Systemic Responses to Pain

SYSTEMIC RESPONSES TO PAIN

Systemic Responses to Acute Pain

Acute pain is typically associated with a neuroendo-crine stress response that is proportional to pain intensity. The pain pathways mediating the afferent limb of this response are discussed above. The efferent limb is mediated by the sympathetic nervous and endocrine systems. Sympathetic activation increases efferent sympathetic tone to all viscera and releases catecholamines from the adrenal medulla. The hormonal response results from increased sym-pathetic tone and from hypothalamically mediatedreflexes. Moderate to severe acute pain, regard-less of site, can affect the function of nearlyevery organ and may adversely affect perioperative morbidity and mortality.

A. Cardiovascular Effects

Cardiovascular effects are often prominent and include hypertension, tachycardia, enhanced myo-cardial irritability, and increased systemic vascular resistance. Cardiac output increases in most normal patients but may decrease in patients with compro-mised ventricular function. Because of the increase in myocardial oxygen demand, pain can worsen or precipitate myocardial ischemia.

B. Respiratory Effects

An increase in total body oxygen consumption and carbon dioxide production necessitates a con-comitant increase in minute ventilation. The lat-ter increases the work of breathing, particularly in patients with underlying lung disease. Pain due to abdominal or thoracic incisions further com-promises pulmonary function because of guard-ing (splinting). Decreased movement of the chest wall reduces tidal volume and functional residual

D. Endocrine Effects

Stress increases catabolic hormones (catecholamines, cortisol, and glucagon) and decreases anabolic hor-mones (insulin and testosterone). Patients develop a negative nitrogen balance, carbohydrate intoler-ance, and increased lipolysis. The increase in cortisol, renin, angiotensin, aldosterone, and antidiuretic hor-mone results in sodium retention, water retention, and secondary expansion of the extracellular space.

E. Hematological Effects

Stress-mediated increases in platelet adhesiveness, reduced fibrinolysis, and hypercoagulability have been reported.

F. Immune Effects

The neuroendocrine stress response produces leuko-cytosis and has been reported to depress the reticu-loendothelial system. The latter predisposes patients to infection. Stress-related immunodepression may also enhance tumor growth and metastasis.

G. Psychological Effects

Anxiety and sleep disturbances are common reac-tions to acute pain. With prolonged duration of the pain, depression is not unusual. Some patients react with frustration and anger that may be directed at family, friends, or the medical staff.

Systemic Responses to Chronic Pain

The neuroendocrine stress response is generally observed only in patients with severe recurring pain due to peripheral (nociceptive) mechanisms and in patients with prominent central mechanisms such as pain associated with paraplegia. It is attenuated or absent in most patients with chronic pain. Sleep and affective disturbances, particularly depression, are often prominent. Many patients also experience significant changes in appetite (increase or decrease) and stresses on social relationships.