Intensive nursing care provided to a patient with permethrin toxicosis

Reason for admission

The patient was found collapsed outside the owner's home and was presented to the hospital with cold extremities, profuse diarrhoea and active muscle tremors. The owner had applied a canine permethrin-based spot on flea treatment the previous evening.

Major body systems assessment

Following presentation to the veterinary practice, the major body systems were assessed.

Veterinary investigations

A blood sample was obtained to provide an emergency database, which enabled evaluation of the patient's clinical status and provided baseline parameters. This included measurement of haematological and biochemical parameters. The emergency database demonstrated a moderate leukocytosis (white blood cell count 28.48 x 10⁹/l (5.0-18.0 x 10⁹/l)) with neutrophilia and lymphopenia; results were consistent with a cortisol-mediated stress leukogram (Gilor and Gilor, 2011). All other parameters were within reference range.

Problem list

After initial patient assessment a medical problem list was generated to enable prioritisation of patient care:

Aims of intensive nursing care

The aims of intensive nursing care were identified as:

Initial management/veterinary interventions

A 22 g intravenous catheter (Jelco, Smiths Medical) was placed in the left cephalic vein. Fluid therapy was initiated at a rate of 60 ml/kg for the first hour, using an isotonic crystalloid solution (compound sodium lac-tate (Aquapharm No11, Animalcare Ltd)). Fluid therapy was administered at incremental doses of 10 ml/kg given over 10 minute intervals. Fluid therapy was administered to clinical effect and evaluated by frequent physical examination to end points of resuscitation, as suggested by Brown and Otto (2008). End points of resuscitation were determined as improvement in mucous membrane colour and capillary refill time, restoration of pulse quality, reduction in heart rate and improvement in patient mentation. Methocarbamol (Robaxin-V; Fort Dodge) 40 mg/kg was crushed with saline and administered rectally, diazepam (Hamelin Pharmaceutical Ltd) 1 mg/kg was administered intravenously; both were administered to reduce muscle tremors through musculoskeletal relaxation.

Discussion

Permethrin is a Type 1 pyrethroid, a synthetic derivative of natural pyrethrins. Permethrin is an active ingredient in some over-the-counter insecticide products (Table 1). Permethrin is considered a neurotoxin (Sutton et al. 2007). Following application permethrin binds to sodium channels in the nerve axon, causing these channels to remain open for longer than normal. This results in changes of sodium movement across the membrane producing repetitive discharge of the nerves, which gives rise to the clinical signs of seizures or tremors observed in permethrin toxicosis (Schleier III and Peterson, 2011). Permethrins are lipophilic compounds (Boland and Angles, 2010) which are metabolised by glucouronide conjugation by the liver (Anadon et al. 2009). Dymond and Swift (2008) suggest cats are more likely than dogs to present with permethrin toxicosis because the feline liver has limited amounts of glucouronide transferase enzyme necessary for permethrin metabolism by glucouronide conjugation. Sutton et al (2007) predicted, based on a 3-month prospective study of reported cases of permethrin toxicosis to the Veterinary Poisons Information Service (VPIS) London and assuming that reports remained consistent, that 288 cases of permethrin toxicosis would be reported per annum. These figures are presumptive, and true figures may be under represented. Malik et al (2010) conducted a study of 750 reported cases of permethrin toxicosis to the Australian Pesticides and Veterinary Medicines Authority (APVMA) over 2 years, 22% of which resulted in fatalities. Potential routes of feline exposure include direct application of a permethrin-based product authorised in dogs and ingestion of permethrin-based product, for example contact or grooming of a dog within the household who has had recent application of a permethrin-based product.

When fluid is lost from the extracellular space, for example with gastrointestinal losses (profuse diarrhoea), fluid movement occurs from the intravascular space as a compensatory response to maintain an effective circulating volume (DiBartola, 2012). Further compensatory responses are initiated by stimulation of the sympathetic nervous system including peripheral vasoconstriction and an increase in heart rate to attempt to restore vascular volume and blood pressure therefore improve perfusion (Welsh and Girling, 2004). Dehydration secondary to profuse diarrhoea can cause significant fluid loss from the extracellular space; subsequently hypovolaemia with secondary hypotension may be observed (Brown and Otto, 2008). The therapeutic goal of fluid therapy in this patient was to re-establish normal circulating volume and therefore arterial blood pressure (Boag and Hughes, 2005), rehydrate the patient to restore extravascular volume and correct whole-body fluid homeostasis. Re-establishment of arterial blood volume and home-ostasis will correct local and systemic hypoperfusion.

