Nose and Mouth

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Generalities

If you can excuse the pun, it is wise to be nosy about the nose. In fact, examination of this important facial appendix may reveal unsuspected abnormalities that lead to a diagnosis of either systemic diseases or capital sins (such as cocaine abuse).

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The External Nose

• 1.

  What are the normal structures of the external nose?

  They are shown in Fig. 6.1 :

  • Bridge: located superomedially and representing the bony upper third of the nose

  • Alae ( wings in Latin): cartilages that make up the inferior, medial, and lateral two-thirds of the nose

  • Nares: the paired orifices (i.e., the nostrils)

  • Tip and columella

  

• 2.

  What is rhinophyma?

  From the Greek rhino (nose) and phyma (tumor), this is a variety of acne rosacea characterized by a bulbous and rather prominent nose. It is also referred to as copper-, hammer-, or potato-nose, since the skin is thickened, erythematous, nontender, and often covered with multiple telangiectasias ( rum or gin blossoms ). In fact, other colorful lay terms for this condition include brandy nose, rum nose, and toper’s nose – all paying tribute to its alleged association with the bottle, which is actually rather loose. Pathology shows follicular dilation and sebaceous hyperplasia, with fibrosis and hypervascularity. Of note, rhinophyma may degenerate into basal cell carcinoma.

• 3.

  What are the causes of rhinophyma?

  The ones conventionally blamed are climatic exposure and alcohol, with the best example of gin blossoms being those of the great comedian W.C. Fields, a man whose nose was directly proportional to his affinity for liquor. Rhinophyma is also rather common among politicians, with an early phase of it noted in the 42nd US president, Bill Clinton. If this prompts you to wonder whether Pinocchio had rhinophyma, too, the answer is no . Pinocchio had variable rhinomegaly , a peculiarly reversible condition related to his telling lies.

• 4.

  Is there any scientific basis for the “Pinocchio effect?”

  Yes. Recent evidence indicates that liars may indeed experience nasal changes, resulting in a telltale itch that eventually prompts them to unconsciously touch their nose. To corroborate this phenomenon, Alan Hirsch, director of the Chicago-based Smell and Taste Research Foundation , gathered 23 giveaway signs (both verbal and nonverbal) of “mendacious speech” and recently used them to analyze Bill Clinton’s famous 1998 grand jury testimony on the Lewinsky affair. Overall, Clinton did 20 of the 23 signs, but whenever being particularly untruthful (or “legally accurate”), he consistently touched his nose, which brings us back to Collodi’s Pinocchio and science. The nose contains abundant vascular erectile tissue (an unfortunate property it shares with the penis), which involuntarily dilates whenever a person lies, thus making the node redder, bigger, and itchy. Hence, the repetitive nose-touching of liars. Hirsch honored Collodi’s insight by naming this phenomenon the “Pinocchio effect.” His observation has been confirmed in other famous cases. For example, even O.J. Simpson touched his nose rather frequently during trial when describing Nicole Brown Simpson’s murder. Hence, simple observation might allow policemen, attorneys, psychiatrists, and everyone else to tell whether someone is lying. Or, as Yogi Berra used to say, “You can observe a lot by watching.”

• 5.

  What is a saddle nose ? Does it really exist outside of board questions?

  A saddle nose is the congenital (or acquired) erosive indentation of the nasal bone, turning the distal tip of the nose upward and outward. A true saddle nose (caused by destruction of the bony portion of the nose) is typical of congenital lues , but actually more frequent in Wegener’s granulomatosis. Given the increasing availability of good therapy for both of these conditions, a saddle nose has now become less common. A pseudo-saddle nose is instead a feature of relapsing polychondritis , although the destruction in this case involves cartilage and not bone.

• 6.

  What are nasal fractures?

  They are the most common trauma-related disorders of the nose. They present with severe pain and anterior epistaxis , often from both nares. Periorbital ecchymoses invariably develop 24 hours after trauma, along with significant sequelae, such as septal hematoma or septal deviation. Because these fractures are open , antibiotics are necessary to prevent osteomyelitis.

• 7.

  What is a septal hematoma? How does it differ from septal deviation?

  A hematoma is a purple and painful nodule in the nasal septum, easily spottable through the nostril. Conversely, traumatic displacement of the nasal septum (i.e., septal deviation ) may be difficult to see until later, since edema of the early posttraumatic stages makes physical exam difficult to perform. Both of these complications require referral to an ear-nose-throat (ENT) specialist for drainage or reduction. If undrained, the hematoma may cause the septal cartilage to become ischemic and necrotic, with a resulting permanent nasal deformity.

• 8.

  What is lupus pernio ?

