Common Health Problems and Diseases Information

Wounds - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:43:00 +0000

Overview
Definition

A wound is any injury causing an interruption of the normal continuity of affected structures or tissues, most often the skin. The skin, the outer integument, is the first line of defense against microorganisms; its loss facilitates entry of microorganisms into wounds. Wounds are classified as incised (made with a sharp object that creates a clean cut, such as bites, knives, scalpel), contused (made by a blunt object that may not break the skin but may cause significant damage, such as bumping the head when falling); lacerated (made by an object such as barbed wired that creates a jagged, irregular cut); puncture (made by a pointed object such as an ice pick or bullet), or thermal and chemical burns (made by scalds, fires, flammable liquids, gases, electricity, and chemicals), and decubitus ulcers (bed sores or diabetic ulcers).
Etiology

* Blunt or penetrating trauma
* Surgery
* Chemical injury
* Thermal injury
* Temperature extremes (e.g., burns, frostbite)
* Ionizing radiation
* Tissue breakdown due to malnutrition or diabetes

Risk Factors

* Age (e.g., elderly)
* Malnourishment, especially protein depletion
* Trace element deficiencies, especially zinc
* Vitamin deficiencies, especially vitamin C
* Compromised general health
* Location and severity of the wound
* Steroid use
* Radiation and chemotherapy
* Diabetes mellitus
* Smoking
* Weight loss or obesity

Signs and Symptoms

* Erythema
* Edema
* Pain and tenderness
* Heat
* Possible fever with infection
* Serous, sanguineous, serosanguineous, or purulent exudate
* Loss of function (or mobility)
* Foul smell (in infected wounds only)

Diagnosis
Physical Examination

A complete assessment, with a history of the insult event, is essential to determine the extent and severity of the injury, possible contamination, and conditions that might complicate the clinical course and treatment. Wound healing is often divided into three types: (1) first intention healing in which the edges of a wound are approximated and closed with sutures (e.g., laceration), thus scarring is usually minimal; (2) second intention healing in which the edges of a wound are not approximated and the wound is left open to granulate (e.g., burns, ulcers), thus scarring is often wide and deep; and (3) third intention healing in which a wound is left open initially because of contamination and then subsequently closed surgically. Astute clinical observation is essential to diagnose possible wound infection, particularly with human bites.
Laboratory Tests

* Complete blood count, to monitor leukocytosis (white blood count should stay between 5,000 and 10,000/mm3), which may herald the development of sepsis
* Urinalysis, blood urea nitrogen (BUN), and serum creatinine, to monitor renal function
* Wound cultures, to measure the number of bacteria (<105 organisms per gram of tissue)
* Sedimentation rate
* Electrolytes

Pathology/Pathophysiology

There are generally four stages of wound healing: (1) vascular response (immediately for about 10 minutes) characterized by blood vessel constriction, smooth muscle contraction, platelet aggregation, blood coagulation, followed by vasodilation, processes that are mediated by histamine release; (2) inflammatory response (days 1 to 5) characterized by infiltration by neutrophils, monocytes, macrophages, and lymphocytes to protect against invasion by microorganisms; (3) proliferative phase (days 5 to 20, depending on the amount of necrotic material and infection) characterized by formation of granulation tissue, collagen synthesis, angiogenesis, and wound contraction, processes that are mediated by cytokines and growth factors; (4) maturation stage (day 20 to resolution, which could take months or years) characterized by remodeling of scar tissue, the basic component of which is collagen, a sturdy structural protein found throughout the body. Scar tissue is only 80% as strong as normal tissue.
Treatment Options
Treatment Strategy

Treatment depends on the type and severity of the wound. Some wounds are characterized by a loss of tissue, requiring grafting to repair, and others, including clean lacerations, result in no tissue loss. It is important to determine at the outset, based on the history and physical, whether or not the wound can be closed immediately either by suturing or grafting, or delayed because of contamination. A contaminated wound can be cleaned sufficiently so that it can be closed, but infected wounds are never closed until the infection has been successfully treated. Wounds must be protected from additional physical, chemical, or bacteriologic complications.
Drug Therapies

* Analgesics, for comfort especially before wound closure or dressing changes
* Antiseptics (e.g., povidone iodine), to clean contaminated wounds
* Systemic antibiotics for wound infections; broad-spectrum antibiotics for sepsis
* Amoxicillin/clavulanic acid (250 to 500 mg orally tid) or ampicillin/sulbactam (1.5 to 3.0 g intravenously every six hours) for animal bites (clindamycin or ciprofloxacin can be substituted for penicillin-allergic patients)
* Medicated dressings (e.g., gauze impregnated with topical antimicrobial agents such as silver sulfadiazine cream, mafenide cream, silver nitrate), to aid healing and make dressing changes less disruptive to epithelialization
* Triamcinolone (10 mg/mm3), to ameliorate hypertrophic scar formation (keloid)
* Tetanus immune globulin, for tetanus prophylaxis; penicillin (10 to 12 million units intravenously for 10 days); metronidazole (500 mg every 6 hours or 1 g every 12 hours) for tetanus infection
* Exogenous growth factors (e.g., epidermal growth factor [EGF], transforming growth factor-beta [TGF-beta], platelet-derived growth factor [PDGF]), to accelerate normal healing (experimental)

Surgical Procedures

* Surgical excision of burned tissue and wound debridement (removal of devitalized or contaminated tissue or foreign bodies)
* Skin grafting
* Excision and drainage, for wound abscesses
* Intubation or tracheostomy, for hypoventilation associated with severe tetanus or pneumonia associated with burn patients
* Splinting, to inhibit contraction, the movement of adjacent skin to close an open wound; in some parts of the body contraction can cause deformity and immobility

Complementary and Alternative Therapies

Homeopathic remedies may provide excellent relief of acute trauma. In addition, nutrients and herbs can help reduce inflammation, speed healing, and minimize the risk of secondary infection.
Nutrition

These supplements can also be taken before surgery to reduce healing time. Lower dose or discontinue when wound has healed.

* Beta-carotene (250,000 IU/day) or vitamin A (50,000 IU/day) promote healthy scar tissue. These are high doses and should not be taken for longer than one to two weeks without physician supervision. Reduce dose to 50,000 IU of beta-carotene and 15,000 to 25,000 IU of vitamin A daily after two weeks. Vitamin A should be avoided by women who are pregnant or trying to conceive.
* Vitamin C (500 to 1,000 mg tid) enhances tissue formation and strength.
* Vitamin E (400 to 800 IU/day) promotes healing when taken internally. May also be used externally once the acute phase has passed and new skin has formed. Higher doses may be beneficial for burn victims.
* Zinc (10 to 30 mg/day) stimulates wound healing.
* Bromelain (250 mg tid between meals) is a proteolytic enzyme and an anti-inflammatory that has been shown to reduce postsurgical swelling, bruising, healing time, and pain.
* Seacure (3 capsules bid to tid) is hydrolized whitefish protein that provides absorbable protein necessary for wound healing.

Herbs

Herbs may be used as dried extracts (pills, capsules, or tablets), teas, or tinctures (alcohol extraction, unless otherwise noted). Dose for teas is 1 heaping tsp. herb/cup water steeped for 10 minutes (roots need 20 minutes).

* Turmeric (Curcuma longa) is an anti-inflammatory that potentiates bromelain. Use the dried extract 250 to 500 mg tid.
* Gotu kola (Centella asiatica) promotes connective tissue repair, supports normal wound healing, and prevents scar hypertrophy and keloid formation. For best results, use a standardized extract 60 mg one to two times daily. For tincture, take 60 drops tid to qid. Gotu kola may also be used topically as a wash for burns to minimize skin shrinking. Note: in some patients gotu kola can cause insomnia, agitation, or overstimulation of the sympathetic nervous system. Reduce dose accordingly.
* Coneflower (Echinacea purpurea) increases macrophage activity. Goldenseal (Hydrastis canadensis) is an antimicrobial that enhances healing. Use them together to protect against secondary infection. Equal parts of tincture may be taken 30 to 60 drops tid to qid.
* Powders of goldenseal, comfrey (Symphytum officinale), and marshmallow root (Althea officinalis) may be applied topically to enhance healing and minimize infection. Washes or compresses of cooled tea containing these herbs may also be used.
* St. John's wort (Hypericum perforatum) oil applied topically helps prevent postsurgical adhesions and may relieve nerve pain.
* Aloe vera gel applied to burns and wounds provides excellent pain relief and speeds healing.
* Marigold (Calendula officinalis) and plantain (Plantago major) aid in healing and can be used topically as salves or creams. These should only be used in incisional or "clean" wounds. Due to their fast action, they could encapsulate an infection.
* Granulated or confectioner's sugar applied topically to decubitus ulcers speeds wound healing. Safe for diabetic ulcers.

Homeopathy

Some of the most common acute remedies are listed below. Acute dose is three to five pellets of 12X to 30C every one to four hours until symptoms resolve.

* Arnica for bruised feeling and grief and/or shock from trauma
* Staphysagria for pain from laceration or surgical incisions
* Symphytum for wounds which penetrate to and involve bone
* Ledum for puncture wounds
* Urtica for burns
* Hypericum for injuries and trauma to nerves
* Keloid gel (Wala) for keloids

Patient Monitoring

Patients must be monitored for signs of bleeding, discoloration, or swelling in and around the wound. Fever, increasing pain, and the development of purulent drainage all indicate the presence of local infection and possible sepsis. Attention to nutritional status and positioning (to avoid undue pressure on the wound) are critical to healing.
Other Considerations
Prevention

Most wounds are accidental and often preventable. Wound infection and other complications can be prevented by careful aseptic technique and prophylactic antibiotics.
Complications/Sequelae

* Keloid scar tissue formation is an overgrowth of scar tissue that can be deforming. A keloid scar often returns even if excised.
* Wound contamination (10% if wounds), for example by Clostridia, Staphylococcus, Pseudomonas, Proteus, and Klebsiella, can occur in three stages: simple contamination, cellulitis, and myonecrosis (gas gangrene). Treatment consists of drainage, surgical debridement, and in severe cases, amputation. Fungal infections (e.g., Candida, Aspergillus) and herpes simplex can also compromise wound healing.
* Wound hemorrhage, usually a result of poor technique.
* Burn wound sepsis occurs when microorganisms invade subeschar tissue. Because most burn wounds are avascular, antibiotics do not adequately suppress microbial growth. Pneumonia is one of the most common infectious complications in burn patients.
* Tetanus (Clostridium tetani) occurs most often in mild penetrating injuries as a result of splinters, thorns, rusty nails, or dirty abrasions and lacerations, often because these mild injuries are ignored. Trismus (lockjaw) is pathognomonic. The mortality rates are as high as 30%, but for patients who recover, recovery is total. Human tetanus immune globulin (TIG) can prevent tetanus.

Prognosis

Prognosis is dependent on the extent and severity of the initial wound, as well as of any subsequent infection.
References

Black JM, Matassarin-Jacobs E. Medical-Surgical Nursing: Clinical Management for Continuity of Care. 5th ed. Philadelphia, Pa: W.B. Saunders Co; 1997.

Blumenthal M, ed. The Complete German Commission E Monographs. Boston, Mass: Integrative Medicine Communications; 1998:432.

Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:837, 839, 902-905, 947, 968.

Hardy JD, et al. Hardy's Textbook of Surgery. 2nd ed. Philadelphia, Pa: J.B. Lippincott; 1988.

Kruzel T. The Homeopathic Emergency Guide. Berkeley, Calif: North Atlantic Books; 1992:312, 314, 316.

Murray MT. The Healing Power of Herbs. Rocklin, Calif: Prima Publishing; 1991:184, 185, 207.

Nettina SM. The Lippincott Manual of Nursing Practice. 6th ed. Philadelphia, PA: J.B. Lippincott; 1996:90-91.

Reeves CJ, et al. Medical-Surgical Nursing. New York, NY: McGraw-Hill; 1999:535, 542-546, 551-553, 567-568.

Schwartz SI, et al. Principles of Surgery. 5th ed. New York, NY: McGraw-Hill; 1989:201-205, 301-302, 320-323, 470-473.

Thompson JM, et al. Mosby's Clinical Nursing. 4th ed. St. Louis, Mo: Mosby; 1997:461-462, 1099-1100, 1160, 1441.

Warts - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:42:00 +0000

Overview
Definition

Warts (verrucae) are small, benign, usually painless, and sometimes self-limiting growths on the skin caused by human papillomaviruses (HPV).

* Common warts (Verruca vulgare)
* Flat warts (Verruca plana)
* Genital warts (Condyloma acuminatum)
* Plantar warts (Verruca plantaris)

Although prevalence is highest in children and lowest in the elderly, warts affect all age groups. Genital warts are contagious; common, flat, and plantar warts generally are not. All warts can spread from one part of the body to another. Warts can disappear without treatment, and reappear.
Etiology

Human papillomaviruses (HPV)
Risk Factors

* Contact with affected persons or shed skin with HPV (particularly for genital warts)
* Trauma
* Immunosuppressive diseases (e.g., AIDS) and drugs
* Atopic dermatitis
* Communal facilities (locker rooms)

Signs and Symptoms

General characteristics:

* Appear singularly, clustered
* Sometimes painful

Common warts:

* Round and asymmetric
* Can grow from tiny (1 mm), smooth, flesh-tone papules to large (5 to 10 mm), thick, rough plaques
* May form mosaics (1 to 3 cm in diameter)
* Found anywhere, but generally on the hands

Flat warts:

* Small (1 to 3 mm) papules with flat tops
* Usually flesh-tone or pink
* Sometimes itchy
* Generally found on the face and back of hands

Genital warts (venereal warts):

* Tiny flat papules that grow to resemble common warts
* Generally found on external genitalia, pubic, and perineal regions
* May be found intravaginally and in the anal canal

Plantar warts:

* Rough, thickened, scarcely elevated papules
* Sometimes exhibiting black dots, indicating thrombosed capillaries
* Often quite tender, possible leg/back pain from disrupted posture
* Found on the sole of the foot, sometimes completely covering the heel or plantar region

Differential Diagnosis

* Corns or clavi Scar tissue
* Skin tags Molluscum contagiosum
* Moles Condyloma latum
* Calluses Seborrheic keratoses
* Skin cancer

Diagnosis
Physical Examination

General clinical characteristics of warts include:

* Disturbed skin lines
* Tiny black dots (thrombosed capillaries)
* Previous trauma to sites (e.g., fingers, nails, knees, face, scalp)

Other Diagnostic Procedures

* Warts usually can be diagnosed by location, appearance, and, if necessary, paring or debridement.
* Genital warts: Check intravaginally and in the anal canal.
* Plantar warts: To confirm diagnosis (vs. corns or clavi), pare lesion and look for characteristic black dots (thrombosed capillaries).
* Electron microscopy
* Immunohistochemistry
* Nucleic acid hybridization

Treatment Options
Treatment Strategy

Although asymptomatic warts can be ignored (with some risk of spreading), treatment may be desirable because warts can be embarrassing and disfiguring.

A number of treatments are available, including drug therapy (usually the initial therapy), cryosurgery (minimal scarring), electrosurgery, laser vaporization, curette and desiccation (scarring possible), and excision (scarring possible). Actual treatment depends on the location, type, and severity of warts. Because warts are benign, avoid treatments that could be harmful or could result in scarring.

Advise patients not to self-treat warts on mucous membranes or genitals and to be aware of scarring when treating warts on the face. Also, advise patients to keep warts covered during treatment.
Drug Therapies

Common, flat, and plantar warts: 12% to 40% salicylic acid, sometimes paired with lactic acid, qid (OTC). To optimize treatment, review guidelines with patients:

* Soak wart in warm water or bathe before treatment.
* Dry wart area.
* Apply medication per manufacturer's instructions.
* Keep area dry during treatment.

Some practitioners advise filing (pumice stone) before application.

Less common drugs include trichloroacetic acid or cantharidin (common warts), tretinoin (retinoic acid, Retin-A) (flat warts, notably on the face), benzoyl peroxide, bleomycin (intradermal injection), and cimetidine.

Genital warts: physician-applied podophyllin 25% in tincture of benzoin weekly or patient-applied podofilox 0.5 bid three days/rest four days, repeat up to four cycles. U.S. FDA-approved intralesional interferon alfa-n3 can be effective for persistent and recurring external genital warts. Covering warts for a week at a time with waterproof tape can cure warts by preventing viral growth. Plantar warts sometimes respond to hot-water soaks, 113?F water for 30 to 45 minutes, two to three times/week for six to eight weeks.
Complementary and Alternative Therapies

Nutritional and herbal support may enhance immune function and minimize recurrence of HPV. Some cases of HPV may respond to alternative therapies alone.
Nutrition

* Eliminate caffeine, alcohol, refined foods, and sugar.
* Avoid saturated fats, which increase inflammation (animal protein and dairy products).
* Increase whole grains, fresh vegetables, fruits, legumes, and essential fatty acids (nuts, seeds, and cold-water fish).
* Vitamin C (1,000 to 1,500 mg tid), beta-carotene (100,000 IU/day), vitamin E (400 IU/day), and zinc (15 to 30 mg/day) support immune function. Vitamin E may also be used topically to treat warts.
* B complex (50 to 100 mg/day) helps to reduce the effects of stress, which can weaken the immune system. Folic acid (800 mcg/day) is especially recommended for cervical HPV.
* Selenium (200 mcg/day) has antioxidant activity and supports immune function.

Herbs

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. of herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

Antiviral herbs that support the immune system. Combine tinctures of 1 part of goldenseal (Hydrastis canadensis) with 2 parts each of the following: lomatium (Lomatium dissectum), licorice root (Glycyrrhiza glabra), coneflower (Echinacea purpurea), osha (Ligusticum porteri), thuja leaf (Thuja occidentalis). Take 30 drops bid.

Topical applications are most effective for eradicating warts. Discontinue any topical application if irritation should develop in the surrounding skin.

For plantar, flat, and common warts use one or more of the following applications. The application may need to be repeated nightly for up to three weeks. Wart will turn black as it begins to die.

* Peel patch. Cut a piece of banana peel and place over wart before going to bed. Tape in place.
* Raw garlic patch. Cover wart and surrounding skin with a thin layer of castor or olive oil. Apply a thin slice of fresh garlic; tape in place.

To maximize benefit, place 2 to 4 drops of tincture of thuja or greater celandine (Chelidonium majus) on the wart before application.

For genital HPV, paint the warts with vitamin A or beta-carotene once or twice daily. Add 3 to 4 drops each of thuja, echinacea, and lomatium for best results. Cervical involvement may need to be treated under the supervision of a physician. A retention douche with 1 tsp. each of thuja, echinacea, and lomatium in 2 cups of water may be helpful in resolving superficial warts.
Homeopathy

Thuja is the classic remedy for warts, although by no means the only remedy that expresses warts. For the greatest benefit, an experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency.
Acupuncture

May be helpful in stimulating immune system.
Patient Monitoring

Monitor patients with diabetes or poor circulation for infections.
Other Considerations
Prevention

* Avoid contact with warts, particularly genital warts.
* Cover warts during treatment and avoid wound fluid.
* Use footwear in public areas.
* Do not scratch, pick, or bite warts.
* Do not share towels and washcloths with affected persons.

Complications/Sequelae

All warts: auto inoculation, scars

Common warts: nail deformity

Plantar warts: chronic pain from plantar wart removal

Genital warts: intraepithelial neoplasms
Prognosis

Although some warts will disappear without treatment, usually within 6 to 24 months, resolution without remission cannot be guaranteed.

With treatment, resolution for common, flat, and plantar warts can be six weeks or more; for genital warts, 20 weeks or more. If treatments are unsuccessful, first consider cryosurgery (multiple treatments may be needed) and then consider electrosurgery, laser vaporization, curette and desiccation, or excision.
Pregnancy

High doses of vitamins and herbs are contraindicated in pregnancy. Topical applications are safe. Pregnant women should not use podophyllin.
References

Barker LR, et al., eds. Principles of Ambulatory Medicine. 4th ed. Baltimore, Md: Williams & Wilkins; 1995:1467-1469.

Berkow R, Beers MH. The Merck Manual of Medical Information. Whitehouse Station, NJ: Merck Research Laboratories; 1997:984-985.

Brodell RT. Infect Med. SCP Communications, Inc.; 1996:13:56-60, 66.

Dambro MR, ed. Griffith's 5 Minute Clinical Consult. Baltimore, Md: Lippincott Williams & Wilkins; 1999:1166-1169.

Duke JA. The Green Pharmacy. Emmaus, Pa: Rodale Press; 1997: 452-455.

Ewald GA, McKenzie CR, eds. Manual of Medical Therapeutics. 28th ed. Boston, Mass: Little, Brown and Company; 1995:20-21.

Lockie A, Deddes N. The Complete Guide to Homeopathy. New York, NY: DK Publishing Inc; 1995:187, 189, 227.

Ody P. The Complete Medicinal Herbal. New York, NY: DK Publishing Inc; 1993:160-161.

Pray WS. Nonprescription Product Therapeutics. Baltimore, Md: Lippincott Willliams & Wilkins, in press.

Scalzo R. Naturopathic Handbook of Herbal Formulas. 2nd ed. Durango, Colo: Kivaki Press; 1994:73.

Walker LP, Brown EH. The Alternative Pharmacy. Paramus, NJ: Prentice Hall Press; 1998:353-354.

Varicose Veins - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:39:00 +0000

Overview
Definition

Varicose veins are large, dilated, tortuous, elongated superficial veins exhibiting reflux or retrograde flow as a result of valvular incompetence, weakness of the venous walls, or increased intraluminal pressure. They occur in 10% to 20% of the population, most commonly in the greater and lesser saphenous veins and their tributaries in the legs. Varicose veins may appear at any age, but the peak incidence is between 50 and 60 years of age. Varicose veins must be distinguished from spider veins or telangiectases, which are tiny, dilated, superficial veins visible on the skin surface.
Etiology

Primary varicose veins result from intrinsic weakness in the walls of the veins coupled with incompetent, perforating veins; 50% of these cases are familial (genetic). Secondary varicose veins are most often caused by post-thrombotic deep venous insufficiency and the resulting diversion of flow into superficial collateral vessels. They may also arise from superficial thrombosis. Less often, they are caused by arteriovenous fistulas.
Risk Factors

* Primary varicose veins
* Family history of varicose veins (50%)
* Female gender (three times more common in women)
* Pregnancy
* Occupations requiring prolonged standing
* Obesity
* Secondary varicose veins
* Proximal obstructing lesions (e.g., tumor)
* Conditions predisposing to deep venous thrombosis, such as surgery or immobilization, hereditary thrombophilia (e.g., protein C or S deficiency, factor V Leiden), acquired thrombophilia (e.g., malignancy), trauma, and arteriovenous fistulas

Signs and Symptoms

Primary varicose veins are often asymptomatic, causing only cosmetic concerns. Secondary varicose veins are more likely than primary varicose veins to be accompanied by the following.

* Chronic pain or heaviness or aching in the legs, relieved by elevation
* Ankle edema
* Skin ulcerations
* Superficial thrombosis
* Rupture with bleeding after minor trauma (rare)

Differential Diagnosis

Differentiating between primary and secondary varicose veins is critical before invasive therapy is attempted. Chronic venous insufficiency may develop if varicose veins are ablated when the deep venous system is obstructed. Chronic leg pain may not be due to the varicose veins themselves but to superficial or deep venous thrombosis. Additional causes of leg pain that must be considered include the following.

* Sciatica
* Peripheral neuropathy
* Arthritis of hip or knee
* Baker's cyst

Diagnosis
Physical Examination

The physician must conduct the examination while the patient is standing position so that the veins distend and are therefore easily seen and palpated. The following three tests may be helpful to distinguish primary and secondary varicosities.

* Brodie-Trendelenberg test to determine valvular incompetence in the saphenofemoral system
* Percussion test to determine valvular competence in the great saphenous vein
* Perthes test to determine valvular competence in the deep femoral vein

Imaging

* Doppler ultrasound to determine the relationship of varicosities to the saphenous system; to assess competence of the greater and lesser saphenous systems; to rule out deep venous obstruction and arterial occlusive disease
* Duplex ultrasound scanning with color-flow imaging used for the same purpose as Doppler ultrasound but may also permit more complete and accurate diagnosis, especially in obese patients.
* Venography to visualize veins filled with a contrast medium; most commonly used to detect thrombophlebitis
* Photoplethysmography to quantitatively measure venous function; to assess the severity of chronic venous insufficiency

Treatment Options
Treatment Strategy

Conservative (noninvasive) therapy is the initial treatment of choice for all patients and may be the only treatment ever needed for all but the most severe cases. These measures include the following.

* Avoidance of prolonged sitting, standing, or walking
* Regular exercise since action of the calf and other leg muscles increases venous return
* Periodic elevation of the legs
* Graduated compression stockings
* Ablative (invasive) procedures, including sclerotherapy and surgery, are indicated for superficial varicose veins accompanied by chronic pain; chronic venous insufficiency with edema, ulceration or other skin changes; and recurrent superficial vein thrombosis.
* Such treatment may also be indicated purely for cosmesis.

Surgical Procedures

Sclerotherapy involves injection of a sclerosing solution (e.g., sodium tetradecyl sulfate) into a varicosity, followed by application of a compression dressing. This produces inflammation in the vessel wall, which leads to fibrosis with obliteration of the vessel lumen. It is used most often for spider veins (telangiectases) and smaller, nonsaphenous varicose veins. Use of sclerotherapy alone and in combination with surgery to treat larger, more extensive varicosities of the greater and lesser saphenous veins is controversial in the U.S.

Phototherapy employs laser or high-intensity pulsed light to destroy telangiectases. It is not used to treat varicose veins per se. Radiofrequency ablation uses a catheter threaded into the varicose vein to heat the vein wall either to obliterate the lumen or shrink it enough to restore valve competence. It is suitable for treating large varicosities in the saphenous system, yet it is a relatively new technique where long-term results are unknown.

Surgical therapy involves removal of varicose veins by various techniques including classic stripping and ligation and the more recently developed stab-avulsion technique, which uses smaller incisions.
Complementary and Alternative Therapies

Nutritional supplements and herbs may be beneficial in enhancing the integrity of the vasculature, stimulating circulation, and relieving discomfort.
Nutrition

* Include dietary fiber in the form of complex carbohydrates (e.g., whole grains) to avoid constipation, which may contribute to venous congestion. Include foods rich in bioflavonoids, such as dark berries, dark leafy greens, garlic, and onions, which strengthen collagen tissues. Drinking fluids and getting regular exercise also help prevent constipation.
* Vitamin C (500 to 1,000 mg tid), vitamin E (200 to 600 IU/day), and zinc (15 to 30 mg/day) are essential for vascular health.

Herbs

Herbs may be used as dried extracts (pills, capsules, or tablets), teas, or tinctures (alcohol extraction, unless otherwise noted). Dose is 1 heaping tsp. herb/cup water steeped for 10 minutes (roots need 20 minutes). Commercial preparations often contain a combination of the following herbs. They may also be taken individually, as noted.

* Horse chestnut (Aesculus hippocastanum) 500 mg tid or standardized Aescin 10 mg tid
* Butcher's broom (Ruscus aculeatus) standardized extract (9% to 11% ruscogenin) 100 mg tid
* Gotu kola (Centella asiatica) 1,000 mg bid to qid or standardized extract (asiaticoside 40%, Asiatic acid 30%, madecassoside 1% to 2%) 60 mg once to twice daily
* Bilberry (Vaccinium myrtillus) standardized extract (25% anthocyanoside) 80 to 160 mg tid

Combine the following in equal parts to support the vasculature and tone the circulatory system: yarrow (Achillea millefolium), hawthorn (Crataegus monogyna), ginkgo (Ginkgo biloba), marigold (Calendula officinalis), horse chestnut (Aesculus hippocastanum), and ginger (Zingiber officinalis). Take 30 to 60 drops tincture bid to tid or drink three to four cups of tea daily.
Homeopathy

An experienced homeopath would consider the individual's constitution. Some of the most common acute remedies are listed below. Acute dose is three to five pellets of 12X to 30C every one to four hours until symptoms resolve.

* Aesculus for generalized venous congestion, especially with hemorrhoids and constipation
* Fluoricum acidum for painful varicose veins and sensation of heat
* Hamamelis for weak veins and easy bruising or bleeding; varicose veins with stinging pains
* Secale for varicosities with burning, constricting pains that are worse with exertion

Physical Medicine

Cold compresses of witch hazel (Hamamelis virginiana) and yarrow (Achillea millefolium) tea may provide temporary relief.
Acupuncture

May be helpful in improving the overall circulatory system and reducing venous congestion.
Massage

May be beneficial in alleviating venous congestion and mechanically stimulating circulation.
Patient Monitoring

Varicose veins, while treatable, will eventually recur and progress regardless of the treatment chosen. Recurrences may develop in residual varicose veins not completely removed by surgery or obliterated by sclerotherapy or in veins not previously affected. This may be assessed by periodic monitoring.
Other Considerations
Prevention

Regular exercise increases venous return. Both weight loss and exercise decrease the likelihood of thrombosis.
Complications/Sequelae

Both primary and secondary varicose veins develop progressively. Once a vein segment dilates, valvular incompetence develops and blood refluxes distally. This increases hydrostatic pressure distally, causing further vein dilation and elongation. Eventually this process may propagate throughout the length of the vein and into peripheral branches and perforating veins. Varicose veins are not thought to lead to venous ulceration unless accompanied by deep venous or greater or lesser saphenous vein insufficiency. Thus, varicose veins may account for only 20% to 30% of venous ulcers.

Complications of sclerotherapy include cutaneous hyperpigmentation; allergic reactions to sclerosing agents; thrombus formation; edema; telangiectatic matting; cutaneous necrosis; and ulceration. Arterial injection with sclerosing agents may lead to limb amputation; pulmonary embolism; deep venous thrombosis; and nerve damage.
Prognosis

Varicose vein disease is a chronic condition. New varicosities often occur after treatment, such as residual varicosities from incomplete surgery or sclerotherapy.
Pregnancy

The incidence of varicose veins during pregnancy varies from 8% to 20% and is most common in multiparous women. These varicosities may be caused by compression of the iliac veins by the uterus, which results in increased pressure in the lower veins, or by the effects or estrogen and progesterone, which make the walls of the veins more pliable. Elevation of legs may be particularly effective.
References

Bergan JJ, Yao JST. Venous Disorders. Philadelphia, PA: Saunders; 1991: 201 215.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:99, 149, 432.

Branch WT Jr. Office Practice of Medicine. 3rd ed. Philadelphia, PA: Saunders; 1994: 144 146.

Fauci AS. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998: 1405.

Goldman MP, Weiss RA, Bergan JJ. Varicose Veins and Telangectasias: Diagnosis and Treatment. 2nd ed. St. Louis, MO: Quality Medical; 1999: 3 41, 110 124, 164 174, 175 264, 414 424, 470 497.

Gruenwald J, Brendler T, et al, eds. PDR for Herbal Medicines. Montvale, NJ: Medical Economics Company; 1998:729-730.

Hoffman D. The New Holistic Herbal. New York, NY: Barnes & Noble Books;1995: 31.

Morrison, R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993.

Murray MT, Pizzorno JE. Encyclopedia of Natural Medicine. Rocklin, Calif: Prima Publishing; 1998: 540.

Rosen P, et al. Emergency Medicine: Concepts and Clinical Practice. 4th ed. Vol 2. St. Louis, MO: Mosby; 1998: 1862 1863.

Vaginitis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:37:00 +0000

Overview
Definition

Vaginitis is the inflammation of the femal vagina, of which there are various types. Some are caused by an increase in abnormal organisms (e.g., trichomonads) and others by an increase in normal flora (e.g., Candida, Gardnerella vaginalis, anaerobes). Candidiasis in the vaginal tract is called vulvovaginitis and is the most common cause of vaginal discharge in women. The Candida yeast-like fungus causes approximately 40% of all vaginitis, and about 75% of women get Candida vaginitis at some time.
Etiology

Candida vaginitis is primarily caused by Candida albicans but may be caused by C. tropicalis or C. glabrata. Yeast is a part of the normal flora of the vaginal tract in nearly one-third of women; infection occurs when there are changes in host resistance or bacterial flora. A small amount of vaginal discharge is normal at midcycle and should not be confused with vaginitis.
Risk Factors

* Antibiotic therapy especially with broad spectrum types
* Pregnancy from increased heat and moisture and hormonal shifts
* Diabetes
* Corticosteroid use
* Immunosuppressive drugs and conditions
* Human immunodeficiency virus (HIV) infection frequent candidiasis can be an early sign of HIV in women
* Anemia
* Hypothyroidism
* Oral contraception controversial, predominately for recurrence
* Being overweight
* High sugar intake
* Use of panty hose, constrictive clothing, or underwear that is not cotton

Signs and Symptoms

* Vaginal and vulvar pruritus (proportional to the number of organisms)
* Thin, creamy, or curd-like vaginal discharge; more copious during pregnancy; nonodorous
* Red, swollen, painful vaginal mucous membranes and external genitalia
* Satellite lesions (tender, red, discrete pustules that spread to thighs and anus)

Differential Diagnosis

* Trichomoniasis
* Gardnerella vaginalis
* Anaerobes
* Vaginal foreign bodies (retained tampons)
* Allergic reaction to douching or vaginal contraception
* Gonorrhea (especially in prepubertal girls)
* Contact dermatitis/vaginitis, including latex in condoms

Diagnosis
Physical Examination

* Vagina may appear hyperemic, bright red, with dry, white, and curd-like plaques or may have no erythema
* Vulva may have fissures, edema, and erythema
* Discharge appears creamy or curd-like

Laboratory Tests

* Microscopic wet mount scraping of vaginal plaque, discharge, or vulva scraping mixed with 10% potassium hydroxide (KOH) shows yeast, spores, and/or pseudohyphae; 50% to 70% accuracy rate.
* Gram's stain is more sensitive; identifies both mycelial and blastospore forms.
* pH
* Wet prep for trichomonas.

For recurrent infections (vaginal pH <4.5):

* Culture's findings on Nickerson's or Sabouraud's media
* Glucose tolerance test rules out diabetes
* HIV testing
* Possibly obtain endocervical swabs for chlamydia and gonorrhea detection assays

Pathology/Pathophysiology

* Pustule lesion dissects horizontally under the stratum corneum and peels it away; may appear like hyperplastic indurated plaques, atrophic inflamed plaques, or a leukoplakic area
* Accumulation of scale and inflammatory cells
* The pH of discharge is normal

Treatment Options
Treatment Strategy

Topical treatment is initiated before systemic, but patient preference may influence choice. Length of treatment and dose are both typically increased for chronic infection. Patients should avoid excessive exertion and sweating, keep vaginal area as dry as possible during infection, avoid sexual relations until symptoms clear, take showers instead of baths, and use unscented soap. Use proper hygiene when cleansing after bowel movement by wiping from front to back. Wear cotton underwear and avoid pantyhose and tight-fitting pants.
Drug Therapies

Topical and oral therapies are considered to be almost equally effective.

* Topical therapies may initially cause burning from inflammation: polyenes (nystatin) one tablet bid for two weeks placed high in the vagina with applicator; 70% to 80% effective; no systemic side effects. Azole derivatives such as imidazole (e.g., miconazole, butoconazole) and triazole (e.g., fluconazole, terconazole) intravaginal cream one to five days, also may be used externally for satellite lesions; 85% to 90% effective; no systemic side effects.
* Oral therapies: fluconazole 75% to 92% effective; 150 mg once; often considered the treatment of choice; contraindicated during pregnancy; appears to help HIV infected women. Ketoconazole 83% effective, but higher rate of recurrence with cessation of short- and long-term therapy; 400 mg/day for five days, or for two weeks with recurrent infection. Oral nystatin helps reduce intestinal colonization.

Complementary and Alternative Therapies

With the exception of pelvic inflammatory disease, gonoccocal, and chlamydia infections, alternative therapies for acute and chronic vaginitis can be effective for treating both symptoms and causes. Begin with a douche and an acidophilus supplement. For chronic or recurrent vaginitis, also incorporate vitamins, minerals, and herbs into the treatment plan.

Topical Applications: Use only one of the following douches at one time. Do not douche during menstrual flow. For first time or acute infection try the vinegar douche or boric acid capsules. For chronic vaginitis, use the herbal combination douche. For recurrent vaginitis, use the Betadine douche. Discontinue douching immediately if there is pain or exacerbation of symptoms.

* White vinegar: 1 to 2 tbsp. white vinegar to 1 pint of water. Douche daily for 10 to 14 days.
* Boric acid: One capsule (600 mg) inserted daily for 10 to 14 days. May cause irritation or problems from systemic absorption.
* Herbal combination: Mix equal parts of oregano leaf (Oreganum vulgare), goldenseal root (Hydrastis canadensis), and coneflower (Echinacea purpurea). Steep 1 heaping tbsp. of herbal mixture in one pint of water. Cool and douche daily for 10 to 14 days.
* Povidone iodine (Betadine): Douche with one part iodine to 100 parts water twice daily for 10 to 14 days. Prolonged use can suppress thyroid function.

Nutrition

* Avoid simple and refined sugars (breads, pasta, baked goods, sweets), dairy products, alcoholic beverages, peanuts, fresh or dried fruit, fruit juice, and all known food allergens. Eat whole foods with plenty of protein, fresh vegetables, and grains.
* Lactobacillus acidophilus reestablishes normal flora in the body and prevents the overgrowth of Candida. Take one capsule orally bid to tid, and insert one capsule into the vagina nightly (not to exceed 14 nights).
* Vitamin A (10,000 IU/day) or beta-carotene (50,000 IU/day) enhances the integrity of the vaginal mucosa. Required for proper immune functioning. Avoid high doses of vitamin A in pregnant patients or those who plan to get pregnant within three months.
* Zinc (30 mg/day) and vitamin E (400 to 800 IU/day) are essential for immune function.
* Vitamin C (1,000 mg tid to qid) optimizes immunity and helps to restore the integrity of vaginal mucosa.

Herbs

Ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

* Pau d'arco tea has antifungal effects. Drink 2 to 4 cups/day.
* Garlic (Allium sativum) has antimicrobial, antifungal, and immune stimulating properties. Prepare a tea with two cloves of garlic. Drink 2 to 4 cups/day. May add lemon and honey for flavor.

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

* Calcarea carbonica for intense itching with thick white or yellowish discharge that is worse before menses.
* Borax for burning pains with egg-white colored discharge that occurs midcycle.
* Sepia for burning pains with milky white discharge and pressure in vaginal area. Depression and irritability are usually present.
* Graphites for backache with thin white discharge that is worse in the morning and when walking.
* Arsenicum album for burning, offensive discharge in a patient who is easily chilled.
* Homeopathic combinations are also available as creams to apply intravaginally.

Acupuncture

Acupuncture may relieve pelvic congestion and improve immune function.
Patient Monitoring

Patients should be educated about the various risks for infection. Strict diabetic control is essential for diabetic patients. There is no specific follow-up unless infection persists. Repeat pelvic examination and a culture is then warranted. Treating the partner will minimize the possibility of reinfection.
Other Considerations
Prevention

* Avoid risks (see above).
* Avoid sweating, overheating, and sexual relations until symptoms clear.
* Use unscented soap, take showers instead of baths, and follow proper hygiene.

Complications/Sequelae

* Chronic candida vaginitis no definitive cure
* Often a result of persistent yeast in vagina, not recurrent infection
* Use oral and topical therapies together in higher doses for two to three weeks; maintenance therapy with azoles.
* Additional risk factors include oral contraception, vaginal douching, increased frequency of sexual intercourse.
* Fifteen percent of men have symptomatic balanitis and should be treated to prevent recurrent female infection.
* Antifungal therapy or acidophilus supplementation is started prophylactically with known antibiotic-associated candida vaginitis.
* HIV infection and diabetes predispose patients to chronic infections.
* Secondary bacterial infections

Prognosis

Some cases of candida vaginitis resolve spontaneously while others progress or become chronic. Recurrence is common. Chronic cases should be evaluated for systemic infections.
Pregnancy

Treatment should only be conducted under the supervision of a physician.
References

Dambro MR, ed. Griffith's 5 Minute Clinical Consult. Baltimore, Md: Lippincott Williams & Wilkins; 1999:358-361.

Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998.

Habif TP. Clinical Dermatology. 3rd ed. St. Louis, Mo: Mosby-Year Book; 1996.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:43, 69, 85, 171, 346.

Murray MT, Pizzorno JE. Encyclopedia of Natural Medicine. 2nd ed. Rocklin, Calif: Prima Publishing; 1998:530-535.

Uveitis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:37:00 +0000

Overview
Definition

Uveitis is characterized by inflammation of one or all parts of the uveal tract (iris, ciliary body, choroids). The most common form is anterior uveitis (iritis, iridocyclitis); posterior uveitis (choroiditis, chorioretinitis) is uncommon and found mostly in persons with AIDS who have cytomegalovirus (CMV) infection. Uveitis occurs in acute (<6 weeks) and chronic forms. The cause is often unknown but may result from either ocular trauma (e.g., chemical exposure) or an underlying systemic disease; the latter accounts for 40% of all cases (see section entitled Etiology for more details). Rate of incidence in both the U.S. and worldwide is 8 to 15 cases per 100,000. Uveitis occurs in men and women of all ages, with most patients presenting between 20 and 50 years of age; peak incidence is during the third decade of life.
Etiology

* Infection, including viral, bacterial, spirochetal, parasitic, and fungal infections (e.g., syphilis, tuberculosis, CMV, Lyme disease, histoplasmosis); toxoplasmosis is common cause of congenital posterior uveitis
* Masquerade syndromes (syndromes that simulate uveitis) include leukemia, lymphoma, retinitis pigmentosa, retinoblastoma, and malignant melanoma of the choroid
* Systemic disease, including suspected immune-mediated disorders (e.g., Behcet's and Crohn's disease, juvenile rheumatoid arthritis, multiple sclerosis, Reiter's syndrome, sarcoidosis); HLA-B27 genotype on chromosome 6 is present in some patients with acute anterior uveitis associated with ankylosing spondylitis, Reiter's syndrome, inflammatory bowel disease, psoriatic arthritis, and recurrent anterior uveitis
* Ocular trauma
* Idiopathic and/or confined to the eye, as in the case of acute retinal necrosis, birdshot choroidopathy, multifocal choroiditis, pars planitis, and Fuchs' heterochromic iridocyclitis
* Some drugs may cause uveitis; rifabutin, for example, has been identified in at least 113 cases by the FDA. Other drugs associated with uveitis include cidofovir, pamidronic acid, and sulfonamides.

Risk Factors

Forms of uveitis are geographically endemic (e.g., histoplasmosis in Ohio and Mississippi Valleys and Lyme disease in the northeastern, north central, and western U.S.). Uveitis due to toxoplasmosis is sometimes associated with pets. General risk factors include the following:

* History of autoimmune disease
* Infections
* Other eye diseases

Signs and Symptoms

* Painful eye(s)
* Conjunctival redness
* Photophobia
* Blurred or decreased vision
* Tearing
* Redness
* Floaters (posterior)

Differential Diagnosis

* Corneal abrasion or ulceration
* Ulcerative or ultraviolet keratitis
* Glaucoma
* Scleritis
* Conjunctivitis

Diagnosis
Physical Examination

Complete history and physical exam are required to identify possible underlying systemic disease. Signs of systemic disease include joint deformities (arthritis), oral or genital lesions (Reiter's and Behcet's syndromes), low back pain (ankylosing spondylitis), breathing problems (sarcoidosis), rash, and nail pitting (psoriasis). An ophthalmologic examination may reveal the following:

Anterior:

* Pupil contraction
* Inflammatory cells visible via slit-lamp examination
* Keratic precipitates on posterior corneal surfaces

Posterior:

* Inflammatory cells
* Fuzzy white retinal lesions
* Retinal and/or choroid inflammation (may be localized, diffuse, or multifocal)

Laboratory Tests

Laboratory tests should be tailored toward specific signs and symptoms when an underlying etiology is suspected.

