Chemical, toxic and physical dermatoses

12 Chemical, toxic and physical dermatoses

Skin trauma can be primary (caused by direct physical insult, chemical applications) or secondary when the insult itself would normally have no material effect. The damage is a combined result of an insult and a predisposing pathology. Primary injury can be a result of obvious traumatic damage, or application of or accidental contact with damaging/caustic chemicals. Perhaps the best example of secondary damage is the photosensitization that is a result of liver failure and the ingestion of photodynamic plants. Without the sunlight exposure the damage would not occur even though the underlying pathology/toxin is present.

Chemical and toxic dermatoses are rare in horses but arise from systemic poisoning or from direct application of toxic chemicals to the skin. The occurrence of systemic toxicity is singularly rare but recognition of the disorders is important if only because of the strong tendency that owners have to blame some form of ‘outward’ interference in the health of the horse.

The disorders that result from some external application or in particular circumstances when the toxicity is either driven by some external factor such as sunlight or is exacerbated by management procedures are more common.

Owners may not readily appreciate the risks of plant or chemical poisonings or may be inclined to blame agents that in fact have no material implication. Where poisonings are suspected the clinician really needs to be very careful before making a confirming statement.

Traumatic damage to the skin also occurs from direct injuries and there are some important dermatological states that have a physical aetiology. Some of these such as burns and scalds have obvious causes but their management is a dermatological concern. However, it is important to realize that skin wound healing is a dermatological matter in the final analysis. Many of the problems faced in wound healing are surmountable if the clinician has a detailed knowledge of the structure and function of skin.

Chemical trauma

Profile

History of application of ‘pour-on’ or topical medications such as antiseptics, insecticides or fungicides (or other materials) is usually obtained. Application of over-strength medication or of normal-strength medication on an oversensitive skin is a common feature. Application of blisters, counterirritants and vesicants is a common iatrogenic cause of this response, where it is regarded as a good therapeutic effect (see Fig. 12.12). Prolonged skin contact with surgical spirit or other chemicals may arise during general anaesthesia (recumbency) and can cause serious problems which are actually ‘chemical burns’. Historically, old/used engine oil has been used to treat lice and insect bite (Culicoides) hypersensitivity (sweet itch) and this can cause extensive and severe damage to skin and has serious potential systemic toxicity.

Key points: Chemical trauma

1. Common result of inappropriate applications of chemicals to the skin. Mistakes made with calculating concentrations of chemicals or application of misguided ‘cures’. Damage can be severe and is often permanent.

2. Exudative or necrotizing dermatitis following known (or suspected) applications of skin chemicals. Usually lesions are confined to the area of application but systemic effects can be induced. Ingestion by licking of the damaged skin can result in oral ‘burns’ , oesophageal ulceration or necrosis and gastrointestinal damage. Strong chemicals such as arsenicals and oils can cause skin necrosis and severe systemic effects.

3. Diagnosis may be more difficult than it seems because many owners will not readily admit to having caused the damage. Histology is sometimes helpful

4. Treatment depends on removing the chemical as soon as possible using suitable solvents and washes without further skin injury and application of wound management procedures. Systemic effects will require more supportive management.

5. The prognosis is variable depending on the type and extent of the damage and the implications for the anatomical region. Many cases have persistent problems with hyperaesthesia and recurrent infections.

Exposure to inappropriate washing materials such as detergent washing powders, bleach and other materials can leave a serious long-term skin change. Often the consequences are detected some weeks after the exposure.

Acute cases show marked moist, exudative dermatitis with matting of hair (Fig. 12.1). Extensive generalized dermatitis such as is caused by application of engine oil causes severe hair loss and a fragile skin which is easily traumatized. Hair loss (Fig. 12.2) and sometimes even open wounds are common consequences.

Figure 12.1 Accidental chemical burn causing matting and exudation of the skin.

Figure 12.2 Extensive hair loss and generalized dermatitis arising from the ill-advised application of hot engine oil in a misguided attempt to treat louse infestation.

Chronic or mild recurrent skin insult causes fine to coarse scaling and (temporary) loss of hair (alopecia) over the affected area, often well demarcated over the area of application (e.g. following therapeutic blisters).

