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2 Nose, Nasal Sinuses, and Face

2.1 Applied Anatomy and Physiology

2.1.1 Basic Anatomy

2.1.1.1 External Nose

The supporting structure of the nose consists of bone, cartilage, and connective tissue. ▶ Fig. 2.1 shows the most important elements. The bony superior part of the nasal pyramid is often broken in typical fractures of the nasal bones, but it may also be fractured in injuries to the central part of the face. The cartilaginous inferior portion is less at risk, at least in mild blunt trauma, because of its elastic structure, but it is endangered in stab wounds, lacerations, and gunshot injuries. The shape, position, and properties of the bone and cartilage of the nose have a considerable influence on the shape and esthetic harmony of the face (see ▶ p. 236) and on the function of the nasal cavity.

The following blood vessels in the external nose are of practical importance:

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  Facial artery and its branches

  
  
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  Dorsal nasal artery, arising from the ophthalmic artery

Profuse hemorrhage can arise from these vessels when the central part of the face is injured.

The angular vein is also clinically important. Thrombophlebitis arising from a furuncle of the upper lip or the nose can spread via the ophthalmic vein to the cavernous sinus, causing a cavernous sinus thrombosis (see ▶ p. 210 and ▶ Fig. 2.2).

The external nose derives its sensory nerve supply from the first and second branches of the trigeminal nerve. The muscles derive their motor nerve supply from the facial nerve.

2.1.1.2 Nasal Cavity

The interior of the nose is divided by the nasal septum into two cavities, which are usually unequal in size. Each side may be divided into the nasal vestibule and the nasal cavity proper ( ▶ Fig. 2.3). The nasal vestibule is covered by epidermis containing hairs (vibrissae) and sebaceous glands. The latter are the site of origin of a nasal furuncle, which can thus only develop in the nasal cavity in the vestibule.

The medial wall of the nasal vestibule encloses the supporting structure of the anterior part of the cartilaginous septum and the membranous septum (i.e., the columella.) The roof of the vestibule is formed by the bird wing–shaped lower lateral or alar cartilage, the medial crus of which extends into the columella and the lateral crus of which supports the external wall of the vestibule ( ▶ Fig. 2.1 and ▶ Fig. 2.3). The alar cartilage determines the shape of the nasal tip and the nasal apertures. Correcting this area is often an important part of rhinoplasty.

The internal nasal valve or limen nasi is a very important structure from the physiologic point of view. It lies at the junction of the vestibule and the nasal cavity. It is formed by a prominence of the anterior edge of the upper lateral or triangular cartilage on the lateral wall of the nose ( ▶ Fig. 2.3a). The internal nasal valve is normally the narrowest point in the entire cross-section of the nasal cavity, making it an important factor in nasal respiration (see ▶ p. 152).

The nasal cavity extends from the internal nasal valve to the choana. The structure of the floor and roof of the nose, the medial wall, and the nasal septum are shown in ▶ Fig. 2.3.

The outline of the lateral wall of the nasal cavity is more complex than that of the medial wall. It contains several structures that are important in the functioning of the nose and nasal cavity ( ▶ Fig. 2.4):

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  Three nasal turbinates (superior, middle, and inferior).

  
  
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  Drainage of the paranasal sinuses (frontal sinus and maxillary sinus through the hiatus semilunaris in the middle meatus, located between the inferior and middle turbinate; the sphenoid sinus has an ostium of its own in the sphenoethmoidal recess).

  
  
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  Opening of the nasolacrimal duct into the inferior meatus.

The superior, middle, and inferior meatus are located inferior to the three turbinates ( ▶ Fig. 2.4); the paranasal sinuses and the nasolacrimal duct open into them. These openings are of diagnostic and therapeutic importance.

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  The inferior meatus, located between the floor of the nose and the insertion of the lower turbinate, lacks a sinus ostium, but contains the opening of the nasolacrimal duct ≈3 cm posterior to the external nasal opening and 3 mm posterior to the head of the inferior turbinate ( ▶ Fig. 2.4).

  
  
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  The middle meatus, between the inferior and middle turbinate, is of clinical importance because the frontal recess, the anterior ethmoid cells, and the maxillary antrum open into it ( ▶ Fig. 2.4).

  
  
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  The superior meatus, between the middle and superior turbinate, contains the opening for the posterior ethmoid cells. The sphenoid ostium is located on the anterior wall of the sphenoid sinus, at the level of the superior meatus ( ▶ Fig. 2.4).

The nasal cavity is lined by two types of epithelium: respiratory and olfactory ( ▶ Fig. 2.5 and ▶ Fig. 2.6). Respiratory epithelium coats the entire airway and its projections and extensions (e.g., the paranasal sinuses and the middle ear), from the nasal introitus to the bronchi. It shows morphologic variation in different parts of the respiratory tract. ▶ Fig. 2.5c, d shows the structure of the respiratory epithelium of the nasal cavity. The epithelium is columnar-ciliated with goblet cells and a layer of mixed glands, a fairly well-demarcated lymphoid cell zone and well-developed venous cavernous spaces in the turbinates and around the ostia ( ▶ Fig. 2.5a).

The olfactory mucosa, innervated by fibers of the olfactory nerve, covers the area of the olfactory cleft, the cribriform plate, part of the superior turbinate, and the part of the septum lying opposite it. The structure is shown in ▶ Fig. 2.5d, and its topographic extent in ▶ Fig. 2.5c. Bowman glands occur specifically in this area. They produce a lipo-lipid secretion that covers the olfactory region and aids in olfactory perception due to the enzymes it contains. It is entirely dissimilar to the secretion of the glands of the respiratory epithelium.

2.1.1.3 Paranasal Sinuses

The paranasal sinuses are pneumatized cavities in the bone adjacent to the nose ( ▶ Fig. 2.7).

Sinus Embryology and Development

Unlike all the other nasal sinuses, the ethmoid labyrinth is fully formed at birth. It is derived from an embryonic paired anlage that coalesces in the first year of life to form a single ethmoid cell.

Before the second dentition erupts—i.e., until about the seventh year of life—the maxillary sinuses are usually very small, since the maxilla contains the tooth buds of the second dentition. The maxillary sinus does not develop its final form and size until after the second dentition appears.

The frontal sinuses form after birth and are not completely developed until the second decade of life.

The sphenoid sinus does not begin to develop until the age of 5 years.

Ostiomeatal Complex

The ostiomeatal complex is a functional entity in the anterior ethmoid complex that represents the final common pathway for drainage and ventilation of the frontal, maxillary, and anterior ethmoid cells (see ▶ Fig. 2.9). Any or all cells, clefts, and ostia, as well as their dependent sinuses, can become diseased, contributing to the symptoms and pathophysiology of sinusitis.

Ethmoidal Labyrinth

The central structure in this system of pneumatized cavities is the ethmoid bone. The anterior ethmoid is the morphologic connection and secretion channel between the nose and the frontal and maxillary sinuses. The tight spaces and clefts normally ensure ventilation and drainage of the sinus mucosa. The anterior ethmoid is central to the pathogenesis of acute, recurrent, and chronic inflammations of the frontal and maxillary sinuses, since ≈90% of all diseases of the frontal and maxillary sinuses begin here.

The central part of the ethmoid bone is T-shaped. In the median plane, the crista galli projects into the anterior fossa ( ▶ Fig. 2.8). The falx cerebri inserts here. The perpendicular plate (lamina perpendicularis) abuts anteriorly onto the septal cartilage and dorsally onto the vomer. The paired ethmoidal labyrinth is situated between the nose and orbit. It consists of 10 to 15 pneumatized cells lined with respiratory epithelium. The volume varies between individuals; roughly, it is the size of a small matchbox standing on its short side.

The lamina cribrosa passes into the ethmoidal notch (incisura ethmoidalis) of the frontal bone. The olfactory nerves extend from the olfactory rim to the olfactory bulb.

The ethmoid air cells are differentiated into anterior and posterior groups. There are often also common ostia for the anterior ethmoid complex in the middle meatus and for the posterior ethmoid complex in the superior meatus (see ▶ Fig. 2.4).

Superiorly, it is related to the anterior part of the base of the skull and is an avenue of spread for rhinogenous intracranial infections. The cranial closure of the ethmoidal labyrinth is formed by frontal bone.

Laterally, the lamina papyracea separates the ethmoid cells from the orbital cavity and is a pathway of spread for orbital complications. It is very thin in children.

Posteriorly, the ethmoid labyrinth is related to the sphenoid sinus. The posterior closure of the ethmoid labyrinth is formed by the sphenoid bone. The optic nerve often runs very close to the posterior ethmoid cells, or even within them. This may explain some cases of retrobulbar neuritis.

Medially, the ethmoid labyrinth is related to the middle and superior turbinates.

Maxillary Sinus

The maxillary sinus is the largest sinus, with an average volume of 15 mL. The paired sinuses often develop asymmetrically, and the resulting differences in the thickness of the bony wall may give rise to incorrect radiologic diagnoses. The sinus usually consists of a single chamber, but it may have recesses and may even contain separate loculi. This can give rise to difficulties in diagnosis and treatment.

The ostium of the maxillary sinus occupies the superior part of the medial wall of the sinus; it opens not directly into the nose, but sagittally into a three-dimensional space, the ethmoidal infundibulum. The infundibulum opens into the nose in the hiatus semilunaris in the middle meatus ( ▶ Fig. 2.9).

The superior or orbital wall of the maxillary sinus also forms the floor of the orbit. The infraorbital nerve passes through it.

The medial wall is also the lateral wall of the nasal cavity. The anterior wall contains the infraorbital foramen.

The posterior wall separates the sinus from the pterygopalatine fossa. The maxillary artery, the pterygopalatine ganglion, and branches of the trigeminal nerve and autonomic nervous system lie within the pterygomaxillary fossa (see ▶ Fig. 2.11).

The floor of the maxillary sinus is related to the dental roots in the alveolus, particularly those of the second premolar and the first molar. Odontogenic sinusitis can originate from this site.

Frontal Sinus

The frontal sinus varies in shape and extent more than the maxillary sinus. The average frontal sinus has a capacity of 4 to 7 mL. There is often a considerable difference in size between the right and left cavities in the same person. The frontal sinuses may be completely absent on one or both sides in 3 to 5% of individuals, but they may also be very extensive and contain loculi. The latter favor the development of inflammatory complications. In the drainage system of the frontal sinus, the frontal infundibulum merges into the frontal recess (ethmoidal bone) at the hiatus semilunaris in the middle meatus.

A bony septum separates the two sinuses. The floor of the frontal sinus forms part of the roof of the orbit and is a pathway for the spread of inflammatory orbital complications. The canal of the supraorbital nerve traverses the floor of the frontal sinus.

The posterior wall of the frontal sinus forms part of the bony anterior cranial fossa, making it a typical pathway for the spread of rhinogenous intracranial complications due to either frontonasal injury or as a complication of sinusitis (see ▶ p. 209).

Sphenoid Sinus

The sphenoid is the most posterior of the sinuses. It occupies the skull base at the junction of the anterior and middle cranial fossae in the body of the sphenoid bone. There are marked individual variations in shape and size, and the capacity of the sinus is 0.5 to 3.0 mL. The sphenoid sinus may be entirely absent in 3 to 5% of individuals. The ostium of the sphenoid sinus lies on the anterior wall of the body of the sphenoid bone in the sphenoethmoidal recess, behind and somewhat above the superior turbinate (see ▶ Fig. 2.4).

The superior wall of the sphenoid sinus is related to the anterior and middle cranial fossae and is a pathway of spread for rhinogenous intracranial complications. The optic chiasm and optic foramen are closely related. The sella turcica and pituitary gland lie on the roof of the sphenoid sinus, which can therefore be used for surgical access to the pituitary.

On the lateral wall of the sphenoid sinus lie the cavernous sinus, the internal carotid artery, and the second, third, fourth, fifth, and sixth cranial nerves. The optic canal may lie freely in the lateral wall of the sphenoid sinus, as may the internal carotid artery and the third and sixth cranial nerves.

