Pericardial anti-adhesion patch

Details Pericardial anti-adhesion patch Pericardial anti-adhesion patch

2001-08-17

2003-07-29

Kishore, Gollamudi S. (Department: 1615)

Drug, bio-affecting and body treating compositions

Preparations characterized by special physical form

Web, sheet or filament bases; compositions of bandages; or...

C424S443000, C424S444000, C424S422000, C424S423000, C424S426000

Reexamination Certificate

active

06599526

ABSTRACT:

FIELD OF THE INVENTION
The present invention generally relates to tissue equivalent technology. Particularly, the present invention relates to a pericardial anti-adhesion patch (PAP), a preformed loose collagenous acellular tissue, which comprises a collagen and at least one non-living cellular component that is reorganized prior to implantation into a patient. The patch prevents tissue adhesions between organs and other tissues being operated upon during surgical procedures and has to be maintained in place during the post-operative period when the mechanisms of adhesion formation are the most active (initial 2-3 weeks). Thereafter PAP diverts the wound healing process into the remodeling phase during which the anti-adhesion patch will be dissolved to component amino acids, predominantly prolyne and lysine.
DESCRIPTION OF THE PRIOR ART
Opening and entering of the body cavities is an intrusive event that exposes the surfaces of internal organs to a variety of traumatic conditions. The severity of trauma or injuries may range from desiccation and undue handling of the tissues, inadequate hemostasis, prolonged contact with foreign materials, misalignment of tissue planes in anastomosis, and failure to remove all abnormal tissues. During cardiothoracic surgery access to the coronary vasculature and the heart requires incision in the pericardial sack (i.e., pericardium) which envelops and isolates the heart from the chest walls and surrounding internal organs (e.g. lungs). Following such procedures, adhesions routinely form between the epicardium and the pericardium, sternum, pleura and other adjacent structures. Retrosternal adhesions cause injury to right ventricle, aorta, right atrium, innominate vein, and aortocoronary by-pass graft. In general, adhesion formation after cardiac surgery is associated with high morbidity and cannot usually be avoided. Once the surgery is complete, the chest cavity is closed but the incision (slit) in the pericardium may be loosely closed or left open. In either case due to post-surgical edema this incision usually becomes an oval opening. During the healing process the flaps of the pericardium adhere (“scar down”) to the chest wall, the lungs and the heart itself. These adhesions occur in 100% of the cases and are a serious risk factor when there is a need for repeated surgeries. As repeated surgeries are now on the increase, there is a serious need for a method to prevent formation of pericardial adhesions in order to improve the success of the procedure. There are no devices approved by the FDA to prevent pericardial adhesions. Adhesions may also be ophthalmic, orthopedic, central nervous system, and intrauterine. It is therefore desirable to prevent post-operative adhesions not only in the thoracic cavity but also in all anatomical locations.
The surgical trauma involves tissue damage ranging from the incision itself to the loss of the measothelial cells that line the body cavity. Measothelial cells secrete fibrinolysin, an enzyme that dissolves fibrin. Inadequate hemostasis causes accumulation of blood and blood clots, and leads to formation and deposition of fibrin, which accumulates at the sites of injuries in the absence of measothelial cells. Fibrin is a very adhesive protein and glues injured surfaces together. Ischemia caused by surgery, although transient, allows the fibrin matrix to persist and gradually becomes populated by macrophages, fibroblasts, and giant cells. The initial adhesion matures as fibrin becomes fibrinous band with calcification nodules, and is often covered by measothelium which is formed after 4-5 days (complete in 10 days post-operatively). The adhesions can vascularize and even innervate, and in the last stages of maturation the adhesion becomes collagenized. This process involves activation of the principal connective tissue cells, which are involved in tissue repair, the fibroblasts, as well as the circulating immune system cells (macrophages). These cells begin to divide and migrate into the injured area as a part of a general inflammatory response. The fibroblasts secrete collagen (collagenization) and finally contract the collagen (fibrin) mass into a dense tissue. This contraction process further intensifies scar formation, forming stronger “adhesions” that “join” or “weld” the adjacent tissue surfaces, which were previously well separated. In time the adhesions become increasingly fibrous and may even calcify. Calcification is a highly undesirable aspect of adhesion formation. Some individuals (particularly of African American and Hispanic ethnicity) are genetically predisposed to severe scarring and therefore adhesion formation. These individuals are also at high-risk for cardiac problems which require surgical intervention. It is critical that the high-risk groups be protected from adhesion formation.
Prevention of adhesions has been a problem for a number of years and the most consistently applied strategy to prevent their formation has been to separate, physically, with “a barrier”, the tissue surfaces which are likely to adhere. The anti-adhesion barriers were initially quite primitive (e.g. fine surgical steel wire mesh) and mostly biocompatible but non-biodegradable. In recent years, interest in more effective and biodegradable anti-adhesion barriers has intensified. However, a totally satisfactory solution is still to be found and development of new approaches is highly desirable. Particularly desirable are the strategies which may lead to a general solution to the problem of adhesion formation and which would prevent them in any anatomical location in the body. Advances in methodologies used for harvesting and culturing a wide variety of normal human cells and incorporation of these cells into three-dimensional matrices to form primitive tissue, now offer new opportunities for advances in adhesion prevention and design of a new generation of anti-adhesion barriers.
SUMMARY OF THE INVENTION
The present invention is directed to an anti-adhesion patch (Patch) and a method for constructing the Patch disclosed herein. Specifically, PAP is engineered tissue equivalent whose mechanical and optical properties arise from organization of collagen type I gel by human fibroblasts, but which in its final form is acellular. In detail, the Patch is constructed by mixing normal human connective tissue cells, preferably fibroblast, or vascular smooth muscle cells, and a collagen such as collagen type I solution. The resulting mixture is incubated to stimulate the cells to adapt to and organize the collagen gel matrix into a mono-cellular tissue equivalent (MCTE) having desirable dimensions and mechanical properties.
The present invention is further directed to a method of preventing tissue adhesions between organs and other tissues being operated upon during surgical procedures by utilizing the anti-adhesion patch disclosed herein.
Other and further aspects, features, and advantages of the present invention will be apparent from the following description of the presently preferred embodiments of the invention given for the purpose of disclosure.


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Peritoneal Surgery, Chapter 35, “Adhesion Prevention: Past the Future” by David M. Wiseman, pp. 401-417A, (1999).
Archives of Othopaedic and Traumatic Surgery1987, “Decreased Adhesion Formation in Flexor Tendons by Topical Application of Enriched Collagen Solution—A Histological Study”, Nyska et al., pp. 192-194.
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Journal of Biomedical Materials Research, vol. 24, 291-297 (1997), “In vivo evaluation of a collagenous memb

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