The removal of the ear canal wall results in: 

a space, the "mastoid cavity", which is less likely than the original ear canal to resist infection;
exposure of the ossicles, which may allow the subsequent formation of a new cholesteatoma deep to the ossicles. To prevent this, these ossicles must be removed, which may diminish the patients hearing.The formation of a mastoid cavity by removal of the canal wall is the simplest and most effective procedure for facilitating the removal of cholesteatoma, but may bestow the most lasting infirmity due to loss of ear function upon the patient treated in this way. The following strategies are employed to mitigate the effects of canal wall removal:

Careful design and construction of the mastoid cavity. This is essential for the health and integrity of the protective sheet of migrating, keratising epithelium which lines the distorted ear canal. This requires the surgeon to saucerise the cavity. A high facial ridge and an inappropriately small cartilaginous meatus are obstructions to epithelial migration and are particularly high risk factors for failure of the self-cleaning mechanism of the external ear. Partial obliteration of the mastoid cavity. This can be performed using a wide range of materials. Many of these resorb in time, which means that the long-term results of such surgery are poorer than the short-term results. Reconstruction of the ear canal wall. Canal wall reconstruction has been performed using ear canal skin alone, fascia, cartilage, titanium as well as by replacing the original intact wall.
Hypothermia, thrombocytopenia, leukopenia, hypocalcemia, and bleeding in the lungs are often results of IUGR.Infants with IUGR are at increased risk of perinatal asphyxia due to chronic hypoxia, usually associated with placental insufficiency, placental abruption, or a umbilical cord accident. This chronic hypoxia also places IUGR infants at elevated risk of persistent pulmonary hypertension of the newborn, which can impair an infants blood oxygenation and transition to postnatal circulation.If the cause of IUGR is intrinsic to the fetus, growth is restricted due to genetic factors or as a sequela of infection. IUGR is associated with a wide range of short- and long-term neurodevelopmental disorders. Cardiovascular
In IUGR, there is an increase in vascular resistance in the placental circulation, causing an increase in cardiac afterload. There is also increased vasoconstriction of the arteries in the periphery, which occurs in response to chronic hypoxia in order to preserve adequate blood flow to the fetus vital organs. This prolonged vasoconstriction leads to remodeling and stiffening of the arteries, which also contributes to the increase in cardiac afterload. Therefore, the fetal heart must work harder to contract during each heartbeat, which leads to an increase in wall stress and cardiac hypertrophy. These changes in the fetal heart lead to increased long-term risk of hypertension, atherosclerosis, cardiovascular disease, and stroke. Pulmonary
Normal lung development is interrupted in fetuses with IUGR, which increases their risk for respiratory compromise and impaired lung function later in life.