Concurrent dorsal dislocations and fracture-dislocations of the index, long, ring, and small (second to fifth) carpometacarpal joints.

OBJECTIVE: To review the outcome of patients with concurrent dorsal dislocations and fracture-dislocations of the second, third, fourth, and fifth carpometacarpal (CMC) joints treated with open reduction and internal fixation (ORIF). DESIGN: Retrospective review. SETTING: Level 1 trauma center. PATIENTS: Between 1991 and 1997, twelve multiply injured patients with the described CMC injury complex (one open injury) were treated with ORIF (eleven patients) or percutaneous wire fixation (one patient) by the same surgeon. INTERVENTION: Treatment consisted of ORIF with Kirschner wires followed by splints and immediate metacarpophalangeal and interphalangeal joint range of motion exercises. MAIN OUTCOME MEASUREMENTS: Grip strength, wrist and finger range of motion, pain, need for additional surgery, and return to work. RESULTS: Of the ten patients available for follow-up (mean, three years), all had been treated with ORIF (eight within forty-eight hours of injury and two had treatment delayed for four weeks because of delayed diagnosis and management of more serious injuries). Three patients had additional surgery (planned secondary second and third CMC arthrodeses). Grip strength of the operated hand in the five patients with JAMAR testing was 50 percent (n = 3), 75 percent (n = 1), and 90 percent (n = 1) of that in their contralateral hands. Five patients were pain-free, and five reported occasional, activity-related pain. The five patients who worked before the injury returned to their previous occupations (one with slightly modified duties). CONCLUSION: This is the largest series of patients with this CMC injury complex and the first report of open CMC dorsal dislocations and fracture-dislocations. Although early ORIF is suggested, delay of up to four weeks did not adversely affect results.

Challenging fractures of the foot and ankle.

The foot and ankle is one of the most imaged parts of the body. Although most plain radiographs reveal no bony injury, subtle fractures can be overlooked. Because it is important to detect these fractures at the time of injury, a review of the most commonly missed foot and ankle fractures is presented.

Prostaglandin production in cultured cerebral microvascular smooth muscle is serum dependent.

To expand the understanding of cerebrovascular eicosanoid metabolism, the ability of smooth muscle isolated from murine cerebral microvessels to produce prostaglandins (PGs) was studied in vitro. Cultures from SJL and BALB/c mice produced primarily prostaglandin E2 (PGE2) and I2 (PGI2) in response to exogenous arachidonate and calcium ionophore as well as the agonists acetylcholine and epinephrine. Subconfluent smooth muscle cultures demonstrated a two- to threefold increased capacity to produce PG compared with confluent cultures. In contrast, serum deprivation of smooth muscle caused an 80-90% diminution in both PGE2 and PGI2 production but had no effect on PG release in cerebromicrovascular endothelium. Reintroduction of serum to smooth muscle restored PG production within 6h, and the restoration was inhibited by 1 microM dexamethasone. Message for both prostaglandin H synthase (PGHS)-1 and -2 was detectable in smooth muscle grown in the presence of serum, but PGHS-2 message was not present in serum-deprived cultures. Furthermore, readdition of serum induced a massive increase in PGHS-2 mRNA with only a small increase in PGHS-1 message. The serum induction of PGHS-2 was corroborated by immunohistochemistry and Western blotting. Thus cerebromicrovascular smooth muscle may contribute significantly to the formation of PG under circumstances likely to be present during central nervous system pathologies. The induction of PGHS, particularly PGHS-2, may play a key role in this process.

Segmental bone deficiency after acute trauma. The role of bone transport.

Bone transport, along with allied techniques of compression distraction, offer exciting new treatment alternatives for the difficult problem of segmental bone loss from acute trauma. Many factors must be considered before indicating these treatment methods, because it is clear that many of the problems that existed with more conventional methods also exist with these techniques. The indications for amputation vs. limb salvage must always be considered in these severe injuries. In less severe injuries with minimal bone loss and soft-tissue injury exposing well-vascularized segments of bone, traditional methods of stabilization, soft-tissue coverage, and grafting lead to more rapid healing times and return to function for patients. These techniques are reserved for the most severe type of injuries for which treatment times are long and complications not infrequent. Therefore, methods to speed treatment, avoid complications, and increase patient acceptance should be actively sought. The great advantage of these techniques is that the vast majority of the reconstruction is done on the injured limb segment, with minimal need for extensive donor-site defects.

Chronic infected tibial nonunions with bone loss. Conventional techniques versus bone transport.

Twenty-five patients with infected nonunions of the tibia and segmental bone loss were treated by one of two methods: resection and bone transport, or conventional treatment using less extensive debridement, external fixation, bone grafting, and soft-tissue coverage. The two groups were comparable except for gender distribution. Each group experienced similar rates of healing; eradication of infection; treatment time; final angulation; number of complications; and total number of surgical procedures. However, the final limb-length discrepancy was significantly less in the bone transport group.

Murine cerebral microvascular endothelium incorporate and metabolize 12-hydroxyeicosatetraenoic acid.

Cultured murine cerebromicrovascular endothelial cells were employed to study the metabolism of 12-hydroxyeicosatetraenoic acid (12-HETE) in an in vitro model of the blood-brain barrier. These endothelial cells convert 12-HETE to at least four, more polar compounds. Analysis of the least polar and predominant metabolite by gas chromatography combined with chemical ionization and electron impact mass spectrometry of reduced and nonreduced derivatives indicate that the compound is 8-hydroxyhexadecatrienoic acid (8-HHDTrE). The uptake of 12-HETE into cell phospholipids peaks at 2 hr, and is not saturable up to the highest concentration tested, 5 microM. Seventy-five to 92% of this 12-HETE is incorporated into phosphatidylcholine, while the remainder is divided between the inositol and ethanolamine phospholipids. Incorporation into neutral lipids is slower, with radioactivity gradually accumulating in triglycerides over 24 hr. Saponification of cell lipids demonstrated that not only 12-HETE, but also its major metabolite, 8-HHDTrE, is incorporated into the cell lipids. Prostacyclin and prostaglandin E2 production by the cerebral endothelial cells is inhibited by up to 56% with 1 microM and 90% with 5 microM 12-HETE. These data demonstrate that 12-HETE is actively metabolized by cerebral endothelium and suggest at least two mechanisms through which 12-HETE may alter cerebromicrovascular function: 1) incorporation into cerebral endothelial membranes and 2) inhibition of cerebral endothelial prostaglandin production. Conversion of 12-HETE to more polar compounds, particularly 8-HHDTrE, may be interpreted as either the inactivation of 12-HETE or the production of additional, biological mediators.