Veterinary Medicine

Ventricular arrhythmias

Site shows some of the common clinical situations associated with ventricular arrhythmias. As can be seen, many cardiac and extracardiac conditions which compromise oxygen supply to cardiac muscle leading to ischaemia, or which increase sympathetic stimulation to the heart or generate factors which are toxic to the myocardium, commonly give rise to ventricular arrhythmias. If cardiac muscle is abnormal or diseased in some way the chances of arrhythmias developing and being sustained are greater when compared to animals with a normal myocardium. It is important to distinguish between ventricular escape beats which occur due to failure of generation and or conduction of impulses from the sinoatrial node (which are preceded by a pause) and ventricular premature contractions () which occur prematurely after the preceding sinus beat. Escape complexes should never be suppressed by the use of antidysrhythmic drugs.

Having diagnosed the presence of ventricular premature contractions (VPCs) or bouts of ventricular tachycardia, the next decision to make is whether or not drug treatment is indicated to suppress that arrhythmia. Obviously, where there is an underlying predisposing condition for which there is appropriate treatment then this should be administered (for example fluid therapy to treat hypovolaemic shock and / or to correct acid-base and electrolyte disturbances, oxygen therapy to treat hypoxia, blood transfusion to increase oxygen-carrying capacity in severe anaemia). It is important that plasma electrolytes are measured in animals with cardiac arrhythmias since not only can abnormalities contribute to arrhythmogenesis but the efficacy and toxicity of antiarrhythmic drugs will be affected by electrolyte disturbances, particularly of potassium ion concentration. The danger with ventricular arrhythmias is that they may progress to ventricular fibrillation which leads to death very rapidly.

When should a ventricular arrhythmia be treated?

It is not possible to predict which patterns of ventricular arrhythmia are most likely to progress to ventricular fibrillation. The recommendations for treating or not treating a specific ventricular arrhythmia are therefore not based on controlled scientific studies but more on intuition. The importance of this decision is that many of the antidysrhythmic drugs used to treat ventricular arrhythmias have pro-arrhythmogenic potential and so could make the situation worse.

The decision to give drugs to suppress a ventricular arrhythmia is probably best made by assessing whether or not the rhythm disturbance is resulting in haemodynamic abnormalities. Those animals with weak pulses, poor peripheral perfusion and signs of muscle weakness and mental depression which can be attributed to the arrhythmia, should be treated. In addition, it is thought that frequent ventricular premature contractions (more than 20 per minute), particularly if they are multiform and are characterized by beats which occur immediately after the previous repolarization phase (the so called Vulnerable period) are more likely to progress to ventricular fibrillation.

Drugs used to treat ventricular arrhythmias

Diazepam, Lignocaine, Procainamide, Propranolol

Veterinary Medicine

Drugs used to treat ventricular arrhythmias

The drugs used most commonly in veterinary practice to treat ventricular arrhythmias are the Class I drugs (local anaesthetic agents) and the Class II drugs (beta-adrenoceptor antagonists). Site shows the ways in which these drugs interfere with the pathological mechanisms involved in arrhythmogenesis. Since the mechanisms involved in the generation of most ventricular arrhythmias cannot be determined from the surface ECG, the choice of drug remains empirical and trial therapy is essentially the only way by which the efficacy of a particular drug can be assessed.

Lignocaine is a Class 1b anti-arrhythmic agent and seems to have the advantage of showing selective suppressant action on damaged and ischaemic cardiac muscle cells with a less negative resting membrane potential while having little or no effect on the automaticity of atria I and normal ventricular myocardial tissue. In most cases. Therefore, it is the first drug of choice for treating serious ventricular arrhythmias. It is essential to ensure preparations of lignocaine without adrenaline are used. Lignocaine is administered as an intravenous bolus injection (given over 1-2 min) at a dose rate of 2 mg kg-1 in the dog and 0.5-1 mg kg-1 in the cat initially. Further boluses may be given (up to 6 mg kg-1 total dose in the dog) if no response is seen initially. Lignocaine toxicity can result in seizures which may be controlled with diazepam. If the plasma potassium concentration is normal, lignocaine will, in most cases, successfully suppress the arrhythmia or at least reduce the frequency of VPCs. A more sustained effect can be achieved by continuous intravenous infusion of lignocaine at a rate of 30-80 μg kg-1 min-1 in the dog and 10-20 μg kg-1 min-1 in the cat. Orally active Class 1b drugs are available and have been shown to be elfective in longer-term therapy (tocainide at a dose of 10-20 mg kg-1 tid, for example).

If lignocaine is not successful, procainamide (Class 1a agent) would be the next drug to try at a dose rate of 5-15 mg kg-1 intravenously or intramuscularly. In an intensive care setting, procainamide can be given by continuous intravenous infusion at a dose of 25-40 μg kg-1 min-1. Oral procainamide can be administered at 10-20 mg kg-1 every 6 h for longer-term therapy. In some cases, administration of propranolol (0.25—1 mg kg-1 orally or 0.1 mg kg-1 intravenously) with lignocaine or procainamide may provide a synergistic effect. Caution must be exercised when using these agents, particularly by the intravenous route, as they all possess the ability to reduce myocardial contractility. In addition, propranolol will reduce the clearance of lignocaine from the circulation, thus potentiating the toxicity of lignocaine, hence the need to reduce the dose of lignocaine if combined with propranolol.

The goals of drug therapy for ventricular arrhythmias should be an improvement of the animal’s haemodynamic status and a reduction in the frequency of VPCs. If this can be achieved and if the underlying disease can be successfully resolved, the need for drug therapy should also disappear. If the underlying problem is not amenable to treatment, long-term drug therapy may be necessary. There is no evidence that anti-dysrhythmic drugs used under these circumstances will prolong the duration of the animal’s life but the quality of life may improve if the frequency and duration of syneopal attacks are reduced. Unfortunately, it is equally possible that some arrhythmias can be worsened by long-term administration of anti-arrhythmic drugs. The significance and incidence of worsening of arrhythmias by the drugs used to treat them can only be assessed by studies which use continuous ambulatory ECG monitoring. The use of two drugs with different mechanisms of action (such as propranolol and procainamide) may produce a synergistic effect. This may allow a reduction in the dosage of the two agents used, which is beneficial since it should reduce the side effects of the drugs, including their pro-arrhythmogenic potential.

Veterinary Procedures

Urine Collection Techniques

Urine can be removed from the bladder by one of four methods: (1) voided (the “free catch”), (2) manual compression of the urinary bladder (expressing the bladder), (3) catheterization, or (4) cystocentesis.


For routine urinalysis, collection of urine by voiding (micturition) is satisfactory. The major disadvantage is risk of contamination of the sample with cells, bacteria, and other debris located in the genital tract and the perineal hair coat. The first portion of the stream is discarded, as it is most likely to contain debris. Voided urine samples are not recommended when bacterial cystitis is suspected.

Manual Compression of the Bladder

Compressing the urinary bladder is occasionally used to collect urine samples from dogs and cats. Critical: Do not use excessive pressure; if moderate digital pressure does not induce micturition, discontinue the technique. Excessive pressure can culminate in forcing contaminated urine (bladder) into the kidneys, or, worse, in patients with a urethral obstruction the urinary bladder can rupture. The technique is most difficult to accomplish in male dogs and male cats.

Urinary Catheterization

Several types of urinary catheters are currently available for use in dogs and cats. The catheter types most often used today are made of rubber, polypropylene, and latex-free silicone. Stainless steel catheters are occasionally used but unless placed with care these can cause damage to the urethra and/or urinary bladder. Generally, urinary catheters serve one of four purposes:

  1. 1. To relieve urinary retention
  2. 2. To test for residual urine
  3. 3. To obtain urine directly from the bladder for diagnostic purposes
  4. 4. To perform bladder lavage and instillation of medication or contrast material

The size of catheters (diameter) usually is calibrated in the French scale; each French unit is equivalent to roughly 0.33 mm. The openings adjacent to the catheter tips are called “eyes.” Human urethral catheters are used routinely in male and female dogs; 4F to 10F catheters are satisfactory for most dogs (Table Recommended Urethral Catheter Sizes for Routine Use in Dogs and Cats). Polypropylene catheters should be individually packaged and sterilized by ethylene oxide gas.

TABLE Recommended Urethral Catheter Sizes for Routine Use in Dogs and Cats

Animal Urethral Catheter Type Size (French Units*)
Cat Flexible vinyl, red rubber, or Tom Cat catheter (polyethylene) 3.5
Male dog (<25 lb) Flexible vinyl, red rubber, or polyethylene 3.5 or 5
Male dog (>25 lb) Flexible vinyl, red rubber, or polyethylene 8
Male dog (>75 lb) Flexible vinyl, red rubber, or polyethylene 10 or 12
Female dog (<10 lb)) Flexible vinyl, red rubber, or polyethylene 5
Female dog (10-50 lb) Flexible vinyl, red rubber, or polyethylene 8
Female dog (>50 lb) Flexible vinyl, red rubber, or polyethylene 10, 12, or 14

*The diameter of urinary catheters is measured on the French (F) scale. One French unit equals roughly 0.33 mm.

Catheterization of the Male Dog

Patient Preparation

Equipment needed to catheterize a male dog includes a sterile catheter (4F to 10F, 18 inches long, with one end adapted to fit a syringe), sterile lubricating jelly, povidone-iodine soap or chlorhexidine, sterile rubber gloves or a sterile hemostat, a 20-mL sterile syringe, and an appropriate receptacle for the collection of urine.

Proper catheterization of the male dog requires two persons. Place the dog in lateral recumbency on either side. Pull the rear leg that is on top forward, and then flex it (). Alternatively, long-legged dogs can be catheterized easily in a standing position.

Before catheter placement, retract the sheath of the penis and cleanse the glans penis with a solution of povidone-iodine 1% or chlorhexidine. Lubricate the distal 2 to 3 cm of the appropriate-size catheter with sterile lubricating jelly. Never entirely remove the catheter from its container while it is being passed because the container enables one to hold the catheter without contaminating it.


The catheter may be passed with sterile gloved hands or by using a sterile hemostat to grasp the catheter and pass it into the urethra. Alternatively, cut a 2-inch “butterfly” section from the end of the thin plastic catheter container. This section can be used as a cover for the sterile catheter, and the clinician can use the cover to grasp and advance the catheter without using gloves.

If the catheter cannot be passed into the bladder, the tip of the catheter may be caught in a mucosal fold of the urethra or there may be a stricture or block in the urethra. In small-breed dogs, the size of the groove in the os penis may limit the size of the catheter that can be passed. One also may experience difficulty in passing the catheter through the urethra where the urethra curves around the ischial arch. Occasionally a catheter of small diameter may kink and bend on being passed into the urethra. When the catheter cannot be passed on the first try, reevaluate the size of the catheter and gently rotate the catheter while passing it a second time. Never force the catheter through the urethral orifice.

Special Considerations

Effective catheterization is indicated by the flow of urine at the end of the catheter, and a sterile 20-mL syringe is used to aspirate the urine from the bladder. Walk the dog immediately after catheterization to encourage urination.

Catheterization of the Female Dog

Patient Preparation

Equipment needed to catheterize a female dog includes flexible urethral catheters identical to those used in the male dog. The following materials also should be on hand: a small nasal speculum, a 20-mL sterile syringe, lidocaine 0.5%, sterile lubricating jelly, a focal source of light, appropriate receptacles for urine collection, and 5 mL of povidone-iodine or a dilute chlorhexidine solution.

Use strict asepsis. Cleanse the vulva with a solution of povidone-iodine or dilute chlorhexidine. Instillation of lidocaine 0.5% into the vaginal vault helps to relieve the discomfort of catheterization. The external urethral orifice is 3 to 5 cm cranial to the ventral commissure of the vulva. In many instances the female dog may be catheterized in the standing position by passing the female catheter into the vaginal vault, despite the fact that the urethral papilla is not visualized directly.


