References

Aldridge P, O'Dwyer LWest Sussex: Wiley-Blackwell; 2013

Bill R Common toxicoses in small animal practice: a guide for the veterinary nurse. The Veterinary Nurse. 2013; 4:(10)610-17

Boag A, Hughes D Fluid therapy. In: King LG, Boag A (eds). Gloucester: BSAVA; 2011

Crandell DE, Weinberg GL Moxidectin toxicosis in a puppy successfully treated with intravenous lipids. J Vet Emerg Crit Care. 2009; 19:(2)181-6

Davis J Decubitus ulcer: risk factors, prevention and treatment. The Veterinary Nurse. 2011; 2:(3)130-9

Duke T Partial intravenous anaesthesia in cats and dogs. Canadian Veterinary Journal. 2013; 54:276-82

Epstein SE, Hollingsworth SR Ivermectin-induced blindness treated with intravenous lipid therapy in a dog. J Vet Emerg Crit Care. 2013; 23:(1)58-62

Parker VJ Nutritional management of hospitalised dogs and cats. The Veterinary Nurse. 2013; 4:(8)478-85

See AM, McGill SE, Raisis AL, Swindells KL Toxicity in three dogs from accidental oral administration of a topical endectocide containing moxidectin and imidacloprid. Aust Vet J. 2009; 87:(8)334-7

Sherman J, Olby N, Halling KB Rehabilitation of the neurological patient. In: Platt S, Olby N (eds). Gloucester: BSAVA; 2013

Snowden NJ, Helyar CV, Platt SR, Penderis J Clinical presentation and management of moxidectin toxicity in two dogs. J Small Anim Pract. 2006; 47:620-4

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Ueda Y, Odunayo A, Mann FA Comparison of heparinzed saline and 0.9% sodium chloride for maintaining peripheral intravenous catheter patency in dogs. J Vet Emerg Crit Care. 2013; 23:(5)517-22

Vanapalli SR, Hung YP, Fleckenstein L, Dzimianski MT, McCall JW Pharmacokinetics and dose proportionally of oral moxidectin in beagle dogs. Biopharm Drug Dispos. 2002; 23:263-72

Weinberg G Lipid rescue resuscitation from local anaesthetic cardiac toxicity. Toxicology review. 2006; 25:(3)139-45

Moxidectin intoxication in a dog — a patient care report

02 April 2016
8 mins read
Volume 7 · Issue 3

Abstract

This article discusses a patient who suffered a moxidectin intoxication from the oral administration of Advocate. Presenting clinical signs, treatment and recovery of the patient will be discussed in reference to the role of the veterinary nurse. This report also highlights the importance of owner education for administering parasitic preventative treatment.

The patient presented as an emergency with an acute onset of tremors, ptyalism, visual impairment and disorientation; all of which started 24–36 hours prior to presentation.

Signalment

  • Species: Canine
  • Breed: Springer Spaniel
  • Sex: Female (neutered)
  • Age: 8 years
  • Weight: 14.6 kg

Patient assessment

On admission to the ward area, the patient was very disorientated, ambulatory but severely ataxic and salivating profusely. The physical examination revealed congested and tacky mucous membranes, pyrexia and tachycardia. The neurological examination revealed moderate tremors, severe ataxia, severe mental depression and hyperaesthesia.

The clinical history revealed that an accidental oral administration of the anti parasitic spot on treatment Advocate® (Bayer) had occurred 48 hours previously. The dog was given Advocate for large dogs which contains 250 mg of imidacloprid and 62.5 mg of moxidectin. The clinical signs and history were therefore suggestive of moxidectin intoxication. The same clinical signs were seen in a canine patient in a case report of accidental oral administration of Advocate reported in Australia (See et al, 2009). The active ingredients are imidacloprid and moxidectin which inhibit acetylcholine binding at the neuromuscular junction's post synaptic membrane and inhibit neurotransmission respectively (See et al, 2009).

In comparison to infectious diseases, the acute onset of clinical signs with toxins is rapid and often a little ambiguous, obtaining a detailed history is therefore crucial to reach an early diagnosis (Bill, 2013).

Veterinary investigations

A blood sample was taken from the patient's left jugular vein to provide an emergency database. The tests included haematology, biochemistry, electrolytes and a coagulation profile. Laboratory findings were normal except for mild hypernatraemia, indicative of free water loss (See et al, 2009).

Nursing interventions

This patient required intense nursing care during the 36-hour hospitalisation period, which involved many different nursing interventions. These included administering and monitoring a propofol (Rapinovet, Norbrook) constant rate infusion (CRI), administering intravenous fluid therapy, nutrition and assisting with mobility.

CRI administration

CRIs are commonly used in veterinary practice and veterinary nurses are often required to set up, administer and monitor these infusions (Taylor, 2014). Following admittance, a cephalic intravenous catheter was placed and the clinician administered a bolus of propofol to effect. The patient was then started on a CRI of propofol which was to be maintained overnight with the use of a syringe driver. This required the author to set the desired infusion rate which was decided by the clinician. Syringe drivers allow the required infusion rate to be programmed and amended easily (Duke, 2013).

