Fever and Chest Pain - Dermatologic Etiologies
Diseases of the skin are usually recognized by patients and often prompt early evaluation since patients’ often have anxiety about diseases they can visualize. The skin should always be examined in the evaluation of fever and chest pain, as infectious rashes and eruptions may be identified. And while the differential diagnosis may not be as broad when rash is combined with fever and chest pain, serious pathology may nonetheless exist. Cellulitis, necrotizing soft tissue infection and herpes zoster represent the most common skin-related causes of fever and chest pain (see Table 7).
Table 7: Dermatologic Etiologies of Chest Pain and Fever
Presentation Management Cellulitis
Intravenous drug use
Diffusely tender area of
erythema, edema & induration
Empiric antibiotic therapy
± Blood cultures
± Removal of implanted device
Skin findings initially
similar to cellulitis with
cyanosis, skin sloughing
± Hypotension, tachycardia
Empiric antibiotic therapy
± Hyperbaric oxygen
Initially, vesicular or pustular
Ulcerated or crusted after 3-5 days
± Superimposed cellulitis
Empiric antiviral therapy
± direct immuno-
fluoresence vs. PCR to confirm etiology
Cellulitis is a diffuse, spreading infection of the dermis and subcutaneous tissue. While more frequently seen in the lower extremities, cellulitis of the chest wall is not uncommon in the setting of certain risk factors. Any type of skin trauma may create a portal of entry for infection. Lacerations, burns, and surgical wounds are common sites for cellulitis. Devices such as cardiac pacemakers, central lines, and implantable defibrillators positioned in the subcutaneous tissue of the chest wall may likewise serve as a nidus for infection. Disruption of lymphatic drainage following axillary node dissection as part of a radical mastectomy or lumpectomy for breast cancer may result in lymphedema, which is a prominent risk factor for cellulitis. Increasing age, obesity, immunosuppression, underlying diabetes mellitus and intravenous drug abuse are all widely recognized risk factors as well. Streptococcus pyogenes and Staphylococcus aureus represent the primary organisms responsible for most cellulitis. Infection with S. aureus may often be complicated by an underlying abscess. In many parts of the United States, community-acquired methicillin-resistant S. aureus (MRSA) is responsible for the majority of skin infections presenting to the emergency department.
Cellulitis typically manifests with poorly-demarcated erythema, edema, induration, and pain. Erysipelas is a specific form of cellulitis that presents with well-circumscribed borders and lymphatic inflammation. In other forms of cellulitis, vesicles, bullae, or pustules (especially Staph aureus) may be present. Likewise, petechiae and ecchymosis may also be noted. The clinical presentation may range anywhere from localized discomfort at the site of infection to a picture of systemic toxicity with fever, tachycardia and hypotension.
Blood cultures are rarely positive in most uncomplicated cases of cellulitis in the general population. Clinical evidence of bacteremia such as high-grade fever, chills and leukocytosis should however warrant blood cultures, especially in the setting of cellulitis superimposed upon preexisting lymphedema.
Antimicrobial therapy should be tailored towards coverage of streptococci and S. aureus with oral penicillinase-resistant penicillin or a first-generation cephalosporin. It is important to consider community-acquired MRSA as well and give some consideration to usage of trimethoprim-sulfamethoxazole, doxycycline, or clindamycin in those patients. In cases of antibiotic-resistant infection requiring hospital admission or allergy to penicillin, treatment with vancomycin or clindamycin may be necessary. Most cases of uncomplicated cellulitis are treated for 7 to 10 days, although evidence suggests that a 5-day course may be equally effective. Cellulitis associated with implanted medical devices may ultimately require removal of the hardware in order for the infection to resolve.
Necrotizing Soft Tissue Infection
In contrast to cellulitis, necrotizing soft tissue infections attack the fascia and subcutaneous tissue. Rapidly progressive and frequently fatal, they often develop as secondary infections in the setting of trauma, surgery, peripheral vascular disease, skin ulcers and diabetes mellitus. Necrotizing fasciitis is a rare infection that spreads along the superficial fascia, compromising the subcutaneous tissue between the skin and underlying muscle. Polymicrobial necrotizing infections (type 1 necrotizing fasciitis) may be caused by a mix of streptococci, staphylococci, enterococci, enteric gram-negative bacteria and anaerobes. Monomicrobial necrotizing infections (type II necrotizing fasciitis) may be caused by group A β- hemolytic streptococci or S. aureus. As in cellulitis, an increasing number of cases of necrotizing fasciitis have been attributed to community-acquired MRSA. Necrotizing fasciitis involving the chest wall is extremely uncommon but bears an especially high mortality. Tube thoracostomy for empyema has been identified as the most common procedure preceding infection in many cases. In at least one case, pneumonia with empyema without prior surgical intervention has also been associated with necrotizing fasciitis.