As recommended by Pachtinger and Drobatz (2008) an isotonic crystalloid solution, compound sodium lactate, was administered which provided replacement of the intravascular volume deficit. The initial volume administered was titrated to effect, a bolus of 10 ml/kg was given over a 10 minute interval and the patient was assessed after each bolus to determine clinical improvement. A reduction in heart rate, restoration of normal mucous membrane colour and capillary refill time, improvement in pulse strength and mentation were considered consistent with improvement in circulating volume, although such variables are considered subjective. More objective assessment of parameters including central venous pressure (CVP), arterial blood pressure (ABP) and quantification of urine output may have been beneficial (Pachtinger and Drobatz, 2008); however the veterinary surgeon (VS) elected not to monitor these parameters during initial stabilisation. A fluid pump was used to ensure accurate administration of fluids and minimise the risk of volume overload.

After initial stabilisation, fluid therapy was continued to provide maintenance requirements and attenuate on-going losses. Dymond and Swift (2008) and Anadon et al (2009), both advocate provision of fluid therapy to maintain intravascular volume, hydration and to prevent renal tubular damage associated with myoglobin breakdown products, which could be released from damaged muscles due to prolonged or severe muscle tremors.

The patient was presented in a hypothermic state (34.1^°C); in response to hypothermia the posterior hypothalamus stimulates peripheral vasoconstriction to conserve core body temperature (Oncken et al. 2001) with consequential hypotension and poor peripheral perfusion (Kirby, 2004). Boland and Angles (2010) also suggest that hypothermia could increase permethrin activity at the sodium channels, which may exacerbate the adverse effects of permethrin toxicosis, although an internal body temperature below 25^°C may be necessary to produce such effects. Re-warming was initiated using a paediatric incubator set to 32^°C and 50-60% humidity, and core body temperature was monitored using an indwelling rectal probe. Armstrong et al (2005) advocate the use of a forced air warming blanket (i.e. Bair Hugger, Advanced Anaesthesia Specialists UK Ltd) to provide active surface warming and minimise heat loss. Although, a Bair Hugger was available it was decided that patient placement in the incubator was preferable. This enabled constant observation of the patient which may have been restricted if the Bair Hugger had been used. Core body temperature monitoring was continued beyond achievement of normothermia as repetitive and vigorous muscular activity due to prolonged or severe muscle tremors, which could also impair adequate ventilation, may predispose the patient to hyperthermia, hypercapnia, hypoxemia and metabolic acidosis (due to lactic acid release) which without intervention could produce central nervous damage (Dymond and Swift, 2008; Anadon et al. 2009).

A number of authors recommend dermal decontami-nation to minimise further exposure to permethrin (Sutton et al. 2007; Dymond and Swift, 2008; Linnett, 2008; Anadon et al. 2009); it is advocated that luke-warm water is used as hot water could cause dilation of the peripheral vessels and potentially increase permethrin absorption. Anadon et al (2009) and Sutton et al (2007) further recommend the use of a mild detergent to aid dermal de-contamination as permethrin is a lipophilic compound insoluble in water. Due to the patient's hypothermic state the patient was bathed only at the site of application using luke-warm water and a mild detergent. The patient was dried thoroughly to prevent further heat loss through evaporation. An Elizabethan collar was placed to prevent self grooming, to minimise the risk of secondary exposure through oral absorption.

