[Periprosthetic fractures of the knee joint]. / Periprothetische Frakturen des Kniegelenks.

Periprosthetic fractures are a challenging problem in view of the demographic development and the increasing number of implanted prostheses. Most of these fractures occur postoperatively after a period of two to four years after implantation of a total knee arthroplasty. They are usually caused by traumata, implantation-specific factors and loosening of the prosthesis. Beside further risk factors osteopenia and a reduced mobility of the prosthesis predispose to these fractures. Numerous classifications which also include a loosening of the prosthesis in the fracture discription are an important tool for planning the therapy. Beside the conservative treatment, the stabilization of the fracture or changing the prosthesis should be considered. The treatment options of periprosthetic fractures of the knee joint are discussed in view of different initial situations with the aim of achieving a load-stable situation.

Complete shutdown of microvascular perfusion upon hepatic cryothermia is critically dependent on local tissue temperature.

Since microvascular dysfunction with complete circulatory arrest and, thus, prolongation of tissue ischaemia is considered a potential mechanism for cell necrosis following hepatic cryosurgery, we determined the temperature necessary for induction of complete nutritive perfusion failure in cryothermia-treated rat livers. After localization of the cryoprobe with seven thermocouples and application of a single or double freeze-thaw cycle, in vivo fluorescence microscopy of the cryoinjured left lobe was performed over a 2-h period using a computer-controlled stepping motor, which guaranteed analysis of the identical liver tissue segments with exact allocation of the thermocouples and thus determination of tissue temperature. Cryothermia resulted in a central non-perfused part of injury, surrounded by a heterogeneously perfused peripheral zone. The non-perfused area after single and double freezing continuously increased over the first 90-min period due to a successive shutdown of perfusion within the peripheral border zone. Analysis of the thermocouples' temperature at the end of freezing revealed the 0 degrees C-front at 11.7 mm (single freeze-thaw cycle) and 12.1 mm (double freeze-thaw cycle) distant from the centre of the cryoprobe, which exactly corresponds with the initial (30 min) expansion of the area with nutritive perfusion failure. The increased non-perfused tissue area at 2 h conformed a critical border temperature between 8.29 +/- 1.63 degrees C and 9.07 +/- 0.24 degrees C. From these findings, we conclude that freezing of liver tissue to temperatures of at least < 0 degrees C causes complete/irreversible perfusion failure, which consequently will result in cell death and tissue necrosis, and may thus be supposed as a prerequisite for the safe and successful application of cryosurgery in hepatic tumour ablation.

Epi-illumination fluorescent light microscopy for the in vivo study of rat hepatic microvascular response to cryothermia.

To elucidate the hepatic microvascular response to cryothermia, we studied the liver microcirculation of Sprague-Dawley rats after one and two 4-minute freeze-thaw cycles using intravital fluorescence microscopy. Irrespective of the number of freeze-thaw cycles applied, the nature of hepatic microvascular injury was characterized by complete stasis of sinusoidal blood flow within the central part of the cryolesions and heterogeneous sinusoidal perfusion in a critically perfused border zone located at the periphery of the lesions. Analysis over time (2 hours) revealed a successive shutdown of sinusoidal perfusion within this critically perfused border zone, which was caused by intravascularly lodging cell aggregates, blocking the lumen of individual sinusoids. The aggregates consisted of parenchymal cells and cell fragments, but did not include leukocytes or platelets. Strikingly, microvascular perfusion failure was associated with Ito cell disintegration and marked dilation of sinusoids (15.6 +/- 0.8 microm vs. 8.8 +/- 0.8 microm; P <.05). This excludes sinusoidal constriction as the cause of nutritive perfusion failure, and may indicate dysfunction of Ito cell-regulated vasomotor control by cryothermia. However, because circulating cell aggregates were frequently observed plugging individual microvessels, dilation of sinusoids may just be the result of passive distension caused by outflow blockade. Analysis of hepatic tissue at 8 weeks after cryothermia did not reveal regeneration and microvascular remodeling, but loss of hepatic tissue, which corresponded well with the tissue area presenting with sinusoidal perfusion failure during the initial observation period after cryothermia. The fact that there was no recovery of sinusoidal perfusion over the initial 2-hour observation period, but loss of tissue after 8 weeks, supports the view that cryothermia induces injury not only by direct low-temperature-mediated action, but also through ischemia caused by irreversible deterioration of the microcirculation.