Chapter 7: The Head and Neck

At least nine clinical specialties have a major focus on the head and neck. Each specialty has developed detailed examinations to meet their needs, often with the use of specialized instruments. We describe examinations that can be made with the resources available to the general clinician. Traumatic disorders are not considered.

Examination of the head, neck, and cranial nerves (CNs) is an essential part of the neurologic examination. Interpretation of physical examination findings is done with an eye to both the local findings and the pattern of neurologic abnormalities. This chapter discusses the symptoms, physical examination, signs, and syndromes related to the head and neck. Symptoms, physical examination, signs, and syndromes primarily of neurologic significance are discussed in Chapter 14. By necessity, these distinctions are somewhat arbitrary.

In the general head and neck examination, the examiner should: (1) identify signs of generalized disease, (2) recognize local lesions within the purview of the generalist, and (3) recognize local lesions requiring specialist care.

The head and neck contain a complicated grouping of major structures all with close proximity to one another. The examiner must always be aware of the anatomy and functional physiology of the superficial and deep structures.

The skull, facial bones, and scalp provide protection and insulation to the deeper structures. The scalp and face are rich in blood vessels that vasodilate in response to cold to maintain normal body temperatures within these vital structures. The head contains the organs of special sense: the eyes, ears, olfactory nerve, and taste buds of the tongue. Impairment of the special senses suggests problems with the sensory organs, their CNs, or the brain. The tongue, pharynx, and larynx are the organs of speech. Changes in articulation suggest anatomic or functional problems with these structures. The nose, mouth, pharynx, larynx, and trachea form the upper airways; any compromise of these structures may impair effective respiration and effect changes in the tone or volume of voice. The mouth, teeth, mandible and maxilla, tongue, salivary glands, pharynx, and upper esophagus are the upper alimentary tract necessary for mastication and swallowing of food. The head and neck are highly vascular. The superficial structures have rich anastomoses from branches of the external carotid, so ischemic injury is unusual. The internal carotid and vertebral arteries supply blood to the brain. The head and neck have a rich lymphatic network draining to discrete regional lymph node beds. The tonsils and adenoids are lymphatic organs surrounding the upper aerodigestive tract. The neck contains the thyroid and parathyroid glands, major structures of the endocrine system.

The Scalp and Skull

The scalp has five layers: the skin, subcutaneous connective tissue, epicranius, a subfascial cleft with loose connective tissue, and the pericranium (Fig. 7-1). Functionally, the outer three are a single thick, tough, and vascular layer. The epicranius is formed by the frontalis muscle attached to the occiput by a large central aponeurosis, the galea aponeurotica. The skin and subcutaneous tissue are tightly bound to the galea by many fibrous bands that sharply limit the spread of blood and pus. The pericranium is the periosteal layer of the skull bones; it dips into the suture lines, limiting spread of subperiosteal blood or pus to the surface of a single bone. Between the pericranium and the galea is a fascial cleft containing loose connective tissue. Because of this layer, the lacerated scalp can be lifted from the skull with minimal effort and blood or pus can spread widely beneath it. A useful pneumonic for remembering this structure is SCALP: Skin, Connective tissue, Aponeurosis, Loose connective tissue, Periosteum.

The scalp has three areas of lymphatic drainage. The forehead and the anterior portion of the parietal bone drain to the preauricular lymph node. The mid-parietal region drains first to the postauricular node and then into the nodes of the posterior cervical triangle. The occipital area drains first into the nodes at the origin of the trapezius and then into the posterior cervical triangle.

The Face and Neck

The facial contour is determined by the frontal bone (forming the forehead and the brows), the maxilla and zygomatic arch (forming the cheeks and inferior orbital rim), the bony and cartilaginous nose, external ears, and mandible. The mandible articulates with the temporal bone anterior to the acoustic canal. The ramus drops inferiorly to the angle of the jaw from which the mandible turns anteriorly and medially with the two halves meeting in the midline to form the chin. The upper and lower teeth contribute to the vertical facial proportions. This bony superstructure is overlaid with muscles and soft tissues, including the lips, which give the face its rounded contours. Mild facial asymmetry is common. The anterior neck is dominated by the thyroid cartilage, which is more prominent in men (the Adam’s apple), the cervical trachea, and the two sternocleidomastoid muscles arising on the mastoid process and inserting on the clavicle and manubrium. The posterior neck is enveloped in thick longitudinal muscles covering the cervical spine from the occiput to the upper back, and the fan-shaped trapezius that forms the posterior lateral contour of the neck.

The Ears

The pinna, or auricle, and the external acoustic canal compose the external ear; the middle ear consists of the tympanic membrane (TM) and the tympanic cavity with its three ossicles. The internal ear, or bony labyrinth, is composed of the cochlea (the organ of hearing) and the semicircular canals (the organ for balance).

The external ear

The pinna or auricle is a flattened funnel with crinkled walls of yellow fibroelastic cartilage. It has a wide external brim that narrows internally to the external acoustic meatus. Several prominent folds are readily identified, although there is considerable individual variation (Fig. 7-2A). The helix originates as the crus, which courses anteriorly and then winds upward, backward, and downward posteriorly to form the funnel’s brim. Above the midpoint of its posterior vertical portion, a fusiform swelling occasionally develops, the Darwinian tubercle. An inner concentric fold, the antihelix, partially surrounding an ovoid cavity, the concha, is divided into an upper and lower portion by the transverse helical crus. From the anterior brim of the funnel, below the crus, the tragus points backward toward the lower concha as a small eminence. From the lower portion of the antihelix, another eminence, the antitragus, points forward across the intertragal notch to the tragus. The deep lower concha forms the external acoustic meatus. At the junction of the inferior limbs of the helix and antihelix is a pendant lobule of adipose and areolar tissue without cartilage, the earlobe.

The external acoustic meatus or canal is approximately 2.5 cm long, extending from the bottom of the concha to the TM (Fig. 7-2B). The lateral one-third of the superficial canal is walled with cartilage; the medial two-thirds runs through the temporal bone. From the concha, the canal forms a gentle S, tending inward, forward, and upward. Approximately 20 mm inside from the concha is a bony constriction in the canal, the isthmus. Ear wax is produced in the cartilaginous canal: it acidifies and protects the epithelium suppressing bacterial overgrowth and capturing particles. The wax is moved to the concha by the outward migration of the canal epithelium.

The middle ear

Within the petrous portion of the temporal bone, the acoustic canal widens to form the tympanic cavity including an attic providing room for movements of the ossicles. Separating the tympanic cavity and the external acoustic meatus is the tympanic membrane (TM), an ovoid biconcave disk slanting across the canal in a plane 35 degrees from the vertical, its posterior superior portion more superficial than the anterior inferior attachment (Fig. 7-2B). The manubrium of the malleus is firmly attached to the inner TM; viewed from outside, the attached portion appears as a smooth ridge forming a radius of the membrane, slanting upward and slightly anterior.

The inner ear

The inner ear, or labyrinth, is contained within the temporal bone adjacent to the middle ear. It consists of the spiral cochlea (the organ of hearing), the semicircular canals, ampullae, utricle and saccule (the organs of balance and position sense of the head), and the acoustic nerve endings of CN VIII. Two windows connect the middle and inner ear: the oval window contains the footplate of the stapes and communicates mechanical vibrations to the inner ear via the scala vestibuli; the round window covers the origin of the scala tympani.

The Eyes

The orbits

The bony orbits are quadrilateral pyramids with bases facing anteriorly and apices pointing backward and medially. Their medial sides are parallel, whereas the lateral walls form a 90-degree angle (Fig. 7-3). Seven bones form each orbit. The orbital roof is formed by the frontal bone and the lesser wing of the sphenoid bone. The medial wall is formed from portions of the ethmoid, maxillary, lacrimal, and sphenoid bones; the front of this wall contains the lacrimal groove for the lacrimal sac. The lateral wall is composed of the zygomatic bone and the greater sphenoid wing. The orbital floor contains the maxillary, palatine, and zygomatic bones. Several foramens open into the orbit. The optic foramen, at the posterior orbital apex within the lesser sphenoid wing, leads into the optic canal containing the optic nerve (CN II), ophthalmic artery, and sympathetic nerves. The superior orbital fissure divides the lesser and greater wings of the sphenoid separating the orbit’s roof from its lateral wall. It carries the orbital branches of the middle meningeal artery, the superior ophthalmic vein, and four CNs: the oculomotor (CN III), the trochlear (CN IV), the first (ophthalmic) division of the trigeminal (CN V-1), and the abducens (CN VI).

The eyelids

The area between the opened upper and lower eyelids is the palpebral fissure (Fig. 7-4); the two angles of the fissure are the lateral (temporal) and the medial (nasal) canthi. In the medial canthus is a small protuberance of modified skin, the caruncle; posterior to the caruncle is a tissue fold, the plica semilunaris. Each lid has a punctum along the nasal aspect of the lid margin. These puncta open into the superior and inferior canaliculi, which meet as the common canaliculus and drain into the lacrimal sac. The upper lid extends superiorly from the superior lid margin to the superior rim of the bony orbit, where its tissue merges with the periosteum. The skin overlying the eyelids is the thinnest skin of the body; it is readily moved and picked up. During elevation, the upper eyelid invaginates between the globe and the upper border of the orbit. The lower lid extends inferiorly from the inferior lid margin to merge with the periosteum of the inferior orbital rim; the lower lid is shorter and does not infold. Extension of edema fluid into or from the orbit is limited by the lids’ firm attachments to the orbital rim. Within the lids are circular fibers of the orbicularis oculi muscle, supplied by the facial nerve (CN VII). The upper lid also contains the vertical tendons of the levator palpebrae superioris muscle, which originates in the optic foramen and inserts into the tarsal plate; the levator palpebrae is innervated by the oculomotor nerve (CN III). Posterior to the levator in the upper lid is Müller muscle which is innervated from the cervical sympathetic chain. The lids are stiffened by transverse dense plaques of connective tissue, the tarsal plates, which are adherent posteriorly to the palpebral conjunctiva. The lids contain modified sebaceous glands, the meibomian glands, that empty through pinpoint openings in the lid margins. At the junction of the conjunctiva and skin on the lid margins is a double row of eyelashes with their hair follicles. The hairs are deeply pigmented and curve outward. Deep to the temporal side of the upper lid, beneath the frontal bone, lies the lacrimal gland that produces tears that flush the conjunctival surfaces. There are many accessory lacrimal glands within the conjunctiva that provide baseline tear production. The epicanthal fold is a semicircular, vertical skin fold over the nasal aspect of the lids, partially covering the medial canthus. It is present in approximately 20% of the newborn white children, but it disappears by the age of 10 years in all but 3%. The epicanthus must be distinguished from a horizontal skin fold in Asian patients that originates in the upper lid and overhangs the superior lid to a variable degree.

The conjunctiva and sclera

The palpebral conjunctiva joins the skin at the lid margins. It follows the inner lid surface into the superior and inferior fornices. Although firmly attached to the tarsal plates, it is quite loose in the fornices permitting movement of the globe. At the fornices, the conjunctiva is reflected to cover the sclera as the bulbar conjunctiva. The larger episcleral vessels are, normally, visible peripherally through the transparent bulbar conjunctiva; they may be moved by sliding the conjunctiva over the sclera. The conjunctiva is firmly attached to the sclera at the corneal limbus. The epithelial surface of the cornea is produced from limbal stem cells and is different from the epithelium of the conjunctiva. The superficial vessels of the bulbar conjunctiva run radially in tortuous courses (Fig. 7-31). The deeper vessels are not individually visible; they radiate near the limbus. Commonly a raised horizontal yellow plaque, the pinguecula, results from sun damage to the conjunctival elastic tissue; it is located on either side of the limbus within the interpalpebral fissure.

The cornea

The cornea and anterior eye structures are best examined by slit lamp which allows examination of individual cell layers. The clear convex cornea is composed of five transparent avascular layers. The diameter of the adult cornea is approximately 12 mm. Through it can be seen the anterior chamber, iris, pupil, and lens. The junction of the cornea with the sclera is called the limbus. The anterior chamber is the space between the endothelial surface of the cornea and the anterior surface of the iris. It is filled with aqueous fluid produced by the ciliary body that drains peripherally through the anterior chamber angle at the circumferential junction of the iris and the cornea.

The sclera

The globe beneath the bulbar conjunctiva is covered by a tough, dense, avascular fibrous coat, the sclera. It is china white except for spots of brown melanin, varying in number with the individual’s complexion and race. The sclera is pierced by the scleral foramen, for the optic nerve, the long ciliary arteries and nerves, the short ciliary nerves, and the venae vorticosae. The tendons of the ocular muscles insert into the sclera.

The iris and pupil

The iris is a muscular diaphragm composed of a radial dilating muscle, the dilator pupillae, and a central, circumferential muscle, the sphincter pupillae. These muscles work in concert to control the aperture of the iris, the pupil, in order to regulate the amount of light that passes through the lens to the retina.

The lens

The lens is a flexible transparent structure behind the iris which focuses light on the retina. The anterior and posterior lens’ surfaces are convex; the junction of the two curved surfaces is the equator. The lens is suspended at its equator by the zonula ciliaris which inserts into the ciliary body (Fig. 7-5). When the eye is at rest for distant vision, the ciliary muscle relaxes increasing tension on zonula peripherally which flattens the flexible crystalline lens centrally and decreases its refractive power of the lens. During near focus the ciliary muscle contracts decreasing the tension on the zonules allowing the elastic lens to become more spherical and thicken centrally, which increases the power of the lens; this process is accommodation.

The vitreous body

The clear, gelatinous tissue behind the lens is the vitreous. Anteriorly, the vitreous is attached in a circumferential fashion to the peripheral pars plana and retina (vitreous base), and posteriorly it is attached to the optic nerve head, vessels, and macula. The vitreous partially liquefies with age. Traction at the vitreous base can tear the retina, allowing liquid vitreous into the subretinal space causing a retinal detachment. The vitreous also provides a scaffold for fibrous tissue and proliferating blood vessels in ischemic retinal disease, which can contract and tear the retina.

The retina, choroid, and optic nerve

To understand the anatomy of the posterior ocular segment, consider the structures from the inside out. The retina loosely lines the inside of the globe, attaching anteriorly to the peripheral ciliary body at the pars plana. The nerve fiber layer of the retina coalesces to form the optic nerve, which runs through a lattice-like opening in the posterior sclera, the lamina cribrosa, to exit the globe. The central retinal artery and vein run within the optic nerve, branching out on the retina to form a superior and inferior temporal arc around the macula. The center of the macula, the fovea, allows the eye to have detailed vision. The nasal vascular arcades supply the nasal retina, which provides indistinct temporal peripheral vision. The deepest retinal structure, the retinal pigment epithelium, shuttles nourishment and waste between the overlying retinal ganglion cells and underlying choroid containing the net-like blood vessels. External to the choroid is the fibrous sclera.

The Nose

The external nose is a triangular pyramid with one side adjoining the face (Fig. 7-6). The upper angle is the root, connected with the forehead. The two lateral sides join in the midline to form the dorsum nasi; its superior portion is the bridge of the nose. The free angle or apex forms the tip of the nose. The triangular base is pierced on either side by an elliptic orifice, the naris (plural nares), separated in the midline by the columella, which is continuous internally with the nasal septum. Still hairs, the vibrissae, line the margins of the nares to inhibit inhalation of foreign bodies. The lateral nasal surface ends below in a rounded eminence, the ala nasi (plural, alae nasi).

The upper third of the lateral nasal wall is supported medially by the nasal bone and laterally by the nasal process of the maxilla. The lower two-thirds is supported by a framework of lateral cartilage, the greater alar cartilage, and several lesser alar cartilages. The nasal passages are separated anteriorly by the cartilaginous nasal septum and posteriorly by bone, the vomer.

The nasal septum divides the nasal cavity into symmetrical air passages. Each passage begins anteriorly at the naris (Fig. 7-7) and widens into a vestibule before passing into a high, narrow passage that communicates posteriorly with the nasopharynx by an oval orifice, the choana. The septum is a vertical plane, whereas the lateral nasal surface has three horizontal, parallel, downward curving bony plates, the superior, middle, and inferior turbinates or conchae. The mucous membranes of the inferior turbinate are highly vascular and semi-tumescent: vasoconstrictor drugs reduce blood flow thereby decreasing tumescence. Under each turbinate is a groove, the superior, middle, and inferior meatus. Superior and posterior to the superior turbinate is the opening of the sphenoid sinus. The superior meatus contains the orifices of the posterior ethmoid cells. The middle meatus receives drainage from the maxillary sinus, the frontal sinus, and the anterior ethmoid cells. The inferior meatus contains the orifice of the nasolacrimal duct. The auditory (Eustachian) tube opens into the nasopharynx just behind and lateral to the choana at the level of the middle meatus. In the posterior nasopharynx is an aggregation of lymphoid tissue, the pharyngeal tonsil, or adenoids.

The endings of the olfactory nerve (CN I) are located high in the nasal chamber, above the superior turbinate. A vascular network on the anterior nasal septum called Kiesselbach plexus is noteworthy because it is the site of most nosebleeds.

