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Vaginal bleeding, postmenopausal
Postmenopausal vaginal bleeding—bleeding that occurs 6 or more months after menopause—is an important indicator of gynecologic cancer. But it can also result from infection, a local pelvic disorder, estrogenic stimulation, atrophy of the endometrium, and physiologic thinning and drying of the vaginal mucous membranes. Sometimes, what appears to be bleeding from the vagina is actually bleeding from another gynecologic location—such as the ovaries, fallopian tubes, uterus, or cervix—that exits the body through the vagina. Vaginal bleeding usually occurs as brown or red spotting that either develops spontaneously or follows coitus or douching, but it may also occur as oozing of fresh blood or bright red hemorrhaging. Many patients—especially those with a history of heavy menstrual flow—minimize the importance of vaginal bleeding, thus delaying diagnosis.
HISTORY AND PHYSICAL EXAMINATION
Determine the patient’s age and her age at menopause. Ask when she first noticed the abnormal bleeding. Then obtain a thorough obstetric and gynecologic history. When did she begin menstruating? Were her periods regular? If not, ask her to describe any menstrual irregularities. How old was she when she first had intercourse? How many sexual partners has she had? Has she had any children? Has she had fertility problems? If possible, obtain an obstetric and gynecologic history of the patient’s mother, and ask about a family history of gynecologic cancer. Determine if the patient has any associated symptoms and if she’s taking estrogen.
Observe the external genitalia, noting the character of any vaginal discharge and the appearance of the labia, vaginal rugae, and clitoris. Carefully palpate the patient’s breasts and lymph nodes for nodules or enlargement. The patient will require pelvic and rectal examinations.
MEDICAL CAUSES
♦ Atrophic vaginitis. When bloody staining occurs in this disorder, it usually follows coitus or douching. The characteristic watery white vaginal discharge may be accompanied by pruritus, dyspareunia, and a burning sensation in the vagina and labia. Sparse pubic hair, a pale vagina with decreased rugae and small hemorrhagic spots, clitoral atrophy, and shrinking of the labia minora may also occur.
♦ Cervical cancer. Early invasive cervical cancer causes vaginal spotting or heavier bleeding, usually after coitus or douching but occasionally spontaneously. Related findings include a persistent, pink-tinged, and foul-smelling vaginal discharge and postcoital pain. As the cancer spreads, back and sciatic pain, leg swelling, anorexia, weight loss, hematuria, dysuria, rectal bleeding, and weakness may occur.
♦ Cervical or endometrial polyps. These small, pedunculated growths may cause spotting (possibly as a mucopurulent pink
discharge) after coitus, douching, or straining at defecation. However, many endometrial polyps produce no symptoms.
discharge) after coitus, douching, or straining at defecation. However, many endometrial polyps produce no symptoms.
♦ Endometrial hyperplasia or cancer. Bleeding occurs early in these disorders; it can be brownish and scant or bright red and profuse, and usually follows coitus or douching. Bleeding later becomes heavier and more frequent, leading to clotting and anemia. It may be accompanied by pelvic, rectal, low back, and leg pain and an enlarged uterus.
♦ Ovarian tumors (feminizing). Estrogenproducing ovarian tumors can stimulate endometrial shedding and cause heavy bleeding that isn’t associated with coitus or douching. A palpable pelvic mass, increased cervical mucus, breast enlargement, and spider angiomas may be present.
♦ Vaginal cancer. Characteristic spotting or bleeding may be preceded by a thin, watery vaginal discharge. Bleeding may be spontaneous but usually follows coitus or douching. A firm, ulcerated vaginal lesion may be present; dyspareunia, urinary frequency, bladder and pelvic pain, rectal bleeding, and vulvar lesions may develop later.
OTHER CAUSES
♦ Drugs. Unopposed estrogen replacement therapy is a common cause of abnormal vaginal bleeding. This can usually be reduced by adding progesterone (in women who haven’t had a hysterectomy) and by adjusting the patient’s estrogen dosage.
SPECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, such as ultrasonography to outline a cervical or uterine tumor; endometrial biopsy, colposcopy, or dilatation and curettage with hysteroscopy to obtain tissue specimens for histologic examination; testing for occult blood in the stool; and vaginal and cervical cultures to detect infection. Discontinue estrogen until a diagnosis is made.
