Superabsorbent dressings for copiously exuding wounds.

Exudate control is important in the management of both acute and chronic wounds. A new category of absorbent dressings that contain superabsorbent particles promises high absorbency. The aim of this multicentre, prospective, non-comparative observational study was to evaluate the clinical efficacy and absorbent capacity of a superabsorbent dressing. Fifteen inpatients and outpatients with highly exuding wounds were included. Most patients (n=8) (53%) had chronic wounds; 20% (n=3) had ulcerating tumours. The superabsorbent dressing was used as a primary or a secondary dressing. Assessment was on day 0 (start), day 3 and day 7 (end of study). The study looked at wound bed and periwound skin condition, exudate production, pain upon dressing removal, reason for dressing removal, and frequency of dressing changes. A clinical visual scoring tool was used, together with digital photographs, which were assessed by the same experienced clinician. All 15 patients completed the study, during which no adverse events were noted. At day 7, maceration had reduced from 46.7% (n=7) at day 0 to 6.7% (n=1). After only 3 days, dressing change frequency was reduced from once daily to twice weekly in 80% (n=12) of patients. The superabsorbent dressing seems to reduce complications associated with exudate production, stimulate wound healing and increase patient comfort; it may also save time and costs for caregivers.

[Physiopathological data of Horton's syndrome]. / Données physiopathologiques de la maladie de Horton.

GREAT PROGRESS: The understanding of the physiopathology of Horton's syndrome has been made in view of the prevalence of the disease, the access to affected tissue and new molecular biology techniques. And it is now possible to specify the intricacy between the genetic, immunological and vascular components. HORTON'S SYNDROME, A GENETIC DISEASE: The preferential association of the disease with some alleles pf the HLA DR4 group has helped to emphasize the fundamental role of a few amino acids of the second hypervariable area of the HLA-DR molecule. An immunogenetic predisposition appears favourable, or even necessary, for the development of the disease. HORTON'S SYNDROME, AN IMMUNOLOGICAL DISEASE: The temporal arteries of patients presenting with Horton's syndrome are infiltrated by polymorphous inflammatory cells, fundamentally including CD4 T-cell lymphocytes, macrophages, and a few giant cells. Some CD4 lymphocytes have undergone clonal proliferation and show signs of recent antigenic recognition. A fraction of them secrete interferon gamma, which plays a crucial role in the onset, maintenance and orientation of the immunological response. The macrophages play multiple roles notably in maintaining the inflammatory reaction, but also in the destruction of certain structures of the arterial wall. HORTON'S SYNDROME, A VASCULAR DISEASE: The destruction of the arterial wall at the acute stage of the disease appears responsible, sometimes later on, for aneurismal dilatations observed on the aorta of certain patients. Moreover, intimal hyperplasia (mediated by the PDGF (platelet derived growth factor) A and B) and thrombosis (related to the inflammation) join up in reducing the arterial flow and enhancing the risk of ischemic complications during the acute stage. PATHOGENESIS, HYPOTHESES: Various candidate-antigens have been incriminated in the onset of the inflammatory reaction during Horton's syndrome. Some epidemiological and molecular studies are in favour of an exogenous antigen, possibly infectious, but no evidence has been demonstrated in the studies published. A parietal, endogenous antigen might also be at the origin of the cascade of events described during this disease.