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TREATMENT of TICK PARALYSIS caused by Ixodes holocyclus in DOGS AND CATS

Disclaimer

Knowledge concerning management of paralysis tick poisoning in dogs is being added to constantly, especially in recent years (2002-03). Whilst I endeavour to keep up to date with developments, information on this page cannot be guaranteed to be the very latest available.

The information presented is intended for perusal, discussion and debate amongst veterinarians. The greater part of the information is derived from published sources. Whilst I have made efforts to be accurate and impartial in this presentation, ultimate responsibility for treatment modalities used rests with the clinician. I would very much appreciate comments and ideas from veterinarians to expand on and refine the information presented. Anecdotal comments are most welcome as they expand the knowledge base and may give rise to well-directed future research. The aim is NOT to promote any one treatment regime but to improve generally the success rate of treating severe cases and reduce the obvious suffering of our animal patients (and their owners).

Staging the severity
Prognosis
First Aid and Transportation
Tick Removal
Nursing Care
Tick Antiserum
Monitoring
Supportive Therapies
Summary of a Treatment Protocol for DOGS (by Michael Fitzgerald, Alstonville Veterinary Hospital NSW 2477)
Summary of a Treatment Protocol for CATS by Richard Malik (Sydney University Veterinary Teaching Hospital, Specialist in Feline Medicine)
Other Treatment Protocols

This page will aim to reflect some of the protocols used by veterinarians to treat tick paralysis in domestic animals- particularly dogs and cats. By no means is there a single correct method of handling these cases. Protocols may vary widely according to circumstances of the patient and owner, the medications used, the facilities for monitoring the patient and the local knowledge.

Staging the severity

The initial treatment is instituted according to severity of the clinical signs. Affected animals can be assigned to one of 5 categories (as classified by Ilkiw, Turner and Howlett (1988) although overlap may exist. See Staging of tick paralysis. Most small animals presented to veterinarians will fall into stages 1, 2 and 3 and can be treated relatively simply.

Prognosis

The prognostic information I have so far found:

• "Untreated dogs usually die within 24 to 48 hours of the onset of obvious clinical signs" (Malik and Farrow, 1991 citing Ilkiw, Turner and Howlett, 1987, and Ross, 1926). In Ilkiw's (1987) experimental study eight crossbred dogs of unknown history, ranging from 20.7 to 32.0 kg, were, under the restraint of general anaesthesia, applied with unfed adult female Ixodes holocyclus ticks. The ticks had been caught in Lismore and flown to Sydney. The ticks were attached to the inside of the ear. Four ticks were attached to each of six dogs whilst two dogs were each infested with three ticks. Seven of the dogs developed signs of tick paralysis and died. One dog showed no clinical signs. It was postulated that the dog which survived may have had a previously acquired immunity or that the three ticks applied to it lacked toxicity. The period elapsing between attachment of the ticks and onset of clinical signs varied from 5.5 to 7 days, while the mean duration of the disease was 23.3 hours.
• "In dogs with tick paralysis caused by Ixodes holocyclus, the disease progresses in stages from weakness, inability to walk, inability to right, and loss of withdrawal reflexes, to a moribund state, with death following within 2 hours" (The Merck Manual, 1998).
• Robert Wylie of Ulladulla Veterinary Hospital has provided the following statistics from his veterinary practice.
  " Some animals which are only mildly affected may recover without treatment by a veterinarian. However to leave an animal untreated is taking a risk with the life of the animal. If you are thinking of NOT treating, at least contact a veterinary clinic for advice and preferably have the animal examined by a veterinarian. Veterinary treatment will significantly improve the chances of survival of any affected animal. However some will die even with the best treatment. The ones which die usually have had a larger amount of toxin injected than normal (as occurs if more than one tick is present) or have been left too long and become severely ill before the owner presents the pet for treatment. Very young and very old animals also tend to be more severely affected, or animals suffering from any other disease or stress at the same time.
  In my early years of treating dogs and cats with tick paralysis I had 41 deaths out of 415 cases presented (10.1%) over a three year period. In later years I got this down to 36 deaths out of 691 treated (5.2%) over a six year period.
  In every case the more severely affected the animals were when presented for treatment, the higher the mortality rate. Treatment of animals showing only mild wobbliness of the legs was 100% successful, with no failures. The most seriously affected group (animals which were paralysed and unable to lift their head at time of presentation for treatment) had a 36% mortality rate despite treatment. However we still saved 64% of these severely affected animals, all of which would certainly have died without treatment".
• With current (1999) treatment regimes around 5% of tick victims die despite treatment (source: The Veterinarian, Dec-Jan 2000, p1, article by Jonica Newby, quoting research by Dr Rick Atwell, University of Queensland). This figure of 5% was also presented at the National Tick Paralysis Forum No.2 (Feb 2000) based on a national survey (Atwell et al, 2000). Some practices report that the mortality rate seems to vary from year to year (David Johnson, Coffs Harbour, at NTPF No. 2, 2000) but it is unknown whether this variation is outside statistical deviations. More intensive management using artificial ventilators might further reduce the mortality rate but at a considerably increased labour and equipment cost (Mike Fitzgerald, Alstonville, pers com). Applying pharmacological methods of reducing pulmonary oedema and oesophageal dysunction is a current the focus of interest in treatment strategies.

First aid and transportation

Under natural circumstances a tick poisoned animal is found to be in a state of gradual deterioration. Transportation to the veterinary clinic may stress the tick poisoned animal by increasing the anxiety and temperature and hence the oxygen demand and levels of catecholamines (adrenaline etc). This may well be enough to cause decompensation to a state of hypoxia. Whilst treatment should be sought as soon as possible, stressful transportation is more counterproductive than taking an extra 30 minutes or so to ensure that the trip is without excessive restraint and in a cool vehicle. The animal should be handled as little as possible and allowed to recover from handling when a new environment is reached. The vehicle would preferably be air-conditioned. Heat stressed animals may benefit from wetting bare skin or short haired areas and applying a light airflow with a fan. No food or water should be given. Airway patency. Owner consent.

Searching

It has been claimed that more than 90% of ticks are found from the shoulders forward but they can be found anywhere on the integument- occasionally inside the mouth (even under the tongue!), nostril, ears, vulva and anus. The predilection for the head and forequarter sites is also seen when ticks are artificially placed on the backs of dogs (National Tick Paralysis Forum, Bulletin No. 1, 1999). In a national survey (Atwell RB et al, 2000) the dogs with longer coats had greater numbers of ticks but clipping dogs to search for ticks did not improve survival rate.

Searching is best performed using two hands and running the fingers through the coat symmetrically, starting from the muzzle and working back over the head and ears, down around the neck , then chest and front legs. Pay attention to the lips folds, the face around the eyes and inside the earflaps. Also check carefully around the carpal pads and digits. The neck area may require repeated searches because of the loose skin folds here. Then search the remainder of the torso and hind legs, and around the anus or vulva/prepuce. On the abdomen nipples can often be confused with ticks- one should be able to part the hair and check. Clipping away hair or matting it down with water may help to identify suspicious nodules. If multiple skin tumours are present they can also make searching difficult and full body clipping may be required.

Tick removal

See Tick Removal for a detailed discussion of the methods of removal. Based on a recent survey (Atwell RB et al, 2000) neither the chemical pre-killing of ticks nor the injecting of antiserum under the tick lesion improved mortality or recovery time. The severe anaphylactic reactions that occur when ticks are removed from humans have not been reported in dogs (NTPF Bulletin No.1). Whether squeezing the body of the tick as it is being removed causes the injection of more toxin is so far a theoretical concern in dogs. Similarly whether it might increase the chance of injecting tick-borne microbial disease organisms in dogs in Australia also unknown. Nevertheless, it may still be a reasonable precaution to grasp as close to the skin as possible when attempting removal.

