What Disease Results In Red Raised Bumps, Fever, Chills And May Require Topical Or Skin Cream.
Evaluating the Febrile Patient with a Rash
Am Fam Md. 2000 Aug 15;62(4):804-816.
Article Sections
- Abstruse
- History
- Physical Test
- Laboratory Data
- Maculopapular Rashes
- Petechial Eruptions
- Diffuse Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
The differential diagnosis for delirious patients with a rash is all-encompassing. Diseases that present with fever and rash are usually classified according to the morphology of the main lesion. Rashes can exist categorized as maculopapular (centrally and peripherally distributed), petechial, diffusely erythematous with desquamation, vesiculobullouspustular and nodular. Potential causes include viruses, leaner, spirochetes, rickettsiae, medications and rheumatologic diseases. A thorough history and a careful physical test are essential to making a correct diagnosis. Although laboratory studies tin be useful in confirming the diagnosis, test results often are not available immediately. Because the severity of these illnesses can vary from minor (roseola) to life-threatening (meningococcemia), the family doc must make prompt management decisions regarding empiric therapy. Hospitalization, isolation and antimicrobial therapy often must exist considered when a patient presents with fever and a rash.
Evaluating the patient who presents with fever and a rash tin be challenging because the differential diagnosis is extensive and includes minor and life-threatening illnesses. In addition, the clinical moving-picture show can vary considerably, and the family unit medico may demand to quickly decide about initiating empiric therapy or isolation. This article reviews mutual diagnoses for fever and a rash and suggests a logical approach to obtaining the correct diagnosis.one–3
History
- Abstract
- History
- Physical Examination
- Laboratory Data
- Maculopapular Rashes
- Petechial Eruptions
- Diffuse Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
A detailed history can exist quite helpful in identifying the crusade of fever and a rash. A history of contempo travel, woodland or brute exposure, drug ingestion or contact with ill persons should be noted. The fourth dimension of twelvemonth tin be a clue to certain diagnoses.2–4
A consummate medical history can help to make up one's mind whether the patient is at increased risk for specific conditions associated with valvular heart disease, sexually transmitted diseases or immunosuppression from chemotherapy. Immune status is especially important because many of the diseases that result in fever and a rash present differently in immunocompromised patients.2–4
Details about the rash should include site of onset, rate and management of spread, presence or absence of pruritus, and temporal relationship of rash and fever.2–5 Information technology is also important to know whether any topical or oral therapies accept been attempted.
Physical Exam
- Abstruse
- History
- Physical Exam
- Laboratory Data
- Maculopapular Rashes
- Petechial Eruptions
- Diffuse Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
A basic understanding of the various types of rashes is essential in making an authentic assessment and determining the severity and acuteness of the patient's illness. Brief descriptions of common primary peel lesions are presented in Table i.1,half dozen
The physician should identify the principal lesion only also note the presence of secondary lesions. Important features include the distribution, configuration and organisation of the lesions.2
In improver to evaluating the patient's vital signs and full general appearance, the physician should look for the following: signs of toxicity, adenopathy, oral, genital or conjunctival lesions, hepatosplenomegaly, evidence of excoriations or tenderness, and signs of nuchal rigidity or neurologic dysfunction.ii,iv
Table 1
Common Chief Skin Lesions
| Lesion type | Description |
|---|---|
| Macule | Circumscribed area of change in normal skin colour, with no skin elevation or depression; may exist whatever size |
| Papule | Solid, raised lesion up to 0.five cm in greatest diameter |
| Nodule | Similar to papule merely located deeper in the dermis or subcutaneous tissue; differentiated from papule by palpability and depth, rather than size |
| Plaque | Summit of skin occupying a relatively large area in relation to meridian; oft formed by confluence of papules |
| Pustule | Circumscribed tiptop of skin containing purulent fluid of variable character (i.e., fluid may be white, yellowish, green or hemorrhagic) |
| Vesicle | Circumscribed, elevated, fluid-containing lesion less than 0.5 cm in greatest diameter; may be intraepidermal or subepidermal in origin |
| Bulla | Aforementioned as vesicle, except lesion is more than than 0.5 cm in greatest diameter |
Laboratory Data
- Abstract
- History
- Physical Test
- Laboratory Data
- Maculopapular Rashes
- Petechial Eruptions
- Diffuse Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
Laboratory data are not usually available during the initial evaluation. The complete blood count with differential, an erythrocyte sedimentation rate, a chemistry panel, liver function tests, and blood and urine cultures may prove useful in identifying organisms or illness processes.i
Aspirates, scrapings and pustular fluid may exist obtained for Gram staining and culture. When a herpes simplex virus infection is suspected, a Tzanck test may be performed by unroofing a lesion and taking a scraping of the lesion base. Biopsy samples should exist obtained from nonhealing or persistent purpuric lesions. Biopsy of inflammatory dermal nodules and ulcers should also be considered.1
Specific diagnoses that may be confirmed histologically include Rocky Mountain spotted fever, herpetic infections, systemic lupus erythematosus, erythema multiforme, allergic vasculitis, secondary syphilis and deep fungal infections.ane,6,7
Although serologic tests are non helpful in the acute setting, they can be used to confirm or support the diagnosis of atmospheric condition such as systemic lupus erythematosus, syphilis, rheumatoid arthritis and human immunodeficiency virus infection.1,half dozen,seven
Diseases that present with fever and rash are summarized in Table 21,ii and discussed by rash type in the following sections.