Alopecia, pigmentary changes and overt scarring are often induced when deeper damage has been caused by prolonged contact with chemical substances. Pruritus and self-inflicted trauma may be marked. Longer-term effects include skin thickening with lichenification and rugae formation.

Focal application of strong chemicals, focal burns or physical cautery to the skin may result in a dense, coagulated slough (eschar) which may remain in situ for prolonged periods (a ‘sitfast’) (Fig. 12.3) and inevitably leaves a scar.

Figure 12.3 Application of a strong arsenic powder caused cutaneous coagulative necrosis. The large eschar sloughed slowly, leaving a large cicatrized scar.

The long-term results of chemical damage to the skin can be marked. Inappropriate washing materials such as detergent powders and engine cleaners, etc. can cause an immediate problem, of course, but the long-term damage to the skin is often much more important. Skin pain, sensitivity to sunlight, or even inflammatory damage from basic grooming are all possible (Fig. CD12 • 1A–E). Affected horses usually have varying periods when they are better and worse but may never be normal again.

Skin scalding (diarrhoea/urine or wound exudate)

Profile

The skin does not tolerate persistent soaking in body fluids such as urine, milk, plasma, serum, lacrimal secretions, synovial fluid or saliva. These body fluids and prolonged or irritant diarrhoea can lead to marked hair matting, scalding and hair loss in the affected skin. These conditions are therefore usually secondary to other pathological disorders. Secondary infections are common.

Wound fluids (whether infected or not) may cause serious excoriation and loss of hair.

Diarrhoea in foals causes severe perineal dermatitis – the prolonged exposure of the dermis to infective agents can lead to significant infection but this is remarkably rare. In adult horses with diarrhoea or those subjected to repeated rectal examinations the perineal region can become tender and mildly inflamed. Often this passes unnoticed.

Urine scalding can occur quickly depending on whether the flow is intermittent/splashing or soaking. Geldings with neurogenic urinary tract disorders including fractures of the sacrum, polyneuritis equi (cauda equina syndrome) or poliomyeloencephalopathy (such as occurs in the neurogenic form of equine herpesvirus infection) and those with idiopathic bladder paralysis syndrome may persistently drip urine onto the hind legs. Usually this causes severe persistent dermatitis (often with secondary infections) and crystallization on the hair which hair smells strongly of urine. In mares the dermatitis caused by the same group of conditions results in perineal skin damage – usually in an obvious flow pattern from the ventrum commissure of the vulva. Crystallization on the hair indicates chronicity and severity. Milder splashing may cause some localized transient inflammation but seldom extensive dermatitis.

Key points: Cheek abscess

1. The skin does not tolerate persistent bathing in body fluids such as lacrimal secretion, blood, serum/plasma, urine or milk. Diarrhoea also causes skin damage, particularly in foals.

2. Signs are associated with bathing in obvious body fluids. Hair matting commonly occurs first. Mild to moderate dermatitis occurs with hair loss and secondary infection.

3. Diagnosis is usually simple. Urine has a characteristic odour and crystallized calcium carbonate is attached to the hair.

4. Treatment is dependent on stopping the contact between the skin and the fluid either by correcting the cause or by protecting the skin in some way. Initially the skin should be cleansed carefully with minimal extra trauma. Dead hair and skin should be removed and the infection controlled appropriately. Thereafter the area should be protected with emollient and soothing water repellent creams or petroleum jelly to allow healing.

5. The prognosis for the skin is good (provided that the primary cause can be managed) but in long-standing cases there may be some persistent changes in hair coat and skin thickness and flexibility.

One of the most damaging materials for the skin is wound exudate. Blood and fresh plasma are not significant irritants to the skin but wound exudate is. Often this has altered acidity and may be laden with bacteria.

Tear overflow can also cause superficial dermatitis and this is a primary aspect of facial Habronema infection (see p. 217).

