Visceral Surgery & Osteopathy

Ricerca e scienza

di Maximilien Girardin

Bridging the Medical and the Osteopathic world

by Frédéric Dumunier D.O.(Fr),

consultant Maximilien Girardin D.O.m.R.O., Evost Fellow, Prosector Anatomist.

The most common complications after abdominal or pelvic surgeries are the peritoneal adhesions in at least 90% of the cases. It was demonstrated that the healing mechanisms of the peritoneum differs from that of the skin. Even if this tissue looks like an epithelium, it reacts and heals as a connective tissue which means it is very adaptive. Adhesions develop through fibrin bridges which reinforce themselves steadily as the process goes on and could look like ‘new formed-ligaments’. This problem has already been well studied and can be assessed via the visceral sliding range measured by ultrasound. The assumption is that more the organ or viscera’s move, the less adhesions are present. Visceral Osteopathy claims to improve the visceral sliding or so-called organ mobility. This paper, through an anatomic and evolutionary physiological review, tends to enlighten the place of Osteopathy in the pre- and post-surgery care at the hospital, with the aim to decrease the post-surgical adhesions.

Key words: Visceral Osteopathy/Post-surgical adhesions/Peritoneal repair

Table of contents

  1. Introduction
  2. Environment
  3. Osteopathy in the Visceral field
  4. Anatomy & Physio-pathology
  5. Adhesions genesis
  6. Abdominal-pelvic surgery
  7. Observation
  8. Recommendation
  9. Conclusion

In collaboration with:

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1. Introduction

Since many years now, we have the chance to work at the Hospital Albert Schweitzer (HAS), located at Deschapelles, in Haiti. We have access to every department of the hospital where we are working in collaboration with the medical staff.

HAS disposes of 131 beds occupied at about a 150% rate. Hence not all treatments were on professional beds or tables (especially at the Dispensaries all over the Island – country; but that only demonstrates the flexibility possibilities of Osteopathic treatment. (Note some of these circumstances are very probably extremely similar to A.T. Still’s early working conditions, and demonstrate the power of them, A.T. Still became popular and known for his treatments of real pathology and not because of leisurely physiotherapy)

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The surgical department does almost 9 000 consultations and admits more that 2 000 patients per year. In the light of the positive results acquired during the previous years, the Medical Director of the hospital wanted to learn more about Osteopathy in the visceral field.

Thus, we looked at the possible role for the prevention and treatment of post operative adhesions in abdominal-pelvic surgeries.

We started by a quick presentation of Osteopathy and its possible work on the visceral component, then a deep review on the Anatomy and Physio-pathology of the abdomen and the chronology of the post operative adhesions genesis. We complete our review by a brief description of surgical interventions and then our clinical observation followed by our recommendations to define the place of the Osteopath in this process.

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The purpose of this paper is to think about a way, to adapt efficiently Osteopathic care to the pre- and post- surgery patients, in order to prevent post surgical adhesions. This reasoning is based upon anatomy, evolutionary physiology and physio-pathology and our previous experience.

2. Environment

Our reflections are mainly based upon the Anatomy, Histology and Evolutionary Physiology courses, as taught by Maximilien Girardin D.O., Evost Fellow and Prosector Anatomist in Morphologicum; and our personal experiences combined.

(WWW.MORPHOLOGICUM.ORG)

The principle of FORM in all dimensions is a central element: the structure and the function (behavior) are interdependent and must thus be seen as one inseparable whole in constant process or change. The enforcement of this principle guaranties to stay as close as possible to our palpation reality and to keep as close as possible to the purity of A.T. Still’s osteopathic philosophy.

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Under these conditions, the study of the structure allows us to deduce its function or its behavior and thus to chose wisely the therapeutic approach that we should use.

We collected data from HAS patients including, the ones operated a few days to several months or even years ago.

In order to have the most objective way of measurement, we chose as frame of reference the mobility of the abdominal organs and viscera during the breathing phases.

They are well-known by Medicine and were studied in a decades long osteopathic research-study[1]. The adhesions lead to a decreased mobility of one or several organs or viscera observable by ultrasound[2],[3].

Starting from these conclusions, we use as hypothesis that the conservation of this mobility is an indicator of small number of adhesions.

3. Osteopathy in the Visceral Field

3.1. Generality

           Osteopathy is a philosophy based on a deep knowledge of human FORM meaning anatomy and physiology in all their dimensions. It allows, with observation, the research of the causes that often result in alterations of health.

It uses for treatment a “ten fingers medicine” (manual therapy) approach, working on the entire body. Osteopathy applies the same principle of wholeness and mobility to all systems composing the human body; thus including the visceral system.

The goal is always to normalize tissue tensions as well as their mobility, encourage fluids circulation and guaranty optimal innervation among others in order to maintain optimal homeostasis.

Our approach includes a general assessment by observation, auscultation, palpation and percussion as learned on the course Visceral Form and Palpatory differentiation,without spending too much time to talk about techniques[4],[5].

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In the working field of the osteopath, anatomy, manual diagnostic and their interpretation, plays a central or crucial role for treatment. Hereby we can pose the following questions:

  • to what extent are the classic anatomical references in our mind concordant with the real anatomical situation of the patient?
  • As to what extent the manual intervention angle and tension are tuned into the real situation of the patient’s visceral system and tissues?

In the course “Visceral Form”, we had learned to readapt our anatomical image to the reality of the patients anatomy, verified by ultrasound. That was extremely useful and confidence building for our research and daily osteopathic practice.

We leave to the therapist the choice of the technique to use. However, we prefer the gentle and superficial approach from G. Finet & Ch. Williame during the first days in post-surgery.

  Finet & Williame made use of ultrasound[6] and X-rays to study the visceral movements induced by the diaphragm during breathing. They conclude that an “organized and repetitive dynamic exists in the visceral system”[7]. They established global and specific tests to each organ. The assessment is quantitative as well as qualitative. Indeed, according to them, an organ may lose its mobility, possibly entirely or have it modified in comparison to the natural-physiological one. In both cases this state may cause functional problems.

           The goals in each of our treatments is to decrease local tensions and foster the circulation, while preserving the tissues from mechanical stress. We will come back extensively to this notion that seems the essence of the post surgical work for us osteopaths.

3.2. Nomenclature and techniques

The nomenclature is very different compared to the classic musculoskeletal system, we talk about sliding planes instead of joints, the attachment system is still composed by ligaments but we will also mention other connexions like: ‘omenta and meso’s’. We take into account ‘new modalities’ such as fluid circulation, pressures or yet the viscoelasticity of the tissue[8].

We decided to not keep the usual classic visceral manipulation nomenclature (Tissue, Mobility and Motility) but to prefer oursWe excluded motility and kept the mobility as assessment tool but not as treatment. The definition for tissue manipulation is modified compare to the one traditionally used in visceral courses.

This is the nomenclature we will use:

–      Tissueviscoelastic quality of the tissue. Describes the direct loco-regional work on the area or structure. The goal is to bring the quality of the treated tissues (tension/pressure) as close as possible to their natural.

–      Circulatory: veino-lymphatic drainage and arterial supply. At the same time local and remotely, to first guaranty the drainage of the treated area before investigation of the arterial supply. (hierarchy – chronology)

–      Neuro-vegetative: innervation of the organ or viscera (Autonomous Nervous system). Landmarking and work on the spine level and/or on the cranial and peripheral nerves. (The eye opening ‘Golden triangle’ from the Evolutionary Physiology course, see also mention in https://www.linkedin.com/pulse/annus-horribilis-max-girardin/ and www.linkedin.com/pulse/nutritional-nonsense-scourge-trendy-mediatised-times-max-girardin/ and www.linkedin.com/pulse/help-something-deeply-wrong-anatomy-max-girardin/).

