Classification of Pressure Ulcers-Reply

Abstract

In Reply. \p=m-\We agree with the authors that when eschar is present d\l=e'\bridementis often necessary to determine the extent of the ulceration and that palpation may assist as well.Our classification of red areas' reflects our clinical practice of intervening if hyperemia persists for greater than 30 minutes.2 It is not necessary to wait for greater than 24 hours to institute therapeutic measures. Our approach is, in fact, more conservative than the authors outline. Of course, if their method has proven successful in their institutions, it can be used as long as there is sufficient interrater reliability. Muscle is frequently observed at the base of pressure ulcers. These ulcerations may occur in both common and uncommon areas and a classification including muscle is needed to classify all possible lesions. Patients who have had musculocutaneous flaps will certainly have muscle exposed if pressure ulcerations reoccur. We find grade IV to be useful and would not eliminate it from the classification. With Lipodermatosclerosis and Venous UlcerationTo the Editor.\p=m-\Iread with interest the article by Falanga et al1 on the potential association of protein S and protein C with venous ulceration and lipodermatosclerosis. Although I applaud the effort, I wish to caution interpretation of hypercoagulable evaluations analyzing isolated defects. Clot formation and dissolution is a very dynamic and complex process, and studies attempting to show a cause-and\x=req-\ effect relationship must exclude other potential factors. The authors state "One proposed hypothesis suggests that the sustained elevation of venous pressure (venous hypertension), resulting from inadequate functioning of the "calf muscle pump," lends to dermal pericapillary deposition of fibrin, which alters the interactions between vasculature and dermis." They further state: "Thus, an increased pro-pensity for deep vein thrombosis, as could occur in the setting of protein C or protein S deficiency, and perhaps in combination with a faulty fibrinolytic system, may lead to the development of venous occlusion and venous hypertension." Protein C and protein S are vitamin K-dependent natural anticoagulants produced by the liver, and activation is dependent on the presence of thrombin and an endothelial cell surface receptor (thrombomodulin).2 Know¬ ing that there is a poor association between depressed pro¬ tein C and protein S levels in the general population and thrombotic tendencies it is much more likely that an endo¬ thelial defect exists secondary to venous hypertension resulting in decreased protein C activation. If this is the case, then one should include tissue plasminogen activator (TPA) and tissue plasminogen activator inhibitor (TPAI-1) in the study since defects in this arm of anticoagulation may produce significant thrombosis. Both TPA and TPAI-1 are produced by endothelial cells.2 Up to 70% of individuals with idiopathic venous thrombosis have been shown to have ab¬ normal TPA results, suggesting that decreased TPA activ¬ ity may be a major com...