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Chapter 37  •  Vaginal Discharge and Itching
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examination is the frog leg position. Have the parent sit on a chair and then have the patient sit on her parent’s lap for the examination. The most common problem (vulvovaginitis) of the younger child requires only the lower third of the vagina to be visualized. A more de­tailed visual examination requires labial separation and labial traction.
Perform an Internal Vaginal Examination
Note the condition of the vaginal walls. A plastic speculum makes vaginal wall inspection easy and helps in the identication of a foreign body for re­moval. In children, the knee-chest position is useful for inspecting the vagina. If a foreign body is suspected in children, removal is done using sedation. Pale or mot­tled red splotches of the vaginal mucosa with a sticky, yellow-brown discharge are associated with atrophic vaginitis. In severe cases of atrophic vaginitis, the pale, thin mucosa may have adhered to the opposing vaginal wall, and the speculum examination often causes an oozing bloody discharge.
The appearance of the cervix should be noted. A friable or “strawberry” appearance of cervical petechiae with a frothy, foul-smelling discharge is descriptive of a trichomonas infection. A mucopuru­lent discharge from the cervical os is an indication to obtain an endocervical sample for gonorrhea and chlamydia testing. This discharge is yellowish-green when collected on an endocervical swab. The charac­ter of the discharge does not consistently identify common infectious causes of vaginitis. Treat vaginal infections before the Papanicolaou test is obtained because BV and trichomoniasis may cause inamma­tory atypia results.
Obtain a sample for testing. The wet mount is a valu­able diagnostic tool, and a sample of vaginal discharge is best obtained from the lateral vaginal fornices. Three positive characteristics for any one etiology can cor­rectly identify the causative agent (e.g., increased pH; the presence of “clue cells,” which are epithelial cells full of bacteria that obscure the cell border; and a thin gray discharge seen in BV) (see Differential Diagno­sis). DNA testing and/or culture may also be indicated (see Laboratory and Diagnostic Studies). Cultures for BV, fungal infections, and T. vaginalis are not routinely recommended and are usually reserved for determining resistant organisms.
Perform a Bimanual Examination
Assess the condition of the uterus, fallopian tubes, and ovaries by checking for uterine and cervical motion
tenderness (CMT), ovarian size, and presence of masses. CMT or pain on palpation of the uterus and adnexa conrms the spread of vaginitis or cervicitis to the upper genital tract and results in PID. This warrants immediate evaluation and treatment or refer­ral to prevent tubal scarring, ectopic pregnancy, and infertility.
Perform a Vaginal-Rectal Examination
Vaginal-rectal examination is an important technique in assessing the posterior uterus and condition of the cul-de-sac as well as the rectum. The internal examina­tion glove must be changed before rectal insertion to prevent contamination of the rectum with vaginal discharge organisms. A rectal examination, using the fth digit, is used to palpate a foreign body and to check pelvic anatomy in the child.
LABORATORY AND DIAGNOSTIC STUDIES
Potassium Hydroxide and Wet Mount/Preparation
Obtain a discharge sample from the lateral fornices of the vagina using a cotton-tipped applicator. There are several acceptable techniques for preparing a diagno­ses and wet mount. One is to prepare two slides with a smear of vaginal discharge. To one slide, add a drop of 10% KOH and put a coverslip in place. To the other slide, add a drop of normal saline and put a coverslip in place. The whiff test is positive when the addition of the 10% KOH produces a shy odor, which is caused by the release of amines. The whiff test has a positive predictive value of 76% for BV. Look under the micro­scope at the KOH slide for the presence of branching and budding hyphae that are characteristic of yeast in­fection. Examine the saline wet mount microscopically for motile trichomonads that signal the presence of trichomonas. Clue cells are characteristic of BV (see
Figure 37-1).
Test for pH
Most litmus paper reads the pH range from 3.0 to 9.0. This is a simple inexpensive test to aid in determining the cause of the vaginal discharge. Normal vaginal se­cretions have a pH less than 4.5. A pH greater than 4.5 is consistent with BV, trichomoniasis, or atrophic vaginitis.
Fungal Culture or Sabouraud Agar Culture
Fungal culture may be needed in the diagnosis of non-Candida albicans (e.g., C. glabrata, C. tropicalis, C. krusei) that are refractory to medication regimens.