The floor of the sphenoid sinus is related to the roof of the nasopharynx and the choana (see ▶ Fig. 2.4).

Mucosa of the Paranasal Sinuses

The mucosa of the paranasal sinuses (see ▶ Fig. 2.13) consists of respiratory epithelium. Goblet cells and seromucous glands produce a secretion forming a two-layered film on the mucosa surface.

The lining of the paranasal sinuses is simpler than that of the nasal cavity. Cavernous erectile tissue may be found in the mucosa around the ostia, and this can affect the patency of the ostia (see ▶ p. 135). This variability in the opening of the ostia is supplemented by simultaneous variations in the volume of the neighboring turbinates (see ▶ Fig. 2.5a). Functionally, they form the ostiomeatal unit.

Blood Supply

The blood supply to the nasal cavity and nasal sinuses is provided by both the internal and external carotid arteries and their accompanying veins. ▶ Fig. 2.10 shows the blood supply of the medial nasal wall. ▶ Fig. 2.95 shows the origin of the blood supply to the lateral nasal wall.

The external carotid artery supplies the nose internally via the internal maxillary artery and externally via the facial artery. The sphenopalatine artery (SPA) is an important branch of the internal maxillary artery.

The internal carotid artery gives rise to the ophthalmic artery, and from there to the anterior and posterior ethmoidal arteries.

There is a particularly rich and relatively superficial plexus of small vessels (the Kiesselbach plexus) located on the anterior part of the nasal septum ( ▶ Fig. 2.9). It is supplied ultimately by both the internal and external carotid arteries.

Venous drainage is provided by the ophthalmic and facial veins and the pterygoid and pharyngeal plexuses. It is therefore located both partially intracranial to the cavernous, coronary, and transverse sinuses, and partially extracranial (see ▶ Fig. 2.2).

The cavernous spaces within the mucosa of the nasal turbinates are very important clinically, as are those on the nasal septum and around the ostia of the nasal sinuses. The filling of these spaces with venous blood is highly variable and is under autonomic control. By regulating the thickness of the mucosa, the cavernous spaces of the turbinates can change the cross-sectional areas of the nasal cavity and of the ostia of the nasal sinuses, thus controlling respiration, ventilation, and drainage (see ▶ Fig. 2.5a).

Lymphatic Drainage

The lymphatic drainage consists of two parts: an anterior system, which collects the lymph from the nasal pyramid and drains to the submandibular superficial cervical lymph nodes; and a posterior system, which drains the posterior part of the nasal cavity and the nasopharynx to the retropharyngeal lymph nodes and jugular nodes.

Nerve Supply

The nasal cavity and nasal sinuses have a sensory and autonomic (secretory and vasomotor) nerve supply. In addition, they include the special sensory function of the olfactory nerve.

The sensory nerve supply is provided by the first and second branches of the trigeminal nerve. The complex autonomic innervation for secretion and vasomotor supply is shown in ▶ Fig. 2.11.

Autonomic innervation: The sympathetic fibers for vasoconstriction arise from the first to the fifth thoracic segments of the spinal cord, and synapse in the superior cervical ganglion. The postganglionic fibers follow the blood vessels to the mucosa of the nose and nasal sinuses. Some fibers run through the pterygopalatine ganglion without synapsing.

The pathway for the parasympathetic fibers for vasodilation is from the lacrimomuconasal nucleus along the intermediate nerve to the geniculate ganglion and then along the facial nerve, the greater superficial petrosal nerve, and the nerve of the pterygoid canal to the pterygopalatine ganglion.

The preganglionic parasympathetic fibers synapse in the pterygopalatine ganglion. From there, they supply the mucosa of the nose and nasal sinuses with secretory and vasodilator fibers.

The pterygopalatine or sphenopalatine ganglion plays a key role in the functioning of the nose and nasal sinuses. It is the main site of its autonomic innervation and has three roots:

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   Parasympathetic fibers, which supplement secretory and vasodilator functions.

   
   
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   Sympathetic fibers for vasoconstriction and inhibition of secretion.

   
   
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   Sensory fibers from the trigeminal nerve, which arise in the trigeminal ganglion and run in the maxillary nerve.

The nose and maxillary sinus are closely related both anatomically and functionally to the maxilla. This bone forms the upper half of the masticatory system and also forms the main part of the middle-third of the facial skeleton. The upper jaw is important in diseases of the nose, due to its immediate relationship to the nose and nasal sinuses.

2.1.2 Basic Physiology and Pathophysiology

The nose is both a sensory organ and a respiratory organ. In addition, the nose performs an important function for the entire body by providing both physical and immunologic protection from the environment. Finally, it is also involved in the formation of speech sounds. The nose is also a major esthetic unit in the center of the face. It balances and unites the other esthetic units, paired and unpaired, such as brows, cheeks, forehead, and lips.

2.1.2.1 The Nose as an Olfactory Organ

The human sense of smell is poorly developed in comparison with that of most mammals and insects. Nevertheless, it is still very sensitive and almost indispensable for the individual. For example, taste is only partly a function of the taste buds, which can only recognize the qualities of sweet, sour, salty, and bitter. All other sensory impressions caused by food, such as aroma or bouquet, are mediated by olfaction. This gustatory olfaction is due to the fact that the olfactory substances of food or drink pass through the olfactory cleft during expiration while eating or drinking. The sense of smell can stimulate appetite but can also depress it. It also provides a warning against spoiled or poisonous foods and toxic substances (e.g., gas). The sense of smell is particularly important in the field of psychology; marked affects may be induced or inhibited by smells. It should also be remembered that a good sense of smell is essential for people in certain occupations (e.g., cooks and confectioners; wine, coffee, and tea merchants; perfumers; tobacco blenders; and chemists). Finally, physicians need a “clinical nose” for making diagnoses.

The olfactory area of the nose is relatively small, at ≈2 to 5 cm². The cell bodies of the olfactory cells are located in the olfactory epithelium covering the superior nasal passage, the cranial nasal septum, and the middle turbinate (see ▶ Fig. 2.5c). The olfactory cells are primary sensory cells that project directly into the olfactory bulb. Their axons are bundled into the olfactory filaments, which pass through the cribriform plate to the olfactory bulb. Between a hundred and a thousand axons together reach each mitral cell. Glutamate is the neurotransmitter between the sensory cells and mitral cells and the messenger of the mitral cells. Other neurotransmitters are γ-aminobutyric acid and dopamine. Important ganglia for further processing within the central nervous system are located in the hippocampus and amygdala, which are responsible for processing emotions and memory content. Finally, conscious olfactory perception occurs at the level of the cortex (superior temporal gyrus, orbitofrontal cortex, insula region).

The olfactory epithelium can regenerate within 100 days, which is unique for sensory organs.

During olfaction, scents first dock onto the olfactory-binding protein in the olfactory region. In this way, they reach the scent receptors located on the bipolar olfactory receptor neurons. The receptors are located within the membrane, where they bind to a specific olfactory G protein (second messenger; cyclic adenosine monophosphate).

Richard Axel and Linda Buck were the first to examine the sense of smell at the molecular level. They discovered that every olfactory cell is specialized for only a single class of scent and is equipped with only one type of receptor. Human beings have 350 types of receptor. One receptor can recognize up to a hundred molecules with structural similarities. Scent molecules have to fit into a receptor like a key into a lock. Docking of a molecule activates a chemical cascade. The scent is transformed into an electrical signal, which is transmitted to a scent center in the brain. The two scientists were awarded the Nobel Prize in 2005 for this discovery.

Only volatile substances can be smelled by humans. These substances have to be soluble in water and lipids. Only a few molecules can be sufficient to stimulate the sense of smell. On average, 10⁻¹⁵ molecules per milliliter of air are enough to exceed the stimulation threshold.

It is said that there are ≈30,000 different olfactory substances in the atmosphere; of these, humans can perceive ≈10,000 and are able to identify ≈200.

The sense of smell, like other senses, demonstrates the phenomenon of adaptation. The sensitivity of the olfactory organ is also dependent on hunger. A very hungry individual can perceive several olfactory stimuli better than one who has just eaten, and this is a useful physiologic regulating mechanism.

Olfactory Disorders ( ▶ Table 2.1 )

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  Disorders of the sense of smell have an increasing incidence.

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Table 2.1 Disorders of olfaction—dysosmias

  Quantitative disorders	Hyperosmia—oversensitivity
  	Normosmia—normal sensitivity
  	Hyposmia—reduced sensitivity
  	Anosmia—complete inability to perceive scents
  Qualitative disorders	Parosmia—altered perception of scents in the presence of a stimulus
  	Phantosmia—perception of scent in the absence of a stimulus
  	Anosmia—inability to identify perceived scents

  
  
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  They can be a symptom of nasal disorders or a key symptom of other general diseases.

  
  
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  A functional and differential diagnosis is required in every case.

  
  
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  What makes it more difficult is that the desire to seek is very different from one to the next.

  
  
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  While French perfumers can smell around 3500 nuances, ordinary people sometimes have problems with eight qualities in the smell test.

Causes and Classification of Olfactory Loss

Olfactory dysfunction secondary to sinonasal disease: These are the most common disorders encountered in otolaryngology. Inflammatory or noninflammatory changes impede the transportation of scents to the olfactory cleft or damage the olfactory epithelium directly.

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  Infectious causes: chronic recurrent rhinosinusitis.

  
  
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  Noninfectious causes: allergies, polyposis, hyperplastic rhinosinusitis, postirritative and toxic, postinfectious, rhinitis sicca.

  
  
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  Noninflammatory causes: anatomic (malignant and benign tumors, stenoses, choanal atresia, adhesions, septum deviations) or nasal congestion, nerve reflexes, idiopathic rhinitis (formerly called nasal hyperreactivity), side effects of drugs.

  
  
  
  

  
  

  Note: Esthesioneuroblastoma (olfactory neuroblastoma) is a highly malignant lesion and the most serious tumor that can affect the olfactory epithelium. It needs to be considered in every patient with an olfactory disorder.

Olfactory dysfunction not associated with sinonasal disease: Viral infections can lead to primary damage to the olfactory cells. Typically, patients experience a subjective loss of the sense of smell immediately after an infectious disease.

A clear example of this is infection by the recent coronavirus SARSCoV-2 leading to COVID-19. Patients report acute onset of complete loss of smell and taste, which recovers in most cases. While taste would be expected to decrease with anosmia, it is likely in COVID-19 that taste is also affected directly by viral damage to taste receptors.

Neurologic, congenital, toxic, and psychiatric conditions may involve olfactory disorders, as well as head injuries. Dysosmias may be an initial symptom of Alzheimer disease, preceding the loss of cognition and abnormal behavior. In Parkinson disease, olfactory disorders often occur before movement disorders. Noxious substances such as carbon dioxide, formaldehyde, or tobacco smoke can directly damage the olfactory cells. Congenital dysosmias (e.g., Kallmann syndrome) are rare.

A large body of clinical evidence suggests that olfactory disorders are associated with certain neurological and psychiatric diseases ( ▶ Table 2.2 ), and as such may be associated with pronounced emotional changes. One of the most common findings is temporal lobe epilepsy, which is associated with an olfactory aura. Olfactory hallucinations are usually unpleasant and lead to corresponding emotional effects, frequently with feelings of “déjà vu,” which in turn elicit motor and sensory phenomena.

An olfactory disorder is regarded as idiopathic if all other causes have been ruled out.

Pheromones and the Vomeronasal Organ

A pheromone is a chemical that when produced by a species evokes a specific reaction in the same species or, in some cases, a different species such as a predator. These pheromone chemicals induce set patterns of social and mating behavior that are generally important for survival.

The vomeronasal organ (VNO or Jacobson organ) is considered to be a pheromone receptor that is part of an accessory olfactory system with separate central connections. The VNO is described as a small, bilateral structure with blind channels located low in the nasal chambers of most mammals, reptiles, and amphibians. In mammals it is normally located on the nasal septum, but the structure is vestigial in humans. The place and function of pheromones in humans is highly controversial.

