to be abating, she developed pain on the left side of her face. She saw her dentist, who referred her to me. Examination of the nose was normal, the oropharynx revealed a mucopurulent postnasal discharge. Her temperature was 101°F orally. Finger percussion over the left maxilla elicited pain. A clinical diagnosis of acute maxillary sinusitis was made. The patient was given a prescription for amoxicillin 500 mg po three times a day for 10 days and advised to use Sudafed? for nasal stuffiness. The patient was also told to mix 1 teaspoon of salt in a glass of water and to put two drops of this solution into each nostril four times a day. She was to sniff this in and then blow it out. She was instructed not to return if the symptoms abated. However, if the symptoms persisted, recurred, or increased she should return immediately. The patient returned 2 weeks later stating that the symptoms had disappeared on the antibiotic therapy but as soon as she stopped taking the amoxicillin the symptoms returned. The ex- amination showed the same results. This is an older case, and at this time plain sinus X rays were used to evaluate and diagnose inflammatory sinus illness. Figure 3.2 shows skull positioning for the four standard sinus X rays. Figure 3.3 shows a normal sinus series. While I virtually never order these, today there is useful anatomy to be learned. The patient's Waters' view (Figure 3.4) showed an air-fluid level on the left side and an opacified sinus on the right side. To document this as an air-fluid level the patient's head was tilted slightly to the right, and the repeat Waters view showed a shift in the air-fluid level. The patient was placed on amoxicillin with clavulanic acid 875 mg p.o. bid. The symptoms did not recur. If the second line antibiotics had failed to clear the infection, a nasal work-up would have been initiated and, based on the findings of that work-up, appropriate therapy recommended. As has been stated, plain sinus radiographs are no longer used to evaluate acute sinus disease, and when, in fact, a radio¬ graph is indicated. sinus CTs are ordered. Figure 3.4C is a coronal CT that demonstrates the kind of findings that might commonly be observed in an individual with acute maxillary sinusitis. Note that the primary disease is in the anterior ethmoids in the area called the ostiomeatal complex. It is because of the disease in this region that the natural sinus ostia for the maxillary sinuses are obstructed and, therefore, fluid and infection has accumulated in the maxillary sinus. Because the patient is positioned upside down, air-fluid levels are now seen at the top of the sinuses. Figure 3.2A. Figure 3.2B. Figure 3.2C. Figure 3.2D. Figure 3.2. Views of the skull showing position of the head for each of the four standard sinus X rays, assuming that the x ray beam is horizontal. (A) Posteroanterior view. (B) Waters’ view. (C) Lateral view. (D) Submental vertical view. Figure 3.3A. Figure 3.3B. Figure 3.3C. Figure 3.3D. Figure 3.3. Normal results of sinuses series of X rays. Sinus films are taken with the patient upright, in a coned-down focus, and with soft-tissue penetration. (A) Posteroanterior view. (B) Waters’ view. (C) Lateral view. (D) SMV view. F = frontal sinus, E = ethmoid sinus, M = maxillary sinus, S = sphenoid sinus. Figure 3.4A. Figure 3.4B. Figure 3.4C. Figure 3.4. X rays of acute maxillary sinusitis. (A) Waters’ view showing showing an air-fluid level in the left maxillary sinus and opacification of the right maxillary sinus. Note the small air bubble in the superior medial corner of this sinus. (B) Waters’ view with the head tilted to the right. Note how the air-fluid level orientation changes in the left maxillary sinus. (C) Coronal CT on an individual with symptoms of acute maxillary sinusitis. Note the extensive anterior ethmoidal disease obstructing the ostial meatal complex and the accumulation of fluid in both maxillary sinuses. An algorithm for the evaluation and treatment of sinus infection is shown in Figure 3.5. Sometimes the disease is not cleared; it becomes indolent and presents as chronic sinusitis. Chronic sinusitis includes that disease that has been refractory to prior treatments and disease that has been indolent and has become a bothersome problem. These individuals require a more complex and thorough work-up. The nature and degree of this work-up differs among both physicians and institutions. Table 3.2 lists those tests that can be performed at the UCSD Nasal Dysfunction Clinic and not all are required for each patient. A history is appropriate. The physical examination should include endoscopic rhinoscopy. Rigid endoscopy is preferable to flexible rhi¬noscopy. The oropharynx should be examined. Important findings in the nose are patency of the airway and presence or absence of a septal deviation, particularly if obstructive to breathing. The mucosa of the inferior turbinate is reflective of the mucosa of the reminder of the nasal cavity. If this is inflamed, it implies a bacterial infection; if it is edematous and either pale or bluish in color, this is most consistent with an allergic problem. The presence of blood or of a tumor is a significant finding, as is presence of polyps. The presence of secretions is also a pertinent finding. Clear or white secretions are found in allergic rhinitis. Purulent secretions are found in bacterial rhinitis. Dry, shrunken mucosa suggests an atrophic rhinitis. Figure 3.5. Algorithm for the evaluation and treatment of sinusitis. Table 3.2 Evaluation for Nasal Dysfunction History Anterior rhinoscopy Oropharyngeal examination Nasal endoscopy Olfactory testing Rhinomanometry Nasal cytology Serum IgE level RAST inhalant panel screen Sinus CT Consultation: Pansinusitis and Asthma A 49-year-old woman enjoyed excellent health throughout her childhood and early adult life. Approximately 1 year ago, she developed asthmatic symptoms and initiated therapy. Four months ago the asthma worsened and she required hospitalization for systemic steroids and bronchodilators. Around this time, she noted difficulty with nasal breathing that progressed to symptoms of sinus disease including pain and pressure over the sinuses and finally a purulent postnasal discharge. The symptoms progressed to the point where she was unable to breathe through her nose. Medications included doxycycline, astemizole, Actifed® theophylline, albuterol, ipratropium bromide, Afrin?, intranasal steroids, and cromolyn sodium. She had no known medical allergies. Anterior rhinoscopy revealed the nose totally obstructed by polypoid tissue. Endoscopy was not possible. The oropharynx showed an edematous mucosa consistent with an allergic disease. Rhinomanometry was attempted. No measurable airflow was possible prior to decongestants. Following decongestant spray, resistances in the right and left nostril, respectively, were 4.2 cm and 4.7 cm of H2O/L/sec. These are normal. The nasal cytogram revealed numerous eosinophils with basophilic cells and neutrophils. Few bacteria were present. The IgE was 180 U/mL with the upper limits of normal being 40 U/mL. The RAST inhalant panel revealed no sensitivities to grasses, trees, animal danders, mites, or fungi. The CT scan shown in Figure 3.6 demonstrated diffuse mucoperiosteal thickening involving the sphenoid sinuses, the ethmoid sinuses, and the maxillary sinuses. Diffuse mucus membrane thickening was seen in the nasal cavity. Surgery was recommended and accepted. A septoplasty was performed, in part to improve the anatomic airway and in part to improve endoscopic access to the ethmoid sinuses. Endoscopic sinus surgery was performed. Both an anterior and a posterior ethmoidectomy were performed. The natural maxillary sinus ostia were enlarged. The frontal recess cells were resected, and drainage was established to the frontal sinuses. The