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Herpes Viral Culture
Viral culture is the most specic method of diagnosing herpes. Results may take from 1 to 7 days, with maxi­mum sensitivity achieved at 5 to 7 days. The herpes culture will probably not be able to identify the caus­ative agent if the specimen is taken from a lesion that is 5 or more days old. It is important to document positive genital herpes infections in the pregnant woman and in skin lesions of the newborn. Collect cells or uid from a fresh sore with a cotton swab and place them in the culture container. You may need to unroof a vesicle to obtain a specimen.
Herpesvirus Antigen Detection Test
This test detects antigens on the surface of cells in­fected with the herpes virus. Cells from a fresh sore are scraped off and then smeared onto a microscope slide. This test may be done in addition to or in place of a viral culture.
Tzanck Smear
Characteristic ndings of a Tzanck smear are multi­nucleated giant cells that are likely to be found if the specimen is from an intact herpes lesion. Prepare the Tzanck smear by removing the roof of the vesicle and scraping the skin with a scalpel blade. Make sure that the base and the margins of the vesicle are scraped. Do not use the vesicular uid for this specimen. The cellular material is spread onto a glass slide, xed with absolute alcohol for 1 minute, and then stained with Wright stain. Alternative staining methods are available, and guidelines can be obtained from local laboratories.
Modified Diamond Culture
Diamond culture is used to identify Trichomonas species, but it is seldom needed to make the diagnosis.
Thayer-Martin Culture
Thayer-Martin medium is a bacterial culture that iden­ties gonococcal infections. A culture is taken from the endocervical canal of the uterine cervix. First remove excess mucus from a portion of the cervix using a cot­ton ball held in ring forceps or a large cotton-tipped procto-swab. Insert a sterile cotton-tipped applicator (Q-tip) into the endocervical canal and allow it to ab­sorb the mucus for 10 to 30 seconds before inoculating the medium. Inoculate the medium bottle or plate in a zigzag manner while simultaneously rolling the small cotton-tipped applicator. When opening the Thayer­Martin culture bottle, avoid holding the bottle totally upright, which will allow for the loss of the carbon dioxide from the specimen collection bottle.
DNA Testing for Infectious Organisms
DNA testing using a sample taken from the vagina provides rapid, sensitive, and specic results. A num­ber of products are available. DNA tests include DNA probes, nucleic acid amplication tests (NAATs), and polymerase chain reaction assays. Tests are available for Chlamydia trachomatis, N. gonorrhoeae, T. vagi- nalis, Gardnerella vaginalis, Candida species, and herpes simplex virus. Samples for chlamydia and gon­orrhea testing can be obtained by the practitioner or by the patient. Urine NAATs can be used to screen for possible STIs in children. A positive test result must be followed up with a culture for denitive diagnosis.
Syphilis Testing
Serology tests are used for screening and diagnosing syphilis and are recommended if other STIs are found or suspected. The screening tests are nontreponemal and include VDRL (Venereal Disease Research Laboratory), RPR (rapid plasma reagin), and EIA (enzyme immuno­assay) tests. Diagnostic tests are T. pallidum-specic
EVIDENCE-BASED PRACTICE
This study  of women in  the United Kingdom  compared self­swabbing vulvovaginal samples for sexually transmitted infec­tions  (STIs)  with  clinician-obtained  endocervical  samples.  The authors  found that in  women with symptoms  suggestive  of gonorrheal infection, the DNA assays—both clinician- and  self-collected—were equivalent and more sensitive than gon­orrhea  culture.  For  chlamydia,  self-collected  vulvovaginal  swabs  were  significantly  more  sensitive  than  clinically  ob­tained  endocervical  swabs  (97%  vs  88%)  and  had  equal 
Copyrighted 2015. IMNG. 116311:0315BN
Self-swabbing for Sexually Transmitted Infections
specificity  (99.9%  vs  100%).  In  women  with  symptoms  of   an  STI,  the  sensitivity  was  97%  vs  88%;  in  those  with  no  symptoms,  the  sensitivity  was  97%  vs  89%.  The  authors  concluded  that  self-collected  vulvovaginal  swabs  are  the  sample of choice for both chlamydia and gonorrhea testing in  women, regardless of  whether  or  not symptoms are present.  When a clinical examination is performed, either the clinician  or the patient can collect a vulvovaginal swab sample.
