NPLEX Combination ReviewEENT - 2

Paul S. Anderson, ND

Medical Board Review Services

Copyright MBRS

Internal Pathology: Macular Degeneration

Normal Fundus Early ARMD with Drusen

Early ARMD with Drusen Same fundus on angiography

Macular Degeneration: Pathogenesis• All forms of Age-related Macular Degeneration (AMD, or

ARMD) have initial, common destructive changes in the macular Retinal Pigment Epithelium (RPE).

• A postulation is that there are isolated choriocapillaris sections that have vascular failure, leading to RPE degeneration, and the loss of photoreceptors. As the inner photoreceptive layers collapse, they bring the outer layers with them, causing the internal spread of the degeneration.

• Many believe the root cause to be Oxidative damage, secondary to Ultraviolet Radiation, and Free Radical formation. – The Dry form of the disease has all of the above attributes. – The Wet form of the disease (Wet AMD) also has a neovascularization

component, which causes a leakage of plasma, lipid, glucose, and other fluid constituents into the choroid and retina. This ultimately leads to fibrous disciform scar formation.

Vision Loss Patterns:

• Macular Degeneration:– Central Vision Loss

• Decrease in eye chart acuity and Amsler’ Grid• Decrease in central vision on perimetry

• Glaucoma:– Peripheral Vision Loss “tunnel vision”

• Decrease in peripheral vision on perimetry

Naturopathic Treatment:1.       Taurine – found in high concentrations in the eye, may be protective on retina – Marz

2.       Zinc (90-120 mg zinc picolinate) – Marz

3.       Selenium IV or oral – Marz

4.       Anti-oxidants: protective against oxidative damage, low levels may increase risk

5.       Carotenoids: Protective effect on retina.

6.       Vitamin C & E

7.       Vitamin E

8.       IV therapy of Se 400 mcg, Zinc 10 mg. in 150 cc of 0.5 N saline or Ringer’s lactate (infused over 30 minutes twice weekly).

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Dr. Andersons IV Rx: Se: 800 mcg / Cr: 600 mcg / Zinc 75 mg / C-500 50cc / Bicarb. 25cc/ MgSO4 2 grams / Cal. Gluc. 5 cc / KCL 3 cc / Taurine 200 mg / Carnitine 50 mg

Infused in 500 cc ½ NS over 1 – 2 hours. Repeat weekly at least 6 times.

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In addition, oral administration of selenium 200-300 mcg qd, Zinc picolinate 60-mg. qd, Vitamin E 800 iu qd and Taurine 1 gm bid (avoid protein 1 hr pre and post). After 8 weeks of the study most patients were able to d/c injections. Nut. Infl on Illness, Werbach; J Nutr Med 1:133-8, 1997

Botanicals; Vaccinum myrtilus (25% extract – anthocyanidin) 160-480 mg qd Gingko Biloba & Crategus Sanum: Pleo-Muc eye drop

Lifestyle: Stop smoking

Diet: Increase intake of dark leafy vegetables, especially collards and spinach

Internal Vascular Changes• Arteriosclerosis

– Visual inspection of vessel color– The more reflection the more “white” in color– Old terminology

• “Copper Wire, Silver Wire”

• Artery to Vein Crossings– The crossing shows the effect of pressure on the vessels– Encroachment of the Artery on the Vein shows forms of

“Nicking”

• Artery to Vein Size Ratio– Generally the Artery is 1/5 smaller than the Vein (so the Vein

is 5/5 and the Artery is 4/5)– So: A normal ratio is Artery to Vein 4/5– The more arteriosclerotic the smaller the Artery becomes so

the ratio is wider (3/5, 2/5, 1/5).

