SINUS/RHINITIS
Vascular supply-primarily the facial and opthalmic arteries
1. The external and internal carotid arteries supply the nose via their terminal branches.
2. The anterior and posterior ethmoidal arteries supply the region above the root of the
middle turbinate.
3. The sphenopalatine and labial arteries supply the remaining structures.
4. Venous drainage of the external nose is via the facial and ophthalmic veins to the
cavernous sinus [therefore, a superficial infection of the nasal lining may involve the
cavernous sinus].
Neurologic supply-primarily the opthalmic and maxillary nerves
The primary sensory supply is via the maxillary division of the trigeminal nerve.
The other sensory supply is via the facial nerve.
The pterygopalatine ganglion supplies the sympathetic and parasympathetic supply.
Secretory glands are under the command of the autonomic system.
The nasal vascular supply is constricted by the sympathetic system and dilated by the
parasympathetic system.
Important anatomical notes
The ethmoid sinus walls are very thin and thus allow easy spread of infection and tumor to
adjacent structures.
The sphenoid sinus is adjacent to the internal carotid artery, optic nerve and cavernous sinus.
The cavernous sinus contains the occulomotor, trochlear, abducens and the 1st and 2nd divisions
of the trigeminal nerves. The pituitary fossa lies posteriorly.
General: possible signs and symptoms
facial pain
otological symptoms [otalgia, hearing loss, crackling, etc.]
disorders of smell
halitosis-bad breath
blockage
discharge
sneezing
post-nasal drip fever
Facial pain-due to distribution of the trigeminal nerve via the ophthalmic and maxillary
nerves-supplying the face, nose and paranasal sinuses
Otologic symptoms-due to disruption of the function of the Eustachian tube. Polyps, edema from
allergies, tumors and post-nasal drip can physically block the tube
Halitosis-most often from poor dental hygiene and poor diet, but may be due to chronic sinusitis
and post-nasal drip
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There are several primary considerations involved when you include sinusitis/rhinitis in your
diagnosis: timing, discharge, location, presence/absence of fever and the pain. The history, of
course, is of primary importance in your work-up of the patient. It is vital that a proper
examination is performed along with this. Please note that sinusitis may progress to several
serious and, even deadly illnesses, so do not take these complaints lightly. Conservative
management is useful in many cases but it should be monitored.
Work-up: history & physical examination: nasal illumination, palpation, visual inspection,
observe eyes for bulging or displacement, sinus transillumination, radiography,
laboratory
Transillumination of the sinuses-has been found to not be a reliable method for detecting fullness
of the sinuses In a research study that compared general practitioners and specialists in the field
of EENT. Radiography of the sinuses is more reliable if you question your examination results.
Nasal illumination-Inspect the nasal passages for polyps, drainage, color of mucosa, swelling,
and foreign objects
Laboratory-performed by nasal swabmost common organisms: strep. pneumo, hemophilus influenza, staph. aureus, beta strep.
eosinophilia-greater than 400-500 (cells/mm3) will support but not confirm a diagnosis of allergy
Hansel's Stain - used for leukocytes and eosinophils-Therefore, this stain will help you
differentiate an infection from an allergy.
Skin tests- false negative results on skin tests are not infrequent. A negative response does not
exclude allergy, and a positive response is not absolute proof that the specific allergen is causing
the symptoms.
Location of Pain-you must know this!!!
ETHMOID-pain at bridge of nose
most frequent sinus involved
occurs especially in kids
also may have pain on eye movement
MAXILLARY-pain In teeth and cheeks
10% from dental infections
pain in several teeth, not just one
also after cold/flu
teeth painful on percussion
face may be puffy
Innervated by the infraorbital nerves
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SPHENOID-occipital pain
may have dizziness
Innervated by the ophthalmic and maxillary nerves
supplied by the internal carotid artery
FRONTAL- pain on eye motion, supraorbital ache
also after cold/flu
severe in mid-day and then gets better
edema in eyelids
pain aggravated by postural changes
innervated by the supra-orbital nerve
Definitions:
Rhinitis-inflammatory state of the anterior nasal passages, the sinuses are spared.
Can be due to allergic, viral, hormonal or bacterial etiology. Simple allergic or viral
rhinitis may respond well to OTC nasal sprays and decongestants.
Sinusitis-inflammatory state of the sinuses can be due to allergic, viral, hormonal, tumor or
bacterial etiology. The primary cause of this condition is BLOCKAGE of the sinuses preventing
them from draining the discharge that is produced from any irritant. Nine out of ten people
presenting with complaints of sinusitis actually have rhinitis. Sinusitis does not readily respond
to nasal sprays and decongestants, despite the advertising.
Epistaxis-nosebleed.
Rhinorrhea- the watery discharge from the nasal passages one of the most common complaints
The nose produces 1-1.5 pints of mucous per day. Most of this mucous drains down the posterior
nasopharynx where the cilia push it along. Smokers and city dwellers have more irritation and
produce more mucous.
Anterior rhinorrheas-conditions of the anterior nose causing increased rhinorrhea. These Include
excessive mucous production (infection, presence of a polyp, foreign object, etc.), ciliary
abnormality (smoking), and nasal blockage.
Allergen- substance that elicits an allergic response-pollen from trees, grass and weeks, dust,
mold, food and dander from animals
Allergic rhinitis- Includes hay fever, mold and dust allergies and other upper respiratory
allergies. Symptoms include runny nose, sneezing and itchy, watery eyes.
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Histamine- chemical produces by the body and released during allergic reactions. When released,
it causes the dilation of blood vessels and contraction of muscles. Permeate nasal tissue and
cause capillaries to swell and ooze. Fluid from capillaries passes through tissue into nasal cavity.
A runny nose results.
Antihistamine-chemical treatment that actually thickens the discharge by decreasing its water
content; so it gets thicker and decreases the drainage. They may be taken Initially but then the
patient should get off them or they will stop the drainage and make the problem worse.
Immunotherapy- typically administered in allergy shots. Injections of Increasing doses of an
allergen to which the patient is sensitive. The pt. gradually becomes less sensitive.
Mast cells- large cells In connective tissue which release histamines during the allergic response,
below epithelial cells become swollen with histamines and release histamines and other
inflammatory chemicals
Pollen- microscopic round or oval grains that fertilize flowers. Particles from wind pollinated
plants are lighter and smaller and tend to be more allergenic than those from bee-pollinated
plants.
