Cholecalciferol (vitamin D3) is used
both as a dietary supplement and a rodenticide. It appears to be toxic at a much
lower dose when consumed in a bait form than when ingested as a technical grade
agent. Most rodenticide baits contain 0.075% cholecalciferol. Incidence of vitamin
D3 toxicosis in animals is relatively less than that of
anticoagulant and bromethalin toxicosis. Relay toxicosis from vitamin
D3 has not been documented. One international unit (1 IU)
of vitamin D3 in nutritional supplement is equivalent to
0.025 mcg of cholecalciferol.
Cholecalciferol toxicosis is characterized by
hyperphosphatemia and hypercalcemia, leading to renal failure, cardiac
abnormalities, hypertension, CNS depression, anorexia, vomiting, diarrhea, and
lethargy. The increased calcium and phosphorus can lead to calcification of soft
tissue, notably the highly vascular areas of kidneys and lungs, as well as within
the walls of the great blood vessels.
Clinical signs generally develop within 18–36 hr of
ingestion; initial signs can include depression, anorexia, polyuria, and polydipsia.
The serum phosphorus more commonly rises first, at ~12–24 hr after ingestion, with
serum calcium levels rising within another 12–24 hr. Nausea, vomiting, hematemesis,
and depression are common as the clinical signs progress. It is important to obtain
a baseline biochemistry profile as early as possible after the exposure, so that
each animal can be monitored based on individual values.
Ingestion of vitamin D3 at >0.1
mg/kg may require decontamination (induction of emesis and administration of
activated charcoal) and monitoring of serum calcium, phosphorus, and renal values.
Emesis can be induced within 2 hr of exposure with 3% hydrogen peroxide or
apomorphine in dogs and xylazine in cats. Activated charcoal at 1–2 g/kg is an
appropriate initial dose for decontamination, and a second half dose after ~6–8 hr
may be helpful. In addition, use of cholestyramine, a bile acid sequestrant, may be
useful to decrease the body burden of vitamin D3 that
undergoes enterohepatic recirculation with bile acids. However, the efficacy of
cholestyramine to reduce vitamin D3 levels in dogs has not
been determined. The recommended dosage is 0.3–0.5 g/kg, dissolved in liquid and
administered orally every 6–8 hr for 3–5 days, depending on the initial dose of
cholecalciferol ingested. Premature initiation of calciuresis (see below) may
disrupt normal calcium-phosphorus metabolism, triggering osteoclasts to move
additional calcium into the blood stream, artificially increasing serum calcium and
phosphorus levels and mimicking vitamin D3 toxicosis.
Once the biochemical values begin to increase, there are two
approaches to management. The first is to promote calciuresis by administering
normal (0.9%) saline at 2–3 times normal rates. Furosemide at 2.5–4.5 mg/kg, PO,
every 6–8 hr promotes calcium excretion but can also increase fluid loss (so
hydration status should be monitored). Prednisolone at 1–3 mg/kg, PO, bid-tid, can
reduce bone resorption as well as decrease calcium absorption from the intestine.
Treatment with a phosphate binder (aluminum hydroxide 30–90 mg/kg, PO, in divided
doses) to decrease phosphorus absorption and feeding a diet low in calcium should
also be considered.
The preferred treatment for persistent significant
hypercalcemia is pamidronate, an
injectable bisphosphonate that inhibits osteoclastic bone resorption. It is
administered at 1.3–2 mg/kg via slow IV infusion in saline over 2 hr. After
administration, as the calcium and phosphorus levels start to decrease, supportive
therapies (furosemide, prednisolone) should be tapered. A repeat dose may be
required if significant hypercalcemia redevelops.
In the past, use of salmon calcitonin (administered at 4–6
IU/kg, SC, every 2–3 hr) has been suggested to decrease calcium and phosphorus
levels, but this treatment is no longer used commonly. The two major disadvantages
are that some animals may become refractory to calcitonin, and that once this
therapy is instituted the use of pamidronate is not helpful.
Calcium and phosphorus levels should be monitored and treated
until they return to baseline. Treatment may have to be continued for days or weeks
because of the lipophilic nature of vitamin D3. Renal
function should be monitored, and other signs treated as needed.
Last full review/revision October 2014 by Safdar A. Khan, DVM, MS, PhD, DABVT; Mary M. Schell, DVM, DABVT, DABT