  It is a chronic, nonblanching, diffuse, and purple skin discoloration of the external nose, in the absence of true nasal enlargement ( Fig. 6.2 ). Hence, it differs from rhinophyma. A sign of active sarcoid, it may occur with uveitis, erythema nodosum, and pulmonary involvement. It may also coexist with lesions of the ears, cheeks, hands, and fingers. The term lupus refers to any disfiguring skin condition that, like a wolf ( lupus in Latin), “devours” the patient’s facial features. It is thus used with modifying terms to designate various disfiguring skin diseases, such as lupus verrucosus, lupus erythematosus, lupus tuberculosis, lupus vulgaris, and, of course, lupus pernio. Pernio is Latin for frostbite and refers to the peculiar violet-bluish hue of the condition (see Chapter 3 , The Skin, Question 255).

  

• 9.

  What did Rudolph of the reindeer story really have?

  Probably rhinophyma, but that begs the question: Did Santa spill the grog while feeding his reindeer?

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The Internal Nose

• 10.

  What are the normal structures of the internal nose?

  The normal internal structures are shown in Fig. 6.3 :

  

  The vestibules . As indicated by the term, these are paired internal widenings, immediately beyond each naris. They are delimited:

  • Medially by the septum. Like the external nose, this is partly bony and partly cartilaginous. The word septum is an anglicized adaptation of the Latin saepire , “to erect a hedgerow.” Indeed, the function of the septum is to provide a medial boundary to each vestibule.

  • Laterally by a wall of cartilage.

  • Deeply beyond the vestibules are the turbinates , or conchae . These are curving bony structures that project into the internal nose. There are three turbinates (and three corresponding meatuses) in each nasal cavity: superior, middle, and inferior. Their main function is to increase the nasal surface for humidification, temperature control, and filtering of inhaled air. To do so, they are covered by a well-vascularized and erectile mucosa.

  Pearl

  On routine examination by either otoscope or Vienna speculum, one can only inspect the vestibule, anterior portion of the septum, and the inferior and middle turbinates.

• 11.

  What are paranasal sinuses ?

  They are the frontal, maxillary, ethmoid, and sphenoid sinuses: four hollow and air-filled paired cavities that open through small ostia into recesses of the nasal cavities called meatuses. These are covered by bony shelves lined by erectile soft tissue (the turbinates) – three on each side.

• 12.

  And what about the adenoids ?

  They are aggregates of lymphatic tissue located on the roof of the nasopharynx, just below the sphenoid sinus. They typically regress with puberty and so in adults are usually absent. Yet in infants and children, they may enlarge considerably and cause nasal obstruction, nasal voice, snoring, restless sleep, and mouth breathing. Since mouth breathing in times of facial formation may result in bony changes, affected children often develop an adenoid facies , with a high, arched palate; prominent upper teeth; pinched-in nose; shortened upper lip; a staring expression of the eyes; and a slightly elongated face. Adenoidal hypertrophy also may obstruct the eustachian tubes and thus result in recurrent middle ear effusions and otitis media.

• 13.

  What is the significance of flaring of the nostrils ?

  Flaring of the nostrils (i.e., of the alae of the nose) is a sign of increased work of breathing, typical of impending respiratory failure. It is often associated with other findings of distress, such as respiratory alternans and abdominal paradox (see Chapter 13 , Chest Inspection, Palpation, and Percussion, Questions 52–58). It also can occur in peritonitis as a result of impaired and painful excursion of the diaphragm.

• 14.

  What are the best tools for inspecting nares and internal nose?

  • Otoscope: this can be mounted with a nasal speculum (instead of an ear speculum) and thus used to shine a light directly into each vestibule.

  • Handheld Vienna nasal speculum: this is a speculum that opens upon closure of the handles. It is commonly used with a head mirror ( Fig. 6.4 ).

    

  In the absence of these tools, you may simply use fingers and penlight. Either way, always instruct the patient to first blow the nose (gently but forcibly) to expel any mucus.

• 15.

  Is inspection of nasal secretions useful?

  Yes. In fact, there is quite some value in snot , the colloquial term for excessive flow of nasal mucosa. Although the butt of vulgar jokes, snot is actually noble in origin, going all the way back to the Old English gesnot . It also retains diagnostic value, since different diseases tend to produce different snots.

  • A clear discharge is suggestive of viral or atopic rhinitis.

  • A yellow discharge may instead indicate an early suppurative process.

  • A green discharge is quite consistent with purulent sinusitis.

  • Obviously, a bloody discharge suggests anterior epistaxis.

  • A dark and almost black discharge (especially in comatose diabetics) argues for mucormycosis.

• 16.

  What is an abscess of the nasal vestibule?

  It is a superficial abscess of hair follicles (furunculosis) , usually caused by Staphylococcus aureus and not uncommonly located in the nasal vestibule or septum. Quite painful, it presents as an erythematous and fluctuant nodule in the septal mucosa. Usually treated with antibiotics and warm compresses, it may require incision and drainage to avoid cavernous sinus thrombosis.