Hay fever- type of allergic rhinitis, seasonal-ragweed most common cause. Season runs until
October, and ends at first frost, warm humid air and lack of breeze traps the airborne allergens in
the area-uncontrolled, allergies can lead to upper-respiratory infections and serious bouts of
asthma-IF symptoms continue past first frost, then possibly sensitive to mold spores
Vasoconstrictor Treatment used to constrict vessels in nasal passages to decrease the
amount of fluid passing from them to the mucosa to decrease inflammation. Long term use can
lead to "Rebound Phenomenon
Rebound Phenomenon-nasal passage swelling due to long term use of vasoconstrictors.
Normal utilization is 4-7 days to shrink mucosa and allow drainage, over 4-7 days can lead to
this phenomenon, leading to blockage. This phenomenon is called Rhinitis Medicamentosa.
Rhinitis Medicamentosa-constant reactive vasodilation of the nasal mucosa due to an
acquired sensitivity of the nasal ling to prolonged use of topical drops and sprays. Many OTC
drugs due fall into the category. Topical steroids may be needed to wean the patient off or will
have severe blockage.
Polyps-sessile or pedunculated overgrowths of mucosa due to recurrent episodes of mucosal
edema, frequently seen in long-standing allergic rhinitis. Typically found bilaterally with the
cardinal symptom of progressive nasal obstruction. Most frequently they are found protruding
from the middle meatus as smooth, gray, pale, spherical masses of mucosa, that are mobile and
insensitive to a probe (which distinguishes them from swollen turbinates) and do not bleed. They
frequently recur after removal.
Note: polyp-When found in children, consider performing a chloride sweat test to rule out cystic
fibrosis and if found in an adult, consider the possibility of a neoplasm.
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Halitosis-bad breath
Discharge from the nose
Blood – (epistaxis) Typically a trivial occurrence due to nose picking or trauma leading to
bleeding from Kiesselbach's plexus, a vascular network in the anterior nasal septum. It can also
be due to anemias, Infections and hypertension. The vessels in the posterior nose belong to the
external carotid artery system. Therefore, if the site of bleeding cannot be seen, consult one of
your texts or send for concurrent management.
Clear - allergic, hormonal, polyps, adenoids, HTN, foreign object, neoplasm, asthma, CSF [CSF
will dry soft and not crusty as normal mucous does]
white to yellow - viral, possibly associated with low-grade fever (less than 101 degrees)
yellow to green-bacterial, possibly associated with a fever, may be atrophic sinusitis or foreign
object or polyp degeneration, may be fungal infection, especially in immunocompromised
patients (diabetics) may appear at the end of a cold-smear would show lots of leukocytes
clear with red streaks-CSF (on a white cloth, a halo will develop)
brown - smokers
SINUSITIS: inflammation of the sinuses
Primary Cause: anything that obstructs the nose
Pain: location of pain typically tells the site of the sinus involved
Treatments: objective is to open sinuses, keep nose open to let air in
1. antihistamines actually thicken the discharge and decrease the drainage, they can be
used initially but should be discontinued ASAP
2. moist heat or diathermy if it is not bacterial
3. vasoconstrictors- spray once, wait five minutes and spray again, then the patient is to
breath through a wet, steamy towel or use a steam apparatus to increase the fluid in the
mucous and increase drainage. Use a vasoconstrictor for 4-7 days to shrink the mucous and
allow drainage. If used over 4-7 days, the patient may have Rebound Phenomenon
4. hang head over edge of bed to promote drainage with affected sinus up for 5
minutes, 3 times a day, for 3-4 weeks.
5. saline spray-may be used to thin mucus and lead to drainage
6. vitamin therapy
7. antibiotics-if bacterial infection
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TYPES OF SINUSITIS and RHINITIS
first the basic things you should already know...
Allergic Sinusitis- the pt. may not have nasal obstruction or nasal discharge. If there is discharge.
it will be clear. You may find copious amounts of this discharge draining down the posterior
pharynx. Watch for timing and look for allergens. The patient will have pain and full feeling In
the involved sinus. The patient will not demonstrate fever or body pains but may have itchy,
watery, red eyes and/or coughing/sneezing. The sinus pain may become severe and debilitating.
If the head pain gets severe enough, a tension headache may overlay the original pattern and
make your diagnostic efforts more complicated. Nasal smear should be performed with Wrights
or Hansel's stain for eosinophils. A count of more than 10% confirms the diagnosis of allergy.
Allergic rhinitis-nasal discomfort and clear discharge (rhinorrhea) without a fever or body pain.
It may be accompanied by itchy, red eyes &/or coughing, sneezing, etc. It is important to track
the cause of the discharge, watching for timing and possible allergens.
Chronic sinusitis-a complication of any acute sinusitis. The pain will be worse on arising in the
morning as there is less drainage while lying down. The pain will be less pronounced during the
day because movement promotes drainage. The tenderness over the sinus will be minor and the
patient will have a normal temperature.
Acute Bacterial Sinusitis-typically there is a hx of an URI. The pt. will have pain in the area of
the involved sinus and possibly redness and tenderness over it and fever. The mucosa will be
swollen and angry red with inflamed turbinates. Copious purulent discharge will be noted that
when checked on nasal smear will show neutrophils. An x-ray will show clouding of the
sinus(es) involved or even a fluid line. always culture (typically gram+ strep. pneumococcus
Infection). These Infections are very resistant to antibiotics and may require several
prescriptions. Can have severe complications.
COMPLICATIONS OF BAC'IERIAL SINUSITIS
The location of the primary Infection will typically dictate what the complication will be. The
following is a list of the primary sinus that was Infected and what is (are) the most likely
complication(s).
Ethmoid sinus > orbital cellulitis, periorbital abscess
Frontal sinus
> meningitis, osteomyelitis, brain abscess
Sphenoid sinus > meningitis
Maxillary sinus---->
ANY sinus
> cavernous sinus thrombosis
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Periorbital abscess-pus extends through the lateral wall of the sinus to form an abscess between
the ethmoid plate and the fascia lining the orbit.