In the spayed female dog, in which blind catheterization may be difficult, the use of a sterilized otoscope speculum andlight source (), vaginal speculum, or anal speculum with a light source will help to visualize the urethral tubercle on the floor of the vagina. In difficult catheterizations it may be helpful to place the animal in dorsal recumbency (). Insertion of a speculum into the vagina almost always permits visualization of the urethral papilla and facilitates passage of the catheter. Take care to avoid attempts to pass the catheter into the fossa of the clitoris because this is a blind, possibly contaminated cul-de-sac.

Catheterization of the Male Cat

Patient Preparation

Before attempting urinary bladder catheterization of the male cat, administer a short-term anesthetic (e.g., ketamine, 25 mg/kg IM), but only after a careful assessment of the cats physical, acid-base, and electrolyte status (see treatment of hyperkalemia).

In some cases, drugs to treat hyperkalemia may be required before anesthetic induction. Once the patient’s electrolyte status has been evaluated and hyperkalemia, if present, addressed appropriately, anesthesia can be induced with a combination of propofol (4 to 7 mg/kg intravenously [IV]) and diazepam (0.1 mg/kg IV); then the patient is intubated and maintained on gas anesthesia.


Place the anesthetized patient in dorsal recumbency. Gently grasp the ventral aspect of the prepuce and move it caudally in such a manner that the penis is extruded. Withdraw the penis from the sheath and gently pull the penis backward. Keeping sterile catheters in a freezer will help them become more rigid to facilitate passage into the urethra. Pass a sterile, flexible plastic or polyethylene (PE 60 to 90) catheter or 3- to 5-inch, 3.5F urethral catheter into the urethral orifice and gently into the bladder, keeping the catheter parallel to the vertebral column of the cat.

Caution: Never force the catheter through the urethra. The presence of debris within the urethral lumen may require the injection of 3 to 5 mL of sterile saline to back-flush urinary “sand” or concretions so that the catheter can be passed. In some instances the presence of cystic and urethral calculi will prevent the passage of a catheter into the urethra. For this reason a lateral radiograph of the penis, with the patients hindlimbs pulled caudally, may help document the presence of a urethral stone.

Catheterization of the Female Cat

Patient Preparation

Urinary bladder catheterization of the female cat is not a simple procedure. When indicated, and after a preanesthetic examination has been performed, attempt the technique only in the anesthetized cat. Urinary bladder catheterization can be accomplished with the use of a rubber or plastic, side-hole (blunt-ended) urinary catheter. The same catheter type used in male cats is effective in female cats. Instilling lidocaine 0.5% has been recommended as a means of decreasing sensitivity to catheter insertion in sedated (not recommended) cats. Cleanse the vulva with an appropriate antiseptic.


Catheterization can be accomplished with the cat in dorsal or ventral recumbency.

Experience and size of the cat dictate which technique works best.

After cleansing of the perineum and vaginal vault, place the patient in sternal recumbency, and gently pass the catheter along the ventral floor of the vaginal vault. Conversely, if the patient is placed in dorsal recumbency, direct the catheter dorsally along the ventral vaginal floor. If a catheter cannot be placed blindly, a small otoscopic speculum can be placed into the vagina, and the catheter pushed into the urethral papilla once it is visualized directly.

Indwelling Urethral Catheter

Patient Preparation

For continuous urine drainage in the awake, ambulatory patient, use a closed collection system to help prevent urinary tract infection. A soft urethral or Foley catheter can be used, and polyvinyl chloride tubing should be connected to the catheter and to the collection bag outside the cage. The collection bag should be below the level of the animal’s urinary bladder. Place an Elizabethan collar on the animal to discourage chewing on the catheter and associated tubing.


The urinary bladder is catheterized as described previously. Despite the quality of care of the catheter, urinary tract infection still may develop in any patient fitted with an indwelling urinary catheter. Ideally, remove the catheter as soon as it is no longer necessary, or if there are clinical signs of a urinary tract infection or previously undiagnosed fever. A urinary catheter is generally changed after it has been in place for more than 48 hours.

Special Considerations

Observe the patient for development of fever, discomfort, pyuria, or other evidence of urinary tract infection. If infection is suspected, remove the catheter and submit urine for culture and sensitivity or determination of minimum inhibitory concentration (MIC). Previously, culture of the catheter tip was recommended to diagnose a catheter-induced infection. However, culture of the catheter tip is no longer recommended, as it may not accurately reflect the type of microorganisms in a urinary tract infection. The empiric use of antibiotics to help prevent catheter-induced infection is not recommended, as their use can allow colonization of resistant nosocomial bacteria in the patient’s urinary tract.


Patient Preparation

Cystocentesis is a common clinical technique used to obtain a sample of urine directly from the urinary bladder of dogs and cats when collecting a voided, or free-catch, aliquot is not preferred. The procedure is indicated when necessary to obtain bladder urine for culture purposes. Urine that is collected by free catch has passed through the urethra and may be contaminated with bacteria, thereby making interpretation of the culture results difficult. Cystocentesis also is performed as a convenience when it is desirable to obtain a small sample of urine but the patient is not ready or cooperative.

Cystocentesis involves insertion of a needle, with a 6- or 12-mL syringe attached, through the abdominal wall and bladder wall to obtain urine samples for urinalysis or bacterial culture. The technique prevents contamination of urine by urethra, genital tract, or skin and reduces the risk of obtaining a contaminated sample. Cystocentesis also may be needed to decompress a severely overdistended bladder temporarily in an animal with urethral obstruction. In these cases, cystocentesis should be performed only if urethral catheterization is impossible. Warning: Penetration of a distended (obstructed) urinary bladder with a needle could result in rupture of the bladder.


To perform cystocentesis, palpate the ventral abdomen just cranial to the junction of the bladder with the urethra, and trap the urinary bladder between the fingers and the palm of the hand. Use one hand to hold the bladder steady within the peritoneal cavity while the other guides the needle. Next, insert the needle through the ventral abdominal wall into the bladder at a 45-degree angle (). Although this procedure is relatively safe, the bladder must have a reasonable volume of urine, and the procedure should not be performed without first identifying and immobilizing the bladder. For the procedure to be performed safely and quickly, the patient must be cooperative. If collection of a urine sample by cystocentesis is absolutely necessary, sedation may be indicated to restrain the patient adequately for the procedure.

Special Considerations

Generally, cystocentesis is a safe procedure, assuming the patient is cooperative and the bladder can be identified and stabilized throughout the procedure. However, injury and adverse reactions can occur. In addition to laceration of the bladder with the inserted needle (patient moves abruptly), the needle can be passed completely through the bladder and into the colon, causing bacterial contamination of the bladder or peritoneal cavity. There is also risk of penetrating a major abdominal bloodvessel, resulting in significant hemorrhage.


Aminophylline Theophylline

Phosphodiesterase Inhibitor Bronchodilator

Highlights Of Prescribing Information

Bronchodilator drug with diuretic activity; used for bronchospasm & cardiogenic pulmonary edema

Narrow therapeutic index in humans, but dogs appear to be less susceptible to toxic effects at higher plasma levels

Therapeutic drug monitoring recommended

Many drug interactions

What Is Aminophylline Theophylline Used For?

The theophyllines are used primarily for their broncho dilatory effects, often in patients with myocardial failure and/or pulmonary edema. While they are still routinely used, the methylxanthines must be used cautiously due to their adverse effects and toxicity.


The theophyllines competitively inhibit phosphodiesterase thereby increasing amounts of cyclic AMP which then increase the release of endogenous epinephrine. The elevated levels of cAMP may also inhibit the release of histamine and slow reacting substance of anaphylaxis (SRS-A). The myocardial and neuromuscular transmission effects that the theophyllines possess maybe a result of translocating intracellular ionized calcium.

The theophyllines directly relax smooth muscles in the bronchi and pulmonary vasculature, induce diuresis, increase gastric acid secretion and inhibit uterine contractions. They have weak chronotropic and inotropic action, stimulate the CNS and can cause respiratory stimulation (centrally-mediated).


The pharmacokinetics of theophylline have been studied in several domestic species. After oral administration, the rate of absorption of the theophyllines is limited primarily by the dissolution of the dosage form in the gut. In studies in cats, dogs, and horses, bioavail-abilities after oral administration are nearly 100% when non-sustained release products are used. One study in dogs that compared various sustained-release products (), found bioavailabilities ranging from approximately 30-76% depending on the product used.

Theophylline is distributed throughout the extracellular fluids and body tissues. It crosses the placenta and is distributed into milk (70% of serum levels). In dogs, at therapeutic serum levels only about 7-14% is bound to plasma proteins. The volume of distribution of theophylline for dogs has been reported to be 0.82 L/kg. The volume of distribution in cats is reported to be 0.46 L/kg, and in horses, 0.85-1.02 L/kg. Because of the low volumes of distribution and theophylline’s low lipid solubility, obese patients should be dosed on a lean body weight basis.

Theophylline is metabolized primarily in the liver (in humans) to 3-methylxanthine which has weakbronchodilitory activity. Renal clearance contributes only about 10% to the overall plasma clearance of theophylline. The reported elimination half-lives (mean values) in various species are: dogs = 5.7 hours; cats = 7.8 hours, pigs = 11 hours; and horses = 11.9 to 17 hours. In humans, there are very wide interpatient variations in serum half-lives and resultant serum levels. It could be expected that similar variability exists in veterinary patients, particularly those with concurrent illnesses.

Before you take Aminophylline Theophylline

Contraindications / Precautions / Warnings

The theophyllines are contraindicated in patients who are hypersensitive to any of the xanthines, including theobromine or caffeine. Patients who are hypersensitive to ethylenediamine should not take aminophylline.

The theophyllines should be administered with caution in patients with severe cardiac disease, seizure disorders, gastric ulcers, hyperthyroidism, renal or hepatic disease, severe hypoxia, or severe hypertension. Because it may cause or worsen preexisting arrhythmias, patients with cardiac arrhythmias should receive theophylline only with caution and enhanced monitoring. Neonatal and geriatric patients may have decreased clearances of theophylline and be more sensitive to its toxic effects. Patients with CHF may have prolonged serum half-lives of theophylline.

Adverse Effects

The theophyllines can produce CNS stimulation and gastrointestinal irritation after administration by any route. Most adverse effects are related to the serum level of the drug and may be symptomatic of toxic blood levels; dogs appear to tolerate levels that may be very toxic to humans. Some mild CNS excitement and GI disturbances are not uncommon when starting therapy and generally resolve with chronic administration in conjunction with monitoring and dosage adjustments.

Dogs and cats can exhibit clinical signs of nausea and vomiting, insomnia, increased gastric acid secretion, diarrhea, polyphagia, polydipsia, and polyuria. Side effects in horses are generally dose related and may include: nervousness, excitability (auditory, tactile, and visual), tremors, diaphoresis, tachycardia, and ataxia. Seizures or cardiac dysrhythmias may occur in severe intoxications.

Reproductive / Nursing Safety

In humans, the FDA categorizes this drug as category C for use during pregnancy (Animal studies have shown an adverse effect on the fetus, hut there are no adequate studies in humans; or there are no animal reproduction studies and no adequate studies in humans.)

Overdosage / Acute Toxicity

Clinical signs of toxicity (see above) are usually associated with levels greater than 20 mcg/mL in humans and become more severe as the serum level exceeds that value. Tachycardias, arrhythmias, and CNS effects (seizures, hyperthermia) are considered the most life-threatening aspects of toxicity. Dogs appear to tolerate serum levels higher than 20 mcg/mL.