The Mouth and Oral Cavity

The mouth is surrounded by two fleshy lips; the vermillion border marks the transition from cornified epithelium of the skin to the noncornified squamous epithelium of the mouth. The philtrum is a vertical groove from columnella downward to vermilion border of the upper lip. Contraction of the orbicularis oris, a circular band of muscle surrounding the mouth and innervated by the facial nerve (CN VII), closes and protrudes the lips. Each lip is anchored to its adjacent gum by a fold of mucosa, the labial frenulum. The oral cavity is a short tunnel with an arched roof formed by the hard and soft palate, walls of the cheeks and lateral teeth, and with a floor formed by the tongue. The lips and teeth are separated by a shallow vestibule. The tunnel’s exit is the isthmus faucium between the faucial pillars; it opens into a vertical passage, the oropharynx, continuous superiorly with the nasopharynx.

The anterior two-thirds of the roof is formed by the hard palate, comprises maxilla and palatine bone covered by mucosa with a median raphe. A fold of mucosa and muscle, the soft palate, continues the roof posteriorly. It hangs free forming a curtain in the isthmus faucium. From the midline of its free border is suspended the conical or bulbous uvula. The lateral border of the soft palate splits into two vertical folds, the tonsillar pillars. Between the anterior and posterior pillars lies the palatine tonsil, a mass of lymphoid tissue containing deep crypts or clefts. Similar lymphoid tissue lies in the base of the tongue, the lingual tonsil.

The teeth

Upper and lower semicircles of teeth are set in the maxilla and mandible. The bony dental ridges and necks of the teeth are covered by tough fibrous tissue and mucosa; the gums. The gum borders are called the gingival margins.

A child develops 20 deciduous teeth: from the midline on each side, uppers and lowers, there are two incisors, one canine, and a first and second molar. Gradually, these teeth are lost that are to be replaced by permanent teeth with the addition of a first and second premolar or bicuspid and a third molar, making a total of 32 (Table 7-1). Dentists use a universal numbering system starting with the right upper third molar as 1 and counting left to the opposite upper third molar as 16, then continuing down to the left lower third molar as 17 and counting right to 32 at the mandibular third molar. The eruption times of various teeth are shown in Table 7-1.

The tongue

The tongue lies within the horseshoe curve of the mandible; its dorsal surface forms the floor of the oral cavity. The tip or apex is thin and narrow, resting against the lingual surface of the lower incisors. Posteriorly and inferiorly is the root, composed of muscle masses and their bony attachments. The tip and dorsal surface of the tongue is the visible portion of a much larger muscular mass. The extrinsic muscles extend between the symphysis mentis of the mandible, the hyoid bone, and the styloid process of the temporal bone; they cause protrusion and retraction of the tip, convex and concave curving of the dorsum, and move the root upward and downward. The intrinsic muscles alter the length, width, and curvature of the dorsal surface. The lingual muscles are innervated by the hypoglossal nerve (CN XII).

The tongue is free at its tip, dorsum, sides, and anteroinferior surface (Fig. 7-8). A midline fold of mucosa, the lingual frenulum, attaches the tongue to the floor of the mouth and the lingual surface of the lower gum. Near its base, the frenulum swells to form twin eminences, the carunculae sublingualis, each surmounted by the orifice of a submandibular duct (Wharton duct). Running from the carunculae laterally and posteriorly around the tongue base is a ridge of mucosa, the plica sublingualis, punctured at intervals by the duct orifices from the sublingual gland, lying deep to the ridges.

The dorsum of the tongue extends from its tip to the epiglottis. The median sulcus bisects the dorsum from tip to the posterior third, where it ends in a depression, the foramen cecum, at the closure site of the embryonal thyroglossal duct. A sulcus terminalis extends forward and laterally from either side of the foramen cecum to form a V whose apex is posterior. Slightly anterior and parallel is another V formed by a row of 8 to 12 vallate papillae. The vallate papillae are round, discrete eminences with concentric fossae. The anterior two-thirds of the dorsum is textured like velvet by microscopic filiform papillae. These papillae catch desquamated cells, bacteria, and particles of food to form the coating of the normal tongue. Scattered among the filiform papillae, at the tip and sides of the tongue, are the less numerous fungiform papillae. They are readily identified with the unaided eye as large, raised, rounded, and deeper red. Microscopic taste buds are numerous in the vallate and fungiform papillae, on the sides and back of the tongue, in the soft palate, and on the posterior surface of the epiglottis. The sensory root of the facial nerve (CN VII), via the chorda tympani, supplies the taste buds in the anterior two-thirds of the tongue; the posterior third is innervated by the glossopharyngeal nerve (CN IX).

The Larynx

The larynx is immediately behind and below the oral cavity; the epiglottic tip is often visible through the mouth. Because the larynx is on the anterior wall of the pharynx with the sloping plane of its rim facing posteriorly, it is easily viewed by a laryngeal mirror held behind it (Fig. 7-9). The laryngeal apparatus may be visualized as three parallel stacked incomplete rings, one atop the other, held together by ligaments. Topmost is the arched hyoid bone, which opens posteriorly; suspended below are the arched thyroid cartilage, which also opens posteriorly and the cricoid cartilage, which is a complete ring affixed to the tracheal rings below. Although these structures are practically subcutaneous and palpable in the neck, their openings are posterior and well protected.

The ability to phonate depends on the shape, position, and action of the two arytenoid cartilages (Fig. 7-10). Each is a three-sided pyramid with a triangular base. The base is slightly concave to glide on a convex joint surface on the posterior rim of the cricoid cartilage, the cricoarytenoid joint, which is surrounded by a capsule. The two pyramids stand erect on either side of the midline of the cricoid. Muscles pull on the various faces of the pyramids, causing their bases to rotate in the joints. The apex of each pyramid is surmounted by a horizontal crescent of small cartilages and ligaments pointing medially toward its opposite and curving anteriorly. From the curve of each crescent, a tough fibroelastic band, the true vocal cord (vocal fold), extends forward to the midline of the thyroid cartilage. The two vocal cords thus form an opening into the trachea, the rima glottidis. When open, the rima is an isosceles triangle, with apex anterior beneath the epiglottis and base posterior, formed by the tissue bridge between the two arytenoid crescents. Rotation of the arytenoids brings the legs of the triangle together posteriorly to approximate the cords over their entire length, closing the airway.

Lateral, parallel to, and above the true cords is a pair of tissue folds, the false vocal cords (ventricular folds). A membrane covers the epiglottis and continues around posteriorly to envelop the crescents of the arytenoids, forming the aryepiglottic folds. Because the larynx protrudes slightly from the anterior pharyngeal wall, several pockets are formed: two valleculae between the epiglottis and the base of the tongue, and two piriform sinuses, one on either side of the cricoid. Most of the intrinsic muscles of the larynx are supplied by fibers of the recurrent laryngeal nerve; a branch of the vagus nerve (CN X).

The Salivary Glands

Parotid glands

This is the largest salivary gland. Normally, it is not palpable as a distinct structure, but its location and extent must be known to recognize parotid enlargement (Fig. 7-11). A superficial portion lies subcutaneously extending from the zygomatic arch superiorly to the angle of the mandible inferiorly and from the external auditory canal posteriorly to the midportion of the masseter muscle anteriorly. A tail portion wraps around the angle and horizontal ramus of the mandible in the upper neck, and a deep lobe extends from the tail medial to the stylomandibular ligament and styloid muscles. The parotid (Stensen) duct is approximately 5 cm long and runs forward horizontally on the superficial surface of the masseter muscle, approximately one fingerbreadth below the zygomatic arch, in a line drawn from the inferior border of the concha of the ear to the commissure of the lips. At the masseter’s anterior border, it pierces the buccinator muscle to reach its orifice in a papilla on the buccal mucosa opposite the upper second molar.

Submandibular glands

Approximately the size of a walnut, the gland lies medial to the inner surface of the mandible; its lower portion can be palpated beneath the inferior mandibular border somewhat anterior to the angle of the jaw. The submandibular (Wharton) duct is about 5 cm long; it runs upward and forward to the floor of the mouth, where its orifice is crowned by the caruncula sublingualis, beside the lingual frenulum.

Sublingual glands

The smallest of the glands, it lies beneath the floor of the mouth, near the symphysis mentis. It empties through several short ducts, some with orifices in the plica sublingualis, some entering the submandibular duct.

The Thyroid Gland

Knowledge of thyroid embryology is necessary to understand thyroid disorders. A median diverticulum, evaginating from the ventral pharyngeal wall (the future foramen cecum in the tongue), goes downward and backward in front of the trachea as a tubular duct (the thyroglossal duct), bifurcating and further dividing into cords that later fuse to form the thyroid isthmus and lateral lobes. Normally, the thyroglossal duct is obliterated, but remnants may persist in the adult to form thyroglossal sinuses or cysts. At the duct’s superior end, a normally functioning lingual thyroid gland may form. Inferiorly, ductal tissue frequently forms a pyramidal lobe arising from the isthmus or a lateral lobe, usually the left. The pyramidal lobe may ascend in front of the thyroid cartilage as high as the hyoid bone. Occasionally, a normal glandular component, such as the isthmus or lateral lobe, may fail to develop. Rarely, the lingual growth may be the only active thyroid tissue in the body.

The thyroid is the largest endocrine gland. It consists of two lateral lobes whose upper halves lie on either side of the projecting prow of the thyroid cartilage; the lower halves are at the sides of the trachea (Fig. 7-12). A flat band of isthmus passes in front of the upper tracheal rings, joining the lateral lobes at their lower thirds. The major outline of the gland is trapezoidal, with a parallel top and bottom, and with the sides converging downward. The normal adult gland weighs approximately 25 to 30 g; it is slightly larger in the female. Each lateral lobe is an irregular cone approximately 5 cm long; the greatest diameter is approximately 3 cm, the thickness approximately 2 cm. The right lobe is, normally, one-fourth larger than the left. The lateral posterior borders touch the common carotid arteries. Usually, on the posterior lateral surfaces are the parathyroid glands. The recurrent laryngeal nerves lie close to the medial deep surface. Each lobe is covered anteriorly by the respective sternocleidomastoid, whereas the isthmus lies on the tracheal rings and is practically subcutaneous. Pairs of superior and inferior thyroid arteries supply an exceedingly vascular parenchyma. The gland is firmly fixed to the trachea and larynx, so that it ascends with them during swallowing; this movement distinguishes thyroid structures from other masses in the neck. The thyroid actually lies in the upper anterior mediastinum. Enlargement by downward growth extends behind the sternum, a retrosternal goiter. The thymus gland also occupies the anterior mediastinum. Thus, a tumor of the anterior mediastinum may arise from either gland.

Examination of the Scalp, Face, and Skull

Examination is by inspection and palpation. Inspect for asymmetry of the skull, ears, eyes, nose, mouth, jaw, and cheeks. Use a tongue blade in the sagittal plane from the midline of the glabella to the midline of the lips to detect nasal deformity. Observe the position of the ears, viewing from the front. Note any masses or deformities. Inspect the skin of the scalp by displacing the hair sequentially to reveal the roots. Inspect for actinic changes and lesions on the sun-exposed skin, especially the helix of the ear, the temples above the zygoma, the forehead, cheeks, and lips. Gently palpate the skull for irregularities. Run a fingertip around the orbital rim and along the zygoma on each side. Palpate the ramus, angle, and arch of the mandible.

Examination of the Ears, Hearing, and Labyrinthine Function

The ears

Pinna

Inspect the pinna for size, shape, and color. Note discharges from the meatus. Palpate the consistency of the cartilages and any swellings. Assess for pain with movement of the pinna and tragus.

External acoustic meatus

Prepare the canal for inspection by taking time to clean it properly. Remove liquid material with a cotton applicator. Remove solids through an ear speculum with either a cotton applicator or a cerumen spoon under direct vision. Use a speculum attached to a lighted otoscope or a speculum and a headlamp. Select the largest speculum that will fit the cartilaginous canal. Tip the head toward the opposite shoulder to bring the canal horizontal. Insert the speculum while retracting the pinna upward and backward for adults so that the flexible cartilaginous canal aligns with the axis of the bony canal; use downward traction for infants and young children (Fig. 7-13). The lining epithelium of the bony canal is very sensitive, so be gentle.

TM and middle ear

When light shines on the TM, it reflects a brilliant wedge of light, the light reflex, whose apex is at the center or umbo with its legs extending radially in the anterior inferior quadrant of the membrane, approximately at a right angle to the manubrium. Examine the normal landmarks of the drumhead: the manubrium of the malleus that forms a smooth ridge from the umbo or center and runs radially upward and forward toward the circumference and ends in the knob of the short process; the two mallear folds, diverging from the knob to the periphery; the shadow of the incus, often showing through the membrane in the upper posterior quadrant; and, finally, look carefully around the entire circumference of the annulus for perforations just inside its border. Note the color and sheen of the membrane, which should be shiny and pearly gray. Serum in the middle ear colors it amber or yellow and air bubbles may be seen; pus shows as a chalky white membrane; blood appears blue. Note changes in the definition of the manubrium; a bulging membrane makes the landmarks indistinct or completely obscures them completely. Inadequate auditory (Eustachian) tube function produces retraction of the membrane sharpening the outline of the manubrium and mallear folds. With either bulging or retraction the light reflex will be distorted or absent. When the incus is visible through the membrane, a normal middle ear is fairly certain.

Rough quantitative test for hearing loss

Difficulty understanding spoken questions during history taking may alert you to hearing loss. Test with the whispered voice at the patient’s side approximately 60 cm (2 ft) from his/her ear. Cover the far ear and whisper test numbers that the patient should repeat or whisper questions that cannot be answered yes or no. Test with loud, medium, and soft tones. Alternatively, use the same intensity for all tests and find the maximal distance from the ear at which the whisper may be understood. Hearing acuity may be tested with a tuning fork with a frequency from 256 to 1024 cycles per second; the 128-cycle fork for testing vibratory sense is too low pitched.

Distinguishing neurosensory and conductive hearing loss

Use a tuning fork with frequencies of 256 to 1024 cycles per second. Set the fork in motion by gently tapping the base of the other hand. The Weber test (Fig. 7-14A). Place the handle of the vibrating fork against the midline of the skull and ask the patient whether the sound is louder in one ear than in the other. With normal neurosensory hearing and no conductive loss, the sounds are equal in both ears. The Rinne test (Fig. 7-14B) is done in each ear sequentially. First, press the tuning fork against the mastoid process (bone conduction) and then place the tines near the ear canal (air conduction). Ask, if it was louder behind the ear or at the ear canal. When air conduction is louder than bone conduction, the test is arbitrarily said to be Rinne-positive, a normal result. The test is Rinne-negative when bone conduction is louder than air conduction. Have the patient indicate when they can no longer detect the sound by air conduction; see if you can hear the vibrating fork to compare their hearing to yours.

Testing Labyrinth Function

Testing vestibular function: test for positional nystagmus, the Dix–Hallpike maneuver

Have the patient sit on the examination table and inspect the eyes carefully for spontaneous nystagmus. Then, keeping the eyes open, have the patient lie supine with the head extending beyond the end of the table, the chin elevated approximately 30 degrees and the head turned 45 degrees to the right. Observe the eyes for 30 seconds looking for nystagmus. Return the patient to the sitting position. After a short rest, repeat the test with the head turning to the left. Have the patient sit up and inspect the eyes for 30 seconds. A positive test induces nystagmus, often accompanied by intense nausea. The slow component of the nystagmus is in the direction of the endolymph flow; the nystagmus is named for its fast component. Test for Past Pointing. Have the patient sit facing you, pointing his forefingers toward you with his eyes closed (Fig. 7-15). Place your forefingers lightly under his and hold them there. Ask the patient to raise his arms and hands, and then return his fingers to yours. Normally, this maneuver can be performed accurately. Past pointing indicates either loss of positional sense or labyrinthine stimulation. Romberg Test for Falling: Have the patient stand with the heels and toes close together (Fig. 7-16). Assure the patient that you will not let him fall, and be prepared to catch him should he fall. Have the patient close his eyes and observe for several seconds. Normally, patients will be steady, even with gentle, forewarned, pushes on the trunk. Falling during the test is the Romberg sign.

Examination of the Eyes, Visual Fields, and Visual Acuity

Examine the palpebral fissures and position of the globe

From a distance, note the width and symmetry of the palpebral fissures. Look for protrusion or recession of one or both globes by inspecting the eyes from the front, from the profile, and from above (looking downward over the forehead), or from below (looking up over the cheekbones). A Hertel exophthalmometer accurately measures the distance from the outer edge of the bony orbit to the anterior surface of the cornea. This can be used to document suspected proptosis (protrusion) of an eye. Individual variation is great, and there are familial and racial trends toward proptosis. Pathologic exophthalmos is likely if a series of accurate shows progressive anterior displacement.

Inspect for inflammation

Inspect for redness and or swelling: Is it in one or both eyes? Does it involve the eyelid and/or the ocular surface?

Test for lid lag, lid retraction, and scleral show

Use your finger or a penlight as a target. Start above eye level, approximately 50 cm (20 inch) away, moving the target slowly and repeatedly up and down in the midline (Fig. 7-17). A lag is indicated by the upper lid lagging, often in a ratcheting pattern, behind the upper limbus, allowing the white sclera to appear between lid margin and limbus. Lid retraction is the dynamic elevation of the upper lid on gaze at an object, and scleral show a more constant exposure of the upper sclera. The inferior sclera may be seen below the limbus in normal individuals depending on the anatomy of their orbit and midfacial architecture.

Tests for Strabismus (Heterotropia): Be sure that the patient has useful vision in each eye.