Clinical signs

Diarrhoeic animals (particularly foals) may have mild-to-moderate perineal skin inflammation and temporary loss of hair (Fig. 12.4). The cause of the problem is usually obvious and although it can be significant, controlling the primary cause is the most important aspect of this. Repeated rectal examinations also causes some local irritation and inflammation.

Figure 12.4 A Mild early perineal dermal inflammation caused by diarrhoea. B Later on the hair falls out and the bald skin heals eventfully with full hair growth.

Urine scalding usually occurs around caudal area of hind legs of mares or the lower regions of the hind legs in geldings with urinary incontinence (Fig. 12.5). Where urine is responsible an obvious stale, ammoniacal, urinary smell on legs can be detected. Urine and faeces may contain blood and this can be obvious. Skin may be extensively damaged and exudative.

Figure 12.5 Urine scalding dermatitis affecting the dorsal aspects of the hind cannons in a gelding with urinary incontinence. Similar effects are encountered in the perineal region of mares with neurological problems in the bladder and vagina.

Hair matting is more obvious with wound fluids; serum exudate appears to induce a moderate or severe dermatitis and this also seems to encourage the development of skin infections. Secondary Habronema musca infestation can occur with wound exudate or lacrimal secretions on the face (see p. 217).

Differential diagnosis

• Dermatophilosis: characteristic distribution and epidemiology affecting horses in poor conditions and subjected to persistent wetting. D. congolensis can be detected in scrapings and smears of exudate and crust.

• Dermatophytosis: localized crusting and scaling dermatosis with characteristic epidemiology and mycology. Most cases spontaneously resolve or respond rapidly to specific treatment.

• Chemical irritants (e.g. strong iodine/disinfectants, mercurial blister): history of application is usually available; characteristic pattern and anatomic distribution corresponding to applications.

• Allergic dermatitis: exudative and no obvious instigatory factors – signs usually restricted to contact regions.

Diagnostic confirmation

• Almost all cases are secondary to other pathology which is usually obvious. A full history and clinical assessment may establish the primary cause.

• If urinary problems are suspected, examine the entire urinary tract to determine whether retention with overflow or cystic calculi is the primary cause.

• Urinary incontinence can be due to sorghum feed poisoning, cauda equina neuritis, rabies, sacral or spinal fracture or the neurological form of equine herpesvirus 1 (EHV1) infection.

• History of foaling accident, trauma to hindquarters, e.g. rearing over backwards and landing on sacrum or spontaneous sacral fractures in racing horses.

• Primary diarrhoea from any cause (especially in foals).

Treatment

The primary condition should be managed to prevent deterioration but the local effects of skin inflammation and excoriation must also be managed. Early cases with transient primary signs relating to diarrhoea, lacrimation and wound exudate are not usually a major clinical problem; Protective jellies such as petroleum jelly (Vaseline) can be applied to limit the damage. Antiseptic creams such as human baby nappy cream can be very helpful. It is important to wash off all faecal material before applying anything to the skin.

Where treatment of the primary problem is likely to be ineffective, persistent skin care is required, e.g. if there is neurogenic damage or persistent/chronic diarrhoea or wound exudate. The anatomic location of the dermatitis is also an issue. The skin of the distal limb is easily damaged and is liable to infection so this can result in a long-term management problem. Neurological disorders may be permanent and strategies have to be formulated to minimize the secondary consequences. Repeated severe washing with cold water and antiseptic shampoos is not ideal. In some cases repeated washing can in itself be harmful to equine skin. Even surface application of petroleum jelly can eventually be detrimental to skin health.

When the primary cause is controlled, hair and skin return to normal rapidly. If treatment is ineffective, local protectants are helpful, e.g. petroleum jelly or waterproof barrier creams with antiseptic and soothing properties (emollient creams, zinc oxide cream). Corticosteroid and local anaesthetic creams can be helpful but should not be overused in case they impair local cutaneous immunity.