TABLE two
Diseases Presenting with Fever and Rash
| Disease | Etiology | Description of rash | Epidemiology | Diagnostic clues | Footing for diagnosis |
|---|---|---|---|---|---|
| Rubeola | Measles virus | Macular-papular rash that may become confluent; begins on face, cervix and shoulders and spreads centrifugally and inferiorly; fades in iv to 6 days | Nearly common in children 5 to nine years of age, nonimmune persons | Prodrome consisting of symptoms of upper respiratory tract infection, coryza, bark-similar cough, angst, photophobia and fever; Koplik's spots (prodromal stage); development of exanthem on fourth febrile day; belatedly winter through early jump | Serology |
| Rubella | Rubella virus | Pink macules and papules that develop on brow and spread inferiorly and to extremities within one mean solar day; fading of macules and papules in reverse order by third day | Young adults, nonimmune persons | Prodrome uncommon, especially in children; petechiae on soft palate (Forschheimer'southward spots); in adults: anorexia, angst, conjunctivitis, headache and symptoms of balmy upper respiratory infection | Serology |
| Erythema infectiosum (fifth affliction) | Human parvovirus B19 | Begins every bit classic bright-red facial rash ("slapped cheek") and progresses to lacy reticular rash; may wax and wane for 6 to viii weeks | Children three to 12 years of age | Can present as rheumatic syndrome in adults; prodrome of fever, anorexia, rash typically beginning subsequently resolution of fever [ corrected] | Serology |
| Roseola | Human being herpes-virus 6 | Diffuse maculopapular eruption, usually sparing face up | Children 6 months to 3 years of historic period | Fever lasting iii to 4 days, followed within 2 to three days past the rash, which resolves spontaneously in several days; about always a cocky-limited benign illness; temporal relationship of fever followed by rash is helpful in making the diagnosis | Clinical findings, serology |
| Lyme disease | Borrelia burgdorferi | Macule or papule at site of tick seize with teeth, progressing to pathognomonic erythema migrans | All ages at risk for tick exposure in endemic areas | History of tick exposure; secondary erythematous, macular lesions; Borrelia lymphocytoma; highest incidence: May through September | Clinical findings, serology, polymerase chain reaction examination |
| Erythema multiforme | Idiopathic in 50 percent of cases (encounter Tabular array three) | Dull-blood-red macules developing into papules with primal vesicles or bullae; common on dorsa of hands, palms, soles, arms, knees, penis and vulva; ofttimes bilateral and symmetric | Adults twenty to 30 years of historic period; men affected more than oft than women | Major and minor forms; major form ever with mucous membrane involvement and usually the effect of drug reaction; minor class ofttimes associated with herpes simplex outbreak; rarely life-threatening | Clinical findings |
| Secondary syphilis | Treponema pallidum | Diverse presentations; dark-brown-red or pink macules and papules; generalized eruption or localized eruption on caput, neck, palms or soles; condyloma lata mutual | Adolescents and adults xv to 49 years of historic period; females affected more ofttimes than males | Develops 2 to 10 weeks after primary chancre; presents with or without fever; may have generalized lymphadenopathy and splenomegaly; may have recurrent eruptions with symptom-free periods | Dark-field examination, serology |
| Meningococcemia (astute) | Neisseria meningitidis | Variety of lesions only, characteristically, petechial lesions distributed on the trunk and extremities (although the lesions can be located anywhere); petechiae on mucous membranes | Highest incidence in children half dozen months to 1 year of age | Acutely ill patient; high fever, tachypnea, tachycardia, mild hypotension; leukocytosis; meningitis develops in more than than 50 percent of patients | Oftentimes, clinical findings; claret cultures |
| Meningococcemia (chronic) | Northward. meningitidis | Intermittent maculopapular lesions, often on a painful joint or pressure betoken; may have nodules on calves | Same as for astute form | Fever, myalgias, arthralgias, headache, anorexia; may recur for weeks or months, with average duration of 8 weeks; may progress to astute meningococcemia, meningitis or endocarditis | Claret cultures |
| Rocky Mountain spotted fever | Rickettsia rickettsii | Rash evolving from pinkish macules to ruby-red papules and finally to petechiae; rash first on wrists and ankles and spreading centripetally; involvement of palms and soles late in illness | Young adults with tick exposure; men affected more often than women | Onset typically abrupt; fever, astringent headache and myalgias are prominent; rash appearing around quaternary twenty-four hour period of illness; may have relative bradycardia and leukopenia | Clinical findings, serology |