This change reflects, a will to stay as close and coherent as possible, to our practical reality and in accordance with the operating anatomy and physiology of the patients Form. This new approach allows, also to avoid to use an erratic ‘osteopathico-osteopathic-osteopathicism’ nomenclature which is badly, to even not at all understood by our colleagues and by the medical corps at the hospital. (Note: because of the completely different frames of reference standards, in use)

Note that our nomenclature describes the level on which we want to work and not a type of manipulation. In fact, the choice of using a structural, functional, fluidic, muscular or any other kind of technique is to the osteopath’s responsibility and especially their ‘good old common sense’.

4. Anatomy & Physio-pathology

4.1. Anatomy

The abdominal-pelvic zone and especially the peritoneal cavity is of interest for us because it is within it that adherences are formed.

The abdominal cavity is limited:

–      At the top with the diaphragm and its costo-sternal and lumbar insertions,

–      Forward with the musculus rectus abdominis and the fasciae of the abdominal muscles,

–      On the sides with the abdominal muscles (external/internal obliques and transversus abdominis) and the transversalis fasciae,

–      Backward with the lumbar spine, pelvis, iliopsoas, iliac and quadratus lumborum muscles as well as the thoraco-lumbar and iliaca fasciae,

–      At the bottom with the pelvic floor and pelvic diaphragm.

4.2. General anatomy of the peritoneum

The peritoneum is a continuous, thin and a translucent unicellular layer lining on the abdominal-pelvic cavity and the organs. The histological name is ‘simple squamous epithelium’ or mesothelium[9]. To give an idea of the size, the total surface of the peritoneum is about the skins[10]. It shapes a space called peritoneal cavity (or peritoneal bag in current language)

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This image is the doubled layer peritoneum as seen, on fresh deer dissection, before the complete field dressing, of an Omentum Majus. (Two layers of peritoneum or mesothelium and in between them an extremely fine layer of two Laminae Basales and a whiff of connective tissue, around the blood vessels there is some fat storing Adipocytes. Not really a sturdy mechanical tissue function!) Courtesy of Jane Stark D.O.M.P., MS, D.Sc.O., Evost Fellow.

In accordance with anatomists, the peritoneum can be described as two (visceral / parietal) or three (primitive parietal (blue) meso-gastrum (red), intestinal (yellow)) sheets, like on the Picture 1, sometimes more.

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Peritoneum, here in color, male subject in sagittal cross view. C. Toldt translated from German by M. Lucien, Atlas d’anatomie humaine TOME IV (1912) p456. Toldt

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This structuring could be confusing sometimes, we remind that from a morphological-anatomical-histological point of view, there is only one peritoneum without discontinuity lining on organs, viscera’s and abdominal-pelvic muscles[11],[12] but composed by numerous folds.

We decided to use the terms visceral and parietal peritoneum. This choice is based on their embryologic developments that differ around day 19 [13]. Here some important characteristics[14],[15]:

Visceral sheet:

Lines on and around organs and viscera’s,

Vascularized by celiac, mesenteries and visceral pelvic plexus (same as the digestive system),

Venous drainage provided mainly via the portal system, (hepato-caval bypasses)

Innervation assured by the splanchnic, celiac and mesenteric plexus.

Parietal sheet:

Lines most of the abdominal cavity,

Vascularized by abdominal and pelvic branches,

Venous drainage provided mainly via the caval system,

Innervation assured by the phrenic, thoraco-abdominal, subcostal and lumbar nerves

The lymphatic drainage is the same, mainly provided by the thoracic duct in the end[16].

4.3. Micro-anatomy of the peritoneum

At a micro-anatomic scale, the both visceral and parietal sheet are similar, composed by a mesothelium lining on a basal membrane. They are supported by connective tissue of variable thickness deriving from the mesoderm[17], which lines on muscle-fascia tissue[18]. The mesothelial cells are also issued from the mesoderm. They have apical microvilli[19] oriented to the peritoneal cavity, characterized by their fragility and high turnover[20]. To summarize the peritoneum is a thin translucent layer of mesothelial cells supported by a loose connective tissue[21]. (Not really a solid mechanical tissue)

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Courtesy of Manumanu, www.intellego.fr/doc/19985. Red arrow translucent double layered mesothelium, of the peritoneal meso

4.4. Peritoneal cavity

The female peritoneal cavity has an opening through the Ostium (uterine tube)[22], although it is totally closed in males[23]. The other difference is that the ovaries are really intra-peritoneal (only organ in this case) and surrounded by a thin layer of mesothelial cells looking like peritoneum[24] but slightly different (cuboidal epithelia cells[25]). Note that the bottom part of the peritoneum, covering the reproductive organs of the female, is called broad ligament[26]. This part is always the most affected during pelvic surgeries[27].

In the peritoneal cavity persists a little quantity of liquid (5 to 20mL) which essentially sustains the organ and viscera sliding[28]. It is principally secreted by mesothelial cells from the plasma filtration (transudate) and the exudate production from the ovaries[29] as well as other secondary sources (macrophage secretion, tubes fluids…)[30]. Thus, we understand why the quantity of peritoneal liquid vary during the menstrual cycle to reach its maximum just after the ovulation (20mL). Then, it progressively decreases during the luteal phase (5mL)[31].

This peritoneal fluid is constantly secreted and reabsorbed by the peritoneum and renewal occurs every 1 to 2 hours[32]. This continuous exchange with the blood is primordial to ensure the behavior and guarantees the frictionless mobility of the organs, exchange of nutriments, removing waste products or pathogens and allows reparative events(19).

It contains nutriments, monocytes and macrophages (represents 50-90% of the leukocytes[33]), mesothelial cells, cytokines, chemokynes, lymphocytes, eosinophils, mastocytes, histamins, growth factors and even a little quantity of granulocytes[34]. This non-exhaustive list shows that it plays a crucial role in the immune response. We can add collagen fibers, fibrins, fibronectins and glycoproteins to this list[35]. The peritoneal liquid should be seen as a crossroad or linking-field between the digestive, immune and reproductive systems[36].

4.5. Clarification on organ position

Classically, organs and viscera’s are said, either intra-peritoneal, implied inside the peritoneum (liver, stomach, small intestine…), or either extra-peritoneal, implied outside of the peritoneum (pancreas, kidneys, uterus…). But this classification let us insidiously think that for example the small intestine is located inside the peritoneal cavity, such mental images are false like we saw previously.

The small intestine, like all the abdominal-pelvic organs and viscera’s except the ovaries are retro-peritoneal but covered by it. The peritoneum does not cover the entire structure. Thus, it stays outside the peritoneal cavity which is a continuous and closed space (except the Ostium in female).

We prefer to use the living images: superficial- (liver, stomach, intestine and colon) and deep- (spleen, gallbladder, duodenum, pancreas, kidneys, rectum, uterus, bladder and prostate) -organs depending on their locations and their behavior (the superficial ones are easier to palpate and usually more mobile).

4.6. Intra-abdominal suspensory system

The suspensory system of the abdominal-pelvic organs and viscera’s could be divided in two categories:

(Notewhereby this classical used terminology carries inherently a deceitful image, ‘suspensory’ carries unconsciously the image of ‘hanging on – suspended’ while reality is that the Meso’s and ligaments demonstrate a more steering or directing behavior than real suspension!)

–      Ligament: composed by the tissues rich in collagen fibers (fasciae or ligaments) having functions such as mechanical resistance ( that is the mechanism how they came to be), for example the connexion between the liver and the diaphragm provided by the triangular ligaments of the liver or the fasciae such as Treitz and Toldt for the pancreas-duodenum or colon respectively.

–      Non-Ligament: composed by tissues practically deprived of mechanical stress resistance (mesos or omenta), such as the Omentum Majus, inter-organ connexions or organ-peritoneum connections containing the big vessels, lymphatics channels and their innervations.

