Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Anosmia Chemosensory disorders affect approximately two million adults in the U.S. It was found that from 1975 to 1976, over 500,000 visits to physician's offices were for evaluation of possible chemosensory dysfunction. Not until this past decade, has a focused, scientific effort been directed to the study of chemosensory disorders and their diagnosis and treatment. The NIH, in 1979, funded the establishment of several chemosensory research centers. It is through the efforts of these centers that a comprehensive understanding of the diagnosis and treatment of smell disorders have been obtained. In evaluating a patient who may have a possible olfactory disorder, the clinician has at his disposal these six tools. Of this group, the first four, i.e., history, physical exam, and olfactory testing and taste testing, offer the most revealing information as to the etiology of the possible anosmia. Several of the most common causes of anosmia carry with their diagnosis unique histories of events or conditions that occurred prior to the onset of the reported dysfunction. A physical exam helps to differentiate conductive form sensorineural etiologies for smell dysfunction. Should this examination of the nasal cavity fail to demonstrate a conductive pathology, then a sensory neural process should be suspected and olfactory testing initiated. When clinically indicated, thyroid tests, adrenal function tests, serum glucose, serum creatinine, erythrocyte sedimentation rate, and CBC are helpful. However, these tests should not be used in a shotgun approach. Finally, diagnostic radiology has a role in the work-up of anosmia, but these studies should be reserved for specific indications. Plain films are useful in diagnosing ethmoid sinus disease. CT scans, are indicated if an intracranial lesion is suspected or to define specific sinus disease more accurately. The recommendations of the Rocky Mountain Taste and Smell Center at the University of Colorado are for the use of CT scans for the evaluation of sinus disease or with patients who have a neurologic sign or symptom, such as headaches or abducens palsy, in association with an olfactory dysfunction. The role of MRI is more limited in its usefulness. Its role should be limited to the evaluation of intracranial processes that are not easily evaluated with CT scans, such as Multiple Sclerosis or when tumor extension into the cranial cavity, especially in the region of the skull base. Other than these specific indications, the routine use of these expensive diagnostic tests has an extremely low cost-benefit ratio and should not be used. The cornerstone for the diagnosis of olfactory dysfunction is olfactory testing and taste testing. The discrimination of taste from smell dysfunction is important because the two senses are integrally related in their ability to providing chemosensory information. Deems et al analyzed 750 patents evaluated at the University of Pennsylvania Smell and Taste Center. This study thus amplifies the divergence between a patient's sense of chemosensory dysfunction and the actual dysfunction that is present. Thus, no diagnosis of a taste or smell disorder should be made without the use of accepted chemosensory testing methods. Because taste disorders are rare, a simple taste test may be performed to rule out this diagnosis. Through the use of liquids that utilize the sense of taste for salty, sweet, sour, and bitter flavors, a patient's inability to detect one or more flavors is identified. This test, known as the Taste-and-Spit test, provides an excellent screen for the diagnosis of taste disorders. Olfactory testing, once a very complex and cumbersome task reserved for research investigations, has become readily available to the clinical physician. No longer must machines like this olfactometer. Today, modern clinical olfactory testing is usually done with two commercially available tests: UPSIT Scratch and Sniff test and the Connecticut Chemosensory test. The UPSIT test, developed by Dr. Richard Doty, is a standardized 40 stimulus microencapsulated "scratch and sniff" test. This test is very portable and no trained personnel or equipment are required for the test to be administered. In fact, the patient may self administer the test at home or in the physician's office. The advantages of this test are that normative data from over 1500 subjects are available for males and females separately, and the relationship between smell ability and age has been determined. Finally, the forced choice design helps to identify malingering. The Connecticut Chemosensory Test, or CCCRC, is designed for unilateral smell assessment offers the ability to detect both olfactory threshold and the ability to identify odors. This test does require a trained administrator to deliver the test protocol. The