Necrotizing fasciitis is often mistaken for cellulitis in its early stages. In fact, almost two-thirds of cases of necrotizing fasciitis are initially misdiagnosed as either cellulitis or abscess. Skin discoloration, warmth, induration, and edema are common findings, but fail to resolve with antibiotic therapy. The affected area may be firm, with a wooden consistency, in contrast to the fleshy consistency of cellulitis. A paucity of skin findings in the early stages of infection is equally likely. In these instances, pain disproportionate to the physical findings may serve as a helpful clue to a deeper infection. As the illness progresses, development of violaceous bullae, diffuse ecchymosis, cyanosis, and skin sloughing signify tissue necrosis below the skin. The hemorrhagic fluid in the bullae may evolve into a gray, foul-smelling fluid, frequently referred to as “dishwater pus.” Skin anesthesia may result from cutaneous nerve destruction. Crepitus may be palpated in polymicrobial infections. Fever, hypotension and mental status change herald bacteremia and sepsis.
The diagnosis of necrotizing fasciitis remains one that is heavily based upon history and clinical examination. Surgical exploration with direct inspection of the fascia is the most expeditious means to confirm the diagnosis. Fascial planes are easily separated using a blunt probe as a result of extensive tissue necrosis. Laboratory evaluation may reveal leukocytosis and elevated sedimentation rate, though both may be nonspecific. Hypocalcemia may arise from extensive fat necrosis. Worsening renal and hepatic indices may signal multiorgan failure from sepsis. Blood cultures are warranted and deep incisional tissue biopsy with aerobic and anaerobic cultures may aid in identifying causative organisms. Conventional radiography may be notable for subcutaneous gas, though CT is more sensitive. Magnetic resonance imaging (MRI) has proven useful in identifying the extent of deep fascial involvement in necrotizing infection, though its sensitivity exceeds its specificity and may result in overestimation. Given the rapid nature of necrotizing fasciitis, imaging should never delay prompt surgical evaluation.
Extensive surgical debridement coupled with fasciotomy is crucial to survival. In many cases, multiple debridements in the operating theater may be necessary. Polymicrobial infections should be treated with a combination of ampicillin-sulbactam, clindamycin and ciprofloxacin for broad aerobic and anaerobic coverage. Monomicrobial infection from group A streptococci should be treated with clindamycin and penicillin. The addition of vancomycin or newer antibiotics such as linezolid may be necessary for infections involving MRSA with resistance to clindamycin. The role for hyperbaric oxygen therapy in the treatment of necrotizing fasciitis is not well established, though it is frequently employed as an adjunct to surgical and antimicrobial therapy at institutions where it is available.
In those who have had a primary infection with varicella-zoster virus in the past, reactivation of latent virus in the dorsal root ganglia clinically manifests itself as a painful vesicular rash known as herpes zoster. More than 90% of adults in the United States have been exposed to varicella-zoster virus and, as a consequence, more than 500,000 cases of herpes zoster are estimated to occur annually. Naturally waning cell-mediated immunity with increasing age is one of the primary risk factors for developing herpes zoster. Patients on immunosuppressive therapy, including corticosteroids and chemotherapy, are likewise at increased risk, as are those with immune systems compromised by lymphoma or HIV.
Herpes zoster frequently occurs along the distribution of a thoracic nerve, resulting in a rash with a unilateral dermatomal distribution across one side of the chest and back that does not cross the midline. A prodrome of pain and paresthesia in the affected sensory nerve may precede the rash by two to three days along with fever, headache and malaise. The rash progresses from macular to vesicular to pustular and finally ulcerates and then crusts after three to five days. Recurrent pain along the course of the affected nerve more than a month after the rash has healed is classified as post-herpetic neuralgia. Affected areas of skin may be at higher risk for cellulitis by superinfection with staphylococci and streptococci.
Although herpes zoster is a clinical diagnosis for the most part, it may be confirmed by direct immunofluorescence assay of fluid from a cutaneous lesion. The important aspect of the physical examination is a thorough skin examination to ensure no herpetic lesions exist outside of the affected dermatome. Immunosuppressed patients (e.g. HIV, chronic steroids, neutropenic) are at risk of disseminated herpes zoster with a significantly increased morbidity and mortality.
Treatment for herpes zoster begins with antiviral therapy. Oral antiviral medications such as acyclovir, valacyclovir and famciclovir may reduce the severity and duration of herpes zoster-related pain if initiated within seventy-two hours of onset of the rash, while viral replication is still ongoing. Concomitant administration of corticosteroids may further accelerate healing and attenuate pain. Immunosuppressed patients or those with any indications of disseminated herpes zoster should be given strong consideration for intravenous therapy and admission to the hospital.