Managing Back Pain During Pregnancy.

The incidence of low-back pain during pregnancy is thought to be about 50%. It occurs most commonly after the sixth month and can last until the sixth month postpartum. The major predictors are back pain prior to pregnancy and multiparity. Several biomechanical and physiologic changes during pregnancy contribute to back pain. As the woman's abdominal muscles are stretched and tone is diminished, they lose their ability to contribute to neutral posture. During pregnancy, production of the hormone relaxin increases ten-fold. The hormone creates joint laxity, which not only allows the pelvis to accommodate the enlarging uterus, but also weakens the ability of static supports in the lumbar spine to withstand shearing forces. In the pelvis, joint laxity is most prominent in the symphysis pubis and the sacroiliac joints. On physical exam, neither lumbar nor sacroiliac back pain is generally associated with any evidence of neurologic deficit or hip pathology. In cases of lumbar back pain, the physical exam will be most consistent with discogenic pain and/or facet element pain. Therefore, a pregnant woman's pain may be most pronounced on flexion and standing. Among the tests that can be used to evaluate lower-back pain are the posterior pelvic provocation test; ventral gapping test; dorsal gapping test; sacroiliac joint fixation test; Patrick's test, or FABERE's maneuver (flexion, abduction, external rotation, and extension); and Derbolowski's test. The most common types of back pain during pregnancy are lumbar pain, sacroiliac pain, and nocturnal back pain.

Special Issue Introduction: Keeping Pace With Today's Active Women.

If every other patient who walked through your office door were an elite marathoner, you would do everything possible to hone your skills at treating this population. You would assiduously study the sport, the inherent stresses involved, typical physical characteristics of endurance athletes, and common running injuries.

Back pain and pregnancy: active management strategies.

For about half of all pregnant women, low-back pain is inevitable. Physicians who can specify what type of back pain the patient has - lumbar, sacroiliac, or nocturnal - can institute targeted treatment that addresses the relevant pathophysiology. Acetaminophen and certain modalities such as icing the area are the basis of acute treatment in conjunction with ergonomic adaptation and a good low-back exercise program. This will help decrease stress on the low back, making back pain less likely. Before a woman becomes pregnant, encouraging her to become fit and resolving existing back problems is the key to back pain prevention.

Pregnant with back pain? Suggested comfort tactics.

Pregnancy, especially the later stages, is fertile ground for back pain. Your center of gravity shifts because your uterus expands. Your abdominal muscles lose tone. And hormonal changes temporarily loosen important support structures - ligaments and tendons - leaving you with joints and muscles in the back and pelvis that seem to groan under the stress of increased weight.

Ionized calcium, parathormone, and mortality in critically ill surgical patients.

A prospective study measured ionized calcium and parathormone sequentially at 48- to 72-hour intervals in 25 surgical intensive care unit patients. Twelve patients (48%) died at mean day 40 and median day 26. Levels of ionized calcium, parathormone, blood urea nitrogen, creatinine, albumin, magnesium, and phosphate for patients who lived were compared with levels for patients who died. The incidence of hypotension, renal failure (creatinine greater than or equal to 3.0), and bacteremia, as well as the amount of red cell, crystalloid, and colloid administration for the two groups was compared. Hypotension, bacteremia, red cells, crystalloid, and colloid were no different. On days 1 and 2 ionized calcium levels were significantly lower and parathormone levels significantly higher in nonsurviving patients; this difference persisted through days 3 and 4. Blood urea nitrogen and creatinine levels increased early in nonsurviving patients but renal failure, which occurred in nine nonsurviving patients, did not develop until mean day 14, median day 18. The phosphate level was slightly higher but still within normal range in nonsurviving patients. By days 5 and 6 ionized calcium and parathormone levels were no different in nonsurviving patients, despite there being no improvement in renal function. Magnesium and albumin levels were no different between groups. Ionized calcium levels are lower and parathormone levels higher early in nonsurviving patients. This difference is not readily explained by associated clinical conditions, including renal dysfunction. Although etiology remains unclear, low ionized calcium and elevated parathormone are early predictors of mortality in critically ill surgical patients.

Modulation of acetyl-CoA carboxylase by inhibitors of IMP dehydrogenase: implications for insulin regulation.

The activity of acetyl-CoA carboxylase (ACC), the rate-limiting enzyme of fatty acid biosynthesis, can be regulated by both adenine and guanine nucleotides in vitro. We have employed two inhibitors of IMP dehydrogenase, ribavarin and tiazofurin, to investigate a possible role for intracellular nucleotides in ACC regulation in rat adipocytes. Ribavarin, but not tiazofurin, leads to a profound time-dependent inhibition of ACC activity that is associated with a decrease in both intracellular ATP and GTP. This inactivating effect is largely reversed with guanosine, accompanied by increases in both ATP and GTP levels. Epinephrine-mediated inactivation of ACC in intact cells is not altered by ribavarin incubation. However, in these experiments, insulin-mediated activation is observed only after ribavarin-induced inhibition of the enzyme. These data suggest that nucleotides may modulate ACC activity and influence is regulation by insulin in intact cells. The possible mechanisms underlying the insulin activation of ACC and the role of intracellular nucleotides in insulin action are discussed.

Phorbol esters, but not insulin, promote depletion of cytosolic protein kinase C in rat adipocytes.

The tumor-promoting phorbol esters have insulinomimetic effects in several tissues. Employing two different assay systems, we have compared the effects of phorbol ester and insulin on the activity and intracellular distribution of the Ca++ and phospholipid dependent protein kinase (protein kinase C) in isolated rat adipocytes. Phorbol ester leads to a prompt depletion of kinase activity from the cytosolic fraction and appearance of activity in membrane extracts; neither of these effects is mimicked by insulin. These results, taken together with other data, emphasize important divergences between the actions of these agonists and suggest that changes in protein kinase C activity or intracellular distribution are not a necessary concomitant of the cascade of insulin action.

Assay of protein kinase C with an N-bromosuccinimide-cleavage fragment of histone H1.

N-Bromosuccinimide cleavage of a lysine-rich histone fraction (histone III-S) yields a peptide substrate, purified by reverse-phase h.p.l.c., for the Ca2+ + phospholipid-dependent protein kinase (protein kinase C). This substrate displays no reactivity with the cyclic AMP-dependent protein kinase, and may prove useful for the detection of protein kinase C activity in crude tissue extracts.