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Red arrow the doubled peritoneum, yellow the mesentery part with vessels and Fat storing Adipocytes (Rat fresh dissection)

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Red arrow translucent doubled layer of mesothelial peritoneum. Yellow arrow Blood vessels, Nerves and Lymphatics, and some fat storing adipocytes.

We chose this classification, in order to choose and use tissue techniques wisely on tissues that are able to bear mechanical stress (ligament) and avoid to injure the other ones (non-ligament).

We said in the introduction that the principle of FORM implies structure and function constant interdependency. On the following photography, we all understand by seeing the peritoneal tissue structure that its function could not be to support mechanical stress. The peritoneal sheets are so thin that we can see through them . The peritoneum belongs to non-ligament tissue upon which mechanical approach is to avoid.

It is interesting to note that the connective tissue layer in between the two sheets is so thin that it appears almost invisible. This one gets thicker and is full of fat surrounding the vessels

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Courtesy of Manumanu, www.intellego.fr/doc/19985.

4.7. Mobility of the abdominal Forms

The major driving force of the visceral mobility is the diaphragm, and the secondary respiratory muscles in general play a role as well with deep breathing. It is one of the drivers of internal pressure changes within the abdomen, as are the quality of the digestive processes and circulation or smooth muscles tensions, but the diaphragm is the main motor in normal conditions[37]. We use it as a reference, particularly in case of the lack of ultrasound to objectify the visceral mobility. In this case, all increase of the amplitude and/or movement quality will be consider as moving toward a non-objective improvement. 

           Here, we describe the organ movements while the diaphragm is moving downward during the inhalation in accordance with the work of Finet & Williame. It should be noted that the sub-diaphragmatic organs have the greater mobility “les valeurs de déplacements diminuent dans les segments les plus inférieurs…”(6) (The range of motion gradually diminishes in the inferior segments). Moreover, they say that the organs should be able not only to move but to move and slide between each other.

The global movement is downward/left side bending, including these specific movements:

–      Stomach ‘collapses’ on its great curvature,

–      Duodenum ‘closes up’ on the pancreas head,

–      Small intestine ‘spreads out’ toward the outside,

–      Colon ‘closes’ up on the inside,

–      Caecum and sigmoid ‘spread out’ toward the outside.

The global movement of the organs is downward, more precisely:

–      Liver, pancreas and right kidney mainly go down,

–      Spleen and left kidney go down and side bend to the left.

Visceral mobility is well known by gastroenterologists who talk about “visceral sliding” observable by ultrasound[38]. They demonstrated that visceral sliding impairment is significantly related with abdominal-pelvic pains[39], obstructions and even bowel occlusions[40] and some cases of infertility[41],[42]. It could be an important co-factor in several digestive functional pathologies such as the irritable bowel syndrome[43]. The loss of these visceral sliding can be due to adhesion genesis within the peritoneum from an inflammatory response (like in the irritable bowel syndrome, even if we do not forget the inferior dimensions, up to the biochemistry, that play a major role in this pathology) or post surgery[44] (abdominal-pelvic).

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4.8. Epithelial healing mechanisms

           The healing mechanism is different from the superficial layer (cutaneous, the skin) to the deep (peritoneum). To understand this difference, we should present the involved tissues.

At the superficial layer, the skin is composed by several stratified epithelial cell layers forming a frontier tissue with the outside. This tissue adheres to the connective tissue via its lamina basalis. The epithelium is avascular, its cells depend on the exchanges with the underlying Lamina Basalis and Connective Tissue. Connective Tissue, which is vascularized, and thus serves as exchange field for as well the necessary supplies for the Epithelial’s metabolism as to drain its waste products. 

In case of epithelial tissue damage, the healing process takes place from the edges of the wound towards the center by a so-called ‘complex sliding process’ from granulation tissue[45]. This mean that wider is the wound, the longer the healing process time will be. One of the reasons, why a suture is made after a surgery: is to bring the wound edges closer as to decrease the distance for the granulation tissue.

4.9. Peritoneal healing mechanisms

We previously mention the peritoneum; this unicellular layer looks like an epithelium but it is not! The way classic Histology defines and classifies tissues may seem a bit confusing. (Note see: One of the big problems from the way classic Histology defines and classifies tissues. From an embryological point of view it comes from the mesoderm. Therefore, it is a specialized connective tissue (crucial point here for the understanding of the healing process, like we will see later). Its main behavior is maintaining homeostasis in the peritoneal cavity, as a result.

It acts like a kind of thin, translucent biochemical and cellular filter (not a musculoskeletal ligament!) from which the peritoneal liquid guarantees a harmonious organ sliding as well as playing a role in the local immune response[46].

In case of peritoneal damage (inflammation or surgery), the healing process uses a mechanism used to be called regeneration[47]. After the tissue injury, coagulation occurs by fibrin deposit. This normal step, during the healing process, is normally followed by fibrin destruction (fibrinolysis).

This balance between the fibrin deposition and degradation is the most important modality that conducts to either normal peritoneal healing or adhesion genesis.

Before going into much details about pathologic healing, here the different steps for a normal physiological peritoneal recovery after injury.

Small islets composed by primitive mesenchymal cells (undifferentiated mesenchymal cells), coming directly from the underlying connective tissue, quickly constitutes a continuous membrane covering the entire wounded area(24). The healing time becomes totally independent from the wound surface but rather depend on the patient ‘general health’ condition[48]. Some authors report that normal healing times go from 5 to 10 days[49],[50].

The different parts of the peritoneum do not heal at the same rate. It looks like the part having a though connective support (liver’s capsule for instance) heals faster that the ones having a weaker or less dense connective support (caecum or visceral peritoneum)[51]. This observation exists but is still subject to more confirmation.

This is a summary of the A. T. Raftery work about the successive steps toward the normal healing process of the peritoneal tissue[28].. We decided to present separately what happening in the superficial (facing the peritoneal cavity) and deep (contacting the underlying connective tissue) layers for a better understanding. As a reminder, the peritoneal layer is composed by mesothelial cells supported by a lamina basalis and an elusive thin (translucent) connective tissue layer, only visible with the naked eye around the blood vessels, thanks to the presence of adipocytes. (Adipocytes are resident cells of connective tissue)

Note that the length of the different steps may vary, it is indicated here only to have an idea of the chronology in approximate day’s (D):

D0 – D2:

Superficial layer: appearance and proliferation of macrophages shaping a unicellular sheet supported by a layer of fibrins,

Deep layer: visible appearance of primitive mesenchymal cells.

D3:

Superficial layer: macrophage still in majority and appearance of primitive mesenchymal cells,

Deep layer: cover by primitive mesenchymal cells and some fibroblasts.

D4:

Superficial layer: macrophage population declining, fibroblasts and primitive mesenchymal cells become superficial, beginning of differentiation into mesothelial cells,

Deep layer: lamina basalis not visible yet, in construction on molecular level.

D5 – D6:

Superficial layer: number of macrophages heavily decreased, mesothelial cells cover almost entirely the superficial layer,

Deep layer: presence of fibroblast and lamina basalis formation.

D7 – D9:

Superficial layer: continuous mesothelial cells layer,

Deep layer: discontinuous lamina basalis.

D10:

Superficial layer: mature mesothelial membrane (peritoneum),

Deep layer: continuous lamina basalis with fibroblasts angled parallel to the surface and linked by collagen fibers.

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We decided to put in the spotlights 5 important points of the healing process that we roughly classify into 3 phases following the traumatic injury of the peritoneum (in this case surgery) and leading to a mature peritoneum.

This classification is not the complete chronology of the healing process, in reality it is much more complex, but a simplification allows us to have a better understanding on what environment we are working on.