If the animal has not yet shown signs of tick paralysis, removal of the tick may prevent development of the disease. However, if the animal is showing any signs then removal of the tick is not sufficient, because the disease is very likely to progress for up to 48 hours in the absence of specific therapy, possibly resulting in death of the animal. [Occasionally veterinarians will permit a dog which is being repeatedly infected with paralysis ticks and may have some degree of immunity derived from recent prior exposure to be observed and not treated with antiserum, despite the presence of early signs. It is important to note that immunity is short-lived and may not last more than a few months. There is always a risk in trying this as there is no established means of assessing the immune status. Perhaps such a test will become available in the future. Not treating a dog with antiserum when it is showing clinical signs is risking the life of that animal; it is a decision usually made because of economic circumstances or because of some other concern with repeated dosing with antiserum].

Searching the animal for ticks is done with minimal stress. Clipping the coat may be necessary in animals with a dense or matted coat. Some veterinarians use acaricidal sprays or rinses. [Subcutaneous injection of ivermectin for the killing of undetected ticks is performed in other species but this has not been evaluated in dogs or cats to my knowledge]. Animals in anxious respiratory distress are best sedated with acepromazine before attempting tick removal. This is particularly the case with cats which can develop a state of frenzied gagging and struggling with handling. Atropine has also been recommended for cats in this state [the salivary and respiratory secretions may precipitate laryngospasm or aspiration of plugs of mucus (see caution on using atropine).]

Nursing (with Tender Loving Care)

Animals must be kept in a comfortable, quiet, stress-free environment. This can mean the difference between life and death. Animals are often in respiratory distress and may have little compensatory reserve to cope with further oxygen demands brought about by anxiety.

The sternal position is probably best for easing respiration and reducing hypostatic congestion. If the animal is in lateral recumbency it should be turned at least every 4 hours to prevent development of hypostatic pneumonia (Ilkiw, 1980). This has however been questioned because some practitioners (Fitzgerald, 1998) report that patients often reapidly deteriorate and even die after turning. They advocate never turning recumbent patients, however, it may be preferable to turn more frequently whilst paying careful attention to any decline in oxygenation (using pulse oximetry) and providing oxygen support where necessary.

Food and water are initially withheld whilst the animal is paralysed because pharyngeal dysfunction, megaoesophagus, laryngeal paresis and a weak cough all predispose aspiration pneumonia.

There are theoretical grounds for preventing tick patients from becoming overheated, and perhaps even for having them in a state of mild hypothermia (see note 4). Additionally, paralysed animals are unable to thermoregulate normally because they cannot readily shiver nor seek warmer or cooler places nor adopt heat conserving/releasing postures. Therefore core temperature needs to be monitored and controlled artificially. Both hyperthermia and hypothermia are possible problems depending on the ambient temperatures and other factors (eg brachycephalics are prone to hyperthermia). In most cases hospital ambient temperature should be slightly cooler than normal room temperature. However, the animal should not be trying to shiver. A slightly cool and de-hu midified air-conditioned environment is usually ideal. Sedation and anesthesia promote hypothermia and this needs to be anticipated. Whilst mild controlled hypothermia may be beneficial, one should not allow core temperature to drop below 34-36° C. Numerous complications are possible with hypothermia (see note 3) and these may be just as life threatening as the tick paralysis itself.

Good comfortable bedding which drains away urine and helps prevent pressure sores is recommended. Towels and sandbags may be useful to stabilise an animal in the sternal position. The pharynx should be swabbed clean after episodes of vomiting or regurgitation to minimise the risk of aspiration. Calm reassurance may benefit some dogs [?cats].

Food and water should be withheld until the patient is mobile and has not vomited for 24 hours. Water can then be given in small amounts, and food can be offered thereafter if there is no vomiting.

After recovery, a period of convalescence should be imposed. Exercise should be restricted and high ambient temperatures avoided. Violent exercise within a day of complete recovery from tick paralysis has resulted in collapse and sudden death, and extremes of heat may cause recovered animals to relapse into paralysis.

Tick antiserum

Dosage
Premedication for serum reaction
Differentiating and treating Bezold-Jarisch and anaphylactic reactions
Warming, dilution and antiemetics
Routes of injection in different species

Hyperimmune serum is derived from dogs deliberately but carefully infected with paralysis ticks. It is available for injection to neutralise circulating toxins. It is much more effective if given early in the course of paralysis whilst toxin is still either circulating or in the tick lesion, that is, before it has bound to its site of action at the neuromuscular junction (and possibly other) receptors. This becomes all the more important when one realises that there is a delay of 8-12 hours before signs of reversal of paralysis are seen (see note 2). Placement of an indwelling intravenous catheter facilitates slow intravenous injection of the antiserum and any fluids and adjunctive drugs.

Dosage

The efficacy of hyperimmune serum has in the past varied between manufacturers and between batches and so precise doses were difficult to recommend. The traditional rule of thumb was to give 0.5 mL/kg body weight to dogs but this dosing method has been questioned (Atwell and Fitzgerald, 1994). Tick antisera are now standardised to contain at least 500 CSIRO neutralising units per mL. Generally, higher doses (1.0 mL/kg) are given to severely affected animals and in these animals many veterinarians give as much anti-tick serum as an owner can afford- even 2mL/kg. Perhaps the only limitation here is the potential for vascular overload if it is given too quickly. Smaller animals may benefit from relatively larger doses as it is reasoned that it is a given amount toxin that requires neutralizing, rather than a given weight of animal. On the other hand larger dogs have the antiserum diluted in a larger volume of body mass and so the reaction of antibody and toxin may be lessened, necessitating higher doses for larger animals. A combination of dosing strategies is probably required. [NF: Perhaps a dose based on surface area has some merit?]

The makers of one antiserum (AVSL) recommend a starting "dose of 10 mL of their serum given IV to counter Stage 3 paralysis (unable to maintain sternal recumbency) caused by one tick in a suseptible 20 kg dog". Thus some veterinarians administer a larger quantity to cases which present with more than one engorging tick. At least 0.5 mL of antiserum can be injected at and around the site of tick attachment (preferably, perhaps, before it is removed) (see AVSL antiserum literature). Lismore Supreme Serums (see Lismore Supreme Serums literature) recommend a starting dose of 10-20 mL for dogs (IV) and 5 mL for cats (IP) for their regular antiserum and for their "despecified" antiserum 5-12 mL IV for dogs and 1-4 mL IV for cats. In humans, a minimum dose of 20 mL is recommended. (see CSL antiserum literature) Yet another serum manufacturer (see North Coast Serum Products literature) suggests its own guidelines for a serum which is claimed to contain 1000 units per mL. They recommend 10-30 mL IV for dogs and 10 mL for cats (half IV and the other half SC). At the Animal Emeregency Centre in Brisbane a policy of using 20 mL of antiserum per engorged tick is apparently being employed (Coralie Endean, pers. com., 1998, email). Fitzgerald (1998) has a regime of giving at least 1 mL/kg with a minimum of 10 mLs per dog. He does not feel confident with doses of less than 0.75 mL/kg.

Should early or "mild" cases receive any less antiserum? As a comparison, would we give an early case of snake poisoning less antiserum simply because the signs seen were initially mild? Should we assume that just because signs of tick paralysis are mild that the dose of toxin is smaller? Perhaps we should be cautious and assume that in many cases we are fortunate in seeing the case early. In my opinion [NF] the overall outcome of cases seems to be better when one gives large doses of antiserum per the number of engorged ticks, even when the signs are "mild" (ie early) (see the discussion in the page "Immunology of Tick Paralysis") (eg 10-15 mL per engorged tick in cats and small dogs, 15-20 mL per tick in larger dogs). The initial additional cost of antiserum is perhaps countered by shorter hospitalisation and secondary support costs.

Premedication for serum reactions

Reactions to administration of antiserum may be divided into two broad categories: physico-chemical and immunological. Physico-chemical reactions include the Bezold-Jarisch Reflex (mediated via receptors in the left ventricular outflow tract), anaphylactoid reactions (mediated via non-Ab-dependent mast cell degranulation), and nausea reactions (mediated via the chemoreceptor trigger zone (CTZ) in the brain).

True immunological reactions are usually anaphylactic (mediated via Ab-dependent mast cell degranulation). The distinction between anaphylactic and anaphylactoid reactions is esoteric in the emergency context- the clinical signs are identical and they are managed similarly.

The Bezold-Jarisch Reflex (B-J Reflex) is a syndrome of depression, hypotension and bradycardia mediated by receptors in the left ventricular outflow tract. In injection reactions it is believed to be an effect mediated by the rate of injection and the temperature of injected fluid. Atropine protects against the reaction but adrenaline does not.

