McCarter 1997 characterizes the phenotype.
The cause of the miniature embryo phenotype appears to be severing of the oocyte during or following ovulation. Oocyte fragments (with and without egg shells) should be visible in the uterus. The most direct method to confirm the phenotype is to use time-lapse imaging of the ovulation and the spermathecal transit. Of course, the oocyte size could be causing the phenotype.
Take a look at Kovacevic 2010 and Kariya 2004 for examples of genes (fln-1 and plc-1) that have the mini embryo phenotype due to spermathecal transit issues. Deformed embryos (round, elongated, or pinched) can also be caused by spermathecal defects.
Ismar
McCarter, J., Bartlett, B., Dang, T., & Schedl, T. (1997). Soma-germ cell interactions in Caenorhabditis elegans: multiple events of hermaphrodite germline development require the somatic sheath and spermathecal lineages. Dev Biol, 181(2), 121–143.
Kovacevic, I., & Cram, E. J. (2010). FLN-1/filamin is required for maintenance of actin and exit of fertilized oocytes from the spermatheca in C. elegans. Dev Biol, 347(2), 247–257.
Kariya, K.-I., Kim Bui, Y., Gao, X., Sternberg, P. W., & Kataoka, T. (2004). Phospholipase Cepsilon regulates ovulation in Caenorhabditis elegans. Dev Biol, 274(1), 201–210.