DIFFERENTIAL DIAGNOSIS
N/A
DIAGNOSTICS
Detection of hypoglycemia in a clinically healthy animal should not cause concern.
In animals with clinical signs and hypoglycemia, attempts should be made to rule out septicemia, hepatobiliary disease, and pancreatic neoplasia.
Glucose may be artificially low in blood samples stored for a prolonged period prior to separation of plasma/serum.
PATHOLOGICAL FINDINGS
Depends on underlying etiology
• The pancreas should be thoroughly evaluated.
APPROPRIATE HEALTH CARE
N/A
NUTRITIONAL SUPPORT
Consider energy‐rich nutritional support by stomach tube in cases of anorexia.
CLIENT EDUCATION/HUSBANDRY RECOMMENDATIONS
If related to poor nutrition and management, educate clients on appropriate feeding practices.
DRUG(S) OF CHOICE
Treat underlying disease
Supportive administration of glucose or dextrose parenterally (e.g., 2.5% in 0.45% saline, 20–40 mL/kg SC) or orally (3 g/kg PO) may be indicated.
PRECAUTIONS/INTERACTIONS
N/A
PATIENT MONITORING
Monitor glucose levels and clinical signs.
EXPECTED COURSE AND PROGNOSIS
If related to nutritional status prognosis is good.
If secondary to severe systemic disease prognosis is poor.
COMMENTS
N/A
ZOONOTIC POTENTIAL
N/A
SYNONYMS
N/A
ABBREVIATIONS
PO = per os
SC = subcutaneous
INTERNET RESOURCES
Kaplan M. Hypoglycemia and Hyperglycemia in Reptiles. Melissa Kaplan’s Herp Care Collection, January 1, 2014. 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; 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)
Hypovitaminosis A
DEFINITION/OVERVIEW
Hypovitaminosis A is a well‐recognized health concern in pet carnivorous, insectivorous, and omnivorous chelonians. The primary cause is feeding food items deficient in the correct form of vitamin A for the species or in under/incorrectly supplementing vitamin A.
ETIOLOGY/PATHOPHYSIOLOGY
In vertebrates, vitamin A forms are trans‐ retinyl esters, trans‐retinol, ‐retinal and ‐retinoic acid (99% of all vitamin A present in body), while the major dietary provitamin A carotenoid is beta carotene.
The all‐trans‐vitamin A isomers are the only forms used physiologically.
Carnivores, insectivores, and possibly omnivores need these forms in their diet.
While reptile herbivores can convert carotenoids lutein and canthaxanthin into trans‐retinyl esters, beta carotene does not convert as well.
Hypovitaminosis A in herbivores is extremely unlikely, excepting after long periods of anorexia.
The liver absorbs and stores preformed vitamin A. Other storage sites include adipose, lung, and kidney.
In humans, 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 night blindness, impaired immune function, cancer, and birth defects.
SIGNALMENT/HISTORY
First‐time owner of reptiles/species.
Supplementing with beta carotene‐based vitamin A or no supplementation.
Box turtles (Terrapene carolina sp.) and sliders (Trachemys scripta sp.) may present more commonly.