Propofol is commonly used to induce anaesthesia and therefore can be administered as a total intravenous anaesthesia agent (TIVA); it can also be used as a partial intravenous anaesthesia agent (PIVA) (Taylor, 2014). Critical care settings have demonstrated the use of propofol using low infusion rates, to achieve a sedation level of central nervous system (CNS) depression rather than an anaesthetic level (Duke, 2013). It was necessary for this patient to ensure the CNS dysfunction was treated with an anaesthetic agent, at a rate that diminished clinical signs without causing adverse effects to the cardiovascular or respiratory system (Snowden et al, 2006). Critical nursing care was required to monitor this patient on the propofol CRI which was being administered as a PIVA. It was essential to maintain a level of sedation that prevented the clinical signs from returning. A dedicated nurse remained with this patient overnight recording hourly vital parameters and observations of the patient's clinical status.

The following day the propofol CRI was stopped by the clinician as the patient was more alert and responsive. The pyrexia and tachycardia had resolved but the ataxia was still severe. Another peripheral intravenous catheter was placed in the remaining cephalic vein, to administer a bolus and CRI of 10% Intralipid® (Fresenius Kabi) emulsion. This lipid emulsion contains soyabean oil which is often used as the fat component for parenteral nutrition (Crandell and Weinberg, 2009). Moxidectin is reported to be lipophilic in nature and is stored in fat (Vanapalli et al, 2002); this makes intralipid an appropriate treatment to remove the moxidectin from the dog's plasma.

The bolus of intralipid given was 3 ml/kg over 10 minutes and the CRI 0.5 ml/kg/minute for 30 minutes. A case report that used intralipid emulsion for a dog that ingested ivermectin used a 20% solution with a bolus of 1.5 ml/kg over 10 minutes and a CRI at 0.25 ml/kg/minute, demonstrating a similar treatment protocol (Epstein and Hollingsworth, 2013). The optimal doses required for canine patients are unknown and based on human literature for treatment of local anaesthetic toxicities (Epstein and Hollingsworth, 2013).

After the intralipid CRI finished, the patient's coordination had greatly improved and the only remaining clinical sign was mild tremors in the hind limbs. The patient began interacting with people once the visual impairment resolved. In a case report of ivermectin-induced blindness in a dog, it was reported the patient's sight returned following intralipid administration (Epstein and Hollingsworth, 2013).

Fluid therapy and nutrition

During the physical examination, dehydration was apparent as the patient presented with tacky mucous membranes, tachycardia and hypersalivation and had not consumed food or water for more than 24 hours. Moxidectin and imidacloprid are reported to have a rapid gastrointestinal absorption, and peak plasma concentrations are reached within 3 hours (Vanapalli et al, 2002). Intravenous fluid therapy (IVFT) was therefore initiated at the same time as the propofol CRI. The isotonic crystalloid solution Lactated Ringer's solution (Hartmanns, Aquapharm) was administered at the maintenance rate of 2 ml/kg/hour. This treatment was indicated to restore normal water balance in the patient (Boag and Hughes, 2011), in addition to the propofol CRI preventing food and water being offered overnight.

Nursing care was required to ensure safe administration of the fluid was maintained. To minimise the risk of fluid overload, a fluid pump was used to ensure accurate administration. Complications with administering fluid therapy can include catheter occlusion and phlebitis (Ueda et al, 2013). Catheter occlusion is believed to arise for reasons such as catheter site infection and prolonged catheterisation (Ueda et al, 2013). The intravenous catheters were in situ for 24 hours so no complications arose. Daily checks of the intravenous catheter were made to ensure patency and cleanliness. This included a protective bandage that was replaced twice daily and if it became soiled. The catheter site was checked for oedema and signs of infection which never became apparent.

IVFT was continued throughout most of the 24 hour hospitalisation of this patient. The hydration status greatly improved within 12 hours which was evident by a decrease in heart rate and a normal mucous membrane appearance. The propofol CRI was stopped after 12 hours and the decision was made to wake the patient up and attempt to encourage them to eat. If this was unsuccessful, the placement of a feeding tube would be considered. Voluntary food and water intake returned after approximately 18 hours of hospitalisation. Nutritional support for hospitalised patients is essential, to ensure they are provided with an appropriate calorie and nutrient intake (Parker, 2013).

Recumbency

Although the patient was ambulatory on admission, the ataxia was quite severe and therefore prevented adequate coordination. Vision impairment was also a contributing factor to the reduced mobility. The first day of hospitalisation did not permit exercise due to the propofol CRI. The patient was therefore recumbent during the first 15 hours and as a result was at risk of secondary problems developing such as atelectasis and decubitus ulcers. Patient positioning for recumbent patients is a very important nursing consideration to maximise oxygen exchange and prevent decubitus ulceration (Aldridge and O'Dwyer, 2013).