GERIATRIC POINTERS
About 80% of cases of postmenopausal vaginal bleeding are benign, caused primarily by endometrial atrophy. However, malignancy should still be ruled out.
PATIENT COUNSELING
Reassure the patient that most cases of postmenopausal vaginal bleeding are benign and not cancer related.
Vaginal discharge
Common in women of childbearing age, a physiologic vaginal discharge is mucoid, clear or white, nonbloody, and odorless. Produced by the cervical mucosa and, to a lesser degree, by the vulvar glands, this discharge may occasionally be scant or profuse because of estrogenic stimulation and changes during the patient’s menstrual cycle. However, a marked increase in discharge or a change in discharge color, odor, or consistency can signal disease and may result from infection, sexually transmitted disease, reproductive tract disease, fistulas, and the use of certain drugs. In addition, the prolonged presence of a foreign body, such as a tampon or diaphragm, in the patient’s vagina can cause irritation and an inflammatory exudate, as can frequent douching and the use of feminine hygiene products, contraceptive products, bubble baths, and colored or perfumed toilet papers.
HISTORY AND PHYSICAL EXAMINATION
Ask the patient to describe the onset, color, consistency, odor, and texture of her vaginal discharge. How does the discharge differ from her usual vaginal secretions? Is the onset related to her menstrual cycle? Also, ask about associated symptoms, such as dysuria and perineal pruritus and burning. Does she have spotting after coitus or douching? Ask about recent changes in her sexual habits and hygiene practices. Is she or could she be pregnant? Next, ask if she has had a vaginal discharge before or has ever been treated for a vaginal infection. What treatment did she receive? Did she complete the course of medication? Ask about her current use of medications, especially antibiotics, oral estrogens, and hormonal contraceptives.
Examine the external genitalia and note the character of the discharge. (See Identifying causes of vaginal discharge, page 688.) Observe vulvar and vaginal tissues for redness, edema, and excoriation. Palpate the inguinal lymph nodes to detect tenderness or enlargement, and palpate the abdomen for tenderness. A pelvic examination may be required. Obtain vaginal discharge specimens for testing.
MEDICAL CAUSES
♦ Atrophic vaginitis. In this disorder, a scant, watery white vaginal discharge may be accompanied by pruritus, burning, tenderness, and bloody spotting after coitus or douching. Sparse
pubic hair, a pale vagina with decreased rugae and small hemorrhagic spots, clitoral atrophy, and shrinking of the labia minora may also occur.
pubic hair, a pale vagina with decreased rugae and small hemorrhagic spots, clitoral atrophy, and shrinking of the labia minora may also occur.
Identifying causes of vaginal discharge
The color, consistency, amount, and odor of your patient’s vaginal discharge provide important clues about the underlying disorder. For quick reference, use this chart to match common characteristics of vaginal discharge and their possible causes.
Characteristics | Possible causes |
Scant thin, watery white discharge | Atrophic vaginitis |
Thin, green or gray-white, foul-smelling discharge | Bacterial vaginosis |
Profuse white curdlike discharge with yeasty, sweet odor | Candidiasis |
Mucopurulent, foul-smelling discharge | Chancroid |
Yellow, mucopurulent, odorless or acrid discharge | Chlamydial infection |
Scant serosanguineous or purulent discharge with foul odor | Endometritis |
Copious mucoid discharge | Genital herpes |
Profuse mucopurulent discharge, possibly foul smelling | Genital warts |
Yellow or green, foul-smelling discharge from the cervix or occasionally from Bartholin’s or Skene’s ducts | Gonorrhea |
Chronic, watery, bloody or purulent discharge, possibly foul smelling | Gynecologic cancer |
Frothy, green-yellow, and profuse (or thin, white, and scant) foul-smelling discharge | Trichomoniasis |
♦ Bacterial vaginosis. This infection, caused by Gardnerella vaginalis, results from an ecozogic disturbance of the vaginal flora. It produces a thin, foul-smelling, green or gray-white discharge that adheres to the vaginal walls and can be easily wiped away, leaving healthy-looking tissue. Pruritus, redness, and other mild signs of vaginal irritation may also occur.
