The Next Era in GI Surgery BioDynamix TM Anastomosis The Colon Ring IMPERATIVES OF THE Healing Process Clinical Training Team
Healing in Gastrointestinal Anastomoses• Optimal gastrointestinal anastomosis is a basic ingredient of successful GI surgery.• Connecting bowel, esophagus or stomach involves a complicated wound healing process.• Careful, meticulous technique and adherence to sound surgical principles is critical, but may not prevent anastomotic leaks.• Anastomotic leakage can result in serious morbidity and mortality.
Healing in Gastrointestinal Anastomoses • Failure of wound-healing leads to: – Life-threatening complications, – Additional surgical procedures, – Increased length of hospital stay, – Increased cost, and – Long-term disability. • Despite advances in surgical technology, anastomotic disruptions and strictures still occur. • In this presentation the biological response to injury is reviewed, and we will discuss the differences in the wound healing process between Compression and Sutured/Stapled anastomoses.
Healing in Gastrointestinal Anastomoses• Optimizing the management of acute wounds has been a major goal of surgical science over the past 100 years.• Primary strategies have relied mainly on mechanical approaches to the problem and have often ignored the important role of the biological response of injured tissue.• There is a need to translate the improved understanding of wound healing to better outcomes in surgical procedures.• Our approach, although still mechanical, emphasizes the primary role of facilitating biologic healing of the anastomosis.• Successful surgical therapy depends on predictable and reliable wound healing.
Definitions : Acute Wound and Acute Wound Healing• An acute wound is defined as a traumatic loss of normal structure after a noxious insult.• Acute wound healing is a series of carefully regulated steps activated at the time of acute injury, designed to re-establish an immune barrier, and resulting in a time-dependent but predictable and orderly pattern of tissue repair.
Mechanism of Acute Wound HealingThere are three primary phases involved in the healing of an acute wound: Phase I Inflammation (Lag) Phase II Proliferation (Fibroblastic) Phase III Remodeling
Mechanism of Acute Wound Healing• I -- Inflammation (Lag): – Platelets first create hemostasis at the site of the injury by the formation of insoluble fibrin-based clot, and vessels constrict to minimize further bleeding. – Subsequent dilatation of vessels leads to increased permeability of vessels adjacent to the injury which facilitates the efflux of inflammatory cells into the wound. – Neutrophils are initially the dominant cell type, and their role is to rid the wound of invasive microbes and debris. – Within 2-3 days, Monocytes and tissue Macrophages predominate. – Macrophages synthesize and release a multitude of tissue growth factors which are critical to the normal progression of tissue repair.
Inflammation or “Lag” Phase: • First, platelets create hemostasis at the site of injury by formation of an insoluble fibrin-based clot & vessels constrict to minimize further bleeding. • Vessels then dilate, allowing neutrophils to invade the wound to rid it of pathogens and debris. • Within 2-3 days, tissue macrophages predominate, synthesizing and releasing a multitude of tissue and growth factors critical to normal tissue repair.
Mechanism of Acute Wound Healing • I -- Inflammation (Lag) phase prolonged: – Inadequate hemostasis because of platelet dysfunction or poor technique can result in hematoma formation with ensuing disruption of the provisional wound and delay in moving to the next phase. – Delayed or deficient inflammatory responses can result in wound contamination or infection with subsequent delay of progression into the fibroproliferative phase of acute tissue repair. – A prolonged inflammatory response resulting from the presence of foreign material or wound infection delays the progression of acute wound healing into the proliferative phase and can result in breaking down the strength of the wound.
Mechanism of Acute Wound HealingWound healing in the GI tract requires a fine balance during theinflammatory phase between collagen synthesis and collagenolysis. - 70 % of initial strength (colonic anastomosis) 2 5
Mechanism of Acute Wound Healing• II -- Proliferation (Fibroblastic): – Proliferative phase begins with the arrival of fibroblasts at the wound site. – Fibroblasts are the major cell type by day 4, are regulated by various growth factors, and replace the provisional matrix with collagen-rich granulation tissue. – Angiogenesis occurs at this time to allow good oxygenation and to supply essential nutrient building blocks to the healing wound.
Mechanism of Acute Wound Healing• II -- Proliferation (Fibroblastic): – Collagen: • Collagen synthesis is a dynamic process that depends on the balance between collagen lysis and synthesis. • Normal soft tissue contains 80% type I (thick)collagen and 20% type III (thin) collagen. • Collagen is secreted from fibroblasts as type III (thin) collagen. • Acute wound granulation tissue contains approximately 30%-40% type III (thin)collagen.