Terms:

• Arteriosclerosis– Arterio- (trouble is with the artery wall)– “Hardening of the arteries”

• Atherosclerosis– Athero- (“Atheroma” or lesion inside the

vascular lumen)

Artery / Vein Ratio

A/V = 4/5 A/V = 2/5

Hypertensive Retinopathy

The Nerve Head with Papilledema

Hypertensive retinopathySigns and Symptoms

The patient with hypertensive retinopathy, as expected, suffers from hypertension. However, the hypertension may be unknown to the patient and the eye exam may yield the first clue to this relative asymptomatic systemic disease. Patients with only hypertensive retinopathy are nearly always visually asymptomatic.

Findings in hypertensive retinopathy include cotton wool spots and flame shaped hemorrhages. In advanced cases, there will be a macular star (ring of exudates from the disc to the macula) and disc edema. Arteriolosclerosis (arteriolar narrowing, arterio-venous crossing changes with venous constriction and banking, arteriolar color changes, vessel sclerosis) is often found concurrently.

PathophysiologyThe findings in hypertensive retinopathy all stem from hypertension-induced changes to the retinal microvasculature. Hypertension leads to a laying down of cholesterol into the tunica intima of medium and large arteries. This leads to an overall reduction in the lumen size of these vessels. In arteriolosclerosis, hypertension leads to focal closure of the retinal microvasculature. This gives rise to microinfarcts (cotton wool spots) and superficial hemorrhages. In extreme cases, disc edema develops. The mechanism behind this phenomenon is poorly understood, but it may be related to a hypertension-related increase in intracranial pressure, and hence is considered true papilledema.

Arteriolosclerotic changes in the retinal microvasculature persist even with the reduction of systemic blood pressure. However, hypertensive retinopathy changes resolve over time with the reduction of systemic blood pressure (BP). Cotton wool spots develop in 24 to 48 hours with the elevation of BP, and resolve in two to 10 weeks with the lowering of BP. A macular star develops within several weeks of the development of elevated BP and resolves within months to years after the BP is reduced. Papilledema develops within days to weeks of increased BP and resolves within weeks to months following BP lowering.

Effects of arteriosclerosis/hypertension on the retina• Narrowing of the arterioles (generalized with

straightening or focal)There may be an observable change in "a/v" ratio

from the "normal“ 4:5 Ratio (2:3)

Pathological changes include: a. copper wire b. silver wire… both (a) and (b) denote an increase

in the relative width of the reflex associated with thickening and hyaline degeneration of the arterial media.

c. Irregularities d. vessel sheathing

• A/V crossing changesa. deflection… depression/humping/ ‘U’ or ‘S’

shaped deflection b. apparent nicking (GREEN ARROW) c. ‘right angling’ (WHITE ARROW)

The arteries are the smaller vessels. The upper artery is “silver wire” and the lower is “copper wire” in appearance. The “A/V” ratio here has decreased from 4/5 (normal) to approximately 2/5 or 3/5.

Clinical Pearls : Hypertensive retinopathy • Grading:

– 1: Arteries ¾ of normal caliber– 2: Arteries ½ of normal caliber “Copper Wire”– 3: Arteries 1/3 of normal caliber “Copper / Silver Wire”

– 4: Arteries not visible / Threadlike “Silver Wire”• In order for cotton wool spots to develop from hypertension, auto regulatory

mechanisms must first be overcome. For this to happen, the patient must have at least 110mmHg diastolic readings.

• Patients who develop papilledema from hypertension have malignant hypertension and typically have BP in the range of 250/150mmHg

• Fluorescein angiography is not indicated in cases of hypertensive retinopathy as it yields no diagnostic information.

• Hypertensive retinopathy presents with a ‘dry’ retina (few hemorrhages, rare edema, rare exudate, and multiple cotton wool spots) whereas diabetic retinopathy, in comparison, presents with a ‘wet’ retina (multiple hemorrhage, multiple exudate, extensive edema, and few cotton wool spots).

DIABETIC RETINOPATHYPathogenesis:

The diabetic biochemistry is predisposed to the production of sorbitol, which destroys the pericyte cells that support the vascular endothelium.