2.1.2.2 The Nose as a Respiratory Organ

In humans, the only physiologic respiratory pathway is via the nose. Mouth breathing is abnormal and is activated only as an emergency supplement to nasal respiration. The physiology of the airstream through the normal nose during inspiration and expiration can be summarized as follows. Average ventilation through a normal nose is 6 L/min during normal breathing, and 50 to 70 L/min during maximum ventilation. The internal nasal valve or limen nasi is the narrowest point in the normal nose. It acts as a nozzle, and the speed of the airstream is very high at this point ( ▶ Fig. 2.12a, b).

The nasal cavity between the valve and the head of the turbinates acts as a diffuser (i.e., it slows the air current and increases turbulence). The central part of the nasal cavity, with its turbinates and meatus, is the most important part for nasal respiration. The column of air consists of a laminar and a turbulent stream. The ratio of laminar to turbulent flow considerably influences the functioning and condition of the nasal mucosa.

The airstream passes in the reverse direction through the nasal cavities during expiration. The expiratory airstream shows much less turbulence in the central part of the nose, reducing the exchange of heat and products of metabolism between the airstream and the nasal wall in comparison with inspiration and enabling the nasal mucosa to recover during the expiratory phase. Inspiration through the nose followed by expiration through the mouth causes the nasal mucosa to dry out rapidly.

Nasal resistance (i.e., the difference in pressure between the nasal introitus and the nasopharynx) is normally between 8 and 20 mm H₂O. If resistance exceeds 20 mm H₂O, the internal nasal valves expand during breathing. Supplemental mouth breathing begins at levels exceeding 40 mm H₂O.

Complete exclusion of the nose from breathing leads in the long-term to deep-seated mucosal changes. Mechanical obstruction within the nose (e.g., due to septal deviation, hypertrophy of the turbinates, stenoses from scarring, etc.) can lead to mouth breathing and the resulting deleterious effects, as well as causing mucosal diseases of the nose and the paranasal sinuses.

Computational fluid dynamics (CFD)—simulation of nasal airflow: CFD is the most recent digital method for fluid examination. It can be used to analyze airflow phenomena in the nose ( ▶ Fig. 2.12a, b). It provides data on the important value of integral pressure loss, as well as extensive information about flow, involving velocity vectors, pressure, and turbulences with high resolution, providing detailed information about the fluid flow.

CFD requires five working steps:

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   Creating a geometric model (computed tomography).

   
   
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   Generating a computational grid.

   
   
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   Preprocessing (physical modeling).

   
   
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   Executing calculations (mathematical modeling, equation solving).

   
   
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   Postprocessing (graphic and quantitative analysis of results).

In the future, CFD may become an important tool for testing and designing prototypes for the shape of the nasal airway before surgical correction.

Nasal patency: Nasal patency can be influenced by many different factors, including the temperature and humidity of the surrounding air; the position of the body; physical activity; changes in body temperature; the effect of cold on different parts of the body, such as the feet; hyperventilation; and psychological stimuli. The state of pulmonary function and of the heart and circulation, endocrinologic conditions such as pregnancy, hyperfunctioning or hypofunctioning of the thyroid gland, and some topical, oral, or parenteral drugs may have a considerable influence on the patency of the nose. Methods of measuring nasal patency are described on ▶ p. 152.

During normal nasal respiration, the inspired air is warmed, moistened, and purified as it passes through the nose.

The warming of air inspired through the nose is very effective, and the constancy of the temperature in the lower airways is remarkably stable. The nasal mucosa humidifies and warms the air. The temperature in the nasopharynx during normal (exclusively nasal) respiration is constant at 31 to 34 °C, independently of the external temperature. The heat output of the nose increases as the external temperature falls, so that the lower airways and lungs can function at the correct physiologic temperature.

The optimal relative humidity of ambient air for subjective well-being and function of the nasal mucosa lies between 50% and 60%. The water vapor saturation of inspired air in the nasopharynx is 80% to 85%, and in the lower airway it is fairly constant at between 95% and 100%, independent of the relative humidity of the surrounding air. The amount of water vapor secreted by the entire respiratory tract per 1,000 L of air can reach 30 g, most of it supplied by the nose. However, the mucous blanket provides a barrier that prevents the release of too much water into the air and consequent drying of the mucosa.

The cleansing function of the nose includes firstly, clearing the inspired air of foreign bodies, bacteria, dust, etc., and secondly, cleansing the nose itself (see below). About 85% of particles larger than 4.5 μm are filtered out by the nose, but only ≈5% of particles less than 1 μm in size are removed.

Foreign bodies entering the nose come into contact with the moist mucosal surface and the mucous blanket, which continually sweeps foreign bodies away. The details are described in the next section.

2.1.2.3 The Nasal Mucosa as a Protective Organ

In addition to warming, humidifying, and cleansing the inspired air, the nose also has a protective function, consisting of a highly differentiated, efficient, and polyvalent resistance potential against environmental influences on the body. A basic element of this defensive system is the mucociliary apparatus ( ▶ Fig. 2.13) (i.e., the functional combination of the secretory film and the cilia of the respiratory epithelium), by which the colloidal secretory film is transported continuously from the nasal introitus toward the choana. A foreign body is carried from the head of the inferior turbinate to the choana in ≈10 to 20 min. The efficiency of this cleansing system depends on several factors, such as pH, temperature, the condition of the colloids, humidity, the width of the nose, or the presence of toxic gases. Disturbances in the composition or physical characteristics of the mucous blanket or of ciliary activity can markedly influence the physiology of the nasal cavity. The nasal mucosa protects the entire body by making contact with and providing resistance against animate and inanimate foreign material in the environment.

Local specific immune defense of the nasal mucosa is ensured by humoral and cellular mechanisms (antibodies and immunologically competent cells).

Humoral defense mechanisms: Paraglandular plasma cells produce antibodies—immunoglobulin A(IgA), IgM, and IgG. The glands of the lamina propria absorb the immunoglobulins (IgA) and then release them as secretory antibodies (sIgA) at the epithelial surface.

Cellular defense mechanisms: The main forces of cellular defense are neutrophilic, basophilic, and eosinophilic granulocytes, macrophages, mast cells, and T and B lymphocytes. B lymphocytes are able to differentiate into plasma cells, which can secrete immunoglobulins. Neutrophils are increased in chronic rhinosinusitis (CRS), eosinophils predominate in CRS with polyposis, and degranulating mast cells and basophils are important in type I allergic reactions. Intercellular adhesion molecule-1 (ICAM-1) is expressed by the epithelium of the nasal mucosa; it serves as a receptor for viruses (rhinoviruses). Cells of the vascular endothelium are stimulated by inflammation mediators such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) to express adhesion molecules that ensure diapedesis by immunologically competent cells.

2.1.2.4 The Nose as a Reflex Organ

Specific nasal reflex mechanisms can arise:

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  Within the nose and affecting the nose itself.

  
  
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  In other parts of the body or organs and affecting the nose.

  
  
• 
  

  In the nose and affecting other parts of the body.

The nasal cycle is a reflex system that is obviously confined to the nose, but its purpose is unknown. One cycle lasts between 2 and 6 hours. If both halves of the nasal cavity are of normal patency, the lumen widens and narrows alternately, lowering or increasing respiratory resistance in each half of the nose. Ideally, the resistance of the entire nose remains constant. This reflex phenomenon is controlled by the action of the autonomic nervous system on the cavernous spaces of the vascular system of the nasal mucosa.

Nasopetal reflexes arise in situations such as cooling of the extremities, which changes the respiratory resistance. They may also arise from the lungs and bronchi and from other autonomic control points.

Important nasofugal communications exist between the nose and the lung, the heart and circulation, the metabolic organs, and the genitals.

In addition, there are sneezing, lacrimal, and cough reflexes, and in certain emergency situations, reflexive respiratory arrest.

2.1.2.5 Influence of the Nose on Speech

The nose influences the sound of speech. During the formation of the resonants “m,” “n,” and “ng,” for example, the air streams through the open nose, whereas during the formation of vowels the nose and nasopharynx are more or less closed off by the soft palate from the resonating cavity of the mouth.

2.1.2.6 Function of the Nasal Sinuses

The function of the paranasal sinuses is one of the oldest and most fascinating controversies in medicine. Many theories have been proposed, e.g., that they serve to reduce the weight of the facial skull, provide resonation spaces for the voice, absorb facial trauma forces, moisturize and warm inspired air, provide olfactory function and thermic insulation, are functionless hollows, or provide a source of secretions for the main nasal cavity.

In an experimental study, one important question was answered in 1990. The mucosa of the paranasal sinuses plays a role in secretion production and control of the nasal mucosa. In other words, when the human organism needs higher humidity to moisten the incoming air, such as during sports activity, the sinuses increase secretion and convection through the ostium to the lateral wall mucosa.

The presence of the ostia causes particular pathophysiologic problems affecting ventilation and drainage. Ostial obstruction interrupts the self-cleansing mechanism of the affected sinus, causing the secretions to stagnate and change in composition. The retained secretions are an ideal medium for saprophytic bacteria, which are often present in normal sinuses. Ostial obstruction can lead to a vicious circle, as illustrated in ▶ Fig. 2.14.

The main cause of closure of the ostium is rhinogenous swelling due to a reaction or infection in the nasal mucosa. Ninety percent of all sinusitis cases begin in the anterior ethmoid (ethmoidal infundibulum, facial recess, and middle meatus). The closure mechanism can be induced by viral or bacterial infection of the nose, barotrauma, hyperreactivity, environmental factors such as relative dryness of the nose, toxic gases, or airborne toxic agents. Other causes include localized congenital or acquired anomalies such as deviation of the septum, scars, lesions of the turbinates, infections of the nose or nasal cavities, allergic diseases of the nose or nasal sinuses (particularly in children), vasomotor dysfunction due to neurogenic or hormonal factors, metabolic diseases such as vitamin deficiencies, diabetes, electrolyte disorders, mechanical obstruction due to crusts, ethmoidal polyps, foreign bodies, prolonged use of a nasogastric tube or prolonged nasal tracheal intubation, and benign and malignant tumors.

The vicious circle of ostial occlusion can only be broken in the long-term by treating the causative factors with appropriate medical or surgical measures ( ▶ Fig. 2.14).

The nasal sinuses are only minimally involved in respiratory phases in the nasal cavity. Only slight changes in pressure are recorded in the sinuses during respiration. When the ostium is occluded, a relatively small drop in pressure in the sinuses (from –20 to –50 mm H₂O) occurs, which is enough to elicit the symptoms of what has been inappropriately termed vacuum sinusitis. The symptoms include moderately severe headaches, which disappear when ventilation of the sinus is restored.

2.2 Methods of Examining the Nose, Paranasal Sinuses, and Face

2.2.1 External Inspection and Palpation

During external examinations, attention is given to the following points:

• 
  

  The properties of the overlying skin (e.g., hardness, firmness, discolorations, inflammatory swellings, and tenderness to pressure).

  
  
• 
  

  Externally visible changes in shape of the cartilaginous or bony structure due to congenital or acquired deformities (e.g., saddle nose, hump nose, broad nose, or scoliotic nose; the early or late results of trauma; painful swelling due to inflammation; nonpainful swelling due to tumor).

  
  
• 
  

  Palpable masses in neighboring structures (e.g., the forehead, cheeks, upper lip, or eyelids; proptosis, displacement of the bulb or limitation of its movement).

  
  
• 
  

  The nasal alae during respiration, inspection for indrawing or flaring of the ala.

  
  
• 
  

  The nasal vestibule, the anterior border of the nasal septum, the roof of the vestibule, and the internal part of the nasal cavity, inspected by lifting the tip of the nose.

  
  
• 
  

  Crepitation and mobility of the nasal bony framework.

  
  
• 
  

  The sites of exit of the various nerves ( ▶ Fig. 2.15).

  
  
  
  

  Fig. 2.15 Clinically important nerve exit sites. (a) At the occiput: 1, lesser occipital nerve; 2, greater occipital nerve. (b) On the face: 3, supraorbital nerve; 4, infraorbital nerve; 5, mental nerve.

