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Anesthesia & Analgesia:
doi: 10.1213/ANE.0b013e3182860fff
General Articles: Special Article

An Overview of Cytoreductive Surgery and Hyperthermic Intraperitoneal Chemoperfusion for the Anesthesiologist

Webb, Christopher Allen-John MD; Weyker, Paul David MD; Moitra, Vivek K. MD; Raker, Richard K. MD

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From the Department of Anesthesiology, Columbia University College of Physicians & Surgeons, Columbia University Medical Center, New York, New York.

Accepted for publication December 17, 2012.

The authors declare no conflicts of interest.

Reprints will not be available from the authors.

Address correspondence to Richard K. Raker, MD, Department of Anesthesiology, Columbia University College of Physicians & Surgeons, Columbia University Medical Center, 622 West 168th St., PH 5-505, New York, NY, 10032. Address e-mail to rkr1@columbia.edu.

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Abstract

Anesthesiologists face several perioperative challenges when patients need cytoreductive surgery and hyperthermic intraperitoneal chemoperfusion. To adequately care for these patients, anesthesiologists must understand the goals and objectives of the operation in addition to having a basic knowledge of the chemotherapeutic drugs that are frequently used. Optimal anesthetic management of patients treated with cytoreductive surgery and hyperthermic intraperitoneal chemoperfusion requires control of a complex interplay of physiologic mechanisms, including hyperthermia, abdominal hypertension, electrolyte abnormalities, coagulopathies, increased cardiac index, oxygen consumption, and decreased systemic vascular resistance. As this surgery continues to gain popularity among oncologic surgeons, further studies that clearly define the chemistry, pharmacokinetics, pharmacodynamics, and end points of efficacy need to be performed to elucidate optimal perioperative management.

Peritoneal surface oncology is a rapidly evolving subspecialty that manages a group of neoplasms collectively termed peritoneal surface malignancies. Clinically, this group of malignancies is categorized into peritoneal carcinomatosis secondary to abdominal, pelvic, or extraabdominal malignancies; pseudomyxoma peritonei; and primary peritoneal tumors.1 Current treatments combine cytoreductive surgery (CRS) with hyperthermic intraperitoneal chemoperfusion (HIPEC).2–5 In our opinion, there is insufficient information available within the anesthesiology literature to educate anesthesiologists on the goals and objectives of the operation, the anticipated metabolic and physiologic derangements, and the potential chemotherapeutic toxicities. In this article, we present an overview of the current literature as well as the anesthetic considerations and perioperative management of the patient undergoing CRS and HIPEC for peritoneal surface malignancies.

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PERITONEAL SURFACE MALIGNANCIES

Peritoneal surface malignancies are categorized as peritoneal carcinomatosis, pseudomyxoma peritonei, or primary peritoneal tumors.1

Peritoneal carcinomatosis is a tumor that spreads over the peritoneal surfaces secondary to gynecologic (frequently ovarian tumors) and nongynecologic tumors (frequently gastric and colorectal cancer) that seed the peritoneum. Although the use of HIPEC is still rare, these diseases are not.2,6 There are 20,000 ovarian carcinomas in the United States per year, 60% presenting as stage III or IV (most of these with carcinomatosis),7 and 140,000 colorectal cancers in the United States per year, approximately 10% presenting with carcinomatosis.7 Nongynecologic tumors that metastasize to the peritoneum are usually gastrointestinal in origin, with gastric cancer and colorectal cancer being the more common causes of secondary peritoneal carcinomatosis.2,6 Median survival rates in patients with untreated peritoneal carcinomatosis are less than 7 months for nongynecologic tumors and less than 15 months for gynecologic tumors.8

Pseudomyxoma peritonei is a rare disease that frequently arises from mucinous appendiceal tumors and is characterized by mucinous ascites and peritoneal implants.6,9–12 This cancer often presents with progressive abdominal distention caused by the accumulation of mucinous ascites. Five-year survival rates are improved with CRS and HIPEC treatment compared with treatment with systemic chemotherapy alone (86% vs 44%).11

Primary peritoneal tumors are usually diffuse malignant peritoneal mesotheliomas, an uncommon yet fatal group of cancers that account for 10% to 30% of all mesotheliomas diagnosed in the United States with up to 400 new cases in the United States every year.1,5,13,14 Median survival rates range from 9 to 15 months in patients with these mesotheliomas who are treated with palliative surgery with or without systemic chemotherapy.14

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Surgical Evaluation

Successful management of patients who have peritoneal surface malignancies with CRS and HIPEC involves assessment of the extent of systemic disease via positron emission tomography and computerized tomography scans of the chest, abdomen, and pelvis.15 In the setting of peritoneal carcinomatosis of colorectal origin, patients with fewer than 3 small hepatic metastases, absence of biliary obstruction, and a successful response to systemic chemotherapy are the most optimal candidates for CRS and HIPEC.15 Selection criteria for CRS and HIPEC include medical optimization with no active cardiac conditions as defined by the American Heart Association guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery; absence of extraabdominal disease, extensive hepatic metastases, and significant retroperitoneal disease; age younger than 70 years; and peritoneal disease that is either amendable to complete or near complete resection.16–18

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Cytoreductive Surgery

CRS, a group of parietal and visceral peritonectomy procedures, is performed in series or during a single operation to excise intraabdominal macroscopic tumors.12,15,19,20 CRS can range from an isolated omentectomy to complete resection of multiple abdominal organs, including the gastrointestinal tract, pancreas, spleen, gallbladder, uterus, ovaries, and portions of the liver.19,21 The peritoneal cancer index, determined at the time of abdominal exploration, estimates the success of CRS and 5-year survival rates.22 Similar to other assessments of carcinomatosis, this index attempts to categorize the extent of tumor involvement.23 Removal of all macroscopic tumors is not always possible. Therefore, the ultimate surgical goal is to debulk the majority of tumors until the nodules are 2.5 mm to ensure that cytotoxic drugs will penetrate those that remain.11,24,25

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Hyperthermic Intraperitoneal Chemotherapy

Directly infusing chemotherapeutic drugs into malignant effusions was described in 1955 when mustard nitrogen was injected into pericardial and peritoneal effusions.26 In 1977, the effects were reported regarding the use of hyperthermic peritoneal perfusion with sterile normal saline warmed to 41°C.27