S&S: some increase in fever, pain on movement of the eye, edema between the inner canthus and
the bridge of the nose, tenderness of the edematous region, the pus may push the eye slightly
down and laterally. No chemosis (swelling of the conjunctiva) is present.
Orbital cellulitis-A periorbital abscess may extend to produce a diffuse cellulitis of the orbital
tissue. Invasion may be heralded by a chill, high fever and dull pain in the eye. There is still
pain on ocular motion. The eyelids (especially the upper lid) are edematous, especially at the
inner canthus. Chemosis (swelling of the conjunctiva around the cornea) develops, which
begins at the medial canthus. Ultimately the eye will become fixed. The patient appears very ill
and requires immediate surgery.
Meningitis-The Infection travels through the perforations of the bones along veins between the
periosteum. The patient will have daily spiking fever, stiff neck. Immediate intervention is
required.
Brain abscess-The infection uses the same route as for meningitis, along the veins, to penetrate
the dura and arachnoid layers. The patient will demonstrate weight loss and anorexia, vomiting
and nausea, headache and a low-grade afternoon fever.
Frontal osteomyelitis-redness and swelling of the frontal bone, exquisitely tender! Can look like
acute bacterial infection, just hurts MORE!
Cavernous sinus thrombosis-The patient is VERY ILL! This is the most feared complication of
nasal Infections, the mortality rate is over 50%. The Infection spreads from the nose through the
angular vein to the cavernous sinus, where septic thrombosis occurs. The patient will complain of
deep pain in the eyes, headaches, rigors. The patient is prostrated and may rapidly become
comatose. Early on, selective occular palsy involving one of the nerves in the cavernous sinus,
either the occulomotor (3) or the trochlear (4) or the abducens (6). As this progresses,
exophthalmos can develop. Later, both eyes will become Involved with them being immobilized
and demonstrate proptosis and chemosis. (This can also be a complication of infected facial
wounds, a retrograde infection via the facial veins) High-dose antibiotics may help.
NOTE: Selective ocular palsy occurs early in cavernous sinus thrombosis, whereas orbital
abscess produces complete immobilization of the globe gradually, without preliminary disorder
of a single nerve.
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Clear sinus discharge
Clear sinus discharge can occur with allergies, atrophy, foreign object, hormonal dysfunction and
tumors.
1.Vasomotor rhinitis
-mucosa appears hypertrophic
-profuse, watery discharge
-decreased airway-unilateral or bilateral
-swollen turbinates, esp Inferior
-deep pink to dusky red mucosa due to vasodilation
-hypertrophic changes (mulberries) seen on Inf turbinates seen on post. rhinoscopy
-neurovascular-type reaction
-predisposing factor-STRESS, psychological, endocrine, genetic, allergy
-20-40 yr old esp females
-stimulation of parasympathetics or depression of sympathetics leading to vasodilation and
subsequent increase in secretion, associated with sneezing
-assoc with hormonal changes-puberty, pregnancy, menses, etc.
2. nasal polyp
often associated with vasomotor rhinitis and allergic rhinitis breathing difficulty, Increase
discharge, may need x-ray and post exam see earlier information in Definitions Section
3. CSF rhinorrhea
-CSF leakage due to trauma to subarachnoid space
- intermittent- when the head in forward position
- fluid dries softly
- has a lot of glucose-use a dipstick
must be treated in ER
4. atrophic rhinitis-characterized by copious amounts of dry crusted material with dry crusted
nasal membranes and atrophy of the membranes and turbinates. The patient is also anosmia [loss
of sense of smell] so the patient cannot tell that the breath is fetid [rotten] due to the lack of
mucus. Treatment with syringing the nose 3-4 TID with a syringe or water-pick, steam
inhalations, glucose in glycerine drops. May be associated with syphilis or tuberculosis.
5. systemic [HTN, thyroid], drugs [cocaine], trauma
6. allergic rhinitis
-seasonal, mucosa is edematous and bluish color
-primary symptoms are nasal obstruction from engorged and swollen Inferior turbinates profuse,
thin, mucoid drainage from the ant and post nose, lacrimation, puffiness and discoloration around
the eyes, glossy and swollen mucosa (pale and boggy), sneezing can be year round, if so then
S&S are less severe
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allergen causes vasodilation leading to increased capillary permeability leading to edema leading
to persistent edema leading to prolapse of tissue leading to polypoid development leading to
polyp formation leading to Increase secretion of seromucinous glands
DD: check hx carefully, family, onset, HTN, thyroid disease, cocaine, URI effusions and
perforation of the tympanic membrane
ALLERGIES
10-20% of the population suffer to some degree form nasal manifestations of an antigen/antibody
type 1 hypersensitivity reaction
The symptom complex, nasal obstruction due to mucosal vasodilatation and edema, rhinorrhea,
paroxysms of sneezing due to mucosal stimulation, is produced by allergen binding on to
immunoglobulin E (IGE), which In turn is bound to mast cells. This binding causes
degranulation of mast cells and the release of mediator substances such as histamine,
leukotrienes and SRSA. Many patients will also have a history of asthma, eczema, allergic
dermatitis, drug allergies, aspirin sensitivity.
Allergy myths- allergies are psychosomatic moving to Arizona will help, shorthaired pets do not
cause allergies, allergies are all sniffles and scratches, but no one ever dies from them you
can catch poison ivy by just standing near the plant
Types of Allergies
1. seasonal allergic rhinitis
-primarily caused by tree pollens such as olive, elm and oak and grass pollens such as bermuda
-symptoms-watery, runny nose and/or eyes, sneezing, itching in nose, throat, roof of mouth or
deep in ears
-Condition is aggravated by low humidity, dust, wind and pollution.
2. perennial allergic rhinitis
-caused by house dust, dust mites, mold spores, pet dander, saliva and urine, feather pillows,
pollens, foods and aggravated by pollution
-symptoms-same as seasonal but constant and less dependent on season.
-note-wheat, eggs, milk and nuts may also be culprits
3. occupational allergic rhinitis
-caused by fumes from cleansers, solvents and industrial chemicals and molds, pollens and dust
as they collect on furniture or in air ducts
-symptoms-sneezing, watery eyes, runny nose, headaches, and dry scratchy throat only while in
work environment.
-Commuters exposed to pollens and smog on the way to work may mistakenly attribute
symptoms to the workplace.