Let’s emphasis that Chart 1 is a simplification of a process running in perfect conditions.

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5. Adhesions genesis

According to the previous chronology, the peritoneal tissue heals quickly and recovers almost all of its initial characteristics. But several steps may potentially go wrong. The connective tissue is very adaptive to its environment, depending on the constraints, it is able to differentiate itself in different kinds of tissues. This property can create a situation considered as pathologic, like in the case of adhesions where the mesothelial tissue is replaced by fascia in response to the mechanical stress.

As we already mentioned, the most sensitive step is the fibrin destruction (between Phase 1 and 2 in Figure 1). We notice that the quantity of fibrins increases during the first two days and then quickly diminishes normally[52], as seen on Chart 1.

In fact, the inflammatory response, following the surgical acts, increases the vascular permeability, then fibrins slowly colonize the entire wounded area. This step is important because it will stabilize the area. The fibrins build bridges between the injured parts of the peritoneal layer. The future adhesions grow only if at least two wounded surfaces are in contact. The fibrin bridges, then, form an anchor point which generates a mechanical stress upon the surrounding connective tissue. The connective tissue reacts to the local stress by favoring the fibroblast proliferation within the fibrin bridges[53].

The fibrinolysis is done by plasmins coming from the blood. The healthy mesothelial cells play, secretes stimulating factors for plasminogen[54] (inactive form of plasmin).

If this crucial step is not well realized, fibrin matrix will become like a scaffold for fibroblasts. Adding the mechanical stress, mesenchymal cells tend to differentiate rather into fibroblasts than mesothelial cells to response to the mechanical load, or even into myofibroblasts if the stress load increases or lingers[55]. Mesothelial cells (via mesothelial-to-mesenchymal transition[56]) or other differentiated cells (via metaplasia[57]) tend to become fibroblasts and later myofibroblasts[58]. Myofibroblasts genesis is really bad news for the normal peritoneal healing process.

The mechanical stress induces fibroblasts differentiate into proto-myofibroblasts and in case of severe levels into myofibroblasts (strain and speed of strain). These cells increase their fibers secretion and thus change the extra-cellular matrix that becomes thicker and stiffer[59]. This vicious cycle reinforces itself by producing and carrying-deviating more mechanical stress within the local environment. With time, the extracellular matrix ends up forming immature adhesions[60] (Behavior or function creating structure). But if the stress is diminished, proto-myofibroblasts and myofibroblast tend to disappear by apoptosis[61].

At this moment, this new matrix could still be destroyed by enzymes: such as for example (Matrix Metalloproteinases or MMPs) secreted by as well the peritoneum as the present macrophages[62]. If it is not the case, the maturation of the neo-fascia will keep densifying itself leading to the genesis of mature peritoneal adhesions.

The maturation continues with vessel formations (neo-angiogenesis) around the main current fluidic trajectories or pathways in the connective tissue (capillaries, arterioles, venules…)(30) and even in two third of the cases, innervation composed by myelinated and non-myelinated fibres occurs[63]Nevertheless, neither correlations exist between the existence of nervous fibers within the adhesions and painful symptoms[64]. When this stage is reached, the adhesions look like a neo-ligament called peritoneal bridles (“brides” in french).

Important fact is that fibrins are able to move within the peritoneal liquid and create adhesions sometimes far away from the surgical site[65]. The quality and quantity of the peritoneal liquid is thus an important variable but its proper circulation is crucial for the good immune system response. We remind that it could be renewed every 1 to 2 hours. We use visceral mobility to maintain motion within the peritoneal liquid and enable the fibrinolysis. If this step is well enough managed, the healing process should follow a normal course (Chart 1) and we should expect only a limited quantity of adhesions.

 The adhesions can be like fibrous and firm cylinders held through the abdominal cavity. This change of form is sometimes called “bridle”[66].

During our dissections, we noticed that the adhesions are more or less easy to break down by stretching the tissues with our fingers!

It is the opposite for the bridle that look more like neo-ligament or neo-meso and are impossible to break without severely damaging the tissues.

The adhesion genesis can start just 2 hours after the surgery[67], hence the need for a fast and adapted care. Their density is maximal between day 10 and 15 post surgery[68]. Just a part of these immature adhesions will be deteriorated.

The problem is well known and is a major public health issue like these numbers from different studies are showing:

–      90% of peritoneal adhesions come from post surgery (versus inflammation or radiation)[69],

–      90% of the time, at least, abdominal surgery generates adhesions[70],

–      55% – 100% of women develop adhesions following pelvic surgery[71],

–      440 000 adhesiolysis procedures are performed in the US per year[72],

–      67% of the time, adhesions involve the great omentum and/or the small intestine[73], some studies found the great omentum involved 92%[74] or even 100%46 of the time,

–      74% of bowel occlusions would be due to adhesions[75],

–      3% of laparotomies result from bowel occlusions due to adhesions[76],

–      1 billion USD, the cost of surgeries for abdominal-pelvic adhesions in the US per year[77].

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6. Abdominal-Pelvic Surgery 

There are two types of abdominal-pelvic surgery procedure: laparotomy and laparoscopy.

The laparotomy is a surgical procedure involving the incision of the abdomen.

As the laparoscopy is a so called “mini-invasive” technique. A fiber-optic camera and trocars are inserted inside the abdomen through very small cutaneous incisions.

In order to freely move the instruments, the peritoneal walls are spread apart by carbon dioxide injection. At the superficial level of the skin, it is true that the scars are minimal but not at the connective tissue level.

The laparotomy is the oldest technique and very early the surgeons find out a very common post surgical complication: the adhesions [60]. They can cause abdominal-pelvic pain and some functional pathologies but the worst complication stays the intestinal occlusion that could be fatal in 4,3% to 13% of the case[78].

A study including 54 000 patients in post surgery during a period of 10 years showed that 30% to 35% of the re-admissions were potentially due to adhesion complications including 5% proven[79],[80]. The treatments sometimes included a new surgery, this procedure is called adhesiolysis. The goal is to cut the adhesions by laparoscopy. This new surgery requires the re-opening of the peritoneum and thus will have the same complications than the previous one[81]. The rate of previous adhesion reconstitution goes up to 90% and even new sites are created +10%[82]. Despite the improvement of the laparoscopic procedures which become less and less invasive according to the surgeons, this technique still does not allow to avoid them[83]. In 90% to 97% of the cases, an abdominal-pelvic procedure causes adhesions[84],[85].

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Colonic adhesions in a dissection on an embalmed human body

The increased abdominal pressure by carbon dioxide injection disturbs the healing process of the peritoneum[86] and could be linked with adhesion genesis.

As well, the electrocautery delays the healing process, increases the length of the inflammatory response and lets necrotic tissues up to several weeks post surgery[87]. This chemically stimulates a local inflammatory response which can evenso increase the problems.

To summarize, CO2 injection and electrocautery are much more traumatizing for the peritoneum than a local incision made by a scalpel[88].

At the time, we are writing this article no definitive strategy to prevent adhesion has been adopted yet[89].

At the HAS, only laparotomy is practiced. During our stay, we were able to follow a patient who had several surgeries because of bowel occlusions due to adhesions. This case is not uncommon, that is why we think that osteopathic care can play a important role in the treatment and prevention of adhesions, to decrease the risks for patient in post-surgery.

8. Observation

8.1. General observation

We saw 6 patients about one-week post-surgery including 3 appendectomies with peritonitis, 1 ilieal resection after an intestinal occlusion, 1 duodenal ulcer and 1 explorative surgery, here our observations commune to all of them:

1.    Hypo-mobility of the diaphragm in high position,

2.    Stomach mobility at the opposite of its physiology according to Finet & Williame,

3.    Motionless caecum (abdominal probe at this level),

4.    Tension and hypo-mobility of the ascending colon and sigmoid.

Note that the left side of the abdomen seems more affecter that the right. The stomach and the left colon were found hypo-mobile in all the patients tested.

