hi i'm dr carrie hemelgarn i just wanted to introduce you to module 5.
this module we're going to be talking about rodenticides the different types
how we're going to treat it and the overall prognosis thank you for joining us
so for module 5 we're going to talk about rodenticides we're going to talk about the
anticoagulant type bromethylene zinc phosphide and cholecalciferol there are four main categories of
rodenticides that they fall into and that's based on their mechanism of action in 2008 the u.s epa
issued a decision to prohibit second generation anticoagulant rodenticide in residential sites
this causes a change in the rodenticide exposure that we see in our pets ideally we would like to
see more anticoagulant redenticide used if any were going to be used but that's not where the
epa trends are falling so the four categories of rodenticide are anticoagulant rodenticide
bromethylin cholecalciferol and phosphides decontamination is the same for all four
rodenticides emissions should be induced if the ingestion was recent usually we say if that's
less than two hours if it's been greater than two hours since ingestion emesis may not be useful
but if a large dose was ingested we may still recommend to hopefully get anything out we can
activated charcoal is recommended post-semesis to prevent further exposure
if the type of rodenticide is known then treatment recommendations should be followed for that type
of rodenticide and based off of clinical signs and a quantity of that rodenticide that could have
potentially been adjusted unfortunately we don't always know what type of identicide they get into
and all of them look very similar as in they are a small green turquoise colored block
if the type is unknown then they have to be treated for all four types of rodenticide
anticoagulant rodenticides are divided into group on how long they stay in an animal system
the first generation of anticoagulant rodenticides lasts for 14 days and that's going to be warfarin
cumural for all and pinadione
bromadialone lasts for 21 days in their system and that's a second generation and other types
of second generation anticoagulants can last up to four weeks in their system the second generation
anticoagulants include comb chlorophenous ion diaphinicom diaphenolone diaphenodione and
valone anticoagulant rodenticides work to inhibit the production of clotting factors 2 7 9 and 10
by inhibiting the vitamin k1 epoxide reductase the first clotting factor affected is factor 7
because it is the shortest half-life and if coagulopathy is going to be seen
it would be within 36 to 72 hours of ingestion of the anticoagulant rodenticide
if a patient has recently ingested anticoagulant rodenticide emesis and activated charcoal should
be given and the patient should be started on vitamin k1 oral therapy for 30 days
usually recommended at 2.5 mix per kid twice a day or five migs per keg once a day as a daily dose
then have clotting factors checked 48 hours after the last dose so that's 32 days post-ingestion
coagulation testing should not be done at presentation if a pet has just ingested the
rodenticide if a patient presents with hemorrhage or concerns for coagulopathy and rodenticide
is a possibility then clotting time should be checked in these cases the patient should have
clotting times particularly their pro-thrombin time to see if it's prolonged if it's prolonged
it's potentially consistent with rodenticide toxicity if there's any possible exposure
pending the patient's cardiovascular stability packed red blood cell transfusions may be needed
if anemic and if are symptomatic for their anemia if the patient is not anemic or symptomatic but
has prolonged clotting times we normally consider that greater than 1.5 times the baseline then
fresh frozen plasma is indicated in these patients and if they are anemic they may need fresh frozen
plasma and a packed red blood cell transfusion a coagulopathy should be corrected before doing
advanced procedures such as a thoracocentesis for pleural effusion as you can cause worsening
bleeding if we have not corrected their clotting factor deficiency these patients also need to be
started on oral or injectable vitamin k1 therapy for 30 days and again they need to have their
clotting factors checked 48 hours after the last dose bromethylene is a neurotoxic rodenticide
its mechanism of action is that it affects the mitochondria in the liver and the brain
it causes decreased atp production which causes sodium and potassium pumps
to fail and lead to intracellular sodium buildup that is responsible for seeing neurologic signs
the intracellular sodium buildup leads to cellular death and associated cellular edema unfortunately
unlike the anticoagulant rodenticides there is no antidote for this toxicity so
early emesis and decontamination with activated charcoal is incredibly important to try to
minimize this toxicity the median lethal dose per pet poison hotline for dogs is 2.38 to 3.65