sphenoid sinus ostia were identified and opened, thereby draining the sphenoid sinuses into the posterior naval cavity. All the nasal polyps were resected. Postoperatively, the patient made an uneventful recovery. The nasal packing was removed on postoperative day 3. Nasal irrigations using a Water Pik? with an Ethicore? nasal adaptor were initiated on postoperative day 10, and the patient began nasal medications, including nasal steroids and cromolyn sodium, 3 weeks following surgery. Immediately following surgery the patient's lungs made a dramatic improvement, and within l or 2 weeks she could tell that her nose and paranasal sinuses felt dramatically better. She had an overall sense of once again being healthy. Not all asthmatics have sinus disease, and not all asthmatics with sinus disease require endoscopic sinus surgery. However, some asthmatics clearly deteriorate when their nasal and paranasal sinus disease exacerbates, as typified by the above individual who made dramatic pulmonary improvement with appropriate management of her sinus disease. Rhinoscopy should examine the entire nasal cavity, with particular attention to the middle meatus. Purulent secretions emanating from the middle meatus or from the sinus ostia indicate a bacterial sinus infection. The oropharynx is a good indicator of nasal pathology. The majority of nasal secretions are transported posteriorly and flow down the posterior and lateral oropharyngeal walls. In allergic conditions, the mucosa will be pale and edematous. In bacterial conditions, the mucosa will appear red and inflamed. Clear secretions indicate an allergic or vasomotor condition; purulent secretions indicate a bacterial condition. Although the remainder of the head and neck examination is important for all patients presenting to an otolaryngologist, it does relatively little to better define the nasal condition. 3.6A 3.6B Figure 3.6. (A) Coronal computed tomography (CT) scan demonstrating extensive nasal and paranasal sinus disease. The ethmoid sinuses are completely filled with inflammatory tissue. One cannot differentiate fluid from soft tissue. The olfactory cleft is obstructed. The left maxillary sinus appears to be filled with fluid or soft tissue swelling. The right maxillary sinus shows extensive mucosal swelling. The nasal cavity is also filled with swollen, inflamed tissue. At this particular time, the right nasal cavity appears worse than the left. However, both are severely diseased. (B) Axial CT scan demonstrating extensive ethmoidal disease involving both the anterior and posterior ethmoid sinuses. Mucosal swelling is seen in the sphenoid sinuses. Consultation: Revision Sinus Surgery The patient was a 32-year-old software engineer with a long history of sinusitis, difficulty breathing through his nose, nasal polyps, and asthma. His asthma was, to a large degree, affected by the condition of his paranasal sinuses, and hence 3 years previously, he underwent extirpative sinus surgery including a Caldwell-Luc and antral windows. He also had bilateral intranasal ethmoidectomies. In the early postoperative period, he felt better, feeling that both his allergies and his asthma were symptomatically improved. However, over the course of several years, the asthmatic symptoms worsened and his exercise tolerance decreased. He also had recurrent episodes of sinusitis and had required repeated, prolonged antibiotic therapy. He was referred to the UCSD Nasal Dysfunction Clinic. The only additional pertinent history was an awareness of a diminution in his sense of smell 5 years previously, with a marked increase in this loss immediately following the previous ethmoid surgery. He had no parosmia, but had had occasional phantosmias, usually a gasoline smell. Olfactory and odor-identification testing indicated mild hyposmia in the left nostril and anosmia or severe hyposmia in the right nostril. Both airways were reasonably patent after decongestants. The nasal cytogram revealed significant numbers of eosinophils and a few basophilic cells. There was no evidence of infection. An IgE was 40 U/mL, which is at the upper limits of normal. The RAST inhalant screen was negative. Nasal endoscopy revealed a posterior septal deflection and an ostiomeatal complex filled with mucopus and inflammatory tissue. The nose was clearly malodorous, and the middle turbinates were strikingly absent, a consequence of the previous intranasal ethmoidectomy. The CT scan is shown in Figure 3.7. Septoplasty and endoscopic sinus surgery were performed. At the time of surgery, the nasal cavity was filled with mucopurulent polypoid material. This material was carefully removed. Additional ethmoid sinuses were opened and drainage facilitated. The natural middle meatal maxillary sinus ostia were large, however, obstructed by polypoid tissue. This polypoid tissue was resected. The agger nasi cells surrounding the frontal sinus drainage contained mucopurulent material. These cells were resected, and the frontal sinus drainage reestablished. The patient's postoperative recovery was uneventful. The nasal packing was removed after 3 days. Nasal irrigations with a Water-pik® and an Ethicore® nasal adaptor were initiated on postoperative day 10. The patient was maintained on his asthmatic medicines throughout surgery and the postoperative period and was begun on intranasal steroids 3 weeks postoperatively. His sense of smell has not returned substantially, probably because the olfactory epithelium was inadvertently destroyed at the previous sinus surgery. His asthma and exercise tolerance have improved dramatically. His nose has remained clean and he has felt well. Twice daily nasal irrigation plus nasal steroids are recommended for life. Figure 3.7 Legend for CT scans. Coronal CT scans of a patient with sinusitis. This is a unique scan, for the right side is essentially normal and the left side is severely diseased. The contrast of the two sides is a useful learning experience. Figure 3.7A. Figure 3.7B. Figure 3.7C. (A) Lateral scout film (B) Lateral scout film. Each dotted line representatives coronal CT scan sliced. In this case each slice is taken at 3 mm separation. (C) One sees the frontal bone, the bridge of the nose and the cartilaginous nasal septum. Figure 3.7D. Figure 3.7E. Figure 3.7F. (D) The anterior frontal sinuses are now evident. The soft tissue density with pockets of air, are suggestive of infection and is present in the left frontal sinus. The right frontal sinus is clear. Note the swelling of the turbinate immediately beneath the nasal bones. This is an area called the septal turbinate. (E) Frontal sinus infection is present on the left. Normal, air-filled frontal sinus on the right. (F) Frontal sinus disease persists the very beginning of the anterior superior ethmoids is evident. The central incisor maxillary teeth are also seen. Figure 3.7G. Figure 3.7H. Figure 3.7I. (G) Frontal sinuses extending over the orbits. The ethmoid sinuses can be seen. The beginning of the maxillary sinuses are seen. The lateral maxillary incisors are evident. (H) Supraorbital frontal sinuses are seen the proximity of the orbit, both superiorly and medially to the frontal sinus. Maxillary sinusitis is evident and infection in the superior anterior ethmoids is also evident on the patient’s left. The same area is clear on the right. (I) Severe ethmoid disease is evident. The turbinates are seen. The very beginning of a pneumatized Crista galli is evident. Figure 3.7J. Figure 3.7K. Figure 3.7L. (J) Maxillary and ethmoid sinusitis. Crista galli is well seen. (K) Frontal sinuses are gone, supraorbital ethmoids persist. Maxillary and ethmoid diseases are evident. Note the normal inferior and beginnings of the middle turbinate on the patient’s right side. (L) Maxillary and ethmoid sinus opacification is very evident. Note