Minimally invasive and open surgical treatment of proximal tibia fractures using a polyaxial locking plate system: a prospective multi-centre study.

PURPOSE: The purpose of this study was to determine whether a polyaxial locking plate of the latest generation (NCB PT(®), Zimmer Inc.) which can be applied both open and minimally invasively, can be used as a routine method of treatment for proximal tibia fractures. METHODS: Eighty-six patients (35 women, 51 men; mean age 51 years) were enrolled in this prospective multicentre trial. Ninety-six percent of the fractures were intra-articular (AO type B and C); 36 % were treated open and 64 % minimally invasively. Follow-up was obtained three, six and 12 months after surgery. RESULTS: No implant failure occurred. At 12 months, the functional result using a knee-specific score was good to excellent in 95 %, and 99 % of the fractures were radiologically healed. CONCLUSION: The system is a versatile implant for proximal tibia fracture treatment. Polyaxiality and a specific locking mechanism are compatible with different fracture patterns. The minimally invasive technique effectively protects soft tissues but should not be performed at the expense of fracture reduction. Early functional results and complication rate are comparable to those in the literature.

Isolated closed minor-muscle injury of the lower leg did not cause an obvious systemic immune response.

OBJECTIVE: A common consequence in patients with blunt trauma is a deterioration of the immune system. The specific impacts of a frequently occurring isolated soft tissue trauma on the immune response are described. However, the dimension of trauma needed to cause systemic effects has not been definitely elucidated. METHODS: Mice were traumatized on the lower leg. The extent of soft tissue trauma was quantified by determination of the wet/dry ratio, magnetic resonance imaging (MRI), and serum content of muscle proteins. Five minutes, 3, 24, 36, 48, and 72 h after trauma (a.t.) the ex vivo cytokine-expression of immune-competent cells were measured. RESULTS: Trauma resulted in an early edema that could be quantified by MRI and wet/dry ration. Release of muscle-specific proteins was detected 5 min a.t. The trauma did not cause significant changes of TNF-alpha response of isolated cells to endotoxin. IL6-response of splenocytes to endotoxin was slightly increased 72 h a.t., while IL6-response of peritoneal macrophages to endotoxin was decreased 36 h a.t. CONCLUSION: We describe a standardized trauma model for minor soft tissue injury in mice. Systemic effects on the immune system by traumatized lower leg were not found on the level of circulating cytokines or cellular responses to endotoxin.

Microcirculatory alterations of hepatic and mesenteric microcirculation in endotoxin tolerance.

LPSs getting access to the circulation of mammalian organisms cause typical systemic inflammatory reactions with symptoms characteristic for acute sepsis. One possibility to attenuate LPS effects is to expose a host to a challenge with low LPS doses, which results in the establishment of "endotoxin tolerance" (ET). Because the microcirculation is of particular importance in LPS action, it seemed of interest to analyze leukocyte-endothelial interactions in the mesentery and liver once endotoxin tolerance has been established and are challenged with LPS. The mesenteric and hepatic microcirculation was investigated by intravital microscopy. After induction of ET LPS, shock was induced by i.v. injection of LPS, and microcirculation of the mesentery and liver was examined. Endotoxin tolerance resulted in reduced ex vivo TNF-alpha synthesis of whole blood. In vivo LPS caused no increase of body temperature. In sinusoids, LPS challenge increased adherence of leukocytes in naive rats, which was almost completely prevented by ET induction. In contrast, in postsinusoidal venules, leukocyte adherence was more intense after ET induction and subsequent to LPS application. Similarly, in postcapillary mesenteric venules, increased adherence of leukocytes after LPS challenge in the ET group was observed. After LPS injection, the endothelial barrier was more disturbed in the nontolerant group when compared with the ET group. Soluble L-selectin and intercellular adhesion molecule were elevated in both ET and untreated rats. Endotoxin tolerance influences leukocyte-endothelial interaction differentially depending on organ and vessel area.

Haemorrhagic shock in mice--intracellular signalling and immunomodulation of peritoneal macrophages' LPS response.

Haemorrhagic shock leads to decreased proinflammatory cytokine response which is associated with an increased susceptibility to bacterial infections. In the present study, the effect of GM-CSF on lipopolysaccharide (LPS)-induced TNF-alpha release and MAPkinase activation was analysed on the background of a possible immunostimulating activity of this substance. Male BALB/c mice were bled to a mean arterial blood pressure of 50 mmHg for 45 min followed by resuscitation. Peritoneal macrophages were isolated 20 h after haemorrhage and incubated with 10 ng/ml GM-CSF for 6h before LPS stimulation. TNF-alpha synthesis was studied in the culture supernatants using ELISA. Phosphorylation of ERK, p38MAPK and IkappaBalpha was detected by Western blotting. LPS-induced TNF-alpha production of peritoneal macrophages was significantly decreased 20 h after haemorrhage in comparison to the corresponding cells of sham-operated mice. In parallel the phosphorylation of IkappaBalpha was less in LPS-stimulated peritoneal macrophages from haemorrhagic mice. LPS-induced phosphorylation of ERK1/2 was also decreased in peritoneal macrophages isolated after haemorrhagic shock. In contrast, p38MAPK was phosphorylated more intensely after LPS-stimulation in macrophages collected from shocked mice. GM-CSF incubation elevated LPS-induced TNF-alpha response of macrophages from both sham-operated and shocked mice which was accompanied by an elevated IkappaB and ERK phosphorylation. In general, GM-CSF treatment in vitro enhanced peritoneal macrophages LPS-response both in terms of TNF-alpha synthesis and IkappaB and MAPK signalling, but the levels always stayed lower than those of GM-CSF-treated cells from sham-operated animals. In conclusion, GM-CSF preincubation could partly reactivate the depressed functions of peritoneal macrophages and may therefore exert immunostimulating properties after shock or trauma.

Dopamine affects cellular immune functions during polymicrobial sepsis.

OBJECTIVE: To determine whether infusion of dopamine modulates cellular immune functions and survival during systemic inflammation. DESIGN AND SETTING: Randomized animal study, university research laboratory, Level I trauma center. SUBJECTS: Male NMRI mice. INTERVENTIONS: Mice were subjected to laparotomy (sham intervention, LAP) or polymicrobial sepsis induced by cecal ligation and puncture (CLP). Mice in each of these conditions received either an intraperitoneal infusion of 0.9% saline (CLP/saline; LAP/saline) or an intraperitoneal infusion of dopamine (1.0 microg/kg/min i.p., CLP/DOP; LAP/DOP). Metabolic data and survival were monitored 24 h and 48 h after onset of sepsis, and animals were terminated 48 h after induction of sepsis to determine splenocyte apoptosis (Annexin V binding capacity), splenocyte proliferation (3H-Thymidine incorporation assay), splenocyte IL-2, IL-6 and IFN-gamma release (ELISA) and leukocyte distribution (WBC; CD3, CD4, CD8, B220, F4/80, NK1.1). MEASUREMENTS AND RESULTS: Infusion of dopamine in septic mice increased splenocyte apoptosis and decreased splenocyte proliferation and IL-2 release of septic mice. Furthermore, an inhibitory effect of dopamine infusion on splenocyte proliferation and the release of the TH1-cytokines IL-2 and IFN-gamma was observed in sham operated control mice. These effects were paralleled by a decreased survival of dopamine-treated septic animals (47% vs. 67%). Treatment with DOP did not affect sepsis-induced changes of leukocyte distribution. CONCLUSIONS: We conclude that dopamine is capable of modulating cellular immune functions in a murine model of sepsis.