Science topic
Peritonitis - Science topic
INFLAMMATION of the PERITONEUM lining the ABDOMINAL CAVITY as the result of infectious, autoimmune, or chemical processes. Primary peritonitis is due to infection of the PERITONEAL CAVITY via hematogenous or lymphatic spread and without intra-abdominal source. Secondary peritonitis arises from the ABDOMINAL CAVITY itself through RUPTURE or ABSCESS of intra-abdominal organs.
Questions related to Peritonitis
A very Emergency case, The Mother of my best friend, the results of her MRI said that she had nodular peritoneal thickening that suggested peritoneal serosal carcinoma, and ovarian cancer, also she has ascites, what is the source of ascites in case of high CA-125? We are suggesting a surgery to remove the ovarian, peritoneal biopsy and taking different samples to histology laboratory for culture and characterization, Any Informations would be helpful and well Appreciated, Many Thanks
Ali

With regard to patients suffering form spontaneous bacterial peritonitis, it seems counterintuitive that those patients tend to NEVER have anerobes as the causative agents despite the common leakage theory that should allow anerobes (that fill the gut) to leak whenever the opportunity is present? Is the leakage theory a sloppy theory? Do we need to tinker it a little bit? Should we adapt a new theory?! Or, should we go playing more in our labs hoping to uncover the real etiology and decipher this anerobes enigma?
I am trying to establish an ovarian cancer preclinical model through peritoneal injection into C57BL/6 mice.
The parental ID8 p53-/- cell line was modified through lentiviral infection in order to express OVA peptide and GFP-luciferase. We injected 5·10e^6 cells per mice.
In day 40 after injection we did not get any tumor in any of the mice.
Hello!
My SR with meta-analysis will be looking at risk-reducing salpingo oophorectomy on ovarian/peritoneal/falloptian tube cancer risks, as well as risk-reduction mastectomy on breast cancer risks in BRCA2+ carriers.
For the inclusion criteria, am I allowed to include people who previously had breast cancer in my search for the ovarian cancer risk-reducing salpingo-oophorectomy data and people who never had breast cancer before for the breast cancer mastectomy data?
Meaning, am I allowed to have two types of inclusion criteria in one SR as I have two study types being analyzed, or must it only contain people with/without breast cancer? The unifying factor is that all participants are BRCA2+ carriers and are women.
I hope this makes sense!!
I'm pretty sure they are mostly macrophages since after a 2 hour incubation in M199 they are stuck with pseudopodia. My slides just aren't pretty enough for me. I'm using Fisherbrand Wight-Giemsa Stain on rabbit cells from a peritoneal wash (days after drawing monocytes to the location with a peritoneal proteose peptone injection). But my concern is that at some point my counts are off because I can't distinguish between macrophages and other large multi-nucleated cells.
My method:
20uL of 10^6 Trypan blue visualized cells are spread, dried using a Bunsen burner, and then fixed with Methanol for 60s.
Slide is flooded with 1mL Wright-Giemsa Stain and incubated 2 minutes.
Add 1.5mL 1X PBS at pH 7. Gently tipped to mix, for 1 minute.
Stands for 2min.
Rinsed well with De-Ionized water.
Dried and visualized at 400X.
Does it have to air dry rather than use a flame?
I am just having a hard time with the outer membranes. Should I use a different method?
Any help is appreciated!
Women undergoing risk reducing bilateral salpingo-oophorectomy especially if they are BRCA1 or BRCA2 pathogenic variant carriers are warned of a residual risk of primary peritoneal cancer. A meta-analysis of studies showed only a 79% reduction in risk of ovarian type cancer after BSO in BRCA1 and BRCA2 carriers. Meaning for a BRCA1 carrier there could still be a 10% risk of primary peritoneal cancer with a high likely mortality rate. Having been involved in referring women to a gynaecological service that undertakes very careful surgery with bagging of the tubes and ovaries we have only now seen our first primary peritoneal cancer after more than 38 years of operations on nearly 600 carriers. Given that it is now thought that the great majority of high grade serous ovarian cancers originate from fimbrial precursor cells rather than for instance ovarian rest cells we feel that if careful surgery is undertaken early enough before the main risk period that this risk reduction is likely to be >95% rather than only 79%. This means a residual risk of only around 2% for BRCA1 and 1% for BRCA2. Do fellow clinicians agree?
I am studying phagocytosis/efferocytosis in vivo and have been using the peritoneum as a source of cells, but have a very low yield of dendritic cells. I also have a lot of CD19+ B-cells that take up 50-60% of the peritoneal exudate cells.
What would be the best tissue site for studying dendritic cell phagocytosis in vivo so that I can get a good yield.
Most protocols that use the peritoneum focus on macrophages.