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and include FTA-ABS (uorescent treponemal antibody absorption test) and TPPA (T. pallidum particle aggluti- nation assay). Detection of T. pallidum can also be done using polymerase chain reaction DNA testing.
Urinalysis
Urinalysis should be obtained if the patient has dys­uria. However, external pain on urination may origi­nate from urine on inamed vulvar tissue, eliminating the need for urinalysis.
Microscopy and Skin Scraping
Viewing a skin scraping under the microscope is used to assist with the differential diagnosis of scabies and pubic lice (see Chapter 28).
Scotch Tape Test
Use this test when you suspect pinworms (Enterobius vermicularis), which occur most commonly in chil-
dren. Instruct the adult to apply adhesive cellophane tape to the child’s perianal region early in the morning when the child awakens. The tape is then removed, placed in a plastic bag, and brought in to the clinic. Place it on a glass slide and examine under a micro­scope for the presence of eggs. Parents may also be able to see the worms by shining a ashlight on the external anus of the child at night. The female worm is about 10 mm long (see Figure 37-2).
macular or papular border. The surface will appear ver­rucous. False-positive results can occur with candidia­sis, psoriasis, lichen planus, and sebaceous glands.
Follicle-Stimulating Hormone
Follicle-stimulating hormone (FSH) levels that are greater than 30 mU/mL are diagnostic of perimeno­pause, and levels of 40 mU/mL or higher represent menopause. This test is particularly helpful in estab­lishing the hypoestrogenic status of a young woman who is experiencing premature menopause and atro­phic vaginitis (see Evidence-Based Practice box).
DIFFERENTIAL DIAGNOSIS
Discharges
Physiological Discharge
Normal vaginal discharge, produced by the cervical and vulvar glands, is mucoid, clear or white in color, and has no foul odor. The amount varies from scant to profuse, depending on the amount of estrogen stimula­tion to the tissues. On occasion, physiological dis­charge can lead to slight vulvar irritation and mild itching secondary to wetness. The vaginal pH is less than 4.5. Wet mount reveals up to 3 to 5 white blood cells (WBCs)/high-power eld (HPF) and the presence of epithelial cells and lactobacilli.
Acetic Acid Test (Acetowhite)
The acetic acid test is best used to detect subclinical lesions caused by human papillomavirus when a geni­tal wart has been identied, when there has been sexual contact, or when the Pap test indicates dysplasia. The application of 5% acetic acid (vinegar) to the cervix, labia, or perianal area causes the lesion to turn white (acetowhite). Saturate a gauze pad with vinegar and place on the lesion for 5 to 10 minutes. After this soak­ing, the white wart will have a sharp circumscribed
EVIDENCE-BASED PRACTICE
According  to  this  systematic  review,  approximately  33%  of  patients with  vaginal discharge  will have bacterial vaginosis,  25% will  have  candidiasis,  and 10% will have  trichomonia­sis.  The  lack  of  a  perceived  odor  makes  candidiasis  more  likely (LR, 2.2), but the absence of the symptom is not con­clusive. No symptoms reliably identify trichomoniasis. A thick  or “curdy”  discharge  is  compatible with yeast, but  does  not 
Data from Piscitelli JT, Simel DL: Update:  Vaginitis. In Simel DL, Drummond  R (eds.): The rational clinical examination: Evidence based clinical
, New York, 2009, McGraw  Hill.
diagnosis
Bacterial Vaginosis
BV is the most common cause of vaginal discharge and is considered a disturbance in normal vaginal ora. It is often found after intercourse with a new partner or in conjunction with other STIs. Fifty percent of women are asymptomatic; infection is associated with in­creased preterm labor in pregnant women and patients undergoing vaginal surgical procedures (increased infection). Symptoms include a thin homogeneous white, gray, green, or brownish discharge that has a
Clinical Diagnosis of Vaginitis
rule  out  additional  infection.  Microscopic  evaluation  is   required  to  identify  clue  cells  (bacterial  vaginosis),  yeast  forms (vaginal  candidiasis),  or  trichomonads (vaginal tricho­moniasis).  The  authors  concluded  that  diagnosis  is  best   established by measuring the pH of the discharge, performing  the whiff test, and using microscopic examination.
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foul odor; there can be pelvic tenderness or pain but no CMT. The vaginal pH is greater than 4.5. Wet mount shows clue cells and a few lactobacilli; the “whiff” test is positive (see Figure 37-1).
