eMedicine Specialties > Oncology > Carcinomas of the Gastrointestinal Tract

Peritoneal Cancer

Wissam Bleibel, MD, Staff Physician, Department of Internal Medicine, Caritas Carney Hospital, Tufts University School of Medicine
Olga Kozyreva, MD, Fellow, Department of Hematology-Oncology, Tufts University School of Medicine; Sarah K May, MD, Consulting Staff, Department of Hematology-Oncology, Caritas Carney Hospital, Commonwealth Hematology-Oncology PC; Daniel Efiom-Ekaha, MD, Fellow in Hematology/Oncology, Department of Internal Medicine, State University of New York-Downstate; Arunbhai G Patel, MD, Chief, Department of Internal Medicine, Division of Hematology-Oncology, Brooklyn Hospital Center; Adekunle Kuku, MD, Staff Physician, Department of Internal Medicine, Brooklyn Hospital Center

Updated: Jul 23, 2007

Introduction

Background

The peritoneum is a serous lining of mesothelial cells with rich vascular and lymphatic capillary network that covers the abdominal and pelvic walls and organs. Peritoneal neoplasia can originate de novo from the peritoneal tissues (primary) or invade or metastasize into the peritoneum from adjacent or remote organs (secondary).

A number of primary cancers have been described to originate from the peritoneum, some of which have been implicated in many cases of carcinomas of unknown primary origin. Ovarian cancer arising in women several years after bilateral oophorectomy is believed to be one of these primary peritoneal cancers. Other described primary peritoneal cancers and tumors include malignant mesothelioma, benign papillary mesothelioma, desmoplastic small round cell tumors, peritoneal angiosarcoma, leiomyomatosis peritonealis disseminata (LPD), and peritoneal hemangiomatosis.

Pathophysiology

The peritoneal cavity, enclosed by visceral and parietal peritonea, is the largest potential space in the body. Any pathologic process involving the peritoneal cavity can easily disseminate throughout this space by means of unrestricted movement of fluid and cells.

Primary malignant diseases arising from the peritoneal cavity include malignant mesothelioma, cystic mesothelioma, primary peritoneal carcinoma, and desmoplastic small round cell tumor. 

Malignant mesothelioma

Malignant peritoneal mesothelioma is a rare but aggressive tumor derived from the peritoneal mesothelium. Although most mesotheliomas involve the pleural surface, 20-30% arise from the peritoneum and are associated with asbestos exposure and abdominal therapeutic radiation. Association of malignant peritoneal mesothelioma and asbestos exposure has been reported to be as high as 83%.

Mesotheliomas are composed of strands of connective tissue covered by cells that react positively to periodic acid-Schiff staining in the cytoplasm. These cells grow in multiple layers, forming papillary or tubular formations. Histologically malignant mesothelioma is classified into epithelial, sarcomatoid, and mixed. Clinical features of malignant mesothelioma include abdominal pain, abdominal or pelvic masses, and thrombocytosis with ascites being the major factor in the disease morbidity and mortality. Rarely, the tumor tends to spread into the pleural space.

On CT scan, this neoplasm can appear as peritoneum-based masses or abdominal ascites with associated nodular or diffuse peritoneal thickening.

This locally aggressive disease is difficult to treat or palliate and, commonly, treatment regimens combine aggressive cytoreductive surgery with intraperitoneal chemotherapy.

Thorough cytoreductive surgery is the cornerstone of current treatment, while hyperthermic intraoperative intraperitoneal chemotherapy (HIIC) is a promising strategy in suitable patients.

Cystic mesothelioma

Cystic mesothelioma is a rare intermediate-grade tumor with a predilection for surfaces of the pelvis. Typically, these lesions consist of multiple grapelike clusters of mesothelium-lined cysts separated by fibrous tissue. The nomenclature for this entity is confusing, and several synonyms (eg, multilocular peritoneal inclusion cyst, cystic mesothelioma) are used interchangeably in the literature.

This rare tumor commonly occurs in young to middle-aged women and typically presents with abdominal pain, tenderness, or distension.

Radiologic tests demonstrate thin-walled cysts containing watery secretions, easily seen on ultrasound, CT scan, and MRI.

Some authors reported effective intraperitoneal chemotherapy, but no clinical study is available about long-term outcome. The short-term prognosis is favorable, although it can recur in 25–50% of cases.