the thin lamina papyracea, note the normal middle and inferior turbinates. The olfactory groove just above the cribriform plate is now seen. The olfactory bulb resides in this area. Figure 3.7M. Figure 3.7N. Figure 3.7O. (M) Persistent maxillary and ethmoid sinus disease. (N) Persistent maxillary and ethmoid sinus disease. Note the deviated septum in the area of the osteomeatal complex. (O) Persistent maxillary and ethmoid sinus disease. Deviated septum. The olfactory grooves continue. The olfactory cleft can see wherein the olfactory epithelium resides, lies immediately beneath the olfactory grooves. This is separated by a thin shell of bone, known as the cribriform plate. The cribriform contains both the horizontal and a vertical portion. These are evident in this slice. Figure 3.7P. Figure 3.7Q. Figure 3.7R. (P) Maxillary disease persists. This is an opacified maxillary sinus. Some posterior ethmoid disease is evident. (Q) Persistent maxillary sinus disease. The posterior ethmoids in this region seem clear. (R) Persistent maxillary sinus disease is also shown. The posterior ethmoids in this region are also clear. Figure 3.7S. Figure 3.7T. Figure 3.7U. (S) Persistent maxillary sinus disease is shown in this image as well. The posterior ethmoids in this are seem clear. (T) The posterior end of the maxillary sinus is seen. The posterior ethmoids are now transitioning into the sphenoid sinus. This is clear bilaterally. (U) Posterior choana. The middle turbinates are all but gone and all one sees is the inferior turbinates. A large sphenoid sinus is evident. Figure 3.7V. Figure 3.7W. Figure 3.7X. (V) Large sphenoid sinus. Posterior choana. Note the wings of the sphenoid. (W) The inferior turbinates are gone. Posterior choana is transitioning into the nasal pharynx. (X) The posterior choana is transitioning into the nasal pharynx. Figure 3.7Y. Figure 3.7Z. Figure 3.7AA. (Y) This is the nasal pharynx. The eustachian tubes lie on either side of the nasal pharynx. (Z) Nasal pharynx. The eustachian tubes ae seen. The back of the soft palate with the uvula is seen. (AA) The eustachian tube orifices are gone. Sphenoid sinuses, soft palate and uvula are evident. Figure 3.7BB. Figure 3.7CC. Figure 3.7DD. (BB) The posterior sphenoid sinus’s soft palate and uvula are evident as well. (CC) The raised tissue in the nasal pharynx is probably adenoid tissue. The tongue base can be seen. (DD) Large adenoid tissue is evident. The beginning of the epiglottis is seen. The sphenoid sinus is absent. Figure 3.7EE. Figure 3.7FF. (EE) The oropharynx and the epiglottis are seen. (FF) The oropharynx and the epiglottis are seen. Consultation: Vasomotor Rhinitis Mr. X was a 45-year-old man referred for evaluation of sinus headaches. He had been to many physicians, none of whom had been able to help and, hence, was referred to the UCSD Nasal Dysfunction Clinic. The history was that of episodic facial and forehead pain. This usually began in the afternoon and normally would persist into the evening in spite of analgesics or antihistamines. It often had a profuse, watery, nasal discharge associated with the pain and it totally incapacitated his ability to function at work. The entire head and neck examination at this time was normal. A complete nasal dysfunction work-up was ordered. The nasal physiology, the sinus CT, the IgE, and the RAST screens all were normal. It was suggested that this was a vasomotor rhinitis, which is a true psychosomatic disorder and one that needs to be dealt with psychiatrically. We explored some of the stresses in his life. I referred him to a psychiatrist. During counseling, it was revealed that he was the child of alcoholic parents and suffered from all the problems associated therewith. He became involved in some short-term counseling and also became involved in a group of adult children of alcoholic parents. He quickly gave up the nasal steroids and decongestants that I had recommended. I didn't see him in follow-up for 3 months. He had pursued the counseling and group therapy actively and stated that he was truly a new man. He was now sleeping at night, he was happy at home, and was both happy and productive at work. Consultation: Allergic Rhinitis A 30-year-old nurse complained that she couldn't breathe through her nose. This was readily evident for she was an obligate mouth breather. The history was classic for allergic rhinitis because the problem was worse in the spring and the fall. Her nose itched, as did her eyes. There was no infectious component and both sides of her nose seemed to be equally involved. Nasal examination revealed a swollen, bluish mucosa, almost totally occluding the airway. The posterior oropharynx was pale and edematous. A nasal cytology was loaded with eosinophils and basophils. The serum IgE was markedly elevated, and the RAST screen showed mild allergy to molds and grasses and a very strong reaction to cat epithelium. However, the woman would not consider giving up her cat. Nasal steroids were prescribed and she was advised to do whatever she could to reduce the allergic load in the environment. At follow-up visit 6 weeks later, she had made some improvement on nasal steroids and environmental control. The cat remained in the house and her nose, for the most part, remained extremely stuffy. Again it was affirmed that if she really wished to be better, she would need to get rid of the cat. She reaffirmed that this was not going to occur. She returned once again, 3 months later. At first glance she was still an obligate mouth breather, and the allergic rhinitis persisted. She then related that her 16-month-old daughter had developed asthma, and her pediatrician had now advised her that she had to get rid of the cat. In the interest of both daughter and patient this was done. The daughter's asthma improved, the patient's allergic rhinitis diminished and my son and I have a beautiful Persian cat. Minimal disease will be seen solely in the ostiomeatal complex. More advanced disease may involve the maxillary sinuses, all of the ethmoid sinuses, and the frontal sinus. The sphenoid sinus is isolated and may or may not be involved. Without allergy, the IgE will be normal. Some individuals will have selective immunoglobulin deficiencies, and certainly if the history so dictates this should be looked for. Initial treatment for a bacterial infection is prolonged use of antibiotics. Typically, the cilia have been so damaged that even though the sinus is sterilized with l or 2 weeks of antibiotic therapy, the cilia have not recovered and, therefore, the sinus is not functioning physiologically. Reinfection usually occurs in several days. Success depends not on the strength of the antibiotic but rather on its duration of use. The key to success is the administration of an antibiotic for an extended period. Amoxicillin 250mg po tid for 6-12 weeks is prescribed. For those who are penicillin allergic, 6-12 weeks of erythromycin 250 mg, three or four times daily, or doxycycline 100 mg, twice daily is recommended. One or two refills are indicated and the patients should be advised to take the antibiotics until they are well and then half again as long. Many patients do not get well for 5 to 8 weeks, and if it takes them 6 weeks to get well, they will need to continue the antibiotics for a full 9 weeks. If it takes them 8 weeks to get well they should continue to take the antibiotics for the full 12 weeks. There is a new explanation for chronic sinusitis. The disease is now called chronic rhinosinusitis (CRS). Early research suggests that fungal spores and hyphae present in the air we breathe, are trapped in the nasal mucus. Eosinophils are attracted to the fungus. This requires their crossing the upper respiratory tract mucosa. The eosinophil attacks the fungus and degranulates. Major basic protein is released