Cover–uncover test

Ask the patient to fix gaze on an object at the end of the room, or at a near target such as the examiner’s nose. First, cover the patient’s left eye with your right hand (Fig. 7-18). Watch the uncovered right eye to see if it moves to take up fixation. Uncover the left eye and allow the patient to look with both eyes. Then cover the right eye watching the uncovered left eye to see if it moves to fixation. If there is fixation movement, the patient has heterotropia (strabismus, squint). A constant misalignment of this type is known as manifest deviation or tropia.

Alternate cover test

While the patient is holding visual fixation, alternately and repeatedly swing to cover each eye in sequence. If the eyes start to alternately move to pick up fixation when they are uncovered, but they did not have a manifest deviation by the first cover/uncover test, then they were initially aligned by the central nervous system’s ability to fuse the image, but have a latent deviation uncovered by breaking that fusion. This latent misalignment is also known as a phoria. This is also demonstrated by having the patient fix on the object with both eyes; cover one eye for a few seconds, then uncover it while observing to see if it moves to reestablish fixation. If there is fixation movement, the eye has heterophoria.

Naming the deviation

If the eye swings inward to pick up fixation, it was initially deviated outward (exotropia or exophoria). If the eye swings outward, it was initially deviated inward (esotropia, esophoria).

To determine if the heterotropia is comitant or incomitant, ask the patient to follow your penlight in the six cardinal directions of gaze. If the eyes move equally without restriction, the deviation is comitant. If one eye over-shoots and the other fails to look the entire distance in one or more directions, the deviation is incomitant and may represent either a paralytic or restrictive misalignment. A paralytic misalignment is pathological and could represent ischemia (stroke) or compression (tumor); restrictive misalignments can be caused by scarring or by fibrosis, as seen in thyroid eye disease.

Examination of the eyelids

Look for swelling about the lids, above, below, and near the canthi. Note inversion or eversion of the lid margins. Examine the lid margins for scaling, normal secretions, exudate, papules, or pustules. Look for lashes turned inward (trichiasis). Press on the lacrimal sac; if fluid can be expressed through the punctum, the tear duct is obstructed.

Examination of the bulbar conjunctiva and sclera

Gently retract the lids with the thumb and forefinger. Note the color of the sclera, any pigment deposits, vascular engorgement, or vascular pterygium (versus the avascular pinguecula).

Examination of the palpebral conjunctiva

To evert the lower lid (Fig. 7-19A) place the thumb tip on the loose skin beneath the lid margin and slide the skin down, pressing it gently into the orbit) and ask the patient to look up. Look for congestion, discharge, and other lesions. If indicated, evert the upper lid (Fig. 7-19B). Face the patient asking her to look downward and keep both eyes open to prevent elevation that accompanies lid closure. Pinch the lashes of the upper lid and pull it gently downward and away from the globe. Press the tip of an applicator against the upper lid just above the tarsal plate. Using this as a fulcrum, pull the eyelid quickly upward so that the tarsal plate everts. After the lid has been everted, stabilize it with the fingers. Have the patient glance upward to return the lid to its normal position.

Examination of the cornea

Shine a light obliquely on the cornea to search for scars, abrasions, or ulcers. The corneal light reflex should look smooth and regular as you play the light over the surface. Abrasions are readily demonstrated by fluorescein staining. Place the tip of a moistened fluorescein strip in the inferior fornix. After removing it, ask the patient to blink. Observe with a blue light; corneal abrasions appear green. The cornea may also be examined with a lens.

Examination of the iris, pupils, and lens

Note the clarity of the iris, whether it appears distinct or muddy. Look for new vessels and deposits. Note the size, shape, and equality of the pupils. Test the pupil’s reaction to light by having the patient fix on a distant object (>3 m [10 ft] away). Shine a light into the right pupil from the side (Fig. 7-19C) while observing the direct pupillary reaction; remove the light and repeat the process on the left eye. Now swing the light back to the right eye but continue to observe the left pupil. In a normal eye, as the flashlight is swung toward the right eye from the left, there is a minimal dilatation followed by constriction of the left pupil, the normal consensual reaction. Repeat the latter process this time observing the right pupil for the normal dilation followed by constriction as the light is moved back to the left eye. This is the swinging light test for a relative afferent pupillary defect (RAPD). Test pupillary reaction to near point by having the patient fix on his/her own finger as it is gradually brought closer to his/her nose. Shine the penlight obliquely through the lens to discover deposits on the surface and opacities in the matrix such as cataracts.

Schirmer test of tears

A thin strip of filter paper is folded over the lower eyelid without anesthesia. Wetting extending less than 10 mm after 5 minutes indicates decreased tear formation, keratoconjunctivitis sicca (Fig. 7-33D).

Examination with the ophthalmoscope

Ophthalmoscopic examination requires considerable practice in order to obtain useful information. Examine the right eye observing with your right eye and using your right hand to manipulate the ophthalmoscope; examine the left eye using your left eye with the ophthalmoscope in your left hand (Fig. 7-20). Undilated examination of the right eye is described. Grasp the instrument with your right hand, your forefinger on the disk of lenses. Rest your left hand on the patient’s forehead so that your thumb can pull up the upper lid slightly to uncover the pupil and prevent excessive blinking. Ask the patient to fix her eyes straight ahead on a distant object.

The media

Place the +8 or +10 diopter lens in the sight hole, bring it close to your eye or glasses, and move forward to approximately 30 cm (12 inch) in front of the patient’s eye. Shine the light into his/her pupil to see the red retinal reflex. A dull red or black reflex is produced by diffuse dense opacities. Look for black spots showing against the red; these are the shadows of opacities in the lens or vitreous made by the light reflected from the retina. Move forward or backward until the spots are clearly focused. While watching the opacities, ask the patient to elevate the eyes slightly; if the spots move upward, they are on the cornea or anterior part of the lens; little movement occurs when the location is near the lenticular center; downward movement indicates a location in the posterior lens or vitreous. Vitreous opacities appear more distinct when viewed obliquely with the white optic disk as a background.

The fundus (Plate 11)

Hold the instrument approximately 5 cm (2 inch) from the patient’s eye with your forehead near or touching your hand on the patient’s forehead. The left hand rests on the forehead with the thumb gently retracting and holding the upper lid to prevent excessive blinking. Adjust the lenses to find the optimal focus to view the retina; the setting is governed by the refractive error and the degree of accommodation in both patient and examiner. In the absence of both factors, the best view should be obtained at zero. Minus lenses are required to correct for involuntary accommodation. When a cataract has been extracted without intraocular lens replacement, approximately +10 is needed for correction. High astigmatism cannot be corrected with the spherical lenses of the instrument, you must examine through the patient’s glasses. When the correct setting is found, examine the following regions (Plate 11 and Fig. 7-35A).

Optic disk

The optic disc lies 10 degrees into the nasal retina and slightly inferior to the visual axis. Therefore, angle the ophthalmoscope 10 degrees nasally from the line of sight to be in the vicinity of the optic disc. Note the shape and color of the optic disk. The shape is round or oval vertically. Most of the disk is red-orange, the color imparted by the capillaries around the nerve fibers. The physiologic cup is a pale area in the center of the disk devoid of nerve fibers; it forms a depression whose base is the nonvascular lamina cribrosa. The size and shape of the cup vary greatly in normal eyes. It is measured by the cup-to-disk ratio. If the cup is not circular, the vertical ratio is used. The site of ingress and egress of vessels, called the vessel funnel, also lacks nerve fibers, so it is pale and white. The borders of the disk may merge gradually into the surrounding retina, or they may be sharply demarcated by a white scleral ring. Outside the ring, on the temporal side, a crescent of pigment may occur.

Retinal vessels

The arteries are bright red with a light reflex, the central stripe. Note the width of the reflex stripe. Normally, the veins are wider than the arteries in a ratio of approximately 4:3; they are darker red and lack a stripe. The vessel branching pattern shows great individual variation. As they emerge from the disk, the afferent vessels are true arteries; branches beyond the second bifurcation, approximately 1 disk diameter from the disk margin, are arterioles. Look for sheathing of the arteries. Observe the veins carefully at the arteriovenous crossings for nicking, deviation, humping, tapering, sausaging, or banking. Retinal veins, normally, pulsate; arteries in the retina do not.

Retina

The amount of pigmentation corresponds to the patient’s complexion and race. The retina is thinner in the nasal periphery and therefore paler. Note areas of white or pigment from scarring. Look for hemorrhages and exudates. Express the size of abnormalities in disk diameters. Measure depression or elevation by the diopters of correction required to focus on an arterial reflex in the area.

Macula

The macula is slightly below the horizontal plane of the disk and from 2 to 3 disk diameters to the temporal side of its margin. Examination of the macula is usually fleeting because illumination of this region produces discomfort; examine it last. In the center of the macula, the fovea appears as a small darker red area, set apart from visible vessels. In its center appears a small darker spot, the foveola, whose center gives off a speck of reflected light.

Bedside tests for visual acuity

Gross tests for visual acuity can be made without special equipment. Test a single eye at a time. Show the patient a newspaper or magazine, testing first with the fine print. If this is not perceived, show the larger letters. If the patient fails on large letters, hold up several fingers 1 m (3 ft) away and ask the patient to count them. If the patient cannot count them, determine if the patient can see movements of the hand. Failing this, flash a light beam into the eye, asking the patient to indicate when it appears. Test whether the patient can perceive the direction of the light source.

When gross visual acuity is fair, more accurate tests can be made with the standard Snellen charts. Be sure there is adequate illumination and the appropriate distance to the chart. Determine the smallest line of letters the patient can read without error with each eye, and then with both eyes together. Express the reading as a ratio of the distance at which the test is conducted and the distance at which the line of letters should be read by a normal eye. The distance is expressed in feet or meters; 20/20 ft and 6/6 m are normal. If the patient could only read the line for 40 ft, his/her acuity is expressed as 20/40.

It should always be noted whether the patient’s optical correction (glasses or contact lens) were used. If the visual acuity is abnormal, the potential acuity from an improved optical correction using lenses can be estimated by using the pinhole test. To perform this, a 1-mm hole (or series of holes) is made in a card. The patient is asked to read a Snellen chart through the pinhole. The patient then selects only those rays of light that are in focus. A close approximation to the patient’s best-corrected visual acuity can then be recorded.

Tests for color vision

Ask the patient to identify the colors of objects immediately available. For more precise testing, use a book of Ishihara plates. Remember that color vision is a mixture of red, blue, and green.

Slit-lamp microscopy

Slit-lamp examination is reserved for an experienced user or ophthalmologist. A powerful light is focused in a narrow slit upon the various layers of the cornea, the anterior chamber, the lens, and the anterior third of the vitreous chamber, whereas the objects are examined through a corneal microscope. Accurate inspection of opacities and minute foci of inflammation can be made.

Examination of the Nose and Sinuses

Routinely inspect the nasal profile, contour and symmetry. Test the patency of each naris by closing the other while the patient inhales with the mouth closed. Transilluminate the nasal septum: push the nasal tip upward while a penlight in the other illuminates one naris (Fig. 7-21A); view the transilluminated septum through the opposite nares for deviations, perforations, and masses. Palpate the cheeks and supraorbital ridges over the maxillary and frontal sinuses for tenderness. If abnormalities are found on the screening examination, a more thorough examination is required.

Examination with the nasal speculum

Examine the anterior nasal chambers with a nasal speculum and a head mirror or head lamp. Hold the speculum in the left hand (Fig. 7-21B) so that the right hand is free to position the head or hold instruments. Insert the closed blades approximately 1 cm into the vestibule; open the blades vertically, in the plane of the septum, with the left forefinger anchoring the ala nasi against the superior blade to avoid pressure on the septum. Reposition the speculum and the patient’s head to see each structure. Examine the vestibule for folliculitis and fissures. Note the color of the mucosa and any swelling. Inspect the nasal septum for deviation, ulcer, or hemorrhage. Examine the inferior turbinate on the lateral wall for swelling, increased redness, pallor, or blueness. Identify the middle turbinate; inspect the middle meatus for purulent discharge from frontal, maxillary, and anterior ethmoid sinuses.

Mirror examination of the nasopharynx

A head mirror or headlamp is required for illumination. Warm a No. 0 (small) postnasal mirror in warm water; touch it with your hand to check its temperature. Depress the tongue as described for the oropharyngeal examination, inserting the blade from the corner of the mouth (Fig. 7-22A). Hold the mirror like a pencil, steadying your hand against the patient’s cheek. Insert the mirror from the side opposite the tongue blade; keep the mirror upright, avoiding contact with tongue, palate, and uvula. Position it behind the uvula near to the posterior pharyngeal wall. Turn the mirror upward, focus the light on it, and adjust it to view the choana (Figs. 7-22B and C). Locate the posterior end of the nasal septum, the vomer, in the midline. Identify the middle meatus; pus draining posteriorly from this region comes only from the maxillary sinus. The inferior meatus is not well visualized posteriorly. The orifices of the auditory (Eustachian) tubes are behind and lateral to the middle meatus. The orifice appears pale or yellow and is approximately 5 mm in diameter. The tubes are closed except during swallowing or yawning. Look for the pharyngeal tonsil (adenoids) hanging from the roof into the fossa. Examine for inflammation, exudate, polyps, and neoplasms in the nasopharynx. If available, a fiberoptic instrument will simplify your examination.

Transillumination of the sinuses

Use a cool light in a fully darkened room. For the maxillary sinuses, press a cool light against the each maxilla while observing the hard palate through the mouth for transmitted light. For the frontal sinuses, place the light under the nasal half of the supraorbital ridge while shielding the orbit to the eyebrows. Look for bright areas in the forehead. Asymmetry of transillumination is most significant.

Examination of the Lips, Mouth, Teeth, Tongue, and Pharynx

Inspect using a tongue blade and penlight. Use of headlamp or mirror frees one hand to hold instruments. Completely inspect the oral cavity before beginning palpation.

Lips

Look for congenital and acquired defects. Note the lip color and look for angular stomatitis, rhagades, ulcers, granulomas, and neoplasms. Have the patient attempt to whistle to reveal weakness of the facial nerve (CN VII). Inspect the inner surface of the lips by retracting them with a tongue blade while the teeth are approximated.

Teeth

Note the absence of teeth and the presence of caries, discoloration, fillings, and bridges. Note abnormal shapes, such as notching. Tap each tooth for tenderness.

Gums

Have the patient remove any dental appliances. Look for retraction of the gingival margins, pus in the margins, gum inflammation, spongy or bleeding gums, lead or bismuth lines, or localized gingival swelling.

Breath

Smell the breath for acetone, ammonia, or fetor.

Tongue

Inspection

Have the patient protrude his tongue. Assess its size and note deviation from the midline or restricted protrusion. Examine the dorsal surface coat for color, thickness, and adhesiveness. Have the patient raise the tip to the roof of the mouth; inspect the undersurface, including frenulum and carunculae sublingualis. Palpation. Palpate the accessible portions of a tongue that is painful or has restricted motion for deep-seated masses. Have the tongue inside the teeth when palpating to relax the muscles. While wearing gloves, have the patient open his mouth wide. To avoid having your fingers bitten, push a fold of the patient’s cheek between their teeth. Insert your forefinger to the back of the mouth and palpate the roof of the tongue, the valleculae, and the tonsillar fossae (Fig. 7-23). Palpate the sublingual salivary glands and the submandibular ducts for calculi. If the patient gags readily, spray the throat with a topical anesthesia; otherwise, proceed without anesthesia.

Examination of a lingual ulcer

Dry the ulcer gently with a cotton sponge and then inspect it carefully. Palpate the surrounding and underlying tissue with gloved fingers. The pain from lingual lesions may be referred to the ear.

Buccal mucosa

Retract the cheek with the tongue blade. Look for melanin deposits, vesicles, petechiae, Candida, Koplik spots, ulcers, neoplasms. Examine the orifice of the parotid duct opposite the upper second molar.

Oropharynx

Hold a tongue blade with the thumb underneath and the index finger and long finger on top. The patient should breathe steadily through the nose keeping the mouth open. Have the patient relax the tongue tip behind the lower incisors. Press the midpoint of the tongue downward and forward with the tip of the blade by depressing the middle with the two fingers while the thumb pushes upward on the end (Fig. 7-24A). Pressing farther back causes gagging, whereas pressing anteriorly causes posterior bulging. Steady the other hand with the ring and little fingers on the patient’s cheek. An optimal view may require several placements of the blade transversely at the midpoint. Test for vagal nerve (CN X) paralysis by noting whether the uvula is drawn upward in the midline when the patient says “e-e-e.”

Tonsils

For adequate examination, take a tongue blade in each hand; depress the tongue with one and retract the anterior faucial pillar laterally with the other to disclose the anterior tonsillar surface. Normally, the color of the tonsil matches the surrounding mucosa. Look for hyperplasia, ulcers, membrane, masses, and small, submerged tonsils.