* Angiotensin-converting enzyme (sarcoidosis)
* Antinuclear antibody testing (autoimmune diseases)
* Complete blood count (bacterial or viral etiology)
* Enzyme-linked immunosorbent assay (Lyme disease)
* Erythrocyte sedimentation rate (systemic disease)
* Human leukocyte antigen-B27 (HLA-B27)
* Syphilis serology; RPR and VDRL may also be associated with granulomatous uveitis; FTA-ABS and microhemagglutination assay for antibodies to Treponema pallidum are more specific for syphilis
* Purified-protein derivative skin test (tuberculosis)
* Skin test for anergy

Pathology/Pathophysiology

Although specific pathophysiology is unknown, the most common cause is an immune reaction against foreign molecules or antigens, which may also cause direct injury to uveal vessels and cells. In the case of autoimmune disorders, immune complexes may deposit in the uveal tract. Findings may include the following:

* Inflammation of ocular structures
* Small, white (not mutton-fat) keratic precipitates without iris nodules (nongranulomatous anterior uveitis)
* Large mutton-fat keratic precipitates and iris nodules (granulomatous anterior uveitis)

Imaging

* Chest X ray (tuberculosis and sarcoidosis)
* Joint X rays (juvenile rheumatoid arthritis and ankylosing spondylitis)
* Fluorescein angiography (may reveal late hyperfluorescence associated with cystoid macular edema)

Other Diagnostic Procedures

* Slit-lamp examination helps confirm diagnosis by revealing leukocytes and increased protein (flare) in aqueous humor
* Gonioscopy determines the presence of progressive peripheral anterior synechia?
* Tonometry measured intraocular pressure

Treatment Options
Treatment Strategy

Prompt treatment is required to preserve vision. Conventional practitioners recommend warm compresses to help relieve symptoms; naturopathic doctors may recommend the addition of herbs, such as eyebright, goldenseal, or marigold (Calendula officinalis) to the water used to make the compress. Sunglasses can protect for light sensitivity. In posterior uveitis, the goals are to determine and treat the systemic cause of the inflammation.
Drug Therapies

* Corticosteroids (topical or systemic) (e.g., prednisone, 0.125% to 1%; fluorometholone; 0.1% to 0.25%) to reduce inflammation and pain, stabilize cell membranes, inhibit release of lysozyme by granulocytes, and suppress lymphocyte circulation; oral prednisone or intraocular injections may be used in recalcitrant cases; contraindicated in patients with viral, fungal, and tubercular infections; can lead to increased intraocular pressure; posterior subcapsular cataracts associated with chronic topical use
* Cyclopegics (e.g., cyclopentolate, 0.5% to 2%; homatropine, 2% to 5%) block neurotransmission to the ciliary muscle, reduce pain, prevent adhesion of the iris to anterior lens capsule, stabilize blood-aqueous barrier, and help prevent continued protein leakage (flare); contraindicated in patients with narrow-angle glaucoma; toxic anticholinergic side effects are rare and occur most often in children; side effects include loss of accommodation (difficulty reading closeup)
* Antimicrobials
* Anti-inflammatories
* Oral immunosuppressants require close monitoring of side effects
* Humanized anti-Tac monoclonal antibody (daclizumab; approved now for immunosuppression in the case of kidney transplantation) phase I/II clinical trial conducted by the National Eye Institute (NEI) of the NIH suggests that this treatment, given IV one time per month, controlled uveitis as effectively as standard treatment with a marked decrease in side effects for the small group of patients studied; the next phase of research for daclizumab is to test the treatment on patients with Behcet's disease followed by a large, multicenter trial

Surgical Procedures

Surgery is used to repair ocular damage, such as glaucoma, cataracts, or detached retina.
Complementary and Alternative Therapies

CAM therapies may be beneficial in reducing the severity of systemic diseases whose sequelae include uveitis. Reducing free radical damage with herbs and nutrients may prevent or slow the progression of uveitis.
Nutrition

Flavonoids are highly concentrated in the eye. They inhibit neutrophil respiratory burst and superoxide production, both of which can create free radical damage in ocular tissues. In one study, the flavonoid, quercetin, decreased intraocular inflammation, reduced hemorrhagic changes, and minimized choroidal thickening in rats with S-antigen-induced uveoretinitis (Romero et al. 1989). High concentrations of flavonoids are found in red grapes, blueberries, cherries, and onions. Quercetin, 200-400 mg tid with meals, may also be taken as a supplement, often with bromelain to enhance function. Carotenoids are also thought to have antioxidant activity, particularly in the eye. Orange, yellow, and dark green vegetables contain a lot of dietary carotenoids. Supplement forms include mixed natural carotenoids (50,000 IU/day) and the carotenoid lutein (5 mg/day); the latter is considered to have a particular affinity for the eyes. Food to avoid that may be pro-inflammatory include saturated fats, fried foods, dairy products, and refined foods; anti-inflammatory foods include flaxseed, fatty fish, and other forms of essential fatty acids.

A randomized, double-blind, placebo-controlled trial evaluated the effects of vitamins C (1,000 mg/day) and E (200 IU/day) in patients with a first or recurrent episode of acute anterior uveitis. A total of 130 patients completed the study. Patients were evaluated for changes in anterior segment inflammation, measured by a laser cell flare meter. Clinical assessments included best-corrected visual acuity (VA), scores on the Hogan-Kimura scale for uveitis, and the number of drops of prednisolone and mydriatic administered (van Rooij et al. 1999).

Upon completion of the study, no significant differences in laser flare and cell measurements were detected between the vitamin and placebo groups, possibly because all patients were also treated with steroids. However, average visual acuity was better on all points in the vitamin group as compared to the placebo group. The investigators suggest that oral vitamins C and E protect photoreceptors from free radical damage and, in this manner, help preserve visual acuity. In addition, vitamin E may play a role in protecting against cystoid macular edema. CME can lead to loss of visual acuity in uveitis patients (van Rooij et al. 1999).
Herbs

Curcumin, the primary active substance in turmeric, has been reported to have anti-inflammatory effects including inhibition of prostaglandin synthesis and stabilization of lysosomal membranes. Specific application for uveitis is not definitive but results of a recent preliminary study are intriguing. In a three-year study following 32 patients with chronic anterior uveitis, researchers report that curcumin (Curcuma longa) showed effects comparable to those of corticosteroid therapy but had none of the adverse effects associated with steroid use. Patients received curcumin, along with topical mydriatics and warm compresses for spasm and pain relief. Antitubercular drugs were added to the regimen if the person had a strongly positive PPD (Purified Protein Derivative, a substance used to measure reactivity to tuberculosis). Curcumin 375 mg po tid was administered to patients for 12 weeks. Antitubercular therapy was continued for one year. Although patients in both groups had recurrences of anterior uveitis (55% in those receiving curcumin alone and 36% in those with the addition of anti-TB drugs), each group showed noticeable improvement. In addition, according to the authors, the rates of both recurrence and complications secondary to the uveitis for all 32 patients on curcumin, with or without anti-TB medications, were similar to these figures for patients taking corticosteroids to treat uveitis. Finally, none of the participants complained of side effects from the curcumin (i.e., any side effects experienced were in the anti-TB drug group and were attributable to those medications) (Lal et al. 1999).

Similar to particular foods (see Nutrition section), herbs with concentrated amounts of flavonoids, such as ginkgo (Ginkgo biloba) and bilberry (Vaccinium myrtillus), have a long tradition of use in treating diseases of the eye. However, their use in the treatment of uveitis specifically has not yet been validated by scientific studies (Blumenthal et al. 2000).
Homeopathy

Homeopathic treatment can address both constitutional?and acute aspects of disease in general. In homeopathic terminology, the constitutional state reflects a pattern of underlying vulnerability or weakness that is unique to the individual and persists throughout that person's life. Symptoms tend to alternate over time and treatment consists of selecting the appropriate remedy specific for the patient's constitutional type. By contrast, in acute conditions a remedy can be administered without reference to any particular constitutional state (Ullman 1995). Although there are no known scientific studies evaluating the utility of specific homeopathic remedies for treating uveitis, acute homeopathic remedies may be beneficial in providing symptomatic relief.
Acupuncture

Acupuncture has been shown to be effective in the treatment of other ocular diseases (see Macular Degeneration monograph, for example) but has not been fully assessed in the treatment of uveitis.
Massage

N/A
Patient Monitoring

Slit-lamp and intraocular pressure measurements every 1 to 7 days in acute phase, with follow up every 1 to 6 months.
Other Considerations
Prevention

There are no known preventive measures for uveitis. However, regular eye exams can screen for chronic asymptomatic uveitis. Treatment of causative disorders may help prevent onset.
Complications/Sequelae

* Glaucoma
* Cataracts due to neovascularization
* Permanent partial vision loss
* Retinal detachment
* Band keratopathy
* Cystoid macular edema
* Macula scarring impairs central vision

Prognosis

* Prognosis is good with early diagnosis and treatment; anterior uveitis tends to respond to treatment in days to weeks
* Outcome may be dependent on underlying condition
* Chronic uveitis (defined as presence of inflammation >6 weeks) may require long-term low-dose topical steroid use and can lead to ocular scarring and vision loss

Pregnancy

Safety of topical steroid use in pregnant women has not been established.
References

Alexander KL, Dul MW, Lalle PA, Magnus DE, Onofrey B. Optometric Clinical Practice Guideline: Care of the Patient with Anterior Uveitis. 2nd edition. American Optometric Association; 1997. Accessed at: www.aoanet.org/cpg-7-au.html on February 8, 2000.

Berkow R, Fletcher AJ, Beers MH, eds. The Merck Manual. Rahway, NJ: Merck & Co.; 1992:2380-2382.

Blumenthal M, Goldberg A, Brinckmann J, eds. Herbal Medicine: Expanded Commission E Monographs. Newton, Mass: Integrative Medicine Communications; 2000:18, 165-166.

Dunn JP, Nozik RA. Uveitis: role of the physician in treating systemic causes. Geriatrics. 1994;49(8):27-32.

Fraunfelder FW, Rosenbaum JT. Drug-induced uveitis. Incidence, prevention and treatment. Drug Saf. 1997;17(3):197-207.

Gordon K III. Iritis and uveitis. In: Adler J, Brenner B, Dronen S, et al. Emergency medicine: An On-line Medical Reference. Accessed at http://emedicine.com/cgi-bin/foxweb.exe/showsection@d:/em/ga?book=emerg&topicid=276 on August 17, 2000.

Lal B, Kapoor AK, Asthana OP, et al. Efficacy of curcumin in the management of chronic anterior uveitis. Phytother Res. 1999;13(4):318-322.

No author listed. Drug-induced uveitis can usually be easily managed. Drugs Ther Perspect. 1998;11(10):11-14.

Nussenblatt RB, Fortin E, Schiffman R, et al. Treatment of noninfectious intermediate and posterior uveitis with the humanized anti-Tac mAb: a phase I/II clinical trial. Proc Natl Acad Sci USA 1999;96(13):7462-7466.

Romero J, Marak GE Jr, Rao NA. Pharmacologic modulation of acute ocular inflammation with quercetin. Ophthalmic Res. 1989;21(2):112-117.

Sowka JW, Gurwood AS, Kabat AG. Anterior Uveitis. In: Handbook of Ocular Disease Management. Review of Optometry Online. Accessed at www.revoptom.com/handbook/sect4e.htm on February 8, 2000.

Ullman D. The Consumer's Guide to Homeopathy. New York, NY: Tarcher/Putnam; 1995.

van Rooij J, Schwartzenberg SG, Mulder PG, Baarsma SG. Oral vitamins C and E as additional treatment in patients with acute anterior uveitis: a randomised double masked study in 145 patients. Br J Ophthalmol. 1999;83(11):1277-1282.

Urolithiasis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:32:00 +0000

Overview
Definition

Also called nephrolithiasis or kidney stones, urolithiasis is the presence of calculi in the urinary tract. The male-to-female incidence ratio is 4:1, with 240,000 to 720,000 Americans affected yearly. Eighty percent of calculi are composed of calcium (either oxalate or phosphate), with others composed of struvite, uric acid, or cystine.
Etiology

Type of stone indicates cause.

* Calcium type I increased small bowel absorption of calcium unrelated to intake
* Calcium type II increased dietary calcium intake
* Calcium type III increased vitamin D synthesis (secondary to renal phosphate loss)
* Calcium oxalate idiopathic in origin, or through primary intestinal disorders, chronic diarrhea with inflammatory bowel disease or steatorrhea
* Struvite (magnesium ammonium phosphate) mainly in women and can be large, stag's horn shape; secondary to infection with urease-producing organisms (Proteus, Pseudomonas, Providencia, and less commonly Klebsiella)
* Uric acid metabolic defects or dietary excess of uric acid; bowel disease or chemotherapy
* Cystine secondary to chronic diarrhea, type I renal tubular acidosis, chronic hydrochlorothiazide treatment, idiopathic

Risk Factors

* Excess intake of calcium, oxalate, or purines in predisposed individuals
* Inadequate fluid intake
* Sedentary occupation
* Area of high humidity, elevated temperatures (summer)
* Hyperparathyroidism
* Renal tubule defects (renal tubule acidosis)
* Bowel disease
* Ileal bypass for obesity
* Genetics cystinuria is an autosomal recessive disorder and homozygous type has markedly increased cystine excretion
* Excessive intake of certain vitamins and minerals
* Gout
* Use of certain diuretics

Signs and Symptoms

May be asymptomatic, but the following are usually seen.

* Sudden onset of severe flank pain
* Nausea and vomiting
* Patient in constant motion in attempt to lessen the pain
* Pain referred to testes or labium as the stone moves
* Fever and chills (infection)
* Pain radiating anteriorly over the abdomen

Differential Diagnosis

* Urinary tract infection
* Pyelonephritis
* Diverticulitis
* Pelvic inflammatory disease
* Ovarian pathology
* Drug addiction
* Appendicitis
* Small bowel obstruction
* Ectopic pregnancy
* Cadmium toxicity

Diagnosis
Physical Examination

Patient is in extreme pain and constantly moving. Pain occurs episodically as the stone moves down the ureter and may be referred. Severity of symptoms does not reflect stone size. Patient may be asymptomatic, with stone found incidentally on plain film.
Laboratory Tests

* Urinalysis Possibly microscopic or gross hematuria, but absence does not exclude stones. Exclude infection.
* Urine pH Persistent urinary pH <5.0>7.5 indicates struvite stone.
* Urine culture and sensitivity tests
* Serum chemistries for calcium, electrolytes, phosphate, and uric acid
* 24-hour urine collection for calcium, uric acid, phosphate, oxalate, citrate excretion (recurrent cases only), and to collect stones for analysis

Pathology/Pathophysiology

Analysis of stone to determine type 60% to 80% are calcium, 15% to 20% struvite, 5% uric acid, and 1% to 3% cystine.
Imaging

* Plain abdominal film and renal ultrasound radiopaque stones
* Ultrasound with a full bladder to confirm stone in the ureterovesical junction
* Intravenous urography to confirm diagnosis
* Intravenous pyelogram to determine size and location of stone and degree of obstruction
* Unenhanced helical CT scan rim sign or halo of the calculus

Other Diagnostic Procedures

Metabolic evaluation for recurrent stone formation:

* 24-hour urine collection to check volume, urinary pH, calcium, uric acid, oxalate, and citrate excretion
* Second collection on restricted calcium (400 mg/day), sodium (100 mEq/day), and oxalate diet
* Serum parathyroid hormone and calcium load tests at third visit

Treatment Options
Treatment Strategy

Usually conservative management eventually results in stone passage. Treatment depends on type of stone, ability or inability to pass, and presence of complications. All patients should drink at least six to eight glasses of water daily plus one at bedtime and one during the night. For calcium type II stones, follow a low-calcium diet, restrict sodium to 1 g/kg daily, and increase bran intake.
Surgical Procedures

Surgery is recommended for patients with severe pain unresponsive to medications, serious bleeding, and persistent fever, nausea, or significant urinary obstruction. If no medical treatment is provided after surgery, stones recur in 50% of patients within five years.

* Extracorporeal shock wave lithotripsy (ESWL) outpatient procedure that shatters stones under 2 cm and without complications
* Urethroscopy for stones in lower third of ureter
* Percutaneous nephrolithotomy when in upper two-thirds of ureter and greater than 2 cm in size

Drug Therapies

* Narcotics as needed to control acute severe pain
* Allopurinol for uric acid calculi; 100 to 300 mg/day to control hyperuricemia
* Potassium citrate for uric acid calculi; 100 mEq tablets bid to raise urinary pH
* Hydrochlorothiazide for calcium type I stones; 25 to 50 mg/day.
* Cellulose phosphate for calcium type I stones; 10 g/day to decrease bowel absorption
* Orthophosphates for calcium type III stones; to inhibit vitamin B synthesis

Complementary and Alternative Therapies

Symptomatic urolithiasis requires medical attention. Alternative therapies aid in preventing recurrent episodes and increasing the overall vitality of the urogenital system. Start with nutritional guidelines for prevention of recurrence. Herbs and homeopathics can be used for acute pain relief and long-term tonification of the urinary tract.
Nutrition

* Reduce intake of sugar, refined foods, animal products (meats and dairy), caffeine, alcohol, soft drinks, and salt.
* Increase intake of water, fiber, vegetables, whole grains, and vegetable proteins.
* Minimize oxalate-containing foods such as spinach, rhubarb, beets, nuts, chocolate, black tea, wheat bran, strawberries, and beans.
* Include foods rich in magnesium and low in calcium, such as barley, bran, corn, rye, oats, soy, brown rice, avocado, banana, and potato.
* Magnesium citrate (200 to 400 mg/day) may increase the solubility of calcium oxalate and calcium phosphate.
* Pyridoxine (B6, 10 to 100 mg/day) is essential for the metabolism of oxalic acid.
* Folic acid (5 mg/day) for uric acid stones.

Herbs

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites, or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 10 to 20 minutes and drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

* For acute pain relief, combine tinctures of wild yam (Dioscorea villosa), cramp bark (Viburnum opulus), kava (Piper methysticum), and Jamaica dogwood (Piscidia piscipula). Take 15 drops every 15 minutes for up to 8 doses.
* Drink an infusion of equal parts of gravel root (Eupatorium purpureum), corn silk (Zea mays), pipissewa (Chimaphila umbellata), and kava 1 tsp./cup, 3 to 4 cups/day.

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

Remedies that may be considered for acute pain relief include the following.

* Berberis for sharp, stitching pains that radiate to groin
* Colocynthis for restlessness with pains that feel better bending forward
* Ocimum for nausea and vomiting from the pain

Physical Medicine

Castor oil pack. Used externally, castor oil is a powerful anti-inflammatory. Apply oil directly to skin, cover with a clean soft cloth (e.g., flannel) and plastic wrap. Place a heat source (hot water bottle or heating pad) over the pack and let sit for 30 to 60 minutes. For best results, use for three consecutive days.
Patient Monitoring

Fifty percent of patients pass the stone within 48 hours. For complications or recurrences, refer patient to a urologist. Admit patients to the hospital when they have persistent vomiting, suspected urinary tract infection, pain unresponsive to oral analgesics, or obstructing calculus with a solitary kidney.
Other Considerations
Prevention

Maintain proper hydration and dietary restrictions to avoid future development of stones. Determine and treat underlying cause. Alkalinize urine (maintain pH >7.5 with cautious use of penicillamine) in patients with recurrent cystine stones.
Complications/Sequelae

Urinary tract infection and obstruction can result in extensive kidney damage.
Prognosis

Annual rate of recurrence after first stone is 3%, after second stone 6%. This condition is painful but usually produces no permanent damage. Majority of patients will pass the stone within 48 to 72 hours of onset of symptoms.
Pregnancy

Do not perform ESWL on women of childbearing age who have a stone in the lower ureter; the effect on the ovary is not known. Rule out ectopic pregnancy and/or ruptured ovarian cyst.
References

The Burton Goldberg Group, compilers. Alternative medicine: The Definitive Guide. Tiburon, Calif: Future Medicine Publishing; 1997.

Ferri FF. Ferri's Clinical Advisor: Instant Diagnosis and Treatment. St Louis, Mo: Mosby-Year Book; 1999.

Grases F, et al. Urolithiasis and phytotherapy. Int Urol Nephrol. 1994;26:507-511.

Larson DE, ed. Mayo Clinic Family Health Book. 2nd ed. New York, NY: William Morrow and Company; 1996.

Scalzo R. Naturopathic Handbook of Herbal Formulas. Durango, Colo: 2nd ed. Kivaki Press; 1994.

Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment 1994. Norwalk, Conn: Appleton & Lange; 1994.

Urinary Incontinence - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:30:00 +0000

Overview
Definition

Urinary incontinence (inability to control urination or the involuntary loss of urine from the bladder) afflicts more than 13 million people in the United States of both sexes and all age groups. Incidence is higher in the elderly and twofold greater in women. Exercise and behavioral therapies have a high degree of success; medication and surgery are effective in a select group over the short-term. Many drugs have unwanted and/or serious side effects. Surgery should be considered only when other treatment options fail. Diagnostic categories are:

* Stress incontinence (SUI): Most common form among women primarily due to pregnancy, childbirth, menopause. Weakened pelvic floor muscles fail to support bladder and resultant pressure interferes with muscles that close the urethra. Leakage occurs with physical stress (e.g., coughing, sneezing).
* Urge (or reflex) incontinence (UI): Leakage accompanied by sudden unexplained need to urinate (e.g., when touching water). May be due to nerve damage (e.g., from Alzheimer's disease, stroke, brain tumor, injury, surgery).
* Overflow incontinence (OI): Rare in women. Bladder overextension due to blocked urethra or inability of bladder muscles to expel urine. Caused by neurological damage (e.g., from diabetes), tumors, urinary stones, enlarged prostate.
* Mixed incontinence (MI): SUI/UI in combination.
* Functional incontinence (FI): Impaired cognitive abilities and/or restricted movement (e.g., confined to a wheelchair) prevents timely access to toilet.
* Transient incontinence (TI): Triggered by medication, UTIs, restricted mobility, stool impaction.

Etiology

* Neurological damage/disorders (dementia, spinal cord injury, multiple sclerosis, stroke)
* Low estrogen levels in women
* Physical changes (from pregnancy or enlarged prostate, stool impaction, tumor)
* Medications
* Urinary tract infections (UTIs)
* Weak urethral sphincter
* Weak pelvic floor muscle

Risk Factors

* Overweight
* Hysterectomy before age 45
* At least one live birth
* Labor exceeding 24 hours
* Prostate disease or hypertrophy in males
* Physical problems associated with age/debility
* Neurologic damage or disorders

Signs and Symptoms

* Involuntary urination Perineal irritation
* Frequent and unusual urinary urge

Differential Diagnosis

* Vaginal discharge in women UTIs
* Urethral discharge in men Medication effects (diuretics)

Diagnosis
Physical Examination

* Urine leakage
* Findings specific to risk factors

Laboratory Tests

Urinalysis to determine urinary tract/bladder infection, urinary stones, diabetes, glomerular disease, tumor.
Pathology/Pathophysiology

* Urethral sphincter incompetence Prostatic hypertrophy
* Bladder tumor UTI

Imaging

* Pelvic ultrasound Renal ultrasound
* Transrectal ultrasound (prostate)

Other Diagnostic Procedures

* Physical examination
* Neurological assessment
* Medical history
* Interview for pattern of voiding/leakage, straining/discomfort associated with urination
* Test for stress incontinence (e.g., vigorous coughing to detect urine loss)
* Urodynamics
* Voidin cystourethrogram

Treatment Options
Treatment Strategy

Along with the drug therapies and surgical procedures listed below, the following may be necessary.

* Catheters Urethral plugs
* Condom catheters Absorbent pads, undergarments, diapers

Drug Therapies

* Antibiotics: For UTIs or sexually transmitted diseases
* Anticholinergics: For UI, reduce detrusor muscle contractions/increase urethral resistance (imipramine [Tofranil] 10 to 25 mg up to tid; oxybutinin [Ditropan] 2.5 to 5 mg up to tid; hyoscyamine [Cystospaz], hyoscyamine sulfate [Levsin/Levsinex, Cystospaz-M], and flavoxate [Urispas] all 100 to 200 mg tid or qid). High instance of undesirable/intolerable side effects
* Antimuscarinic/ganglionic-blockers: Propantheline (Pro-Banthine) 15 to 30 mg every four to six hours. High incidence of side effects including confusion, agitation, coronary artery disease, especially in the elderly.
* Cholinergics: For underactive detrusor, bethanechol (Duvoid, Myotonachol, Urecholine); contraindicated with asthma, bradycardia, Parkinson's disease. Can produce intolerable sweating/excessive salivation.
* Sympathomimetics: For SUI, phenylpropanolamine (found in Ornade) 25 to 100 mg bid; or pseudoephedrine (found in Sudafed) 15 to 30 mg tid; caution with hypertension, angina, hyperthyroidism, diabetes
* Hormones: SUI in women, increase urethral resistance (conjugated estrogens [Premarin] 1.25 to 2.5 mg/day in cream; 0.3 to 0.625 mg/day orally with estradiol [Estrace]); increased risk of endometrial cancer, particularly with unopposed estrogen

Surgical Procedures

Success rate higher in younger patients; effectiveness deteriorates over time; long-term success rate estimated at 75% to 90% for five years.

* Artificial sphincter: Inflatable cuff surrounding bladder neck activated by mechanism implanted in scrotum or labia.
* Supportive devices: String secured to the bladder and attached to muscle, bone, or ligament; in severe SUI, a wide sling elevates bladder.

Complementary and Alternative Therapies

The main thrust of alternative therapies is Kegel exercises, biofeedback, and preventing any exacerbating conditions. Underlying conditions (e.g., malnutrition, dementia, prostatitis, and UTIs) need to be addressed. Yoga may be beneficial. Habit training (establishing toilet times to increase regularity of voiding) may also help treat this condition.
Nutrition

* Eliminate caffeine, alcohol, sweetener substitutes, simple sugars.
* Cranberries and blueberries contain substances which inhibit the adhesion of bacteria to bladder tissue. This may be useful in preventing infections which can exacerbate incontinence. Also helps to deodorize urine.
* Vitamin C (1,000 mg tid) acidifies urine, which inhibits bacterial growth.
* Beta-carotene (25,000t to 50,000 IU/day) is necessary for immune function and mucous membrane integrity.
* Zinc (30 mg/day) supports immune function, often deficient in the elderly.
* Calcium (1,000 mg/day) and magnesium (500 mg/day) together may help to improve sphincter control.

Herbs

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

Urinary astringents have been used historically for sphincter tone and connective tissue integrity. Demulcents soothe irritated tissue and may decrease spasm of the bladder.

These urinary astringents tone and heal the urinary tract and can be taken long term at 1 cup/day or 30 drops tincture/day.

* Horsetail (Equisetum arvense) also helps with connective tissue integrity.
* Plantain (Plantago major) is an astringent and demulcent.

Marshmallow root (Althaea officinalis) is a urinary demulcent, best used alone in a cold infusion. Soak 1 heaping tbsp. of marshmallow root in 1 quart of cold water overnight. Strain and drink during the day in addition to other teas.
Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

* Causticum for SUI, especially with retention from holding the urine and frequent urges to urinate
* Natrum muriaticum for SUI, vaginal dryness, painful coitus, especially with a history of grief
* Pareira for retention of urine from an enlarged prostate
* Sepia for SUI with sudden urging, especially with prolapsed uterus and vaginitis
* Zincum for SUI, urinary retention from prostate problems, unable to urinate standing, must sit

Acupuncture

May be of help, depending on cause.
Patient Monitoring

Compliance with behavioral techniques is essential and may require close monitoring and reinforcement. Physician must be alert to and monitor side effects of medications, or for infections following implants/surgery.
Other Considerations

Early treatment is most beneficial; embarrassment often causes delay in seeking help.
Prevention

* Pelvic muscle strengthening (Kegel) exercises during and after pregnancy
* Maintenance of healthy prostate in men; maintenance of healthy pelvis in women
* Maintenance of optimal body weight for height/age

Complications/Sequelae

* Drugs: Considerable risk of unwanted, intolerable and/or serious side effects; contraindication with other medications
* Surgery: Possible complications
* Catheters: UTIs

Prognosis

Most cases can be vastly improved with appropriate management; effectiveness may deteriorate with age.
Pregnancy

Pregnancy increases risk of incontinence; effect of drugs upon fetus must be determined before being administered during pregnancy.
References

Bartram T. Encyclopedia of Herbal Medicine. Dorset, England: Grace Publishers; 1995:247.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:432.

Dambro MR, ed. Griffith's 5 Minute Clinical Consult. Baltimore, Md: Williams & Wilkins; 1998.

Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:1466-1468.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:111-113, 258-261, 286, 402.

Olshevsky M, Noy S, Zwang M, et al. Manual of Natural Therapy. New York, NY: Facts on File Inc; 1989.

Thom DH, Van den Eeden SK, Brown JS. Evaluation of parturition and other reproductive variable as risk factors for urinary incontinence. Obstet Gynecol. 1997;90:983-989.

Ullman D. The Consumer's Guide to Homeopathy. New York, NY: The Putnam Publishing Group; 1995.

Urethritis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:29:00 +0000

Overview
Definition

Urethritis is infection and inflammation of the urethral lining caused by bacterial infections, and may involve the bladder, prostate, and reproductive organs. Urethritis can affect males and females of all ages; however, females are at higher risk due to proximity of urethral opening to anus and vagina, increasing the likelihood of bacterial contamination.

Sexually transmitted pathogens Chlamydia trachomatis, Neisseria gonorrhoeae (co-infection common), and herpes simplex are primary causes of urethritis, particularly in men; however, often no infection can be documented. Vaginitis triggered by Candida albicans or Trichomonas vaginalis, and bacterial vaginosis, are also contributing causes for women. In bacteria-negative cultures, urethritis and vaginitis account for most urinary disorders in women.

Of the organisms which cause nongonococcal urethritis (NGU), chlamydia is the most common and most serious, with 75% of infected women and 50% of infected men remaining asymptomatic. Left untreated, it can lead to permanent damage of reproductive organs in both men and women. Implications tend to be more severe in women due to the internal nature of the infection, which often goes without notice until complications arise.
Etiology

* Bacteria and other organisms entering the urethra, including Chlamydia trachomatis, Neisseria gonorrhoeae, Ureaplasma urealyticum, Mycoplasma hominis, Candida albicans, Trichomonas vaginalis, and herpes viruses
* Bruising during sexual intercourse (women)
* Infection reaching the urethra via venous system from prostate gland or through the penis opening; in older men, classic urinary tract pathogens are a more common cause than STDs
* Bacterial infection following course of antibiotics
* Reiter's syndrome

Risk Factors

* Unprotected sex
* History of sexually transmitted diseases
* Multiple sex partners, or sexual relations with individual who has multiple sex partners
* Urinary catheter or instrumentation
* Bacteria-resistant drugs
* Prior history of kidney stones, prostatitis, epididymitis, genital injury
* Reiter's syndrome, which has a genetic predisposition
* Increased caffeine intake

Signs and Symptoms

In both sexes but particularly women, the disease may be asymptomatic.

In men:

* Burning during urination
* Purulent or whitish-mucus urethral discharge
* Burning or itching around the penile opening

In women:

* Painful urination and/or unusual vaginal discharge
* Cervicitis
* Salpingitis
* Pelvic inflammatory disease

Differential Diagnosis

* Reiter's syndrome
* Gonorrhea
* Allergic reactions
* Other urinary tract infections

Diagnosis
Physical Examination

* Watery and thin discharge (Chl. trachomatis)
* Purulent discharge (N. gonorrhoeae)
* Inflammation of penile opening

Laboratory Tests

* Presence of white blood cells in urine specimen
* Gram's stain of urethral discharge which shows >4 WBCs per HPF
* Intracellular gram-negative diplococci strongly suggests gonorrhea
* Absence of gram-negative cocci strongly suggests NGU (Gram's stains are less than 100% sensitive for chlamydial infections)
* Syphilis and HIV serology to rule out other STDs

Pathology/Pathophysiology

* Unusual urethral/vaginal discharge in 50% to 75% of cases
* In males, possible inflammation and irritation at penis opening
* Urethral strictures

Other Diagnostic Procedures

* Thorough medical and sexual history, including date of symptom onset and prior history of STDs
* Genital examination
* Evaluation of laboratory evidence for infection (Chl. trachomatis requires specimen of intracellular and urethral cellular material; collect specimen with calcium alginate swab inserted two to three cm into urethra)
* Evaluation of sexual partners may aid diagnosis in asymptomatic disease

Chl. trachomatis:

* Immunofluorescent testing
* Enzyme-linked immunoassay
* DNA probing of cervical samples

Treatment Options
Treatment Strategy

* Therapy must often be administered presumptively.
* Antimicrobial therapy directed against etiologies.
* Chlamydial disease may persist even after successful treatment of gonococcal component.
* Impress upon patient importance of treatment compliance.
* All sex partners should be treated.
* Sexual abstinence recommended until treatment regimen is completed, as disease can remain active even after symptoms have disappeared.

Drug Therapies

Urethritis:

* Tetracycline (500 mg qid for seven days)
* Erythromycin (500 mg qid for seven days; preferred in pregnancy)

N. gonorrhoeae:

* Ceftriaxone (250 mg IM once a day)
* Ofloxacin (400 mg once a day)
* Ciprofloxacin (500 mg once a day)

Chl. trachomatis:

* Doxycycline (100 mg bid for 10 days)
* Ofloxacin (300 mg orally bid for 10 days)

Trichomonas urethritis/vaginitis:

* Metronidazole (2 g orally once a day; contraindicated in pregnancy)
* Clindamycin (300 mg orally bid for seven days)

Herpes simplex:

* Acyclovir (400 mg orally tid for 10 days)
* Famciclovir (250 to 500 mg orally bid for 10 days)
* Valacyclovir (1,000 mg orally bid for 10 days)

Persistent/recurrent disease:

* Retreatment with antimicrobials

Complementary and Alternative Therapies

Nutrition, herbs, and homeopathic remedies are useful in fighting infection, relieving pain, and tonifying the urinary system.
Nutrition

* Eliminate any known food allergens. Food allergies can be tested for using an IgG ELISA food allergy panel, or by an elimination diet.
* Eliminate refined foods, fruit juices, caffeine, alcohol, and sugar, which may compromise immune function and irritate the urinary tract.
* Cranberries and blueberries contain substances that inhibit the adhesion of bacteria to the urinary tract.
* Vitamin C (1,000 mg tid) stimulates immune system and acidifies urine, which inhibits bacterial growth.
* Beta-carotene (25,000 to 50,000 IU/day) is necessary for immune function and mucous membrane integrity.
* Zinc (30 to 50 mg/day) supports immune function.

Herbs

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

Herbal therapy should be instituted at the first sign of symptoms and continued for three days beyond resolution of symptoms. Treatment of infectious urethritis is best accomplished through teas because of the flushing action of the additional fluid intake. Combine two herbs from each of the following categories and drink 4 to 6 cups/day.

Urinary antiseptics are antimicrobial and include the following.

* Uva ursi (Arctostaphylos uva ursi)
* Buchu (Agathosma betulina)
* Thyme leaf (Thymus vulgaris)
* Pipissewa (Chimaphila umbellata)

Urinary astringents tone and heal the urinary tract and include the following.

* Horsetail (Equisetum arvense)
* Plantain (Plantago major)
* Cleavers (Galium aparine)

Urinary demulcents soothe the inflamed urinary tract and include the following.

* Corn silk (Zea mays)
* Couch grass (Agropyron repens)
* Marshmallow root (Althaea officinalis) is best used alone in a cold infusion. Soak 1 heaping tbsp. of marshmallow root in one quart of cold water overnight. Strain and drink during the day in addition to the other urinary tea.

For advanced or recurrent infections, prepare a tincture of equal parts of goldenseal (Hydrastis canadensis) and coneflower (Echinacea purpurea). Take 30 drops four to six times/day in addition to the urinary tea.

For noninfectious urethritis or for urethritis with severe pain and spasm, add kava kava (Piper methysticum) to any of the above formulas.

A periwash may be helpful in reducing pain with urination. Place 1 tsp. of the coneflower/goldenseal tincture in an 8-oz. peri bottle. Fill with water. Rinse off after each urination.
Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

* Staphysagria for urinary infections associated with sexual intercourse
* Apis mellifica for stinging pains that are exacerbated by warmth
* Cantharis for intolerable urging with "scalding" urine
* Sarsaparilla for needing to stand to urinate, with burning after urination

Acupuncture

May be helpful in enhancing immune function.
Patient Monitoring

* Recurrent or persistent symptoms require careful reevaluation and re-treatment with antimicrobials when urethral discharge tests positive or demonstrates increased numbers of polymorphonuclear leukocytes.
* Monitor general condition/medications.
* Encourage patient self-care.
* Monitor closely for treatment compliance, particularly for STD-related urethritis.

Other Considerations

Treat patient's sexual partner(s) if STD-related.
Prevention

* Wipe from front to back following bowel movement, wash genitalia with soapy water, shower rather than bath (for women only).
* Drink eight glasses of water daily.
* Protected sex with latex condom when outside of a monogamous relationship

Complications/Sequelae

* When left untreated, gonococcal urethritis common in men may cause urethral stricture with increased risk of periurethral abscess; may perforate the peritoneal scrotum, causing urethral fistula.
* Untreated chlamydia increases risk of acquisition/transmission of HIV, causes pelvic inflammatory disease (PID) in women, and in men affects the testicles, which leads to complications and possible infertility.
* Infection spread to ureters/kidneys

Prognosis

* When associated with low-grade infection and treated appropriately, seldom produces long-term illness; however, recurrence is common.
* STDs or NGU can be effectively treated with antibiotic medication. When asymptomatic or left untreated, complications including infertility may result, and disease transmission to sex partners is inevitable.

Pregnancy

NGU:

* Permanent damage to reproductive organs/infertility in both sexes.
* Difficulties during pregnancy, premature delivery, low birth weight.
* Ear, eye, and lung infections in newborns. (Resultant neonatal conjunctivitis can permanently damage eyesight.)
* Nutritional guidelines are safe to follow in pregnancy. Herbal therapies should be used only with physician supervision.
* Avoid tetracyclines.

References

Bartram T. Encyclopedia of Herbal Medicine. Dorset, England: Grace Publishers; 1995:436-437.

Berkow R, Beers MH. The Merck Manual of Diagnosis and Therapy. Rahway, NJ: Merck and Company; 1992.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:432.

Bowie WR. Approach to men with urethritis and urologic complications of sexually transmitted diseases. Med Clin North Am. 1990;74:1543-1557. Accessed at www.thriveonline.com.

Hoffman D. The New Holistic Herbal. New York, NY: Barnes & Noble Books; 1995:109-110.

Kruzel T. The Homeopathic Emergency Guide. Berkeley, Calif: North Atlantic Books; 1992:98-102.

Shealy CN. The Illustrated Encyclopedia of Healing Remedies. Boston, Mass: Element Books Limited; 1998.

Tierney LM Jr, et al., ed. Current Medical Diagnosis & Treatment 1999. 38th ed. Stamford, Conn: Appleton & Lange; 1999.

Virtual Hospital: University of Iowa Family Practice Handbook. 3rd ed. Available at www.vh.org.

Ulcerative Colitis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:26:00 +0000

Overview
Definition

Ulcerative colitis (UC) is a chronic nonspecific inflammatory bowel disease (IBD) involving the mucosa and submucosa of the colon. It involves the rectum and is characterized by ulceration, bloody diarrhea, and rectal bleeding. Disease severity depends on degree and extent of inflammation and proximal colonic involvement. UC may present at all ages, but onset peaks between 15 and 30 years with a secondary onset peak between 60 and 70; it is a serious, relapsing remitting disease with significant morbidity and mortality affecting at least 50 per 100,000 people in the United States. Higher incidence in Jewish population. Familial incidence is established; 10% to 20% of UC patients have at least one family member affected with IBD. Medical management controls symptoms in most cases, but colectomy is necessary in about 25% of those affected.
Etiology

Unknown. Infectious, genetic, immunologic, and psychological causes likely.
Risk Factors

* Jewish ethnicity (Ashkenazi Jews in particular)
* Positive family history
* A diet high in margarine or chemically modified fat (diet of combined western foods)
* Psychological disturbances

Signs and Symptoms

UC typically manifests as bloody diarrhea interspersed with asymptomatic intervals. Onset may be acute and fulminant, but more often is insidious, with progressively severe urgency to defecate, mild abdominal cramps, and blood and mucus in stools. Symptoms may include violent diarrhea, high fever, malaise, abdominal tenderness or pain, anemia, anorexia, weight loss, and arthralgias. In UC confined to the rectosigmoid area, stool may be normal or hard and dry, with mucus discharged between or accompanying bowel movements. Stool abnormality increases with proximal involvement, with up to 20 bowel movements a day, diffuse cramping, distressing tenesmus, passage of pus, nocturnal sweats, pain, and diarrhea.
Differential Diagnosis

* Crohn's disease
* Hemorrhoids
* Viral, bacterial, and parasitic infections
* Diverticulitis
* Irritable bowel syndrome
* Radiation proctitis
* Drug- or toxin-induced enterocolitis
* Vasculitis of the intestinal tract
* Colonic carcinoma
* Tuberculosis
* Diarrhea associated with infection
* Diarrhea associated with antibiotics

Diagnosis
Physical Examination

Patients with mild or moderate disease usually look well and exhibit few abnormal signs; bowl sounds and rectal exam (apart from blood) are often normal. Those with severe disease may also look deceptively well, but usually exhibit tachycardia, tender colon, and systemic complications. Diagnosis is made on the basis of history, absence of fecal pathogens, and endoscopic and histological appearances of the colon.

Mild inflammatory changes include the following.

* Loss of normal vascular pattern
* Fine granularity of mucosa
* Pinpoint hemorrhage to mucosal swabbing
* Exudation of mucopus

Progressive inflammatory changes include the following.

* Coarse granularity and pinpoint ulceration
* Confluent hemorrhage
* Confluent mucopus progressing to gross ulcerations
* Spontaneous hemorrhage
* Exudation of pus
* Pseudopolyps
* Epithelial dysplasia

Acute disease stage includes the following.

* Loss of haustrations
* Thickening of smooth muscle of colon
* "Lead pipe" appearance of colon
* Occasional colonic stricture

Laboratory Tests

* Nonspecific Iron-deficiency anemia
* Leukocytosis Hypoalbuminemia
* Elevated ESR Electrolyte imbalance

Pathology/Pathophysiology

Endoscopic appearance of mucosa ranges from normal-appearing to complete denudation; UC is characterized by an even "microcarpet" of tiny ulcers. Sigmoidoscopic appearance is rarely normal even during asymptomatic intervals. Pathologic changes include:

* Degeneration of reticulin fibers beneath mucosal epithelium
* Occlusion of subepithelial capillaries
* Infiltration of lamina propria with plasma cells, eosinophils, lymphocytes, mast cells, and polymorphonuclear leukocytes
* Crypt abscesses, epithelial necrosis, and mucosal ulceration

Imaging

* Radiography (plain view of abdomen)
* Air contrast barium enema
* Ultrasonography and CT may help determine extent of disease and complications

Other Diagnostic Procedures

* Stool samples
* Rectal exam
* Endoscopy with biopsy
* Presence of IL-1ra allele 2 gene is marker for disease severity
* State-Trait Anxiety Inventory (Form Y); Sacks' sentence completion tests (psychological influences)

Treatment Options
Treatment Strategy

The goal of treatment is to control inflammation, prevent complications, and replace nutritional and blood losses. Severe cases may require hospitalization; perforations and hemorrhage may occur without warning. Control of active disease with drug therapy depends upon extent and severity of mucosal ulceration. Most widely used are steroids and 5-aminosalicylic acid (5-ASA) drugs. Corticosteroids can induce remissions but do not prevent relapses. When indicated, total proctocolectomy with ileoanal pull through and pouch is the preferred surgical procedure. Indications for surgery include:

* Severe inflammation unresponsive to medical therapy
* Chronic active disease
* Cancer prophylaxis
* Growth retardation in children

Drug Therapies

Sulfasalazine is the treatment of choice for flare-ups, chronic treatment, and to reduce frequency of relapse (1 to 4 g/day). Diarrhea may be treated cautiously with diphenoxylate, loperamide, or opiates. Use of antidiarrheal agents in severe disease could precipitate toxic megacolon. Toxic megacolon requires immediate surgery if no improvement within 24 hours after hospitalization.

