Tier II: Ears, Nose & Throat

There are eight common complaints of the head and neck.

1. Loss of hearing

2. Ear pain

3. Facial Trauma and Nose bleeding

4. Rhinitis

5. Mouth pain

6. Mass in the neck/jaw

7. Diplopia

8. Eye pain

9. Abnormal vision

10. Headache

I. Loss of hearing

The ear receives sound vibrations through the external auditory canal; they are received by the tympanic membrane, amplified by the middle ear bones (conduction system) to the cochlea that registers the sounds (nerve system). CN VIII takes the sound to the brainstem. To diagnose loss of hearing, follow sound from the source through each of these steps.

A. External ear: look in the external ear for cerumen impaction or foreign bodies. Place the otoscope flat on the table. Keep it parallel to the floor throughout the exam. Start with the good ear. If you are examining the left ear, pick up the otoscope with your left hand using three fingers. This will keep you from wrenching the otoscope around in the patient’s ear. Use you right hand to grasp the pinna. Place the tip of the otoscope in the ear and have a look; use your right hand to move the pinna to straighten out the EAC until you can see the TM. There is no vertical dimension to this; if you keep the otoscope parallel to the floor, the patient will have no pain.

B. Tympanic membrane. The normal TM is like a transparent sail. The pressure behind the TM buldges the center of the TM towards you to form a subtle cone. The light from your scope bounces to all sides of the cone, creating a slight light reflex (Figure 31.1).

1. Perforation will appear as a visable hole in the TM.

2. Bullous meringitis is due to a Mycoplasma infection. It will appear as vesicles on the TM.

3. Otisis media is inflammation in the middle ear (behind the TM). The TM will appear red and inflamed. Obstruction of the eustacian tubes traps oral anerobic bacteria in this enclosed space, leading to infection. Children have frequent middle ear infections as the eustacian tubes develop. When examining a child, always look in the ears last unless you think the examination will induce crying. The act of crying will inflame the TM in a child, and this can deceive you into thinking an otitis media is present. In this case, use an insuffalation device (a bulb attached to the otoscope) to insert air into the EAC. A normal TM will move back and forth like a sail. Inflammation behind the TM (in otitis media) will prevent this movement.

4. Pus behind the TM (purulent otitis media) will appear as a completely white TM.

5. Serous otitis is non-infected fluid trapped behind the TM. econgestants will open the eustacian tube to drain the fluid.

C. Middle ear bones to the cochlea. It is hard to see abnormalities of the cochlea, but you can do a simple test to evaluate if it is working properly. Remember there are two components of hearing: 1) Conduction from the EAC to the cochlea and 2) Nerve transmission from the cochlea to the brainstem. 

1. The Webber Test distinguishes between a conduction deficit vs a nerve deficit. Ask the patient to identify which ear has the hearing deficit. If both ears have abnormal hearing, skip to the next test (Rine test). Look in this ear to exclude the obvious EAC obstruction. If this is normal, strike a tuning fork on your hand and place it on the center of the top of his head (or just ask the patient to hummm). The tuning fork vibration travels through the bone to both cochlea. Ask him to identify which ear detects the vibration the greatest.

a. If the hearing deficit is due to a nerve defect, the bad ear will not detect the vibration, and the tuning fork vibration will be best felt (heard) in the opposite (good) ear.

b. If the bad ear has a conduction deficit, all external sound will be eliminated. This will optimize the bone vibration, and the bad hear will detect the vibration the greatest. You can convince yourself by applying the same test on yourself. Put your finger in your right ear while you humm. You will feel the vibration the strongest in your obstructed right ear. (right).

2. Rine test. Strike the tuning fork and placed the single end on the mastoid (behind the ear). These vibrations through the bone will bypass the conduction system and go straight to the cochlea. Now set the forked part of the tuning fork next to the external ear. Ask the patient which sounds stronger. Although solids conduct vibration better the air, the amplification system of the normal ear (the middle ear bones) makes air conduction greater than bone conduction (AC>BC). This is true unless the amplification system is broken, in which case BC>AC.

a. If the deficit is due to a conduction deficit, bone conduction will be greater than air conduction.

b. If the deficit is due to a nerve deficit, the normal pattern is preserved, but at a lower level of volume (AC>BC).

3. The other clue to the cause of the hearing loss is listening to the patient talk. If the patient has a conduction deficit, he will still feel the volume of his voice through bone conduction as he speaks. His voice volume will be normal. If he has a nerve deficit, he cannot determine the loudness of his voice and he will speak very loudly.

