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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Photosensitization is defined as UV-induced dermatitis caused by a photodynamic agent in the skin which increases the sensitivity of the skin to sunlight
  • Decreased skin pigmentation and hair cover facilitate cutaneous penetration of UV

Pathophysiology!!navigator!!

  • Upon exposure to UV, molecules of the photodynamic agent enter an excited or high-energy state. These excited molecules may cause skin damage directly but damage occurs mostly through the production of reactive oxygen metabolites and free radicals
  • Photosensitization in horses generally fits into 1 of 2 categories: (1) primary photosensitization, which is caused when a preformed or metabolically derived photodynamic agent (e.g. plant or fungal products or chemicals) reaches the skin by ingestion, injection, or contact; and (2) secondary (hepatogenous) photosensitization, which occurs in cases of liver disease when phylloerythrin acts as a photodynamic agent
  • Phylloerythrin, a porphyrin compound formed by microbial degeneration of chlorophyll in the intestine, is normally conjugated in the liver and excreted in the bile. Liver dysfunction and/or biliary stasis may result in the accumulation of phylloerythrin in the blood and body tissues, including the skin. Some toxins derived from grasses are directly phototoxic and hepatotoxic, which makes the above classification of photosensitization less clear

Systems Affected!!navigator!!

  • Skin/exocrine—lesions usually restricted to light-skinned, sparsely haired areas such as the coronary band, muzzle, ears, eyelids, tail, and vulva
  • Hepatobiliary—secondary photosensitization can be associated with any cause of hepatic insufficiency. However, it appears to be more commonly associated with hepatic insufficiency caused by the ingestion of hepatotoxic plants

Genetics!!navigator!!

N/A

Incidence/Prevalence!!navigator!!

N/A

Geographic Distribution!!navigator!!

More common in sunny areas.

Signalment!!navigator!!

  • All ages and breeds are susceptible
  • Light-skinned horses will have the most severe lesions

Signs!!navigator!!

Historical Findings

  • Initial signs noted are restlessness and scratching and rubbing of the ears, eyelids, and muzzle
  • Shade-seeking behavior
  • Demarcated skin lesions characterized by redness, blister formation; weeping, and crusting
  • In cases of secondary photosensitization owners may notice signs suggestive of liver failure (e.g. altered mentation, weight loss, abdominal pain, diarrhea, etc.)

PhysicalExamination Findings (Web Figures 3 and 4)

Cutaneous Lesions (Primary and Secondary Photosensitization)

  • Usually restricted to sparsely haired, light-skinned areas on the dorsal aspects of the body (e.g. face, muzzle, eyelids, ears, coronary bands, vulva, and tail), but in severe cases can extend to dark-skinned areas
  • Demarcation between lesions and normal skin is quite clear, particularly in multicolored animals
  • Acute signs include erythema, edema, serous exudation, and crust formation; lesions may be sensitive to touch and/or pruritic
  • As lesions become more chronic, crust formation and sloughing of the skin is noted
  • Conjunctivitis, keratitis, and corneal edema may be seen

Liver Failure Signs (May Accompany Cutaneous Lesions in Cases of Secondary Photosensitization)

  • Icterus
  • Pruritus
  • Weight loss
  • Diarrhea
  • Abdominal pain
  • Altered mentation

Causes!!navigator!!

Causes of Primary Photosensitization

  • Associated with ingestion, injection, or contact with a photodynamic agent
  • Photodynamic plants (e.g. St. John's wort (Hypericum perforatum), buckwheat (Fagopyrum esculentum), perennial ryegrass (Lolium perenne), burr trefoil (Medicago denticulata), spring parsley (Cymopterus watsoni), bishop's weed (Ammi majus), oat grass (Avena fatua), rape (Brassica spp.), Dutchman's breeches (Thamnosma texana), alsike clover (Trifolium hybridum), alfalfa (Medicago spp.), vetches (Vicia spp.), hogweed (Heracleum sphondylium), gluten, etc.)
  • Chemicals (e.g. phenothiazines, thiazides, acriflavines, methylene blue, sulfonamides, tetracyclines, coal tar derivatives, furosemide, promazine, chlorpromazine, quinidine, rose bengal, etc.)
  • Mycotoxins (e.g. phycocyanin produced by blue-green algae and phytoalexins produced by celery and parsnip)

Causes of Secondary Photosensitization

  • Associated most often with chronic liver failure or conditions that result in biliary obstruction
  • Chronic active hepatitis
  • Hepatic abscessation
  • Neoplasia (cholangiocellular carcinoma, lymphosarcoma)
  • Chronic megalocytic hepatopathy (Senecio spp., Crotalaria spp., Heliotropium spp.)
  • Burning bush, fireweed (Kochia scoparia)
  • Mycotoxicoses (blue-green algae (Microcystis spp.), Phomopsis leptostromiformis (on lupines))
  • Cholelithiasis/cholangitis

Risk Factors!!navigator!!

  • Exposure to plants and chemicals that cause primary photosensitization
  • Chronic liver failure or biliary obstruction
  • Lack of skin pigment and/or sparse hair cover
  • Exposure to sunlight

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

The clinical signs in cases of photosensitization are identical regardless of the etiology. History and clinical findings can aid in the differentiation of primary vs. secondary photosensitization.

Primary Photosensitization

A history of exposure to plants (e.g. St. John's wort, buckwheat) or chemicals (phenothiazines, tetracyclines) known to cause primary photosensitization, and absence of liver failure signs, will support a tentative diagnosis of primary photosensitization.

Secondary Photosensitization

Photodermatitis accompanied by liver failure signs (e.g. icterus, weight loss, diarrhea, abdominal pain, neurologic lesions) should prompt the clinician to consider secondary photosensitization.

