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Table 47–1Common dermatoses in the ICU setting.
Figure 47–1

Contact dermatitis. Typical geometric shape due to adhesive tape.

Figure 47–2

Miliara crystillina. Clear vesicles on the back.

Skin Infections

Any systemic infection can have cutaneous manifestations that are often nonspecific. The discussion will be focused on life-threatening infections with distinctive skin findings.

Staphylococcal Scalded Skin Syndrome


Staphylococcal scalded skin syndrome (SSSS) is caused by an exfoliative toxin producing staphylococcal species which bind and cleave desmoglein 1, an adhesion molecule that binds keratinocytes. This explains the clinical manifestation of widespread flaccid bullae and exfoliation. Although primarily a disease of infants and young children, adults with renal failure or immunosuppression are at risk for developing SSSS. The initiating event in adults is often a staphylococcal pneumonia or bacteremia.

Clinical Features

SSSS begins with widespread erythema beginning on the head and intertriginous areas which then generalize within 48 hours. There is often a preceding prodrome of fever, malaise, and skin tenderness. The skin then takes on a wrinkled appearance due to the superficial flaccid bullae with subsequent exfoliation (Figure 47–3). There are no mucosal lesions distinguishing it from Stevens–Johnson syndrome/toxic epidermal necrolysis (SJS/TEN).

Figure 47–3

Staphylococcal scalded skin syndrome. Peeling of the hands.

Workup and Differential Diagnosis

SSSS is a clinical diagnosis. Since the condition is due to distant foci of infection, skin cultures are generally negative. However, blood cultures may be positive. A skin biopsy can be useful and will show disadhesion of keratinocytes due to cleavage of desmoglein 1. Other conditions to consider are extensive sunburns, toxic shock syndrome (TSS, staphylococcal), SJS/TEN, and autoimmune blistering dermatoses.


Patients generally require supportive skin care which may best be handled in a burn unit. Parenteral antibiotics with beta-lactamase–resistant penicillins such as dicloxacillin or cephalexin should be given. Clindamycin reduces toxin production and is, therefore, recommended.

Toxic Shock Syndrome


Toxic shock syndrome (TSS) is a severe, multisystem disease characterized by fever, hypotension, and multiorgan involvement with skin findings. There are 2 types: (1) classic TSS caused by staphylococcus and (2) streptococcal TSS (sTSS) which is more severe and has a mortality rate of up to 50%. Both tend to affect young healthy adults. Classic TSS was previously associated with tampon use but most recently is associated with surgical (particularly nasal) packing and abscesses, whereas, sTSS is associated with disruption of the skin barrier due to lacerations or bites. Both are due to elaboration of toxins that stimulate massive cytokine release.

Clinical Features

Classic TSS begins with a sudden onset of headache, fever, malaise, myalgias, vomiting, and diarrhea. This can rapidly progress to hypotension and frank shock. Patients generally also have generalized erythema and/or a scarlatiniform exanthema. Conjunctivitis, a red tongue, mucosal involvement and the hands and feet may also be involved.

sTSS often begins with severe pain in an extremity. sTSS is usually due to an invasive soft tissue infection but up to 50% of patients may have only severe extremity pain as the initial symptom. Other nonspecific symptoms such as fever, malaise, myalgias, and diarrhea may also be present. Unlike classic TSS, widespread erythema is often not present. The disease progresses very rapidly with multiorgan failure ensuing in 48 to 72 hours. Disseminated intravascular coagulation (DIC) and acute respiratory distress syndrome may also develop. In both types, desquamation of the hands and feet occur a few weeks after disease onset.

Workup and Differential Diagnosis

Because this condition can progress very rapidly a high index suspicion is needed. Blood cultures and cultures of any visible skin wounds or skin infections should be performed but are often negative in both TSS and sTSS. Laboratory findings may include an elevated creatinine and an elevated white blood count. Other conditions to consider are SSSS and TEN.