Candida Vulvovaginitis
Ninety percent of women with candida vulvovaginitis present with vulvar pruritus. In children, it may be ac­companied by oral thrush. The discharge is often thick, white, and “curdy;” the labia are erythematous and edematous. Vaginal pH is 4.0 to 4.7. A KOH wet mount shows pseudohyphae and spores (see Figure 37-1).
Trichomoniasis
Trichomoniasis is asymptomatic in about half of the women and 90% of the men affected. It is usually transmitted via sexual contact but can also be spread by fomites. Women with chronic infections will have copious amounts of discharge and little or no inam­mation of the vaginal tissues. When there is an acute infection, they will report vulvar itching, swelling, and redness. The pH is greater than 5; the discharge is white, grayish-green, or yellow, and sometimes frothy; infrequently there will be a “strawberry cer­vix” (cervical petechiae). If the woman has douched within the past 24 hours, the sensitivity of tests will be greatly decreased. Wet mount shows “gyrating” motile protozoa and often greater than 10 WBCs/HPF (see Figure 37-1).
Atrophic Vaginitis
In atrophic vaginitis, there is a dry (shiny), pale, thin vaginal wall caused by an insufcient amount of endogenous estrogen. During menopause, the vaginal mucosa and vulva, which lack glycogen, become frag­ile and are susceptible to injury and infection. Patients may experience burning, dryness, irritation, or dyspa­reunia. This also occurs in postpartum women, those who are breastfeeding, and prepubertal girls. The pH is alkaline and ranges from 6.5 to 7.0. Wet mount shows a few WBCs and is negative for pathogens.
Allergic Vaginitis
The causes of allergic vaginitis are different in children and adults. In the child, the most common offending agents are bubble baths and perfumed soaps. Adult vulvovaginitis involves any harsh or caustic substance that has direct contact with the area. Often a new brand of vaginal lubricant, douche, spermicide, or condom will cause the inammation and edema. Vinegar douches stronger than 1 to 2 tablespoons per quart
of water may also irritate tissues. The wet mount is positive for WBCs and negative for pseudohyphae.
Foreign Body
The presenting symptom in foreign body retention is a very malodorous, whitish discharge. In children, the for­eign body is as variable as those objects found in the ears and nose. However, children younger than 12 months do not have the coordination to insert anything into their va­gina, so suspect child abuse in such cases and inspect for bruising or excoriations. Wet mount reveals many WBCs.
Chlamydia
Chlamydia is the most prevalent STI in the United States. About 30% of infected women are asymptom­atic. Gonorrhea and chlamydia coexist in up to 60% of patients. Women with chlamydia have an increasing amount of vaginal discharge and bleeding after inter­course. Those at greatest risk for infection are younger than 25 years, sexually active with three or more part­ners, and not using barrier methods of contraception. Wet mount shows greater than 10 WBCs/HPF and few microscopic bacteria. DNA testing conrms the diag­nosis. Except for perinatal syndromes, nonsexual transmission has not been reported; therefore, suspect child abuse in children with chlamydia infection.
Gonorrhea
Gonorrhea is one of the most common reportable diseases. Women are asymptomatic 50% to 80% of the time. However, the patient may have purulent discharge that originates from the endocervical co­lumnar and transitional cells. Patients often experi­ence inammation of Skene glands, Bartholin glands, or the urethra, which causes pain and dysuria. Culture or DNA testing conrms the diagnosis. A nding of gonorrhea in children is considered specic evidence of sexual abuse.
Pelvic Inflammatory Disease
PID is most commonly caused by Chlamydia tracho­matis and N. gonorrhoeae (see Chapter 3) and can
produce bleeding, abdominal pain, fever, and vaginal discharge. Women with PID have an increasing amount of vaginal discharge and bleeding after intercourse. Infection begins intravaginally in most cases and then spreads upward, causing salpingitis. In the early stages, women may be asymptomatic. Patients may have a purulent discharge that originates from the endocervi­cal columnar and transitional cells. With gonorrhea, patients often experience inammation of Skene
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glands, Bartholin glands, or the urethra, which causes pain and dysuria. On examination, abdominal tender­ness, CMT, and adnexal tenderness are present. As with peritonitis, patients may also have guarding and rebound tenderness. WBCs and erythrocyte sedimenta­tion rate are usually elevated. Cultures, Gram staining, and DNA testing can assist with diagnosis. Women with suspected PID should have a pregnancy test to rule out ectopic pregnancy and complications of an intrauterine pregnancy. All patients diagnosed with acute PID should also be tested for HIV infection.