Treatment of theophylline toxicity is supportive. After an oral ingestion, the gut should be emptied, charcoal and a cathartic administered using the standardized methods and cautions associated with these practices. Patients suffering from seizures should have an adequate airway maintained and treated with IV diazepam. The patient should be constantly monitored for cardiac arrhythmias and tachycardia. Fluid and electrolytes should be monitored and corrected as necessary. Hyperthermia may be treated with phenothiazines and tachycardia treated with propranolol if either condition is considered life threatening.

How to use Aminophylline Theophylline

Note: Theophyllines have a low therapeutic index; determine dosage carefully. Because of aminophylline/theophylline’s pharmacokinet-ic characteristics, it should be dosed on a lean body weight basis in obese patients. Dosage conversions between aminophylline and theophylline can be easily performed using the information found in the Chemistry section below. Aminophylline causes intense local pain when administered IM and is rarely used or recommended via this route.

Aminophylline Theophylline dosage for dogs:

a) Using Theochron Extended-Release Tablets or Theo-Cap Extended-Release Capsules: Give 10 mg/kg PO every 12 hours initially, if no adverse effects are observed and the desired clinical effect is not achieved, give 15 mg/kg PO q12h while monitoring for adverse effects. ()

b) For adjunctive medical therapy for mild clinical signs associated with tracheal collapse (<50% collapse): aminophylline: 11 mg/kg PO, IM or IV three times daily. ()

c) For adjunctive therapy of severe, acute pulmonary edema and bronchoconstriction: Aminophylline 4-8 mg/kg IV or IM, or 6-10 mg/kg PO every 8 hours. Long-term use is not recommended. ()

d) For cough: Aminophylline: 10 mg/kg PO, IV three times daily ()

e) As a broncho dilator tor collapsing trachea: 11 mg/kg PO or IV q6- 12h ()

Aminophylline Theophylline dosage for cats:

a) Using Theo-Dur 20 mg/kg PO once daily in the PM; using Slo-Bid 25 mg/kg PO once daily in the PM (Johnson 2000) [Note: The products Theo-Dur and Slo-Bid mentioned in this reference are no longer available in the USA. Although hard data is not presently available to support their use in cats, a reasonable alternative would be to cautiously use the dog dose and products mentioned above in the reference by Bach et al — Plumb]

b) Using aminophylline tablets: 6.6. mg/kg PO twice daily; using sustained release tablets (Theo-Dur): 25-50 mg (total dose) per cat PO in the evening ()

c) For adjunctive medical therapy for mild clinical signs associated with tracheal collapse (<50% collapse): aminophylline: 5 mg/kg PO, two times daily. ()

d) For adjunctive therapy for bronchoconstriction associated with fulminant CHF: Aminophylline 4-8 mg/kg SC, IM, IV q8-12h. ()

e) For cough: Aminophylline: 5 mg/kg PO twice daily ()

Aminophylline Theophylline dosage for ferrets:

a) 4.25 mg/kg PO 2-3 times a day ()

Aminophylline Theophylline dosage for horses:

(Note: ARCI UCGFS Class 3 Aminophylline Theophylline)

NOTE: Intravenous aminophylline should be diluted in at least 100 mL of D5W or normal saline and administered slowly (not >25 mg/min). For adjunctive treatment of pulmonary edema:

a) Aminophylline 2-7 mg/kg IV q6- 12h; Theophylline 5-15 mg/kg PO q12h ()

b) 11 mg/kg PO or IV q8-12h. To “load” may either double the initial dose or give both the oral and IV dose at the same time. IV infusion should be in approximately 1 liter of IV fluids and given over 20-60 minutes. Recommend monitoring serum levels. ()

For adjunctive treatment for heaves (RAO):

a) Aminophylline: 5-10 mg/kg PO or IV twice daily. ()

b) Aminophylline: 4-6 mg/kg PO three times a day. ()


■ Therapeutic efficacy and clinical signs of toxicity

■ Serum levels at steady state. The therapeutic serum levels of theophylline in humans are generally described to be between 10-20 micrograms/mL. In small animals, one recommendation for monitoring serum levels is to measure trough concentration; level should be at least above 8-10 mcg/mL (Note: Some recommend not exceeding 15 micrograms/mL in horses).

Client Information

■ Give dosage as prescribed by veterinarian to maximize the drug’s benefit

Chemistry / Synonyms

Xanthine derivatives, aminophylline and theophylline are considered to be respiratory smooth muscle relaxants but, they also have other pharmacologic actions. Aminophylline differs from theophylline only by the addition of ethylenediamine to its structure and may have different amounts of molecules of water of hydration. 100 mg of aminophylline (hydrous) contains approximately 79 mg of theophylline (anhydrous); 100 mg of aminophylline (anhydrous) contains approximately 86 mg theophylline (anhydrous). Conversely, 100 mg of theophylline (anhydrous) is equivalent to 116 mg of aminophylline (anhydrous) and 127 mg aminophylline (hydrous).

Aminophylline occurs as bitter-tasting, white or slightly yellow granules or powder with a slight ammoniacal odor and a pKa of 5. Aminophylline is soluble in water and insoluble in alcohol.

Theophylline occurs as bitter-tasting, odorless, white, crystalline powder with a melting point between 270-274°C. It is sparingly soluble in alcohol and only slightly soluble in water at a pH of 7, but solubility increases with increasing pH.

Aminophylline may also be known as: aminofilina, aminophyllinum, euphyllinum, metaphyllin, theophyllaminum, theophylline and ethylenediamine, theophylline ethylenediamine compound, or theophyllinum ethylenediaminum; many trade names are available.

Theophylline may also be known as: anhydrous theophylline, teofillina, or theophyllinum; many trade names are available.

Storage / Stability/Compatibility

Unless otherwise specified by the manufacturer, store aminophylline and theophylline oral products in tight, light-resistant containers at room temperature. Do not crush or split sustained-release oral products unless label states it is permissible.

Aminophylline for injection should be stored in single-use containers in which carbon dioxide has been removed. It should also be stored at temperatures below 30°C and protected from freezing and light. Upon exposure to air (carbon dioxide), aminophylline will absorb carbon dioxide, lose ethylenediamine and liberate free theophylline that can precipitate out of solution. Do not inject aminophylline solutions that contain either a precipitate or visible crystals.

Aminophylline for injection is reportedly compatible when mixed with all commonly used IV solutions, but may be incompatible with 10% fructose or invert sugar solutions.

Aminophylline is reportedly compatible when mixed with the following drugs: amobarbital sodium, bretylium tosylate, calcium gluconate, chloramphenicol sodium succinate, dexamethasone sodium phosphate, dopamine HCL, erythromycin lactobionate, heparin sodium, hydro cortisone sodium succinate, lidocaine HCL, mephentermine sulfate, methicillin sodium, methyldopate HCL, metronidazole with sodium bicarbonate, pentobarbital sodium, phenobarbital sodium, potassium chloride, secobarbital sodium, sodium bicarbonate, sodium iodide, terbutaline sulfate, thiopental sodium, and verapamil HCL

Aminophylline is reportedly incompatible (or data conflicts) with the following drugs: amikacin sulfate, ascorbic acid injection, bleomycin sulfate, cephalothin sodium, cephapirin sodium, clindamycin phosphate, codeine phosphate, corticotropin, dimenhydrinate, dobutamine HCL, doxorubicin HCL, epinephrine HCL, erythromycin gluceptate, hydralazine HCL, hydroxyzine HCL, insulin (regular), isoproterenol HCL, levorphanol bitartrate, meperidine HCL, methadone HCL, methylprednisolone sodium succinate, morphine sulfate, nafcillin sodium, norepinephrine bitartrate, oxytetracycline, penicillin G potassium, pentazocine lactate, procaine HCL, prochlorperazine edisylate or mesylate, promazine HCL, promethazine HCL, sulfisoxazole diolamine, tetracycline HCL, vancomycin HCL, and vitamin B complex with C. Compatibility is dependent upon factors such as pH, concentration, temperature, and diluent used and it is suggested to consult specialized references for more specific information.

Dosage Forms / Regulatory Status

Veterinary-Labeled Products: None

The ARCI (Racing Commissioners International) has designated this drug as a class 3 substance. See the appendix for more information.

Human-Labeled Products:

The listing below is a sampling of products and sizes available; consult specialized references for a more complete listing.

Aminophylline Tablets: 100 mg (79 mg theophylline) & 200 mg (158 mg theophylline); generic; (Rx)

Aminophylline Injection: 250 mg (equiv. to 197 mg theophylline) mL in 10 mL & 20 mL vials, amps and syringes; generic; (Rx)

Theophylline Time Released Capsules and Tablets: 100 mg, 125 mg 200 mg, 300 mg, 400 mg, 450 mg, & 600 mg. (Note: Different products have different claimed release rates which may or may not correspond to actual times in veterinary patients; Theophylline Extended-Release (Dey); Theo-24 (UCB Pharma); Theophylline SR (various); Theochron (Forest, various); Theophylline (Able); Theocron (Inwood); Uniphyl (Purdue Frederick); generic; (Rx)

Theophylline Tablets and Capsules: 100 mg, 200 mg, & 300 mg; Bronkodyl (Winthrop); Elixophyllin (Forest); generic; (Rx)

Theophylline Elixir: 80 mg/15 mL (26.7 mg/5 mL) in pt, gal, UD 15 and 30 mL, Asmalix (Century); Elixophyllin (Forest); Lanophyllin (Lannett); generic; (Rx)

Theophylline & Dextrose Injection: 200 mg/container in 50 mL (4 mg/mL) & 100 mL (2 mg/mL); 400 mg/container in 100 mL (4 mg/ mL), 250 mL (1.6 mg/mL), 500 mL (0.8 mg/mL) & 1000 mL (0.4 mg/mL); 800 mg/container in 250 mL (3.2 mg/mL), 500 mL (1.6 mg/mL) & 1000 mL (0.8 mg/mL); Theophylline & 5% Dextrose (Abbott & Baxter); (Rx)


Alprazolam (Xanax)

Benzodiazepine Sedative / Tranquilizer

Highlights Of Prescribing Information

Oral benzodiazepine that may be useful for unwanted behaviors in dogs or cats

Contraindications: Aggressive animals (controversial), benzodiazepine hypersensitivity

Caution: Hepatic or renal disease

Adverse Effects: Sedation, behavior changes, & contradictory responses; physical dependence is a possibility; may impede training

C-IV controlled substance

What Is Alprazolam Used For?

Alprazolam may be useful for adjunctive therapy in anxious, aggressive dogs or in those demonstrating panic reactions. (Note: Some clinicians believe that benzodiazepines are contraindicated in aggressive dogs as anxiety may actually restrain the animal from aggressive tendencies). It may be useful in cats to treat anxiety disorders.

Alprazolam may have less effect on motor function at low doses than does diazepam.


Subcortical levels (primarily limbic, thalamic, and hypothalamic) of the CNS are depressed by alprazolam and other benzodiazepines thus producing the anxiolytic, sedative, skeletal muscle relaxant, and anticonvulsant effects seen. The exact mechanism of action is unknown, but postulated mechanisms include: antagonism of serotonin, increased release of and/or facilitation of gamma-aminobutyric acid (GABA) activity, and diminished release or turnover of acetylcholine in the CNS. Benzodiazepine specific receptors have been located in the mammalian brain, kidney, liver, lung, and heart. In all species studied, receptors are lacking in the white matter.


The pharmacokinetics of alprazolam have not been described for either dogs or cats. In humans, alprazolam is well absorbed and is characterized as having an intermediate onset of action. Peak plasma levels occur in 1-2 hours.

Alprazolam is highly lipid soluble and widely distributed throughout the body. It readily crosses the blood-brain barrier and is somewhat bound to plasma proteins (80%).