In a stab or gunshot wound, is peritoneal violation alone (without any intra-abd. organ injuries) an indication for laparotomy? Previously I was under the impression that any time a non-sterile object is introduced into the peritoneum, it WILL get infected and cause peritonitis, and so you had to wash out the abdomen. However, it seems some stab wounds can be managed conservatively, even if it enters the peritoneum. So what is the general principle here?
by lavage peritoneal, could i get macrophages in high purity? and how many macrophages can i get by this procedure?
Please share your experience that may helpful to my experiment. Thanks.
Cause : Usage of Asbestos as insulator . Effect : Mesothelioma cancer ; Lung / peritoneal /larynx and ovary (8) cancer .
Hi!
Can anyone suggest a protocol for intracellular staining of peritoneal mast cells for cytokine detection by flow cytometry?
I wish to know if peritoneal injection of MSU in mice is proper study model for gout? Most common are air pouch model or ankle inflammation. Is peritoneal based gout model are clinically relevant?.
Hi!
In our lab, we are currently having a lot of trouble with extracting RNA from rat peritoneal mast cells. Mast cells were isolated from rat peritoneum and a method of Chomczynski was used to extract the RNA. We have obtained yields of 0.8 ug/uL RNA (from 0.5x106mast cells); A260/280 ~ 1,99. But in qRT-PCR we obtained unsatisfactory results.
Thanks a lot.
Elzbieta
a patient in septic shock on high vasopressors due to secondary peritonitis(?diverticular rupture) ,cannot be mobilized to CAT scan as surgeons requested
the ultrasound showed fluid with floating debris and sediment
can the drainage of the peritoneal cavity help to stabilize the patient even temporarily?
Are abdominal carcinoid carcinomas having peritoneal mets sensitive to chemotherapy agents used intraoperatively? Is cytoreduction surgery of peritoneal mets in carcinoid carcinomas complicated by potential for initiating neuroendocrine syndrome?
Hello,
We test the effect of different substances on the immune cells of the peritoneum. After activation we sort them and we now want to run a gene expression array.
The problem is that after they are activated cells of course start to migrate. This is especially problematic for the macrophages (they migrate super fast).
SO...
1. How do I block the migration of the macrophages?
2. How do I block migration of the B1a cells?
Your response would be very very very much appreciated!
Cheers!
Lambeck et al., (2007) detected that the median concentration of serum IL-7 in healthy patients is 2.9pg/ml. They have also detected that the median concentration of serum IL-7 in ovarian cancer patients is 5.3 pg/ml.
While Xie et al., (2004) have estimated that the median serum level of IL-7 in ovarian cancer patients is 32.49 pg/ml, and the median peritoneal level of IL-7 (mainly by tumor cells) in ovarian cancer patients is 17.39 pg/ml.
I need both the shedding rate and shedding fraction for IL-7, can I get them from its level (conc.) in the serum or the peritoneal fluid?
Trinder et al., (1999) have estimated that the production rate for IL-7 in renal cancer cell lines is ranging from 3.9 to 15.1 pg/ml/10^(6) cells/day. Can I benefit from this information in estimating the production rate for IL-7 in ovarian cancer?
Thanks in advance.
I wanted to stain for B-1 Cells in mouse peritoneal cryo samples. I dont know which antibodies should i use for the classification , B220 and CD5 are one which i thought i could use? Does anyone knows the sure/ correct method for the labelling of B1 cells in IHC..
Thank you
seeking your kind assistance...
Distinguishing between peritoneal and other (liver, lung, brain and bone) metastases for metastatic stomach adenocarcinomas can be important in directing chemotherapy. Was there a way to distinguish peritoneal metastases from the other metastatic sites using SEER data before 2010?
I want culture macrophage from peritoneal rat with alternative natural product than RPMI
Would this patient be at risk for peritonitis?
46year old woman who underwent open resection of Fundus for GIST 4years ago with recurrence at the site and two peritoneal nodules near the spleen.Ever since surgery she is being followed by a medical oncologist.Pet scan one year ago was normal.
36 years old male with advanced splenic flexure carcinoma with involvement of the anterior abdominal wall, stomach and small bowel. HPE revealed moderately differentiated (Greade 2 to 3) adenocarcinoma. pT4bN1bMx. Received 12 cycles of Folfurie with avastin. Now PET CT shows Hypermetabolic spots, one 1.4X1.6 cms at anastomotic site and another 1.4X1.5 at left hypochondrium region(Peritoneal deposits).
How often you meet false negative results at the relatively low but pathological levels of PMN in ascitic fluid (for example, polymorphonuclear cell count <500 cells/mm3)?
