Necrotizing Skin Diseases

Chapter 49 Necrotizing Skin Diseases



Gail A. Kunkle


Necrotizing dermatitis refers to those skin conditions in which there is death of tissue. With many cases of necrotizing dermatitis, eschar (slough) formation and ulceration is often the visible clinical sign, and it occurs when there is cell death, especially within the epidermis and the hair follicles. In other necrotizing skin diseases, the tissue destruction may arise in the dermis or even from compromise of deeper vessels. In these cases the first clinical signs may be discoloration, swelling, or coolness to the skin followed later by cutaneous ulceration. Causes of necrotizing skin disease are categorized in Table 49-1.


Table 49-1 CLASSIFICATION AND CAUSES OF NECROTIZING DERMATOSES






































































































Category Cause
Vasculitis Sepsis
Systemic infectious disease
Drug-induced
Neoplasia
Immune-mediated
Focal (rabies vaccination)
Post-vaccination ischemic dermatopathy
Dermatomyositis
Idiopathic
Neoplasia Squamous cell carcinoma (see Chapter 30)
Mast cell (see Chapter 28)
Lymphoma (see Chapter 27)
Lymphatoid granulomatosis
Other tumors (see Chapter 30)
Drug-induced Antibiotics
Biologicals
Barbiturates
Phenylbutazone
Gold salts
Toxic epidermal necrolysis Drug-induced
Systemic disease
Erythema multiforme Neoplasia
Idiopathic
Superficial necrolytic dermatitis Glucagonoma
Hepatopathy
Environmental Contact irritant
Snake bite
Spider bite
Radiation
Burns
Frostbite
Decubitus ulcers
Immune-mediated Systemic lupus erythematosus (see Chapter 24)
Bullous pemphigoid (see Chapter 24)
Pemphigus complex (see Chapter 24)
Cold agglutinin disease
Vasculitis
Vesicular cutaneous lupus erythematosus
Infectious Bacterial cellulitis (see Chapter 38)
Deep fungal infection (see Chapter 40)
Vascular compromise Thrombovascular necrosis
Mechanical occlusion
Diabetes mellitus (see Chapter 34)



Key Point


Dependent on the depth of necrosis or the percentage of surface area which is ulcerated, necrotizing dermatoses can be life-threatening.


An overview of necrotizing dermatitis will be presented in this chapter, followed by discussion of the specific diseases that cause the disorder.



CLINICAL SIGNS


Necrotizing skin diseases are characterized clinically by well-defined areas of devitalized skin (eschar), which may vary from pinpoint sized to involving of a large portion of the skin surface. The area may be discolored, ranging from dark red to purple to yellow to black. There may be swelling and even gas production within the tissues. In time, the devitalized skin develops into a thick adherent crust, revealing deep ulceration if removed. Common sequelae are systemic signs of toxicity.



Principles of DIAGNOSIS


Significant necrosis of the skin is a dermatologic emergency and may result in death; thus, initiate the diagnostic approach to necrotizing skin disease as quickly as possible.


Early identification of an underlying cause and specific treatment generally allows a better clinical outcome. The diagnostic approach should be as thorough as possible from the outset to increase the chance of a definitive diagnosis.




Key Point


Specific diagnosis is best made by routine histopathology from representative primary skin lesions and/or tissue samples adjacent to necrosis, in conjunction with a careful history and thorough physical examination.




History



• Identify or exclude several of the potential causes of necrotizing dermatoses.

• Record a thorough drug history and take note of environmental factors.

• Record a careful timetable of events in addition to the owner’s description of the earliest cutaneous lesions and their temporal relationship to any noted systemic signs.


Physical Examination



• Thoroughly examine all of the skin, including the inside of the ears, the oral cavity (and other mucosal surfaces), and haired as well as non-haired skin.

• Note any primary lesions.

• Look for secondary lesions and for evidence of how they may have developed.

• Palpate all peripheral lymph nodes for enlargement.

• Take the body temperature.

• Perform a general physical examination, including examination of the eyes, auscultation of the thorax and palpation of the abdomen, to evaluate for systemic signs.


Serum Biochemical Profile, Urinalysis, and Complete Blood Count



• Evaluate these in animals with systemic signs such as anorexia, fever, and depression. This minimum database may even be justified in animals with extensive necrotizing dermatitis but without overt clinical signs of systemic disease.

• Use these as baseline information when progressive disease is suspected.


Tests for Systemic Immune-Mediated Diseases



• When clinical signs suggest systemic disease, perform antinuclear antibody (ANA) testing of serum to assess the presence or absence of antibodies directed against multiple nuclear antigens.

• Other immune tests such as Coombs testing and cryoglobulin identification may be indicated in cases in which specific diseases are suspected.

• See Chapter 24 for further discussion of testing for systemic immune-mediated diseases.


Skin Biopsy



• Skin biopsy is usually a critically important diagnostic tool in necrotizing skin diseases (see Chapter 37). Sampling of early primary lesions is most likely to be rewarding. When vasculitis is suspected, obtain deep wedge biopsies for diagnosis—deep tissue may not be obtained if only punch biopsy tissue specimens are collected.

