eMedicine Specialties > Emergency Medicine > Infectious Diseases

Staphylococcal Scalded Skin Syndrome

Randall W King, MD, Assistant Clinical Professor of Emergency Medicine, The University of Toledo College of Medicine; Program Director Emergency Medicine Residency, Associate Chair, Department of Emergency Medicine, St Vincent Mercy Medical Center
Paul R de Saint Victor, MD, FACEP, Chief of Staff, St Vincent Mercy Medical Center, Toledo

Updated: Jun 18, 2009

Introduction

Background

Staphylococcal scalded skin syndrome (SSSS), also known as Ritter von Ritterschein disease (in newborns), Ritter disease, and staphylococcal epidermal necrolysis, encompasses a spectrum of superficial blistering skin disorders caused by the exfoliative toxins of some strains of Staphylococcus aureus.

It is a syndrome of acute exfoliation of the skin typically following an erythematous cellulitis. Severity of staphylococcal scalded skin syndrome varies from a few blisters localized to the site of infection to a severe exfoliation affecting almost the entire body.

Pathophysiology

Staphylococcal scalded skin syndrome (SSSS) is caused by an exfoliative toxin produced by roughly 5% of Staphylococcus aureus. As the syndrome evolves, an initial infection occurs, commonly at a site such as the oral or nasal cavities, throat, or umbilicus.¹ Epidermolytic toxins are produced by the infecting Staphylococcus species; these toxins act at a remote site leading to a red rash and separation of the epidermis beneath the granular cell layer. Bullae form, and diffuse sheetlike desquamation occurs. Two types of staphylococcal scalded skin syndrome are thought to exist: a localized form, in which there is only patchy involvement of the epidermis, and a generalized form, in which significant areas of are involved, remote from the initial site of infection.

Two exfoliative toxins (ETA and ETB) have been isolated and characterized, but the exact mechanism by which they cause exfoliation had until recently been uncertain. The toxins likely act as proteases that target the protein desmoglein-1 (DG-1), an important cell-to-cell attachment protein found only in the superficial epidermis.^2,3,4 The relative quantity of DG-1 in the skin differs with age and may partially explain the increased frequency of staphylococcal scalded skin syndrome in children younger than 5 years. It is theorized that immature renal function in this age group may contribute to impaired clearance of circulating exotoxins, contributing to more extensive disease. Another theory suggests that the exfoliative toxins may possess a superantigenic activity.

The decrease in frequency of staphylococcal scalded skin syndrome (SSSS) in adults is thought to be explained by the presence of antibodies specific for exotoxins and also improved renal clearance of toxins that are produced.

Initial studies suggested that phage lytic group II S aureus (subtypes 3A, 3B, 3C, 55 and 71) were solely responsible for exfoliative toxin production, but it is now known that all phage groups are able to produce exfoliative toxin and cause staphylococcal scalded skin syndrome.

Staphylococcal scalded skin syndrome differs from bullous impetigo. Both are blistering skin diseases caused by staphylococcal exfoliative toxin. However, in bullous impetigo, the exfoliative toxins are restricted to the area of infection, and bacteria can be cultured from the blister contents. In staphylococcal scalded skin syndrome, the exfoliative toxins are spread hematogenously from a localized source potentially causing epidermal damage at distant sites.

Frequency

United States

Staphylococcal scalded skin syndrome (SSSS) is most common in children and neonates. Staphylococcal scalded skin syndrome is rarer in adults, but it has been described in adults with renal failure, immunologic deficiency, and other chronic illness.⁵

International

Internationally, predominance is in children as well. Overall incidence is higher in developing countries and wherever the incidence of staphylococcal infections is higher. Additionally, some geographic difference exists in the incidence of staphylococcal strains and the types of exotoxins produced.⁶

Mortality/Morbidity

The mortality rate from staphylococcal scalded skin syndrome (SSSS) in children is very low (1-5%), unless associated sepsis or an underlying serious medical condition exists. The mortality rate in adults is higher (as high as 50-60%), although this may be a reflection of the underlying disorder, which increased susceptibility to SSSS, and not SSSS itself.^7,8,9 Significant morbidity can result from hematologic or local spread of infection.¹⁰ Complications are usually the result of sepsis, superinfection, and dehydration or electrolyte imbalance due to denuded skin.

