[Labor pain-causes, pathways and issues]

Abstract

In the first stage of labor, pain is caused by distension of the cervix and low uterine segments in combination with isometric contraction of the uterus. Pain in the second stage of labor is dominated by tissue damage in the pelvis and perineum. Labor pain is due to an activation of nociceptors partly resulting from ischemia. The impulses thus generated are conducted into the spinal cord by afferent C fibers from the cervix and lower uterine segments, and by afferent Adelta and C fibers from the pelvis, pelvic organs and perineum. Labor pain is referred to the dermatomes T(11) and T(12) in the early stage of labor. It spreads to the neighboring dermatomes T(10) and L(1) and eventually involves the dermatomes S(2-4) during the second stage of labor and delivery. As in any other type of pain, labor pain stimulates respiration. This reduces the CO(2) concentration in the blood so that, in pain-free periods, respiratory stimulation is lacking and, in consequence, oxygen concentration in maternal and fetal blood is lowered. Pain-induced sympathetic activation will increase cardiac output in a way that may be deleterious in parturients with heart disease, eclampsia and anemia. Moreover, slowing of gastric emptying may cause nausea and vomiting, and slowing of intestinal propulsive movements may result in ileus and oliguria. An increase in plasma catecholamines and glucocorticoids influences uterine contractions. The amount of beta-endorphin released from the pituitary and placenta into the blood is relatively high but obviously not sufficient to depress pain effectively. Adequate nerve block and epidural anesthesia, as well as measures to relieve anxiety, will help markedly to reduce the risks associated with labor pain.