Examination of the Larynx

Mirror laryngoscopy

This has been replaced by the use of flexible fiberoptic instruments, if available. Use a head mirror or head lamp so both hands are free. To use a mirror, seat the patient with a bright light source immediately behind and to the side of the head. Reflect this light with your head mirror; practice is required. Have the patient sit erect with the chin somewhat forward. Seat yourself in front of the patient with your knees outside the patient’s knees. Explain exactly what you are about to do. Have the patient concentrate on breathing softly and regularly through the mouth (Fig. 7-9A). Have the tongue protrude maximally over the lower teeth; with your left hand, wrap a piece of gauze over the tongue, grasp the wrapped portion between thumb and middle finger, bracing your hand against the patient’s upper teeth with the forefinger; pull the tongue gently to the side. Hold a No. 5 (large) laryngeal mirror like a pencil at the midpoint of the handle. Warm the mirror in warm water to avoid condensation; check its temperature on your wrist. Brace your fourth and fifth fingers against the patient’s cheek; insert the mirror from the side, with the face of the mirror downward and parallel to the tongue surface. Move it posteriorly until its back rests against the anterior surface of the uvula. Press the uvula and soft palate steadily upward; to prevent gagging, avoid touching the back of the tongue. Have the patient breathe steadily while you inspect the larynx. While still viewing the vocal cords, ask the patient to say “e-e-e” or “he-e-e” in a high-pitched voice. Sing along with him in the desired pitch and for the proper duration. When viewing in the mirror, remember that upward is anterior, downward is posterior. Examine the vallate papillae, lingual tonsils, valleculae, and epiglottis (Fig. 7-9B). Then look at the false cords, true vocal cords, arytenoids, and piriform sinuses. Finally, observe the true vocal cords during quiet respiration when the rima is tent shaped. During phonation, watch the cords meet in the midline.

Examination of the Salivary Glands

Parotid glands

When fullness is present anterior to the tragus, ascertain whether it is continuous with the inferior mass, as in parotid swelling, or discontinuous, as in swelling of a preauricular lymph node. Swelling from the parotid gland is seen in front of the tragus and earlobe and behind the lower ear, pushing the pinna outward. Have the patient clench his teeth to tense the masseter muscle; palpate against the hard muscle to determine extent, consistency, and tenderness of the mass. Feel for swelling behind the mandibular ramus, which is always present in parotid enlargement. Palpate for calculus in the parotid duct. The normal duct is thick enough to be felt when rolled against the tensed masseter. Inspect the orifice of the parotid duct; while watching the orifice, press the cheek looking for discharge from the duct. With a gloved finger, palpate the orifice and posteriorly for calculus or other mass.

Submandibular glands

It is felt as a swelling under the mandible slightly anterior to the angle of the jaw. Bimanual palpation is done with a gloved finger in the floor of the mouth and the opposite hand under the jaw. The gland has a finely lobulated feel. To test for secretion place cotton gauze under the tongue, have the patient sip lemon juice, and then remove the gauze watching for saliva flowing from each orifice.

Examination of the Temporomandibular Joint

Palpate over the temporomandibular joint (TMJ), anterior to the tragus, while the patient opens and closes the mouth, feeling for clicking or crepitus (Fig. 7-25). Corresponding noises may be heard by placing the bell of the stethoscope over the joint during movement. To elicit joint tenderness, place the tips of your index fingers in each external acoustic meatus. Press forward while the mouth is opened and closed.

Examination of the Neck

Examination of the cervical muscles and bones

In trauma cases or if cervical fracture is suspected, immobilize the patient and obtain X-rays before trying to elicit physical signs. Have the patient’s neck and shoulders uncovered. Face the patient looking for any swellings, especially in the sternocleidomastoideus and the cervical spine. Note any asymmetry of shoulder height and clavicles, or fixed neck posture. Note the range of movement and pain elicited by cervical flexion, extension, lateral bending, and rotation. Palpate the cervical vertebrae and muscles for tenderness, tightness, and masses.

Examination of the thyroid gland

The normal adult thyroid is often not palpable. In a thin neck, the normal isthmus may be felt as a band of tissue that just obliterates the surface outlines of the tracheal rings. A goiter is any enlarged thyroid gland. Inspection. With the patient seated in a good cross-light, inspect the lower half of the neck in the anterior triangles. Have the patient swallow looking for an ascending mass in the midline or behind the sternocleidomastoid. If the patient is obese or has a short neck, tilt the patient’s neck back and have them support their occiput with their clasped hands; ask the patient to swallow while in this posture. Palpation from behind. Place yourself behind the seated patient. Lower their chin to relax the neck muscles. Place your thumbs in back of the neck, curling your fingers anteriorly so long and ring finger tips just touch while resting over the upper tracheal rings (Fig. 7-26A). Have the patient hold some water in her mouth and swallow when asked. Locate the thyroid and cricoid cartilages and tracheal rings. The lateral lobes are on either side of the trachea and will rise under your fingers during a swallow. Feel for tissue overlying the tracheal rings; it is likely to be a hyperplastic thyroid isthmus. Palpate systematically the lower poles of both lateral lobes. During the examination, shift the inclination of the patient’s head to relax the neck muscles, and have the patient swallow to test the adherence of palpated masses to the trachea. Palpate the anterior surface of each lateral lobe through the sternocleidomastoid with the patient’s head slightly inclined toward the side being examined. Occasionally, the thyroid is more easily felt when the neck is dorsiflexed. Palpation from the front. Place the fingers of one hand behind the neck with the thumb on the base of the thyroid cartilage (Fig. 7-26B) pushing the trachea gently away from the midline. The fingers of the other hand palpate behind the opposite sternocleidomastoid for the posterior aspect of the lateral lobe while the thumb palpates the anterior surface medial to the muscle. Having the patient swallow or depress the chin may assist the examination. Palpate the other lateral lobe in the same manner with the tasks of the two hands reversed. Auscultation of a goiter. Use the bell of the stethoscope to auscultate a goiter for a bruit.

Examination of the Lymph Nodes

See Chapter 5.

Examination of the Vascular System

See Chapter 8.

General Symptoms

Headache

See Chapter 14.

Skull, Scalp, and Face Symptoms

Blushing and flushing

Transient dilation of the superficial blood vessels of the head, face, and neck occurs with emotional, pharmacological, or physical stimulation. Flushing is a normal response to exercise, hot environments, and ingestion of vasoactive substances such as alcohol or capsaicin in hot peppers. Flushing is common in patients with rosacea or carcinoid syndrome and in women at the menopause. Blushing is a term usually reserved for flushing associated with embarrassment or self-consciousness.

Pain in the face

Facial pain is usually well localized, indicating the structure involved. In some cases, it may present a difficult diagnostic problem.CLINICAL OCCURRENCE: An anatomic approach to identifying the cause is useful. Sort the likely causes by the structure involved: Nerves: trigeminal neuralgia, postherpetic neuralgia; Blood Vessels: temporal arteritis, cavernous sinus thrombosis; Teeth: periapical abscess, periodontitis, unerupted teeth; Bones: sinusitis, osteomyelitis; Joints: temporomandibular arthritis; Salivary Glands: parotitis.

Trigeminal neuralgia (tic douloureux)

see Chapter 14.

Herpes zoster

See Chapter 6. Sharp burning pain occurs unilaterally in the distribution of one trigeminal nerve branch 2 to 3 days before vesicles appear. Persistent pain after resolution of the skin lesions is postherpetic neuralgia.

Acute suppurative sinusitis, orbital cellulitis

See Suppurative paranasal sinusitis and Orbital cellulitis.

Spasms of the jaw muscles—trismus

See Trismus.

Pain with chewing—masseter claudication

Ischemia of the masseter and/or temporalis muscles is induced by chewing, especially tough meats, and is relieved by rest. The patient may have altered their diet to avoid the pain. Giant cell arteritis should be suspected.

TMJ pain

Symptoms include pain, which may be felt in the ear or temple, clicking, and occasionally locking. Trauma is associated with injury and crepitation. See TMJ pain.

Numb chin syndrome

Invasion of the mental or inferior alveolar nerve causes numbness in the chin. Patients present with a complaint of numbness of the chin; no other symptoms or signs may be present. If a thorough oral examination does not identify a local cause of nerve injury, a search for neoplastic disease is indicated.

Ear Symptoms

Tinnitus

Ringing in the ears or tinnitus is often sufficiently distressing to bring the patient to the physician [Lockwood AH, Salvi RJ, Burkard RF. Tinnitus. N Engl J Med. 2002;347:904–910]. Unilateral tinnitus may be the first symptom of an acoustic neuroma. CLINICAL OCCURRENCE: Outer Ear: Cerumen, foreign body or polyp in the external meatus; Middle Ear: inflammation, otosclerosis, polychondritis; Inner Ear: Meniere disease, syphilis, fevers, suppuration of the labyrinth, basilar skull fracture, acoustic neuroma, trauma; Drugs: Quinine, salicylates, aminoglycoside antibiotics.

Temporary altered hearing

Eustachian tube dysfunction causes the patient to experience mild intermittent pain, a feeling of fullness in the ear, and altered hearing. The patient may hear a popping sound on swallowing or yawning. Inspection of the eardrum may show retraction (Fig. 7-27B).

Earache

The middle ear arises from the first and second pharyngeal pouches. Pain may arise from inflammation of structures in the ear or be referred from other pharyngeal sites, including the thyroid. Although the cause of acute pain in the ear is usually readily discovered, chronic earache may offer considerable challenge to diagnosis. CLINICAL OCCURRENCE: Auricle: Trauma, hematoma, frostbite, burn, epithelioma, perichondritis, gout, eczema, impetigo, insect bites, carcinoma, herpes zoster; Meatus: External otitis, malignant external otitis, carbuncle, meatitis, eczema, hard cerumen, foreign body, injury, epithelioma, carcinoma, insect invasion, herpes zoster, trigeminal neuralgia (CN V3); Middle Ear: Acute otitis media, acute mastoiditis, cholesteatoma, malignant disease; Referred Pain: (through CN V, IX, and X and the second and third cervical nerves) unerupted lower third molar, carious teeth, arthritis of TMJ, tonsillitis, carcinoma or sarcoma of pharynx, ulcer of epiglottis or larynx, cervical lymphadenitis, subacute thyroiditis, trigeminal neuralgia.

Dizziness and vertigo

See Dizziness and Vertigo.

Eye Symptoms

Double vision—diplopia

Perception of two visual images results from abnormalities of refraction or, less commonly, nonconjugative gaze. A careful history should determine the pattern of the symptom (e.g., vertical or horizontal), precipitating activities, the field of vision where the diplopia is apparent, and the head position or gaze that relieves the diplopia. If the patient reports monocular diplopia or diplopia when one eye is covered, the cause is nearly always refractive. Binocular diplopia: see Chapter 14.

Dry eyes

See Keratoconjunctivitis sicca.

Blurred vision

Loss of sharp focus of light on the retina occurs with inability of the eye to accommodate the shape of the lens to near or far vision, or scattering of light as a result of opacities in the cornea, lens, or vitreous. The history is the key to identifying the etiology. Pain in the eye suggests inflammation (keratitis, iritis and uveitis) or acute angle closure glaucoma. Abnormality of the oils in the tear film is a frequent cause of visual aberration. Use of topical and systemic drugs, especially anticholinergics, results in decreased accommodation and dilation of the pupil. Loss of vision in one eye may also be described as “blurred vision,” meaning the vision is less distinct than normal with loss of binocular sight. The pinhole test (Bedside tests for visual acuity) can be used to determine if the blurred vision is refractive [Shingleton GJ, O’Donoghue MW. Blurred vision. N Engl J Med. 2000;343:556–562].

Pain in the eye

Pain in the eye results from inflammation, infection, trauma, and increased intraocular pressure. Inspect the lids, conjunctivae, and sclera for lesions. Careful examination of the cornea, anterior chamber, iris, and retina are mandatory. Always assess visual acuity in each eye. Optimal examination requires an ophthalmologist. CLINICAL OCCURRENCE: Idiopathic: cluster headache; Inflammatory/Immune: hordeolum (sty), chalazion, interstitial keratitis, iritis, iridocyclitis, episcleritis, scleritis, band keratopathy, optic neuritis; Infectious: infective keratitis (herpes simplex, zoster and others), sinusitis (ethmoid, frontal, sphenoid); Mechanical/Trauma: foreign body, corneal abrasion, entropion, glaucoma, eye strain.

Visual loss

Injury or impairment to any portion of the visual pathways can lead to visual loss. Acute loss of vision is a medical emergency (see Monocular visual loss—amblyopia). Chronic progressive loss of vision is common with diseases of the cornea, lens, or retina. Standard tests of visual acuity will quantitate the degree of impairment and formal visual field testing is required. Referral to an ophthalmologist is indicated.

Nose Symptoms

Loss of smell—anosmia

See Anosmia.

Abnormal smell or taste—dysgeusia

This is a common complaint in patients who have loss of smell (anosmia). If it is paroxysmal and associated with behavioral symptoms, it suggests complex partial seizures.

Lip, Mouth, Tongue, Teeth, and Pharynx Symptoms

Sore throat

See syndromes, pharyngitis Oral Syndromes (Lips, Mouth, Tongue, Teeth, and Pharynx).

Soreness of tongue or mouth

Pain or tenderness in the tongue or mouth is a presenting symptom for a number of disorders. Inspection and palpation assist in the differential diagnosis [Drage LA, Rogers RS. Clinical assessment and outcome in 70 patients with complaints of burning or sore mouth symptoms. Mayo Clin Proc. 1999;74:223–228]. CLINICAL OCCURRENCE: No Lesions: tobacco smoking, early glossitis from all causes, menopausal symptom, heavy metal poisoning; Deep Lesions: calculus in duct of submaxillary or sublingual gland, foreign body, myositis of lingual muscles, trichinosis, periostitis of hyoid bone, neoplasm of lingual muscles; Localized Superficial Lesions: biting the tongue, trauma to lingual frenulum, dental ulcer, injury while under anesthesia, foreign body (e.g., fish bone), epithelioma or carcinoma, ranula, tuberculous ulcer, herpes, Vincent stomatitis, leukoplakia, thrush; Generalized Disease: pellagra, riboflavin deficiency, scurvy, pernicious anemia, atrophic glossitis, leukemia, exanthematous disorders, collagen diseases, pemphigus, cicatricial pemphigoid, lichen planus, heavy-metal poisoning, phenytoin, uremia, cancer chemotherapy, drug sensitivity; systemic fungal infections, for example, histoplasmosis; Irradiation: Therapeutic irradiation for head and neck malignancy causes temporary or permanent loss of saliva production. Within 2 to 4 weeks of the beginning of treatment, and lasting 6 or more weeks, patients experience increasing dryness and generalized soreness of the mouth and throat.

Difficult or painful swallowing—dysphagia and odynophagia

A disorder in swallowing is termed dysphagia. With oropharyngeal dysphagia the patient describes difficulty initiating a swallow or choking and coughing with swallowing. With esophageal dysphagia, the patient experiences a sense of obstruction at a definite level when fluid or a bolus of food has been swallowed. Neurogenic dysphagia may be accompanied by regurgitation through the nose. Some varieties of dysphagia may cause localized pain (odynophagia); others are painless. Deglutition involves muscles in both the oropharynx and the esophagus. Pain from the oropharynx is accurately localized, but esophageal pain is dispersed in the thoracic six-dermatome band, presenting as chest pain (see Deep retrosternal or precordial pain and the six-dermatome band and Chapter 9). CLINICAL OCCURRENCE: Oropharynx—Painful Dysphagia from Intrinsic Lesions: glossitis, tonsillitis, stomatitis, pharyngitis, laryngitis, lingual ulcer, carcinoma, pemphigus, erythema multiforme, Ludwig angina, mumps, bee sting of the tongue, angioedema, candidiasis, sometimes Plummer–Vinson syndrome; Painful Dysphagia from Local Extrinsic Lesions: cervical adenitis, subacute thyroiditis, carotid arteritis, infected thyroglossal cysts or sinuses, pharyngeal cysts or sinuses, carotid body tumor, spur in cervical spine, pericarditis; Painful Dysphagia from Systemic Conditions: rabies, tetanus; Painless Dysphagia from Intrinsic Lesions: cleft palate, flexion of the neck from cervical osteoporosis, xerostomia in Sjögren syndrome, and magnesium deficiency; Painless Dysphagia from Neurogenic Lesions: CN-IX or CN-X damage, globus hystericus, postdiphtheritic paralysis, bulbar paralysis, West Nile virus, myasthenia gravis, amyotrophic lateral sclerosis, Wilson disease, syphilis, parkinsonism, botulism, poisoning (lead, alcohol, fluoride); Esophagus—Painful Dysphagia from Intrinsic Lesions: (see Chapter 8 and Chapter 9) foreign body, carcinoma, esophagitis, diverticulum, hiatal hernia; Painless Dysphagia from Intrinsic Lesions: achalasia, congenital stricture, stricture, scleroderma, dermatomyositis; Sjögren syndrome, amyloidosis, thyrotoxicosis; Painless Dysphagia from Extrinsic Lesions: aortic aneurysm, aberrant right subclavian artery (Aberrant right subclavian artery (dysphagia lusoria)), vertebral spurs, enlarged left atrium.

Larynx Symptoms

Hoarseness

See Hoarseness.

Salivary Gland Symptoms

Dry mouth—xerostomia

See Dry mouth—xerostomia.

