Ovarian dermoid cysts, also called mature cystic teratomas (MCTs), account for 69% of ovarian germ cell tumors in young women. The tumors are formed by tissues derived from three germ layers, and sebaceous materials are most commonly seen. The origin of MCTs is widely considered to be the germ cell origin, which completes meiosis I. The clinical symptoms vary widely, but 20% of tumors could be asymptomatic. The diagnosis of MCTs is usually made without difficulty by ultrasound and confirmed by histopathology post-operatively. The imaging findings have a high diagnostic value. The typical characteristics present in the sonographic images, including a dermoid plug or Rokitansky nodule, are considered strong evidence for a teratoma. Although the malignant transformation of MCTs is rare, it can occur in some cases, especially in women of advanced age. The treatment of MCTs depends on the risk of malignancy, the age of the patient, and the patient's fertility reserve requirement. In this article, we review the epidemiology, clinical symptoms, diagnosis criteria, cellular origin, and treatment of mature cystic teratomas.

Mature cystic teratomas (dermoid cysts) are the most common germ cell tumours with 10-25% incidence of adult and 50% of paediatric ovarian tumours. The aetiology of dermoid cysts is still unclear, although currently the parthenogenic theory is most widely accepted. The tumour is slow-growing and in the majority of cases it is an accidental finding. Presenting symptoms are vague and nonspecific. The main complication of a dermoid cyst is cyst torsion (15%); other reported complications include malignant transformation (1-2%), infection (1%), and rupture (0.3-2%). Prolonged pressure during pregnancy, torsion with infarction, or a direct trauma are the main risk factors for a  spontaneous dermoid rupture that can lead to acute or chronic peritonitis. The diagnosis of mature cystic teratoma is often made in retrospect after surgical resection of an ovarian cyst, because such imaging modalities as ultrasound, computer tomography, or magnetic resonance imaging cannot yet accurately and reliably distinguish between benign and malignant pathology.

We present a report of a clinical case of a 35-years-old female, who was referred to the hospital due to abdominal pain spreading to her feet for three successive days. She had a history of a normal vaginal delivery one month before. Abdominal examination revealed mild tenderness in the  lower abdomen; no obvious muscle rigidity was noted. Transvaginal ultrasound showed a multiloculated cystic mass measuring 16 × 10 cm in the pelvis. In the absence of urgency, planned surgical treatment was recommended. The next day the patient was referred to the hospital again, with a complaint of stronger abdominal pain (7/10), nausea, and vomiting. This time abdominal examination revealed symptoms of acute peritonitis. The ultrasound scan differed from the previous one. This time, the transvaginal ultrasound scan revealed abnormally changed ovaries bilaterally. There was a large amount of free fluid in the abdominal cavity. The patient was operated on - left laparoscopic cystectomy and right adnexectomy were performed. Postoperative antibacterial treatment, infusion of fluids, painkillers, prophylaxis of the thromboembolism were administered. The patient was discharged from the hospital on the seventh postoperative day and was sent for outpatient observation.

Ultrasound is the imaging modality of choice for a dermoid cyst because it is safe, non-invasive, and quick to perform. Leakage or spillage of dermoid cyst contents can cause chemical peritonitis, which is an aseptic inflammatory peritoneal reaction. Once a rupture of an ovarian cystic teratoma is diagnosed, immediate surgical intervention with prompt removal of the spontaneously ruptured ovarian cyst and thorough peritoneal lavage are required.

Rupture of a benign cystic ovarian teratoma may result in severe chemical granulomatous peritonitis, a condition mimicking peritonitis carcinomatosa, with patients complaining of common abdominal symptoms. As the precipitating cause of rupture is often indeterminate and the rupture itself is hard to recognize, it is difficult to differentiate from peritonitis of other etiologies, such as gastrointestinal malignancy. We report the case of a 72-year-old female who presented with recurrent pyrexia and abdominal distension. Laboratory data showed signs of inflammation and a high level of carbohydrate antigen 125. Imaging examinations showed left-side-dominant pleural effusion, ascites with peritoneal adhesions, and a left cystic ovarian teratoma. Repeat paracentesis of both the pleural effusion and ascites demonstrated exudative characteristics, but there was no indication of malignancy or signs of infection, including those of tuberculosis. Although exploratory laparotomy was then recommended for conclusive diagnosis and ruling out such gynecological malignancy, the patient declined. Fortunately, laboratory data, radiological images, and other clinical findings gradually improved over the following 12 months. Moreover, a retrospective review of the computed tomography images revealed lipid particles in the ascites, indicative of teratoma rupture. The final diagnosis was chemical peritonitis and pleuritis caused by spontaneous rupture of the benign cystic teratoma. The present case was extremely rare with regard to its diagnosis and clinical progression. Our experience suggests that chemical peritonitis should be included in the differential diagnosis of peritonitis.