What to Expect the Toddler Years (257 page)

How common is it?
1 in 133 people in the U.S. has celiac disease, but the odds increase if the person has other autoimmune conditions (1 in 56) or has a parent, child, or sibling with the disease (1 in 22). It is less prevalent in African-, Hispanic-, or Asian-Americans (1 in 236).

Who is susceptible?
It’s not clear; children with affected family members have a slightly increased risk.

What causes it?
Also unclear. Most likely some combination of environmental factors and genetic predisposition is involved.

Related problems.
Lactose intolerance in some children; malabsorption of fat; fluid retention; developmental delays; late teething; rickets.

Treatment/management.
Once the diagnosis has been confirmed via a biopsy of
the small bowel (intestine), a gluten-free diet is prescribed, along with extra calories and vitamin and mineral supplementation to help the child catch up growthwise. Baked goods and pasta made with rice, corn, soy, potato, or other gluten-free flours replace the traditional grains. Grain by-products such as malt, hydrolized vegetable protein, modified starches, vegetable gums, MSG, and vinegar are also avoided. Another biopsy may be done after six to twelve months on the diet to see if it is working. If the bowel appears normal at that time, gluten may be reintroduced into the diet. After two years, or as soon as symptoms reappear, another bowel biopsy is performed. A positive biopsy confirms the diagnosis, and the gluten-free diet is resumed. Although continuing this diet for a lifetime has long been recommended, some experts believe that such an extreme approach may not be necessary.

Prognosis.
The gluten-sensitive individual can live a perfectly normal life as long as gluten products are avoided. Since there are now many gluten-free products on the market, this is easier to do than it was in the past. If a mild case of GSE is missed and untreated in childhood, the individual may not grow to full genetic height.

What is it?
Also called static encephalopathy, CP is a neuromuscular disorder. It’s nonprogressive (which means it doesn’t get worse, although its manifestations may change) and is divided into three types: spastic, athetoid, and ataxic. Signs of a problem may not be noted until a child is six or seven months old and diagnosis may not be made until midway through the second year of life or later.

Symptoms vary from mild to severe and may differ from case to case, depending on the type of CP. In toddlers symptoms often include: a history of delayed development (the child didn’t sit, stand, walk, talk at the usual ages); poor motor control with diminished (floppy) or excessive (stiff) muscle tone; spasticity.

How common is it?
CP is the most common movement disorder of childhood, with an estimated incidence of about 2 to 3 per 1,000 births.

Who is susceptible?
Very low-birth-weight babies (under 3
¹
/
₂
pounds or 1,500 grams); boys slightly more often than girls; white infants more often than black; twins, triplets, and quadruplets more than singletons; and children with other major or minor physical malformations.

What causes it?
Most often, probably damage to the developing nervous system during the prenatal period. A wide range of possible agents have been suggested, including: maternal smoking or drug or alcohol abuse; Rh incompatibility; and maternal hyperthyroidism. Though it’s also been suggested that some cases may be genetic, this isn’t entirely clear. Studies have found that an association between CP and a lack of oxygen or other trauma during childbirth only account for 5 to 10 percent of cases. Other cases of CP result from brain damage (due to a head injury or illness, such as meningitis) early in childhood. Many cases of CP have no identifiable cause.

Related problems.
Sometimes, seizures; also communication (speech, vision, and hearing) disorders; dental defects; mental retardation; learning disabilities.

Treatment/management.
No cure, but early detection and therapy can help a child reach his or her potential. Treatment plans should stress the whole child, and may include: surgery to reduce spasticity
or otherwise improve functioning; medication; physical therapy, and training in alternative modes of movement; speech therapy, and training in alternative modes of communication, such as computer-synthesized communication; occupational therapy; braces, splints, or other orthotics; special furniture and utensils, and training in self-sufficiency. Reduction of sudden noise in the environment may be helpful when the child is noise-sensitive.

