- 19 UNIT III - HEAD AND NECK
Clinical Content
1. Name the most common types of mandibular fractures and describe the surrounding
structures most commonly injured with these fractures.
“A fracture of the mandible usually involves two fractures, which frequently
occur on opposite sides of the mandible; thus if one fracture is observed, a search should
be made for another. For example, a hard blow to the jaw often fractures the neck of the
mandible and its body in the region of the opposite canine tooth.
“Fractures of the coronoid process are uncommon and usually single (Fig. B7.2).
Fractures of the neck of the mandible are often transverse and may be associated with
dislocation of the temporomandibular joint (TMJ) on the same side. Fractures of the
angle of the mandible are usually oblique and may involve the bony socket or alveolus of
the 3rd molar tooth (Fig. B7.2, line C). Fractures of the body of the mandible frequently
pass through the socket of a canine tooth (Fig. B7.2, line D).” (COA pp 837-838)
FIGURE B7.2. Fractures of mandible. Line A, Fracture of
the coronoid process; line B, fracture of the neck of the
mandible; line C, fracture of the angle of the mandible; line
D, fracture of the body of the mandible.
2. Describe the most common types of bleeding that can occur with ocular/orbital trauma
and how these clinical scenarios are managed.
“Orbital fractures often result in intraorbital bleeding, which exerts pressure on
the eyeball, causing exophthalmos (protrusion of the eyeball). Any trauma to the eye may
affect adjacent structures—for example, bleeding into the maxillary sinus, displacement
of maxillary teeth, and fracture of nasal bones resulting in hemorrhage, airway
obstruction, and infection that could spread to the cavernous sinus through the
ophthalmic vein.” (COA p 909)
“Hemorrhage within the anterior chamber of the eyeball (h y p h e ma or hy phe mi a )
usually results from blunt trauma to the eyeball, such as from a squash or racquet ball or a
hockey stick (Fig. B7.29). Initially, the anterior chamber is tinged red but blood soon
accumulates in this chamber. The initial hemorrhage usually stops in a few days and
recovery is usually good.” (COA p 912)
“Trauma to the Orbit: Conservative medical management of orbital fractures
consists of broad spectrum oral antibiotics and nasal decongestants, particularly with CT
evidence of disease of the paranasal sinuses or evidence of foreign body penetration into
the orbit. If the patient has no complaints of diplopia and very little restriction of ocular
motility, surgical intervention is not indicated and the patient can be observed weekly.
The findings that require immediate repair (within 24 hours) are the white-eyed blowout
fracture (normal appearing eye with marked restriction of motility) and fractures with
evidence of entrapment clinically and on CT that are associated with nonresolving
bradycardia, heart block, nausea, vomiting, or syncope (the oculo-cardiac reflex).
Fractures of the orbital roof, fractures associated with CSF rhinorrhea and orbital
fractures associated with intracranial hemorrhage require neurosurgical evaluation, and
often are repaired collaboratively by neurosurgery and ophthalmology.[12]
“Retrobulbar hemorrhage is diagnosed by the presence of significant proptosis
and elevated intraocular pressure in the presence of a tight orbit (very tense eyelids) and
evidence of retrobulbar bleeding on orbital CT. If the clinical suspicion is high, a lateral
canthotomy and cantholysis can be performed primarily and the orbital CT can be
obtained afterward. Performing a lateral canthotomy and cantholysis requires application
of local anesthetic and the use of toothed forceps and straight scissors. The lateral orbital
rim is palpated and the tissue extending from the lateral canthal angle to the orbital rim is
cut in a vertical fashion, splitting the upper and lower connection of the eyelids. The
lower lid is grasped with the forcep and tension is placed on the canthal tendon. The
tendon can be identified by strumming with scissors and the tendon is cut as close to the
orbital rim as possible (Figure 21). The same approach is taken to locating and incising
the upper canthal tendon. Many physicians take a step-wise approach to performing this
procedure by cutting the lower canthal tendon and re-measuring the intraocular pressure.
If the pressure normalizes by this step alone, cutting the upper canthal tendon can be
deferred. Intraocular pressure lowering agents consisting of intravenous or oral carbonic
anhydrase inhibitors, topical beta-blockers, and hyperosmotic agents should be
initiated.[12] On completion of this procedure, there is often a release of blood from the
retrobulbar space and the eye becomes even more proptotic. However, the result should
be the lowering of intraocular pressure and re-establishment of normal blood flow to the
eye.
“The treatable causes of an afferent pupillary defect in cases of trauma include
orbital compartment syndrome, mechanical optic nerve compression (by a bone fragment
or foreign body), or traumatic optic neuropathy. Central retinal artery occlusion, optic
nerve avulsion, and damage to the nerve within the optic canal (fracture or compression
within the canal) are less amenable to medical or surgical intervention. Traumatic optic
neuropathy (TON) is the diagnosis of exclusion once the other causes have been ruledout. If TON is suspected, the recommended treatment involves intravenous SoluMedrol,
5.4 mg/kg every 6 hours over 3 days in 12 divided doses.[12] No oral steroid taper is
necessary with this regimen. This treatment has been extrapolated from the results of the
spinal cord treatment trial, which showed limited benefit for recovery of function in
patients who sustained spinal cord injuries when treated with systemic steroids.[24,][25]
Studies published in the ophthalmic literature do not conclusively show a benefit of
systemic steroids in treating traumatic optic neuropathy, but this approach is widely
accepted.[26] Because of the questionable benefit and significant side-effect profile, this
treatment is used with the utmost caution in young children, the elderly, patients with
brittle diabetes, and patients predisposed to infection.
“An additional consideration in patients with orbital trauma is the presence of
lacerations to the eyelids and surrounding soft tissues. Emergency physicians and trauma
surgeons are capable of suturing the majority of these lacerations. Exceptions include
lacerations involving the eyelid margin and the lacrimal drainage system (punctum and
canaliculus) associated with ptosis (droopy eyelid) and with exposed orbital fat. Repair of
these injuries must often be done in the operating room and are often associated with
trauma to the eye. Consider tetanus prophylaxis and systemic antibiotics if contamination
is suspected (e.g., animal bite). Fast-absorbing suture should be used for the deep aspect
of the wound, and slow-absorbing suture for the superficial aspect (e.g., 6-0 Vicryl),
particularly if removal after 7–10 days proves to be difficult (e.g., children or patients
where follow-up may be questionable). (Asensio: Current Therapy of Trauma and
Surgical Critical Care, 1st ed.)
3. Describe the type of head trauma most likely to lead to a pterion fracture and the vessel
most at risk for injury.
“Fracture of the pterion can be life threatening because it overlies the anterior
branches of the middle meningeal vessels, which lie in grooves on the internal aspect of
the lateral wall of the calvaria (Fig. 7.30). The pterion is two fingers' breadth superior to
the zygomatic arch and a thumb's breadth posterior to the frontal process of the
zygomatic bone (Fig. B7.16A). A hard blow to the side of the head may fracture the thin
bones forming the pterion (Fig. 7.4A), producing a rupture of the anterior branch of the
middle meningeal artery crossing the pterion (Fig. B7.16B). The resulting hematoma
exerts pressure on the underlying cerebral cortex. An untreated middle meningeal artery
hemorrhage may cause death in a few hours.” (COA pp 874-875)
FIGURE B7.16.
4. Describe the specific injury, the most common cause and clinical implications of the
following cervical spine injuries:
(A) Traumatic spondylolysis of C2 (axis): “Fractures of the vertebral arch of the
axis are one of the most common injuries of the cervical vertebrae (up to 40%) (Yochum
and Rowe, 2004). Usually the fracture occurs in the bony column formed by the superior
and inferior articular processes of the axis, the pars interarticularis (Fig. 4.5A). A
fracture in this location, called a traumatic spondylolysis of C2 (Fig. B4.5A, B, & D),
usually occurs as a result of hyperextension of the head on the neck, rather than the
combined hyperextension of the head and neck, which results in whiplash injury.
“Such hyperextension of the head was used to execute criminals by hanging, in
which the knot was placed under the chin before the body suddenly dropped its length
through the gallows floor (Fig. B4.5C); thus this fracture has been called a hangman's
fracture.
“In more severe injuries, the body of the C2 vertebra is displaced anteriorly with
respect to the body of the C3 vertebra. With or without such subluxation (incomplete
dislocation) of the axis, injury of the spinal cord and/or of the brainstem is likely,
sometimes resulting in quadriplegia (paralysis of all four limbs) or death. Fractures of
the dens are also common axis injuries (40-50%), which may result from a horizontal
blow to the head or as a complication of osteopenia (pathological loss of bone mass)”
(COA pp 459-460)
(B) Dens fracture: “The transverse ligament of the atlas is stronger than the dens
of the C2 vertebra. Fractures of the dens make up about 40% of fractures of the axis.
