Charles E. Short

Fundamentals of pain perception in animals

Abstract Pain is mediated by functionally distinctive components. It may involve acute high threshold afferent stimuli (thermal, mechanical or chemically damaged tissue), protracted afferent input (long-lasting hyperalgesia) or low-threshold input (allodynia as related to pain from light touch). Behavioral patterns will be associated with the effects of noxious stimulus on excitatory transmitters. Humane studies using mechanical, thermal (cold pressor test), audio-evoked potentials, or other noxious stimuli during anesthesia and analgesia provide clues to perception of pain in animals and help us determine guidelines for the clinical relief of animal pain. There is a better understanding of cutaneous somatosensory responses than for deep sensation (e.g., subcutaneous tissue, muscle, bone, viscera). The prevention or treatment of pain can best be accomplished when there is a diagnosis of the neuroanatomical distribution of the pain based on evidence of sensory dysfunction involving a peripheral nerve, plexus, nerve root or central pathway using different modalities for quantitative sensory testing. Anatomical studies have demonstrated that unmyelinated primary afferent fibers contain a variety of neuroactive substances which may be released by high-intensity peripheral stimulation. Fast depolarization of the dorsal horn nociresponsive neurons is mediated by tissue damage. These neuroreceptors may be activated by glutamate, substance P, and neurokinin A. The major ascending pathway relaying nociceptive information relating to pain is the spinothalamic tract. Most of the neurons in this tract are nociceptive or thermoreceptive. The thalamus is the final relay nucleus for all the sensory systems, except olfactory tissue. Injury or disease processes in deeper tissue or visceral areas with extensive innervation may result in pain thresholds not adequately controlled by current available analgesics or at their recommended dosage levels. These issues are complex and diagnosis is even more difficult due to species and breed differences in outward expression to painful insult. Medications can now be targeted for specific receptors.

The use of propofol for induction of anaesthesia in dogs premeditated with acepromazine, butorphanol and acepromazine-butorphanol

Cardiovascular, pulmonary and anaesthetic-analgesic responses were evaluated in 18 male and female dogs to determine the effect of the injectable anaesthetic propofol used in conjuction with acepromazine and butorphanol. The dogs were randomly divided into three groups. Dogs in Group A were premeditated with 0.1 mg/kg of intramuscular acepromazine followed by an induction dose of 4.4 mg/kg of intravenous propofol; Group B received 0.2 mg/kg of intramuscular butorphanol and 4.4 mg/kg of intravenous propofol; dogs in Group AB were administered a premeditation combination of 0.1 mg/kg of intramuscular acepromazine and 0.2 mg/kg of intramuscular butorphanol, followed by induction with 3.3 mg/kg of intravenous propofol. The induction dose of propofol was given over a period of 30-60 seconds to determine responses and duration of anaesthesia. Observations recorded in the dogs included heart and respiratory rates, indirect arterial blood pressures (systolic, diastolic and mean), cardiac rhythm, end-tidal CO, tension, oxygen saturation, induction time, duration of anaesthesia, recovery time and adverse reactions. The depth of anaesthesia was assessed by the response to mechanical noxious stimuli (tail clamping), the degree of muscle relaxation and the strength of reflexes. Significant respiratory depression was seen after propofol induction in both groups receiving butorphanol with or without acepromazine. The incidence of apnea was 4/6 dogs in Group B, and 5/6 dogs in Group AB. The incidence of apnea was also correlated to the rate of propofol administration. Propofol-mediated decreases in arterial blood pressure were observed in all three groups. Moderate bradycardia (minimum value > 55 beats/min) was observed in both Groups B and AB. There were no cardiac dysrhythmias noted in any of the 18 dogs. The anaesthetic duration and recovery times were longer in dogs premeditated with acepromazine/butorphanol.

Pharmaceutical control of pain in large animals

Abstract Pain may result in tissue ischemia, tissue hypoxia, shock, severe cardiac arrhythmias, atelectasis, renal failure, and a catabolic state. Hence, veterinarians are expected to treat pain in animals for ethical reasons and to improve wound healing. Adequate treatment of pain requires recognition of a variety of cardiovascular, respiratory, neuroendocrine, and behavioral changes associated with pain in animals. Pain treatment can be directed at the periphery, at sensory axons, or at central neurons. Drugs that are used to interfere at one or more of these sites include non-steroidal anti-inflammatory drugs (NSAIDs), opioids, α 2 -adrenoceptor-agonists, and local anesthetics administered systemically, locally, epidurally, or intrathecally. The dose rates and frequency of administration of each analgesic drug are highly dependent on animal species and route of drug administration.