  
  

  

  
  
• 
  

  Sensitivity to pressure on the forehead, cranial vault, or cheek.

2.2.2 Anterior Rhinoscopy

Anterior rhinoscopy using a nasal speculum, a strong light source, and a head mirror or headlamp is only carried out after inspection without instruments ( ▶ Fig. 2.16). The method of using the nasal speculum is shown in ▶ Fig. 2.17. Usually, the left hand holds the speculum when inspecting both nasal cavities. Anterior rhinoscopy alone is now considered insufficient, but it is the first step in examining the nose.

Technique: The speculum is introduced into the nasal vestibule with its blades together. The point of the speculum is directed slightly laterally in the nasal vestibule.

The speculum blades are then spread within the nasal vestibule and fixed to the nasal ala with the index finger. The instrument is held slightly open when it is being removed, to prevent pain due to avulsion of vibrissae. The right hand is used to adjust the position of the face and head. As shown in ▶ Fig. 2.17a, the patient’s head is initially in the vertical position, so that the examiner’s gaze is parallel to the floor of the nose and along the inferior turbinate and the inferior meatus (position I). If the nasal cavity is wide, the choana and the posterior wall of the nasopharynx can be seen in this position. To allow inspection of the upper part of the nasal cavity, the patient’s head is tilted slightly backward. The middle meatus, which is very important clinically, and the middle turbinate are thus brought into view (position II) ( ▶ Fig. 2.17b). If the head is tilted far backward, the olfactory cleft may also be visible.

Small children and infants, it is advisable to use an otoscope rather than a nasal speculum for anterior rhinoscopy.

When the head position has been adjusted satisfactorily, the hand holding the speculum can be used simultaneously to fix the head, leaving the right hand free for manipulating instruments, performing aspirations, etc., within the nasal cavity.

The following are noted during anterior rhinoscopy:

• 
  

  Nasal secretions, their color, quantity, and properties; mucus, pus, and crust formation.

  
  
• 
  

  Location of abnormal secretion.

  
  
• 
  

  Swelling of the turbinates, narrowing or widening of the nasal meatus.

  
  
• 
  

  Properties of the mucosal surface (including its color—e.g., whether it is moist, dry, smooth, cornified, or uneven.

  
  
• 
  

  Position of the nasal septum and septal deformities.

  
  
• 
  

  Sites of major blood vessels (e.g., Kiesselbach plexus).

  
  
• 
  

  Abnormal pigmentation or color of the mucosa.

  
  
• 
  

  Presence of abnormal tissue.

  
  
• 
  

  Ulcerations or perforations.

  
  
• 
  

  Foreign bodies.

The clinically important region of the middle meatus may be anatomically narrow and difficult to examine. It can be visualized by using a long Killian nasal speculum, provided that local anesthesia of the nasal mucosa has been induced (e.g., by local application of lidocaine [Xylocaine]; or 1% pantocaine with 1:1,000 epinephrine, one drop to 1 mL of anesthetic solution; or with a 5% lidocaine and 0.5% phenylephrine spray). Gustav Killian (1860–1921) developed this instrument for the medial rhinoscopy technique, having recognized as early as 100 years ago that the lateral nasal wall is important in pathogenesis. The technique of anterior rhinoscopy using nasal endoscopy was added more recently.

2.2.3 Posterior Rhinoscopy

▶ Fig. 2.18 shows the method of examining the nasopharynx with a mirror, with a composite view of the inspected region. Posterior rhinoscopy is used to examine the posterior part of the nasal cavity: the choana, the posterior ends of the turbinates, the posterior margin of the septum, and the nasopharynx, including its roof and the ostia of the eustachian tube. The advent of flexible nasal endoscopy has resulted in the loss of the skill of examination with a mirror, but it is important to try and preserve this skill to ensure that we can cover all eventualities. However, COVID-19 has changed clinical practice, and should a clinician carry out such a diagnostic examination now, we would strongly recommend that appropriate personal protective equipment is worn.

Nasal endoscopy, including the nasopharynx, should nowadays be an integral part or an adjunctive measure in any examination assessing an otorhinolaryngology patient. It has superseded posterior rhinoscopy and can be regarded as the gold standard for obtaining nasal findings, regardless of the further management.

Technique: Posterior rhinoscopy requires a considerable amount of practice on the part of the examiner, as well as cooperation by the patient. A tongue depressor is placed on the center of the base of the tongue with one hand, and the base of the tongue is pressed slowly downward, increasing the distance between the surface of the tongue and the soft palate and posterior pharyngeal wall. The glass side of a small mirror is warmed and then tested on the hand to make sure it is not too hot. The other hand is used to introduce the mirror into the space between the soft palate and the posterior pharyngeal wall. The mirror must not touch the mucosa, otherwise it will elicit the gag reflex. If the soft palate remains tense, the patient is asked to breathe gently through the nose, to sniff, or to say “ha,” causing the palate to relax and providing an unobstructed view into the nasopharynx. A view of the various parts of the nasopharynx is obtained by moving and tilting the mirror ( ▶ Fig. 2.18b). The vertical posterior edge of the septum is used for orientation to locate the normal structures. If a satisfactory view cannot be obtained due to the gag reflex, a successful examination can often be achieved by applying a local anesthetic (e.g., a 1% lidocaine spray) to the oropharynx, particularly to the soft palate and posterior wall of the pharynx.

If it is not possible to examine the nasopharynx with this method, either endoscopy or palatal retraction (or both combined) can be carried out, although endoscopy has now made palatal retraction largely obsolete.

The following should be noted during posterior rhinoscopy ( ▶ Fig. 2.19):

• 
  

  The opening and width of the choanae.

  
  
• 
  

  The shape of the posterior end of the inferior and middle turbinates.

  
  
• 
  

  Scars or deformities in the nasopharynx (e.g., due to trauma).

  
  
• 
  

  The shape of the posterior part of the nasal septum.

  
  
• 
  

  Nasal polyps.

  
  
• 
  

  The shape of both tubal ostia and the Rosenmüller fossa (pharyngeal recess).

  
  
• 
  

  Obstruction of the nasopharynx by enlarged adenoids in children.

  
  
• 
  

  Tumors of the nasopharynx.

  
  
• 
  

  Abnormal secretions in the choanae.

  
  
• 
  

  The properties of the mucosa of the posterior part of the nose and the nasopharynx (e.g., for moisture, dryness, thickening, and color).

Computed tomography (CT) is used to evaluate the spread of paranasal sinus lesions to adjacent structures, particularly the skull base, cranial cavity, retromaxillary space, and orbits. Also used in trauma patients, CT is indispensable for differentiated evaluation of bony structures. It is supplemented by magnetic resonance imaging (MRI) for soft tissue investigations.

2.2.4 Nasal Endoscopy

The principle used in the rod lens system was submitted to the Patent Office in the United Kingdom by its inventor, the English physicist Harold Horace Hopkins (1918–1994), on July 16th, 1959. The rod lens system uses precision-polished glass rods with optically processed ends instead of conventional lenses. The system has substantial advantages over conventional lens systems: better resolution and contrast, a wider angle of view, and extremely clear and bright images that resolve even the smallest details throughout the entire field of view.

The German inventor Karl Storz (1911–1996) introduced the system into otorhinolaryngology and developed cold light illumination. This marked the beginning of a new era in otorhinolaryngology—the era of endoscopy.

The Austrian physician Walter Messerklinger (1920–2001) studied mucociliary transport in the paranasal sinus mucosa over a period of several years. He used the new scopes to explore the lateral nasal wall and obtained significant pathogenetic findings:

• 
  

  The vast majority of cases of recurrent and chronic sinusitis are rhinogenous in origin.

  
  
• 
  

  Inconspicuous signs of mucosal disease or anatomical configurations predisposing to sinusitis are detectable with endoscopy.

  
  
• 
  

  The endoscope is thus an important optical device for elucidating the spreading pathway of spread of rhinogenous sinusitis.

  
  
• 
  

  Endoscopic devices have therefore made new surgical approaches possible. Endoscopic surgery can be directed at the central pathogenetic mechanism of recurrent or chronic sinusitis (see functional endoscopic sinus surgery, ▶ p. 192).

Nasal endoscopy is the most important method for evaluating intranasal findings ( ▶ Fig. 2.20a–d).

Clinical indications for nasal endoscopy: These include acute, recurrent, and chronic sinusitis; head and facial pain; chronic nasal catarrh; epistaxis; epiphora; chronic pharyngitis and laryngitis; epipharyngeal disease; chronic otitis media; hyposmia and anosmia; suspected or known cerebrospinal fluid (CSF) rhinorrhea; foreign-body removal; sample biopsies; and sleep disorders.

Normal mucosal findings during nasal endoscopy: The mucosa has a pale pink color and a moist consistency.

The diagnostic evaluation criteria in nasal endoscopy are shown in ▶ Table 2.3 .

Technique: The examination is carried out with the patient in a sitting, semireclining, or fully reclined position, without premedication. If the mucosa is severely swollen, vulnerable, or sensitive, it can be decongested and anesthetized with a 5% lidocaine and 0.5% phenylephrine spray, or with a single puff of tetracaine plus epinephrine. It is useful to soak a few cotton swabs in a solution of this type for 5 min before the examination. Swabs should be inserted under endoscopic guidance to prevent mucosal injury.

The endoscopic examination should follow a systematic approach in which different regions are explored ( ▶ Fig. 2.19 and ▶ Fig. 2.21). The 0-degree wide-angle scope (4 mm) is the standard instrument for all endoscopic nasal examinations. Small-diameter endoscopes should be used only if access is limited due to substantial deviation of the anterior septum, or in small children (2.7 mm, 1 mm).

Step 1: 0-degree scope: Initially, the nasal vault and nasal isthmus are inspected. Positioning the endoscope in front of the nasal cavity or the isthmus region—without deforming the nostrils by using a nasal speculum—makes it possible to evaluate the functional condition as well as low-pressure phenomena of the alar cartilages during normal and forced nasal breathing, in physiological conditions.

The endoscope is advanced into the nasal cavity to visualize the nasal floor. It is then carefully positioned between the septum and body of the lower turbinate, to advance toward the choanae. The lower turbinate and pharyngeal tubal ostium have the same orientation. The nasopharynx, soft palate motility, and function of the pharyngeal tubal ostium should be inspected. In children, the size and status of the adenoids need to be evaluated.

Step 2: 0-degree scope: The endoscope is now moved backward to visualize the middle nasal meatus, the “window to the ethmoid.” This is particularly important, as sinusitis may originate here. The middle turbinate may be pneumatized by a system of ethmoidal cells and may be quite large (in the case of concha bullosa); it may also be the site of origin for recurrent sinusitis.

Step 3: 0-degree scope: Gentle medialization of the middle turbinate using a Freer elevator provides a view of the typical relief structure of the lateral nasal wall. The uncinate process is situated ventral to the ethmoidal bulla, the size of which varies depending on its degree of pneumatization. The inferior semilunar hiatus is situated between the posterior margin of the uncinate process and the anterior surface of the ethmoidal bulla. The ethmoidal infundibulum extends in a sagittal direction and opens into the inferior semilunar hiatus. Advancing cranially from the semilunar hiatus, one approaches the frontal recess.

Step 4: 30- or 45-degree scope: The sphenoethmoidal recess and sphenoid sinus ostium can be inspected with a 30- or 45-degree scope. The endoscope is advanced along the nasal floor in a cranial direction until the choana is reached. A 45- or 70-degree scope can be inserted underneath the entire middle nasal meatus; it is used to inspect this area endoscopically in a cranial direction. The olfactory cleft can also be inspected (e.g., to distinguish sensorineural from respiratory hyposmia or anosmia). Angled endoscopes are suitable for inspection of the nasal ostium, which contains the nasolacrimal duct. The ostium is oval in shape and is located just a few millimeters dorsal to the anterior insertion of the lower turbinate.

2.2.5 Assessment of Nasal Patency

Rhinomanometry is the gold standard method for measuring nasal patency and airway resistance or “obstruction” of the nose as the narrowest part of the entire airway.