Sex

No gender predilection is documented in children. In adults, the male-to-female ratio is approximately 2:1.

Age

Staphylococcal scalded skin syndrome (SSSS) primarily is a disease of children.

• Children are more at risk because of lack of immunity and immature renal clearance capability (exfoliative toxins are renally excreted). Maternal antibodies transferred to infants in breastmilk are thought to be partially protective, but neonatal disease can still occur possibly as a result of inadequate immunity or immature renal clearance of exotoxin. 
• SSSS can occur individually or as outbreaks in nurseries.  Outbreaks are usually due to asymptomatic carriers who spread the disease to susceptible individuals. 
• Most children (62%) are younger than 2 years, and almost all (98%) are younger than 6 years. 
• SSSS is rare in adults, with fewer than 50 cases formally reported in the literature. Adults with SSSS are most often chronically ill, are immunocompromised, or have renal failure. SSSS can also appear in adults in cases with a high burden of staphylococcal infection where the quantity of exotoxin is significant.

Clinical

History

• Staphylococcal scalded skin syndrome (SSSS) presents as a red rash followed by diffuse epidermal exfoliation. 
• A prodromal localized S aureus infection of the skin, throat, nose, mouth, umbilicus, or GI tract occurs. Such an infection often is not apparent before the SSSS rash appears.
• General malaise
• Fever
• Irritability
• Skin tenderness

Physical

• Fever, although patients may be afebrile
• Tenderness to palpation
• Warmth to palpation
• Diffuse erythematous rash (see Media file 1)
  
  

  

  Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

  
  
  • Often begins centrally
  • Sandpaperlike, progressing into a wrinkled appearance
  • Accentuated in flexor creases (see Media file 2)
    
    

    

    Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

    
    
• Bullae (see Media file 3)
  
  

  

  Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

  
  
  • Flaccid
  • Ill-defined
• Nikolsky sign (gentle stroking of the skin causes the skin to separate at the epidermis)^11,12
• Exfoliation of skin, which may be patchy or sheetlike in nature (see Media files 4-6)
• Facial edema
• Perioral crusting
• Most patients do not appear severely ill.
• Dehydration may be present and significant.

Causes

• Infection by group 2 phage S aureus (several types) leads to release of exotoxin.
  • Exotoxin is a protein and is classified as either type A or B. Most are type A.
  • Exotoxin causes separation of the epidermis beneath the granular cell layer.
  • Cases of staphylococcal scalded skin syndrome (SSSS) have been reported among infants who have breastfed from mothers with S aureus breast abscess.
  • A case has been reported of neonatal staphylococcal scalded skin syndrome secondary to maternal-fetal transmission at birth.
  • Outbreaks have been reported in neonatal and newborn nurseries.
  • Reports implicating MRSA and community-acquired methicillin Staphylococcus aureus (CA-MRSA) as a cause of staphylococcal scalded skin syndrome are increasing.^13,14,15

Differential Diagnoses

Workup

Laboratory Studies

• White blood count (WBC) may be elevated; however, often WBC is normal.
• Erythrocyte sedimentation rate (ESR) frequently is elevated.
• Electrolytes and renal function should be followed closely in severe cases where fluid losses and dehydration via denuded skin are a concern. 
• A polymerase chain reaction (PCR) serum test for the toxin is available.
• Typing of staphylococcal isolates for phage and subtype and the presence of exotoxin production is usually not necessary but is available at some centers
• Cultures of bullae are negative in the absence of contamination.
• Blood culture
  • Usually negative in children (but positive in bullous impetigo)
  • Usually positive in adults
• A Gram stain and/or culture from the remote infection site may confirm staphylococcal infection.

Imaging Studies

• A chest radiograph should be considered to rule out pneumonia as the original focus of infection.