NUGGET: Cerumen is easily removed with a warm hydrogen peroxide-saline mixture. Remove the needle from an angiocath (IV). Attach the tubing to a 50 cc syringe and place it in the ear. Repeatedly squirt the mixture into the ear (it may take a liter or so), until the cerumen falls out. Do not try to scrape it out; you will only pack it deeper.

NUGGET: the most common foreign body is a bug (baby cockroach). Fill the EAC with lidocaine before removing the bug; this will paralyze it so it will not resist you pull, preventing the removal of half a bug.

II. Ear pain. Start with the external ear and work in.

A. Pinna: Erythema of the external ear is due to either:

1. Califlower ear. Trauma to the ear (wrestling) causes a hematoma between the cartilage and the skin. There is little to be done for chronic califlower ear, but an acute hematoma should be drained since blood is toxic to the cartilage.

2. Malignant external otitis. This rare infection is due to pseudomonas and is seen in diabetics due to their impaired poly function. The infection begins as an external otitis, extending to the skin around the ear and potentially to the mastoid sinus The next step is to the brain: death.

3. Relapsing polychondritis is a rare auto-immune disease in which the body destroys its own cartilage. The key finding is involvement of other cartilage structures: the nose and larynx. Early steroid therapy is important to prevent tracheomalacia (softening of the trachea) and respiratory obstruction.

B. External auditory canal: External otitis (swimmer’s ear). The external ear will be erythematous and tender. Treat with antibiotic drops with or without steroids.

C. Tympanic membrane (see above)

D. Middle ear (see above)

E. Inner ear (cochlea) infections are usually viral, and do not hurt. The symptoms are vertigo as the ear is fooled into thinking that it is constantly spinning. See chapter 36.

III. Facial trauma and nose bleeding

A. Nosebleeds. There are two types of nosebleeds:

1. Anterior nosebleeds are due to trauma of the turbinates. The number one cause is nose picking (Don’t pick your nose). The bleeding is primarily through the nares, and the source can be touched by a Q-tip. It is thus amenable to packing.  To treat an anterior nosebleed, tell the patient to blow his nose. The residual clot continues to irritate the lesion, paradoxically perpetuating the bleeding. Then tape two tongue depressors together to form a pincher. Maximally extend the patient’s head, and place the pincher on the nose.

2.Posterior nosebleeds are due to medical disease such as hypertension or a bleeding diathesis. Call ENT immediately, since posterior packing is required. If you are in a pinch, you can insert a urinary (Foley) catheter into the nose until you see it appear in the pharynx. Blow up the balloon, and pull backwards. This puts pressure on the posterior nares and tamponades the bleeding. Treat the disease.

B. Other facial trauma. The key to facial trauma is to make sure nothing vital has been broken. Follow this method:

1. Ask the patient to close his jaw tightly. The teeth should align. If not, the jaw is either broken or dislocated (see below).

2. Look in the nose. Make sure the septum has not deviated to obstruct one of the nares. An obstructing septum requires surgical correction.. Otherwise, the broken nose is a cosmetic issue. Do not try to pop it back into place as in the movies. Let ENT have a look.

3. Carefully examine the extra-occular muscles. See above. Lower maxillary trauma can fracture the floor of the ocular orbit, trapping the inferior rectus muscle. .

4. Examine visual acuity. Damage to the eye including posterior vitreous/anterior chamber bleeding can take a while to become apparent; both will affect visual acuity.

5. Examine the zygomatic arches. These bridges along the lateral face are highly susceptible to injury. There will be tenderness along the bone and jaw mal-alignment. Surgical correction is required.

6. Look in the external auditory canals. Sufficient forward force can dislodge the jaw into the EAC. Blood will be apparent.

7. Look for loose or dislocated teeth. These are an aspiration risk. If a tooth is loose or cracked, consult the dentist immediately. A cracked tooth will ultimately abscess unless removed or capped.

8. Know what to expect. Swelling of the eye and sub-conjunctival hemorrhage (homogenous redness of the white of the eye) are expected findings following trauma. Black eyes or Battles sign (blood behind the ear) usually occur 24-48 hours after the injury. If you see them in the setting of acute trauma, suspect that this is the second episode of trauma. Suspect domestic abuse. In fact, have a high suspicion for domestic abuse in all patients with facial trauma. Examine the patient alone.

IV. Rhinitis. Look in the nose with the nasal speculum. Remember that the nose goes straight back into the head, parallel to the floor. Lift the tip of the nose with your finger and insert the nasalscope directly back.

A. Allergic rhinitis (hayfever). The mucosa of the nose will be pale white. Treat with antihistamines.

B. Viral rhinitis. The nasal mucosa will be inflamed and red. Treat with decongestants.

C. Bacterial rhinitis/sinusitis. Pus in the nose is suggestive of a bacterial sinusitis. Treat with decongestants and antibiotics.