We kept our osteopathic approach and tested globally the patient. Two other common points were found: hypo-mobility of the sterno-clavicular joint as well as the cervico-thoracic junction.

We think this could be explained by the position of the patient during the surgery, the arms are maintained in abduction about 90ᴼ angle for an extended period of time under anesthesia. Theses restrictions may have a negative impact on the lymphatic system which connects to the Caval system by the sub-clavicular veins.

As a reminder, the thoracic duct (drains the entire trunk, its viscera and lower limbs) passes in front of the superior thoracic vertebral bodies before diving into the left sub-clavicular vein. Knowing that this lymphatic system is a low-pressure system, it is reasonable to assume that any increased tension at this level (due to an articular blockage, increased fascia tension or a muscle hypertonia for instance) would have a negative impact on its flow rate.

In our approach, we want to avoid lymphatic stasis and encourage the free fluids flow. To do so, some articular techniques could be advised, we will get back to it.

In addition to the post-surgery patients, we tested out patients who received a surgery several months to years ago. Their surgeries were similar to our post-surgery patients. We tested a dozen of patients, all including a digestive complaint to their reasons for consultation, from bloating to constipation (we keep in mind that these symptoms are also related to the diet). We found a common point in almost all our patient: stomach, caecum, descending colon and sigmoid hypo-mobility. In addition, we notice that the superficial scars were difficult to move with at least one area very bonded in the depth. With this observation, we decided to include, work on the scar tissues first if needed.

8.2. Pre-surgery

           Numerous surgical, medical and non-medical treatment already exist to prevent or to treat the adhesions but with more or less success[90]. Quoting several studies “Prevention is the key”[91],[92],[93], point on which we totally agree.

The hydration of the patient is the primary variable based on the fact that water is the environment of all the tissues and cells previously mentioned. The advantage is that in the pre and post surgery, we are able to have a quick and simple impact. We advice very frequent (every half hour) body temperature water income but each time in small quantity (2 to 3 sips) to ensure the best absorption possible without adding mechanical stress. Note that the water needs to be neutral (chemically and temperature) to avoid a stimulation of the stomach and slow the absorption down.

We also mention the importance of the peritoneal fluid, knowing that the maximal quantity is reached just before the ovulation, it should be interesting to schedule the intervention during this time if possible. It is true that the fluctuation is only 14mL (20mL maximum and 6mL minimum during the luteal phase) but it represents a 230% variation, which is not marginal. This little advantage may be of a great help for the osteopathic work on the circulation.

Still for the pre-surgery, the observation of the physiologic condition of the patient seems fundamental. Indeed, the different steps described in Figure 1 and 2, involve the basic elements such as protein, fat and sugar. Any deficiencies or special conditions affecting their physiology have a direct impact on the healing process[94], which we should try to fix before the surgery if possible, or at least to take them into account for the treatment.

8.3. Post-surgery

In the literature, we found some studies showing the benefits of abdominal massages and visceral mobilizations in post surgery. As early as 1899, the positive effects of post-surgical visceral massages are described[95]. Closer to us in 2002, a study concluded that abdominal massages can decrease pain after an ileal surgery[96]. These massages were done by a massage device (LPG, or Endermology machine). The principle is to use a suction effect to separate the different tissue layers, decreasing their viscosity and enable the fluid circulation. Point on which we are focusing our work too.

Another study, performed on animals showed that the early post-operative strolls have the tendency to decrease the adhesions compared to the ones whom stay immobile[97]. A study on rats showed that visceral mobilizations decreased in a significative way the adhesions[98].

8.3 Osteopathic approach

These few conclusions, encourage us to think that osteopathic care including gentle visceral manipulations (Finet & Williame like) aiming to work at a circulatory level, starting first far from the surgical site and then slowly coming closer, could make the difference by maintaining veino-lymphatic and peritoneal fluids circulation in post-surgery.

We remind that in Haiti, it is difficult to benefit from the last breakthroughs in term of post-surgery treatment and the human and economical cost of a surgery is to be kept in mind.

This is why we are convinced that Common sense and Evolutionary Osteopathy have their place in prevention, even more here and in other economically challenged places.

Our hypothesis is to maintain the visceral mobility in order to have an impact on adhesions. But before using any manipulations, we have to take the healing process delay into account. The problem is to maintain the structures involved mobile between each other in order to:

1.    Guaranty ideal fluid circulation (peritoneal and veino-lymphatic) and avoid stasis leading to clotting, mechanical stress… favorable ground to the fibroblasts and myofibroblasts proliferation.

2.    Maintain diaphragm mobility as much as possible to reach the same goal, stimulation of the fluid circulation, including the air like a way of excretion of waste product.

3.    Decrease the mechanical tensions under the wounded areas for the reasons already exposed.

This, without imposing any mechanical stress upon the immature connective tissue to avoid creating line of forces stimulating fascial instead of mesothelial genesis.

(Note of Max Girardin: so please refrain- , or even better, -stop reasoning about the peritoneum, and visceral area in musculo-skeletal images…PLEASE, because how you think, and the images you have in your mind affects how your fingers and palpation act!) See: https://www.linkedin.com/pulse/osteopathy-tissue-knowledge-max-girardin/

The patient’s pain is primordial during this kind of work.

We should stay under their pain thresholds the entire time.

The risk is, first and foremost to injure the patient, but as well as initiate a tissular and body defense reaction which could increase the intra-abdominal pressure, thing that we want to avoid at all costs.

9. Recommendation

9.1. Treatment outcomes

           We saw 6 patients every day during 4 to 8 days depending on the case. The treatment occurred after the visit of the surgeon, here are our observations:

–      There is no need to treat the patient everyday, sometimes the manual tests were satisfying enough and this for one to several days,

–      The stomach was able to recover its normal mobility after just a few sessions,

–      Increased mobility for the diaphragm and the treated organs,

–      Decreased pain perception for all our patients.

We want to keep our approach and respect the osteopathic philosophy,

that is why we do not want to describe a stereotyped protocol but rather recommendations to frame our work.

The first remark, the length of the treatment is much shorter that a classic osteopathic session, between 10 and 20 min. Their frequency depends on the improvements of each patient. The purpose is always to maintain the optimal mobility as long as possible. We sometimes can treat a patient several times a day if we detect increased restrictions.

Note that until about week 2, the techniques used, stay very superficial such as the techniques developed by Finet & Williame (1) and using the natural movement of the diaphragm. We want to keep this superficial approach to encourage the circulatory function of the diaphragm without putting mechanical constraints on the surgical site.

9.2. Treatment proposed

We start far from the surgical site and come closer. This approach allows us a continuous manual assessment. It has a comforting effect on the patient who is sometimes nervous after the intervention as well.

The treatment of the cutaneous scars includes stretchings, detachments and mobilizations of the area. The efficiency of the manual massage for the treatment of the scars is weak[99]. We prefer the massage suction machines such as LPG (Endermology) for their benefits previously described.

Here the chronology of our treatment:

Pre-surgery:

–      Full osteopathic treatment, (preparing the organism for the stress-injury to come)

Few hours post-surgery:

–      Rest,

Step 1:

–      Maintain organ mobilities and diaphragm help

–      Treatment remotely (closer and closer),

Step 2 (superficial healing finished):

–      Treatment of the superficial scare,

–      Control and treatment of the mobility,

Step 3:

–      Full osteopathic treatment.

On purpose, we do not talk about time scale because it depends entirely on the patient’s condition. The osteopath should use parsimony and judge first with palpation, on the benefit of the technique to use.