♦ Candidiasis. Infection with Candida albicans causes a profuse, white, curdlike discharge with a yeasty, sweet odor. Onset is abrupt, usually just before menses or during a course of antibiotics. Exudate may be lightly attached to the labia and vaginal walls and is commonly accompanied by vulvar redness and edema. The inner thighs may be covered with a fine red dermatitis and weeping erosions. Intense labial itching and burning may also occur. Some patients experience external dysuria.
♦ Chancroid. This rare but highly contagious sexually transmitted disease produces a mucopurulent, foul-smelling discharge and vulvar lesions that are initially erythematous and later ulcerated. Within 2 to 3 weeks, inguinal lymph nodes (usually unilateral) may become tender and enlarged, with pruritus, suppuration, and spontaneous drainage of nodes. Headache, malaise, and a fever as high as 102.2° F (39° C) are common.
♦ Chlamydial infection. This infection causes a yellow, mucopurulent, odorless or acrid vaginal discharge. Other findings include dysuria, dyspareunia, and vaginal bleeding after douching or coitus, especially after menses. Many women, however, remain asymptomatic.
♦ Endometritis. A scant serosanguineous discharge with a foul odor can result from bacterial invasion of the endometrium. Associated findings include fever, low back and abdominal pain, abdominal muscle spasm, malaise, dysmenorrhea, and an enlarged uterus.
♦ Genital warts. These mosaic, papular vulvar lesions can cause a profuse mucopurulent vaginal discharge, which may be foul smelling if the warts are infected. Patients commonly complain of burning or paresthesia in the vaginal introitus.
♦ Gonorrhea. Although 80% of women with gonorrhea are asymptomatic, others have a foul-smelling yellow or green discharge that can be expressed from Bartholin’s or Skene’s ducts. Other findings include dysuria, urinary frequency and incontinence, bleeding, and vaginal redness and swelling. Severe pelvic and lower abdominal pain and fever may develop.
♦ Gynecologic cancer. Endometrial or cervical cancer produces a chronic, watery, bloody or purulent vaginal discharge that may be foul smelling. Other findings include abnormal vaginal bleeding and, later, weight loss; pelvic, back, and leg pain; fatigue; urinary frequency; and abdominal distention.
♦ Herpes simplex (genital). A copious mucoid discharge results from this disorder, but the initial complaint is painful, indurated vesicles and ulcerations on the labia, vagina, cervix, anus, thighs, or mouth. Erythema, marked edema, and tender inguinal lymph nodes may occur with fever, malaise, and dysuria.
♦ Trichomoniasis. This infection can cause a foul-smelling discharge, which may be frothy, green-yellow, and profuse or thin, white, and scant. Other findings include pruritus; an inflamed, erythematous vagina with tiny petechiae; dysuria and urinary frequency; dyspareunia; postcoital spotting; and menorrhagia or dysmenorrhea. About 70% of patients are asymptomatic.
OTHER CAUSES
♦ Contraceptive creams and jellies. These products can increase vaginal secretions.
♦ Drugs. Drugs that contain estrogen, including hormonal contraceptives, can cause a mucoid vaginal discharge. Antibiotics such as tetracycline may increase the risk of a candidal vaginal infection and associated discharge.
♦ Radiation therapy. Irradiation of the reproductive tract can cause a watery, odorless vaginal discharge.
SPECIAL CONSIDERATIONS
Teach the patient to keep her perineum clean and dry. Also, tell her to avoid wearing tight-fitting clothing and nylon underwear and to instead wear cotton-crotched underwear and pantyhose. If appropriate, suggest that the patient douche with a solution of 5 tbsp of white vinegar in 2 qt (2 L) of warm water to help relieve her discomfort.
If the patient has a vaginal infection, tell her to continue taking the prescribed medication even if her symptoms clear or she menstruates. Also, advise her to avoid intercourse until her symptoms clear and then to have her partner use condoms until she completes her course of medication. If her condition is sexually transmitted, teach her about safer sex methods.
