Acute Pain Sequence of Changes in the Body

Pain as a warning symptom directs the individual's attention to the injury, so that protective measures are taken and everything is done to avoid further damage. However, defensive physical reactions can result in an overcompensation of the individual's capabilities and an additional burden. Thus, pain and fear lead to the release of adrenaline and noradrenaline via an increase of activity of the adrenergic nervous system. Activation of the cortex-hypothalamus-pituitary-axis results in the release of ACTH, inducing a simultaneous rise in the level of gluco- and mineral-corticoids from the adrenal body. Pain and the accompanying stress reaction induce secretion of ADH (antidiuretic hormone) and STH (somatotropic hormone) from the posterior lobe of the pituitary. This is followed by a defense mechanism of the cardiovascular system with:

• vasoconstriction (peripheral and the splanchnic area),

• increase of heart work,

• rise in cardiac excitability, and

• increase in myocardial oxygen demand (MVO2).

In addition to catecholamine-related cardiovascular effects, also humeral changes can be observed:

• increase in blood volume

• increase in blood viscosity,

• hyperglycemia (glucocorticoid and adrenaline effect),

• excess formation of lactic acid (hyperlactemia),

• increase of free fatty acids in the plasma (noradrenaline effect),

• reduction in sodium secretion and

• increase of potassium loss (aldosterone effect).

Aside from hormonal changes, as they can be observed in acute pain, particularly in the postoperative period or after acute trauma, such negative effects can result in the malfunctions of organs and organ systems:

• Suppression of immune function, which is due to a long lasting consequence of glucocorticoids with a concomitant rise in the susceptibility for bacterial and viral infections (Figure I-1).

• A raise in the vulnerability of the myocardial conduction system with an ensuing ventricular arrhythmia and/or fibrillation.

• Pulmonary dysfunctions are one of the main postoperative complications, especially after thoracic and intra-abdominal surgery [2, 3]. Due to insufficient ability to cough, atelectasis develops, which, beside an inadequate ventilationperfusion-ratio with hypoxia, may result in the development of pneumonia,

• Circulatory and metabolic dysfunction lead to an elevation of stroke volume, blood pressure, myocardial metabolism as well as an increase in myocardial oxygen demand,

• Gastrointestinal and urological complications originate in an inhibition of reflex motility, resulting in nausea, emesis and ileus. Pain also induces a reflex-induced hypomotility of the urinal tract, with the sequealae of urinary retention and infection.

• Reflex vasoconstriction in the area of the large joints leads to neglect of use and atrophy with joint stiffening [4].

• Hormonal-related increase in blood viscosity with a decrease in fibrinolysis, especially in the postoperative period in the lower extremities results in the formation of thromboemboli and subsequent pulmonary emboli [4, 5].

• Electrophysiological and morphological changes within the nociceptive system results in the chronification of pain, which may even outlast the actual event [6].

Later, when chronification of pain has developed, it may even become difficult to link it with the actual source [7]. Despite removal of the actual cause, chronification leads to a pain behavior, which requires the entire attention of the patient. Thus, chronified pain has lost its actual function as an alarm signal, because it accompanies the patient over years and even decades [8, 9, 10].

The importance of pain transmission is underlined by the fact that half of all skin nerve fibers with their peripheral nociceptors can be activated by means of thermal (heat or cold), mechanically (push, pressure), and even chemically (acids, lye) stimuli. This for instance is highlighted by the affection of locomotion, where pain has warning function. For instance, after trauma such as bruise, strain, inflammation as well as thermal or electric injury a barrage of so-called pro-nociceptive compounds are being released, which excite the peripheral nociceptors (anatomically free nerve endings). These nociceptors are activated directly or indirectly through different kinins, such as bradykinin, kallidin, T-kinin and/or prostaglandin E. The kinins are body-made compounds the concentration of which is increased through inflammation, tissue damage, or directly through trauma. It is only by inhibition of the enzyme, cyclooxygenase (COX), a necessary step in the formation of prostaglandin from arachidonic acid, peripheral analgesics (NSAIDs) induce their

Figure 1-2. Decrease in prefrontal and thalamic gray matter during chronic pain Adapted from [12]

action. In addition, it has been demonstrated, that aside from their peripheral mode of action, peripheral analgesics also induce a centrally related analgesic effect [11].

Following transition from acute to chronic pain, it can be regarded as an ailment of itself and has to be treated accordingly. This has been demonstrated in patients with chronic pain. By using magnetic resonance imaging (MRI) an irreversible loss of brain tissue has been demonstrated. For instance patients with long-lasting neuropathic pain, showed a reduction in neocortical tissue (prefrontal cortex and thalamus) by as much as 11%, which is equivalent to a loss in the grey matter following 10-20 years of normal ageing. In addition, cortical tissue loss was directly related to the duration of pain. These findings are in accordance with other imaging studies that demonstrated a decrease in brain tissue in the specified areas. These studies provide compelling evidence for the early identification and appropriate management of pain (Figure I-2).

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