Septic vasculitisI77.6

Author:Prof. Dr. med. Peter Altmeyer

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Last updated on: 24.08.2022

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Synonym(s)

Septic vasculitis, septic vasculitis; Vasculitis and sepsis; Vasculitis in sepsis

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DefinitionThis section has been translated automatically.

Rare skin symptoms in sepsis caused mainly by meningococcus, gonococcus and Pseudomonas aeroginosa, either by haematogenic pathogen seeding or infectious-allergic or toxic (bacterial toxins) etiology. Mostly occurs in immunocompromised patients.

PathogenThis section has been translated automatically.

Gonococci, meningococci, streptococci in the setting of endocarditis lenta, pseudomonads.

EtiopathogenesisThis section has been translated automatically.

Bacterial decomposition products (endotoxins, superantigens) or released mediators cause fatal damage to the vessel wall with unphysiological activation of the coagulation system (disseminated intravascular coagulation; consumption coagulopathy).

ManifestationThis section has been translated automatically.

Occurs in young adults of both sexes.

LocalizationThis section has been translated automatically.

Predominantly acral lesions.

Clinical featuresThis section has been translated automatically.

Usually accompanied by life-threatening, severe general symptoms (high fever, somnolence, drop in blood pressure, tachycardia), shooting up within a few hours, acrally localized, widely spread, 1-2 mm large hemorrhagic spots or papules, more rarely pustules with erythematous margins. Often central necrosis, also splinter hemorrhages.

See below for details. Purpura fulminans, Waterhouse-Friderichsen syndrome, consumption coagulopathy,

S.a. under sepsis, skin lesions.

LaboratoryThis section has been translated automatically.

Signs of consumption coagulopathy, fibrinolysis, thrombosis and bleeding are to be searched for.

Furthermore, determination of fibrin monomers, fibrinopeptide A (indicating intravascular coagulation), D-dimers (reactive hyperfibrinolysis), platelets, fibrinogen and antithrombin (indicating severity of consumption coagulopathy).

HistologyThis section has been translated automatically.

Conspicuous are hyaline thrombi in the lumen of postcapillary venules. Perivascular oedema; erythrocyte extravasations. Moderately dense, superficial, perivascularly stored, inflammatory infiltrate of neutrophil granulocytes, lymphocytes, more rarely plasma cells. The epidermis may show incipient necrosis. Bacterial clusters in the vascular lumens are rarely detectable. The exudation can be so strong that subepidermal blistering can occur.

Differential diagnosisThis section has been translated automatically.

Leucocytoclastic vasculitis; vasculitis with essential cryoglobulinemia; disseminated intravascular coagulopathy (see coagulopathies below).

TherapyThis section has been translated automatically.

Immediate intensive care: treatment of septic shock and consumer coagulopathy.

Progression/forecastThis section has been translated automatically.

Very serious. Fatal course is possible within hours (multiorgan failure). Chronic recurrent courses, in which the described severe general symptoms are missing, are described.

Note(s)This section has been translated automatically.

In case of foudroyantly developing large-area purpura with rapidly deteriorating AZ, sepsis must be considered.

LiteratureThis section has been translated automatically.

  1. Sundkötter C et al (2004) Leucocytoclastic vasculitis. Dermatologist 55: 759-783
  2. Tomasini C (2015) Septic vasculitis and vasculopathy in some infectious emergencies: theperspective
    of the histopathologist. G Ital Dermatol Venereol 150:73-85.

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Last updated on: 24.08.2022