* Ulcerative proctitis and proctosigmoiditis may be treated topically with corticosteroid or mesalamine enema, foam, or suppository; oral prednisone if refractory (20 to 60 mg/day); osmotic purgation to relieve constipation.
* Parenteral or oral corticosteroids (prednisone 20 to 60 mg/day) for more severe flare-ups; patients with chronic activity (10% to 15%) require continuous low-dose corticosteroids.
* Immunomodulators such as 6-mercaptopurine and azathioprine reduce need for corticosteroids .
* Oral prednisone (20 to 60 mg/day) or parenteral corticosteroids and sulfasalazine (1 g bid or tid) and parenteral ACTH are useful in severe active disease; iron and parenteral hyperalimentation if indicated; antibiotics in toxic megacolon.
* A new class of topically-acting corticosteroids (budesonide, fluticasone, beclomethasone dipropionate, prednisolone-21-methasulphobenzoate, tixocortol pivalate) is an alternative in treating active UC.
* Cyclosporine may induce remission.
* Nicotine patches may induce remission but are not helpful in maintaining remission.

Complementary and Alternative Therapies

Nutritional and herbal support, mind-body techniques, and physical aids can help reduce the frequency and severity of ulcerative colitis as well as improve the integrity of intestinal mucosa and correct nutritional deficiencies. Stress reduction techniques through biofeedback, hypnosis, or counseling can help patients to deal productively with stress. Other mind-body therapies such as: yoga, tai chi, meditation, psychotherapy; stress management such as yoga, deep breathing, stretching, regular exercise (walking), meditation, prayer, visualization, and hypnotherapy; and support groups such as the Crohn's-Colitis Foundation of America (CCFA) may also be helpful.
Nutrition

* Decrease refined foods, sugars, and saturated fats.
* Eliminate all food allergens from the diet. The most common allergenic foods are dairy, soy, citrus, peanuts, wheat, fish, eggs, corn, and tomatoes. An elimination/challenge trial may be helpful in uncovering sensitivities. Remove suspected allergens from the diet for two weeks. Re-introduce foods at the rate of one food every three days. Watch for reactions which may include gastrointestinal upset, mood changes, headaches, flushing, and exacerbation of symptoms.
* A rotation diet, in which the same food is not eaten more than once every four days, may be helpful in reducing symptoms.
* Specific foods that may exacerbate ulcerative colitis are dairy, Brassica vegetables (cabbage, brussels sprouts, broccoli, cauliflower, and kale) and gluten-containing grains (wheat, oats, barley, triticale, rye).
* Fiber supplementation can help reduce abdominal pain, cramping, and gas. These supplements include psyllium, flaxmeal, slippery elm (Ulmus fulva) powder, and marshmallow root (Althaea officinalis) powder. There may be increased bloating and gas initially but this should resolve within 7 to 10 days.
* Pro-flora supplements taken bid to tid can help to rebalance normal bowel flora and reduce gas and bloating.
* Essential fatty acids may be protective of intestinal mucosa. Max-EPA or fish oil (3 to 4 g, up to 18 g/day).
* Bromelain (250 to 500 mg between meals) is a proteolytic enzyme that reduces inflammation.
* Minimum 48 oz. of water/day
* Eliminate caffeine and alcohol.

IBD is associated with low levels of the following nutrients due to poor absorption, competitive inhibition from medications, or increased requirement.

* Biotin (300 mcg/day)
* Beta-carotene (50,000 IU/day)
* Vitamin A (50,000 IU/day for one month, then 10,000 IU/day)
* Vitamin C (1,000 mg tid)
* Vitamin D (100 to 200 IU/day) is associated with secondary hyperparathyroidism and osteomalacia, possibly due to poor calcium absorption and utilization.
* Vitamin K (10 mg/day) may help normalize prothrombin levels and decrease bleeding.
* B vitamins, specifically thiamine (100 to 250 mg/day), pantothenic acid (100 mg/day), riboflavin (50 mg/day), B12 (1,000 mcg/day), and folic acid (800 mcg/day). Folic acid may be depleted with sulfasalazine use, which is a competitive inhibitor with folic acid.
* Magnesium (200 mg bid to tid) is associated with weakness, hypotension, and tetany.
* Calcium (1,000 mg/day)
* Zinc (100 mg bid for one month, then 20 to 30 mg/day)
* Elemental iron (30 mg bid), especially with chronic blood loss. Glycinate form is least constipating and 30% more absorbable than ferrous sulfate.
* Selenium (200 mcg/day) protects against oxidative damage.

Herbs

Ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted. The goal of herbal therapy is to relieve spasm, reduce inflammation, and encourage healing of the intestinal mucosa.

* Enteric-coated peppermint oil: one to two capsules (0.2 ml peppermint oil/capsule) tid after meals. Peppermint oil (Mentha piperita) is a potent spasmolytic that reduces bowel irritability.
* A tincture of equal parts of the following herbs may be taken before meals (20 to 30 drops tid): Cramp bark (Viburnum opulus), passionflower (Passiflora incarnata), meadowsweet (Filipendula ulmaria), wild yam (Dioscorea villosa), valerian (Valeriana officinalis), and lemon balm (Melissa officinalis). Combined, they enhance digestion and relieve spasm.
* For acute exacerbation with bleeding, use equal parts of the following herbs in a tincture (30 drops qid): coneflower (echinacea purpurea), goldenseal (Hydrastis canadensis), and geranium (Geranium maculatum)
* Licorice root (Glycyrrhiza glabra) and marshmallow root (Althaea officinalis) are soothing and promote healing of gastrointestinal mucosa. Make a tea of licorice root by steeping 1 tsp. in one cup of hot water for 20 minutes. Drink 3 cups/day. (Contraindicated in hypertension.) For marshmallow root tea, soak 1 heaping tbsp. of root in one quart of cold water overnight. Strain and drink throughout the day.
* Quercetin (250 to 500 mg before meals) may help reduce reactions to food sensitivities.

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

* Arsenicum album for intense cramping and burning, with scanty dark blood in stool. Patient is restless, chilly, and anxious about their health.
* China for extreme bloating and gurgling in abdomen; bloody stools and exhaustion.
* Phosphorus for painless diarrhea with prostration and thirst for cold drinks.
* Sulphur for morning diarrhea that drives patient out of bed.
* Mercurius vivus for IBD associated with canker sores and metallic taste.

Physical Medicine

Castor oil pack. Used externally, castor oil is a powerful anti-inflammatory. Apply oil directly to skin, cover with a clean soft cloth (e.g., flannel) and plastic wrap. Place a heat source (hot water bottle or heating pad) over the pack and let sit for 30 to 60 minutes. For best results, use for three consecutive days.
Acupuncture

Ulcerative colitis may respond to acupuncture, which can help alleviate spasm and normalize digestive function.
Patient Monitoring

Regularly scheduled appointments to evaluate disease activity, and psychological well-being. The extreme variability and high incidence of relapse and morbidity predispose patients to anxiety and depression.
Other Considerations
Prevention

Severely ill patients must be monitored closely for peritonitis, perforation, and toxic megacolon; long-term patients for epithelial dysplasia and cancer. Annual liver tests and cholangiography for cholestasis are recommended. Laboratory parameters measured serially during treatment are useful indicators of disease activity.
Complications/Sequelae

Local:

* Hemorrhage
* Perforations
* Peritonitis
* Strictures
* Perianal abscesses
* Rectovaginal fistulas
* Pseudopolyposis
* Toxic megacolon
* Carcinomatous changes
* Colon cancer

Systemic:

* Peripheral arthropathy
* Ankylosing spondylitis
* Erythema nodosum
* Pyoderma gangrenosum
* Episcleritis
* Aphthous ulceration of the mouth
* Fatty liver
* Primary sclerosing cholangitis
* Cholangiocarcinoma
* Growth retardation in children
* Depression and anxiety

Prognosis

The typically relapsing remitting course of UC depends upon severity of initial attack, extent of proximal colonic involvement, and response to medical treatment. There is no cure excepting colectomy. Left-sided and ulcerative proctitis have the most favorable prognosis. Drug treatment is effective for about 70% to 80% of patients; surgery becomes necessary in the remaining 20% to 30%. About 45% of patients are symptom-free at any given time; most suffer at least one relapse in any 10-year period. About 5% succumb to fulminant UC or require immediate colectomy; a smaller percentage have a single attack without recurrence; and about 15% experience continuous symptoms refractory to medication and rarely achieve full remission. In the 25% of patients with ulcerative proctitis (disease localized to the rectum), 10% to 30% experience late proximal spread. UC in children affects the entire colon in 50% of cases. The prognosis is affected by the extent and the severity of the disease, and by the physical condition of the patient.
Pregnancy

Maintenance treatment should be continued, with pregnancy timed to inactive phase of disease and relapses treated aggressively with corticosteroids. Corticosteroids and sulfasalazine are safe and nonteratogenic; immunosuppressive agents are not recommended. Goldenseal, geranium, and quercetin are contraindicated in pregnancy. In addition, high doses of vitamins should be avoided.
References

Berkow R, ed. The Merck Manual of Diagnosis and Therapy. 16th ed. Rahway, NJ: Merck Research Laboratories; 1992.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:427-428, 432.

Greenfield SM, et al. A randomized controlled study of evening primrose oil and fish oil in ulcerative colitis. Aliment Pharmacol Ther. 1993;7:159-166.

Roediger WE, Moore J, Babidge W. Colonic sulfide in pathogenesis and treatment of ulcerative colitis. Dig Dis Sci. 1997;42:1571-1579.

Weatherall DJ, Ledingham JGG, Warrell DA, eds. Oxford Textbook of Medicine. 3rd ed. New York, NY: Oxford University Press; 1996.

Werbach M. Nutritional Influences on Illness. New Canaan, Conn: Keats Publishing; 1988:424-427.

Wyngaarden JB, Smith LH, Bennett JC, eds. Cecil Textbook of Medicine. Philadelphia, Pa: WB Saunders Co; 1992.

Tuberculosis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:23:00 +0000

Overview
Definition

Tuberculosis remains a leading cause of infectious morbidity and mortality worldwide. In 1993, the World Health Organization (WHO) called tuberculosis a "global emergency." There are an estimated 8 million new cases of tuberculosis each year. Tuberculosis is a slow-growing disease that primarily affects the pulmonary system. In 15% of patients it manifests as an extrapulmonary disease, including lymphadenitis, pleurisy, and meningitis as well as renal, genitourinary, thyroid (rarely), and bone and joint involvement. Tuberculosis is most frequently transmitted via airborne droplets expelled when an infected person coughs, sneezes, or talks. When these droplets evaporate, the desiccated bacilli remain airborne, finding their way to the distal alveoli of a new host. There is typically a prolonged latency period between initial infection and overt disease.

The incidence of tuberculosis peaked in the United States in the early 1900s. With the advent of antibiotics, the number of cases steadily declined from the early 1950s to 1984. In 1985, the trend reversed. This increase has been attributed both to the premature abatement in government control programs and to the human immunodeficiency virus (HIV) epidemic. Since that time, effective public health programs have once again reversed this trend; since 1993, tuberculosis has declined.

Miliary tuberculosis is a systemic version of TB affecting many organ systems due to hematogenous spread.
Etiology

* Mycobacterium tuberculosis the major etiologic agent worldwide; humans are the sole reservoir
* M. bovis transmitted from milk of infected cows; rare since institution of pasteurization
* M. africanum rare; only in Africa

Risk Factors

* Occupational: healthcare workers airborne transmission, infection from extrapulmonary disease such as draining an abscess, autopsies; embalmers from body fluids generating infectious aerosols
* Contact with infected person
* Location of birth: Asia, Africa, Latin America
* HIV infection
* Residence in a long-term care facility
* Immunosuppressive therapy
* Tuberculosis infection: increases likelihood of developing active disease within two years
* Low income, medically underserved individuals
* In areas with a high incidence of TB, exogenous re-infection is a major cause of recurrence after effective treatment.

Signs and Symptoms

* Asymptomatic especially from initial infection
* Mild fever, headache, chills, night sweats
* Malaise, fatigue
* Anorexia, weight loss
* Cough nonproductive or mucopurulent
* Hemoptysis
* Pleuritic chest pain
* Dyspnea
* Adenopathy
* Children asymptomatic and extrapulmonary manifestations are more frequent than in adults; look for signs of meningitis, adenopathy

Differential Diagnosis

* Bacterial pneumonia
* Other nontubercular mycobacterial infections
* Lymphomas
* Sarcoidosis
* Lung abscess

Diagnosis
Physical Examination

With pulmonary disease, post-tussive rales or amphoric breath sounds may be heard. Keratoconjunctivitis may be apparent. Marked general ill health and possibly pallor from anemia are the most common general findings. Positive tuberculin skin test such as purified protein derivative (PPD).
Laboratory Tests

* Acid-fast bacillus microscopy sputum (take three specimens from three different days) or smear mycobacteriologic studies with stains; 10,000 bacilli/mL yields a positive microscopy result; negative result does not rule out tuberculosis.
* M. tuberculosis culture more sensitive than sputum; radiometric culture permits detection in 7 to 14 days; also tests for drug resistance of the M. tuberculosis

Pathology/Pathophysiology

* M. tuberculosis droplets are engulfed by an alveolar macrophage (phagocytized) and destroyed by a resistant host (95% of cases), or progress in an immunocompromised host.
* Macrophage lyses from replicating bacilli; circulating monocytes differentiate into macrophages, which ingest but cannot inhibit the logarithmic growth of the bacilli; infected macrophages are transported by lymphatics to the bloodstream.
* Infected macrophages release cytokines that attract T cells.
* CD4 helper T cells secrete various cytokines (cell-mediated immunity), activating the macrophages to kill the bacilli; local tissue also destroyed.
* Tubercle bacilli can survive dormant and walled off by epithelioid cells for years cell walls contain high concentrations of lipids or waxes (resistant to standard staining); may be evidenced by a positive PPD 4 to 6 weeks after infection.
* Primary tuberculosis uncontrolled tubercles and disseminated M. tuberculosis; granulomatous lung foci
* Liquefaction and cavity formation may occur from reactivation of dormant M. tuberculosis foci causing bronchopneumonia.
* Extrapulmonary relative paucity of bacilli; giant cell granulomas with caseating necrosis

Imaging

* Chest X ray upper lobe with fibronodular shadowing, infiltrates, and cavities; may be normal even with active M. tuberculosis; hilar lymphadenopathy often seen in children
* CT or MRI for meningitis

Other Diagnostic Procedures

PPD skin test

* Induration ³5 mm is positive for patients with a close contact who is infected or a patient with HIV
* Induration ³10 mm is positive for high-risk, high-prevalence groups
* Induration ³ 15 mm is positive for anyone
* False negatives may occur with immunosuppression even in the presence of overwhelming disease
* False positives may occur in the case of bacilli Calmette-Gu?rin (BCG) vaccine recipient

DNA detection by polymerase chain reaction (PCR)

* Rapid; problems of false positives may be resolved; specimen preparation problems, though, still do exist?

Treatment Options
Treatment Strategy

In the case of hemoptysis, the patient must be treated emergently to prevent asphyxiation. Chest x-ray, sputum, and culture tests are administered when diagnosis is suspected. Patients are often treated presumptively until results of lab tests return. Multidrug, not single-drug, antituberculous agents are prescribed. The 1998 consensus statement of the Public Health Tuberculosis Guidelines Panel found that rates of treatment completion are most likely to exceed 90% with directly observed therapy (DOT). The more action that is taken to administer medications, the higher the completion rates. Directly observed therapy should be employed whenever possible.
Drug Therapies

The patient is tested for drug resistance to determine the most effective combination of medications. Multidrug regimens taken regularly and for a sufficient period of time are required to effectively eradicate M. tuberculosis. Drug therapy regimens last 6 to 9 months for most patients, 9 to 12 months for HIV-infected patients, and a minimum of 12 months with extrapulmonary tuberculosis. For patients with HIV, preventive therapy reduces incidence of active tuberculosis and decreases mortality rates for those with positive skin tests. Drug regimens are divided into an initial bactericidal phase followed by a sterilization phase.

Standard antibiotics for tuberculosis include:

* Isoniazid adults 5 mg/kg/day, children 10 to 20 mg/kg/day, 300 mg maximum for both; side effects: hepatitis (risk increased with alcohol consumption), peripheral neuropathy, rash, fever; additional drug interactions and toxicity for patients with HIV
* Rifampin adults 10 mg/kg/day, maximum 600 mg/day, children 10 to 20 mg/kg/day; side effects: gastrointestinal upset, hepatitis, orange discoloration of body fluids (and contact lenses); additional drug interactions and toxicity for patients with HIV
* Pyrazinamide 15 to 30 mg/kg/day, 2 g maximum; side effects: hepatitis, hyperuricemia possibly with polyarthralgias (both reduced by concurrent rifampin administration)
* Ethambutol least potent against M. tuberculosis; 15 to 25 mg/kg/day for 2 months, then reduce to 15 mg/kg/day; side effects: retrobulbar optic neuritis and color perception problems, avoid with children
* Streptomycin used least often because of toxicity; intramuscular or intravenous administration of 10 to 15 mg/kg/day, maximum 1 g/day, up to 5 times per week for adults, 20 to 40 mg/kg/day with 1 g/day maximum for children; side effects: ototoxicity (both hearing loss and vestibular dysfunction), nephrotoxicity, teratogenic
* Pyridoxine (vitamin B6) added to regimen particularly in populations at risk for vitamin deficiency (e.g., malnourished, alcoholics, elderly, pregnant and nursing mothers) or at risk for neuropathy (diabetics, HIV, chronic renal failure)

Experimental drugs:

* Rifapentine longer acting, allowing dosing twice a week
* Fluoroquinolones (e.g., ciprofloxacin) antibacterial; concentrations higher in respiratory secretions than in serum; well tolerated, but insufficient data to use as standard treatment; less effective with HIV
* Rifabutin as effective as rifampin with concurrent HIV, but reduces time to sputum conversion; 150 mg/day associated with fewest adverse effects; possible role with multidrug resistance

Surgical Procedures

* Bone and joint: curettage and bone grafting of extra-articular lesions; joint or bone resection; excision of soft tissue abscess; amputation

Complementary and Alternative Therapies

The control of tuberculosis worldwide depends on the effectiveness of vaccination programs and antibiotic therapy. Recent studies have determined that dietary deficiencies of proteins, zinc, and vitamins A, C, and D are linked to multiple abnormalities in immune function; these abnormalities may result in a poor immunologic response to tuberculosis and to the BCG vaccine, especially among the elderly, children, alcoholics, the homeless, and HIV-infected individuals.

Although the antimicrobial properties of plant species are not comparable to the potency of antimicrobial agents produced by microorganisms, researchers continue to conduct in vitro studies in an effort to uncover effective plant compounds that will inhibit M. tuberculosis. A definitive review of this research was compiled by Newton and her colleagues (2000).
Nutrition

Most data concerning nutrients and tuberculosis are derived from animal studies and in vitro experiments using cultured macrophages infected with M.?tuberculosis. Extrapolating relevant data for human subjects must therefore be done cautiously.

Protein Deficiency

Protein deficiency in guinea pigs resulted in (McMurray et al. 1990):

* Loss of protection from BCG vaccine
* Reduction in E rosette-forming T cells
* Loss of PPD-lymphocyte responses
* Altered production of interleukin-2 (IL-2)

A reversal of all immune dysfunction occurred after good nutrition was reestablished.

Vitamins B12

The high incidence of tuberculosis among a vegetarian population was attributed to defective macrophage killing of M. tuberculosis secondary to vitamin B12 (cyanocobalamin) deficiency. Levels of methylmalonic acid (MMA) tend to accumulate in cases of B12 deficiency and MMA can be used by mycobacteria for constructing their cell walls. The authors hypothesized, therefore, that chronic vitamin B12 deficiency may predispose individuals to infection by mycobacteria (Chanarin and Stephenson 1998).

Vitamin D Deficiency

Vitamin D deficiency results in (McMurray et al. 1990):

* Reduced tuberculin skin reactions
* Impaired PPD-induced lymphocyte proliferation
* Inability to control M. tuberculosis infection?

Results of a hospital-based, case-controlled study in Asia suggest that persons with tuberculosis who are vitamin D (25-hydroxycholecalciferol) deficient are more susceptible to tuberculosis. Undetectable levels of vitamin D were associated with the highest risk (Wilkinson 2000). In a previous study, an active metabolite of vitamin D (1,25-dihydroxyvitamin D3) was reported to help mononuclear phagocytes restrict the intracellular growth of M. tuberculosis in vitro; the combination of 1,25-dihydroxyvitamin D3 with gamma interferon appears to potentiate this growth inhibition further. These findings may help explain case reports of the value of vitamin D as adjunctive treatment for tuberculosis (Rook et al. 1986).

Zinc Deficiency

The results of studies concerning the role of zinc supplementation on immune cell function are somewhat controversial. Zinc deficiency is thought to result in (McMurray et al. 1990):

* Impaired thymic function
* Loss of T-cell mediated responses
* Subsequent increased susceptibility to infection

Respiratory infection with virulent M. tuberculosis in zinc-deficient guinea pigs led to:

* Tuberculin anergy?
* Decreased numbers of circulating E rosette-forming T cells
* Decreased response of peritoneal exudate cells to PPD in vitro?

In addition, recent human studies demonstrated that immune system function in patients with acute respiratory disease (e.g., tuberculosis, bacterial pneumonia) is dependent on zinc levels. Zinc has been shown to regulate the production of interleukin-1 alpha by alveolar macrophages in patients with tuberculosis and bacterial pneumonia. Zinc in concert with interleukin-1 (IL-1) is thought to stimulate other mediators that help regulate the host immune system, such as IL-2, IL-6, and IL-8 (Abul et al. 1995). However, the dose and stage of infection during which zinc is administered may be critical for determining whether immunologic responses to antigen are evoked or inhibited (Abul et al. 1995).

Essential Fatty Acids: Omega-3

Animal studies suggest that tuberculosis is more severe in guinea pigs fed omega-3 polyunsaturated fatty acids (e.g., eicosapentaenoic acid, docosahexaenoic acid) than in guinea pigs fed saturated fatty acids or omega-6 fatty acids (Paul et al. 1997). Omega-3 fatty acids impair the intracellular killing of mycobacteria in general, and this may account for the reduced resistance to M. tuberculosis (Rastogi and David 1988).

Vitamin A

A double-blind clinical trial sought to determine the effect of vitamin A repletion therapy in a pediatric population with pulmonary tuberculosis and vitamin A deficiency (<20 mcg/dL). The researchers found that while vitamin A therapy had no effect on the outcome of the tuberculosis, after 6 weeks the respiratory status of the placebo group had improved in significantly more children than in the treatment group, leading to the conclusion that there may be adverse effects to vitamin A therapy (Hanekom et al. 1997).
Herbs

Garlic

The antibacterial properties of garlic (Allium sativum) are well documented. The antimicrobial component of garlic oil is allicin (diallyl thiolsulfinate). In vitro studies have demonstrated that garlic extract inhibits the growth of 17 species of mycobacteria. However, high concentrations of garlic extract (1.34 to 2.68 mg/mL) were required to exert this effect on the various strains of M. tuberculosis tested. Such high serum levels could prove toxic to humans and animals. Further study is necessary to determine safe but efficacious levels of garlic extract for treatment of tuberculosis (Delaha and Garagusi 1985).

A recent animal study indicates that garlic oil also has an inhibitory effect on M. tuberculosis. In a study on guinea pigs inoculated with M. tuberculosis, the viscera of the inoculated animals showed markedly reduced tubercular lesions compared to controls (Jain 1998). It may be that a combination of garlic extract with antituberculous agents will prove to be an effective synergistic treatment for mycobacterial infections (Delaha and Garagusi 1985).

Other Herbs?

Other herbs that may be helpful include (Wagner 1999):

* Echinacea (Echinacea spp.)
* Tamarisk?(Tinospora cordifolia)??

In vitro study of the following root extracts suggest that active fractions had a significant inhibitory effect against M. tuberculosis (Cantrell et al. 1999):

* Elecampane (Inula helenium); used by Native Americans for lung disorders including tuberculosis
* Sweet coneflower (Rudbeckia subtomentosa)

Analysis of the active fractions resulted in the identification of such known sesquiterpene lactones as alantolactone, isoalantolactone, alloalantolactone, 3-oxoalloalantolactone, and 11 alpha H,13-dihydroisoalantolactone.
Patient Monitoring

* Adherence to treatment is essential directly observed therapy (now the standard approach to drug administration in the United States for treating tuberculosis) insures compliance and reduces the possibility of drug-resistant strains.
* Sputum samples should be collected monthly; if still positive after 3 months, drug resistance and treatment failure is assumed.
* U.S. public health policy mandates patients with communicable tuberculosis be treated or quarantined; it is a reportable disease in all states.
* Isolation from any new contacts for at least 2 weeks is very important.
* Hospitalization is required for the elderly, acutely ill, and for those with drug-resistant tuberculosis for at least the first few days of treatment.
* Monitor patients carefully for adverse drug reactions.

Other Considerations
Prevention

* BCG vaccine from M. bovis efficacy 0% to 80%; used at birth in high risk countries
* Isoniazid used alone for preventive therapy (300 mg/day for 6 months for adults or 10 to 15 mg/kg/day for 9 months for children; 12 months with HIV, may extend survival time with HIV; supervised prophylactic dose is 900 mg two times per week)
* Rapid diagnosis and appropriate treatment
* Patient and health care worker education
* Surgical masks limit patients' transmission of M. tuberculosis; dust-mite respirators must be used by medical staff for high-risk procedures.
* Ultraviolet radiation tends to destroy M. tuberculosis.
* All patients with tuberculosis should be tested for HIV infection.

Complications/Sequelae

* Drug-resistant tuberculosis defined as resistance to two or more antituberculous agents; occurs from inadequate treatment that may be due to irregular drug availability, inappropriate regimens, or poor compliance; also results from transmission of drug-resistant M. tuberculosis; potentially lethal; isolate patient; 96% cure rates with prompt recognition
* Extrapulmonary disease increased at faster rate than pulmonary tuberculosis since 1984; frequently associated with HIV
* Tuberculosis meningitis in children basilar meningitis, infarction, vasculitis; affects 1% to 2% of untreated cases
* Pneumothorax
* Massive hemoptysis possibly caused by aspergilloma
* Lymph nodes that rupture into the pericardium

Prognosis

* Complete resolution with full course of therapy and lack of drug resistance
* Patients with miliary disease, drug-resistant strains, extrapulmonary disease, and HIV or the acquired immunodeficiency syndrome (AIDS) have less promising prognoses, as do the elderly.

Pregnancy

* Tuberculosis does not alter the course of pregnancy with the exception of extrapulmonary tuberculosis that extends beyond the lymph nodes; most infants acquire infection postpartum.
* Infant of contagious mother should be separated until mother is not contagious; test infant at 4 to 6 weeks and 3 to 4 months.
* Noninfectious, compliant mother is not separated from infant.
* Treatment for tuberculosis is not contraindicated in pregnancy or when breast feeding; the mother must be treated; treatment of choice is isoniazid and rifampin for 9 months with ethambutol for the first 2 months. Streptomycin is contraindicated due to risk of congenital deafness for the fetus. Pyrazinamide should be avoided but may be necessary to take.

References

Abul HT, Abul AT, Al-Althary EA, Behbehani AE, Khadadah ME, Dashti HM. Interleukin-1 alpha (IL-1 alpha) production by alveolar macrophages in patients with acute lung diseases: the influence of zinc supplementation. Mol Cell Biochem. 1995;146(2):139-145.

Agrons GA, Markowitz RI, Kramer SS. Pulmonary tuberculosis in children. Semin Roentgenol. 1993;28(2):158-172.

Barry CE. New horizons in the treatment of tuberculosis. Biochem Pharmacol. 1997;54(11):1165-1172.

Bastian I, Colebunders R. Treatment and prevention of multidrug-resistant tuberculosis. Drugs. 1999;58(4):633-661.

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Cantrell CL, Abate L, Fronczek FR, Franzblau SG, Quijano L, Fischer NH. Antimycobacterial eudesmanolides from Inula helenium and Rudbeckia subtomentosa. Planta Med. 1999;65(4):351-355.

Cecil RI, Plum F, Bennett JC, eds. Cecil Textbook of Medicine. 20th ed. Philadelphia, Pa: W.B. Saunders; 1996.

Chanarin I, Stephenson E. Vegetarian diet and cobalamin deficiency: their association with tuberculosis. J Clin Pathol. 1998;41(7):759-762.

Chaulk CP, Kazandjian VA. Directly observed therapy for treatment completion of pulmonary tuberculosis: Consensus statement of the Public Health Tuberculosis Guidelines Panel. JAMA. 1998;279(12):943-948.

Curtis AB, Ridzon R, Vogel R, et al. Extensive transmission of Mycobacterium tuberculosis from a child. N Engl J Med. 1999;341(20):1491-1495.

Dambro MR, ed. Griffith's 5 Minute Clinical Consult. Baltimore, Md: Lippincott Williams & Wilkins, Inc.; 1999.

Delaha EC, Garagusi VF. Inhibition of mycobacteria by garlic extract (Allium?sativum). Antimicrob Agents Chemother. 1985;27(4):485-486.

Douglas JG, McLeod MJ. Pharmacokinetic factors in the modern drug treatment of tuberculosis. Clin Pharmacokinet. 1999;37(2):127-146.

Elder NC. Extrapulmonary tuberculosis. A review. Arch Fam Med. 1992;1(1):91-98.

Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998.

Gillespie SH, Kennedy N. Fluoroquinolones: a new treatment for tuberculosis? Int J Tuberc Lung Dis. 1998;2(4):265-271.

Grassi C, Peona V. Use of rifabutin in the treatment of pulmonary tuberculosis. Clin Infect Dis. 1996;22(suppl 1):S50-S54.

Hanekom WA, Potgieter S, Hughes EJ, Malan H, Kessow G, Hussey GD. Vitamin A status and therapy in childhood pulmonary tuberculosis. J Pediatr. 1997;131(6):925-927.

Havlir DV, Barnes PF. Tuberculosis in patients with human immunodeficiency virus infection. N Engl J Med. 1999;340(5):367-373.

Hirsch CS, Johnson JL, Ellner JJ. Pulmonary tuberculosis. Curr Opin Pulm Med. 1999;5(3):143-150.

Jain RC. Anti tubercular activity of garlic oil [letter]. Indian J Pathol Microbiol. 1998;41(1):131.

Jana N, Vasishta K, Saha SC, Ghosh K. Obstetrical outcomes among women with extrapulmonary tuberculosis. N Engl J Med. 1999;341(9):645-649.

Mbala L, Matendo R, Nkailu R. Is vitamin B6 supplementation of isoniazid therapy useful in childhood tuberculosis? Trop Doct. 1998;28(2):103-104.

McMurray DN, Bartow RA, Mintzer CL, Hernandez-Frontera E. Micronutrient status and immune function in tuberculosis. Ann NY Acad Sci. 1990;587:59-69.

Nakamura T, Shiraishi N, Aono K. Effects of in vitro and in vivo supplementation with zinc on superoxide anion production in leukocytes. Physiol Chem Phys Med NMR 1987;19(3):147-151.

Newton SM, Lau C, Wright CW. A review of antimycobacterial natural products. Phytother?Res. 2000;14(5):303-322.

Pablos-Mendez A, Raviglione MC, Laszlo A, et al. Global surveillance for antituberculosis-drug resistance, 1994 1997. N Engl J Med. 1998;338(23):1641-1649.

Paul KP, Leichsenring M, Pfisterer M, et al. Influence of n-6 and n-3 polyunsaturated fatty acids on the resistance to experimental tuberculosis. Metabolism. 1997;46(6):619-624.

Petersen L, Mommsen S, Pallisgaard G. Male genitourinary tuberculosis. Report of 12 cases and review of the literature. Scand J Urol Nephrol. 1993;27(3):425-428.

Rakel RE, ed. Conn's Current Therapy. 51st ed. Philadelphia, Pa: W.B. Saunders; 1999.

Ramadan HH, Tarazi AE, Baroudy FM. Laryngeal tuberculosis: presentation of 16 cases and review of the literature. J Otolaryngol. 1993;22(1):39-41.

Rastogi N, David HL. Mechanisms of pathogenicity in mycobacteria. Biochimie. 1988;70(8):1101-1120.

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Transient Ischemic Attack - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:17:00 +0000

Overview
Definition

Transient ischemic attacks (TIAs), defined as neurologic deficits with complete clinical resolution within 24 hours, usually last only 10 to 15 minutes. The deficits generally occur when platelet aggregates form on atheromatous plaques, cause embolization, and temporarily occlude a distal cerebral or ophthalmic arteriole. Stroke from occlusive carotid disease is preceded by TIAs in 50% to 75% of patients. Up to 64% of patients with complete resolution of symptoms within 24 hours still have radiographic evidence of infarction by computed tomography (CT) scan; the distinction, therefore, between TIA, cerebral infarct with transient signs and symptoms, and stroke has become increasingly difficult with the use of both CT scans and magnetic resonance imaging (MRI).
Etiology

* Emboli of platelets and fibrin or atheromatous plaques or emboli from cardiac lesions secondary to mitral valve pathology; ventricular aneurysm, clot, or dyskinesia; atrial fibrillation or clot; interarterial shunts temporarily occlude a distal cerebral or ophthalmic artery
* Carotid stenosis with >70% occlusion in conjunction with transient hypotension
* Coagulation abnormalities (especially in young people); antiphospholipid antibodies; protein C or S deficiency; oral contraceptives; rare association with stroke which is more likely to occur when other co-founding risk factors exist such as HTN, smoking, and/or age > 35
* Chlamydia pneumoniae IgG antibody titers is associated with stroke and TIA

Risk Factors

Non-modifiable:

* > 65 risk doubles each decade over 65 years of age
* Men > women
* Family history
* Race-ethnicity: African-American and Japanese-American > Caucasian

Modifiable:

* Hypertension
* Diabetes
* History of stroke
* Cardiac disease, including atrial fibrillation
* Hyperlipidemia/hypercholesterolemia
* Smoking
* Heavy alcohol consumption
* Physical inactivity

Signs and Symptoms

Carotid symptoms, more focal:

* Transient monocular blindness
* Dysphasia, aphasia
* Amaurosis fugax
* Hemiparesis, clumsiness, weakness
* Carotid bruit

Vertebrobasilar symptoms, more general:

* Visual blurring binocular
* Vertigo
* Paresthesias
* Ataxia
* Dysarthria
* Diplopia
* Weakness
* Loss of consciousness
* Transient global amnesia

Brain stem involvement:

* Headache
* Vomiting
* Ataxia

Differential Diagnosis

* Thrombocytosis
* Mass lesions e.g. meningiomas
* Subdural hematomas
* Cerebral hemorrhage
* Focal seizures
* Migraine
* Protruding cervical disk
* Infection e.g. endocarditis, sepsis; rarely, cryptococcal meningitis or meningoencephalitis; syphilis
* Hypoglycemia
* Drug use e.g. cocaine, crack, amphetamines, LSD, PCP, heroin; sharing unclean needles may precipitate infections (see above)

Diagnosis
Physical Examination

Focal deficits should be noted, and accurate neurologic examination performed. Airway, breathing, circulation, vital signs as well as presence of heart murmurs, dysrhythmias, and hypertension require immediate assessment. Carotid arteries are gently auscultated for presence of a bruit. The head is examined for trauma and the arms for signs of needle tracks. Signs of systemic disease should be evaluated as well, including petechiae and ecchymosis.
Laboratory Tests

* Blood sugar evaluation
* Complete blood count (CBC) with platelet count (identifies thrombocytosis, thrombocytopenia); coagulation studies; toxicology screening
* Blood cultures should be considered in appropriate clinical setting
* VDRL should be considered

Pathology/Pathophysiology

* See etiology

Imaging

* CT scan, noncontrast, differentiates hemorrhagic from ischemic infarction (ischemic strokes not visualized for at least six hours 5% visualized by CT within 12 hours; 50% between 24 and 48 hours; 90% within seven days); identifies abscesses, tumors, hematomas
* MRI identifies ischemic infarcts faster than CT scans; able to show silent or prior infarction
* Magnetic resonance angiography (MRA) for large-vessel occlusion at base of skull; images blood flow
* Angiogram detects subtle abnormalities, stenosis (distinguishes 95% from complete occlusion), occlusion, subarachnoid hemorrhage, aneurysm; screen prior to endarterectomy and/or with borderline stenoses to determine endarterectomy vs. anticoagulation
* Doppler and B-mode ultrasound reveals carotid arterial lesion, lumen size; differentiates occlusion from tightly stenosed carotid artery

Other Diagnostic Procedures to consider

* National Institutes of Health (NIH) stroke scale
* Funduscopy looking for hypertensive changes, papilledema, diabetic retinopathy, bacterial endocarditis, retinal artery branch embolism
* More detailed and extensive neurologic examination of cranial nerve, brain stem, cortical, motor, sensory, sensorimotor, cerebellar
* ECG to identify MI and atrial fibrillation
* Transesophageal echocardiogram detects intracardiac and aortic embolisms
* Holter monitor may be indicated to r/o arrhythmia
* Antiphospholipid antibodies

Treatment Options
Treatment Strategy

Treatment strategy depends on clinical presentation and evaluation including physical exam, lab work, and radiologic tests. It is often desirable that patients be admitted to an acute care facility; Henneman and Lewis, writing in Annals of Emergency Medicine, conclude that admitting all patients with TIA is medically justified because ER evaluation cannot reliably identify which patients' conditions are likely to worsen. The 1994 American Heart Association (AHA) guidelines for treatment of TIAs conclude that hospitalization is often justified to expedite evaluation and lessen the possibility of stroke; this is particularly true when a patient is seen within one week of a TIA since the guidelines recommend that the work-up be completed within one week or less. The 1999 AHA update with new guidelines for treatment does not specifically address this recommendation, implying that the approach to hospital care remains the same.

Patient may require oxygen to aid breathing; in addition, oxygen supplementation may be necessary to lessen effects of ischemia. Intubation may be needed if patient loses consciousness or is unable to breathe on his or her own. Medical risk factors, such as volume overload, dehydration, hypoglycemia, and hypertension, need immediate control.
Drug Therapies

Antiplatelet agents:

* Aspirin 25 mg/day to 1300 mg/day decreases risk of TIA, stroke and MI; generally, reduces stroke risk by 15%; no linear dose-response level effect has been established for ASA, supporting low-dose ASA whenever possible; the lowest effective dose has not been established
* Ticlopidine 250 mg/bid; thought to be superior to aspirin for prevention of stroke following TIA; however, side effect profile limits use; generally reserved for aspirin failures or aspirin intolerance; may cause neutropenia (2.4% of those taking ticlopidine) requiring CBC every two weeks for initial three months; thrombotic thrombocytopenic purpura (TTP) reported
* Clopidogrel 75 mg QD; potentially better side-effect profile than ticlopidine
* Dipyridamole 200 mg QD to BID, extended release; in combination with ASA; 1994 AHA recommendations concluded no evident benefit over ASA alone or ticolopidine; 1999 AHA update reports European Stroke Prevention Study (ESPS-2) showing marked improvement over ASA or dipyridamole alone; AHA update states that dipyridamole and ASA combination has greater stroke risk reduction than clopidogrel
* Anticoagulant INR should generally be between 2.0 and 3.0; therapy of choice for atrial fibrillation with TIA; appropriate in case of TIA when at high risk for cardiac embolization e.g. mechanical prosthetic heart valve, recent MI, LV thrombus, dilated cardiomyopathy; INR > 3.0 is not safe in case of recent TIA d/t risk of hemorrhage; studies with low dose anticoagulation (INR 1.4 to 2.8) in combination with ASA for stroke prevention are currently under way; may be indicated while awaiting endarterectomy when stenosis is severe or in case of antiphospholipid antibody syndrome

Surgical Procedures

* Carotid endarterectomy is procedure of choice if >70% stenosis and one or more TIAs in last two years; determine surgical candidacy (cardiac risk); superior to medical management with > 70% stenosis and in the hands of a skilled surgeon; should be considered in the case of recent TIA even with stenosis between 50% and 69% because reduced stroke rate has been suggested by research compared to medical management, particularly for men and patients with hemispheric symptoms; women benefit much less from surgery
* Angioplasty and stent placement for carotid stenosis under investigation
* Extracranial-intracranial bypass high patency rate of the bypass; however, no benefit over medical therapy has been demonstrated to date

Complementary and Alternative Therapies

Dietary factors figure prominently in the prevention and treatment of vascular disease. Specific nutrients and herbs may provide protection against oxidative stress and ischemic injury. Acupuncture plays a role in altering cerebral hemodynamics and in reducing adverse effects of reperfusion.
Nutrition

In the Framingham Study (a pivotal, population-based, longitudinal study which has been ongoing since 1948), researchers investigated the association of diet and relative risk of transient ischemic attacks (TIAs) and completed stroke in 832 men aged 45 to 65 with no known history of vascular disease. Increased intake of fruits and vegetables was associated with a decreased overall risk of all causes of stroke and TIAs. Age-adjusted risk of stroke decreased as the quintiles of servings of fruits and vegetables per day increased (Gillman et al. 1995).

As part of the Physicians' Health Study, a prospective study of 14,916 male subjects aged 40 to 84, the relationship of homocysteine to ischemic stroke using a nested case-control design was examined. Subjects, who had no prior history of stroke or related incidents, provided baseline blood samples and were followed for 5 years. Although not statistically significant, homocysteine levels assayed in samples from 109 subjects who subsequently developed ischemic stroke were slightly higher than the 427 controls (11.1 +/- 4.0 nmol/mL compared to 10.6 +/- 3.4 nmol/mL respectively). In subgroup analyses, homocysteine levels seemed to be a better predictor of stroke risk in normotensive individuals and men <= 60 years old than the group at large (Verhoef et al. 1994). Folic acid, vitamin B6, vitamin B12, and betaine are essential to homocysteine metabolism; therefore, supplementation with these nutrients is thought to be beneficial for controlling homocysteine levels (Miller and Kelly 1997). Please see individual monographs on folic acid and vitamins B6 and B12 for detailed information about these supplements.

A review of the role of magnesium in vascular disease shows a strong association between the dietary intake of magnesium, the concentration of magnesium in the myocardium and vasculature, and the risk for development of TIAs and other vascular pathologies (Altura and Altura 1985).

Acetyl-L-carnitine has been found to improve cerebral blood flow in patients with cerebrovascular disease. Ten patients, who had suffered an ischemic stroke at least six months before the study, were administered acetyl-L-carnitine (1.5 g IV) and evaluated with Single Photon Emission Computerized Tomography (SPECT scan) before and after injection. Cerebral blood flow improved in the areas surrounding the ischemic site but not in the stroke corresponding zone itself (Postiglione et al. 1990). In an animal model, pre-ischemic treatment with acetyl-L-carnitine (100 mg/kg) provided neuronal protection (Shuaib et al. 1995). This supplement may hold potential benefit as primary prevention for high-risk patients and/or secondary prevention for those who have already suffered from a TIA or ischemic stroke.

Free radical damage and lipid peroxidation play a crucial role in the pathogenesis of cerebral ischemia (van der Worp et al. 1999). Vitamin E inhibits platelet adhesion and platelet-induced lipid peroxidation (Steiner et al. 1995). A randomized, double-blind, controlled study of 100 patients with a history of cerebrovascular events was performed over a period of two years. Patients received either aspirin (325 mg/day) monotherapy or aspirin combined with vitamin E (alphatocopheral) (400 mg/day). The combination of alpha-tocopherol (antiadhesive) and aspirin (antiaggregating) therapy reduced platelet adhesion by 40% and significantly reduced the incidence of ischemic events in patients with history of ischemic cerebrovascular disease (Steiner et al. 1995). Several animal studies have also supported findings of the protective effect of vitamin E alpha-tocopherol on the effects of ischemia (Altura and Gebrewold 1996; Hara et al. 1990; van der Worp et al. 1999). Vitamin E inhibited neuronal damage secondary to pro-oxidant events such as alcohol-induced cerebrovascular and brain damage, common carotid artery occlusion, and iron-induced lipid peroxidation.

Other areas of animal research which may prove beneficial to the treatment of TIAs in humans include post-ischemia treatment with nicotinamide (vitamin B3). In rat studies using models of permanent middle cerebral artery occlusion, post-ischemia treatment with vitamin B3 was neuroprotective and reduced the infarct volume; the theory is that ischemia depletes ATP and that nicotinamide, a precursor of NAD+, helps regenerate ATP or energy reserve, which, in turn, is neuroprotective (Sakakibara et al. 2000).
Herbs

Ginkgo (Ginkgo biloba) increases cerebral circulation, improves hypoxic tolerance in cerebral tissues, inhibits cerebral edema, improves cognitive function, provides neuronal protection, and inhibits platelet-activating factor (Blumenthal et al. 1998). It is often used in a standardized form, EGb 761.