The main recommendation after this work is caution about early tissue manipulation in post-surgery. As well as too early manipulation of the superficial scars. We already explained the negative effects of a mechanical stress during the very first day post surgery. They can have a harmful impact and at best create new adhesions or at worst lead to peritoneal lesions potentially be life-threatening for the patient!

10. Conclusion

           This paper aims to show the possibilities that can be offered by Osteopathy at the hospital. We are working with the HAS every year, for 4 years now. This year, we gave surveys to the Medical Director (16 years experience), the Chief of Surgery (31 years experience) and Chief of Rehabilitation Department (10 years experience). To the question, “do you see an interest for Osteopathy to be present at the hospital and if yes in which service”, here their answers:

–      Medical Director: YES, Maternity, Intern Medicine, Surgery.

–      Chief of Surgery: YES, Every Service.

–      Chef of Rehabilitation Department: YES, Surgery and Medicine.

These answers and the work in collaboration between our group of osteopaths and the medical staff during all these years, allows us to have certainty that Osteopathy has its place at the hospital.

In Haiti and within the HAS this statement is even more true, this is why we are transmitting our osteopathic approach to the rehabilitation team.

No alt text provided for this image

For the pre and post-surgery patient care, we build a treatment chronology which seems coherent to our experience and easy to follow. It integrates both the specificity of each patient as well as a post-surgery follow up in the long term.

The patient outcomes were all positive which encourage use to work this way like other authors: « If further experiments confirm and extend our initial findings, visceral mobilization could readily be implemented into post surgical care and patient education. It is possible that visceral mobilization could become an economic and effective way of preventing and treating abdominal adhesions.[46]”.

This exceptional experience allows us to work, in collaboration with a high-quality staff, on patients who we would ordinarily not have access too. There were sad stories but also many successes and a lot of future projects. We would like to thank once again The Hospital Albert Schweitzer for the outstanding trust in Osteopathy.

Professionals which were interested by this article stay on the look out for the complete monograph, which will follow, this is just a short version.

The long version is full throttle, with everything on and around, a relish for die hard Osteopaths loving tissue and Osteopathy in the visceral field.

We will publish the full monograph in French and English when the editing is done.

Keep up the good work!

Cheers Brothers and Sisters

REFERENCE

[1] Finet, G. DO, Williame, C. DO (1985-2016). « Traité d’Ostéopathie ».

[2] Kodama, I., Loiacono, L. A., Sigel, B., Machi, J., Golub, R. M., Parsons, R. E., … & Sachdeva, A. K. (1992). Ultrasonic detection of viscera slide as an indicator of abdominal wall adhesions. Journal of clinical ultrasound20(6), 375-380.

[3] Tan, H. L., Shankar, K. R., Ade-Ajayi, N., Guelfand, M., Kiely, E. M., Drake, D. P., … & Gent, R. (2003). Reduction in visceral slide is a good sign of underlying postoperative viscero-parietal adhesions in children. Journal of pediatric surgery38(5), 714-716.

[4] Jordan, T., & Schuster, R. (1994). Selected writings of Carl Philip McConnell.

[5] McConnell, C. P. DO, Teall, C. C. DO. (1920). The practice of Osteopathy. Journal printing CO.

[6] Kolecki, R. V., Golub, R. M., Sigel, B., Machi, J., Kitamura, H., Hosokawa, T., … & Zaren, H. A. (1994). Accuracy of viscera slide detection of abdominal wall adhesions by ultrasound. Surgical endoscopy8(8), 871-874.

[7] Finet, G. DO, Williame, C. DO (1992). Treating Visceral Dysfunction: An Osteopathic Approach to Understanding and Treating the Abdominal Organs. Stillness Press.

[8] Chila, A. (2012). Foundations of osteopathic medicine. LWW.

[9] Victor, P. E. (2017). Atlas of Histology with Functional Correlations. New York: AW olters Kluwer Company, 125-128.

[10] diZerega, G. S., & Rodgers, K. E. (1992). Intraperitoneal adhesions. The peritoneum. New York: Springer-Verlag, 274-306.

[11] Coffey, J. C., Dillon, M., Sehgal, R., Dockery, P., Quondamatteo, F., Walsh, D., & Walsh, L. (2015). Mesenteric-based surgery exploits gastrointestinal, peritoneal, mesenteric and fascial continuity from duodenojejunal flexure to the anorectal junction-a review. Digestive surgery32(4), 291-300.

[12] Coffey, J. C., & O’Leary, D. P. (2016). The mesentery: structure, function, and role in disease. The lancet Gastroenterology & hepatology1(3), 238-247.

[13] Sadler, T. W. (2010, August). The embryologic origin of ventral body wall defects. In Seminars in pediatric surgery (Vol. 19, No. 3, pp. 209-214). WB Saunders.

[14] Khanna, R., & Krediet, R. T. (2009). Chapter 4: the peritoneal microcirculation in peritoneal dialysis. Nolph and Gokal’s Textbook of Peritoneal Dialysis, ed3.

[15] Snell, R. S. (2011). Clinical anatomy by regions. Lippincott Williams & Wilkins.

[16] Aguirre, A. R., & Abensur, H. (2014). Physiology of fluid and solute transport across the peritoneal membrane. Brazilian Journal of Nephrology36(1), 74-79.

[17] Ansaloni, L., & Piso, P. (2016). The peritoneum, a still neglected organ. Its rediscovery through a new scientific journal: the Journal of Peritoneum (and other serosal surfaces). Journal of Peritoneum (and other serosal surfaces).

[18] Michailova, K. N., & Usunoff, K. G. (2006). Introduction and Review of the Literature (pp. 1-17). Springer Berlin Heidelberg.

[19] Wilkosz, S., Ireland, G., Khwaja, N., Walker, M., Butt, R., de Giorgio-Miller, A., & Herrick, S. E. (2005). A comparative study of the structure of human and murine greater omentum. Anatomy and embryology209(3), 251-261.

[20] Di Paolo N, Sacchi G. Atlas of peritoneal histology. Perit Dial Int 2000; 20 Suppl 3: S5-96.

[21] Di Paolo N, Nicolai GA, Garosi G. The peritoneum: from histological studies to mesothelial transplant through animal experimentation. PeritDial Int 2008; 28 Suppl 5: S5-9.

[22] Blackburn SC, Stanton MP. Anatomy and physiology of the peritoneum. Semin Pediatr Surg 2014;23:326-30.

[23] Di Paolo N, Sacchi G. Anatomy and physiology of the peritoneal membrane. Contrib Nephrol 1990;84:10-26.

[24] Blaustein, A. (1984). Peritoneal mesothelium and ovarian surface cells–shared characteristics. International journal of gynecological pathology: official journal of the International Society of Gynecological Pathologists3(4), 361-375.

[25] Eroschenko, V. P., & Di Fiore, M. S. (2013). DiFiore’s atlas of histology with functional correlations. Lippincott Williams & Wilkins.

[26] Miller, A., Hong, M. K. H., & Hutson, J. M. (2004). The broad ligament: a review of its anatomy and development in different species and hormonal environments. Clinical Anatomy: The Official Journal of the American Association of Clinical Anatomists and the British Association of Clinical Anatomists17(3), 244-251.

[27] Craig, M. E., & Billow, M. (2018). Anatomy, Pelvis, Ligaments, Broad. In StatPearls [Internet]. StatPearls Publishing.

[28] Jacquet, P., & Sugarbaker, P. H. (1996). Peritoneal-plasma barrier. In Peritoneal carcinomatosis: principles of management (pp. 53-63). Springer, Boston, MA.

[29] Koninckx, P. R., Renaer, M., & Brosens, I. A. (1980). Origin of peritoneal fluid in women: an ovarian exudation product. BJOG: An International Journal of Obstetrics & Gynaecology87(3), 177-183.