Itching and Lesions
Syphilis
The chancre of primary syphilis is an ulcerative lesion that most often develops at the site of initial inocula­tion. The syphilitic chancre begins as a papule and progresses to a painless, tender, hard, indurated ulcer. The infection causes inguinal lymphadenopathy. Even without treatment, the lesion will heal in 3 to 6 weeks. Many chancres go unnoticed until the appearance of condylomata lata, the warty papule of secondary syph­ilis, or a maculopapular rash on the palms of the hands and soles of the feet. Diagnosis is conrmed with sero­logical or DNA testing for syphilis.
Genital Warts
Genital warts (condylomata acuminata) are caused by the human papillomavirus and may be precursors to genital cancers. The warts may involve the vagina, cervix, perineum, or perianal areas. Condylomata can be at or raised verrucous lesions (Figure 37-3). The patient usu- ally notices a bump in the genital region accompanied by itching and leukorrhea. A wet mount should be performed to rule out any coexisting vaginal infections. An acetic acid test is helpful in identifying at warts. Referral to a dermatologist or gynecologist is indicated for treatment of warts of the urethra or anus. High-risk human papilloma­virus testing of genital warts is not recommended.
FIGURE 37-3 Condylomata acuminata. (From Morse SA, Holmes
KK, Ballard R: Atlas of sexually transmitted diseases and AIDS, ed. 3, St Louis, 2003, Mosby.)
FIGURE 37-4 Herpes. (Left from Habif. TP: Clinical dermatology, ed 4, St. Louis, 2004, Mosby. Right from
Morse SA, Holmes KK, Ballard R: Atlas of sexually transmitted diseases and AIDS, ed. 3, St Louis, 2003, Mosby.)
Herpes
Herpetic lesions can be difcult to distinguish from ulcerative lesions. The most typical presentation is that of grouped vesicles on an erythematous base that rupture and erode (Figure 37-4). A prodrome of
BA
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Chapter 37  •  Vaginal Discharge and Itching
tingling or itching occurs before the outbreak of the vesicles. On the vulva, the erosions are covered with a whitish, exudative layer. Herpetic outbreaks can involve the cervix, vagina, vulva, anus, or extra­genital organs, like the pharynx. Culture, antigen test, Tzanck smear, or DNA testing conrms the diagnosis.
If the mother has an active primary herpes simplex
virus infection at the time of birth, the infant has a 50% risk of becoming infected. Recurrent maternal infections impart a less than 5% risk of transmission. Clinical signs of the infant’s infection become appar­ent in the rst week of life and pose the possibility of death.
Molluscum Contagiosum
Molluscum are small (2 to 5 mm in diameter), umbili­cated, esh-tone papules (Figure 37-5). These charac­teristic lesions are the hallmark of the diagnosis. Scratching can spread them. Molluscum is an STI of adults and a likely nding in HIV-infected patients. When children are found to have genital molluscum, suspect child abuse.
FIGURE 37-5 Molluscum contagiosum. (From Black M,
Ambros-Rudolph C, Edwards L, et al: Obstetric and gynecologic dermatology, London, 2008, Mosby.)