The goal of intraperitoneal perfusion of chemotherapeutic drugs is to maximize exposure of the involved tissue to high concentrations of chemotherapeutic drugs (20–1000 times greater than plasma levels), while minimizing exposure of the normal tissue.2,28–30 HIPEC drugs are high-molecular-weight hydrophilic drugs that are unable to cross the peritoneal fluid–plasma barrier and demonstrate slow peritoneal clearance.31–34

Through inhibition of DNA repair mechanisms, denaturing of proteins, and activation of heat shock proteins, hyperthermia not only exhibits a direct cytotoxic effect but also causes an immune-mediated attack on tumor cells.35,36 HIPEC is most successful in treating tumors when the perfusion is administered immediately after CRS and before any gastrointestinal tract reconstruction to prevent enclosure of malignant cells within scar tissue, adhesions, or anastomosis sites.37,38

Typically, HIPEC is performed with a closed abdominal technique in which a suprahepatic inflow cannula and a pelvic outflow cannula are connected through a recirculating perfusion circuit driven by a roller pump heat exchanger.39 Perfusion of cytotoxic drugs for 60 to 120 minutes is followed by abdominal lavage, drainage, and abdominal closure.21,30,32 An open technique can also be performed whereby the abdomen remains open during chemoperfusion. In absence of peritoneal cavity expanders, leaving the abdomen open may prevent an increase of intraabdominal pressure and the associated complications including decreased renal perfusion. Another advantage is that perfusate is not reused and therefore there is less spreading of tumor cells throughout the cavity.21 However, open techniques also increase risk of exposure of chemotherapeutic drugs to operating room personnel.40

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Carrier Solutions

The anesthesiologist should be familiar with the toxicity profiles of the various chemotherapeutic drugs (Table 1) and understand how the type and volume of carrier fluid affects the pharmacokinetics and ultimately the systemic absorption of these cytotoxic drugs. The carrier solution for HIPEC is dependent on the cytotoxic drug used for chemoperfusion. Currently, the solutions of choice are either isotonic saline or dextrose-based peritoneal solutions. Of the currently used drugs, only oxaliplatin is used in 5% dextrose-based water solutions because the presence of chloride ions degrades oxaliplatin into less-cytotoxic metabolites.41,42 Although most centers use 1.5% dextrose isotonic peritoneal dialysis solutions, some institutional protocols suggest regular crystalloids such as lactated Ringer’s solution.37 These isotonic low-molecular-weight solutions are readily absorbed from the peritoneal cavity, resulting in both an uneven distribution and varied concentration of cytotoxic drugs in the peritoneal cavity because of the loss of carrier solution.32,43 However, given the short duration of HIPEC and the ability to adjust flow rates intraoperatively, the role of carrier solutions becomes less important.32 Alternative carrier solutions are currently being investigated. Animal studies using high-molecular-weight, isomolar glucose polymer solutions such as hetastarch demonstrated a prolonged exposure of intraperitoneal tumor cells to cytotoxic drugs.32,44 The systemic absorption of 5% dextrose solutions can lead to severe hyperglycemia and hyponatremia. In contrast to animal studies, human studies using hypotonic solutions failed to demonstrate increased tumor cell penetration. Patients in this study had an increased incidence of intraperitoneal hemorrhage and thrombocytopenia compared with patients treated with hypertonic solutions.45

Table 1
Table 1
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Preoperative Anesthetic Management

Anesthesiologists face several perioperative challenges when patients with peritoneal surface malignancies need surgery. Surgical and anesthetic management are complicated by systemic absorption of peritoneal fluid, with blood loss, acute kidney injury, electrolyte abnormalities, ascites, hypothermia, and hyperthermia. Physiologic perturbations during the perioperative period may precipitate multisystem organ failure.

The cardiac risk of patients undergoing CRS is comparable to the risk for patients who undergo other types of major abdominal surgery.46,47 Cardiopulmonary assessment should focus on the ability of the patient to compensate for the anticipated physiologic derangements, including tachycardia, increased cardiac index, and increased oxygen consumption.48,49 Electrolyte, blood urea nitrogen, creatinine, albumin, bilirubin, and complete blood count levels, as well as coagulation variables and glucose values, should be obtained.

Patients of advanced age or those with risk factors may undergo cardiopulmonary testing as guided by the American College of Cardiology/American Heart Association guidelines for patients undergoing noncardiac surgery.18 The goals of patient selection include identifying patients with multiple comorbidities that contribute to unacceptably high perioperative mortality rates.

Preoperative renal assessment in the form of calculated glomerular filtration rate identifies patients at risk for postoperative renal injury. Although acute kidney injury from HIPEC may be reversible,21 patients with preoperative renal dysfunction are at increased risk for perioperative cardiovascular events.50

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Intraoperative Anesthetic Management

Temperature Management The carrier solution for HIPEC is heated to 40°C to 43°C, putting the patient at significant risk for hyperthermia. Hyperthermia may cause consumptive coagulopathies, arrhythmias, liver/renal injury, peripheral neuropathies, and seizures.35 Before initiation of HIPEC, controlled hypothermia (decreased room temperature, avoiding surface air heating, cool IV fluids) should be used to avoid severe hyperthermia. The risks of hypothermia include alteration of pharmacokinetics of frequently used anesthetic drugs and increased risk of blood loss, surgical wound infections, and adverse myocardial events.51 Therefore, temperature management weighs the risks of hypothermia versus those of hyperthermia.

