Updated: Aug 12, 2009
Vulvovaginitis is common, affecting women of all ages. Vulvovaginitis is an inflammation of the vagina and vulva, most often caused by a bacterial, fungal, or parasitic infection. Vulvovaginitis, one of the most common reasons why women visit their gynecologist, causes vaginal discharge, irritation, and itching. Normally, a woman may have a vaginal discharge, the amount and consistency of which varies during the course of the menstrual cycle; however, vulvovaginitis causes a symptomatic increased vaginal discharge. Other symptoms associated with this condition are dyspareunia, dysuria, and odor.
Women with vulvovaginitis tend to be embarrassed or are worried about sexually transmitted diseases (STD). Self-treatment is usually the norm and close to 50% ineffective.1 In this country alone, millions of dollars are wasted on over-the-counter antifungals because of self-treatment for candidiasis.2 Providers may also be uncomfortable or do not have adequate time to diagnose the true etiology and may treat the wrong condition. Thus, vulvovaginitis is probably underdiagnosed.
Etiologies and the approach of management for a patient with vulvovaginitis are age dependent. Vulvovaginitis can be divided into 3 age categories: premenarchal, childbearing, and postmenopausal.
The normal vaginal epithelium cornifies (develops into a thickened layer of epithelial cells) under the influence of estrogen, protecting women against infection. A normal vaginal discharge consists of 1-4 mL of fluid that is white or transparent, thick, and odorless. This physiologic discharge is formed by sloughing epithelial cells, normal bacteria, and vaginal transudate. The discharge may be noticeable during pregnancy, oral contraceptive pill use, or at mid menstrual cycle, close to the time of ovulation.
The normal pH of vaginal secretions is 4.0-4.5.3 The pH is maintained by lactobacillus, which produces hydrogen peroxide and lactic acid; diphtheroids; and Staphylococcus epidermidis.2 Lactobacillus is found in 62-88% of women.3 Vaginal pH may increase with age, phase of menstrual cycle, sexual activity, contraception choice, pregnancy, presence of necrotic tissue or foreign bodies, and use of hygienic products or antibiotics.3
Bacterial vaginosis is secondary to bacterial overgrowth and not due to tissue inflammation. The organisms associated with bacterial vaginosis are Gardnerella vaginalis, Mycoplasma hominis, and Mobiluncus, a facultative anaerobe.4,5 Summarizing, practically any condition changing the vaginal milieu may result in vulvovaginitis.
Premenarchal
Vulvovaginitis is the most common gynecologic problem affecting prepubertal girls and is responsible for the largest number of visits to the gynecologist.
Childbearing age
Bacterial vaginosis is the most important cause of vulvovaginitis. Estimating the number of patients presenting with bacterial vaginosis is difficult because G vaginalis can be recovered from the vagina in 30-50% of asymptomatic women.6
Trichomonas vaginalis affects 2-3 million women annually in the United States. The organism also is detected in 30-40% of men who are exposed to women with T vaginalis.3 The prevalence of T vaginalis infection at clinics treating sexually transmitted diseases (STDs) varies from 8-31%. In men, T vaginalis may account for as many as 17% of cases of nongonococcal, nonchlamydial urethritis. T vaginalis infection appears to be more common in the southern United States.
Candidal vulvovaginitis is considered slightly less common than bacterial vaginosis, yet, 3 out of every 4 women in the United States will have at least 1 bout of vulvovaginal candidiasis (VVC) during their lifetime.4,6 Patients with recurrent or severe vulvovaginal candidiasis warrant a screening test for diabetes mellitus.
Postmenopausal
After menopause, most women experience some vaginal atrophy as estrogen levels fall. Incidence of atrophic vaginitis depends on how it is defined. Vulvovaginitis related to infection is much less common after menopause. Desquamative inflammatory vaginitis, an exception, has an unknown etiology, but a Gram stain of culture often reveals streptococci. This is treated with intravaginal clindamycin cream or a topical or intravaginal steroid.7 Postirritation vulvovaginitis may occur in women undergoing pelvic irradiation for cancer.
Bacterial vaginosis is the most common cause of vaginitis in women of childbearing age, with prevalence of 50-60% across the globe.
Trichomoniasis affects 180 million women worldwide.
No mortality has been documented primarily from vulvovaginitis.
Vulvovaginitis does not occur in males. Males may be carriers of G vaginalis and T vaginalis.