The most common dens fracture occurs at its base—that is, at its junction with the body
of the axis (Fig. B4.13A). Often these fractures are unstable (do not reunite) because the
transverse ligament of the atlas becomes interposed between fragments (Crockard et al.,
1993) and because the separated fragment (the dens) no longer has a blood supply,
resulting in a v a sc u la r n ec r os is (G., death). Almost as common are fractures of the
vertebral body inferior to the base of the dens (Fig. B4.13B-E). This type of fracture heals
more readily because the fragments retain their blood supply. Other dens fractures result
from abnormal ossification patterns.” (COA p 476)
(C) Atlantoaxial subluxation: “When the transverse ligament of the atlas ruptures,
the dens is set free, resulting in atlanto-axial subluxation—incomplete dislocation of the
median atlanto-axial joint (Fig. B4.14A). Pathological softening of the transverse and
adjacent ligaments, usually resulting from disorders of connective tissue, may also cause
atlanto-axial subluxation (Bogduk and Macintosh, 1984); 20% of people with Down
syndrome exhibit laxity or agenesis of this ligament. Dislocation owing to transverse
ligament rupture or agenesis is more likely to cause spinal cord compression than that
resulting from fracture of the dens (Fig. B4.14B). In a fracture of the dens, the dens
fragment is held in place against the anterior arch of the atlas by the transverse ligament,
and the dens and atlas move as a unit.
“In the absence of a competent ligament, the upper cervical region of the spinal
cord may be compressed between the approximated posterior arch of the atlas and the
dens (Fig. B4.14A), causing paralysis of all four limbs (quadriplegia), or into the medulla
of the brainstem, resulting in death. Steele's Rule of Thirds: Approximately one third of
the atlas ring is occupied by the dens, one third by the spinal cord, and the remaining
third by the fluid-filled space and tissues surrounding the cord (Fig. B4.14C & D). This
explains why some people with anterior displacement of the atlas may be relatively
asymptomatic until a large degree of movement (greater than one third of the diameter of
the atlas ring) occurs. Sometimes inflammation in the craniovertebral area may produce
softening of the ligaments of the craniovertebral joints and cause dislocation of the
atlanto-axial joints. Sudden movement of a patient from a bed to a chair, for example,
may produce posterior displacement of the dens and injury to the spinal cord.” (COA p
477)
FIGURE B4.14. Rupture of transverse ligament of atlas. A. This left lateral view
demonstrates that subluxation of the median atlanto-axial joint results from rupture of the
transverse ligament. The atlas moves but the dens is fixed. B. This left lateral view of a
fracture of the dens shows that the dens and atlas move together as a unit because the
transverse ligament holds the dens to the anterior arch of the atlas. C and D. Inferior view of
transverse CT scan and interpretive drawing showing a normal median atlanto-axial joint and
demonstrating Steele's Rule of Thirds.
5. Describe the layers of the scalp and why an infection in one of the layers is potentially
very dangerous.
“The scalp is composed of five layers, the first three of which are connected
intimately and move as a unit (e.g., when wrinkling the forehead and moving the scalp).
Each letter in the word scalp serves as a memory key for one of its five layers (Fig.
7.15A):
 Skin: thin, except in the occipital region, containing many sweat and sebaceous
glands and hair follicles. It has an
 abundant arterial supply and good venous and lymphatic drainage.
 Connective tissue: forms the thick, dense, richly vascularized subcutaneous layer
that is well supplied with cutaneous nerves.
 Aponeurosis (epicranial aponeurosis): the broad, strong, tendinous sheet that
covers the calvaria and serves as the attachment for muscle bellies converging
from the forehead and occiput (the occipitofrontalis muscle) (Fig. 7.15B) and
from the temporal bones on each side (the temporoparietalis and superior
auricular muscles). Collectively, these structures constitute the


musculoaponeurotic epicranius. The frontal belly of the occipitofrontalis pulls
the scalp anteriorly, wrinkles the forehead, and elevates the eyebrows; the
occipital belly of the occipitofrontalis pulls the scalp posteriorly, smoothing the
skin of the forehead. The superior auricular muscle (actually a specialized
posterior part of the temporoparietalis) elevates the auricle of the external ear. All
parts of the epicranius are innervated by the facial nerve.
Loose areolar tissue: a sponge-like layer including potential spaces that may
distend with fluid as a result of injury or infection. This layer allows free
movement of the scalp proper (the first three layers—skin, connective tissue, and
epicranial aponeurosis) over the underlying calvaria.
Pericranium: a dense layer of connective tissue that forms the external periosteum
of the neurocranium. It is firmly attached but can be stripped fairly easily from the
crania of living persons, except where the pericranium is continuous with the
fibrous tissue in the cranial sutures.” (COA pp 843-844)
“The loose connective tissue layer (layer four) of the scalp is the danger area of
the scalp because pus or blood spreads easily in it. Infection in this layer can also pass
into the cranial cavity through emissary veins, which pass through parietal foramina in
the calvaria, and reach intracranial structures such as the meninges (Fig. 7.8A & C). An
infection cannot pass into the neck because the occipital bellies of the occipitofrontalis
muscle attach to the occipital bone and mastoid parts of the temporal bones. Neither can a
scalp infection spread laterally beyond the zygomatic arches because the epicranial
aponeurosis is continuous with the temporal fascia that attaches to these arches.
“An infection or fluid (e.g., pus or blood) can enter the eyelids and the root of the
nose because the frontalis inserts into the skin and subcutaneous tissue and does not
attach to the bone. The skin of the eyelid is the thinnest of the body and is delicate and
sensitive. Because of the loose nature of the subcutaneous tissue within the eyelids, even
a relatively slight injury or inflammation may result in an accumulation of fluid, causing
the eyelids to swell. Blows to the periorbital region usually produce soft tissue damage
because the tissues are crushed against the strong and relatively sharp margin.
Consequently, “black eyes” (periorbital ecchymosis) can result from an injury to the
scalp and/or the forehead (Fig. B7.12). Ecchymosis, or purple patches, develop as a
result of extravasation of blood into the subcutaneous tissue and skin of the eyelids and
surrounding regions.” (COA p 860)
6. Describe the anatomical location of the following lymph nodes that are routinely
palpated during a physical examination:
(A) “Occipital – base of the skull
(B) Postauricular – superficially over the mastoid process
(C) Preauricular – in front of ear (over canal)
(D) Buccal – (just posterior to corner of mouth)
(E) Submental – (just posterior to chin)
(F) Submandibular – halfway between the angle and the tip of the mandible
(G) Anterior Cervical – along the sternocleidomastoid muscle
(H) Posterior Cervical – along the anterior border of the trapezius muscle
(I) Supraclavicular – deeply in the angle formed by the clavicle and the
sternocleidomastoid muscle” (SPETA outline)
FIGURE 7.26. Lymphatic drainage of face and scalp. A. Superficial drainage. A
pericervical collar of superficial lymph nodes is formed at the junction of the head and
neck by the submental, submandibular, parotid, mastoid, and occipital nodes. These
nodes initially receive most of the lymph drainage from the face and scalp. B. Deep
drainage. All lymphatic vessels from the head and neck ultimately drain into the deep
cervical lymph nodes, either directly from the tissues or indirectly after passing through
an outlying group of nodes. (COA p 859)
FIGURE 8.48. Lymphatic drainage of head and neck. A and B. The pathways of the superficial and
deep lymphatic drainages are shown, respectively. C. The lymph nodes, lymphatic trunks, and thoracic
duct are shown.
7. Describe the structures most at risk for injury during surgery on the salivary (ie
parotid, submandibular and sublingual) glands.
“About 80% of salivary gland tumors occur in the parotid glands. Most tumors of
the parotid glands are benign, but most salivary gland cancers begin in the parotid.
Surgical excision of the parotid gland (parotidectomy) is often performed as part of the
treatment. Because the parotid plexus of CN VII is embedded in the parotid gland, the
plexus and its branches are in jeopardy during surgery. An important step in
parotidectomy is the identification, dissection, isolation, and preservation of the facial
nerve. A superficial portion of the gland (often erroneously referred to as a “lobe”) is
removed, after which the parotid plexus, which occupies a distinct plane within the gland,
can be retracted to enable dissection of the deep portion of the gland.
The parotid gland makes a substantial contribution to the posterolateral contour of the
face, the extent of its contribution being especially evident after it has been surgically
removed.” (COA p 926)
“Excision of a submandibular gland because of a calculus (stone) in its duct or a
tumor in the gland is not uncommon. The skin incision is made at least 2.5 cm inferior to
the angle of the mandible to avoid injury to the marginal mandibular branch of the facial
nerve. Caution must also be taken not to injure the lingual nerve when incising the duct.