Alprazolam is metabolized in the liver to at least two metabolites, including alpha-hydroxyalprazolam which is pharmacologically active. Elimination half-lives range from 6-27 hours in people.

Before you take Alprazolam

Contraindications / Precautions / Warnings

Some clinicians believe that benzodiazepines are contraindicated in aggressive dogs as anxiety may actually restrain the animal from aggressive tendencies. This remains controversial. Alprazolam is contraindicated in patients with known hypersensitivity to the drug. Use cautiously in patients with hepatic or renal disease, narrow angle glaucoma and debilitated or geriatric patients. Benzodiazepines may impair the abilities of working animals.

Adverse Effects

Benzodiazepines can cause sedation, increased appetite, and transient ataxia. Cats may exhibit changes in behavior (irritability, increased affection, depression, aberrant demeanor) after receiving benzodiazepines.

Dogs may rarely exhibit a contradictory response (CNS excitement) following administration of benzodiazepines.

Chronic usage of benzodiazepines may induce physical dependence. Animals appear to be less likely than humans to develop physical dependence.

Benzodiazepines may impede the ability of the animal to learn and may retard training.

Reproductive / Nursing Safety

Diazepam and other benzodiazepines have been implicated in causing congenital abnormalities in humans if administered during the first trimester of pregnancy. Infants born of mothers receiving large doses of benzodiazepines shortly before delivery have been reported to suffer from apnea, impaired metabolic response to cold stress, difficulty in feeding, hyperbilirubinemia, hypotonia, etc. Withdrawal symptoms have occurred in infants whose mothers chronically took benzodiazepines during pregnancy. The veterinary significance of these effects is unclear, but the use of these agents during the first trimester of pregnancy should only occur when the benefits clearly outweigh the risks associated with their use. In humans, the FDA categorizes this drug as category D for use during pregnancy (There is evidence of human fetal risk, hut the potential benefits from the use of the drug in pregnant women may he acceptable despite its potential risks.)

Overdosage / Acute Toxicity

When administered alone, alprazolam overdoses are generally limited to significant CNS depression (confusion, coma, decreased reflexes, etc.). Hypotension, respiratory depression, and cardiac arrest have been reported in human patients but apparently, are quite rare. The reported LD50 in rats for alprazolam is >330 mg/kg, but cardiac arrest occurred at doses as low as 195 mg/kg.

There were 935 exposures to alprazolam reported to the ASPCA Animal Poison Control Center (APCC; during 2005-2006. In these cases 863 were dogs with 208 showing clinical signs, 63 were cats with 20 showing clinical signs, 3 were rodents with 1 reported as having clinical signs, and 2 cases were rabbits with 1 reported as having clinical signs. Common findings in dogs recorded in decreasing frequency included ataxia, lethargy, hyperactivity, disorientation, depression. Common findings in cats recorded in decreasing frequency included ataxia disorientation, sedation, hyperactivity and restlessness. Common findings in rodents recorded in decreasing frequency included ataxia, somnolence and vomiting. Common findings in lagomorphs recorded in decreasing frequency included ataxia and lethargy.

Treatment of acute toxicity consists of standard protocols for removing and/or binding the drug in the gut if taken orally and supportive systemic measures. Flumazenil (see separate monograph) may be employed to reverse the sedative effects of alprazolam, but only if the patient has significant CNS or respiratory depression. Seizures may be precipitated in patients physically dependent. The use of analeptic agents (CNS stimulants such as caffeine) is generally not recommended.

How to use Alprazolam

Alprazolam dosage for dogs:

a) For treatment of canine anxiety disorders: 0.01-0.1 mg/kg PO as needed for panic, not to exceed 4 mg/dog/day. Start with 1-2 mg (total dose) for a medium-sized dog. ()

b) For separation anxiety: 0.25 mg-2 mg (total dose) once daily to three times daily PO. ()

c) For storm phobias: 0.02 – 0.4 mg/kg PO q4h as needed; helps to minimize impact of experiencing a severe storm ();

0.02 mg/kg PO as needed one hour before anticipated storm and every 4 hours as needed; used as an adjunct after behavior modification and prior clomipramine treatment (see clomipramine monograph for further information) ()

d) For phobias, night waking: 0.01-0.1 mg/kg or 0.25-2 mg (total dose) per dog PO q6- 12h PO ()

Alprazolam dosage for cats:

a) For treatment of feline anxiety disorders: 0.125-0.25 mg/kg PO q12h (Start at 0.125 mg/kg PO) ()

b) For refractory house soiling: 0.1 mg/kg or 0.125-0.25 mg (total dose) per cat PO q8- 12h ()

c) For urine marking: 0.05-0.2 mg/kg PO ql2-24h ()

d) For fears/phobias/anxieties: 0.125-0.25 mg (total dose) PO once to three times a day. ()


■ Efficacy

■ Adverse Effects

■ Consider monitoring hepatic enzymes particularly when treating cats chronically

Client Information

■ Try to dose approximately one hour in advance of storms or other anticipated stimuli that evokes negative responses

■ If difficulty with pilling the medication occurs, consider using the orally-disintegrating tablets; hands must be dry before handling

■ If excessive sedation or yellowing of the whites of eyes (especially in cats) occurs, contact veterinarian

Chemistry / Synonyms

A benzodiazepine, alprazolam occurs as a white to off-white, crystalline powder. It is soluble in alcohol and insoluble in water.

Alprazolam may also be known as D65 MT, U 31889, or alprazolamum; many trade names available internationally.

Storage / Stability

Alprazolam tablets should be stored at room temperature in tight, light-resistant containers. The orally disintegrating tablets should be stored at room temperature and protected from moisture.

Dosage Forms / Regulatory Status

Veterinary-Labeled Products: None

The ARCI (Racing Commissioners International) has designated this drug as a class 2 substance. See the appendix for more information.

Human-Labeled Products:

Alprazolam Tablets: 0.25 mg, 0.5 mg, 1 mg & 2 mg; Xanax (Pfizer); generic; (Rx; C-IV)

Alprazolam Extended-release Tablets: 0.5 mg, 1 mg, 2 mg, & 3 mg; Xanax XR (Pfizer); generic; (Rx; C-IV)

Alprazolam Orally Disintegrating Tablets: 0.25 mg, 0.5 mg, 1 mg, & 2 mg; Niravam (Pfizer); (Rx; C-IV)

Alprazolam Oral Solution: 1 mg/mL in 30 mL; Alprazolam Inten-sol (Roxane); (Rx; C-IV)




Acepromazine Maleate (PromAce, Aceproject)

Phenothiazine Sedative / Tranquilizer

Highlights Of Prescribing Information

Negligible analgesic effects

Dosage may need to be reduced in debilitated or geriatric animals, those with hepatic or cardiac disease, or when combined with other agents

Inject IV slowly; do not inject into arteries

Certain dog breeds (e.g., giant breeds, sight hounds) may be overly sensitive to effects

May cause significant hypotension, cardiac rate abnormalities, hypo- or hyperthermia

May cause penis protrusion in large animals (esp. horses)

What Is Acepromazine Used For?

Acepromazine is approved for use in dogs, cats, and horses. Labeled indications for dogs and cats include: “… as an aid in controlling intractable animals… alleviate itching as a result of skin irritation; as an antiemetic to control vomiting associated with motion sickness” and as a preanesthetic agent. The use of acepromazine as a sedative/tranquilizer in the treatment of adverse behaviors in dogs or cats has largely been supplanted by newer, effective agents that have fewer adverse effects. Its use for sedation during travel is controversial and many no longer recommend drug therapy for this purpose.

In horses, acepromazine is labeled “… as an aid in controlling fractious animals,” and in conjunction with local anesthesia for various procedures and treatments. It is also commonly used in horses as a pre-anesthetic agent at very small doses to help control behavior.

Although not approved, it is used as a tranquilizer (see doses) in other species such as swine, cattle, rabbits, sheep and goats. Acepromazine has also been shown to reduce the incidence of halothane-induced malignant hyperthermia in susceptible pigs.

Before you take Acepromazine

Contraindications / Precautions / Warnings

Animals may require lower dosages of general anesthetics following acepromazine. Use cautiously and in smaller doses in animals with hepatic dysfunction, cardiac disease, or general debilitation. Because of its hypotensive effects, acepromazine is relatively contraindicated in patients with hypovolemia or shock. Phenothiazines are relatively contraindicated in patients with tetanus or strychnine intoxication due to effects on the extrapyramidal system.

Intravenous injections should be made slowly. Do not administer intraarterially in horses since it may cause severe CNS excitement/depression, seizures and death. Because of its effects on thermoregulation, use cautiously in very young or debilitated animals.

Acepromazine has no analgesic effects; treat animals with appropriate analgesics to control pain. The tranquilization effects of acepromazine can be overridden and it cannot always be counted upon when used as a restraining agent. Do not administer to racing animals within 4 days of a race.

In dogs, acepromazine’s effects may be individually variable and breed dependent. Dogs with MDR1 mutations (many Collies, Australian shepherds, etc.) may develop a more pronounced sedation that persists longer than normal. It may be prudent to reduce initial doses by 25% to determine the reaction of a patient identified or suspected of having this mutation.

Acepromazine should be used very cautiously as a restraining agent in aggressive dogs as it may make the animal more prone to startle and react to noises or other sensory inputs. In geriatric patients, very low doses have been associated with prolonged effects of the drug. Giant breeds and greyhounds may be extremely sensitive to the drug while terrier breeds are somewhat resistant to its effects. Atropine may be used with acepromazine to help negate its bradycardic effects.

In addition to the legal aspects (not approved) of using acepromazine in cattle, the drug may cause regurgitation of ruminal contents when inducing general anesthesia.

Adverse Effects

Acepromazine’s effect on blood pressure (hypotension) is well described and an important consideration in therapy. This effect is thought to be mediated by both central mechanisms and through the alpha-adrenergic actions of the drug. Cardiovascular collapse (secondary to bradycardia and hypotension) has been described in all major species. Dogs may be more sensitive to these effects than other animals.

In male large animals acepromazine may cause protrusion of the penis; in horses, this effect may last 2 hours. Stallions should be given acepromazine with caution as injury to the penis can occur with resultant swelling and permanent paralysis of the penis retractor muscle. Other clinical signs that have been reported in horses include excitement, restlessness, sweating, trembling, tachypnea, tachycardia and, rarely, seizures and recumbency.

Its effects of causing penis extension in horses, and prolapse of the membrana nictitans in horses and dogs, may make its use unsuitable for show animals. There are also ethical considerations regarding the use of tranquilizers prior to showing an animal or having the animal examined before sale.

Occasionally an animal may develop the contradictory clinical signs of aggressiveness and generalized CNS stimulation after receiving acepromazine. IM injections may cause transient pain at the injection site.

Overdosage / Acute Toxicity

The LD50 in mice is 61 mg/kg after IV dosage and 257 mg/kg after oral dose. Dogs receiving 20-40 mg/kg over 6 weeks apparently demonstrated no adverse effects. Dogs gradually receiving up to 220 mg/kg orally exhibited signs of pulmonary edema and hyperemia of internal organs, but no fatalities were noted.

There were 128 exposures to acepromazine maleate reported to the ASPCA Animal Poison Control Center (APCC; during 2005-2006. In these cases, 89 were dogs with 37 showing clinical signs and the remaining 39 reported cases were cats with 12 cats showing clinical signs. Common findings in dogs recorded in decreasing frequency included ataxia, lethargy, sedation, depression, and recumbency. Common findings in cats recorded in decreasing frequency included lethargy, hypothermia, ataxia, protrusion of the third eyelid, and anorexia.