| Blood-red fever | Beta-hemolytic Streptococcus pyogenes | Punctate erythema beginning on torso and spreading to extremities, becoming confluent; flushed face with perioral pallor; rash fading in 4 to v days and followed by desquamation | Children | Acute infection of tonsils or pare; linear petechiae in antecubital and axillary folds (Pastia's sign); rash actualization two to three days after infection; initially, "white strawberry tongue" but by fourth or 5th twenty-four hours, "red strawberry tongue" | Rapid strep test, wound or throat civilisation, antistreptolysin O titers |
| Toxic shock syndrome | Staphylococcus aureus | Diffuse "sunburn" rash that desquamates over 1 to 2 weeks | All ages, but most common in menstruating females | High fever, hypotension and involvement of three or more than organ systems; about 50 per centum of cases occurring in menstruating women around onset of menstruum; postoperative patients at increased risk; condition out of proportion to wound appearance | Clinical criteria, vaginal and wound cultures |
| Kawasaki's disease | Idiopathic | Erythematous rash on hands and feet; morbilliform, scarlatiniform rash on trunk and perineum; hyperemic lips | Children less than eight years of age, with peak incidence at 1 year; boys affected more often than girls | Winter and leap; high fevers, cervical lymphadenopathy, arthritis, arthralgias, cardiac involvement, mucous membrane involvement; can be complicated by coronary artery abnormalities in twenty to 25 percent of cases | Specific clinical criteria |
| Chickenpox | Varicella-zoster virus | Initially, papules, which evolve into vesicles ("dewdrops on a rose petal") and eventually into pustules and crusts; rash offset on face up and spreading inferiorly to trunk and extremities | xc percent of cases in children less than 10 years of age; v percent of cases in persons older than 15 years | Prodrome consisting of headache, general aches, backache and malaise is typically absent-minded in children; exposure history; may accept all forms of lesions at the aforementioned time; vesicles evolving to shallow erosions common on mucous membranes of palate; may also accept vesicles on nasal, conjunctival, gastrointestinal tract and genital mucosa | Clinical findings, confirmed by Tzanck examination |
| Canker zoster (shingles) | Varicella-zoster virus | Begins as erythematous maculopapular eruption, rapidly evolves to vesicles | All ages, simply incidence increases with age and immunosuppression | Prodrome of unusual skin sensations; dermatomal pattern, with lesions rarely crossing midline; pain frequently severe; more than common in thoracic and facial dermatomes | Clinical findings, confirmed by Tzanck exam |
| Rickettsialpox | Rickettsia akari | Generalized maculopapular- vesicular exanthem; possible interest of mucous membranes; no involvement of palms or soles | All ages; urban settings | Transmitted from mice to humans via mites; formation of papules vii to 10 days after initial seize with teeth; typically, germination of a blackness eschar over healing lesion; febrile stage occurring iii to 7 days after initial lesion and lasting upward to a week; self-express, usually mild course | Serology |
| Erythema nodosum | Various causes (run into Table four) | Bright-ruddy nodules (3 to twenty cm in diameter) scattered bilaterally only not symmetric; most ofttimes on lower legs but as well establish on knees and arms; rarely institute on face up and neck; lesions oft tender and indurated | Adolescents and young adults 15 to xxx years of age; females affected more than often than males | Thorough history and physical examination to identify known causes; throat culture for grouping A beta-hemolytic streptococci; chest radiograph to rule out sarcoidosis; arthralgias present in 50 pct of cases; fever and malaise common | Clinical findings |
Maculopapular Rashes
- Abstract
- History
- Concrete Examination
- Laboratory Data
- Maculopapular Rashes
- Petechial Eruptions
- Diffuse Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
Maculopapular eruptions are most oftentimes seen in viral illnesses (Figure 1) and allowed-mediated syndromes. These eruptions can accept many causes, including drug reactions and bacterial infections. Infectious exanthems are mutual and are divers as generalized cutaneous eruptions associated with a systemic infection. Information technology is helpful to consider centrally and peripherally distributed eruptions separately because each type has its own differential diagnosis.2
Effigy one.
Maculopapular rash in a nonspecific viral exanthem.
CENTRALLY DISTRIBUTED ERUPTIONS
Centrally distributed maculopapular eruptions are more common than peripheral eruptions.2 These eruptions include rashes that begin centrally, kickoff affecting the head and cervix, and so progress peripherally.