The differential diagnoses include lymphangioma, mesenteric-omental cysts, ovarian cystadenoma and cystadenocarcinoma, cystic teratoma, pseudomyxoma peritonei, cystic smooth muscle tumors, visceral cysts, and endometriosis.

Primary peritoneal carcinoma

Primary peritoneal carcinoma (ie, serous surface papillary carcinoma) arises primarily from peritoneal cells. The mesothelium of the peritoneum and the germinal epithelium of the ovary arise from the same embryologic origin; therefore, the peritoneum may retain the multipotentiality allowing the development of a primary carcinoma.

This rare malignancy predominantly affects postmenopausal women typically with multicentric peritoneal and omental involvement. It resembles papillary serous ovarian carcinoma in pathological and clinical aspects. This malignancy is differentiated from its ovarian counterpart by the fact that it involves the extraovarian peritoneum significantly and the ovarian surface minimally or not at all. Extensive calcification or omental caking is present in many cases and is a useful CT finding to exclude mesothelioma. The absence of an ovarian mass is critical for excluding metastatic papillary serous ovarian carcinoma, which otherwise has a similar CT appearance.

Treatment of this malignancy is very similar to that of epithelial ovarian cancer, which includes combination chemotherapy after optimal cytoreductive surgery.

Desmoplastic small round cell tumor

This tumor is a highly aggressive malignancy that has recently been described. It involves the peritoneal cavity in most cases. Unlike the other primary peritoneal neoplasms, desmoplastic small round cell tumor (DSRCT) most often affects young adults. This malignancy extensively and rapidly invades the peritoneal surfaces with hematogenous metastasis to the liver, lungs, and lymph nodes.

Cytologically, DSRCT is a highly cellular tumor composed of small round cells with granular chromatin, nuclear molding, and inconspicuous nucleoli that are arranged singly and in clusters. This tumor exhibits a unique immunohistochemical profile, characterized by coexpression of epithelial (keratin and epithelial membrane antigen), neural (neuron-specific enolase and CD56), mesenchymal (vimentin), and myogenic (desmin) markers. The reciprocal chromosomal translocation t (11; 22)(p13; q12) is also specific for DSRCT.

Radiological investigation shows multiple rounded peritoneal masses with or without ascites. The omentum and paravesical regions are often involved.

The recommended treatment is a combination of multiagent chemotherapy with adjuvant surgery and radiation. The overall survival for people with this disease is poor despite aggressive treatment.

Other neoplasms

In addition to the above-mentioned primary peritoneal malignancies arising from the peritoneal lining, various types of neoplasms may develop from mesenchymal and lymphatic tissues of the abdominal and pelvic cavities. This includes different forms of sarcomas, histiocytoma, gastrointestinal stromal tumors (GIST), and lymphoproliferative malignancies. Moreover, the differential of peritoneal malignancies includes many benign tumors derived from lymphatic, vascular, neuromuscular, or fatty tissues.

Frequency

United States

All of the primary peritoneal cancers are rare. Primary peritoneal carcinoma is very uncommon. Peritoneal mesotheliomas are also rare, with 2 cases per 1 million population reported each year. However, the incidence appears to be increasing. Based on the prior use of asbestos, more than 8 million people in the United States were exposed and at risk. Benign cystic peritoneal mesotheliomas are rare.

Mortality/Morbidity

• Survival is poor for patients with primary peritoneal carcinoma, with 100% mortality; the median survival reported is 12-25 months, even with extensive surgery and chemotherapy.
• Benign cystic peritoneal mesotheliomas are associated with prolonged survival despite bulky disease.
• Desmoplastic small round cell tumors are associated with a reported median survival of 17 months.

Sex

• Primary peritoneal carcinoma is a rare tumor that occurs almost exclusively in women.
• Malignant mesotheliomas show extreme male predominance (93% in one series).

Age

• Patients with primary peritoneal carcinoma are older than patients with epithelial ovarian cancers.
• Desmoplastic small round cell tumors occur in adolescent persons and young men.
• Benign cystic peritoneal mesotheliomas are rare and are found predominantly in younger women.
• Most cases of leiomyomatosis peritonealis disseminata have been discovered in reproductive-aged women (mean age 37 y), in young pregnant women, and in women who have hormonal excess for any other reason. In most reported cases, nodules either regress or exhibit growth once the hormonal stimulation has been removed.

