Chronic Granulomatous Peritonitis From Recurrent Bilateral Ovarian Mature Cystic Teratomas Masquerade as Peritoneal Carcinomatosis

ABSTRACT

Although rare, ruptured mature cystic teratoma (MCT) can cause chronic granulomatous peritonitis that mimics peritoneal carcinomatosis. In patients with a history of cystectomy for MCT, careful clinicoradiologic and histopathologic correlation is essential to avoid misdiagnosis and unnecessary aggressive treatment.

1. Introduction

One of the most prevalent ovarian neoplasms in women of reproductive age is mature cystic teratoma (MCT). Because of its pluripotent germ cell origin, this tumor commonly contains keratin, fat, hair, and occasionally bone or teeth [1]. Mature cystic teratomas are about 10%–15% bilateral, and they are typically discovered incidentally on imaging [2]. Although MCTs are usually benign, they may be associated with several complications, including torsion, rupture, infection, hemorrhage, and rarely, malignant transformation [3]. In addition, atypical presentations have been reported, including ovarian tumor‐related anti‐N‐methyl‐D‐aspartate receptor encephalitis and a massive MCT mimicking advanced ovarian malignancy [4, 5].

Due to the thick capsule of the cyst, spontaneous rupture is a very rare complication, occurring in only 1%–2% of cases [6]. Rupture has been documented in a number of clinical settings, including pregnancy (across all trimesters and the postpartum period), ovarian torsion, malignant transformation, trauma or intense physical activity, infection, and idiopathic causes [2]. Sudden rupture typically leads to acute chemical peritonitis due to the spillage of sebaceous contents into the peritoneal cavity. Furthermore, dissemination of tumor contents can induce a more widespread peritoneal inflammatory response [7]. In contrast, chronic granulomatous peritonitis results from the slow, gradual leakage of sebaceous material, reflecting a prolonged course. This chronic process is characterized by multiple small white peritoneal implants, dense adhesions, and variable degrees of ascites. Consequently, adhesions from chemical peritonitis can cause subsequent bowel obstruction—a potentially serious complication. Complete removal of cystic contents and copious peritoneal lavage are recommended to prevent the formation of new adhesions and peritoneal granulomas; this approach has been successful in treating chemical peritonitis caused by a ruptured ovarian teratoma [8].

Clinically and radiologically, granulomatous peritonitis from cystic rupture can mimic other disease processes, such as gynecologic, pelvic, or gastrointestinal malignancies and warrants multidisciplinary management. Herein, we report a rare diagnostically challenging case of recurrent bilateral mature cystic teratomas complicated by chronic granulomatous peritonitis that mimicked peritoneal carcinomatosis on imaging.

2. Case History/Examination

A 43‐year‐old gravida 2, para 2 woman with a history of type 2 diabetes mellitus and hypertension presented with chronic pelvic pain and progressively worsening abdominal bloating. Her family history was notable for gastric cancer in her maternal grandmother, diagnosed at age 65. Approximately 18 months prior, imaging performed for upper abdominal pain and symptomatic gallstones incidentally identified bilateral ovarian MCT. She subsequently underwent laparoscopic cholecystectomy, and 1 month later laparoscopic bilateral ovarian cystectomy, which was complicated by intraoperative cyst rupture. Histopathologic examination confirmed MCT.

Postoperatively, the patient experienced persistent fevers and abdominal pain. A follow‐up computed tomography (CT) scan demonstrated an intra‐abdominal fluid collection, prompting pelvic drain placement. Due to persistent symptoms, she underwent a second surgical intervention the following month to aspirate fluid collection, and the cytologic examination was unremarkable. Three months later, follow‐up pelvic magnetic resonance imaging (MRI) revealed a 3 cm recurrent left ovarian cyst radiologically consistent with dermoid cyst, a 3 cm right ovarian follicular cyst, and multiple small uterine fibroids. At that time, her symptoms gradually improved, although she continued to experience chronic left‐sided pain and bloating.

3. Differential Diagnosis, Investigations, and Treatment

Approximately 1 year after the initial follow‐up MRI, a repeat MRI demonstrated a multiloculated left ovarian cystic lesion adherent to the sigmoid colon and a complex right ovarian cystic lesion closely associated with a loop of small bowel. Additionally, T2‐weighted images showed multiple new cystic lesions with restricted diffusion throughout the pelvis, involving the uterine serosa and bilateral parametria. Multiple nodules suspicious for mesenteric, omental, and serosal peritoneal implants were also identified within the pelvis and lower abdomen, accompanied by trace pelvic fluid (Figure 1A–E).