Procedures

• Skin biopsy: A biopsy of the affected area will demonstrate separation of the epidermis at the granular layer. An inflammatory cell infiltrate is typically not present. Immunofluorescence and the presence of antibodies that are common in pemphigus foliaceous are not present in staphylococcal scalded skin syndrome (SSSS). In toxic epidermal necrolysis (TEN), an inflammatory (lymphocytic) infiltrate is present, and the plane of separation is deeper, at the level of the basement membrane. 
• Frozen section of the peeled skin confirms the site of cleavage as superficial. Toxic epidermal necrolysis (TEN) shows deeper cleavage below the epidermis.

Treatment

Prehospital Care

In the prehospital phase, treatment will be likely limited to antipyretic therapy and treatment of the dehydration with intravenous fluid therapy during transport. Most patients are brought to the emergency department by parents or caregivers.

Emergency Department Care

• The major focus of ED care should be to identify staphylococcal scalded skin syndrome (SSSS) and to stabilize the patient's condition.
• Once SSSS is diagnosed, the treatment consists of supportive care and eradication of the primary infection.
• Patients need fluid rehydration, topical wound care similar to the care for thermal burns, and parenteral antibiotics to cover S aureus.
• Consideration must be given for the sharply increasing rates of community-acquired S aureus infection (CA-MRSA). Prompt treatment with parenteral anti-staphylococcal antibiotics is essential. Most staphylococcal infections implicated in staphylococcal scalded skin syndrome have penicillinases and are resistant to penicillin. Nafcillin, oxacillin, or vancomycin is indicated.
• Clindamycin may also be used to inhibit bacterial ribosomal production of exotoxin.
• Fluid rehydration is initiated with Lactated Ringer solution at 20 mL/kg initial bolus. Repeat the initial bolus, as clinically indicated, followed by maintenance therapy with consideration for fluid losses from exfoliation of skin being similar to a burn patient.
• Topical wound care, in severe cases, in a dedicated burn center should be provided.
• Cultures from the exfoliated sites as well as nose, throat, and other potential sites of the original focus of infection should be performed.
• A chest radiograph should be considered to rule out pneumonia as the original focus of infection.
• Steroids are not indicated and may worsen immune function.
• Nonsteroidal anti-inflammatory agents and other agents that potentially reduce renal function should be avoided
• Differentiating staphylococcal scalded skin syndrome (SSSS) from toxic epidermal necrolysis (TEN), which carries a much higher mortality, is important. In SSSS, the mucous membranes are spared. In TEN, the mucous membranes are almost always affected (mouth, conjunctiva, trachea, esophagus, anus, vagina).

Consultations

• Pediatrician
• Dermatologist
• Possibly, infectious disease and burn specialists (eg, plastic surgeon)

Medication

Drug therapy for staphylococcal scalded skin syndrome (SSSS) consists of parenteral antibiotics to cover S aureus, which is considered the primary source of the toxin-mediated syndrome.

Topical therapy with agents, such as fusidic acid and/or mupirocin, can be used as adjuncts to parenteral antibiotics, but they should not be used alone in true cases of staphylococcal scalded skin syndrome (SSSS).

Antibiotics

When the susceptibility of the organism is not yet known, the DOC is a penicillinase-resistant synthetic penicillin (eg, nafcillin). However, should the organism show susceptibility to penicillin G, then that drug should be chosen as the main course of therapy. A first-generation cephalosporin can be used as an alternative. In penicillin-allergic patients, macrolides or aminoglycosides may be substituted. Increasing rates of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) associated infections warrants consideration for vancomycin therapy in patients who initially appear toxic or who fail to respond to nafcillin.

Sulfamethoxazole and trimethoprim (Bactrim, Bactrim DS, Cotrim, Cotrim DS, Septra, Septra DS)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Dosing

Adult

8-10 mg/kg/d IV divided q6-12h

Pediatric

<2 years: Do not administer
>2 years: 8-10 mg/kg/d IV divided q6-12h

Interactions

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Contraindications

Documented hypersensitivity; megaloblastic anemia due to folate deficiency; age <2 mo

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use during last trimester of pregnancy due to potential toxicity to newborn (eg, jaundice, hemolytic anemia, kernicterus)
Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: Recommended IV dose q18h
CrCl 50-10: Recommended IV dose q24h
CrCl <10: Not recommended
HD: 4-5 mg/kg after HD
During peritoneal dialysis: 0.16-0.8 g q48h
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholics, elderly persons, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in G-6-PD deficient individuals; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation

Nafcillin (Nafcil, Unipen)

Treats infections caused by penicillinase-producing staphylococci, and thus is DOC for penicillin G-resistant staphylococcal infections. Do not use for treatment of penicillin G-susceptible staphylococci. Use parenteral therapy initially in severe infections, using very high doses for very severe infections.