Two classic laws of physics and psychophysics should be known because both principles determine the indication and success of surgery or other types of treatment for nasal obstruction.

The Hagen-Poiseuille law describes the relationship between resistance and length and width in a tubular cavity: R= 8ηl/(πr⁴).

This classical law is of eminent practical importance. The resistance depends on the viscosity and grows linearly with the length of a tube, which is trivial. However, reducing the radius by half increases the resistance by a factor of 16. This means that only a small decongestion of the nasal mucosa with decongestants or by widening the nasal entrance with a well-planned septoplasty can reduce the resistance with a minimally extended operation. The human eye cannot estimate this relationship.

The second law is the basic law of psychophysics by Weber and Fechner, which states that the sensation of a stimulus follows the logarithm of the stimulus strength. ENT specialists know this relationship very well from the dB scale in audiology and everyone knows it from the sensation of smells. The sensation of nasal resistance is a summary of the sensation of the force required for nasal breathing, the temperature difference between the inside and outside of the nose, and the so-called wall shear stress.

Four-phase rhinomanometry as the physically and statistically based international standard of rhinomanometry (Vogt 2018) determines the Logarithmic Effective Resistance (LReff) and the Logarithmic Vertex Resistance (LVR) instead of the flow rates at a single pressure level. The major advantage of this method of assessment is the correlation of the measured values with the patient’s subjective perception of obstruction and the relationship to the physical data of computational fluid dynamics (CFD) as an expected upcoming routine method. Furthermore, loops in the x/y curve show the onset of movement of the lateral nasal wall, the so-called “nasal valve”.

A classification of nasal obstruction based on thousands of measurements in Caucasians is shown in ▶ Fig. 2.22b. Of clinical interest are the “temporary” and “permanent” resistances that can be determined as a standard test to distinguish nasal obstruction caused by mucosal swelling from skeletal obstructions such as septal deviation.

In sleep medicine, the influence of body position on nasal breathing is important because of the topical analysis of sleep-related breathing disorders. Rhinomanometry is also a preferred quantitative method to measure the increase in resistance in nasal provocation tests (NPT) ( ▶ Fig. 2.22, ▶ Fig. 2.23).

Peak nasal inspiratory flow (PNIF): PNIF is a simple diagnostic procedure which can be used by patients to measure the effect of drugs or allergens in the environment or by nonspecialists as an information resource on complained obstruction of the nose or the effect of allergens after nasal provocation. Normal values or a classification do not exist. The method is not suitable as preoperative diagnostic in functional surgery of the internal or external nose.

Acoustic rhinometry: This method uses acoustic reflection for separate measurements on each side of the cross-sectional area of the nose, from the vestibule to the nasopharynx. In contrast to rhinomanometry, it assesses the cross-sectional area of various parts of the nose, rather than flow parameters in the nose. Another difference is that it also serves to determine static parameters without the need for patient cooperation.

Glatzel-test: An approximate qualitative test of nasal patency can be achieved by holding a polished metal plate in front of the nose during inspiration and expiration. The surface area of the resulting fogging gives an approximation of the patency of the two sides of the nose.

In infants, nasal patency is tested by holding a wisp of cotton wool or a feather in front of the nose.

Computational fluid dynamics (CFD): In the future, computational fluid dynamics (CFD) might become part of a new methodology to assess nasal breathing. CFD is already established in the industry as well as in the medical field of cardiology. Currently, there is also an increasing interest in rhinology to analyze the intranasal airstream ( ▶ Fig. 2.23). CFD provides airflow parameters, such as velocity, pressure, and wall shear stress, with a high spatial and temporal resolution. A DICOM data set of a CT scan or DVT of the paranasal sinuses that captures the entire nasal cavity from the nasal tip up to the choana is the only requirement.

2.2.6 Olfactometry

First, a precise case history is taken that includes triggering events, associated symptoms, relevant illnesses, operations, medications, and noxious influences. This is followed by nasal endoscopy, with exploration of the nasopharynx and the olfactory cleft.

Assessment of olfactory function is based on a standardized, validated test. The following olfaction tests are available and widely used:

• 
  

  Sniffin’ Sticks: Sixteen scents on felt-tip pens are presented to the patient, who is asked to identify them. This test is widely used in Europe. It combines threshold, identification, and discrimination of scents; the identification test is suitable for screening.

  
  
• 
  

  University of Pennsylvania Smell Identification Test (UPSIT): Forty scents in microcapsules are deposited on paper, where they can be released mechanically by rubbing. The individual scents have to be identified from a list, with four alternatives each. The cross-cultural smell identification test (CCSIT) is a simplified version of this.

  
  
• 
  

  Connecticut Chemosensory Clinical Research Center Test (CCCRC): This is a combination of a threshold test for butanol and an identification test for ten scents. The scents are contained in polypropylene flasks that can be pressed open. A disadvantage with this test is low validation.

  
  
• 
  

  Evoked response olfactometry (ERO): Objective assessment of olfactory disorders is possible by analyzing the potentials evoked by olfactory stimuli. Derivation of olfactory evoked potentials is the only validated method of confirming a loss of the sense of smell objectively. ERO involves application of chemosensory stimuli via a tube inserted into the middle nasal meatus, at intervals averaging 20 to 40 seconds. Each stimulation lasts 250 ms. Phenylethyl alcohol or hydrogen sulfide can be used as scents.

The ability to identify different substances may be of importance in neurologic differential diagnosis ( ▶ Table 2.4 ).

Two different parameters can be tested:

1. 
   

   The threshold at which the substance is perceived.

   
   
2. 
   

   The threshold at which it is recognized.

The former threshold is lower than the latter. Apart from ERO, all of the methods mentioned above depend on cooperation from the patient, and the results are therefore largely subjective. Objective results can only be obtained with ERO.

Tests for simulation include ERO and the cinnamon test. The taste of cinnamon is mediated by the olfactory nerve. Cinnamon cannot be recognized in the absence of the ability to smell.

Anosmia is complete loss of the ability to smell; hyposmia is a reduced ability to smell; and parosmia refers to a state in which the subjective impression does not correspond to the substance offered. Phantosmia describes the perception of smell in the absence of olfactory stimulation. Smells are typically perceived as being offensive in both parosmia and phantosmia, and the two descriptions can occasionally coexist. The terminology is sometimes confusing and parosmia is often referred to as dysosmia, cacosmia, euosmia or troposmia. (see also ▶ Table 2.1 ).

2.2.7 Diagnostic Imaging of the Nose and Sinuses

Diagnosis of diseases of the nasal sinuses is hardly possible without the use of radiology.

Conventional radiology: Radiographs of the nose in the lateral projection are necessary to demonstrate a fracture of the nasal bone. They can also be used if an intranasal foreign body is suspected.

Plain sinus radiography ( ▶ Fig. 2.24a, b): The diagnostic value of plain sinus radiographs is controversial today. Proponents of plain sinus radiography say the films provide rapid, noninvasive evaluation of the lower third of the nasal cavity and the maxillary, frontal, sphenoid, and posterior ethmoid sinuses. Plain films are neither useful nor cost-efficient for evaluating the anterior ethmoid air cells, the upper two-thirds of the nasal cavity, or the infundibular, middle meatal, and frontal recess air passages. The clinical role of plain films is thus at best limited to documenting acute maxillary or frontal sinusitis and, if baseline films are available, to following the course of infection and the response to treatment. Detection of air-fluid levels warrants evaluation by CT or nasal endoscopy.

Computed tomography: A multiplanar spiral CT scan is the imaging modality of choice for demonstrating the anatomy and extent of pathology. It helps in understanding the functional sinus anatomy of the individual patient, the extent of the pathology, anatomical anomalies, or bony dehiscence. Most CT sinus scans are done without contrast.

It is important to ensure that a CT sinus scan includes a complete view of all of the paranasal sinuses such as the superior aspect of the frontal sinus, the inferior aspect of the maxillary sinuses, and the whole of the sphenoid sinus. For navigation purposes during image guidance surgery, the nasal tip must be included for surface matching during the registration of optical systems.

Indications: Inflammatory rhinosinusitis, such as recurrent acute and chronic rhinosinusitis, that fails to respond to appropriate medical therapy; benign and malignant sinonasal tumors; facial trauma and complex fractures. A CT sinus scan is essential in all patients undergoing endoscopic sinus surgery or anterior skull base surgery ( ▶ Fig. 2.25).

Digital volume tomography (DVT), or cone beam computed tomography (CBCT), is a three-dimensional diagnostic imaging especially for structures with high contrasts. It is useful in the dialog between implantologists and rhinologists to decide about the interdisciplinary individual concepts in patients with sinus problems and the need for sinus lift and dental implants.

Magnetic resonance imaging: MRI is an excellent adjunct to a CT sinus scan for some conditions, but not the primary imaging modality for chronic rhinosinusitis ( ▶ Fig. 2.26a, b). It is indicated in the management of sinonasal tumors, cerebrospinal fluid rhinorrhea, and complications of sinusitis (intracranial abscess; orbital cellulitis). A gadolinium contrast agent may be required, and renal function must be assessed before the contrast agent is administered.

Magnetic resonance angiography (MRA): This helps clarify the hemodynamic activity of a tumor or vascular anomaly.

Angiography/digital subtraction angiography: In addition to visualization of the blood vessels, this allows preoperative embolization of the arteries that supply a tumor. This is a prerequisite for endonasal endoscopic surgical resection of a juvenile angiofibroma.

Ultrasound in A or B mode: While this modality has been considered, it is not accepted as a standard way of imaging sinuses.

2.2.8 Lavage of the Sinuses

The maxillary sinus, frontal sinus, and sphenoid sinus can be irrigated, but not the ethmoid sinuses. There are two reasons for irrigating the sinuses:

1. 
   

   For diagnostic purposes, to allow aspiration and lavage of abnormal secretions, bacteriologic and cytologic examination of the secretions, and possibly the introduction of a contrast medium for radiography.

   
   
2. 
   

   The sinuses can be irrigated for therapeutic purposes, to allow drainage of abnormal secretions and introduction of locally active substances into the sinuses.

Although lavage of the sinuses was commonly used to treat maxillary empyema up until just a few decades ago, it is rarely done today. Drainage of the frontal sinus using the Kümmel and Beck method is now practically obsolete, having been replaced by endoscopic endonasal microsurgery. However, the otolaryngologist should be familiar with these techniques to avoid complications of infection, should modern endoscopic methods be unavailable: ubi pus, ibi evacua.

Lavage of the Maxillary Antrum: Two methods are routinely used:

1. 
   

   Access via the inferior meatus (sharp puncture).

   
   
2. 
   

   Access via the middle meatus (blunt puncture) after fenestration during functional endoscopic surgery.

Principle of lavage via the inferior meatus: Local anesthesia of the inferior meatus is induced. A Lichtwitz trocar is placed against the lateral nasal wall beneath the origin of the inferior turbinate. After the cannula has been pushed through this part of the lateral nasal wall, which is usually thin, it can be used for aspiration, lavage, or the introduction of drugs.

A long-term drain can be introduced for conservative treatment, especially in children (see ▶ Fig. 2.27).

The Sinus Trocar lavage system for the maxillary sinus ( ▶ Fig. 2.27a, b) is an optimized drainage system. During puncture of the maxillary sinus with a trocar in the middle nasal meatus, a 3-mm plastic tube equipped with a plastic hull (1 cm long, 1.5 mm thick) is inserted into the maxillary sinus. The trocar is then removed; two small barbs keep the self-retaining catheter from slipping away from the wall of the maxillary sinus. For repeated lavage, the self-retaining catheter is attached to an adapter tube (19 cm long, Luer-Lok, or cone connection).

Complications during blunt puncture are very unlikely if it is performed expertly. During sharp puncture, the point of the cannula may be pushed inadvertently into the soft tissues of the cheek, pterygopalatine fossa, or orbit if the technique is incorrect.