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GLOSSARY
Timing
August and September-WEEDS, chiefly ragweed and lamb's quarter
Mostly in winter, but all year-molds, as in damp basement and air-borne
March through May, tree pollens are heaviest now
June on to first frost-grasses
pollen counts are highest from 1 AM to 9 AM
pollen counts are lowest in the late afternoon and evening
Rx/TX
-Mast cell stabilizers- block the release of histamines and other chemicals by mast cells
-antihistamines-prevent histamine from acting on nasal tissue
-decongestant sprays-shrink blood vessels to reduce swelling caused by histamines
-oral decongestants-shrink blood vessels in the nose, reducing swelling
-corticosteroids- shut off nasal inflammation
Other tx
desensitization-injections working on the principle of producing IgG antibody that prevents
antigen binding to IgE. The treatment is only of value if specific allergens can be identified, and
it is essential to commence the series of injections well in advance of exposure.
Information:
allergies and asthma Asthma and allergy foundation 692-2422
pollen and mold counts St. Louis County Health Dept. 854-6825
CERUMEN-Ear wax
Cerumen is produced by seromucinous glands. These secretions combine with desquamated cells
and debris to form wax. Most people are obsessive about it. Tell them to relax. Production of
cerumen appears to be partly controlled by circulating catecholamines. An over production of
wax is often found in patients with essential fatty acid deficiency and can also indicate
atherosclerosis (perform a SMAC)
Appearance of cerumen: Cerumen is shiny and when it builds up it looks lumpy. These are
constants. The color of cerumen is not constant.
white, shiny = water logged
pale yellow, shiny = new cerumen
golden, shiny = been around awhile
amber, shiny = been around awhile longer
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blood-colored, shiny = been around even longer
scab-colored, shiny = boy, it's been there so long, we should name it
brown, shiny = it's been around so long, it should get a job
black, shiny = it's been around so long, it should get a medal
Differentiating a tumor, blood, fungus, or other discharge from the ear from cerumen
ONLY CERUMEN WILL REMAIN SIIINY AND LUMPY
Removal of ear wax [cerumen]
Using a syringe filled with tap water at body temperature, the pinna is pulled to straighten the
EAM, the syringe is tilted to the superior wall of the EAM [never at the tympanic membrane],
and examine the canal after. Be sure to drape the patient and place a bowl under the ear to catch
the fluid. This should not be done if there is a possibility of a perforated tympanic membrane or
if the debris is likely to swell. A curette or spoon may sometimes be used if you can control the
patient and are sure not to touch the highly sensory innervated walls of the EAM as it may cause
the patient to cough and have severe pain Further, the tissue is very fragile and you can cause
severe tearing if you scrape the walls. Never use a curette if the object or wax is very dry. If it is
very dry, then when you try to remove it, it will be like pulling off a scab and tear the EAM.
Very dry cerumen should be hydrated for several days [7-10] with Sweet Oil [special virgin olive
oil], a solution of one part alcohol and two parts water or an over the counter product. Patience is
necessary.
A build up of cerumen is frequently due to dust, hair spray and other environmental debris. More
frequently it is due to cotton swabs being pushed into the canal causing a bit of cerumen to be
pushed in and creating a dam effect.
TINNITUS-use a 512 cps tuning fork
Definition: noises in the ear, real or imagined.
[Most common in patients who have been exposed to long-term, high level intensity noise. The
TMJ, eustachian tube and carotid artery can produce sounds which are usually innocent and can
be heard by the examiner also (objective tinnitus). ototoxicity, neurologic or mechanical
etiologies can also be at fault.]
Rule of thumb:
high pitched tinnitus-typically due to neurologic etiology, includes chemical toxicity.
-sensorineural hearing loss can also be described as a rushing, hissing or buzzing by the patient
low pitched tinnitus-typically due to mechanical etiology, includes middle and outer ear
problems.
Why do you need to understand this condition? 35 million people are afflicted with tinnitus
annually
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Systemic causes and their pictures: typically high pitched
1. Costen's Syndrome: typically in menopausal females
the patient may present with ear discomfort and Slight deafness with tinnitus
the tinnitus is due to abnormal stresses of the TMJ
a general picture will present with dryness of the eyes and mouth, sialoadenitis, recurrent attacks
of arthritis
2. Diabetes neuritis-unilateral sensorineural deafness with tinnitus of course, other systemic signs
will be seen
don't forget to check the PDR for the influence of any medication
3. Syphilis-unilateral sensorineural deafness with tinnitus vertigo is present
other systemic signs and symptoms will also be present
4. cerebral tumor-intermittent tinnitus associated with aura and seizure
5. persistent noise exposure-ringing or cricket sounds
If the patient has had short4erm exposure to noise, the sound may be temporary.
It would be wise to have the patient's hearing screened by an audiologist to monitor for
sensorineural hearing loss
6. acoustic neuroma-constant tinnitus. begins faint and gets louder as the tumor grows, vertigo
accompanies this condition. The vertigo comes on gradually, as does the tinnitus, so the
patient may be able to compensate fairly well, so you may see some ataxia.
Acoustic Neuroma-a benign, expansile lesion located anywhere along the 8th cranial nerve
from the cochlea to the brainstem.
The patient can have other signs and symptoms depending on the location and the size of
the tumor. If the patient has loss of the corneal reflex, then the growth of the tumor is
compromising the 5th cranial nerve.
If the patient is experiencing facial Palsy, then the growth of the tumor is compromising the
7th cranial nerve. Though this is a benign tumor, death may occur, if the tumor gets large
enough, it can significantly increase intracranial pressure.
7. Hypertension constant tinnitus
may be due to hypoxia from the typically associated atherosclerosis
8. Anemias constant tinnitus due to hypoxia
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9. Presbycusis-YOU MUST KNOW THIS DEFINITION -tinnitus due to aging. It is typically
associated with sensorineural hearing loss and therefore; typically high pitched.
An interesting point-Due to the gradual onset, the patient may be unaware of the noise
until a heavy cold produces a temporary conductive hearing loss, which highlights the
tinnitus. With aging, there is degeneration of the hair cells of the Organ of Corti and
the cochlear nerve fibers.
Examination is negative.
The patient will play the TV loudly, complain that people mumble.
Masking is helpful with most to cover the tinnitus if it disturbs sleep.
