Peritoneal metastases
Anju Sahdev, Sarah J. Vinnicombe in Husband & Reznek's Imaging in Oncology, 2020
The peritoneal cavity is a serous sac (or coelom) lying between the parietal and visceral peritoneum (Figure 33.1). It consists of a series of communicating potential spaces not normally seen on imaging unless distended by fluid or air. The visceral peritoneum covers the abdominal organs, and the parietal peritoneum lies against the abdominal wall and retroperitoneum, resulting in an extensive surface area as a potential site of tumour deposition. The greater omentum consists of four layers of peritoneum, two from the greater curve of the stomach and two from the transverse mesocolon, which fuse and pass anterior to the small bowel—this is often involved by metastases. The lesser omentum (or gastrohepatic ligament) joins the lesser curve of the stomach to the liver. Ligaments are peritoneal folds connecting abdominal organs. A mesentery is a peritoneal fold joining the small bowel or parts of the colon to the posterior abdominal wall and containing blood vessels, lymphatics, and nerves (3). Ligaments and mesenteries are suspended by the visceral peritoneum and so are not truly intraperitoneal (4). The transverse mesocolon is the main dividing barrier, separating the supracolic and infracolic compartments. The left infracolic space is divided from the right by the small bowel mesentery and communicates inferiorly with the right pelvis. The peritoneal cavity normally contains less than 100 mL of serous fluid, which circulates and is preferentially drawn up to the right subphrenic space where it is absorbed (4).
The peritoneum, omentum, mesentery and retroperitoneal space
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
Ultrasonography and CT scanning will demonstrate the lesion and may allow diagnosis of cyst type (Figure 61.13 a and b). There are no suitable medical therapies. The goal of surgical therapy is complete excision of the mass. The preferred treatment of mesenteric cysts is enucleation, although bowel resection is frequently required to ensure that the remaining bowel is viable. Bowel resection may be required in 50-60%of children with mesenteric cysts, whereas resection is necessary in about a third of adults (Figure 61.13c). If enucleation or resection is not possible because of either the size of the cyst or its location deep within the root of the mesentery, the third option is partial excision with marsupialisation of the remaining cyst into the abdominal cavity. Approximately 10% of patients require this form of therapy. If marsupiali- sation is performed, the cyst lining should be sclerosed with 10% glucose solution, diathermy or tincture of iodine to minimise recurrence. Recurrence rates vary from 0% to 13%.
Applied radiological anatomy of the peritoneal cavity
Wim P. Ceelen, Edward A. Levine in Intraperitoneal Cancer Therapy, 2015
These terms are used to describe the parts of the peritoneum connecting organs with each other or to the abdominal wall. A mesentery is a double layer of peritoneum suspending the small or large bowel from the posterior abdominal wall. It acts as a conduit for neurovascular and lymphatic structures between the organ and the subperitoneal space. True mesenteries connect directly to the posterior abdominal wall, whereas specialized mesenteries (the omenta and mesoappendix) are not attached to the posterior abdominal wall (Figure 3.2). A peritoneal ligament is formed by two layers of peritoneum and supports a structure within the peritoneal cavity. Ligaments are named according to the structures they connect. For example, the gastrosplenic ligament connects the stomach to the spleen; the splenorenal ligament connects the kidney to the spleen (Figure 3.1). An omentum refers to a double-layered continuation of peritoneal ligaments joining the stomach and proximal duodenum to adjacent structures. The greater omentum extends from the greater curvature of the stomach and consists of the gastrocolic ligament, the gastrosplenic ligament, and the gastrophrenic ligament. Its descending and ascending layers fuse, forming a four-layered structure in continuity with the lesser sac [2] (Figure 3.2). It drapes over the transverse colon and hangs down a variable length anteriorly as an apron of fat, covering the small bowel allowing free peristalsis. The greater omentum is easily identifiable at surgery but difficult to see on cross-sectional imaging when normal, as it cannot be differentiated from the surrounding mesenteric fat.
The mesentery: an ADME perspective on a ‘new’ organ
Published in Drug Metabolism Reviews, 2018
Aneesh A. Argikar, Upendra A. Argikar
With the inclusion of mesentery, the total number of human organs has recently increased by one. The mesentery was formerly construed to be a complex, discontinuous anatomical structure simply serving as a support for organs in abdominal cavity. However, recent research has established the mesentery to be a far more simple and unfragmented organ. Newly emerging information on the mesentery has challenged some older pathophysiological concepts. This review briefly discusses the anatomy of the mesentery, historical perspective on the mesentery, embryology, drug metabolizing enzymes and transporters of the mesentery, and the mesentery’s role in diseases. The possible impact of the mesentery on absorption, distribution, metabolism, and excretion (ADME) is also discussed.
Strain Differences in the Facilitatory Action of Angiotensin on Noradrenergic Transmission in the Rat Mesentery
Published in Clinical and Experimental Hypertension, 1981
D. C. Eikenburg, R. D. Ekas, M. F. Lokhandwala
The isolated perfused rat mesenteric vasculature preparation was used to assess the contributions of presynaptic as well as postsynaptic mechanisms in the adrenergic potentiating action of angiotensin II in different rat strains. Angiotensin II (3 ng/ml; 2.5×10 12M) potentiated vasoconstrictor responses to periarterial nerve stimulation in mesentery obtained from Sprague-Dawley (SD) rats by 102.5±6.2% (p < .05) but did not significantly affect responses in mesentery from Wistar (W) rats. Responses to nerve stimulation were increased in W rats by 22.6±12.9% (p < .05) at higher concentrations of angiotensin II (10 ng/ml; 8.5×10-12M). The facilitatory actions of angiotensin II on nerve stimulation responses were antagonized by saralasin. Angiotensin II (2.5 or 8.5×10 12M) had little or no effect on responses to norepinephrine in mesentery from either SD or W rats. Blockade of neuronal and extraneuronal uptake potentiated the effects of angiotensin II on the responses to nerve stimulation in mesentery from W rats but not in mesentery from SD rats. The data suggest that angiotensin II increases norepinephrine release during nerve stimulation in mesentery obtained from SD and W rats. However, due to differences in the ability of the two strains of rats to compensate for the effect through increased neurotransmitter reuptake, the net effect on nerve stimulation responses is a large increase (100–110%) in SD rats as opposed to only a slight increase (15–20%) in W rats.
Mast Cell Degranulation and Parenchymal Cell Injury in the Rat Mesentery
Published in Microcirculation, 1999
JENNIFER J. COSTA, ANTHONY G. HARRIS, FRANK A. DELANO, BENJAMIN W. ZWEIFACH, GEERT W. SCHMID-SCHÖNBEIN
Objective:The objective of this study was to explore the degree of parenchymal cell injury after mast cell degranulation by application of compound 48/80 (CMP 48/80) in the absence of adherent leukocytes in the rat mesentery. Methods:Rats were rendered leukopenic by injection of an antibody against leukocytes, and the mesentery was superfused with CMP 48/80 during intravital microscopy. The extent of cell injury was determined using a fluorescent cellviability indicator, propidium iodide (PI). In an additional group, mast cell degranulation with CMP 48/80 was prevented by using the mast cell stabilizer Ketotifen. Results:After a reduction in the number of circulating leukocytes, mast cell degranulation produced a mild increase in parenchymal cell injury. The injury levels significantly increased when individual regions of the mesentery were compared. Stabilization of the mast cells with Ketotifen reduced the injury to below baseline values. Conclusions:In the absence of leukocyte adhesion to the endothelium, mast cell degranulation contributes to parenchymal cell injury in the mesentery.