In patients with cerebrovascular ischemia secondary to developmental anomalies and deformities of major brain arteries, blood serum antioxidant activity increased and cognitive measures improved after administration of the preparation Tanakan, also known as EGb 761 (Dziak and Golik 1998). In animal models, pre-treatment with ginkgo (EGb 761) prior to intentional ischemic injury preserves membrane integrity, presumably by preventing Na,K-ATPase injury and by reducing lipoperoxidation induced by ischemia (Pierre et al. 1999).
Homeopathy

Although there is no known literature specifically evaluating the application of homeopathy for?prevention or treatment of TIAs, a trained specialist would determine value and appropriateness of this approach on a case by case basis. Homeopathic treatment can address both constitutional and acute aspects of disease in general. In homeopathic terminology, the constitutional state reflects a pattern of underlying vulnerability or weakness that is unique to the individual and persists throughout that person's life. Symptoms tend to alternate over time, and treatment consists of selecting the appropriate remedy specific for the patient's constitutional type. By contrast, in acute conditions a remedy can be administered without reference to any particular constitutional state (Ullman 1995).
Acupuncture

In an animal study of focal cerebral ischemia, scalp acupuncture improved neurologic symptoms, promoted proliferation and repair of neogenetic capillaries and gliocytes in necrotic regions, and reduced blood viscosity, infarct size, edema, and inflammatory changes at the necrotic site (Lei et al. 1997). In patients with cerebrovascular disease, electro-acupuncture (EA) stimulation induced greater change in cerebral blood flow compared to needle retention, assessed via SPECT scan (Wang and Jia 1996). Animal studies have confirmed the benefit of electro-acupuncture, indicating that it could reduce EEG inhibition during global ischemia and improve recovery after reperfusion (Ying and Cheng 1994).

Pointed massage, or massage on acupuncture points (such as that performed in the practice of acupressure), improved cerebral blood flow in 120 patients with encephalopathy due to poor circulation and a history of TIAs in the vertebrobasilar bed (Gusarova et al. 1997).

Oren-gedo ku-to (TJ15), a Chinese herbal preparation, reduced neuronal damage in mice with oxidative stress induced by transient forebrain ischemia (Kondo et al. 2000)?. An acupuncturist trained in Chinese approach and technique would determine if this herb or others are appropriate for a particular person with history of TIA or stroke.
Patient Monitoring

Following TIAs, 50% of strokes occur within a year, 20% within five months. Patient monitoring is essential for stroke and MI prevention.
Other Considerations
Prevention

* Lifestyle factors no smoking, regular exercise, dietary factors (e.g., reducing homocysteine levels with folate, vitamins B6 and B12; AHA Step II diet), maintain ideal body weight
* Eliminate excessive alcohol intake (definied as ³ seven drinks per day) moderate alcohol consumption (no more than two drinks per day) may confer benefit for prevention of ischemic stroke only
* Control hypertension regular screenings; weight control; antihypertensive drugs; SBP should be maintained below 140 mm Hg and DBP below 90 mm Hg, for diabetics these numbers should be 130 and 85 mm Hg respectively
* Modify other risks of CAD as well e.g. lipid-lowering agents decrease risk of stroke, TIAs following MI; FDA has approved pravastatin, simvastatin
* Control diabetes control blood sugar levels; controlling co-morbidity is particularly important for diabetics to reduce the risk of stroke and TIA
* Treat carotid artery disease consider endarterectomy; see section entitled "Surgical Procedures" for indications; can be considered for > 50% stenosis, particularly for men
* Treat CAD, cardiac arrhythmias, CHF and valvular disease appropriately
* Maintenance of Hormone Replacement Therapy (HRT) if already on it i.e. discontinuation not recommended

Complications/Sequelae

* TIAs warning signs of stroke
* Myocardial Infarction more patients with TIA die from MI than stroke
* Incapacitated stroke victim may be found one to two days following event results in complications, including pneumonia, hypothermia, dehydration, rhabdomyolysis
* Brain stem lesions airway compromised
* Hemorrhaging transformation several days following stroke presentation; may be clinically silent
* Cerebral edema occurs one to two days after TIA
* Multiple strokes increase risk of seizure, pulmonary embolism, thrombosis, dementia

Prognosis

* Interval between TIAs seems to be most important predictor of stroke; frequency of TIAs as well as location or duration of symptoms are not predictive of stroke risk
* Severity of carotid stenosis predictor of stroke (e.g., lumen < 1 mm)
* Carotid disease is more likely cause of stroke than vertebrobasilar disease

Pregnancy

Hypercoagulability during pregnancy increases risks.
References

Abou-Zamzam AM, et al. Extrathoracic atrial grafts performed for carotid artery occlusive disease not amenable to endarterectomy. Arch Surg. 1999;134:952-957.

Albers GW, Hart RG, Helmi LL, Newell DW, Sacco, RL. AHA Scientific Statement Supplement to the guidelines for the management of transient ischemic attacks: A statement from the ad hoc committee on guidelines for the management of transient ischemic attacks, stroke council, American Heart Association. Stroke. 1999;30:2502-2511.

Altura BM, Altura BT. New perspectives on the role of magnesium in the pathophysiology of the cardiovascular system. Magnesium. 1985;4(5-6):226-244.

Altura BM, Gebrewold A. Alpha-tocopherol attenuates alcohol-induced cerebral vascular damage in rats: possible role of oxidants in alcohol brain pathology and stroke. Neurosci Lett. 1996;220(3):207-210.

Blumenthal M, Busse WR, Goldberg A, et al., eds.?The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass:Integrative Medicine Communications; 1998: 136-138, 159-160, 172, 197.

Caplan LR, et al. Should thrombolytic therapy be the first-line teatment for acute ischemic stroke? N Engl J Med. 1997;337:1309-1310.

Cecil RI, Plum F, Bennett JC, eds. Cecil Textbook of Medicine, 20th ed. Philadelphia, Pa: W.B. Saunders, 1996.

Dambro MR, ed. Griffith's 5 Minute Clinical Consult. Baltimore, Md: Lippincott Williams & Wilkins; 1999.

Dziak LA, Golik VA. [The efficacy of treating cerebral ischemia due to changes in the major cerebral arteries by using the preparation Tanakan (EGB 761).] Lik Sprava. 1998; August(6):125-127.

Gillman MW, Cupples LA, Gagnon D, et al. Protective effect of fruits and vegetables on development of stroke in men. JAMA. 1995;273(14):1113-1117.

Goroll AH, ed. Primary Care Medicine. 3rd ed. Philadelphia, Pa: Lippincott-Raven Publishers, 1995.

Gusarova SA, Kuznetsov OF, Gorbunov FE, Maslovskaia SG. [The use of point massage in patients with circulatory encephalopathy.] Vopr Kurortol Fizioter Lech Fiz Kult. 1997;(6):11-13.

Hara H, Kato H, Kogure K. Protective effect of alpha-tocopherol on ischemic neuronal damage in the gerbil hippocampus. Brain Res. 1990;510(2):335-338.

Henneman PL, Lewis RJ. Is admission medically justified for all patients with acute stroke or transient ischemic attacks? Ann Emerg Med. 1995;25(4):458-63.

Johnson ES, et al. A metaregression analysis of the dose-response effect of aspirin on stroke. Arch Intern Med. 1999;158:1248-1253.

Kondo Y, Kondo F, Asanuma M, Tanaka K, Ogawa N. Protective effect of oren-gedoku-to against induction of neuronal death by transient cerebral ischemia in the C57BL/6 mouse. Neurochem Res. 2000;25(2):205-209.

Kwiatkowski TG, et al. Effects of tissue plasminogen activator for acute ischemic stroke at one year. N Engl J Med. 1999;340:1781-1787.

Lei XQ, Wang J, Wang YS. [Effects of scalp acupuncture on focal cerebral ischemia in rats.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. 1997;17(9):544-546.

Miller AL, Kelly GS. Homocysteine metabolism: nutritional modulation and impact on health and disease. Altern Med Rev. 1997;2(4):234-254.

National Stroke Association. 1998 consensus statement: prevention of a first stroke. JAMA. 1999;281:1112-1120.

Pierre S, Jamme I, Droy-Lefaix MT, Nouvelot A, Maixent JM. Ginkgo biloba extract (EGb 761) protects Na,K-ATPase activity during cerebral ischemia in mice. Neuroreport. 1999;10(1):47-51.

Postiglione A, Cicerano U, Soricelli A, et al. Cerebral blood flow in patients with chronic cerebrovascular disease: effect of acetyl-L-carnitine. Int J Clin Pharm Res. 1990;10(1-2):129-132.

Rosen P, Barkin R, eds. Emergency Medicine: Concepts and Clinical Management. 4th ed. St. Louis, MO: Mosby-Year Book;1998.

Rowland LP. Merritt's Textbook of Neurology. 9th ed. Baltimore, Md: Lippincott Williams & Wilkins; 1995.

Sacco RL, et al. The protective effect of moderate alcohol consumption on ischemic stroke. JAMA. 1999;281:53-60.

Sakakibara Y, Mitha AP, Ogilvy CS, Maynard KI. Post-treatment with nicotinamide (vitamin B3) reduces the infarct volume following permanent focal cerebral ischemia in female Sprague-Dawley and Wistar rats. Neurosci Lett. 2000:111-114.

Shuaib A, Waqaar T, Wishart T, Kanthan R, Howlett W. Acetyl-L-carnitine attenuates neuronal damage in gerbils with transient forebrain ischemia only when given before the insult. Neurochem Res. 1995;20(9):1021-1025.

Steiner M, Glantz M, Lekos A. Vitamin E plus aspirin compared with aspirin alone in patients with transient ischemic attacks. Am J Clin Nutr. 1995;62(suppl):1381S-1384S.

The Multicenter Acute Stroke Trial Europe Study Group. Thrombolytic therapy with streptokinase in acute ischemic stroke. N Eng J Med. 1998;335(3):145-150.

Tybjaerg-Hansen A, Steffensen R, Meinertz H, Schnohr P, Nordestgaard BG. Association of mutations in the apolipoprotein B gene with hypercholesterolemia and the risk of ischemic heart disease. N Engl J Med. 1998;338(22):1577-1584.

Ullman D. The Consumer's Guide to Homeopathy. New York, NY: Tarcher/Putnam; 1995.

van der Worp HB, Thomas CE, Kappelle LJ, Hoffman WP, de Wildt DJ, Bar PR. Inhibition of iron-dependent and ischemia-induced brain damage by the alpha-tocopherol analogue MDL 74,722. Exp Neurol. 1999;155(1):103-108.

Verhoef P, Hennekens CH, Malinow MR, Kok FJ, Willett WC, Stampfer MJ. A prospective study of plasma homocysteine and risk of ischemic stroke. Stroke. 1994;25(10):1924-1930.

Wang F, Jia SW. [Effect of acupuncture on regional cerebral blood flow and cerebral functional activity evaluated with single-photon emission computed tomography.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. 1996;16(6):340-343.

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Thyroiditis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:15:00 +0000

Overview
Definition

Thyroiditis is an inflammatory condition of the thyroid gland. Patient may present with clinical features of hyperthyroidism or hypothyroidism. There are several types, both common (Hashimoto's, subacute, silent) and rare (suppurative, Riedel's). These vary by cause, course, and histopathology:

* Hashimoto's (struma lymphomatosa, lymphadenoid goiter, chronic lymphocytic thyroiditis): an autoimmune disorder closely related to Graves' disease, with a familial tendency; it is the most common cause of hypothyroidism in patients not previously treated for overactive thyroid.
* Subacute (de Quervain's thyroiditis, granulomatous thyroiditis, giant cell thyroiditis): self-limited inflammation; a prodromal upper respiratory infection is common.
* Silent (acute lymphocytic thyroiditis): related to Hashimoto's; self-limited, usually occurring in young to middle-aged women; hyper- or hypothyroidism may spontaneously resolve.
* Suppurative: rare disorder usually occurring in the course of a systemic infection.
* Riedel's (chronic fibrous thyroiditis, Riedel's struma, wood thyroiditis, ligneous thyroiditis, invasive thyroiditis): rarest form; found most frequently among middle-aged women; may cause both hypothyroidism and hypoparathyroidism.

Etiology

Hashimoto's thyroiditis is an immune disorder, with lymphocytes gradually replacing thyroid tissue; gland enlarges, and hypothyroidism slowly develops. Subacute is most likely a viral infection, with leaked thyroid hormone causing transient thyrotoxicosis, followed by hypothyroidism. The trigger for silent thyroiditis is unknown, but may involve an autoimmune mechanism. The suppurative form is caused by pyogenic organisms. Riedel's thyroiditis is caused by multifocal systemic fibrosis syndrome.
Risk Factors

* Prodromal upper respiratory tract infection (subacute)
* Pregnancy
* Graves' disease (Hashimoto's)
* Positive family history or preceding autoimmune diseases or conditions

Signs and Symptoms

Hashimoto's:

* Firm, symmetrically enlarged, lobulated gland not tender on palpation; few pressure symptoms
* Progressive worsening of hypothyroid symptoms cool, dry skin, slow pulse rate (60 bpm), swelling around eyes, hoarseness, slow reflexes

Subacute:

* Acute, painful enlargement of thyroid; pain possibly radiating to ears or jaw
* Dysphagia
* Malaise and low-grade fever

Silent:

* Mild hyperthyroid symptoms rapid heartbeat, slight nervousness, hyperactivity, weight loss (5 to 10 lbs.), increased perspiration
* Thyroid moderately enlarged and firm but not tender or painful

Suppurative:

* Severe pain, tenderness, redness, fluctuation in thyroid area

Riedel's:

* Thyroid asymmetrically enlarged, stony, adheres to neck structures
* Signs of compression and invasion dysphagia, dyspnea, hoarseness

Differential Diagnosis

* Graves' disease
* Goiter
* Carcinoma
* Thyrotoxicosis
* Sore throat
* Dental problems
* Ear infection

Diagnosis
Physical Examination

With Hashimoto's, the gland is firm, symmetrically enlarged, not tender on palpation, with few pressure symptoms. With subacute, the gland is acutely painful, with pain radiating to the ears and jaw. If no pain is present, silent form is likely. Suppurative produces severe pain and redness. With Riedel's, the enlarged gland is asymmetric and hard.
Laboratory Tests

* TSH and serum T4 and T3 levels: Hashimoto's T4, 5 mcg/100 ml, TSH >5.0 mcU/ml; subacute suppressed TSH (<0.1 mcU/ml), elevated serum or free T4; silent increased T4 and decreased TSH
* Radioiodine uptake: very low to zero in hyperthyroid phase of subacute; high in chronic forms; low in Riedel's
* Thyroid antibody test: high titers in Hashimoto's; possible in other types
* Erythrocyte sedimentation rate: elevated in subacute; markedly elevated in silent
* Biopsy: only if antibodies not detected and no apparent cause for symptoms; see giant cells in silent thyroiditis

Pathology/Pathophysiology

Lymphocyte infiltration, fibrosis, atrophy (lymphocyte), mononuclear cell infiltrate, giant cells (granulomatous)
Imaging

Thyroid radioiodine scan (granulomatous)
Treatment Options
Treatment Strategy

The course of each type of thyroiditis generally involves three phases: hyperthyroid phase, hypothyroid phase, and return to euthyroid status. Treatment is symptomatic and individualized to type and phase.
Drug Therapies

Hashimoto's:

* Levothyroxine: 0.1 to 0.15 mg daily if hypothyroidism or large goiter present

Subacute:

* Aspirin: two tablets (325 mg) three to four times daily as needed to relieve pain and inflammation
* Steroids (such as prednisone or dexamethasone): at lowest dose that relieves pain; gives relief in 24 hours, but continue four to six weeks after pain is gone; severe cases only
* Propranolol: 10 to 40 mg every six hours for thyrotoxic symptoms
* Thyroxine: 0.05 to 0.1 mg/daily for hypothyroidism symptoms

Silent:

* Short-term beta-blockers: as needed for hyperthyroid symptoms
* Levothyroxine: as needed for hypothyroid symptoms

Suppurative:

* Antibiotics and surgical drainage: as needed for marked fluctuation

Riedel's:

* Partial thyroidectomy: to relieve pressure

Complementary and Alternative Therapies

Concurrent therapy with medications may be necessary.
Nutrition

* Foods that depress the thyroid are broccoli, cabbage, brussels sprouts, cauliflower, kale, spinach, turnips, soy, beans, and mustard greens. These foods should be included in the diet for hyperthyroid conditions and avoided for hypothryroid conditions.
* Avoid refined foods, sugar, dairy products, wheat, caffeine, and alcohol.
* Essential fatty acids are anti-inflammatory and necessary for hormone production. Take 1,000 to 1,500 mg flaxseed oil tid.
* Calcium (1,000 mg/day) and magnesium (200 to 600 mg/day) are cofactors for many metabolic processes.

For hyperthyroid conditions:

* Bromelain (250 to 500 mg tid between meals) is a proteolytic enzyme that reduces inflammation.
* Vitamin C (1,000 mg tid to qid) supports immune function and decreases inflammation.

For hypothyroid conditions:

* Vitamin C (1,000 mg tid to qid), vitamin A (10,000 to 25,000 IU/day), B-complex (50 to 100 mg/day), selenium (200 mcg/day), iodine (300 mcg/day), vitamin E (400 IU/day), and zinc (30 mg/day) are necessary for thyroid hormone production.
* L-tyrosine (100 mg bid) also supports normal thyroid function. May exacerbate hypertension.

Herbs

Ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink two to four cups/day. Tinctures may be used singly or in combination as noted.

For hyperthyroid conditions:

* Bugleweed (Lycopus virginica) and lemon balm (Melissa officinalis) help to normalize the overactive thyroid.
* Motherwort (Leonurus cardiaca) relieves heart palpitations and passionflower (Passiflora incarnata) reduces anxiety. Combine two parts of bugleweed with one part each of lemon balm, motherwort, and passionflower in a tincture, 30 to 60 drops tid to qid.
* Quercetin (250 to 500 mg tid) is an anti-inflammatory.
* Turmeric (Curcuma longa) potentiates bromelain and should be taken between meals, 500 mg tid.
* Ginkgo biloba 80 to 120 mg bid.

For hypothyroid conditions:

* A combination that would support thyroid function includes herbs rich in minerals. Combine the following for a tea (3 to 4 cups/day) or tincture (20 to 30 drops tid). Horsetail (Equisetum arvense), oatstraw (Avena sativa), alfalfa (Medicago sativa), gotu kola (Centella asiatica), and bladderwrack (Fucus vesiculosus)

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency.
Physical Medicine

For hyperthyroid conditions: ice packs to the throat for inflammation.

For hypothyroid conditions: contrast hydrotherapy to the neck and throat may stimulate thyroid function. Alternating hot and cold applications brings nutrients to the site and diffuses metabolic waste from inflammation. The overall effect is decreased inflammation, pain relief, and enhanced healing. Alternate three minutes hot with one minute cold and repeat three times. This is one set. Do two to three sets/day. In addition, exercise sensitizes thyroid gland to hormones and improves its function.
Acupuncture

Acupuncture may be helpful in correcting hormonal imbalances and addressing underlying deficiencies and excesses involved in thyroiditis.
Patient Monitoring

* Hashimoto's is associated with other autoimmune diseases (Addison's disease, pernicious anemia, etc.), so monitor the patient for these.
* Because Hashimoto's can progress to hypothyroidism, schedule yearly checkups and begin treatment promptly.
* Repeat thyroid function tests 3 to 12 months in lymphocytic thyroiditis, and every three to six weeks in granulomatous thyroiditis, until euthyroid.

Other Considerations
Complications/Sequelae

* High doses of glucocorticoids can cause stomach ulcers, bone loss.
* Hypothyroidism may develop after silent or Hashimoto's thyroiditis.

Prognosis

Some degree of compromise or disability is expected for 6 to 12 months: hyperthyroid phase, 1 to 3 months; hypothyroid phase, 3 to 6 months, then gradual return to euthyroid.
Pregnancy

Thyroid testing during pregnancy may have variable and unreliable results. Mild pathology may not be detected until after pregnancy.
References

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:432.

The Burton Goldberg Group, compilers. Alternative Medicine: The Definitive Guide. Tiburon, Calif: Future Medicine Publishing Inc; 1997.

Ferri FF. Ferri's Clinical Advisor: Instant Diagnosis and Treatment. St Louis, Mo: Mosby-Year Book;1999.

Hoffman D. The New Holistic Herbal. New York, NY: Barnes & Noble Books; 1995:95.

Murray MT, Pizzorno JE. Encyclopedia of Natural Medicine. 2nd ed. Rocklin, Calif: Prima Publishing; 1998:386-390.

Noble J, ed. Textbook of Primary Care Medicine. 2nd ed. St Louis, Mo: Mosby-Year Book; 1996.

Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment. Norwalk, Conn: Appleton & Lange; 1994.

Tendinitis - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:15:00 +0000

Overview
Definition

Tendinitis is the painful inflammation of a tendon and its attachments to bone. It is most often the result of the stress from a particular occupation (e.g., drywall hangers, musicians, painters) or sport (e.g., baseball, basketball, tennis, swimming). Acute tendinitis may heal within a few days or weeks, but it may also become chronic if it is not treated acutely. Pain may initially be only a dull ache with movement of the affected limb; however, with time, if untreated, it may become severe, allowing only limited movement and causing disability. The areas most commonly affected by tendinitis are the shoulder (e.g., bicipital tendinitis, supraspinatus tendinitis, rotator cuff tendinitis, or impingement syndrome), elbow (e.g., lateral epicondylitis [tennis elbow] or medial epicondylitis [golfer's elbow]), wrist and thumb (e.g., stenosing tenosynovitis [de Quervain's disease]), knee (e.g., patellar tendinitis [jumper's knee]), and ankle (e.g., Achilles and peroneal tendinitis).

Calcific tendinitis, which occurs when calcium deposits in a joint, is not usually preceded by an identified trauma. There is much disagreement over the cause of this type of tendinitis. Although some investigators hypothesize that it results from chronic tendinitis, it appears to be associated with chronic diseases, such as diabetes mellitus. Calcific tendinitis presents as an acute inflammatory reaction, often resembling gout, that is often bilateral (e.g., in both shoulders), progressing to a pattern of exacerbations and remissions.
Etiology

* Sports, with over- or undertraining or poor technique
* Trauma
* Infections (e.g., gonococcal disease)
* Inflammatory conditions (e.g., Reiter's syndrome, ankylosing spondylitis)
* Ill-fitting shoes (Achilles tendinitis)
* Falling
* Carrying or lifting heavy objects

Risk Factors

* Participation in sports activities
* Occupations involving repetitive activities
* Poor ergonomic positioning with office activities
* Alcoholism, because of an inadequate neurologic function
* Diabetes, because of an inadequate vascular supply

Signs and Symptoms

* Edema (usually minimal)
* Localized tenderness
* Pain, which may or may not be present at rest but is always triggered or exacerbated by movement of the affected limb
* Warmth and redness
* Crepitus (crackling)

Differential Diagnosis

It is often difficult to distinguish between tendinitis and bursitis. Bursitis is the inflammation of the small fluid-filled sacs (bursa) located between tendons and bones, which cushion tissues from friction. Bursitis is usually characterized by a dull, persistent ache, while tendinitis typically causes sharp pain on movement. The two conditions often coexist.

* Bursitis inflammation of the bursa (fluid-filled sacs)
* Polyarthritis arthritis in many joints
* Vasculitis inflammation of the blood vessels
* Periosteitis inflammation of the periosteum (connective tissue that covers bone)
* Fibrositis inflammation of muscle sheaths and fascial layers
* Polymyalgia rheumatica severe pain and stiffness in proximal muscle groups
* Diseases of the muscles, bones, or spine (e.g., Reiter's syndrome, gout, rheumatoid arthritis)
* Malingering
* Fibromyalgia
* Carpal tunnel syndrome

Diagnosis
Physical Examination

Pain at the point of inflammation is usually worsened by movement, but there may also be pain at rest. The patient may exhibit crepitus when moving the affected joint and complain of numbness and tingling. Range of motion may be normal or limited because of the pain. Severe swelling is uncommon and may indicate arthritis.
Pathology/Pathophysiology

* Shoulder: impingement of supraspinatus tendon between acromion and greater tuberosity of the humerus, fibrosis and thickening, tear of the rotator cuff, degenerative bony changes (e.g., bony spurs, sclerosis, cyst formation)
* Knee: calcifications, fibrosis of the tendon, degenerative changes, necrotic areas
* Elbow: small tears (microtears) of the tendon of the extensor carpi radialis brevis, inflammation of tendinous sheath over extensor carpi radialis and extensor communis, granulation tissue, degenerative changes
* Wrist and thumb: inflammation of abductor pollicis longus and extensor pollicis brevis tendons, proliferation of fibrous tissue
* Foot: thickening of the Achilles tendon, adhesions between the tendon and tendon sheath

Imaging

* Computed tomography, to evaluate intra-articular abnormalities
* Magnetic resonance imaging, to diagnose tendinitis, tears, or tumors

Other Diagnostic Procedures

* Individual tests, chosen for their specificity, sensitivity, and cost-benefit profile
* X rays, which are often normal in the early stages
* Arthroscopy, to diagnose arthritis, calcific tendinitis, osteonecrosis, and cancer and to treat any abnormalities found
* Arthrography, to establish the correct diagnosis
* Ultrasonography, to diagnose intra-articular abnormalities
* Electromyography, to rule out neurologic problems
* Nerve conduction velocity studies

Treatment Options
Treatment Strategy

In all cases of tendinitis, treatment depends on the severity of the symptoms. Conservative treatment is attempted initially, progressing to surgery if needed. Health care providers will prescribe ice, analgesia, rest, temporary immobilization, massage, steroid injections, light exercise, physical therapy, and finally surgery for refractory cases.
Drug Therapies

* Nonsteroidal anti-inflammatory drugs (NSAIDs): indocin (25 to 50 mg tid) and ibuprofen (200 to 600 mg bid to tid)
* Injection of lidocaine and corticosteroids (1 to 3 ml 1% lidocaine, 1 to 3 ml 0.5% bupivacaine, and 10 to 30 mg triamcinolone). Only three or four injections spaced three weeks apart should be given. Steroid injections directly into weight-bearing tendons are contraindicated because there is a risk of tendon rupture. Injections should be into the tendon sheath or bursa.
* Colchicine (for calcific tendinitis only)

Complementary and Alternative Therapies

A combination of essential fatty acids (EFAs), castor oil packs, and homeopathic treatment is often sufficient for simple tendinitis. Other therapies may be added as needed.

* Ice, especially after the initial injury, to decrease circulation to inflamed tissues and decrease pain caused by congestion
* Rest
* Massage or chiropractic for improved circulation
* Temporary immobilization (e.g., slings, splints, crutches) of the affected limb. The shoulder should not be immobilized for a long period of time because further loss of range of motion (frozen shoulder) may occur from adhesions, capsular tightening, and muscle shortening.
* Flexibility and strengthening exercises after acute phase has passed
* Physical therapy (e.g., range of motion exercises)
* Ultrasonography (phonophoresis with 10% lidocaine cream or arnica gel) high-frequency sound to heat an area and increase the blood supply
* Transcutaneous electrical nerve stimulation (TENS) electricity used to control pain
* Proper occupational ergonomics (i.e., stop repetitive or offending activity)

Nutrition

* Vitamin C (500 to 1,000 mg tid) to aid in healing, increase immune function, and reduce inflammation
* Calcium (1,500 mg/day) and magnesium (750 mg/day) to aid healing of connective tissues and muscles
* Vitamin A (15,000 IU/day) to increase immune function and tissue healing
* Vitamin E (400 to 800 mg/day) to reduce inflammation
* Bromelain (250 to 750 mg tid between meals) to reduce inflammation and prevent swelling after trauma or surgery
* Essential fatty acids (EFAs) (1,000 to 1,500 IU one to three times/day) as an anti-inflammatory

Herbs

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

* Flavonoids (500 to 1,000 mg tid) to reduce inflammation and maintain healthy collagen
* Curcumin, yellow pigment of turmeric (Curcuma longa) (200 to 400 mg tid) between meals to reduce inflammation; serves as an antioxidant
* Willow (Salix alba) bark tea (2 to 3 tsp. per 1 cup of boiling water tid) for analgesic effect (Caution: If allergic to aspirin, do not take aspirin-like herbs.)
* Licorice (Glycyrrhiza glabra) 3 cups tea/day to reduce inflammation (Caution: Long-term use is associated with headaches, water retention, potassium loss, high blood pressure, and lethargy.)
* Comfrey (Symphytum officinale) 1 tsp. per 1 cup boiling water qid to aid healing and for pain relief. Use as the water in contrast hydrotherapy.

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing, use 3 to 5 pellets of a 12X to 30C remedy every 1 to 4 hours until acute symptoms resolve.

Externally:

Homeopathic treatments for tendinitis include creams or gels. Arnica cream by itself or in combination with Calendula officinalis, Hamamelis virginiana, Aconitum napellus, and Belladonna, applied three to six times/day, speeds healing and decreases discomfort. For acute injuries, start with Arnica.

Internally:

* Bryonia for pains that are worse with the slightest motion or when jarred. The pain feels worse with cold and better with heat.
* Phytolacca for tendinitis where the pain is focused at the insertion of the tendons and that feels worse with heat
* Rhus toxicodendron for tendinitis with restlessness that is worse in the morning
* Rhododendron for tendinitis that gets worse with barometric pressure changes

Physical Medicine

* Orthotics or heel lifts and shoe correction (Achilles tendinitis)
* Elbow strap and small (2 lb.) weights (tennis elbow)
* Contrast hydrotherapy. Alternating hot and cold applications brings nutrients to the site and diffuses metabolic waste from inflammation. The overall effect is decreased inflammation, pain relief, and enhanced healing. After first 24 to 48 hours, soak affected part for three minutes in hot water, then 30 seconds in cold water.

Massage

May be helpful for pain relief and improving range of motion.
Patient Monitoring

Tendinitis often presents in three stages: Stage 1, a dull ache precipitated by strenuous activity and resolving with rest; stage 2, pain precipitated by minor movements (e.g., dressing); and stage 3, constant pain. Patients should be seen every three to four weeks until the tendinitis resolves.
Other Considerations
Prevention

Proper stretching and warm-up exercises can be preventive measures for athletes at risk for tendinitis. Braces are used for forearms, knees, and ankles to give added stability and support to reduce recurrences. For occupational injuries, job ergonomics must be reviewed and modified to prevent recurrences.
Complications/Sequelae

* Tendon rupture
* After surgery, some patients do not attain their preinjury functional level.
* Degenerative changes are often seen in patients over 40 with chronic tendinitis.
* After steroid injection, there may be atrophy of the soft tissues surrounding a joint or iatrogenic infections. In addition, steroids may weaken the collagen structure of tendons, potentiating the risk for tendon rupture.

Prognosis

Although most case of tendinitis resolve within a few days to weeks of treatment, recurrences are common, particularly with athletes and individuals in occupations that require overhead or repetitive motions.
Pregnancy

* Stenosing tenosynovitis (de Quervain's disease) is common in pregnancy, but usually resolves spontaneously without treatment.
* A health care provider should be consulted for the proper dosage of vitamin A.

References

Balch JF, Balch PA. Prescription for Nutritional Healing. 2nd ed. Garden City Park, NY: Avery Publishing; 1997:174-175.

Duke JA. The Green Pharmacy. Emmaus, Pa: Rodale Press; 1997:106-109.

Kelly WN, Harris ED Jr, Ruddy S, Sledge CB. Textbook of Rheumatology. 5th ed. Philadelphia, Pa: WB Saunders Co; 1997:372-373, 386, 422-429, 462-463, 486, 558-559, 598-599, 603-606, 642.

Koopman WJ. Arthritis and Allied Conditions: A Textbook of Rheumatology. 13th ed. Baltimore, Md:Williams & Wilkins; 1997:44, 1769-1771, 1795, 1894-1896.

Millar AP. Sports Injuries and Their Management. Sydney, Australia: Maclennan & Petty; 1994:10-14, 84-85, 101-103, 111-112, 118-119, 8830-8831.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:72-74, 298.

Murray MT, Pizzorno JE. Encyclopedia of Natural Medicine. 2nd ed. Rocklin, Calif: Prima Publishing; 1998:805-809.

Noble J. Textbook of General Medicine and Primary Care. Boston, Mass: Little, Brown; 1987:228-229, 288-290, 293-296.

Vinger PF, Hoener EF, eds. Sports Injuries: The Unthwarted Epidemic. Boston, Mass: John Wright; 1982:227, 255.

Temporomandibular Joint Dysfunction - home health advice

noreply@blogger.com (kablogspot) — Wed, 24 Oct 2007 01:12:00 +0000

Overview
Definition

The temporomandibular joint (TMJ) is a synovial joint that involves the masseter, medial pterygoid, and temporalis muscles of the lower jaw movement. TMJ dysfunction, often simply but inaccurately referred to as TMJ, characteristically involves face pain, clicking sounds in the TMJ, and limited movement in the mandibular area. Terminology given to the condition has been confusing and treatment of it diverse. Physicians do not appear to agree on whether TMJ dysfunction should be treated by the medical provider, the dental professional, or both. TMJ dysfunction has a prevalence rate of about 33% in the general population. However, up to 75% percent of the population may have some symptoms with only 5% to 25% seeking treatment. TMJ dysfunction affects people of all ages and women only slightly more than men.
Etiology

Definitive etiology is unknown but probably multifactorial. Contributing causes include the following.

* Malocclusion controversial as a causal factor
* Bruxism (jaw clenching) leading to masticatory muscle fatigue and spasm
* Disk derangement
* Trauma to the area
* Synovitis
* Psychophysiologic factors

Risk Factors

* Women seek treatment twice as often as men
* Age 30 to 50
* Nutritional or metabolic disorders
* Chronic bruxism
* Occlusal problems
* Psychosocial stress especially bereavement, illness, divorce, moving; depression is a risk for chronicity
* Unfavorable incisor relationship overbite, overjet, negative overbite

Signs and Symptoms

* Orofacial pain usually a chronic, unilateral, dull pain that may extend to the eyes and ears; worsens during mastication; masticatory muscle tenderness
* Decreased mandibular range of motion especially in the morning; jaw may lock
* Clicking and/or crepitus noises (however, up to 50% of the population may have such noises without pain or other TMJ dysfunction symptoms)
* Headache often chronic
* Earache, tinnitus, blocked sensations
* Neck pain
* Dizziness, vertigo
* Aggravated by occlusal problems
* Flattened molar prominences from chronic bruxism
* Chewing exacerbates all symptoms

Differential Diagnosis

* Numerous other causes of head, neck, or ear pain (e.g., sinusitis, acute otitis media, acute otalgia, parotitis)
* Neuralgias trigeminal, herpes zoster, geniculate
* Rheumatoid arthritis and osteoarthritis
* Condylar hyperplasia
* Gout, with accompanying tophi
* Odontogenic pain
* Ankylosing spondylitis
* Neoplasia
* Congenital disorders

Diagnosis
Physical Examination

The muscles in the area of the TMJ may be palpated for tenderness and fasciculations or spasms; palpate as the patient opens and closes jaw. Face is checked for asymmetry or inflammation. Joint clicking or scraping sounds may be audible. The patient's mandibular range of motion may be limited. The teeth may show evidence of bruxism or jaw clenching, such as wear facets. A neurological examination should be given if any signs of neurological dysfunction are evident (e.g., numbness).
Pathology/Pathophysiology

* Limited mandibular range of motion: <50 mm opening, <10 mm protusively and laterally
* Intracapsular diseases infection, tissue, or degenerative joint disease
* Spasms of the masseter and internal pterygoid muscles
* Nonserous inflammation from mechanical microlesions of interfibrillar connective tissue
* Inflammation of articular and periarticular tissue
* Release of neuropeptides
* Osteoarthritic joint irregular surfaces, morphologic changes
* Anterior displacement of articular disk within joint, preventing forward translation of mandibular condyle

Imaging

Unless there is suspicion of degenerative disease or disk derangement, imaging should not be performed routinely. Imaging can reveal osseous tumors, articular disk problems, condylar erosion, osteophytes, heterotopic bone, or metastatic disease. Panoramic dental radiographs reveal occlusion or other dental problems. Magnetic resonance imaging is the medium of choice for bony and soft tissue visualization and determination of joint effusion, avascular necrosis, or intracapsular TMJ disease. Arthrography is an invasive technique but allows visualization of the condyle in relationship to the disk through tomography recorded on video camera.
Other Diagnostic Procedures

* Often diagnosed by a dentist
* History and physical examination of the masticatory system

Treatment Options
Treatment Strategy

Many primary physicians see TMJ dysfunction largely as a psychophysiologic condition, while others evaluate it as a dental problem. TMJ dysfunction is treated successfully in 75% of patients who employ multifaceted treatment plans.
Drug Therapies

* Analgesics aspirin or nonsteroidal anti-inflammatory drugs no significant long-term benefits; patient-reported short-term benefit; gastrointestinal side effects
* Minor tranquilizer/muscle relaxants bedtime use reduces spasms and pain; diazepam 2 mg every hour or as needed for three to five days
* Intramuscular injections local anesthetic, longer periods of relief with repeated injections; 2% lidocaine hydrochloride
* Antidepressants for refractory pain; e.g., nortriptyline 25 mg every hour or as needed
* Intra-articular cortisone injections intractable cases only, controversial; side effects include infection, local structure damage, usual systemic effects

Surgical Procedures

* High intracapsular condylectomy, disk correction or replacement; when all other measures have failed
* Arthroscopy less invasive and provides good symptom relief; low incidence of complications; long-term benefit unclear

Complementary and Alternative Therapies

The goal is to decrease inflammation and provide pain relief. Physical approaches can be quite effective. Although research is scanty, a clinical trial of CAM therapies seems reasonable, given the irreversibility of surgery. Biofeedback may be efficacious in treating TMJ and in preventing recurrence.
Nutrition

* Essential fatty acids regulate arachidonic acid metabolites to decrease inflammation; 1,000 to 3,000 mg/day of mixed omega-3 and omega-6.
* Soft foods high in flavonoids provide antioxidants to decrease pain caused by free radical buildup in the joint.
* Avoid saturated fats, fried foods, and caffeine, all of which increase inflammation. Avoid chewing gum.

Herbs

Herbs may be used as dried extracts (pills, capsules, or tablets), teas, or tinctures (alcohol extraction, unless otherwise noted). Dose for teas is 1 heaping tsp. herb/cup water steeped for 10 minutes (roots need 20 minutes).

* St. John's wort (Hypericum perforatum) may improve serotonin levels affected in TMJ. Oil may be applied topically. Oral dose is 250 mg tid.
* Cramp bark (Viburnum opulus) and lobelia (Lobelia inflata) are antispasmodic. Rub 5 drops tincture of each herb into joint. Do not apply to broken skin.

Homeopathy

An experienced homeopath would consider an individual's constitutional type to prescribe a more specific remedy and potency. Some of the most common acute remedies are listed below. Acute dose is three to five pellets of 12X to 30C every one to four hours until symptoms resolve.

* Causticum for burning pains that are better in rainy weather and worse in dry weather
* Hypericum perforatum for sharp shooting pains, especially after an injury or dental work
* Ignatia for tension in the jaw after a grief or conflict
* Kalmia for face pain especially with other joint pains/arthritis
* Magnesia phosphorica for muscle cramps that feel better with heat and pressure
* Rhus toxicodendron for pains that feel better in the morning and in dry weather, and worse after movement or in wet weather
* Ruta graveolens for pains from overuse or injury that are better with rest

Physical Medicine

Contrast hydrotherapy. Alternating hot and cold applications brings nutrients to the site and diffuses metabolic waste to decrease inflammation, provide pain relief, and enhance healing. Use hot packs and ice wrapped in a wash cloth and apply to area. Alternate three minutes hot with one minute cold and repeat three times. This is one set. Do two to five sets/day.
Acupuncture

May help decrease spasm and reduce frequency and intensity of symptoms
Massage

Cranio-sacral and chiropractic manipulation may be useful to decrease muscle spasm, provide pain relief, and prevent recurrence.
Patient Monitoring

Ongoing assessment of conservative therapies is appropriate.
Other Considerations
Prevention

* Stress reduction
* Awareness and efforts to stop bruxism and clenching

Complications/Sequelae

* Prolonged teeth clenching or grinding, trauma, infection, or connective tissue disease may cause severe malocclusion or intracapsular joint derangement, which may result in degenerative joint disease or arthritis. The diagnosis is confirmed by radiologic examination. Although rare, the implications are serious and may require teeth regrinding or surgery. Patients with severe grinding may benefit from nighttime use of a splint or bite guard.
* Severe trismus apply refrigerant spray (e.g., ethyl chloride), then standard therapies
* Arthritic conditions

Prognosis

TMJ dysfunction is almost always self-limiting. Irreversible treatments, such as teeth regrinding and surgery, are rarely called for and have a limited efficacy.
Pregnancy

N/A
References

Challem J. TMJ pain may be aggravated by free radicals, relieved partly by anti-oxidants. The Nutr Reporter. 1998.

Crider AB, Glaros AG. A meta-analysis of EMG biofeedback treatment of temporomandibular disorders. J of Orofacial Pain. 1999;13(1):29-37.

Dambro MR. Griffith's 5-Minute Clinical Consult. 1999 ed. Baltimore, Md: Lippincott Williams & Wilkins, Inc.; 1999.

Ernberg M, Hedenberg-Magnusson B, et al. Pai, allodynia and serum serotonin level in orofacial pain of muscular origin. J Orofacial Pain. 1999; Winter 13(1):56-62.

Goroll A, ed. Primary Care Medicine. 3rd ed. Philadelphia, Pa: Lippincott-Raven Publishers; 1995.

Jagger RG, Bates JF, Kopp S. Temporomandibular Joint Dysfunction. Oxford, England: Wright; 1994.

Koopman WJ, ed. Arthritis and Allied Conditions. 13th ed. Baltimore, Md: Williams & Wilkins, Inc.; 1997.

Marbach JJ. Temporomandibular Pain and Dysfunction Syndrome. Rheum Dis Clin North Am. 1996;22(3).

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:111-114, 185-186, 187-189, 208-209, 237, 324-325, 329-330.

Roberts J, Hedges J, ed. Clinical Procedures in Emergency Medicine. 3rd ed. Philadelphia, Pa: W.B. Saunders; 1998.

Rosen P, ed. Emergency Medicine: Concepts and Clinical Management. 4th ed. St. Louis, Mo: Mosby-Year Book; 1998.

Systemic Lupus Erythematosus - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 21:17:00 +0000

Overview
Definition

Systemic lupus erythematosus (SLE) is a combination of diseases, attributable to a genetically determined production of pathogenic autoantibodies and immune complexes. Immune abnormalities, typically involving antibodies to a number of nuclear or other cellular antigens, result in inflammation and cellular injury. Lupus is characterized by periods of both chronic disease and remission. Prevalence is not well established and ranges from 15 to 50 cases per 100,000 people.
Etiology

There is no known etiology for lupus. However, genetics, immune abnormalities, hormones, and environmental factors all play a role in the etiology or aggravation of lupus.
Risk Factors

* Ultraviolet (UV) light (both UV-A and UV-B) sensitivities
* Females (90% of cases); female:male ratio changes to 3:1 outside of childbearing years
* Genetic predisposition

Signs and Symptoms

Lupus may involve one organ or many, even at onset.