D. Deviated septum. This is a congenital abnormality where the septum deviates into one nare. It requires surgical correction only if it is causing chronic sinusitis or airway obstruction. Always look for this prior to inserting nasogastric tubes.

E. Perforated septum this is seen almost exclusively in cocaine users.

F. Nasal polyps. This will appear as a fleshy, non-tender mass in the nose. Finding them is important, as they should be surgically removed if they obstruct breathing, and they are part of an important triad: asthma, aspirin hypersensitivity and nasal polyps.

V. Mouth pain (see chapter 25)

A. Oral ulcers

B. Gingivitis

C. Oral cancer

D. Cracked teeth

VI. Mass in the neck/jaw

A. Lymph nodes (see chapter 25)

B. Thyroid. Examine the thyroid from behind the patient. Have the patient sit up on the edge of the bed. From behind the patient, with light touch, position your second, third, and fourth fingers below the cricoid cartilage and medial to the lower portion of the sternocleidomatsoid muscles. Your fingers should be just above the clavicles/sternum. Have the patient swallow a drink of water. You may not feel the thyroid; this is normal. If you do feel it, you will feel it move up under your fingers. Note its size, symmetry, and consistency.

1. A solitary nodule should be biopsied, regardless of its I131 uptake status. Cold nodules (no I131 uptake) are more likely to be cancer than hot nodules, but both can be malignant.

2. Multiple nodules are unlikely to be cancer. This is multinodular thyroid disease. Treat with radioactive ablation.

3. A fluctuant thyroid is supparative thryoiditis due to a bacterial infection that has spread contiguous from the pharynx. Surgical consultation and antibiotics are required.

4. A hard, wooden thyroid is Reidel’s struma, or fibrosis of the thyroid gland.

5. A tender, enlarged thyroid is either Graves disease (see below), sub-acute thyroiditis or Hashimoto’s thryoiditis. Hashimoto’s is an autoimmune disease that attacks the whole of the thyroid gland. Acutely, hyperthyroidism results as stored thyroid hormone is released. Later, hypothyroidism results. Sub-acute thryoiditis is due to a viral infection. It can mimick Graves exactly, with the exception of the lack of a bruit.

6. A chronically enlarged gland without tenderness may also be a goiter. A normal thyroid gland without access to iodine will continue to grow under the influence of TSH. The lack of iodine prevents production of T4, which augments more TSH production.

7. Listen over the thyroid for a bruit. This is actually a venous humm due to the arterio-venous connections formed within the gland due to Grave’s disease. This is virtually diagnostic for Graves disease.

C. Thyroglossal cysts. This is a remnant of the branchial clefts. As such, it communicates with the floor of the mouth. Moving the tongue in an out will also move the mass. It is of no clinical significance.

Section II: The Eye

There are three components to the eye exam: extra-occular muscles, the soft tissues of the eye, and the retina/neuro structures of the eye. Pupillary response and abnormal pupils are discussed in chapter 25.

VII. Problem: Diploplia (double vision) is always a disorder of the extra-ocular muscles, either due to neuromuscular disease (see chapter 36), a mass behind the eye (fungus, tumor), or swelling of the extra-occular muscles as occurs with Grave’s disease (the antibodies of Graves attack the extra-ocular muscles). See chapter 25.

VIII. Problem: Red/Painful Eye

Eye pain derives from the peri-ocular structures or the eye itself. Use the following method for discerning abnormalities of the eye.

A. Step 1: Exclude peri-ocular causes of eye pain/redness.

1. Blepharitis is inflammation of the eyelids. Treatment is scrubbing the eyelids with baby shampoo. Look carefully at the lashes to exclude pubic lice. Crabs have to grasp two closely spaced thick hairs to survive; they hone to the eyelashes and pubic hairs..

2. Hodeolum (Sty)is a eyelash follicle that has become plugged (a zit of the eyelash). Warm compresses to the sty are the treatment. Do not try to surgically open the sty.

3. Pre-septal/orbital cellulitis is infection of the skin surrounding the eye. Orbital cellulitis is an emergency requiring aggressive intravenous antibiotics. Because surrounding structures are involved, the patient will have pain with movement of they eye.

