Ovarian cystadenomas are neoplasms that on rare occasions present as extremely large abdominal masses. Few ovarian tumors weighing >45 kg have been reported.1 The anesthesia literature is generally devoid of case reports and guidelines for the perioperative management in this patient population. Similar anesthesia implications in patients with a gravid uterus during pregnancy, such as supine hypotension syndrome, aspiration risk, and rapid hemoglobin oxygen desaturation, are exaggerated in patients with large abdominal masses. We describe a case that was challenging because of the unique anatomical and physiologic changes caused by a massive ovarian neoplasm.
Permission for the publication of this case report was obtained from both the Mayo Clinic IRB and the patient.
A 59-year-old postmenopausal woman presented to the emergency department with a 1-year history of abdominal distention associated with recent postmenopausal vaginal bleeding. At admission, the patient weighed 141.5 kg, which was reported as >50 kg heavier than her usual weight. She had difficulty with ambulation and worsening shortness of breath. The patient’s abdomen was markedly distended and rigid (Fig. 1), exhibiting a fluid wave on examination. Bilateral lower extremity edema was present. A paracentesis was performed to relieve the shortness of breath on her arrival at the emergency department and yielded 10 L of fluid.
Deep vein thrombosis as a cause of the patient’s lower extremity edema was excluded through bilateral lower extremity venous duplex ultrasonography. Transthoracic echocardiography revealed grade 1 diastolic dysfunction and left ventricular concentric remodeling, with a left ventricular ejection fraction of 61%. Mild tricuspid, mitral, and pulmonic valve regurgitation was also found. Laboratory studies showed that levels of all plasma electrolytes, complete blood cell count, creatinine, blood urea nitrogen, prothrombin time, partial thromboplastin time, and urinalysis were within reference limits. An abdominal and pelvic computed tomographic scan showed a large, cystic, well-circumscribed mass involving the entire abdomen and pelvis. In addition, a large anterior abdominal wall defect contained part of the mass and a portion of the transverse colon (Fig. 2).
Before the procedure, the patient received 20 mg of famotidine and 4 mg of ondansetron for aspiration prophylaxis. In the operating room, she was placed in the left lateral decubitus position with a wedge under the right hip to avoid aortocaval compression similar to that seen in pregnant patients. During positioning, the patient’s systolic blood pressure decreased from 140 to 120 mm Hg, which was treated by placing a larger wedge under the hip and administering 5 mg ephedrine. An indwelling left radial arterial catheter, 2 large-bore peripheral IV catheters, and a right subclavian central venous catheter were inserted for hemodynamic monitoring and to help provide fluid resuscitation.
After oxygen administration for 8 minutes, rapid-sequence induction of anesthesia with 140 mg of propofol, 100 mcg of fentanyl, and 120 mg of succinylcholine was performed. Tracheal intubation was performed via direct laryngoscopy using a Macintosh 4 laryngoscope and application of cricoid pressure. Inhaled sevoflurane and IV vecuronium were used for maintenance of anesthesia.
A laparotomy was performed by making a midline vertical incision just above the umbilicus. The surgeon drained the cystic fluid at a slow, continuous rate, yielding 55 L of fluid. The patient became hypotensive during fluid drainage but responded to phenylephrine (650 mcg total) and fluid boluses. She received 2 units of packed red blood cells, 2 L of albumin, and 2.5 L of crystalloid, with an estimated blood loss of 600 mL and urine output of 800 mL. In total, a 56.7-kg cystic mass was removed. Complete hysterectomy and complex wound closure were performed. Frozen section pathologic results showed a diagnosis of benign left ovarian serous cystadenoma.
The patient was positioned supine before extubating the trachea (Fig. 3) in the operating room. Throughout her postoperative course in the intensive care unit, she was able to remain in the supine position without hemodynamic instability. Postoperative analgesia was accomplished with IV hydromorphone delivered via patient-controlled analgesia. Her postoperative course continued to be unremarkable. With the return of bowel function on postoperative day 2, the patient’s medication was transitioned to oral oxycodone/acetaminophen on day 3 for pain control and she was discharged home on postoperative day 4.
Anesthetic implications in this patient included anticipating the physiologic and anatomical changes related to the removal of a large abdominal mass and avoiding hemodynamic instability in the perioperative period.
Aspiration risk is increased because of the increased intraabdominal pressure (IAP). Partial or complete bowel obstruction and intestinal herniation may exist because of the increased IAP. The gastrointestinal system may be compromised by adynamic ileus, resulting in intestinal distention and perforation.2 Intubation may be further complicated by the left semilateral position used to prevent aortocaval compression. When our patient did not present with a difficult airway, rapid-sequence induction of anesthesia for tracheal intubation was recommended to prevent aspiration complications.
