ABSTRACT
BACKGROUND: Frostbite is an uncommon event that can occur from exposure to temperatures below -4 degrees C and can lead to potential serious tissue damage and necrosis. This in turn can result in debilitating amputations in otherwise healthy people. The pathophysiological mechanisms of frostbite have marked similarities to those seen in thermal burns, ischemia/reperfusion injuries and crush injuries--i.e., non-healing wounds and inflammatory processes. These injuries are commonly treated with hyperbaric oxygen therapy. OBJECTIVES: Evidence for treating frostbite with hyperbaric oxygen (HBO2) is scarce, and to date HBO2 is not a standard addition in the multidisciplinary care of freezing injuries. We aim to contribute to the available evidence with a case report and review the literature to reassess the multidisciplinary treatment of frostbite injuries. CASE REPORT AND REVIEW OF LITERATURE: We present a case report of a woman with deep frostbite of the toes treated with hyperbaric oxygen therapy, after a delay of 21 days, with good results. No surgical intervention was needed. A literature search revealed 17 human case reports on frostbite and four animal studies in which hyperbaric oxygen was applied. All case reports showed positive effects, and in none of the cases was amputation necessary. In the animal studies, two showed significant positive results regarding tissue loss and reduction of inflammatory markers, whereas two did not. CONCLUSIONS: Based on our case report as well as the literature and the mechanisms of hyperbaric oxygen, we make the recommendation that this therapy be considered as an addition to the multidisciplinary treatment of frostbite, even after significant delay of treatment.
Subject(s)
Frostbite/therapy , Hyperbaric Oxygenation/methods , Mountaineering/injuries , Toes/injuries , Female , Frostbite/pathology , Frostbite/physiopathology , Humans , Nepal , Time FactorsABSTRACT
Seven consecutive cases of late cardiac tamponade after valvular surgery are reported; all were postoperatively treated with acenocoumarol and 6 had an international normalized ratio peak greater than 6.0 within 3 days preceding tamponade. It is suggested that during this excessive anticoagulation state a hemorrhagic event within the pericardial space precipitates the tamponade. In addition, it is proposed that all valve patients with a postoperative international normalized ratio peak greater than 5.0 within 6 weeks postoperatively should be considered for a transthoracic echocardiogram.
Subject(s)
Acenocoumarol/adverse effects , Anticoagulants/adverse effects , Cardiac Tamponade/diagnosis , International Normalized Ratio , Pericardial Effusion/etiology , Postoperative Complications/diagnosis , Acenocoumarol/administration & dosage , Adult , Aged , Anticoagulants/administration & dosage , Cardiac Tamponade/blood , Cardiac Tamponade/diagnostic imaging , Drainage , Female , Heart Valve Prosthesis Implantation , Humans , Male , Middle Aged , Pericardial Effusion/surgery , Postoperative Complications/blood , Postoperative Complications/diagnostic imaging , Retrospective Studies , Time Factors , UltrasonographyABSTRACT
OBJECTIVE: The mechanisms causing the presence of platelet-derived microparticles in the circulation are unknown. In vitro platelets release platelet-derived microparticles in response to complement activation. This study evaluates the relationship between complement activation and levels of circulating platelet-derived microparticles in patients undergoing cardiac surgery. METHODS: Prospectively, 71 patients were included who underwent elective coronary artery bypass grafting with cardiopulmonary bypass. The patients were randomly allocated to one of the 3 groups: uncoated oxygenator, UnModified Surface (n = 25) or oxygenator coated with either BioPassive Surface (n = 25) or BioActive Surface (n = 21). Platelet-derived microparticles and terminal complement complexes were determined before bypass and after induction of anesthesia, 15 minutes after the start of cardiopulmonary bypass, at the end of cardiopulmonary bypass, and 30 minutes after administration of protamine sulfate. RESULTS: Demographic and cardiopulmonary bypass data were similar for the 3 groups. At the end of cardiopulmonary bypass, platelet-derived microparticle numbers were decreased in all 3 groups. No significant differences were observed among the groups at any sampling point. At the end of cardiopulmonary bypass, terminal complement complex concentrations were increased in all groups (P <.001), and significant differences among the groups were present (P =.002). CONCLUSIONS: Despite significant complement activation, no increase in numbers of circulating platelet-derived microparticles was found in the systemic blood of patients undergoing cardiac surgery with cardiopulmonary bypass. Thus complement activation in vivo does not necessarily affect generation of platelet-derived microparticles.