Different historical aspects should be ascertained depending on what vulvovaginitis category the patient may have.
| Candidiasis | Pediatrics, Child Sexual Abuse |
| Dermatitis, Atopic | Pediatrics, Foreign Body Ingestion |
| Dermatitis, Contact | Pediatrics, Urinary Tract Infections and
Pyelonephritis |
| Dermatitis, Exfoliative | Pelvic Inflammatory Disease |
| Gonorrhea | Trichomoniasis |
| Herpes Simplex | Vaginitis |
| Pediatrics, Child Abuse |
Treatment should be aimed at bacterial, parasitic, or fungal infection.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the clinical setting.25
A 7-day oral course yields a 90% cure, and single oral dose therapy yields an 80% cure. Relapses are common requiring a longer duration of treatment.26 Combinations of antibiotics have no benefit.25,26 If single oral dose therapy is ineffective, either administer a second oral dose in 48 hours or initiate weeklong therapy. Some patients prefer intravaginal medication.10 Treatment of bacterial vaginosis before 20 weeks' gestation may decrease preterm delivery.27 Only those women who are symptomatic from bacterial vaginosis should be screened.10,28,5 Topical metronidazole gel poorly achieves therapeutic concentration in the urethra and Skene's gland and therefore is not indicated in Trichomonas infections.19 Tinidazole may have less side effects than metronidazole and can be used in the rare case of metronidazole resistance.29
Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Indicated for treatment of bacterial vaginosis (formerly referred to as Haemophilus vaginitis, Gardnerella vaginitis, nonspecific vaginitis, Corynebacterium vaginitis, anaerobic vaginosis).
2 g PO once or 500 mg PO bid for 7 d for Trichomonas
For bacterial vaginosis: 500 mg PO bid for 7 d
Alternatively: Metronidazole gel 0.75%, 1 applicatorful (5 g) intravaginally qd for 5 d effective as oral metronidazole
Less efficacious (<50% cure for Trichomonas)
Pregnancy: 500 mg PO bid for 7 d or 250 mg PO tid for 7 days or 2 g PO once for T vaginalis
15-30 mg/kg/d PO divided bid for 7 d; not to exceed 500 mg or 40 mg/kg PO once
Alternatively: Insert 1 applicatorful as in adults
Cimetidine may increase toxicity of metronidazole; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; avoid alcohol during treatment and 24 h after that
Documented hypersensitivity; use of alcohol
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy; known or previously unrecognized vaginal candidiasis may present more prominent symptoms during metronidazole vaginal gel therapy; more than 6% of patients have developed symptomatic candidal vaginitis during or immediately after therapy
Avoid alcohol 24 h before therapy and 72 h after therapy
Indicated when the offending organism is group A streptococci. Inhibits biosynthesis of cell wall mucopeptide and is effective during active replication. Inadequate concentrations may produce only bacteriostatic effects.
500 mg PO q6h for 10 d
<12 years: 40-50 mg/kg/d PO divided tid/qid; not to exceed 3 g/d
>12 years: Administer as in adults
Probenecid can increase penicillin effectiveness by decreasing its clearance; conversely, coadministration of tetracyclines can decrease penicillin effectiveness
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in impaired renal function
5-Nitroimidazole derivative used for susceptible protozoal infections. The mechanism by which tinidazole exhibits activity against Giardia and Entamoeba species is not known.
500 mg PO bid for 5 d
Alternatively, 2 g PO one dose for Trichomonas
<3 years: Not established
>3 years: 50 mg/kg PO qd for 3 d with food; not to exceed 2 g/dose
Limited data exist; interaction information based on experience with other nitroimidazole derivatives (ie, metronidazole); may prolong PT when coadministered with warfarin; avoid alcoholic beverages and preparations containing ethanol or propylene glycol during and 3 d following administration (may cause disulfiramlike reaction); may increase serum levels of lithium, phenytoin, cyclosporine, tacrolimus, and fluorouracil; CYP450 inducers (eg, phenobarbital, rifampin, phenytoin) may increase elimination; CYP450 inhibitors (eg, cimetidine, ketoconazole) may decrease elimination; concurrent administration with cholestyramine may decrease oral bioavailability; oxytetracycline may antagonize effect
Documented hypersensitivity; first trimester of pregnancy; breastfeeding women (recommend interruption during therapy and for 3 d following last dose)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
X - Contraindicated; benefit does not outweigh risk
Caution in blood dyscrasias, organic neurological dysfunction, late trimesters of pregnancy, seizure disorders, and hepatic and renal impairment
Carcinogenicity has been observed in mice and rats treated chronically with metronidazole (another nitroimidazole), although not observed with tinidazole, use cautiously; may cause metallic/bitter taste, nausea, anorexia, vomiting, weakness, fatigue, dizziness, or headache; if administered on day of hemodialysis, administer additional dose equivalent to one-half of recommended dose following dialysis
DOC for penicillin-allergic patients with infections caused by susceptible strains of microorganisms, including group A streptococci. Inhibits RNA-dependent protein synthesis, possibly by stimulating dissociation of peptidyl tRNA from ribosomes, which inhibits bacterial growth.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.