Neck Symptoms

Pain in the neck

Pain in the neck is a common complaint whose cause is often readily diagnosed by a careful history, palpation of the neck, and examination of the oropharynx. Posttraumatic or postural cervical strain is the most common cause. Each anatomic structure should be palpated systematically. Increased pain with specific movements may be helpful in localizing the source of pain. CLINICAL OCCURRENCE: Neck Pain Increased by Swallowing—Pharynx: pharyngitis, Ludwig angina, inflamed thyroglossal duct or cyst; Tonsils: tonsillitis, neoplasm; Tongue: ulcers, neoplasm; Larynx: laryngitis, neoplasm, ulcer, foreign body; Esophagus: inflamed diverticulum, esophagitis; Thyroid: suppurative or subacute thyroiditis, hemorrhage; Carotid Artery: carotodynia, carotid body tumor; Salivary Glands: mumps, suppurative parotitis; Neck Pain Increased by Chewing—Mandible: fracture, osteomyelitis, periodontitis; Salivary Glands: mumps, suppurative parotitis; Neck Pain Increased by Movements of the Head—Sternocleidomastoid: torticollis, hematoma; Nuchal Muscles: viral myalgia, muscle tension; Cervical Spine: herniated intervertebral disk, spinal arthritis, meningitis, meningismus, craniovertebral junction abnormalities; Neck Pain Increased by Shoulder Movement—Superior Thoracic Aperture: cervical rib, scalenus anticus syndrome, costoclavicular syndrome; Neck Pain Not Increased by Movement—Skin and Subcutaneous Tissues: furuncle, carbuncle, erysipelas; Lymph Nodes: acute adenitis. Deep Veins: septic thrombophlebitis of the internal jugular vein (Lemmiere syndrome); Branchial Cleft Remnants: inflamed pharyngeal cyst; Salivary Glands: duct calculus; Subclavian Artery: aneurysm; Nervous System: poliomyelitis, West Nile virus, herpes zoster, epidural abscess, spinal cord neoplasm; Spinal Vertebrae: herniated intervertebral disk, metastatic carcinoma; Referred Pain: Pancoast syndrome, angina pectoris, and other conditions in the six-dermatome band.

Carotodynia

The patient complains of constant or throbbing pain in the anterior lateral neck intensified by swallowing. It may radiate to the mandible or ear. Symptoms frequently follow a viral pharyngitis with fever. Some patients have profound lassitude. Several relapses may occur within a few months. The carotid bulb is exquisitely tender and may seem enlarged with exaggerated pulsations; the common carotid may be tender as well. Carotid compression causes radiation of pain along the branches of the external carotid to the jaw, ear, and temple (Fay sign). One or both common carotid arteries may be involved. The pharynx and larynx are normal or slightly hyperemic and edematous. The diagnosis is made by demonstrating tenderness of the carotid artery.

Neck fullness

Many patients with a goiter complain of a sense of constriction or fullness in the neck. See Salivary Gland Syndromes.

Scalp, Face, Skull, and Jaw Signs

Scalp wounds

Because the scalp is extremely vascular, scalp wounds bleed profusely. Wounds do not gape unless the galea aponeurotica is lacerated. If gaping is noted, an open skill fracture should be suspected.

Fluctuant scalp mass—hematoma, abscess, fracture

When blood or pus accumulates in the skin or subcutaneous layer of the scalp, it is sharply localized and the mass readily slides over the skull. A boggy, fluctuant mass in the entire adult scalp results from blood or pus in the loose connective tissue under the aponeurosis; the same finding in a young child may also be an evidence of parietal bone fracture. A fluctuant mass bounded by the skull suture lines indicates subperiosteal blood or pus or a depressed fracture. A hematoma under the periosteum usually has a soft center that is plastic, whereas the edges are firm and feel much like a depressed fracture.

Scalp cellulitis

The scalp is tender, soft, and boggy. The infection extends rapidly, causing edema of the eyelids and pinnae; regional lymph nodes are tender and swollen.

Sebaceous cyst (wen)

A common lesion, it is either single or multiple. Arising from the skin, it slides easily over the skull. The mass is firm, nontender, and often hemispheric. If infected, it bleeds easily and may be mistaken for a squamous cell carcinoma.

Scalp mass—lipoma

In the subcutaneous layer it feels smooth and soft; the finger slides around its edges. When it occurs beneath the pericranium, its movement is strictly limited, but the finger can detect a smooth, rounded border.

Parotid enlargement

See Enlarged salivary glands.

Preauricular abscess

Suppuration of the preauricular lymph node produces an abscess that may ulcerate. The swelling is localized, tender, and sometimes warm. The source of infection is in the side of the face, pinna, anterior wall of the external acoustic meatus, anterior third of the scalp, eyebrows, or eyelids.

Masseter muscle hypertrophy

One or both masseter muscles undergo spontaneous hypertrophy producing facial swelling mimicking parotid gland swelling. If the entire mass hardens when the patient clench his teeth, it is muscular.

Redness of the cheeks

Erythema, scaling, pustules, and tenderness in a malar distribution may be because of sunburn, cellulitis, rosacea, seborrheic dermatitis, discoid or systemic lupus erythematosus (SLE), or acne vulgaris.

Forehead wrinkles

Absence of normal transverse furrowing with upward gaze is a sign of hyperthyroidism. Deep wrinkling, with longitudinal furrowing and prominence of intervening tissue is the bulldog skin in pachydermatosis. Unilateral loss of wrinkling results from facial nerve (CN VII) paralysis.

Enlarged adult skull—Paget disease

See Paget disease. In addition to bone pain, the patient may complain that his hats have become too small. The calvarium is large compared with the facial bones. A bruit is sometimes heard in the skull.

Mastoid pain and tenderness—mastoiditis

See Acute mastoiditis.

Skull masses—neoplasms

An osteoma frequently occurs in the outer table of the skull, producing a hard, sessile bony eminence. Hard or soft masses in the cranial bones may be a pericranial sarcoma, carcinomatous metastasis, lymphomas, leukemia, or multiple myeloma.

Trismus

Trismus is the forceful closing of the jaws from spasm of the muscles of mastication. Trismus is common with tetanus, but it has many other causes. Failure of the mouth to open from other causes is far more common. CLINICAL- OCCURRENCE: Local Disorders: impacted third molar, TMJ arthritis, malignant external otitis, lymphadenitis, trigeminal neuralgia, scleroderma, dermatomyositis; Disorders With Widespread Muscle Spasm: trichinosis, rabies, tetany, tetanus, strychnine poisoning, typhoid fever, cholera, septicemia; Cerebral Disorders: encephalitis, epilepsy (transient), catalepsy, hysteria, malingering.

Inability to close the jaw—TMJ dislocation

Because the TMJ is a shallow biconcave surface, it can easily partially sublux or completely dislocate. After a yawn or an upward blow on the chin with the mouth wide open, the jaw cannot be closed. The mandible protrudes and the lower teeth override the upper. There is a depression or pit anterior to the tragus that is more obvious when bilateral; in unilateral dislocation, the pretragal depression occurs only on the affected side. No movement of the mandibular head is felt when palpating through the external acoustic meatus on the affected side.

External ear signs

Earlobe crease

A visible crease extending at least one-third of the distance from tragus to posterior pinna has been associated with a higher rate of cardiac events in the patients admitted to the hospital with suspected coronary heart disease [Elliott WJ, Powell LH. Diagonal earlobe creases and prognosis in patients with suspected coronary artery disease. Am J Med. 1996;100:205–211].

Earlobe nodule: gouty tophus

In long-standing gout, accumulations of sodium urate crystals may occur in the helix and antihelix; they also occur in the olecranon bursa, the tendon sheaths, and the aponeuroses of the extremities. The nodules are painless, hard, and irregular. They may open discharging chalky contents.

Darwin tubercle

A developmental eminence in the upper third of the posterior helix, this condition is harmless. It must be distinguished from acquired nodules, such as tophi.

Other nodules

Nontender nodules may be basal cell carcinomas, rheumatoid nodules, or leprosy. Cartilage calcification is a rare complication of Addison disease.

Hematoma

Trauma or a hemostatic defect results in blood accumulating between the cartilage and the perichondrium. There is a tender, blue, doughy mass, usually without spontaneous pain. Prompt incision and drainage avoids suppuration or cauliflower ear.

Recurring inflammation—relapsing polychondritis

There is inflammation and degeneration of cartilage especially of the pinna, nasal septum, laryngeal cartilages, tracheal and bronchial rings; joint cartilages may be affected. The ear is painful, swollen, and reddened, except over the lobule. Hoarseness indicates laryngeal involvement, blindness may result from involvement of the sclerae, and tinnitus and deafness from middle ear involvement. Rarely, degeneration of the aortic or mitral valve ring produces valvular regurgitation or aortic aneurysm.

Dermoid cyst

A favorite site is just behind the pinna. It is soft and slightly fluctuant.

External Acoustic Meatus Signs

Cerumen impaction

The wax of Native Americans and East Asians is often dry and flakey, and more yellow than amber. Excessive wax production or a narrow meatus leads to impacted cerumen and partial or complete obstruction of the canal. When obstruction is complete, partial deafness results. Tinnitus or dizziness may occur. A partial obstruction may suddenly become complete when water enters the meatus during bathing or swimming. The obstructing wax is easily seen in the external meatus.

Discharge from the ear—otorrhea

Discharge from the ear has many causes. The type of discharge suggests the diagnosis: Yellow Discharge: melting cerumen; Serous Discharge: eczema, early ruptured acute otitis media; Bloody Discharge: trauma of the external canal or longitudinal temporal bone fracture causing TM and external canal laceration; Purulent Discharge: chronic external otitis, perforation of acute suppurative otitis media, chronic suppurative or tuberculous otitis media with or without cholesteatoma.

External otitis

See Acute external otitis.

Dermatitis

Seborrheic dermatitis commonly causes scaling and pruritus of the choana and meatus. Medicated eardrops can cause contact dermatitis.

Carcinoma

Either squamous cell or basal cell carcinoma can involve the meatal epithelium. Pain and discharge are the presenting symptoms. In advanced stages, deafness and facial paralysis may occur.

Foreign body

Children often place objects in their ears. A purulent discharge from the canal or an earache may be the first indication.

Polyps

A bulbous, reddened, pedunculated mass arises from the wall or the middle ear. Moving it with forceps may reveal the origin. They cause a foul purulent discharge.

Exostoses and chondromas

Exostoses form nodules in the osseous canal near the TM. They rarely produce obstruction, although the TM may be partially obscured. A single bony osteoma may occur. Rarely, chondromas arise from the cartilaginous canal, usually without obstruction.

Furuncle

A red, tender prominence with or without a pustule forms in the cartilaginous canal producing extreme pain.

Vesicles

Pain in the ear with vesicles in the canal and facial weakness is because of herpes zoster of CN VII (Ramsey–Hunt Syndrome), Chapter 14, Facial Weakness and Paralysis.

TM Signs

Retracted TM

See Otitis Media with Effusion.

Red or bulging TM

See Acute Suppurative Otitis Media.

Vesicles on the TM

Infection with Mycoplasma pneumoniae causes severe ear pain and an inflamed TM with often hemorrhagic vesicles (bullous myringitis).

Perforated TM

A healed suppurative middle ear infection has eroded through the TM leaving an oval hole through which the middle ear cavity is seen. Other than some decrease in auditory acuity, chronic perforations are asymptomatic.

Hearing Signs

Lateralizing Weber test—ipsilateral conductive hearing loss or contralateral neurosensory loss

When neurosensory hearing is intact bilaterally, the sound will lateralize to the side of conductive loss, which loses the masking effect of background noises. Neurosensory loss on one side results in a louder sound on the opposite side. Therefore, lateralization of sound to the right ear means conductive loss on the right or perceptive loss on the left.

Bone conduction greater than air conduction (Rinne-negative test)—conductive hearing loss

When amplification of sound by the TM and ossicles is impaired, direct transmission of vibrations through bone to the cochlea is louder than sound transmitted through air. Conductive hearing loss results from obstruction of the auditory canal, damage to the TM, middle ear fluid, and destruction or ankylosis of the ossicles.

Balance and position Sense signs

See Chapter 14.

Eye Lid Signs

Lacrimation

Lacrimation usually refers to any condition resulting in tears, although strict usage indicates an overproduction. Epiphora means an overflow of tears from any cause. CLINICAL OCCURRENCE: Increased Secretion: weeping from emotion, irritation from foreign body, corneal ulcer, conjunctivitis, coryza, measles, hay fever, poisoning (iodide, bromide, arsenic); Lacrimal Duct Obstruction: congenital, cicatrix, eyelid edema, lacrimal calculus, dacryocystitis; Separation of the Puncta from the Globe: facial paralysis, aging, chronic marginal blepharitis, ectropion, proptosis.

Widened palpebral fissures

The fissures are widened by lid retraction (contraction of Mueller muscle) or protrusion of the globe. With eyes in the primary position the upper lid covers the limbus and a white scleral strip usually shows between limbus and lower lid. Widening of the palpebral fissure uncovers the upper border of the limbus to expose white sclera superiorly. When there is no actual proptosis, widened fissures produce the optical illusion of global protrusion. A few normal persons have widened palpebral fissures.

Exophthalmos (ocular proptosis)

Proptosis is proven by measurement. Unilateral proptosis is recognized by comparing the two eyes. If both eyes seem equally prominent, inspect them in profile (Fig. 7-28). Unilateral proptosis suggests orbital tumor or inflammation. When the globe is displaced medially, disease of the lacrimal gland should be suspected; upward displacement suggests disease in the maxillary sinus; lateral displacement can occur from a lesion in the ethmoid or sphenoid sinus. Graves disease is the most common cause of bilateral proptosis. CLINICAL OCCURRENCE: Unilateral Exophthalmos: Graves disease, mucocele, orbital cellulitis and abscess, cavernous sinus thrombosis, orbital periostitis, myxedema, orbital fracture, hemangioma, orbital neoplasm, arteriovenous aneurysm, fungal infection, histiocytosis; Bilateral Exophthalmos: Graves disease, myxedema, acromegaly, cavernous sinus thrombosis, empyema of the nasal accessory sinuses, lymphoma, leukemia, histiocytosis.

Lid lag

Thyrotoxicosis increases sympathetic stimulation producing contraction of Mueller muscle in the upper lid. Lid lag indicates increased tone even without widened fissures in the primary position. Usually the finding is bilateral; occasionally one fissure is much wider than the other. Other Lid Signs in Hyperthyroidism—Stellwag Sign: infrequent blinking; Rosenbach Sign: tremor of the closed eyelids; Mean Sign: global lag during elevation; Griffith Sign: lag of the lower lids during elevation of the globes; Boston Sign: jerking of the lagging lid; Joffroy Sign: absence of forehead wrinkling with upward gaze, the head being tilted down.

Narrowed palpebral fissures—enophthalmos

The globe is recessed in the orbit. When bilateral, it is usually caused by decreased orbital fat or congenital microphthalmos. Unilateral enophthalmos is caused by trauma or inflammation. Enophthalmos has been described as a sign of Horner syndrome; actually, the accompanying droop of the eyelid merely produces an optical illusion of globe recession.

Failure of lid closure—paralysis of orbicularis muscle

The facial nerve (CN VII) supplies the orbicularis oculi muscle. Damage to CN VII, as in Bell palsy, causes partial or complete paralysis of the orbicularis. When complete, both upper and lower lids remain retracted so the eye is unprotected and tears drain onto the face. Bell phenomenon occurs when the globes elevate during attempted closure of the lids. Failure of lid closure is also present in severe grades of exophthalmos.

Failure of lid opening—ptosis of the lid

The congenital form is usually bilateral from paralysis of or failure to develop the levator palpebrae superioris. The acute acquired condition usually results from disease of the oculomotor nerve (CN III). In the congenital form, the eyelid will show lid lag as the child looks down. With CN III lesion paralysis of other eye muscles may be present.CLINICAL OCCURRENCE: supranuclear lesions (e.g., encephalitis), Horner syndrome, paralysis of the levator muscle, levator dehiscence, thinning of levator tendon (the lid droops but has normal excursion, 15–18 mm).

Blepharospasm

Frequent spasmodic lid closure, either unilateral or bilateral, may progress to the point that it interferes with function. It is a form of focal dystonia. Unilateral disease may follow Bell palsy.

Epicanthal fold—Down syndrome

See Down syndrome.

Shortened palpebral fissures—fetal alcohol syndrome

The combination of shortened palpebral fissures, epicanthic folds, shortened nose with anteverted nostrils, hypoplastic upper lip with thinned vermilion and flattened or absent philtrum, together with mental retardation, is stigmata of fetal alcohol syndrome.

Lid inversion—entropion

Structural changes or muscular contraction turns the eyelashes inward to impinge upon the globe. Spastic entropion occurs only in the lower lid and is caused by increased tone of the orbicularis oculi; the lid turns in only when forcibly closed (Fig. 7-29A). Cicatricial entropion occurs in either lid from contracture of scar tissue, as in trachoma. Irritation from the inverted eyelashes may produce blepharospasm.

Lid eversion—ectropion

The lid turns outward (Fig. 7-29B). Both lids may be affected by spastic or cicatricial ectropion, but paralytic ectropion involves only the lower lid. Senile atrophy of tissues sometimes results in ectropion rather than entropion.

Violaceous lids

Heliotrope or violaceous discoloration of the periorbital skin occurs in dermatomyositis and after chronic quinacrine ingestion.

Lid erythema

Generalized reddening of the lids is nonspecific. Erythema of the nasal half of the upper lid suggests inflammation of the frontal sinus. Disease of the lacrimal sac can cause erythema of the medial lower lid. Hyperemia of the temporal upper lid should suggest dacryoadenitis. The lid is frequently red over a sty.

Lid cyanosis

Blueness of the eyelid occurs from thrombosis of the orbital veins, orbital tumors, and arteriovenous malformations in the orbit.