Clinical

History

• Primary peritoneal carcinoma usually manifests with abdominal distention and diffuse nonspecific abdominal pain secondary to ascites. This tumor is described almost exclusively in women. Atypical presentations of primary peritoneal carcinoma have been described, including a case of severe glandular dysplasia on a screening Papanicolaou test (Pap smear).
• Malignant peritoneal mesothelioma usually manifests with symptoms and signs of advanced disease, including pain, ascites, weight loss, or an abdominal mass.
  • These tumors tend to manifest with diffuse involvement of the peritoneal cavity, including omental caking and diaphragmatic and pelvic tumor deposits.
  • Thrombocytosis is common and is associated with a poor prognosis.
  • Other common clotting abnormalities include phlebitis, emboli, hemolytic anemia, and disseminated intravascular coagulation.
  • Esophageal achalasia, secondary amyloidosis, and dermatomyositis have been reported.
  • Most patients die without metastasis or involvement of the chest.
• Desmoplastic small round cell tumors occur typically in young patients and manifest with extensive involvement of the peritoneal surfaces. Rapid multifocal growth and hematogenous metastasis to the liver, lungs, and lymph nodes are common.
• Leiomyomatosis peritonealis disseminata is found most commonly in women of reproductive age who are pregnant; these patients are usually asymptomatic, have a long-term history of oral contraceptive use, or have uterine leiomyomas at the time of diagnosis. All cases of this disease have been discovered intraoperatively during obstetric and gynecologic surgical procedures.
• Peritoneal hemangiomas are usually associated with hemangiomas of the GI tract. They are rare and can manifest with ascites, anemia (from chronic blood loss), thrombocytopenia, and coagulopathy.

Causes

• A chromosomal translocation, which results in the fusion of the Ewing sarcoma gene with the Wilms tumor gene, has been identified and implicated in desmoplastic small round cell tumors.
• Hereditary predisposition may play a role in primary peritoneal carcinoma because patients with the BRCA1 mutation have an increased risk.
• Although conventional wisdom dictates that asbestos is the environmental factor most commonly associated with mesothelioma, asbestos does not transform human mesothelial cells in tissue culture. This suggests that additional carcinogens act in concert with asbestos to cause mesothelioma.

Differential Diagnoses

Ovarian Cysts

Other Problems to Be Considered

The differential diagnosis of primary peritoneal cancers includes peritoneal metastasis (ie, peritoneal carcinomatosis) from primary sites including the GI tract, ovaries, or breast or as part of the syndrome of adenocarcinomas of unknown primary site. Although the primary histology findings dictate the clinical course, important concepts of diagnosis and treatment are common to all forms. The most important risk factor for developing peritoneal carcinomatosis is the depth of invasion of the primary tumor.

Reactive tumorlike lesions of the peritoneum have been described and should be included in the differential diagnosis of primary peritoneal cancers, as follows:

• Granulomatous lesions
  • Vernix caseosa and meconium peritonitis
  • Granulomatous peritonitis secondary to foreign material, including keratin
  • Necrotic pseudoxanthomatous nodules
  • Postcautery granulomas
• Nongranulomatous histiocytic lesions
  • Ceroid-rich histiocytic infiltrates
  • Peritoneal melanosis
  • Mucicarminophilic histiocytosis
  • Other histiocytic infiltrates
• Fibrosing lesions
  • Sclerosing peritonitis
  • Peritoneal fibrosis nodules
• Mesothelial lesions
  • Mesothelial hyperplasia
  • Peritoneal inclusion cysts

Workup

Laboratory Studies

Malignant peritoneal mesothelioma: Findings from cytologic examination of ascites can suggest the diagnosis, and findings from percutaneous biopsy of the omentum can help verify the diagnosis. This condition is usually confined to the abdomen at the time of diagnosis.

