Before insertion, a pelvic exam is performed to examine the shape and position of the uterus. A current STI at the time of insertion can increase the risk of pelvic infection. However, routine screening for gonorrhea and chlamydia prior to insertion is not recommended. If a person needs screening and there is no evidence of infection on examination or has been previously screened, insertion of the IUD does not need to be delayed. Insertion
During the insertion, the vagina is held open with a speculum, the same device used during a pap smear. A grasping instrument is used to steady the cervix, the length of the uterus is measured for proper insertion with a uterine sound for decreasing chance of uterine perforation with the IUD, and the IUD is placed using a narrow tube through the opening of the cervix into the uterus. A short length of monofilament plastic/nylon string hangs down from the cervix into the vagina. The string allows physicians and patients to check to ensure the IUD is still in place and enables easy removal of the device. Mild to moderate cramping can occur during the procedure, which generally takes five minutes or less. Insertion can be performed immediately postpartum and post-abortion if no infection has occurred.Misoprostol is not effective in reducing pain in IUD insertion. Removal
Removal of the device should also be performed by a qualified medical practitioner. After removal, fertility will return to previous levels relatively quickly. One study found that the majority of participants returned to fertility within three months.
Hennekam syndrome also known as intestinal lymphagiectasia–lymphedema–mental retardation syndrome, is an autosomal recessive disorder consisting  of intestinal lymphangiectasia, facial anomalies, peripheral lymphedema, and mild to moderate levels of growth and intellectual disability.It is also known as "lymphedema-lymphangiectasia-mental retardation syndrome".Hennekam Syndrome is subdivided according to the causative genetic lesion, most (or all) of which are affecting the VEGF-C/VEGFR-3 signaling pathway:

Type 1 (mutations in CCBE1) 
Type 2 (mutations in FAT4)
Type 3 (mutations in ADAMTS3)The first recognition of a genetic association was with CCBE1, published by its namesake, Raoul Hennekam. The molecular mechanism of the lymphedema phenotype in CCBE1-associated cases was identified as a diminished ability of the mutated CCBE1 to accelerate and focus the activation of the primary lymphangiogenic growth factor VEGF-C. Mutations in the FAT4 gene had previously been only associated with van Maldergem syndrome, but the pathogenetic molecular mechanism and the function of FAT4 within lymphangiogenesis are still unknown. References


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