* Fever
* Fatigue
* Malar ("butterfly") rash
* Skin lesions
* Hair loss
* Nausea, vomiting, abdominal pain
* Muscle pain and stiffness
* Arthritis
* Oral/nasopharyngeal ulcers
* Central nervous system (CNS) headaches, migraine, cognitive dysfunction, seizures, stroke, psychosis
* Depression, anxiety, confusion
* Photosensitivity

Differential Diagnosis

* Rheumatoid arthritis
* Multiple sclerosis
* Psychological disorders
* Dermatitis
* Fibromyalgia
* Chronic fatigue syndrome
* Drug-induced lupus
* Discoid lupus
* Hepatitis
* Vasculitis

Diagnosis
Physical Examination

The patient appears pale, may have hair loss, and reports malaise. There is typically joint swelling, mouth sores, or skin rash. The heartbeat is rapid (with or without chest pain), and the patient usually has episodic fever.
Laboratory Tests

* Cerebral spinal fluid elevated protein in 50%, increased mononuclear cells in 30%
* Erythrocyte sedimentation rate assesses clinical activity
* Urinalysis and increased serum creatinine levels proteinuria, cylindruria, hematuria
* Hematology may show anemia, leukopenia, lymphocytopenia, thrombocytopenia
* Elevated number of antinuclear antibodies (ANAs) indicate:
* Diffuse proliferative glomerulonephritis
* Antibodies (depending on disease expression) to cell surface, glomerular, and/or tubular antigens, and endothelial and/or neuronal cells
* Antibodies to double-strand DNA (dsDNA) and Sm relatively specific
* Hypoalbuminuria
* Increased prothrombin time

Pathology/Pathophysiology

* Antigen-specific, polyclonal B and T lymphocyte hyperactivity and lack of regulation
* Immune response switches from IgM to IgA antibodies
* Most common genetic marker C4AQO, a defective class III allele fails to encode C4A protein
* Ischemic necrosis of bone, cellular necrosis
* Perivascular mononuclear cells, lumen obliteration, enlarged endothelial cells, thrombi
* Skin lesions hyperkeratosis, follicular plugging, immune complexes (IC) at dermal epidermal junction, mononuclear infiltrates in upper dermis, lesions show leukocytoclastic angiitis
* Mononuclear cells infiltrate pleura and pericardium
* Renal IC in mesangium and glomeruli basement membrane

Imaging

* Magnetic resonance imaging most sensitive radiographic technique to evaluate CNS changes; reveals avascular necrosis
* Computed tomography and angiograms identify focal neurologic deficits
* Angiograms shows mesenteric vasculitis
* X ray diagnoses lupus pneumonitis; intestinal perforation and vasculitis
* Echocardiogram reveals pericarditis

Other Diagnostic Procedures

* Diagnosis is determined by the 1982 Revised American College of Rheumatology criteria for SLE (97% sensitivity, 98% specificity). A patient must have 4 of the 11 criteria, serially or simultaneously, to be diagnosed with lupus. Broadly, the criteria include: malar rash, discoid rash, photosensitivity, oral and nasopharyngeal ulcers, nonerosive arthritis, serositis (pleuritis, pericarditis), renal disorder (proteinuria), neurological disorder (seizures, psychosis), hematological disorder (hemolytic anemia, leukopenia), immunologic disorder, and antinuclear antibodies.
* Renal biopsy assesses extent of disease for accurate treatment, and lumbar puncture determines presence of infection.
* Electroencephalograms abnormal in 70% of patients

Treatment Options
Treatment Strategy

There is no known cure for lupus. Symptoms are managed and complications or flare-ups are emergently treated. The goal is to prevent organ damage and maintain organ function. Sunscreen and sun avoidance are recommended for photosensitivity.
Drug Therapies

* Glucocorticoids for disabling and organ disease; 1 to 2 mg/kg/day bid or tid, taper with improvement; prednisone 15 mg/day before noon to avoid hypothalamic pituitary axis suppression; intravenous treatment with acute illness; numerous serious side effects
* Nonsteroidal anti-inflammatory drugs and salicylates to alleviate arthralgias, arthritis, myalgias, fever, serositis
* Antimalarials to alleviate arthritis, dermatitis, pleuritis, fatigue, hair loss; e.g., hydroxychloroquine 400 mg/day for at least two years, 6- to 12-week response time; side effects uncommon; monitor retinal toxicity with long-term use
* Cytotoxic agents renal disease, pulmonary hemorrhage, vasculitis, anemia, arthritis; reduces flare-ups and need for steroids; cyclophosphamide (1.5 to 2.5 mg/kg/day) most effective but serious side effects; azathioprine (50 to 200 mg/day) least toxic
* Warfarin for thrombosis

Surgical Procedures

Occasionally for serositis, vasculitis, deforming arthritis, avascular necrosis
Complementary and Alternative Therapies

While CAM is occasionally able to control SLE symptoms, treatments are usually most helpful at minimizing symptoms and/or dosages of pharmaceuticals and at reducing side effects of pharmaceutical interventions. Goal is to decrease immune response cross reactivity.
Nutrition

* Eliminate all suspected allergens, including dairy, wheat (gluten), soy, chocolate, eggs, corn, and preservatives. An ELISA IgG delayed sensitivity food allergy panel is helpful in identifying food sensitivities.
* A modified fast of five to seven days at two-week intervals may be helpful, especially during flare-ups. Modified fast can consist of fruits, vegetables, and fish or vegetable protein.
* Avoid coffee, alcohol, and smoking to decrease toxic load on the body.
* Minimize red meat and saturated fats to decrease inflammation.
* Omega-3 fatty acids such as flaxseed and fish oils (3,000 mg/day) decrease inflammation.
* Beta-carotene (50 mg tid) has cleared some cases of discoid lupus. Some controversy exists about whether vitamin A is helpful or harmful in SLE.
* Vitamin B12 (1,000 mcg IM once or twice a week) increases healing of lesions.
* Vitamin E (800 IU/day) for both discoid lupus and SLE
* Tryptophan should be avoided in SLE. SLE patients may have difficulty converting tryptophan, which may lead to auto-antibody production. Eating alfalfa sprouts has also increased symptoms.
* Hydrochloric acid. SLE sufferers may have a deficiency and supplementation can decrease symptoms.
* DHEA (start at 5 mg tid and work up to 100 mg/day) is especially effective in reducing symptoms in mild to moderate SLE with incremental benefits over 3 to 12 months.
* Melatonin (20 mg before bed) has been shown to be helpful in many autoimmune diseases. Lower dose if drowsiness occurs.
* Methylsulfonylmethane (MSM) (3,000 mg bid) helps prevent joint and connective tissue degeneration.
* Iron leads to increased inflammation and should be avoided if patient is not anemic.

Autoimmune diseases can be viewed as a cross sensitivity to an exogenous antigen that has similar receptor sites to an endogenous antigen. Reducing the exposure of the immune system to exogenous antigens (usually through the gut wall) can help lower the immune response. Agents that strengthen GI mucosa are beneficial. Consider L-glutamine (3,000 mg tid) or quercetin (500 mg tid).
Herbs

Herbs may be used as dried extracts (pills, capsules, or tablets), teas, or tinctures (alcohol extraction, unless otherwise noted). Dose for teas is 1 heaping tsp. herb/cup water steeped for 10 minutes (roots need 20 minutes). Herbs may be useful for treating secondary symptoms, such as depression and insomnia.

Dandelion (Taraxacum officinale), yellowdock (Rumex crispus), echinacea (Echinacea purpurea), and garlic (Allium sativum) are historically used as alteratives (balancing herbs) and may be useful. Equal parts in a tea, 1 cup tid.
Homeopathy

An experienced homeopath would consider an individual's constitutional type to prescribe a more specific remedy and potency. Some of the most common acute remedies are listed below. Acute dose is three to five pellets of 12X to 30C every one to four hours until symptoms resolve.

* Arsenicum album for restless exhaustion that comes on quickly, feels worse with cold
* Calcarea carbonica for overworked, overwhelmed people with poor stamina and low back pain
* Nux vomica for irritable people with constipation and sharp, crampy pains that feel better with heat
* Tuberculinum for repeated chest infections and joint pain with swollen glands

Acupuncture

May help balance immune response during remissions and alleviate acute exacerbations.
Patient Monitoring

Patients need to be closely monitored during flare-ups. Evaluation of specific complications and measurement of erythrocyte sedimentation rates are performed to determine appropriate treatment and induce remission.
Other Considerations
Prevention

* Avoid sun exposure, high-dose oral contraceptives, penicillin, and sulfonamides, as they can exacerbate lupus
* Exercise regularly
* Flu and pneumococcal vaccines generally recommended

Complications/Sequelae

* Arthritis, arthralgias, myalgias, tenosynovitis
* Pericarditis, myocarditis, hypertension, coronary heart disease (especially in long-term disease)
* Pleurisy, pneumonitis, pulmonary embolus
* Nephritis mesangial nephritis, diffuse proliferative nephritis, glomerulonephritis
* Anemia, leukopenia, lymphocytopenia, thrombocytopenia, splenomegaly
* Fibromyalgia
* Vasculitis cerebral, intestinal
* Isolated discoid lesions 10% frequency of developing into lupus
* Subacute cutaneous lupus erythematosus
* Pancreatitis
* Hepatomegaly
* Autophospholipid syndrome false positive syphilis tests
* Orbital myositis, conjunctivitis, cataracts
* Raynaud's phenomenon
* Sj?gren's syndrome
* Coomb's disease
* Osteoporosis from steroid use

Prognosis

* Poor prognosis correlates with high serum creatinine levels, nephrotic syndrome, hypertension, anemia, autoalbuminemia, low socioeconomic status
* Survival rates 10 years, 90%; 20 years, 63% to 75%
* Half of people who go into remission remain so for decades, but 90% of patients have complications
* Symptoms decrease after menopause
* Major cause of death infection

Pregnancy

* Still births and spontaneous abortions 10% to 30% higher than the general population
* Hypertension, renal disease, myocarditis pregnancy contraindicated
* Onset, flare-ups common
* With disease control and absence of serious cardiac or renal involvement two-thirds have safe, full-term pregnancies
* Newborns cardiac arrhythmias; rarely, neonatal lupus (1% to 5%) with skin lesions

References

Bartram T. Encyclopedia of Herbal Medicine. Dorset, England: Grace Publishers; 1995:278.

Cecil R, ed. Cecil Textbook of Medicine. 20th ed. Philadelphia, Pa: W.B. Saunders; 1996.

Dambro MR. Griffith's 5-Minute Clinical Consult. 1999 ed. Baltimore, Md: Lippincott Williams & Wilkins, Inc.; 1999.

Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998.

Koopman WJ, ed. Arthritis and Allied Conditions. 13th ed. Baltimore, Md: Williams & Wilkins, Inc.; 1997.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:39-44, 82-87, 272-276, 390-392.

Val Vollenhoven RD, Engleman, EG, McGuire JL. An open study of dehydroepiandrosterone in systemic lupus erythematosus. Arthritis Rheumatol. 1994;37:1305-1310.

Werbach M. Nutritional Influences on Illness. New Canaan, Conn: Keats Publishing Inc;1987:292-296.

Syncope - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 21:09:00 +0000

Overview
Definition

Syncope is defined as a sudden but brief loss of consciousness with postural collapse, resulting from decreased cerebral blood flow, and spontaneous recovery that does not require resuscitative measures. According to the Framingham Study, syncope occurs in 3% of men and 3.5% of women, especially among the elderly, and is responsible for 3% to 6% of all hospital admissions.
Etiology

Vasovagal (neurocardiogenic) syncope is the most common noncardiac cause (50% of all cases), followed by orthostatic hypotension. Cardiac causes of syncope are either related to obstruction of cardiac output or disturbances of cardiac rhythm. The causes of syncope are often classified into three categories.

* Noncardiac causes vasovagal (vasodepressor) responses; orthostasis; cerebrovascular disease; carotid sinus sensitivity; gastrointestinal hemorrhage, other blood loss or other causes of hypovolemia; situational (cough, micturition, defecation, deglutition, hypoxia, hypoglycemia, hyperventilation, psychogenic, migraine)
* Cardiac causes obstructions: aortic stenosis, pulmonary embolism, pulmonary stenosis, pulmonary hypertension, mitral stenosis, hypertrophied cardiomyopathy, cardiac myxoma, prosthetic valve malfunction; arrhythmias: ventricular tachycardia/fibrillation, sinus bradycardia (sick sinus syndrome), supraventricular tachycardia, atrioventricular block, myocardial infarction, pacemaker malfunction, prolonged QT syndrome
* Unknown cause 30% to 45% of cases?

Risk Factors

* Age (>65 years of age)?
* Preexisting heart disease?
* Recreational drugs (e.g., cocaine)?
* Medications (e.g., antihypertensives, insulin, oral hypoglycemics, diuretics, antiarrhythmics, anticoagulants via blood loss)?

Signs and Symptoms

* Presyncope: lightheadedness, blurred vision, diaphoresis, heaviness in the lower limbs, giddiness, confusion, yawning, nausea, and sometimes vomiting?
* Syncope: pallor, loss of consciousness, loss of postural tone, myoclonic jerks, feeble pulse, low blood pressure, imperceptible breathing, recovery of consciousness within a few seconds to minutes

Differential Diagnosis

Although syncope is a fairly straightforward diagnosis, distinguishing among the numerous causes of syncope can be difficult. It is most important to distinguish syncope from seizures or hypoglycemic reactions in diabetics; after this distinction is made, it is imperative to distinguish cardiac from noncardiac causes.
Diagnosis
Physical Examination

Evaluation of the patient with syncope involves a detailed history, physical examination, and special diagnostic tests, focusing on the symptom complex of the present episode, medications taken, preexisting medical conditions, and descriptions of similar previous episodes. Fainting patients are pale, motionless, diaphoretic, hypotensive, with a weak or absent pulse and shallow respirations. Orthostatic vital signs should be measured as part of the exam, particularly just following an episode when a patient presents to a hospital emergency room or other acute care facility. The patient should also be observed on a cardiac monitor.
Laboratory Tests

The following studies may be warranted depending on clinical circumstances:

* Complete blood count to determine the presence of anemia?
* Serum electrolytes to determine the presence of electrolyte deficiencies that may cause arrhythmias
* Glucose - to assess for hypoglycemia

Pathology/Pathophysiology

* Vasovagal syncope: impaired sympathetic drive, diminished venous return, and venous pooling, resulting in inappropriate vasodilation, bradycardia, and hypotension?
* Cardiac syncope: reduction in cardiac output usually from a cardiac arrhythmia (<35>180 beats/min), resulting in reduction in cerebral perfusion
* Orthostatic hypotension: autonomic dysfunction secondary to diabetes mellitus, syphilis, alcoholism, amyloidosis, or adrenal insufficiency; hypovolemia secondary to hemorrhage, vomiting, diarrhea, drugs, or low fluid or sodium intake

Imaging

The following may be indicated under certain clinical circumstances:

* Magnetic resonance imaging (MRI) of the head or brain to identify focal neurologic deficits or intracranial abnormalities
* Echocardiography to identify cardiac structural or functional abnormalities
* Nuclear lung scan, pulmonary angiography, duplex ultrasound, or venography to look for venous thromboembolic disease?

Other Diagnostic Procedures

The following may be indicated under certain clinical circumstances:

* Tilt table testing with or without isoproterenol (1 to 5 mg/min for 30 min) infusion (to enhance sensitivity) to provoke a neurocardiogenic response?
* Electrocardiogram (ECG) to determine an underlying cardiac problem (e.g., arrhythmia, conduction abnormalities, ventricular hypertrophy, QT prolongation, pacemaker malfunction, myocardial infarction)?
* Transtelephonic ECG monitoring (event recorders) to diagnose causes of syncope over weeks to months?
* Signal-averaged ECG to identify ventricular arrhythmias, especially in patients who have had a myocardial infarction?
* Electroencephalogram (EEG)to differentiate seizures from syncope?
* Electrophysiology studies to determine the presence of cardiac rhythm disturbances, especially ventricular tachycardia?

Treatment Options
Treatment Strategy

Physicians should be alert to the malignant causes of syncope (e.g., internal bleeding, myocardial infarction, complete heart block, ventricular tachyarrhythmia) so that life-threatening situations do not ensue. The benign faint can be treated by placing the patient in a position that increases cerebral blood flow (e.g., head lower than the heart), loosening all tight clothing, applying cold water to the face, and preventing emesis or choking by turning the head to the side.
Drug Therapies

* Beta-adrenergic antagonists, disopyramide, theophylline, scopolamine, ephedrine to treat vasovagal syncope
* Mineralocorticoids and salt loading to correct hypovolemia or venous pooling

Surgical Procedures

Placement of a cardiac pacemaker for symptomatic bradycardia or some tachyarrhythmias.
Complementary and Alternative Therapies

As discussed earlier, syncope may be preceded by a trigger along with warning symptoms. Autogenic training, diaphragmatic breathing, progressive muscle relaxation, and biofeedback have been successfully utilized to increase awareness of presyncopal symptoms and to reduce autonomic activity in the case of vasovagal syncope (McGrady et al. 1997). Nutrition, herbs, and acupuncture may also play a role in the treatment of syncope.
Nutrition

As discussed earlier in the monograph, hypoglycemia may be associated with syncope. Even modest decreases in blood glucose levels can act synergistically with hypotension and hypocapnea in particular to induce a loss of consciousness. In one study, glucose levels were assessed in 16 patients with presumed vasovagal syncope. Hypoglycemia was consistently found in all patients experiencing syncope (Salins et al. 1992), suggesting that low blood sugar may be the etiology at times, rather than the presumed vasodepression. Syncope may be even more prominent in elderly patients with poor glycemic control who commonly suffer from postprandial hypotension (Jansen and Lipsitz 1995). These case reports and the Jansen and Lipsitz trial illustrate the importance of adequate nutritional intake in those with a history of syncope as well as the elderly. In the case of dysglycemia, avoidance of refined foods and sugar as well as eating small, frequent meals high in protein are generally recommended.?
Herbs

Licorice root (Glycyrrhiza glabra) contains mineralocorticoid properties that expand intravascular fluid volume. A case study of a 38-year-old male with a history of vasovagal syncope responded well to a trial of high-salt diet and treatment with licorice root (520 mg bid); resolution of symptoms and syncopal episodes was achieved within one week. A withdrawal of the herb over several days resulted in resumed symptomology. The patient remained normotensive on this therapy and serum electrolytes remained within normal range. While licorice root is often deglycyrrhated to remove the active mineralocorticoid constituent, this property may be of benefit in select populations. This herb is contraindicated in patients with hypertension, hypokalemia, severe kidney disease, and pregnant women (Blythe 1999); even with normotensive patients, blood pressure should be monitored while taking licorice every four to six weeks initially, followed by every three to six months when stable.

Many herbs have cardiotoxic side effects when used indiscriminately. Natural does not necessarily imply safe and herbal therapies should only be used under the supervision of an experienced health care provider. A case of self-medication with tincture of aconite resulted in severe bradycardia, reversible conduction defect, hypotension, and syncope (Guha et al. 1999).

There are some herbal remedies, used alone and in combination, which are considered cardioprotective in general. One example includes hawthorn (Crataegus monogyna). While not specific for cardiac causes of syncope, some clinical experts suggest the value of hawthorn for maintenance of blood pressure, myocardial perfusion, and treatment of arrythmias (Murray and Pizzorno 1999).
Homeopathy

An experienced homeopath would consider the individual's constitution and determine an appropriate treatment. Although no known studies in the literature have specifically tested homeopathic remedies, the following are used clinically by many homeopaths for the treatment of recurrent syncope and pre-syncope:

* Carbo vegetabilis for syncope or lightheadedness after rising in the morning; from loss of fluids; or from becoming overheated. Patients appropriate for this treatment are generally chilly and pale at the time of presentation.
* Opium for syncope due to excitement or fright. Patients appropriate for this treatment are generally sweaty, glassy-eyed, and trembling at the time of presentation.
* Sepia for syncope following prolonged standing, exercise, or secondary to fluid loss from fever. Patients appropriate for this treatment feel hot during the syncope episode but cold immediately afterwards.

Acupuncture

The Chinese medical model of syncope consists of five categories of symptomatology: dying out of yang, dying out of yin, qi syncope, crapulent syncope (due to excess eating or drinking), and phlegm syncope. A clinical analysis of 102 critical cases of syncope treated with acupuncture and moxibustion was presented. Eighty seven patients were considered semi-comatose; fifteen were comatose. Traditional Chinese and Western drugs had been ineffective in reviving these patients. Treatment consisted of regulating yin and yang with acupuncture and reinforcing qi with moxibustion, then regulating qi and blood and dredging the channels to resuscitate the patient. Resuscitation efforts were based on the presenting symptoms. The intent was to evaluate and treat the underlying disease after the patient regained consciousness as well as normal blood pressure, pulse, and respiration (Shifa and Shiping 1990).

Results were reported as follows: "excellent" in 40 patients, "good" in 38, "fair" in 3, and "failed" in 21. In the excellent to good categories, patients were conscious; pulse was either normal or nearly normal and stabilized; and drug intervention was at least partially suspended while treating with acupuncture and moxibustion. ("All drugs" included Traditional Chinese Medicine as well as conventional medications.) Those with "fair" results were conscious; their blood pressure was nearly normal but not stabilized; and their pulse was "scattered and weak." Those whose treatment failed were not able to be resuscitated from the coma and died after all treatments failed Western medication and TCM, including acupuncture and moxibustion (Shifa and Shiping 1990).

The application of acupuncture is known for its virtual absence of side effects and complications; however, it is not uncommon to observe syncope in patients during acupuncture treatments. This type of syncope, called "needle fainting" in Chinese medicine, belongs to the category of vasodepressor syncope. In a year-long clinical study of 28,285 total acupuncture therapy procedures, 49 patients experienced needle fainting once and three patients experienced it twice. Management consisted of immediate removal of all needles and vigorous stimulation of the Jen-Chung point (Gv 26, located between the nose and upper lip), as well as placing the patient in a recumbent position. All of the patients who experienced syncope were upright when the episodes occurred. Patients with anxiety or fears about acupuncture were more likely to faint during the first visit, while patients with underlying cardiovascular complications (e.g., hypertension, arrhythmias) were more likely to faint during subsequent visits. Needle fainting is not a serious complication of acupuncture and may be easily remedied by needling susceptible patients appropriately while in the recumbent position (Fang-Pey et al. 1990).
Massage

No corroborating evidence has been found with respect to massage and syncope.
Patient Monitoring

Many patients, especially the elderly and those with preexisting cardiac disease, may benefit from hospitalization both to prevent further episodes (thereby avoiding serious injury or death) and to perform diagnostic tests. Continuous ambulatory ECG monitoring can identify arrhythmias as a cause of syncope, especially in patients who experience recurrences.
Other Considerations
Prevention

Prevention of syncope is dependent on the cause.

* Vasovagal syncope due to fatigue, hunger, emotional upheaval avoid these circumstances; see the Nutrition section under Treatment Options for more specific ideas.
* Orthostatic syncope avoid changing positions quickly, especially rising from a recumbent position, wear elastic stockings to prevent pooling of blood in the lower legs, and avoid situations requiring prolonged standing; find alternatives to medicines that can cause orthostasis such as diuretics, antidepressants, sympatholytic antihypertensive drugs, and beta-blockers. See also the section under Complementary and Alternative Therapies for more ideas on how to prevent orthostatic syncope.
* Carotid sinus syncope avoid tight clothing around the neck area; turn the whole body, not just the head, when looking around.
* Recurrent syncope cover all floors, including in the bathroom, with thick carpeting and avoid driving or operating mechanical equipment.
* Avoid caffeine which may exacerbate hypoglycemia.
* Avoid alcohol which may lead to hypotension by causing vasodilation.

Complications/Sequelae

Elderly patients are at increased risk for injury after a syncopal episode, especially fractures or intracranial hemorrhage, which in turn may lead to hospitalization, immobility, pneumonia, and even death.
Prognosis

The one-year mortality rate for syncope associated with heart disease is roughly 20% to 30%; for non-cardiac syncope it is 0% to 6%; and with syncope from an undetermined cause, 6%.
Pregnancy

Paradoxically, the normal treatment for syncope (placing the patient in the supine position to increase cerebral blood flow) may actually worsen the inadequate perfusion in the pregnant patient caused by the enlarged uterus, which prevents venous return. The correct position is left lateral decubitus. Varicose veins, which are common in pregnant women, may predispose the pregnant woman to syncopal episodes as they increase the pooling of blood in the extremities.
References

Adams RD, Victor M. Principles of Neurology. 6th ed. New York, NY: McGraw-Hill; 1997:902–912.

Beers MH, et al. The Merck Manual of Diagnosis and Therapy. 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:1651-1654.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:159, 160, 161, 162, 172, 179-180, 226-227.

Blythe SL. Use of licorice root to treat vasovagal syncope. HerbalGram. Spring 1999;(46):24.

Castro M. The Complete Homeopathy Handbook: A Guide to Everyday Health Care. New York, NY: St. Martin's Press; 1990:67-68, 127, 148.

Castro V, Nacht R. Cocaine-induced bradyarrhythmia: an unsuspected cause of syncope. Chest. 2000; 117:275-277.

Fang-Pey C, Hwang SJ, Lee HP, Yang HY, Chung C. Clinical study of syncope during acupuncture treatment. Int J Acupuncture & Electro-Therapeutics Res. 1990;15:107-119.

Fauci AS, Brauwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:100-107.

Gruenwald J, Brendler T, Jaenicke C, et al., eds. PDR for Herbal Medicines. Montvale, NJ: Medical Economics Company; 1998:779,1204-1205.

Guha S, Dawn B, Dutta G, Chakraborty T, Pain S. Bradycardia, reversible panconduction defect and syncope following self-medication with a homeopathic medicine. Cardiology. 1999;91(4):268-271.

Guize L, Iliou MC, Bayet G, Lavergne T, Le Heuzey JY. [Torsades de pointes.] Arch Mal Coeur Vaiss. 1993;86(5 Suppl):769-776.

Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Derm. 1999;41(6):895-906.

Hoffman D. The New Holistic Herbal. New York, NY: Barnes & Noble Books; 1995:215.

Jansen RW, Lipsitz LA. Postprandial hypotension: epidemiology, pathophysiology, and clinical management. Ann Int Med. 1995;122(4):286-295.

Kelley WN, et al. Textbook of Internal Medicine. 3rd ed. Vol. 1. Philadelphia, Pa: Lippincott-Raven Publishers; 1997:343–350.

Kerr D, Sherwin R, Pavalkis F, et al. Effect of caffeine on the recognition of and response to hypoglycemia in humans. Ann Intern Med 1993; 119(8): 799-804.

McGrady AV, Bush EG, Grubb BP. Outcome of biofeedback-assisted relaxation for neurocardiogenic syncope and headache: a clinical replication series. Appl Psychophysiol Biofeedback. 1997;22(1):63-72.

Murray M, Pizzorno J. Crataegus oxyacantha (hawthorn). In: Pizzorno J, Murray M, eds. Textbook of Natural Medicine. Vol 2. 2nd ed. Edinburgh, Scotland: Churchill-Livingstone; 1999: 683-687.?

Murray MT. Encyclopedia of Nutritional Supplements. Rocklin, Calif: Prima Publishing; 1996:296-308.

Murray MT. The Healing Power of Herbs: The Enlightened Person's Guide to the Wonders of Medicinal Plants. Rocklin, Calif: Prima Publishing; 1991:158-164.

Olshansky B. Evaluating syncope: how to do it efficiently and safely. J Crit Ill. 1999;14(8):423-430.

Rosen P, et al. Emergency Medicine. 4th ed. Vol. 2. St. Louis, Mo: Mosby; 1998: 1570-1581.

Salins PC, Kuriakose M, Sharma SM, Tauro DP. Hypoglycemia as a possible factor in the induction of vasovagal syncope. Oral Surgery, Oral Medicine, Oral Pathology. 1992;74(5):544-9.

Schlant RC, et al. Hurst's The Heart. 8th ed. New York, NY: McGraw-Hill; 1994: 927-945.

Shifa D, Shiping D. Resuscitation from syncope using acupuncture and moxibustion: a clinical analysis of 102 cases. Int J Clin Acup. 1990;1(3):251-256.

Stress - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 15:26:00 +0000

Overview
Definition

All individuals experience the typical stresses of life from time to time. According to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), stress disorders occur as a result of experiences of profound trauma, including encountering or witnessing threatened death, death, or serious injury. This must be coupled with a response that exhibits intense fear, helplessness, or horror. Physicians well know that similar reactions are seen in individuals who have endured a major operation or life-threatening disease, such as cancer. Acute stress disorder occurs soon after the traumatic event, resolving in about a month's time. Post-traumatic stress disorder (PTSD) continues for more than three months and may begin within a few days or may have delayed onset of action (possibly as long as 30 to 40 years). The lifetime U.S. prevalence rate for PTSD is 5% to 10% and can be as high as 58% in at-risk populations. Prevalence rates for acute stress disorder are unknown. Individuals of all ages can experience stress disorders.
Etiology

Acute and post-tramatic stress is precipitated by the combination of a traumatic event and a strong reaction to it, which involves feelings of intense fear and helplessness. However, without a stressor the condition does not exist. The trauma of war, rape or any other inappropriate sexual experience, illness, bereavement, or natural disaster can cause stress disorders.
Risk Factors

* Neuroticism, extroversion, poor self-confidence, past history of psychiatric problems, including sexual abuse
* Women > men
* The elderly and children
* Genetic predisposition
* Risk of PTSD increases with the magnitude of and exposure to the trauma
* Feelings of guilt or shame
* Lack of social support or financial security
* Early separation from parents, childhood neglect
* Children of alcoholic parents
* Parental poverty before the trauma

Signs and Symptoms

* Persistent re-experiencing of the trauma flashbacks, dreams, intrusive thoughts, intense distress when relived, accompanying physiologic responses
* Active avoidance of stimuli that prompts recollection inability to recall aspects of the trauma
* Detachment, decrease in emotional responsiveness, restricted range of affect and activity, sense of detachment from the body, alterations in memory or cognition
* Sense of a foreshortened future
* Impulsive and risk-taking behaviors
* Hopelessness akin to major depressive disorders
* Increased arousal, startled response, hypervigilance, insomnia
* Decreased occupational and social functioning
* Stress is also implicated in and can exacerbate illness (e.g., gastrointestinal, cardiac, cancer) as well as recuperation time and outcome

Differential Diagnosis

* Mental disorders such as mood, anxiety, depression, panic, obsessive-compulsive, and psychotic disorders
* Head trauma
* Substance-induced disorder
* Malingering

Diagnosis
Physical Examination

The patient may appear tired, pale, or disoriented.
Pathology/Pathophysiology

Stress disorders are one of only a few conditions for which DSM-IV reviews physiologic reactions.

* Increased release of neurotransmitter norepinephrine at the locus ceruleus (possibly the central nervous system arousal center, containing 50% of all neurons)
* Increased noradrenergic activity at the locus ceruleus afferent projection sites in the amygdala and hippocampus (may encode persisting memories of fear)
* Possible impaired alpha2- and beta-adrenergic receptor binding and feedback from norepinephrine release
* Elevated urinary catecholamines
* Decreased platelet monoamine oxidase (MAO) activity
* Increased sympathetic nervous system activity correlates with increased blood pressure, electromyography, heart rate, and sweat activity (possibly evoking feelings of panic)
* Increased serotonin activity
* Decreased amounts of neurotransmitter gamma-aminobutyric acid in elderly may predispose them to greater anxiety with trauma
* Decreased platelet adenylate cyclase activity
* Decreased cortisol release and increased sensitivity of it to dexamethasone inhibition
* Opioid system abnormalities such as a naloxone-reversible analgesia
* Increased rapid eye movement and decreased stage II sleep
* Elevated epinephrine and growth hormone; decreased prolactin, testosterone, and estrogen

Imaging

Computerized tomography and magnetic resonance imaging can rule out brain damage.
Other Diagnostic Procedures

* Psychiatric exam and psychological testing (e.g., Minnesota Multiple Personality Inventory [MMPI])
* Hypnosis with or without sodium amytal may uncover traumatic material with amnesia
* Electroencephalogram rules out brain damage, diagnoses sleep disorder

Treatment Options
Treatment Strategy

Acute stress is usually self-limiting with symptoms decreasing with time. Chronic stress requires a longer treatment period with most patients being more responsive to a multifaceted approach.

* Crisis intervention provides support, acceptance, education, meets health needs
* Psychotherapy mastering fear and overcoming avoidance behaviors in a phase-oriented approach is correlated with effective outcomes (e.g., cognitive behavioral therapy)

Drug Therapies

Drug therapy for symptom relief none approved for this use by the Food and Drug Administration

* Benzodiazepines more rapid onset of action than antidepressants, often combined with antidepressants; side effects include addiction, sedation, psychomotor impairment, ataxia, disinhibition
* Antidepressants wide spectrum of activity: reduce anxiety, avoidance behavior, intrusive thoughts, impulsiveness; slow onset (two to six weeks); e.g., fluoxetine 20 to 60 mg/day; side effects include nausea, gastrointestinal effects, sexual dysfunction, sleep disturbance
* Sedating antidepressants can relieve insomnia; e.g., trazodone 50 to 150 mg qid

Complementary and Alternative Therapies

Chronic stress may lead to derangements of multiple organ systems and has significant implications for normal physical, mental, and emotional functioning. Psychotherapy (individual and group support) and body-mind techniques such as meditation, cranial-sacral therapy, yoga, tai chi, and breathwork are the cornerstone for treatment of post-traumatic stress disorder and chronic stress. Early intervention has the best results, although support at any time may help. Homeopathy may be used acutely for grief, trauma, and anxiety; nutrition and herbs can provide long-term support and minimize sequelae.
Nutrition

* Avoid refined foods such as sugar and baked goods, as well as pro-inflammatory foods such as caffeine, alcohol, dairy, and animal products, which deplete vitamins and minerals that are mobilized during stress (particularly B-complex and magnesium).
* Increase foods that nourish the nervous system, such as whole grains, fresh vegetables, and foods rich in essential fatty acids such as nuts, seeds, and cold-water fish.
* Digestive enzymes, including betaine HCl, may be necessary to support proper digestive function which may be compromised under stress.
* B-complex (50 to 100 mg/day), calcium (1,000 mg/day), and magnesium (400 mg/day) may be depleted by stress.

Herbs

Herbs may be used as dried extracts (pills, capsules, or tablets), teas, or tinctures (alcohol extraction, unless otherwise noted). Dose for teas is 1 heaping tsp. herb/cup water steeped for 10 minutes (roots need 20 minutes).

A nervine tea or tincture may be indicated for long-term use to nourish and restore normal sympathetic/parasympathetic tone (30 to 60 drops tid). In addition, the tincture may be taken in small amounts (5 to 10 drops as needed) for symptomatic relief. Combine equal parts of passionflower ( Passiflora incarnata), lemon balm (Melissa officinalis) and oatstraw (Avena sativa) with one to three of the following herbs.

* With anxiety: kava kava (Piper methysticum), motherwort (Leonurus cardiaca)
* With insomnia: valerian (Valeriana officinalis), skullcap (Scutellaria laterifolia)
* With depression: St. John's wort (Hypericum perforatum), wood betony (Stachys betonica)
* With digestive upset: wild yam (Dioscorea villosa), chamomile (Matricaria recutita)
* With exhaustion: bladderwrack (Fucus vesiculosus), gotu kola (Centella asiatica)

Siberian ginseng (Eleuthrococcus senticosus) is an important adaptogenic herb that inhibits the alarm phase of stress. It is best taken as a fluid extract (1:1) 1/2 to 1 tsp. bid to tid. This herb may be stimulating to some and should not be taken after 3 pm. Ginseng is best used long-term (four to six months) in order to achieve maximum benefit.
Homeopathy

An experienced homeopath would consider an individual's constitutional type to prescribe a more specific remedy and potency. Some of the most common acute remedies are listed below. Acute dose is three to five pellets of 12X to 30C every one to four hours until symptoms resolve.

* Aconite for panic with heart palpitations, shortness of breath, and fear of death
* Arsenicum for anxiety, especially about health, with restlessness and fear of being alone
* Phosphorous for free-floating anxiety and foreboding; startles easily and feels better with reassurance

Patient Monitoring

Patients are treated on an outpatient basis until symptoms have subsided. With concerns of self-abuse or suicide, inpatient treatment is indicated.
Other Considerations
Prevention

Crisis intervention can prevent PTSD from developing.
Complications/Sequelae

* Greater risk of developing another mood, anxiety, or substance-abuse (especially alcohol) disorder
* Predisposition to comorbidity heart disease, insomnia, gastrointestinal illness
* Suicide

Prognosis

Many people have acute stress disorder or present with similar symptoms after a trauma. For most this is quickly resolved. Optimistic individuals, who can use family, work, humor, art, etc., for recovery, have a better prognosis. A lengthier course and delayed onset correlate with worse prognosis. PTSD appears within the first month in 70% to 90% of patients with the following resolutions.

* Complete recovery 30%
* Partial recovery 40% mild and 20% moderate symptoms
* Recovery failure 10%

References

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.

Blumenthal M, ed. The Complete German Commission E Monographs. Boston, Mass: Integrative Medicine Communications; 1998: 422, 425, 431, 462.

Braunwald E, ed. Heart Disease: A Text Book of Cardiovascular Medicine. 5th ed. Philadelphia, Pa: W.B. Saunders; 1997.

Dambro MR. Griffith's 5-Minute Clinical Consult. 1999 ed. Baltimore, Md: Lippincott Williams & Wilkins, Inc.; 1999.

Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998.

Kaplan HW, ed. Comprehensive Textbook of Psychiatry. 6th ed. Baltimore, Md: Williams & Wilkins; 1995.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:4, 40, 292, 293.

Murray MT. The Healing Power of Herbs. Rocklin, Calif: Prima Publishing; 1991:54-57.

Rakel RE, ed. Conn's Current Therapy. 50th ed. Philadelphia, Pa: W.B. Saunders; 1998.

Rosen P, ed. Emergency Medicine: Concepts and Clinical Management. 4th ed. St. Louis, Mo: Mosby-Year Book; 1998.

Sabiston DC, ed. Textbook of Surgery. 15th ed. Philadelphia, Pa: W.B. Saunders; 1998.

Yamada T, ed. Textbook of Gastroenterology. 2nd ed. Philadelphia, Pa: Lippincott-Raven Publishers; 1995.

Sprains and Strains - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 15:25:00 +0000

Overview
Definition

A sprain is an injury to a ligament or to the site of its attachment to bone, most often the ankle, knee, elbow, or wrist, which usually results in painful swelling.

* Grade 1 least severe type of sprain; minimal or mild pain, swelling, and disability. Edema, tenderness, and function loss is minimal to mild. Joint is stable. The ligament or muscle has less than 20% of its fibers damaged.
* Grade 2 moderate pain, swelling, and disability; moderate edema, tenderness and functional loss. Unstable joint, but flexion of the ligament will result in a solid endpoint. Twenty to 70% tissue fibers damaged.
* Grade 3 severe symptoms in all six categories. Joint is unstable, and flexion of the ligament results in an absent or mushy endpoint. Over 70% of the tissue fibers are damaged, or ligament or muscle is completely ruptured.

A strain is a tear or other injury to muscle tissue or tendon, commonly occurring in the muscles that support the neck, thigh, groin, and ankle.
Etiology

Sprain extrinsic load (i.e., twisting) to a joint, which causes the ligaments to deform past their elastic limit. The extent to which the bones depart from their normal alignment will determine the severity of the injury to the tendon.

Strains tension on a muscle that is stronger than the tensile capacity of its weakest structural element. Usually occurs during activities that require muscle activation and stretching simultaneously.
Risk Factors

* Poor conditioning
* Ill-fitting sports equipment
* Inadequate warm-up before activity

Signs and Symptoms

* Pain
* Stiffness
* Swelling
* Joint instability

Differential Diagnosis

First, differentiation must be made between a sprain and a strain.

Sprains:

* Strain
* Avulsion fracture
* Hairline fracture
* Contusion
* Ecchymosis
* Tendon rupture (especially Achilles)
* Hematoma
* Septic joint
* Inflammatory arthropathies
* Tendinitis

Strains:

* Underlying tumor involving the muscle or its attachment
* Infectious and inflammatory muscle syndromes
* Sprain
* Contusion
* Tendinitis
* Fracture

Diagnosis
Physical Examination

Pain and swelling in the affected area, usually acute within the first 48 hours of the injury
Pathology/Pathophysiology

Damage to the muscle, tendon, or ligament, depending on the severity and grade of the injury
Imaging

X rays may be indicated when the patient suffers from a grade 2 or grade 3 sprain, or is experiencing pain over a bone. The attached ligament can pull a piece of bone off during the injury, resulting in an avulsion fracture. X rays are not useful for strains. Although rarely necessary, a magnetic resonance image (MRI) will reveal complete tears of the ligament, as edema and bleeding and muscle-tendon pathology (Achilles or rotator cuff tear).

Appropriate stress films show ligament instability.
Other Diagnostic Procedures

Determine degree of injury for sprains (see Overview), and extent of pain/tenderness in strains.
Treatment Options
Treatment Strategy

Over several days following injury, RICE treatment rest, ice, compression (tape, etc.), and elevation of the affected joint.

Ice reduces pain, bleeding, and inflammation. It may also reduce secondary damage to other parts of the joint. However, the overall clinical benefit is not known. Bleeding and inflammation may play an important role in the healing process. Wrap the affected area in elastic bandage in more severe cases. Cast may be required to stabilize grade 3 injuries.

Activity that involves the affected area should be limited for an average of seven days.

Physical therapy—Grade 1 injury: strapping/taping or orthotic for two to three weeks. Grade 2: weight-bearing brace/orthotic/cast for four to eight weeks. Grade 3: weight-bearing cast for three to six weeks followed by orthotic or strapping for three to six weeks. Surgery may be indicated. All to be followed by appropriate exercise regimen for return of function.
Drug Therapies

Pain relief through analysis may allow the patient to mobilize the affected area and resume activity. When injuries are more severe or chronic, however, continued use of analgesics may lead to aggravation of the condition. Analgesics should not be used to mask pain so that activity can be resumed without proper immobilization. Reduction in the inflammatory response can also hasten the mobilization of the injured area, but the role of inflammation in healing is unknown and interference could theoretically slow tissue repair. Muscle spasms often accompany sprains and strains and can interfere with rehabilitation.

Over-the-counter pain relievers and anti-inflammatory agents usually help; however, product label dosage recommendations may be inadequate for moderate to severe injuries.

* Aspirin 325 mg, one to two tablets every four hours
* Naproxin 210 mg, two to three tablets every 8 to 12 hours
* Ibuprofen 200 mg, two to three tablets every four to six hours
* Analgesic balms
* Acetaminophen 325 mg, one to two tablets every four hours

Complementary and Alternative Therapies

Specific nutrients and herbs may help restore the integrity of connective tissue, reduce inflammation, and provide pain relief.
Nutrition

* Vitamin C (1,000 to 1,500 mg tid) to reduce inflammation and support connective tissue.
* Bromelain (250 to 500 mg tid between meals) is a proteolytic enzyme that helps to reduce inflammation.
* Beta-carotene (50,000 IU/day) is needed for collagen synthesis.
* Zinc (15 to 30 mg/day) supports immune function and healing.
* Vitamin E (400 IU/day) has antioxidant effects.
* Adequate protein intake is important.

Herbs

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

Flavonoids, a constituent found in dark berries and some plants, have anti-inflammatory properties and strengthen connective tissue by promoting collagen synthesis. The following are flavonoids that may be taken in dried extract form as noted.

* Quercetin: 250 to 500mg tid
* Hawthorn (Crataegus monogyna): 500 mg tid
* Turmeric (Curcuma longa) potentiates the effect of bromelain. Take 250 to 500 mg each of turmeric and bromelain, tid between meals.

The following combination of antispasmodic, analgesic, and circulatory stimulants may help to relieve congestion and provide pain relief. Black cohosh (Cimicifuga racemosa), cramp bark (Viburnum opulus), Jamaica dogwood (Piscidia piscipula), feverfew (Tanacetum parthenium), poke root (Phytolacca americana), and valerian (Valeriana officinalis). Combine equal parts in a tea (1 cup tid to qid), or tincture (15 drops every 15 minutes for acute relief, up to eight doses; or 20 to 30 drops qid).
Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

* Arnica montana for acute injury with bruised sensation and sensitivity to pressure
* Rhus toxicodendron for sprains and strains with great restlessness
* Ruta graveolens for stiffness and pain from injury or chronic overuse

Topical homeopathic creams containing leopard's bane (Arnica montana) and/or St. John's wort (Hypericum perforatum) may provide pain relief. Do not apply over broken skin.