In humans the "vasodepressor reactions" are probably the events most commonly confused with anaphylaxis. These reactions are characterized by pallor, weakness, hypotension, sweating, nausea, sometimes vomiting and almost always bradycardia.

In tick paralysis the Bezold-Jarisch reflex seems to be numerically a much more important problem, occuring in as much as 2.7% of dogs and 3.9% of cats given tick antiserum (Atwell and Campbell, 2001).

This study also found that those animals premedicated with atropine had a much reduced chance of developing such reactions. This benefit may be suffcient to recommend the routine use of atropine before giving tick antiserum in both cats and dogs. Despite this one should be mindful that the resulting increase in cardiac workload is a possible problem. The dose of atropine used to prevent the B-J reflex (0.1-0.2 mg/kg) is much higher than the normal pre-anaesthetic dose (0.04 mg/kg).

Giving the anti-tick serum SLOWLY and PREWARMED are probably just as important as any premedication.

 

Differentiating and treating Bezold-Jarisch and anaphylactic reactions

Measuring the heart rate gives the best clue as to which reaction is occuring. Bradycardia and syncope is more likely a B-J reflex whereas tachycardia with dyspnoea or pruritus more likely to be an anaphylactic reaction.

Visceral signs (ptyalism, vomiting and diarrhoea) are more likely with anaphylactoid reactions but can occur with both vasodepressor and anaphylactic reactions and so are not as useful in differentiation. Furthermore both reactions can occur simultaneously.

The B-J reflex is best treated with atropine, though adrenaline might also be useful if anaphylaxis is suspected.

Anaphylaxis is treated with oxygen, fluids, adrenaline, corticosteroids, antihistamines and possibly aminophyline and dopamine (see table below). [NF: Based on differences in shock organs for dogs and cats, adrenaline/corticosteroid and fluids may be more important in treating dogs, whereas adrenaline/corticosteroid and aminophylline more important in treating cats?]

For recent information on this topic see the article by Atwell and Campbell (2001) on serum reactions.

 

Antibody-dependent anaphylaxis. Being derived from dog serum, anti-tick serum can cause true anaphylactic reactions, particularly in other species. Nevertheless it is reportedly rare in dogs even with multiple exposures, and also rare in those cats receiving the antiserum for the first time.

In the dog the splanchnic viscera and liver are the major "shock organs". Dogs suffering from anaphylaxis commonly exhibit restlessness and excitement, followed by vomiting, diarrhoea (which may be bloody), collapse, convulsions, coma and finally death (Cohen RD, 1995). Typically there is a compensatory tachycardia unless a BJ reaction is concurrent. The entire process may occur in less than an hour.

In cats the respiratory system is the primary "shock organ". Cats often show facial pruritus initially (pawing at the face), followed by ptyalism, vomiting, incoordination, collapse and death. Cats suffer from severe bronchoconstriction, pulmonary haemorrhage and laryngeal oedema (Cohen RD, 1995).

In humans, by comparison, both the circulatory system in general as well as the lungs and the skin are the "shock organs". Urticaria and angioedema are the most common initial signs. The next most common findings are related to the respiratory tract. They consist of manifestations of upper airway edema, shortness of breath and wheeze. Symptoms of hypotension occur next most commonly. These consist of dizziness, syncope, and measurable hypotension. Gastrointestinal findings including nausea, vomiting, diarrhea, and cramping abdominal pain follow in frequency. Rarely, there is rhinitis, headache, substernal pain and pruritus without rash. The most threatening manifestations are airway edema, bronchospasm and cardiovascular shock. Shock is caused by vasodilation and vasopermeability. This increase in vasopermeability produces a shift of fluid from the intravascular to extravascular space and can result in rapid and profound losses of intravascular volume. Up to 50% of intravascular volume can be lost within 10 minutes (Phillip L. Lieberman, MD, University of Tennessee College of Medicine, Medscape article, 1997).

Pretreatment with antihistamines and/or corticosteroids does not prevent anaphylactic reactions but will blunt the physiological response (Cohen RD, 1995). It will also help prevent the "late phase" or "biphasic" anaphylactic response.

In dogs the trend is towards not using corticosteroids routinely because they may cause secondary problems and worsen the outcome if there is aspiration pneumonia (Malik et al, 1991). This issue is not however resolved, as there may be benefits of using glucocorticosteroids unrelated to their suppressing reactions to antiserum (see unresolved issues). Antiserum reactions appear to be quite rare in dogs (even with second treatments). This is in contradistinction to the repeated use of equine anti-snake serum where reactions are a significant risk (Fitzgerald, 1998). One author (Dunsmore and Shaw, 1990), has however reported the rate of anaphylaxis for anti-tick serum to approach 10% although the species was not clearly stated.

In cats, Malik et al (1991) have recommended the routine administration of intravenous hydrocortisone (at 30 mg/kg) prior to the slow intravenous injection of antiserum (5-10 mL). Adrenaline (1.0 mL of 1:10,000 solution) is kept ready in case of an anaphylactic reaction. Other veterinarians give antiserum to cats intravenously after premedicating with acepromazine or antihistamine. Others again give antiserum to cats intraperitoneally. Intravenous administration would be expected to give quicker results but possibly at the cost of increased stress of handling and serum reactions. According to Malik and Farrow (1991) canine hyperimmune serum probably should be initially withheld from mildly affected cats, pending their response to tick removal in hospital. A "despecified" (de-species-fied) tick antiserum which is more purified may be better suited for treating cats.

Fitzgerald (1998) suggests that antiserum is given to dogs intravenously and without premedication. He suggests that it should also be given intravenously to cats but in this instance with premedication to reduce the chances of anaphylaxis. Cats that are only very mildly affected may be given antiserum intraperitoneally.

 

Warming, dilution and antiemetics

Pre-warming of the antiserum may be important in reducing reactions in cats and small dogs. Cold antiserum is more likely to induce a Bezold-Jarisch Reflex.

Similarly, Jones (1991) recommends diluting antiserum in an equal volume of 0.9% NaCl when it is used intravenously for cats and small dogs. (NF comment: the additional load on circulating blood volume may, however, be a consideration, particularly in very small dogs and in cats).

Antiemetics. Slow administration, ie over 15-30 minutes, helps to minimise nausea associated with bolus infusions [NF: it is not unusual to hear borborygmus when giving tick antiserum]. This reaction is probably due to the cresol preservative that is found in the antiserum (R. Sillar pers com, quoted by Fitzgerald, 1998). Premedication with the antiemetic prochlorperazine (Stemetil®) may help to reduce this.

Routes of injection in different species

In dogs the intravenous route has the most acceptance.

In cats both intravenous and intraperitoneal routes are often satisfactory. The intravenous route is probably more effective but is more stressful to administer and perhaps more of a risk for anaphylaxis. Adequate sedation, premedication with adrenaline and hydrocortisone and slow administration of diluted serum might overcome these risks in cats. Intraperitoneal injections are not entirely without risk however. In a struggling patient the antiserum may enter liver, spleen, gravid uterus, bladder and intestine. If the tissue is vascular (eg liver, spleen) the rapid injection may cause an acute reaction similar to an IV reaction. Injection into a hollow viscus (bladder and intestine) may risk causing poor absorption and peritonitis.

Antiserum injection in sheep, goats, calves and foals should be by the intravenous (IV) route, whereas in the lamb, kid and small pigs the intra-peritoneal (IP) route is satisfactory, although it gives a slower response. In koalas and other marsupials, the rabbit and guinea pig the IP or intra-muscular (IM) routes should be used. Because it may take up to 12 hours to be absorbed from the IM route a doubled dose should be used, particularly in severe cases.

In mildly affected animals with a straightforward ascending paralysis, removal of ticks and administration of hyperimmune serum usually results in obvious clinical improvement within 24-48 hours, although there is often little change within the first 12 hours. Failure to respond to hyperimmune serum after an appropriate interval may suggest the presence of undetected ticks.