Lavage of the Frontal and Sphenoid Sinus: Trephination of the anterior wall of the frontal sinus can be performed using a fine drill under local anesthesia. This allows irrigation for both diagnostic and therapeutic purposes, and also prolonged drainage of the frontal sinus for 1 to 2 weeks, allowing daily administration of drugs. The principle of puncture is shown in ▶ Fig. 2.28a–d.

Technique: Anteroposterior and lateral radiographs of the sinuses have to be obtained first. If the frontal sinus has not developed or is very shallow, there is a risk that the frontal lobe may be punctured.

Irrigation of the sphenoid sinus can be performed using a special “sphenoid” cannula.

The ethmoidal labyrinth does not have a defined ostium and therefore cannot be irrigated. However, pathologic secretions can be evacuated using suction.

2.2.9 Specific Diagnostic Methods

Cytology: Smears of secretions or swabs taken from the mucosa can be assessed cytologically. This is useful for differentiating between catarrh, bacterial infection, allergic rhinitis, and mucosal mycoses.

Allergy studies: Investigations performed on patients include skin tests (scratch, prick, intracutaneous, or friction) and provocation tests (conjunctival and intranasal). Laboratory studies include total immunoglobulin E (IgE) in serum (paper radioimmunosorbent test, PRIST); specific IgE in serum (radioallergosorbent test, RAST); eosinophil counts in the blood and nasal secretions.

Biopsy: Biopsy of sinonasal lesions is recommended for diagnostic reasons for both benign and malignant lesions prior to definitive treatment. Nasal mucosal biopsy is also helpful in the management of granulomatous/vasculitic disease affecting the nose, and ideally needs to be performed before medical therapy is instigated.

Beta-2 transferrin: The presence of the polypeptide beta-2 transferrin in fluid dripping from the nose is strong evidence of a CSF leak. The sample should be assayed together with a serum sample to exclude the rare possibility of a false-positive result.

Beta-trace protein is a more recent alternative, sensitive, and specific method of detecting CSF in patients with a suspected CSF leak, but not as freely available as beta-2 transferrin.

2.3 Dermatologic Principles for the Otolaryngologist

Skin lesions and diseases commonly present on the nose, face, and in the head and neck region. This section has therefore been included as an aid to the otorhinolaryngologist. In some areas, such as the external ear canal, the otorhinolaryngologist serves as a “head and neck dermatologist.”

Before the conclusion is made that a skin finding is a localized change limited to the head and neck region, it needs to be considered whether it might be a regional manifestation of a systemic disease such as lupus erythematosus, systemic sclerosis, or pemphigus vulgaris, or whether it is part of a cutaneous-mucosal disease such as lichen planus or erythema multiforme, to cite but a few dramatic examples.

2.3.1 Skin Type

Certain disorders may be more or less common, depending on the skin type. For example, acne vulgaris with follicular comedomes, papules, and pustules is more common in those with oily skin (the seborrheic skin type), as is rosacea, which features facial erythema, papules, pustules, and sebaceous gland hyperplasia. Rosacea appears in adult life and is occasionally called “adult acne”—an incorrect oversimplification. Atopic dermatitis is more common in those with dry skin (the sebostatic skin type). In our experience, healing in oily skin is poorer than in normal or dry skin, an important consideration when planning surgery. The skin type can help one decide to perform a flap rather than primary closure in an oily area.

In describing the skin, a distinction is made between the condition of the skin and its vascular supply. The skin status describes turgor, seborrhea, xerosis, atrophy, actinic damage, hyperhidrosis, and hypohidrosis, while the vascular status includes factors related to blood supply, such as cyanosis, paleness, cold, warmth, edema, and necrosis.

2.3.2 Types of Lesion

Just as the multiplication tables are one of the cornerstones of arithmetic, the terminology and precise description of lesions is a central part of dermatologic knowledge that is necessary for achieving a logical diagnostic approach. Even if the working diagnosis proves to be incorrect, it is easier to advance to the correct diagnosis if the lesions have been precisely and correctly described. If the initial lesions have been poorly described, then it is very difficult to reconstruct a case. The way to describe the different lesions simply has to be learned, therefore—much like learning the words of a foreign language. Describing lesions correctly is extremely important.

A distinction is made between primary and secondary lesions ( ▶ Fig. 2.29a–k).

2.3.2.1 Primary Lesions

• 
  

  Macule (spot), urticaria (hive), papule (small raised lesion), nodule (larger raised lesion), vesicle (small blister), bulla (large blister), pustule (primary pus-filled blister).

2.3.2.2 Secondary Lesions

• 
  

  Pustule (vesicle with secondary pus), crust (mixture of pus and scales), scales, erosion (superficial defect of epidermis), excoriation (self-induced defect in the epidermis and upper dermis), rhagades/fissure (linear tear), ulcer (deeper defect), scar, atrophy, cyst (fluid-filled lesion), and necrosis.

Primary lesions are fresh lesions that appear as the first sign of a skin disease. Secondary lesions are less sharply defined. They may result from secondary changes in primary lesions (a vesicle becomes a pustule), from exogenous damage (erosion or excoriation), or over time (atrophy, scales). It is more important to describe the lesion correctly than to decide whether it is primary or secondary. It should always be possible to identify a pustule; whether it is primary or secondary can remain an open question.

Along with the type of lesion, the pattern of distribution is also of diagnostic significance. The distribution may be strikingly asymmetrical, segmental, symmetrical, or generalized, as well as fitting, light-exposed, hypostatic, or other known patterns. The pattern often facilitates the diagnosis and should therefore always be documented.

Dermatologic differential diagnosis requires a logical approach, as one develops a sense or feeling for the process. At the start, one should consider all the possible diagnoses that fit the morphologic pattern, but always remembering that the most common disorder is the most likely diagnosis. A second important principle is always to consider the possibility of an unusual variation of a common condition; for example, many disorders are more severe or clinically atypical in patients with human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS).

2.3.3 Basics of Topical Dermatologic Therapy

Topical therapy has a special role in treatment. The medication is directly applied to the site of disease, and its effect is easily observed without complex instrumentation. A distinction is made between vehicle, active ingredient, and additives. Most topical agents contain all three components. The active ingredient is the pharmaceutical agent that is to be delivered to the skin in a vehicle. Additives can play many roles, making the vehicles more attractive (with fragrance) or stable (through preservatives). While in the past many formulations contained multiple active ingredients, today most have one or at most two such agents, reducing the likelihood of drug interactions.

Three different types or phases of vehicle are available: solid, liquid, and semisolid. They can all be combined in various ways. A favorite way of visualizing this is using a phase triangle, in which the corners represent the basic phases, while the sides of the triangle signify mixtures of two classes and the center represents a mixture of all three ( ▶ Fig. 2.30).

The vehicles available for topical therapy can also be divided into two groups:

1. 
   

   Primary vehicles (one phase): These are the corners of the phase triangle. They include:

   
   
   
   
   • 
     

     Solids (powders).

     
     
   • 
     

     Liquids (wet soaks, solutions).

     
     
   • 
     

     Semisolids (ointments, petrolatum, oils).

   
   
2. 
   

   Combined vehicles (two or more phases) fall between the corners, depending on their composition:

   
   
   
   
   • 
     

     Emulsions (ointments (oil/water, water/oil), creams).

     
     
   • 
     

     Shake lotions.

     
     
   • 
     

     Pastes.

2.3.3.1 Principles for Choosing a Vehicle

The correct choice of a vehicle can greatly enhance healing, while an inappropriate vehicle can have adverse effects, even if exactly the correct active ingredient has been chosen. One should try to work with as few vehicles as possible, in order to get to know them well and acquire experience in administering them. The choice of vehicle is based on the skin type, involved area, acuteness of inflammation, and type of lesion.

Skin type

Seborrheic skin: Powders, alcoholic solutions, shake lotions, creams; no greasy vehicles.

Sebostatic skin: Ointments, ointment emulsions, soft pastes; no drying or only minimally greasy vehicles.

Special body regions

Scalp: Aqueous or alcoholic solutions, easily washed emulsion creams; no pure ointments (petrolatum), pastes, or shake lotions.

Intertriginous areas: Soft zinc pastes, creams, zinc oils; no shake lotions or thick ointments.

Degree of inflammation

Acute superficial inflammation: Dye solutions, moist dressings, powders, shake lotions, creams. Clearly weeping dermatoses should be treated with wet dressings or greasy-wet dressings (slightly greasy dressing covered with wet soaks). Occlusive dressings should not be used for weeping dermatoses, pyodermas, or fungal infections.

Chronic deeper inflammation: Vehicles are required that can ensure penetration of the active ingredients such as ointments, ointment emulsions, soft pastes, and emollient creams, but no powders, shake lotions, or wet dressings.

Morphology of skin changes

Acute erythema: Powders, shake lotions, creams, wet dressings.

Vesicles and bullae: Shake lotions, creams, moist dressings, greasy-wet system (greasy vehicle covered by wet dressing).

Erosions: Wet dressings (wet or greasy-wet), ointments.

Crusts: Wet dressings (wet or greasy-wet), ointments, emollient ointments, soft pastes.

Scales: Ointments, emollient ointments, soft pastes, greasy-wet dressings.

Chronic infiltrates or lichenification: Ointments, emollient ointment, soft pastes.

Atrophy, scars: Ointments, emollient ointments, soft pastes.

2.3.3.2 Examples of Topical Active Ingredients

Urea: Hygroscopic (binds water), keratolytic, proteolytic, increases penetration, antipruritic and weakly antiproliferative. Nonsensitizing, but irritating, depending on concentration. Indication: dry, pruritic skin.

Salicylic acid: Very keratolytic, weakly anti-inflammatory and antimicrobial, irritating in active inflammation. Usually combined with other active ingredients, such as a topical corticosteroid for pruritic otitis externa.

Corticosteroids: Depending on choice of agent and concentration, varying degrees of effectiveness. Care is also needed on the face, with a preference for lower concentrations and less active agents; in case of infection, corticosteroids should not be used as a single agent, but only as a supplementary anti-infectious therapy. Because they are simply the best topical anti-inflammatory agents, corticosteroids are often used for otorhinolaryngology indications. Formulation (for weeping otitis externa): prednisolone 0.02, ol. zinci oxydat. ad 50.0.

Dyes and antiseptics: Most dye solutions such as brilliant green or Castellani paint with carbol fuchsin are no longer used today due to undesirable drug effects. Methylrosanilinium chloride (also known as gentian violet and crystal violet) is still available. It has a bacteriostatic effect and inhibits the growth of yeasts and dermatophytes. The aqueous solution is used in concentrations of 0.1%, 0.3%, and 0.5% for infections of the skin and oral mucosa.

Antibiotics: The use of topical antibiotics is somewhat controversial in dermatology. The main reasons for this include the development of resistance and allergic sensitization, which can then leave the individual intolerant to the same or related agents administered systemically. There are many alternatives for most forms of topical antibiotic therapy. The active agents that are still in use after a long period of time and have proved their effectiveness include the following (with examples of representative products):

• 
  

  Gentamicin sulfate: Gentamicin cream 0.1%, gentamicin ointment 0.1%.

  
  
• 
  

  Erythromycin: Akne-Mycin ointment or solution, Zineryt (solution with zinc acetate), Clinofug gel 2%/4%.

  
  
• 
  

  Oxytetracycline HCl: Terramycin ointment (with polymyxin B), oxytetracycline ointment 1%.

2.4 Clinical Aspects of Diseases of the Nose, Sinuses, and Face

The main symptoms of diseases of the nose and sinuses are:

• 
  

  Increased nasal secretion

  
  
• 
  

  Nasal obstruction

  
  
• 
  

  Bleeding or hemorrhagic secretion (see ▶ Table 2.12 , ▶ Table 2.13 )

  
  
• 
  

  Fetor

  
  
• 
  

  Altered or absent sense of smell (see ▶ Table 2.1 , ▶ Table 2.2 )

  
  
• 
  

  Pain in the head or face

  
  
• 
  

  Disease of neighboring organs (e.g., teeth, the lacrimal apparatus, eyes, mouth, and throat). Important symptoms of eye disease include abnormalities of refraction, limitation of the visual field, acute loss of vision, and displacement of the orbit. Diseases of the mouth and throat may be symptomatic, or a change in the quality of the voice and speech may be noted.