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B. Step 2: Approach the eye layer-by-layer

1. Conjunctivitis. See chapter 25.

2. Sub-conjunctival hemorrhages. Homogeneous, painless redness of the eye. Chapter 25.

3. Corneal abrasions are common with contact lenses, trauma or a foreign body hitting the eye. The diagnostic clue is redness of the eye, eye pain and a sensation of a retained foreign body. The foreign body is almost never there; the sensation comes from the abrasion. Nonetheless, evert the eyelid with a Q tip to make sure.

a. At the edge of the eyelid is a small cartilage strip. Place the Q tip just above this strip; grasp the eyelashes and pull up. The eyelid will roll over the Q tip, everting the eyelid. Ask the patient to look down during the whole procedure to prevent him from fighting you with eyelid contractions.

b. Use floroscene to reveal any abrasions. Place a drop of alcaine (anesthetic) in the eye, and then touch the eye with a strip of floreisceine (orange strips). Turn out the lights and look at the eye with a Wood’s lamp (black light). An abrasion will hold the florosceine and reveal itself as a yellow line. Abrasions on the front of the cornea require immediate ophthalmologist evaluation, as improper healing can lead to corneal scarring and blindness. Other abrasions can be treated conservatively; antibiotics and eye patches are usually not required but often prescribed for these. Stellate abrasions (like a star in appearance) suggest herpes; these patients require treatment with acyclovir.

c. Consult the ophthalmologist immediately for all welding injuries. The heat of the particles and the speed of impact can penetrate the front of the eye, depositing in the posterior chamber.

4. Other things you might see:

a. Pingueculum/pterygium  are fibrotic streaks on the eye surface. They usually result from previous trauma or exposure to ultraviolet light. They are of no significance unless they extend to the cornea, in which case they need to be surgically removed to prevent blindness.

b. Chemosis. Chapter 25.

5. Iritis is inflammation of the iris. The diagnostic test is to shine a light in the patient’s eye. This will cause pupillary constriction and will increase the pain. The etiology of iritis is almost always rheumatologic (auto-antibodies cause an inflammation of the anterior chamber and involve the iris). The anterior eye is a filter, just like the joints, the lungs and the kidney. As such, it traps the antibody-antigen complexes that are rheumatologic disease. Chronic infections that cause a similar long-standing antibody-antigen complex(syphilis, TB, viruses) are other causes. If the inflammation is long-standing, fibrosis may lock the pupil in position (non-reactive pupil) and form an irregular appearance..

6. Anterior uveititis. The causes of anterior uveitis are the same as with iritis. A hyphema is blood that has pooled in the anterior chamber. You will see a layer of blood sitting in front of the iris. Hypopion is similar to a hyphema, except that it is pus that causes a milky-white layer of fluid in front of the iris. Both are caused by either trauma to the eye or inflammation (auto-immune disease) of the anterior chamber: anterior uveitis.

7. Narrow-angle glaucoma. The anterior chamber fluid is created behind the iris and then travels in front of the lens, through the pupil, to the anterior segment where it is reabsorbed. (Figure 31.2) The iris separates the anterior from the posterior chambers: narrow angle glaucoma is narrowing of the passage between these two segments. When the angle acutely closes, pressure in the posterior chamber builds quickly, causing pain, erythema and, due to a vagal response, abdominal pain and vomiting. This will also hold the pupil in a fixed, mid-position. The only treatment is to create laser-holes in the iris to allow the fluid to escape from behind the iris. Reliably diagnosing non-acute narrow angle glaucoma requires a slit lamp exam where a narrow strip of light (from the slit) is shone across the anterior chamber. The high pressure in the posterior chamber budges the iris forward, obscuring the light as it tries to pass across the anterior chamber. Dilating the eye can cause the iris to constrict, and this may acutely narrow the passage causing acute angle closure glaucoma. You will be warned to not dilate eyes until narrow angle glaucoma is excluded for this reason, but do not be fooled. This may happen, but if it does, you have done the patient a favor by uncovering the abnormality in a medical center where treatment is readily available. The real danger is in not dilating eyes when you feel you need to: if you have a reason to look at the retina, always dilate the eye (see below).

8. Open angle (garden variety) glaucoma is pressure that builds in the eye because the drainage of anterior fluid is obstructed. Over time, the increased pressure on the retina obliterates vascular flow, leading to retinal ischemia and blindness. The smallest vessels are furthest away from the cup/disk (where vascular flow originates, so they are squeezed shut first. Visual loss, therefore, begins at the periphery of the retina working inwards: tunnel vision.  (Figure 34.3). The diagnosis is easily made by palpating the eyeball. Ask the patient to close his eyes. Grasp the patient’s head with both hands as if holding it still. Your fingers should be pointing towards the back of his head, your thumbs should rest gently on the closed eyes. Press gently. The eye-ball should feel like firm ripe grapes; squishy eye balls suggest trauma to the eye, hard rocks suggest glaucoma. Open angle glaucoma is dangerous because it is painless; unless you screen for it, you are unlikely to make the diagnosis until the eye is beyond recovery. Make it a practice to screen for glaucoma; anyone with a family history of glaucoma deserves referral to an ophthalmologist for tonometry (a tonopen that measures the pressure in the eye).