Lid hemorrhage

Trauma to the lids may result in extravasation of blood into the surrounding tissue, colloquially known as a “black eye.” Palpebral hematoma can occur from nasal fracture. The appearance of hematoma many hours after head trauma suggests a skull fracture; the greater the time interval, the more remote the fracture site. Fractures of the basilar skull may produce hematoma of the lid several days later. Involvement of both eyes is called raccoon sign.

Lid edema

Noninflammatory edema is frequent in acute nephritis, but uncommon in chronic nephritis and cardiac failure (Fig. 7-30A). Lid edema occurs early in the course of both myxedema and Graves ophthalmopathy. Palpebral edema is frequent in angioedema and trichinosis. Contact dermatitis frequently involves the lids; the patient may not react to an allergen on the hands, but when transferred to the lids swelling occurs. Local infections cause inflammatory edema of the eyelids, which is readily identified by finding redness, warmth, and pain. More serious causes are thrombosis of the intracranial sagittal sinus or cavernous sinus.

Xanthelasma

Xanthelasma are raised yellow, painless, and nonpruritic plaques on the upper and lower lids near the inner canthi (Fig. 7-30B). They grow slowly and may disappear spontaneously. They are frequently associated with elevated cholesterol.

Blepharitis

Seborrheic blepharitis is an oily inflammation of the lid margins that produces greasy flakes of dried secretion on the eyelashes and reddening of the lid margins. When ulceration of the lid margin occurs, it is usually staphylococcal blepharitis. Angular blepharitis is a specific disease caused by the diplococcus of Morax–Axenfeld, in which the margins near the temporal canthi are inflamed.

External hordeolum (sty)

When a sebaceous gland of an eyelash hair follicle becomes inflamed, a pustule forms on the lid margin (Fig. 7-30C). It may be surrounded by hyperemia and swelling. Many rupture and heal spontaneously.

Internal hordeolum and meibomian cyst (chalazion)

Acute inflammation of a meibomian (tarsal) gland is termed an internal hordeolum or internal sty. A granuloma of the gland is known as a chalazion or meibomian cyst (Fig. 7-30D). These internal sebaceous gland lesions produce localized swelling that frequently causes a protrusion on the lid. Lid eversion shows hyperemia, a localized cyst or enlarged gland.

Dacryoadenitis

Obstruction of the lacrimal duct produces acute inflammation of the lacrimal gland with pain and tenderness within the temporal edge of the orbit. It must be distinguished from orbital cellulitis and upper lid hordeolum (Fig. 7-30E).

Dacryocystitis

Nasolacrimal duct obstruction leads to inflammation and infection. Patients present with pain and an overflow of tears onto the cheek (epiphora). Symptoms are increased by irritants such as wind, dust, or smoke. Tenderness, swelling, and redness are present beside the nose, near the medial canthus (Fig. 7-30F). The swelling is anterior to the eyelid, distinguishing it from hordeolum. Fluid can be expressed with pressure on the duct. Conjunctivitis, blepharitis, and lid edema may be present.

Eye Movement Signs

See Chapter 14, Eye Movement Signs. Abnormalities of eye movements may be caused by either primary disease of the extraocular muscles or disease of the central nervous system and CNs. For the nonspecialist the ability to distinguish neurologic from primary muscle disease is most critical. Therefore, these signs are discussed with the neurologic examination.

Restriction of motion

Movement of the globe may be restricted in all directions by orbital tumor or the increase in orbital contents with Graves disease.

Glaucoma

See Glaucoma.

Conjunctiva Signs

Subconjunctival vessels

The scleral vessels may be prominent in normal individuals. They run in from the sides (Fig. 7-31A).

Subconjunctival hemorrhage

Bleeding under the conjunctiva is obvious and harmless (Fig. 7-31B). It may be induced by coughing, sneezing, weight lifting, or defecation; frequently, the cause is not apparent.

Conjunctival injection

Mild diffuse capillary hyperemia of the scleral and palpebral conjunctivae, without hemorrhage, is common in the coryza phase of respiratory infections or from exposure to direct sunlight or environmental irritants. It may be mildly uncomfortable. Significant pruritus, pain, or discharge should suggest another disorder such as allergic conjunctivitis.

Conjunctival edema—chemosis

The conjunctiva is swollen and transparent; it is usually associated with edema of the lids. The edema may be demonstrated by looking at the globe in profile while pressing the lower lid against the bulbar conjunctiva; the edge of the lid pushes up a wave of edematous bulbar conjunctiva (Fig. 7-31C). It is frequent in Graves ophthalmopathy.

Hyperemia of the globe and ciliary flush

Bulbar conjunctival injection is the dilation of the radial conjunctival vessels and their branches running from the fornices toward the center of the cornea (Fig. 7-32A). When the deeper, net-like episcleral vessels dilate they produce a more violaceous injection, particularly noted as ciliary flush at the corneal limbus (Fig. 7-32B). Suffusion in the conjunctiva blanches with pressure; the ciliary flush does not blanch. Ciliary flush indicates inflammation of the uveal tract (see Uveal tract inflammation—uveitis (iritis, iridocyclitis, and choroiditis)).

Conjunctivitis

Inflammation of the conjunctiva, with or without infection, is conjunctivitis. The patient may awaken with eyelids stuck shut and a gritty or burning sensation with excessive lacrimation. There is marked redness of the eye(s) from hyperemia of the palpebral and peripheral global conjunctival vessels. There are many causes; consider viral and bacterial infections, foreign–body reaction, allergies, and blepharitis. DDX: Awakening with the lids stuck together by purulent discharge increases the probability for bacterial infection; itching suggests a nonbacterial etiology.

Hyperemic conjunctiva with calcification

These lesions occur when the serum calcium–phosphorus product exceeds 70 in renal failure and sarcoidosis. Conjunctiva Lesions: The segments from limbus to canthus at 7 to 10 o’clock and at 2 to 5 o’clock show hyperemic reddening, calcified plaques, and pingueculae. The eyes are painful or feel gritty. The affected areas contain calcium deposits, visible to the unaided eye or through the slit lamp. Cornea Lesions: This is called band keratopathy occurring in hypercalcemia and in renal disease with conjunctival calcification. White material is visible in the limbal arcs at 2 to 5 o’clock and 7 to 10 o’clock. The slit lamp reveals calcium deposits.

Pterygium

Chronic irritation from wind and dust is thought to stimulate the growth of the pinguecula, resulting in the extension of a vascular membrane over the limbus toward the center of the cornea, called a pterygium. This is a raised, subconjunctival fatty structure, growing in a horizontal band toward and over the pupil (Fig. 7-33A); vision may be obstructed. It has a firm attachment to the bulbar surface and is strictly horizontal; it is usually bilateral. A pseudopterygium is a band of scar tissue that may extend in any direction and adhere only partially to the bulbar conjunctiva, so a probe may be passed beneath it.

Pigmented pingueculae

Brownish pigmentation of the pingueculae is one of the few signs of Gaucher disease; others are hepatosplenomegaly, thrombocytopenic purpura, and patchy brown pigmentation on the face and the legs.

Cornea Signs

Hypopyon

Inflammation in the iris or anterior chamber produces a purulent discharge in the anterior chamber. The opaque fluid settles in the dependent portion of the chamber where it is seen as a fluid level behind the cornea (Fig. 7-33B). Iritis is a common cause.

Lusterless cornea—superficial keratitis

Corneal inflammation or drying causes epithelial loss. There is loss of the normal corneal luster with grayness of the anterior stroma. A ciliary flush is often present. Fluorescein staining demonstrates ulceration or denuded epithelium. A corneal ulcer is extremely painful and causes miosis and photophobia. Disruption of the epithelium demands urgent expert therapy, because visual loss can occur rapidly. CLINICAL OCCURRENCE: There are many causes of superficial keratitis including contact lens-related ulcers, infected abrasions, herpes simplex and zoster, corneal exposure, trigeminal nerve (CN V) injury, amiodarone deposits, and spread of infection from the conjunctiva.

Cloudy cornea—interstitial keratitis

The prototype is congenital syphilis, in which interstitial keratitis, deafness, and notched teeth constitute the Hutchinson triad. During the early stages of inflammation, between ages 5 and 15 years, a faint opacity begins in the central zone of the cornea together with a faint ciliary flush. Usually, pain and lacrimation occur as well. Later, the cornea becomes diffusely clouded, so the iris may be obscured. Blood vessels grow into the cornea. After the acute stage, there is permanent corneal opacity. Acquired syphilis and tuberculosis are occasional causes.

Arcus senilis

A gray opaque band in the cornea, 1.0- to 1.5-mm wide, is separated from the limbus by a narrow clear zone (Fig. 7-33C). Early on only a segment of the circumference is involved; later the circle is completed. It is present to some degree in most persons older than 60 years of age; it is bilateral. If seen before age 40, hyperlipidemia should be suspected.

Keratoconjunctivitis sicca—Sjögren syndrome

Lymphocytic infiltration of exocrine glands (lacrimal and salivary) reduces tear flow producing dry inflamed eyes. Sjögren syndrome (Sjögren syndrome—keratoconjunctivitis sicca) is likely if persistent dry eyes, dry mouth, and a positive Schirmer test (Schirmer test of tears and Fig. 7-33D) are present without obvious cause. Similar findings can be seen with HIV infection and sarcoidosis.

Kayser–Fleischer ring—Wilson disease

A 2-mm-wide golden-brown circular band is seen in the peripheral cornea near the limbus. The ring is formed by the copper deposited in Descemet membrane, the basement membrane of the cornea endothelium. This deposit begins superiorly, spreads inferiorly; it accompanies the neurologic manifestations of Wilson disease. A slit lamp is often required to see the ring.

Central corneal opacity

This results from trauma or infection and is seen in 75% of patients with Hurler syndrome.

Dots in the cornea—Fanconi syndrome

Cystine crystals are deposited throughout the stroma with no accompanying inflammatory reaction.

Sclera Signs

Yellow sclera—icterus and fat

In obstructive jaundice (Jaundice) conjugated bilirubin infiltrates all body tissues and fluids; it colors the sclera evenly. The conjunctiva of the fornices is usually deeper yellow because it is thicker. Deposits of fat beneath the conjunctiva commonly impart a yellow color to the periphery, leaving the perilimbal area relatively white. It is more obvious with advancing age and in the patients with anemia.

Red sclera—scleritis and episcleritis

Inflammation of the sclera and/or Tenon capsule can produce loss of scleral integrity. Scleritis may be diffuse or nodular and frequently associated with autoimmune diseases. The patient will have severe, deep, boring pain. In sunlight, the lesion will have a violaceous, red–purple appearance. Suppurative scleritis is rare and usually metastatic. Tuberculosis, sarcoidosis, and syphilis cause a granulomatous scleritis with localized scleral elevation and nodule formation. Scleral thinning may be non-necrotizing (scleromalacia perforans) or necrotizing with acute inflammation surrounding an area of ischemia which may ulcerate. Episcleritis is a much milder form of inflammation involving the fascial sheath of the globe (Tenon capsule) and appears clinically as a diffuse or nodular violaceous injection (Plate 14).

Blue sclera—osteogenesis imperfecta

Light reflecting off the pigmented choroid appears blue through the thinned sclera. This finding is classic for osteogenesis imperfecta; it may be mimicked by minocycline deposits, scleral thinning after scleritis, or age-related calcification of the horizontal rectus muscle insertions.

Brown sclera—melanin or homogentisic acid

Patches of melanin are commonly seen on the conjunctiva of dark-complexioned people, especially blacks. In alkaptonuria with ochronosis wedge-shaped areas of brown homogentisic acid color the sclera near the attachments of the ocular muscles with their apices toward the limbus.

Scleral protrusion—staphyloma

Scleral injury or increased intraocular pressure leads to a protrusion from the surface of the globe. An anterior staphyloma forms near the cornea creating a characteristic profile (Fig. 7-33E).

Pupil Signs

See Chapter 14, The Neurologic Examination.

Lens Signs

Cataract

Discoloration or disruption of the layers of the lens produce focal or diffuse opacities that can obstruct and/or scatter light before it reaches the retina. Because nearly all adults have some lens opacity, a clinical definition of cataract implies interference with vision [Asbell PA, Dualan I, Mindel J, et al. Age-related cataract. Lancet. 2005;365:599–609]. Some cataracts are seen by shining a light beam obliquely through the lens (focal illumination), by ophthalmoscopic inspection against the red retinal reflex with 0 diopter magnification from approximately 40 cm (15.7 inch), or by using + 10 diopter magnification with close inspection (direct illumination). Many can only be identified with the slit lamp. Centrally placed cataracts can be seen without pupillary dilatation; those in the periphery are only visualized with dilation. This discussion is limited to cataracts detectable without mydriatics or the slit lamp.

Anterior and posterior polar cataract

A small congenital white plaque can be seen in the center of the pupil. It results from a congenital defect in the anterior or posterior capsule.

Nuclear cataract

Diffuse yellow to brown discoloration occurs first in the central portion of the lens then gradually becomes diffuse discoloration throughout the lens. There is a black spot centrally against the red retinal reflex.

Cortical cataract

Wedge-shaped anterior or posterior cortical opacities, arranged radially and extending in from the periphery, appear gray with the penlight and black against the red retinal reflex (Plate 16).

Secondary cataract

Fibrosis of the posterior capsule is a common sequela of cataract surgery; the peripheral lens epithelial cells migrate across the capsular bag left to support the intraocular lens implant. This is more correctly an opacified posterior capsule. It appears as dense folds of tissue and clusters of clear vesicles.

Diabetic cataract

Older diabetic patients have an increased tendency to develop nuclear or cortical cataracts with no distinctive character. Juvenile diabetic patients acquire a distinctive snowflake cataract containing chalky white deposits; the entire lens subsequently becomes milky.

Posterior subcapsular cataract

This lesion is commonly seen after long-term use of corticosteroids, with diabetes, and after trauma or uveitis (Plate 17).

Lens subluxation and dislocation

Rupture of the zonula ciliaris (zonule of Zinn) permits the lens to move from its fixed position behind the pupil. Slight displacement, with the lens still backing the pupillary aperture, is termed subluxation (Fig. 7-34A); it is manifested by tremulousness of the iris (iridodonesis), when the eye moves horizontally. Viewed through the ophthalmoscope, the equator of the lens may show as a dark, curved line crossing the pupil; a double image of the retina with different magnifications may be seen, one through the lens, the other without the lens. When the lens is displaced completely it is a dislocation; when it enters the anterior chamber (Fig. 7-34B), it is easily seen. Lenticular displacement is usually caused by trauma. Nontraumatic dislocation occurs in several hereditary conditions including Marfan disease, homocystinuria, and hereditary spherophakia.

Intraocular pressure changes

Increased tension occurs in glaucoma; decreased tension is seen with myotonic dystrophy, globe rupture, and extreme dehydration. Accurate assessment is made by measurement of pressure with the tonometer.

Retina Signs

The following article provides a good review of retinal diseases with pathophysiology and photographs of many retinal signs [D’Amico DJ. Diseases of the retina. N Engl J Med. 1994;331:95–106].

Increased cup-to-disk ratio—glaucoma

See Glaucoma and Plate 17.

Myelinated nerve fibers

Myelination of the optic nerve fibers usually ends at the lamina cribrosa; infrequently myelin sheaths are maintained in the retinal nerve fiber layer (Fig. 7-35B). Semi-opaque white patches emerge from the optic disk spreading into one or two retinal quadrants. The disk margin appears frayed and the underlying vessels are partially or completely obscured. It is a normal variation of no clinical significance. Patches of myelinated nerves may occur remote from the disc.

Disk pallor—optic atrophy

Damage to the optic nerve (compression, ischemia, inflammation, or increased intracranial pressure) leads to atrophy of the nerve fibers and loss of normal vascularity (Fig. 7-35C and Plate 18). The disk is pale pink, yellow, or white; the margins may be less distinct and the physiologic cup and lamina cribrosa are variably seen. The emerging vessels may be surrounded by perivascular glial sheathing, seen as white lines. DDX: Pigmented high water marks around the nerve or residual exudate in the peripapillary retina may indicate previous disc edema, suggesting increased intracranial pressure producing the optic atrophy. It is important to recognize that an atrophic nerve can no longer swell, so cannot be used to monitor the presence of papilledema. A common cause of incidentally found optic atrophy is brain tumor, thus all optic atrophy should be evaluated promptly by an ophthalmologist. In optic atrophy from chorioretinitis, the disk may have a yellow cast, and the surrounding retina may contain hemorrhages, areas of atrophy, and pigment. The distinction between optic atrophy resulting from intrinsic optic nerve lesions versus increased intracranial pressure cannot be made reliably by the physical findings; interestingly, disc pallor does not occur in glaucoma until very late in its course. CLINICAL OCCURRENCE: Intrinsic Optic Nerve Lesions: multiple sclerosis, syphilis; Increased Intracranial Pressure: idiopathic intracranial hypertension, brain tumors; optic nerve compression without increased intracranial pressure.