Dosing

Adult

Parenteral: 500 mg IV/IM q4-6h
Severe infections: 1 g IV/IM q4h
Oral: 250-500 mg PO q4-6h
Severe infections: 1 g PO q4-6h

Pediatric

0-4 kg (neonates): 10 mg/kg IM or 10 mg/kg PO tid/qid; if inadequate, change to parenteral nafcillin sodium
4-40 kg: 25 mg/kg IM bid; alternatively, 100-200 mg/kg/d IV/IM in 4-6 divided doses
Oral: 50 mg/kg/d PO divided qid

Interactions

Associated with warfarin resistance; bacteriostatic action of tetracycline derivatives may decrease effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

To optimize therapy, determine causative organisms and susceptibility; treat for >10 d to eliminate infection and prevent sequelae (eg, endocarditis, rheumatic fever); take cultures after treatment to confirm that infection is eradicated

Penicillin G procaine (Crysticillin, Wycillin)

Long-acting parenteral penicillin (IM only) indicated in treatment of moderately severe infections caused by penicillin G-sensitive microorganisms. Useful in treatment of moderately severe infections of skin and skin structures. In adults, administer by deep IM injection only into upper, outer quadrant of buttock. In infants and small children, midlateral aspect of thigh may be better site for administration.

Dosing

Adult

600,000-1 million U/d IM

Pediatric

<30 kg: 300,000 U/d IM
>30 kg: Administer as in adults

Interactions

Warfarin increases risk of bleeding; ethacrynic acid, aspirin, indomethacin, and furosemide may compete with penicillin G for renal tubular secretion, increasing penicillin serum concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Never use IV route to administer penicillin G procaine; administer >10 d to eliminate organism and prevent complications such as endocarditis and rheumatic fever; perform cultures after treatment to confirm pathogen eradication

Amoxicillin and clavulanate (Clavulin, Augmentin)

Drug combination that extends antibiotic spectrum of this penicillin to include bacteria normally resistant to beta-lactam antibiotics. Indicated for skin and skin-structure infections caused by beta-lactamase-producing strains of S aureus. In children >3 mo, base dose on amoxicillin content. Because of different amoxicillin-to-clavulanic acid ratios in 250-mg tablets (250/125) vs 250-mg chewable tablets (250/62.5), do not use 250-mg tablet until child weighs >40 kg.

Dosing

Adult

500 mg PO q12h or 250 mg PO q8h

Pediatric

<3 months: 125 mg/5 mL PO susp based on amoxicillin; 30 mg/kg/d divided bid
>3 months: if using 200 mg/5 mL or 400 mg/5 mL susp, 45 mg/kg/d PO q12h; if using 125 mg/5 mL or 250 mg/5 mL susp, 40 mg/kg/d PO q8h
>40 kg: Administer as in adults

Interactions

Warfarin or heparin increases risk of bleeding

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Give for minimum of 10 d to eliminate organism and prevent sequelae (endocarditis, rheumatic fever); following treatment, perform cultures to confirm eradication of pathogen

Cefazolin (Ancef, Kefzol, and Zolicef)

First-generation semisynthetic cephalosporin, which, by binding to one or more penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial growth. Primarily active against skin flora, including S aureus. Typically used alone for skin and skin-structure coverage. Total daily dosages are same for IV/IM routes.

Dosing

Adult

250 mg to 2 g IV/IM q6-12h, depending on severity of infection; not to exceed 12 g/d

Pediatric

25-100 mg/kg/d IV/IM divided q6-8h, depending on severity of infection; not to exceed 6 g/d

Interactions

Probenecid prolongs effect; aminoglycosides may increase renal toxicity; may yield false-positive urine dip test for glucose

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy

Cephalexin (Keflex, Biocef)

First-generation cephalosporin that inhibits bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal and effective against rapidly growing organisms forming cell walls. Primarily active against skin flora. Typically used for skin-structure coverage and as prophylaxis in minor procedures.