• 17.

  What are the causes of swelling/bumps in the nasal septum?

  • Septal hematoma

  • Septal abscess

  • Nasal polyps

  • Papillomas

  • Tumors

  All require ENT referral, since an untreated hematoma (or abscess) may result in septal perforation .

• 18.

  What are the most common causes of airflow obstruction in one or both nares?

  In addition to the conditions previously listed, other causes include nasal mucosa edema, septal deviation, and foreign bodies – all diagnosable by exam. Foreign bodies are especially common in children, given their unique penchant for inserting rocks, twigs, and crayons into nares and various body orifices.

• 19.

  What are nasal polyps?

  They are pedunculated, fleshy, and friable structures that hang from the lateral or septal mucosa. Polyps originate from localized swellings of either sinus or nasal mucosa, initially small, but eventually growing with each recurrence of submucosal edema until they may even protrude from the vestibule and cause nasal obstruction. They are often multiple, clearly visible, easy to move back and forth, and not tender (which differentiates them from other internal nasal structures). They are common in chronic (atopic) rhinitis and aspirin sensitivity (often in association with asthma) and can be easily removed through endoscopy.

• 20.

  What is a papilloma of the nasal vestibule?

  It is a wart of the inner nose. In contrast to the more common polyp, papillomas are jagged in appearance and more likely to bleed. Like polyps, they can interfere with the sense of smell and cause obstruction. They are easily visible on exam and must all be removed, since they can undergo neoplastic degeneration . Like warts elsewhere, they often recur.

• 21.

  What is a nasopharyngeal carcinoma (lymphoepithelioma)?

  It is a sequela of Epstein-Barr virus (EBV) infection, rare in Europe but frequent in Southeast Asia, where it represents the third most common cancer. Tumor growth is often asymptomatic, and presentation is late, typically with cervical lymphadenopathy. Hence, the prognosis is poor, even though screening for anti-EBV antibodies may help detect early and treatable disease.

• 22.

  What does a nasal septal perforation look like?

  Like a hole in the septum. This can be demonstrated on inspection or by shining a light into one nostril and seeing it transilluminate both sides.

• 23.

  What are the common causes of a septal perforation?

  The traditional four are:

  • Traumatic: facial injury or self-induced lesions (nose picking/piercing).

  • Iatrogenic: prior septal surgery, nasogastric tube placement, or nasal intubation.

  • Inflammatory/malignant: often the sequela of untreated septal hematomas or abscesses.

  • Cocaine snorting: one of the most frequent causes today, often presenting with large and expanding perforations. Cocaine contains adulterants that may irritate the mucosa, plus has strong alpha-agonist effects (causing vasoconstriction and ischemia of the nasal cartilage).

• 24.

  What are the less-common causes of perforation?

  • Chemical irritants (chromic or sulfuric acid fumes, glass dust, mercurials, and phosphorous)

  • Infections (tuberculosis, syphilis, and, more rarely, leprosy)

  • Collagen vascular diseases (Wegener’s, midline granuloma, systemic lupus erythematosus, rheumatoid arthritis, mixed connective tissue disease, and progressive system sclerosis)

• 25.

  What are the nasal manifestations of a basilar skull fracture?

  In addition to the direct facial trauma, patients often show evidence of nasal fracture, such as periorbital ecchymoses, swelling/tenderness of the nasal bridge, and anterior epistaxis. There also may be cerebrospinal fluid (CSF) rhinorrhea (leakage of CSF through the fracture site). This is a risk factor for the development of meningitis and thus necessitates prompt surgical attention.

• 26.

  How do you recognize CSF rhinorrhea?

  By placing a drop of nasal secretions over a paper tissue. In CSF rhinorrhea, this will serve as a “poor man’s” paper chromatography, showing a clear halo around “nasal” secretions that represent instead spinal fluid leakage. Alternatively, the glucose content of secretions may be measured at the bedside by using a Chemstrip. In patients with CSF rhinorrhea, this will reveal a high glucose concentration, close to spinal fluid levels of 40–80 mg/dL.

• 27.

  What results in swelling of the nasal mucosa?

  One of three causes:

  • Viral: nasal and oropharyngeal infections by either rhinoviruses or adenoviruses.

  • Atopic: pollen or dander exposure causing nasal congestion, allergic (serous) conjunctivitis, and sneezing.

  • Vasomotor: response to a specific inhalant, characterized by boggy edema of the mucosa and marked tearing. Inhalants may either be noxious to all (such as tear gas) or only to some. For example, perfumes may elicit an idiosyncratic response in a few predisposed individuals, causing pronounced swelling of the nasal mucosa.

• 28.

  Can you diagnose the cause of gastrointestinal (GI) bleeding by peeking into the patient’s nose?