The submandibular duct passes directly over the nerve inferior to the neck of the 3rd
molar tooth (Fig. 7.96).” (COA p 950)
“The sublingual glands are the smallest and most deeply situated of the salivary
glands (Fig. 7.96). Each almond-shaped gland lies in the floor of the mouth between the
mandible and the genioglossus muscle. The glands from each side unite to form a
horseshoe-shaped mass around the connective tissue core of the lingual frenulum.
Numerous small sublingual ducts open into the floor of the mouth along the sublingual
folds. The arterial supply of the sublingual glands is from the sublingual and
submental arteries, branches of the lingual and facial arteries, respectively (Fig. 7.92).
The nerves of the glands accompany those of the submandibular gland. Presynaptic
parasympathetic secretomotor fibers are conveyed by the facial, chorda tympani, and
lingual nerves to synapse in the submandibular ganglion (Fig. 7.95).” (COA p 945)
8. Describe the most common physical examination findings of patients with the
following eye related injuries:
(A) Horner's syndrome: “Horner syndrome results from interruption of a cervical
sympathetic trunk and is manifest by the absence of sympathetically stimulated functions
on the ipsilateral side of the head. The syndrome includes the following signs:
constriction of the pupil (miosis), drooping of the superior eyelid (ptosis), redness and
increased temperature of the skin (vasodilation), and absence of sweating (anhydrosis).
Constriction of the pupil occurs because the parasympathetically stimulated sphincter of
the pupil is unopposed. The ptosis is a consequence of the paralysis of the smooth muscle
fibers interdigitated with the aponeurosis of the levator palpebrae superioris that
collectively constitute the superior tarsal muscle, supplied by sympathetic fibers.” (COA
p 913)
(B) Cranial nerve III, IV and VI palsies
“Complete oculomotor nerve (CN III) palsy affects most of the ocular muscles,
the levator palpebrae superioris, and the sphincter pupillae. The superior eyelid droops
and cannot be raised voluntarily because of the unopposed activity of the orbicularis oculi
(supplied by the facial nerve) (Fig. B7.30A). The pupil is also fully dilated and nonreactive because of the unopposed dilator pupillae. The pupil is fully abducted and
depressed (“down and out”) because of the unopposed activity of the lateral rectus and
superior oblique, respectively.” (COA p 913) “Rapidly increasing intracranial pressure
(e.g., resulting from an extradural hematoma) often compresses CN III against the crest
of the petrous part of the temporal bone. Because autonomic fibers in CN III are
superficial, they are affected first. As a result, the pupil dilates progressively on the
injured side. Consequently, the first sign of CN III compression is ipsilateral slowness of
the pupillary response to light.” (COA p 1080)
“CN IV is rarely paralyzed alone. Lesions of this nerve or its nucleus cause
paralysis of the superior oblique and impair the ability to turn the affected eyeball
inferomedially. CN IV may be torn when there are severe head injuries because of its
long intracranial course. The characteristic sign of trochlear nerve injury is diplopia
(double vision) when looking down. Diplopia occurs because the superior oblique
normally assists the inferior rectus in depressing the pupil (directing the gaze downward)
and is the only muscle to do so when the pupil is adducted. In addition, because the
superior oblique is the primary muscle producing intorsion of the eyeball, the primary
muscle producing extorsion (the inferior oblique) is unopposed when the superior oblique
is paralyzed. Thus the direction of gaze and rotation of the eyeball about its
anteroposterior axis is different for the two eyes when an attempt is made to look
downward, and especially when looking downward and medially. The person can
compensate for the diplopia by inclining the head anteriorly and laterally toward the side
of the normal eye.” (COA pp 1080-1081)
“When the abducent nerve (CN VI) supplying only the lateral rectus is paralyzed,
the individual cannot abduct the pupil on the affected side (Fig. B7.30B). The pupil is
fully adducted by the unopposed pull of the medial rectus.” (COA p 913) “Because CN
VI has a long intradural course, it is often stretched when intracranial pressure rises,
partly because of the sharp bend it makes over the crest of the petrous part of the
temporal bone after entering the dura. A space-occupying lesion, such as a brain tumor,
may compress CN VI, causing paralysis of the lateral rectus. Complete paralysis of CN
VI causes medial deviation of the affected eye—that is, it is fully adducted owing to the
unopposed action of the medial rectus, leaving the person unable to abduct the eye.
Diplopia is present in all ranges of movement of the eyeball, except on gazing to the side
opposite the lesion.” (COA p 1081)
TABLE 9.6. SUMMARY OF CRANIAL NERVE LESIONS
Nerve
CN III
Types(s) and/or Site(s) of Lesion
Pressure from herniating uncus on
nerve; fracture involving cavernous
sinus; aneurysms
Abnormal Finding(s)
Dilated pupil; ptosis; eye turns down
and out; pupillary reflex on side of lesion
will be lost
CN IV
Stretching of nerve during its course
around brainstem; fracture of orbit
Inability to look down when eye is
adducted
CN VI
Base of brain or fracture involving
cavernous sinus or orbit
Eye falls to move laterally; diplopia on
lateral gaze (COA p 1079)
9. Describe the physical examination findings (including the affected side based on
head/neck position) most commonly found with an accessory nerve injury.
“Lesions of the spinal accessory nerve are uncommon. CN XI may be damaged
by:
 Penetrating trauma, such as a stab or bullet wound.
 Surgical procedures in the lateral cervical region.
 Tumors at the cranial base or cancerous cervical lymph nodes.
 Fractures of the jugular foramen where CN XI leaves the cranium.
“Although contraction of one SCM turns the head to one side, a unilateral lesion
of CN XI usually does not produce an abnormal position of the head. However, people
with CN XI damage usually have weakness in turning the head to the opposite side
against resistance. Lesions of the CN XI produce weakness and atrophy of the trapezius,
impairing neck movements.
“Unilateral paralysis of the trapezius is evident by the patient's inability to
elevate and retract the shoulder and by difficulty in elevating the upper limb superior to
the horizontal level. The normal prominence in the neck produced by the trapezius is also
reduced. Drooping of the shoulder is an obvious sign of CN XI injury. During extensive
surgical dissections in the lateral cervical region—for example, during removal of
cancerous lymph nodes—the surgeon isolates CN XI to preserve it, if possible. An
awareness of the superficial location of this nerve during superficial procedures in the
lateral cervical region is important because CN XI is the most commonly iatrogenic nerve
injury (G. iatros, physician or surgeon).” (COA p 1009)
10. Describe the physical examination findings of a patient with a cranial nerve VII palsy
and why this patient is at risk for a corneal abrasion.
“Injury to the facial nerve (CN VII) or its branches produces paralysis of some or
all facial muscles on the affected side (Bell palsy). The affected area sags, and facial
expression is distorted, making it appear passive or sad (Fig. B7.13). The loss of tonus of
the orbicularis oculi causes the inferior eyelid to evert (fall away from the surface of the
eyeball). As a result, lacrimal fluid is not spread over the cornea, preventing
adequate lubrication, hydration, and flushing of the surface of the cornea.
“This makes the cornea vulnerable to ulceration. A resulting corneal scar can
impair vision. If the injury weakens or paralyzes the buccinator and orbicularis oris, food
will accumulate in the oral vestibule during chewing, usually requiring continual removal
with a finger. When the sphincters or dilators of the mouth are affected, displacement of
the mouth (drooping of its corner) is produced by contraction of unopposed contralateral
facial muscles and gravity, resulting in food and saliva dribbling out of the side of the
mouth. Weakened lip muscles affect speech as a result of an impaired ability to produce
labial (B, M, P, or W) sounds. Affected persons cannot whistle or blow a wind
instrument. They frequently dab their eyes and mouth with a handkerchief to wipe the
fluid (tears and saliva), which runs from the drooping lid and mouth; the fluid and
constant wiping may result in localized skin irritation.” (COA p 861)
“Corneal Reflex – During a neurological examination, the examiner touches the
cornea with a wisp of cotton (Fig. B7.14). A normal (positive) response is a blink.
Absence of a blink response suggests a lesion of CN V1; a lesion of CN VII (the motor
nerve to the orbicularis oculi) may also impair this reflex. The examiner must be certain
to touch the cornea (not just the sclera) to evoke the reflex. The presence of a contact lens
may hamper or abolish the ability to evoke this reflex.” (COA p 912)
“Corneal Abrasions and Lacerations - Foreign objects such as sand or metal
filings (particles) produce corneal abrasions that cause sudden, stabbing pain in the
eyeball and tears. Opening and closing the eyelids is also painful. Corneal lacerations
are caused by sharp objects such as fingernails or the corner of a page of a book.” (COA
p 912)
“Among motor nerves, CN VII is the most frequently paralyzed of all the cranial
nerves. Depending on the part of the nerve involved, injury to CN VII may cause
paralysis of facial muscles without loss of taste on the anterior two thirds of the tongue or
altered secretion of the lacrimal and salivary glands.
