Skin rash is a common reason why patients visit or consult with a health care practitioner. However, many skin rashes are self-limiting, i.e. Self-limiting rashes subsequently disappear without treatment within two (2) weeks.
There are several principle morphological components of the skin that one may evaluate when considering rashes and other lesions of the skin. They include: 1) Epidermis; 2) Papillary dermis; 3) Reticular dermis; and 4) Subcutis, or subcutaneous fatty tissue. One may readily define each of these components through referencing a basic, general Anatomy and Physiology textbook.
When examining skin tissue under a light microscope, the principle goal is to define the normal histological pattern of skin, and this is based on where the skin is located on the body. The normal histological pattern is assessed primarily to exclude benign and cancerous tumors of the skin, also known as skin neoplasms. Once skin neoplasm has been ruled out by examining the skin under a light microscope, the second step is to consider reactive or inflammatory lesions of the skin also known as skin rashes or dermatitides, and thus, the topic for this discussion.
Reactive or Inflammatory Skin Diseases can be subdivided into acute, sub-acute, and chronic dermatitides, and this categorization of skin inflammatory diseases is based on changes in the epidermis, dermis, and subcutis. Often times, acute inflammatory skin diseases as related to allergy for instance, will disappear within days after contact with allergen or other toxins have been removed; or after appropriate treatment with antiviral, antibacterial, antifungal, etc., medications for another example; or still yet after resolving an acute vascular insult as still another example. Sub-acute and chronic dermatitides generally last longer, and often require expert evaluation by a dermatologist for further therapeutic and prognostic management, generally after a skin biopsy and histological diagnosis have been rendered by a pathologist.
Evaluating the Epidermis:
An acute and/or subacute insult of the epidermis may demonstrate a range of changes from as mild as intracellular edema, also known as spongiosis to as severe as evidence of dead (necrotic) epidermal cells and ulceration (disruption or absence of) lining epithelial cells.
A chronic or long lasting (greater than three months) insult of the epidermis may show similar changes as to the above, in addition to reactive overgrowth also known as hyperplasia (given the two classifications: pseudoepitheliomatous hyperplasia and psoriasiform hyperplasia). The pattern of keratin (hyperkeratosis) may accompany overgrowth of the epidermis, or the presence of parakeratosis may give evidence for rapid or continuous keratin turnover as with pruritus or chronic itching/scratching. Degenerative changes of the basal cells (vacuolar ‘bubbly’ degenerative changes) may also define the dermatitides. Vesicles or bullae may be seen in both acute and chronic dermatitides and the pattern of the bullae, i.e. intra-epidermal and subepidermal, may shed light on specific types of rashes that often times require even specialized studies such as immunohistochemistry to define abnormal autoantibody complexes. The pattern of Intra-epithelial inflammatory cells found within the epidermis and adnexa (sweat glands, sebaceous glands, hair follicules, etc) may also shed light on specific diagnosis of acute and chronic dermatitides. And, finally, specific pathogens such as viruses (viral cytopathic effect, as with Herpetic or Zoster viruses, for example), or Fungi (candida, dermatophytes, etc), or bacteria such as staphylococcus for example, may also be demonstrated as the etiology of the rash.
Evaluating the Dermis:
The inflammatory pattern is one of the most important features when defining rashes, as well as the specific types of inflammatory cells that are present within the dermis. Six (6) patterns are commonly evaluated which include: 1) superficial and/or deep perivascular inflammatory infiltrate with or without eosinophils or mast cells; 2) Superficial and deep perivascular inflammatory infiltrate comprised predominantly of lymphocytes and plasma cells with or without a periadnexal component; 3) Diffuse, mixed inflammatory infiltrate of dermis and/or subcutis; 4) Lichenoid or interface (a linear pattern of inflammation at the junction between the epidermis and dermis);5) Bullous inflammatory infiltrate, and 6) Fibrinoid necrosis (evidence of dead endothelial cells involving cells which line blood vessels) and clots within small blood vessels. Granulomatous inflammatory infiltrate is a specific pattern that may be attributed to deep fungal infection or mycobacterial infection, etc, of the skin or Non-infectious granulomatous infiltrate as seen in sarcoidosis.
Examples of Descriptive Inflammatory Diseases of Skin ( Dermatitides):
Most common, acute rash: Urticarial Reaction; Sub-acute Spongiotic Dermatitis (includes allergy, contact dermatitis, other self-limiting dermatitis); etc:
-Spongiosis with superficial patchy perivascular lymphoplasmacytic and histiocytic inflammatory cell infiltrate with eosinophils and/or mast cells
Acute/Sub-acute rash: Arthropod/Insect Bite; Scabies, fixed drug-eruption, etc
-Spongiosis with superficial and deep lymphoplasmacytic and histiocytic inflammatory cell infiltrate with or without eosinophils.
Chronic rash: psoriasiform dermatitis (requires clinical correlation), includes: Psoriasis (various forms), Neurodermatitis, Superficial fungal infection, etc:
-pseudoepitheliomatous hyperplasia/psoriasiform hyperplasia, plus or minus intraepithelial inflammatory cell infiltrate, with superficial and deep lymphoplasmacytic and histiocytic inflammatory cell infiltrate WITHOUT eosiniphils and/or mast cells
Chronic rash: Lichenoid dermatitis (requires clinical correlation), includes: Lichen Planus, Discoid Lupus, Drug-eruption, etc.:
– Linear, Interface inflammatory lymphoplasmacytic and histiocytic inflammatory cell infiltrate, vacuolar degeneration, with or without superficial and deep lymphoplasmacytic and histiocytic perivascular inflammatory cell infiltrate and/or lymphocytic periadnexal inflammatory cell infiltrate.
The above are just some examples, but there are many other inflammatory dermatitides, including rare and special types such as deep fungal infection, parasitic infection, Herpetic dermatitis, Lyme disease, Sweet’s syndrome, Bullous Dermatitis, Erythema Nodosum, Toxic Epidermal Necrolysis (TEN), etc.
Evaluating the Subcutis:
This is typically a limited evaluation looking for specific diseases related to causes of septal and diffuse panniculitis which tend to be systemic as related to calcium metabolic deposits (saponification), pancreatic and/or kidney diseases for example.
In short, defining rashes can be routine for the general health-care pracitioner. AND, using the above diagnostic evaluation profiles by the laboratory medicine specialist can define many different types of acute, sub-acute and/or chronic rashes (dermatitides). Patients in general can save on health care cost for common rashes by going to visit a general practitioner/laboratory medicine specialist like Dr. Gates prior to consulting with a dermatologist.
Most acute rashes will be self-limiting and typically resolve without therapy once the allergen or toxin has been removed. But in general, most inflammatory dermatitides (skin rashes) can be resolved through corticosteroids, antihistamines, antimicrobials, or other topical and/or systemic chemotherapy agents as predicated by the specific etiology of the rash.
We at MDC-Atlanta remain committed to keeping patients informed for better quality and safe medical care.