Toxic shock syndrome differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Toxic shock syndrome may have a similar presentation to some diseases which present as a rash, fever and hypotension. Some features are unique to toxic shock syndrome and can be used to differentiate it from other diseases.

Differentiating Toxic Shock Syndrome from other Diseases

Toxic shock syndrome requires all 3 manifestations of fever, hypotension and diffuse scarlatiniform rash (innumerable small red papules that are diffusely distributed plus erythema, which blanches and desquamates one or two weeks after onset of illness). It presents with various signs of infection, hemodynamic dysfunction and organ failure.

Clinical presentation of sepsis and rash needs to be differentiated from other diseases like:

• Gram-negative sepsis
• Scarlet fever

• Viral exanthem
• Rickettsial disease
• Kawasaki disease

• Staphylococcal scalded skin syndrome
• Exfoliative erythroderma syndrome
• Erythema multiforme major
• Drug eruption

Disease	Epidemiology	Predisposing factors	Clinical features		Lab abnormalities
			Signs	Symptoms
Toxic shock syndrome	Occurs in both adults and children (9:1 female predominance)	Occurs in association with vaginitis during menstruation following tampon use (S. aureus); as a complication of soft tissue infections (S. pyogenes or GAS) or in females undergoing medical abortion (C. sordellii).	Hypotension, tachycardia, mucous membrane hyperemia (vaginal, oral, conjunctival)	Fever, diarrhea, vomiting, diffuse scarlantiform rash	Hyponatremia and uremia. Hepatic dysfunction (total bilirubin, serum asparate aminotransferase or serum alanine aminotransferase levels >2 times upper normal limit), leukocytosis with a polymorphonuclear shift to the left. Platelets < 100,000 per mm3 (thrombocytopenia), pyuria of renal origin.
Kawasaki disease	Occurs in children, usually age 1-4 years	Interaction of genetic and environmental factors, possibly including an infection in combination with genetic predisposition to an autoimmune mechanism (autoimmune vasculitis)	Non-suppurative, painless bilateral conjunctival inflammation (conjunctivitis), strawberry tongue (marked redness with prominent gustative papillae), deep transverse grooves across the nails may develop (Beau’s lines), lymphadenopathy present(acute, non-purulent, cervical), may lead to coronary artery aneurysms.	High and persistent fever that is not very responsive to normal treatment with acetaminophen or NSAIDs,  diffuse macular-papular erythematous rash	Liver function tests may show evidence of hepatic inflammation and low serum albumin levels, low hemoglobulin and age-adjusted hemoglobulin concentrations, thrombocytosis, anemia. Echocardiographic abnormalities, such as valvulitis (mitral or tricuspid regurgitation) and coronary artery lesions, are significantly more common in Kawasaki disease. Pyuria of uretheral origin.
Scarlet fever	Distributed equally among both genders. Most commonly affects children between five and fifteen years of age.	Occurs after streptococcal pharyngitis/tonsillitis	Pastia's sign (puncta and skin crease accentuation of the erythema), strawberry tongue, cervical lymphadenopathy may be present. Scarlet fever appears similar to Kawasaki's disease in some aspects, but lacks the eye signs or the swollen, red fingers and toes	Characteristic sandpaper-like rash which appears days after the illness begins (although the rash can appear before illness or up to 7 days later), rash may first appear on the neck, underarm, and groin	Leukocytosis with left shift and possibly eosinophilia a few weeks after convalescence. Anti-deoxyribonuclease B, antistreptolysin-O titers (antibodies to streptococcal extracellular products), antihyaluronidase, and antifibrinolysin may be positive.

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