If there is less inflammation, the cholesteatoma may present the appearance of semolina discharging from a defect in the tympanic membrane. The posterior and superior parts of the tympanic membrane are most commonly affected. If the cholesteatoma has been dry, the cholesteatoma may present the appearance of wax over the attic. The attic is just above the eardrum. If untreated, a cholesteatoma can eat into the three small bones located in the middle ear (the malleus, incus and stapes, collectively called ossicles), which can result in nerve deterioration, deafness, imbalance and vertigo. It can also affect and erode, through the enzymes it produces, the thin bone structure that isolates the top of the ear from the brain, as well as lay the covering of the brain open to infection with serious complications (rarely even death due to brain abscess and sepsis). Both the acquired as well as the congenital types of the disease can affect the facial nerve that extends from the brain to the face and passes through the inner and middle ear and leaves at the anterior tip of the mastoid bone, and then rises to the front of the ear and extends into the upper and lower face. Cause
Cholesteatomas occur in two basic classifications:  Acquired cholesteatomas, which are more common, are usually caused by pathological alteration of the ear drum leading to accumulation of keratin within the middle ear. Congenital cholesteatomas are usually middle ear epidermal cysts that are identified deep within an intact ear drum.
Potter analyzed approximately 5000 autopsy cases performed on fetuses and newborn infants over a period of ten years and found that 20 of these infants presented with BRA, all of which had distinctive facial characteristics which did not appear to them to have any specific embryologic correlation with the renal anomaly. It was only much later when she and others attributed the multiple congenital deformities, including the features of Potters facies and also pulmonary hypoplasia, to have been caused by the prolonged severe lack of amniotic fluid. These facial characteristics have subsequently been termed as being known as Potter facies. From her analysis, she was able to deduce the sequence of events that leads to what is now known as Potter sequence.Potter went on to become a pioneer in the field of human renal development and her contributions are still employed and appreciated by clinicians and researchers to this day. Terminology
Potter syndrome is not technically a syndrome as it does not collectively present with the same telltale characteristics and symptoms in each and every case. It is more accurately described as a "sequence" or chain of events  that may have different beginnings (absent kidneys, cystic kidneys, obstructed ureters or other causes), but which all end with the same conclusion (absent or reduced volume of amniotic fluid). This is why Potter syndrome is often called Potter sequence or oligohydramnios sequence by some clinicians and researchers.