250 mg erythromycin stearate/base, or 400 mg ethylsuccinate PO q6h 1 h ac or 500 mg q12h for 10 d
30-50 mg/kg/d PO divided q6-8h for 10 d, not to exceed 2 g/d; double dose for severe infections
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs
Useful as treatment against serious skin and soft tissue infections caused by most staphylococcal strains. Inhibits bacterial protein synthesis by inhibiting peptide chain initiation at the bacterial ribosome, where it preferentially binds to the 50S ribosomal subunit, causing bacterial growth inhibition. Has a 90% cure rate and is used as an alternative to metronidazole.
Cream 2%: 1 applicatorful (5 g)intravaginally hs for 7 d
Alternatively: Administer 300 mg PO bid for 7 d or clindamycin ovules 100 g intravaginally qhs for 3 d
20-30 mg/kg/d PO divided tid/qid for 7 d
None reported
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Avoid contact with eyes; vaginal cream contains ingredients that cause burning and irritation of the eye; in event of accidental contact, rinse eye with copious amounts of cool tap water; use of clindamycin vaginal cream may result in overgrowth of nonsusceptible organisms, particularly yeasts, in vagina; clindamycin cream and ovules are oil-based and might weaken latex condoms and diaphragms; antibiotic-associated colitis has been reported with both oral and topical clindamycin
These agents are used to treat extreme vaginal pruritus. Cream is for symptomatic relief, especially in pediatric vulvovaginitis.
These agents are adrenocorticosteroid derivatives incorporated into a vehicle suitable for application to skin or external mucous membranes.
DOC because of its mineralocorticoid activity and glucocorticoid effects.
Primary therapeutic effects of topical corticosteroids are from their anti-inflammatory activity, which is nonspecific (ie, they act against most causes of inflammation including mechanical, chemical, microbiological, immunological).
Do not use very high or high-potency agents on the face, groin, or axilla.
Apply sparingly bid to vagina in affected areas
Apply as in adults
None reported
Documented hypersensitivity; viral, fungal, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use, applying over large surface areas, applying potent steroids, and using occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria
These agents are used to treat candidal vulvovaginitis. Topical azole antifungals achieve cure rates of 85-95%. Nystatin demonstrates a 75-80% cure rate. Oral fluconazole has a cure rate comparable to topical azole antifungals.30 It may be preferred by patients because of the ease of one-time dosing.
Intravaginal and topical therapies with a variety of antifungals, such as clotrimazole, miconazole, terconazole, and tioconazole, are highly effective. Many of the preparations are now available OTC. 1-, 3-, and 7-day regimens can be used. Cure rates of 90% are reported with longer courses.
Broad-spectrum antifungal agent that inhibit yeast growth by altering cell membrane permeability, which causes fungal cell death.
3-d therapy:
2% cream: Insert 5 g, 1 applicatorful, intravaginally qhs for 3 d
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
If sensitivity or chemical irritation occurs, discontinue use; use only externally; avoid contact with eyes
Broad-spectrum antifungal agent that inhibit yeast growth by altering cell membrane permeability, which causes fungal cell death.
1-d therapy:
6.5% ointment: Insert 5 g, 1 applicatorful, intravaginally once
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
If sensitivity or chemical irritation occurs, discontinue use; use only externally; avoid contact with eyes
Broad-spectrum antifungal agents that inhibit yeast growth by altering cell membrane permeability, which causes fungal cell death.