Because of the apparent relatively low toxicity of acepromazine, most overdoses can be handled by monitoring the animal and treating clinical signs as they occur; massive oral overdoses should definitely be treated by emptying the gut if possible. Hypotension should not be treated with epinephrine; use either phenylephrine or norepinephrine (levarterenol). Seizures may be controlled with barbiturates or diazepam. Doxapram has been suggested as an antagonist to the CNS depressant effects of acepromazine.

How to use Acepromazine

Note: The manufacturer’s dose of 0.5-2.2 mg/kg for dogs and cats is considered by many clinicians to be 10 times greater than is necessary for most indications. Give IV doses slowly; allow at least 15 minutes for onset of action.

Acepromazine dosage for dogs:

a) Premedication: 0.03-0.05 mg/kg IM or 1-3 mg/kg PO at least one hour prior to surgery (not as reliable) ()

b) Restraint/sedation: 0.025-0.2 mg/kg IV; maximum of 3 mg or 0.1-0.25 mg/kg IM; Preanesthetic: 0.1-0.2 mg/kg IV or IM; maximum of 3 mg; 0.05-1 mg/kg IV, IM or SC ()

c) To reduce anxiety in the painful patient (not a substitute for analgesia): 0.05 mg/kg IM, IV or SC; do not exceed 1 mg total dose ()

d) 0.55-2.2 mg/kg PO or 0.55-1.1 mg/kg IV, IM or SC (Package Insert; PromAce — Fort Dodge)

e) As a premedicant with morphine: acepromazine 0.05 mg/kg IM; morphine 0.5 mg/kg IM ()

Acepromazine dosage for cats:

a) Restraint/sedation: 0.05-0.1 mg/kg IV, maximum of 1 mg ()

b) To reduce anxiety in the painful patient (not a substitute for analgesia): 0.05 mg/kg IM, IV or SC; do not exceed 1 mg total dose ()

c) 1.1-2.2 mg/kg PO, IV, IM or SC (Package Insert; PromAce — Fort Dodge)

d) 0.11 mg/kg with atropine (0.045-0.067 mg/kg) 15-20 minutes prior to ketamine (22 mg/kg IM). ()

Acepromazine dosage for ferrets:

a) As a tranquilizer: 0.25-0.75 mg/kg IM or SC; has been used safely in pregnant jills, use with caution in dehydrated animals. ()

b) 0.1-0.25 mg/kg IM or SC; may cause hypotension/hypothermia ()

Acepromazine dosage for rabbits, rodents, and small mammals:

a) Rabbits: As a tranquilizer: 1 mg/kg IM, effect should begin in 10 minutes and last for 1-2 hours ()

b) Rabbits: As a premed: 0.1-0.5 mg/kg SC; 0.25-2 mg/kg IV, IM, SC 15 minutes prior to induction. No analgesia; may cause hypotension/hypothermia. ()

c) Mice, Rats, Hamsters, Guinea pigs, Chinchillas: 0.5 mg/kg IM. Do not use in Gerbils. ()

Acepromazine dosage for cattle:

a) Sedation: 0.01-0.02 mg/kg IV or 0.03-0.1 mg/kg IM ()

b) 0.05 -0.1 mg/kg IV, IM or SC ()

c) Sedative one hour prior to local anesthesia: 0.1 mg/kg IM ()

Acepromazine dosage for horses:

(Note: ARCI UCGFS Class 3 Acepromazine)

a) For mild sedation: 0.01-0.05 mg/kg IV or IM. Onset of action is about 15 minutes for IV; 30 minutes for IM ()

b) 0.044-0.088 mg/kg (2-4 mg/100 lbs. body weight) IV, IM or SC (Package Insert; PromAce — Fort Dodge)

c) 0.02-0.05 mg/kg IM or IV as a preanesthetic ()

d) Neuroleptanalgesia: 0.02 mg/kg given with buprenorphine (0.004 mg/kg IV) or xylazine (0.6 mg/kg IV) ()

e) For adjunctive treatment of laminitis (developmental phase): 0.066-0.1 mg/kg 4-6 times per day ()

Acepromazine dosage for swine:

a) 0.1-0.2 mg/kg IV, IM, or SC ()

b) 0.03-0.1 mg/kg ()

c) For brief periods of immobilization: acepromazine 0.5 mg/ kg IM followed in 30 minutes by ketamine 15 mg/kg IM. Atropine (0.044 mg/kg IM) will reduce salivation and bronchial secretions. ()

Acepromazine dosage for sheep and goats:

a) 0.05-0.1 mg/kg IM ()


■ Cardiac rate/rhythm/blood pressure if indicated and possible to measure

■ Degree of tranquilization

■ Male horses should be checked to make sure penis retracts and is not injured

■ Body temperature (especially if ambient temperature is very hot or cold)

Client Information

■ May discolor the urine to a pink or red-brown color; this is not abnormal

■ Acepromazine is approved for use in dogs, cats, and horses not intended for food

Chemistry / Synonyms

Acepromazine maleate (formerly acetylpromazine) is a phenothiazine derivative that occurs as a yellow, odorless, bitter tasting powder. One gram is soluble in 27 mL of water, 13 mL of alcohol, and 3 mL of chloroform.

Acepromazine Maleate may also be known as: acetylpromazine maleate, “ACE”, ACP, Aceproject, Aceprotabs, PromAce, Plegicil, Notensil, and Atravet.

Storage / Stability/Compatibility

Store protected from light. Tablets should be stored in tight containers. Acepromazine injection should be kept from freezing.

Although controlled studies have not documented the compatibility of these combinations, acepromazine has been mixed with atropine, buprenorphine, chloral hydrate, ketamine, meperidine, oxymorphone, and xylazine. Both glycopyrrolate and diazepam have been reported to be physically incompatible with phenothiazines, however, glycopyrrolate has been demonstrated to be compatible with promazine HC1 for injection.

Dosage Forms / Regulatory Status

Veterinary-Labeled Products:

Acepromazine Maleate for Injection: 10 mg/mL for injection in 50 mL vials; Aceproject (Butler), PromAce (Fort Dodge); generic; (Rx). Approved forms available for use in dogs, cats and horses not intended for food.

Acepromazine Maleate Tablets: 5, 10 & 25 mg in bottles of 100 and 500 tablets; PromAce (Fort Dodge); Aceprotabs (Butler) generic; (Rx). Approved forms available for use in dogs, cats and horses not intended for food.

When used in an extra-label manner in food animals, it is recommended to use the withdrawal periods used in Canada: Meat: 7 days; Milk: 48 hours. Contact FARAD (see appendix) for further guidance.

The ARCI (Racing Commissioners International) has designated this drug as a class 3 substance. See the appendix for more information.

Human-Labeled Products: None


Stallion Behavior Problems

This post briefly outlines several of the most common behavior problems of breeding stallions. These problems include self-mutilation, inadequate libido, rowdy breeding behavior, specific erection dysfunction, mounting and thrusting difficulties, frenzied hyperactive behavior, and specific ejaculation dysfunction. Also briefly outlined is the common problem of residual stallionlike behavior in geldings.

Inadequate Libido

Specific stallion libido problems include slow starting novices, slow or sour experienced stallions, and specific aversions or preferences. Although certain genetic lines tend to be shy or quiet breeders, the majority of inadequate libido in stallions is man-made in the sense that it is the result of domestic rearing, training, or breeding conditions. Stallions that have been disciplined for showing sexual interest in mares during their performance career, discouraged from showing spontaneous erection and masturbation, or mishandled during breeding under halter are at risk of libido problems. When exposed to a mare for teasing, stallions such as these may simply stand quietly, may appear anxious and confused, or may savage the mare.

Most stallions with such experience-related libido problems respond well to behavior therapy alone or in combination with anxiolytic medication. These stallions typically respond best to continued exposure to mares, initially with minimal human presence, and then with gradual introduction of quiet, respectful, patient, positive reinforcement-based handling. These stallions appear to respond favorably to reassurance for even small increments of improvement. Tolerance of minor misbehavior rather than punishment is often the most effective strategy with low-libido stallions. The anxiolytic diazepam (0.05 mg/kg through slow IV 5-7 min before breeding) is useful in about half of such cases as an adjunct to behavior modification.

Some libido problems are hormone-related, with androgens on the low side of the normal range. These stallions will likely improve with management aimed at increasing exposure to mares and reduced exposure to other stallions. This will typically increase androgen levels, general confidence, as well as sexual interest and arousal. Gonadotropin-releasing hormone (GnRH; 50 μg SQ 2 hr and again 1 hr before breeding) can be useful to boost libido in stallions, particularly in those with low normal levels. In rare cases when more rapid improvement is required to rescue a breeding career, treatment with testosterone can effectively jump-start a slow novice without apparent significant adverse effects on spermatogenesis. Current recommendations are 0.1 to 0.2 mg/kg aqueous testosterone SQ every other day for as long as 2 weeks, with frequent assay of circulating testosterone not to exceed 4 ng/ml.

Specific Erection Dysfunction

Libido-independent erection dysfunction is rare in stallions. The majority of erection dysfunction that does occur is related to traumatic damage of the corpora cavernosa that results in insufficient or asymmetric tumescence (lateral or ventral deviations) that impairs insertion. In some instances, penile injury appears to impair sensory and or proprioceptive feedback from the penis, delaying ejaculation, coupling, or organized thrusting. Common causes include stallion ring injuries, drug-related paralyzed penis and paraphimosis, kick injuries, and self-serve breeding dummy accidents.

An interesting and often confusing type of erection dysfunction involves the folding back of the penis within the prepuce. The behavioral hallmark of this situation is a stallion that appears aroused and ready to mount, without a visible erection. The stallion may also appear uncomfortable or intermittently distracted, pinning the ears, kicking toward the groin, and/or stepping gingerly on the hind legs. Close observation reveals a rounded, full-appearing prepuce, with the skin stretched taut. Resolution usually requires removal of the stallion from the mare until the penis detumesces. Once the penis is fully withdrawn, application of a lubricating ointment to the prepuce facilitates subsequent normal protrusion. This situation tends to repeat occasionally over time, particularly in stallions with profuse smegma production or with dryness of the penis and sheath from frequent cleansing.

Mounting And Thrusting Difficulties

A significant percentage of breeding dysfunction appears to involve neurologic or musculoskeletal problems that affect the stallion’s ability to mount and thrust. Many such stallions can continue breeding with therapy aimed to reduce discomfort and accommodate disabilities during breeding, including adjustments to the breeding schedule aimed at reducing the total amount of work. This author has found that long-term treatment with oral phenylbutazone (2-3 mg/kg orally twice daily) often works well to keep such stallions comfortable for breeding. Certain debilitated stallions can benefit from semen collection while standing on the ground.

Specific Ejaculation Dysfunction

Although any libido, erection, or mounting and thrusting problem can result in failure to ejaculate, stallions also exist in which the dysfunction seems to be specific to ejaculation. Specific ejaculation problems can include apparent

failure of the neural ejaculatory apparatus, physical or psychologic pain associated with ejaculation, and genital tract pathology. Goals of therapy are to address as many contributing conditions as possible, as well as to optimize handling and breeding conditions and maximize musculoskeletal fitness and libido to enhance the stallion’s ability to overcome ejaculatory difficulty. Imipramine hydrochloride (0.5-1.0 mg/kg orally 2 hr before breeding) can effectively reduce the ejaculatory threshold.