PEDIATRIC POINTERS
Female neonates who have been exposed to maternal estrogens in utero may have a white mucous vaginal discharge for the first month after birth; a yellow mucous discharge indicates a pathologic condition. In an older child, a purulent, foul-smelling and, possibly, bloody vaginal discharge commonly results from a foreign object placed in the vagina; in such cases, consider the possibility of sexual abuse.
GERIATRIC POINTERS
The vaginal mucosa becomes thin in postmenopausal women because of their decreased estrogen levels. This mucosal thinning combined with a rise in vaginal pH results in decreased resistance to infectious agents and an increased incidence of vaginitis.
Venous hum
A venous hum is a functional or innocent murmur heard above the clavicles throughout the cardiac cycle. Loudest during diastole, it may be low pitched, rough, or noisy. The hum commonly accompanies a thrill or, possibly, a high-pitched whine. It’s best heard by applying the bell of the stethoscope to the medial aspect of the right supraclavicular area with the patient seated upright, or by placing the stethoscope bell in the second or third parasternal interspace with the patient standing upright. (See Detecting a venous hum, page 690.)
A venous hum is a common, normal finding in children and pregnant women. However, it also occurs in hyperdynamic states, such as anemia and thyrotoxicosis. The hum results from increased blood flow through the internal jugular veins, especially on the right side, which causes audible vibrations in the tissues.
Detecting a venous humTo detect a venous hum, have your patient sit upright and then place the bell of the stethoscope over his right supraclavicular area. Gently lift his chin and turn his head toward the left, which increases the loudness of the hum (top). If you still can’t hear the hum, press his jugular vein with your thumb (bottom). The hum will disappear with pressure but will suddenly return, temporarily louder than before, when you release your thumb—a result of the turbulence created by pressure changes.
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Occasionally, a venous hum may be mistaken for an intracardiac murmur or a thyroid bruit. However, a venous hum disappears with jugular vein compression and waxes and wanes with head turning. In contrast, an intracardiac murmur and a thyroid bruit persist despite jugular vein compression and head turning.
HISTORY AND PHYSICAL EXAMINATION
Determine if the patient has a history of anemia or thyroid disorders. If he does, ask which medications or other treatments he has received. If he doesn’t, ask if he has had associated signs and symptoms, such as palpitations, dyspnea, nervousness, tremors, heat intolerance, weight loss, fatigue, or malaise.
Take the patient’s vital signs, noting especially tachycardia, hypertension, a bounding pulse, and widened pulse pressure. Auscultate his heart for gallops or murmurs. Examine his skin and mucous membranes for pallor.
MEDICAL CAUSES
♦ Anemia. A venous hum is common in severe anemia (hemoglobin level below 7 g/dl). Additional findings include pale skin and mucous membranes, dyspnea, crackles, tachycardia, bounding pulse, atrial gallop, systolic bruits over both carotid arteries, bleeding tendencies, weakness, fatigue, and malaise.
♦ Thyrotoxicosis. This disorder may cause a loud venous hum, audible whether the patient is sitting or in a supine position. Auscultation may also reveal an atrial or ventricular gallop. Additional findings include tachycardia, palpitations, weight loss despite increased appetite, diarrhea, an enlarged thyroid gland, dyspnea, nervousness, difficulty concentrating, tremors, diaphoresis, heat intolerance, and exophthalmos. Women may have oligomenorrhea or amenhorrhea; men, gynecomastia. Both sexes may have a decreased libido.
SPECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, which may include an electrocardiogram, a complete blood count, and thyroid hormone (triiodothyronine and thyroxine) assays.
PEDIATRIC POINTERS
A cervical venous hum occurs normally in more than two-thirds of children ages 5 to 15.
Vertigo
Vertigo is an illusion of movement in which the patient feels that he’s revolving in space (subjective vertigo) or that his surroundings are revolving around him (objective vertigo). He may complain of feeling pulled sideways, as though drawn by a magnet.
A common symptom, vertigo usually begins abruptly and may be temporary or permanent and mild or severe. It may worsen when the patient moves and subside when he lies down. It’s commonly confused with dizziness—a sensation of imbalance and light-headedness that is nonspecific. However, unlike dizziness, vertigo is commonly accompanied by nausea, vomiting, nystagmus, and tinnitus or hearing loss. Although the patient’s limb coordination is unaffected, he may exhibit a vertiginous gait.