“A lesion of CN VII near its origin or near the geniculate ganglion is accompanied
by loss of motor, gustatory (taste), and autonomic functions. The motor paralysis of facial
muscles involves superior and inferior parts of the face on the ipsilateral side.
A central lesion of CN VII (lesion of the CNS) results in paralysis of muscles in the
inferior face on the contralateral side; consequently, forehead wrinkling is not visibly
impaired because it is innervated bilaterally. Lesions between the geniculate ganglion and
the origin of the chorda tympani produce the same effects as that resulting from injury
near the ganglion, except that lacrimal secretion is not affected. Because it passes through
the facial canal in the temporal bone, CN VII is vulnerable to compression when a viral
infection produces inflammation (viral neuritis) and swelling of the nerve just before it
emerges from the stylomastoid foramen.
“Because the branches of CN VII are superficial, they are subject to injury from
knife and gunshot wounds, cuts, and birth injury. Damage to CN VII is common with
fracture of the temporal bone and is usually detectable immediately after the injury. CN
VII may also be affected by tumors of the brain and cranium, aneurysms, meningeal
infections, and herpes viruses. Although injuries to CN VII cause paralysis of facial
muscles, sensory loss in the small area of skin on the posteromedial surface of the auricle
and around the opening of the external acoustic meatus is rare. Similarly, hearing is not
usually impaired, but the ear may become more sensitive to low tones when the stapedius
(supplied by CN VII) is paralyzed; this muscle dampens vibration of the stapes (see
Chapter 7).
Bell palsy is a unilateral facial paralysis of sudden onset resulting from a lesion of
CN VII.” (COA pp 1081-1082)
11. Describe the most common functions disrupted with a temporal bone skull fracture.
“Injury to branches of the facial nerve causes paralysis of the facial muscles (Bell
palsy), with or without loss of taste on the anterior two thirds of the tongue or altered
secretion of the lacrimal and salivary glands (see the blue box “Paralysis of Facial
Muscles,” p. 861). Lesions near the origin of CN VII from the pons of the brain or
proximal to the origin of the greater petrosal nerve (in the region of the geniculate
ganglion), result in loss of motor, gustatory (taste), and autonomic functions. Lesions
distal to the geniculate ganglion, but proximal to the origin of the chorda tympani nerve,
produce the same dysfunction, except that lacrimal secretion is not affected. Lesions near
the stylomastoid foramen result in loss of motor function only (i.e., facial paralysis).
“Facial nerve palsy has many causes. The most common nontraumatic cause of
facial paralysis is inflammation of the facial nerve near the stylomastoid foramen, often
as a result of a viral infection. This produces edema (swelling) and compression of the
nerve in the facial canal. Injury of the facial nerve may result from fracture of the
temporal bone; facial paralysis is evident soon after the injury. If the nerve is completely
sectioned, the chances of complete or even partial recovery are remote. Muscular
movement usually improves when the nerve damage is associated with blunt head
trauma; however, recovery may not be complete (Rowland, 2005). Facial nerve palsy
may be idiopathic (occurring without a known cause), but it often follows exposure to
cold, as occurs when riding in a car with a window open.
“Facial paralysis may be a complication of surgery; consequently, identification
of the facial nerve is essential during surgery (e.g., parotidectomy, removal of a parotid
gland). The facial nerve is most distinct as it emerges from the stylomastoid foramen; if
necessary, electrical stimulation may be used for confirmation. Facial nerve palsy may
also be associated with dental manipulation, vaccination, pregnancy, HIV infection,
Lyme disease (inflammatory disorder causing headache and stiff neck), and infections of
the middle ear (otitis media).
“Because the branches of the facial nerve are superficial, they are subject to injury
by stab and gunshot wounds, cuts, and injury at birth:
 A lesion of the zygomatic branch of CN VII causes paralysis, including loss of
tonus of the orbicularis oculi in the inferior eyelid.
 Paralysis of the buccal branch of CN VII causes paralysis of the buccinator and
superior portion of the orbicularis oris and upper lip muscles.
 Paralysis of the marginal mandibular branch of CN VII may occur when an
incision is made along the inferior border of the mandible. Injury to this branch
(e.g., during a surgical approach to the submandibular gland) causes paralysis of
the inferior portion of the orbicularis oris and lower lip muscles.” (COA p 863)
12. Describe the anatomical basis for Frey's syndrome.
“The risk and the nature of complications following parotidectomy depend on the
experience of the surgeon, extent of parotidectomy, pathology of the tumor, and location
of the tumor within the gland. Potential complications include facial nerve dysfunction,
sensory deficits around the ear and cheek, and Frey's syndrome (discussed below); less
commonly seen are wound infection, salivary leak or fistula formation, hemorrhage or
hematoma.
“Frey's syndrome, also known as auriculotemporal syndrome or gustatory
sweating, is characterized by sweating and flushing of the facial skin over the parotid bed
and neck during mastication. The conjectured pathophysiology entails aberrant
regeneration of cut parasympathetic fibers between the otic ganglion and salivary
tissue which leads to innervation of sweat glands and subcutaneous vessels [24].
Frey's syndrome is reported by approximately ten percent of patients, but rigorous testing
may detect gustatory sweating in as many as 95 percent of patients after parotidectomy.
Due to a latency in the regeneration of parasympathetic nerve fibers, Frey's syndrome
may occur from two weeks to two years after surgery, and the area of involved skin may
increase over time [25,26].
“The incidence of Frey's syndrome is reduced by minimizing the parotid wound
bed, reconstructive techniques such as thick skin flaps, and postoperative RT [24].
Intracutaneous injection of botulinum toxin A is an effective, well-tolerated, and longlasting treatment for symptomatic patients; it may also be repeated for recurrent
symptoms [24,25].” (UpToDate.com)
13. Describe the most common clinical findings in mandibular nerve palsy and trigeminal
neuralgia.
Mandibular nerve palsy: “The mandibular nerve (CN V3) is the inferior and
largest division of the trigeminal nerve (Fig. 7.19A). It is formed by the union of sensory
fibers from the sensory ganglion and the motor root of CN V in the foramen ovale in the
greater wing of the sphenoid, through which CN V3 emerges from the cranium. CN V3
has three sensory branches that supply the area of skin derived from the embryonic
mandibular prominence. It also supplies motor fibers to the muscles of mastication (Fig.
7.19B). CN V3 is the only division of CN V that carries motor fibers. The major
cutaneous branches of CN V3 are the auriculotemporal, buccal, and mental nerves. En
route to the skin, the auriculotemporal nerve passes deep to the parotid gland, conveying
secretomotor fibers to it from a ganglion associated with this division of CN V.” (COA p
853) Thus, palsy of the mandibular nerve would cause trouble with motor function of
“SVE: mylohyoid m., anterior belly of the digastric m.; tensor tympani m., tensor veli
palatini m.; muscles of mastication (temporalis, masseter, medial pterygoid and lateral
pterygoid)” (Mich. Anat Tables) and sensory innervation of “GSA: skin of the lower lip
and jaw extending superiorly above level of the ear; mucous membrane of the tongue and
floor of the mouth; lower teeth and gingiva of the mandibular alveolar arch.” (Mich Anat
Tables)
“Trigeminal neuralgia or tic douloureux is a sensory disorder of the sensory root
of CN V that occurs most often in middle-aged and elderly persons. It is characterized
by sudden attacks of excruciating, lighteninglike jabs of facial pain. A paroxysm
(sudden sharp pain) can last for 15 minutes or more. The pain may be so intense that the
person winces; hence the common term tic (twitch). In some cases, the pain may be so
severe that psychological changes occur, leading to depression and even suicide attempts.
“CN V2 is most frequently involved, then CN V3, and least frequently, CN V1.
The paroxysms of sudden stabbing pain are often set off by touching the face, brushing
the teeth, shaving, drinking, or chewing. The pain is often initiated by touching an
especially sensitive trigger zone, frequently located around the tip of the nose or the
cheek (Haines, 2006). In trigeminal neuralgia, demyelination of axons in the sensory root
occurs. In most cases this is caused by pressure of a small aberrant artery (Kiernan,
2008). Often, when the aberrant artery is moved away from the sensory root of CN V, the
symptoms disappear. Other scientists believe the condition is caused by a pathological
process affecting neurons in the trigeminal ganglion.
“Medical or surgical treatment or both are used to alleviate the pain. In cases
involving the CN V2, attempts have been made to block the infra-orbital nerve at the
infraorbital foramen by using alcohol. This treatment usually relieves pain temporarily.
The simplest surgical procedure is avulsion or cutting of the branches of the nerve at the
infra-orbital foramen.
“Other treatments have used radiofrequency selective ablation of parts of the
trigeminal ganglion by a needle electrode passing through the cheek and the foramen
ovale. In some cases, it is necessary to section the sensory root for relief of the pain. To
prevent regeneration of nerve fibers, the sensory root of the trigeminal nerve may be
partially cut between the ganglion and the brainstem (rhizotomy). Although the axons
may regenerate, they do not do so within the brainstem. Surgeons attempt to differentiate
and cut only the sensory fibers to the division of CN V involved.