Threshold portion of the test consists of 11 plastic squeeze bottles, each with a pop-up spout that is inserted into the external nares for monorhinic testing. Seven of the bottles contain butanol in deionized water and are presented in seven serial dilutions. The remaining four bottles contain distilled water controls. A two bottle, forced-choice, method is used. In a trial, the subject receives two bottles, one with and one without butanol, and chooses which one has the strongest smell. Testing begins with the weakest concentration and progresses to higher concentrations depending on the outcome of each trial. The patient's threshold is defined as the concentration at which the correct bottle is identified four times in a row. The maximum score is 7 (i.e., detection of the 7th serial dilution).A score below 5 is defined as olfactory dysfunction. The second component of the Connecticut test is the odor identification test. In this test, eight plastic jars contain a common odorant. A list of twenty possible common household and food items is also shown. Of these 20, the patient is tested with 8 and the other 12 serve as distracter items. One of the eight odors serves as a stimulant of the trigeminal nerve such as vicks or ammonia. The patient is presented with an odor and asked to identify it. If the subject perceived no odor, no forced response is required and the item is marked as unidentified. The score for the test consists of the number of olfactory items identified correctly out of 7 choices. The trigeminal stimuli is not included in the final score. With these two olfactory tests, the Etiology of Anosmia has been examined. Three of the major smell centers have published data analyzing the most common etiologies of anosmia. The top four causes of anosmia include upper respiratory tract infections, idiopathic etiologies, trauma, and nasal and sinus disease. Of note toxins rarely account for olfactory loss. The incidence of long-lasting olfactory loss after a URI is not known. Nonetheless, this entity accounts for 15-25% of anosmia. In making the diagnosis of an olfactory dysfunction secondary to an upper respiratory infection, the history is almost pathopneumonic. Typically, either a constant foul smell or a distortion in normal smells is reported within 6 months following a URI. This disorder is reported more often in women and occurs within the 4th and 5th decade commonly. Patients usually do not have total anosmia when tested, but instead the demonstrate hyposmia or partial loss of normal smell function. The prognosis for recovery depends on the etiology of the olfactory dysfunction. Conductive disorders will resolve after the URI, allowing a return to normal air flow and olfactory function. However, sensory neural damages of the olfactory neurons tend to be permanent and irreversible. Ultrastructural changes have been demonstrated by electron microscopy, demonstrating the presence of degenerative changes of the ciliated olfactory receptors, and a replacement of the olfactory epithelium with respiratory epithelium. There is no established treatment for anosmia following a URI Commonly prescribed therapies such as zinc, vitamin A, and oral steroids have been shown to provide no greater benefit than placebo in several studies. Head trauma was first reported as a cause of anosmia in 1864. Since that time, it has been recognized that 5% of all head trauma patients exhibit total anosmia and that 30% of patients demonstrate hyposmia. Costanzo et al demonstrated that the prevalence of anosmia is directly proportional to the severity of the head injury. In a review of 493 head injury patients, Costanzo demonstrated a 15.9% incidence of anosmia in Grade I head injury, a 19.4% incidence in Grade II, and a 24.5% incidence in Grade III head injuries. The etiology of the anosmia is most commonly due to shearing of the olfactory filaments at the cribriform plate as a result of Coup and Contracoup forces. Although frontal injuries are more common in head trauma, occipital injuries have the highest incidence of total anosmia. The histopathologic changes result in a loss of olfactory cilia and a disorganization of the olfactory axons. Recovery of olfactory function following a head injury is variable and depends on the pathophysiological mechanism of the loss. Any recovery usually does not occur until after 6-12 months following the injury. Patients with shearing injuries to the fila olfactoria leading to the olfactory bulb have the worst prognosis for recovery. Anosmia secondary to cerebral hemorrhage, hematoma, inflammation, or from blockage of the nasal passages has a fair chance of a complete to partial return of olfaction. Finally, olfactory dysfunction secondary to sinus disease represents the most treatable etiology of anosmia. Usually due to a conductive disorder of nasal air