• Collect lesions that are primary eruptions and/or skin immediately adjacent to necrotic skin.

• Use formalin as a fixative and obtain representative tissue samples from various types of lesions. A pathologist familiar with dermatopathology often can determine if systemic or topical disease is present.

• Most pathologists now use formalin-fixed tissue for immunohistochemistry for the presence of antibody. However, absence of antibody does not rule out autoimmunity as a cause.


Skin and Blood Cultures



• Evaluate the patient for infection by culturing the skin for bacterial (aerobic and anaerobic) and fungal agents.

• For systemic diseases, blood cultures may be indicated.


Other Diagnostic Evaluations



• Evaluate rickettsial serum titers and other disease-specific hematologic tests as indicated.

• Perform liver function tests (pre- and post-prandial serum bile acids) and abdominal ultrasound (to evaluate the liver and pancreas) to assess a suspected case of superficial necrolytic dermatitis.

• Radiography and ultrasonography are useful if cutaneous lesions are suspected to be secondary to malignancy or systemic disease.

• In rare cases, response to therapy or removal of a suspected inciting drug confirms the diagnosis.


Principles of TREATMENT




Key Point


Therapy is most effective when a specific cause is identified; treatment can then be focused on the elimination or modification of the underlying cause.


Cutaneous necrosis is best managed aggressively with treatment directed against a definitive cause. If there is a possibility that drugs are implicated, discontinue all drugs until a definitive or probable diagnosis is established. Secondary infection is likely and best treated with a broad-spectrum antibiotic (preferably one that the patient has not previously received). Toxins associated with tissue necrosis can have systemic effects; therefore, debride tissues and flush frequently with sterile saline. When the cause cannot be identified, supportive care is the mainstay of treatment. Hydration and provision of a high-quality protein diet are important aspects of therapy.



SPECIFIC NECROTIZING DERMATOSES




Vasculitis/Vasculopathy



Etiology


Vasculitis is an inflammatory process that occurs within blood vessel walls and that can lead to necrosis of the vessels and subsequent death of the adjacent tissue. Histopathologic evidence of vasculitis can be subtle and transient. When surrounding tissues suggest vascular compromise or there is vessel wall damage without cells, many pathologists refer to this as vasculopathy. Acute cutaneous vasculitis is most likely to result in necrotizing skin signs including hemorrhage (ecchymoses or purpura), hemorrhagic bullae, necrosis (eschar), and punched out ulcers. Hemorrhage can be confirmed clinically by diascopy (the skin remains discolored when pressure is applied with a glass slide. In comparison, erythema blanches under pressure). Chronic vasculitis or cell-poor vasculitis (vasculopathy) is more likely to present with ischemic changes such as alopecia, scaling, hyperpigmentation and some erythema. Both often involve the ears, tail tip, face, and extremities. Cutaneous vasculitis and vasculopathies are rarely primary in the dog. The list of secondary causes is quite extensive; for prognosis and treatment purposes it is useful to separate these into infectious and non-infectious etiologies. In spite of an extensive search for an underlying cause, many cases are idiopathic.



Non-immunologic Causes


• Necrotizing vasculitis can be seen with a variety of infections caused by bacteria, viruses, disseminated fungi, and tickborne organisms such as Rickettsia rickettsii. Bacteria may directly invade the vessel walls, especially with sepsis. Other infections such as E. coli can produce toxins that result in specific signs of vasculopathy as seen in the cutaneous and renal glomerular vasculopathy of greyhounds.

• Neoplasia can result in vessel wall necrosis through toxin production or direct invasion of the vessel wall by neoplastic cells.

• Specific drugs can induce lesions of vasculitis in animals; the antifungal drug, itraconazole, at a dosage of 5 mg/kg q12h PO has been observed to cause vasculitis in some dogs.


Immunologic Causes


• With autoimmune disease immune complex deposition may occur in vessel walls. Antibodies or cytotoxic cells may attack components of the vessel walls in other connective tissue conditions.

• Focal cutaneous vasculitis has been reported at the site of rabies vaccination. This is usually a deep panniculitis, and the cutaneous clinical sign most often is alopecia instead of necrosis. Similar lesions may develop later at sites distant from the site of vaccination.

• Post-vaccination ischemic dermatopathy and familial dermatomyositis in the acute stages may exhibit erosions or ulcerated lesions on the extremities in association with vasculitis. However, in the majority of these cases the signs are more chronic and are evidence of a vasculopathy.


Clinical Signs



• Vasculitis signs usually consist of necrosis and ulceration. These commonly occur on the pressure points, foot pads, pinnae, and extremities. Mucocutaneous ulcerations may be present as well as fever, lymphadenopathy, anorexia, and depression. Acute signs are more often necrotic or erosive lesions whereas chronic signs may show alopecia and scarring.

Related posts:

  1. Feline Infectious Peritonitis (Feline Coronavirus)
  2. Borreliosis (Lyme Disease)
  3. Immune-Mediated Dermatoses
  4. Canine and Feline Demodicosis

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Necrotizing Skin Diseases

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