Arnica oil may be applied topically for pain relief, provided the skin is not broken.
Physical Medicine

Castor oil pack. Used externally, castor oil is a powerful anti-inflammatory, especially helpful for chronic or severe injury. Apply oil directly to skin, cover with a clean soft cloth (e.g., flannel) and plastic wrap. Place a heat source (hot water bottle or heating pad) over the pack and let sit for 30 to 60 minutes. For best results, use for three consecutive days.
Acupuncture

Acupuncture may provide pain relief and increase local circulation.
Massage

Therapeutic massage is effective at increasing circulation and may relieve spasm in surrounding muscle groups.
Patient Monitoring

Monitor for recurring sprains and strains. Once a muscle or tendon is injured, it is susceptible to reinjury, especially if patient returns to full activity too soon.
Other Considerations
Prevention

Basic physical fitness and strength training are important preventive measures.

Warm-up exercises increase energy output and increase the temperature of muscles, improve coordination between the brain and muscles, reducing uncontrolled muscle movements.

Warm-ups should begin with stretching movements of the large muscle groups that are to be exercised more heavily. Jogging and exercise bikes are good initial exercises, to be followed by exercises more specific to the activity to be pursued. Lastly, the warm-up routine should include event-specific movements, such as throwing a football or swinging a racket. Warm-ups should last 15 or 20 minutes.

Half of all athletic injuries are due to inappropriate training or inadequate warm-up, and most of these errors result from a failure to follow the principle of slow progression. Sudden increases in intensity or duration of an activity often lead to over-use injuries such as sprains and strains.

Preventive training can take the form of muscle training, mobility and flexibility training (flexibility of the joint is limited by tight connective tissue), coordination and propioceptic training, and sport-specific training that reinforces good technique in recurring, stress-inducing movements.

Improper technique often causes excess load on joints, so correction of technique can prevent sprains and strains. Another method for reducing load is to decrease the speed of the activity.

Patient should not return to full activity until the affected joint has returned to 90% strength and flexibility.
Complications/Sequelae

* Strains: recurrent strains and complete muscle tears
* More chronic pain and joint instability
* Recurrent sprains
* Complete tear of muscle or tendon
* Stress fracture
* Degenerative arthritis from chronic joint instability

Prognosis

Inflammation occurs for up to 72 hours, followed by gradual reduction of swelling.

Recovery time is as follows: grade 1, 4 to 6 weeks; grade 2, 2 to 3 months; grade 3, 4 to 6 months. Patient may return to high-impact activity when range of motion, strength, and function of the injured joint is nearly equal to the uninjured side.
Pregnancy

High doses of vitamin C are contraindicated in pregnancy. Bromelain, quercetin, and turmeric should be used with caution.
References

Balch JF, Balch PA. Prescription for Nutritional Healing. Garden City Park, NY: Avery Publishing Group; 1997.

Birrer RB, ed. Sports Medicine for the Primary Care Physician. Boca Raton, Fla: CRC Press; 1994.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:429.

Brown DJ. Herbal Prescriptions for Better Health. Rocklin, Calif: Prima Health; 1996.

Kibler WB, Herring S, Press J, Lee P. Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, Md: Aspen Publishers; 1998.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:38, 326, 330.

Null G. The Clinician's Handbook of Natural Healing. New York, NY: Kensington Publishing Corp; 1997.

Olshevsky M, Noy S, Zwang M, Burger R. Manual of Natural Therapy. New York, NY: Facts on File; 1989.

Strauss RH, ed. Sports Medicine. Philadelphia, Pa: WB Saunders Co; 1991.

Ullmann D. The Consumer's Guide to Homeopathy. New York, NY: G.P. Putnam's Sons; 1995.

Zachazewski JE, Magee DJ, Quillen WS. Athletic Injuries and Rehabilitation. Philadelphia, Pa: WB Saunders Co; 1996.

Spontaneous Abortion - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 15:16:00 +0000

Overview
Definition

Spontaneous abortion, or miscarriage, is defined as the loss of a clinically recognized pregnancy that occurs before 20 weeks of gestation; early miscarriage occurs prior to week 12 while late spontaneous abortion occurs between weeks 12 and 20. Spontaneous abortions are classified as threatened (bleeding or cramping in the first 20 weeks of gestation), inevitable (bleeding that threatens the pregnant woman's health), incomplete (partial expulsion of the products of conception), or complete. Missed abortion refers to a fetus that has died in utero, which can be confirmed by ultrasonography. Habitual spontaneous abortion is defined as three or more consecutive miscarriages. Twenty-two to thirty-three percent of spontaneous abortions occur before clinical recognition as a pregnancy; an additional 9% to 14% of spontaneous abortions occur after pregnancy has been clinically recognized. Therefore, overall rate of loss following implantation is estimated to be one-third to one-half of all pregnancies.
Etiology

Chromosomal abnormalities:

* Up to 60% of spontaneous abortions
* Balanced parental translocation phenotypically normal parents, but abortuses show chromosomal duplications or deficiencies
* Aneuploidy numerical chromosomal abnormalities; trisomies, then monosomy X, most common
* Triploidy early abortions
* Inversions order of genes is reversed

Anatomic:

* Congenital distortion of uterine cavity e.g. mullerian fusion defects septate uteri or small T-shaped uteri; secondary to diethylstilbestrol (DES) exposure; generally a second trimester miscarriage
* Acquired abnormalities: Asherman's Syndrome (intrauterine adhesions from surgery and/or curettage); leiomyomas (rare); adenomyosis; endometriosis; endometritis, which may also cause synechiae; 15% to 30% of those with intrauterine adhesions have repeated spontaneous abortions
* Incompetent internal cervical os DES exposed as well
* Placental abnormalities rare

Endocrine:

* Hyperandrogen disorders including polycystic ovary syndrome
* Hyperthyroidism, hypothyroidism antithyroid antibodies higher in women experiencing repeated fetal loss
* Diabetes mellitus only if poorly controlled
* Hyperprolactinemia
* Luteal phase defects (LPD) inhospitable endometrium possibly from deficient progesterone production; LPD may be associated with hyperprolactinemia; although clinically plausible, currently considered an uncommon even unlikely cause as LPD also exists in fertile women who carry to term and treatment for LPD with progesterone suppositories remains unproven

Infection:

* Directly via bacterial, viral, parasitic, or fungal infection
* Indirectly via fever causing elevated core temperature
* Chlamydia trachomatis commonly associated with endometritis and salpingitis
* Ureaplasma urealyticum and Mycoplasma hominis relationship to spontaneous abortion somewhat controversial
* Herpes simplex may be associated with increased risk for spontaneous abortion
* Human papillomavirus (HPV) more prevalent in spontaneously aborted tissue compared to electively terminated pregnancies
* Septic abortion infected uterine contents occurring before, during, or after an abortion; generally, the woman is acutely ill with chills, high fever, leukocytosis, and signs of septicemia and/or peritonitis; causative agents include E. coli, Enterobacter aerogenes, Proteus vulgaris, hemolytic streptococci, staphylococci, and anaerobic organisms; incidence dramatically reduced with legalization of elective abortions

Autoimmunity:

* Antiphospholipid antibodies (APLA) with high-titer IgG or IgM possibly abnormal when directed against negatively charged phospholipids (e.g., lupus anticoagulant, anticardiolipin)

Anti-Fetal Antibodies:

* Rh-negative (D-negative) women with anti-D antibodies
* Anti-P antibodies in mother rejects Pp fetus early in gestation

Alloimmune:

* Excessive sharing of HLA antigens between mother and father

Other Causes:

* Time of implantation preovulatory oocyte aging and postovulatory gamete aging; conceptus that implants after days 8 to 10 is at increased risk
* Defective spermatozoa
* Stress possibly a psychocytokine mechanism controversial

Risk Factors

* Previous spontaneous abortion
* Increased maternal age
* Cigarette smoking presence of cotinine in urine, smoking half a pack a day significantly increases risk
* Alcohol risk doubles with more than two drinks a day; paternal alcohol use as well
* Caffeine see section entitled Nutrition
* Cocaine hair tests mildly correlate to greater risk but urine tests did not; therefore, this issue is controversial; possible that long-term use is more predictive of miscarriage (as indicated by positive hair tests) than acute exposure
* Increased homocysteine levels (see section entitled Nutrition)
* Exposure to x-rays (greater than 10 rads)
* Environmental excessive exposure to lead, mercury, ionizing radiation, organic solvents
* Intrauterine device increased risk of septic abortion
* Serious maternal illness
* Flight attendants working more than 74 hours/month during pregnancy; possibly secondary to increased gravitational forces, circadian rhythm disruption, noise and vibration, ozone, decompression episodes, fatigue, chemical exposure, ionizing radiation exposure
* Maternal or paternal handling of anti-neoplastic agents

Signs and Symptoms

* Embryonic heart rate below 90 beats per minute at 6 to 8 weeks of gestation
* Bleeding
* Uterine cramping
* Cervical dilation
* Fever
* Shock
* Passage of necrotic fetal tissue

Differential Diagnosis

* Ectopic pregnancy
* Molar pregnancy
* Cervical or vaginal lesions
* Membranous dysmenorrhea

Diagnosis
Physical Examination

* Comprehensive medical, genetic, and social history of both parents
* Assessment for signs of metabolic illness and hyperandrogenism
* Pelvic examination including assessment of uterine size and shape, evidence of DES or trauma

Laboratory Tests

* Human chorionic gonadotropin (hCG) chemical detection of pregnancy; levels >2,000 mIU/ml and lack of gestational sac indicates loss to make the diagnosis
* Karyotyping determines chromosomal abnormalities
* Hematocrit to evaluate extent of bleeding

To evaluate possible etiology:

* Serum assay for thyroid-stimulating hormone (TSH)
* Lupus anticoagulant, IgG and IgM iosotopes of anticardiolipin and of antiphosphatidylserine for immunologic assessment
* Cervical culture, Gram's staining of endometrial smears reveals infection
* Endometrial biopsy examines effect of progesterone on endometrium with luteal phase defects
* Serum progesterone level from mid-luteal phase best predictor of low progesterone

Pathology/Pathophysiology

Necrotic fetal debris with or without chromosomal abnormalities; fetal death may precede miscarriage by several weeks
Imaging

* Ultrasound for uterine and fetal evaluation to make diagnosis of spontaneous abortion; to assess for possible etiology e.g. polycystic ovaries or anatomic abnormality
* Sonohysterography identifies mullerian lesions
* Sonohysterosalpingography differentiates between a bicornuate and septate uterus; reveals tubal patency
* MRI for uterine evaluation may be useful but costly

Other Diagnostic Procedures

* Ultrasound-guided amniocentesis or chorionic villus sampling for prenatal genetic diagnosis or before uterine evacuation to increase likelihood of fetal, not maternal, karyotyping
* Hysteroscopy evaluates uterine cavity
* Laparoscopy differentiates between a bicornuate and septate uterus

Treatment Options
Treatment Strategy

Genetic counseling is advised for parents with inborn chromosomal abnormalities. Necrotic uterine contents must be removed (naturally or surgically) to avoid complications. Recognizing that spontaneous abortion may be associated with a grieving process, counseling both partners during this process is essential. In vitro fertilization, embryo transfer, or artificial insemination are used with unexplained, recurrent loss and parental translocations involving homologous chromosomes.
Drug Therapies

* Anti-D immunoglobulin if only mother is Rh-negative; 50 mcg first trimester, 300 mcg thereafter; plasmapheresis also possibly therapeutic in the case of anti-fetal antibodies
* Antibiotics in case of chlamydia or ureaplasm, should treat both partners with doxycycline 100 mg po bid x 7 days to eradicate infection and avoid spontaneous abortion in the future; if mother is pregnant, use amoxicillin 500 mg po tid x 7 days instead; in case of endometritis, cefoxitin (2 g IV, every 6 to 8 hours) for moderately severe infection; in the case of sepsis or septic shock secondary to septic abortion, clindamycin (900 mg IV, q 8 hours), ampicillin (2 g IV, q 6 hours), and an aminoglycoside; prophylactic antibiotics should be used prior to certain surgeries or procedures such as hysterosalpingogram
* Estrogen supplementation following intrauterine adhesion surgery; 2.5 mg/day for 30 days with 10 mg/day medroxyprogesterone during last 10 days, which stimulates endometrial growth
* Aspirin (81 mg/day) followed by low-molecular-weight heparin (2,500 or 5,000 U/day) after confirmed pregnancy for antiphospholipid syndrome
* Vaginal progesterone suppositories for LPD 25 mg/bid starting at time of basal body temperature elevation, for 6 to 8 weeks
* Immunotherapy with paternal or third-party leukocytes or trophoblast membranes for alloimmune disease; controversial

Surgical Procedures

* D & C to evacuate necrotic debris
* Uteroplasty corrects mullerian fusion defects; controversial
* Resection of intrauterine septum and cervical cerclage with DES exposure, uterine anomalies
* Lysis under hyperscopic visualization followed by an intrauterine device to reduce reapposition for intrauterine adhesions

Complementary and Alternative Therapies

There is a strong association between dietary and lifestyle factors and the risk of spontaneous abortion; preconceptional counseling, therefore, should include discussion of diet and lifestyle in relation to known risk factors including avoidance of caffeine and abstinence from alcohol and recreational drugs. In addition, while there is no definitive scientific support, there are case reports suggesting the usefulness of Chinese herbal medicines in preventing recurrent spontaneous abortions secondary to autoimmune abnormalities.
Nutrition

Clinically, many naturopathic and other doctors recommend the use of vitamin B complex 50 mg per day with additional vitamin B6 and folic acid 800 to 1,000 mcg per day. These practices for prevention of spontaneous abortion are supported by studies suggesting a connection between impaired methionine-homocysteine metabolism and recurrent miscarriages.

Increased homocysteine levels, caused by a dysfunctional methionine-homocysteine metabolism, have been implicated in spontaneous abortion, placental abruption, and neural tube defects. Cofactors in methionine metabolism include folic acid, vitamins B12 and B6, and betaine. The fetus, the neonate, and the pregnant woman all have increased requirements of folic acid and B12; therefore, they are also more likely to be deficient in these vitamins (Miller and Kelly 1996).

Impaired methionine metabolism may negatively impact other important nutritional constituents such as coenzyme Q10 which may not be synthesized in sufficient quantity in the case of too little folic acid, cobalamin and betaine. Two studies comparing women with a threatened or completed spontaneous abortion with women who had a normal, term pregnancy suggest that CoQ10 levels are significantly decreased in women with negative pregnancy outcomes. Supplementation with cofactors for methionine metabolism (e.g., folic acid or its active form folinic acid; vitamin B12 or its active form methylcobalamin together with riboflavin-5'-phosphate) may be useful in preventing spontaneous abortion (Miller and Kelly 1996).

The deleterious effects associated with elevated homocysteine levels have been illustrated in a case report of a woman with five consecutive spontaneous abortions and in a retrospective study of 100 women with recurrent early miscarriages of unknown cause. Evaluations of homocysteine levels in these women revealed significant hyperhomocysteinemia, with levels inversely correlated with serum folate and C677T homozygous genotype carrier status. The C677T mutation occurs in the 5,10-methylene tetrahydrofolate reductase (MTHFR) gene, which plays a central role in folate metabolism. Supplementation for 1 month with 15 mg daily folic acid and 500 mg daily B6 resulted in restoration of normal homocysteine levels and successful pregnancy outcome in the single case study (Quere et al. 1998).

Although supplementation with folic acid prior to and during pregnancy particularly for prevention of neural tube defects is standard practice, it is not entirely without controversy. As one author writes, a few studies have suggested a slightly increased risk of miscarriage among users of prenatal vitamins, multivitamins, or folic acid supplements, particularly if their use began before conception. It is questionable whether supplementation actually increases risk of miscarriage or simply prolongs a pregnancy that might have miscarried earlier; it is also difficult to determine from these particular studies whether it was folate or another factor contributing to the incidence of spontaneous abortion (Windham et al. 2000).

Other nutrients with a potential role in spontaneous abortion include selenium, magnesium, glutathione, beta-carotene, and vitamins A and E. Subacute, chronic, and marginal deficits in magnesium may contribute to impaired reproductive function, including miscarriage. In one small study, six women with a history of unexplained infertility or early miscarriage, whose red blood cell (RBC) magnesium levels failed to normalize after 4 months of oral magnesium supplementation, were compared with a similar group of controls whose levels did normalize. Levels of RBC GSH-Px, a selenium-dependent, antioxidant enzyme, were found to be significantly lower in the non-normalized group, suggesting a role for selenium deficiency in magnesium depletion. Within 8 months of normalizing their RBC-magnesium levels with either magnesium or magnesium/selenium supplements, all 12 of the previously infertile women conceived and delivered normal healthy babies (Howard et al. 1994).

While magnesium deficiency is conventionally managed with magnesium supplementation, these researchers suggest that normalization of magnesium depletion may require supplementation with selenium as well. Magnesium depletion appears to be secondary to increased permeability of cell membranes caused by oxidative damage. According to this explanation, the selenoenzyme GSH-Px is essential to cellular antioxidant activity, and a deficiency of selenium may compromise the integrity of cell membranes. Other possible explanations are that selenium improves magnesium absorption, or that enhanced selenium status optimizes reproductive function by some other mechanism not identified in this particular study (Howard et al. 1994).

Other studies have confirmed the association between antioxidant status and spontaneous abortion. In a preliminary study, 40 women presenting with first trimester miscarriage were matched with 40 nonpregnant healthy volunteers and 40 women in their first trimester of pregnancy. Healthy volunteers had normal blood levels of selenium with the exception of one volunteer with a marginally low level. All women in the healthy pregnant control group delivered healthy babies and had decreased selenium levels compared with nonpregnant controls. However, still lower selenium levels were found in the women who miscarried in the first trimester. The loss of antioxidant activity associated with selenium deficiency may have contributed to miscarriage in this group (Gabbe 1996). Similarly, blood samples of 40 women with habitual spontaneous abortion compared with those of 40 healthy fertile women revealed increased lipid peroxidation and lower levels of vitamins A and E and beta-carotene in the spontaneous abortion group. Levels of glutathione were significantly higher in the women with habitual abortion (Simsek et al. 1998).

Caffeine is known to cross the placenta readily; its impact on pregnancy is not entirely understood. Whereas the plasma half-life of caffeine in healthy adults is 2.5 to 4.5 hours, the half-life increases to 10.5 hours in pregnant women and 32 to 149 hours in the newborn. A prospective cohort study of 3135 pregnant women showed that moderate-to-heavy caffeine users (> 151 mg daily) were significantly more likely to experience late first- or second-trimester spontaneous abortion when compared with nonusers or light users. Light caffeine use (1 to 150 mg daily) was associated with increased risk for abortion only in women for whom there was a history of spontaneous abortion. (Note: one cup of coffee has 107 mg of caffeine, one cup of tea has 34 mg, and one glass of cola has 47 mg.) Coffee was the main source of caffeine in moderate-to-heavy users; light users were more likely to derive caffeine from tea and other sources. It is possible that some other component of coffee other than caffeine is responsible for the increased risk of spontaneous abortion (Srisuphan and Bracken 1986).

Researchers have recently reported on a marked positive dose-response relation between coffee consumption and plasma total homocysteine (Nygard et al. 1997). In view of a role for aberrant homocysteine metabolism in negative pregnancy outcomes (as discussed earlier), a coffee-homocysteine correlation may provide a mechanism for increased risk of spontaneous abortion among heavy coffee drinkers. However, further research is needed to investigate the possible connection between homocysteine levels, coffee consumption, and pregnancy.

A recent retrospective study examining the link between miscarriage and stillbirths and a high intake of persistent organochlorine compounds due to ingestion of contaminated fish found no association (Axmon et al. 2000). Examples of POCs are polychlorinated biphenyls (PCBs) and DDT (dichlorodiphenyltrichlorothane). Higher blood levels of PCBs were previously reported in women hospitalized for miscarriage as compared with women who carried full-term (Leoni et al. 1989).
Herbs

Western herbs may be beneficial in resolving underlying endocrine abnormalities and may also play a role in stress reduction; however, these have not yet been explored in relation to spontaneous abortion specifically.

Autoimmune abnormalities have been successfully treated with Traditional Chinese Medicine. Twelve patients positive for antinuclear antibodies (ANA) and one or more antiphospholipid antibodies (APLA) were admitted into treatment; all had experienced recurrent spontaneous abortion during the first trimester. Preconceptional administration of Sairei-to (a modified, Japanese version of the Chinese herbal preparation Chan ling-tang) resulted in normalization of APLA values in all but one of the patients within 2 months of treatment. Sairei-to was continued throughout the prenatal course and discontinued after delivery. Corticosteroids and aspirin were not administered during this time. In 9 out of 11 patients, these levels continued to be negative throughout the course of Sairei-to. In the other two cases, levels increased and became positive. Ten patients delivered healthy babies following a normal prenatal course. Two of the patients whose APLA re-elevated or remained positive experienced recurrent miscarriage (Takakuwa et al. 1996).

There are case reports in Chinese journals of women with recurrent spontaneous abortion secondary to elevated autoantibodies and/or allo-antibodies including anti-zona pellucida, APLA, and anti-ABO blood group antibodies being treated successfully with Chinese herbal preparations (Li et al. 1997). Such reports suggest that, for the appropriate patient with a history of one or more spontaneous abortions, referral to a traditional medical practitioner is not unreasonable.
Homeopathy

While information regarding the use of homeopathy for prevention of recurrent spontaneous abortion was not found in the literature, a licensed and certified homeopath would evaluate each individual and determine the appropriate constitutional homeopathic treatment, which may be useful in supporting the person's overall health.
Acupuncture

Although not necessarily recorded in the medical literature, acupuncturists report clinical success in treating women with a history of spontaneous abortion leading to future term pregnancies. The mechanism of success is possibly related to resolution of underlying endocrine abnormalities and may also play a role in stress reduction.
Patient Monitoring

* Monitor until miscarriage is complete
* Postconception monitoring is critical

Other Considerations
Prevention

* Avoid known risks as described above
* Abortus karyotyping for clues to etiology and likelihood of recurrence

Complications/Sequelae

* Retained necrotic tissue may become infected and could possibly result in pelvic abscess, septic shock, or death
* Feelings of depression and guilt are quite common, as well as fear and concern with the next pregnancy

Prognosis

* Fetal chromosomal abnormality present in 45% to 60% of first abortus and 75% of second abortuses
* Fetal chromosomal normality second loss has 75% chance of normality
* Recurrent miscarriage approximately 1%; risk for subsequent loss is 24% after two, 30% after three, and 40% after four consecutive losses

References

Axmon A, Rylander L, Stromberg U, Hagmar L. Miscarriages and stillbirths in women with a high intake of fish contaminated with persistent organochlorine compounds. Int Arch Occup Environ Health. 2000;73(3):204-208.

Barrington JW, Lindsay P, James D, Smith S, Roberts A. Selenium deficiency and miscarriage: a possible link? Br J Obstet Gynaecol. 1996;103(2):130-132.

Gabbe SG, ed. Obstretrics Normal and Problem Pregnancies. 3rd ed. New York, NY: Churchill Livingston; 1996.

Howard JM, Davies S, Hunnisett A. Red cell magnesium and glutathione peroxidase in infertile women: effects of oral supplementation with magnesium and selenium. Magnes Res. 1994;7(1):49-57.

Klebanoff MA, Levine RJ, DerSimonian R, Clemens JD, Wilkins DG. Maternal serum paraxanthine, a caffeine metabolite, and the risk of spontaneous abortion. N Engl J Med. 1999;341(22):1639-1644.

Leoni V, Fabiani L, Marinelli G, et al. PCB and other organochlorine compounds in blood of women with or without miscarriage: a hypothesis of correlation. Ecotoxicol Environ Saf. 1989;17(1):1-11.

Li DJ, Li CJ, Zhu Y. Treatment of integrated traditional and western medicine in recurrent spontaneous abortion of immune abnormality type [in Chinese]. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. 1997;17(7):390-392.

Miller AL, Kelly GS. Methionine and homocysteine metabolism and the nutritional prevention of certain birth defects and complications of pregnancy. Altern Med Rev. 1996;1(4):220-235.

Ness RB, Grisso JA, Hirschinger N, et al. Cocaine and tobacco use and the risk of spontaneous abortion. N Engl J Med. 1999;340(5):333-339.

Nygard O, Refsum H, Ueland PM, et al. Coffee consumption and plasma total homocysteine: The Hordaland Homocysteine Study. Am J Clin Nutr. 1997;65(1):136-143.

Quere I, Bellet H, Hoffet M, Janbon C, Mares P, Gris JC. A woman with five consecutive fetal deaths: case report and retrospective analysis of hyperhomocysteinemia prevalence in 100 consecutive women with recurrent miscarriages. Fertil Steril. 1998;69(1):152-154.

Rosen P, Barkin R, eds. Emergency Medicine: Concepts and Clinical Management. 4th ed. St. Louis, Mo: Mosby-Year Book; 1998.

Ryan KJ, ed. Kistner's Gynecology & Women's Health. 7th ed. St. Louis, Mo: Mosby, Inc.; 1999.

Simsek M, Naziroglu M, Simsek H, Cay M, Aksakal M, Kumru S. Blood plasma levels of lipoperoxides, glutathione peroxidase, beta carotene, vitamin A and E in women with habitual abortion. Cell Biochem Funct. 1998;16(4):227-231.

Srisuphan W, Bracken MB. Caffeine consumption during pregnancy and association with late spontaneous abortion. Am J Obstet Gynecol. 1986;154(1):14-20.

Takakuwa K, Yasuda M, Hataya I, et al. Treatment for patients with recurrent abortion with positive antiphospholipid antibodies using a traditional Chinese herbal medicine. J Perinat Med. 1996;24(5):489-494.

Wilcox AJ, Baird DD, Weinberg CR. Time of implantation of the conceptus and loss of pregnancy. N Engl J Med. 1999;340(23):1796-1799.

Windham GC, Shaw GM, Todoroff K, Swan SH. Miscarriage and use of multi-vitamins or folic acid. Am J Med Genet. 2000;90(3):261-262.

Sleep Apnea - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 15:12:00 +0000

Overview
Definition

Sleep apnea is a disorder that involves repeated episodes of upper airway occlusion and transient respiratory arrest during sleep. Types include obstructive (caused by upper airway obstruction, seen in up to 4% of adults), central (caused by CNS's failure to initiate respirations during sleep, termed "Ondine's curse"), and mixed. Apneas have significant adverse cardiovascular effects, create sleep disruptions that cause daytime exhaustion, and are associated with increased mortality.
Etiology

In obstructive apnea, the upper airway is narrowed or obstructed by blocked nasal passages, large tonsils or adenoids, large tongue, short lower jaw, or fatty tissue resulting from obesity. In central apnea, the CNS respiratory control stops working during sleep, possibly an inherited neurologic problem, acquired neuromuscular disorder, or triggered by obstructive apnea.
Risk Factors

* Obesity (67% of patients)
* Insensitive breathing reflex
* Incoordination of breathing muscles
* Male gender (three times more common among men)
* Middle age (can occur at any age, but worsens as patients grow older)
* Drugs such as alcohol, sedatives, hypnotics, short-acting beta-blockers
* Prematurity in infants
* Allergies
* Nasal obstruction

Signs and Symptoms

* Loud, irregular snoring punctuated by quiet periods when patient is not breathing for more than 10 seconds; episodes can occur up to 100 times or more per hour
* Excessive daytime sleepiness and fatigue
* Morning headaches, sore throat, dry mouth, cough
* Personality or behavior change (depression, moodiness, irritability)
* Change in alertness, memory
* Impotence
* Hypertension (in 20% to 30% of hypertensive patients)

Differential Diagnosis

* Narcolepsy
* Insomnia
* Other sleep disorder (periodic leg movement, restless leg syndrome)
* Hypothyroidism
* Temporal lobe epilepsy
* Laryngospasm

Diagnosis
Physical Examination

Daytime sleepiness and/or a partner's report of snoring usually prompt treatment. Check weight and blood pressure. May try overnight oximetry during sleep at home to evaluate O2 levels. If significant pattern of low O2 levels, refer to a sleep clinic.
Laboratory Tests

* Thyroid hormone levels for hypothyroidism
* Allergy panel
* Albumin levels for true hypocalcemia

Other Diagnostic Procedures

* Refer to otolaryngologist to rule out anatomic or inflammatory causes.
* Epworth Sleepiness Scale to evaluate degree of daytime sleepiness. (Eliminate caffeine before taking test.)
* Refer to sleep clinic.
* Portable or ambulatory monitoring. Sleep test done in home; appropriate only if symptoms are obvious and severe and patient requires urgent treatment but cannot come to sleep clinic.
* Multiple Sleep Latency Test. Performed day after all-night sleep study to assess level of daytime sleepiness and rule out other causes.
* Definitive test is polysomnography, all-night observation in a sleep clinic, where the apneic episodes can be detected.

Treatment Options
Treatment Strategy

* Lose weight.
* Decrease or eliminate use of alcohol, antihistamines, tranquilizers, and short-acting beta-blockers.
* Treat allergies and upper respiratory infections.
* Develop regular sleep habits and sleep for sufficient periods.
* Avoid supine posture; sleep sitting up or on side.
* Humidify air at night.
* Gargle with salt (without swallowing) to shrink tonsils.
* Eliminate smoking or other irritants.
* Raise the head of the bed.
* CPAP (continuous positive airway pressure) device for moderate to severe cases
* Surgery for moderate to severe cases (tonsillectomy, nasal surgery, uvulopalatopharyngoplasty)

Drug Therapies

Drugs for treating central apnea include the following.

* Acetazolamide. Results promising.
* Clomipramine. Side effects (e.g., impotence) limit use. Patient may develop tolerance in 6 to 12 months.
* Doxapram. Experimental; side effects are hyperactivity, irregular heart rhythm, increased blood pressure, nausea and diarrhea, urinary retention; not for use in those with cardiac problems.
* Aminophylline, theophylline, almitrine, naloxone, medroxyprogesterone, tryptophan. No appreciable improvement; serious side effects.
* Oxygen. Not consistently effective.

Drugs for treating obstructive apnea include the following.

* Medroxyprogesterone. Somewhat effective; side effects are fluid retention, nausea, depression, excess hair growth, breast tenderness; not for use in patients with blood-clotting disorders, liver disease, breast or genital cancer, or pregnant women.
* Protriptyline. Used rarely; side effects are decreased REM sleep, dry mouth, constipation, urinary hesitancy or frequency, impotence, confusion (elderly); not for use if arrhythmias, very high blood pressure, glaucoma, or prostate disease are present.

Surgical Procedures

Devices for treating central apnea include the following.

* Diaphragmatic pacemaker. Requires delicate surgery with risk of developing obstructive apnea and injuring phrenic nerves; not practical for most patients.
* CPAP ventilator. Keeps airway open to eliminate apneic spells; can be uncomfortable and reduce quality of sleep.
* Negative pressure ventilator (cuirass). Requires tight fit and careful adjustment of rate; can be uncomfortable and reduce quality of sleep.

Devices for treating obstructive apnea include the following.

* CPAP ventilator. Excellent results; pressure settings 5 to 20 cm H2O; side effects are discomfort or claustrophobia wearing mask, inconvenience, nasal congestion, sneezing.
* Tongue-retaining device. Pulls tongue forward; use generally limited to nonobese patients with no nasal obstruction.
* Jaw retainers. Custom-fitted to pull jaw forward; still experimental; side effects are excess saliva, exacerbation of TMJ or dental problems.
* Internal dilators or external nose strips. Available over-the-counter; effectiveness unproven.

Surgery options include the following.

* Nasal surgery. By itself not usually effective; may be needed to allow use of CPAP.
* Uvulopalatopharyngoplasty (UPPP). Smooths and removes excess tissue from soft palate and throat; effectiveness greater than 20%, with success depending on body weight control. Outpatient in healthy uncomplicated cases; one to two days in hospital for others. Risk from anesthesia; results include pain, difficulty swallowing.
* Laser-assisted uvulopalatoplasty (LAUP). Treats snoring, but leaves apnea potential.
* Maxillofacial surgery. Effectiveness not proven; risks include difficulty healing, inconvenience, added orthodontics, possible need for reoperation, effect of general anesthestic on breathing, pneumonia, difficulty swallowing, 50% to 75% failure rate in five years.

.
Complementary and Alternative Therapies

Alternative therapies may be useful in treating the allergic component of this condition. Homeopathy and nutrition could be most likely to have a positive effect. While many supplements are touted as good for weight loss, none have proved to be as effective as decreasing caloric input and increasing exercise.
Nutrition

* Diet: clinical trial of eliminating mucus-producing foods (dairy and bananas) for two weeks, reintroducing them and noticing any difference.
* Essential fatty acids (EFAs) moderate inflammatory response, decrease allergic response; EFAs are found to be low in obese individuals.
* Chromium helps regulate insulin and decrease insulin resistance; may not be effective at burning fat preferentially, but effective at stabilizing blood sugar and decreasing sugar cravings.

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

* Grindelia for sleep apnea with advanced cardiac or respiratory illness, patient starts from sleep with a sensation of suffocation
* Lachesis for sleep apnea, especially if the patient also has frequent nightmares; patient is unable to sleep on their right side, and is very loquacious
* Sambucus nigra for difficulty breathing at night; patient may actually jump up out of bed with a feeling of suffocation, especially with nasal obstruction or asthma
* Spongia tosta for patients with a sense of suffocation that may wake them, constriction, tickling or dryness of the throat, a harsh, dry cough
* Digitalis used homeopathically helps sleep apnea in persons who have a slow heartbeat that may be accompanied by palpitations, and fear of dying from heart problems
* Opium for sleep apnea with loud snoring; heavy sleep that is difficult to disturb, especially if associated with narcolepsy
* Sulphur for sleep apnea with insomnia and nightmares, especially with skin rashes that become worse with heat

Patient Monitoring

* Refer for nutritional counseling or supervised exercise program for weight loss and maintenance.
* Follow-up with sleep clinic or home health care products supplier if using CPAP device.
* Refer to psychological counseling for personality/behavioral problems.
* Suggest support group, such as AWAKE or American Sleep Apnea Association (ASAA).

Other Considerations
Prevention

Weight loss is key in preventing continuance or recurrence of obstructive apnea.
Complications/Sequelae

* Nocturnal sudden death (2,000 to 3,000/year in U.S.)
* Chronic heart enlargement or arrhythmias
* Psychological and memory problems
* Marital discord
* Pulmonary hypertension

Prognosis

With treatment, patients are able to lead normal lives. Untreated, or if treatment is discontinued, significant health issues and even premature death can result.
Pregnancy

* Nasal congestion that produces snoring is common in pregnancy but should not be confused with apnea.
* Apnea may cause fetal distress because of low oxygen supply in the blood; early recognition and treatment are required.

References

Caldwell JP. Sleep: Everything You Need to Know. Buffalo, NY: Firefly Books; 1997.

Dunkell S. Goodbye Insomnia, Hello Sleep. New York, NY: Carol Publishing Group; 1994

Lipman DS. Snoring From A to ZZZZ: Proven Cures for the Night's Worst Nuisance. Portland, Ore: Spencer Press; 1996.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993.

Pascualy RA, Soest SW. Snoring and Sleep Apnea: Personal and Family Guide to Diagnosis and Treatment. 2nd ed. New York, NY: Demos Vermande; 1996.

Smolley LA, Bruce DF. Breathe Right Now: A Comprehensive Guide to Understanding and Treating the Most Common Breathing Disorders. New York, NY: WW Norton & Co; 1998.

Skin Disorders Photodermatitis - home haelth advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 15:10:00 +0000

Overview
Definition

Photodermatitis is an abnormal response to ultraviolet radiation (UVR) that can be acute or chronic. For clinical purposes, photodermatitis is categorized into four groups:

* Idiopathic photodermatoses (e.g., polymorphic light eruption, actinic prurigo, hydroa vacciniforme, chronic actinic dermatitis, solar urticaria), in which the mechanism of photosensitization is unknown;
* Exogenous chemical or drug reactions (e.g., phototoxic reactions, photoallergic reactions), in which photosensitizers (e.g., drugs, fragrances, sunscreens) are externally applied or ingested;
* Metabolic or genetic photodermatoses (e.g., xeroderma pigmentosum, variegate porphyria, pellagra from niacin deficiency, Hartnup's disease a congenital disorder due to a defect in renal tubular absorption of amino acids and excretion of tryptophan derivatives), in which the photosensitizer is endogenously formed and deposited in the skin;
* Systemic and cutaneous diseases exacerbated by UVR (e.g., systemic lupus erythematosus, herpes simplex, acne, rosacea, eczema, pemphigus, dermatomyositis).

UVR is often classified by wavelength ranges; wavelengths ranging from 290 to 400 nm can adversely affect human skin. Categories are as follows:

* UVC is less than 290 nm and is mostly blocked by the ozone layer.
* UVB ranges from 290 to 320 nm and causes sunburn, tanning, aging, and carcinogenic changes to the skin.
* UVA (long wave UV light) ranges from 320 to 400 nm and can cause photoreactions through window glass.

UVR on earth is 90% UVA and 10% UVB. Photoreactions from UVR depend on the season or time of the year, the latitude, thickness of the ozone layer, amount of light reaching the earth, and the topography.
Etiology

More than 115 chemical agents and drugs in the United States taken systemically or applied topically may cause photodermatitis. A certain wavelength of light, usually 320 to 400 nm (UVA), induces sunburn responses and eczematous and urticarial reactions. Phototoxic reactions (nonimmunologic) result from the absorption of UVB light. Phototoxic drugs or chemicals include:

* Coal tar derivatives
* Antipsychotics (e.g., phenothiazines)
* Antimicrobials (e.g., tetracyclines, sulfonamides)
* Antidepressants (e.g., desipramine)
* Anxiolytics (e.g., alprazolam, tetrazepam)
* Antifungals (e.g., griseofulvin)
* Antimalarials (e.g., quinine)
* Thiazide diuretics
* Sulfonylureas
* Dyes (e.g., eosins, methylene blue)
* Chemotherapeutic agents (e.g., 5-fluorouracil, vinblastine)
* Psoralens
* Retinoids
* Nonsteroidal anti-inflammatory drugs (e.g., piroxicam)
* Furocoumarins (i.e., plant derivatives found in limes and celery)

Photoallergic reactions (immunologic) result from absorption of UVA light, causing a delayed hypersensitivity response. Photoallergic drugs or chemicals include fragrances (e.g., methylcoumarin, musk ambrette), sunscreens with p-aminobenzoic acid (PABA) esters, and salicylanilide-containing industrial cleaners.

Immunologic diseases such as systemic lupus erythematosus (SLE), solar urticaria, porphyria cutanea tarda, erythropoietic protoporphyria, pellagra, pemphigus, or polymorphous light eruption may induce photodermatitis or be exacerbated by UVR.
Risk Factors

* Exposure to UVR for 30 minutes to several hours; thus, outbreaks in spring and summer months are characteristic
* Exposure to UV light from 11:00 a.m. to 2:00 p.m., when 50% of the UVR is emitted
* Skin type may influence likelihood of reaction. Skin type I is fair, white; red or blond hair; green or blue eyes; most sensitive. Skin type II is white, blond or light brown hair; blue eyes; minimal tanning

Signs and Symptoms

* Pruritic papules, vesicles, bullae, or plaques
* Eczematous, lichenoid, and hyperpigmented lesions
* Localization of outbreaks to photoexposed areas
* Pain, erythema, and swelling
* Chills, headache, fever, and nausea
* Diminution of symptoms after repeated exposure (60%)

Differential Diagnosis

* Systemic lupus erythematosus (SLE)
* Benign lymphocytic infiltration of skin
* Atopic or seborrheic eczema
* Sunburn of patients with extremely fair skin or xeroderma pigmentosa
* Lymphocytoma cutis
* Sarcoidosis

Diagnosis
Physical Examination

The history and physical examination are the most important diagnostic tools for photodermatitis, particularly when focused on the time of year and duration of exposure leading to eruptions; duration, distribution, and morphology of eruptions; and age, sex, occupation, topical application, skin exposures, medication, recreational activities, and family history of the patient. A review of systems is instrumental in helping to detect an associated connective tissue disease.
Pathology/Pathophysiology

* UV-induced cell damage, caused by energy absorption leading to generation of singlet oxygen, superoxide anion radical, and other free radicals
* Perivascular infiltrate in upper dermis and middle dermis; dominated by T cells with some neutrophils
* Dermal and perivascular edema as well as endothelial swelling
* Spongiosis (intracellular edema), dyskeratosis (abnormal keratinization of keratinocytes), exocytosis (aggregation of leukocytes in epidermis), and basal cell vacuolization (formation of small spaces or vacuoles)

Laboratory Tests

Laboratory tests are used to rule out systemic illness:

* Measurement of antinuclear factor to rule out SLE
* Anti-SSA (Ro) and anti-SSB (La) antibody titers to rule out SLE
* Measurement of porphyrin concentrations of blood, urine, and stool to determine comorbid conditions such as porphyria cutanea tarda or variegate porphyria
* Histologic assessment of skin lesions

Other Diagnostic Procedures

* Immunofluorescence to rule out SLE
* Phototesting and photopatch testing to identify allergens that may exacerbate or induce photosensitivity; to test cross-reactivity of drugs and chemicals

Treatment Options
Treatment Strategy

* Identification and avoidance of the offending agent
* Measures to protect skin from sun exposure
* Cool, wet dressings for vesicular or weepy eruptions
* Desensitization with narrow band 312 nm phototherapy
* Phototherapy UV exposure of prophylactic low-dose psoralen plus UVA light (PUVA) or UVB therapy to control symptoms of polymorphous light eruption

Drug Therapies

* Immunosuppressive therapy with azathioprine (50 to 150 mg/day) for extremely photosensitive patients
* Glucocorticoids (for <1 week) to control eruptions
* Hydroxychloroquine, thalidomide, beta-carotene, and nicotinamide for patients unable to be treated with PUVA

Complementary and Alternative Therapies

Given the immunologic, inflammatory, and often recurrent nature of photodermatitis, it seems logical that certain CAM approaches or modalities would be helpful adjuncts to conventional care, particularly in reducing the frequency and severity of reactions. In fact, some promising results have been published regarding the following antioxidants and other micronutrients:

* Beta-carotene and other carotenoids (see section on Drug Therapies above)
* Fish oil and other forms of omega-3 fatty acids
* Glutathione
* Vitamin B3
* Vitamin B6
* Vitamin C
* Vitamin D
* Vitamin E

See the subsections that follow for details about each of these topics.

In addition, pellagra, one cause of photodermatoses, reflects a niacin deficiency; raising questions about the possibility of other nutrient deficiencies also contributing to photosensitivity as is seen in the case of actinic prurigo associated with protein deficiency.

Similar to some of the nutrients mentioned, green tea contains antioxidants that may also confer photoprotection. Finally, similar to medication that can predispose an individual to photoreactivity, certain herbs can have the same sensitizing effect (see section entitled Herbs).
Nutrition

Beta-carotene and Other Carotenoids

In a trial of 20 healthy subjects randomly assigned to carotenoids, primarily from beta-carotene, or carotenoids plus vitamin E, MED improved when on either carotenoids alone or in combination with vitamin E. Each group served as its own control, comparing MED before and after supplementation. Each group improved significantly from its own baseline, but the two groups did not differ significantly from one another in terms of level of MED at the end of the trial. The implication is that vitamin E did not confer benefit over and above the carotenoid supplement alone (Stahl et al. 2000).

Although beta-carotene is used standardly for treatment of certain types of photodermatitis, results of studies have not all been positive. Following baseline MED determinations, subjects were given either a single oral supplement of 120 mg beta-carotene or placebo and exposed to UV irradiation equivalent to 3xMED. The formation of sunburn cells was not significantly different between the treatment group and placebo. The authors remark that although beta-carotene has been used clinically in treating erythropoietic protoporphyria and other photosensitivity conditions, it may not protect against cutaneous photodamage in normal individuals (Garmyn et al. 1995).

Fish Oil/Omega 3

As indicated in the Overview, polymorphic light eruption (PLE) is a common form of photodermatitis. Thirteen patients with PLE received dietary supplements of fish oil for three months. Photoprovocation testing with UVB and UVA was performed and skin prostaglandin levels were measured in all 13 patients before and after completion of 3 months of supplementation. Following fish oil supplementation, the MED of UVB significantly increased and the median score for provocation of PLE by UVA significantly decreased. Recent evidence suggests an immunologic basis for PLE; modulation of skin prostaglandins with omega-3 oils may be the cause of the photoprotection seen in this trial (Rhodes et al. 1995).

