Pain management in critically ill patients
Abstract
Pain in critical care patients is a frequent occurrence due to surgery, trauma, invasive monitoring, changing dressings, suctioning various fluids and prolonged immobilization. These varied sources of pain make pain in the critical patient one of the most challenging areas of clinical practice for human nurses, and the same is true for veterinary nurses. Pain is defined as an unpleasant sensory and somewhat emotional experience that is typically associated with tissue damage, or is described in terms of actual or potential tissue damage. The body's nociceptive system initially detects a noxious stimulus, such as heat or a surgical incision, and generates a physiological and behavioural response to the injury; this process can also occur following any form of neuroplastic change, even after a wound or injury is considered healed. Pain is a very complicated concept and there are many physiological processes involved, which can make it difficult to assess and understand in animal patients, especially where pain has developed and seems unrelated to any obvious or identifiable physical process or injury. Due to these difficulties in pain assessment in veterinary patients it is recommended to take a liberal approach to analgesic use for their benefit.
Anoxious stimulus activates the body's normal sensory system and there are certain stages identified in the pain pathway; these are transduction, transmission, modulation and perception. There are two types of fibres associated with the transmission of pain: A delta fibres are large in diameter and myelinated, and produce sharp or well-defined pain to a noxious stimulus so fast the body responds immediately; smaller C fibres transmit dull or aching pain, and transmit the pain signal slower than A delta fibres due to their lack of a myelin sheath (Helms and Barone, 2008).
Nociceptors, or primary afferent neurons are activated due to tissue injury caused by mechanical, chemical or thermal sources, and are found in skin, muscles, joints, connective tissue (somatic tissues) and some visceral tissues. Transduction (the first stage in the pain process) occurs when nociceptors are exposed to a sufficient stimulus to cause depolarization of the nerves, and transmission (the second stage) of this impulse generated occurs along the axon of the neuron, which continues to the spinal cord and higher centres (Benson, 2000). Perception is the third stage, where the cerebral cortex receives the signals from the peripheral and spinal nerves in order to formulate a response. Modulation is the final stage of the pain process, where the afferent neurons release substances that expand the nociceptive field to areas adjacent to the original injury; this is essentially the start of ‘wind up’, or secondary hyperalgesia (Figure 1).
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