and causes injury to the upper respiratory tract mucosa. This leaves holes in the mucosa. Bacteria, which are present in the nose, come in contact with the underlying bone through these small holes and bacterial infection which we know as chronic sinusitis ensues. Researchers have been able to culture fungi. Those most commonly present include Penicillium, Alternaria, Cladosporium, Aspergillus and Candida. A myriad of other fungi have also been cultured. Whether this is in fact the pathogenesis of chronic rhinosinusitis is still being explored. Systemic treatment with antifungal agents would not be successful for the antifungal agents would not be transported across the mucus membrane and into the nasal mucus. The above was discovered at the Mayo Clinic and substantiated in an excellent laboratory in Europe. It provides an explanation for a common illness, were explanation has not been obvious. This is certainly a pathogenesis and a treatment which should be considered in cases recalcitrant to other therapies. Our current treatment for those who fail 6 to 12 weeks of amoxicillin, is amphotericin nasal irrigation. The prescription is reproduced in Figure 3.8 When all else fails endoscopic sinus surgery (ESS) is recommended. If there is an allergic component to the disease, the judicious use of nasal steroids may facilitate opening of the ostiomeatal complex and for the most part, as long as the patient is protected with antibiotics, the use of nasal steroids is safe. This is the info on the health care profession section of the website: http://sinuseducation.org/hcp_antifungal.html "Recent cutting-edge research at the Mayo Clinic has introduced a new paradigm for the treatment of chronic rhinosinusitis (CRS). Clinical studies have demonstrated that topical antifungals are effective in treating and altering the disease progression of CRS. In addition to improving symptoms, topical antifungal therapies have demonstrated decreased mucosal thickening on endoscopic exam and CT scan (View image). Antifungal drugs used in the treatment of CRS include: Amphotericin B Itraconazole Voriconazole In CRS, topical application of these drugs is used to avoid side effects, such as those that occur when oral or intravenous formulations are used in the treatment of other diseases or conditions. Topical administration allows a high dose to be applied to the organism while limiting the patient's exposure to the drug. In clinical studies, side effects reported by patients were not different than the symptoms of the disease. In clinical studies, topical antifungals have been used as follows: Amphotericin B: 100 mg/L of sterile water (up to 200 mg/L has been used) Itraconazole: 100 mg/L of sterile water Voriconazole: 1000 mg/L of normal saline With the introduction of topical antifungal therapy, there remains a role for the traditional therapies in the treatment of CRS. Antibiotics are useful in treating acute bacterial infections that may result because of damage to the nasal epithelium. Use of a systemic corticosteroid may be desirable in patients with moderate-severe to very severe disease. In these patients, thickened, inflamed tissue may prevent the antifungal preparation from reaching the entire affected sinus. In studies, pretreatment with a systemic corticosteroid decreased the extent of inflammation and allowed for better distribution of the antifungal. Systemic corticosteroid options include a short course of 7 to 10 days, an extended taper of up to two weeks, or a one-time dose of an intramuscular formulation, such as triamcinolone dosed at 60 to 100 mg. Sinus surgery has shown to be useful to remove obstructions and excess mucus from the frontal and maxillary sinus prior to initiating topical antifungal treatment. Intraoperative irrigation with an antifungal preparation has also been beneficial to reach the remote portions of the sinuses and to remove excess mucus. In addition, the access provided during surgical intervention provided an opportunity for distribution of the antifungal to the complete sinus area. Such thorough distribution is difficult for the patient to achieve using post-operative drug delivery. In studies, following surgery, patients began irrigation with an antifungal preparation as soon as the treatment could be tolerated. This was generally three to seven days post-operatively. Dosing of the antifungal was 20 mL into each nostril given twice daily. Therapy was continued for a minimum of three months. Some patients responded sooner than three months, but patients with severe disease benefited from extended treatment of up to several years." Figure 3.8 Amphotericin prescription. Current Mayo Clinic recommendations. ENDOSCOPIC SINUS SURGERY If the antibiotic therapy fails, endoscopic sinus surgery is indicated, a relatively new but important development in paranasal sinus surgery. Using small endoscopes to look inside the nose, the surgery is directed at opening the natural drainage channels for the maxillary, ethmoid, and frontal sinuses. Older operations made new drainage channels that did not function physiologically and were not effective. The new endoscopic sinus surgery is a more natural procedure, substantially less involved, and is performed under direct vision. Abnormal and obstructive tissues are removed using state-of-the-art microtelescopes and instruments. In most cases, the surgery is performed entirely through the nostrils, leaving no external scars, little swelling and only mild discomfort. Although in the past attention has often been directed toward the removal of all sinus mucosa from the major sinuses, the functional endoscopic approach relies on the principle that sinus disease is reversible if the underlying cause can be identified, corrected, and the natural sinus ostia enlarged to permit drainage of sinus secretions. This procedure takes practice to perfect, but it has become the procedure of choice when sinus surgery is required. It does the least harm, removes the least amount of tissues, and, unarguably, most effectively reestablishes the natural outflow of sinus secretions and the inflow of air. Endoscopic sinus surgery is best performed under general anesthesia. The surgery is performed as an outpatient, meaning the patient goes home the same day. The discomfort is minimal and far less than with the older operations. Potential surgical complications include bleeding, bruising around the eyes, swelling, scarring, and infection. Rare complications include the possibility of intracranial entry and spinal fluid leak. The ethmoid sinus is located under and adjacent to the brain and the CSF fluid that surrounds the brain can leak through the sinuses into the nose. There is then potential for infection that could result in meningitis. Because the endoscopes used in surgery allow improved visualization of the ethmoid sinuses, this complication is uncommon. Double vision and loss of vision have also been reported after ethmoid surgery. Fortunately, these too are rare complications. Because of potential bleeding problems, aspirin, all Cox 1 NSAIDs all anticoagulants must not be used for 10 days preceding and 10 days following surgery. Light red to clear drainage from the nose is normal for 3 to 6 days following surgery. The outside gauze dressing needs to be changed when soiled or saturated. A 2 x 2 gauze pad folded in half over the nostrils and held in place with a strip of paper tape is sufficient. Nasal packing is uncommonly used after surgery. Mild headaches and sinus or nasal pressure/discomfort are common after surgery. Pain relievers are prescribed. Antibiotics are generally unnecessary. A moisturizing saline spray may be used. No swim strenuous activities should be performed for at least 10 to 14 days after surgery, as this might produce bleeding. Diet should be normal. Alcoholic beverages