Rowdy Breeding Behavior

Rowdy, misbehaved breeding stallions in most cases represent a human-animal interaction problem. Most problems can be overcome with judicious, skillful, respectful re-training. Even strong, vigorous, and misbehaved stallions can be brought under control by using consistent positive and negative reinforcement, with very little or no severe punishment. Re-training can be done in a safe and systematic manner without abuse or commotion, usually within a few brief sessions. Some of the most challenging, rowdy stallions may benefit from vigorous exercise under saddle or ground work immediately before breeding. This practice not only fatigues the stallion but also establishes a pattern of the stallion taking direction from a handler. For similar reasons, this author recommends an intensive schedule for breeding shed retraining, with as many as several breedings per day. With fatigue and reduced urgency to breed, many stallions seem more able to abide direction and learn a routine. With rapid repetition, stallions seem to more readily understand the routine. Tranquilization is generally not recommended. Levels of sedation that improve controllability without compromising musculoskeletal stability or ejaculatory function are difficult to achieve. Tranquilizing agents commonly used in stallions, such as xylazine or detomidine, can both facilitate and inhibit erection and ejaculation depending on dose.

Frenzied Behavior

Distinct from simple rowdiness, some stallions are hyperactive or even frenzied. This is typically greater during the breeding season. Some will spend nearly their entire time budget frantically “climbing the walls,” or running a fence line. In general frenzied breeding stallions can benefit from more roughage and less grain in the diet, organized physical work and pasture exercise, and consistent housing in a quiet area. Careful observation (particularly video surveillance) can be useful to identify environmental conditions and events that set off episodes or tend to quiet a stallion. In extreme cases, pasturing directly with mares can effectively quiet or sensibly occupy a frenzied stallion. L-Tryptophan supplementation (1-2 g twice daily in feed) can have a calming effect on such stallions. Tranquilization for this purpose is not recommended in breeding stallions because of risk of paralyzed penis and paraphimosis.


Although not unique to stallions, self-mutilation is a severe and relatively uncommon fertility limiting and/or life-threatening problem. This behavior typically takes the form of self-biting of the flank, chest, or limbs, with violent spinning, kicking, and vocalization. Self-mutilation in horses appears to occur in two distinct forms. One appears to be a severe reaction to irritation or pain, and would be similar in males or females. The self-biting is typically targeted toward the site of discomfort. Another form occurs in males and is reminiscent of stallion intermale aggression. The behavior is targeted at the typically intermale sites of aggression — the groin, flank, knees, chest, and hocks. The sequence of the behavior follows closely to that of two males fighting, with sniffing and nipping of the groin, vocalization, stamping with a fore leg, kicking out with a hind leg, and then taking occasional larger bites from anywhere on the opponent’s body.

Episodes often appear to be stimulated by sight, sound, or smell (feces or oily residues) of another stallion. For some stallions, episodes are set off by sniffing their own excrement or oily residues on stall walls or doorways. Current recommendations to control episodes are as follows: (1) physically protect the stallion from injury by padding walls or limbs, blanketing, and muzzling as effective; (2) aggressively evaluate the housing and social environment to identify exacerbating and ameliorating conditions that may be manipulated for greatest relief; (3) reduce concentrates and increase grass and hay in the diet to increase feeding time and eliminate highly palatable meals (feeding tends to distract and occupy the stallion; concentrate meals tend to increase stereotypic behavior); (4) apply odor-masking agents (Vicks or Acclimate) around the nares; and (5) provide as much organized exercise as possible, also to distract the stallion.

Residual Stallionlike Behavior In Geldings

Castration, regardless of age or previous sexual experience, does not always eliminate stallionlike behavior in horses. If given the opportunity, as many as half of geldings will show stallionlike behavior to mares, many will herd mares, and even mount and appear to breed. Similarly, although castration does tend to “mellow” most horses, it does not eliminate general misbehavior. Traditional behavior modification is usually much more effective in the control of sexual and aggressive behavior in a gelding under saddle or in-hand than it is with an intact stallion. Also, treatment aimed at quieting sexual and aggressive behavior, such as progesterone (e.g., altrenogest, 50-75 mg orally daily), is typically more effective in geldings than in intact stallions. Elimination of stallionlike herding and teasing at pasture is difficult. Separation from mares is recommended.


Neurological Conditions

Afghan myelopathy

A progressive disease of the white matter of the spinal cord. Symptoms include pelvic limb ataxia and paresis progressing to thoracic limb involvement, tetraplegia and eventually death from respiratory paralysis.

Ambylopia and quadriplegia

This is a lethal inherited condition of Irish Setters. Puppies are unable to walk and progression to visual impairment, nystagmus and seizures occurs.

Arachnoid cysts

Arachnoid cysts are a rare cause of focal spinal cord compression in young dogs. Neurological deficits depend on the site of the lesion.

Atlantoaxial subluxation

This is seen primarily in young dogs of Toy breeds which present with neck pain and neurological deficits in all four limbs due to cervical spinal cord compression. A variety of congenital defects including a lack of or hypoplasia of the dens and shortening of the axis lead to instability of the atlantoaxial articulation. The condition may also be acquired in any breed as a result of fracture of the dens or damage to the ligamentous support. (See also Odontoid process dysplasia under Musculoskeletal conditions.)

Birman cat distal polyneuropathy

A degenerative polyneuropathy which results in hypermetria in all limbs, progressive pelvic limb ataxia and a tendency to fall. The condition is believed to be hereditary.

Cerebellar degeneration

Cerebellar cells can undergo premature aging, degeneration and death (termed abiotrophy) leading to signs of cerebellar dysfunction (intention tremor, ataxia, hypermetria and menace deficits). In most cases the condition is believed to be hereditary.

Cerebellar malformation

Congenital malformations of the cerebellum include hypoplasia and aplasia of the whole or part of the cerebellum. Some may have a genetic basis, others result from a teratogen. Clinical signs are seen as soon as the animal becomes mobile and are non-progressive. They include hypermetria, head tremor and a wide-based stance. There is no treatment, but animals may make suitable pets if not severely affected.

Cervical vertebral malformation (wobbler syndrome)

This is a developmental malformation and malarticulation of the caudal cervical vertebrae seen in large- and giant-breed dogs, particularly the Dobermann and Great Dane. Clinical signs result from spinal cord compression and include neck pain and gait abnormalities (e.g. ataxia and paresis) which are worse in the pelvic limbs.

Congenital deafness

This has been observed in numerous breeds (especially Dalmatians and blue-eyed white cats) and usually results from a partial or complete failure of development of the organ of Corti.

Congenital vestibular disease

Young animals may present with signs of peripheral vestibular dysfunction including head tilt, circling, and falling. Nystagmus is not a common feature of the congenital condition. There is no treatment, symptoms may improve with time as the animal compensates.

Vestibular disease may also be acquired secondarily to a variety of causes including middle-ear infections in breeds predisposed to ear disease. An idiopathic form may be seen in older dogs.

Dalmatian leukodystrophy

This rarely reported progressive neurological condition results in visual deficits and progressive weakness. On gross pathology there is atrophy of the brain, lateral ventricle dilation and cavitation of the white matter of the cerebral hemispheres.

Dancing Dobermann disease

This is believed to be a neuromuscular disease of the gastrocnemius muscle, the underlying cause is not known. It has only been reported in Dobermann Pinschers and affected dogs initially flex one pelvic limb whilst standing. As progression occurs to involve the other pelvic limb the dog is seen to alternately flex and extend each pelvic limb in a dancing motion.

Degenerative myelopathy

A degenerative disease primarily seen in German Shepherd Dogs over five years of age. Diffuse degeneration of the white matter of the thora-columbar spinal cord results in progressive pelvic limb ataxia, paresis and loss of conscious proprioception. The cause in unknown.

Demyelinating myelopathy of Miniature Poodles

A rare, possibly inherited condition characterised by diffuse spinal cord demyelination. Pelvic limb paresis progresses to paraplegia and tetraplegia. Spinal reflexes are hyperactive.

Dermoid sinus

A dermoid sinus is a developmental defect arising from the incomplete separation of the skin and neural tube. It may be found midline in the cervical, cranial thoracic or sacrococcygeal regions. In cases where the sinus communicates with the dura mater, neurological signs may be seen. The condition is most commonly found in the Rhodesian Ridgeback and is believed to be hereditary in this breed.


Infection of the intervertebral disc with osteomyelitis of adjoining vertebral bodies. Infection occurs secondarily to spinal surgery, foreign body migration or septic emboli from the skin, urinary/genital tract, or from a concurrent endocarditis. Clinical signs may include pyrexia, anorexia, spinal pain and paresis.

Distal symmetrical polyneuropathy

This distal polyneuropathy has been reported in young adult Great Danes and other large breeds of dog. Symptoms include pelvic limb paresis that progresses to tetraparesis, and atrophy of limb and head muscles. There is no treatment.

Eosinophilic meningoencephalitis

This condition has been reported in six male dogs, three of which were Golden Retrievers. Cerebrospinal fluid analysis demonstrated pleo-cytosis with an eosinophil percentage of 21-98%. There was a concurrent peripheral blood eosinophilia in four of the cases. Symptoms included behavioural abnormalities and seizures.

Episodic falling

Seen in Cavalier King Charles Spaniels in the UK. During exercise, a bounding hind-limb gait develops. This progresses to a bunny-hop with arched spine, and eventually collapse often with the thoracic limbs crossed over the back of the head. There is no loss of consciousness and recovery is rapid. Some improvement may be seen with diazepam. The cause is unknown.

Giant axonal neuropathy

This is a rare inherited neuropathy of German Shepherd Dogs. The cause is unknown. Distal nerves in the pelvic limbs and long tracts of the central nervous system are affected first, giving rise to paresis, loss of spinal reflexes and pain perception in the pelvic limbs. Megaoesophagus and loss of bark occur later. There is no treatment.

Glycogenosis (glycogen storage disease)

A group of rare diseases resulting from a deficiency of one or more enzymes involved in glycogen degradation or synthesis. Glycogen accumulates in a variety of tissues including the central nervous system, muscle and liver resulting in clinical signs including seizures and muscular weakness.

Granulomatous meningoencephalitis

This is an inflammatory condition of unknown cause. The disease may be focal or diffuse and may affect any part of the central nervous system, leading to a wide range of clinical signs including seizures, ataxia, nystagmus and visual deficits. The disease is usually chronic and progressive. Small-breed dogs are most commonly affected with Poodles representing about 30% of diagnosed cases.


Hemivertebrae are congenitally malformed vertebrae most commonly seen at the level of thoracic vertebrae 7-9. Neurological signs, e.g. pelvic limb ataxia, paresis, faecal and urinary incontinence, may result from spinal cord compression.

Hereditary ataxia

Progressive ataxia results from degeneration of the white matter of the cervical and thoracic spinal cord in young Smooth-haired Fox Terriers and Jack Russell Terriers.

Hound ataxia

A degenerative myelopathy seen in Foxhounds and Beagles in the UK. Degenerative changes are most severe in the mid-thoracic spinal cord but may extend to involve the brainstem, caudal cerebellar peduncles or sciatic nerve. Signs include pelvic limb weakness and ataxia. Muscle atrophy and loss of spinal reflexes is not seen. The cause is unknown but a link has been suggested to an all-tripe diet.


Hydrocephalus occurs where there is dilation of all or part of the ventricular system of the brain, and may be congenital or acquired (usually secondary to neoplasia or inflammatory disease). Symptoms include a domed cranium, seizures and altered mental status.

Hyperaesthesia syndromes

Increased sensitivity to tactile and painful stimulation may result in self-mutilation which varies in severity from rippling of the skin when touched or excessive licking to auto-amputation. Some cases are due to underlying neuropathies or are forms of seizure; however, in others no underlying cause is identified. Treatments tried include phenobarbitone, megoestrol acetate and prednisolone. Success has been variable.


Hyperlipidaemia (high blood lipid levels) is a familial condition of Miniature Schnauzers and cats which is believed to be associated with a reduced activity of lipoprotein lipase resulting in defective lipid metabolism. Affected animals may experience seizures as well as abdominal distress and pancreatitis.


