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American Journal of Forensic Medicine & Pathology:
doi: 10.1097/PAF.0b013e318221be82
Case Reports

Massive Ovarian Cyst and Sudden Death

Chute, Dennis J. MD; Stasaitis, Wilma RN

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From the Dutchess County Medical Examiner’s Office, Poughkeepsie, NY.

Manuscript received January 28, 2011; accepted March 31, 2011.

The authors did not receive financial support for this study.

The authors report no conflicts of interest.

Reprints: Dennis J. Chute, MD, 387 Main St, Poughkeepsie, NY 12601. E-mail: dchute@co.dutchess.ny.us.

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Abstract

Abstract: Massive enlargement of an ovarian cyst is an uncommon cause of morbidity and a rare cause of mortality due in large to part to noninvasive imaging techniques that usually permit early detection. When an ovarian cyst reaches giant proportions, it produces abdominal enlargement often with a fluid wave resulting in a condition that mimics ascites, called pseudoascites. Despite their impressive appearances, such cysts often are operable for cure. We describe a case of a middle-aged woman who presented 3 years before her death with symptoms from an undiagnosed giant cyst and given a diagnosis of ascites of undetermined etiology. She subsequently died at home unexpectedly, and at autopsy, she was found to have a massively enlarged but otherwise benign mucinous cystadenoma.

Pseudoascites is a rare condition due to an abnormal accumulation of fluid within a structure, such as an organ, cyst, or pseudocyst, within the abdomen that mimics ascites, the latter is due to free fluid inside the peritoneal cavity.1 Both present with abdominal enlargement, full flanks, and a fluid wave on physical examination. The following entities may cause pseudoascites: bladder distention or diverticulum, hydronephrosis, nonpancreatic pseudocyst, large uterine or ovarian tumors, and giant mesenteric, omental, and echinococcal cysts.2,3 Although massive ovarian cysts may produce pseudoascites, such cases have become less common as modern imaging methods identify them earlier and surgical interventions prevent them from reaching enormous size. We describe a case of a middle-aged white female who died due to a slow enlargement of a mucinous cystadenoma of her left ovary mistaken for a case of ascites.

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CASE REPORT AND RESULTS

A 51-year-old white female with a long history of tobacco use presented to an emergency department 3 years before her death with a complaint of abdominal pain and increasing abdominal girth. Computed tomography (CT) of the abdomen and pelvis was performed to rule out a mass; the study was limited because the patient objected to oral and intravenous contrast. This scan was interpreted as showing a massive amount of fluid, with some loculations, present in the abdomen displacing visceral organs (Fig. 1). The liver had a normal contour. The kidneys were noted to be pushed posteriorly and medially by the fluid. The pancreas, kidneys, spleen, uterus, gallbladder, and urinary bladder were unremarkable. The patient was given a diagnosis of ascites and discharged for outpatient follow-up, but she was noncompliant. Two years later, the patient visited a primary care physician for symptoms of acute maxillary sinusitis at which time her physician began a workup for a suspected ascites and ordered blood test and an ultrasound with paracentesis of the patient’s abdomen. This ultrasound study, although described as extremely limited, showed a large amount of peritoneal fluid of low-level echogenicity and structures containing cystic components in the dependent portion of the peritoneal cavity. Abdominal and pelvic organs were not demonstrable. Paracentesis collected a dark brown fluid. Cytology examination revealed a hypocellular material with few inflammatory cells and reactive mesothelial cells with no evidence of malignancy on the cytospins and cell block. Chemistry results of the paracentesis fluid showed an albumin level of 1.8 g/dL with a calculated serum-ascites albumin gradient of 1.9 g/dL (ie, serum albumin concentration minus paracentesis fluid albumin concentration). Gradients greater than 1.1 g/dL usually infer that ascites is due to portal hypertension. Blood tests included a complete blood cell count; chemistry metabolic profile with liver enzymes, protein, albumin, amylase, lipase, ammonia, CA 19-9, and CA-125; and coagulation parameters (Prothrombin Time, Partial Thromboplastin Time, and International Normalized Ration) with results all within reference limits. A diagnosis of ascites due to portal hypertension of undetermined origin was made but, again, because of noncompliance, the patient was lost to further follow-up. One year later, she complained of abdominal pain to her spouse and had a witnessed sudden, unexpected collapse. She was in asystole when paramedics arrived, and she could not be resuscitated.