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Vaginal Discharge and Itching
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
DISCHARGES
Physiological  
discharge
Bacterial vaginosis Foul-smelling discharge Homogeneous thin white or 
Candida vulvovaginitis
Trichomoniasis Watery discharge; foul odor Profuse, frothy, greenish  
Atrophic vaginitis Dyspareunia; vaginal dryness Pale, thin vaginal mucosa; 
Allergic vaginitis Examples: New bubble bath, 
Foreign body Red and swollen vulva; vaginal 
Chlamydia
Increase in discharge; no foul 
odor, itching, or edema
Pruritic discharge White, curdy discharge;  
soap, douche
discharge; history of tampon,  condom, or diaphragm use
Partner with nongonococcal 
urethritis; asymptomatic;  discharge or bleeding   after intercourse
Clear or mucoid; pH ,4.5
gray discharge; pH .4.5
pH 4.0-5.0
discharge; red friable   cervix; pH 5.0-6.0
pH .4.5
Foul smell, erythema, “lost 
tampon,” pH ,4.5
Bloody, foul-smelling  
discharge
May or may not have  
purulent discharge
Up to 3-5 WBCs/HPF;  
epithelial cells, lactobacilli
Presence of KOH “whiff”  
test; presence of clue   cells; few lactobacilli   (see Figure 37-1)
KOH prep: mycelia, budding, 
branching yeast, pseudohy­phae (see Figure 37-1)
Round or pear-shaped  
protozoa; motile “gyrating”  flagella (see Figure 37-1)
Folded, clumped epithelial 
cells
WBCs
WBCs
DNA testing; .10 WBCs/HPF
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DIFFERENTIAL DIAGNOSIS OF
Common Causes of Vaginal Discharge and Itching—cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
DISCHARGES
Gonorrhea
Pelvic inflammatory 
disease (PID)
ITCHING AND LESIONS
Syphilis
Genital warts Mild-to-moderate itching, foul 
Herpes History of prodromal  
Molluscum  
contagiosum
CMT, Cervical motion tenderness; ESR, erythrocyte sedimentation rate; HIV, human immunodeficiency virus; HPF, high-power field; KOH, potassium  hydroxide; STI, sexually transmitted infection; WBC, white blood cell.
—cont’d
Partner with STI;  
often asymptomatic
Bleeding, abdominal pain,  
fever, and vaginal dis­charge; increasing amount  of vaginal discharge and  bleeding after intercourse
History of painless ulcerative 
lesion; rash on palms and  soles of feet; warty growth  on vagina or anus
vaginal discharge; child:  history of sexual abuse;  adult: new or multiple  partners; history of warts
syndrome, paresthesias,  burning, itching; may   have mucoid vaginal   discharge
History of contact with  
infected person;   if inflamed: itching
Purulent discharge;   
inflammation of S kene/ Bartholin glands
CMT and adnexal tenderness; 
may also have guarding  and rebound tenderness
Chancre: usually one but can 
be more, painless ulcer­ation; condylomata lata:  flat, whitish papule or  plaque; maculopapular  rash: palm, soles, body
Moist, pale-pink, verrucous 
projections on base; lo­cated on vulva, vagina,  cervix, or perianal area
Grouped vesicles on red 
base, erode to an ulcer;   if on mucous membrane,  exudates form; if on skin,  crusts form; redness,  edema, tender inguinal  lymph nodes
Flesh-colored, dome-shaped 
papules, some with umbili­cation; usually 2-5 mm in  diameter
Gram stain; culture;  
DNA testing
WBC; culture; Gram stain; 
DNA testing (chlamydia   and gonococcus), syphilis  testing; ESR, C-reactive  protein; pregnancy, HIV
Syphilis and DNA testing
Acetic acid test: white
Viral culture; Tzanck smear; 
DNA testing
None
References and Readings
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Baron EJ, Miller JM, Weinstein MP, et al: A guide to utilization of
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355:1244, 2006. French L, Horton J, Matousek M: Abnormal vaginal discharge: Using
ofce diagnostic testing more effectively, J Fam Pract 53:805, 2004. Gradison M: Pelvic inammatory disease, Am Fam Physician
85:791, 2012.
Hainer BL, Gibson MV: Vaginitis, Am Fam Physician 83:807, 2011. Jasper J: Vulvovaginitis in the prepubertal child, Clin Pediatr Emerg
Med 10:10, 2009.
Markle W, Conti T, Kad M: Sexuality transmitted diseases, Prim
Care 40:557, 2013.
Mitchell H: ABC of sexually transmitted infections: Vaginal
discharge—causes, diagnosis, and treatment, BMJ 328:1306,
2004.
Page C, Mounsey A, Rowland K: PURLs: Is self-swabbing for STIs
a good idea? J Fam Pract 62:651, 2013.
Piscitelli JT, Simel DL: Update: Vaginitis. In Simel DL, Drummond
R (eds.): The rational clinical examination: Evidence based clini- cal diagnosis, New York, 2009, McGraw Hill.
Quan M: Vaginitis: Diagnosis and management, Postgrad Med
122:117, 2010.
Trent M: Pelvic inammatory disease, Pediatr Rev 34:163, 2013.
