d. Changes in the extremities: erythema of the palms or soles; indurative edema of
the hands or feet; desquamation of the skin of the hands, feet, and perineum
during convalescence
e. Cervical lymphadenopathy: lymph nodes more than 15 mm in diameter- Exclusion of disease with a similar presentation, such as scalded skin syndrome, TSS,
viral exanthems, etc.
Other clinical features include intense irritability (possibly due to cerebral vasculitis),
sterile pyuria, and upper respiratory symptoms (130). The major morbidity of KD is the
development of coronary artery aneurysm(s) that occur in 25% of the cases.
There are no specific or sensitive tests that can be used to diagnose KD. The diagnosis is
made by clinical assessment of the above criteria. The cause of KD is unknown; however, an
infectious etiology is still being sought. KD has seasonal peaks in the winter and spring
months, and focal epidemics occurred in the 1970s and 1980s (131). Treatment with aspirin and
intravenous immune globulin has reduced the development and severity of coronary artery
aneurysms.
Other Causes of Diffuse Erythematous Rashes
Streptococcus viridansbacteremia can cause generalized erythema. Ehrlichiosis can produce a
toxic shock-like syndrome with diffuse erythema. Enteroviral infections, graft versus host
disease, and erythroderma may all present with diffuse erythema (8).
VESICULAR, BULLOUS, OR PUSTULAR RASHES
Vesicles and bullae refer to small and large blisters. Pustules refer to a vesicle filled with
cloudy fluid. The causes of vesiculobullous rashes associated with fever include primary
varicella infection, herpes zoster, herpes simplex, small pox, S. aureus bacteremia,
gonococcemia,V. vulnificus,Rickettsia akari, enteroviral infections, parvovirus B19, and HIV
infection. Other causes that will not be discussed include folliculitis due to staphylococci,
Pseudomonas aeruginosa, andCandida, but these manifestations would not result in admission to
a critical care unit.
Varicella Zoster
Primary infection with varicella (chicken pox) is usually more severe in adults and
immunocompromised patients. Although it can be seen year-round, the highest incidence of
infection occurs in the winter and spring. The disease presents with a prodrome of fever and
malaise one to two days prior to the outbreak of the rash. The rash begins as erythematous
macules that quickly develop into vesicles. The characteristic rash is described as “a dewdrop
on a rose petal.” The vesicles evolve into pustules that umbilicate and crust. A characteristic of
primary varicella is that lesions in all stages may be present at one time (8).
Herpes zoster (i.e., shingles) is caused by the reactivation of the varicella zoster virus
(VZV), which lies dormant in the basal root ganglia (132). The incidence of zoster is greatest in
older age groups because of a decline in VZV-specific cell-mediated immunity. Herpes zoster
also occurs more often in immunosuppressed patients such as transplant recipients (133–135)
and HIV-infected patients (136–138).
Patients often have a prodrome of fever, malaise, headaches, and dysesthesias that
precede the vesicular eruption by several days (139). The characteristic rash usually affects a
single dermatome and begins as an erythematous maculopapular eruption that quickly
evolves into a vesicular rash (Fig. 8). The lesions then dry and crust over in 7 to 10 days, with
resolution in 14 to 21 days (112). Disseminated herpes zoster is seen in patients with solid-
organ transplants, hematological malignancies, and HIV-infection (136,137,140–144). Thirty-
five percent of patients who have received bone-marrow transplants have reactivation of VZV,
and 50% of these patients develop disseminated herpes zoster (142,145,146).
Both immunocompetent and immunocompromised patients can have complications
from herpes zoster; however, the risk is greater for immunocompromised patients (147).
Complications of herpes zoster include herpes zoster ophthalmicus (140,148), acute retinal
36 Engel et al.