Viral Exanthems. Viral etiologies of rashes include rubeola, rubella, erythema infectiosum and roseola.4
The exanthem of rubeola begins effectually the 4th febrile day, with discrete lesions that go confluent as they spread from the hairline downward, sparing the palms and soles. The exanthem typically lasts four to six days. The lesions fade gradually in lodge of appearance, leaving a residual yellow-tan coloration or faint desquamation. Rubeola is as well distinguished by the presence of Koplik's spots in the oral mucosa.1,2
Rubella is similar to rubeola. However, it causes less astringent symptoms, and its exanthem characteristically has a shorter elapsing (two to 3 days).ane,ii
Erythema infectiosum, or fifth disease, is caused by man parvovirus B19. This disease primarily affects children between three and 12 years of historic period, although it can present equally a rheumatic syndrome in adults. The prodrome may consist of fever, anorexia, sore throat and abdominal pain. In one case the fever resolves, the classic vivid-red facial rash ("slapped cheek") appears. Within several days, the exanthem progresses to a diffuse, lacy, reticular rash that may wax and wane for six to eight weeks (Figure 2). Human parvovirus B19 infection is of particular business organisation in pregnant women considering it has been associated with fetal hydrops and subsequent fetal decease.one,four,7,8
FIGURE 2.
Maculopapular rash of erythema infectiosum (fifth illness).
Roseola, or exanthema subitum, is acquired by human herpesvirus half-dozen. This affliction occurs in children less than three years of age. As in 5th illness, the rash appears afterward the resolution of several days of loftier fever. The diffuse maculopapular eruption often spares the face and is of short duration, typically fading inside iii days.7,8
Lyme Disease and Erythema Migrans. Lyme disease is the most commonly reported vector-borne illness in the United States.7 Information technology is acquired by the spirochete Borrelia burgdorferi, which is transmitted by the bite of a tick (Ixodes species). Endemic areas in the United States include the northeastern, mid-Atlantic, northward-primal and far-western regions.ix
Erythema migrans, the pathognomonic rash, develops in about eighty percent of patients with Lyme disease.6 This enlarging, erythematous macular rash begins every bit a macule or papule at the site of inoculation (Figure 3). Systemic symptoms, including fever, chills, myalgias, headaches and arthralgias, often back-trail the rash.1,x
Figure 3.
Erythema migrans on upper arm in Lyme affliction.
The rash is more common on the proximal extremities, in body creases and on the breast. It enlarges over a period of days to weeks, reaching a maximum diameter of 3 to 68 cm (median diameter: 15 cm).1,10
The primary lesion may prove primal clearing, cardinal necrosis, induration or vesiculation. Smaller secondary lesions may develop in up to twenty percent of patients with Lyme disease and may betoken early hematogenous spread.10
Borrelia lymphocytoma is a painless bluish-red nodule or plaque that may develop in early Lyme illness. The lesion is unremarkably located on the earlobe, nipple or scrotum.9
Complications of untreated Lyme disease include carditis, neuroborreliosis, arthritis and acrodermatitis chronica atrophicans.nine
Drug-Related Eruptions. Drug reactions tin present equally whatever dermatologic morphology and prove no predilection for age, gender or race. Exanthematous eruptions well-nigh commonly occur in clan with the assistants of penicillins or cephalosporins. The rash usually appears within the get-go calendar week later on the offending drug is started and typically resolves within days later on the drug is discontinued. Drug-related reactions tin can be difficult to distinguish from viral exanthems, but they may exist more intensely erythematous and pruritic.1,ii,11
PERIPHERAL ERUPTIONS
Erythema Multiforme. The almost common peripheral eruptive maculopapular rash, erythema multiforme occurs more frequently in men than in women and nearly often affects persons between 20 and xxx years of historic period. The rash, which can be recurrent, shows a predilection for palms, soles, knees and elbows. Although erythema multiforme has a number of known etiologies (Table 3),1,4,6 information technology is idiopathic in more 50 pct of affected patients.1,half-dozen
TABLE 3
Etiologies of Erythema Multiforme
| Idiopathic (more than l percent of cases) | |
| Radiations therapy | |
| Medications | |
| Penicillin | |
| Sulfonamides | |
| Phenytoin (Dilantin) | |
| Barbiturates | |
| Phenylbutazone | |
| Infectious causes | |
| Herpes simplex virus | |
| Epstein-Barr virus | |
| Adenovirus | |
| Coxsackievirus B5 | |
| Vaccinia virus | |
| Mycoplasma species | |
| Chlamydia species | |
| Salmonella typhi | |
| Yersinia species | |
| Mycobacterium tuberculosis | |
| Histoplasma capsulatum | |
| Coccidioides immitis | |
Erythema multiforme begins as a macular eruption (Figure iv). The dull-reddish lesions accelerate from macules to papules, with prominence of feature target-shaped lesions. Vesicles and bullae may develop in the center of the papules. In many patients, the mucous membranes of the oral fissure and lips are involved.1
FIGURE 4.
Erythema multiforme associated with sulfa drug assistants.