Cardiovascular Management Patients undergoing total body hyperthermia for treatment of metastatic cancer demonstrate increases in heart rate, cardiac index, and oxygen consumption, as well as decreases in systemic vascular resistance.52 Plasma norepinephrine levels were found to increase linearly parallel to the core body temperature.52

In addition to the monitors recommended by the American Society of Anesthesiologists, a radial arterial catheter is placed for frequent blood sampling. Pulse pressure variation, calculated from the invasive arterial tracing, can be used to assess fluid responsiveness.53 Central venous access may be established to administer vasoactive medications. Central venous pressure monitoring does not reliably measure blood volume or change in blood volume.54

Elevated Abdominal Pressures During intraperitoneal chemoperfusion, perfusate is used to circulate cytotoxic drugs throughout the peritoneal cavity. As the abdominal cavity fills with chemotherapeutic drugs dissolved in carrier fluid, the abdomen becomes distended and parallels physiologic changes found during pneumoperitoneum (compression of the inferior vena cava and decreased preload).40 Depending on perfusion flow rates, volume of perfusate, and surgical use of peritoneal expanders, intraabdominal pressures can vary between 12 and 26 mm Hg.55 The goals are to maintain adequate abdominal perfusion pressure(>60 mm Hg) by increasing the mean arterial blood pressure either through increasing cardiac output by augmenting preload with a normal to slightly increased intravascular volume or by increasing the systemic vascular resistance with vasoactive medications.40,56–58 Additionally, maximizing abdominal relaxation with muscle paralysis is also useful.57,58

Metabolic Response The severity of metabolic changes observed during HIPEC depends on the type of carrier solution and degree of hyperthermia. Hyperthermia increases metabolic activity, heart rate, carbon dioxide production, and ultimately oxygen consumption.40 In contrast to patients who receive HIPEC with lactated Ringer’s solution, patients who receive HIPEC with a 5% dextrose solution may experience hyperglycemia, hyponatremia, and metabolic acidosis.59 Studies report increases of 2 to 4 mmol/L lactate.60 These metabolic changes occur when both glucose and free water are absorbed into the plasma causing hyperglycemia and dilutional hyponatremia. The latter is also due to the excretion of sodium into the peritoneal fluid in patients treated with oxaliplatin.59 Although these changes do not normally lead to increased morbidity and mortality, a few case reports have documented cerebral edema due to severe hyponatremia.59 Hypervolemic hyponatremia can be managed with IV furosemide whereas euvolemic and hypovolemic hyponatremia secondary to peritoneal extraction of sodium and water may be slowly corrected with IV saline replacement. The hyperlactatemia observed during HIPEC procedures may be from type B lactate production, where the increase is a result of hyperglycemia-induced glycolysis rather than type A lactate production, which is due to tissue dysoxia or hypoperfusion.59,60 Intraoperative arrhythmias from cisplatin-induced renal wasting of intracellular magnesium have been reported.61

Fluid and Renal Management Among patients undergoing CRS with HIPEC, 1.3% to 5.7% develop acute kidney injury from nephrotoxic chemotherapeutic drugs, abdominal hypertension, and large fluid shifts resulting in significant intravascular volume depletion.62–64 Renal failure associated with HIPEC is multifactorial, is normally reversible, and is usually associated with use of cisplatin.21,64 A correlation between HIPEC doses of cisplatin >240 mg and increased postoperative serum creatinine levels has been reported.64 When used systemically, mitomycin C has been shown to cause mesenchymal endothelial cell damage, leading to nephrotoxicity.64

Two large-bore peripheral IV catheters should be placed for fluid resuscitation where large, highly vascularized tumors and extensive debulking can lead to significant blood loss.40 The large incision combined with surgery duration of up to 10 hours can cause large evaporative losses. Blood loss during these procedures can range from 0.5 to several liters.30,49 Additionally, peritoneal inflammation that begins during HIPEC continues postoperatively, leading to significant third-space fluid losses of up to 5 L per day.30 Replacement of these fluid losses is achieved through a combination of albumin and crystalloid solutions. Transfusion of fresh frozen plasma is guided by coagulation studies, and transfusion of packed red blood cells is guided by clinical signs and laboratory data suggesting inadequate oxygen delivery. Although studies of optimal replacement fluids in CRS and HIPEC are lacking, a recent meta-analysis of studies of patients with chronic liver disease and ascites found that replacement of ascites with albumin, compared with other intravascular volume expanders, reduced morbidity, mortality, and the incidence of circulatory dysfunction in this population.65 Although numerous studies have been reported on renal protective strategies, maintenance of adequate intravascular volume and renal perfusion may be the best method of preventing acute kidney injury.66,67

At our institution, we use pulse pressure variation, urine output, and point-of-care blood gas chemistries—lactate, base excess, and hemoglobin levels—to guide fluid administration. Although there are no specific guidelines regarding frequency of blood sampling during this procedure, optimal frequency of point-of-care testing depends on the carrier solution of the chemoperfusate and other patient-specific factors. During chemoperfusion, we check blood chemistries as often as every 15 minutes. In the case of hyperglycemia requiring an insulin infusion, we check point-of-care blood chemistries at least hourly.

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Postoperative Management

Anticipated Physiologic Changes After HIPEC, patients are oftentimes admitted to the intensive care unit or remain in the postanesthesia care unit for monitoring of organ function, management of intraoperative complications, and correction of coagulopathy. Regardless of the location, they should be monitored with continuous telemetry and pulse oximetry. Physiologic perturbations during the perioperative period affect the duration of the patient’s stay in the intensive care unit and may precipitate multisystem organ failure. Similar to patients with other intraabdominal surgical procedures, these patients are at risk for bowel perforations, anastomotic leakage, bile leakage, fistula formation, pancreatitis, postoperative bleeding, wound dehiscence, deep vein thrombosis, and pulmonary embolism.21 In fact, the most frequently used drug in HIPEC for pseudomyxoma, mitomycin C, is not only associated with transient postoperative leukopenia and elevated transaminases, but also affects wound healing and results in an increased incidence in anastomotic leaks, especially in patients treated preoperatively with radiation therapy.68

Vasodilation often occurs after HIPEC. Management of the resulting hypotension focuses on expanding the IV volume, administering a vasoconstricting drug such as norepinephrine or vasopressin, and determining the underlying cause of vasodilation to target. Aggressive fluid resuscitation without assessment of fluid responsiveness should be avoided. Administration of excessive intravascular fluid to a nonfluid-responsive patient increases cardiac filling pressures, which in turn can cause pulmonary edema. Ultimately, the length of intensive monitoring will, in large part, be determined by the normalization of electrolyte and hemodynamic abnormalities.

Prevention of postoperative thromboembolic complications is of utmost importance because of the patient’s underlying high risk. Any standard perioperative regimen for prevention of deep venous thrombosis prophylaxis is recommended. Sequential compression devices are placed in the operating room and are continued postoperatively until patients start mobilizing.