Prognosis.
When intelligence is normal, a good long-term outcome can be achieved through providing the child with a way to communicate, a way to get around, and the ability to perform the tasks of daily living. When there is a mental or cognitive (learning) handicap, mild or major, outcomes can vary greatly, depending on the individual case.

What is it?
A condition in which there is a generalized dysfunction of the exocrine glands—the glands that discharge secretions through the skin, the mucous membranes, and the linings of the hollow organs. Because the sweat glands are affected, perspiration is salty and profuse, and the disease is often first diagnosed when parents note the saltiness of the skin on kissing their child (there may even be salt crystals visible). Also invariably involved, to a lesser or greater degree, is the respiratory system. Thick secretions eventually fill the lungs, causing chronic coughing and increased risk of lower respiratory infection. The pancreas is also generally affected. The pancreatic ducts become blocked, pancreatic enzymes become deficient, and as a result, the child cannot digest fats and proteins properly. Undigested material is excreted in stools that are large, bulky, foul-smelling, pale, and fatty. Though appetite is ravenous, weight gain is poor; the child’s abdomen is distended, arms and legs thin, and skin sallow.

How common is it?
It is the most common serious genetic disorder affecting 1 in 3,000 babies. It affects both boys and girls, and is more commonly found in whites. It also affects Latinos and Native Americans, and is less common in African Americans and Asians.

Who is susceptible?
Most often, children of white Anglo-Saxon ancestry.

What causes it?
Autosomal recessive inheritance; both parents must pass on recessive genes for their child to have CF. Since the gene has now been located, testing is often possible to determine whether parents are carriers and whether their unborn children are affected.

Related problems.
If fluids are not adequately replaced, excessive perspiration can lead to dehydration and shock. Pneumonia and other respiratory illnesses are common with lung involvement; diabetes with pancreatic involvement; sinusitis; liver damage; gastro esophageal reflux and other digestive disorders; malnutrition; infertility in most males, and in some females.

Treatment/management.
No cure yet, but early diagnosis (most cases can be diagnosed prenatally) and a comprehensive, intensive therapy program are essential to improving the outlook. Depending on the individual case, the program may include many or all of the following:
Nutritional supplementation
, with about 50% more calories than are normally needed (to fuel growth and activity), a high protein and moderate fat intake, vitamin and mineral supplementation, a copious fluid intake (to help thin secretions), and generous salting of
food and salt supplements in hot weather (to prevent salt depletion).
Pancreatic enzymes
, given by mouth with meals and snacks, for digestive problems.
Respiratory therapy
, including postural drainage to help loosen and remove secretions, given daily for respiratory problems.
Oxygen therapy
, as needed.
Air control
, to keep room air cool, dry, and smoke-free.
Medication
, as needed. Infections are treated with large doses of antibiotics, insulin depletion with insulin.
Surgery
, if rectal prolapse becomes a problem.

A variety of experimental treatments hold promise, including: genetic manipulation; the use of an inhaled enzyme to break up thick secretions in the lungs, the use of anti-inflammatory agents, aerosol therapy, immunotherapy, and a vaccine to prevent infection by
Pseudomonas aeruginosa
.

Prognosis.
Steadily improving. Once, children with CF rarely survived childhood, usually because of respiratory failure. Today, with early diagnosis, aggressive treatment (especially at a major CF center; ask your child’s doctor for a referral to the nearest center), and strong family support, more than half live to the age of twenty-eight, and many more are now reaching their thirties, forties, and fifties, and lead busy, active lives. Some have married, and though males with CF are generally sterile, some women with CF have successfully borne children. The outlook for today’s toddler is even better.

What is it?
Type 1, or insulin-dependent diabetes mellitus (IDDM; also called juvenile-onset diabetes), is an autoimmune disorder in which the body’s immune system attacks the insulin-producing beta (or islet) cells of the pancreas. Insulin is needed to turn sugar into energy that can be used by the cells. When there is inadequate insulin, sugar builds up in the blood, spilling over into the urine and making it sweet—thus the name diabetes mellitus (“mellitus” means sweet). The starving cells, not getting their usual energy source, start to burn fat stores instead. This can lead to serious complications, including a potentially fatal diabetic coma.

