Dermal Changes

Clinically rashes that have a dermal pathology usually are found in the CUL DVA EVIE mnemonic. (See you later at the Dept of Veterans Affairs EVIE where Evie is your girlfriend.)

Histopathologically dermal patterns are due to

1. Infiltrates of cells or substances

2.  Excess or reduction in collagen or elastin

3. Proliferation of nevus cell benign or malignant ,

4. Hair follicle, Apocrine or eccrine gland proliferations,

5.Nerves, lymphatics or blood vessel proliferations

6. Granulomas

7. Perivascular lymphocytic cuffing

8. Vessel damage (Vasculitis)

9. Basal layer infiltrates either Lichenoid or Interface type

When we look at dermal diseases we are looking at anything that is involving the dermal epidermal junction and below as far as the fat layer.   Classically the reaction patterns have then be divided into those that involve a band like infiltrate at the dermal epidermal junction, which is known as a lichenoid infiltrate, those that have more sparse infiltrate but primarily damage to the cells of the dermal epidermal junction, which is then called interface damage and those that have collections of cells in the actual dermis itself.  These cells can be eosinophils, neutrophils, lymphocytes, melanocytes or nevus cells and rarely cells from metastatic disease. 

You can get granulomas occurring and you can obviously get tumours in the dermis where you get hyperproliferation of other tissue cells that are there.  These can be tumours of fibroblasts, nerve or muscle cells and also those derived from hair follicles or eccrine and apocrine glands. 
Most of the pathologies that involve the dermis will give red, non-scaly lesions or skin coloured non-scaly lesions and the fact that they are non-scaly indicates that the epidermis isn't going to be involved. So, if you see that most of the pathology is in the dermis then consider that the clinical morphology is going to be a non-scaly either red or skin coloured lesion. We will show you examples of that when we look at conditions such as granuloma annulare or even some of the atypical mycobacteria or deep fungal infections.  Remember though that sometimes dermal processes can perforate the epidermis.  They can go up through the epidermis as the body tries to get rid of the abnormal tissue.  In those circumstances there will be epidermal involvement and this certainly has to be considered when a predominantly dermal process has an epidermal component as well.

CUL DVA EVIE

Clinically cellulitis presents as a hot red tender spreading plaque on the skin, particularly in the lower legs near the ankles, but it can also occur on the face and other parts of the body.  It is generally due to a staph or strep infection.  There isn't any epidermal involvement and so you would not expect any histological changes there.  What you see histologically is oedema in the dermis and numerous leucocytes interspersed between the collagen bundles in the oedema fluid.  Sometimes the heavy infiltrate of leucocytes will extend deeply even to the septal layer of the fat and give rise to a septal panniculitis.  In the more superficial variant of cellulitis called erysipelas you histologically can see quite a bit of sub epidermal oedema and even a threatening bullous eruption depending on the degree of oedema with a heavy infiltrate of neutrophils.

In urticaria the skin is also red and may be hot but is usually not painful.  It is usually described as being itchy.  It does feel plaque like but histologically this time as well as fluid in between the collagen bundles the cellular infiltrate is mainly eosinophilic.  There are usually also dilated blood vessels and lymphatics associated with this dermal oedema.  The infiltrate of cells isn't as great as an infected process and a large proportion of them are eosinophils, though there may be some neutrophils as well.

 Papular urticaria is a different condition.  Whereas common urticaria is IgE mediated, papular urticaria is generally a Type 4 hypersensitivity reaction to insect bites, particularly fleas and the lesions will arise some hours after the bite reaction. 
Histologically in these circumstances there is both a superficial and deep infiltrate and the infiltrate is of mainly lymphocytes and some eosinophils. Histologically it often has a wedge shaped arrangement.  A similar histological picture may be seen in the pre-bullous phase of bullous pemphigoid which appears to be a dermal hypersensitivity reaction with dermal oedema and eosinophils.  Rarely in early bullous pemphigoid just before the bullae erupt you may see some eosinophilic spongiosis where there is some epidermal involvement, but it is only when an autoimmune attack occurs at the dermoepidermal junction that you get the blisters superimposed on this background of dermal oedema and eosinophils.

The next letter of the mnemonic is L standing for lupus or for polymorphous light eruption.  Now, in these circumstances the damage is going to be at the dermal/epidermal junction with vacuolar damage and some of that damage will extend down the hair follicles.  This is typical in lupus and often you will get some plugging of the hair follicles as well and this is reflected in the carpet tack sign when you remove the scale from the surface of a lesion of lupus.

Lupus also comes up as one of the red scaly diseases, in fact discoid lupus is very scaly, but here we are looking at it under the heading of red non-scaly diseases and so most of the disease process is taking place not in the epidermis but in fact at the dermal/epidermal junction and in the dermis itself.  There is a variant called tumid lupus, particularly affecting the face and upper trunk and this is similar to the histopathology of discoid lupus with vacuolar damage at the dermal/epidermal junction, but there is also a lot of mucin in the dermis and there may be some subepidermal oedema, so there is no real surface scale changes in this variant of lupus.  Jessner's lymphocytic infiltrate looks very similar histopathologically to this condition although the morphology of the lesion is more florid than you see in tumid lupus.  In subacute cutaneous lupus, again the damage is at the dermal/epidermal junction with vacuolar change but this can be more marked in subacute lupus.  There is also a degree of epidermal atrophy, again dermal oedema and mucin and much less of the keratotic epidermal changes that you see in discoid lupus.  There is also a thickening of the basement membrane.  In subacute lupus you may get positive immunofluorescence as well.  Remember that subacute lupus can be due to a variety of drugs as well.  In systemic lupus clinically we see the patient who has a marked erythema, particularly a malar erythema often without much in the way of overlying keratotic changes in the epidermis and histologically this is reflected in the prominent basal layer damage that is occurring.  There may again be dermal oedema and mucin and here you get a lot more damage to blood vessels in the upper parts of the dermis with fibrin deposition in the vessel walls.  As with subacute lupus there is often marked thickening of the basement membrane itself.  Neonatal lupus if you are looking at the biopsy is very similar to subacute lupus.

When you think of lupus in these red non-scaly diseases you also have to consider some of the other collagen disorders such as the dermatomyositis and even scleroderma although morphologically they can look different.  Dermatomyositis can clinically look like lupus and the histopathology also reflects this.  There is the same basement membrane thickening and vacuolar changes at the basement membrane but usually it is only a superficial perivascular infiltrate.  It is not superficial and deep as you tend to get in lupus. You can also get oedema and mucin and a degree of epidermal atrophy and that is reflected later on in the   clinical changes that you will see in dermatomyositis, (poikiloderma) so it can be very difficult histologically to separate dermatomyositis and lupus and in point of fact it is often easier clinically!