Postoperative ileus is a common problem after CRS and HIPEC. Although there are no prospective studies evaluating the ideal postoperative nutrition strategies, a retrospective study by Arakelian et al.69 found that most patients were able to tolerate oral feeding between 7 and 11 days after surgery. To promote healing and improve intestinal transit, early enteral feeding is both safe and beneficial for these patients.70–72 Use of epidural anesthesia has been recommended by some as a strategy to reduce postoperative ileus.69

Pain Management Pain management for CRS and HIPEC is essential for patient comfort and postoperative pulmonary function optimization. Several centers use thoracic epidurals preoperatively for intraoperative and postoperative pain management.73 Other options include spinal morphine and IV opioid-based patient-controlled analgesia. No studies have been done comparing these different modalities. Epidurals can decrease postoperative IV opioid consumption and enhance bowel motility via decreased sympathetic tone. Additionally, adequate analgesia enables these patients to partake in early physical therapy and breathing exercises that aim to prevent postoperative atelectasis and pneumonia. Schmidt et al.40 performed a retrospective analysis of 78 patients treated with CRS and HIPEC in which 72% of patients in the cohort received a thoracic epidural. The researchers found that these patients received less intraoperative opioids and had a decreased period of postoperative intubation. Although no complications were reported from epidural placement, anesthesiologists should evaluate the patient’s platelet count, prothrombin time, and activated partial thromboplastin time before removing the epidural catheter according to the American Society of Regional Anesthesia guidelines.74

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Outcomes and Morbidity and Mortality After CRS and HIPEC

Verwaal et al.75 showed that patients with peritoneal carcinomatosis secondary to colorectal cancer treated with CRS and HIPEC had a significant increase in median survival of 22 months compared with those treated with systemic chemotherapy alone (12 months). Peritoneal carcinomatosis secondary to ovarian cancer is unique in that current management combines CRS with systemic chemotherapy depending on the state at diagnosis.76 In a small prospective study, Spiliotis et al.77 showed that patients with peritoneal carcinomatosis secondary to ovarian cancer treated with CRS and HIPEC followed by systemic therapy demonstrated a significant increase in median survival of 19.5 months and a 3-year survival of 50% compared with patients treated with only CRS and systemic chemotherapy whereby median survival was 11.2 months and 3-year survival was 18%.

A systematic review of patients with pseudomyxoma peritonei treated with CRS and HIPEC demonstrated a median survival ranging from 51 to 156 months with 5-year survival rates ranging from 52% to 96% depending on severity of disease at time of treatment.78,79

In a systematic review involving more than 400 patients by Yan et al.,13 patients with primary peritoneal tumors secondary to diffuse malignant peritoneal mesothelioma treated with CRS and HIPEC demonstrated an overall survival rate of 53 months and a 5-year survival rate of 47%. Currently, CRS and HIPEC are recognized as the standard of care for managing peritoneal carcinomatosis secondary to colorectal cancer and appendiceal neoplasms.80

Given the extensive nature of CRS and HIPEC, it is not surprising that these treatments are associated with significant morbidity and mortality. Risk factors for major morbidity include peritoneal cancer index >21, ASA physical status >III, operation duration of >10 hours, left upper quadrant peritonectomy procedure, colostomy, ileostomy, and transfusion >6 U.81 With an improvement in surgical and perfusion techniques, morbidity and mortality associated with CRS and HIPEC have decreased. Sugarbaker et al.82 prospectively analyzed 350 patients with pseudomyxoma peritonei treated from 1998 to 2004 with CRS and HIPEC with mitomycin C in a single center experienced with peritoneal carcinomatosis. This group demonstrated a decrease in 30-day in-hospital morbidity and mortality from 35% and 5% to as low as 19% and 2%, respectively. It should be noted that these numbers are center-specific and depended not only on surgical volume but also physician and nursing staff expertise in caring for these patients. Data from other centers suggest a morbidity of 27% to 65% and mortality of 0% to 9%.83

Quality of life after CRS and HIPEC is also an important consideration during patient selection. Studies analyzing quality of life in long-term survivors have illustrated that functional status and pain scores return to baseline 4 to 6 months after surgery with quality of life returning to baseline levels 12 to 24 months after surgery.83–85

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Safety Considerations for Operating Room Staff

There are 3 main mechanisms through which intraperitoneal chemoperfusion is accomplished: open abdominal technique, closed abdominal technique, and peritoneal cavity expander technique. Unlike the open and peritoneal cavity expander techniques, only the closed abdominal technique greatly decreases exposure and inhalation of the chemotherapeutic drugs.86–89 Stuart et al.88 analyzed the exposure of the surgeon and perfusionist during an open abdominal, intraperitoneal chemoperfusion of mitomycin C during 10 different cases. Although this was a small, underpowered study, they were unable to detect any significant safety hazard to operating room personnel with maximal exposure to antineoplastic drugs as evidenced by the lack of any detectable mitomycin C in air and urine samples. Additionally, powder-free, latex gloves proved to be a sufficient barrier against skin contact and/or absorption.88 This study also used a smoke evacuation device that was placed in the surgical field to remove any droplets or chemotherapy-contaminated air immediately surrounding the open abdomen.88 Mitomycin C was detected within the filter device but was below the Occupational Safety and Health Administration maximum allowable exposure during an 8-hour period.88 Of note, although not part of the Occupational Safety and Health Administration guidelines, some centers prohibit pregnant women, women trying to become pregnant, women with a history of miscarriages, people with a history of oncologic and immunosuppressant therapy, and those with a hematologic disease from partaking in the intraoperative management of patients undergoing hyperthermic intraperitoneal chemotherapy.86–89

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Knowledge Gap and Future Direction

Designing clinical studies is very challenging in this patient population. Currently, there is no consensus among treatment centers regarding patient selection, optimal duration of HIPEC, perfusate temperature, and choice of cytotoxic drug. Creating a single system has also proven to be a formidable challenge. There are multiple staging systems, which vary in complexity and reproducibility. Thus, depending on the staging system used, a patient may have different degrees of tumor burden. Another challenge, in terms of defining outcomes, is the lack of clearly defined criteria of morbidity. Some centers routinely use the National Cancer Center Institute common toxicity criteria/grading system. Other centers include all postoperative complications, even those not specific to this procedure, when reporting morbidity from CRS and HIPEC. Having a single grading system would allow for the comparison of morbidity rates among centers. Additionally, centers that routinely incorporate adjuvant systemic chemotherapy or even postoperative intraperitoneal chemotherapy will also have differing morbidity rates. Another problem with designing clinical studies for this type of procedure is that standard IV chemotherapy regimens do not exist for all of the cancers that are under peritoneal surface malignancies. This paradigm exists for clinical studies involving isolated peritoneal carcinomatosis. Perhaps the most difficult factors to control for are tumor doubling time and aggressiveness of the cancer cells, both of which greatly affect outcomes. As we move forward, there are many questions that remain to be answered. Is there a role for perioperative chemotherapy, combining systemic and intraperitoneal chemotherapy? Is there a combination of chemotherapeutic drugs that maximizes tumor killing?