Hearing screening is definitely in order.
10.Bell's Palsy-tinnitus with pain around the ear, eyelid fasciculation and facial twitch most
common cause of facial paralysis and is a diagnosis of exclusion. The nerve will swell within the
bony canal causing a conduction block [neuropraxia]. Discomfort or pain around the mastoid
may precede the palsy. Loss of hearing, taste and hyperacusis may be present. When the palsy is
incomplete, 90% of patients have a satisfactory recovery within 6 weeks of onset.
[Note: The facial nerve is a motor nerve which has a complex course from the brain
stem through the temporal bone and the parotid gland, before innervating the muscles
of the face that result in expression. There are also sensory fibers that run along this
nerve for taste from the anterior 2/3 of the tongue and secromotor fibers for the
lacrimal, submandibular and sublingual glands. The site of the lesion of the nerve will
determine the picture the patient will present. For instance, in supranuclear lesions, the
forehead is often spared due to bilateral innervation; infranuclear lesion produce lower
motor neuron paralysis with both the upper and lower facial muscles involved.
Facial palsy can be due to trauma to the facial nerve, herpes zoster oticus,
cholesteatoma, parotid tumor, acoustic neuroma, or facial nerve tumor.]
To differentiate stroke (supranuclear) from Bell's Palsy (infranuclear) check the
frontalis muscle. Always examine all the cranial nerves.
11. ototoxicitv- The active metabolic processes of the inner ear are very susceptible to drugs.
Those that affect the renal system will frequently affect the ear, ie. aminoglycosides and
cytotoxic agents, salicylates and quinine. Typically will be a constant high pitched tinnitus.
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Local causes of tinnitus
1. torus tubaris dysfunction-a blowing or swishing sound is reported by the patient
¾
2. foreign body in the middle ear-a phlebolith can break free and begin moving in the
middle ear. Auscultate the ear while the patient is moving the head.
3. Meniere's Disease or Multiple Sclerosis-unilateral tinnitus with hearing loss, also
vertigo
5. Carotid stenosis, arteriovenous aneurysm, nasopharynx carcinoma-These will
produce a low/pulsing swish that is synchronous with the heartbeat
6. any air conduction hearing loss (ie. otitis media, otitis externa with moderate to
severe swelling, any eustachian tube dysfunction)- low Ditched tinnitus on the side of
involvement, may he intermittent, may be constant. dependent on cause
ie. otitis externa tinnitus accompanied with itching around the ear
ie. foreign body or impacted cerumen~constant, low pitched
ie. perforated tympanic membrane~constant, low pitched, until healing occurs
ie. serous otitis media-may have intermittent low pitched tinnitus if the eustachian tube
drains occasionally
NOTE:
a conductive hearing loss may lead the patient to have tinnitus that is
associated with chewing.
7. myofascitis-typically, trigger points of the masticatory muscles, especially the
upper posterior deep masseter muscle will refer motor unit activity to the stapedius
muscle causing movements of the ossides leading to motion of the oval window
leading to activity in the cochlea resulting in the stimulation of the nerve fibers, There
is not a hearing deficit with this condition.
Causes-cutting thread with teeth, chewing ice, incessant gum chewing, pipe stem
holding with teeth, cracking nuts, mouth breathing, emotional tension [the muscles of
mastication are the first muscles to contract in reaction to tension (fight or flight
response)], occlusal disharmony.
CHECK the TMJ
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OTALGIA
Definition: earache. Diagnosis is made by examination of the pinna, ear canal and
tympanic membrane. If the ear is normal, the pain may be referred by one of several
cranial nerves supplying the external and middle ear or via myofascitis.
Note: Pain can be referred to the ear via
C2 and C3 [cervical spondylosis]
FYI: C2 via the lesser occipital nerve and C2 &~ via the greater auricular nerve
5th cranial nerve [teeth. parotid. TMJ. Tongue, nose and sinuses]
FYI: especially the auriculo-temporal branch of the trigeminal
7th cranial nerve [sensory branch]
9th cranial nerve [oropharynx]
10th cranial nerve [larynx. hypopharynx and esophagus
1.
Otitis externa-Infection or inflammation of the EAM
The patient may have mild to severe pain.
Symptoms are aggravated with movement of the tragus.
Fever is not uncommon.
If swelling is significant, there may be a conductive hearing loss and possible low
pitched tinnitus
S&S: mild itching, swelling, pale to red epithelium, otorrhea is possible,
lymphadenopathy is possible
anterior to the tragus
Note: if the condition is due to frequent water exposure. the condition is called
Swimmer's Ear. The cerumen, which protects the EAM [external auditory meatus], is
washed away frequently allowing drying of the epithelium with resultant irritation and
possible opportunistic infection by streptococci, staphylococci, pseudomonas and fungi.
Therefore, it is important to monitor these cases.
If your patient has Swimmer's Ear-ear plugs should be used to allow the cerumen to build up and protect the ear.
-If water does get in the ear, it should be removed, a hairdryer or 1:2 solution of alcohol,
and
water can be used to remove the water
-Cortisone creams or triple antibiotics may be used
-can irrigate with a solution at 38 degrees Centigrade (body temperature) with 1 part 70 %
peroxide, 2 parts water, 1 part 5% vinegar 3 times per day
2.
furunculosis the infection of a hair follicle in the EAM usually a staph infection
S&S: severe throbbing pain with a red, tender eminence with or without a pustule
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3.
malignant otitis externa-an aggressive form of otitis externa
This pathology commonly occurs in immunocompromised patients.
It is a spreading osteomyelitis and can lead to intracranial infection
S&S: severe pain that extends beyond the ear
4.
myringitis bullosa-a localized form of otitis externa where blisters form on the
tympanic membrane and deep in the external auditory meatus
It is presumed to be a viral infection and treatment is symptomatic
5.
foreign bodies in the EAM-do not flush dried objects The EAM is innervated by:
6. perforations of the tympanic membrane - The patient will initially have pain when the
rupture occurs and then the pain stops. There will be a conductive hearing loss and the
patient will state that it sounds as if they are speaking in a cloud. Tinnitus [low
frequency] is possible. A large perforation will typically heal in six weeks.
7. acute otitis media - overall view
Otitis media is a result of blockage of the eustachian tube allowing build up of the
normally produced serous fluid in the middle ear chamber or the proliferation of viruses
or bacterial in the middle ear.
