Retinopathy of prematurity is a bilateral disease of the retinal vessels present in premature infants, some of whom were exposed to high postnatal oxygen concentrations. High oxygen concentration used in treating premature infants, esp. those weighing less than 1500 grams, causes vasoconstriction of the immature retinal vessels and eventually occlusion of the vessels. Fibrous proliferation and invasion of the vitreous may follow this. Retinal detachment may occur at that time or many years later. Blindness develops within several weeks. Other factors can gave an important role in the pathogenesis of retinopathy of prematurity (ROP). Apnea, asphyxia, sepsis, nutritional deficiencies, and a large number of blood transfusions given over a short period of time have all been related to ROP.

Prevention is possible by using only the lowest possible effective oxygen concentration in treating premature infants. Thus, the lowest level possible without endangering the life of the infant is used. Too severe restriction of oxygen will increase the likelihood of hyaline membrane disease and neurologic disorders. All premature infants treated with supplemental oxygen should have careful examination by an ophthalmologist prior to discharge from the hospital. Once blindness develops, there is no effective treatment.

Infantile apnea is when a baby stops breathing for more than 20 seconds or when a baby stops breathing for less than 20 seconds but has other symptoms at the same time, such as: fainting, pale or blue color skin, or a drop in heart rate below 80.

Some causes of apnea include:
• Infection
• Blocked air passages
• Exposure to drugs while in utero
• Congenital heart defects
• Unbalance of body salts
• Convulsions or seizures
• Low blood sugar
• Anemia

Apnea of the premature infant is the most common type of apnea in the newborn. This occurs because the premature infant’s brain is still developing and is not completely ready to control the baby’s breathing. The apnea stops once the premature baby grows and develops. While the baby is still immature, repeated prolonged apnea may cause low heart rate, fainting, and blueness. These symptoms can lead to low oxygen levels in the blood, possibly causing damage to the baby’s vital organs, including the brain. This is why premature babies in the nursery are monitored and treated for apnea with stimulation, medication or even sometimes with respirator support. The apnea monitor alerts us to apnea before it becomes prolonged, so that we may help the baby begin breathing again and avoid symptoms that are more serious.

Apnea monitor use

The reason the baby needs to be on an apnea monitor and the length of the time the monitor is needed depends on the cause of the apnea, and how long it has been since any apnea has occurred. The decision to stop using the apnea monitor is a serious one and needs to be made by the baby’s physician. Generally, the monitor is continued until the baby has been apnea free for two months. Siblings of SIDS victims are often monitored until 6 months of age, or two months past the age at which the sibling died. Most premature infants will outgrow the need for a monitor by the time they are 3 to 4 months of age.

Retinopathy of prematurity is a bilateral disease of the retinal vessels present in premature infants, some of whom were exposed to high postnatal oxygen concentrations. High oxygen concentration used in treating premature infants, esp. those weighing less than 1500 grams, causes vasoconstriction of the immature retinal vessels and eventually occlusion of the vessels. Fibrous proliferation and invasion of the vitreous may follow this. Retinal detachment may occur at that time or many years later. Blindness develops within several weeks. Other factors can gave an important role in the pathogenesis of retinopathy of prematurity (ROP). Apnea, asphyxia, sepsis, nutritional deficiencies, and a large number of blood transfusions given over a short period of time have all been related to ROP.

Prevention is possible by using only the lowest possible effective oxygen concentration in treating premature infants. Thus, the lowest level possible without endangering the life of the infant is used. Too severe restriction of oxygen will increase the likelihood of hyaline membrane disease and neurologic disorders. All premature infants treated with supplemental oxygen should have careful examination by an ophthalmologist prior to discharge from the hospital. Once blindness develops, there is no effective treatment.

Hydrocephalus means an enlargement of the ventricles in the brain. This is caused by an obstruction of the flow of the cerebrospinal fluid. The fluid will build up and cause the ventricles to enlarge. If the ventricles continue to enlarge, the brain tissue will be compressed. Sometimes hydrocephalus will stop and surgery is not needed. If it does not stop on its own, a thin tube called a “shunt” is inserted through the brain into the ventricle; the other part of the tube is passed beneath the skin into the abdominal cavity. This is called a ventriculoperitoneal shunt (V-P shunt). This shunt will drain the cerebrospinal fluid, when it starts to build up, into the abdomen where it is reabsorbed. In infants, the unmistakable sign of hydrocephalus is enlargement of the head clearly disproportionate to the infant’s growth. Other characteristic changes include distended scalp veins; thin, fragile and shiny looking scalp skin; and underdeveloped neck muscles. In severe cases, the eyes are displaced downward, and the sclera is prominent (sunset eyes, setting-sun sign). A high-pitched, shrill cry; abnormal muscle tone of the legs; irritability; anorexia; and projectile vomiting often occur. The major complications of VP shunts are infection and malfunction. All shunts are subject to mechanical difficulties, such as kinking, plugging, or separation or migration of the tubing. Malfunction is most often caused by mechanical obstruction either within the ventricles from particulate matter (tissue or exudate) or at the distal end from thrombosis or displacement because of growth. The most serious complication, shunt infection, can occur at any time but the period of greatest risk is 1 to 2 months following placement. An infection is treated with massive doses of antibiotics administered by the intravenous route or directly into the ventricles via the shunt reservoir. A persistent infection requires removal of the shunt until the infection is controlled.

1. Swelling along shunt tract.
2. High-pitched cry.
3. Bulging fontanels.
4. Prominent scalp veins.
5. Irritability when awake.
6. Increased frontal occipital circumference.
7. Projectile vomiting.
8. Change in appetite.
9. Lethargy.
10. Lower extremity spasticity.
11. Elevated temperature.

The infant with a shunt obstruction or infection often presents as an emergency with clinical manifestations of increased intracranial pressure, frequently accompanied by worsening neurologic status.