Optimal anesthetic management of patients being treated with CRS and HIPEC requires control of a complex interplay of physiologic mechanisms, including hyperthermia, abdominal hypertension, electrolyte abnormalities, coagulopathies, increased cardiac index, oxygen consumption, and decreased systemic vascular resistance.

Use of CRS and HIPEC presents a challenge to anesthesiologists. As this surgery continues to gain popularity among oncologic surgeons, further studies that clearly define the chemistry, pharmacokinetics, pharmacodynamics, and end points of efficacy need to be performed to elucidate optimal perioperative management.

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DISCLOSURES

Name: Christopher Allen-John Webb, MD.

Contribution: This author helped write the manuscript.

Attestation: Christopher Allen-John Webb approved the final manuscript.

Name: Paul David Weyker, MD.

Contribution: This author helped write the manuscript.

Attestation: Paul David Weyker approved the final manuscript.

Name: Vivek K. Moitra, MD.

Contribution: This author helped write the manuscript.

Attestation: Vivek K. Moitra approved the final manuscript.

Name: Richard K. Raker, MD.

Contribution: This author helped write the manuscript.

Attestation: Richard K. Raker approved the final manuscript.

This manuscript was handled by: Steven L. Shafer, MD.

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ACKNOWLEDGMENTS

We thank Joshua Leinwand and Robert Taub, MD, PhD, in the Division of Hematology/Oncology at Columbia University College of Physicians & Surgeons; John Chabot, MD, from the Department of Surgery and Sharyn Lewin, MD, from the Department of Obstetrics & Gynecology, Division of Gynecologic Oncology at Columbia University College of Physicians & Surgeons; and Charles Emala, MS, MD, from the Department of Anesthesiology at Columbia University College of Physicians & Surgeons, for reviewing the manuscript.

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REFERENCES

1. Macrì A. New approach to peritoneal surface malignancies. World J Gastrointest Oncol. 2010;2:9–11

2. Al-Shammaa HA, Li Y, Yonemura Y. Current status and future strategies of cytoreductive surgery plus intraperitoneal hyperthermic chemotherapy for peritoneal carcinomatosis. World J Gastroenterol. 2008;14:1159–66

3. Chu DZ, Lang NP, Thompson C, Osteen PK, Westbrook KC. Peritoneal carcinomatosis in nongynecologic malignancy: a prospective study of prognostic factors. Cancer. 1989;63:364–7

4. Davies JM, O’Neil B. Peritoneal carcinomatosis of gastrointestinal origin: natural history and treatment options. Expert Opin Investig Drugs. 2009;18:913–9

5. Sugarbaker PH, Yan TD, Stuart OA, Yoo D. Comprehensive management of diffuse malignant peritoneal mesothelioma. Eur J Surg Oncol. 2006;32:686–91

6. Teo M. Peritoneal-based malignancies and their treatment. Ann Acad Med Singapore. 2010;39:54–7

7. American Cancer Society. Cancer Facts & Figures 2012. 2012 Atlanta American Cancer Society

8. Chua TC, Liauw W, Saxena A, Al-Mohaimeed K, Fransi S, Zhao J, Morris DL. Evolution of locoregional treatment for peritoneal carcinomatosis: single-center experience of 308 procedures of cytoreductive surgery and perioperative intraperitoneal chemotherapy. Am J Surg. 2011;201:149–56

9. Miner TJ, Shia J, Jaques DP, Klimstra DS, Brennan MF, Coit DG. Long-term survival following treatment of pseudomyxoma peritonei: an analysis of surgical therapy. Ann Surg. 2005;241:300–8

10. Butterworth SA, Panton ON, Klaassen DJ, Shah AM, McGregor GI. Morbidity and mortality associated with intraperitoneal chemotherapy for pseudomyxoma peritonei. Am J Surg. 2002;183:529–32

11. Sugarbaker PH. Cytoreductive surgery and peri-operative intraperitoneal chemotherapy as a curative approach to pseudomyxoma peritonei syndrome. Eur J Surg Oncol. 2001;27:239–43

12. Cioppa T, Vaira M, Bing C, D’Amico S, Bruscino A, De Simone M. Cytoreduction and hyperthermic intraperitoneal chemotherapy in the treatment of peritoneal carcinomatosis from pseudomyxoma peritonei. World J Gastroenterol. 2008;14:6817–23

13. Yan TD, Deraco M, Baratti D, Kusamura S, Elias D, Glehen O, Gilly FN, Levine EA, Shen P, Mohamed F, Moran BJ, Morris DL, Chua TC, Piso P, Sugarbaker PH. Cytoreductive surgery and hyperthermic intraperitoneal chemotherapy for malignant peritoneal mesothelioma: multi-institutional experience. J Clin Oncol. 2009;27:6237–42

14. Deraco M, Baratti D, Cabras AD, Zaffaroni N, Perrone F, Villa R, Jocollè J, Balestra MR, Kusamura S, Laterza B, Pilotti S. Experience with peritoneal mesothelioma at the Milan National Cancer Institute. World J Gastrointest Oncol. 2010;2:76–84