Imaging Studies

• Standard imaging tests, including ultrasonography and helical CT scans, are notably insensitive for the detection of peritoneal tumors.
  • The sensitivity of CT scans for peritoneal nodules measuring smaller than 1 cm is approximately 15-30%.
  • Ultrasonography is similarly insensitive; therefore, considering findings, rather than solid tumor detection, that may suggest the presence of peritoneal lesions is important. These include the presence of ascites, fixing together of bowel loops, thickening of mesentery, and omental matting.
• CT scan findings are nonspecific in primary papillary serous carcinoma of the peritoneum. Consider this diagnosis when findings include ascites, omental caking, and diffuse enhancement with nodular thickening of the parietal peritoneum of the pelvis observed with normal-sized ovaries, with or without a fine enhancing surface nodularity of the ovary.
• Some studies show that MRI is superior to helical CT scan for the detection of peritoneal and bowel wall abnormalities.
• Positron emission tomography imaging has not been shown to be sensitive for lesions smaller than 1 cm in the abdominal cavity.
• Findings from radionuclide scan studies can help confirm the diagnosis of peritoneal hemangiomas; the isotope concentrates in the area where platelets are being sequestered. A CT scan and ultrasound also may detect larger hemangiomas. Angiographic evaluation is a more precise, although invasive, procedure when radionuclide scans, CT scan, and ultrasound findings are negative.

Procedures

• Procedures for the workup of peritoneal lesions include peritoneal lavage cytology. This can be performed using a cutaneous closed technique or at the time of laparoscopy or laparotomy. The sensitivity of the test results depends on the ability to completely lavage all regions of the peritoneal cavity and the ability to detect cancer cells being shed into the peritoneal cavity by the tumor.
• Direct visualization of the peritoneal surfaces along with palpation of the abdominal contents is by far the most sensitive modality for detecting peritoneal cancer. This can be accomplished with a minimally invasive approach (ie, laparoscopy), which allows for safe, directed peritoneal lavage for cytology and with open abdominal exploration and palpation of the peritoneal surfaces. Open abdominal exploration and palpation are extremely sensitive for 1- to 2-mm peritoneal nodules.

Histologic Findings

Primary peritoneal carcinoma is histologically indistinguishable from primary epithelial ovarian carcinoma; however, primary ovarian cancer can be excluded based on certain criteria. First, both ovaries must be of normal in size. Second, the extraovarian involvement must be greater than the involvement on the surface of the ovary. Third, the ovarian component must be smaller than 5 by 5 mm within the ovary or confined to the ovarian surface. Finally, the cytologic characteristics must be of the serous type.

Treatment

Medical Care

• The therapeutic approach of peritoneal mesothelioma involves surgical cytoreduction followed by one of various regimens of intraperitoneal hyperthermic chemotherapy. In addition to the intraoperative use of heated chemotherapeutic drugs such as cisplatin, mitomycin, or doxorubicin, newer techniques include adding immunotherapeutic agents such as interleukins and interferons. Multimodality therapy is currently the most commonly accepted therapeutic approach. This includes using combined therapeutic methods such as cytoreduction, intraperitoneal perioperative chemotherapy, and hyperthermia. Intraperitoneal chemotherapy greatly enhances drug concentrations in the peritoneal cavity and decreases its systemic toxicity. While the median survival with traditional therapeutic options ranges between 4 and 12 months, the application of multimodality therapy has shown promising results with increased survival approaching 60 months.
• For patients with unresectable or recurrent disease malignant mesothelioma, palliative systemic chemotherapy (with different regimens such as cisplatin plus pemetrexed) should be considered. Other antineoplastic agents that may be used include cisplatin plus paclitaxel or mitomycin, doxorubicin, and irinotecan. Furthermore, intraperitoneal instillation of radioactive colloidal gold Au 198 has been reported to improve symptoms of peritoneal mesothelioma.
• Primary peritoneal carcinoma is treated similarly to ovarian cancer, with cytoreduction and chemotherapy. The multimodality treatment consisting of debulking of the tumor followed by 5-fluorouracil-, doxorubicin-, or cisplatin-based regimens has been shown to have high response rate and improvement of median survival. Furthermore, the use of single newer antineoplastic agents such as taxanes, topoisomerase I inhibitors, gemcitabine, and vinorelbine or their combinations (gemcitabine/cisplatin, irinotecan/cisplatin, docetaxel/gemcitabine, gemcitabine/carboplatin) has increased median survival to 8-11 months. In addition to the use of chemotherapeutic agents, recent studies have shown some benefit of antiangiogenic drugs such as bevacizumab and erlotinib.
  