  Yes, bleeding in the gut may indeed be linked to the nose. The most common reason is simple epistaxis , wherein patients swallow nasal blood, resulting in guaiac-positive stools and even melena. More rare are the multiple nasal telangiectasias of Osler-Weber-Rendu syndrome, an autosomal dominant disorder characterized by multiple (and often bleeding) vascular lesions of the gut, mouth, face, extremities, and chest. The tongue and lips also may have telangiectasias.

• 29.

  Who was Rendu?

  Henry J.L. Rendu (1844–1902) was the grandson of a distinguished Parisian painter and the son of an agricultural inspector. An art lover, he was so fascinated by his father’s profession as to pursue a medical career only after a stint in agriculture, geology, and botany. Still, he never lost his passion for plants and eagerly maintained it as a lifelong hobby. At age 43, he finally joined the staff of the Necker Hospital in Paris (the same one where Laënnec had been chief of chest medicine), rapidly gaining fame as a charismatic lecturer and gifted clinician.

• 30.

  Who was Weber?

  Frederick P. Weber (1863–1962) was a British physician, already encountered in the ear chapter because of Sturge-Weber disease. Educated in Cambridge, Vienna, and Paris, Weber cultivated throughout his life an interest in medical philosophy, the arts, and numismatics, which he then expressed in many books and articles. His father was Herman D. Weber (1823–1918), himself a famous and long-lived physician (he is the same Weber who described the midbrain syndrome that still carries his name). Weber père was a charming man with many interests, who taught himself English so that he could read Shakespeare and befriend, among others, Addison, Carlyle and several Waterloo veterans (including the famous Sir Peregrine Maitland of Wellington’s cry: “Now it’s your time, Maitland, now it’s your time!”). Increasingly fascinated by England, Weber senior eventually moved there in 1854, married an Englishwoman, and became a member of the Royal College of Physicians. Both father and son were avid climbers and advocates of physical exercise as key to long and productive lives (which served them well, since both lived well into their 90s). The older Weber climbed several mountains in the Italian Alps (including one for his 80th birthday) and walked 40–50 miles/week.

• 31.

  Who was Osler?

  Sir William Osler (1849–1919) is such a legend that a few lines in this chapter will do him a disservice. Born in the backwoods of Canada as son of a missionary, Osler was so spiritual that early in life he even considered joining the clergy. A charming and compassionate man with a prankish twist, he was a charismatic teacher, a superb bedside diagnostician, and a good person who never lost his respect for patients as fellow humans in need of help. After teaching in Canada and the United States, he moved to England, where he became Regius Professor of Medicine at Oxford. The last part of his life was unfortunately quite sad, tormented by the memory of his only son, who had died in Flanders toward the end of World War I.

• 32.

  What is anosmia?

  It is the congenital or acquired absence of smell (from the Greek an , lack of, and osme , smell).

  • Acquired anosmia may result from a long list of disease processes, affecting either the central nervous system or nose. Among them are multiple sclerosis, Parkinson’s disease, diabetes mellitus, pernicious anemia, liver cirrhosis, chronic renal insufficiency, Cushing’s syndrome, cystic fibrosis, sarcoidosis, allergic rhinitis, nasal polyposis, and zinc deficiency. Still, sequelae of a viral infection are often the most common reasons for acquired reversible anosmia, and has been recognized as a common symptom in COVID-19 patients.

  • Congenital anosmia is almost always caused by Kallmann’s syndrome. Described by the German psychiatrist Franz J. Kallmann (1897–1965), this consists of familial hypogonadotropic hypogonadism with or without anosmia (usually characterized by congenital absence of olfactory lobes). Kallmann’s is inherited through sex-linked recessive or autosomal transmission, with expression mostly in males. It can be treated with gonadotropins.

• 33.

  Do smell and taste interact?

  Yes. Patients whose olfaction is weakened or absent (hyposmia or anosmia) can only taste the five fundamental sensations of sweet, sour, bitter, salty, and umami (i.e., the taste of glutamate). This is because flavor results from oral combination of the five basic tastes plus the foodstuff’s odor and various chemical characteristics, such as texture, temperature, and other sensations. Hence, flavor is typically absent when olfaction is also absent. Overall, smell disorders are more common than isolated taste disorders (such as hypogeusia and ageusia ). Perversion of taste can also occur, with misreadings and distortions, such as foul tastes from otherwise pleasant substances.

• 34.

  Is perception of alcohol odor an indication that the sense of smell is intact?

  No. Alcohol is an irritant . Hence, it stimulates the trigeminal rather than the olfactory endings of the nasal mucosa. That is why even patients without olfactory lobes (such as those with Kallmann’s syndrome) can “feel” an alcohol sponge. Same is true for other irritants, such as ammonia and pepper. To test the sense of smell, you should use nonirritating substances with strong odors. Coffee and spices (such as cinnamon, cloves, and nutmeg) are excellent choices.