Symptoms of high blood sugar in a toddler include frequent urination (difficult to judge in one still in diapers), excessive thirst, excessive appetite coupled with poor weight gain, and, sometimes, lethargy.

How common is it?
One child in 500 is diagnosed with Type 1 diabetes each year—that’s more than 15,000, or about 40 per day. Type 1 is most commonly diagnosed in childhood and teenage years, although the disease can develop in a person in their 20s, 30s, or 40s.

Who is susceptible?
Most often, children with a family history of IDDM.

What causes it?
Destruction of the insulin-producing beta cells. Just which component or components of the immune system are responsible for this destruction is still to be definitely determined. The disease is not passed on via a single gene, but there appears to be an inherited susceptibility toward developing it. Other factors are apparently also involved, though it isn’t clear what they are. The theory, suggested by one study, that for susceptible children, cow’s milk in the first year of life could be a triggering factor and that breast milk could be protective, has not been confirmed.

Related problems.
Retinopathy (damage to the retina of the eye); nephropathy (kidney damage); neuropathy (nervous system damage); premature coronary artery disease; poor circulation to hands
and feet. The risk of such complications can be greatly reduced with very careful control of blood sugar levels; about 1 in 4 diabetics never develop a complication.

Treatment/management.
Aimed at keeping blood sugar at normal levels, treatment usually includes: administration of insulin, home glucose monitoring, exercise (which, among other benefits, helps burn excess sugar and maintain normal circulation to the feet), and dietary management. Dietary management is necessary both to keep blood sugar from soaring too high (by limiting the intake of sugary foods) and to keep it from dropping too low (by serving meals and snacks at regular hours and avoiding long periods without food). Though diets must be individually tailored, the recommended diet for children with diabetes is typically 50% complex carbohydrates, 20% protein, and 30% fat. Pancreas transplants, sometimes recommended for adults, are not recommended for children—the surgery and the required immunosuppression are too risky.

Clinical studies in the works that hold promise include: early suppression of the immune cells to prevent further destruction of beta cells; transplantation of beta cells, which might end the need for insulin shots and prevent or reverse many of the serious complications of diabetes; an implantable insulin pump and an automatic glucose sensor, which together will be able to monitor blood sugar and administer insulin as needed. Meanwhile, parents of toddlers (and other caregivers) will have to take charge of this insulin monitoring and administration process—until the children are old enough to take over.

It’s important for parents to keep in mind that on beginning treatment, newly diagnosed IDDM patients often seem to get better, even to need less insulin. That’s because some insulin-producing cells are still working and when outside insulin is administered, they seem to perk up. But this “honeymoon” period doesn’t last more than a year or two (the cells eventually stop producing insulin entirely), and parents should not become lax in attention to treatment during this time.

Prognosis.
For children who are able to maintain good control of their disease (with adult help during childhood), the prognosis for a normal life is excellent.

Prevention.
Still experimental. It is hoped that once tests that screen close relatives of diabetics for antibodies that damage insulin-producing beta cells are refined, accurate prediction of who is likely to eventually develop diabetes will be possible. Those who test positive for the antibodies could then be treated with immunosuppressive therapy aimed at preventing the damage they do.

What is it?
A set of signs and symptoms that usually include delayed development, oval-shaped eyes, an oversized tongue, and a short neck. Children with Down syndrome may also have a flat back of the head, small ears (sometimes folded a little at the tops), a flat, wide nose; short, wide hands; short stature; poor muscle tone; and a sweet, loving, and lovable personality. Characteristics may vary depending on the type of chromosome abnormality. There may also be a variety of related problems (see below). Though it has long been believed that Down syndrome was synonomous with mental retardation, early intervention has shown that some children with Down syndrome have normal IQs; most others have only mild to moderate retardation.