Similarly, two out of three case reports of children with hydroa vacciniforme, a rare scarring photosensitivity disorder also mentioned in the Overview, suggest possible benefits of supplementation with omega-3 oils. Fish oil supplementation in the first child demonstrated clinically pronounced improvements despite sun exposure. Fewer lesions than normal appeared in summer and no new scarring occurred. A challenge with UVA radiation provoked no response following fish oil supplementation. In the second child, mild clinical improvement was observed. Vesicles still appeared, although they were of shorter duration and less prone to scarring. Provocation test was positive but fewer lesions were provoked compared to baseline. No clinical improvement was seen in the third patient (Rhodes and White 1998).

Glutathione

In an animal study, glutathione demonstrated some protection against light induced oxidation (Kamat and Devasagayam 1996). How this translates to humans is not known at this time.

Protein

Primarily seen in malnourished populations, actinic prurigo (see section entitled Overview) is hypothesized to be related to a diet deficient in protein or a specific amino acid. Patients treated with a high-protein diet have reportedly had good response for treatment of actinic prurigo, although patients tend to relapse a few weeks after returning to their standard diet (Magaña-Garcia and Magaña 1993).

Vitamin B3

In a pilot study, 42 patients with polymorphous light eruption were treated with oral nicotinamide (the biologically active form of niacin), 3 g/day for 2 weeks. Despite extensive sun exposure, 25 subjects remained lesion-free (Neumann et al. 1986). Another more recent study of rats illustrated how nicotinamide may be conferring protection. Nicotinamide, acting as an antioxidant and free radical scavenger, showed inhibition of singlet oxygen in the animal study (Kamat and Devasagayam 1996).

Vitamin B6

Two case reports describe marked reduction in erythropoietic protoporphyria associated phototoxicity by pyridoxine (vitamin B6). Two children with erythropoietic protoporphyria and significant photosensitivity were administered high doses of pyridoxine with marked reduction of symptoms. Because pyridoxal phosphate promotes the enzymatic conversion of tryptophan to nicotinic acid, the authors speculate that the effects of high-dose pyridoxine are due to enhanced nicotinamide synthesis (Ross and Moss 1990). However, pyridoxine hydrochloride has also been implicated in photoallergic drug eruptions, although such cases seem very rare. Three case reports describe discrete episodes of photoallergic dermatitis following injection or oral administration of pyridoxine hydrochloride, which resolved upon withdrawal of the substance (Murata et al. 1998; Tanaka et al. 1996).

Vitamin D

Mice pretreated either systemically or topically with 1,25-dihydroxyvitamin D3 showed significant dose-dependent protection against UVB-induced damage. Rat keratinocytes treated with 1,25-dihydroxyvitamin D3 showed increased survival rates compared to controls. The authors suggest that the efficacy of low-dose vitamin D3 against UVB-induced cytotoxicity is indicative of a natural defense system whereby derivatives of photochemically produced vitamin D3 promote the synthesis of endogenous metallothionein (MT, a cysteine-rich antioxidant protein found in epidermal cells) (Hanada et al. 1995). It is not clear if this information will translate to humans and how it will do so. Future research should be conducted regarding photoprotection of vitamin D supplementation in humans.

Vitamins C and E

Given the connection between formation of free radicals and damage to the skin (see section entitled Pathology/Pathophysiology), reactive oxygen scavengers (such as the antioxidant vitamins C and E) may be employed to reduce UV-induced skin reactions. In a double-blind, placebo-controlled study, 20 subjects were randomized to take either 2 g ascorbic acid and 1,000 IU of d-alpha-tocopherol or placebo for 8 days. The treatment and control groups had equivalent minimal erythema dose (MED) at baseline. At the end of 8 days of supplementation, the vitamin group showed an increased MED (indicating less photosensitivity) in 80% of the subjects compared to no change in the placebo group (Eberlein-König et al. 1998).

The possible synergistic effects of vitamins C and E were examined further in a randomized, placebo-controlled study of 40 subjects with skin type II (see section entitled Risk Factors for definition) taking either 2 g (3,000 IU) per day of d-alpha-tocopherol (group 1), 3 g per day of ascorbic acid (group 2), 2 g (3,000) per day of d-alpha-tocopherol combined with 3 g per day of ascorbic acid (group 3), or placebo (group 4) for 50 days. Only group 3 showed statistically significant increases in MEDs after supplementation. These results suggest that vitamins C and E may have synergistic protective effects, although supplementation only achieved a sun protection factor (SPF) of approximately 2 (Fuchs and Kern 1998).

Treatment with vitamin E may also be beneficial in cases of actinic prurigo (see section entitled Overview). A comparison study of patients treated for six months with either 100 IU daily of vitamin E or 500 mg tid of tetracycline showed similar results; tetracycline is thought to be beneficial in this condition because of its suppression of oxygen radical activity. Two groups of eight patients were observed under treatment. Efficacy was analyzed for cheilitis, papules, infiltrates, plaques, lichenification, and pruritus, the primary signs and symptoms of actinic prurigo. Although cheilitis, infiltrates, and plaques did not show significant changes throughout the study, lichenification and pruritus demonstrated remarkable improvement in both the vitamin E and tetracycline groups (Durán et al. 1996).
Herbs

* Green Tea Antioxidant properties in green tea may provide protection against UV-light induced erythema. Epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent of green tea (Camellia sinensis), has demonstrated photoprotection in previous animal models. In a human study, volunteers were subjected to UVB radiation equal to a 4 MED dose, delivered to buttock skin with or without topical EGCG applied 30 minutes before exposure. Skin punch biopsies were obtained from the treated areas and nontreated control areas and evaluated for myeloperoxidase and cyclooxygenase activities. While EGCG does not block UVB absorption, it appears to act indirectly. In this study, EGCG significantly inhibited erythema formation and myeloperoxidase and cyclooxygenase activities; it also protected against leukocyte infiltration, prostaglandin metabolite formation, and cellular oxidative damage (Katiyar et al. 1999).
* St. John's wort (Hypericum perforatum) is known to exhibit phototoxic properties when large amounts are ingested or when combined with photosensitizing drugs.

In addition to St. John's wort, other possible photosensitizing herbs include:

* Angelica seed and root (Angelica archangelica) (Blumenthal et al. 1998)
* Celery stems (Apium graveolens) (Newall et al. 1996)
* Rue (Rutae folium) (Blumenthal et al. 1998)
* Lime oil/peel ( Citrus aurantifolia) (Leung and Foster 1996)

Homeopathy

Anecdotal reports suggest that individualized homeopathic remedies may be a useful adjunct to the prevention and treatment of photodermatitis; however, potential benefits in this area have not yet been subjected to scientific inquiry.
Patient Monitoring

Patients who require steroids for photosensitivity reactions must be monitored closely. In addition, anyone with a history of photodermatitis or photoreactivity should monitor frequency and duration of eruptions. This information can help determine etiology and treatment.
Other Considerations
Prevention

* Limit skin exposure especially at peak ultraviolet intensity.
* Use broad-spectrum sunscreens, especially against UVA, with a sun protection factor (SPF) of 30 to 50.
* Cover up with long-sleeved shirts, long pants, and wide-brimmed hats.
* Discontinue use of the photosensitizing drug or agent.

Complications/Sequelae

* Persistence of photosensitivity, resulting in chronic actinic dermatitis
* Postinflammatory hyperpigmentation
* Premature aging of the skin
* Squamous cell and basal cell carcinomas
* Increased UV exposure after PUVA and UVB phototherapy
* Melanoma

Prognosis

Most photosensitivity reactions are benign and self-limited; however, symptoms can be severe when associated with a systemic disorder or when the exposure has been severe. Some photosensitivity reactions can continue for years after exposure has discontinued.
References

Abramowitz AI, Resnik KS, Cohen KR. Margarita photodermatitis [letter]. N Engl J Med. 1993;328(12):891.

Adamski H, Benkalfate L, Delaval Y, et al. Photodermatitis from non-steroidal anti-inflammatory drugs. Contact Dermatitis. 1998;38(3):171-174.

American Academy of Pediatrics. Ultraviolet light: a hazard to children. Pediatrics. 1999;104(2):328-333.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines.Boston, Mass: Integrative Medicine Communications; 1998:35-36; 214-215; 245-249.

Callen JP. Photodermatitis in a 6-year-old child. Arthritis Rheum. 1993;36(10):1483-1485.

Darr D, Dunston S, Faust H, Pinnell S. Effectiveness of antioxidants (vitamin C and E) with and without sunscreens as topical photoprotectants. Acta Derm Venereol (Stockh). 1996;76(4):264-268.

Durán MM, Ordoñez CP, Prieto JC, Bernal J. Treatment of actinic prurigo in Chimila Indians. Int J Dermatol. 1996;35(6):413-416.

Eberlein-König B, Placzek M, Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin E). J Am Acad Dermatol. 1998;38(1):45-48.

Enta T. Dermacase. Contact photodermatitis. Can Fam Physician. 1995;41:577, 586-587.

Enta T. Dermacase. Photodermatitis reaction to chlorothiazide. Can Fam Physician. 1994;40:1269, 1276.

Fernandez de Corres L, Diez JM, Audicana M. Photodermatitis from plant derivatives in topical and oral medicaments. Contact Dermatitis. 1996;35(3):184-185.

Freedberg IM, Eisen AZ, Wolff K. Fitzpatrick's Dermatology in General Medicine. Vol. 1. 5th ed. New York, NY: McGraw-Hill; 1996:1573-1586.

Fuchs J, Kern H. Modulation of UV-light-induced skin inflammation by D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated radiation. Free Radic Biol Med. 1998;25(9):1006-1012.

Garmyn M, Ribaya-Mercado JD, Russell RM, Bhawan J, Gilchrest BA. Effect of beta-carotene supplementation on the human sunburn reaction. Exp Dermatol. 1995;4(2):104-111.

Goldman L, Bennett JC. Cecil Textbook of Medicine. 21st ed. Philadelphia, Pa: W.B. Saunders; 2000:2295-2296.

Hadshiew I, Stäb F, Untiedt S, Bohnsack K, Rippke F, Hölzle E. Effects of topically applied antioxidants in experimentally provoked polymorphous light eruption. Dermatology. 1997;195(4):362-368.

Hanada K, Sawamura D, Nakano H, Hashimoto I. Possible role of 1,25-dihydroxyvitamin D3-induced metallothionein in photoprotection against UVB injury in mouse skin and cultured rat keratinocytes. J Dermatol Sci. 1995;9(3):203-208.

Kamat JP, Devasagayam TP. Methylene blue plus light-induced lipid peroxidation in rat liver microsomes: inhibition by nicotinamide (vitamin B3) and other antioxidants. Chem Biol Interact. 1996;99(1-3):1-16.

Katiyar SK, Matsui MS, Elmets CA, Mukhtar H. Polyphenolic antioxidant (-)-epigallocatechin-3-gallate from green tea reduces UVB-induced inflammatory responses and infiltration of leukocytes in human skin. Photochem Photobiol. 1999;69(2):148-153.

Leroy D, Dompmartin A, Szczurko C, Michel M, Louvet S. Photodermatitis from ketoprofen with cross-reactivity to fenofibrate and benzophenones. Photodermatol Photoimmunol Photomed. 1997;13(3):93-97.

Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: Wiley and Sons; 1996.

Magaña-Garcia M, Magaña M. Actinic prurigo. The possible etiologic role of an amino acid in the diet. Med Hypotheses. 1993;41(1):52-54.

Moschella SL, Hurley HJ. Dermatology. 3rd ed. Philadelphia, Pa: W.B. Saunders; 1992:507-530.

Murata Y, Kumano K, Ueda T, Araki N, Nakamura T, Tani M. Photosensitive dermatitis caused by pyridoxine hydrochloride. J Am Acad Dermatol. 1998;39(2 pt 2):314-317.

Neumann R, Rappold E, Pohl-Markl H. Treatment of polymorphous light eruption with nicotinamide: a pilot study. Br J Dermatol. 1986;115(1):77-80.

Newall CA, Anderson LA, Phillipson JD. Herbal Medicine: A Guide for Health-care Professionals. London: The Pharmaceutical Press; 1996.

Pigatto PD, Legori A, Bigardi AS, et al. Multicenter study of allergic contact photodermatitis: epidemiological aspects. Am J Contact Dermat. 1996;7(3):158-163.

Quinones D, Sanchez I, Alonso S, et al. Photodermatitis from tetrazepam. Contact Dermatitis. 1998;39(2):84.

Rhodes LE, Durham BH, Fraser WD, Friedmann PS. Dietary fish oil reduces basal and ultraviolet B-generated PGE2 levels in skin and increases the threshold to provocation of polymorphic light eruption. J Invest Dermatol. 1995;105(4):532-535.

Rhodes LE, White SI. Dietary fish oil as a photoprotective agent in hydroa vacciniforme. Br J Dermatol. 1998;138(1):173-178.

Ross JB, Moss MA. Relief of the photosensitivity of erythropoietic protoporphyria by pyridoxine. J Am Acad Dermatol. 1990;22(2 pt 2):340-342.

Scholzen TE, Brzoska T, Kalden DH, et al. Effect of ultraviolet light on the release of neuropeptides and neuroendocrine hormones in the skin: mediators of photodermatitis and cutaneous inflammation. J Investig Dermatol Symp Proc. 1999;4(1):55-60.

Stahl W, Heinrich U, Jungmann H, Sies H, Tronnier H. Carotenoids and carotenoids plus vitamin E protect against ultraviolet light-induced erythema in humans. Am J Clin Nutr. 2000;71(3):795-798.

Tanaka M, Niizeki H, Shimizu S, Miyakawa S. Photoallergic drug eruption due to pyridoxine hydrochloride. J Dermatol. 1996;23(10):708-709.

Tierney LM, McPhee SJ, Papadakis MA. Current Medical Diagnosis and Treatment 2000. New York, NY: Lange Medical Books/McGraw-Hill; 2000:177-178

Skin Disorders Erythema - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 15:02:00 +0000

Overview
Definition

Erythema is defined as redness of the skin, resulting from congestion of the capillaries. There are many causes and manifestations of erythema; some examples include photosensitivity, erythema multiforme and erythema nodosum. Erythema multiforme is a an acute inflammatory eruption of the skin and/or mucosal membranes. Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) have been historically considered severe forms of erythema multiforme, although some people view them as separate but related conditions. Erythema nodosum (also called subacute migratory panniculitis) is a nodular erythematous eruption that is typically limited to the extremities. The following sections address background and treatment information about erythema multiforme and erythema nodosum; the complementary and alternative therapies section also covers approach for adjunctive treatment of erythema in general, particularly photosensitivity.
Etiology

Erythema multiforme

* Idiopathic 50% of cases
* Infectious primarily herpes simplex virus (HSV) and mycoplasma pneumonia, but numerous others (e.g., Epstein-Barr virus, hepatitis B, influenza A, Salmonella, Streptococcus pyogenes, Trichomonas vaginalis)
* Drugs including sulfonamides, anticonvulsants, penicillin, poliomyelitis vaccine, 5-fluorouracil
* Radiation therapy
* Malignancies
* Serum sickness
* Erythema infectiosum (fifth disease) human parvovirus B19
* Chemicals

Erythema nodosum

* Idiopathic 50% of cases
* Tuberculosis
* Streptococcal infection
* Sarcoidosis
* Systemic lupus erythematosus (SLE)
* Ulcerative colitis
* Pregnancy
* Drugs especially oral contraceptives, sulfonamides, bromides
* HSV
* Leprosy (usually after initiation of antimicrobial therapy)

Risk Factors

Erythema multiforme

* Previous history
* Males at greater risk than females
* Sun exposure

Erythema nodosum

* Familial
* Females at greater risk than males

Signs and Symptoms

Erythema multiforme

* Prodromal symptoms malaise, fever, sore throat, cough, and itching or burning at impending site
* Sudden onset
* Target lesions and papules central erythema surrounded by normal skin, which is surrounded by erythematous ring; central portion dusky red, 1 to 3 cm circumference, may become cyanotic, purpuric, or vesicular; heal without scarring; hyperpigmentation or hypopigmentation common
* Knees, elbows, palms, soles; oral lesions appear in 25% of cases; trunk in severe cases
* Lesions recur in crops
* Erythema infectiosum facial "slapped cheek" rash; reticulated rash (upper extremities) lasting about 2 weeks
* SJS upper respiratory infection; flat atypical targets on trunk; mucosal involvement (oral blisters, conjunctivitis, nares, anorectal junction, vulvovaginal region); hacking cough; fever
* TEN initial SJS-type symptoms progress to generalized detachment of the epidermis; sepsis, fluid loss; death

Erythema nodosum

* Prodromal symptoms fatigue, malaise, upper respiratory infection; low-grade fever, flu-like symptoms
* Tender nodules 2 to 6 cm in diameter; resolve without scarring or joint damage
* Lesions change from red, hard, and painful to fluctuant and bluish, fading to yellowish or brown
* Arthralgias
* Arthritis
* Typically in crops, may be solitary
* Shins, forearms, thighs, trunk
* Leprosy severe and systemic

Differential Diagnosis

Erythema multiforme

* Kawasaki disease
* Behcet's syndrome
* Urticaria
* HSV
* Stomatitis

Erythema nodosum

* Nodular nonsuppurative panniculitis (Weber-Christian disease)
* Thrombophlebitis
* Erysipelas
* Cellulitis
* Arteriosclerosis obliterans

Diagnosis
Physical Examination

Clinical appearance helps to identify the type of erythema. Physical examination may identify underlying disease. A thorough history can reveal agents.
Laboratory Tests

Erythema multiforme

* Skin biopsy may reveal HSV-specific DNA
* Immunoglobulin (IgM) antibody to B19 fifth disease
* Immunofluorescence SJS
* Test for lymphopenia TEN

Erythema nodosum

* Elevated erythrocyte sedimentation rate
* Mild leukocytosis
* For differential diagnosis: throat culture, stool culture, tuberculin skin test

Pathology/Pathophysiology

Erythema multiforme

* Circulating immune complexes and mononuclear and T lymphocyte-rich cell infiltrates around upper dermal blood vessels
* Increased expression of intracellular adhesion molecule 1 (ICAM-1)
* TEN keratinocyte necrosis

Erythema nodosum

* Lymphohistiocytic infiltrate
* Granulomatous inflammation
* Fibrosis in the septa of subcutaneous fat

Imaging

X ray bilateral hilar adenopathy with erythema nodosum, related to a particular disease or may be nonspecific reaction
Other Diagnostic Procedures

* Excisional biopsy

Treatment Options
Treatment Strategy

Underlying disease is treated and causative drugs stopped. Measures to control symptoms are instigated. While mild cases need not be treated, bed rest and medication are used for moderate or severe cases.
Drug Therapies

Erythema multiforme

* Prednisone high dose for 1 to 3 weeks until controlled, then taper quickly; prevents recurrence; use is controversial
* Acyclovir (400 mg bid for 6 months) continual use prevents HSV-related lesions
* Valacyclovir (500 mg/day) or famciclovir (250 mg bid) newer antiviral agents
* Azathioprine (100 to 150 mg/day) anecdotal reports of efficacy; however, recurs upon discontinuation
* Thalidomide (100 mg/day, then titrate to effective level) for refractory cases; severely teratogenic
* Levamisole hydrochloride (150 mg/day for 3 days) for oral lesions
* Antihistamines control pruritus
* Burrow's compresses for cutaneous blisters
* Analgesics preferably not NSAIDs
* Topical steroids for papules and plaques
* Antibiotics for secondary infection, avoiding drugs associated with erythema
* Human intravenous immunoglobulin promising experimental treatment for SJS and TEN

Erythema nodosum

* Intralesional triamcinolone acetonide (2.5 to 5 mg/mL) for symptom relief
* Corticosteroids reduces symptoms; masks underlying disease; recurs on discontinuation
* Antibiotics for underlying infections
* Thalidomide (200 mg bid for 2 to 3 days, then reduce) for leprosy; severely teratogenic

Complementary and Alternative Therapies

Treatment of any type of erythema is dependent upon the underlying cause. Certain CAM therapies may:

* Reduce inflammation
* Support the immune system
* Help prevent secondary infections

Antioxidant compounds, for example, have demonstrated protective effects for the skin against ultraviolet-induced damage in clinical trials. Therefore, the question raised is whether antioxidants may confer protection to the skin from other sources of damage. In addition, because sun exposure is one of the risk factors for erythema multiforme, photoprotective antioxidants may, theoretically, confer some protection against this disease process.
Nutrition

According to scientific studies, dietary supplementation or topical administration of antioxidants provides some protection against damage to the skin, such as that which ultraviolet radiation may cause. The mechanism of action is not entirely understood but antioxidants are scavengers of ROS (reactive oxygen species). ROS and oxygen-derived free radicals cause damage to the skin by depleting it of important protective antioxidants. These reactive substances also interact with lipids, proteins, and other biomolecules and, in the process, make the skin tissue more susceptible to damage (Dreher et al. 1998).

The studies described in the following subsections suggest that supplementation with antioxidants may provide at least modest photoprotective benefit when used prior to exposure. It is not clear from the data whether topical or oral antioxidants confer protection to the skin from other types of damage leading to erythema multiforme, erythema nodosum, or other forms of erythema; such protection, though, seems plausible. Supplements with antioxidant properties that have been investigated include:

* Carotenoids
* Vitamin C
* Vitamin E
* Melatonin
* Zinc

Caution should be exercised when considering supplementation with megadoses of vitamins. Although they may provide photoprotection, the impact of long term supplementation is unknown. In addition, the results are not yet conclusive and more research is needed.

Carotenoids

Carotenoids are highly effective natural scavengers of ROS. Several small studies have investigated whether carotenoids help to protect against UV-light-induced erythema and have reported positive results. In one study, for example, twenty healthy subjects, ages 20 to 57, were randomly assigned to two groups:

* Group one received 25 mg of carotenoids (primarily beta-carotene) daily for 12 weeks
* Group two received the same oral carotenoid supplementation together with 500 IU alpha-tocopherol (vitamin E)

Subjects were categorized by skin type:

* Type I (fair, white skin; red or blonde hair; green or blue eyes; extremely sensitive to sun exposure; absence of tanning)
* Type II (white skin, blonde or light brown hair, blue eyes; sensitive to sun exposure; and minimal tanning).

In both groups, participants' unprotected skin response prior to supplementation was used as the control. Both groups experienced greater protection against erythema formation during supplementation, as indicated by higher MED (minimal erythema dose) levels than baseline values. Group two showed less erythema formation than group one, indicating a possible additional protection from vitamin E, although this difference was not statistically significant (Stahl et al. 2000).

Vitamins C and E

A few small studies suggest that vitamins C and E, taken in combination, may have photoprotective properties. In one double-blind, placebo-controlled study, for example, 10 subjects took the following for eight days:

* Ascorbic acid 2 g
* d-alpha-tocopherol 1,000 IU

MEDs were assessed before and after the trial. In the vitamin group, MED level increased in eight subjects following eight days compared to no change in the placebo group (Eberlein-König et al. 1998).

These synergistic effects were further examined in a prospective, randomized, placebo-controlled study of 40 healthy volunteers. Results showed that oral supplementation with megadoses of vitamins C and E (3 grams and almost 3,000 IU respectively), in combination, achieved greater photoprotective effects than supplementation with either vitamin alone (Fuchs and Kern 1998). As stated earlier, though, caution must be exercised when using megadoses of vitamins because of lack of knowledge regarding long term safety.

Melatonin

A small scale study suggests that topical melatonin may confer added photoprotection when combined with both vitamin C and vitamin E in topical form (Dreher et al. 1998). In this study by Dreher et al (1998), significant differences were also seen when vitamin E was combined with either melatonin or vitamin C. Even melatonin alone achieved significant dose-dependent effects compared to placebo. Vitamin C or vitamin E alone, however, demonstrated only modest to no effect.

Given the size of the melatonin, vitamin C and vitamin E studies to date, more research is required before drawing conclusions about efficacy or even safety of these substances for skin protection from the sun or other damaging processes.

If there are benefits to topical antioxidants in protecting against sun damage to the skin, it seems that these free radical scavengers should be used prophylactically rather than as treatment. Six volunteers applied topical vitamin C, vitamin E, melatonin, or placebo cream alone or in combination following UV-light irradiation. (An unexposed and untreated skin area served as a negative control for each subject.) Significant reductions in erythema response were not observed with single antioxidants or combinations, nor with single or multiple applications. The authors concluded that the benefits of topical antioxidants in erythema suppression appear to be limited to preparations applied prior to, not following, UV exposure. The authors suggest that oxidative skin damage is a rapid event and that antioxidants can help prevent such damage only when present in UV-exposed skin prior to and during exposure (Dreher et al. 1999).

Zinc Sulfate

A review article describes seven known cases of necrolytic acral erythema (NAE; a condition akin to TEN as described earlier) and adds an eighth case. Dosages of oral zinc sulfate (60 to 440 mg/day), administered alone or in combination with interferon, were reported to be effective for five of the eight patients (Sinclair and Reynolds 1997).

Flavonoids

In theory, flavonoids confer a benefit for erythematous skin conditions such as erythema multiforme and erythema nodosum because they act as anti-inflammatories and strengthen connective tissue. Examples include (Murray 1996):

* Quercetin 200 to 400 mg tid 20 minutes prior to meals
* Rutin 50 to 250 mg bid to tid
* Hesperidin 250 mg bid to tid

Herbs

Green Tea

Antioxidant properties in green tea may provide protection against UV-light-induced erythema. Epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent of green tea (Camellia sinensis), has demonstrated photoprotection in previous animal models. In a human study, volunteers were subjected to UVB radiation equal to a 4 MED dose, delivered to buttock skin with or without topical EGCG applied 30 minutes before exposure. Skin punch biopsies were obtained from the treated areas and nontreated control areas. EGCG significantly (Katiyar et al. 1999):

* Inhibited erythema formation
* Reduced myeloperoxidase and cyclooxygenase
* Protected against leukocyte infiltration
* Diminished prostaglandin metabolite formation
* Reduced cellular oxidative damage

Other Herbs

Although not studied scientifically, herbs used traditionally to promote dermal healing, stimulate lymphatic circulation, and possibly help treat the underlying cause include the following examples:

* Burdock root (Arctium lappa) can be used topically for skin inflammation and wound healing (Blumenthal et al. 2000)
* Goldenseal (Hydrastis canadensis) for an infectious etiology
* Lemon balm (Melissa officinalis) cream or wash can be applied to HSV lesions (which may cause erythema multiforme see section entitled Etiology) (Blumenthal et al. 2000).
* Licorice root (Glycyrrhiza glabra) in the case of a virus; contraindicated with hypertension (Blumenthal et al. 2000)
* Meadowsweet (Filipendula ulmaria) for pain, particularly arthralgias (as may be seen with erythema nodosum) (Blumenthal et al. 2000)
* Milk thistle (Silybum marianum) for a chemical etiology (Blumenthal et al. 2000)
* Slippery elm (Ulmus fulva) may be combined with goldenseal root and applied topically for treatment of an open wound (Blumenthal et al. 2000)
* Yarrow (Achillea millefolium) can be used topically for skin inflammation and wound healing (Blumenthal et al. 2000)

Homeopathy

Independent studies published by two groups of researchers have demonstrated positive photoprotective effects of homeopathic treatment with Apis in albino guinea pigs subjected to radiation. Although neither of these studies was methodologically rigorous, both reported positive results (Vickers 1999).

Additional remedies commonly used in clinical practice for skin conditions include:

* Chininum sulphuricum
* Rhus toxicodendron -- used in the case of blisters and vesicles accompanied by intense itching that worsens at night and improves with the application of heat; the appropriate patient is generally restless and unable to get comfortable at night

Massage

Should be avoided in the case of acute erythematous skin conditions
Patient Monitoring

Erythema multiforme

* Burn unit preferred when 20% of body affected
* Monitor fluid and electrolyte abnormalities, protein loss, organ damage

Other Considerations
Prevention

* Treat underlying disease
* Avoid known triggers
* Acyclovir with HSV

Complications/Sequelae

* SJS may lead to blindness
* TEN may lead to death (see Prognosis section below)
* Erythema nodosum pulmonary hilar adenopathy

Prognosis

Erythema multiforme

* Episodes generally resolve in 4 to 6 weeks

SJS and TEN

* SJS generally resolves in 1 month without complication; 10% mortality with extensive disease
* TEN 34% to 40% overall mortality; 25% to 100% with full-thickness epidermal loss
* Prompt withdrawal of causative drug decreases mortality

Erythema nodosum

* Recurs for months; may persist for 2 years

Pregnancy

* Thalidomide severely teratogenic
* Precipitating factor with erythema nodosum
* Erythema infectiosum can lead to fetal infection, causing fetal anemia, heart failure, fetal hydrops, death

References

Beers MH, Berkow R, eds. The Merck Manual of Diagnosis and Therapy. 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999.

Blumenthal M, Goldberg A, Brinckmann J, eds. Herbal Medicine: Expanded Commission E Monographs. Newton, Mass: Integrative Medicine Communications; 2000:230-239, 253-263, 419-423.

Dambro MR. Griffith's 5 Minute Clinical Consult. Baltimore, Md: Lippincott Williams & Wilkins, Inc.; 1999.

Dreher F, Denig N, Gabard B, Schwindt DA, Maibach HI. Effect of topical antioxidants on UV-induced erythema formation when administered after exposure. Dermatology. 1999;198(1):52-55.

Dreher F, Gabard B, Schwindt DA, Maibach HI. Topical melatonin in combination with vitamins E and C protects skin from ultraviolet-induced erythema: a human study in vivo. Br J Dermatol. 1998;139(2):332-339.

Eberlein-König B, Placzek M, Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol. J Am Acad Dermatol. 1998;38(1):45-48.

Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998.

Fuchs J, Kern H. Modulation of UV-light-induced skin inflammation by D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated radiation. Free Radic Biol Med. 1998;25(9):1006-1012.

Garcia-Doval I, LeCleach L, Bocquet H, Otero XL, Roujeau JC. Toxic epidermal necrolysis and Stevens-Johnson syndrome: does early withdrawal of causative drugs decrease the risk of death? Arch Dermatol. 2000;136(3):323-327.

Garcia-Porrua C, Gonzalez-Gay MA, Vazquez-Caruncho M, et al. Erythema nodosum: etiologic and predictive factors in a defined population. Arthritis Rheum. 2000;43(3):584-592.

Habif TP. Clinical Dermatology. 3rd ed. St. Louis, Mo: Mosby-Year Book; 1996.

Halliday GM, Yuen KS, Bestak R, Barnetson RS. Sunscreens and vitamin E provide some protection to the skin immune system from solar-simulated UV radiation. Australas J Dermatol. 1998;39(2):71-75.

Katiyar SK, Matsui MS, Elmets CA, Mukhtar H. Polyphenolic antioxidant (-)-epigallocatechin-3-gallate from green tea reduces UVB-induced inflammatory responses and infiltration of leukocytes in human skin. Photochem Photobiol. 1999;69(2):148-153.

Khanna VJ, Shieh S, Benjamin J, et al. Necrolytic acral erythema associated with hepatitis C: effective treatment with interferon alfa and zinc. Arch Dermatol. 2000;136(6):755-757.

Lee J, Jiang S, Levine N, Watson RR. Carotenoid supplementation reduces erythema in human skin after simulated solar radiation exposure. Proc Soc Exp Biol Med. 2000;223(2):170-174.

Lo SK, Yip D, Leslie M, Harper P. 5-flourouracil-induced erythema multiforme. Int J Clin Pract. 1999;53(3):219-221.

Mandell GL, Bennett JE, Dolin R, eds. Principles and Practices of Infectious Diseases. 5th ed. Philadelphia, Pa: Churchill Livingstone, Inc.; 2000.

Martinez AE, Atherton DJ. High-dose systemic corticosteroids can arrest recurrences of severe mucocutaneous erythema multiforme. Pediatr Dermatol. 2000;17(2):87-90.

Murray M. Encyclopedia of Nutritional Supplements. Rocklin, Calif: Prima Publishing; 1996:320-335.

Rakel RE, ed. Conn's Current Therapy. 51st ed. Philadelphia, Pa: W.B. Saunders; 1999.

Sinclair SA, Reynolds NJ. Necrolytic migratory erythema and zinc deficiency. Br J Dermatol. 1997;136(5):783-785.

Stahl W, Heinrich U, Jungmann H, Sies H, Tronnier H. Carotenoids and carotenoids plus vitamin E protect against ultraviolet light-induced erythema in humans. Am J Clin Nutr. 2000;71(3):795-798.

Stern RS. Improving the outcome of patients with toxic epidermal necrolysis and Stevens-Johnson syndrome. Arch Dermatol. 2000;136(3):410-411.

Vickers AJ. Independent replication of pre-clinical research in homoeopathy: a systematic review. Forsch Komplementarmed. 1999;6(6):311-320.

Sinusitis - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 14:56:00 +0000

Overview
Definition

Sinusitis is an inflammation and infection of the paranasal sinuses that causes impaired sinus mucociliary clearance. It affects approximately 31 million adults and children in the United States. Sinusitis has many similar characteristics to rhinitis, and can also be called rhinosinusitis.
Etiology

Sinusitis is most often caused by an upper respiratory tract infection or through bacterial infection (Streptococcus pneumoniae, Haemophilus influenzae, or by fungal or viral entities). This is followed by allergic rhinitis, dental infection or manipulation, and trauma to the sinuses. Disease of the anterior ethmoid-middle meatal complex (ostiomeatal complex) is the most frequent local cause of chronic sinusitis.
Risk Factors

* Upper respiratory infections
* Allergic rhinitis
* Immunodeficiency, Kartagener's syndrome, and cystic fibrosis
* Nosocomial sinusitis from foreign nasal bodies
* Nasal polyps, nasal septal deviation, and spurs
* Anatomic abnormalities that narrow the ostiomeatal channels
* Cold air, cigarette smoke, decongestants, and metal vapors

Signs and Symptoms

* Inflammation and edema of nasal mucosa, purulent sinonasal secretion (yellow or green), or postnasal drip
* Headache, pain, sinus tenderness, or toothache
* Cough or pharyngitis
* Fever, in half of patients
* Loss of smell
* General malaise

Differential Diagnosis

* Upper respiratory tract infection (common cold)
* Tension and vascular headaches
* Meningitis
* Brain and epidural abscesses
* Viral, allergic, or vasomotor rhinitis
* Tumors or cysts

Diagnosis
Physical Examination

Physical findings may include tenderness, purulent sinonasal obstruction and secretion, and postnasal drip. Look for three of the following findings: maxillary toothache, colored nasal discharge, poor response to nasal decongestants, abnormal sinus transillumination, purulent secretions
Laboratory Tests

* Culture and biopsy for chronic and fungal sinusitis
* Microscopic examination shows sheets of polymorphonuclear neutrophils as well as bacteria
* Skin test to determine underlying allergy
* Blood test to reveal immunoglobulin serum levels and antibody response to specific antigens (i.e., allergies)
* Nasopharyngeal culture

Pathology/Pathophysiology

* Bacterial titers exceeding 1,000 CFU per ml, primarily S. pneumoniae, H. influenzae, and Branhamella (Moraxellla) catarrhalis for acute sinusitis
* Anaerobes of the Bacteroides, Fusobacterium, Streptococcus, Veillonella, and Corynebacterium species as well as anaerobic gram-positive cocci for chronic sinusitis (some studies show this to be inaccurate with anaerobes found in as few as 7.6% of cases)
* Gram-negative bacteria, such as Pseudomonas aeruginosa, Klebsiella pneumoniae, and Enterobacter species for nosocomial sinusitis
* Normal ciliated epithelium replaced by stratified squamous epithelium in chronic sinusitis
* Goblet cell hyperplasia, mononuclear cell infiltration, and basement membrane thickening
* Edema, inflammation, and thickened mucosa

Imaging

* Computed tomography (CT) shows the ostiomeatal complex as well as other sinuses; evaluates disease, anatomic obstructions, fine bony structure, and soft-tissue complications; diagnoses fungal sinusitis
* Conventional sinus radiograph diagnoses maxillary and frontal sinus disease; poor for ostiomeatal complex
* Flexible fiberoptic rhinoscopy reveals purulent drainage in sinus ostia
* Transillumination maxillary and frontal sinuses; often inaccurate

Other Diagnostic Procedures

* Endoscopy exam differentiates between purulence and allergic mucosal thickening; reveals ostiomeatal disease
* Irrigation of the maxillary antrum distinguishes between purulence and allergic mucosal thickening; identifies tumors

Treatment Options
Treatment Strategy

Nonsurgical treatment includes antibiotics, decongestants, avoiding allergens, steam or mist inhalation for drainage and symptom relief, and hydration to thin secretions. Surgical treatment for restoration of ventilation and mucociliary functioning is attempted when nonsurgical measures have failed.
Drug Therapies

* Antibiotics For first cases of sinusitis, amoxicillin (500 mg tid) is generally used. With penicillin resistance and treatment failure, use broad-spectrum antibiotics such as cefuroxime (Ceftin, 250 to 500 mg bid), cefaclor (Ceclor, 500 mg bid), amoxicillin/clavulanic acid (Augmentin, 500 mg bid), clarithromycin (Biaxin, 250 to 500 mg bid), or an azithromycin (Zithromax) pack for patients allergic to penicillins. Antibiotics are taken for 10 to 14 days in acute cases and for up to six weeks in chronic cases.
* Decongestants Oral decongestants, such as pseudoephedrine (60 mg tid to qid), cause urinary retention in older male patients; monitor their use with hypertensive patients. Nasal sprays, such as oxymetazoline (Afrin, tid), should be used for three to five days only; there is a risk of tachyphylaxis and rebound if used longer.
* Nasal steroid spray for allergic/chronic sinusitis (e.g., triamcinolone)

Surgical therapies include functional endoscopic surgery (FESS) to remove diseased tissue (reduced comorbidity and damage to normal anatomy compared to external surgery); external surgery for osteomyelitis, orbital or intracranial complications, and failure of FESS
Complementary and Alternative Therapies

A combination of physical medicine and herbal or homeopathic treatment is often effective for treating both acute and chronic rhinosinusitis.
Nutrition

* Vitamin C (1,000 mg tid), zinc (30 to 60 mg/day ), beta-carotene (15,000 IU/day) to support immunity.
* Bromelain (500 mg tid between meals) and quercetin (500 mg tid between meals) are anti-inflammatory
* Avoid mucus-producing foods, such as dairy products, bananas and any known allergens. Drink plenty of fluids. Decrease sugar intake.

Herbs

Ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

* Wild indigo (Baptisia tinctoria) specific for upper respiratory and sinus infections, increases phagocytosis
* Eyebright (Euphrasia officinalis) anticatarrhal, specific for sinus
* Licorice (Glycyrrhiza glabra) antiviral, soothing, especially with exhaustion and/or heartburn; avoid with hypertension
* Coneflower (Echinacea purpurea) stimulates the immune system
* Goldenseal (Hydrastis canadensis) antiviral, antibacterial, digestive tonic

A combination of all of the above herbs, equal parts, may be very effective. 1 cup tea or 30 to 60 drops tincture every two to four hours. May add:

* Jamaica dogwood (Piscidia piscipula) or St. John's wort (Hypericum perforatum), in equal parts, may be added for pain relief.
* Garlic/Ginger tea two to three cloves of garlic (Allium sativum) and two to three slices of fresh ginger (Zingiber officinale). Steep 5 to 15 minutes and drink, breathing in the steam. Stimulates immune system and stimulates drainage, prevents sinus problems from extending into lungs.
* Essential oils for bath or steam. For a steam, place 2 to 5 drops in a pot, bring to a simmer and hold head over the pot. For a bath, add 5 to 10 drops of oil to the bath. Eucalyptus (Eucalyptus globulus), lavender (Lavandula angustifolia), and thyme (Thymus vulgaris) are specific for upper-respiratory infections. Lavender and rosemary (Rosmarinus officinalis) are also calming. These essential oils have antiseptic properties.

Homeopathy

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

* Arsenicum album for sinusitis with watery, excoriating discharge
* Kali bichromicum for sinusitis with thick "gluey" discharge, postnasal drip, especially with ulceration
* Pulsatilla for thick, bland, greenish discharge, especially if patient is weepy and is not thirsty
* Nux vomica for sinusitis with coryza, and a stopped up feeling, especially if patient is impatient and/or angry

Physical Medicine

* Contrast hydrotherapy. Alternating hot and cold applications brings nutrients to the site and diffuses metabolic waste from inflammation. Use washcloths over the sinus area. Alternate three minutes hot with one minute cold. Repeat three times to complete one set. Do two to three sets/day.
* Nasal lavage to shrink membranes/increase drainage. Mix salt and water to taste like tears. Rinse each nostril by holding head over sink and letting water run from upper nostril to lower nostril. Keep nostrils lower than throat to prevent salt water draining into back of throat.
* Craniosacral therapy (osteopathic/chiropractic) can be very effective at decreasing the frequency of infections/headaches.

Acupuncture

May be helpful for both acute and chronic sinusitis.
Patient Monitoring

Patients not responding to therapy should see an otolaryngologist.
Other Considerations

Fungal sinusitis should be suspected for patients who do not respond to antibiotic therapy and for immunocompromised patients.
Prevention

Avoid known allergens, cold air, cigarette smoke, topical drugs, swimming, and metal vapors, and follow a diet that reduces mucus production.
Complications/Sequelae

Orbital infection from acute ethmoid sinusitis requires hospitalization, surgical drainage, and intravenous culture-specific antibiotics.

* Osteomyelitis of the frontal bones (Pott's puffy tumor), especially in children
* Intracranial spread of infection results in meningitis, subdural empyema, and abscesses; male adolescents are most at risk.
* Sphenoid sinusitis delayed diagnosis is associated with serious morbidity and mortality.
* Otitis media frequently present with children
* Abscess extradural, subdural, brain, or retrobulbar

Prognosis

An acute sinus infection lasts no longer than 8 weeks; a chronic sinus infection lasts for at least 4 weeks after initiation of treatment.
Pregnancy

Tetracycline is contraindicated in pregnancy.
References

Barkin R, Rosen P, eds. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, Mo: Mosby-Year Book; 1996.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:122-123.

Gruenwald J, Brendler T, Jaenicke C, et al., eds. PDR for Herbal Medicines. Montvale, NJ: Medical Economics Co; 1998:684-685.

Kruzel T. The Homeopathic Emergency Guide. Berkeley, Calif: North Atlantic Books; 1992:286-290.

Middleton E, ed. Allergy: Principles and Practice. 5th ed. St. Louis, Mo: Mosby-Year Book; 1998.

Rakel RE. Conn's Current Therapy. 50th ed. Philadelphia, Pa: WB Saunders Co; 1998.