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ision loss is a condition that ranges from vision
V
impairment to total blindness. For vision to oc­cur, light is transmitted through the eye to photore­ceptors in the retina that collect light and send neural impulses to the brain. These impulses are then processed to give information on what is being seen. Vision loss occurs with any interruption in this visual pathway, such as opacication of the cornea, lens, or vitreous body (see Chapter 30, Figure 30-1 for the anatomical structures of the eye). Vision loss also occurs when light energy cannot be converted into neural impulses, such as in glaucoma, retinal detach­ment, ischemic optic nerve atrophy, and pituitary or occipital tumors. Because vision loss is a self­reported condition, functional causes, formerly called malingering or hysteria, can be considered.
The most common causes of vision loss in adults are refractive errors, cataracts, glaucoma, age-related macular degeneration (AMD), and diabetic retinopa­thy. In all cases, impaired vision requires evaluation by an ophthalmologist. However, knowledge of the causes of vision loss can provide important clues to the diagnosis of these conditions.
Vision Loss
Blurring of Vision
Distinguish between loss of vision and loss of visual acuity. Vision loss is the absence of vision, completely or partially, in one or both eyes. Blurriness refers to a change in the acuity of vision. The most common cause of visual acuity change is refractive error.
Ability to Focus
Patients who are without sight have no ocular align­ment and commonly manifest a gross searching and wandering nystagmus. Nystagmus in the rst year of life suggests bilateral vision loss until proved other­wise. In infancy, vision loss is a common cause of nystagmus.
Visual Fixation
Even though the visual system is incompletely devel­oped at birth, most infants can see and will demon­strate visual interest when stimulated by a human face. At birth the infant will have visual xation present, and by 2 months of age xation will be well developed. Any parental concern about a child’s visual functioning is an important history nding.
DIAGNOSTIC REASONING: FOCUSED HISTORY
What is the extent of vision loss?
Key Questions
l
What can you see? Can you detect light?
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Is your vision blurred?
l
To self: Does the patient look at me?
l
If a child: Does the child’s eye wander?
Total Absence of Vision
Disease that affects the optic nerve or retina, such as retinal detachment, leads to total loss of vision. Blindness is a complete lack of form and visual light perception.
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Is this an emergency that requires immediate intervention?
Key Questions
l
Was the loss of vision sudden?
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Is the loss in one or both eyes?
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Is the loss complete or partial?
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Is there any pain with the loss of vision?
l
Are there other symptoms associated with the loss,
such as a ash of light?
l
Was the loss momentary or persistent?
Onset
Sudden loss of vision suggests a vascular etiology, spe­cically occlusion of the central retinal artery until proven otherwise. In occlusion of the central retinal artery, the
Chapter 38  •  Vision Loss
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patient notes that vision is lost suddenly, and light cannot
be distinguished from dark. Loss of vision in one eye in-
dicates that the problem is anterior to the chiasm; hemi-
anopic eld defects in both eyes suggest a postchiasmal
lesion (Figure 38-1). Occlusion of the central retinal ar-
tery is an emergency and requires immediate treatment.
Pain
Sudden loss of vision with eye pain and photophobia
indicates pathology of the cornea, iris, and ciliary
body. Sudden loss of vision with a red painful eye may
indicate acute-angle glaucoma (see Chapter 30).
Inammation, demyelinization, or degeneration of the
optic nerve causes pain on movement of the eye and is
thought to be the result of general inammation of
the posterior portion of the orbit or inammation of the
optic nerve (cranial nerve II). Retrobulbar neuritis is
the most common disease in this category.
A common cause of sudden loss of vision without pain is vitreous hemorrhage. The patient describes oat­ers that begin to drift in front of the eye, followed by a red glow. The vision gradually fades until only light and
LEFT RIGHT
dark are distinguished. Painless vision loss is also associ­ated with macular degeneration, retinal detachment, dia­betic retinopathy, and anterior ischemic optic neuropathy.
Children
In children, acute optic neuritis rarely occurs as an isolated condition and is usually a manifestation of a neurological or systemic disease such as meningitis, viral infection, or demyelinizing diseases. It may also be as­sociated with lead poisoning and long-term use of certain drugs, most notably chloramphenicol or vincristine.
Flash of Light With Loss of Vision
Patients who have retinal detachment describe a ash of light shortly before loss of vision. Some patients describe a veil over the eye either just before or immediately after the ash. The reason for the ashes is that detachment of the retina causes mechanical stimulation of the rods and cones as it tears away from the pigment epithelium and oats free.