NUGGET: Superficial eye pain (conjunctivitis, scleritis) will abate with topical alcaine; deeper causes of eye pain (anterior uveititis, iritis) do not.

NUGGET: Never prescribe eye-drop anesthetics. In fact, never leave the bottle unguarded. The pain relief with alcaine will be so dramatic that patients will want (perhaps steal) the anesthetic to relieve the eye pain. Pain is your friend, however, as worsening pain heralds worsening eye disease. The anesthetic will mask this warning sign until it is too late.

IX. Problem: Abnormal Vision. Approach this with a step-by-step process following the path by which light travels through the layers of the eye. Approach each layer one at a time. Before you begin, assess the patient’s visual acuity. This is the single most important part of the examination. Visual acuity is expressed as OD, OS or OU. Ocular dextra refers to the right eye (dextra- (L) right, as in dextracardia or ambidextrious (two right hands)). Ocular sinster refers to the left eye (sinster- (L) left; left handed people were thought to be witches, cursed, and otherwise sinister). Ocular ubiquitous refers to both eyes. A score will be given for each eye or both if the score is the same for both. Ask the patient to stand 20 feet from the vision chart, or if you have a visual acuity card, to hold the card one foot from the face. The top number is the distance at which the patient can read the top letter on the chart; the bottom number is the distance at which a patient with normal visual acuity could read the same letter. 

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A. Cornea. See above. Corneal scarring or damage refracts light, but allows it to pass, resulting in blurry vision.

B. Anterior chamber. Anterior uveitis. As with corneal damage, light passes but is refracted as it passes: blurry vision.

C. Vitreous chamber. There are few diseases that affect the posterior chamber. The most common are:

1. Bleeding in the vitreous from a detached retina. Severely myopic patients are at risk for this as the oval eyeball puts tension on the retina. A sudden scintillating flash of light with visual loss suggests the diagnosis.

2. Floaters are tiny pieces of retinal tissue that have broken free and float in the vitreous fluid. Patients will complain of “a spot” in their vision that persists even with eye movement. There is no clinical significance to this.

D. Retina. A vision of scintilating light suggests a sudden retinal disease. You can mimick this by creating temporary ischemia on your own retina by rubbing your eyes vigerously for a few seconds.

E. Optic nerve. Inflammation of the optic nerve is almost always due to multiple sclerosis. See chapter 36.

F. Optic nerve tracks and the brain. See below for details on visual field deficits.

X. Retinal exam. If you are serious about looking at the retina, dilate the eyes. Always dilate both eyes, lest someone will think your patient has suffered a cerebral herniation causing a unilateral pupilary dilation.

A. Standard ophthalmoscope

1.First, get a dark room. You do not want to fight the pupil constriction as you try to look at the retina.

2.Place an X on the wall about 7 feet up so that the patient is gazing slightly superiorly.

3.Place the ophthalmoscope so the top of it rests flush against your eyebrow. Consider the scope a part of your head; once it is fixed to your eyebrow, it should not move at all. Fixing the scope to your head allows you to make very fine adjustments while looking at the retina by moving your head slightly.

4.  Look through the scope and focus (at 6 inches away) on the wrinkles of your palm. Turn the dial on the scope until the lines are clear. Note the number at the bottom of the scope. This will be your number for all eye exams. After this point, do not mess with the dial.

5. Now dial down the light on the scope to its lowest level. The back of the eye is dark: you won’t need much light. A bright light will only cause papillary constriction to oppose your efforts.

6. Stand in front and a couple of feet away from the patient at a 30 degree angle. Look through the scope with your medial eye until you see a red reflex from his retina (like the “red eye” you see in bad photography). Once you have the red eye in sight, you are on the right angle. Follow that angle all the way to the patient’s eye.

7. Before you move in with the scope, take your lateral hand (your medial hand should be holding the scope) and place it on the patient’s forehead with your thumb pointing down. Place your thumb on his eye-lid and lift up. Your hand on his head will keep your from ramming the scope into his eye. Your thumb will keep him from blinking.

8. Now move in with the scope. You have to get very close (a centimeter or less away from the eye). Close the medial part of your mouth and breath out the lateral side. This will keep you from breathing on him.

9. You are not going to see the nice view of the retina depicted in the textbooks. Instead, you will only see one circles’s worth of the retina. Make fine movements with your head to move around the retina, mentally putting the circle pieces together until you have a complete (collage) picture of the retina. The next section will tell you what to look for.

