T

Tattoos

What is a tattoo?
Who gets a tattoo?
What are the medical risks of a decorative tattoo?
What are the non-medical risks of a decorative tattoo?
How is a tattoo removed?
Links to other information

Paul Gillum, M.D.
Aurora/Parker Skin Care Center
Aurora, Colorado

What is a tattoo?
A “tattoo” refers to any permanent mark made by placing colored material (“pigment”) under the skin surface. The pigment can be nearly any substance, including ink, dye, carbon, or metal. Most decorative tattoos are made by intentionally injecting pigment under the skin surface to create permanent artistic designs. Sometimes, tattoos are made when the pigment is accidentally pushed into the skin. For example, ear piercing, a gunpowder explosion, or a “road rash” could make an accidental tattoo.

Who gets a tattoo?
Decorative tattoos are by far the most common. Tattoos are an artistic expression of individual taste and style. In the last few years, tattooing has become a popular way to apply permanent “make-up,” such as eyeliner. Not all tattoos are decorative. Sometimes, doctors use small tattoos to permanently mark the skin to help give medical treatments at exactly the same spot every time. Tattoos also are used to identify members of a group, such as prisoners, social groups, or gang members.

What are the medical risks of a decorative tattoo?
Because needles and injections are used in tattooing, improperly sterilized equipment can spread viruses. Getting a tattoo significantly increases a person’s risk of contracting viral hepatitis. Although possible, there are no documented cases of HIV linked to tattoo needles. Since tattoos create a wound in the skin, there is a small risk of bacterial infection, scar formation, or a keloid.
Allergic reactions to the ink or pigment are possible, and the allergy may not s unless the tattoo is removed. There are many reports of skin cancer occurring in a tattoo. Tattooing can spread warts and molluscum (a skin disease that is characterized by soft, round masses).

What are the non-medical risks of a decorative tattoo?
Many people get tattoos impulsively and without much thought. Later, some people regret getting them or regret the location or design. Several articles document that it is harder to leave a gang lifestyle once the members are tattooed. A recent study surveyed individuals responsible for hiring new employees and found that many of them would not hire a person with visible tattoos.

How is a tattoo removed?
In most decorative tattoos, the pigment is found in the upper part of the skin, called dermis. The earliest methods of tattoo treatment simply removed the layers of skin where the pigment was located.
Salabrasion uses salt particles to rub away the upper skin and the pigment. Immediately after treatment, the skin looks and feels like a “road rash.” Although this method is inexpensive, it always leaves a significant scar, and it can be quite painful. Dermabrasion is a similar technique that uses a high-speed rotating sanding bit.
Small tattoos can be cut out surgically and then stitched closed. This leaves a surgical scar. Some locations, like the face, heal very well. If the tattoo is located on an area of the skin with a lot of movement or tension (e.g., hips, knees, or shoulders), the surgical scar will usually widen, or there may be stretch marks around the incision. Sometimes, large tattoos are cut out in stages over several sessions. Again, there is often a significant surgical scar.
The dermaplane is a tool that shaves off the layer of the skin. This tool is often used to harvest skin for skin grafting. Amateur tattoos are frequently placed irregularly and deeper, so this technique may not go deep enough to remove all the color. As with the other surgical techniques, this often leaves a scar.
Several different LASER systems are now available for tattoo removal. The carbon dioxide (CO2) LASER simply burns off the of the skin, one layer at a time, until all the color is gone. There is always scarring, resembling other kinds of burn scars.
Newer LASER systems use special types of light energy to instantaneously heat and destroy the tattoo pigment without damaging the surrounding skin. Some systems even have a device attached that keeps the surface of the skin cool to avoid a heat injury or burn. Some LASER systems work best for black pigment, while other systems work better for red or green pigments. This method of treatment is much less likely to cause pain or scarring. However, most LASER systems require multiple treatment sessions, and it may cost several hundred dollars per session.
When considering tattoo removal, discuss all of the methods, risks, costs, and alternatives with us.

Links to other information
For medical articles about tattoos, log on to: http://www.ncbi.nlm.nih.gov/PubMed/medline.html”>
As an alternative to permanent tattoos, consider Henna:
http://dir.yahoo.com/Business_and_Economy/Companies/Arts_and_Crafts/Visual_Arts/Body_Art/Tattoos/Henna_Tattoos/

Yahoo search results on henna tattoos

For the history of tattooing, go to: http://tattoos.com/jane/steve/toc.htm

History of Tattooing

About the Author
After finishing medical school and dermatology training at the University of Oklahoma, Dr. Gillum came to Colorado to further his knowledge in this specialty. He is board certified in Dermatology and Dermaathology.
He works at a busy private practice with offices in Aurora and Parker, Colorado. He also teaches at the University of Colorado Department of Dermatology and volunteers his time working with gang members to have their tatoos removed.
Copyright 2012 Paul Gillum, M.D., All Rights Reserved

Tear Duct, Blocked

What is a Blocked Tear Duct?
What Causes a Blocked Tear Duct?
Who gets a Blocked Tear Duct?
What are the Symptoms of a Blocked Tear Duct?
How is a Blocked Tear Duct Diagnosed?
How is a Blocked Tear Duct Treated?
What are the Complications of a Blocked Tear Duct?

What is a Blocked Tear Duct?
When an obstruction occurs in the duct system which carries tears away from the surface of the eye to the nose, it is called a blocked tear duct or nasolacrimal duct obstruction.