Vertigo may result from a neurologic or otologic disorder that affects the equilibratory apparatus (the vestibule, semicircular canals, eighth cranial nerve, vestibular nuclei in the brain stem and their temporal lobe connections, and eyes). However, this symptom may also result from alcohol intoxication, hyperventilation, postural changes (benign postural vertigo), and the effects of certain drugs, tests, or procedures.
HISTORY AND PHYSICAL EXAMINATION
Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he’s ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note any evidence of alcohol abuse.
Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient’s gait and posture for abnormalities.
MEDICAL CAUSES
♦ Acoustic neuroma. This tumor of the eighth cranial nerve causes mild, intermittent vertigo and unilateral sensorineural hearing loss. Other findings include tinnitus, postauricular or suboccipital pain, and—with cranial nerve compression—facial paralysis.
♦ Benign positional vertigo. In this disorder, debris in a semicircular canal produces vertigo lasting a few minutes when the patient changes head position. This type of vertigo is usually temporary and can be effectively treated with positional maneuvers.
♦ Brain stem ischemia. This condition produces sudden, severe vertigo that may become episodic and later persistent. Associated findings include ataxia, nausea, vomiting, increased blood pressure, tachycardia, nystagmus, and lateral deviation of the eyes toward the side of the lesion. Hemiparesis and paresthesia may also occur.
♦ Head trauma. Persistent vertigo, occurring soon after a head injury, accompanies spontaneous or positional nystagmus and, if the temporal bone is fractured, hearing loss. Associated findings include headache, nausea, vomiting, and decreased level of consciousness. Behavioral changes, diplopia or visual blurring, seizures, motor or sensory deficits, and signs of increased intracranial pressure may also occur.
♦ Herpes zoster. Infection of the eighth cranial nerve produces sudden onset of vertigo accompanied by facial paralysis, hearing loss in the affected ear, and herpetic vesicular lesions in the auditory canal.
♦ Labyrinthitis. Severe vertigo begins abruptly in this inner ear infection. Vertigo may occur in a single episode or may recur over months or years. Associated findings include nausea, vomiting, progressive sensorineural hearing loss, and nystagmus.
♦ Ménière’s disease. In this disease, labyrinthine dysfunction causes abrupt onset of vertigo, lasting minutes, hours, or days. Unpredictable episodes of severe vertigo and unsteady gait may cause the patient to fall. During an attack, any sudden motion of the head or eyes can precipitate nausea and vomiting.
♦ Motion sickness. This condition is characterized by vertigo, nausea, vomiting, and headache in response to rhythmic or erratic motions.
♦ Multiple sclerosis (MS). Episodic vertigo may occur early and become persistent in MS. Other early findings include diplopia, visual blurring, and paresthesia. MS may also produce nystagmus, constipation, muscle weakness, paralysis, spasticity, hyperreflexia, intention tremor, and ataxia.
♦ Posterior fossa tumor. This type of tumor may produce positional vertigo that lasts for a few seconds as well as papilledema, headache,
memory loss, nausea, vomiting, nystagmus, apneustic or ataxic respirations, and increased blood pressure. The patient may also fall sideways.
memory loss, nausea, vomiting, nystagmus, apneustic or ataxic respirations, and increased blood pressure. The patient may also fall sideways.
♦ Seizures. Temporal lobe seizures may produce vertigo, usually associated with other symptoms of partial complex seizures.
♦ Vestibular neuritis. In this disorder, severe vertigo usually begins abruptly, lasts several days, and isn’t accompanied by tinnitus or hearing loss. Other findings include nausea, vomiting, and nystagmus.
OTHER CAUSES
♦ Diagnostic tests. Caloric testing (irrigating the ears with warm or cold water) can induce vertigo.
♦ Drugs and alcohol. High or toxic doses of certain drugs or alcohol may produce vertigo. These drugs include salicylates, aminoglycosides, antibiotics, quinine, and hormonal contraceptives.
♦ Surgery and other procedures. Ear surgery may cause vertigo that lasts for several days. Administration of overly warm or cold eardrops or irrigating solutions can also cause vertigo.