B. Pan-optic scope. The single best thing you can do for the retinal exam is to buy the Pan-Optic scope.

1. Get the room dark.

2. Look through the scope with your medial eye and focus on something ten feet away. Do not make any further adjustments to the scope. Turn down the light to its lowest level.

3. Do all of the above steps above, except with the pan-optic you will be placing the soft rubber cup over the patient’s eye. You will be amazed at how much better this scope is.

NUGGET: Do not carry your ophthalmoscope on the wards. The weight of the scope will tempt you to take it out of your coat and set it down. Once you do, it is stolen. Put it in a locked locker. If there is no locked locker, keep it in your car. You can always go get it when you need it. You’ll need this time anyway to wait for the pupil to dilate after you have placed the pilocarpine drops.

C. What to look for:

1. First, find the optic cup and disk. If you are on a part of the retinal that is not the cup/disk, find the veins-arteries. Follow the direction of their branch points: like little arrows, they will point you towards the cup/disk. The optic disk is the end of the optic nerve and it sets in a small depression of the retina that is the cup. The two will appear as two yellow circles; one on top of the other. The cup should be three times the size of the cup. Abnormalities:

a. If there is only one circle, the optic nerve has been pushed through the cup towards you. This means there is elevated pressure in the head (cerebral edema) that has pushed it forward. This is papiledema.

b. If the disk is bigger than it should be (i.e., the cup to disk ratio is less than 3:1), the optic nerve is inflamed and partially moved forward. This is optic neuritis (see above).

c. Glaucoma is pressure inside the eye. This pressure will push the optic nerve head (the disk) back towards the brain and make the cup deeper. Without a 3-D scope, assessing the depth of the cup is difficult, but there is a useful clue. Some of the veins/arteries originate from inside the cup. Normally, these vessels approach the cup and gradually disappear into it. If the cup is deep, the vessels will approach the lip of the cup and suddenly disappear. A sharp fall-off (demarcation) of the vessels as they approach the cup suggests glaucoma.

2. Next, inspect the retinal veins/arteries.

a. A retinal vein occlusion causes all of the veins to dilate. The retinal veins will look like a cluster of worms. Thunder and lightening is used to described  RVO because of its dramatic appearance.

b. A retinal artery occlusion causes palor of the retina. The vessels will not be apparent. There will be a cherry-red spot that represents the artery just to the point of occlusion. The surrounding palor is a function of the decreased blood flow to the retina.

c. Look for the color of the retinal veins/arteries. The normal vessels appear red because the vessel is 1/10^th vessel wall (white) and 9/10^th blood inside the vessel (red). When the vessel wall hypertrophies (See equation 9 for why long standing hypertension would cause the vessel wall to hypertrophy), there is more white than red: the copper wire appearance of the vessel is due to the hybrid of the two. If vessel wall hypertrophy continues, the vessel becomes mostly white: silver wire in appearance.

d. Look for new vessels. The sugar-coated proteins of diabetes plug up the retinal vessels causing occlusion. This stimulates the retina to grow new vessels: neovascularization . These new vessels, however, begin to obscure the retina, and because they are more fragile than normal vessels, are at greater risk of rupture. 

e. Look for other abnormalities

i. Flame hemorrhages are busted vessels due to hypertension (equation 9) or diabetes.

ii. cotton wool spots look like little patches of cotton. They represent embolic material (i.e., from endocarditis) that has plugged the vessel. 

3. Macular degeneration is the most common cause of blindness in the US. It is difficult to diagnose without the benefit of the ophthalmologist’s indirect ophthalmoscope. Know about it, but do not expect to see in on your direct retinal exam.

V. Visual field defects. Sit in front of the patient, two feet apart. Ask the patient to stare straight at your nose; you stair straight at this nose. Put your arms straight out to your side with your hands behind your head where you cannot see them. Extend one finger in your left hand and two fingers in your right. Slowly move your hands forward. Ask the patient to tell you when he can first see your fingers and to tell you how many total fingers you have up (right plus left hand). If he answers 3 at the same time you begin to see your fingers, the visual fields are normal. If he answers four, his right lateral visual field is out (he sees two in your right hand (his left) and he assumes that your other hand also has two fingers extended). If he answers two, his left visual field is out. If he does not see any fingers after you are able to see your fingers, both lateral fields are out. Figure 34.3 will help you localize the deficit. Remember in these diagrams, the black part of the circle is the part the world the patient does not see (as if he were looking through binoculars). Since light crosses as it enters the eye, the damaged part of the retina/nerve is opposite of what he does not see in the world(i.e., if the right half of a circle is black, it is the left part of that retina that is damaged).