Monitoring therapy

The adequate monitoring of the response to treatment and to nursing care is critical in severe cases. The level of nursing care and the types of ancillary drugs required may vary throughout the course of treatment. For this reason hospitalisation of cases until animals are able to stand and consume oral food or liquid is to be recommended. An owner caring for a patient at home may not be able to appreciate changes in respiration (pulmonary oedema, aspiration pneumonia and ventilatory failure), pharyngeal saliva accumulation, temperature, arterial pulse rate and pressure and mucous membrane colour and refill, PCV/TPP and Hb oxygen saturation all of which may dictate management.

Physical exam and PCV/TPP

After initial survey and stabilisation Dr Mike Fitzgerald (1998) routinely attempts a full physical examination, including tests for cranial nerve function. He then also obtains a more detailed history. An intravenous line is placed for ready access and blood withdrawn for PCV and TPP (see note 1).

Thoracic radiography

A chest radiograph can often be taken if it is not too stressful- either dorsoventral and/or lateral. This may reveal pulmonary changes due to oedema or aspiration, or a dilated oesophagus. According to Fitzgerald (1998) most of the dogs he has seen exhibiting gagging/retching of white froth have had evidence of megaoesophagus on a plain lateral thoracic radiograph.

Pulse oximetry

Pulse oximetry may be very useful for monitoring. Negative trends can be acted upon by oxgen supplementation, evacuation of obstructive fluids or treatment of pulmonary oedema, particularly when SpO2 declines below 90%. Sedated animals can have the transmittance (clip-on) probe attached to the tongue but they can also be applied to the lip, the ear, the paw of a cat, across a dog's toe and onto the thin skin folds above the hock caudal to the tibia. They should be applied to unpigmented skin.

The reflectance probe can be taped to a hairless skin surface such as under the tail or onto a mucosal surface such as in the mouth. Placement in the rectum may not work well because faecal material interferes with light transmission and because probe movement causes mucosal vasoconstriction.

Pulse oximeters are useful because cyanosis does not becaome clinically apparent until there is more than 50 g/L of desaturated Hb. This, in an animal with both a normal PCV and normal peripheral perfusion, corresponds to a Hb saturation of approximately 66% which is extremely low. In anaemic animals other signs of hypoxia are tachycardia (follwed by bradycardia just before cardiac arrest), hypertension (initially), mucous membrane pallor and increased respiratory efforts.

Blood pressure measurement

Where the dog is compliant, a systolic arterial blood pressure reading can be taken using either an ultrasonic movement detector (Doppler) or an oscillometric pressure detector (manual or automated-transducer sphygmomanometer).

Capnography

Nasal end-expiratory capnography. This would be useful in the advanced cases when hypoventilation becomes significant.

Supportive therapies

Anxiolytics (acetylpromazine, benzodiazepines, opioids), Vasodilators (phenoxybenzamine, acetylpromazine, hydralazine), Diuretics, Bronchodilators, Anaesthetics, Analgesics, Oxygen, Ventilator, Fluids, Antibiotics, Glucocorticosteroids, Antiemetics, H2 blockers, Antisialics, Oesophageal Suctioning, Physical therapy.

Anxiolytics

The need for calming or sedation varies with the individual animal. By reducing anxiety one may reduce oxygen demand and the release of catecholamines. However, use of some tranquillizers may also have some undesirable effects such as CNS depression, respiratory depression and hypotension.

Phenothiazines

For dogs the alpha-adrenegic antagonists (alpha blockers) acetylpromazine and phenoxybenzamine have a beneficial tranquillizing effect as well as being commonly used for their vasodilating effects (see below). However, one needs to take into account factors such as age and concurrent disease before automatically using the alpha blockers. The doses used in clinical practice are usually well below those required to achieve significant vasodilation.

Benzodiazepines

Benzodiazepines (diazepam and midazolam) may be useful in conjunction with low dose opiate administration to relieve distress and facilitate ventilatory support (even permitting intubation in advanced cases). The respiratory rate and tidal volume are minimally affected by benzodiazepines. Some individuals may show paradoxical increases in anxiety so concurrent use of other sedatives at reduced doses may be warranted (Fitzgerald, 1998).

Opioids

Opioids (eg morphine, methadone, pethidine) produce excellent sedation but with a dose dependent respiratory depression. Both tidal volume and respiratory rate decline at high doses. Respiratory centre responsivenes to elevated CO2 is suppressed. Because of this respiratory depression only low doses should be used, preferably in combination with either a phenothiazine or benzodiazepine. Morphine may have additional benefits in treating pulmonary oedema, by acting as a mild venodilator. Morphine dose rate is usually 0.25 - 1.0 mg/kg in dogs but it may be advisable to start with a very low dose of 0.1 mg/kg. The normal dose is 0.05 - 1.0 mg/kg in cats but again it may be advisable to use the lowest dose rate in tick poisoning.

Sedation of cats

Most cats seem to benefit from sedation. It may be wise to sedate cats on admission as they are highly susceptible to developing a frenzied panic state precipitating acute hypoxia and cyanosis. Fizgerald (1998) finds the use of ACP in combination with ketamine (10-15 mg [0.10-0.15 mL]/5 kg cat) IM, sometimes with atropine to be very effective. This reduces panic, improves dyspnoea, and facilitates placement of an IV catheter or needle. Ketamine would be contraindicated in cats with hyperthyroidism or hypertrophic cardiomyopathy. Alternatively ACP could be combined with an opiate (eg buprenorphine, Temgesic®) or benzodiazepene (diazepam, Valium®). Propofol (Diprivan®) , alphadaxalone (Saffan®) and thiopentone (Pentothal®) could also be used (Fitzgerald, 1998).

Vasodilators

Animals with more advanced paralysis may benefit from the administration of drugs that reduce peripheral vascular resistance, thereby perhaps relieving the respiratory distress associated with pulmonary congestion and oedema. Two drugs, phenoxybenzamine (Phenoxyl®) and acetylpromazine have traditionally been advocated for this purpose. However conflicting data has confused the issue. Earlier experiments (on a small number of highly instrumented dogs) by Ilkiw suggested that hypertension and increased systemic vascular resistance were causing pulmonary oedema. More recent findings (cardiac ultrasound) have indicated that primary myocardial dysfunction and hypotension are the norm. Hence the routine use of both phenoxybenzamine and acepromazine are being questioned.

Phenoxybenzamine

The success of phenoxybenzamine is controversial. In people phenoxybenzamine acts as an alpha blocker (alpha-adrenoreceptor antagonist) BUT it causes reflex beta-receptor activated hypertension, acting both centrally and peripherally. In the complex milieu of various sympathetic receptors it may be that the net effect of phenoxybenzamine may vary with the stage of disease, dosing regime, sympathetic tone and species. From Ilkiw's original experimental work it is unclear whether phenoxybenzamine gave benefit through an antihypertensive effect or through another mechanism. The dose recommended is 1mg/kg diluted into at least 20 mL of 0.9% NaCl given slowly (over 20 minutes) and repeated every 12-24 hours if necessary. A low-dose regime has also been advocated. In this regime, which has apparently been clinically successful, the phenoxybenzamine is given at almost a quarter of the Phenoxyl® label dose and mixed in with the antiserum.

In more recent discussions (Atwell, 2001) the routine use of phenoxybenzamine appears to be losing favour. The recent findings of primary cardiac dysfunction and hypotensive tendencies lend theoretical support to this.

Acetylpromazine

Acetylpromazine has perhaps found greater acceptance amongst veterinarians than phenoxybenzamine. Its tranquillizing effects (not just sedating but actually reducing responsiveness to stimuli?), its predictable hypotensive effects and perhaps even its anti-arrhythmic effects are all of potential benefit. Relatively high doses (0.05-0.10 mg/kg every 6-12 hours SC or IM) have been used most frequently for this purpose. Recently, however, a low-dose regimen for ACP is also being proposed (E. Court pers. com.)- in this case 0.1-0.2 mL of 2mg/mL solution is given per animal. Acetylpromazine's calming effect is thought to be mediated by by depression of the reticular activating system and anti-dopaminergic actions in the CNS. The anti-dopaminergic effect in the medullary chemoreceptor trigger zone (CTZ) gives an anti-emetic effect. Brain stem effects may cause a loss of vasomotor regulation. Catecholamine release is depressed both centrally and peripherally (ganglionic and adrenal), which gives an anti-arrhythmic benefit. ACP causes alpha-adrenergic blockade producing hypotension in excited or apprehensive animals, resulting in a compensatory reflex tachycardia. Respiratory rate falls first, and then higher doses may also decrease respiratory depth (tidal volume). Respiratory centre sensitivity to CO2 is reduced. ACP interferes with normal thermoregulation. The phenothiazines generally have weak antihistamine effects. They potentiate the depressant effects (cardiovascular and respiratory) of alpha2-agonists, opioids and general anaesthetic drugs.