A high number of emergency patients are recumbent for part of their hospitalisation period which is either medically induced or caused by a condition or disease process. In this case, the propofol CRI was intended to sedate the patient for the first night and therefore atelectasis was a risk. Collapsing of the lung lobes can result from remaining in lateral recumbency for a prolonged period of time and therefore reducing gaseous exchange (Aldridge and O'Dwyer, 2013). The patient was propped in sternal recumbency and the back end was turned every 4 hours alternating from right and left lateral for the prevention of both atelectasis and to help prevent ulcers (Sherman et al, 2013).

Decubitus ulcers can appear from prolonged pressure on an area of skin where the weight of the patient exerts pressures on their joints or muscles against a surface, most commonly in recumbent patients (Davis, 2011). Identifying patients that are at risk, helps prevent the problem occurring (Davis, 2011). Prevention of decubitus ulcers can be easily achieved by the veterinary nurse, by ensuring the patient has adequate bedding material and is not left in the same position for more than 2 hours. Prevention is better than cure (Sherman et al, 2013). The patient in this report was therefore provided with an orthopaedic mattress with a thick vet bed, which also prevented urine scalding as they are made from a wicking material so therefore soak up any bodily fluids (Tompkins, 2013). Bedding was checked every 2 hours to ensure the patient's skin was not in contact with any excrement.

Once the propofol infusion had been stopped, the nursing team encouraged the patient to walk voluntarily to observe the level of ataxia and record any improvements seen. With regards to the patient's demeanour — she was more alert and aware of her surroundings which helped with her walking but the ataxia was still quite severe. Following the intralipid CRI the ataxia greatly reduced and was no longer present at time of discharge. The patient's sight had also fully returned. The total hospitalisation period for this patient was only 24 hours from initial presentation and there have been no long-term clinical abnormalities. The time period of hospitalisation in a study of three dogs suffering from oral administration of moxidectin was similar to this patient. The time ranged from 12–42 hours post admittance also with no long-term clinical abnormalities (See et al, 2009).

Moxidectin

Moxidectin is a macrocyclic lactone of the milbemycin family and is closely related structurally to the avermectin family, an example is ivermectin (Snowden et al, 2006).

The mechanism of parasiticide action is by selectively binding to a parasite's glutamate-gated chloride ion channels, therefore inhibiting neurotransmission (See et al, 2009). It is used in veterinary medicine for canine heartworm prophylaxis and large animal endoparasitism (Crandell and Weinberg, 2009).

In this case, the dog ingested moxidectin due to incorrect administration of the drug by the owner. Toxicity can also be caused from ingestion of faeces from animals that have been treated with the drug, or from consuming food that contains the drug. Moxidectin used in horses as an anti-parasitic is palatable to dogs and therefore toxicity may be more commonly seen with dogs in close contact with horses (Snowden et al, 2006).

Recommendations for future practice

Client education on how to administer anti-parasitic drugs is essential to prevent scenarios like the one described in this patient care report. Despite cautionary labelling such as ‘Spot on treatment’ and ‘External use only’ being printed on the packaging, perhaps a warning sign or a message is necessary to increase awareness of the life-threatening complications that can arise from incorrect administration of the drug. A published article discusses a clinical case where a feline patient was administered a canine spot on flea treatment containing permethrin, despite the packaging displaying a warning sign that reads ‘do not use on cats’ (Tompkins, 2013). This article discusses research that highlights a large number of cases of toxicosis from this drug, some of which resulted in fatalities.

The true number of cases that present with toxication of parasitic treatments will always likely exceed the reported figure, due to a number of cases not being reported or incorrect diagnoses being made due to a lack of patient history. The author believes that future cases of moxidectin toxicity should be actively reported, to enable a more accurate representation of the frequency and number of companion animals that are affected by incorrect administration of Advocate and other antiparasitic treatments. The main priority should however be focusing on owner education and increasing awareness which will hopefully reduce the number of affected animals.

Identifying the cause of the neurotoxicity and treating appropriately is paramount, to increase the prognosis for the affected canine patients (Snowden et al, 2006).

Conclusion

Intravenous lipid therapy rapidly reversed the signs of toxicity in this patient and there is some research supporting its use for treating patients that have ingested moxidectin and/or ivermectin. Crandell and Weinberg (2009) believe that a puppy suffering from moxidectin toxicosis made a complete recovery from the clinical signs of toxicity in a short time period due to intralipid administration. Human literature has also demonstrated the use of intralipid therapy for local anaesthetic toxicities and other fat soluble toxins (Weinberg, 2006).

Key Points

  • Client education on how to correctly administer anti-parasitic drugs is essential.
  • Intravenous intralipid therapy can rapidly reverse neurotoxicities resulting from an intoxication.
  • Critical nursing greatly aids a patient's recovery and prognosis.