Problem: Headache

To diagnosis the cause of a headache, work inside-out, starting with the vessels in the brain, the sub-arachnoid space, the meninges, the sub-dural space, the epidural space, the skull, the muscles, the vessels and then the skin.

I., The brain tissue. The brain does not have sensory fibers of its own; headache results only when the brain is forced against the skull wall, or if the sensory fibers around intra-cerebral vessels are distended.

A. Migraine headache:

(heMi- half; cranium= head; “half the head.”) Migraine headaches result from an abnormal constriction of a vessel, followed by hyper-dilation of that distends pain fibers. It occurs on the side of the head corresponding to the side of the distended vessel. Migraines are sudden (occurring over minutes to hours) and may last hours to days. They are brought on by stress or drugs that cause vasoconstriction (caffeine, chocolate). The first onset of migraine usually occurs before the age of 21, and there is a tight association with motion sickness as a child. Patients who develop headaches after the age of 21 should prompt suspician for other non-migraine causes of the headache. The medications to treat migraine are vasoconstrictive medications (ergotomine, sumatriptan).

1. The Classic migraine is preceeded by an aura that corresponds to the location of the constricted vessel.  Common auras include flashing lights, abnormal sensation, or motor deficits.

2. The Common migraine, however, has no aura; pain only. 

3. The Complicated migraine is associated with neurologic deficits that resolve as the headache resolves.

4. Catemenial migraines are associated with menses.

The ice-cream headache is similar in that it results from cerebral vasoconstriction followed by vasodilation due to excessive cold stimulation of the carotid receptors in the back of the throat.

B. Cluster headaches occur in clusters: several headaches in a two-week period followed by no headaches for several months. They usually occur in 30-50 year-old men and are characterized by retro-orbital pain associated with unilateral tearing. Oxygen helps.

C. Tumor Headaches are due to increased cerebral pressure due to the tumor in the brain. They are insidious, occurring over months as the tumor enlarges. They are worse in the morning (lying down at night increases the pressure in the head), and are made worse with increasing intracerebral pressure (coughing, sneezing). They are associated with nausea and vomiting and occasionally focal neurologic deficits.

II. The sub-arachnoid space. Sub-arachnoid bleed: “The worst headache of my life.” This is due to a rupture of an intra-cerebral arterial aneurysm. The headache is sudden; the pressure from the bleed may cause herniation of the brain and neurologic deficits. Older patients may present with more subtle signs manifest only as a blank stare with a retarded, though appropriate response to questions (the Wiese pause). A CT or a lumbar puncture will show blood in the CSF.

III. The sub-dural space. A sub-dural bleed is a venous bleed following head trauma. Alcoholics and the elderly are particularly at risk due to cerebral atrophy (the brain bounces around inside the head like a small walnut in a large walnut shell). Neurologic deficits are rare; reduced cognition is common.

IV. The meninges. Meningitis comes in four flavors: bacterial, aseptic drug, aseptic viral and cancer. Ask the patient to touch his chin to his chest. This stretches the meningeal lining of the brain, worsening the pain. The inability to touch the chin to the chest due to rigidity suggests meningitis.

A. Kernig’s: Lay the patient flat on the bed and flex his legs at the hip. This stretches the meninges. In a positive test, the patient will flex his neck (raise his head off the bed) to reduce this stretch.

B. Brudzinski’s is the opposite of Kernig’s. With the patient flat on the bed, flex his neck. The patient will flex his hips to reduce the meningeal stretch.

C. Jolt-acceleration. With the patient facing you, rapidly turn the head side to side (make sure you have excluded spinal trauma) for 30 seconds. Progressively increasing pain indicates meningitis.

D. Infectious meningitis is a medical emergency. The lumbar puncture is the key to diagnosis, and should be performed immediately. If herniation of the brain is a concern, get a CT before the LP, but do not delay empiric antibiotics. Give the antibiotics, get the CT, then do the LP. You have 4-6 hours before the antibiotics will taint the CSF cultures.

1. Bacteria (S. Pneumo, N. Meningidities). Bacteria are protein containing organisms that consume glucose: the CSF protein will be high and the glucose will be low. The CSF WBC will be elevated with polys.

2. Viruses are intracellular: they do not introduce more protein to the CSF and they do not consume glucose. The CSF protein and glucose will be normal. The WBC count will be elevatedwith lymphocytes, though the acute phase will be polys.