Figure 1
Figure 1
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AUTOPSY RESULTS

External examination showed a well-developed, thin, white female, 65 in in height, 120 lb with a markedly distended, tense abdomen, and a demonstrable fluid wave (Fig. 2A). Icterus, spider angiomata, periumbilical varices, and external hemorrhoids were not noted. Internal examination was remarkable for a massively enlarged left ovarian cyst adhering to the serosal surface of the abdomen and the greater omentum. The outside of the cyst was gray-white, firm with a tough resiliency, consistent with dense connective tissue. Abdominal viscera were displaced superiorly and posteriorly by this cyst to the extent that the hemidiaphragms seemed to compromise the chest cavities. The ovarian cyst contained 26 L of amber- to dark brown–colored, slightly viscous fluid. The overall dimensions of the collapsed cyst, that is, after the fluid was removed, were 35.5 × 23 × 20 cm (Fig. 2,B and C). The cyst wall was 0.5 cm in average thickness, with a glistening inner lining that contained a few nodular structures toward the pelvic area. On cut section, these nodules showed multiloculated cysts that contained similar amber-colored viscous fluid and a glistening inner lining. In some foci, the inner lining was covered by a smear of brown pastelike material consistent with old hemorrhage and hemolysis. In no area was there evidence of infiltration of tumor through the wall of the cyst into the surrounding peritoneum; no satellite cyst, nodule, or retroperitoneal lymphadenopathy was noted. Histologic examination of the cyst wall showed a simple columnar epithelial lining, with basally oriented uniform nuclei resembling endocervical epithelium resting on a fibrotic stroma with relatively sparse chronic inflammatory cell infiltration (Fig. 3). There was no evidence of malignancy or atypical pseudostratification. The diagnosis was a massively enlarged benign mucinous cystadenoma. Additional findings were focal atherosclerotic coronary artery disease and a 12 × 6 × 4-cm adenocarcinoma of the upper lobe of the right lung that infiltrated into the midesophagus where it produced a malignant ulcer with local metastatic adenopathy. The cause of death was certified as due to complications of a mucinous cystadenoma of the left ovary with the adenocarcinoma of the right lung and coronary arteriosclerosis as contributory.

Figure 2
Figure 2
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Figure 3
Figure 3
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DISCUSSION

Mucinous cystadenomas of the ovary are much more common in adults than in adolescents and children. Massive enlargement of an ovarian cyst is a rare occurrence that typically happens under circumstances of neglected medical care or lack of follow-up. These giant abdominal cysts are known to produce cardiovascular, pulmonary, and circulatory problems4 and have also been associated with the abdominal compartment syndrome.5 The latter condition is defined as an intra-abdominal pressure (IAP) of 20 mm Hg or greater associated with new organ dysfunction or failure.6

The pathophysiologic mechanisms that contributed to her death are probably multifactorial. Her massive ovarian cyst, similar to a patient with tense ascites, increased her IAP and produced a cephalic shift in her diaphragm. To varying degrees, comparable effects occur in other conditions, for example, pneumoperitoneum during laparoscopy, continuous ambulatory peritoneal dialysis, and the abdominal compartment syndrome. Elevation of the diaphragm and increasing abdominal pressure may adversely affect the cardiovascular and respiratory systems by (a) decreasing respiratory compliance, (b) increasing the respiratory rate, (c) increasing peak inspiratory pressure, (d) increasing the heart rate, (e) increasing mean arterial pressure and systemic vascular resistance, (f) reducing femoral venous return, and (g) compressing the inferior vena cava.7 Animal studies suggest that chronic abdominal loading leads to a biochemical remodeling of diaphragmatic muscle from fibers that are slow-twitch fatigue resistant to fibers that are fast-twitch fatigue vulnerable.8 In animals, an increase in IAP also raises systolic and diastolic blood pressures and upregulates the renin-angiotensin-aldosterone system.9,10 Furthermore, several studies have shown that patients with tense ascites decompressed by large-volume paracentesis significantly improve lung volumes and ventilatory function and decrease their systemic vascular resistance.11–14 As our patient’s IAP slowly increased, her cardiopulmonary reserve would have diminished. We speculate that, together with her underlying coronary artery disease and lung tumor, she became more and more susceptible to hypoxia and went into a sudden lethal dysrhythmia.

