**3. Etiology**

The etiopathology of catamenial pneumothorax remains unclear, but there are some theories explaining the etiopathogenesis of catamenial pneumothorax. These theories include physiological, migrational, microembolic-metastatic, and the diaphragmatic theory of air passage [17] (**Table 1**).

According to the physiologic hypothesis, high levels of circulating prostaglandin F2 during menstrual cycle cause vasoconstriction and this induces alveolar rupture and pneumothorax. Pulmonary bullae blebs may be more sensitive to ruptures during hormonal changes. There are no pathognomonic lesions in such cases and this issue supports the physiologic theory [4, 7, 8, 24, 31].

In metastatic or lymphovascular microembolization theory, endometrial tissue spread through the venous and/or the lymphatic system to the lungs, and subsequent catamenial necrosis of endometrial parenchymal site adjacent to visceral pleura causes pneumothorax. If parenchymal endometrial focus is located centrally, hemoptysis may be present as a symptom [3, 4, 7, 8, 22, 24, 30–32]. Endometrial tissue can be detected in the lung parenchyma, at knee, in the brain, and in the eye. This supports the metastatic theory [12].

According to the transgenital-transdiaphragmatic passage of air theory, absence of cervical mucus during menstruation provides air passage from the vagina to the uterus, through the cervix. Then, air enters the peritoneal cavity straight through the fallopian tubes and reaches to the pleural space by diaphragmatic defects [4, 7, 8, 22, 24, 31]. This passage is facilitated by the difference in atmospheric pressures between pleural space and peritoneal space since the atmospheric pressure in the pleural cavity is less than the pressure in the peritoneal cavity.

**43**

pneumothorax.

*Catamenial Pneumothorax*

Metastatic or lymphovascular microembolization hypothesis

transdiaphragmatic passage

Transgenital-

*passage.*

**Table 1.**

of air hypothesis

*DOI: http://dx.doi.org/10.5772/intechopen.82564*

can be explained by this theory [7, 24, 29, 36].

*etiopathogenesis of catamenial pneumothorax.*

**4. Clinical manifestations and diagnosis**

There are few reports in the literature regarding transgenital-transdiaphragmatic passage of air theory. There are rare cases reporting simultaneous [33, 34] or undulating episodes CPX and pneumoperitoneum [35], and also case reports defining radiologic findings of small diaphragmatic defects associated with ipsilateral CPX [21]. But repeated episodes of pneumothorax after hysterectomy, fallopian tube ligation, and diaphragmatic resection provide evidence that all the CPX cases

*The etiopathology of catamenial pneumothorax remains unclear, but there are some theories explaining the* 

underlying alveoli, and pneumothorax occurs.

*These theories include physiological, migrational, microembolic-metastatic, and the diaphragmatic theory of air* 

Physiological hypothesis High levels of circulating prostaglandin F2 during menstrual cycle cause

by diaphragmatic defects. Migration hypothesis Following catamenial necrosis of this diaphragmatic endometrial

vasoconstriction, and this induces alveolar rupture and pneumothorax.

Absence of cervical mucus during menstruation provides air passage from the vagina to the uterus, through the cervix. Then air enters the peritoneal cavity straight through the fallopian tubes and reaches to the pleural space

implants results in diaphragmatic perforations. Endometrial tissue then passes through this diaphragmatic perforation and spreads into the thoracic cavity. Ectopic endometrial tissue implants to the visceral pleura and following catamenial necrosis of this tissue causes rupture of the

Endometrial tissue spreads through the venous and/or the lymphatic system to the lungs, and subsequent catamenial necrosis of endometrial parenchymal site adjacent to visceral pleura causes pneumothorax

Migration theory is based on retrograde menstruation which causes in pelvic seeding of endometrial tissue and migration of this tissue to the subdiaphragmatic sites through the peritoneal fluid flow. Endometrial tissue is mostly implanted to the right hemidiaphragm because peritoneal circulation prefers a clockwise flow through the right paracolic gutter to right hemidiaphragm and the liver facilitates flow with its piston-like activity. Catamenial necrosis of this diaphragmatic endometrial implants results in diaphragmatic perforations. Endometrial tissue then passes through this diaphragmatic perforation and spreads into the thoracic cavity. Ectopic endometrial tissue implants to the visceral pleura and following catamenial necrosis of this tissue cause rupture of the underlying alveoli, and pneumothorax occurs [3, 4, 7, 8, 22, 24, 30, 31]. Endometrial diaphragmatic implants exist along with diaphragmatic perforations [37], and endometrial tissue can be seen at the edges of the diaphragmatic perforations in many cases of CPX [22]; these findings may support the migration theory in the etiopathology of catamenial

The typical clinical manifestations of CPX include spontaneous pneumothorax

with or before menses presented with pain, dyspnea, and cough. Scapular and thoracic pain may also be present before or during menstruation. There may also be a history of previous episodes of spontaneous pneumothorax, history of previous uterine surgery, primary or secondary infertility or uterine scratching, pelvic