In tick paralysis the benefits of being anxiolytic (even this has been questioned), anti-emetic, anti-arrhythmic, hypotensive and hypothermic need to be weighed against the possible problem of severe hypotension, severe hypothermia and severe respiratory depression. One also has to be very careful in dogs with brachycephalic airway syndrome in which any relaxation of laryngopharyngeal tone could precipitate upper airway obstruction, in turn also compounding pulmonary oedema.

ACP seems to have a place in many cases but needs to be used judiciously and perhaps starting with lower doses.

In recent discussions (Atwell, 2001) the routine use of ACP in dogs is being questioned, and it was stressed that clinical judgement and discretion are required. In cats, however, the tranquillisation effect may have greater relevance.

Hydralazine and Sodium Nitroprusside

Afterload reducers, such as hydralazine (arteriolar dilator) and sodium nitroprusside (arteriolar and venular dilator) have not been evaluated clinically or experimentally in animals with tick paralysis.

Nitroglycerine

The preload reducer (venodilator) and human angina medication nitroglycerine ointment (Nitro-Bid®) administered topically has anecdotal support amongst some veterinarians. Nitrate compounds are believed to induce venous smooth muscle relaxation through the release of nitric oxide. Nitroglycerin may have a beneficial effect in acute congestive heart failure. It is readily administered on the pinna, in the axilla or in the inguinal region. The dose is 1/8 th to 1 inch of the 2% ointment (Marks and Abbott, 1998). Dr G Maskiell of Caboolture uses the following regime routinely in all cases, applied to the skin in clipped areas:

• cats and small dogs 2 cm
• medium dogs 5 cm
• large dogs 7-10 cm

"Seems to last 3-5 hours, can be repeated"

Furosemide

Furosemide (a strong diuretic and mild vasodilator) should also help with pulmonary oedema (whether cardiac or vascular in origin) see further discussion below.

Calcium Channel blockers (diltiazem etc)

Diltiazem, a mild negative inotrope, negative chronotrope and arterial vasodilator may have a role in tick poisoning but has not been investigated. The calcium channel blockers also have anti-arrhythmic properties ude to effects on the specialised conduction system. Whilst the effect on heart rate is modest the drug may have a positive lusitropic effect, that is it may improve ventricular filling by assisting myocardial relaxation, a property known to be of benefit in hypertrophic cardiomyopathy and possibly those with restrictive cardiomyopathy (Marks and Abbott, 1998).

Angiotensin Converting Enzyme Inhibitors (enalapril, benazepril)

Enalapril, a balanced arterial and venous vasodilator) may have a role in tick poisoning but has not been investigated.

Phlebotomy

Reducing blood volume may be of benefit in cases of advanced pulmonary oedema that is unresponsive to other medical therapies. Some vets say this can save a moribund case. Ten to fifteen percent of blood volume is taken from a jugular vein. This should be saved as it can be administered to the same animal later (Maskiell, 2000).

Diuretics

Furosemide (a strong diuretic and mild vasodilator) should also help with pulmonary oedema (whether cardiac or vascular in origin). This treatment deserves further critical evaluation in the light of the recent demonstration of cardiac dysfunction (presented by F Campbell at TPF II, 2000). In the past there has perhaps been reticence in using diuretics because of the PCV elevation seen in tick poisoning. Yet from measurements of glomerular filtration rate (GFR, via creatinine) and electrolytes it appears that this haemoconcentration does not necessarily correlate with reduced renal perfusion or total body dehydration and probably represents a fluid shift. Whilst severe haemoconcentration causes its own problems and needs to be monitored, the consequences of pulmonary oedema are probably more deleterious. The use of furosemide needs more investigation and perhaps deserves a higher profile in the treatment regime for severely dyspnoeic animals. Furosemide can be used at a dose of 1-5 mg/kg IV every 2 hours if severe pulmonary oedema is present. Intravenous furosemide may lead to relief of dyspnoea prior to diuresis due to venodilation and preload reduction (Marks and Abbott, 1998).

Bronchodilators

Theophylline, etamiphylline and aminophylline

Methylxanthines such as theophylline, etamiphylline (Millophyline-V®) and aminophylline have been empirically used by some veterinarians in the treatment of respiratory distress associated with tick paralysis. Theoretically their use would be controversial. Etamiphylline, for example, exerts positive inotropic effects on the heart and possesses bronchodilator activity similar to that of theophylline; in contrast to theophylline, however, etamiphylline does not increase the heart rate; cardiovascular effects include increased cardiac amplitude and cardiac output (stroke volume); respiratory effects include increased rate and depth of respiration by strengthening respiratory muscles, and the relaxation of bronchial and bronchiolar smooth muscle. This class of drugs may also have some mild diuretic properties. They may, however, also be arrhythmogenic (Marks and Abbott, 1998).

Contrary to the traditional view that aminophylline is primarily a bronchodilator, aminophylline may actually improve tidal volume mainly by increasing diaphragmatic excursions (W Lamb, 2000; Novartis Cardial Pursuit III, Wollongong).

Anaesthetics

Barbiturates

Anecdotal use of barbiturate anaesthetics such as pentobarbitone or thiopentone exist. This method may occasionally be used to take control of a dog struggling violently as it is choking- permitting rapid intervention by intubation and ventilation. Anaesthesia may also be necessary for intubation/tracheostomy and ventilation. For rapid induction thiopentone may be used. For maintenance of anaesthesia (for the purpose maintaining an endotracheal tube) pentobarbitone can be used by continuous rate infusion at 1 mg/kg/hr combined with morphine (or methadone) and diazepam which are added to effect (Fitzgerald, 1998).

Propofol

Propofol (Diprivan®) has also been used to maintain enough sedation to maintain a dog with an endotracheal tube on a ventilator.

Volatile (inhalation) anaesthetics

On the use of volatile anaesthetics there is so far no information to hand.

Analgesics

[Their use has not been investigated to my knowledge but paralysed patients may experience significant discomfort in their recumbency, adding to the overall stress; opiates have the potential benefit of concurrent sedation but may suppress ventilation and the cough reflex. Worth more investigation.].

Oxygen

The question of whether hypoxaemia (low O2) or hypoventilation (high CO2) or both hypoxaemia and hypoventilation are of primary importance was again raised at the Tick Paralysis Forum (David Johnson, pers com, 2002). Ilkiws original work suggested that ventilatory failure (rising CO2) only develops in the latest stages after the fall in arterial oxygen tension develops and the alveolar-arterial oxygen tension difference rises- but this finding may need to be revisited perhaps by checking CO2 in a larger number of patients.

Supplementary oxygen (and possibly ventilation) may be necessary when the pulse oximeter (SpO2) reading drops below 89% (see monitoring). Patient stress, invasiveness and costs need to be considered when deciding on the oxygen delivery method. Fully ventilated oxygen supplementation is the theortical ideal but not often necessary or manageable.

Sedation and other means of stress minimisation help to reduce oxygen demand. When this is insufficient a source of enriched oxygen is required. Room air provides approximately 21% inspired O2. The method of O2 administration used is determined by the extent of the patient's need, the patients tolerance, the practitioner's preference and familarity, the equipment available, the human resources available and the owner's financial resources (Fitzgerald, 1998).