Disk edema—papillitis, optic neuritis

When optic neuritis involves the portion of the optic nerve within the globe, papillitis, with loss of vision, is produced (Fig. 7-35D) with disk edema indistinguishable from papilledema. Visual loss occurs early in optic neuritis and usually later with papilledema. The disk is hyperemic and its margins may be indistinct from edema in the peripapillary nerve fiber layer. The disk surface may be elevated above the surrounding retina (a + 1 or + 2 lens correction is required to focus on the disk) [Balcer LJ. Optic neuritis. N Engl J Med. 2006;354:1273–1280]. CLINICAL OCCURRENCE: ocular inflammation (e.g., uveitis, retinitis, sympathetic ophthalmia), intrinsic inflammation of the optic nerve (e.g., demyelinating optic neuritis in multiple sclerosis, neuromyelitis optica—Devic syndrome), intracranial inflammation (e.g., meningitis, venous sinus thrombosis), infections (e.g., syphilis, tuberculosis, influenza, measles, malaria, mumps), and intoxications (e.g., methyl alcohol).

Anterior ischemic optic neuropathy (AION)

Infarction of the optic nerve head results from inadequate perfusion of the posterior ciliary arteries. AION occurs in two forms, the arteritic, related to giant cell arteritis, and the nonarteritic, which occurs in patients with vasculopathies such as hypertension or diabetes mellitus and intercurrent hypotension. The onset is usually sudden and painless, with profound visual loss, typically altitudinal, involving the upper and lower field. The optic nerve appears edematous, with scant hemorrhage and more pallor than typical for papilledema. DDX: In a patient of age >55 years, it is imperative to search for giant cell arteritis. The nonarteritic form is commonly accompanied by a small to absent optic cup in the uninvolved eye and often a period of systemic hypotension.

Papilledema

Increased intracranial pressure causes the cerebrospinal fluid (CSF) to compress the optic nerve within its sheath resulting in axoplasmic flow stasis and ischemia (Fig. 7-36A). Early papilledema causes a C-shaped halo of nerve fiber layer edema that surrounds the disc with a gap temporally (Plate 19). With more advanced papilledema, the halo becomes circumferential. Next there is obscuration of major vessels as they leave the disc; and later there is obscuration of vessels on the optic disc. The emerging vessels bend sharply in passing over the elevated disk edge (Plate 20). Macular retinal edema creates traction folds (choroidal folds), seen as white lines radiating from the macula (Fig. 7-36B). Patients with papilledema will have an enlarged physiologic blind spot documented with formal visual field testing. DDX: In contrast to papillitis, central vision is unimpaired, but, like glaucoma, there is usually peripheral visual loss. CLINICAL OCCURRENCE: The principal causes are brain tumor and idiopathic intracranial hypertension. Less common causes are hydrocephalus, malignant hypertension, subarachnoid hemorrhage, meningitis, and salicylate poisoning.

Pseudopapilledema—drusen bodies

These are granular deposits in the optic disk that cause pseudopapilledema. The distinctions between early papilledema and drusen bodies are reported as follows: drusen cause obvious irregular, lumpy, bumpy elevation of the disk; drusen are pink or yellow, the surface of papilledema is hyperemic; drusen cause the nerve fiber layer to glisten and often show a halo of feathery reflections, whereas the layer in papilledema is dull; drusen are in the disk center; in papilledema, the vessels show absence of venous pulsation and the light reflexes are dulled; drusen make the disk outline irregular and are more frequent in small, hypermetropic eyes.

Venous engorgement

Distention of retinal veins suggests retinal vein occlusion, polycythemia vera, cyanotic congenital heart disease, leukemia, and macroglobulinemia.

Retinal hemorrhage

Hemorrhage may occur in any layer of the retina. The shape of the hemorrhage frequently reveals its depth. A large, deep hemorrhage in the choriocapillaris produces a dark, elevated area that looks like a melanotic tumor (Fig. 7-37A); you should suspect a subretinal vascular membrane seen in association with macular degeneration. A smaller, more superficial hemorrhage appears as a round red spot, with blurred margins, called a blot hemorrhage (Fig. 7-37B). Microaneurysms are also round red spots, but their borders are sharp, they are not reabsorbed like hemorrhages, and they may occur in clusters about vascular sprigs (Fig. 7-37C). Flame-shaped hemorrhages occur in the nerve fiber layer of the retina; they are red and striated (Fig. 7-37D and Plate 23). In the subhyaloid or preretinal hemorrhage, a pool of blood accumulates between the retina and the hyaloid membrane forming a boat-shaped hemorrhage appearing as a turned-up half-moon; the straight upper border is a fluid level (Fig. 7-37E). A small hemorrhagic spot with a central white area is called a Roth spot, (Fig. 7-37F) classically seen in subacute bacterial endocarditis and leukemia. CLINICAL OCCURRENCE: Many conditions produce retinal hemorrhages, examples are hypertension, diabetes mellitus, papilledema, retinal vein occlusion, SBE, HIV, SLE, Takayasu arteritis, macroglobulinemia, thiamine deficiency, leukemia, polycythemia, sickle cell disease, and sarcoidosis.

Diabetic retinopathy

Diabetic retinopathy often leads to blindness from damage to the macular region. Microaneurysms occurring around the macula need to be distinguished from blot hemorrhages. With advanced diabetic retinopathy there are white or yellow waxy exudates having distinct, often serrated, borders (Plate 24). The exudates gradually coalesce to form a broken circle around the macula. Neovascularization of the disk or neovascularization elsewhere in the retina is an ominous sign requiring laser phototherapy (Plates 25 and 26). The signs of atherosclerosis and hypertension are sometimes superimposed [Frank RN. Diabetic retinopathy. N Engl J Med. 2004;350:48–58]. DDX: Although microaneurysms around the macula are characteristic of diabetes, retinal microvasculopathy with cotton–wool spots, intraretinal hemorrhages, and microaneurysms occurs in radiation retinopathy and in some patients with HIV-AIDS.

Arterial occlusion

Sudden loss of vision occurs when the central retinal artery is occluded, usually from thrombosis or embolism. Early the retina is very pale from ischemic edema; the arteries are extremely narrowed, and the smaller ones are invisible (Fig. 7-38A and Pate 21). Although the veins are full, they are pulseless. The lack of circulation is demonstrated by the absence of induced pulsation in either artery or vein with pressure on the eyeball. Retinal edema initially causes macular pallor that is less dense over the fovea because of an anatomical lack of the nerve fiber layer at this location. The fovea appears as a cherry red spot because of the visualization of the choroidal blood flow within the macular edema; this finding will disappear as the edema resolves over weeks. Occlusion of a branch artery causes findings limited to its distribution area. CLINICAL OCCURRENCE: Common causes are vascular disease, cardiac valve disease or vegetations, rheumatic fever, and vasculitis, most commonly temporal arteritis. Rarely, it is a complication of SLE, sickle cell disease, cryoglobulinemia, syphilis, or thromboangiitis obliterans.

Venous occlusion

Central retinal vein thrombosis is followed by engorgement and tortuosity of all visible veins (Fig. 7-38B). Significant nerve fiber layer and blot hemorrhages appear throughout the retina. Edema of the macula and disk is commonly present. Occlusion of a branch of the central vein produces findings limited to its drainage area. CLINICAL OCCURRENCE: Venous occlusive disease is most associated with hypertension, as the stiffened arterioles will compress the more compliant retinal veins as they cross in their common sheath. Hypercoagulable states can also cause venous occlusion from sluggish blood flow and can be seen in polycythemia, multiple myeloma, macroglobulinemia, and leukemia. In sickle cell disease, multiple venous thromboses may be accompanied by neovascularization.

Arteriolar sclerosis

The degree of involvement of the retinal vessels by the arteriolar sclerotic process has been variously scored. Table 7-2 represents the Kirkendall and Armstrong modification of the Scheie classification. The retinal changes do not necessarily parallel atherosclerotic disease elsewhere in the body.

Arterial stripe

Normal retinal arteries show a central bright stripe from light reflecting off the curved blood column. Increases in wall thickness cause widening of the stripe and brightening of the reflex. In moderate disease, the walls look like burnished copper (copper wire reflex); in advanced disease, the entire width of the artery reflects as a white stripe (silver wire reflex).

Vessel sheaths

Normal vessel walls are invisible. Wall thickening with lipid infiltration produces a milky white streak on either side of the blood column called pipestem sheathing.

Arteriovenous crossings

As the arterial and arteriolar walls become denser and less compliant, arteriovenous crossing signs are produced (Fig. 7-39A). Arteriovenous nicking (Fig. 7-39B) occurs when the thickened arterial sheath obscures a short segment of the more compliant vein, seen as a notch on either side of the artery at their crossing. Deviation of the vein is produced when the stiffened artery causes the vein to assume a 90 degrees crossing angle (Fig. 7-39C); the normal angle is acute. When an overlying vein is elevated by the thickened artery, it is called humping (Fig. 7-48D). Tapering of the veins results if the artery compresses the vein (Fig. 7-39E). When venous flow is partially obstructed, the vein dilates upstream from the artery, called banking (Fig. 7-39F), which may induce a retinal vein occlusion.

Hypertensive retinopathy

Arterial hypertension produces distinctive retinal signs that often coexist with the signs of arteriolar sclerosis (Plates 22 and 23). For example, the appearance of a retina may be classified as “grade 3 arteriolosclerosis, grade 4 hypertension.” The signs attributed to hypertension may also be graded by using the classification of Kirkendall and Armstrong (Table 7-3) [Wong, T, Mitchell P. The eye in hypertension. Lancet. 2007;369:425–435]. Most ophthalmologists will simply describe the retinal and vascular finding without the use of these grading scales.

Retinal spots

Many diseases and pathogenic process leave their marks in the retina as scars, deposits, pigmentation, etc. In addition, active retinal disease and systemic diseases with retinal manifestations can appear as unifocal or multifocal spots against the normal retina. Careful retinal examination of patients with confusing systemic disease may assist in diagnosis. The clinician’s first task is to distinguish active disease from the residuals of past events.

Cholesterol emboli

Ulcerated atherosclerotic plaque in the aorta or carotid artery sheds cholesterol crystals that become lodged at the bifurcations of retinal vessels. Patients may be asymptomatic or present with transient monocular visual loss, amaurosis fugax, or transient ischemic neurologic attacks (TIA) in a carotid distribution. Finding cholesterol emboli proves plaque rupture with embolization. It is difficult, if not impossible, to differentiate cholesterol emboli from calcific emboli in the diseased heart valves.

Cotton wool patches

Thickening and swelling of the terminal retinal nerve fibers results from ischemic infarcts. Gray to white areas with ill-defined fluffy borders occur within the posterior pole of the retina (Plate 22). They are often accompanied by microaneurysms that may rupture producing small striate hemorrhages known as flame hemorrhages. CLINICAL OCCURRENCE: Hypertension, diabetes, SLE, HIV, central retinal vein occlusion, papilledema.

Hard exudates

This is lipid deposition from leaking capillaries left behind as a high water mark after the retinal pigment epithelium resorbs the associated serous fluid. These are small white spots with sharply defined edges. They are deeper than the superficial retinal vessels and the superficial cotton wool patches.

Pigmented spots

Old inflammation or scarring may appear as a pigmented region of the retina.

Talc deposits

White or yellow spots are seen in the retinae of intravenous drug users who have injected ground-up tablets containing talc.

Cytomegalovirus (CMV) retinitis

Advanced immunosuppression from HIV infection is frequently accompanied by cytomegalovirus infection of the retina. Patients describe visual loss, blurring, floaters, and flashes of light. Look for whitening of the retina, cotton-wool spots, and intraretinal hemorrhages. Although less common, consider varicella zoster infection, toxoplasmosis, and syphilis [Cunningham ET, Margolis TP. Ocular manifestations of HIV infection. N Engl J Med. 1998;339:236–244]. CMV retinitis has become less common with the advent of highly active antiviral therapy.

Candida endophthalmitis

Systemic Candida infection associated with immunosuppression and indwelling venous catheters can be difficult to diagnose. Patients have fever, but blood cultures are often negative. Small white patches on the retina may be the only sign of disease. With advancing disease, there is pain, visual disturbance, and large white globular lesions are seen invading the vitreous.

Macular degeneration

Although vision is much reduced, the only visible sign may be a few spots of pigment near the macula and blurring of the macular borders. In other cases, subretinal hemorrhages, patches of retinal atrophy, yellow drusen, and pigmented areas may be seen.

Retinitis pigmentosa

Inherited singly or as a component of several syndromes, retinitis pigmentosa is manifested by arteriolar narrowing, waxy pallor of the optic disc, and perivascular retinal pigmentation. Night blindness is the earliest symptom; later, all types of vision are greatly impaired as the retinal degeneration progresses from the periphery to the posterior retina. Spidery strands of pigmented spots form a girdle about the global equator (Fig. 7-40A).

Angioid streaks

These probably represent elastic tissue degeneration. Broad lines of pigment radiate from the optic disk, branching like blood vessels (Fig. 7-40B). They occur in Paget disease and in pseudoxanthoma elasticum.

Retinal detachment

Retinal detachments may be symptomatic or asymptomatic. Patients complain of flashing lights followed by floaters and then a curtain crossing their vision. The earliest sign is elevation of a retinal area so that it is out of focus with the surrounding structures. The arteries and veins in the separated membrane appear elevated (Fig. 7-41). When widely separated, the retinal sheet is gray and frequently folded. Underlying inflammation may produce areas of choroiditis and vitreous opacities. A torn edge may be encountered, often shaped like a horseshoe. The cause of detachment is often undetermined.

Nose and Sinus Signs

Epistaxis (nosebleed)

In the anterior nose, the most common site of bleeding is Kiesselbach plexus, a vascular network in the anterior nasal septum. Posteriorly, hemorrhage occurs frequently at the back third of the inferior meatus; vessels in the region are large and belong to the external carotid artery system. In some cases, there are multiple oozing points in the mucosa. Nosebleed can be a spontaneous and trivial occurrence or a sign of serious local or generalized disease. Hemorrhage from the external nares is obvious, but bleeding from the choana must be distinguished from hemoptysis and even hematemesis. The first problem is to ascertain the bleeding site and judge whether trauma or some predisposing disease is present. Inquire about trauma, predisposing local or systemic disease, and the amount of blood lost. To examine the patient observe universal precautions: use gloves, gown, and face protection to avoid blood contamination. Remove the clots by suction or have the patient clear the nose by blowing. Inspect the anterior nasal chambers, especially the septum. If hemorrhage is so profuse as to obscure the site, advance the sucker tip backward in small increments, clearing the blood at each step, until a point is reached where the passage immediately fills after clearing; this is the bleeding site. Blood-tinged fluid suggests a CSF leak. Consult textbooks for methods of arresting hemorrhage. CLINICAL OCCURRENCE: Local Causes: coughing, sneezing, nose picking, fractures, lacerations, foreign bodies, adenoid growth, nasopharyngeal fibroma, angioma, rhinitis sicca. Generalized Causes: Congenital: hereditary telangiectasia; Inflammatory/Immune: Granulomatosis with polyangiitis (Wegener), lethal midline granuloma; Infectious: viral rhinitis, typhoid fever, scarlet fever, influenza, measles, infectious mononucleosis, diphtheria, pertussis, psittacosis, Rocky Mountain spotted fever, erysipelas, mucosal leishmaniasis; Metabolic/Toxic: pernicious anemia, aspirin, scurvy; Mechanical/Trauma: (see local causes) changes in atmospheric pressure (mountain climbing, caisson disease, flying) exertion; Neoplastic: nasopharyngeal carcinoma, squamous cell carcinomas, leukemia; Vascular: coagulopathy, cirrhosis, uremia, hemophilia, von Willebrand disease, thrombocytopenia; Elevated Arterial Pressure: hypertension, aortic coarctation; Elevated Venous Pressure: cor pulmonale, congestive heart failure, superior vena cava syndrome.

Nasal and maxilla fracture

Nasal fractures are simple or comminuted; seldom are they compound. A blow from the side displaces both nasal bones to the opposite side, producing an S-shaped curve in the dorsum nasi. The septum may be fractured with or without nasal bone fracture. Frontal blows depress the nasal bones. Palpation along the inferior border of the orbit may disclose an irregularity indicating fracture of the maxilla; a fragment may displace downward into the sinus. Malocclusion of the teeth indicates displacement of the maxilla. Fracture of the zygoma produces flattening of the cheek.

Anosmia

Lesions of CN I, often shearing of the nerve ending passing through the cribriform plate, or nasal obstruction produce loss of smell. Anosmia is invariably accompanied by a perceived change in the taste of food, which seems bland and unpalatable. The most common identified cause is closed head trauma.

Congenital nasal deformities

Disturbances in development of the nose are myriad, but they pose little problem in diagnosis. Perhaps the most common is cleft nose from incomplete fusion at the tip and dorsum (Fig. 7-42B).

Acquired nose deformities

Acquired deformities are commonly the result of trauma, infection, or neoplasms. Rhinophyma is an erythematous bulbous enlargement of the distal two-thirds of the nose from multiple sebaceous adenomas (Fig. 7-42A). It may follow longstanding rosacea. Saddle nose is distinguished by the sunken bridge (Fig. 7-42C) that results from loss of cartilage; common causes are septal hematoma or abscess. Rarely, it can follow relapsing polychondritis, granulomatosis and polyangiitis (Wegener), or congenital or acquired syphilis. A crooked nose results from fracture.

Vestibule folliculitis

Mild inflammation around the hair follicles is evident on inspection.

Vestibule furunculosis

A small superficial abscess forms in the skin or mucous membrane. The area is extremely tender, swollen, and reddened. Swelling may involve the nasal tip, alae nasi, and upper lip (Fig. 7-43A). Avoid instrumentation or other trauma to pyogenic lesions within the triangle anterior to a line from the corners of the mouth to the glabella; this may cause spread of the infection directly to the cavernous sinus.