2.4.1 Inflammatory Diseases of the Nose and Paranasal Sinuses

2.4.1.1 Inflammations Confined Mainly to the External Nose

The skin of the nose and the face may be affected by the same common typical skin diseases that affect the rest of the skin, such as impetigo, acne, trichophyton, rosacea, and lupus erythematosus. These diseases are treated using the appropriate dermatologic methods.

Other skin diseases that are particularly important in the nasal area are described in the following text.

Nasal Eczema

Clinical features: The disease is moist in the early phases, with vesicles and pustules. Later, crusts form, followed by painful cracks. In the chronic stage, there is itching, burning, and desquamation. The disease is localized to the external nose and the skin of the nasal vestibule and never affects the nasal mucosa.

Pathogenesis: The disease is often caused by abnormal nasal secretions, but may also be due to a contact allergy (sensitivity testing should be carried out). Promoting factors include diabetes mellitus, generalized eczema, and dietary sensitivity in children.

Treatment: The crusts should be softened with a mild greasy ointment followed by a corticosteroid (hydrocortisone). The use of stronger steroids should be avoided on facial skin. Cracks are treated with 5 to 10% silver nitrate solution. The cause should be looked for and treated or eliminated.

Folliculitis of the Nasal Vestibule (Sycosis) and Nasal Furuncle

Clinical features: Increasing pain, marked sensitivity to pressure, and a feeling of tension in the tip of the nose are followed by reddening and swelling of the tip of the nose, of the nasal ala, and of the upper lip ( ▶ Fig. 2.31a, b). The area becomes edematous, and the patient may have fever. The swelling may begin to resolve before suppuration occurs. Otherwise, a typical furuncle forms, containing pus and a central necrotic core.

Diagnosis: An ascending infection via the facial vein has to be ruled out by testing the medial angle of the eye for tenderness.

Pathogenesis: A pyoderma, usually due to staphylococcal infection, arises from the hair follicles of the nasal vestibule or the upper lip, often close to the nasal tip. The disease is always limited to the skin and never affects the mucosa.

Treatment: Antibiotic creams, such as 2% mupirocin (Bactroban) or 0.1% chlorhexidine/0.5% neomycin (Naseptin) cream or ethacridine lactate solution, are applied to the nasal vestibule as long as the disease remains a circumscribed folliculitis. Manipulation in the nose is contraindicated. If it is suspected that a furuncle is forming, high-dose oral or parenteral antibiotics are given, if necessary in combination with topical antibiotics. The antibiotics of choice for systemic bactericidal therapy are cefadroxil, flucloxacillin (floxacillin), or doxycycline; in severe cases, cefazolin or an aminopenicillin with a β-lactamase inhibitor. Antibiotics must be continued for several days after the symptoms have subsided; they should not be discontinued too early or used at too low a dosage. If an infection is severe, the patient will need hospital admission and intravenous antibiotic and fluid administration.

If there is tenderness in the medial angle of the eye, the facial artery and vein must be ligated.

Frostbite and Burns

The nose is particularly at risk for frostbite and sunburn in extremes of weather and temperature. The injury is divided into three degrees of severity, with the most severe being dry or moist tissue necrosis.

Treatment: As for thermal damage to other parts of the body.

Erysipelas

Clinical features: The incubation period lasts several hours to 2 days. The disease starts with high fever and possibly chills. There is marked pain and sharply demarcated reddening of the edematous skin. Often there is extension on both sides of the nasal pyramid in a butterfly configuration. The disease usually resolves within 1 week with proper treatment. Treatment must be energetic and high-dose, as the disease tends to recur ( ▶ Fig. 2.32a, b).

Pathogenesis: The causative organism is usually a streptococcus. The portal of entry is often a small abrasion on the skin.

Differential diagnosis: Angioneurotic edema, acute dermatitis, and herpes zoster must be considered.

Treatment: Penicillin is the first-line drug. It should be given intravenously to begin with, and continued for 10 days. In severe cases, 10 million IU per day may be required. Alternatively, erythromycin, cephalosporins, or macrolides may be given. Antibiotics are continued for 8 days after the eruptions subside, and local moist dressings are applied.

Prognosis: Good.

Rhinophyma

Clinical features: The condition starts with coarsening of the skin over the cartilaginous part of the nose. A lumpy, bluish-red pseudotumor develops and slowly progresses to become a markedly protuberant lobular swelling of the anterior part of the nose, which may even obstruct breathing and eating. This disease usually occurs in older men ( ▶ Fig. 2.33).

Pathogenesis: Rhinophyma is due to hypertrophy of the sebaceous glands. It is associated with acne rosacea.

Treatment: The disease is treated surgically. The tissue is removed in layers with a scalpel, CO₂ laser, or by dermabrasion, and is shaved down to the level of the normal nasal contour. The area is then allowed to heal spontaneously, or is covered with a split-skin graft.

Tuberculosis and Nasal Lupus Vulgaris

Tuberculosis of the nose is now rare, but exists in two forms: lupus vulgaris and exudative ulcerative mucosal tuberculosis.

The latter is due to hematogenous or intraluminal spread of pulmonary TB. Diagnosis is confirmed by biopsy and bacteriology from the mucosal ulcerations.

Clinical features of lupus: Fine red nodules are found on the nasal vestibule, the head of the inferior turbinate, and the septum lying opposite to it. The nodular stage is followed by central necrosis of the nodules, with ulceration and formation of granulomas, and finally scarring with deformity of the underlying cartilage. The nasal introitus becomes stenosed, and the cartilaginous framework of the nose collapses ( ▶ Fig. 2.34).

Pathogenesis: The disease is due to tuberculous infection in the presence of relatively robust immunologic resistance (the proliferative form). The organism responsible is Mycobacterium tuberculosis, either the human or bovine type.

Diagnosis: The diagnosis is reached by demonstrating the infectious agent and by biopsy. Diagnosis of the disease is notifiable. Characteristic findings are intradermal papules that ulcerate, leaving scars.

Differential diagnosis: Eczema of the nasal introitus, anterior rhinitis sicca, perforating ulcer of the septum, syphilis, mycosis, lupus erythematosus, sarcoid, and malignancy. Tuberculosis usually affects the cartilaginous parts of the nose, whereas syphilis attacks the bony part.

Treatment: Long-term triple combinations of tuberculostatic drugs and vitamin D₂ are given.

Sarcoidosis (Besnier-Boeck-Schaumann Disease)

Clinical features: Sarcoidosis is a multisystem disorder of unknown etiology that may occur as an isolated lesion in the nose. Nasal sarcoid presents with nasal obstruction, recurrent epistaxis, crusting, and/or anosmia. Examination may show red nodules within the nasal mucosa, giving the appearance of strawberry skin, nasal tenderness, and occasionally infiltration of the facial skin. There may also be a saddle deformity and septal perforation and facial swelling. There may also be associated sinusitis. Regional lymph nodes may be firm and enlarged.

Diagnosis: If nasal sarcoidosis is suspected, a vasculitic screen should be instigated. This should include a full blood count; erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); serum biochemistry and calcium; angiotensin-converting enzyme (ACE); antineutrophil cytoplasmic antibody (ANCA) and syphilis serology. Urine should be checked for blood and protein and a 24-hour urinary calcium assessment.

The serum ACE diagnosis is usually elevated in active sarcoidosis but is a nonspecific nondiagnostic test. The diagnosis relies on obtaining a biopsy that shows noncaseating granulomata. A chest radiograph and/or chest CT should also be requested.

Differential diagnosis: This includes rhinophyma, lupus, syphilis, and malignancy.

Treatment: Systemic steroids are the mainstay of treatment for active disease and should be administered under supervision of a rheumatologist. Immunosuppressive or immunomodulation medication such as methotrexate or an anti-TNF alpha blocker (infliximab) can be helpful in limiting systemic steroid use. Surgery may be considered for sinusitis or to reduce the obstruction from large inferior turbinates, but septal/reconstructive surgery can induce further inflammatory change within the nose and is best deferred until the condition becomes less active.

Syphilis

Syphilis became a rarity after the advent of penicillin, but it has become quite common again and its incidence is increasing.

Clinical features: Stage 1 is usually marked by the appearance of a single sore (chancre), but there may be multiple sores. Stage 2 begins ≈9 weeks after the infection. It is characterized by bacteremia, generalized exanthema, mucous membrane lesions, flulike systemic signs and symptoms, and the production of antibodies. Stage 3 occurs more than 2 years after the primary infection and shows gummatous infiltration with painful swelling of the bony part of the nose, foul-smelling secretions, formation of sequestra, sharply demarcated ulceration, and usually regional lymphadenopathy. Finally, the typical saddle nose develops, affecting the bony part of the nose, and firm, radiating scars form within the nose ( ▶ Fig. 2.35).

Pathogenesis: This illness is due to an infection with Treponema pallidum. Intrauterine infection may cause early congenital syphilis within the first months of life, or late congenital syphilis beginning between the age of 3 years and puberty, but accompanied by the triad of interstitial keratitis, Hutchinson teeth, and inner ear deafness. The infection may also be acquired (extrauterine) after birth.

Diagnosis: This is based on the history, serology (which is not always positive in stage 3), Nelson test (Treponema pallidum immobilization test, TPI), and biopsy.

Differential diagnosis: Tuberculosis and malignancy must be considered.

Treatment: Antibiotics are administered under the supervision of a venereologist. Local treatment may be required in stage 3. Once the lesion has healed, reconstruction of the defect may be required. The antibiotic of choice is penicillin. In the early stage, benzathine penicillin should be administered intramuscularly at a dose of 2.4 million IU (1.2 million IU in each buttock) as a single dose. In case of penicillin allergy, doxycycline is the usual choice (100mg b.i.d. p.o. for 14 days); alternatively, erythromycin (500mg q.i.d. p.o. for 14 days) can be used. In the late stage, the same dose of benzathine penicillin is injected intramuscularly on days 1, 8, and 15. Alternatively, doxycycline (200mg b.i.d. p.o. for 28 days) or erythromycin (2g i.v. daily for 21 days) may be given.

Rhinoscleroma

Epidemiology: This disease occurs in eastern Europe, North Africa, Central and South America, and Asia.

Clinical features: The disease starts with an atypical rhinitis with purulent secretion and crusts. A flat, nodular infiltrate then appears in the nasal mucosa. There is increasing coarsening of the external nose (tapir nose). The lesion heals with extensive scarring ( ▶ Fig. 2.36).

Pathogenesis: The infectious organism is Klebsiella rhinoscleromatis.

Diagnosis: This depends on the history, with particular attention to foreign travel, and on the results of biopsy and microbiologic studies.

Differential diagnosis: This consists of tuberculosis, syphilis, sarcoid, mycoses, and Hodgkin disease.

Treatment: Antibiotics are given, as dictated by culture and sensitivity tests.

Prognosis: The outcome is uncertain and recurrence is possible.

Leprosy

Epidemiology: The disease occurs in tropical and subtropical regions.

Clinical features: A bulbous thickening in the nasal vestibule, obstruction of the nasal cavity, extensive crusting, fetid secretion, ulceration and liquefaction of the nasal framework, and leonine facies may occur.

Pathogenesis: The disease is due to an infection with Mycobacterium leprae (Hansen).

Diagnosis: This is based on history of contact, symptoms of infection of other parts of the body, and neurologic lesions that are exclusively sensory. Culture and the lepromin reaction also form part of the investigations.

Treatment: Single skin lesions: rifampicin 600 mg as a single dose. Paucibacillary disease (tuberculoid leprosy): dapsone 100 mg daily and rifampicin monthly for 6 months. Multibacillary disease (lepromatous leprosy): rifampicin 600 mg and clofazimine 300 mg, both monthly for 12 months.

