Possible problems include:

Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
Damage to the eye: optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts, chorioretinitis, optic atrophy
Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horners syndrome
Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction
Skin disorders: (cicatricial) skin lesions, hypopigmentationInfection late in gestation or immediately following birth is referred to as "neonatal varicella". Maternal infection is associated with premature delivery. The risk of the baby developing the disease is greatest following exposure to infection in the period 7 days before delivery and up to 8 days following the birth. The baby may also be exposed to the virus via infectious siblings or other contacts, but this is of less concern if the mother is immune. Newborns who develop symptoms are at a high risk of pneumonia and other serious complications of the disease. Pathophysiology
Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), postherpetic neuralgia, and sometimes Ramsay Hunt syndrome type II.
Some countries require the varicella vaccination or an exemption before entering elementary school. A second dose is recommended five years after the initial immunization. A vaccinated person is likely to have a milder case of chickenpox if they become infected. Immunization within three days following household contact reduces infection rates and severity in children. Being exposed to chickenpox as an adult (for example, through contact with infected children) may boosts immunity to shingles. So it was thought, that when the majority of children are vaccinated against chickenpox, adults might lose this natural boosting, so immunity would drop and more shingles cases would occur. On the other hand, current observations suggest that exposure to children with varicella is not a critical factor in the maintenance of immunity. Multiple subclinical reactivations of varicella zoster virus may occur spontaneously and, despite not causing clinical disease, may still provide an endogenous boost to immunity against zoster.It is part of the routine immunization schedule in the US. Some European countries include it as part of universal vaccinations in children, but not all countries provide the vaccine. In the UK as of 2014, the vaccine is only recommended in people who are particularly vulnerable to chickenpox. This is to keep the virus in circulation thereby exposing the population to the virus at an early age, when it is less harmful, and to reduce the occurrence of shingles in those who have already had chickenpox by repeated exposure to the virus later in life.