should be avoided. When directed, saline irrigations are recommended to reduce crusting and to keep sinus openings clear. We use 1 teaspoon of salt in 1 quart (500cc) of warm water. This is delivered via pulsatile nasal irrigator such as the WaterPik®. Using a nasal adaptor such as the Ethicore or Grossan (Hydropulse), the patient leans over a sink and irrigates both nasal passages. Irrigate twice a day, morning and evening. For additional information on nasal irrigation the reader should read the Handbook of Nasal Disease. For additional information on clinical indications for sinusitis and the surgical information for sinus surgery click on Consultation for Sinusitis. ALLERGIC RHINITIS The most common inflammatory nasal disorder is allergic rhinitis. Allergic rhinitis presents with itchy nose, sneezing, itchy eyes, congestion and a clear or white nasal discharge. The condition may be seasonal or perennial. Rhinoscopy reveals a swollen pale or blue mucosa. The oropharynx is pale and edematous, and clear or white secretions may be seen flowing down the pharyngeal walls. Nasal cytology typically, but not necessarily, shows basophils or eosinophils. There may or may not be an obstructive septal component, but typically, airway resistance diminishes (airflow improves) after the mucosa is vasoconstricted with phenylephrine. In IgE-mediated allergy, the serum IgE will be elevated and often specific allergens will be identified on the RAST panel. Classically, the CT scan will be normal. Treatment involves nasal irrigation, and environmental control. First and foremost is environmental control. If specific allergens such as pets are present in the house, they should be removed, but in addition, almost everyone with an allergic diathesis has sensitivity to molds, fungi, mites, dust, and so forth, and to whatever degree the home and work environment can have their allergic load reduced, the patient will do better. The most powerful allergic nasal medications available today are the nasal steroids. Eighty µg of beclomethasone (two puffs) is typically instilled in each nostril two times daily. Newer nasal steroids include –budesonide (Rhinocort®) and fluticasone (Flonase®). Patients normally use 1-2 puffs per nostril once a day. If the aforementioned regimen is not efficacious, referral to an allergist is appropriate. Specific sensitivities are determined and the patient is administered measured doses of the respective allergens in an effort to desensitize the patient to the particular allergen. In some individuals this is effective, and in others the efficacy is uncertain. Desensitization requires intradermal injections that are typically administered three times a week. There is no surgical therapy for allergy, but those individuals with compounding problems such as a deviated nasal septum or bacterial sinusitis may be advised to consider surgical correction of those problems. For additional information on allergy, review the NIH Advances in Allergic Diseases. For additional information on environmental control you can review this section in the Handbook of Nasal Disease. Vasomotor Rhinitis Stress is a common problem presenting as nasal disease. Vasomotor rhinitis is a psychosomatic disease. It is parasympathetic mediated, as are other psychosomatic illnesses. In response to stress, the parasympathetic system is stimulated. The identified target organ is the nasal and paranasal sinus mucosa. The mucosa swells and secretions are induced. The nose becomes congested and anterior or posterior rhinorrhea may be evident. Nasal endoscopy is normal, the IgE and RAST are normal, and the CT scan is normal. History confirms stress in the patient's life either at home or at work. Typically, the sinus problems come on for a short period. For some individuals, they may begin in the afternoon; for other individuals, they may wake up with them; for some, they are weekend problems similar to migraine headaches. Antihistamine decongestants, decongestants alone, or nasal steroids may lessen the symptomatology; however, optimal therapy is to identify this as a psychosomatic disorder, appropriately instruct the patient, and have him or her seek help either in stress reduction or in more aggressive psychotherapy. NASAL OBSTRUCTION Consultation: Nasal Obstruction 1 A psychology student had such severe nasal obstruction that he was an obligate mouth breather. He had lived with this all his life but recently had met a new girlfriend who loved kissing. Because he could not breathe through his nose, he was having obvious problems. He denied any history of nasal injury and did not have any symptoms of nasal allergy. The external nose was straight with a rather prominent hooked dorsum. The septum was horribly crooked. I advised the patient that he would need a septoplasty to correct the breathing. I also told him that if he wished to have a rhinoplasty, this would be a good time, because the two operations should be done simultaneously. He eagerly requested both procedures. A septorhinoplasty was performed and a good functional and cosmetic result was obtained. Various degrees of nasal obstruction occur and they rarely are all-or-none phenomena. Why does a patient with nasal obstruction suddenly decide to seek medical care? Sometimes the obstruction becomes noticeably worse or the patient becomes more aware of the problem. Once attention is focused on the obstruction, it can seem increasingly problematic. Patients who develop acute nasal obstruction from nasal trauma are also acutely aware of their problem and anxious to have it corrected. They may complain of a dry mouth or of an obstruction to breathing. History is the key to diagnosis. Which side of the nose is obstructed? Is it always obstructed or does the obstruction come and go? What brings it on, and what relieves it? An algorithm to approach nasal obstruction is shown in Figure 3.9. The nose should be examined carefully. Unilateral obstruction is usually constant and implies an anatomic basis. This may be a foreign body, a nasal polyp, a nasal tumor, or most commonly, an obstructive nasal septal deviation. Bilateral obstruction can be caused by polyps, tumor, nasal septal deviation, or merely from drooping of the nasal tip associated with the aging process. Allergic rhinitis will also present as nasal obstruction. In this case, the obstruction is generally bilateral and will fluctuate. Many patients complain that when they lie down, one side of their nose becomes obstructed. It is always the lower most or downside, and if they turn over, the nose clears and the other side becomes obstructed. This is a normal physiologic response, and the patient should be so advised. No treatment is necessary. Figure 3.9. Algorithm for the evaluation of nasal obstruction. The nose is a dynamic organ, responsible for filtering, warming, and humidifying inspired air and, to some degree, recapturing the humidity on expiration as well as preserving some of the heat. Because this is an intense process, the nose goes through a nasal cycle in which one side congests while the other side decongests. The decongested side is then responsible for the majority of the work, while the congested side has opportunity to rest. Most individuals cycle approximately four times a day. In some individuals, this normal nasal cycle is exaggerated or, at least, it comes to their attention and they find it to be bothersome. Those who complain to their physicians should be evaluated to rule out other problems such as anatomic obstruction or inflammatory disease. A good explanation will help patients understand what is happening, and will assure them that this is not a problem to be further pursued. The physician's responsibility is, of course, to recognize the normal nasal cycle and resist the temptation to treat with unnecessary surgery or