15. Esquivel J, Sticca R, Sugarbaker P, Levine E, Yan TD, Alexander R, Baratti D, Bartlett D, Barone R, Barrios P, Bieligk S, Bretcha-Boix P, Chang CK, Chu F, Chu Q, Daniel S, de Bree E, Deraco M, Dominguez-Parra L, Elias D, Flynn R, Foster J, Garofalo A, Gilly FN, Glehen O, Gomez-Portilla A, Gonzalez-Bayon L, Gonzalez-Moreno S, Goodman M, Gushchin V, Hanna N, Hartmann J, Harrison L, Hoefer R, Kane J, Kecmanovic D, Kelley S, Kuhn J, Lamont J, Lange J, Li B, Loggie B, Mahteme H, Mann G, Martin R, Misih RA, Moran B, Morris D, Onate-Ocana L, Petrelli N, Philippe G, Pingpank J, Pitroff A, Piso P, Quinones M, Riley L, Rutstein L, Saha S, Alrawi S, Sardi A, Schneebaum S, Shen P, Shibata D, Spellman J, Stojadinovic A, Stewart J, Torres-Melero J, Tuttle T, Verwaal V, Villar J, Wilkinson N, Younan R, Zeh H, Zoetmulder F, Sebbag GSociety of Surgical Oncology Annual Meeting. . Cytoreductive surgery and hyperthermic intraperitoneal chemotherapy in the management of peritoneal surface malignancies of colonic origin: a consensus statement. Society of Surgical Oncology. Ann Surg Oncol. 2007;14:128–33

16. Stewart JH IV, Shen P, Levine EA. Intraperitoneal hyperthermic chemotherapy for peritoneal surface malignancy: current status and future directions. Ann Surg Oncol. 2005;12:765–77

17. Spiliotis JD. Peritoneal carcinomatosis cytoreductive surgery and HIPEC: a ray of hope for cure. Hepatogastroenterology. 2010;57:1173–7

18. Fleisher LA, Beckman JA, Brown KA, Calkins H, Chaikof E, Fleischmann KE, Freeman WK, Froehlich JB, Kasper EK, Kersten JR, Riegel B, Robb JF, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Antman EM, Buller CE, Creager MA, Ettinger SM, Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Lytle BW, Nishimura R, Ornato JP, Page RL, Riegel B, Tarkington LG, Yancy CW. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: executive summary—a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg. 2008;106:685–712

19. Sugarbaker PH. Peritonectomy procedures. Ann Surg. 1995;221:29–42

20. Eisenkop SM, Friedman RL, Wang HJ. Complete cytoreductive surgery is feasible and maximizes survival in patients with advanced epithelial ovarian cancer: a prospective study. Gynecol Oncol. 1998;69:103–8

21. Witkamp AJ, de Bree E, Van Goethem R, Zoetmulder FA. Rationale and techniques of intra-operative hyperthermic intraperitoneal chemotherapy. Cancer Treat Rev. 2001;27:365–74

22. Esquivel J, Averbach A, Chua TC. Laparoscopic cytoreductive surgery and hyperthermic intraperitoneal chemotherapy in patients with limited peritoneal surface malignancies: feasibility, morbidity and outcome in an early experience. Ann Surg. 2011;253:764–8

23. Harmon RL, Sugarbaker PH. Prognostic indicators in peritoneal carcinomatosis from gastrointestinal cancer. Int Semin Surg Oncol. 2005;2:3

24. Los G, Mutsaers PH, van der Vijgh WJ, Baldew GS, de Graaf PW, McVie JG. Direct diffusion of cis-diamminedichloroplatinum(II) in intraperitoneal rat tumors after intraperitoneal chemotherapy: a comparison with systemic chemotherapy. Cancer Res. 1989;49:3380–4

25. van de Vaart PJ, van der Vange N, Zoetmulder FA, van Goethem AR, van Tellingen O, ten Bokkel Huinink WW, Beijnen JH, Bartelink H, Begg AC. Intraperitoneal cisplatin with regional hyperthermia in advanced ovarian cancer: pharmacokinetics and cisplatin-DNA adduct formation in patients and ovarian cancer cell lines. Eur J Cancer. 1998;34:148–54

26. Weisberger AS, Levine B, Storaasli JP. Use of nitrogen mustard in treatment of serous effusions of neoplastic origin. J Am Med Assoc. 1955;159:1704–7

27. Spratt JS, Adcock RA, Sherrill W, Travathen S. Hyperthermic peritoneal perfusion system in canines. Cancer Res. 1980;40:253–5

28. Armstrong DK, Bundy B, Wenzel L, Huang HQ, Baergen R, Lele S, Copeland LJ, Walker JL, Burger RAGynecologic Oncology Group. . Intraperitoneal cisplatin and paclitaxel in ovarian cancer. N Engl J Med. 2006;354:34–43

29. Miao N, Pingpank JF, Alexander HR, Royal R, Steinberg SM, Quezado MM, Beresnev T, Quezado ZM. Cytoreductive surgery and continuous hyperthermic peritoneal perfusion in patients with mesothelioma and peritoneal carcinomatosis: hemodynamic, metabolic, and anesthetic considerations. Ann Surg Oncol. 2009;16:334–44

30. Ahmed S, Oropello JM. Critical care issues in oncological surgery patients. Crit Care Clin. 2010;26:93–106

31. Sugarbaker PH, Stuart OA, Vidal-Jove J, Pessagno AM, DeBruijn EA. Pharmacokinetics of the peritoneal-plasma barrier after systemic mitomycin C administration. Cancer Treat Res. 1996;82:41–52

32. de Bree E, Tsiftsis DD. Principles of perioperative intraperitoneal chemotherapy for peritoneal carcinomatosis. Recent Results Cancer Res. 2007;169:39–51

33. Rampone B, Schiavone B, Martino A, Confuorto G. Current role of hyperthermic intraperitoneal chemotherapy in the treatment of peritoneal carcinomatosis from colorectal cancer. World J Gastroenterol. 2010;16:1299–302

34. Piché N, Leblond FA, Sidéris L, Pichette V, Drolet P, Fortier LP, Mitchell A, Dubé P. Rationale for heating oxaliplatin for the intraperitoneal treatment of peritoneal carcinomatosis: a study of the effect of heat on intraperitoneal oxaliplatin using a murine model. Ann Surg. 2011;254:138–44

35. Christophi C, Winkworth A, Muralihdaran V, Evans P. The treatment of malignancy by hyperthermia. Surg Oncol. 1998;7:83–90

36. Dahl O, Dalene R, Schem BC, Mella O. Status of clinical hyperthermia. Acta Oncol. 1999;38:863–73

37. González-Moreno S, González-Bayón LA, Ortega-Pérez G. Hyperthermic intraperitoneal chemotherapy: rationale and technique. World J Gastrointest Oncol. 2010;2:68–75

38. Maggiori L, Elias D. Curative treatment of colorectal peritoneal carcinomatosis: current status and future trends. Eur J Surg Oncol. 2010;36:599–603