1. Flow-By. The tube is placed in front of the nares to that the flow is perpendicular to the nasal cavity. This is a good initial method as the stress on the animal is minimal.
2. Chamber. In small patients additional O2 is readily provided by piping 100% oxygen into a cat induction chamber through a disposable plastic nebuliser. Dedicated O2 cages achieve 60-70% inspired O2 however there is a serious risk of hyperthermia. Cage humidity should not exceed 50% and temperature should not exceed 25C. Disadvantage is the cost of equipment (when a dedicated chamber is used) and poor access to patient whilst maintaining O2 therapy.
3. E-collar. A method of using an Elizabethan collar draped with transparent plastic film into which oxygen is piped from under the collar has also been described. Hyperthermia and failure to remove CO2 are potential
4. Intranasal. In larger patients humidified intranasal oxygen may be useful. Inspired O2 achieved varies with patient size and flow rate. A 6 French tube in cats and small dogs and a 10 French tube in larger dogs inserted to level of carnassial tooth under topical anaesthesia (eg 0.5-1.0 mL Ophthaine® or lignocaine). The largest comfortable tube is used.
   
   

   Nasal Catheter oxygen catheter flow rates required (L/min) to achieve various inspired oxygen concentrations (FIO2)
   	O2 flow rates required (L/min) to achieve FIO2 %
   weight (kg)	30 - 50 %	50 - 75 %	75 - 100 %
   0 -10	0.5 - 1.0	1 - 2	3 - 5
   10 - 20	1 - 2	3 - 5	>5
   20 - 40	3 - 5	>5	?
   from Court MH: Respiratory support of the critically ill small animal patient. In Murtaugh RJ, and Kaplan PM (eds): Veterinary Emergency and Critical Care Medicine. St Louis, Mosby Year Book, 1992, p 575.

   Red rubber or silicone feeding tubes (Cook®) can be used. Having side holes minimises noise (which can be quite loud for the patient) and jetting lesions. Depth is measured to the medial canthus. Tubes are secured with cyanoacrylate glue or nylon suture at the side of the face close to the nare (avoid whiskers in cats!). Where high rates of FIO2 are required, bilateral catheters may be preferable to using very high flow through a single catheter. An Elizabethan collar may be required. Humidification is essential to prevent drying of the respiratory mucosa. Humidification can be improvised by bubbling the oxygen through a bottle containing warmed sterile water. Some animals don't tolerate these tubes and appear stressed in their attempts to dislodge them. Local complications include haemorrhage and infection, and gastric distension with flow rates greater than 500 mL/kg/min. Not to be used if pre-existing nasal trauma or infection or haemorrhagic diathesis. The catheter should be replaced every 48 hrs, into the oppsosite nare where possible.

5. Face Mask. Masked oxygen (at > 10L/min !, achieving inspired O2 of 50%, via a face mask that is loose fitting to permit escape of exhaled C02) may help some patients but may also be stressful.
6. Intratracheal. Tracheal catheters (either transtracheal or nasotracheal) via 16 g IV catheters with side holes flowing at 1-2 L/min with humidified O2 provide an inspired O2 of 30-40%. Local anaesthesia or short general anaesthesia (propofol, thiopentone) may be used to permit placement. The transtracheal catheters may be passed either through the cricothyroid membrane or between tracheal rings. Placed to level of carina (~5th intercostal space). Jet lesions and tracheitis are possible complcations. Silicone feeding tubes (Cook) are preferred because they are pliable and less likely to kink. A less invasive method but one that requires heavy sedation or general anaesthesia to be maintained involves placement of the tracheal catheter through a cuffed endotracheal tube to the level of the carina. This may reduce dead space in animals reliant on self-ventilation.
7. Tracheostomy tube. This is useful in brachycephalic breeds, but, like endotracheal tube placement, can be labour intensive.
8. Endotracheal tube. This requires continued general anesthesia or very heavy sedation but can be combined with positive pressure ventilation (PPV) which may include maintaining a positive end-expiratory pressure (PEEP).

Weaning from Oxygen

Abrupt cessation of oxyen supplementation can result in rapid respiratory decompensation, even when the patient is receiving a low FlO2 (Drobatz et al, 1995). An FlO2 as low as 0.3 can mask the hypoxic effects of lung areas with low ventilation/perfusion ratios. It is thus prudent to reduce the FlO2 gradually over 24-48 hrs depending on the patients response.

Oxygen toxicity

"Absolute" oxygen toxicity. The principal pathology is thought to involve endothelial cells and Type 1 & 2 epithelial cells of respiratory system. Cellular damage is caused by oxygen free radicals and may become a problem after 8-12 hours of continuous inhalation of 100% oxygen. Therefore the O2 concentration should be reduced when SPO2 is normalised.

"Relative" oxygen toxicity. It has been pointed out that providing enriched oxygen to a hypoventilated patient could actually be detrimental (David Johnson, group discussion, National Tick Paralysis Forum, 2002). Hypercapnia together with increased inspired oxgen concentration may worsen respiratory acidosis. More research (particularly using capnography) is required.

Ventilators

In some dogs paralysis or "fatigue" of the intercostal muscles and diaphragm may cause ventilatory failure, with or without simultaneous pulmonary oedema. A central respiratory centre depression has also been postulated (Ilkiw and Turner, 1987b). These animals require intermittent positive pressure ventilation (IPPV). Those that have reached this stage should be easy to intubate because of lack of jaw tone and do not tend to fight the ventilator. Fitgerald (1998) has found that ventilation, once required, usually needs to be continued for at least 8 and up to 30 or more hours. Malik et al (1991) have successfully ventilated such a dog for 60 hours by which time acceptable ventilation had developed. This requires continuous monitoring. Referral to a specialist emergency centre may be advisable where available. A volume regulated (cf pressure regulated) ventilator may be more useful theoretically when lung mechanics and pulmonary compliance changes due to congestion/oedema are present. A pressure regulated respirator, however, may be somewhat safer. Oxygen toxicity (the principal pathology being on endothelial cells and Type 1 & 2 epithelial cells of respiratory system; caused by oxygen free radicals) may become a problem after 8-12 hours of continuous inhalation of 100% oxygen. Therefore the O2 concentration should be reduced when SPO2 is normalised. Airway pressure therapy during inspiration, expiration or both inspiration and expiration is possible in the intubated patient and helps to increase alveolar distending pressure in cases of pulmonary atelectasis.

Tracheostomy tubes may be required in brachycephalic breeds to circumvent upper respiratory tract obstruction (stenotic nares, pharyngeal folds, relatively elongated soft palate, everted laryngeal ventricles and laryngeal collapse). Peroral endotracheal intubation however may provide such relief to these dogs that it is tolerated with minimal sedation.

Fluids

Dogs with tick paralysis are not usually dehydrated on presentation. This may not apply to those occasional cases that have had excessive vomiting/drooling or are presented late in the course of their toxicity.

Unfortunately, the measuring of packed cell volume (PCV) alone can be misleading in regard to reflecting total body dehydration. In fact, PCV elevation at a rate greater than total protein (TP) elevation, is more likely to reflect a pulmonary fluid shift than dehydration. If such fluid shifts are occurring, then initially neglecting the administration of fluids is probably indicated. In fact such patients might actually benefit from the use of diuretics (eg furosemide) to help them through the most immediate risk of pulmonary oedema. If any fluids are used at all, then colloidal fluids may be less likely to exacerbate pulmonary oedema than crystalline fluids, but this has not been measured.

The situation is however dynamic. The severely affected patient may quickly change from requiring no fluids for the 48 hours, to then requiring fluids to maintain renal perfusion and preventing hyperviscosity, especially if diuretics have been used. It is worth noting that dyspnoea alone cannot be relied upon in judging that fluids are not required. This is because the initial slower cardiogenic dyspnoea may change to a more rapid dyspoea caused by a secondary pneumonia. Such toxaemic animals may then require even more than maintenance fluids, as well as antibiotics etc.

In summary, fluids are not initially required in most presented cases and in fact they may be detrimental to those with pulmonary oedema. An emphasis on monitoring of hydration is required- using clinical signs and whatever laboratory means are considered valuable without presenting undue stress to the animal (weighing, creatinine, serum osmolality, PCV, TP etc). Fluids are then given to match the need.

Antibiotics

Prophylactic antibiotics are not appropriate for most cases of tick paralysis. Antibiotics are warranted if aspiration pneumonia is suspected. In general, pathogens from dogs with pneumonia in decreasing frequency are Streptococcus spp (haemolytic and non haemolytic), Escherichia coli, anaerobes, Pasteurrella spp, Klebsiella spp, Staphylococcus spp, and Bordetella spp. A single species is isloated in about 60% of cases whereas the remainder have two or more organisms.