As the endothelium declines, there is an increased leakage of blood, protein, and lipid. This leakage, along with the high glucose levels in the blood, produces vascular insufficiency, capillary non-perfusion, retinal hypoxia, and resultant altered structure and function.

These factors are compounded by the release of angiogenic factors, which create neovascularization. The new vessels are not only ectopic, but are of poor quality and leak, causing the cycle to propagate.

FRUCTOSE METABOLISM

In Muscle

Acetyl S~CoA KREBS CYCLE

DIABETIC RETINOPATHYDiagnostic information:A. Sn / Sx: In addition to the common systemic symptoms of Diabetes (polyphagia,

polydypsia, polyuria), the patient may have had long standing conjunctival injection, visual acuity fluctuations, and symptoms of lens opacity. On ophthalmoscopic exam “dot and blot” intraretinal hemorrhages will be seen, along with microaneurysms, neovascularization, edema, and cotton wool infarcts. Cranial nerve 3, 4, and 6 palsies may result from longstanding diabetes.

Proliferative diabetic retinopathy will show neovascularization of the optic disc, iris, and other retinal sites.

**A neovascular ring around the pupillary border of the iris should prompt further exploration into the retinal health of the patient.

B. DDX: Macular degeneration, Cataract.

C. Lab Dx: Glyco-hemoglobin, Oral GTT, Fasting blood glucose with Chem panel and lipids. Fluorescein Angiography is not a diagnostic test in this condition, but is used to guide laser treatment.

Referral information: These patients should be under regular observation by an Ophthalmologist or Optometrist to chart the progression of the disease, and any treatment gains made.

Standard treatment: In patients who have quickly proliferating neovascularization, or in whom the retinopathy threatens the macula, laser photocoagulation is typically ordered.

DIABETIC RETINOPATHY• Major cause of blindness especially in juvenile IDDM or chronic NIDDM.

Appears more related to duration than stability. Changes include cataracts and retinopathy

– Symptoms: 5-15% note visual changes due to clinically significant macular edema

– Signs: First signs opthalmoscopically: venous dilation, small red dots in post-retinal pole.

• Non-proliferative type – increased capillary permeability, microaneurysms, hemorrhages, exudate (cotton-wool spots), edema causing yellow exudates from damaged capillaries.

• Proliferative retinopathy has neovascularization of the retina and scarring of the posterior pole.

EXAM SCHEDULE FOR DIABETIC PATIENTS:

1: Annual visits within five years of diagnosis if thirty years or younger, within a few months of diagnosis if thirty or older.

2: Immediately if visual changes affect only one eye, last more than a few days and are unassociated with change in blood sugar.

DIABETIC RETINOPATHYTreatment: (Obviously, treat the underlying

diabetes…)1.       Lower sorbitol:

(Ascorbate may help)2.      Control blood glucose:

chromium, vanadium, zinc, gymnema sylvestre, fenugreek seeds

3.      Control serum lipid levels4.      Protect endothelial cells:

Favinoids, (rutin) vaccinium myrtilus, beta carotene, lutein

8.      Prevent retinopathy:Magnesium 300 - 500 mg/day

DIABETIC RETINOPATHY-- Vitamin C to bowel tolerance-- Bioflavinoids, especially Rutin,

@ 1000 to 2000 mg / tid-- Vitamin E @ 800 to 1200 iu / d-- Co-Q-10 @ 75 - 200 mg / d-- Taurine @ 1000 mg / bid-- EPA / DHA 2 – 6 grams daily-- Chromium @ 300 to 450 mcg / bid - tid-- Zinc @ 50 to 100 mg / bid-- Magnesium (citrate) @ 150 to 250 mg / bid-- Selenium @ 100 mcg / bid

Diabetic Retinopathy: macular edema and micro-aneurysms

RETINAL DETACHMENT Pathogenesis: During the course of a posterior vitreous detachment

(described below) the vitreous is pulled from the retina. At certain points (nerve head, vessel attachment, old scars) the vitreous is attached more firmly to the retina. It is at these points that the vitreous can pull with more force, and pull the retina away from the retinal pigment epithelium, causing a tear or detachment. This is commonly precipitated by trauma.