flow, there is rarely any pathologic changes of the olfactory epithelium itself. Therapy is usually directed to the removal of the anatomic obstruction. Anosmia secondary to chronic sinus disease has been shown to be responsive to steroid therapy as the reduction in mucosal edema increases the inspiratory intranasal air flow. The prognosis for a return to normal olfactory function is greatest in this group compared to the previous described etiologies. Anosmia is an important disorder that the otolaryngologist must recognize and properly diagnose. The psychological impacts of anosmia are well documented, as are the health hazards resulting from this disorder. Patients who are evaluated and found to have olfactory dysfunction need counseling for dietary modification and on lifestyle adjustments to avoid the hazards of exposure to toxic fumes and natural gas. It would be wise to advise patients with total anosmia to switch from gas appliances to electric so as to minimize the risk of undetectable natural gas leaks. Great steps have been taken over the past 15 years to better understand and diagnose this disorder. Perhaps the future will bring improved methods of treatment. Case Presentation A 69-year-old white female presented with the complaint of an inability to smell or taste. The patient stated that these symptoms had been present for over a year following an upper respiratory tract infection. Initially, normal odors became distorted, and a constant foul smell was detected for approximately 6 months after the infection, followed by a sense of total smell loss and altered taste. During the initial work-up, the patient was started on oral steroids for 1 week without resolution of her symptoms. She was then placed on nasal Beconase spray and reported no improvement in her symptoms. She has lost over 30 pounds in one year and suffers from periods of depression that had not been present before her reported anosmia. Her only current medication consists of Beconase nasal spray twice daily. The patient's past medical history is unremarkable and no history consistent with allergy, chronic nasal disease, or sinus infection was present. The physical examination demonstrated no evidence of sinusitis, nasal polyps, septal deviation, or dental caries. A sed rate, CBC and blood chemistries were within normal limits. A plain film sinus series showed minimal mucosal thickening. A CT scan and MRI confirmed the presence of mild sinus mucosal thickening and no intracranial pathology. The patient underwent formal smell and taste testing via the UPSIT Scratch and Sniff test and a variant of the Spatial Q-Tip test. The patient scored 27 out of a possible 40 on the UPSIT test and had normal taste sensation. The trigeminal nerve was tested with ammonia and was intact. The patient was diagnosed with hyposmia secondary to a viral upper respiratory tract infection and the nasal steroid spray was discontinued. A dietary consult was obtained to aid in maximizing the sensation of flavor in order to improve the patient's appetite. Counseling on the risks of undetectable natural gas leaks, fires and other hazardous odors was offered and the patient was advised to obtain smoke detectors for her home, and to change her appliances from gas to electric. Bibliography Cain WS. Testing olfaction in a clinical setting. Ear Nose Throat J 1989;68:322-328. Cain WS, Gent JF, Goodspeed RB, Leonard G. Evaluation of olfactory dysfunction in the Connecticut chemosensory clinical research center. Laryngoscope 1988;98:83-88. Costanzo RM, Becker DP. Smell and taste disorders in head injury and neurosurgery patients. In: Meiselman HL, Rivlin RS, eds. Clinical Measurement of Taste and Smell. New York: Macmillian, 1990:565-578. Doty RL. A review of olfactory dysfunctions in man. Am J Otolaryngol 1979:1:57-79. Doty RL, Shaman P, Kimmelman CP, Dann MS. 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Report of the Panel on Communication Disorders to the National Advisory Neurological and Communicative Disorders and Stroke Council. Washington D.C.: Public Health Service, NIH Publication No. 79-1914;1979:319. Scott AE. Clinical characteristics of taste and smell disorders. Ear Nose Throat J 1989;68:423-427. Seiden AM, Duncan HJ, Smith DV. Office management of taste and smell disorders. Otolaryngol Clin North Am 1992;25:817-835. Smith DV. Assessment of patients with taste and smell disorders. Acta Otolaryngol Suppl 1988;458:129-133. Tichman RA, Post EM, Sheehe PR, Wright HN. Olfactory performance during childhood. I. Development of an odorant identification test for children. J Pediatr 1992;121:908-911. Yamagishi M, Hasegawa S, Nakano Y. Examination and classification of human olfactory mucosa in patients with clinical olfactory disturbances. Eur Arch Otorhinolaryngol 1988;245:316-320. 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