This case is instructive because the patient presented with an enlarged ovarian cyst 3 years before her death, at a time when surgical intervention, either by laparotomy or by laparoscopy, may have been curative.4,15,16 Review of the CT scan of the abdomen/pelvis and the abdominal ultrasound examinations left clues to the actual underlying pathology. On CT scan, it is atypical to note displacement of abdominal viscera by ascites, with the exception of so-called tense ascites, whereas this is a common finding in massive ovarian cysts.17 Furthermore, fluid was not noted about the lateral aspects of the liver, typically seen in ascites.18 In addition, the contour of the liver was normal, as were her liver enzymes, coagulation studies, and renal functions. On ultrasound examination, an inability to observe abdominal viscera with an ability to identify loculated structures is also consistent with features of a multiloculated ovarian cyst. Paracentesis did not support an ongoing malignant or infectious process. In this case, an elevated serum-ascites albumin gradient falsely supported a working diagnosis of ascites due to portal hypertension. However, the paracentesis collected pseudoascitic fluid not ascitic fluid. Despite their impressive size, such cysts have been safely resected, relieving symptoms and lowering morbidity. There is currently a debate as to whether presurgical removal of some fluid is necessary.19 In brief, this case of a middle-aged female is brought to the attention of forensic and autopsy pathologists to alert them to the unusual condition known as pseudoascites in patients who present with a markedly increased abdominal girth, fluid wave, and sudden death.

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REFERENCES

1. Shilo L, Hirsch D, Ellis M, et al.. Pseudoascites—still a diagnostic pitfall. Isr Med Assoc J. 2001; 3: 770–771.

2. Kaya M, Sakarya MH. Pseudoascites: report of three cases. Turk J Gastroenterol. 2009; 20: 224–227.

3. Fiedorek SC, Casteel HB, Reddy G, et al.. The etiology and clinical significance of pseudo ascites. J Gen Intern Med. 1991; 6: 77–80.

4. Kim YT, Kim JW, Choe BH. A case of huge ovarian cyst of 21-year-old young woman. J Obstet Gynaecol Res. 1999; 25: 275–279.

5. Chao A, Chao A, Yen YS, et al.. Abdominal compartment syndrome secondary to ovarian mucinous cystadenoma. Obstet Gynecol. 2004; 104: 1180–1182.

6. Malbrain MLNG, Cheatham ML, Kirkpatrick A, et al.. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. I. Definitions. Intensive Care Med. 2006; 32: 1722–1732.

7. Nguyen NT, Wolfe BM. The physiologic effects of pneumoperitoneum in the morbidly obese. Ann Surg. 2005; 241: 219–226.

8. Papavramidis TS, Kotidis E, Ioannidis K, et al.. Diaphragmatic adaptation following intra-abdominal weight charging. Obes Surg. 2010. [Epub ahead of print] PubMed PMID: 21153889.

9. Bloomfield GL, Sugerman HJ, Blocher CR, et al.. Chronically increased intra-abdominal pressure produces systemic hypertension in dogs. Int J Obes Relat Metab Disord. 2000; 24: 819–824.

10. Bloomfield GL, Blocher CR, Fakhry IF, et al.. Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels. J Trauma. 1997; 42: 997–1004.

11. Berkowitz KA, Butensky MS, Smith RL. Pulmonary function changes after large volume paracentesis. Am J Gastroenterol. 1993; 88: 905–907.

12. Chao Y, Wang SS, Lee SD, et al.. Effect of large-volume paracentesis on pulmonary function in patients with cirrhosis and tense ascites. J Hepatol. 1994; 20: 101–105.

13. Coll S, Vila MC, Molina L, et al.. Mechanisms of early decrease in systemic vascular resistance after total paracentesis: influence of flow rate of ascites extraction. Eur J Gastroenterol Hepatol. 2004; 16: 347–353.

14. Cabrera J, Falcón L, Gorriz E, et al.. Abdominal decompression plays a major role in early postparacentesis haemodynamic changes in cirrhotic patients with tense ascites. Gut. 2001; 48: 384–389.

15. Ueda S, Yamada Y, Tsuji Y, et al.. Giant abdominal tumor of the ovary. J Obstet Gynaecol Res. 2008; 34: 108–111.

16. Postma VA, Wegdam JA, Janssen IM. Laparoscopic extirpation of a giant ovarian cyst. Surg Endosc. 2002; 16: 361.

17. Mikos T, Tabakoudis GP, Pados G, et al.. Failure of ultrasound to diagnose a giant ovarian cyst: a case report. Cases J. 2009; 2: 6909.

18. Jolles H, Coulam CM. CT of ascites: differential diagnosis. AJR Am J Roentgenol. 1980; 135: 315–322.

19. Einenkel J, Alexander H, Schotte D, et al.. Giant ovarian cysts: is a pre- and intraoperative drainage an advisable procedure? Int J Gynecol Cancer. 2006; 16: 2039–2043.

Keywords:

pseudoascites; ovarian cyst

© 2012 Lippincott Williams & Wilkins, Inc.

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