Diagnostic information:A. Sn / Sx: Reports of sudden onset of single or multiple floating spots, and

flashes of light. Recent Hx of trauma to the head or eye is common. A vitreous hemorrhage will produce multiple floaters. The vision loss will range from severe to none.

B. DDX: Posterior vitreous detachment. C. Lab Dx: No serology. Binocular indirect ophthalmoscopy.

Referral information: This requires direct referral. If the patient is experiencing symptoms, have them lie supine and wait for ambulance transport to an Ophthalmic surgery center, or ER.

RETINAL DETACHMENT

Standard treatment: Laser photocoagulation, or cryoretinopexy, are the most common treatments.

Complementary treatments:-- All standard dietary, supplemental, and lifestyle

modifications are appropriate.-- Collagen C -S, 6 tablets, tid X 12 weeks, then 4 bid

for maintenance.-- Vitamin C to bowel tolerance-- Glucosamine Sulfate, 500 mg tid-- UNDA homeopathic Retininum, and #42-- 2 – 4 grams of EPA / DHA-- Bilberry 120 mg (25% extract) tid for 12 weeks

POSTERIOR VITREOUS DETACHMENT Pathogenesis: During aging, the hyaluronic acid levels in the vitreous

decrease, causing a lack of collagen integrity. The vitreous will then collapse forward (away from the retina).

Diagnostic information:A. Sn /Sx: The typical patient will be over the age of 50, and present with an

acute onset of floaters. There will typically be one large floating spot, which prompts the visit to the doctor. If there is decrease in vision, suspect vitreous hemorrhage.

B. DDX: Retinal detachment.C. Lab Dx: See Retinal detachment.

Referral information: This requires direct referral for evaluation.Standard treatment: If no retinal break is present, the patient is seen again in

six weeks. If breaks are present, photocoagulation is necessary in most cases.

Complementary treatments:-- See retinal detachment.

Lipemia RetinalisHigh Blood Lipids!

RETINITIS PIGMENTOSA

RETINITIS PIGMENTOSA• Pathogenesis: Thought to be a hereditary degenerative process of the rod cells. • Diagnostic information:

– A. Sn / Sx: Slowly progressive, bilateral, loss of night vision. A ring scotoma is often present on perimetry, which tends to widen, decreasing central vision. Dark “bone- spicule” pigmentary changes are often present in the retina.

• DDX: Syphilis, Rubella, Chloroquine toxicity.

• Lab Dx: Perimetry, Dark adaptation testing, ERG studies.

• Referral Information: Should be co-managed, as with all retinopathies.

• Standard treatment: None (Some researchers use Vitamin A)

• Complementary treatments:-- In addition to optimization of diet, lifestyle, supplements, etc.:-- Vitamin A @ 15,000 iu / d (Berson, et.al.,1993) -- Bilberry / Other flavinoids

-- Use any extra (over 200 – 400 iu.) Vitamin E with care as it was shown to have a negative effect;

– There is some concern over Vitamin E use with the Vitamin A therapy in Retinitis Pigmentosa, as one study (Berson, et.al.,1993) found a negative outcome in the Vitamin E supplemented groups. This information should be considered and explored before giving vitamin E to these patients.

Pathology as found in aberrant EOM function

Pathology noted in painful EOM function

• Retrobulbar (Optic) Neuritis– Pain on eye rotation– Inflammatory disorder– Typically self limiting– May indicate systemic disease

• Orbital Cellulitis (includes swelling)• Other Neuritides

• Migraine / Headache– May exhibit pain with eye movement– May be photophobia

• DDX by doing EOM in darkened room

Strabismus

Discharge

• Lid Abnormalities– Chalazia– Hordeola– Blepharitis

• Allergic discharge– Treatment discussed in ENT section on

Allergy.