Dosing

Adult

250-1000 mg PO q6h; not to exceed 4 g/d

Pediatric

25-50 mg/kg/d PO q6h; not to exceed 3 g/d

Interactions

Aminoglycosides increase nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment

Clindamycin (Cleocin)

Lincosamide useful as treatment against serious skin and soft-tissue infections caused by most staphylococci strains. Inhibits bacterial protein synthesis by inhibiting peptide chain initiation at bacterial ribosome, where it binds preferentially to 50S ribosomal subunit, inhibiting bacterial growth.

Dosing

Adult

600-1200 mg/d IV divided q6-8h, depending on degree of infection

Pediatric

8-16 mg/kg/d IV divided tid/qid
Severe infections: May increase dose to 16-20 mg/kg/d IV divided tid/qid

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Contraindications

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

Gentamicin (Garamycin, Gentacidin)

Aminoglycoside antibiotic used for gram-negative bacterial coverage. Commonly used in combination with both agent against gram-positive organisms and one that covers anaerobes.
Not antibiotic of first choice. Consider using only if penicillins or other less toxic drugs are contraindicated, when bacterial susceptibility tests and clinical judgment indicate its use, and in mixed infections caused by susceptible strains of staphylococci and gram-negative organisms.
Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution, as well as body space into which agent needs to distribute. Dose of gentamicin may be given IV/IM. Each regimen must be followed by at least trough level drawn on third or fourth dose, 0.5 h before dosing; may draw peak level 0.5 h after 30-min infusion.

Dosing

Adult

Serious infections and normal renal function: 3 mg/kg/d IV q8h
Extended-dosing regimen for life-threatening infections: 5 mg/kg/24 h IV q6-8h
Loading dose: 1-2.5 mg/kg IV q8h
Maintenance dose: 1-1.5 mg/kg IV q8h

Pediatric

<5 years with normal renal function: 2.5 mg/kg/dose IV/IM q8h
>5 years: 1.5-2.5 mg/kg/dose IV q8h or 6-7.5 mg/kg/d IV divided q8h; not to exceed 300 mg/24 h

Interactions

Other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus prolonged respiratory depression may occur; loop diuretics may increase auditory toxicity—possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Contraindications

Documented hypersensitivity; non-dialysis–dependent renal insufficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment

Tobramycin (Nebcin)

Used in skin, bone, and skin-structure infections caused by S aureus, Pseudomonas aeruginosa, Proteus species, Escherichia coli, Klebsiella species, and Enterobacter species. Indicated in serious staphylococcal infections when penicillin or other potentially less toxic drugs contraindicated and when bacterial susceptibility testing and clinical judgment indicate use. To prevent increased toxicity caused by excessive blood levels do not exceed 5 mg/kg/d, unless serum levels monitored.

Dosing

Adult

Serious infection: 3 mg/kg/d IV/IM divided tid
Life-threatening infection: Up to 5 mg/kg/d IV/IM divided tid/qid; reduce to 3 mg/kg/d as soon as clinically indicated

Pediatric

6-7.5 mg/kg/d IV/IM divided tid/qid (2-2.5 mg/kg q8h or 1.5-1.9 mg/kg q6h)

Interactions

Increases effects of neuromuscular blockers and potentiates effect of extended-spectrum penicillins; amphotericin B, cephalosporins, and loop diuretics increase risk of nephrotoxicity

Contraindications

Documented hypersensitivity; renal impairment; preexisting auditory or vestibular impairment; neuromuscular disorders

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Avoid in renal impairment, preexisting auditory or vestibular impairment, and neuromuscular disorders; associated with nephrotoxicity and ototoxicity

Erythromycin (E-mycin, Ery-Tab, Erythrocin)

Indicated for treatment of infections caused by susceptible strains including S aureus. Inhibits RNA-dependent protein synthesis, possibly by stimulating dissociation of peptidyl t-RNA from ribosomes. This inhibits bacterial growth.
Age, weight, and severity of infection determine proper dosage. When bid dosing desired, half of total daily dose may be taken q12h. For more severe infections, double dose.