FIGURE 1.

Pelvic magnetic resonance imaging (MRI) findings. (A) Axial T2‐weighted image showing complex cystic lesions arising from the right ovary (2.7 × 1.6 cm) and left ovary (5.3 × 4.5 cm). (B) Axial high b‐value diffusion‐weighted imaging (DWI) showing restricted diffusion. (C) Coronal T2‐weighted image demonstrating adhesion of the left ovary to the sigmoid colon. (D) Axial T2‐weighted image showing a cystic peritoneal lesion in the left anterior pelvis. (E) Corresponding axial high b‐value DWI showing restricted diffusion within the same lesion. A white arrow indicates all described lesions.

Overall, the MRI findings were highly concerning for malignancy, with features suggestive of peritoneal carcinomatosis. The differential diagnosis included recurrent MCT, primary ovarian malignancy, and other pelvic neoplasms. Her documented last menstrual period was approximately 6 weeks prior to surgery, and preoperative quantitative serum beta‐human chorionic gonadotropin (β‐hCG) was negative (< 1 mIU/mL). The serum tumor markers, including cancer antigen 125 (CA‐125), carbohydrate antigen 19‐9 (CA 19‐9), carcinoembryonic antigen (CEA), and human epididymis protein 4 (HE4), were all within normal ranges. Consequently, the patient underwent robotic‐assisted hysterectomy, bilateral salpingo‐oophorectomy, lysis of dense adhesions, omental biopsy, and pelvic washings with intraoperative frozen section consultation to direct further surgical management (Figure 2A,B).

FIGURE 2.

Intraoperative images of ovarian lesions. Intraoperative views of the left ovary (A) and right ovary (B) show ovarian lesions with dense adhesions to the pelvic sidewall and peritoneum. The black arrow highlights the adherent surface of the left ovarian lesion, and the white arrow indicates white peritoneal nodules/implants from which biopsies were obtained during surgery.

4. Results and Conclusion

On gross inspection, the left ovary (6.5 × 5.5 × 4.5 cm) had a smooth external surface with both cystic and solid components. Sectioning revealed cysts containing soft, yellow, sebaceous material without identifiable hair, bone or teeth. The right ovary (2.7 × 2.0 × 1.7 cm) was densely covered by adhesions and showed solid and cystic components filled with sebaceous material and hair. Microscopic examination of both ovaries revealed a well‐differentiated mixture of mature tissues derived from all three germ layers, including keratinizing stratified squamous epithelium with sebaceous material (ectoderm), mature adipose tissue (mesoderm), and columnar mucinous epithelium resembling gastrointestinal mucosa (endoderm) (Figure 3A,B). Multiple peritoneal and omental biopsies revealed an exuberant foreign‐body giant cell reaction with non‐necrotizing granulomas, epithelioid histiocytes, multinucleated giant cells, chronic lymphoplasmacytic infiltrates, and foreign material consistent with keratin and hair debris (Figure 4A,B). Notably, the left ovary demonstrated a dense plasma cell infiltrate, initially raising concern for plasma cell neoplasia. However, immunohistochemical workup confirmed polyclonality, consistent with a prominent reactive inflammatory response to foreign material secondary to MCT (Figure 5A–E). There was no clinical or histopathologic suspicion of infection; therefore, special stains for microorganisms (e.g., Ziehl‐Neelsen, PAS, and GMS) were not performed. Pelvic washings obtained intraoperatively were negative for malignant cells and lacked significant inflammation or granulomas.

FIGURE 3.

Histopathologic features of bilateral mature cystic teratomas. Hematoxylin and eosin (H&E) sections show mature squamous epithelium with keratinous material (black arrow) and corpus albicans (white arrow) (A). Additional sections show mature squamous epithelium with keratinous material (black arrow) and sebaceous glands (red arrow) (B). The upper‐right inset highlights the associated plasma cell‐rich inflammatory infiltrate.

FIGURE 4.

Histopathology of peritoneal implants associated with teratoma. Low‐ and high‐power hematoxylin and eosin (H&E) images show peritoneal implants containing hair shaft fragments/keratinous material with surrounding foreign‐body giant cell reaction and chronic inflammation (A, B). The black arrow indicates a multinucleated giant cell (B).

FIGURE 5.