SPECIAL CONSIDERATIONS
Place the patient in a comfortable position, and monitor his vital signs and level of consciousness. Keep the side rails up if he’s in bed, or help him to a chair if he’s standing when vertigo occurs. Darken the room and keep him calm. Administer drugs to control nausea and vomiting and meclizine or dimenhydrinate to decrease labyrinthine irritability.
Prepare the patient for diagnostic tests, such as electronystagmography, EEG, and X-rays of the middle and inner ears.
PEDIATRIC POINTERS
Ear infection is a common cause of vertigo in children. Vestibular neuritis may also cause this symptom.
Vesicular rash
A vesicular rash is a scattered or linear distribution of blisterlike lesions that are sharply circumscribed and filled with clear, cloudy, or bloody fluid. The lesions, which are usually less than 0.5 cm in diameter, may occur singly or in groups. (See Recognizing common skin lesions, pages 518 and 519.) They sometimes occur with bullae—fluid-filled lesions larger than 0.5 cm in diameter.
A vesicular rash may be mild or severe and temporary or permanent. It can result from infection, inflammation, or allergic reactions.
HISTORY AND PHYSICAL EXAMINATION
Ask your patient when the rash began, how it spread, and whether it has appeared before. Did other skin lesions precede eruption of the vesicles? Obtain a thorough drug history. If the patient has treated the rash with a topical medication, what type did he use and when did he last apply it? Also, ask about associated signs and symptoms. Find out if he has a family history of skin disorders, and ask about allergies and recent infections, insect bites, or exposure to allergens.
Examine the patient’s skin, noting if it’s dry, oily, or moist. Observe the general distribution of the lesions and record their exact location. Note the color, shape, and size of the lesions, and check for crusts, scales, scars, macules, papules, or wheals. Palpate the vesicles or bullae to determine if they’re flaccid or tense. Slide your finger across the skin to see if the outer layer of epidermis separates easily from the basal layer (Nikolsky’s sign).
MEDICAL CAUSES
♦ Burns (second-degree). Thermal burns that affect the epidermis and part of the dermis cause vesicles and bullae along with erythema, swelling, pain, and moistness.
♦ Dermatitis. In contact dermatitis, a hypersensitivity reaction produces an eruption of small vesicles surrounded by redness and marked edema. The vesicles may ooze, scale, and cause severe pruritus.
Dermatitis herpetiformis, a skin disease that is most common in men between ages 20 and 50 (and is occasionally associated with celiac disease, organ malignancy, or immunoglobulin A immunotherapy), produces a chronic inflammatory eruption marked by vesicular, papular, bullous, pustular, or erythematous lesions. The rash is usually distributed symmetrically on the buttocks, shoulders, and extensor surfaces of the elbows and knees, but it may sometimes appear on the face, scalp, and neck. Other symptoms include severe pruritus, burning, and stinging.
In nummular dermatitis, groups of pinpoint vesicles and papules appear on erythematous or pustular lesions that are nummular (coinlike) or
annular (ringlike). The pustular lesions commonly ooze a purulent exudate, itch severely, and rapidly become crusted and scaly. Two or three lesions may develop on the hands, but the lesions typically develop on the extensor surfaces of the limbs and on the buttocks and posterior trunk.
annular (ringlike). The pustular lesions commonly ooze a purulent exudate, itch severely, and rapidly become crusted and scaly. Two or three lesions may develop on the hands, but the lesions typically develop on the extensor surfaces of the limbs and on the buttocks and posterior trunk.
♦ Dermatophytid. This allergic reaction to a fungal infection produces vesicular lesions on the hands, usually in response to tinea pedis. The lesions are extremely pruritic and tender and may be accompanied by fever, anorexia, generalized adenopathy, and splenomegaly.
♦ Erythema multiforme. This acute inflammatory skin disease is heralded by a sudden eruption of erythematous macules, papules and, occasionally, vesicles and bullae. The characteristic rash appears symmetrically over the hands, arms, feet, legs, face, and neck and tends to reappear. Although vesicles and bullae may also erupt on the eyes and genitalia, vesiculobullous lesions usually appear on the mucous membranes— especially the lips and buccal mucosa—where they rupture and ulcerate, producing a thick, yellow or white exudate. Bloody, painful crusts, a foul-smelling oral discharge, and difficulty chewing may develop. Lymphadenopathy may also occur.