Supportive care and intensive monitoring are the hallmarks of treatment. Hypotension may require aggressive intravenous fluid resuscitation and vasopressors. In addition parenteral clindamycin should be considered since it reduces toxin load, otherwise a beta-lactamase–resistant penicillin should be given. Surgical packing, if present, should be removed. The use of intravenous immunoglobulin (IVIG) may neutralize toxin.

Necrotizing Fasciitis


Necrotizing fasciitis (NF) is a rapidly progressive and life-threatening disease of the subcutaneous fat and fascia. Prompt recognition with surgical intervention and parenteral antibiotics are the mainstay of treatment. Risk factors for NF include diabetes mellitus, immunosuppression, renal failure, peripheral vascular disease, recent surgery and intravenous drug use. NF may also follow penetrating injuries. Mortality is up to 40%. It is generally caused by a polymicrobial infection including streptococci, staphylococci, E. coli, Bacteroides, and Clostridium.

Clinical Features

NF begins with severe pain, erythema and edema often in an extremity. Initially the skin is taut and shiny. As the condition evolves, the skin then becomes gray-blue with progression to frank necrosis. Hemorrhagic bullae may also form (Figure 47–4). As necrosis of the fascia ensues, a characteristic, malodorous, watery discharge is produced. Anesthesia is a late finding from destroyed nerves. Patients are toxic appearing with fevers, chills, and symptoms of septic shock. A key feature of this condition is pain out of proportion to the clinical exam on initial presentation. Fournier's gangrene refers to NF of the perineum and genitalia that rapidly spreads to the anterior abdominal wall.

Figure 47–4

Necrotizing fasciitis. Confluent bullae. Note the grey-tan color.

Workup and Differential Diagnosis

NF is often mistaken for cellulitis. However, the patient's condition continues to rapidly deteriorate and characteristic skin changes ensue despite antibiotic therapy. Initial evaluation should include a complete white blood cell count, creatinine, electrolytes, and C-reactive protein. Blood cultures and culture of any visible drainage should also be done. NF can be confirmed with MRI but this may not be practical and often a CT scan or echo will show fascial edema.


Broad spectrum parenteral antibiotics should be started immediately as workup is in progress and tailored as the causative organism(s) are identified. Surgical debridement is the mainstay of treatment. Amputation may be necessary.



Meningococcemia is a severe presentation of an infection by Neisseria meningitidis. Infections can range from mild upper respiratory infections to meningitis to purpura fulminans. Functional complement is necessary to fight N. meningitidis.

Clinical Features

Up to 1/3 of patients with acute meningococcemia will present with a petechial eruption on the trunk and extremities (Figure 47–5). These lesions can progress to large purpuric lesions that are often retiform with a characteristic gunmetal grey color centrally. Bullae may form within these lesions. More extensive and severe skin lesions portend the onset of purpura fulminans.

Figure 47–5

Meningococcemia. Petechial macules on the lower extremity.

Patients will have fever and hypotension. Other complications include arthritis, myocarditis, and meningeal symptoms. Of note, meningeal symptoms are usually absent in the severe cutaneous presentations of meningococcemia.

Workup and Differential Diagnosis

Diagnosis is made by confirmation of the organism by culture or gram stain. Blood cultures and CSF fluid should be sampled. Other laboratory findings are generally nonspecific except an elevated white blood cell count. Patients with extensive petechial or purpuric lesions should be evaluated for the development of DIC.

Meningococcemia should be considered in any patient with fever and petechial rash. Rocky Mountain spotted fever and West Nile virus and other causes of meningitis also need to be considered.


Treatment for acute meningococcemia is high dose intravenous penicillin. Third generation cephalosporins may also be used. Unfortunately, in severe cases, patients may deteriorate rapidly despite aggressive IV antibiotic therapy. All close contacts require prophylaxis with ciprofloxacin or rifampin.

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