2.4.1.2 Acute and Chronic Inflammations of the Internal Nose

Acute Rhinitis and Common Cold

Clinical features: Since the common cold can be caused by different organisms, the symptoms are not uniform. In the common form, there is a dry prodromal stage with generalized symptoms, including chills and a feeling of cold alternating with a feeling of heat, headache, fatigue, loss of appetite, possibly subfebrile temperature, but often a high temperature in children, as well as itching, burning, a feeling of dryness in the nose and throat, and nasal irritation. The nasal mucosa is usually pale and dry. The catarrhal stage usually begins a few hours later, with watery secretions, nasal obstruction, temporary loss of smell, lacrimation, rhinolalia clausa, and worsening of the constitutional symptoms. The nasal mucosa is deep red in color, swollen, and secretes profusely. After several days, the disease changes to a mucous phase. The generalized symptoms begin to improve, the secretions thicken, the sense of smell improves, and local symptoms gradually regress. Resolution should be achieved within a week. The common cold, or viral rhinosinusitis, is defined as duration of symptoms for less than 10 days.

Secondary bacterial infection may occur. The secretions then turn greenish-yellow, and the disease resolves more slowly. Acute intermittent nonviral rhinosinusitis is defined as an increase in symptoms after 10 days, with a duration of less than 12 weeks ( ▶ Fig. 2.37).

Initial catarrh occurs in influenza and infection with other types of viruses such as parainfluenza virus, adenovirus, reovirus, coronavirus, enterovirus, myxovirus, and respiratory syncytial virus. The symptoms are as described above, but are complicated by other manifestations such as involvement of the entire respiratory tract, the gastrointestinal tract (causing diarrhea), the meninges, the pericardium, the kidneys, and the muscles.

Pathogenesis: The infection is often caused by a rhinovirus. More than 100 types belonging to the picornavirus group have been isolated. The disease may also be caused by numerous other viruses. The incubation period of the rhinovirus is from 1 to 3 days. The disease is spread by droplet infection and is exacerbated by cooling of the body.

The most common pathogens in purulent bacterial rhinosinusitis are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, Streptococcus pyogenes, and various anaerobes.

Diagnosis: The diagnosis may not be clearly apparent during the early phase of the condition, but this becomes clearer within a couple of days.

Differential diagnosis: The initial phase of influenza or coronavirus infection should be considered. Acute allergic rhinitis is possible.

Treatment: Treatment is symptomatic and includes decongestant nose drops or oral decongestants. Antibiotics should only be given for secondary bacterial infection, and culture and sensitivity tests should be carried out beforehand. Steam inhalations, treatment with infrared lamps, analgesics, and bed rest should be prescribed if necessary.

Prevention: While there is no scientific evidence that prevention is possible, measures to improve general health may be helpful. These include building up the patient’s overall resistance using sauna baths, therapeutic regimens at health resorts, hydrotherapy, participation in sports, administration of vitamin C, and scrupulous hygiene, especially in contact with young children. Adenoidectomy may be necessary in children (see ▶ p. 269). Immunization against rhinoviruses is not yet possible, but there are vaccines against influenza.

Allergic Rhinitis

Allergic Rhinitis may present with acute intermittent symptoms, seasonal variation or acute exacerbations within a background of chronic perennial symptoms. It is mainly a type I allergic reaction. In this type of anaphylactic hypersensitivity reaction, cutaneous or mucocutaneous symptoms develop either immediately or within a few minutes after exposure. The most common form is hay fever, but other allergens may be responsible.

Clinical features: These include itching in the nose, nasal obstruction, sneezing attacks, and a clear, watery nasal discharge. The patient may also have a feeling of stuffiness and irritation of the entire head, possibly conjunctivitis, malaise, temporary fever, loss of appetite, autonomic symptoms, possibly inability to work, and temporary hyposmia or anosmia. Secondary infection is possible.

Pathogenesis: An inhalation allergy is the cause. The shock organ is usually the nasal mucosa, but it may also be the conjunctiva or other mucous membranes. Predisposition for the disease may be hereditary.

Seasonal allergic rhinitis is caused by pollen ( ▶ Fig. 2.38).

Perennial allergic rhinitis is due to an inhaled allergen, regardless of the season. The allergens include fungi, animal hair, house dust mites, house-plants such as primroses and roses, and also foods such as fish, strawberries, nuts, eggs, milk, and flour. There are occupational allergies (e.g., to flour for bakers, to hair and epithelial scales for hair-dressers, etc.) and other allergies to bacteria and parasites.

Infection and allergy: Bacteria and viruses can act as allergens, but the practical significance of this is still controversial. Three pathogenetic mechanisms are possible:

1. 
   

   An allergic reaction to bacteria or viruses without clinical infection (e.g., to nasal saprophytes).

   
   
2. 
   

   An allergic reaction to bacterial or viral infection(e.g., chronic bacterial rhinitis or sinusitis with resultant sensitivity to the causative organism).

   
   
3. 
   

   Secondary infection in tissue already altered by allergic reaction. In this case, the infective agent is not the same as the antigen.

The second form corresponds to the term “infection allergy.” Its time course classifies it as a late allergic reaction.

If an infective allergy is suspected, tests should be carried out for the antigen (i.e., a positive cutaneous late reaction to a bacterial extract), and antibiotics should be given depending on the sensitivity tests. The long-term value of hyposensitization has not yet been confirmed in clinical practice.

Diagnosis: This is made primarily on the basis of the history. Investigations include cytology of the nasal secretions, intracutaneous tests, prick tests, and patch tests, intranasal challenge with rhinomanometry, olfactometry, measurement of serum and secretion IgE, and RAST.

Local findings: The nasal mucosa is livid and pale. In acute stages, the mucosa may also be deep red. The turbinates are swollen, and there are copious amounts of clear secretion.

Differential diagnosis: Nasal hyperreactivity/idiopathic rhinitis and acute rhinitis (coryza) must be considered.

Treatment: Symptomatic: The World Health Organization (WHO) has published guidelines on Allergic Rhinitis and its Impact on Asthma (ARIA)—2016 revision. The classification has changed from seasonal (SAR), perennial (PAR), and occupational allergic rhinitis (AR) to “intermittent” and “persistent” AR ( ▶ Table 2.5 ). The recommendations apply to moderate-to-severe AR and the old classification is retained for clarity.

• 
  

  Mild-to-moderate symptoms (e.g., first manifestation of allergic rhinoconjunctivitis): A third-generation oral antihistamine (e.g., levocetirizine, desloratadine) or a topical antihistamine (e.g., an azelastine nasal spray), if necessary with concomitant use of antihistamine eyedrops.

  
  
• 
  

  Marked nasal symptoms: A combination of an oral antihistamine and a topical steroid (e.g., mometasone, fluticasone, triamcinolone).

  
  
• 
  

  Severe nasal obstruction: Brief application of a nasal decongestant containing an asympathomimetic drug.

  
  
• 
  

  Hyposensitization: Short-term titration and coseasonal hyposensitization treatment.

  
  
• 
  

  Causative therapy: Specific immune therapy is the only treatment modality to address the underlying cause. It can prevent the development of allergic asthma.

Principle of specific immune therapy: Standardized allergen extracts of dominant single allergens (major allergens), native, or polymerized (chemically modified) extracts (so-called allergoids) are used. They are bound to a carrier such as aluminum hydroxide, tyrosine, or calcium phosphate. Application may be subcutaneous (subcutaneous immune therapy, SCIT) or sublingual (sublingual immune therapy, SLIT).

Immunologic effects: T lymphocytes are influenced by the activation of regulatory CD4⁺ T cells (IL-10, transforming growth factor β), inducing immediate hyposensitivity (lowered cytokine production) and replacement of T-helper subset 2 (TH2) dominance (IL-4, IL-5, IL-13) with a TH1 response. This in turn affects the production of immunoglobulins by B lymphocytes and inhibits effector cells (e.g., mast cells, basophilic leukocytes, and eosinophilic granulocytes).

Effectiveness: Pollen allergy: symptoms decreased in 30%; grass and birch allergies in 45%; dust allergies in 30%.

Surgery: Indications for surgery have to be established in septal deviation, turbinate hyperplasia, nasal polyps, rhinosinusitis, or adenoids.

Prognosis: This is generally good. The disease gradually regresses as the patients get older, but progression to bronchial asthma (or vice versa) is possible.

Complications: Involvement of the nasal sinuses and the lower respiratory tract, and polyps of the nose and sinuses are possible.

Chronic Rhinitis: Nonallergic, Nonspecific Inflammation of the Nose

The WHO’s ARIA guidelines recommend that the term “idiopathic rhinitis” should be used instead of noninfectious and vasomotor rhinitis. The synopsis of classifications in the ARIA report and the consensus report on nasal hyperreactivity defines idiopathic rhinitis as a group of nasal oversensitivity syndromes due to unknown pathomechanisms. Idiopathic rhinitis is a diagnosis of exclusion; it is considered present if the forms of rhinitis and differential diagnoses listed in ▶ Table 2.6  can be ruled out.

Clinical features: The International Consensus Report on the Diagnosis and Management of Rhinitis (1994) requires at least two symptoms from the group: urge to sneeze, runny nose, nasal obstruction, and/or itching, lasting for more than 1 h per day. Healthy individuals may sneeze or wipe their noses up to four times daily.

Pathogenesis: There are three pathogenic mechanisms:

1. 
   

   Neuronal dysfunction ( ▶ Fig. 2.39): Neurogenic inflammation is mediated by neurotransmitters and interacts in many ways with the immune system. Activation of neuro-kinine-1 receptors in the airways causes contraction of smooth muscles, dilation of blood vessels, glandular secretion, and extravasation of plasma proteins. Activation of neurokinine-2 receptors causes bronchoconstriction and stimulates afferent nerves. Hyposympathicotonia or hyperparasympathicotonia leads to obstruction and hypersecretion.

   
   
   
   

   Fig. 2.39 Diagram of neural regulation of the nasal mucosa and its disorders in idiopathic rhinitis. 1, Enhanced, 2, reduced neural activity; increased density of innervation or release of neurotransmitters; 3, glands of the nasal mucosa; 4, blood vessels, vasodilation. SP, Substance P; NKA, neurokinin A; CGRP, calcitonin gene-related peptide; GRP, gastrin-releasing peptide; NOR, norepinephrine; NPY, neuropeptide Y; Ach, acetylcholine; VIP1, vasoactive interstitial peptide + VIP-like peptide. (Adapted from Damm M. Idiopathic Rhinitis. Laryngo-Rhino-Otol. 2006; 85:365.)

   
   

   

   
   
2. 
   

   Immune inflammatory disorders: Among others, CD3⁺, CD25⁺, CD8⁺, CD45RA⁺, and T cells, eosinophils, and mast cells are increased.

   
   
3. 
   

   Mucosal damage, with increased permeability for irritants.

Diagnosis: History, nasal endoscopy, rhinomanometry, acoustic rhinometry, allergy tests.

Treatment:

Medical:

• 
  

  Ipratropium bromide (anticholinergic, 80–100 mg/d) is effective against rhinorrhea.

  
  
• 
  

  Topical corticosteroids are effective against symptoms such as obstruction, rhinorrhea, and postnasal drip.

  
  
• 
  

  Azelastine (antihistamine, 1.1 mg/d) works well against rhinorrhea, sneezing, obstruction, and postnasal drip.

  
  
• 
  

  An isotonic salt-water spray may be an effective treatment in mild cases.

Surgical: Invasive and surgical measures are considered only after conservative treatment has failed. Severing the nerve of the pterygoid canal (vidian nerve) used to be done to interrupt the parasympathetic innervation of the nose. This treatment option should first be simulated by reversible and repeatable blockade of the sphenopalatine ganglion.

Reduction of the erectile cavernous tissue in the inferior turbinate should relieve nasal obstruction and possibly hypersecretion. There are various techniques for reducing the inferior turbinates: submucosal reduction with a mini-microdebrider, submucosal radiofrequency therapy/coblation, laser reduction therapy, partial excision or reduction by a microdebrider.

Foreign Bodies in the Nose

Foreign bodies are found in children in most cases and may have been retained for a very long time ( ▶ Fig. 2.40). They include coins, metal fragments, peas, etc.

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