[30] Oral, E., Olive, D. L., & Arici, A. (1996). The peritoneal environment in endometriosis. Human Reproduction Update2(5), 385-398.

[31] Alfonsin, A. E., & Leiderman, S. (1980). Peritoneal fluid throughout the cycle. Obstet y Gin Lat Amer38, 53-56.

[32] Krediet, R. T., Lindholm, B., & Rippe, B. (2000). Pathophysiology of peritoneal membrane failure. Peritoneal Dialysis International20(Suppl 4), S22-S42.

[33] Heel, K. A., & Hall, J. C. (1996). Peritoneal defences and peritoneum‐associated lymphoid tissue. British journal of surgery83(8), 1031-1036.

[34] Gazvani, R., & Templeton, A. (2002). Peritoneal environment, cytokines and angiogenesis in the pathophysiology of endometriosis. Reproduction123(2), 217-226.

[35] Fallowfield, J. A. (2015). Future mechanistic strategies for tackling fibrosis–an unmet need in liver disease. Clinical medicine15(Suppl 6), s83-s87.

[36] Ramey, J. W., & Archer, D. F. (1993). Peritoneal fluid: its relevance to the development of endometriosis. Fertility and sterility60(1), 1-14.

[37] Hodges, P. W., Cresswell, A. G., Daggfeldt, K., & Thorstensson, A. (2001). In vivo measurement of the effect of intra-abdominal pressure on the human spine. Journal of biomechanics34(3), 347-353.

[38] Goksel, O., Vishnevsky, V., Carrillo, A. G., & Tanner, C. (2016, April). Imaging of sliding visceral interfaces during breathing. In 2016 IEEE 13th International Symposium on Biomedical Imaging (ISBI) (pp. 298-301). IEEE.

[39] Corfman, R. S., Badram, O. (1994). Effect of pelvic adhesions on pelvic pain and fertility. In Adhesions. R.E. Leach, Ed. Infertil. Reprod. Med. Clin. N. Am. 5(3): 405–411.

[40] Van Goor, H. (2007). Consequences and complications of peritoneal adhesions. Colorectal Disease9, 25-34.

[41] Vrijland, W. W., Jeekel, J., Van Geldorp, H. J., Swank, D. J., & Bonjer, H. J. (2003). Abdominal adhesions: intestinal obstruction, pain, and infertility. Surgical Endoscopy and Other Interventional Techniques17(7), 1017-1022.

[42] Mahadevan, M. M., Wiseman, D., Leader, A., & Taylor, P. J. (1985). The effects of ovarian adhesive disease upon follicular development in cycles of controlled stimulation for in vitro fertilization. Fertility and sterility44(4), 489-492.

[43] Chegini, N. (2002). Peritoneal molecular environment, adhesion formation and clinical implication. Front Biosci7(16), 91-115.

[44] Hellebrekers, B. W. J., & Kooistra, T. (2011). Pathogenesis of postoperative adhesion formation. British journal of Surgery98(11), 1503-1516.

[45] Sorg, H., Tilkorn, D. J., Hager, S., Hauser, J., & Mirastschijski, U. (2017). Skin wound healing: an update on the current knowledge and concepts. European Surgical Research58(1-2), 81-94.

[46] Brulez, H. F., & Verbrugh, H. A. (1995). First-line defense mechanisms in the peritoneal cavity during peritoneal dialysis. Peritoneal dialysis international15(Suppl 7), S24-S33.

[47] Ellis, H., Harrison, W., & Hugh, T. B. (1965). The healing of peritoneum under normal and pathological conditions. British journal of Surgery52(6), 471-476.

[48] DiZerega, G. S. (1990). The peritoneum and its response to surgical injury. Progress in clinical and biological research358, 1.

[49] Glucksman, D. L. (1966). Serosal integrity and intestinal adhesions. Surgery60(5), 1009-11.

[50] DeCherney, A. H. (1997). Clinical problem of intraperitoneal postsurgical adhesion formation following general urgery and the use of adhesion prevention barriers. Surgical Clinics of North America77(3), 671-688.

[51] Raftery, A. T. (1973). Regeneration of parietal and visceral peritoneum: an electron microscopical study. Journal of anatomy115(Pt 3), 375.

[52] DiZerega, G. S. (2000). Peritoneum, peritoneal healing, and adhesion formation. In Peritoneal surgery (pp. 3-37). Springer, New York, NY.

[53] DiZerega, G. S., Campeau, J. D. (2001). Peritoneal repair and post-surgical adhesion formation. Human reproduction update7(6), 547-555.

[54] Sikkink, C. J., Reijnen, M. M., Falk, P., van Goor, H., & Holmdahl, L. (2005). Influence of monocyte-like cells on the fibrinolytic activity of peritoneal mesothelial cells and the effect of sodium hyaluronate. Fertility and sterility84, 1072-1077.

[55] Hinz, B., Mastrangelo, D., Iselin, C. E., Chaponnier, C., & Gabbiani, G. (2001). Mechanical tension controls granulation tissue contractile activity and myofibroblast differentiation. The American journal of pathology159(3), 1009-1020.

[56] Wei, Mingtian, et al. “Malignant ascites-derived exosomes promote proliferation and induce carcinoma-associated fibroblasts transition in peritoneal mesothelial cells.” Oncotarget 8.26 (2017): 42262.

[57] Ibrahim, M. G., Sillem, M., Plendl, J., Taube, E. T., Schüring, A., Götte, M., … & Mechsner, S. (2018). Arrangement of myofibroblastic and smooth muscle-like cells in superficial peritoneal endometriosis and a possible role of transforming growth factor beta 1 (TGFβ1) in myofibroblastic metaplasia. Archives of gynecology and obstetrics, 1-11.

[58] Yáñez-Mó, M., Lara-Pezzi, E., Selgas, R., Ramírez-Huesca, M., Domínguez-Jiménez, C., Jiménez-Heffernan, J. A., … & Castro, M. A. (2003). Peritoneal dialysis and epithelial-to-mesenchymal transition of mesothelial cells. New England Journal of Medicine348(5), 403-413.

[59] Arora, P. D., Narani, N., & McCulloch, C. A. (1999). The compliance of collagen gels regulates transforming growth factor-β induction of α-smooth muscle actin in fibroblasts. The American journal of pathology154(3), 871-882.

[60] Diamond, M. P., & Freeman, M. L. (2001). Clinical implications of postsurgical adhesions. Human Reproduction Update7(6), 567-576.

[61] Schmid, P., Itin, P., Cherry, G., Bi, C., & Cox, D. A. (1998). Enhanced expression of transforming growth factor-beta type I and type II receptors in wound granulation tissue and hypertrophic scar. The American journal of pathology152(2), 485.

[62] Elkington, P. T., Green, J. A., Friedland, J. S. (2009). Analysis of matrix metalloproteinase secretion by macrophages. In Macrophages and Dendritic Cells (pp. 253-265). Humana Press.

[63] Herrick, S. E., Mutsaers, S. E., Ozua, P., Sulaiman, H., Omer, A., Boulos, P., … & Laurent, G. J. (2000). Human peritoneal adhesions are highly cellular, innervated, and vascularized. The Journal of pathology192(1), 67-72.

[64] Tulandi, T., Chen, M. F., Al-Took, S., Watkin, K. (1998). A study of nerve fibers and histopathology of postsurgical, postinfectious, and endometriosis-related adhesions. Obstetrics & Gynecology92(5), 766-768.

[65] Pattinson, H. A., Koninckx, P. R., Brosens, I. A., Vermylen, J. (1981). Clotting and fibrinolytic activities in peritoneal fluid. BJOG: An International Journal of Obstetrics & Gynaecology88(2), 160-166.

[66] Arung, W., Meurisse, M., & Detry, O. (2011). Pathophysiology and prevention of postoperative peritoneal adhesions. World journal of gastroenterology: WJG17(41), 4545.

