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Combined 11 clinical training--healing process
1. The Next Era in GI Surgery
BioDynamix TM
Anastomosis
The Colon Ring
IMPERATIVES
OF THE
Healing Process
Clinical Training Team
2. 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.
3. 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.
4. 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.
5. 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.
6. Mechanism of Acute Wound Healing
There are three primary phases involved in the healing of an acute
wound:
Phase I Inflammation (Lag)
Phase II Proliferation (Fibroblastic)
Phase III Remodeling
7. 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.
8. 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.
9. 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.
10. Mechanism of Acute Wound Healing
Wound healing in the GI tract requires a fine balance during the
inflammatory phase between collagen synthesis and collagenolysis.
- 70 % of initial strength (colonic anastomosis)
2 5
11. 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.
12. 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.
13. 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.
14. 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.
15. 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.
16. 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.
17. 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.
18. 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.
19. 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.
20. 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.
21. 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.
23. 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
24. Anastomotic Index
3 Months ColonRingTM
3 Months Staples
No narrowing
Narrowing
25. 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.
30. Anastomoses at Two Weeks – Staples
Images of staple formation demonstrates the “bad” scarring due to tissue
healing with embedded foreign material.