CBC/Biochemistry/Urinalysis!!navigator!!

Primary Photosensitization

Liver enzyme activities (SDH, GGT, AST, ALP), bilirubin, and bile acid concentration are usually normal.

Secondary Photosensitization

Increased liver enzyme activities (SDH, GGT, AST, ALP), hyperbilirubinemia, and/or bilirubinuria will support a diagnosis of secondary or hepatogenous photosensitization.

Other Laboratory Tests!!navigator!!

Increased serum bile acid concentration, prolonged clearance of foreign dyes such as bromosulfophthalein, and abnormal findings on a liver biopsy indicate a diagnosis of secondary photosensitization.

Imaging!!navigator!!

US

May detect changes in liver size and abnormalities in the hepatic parenchyma (e.g. abscesses, neoplastic masses, dilated bile ducts, choleliths) in cases of secondary photosensitization.

Other Diagnostic Procedures!!navigator!!

Liver Biopsy

  • May yield diagnostic, prognostic, and therapeutic information in cases of secondary photosensitization
  • Samples obtained using US-guided or blind techniques; placed in formalin for histopathology, transport medium for microbiology
  • Complications—hemorrhage, pneumothorax, spread of infectious hepatitis, peritonitis (e.g. bile or ingesta contamination)
  • Complications minimized by performing hemostasis profile, using US guidance

Pathologic Findings!!navigator!!

Primary Photosensitization

Lesions are limited to the skin and include edema, serous exudate, scab formation, and skin necrosis.

Secondary Photosensitization

Dependent on primary disease process.

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

Dependent on primary disease process.

Nursing Care!!navigator!!

  • Identify and eliminate source of photodynamic agent
  • Administer laxatives (mineral oil) and/or adsorbents (activated charcoal) to prevent further toxin absorption from the gastrointestinal tract
  • IV fluids may be required in severely affected animals

Activity!!navigator!!

Restrict activity and avoid exposure to sunlight.

Diet!!navigator!!

For secondary photosensitization, a diet that provides 40–50 kcal/kg body weight in the form of a low-protein, high-energy feed is recommended (e.g. milo, Sorghum, beet pulp).

Client Education!!navigator!!

  • Identification and removal of any plants causing primary or secondary photosensitization
  • Knowledge of drug sensitivities to prevent further occurrences
  • Management of specific disease process(es) for secondary photosensitization

Surgical Considerations!!navigator!!

Surgical debridement is indicated to manage skin necrosis.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

Medications for Cutaneous Lesions

  • Use anti-inflammatory drugs (prednisolone 1.1 mg/kg PO every 24 h or flunixin meglumine 1.1 mg/kg PO, IV every 12 h) to decrease severity of inflammation in early stages
  • Topical antibiotic—corticosteroid creams may be applied to affected areas
  • Systemic antibiotics are indicated to manage secondary bacterial infections

Treatment for Hepatic and Extracutaneous Disorders

Treat underlying liver disease.

Contraindications, Precautions, Possible Interactions!!navigator!!

Primary Photosensitization

Avoid use of drugs that may promote further photosensitization (e.g. tetracyclines, sulfonamides, or phenothiazines).

Secondary Photosensitization

  • Avoid use of drugs metabolized primarily by the liver (e.g. anesthetics, barbiturates, or chloramphenicol)
  • Sedatives metabolized by the liver (e.g. xylazine or diazepam) may have to be used at reduced dosages

Alternative Drugs!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Primary Photosensitization

Evaluate skin lesions every few days and debride necrotic lesions as required.

Secondary Photosensitization

  • Manage skin lesions as for primary photosensitization
  • Monitor liver enzyme activities, serum bile acids, and bilirubin concentration weekly until improvement is noted
  • Repeat liver biopsy in 4–6 weeks to monitor disease progression

Prevention/Avoidance!!navigator!!

Identify and eliminate photodynamic agent from environment.

Possible Complications!!navigator!!

  • Patients with secondary photosensitization often succumb to underlying liver disease
  • Rubbing and biting of affected areas may cause secondary self-trauma and bacterial infections

Expected Course and Prognosis!!navigator!!

In general, prognosis is favorable for primary photosensitization and poor for secondary photosensitization.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Local edema of nostrils, lips, and eyelids can cause dyspnea, abnormal feed prehension, or lacrimation
  • Mares with teat lesions may not allow their foals to nurse, causing starvation
  • Secondary septicemia may develop in severe cases

Age-Related Factors!!navigator!!

Factors leading to secondary photosensitization are generally seen in adult horses.

Abbreviations!!navigator!!

  • ALP = alkaline phosphatase
  • ASP = aspartate aminotransferase
  • GGT = γ-glutamyltransferase
  • SDH = sorbitol dehydrogenase
  • US = ultrasonography, ultrasound
  • UV = ultraviolet

Suggested Reading ⬆ ⬇

Peterson AD, Schott AC. Cutaneous markers of disorders affecting adult horses. Clin Tech Equine Pract 2005;4:234–388.

Rashmir-Raven A, McConnico RS. Photosensitization. In: Sprayberry KA, Robinson NE, eds. Robinson's Current Therapy in Equine Medicine, 7e. St. Louis, MO: WB Saunders, 2015:536–542.

Scott DW, Miller WH. Environmental skin diseases. In: Scott DW, Miller WH, eds. Equine Dermatology, 2e. Maryland Heights, MO: Elsevier Saunders, 2011:398–420.

Author(s) ⬆

Authors: Emily E. John and Jeanne Lofstedt

Consulting Editors: Michel Levy and Heidi Banse