[67] Hellebrekers, B. W. J., Trimbos-Kemper, G. C. M., Bakkum, E. A., Trimbos, J. B. M. Z., Declerck, P. J., Kooistra, T., & Emeis, J. J. (2000). Short-term effect of surgical trauma on rat peritoneal fibrinolytic activity and its role in adhesion formation. Thrombosis and haemostasis84(05), 876-881.

[68] Alexandre, J. H., Cachera, J. P., & Cukier, J. (1978). Occlusions intestinales. Patel JC, Pathologie Chirurgicale. Paris: Masson, 836-7.

[69] Szomstein S., Lo Menzo E., Simfenendorfer C. Laparoscopic lysis of adhesions. World J. Surg. 2006 Apr;30(4):535–540.

[70] Kössi, J., Salminen, P., Rantala, A., & Laato, M. (2003). Population‐based study of the surgical workload and economic impact of bowel obstruction caused by postoperative adhesions. British journal of surgery90(11), 1441-1444.

[71] Liakakos, T., Thomakos, N., Fine, P. M., Dervenis, C., & Young, R. L. (2001). Peritoneal adhesions : etiology, pathophysiology, and clinical significance. Digestive surgery18(4), 260-273.

[72] Adhesiolysis, P. (1994). National Inpatient Profile 1993. Baltimore, HCIA427, 653-5.

[73] Luijendijk, R. W., de Lange, D. C., Wauters, C. C. A. P., Hop, W. C. J., Duron, J. J., Pailler, J. L., … & Jeekel, J. (1996). Foreign material in postoperative adhesions. Annals of surgery223(3), 242.

[74] Weibel, M. A., & Majno, G. (1973). Peritoneal adhesions and their relation to abdominal surgery: a postmortem study. The American Journal of Surgery126(3), 345-353.

[75] DeWilde, R. L., & Trew, G. (2007). Postoperative abdominal adhesions and their prevention in gynaecological surgery. Expert consensus position. Part 2—steps to reduce adhesions. Gynecological surgery4(4), 243-253.

[76] Menzies, D., Ellis, H. (1990). Intestinal obstruction from Adhesions how big is the problem? Ann R Coll Surg Engl 72(1):60 – 63.

[77] Ray, N. F., Denton, W. G., Henderson, S. C., & Seymour Perry MD, M. A. C. P. (1998). Abdominal adhesiolysis: inpatient care and expenditures in the United States in 1994. Journal of the American College of Surgeons186(1), 1-9.

[78] Nieuwenhuijzen, M., Reijnen, M. M. P. J., Kuijpers, J. H. C., & Van Goor, H. (1998). Small bowel obstruction after total or subtotal colectomy: a 10‐year retrospective review. British journal of surgery85(9), 1242-1245.

[79] Ellis, H., Moran, B. J., Thompson, J. N., Parker, M. C., Wilson, M. S., Menzies, D., … & Buchan, S. (1999). Adhesion-related hospital readmissions after abdominal and pelvic surgery: a retrospective cohort study. The Lancet353(9163), 1476-1480.

[80] Lower, A. M., Hawthorn, R. J., Emeritus, H. E., O’Brien, F., Buchan, S., & Crowe, A. M. (2000). The impact of adhesions on hospital readmissions over ten years after 8849 open gynaecological operations: an assessment from the Surgical and Clinical Adhesions Research Study. BJOG: An International Journal of Obstetrics & Gynaecology107(7), 855-862.

[81] Diamond, M. P., Daniell, J. F., Feste, J., Surrey, M. W., McLaughlin, D. S., Friedman, S., … & Martin, D. C. (1987). Adhesion reformation and de novo adhesion formation after reproductive pelvic surgery. Fertility and sterility47(5), 864-866.

[82] Operative Laparoscopy Study Group. (1991). Postoperative adhesion development after operative laparoscopy: evaluation at early second-look procedures. Fertility and Sterility55(4), 700-704.

[83] Milingos, S., Kallipolitis, G., Loutradis, D., Liapi, A., Mavrommatis, K., Drakakis, P., … & Michalas, S. (2000). Adhesions: laparoscopic surgery versus laparotomy. Annals of the New York Academy of Sciences900(1), 272-285.

[84] Fevang, B. T. S., Fevang, J., Lie, S. A., Søreide, O., Svanes, K., & Viste, A. (2004). Long-term prognosis after operation for adhesive small bowel obstruction. Annals of surgery240(2), 193.

[85] Menzies, D., & Ellis, H. (1990). Intestinal obstruction from adhesions–how big is the problem?. Annals of the Royal College of Surgeons of England72(1), 60.

[86] Gurusamy, K. S., Vaughan, J., & Davidson, B. R. (2014). Low pressure versus standard pressure pneumoperitoneum in laparoscopic cholecystectomy. Cochrane Database of Systematic Reviews, (3).

[87] Bellina, J. H., Hemmings, R., Voros, J. I., & Ross, L. F. (1984). Carbon dioxide laser and electrosurgical wound study with an animal model: a comparison of tissue damage and healing patterns in peritoneal tissue. American Journal of Obstetrics & Gynecology148(3), 327-334.

[88] Montgomery, T. C., Sharp, J. B., Bellina, J. H., & Ross, L. F. (1983). Comparative gross and histological study of the effects of scalpel, electric knife, and carbon dioxide laser on skin and uterine incisions in dogs. Lasers in surgery and medicine3(1), 9-22.

[89] Arung, W., Meurisse, M., & Detry, O. (2011). Pathophysiology and prevention of postoperative peritoneal adhesions. World journal of gastroenterology: WJG17(41), 4545.

[90] Robertson‐Malt, S. (2011). Intra‐peritoneal Prophylactic Agents for Preventing Adhesions and Adhesive Intestinal Obstruction. Aorn Journal94(5), 498-499.

[91] Canis, M., Botchorishvili, R., Wattiez, A., Rabischong, B., Houlle, C., Mage, G., … & GOMEL, V. (2001). Prévention des adhérences péritonéales. Commentaire. Journal de gynécologie obstétrique et biologie de la reproduction30(4), 305-324.

[92] Gomel, V., Urman, B., & Gurgan, T. (1996). Pathophysiology of adhesion formation and strategies for prevention. The Journal of reproductive medicine41(1), 35-41.

[93] Scott-Coombes, D. M., Vipond, M. N., & Thompson, J. N. (1993). General surgeons’ attitudes to the treatment and prevention of abdominal adhesions. Annals of the Royal College of Surgeons of England75(2), 123.

[94] Arnold, M., & Barbul, A. (2006). Nutrition and wound healing. Plastic and reconstructive surgery117(7S), 42S-58S.

[95] Haberlin, H. (1899). Die massage bei postoperativem ileus. Cen-tralblatt fur Gynäkologie 42, 1164e1167.

[96] Le Blanc-Louvry, I., Costaglioli, B., Boulon, C., Leroi, A. M., & Ducrotte, P. (2002). Does mechanical massage of the abdominal wall after colectomy reduce postoperative pain and shorten the duration of ileus? Results of a randomized study. Journal of Gastrointestinal Surgery6(1), 43-49.

[97] Das, K., Penney, L. L., & Critser, J. K. (1990). Effects of passive motion and early vs. delayed ambulation on adhesion formation in rat uterine surgery. International journal of fertility35(4), 245-248.

[98] Bove, G. M., & Chapelle, S. L. (2012). Visceral mobilization can lyse and prevent peritoneal adhesions in a rat model. Journal of bodywork and movement therapies16(1), 76-82.

[99] Shin, T. M., & Bordeaux, J. S. (2012). The role of massage in scar management: a literature review. Dermatologic Surgery38(3), 414-423.


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