ChalazionPathogenesis: Chalazia- Non-infectious, granulomatous inflammation of the Meibomian glands.

May develop secondary to hordeola, or from Meibomian secretion retention.

A. Sn / Sx:

Hordeola- Acutely swollen and edematous lid. Lid is sensitive to palpation. Commonly a pimple like lesion at the lid margin. May be associated conjunctivitis, and discharge. Vision is unaffected.

Chalazia- Single or multiple hard, painless nodules in the lid or lids. Possible Hx of lid infection, or blepharitis.

B. DDX: Preseptal cellulitis, will have greater lid involvement, usually more pain, and no pimple like lesion.

Primary DDX for Chalazia and Hordeola is pain on palpation; positive in Hordeola, negative in Chalazia.

C. Lab Dx: Biopsy recurrent Chalazia, to R/O Sebaceous gland carcinoma.

D. Referral information: None, unless Hordeola is progressing to cellulitis and patient is not improving with treatment. 

E. Standard treatment:1. First, Hot compress, followed by digital massage to the chalazion to break up and express the

nodule, up to qid.

2. Intralesional steroid injection [Kenalog @ 10mg/ml] .05 to .30 ml.

3. Trial of Tetra / Doxy / Minocycline to thin secretions

4. Excision and curettage for unresponsive lesions.

Chalazion

Chalazion: Complementary treatments:• PO Herbs: Chamomile, Euphrasia, Berberis, Fennel, Hamamelis,

Hydrastis, Juglens, Qurecas, Ginger, Achillea, Bilberry,& Pulsatilla (synergist)

• Vitamin A 50,000 – 150,000 iu qd X 2-4 weeks (Used to thin secretions, as in antibiotic therapy)

• Botanicals: Used as compresses.

Hydrastis Canadensis Calendula officinalis

Hamamelis Mahonia aquafolium (Berberis) Symphytum officinalis

Botanical formula (Jill Stansbury, ND)Calendula off 1 TBS flowers Berberis 1 tsp. powder

Euphrasia off 1TBS leaves Symphytum off 1 TBS root chopped finely

Infuse the herbs in two cups isotonic saline. Strain well with mesh filter. Use within 24 hours as a hot or cold compress

• Local and systemic Hydrotherapy • Poultice of fresh green clay, potato, or carrot • Silica and Nat. Sul. Cell salts

BLEPHARITIS:• Inflammation of the lid margins. Bacterial cause is

most common.• Differential Diagnosis: sebaceous cell carcinoma

or squamous cell carcinoma should be ruled out in chronic, unilateral blepharitis

• Treatment:– Hot and cold contrasting compresses– Same herbal topical Tx. as Chalazion below– Cleanse the eyelids:

1. Wash with aloe based shampoo and apply combination of tea tree, lavender oil, Vitamin E and olive oil and let sit.

2. Johnsons baby shampoo3. Antidandruff shampoo

– Allopathic treatment: 1. Antibiotic ointment. 2. Preventative antibiotic / sebulytic use

HORDEOLUM (STYE)

HORDEOLUM (STYE)

• A type of furuncle occurring in the sebaceous glands or hair follicle of the upper or lower lid. Acute localized bacterial infection– 2 typesa. External: involves glands of Zeis or Mollb. Internal: involves Meibomian glands

• Differential Diagnosis: rare meibomian gland or squamous cell carcinoma

• Standard treatment:– Oral antibiotics; Cold packs; I&D if necessary.

• Complementary treatments:– Consider herbs: Chamomile, Euphrasia, Berberis, Fennel,

Hamamelis, Hydrastis, Juglens, Qurecas, Ginger, Achillea, Bilberry, and Pulsatilla (synergist)

– Local and systemic Hydrotherapy– Silica and Nat. Sul. Cell salts– Maximize Antioxidants, B-Complex.

Dilated Pupils

(MYDRIASIS)

DIPLOPIA