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Case Report
Journal of Veterinary Emergency and Critical Care
23(1) 2013, pp 58–62
doi: 10.1111/vec.12016
Ivermectin-induced blindness treated with
intravenous lipid therapy in a dog
Steven E. Epstein, DVM, DACVECC and Steven R. Hollingsworth, DVM, DACVO
Abstract
Objective – To report a case of blindness due to the ingestion of ivermectin and subsequent successful treatment
with intravenous lipid (IVL) therapy.
Case Summary – A female neutered Jack Russell Terrier was examined for acute onset of apparent blindness
after being exposed to ivermectin the previous day. The dog appeared to be blind during initial examination.
Pupillary light reflex, menace response, and dazzle reflex were not present in either eye. Fundic examination
revealed small areas of linear retinal edema. Electroretinography (ERG) showed diminished activity in both
eyes. Ivermectin was present in the serum on toxicological assay. Approximately 20 hours after exposure, IVL
was infused. Within 30 minutes of initiating the infusion, the pupillary light reflexes returned in both eyes, and
by the end of the infusion the patient behaved as if sighted. Fundic examination and ERG were unchanged at
this time. The dog was tested for the multidrug resistance gene mutation and was unaffected.
New or Unique Information Provided – Ivermectin toxicity occurs in dogs with apparent blindness being a
common clinical sign. This is the first case report of ivermectin-induced blindness evaluated with ERG before
and after treatment with IVL in a dog unaffected by the multidrug resistance gene mutation. Treatment with an
infusion of IVL therapy appeared to shorten the clinical course of disease in this patient without affecting ERG
results.
(J Vet Emerg Crit Care 2013; 23(1): 58–62) doi: 10.1111/vec.12016
Keywords:
intralipid, neurotoxin, toxicology
Introduction
An 11-year-old 10 kg female neutered Jack Russell Ter-
rier presented to the Small Animal Emergency Service
at the William R. Pritchard Veterinary Medical Teaching
Hospital of the University of California, Davis, for acute
onset blindness. The owners reported that the evening
prior to presentation the farrier was de-worming horses
with a product containing 1.87% ivermectinawith the
dog present in the pen. No abnormalities were noted
with the dog on the previous day. General physical ex-
amination findings on presentation were unremarkable.
The initial ophthalmic examination revealed a patient
who behaved as if unsighted; no menace response was
present in either eye and the patient ran into obstacles un-
der both photopic and scotopic conditions. Both pupils
From the Department of Surgical and Radiological Sciences, School of Vet-
erinary Medicine, University of California, Davis, CA.
The authors declare no conflict of interest.
Address correspondence and reprint requests to
Dr. Steven E. Epstein, Department of Surgical and Radiological Sciences,
School of Veterinary Medicine, University of California, Davis, CA 95616,
USA.
Email: seepstein@ucdavis.edu
Submitted September 25, 2011; Accepted November 25, 2012.
Abbreviations
ERG electroretinography
IVL intravenous lipid
GABA gamma-aminobutyric acid
MDR-1 multidrug resistance gene
PLR pupillary light reflex
were mydriatic in ambient light and the pupillary light
reflexes (PLRs) were absent.
A board certified ophthalmologist performed a com-
plete ophthalmic examination approximately 2 hours
after presentation to the emergency service, including
slit lamp biomicroscopy, indirect ophthalmoscopy, and
electroretinography (ERG).bBoth eyes were open and
appeared comfortable. No PLRs (either direct or consen-
sual), menace responses, nor dazzle reflexes were present
in either eye. No abnormalities were detected in the an-
terior segment or vitreous humor of either eye.
Fundic examination revealed small areas of linear reti-
nal edema ventral and medial to optic disk in the non-
tapetal area of both eyes (Figure 1). Following a 25-
minute period of dark adaption, an ERG was performed
58 CVeterinary Emergency and Critical Care Society 2013
Ivermectin-induced blindness treated with intralipid therapy
Figure 1: Retinal examination of dog with ivermectin-induced
blindness. The image depicts areas of retinal edema, right eye.
without sedation. Retinal responses from each eye were
assessed separately by use of a series of 8 red-light flashes
(findings were averaged). The b-wave amplitude was
75.56 v in the right eye and 33.89 v in the left (nor-
mal retinal function for this unit is >100 v). While the
specific origin of the ERG b-wave is controversial, it is
currently thought to be the result of retinal bipolar cell
activity.1, 2 In common practice, b-wave amplitude is con-
sidered the key indicator of retinal function.1–3
Results of a CBC were unremarkable. Serum biochem-
ical analyses showed no clinically significant abnormal-
ities. Serum was analyzed for macrocyclic lactones via
liquid chromatography-mass spectrometry with results
returning the following day positive for ivermectin at
1,500 parts per billion, but negative for abamectin, mox-
idectin, and selamectin. Testing for ABCB1-1or multi-
drug resistance (MDR)-1 allele mutation later revealed
that the dog was unaffected.
