Non-immune hydrops fetalis is a severe fetal condition defined as the excessive accumulation of fetal fluid within the fetal extravascular compartments and body cavities. The prevalence of non-immune hydrops fetalis is unknown. Currently, about 90% of cases of hydrops fetalis are non-immune hydrops fetalis. Non-immune hydrops fetalis causes are multi-factorial. The pathophysiological mechanism of non-immunologic hydrops fetalis is related to abnormal fluid transportation between plasma and tissues. This is due to the increase in hydrostatic capillary pressure and capillary permeability and a reduction of the plasma osmotic pressure or lymphatic flow. A variety of viral infection agents have been associated with non-immune hydrops fetalis like parvovirus B19, herpes simplex virus, cytomegalovirus, Toxoplasma gondii, Treponema pallidum, but even other viruses that attack the maternal and fetus during pregnancy cannot be excluded as possible causes of non-immune hydrops fetalis. We present one case of non-immune hydrops fetalis who was diagnosed intra-uterine, three weeks after recovery from Coronavirus disease (COVID-19). After much investigation, we could not find any known factor that may be the cause of non-immunologic hydrops fetalis. Therefore, we predisposed a possible causal connection between nonimmunologic hydrops fetalis and Coronavirus disease (COVID-19).

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A 37-year-old woman presented in the Obstetrics and Gynecology Clinic, for the evaluation of pregnancy, which was in the 20 th week of gestation. The patient had received a diagnosis for congenital fetal anomalies, by her doctor, who had followed her pregnancy. The patient had no earlier personal history of congenital fetal anomalies, and she had no family history of congenital anomalies. Ultrasound examination showed a skull defect, localized in the occipital region that was a cystic formation or cephalocele. This anomaly was shown with a transthalamic view. The condition is characterized by protrusion of intracranial structures through a cranial bone defect. The herniated anatomic structures can consist of meninges only (meningocele) or meninges plus cerebral tissue (encephalomeningocele). The most common location of cephaloceles is occipital region, but it can also be on frontal region, parietal, occipital, frontoethmoidal, etc. There is an incidence around 1 in 5000 to 1 in 100 000 at birth, but decreasing due to prenatal diagnosis. It is generally thought that cephalocele is caused by a lack of fusion of the neural tube in its specific closing sites. For a correct evaluation of the encephalic structures, apart ultrasound examination in different plans often needed an MRI-scan. During differential diagnosis, the most important lesions to differentiate from occipital meningocele are cystic hygroma, teratoma, and hemangioma. When we have a cephalocele be detected in a fetus, a thorough search for possibly associated structural anomalies has to be carried out (Figure 1). Delivery by cesarean section is advisable to avoid trauma and infection (through the delivery canal) of the exposed brain tissue. Small cephaloceles can be corrected surgically. Very large lesions have an unfavorable prognosis hence there is no benefit from treatment. The postnatal mortality rate varies from 30% to 50%, depending on the dimensions and the location of the lesion, in the presence of cerebral tissue in the herniated sack, etc. Figure 1: A) and B) Two views to occipital cephalocele.