No abstract

These in vitro results, if extrapolated to catheter interventions, suggest that thermal injury to the vessel wall by laser angioplasty or other thermal angioplasty methods may provide a basic and clinically relevant advantage over mechanical angioplasty modalities, because of a potentially reduced risk of complications related to platelet adhesion.

Acute occlusion and restenosis are the major complications of percutaneous transluminal coronary balloon angioplasty. Application of heat during balloon dilation was postulated to reduce these complications. We evaluated thrombogenicity and intimal hyperplasia of normal rabbit iliac arteries after conventional (37 °C) and thermal balloon dilation. Thermal dilation was performed with a radio-frequency-heated balloon, provided with three thermocouples attached to the inside of the balloon skin. In a previous in vitro study, thrombogenicity of human subendothelium was increased at 55°C and greatly decreased at temperatures over 70°C. Thermal balloon dilation was therefore performed at 55 and 90°C in vivo. Rabbits survived 2 h for evaluation of platelet adhesion or either 3 or 8 weeks for intimal hyperplasia. Angiograms revealed no occlusions or thrombi after any procedure. Platelet adhesion was quantified on 20 scanning electron microscopic pictures per balloon dilation site and was expressed as the percentage of the luminal surface covered by platelets. Platelet adhesion was similar in all groups, although large thrombi were present in the 90°C group. Intimal hyperplasia was measured morphometrically at regular intervals over the balloon site. After 3 weeks, the average intimal hyperplasia was significantly reduced in the 90°C balloon dilation group, which was mainly due to the absence of intimal hyperplasia in the mid-part of these segments. After 8 weeks, intimal hyperplasia was equal in all groups. Thus, in the applied model, platelet coverage was equal after conventional balloon angioplasty and after 55 and 90°C balloon angioplasty. Our data suggest that intimal hyperplasia is delayed but not diminished after balloon dilation at 90°C.

Objective To describe a case of massive transfusion using unwashed, non‐anticoagulated, nonsterile autologous blood in a dog with catastrophic hemorrhage from a peripheral vessel during orthopedic surgery. A damage control surgical strategy was also employed. Case Summary A 6‐year‐old, 48 kg neutered male Labrador Retriever experienced massive hemorrhage after transection of a large blood vessel while undergoing femoral head and neck osteotomy. Blood was collected from clean, but not sterile, suction canisters and clots were skimmed off. The blood was then transfused back to the dog using a standard in‐line blood filter. Approximately 58% of the dog's blood volume was autotransfused in less than 2 hours, thereby meeting the criteria for massive transfusion. Surgery was aborted after hemostasis was achieved by ligation of the vessel and packing of the surgical site. Two units of fresh frozen plasma were administered postoperatively due to the development of a coagulopathy. Hemoglobinuria developed but resolved within 18 hours. Three days later, completion of the surgical procedure was performed without incident. The dog was discharged 4 days after the initial surgery. Marked swelling of the affected limb developed, but resolved after the sixth day. No other significant complications developed. New or Unique Information Provided In this case report, the authors describe the successful management of catastrophic hemorrhage with autotransfusion performed in the absence of sterile collection, cell washing, or anticoagulation. Although not ideal, autotransfusion under these conditions can be lifesaving in situations of massive hemorrhage. This case also highlighted the employment of a damage control surgical strategy.

In vitro platelet adhesion to human subendothelium is reduced by more than 50% after heating it briefly to more than 74 degrees C. Temperatures in excess of 80 degrees C reduce platelet adhesion by at least 85%. Thermal denaturation of von Willebrand factor is responsible not only for the decreased thrombogenicity above 71 degrees C but also for the increased thrombogenicity near 55 degrees C, provided that the von Willebrand factor concentration is low.