  
  • It is generally accepted that all patients with good performance status should be considered for a trial of empiric chemotherapy, preferably with a regimen containing newer drugs. The combination of paclitaxel and carboplatin is a reasonable first-line therapy with possible benefit from adding a third agent (etoposide or gemcitabine).
  • Supportive measures should be considered in patients with poor performance status.

Surgical Care

• Treatment of primary peritoneal carcinoma consists of total abdominal hysterectomy and bilateral salpingo-oophorectomy as needed, with debulking of tumor and follow-up chemotherapy.
• Treatment of malignant peritoneal mesothelioma consists primarily of surgical palliation. Complete surgical resection is rarely, if ever, feasible and has not been shown to afford a survival benefit in the absence of additional therapy. If laparoscopy is used to help make the initial diagnosis, confine port sites to the abdominal midline because port site recurrence has been described, requiring extensive abdominal wall resection.
• Benign cystic mesothelioma tends to recur even with aggressive surgical removal; however, among recorded cases, no deaths have been attributable to this process.
• A combination of aggressive surgical debulking and systemic chemotherapy with cyclophosphamide, doxorubicin, and vincristine interspersed with ifosfamide, etoposide, and mesna (P6 protocol) appears to lead to an improved outcome in patients with desmoplastic small cell tumors.
• Treatment of peritoneal and GI hemangiomas has involved surgical removal.

Medication

The goals of pharmacotherapy are to induce remission, to prevent complications, and to reduce morbidity.

Chemotherapeutic agents

These drugs inhibit cell growth and proliferation. Agents used include cisplatin, doxorubicin, cyclophosphamide, carboplatin, and paclitaxel.

Cisplatin (Platinol)

Inhibits DNA synthesis and thus cell proliferation by causing DNA cross-links and denaturation of double helix.

Dosing

Adult

75-100 mg/m² q3wk IV; 90-270 mg/m² IP; retain 4 h before draining with systemic sodium thiosulphate

Pediatric

30-100 mg/m² IV q2-3wk

Interactions

Increases toxicity of bleomycin and ethacrynic acid

Contraindications

Documented hypersensitivity; preexisting renal insufficiency, myelosuppression, and hearing impairment

Precautions

Pregnancy

D - Unsafe in pregnancy

Precautions

Administer adequate hydration before and 24 h after dosing to reduce risk of nephrotoxicity; hyperuricemia, nausea and vomiting, myelosuppression, anemia, peripheral neuropathy, ototoxicity, nephrotoxicity, acute renal failure, bradycardia, arrhythmia, mild alopecia, SIADH, hypomagnesemia, hypocalcemia, hypokalemia, hypophosphatemia, mouth sores, elevated liver enzymes, phlebitis, optic neuritis, blurred vision, and papilledema may occur; symptoms of overdosage include severe myelosuppression, intractable nausea and vomiting, kidney and liver failure, deafness, ocular toxicity, and neuritis; use proper handling and disposal

Doxorubicin (Adriamycin, Rubex)

Inhibits topoisomerase II and produces free radicals, which may cause the destruction of DNA. Combination of these events can, in turn, inhibit the growth of neoplastic cells.

Dosing

Adult

60-75 mg/m² IV as single dose, repeat q21d; 20-30 mg/m²/d IV for 2-3 d, repeat in 4 wk; or 20 mg/m² IV once/wk

Pediatric

35-75 mg/m² IV as single dose, repeat q21d; 20-30 mg/m² IV once weekly; or 60-90 mg/m² continuous IV infusion over 96 h q3-4wk

Interactions

May decrease phenytoin and digoxin plasma levels; phenobarbital may decrease plasma levels; cyclosporine may induce coma or seizures; mercaptopurine increases toxicity; cyclophosphamide increases cardiac toxicity

Contraindications

Documented hypersensitivity; severe heart failure; cardiomyopathy; impaired cardiac function; preexisting myelosuppression