Actinic dermatoses

Profile

Sunlight (and light derived from other sources) in the ultraviolet part of the spectrum combines short, medium and long wavelengths (UVc, UVb and UVa, respectively). Damage can be caused directly by simple actinic exposure (sunburn) or the various wavelengths of light can react with abnormal (exogenous or endogenous) photosensitizing proteins deposited in the skin (Fig. 12.6). The abnormal response in the latter case is usually much more severe. Melanin protects pigmented skin from the damaging effects of ultraviolet light by absorbing and scattering the ultraviolet light and where skin has little or no melanin the cells can be significantly damaged. All the significant light-related dermatoses are exaggerated in regions lacking in pigment and hair.

Figure 12.6 Light-related skin disorders. Note the aetiopathogenesis of the various types of light-related dermatosis.

Actinic dermatitis may be acute or chronic and falls into two distinct categories:

1. Sunburn (excessive exposure to UV light) with an expected (understandable) outcome. The severity of the damage is dependent upon the strength of the radiation and the sensitivity of the skin to the damage. Pale-skinned horses are far more liable to sunburn than black-skinned horses.

2. Photosensitization (normal exposure to UV light) with unexpected or disproportionate response. In this case even mild exposure causes severe (disproportionate) damage.

Sunburn is a primary event that follows exposure to strong sunlight. Some individual horses are more liable to the condition and usually these are horses with little pigment in the skin. Susceptible areas that are not protected by hair are even more liable and that is why many cremello/albino and white-faced horses are affected by sunburn on the muzzle. Repeated exposure over the short term and repeated exposure year on year result in chronic skin changes recognized as solar keratosis. This change can be recognized as an early pre-carcinomatous change particularly in the intraepithelial forms of squamous cell carcinoma (in-situ carcinoma) that are found on the cornea and conjunctiva and the face/eyelids in particular.

Photosensitization requires three factors:

• the presence of a photodynamic agent in the skin (Table 12.1)

• exposure to sunlight or certain wavelengths of ultraviolet light

• cutaneous absorption of ultraviolet light.

Table 12.1 Agents associated with photodermatoses in horses

Photosensitization occurs in three forms:

1. Type 1 (primary) photosensitization. This form is encountered as a result of the ingestion of preformed photodynamic substances such as those found in certain plants (e.g. St John’s wort (Hypericum perforatum); Table 12.1) and some chemical ‘poisonings’ (e.g. phenothiazine anthelmintic). The ingested photodynamic agent is absorbed directly from the digestive tract and is delivered to the skin without any hepatic detoxification or alteration. The result is predictable in most horses and is seldom severe.

Primary photosensitization may be involved in some variants of photoactivated pastern and cannon leukocytoclastic vasculitis. In this condition photodynamic complexes may be formed through combination between tissue proteins and plant proteins on the surface of the skin. In these cases the effects can be more severe but remain localized to the exposed regions (see p. 305).

2. Type 2 (endogenous) photosensitization. In these cases endogenously derived metabolites act as photodynamic agents. Examples include porphyrins. This form has not been reported in horses.

3. Type 3 (secondary) photosensitization. Digestion of chlorophyll produces a potent photodynamic agent, phylloerythrin, which is normally detoxified and excreted by the liver. Severe/advanced liver failure allows the substance to pass into the bloodstream unchanged. It accumulates in the skin where it becomes a highly reactive material when exposed to UV light. Severe/extreme actinic damage that is disproportionate to the amount of sunlight applied to the skin is the common presentation. The aetiopathogenesis is related to concurrent hepatic failure and is therefore unpredictable – failure to recognize the primary hepatic disease leads to recurrent episodes and continued suffering.

Most of the primary photosensitizing plants and the hepatotoxic plants are only marginally palatable, but signs can be seen during periods of ingestion of the plant, i.e. during grazing in summer months. Significant ingestion of hepatotoxic plants such as Senecio spp. or Lantana spp. is unusual from grazing situations but horses are unable to identify and reject the plants in preserved forage (hay or silage). Thus, most cases develop in late winter and spring and manifest when the ultraviolet light levels increase in early summer.

Specific primary and hepatotoxic plants are probably well known to veterinarians practising in the areas concerned. Almost every country has examples of both types of plant.

There are circumstances when the tissue-toxic photoactivity results when a combination of antibody and a photodynamic agent is deposited in dermal and subcutaneous blood vessel walls and the dermis. In this case the response is complicated by autoimmune or other immunological responses that, in horses at least, are poorly understood. An example of this response may be seen in pastern and cannon leukocytoclastic vasculitis (see p. 273).

