(Consecutive exotropia may however also spontaneously develop from esotropia, without surgery or botulinum toxin treatment.) Because of the risks of surgery, and because about 35% of people require at least one more surgery, many people try vision therapy first. This consists of visual exercises. Although vision therapy is generally not covered by American health insurance companies, many large insurers such as Aetna have recently begun offering full or partial coverage in response to recent studies. Strabismus surgery is sometimes recommended if the exotropia is present for more than half of each day or if the frequency is increasing over time. It is also indicated if a child has significant exotropia when reading or viewing near objects or if evidence shows that the eyes are losing their ability to work as a single unit (binocular vision). Finally, if there is a complaint of headaches, and no other cause for the headaches can be found, then these headaches could be because the child or adult is trying to control the exotropia. If none of these criteria are met, surgery may be postponed pending simple observation with or without some form of eyeglass and/or patching therapy. In very mild cases, a chance exists that the exotropia will diminish with time. The long-term success of surgical treatment for conditions such as intermittent exotropia is not well proven, and surgery can often result in a worsening of symptoms due to overcorrection. Evidence from systematic reviews of interventions show clinical benefits for patching for children ages 12 months to ten years.
Glutaric acidemia type 2 is an autosomal recessive metabolic disorder that is characterised by defects in the ability of the body to use proteins and fats for energy. Incompletely processed proteins and fats can build up, leading to a dangerous chemical imbalance called acidosis. Genetics
Mutations in the ETFA, ETFB, and ETFDH genes cause glutaric acidemia type II. Mutations in these genes result in a deficiency in one of two enzymes that normally work together in the mitochondria, which are the energy-producing centers of cells. The ETFA and ETFB genes encode two subunits of the enzyme electron transfer flavoprotein, while the ETFDH gene encodes the enzyme electron-transferring-flavoprotein dehydrogenase. When one of these enzymes is defective or missing, the mitochondria cannot function normally, partially broken-down proteins and fats accumulate in the cells and damage them; this damage leads to the signs and symptoms of glutaric acidemia type II.This condition is inherited in an autosomal recessive pattern, which means the defective gene is located on an autosome, and two copies of the gene – one from each parent – are needed to inherit the disorder. The parents of an individual with an autosomal recessive disorder are carriers of one copy of the defective gene, but do not show signs and symptoms of the disorder themselves. Diagnosis
Glutaric acidemia type 2 often appears in infancy as a sudden metabolic crisis, in which acidosis and low blood sugar (hypoglycemia) cause weakness, behavior changes, and vomiting.