It occurs most often in infants UD to 4 years old due to the horizontal orientation of the
eustachian tube.
Pain will occur when pressure in the middle ear develops and will resolve upon
spontaneous rupture of the drum.
first, a rule of thumb. Once a child has had a middle ear infection, serous or purulent, the
child will have more bouts of this.
Second, prevent this in your patients. An infant should not be fed with a bottle lying
down or given a bottle while in its crib. The milk will pool and block the torus tubaris
leading to eustachian tube dysfunction.
Third, if your young patient has allergies or recurrent bouts of otitis media, discuss the
utilization of decongestants with the concurrent care provider or home therapy to open
the eustachian tube. If the child is old enough, regular gargling several times per day to
dear the mucus from the torus tubaris may be of great assistance in preventing otitis
media or even resolving it.
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note:
blue posterior to the tympanic membrane = blood
white = pus, purulent otitis media
bubbles with fluid line = fluid, serous otitis media
Antibiotics are frequently prescribed, even for the serous type. It is thought that this is
leading us to super infections.
Antihistamines in some studies have proven to be effective.
A pharyngeal sweep, from superior to inferior, can prove to be effective by pulling the
fascia surrounding the torus tubaris open and removing mucus from the t. tubaris. This
must be done repeatedly if the patient is having significant post-nasal drainage.
[Pharyngeal sweep-slide your gloved finger along the gums or molars toward the back of the
throat, move your finger slightly medially to pass around the pharyngeal fold and the tonsil,
move your finger superiorly to just above the hard palate and sweep firmly inferiorly to the oral
pharynx. This can have a high success rate with just one treatment. Be sure to warn the
patient/parent that the patient may gag. Be forewarned, you may get bitten. With very small
children, you may wish to do this only when other treatments have been unsuccessful. If you can,
you may wish to sweep/massage the posterior pharyngeal area with your finger to massage the
lymph chain.]
Cervical spine adjustments may be helpful by increasing blood flow to the area to dear the
infection and the by-products of infection from the area, by decreasing the inflammatory
chemical concentrations and increasing the lymphatic flow.
NOTE: There are multiple complications of the purulent middle ear infection. Extracranial
complications of otitis media
1. mastoiditis- still the most common complication and mostly in children severe pain, usually
localized over the mastoid process
Early signs of mastoiditis include a sagging or swollen posterior EAM wall and edema over the
mastoid and zygomatic areas. Eventually the pinna will be pushed anterior and inferior by a
subperiosteal abscess.
2. facial paralysis-if the facial nerve in the middle ear is not covered by bone in your patient,
there may be enough pressure developed to cause a neuropraxia
3. labyrinthitis-A giddiness and loss of balance with nausea and vomiting, and sensorineural
hearing loss following a bout of otitis media. The patient will lie in bed with the affected ear up
to decrease the 5 sensations.
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Intracranial complications of otitis media
1. Intracranial suppuration-a significant mortality rate,
2. Meningitis-headache, fever; later-stiff neck, irritability, confusion
3. Cerebellar abscess-nystagmus, past pointing and ataxia with headache
4. Temporal lobe abscess-headache, rigors, fever and vomiting (cerebritis) then after several
weeks present with paralysis or visual field changes or "fits"
5. Thrombosis of lateral venous sinus-due to the infection passing through the mastoid. A clot
will develop until the lumen is occluded. S&S: rigors and high fever
Hearing Loss
Sensorineural hearing loss-loss of sound perception due to any disorder from the oval or round
window to the brain due to trauma, infection, congenital, etc. causes
Conduction hearing loss-loss of sound perception due to the blockage of the sound waves
reaching the receptor organ. Due to blockage, infection, trauma or congenital malformation.
Tuning fork tests
Best performed with a 512 cps tuning fork, a 256 cps tuning fork is acceptable.
Rinne Test Normal AC > BC positive
Abnormal AC < BC negative
Weber Test lateralized sound to one ear
The sound will be heard in the good ear with a sensorineural lossThe sound will be heard in the bad ear with a conduction loss-
TRAUMA to the head
Mandibular fractures-typical site it the condylar neck
--the patient will have severe trismus
Malar fractures typically due to a blow to the cheek
---the fracture will produce a depression that may be obscured by swelling
---palpation may reveal a step over the infraorbital ridge, if the infraorbital nerve has
been insulted, then the cheek may display sensory loss
Maxillary fractures-Le Fort I, II and III
---severe hemorrhage and fatal airway obstruction can complicate these fractures
---palpation reveals bony irregularities
Orbital blow-out fractures-a blow that pushes the eye into the orbit
---the orbital floor is fractured
---limited eye movement
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Nasal fractures-most are lateral
---a lateral fracture may have to wait 7 days for correction due to swelling
---an anterior fracture may have to wait10 days for correction
It is important to note that a fracture anywhere in the skull may cause one or both eves
to blacken.
EQUILIBRIUM
1.EYES
2.PROPRIOCEPITON
3. VESTIBULAR APPARATUS [SEMICIRCULAR CANALS, ETC]
Vestibular apparatushair cells >neurons->vestihular [Scarpi's] ganglion~>cerebellum
[fastigial nucleus]
[flocculonodular lobe]
[nuclei of cranial nerves III, IV and VII
[spinal cord-primarily the vestibulospinal tract]
the eyes reflex [as in nystagmus] along the medial longitudinal fasciculus
Proprioceptive input
upper cervical is actually more responsive due to the more direct neural communication
Cl -C2 lateral cervical nerve - nerves are monsynaptic and have direct connections to the spinal cord
stimulation of muscles innervated by these nerves can cause nystagmus [splenius capitus]
C2 dorsal root ganglia-takes sensory information from the joints and muscles
-has direct connection with the spinal cord and brainstem nuclei [medullary nuclei-inc. vestibular
nuc, cuneatus]
stimulation of traumatized cervical muscles can cause nystagmus
It is assumed that you realize that trauma to the head and neck can cause significant
neurologic, vascular and soft tissue problems. Further information on this will not be
pursued in this course. It is your responsibility to seek out this information.