3. TB and fungal meningitis can occur in all patients, but occur more commonly in the immunosuppressed. TB contains protein and consumes glucose, so the protein will be high and the glucose low. The WBC response is lymphocytes. It has a predilection for the basal meningies, and can “pick off” cranial nerves as they leave the brainstem, resulting in cranial nerve defects.  Meningitis with cranial nerve abnormalities should prompt suspicion for either TB meningitis or carcinomatous (cancer to the brain) meningitis.

4. Carcionmatous meningitis is a cancer that has gone to the CSF space. All cancers can do this, but leukemia and lung cancer are the most common. The cancer contains protein and consumes glucose (protein high, glucose low). The diagnosis is made by finding cancer cells in the CSF or finding the cancer elsewhere in the body. It behaves exactly like TB meningitis. TB meningitis is less common as patients age, and cranial nerve deficits in the setting of meninigitis in an elderly patient should raise suspicion for carcinomatous meningitis.

E. Drug-induced aseptic meningitis. Non-steroidals and sulfa drugs are the most common. The protein will be low, the glucose will be normal.

V. The epidural space. An epi-dural bleed is due to rupture of the middle meningeal artery as it is displaced from its groove in the temporal bone. The diagnosis is usually obvious as this is usually associated with a displaced skull fracture. Patients will lose consciousness, then awake,  and then gradually lose consciousness over minutes to hours as the arterial bleed increases.

VI. The skull and neck

A. Sinus headaches may affect the whole head. While facing the patient, grasp the back of his head with both hands, placing your fingers on the back of the head so that your thumbs are on the maxillary bones. Squeeze. Do the same with your thumbs on the frontal sinuses (just over the eyes). All patients may have some tenderness; sinusitis patients will have exquisite tenderness.

B. Mastoiditis. This is a sinusitis of the mastoid sinuses. Like frontal sinusitis, the danger is in extension via venous drainage to the brain.

C. Fracture. Fracture to the face, scalp and spine follows trauma to the area. When in doubt, exercise extreme caution and use X-rays/CT’s instead of the physical exam to make the diagnosis.

1. When there is very low suspicion for a fracture, a cervical spine fracture can be excluded by the absence of spinal tenderness with palpation. If there is moderate suspicion, however, cervical neck X-rays should superceed the exam. Never flex the patient’s neck if a neck fracture is suspected.

2. Look for signs of head trauma. Superior and lateral skull fractures are usually obvious. Basilar skull fractures, however, are occult because you cannot palpate it. A fracture of the head or neck will induce hemorrhage, just as in any fracture.

a. Battle’s sign is ecchymosis from the fracture depositing to the skin behind the ear. Like a black eye, it will not appear until 24 hours after the fracture, however. Do not rely on Battle’s sign or Raccoon eyes in the setting of acute trauma.

b. Raccoon eyes is ecchymosis from the fracture draining to the skin around the eyes (black eyes).

c. Blood in the external auditory canal.

d. Cerebrospinal fluid draining from the nose or in the external ear. This fluid will be clear, and unlike nasal drainage, will be high in glucose (it will test positive for glucose on a urine dipstick)

VII. The muscles, sub-dermal vessels and skin

A. Tension headache occurs in response to neck strain or stress, usually occurring at the end of the day when stress has been maximal. The neck muscles begin at the posterior neck and insert over the top of the head. The pattern of pain follows this course, radiating from the neck over the top of the head. Do not be fooled by non-tender neck muscles, as the day long tension on the top of the head may be sufficient to cause and continue the headache even after the neck muscles have relaxed (like wearing a baseball hat that is too small).

B. Inflammatory headaches: Temporal arteritis (also know as Giant Cell Arteritis or polymyalgia rheumatica (PMR)). This is a vasculitis that affects the temporal artery. It is characterized by headache, jaw claudication and (if not treated immediately) loss of vision (blood flow to the anterior ophthalmic artery is lost). A new onset headache in the elderly should raise suspicion for GCA. An ESR greater than the patient’s age in the setting of headache should prompt a temporal artery biopsy to exclude the diagnosis. Empiric steroids should be started until the diagnosis is excluded.

C. Herpes Zoster/Shingles. This is due to a varicella virus that is reactivated in the dermatomal nerve root. The word origin describes the course: Herpes= to crawl (as in herpetology), zoster (G)= like a girdle; cingella (L)= like a girdle (from which we get shingles). As the virus craws out along the sensory nerve root, the pain begins. Vesicles may be delayed for a day after the headache. If this affects CN V1 (ophthalmic branch) the patient must be hospitalized for IV acyclovir to prevent involvement of the cornea (remember, CN V is the corneal reflex). Ramsey-Hunt is the same disease involving CN VII, leading to pain around the external ear and facial paralysis. In all cases, the headache is one sided (only one nerve is involved), and the skin is exquisitely sensitive to light palpation

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