medication. Allergic rhinitis may also present with a runny nose. The common symptoms of allergic rhinitis are nasal obstruction, sneezing, tearing, and runny nose. The symptoms are seasonal or perennial. Allergic rhinitis may be associated with sinus disease and often occurs in conjunction with nasal polyps. The diagnosis is made initially by history. Examination reveals swollen, often bluish-purple mucosa. The treatment has been discussed. Consultation: Nasal Obstruction 2 A 7-year-old girl presented with a 5¬ to 6-month history of nasal stuffiness with a diminishing sense of smell and associated loss of appetite and resultant weight loss. She also complained of severe tiredness, and her mother noted some sluggishness. There were no other complaints, except a headache associated with a recent upper RTI. There was no family history of allergy, no history consistent with infection, and no history of nasal disease prior to the present illness. Examination revealed a normal 7-year-old child. The anterior nares were filled with a mucoid material and it was impossible to see deeper into the nasal cavity. The oropharynx, oral cavity, and remainder of the head and neck examination were all within normal limits. A nasal work-up was initiated. Rhinomanometry revealed an infinite resistance in both nostrils; that is, the nose was totally occluded, even after it was sprayed with phenylephrine. Nasal cytology revealed a few polymorphonucleocytes and a few bacteria. The IgE was within normal limits, and the inhalant RAST panel was negative. A CT scan revealed a large cystic mass involving the mid-portion of the nasal cavity and nasopharynx. The mass was seen to bulge into the anterior cranial fossa, extending into the sphenoid sinus. A neurosurgical consultation was obtained, which confirmed the history and physical examination. Her mental status, cranial nerves, motor, coordination, and gait examinations were all within normal limits. An MRI was obtained, which is shown in Figure 3.10. This revealed a large midline cystic lesion involving her sphenoid, with extension through the plana sphenoidal into the sphenoid. This latter extension was minimal; nonetheless, the gyrus rectus appeared to be elevated. The diagnostic impression was that this was a sphenoid sinus mucocele. The patient was brought to the operating room where a ¬sublabial approach to the nasal cavity was made. The cystic mass was easily identified. The fluid was evacuated, and the cyst dissected from the septum, nasopharynx, and superior nasal cavity. A small dehiscence in the clivus was noted, beneath and posterior to the pituitary. Dissection was completed using a microscope. The lesion was completely removed and there was no evidence of intracranial involvement. The frozen section diagnosis was a craniopharyngioma. This was confirmed on permanent evaluation. The patient made an uneventful recovery with no neurologic, nasal, or endocrine dysfunction. Occasionally, nasal secretion, stuffiness, or obstruction is more than just allergic rhinitis. In this case, it was a tumor that was diagnosed before it eroded into and caused central nervous system disease. Once again, the necessity of a thorough work-up for patients with chronic, complex nasal dysfunction is important. Figure 3.10A. Figure 3.10B. Figure 3.10. (A) T1 magnetic resonance imaging (MRI) scan, sagittal view, no contrast: high-signal intensity mass extending from clivus, sphenoid sinus, and floor of anterior cranial fossa. (B) T2 MRI scans, axial view, no contrast: high-signal intensity mass occupying sphenoid sinus, posterior ethmoids, and posterior nasal airway. RHINORRHEA A runny or drippy nose is a common complaint. Frequently, it is a short-term problem often associated with an upper RTI. However, the runny nose can be a chronic condition. Table 3.3 lists the differential diagnosis for rhinitis. The diagnosis is generally made by a careful history and physical examination. Allergic evaluation and nasal cytology may help distinguish some causes. The algorithm shown in Figure 3.9 will help distinguish the causes of obstruction and discharge. SMELL LOSS The most important chemical sense is olfaction. It is currently estimated that 1% to 2% of the American population suffer from the loss of the sense of smell and if one includes dementia, the number approaches 5% and if one includes allergic rhinitis and hyposmia, the number must approach 20%. For these millions of individuals the world has lost some of its excitement. The most obvious and primary complaint is that food no longer has a taste, because, 95% of the sensory input received from food (that which allows us to distinguish a good steak from a bad steak, a tasty pasta from wet cardboard) is the sense of smell. But smell means a great deal more than just the ability to taste and enjoy food. First and foremost, it is a warning sign. Smoke is an early warning of fire. Most gasolines are odorized, and a natural/home gas leak is detected by its noxious mercaptan smell. Spoiled food smells horrible, and those without a sense of smell cannot protect themselves from food poisoning. Table 3.3 Differential Diagnosis for Rhinitis Acute viral upper respiratory tract infection (common cold) Allergic rhinitis Bacterial rhinosinusitis Atrophic rhinitis E. Vasomotor rhinitis Irritative rhinitis (tobacco, poor air quality, smoke, gases, chemicals) Hormonal rhinitis (pregnancy, menstruation, endocrine) Cold-induced rhinitis (skier’s nose) Gustatory rhinitis Drug-induced rhinitis Rule out CSF leak RAST = Radio Allergo Sorbent Test CSF = cerebrospinal Fluid Smell is a major pleasure sense, and when one smells the fragrance of cut grass, of flowers, of a wet forest, of autumn or of spring, one derives not only information, but pleasure. We all know the smell of our loved ones. The sense of smell plays an important role in sexual excitement, and although Americans have done a great deal to camouflage body odor and sexual smells, they are still perceived and remain important. The sense of smell is necessary for body hygiene. How would one know when to change ones underwear or take a shower without the sense of smell? The sense of smell, second only to hearing, is a strong component of memory. For example, the smell of cut grass brings back memories of K1-12 sports such as football, soccer and baseball. The smell of grandfather's fishing vest brings back the smells of summer vacations. The smell of the kitchen brings back the smell of home and the smell of cooking brings the memories of festive holidays. The loss of the sense of smell has not received the same attention that loss of vision and loss of hearing have, and hence, less is known about it, and patients know even less about what has happened to them. The nomenclature of smell is listed in Table 3.4 and includes definitions for anosmia, hyposmia, phantosmia, parosmia, presbyosmia and dysosmia. The differential diagnosis for smell loss is long. The most important causes are described. Inflammatory nasal disease is responsible for approximately one third of the patients complaining of smell loss. Whether this is a chemical inhibition of olfactory epithelial function in the olfactory cleft or whether it represents a simple obstruction to air passage in the olfactory cleft is unknown. Inflammation can be caused by infection and/or allergy, if the inflammation is appropriately treated, the sense of smell can often be restored. Allergic rhinitis is increasing in prevalence and severity many with allergic rhinitis suffer hyposmia. Head trauma results in impaired olfaction in approximately 10% of cases, particularly with frontal and occipital trauma. The brain is jarred relative to the cribriform plate, and the delicate olfactory nerves penetrating the cribriform are stretched or sheared. If stretched, the sense of smell returns. This occurs in approximately one third of cases. 