In addition to the primary and secondary photosensitization conditions that are described below, there are several skin disorders that are exacerbated by exposure to sunshine/UV light. It is suggested that cytokines released by keratinocytes act as the photodynamic agents. Interestingly, sun exposure is usually necessary for the conditions to develop initially; most cases develop in summer months at grass. Once instigated, removal from the sun may have little initial benefit and the condition may persist thereafter without sunlight exposure. Even minor sunlight will trigger exacerbation. These conditions include systemic lupus erythematosus-like syndrome (see p. 276), and discoid lupus (see p. 270).

Key points: Actinic dermatoses

1. Dermatitis of varying severity is caused either directly by the action of ultraviolet light on skin (sunburn) or through the effects of a photodynamic chemical or metabolite deposition in the skin deposited in or on the skin. Endogenous photosensitization as a result of porphyrins etc. has not been reported in horses but some drugs such as phenothiazine can cause the problem.

2. Mild to extreme necrotizing dermal inflammation is characteristic. The proportionality of the damage to the degree of sunlight provides the best indicator of the likely type of photosensitization present. White-skinned areas and pale glabrous (hairless) skin are most liable to the condition.

3. Diagnosis is relatively easy when the dermatitis is restricted to non-pigmented skin in summer months. Histologically the changes are not pathognomonic.

4. Primary sunburn is easily managed by avoidance or sunscreen creams, but the risks associated with repeated exposure should be considered. Type 2 primary photosensitization will resolve if the causative plant/agent is eliminated. For secondary photosensitization as a result of hepatic failure, treatment is usually supportive. Antibiotic treatment and avoidance of sunlight exposure are always sensible. High factor suncreams are not really the answer because they may be used as an excuse to avoid management strategies which are far more effective. Avoidance of any defined causative plant/toxin is essential.

5. The prognosis for primary photosensitization is good. For advanced hepatic failure the prognosis is hopeless.

Ultraviolet light is also potentially mutagenic and carcinogenic but it can also suppress skin inflammation. Therefore sunlight can be both harmful and beneficial. Certain skin tumours, in particular squamous cell carcinoma, are thought to be precipitated by exposure to ultraviolet light and certainly the cutaneous and conjunctival forms of this neoplasm (see p. 427) are much more common in non-pigmented tissues and in regions where more sunlight exposure occurs.

The tissue toxicity effects of light and photodynamic compounds can be used therapeutically in photodynamic therapy (see p. 126).

Clinical signs

Cutaneous lesions vary widely in both severity and extent but are usually restricted to light skin or hairless areas.

1. Simple sunburn (Fig. 12.7) can be difficult to differentiate from the more serious forms of actinic dermatitis but the horse is usually clinically normal and often has very pink skin with minimal hair cover over the muzzle and face. The extent of the damage is usually much less severe than in true photosensitization but repeated exposure can cause significant exacerbation. Most prominent signs are found on the face, commonly around lips, nose and eyelids. If there is significant exudation there may be a complicating superficial infection with Dermatophilus congolensis (see Fig. 6.22). A history of previous problems during summer months is often given. Most (if not all) cases improve quickly when removed from exposure and the skin rapidly returns to normal.

2. The more severe, systemically mediated condition (either from direct photodynamic agents or hepatic failure) is usually much more serious and has a much more destructive nature. Again, the lesions are typically restricted to the white areas on the face and elsewhere (Fig. 12.8) and are always sharply restricted to the non-pigmented skin (Fig. 12.9). Severe cases may have lesions which just overlap into dark-skinned, well-haired areas. Conjunctivitis, skin oedema, erythema, pruritus and pain are usually present as the skin becomes necrotic. The perineum and coronary band region may be severely affected (Fig. 12.8). Extensive sloughing of skin occurs in most severe cases. Concurrent systemic signs of hepatic disease may be present (ventral oedema, hepatoencephalopathy, icterus and weight loss) with biochemical evidence of hepatic failure.