“The same result may be achieved by sectioning the spinal tract of CN V
(tractotomy). After this operation, the sensation of pain, temperature, and simple (light)
touch is lost over the area of skin and mucous membrane supplied by the affected
component of the CN V. This loss of sensation may annoy the patient, who may not
recognize the presence of food on the lip and cheek or feel it within the mouth on the side
of the nerve section, but these disabilities are usually preferable to excruciating pain.”
COA p 862)
14. Describe the structures most at risk for injury with a cheek laceration.
“There are two major structures underlying the cheek area, just anterior to the ear,
that can be injured by penetrating lacerations: the parotid gland and the facial nerve (Fig.
12-8). If the parotid gland is injured, salivary fluid can be seen leaking from the wound.
Inspection of the inside of the mouth often reveals bloody fluid coming from the opening
of the parotid duct located on the buccal mucosa of the cheek at the level of the upper
second molar tooth.
Figure 12-8 The parotid gland and facial nerve underlie the zygomatic
and cheek areas. Any lacerations anterior to the ear must be assessed
carefully for injuries to the various branches of the facial nerve, parotid
gland, or parotid duct.
“Lacerations of this region also can injure the facial nerve. It is necessary to test
all five branches of the nerve to ensure that each one is intact. The temporal branch is
tested by having the patient contract his or her forehead and elevate the brow. The
function of the zygomatic branch is observed by having the patient open and shut his or
her eyes. The act of sniffing with flaring of the nasal alae is also evidence for preserved
function of that branch. Buccal and mandibular branches innervate the lips during the acts
of smiling and frowning. Finally, the cervical branch is tested by having the patient shrug
the neck through contraction of the platysma muscle.” (Trott: Wounds and Lacerations:
Emergency Care and Closure, 3rd ed.)
- 20 15. Describe the most common causes, presentations (including radiographic findings),
vessels disrupted and treatments in the following conditions:
(A) Subdural hematoma: “A dural border hematoma is classically called a
subdural hematoma (Fig. B7.19B); however, this term is a misnomer because there is no
naturally occurring space at the dura-arachnoid junction. Hematomas at this junction are
usually caused by extravasated blood that splits open the dural border cell layer. The
blood does not collect within a preexisting space, but rather creates a space at the duraarachnoid junction (Haines, 2006). Dural border hemorrhage usually follows a blow to
the head that jerks the brain inside the cranium and injures it. The precipitating trauma
may be trivial or forgotten. Dural border hemorrhage is typically venous in origin and
commonly results from tearing a superior cerebral vein as it enters the superior sagittal
sinus (Fig. 7.29B) (Haines et al., 1993).” (COA pp 876-877)
(B) “Subarachnoid/intra-cranial hemorrhage: “Subarachnoid hemorrhage is an
extravasation of blood, usually arterial, into the subarachnoid space (Fig. B7.19C). Most
subarachnoid hemorrhages result from rupture of a saccular aneurysm (sac-like dilation
on the side of an artery), such as an aneurysm of the internal carotid artery (see the blue
box “Strokes,” p. 887).
“Some subarachnoid hemorrhages are associated with head trauma involving
cranial fractures and cerebral lacerations. Bleeding into the subarachnoid space results in
meningeal irritation, severe headache, stiff neck, and often loss of consciousness.” (COA
p 877)
(C) Epidural hematoma: “Extradural or epidural hemorrhage is arterial in origin.
Blood from torn branches of a middle meningeal artery collects between the external
periosteal layer of the dura and the calvaria. The extravasated blood strips the dura from
the cranium. Usually this follows a hard blow to the head, and forms an extradural or
epidural hematoma (Fig. B7.19A & B). Typically, a brief concussion (loss of
consciousness) occurs, followed by a lucid interval of some hours. Later, drowsiness and
coma (profound unconsciousness) occur. Compression of the brain occurs as the blood
mass increases, necessitating evacuation of the blood and occlusion of the bleeding
vessels.” (COA p 876)
(D) Scalp hematoma: Cephalhematoma – “Sometimes after a difficult birth,
bleeding occurs between the baby's pericranium and calvaria, usually over one parietal
bone. Blood becomes trapped in this area, causing a cephalhematoma. This benign
condition frequently results from birth trauma that ruptures multiple, minute periosteal
arteries that nourish the bones of the calvaria.” (COA p 861)
“Caput succedaneum — Caput succedaneum is an edematous swelling of the
scalp above the periosteum, which is occasionally hemorrhagic (show figure 1). It
presents at birth after prolonged engagement of the fetal head in the birth canal or after
vacuum extraction. Unlike cephalohematoma, it extends across the suture lines. Caput
succedaneum is generally a benign condition, and it usually resolves within a few days
and requires no treatment.
“There are reported rare complications in infants with caput succedaneum that
include necrotic lesions resulting in long-term scarring and alopecia [11], and an
associated case of Escherichia coli infection [12]. These reported complications were
seen in preterm infants who were delivered by vacuum extraction.
“Cephalohematoma — Cephalohematoma is a subperiosteal collection of blood
caused by rupture of vessels beneath the periosteum (usually over the parietal or occipital
bone), which presents as swelling that does not cross suture lines (show figure 1). The
swelling may or may not be accompanied by discoloration, rarely expands after delivery,
and does not generally cause significant blood loss. Cephalohematoma is estimated to
occur in 1 to 2 percent of all deliveries and is much more common when forceps or
vacuum delivery is performed (show table 2). (See "Operative vaginal delivery", section
on Complications).
“The majority of cephalohematomas will resolve spontaneously over the course of
a few weeks without any intervention. However, calcification of the hematoma can occur
with a subsequent bony swelling that may persist for months. Significant deformities of
the skull may occur when calcification or ossification of the cephalohematoma occurs
(show figure 2). Case reports have demonstrated successful surgical excision of these
calcified or ossified hematomas [13,14].
“Other complications of cephalohematoma include infection and sepsis, with
Escherichia coli being the most commonly reported causative agent. Infected
cephalohematomas present as erythematous, fluctuant masses that may have expanded
from their baseline size. Imaging with computed tomography (CT) or magnetic resonance
imaging (MRI) is helpful in making the diagnosis. Needle aspiration and culture of the
hematoma are considered to be mandatory for suspected cases [15]. Osteomyelitis is a
reported complication of an infected cephalohematoma [16]. In these affected infants,
treatment includes incision and drainage of the abscess with debridement of the necrotic
skull and a prolonged course of parenteral antibiotics (eg, vancomycin, gentamycin, and
cephotaxime).
“Subgaleal hemorrhage — Subgaleal hemorrhage (SGH) develops when blood
accumulates in the loose areolar tissue in the space between the periosteum of the skull
and the aponeurosis (show figure 1). The injury occurs when the emissary veins between
the scalp and dural sinuses are sheared or severed as a result of traction on the scalp
during delivery. The incidence of SGH has been estimated to occur in 4 of 10,000
spontaneous vaginal deliveries and 59 of 10,000 vacuum-assisted deliveries [17].
“The potential for massive blood loss (20 to 40 percent of a neonate's blood
volume resulting in a loss of 50 to 100 mL [18]) into the subgaleal space contributes to
the high mortality rate associated with this lesion. The subgaleal space extends from the
orbital ridges anteriorly to the nape of the neck posteriorly and to the level of the ears
laterally. In infants with SGH, the reported mortality is about 12 to 14 percent [19,20].
Infants who died had massive volume loss resulting in shock and coagulopathy [20].
SGH presents as a diffuse, fluctuant swelling of the head that may shift with movement.
Expansion of the swelling due to continued bleeding may occur hours to days after
delivery. Affected neonates may have tachycardia and pallor due to blood loss, although
blood loss may be massive before signs of hypovolemia become apparent.
“Early recognition of this injury is crucial for survival [21]. Infants who have
experienced a difficult operative delivery or are suspected to have a SGH require ongoing
monitoring including frequent vital signs (minimally every hour) and serial
measurements of hematocrits and their occipital frontal circumference, which increases 1
cm with each 40 mL of blood deposited into the subgaleal space. Head imaging, using
either CT or MRI, can be useful in differentiating subgaleal hemorrhage from other
cranial pathologic conditions. Coagulation studies are required to detect coagulopathy
that may be associated with the bleeding.