Histopathology and immunohistochemical evaluation of plasma cell infiltration in ovarian teratoma. Low‐power hematoxylin and eosin (H&E) image shows mucinous epithelium within the teratoma, indicated by the black arrow (A). High‐power H&E image demonstrates prominent plasma cell‐rich inflammation (B). Immunohistochemical stains show kappa (C), lambda (D), and multiple myeloma oncogene 1 (MUM1) (E) expression.

Overall, the histologic findings supported a diagnosis of chronic granulomatous peritonitis secondary to MCT rupture, with no evidence of malignancy. At approximately 9 months postoperatively, the patient reported persistent abdominal bloating and discomfort without associated pain. Physical and pelvic examination revealed no palpable or concerning masses. A follow‐up CT of the abdomen and pelvis demonstrated a decreased small focus of probable fat necrosis without fluid collection, abscess, or lymphadenopathy. The patient remains under close clinical surveillance.

5. Discussion

Rupture of a MCT is rare, occurring in approximately 0.3%–2% of cases [9]. While acute rupture causes rapid‐onset chemical peritonitis, a micro‐perforation or subtle tear produces a slow leakage of cyst contents, precipitating chronic granulomatous peritonitis. The most common cause of MCT‐associated peritonitis is iatrogenic spillage during laparoscopic cystectomy, where accidental rupture or perforation releases sebaceous material, keratin debris, and hair into the abdominal and peritoneal cavity. In a retrospective review of 496 laparoscopic dermoid cystectomies by Shawki et al., intraoperative spillage occurred in 324 cases (65.3%). Despite this high spillage rate, granulomatous peritonitis remained an exceedingly rare complication, developing in only one patient (0.2%) [10].

During the initial phase of chemical peritonitis, clinical features are often nonspecific; however, patients may develop gastrointestinal symptoms alongside progressive abdominal distension and lower abdominal or pelvic pain. Previously reported cases typically described patients presenting within days to weeks with acute or subacute abdominal pain, occasionally accompanied by fever [7, 8, 11, 12]. However, Rai et al. reported a 40‐year‐old woman who developed chronic granulomatous peritonitis mimicking carcinomatosis 2 years after rupture of a unilateral ovarian MCT, underscoring the potential for an insidious and delayed presentation [1]. A focused narrative literature search of PubMed and Google Scholar was performed for articles published between 2010 and 2025 using the search terms “bilateral ovarian dermoid cyst,” “mature cystic teratoma,” “rupture,” “spillage,” “granulomatous peritonitis,” “chemical peritonitis,” and “peritoneal carcinomatosis.” Relevant reports describing bilateral MCT rupture or intraoperative spillage associated with chemical or granulomatous peritonitis—particular those mimicking peritoneal carcinomatosis—are summarized alongside the present case in Table 1.

TABLE 1.

Reported cases and the present case of bilateral ruptured ovarian dermoid cysts presenting with granulomatous/chemical peritonitis and clinically or radiologically mimicking peritoneal carcinomatosis.