90% of those who recover recognize the return of olfaction within the first year post trauma. If the nerves are sheared, olfaction does not return. These patients often experience phantosmias, much like a phantom limb complaint following an amputation. Another third of smell impairments are post¬viral in nature. Certain viruses, particularly of the influenza group, injure the olfactory epithelial cells and render the patient hyposmic and sometimes anosmic. Once this occurs, there is no known treatment and prognosis for recovery is poor. Certain toxins are known to destroy the olfactory epithelium. Ammonia is probably the most common, but other cleaning solvents have been reported as well. Table 3.4 The Nomenclature of Osmia Normosmia-A normal sense of smell Anosmia-An absent sense of smell Hyposmia-A diminished sense of smell Parosmia-A distorted sense of smell Phantosmia-A phantom sense of smell Presbyosmia-Hyposmia associated with aging Dysosmia –Any abnormality of olfaction Some patients have a congenital loss of the sense of smell. For these individuals, the loss is not as great because it is a sense that they never had. The true incidence of congenital anosmia is not known, because many of the patients never complain and those that do are rarely reported. Presbyosmia is the loss of the sense of smell with aging. As the geriatric population increases, this becomes increasingly important, as there is concern that the sense of smell diminishes with age. It diminishes faster in males and in those who smoke tobacco products. Certain endocrine dysfunctions are associated with smell impairment. The sense of smell is a primitive and basic sense and it is often associated with psychiatric illness. Some patients at a smell dysfunction clinic will, in fact, have a normal sense of smell and will have a mental health illness. There are many other causes, but the frequency of these is small. The work-up for smell loss begins with an olfactory test. Several are available. The most rudimentary is the Alcohol Sniff Test. Commercially available is a scratch and sniff test called the UPSIT the acronym for the University of Pennsylvania Smell Identification Test. The most sophisticated test is the olfactory-threshold and odor-identification test. The work-up should also include an evaluation for abnormal physiology, which can include such tests as nasal cytology, rhinomanometry, and IgE and RAST screens or skin tests for allergic rhinitis. The examination should include rhinoscopic endoscopic examination of the olfactory cleft and a sinus CT scan for paranasal sinus disease, olfactory cleft obstruction, and, occasionally, tumor. For those with an inflammatory etiology, rigorous treatment can be prescribed. For all others, that is, those with a nonreversible cause, the patient is counseled. The most important counseling is educating the patient in the cause and reality that the sense of smell is, in fact, diminished or absent. Patient instructions are important for those with a diminished or absent sense of smell. They must have smoke detectors in all rooms in which they cook, burn fires, or sleep. Gas detectors must be present in all areas in which gases may be present, because if one is to light a match in a gas-filled room, the resultant explosion can be fatal. Because smell-impaired individuals cannot detect spoiled or rotten food, they must maintain a rather rigorous leftover-food discard schedule, and it is always best if their food is sniffed or tasted by someone with a normal sense of smell before they eat it. Without question, the greatest loss is the pleasure derived from eating. One invariably invites friends over for brunch, lunch, dinner, snacks, or "lets just eat anyway." In any case, food, its preparation, and its consumption are a major American pleasure. Rehabilitation in this regard is difficult. The patient may learn to focus on the other aspects of food, such as color, the pre¬sentation, and the texture, but these fall far short of the aromatic pleasures they once enjoyed. For some, the addition of hot trigeminal stimulants returns some interest in food. Pepper and curry are the two major hot trigeminal cuisine stimulants and for many individuals,spicy Mexican or Asian or Indian food becomes interesting. If little is known about olfaction, even less is known about taste. The chemical tastes on the tongue, modulated primarily by the seventh and ninth cranial nerves, are sweet, sour, salt, and bitter. The true incidence of chemical taste impairment is unknown. Although some purport it to be a large number with a complex work-up and a lengthy differential diagnosis, others consider this a rather infrequent problem and that those seriously concerned about their taste dysfunction generally have psychiatric rather than physiologic causes. Nonetheless, there are some physiologic problems that impair the sense of taste. Certainly, injury to the taste fibers in the ear at the chorda tympani or any site distal will alter the sense of taste. Certain drugs, such as metronidazole, will cause a metallic taste in the mouth, and although this is not truly a taste dysfunction, it is an abnormal taste, and fortunately one that disappears when the drug is discontinued. Many patients complain of an electric taste in their mouth. For some, this is caused by different metals used in dental restoration and thus a small battery is active in the mouth. This is almost impossible to document and normally requires removing all the dental work and then redoing it with a single compound. The sense of taste can be tested by applying sweet, salty, bitter, and sour compounds to the tongue. Intensity can also be measured but it is more difficult and requires a clinic setup to do so. For the majority who have lost their sense of taste, the impairment is small, and it may be that the majority never even come to medical attention because they adapt to the loss. Each patient deserves a work-up excluding tumors, gastric reflux, postnasal discharge, and obvious intraoral pathology. Psychiatric consultations should be obtained early, and the astute clinician should not pursue organic causes for a complaint that is often psychogenic. Dysgeusia and burning mouth syndrome are often related to depression and may be improved with SSRI inhibitor antidepressants. The following letter submitted by one of my patients describes one person’s loss. Dear Lorraine, I have to tell you that I CAN smell the roses and not to give up hope. But before I continue with that, I need to ask a favor: I don’t remember where I posted my loss of sense of smell story and I need to update it. You wouldn’t believe how many people I’ve heard from! Can you tell me which site to go back to? When I was first told I had anosmia, by my primary care physician, he tried treating me with prednisone. I don’t remember the dosage, but he prescribed a packet where the first day there were five or six pills, the second day one pill less, and so on for about a week. No change. I read as much as I could find, most of it discouraging, but I felt I should not give up without a fight. I had found the University of California San Diego Nasal Dysfunction Clinic site in my search. I emailed Dr. Davidson and waited. And waited. And waited. Finally I went back to the site, got the phone number and called and spoke with one of the staff. Dr. Davidson called me back and told me what would be entailed in an evaluation and exam and what I would need beforehand. The clinic arranged a schedule for me where I could get the CT scans of my nasal sinuses when I arrived, then be given two different kinds of tests to determine how much I could still smell, if anything, and then I would be seen by the doctor. My insurance covered all of this. I live in Northern California, so