migs per gig with a minimum lethal dose has been noted as little as 2.5 migs per kick
cats unfortunately are more susceptible and need a lower dose of this rodenticide to cause clinical
signs and the medium median lethal dose in cats is .45 megs per gig clinical signs can occur within
two hours but can last up to and potentially not be seen for up to 24 hours after ingestion
and the clinical signs we're expecting to see is ataxia depression hyperaesthesia seizures and in
some cases coma some dogs that get into sublethal doses can have delayed onset of clinical signs
and it can take days after ingestion for the same clinical signs to appear
or that they can show up weeks after ingestion sometimes the clinical signs can appear and then
progress for one to two weeks after ingestion so there's a few different clinical manifestations
lastly some pets can develop delayed paralysis which is a coma-like state
that can take them weeks to recover from when they ingest from methylene treatment
involves early emesis and decontamination with multiple doses of activated charcoal
if clinical signs appear treat supportively with iv fluids anti-seizure medications and
if there is concern for intracranial edema then corticosteroid dose would be recommended
if there's concern for intracranial hypertension a dose of mannitol could be recommended and
unfortunately the prognosis is very poor once neurologic signs have been present and
unfortunately if the signs are progressive then it is most likely going to be fatal
cholecalciferol or vitamin d3 is another type of rodenticide and it's become more popular
as anticoagulant rodenticides are slowly being phased out in residential areas cholecalciferol
is involved in the calcium hemostasis in our body when this rodenticide is ingested
it causes unregulated calcium absorption from the gi tract and their bones and this leads
to marked hypercalcemia and hyperphosphatemia in our pets these electrolyte changes unfortunately
lead to ultimately why we see neurology why we see clinical signs which is that these electrolyte
changes lead to acute kidney failure and soft tissue mineralization within days after ingestion
clinical signs that we can see with cholecalciferol toxicity include depression
weakness anorexia vomiting increased thirst increased urination and pretty severe dehydration
the blood work is going to show what we would expect for it to show which is elevated calcium
phosphorus and esotemia secondary to acute kidney failure
treatment if known ingestion has happened recently then emesis has recommended
and activated charcoal administration to try to prevent any further absorption
the toxic dose in our pets can be as little as 50 micrograms per kilogram so a very small amount
if clinical signs are present treatment involves iv fluids anti-aemetics sometimes corticosteroids
loop diuretics and bisphosphonates as clinically indicated the prognosis is good with early
treatment before hypercalcemia and azatemia are noted but it's guarded to very poor if
these are already noted when we diagnose pets with this the last rodenticide we're going to
talk about is phosphide rodenticide which is a rare rodenticide thankfully when zinc phosphide
is ingested it interacts with our gastric acid and creates phosphine gas which is incredibly
toxic phosphine gas is absorbed across the gastric mucosa and absorbed throughout the body but its
most concentrated toxic effect that we note is on tissues that have a really high oxygen demand
so the tissues that we're talking about that are most affected by this toxicity
is going to be our brain our lungs liver kidneys and unfortunately the central nervous system
clinical science can occur hours after ingestion which include profuse vomiting depression
dull quiet or abnormal mentation lethargy tachypnea and tachycardia this is one that
we talked about in the first or in the second module in that we have to take extreme care if
we think pets have gotten into this when we induce vomiting in a veterinary hospital because it is
something that that phosphine gas can be inhaled by our veterinary team and cause clinical signs
so we need to take care that if we are going to induce vomiting in a patient that could
have eaten i think phosphide bait that the gas is toxic and therefore we need to do this in an open
well ventilated area so potentially outside or in an area that has fans going to increase
air circulation treatment is supportive for the clinical science and the prognosis is good if
the pet is asymptomatic 8 to 12 hours after ingestion the prognosis is variable depending
on the severity of clinical signs but if the security of clinical signs is very poor then
unfortunately there is possibilities that this can be fatal in pets so this finishes
up our module on rodenticides thank you so much for joining us the next module is going
to be on human medications over the counter and prescription that pets potentially could ingest
you