Author/year	Age	Presenting symptoms	Pre‐op imaging findings	Tumor markers	Intra‐op findings	Pathology finding	Management	Post‐op outcome/follow‐up
Present case	43	Chronic pelvic pain and progressive abdominal bloating	MRI: bilateral recurrent ovarian cystic lesions with peritoneal/omental implants and trace ascites.	Normal CA‐125, CA 19‐9, CEA, and HE4; negative β‐hCG	Dense adhesions; bilateral ovarian cystic‐solid lesions with sebaceous material/hair; white peritoneal nodules	Bilateral mature cystic teratomas with chronic granulomatous peritonitis/foreign‐body giant cell reaction; no malignancy	Robotic hysterectomy, bilateral salpingo‐oophorectomy, lysis of adhesions, omental/peritoneal biopsies, and pelvic washings	No malignancy identified, persistent bloating but no pain, under follow‐up
Kudo et al., 2025 [11]	30	Acute pain and fever at POD 20	CT: bilateral tumors with calcifications, fat, small ascites	Elevated (CA‐125 and CA19‐9)	Rupture capsular rents and chemical peritonitis	Mature cystic teratoma (hair, fat, keratinized squamous epithelium, cartilage, adipose tissue)	Laparoscopic removal, lavage, antibiotics, steroids for recurrence	Improvement: recurrence treated; recovered by POD 37
Yamawaki et al., 2025 Case 1 [12]	45	Lower abdominal pain at POD 30	CT: pelvic fat stranding, peritoneal thickening, residual hair and fat implants	Mildly elevated (CA19‐9: mild elevation)	Intra‐abdominal fat and hair remnants; chemical peritonitis	Mature cystic teratoma; chemical peritonitis	Peritoneal lavage via laparoscopic appendectomy	Symptoms improved; no recurrence reported
Yamawaki et al., 2025 Case 2 [12]	28	Lower abdominal pain at POD 27	MRI: diffuse fat deposition and inflammation in pelvis and around liver	Elevated (CA19‐9: 107 U/mL)	Ruptured left ovarian teratoma; widespread fatty and hair deposits; chemical peritonitis	Mature cystic teratoma; chemical peritonitis	Aggressive peritoneal lavage; low‐dose oral steroid therapy	Symptoms improved; no recurrence at follow‐up
Wong et al., 2019 [7]	35	Insidious upper abdominal pain, spontaneous rupture	CT: bilateral ovarian cysts with fat‐fluid level, calcifications, Rokitansky protuberance; fatty pockets at bilateral subphrenic space	N/A	Flimsy adhesions and sebum‐like peritoneal implants	Mature cystic teratomas (benign), no malignancy	Bilateral cystectomy and peritoneal lavage	Symptoms resolved; mild progression of fat implants; chronic peritonitis
Shamshirsaz et al., 2011 [8]	41	Pelvic pain, dyspareunia, fever, anorexia at POD 3	Ultrasound: bilateral ovarian dermoid cysts (left 3.5 × 3.5 cm; right 2.8 × 2.3 cm)	N/A	Residual dermoid contents, extensive filmy adhesions of bowel and omentum	Dermoid cyst contents with chemical peritonitis; no malignancy	Bilateral salpingo‐oophorectomy, partial omentectomy	Excellent recovery; afebrile by POD 2, WBC normalized by POD 4, symptom‐free at 6 months

Abbreviations: CA, cancer antigen; CT, computed tomography; MRI, magnetic resonance imaging; N/A, not available; POD, postoperative day; WBC, white blood cell.

Our patient experienced two distinct recurrences following her initial surgery. The first occurred acutely after the laparoscopic bilateral ovarian cystectomy, which was complicated by intraoperative rupture and resulted in persistent abdominal pain and an intra‐abdominal fluid collection requiring percutaneous drainage and subsequent reoperation. The second recurrence developed insidiously over the subsequent 1.5 years. This prolonged latency, indolent progression and concurrent development of recurrent bilateral teratomas distinguish this case from previously reported cases.

As seen in our patient, ruptured or leaking MCTs can closely mimic peritoneal carcinomatosis on preoperative imaging and intraoperatively due to multiple fat‐fluid levels, scattered calcifications, and nodular peritoneal implants with filmy bowel and omental adhesions. The chronicity and distribution of implants in our patient were markedly more extensive than those previously reported, highlighting the critical need to correlate these imaging findings with the clinical history and histopathologic features to avoid misdiagnosis.

Typical histopathologic features of MCT‐associated chronic granulomatous peritonitis include a foreign‐body giant cell reaction to keratin and hair debris accompanied by chronic inflammation and fibrosis [13]. In addition to the foreign‐body reaction, our patient's left ovary demonstrated an unusually dense plasma cell infiltrate, reflecting a chronic, prolonged immune response rather than a neoplastic process. This histopathologic feature has not been previously reported and expands the known morphologic spectrum of chemical peritonitis secondary to MCT rupture.

Given these diagnostic challenges and pitfalls, clinicians need to expand the differential diagnosis beyond malignancy and consider chronic granulomatous peritonitis in patients presenting with peritoneal nodules who have a history of MCT. To minimize the risk of spillage and subsequent inflammatory complications, surgeons should employ a meticulous, atraumatic technique during cystectomy. Although peritonitis following MCT rupture is exceedingly rare, clinical awareness of this presentation is essential for achieving an accurate diagnosis and guiding appropriate management.

Author Contributions

Zohre Sadeghian: conceptualization, investigation, writing – original draft. Joel Cardenas: data curation, investigation. Kirill Lyapichev: investigation, writing – review and editing. Albert Parlade: investigation, methodology. Elvia Goez‐Gutierrez: investigation, resources. Amir Behdad: supervision, writing – review and editing. Esther Yoon: investigation, resources, supervision, writing – review and editing.

Funding

The authors have nothing to report.

Ethics Statement

As per the policy of our institution, technical notes and case reports involving three or fewer patients do not require formal IRB approval. The authors have fulfilled all ethical standards relevant for this manuscript.

Consent

Written informed consent to publication was obtained from the patient.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author.