“Treatment includes volume resuscitation with packed red blood cells, fresh
frozen plasma, and normal saline as appropriate for ongoing bleeding and coagulopathy
correction. Rarely has brain compression been reported that required surgical evacuation
of the hematoma [22].” UpToDate.com
UpToDate.com
(E) Occipital lobe (visual cortex) cerebral vascular accident ("Stroke"): “A
syndrome of agitated delirium, visual hallucinations, and hemianopia can also be
produced by lesions (usually stroke) affecting the medial aspect of the occipital lobe, the
parahippocampal gyrus, and hippocampus [11]. This can be difficult to distinguish from
acute toxic metabolic encephalopathy.” UpToDate.com
“Vertebrobasilar ischemia — Ischemia to the visual cortex may result in TBVL
(transient binocular visual loss). If only one hemisphere is ischemic, the patient will
experience homonymous visual field loss contralateral to the lesion. Visual loss may be
an isolated symptom or may be accompanied by symptoms of brainstem ischemia
(dysarthria, dysphagia, vertigo, diplopia) or cerebral ischemia (hemiparesis, hemisensory
loss, aphasia). Isolated visual symptoms are usually the result of occipital lobe ischemia
secondary to posterior cerebral artery occlusion. Difficulty seeing to one side is the most
common symptom; lateralized flashing lights (photopsias) are also common [84,85].”
UpToDate.com
“Occlusive disease of the posterior cerebral arteries (PCAs) causes visual and
somatosensory symptoms due to loss of function in the lateral thalamus and occipital lobe
regions supplied by the PCAs.” UpToDate.com
(F) Epistaxis: “Epistaxis (nosebleed) is relatively common because of the rich
blood supply to the nasal mucosa. In most cases, the cause is trauma and the bleeding is
from an area in the anterior third of the nose (Kiesselbach area). Epistaxis is also
associated with infections and hypertension. Spurting of blood from the nose results from
rupture of arteries. Mild epistaxis may also result from nose picking, which tears veins in
the vestibule of the nose.” (COA p 964)
FIGURE B7.19. Intercranial hemorrhages. A and B. Extradural (epidural) hemorrhage. C. Dural
border (subdural) hematoma. D. Subarachnoid hemorrhage.
16. Compare/contrast the type of hematoma most often associated with the following
conditions:
(A) "Shaken baby" syndrome: subdural hematoma “Cranial injury may be
inflicted by blunt force trauma, shaking, or a combination of forces [3]. The classic injury
pattern that is associated with shaking includes diffuse unilateral or bilateral subdural
hemorrhage, diffuse multilayered retinal hemorrhages, and diffuse brain injury. This
pattern has been referred to as the "shaken baby syndrome" and "shaken/impact
syndrome" [4,5]. The absence of a history of trauma and a paucity of external
manifestations of injury, can make recognition of the inflicted nature of these injuries
difficult.” UpToDate.com
(B) "Worst headache of my life": subarachnoid hematoma “Subarachnoid
hemorrhage — Rupture of an aneurysm releases blood directly into the cerebrospinal
fluid (CSF) under arterial pressure. The blood spreads quickly within the CSF, rapidly
increasing intracranial pressure. Death or deep coma ensues if the bleeding continues.
The bleeding usually lasts only a few seconds but rebleeding is very common. With
causes of SAH other than aneurysm rupture, the bleeding is less abrupt and may continue
over a longer period of time.
“Symptoms of SAH begin abruptly in contrast to the more gradual onset of ICH.
The sudden increase in pressure causes a cessation of activity (eg, loss of memory or
focus or knees buckling). Headache is an invariable symptom and is typically
instantly severe and widespread. There are usually no important focal neurologic signs
unless bleeding occurs into the brain and CSF at the same time (meningocerebral
hemorrhage).
“Onset headache is more common in SAH than in ICH, whereas the combination
of onset headache and vomiting is infrequent in ischemic stroke (show figure 2).”
UpToDate.com
(C) Alcoholism: subdural hematoma: “Head trauma is the most common cause of
SDH, with the majority of cases related to motor vehicle accidents, falls, and assaults
[10].
“Patients with significant cerebral atrophy are at high risk for SDH. This category
includes the elderly, those with a history of chronic alcohol abuse, and those with
previous traumatic brain injury. In such patients, trivial head trauma or even pure
whiplash injury in the absence of physical impact may produce an SDH [7,11]. Thus,
SDH, particularly chronic SDH, is seen in older adults more commonly than younger
adults. However, when limited to acute SDH cases caused by mild to severe head
injuries, the mean age of affected patients is between 31 and 47 years old, and the
majority are men [10,12-15].” UpToDate.com
17. Describe the anatomic defect in each of the following conditions:
(A) Cleft lip: “Cleft lip (harelip) is a congenital anomaly (usually of the upper lip)
that occurs in 1 of 1000 births; 60-80% of affected infants are males. The clefts vary from
a small notch in the transitional zone of the lip and vermilion border to a notch that
extends through the lip into the nose (Fig. B7.32). In severe cases, the cleft extends
deeper and is continuous with a cleft in the palate. Cleft lip may be unilateral or
bilateral.” (COA p 946)
(B) Cleft palate: “Cleft palate, with or without cleft lip, occurs in approximately 1
of 2500 births and is more common in females than in males (Moore and Persaud, 2008).
The cleft may involve only the uvula, giving it a fishtail appearance, or it may extend
through the soft and hard regions of the palate (Fig B7.37). In severe cases associated
with cleft lip, the cleft palate extends through the alveolar processes of the maxillae and
the lips on both sides. The embryological basis of cleft palate is failure of mesenchymal
masses in the lateral palatine processes to meet and fuse with each other, with the nasal
septum, and/or with the posterior margin of the median palatine process.” (COA p 949)
(C) Thyroglossal duct cyst: “Development of the thyroid gland begins in the floor
of the embryonic pharynx at the site indicated by a small pit, the foramen cecum, in the
dorsum of the postnatal tongue (Chapter 7, p. 940). Subsequently, the developing gland
relocates from the tongue into the neck, passing anterior to the hyoid and thyroid
cartilages to reach its final position anterolateral to the superior part of the trachea.
During this relocation, the thyroid gland is attached to the foramen cecum by the
thyroglossal duct. This duct normally disappears but remnants of epithelium may remain
and form a thyroglossal duct cyst at any point along the path of its descent (Fig. B8.6A).
The cyst is usually in the neck, close or just inferior to the body of the hyoid bone and
forms a swelling in the anterior part of the neck. Surgical excision of the cyst may be
necessary. Most thyroglossal duct cysts are in the neck, close or just inferior to the body
of the hyoid bone (Fig. B8.6B).” (COA p 1041)
(D) Tracheoesophageal fistula: “The most common congenital anomaly of the
esophagus is tracheo-esophageal fistula (TEF). Usually, it is combined with some form
of esophageal atresia. In the most common type of TEF (approximately 90% of cases),
the superior part of the esophagus ends in a blind pouch and the inferior part
communicates with the trachea (Fig. B8.17A). In these cases, the pouch fills with mucus,
which the infant aspirates. In some cases, the superior esophagus communicates with the
trachea and the inferior esophagus joins the stomach (Fig. B8.17B), but sometimes it does
not, producing TEF with esophageal atresia (Fig B8.17C). TEFs result from
abnormalities in partitioning of the esophagus and trachea by the tracheo-esophageal
septum.” (COA p 1049)
18. Identify the location (on a coronal CT scan) and most common presenting symptoms
of sinusitis of the following sinuses:
(A) Frontal
(B) Ethmoidal
(C) Maxillary
(D) Sphenoidal
Symptoms of Sinusitis by Specific Site
Site
Acute Symptoms
Chronic Symptoms
ETHMOID SINUSITIS
Ethmoid sinuses are
Nasal congestion.
Chronic nasal discharge,
located between the
obstruction, and low-grade
eyes. They resemble a
discomfort usually across the
honeycomb and are
bridge of the nose.
vulnerable to
Nasal discharge or postnasal drip.
Symptoms worse in the late
obstruction. This is a
morning or when wearing
common location for
glasses.
sinusitis in children.
Pain or pressure around the inner corner Chronic sore throat and bad
of the eye or down one side of the nose. breath.
Headache in the temple or surrounding
Sinusitis also can recur in
the eye.
other sites.
Symptoms worse when coughing,
straining, or lying on the back and better
when the head is upright.
Fever.
Symptoms of maxillary sinusitis often
occur.
Symptoms indicating medical
emergency:
Increasing severity of symptoms.
Fever, swelling and drooping eyelid,
loss of eye movement (possible orbital
infection, which is in the eye socket).
Fever, vision changes, pupil fixed or
dilated. Symptoms spreading to both
sides of face (may indicate blood clot).
ACUTE MAXILLARY SINUSITIS
Maxillary sinuses are
Pain across the cheekbone, under or
located behind the cheek around the eye, or around the upper
bones. They are present
teeth; may occur on one or both sides of
at birth and continue to
the face.
develop as long as teeth Area over the cheekbone is tender and
erupt. Tooth roots, in
may be red or swollen.
some cases, can
Possibly tooth pain.
penetrate the floor of
these sinuses.
Symptoms are worse when the head is
upright and improve when patient
reclines.
Nasal discharge or postnasal drip.