1-d therapy:
500-mg tab: Insert 1 applicatorful intravaginally once
3-d therapy:
100-mg tab: Insert 2 tab intravaginally qhs for 3 d
7-d therapy:
Applicator: Insert 5 g, 1 applicatorful, of 1% vaginal cream intravaginally qhs for 7-14 d
Vaginal tab: Insert 1 tab (100 mg) intravaginally qhs for 7 d
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
If irritation (5%-10% will have local burning)or sensitization occurs, discontinue use; chronic or recurrent candidiasis may be a symptom of unrecognized diabetes mellitus or a damaged immune system (including HIV infection); persistently resistant infections may be re-infections, thus evaluate sources of re-infection; if lack of response, repeat microbiologic studies to confirm diagnosis and exclude other pathogens before re-instituting antifungal therapy; do not use creams in mouth or eyes; no well-controlled studies have been performed during first trimester of pregnancy; these products may compromise condoms and diaphragms
Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation. Consider ease of use, although direct cost may be a limiting factor. Do not recommend PO antifungals in pregnancy.
1-d therapy:
150 mg PO once may repeat on the third day if infection not improved
3-6 mg/kg PO qd for 14-28 d, depending on severity of infection
Levels may increase with hydrochlorothiazides; levels may decrease with chronic coadministration of rifampin; coadministration of fluconazole may decrease phenytoin concentrations; may increase concentrations of theophylline, tolbutamide, glyburide, and glipizide; effects of anticoagulants may increase with fluconazole coadministration; increases in cyclosporine concentrations may occur when administered concurrently
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Monitor closely if rashes develop and discontinue drug if lesions progress; may cause clinical hepatitis, cholestasis, and fulminant hepatic failure (including death) with underlying medical conditions such as AIDS or a malignancy and while taking multiple concomitant medications; not recommended for women who are breastfeeding
Broad-spectrum antifungal agent that inhibit yeast growth by altering cell membrane permeability, which causes fungal cell death.
3-d therapy:
200-mg vaginal suppository: Insert 1 supp intravaginally qhs for 3 d
7-d therapy:
2% cream: Instill 5 g, 1 applicatorful, intravaginally qhs for 7 d
100-mg vaginal supp: Insert 1 supp intravaginally qhs for 7 d
Administer as in adults
May impair barrier contraceptives
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
If sensitivity or chemical irritation occurs, discontinue use; use only externally; avoid contact with eyes; adverse effects include vaginal burning, irritation, and dyspareunia
Broad-spectrum antifungal agent that inhibit yeast growth by altering cell membrane permeability, which causes fungal cell death.
3-d therapy:
0.8% cream: Insert 5 g, 1 applicatorful, intravaginally qhs for 3 d
80-mg vaginal supp: Insert 1 supp intravaginally qhs for 3 d
7-d therapy:
0.4% cream: Insert 5 g, 1 applicatorful, intravaginally for 7 d
Tab: Insert 2 tab (100 mg each) intravaginally qhs for 3 d or a 500-mg tab intravaginally once
1% vaginal cream: Apply to external genitalia bid
Not established
May impair barrier contraceptives
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
If sensitivity or chemical irritation occurs, discontinue use; use only externally; avoid contact with eyes; high doses may cause fever or flulike symptoms
Broad-spectrum antifungal agents that inhibit yeast growth by altering cell membrane permeability, which causes fungal cell death.
2% cream: Rub gently into affected area qd/bid
Not established
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
If sensitivity or irritation develops, discontinue use; for external use only; avoid contact with eyes
Broad-spectrum antifungal agent that inhibit yeast growth by altering cell membrane permeability, which causes fungal cell death.
Insert 1 vaginal tab (100,000 U) qhs for 2 wk
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use to treat systemic mycoses
These agents are used in treatment of atrophic vaginitis in postmenopausal women. Oral estrogen replacement also is effective and has other health benefits. Oral estrogen therapy generally should be initiated by a primary care provider rather than an ED clinician.
Several topical steroid preparations are available, including equine estrogen, estradiol, and dienestrol. Estrogens are indicated for atrophic vaginitis and atrophic urethritis associated with menopause.