Glucocorticosteroids

Although glucocorticosteroids (eg dexamethasone 0.5 mg/kg) have been shown to be of some value in advanced cases of tick paralysis in a small study, their routine use may be unwarranted in dogs because of the risk of aspiration pneumonia (Malik, 1991). The most common rationale for their use is in protection against serum reactions even though these are quite rare (see premedication for serum reactions above). [NF: They may also complicate many other systems eg. gastritis, pancreatitis, colonic perforation, catabolism, latent infections etc]. Their routine prophylactic use has, however, been recommended in cats which are at greater risk of anaphylactic reactions to antiserum. [Some veterinarians also find that small dogs are at greater risk of reactions; use of glucocorticosteroids, dilution, adequate warming and slow injection of the antiserum may help to counter this problem].

Antiemetics

Tick poisoned animals frequently suffer from both regurgitation and true vomiting. The cause of true vomiting is not known but could be from direct effect of toxin on the chemoreceptor trigger zone (CRTZ), or a vagal reflex or a physical response to atonic distension.

Recumbency, pharyngeal dysfunction and laryngeal dysfunction heighten the associated risk of aspiration pneumonia. In humans, nausea (along with headache) is also a consistent symptom. The pre-existing risk of vomiting and regurgitation is actually increased by treatment with a bolus of antiserum (this reaction may be due to the cresol preservative used in antisera).

The role and effectiveness of antiemetics such as metoclopramide (Maxolon®), chlorpromazine (Largactil®) and prochlorperazine (Stemetil®) has not been established. Theoretically, helping to increase gastric emptying and increasing lower oeseophageal tone would be beneficial in reducing oesophagitis, excessive drooling and aspiration pneumonia as well as reducing anxiety and making the patient more comfortable.

Phenothiazines

The phenothiazine derivatives (acepromazine, chlorpromazine and prochlorperazine) are antagonists of alpha-1 and alpha-2, D-2 dopamine, H-1 and H-2 histamine, and muscarinic ACh receptors. They block vomiting at both the neural vomiting centre and at the chemoreceptor trigger zone. Stemetil® probably has the least sedating effects. It is also available in suppository form (Fitzgerald, 1998).

Metoclopramide

Metoclopramide (Maxolon®, Metomide®) is an antagonist of D-2 dopamine and 5HT-3 serotonin receptors but an agonist of peripheral ACh receptors. The cholinergic effect results in an increase in lower oesophageal tone and increased strength of oesophageal contractions, so improving the competence of the lower oesophageal "sphincter" zone. There is also an increase in gastric antral contractions, a relaxation of the pylorus, and an increase in contractions in the proximal small intestine. Gastric emptying is accelerated. It is not known whether it is effective in cases of tick-induced megaoesophagus (cholinergic drugs are apparently not effective in the megaoesophagus seen with myasthenia gravis). Metoclopramide is perhaps best avoided or at least used cautiously when using phenothiazines (ie ACP) due to enhanced risk of behavioural changes (eg disorientation; in humans metoclopramide has effects additive to the sedative and extrapyramidal effects of phenothiazines). Atropine may block the beneficial cholinergic effects of metoclopramide (Fitzgerald, 1998).

H2 blockers

The gastric antacids such as the H2-blockers cimetidine and ranitidine may, like the emetics, be be used to reduce nausea and the risks of oesophagitis and aspiration pneumonia. [There may be value in the prophylactic use of such medications. They are registered for slow IV use in humans when diluted in crystalline fluids. For tick cases I find it convenient to dilute with the anti-tick serum as this also is given slowly IV, although I cannot determine if there are any pharmacological reasons to avoid doing so]

Antisialics

Atropine

Drooling of saliva is thought to result from loss of pharyngeal tone and the swallowing reflex. It may exacerbate the dyspnoea and distress of a paralysed animal. Atropine, however, has been shown to be probably contraindicated in tick paralysis because of it's potentially haemodynamic and cardiotoxic effects (Malik and Farrow,1991). Nevertheless Jones (1991) suggests using atropine sulphate (dogs 0.05 mg/kg, cats 0.025 mg/kg, in both cases combined with acepromazine 0.1 mg/kg) when the patient is presented with saliva drooling from the mouth and has a bubbling sterterous breathing.

Hyoscine hydrobromide and chlorpheniramine maleate

Others have used hyoscine hydrobromide or the anthihistamine chlorpheniramine maleate.

[If drooling is due to reflux oesophagitis then antiemetics and H2 blockers may be safer and more appropriate, see Oesophageal suctioning]

Oesophageal Suctioning

In dogs a striated type of oesophageal musculature is much more predisposed to the paralysing effects of the tick toxin(s). This results in a megaoesophagus in most, if not all cases of tick paralysis in dogs (Mike Fitzgerald, pers com). Combined with a dilated pharynx and loss of a functional gag reflex this results in marked salivary pooling which may be sufficient to cause laryngeal obstruction and/or aspiration through a paralysed larynx. The choking effect causes great distress and anxiety in some dogs and is in itself potentially life-threatening.

Salivation may be compounded by gastro-oesophageal reflux. This is because the resulting acid-induced esophagitis stimulates a reflex salivation.

Regular suctioning with a suitably sized oesophageal or orogastric tube is recommended in dogs where salivation and attempts at gagging are pronounced (Atwell, 2000).

Body positioning may also be helpful- in lateral recumbency the high point should be shoulder to ensure natural clearance (Atwell, 2000 citing T. King pers com). Ideally, however, a sternal recumbency with head down position is maintained to assist both in fluid clearance and in ventilation.

Physical therapy

Assisted coughing

When positive pressure ventilation is not feasible intermittent physical chest compressions timed with normal exhalation may clear areas of dead space ventilation and provide "assisted coughing". With assisted coughing the animal is in lateral recumbency and one hand applies pressure in the epigastric region. During expiration the lateral chest wall is compressed downward and and the abdomen pushed toward the diaphragm, thus increasing the force of expired air and mobilising secretions (Manning et al, 1997). Whether this can worsen pulmonary oedema needs to be ascertained, but it might be at least be a useful technique in the later stages when pulmonary oedema is under control but aspiration pneumonia has developed.

Postural drainage

If pulmonary secretions are suspected, postural drainage in various recumbent positions (left and right lateral and ventral and dorsal, head both elevated and lowered), combined with chest percussion may help- provided they do not cause obvious additional stress. NB: the dependent lung has the most efficient ventilation/perfusion ratio and so when a collapsed/atelectatic lung is causing hypoxaemia it is best to place the healthy lung in the dependent position.

Chest percussion

Chest percussion with cupped hands is also useful (cupping the hands transmits energy to underlying lung rather than just the chest wall, as happens with a flat hand). It is performed during both inspiration and expiration. Frequent chest percussion stimulates coughing as mucous plugs are dislodged. It is possible that physical therapy may cause the animal stress and and it should therefore be employed with caution.