[ corrected] The affliction is classified as minor or major, depending on severity. In erythema multiforme small-scale, bullae and systemic symptoms are absent-minded. The eruption is typically confined to the extensor surfaces of extremities and just rarely involves the mucous membranes. Recurrent episodes of erythema multiforme minor commonly precede an outbreak of canker simplex by several days. Recurrences may be prevented with chronic acyclovir (Zovirax) therapy.1
Erythema multiforme major most often results from a drug reaction. Mucous membranes are always involved. The eruption tends to get bullous and systemic symptoms, including fever and prostration, are nowadays. Eating may be complicated by cheilitis and stomatitis, and micturition may be hard considering of balanitis and vulvitis. Conjunctivitis may exist severe and can lead to keratitis and ulceration. Lesions may besides be plant in the throat, larynx and trachea. Rarely, erythema multiforme major tin be life-threatening and tin progress to necrotizing tracheobronchitis, meningitis, blindness, sepsis and renal tubular necrosis.ane,4,vi
Secondary Syphilis. The rash of secondary syphilis can be lengthened, with localized eruptions often occurring on the head, neck, palms and soles. The lesions are typically dark-brown-red or pink macules and papules, but they may be papulosquamous, pustular or acneiform. The eruption ordinarily occurs two to six months afterward the primary infection and 2 to x weeks after the primary chancre.12
Patients often present with acute constitutional symptoms, and asymptomatic flat-topped macules and papules (mucous patches) are normally constitute on the oral and genital mucosa. Archetype condyloma lata may besides exist found in the perineum.1,6,12
Others. Meningococcemia, Rocky Mountain spotted fever and dengue fever—all potentially life-threatening infections—may initially present with erythematous maculopapular lesions before advancing to a petechial exanthem.3,thirteen
Petechial Eruptions
- Abstract
- History
- Physical Examination
- Laboratory Information
- Maculopapular Rashes
- Petechial Eruptions
- Lengthened Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
Petechial rashes warrant immediate evaluation to rule out severe, life-threatening illness. For proper assessment of an acutely ill patient with a petechial rash, the physician must exist familiar with the common infectious and noninfectious etiologies. Prompt, accurate diagnosis and early handling can exist life-saving in patients with meningococcemia, rickettsial infections and bacteremia.3,13
MENINGOCOCCEMIA
Meningococcal infections are a worldwide business organization. These infections occur sporadically or in epidemics, about commonly in the midwinter months.1 Seeding of Neisseria meningitidis from the nasopharynx may result in acute meningococcal septicemia, meningococcal meningitis or chronic meningococcemia. The risk of meningococcal affliction is highest in infants, asplenic patients, alcoholics and patients with a complement deficiency (particularly C5 to C8).i
In some patients, the typical prodrome of cough, headache, sore throat, nausea and vomiting may exist of short duration. Patients with acute meningococcemia appear ill and unremarkably present with a characteristic petechial rash (Figure five), a high, spiking fever, tachypnea, tachycardia and mild hypotension. In the early stages of disease, the rash may be maculopapular.14 Signs and symptoms of meningeal irritation may exist helpful, given that up to 88 percent1 of patients with meningococcemia develop meningitis.1,13–15
FIGURE 5.
Petechiae in meningococcemia.
Chronic meningococcemia is a rare condition. Patients may present with intermittent rash, fever, arthritis and arthralgias occurring over a menses of weeks to several months. In some patients, the chronic class advances to acute meningococcemia.1 The rash may be polymorphous, with maculopapular lesions commonly located around a painful articulation or pressure signal, nodules on the lower extremities and petechiae of variable size.one,4,vii,13–15
ROCKY Mountain SPOTTED FEVER
Rocky Mountain spotted fever is the nearly common rickettsial illness in the U.s..16 It is caused past Rickettsia rickettsii, which is transmitted through a tick bite or contact with tick feces or tissue juices.1
The disease occurs well-nigh often in young men betwixt April and September.16 In the United States, the areas with the highest prevalence of Rocky Mountain spotted fever are Oklahoma and the southern Atlantic states.6
The prodrome may include malaise, chills, a feverish feeling, anorexia and irritability. The onset of symptoms may be abrupt, with the predominant features beingness fever (94 percent), severe headache (86 percentage), generalized myalgia (83 pct), shaking rigor, photophobia, prostration and nausea. The diagnosis can be hard when the onset is gradual and no rash is present, every bit is the case in upward to 20 per centum of adults and five per centum of children with Rocky Mount spotted fever.16
When rash is present, it develops on approximately the fourth day of illness. Its appearance, combined with the temporal evolution, is characteristic of Rocky Mountain spotted fever. The rash typically begins as pink macules, 2 to 6 mm in diameter, located on the wrists, forearms, ankles, palms and soles. Within six to 18 hours, the rash spreads centrally to involve the artillery, thighs, trunk and face up. In the ensuing one to three days, the lesions evolve into deep-cerise papules. Within two to iv days after onset of the rash, the lesions get petechiae.one,4,seven,13,16,17
OTHER CAUSES
Viral illnesses known to cause petechial rashes include coxsackievirus A9, echovirus 9, Epstein-Barr virus and cytomegalovirus infections, atypical measles and viral hemorrhagic fevers caused past arboviruses and arenaviruses. Coxsackievirus and echovirus infections in children can produce severe affliction and, at times, are difficult to distinguish from meningococcemia.four
Included in the differential diagnosis of petechial rash are disseminated gonococcal infections, bacteremia, staphylococcemia and thrombotic thrombocytopenic purpura.