the greatest out-of-pocket cost for me was getting a round-trip ticket from San Francisco to San Diego. It was money and time very well spent. First of all, I found out I was hyposmic (reduced sense of smell), not anosmic (total loss of sense of smell), and that my case was considered to be “mild.” I wondered what it must be like for someone with “moderate” let alone “severe” hyposmia. I also found out that there was nothing physically wrong with my nasal sinuses, no evidence of other disease, blockage or damage, and that the cause of my loss of what I felt was most of my sense of smell was definitely a post- viral infection. The physician examination of my nasal passages and sinuses(?) involved endoscopy, which was painless. At the end of the exam, Dr. Davidson told me the condition was treatable with prednisone and that the dosage my physician had used had not been high enough. He also told me that I would soon notice improvement and that my sense of smell would continue to improve over the coming months. When I left the clinic that evening, I had something priceless: hope. I returned to the airport with plenty of time to have dinner before my flight. I didn’t care what I ate, except that I followed the healthy eating program of Weight Watchers. Beyond that, I couldn’t taste much. At first I didn’t notice that I could smell some of the food in the food court. When I realized I was smelling the aromas of grilled meat at the “healthy” Mexican food stall, I was amazed and seized the moment to have something I could taste almost fully. I suspect that my being able to smell things at that time may have had something to do with the solutions put into my nose to prep me for the endoscopy—something to do with moisturizing the nasal passages. The following week proved Dr. Davidson correct. I did notice some improvement in my sense of smell. I had taken the prednisone for five days and I had begun the prescribed regiment of irrigating my nose twice a day using a salt-water solution and a nasal irrigator with a special attachment I was able to purchase from the clinic. ( I thought of it as bush my teeth, clean my face and wash my nose. I bet almost everyone who does this has had the same thought.) I did well for about two to three weeks. Then, another sinus infection interfered with my progress. Please understand that my ability to smell aromas didn’t happen overnight, and I thought Dr. Davidson was wrong when I had the setback. But it turned out to be only a setback, no more. What Dr. Davidson and I did not know was that a month later I would be diagnosed with a non-Hodgkin’s lymphoma (cancer of the lymphatic system, which is the immune system). My type of lymphoma is considered “indolent,” a slow-growing cancer, and I was told that I have had the disease for many years, even though I had no symptoms. (I was checked out after I discovered a lump on my chest wall.) Because people with lymphomas are prone to upper respiratory infections, I believe the susceptibility I’ve had to bronchitis and sinusitis problems in the last few years was probably due to the underlying lymphoma. My immune system being reduced in effectiveness, I was most likely a prime host of the virus that attacks the olfactory nerve. THIS IS NOT TO SAY THAT YOU HAVE OR MAY HAVE LYMPHOMA. You probably don’t—it’s a whole other story. But for me, it makes my experience make more sense. By the time I was diagnosed, I had so much of the cancer in my body that I was given less than a year to live unless I began chemotherapy immediately. So I did. And guess what? That therapy included very high doses of prednisone (which kills lymphoma and leukemia cells of certain types). I am convinced that the very high doses of prednisone hastened the return of most of my sense of smell. I can taste food, smell flowers and distinguish between socks that have been laundered and those that have not. I can smell dinner burning and the additive put into natural gas. I can enjoy being put off by the unpleasant odors of sewer gases and cap poop. So, Lorraine, don’t give up hope unless it is absolutely certain that there’s a reason to do so. Go to the UCSD site on anosmia if you haven’t been there already. Read everything. Then find a smell/taste dysfunction clinic near you and make an appointment to be seen. Failing that, find the nearest specialist in nasal dysfunction—an otolaryngologist (ear/nose/throat) specialist who truly cares about lessened or lost sense of smell/taste (many don’t care or know much about this problem, their practices focus on other nasal diseases and conditions). Then and only then will you have the best help. People like me can be great emotional support, but we can’t diagnose you or provide you with appropriate treatment. For getting the most of every day, you have to learn to change your perspective. You can still see, hear and feel the glory of the world around you—even the flowers and plants. Feel the textures, absorb the splendor of the colors and shapes, listen to the leaves rustle in the wind. Learn to taste in food in new ways: savor texture, colors and what you can sense with your tongue: sweet, sour, salt and bitter. (My favorite dinner was refried beans into which I mixed chopped farmer’s market tomatoes and thinly sliced serrano chilies. I topped this with a couple of tablespoons of low-fat sour cream. Great texture with sweetness, bite, and a distinctive flavor. If you don’t like refried beans, you can mash or puree canned white beans or kidney beans or pinto beans and mix them with tomatoes, chilies, sweet fresh corn taken off the cob or other things your tongue can taste.) Most herbs and spices won’t register. Mint might, and cumin. Dr. Davidson advised me to use curry powder (which usually contains cumin) the way other people use salt. Experiment and never let yourself be disappointed if you can’t taste something—but always let yourself be delighted when you can (even if you wouldn’t choose to taste whatever it was again). For summer, try icy cold slices of cucumber in a dressing of rice vinegar (sour) or lime juice with a little sugar and chopped fresh mint. Eat fresh crunchy vegetables (lettuce, mung bean sprouts, cucumber) and combine them with sweet vegetables and fruits (tomatoes, carrots, pieces of mango or papaya or peach, sliced grapes or apples or pears. Add crushed toasted corn tortilla pieces for more crunch or whatever you can think of to add another textural or tongue-taste dimension.) You’ll enjoy the creativity of the effort. I don’t talk much about meat because I found it unpleasant, except for an Indian meal with lamb curry. Stay away from canned tuna fish! Watch expirations dates, especially on yogurt and milk. Make friends with someone responsible for the produce section in your market and tell that person and the vendors at farmer’s markets what is going on so they can help you get the sweetest melons, mangoes, strawberries, pears, peaches, nectarines and anything else where selection has as much to do with aroma as with color or feel (a good ripe honeydew melon has a creamy color and feels velvety, but let your new produce friends select the cantaloupe, mangoes peaches, strawberries, etc.) Invited to a potluck? Bring the bread and cheese. Want to make dinner for company? Use tried and true recipes or even try something new and have someone in your household taste for seasoning. Although I went through the kind of loss behavior in losing my sense of smell that usually occurs with people newly diagnosed with cancer (grieving, anger, resignation), I found that life and the pleasures of life remain and are forever open to discovery, often giving back wonderful surprises. When I was diagnosed with cancer I didn’t grieve: been there, done that. I just got on with getting treated and getting well. Wishing you all the best, Penny