39. Sarnaik AA, Sussman JJ, Ahmad SA, McIntyre BC, Lowy AM. Technology for the delivery of hyperthermic intraoperative intraperitoneal chemotherapy: a survey of techniques. Recent Results Cancer Res. 2007;169:75–82

40. Schmidt C, Creutzenberg M, Piso P, Hobbhahn J, Bucher M. Peri-operative anaesthetic management of cytoreductive surgery with hyperthermic intraperitoneal chemotherapy. Anaesthesia. 2008;63:389–95

41. Jerremalm E, Hedeland M, Wallin I, Bondesson U, Ehrsson H. Oxaliplatin degradation in the presence of chloride: identification and cytotoxicity of the monochloro monooxalato complex. Pharm Res. 2004;21:891–4

42. Curis E, Provost K, Bouvet D, Nicolis I, Crauste-Manciet S, Brossard D, Bénazeth S. Carboplatin and oxaliplatin decomposition in chloride medium, monitored by XAS. J Synchrotron Radiat. 2001;8:716–8

43. Pestieau SR, Schnake KJ, Stuart OA, Sugarbaker PH. Impact of carrier solutions on pharmacokinetics of intraperitoneal chemotherapy. Cancer Chemother Pharmacol. 2001;47:269–76

44. Mohamed F, Marchettini P, Stuart OA, Yoo D, Sugarbaker PH. A comparison of hetastarch and peritoneal dialysis solution for intraperitoneal chemotherapy delivery. Eur J Surg Oncol. 2003;29:261–5

45. Elias D, El Otmany A, Bonnay M, Paci A, Ducreux M, Antoun S, Lasser P, Laurent S, Bourget P. Human pharmacokinetic study of heated intraperitoneal oxaliplatin in increasingly hypotonic solutions after complete resection of peritoneal carcinomatosis. Oncology. 2002;63:346–52

46. Vanacker B. Anaesthetic issues in women undergoing gynaecological cytoreductive surgery. Curr Opin Anaesthesiol. 2009;22:362–7

47. Auerbach A, Goldman L. Assessing and reducing the cardiac risk of noncardiac surgery. Circulation. 2006;113:1361–76

48. Kanakoudis F, Petrou A, Michaloudis D, Chortaria G, Konstantinidou A. Anaesthesia for intra-peritoneal perfusion of hyperthermic chemotherapy: haemodynamic changes, oxygen consumption and delivery. Anaesthesia. 1996;51:1033–6

49. Esquivel J, Angulo F, Bland RK, Stephens AD, Sugarbaker PH. Hemodynamic and cardiac function parameters during heated intraoperative intraperitoneal chemotherapy using the open “coliseum technique.” Ann Surg Oncol. 2000;7:296–300

50. Brosius FC III, Hostetter TH, Kelepouris E, Mitsnefes MM, Moe SM, Moore MA, Pennathur S, Smith GL, Wilson PWAmerican Heart Association Kidney and Cardiovascular Disease Council; Council on High Blood Pressure Research; Council on Cardiovascular Disease in the Young; Council on Epidemiology and Prevention; Quality of Care and Outcomes Research Interdisciplinary Working Group. . Detection of chronic kidney disease in patients with or at increased risk of cardiovascular disease: a science advisory from the American Heart Association Kidney and Cardiovascular Disease Council; the Councils on High Blood Pressure Research, Cardiovascular Disease in the Young, and Epidemiology and Prevention; and the Quality of Care and Outcomes Research Interdisciplinary Working Group—developed in collaboration with the National Kidney Foundation. Circulation. 2006;114:1083–7

51. Reynolds L, Beckmann J, Kurz A. Perioperative complications of hypothermia. Best Pract Res Clin Anaesthesiol. 2008;22:645–57

52. Kim YD, Lake CR, Lees DE, Schuette WH, Bull JM, Weise V, Kopin IJ. Hemodynamic and plasma catecholamine responses to hyperthermic cancer therapy in humans. Am J Physiol. 1979;237:H570–4

53. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology. 2005;103:419–28

54. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134:172–8

55. Tsiftsis D, de Bree E, Romanos J, Petrou A, Sanidas E, Askoxylakis J, Zervos K, Michaloudis D. Peritoneal expansion by artificially produced ascites during perfusion chemotherapy. Arch Surg. 1999;134:545–9

56. Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF. Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49:621–6

57. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh Z, Leppäniemi A, Olvera C, Ivatury R, D’Amours S, Wendon J, Hillman K, Johansson K, Kolkman K, Wilmer A. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med. 2006;32:1722–32

58. Cheatham ML, Malbrain ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh Z, Leppäniemi A, Olvera C, Ivatury R, D’Amours S, Wendon J, Hillman K, Wilmer A. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med. 2007;33:951–62

59. Rueth NM, Murray SE, Huddleston SJ, Abbott AM, Greeno EW, Kirstein MN, Tuttle TM. Severe electrolyte disturbances after hyperthermic intraperitoneal chemotherapy: oxaliplatin versus mitomycin C. Ann Surg Oncol. 2011;18:174–80

60. De Somer F, Ceelen W, Delanghe J, De Smet D, Vanackere M, Pattyn P, Mortier E. Severe hyponatremia, hyperglycemia, and hyperlactatemia are associated with intraoperative hyperthermic intraperitoneal chemoperfusion with oxaliplatin. Perit Dial Int. 2008;28:61–6

61. Thix CA, Königsrainer I, Kind R, Wied P, Schroeder TH. Ventricular tachycardia during hyperthermic intraperitoneal chemotherapy. Anaesthesia. 2009;64:1134–6

62. Glehen O, Osinsky D, Cotte E, Kwiatkowski F, Freyer G, Isaac S, Trillet-Lenoir V, Sayag-Beaujard AC, François Y, Vignal J, Gilly FN. Intraperitoneal chemohyperthermia using a closed abdominal procedure and cytoreductive surgery for the treatment of peritoneal carcinomatosis: morbidity and mortality analysis of 216 consecutive procedures. Ann Surg Oncol. 2003;10:863–9

63. Verwaal VJ, van Tinteren H, Ruth SV, Zoetmulder FA. Toxicity of cytoreductive surgery and hyperthermic intra-peritoneal chemotherapy. J Surg Oncol. 2004;85:61–7