Precautions

Pregnancy

D - Unsafe in pregnancy

Precautions

Extravasation may result in severe local tissue necrosis; reduce dose in patients with impaired hepatic function; use proper handling and disposal; total dose not to exceed 550 mg/m² or 400 mg/m² in patients with previous or concomitant treatment (ie, with daunorubicin, cyclophosphamide, or irradiation of the cardiac region); alopecia, nausea and vomiting, mucositis, ulceration and necrosis of the colon, anorexia and diarrhea, stomatitis, esophagitis, red discoloration of urine, myelosuppression, and cardiac toxicity may occur
Acute arrhythmia, heart block, pericarditis-myocarditis, and chronic cardiac toxicity as congestive cardiac failure may occur; facial flushing, hyperpigmentation of nail beds, erythematous streaking along the vein if administered too rapidly, hyperuricemia, fever, chills, urticaria, conjunctivitis, allergic reaction, and anaphylaxis may occur; radiation recall noticed in patients who have had prior irradiation; symptoms of overdosage include myelosuppression, nausea, vomiting, and myocardial toxicity

Carboplatin (Paraplatin)

Analog of cisplatin. Has same efficacy as cisplatin but with better toxicity profile.
Dose is based on following formula:
Total dose (mg) = (target AUC) X (GFR = 25), where AUC (area under plasma concentration-time curve) is expressed in mg/mL/min and GFR (glomerular filtration rate) is expressed in mL/min.

Dosing

Adult

360 mg/m² IV q3wk as monotherapy or 300 mg/m² q4wk as combination therapy

Pediatric

300-600 mg/m² IV q4wk

Interactions

Nephrotoxicity increases with aminoglycosides and other nephrotoxic drugs

Contraindications

Documented hypersensitivity; bone marrow suppression

Precautions

Pregnancy

D - Unsafe in pregnancy

Precautions

Monitor bone marrow function; use proper handling and disposal; high doses have resulted in severe LFT abnormalities; increased risk of allergic reactions if previously exposed to platinum therapy; hypocalcemia, hypomagnesemia, hyponatremia, hypokalemia, nausea, vomiting, stomatitis, myelosuppression, asthenia, alopecia, diarrhea, anorexia, peripheral neuropathy, and ototoxicity may occur; symptoms of overdosage include bone marrow suppression and hepatic toxicity

Cyclophosphamide (Neosar, Cytoxan)

Chemically related to nitrogen mustards. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Dosing

Adult

50-100 mg/m²/d PO continuous therapy or 400-1000 mg/m² PO in divided doses 4-5 d intermittent therapy

Pediatric

Administer as in adults

Interactions

Allopurinol may increase risk of bleeding or infection and enhance myelosuppressive effects; may potentiate cyclophosphamide-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones; chloramphenicol may increase half-life while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Contraindications

Documented hypersensitivity; severely depressed bone marrow function

Precautions

Pregnancy

D - Unsafe in pregnancy

Precautions

Regularly examine hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine urine for RBCs, which may precede hemorrhagic cystitis; use proper handling and disposal
Adverse effects include alopecia, sterility, nausea and vomiting, diarrhea, stomatitis, mucositis, jaundice, headache, skin rash, facial flushing, myelosuppression, cardiac dysfunction, dizziness, darkening of skin/fingernails, hyperglycemia, hypokalemia, hyperuricemia, SIADH, acute hemorrhagic cystitis, hepatic toxicity, renal tubular necrosis, nasal congestion, interstitial pulmonary fibrosis, and secondary malignancy (alone or in combination with other antineoplastics)
Both bladder carcinoma and acute leukemia are well documented; symptoms of overdosage include myelosuppression, alopecia, nausea, and vomiting

Paclitaxel (Taxol)

Mechanisms of action are tubulin polymerization and microtubule stabilization.

Dosing

Adult

175 mg/m² IV over 3 h q3wk; alternatively, 135 mg/m² IV over 24 h q3wk

Pediatric

Not established

Interactions

Coadministration with cisplatin may further increase myelosuppression

Contraindications

Documented hypersensitivity to paclitaxel or polyoxyethylated castor oil; peripheral neuropathy; bone marrow suppression; liver failure; severe cardiac disease

Precautions

Pregnancy

D - Unsafe in pregnancy

Precautions

Premedicate with steroids, H1 blockers, and H2 blockers to decrease risk of hypersensitivity reactions; current evidence indicates that prolongation of infusion >6 h plus premedication may minimize this effect; adverse reactions include hypotension, abnormal ECG tracings, alopecia, nausea and vomiting, diarrhea, mucositis, bleeding anemia neutropenia, thrombocytopenia, abnormal LFT results, peripheral neuropathy, myalgia, bradycardia, and radiation pneumonitis in patients receiving concurrent radiotherapy

Follow-up

Further Inpatient Care

• Follow up to evaluate patients for complications of the cancer, spread of the cancer, and possible complications of therapy.
• Screening is also essential to help rule out known associated cancers and cancer syndromes.

