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1039.e4 Vitamin A Toxicosis

Vitamin A Toxicosis
VetBooks.ir Etiology and Pathophysiology

BASIC INFORMATION
Source: vitamin A toxicosis [hepatotoxicosis] is very
uncommon)
Definition • Vitamin A and its congeners are not produced
• Chronic toxicosis occurs in animals that endogenously and must be supplied by differ- Initial Database
repeatedly ingest high doses of vitamin A. ent sources (dietary or oral supplementation). • CBC: nonspecific changes or no significant
Characterized by lethargy, anorexia, weight • Beta-carotene is a plant pigment found in a changes expected
loss, exostoses (most prominent in cervical number of foods. It is converted to retinol • Serum biochemistry profile: liver enzymes
and thoracic spine), cervical neck pain, in the intestine and is further oxidized to elevated with acute intoxication
skin conditions, and possibly reproductive retinoic acid and retinol. • Urinalysis: generally unremarkable
problems. • Acidic forms of vitamin A (cis- or trans- • Cervical radiographs may show bone-density
• Acute intoxication can cause ptyalism, retinoic acid), vitamin A derivatives (retinol, cervical mass ventral to C1-C2 intervertebral
anorexia, vomiting, diarrhea, abdominal trans-retinyl palmitate, retinyl stearate), space.
pain, peeling skin, tremors, convulsions, synthetic retinoids (tretinoin, isotretinoin,
hepatitis (rare), and death. etretinate), and vitamin A capsules, tablets, Advanced or Confirmatory Testing
and injections all represent potential phar- • Cats: serum/plasma retinol level > 3145 mcg/L
Synonyms maceutical sources of vitamin A. is considered toxic (normal: 200-1600 mcg/L).
Retinoids (vitamin A derivatives), hypervita- • Liver (typically from chicken, beef, or fish) • Toxic levels in feline liver (postmortem):
minosis A is a common nutritional source of vitamin 8590-39,570 mcg/g wet weight
A. • In dogs, serum/plasma retinol > 20,000 mcg/L
Epidemiology • Large, acute ingestion of multivitamin is considered toxic (normal: 300-1000 mcg/L).
SPECIES, AGE, SEX formulations containing vitamin A or vitamin
All mammals are susceptible; chronic intoxi- A creams are not expected to cause acute TREATMENT
cation occurs mainly in the cat from eating vitamin A toxicosis (may see some GI signs
diet largely consisting of liver (raw); dogs are such as vomiting and diarrhea, but systemic Treatment Overview
overrepresented in acute toxicosis effects are not expected). With acute intoxication, general decon-
• Excessive cod liver oil supplementation in tamination procedures are sometimes indicated,
Clinical Presentation cats can cause vitamin A toxicosis. whereas with chronic toxicosis, treatment
DISEASE FORMS/SUBTYPES Mechanism of toxicosis: consists of removing the source of excess vitamin
• Acute: rare to see anything more than mild • Vitamin A plays an essential role in normal A and providing supportive care. There is no
gastrointestinal (GI) signs night vision, reproductive processes, main- antidote.
• Chronic: after consumption of high tenance of epithelial and cell membrane
levels of vitamin A–containing diet for structure, normal cellular growth, and Acute General Treatment
months immune functions. • Decontamination of patient (p. 1087)
• Hypervitaminosis A can inhibit keratinization ○ Remove source (excess vitamin A)
HISTORY, CHIEF COMPLAINT of epithelial cells, which can lead to skin ○ Induction of vomiting (p. 1188) if large
• History of chronic exposure to a high problems. amount of pills or cream is ingested and
vitamin A–containing product (capsules) • High concentrations of vitamin A induce animal is asymptomatic
or diet (mainly/exclusively raw liver diet: chondrocytes to produce more extracel- ○ Activated charcoal 1-2 g/kg PO if recent
most common) lular matrix, which forms a framework for large ingestion (within few hours); rarely
○ Chronic: lethargy, anorexia, weight loss, mineralization (exostoses: abnormal bone needed
reluctance to walk, lameness, gingivitis, growth, cervical spondylosis). • Supportive care
matted haircoat, irritability, resentment • Toxicosis can occur in adult cats that eat a ○ IV fluids if needed to correct dehydration
of handling; signs typically develop over diet of raw liver 4 days per week. from vomiting (or rarely, if liver injury
several months. • In puppies, feeding > 400,000 IU/kg in the occurs from massive intoxication)
• Acute (rare): self-limited mild vomiting, diet (dry matter) for 6 months (and in adult ○ Vomiting may be controlled with maropi-
ptyalism, diarrhea, anorexia, depression dogs, > 787,000 IU/kg for 1 year) did not tant 1 mg/kg SQ q 24h or metoclopramide
• Pregnant animals: teratogenicity (cleft palate, produce signs of toxicosis. 0.1-0.4 mg/kg body weight PO, SQ, or
hydrocephalus, microencephaly), reproduc- • In humans, neurotoxicosis is seen due to IM q 8h.
tive failure increased intracranial pressure. ○ Management of liver damage (rare) as
needed (p. 442)
PHYSICAL EXAM FINDINGS DIAGNOSIS
• Neck and limb rigidity due to cervical Chronic Treatment
spondylosis or exostosis (proliferation of Diagnostic Overview Remove the source (liver in the diet)
bone) Clinical diagnosis is based almost entirely on
• Tense musculature unusual nutritional/dietary supplement history Drug Interactions
• Neck ventroflexion possible and characteristic exostotic bony changes on Hypervitaminosis A can interfere with the
○ In contrast to neck ventroflexion from radiographs (especially cervicothoracic verte- action of other fat-soluble vitamins.
hypokalemia or thiamine deficiency brae) and is confirmed by elevated serum levels
(characterized by a flaccid neck), in of retinol. Recommended Monitoring
patients with vitamin A intoxication, • Serum biochemistry profile: liver enzymes
ventroflexion is stiff (caused by bony Differential Diagnosis • Body weight
exostoses). Other causes of acute GI signs (vomiting,
○ Exfoliation, matted coat diarrhea) or liver damage (rare because acute

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