Approximately 20 hours after exposure and 3.5 hours
after clinical signs were noted, an IV catheter was
placed, and a 20% intralipid emulsioncwas administered
(1.5 mL/kg over a 10-minute period, then 0.25 mL/kg/
min for a 90-minute period). Thirty minutes after initi-
ation of the infusion, slight PLRs and a positive dazzle
reflex were noted. At the end of the infusion the patient
appeared to be sighted navigating around obstacles and
avoiding walls, had a positive menace response, but still
had bilateral mydriasis in ambient light. The linear ar-
eas of retinal edema were also still present. The ERG
was repeated and the b-wave amplitudes were similar
to the previous recordings with 55.83 v for the right eye
and 39.44 v for the left eye. The dog was discharged to
the owner the same day and has remained sighted ever
since.
Figure 2: Follow-up retinal examination of dog with ivermectin-
induced blindness. Same area of right eye as depicted in
Figure 1, 9 months after toxic event.
Approximately 9 months after initial evaluation the
dog was reexamined. General physical examination was
unremarkable except for a healing wound on the right
antebrachium. Ophthalmic examination revealed nor-
mal pupil size in ambient light, present and brisk direct
and consensual PLRs, and a positive menace response
and dazzle reflex in both eyes. There was no evidence
of any intraocular inflammation and the areas of retinal
edema had resolved (Figure 2). The patient easily navi-
gated a maze under both photopic and scotopic condi-
tions. An ERG was not repeated at this time due to equip-
ment malfunction. The patient subsequently returned for
an ERG 2 months later (approximately 11 months after
the initial evaluation). The b-wave amplitudes had im-
proved in both eyes to 86.39 v in the right eye and
84.17 v in the left.
Discussion
Ivermectin toxicosis is well described in dogs.4–10 A wide
variety of clinical signs can occur including blindness,
mydriasis, hypersalivation, ataxia, tremors, respiratory
failure, obtundation, and death. Some intoxicated ani-
mals may show apparent blindness with or without the
other generalized signs. The first reported retinal lesions
with presumed ivermectin toxicosis were in 2 dogs in
198911 and have been subsequently reported in another
dog with presumed ivermectin toxicosis12 and in 2 dogs
with confirmed ivermectin toxicosis.13 Blindness due to
suspected ivermectin ingestion has also been reported in
a mule foal.14
Ivermectin, avermectin, milbemycin, and moxidectin
are macrocyclic lactones and are commonly used in
CVeterinary Emergency and Critical Care Society 2013, doi: 10.1111/vec.12016 59
S. E. Epstein and S. R. Hollingsworth
veterinary medicine. Gamma-aminobutyric acid
(GABA) is an inhibitory amino acid neurotransmitter.
GABA receptors, when activated by either endogenous
GABA or ivermectin, cause cell membrane hyperpo-
larization via increased postysynaptic permeability to
chloride ions. This effect is resolved with the application
of picrotoxin, a GABA antagonist.16 A second proposed
mechanism for the action of ivermectin is by binding
glutamate gated chloride channels which similarly
causes inhibition of excitatory motor neurons.16 In
nematodes ivermectin results in rapid paralysis of
movement and inability to feed due to pharyngeal mus-
cle weakness resulting in death of the parasite.15 Clinical
signs of ivermectin toxicity in mammals are attributed
to this enhancement of neuronal inhibition.17,18
In mammals GABA mediated interneurons are largely
present within the CNS, but may also be present on
skeletal muscle and intestines.19 P-glycoprotein (P-gp)
is a large transmembrane protein encoded by the MDR-
1 gene, and is responsible for limiting the penetration
of ivermectin into the CNS. Toxicity in mammals re-
quires a much larger dose as compared with that ob-
served in nematodes.15 The exceptions are dogs with a
homozygous mutation in the ABCB1-1allele that show
increased sensitivity to ivermectin toxicosis.20 In dogs
without the ABCB1-1polymorphism, clinical signs of
toxicosis can occur at doses of 2.5 mg/kg.21 In this Jack
Russell Terrier who was negative for the ABCB1-1
polymorphism, the ingested dose was unknown.