Prognosis

• Patients with peritoneal mesothelioma generally have a better prognosis than those with pleural mesothelioma. Original reports suggest a median survival of less than 1 year from the time of diagnosis; however, multiple varied treatment approaches may prolong long-term survival.
• For further information about survival of particular peritoneal malignancies, refer to Mortality/Morbidity.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose and appropriately treat cancers and precancerous lesions
• Failure to monitor to detect cancer recurrence and complications
• Failure to detect adverse effects and complications of therapy
• The diagnosis of malignant peritoneal mesothelioma could be work-related, and a thorough discussion with the patient is warranted.
• In case of malignant peritoneal mesothelioma, the legal implications are tremendous, primary prevention is important, and employers should limit the amount of asbestos exposure to the lowest levels possible. Having work standards in place is important.

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Keywords

ovarian cancer, malignant mesothelioma, benign papillary mesothelioma, desmoplastic small round cell tumors, DSRCT, peritoneal angiosarcoma, leiomyomatosis peritonealis disseminata, LPD, peritoneal hemangiomatosis, primary peritoneal cancer, peritoneal malignancy, peritoneum, peritoneal carcinoma, peritoneal carcinoma, abdominal therapeutic radiation, radiation therapy, asbestos exposure, cystic mesothelioma, multilocular peritoneal inclusion cyst, primary peritoneal carcinoma, serous surface papillary carcinoma

Contributor Information and Disclosures

Author

Wissam Bleibel, MD, Staff Physician, Department of Internal Medicine, Caritas Carney Hospital, Tufts University School of Medicine
Wissam Bleibel, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Olga Kozyreva, MD, Fellow, Department of Hematology-Oncology, Tufts University School of Medicine
Disclosure: Nothing to disclose.

Sarah K May, MD, Consulting Staff, Department of Hematology-Oncology, Caritas Carney Hospital, Commonwealth Hematology-Oncology PC
Sarah K May, MD is a member of the following medical societies: American Society of Clinical Oncology
Disclosure: Nothing to disclose.

Daniel Efiom-Ekaha, MD, Fellow in Hematology/Oncology, Department of Internal Medicine, State University of New York-Downstate
Daniel Efiom-Ekaha, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.

Arunbhai G Patel, MD, Chief, Department of Internal Medicine, Division of Hematology-Oncology, Brooklyn Hospital Center
Arunbhai G Patel, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.

Adekunle Kuku, MD, Staff Physician, Department of Internal Medicine, Brooklyn Hospital Center
Disclosure: Nothing to disclose.

Medical Editor

Robert C Shepard, MD, FACP, Associate Professor of Medicine in Hematology and Oncology at University of North Carolina at Chapel Hill; Vice President of Scientific Affairs, Therapeutic Expertise, Oncology, at PRA International
Robert C Shepard, MD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physician Executives, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Medical Association, American Medical Informatics Association, American Society of Clinical Oncology, American Society of Hematology, Association of Clinical Research Professionals, Eastern Cooperative Oncology Group, European Society for Medical Oncology, Massachusetts Medical Society, and Society for Biological Therapy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Benjamin Movsas, MD, Vice-Chairman, Department of Radiation Oncology, Fox Chase Cancer Center
Benjamin Movsas, MD is a member of the following medical societies: American College of Radiology, American Radium Society, American Society for Therapeutic Radiology and Oncology, and American Society of Clinical Oncology
Disclosure: Nothing to disclose.

CME Editor

Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD, Visiting Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine at Tucson; Consulting Staff, Arizona Cancer Center
Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Federation for Clinical Research, American Society of Clinical Oncology, American Society of Hematology, Central Society for Clinical Research, Society for Biological Therapy, and Society for Leukocyte Biology
Disclosure: GlobeImmune Salary Consulting; Amplimed Consulting fee Consulting

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