Lengthened Erythema with Desquamation
- Abstract
- History
- Physical Examination
- Laboratory Information
- Maculopapular Rashes
- Petechial Eruptions
- Diffuse Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
SCARLET FEVER
Ruddy fever provides the archetype example of an erythematous rash with subsequent desquamation. Most common between one and 10 years of age,eighteen scarlet fever unremarkably follows an astute infection of the tonsils or pare past group A beta-hemolytic streptococci that produce an erythrogenic exotoxin.2 Patients may appear acutely sick and have fever, sore throat, headache, chills, nausea and vomiting.1,18
The rash begins as finely punctate erythema on the superior torso and face up two to iii days subsequently the onset of illness. The erythema rapidly spreads to the extremities. When nowadays, petechiae in the antecubital and axillary skin folds (Pastia's lines) can be helpful in making the diagnosis.1,2
Initially, the tongue may appear white, with red, swollen papillae (white strawberry tongue), but past the fourth or fifth day, it becomes brilliant carmine (reddish strawberry tongue). The oral mucosa may take punctate erythema or petechiae, and the tonsils may be acutely infected.i
The exanthem varies in intensity. Withal, it normally fades in four to five days and is followed by diffuse desquamation.ane
The infection may exist mild, and patients may nowadays with just complaints of desquamation. Rarely, the streptococcal infection may produce a toxic-shock–like picture show that results in hypotension and multisystem failure. Many of these patients have a localized tissue infection that progresses to necrotizing fasciitis, which usually warrants firsthand surgical intervention.one,ii
TOXIC SHOCK SYNDROME AND SCALDED Pare SYNDROME
Staphylococcus aureus is the organism responsible for classic toxic shock syndrome and scalded skin syndrome. Toxic shock syndrome can present with hypotension, erythema, fever and multisystem dysfunction.3 Most cases of nonmenstrual toxic shock syndrome occur in the postoperative setting.one
Several dissimilar staphylococcal exotoxins take been implicated. The syndrome may upshot from infection, or it may occur because of simple colonization with S. aureus.three Staphylococcal scalded skin syndrome occurs in infants, immature children and adults with immunosuppression or renal damage.i
The rash is ordinarily diffuse and can present equally bullous impetigo, scarlatiniform lesions or diffuse erythema (Figure 6). The mucous membranes are spared in most patients. During the physical examination, the physician should effort to elicit Nikolsky's sign (shearing of the skin with gentle lateral pressure).1,3,4
Figure 6.
Diffuse erythema in toxic shock syndrome.
KAWASAKI'Due south DISEASE
Kawasaki'south disease, or mucocutaneous lymph node syndrome, is an acute delirious illness that affects infants and young children (mean age: 2.6 years). The disease is uncommon afterwards the age of 12 years.half dozen
In patients with Kawasaki'due south disease, fever begins abruptly, and the temperature is typically higher than forty°C (104°F). The fever lasts v to 30 days (hateful elapsing: 8.5 days) and does not respond to antibiotics and antipyretics.half-dozen,8
The rash appears within three days of the onset of fever and can vary in character. Ofttimes, the rash is scarlatiniform on the body and erythematous on the palms and soles, with subsequent distal desquamation. Mucous membrane interest is common and includes hyperemic bulbar conjunctiva, injected oropharynx, dry, cracked lips and a strawberry tongue.1,six
The physical examination may reveal non-suppurative cervical lymphadenopathy (more than 1.5 cm in bore). Coronary avenue abnormalities develop in 20 to 25 percent of patients with Kawasaki's affliction.nineteen Cardiovascular complications are the major cause of short-term and long-term morbidity and mortality.1,6,viii,19
OTHER CAUSES
Ehrlichiosis, a rickettsial-like infection, can occasionally exist associated with a clinical picture like to toxic daze syndrome, including lengthened erythema. Streptococcus viridans bacteremia is another rare crusade of generalized erythema. Finally, enteroviral infections, toxic epidermal necrolysis, graft-versus-host reaction, erythroderma and generalized pustular psoriasis (von Zumbusch's psoriasis) may present with lengthened erythema.one,3
Vesiculobullous-Pustular Eruptions
- Abstract
- History
- Physical Test
- Laboratory Information
- Maculopapular Rashes
- Petechial Eruptions
- Diffuse Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
VARICELLA-ZOSTER VIRUS INFECTIONS
Varicella-zoster virus is the near infectious of the human herpesviruses. Information technology is responsible for varicella (chickenpox) and canker zoster (shingles).twenty
Varicella. Primary infection with varicella-zoster virus results in chickenpox, a common childhood illness. Its highest incidence is in belatedly winter and spring.two The disease is typically more severe in adults and immunocompromised patients.1,6
The clinical presentation consists of rash, fever and general malaise.2 A mild prodrome lasting one to 2 days before appearance of the rash is not uncommon. The rash typically begins on the face, scalp or trunk and so spreads to the extremities.8
The lesions appear every bit erythematous macules and progress to papules with an edematous base (Figure seven). The papules quickly evolve into vesicles, with each vesicle initially having the appearance of "a dewdrop on a rose petal."1 The vesicles evolve into pustules, which get umbilicated and afterwards crust over in the ensuing viii to 12 hours. An enanthema may be noted, and vesicles may evolve to shallow erosions, primarily on the palate. On physical examination, lesions in all stages may be present.1
Effigy 7.