Fever.
FRONTAL SINUSITIS
Frontal sinuses are
Severe headache in the forehead.
located on both sides of
the forehead. These
Fever (common but not always present).
sinuses are late in
developing, so infection
Symptoms are worse when lying on the
here is uncommon in
back and when pressing against the area
children.
over the eye on the side closest to the
nose.
Symptoms are better when the head is
upright.
Nasal discharge or postnasal drip.
Symptoms indicating medical
emergency:
Increasing severity of symptoms,
particularly severe headache, altered
vision, mild personality or mental
changes (may indicate spread of
infection to brain).
Fever, vision changes, fixed or dilated
pupil. Symptoms spreading to both
sides of face (may indicate blood clot).
Discomfort or pressure below
the eye.
Chronic toothache.
Symptoms become worse with
colds, flu, or allergies.
Discomfort increases during
the day.
Coughing increases at night.
Persistent, low-grade headache
in the forehead.
History of physical injury or
other damage to the sinus area.
Headache, fever, along with a soft
swelling over the bone (may indicate
bone infection).
SPHENOID SINUSITIS
Sphenoid sinuses are
located behind the eyes.
They usually are present
by age 3 and are fully
developed by age 12.
Deep headache with pain in many
Low grade, general headache
places, including the back and top of the (although not always present).
head, across the forehead, and behind
the eye.
Fever.
Symptoms are worse when lying on the
back or bending forward.
Nasal discharge or postnasal drip.
Symptoms indicating medical
emergency:
Increasing severity of symptoms,
particularly severe headache, altered
vision, mild personality or mental
changes (may indicate spread of
infection to brain).
(Adapted from: Sinus Disease: Guide to First-line Management. D. Kennedy, ed. © 1994 Health
Communications, Inc. Adrian, CT.)
(Grant’s Atlas)
The labeled features include the ethmoidal cells (E), sphenoidal (S) and maxillary (M)
sinuses, the hypophyseal fossa (H) for the pituitary gland, the petrous part of the
temporal bone (T), mastoid cells (Mc), grooves for the branches of the middle
meningeal vessels (Mn), arch of the atlas (A), internal occipital protuberance (P), and
the nasopharynx (N). (Grants Atlas 12 ed p. 622)
UpToDate.com
Coronal CT demonstrated air-fluid level and gaseous bubbles within the maxillary sinuses in a
patient with acute bacterial rhinosinusitis
CT scan of normal paranasal sinuses
UpToDate.com
This coronal CT image shows normal maxillary and ethmoid sinuses, with the ostio-meatal
complexes widely patent bilaterally. Courtesy of Marilene B Wang, MD.
UpToDate.com
Sinus CT scan of a patient with allergic fungal rhinosinusitis (AFRS) showing complete
opacification of both anterior ethmoid and maxillary sinuses and hyperdensities within these
same areas. Courtesy of Daniel Hamilos, MD
UpToDate.com
Radiographic features of CRS without NP
Sinus CT scan of a 35-year-old female with CRS without NP before and immediately following
intensive medical treatment. The pretreatment sinus CT scan shows near total opacification of
both maxillary and anterior ethmoid sinuses. The post treatment sinus CT scan shows
complete resolution of these findings. The patient's CRS symptoms completely resolved.
Reproduced with permission from: Subramanian, HN, Schechtman, KB, Hamilos, DL. A
retrospective analysis of treatment outcomes and time to relapse after intensive medical
treatment for chronic sinusitis. Am J Rhinol 2002; 16:303. Copyright ©2002 Oceanside
Publications.
19. Define Ludwig's angina and explain (using anatomical planes) how this infection can
spread to the neck and chest.
“Submandibular space infections (Ludwig's angina) — The prototypical
infection of the submandibular space is known as Ludwig's angina. In 1836, von Ludwig
described five patients with "gangrenous induration of the connective tissues of the neck
which advances to involve the tissues that cover the small muscles between the larynx
and the floor of the mouth". Although the term Ludwig's angina has been loosely applied
to a heterogeneous array of infections involving the sublingual, submaxillary, and
submandibular spaces, this diagnosis should be restricted to the following classical
description:
 The infection is always bilateral.
 Both the submandibular and sublingual spaces are involved.
 The infection is a rapidly spreading cellulitis without abscess formation or
lymphatic involvement.
 The infection begins in the floor of the mouth. It is characteristically an
aggressive, rapidly spreading "woody" or brawny cellulitis involving the
submandibular space.
“Location of infection and mechanisms of spread — Although the
submandibular space is further divided by the mylohyoid muscle into the sublingual
space above and the submylohyoid space below, it can be considered as a single unit due
to a direct communication around the posterior aspect of the mylohyoid muscle (show
figure 2). Seventy to 85 percent of cases of Ludwig's angina follow infection of the
second or third mandibular molar teeth. The submylohyoid space is initially involved,
since the roots of these teeth are located below the attachments of the mylohyoid muscle
to the mandible. (See "Epidemiology, pathogenesis, and clinical manifestations of
odontogenic infections").
“Medial spread of infection is facilitated because the lingual aspects of
periodontal bone around these teeth are thinner. Infection extends contiguously to involve
the sublingual and thus the entire submandibular space in a symmetrical manner. If
infection were instead spread via the lymphatics, involvement would be unilateral instead
of bilateral as is observed. An identical process, initially involving the sublingual space,
can arise less commonly from infection of the premolars and other teeth or from trauma
to the floor of the mouth.
“Once established, infection evolves rapidly. The tongue may enlarge to two or
three times its normal size and distend posteriorly into the hypopharynx, superiorly
against the palate, and anteriorly out of the mouth. Immediate posterior extension of the
process will directly involve the epiglottis. There exists a little regarded dangerous
connection between the submandibular and parapharyngeal spaces known as the
buccopharyngeal gap (show figure 2). This is created by the styloglossus muscle as it
leaves the tongue and passes between the middle and superior constrictor muscles to
attach on the styloid process. Thus, cellulitis of the submandibular space may spread
directly into the parapharyngeal space and from there to the retropharyngeal space and
the superior mediastinum.
“Clinical features — Clinically, the patient is febrile and complains of mouth
pain, stiff neck, drooling, and dysphagia, leaning forward to maximize the airway
diameter. A tender, symmetric and indurated swelling, sometimes with palpable crepitus,
is present in the submandibular area. The mouth is held open by lingual swelling.
As the illness progresses, respirations may become difficult; stridor and cyanosis are
considered ominous signs. Radiographic views of the teeth may indicate the source of
infection, and lateral views of the neck will demonstrate the degree of soft tissue swelling
around the airway and possibly submandibular gas. The development of significant
asymmetry of the submandibular area should be viewed with great concern since it may
be indicative of extension to the parapharyngeal space. Surgical drainage will reduce the
risk of spread to this space and subsequently to the superior mediastinum [22].
“Treatment — The therapy of Ludwig's angina has undergone a number of
modifications since its initial description [23]. While maintenance of an adequate airway
is the primary concern and may necessitate urgent tracheostomy, most cases can be
managed initially by close observation and intravenous antibiotics. If cellulitis and
swelling continue to advance or if dyspnea occurs, artificial airway control should be
gained immediately before the onset of stridor, cyanosis, and asphyxia, which would
require tracheostomy under emergency conditions.” (UpToDate.com)
UpToDate.com
20. Describe the most common clinical findings with otitis media and mastoiditis.
“An earache and a bulging red tympanic membrane may indicate pus or fluid in
the middle ear, a sign of otitis media (Fig. B7.43A). Infection of the middle ear is often
secondary to upper respiratory infections. Inflammation and swelling of the mucous
membrane lining the tympanic cavity may cause partial or complete blockage of the
pharyngotympanic tube. The tympanic membrane becomes red and bulges, and the
person may complain of “ear popping.” An amber-colored bloody fluid may be observed
through the tympanic membrane. If untreated, otitis media may produce impaired hearing
as the result of scarring of the auditory ossicles, limiting their ability to move in response
to sound.” (COA p 978)
“Infections of the mastoid antrum and mastoid cells (mastoiditis) result from a
middle ear infection that causes inflammation of the mastoid process (Fig B7.44).
Infections may spread superiorly into the middle cranial fossa through the petrosquamous
fissure in children and cause osteomyelitis (bone infection) of the tegmen tympani. Since
the advent of antibiotics, mastoiditis is uncommon. During operations for mastoiditis,
surgeons are conscious of the course of the facial nerve to avoid injuring it. One point of
access to the tympanic cavity is through the mastoid antrum. In children, only a thin plate
of bone must be removed from the lateral wall of the antrum to expose the tympanic
cavity. In adults, bone must be penetrated for 15 mm or more. At present, most
mastoidectomies are endaural (i.e., performed through the posterior wall of the external
acoustic meatus).” (COA p 979)
Mastoiditis
21. Describe the nerve branch and artery most at risk for injury during placement of
tympanic tubes in children for treatment of recurrent ear infections.