Mechanism of Acute Wound Healing• II -- Proliferation (Fibroblastic) phase prolonged: – Local infection increases collagenase activity, prolonging the proliferative phase and delaying progression into the next phase of wound healing. – Delayed fibroblast responses impede the establishment of a strong wound matrix and the laying down of an early scar, prolonging the period that a wound is subjected to increasing mechanical loads and remains dependent predominantly on mechanical means of support (ColonRingTM, staples, or suture material) for strength.
Mechanism of Acute Wound Healing • III -- Remodeling: – Granulation tissue undergoes remodeling, and the density of macrophages and fibroblasts is reduced. – Thin collagen fibers transform into thick bundles. – Wound contraction occurs as fibroblasts pack thick collagen bundles into contractile units.
Summary of Wound Healing Physiology • Healing starts with inflammation, an initial hemostatic response with vasoconstriction, and is followed by increased vessel permeability. • This facilitates the efflux of inflammatory cells (neutrophils) into the wound with lysis of old collagen. • Shortly, macrophages can be seen in the anastomotic site, where they synthesize and release tissue growth factors. • Granulation tissue in the anastomosis marks the beginning of the proliferation phase, and new collagen is synthesized. • In the remodeling phase the density of macrophages and fibroblasts decreases, and newly formed collagen transforms into thick bundles and contractile units.
Physiology of Anastomotic Healing• Anastomotic strength is derived from collagen fibrils in the submucosal layer.• Anastomotic strength is low during the first postoperative days as collagen is degraded by collagenase activity at the site of the injury.• Early anastomotic strength depends on suture- or staple-holding capacity of existing collagen until a large amount of new collagen can be synthesized by both fibroblasts and smooth muscle cells.• Anastomosis is weakest post operatively for 3 or 4 days until this occurs.
Mechanism of Acute Wound Failure• Biologic Response – Successful acute wound healing depends on timely, effective and regulated hemostasis, inflammation, proliferation and remodeling. – Acute wounds are totally dependent on staples/sutures until breaking strengths are achieved that are capable of off- setting the increased loads placed on the acute wound. – Acute wound healing failure occurs when the load placed across the wound exceeds the resistive capacity of the suture/staple line and the provisional matrix. Usually this situation occurs when there is abnormal progression through the integrated phases of acute tissue repair.
Mechanism of Acute Wound Failure • Wound healing failure occurs when there is abnormality in either the degree or the duration of one of the components of tissue repair. • Local and systemic factors may cause failure of GI healing.
Compression vs. Stapled/Sutured Anastomoses? • A compression device mechanically compresses the blood vessels, creating an immediate and almost complete hemostasis; while in the case of a sutured anastomosis, platelets create hemostasis by the formation of a fibrin-based clot, thus lengthening the time to achieve hemostasis. • Compression anastomosis (CA), which is a sutureless anastomosis, differs from sutured anastomoses (both manual and stapled) in the absence of a great number of through-the-wall punctures in the anastomosed organs. • Circular stapled anastomoses usually have 26 staples, each with 2 limbs, which pierce complete layers of both proximal and distal bowel (usually twice), creating approximately 200 additional wounds. • CA device requires no foreign bodies (sutures, staples) to remain in the healing zone after the clamping element is expelled. • The result is full recovery of the natural multi-layer tissue structure and normal lumen size.
Constancy of the Anastomosis • Staplers treat various thicknesses identically – the gap always remains the same without any adjustment. • The ColonRingTM adjusts to all kinds of tissues, providing the same compression regardless of the thickness of the tissue or stage of ischemia/necrosis. • Furthermore, we have found the ColonRingTM measurements much more stable and constant overall than those of the staplers.
Definitions: Measurements• Methods to quantify anastomotic strength : – Bursting strength/pressure: maximum intracolonic pressure when inflating an anastomosed segment which leads to disruption. – Hydroxiproline contents: can be measured by a blood test.
Comparison Study: ColonRing™ vs. Stapling • Burst pressure is higher in compression anastomoses than in stapled anastomoses at zero-time and even at 3 months. mmHg Burst Pressure 225 210 215 192 200 175 168 167 150 151 125 112 105 100 96 75 50 25 32 0 Time "0" 2-3 Days 7-10 Days 1 Month 3 Months POD Stapler CAR
Anastomotic Index 3 Months ColonRingTM 3 Months Staples No narrowing Narrowing
Anastomotic Strength By the time that ring detaches, the tissue strength is sufficient to adequately maintain the anastomosis. Histologically- The use of compression promotes tissue healing in different ways: – Early epithelialization of the mucosa, – Collagen formation in the submucosa, and – Full adaptation of the layers of the anastomosed tissue.