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Vestibular System (see table 22C in class file)
Equilibrium-maintained by three sources: eyes, proprioception and vestibular apparatus in inner
ear
-for instance, a person with congenital atresia of the labyrinth system will be able to
accommodate due to vision, but in the dark or swimming, the person will be disoriented
-vestibular impulses caused by motion of the head help the eyes fixate on an object
-it is thought that loss of proprioception or vision causes more significant balance and equilibrium
problems, if both vestibular systems were congenitally absent or ablated, the patient would have
problems in the dark or on a soft surface.
Vestibular System-the righting mechanism, a function of the vestibular division of the VIIIth
cranial nerve, the acoustovestibular nerve. The vestibular system is part of the extrapyramidal
tract as it does not involve the cerebral motor cortex and it is reflexive.
The vestibular System called the labyrinth is comprised of the three interconnected structures of
different function, which can be divided into two Systems.
1. for linear acceleration-the utricle and the saccule [two fluid-filled sacs]
a. the utricle-position of the head relative to gravity b. the saccule-same-but for high
velocities
b.
2. for rotation of the head-the three semicircular canals [fluid-filled and perpendicular to each
other]. They have hair cells [receptor cells] that wave in the fluid currents of the endolymph that
moves when the head moves.
The semicircular canals begin and end at the utricle. At the origin of each canal is an enlarged
area or dilation called the ampulla [containing the end organ of balance, the crista] The receptors,
linings and endolymph are the same throughout the system except for their organization, giving
them different functions. In the ampulla is the crista, lying Perpendicular to the orientation line of
the semicircular canals. On top of the crista, are hair cells with a gelatinous cap that forms a
valve-like structure that is sensitive to the smallest motion of the endolymph. They stay behind or
lag when movement is initiated by the head; so you get a lag in the sensory input from this
system which conflicts with the proprioceptive and visual input you are getting at the same time.
The receptors in the saccule and the utricle respond to the pull of gravity and to the inertial
movement caused by linear acceleration and deceleration.
The ampullae receptors in the semicircular ducts respond to the rotation of the head in any
plane.
The hair cells in the vestibule contact dendrites of neurons in the vestibular ganglion. Most of the
axons of these neurons end in the vestibular nuclei, but a few go directly to the cerebellum.
Neurons in the vestibular nuclei have axons that end in the vestibulocerebellum [fastigial nucleus
and flocculonodular lobe], the nuclei of cranial nerves Ill, IV and VI; and the spinal cord. There
also is a pathway to the thalamus and cerebral cortex.
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Reflex movements of the eyes in response to stimulation of the kinetic labyrinth require the
integrity of a reflex arc that includes fibers in the medial longitudinal fasciculus.
You can test the vestibular apparatus with rotation, caloric or galvanic stimulation.
Vestibular nystagmus occurs when the semicircular canal system is overstimulated. It is seen as
the slow phase of the nystagmus and the brain causes the fast [snap back] portion of the
nystagmus, as seen with rapid spinning.
With caloric testing, warm or cold water is placed in the EAM, the temperature being transmitted
through the bone to die semicircular canals. Since the horizontal semicircular canal is closest to
the water, it is most affected, therefore, you will see most of the effect in the horizontal plane.
The ampulla lies medially and anterior [superior when supine] to the semicircular canal.
Placing the patient supine with 30 degrees of head flexion [bringing the horizontal semicircular
canal to a vertical position], the cool water irrigating the EAM will cool the endolymph,
especially of the horizontal canal. The endolymph gets denser and its fluid level falls decreasing
the stimulation to the crista in the ampulla, causing the eyes to rotate toward the cool water
irrigated ear. This is due to the sensation that you have rotated your head in the opposite
direction. You will see a slow motion of the eyes toward that ear [vestibular phase] and a fast
motion away brain phase]. If the ear is irrigated with warm water, making the endolymph less
dense and stimulating the crista in the eyes will move away from that ear, endolymph and an
imbalance between the two ears giving a sensation that yon have turned your head in the opposite
direction. In short, the eyes move opposite the side of stimulation which is the Opposite of head
movement.
COWS - cold opposite, warm toward as the nystagmus is named for the fast phase
Neurology of this system - an afferent reflex input to the motor system
Stimulation of the labyrinth [vestibular system] leads to
stimulation of the vestibular ganglion (Scarpi's] in the internal auditory canal
1. going to the vestibular nuclei ~ the medulla and pons
the medial and superior vestibular nuclei project via the ascending medial
longitudinal fasciculus to the oculomotor nuclei of the 3, 4, and 6th cranial nerves
vestibuloocular reflex
(note the medial vestibular nuclei also sends descending projections via the medial
vestibulospinal tracts in the medial longitudinal fasciculus to cervical musculature]
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2.
some fibers go directly to the cerebellum in the area of the fastigial nuclei
flocculonodular lobe, inferior vermis. This area also receives direct fibers of the
vestibular nerve. The vestibulocerebellum also has efferent fibers that terminate with the
vestibular nuclei.
The role of the cerebellum in maintaining equilibrium is exerted mainly through
pathways from the vestibular nuclei to the spinal cord via the vestibulospinal tract. The
fibers originate in the lateral vestibular nucleus descend in the medulla into the ventral
funiculus of the spinal cord, terminating in the medial part of the ventral horn mostly in
the lumbar and cervical regions. Therefore, the vestibulospinal tract is important in the
regulation of the tone of muscles in posture for balance. Stimulation of the vestibular
nucleus on that side will stimulate the extensors in that limb and inhibit the flexors,
causing the foot to press into the ground.
The symptoms of nausea and vomiting are from excessive or prolonged stimulation of
the vestibular system with efferent fibers from the vestibular nuclei with collateral
branches ending in visceral centers and parasympathetic nuclei in the brain stem.
VERTIGO-the illusion of movement
The cause of vertigo may be peripheral [otological] or central (brainstem]
The peripheral system of the ear receives input from the ear, eye, joint proprioceptors,
and cerebellum
Examination :Cranial nerves, otoscopic, tuning fork, ophthalmoscopic,
Romberg's Test, gait, vitals
Otoscopic exam may reveal-middle ear disease
Romberg's Test may reveal that the patient sways when the eyes are closed which
deprives the patient of this sensory input. This is positive with loss of joint proprioception
or peripheral vestibular disturbance. Blood pressure-may reveal postural hypotension
Positional Test-From an erect position on a couch, the patient lies down with the head
turned to one side. The onset of vertigo is noted. Have any feeling of vertigo or signs of
nystagmus settle prior to having the patient sit up. Have the patient sit up and repeat with
the head turned to the opposite side. This test differentiates vertigo of the peripheral
apparatus vs. a central cause.
