Pain is defined by the International Association for the Study of Pain (IASP) as:
An unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such
damage. Controlling pain is a vital role for clinicians.
Types of Pain
Physiologic: High intensity fibers that act to protect by warning of contact w/ tissue damaging stimuli
Pathologic (clinical): Produced by peripheral tissue injury or damage to nervous system, and can be inflammatory (visceral/somatic)
Idiopathic: Pain that persists in absence of identifiable substrate
Hyperalgesia is characterized by an increased response to a noxious stimulus, without a change in nociceptor threshold. This is illustrated
by the slope of the line being greater than normal. Allodynia on the other hand is characterized by a decrease in the nociceptor threshold required to produce a response, (ie a non painful
stimuli can induce a painful response).
Nociception is the process of detecting pain via pain receptors (nociceptors) and signaling noxious stimulus, it consists of transduction,
transmission, modulation which leads to conscious perception of pain.
Transduction is the process that involves translation of noxious stimuli into electrical activity at sensory nerve endings. Nociceptors
respond to thermal, mechanical, and chemical stimulation. Transmission is the process of sending the impulses throughout the sensory nervous system. Afferent signals from the periphery are relayed
through the dorsal root ganglia to the dorsal horn of the spinal cord where sensory input can be modulated. Information then
travels rostrally, finally reaching the cerebral cortex.
Modulation is the modification of nociceptive transmission. The body can regulate and modify incoming impulses at the dorsal horn.
Perception of pain can only occur in a conscious animal and is a result of the interaction of transduction, transmission, and modulation.
The concepts of peripheral and central sensitization explain a great deal about an animal's response to an injury and also
pave the way for better pain management. Surgery produces inflammation and a change in sensitivity to noxious stimuli. As
the local area of tissue injury becomes more sensitive, the threshold for subsequent stimuli decreases (termed hyperalgesia).
The hypersensitivity is not localized just to the original site of injury; it spreads to other parts of the body, which is
termed secondary hyperalgesia. When neurons in the dorsal horn are repeatedly stimulated, their rate of discharge dramatically
increases with time, and this is central hypersensitization. The barrage of signals that arrive in the spinal cord causes
changes in the dorsal horn neurons, which become "wound up." The neurons are hypersensitive even after the noxious stimulus stops. Specific receptors are involved in the process of "wind-up";
one is the N-methyl-D-aspartate (NMDA) receptor in the spinal cord. Ketamine is a noncompetitive NMDA antagonist, and this
has resulted in numerous studies on ketamine's ability to prevent or treat pain, particularly when given prior to the painful
Clinical Signs of Pain
Tachycardia, hypertension, dilated pupils, tachypnea, behavioral changes, vocalization, and abnormal posture/gait
Physiologic Consequences of Pain
Increased sympathetic tone, vasoconstriction, increased systemic vascular resistance, increased cardiac output, increased
myocardial work, decreased gastro-intestinal tract tone, catabolic state, increased blood glucose, increased protein catabolism
and lipolysis, and renal retention of H20 and Na with increased K excretion and decreased GFR. Coagulation abnormalities include
increased blood viscosity, prolonged PT/PTT, fibrinolysis and platelet aggregation.
Non-pharmacologic Treatment of Pain
Caring and supportive (environment clean and dry environment), visiting with family and familiar objects, and giving cats
a place to hide. Direct drug therapy at the four steps in the nociceptive.
Options for therapy
Anesthetics, opiods, α2 agonists, benzodiazepines, phenothiazines, local anesthetics, NSAIDS, NMDA antagonists, TCA, anticonvulsants,