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A Journal on Heart and Vascular Diseases
Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752
Minerva Cardioangiologica 2002 June;50(3):239-44
Evaluation of cutaneous necrosis risk in peripheral arterial diseases
D'Eri A., Martini R., Cordova R. M., Trevisan G., Andreozzi G. M.
Background. In the last years the surgical and pharmacological treatment of critical limb ischaemia has been significantly modified, increasing the reduction of amputation and/or the increase of limbs recovery. However, neither survival nor incidence of amputations changed. This , probably has been related to an inadequate therapy after revascularization procedures or to an increase of complications. The assessment of cutaneous necrosis risk and of the recovery possibility of the ischemic limb can positively influence the therapeutic strategy, in these patients. The aim of this paper is to identify the reference parameters that can represent objectively the limit for cutaneous ischemic suffering, improving the physiological knowledges of critical limb ischemia.
Methods. In the first phase of our study 56 patients, in different stages of peripheral arterial disease have been, submitted to microcirculatory assessment measuring the pattern of TcPO2 and TcPCO2 in correlation with walking performance expressed as ACD at treadmill test (2.5 Km/h gradient 12.5%). The second phase assesses the clinical outcome after three months of 12 among 19 patients with critical limb ischemia, measuring the changes of TcPO2 and TcPCO2 with postural test and after infusion with prostanoids of two weeks.
Results. A reduction of the TcPO2 and an increase of the acidosis from stable to invalidant claudication have been observed, with a progressive loss of direct correlation between ACD and TcPO2, and an increase of the inverse correlation of the ACD with TcPCO2. In the CLI we found a very low TcPO2 levels with a TcPCO2 levels ( about 120 mmHg) with no correlation of ACD with TcPO2 and TcPCO2. The good clinical outcome was related to an increase of the TcPO2 and to a reduction of the TcPCO2 after postural stimulation and after therapy. In the patients with a bad response to the postural test, a possibility of recovery was observed only in those with a positive answer to therapeutic treatment.
Conclusions. The invalidant claudication phase can be considered a point of physiopathological change from relative to absolute ischemia that is clinically equivalent to early sign of ischemia. The identification of recoverable patients seems to be related to postural test and pharmacological treatment with an increased values. Viceversa, it is still difficult to identify as non-responders, those patients with a bad postural test , or with a little improvement after pharmacological treatment, as those with an indication to primary amputation. More observations, evaluation data will contribute to a better definition of a negative trend.