Rash of varicella (chickenpox).
Complications are unusual in immunocompetent patients. In children, the most common complication is secondary bacterial infection of excoriated lesions.7
The cardinal nervous arrangement (CNS) is the most common site of extracutaneous involvement in children. Cerebellar ataxia is the well-nigh oft encountered syndrome. Other possible CNS complications include encephalitis, meningitis, transverse myelitis and, rarely, Reye'due south syndrome (especially subsequent to aspirin use). Varicella pneumonia and encephalitis tin can be serious complications in adults. Additional rare complications in children and adults include myocarditis, corneal lesions, nephritis, arthritis, haemorrhage diatheses, acute glomerulonephritis and hepatitis.1,2,7,21
Herpes Zoster. Afterwards the primary infection, the varicella-zoster virus lies dormant in the dorsal root ganglia. Herpes zoster is acquired by reactivation of the virus.20 Although shingles tin occur at any age, its incidence increases significantly with historic period and in immunocompromised patients. An estimated ten to 20 percentage of the general U.Southward. population volition have herpes zoster at some time in life.20
The characteristic vesicular rash of canker zoster usually affects a single dermatome and rarely crosses the midline (Figure 8). The most common locations are the chest (approximately l percentage of cases) and the face (approximately xx percentage of cases).xx A prodrome of unusual skin sensations may evolve into hurting, burning and paresthesias, which precede the rash past two to iii days.
Figure eight.
Dermatomal distribution of rash in canker zoster.
The rash begins as an erythematous maculopapular eruption that rapidly evolves to a vesicular rash.21 In about five percent of patients, the rash may exist accompanied by headache, malaise and fever.ane Drying of the lesions with chaff formation more often than not occurs in 7 to ten days, and the lesions ordinarily resolve in 14 to 21 days.20
Pain is the most debilitating feature of herpes zoster, and postherpetic neuralgia is the virtually common long-term complexity. Post-herpetic neuralgia is uncommon in young patients just may bear on as many equally l percent of patients more 50 years of age.21
Other potential complications of herpes zoster include secondary infection, meningo-encephalitis, transverse myelitis, pneumonitis, hepatitis, myocarditis, pancreatitis, esophagitis, cystitis, granulomatous arteritis, conjunctivitis and Ramsay Hunt syndrome (herpes zoster involving the facial and auditory fretfulness). When herpes zoster affects the middle (herpes zoster ophthalmicus), an ophthalmologist should always exist consulted.one,twenty,21
OTHER CAUSES
Staphylococcal bacteremia may nowadays with a widespread pustular eruption. Gonococcemia may also produce a pustular rash, although other lesion types, such as macules, petechiae and papules, are commonly present.iii
In immunocompromised patients, disseminated herpes simplex virus infection must be considered. Patients with underlying liver disease, renal dysfunction or diabetes are particularly susceptible to infection with Vibrio vulnificus, which is acquired from eating seafood, exposure to ocean water or injury when treatment crabs. Rickettsia akari, transmitted by a house mite, is the cause of rickettsialpox, a mild disease characterized past a local eschar, a papulovesicular rash and a mild clinical course.1–four,12
Nodular Eruptions
- Abstract
- History
- Physical Exam
- Laboratory Information
- Maculopapular Rashes
- Petechial Eruptions
- Lengthened Erythema with Desquamation
- Vesiculobullous-Pustular Eruptions
- Nodular Eruptions
- References
ERYTHEMA NODOSUM
Erythema nodosum is an acute inflammatory and immunologic process involving the panniculus adiposus (the fatty tissue layer underlying the skin).1 A number of etiologies take been identified (Tabular array 4).1,iv This status is more common in women than in men.
Table 4
Etiologies of Erythema Nodosum
| Idiopathic (40 pct of cases) | ||
| Infectious causes | ||
| Beta-hemolytic streptococci | ||
| Yersinia species | ||
| Hepatitis C virus | ||
| Mycobacterium species | ||
| Chlamydia trachomatis | ||
| Coccidioides immitis | ||
| Noninfectious causes | ||
| Medications | ||
| Sulfonamides | ||
| Oral contraceptives | ||
| Systemic lupus erythematosus | ||
| Sarcoidosis | ||
| Ulcerative colitis | ||
| Behçet'south syndrome | ||
| Pregnancy | ||
Presenting features often include fever, malaise and arthralgias. The characteristic nodules are painful and tender. The lesions most often develop on the lower legs, knees and arms (Effigy 9). The course of erythema nodosum depends on the specific cause, but spontaneous resolution can be expected inside half dozen weeks.1,2
FIGURE ix.