♦ Herpes simplex. This common viral infection produces groups of vesicles on an inflamed base, most commonly on the lips and lower face. In about 25% of cases, the genital region is involved. Vesicles are preceded by itching, tingling, burning, or pain; develop singly or in groups; are 2 to 3 mm in diameter; and don’t coalesce. Eventually, they rupture, forming a painful ulcer followed by a yellowish crust.
♦ Herpes zoster. A vesicular rash is preceded by erythema and, occasionally, by a nodular skin eruption and unilateral, sharp pain along a dermatome. About 5 days later, the lesions erupt and the pain becomes burning. Vesicles dry and scab about 10 days after eruption. Associated findings include fever, malaise, pruritus, and paresthesia or hyperesthesia of the involved area. Herpes zoster involving the cranial nerves produces facial palsy, hearing loss, dizziness, loss of taste, eye pain, and impaired vision.
♦ Pemphigoid (bullous). Generalized pruritus or an urticarial or eczematous eruption may precede the classic bullous rash. Bullae are large, thick walled, tense, and irregular, typically forming on an erythematous base. They usually appear on the lower abdomen, groin, inner thighs, and forearms.
♦ Pemphigus. In chronic familial pemphigus, groups of tiny vesicles erupt on normal skin or mucous membranes. The vesicles are thin walled, flaccid, and easily broken, producing small denuded areas that become covered with crust and typically itch and burn. The eruption remits spontaneously but recurs.
Pemphigus foliaceus usually develops slowly and may begin with bullous lesions, commonly on the head and trunk. As these lesions spread to other areas, they become moist, scaly, and foul smelling. Nikolsky’s sign is present, and denudation of lesions results in extensive erythema, with large, loose scales and crusts. Pruritus and burning are common.
Pemphigus vulgaris may be acute and rapidly progressive or chronic. The typically flaccid bullae may be tender or painful and large or small. When they rupture, denuded skin exudes a clear, bloody, or purulent discharge. Commonly, the bullae first erupt in a specific location, such as the mouth or scalp, and eventually become widespread. Nikolsky’s sign and pruritus may be present.
♦ Pompholyx (dyshidrosis or dyshidrotic eczema). This common, recurrent disorder produces symmetrical vesicular lesions that can become pustular. The pruritic lesions are more common on the palms than on the soles and may be accompanied by minimal erythema.
♦ Porphyria cutanea tarda. This disorder, resulting from abnormal porphyrin metabolism, produces bullae—especially on areas exposed to sun, friction, trauma, or heat—and photosensitivity. Papulovesicular lesions may evolve into erosions or ulcers and scars. Chronic skin changes include hyperpigmentation or hypopigmentation, hypertrichosis, and sclerodermoid lesions. Urine is pink to brown.
♦ Scabies. In this disorder, mites that burrow under the skin cause small vesicles to erupt on the webs of the fingers, wrists, elbows, axillae, and waistline; the glans, shaft, and scrotum in males; and the nipples in females. The lesions are a few millimeters long, with a swollen nodule or red papule that contains the mite. Pustules and excoriations may also occur. Associated pruritus worsens at night and with inactivity and warmth.
♦ Smallpox (variola major). Initial signs and symptoms include high fever, malaise, prostration, severe headache, backache, and abdominal pain. A maculopapular rash develops on the mucosa of the mouth, pharynx, face, and forearms and then spreads to the trunk and
legs. Within 2 days, the rash becomes vesicular and later pustular. The lesions develop at the same time, appear identical, and are more prominent on the face and extremities. The pustules are round, firm, and deeply embedded in the skin. After 8 to 9 days, the pustules form a crust, which later separates from the skin leaving a pitted scar. Death may result from encephalitis, extensive bleeding, or secondary infection.
legs. Within 2 days, the rash becomes vesicular and later pustular. The lesions develop at the same time, appear identical, and are more prominent on the face and extremities. The pustules are round, firm, and deeply embedded in the skin. After 8 to 9 days, the pustules form a crust, which later separates from the skin leaving a pitted scar. Death may result from encephalitis, extensive bleeding, or secondary infection.
Drugs that cause toxic epidermal necrolysis
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