Adequate oxygen administration is crucial in this surgical setting. As seen in patients with gravid uterus or morbid obesity, decreased compliance of the chest wall reduces total respiratory compliance, which leads to decreases in functional residual capacity (FRC), vital capacity, and total lung capacity,3 all of which contribute to rapid hemoglobin oxygen desaturation. Reduced FRC also results in lung volumes below closing capacity during normal tidal ventilation, which can lead to ventilation–perfusion mismatch, intrapulmonary shunting, and arterial hypoxemia.3 In addition to the arterial hypoxemia, decreased compliance may present as high intrathoracic pressures, increased peak airway pressures, and hypercapnia.4 Patients may also continue to derecruit gas exchange units while undergoing anesthesia.5 Because of these changes, application of 5 to 10 cm H2O of positive end-expiratory pressure may be used to decrease atelectasis.6
IAP ranges from approximately 5 to 7 mm Hg in adult patients, but variations of up to 15 mm Hg can be seen in the postlaparotomy state, secondary to edema of the abdominal contents. A large abdominal or pelvic mass can further increase IAP, which may produce clinically significant end-organ dysfunction, organ failure, or even patient death due to hypoperfusion or ischemia of abdominal viscera.4
Reverse Trendelenburg position used to minimize the reduction of FRC by the large abdominal mass and the weight of the mass compressing the abdominal aorta in a supine patient may, in combination with the effects of anesthetic drugs, also reduce cardiac output substantially. This decrease in cardiac output may be amplified further by the application of positive end-expiratory pressure.6 Right hip elevation may reduce aortocaval compression caused by the abdominal mass.7 However, large hemodynamic changes may still occur during the induction of anesthesia because of the cardiac depressant effects of medications used during induction of anesthesia.8 With the administration of muscle relaxants, the weight of the mass may redistribute to the major blood vessels after the loss of muscle tone, despite optimal positioning.9
An intraarterial catheter should be inserted before induction to provide adequate hemodynamic monitoring during induction. Patients should also have adequate IV access if large fluid resuscitation is needed at any time during the perioperative period. If the patient has any previous cardiac disease or recent cardiovascular decompensation caused by the abdominal mass, a central venous catheter or a pulmonary artery catheter placed before induction may be warranted for close monitoring of cardiac function. We recommend that transthoracic echocardiography be performed before surgery, to assess left ventricular function and exclude valvular abnormalities and pulmonary hypertension.
Maintenance of anesthesia should be conducted using short-acting opiates for analgesia to minimize hemodynamic instability. The patient is at risk for acute arterial blood pressure changes, and neuraxial anesthesia should be avoided intraoperatively because sympathetic denervation may contribute to arterial hypotension that is unresponsive to fluid therapy.10
Rapid decompression of a large abdominal mass can cause acute arterial blood pressure changes. These changes depend on whether increased venous pooling or splanchnic pooling dominates after the tumor removal, which can occur up to 72 hours postoperatively.11 The release of the abdominal aortic compression can produce a sudden decrease in peripheral resistance.7 Cooperation with the surgeon to decompress the mass slowly may allow adequate time for fluid resuscitation and restoration of peripheral arterial tone. The surgical team may need to temporarily reverse the sudden decrease in IAP by applying pressure manually on the major vessels. When simple manual application of pressure is not sufficient, sterile bags of IV fluids may be placed in the abdominal cavity to provide additional pressure. The possible delayed hemodynamic changes in the postoperative period necessitate the need for continued close monitoring in the intensive care unit.
The recovery period can be uniquely challenging because of the anatomical, physiologic, and even psychological changes. Postoperative neuraxial anesthesia may be considered in hemodynamically stable patients to reduce postoperative pulmonary complications and ileus. An opiate-only epidural infusion may be considered to prevent substantial hemodynamic changes. Physical therapy may be needed beyond the initial postoperative period because bony structures may have undergone hyperplastic changes during the disease process, thereby modifying not only the patient’s anatomy but also the patient’s center of balance and gait.2 In addition, with the removal of the large abdominal mass, excessive skin and tissue are likely to require reconstructive surgery (Fig. 3). The abrupt change in physical appearance may also require psychiatric intervention.11
This case demonstrates that, although large intraabdominal masses pose a challenge to perioperative patient management, major adverse outcomes may be circumvented with a clear understanding of the pathologic process.
1. Hunter DJ. Management of a massive ovarian cyst. Obstet Gynecol. 1980;56:254–5
2. Kincey J, Westin SN, Zhao B, Curtis MG, Ramondetta L. Surgical removal of a gigantic abdominal mass: a multidisciplinary approach. Obstet Gynecol. 2011;117:508–12
3. Ogunnaike BO, Whitten CWBarash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Anesthesia and obesity. Clinical Anesthesia. 20096th ed Philadelphia, PA Wolters Kluwer Health/Lippincott Williams & Wilkins:1230–46
4. Vegar-Brozovic V, Brezak J, Brozovic I. Intra-abdominal hypertension: pulmonary and cerebral complications. Transplant Proc. 2008;40:1190–2
5. Jense HG, Dubin SA, Silverstein PI, O’Leary-Escolas U. Effect of obesity on safe duration of apnea in anesthetized humans. Anesth Analg. 1991;72:89–93
6. Perilli V, Sollazzi L, Modesti C, Annetta MG, Sacco T, Bocci MG, Tacchino RM, Proietti R. Comparison of positive end-expiratory pressure with reverse Trendelenburg position in morbidly obese patients undergoing bariatric surgery: effects on hemodynamics and pulmonary gas exchange. Obes Surg. 2003;13:605–9
7. Hoile RW. Hazards in the management of large intra-abdominal tumours. Ann R Coll Surg Engl. 1976;58:393–7
8. Searle NR, Sahab P. Propofol in patients with cardiac disease. Can J Anaesth. 1993;40:730–47
9. Hedenstierna G, Edmark L. The effects of anesthesia and muscle paralysis on the respiratory system. Intensive Care Med. 2005;31:1327–35
10. Richards ER, Kabir SI, McNaught CE, MacFie J. Effect of thoracic epidural anaesthesia on splanchnic blood flow. Br J Surg. 2013;100:316–21
11. Buller RE, Holter H, Laros RK Jr, Hanson KH, Abele J. Massive ovarian mucinous cystadenoma of low malignant potential. Obstet Gynecol. 1982;59:112S–6S