Blackwell's Five-Minute Veterinary Consult: Reptile and Amphibian. Javier G. Nevarez

hyperglycemia is likely insignificant, while chronically elevated levels carry a poor prognosis.

MISCELLANEOUS

      COMMENTS

      N/A

      ZOONOTIC POTENTIAL

      N/A

      SYNONYMS

      N/A

      INTERNET RESOURCES

      Melissa Kaplan’s Herp Care Collection. Hypoglycemia and Hyperglycemia in Reptiles. http://www.anapsid.org/diabetes.html

Suggested Reading

      1 Campbell TW. Clinical pathology. In: Mader DR, Divers SJ, eds. Current Therapy in Reptile Medicine and Surgery. St. Louis, MO: Elsevier Saunders; 2014:70–92.

      2 Stahl SJ. Hyperglycemia in reptiles. In: Mader DR, ed. Reptile Medicine and Surgery. 2nd ed. St. Louis, MO: Elsevier Saunders; 2006:822–830.

      Author Mads F. Bertelsen, DVM, DVSc, DACZM, DECZM (Zoo Health Management)

      Hypervitaminosis A

      

BASICS

      DEFINITION/OVERVIEW

      Hypervitaminosis A is well recognized health concern in chelonians. It can be caused by OTC supplements provided by well‐ meaning owners, parenteral overdosing by veterinarians, or diets with high animal vs. plant‐based (beta carotene) vitamin A levels.

      ETIOLOGY/PATHOPHYSIOLOGY

       In vertebrates, the vitamin A forms are trans‐retinyl esters, trans‐retinol, ‐retinal and ‐retinoic acid (99% of all vitamin A present in the body), while the major dietary provitamin A carotenoid is beta carotene.

       The all‐trans‐vitamin A isomers are the only forms used physiologically.

       The liver absorbs and stores preformed vitamin A; at a certain point, storage capacity is reached and toxicity occurs. Other storage sites include adipose tissue, lung, and kidney.

       In humans, the retinoid delivery pathway to tissues involves primarily retinol bound to retinol‐binding protein; chylomicrons, very low density lipoprotein, low density lipoprotein, and albumin also provide transport.

       Adverse effects in humans include increased bone turnover by suppressing osteoblast activity and stimulating osteoclast formation. This can lead to hypercalcemia, osteoporosis, pathologic fractures, altered skeletal development in children, and skeletal pain.

       Vitamin A is fat soluble and high levels can affect metabolism of other fat‐soluble vitamins (D, E, K); with the effects on vitamin D contributing to the aforementioned bone pathology, although stimulation of bone resorption by vitamin A is reported independent of effects on vitamin D.

       Vitamin A can have a toxic effect on mitochondrial function and is reported to cause hypothyroidism in mice.

      SIGNALMENT/HISTORY

       First time owner of reptiles/species and young animals.

       Owner using OTC vitamin A drops, OTC multivitamin with vitamin A in formulation other than beta carotene, using cod liver oil or feeding liver to a carnivorous/omnivorous animal.

       Occasional issues with extruded diets with inadvertent toxic levels of non‐beta carotene vitamin A.

      CLINICAL PRESENTATION

       Patients present with vague signs such as anorexia, dehydration, lethargy.

       Usually has a dermatological component including: dysecdysis, epidermal flakiness, ulceration, and sloughing.

       Bilateral epiphora and periorbital edema may be noted.

       Ulcerative stomatitis can be seen.

       Secondary bacterial and fungal infections can occur.

       Based on pathophysiology, suspect that metabolic bone disease may have interplay with hypervitaminosis A.

      RISK FACTORS

       Juvenile animal

       Reproductively active female

       Liver disease

       Husbandry

      N/A

       Others

      Iatrogenic dietary or parenteral over supplementation of non‐beta carotene vitamin A.

DIAGNOSIS

      DIFFERENTIAL DIAGNOSIS

       Hypovitaminosis A

       Infection

       Hepatic or renal disease

       UVB or thermal burns

       Poor overall husbandry or diet

       Improper conspecific arrangement

       Metabolic bone disease

      DIAGNOSTICS

       Liver biopsy for histopathology and testing vitamin A levels (need normal values for the species).

       Presumptive diagnosis based upon history and clinical presentation.

      PATHOLOGICAL FINDINGS

       Hepatic fibrosis

       Osteoporosis

       Decreased or abnormal bony growth in juvenile animals.

       Epidermal ulceration

TREATMENT

      APPROPRIATE HEALTH CARE

      N/A

      NUTRITIONAL SUPPORT

      Often need assisted feeding

      Esophageal feeding tube is often recommended, especially in chelonians with skin sloughing, which makes it difficult to manipulate the head and neck.

      CLIENT EDUCATION/HUSBANDRY RECOMMENDATIONS

       Proper education about the correct diet and formulation of vitamin A for the species.

       Education about differences between water soluble and fat‐soluble vitamins.