A condition seen in Domestic Short Hair cats in which young cats develop acute renal failure and neurological disease. Signs include anorexia, depression, enlarged painful kidneys, weakness, reduced spinal reflexes and poor response to pain. Oxalate crystals are found deposited in the kidney tubules, and swellings of the proximal axons of the ventral horn cells are found in the spinal cord on post-mortem. There is no treatment and the condition carries a grave prognosis.

Hypertrophic neuropathy

An inherited neuropathy reported in the Tibetan Mastiff which results in generalized weakness, hyporeflexia and dysphonia from seven to ten weeks of age. There is no treatment and the prognosis is guarded.


Hypoglycaemia is a common metabolic cause of seizures. It may result from a variety of causes including insulinoma, hypoadrenocorticism, severe liver disease and sepsis. Young dogs of Toy breeds may develop hypoglycaemia easily when stressed, fed an inadequate diet or affected by gastrointestinal disease. Hunting dogs which are not fed on the morning of a hunt may also be predisposed to hypoglycaemia as a result of physical exertion.


Hypomyelination of the central nervous system has been seen in several breeds of dog and is known to be hereditary in some cases. Signs usually start at a few weeks of age with generalized body tremors which worsen with excitement. Hypomyelination of the peripheral nervous system has been seen in two Golden Retriever litter-mates with pelvic limb weakness and depressed spinal reflexes.

Idiopathic facial paralysis

Paralysis of the facial nerve results in drooping of the lip, paralysis of the eyelids and impaired ear movement on the affected side. Acute onset facial paralysis may occur in adult dogs without evidence of an underlying cause.

Intervertebral disc disease

Degeneration of the intervertebral discs resulting in extrusion or protrusion of the nucleus pulposus may result in spinal cord compression and pain/paresis. Nuclear extrusion occurs early in chondrodystrophoid breeds, e.g. Pekingese, Dachschunds, Beagles, Welsh Corgis, French Bulldogs, some Spaniels and Basset Hounds giving rise to signs in younger dogs.

Leukoencephalomyelopathy of Rottweilers

This is believed to be an inherited condition. Degeneration of the myelin of the spinal cord, brainstem, cerebellum and sometimes optic tracts results in ataxia, tetraparesis and loss of conscious proprioception, with increased spinal reflexes and muscle tone. Vision is usually unaffected. The condition progresses over 6-12 months.


A developmental anomaly where the cerebral cortex has reduced or absent gyri or sulci resulting in a smooth appearance. Clinical signs are usually seen from a few months of age and may include behavioural abnormalities, lack of training, aggressive behaviour, visual deficits and seizures.

Lumbosacral stenosis

Stenosis (narrowing) of the lumbosacral vertebral canal and/or intervertebral foramina causes compression of the lumbosacral nerve roots. Clinical signs may include pain on palpation of the area, pelvic limb paresis or lameness, tail paralysis, hypotonia of the anal sphincter and bladder atonicity (‘lumbosacral syndrome’). It is most commonly seen in adult German Shepherd Dogs.

Lysosomal storage diseases

These rare diseases result from a failure of normal metabolic processes due to a deficiency of an enzyme within the lysosomes of neuronal tissues. As a result, substrate accumulates, causing cellular dysfunction and eventually death. One of a variety of lysosomal enzymes may be affected. Symptoms usually occur before one year of age and may include ataxia, tremors, seizures, dementia and blindness. Most lysosomal storage diseases are believed to be inherited as an autosomal recessive trait.

Meningitis and polyarteritis

This is a vasculitis of meningeal arteries which results in clinical signs of recurrent fever, anorexia and cervical rigidity. In some cases paresis or tetraparesis may be seen. An immune-mediated aetiology has been suggested and some cases may respond to high-dose, long-term prednisolone treatment.


A lethal malformation where part of the brain and meninges is herniated through a defect in the skull.

Multisystem neuronal degeneration

A slowly progressive degenerative disease of young Cocker Spaniels. Diffuse neuronal loss throughout the subcortical, brainstem and cerebellar nuclei results in symptoms including loss of recognition of the owner, apathy, hyperactivity, hypersexuality and aggression.

Muscle cramping

An inherited disorder of Scottish Terriers. Affected dogs are normal at rest but exercise may provoke muscle spasms which in its mildest form appear as pelvic limb stiffness. Severe attacks cause rigidity of all muscles including facial muscles causing the dog to fall over into a tightly curled ball. Consciousness is maintained and the animal makes a spontaneous recovery. The cause is unknown but it is believed to be a disorder of central nervous system neurotransmitters. A similar condition has been reported in Dalmatians and Norwich Terriers.

Myasthenia gravis

Decreased numbers of acetylcholine receptors on the post-synaptic muscle membrane leads to defective neuromuscular transmission. The disease can be congenital or acquired. Clinical signs in dogs include muscle weakness on exercise which improves with rest, and megaoesophagus. The onset may be chronic or acute and the condition can be generalised or focal. Signs in cats include drooling, ventroflexion of the neck, regurgitation, weakness and lameness.


Narcolepsy is characterised by excessive sleepiness at inappropriate times, whilst cataplexy is acute flaccid paralysis from which the animal makes a complete recovery after a few seconds to several minutes. In dogs, cataplexy seems to be the more prominent and is often associated with excitement, e.g. eating or playing.

Neuroaxonal dystrophy

A degenerative central nervous system disorder of unknown cause, seen primarily in Rottweilers. Pathological findings include swellings of the distal axons within the central nervous system and cerebellar atrophy. Symptoms include ataxia, hypermetria and intention tremors which may be slowly progressive over several years.

Partial seizures

Partial seizures result from a focal discharge from the brain. The appearance of the seizure varies with the location of the discharge but may include fly-biting, star-gazing, tail-chasing or self-mutilating behaviour.


This is an inflammatory condition affecting multiple nerve roots resulting in pelvic limb weakness which rapidly progresses to quadriplegia. An idiopathic form may be seen in any breed, however the condition has been seen following raccoon bites in hunting breeds such as the Coonhound. An immunological reaction to raccoon saliva may be the underlying cause in these cases.

Primary brain tumours

Primary brain tumours are derived from tissues of the nervous system including nerve cells, glial cells, meninges and neuroepithelial cells. They are generally solitary and most cases will present with signs of a space-occupying lesion in the brain, the specific signs varying with the location. Meningiomas and gliomas are the most common primary brain tumours in dogs. Meningiomas are the most common primary brain tumours in the cat and may be single or multiple in this species.

Progressive axonopathy

See Sensory neuropathy.

Pug encephalitis

A rare, necrotising meningoencephalitis of unknown aetiology seen in Pugs. Symptoms are often acute in onset and include seizures, depression, head-pressing, circling, blindness with normal pupillary reflexes and opisthotonus. The condition is progressive and there is no treatment. Most cases are euthanased.

Pyogranulomatous meningoencephalomyelitis

An acute, rapidly progressive disease of unknown cause seen in mature Pointers. Mononuclear and polymorphonuclear inflammatory infiltrates are found throughout the central nervous system but especially in the cervical spinal cord and lower brainstem. Dogs suffer from cervical rigidity, ataxia and sometimes seizures. The prognosis is poor. A temporary remission in response to antibiotics may be seen.

Rottweiler distal sensorimotor polyneuropathy

A polyneuropathy of Rottweilers resulting in paraparesis progressing to tetraparesis, reduced spinal reflexes, hypotonia and neurogenic atrophy of limb muscles. The condition progresses over twelve months.

Sacrocaudal dysgenesis

Congenital malformation of the sacrococcygeal spinal cord and vertebral column which results in locomotor problems in the hind legs and faecal and urinary incontinence.

Sensory neuropathy

Sensory neuropathies have been seen in a number of breeds. In Pointers signs of self-mutilation associated with loss of pain sensation predominate, whereas in Dachshunds loss of proprioception and ataxia may be seen. In Boxers the condition is termed progressive axonopathy and is characterised by pelvic limb hyporeflexia, hypotonia and proprioceptive loss.

Shaker dog disease

This condition has been most commonly observed in dogs with white hair coats, particularly Maltese and West Highland White Terriers. Dogs develop a fine whole-body tremor which may worsen with excitement and stress. Other signs may include nystagmus, menace deficits, proprioceptive deficits and seizures. There may be an underlying mild lymphocytic encephalitis and affected animals are usually responsive to immunosupressive doses of corticosteroids with benzodiazepines.

Spina bifida

This is a developmental defect resulting from the failure of the two halves of the dorsal spinous processes to fuse, most commonly in the lumbar spine. Protrusion of the spinal cord or meninges may result in symptoms including pelvic limb ataxia, paresis and urinary or faecal incontinence. If no protrusion occurs the condition is termed ‘spina bifida occulta’.

Spinal dysraphism

This is a congenital malformation of the spinal cord resulting in a wide-based stance and bunny-hopping gait of the hind-limbs. It may be associated with hemivertebrae or spina bifida. The condition is non-progressive.

Spinal muscular atrophy

This is a condition where premature degeneration of various neuronal cell populations of the brainstem and ventral horn of the spinal cord result in generalised weakness which may progress to muscular atrophy and tetraparesis/plegia.

Spongiform degeneration

Spongiform degenerations are rare disorders resulting in vacuolation of the brain and spinal cord which may result in a wide variety of neurological signs.

Springer Spaniel rage syndrome

Seen in young adult Springer Spaniels which become aggressive to people including their owners. No intracranial lesion has been found to explain this behaviour.

True epilepsy

Recurrent seizures caused by functional disorders of the brain. The high incidence in certain breeds of dog suggests an inherited basis.

Veterinary Medicine

Aspects Of Chemical Restraint

Chemical restraint is often necessary in reptile medicine to facilitate procedures from simply extracting the head of a leopard tortoise or box turtle, to enable a jugular blood sample to be performed, to coeliotomy procedures such as surgical correction of egg-binding.

Before any anesthetic / sedative is administered, an assessment of the reptile patient’s health is necessary. Is sedation / anesthesia necessary for the procedure required? Is the reptile suffering from respiratory disease or septicaemia, i.e. is the reptile’s health likely to be made worse by sedation / anesthesia?

Before any attempt to administer chemical restraint the reptilian respiratory system should be understood.

Overview of reptilian anatomy and physiology relevant to anesthesia

The reptilian patient has a number of variations from the basic mammalian anatomical and physiological systems. Starting rostrally:

(1) Reduced larynx: The reptile patient does have a glottis similar to the avian patient, which lies at the base of the tongue, more rostrally in snakes and lizards and more caudally in Chelonia. At rest the glottis is permanently closed, opening briefly during inspiration and expiration. In crocodiles the glottis is obscured by the basihyal valve which is a fold of the epiglottis that has to be deflected before they can be intubated.

(2) The trachea varies between orders: The Chelonia and Crocodylia have complete cartilaginous rings similar to the avian patient, with the Chelonia patient having a very short trachea, bifurcating into two bronchi in the neck in some species. Serpentes and Sauria have incomplete rings such as is found in the cat and dog, with Serpentes species having a very long trachea. Many Serpentes species have a tracheal lung – an outpouching from the trachea as a form of air sac.

(3) The lungs of Serpentes and saurian species are simple and elastic in nature. The left lung of most Serpentes species is absent or vestigial but may be present in the case of members of the Boid family (boa constrictors etc.). The right lung of Serpentes species ends in an air sac. Chelonia species have a more complicated lung structure, and the paired lungs sit dorsally inside the carapace of the shell. Crocodylia have lungs not dissimilar to mammalian ones and they are paired.

(4) No reptile has a diaphragm: Crocodylia species have a pseudodiaphragm, which changes position with the movements of the liver and gut, so pushing air in and out of the lungs.