SUMMARY OF A TREATMENT PROTOCOL FOR DOGS [by Michael Fitzgerald (1998)]

1. Treat acute respiratory distress if present. Oxygen, minimise stress, sedation.
2. Confirm diagnosis and assess stage: paresis and respiratory compromise.
3. Premedicate: sedate if necessary ACP or other. Antiemetics if appropriate. Corticosteroids and antihistamines commonly used but not by this author.
4. Place IV line. Prepare TAS: dilute & warm. Flow-by oxygen if dyspnoeic. Institute whatever ventilatory support is indicated. Take blood for PCV and TPP.
5. Kill tick in situ: solvent (e.g. methylated spirit, turpentine), non-OP insecticide (fipronil or pyrethroid) or by freezing (cryosurgery aerosol "Histofreezer®"). Don't "annoy" the tick by handling it, just kill it.
6. Once stabilised administer TAS slowly- be patient. There is no hurry regarding this step. Give ample early.
7. Administer between 0.5 & 5 mLs subcutaneously at the tick site. This may or may not make a difference but will not hurt.
8. Place in cool cage (air-conditioning if available) and continue frequent observations. Monitor haemoglobin saturation, core temperature, respiratory rate & pattern, HR, BP, Mucous membrane colour & refill. Frequently check for airway patency, positioning, suctioning as necessary. Make sure temperature does not keep falling below say 36⁰C.
9. Provided animal is stable, perform search for further ticks and apply tickicide to kill any unfound ticks. ( whole body rinse/hydrobath, Frontline® spray). Clip whole body if this appears necessary and if it does not add to stress level.
10. Administer adjunctive drugs as necessary: e.g. diuretics and venodilators to reduce cardiac preload (furosemide, Nitro-Bid Lingual spray or ointment); bronchodilators; antibiotics for prevention of bacterial pneumonia secondary to aspiration pneumonitis; alpha-adrenergic blockers (ACP, phenoxybenzamine) to reduce sympathetic drive if excessive (^ HR, BP) and reduce afterload.
11. Administer crystalloid fluids cautiously IV if ^ PCV AND ^ TPP (avoid lactate-containing fluids) or colloids if available if pulmonary oedema present or if ^ PCV and normal TPP. Maintain oncotic pressure gradient.
12. If decompensating, administer ultrashort GA intubate, oxygenate and place on whatever 02 support is appropriate - see above.
13. Plan for further deterioration to some degree for about 12 hours after administration of TAS
14. Monitor fluid balance, progress of reversal of neuromuscular paralysis after 12 hours, oxygenation/ventilation, core temperature, PCV, nursing care, respiratory mucosal integrity, heart rate/rhythm, blood pressure, degree of distress and need for further sedation.
15. Reassess at 24 hrs. Slow recovery should prompt re-checking for further ticks and other underlying disease.
16. Gagging and retching that persists for several days after recovery of limb strength can be due to ongoing oesophagitis which on its own can reduce oesophageal tone. Consider antibiotics and analgesics (NSAIDS). A severe fibrinous oesophagitis may be observed endoscopically. (D. Deeley pers. com.)

 

SUMMARY OF A TREATMENT PROTOCOL FOR CATS by Richard Malik (1998)

This protocol was developed by R Malik over several years of treating cases at SUVTH (Malik, 1998). The contribution of Donna Bruhl is also acknowledged by the author.

1. after discovering a tick the cat is given acepromazine 0.05 mg/kg (usually 0.1 mL of 2mg/mL solution per cat) for it's sedative, hypotensive and antihistaminic actions.
2. cat is placed in a quiet, dark and preferably cool room; emergency drugs and equipment are readied whilst sedation is taking effect- these include infusion pump, Hartmanns solution, face mask, tick antitoxin, adrenaline 1:10,000, anaesthetic machine for O2 delivery, endotracheal tube (just in case), soluble prednisolone and fipronil (Frontline®)
3. the tick is removed using partially opened scissor tips as a lever (it is mentioned that Bernard Stone recommends pre-killing in situ before removal)
4. the cat is given 10 mg/kg soluble prednisolone (Solu-delta cortef) SC
5. after usual aseptic preparation an IV catheter is placed into a cephalic vein and IV infusion of Hartmanns is commenced at a rate of 2 mL/hour
6. 1 mL/kg of antitoxin is diluted out to 20 mL with Hartmanns solution
7. an assistant gently restrains the cat with the head sitting comfortably in a face mask, with oxygen flow at 2-3 L/min- the cats usually tolerate this very well when well sedated
8. 3 mL of adrenaline 1:10,000 (or 0.3 mL of 1:1000) is administered subcutaneously; an identical amount is drawn up ready to give in a syringe just in case it is needed later
9. about 3-4 minutes after the adrenaline injection (tachycardia should have developed) the antitoxin is administered slowly, over 1-2 minutes, into the injection port of the IV infusion line. If the cat collapses the same dose of adrenaline is administered but this time intravenously and the remaining antitoxin is then still given. Even if the cat collapses, usually the cardiovascular system settles down after 1-2 minutes
10. if dyspnoea is worrying, 1mg/kg of frusemide is administered intravenously
11. intravenous fluids are continued at the rate of 2 mL/hr/cat for the first 12-24 hours, which is just enough to keep the line open. After this time the fluid rate is increased to maintenance levels, usually 10-15 mL/hr/cat, and changed to a maintenance type such as 0.45% NaCl and 2.5% dextrose containing 20 mmol/L of KCl/L
12. cat is searched for more ticks and sprayed with Frontline which is combed through the coat to kill any missed ticks. Then 0.5-1.0 mL of tick antitoxin is injected underneath the tick lesion
13. the cat is then taken back to the cool, dark and quiet part of the hospital and if necessary positioned in sternal recumbency with towels. The cat's head is in a somewhat extended position. At the time of writing no feline cases had required ventilation by the author (R Malik). Whilst severely affected cats had a marked end-expiratory grunt, this usually became less marked about 4-6 hours after implementation of therapy.

Other Treatment Protocols

Please note that these protocols are given for purposes of providing a broad perspective and should be seen as giving anecdotal information only.

Alfaxan/Saffan:

"Alfaxan/Saffan has to be the best thing since sliced bread when it comes to treating cats with tick paralysis. Over the last four years I've been using it as part of my treatment with great success. All cats showing signs of tick paralysis from virtually no signs to the "near death syndrome" get the same protocol. 1/2ml Ace S/C, 1ml Histamil I/M, usually wait for 10 - 15 minutes then give saffan/alfaxan I/V. The dose varies from 1/3ml for the" near death" cat to 1ml for the cat showing few signs. A.V.S.L. tick antivenom given at 1ml per kg mixed with equal parts saline is given slowly I/V over 10 minutes. No nasty reactions seen and only 1 person needed to administer. Usually recover and go home in 24 - 48 hours. If the tick is still on the cat inject 1/2ml of antivenom S/C under tick and kill with permoxin. The tick is left in situ and falls off in 2-3 days. Over 4 years I have only lost one cat using this protocol, (usually see 4-8 per week at the height of the season)." From: Brian Roberts supervet@bigpond.com To: avalist@farmwide.com.au Sent: Wednesday, 13 September 2000 14:24 Subject: Alfaxan/Saffan, tick paralysis cats.

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Note 1. Some cases have had a high PCV ranging 0.65-0.82 L/L but concurently a normal TPP; possibly due to "third spacing" to body cavities or to interstitium such as pulmonary oedema or perhaps due to splenic contraction; transcapillary fluid shift into the extravascular space is also seen in the severe vasoconstriction of hypothermia, which is sometimes also present in tick paralysis; regardless of the cause, the resultant hyperviscosity increases cardiac workload and decreases microperfusion, and so may warrant the parenteral administration of colloid or crystalloid fluids.

Note 2. Why there is a delay in onset in action for the Ixodes holocyclus antiserum is not known. It could be that toxin bound to receptors is either inaccessible or takes longer for antibodies to reach (Fitzgerald, 1998). Given that the toxin somehow has a slow onset of action it is also possible that a slow sequence of events not helped by antiserum has already been initiated [see toxicology NF].

Note 3. When temperatures drop below 32° C one sees sinus bradycardia, depressed respiration and hypotension. Peripheral vasoconstriction leads to increased blood viscosity, capillary sludging, increased afterload and reduced cardiac output. Although dogs with core temperature at 30° C have oxygen consumption just 50% of normal, concurrent alveolar hypoventilation, decreased dissociation of oxyhaemoglobin and capillary sludging reduce the oxygen delivery. As hypothermia progresses, consciousness fades and the reduced respiratory rate can cause respiratory acidosis. Further respiratory compromise can occur with fluid shifts into pulmonary alveolar and interstitial spaces. Bronchial secretions become thick and tenacious and predispose to bacterial infections. Atrial irritability is seen early in hypothermia and ventricular irritability later, with a risk of developing PVCs and ventricular tachycardia. Platelet dysfunction and DIC are further serious risks with hypothermia. All these problems are likely to aggravate and even mask tick paralysis (Fitzgerald, 1998).

Note 4. According to Cooper's original research, not only was the neuromuscular blockade increased with increased temperatures but additionally survival in tick paralysed mice was reduced as ambient temperatures were raised to 25-27° C.

 

 

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