Dosing

Adult

250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) PO q6h 1 h ac, or 500 mg PO q12h; alternatively, 333 mg PO q8h; increase up to 4 g/d

Pediatric

30-50 mg/kg/d (15-25 mg/lb/d) PO in divided doses

Interactions

May increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; lovastatin and simvastatin increase risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Vancomycin (Vancocin)

Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci. To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use creatinine clearance to adjust dose in patients diagnosed with renal impairment.
Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures.

Dosing

Adult

1 g or 15 mg/kg IV q12h

Pediatric

30-40 mg/kg/d IV in 2 doses

Interactions

Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal failure, neutropenia; red man syndrome is caused by too rapid IV infusion (dose given over a few min) but rarely happens when dose given IV over 2-h administration or as PO or IP administration; red man syndrome is not an allergic reaction

Follow-up

Further Inpatient Care

• Further inpatient care for patients with staphylococcal scalded skin syndrome (SSSS) involves fluid rehydration, local burn/wound care, and eradication of the underlying infection.

Transfer

• Patients with severe disease may require ICU or burn unit care.

Deterrence/Prevention

• Avoidance of the primary staphylococcal infection that may lead to the toxic syndrome
• Timely treatment of established staphylococcal infections
• Identification and treatment of asymptomatic carriers

Complications

Complications of staphylococcal scalded skin syndrome may include the following:

• Dehydration
• Shock
• Hypothermia
• Generalized bacteremia and/or sepsis
• Local or remote spread of infection
• Secondary infections
• Scarring, disability, and death

Prognosis

• Prognosis of staphylococcal scalded skin syndrome (SSSS) in children is excellent, with complete healing typically occurring in 10 days without significant scarring.
• Prognosis of staphylococcal scalded skin syndrome in adults depends on the host's immune status, the speed in initiating proper treatment, the course of the infection, and the occurrence of complications. Staphylococcal scalded skin syndrome in adults carries significant rates of morbidity and mortality.

Miscellaneous

Medicolegal Pitfalls

• Differentiating between staphylococcal scalded skin syndrome (SSSS) and more dangerous dermatologic conditions, such as toxic epidermal necrolysis (TEN) and pemphigus in the early stages of disease, can be difficult. Care should be taken to establish the correct diagnosis and as well to have a low threshold for specialty consultation as well as ICU and/or burn unit care. 
• In outbreaks of staphylococcal infections and staphylococcal scalded skin syndrome (SSSS), identifying and treating asymptomatic carriers is imperative. Universal precautions should be used at all times.

Multimedia

Media file 1: Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

Media file 2: Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

Media file 3: Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

Media file 4: Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

Media file 5: Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

Media file 6: Staphylococcal scalded skin syndrome. Photograph by David Effron, MD, FACEP.

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Keywords

staphylococcal scalded skin syndrome, SSSS, blistering skin, Ritter von Ritterschein disease, Ritter disease, Ritter’s disease, Lyell disease, Lyell’s disease, skin disease, skin condition, treatment, symptoms, causes, exfoliative toxins, toxin-mediated syndrome, staphylococcal epidermal necrolysis, acute exfoliation of the skin, staphylococcal infection, erythematous cellulitis, phage group 2 Staphylococcus aureus, S aureus, epidermolytic toxins

Contributor Information and Disclosures

Author

Randall W King, MD, Assistant Clinical Professor of Emergency Medicine, The University of Toledo College of Medicine; Program Director Emergency Medicine Residency, Associate Chair, Department of Emergency Medicine, St Vincent Mercy Medical Center
Randall W King, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Ohio State Medical Association, and Society for Academic Emergency Medicine
Disclosure: Challenger corporation None Other

Coauthor(s)

Paul R de Saint Victor, MD, FACEP, Chief of Staff, St Vincent Mercy Medical Center, Toledo
Paul R de Saint Victor, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Heart Association, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Associate Professor, Department of Emergency Medicine, University of Texas-Houston
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor

Jeter (Jay) Pritchard Taylor III, MD, Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist
Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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The authors and editors of eMedicine gratefully acknowledge the medical review of this article by Joseph U Becker, MD.

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