(5) Most reptiles use intercostal muscles to move the ribcage in and out, as with birds: The exception being the Chelonia. These species require movement of their limbs and head into and out of the shell in order to bring air into and out of the lungs. This is important when they are anesthetised as such movements, and therefore breathing, cease.

(6) Some species can survive in oxygen-deprived atmospheres for prolonged periods: Chelonia species may survive for 24 hours or more and even green iguanas may survive for 4-5 hours, making inhalation induction of anesthesia almost impossible in these animals.

(7) Reptiles have a renal portal blood circulation system: This means that the blood from the caudal half of the body can pass through the kidney structure before passing into the caudal major veins and entering the heart. Therefore, if drugs that are excreted by the kidneys are injected into the caudal half of the body, then they may be excreted before they have a chance to work systemically (e.g. ketamine). In addition, if a drug is nephrotoxic (e.g. the aminoglycosides) then injection into the caudal half of the body may increase the risk of renal damage.

Pre-anesthetic preparation

Blood testing

It is useful to test biochemical and haemocytological parameters prior to administering chemical immobilising drugs. Blood samples may be taken from the jugular vein or dorsal tail vein in Chelonia, the ventral tail vein, palatine vein or by cardiac puncture in Serpentes and the ventral tail vein in Crocodylia and Sauria. Minimal testing advised is a haematocrit, blood calcium levels, blood total protein levels, aspartate transaminase (AST) levels for hepatic function and uric acid levels for renal function.


This is necessary prior to anesthesia in Serpentes (for a period of 2 days in small snakes up to 1-2 weeks for the larger pythons) to prevent regurgitation and pressure on the lungs / heart. Chelonia rarely regurgitate and do not need prolonged fasting. It is important not to feed live prey to insectivores (e.g. leopard geckos) within 24 hours of anesthesia as the prey may still be alive when the reptile is anesthetised!

Pre-anesthetic medications

Antimuscarinic drugs

Atropine (0.01-0.04mg / kg intramuscularly (IM)) or glycopyrrolate (0.01 mg / kg IM) can reduce oral secretions and prevent bradycardia. However, these problems are rarely of concern in reptiles.


Midazolam has been used in red-eared terrapins at 1.5 mg / kg as a premedicant and produced adequate sedation to allow minor procedures and induction of anesthesia.


Acepromazine (0.1-0.5 mg / kg intramuscularly (IM)) may be given 1 hour before induction of anesthesia to reduce the dose of induction agent required. Diazepam (0.22-0.62mg / kg IM in alligators) and midazolam (2mg / kg IM in turtles) are also useful.

Alpha-2 adrenoceptor agonists

Xylazine can be used 30 minutes prior to ketamine at 1 mg / kg in Crocodylia to reduce the dose of ketamine required. Medetomidine may be used at doses of 100-150 μ.g / kg, also reducing the required dose of ketamine in Chelonia, and it has the advantage of being reversible with atipamezole at 500-750 µg / kg.


Butorphanol (0.4mg / kg intramuscularly (IM)), can be administered 20 minutes before anesthesia, providing analgesia and reducing the dose of induction agent required. It may be combined with midazolam at 2mg / kg.

Induction of Anesthesia

Maintenance of anesthesia with injectable agents


This may be used on its own for anesthesia at doses of 55-88 mg / kg intramuscularly (IM). As the dose increases, so the recovery time also increases, in some instances to several days; doses above 110 mg / kg will cause respiratory arrest and bradycardia.

Ketamine may be combined with other injectable agents to provide surgical anesthesia.

Suitable agents include: midazolam at 2 mg / kg intramuscularly (IM) with 40 mg / kg ketamine in turtles; xylazine at 1 mg / kg IM, given 30min prior to 20mg / kg ketamine in large crocodiles and medetomidine at 0.1mg / kg IM with 50mg / kg ketamine in king snakes.

Ketamine at 5mg / kg has been combined with medetomidine at 0.1mg / kg intravenously (IV) to produce a short period of anesthesia in gopher tortoises although some hypoxia was observed and supplemental oxygen is advised.


Propofol may be used to give 20-30 min of anesthesia, which may allow minor procedures. It may be topped up at 1 mg / kg / min IV or intraosseously. Apnoea is extremely common and intubation and ventilation with 100% oxygen are advised.

Maintenance of anesthesia with inhalational agents

Maintaining Anesthesia

Veterinary Medicine

Hepatic Lipidosis And Acute Hepatitis

1. What is hepatic lipidosis?

Hepatic lipidosis is a common disease of cats in which excessive fat accumulates in hepatocytes and may lead to severe intrahepatic cholestasis and progressive liver failure. Most cases in cats are idiopathic. Diabetes mellitus, pancreatitis, cholangiohepatitis, hyperthyroidism, hypertrophic cardiomyopathy, renal disease, chronic cystitis, chronic upper respiratory infections, hyperadrenocorticism, and neoplasia also have been detected in some cats with hepatic lipidosis. Most dogs with hepatic lipidosis have another underlying disease process.

2. What is acute hepatitis?

Acute hepatitis refers to any condition that causes inflammation and swelling of the liver. Injury may be precipitated by drugs, trauma, toxins, and infectious agents. In addition, immune-mediated diseases, inborn errors of metabolism (copper toxicity in Bedlington terriers is an example), and neoplastic diseases may result in acute hepatitis. Acute hepatitis also accompanies acute pancreatitis in both dogs and cats.

3. What historical questions should be asked of clients with animals with suspected acute hepatitis?

Drug administration, trauma, and toxin exposure should be ruled out by history. Many drugs, including potentiated sulfonamides, carprofen, anthelmintics such as metronidazole, and benzodiazepines have been associated with acute hepatitis or acute hepatic necrosis. It should be determined whether the animal has ingested moldy food; aflatoxins produced by some fungi are potent hepatotoxins. Travel and vaccination histories are important; leptospirosis may result in acute hepatitis in dogs and is a direct zoonosis.

4. What population of cats typically develops idiopathic hepatic lipidosis?

Middle-aged cats are primarily affected, but cats of any age may develop hepatic lipidosis. There does not appear to be a breed or sex predisposition. A large percentage of affected cats are obese before onset of clinical signs.

5. What historical complaints are commonly associated with acute hepatitis or lipidosis?

Anorexia occurs in most animals. In cats with idiopathic lipidosis, a stressful episode such as surgery, boarding, moving, or a new member in the household may precede appetite loss. Lethargy, depression, icterus, ptyalism, and vomiting are also commonly reported with acute hepatic diseases. Diarrhea is uncommon with idiopathic lipidosis but occurs in some animals with acute hepatitis. Hepatic encephalopathy (HE), characterized by head pressing, stupor, and coma, occurs in some animals with acute hepatic diseases.

6. What physical abnormalities are commonly detected in animals with acute hepatitis or lipidosis?

Depression, icterus, and dehydration are common. At presentation, most cats with idiopathic hepatic lipidosis have lost as much as 25-50% of their previous body weight. Most animals with acute hepatitis have clinical signs of shock, including elevated heart rate, pale mucous membranes, increased capillary refill time, and weak pulse. Liver size may be normal, increased, or decreased, depending on the primary cause and duration of the disease process before acute presentation. Animals with chronic hepatic disease that present with an acute exacerbation may have abdominal distention due to sustained portal hypertension or hypoalbuminemia-associated transudative ascites.

7. What diagnostic tests should be considered for animals with suspected acute hepatitis or lipidosis?

Complete blood count, platelet count, serum biochemistry panel, activated clotting time, and urinalysis should be assessed on admission. Packed cell volume, total protein, blood glucose, electrolytes, and coagulation should be assessed as soon as possible and emergency treatment initiated as indicated. Coagulation should be assessed because hepatic aspiration or biopsy is often indicated and disseminated intravascular coagulation is common, particularly in animals with acute hepatitis.

8. What routine laboratory abnormalities are most consistent with acute hepatitis or lipidosis?

Although no pathognomonic changes in complete blood count are associated with hepatic lipidosis, mild nonregenerative anemia, neutrophilia, or neutropenia may be noted. Increases in liver enzyme activities are common; any combination of increased activity of alanine transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), or gamma-glutamyl transferase (GGT) may occur. In most cats, increases in ALP and GGT activities are greater than increases in ALT and AST activities. Lack of increased liver enzyme activities does not exclude the diagnosis of idiopathic hepatic lipidosis. Hyperbilirubinemia and bilirubinuria occur in most cats with idiopathic hepatic lipidosis. Findings are similar with acute hepatitis, but increases in alanine transferase and aspartate aminotransferase activities are usually greater than increases in alkaline phosphatase and gamma-glutamyl transferase activities.

9. What ancillary diagnostic tests help to determine the cause of liver disease in animals with suspected acute hepatitis or lipidosis?

Fasting and postprandial serum bile acids are usually markedly increased but do not need to be measured if hyperbilirubinemia is present. Fasting serum ammonia concentrations may be elevated and can be used for indirect assessment of the presence of hepatic encephalopathy. Abdominal radiographs, hepatic ultrasound, pancreatic ultrasound and trypsin-like immunoreactivity (TL1) tests may be used to narrow the differential list in animals with acute hepatic disease.

10. Do I need to perform a hepatic biopsy for all animals with suspected acute hepatitis or lipidosis?

A presumptive diagnosis of idiopathic hepatic lipidosis in cats may be made by the combination of appropriate history, laboratory abnormalities, and vacuolated hepatocytes on cytologic evaluation of a fine aspirate of the liver. If the cause of hepatitis is determined by history (trauma, drugs, toxins) or other findings (pancreatitis), biopsy may not be needed. However, the reference test for hepatic diseases is hepatic histologic evaluation. If hepatic aspiration or biopsy is performed, samples should be cultured for aerobic and anaerobic bacteria.

11. What immediate supportive care should be provided to animals with suspected acute hepatitis or lipidosis?

Fluid, electrolyte, acid-base, coagulation, and glucose abnormalities should be corrected as discussed in other chapters. Depending on acid-base and electrolyte status, 0.45% NaCl and 2.5% dextrose or Normosol-R are appropriate fluid choices. Potassium supplementation is required for most cases. Antibiotics should be administered to all animals with suspected acute hepatitis because bacterial translocation from the intestines into the liver is common. Penicillin derivatives or first-generation cephalosporins administered parenterally are adequate if clinical findings of sepsis are not present. Enrofloxacin should be considered in animals with suspected gram-negative sepsis. Vitamin K should be given subcutaneously to animals with increased activated clotting time. Supplementation with B vitamins is suggested for most cases. Hepatic encephalopathy, if present, is managed as described for portosystemic shunts (see chapter 83). Appetite stimulants, including cyproheptadine and benzodiazepams, generally are not successful alone. Benzodiazepams may lead to severe sedation if hepatic dysfunction is severe and have been associated with liver failure.

Whether enteral feeding is indicated depends on the cause of the disease. Early, aggressive nutritional therapy is the key to successful treatment of idiopathic hepatic lipidosis in cats. Initial short-term nutritional support may be provided by a nasoesophageal tube. However, because nutritional support is required for at least 3-6 weeks in most cases, a gastrostomy tube is strongly recommended. Multiple small meals should be fed to cats to provide a total of 60-80 kcal/kg/day. Most full-grown cats can handle 50-80 ml of food per feeding when the volume of food at each meal is gradually increased over several days. Protein should not be restricted unless signs of hepatic encephalopathy are present. Food should always be offered by mouth; the tube can be pulled after eating begins and liver enzymes have returned to normal.

12. What is the prognosis for recovery from idiopathic hepatic lipidosis?

The prognosis is guarded to fair, depending on how early the disease is recognized. The conditions can be reversed with aggressive nutritional therapy. Owners must be counseled that recovery may require up to 20 weeks before spontaneous eating occurs. Without treatment, hepatic lipidosis is usually fatal, leading to progressive liver failure.