Causes (See table 21B in class file)
1. Meniere’s Disease – an endolymphatic imbalance that occurs in periodic clusters
affects young and middle aged adults, cause unknown, tinnitus with sensorineural
hearing loss will begin as fluctuating and become constant and herald the onset of
vertigo.
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2. Acoustic neuroma-benign expansile tumor of the eighth cranial nerve anywhere from
the brainstem to the ear
The tinnitus will begin as faint and get louder.
Vertigo-You may see more Ataxia than vertigo because the slow growing lesion allows
the patient to accommodate.
3 proprioceptive vertigo-commonly seen in whiplash injuries, discogenic spondylosis,
cervical disc injuries and myofascitis
Proprioceptors orient the head to the body whereas the vestibular apparatus orients the
body to space
3a. myofascial proprioceptive vertigo typically the clavicular division of the SCM*
The patient will have the illusion of disagreeable motion that occurs with a sudden
turning of the head or other motions.
The patient may fall when bending forward, stooping or be ataxic.
The patient may simply feel like falling backwards when looking up and visa versa.
These attacks can last just a few seconds [or last for hours]
Nausea is common
Other symptoms include: carsickness, frontal headaches, dizziness, turning in bed,
holding the phone with the shoulder.
Activated by painting, sleeping on two pillows, sports, scoliosis, emphysema, neckties.
The key is: DRAMAMINE RELIEVES NAUSEA BUT NOT DIZZINESS
Another myofascial proprioceptive vertigo is EAGLE Syndrome
The styloid process is elongated by calcification of the stylohyoid ligament
There are trigger points in the posterior belly of the digastric and medial pterygoid
muscles
Note: There are typically concurrent trigger points in the SCM
S&S: dizziness, visual blurring with decreased vision on the same side.
Pain and dizziness on extreme rotation of the head
This may give suspiciously positive signs like a + George’s Test.
but there is no nystagmus and does give pain.
3b. spondylosis
3c. cervical muscle strain and joint sprain
4. Hypoglycemia-mostly the complaints are of a lightheadedness nature.
The complaints will typically be in the morning or 3A hours post-prandial.
A serum glucose test should be performed while the patient is symptomatic.
If the results are positive, Then, you order a glucose tolerance test.
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5. Vestibular neuronitis-A viral infection of the vestibular nerve
There is often a history of an upper respiratory infection 2-3 weeks prior to the onset of
symptoms
There is a sudden onset of dizziness and sometimes nausea.
The patient may complain of feeling the earth move.
The episodes may be short and mild or long and severe
The viral infection typically clears in 3 weeks to 3 months.
6. (demyelinating disease- nystagmus, sensorineural hearing loss, dizziness, etc. what you
see here is a global pattern that involves several systems.
7. Benign postural hypotension - take the blood pressure sitting, standing and recumbent
8. middle ear disease - unsteadiness on the feet, true vertigo
9. Benign paroxysmal positional vertigo-An episodic vertigo, usually dramatically described as
occurring on turning the head, particularly in bed. It can follow an upper respiratory tract
infection or head injury, but there may be no preceding illness. The vertigo lasts several seconds
and fatigues with repetitive stimulation such as repeated positional testing. These typically
resolve spontaneously.
10. aging -loss of balance due to failing eyesight and hearing. Cervical spondylosis and
vertebrobasilar ischemia and atherosclerosis or the cerebral arteries. There may also be postural
hypotension and cardiac arrhythmias. A medication may also be at fault, ie. antihypertensives.
11. Migraine -only unsteadiness and imbalance, not a true vertigo
12. Transient ischemic attacks- sense of imbalance associated with other neurologic signs that
last 24 hours
Vertigo-Testing - Always perform complete HEENT Exam
1. OBSERVATION-while going to room gait-unsteadiness or leaning mood-anxiety,
moodiness, confusion
2.
CRANIAL NERVESwhile testing, observe facial movements-could be indicative of acoustic neuroma,
stroke checking peripheral vision, vision loss, blurring-tumor, trauma, MVA
3. EAR otitis externa, otitis media, cholesteoma
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4. PALPATION
cervical lymph nodes, trigger points
5. AUSCULTATION
posterior to mastoid if tinnitus timed with pulse~arterivenous aneurysm
cervical vessels-bruit
6. BLOOD PRESSURE
positional, antihypertensives
7.
NEUROLOGIC TESTING
DTR [increased with UMNL], Dermatomes [checking for numbness], Myotomes
Nylen-Barany or Barany or Halipike or Dix-Hallpike Test for dx of BPPV
pt. seated then lie the pt. down with head in extension 30-45 degrees and 30-45 degrees
rotation
a. BPPV-vertigo and nystagmus appear after 3-4 seconds and will decrease and stop
after 10-60 seconds
slow phase of nystagmus goes down toward the downward ear
[R ear down = eyes R]
1. peripheral cause - decrease with repetition
2. central cause-no decrease in vertigo or nausea
b. Have patient stand on one foot with eyes closed, and then other foot-if can do then
EN [uemura]
c. Have pt. hop on one foot-difficulty hopping if cerebellar dysfunction on the same
side as the foot being hopped on
d. Tandem Romberg-have the patient read a sign over the shoulder while walking the
other direction
e. Sharpened Romberg-have the patient stand with arms across chest with eyes closed
and head rotated as if reading over the shoulder [Tandem Romberg position]
normal-can maintain position > 30 seconds purpose-vestibular systems screen
f. stepping test-marching in place 50 x at same speed as in walking watch for turning
of head, position of arms/body or sway ABN = > 30 body rotation or 1 meter of body
movement from starting place. The key here is nystagmus.
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THROAT
Sore throats-patients describe a sore throat ranging from dryness to pain.
Important !!!When do you need to culture a sore throat
1. if there is a history of exposure to strep
2. if there is a fever over 101 degrees
3. if there is tonsillar or pharyngeal exudate
4. if there is tender, cervical lymphadenopathy
5. if the condition is not resolving
6. if the condition is worsening
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