The mechanism for ivermectin-induced blindness is
not known at this time. Reports in dogs suggest that reti-
nal pathology is involved in the process, but there may
be a nerve and cortical component as well. Most cell
types within the retina express GABA-ergic receptors22
and GABA is considered the primary inhibitory neuro-
transmitter of the mammalian retina.23 It is possible that
if ivermectin crosses the blood-retinal barrier, neurons
originating in the retina may be affected in a manner
similar to the CNS.
This case report is of particular interest for a number of
reasons. Because the dog had participated in a noninva-
sive clinical study about 6 months prior to the toxic event,
the dog had received a complete ophthalmic examina-
tion by the same veterinary ophthalmologist who later
examined this dog in connection with the toxic episode.
The dog had been found to be free of any ophthalmic
abnormalities at that time, although an ERG was not
performed. Similar to 1 dog in a previous report,13 and
a mule foal14 with suspected ivermectin-induced blind-
ness, this patient did not exhibit an extinguished ERG
reading even at presentation when she was blind and
lacked PLRs. This would seem to eliminate the retina
as the sole location for the changes in PLRs and vi-
sion loss and imply a multifactorial anatomic basis of
this disease. Additionally, after the administration of
intravenous lipid (IVL) therapy and subsequent return
of vision, this patient did not demonstrate a significant
change in fundic signs or ERG readings, and only a min-
imal improvement in PLRs. The fact that the dog had
a return to vision without a significant change in PLRs
would tend to rule out cranial nerve II as the location
of the toxic effect as a lesion here would probably af-
fect both PLRs and vision. Cranial nerve III dysfunction
could cause PLR abnormalities without affecting vision.
However, this would necessitate a lesion relatively dis-
tal in the course of the nerve, as more proximal lesions
would also cause ptosis and strabismus, or ivermectin
only affecting the superficial and medial layers of the
nerve. Taken together, this would suggest that the blind-
ness associated with ivermectin toxicity is not entirely
retinal in origin and likely partially cortical in origin,
with the PLR effects due to effects elsewhere.
Ivermectin-induced blindness occurred in 22% of sus-
pected or diagnosed canine ivermectin toxicosis cases re-
ported to the Animal Poison Control Center.24 The dog
in this report had exposure to ivermectin with simul-
taneous positive plasma levels for ivermectin confirm-
ing ingestion. Positive plasma levels may only be used
to confirm ingestion and are less important than brain
concentrations because the latter correlate more directly
with the clinical consequences of intoxication.25, 26 Cur-
rent treatment recommendations for ivermectin toxicity
are supportive in nature. Picrotoxin, a GABA antagonist,
was reported to aid the recovery of 1 dog with ivermectin
toxicity, but caused violent seizures and tachycardia and
is not currently recommended.27 Vision loss associated
with ivermectin toxicity is temporary, and anecdotally,
recovery is expected in 2–10 days28 although the exact
recovery time is unknown. As blindness can last many
days, animals are typically discharged to owners to wait
for vision to return which can create anxiety for owners
and potentially the patient. In this case, IVL therapy was
used, which was associated with a rapid return of vision
in less than 90 minutes.
The treatment of ivermectin toxicosis with IVL has re-
cently been described29, 30 although there are anecdotal
reports of its use for years. In one case of an ABCB1-1
unaffected Border Collie31 that presented with both oph-
thalmologic and neurologic symptoms, the dog’s dazzle
response returned within 6 hours. The PLR was incom-
plete and visual ability improved over the next 24 hours.
The return to vision appeared to take longer than the
time course for the case reported here, but in both cases
the dazzle response returned within hours of initiating
IVL therapy.
