Treatment of osteitis pubis in athletes. Results of corticosteroid injections.

This study presents the results of treatment of osteitis pubis in 12 intercollegiate athletes. Early in this series, athletes were treated with prolonged rest, oral antiinflammatory medications, and hip-stretching exercises. Of the nine athletes treated in this manner, only one resumed symptom-free activity after 16 weeks of therapy; eight remained symptomatic and subsequently received a corticosteroid injection (1 ml 1% lidocaine, 1 ml 0.25% bupivacaine, and 4 mg dexamethasone) into the pubic symphysis. Of these eight athletes, three returned to full participation within 3 weeks of injection, four required a second injection to alleviate their symptoms, and one was unable to resume athletic activities despite two injections and an inguinal herniorrhaphy. In recent years, we have recommended an injection if treatment. Three athletes received a corticosteroid injection when their symptoms did not resolve. All three returned to full athletic competition within 2 weeks of the injection. The results of our study suggest that a more rapid return to intercollegiate athletics can be achieved through the judicious use of corticosteroid injections.

Failure of heparin, superoxide dismutase, and catalase to protect against decompression sickness.

The effects of heparin (HEP), superoxide dismutase (SOD), and catalase (CAT) on the course of decompression sickness (DCS) were studied in anesthetized dogs (Canis familiaris). Animals were divided into 4 groups: a drug assay group (n = 4) received HEP + SOD or HEP + SOD + CAT but were not dived; a control group (n = 14) was dived without drug treatment; a HEPSOD group (n = 11) received HEP + SOD predive and postdive; and a HEPSODCAT group (n = 15) received HEP + SOD + CAT before diving. All dived animals were subjected to repetitive air dives to 10 ATA until pulmonary artery pressure at least doubled within 10 min postdive. Physiologic variables were measured for 3 h postdive or until death. Animals were not recompressed. More early deaths occurred in the HEPSOD (7/11) and HEPSODCAT (8/15) groups than in the control group (5/14). All dived animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, acidosis, hypoxemia, and interstitial pulmonary edema postdive. Drug therapy did not alter these responses to decompression. We conclude that without recompression, treatment with either HEP + SOD OR HEP + SOD + CAT does not improve the outcome of severe DCS in this animal model.

Effects of He-O2 breathing during experimental decompression sickness following air dives.

The effects of ventilation with He-O2 during decompression sickness (DCS) and venous air embolism were studied. Fifteen anesthetized dogs were mechanically ventilated and subjected to repeated air dives until pulmonary artery pressure at least doubled within 10 min postdive. At 30 min postdive, ventilation was either continued with air (controls, n = 7) or changed to He-O2 (n = 8) for an additional 90 min. All animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, hypoxemia, hypercarbia, and pulmonary edema. Breathing air or He-O2 postdive did not alter these responses, but He-O2 breathing produced an 11% increase in pulmonary vascular resistance (PVR). In 3 other anesthetized dogs that were not subjected to dives, ventilation was changed to He-O2 at various times during an intravenous infusion of air; He-O2 breathing caused a 22% increase in PVR. We conclude that breathing He-O2 during DCS resulting from air dive can intensify pulmonary vascular obstruction.