Fissure

Fissures often develop at the mucocutaneous junction. They become overlaid with crusts that cover tender surfaces.

Deviated septum

In the adult the nasal septum is seldom precisely a midline structure. The cartilaginous and bony septum may deviate as a hump, spur, or shelf to encroach on one nasal chamber, occasionally causing obstruction. Columnar dislocation of the septum may occur.

Perforated septum

The cartilaginous septum is usually involved. Perforation is commonly caused by chronic infection, repeated trauma in picking off crusts, as a result of nasal or transphenoidal pituitary surgery, or cocaine abuse. Perforation is readily demonstrated by looking in one naris while a light shines in the other (Fig. 7-43B).

Septal hematoma

Even slight trauma to the nose may produce bleeding under the mucoperichondrium, usually causing bilateral hematomas. Nasal obstruction necessitates breathing through the mouth. The hematoma is seen as a violaceous, compressible, obstructive mass. The columella may be widened; the nasal tip pales from stretching of the skin. Pressure by the hematoma on the anterior ethmoidal nerve may cause anesthesia of the tip. Long-standing hematomas interfere with the blood supply of the septum, causing slow necrosis of the cartilage and a saddle nose deformity.

Septal abscess

The septum swells into both nasal chambers, and the mucosa is edematous. Infection of a septal hematoma invariably results in loss of cartilage; it must be immediately incised, drained, and treated with appropriate antibiotics. There is risk of progression through the angular veins to produce cavernous sinus thrombosis.

Foreign body

Children frequently put objects into the nose that remain for long periods and produce foul, purulent unilateral discharge.

Neoplasm

Sinus carcinomas cause obstruction, bloodstained discharge, and constant, boring pain. They invade bone: in the orbit, they may cause ocular disturbances; in the maxillary antral floor, upper teeth may become loose, a denture may no longer fit properly, or bulging and softness of the hard palate is seen.

Cerebrospinal rhinorrhea

A traumatic fistula occurs between the subarachnoid space and the nasal cavity. A unilateral discharge of clear spinal fluid occurs after head injury or surgery. The fluid may be blood tinged but is easily distinguished from nosebleed. Jugular vein compression increases the flow. If spinal fluid is suspected, the specimen should be tested for b₂-transferrin. There is substantial risk for meningitis; recurrent meningitis should lead to a search for CSF leak.

Nasal discharge—acute suppurative sinusitis

See Suppurative paranasal sinusitis.

Nasal discharge—chronic suppurative sinusitis

See Suppurative paranasal sinusitis.

Sinusitis and periorbital edema—periorbital abscess

See Periorbital abscess.

Sinusitis and periorbital edema—orbital cellulitis

See Orbital cellulitis.

• Sinusitis and ocular palsies—cavernous sinus thrombosis. See Sinusitis and ocular palsies—cavernous sinus thrombosis and Figure 7-44A.

Nasal polyps

Nasal polyps are sessile or pedunculated mucosal overgrowths developing after recurrent episodes of mucosal edema. They are frequently seen in long-standing allergic rhinitis, aspirin-sensitive asthma, and cystic fibrosis. Polyps are commonly multiple, most frequently protruding from the middle meatus as smooth, pale, spheric mucosal masses (Fig. 7-44B). Polyps may enlarge to obstruct the air passages; they frequently recur after removal. DDX: they are mobile and insensitive, distinguishing them from swollen turbinates.

Periorbital masses—mucocele and pyocele

Permanent obstruction of the frontal or ethmoid sinus orifices causes mucus secreted by their mucosae to accumulate. The resulting sac, or mucocele, slowly enlarges; the pent-up mucus exerts pressure on the surrounding structures and erodes bone, behaving like a neoplasm. The sac may eventually erode through the floor of the frontal sinus or the lateral ethmoid wall producing a painless swelling beneath the supraorbital ridge, medial to the ocular globe (Fig. 7-45). The painless mass feels rubbery and slightly compressible. The globe is pushed downward and laterally, causing diplopia; proptosis may also occur. Upward and medial motions of the eye are restricted. Intranasal examination may be negative. An infected mucocele is termed a pyocele. DDX: Swelling from the mucocele occurs above the inner canthus; dacryocystitis forms a swelling below the canthus.

Papillomas

Benign papillomas are often found in the vestibule. Slow-growing, benign neoplasms of the sinuses are usually osteomas or chondromas. They grow slowly and cause no symptoms until air passages or a sinus orifice is obstructed. Inverted papillomas grow downward into the underlying tissues so are difficult to resect.

Midline granuloma

The cause is unknown, but some classify it as one of the angiocentric immunoproliferative lesions. The inflammation is attended by granuloma formation. It is most common in fifth and sixth decades, with a slight preference for women. Symptoms include sneezing, nasal stiffness, obstruction, and pain. Signs are rhinorrhea, nasal congestion, and paranasal sinusitis progressing to inflammation and ulcerations of the nasal septum, palate, and nasal ali. Advanced disease is indicated by destruction of midfacial structures including pharynx, mouth, sinuses, and eyes with death from cachexia, pneumonia, meningitis, or hemorrhage. Indolent ulceration and mutilation suggest the diagnosis. DDX: Unlike Wegener granulomatosis, here there is no systemic involvement or primary vasculitis.

Granulomatosis and polyangiitis (Wegener)

See Chapter 8.

Breath Signs

Breath odor is an important diagnostic sign. There is great variation in olfactory acuteness, and description of odors is meaningless; experience is necessary. A foul breath odor, fetor oris, is common in infection (dental, tonsillar) atrophic rhinitis, putrefaction of food (achalasia, esophageal diverticula, pyloric obstruction), and infected sputum (bronchiectasis, lung abscess). Acetone on the breath indicates ketonemia in diabetic or starvation acidosis. In some patients with uremia, ammonia is detected. A curious musty odor occasionally is smelled in patients with severe liver disease. When a person has inhaled or swallowed volatile hydrocarbons, the odor is detectable in the exhaled air. Alcohol on the breath indicates recent ingestion, but medical illness, trauma, or the ingestion of other drugs must be excluded as comorbid conditions. A few patients in coma have no alcohol odor on the breath, whereas the aspirated gastric contents smell strongly of alcohol. The chronic alcoholic may smell of acetaldehyde instead of alcohol. When garlic is eaten, the methyl mercaptan causing its odor excreted from the lungs for more than 24 hours.

Lip Signs

Cleft lip

In the embryo, incomplete fusion of the frontonasal process with the two maxillary processes leaves a persistent cleft in one or both sides of the upper lip. Cleft lip is sometimes accompanied by cleft palate.

Lip enlargement

The lips may appear large in cretinism, myxedema, acromegaly, and collagen injections.

Labial vesicles—herpes simplex (cold sores, fever blisters)

Latent herpes simplex virus is reactivated producing local inflammation when the carrier develops another infectious disease, has local trauma, or is exposed to sunlight. Groups of vesicles containing clear fluid are surrounded by areas of erythema. Frequently, they occur on the lips. The lesions may burn or smart.

Cheilosis (angular stomatitis)

Maculopapular and vesicular lesions are grouped on the skin at the corners of the mouth and the mucocutaneous junction (Fig. 7-46A). Irritation of the skin leads to crusting and fissuring. Often accompanying profuse salivation from any cause, it is specifically associated with riboflavin deficiency or ill-fitting dentures; secondary Candida infection is common (perlèche). The entire labial surface may be inflamed from overexposure to sunlight, actinic cheilosis.

Carbuncle

Painful localized swelling with erythema and increased skin warmth suggests early cellulitis or carbuncle. When it occurs on the upper lip, it may be exceedingly dangerous, because the veins drain into the cavernous sinus.

Carcinoma of the lip

An early lesions is indurated and discoid; later, it becomes warty and crusted, forming a shallow ulcer that slowly extends. The ulcerated border is elevated, sometimes pearly (Fig. 7-46B). Regional lymph nodes are involved late. It is more frequent in men and 95% of the cases are on the lower lip. Biopsy all the ulcers that are more than 2 weeks old.

Lip chancre

The initial lesion of syphilis occurs at the inoculation site. The lip is the most common extragenital site of primary syphilitic chancre; usually the upper lip is involved. The lesion is discoid, without sharply defined borders and can be moved over the underlying tissues. It soon ulcerates to exude a clear fluid teeming with Treponema pallidum. The regional lymph nodes are involved early and feel larger and softer than carcinomatous nodes. Serologic tests for syphilis are frequently negative while the chancre is present.

Molluscum contagiosum

A nodular growth in the lip may ulcerate to discharge caseous material. The ulcer border may be elevated. The lesion is caused by Molluscipoxvirus. The resemblance to carcinoma may be striking, so biopsy may be required.

Rhagades

The white radial scars about the angles of the mouth are stigmata of previous syphilitic lesions (Fig. 7-46C).

Actinic keratosis

A dry, flat, light-colored precancerous growth occurs on the lip and produces scaling; it bleeds easily.

Lip pigmentation—Peutz–Jeghers syndrome

Multiple pigmented brown to black spots on the lips resemble freckles (Fig. 7-46D); freckles are uncommon on the mucosa. This autosomal dominant syndrome is associated with intestinal polyposis and an increased risk for gastrointestinal cancer.

Lip telangiectasias—hereditary hemorrhagic telangiectasia

The most obvious lesions may occur on the buccal mucosa, tongue, and lips. See Hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu disease).

Oral mucosa and palate signs

Xerostomia, Sjögren syndrome

See Sjogren Syndrome and Xerostomia.

Buccal pigmentation—Addison disease

Small patches of pigment in the buccal mucosa are common in blacks and other darkly pigmented races. In whites, however, dappled brown pigment in the lining of the cheek strongly suggests Addison disease or Peutz–Jeghers syndrome.

Retention cyst

An obstructed mucous gland produces a blue-domed translucent cyst anywhere on the buccal surface.

Mucosal sebaceous cysts (Fordyce spots)

The lip, cheek, and tongue mucosa show isolated white or yellow, sometimes slightly raised, spots <1 mm in diameter. Often a bit of white sebum may be expressed from the lesion. They are painless and harmless.

Koplik spots (measles)

Koplik spots are the earliest diagnostic sign of the measles; they are pathognomonic. One or two days before the exanthem appears, small white spots appear opposite the molars, and sometimes elsewhere, on the buccal mucosa (Fig. 7-47B). Each is surrounded by a narrow red areola.

Lichen planus

The lesions are thin, bluish-white, spiderweb lines resembling leukoplakia. Circumscribed areas of flattened papules on the flexor surfaces of the wrists and the middle of the shins strengthen the diagnosis of lichen planus (Lichen planus).

Leukoplakia

This often occurs at the site of chronic irritation from ill-fitting dentures or smokeless tobacco; it is precancerous. Tobacco and alcohol are cocarcinogens. The first lesion is a whitened hyperkeratotic plaque. On the tongue, one or more areas on the dorsal surface show obliteration of the papillae with thin white lesions that are wrinkled and sometimes pearly. Early lesions coalesce; as they persist and enlarge, they become chalk white and thick and are palpably more firm than the adjacent mucosa. Biopsy is indicated.

Thrush, candidiasis

Infection of the oral mucosa with Candida spp. occurs in patients who are diabetic, immunosuppressed (e.g., HIV, immunosuppressant drugs), or have received broad spectrum antibiotics. The lesions may be painless or cause mouth soreness. Examination reveals white plaques that are easily removed with a tongue blade. Less commonly, the mucosa is erythematous and thin, without the white plaques. Pain with swallowing suggests concomitant Candida esophagitis.

Telangiectasias—hereditary hemorrhagic telangiectasia

Early and obvious lesions occur on the buccal mucosa, tongue, and lips. See Hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu disease).

Oral vesicles, blisters, and ulcers

Several diseases result in oral vesicles or bullae, often with multiple ulcerations. The major mechanisms of disease are infection- and immune-mediated processes. Larger ulcers result from tissue destruction because of infectious, neoplastic, or metabolic causes.

Herpes simplex

Primary infection with herpes simplex causes severe stomatitis with painful vesicles that rupture to form shallow ulcers, which heal slowly.

Herpangina

Infection with coxsackievirus 16 results in fever and sore throat. On examination, there are small vesicles or whitish papules on the soft palate.

Lichen planus

Painful chronic ulcers may be surrounded by the characteristic lacy white mucosal lines.

Disseminated histoplasmosis

A persistent oral ulcer can be the presenting sign of disseminated histoplasmosis. Diagnosis is made by biopsy.

Cicatricial pemphigoid

Autoantibodies directed against hemidesmosomes in the basal layer of the mucosa and skin lead to the separation of the epithelial layers with blister formation. Pain is mild to moderate. The incidence increases with age. Oral lesions may be accompanied by skin lesions (Fungal Infections). The course is chronic and recurrent. It must be distinguished from pemphigus vulgaris (Fungal Infections).

• Stevens–Johnson syndrome. This is a severe allergic reaction with generalized involvement of the skin and mucous membranes. The most common cause is medication exposure. Early recognition, withdrawal of the offending agent, and supportive therapy may be lifesaving.

Aphthous ulcer (canker sore)

A few small vesicles appear in crops on the tip and sides of the tongue and on the labial and buccal mucosa. After vesicle has ruptured, the lesion is a small, round, painful ulcer with a white floor, yellow margins, and surrounding narrow erythematous areola. The cause is unknown. Recurrent or persistent aphthous ulcers are seen in Crohn disease and Behçet syndrome [Scully C. Aphthous ulceration. N Engl J Med. 2006;355:165–172].

Mucous patches (condyloma latum)

This is the common lesion of secondary syphilis, occurring on the tongue and the buccal and labial mucosa regardless of the site of the primary lesion. The patches are round or oval, 5 to 10 mm in diameter, slightly raised, and covered by gray membrane. They may ulcerate slightly. They feel indurated and are painless. Regional lymphadenopathy is common.

Osteonecrosis

Ionizing irradiation, especially of the mandible, leads to suppression of bone turnover and acute or delayed necrosis of bone with ulceration of the overlying mucosa. Bisphosphonate therapy (especially intravenous bisphosphonates for malignant hypercalcemia and myeloma) also suppresses bone turnover and is associated with bone necrosis and ulceration of the overlying mucosa. Patients present with one or more slowly progressive often painful ulcerations exposing underlying bone. A history of irradiation or bisphosphonate use is essential for making the diagnosis. Formerly, exposures to white phosphorus in the munitions industry caused a similar syndrome known as phossy jaw [Woo SB, Hellstein JW, Kalmar JR. Bisphosphonates and osteonecrosis of the jaws. Ann Intern Med. 2006;144:753–761].

Mucositis

The bone marrow and oral and intestinal mucosa are the most rapidly proliferating tissues in the body. Cytotoxic chemotherapy transiently stops proliferation and leads to impaired mucosal repair. Mouth ulcers commonly occur 5 to 10 days after intermittent bolus cytotoxic chemotherapy. They can occur anytime in the course of chronic oral therapy with alkylating agents or antimetabolites.

Reddened parotid duct orifice—mumps

The parotid (Stensen) duct orifice, opposite the upper second molar, may become reddened in mumps or other acute parotitis.

Bony palate protuberance—torus

This is a common anatomic variation; a bony knob or ridge occurs in the midline of the hard palate. It is harmless.

Arched palate

There are many causes for high-arched palate. It is common in Marfan and Turner syndromes.

Cleft palate

A midline opening in the hard palate results from congenital failure of fusion of the maxillary processes. It is usually associated with cleft lip but also occurs in isolation. Its severity varies from a complete cleft of the entire soft and hard palate, including the alveolar ridge, to a partial cleft of the soft palate alone.

Bifid uvula

This results from incomplete cleft of the soft palate and may be accompanied by disoriented palatal muscles. Test for elevation of the uvula; deviation of the uvula and asymmetry of the soft palate suggest muscular abnormality.

Teeth and Gum Signs

Wide interdental spaces

This may occur congenitally or be acquired as the jaw enlarges in acromegaly.

Caries

Usually the presence of cavities in the teeth is obvious. Decreased saliva production following irradiation or with sicca syndrome is associated with an increased risk for caries.

Loss of enamel

Loss of dental enamel results from erosion by regurgitated acidic stomach contents in patients with bulimia nervosa and by acid water in swimming pools with excessive chlorination.

Fluoride pits

Opaque chalk-white spots, 1 to 2 mm in diameter, are seen scattered on the surface of multiple teeth. This is a harmless condition found exposure to large amounts of fluoride in the water during childhood.

Notched teeth—Hutchinson teeth

This results from congenital syphilis. The permanent upper central incisors are misshapen (Fig. 7-48A). They are smaller than normal and peg topped, resembling the frustum of a cone; the tips are notched. Notching is one component of the Hutchinson triad, together with interstitial keratitis and labyrinthine deafness.

Periapical abscess

An abscess forms at the root tip within the bone. The inflammation produces a very painful increase in intraosseous pressure. An abscess suspected when toothache pain is accentuated by tapping the tooth with a tongue blade or probe. Tender swelling occurs in the adjacent gum and a draining sinus tract may form.

Bleeding gums

Gum bleeding signals local gum lesions or generalized disorders of the blood vessels or hemostasis. The patient may complain of bleeding accompanying brushing or may notice blood in expectorated phlegm. Other signs of a systemic vascular or hemostatic process should prompt direct questioning about bleeding from the gums because many patients do not consider this abnormal.