This seemingly positive response to lipid therapy was
not appreciated in 3 dogs that were homozygous for
the ABCB1-1gene mutation.30 This patient and the
60 CVeterinary Emergency and Critical Care Society 2013, doi: 10.1111/vec.12016
Ivermectin-induced blindness treated with intralipid therapy
Border Collie were negative for the mutation, yet both
appeared to have a clinical response to IVL therapy,
while 3 homozygous dogs did not. This raises the pos-
sibility that IVL therapy may only be helpful if the dog
is not a homozygous mutant. Possible support for this is
that P-gp is expressed in renal tubular epithelial and bil-
iary canalicular cells,31 which may reduce the excretion
rates during ivermectin toxicosis in ABCB1-1homozy-
gous mutant dogs. P-gp also transports ivermectin from
the brain into the blood. Without this ability, homozy-
gous mutant dogs would rely solely on a concentration
gradient for diffusion of ivermectin from the brain into
the infused lipid. Without P-gp, the ivermectin parti-
tioned in the circulating lipid could back diffuse into
the brain, limiting the potential helpful effects of IVL
therapy. In wild type dogs, ivermectin transport into cir-
culating lipid may be an active process and back diffu-
sion into the brain would be limited. Further investiga-
tions are needed to investigate the role of IVL therapy in
ABCB1-1homozygous mutant dogs.
Intravenous lipid has also been used in the treatment
of moxidectin toxicosis in a puppy, which may have
shortened the clinical course of disease,32 and recently
IVL therapy was used to treat successfully lidocaine tox-
icity in a cat.33 In human medicine, IVL infusions have
been used to treat toxicities for lipid soluble drugs such as
local anesthetics,34, 35 a severe case of organophosphate
poisoning,36 antidepressants,37–40 and cardiac drugs.41–43
The mechanism by which lipids improve clinical signs
of toxicity associated with the macrocyclic lactones is
unclear. A proposed mechanism is through a “lipid
sink” where ivermectin is removed from the CNS or
retina by sequestering it into the plasma lipid phase. If
a drug is lipophilic, theoretically this allows a higher
drug concentration in the plasma with less available
to be toxic in the tissues. A drug is deemed lipophilic
if its log Pis >1.0. This “lipid sink” theory is sup-
ported with increasing plasma levels of clomipramine,37
mepivacaine,44 bupropion,39 and ivermectin29 when tox-
icoses are treated with lipid emulsions. The log Pfor
these drugs are 3.30, 1.89, 3.47, and 3.50, respectively.45
Although 20% intralipid solutions have been used in
parenteral nutrition safely, there is no clinical evidence
on safety of short-term large boluses of lipid solutions.
Short-term infusions of soybean oil-based lipid emul-
sions have been shown to decrease neutrophil function
in dogs.46 Other potential adverse effects are pancreati-
tis, fat emboli, phlebitis, and hypersensitivity reactions.
However, no adverse outcome related to IVL therapy
for the treatment of intoxication has been reported ex-
cept for laboratory difficulty in analyzing lipemic blood
samples.47
The optimal dose of intralipid for IVL therapy
is unknown. The dose of 1.5 mL/kg bolus then
0.25 mL/kg/min was chosen based on this being the
most commonly cited dose in human case reports. A re-
view of IVL therapy to treat local anesthetic toxicity in
humans suggests a dose of 1.5 mL/kg bolus that can be
repeated up to 3 times in cardiac arrests then 0.25–0.5
mL/kg/min.48 On this basis it is reasonable to use this
dose in veterinary medicine as well until further studies
show an optimal dose.
The present case report shows a definitive diagnosis of
ivermectin ingestion with acute onset of blindness that
resolved temporally after a lipid infusion. The patient’s
fundic changes were not altered with lipid therapy, nor
were the ERG results different, despite an apparent clin-
ical improvement. The improvement observed in this
patient however cannot definitively be attributed to the
IVL therapy. Further assessment of plasma levels would
have been useful to support a “lipid sink” theory, but
as they do not necessarily correlation to brain levels or
clinical signs, they were not performed. At this time IVL
therapy appears to be a reasonable treatment option for
ivermectin-induced blindness although its safety and ef-
ficacy in canine patients has not been fully determined
at this time. Further studies on the benefit of lipid emul-
sions to treat lipid soluble toxicities such as ivermectin
are indicated.
Footnotes
aDuramectin Paste, Durvet, Blue Springs, MO.
bRetinoGraphics, Inc., Norwalk, CT.
cIntralipid, for Baxter Healthcare Corporation by Fresenius Kabi, Uppsala,
Sweden.
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62 CVeterinary Emergency and Critical Care Society 2013, doi: 10.1111/vec.12016