As the patient was initially non ambulatory and recumbent, padded and absorbent bedding was provided to optimise patient comfort and minimise soiling in the event of urination. The patient was placed on a VetBed (Petlife International Ltd) to ensure provision of padded bedding and enable any urine passed to wick away from the patient. Patient bedding was checked at regular intervals to ensure any urine or faeces passed were removed to prevent urine and faecal scalding, and minimise moisture contact with the patient's skin. The patient was turned every 2 hours to prevent the development of hypostatic pneumonia, atelectasis and decubitus ulcers. Hypostatic pneumonia is caused by reduced pulmonary perfusion, commonly attributed to prolonged pressure as a result of gravity on a dependent side which decreases pulmonary blood flow and can promote atelectasis and possibly pulmonary oedema if the thin-walled pulmonary venous vasculature is compressed (Elphee, 2011). Tefend (2002) and Boland and Angles (2010) both suggest that the patient should be positioned and supported in sternal recumbency, to facilitate respiration and mini-mise hypostatic congestion, however, with seizure activity and frequent muscle tremors it was difficult to maintain the patient in a sternal position. It was decided that frequent turning and placement of the patient in lateral recumbency with head and neck extended, to maintain airway patency, was preferable. Decubitus ulcers can occur as a consequence of a patient's bodyweight exerting pressure on the skin over a bony prominence resulting in local or regional tissue ischaemia and necrosis (Tefend, 2002). Although, this may be considered of greater relevance in patients with a larger bodyweight than a feline patient it is an important consideration for any patient with prolonged episodes of recumbency. Friction, shearing, moisture and ischaemia may also provide further contributing factors in the formation of decubitus ulcers (Campbell and Parish, 2010). If a patient is immo-bile for more than 2 hours the patient may be at risk of decubitus ulcer formation (Bansal et al. 2005). Campbell and Parish (2010) consider that the intervention of repositioning a patient every 2 hours is based on anecdotal evidence and suggest further research and evaluation is necessary to provide an evidence base and determine the optimal frequency of repositioning. However, frequent patient repositioning will minimise the potential for complications associated with prolonged recumbency and pressure on a dependent side. An ocular lubricant carbomer (Gel Tears; Chauvin Pharmaceuticals Ltd) was applied every 4 hours to prevent corneal drying and ulceration (Boland and Angles, 2010).

Recommendations for practice

Despite current cautionary labelling (Figure 1) as suggested by Sutton et al (2007) an estimated 288 cases of permethrin toxicosis are reported per year. With one fifth of cases reported resulting in fatalities (Malik et al, 2010). However, these figures are presumptive and the true number of cases presented is likely to exceed this figure. Permethrin-based products are often sold in over-the-counter presentations and as such may lack appropriate professional guidance with regard to correct use and application. The author suggests that there is a need to raise awareness of the potential of life-threatening complications associated with permethrin exposure in cats. In the patient described, and in other cases of feline permethrin toxicosis presented to the author's practice, the suspected adverse reactions observed were not reported. The author considers that in future cases and as a profession, active reporting of suspected adverse reactions to permethrin-based products should be encouraged to enable quantification and evaluation to the true extent of permethrin toxicosis and potentiate intervention as appropriate. Suspected adverse reactions may be reported to the product manufacturer, the Suspected Adverse Reaction Surveillance Scheme administrated by the Veterinary Medicines Directorate or Veterinary Poisons Information Service.

Case reflection

Within the author's practice this case represents one of six cases presented within a 4-week period. Five of these cases were related to owner error and one was as a result of ingestion of a permethrin-based cat flea collar. Patient presentation, level of veterinary intervention and intensive nursing care required was variable. One patient exhibited minimal muscle tremors and was treated on an outpatient basis. Three patients, including the case discussed, required intensive nursing care and observation for a 48-hour period. One patient was presented with severe muscle tremors and hyperthermia, sedation using a constant rate infusion of propofol (Vetofol, Norbrook) was necessary to control muscle tremors and reduce core body temperature, the patient was discharged 4 days after initial presentation. All patients described recovered fully and required no further treatment.

Conclusion

The requirement of intensive nursing care for patients with permethrin toxicosis should prompt veterinary nurses to consider the potential complications of prolonged recumbency and muscle tremors, and ensure provision of supportive care to maintain hydration, normovolaemia, normothermia and patient comfort. Veterinary professionals should encourage an increased public awareness of the potentially life-threatening complications of permethrin toxicosis and actively report suspected adverse reactions to enable effective monitoring and intervention.