Erythema nodosum.
OTHER CAUSES
In immunocompromised patients, disseminated fungal infections may produce nodular lesions. Disseminated candidiasis may present with diffuse nonerythematous nodules in an immunocompromised patient who has fever and myalgias. Other fungal infections to consider include cryptococcosis, blastomycosis, histoplasmosis, coccidioidomycosis and sporotrichosis.2
Rarely, bacteria such as Nocardia, Pseudomonas and Mycobacterium species may produce nodular lesions.one,four
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REFERENCES
evidence all references
i. Fitzpatrick TB, et al. Color atlas and synopsis of clinical dermatology: mutual and serious diseases. 3d ed. New York: McGraw-Hill, Wellness Professions Division, 1997. ...
ii. Kaye ET, Kaye KM. Fever and rash. In: Fauci Equally, et al., eds. Harrison'due south Principles of internal medicine. 14th ed. New York: McGraw-Hill, Health Professions Division, 1998.
3. Schlossberg D. Fever and rash. Infect Dis Clin North Am. 1996;10:101–10.
iv. Weber DI, Cohen MS, Fine JD. The acutely ill patient with fever and rash. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett'south Principles and practice of infectious diseases. 5th ed. Philadelphia: Churchill Livingstone, 1999:633–fifty.
five. Nichol KL, MacDonald R, Hauge Thou. Side effects associated with pneumococcal vaccination. Am J Infect Control. 1997;25:223–8.
6. Habif TP. Clinical dermatology: a color guide to diagnosis and therapy. 3d ed. St. Louis: Mosby, 1996.
7. American Pharmaceutical Association. Infectious diseases handbook: including antimicrobial therapy & diagnostic tests/procedures. 2nd ed. Hudson, Ohio: Lexi-Comp, 1996.
8. Nelson We, Behrman RE, Kliegman RM, Arvin AM, eds. Nelson Textbook of pediatrics. 15th ed. Philadelphia: Saunders, 1996.
9. Nadelman RB, Wormser GP. Lyme borreliosis. Lancet. 1998;352:557–65.
10. Edlow JA. Lyme disease and related tick-borne illnesses. Ann Emerg Med. 1999;33:680–93.
11. Romano A, Quaratino D, Papa G, Di Fonso M, Venuti A. Aminopenicillin allergy. Arch Dis Child. 1997;76:513–seven.
12. Joklik WK, et al., eds. Zinsser Microbiology. 20th ed. Norwalk, Conn.: Appleton & Lange, 1992:659–63,707–8.
thirteen. Cunha BA. Rash and fever in the critical care unit. Crit Care Clin. 1998;fourteen:35–53.
xiv. Pollard AJ, Britto J, Nadel S, DeMunter C, Habibi P, Levin G. Emergency management of meningococcal disease. Curvation Dis Child. 1999;lxxx:290–6.
15. Granier Southward, Owen P, Pill R, Jacobson Fifty. Recognising meningococcal illness in primary intendance: qualitative written report of how general practitioners process clinical and contextual data. BMJ. 1998;316:276–9.
xvi. Abramson JS, Givner LB. Rocky Mount spotted fever. Pediatr Infect Dis J. 1999;xviii:539–twoscore.
17. Thorner AR, Walker DH, Petri WA. Rocky mount spotted fever. Clin Infect Dis. 1998;27:1353–ix.
eighteen. Manders SM. Toxin-mediated streptococcal and staphylococcal disease. J Am Acad Dermatol. 1998;39:383–98.
xix. Rubin B, Cotton wool DM. Kawasaki disease: a dangerous astute babyhood illness. Nurse Pract. 1998;23:3437–viii.
twenty. Morgan R, King D. Shingles: a review of diagnosis and management. Hosp Med. 1998;59:770–half dozen.
21. Whitley R. Varicella-zoster virus. In: Fauci Every bit, et al., eds. Harrison's Principles of internal medicine. 14th ed. New York: McGraw-Hill, Health Professions Partitioning, 1998.
Members of various family exercise departments develop articles for "Trouble-Oriented Diagnosis." This article is one in a series coordinated by the Department of Family Medicine at the Uniformed Services University of the Health Sciences, Bethesda, Md. Guest editors of the serial are Francis G. O'Connor, LTC, MC, Usa, and Jeannette E. South-Paul, COL, MC, USA.
Copyright © 2000 by the American Academy of Family unit Physicians.
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What Disease Results In Red Raised Bumps, Fever, Chills And May Require Topical Or Skin Cream.,
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