“Perforation of the tympanic membrane (“ruptured eardrum”) may result from
otitis media and is one of several causes of middle ear deafness. Perforation may also
result from foreign bodies in the external acoustic meatus, trauma, or excessive pressure
(e.g., during scuba diving). Minor ruptures of the tympanic membrane often heal
spontaneously. Large ruptures usually require surgical repair. Because the superior half
of the tympanic membrane is much more vascular than the inferior half, incisions to
release pus from a middle ear abscess (myringotomy), for example, are made
posteroinferiorly through the membrane (Fig. B7.43B). This incision also avoids injury to
the chorda tympani nerve and auditory ossicles. In persons with chronic middle ear
infections, myringotomy may be followed by insertion of tympanostomy or pressureequalization (PE) tubes in the incision to enable drainage of effusion and ventilation of
pressure (Fig. B7.43C).” (COA p 978-979)
Chorda tympani nerve “Tympanic membranes generally are translucent,
occasionally allowing for visualization of several middle ear structures (umbo,
manubrium of the malleus, round window niche, pars flaccid, and chorda tympani
nerve).” UpToDate.com
Anterior tympanic a. of maxillary a. (“anterior tympanic a. passes through the
petrotympanic fissure along with the chorda tympani n.” Mich Anat Tables); supplies
blood to middle ear
22. Describe how to access hearing with the following physical examination tests:
(A) Weber: “Assess hearing w/Weber test
 Place vibrating tuning fork on the top of the head
 Ask the patient if the sounds can be heard the same in both ears of better in
one
 Testing lateralization
(B) Rinne: “Assess hearing with Rinne test
 Place vibrating tuning fork on the mastoid bone of each ear
 The examiner asks the patient to tell them when they can no longer hear the
sound
 Then move the tuning fork in front of the ear and ask the patient to tell you
when he can no longer hear it
 Air conduction should be longer than bone conduction” (SPETA outline)
23. Describe the nerves at risk for injury during thyroid surgery and the clinical findings
associated with these injuries.
“Excision of a malignant tumor of the thyroid gland, or other surgical procedure
sometimes necessitates removal of part or all of the gland (hemithyroidectomy or
thyroidectomy). In the surgical treatment of hyperthyroidism, the posterior part of each
lobe of the enlarged thyroid is usually preserved, a procedure called near-total
thyroidectomy, to protect the recurrent and superior laryngeal nerves and to spare
the parathyroid glands. Postoperative hemorrhage after thyroid gland surgery may
compress the trachea, making breathing difficult. The blood collects within the fibrous
capsule of the gland.
“The risk of injury to the recurrent laryngeal nerves is ever present during neck
surgery. Near the inferior pole of the thyroid gland, the right recurrent laryngeal nerve is
intimately related to the inferior thyroid artery and its branches (Fig. B8.10). This nerve
may cross anterior or posterior to branches of the artery, or it may pass between them.
Because of this close relationship, the inferior thyroid artery is ligated some distance
lateral to the thyroid gland, where it is not close to the nerve. Although the danger of
injuring the left recurrent laryngeal nerve during surgery is not as great owing to its more
vertical ascent from the superior mediastinum, the artery and nerve are also closely
associated near the inferior pole of the thyroid gland (Fig. 8.27). Hoarseness is the usual
sign of unilateral recurrent nerve injury; however, temporary aphonia or disturbance of
phonation (voice production) and laryngeal spasm may occur. These signs usually result
from bruising the recurrent laryngeal nerves during surgery or from the pressure of
accumulated blood and serous exudate after the operation.
“The variable position of the parathyroid glands, especially the inferior ones,
puts them in danger of being damaged or removed during surgical procedures in the neck.
The superior parathyroid glands may be as far superior as the thyroid cartilage, and the
inferior ones may be as far inferior as the superior mediastinum (Fig. 8.30). The aberrant
sites of these glands are of concern when searching for abnormal parathyroid glands, as
may be necessary in treating parathyroid adenoma, an ordinarily benign tumor of
epithelial tissue associated with hyperparathyroidism.
“Atrophy or inadvertent surgical removal of all the parathyroid glands results in
tetany, a severe neurologic syndrome characterized by muscle twitches and cramps. The
generalized spasms are caused by decreased serum calcium levels. Because laryngeal and
respiratory muscles are involved, failure to respond immediately with appropriate therapy
can result in death. To safeguard these glands during thyroidectomy, surgeons usually
preserve the posterior part of the lobes of the thyroid gland.
“In cases in which it is necessary to remove all of the thyroid gland (e.g., because
of malignant disease), the parathyroid glands are carefully isolated with their blood
vessels intact before removal of the thyroid gland. Parathyroid tissue may also be
transplanted, usually to the arm, so it will not be damaged by subsequent surgery or
radiation therapy.” (COA p 1043-1044)
24. Describe the preferred locations for performing emergent and non-emergent
tracheostomies. Describe the anatomic basis for the different preferred locations. Name
the structures/layers that are passed through during this surgery.
“A transverse incision through the skin of the neck and anterior wall of the
trachea (tracheostomy) establishes an airway in patients with upper airway obstruction or
respiratory failure (Fig. B8.13). The infrahyoid muscles are retracted laterally, and the
isthmus of the thyroid gland is either divided or retracted superiorly. An opening is made
in the trachea between the first and second tracheal rings or through the second through
fourth rings. A tracheostomy tube is then inserted into the trachea and secured. To avoid
complications during a tracheostomy, the following anatomical relationships are
important:
 The inferior thyroid veins arise from a venous plexus on the thyroid gland and
descend anterior to the trachea.
 A small thyroid ima artery is present in approximately 10% of people; it ascends
from the brachiocephalic trunk or the arch of the aorta to the isthmus of the
thyroid gland.
 The left brachiocephalic vein, jugular venous arch, and pleurae may be
encountered, particularly in infants and children.
 The thymus covers the inferior part of the trachea in infants and children.
 The trachea is small, mobile, and soft in infants, making it easy to cut through its
posterior wall and damage the esophagus.” (COA p 1045)
FIGURE B8.13. Tracheostomy.
25. Describe the most common clinical findings with a carotid body tumor and the most
common complications encountered during surgical removal of this tumor.
“A firm, lateral neck mass which moves from side-to-side but not up and down
indicates involvement with the carotid sheath, such as a carotid body tumor or vagal
schwannoma.” UpToDate.com
Carotid Body Tumor: “A chemodectoma of the carotid body chemoreceptor, may
present as a pulsatile anterior triangle mass.
Features
 Usually presents with a slow-growing mass in the carotid triangle of the neck
 Patients may complain of pulsatile tinnitus
 Mass can usually be displaced in a lateral to medial direction but not up and down
 Diagnostic imaging includes CT and angiography
 Usually a surgical disease” MDConsult
“The vast majority of carotid body paragangliomas present as slowly
enlarging(~5mm per year), non-tender neck masses located just anterior to the
sternocleidomastoid muscle at the level of the hyoid. The classic finding is a mass in this
location that is mobile in the lateral plane but limited in the cephalocaudal direction.
Occasionally the mass may transmit the carotid pulse or demonstrate a bruit or thrill. As
these tumors enlarge, progressive symptoms of dysphagia, odynophagia, hoarseness and
other cranial nerve(IX-XII) deficits appear. The history should include questioning as to
the presence of similar lesions in family members and symptoms associated with
catecholamine production such as fluctuating hypertension, blushing and palpitations.”
(UTMB)
“In the majority of patients (60 to 70 percent), resection of the tumor can be
accomplished without concomitant repair or resection of the carotid artery. In
approximately 10 percent of cases, a simple suture repair of the carotid artery is required.
“More complicated carotid artery repair may be necessary in up to 25 percent of
patients. The type of repair depends on the type of defect created by resecting the tumor,
and may include “patching” of a hole created by tumor resection, or replacing a segment
of the carotid artery with a bypass graft. In situations of more complex repairs, a
temporary shunt is placed in the carotid artery to allow for continuous flow of blood to
the brain during repair.
“One possible complication of resection of carotid body tumors is stroke, but it
occurs in less than 5 percent of patients. Most strokes are associated with large tumors
requiring vascular repair or replacement. Some tumors involve the nerves that lie near the
carotid artery, such as the vagus nerve. Curative resection, in these cases, requires
concomitant resection of the vagus nerve, which may result in dysfunction of the nerve.
Other nerves that may be involved include the facial nerve and the hypoglossal nerve
(which controls the tongue). The risk of nerve involvement correlates directly to the size
of the tumor.
“Approximately 20 percent of patients develop a permanent cranial nerve
dysfunction, but this varies depending on the size of the tumor. Metastatic disease
develops in less than 5 percent of patients, and recurrence can occur in 5 to 10 percent of
patients.” (ClevelandClinic)