Shock - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 14:53:00 +0000

Overview
Definition

Shock is a "circulatory collapse" characterized by inadequate blood flow and inability to maintain cellular perfusion of peripheral tissues. Shock as a syndrome is defined by a group of clinical signs arising from any of a number of causes and is usually associated with hypotension and oliguria. A life-threatening medical emergency, shock occurs in both sexes and all ages. Although prevalence is not well established, an estimated 71,000 hospitalized patients develop cardiogenic shock each year.
Etiology

Cardiogenic shock:

* Myocardial ischemia or infarction, particularly if > 40% of left ventricular muscle mass is involved; most common cause of cardiogenic shock; can also occur with right ventricular failure
* Ruptured interventricular septum
* Ventricular aneurysm
* Prolonged cardiopulmonary bypass; myocardium may be stunned for hours to days
* Severe cardiomyopathy or myocarditis
* Arrhythmia
* Acute mitral or aortic regurgitation or acute ventricular septal defect
* Aortic stenosis leading to decreased cardiac output and stroke volume
* Prosthetic valve malfunction
* Outflow obstruction e.g., hypertrophic cardiomyopathy (IHSS)

Extra cardiac obstructive shock:

* Pericardial tamponade impairs ventricular diastolic filling causing decreased cardiac output, diminished stroke volume, and reduced preload
* Massive pulmonary embolism
* Tension pneumothorax diminishes venous return to the heart
* Severe pulmonary hypertension

Hypovolemic shock :

* Acute hemorrhage due to trauma or preexisting disease (e.g., peptic ulcer or aortic aneurysm)
* Massive fluid depletion e.g., severe vomiting or diarrhea; or extreme insensible losses as in the case of burns
* Diabetes insipidus

Distributive shock (tissue perfusion due to abnormal shunting of a normal or increased cardiac output):

* Bacteremic or septic shock
* Drug overdose
* Anaphylaxis
* Neurogenic shock
* Addisonian crisis

Risk Factors

* Serious injury and trauma
* Cardiogenic disorders (e.g., acute myocardial infarction, cardiomyopathy)
* Surgery
* Bacteremia
* Hemorrhage
* Large volume loss from excessive diarrhea or vomitting
* Excess alcohol consumption
* Anemia
* Allergic reactions to medication(s)
* Drug overdose

Signs and Symptoms

* Low or unobtainable BP; often <60 mm Hg systolic in adults; regardless of absolute number, reduction of mean arterial pressure by 40 mm Hg also indicative of shock
* Lethargy, confusion, and somnolence
* Cold, moist, and often cyanotic and pale hands and feet
* Weak and/or rapid pulse
* Tachypnea and hyperventilation
* Oliguria
* Shaking chills, rapid temperature increase, warm flushed skin, hyperdynamic syndrome (septic shock)
* Engorged neck veins (cardiogenic and extra cardiac obstructive)
* Pulmonary congestion (cardiogenic)
* Gallop rhythm (cardiogenic)
* Systolic murmur (cardiogenic) new
* Pulsus paradoxus pericardial tamponade

Diagnosis
Physical Examination

Shock is an emergency that requires rapid evaluation based on "limited" history and physical signs and symptoms (e.g., cold and sweaty skin, weak and rapid pulse, irregular breathing, dry mouth, dilated pupils) and rapid initiation of treatment. Further diagnostic procedures (e.g., right heart catheterization) should determine cause and severity of shock. Specific diagnostic criteria include the following:

* Hypotension
* Tachycardia
* Diminished sensorium
* Oliguria

Also, listen for heart murmer, gallop rhythm, and pulmonary congestion (signs of cardiogenic shock). Distant heart sounds and presence of pulsus paradoxus suggest pericardial tamponade.
Laboratory Tests

Must be monitored closely and continuously in an intensive care setting:

* Arterial blood gas likely to reveal a metabolic acidosis from lactate
* CBC, PT, PTT
* Blood chemistry (electrolytes including calcium, magnesium, and phosphorus, as low levels depress myocardial and respiratory function)
* In the case of septic shock blood cultures, urinalysis, and urine cultures (if urine can be obtained), sputum cultures if any respiratory secretions

Pathology/Pathophysiology

Cardiogenic and hypovolemic shock result in decreased tissue perfusion. Distributive shock results from decreased arterial pressure due to systemic vascular resistance. Recent studies indicate two modes of gene expression in stress (acute-phase and heat-shock response), which may be harmful in shock. Common findings include decreased arterial pressure and often multiple organ system failures. Specific findings per type of shock include the following:

Cardiogenic:

* Myocardial injury or necrosis
* Reduced systolic performance
* Low cardiac output

Hypovolemic:

* Reduced preload
* Low cardiac output

Distributive:

* Decreased systemic vascular resistance
* Myocardial dysfunction
* High or normal cardiac output
* Maldistribution of blood flow in microcirculation
* In the case of septic shock, cardiovascular decompensation is due to the organism itself, endotoxins, or exotoxins

Extra cardiac obstructive:

* Reduced filling pressure
* Low cardiac output

Imaging

* Chest X ray to look for interstitial edema and thickening and loss of definition of pulmonary vasculature shadow, characteristic appearance of Kerley A and B lines
* Echocardiography to evaluate for valvular disease and vegetation, wall-motion abnormalities, LV function, and cardiomyopathy
* Coronary angiography may be warranted in the case of cardiogenic shock

Other Diagnostic Procedures

* Electrocardiogram (ECG) to diagnose myocardial damage; help identify arrhythmias
* Right heart catheterization for hemodynamic assessment and monitoring therapy

Treatment Options
Treatment Strategy

Primary goals are to maintain mean arterial pressure (at least 60 mm Hg) and to ensure adequate perfusion and oxygen delivery. Initial first-aid therapy includes covering for warmth, raising legs to improve venous return, stopping hemorrhage, and CPR/ACLS if needed. Oxygen should be given via nasal cannula or mask. Once patient reaches intensive care, continuous ECG monitoring, careful monitoring of oxygenation, and right heart catheterization should be instituted. Mainstay therapy in the case of hypovolemic shock is volume repletion; in the case of hemorrhage, this should be done with packed RBCs; fluids also used for septic shock even if edematous.
Drug Therapies

* Ionotropic agents dopamine, dobutamine, norepinephrine intravenous to augment arterial pressure and cardiac output in cardiogenic shock
* Vasodilators to decrease afterload and thereby decrease LV work in the case of cardiogenic shock
* Vasopressors often necessary for septic shock e.g., dopamine, norepinephrine
* Corticosteroids (e.g., hydrocortisone, 2 to 10 gm IV) for anaphylactic shock; to stabilize patient, prevent recurrence, and block late-phase reactants
* Antimicrobials (septic shock) initial broad-spectrum regimen to cover wide range of causative microorganisms in infections
* Morphine serves as venodilator and to decrease anxiety
* Thromobolytic therapy should be considered in the case of myocardial infarction or pulmonary embolism

Surgical Procedures

* Surgery may be necessary in cases such as valvular heart disease or ventricular septum rupture after myocardial infarction
* Emergency angioplasty or coronary bypass surgery may improve survival at 6 months in patients with acute myocardial infarction complicated by cardiogenic shock
* Placement of intra-aortic balloon pump may be necessary in the case of cardiogenic shock
* Emergency pulmonary embolectomy in the case of pulmonary embolism, particularly if thrombolytic therapy is contraindicated

Complementary and Alternative Therapies

While shock is a life-threatening condition requiring emergent attention and treatment, some CAM modalities may provide adjunctive care. Nutritional manipulation, for example, has demonstrated some protection against the deleterious effects of shock and improvement in outcome, including possible roles for:

* Omega 3 fatty acids
* L-acetyl carnitine
* Glutamine
* Coenzyme Q10
* N-acetylcysteine
* Nicotinamide
* Vitamin B12
* Vitamin C
* Vitamin E

See details in the respective subsections.
Nutrition

Oxidative stress has been implicated as a contributor to the development of shock (e.g., cardiogenic shock from myocardial ischemia as well as septic shock from bacterial endotoxins). Several studies have suggested that treatment with antioxidants and free radical scavengers may have protective effects against developing these shock syndromes. See subsections entitled Coenzyme Q10, Vitamin C, and Vitamin E for more information.

Arginine, Omega-3 Fatty Acids, and Nucleotide Supplement

Nutritional supplementation has been examined for benefits in the correction or inhibition of inflammation and metabolic derangements that accompany shock. A prospective, randomized, double-blind, controlled study of 32 patients with severe multiple trauma compared possible benefits from a nutritional formulation containing arginine, omega-3 fatty acids, and nucleotides with those from an isonitrogenous isocaloric control diet. Although no significant difference was seen in mortality or hospital stay (the sample size was too small to test for these parameters adequately), patients in the test group developed significantly less systemic inflammatory response syndrome (SIRS), a condition that can induce multiple organ failure (MOF). SIRS is defined according to criteria determined at the Society of Critical Medicine Consensus Conference and is related to body temperature, heart rate, respiratory rate, WBC count, and band formation of WBCs. The authors conclude that critically ill patients due to trauma and other causes may benefit from the addition of arginine, omega-3 fatty acids, and ribonucleotides to enteral nutrition (Weimann et al. 1998).

An earlier, prospective, randomized study of critically injured patients compared a standard diet and an experimental diet supplemented with arginine, omega-3 fatty acids, and trace elements. Over time, the group on the experimental diet showed a trend toward normal levels of immune mediators (e.g., tumor necrosis factor and prostaglandin E2) in comparison with patients on the standard diet (Mendez et al. 1996).

Omega-3 vs. Omega-6 Fatty Acids

Animal studies investigating the role of essential fatty acids in the clinical outcomes from shock show positive benefits from omega-3 essential fatty acids and negative outcomes associated with omega-6 essential fatty acids. These data are consistent with other scientific information suggesting that omega-3 essential fatty acids are anti-inflammatory while omega-6 essential fatty acids are pro-inflammatory. Perinatal supplementation with omega-3 polyunsaturated fatty acids significantly decreased mortality from endotoxic shock in newborn rats (Farolan et al. 1996). Guinea pigs fed an intravenous diet containing black currant oil (rich in omega-6 gamma linolenic acid namely, 20% GLA) showed no improvement in resistance to shock; in fact, they exhibited a more rapid onset of metabolic acidosis and increased mortality compared with guinea pigs getting soy supplementation (0% GLA) (Hirschberg et al. 1990). The results of these two animal trials suggest that a diet rich in omega-3 essential fatty acids compared with omega-6 fatty acids may prove protective against the deleterious effects of septic shock following exposure to the endotoxin i.e., a potential prophylactic use. Diets in the United States and some other industrialized countries tend to be high in omega-6 fatty acids and low in omega-3.

Carnitine

A multi-center, double-blind clinical study of 115 patients with septic, cardiac, or traumatic shock investigated the effects of acetyl-L-carnitine infused for 12 hours after a single intravenous bolus. Clinical improvements were seen in patients with all three conditions (Gasparetto et al. 1991):

* Cardiogeneic shock -- heart rate decreased to normal values; oxygen saturation improved; right atrial pressure diminished
* Septic shock -- systolic arterial pressure increased; oxygen saturation improved
* Traumatic shock -- right arterial and mean arterial pressures improved

Intravenous administration of L-carnitine may also prevent cardiogenic shock in patients suffering from acute myocardial infarction. An open pilot study of 27 patients hospitalized with acute MI evaluated the effects of standard treatment, an intravenous bolus of L-carnitine, and subsequent continuous infusion of the supplement. According to hemodynamic measurements (via Swan-Ganz catheter), blood-gas analysis, and biochemical parameters, L-carnitine had a beneficial effect (Corbucci and Loche 1993). The supplement appeared to:

* Oppose the metabolic derangements induced by acute ischemia
* Protect cardiac function
* Improve outcome of acute MI

Carnitine may also ameliorate the response of cachexia from sepsis and other causes, as suggested by a controlled animal study. Cachexia, a complication of septic shock, is accompanied by:

* Protein wasting
* Lipogenesis
* Reduced fatty acid oxidation
* Hypertriglyceridemia

Carnitine supplements administered in the feed of rats with cachexia from septic shock had a normalizing effect on lipid metabolism compared with controls. The authors of this trial propose that the improvement in metabolism in cachectic animals may contribute to reduction in mortality rate seen in earlier studies of septic rats supplemented with carnitine (Winter et al. 1995).

Coenzyme Q10

Coenzyme Q10 (CoQ10) is a lipophilic antioxidant that has been shown to protect cellular and subcellular membranes from lipid peroxidation. A small controlled canine study evaluated the effects of CoQ10 against hemorrhagic shock. Pretreatment with CoQ10 before induction of hemorrhagic shock moderated the accumulation of lactate and metabolic acidosis and was responsible for returning catecholamine levels to baseline more quickly than in the control group. Histamine levels, chemical mediators that may be reduced during hemorrhagic shock, were found to be higher in the treatment group; the author to speculates that the maintenance of normal histamine levels by CoQ10 (Yamada 1990):

* Prevents vasoconstriction
* Supports microcirculatory blood flow
* Promotes survival by maintaining histamine levels

Other studies of endotoxic shock have reported that CoQ10 pretreatment improves pulmonary function by decreasing histamine levels. When considering these results and the present findings, the author proposes that CoQ10 administration has protective effects in both hemorrhagic and endotoxic shock and it works by different mechanisms in the two related but distinct clinical circumstances. The beneficial effects of CoQ10 in each type of shock are dependent on factors in addition to the impact of the supplement on histamine levels in the respective clinical settings (Yamada 1990).

A similar study that evaluated the effects of CoQ10 on puppies with induced septic shock showed the following beneficial changes (Lelli et al. 1993):

* Improvement in cardiovascular hemodynamics including enhanced cardiac output and improved mean arterial pressure
* Inhibition of free radical-mediated lipid peroxidation.
* Prevention of early hypotension

Glutamine

The addition of glutamine to parenteral nutrition may have the following beneftits:

* Preservation of the integrity of the gut
* Maintenance of mucosal weight and villous height
* Possible prevention of bacterial translocation and septic complications
* Decreased mortality among critically ill patients

Glutamine is thought to be a safe adjunctive therapy without significant side effects (Felbinger et al. 1999).

Nicotinamide

At least two animal studies have suggested a protective effect from nicotinamide (the biologically active amide of niacin or vitamin B3; also called niacinamide) following exposure to bacterial endotoxin (LeClaire et al. 1996; Zingarelli et al. 1996). The significant results seen in the treatment group compared to controls include:

* Improved survival
* Reduced hypotensive response

The authors suggest that benefits are conferred by:

* Reduction of cytokine activity
* Protection from nitric oxide mediated vascular failure

Vitamin B12

Animal studies suggest that hydroxycobalamin (vitamin B12) may attenuate the hypotensive response to E. coli endotoxin through mechanisms similar to those conferred by nicotinamide (see previous subsection of this title) (Greenberg et al. 1995).

Vitamin C

Reactive oxygen species (ROS) production from phagocytes, such as superoxide anions, has been implicated as contributing to the high mortality rate from septic shock. Administration of ascorbic acid to in vitro macrophages taken from mice suffering from endotoxic shock reduced adherence, ingestion, and superoxide production by the phagocytes. The authors speculate that this may ultimately translate into vitamin C attenuating the severity of septic shock (Victor et al. 2000). More research is needed.

Vitamin E

In a controlled study comparing elderly men with younger subjects, administration of a daily dose of 200 mg of vitamin E for 3 months decreased lymphocyte adherence (initially very high) and stimulated lymphoproliferation; each of these processes may be disturbed in the course of aging. Ingestion of vitamin E appeared to restore immune balance in the older male subjects (De la Fuente and Victor 2000). It is unclear what exact conclusions can be drawn in terms of the clinical application for vitamin E supplementation in the case of shock. One implied suggestion is that older men who use this antioxidant may be protecting their immune system and, thereby, may be less susceptible to the damaging effects of bacterial endotoxins at the time of exposure i.e., a prophylactic use.

N-acetylcysteine

N-acetylcysteine (NAC), administered to mice with septic shock secondary to bacterial endotoxin, decreased lymphocytic adherence and increased chemotaxis compared with mice not given the supplement. The authors conclude from the animal study that NAC seems to preserve adequate immune function against imbalances such as those caused by endotoxic shock (De la Fuente and Victor 2000). Following further research in humans, there may be an adjunctive role for NAC supplementation following endotoxin exposure and development of septic shock.
Herbs

The immunomodulatory effects of plant-based medicines may be beneficial in the treatment of systemic septic shock. An Ayurvedic formula was evaluated in a controlled animal study investigating septic shock; the formula contains:

* Tinospora cordifolia (Tamarisk)
* Withania somnifera (Ashwagandha)
* Phyllanthus emblica (Indian gooseberry)
* Ocimum sanctum (Sweet basil)

All of the mice were administered lethal doses of E. coli and development of bacteremia was reduced in the treatment group. The authors conclude that the protective effect of this Ayurvedic herbal formula may be due to indirect enhancement of antimicrobial defenses as well as direct enhancement of macrophage response (Mitra et al. 1999).

A series of new herbal preparations based on Traditional Chinese Medicine were evaluated for their ability to improve outcomes in 183 cases of septic shock. Injections of the following herbs which regulate the flow of qi, appeared to promote blood circulation and enhance the body's resistance to circulatory collapse:

* Kangjue tongma
* Yiqi jiuyin
* Yiqi huiyang

Injections were also reported to significantly improve mortality in the treatment group (4.4%) as compared to controls (23.0%). Blood pressure was stabilized, renal blood flow was enhanced, and blood viscosity was lowered. An additional animal study of the remedies reported reduced lipid peroxidation and stabilization of cellular membranes (Jin et al. 1995).
Homeopathy

Scientific investigations of homeopathic remedies for the treatment of shock specifically have not been conducted. The remedy Aconite, however, is frequently used by homeopathic doctors for acute, emergent conditions which might include shock (Jack 1986)
Acupuncture

In rabbits with induced hemorrhagic shock, electroacupuncture of Neiguan (P 6) (Song et al. 1993):

* Raised blood pressure
* Protected cardiac pump function
* Normalized serum levels of angiotensin II, atrial natriuretic peptide, serotonin, and thromboxane B2

While the most common adverse events related to acupuncture are forgotten needles, near syncope, and needle pain, there have been rare case reports of acupuncture producing serious side effects including one mortality secondary to septic shock (Ernst and White 2000). Nonfatal cardiac tamponade is extremely rare, but has been reported to follow acupuncture treatments in at least three cases (Kirchgatterer et al. 2000).
Patient Monitoring

Hospitalization including admission to an intensive care unit is critical with careful monitoring of the following:

* Continuous cardiac monitoring and serial 12-lead ECGs
* Arterial BP
* Ventricular filling pressure via right heart catheterization
* Urine flow
* Arterial blood pH
* Body temperature
* Overall clinical status

Other Considerations
Prevention

* Treatment of related disorders may reduce risk
* Avoid allergens to prevent anaphylactic shock; carry epinephrine pen

Complications/Sequelae

* Damage to organs, including kidney, brain, liver
* Cardiac arrest
* Respiratory arrest
* Death

Prognosis

Outcome depends on immediate and proper treatment in most cases. Cure may occur with early diagnosis and treatment. However, all causes of shock have very high rates of morbidity and mortality. Immediate treatment for anaphylactic shock usually results in complete recovery. Mortality in elderly patients due to septic shock is particularly high.
Pregnancy

Childbirth is a risk factor for shock.
References

Berkow R, Fletcher AJ, Beers MH, eds. The Merck Manual. Rahway, NJ: Merck & Co.; 1992:437-443.

Bochan M. Hypersensitivity reactions, immediate. In: Cunha BA, Geibel J, Griffing GT, et al., eds. Medicine, Ob/Gyn, Psychiatry, and Surgery: An On-line Medical Reference. Accessed at www.emedicine.com/cgi-bin/foxweb.exe/showsection@d:/em/ga?book=med&topicd=1101 on August 29, 2000.

Corbucci GG, Loche F. L-carnitine in cardiogenic shock therapy: pharmacodynamic aspects and clinical data. Int J Clin Pharmacol Res. 1993;13(2):87-91.

De la Fuente M, Victor VM. Anti-oxidants as modulators of immune function. Immunol Cell Biol. 2000;78(1):49-54.

National Heart, Lung, and Blood Institute. Emergency Angioplasty or Bypass Surgery Saves Lives of Heart Attack Patients with Cardiogenic Shock. National Institutes of Health. Accessed at www.nhlbi.nih.gov/new/press/aug25-99.htm on February 15, 2000.

Ernst E, White AR. Acupuncture may be associated with serious adverse events [letter]. BMJ. 2000;320(7233):513-514.

Farolan LR, Goto M, Myers TF, Anderson CL, Zeller WP. Perinatal nutrition enriched with omega-3 polyunsaturated fatty acids attenuates endotoxic shock in newborn rats. Shock. 1996;6(4):263-266.

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Sexually Transmitted Diseases - home health advice

noreply@blogger.com (kablogspot) — Mon, 22 Oct 2007 14:40:00 +0000

Overview
Definition

Sexually transmitted diseases (STDs) are a group of diverse infections caused by heterogeneous microbial agents. While sexual contact is epidemiologically important and a frequent mode of transmission, it is not the only mechanism by which certain conditions classified as STDs may be spread. The full range of sexual conduct must be considered in diagnosing STDs, including heterosexual and homosexual genital, oral genital, oral anal, and genital anal behaviors. Common clinical features across infectious agents allow groupings of vaginitis, cervicitis, urethritis, and genital lesions as STDs.

Note: For information on HIV infection, AIDS, and Hepatitis, please see the Integrative Medicine Access monographs entitled "HIV and AIDS" and "Hepatitis, Viral."
Etiology

Vaginitis:

* Candida spp, primarily albicans; sexual transmission is not the only or even the main mode of contraction
* Trichimonas vaginalis; may be asymptomatic
* Gardnerella vaginalis and other forms of bacterial vaginosis including mycoplasma; associated with risks for STDs but not necessarily sexually transmitted
* Herpes simplex virus (HSV)

Cervicitis:

* Neisseria gonorrhea
* Chlamydia trachomatis most common cause of cervicitis by identified organism
* Herpes simplex virus (HSV)
* Idiopathic i.e., organism not identified; up to 50% of cases

Urethritis:

* Gonococcal urethritis N. gonorrhea; decreased incidence in industrialized countries over the last decade
* Nongonococcal urethritis all other etiologies, including C. trachomatis (30-40% of cases of nongonococcal urethritis), Ureaplasma urealyticum, Trichomonas vaginalis, HSV, Mycoplasm genitalium
* Reiter's syndrome, sporadic form of chlamydial infection

Genital lesions:

* HSV
* Syphilis Treponema pallidum
* Chancroid gram-negative rod Haemophilus ducreyi; common in Africa and Asia
* Genital warts Human papillomavirus (HPV)
* Scabies Sarcoptes scabiei
* Lymphogranuloma venereum (LGV) and Granuloma inguinale very rare in Europe and North America
* Trauma rarely causes genital ulcers (See section entitled Differential Diagnosis)

Risk Factors

* Sexual partner with known history of STD
* Asymptomatic sexual partner with undiagnosed STD
* Multiple sexual partners, or a partner with multiple sexual partners
* Unprotected intercourse or sexual practices
* H/O one STD increases the likelihood (up to 60%) of contracting another, including HIV
* Adolescents have highest risk for new acquisition
* Lower socioeconomic status, inner city, racial minorities e.g., syphilis and chancroid
* Homosexuality for HIV, gonorrhea, hepatitis, syphilis
* Immunosuppressive diseases
* Prostitution
* Illicit drug use

Signs and Symptoms

Vaginitis:

* Vaginal and vulvar pruritus, irritation, burning
* Creamy or curd-like vaginal discharge; nonodorous; increased amount of discharge
* Red, painful vaginal mucous membranes
* Dysuria
* Dyspareunia
* Satellite lesions (pustules spreading to thighs and anus)

Cervicitis:

* May be asymptomatic
* May have normal-appearing cervix or erythema around cervical os or diffusely friable cervix with exocervical ulcers as in the case of HSV
* Purulent or mucopurulent discharge coming from the cervical os gonococcal or chlamydial infection
* Hypertrophic cervicitis erythema, bleeding lesion; often with chlamydial infection
* Abdominal pain suggestive of HSV
* Rectal infection and proctitis gonorrhea

Urethritis:

* May be asymptomatic
* Men mucopurulent discharge, erythema at the meatus, dysuria with pruritus
* Women often unaware of discharge; dysuria and frequent urination; pyuria
* Rectal infection and proctitis gonorrhea

Genital lesions:

* HSV fever, myalgias; pruritus; dysuria; vaginal and urethral discharge; inguinal lymphadenopathy; vesicular lesions of the external genitalia, cervix, and urethra; pain and/or burning preceding the appearance of lesions
* Syphilis ulcerative lesions (chancres) on the genitalia, mouth, anus; regional, generally painless, adenopathy. Secondary syphilis systemic illness, maculopapular rash, contagious lesions (Condylomata lata). Late-stage syphilis destructive lesions of skin and bone, dementia; lymphocytic meningitis
* Chancroid painful ulcers and inguinal adenopathy; fluctuant or ruptured nodes
* Genital warts soft, small papules on external genitalia, urethra, vagina, cervix, or pubic or perianal regions
* Scabies mite in unexcoriated papules or burrows, causing severe pruritus

Differential Diagnosis

* Vaginitis gonorrhea; cystitis
* Cervicitis mucopurulent cervicitis clinically similar to urethritis; cystitis
* Urethritis with gonococcal diagnosis, concurrent diagnosis of nongonococcal urethritis must be assumed; epidydimitis; disseminated gonococcal infection; cystitis; prostatitis; pyelonephritis
* Genital lesions clinical overlap among lesion types; morphologic features are important; chancroid often over diagnosed; vaginitis; malignant lesions; trauma

Diagnosis
Physical Examination

(See section entitled Signs and Symptoms for additional information)

Vaginitis:

* Vagina hyperemic, bright red, with curd-like plaques or without erythema
* Discharge creamy or curd-like; may be yellow or gray in color

Cervicitis:

* Cervix normal, erythematous, or displaying ulcers in the case of HSV; discharge visible from cervical os, yellow and mucopurulent
* Friable cervix that bleeds easily with gentle swabbing particularly in case of HSV

Urethritis:

* Men mucopurulent discharge occurs with both gonococcal and nongonococcal urethritis; in nongonococcal type, the discharge is completely clear or there is a crusting at the meatus; stained underwear; discharge is extracted by gently stripping the urethra
* Women dysuria with urethritis (internal) and vulvovaginitis (external)

Genital lesions:

* History, incubation period
* Presence or lack of pain
* Cyclic or persistent lesions

Laboratory Tests

Vaginitis:

* Microscopic wet mount one scraping of vaginal plaque, discharge or vulva is mixed with 10% potassium hydroxide (KOH), another with saline; examine for WBC's, yeast, spores, pseudohyphae, motile trichomonoas (easy to miss), and clue cells; 50% to 70% accuracy rate
* Gram's stain
* pH

Cervicitis:

* Gram's stain inaccuracies dictate treatment for both gonorrhea and chlamydia
* Pap smear may reveal infection
* Culture for gonorrhea, HSV
* Chlamydial culture using fluorescein-conjugated monocolonal antibody requires experienced technician

Urethritis:

* Culture
* Gram's stain of swab inserted into urethra looking for presence (gonococcal) or absence (nongonococcal) of intracellular gram-negative diplococci
* Nongonococcal urethritis nucleic acid hybridization test
* Polymerase chain reaction (PCR)
* Voided urine can be examined for WBC's

Genital lesions:

* HSV culture shows multinucleated giant cells; PCR for CNS infections; serologic assays; Tzank prep only sensitive in presence of intact vesicles
* Syphilis serologic tests include nontreponemal tests (Venereal Disease Research Laboratory [VDRL] and rapid plasma reagin [RPR]); and treponemal tests (fluorescent treponemal antibody absorption [FTA-ABS] test most sensitive); dark-field microscopic examination; if tests negative and no other organism identified, repeat in 1 to 2 weeks and again in 6 weeks
* Chancroid culture for H. ducreyi; Gram's staining
* Genital warts biopsy; 3% to 5% acetic acid swab of epithelial turns infected area white
* Scabies shave biopsy and light microscopic examination

Pathology/Pathophysiology

Vaginitis:

* Pustule lesion appears like hyperplastic indurated plaques, atrophic inflamed plaques, or a leukoplakic area
* Accumulation of scale and inflammatory cells
* pH discharge normal

Cervicitis:

* Gram-negative intracellular diplococci gonococcal
* Pap test to identify cervical changes associated with HPV
* Presence of polymorphonuclear neutrophils (PMNs)

Urethritis:

* Presence of PMNs
* Gram-negative intracellular diplococci in gonococcal urethritis

Genital lesions:

* HSV latent state maintained by nerve ganglion cells
* Syphilis multiplication of spirochetes; regional adenopathy can be aspirated and cultured
* Chancroid inguinal adenopathy; purulent granulated tissue
* Genital warts papillomavirus DNA identifiable near lesion

Other Diagnostic Procedures

Cervicitis:

* Immunofluorescence microscopy chlamydia, HSV
* DNA probes chlamydia

Urethritis:

* Nongonococcal: Enzyme-linked immunosorbent assay (ELISA); immunofluorescent testing; DNA probe
* Examination of synovial fluid if signs of acute arthritis present

Genital lesions:

* HSV testing of cerebrospinal fluid (CSF) and imaging in case of suspected encephalitis and/or meningitis
* Syphilis testing of CSF when there are neurologic signs
* Genital warts electron microscopy; immunohistochemistry; nucleic acid hybridization
* Scabies hand lens

Treatment Options
Treatment Strategy

Presumptive therapy is generally given to sexual partners. Because of increased association and susceptibility, HIV testing is encouraged for patients with any STD. Importance of compliance with treatment must be stressed. Sexual abstinence or use of condoms is typically recommended until infection resolves. Drug treatment is administered. Whenever gonorrhea is identified, simultaneous treatment for chlamydia should be given.
Drug Therapies

Vaginitis:

* Candidal infections topical polyenes (e.g., nystatin) 1 vaginal suppository bid for 2 weeks or azole (e.g., miconazole) derivative cream for 1 to 5 days; oral treatment of choice is fluconazole (150 mg given once)
* Trichimonas metronidazole 2.0 gm po x one dose or 500 mg po bid x 7 days; during pregnancy, clotrimazole vaginal suppository qhs x 2 weeks should be used instead
* Gardnerella metronidazole 500 mg po bid x 7 days or metronidazole gel 1 applicator applied intravaginally bid x 5 days; during pregnancy, clindamycin 2% cream bid x 1 week

Cervicitis treated based on clinical diagnosis, i.e. before presence of organism is confirmed:

* Gonorrheal ceftriaxone (125 to 250 mg IM) given once; plus treatment for chlamydia
* Chlamydial doxycycline (100 mg bid x 7 days); azithromycin 1.0 gm po x one dose; during pregnancy, erythromycin 500 mg qid x 7 days
* Sexual partners should be examined and treated

Urethritis:

* Gonococcal ceftriaxone (125 to 250 mg IM once); plus treatment for nongonococcal urethritis; same treatment for anogenital or pharyngeal gonococcal infection
* Nongonococcal doxycycline (100 mg bid x 10 days); azithromycin 1.0 gm po x one dose; during pregnancy, erythromycin 500 mg qid x 7 days

Genital lesions:

* HSV acyclovir 200 to 400 mg/tid for 10 days; in the case of HSV encephalitis, acyclovir 10 mg/kg IV q 8 hours for 14 to 21 days
* Syphilis benzathine penicillin G (2.4 million units IM) given once or once a week for 3 consecutive weeks for syphilis extending beyond a year; aqueous crystalline penicillin G (12 to 24 million units IV) given for up to 14 days with neurosyphilis
* Chancroid ceftriaxone (250 mg IM) given once; erythromycin 500 mg po qid x 7 days; azithromycin 1.0 gm po given once
* Genital warts physician-applied podophyllin; podofilox 0.5% solution bid for 3 days, then none for 4 days; repeat cycle up to four times; cryotherapy, surgical removal, or electrocautery may be performed by a specialist; intralesional interferon alfa-n3 for refractory cases
* Scabies apply to all areas of the body: permethrin 5% cream for 8 to 14 hours; lindane 1% lotion or cream for 8 hours
* LGV doxycycline 100 mg po bid x 21 days; erythromycin 500 mg qid x 21 days
* Granuloma inguinale doxycycline 100 mg po bid x 1 to 4 weeks; during pregnancy, erythromycin 500 mg qid x 14 days

Complementary and Alternative Therapies

CAM therapies show promise in the treatment of STDs, including those that have become resistant to conventional drugs. Combining antioxidant nutrients with herbs, acupuncture, or conventional medications may effectively treat many STDs.
Nutrition

Chlamydia trachomatis infections have been shown to generate reactive oxygen species associated with the formation of lipid peroxides in host cell membranes. Experimental studies have demonstrated the release of highly reactive oxygen species with marked peroxidation of host membrane lipids in chlamydial infections. Treatment of infected cells with ascorbic acid, a powerful antioxidant, prevented such lipid peroxidation. This study suggests, therefore, that ascorbic acid, as well as other antioxidant nutrients known for their free radical scavenging abilities, may ultimately prove useful for improving treatment outcomes of chlamydial infections when taken in conjunction with standard antibiotic therapy (Azenabor and Mahony 1999).

Clinically, many recommend Lactobacillus acidophilus in either food or supplement form to aid in restoration of normal flora in the case of candidal infections or following antibiotic use; please see the monograph on Lactobacillus acidophilus for additional information.
Herbs

Several antimicrobial herbal formulations have demonstrated effectiveness in the treatment and/or prevention of STDs. For example, studies performed using Praneem polyherbal vaginal suppository (PR-048), containing purified leaf extract from Azadirachta indica, purified saponins from Sapindus mukerossi, and Mentha citrata oil as well as polyherbal cream (CH-005), containing purified saponins from Sapindus mukerossi, Mentha citrata oil, and a natural polycationic polymer evaluated effectiveness of these substances against cultures of clinical isolates containing various pathogenic strains inoculated in mouse vaginal models. PR-048 did not demonstrate activity against Candida species; however, the CH-005 cream was found to be effective against C. albicans, C. krusei, and C. tropicalis. Both formulations inhibited all strains of urinary tract E. coli, including those that were multidrug resistant, and they both exhibited anti-HIV activity in vitro. In addition, mouse vaginal models pretreated with the herbal formulations were less likely to become infected when challenged with C. trachomatis or HSV-2. In fact, vaginal application of the herbal formulations prevented the formation of herpes lesions. Both inhibited the growth of clinical isolates of N. gonorrhea, including penicillin-resistant strains. While the clinical application is not yet completely understood from these animal models, these formulations show great potential for speeding recovery, arresting growth, and inhibiting the transmission of STDs (Talwar et al. 2000).

Propoli is rich in flavonoids and has antimicrobial and anesthetic properties, making it a potentially ideal topical treatment for herpes infections. A single-blind, randomized, controlled multicenter study was undertaken to compare the effectiveness of a Canadian propolis ointment to acyclovir as well as placebo ointments in 90 patients with recurrent chronic genital HSV-2. Treatment began in the blister phase of infection and patients were assessed on the 3rd, 7th, and 10th days of treatment. Propolis was found to be markedly superior to both acyclovir and placebo in resolution of lesions and decreased time to heal (Vynograd et al. 2000).

An herbal immunoadjuvant and antitumor formula was evaluated for effectiveness against active herpes lesions. WTTC, containing Wisteria floribunda, Terminalia chebulae, Trapa natans, and Coicis semen was combined with Ganoderma lucidum and Elfuinga applanata. Oral administration of the formula to four patients with recurrent herpes labialis and one with genital herpes resulted in complete recovery within 3 to 7 days. The authors suggest that the combined extracts may be helpful in inhibiting reactivation of HSV, reducing pain, and hastening recovery (Hijikata and Tsukamoto 1998).

Topical herbs used in clinical practice that have not yet been validated by scientific investigation include licorice root (Glycyrrhiza glabra) and lemon balm (Melissa officinalis) for HSV; thuja (Thuja occidentalis) for HPV; and garlic (Allium sativum) and essential oils of oregano (Oreganum vulgare), lavender (Lavandula augistifolia), and tea tree (Melaleuca alternifolia) for HPV and Candida species. For best care, patients with STDs should be advised to see a licensed naturopathic doctor or other specialist trained and certified in the use of herbal remedies.
Homeopathy

Homeopathic remedies are widely used in clinical practice for the treatment of STDs although scientific studies have not yet investigated this modality for such use. Patients should be referred to a licensed, certified homeopathic doctor who can help in both the acute and chronic phases of many STDs.
Acupuncture

Four hundred five reports of men with nongonococcal urethritis treated with acupuncture were considered cured or significantly improved in 86% of cases. Cases were collected over a 21-month period from June 1988 to April 1990. During a daily treatment lasting 1 hour, needles were inserted into four particular acupuncture points and manipulated every 10 minutes. Points that were needled were zhaohai (KI 6, bilateral, by the reduction method), zhongji (RN 3, by the reinforcing method), taichong (LR 3, bilateral, by the reduction method), and sanyinjiao (SP 6, bilateral, by the reinforcement method). Following each course of 10 treatments, a urethral smear was evaluated and a 5-day rest period was instituted before commencing the next course. Patients were asked to abstain from all sexual activity during treatment and for 1 month following the completion of treatment; in addition, the patients' sexual partners were treated as well (Wang 1997).

Of the 405 cases, 261 (64.4%) were cured (i.e., clinical symptoms resolved, urine became clear, and smear of fluid obtained from prostatic massage was negative). Treatment appeared markedly effective in 50 of the 405 subjects (12.4%) (i.e., symptoms resolved, urine was clear, and prostatic massage secretion showed only a very small amount of bacteria). Thirty-seven (9.1%) cases were considered improved (i.e., symptoms markedly reduced except rare urethral secretions persisted). Smears of prostatic fluid were weakly positive, e.g., some baccilli. Fifty-seven (14.1%) cases failed (i.e., symptoms alleviated by less than one-third and positive or strongly positive prostatic smears). The total rate of some degree of effectiveness was 85.9% (348 cases) (Wang 1997).

Several successful cases of treatment of herpes simplex viral infections with acupuncture have been reported in the literature. For example, two researchers report their findings treating two patients with herpes oral-labialis and three with herpes genitalis. The acupuncture points were selected from those generally employed for treatment of skin conditions, including dazhui (DU 14), fengmen (UB 12), fengchi (GB 20), huantiao (GB 30), fengshi (GB 31), yangfu (GB 38), xuanzhong (GB 39), hegu (LI 4), quchi (LI 11), jianyu (LI 15), zhongwan (REN 12), zusanli (ST 36), sanyinjiao (SP 6), xuehai (SP 10), quze (P 3), and weizhong (UB 40). Resolution of active recurrent infections in this group of patients required between one and four sessions. Although these findings are too preliminary to generalize, the results suggest that acupuncture helped to promote the healing of skin lesions, lengthen remission, and inhibit recurrences in the five patients studied with HSV infections (Liao and Liao 1991).

One hundred sixteen patients with gonococcal arthritis (see section entitled Complications/Sequelae) were treated with a combination of acupuncture (dazhui, DU 14; quchi, LI 11; zusanli, ST 36), garlic moxibustion, pricking bloodcupping, and joint aspiration. Of the 116 patients, 74 were considered cured (63.8%) (defined as complete disappearance of clinical symptoms, restoration of normal function, and negative joint aspiration); treatment was markedly effective in 13 (11.2%) (defined as resolution of clinical symptoms, recovery of normal function, but joint aspiration weakly positive); 11 improved (9.5%) (defined as improvement in clinical symptoms, recovery of function, but weakly positive or positive joint aspiration); and 18 failed (15.5%) (less than 30% resolution of symptoms and return of function with persistently positive joint aspiration). A therapeutic course consisted of 10 days of treatment with a 2- to 3-day interval between courses. Of the 74 patients who were cured, 21 (28.4%) recovered after one course; 34 (45.9%) after two courses, and 19 (25.7%) after three courses (Wang 1996).

[Note: Reinforcing or tonifying in acupuncture refers to the building up of deficient yin, yang, or qi in an organ by a needling technique that stimulates energy flow in the corresponding meridian. Reducing or dispersing refers to the opposite, i.e., the draining away of excessive or stagnant energy that has accumulated because of blocked circulation in the affected area (Kaplan 2000).]
Patient Monitoring

Women should have regular pap smears annually if sexually active, particularly with more than one partner and/or with change of partner; consider routine screening for certain STDs in sexually active young men and women between the ages of 14 and 20 as well as older adults with more than one partner and/or other risk factors.

Vaginitis:

* Monitor for recurrence only
* Strict control for diabetics is critical

Cervicitis and urethritis:

* Gonorrhea is reportable in all U.S. states
* Monitor for recurrence and noncompliance with treatment

Genital lesions:

* Syphilis follow-up serologic tests at 3 and 6 months until titers stabilize; every 6 months thereafter
* Chancroid draining of fluctuant buboes prevents rupture
* Genital warts patients with diabetes or poor circulation should be monitored for infection
* Scabies retreatment in 1 week is generally recommended if pruritus is not improved (but pruritus can continue for weeks despite adequate treatment)

Other Considerations
Prevention

* Education modes of disease transmission, risk reduction, recurrence patterns
* Assumptive treatment of sexual partner
* Detection of asymptomatic partner
* Sexual abstinence for some infections (e.g., HSV) is essential as condoms do not necessarily prevent transmission
* Use of condoms and other prophylactic devices
* Treat symptomatic balanitis in men to prevent vaginitis in women
* Reduction of number of sexual partners as well as decreased rate of change in sexual partners
* Early detection and treatment
* Screening of high risk individuals during routine exams
* Wise use of prophylactic antibiotics prevents development of resistant strains

Complications/Sequelae

* Antibiotic resistance of etiologic agent may occur
* Many infectious agents increase the risk of contracting HIV
* Gonococcal infections can result in acute arthritis

Vaginitis:

* HIV infection and diabetes predispose to chronic infections
* May be early sign of Toxic Shock Syndrome
* Presence early in pregnancy may be independent predictor of preterm labor

Cervicitis:

* Uncontrolled chlamydial or gonococcal infections may result in pelvic inflammatory disease (PID), potentially leading to infertility; possible obstetric complications (see section entitled Pregnancy)

Urethritis:

* Gonococcal type can coexist with nongonococcal type; detected by gram-negative diplococci and persistence of PMNs
* PID can lead to infertility or ectopic pregnancy
* Gonococcal urethritis urethral stricture or abscess; perforation of the peritoneal scrotum; pharyngeal infection

Genital lesions:

* HSV primary infections may be associated with encephalitis and meningitis
* Syphilis neurosyphilis occurs more rapidly and is harder to treat with HIV; 50% of patients with primary syphilis and nearly 100% with secondary syphilis have Jarisch-Herxheimer reaction (fever, increased rash, adenopathy) 1 to 6 hours after antibiotic administration; the reaction is self-limited and is treated with anti-pyretics, but patients should be forewarned
* Chancroid predisposes to HIV; lesions spread to other parts of body or coalesce to form giant ulcers
* Genital warts strains of HPV (6 & 11), which commonly cause venereal warts, are generally not associated with cervical cancer; strains of HPV associated with dysplasia and cancer are not usually visible but may cause a mild cervicitis; again, all sexually active women should undergo routine pap smears
* Scabies atypical and severe forms occur with HIV

Prognosis

Vaginitis:

* Candida may resolve spontaneously or may become chronic
* Recurrence is common

Cervicitis: Prognosis is generally good if appropriately treated, but may lead to PID.

Urethritis: Recurrence is common. Prognosis is good if appropriately treated.

Genital lesions:

* HSV recurrences are usually milder; suppressive therapy is considered for when there are more than six episodes a year; resolution without sequelae is typical except in neonates and immuno-compromised persons
* Syphilis chronic infection, earlier stages resolve latently, reappearing in later stage
* Chancroid recurrent episodes lasting 1 to 3 weeks
* Genital warts resolution takes 20 weeks or more; no known therapy to completely eradicate HPV
* Scabies no sequelae with adequate treatment

Pregnancy

Some STDs may result in permanent damage to reproductive organs and infertility, particularly in the case of cervicitis leading to PID. Standard drugs for treatment of STDs may be teratogenic (e.g., metronidazole). Finally, presence of STDs often has potential ramifications for the neonate.

Vaginitis:

* Discharge more copious, incidence twice as high, therapy twice as long
* Fluconazole and metronidazole are contraindicated in pregnancy; see section entitled Drug Therapies for alternatives

Cervicitis:

* Rx of choice during pregnancy for chlamydia erythromycin 500 mg po qid x 7 days; do not use doxycycline
* Perinatal chlamydia can cause neonatal pneumonia or conjunctivitis
* Gonococcal infection may spread to eyes of neonate

Urethritis:

* Rx of choice during pregnancy erythromycin 500 mg po qid x 7 days or Amoxicillin 500 mg po tid x 7 days

Genital lesions:

* HSV primary infection during delivery may result in neurologic defects in the neonate or death of the neonate; if visible lesions present, neonate is delivered via cesarean section
* Syphilis desensitization in case of penicillin allergy; erythromycin unreliable for fetal cure; Jarisch-Herxheimer reaction can precipitate labor
* Chancroid Rx of choice during pregnancy is erythromycin 500 mg po qid x 7 days
* Genital warts avoid podophyllin; vaginally delivered neonate may develop laryngeal papillomatosis; cryotherapy safe during pregnancy
* Scabies avoid lindane

References

Azenabor AA, Mahony JB. Generation of reactive oxygen species and formation of membrane lipid peroxides in cells infected with Chlamydia trachomatis. Int J Infect Dis. 1999;4(1):46-50.

Berger RE. Sexually transmitted diseases: the classic diseases. In: Walsh PC, ed. Campbell's Urology. 7th ed. Philadelphia, Pa: W.B. Saunders Co.; 1998.

Brunham RC. Diseases caused by chlamydiae. In: Cecil RI, Plum F, Bennett JC, eds. Cecil Textbook of Medicine. 20th ed. Philadelphia, Pa: W.B. Saunders Co.; 1996.

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