Hi all, I'm trying to do immunofluorescence on smears from peritoneal fluid, and I get some autofluorescence from eosinophils mainly. Does anyone know any method or something to avoid it? I usually do the washes with PBS+ tween 20 0'5%+ 1% triton-X. What do you think about it? thank you very much in advance.
Plz let me know about incidence(%) of osteomyelitis, Septic arthritis, Peritonitis through all ages in USA and EU.
I study a new vaccine for MRSA ..
I'm looking for a protocol for MGG staining protocol for BAL and peritoneal cells smears for the morphological assessment of the different cell populations.
Is it the same as the standard protocol used for blood smears?
We are studying the IL-1b secretion by TG-elicited mouse peritoneal macrophages, but saw a big variation in the amount of IL-1b secretion after LPS and ATP stimulation. We normalize the cytokine amount to the BCA data, and saw the IL-1b level could range from 30pg to~350pg per ug of cellular protein. We usually flush the peritoneal cells at 72hr after TG ip injection and culture the exudate cells in medium, at 37C overnight to allow macrophages to adhere. The following day, we will wash the cells once with PBS to remove the floating cells and stimulate the adherent macrophages with LPS (4hrs) and ATP(30mins. ATP in small aliquot, no freeze-thaw). The harvested supernatant will then undergo a brief spin (~3000rpm, 5mins) and IL-1b is measured by ELISA (R&D kit for mature mouse IL-1b). We used both male and female mice. But is such big variation in IL-1b level normal?
The peritoneal adhesions have been one of the major challenges for both the surgeons and the patients themselves. All treatment modalities ever suggested to solve the problem show low, if any, effectiveness. On the other hand, the serosal lining disappears on the posterior surfaces of the duodenum, pancreas, and the ascending and descending colon; the mesothelial 'processus vaginalis' in the spermatic cord vanishes as well during the embryonic development governing by some genes. So, one may expect that those very genes might become of use for the peritoneal adhesions to diminish or even to resolve completely.
I'm using REDCap for the first time and wanting to track peritonitis episodes in patients on peritoneal dialysis. These may happen multiple times per patient. There are no strictly defined visits (as there would be in a clinical trial) and there will be indefinite follow-up - I'm therefore using the traditional, and not the longitudinal, REDCap setup.
I'm thinking that I should have a new/different data entry form for each episode of peritonitis e.g. episode1, episode2, etc. This just feels very clumsy though so I would appreciate any other suggestions.
Thanks
Razeen
I want to generate polyclonal sera in mice by injecting hybridomas in peritoneal cavity of mice. Could anybody recommend a simple protocol to isolate the cells from peritoneal cavity once again!
Regards
A lady, 29 years old, five years history of Crohn disease, quite moderate. No family history traced.
The patient referred to the gastroenterologic department on the 6th of May with a vague abdominal pain, subfebrile body temperature, and sulfosalicilates were prescribed 500 mg thrice a day. On the 8th of May, about 7.00 a.m. a bout of severe pain along the whole stomach. A surgeon on duty examination was performed, and the patient was transferred to the 1st department of Surgery at 7.15. A pneumoperitoneum under the diaphragm was recognized on the X-ray upright position. The lady was taken into operation room, and the midline incision was made. Approximately 2 L of the intestinal contents was revealed in the abdominal cavity. Futher examination discovered a loose inflammatory mass in the right iliac fossa, and a perforation of the mesenteric border of the ileum as less as 10 cm from the ileocaecal junction.
I have never met before a perforation into the free abdominal cavity due to the Crohn disease. What would be the best way to complete the operation? What medication would be the best choise for the patient?
Some say, a methylene blue test, but others say it may cause chemical peritonitis.
Is glucose measurement a reliable test?
What are some other diagnostic tests and how are they performed?
Distention of the small intestine loops by liquid and gas content, along with contemporarily disappearance of the colon 'pneumatization', are characteristic for the severe secondary and for the tertiary peritonitis cases. One may suggest that either phenomena are developed due to, or connected, with dramatic changes of both the small and large intestines microflora quantity and quality.
However, I could find no data on this matter. I would be obliged for any help on the topic.
I'm trying to identify the effect of different cytokines on the level of F4/80 expression in macrophages from the peritoneum that may be produced when sterile inflammation is induced. I understand I will be checking in isolation and in vivo, as it maybe different.
One of my 40 year old patients, since 6 months on PD has from the start a complete symptom free phenomenon of a pink bag every morning after the long dwell. He is completely syymptom free, has no secondary symptoms suspicious for malignancy and no weight loss. He has stable blood results including a normal Haemoglobin without EPO. Hardly any WBC, cultures all negative. The exit site looks great and there has been no peritonitis. Abdo US normal with normal catheter position. He is a high average transporter and ultrafiltrates well on low concentration standard dextrose bags.
I tend not to worry about it. Anybody here different opinion and any further explanations?