Patients whose retinae pull away or tear but do not
detach experience the same ash of light as those with
SCOTOMATA
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1
Blind eye
Optic nerve
Optic chiasm
Optic tract
Lower occipital cortex
Upper occipital cortex
FIGURE 38-1 Visual fields and five locations of visual field defects and associated visual field changes.
Examples of visual field defects along the optic nerve, optic chiasm, optic tracts, and optic radiations in the cortex. (From Ferri FF: Ferri’s color atlas and text of clinical medicine, Philadelphia, 2008, Saunders.)
1
2
3
5
Upper occipital radiation
4
Lower occipital radiation
2
Bitemporal hemianopsia
3
Left homonymous hemianopsia
4
Left upper homonymous quadrantanopsia
5
Left lower homonymous quadrantanopsia
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Chapter 38  •  Vision Loss
retinal detachment. They may also experience momen­tary total or partial loss of vision in the affected eye.
Transient Loss of Vision
Some patients with migraine headaches experience a scotoma, or an area of impaired vision within the visual eld, before the onset of the headache. The scotoma may be either positive (the patient sees a light spot or scintillat­ing ashes [scintillating scotoma]) or negative (the patient experiences a blind spot). Scotoma may be prodromal to a migraine headache. Profound anxiety can produce a transient loss of vision or a perceived loss of vision.
Can I rule out trauma?
Key Questions
l
Is there a history of head trauma?
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Is there a history of eye trauma?
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Has there been a chemical or thermal injury?
Head Trauma
Loss of vision is most likely to occur after trauma to the occiput. The vision loss is sudden and complete, but vision usually returns in a matter of hours. Severe head trauma with skull fracture but without direct damage to the eyeball can result in loss of vision that occurs immediately or shortly thereafter. Occasionally a patient can have good vision in the affected eye after the acci­dent and subsequently lose vision as a result of severe retrobulbar hemorrhage. In children, trauma is the most common cause of retinal detachment. Abusive head trauma, called shaken baby syndrome, may result in retinal and vitreous hemorrhage.
Eye Trauma
Blunt trauma occurs when an object impacts the bony orbit of the eye. High-velocity injuries to the eye are not always immediately obvious. Small perforations or penetrations of the cornea may appear similar to corneal abrasions. Sharp trauma includes impact from a sharp object that may perforate the cornea, leaking uid from the eye.
Cataract formation is a result of major trauma to the
eye in children. Opacication of the lens can result from a blunt or penetrating injury.
Chemical or Thermal Trauma
Alkaline burns from household cleaners and lawn and garden products can cause irreversible vision loss. Exposure to extreme heat or ames can damage the cornea and eyelids.
Minutes make a difference with chemical trauma to the eye; treat rst and examine later. Wash the eye with copious amounts of water or normal saline solution immediately for an alkaline burn.
Is the vision loss because of a chronic problem?
Key Questions
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How long has vision loss been present?
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Has vision decreased over time?
Progression of Vision Loss
Slowly progressive degenerative disease of any part of the eye can cause progressive vision loss. Progressive loss of visual acuity and color vision can be seen with optic gliomas, the most frequently occurring tumor of the optic nerve in childhood. A history of neurobromatosis can be found in 25% of patients. Children who have surgery for cataracts are especially at risk for glaucoma. Glaucoma may cause chronic loss of vision. AMD is as­sociated with decreased reading vision (see Chapter 30).
Is this related to a genetic, familial, or intrauterine risk?
Key Questions
l
Is there a family history of vision or eye problems?
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Is there a history of maternal, intrapartum, or neonatal
conditions?
Family History
A family history of retinoblastoma, congenital cata­racts, or metabolic or genetic disease is a risk factor for visual and ocular abnormalities. Retinoblastoma occurs in 12% of children with a family history. Hereditary congenital cataracts occur in 10% to 25% of children with a family history. Autosomal dominant inheritance is the most common cause.
Maternal, Intrapartum, and Neonatal Risks
Infants at risk for vision problems are those who are premature, have been on oxygen therapy, are low birth weight, or have mothers who have had infections related to human immunodeciency virus/acquired immune deciency syndrome or to toxoplasmosis, rubella, cytomegalovirus, or herpes simplex—known as the TORCH complex of infections. These conditions during pregnancy may produce blindness at birth or vision loss later in life. Down syndrome is associated with cataracts. Children with galactosemia develop cataracts in infancy. Children with galactokinase deciency develop cataracts in the rst decade of life.