0.3-1.25 mg PO qd, depending on tissue response of patient
Topical: Insert 2-4 g, 0.5-1 applicatorful intravaginally qhs
Recommendation: Cyclical administration consisting of 3 wk of daily estrogen and 1 wk off
Not established
May reduce hypoprothrombinemic effects of anticoagulants; coadministration of barbiturates, rifampin, and other agents that induce hepatic microsomal enzymes may reduce estrogen levels; pharmacologic and toxicologic effects of corticosteroids may occur as a result of estrogen-induced inactivation of hepatic P450 enzyme; loss of seizure control has been noted when administered concurrently with hydantoins
Documented hypersensitivity; known or suspected pregnancy; breast cancer; undiagnosed abnormal genital bleeding; active thrombophlebitis or thromboembolic disorders; history of thrombophlebitis, thrombosis, or thromboembolic disorders associated with previous estrogen use (except when used in treatment of breast or prostatic malignancy)
X - Contraindicated; benefit does not outweigh risk
Certain patients may develop undesirable manifestations of excessive estrogenic stimulation, such as abnormal or excessive uterine bleeding or mastodynia; estrogens may cause some degree of fluid retention (exercise caution); prolonged unopposed estrogen therapy may increase risk of endometrial hyperplasia
These agents are used to treat parasitic infections. Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.
Indicated drug to treat pinworm. Kills worms by selectively and irreversibly blocking glucose uptake and other nutrients in the susceptible adult intestine where helminths dwell.
100 mg PO once
Alternatively: Administer 100 mg PO bid on 3 consecutive days; second course may be administered if patient is not cured within 3-4 wk
<2 years: Not established
>2 years: Administer as in adults
Carbamazepine and phenytoin may increase mebendazole metabolism, decreasing its efficacy; conversely, cimetidine may increase mebendazole levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid in pregnancy, especially during first trimester; may need to adjust dose in hepatic impairment
Used as an alternative to mebendazole; a depolarizing neuromuscular blocking agent that inhibits cholinesterases, resulting in spastic paralysis of the worm. Active against E vermicularis (ie, pinworm) and Ascaris lumbricoides (ie, roundworm). Also effective against Ancylostoma duodenale (ie, hookworm). Purging is not necessary; may be taken with milk or fruit juices.
11 mg/kg (5 mg/lb) PO not to exceed 1 g once without regard to ingestion of food or time of day
<2 years: Not established
>2 years: Administer as in adults
In ascariasis, pyrantel and piperazine are mutually antagonistic and should not be used concomitantly; theophylline serum levels may increase in pediatric patients following pyrantel pamoate administration
Documented hypersensitivity; hepatic disease
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in liver impairment, anemia, and malnutrition
These agents competitively bind to estrogen receptor, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects.
May be used for women who are very concerned about estrogen exposure. Known to have both estrogen antagonist and agonist effects, depending on target tissue.
10-20 mg PO bid
Not established
May exacerbate hepatotoxic effects of allopurinol; may increase cyclosporine serum levels; increases anticoagulant effects of warfarin; aminoglutethimide reduces serum concentration of tamoxifen; cyclophosphamide, methotrexate, and 5-FU increase thrombotic risk of tamoxifen
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in leukopenia, thrombocytopenia, and hyperlipidemia; decreased visual acuity, corneal changes, and retinopathy may occur with >1 y of use; may induce ovulation
Video available at http://img.medscape.com/pi/emed/ckb/emergency_medicine/756148-794917-797497-1698515.flv.
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vulvovaginitis, vaginitis, vaginal yeast infection, vaginosis, bacterial vaginosis, lactobacillus, inflammation of vagina, inflammation of vulva, vaginal discharge, vaginal itching, vaginal irritation, vaginal fluid, vaginal pH, Gardnerella vaginalis, G vaginalis, Staphylococcus epidermis, S epidermis, Trichomonas vaginalis, T vaginalis, vulvovaginal candidiasis, VVC, candidal vulvovaginitis, desquamative inflammatory vaginitis, atrophic vaginitis, trichomoniasis
Mark J Leber, MD, MPH, Clinical Assistant Professor of Emergency Medicine, Weill Medical College of Cornell University; Consulting Staff, Department of Emergency Medicine, Brooklyn Hospital Medical Center
Mark J Leber, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and American College of Physicians
Disclosure: Nothing to disclose.
Anuritha Tirumani, MD, Research Coordinator, Department of Emergency Medicine, Brooklyn Hospital Center
Disclosure: Nothing to disclose.
David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
David S Howes, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Mark Zwanger, MD, MBA, Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University
Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association
Disclosure: Medicines Company Consulting fee Consulting; Pfizer Salary Employment
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center
Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.