64. Kusamura S, Baratti D, Younan R, Laterza B, Oliva GD, Costanzo P, Favaro M, Gavazzi C, Grosso F, Deraco M. Impact of cytoreductive surgery and hyperthermic intraperitoneal chemotherapy on systemic toxicity. Ann Surg Oncol. 2007;14:2550–8

65. Bernardi M, Caraceni P, Navickis RJ, Wilkes MM. Albumin infusion in patients undergoing large-volume paracentesis: a meta-analysis of randomized trials. Hepatology. 2012;55:1172–81

66. Fleisher LA. Evidence-Based Practice of Anesthesiology. 20092nd ed Philadelphia Saunders/Elsevier

67. Webb TS, Allen DS. Perioperative renal protection. Contin Educ Anaesth Crit Care Pain. 2008;8:176–80

68. Loggie BW, Fleming RA. Complications of heated intraperitoneal chemotherapy and strategies for prevention. Cancer Treat Res. 1996;82:221–33

69. Arakelian E, Gunningberg L, Larsson J, Norlén K, Mahteme H. Factors influencing early postoperative recovery after cytoreductive surgery and hyperthermic intraperitoneal chemotherapy. Eur J Surg Oncol. 2011;37:897–903

70. Tsahalina E, Razvi K, Alkatib M, Shaw C, Chun LY, Barton DP. Early enteral feeding following major abdominal surgery for recurrent gynaecological cancer. J Obstet Gynaecol. 2006;26:457–61

71. Lewis SJ, Egger M, Sylvester PA, Thomas S. Early enteral feeding versus “nil by mouth” after gastrointestinal surgery: systematic review and meta-analysis of controlled trials. BMJ. 2001;323:773–6

72. Moore-Olufemi SD, Padalecki J, Olufemi SE, Xue H, Oliver DH, Radhakrishnan RS, Allen SJ, Moore FA, Stewart R, Laine GA, Cox CS Jr. Intestinal edema: effect of enteral feeding on motility and gene expression. J Surg Res. 2009;155:283–92

73. Schmidt C, Steinke T, Moritz S, Bucher M. Thoracic epidural anesthesia in patients with cytoreductive surgery and HIPEC. J Surg Oncol. 2010;102:545–6

74. Horlocker TT, Wedel DJ, Rowlingson JC, Enneking FK, Kopp SL, Benzon HT, Brown DL, Heit JA, Mulroy MF, Rosenquist RW, Tryba M, Yuan CS. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-Based Guidelines (Third Edition). Reg Anesth Pain Med. 2010;35:64–101

75. Verwaal VJ, van Ruth S, de Bree E, van Sloothen GW, van Tinteren H, Boot H, Zoetmulder FA. Randomized trial of cytoreduction and hyperthermic intraperitoneal chemotherapy versus systemic chemotherapy and palliative surgery in patients with peritoneal carcinomatosis of colorectal cancer. J Clin Oncol. 2003;21:3737–43

76. Spiliotis JD, Halkia EA, Efstathiou E. Peritoneal carcinomatosis 2011; it’s about time for chemosurgery. J BUON. 2011;16:400–8

77. Spiliotis J, Vaxevanidou A, Sergouniotis F, Lambropoulou E, Datsis A, Christopoulou A. The role of cytoreductive surgery and hyperthermic intraperitoneal chemotherapy in the management of recurrent advanced ovarian cancer: a prospective study. J BUON. 2011;16:74–9

78. Yan TD, Black D, Savady R, Sugarbaker PH. A systematic review on the efficacy of cytoreductive surgery and perioperative intraperitoneal chemotherapy for pseudomyxoma peritonei. Ann Surg Oncol. 2007;14:484–92

79. Mohamed F, Cecil T, Moran B, Sugarbaker P. A new standard of care for the management of peritoneal surface malignancy. Curr Oncol. 2011;18:e84–96

80. Sugarbaker PH. Evolution of cytoreductive surgery and perioperative intraperitoneal chemotherapy for peritoneal carcinomatosis: are there treatment alternatives? Am J Surg. 2011;201:157–9

81. Saxena A, Yan TD, Chua TC, Morris DL. Critical assessment of risk factors for complications after cytoreductive surgery and perioperative intraperitoneal chemotherapy for pseudomyxoma peritonei. Ann Surg Oncol. 2010;17:1291–301

82. Sugarbaker PH, Alderman R, Edwards G, Marquardt CE, Gushchin V, Esquivel J, Chang D. Prospective morbidity and mortality assessment of cytoreductive surgery plus perioperative intraperitoneal chemotherapy to treat peritoneal dissemination of appendiceal mucinous malignancy. Ann Surg Oncol. 2006;13:635–44

83. Schmidt U, Dahlke MH, Klempnauer J, Schlitt HJ, Piso P. Perioperative morbidity and quality of life in long-term survivors following cytoreductive surgery and hyperthermic intraperitoneal chemotherapy. Eur J Surg Oncol. 2005;31:53–8

84. McQuellon RP, Loggie BW, Fleming RA, Russell GB, Lehman AB, Rambo TD. Quality of life after intraperitoneal hyperthermic chemotherapy (IPHC) for peritoneal carcinomatosis. Eur J Surg Oncol. 2001;27:65–73

85. Glockzin G, Schlitt HJ, Piso P. Peritoneal carcinomatosis: patients selection, perioperative complications and quality of life related to cytoreductive surgery and hyperthermic intraperitoneal chemotherapy. World J Surg Oncol. 2009;7:5

86. Benoit L, Cheynel N, Ortega-Deballon P, Giacomo GD, Chauffert B, Rat P. Closed hyperthermic intraperitoneal chemotherapy with open abdomen: a novel technique to reduce exposure of the surgical team to chemotherapy drugs. Ann Surg Oncol. 2008;15:542–6

87. González-Bayón L, González-Moreno S, Ortega-Pérez G. Safety considerations for operating room personnel during hyperthermic intraoperative intraperitoneal chemotherapy perfusion. Eur J Surg Oncol. 2006;32:619–24

88. Stuart OA, Stephens AD, Welch L, Sugarbaker PH. Safety monitoring of the coliseum technique for heated intraoperative intraperitoneal chemotherapy with mitomycin C. Ann Surg Oncol. 2002;9:186–91

89. White SK, Stephens AD, Sugarbaker PH. Hyperthermic intraoperative intraperitoneal chemotherapy safety considerations. AORN J. 1996;63:716–24

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