What Causes a Blocked Tear Duct?
Tears are produced in the lacrimal gland located above the lateral aspect of the eye. These tears are secreted and travel across the cornea, exiting via the superior and inferior puncta (holes) on the inner (medial) corner of the eye. Usually, a small tube called the nasolacriminal duct drains the tears from the surface of the eye into the nose. This duct is usually developed by birth but up to 1% to 5% of the population may have a duct that is incompletely developed or obstructed. The nasolacrimal duct has three valves in it and the majority of nasolacrimal duct obstructions occur at the most distal valve that is located in the nose (Hasner’s Valve).
Who gets a Blocked Tear Duct?
Babies begin to produce tears at two days to two weeks after birth. You may notice excessive tearing from one or both of your infants’ eyes during this time. Rarely, adults get a blocked tear duct because of an infection, an injury, or a tumor.
What are the Symptoms of a Blocked Tear Duct?
The main symptom of a blocked tear duct is increased or excessive tearing.
How is a Blocked Tear Duct Diagnosed?
A blocked tear duct is diagnosed after a standard eye exam or an internal examination of the nose. If necessary, the drainage of the tears can be tracked by an eye stain.
How is a Blocked Tear Duct Treated?
Nearly half of the cases of nasolacrimal duct obstruction will resolve spontaneously by 6 months of age. A pediatric ophthalmologist may need to probe your childs eye between 6 to 12 months of age to help open up the obstruction. In rare circumstances, the probing does not fix the problem completely and a silicone stint may have to be placed in the nasolacrimal duct for 1 to 3 months to help keep the duct open.
In the meantime, your health care provider may choose to prescribe antibiotic drops or ointment if your child has persistent yellow drainage from the eye. Some health care providers recommend a massage technique to try to unblock the duct. Two methods have been recommended. You may place a washed finger between the nose and the inner corner of the eye. Massage downward (inferiorly) in an attempt to push the tears through the nasolacrimal duct via its normal path. Another recommendation calls for a superior motion in the same location, pushing the tears out of the duct. You should do this procedure at every other feeding for a newborn.
What are the Complications of a Blocked Tear Duct?
A blocked tear duct can cause a significantly higher amount of eye infections resulting in yellow discharge from the eye. These infections can be treated by antibiotic eye drops or ointment.
Rarely, your child may develop a bluish swelling on the skin between the nose and the inner corner of the eye(an amniotecele). Massage may be attempted. However, if the swollen area becomes red and inflamed, you should contact your health care provider immediately for an abscess may be developing which requires IV antibiotics and probing.
References
Nelson LB, Calhoun LJ, Menduke H. Medical Management of congenital nasolacrimal duct obstruction. Pediatrics 76: 173 1985
Wright, KW. Pediatric Ophthalmology for Primary Care, 2003, American Academy of Pediatrics
Reviewed by: Evan Taragano MD
This Article contains the comments, views and opinions of the Author at the time of its writing and may not necessarily reflect the views of Pediatric Web, Inc., its officers, directors, affiliates or agents. No claim is made by Pediatric Web, the Author, or the Authors medical practice regarding the effectiveness and reliability of the statements contained herein and such individuals and entities disclaim any and all liability for the comments and statements contained in this Article and for any use or misuse of the statements made in this article in any specific medical situations. Further, this Article is intended to be general in nature and shall not be considered medical advice. The statements made are not to be utilized to diagnose and/or treat any individuals medical symptoms. If you or someone you know has symptoms which you believe are similar to this Article, you should discuss such symptoms with your personal physician or other qualified medical practitioner.
Copyright 2012 Pediatric Web, Inc., by Dan Feiten, M.D. All Rights Reserved

Tetralogy of Fallot

What is Tetralogy of Fallot?
How is Tetralogy of Fallot treated?
What are the signs and symptoms of Tetralogy of Fallot?
Diagnosing Tetralogy of Fallot
Helpful resources

What is Tetralogy of Fallot?
Tetralogy of Fallot is a congenital heart condition that involves the incorrect formation of the septum between the right and left ventricles. This condition results in mixing of oxygen-rich and oxygen-poor blood across the ventricular septal defect inside the heart. This causes an overall decrease in the amount of oxygen in the blood.
The four functional heart problems that make up a tetralogy of Fallot are:
A hole between the ventricles, the lower chambers of the heart. This is called a ventricular septal defect(VSD).
A blockage or kink in the pulmonary artery where blood flows from the heart to the lungs
The aorta, the largest blood vessel, lies over the VSD, the hole in the lower chambers of the heart
The muscle surrounding the lower right chamber is too thick
Tetralogy of Fallot is a congenital heart defect, meaning children are born with it. The cause of the condition is not known. In some situations, it may be associated with certain genetic syndromes, like Di George syndrome.
Children usually show symptoms of the condition and are diagnosed shortly after birth. With treatment, kids with tetralogy of Fallot can lead normal, healthy lives. However, if your child has tetralogy of Fallot, he or she will need follow-up care to monitor any changes in the heart.

How is Tetralogy of Fallot treated?
Surgery is the only definitive treatment for children with tetralogy of Fallot. Your doctors will likely schedule your child’s surgery by the time he or she turns one year old.
During the surgery, a pediatric cardiac surgeon will fix the hole between the ventricles (the ventricular septal defect) using a patch. The surgeon will also widen the pulmonary artery and fix any problems with the pulmonary valve. This repair will help more blood reach the lungs. The entire procedure is known as intra-cardiac repair.
If your child is too ill or too small for intra-cardiac repair, surgeons will create a temporary solution called a shunt. This is a bypass from the aorta to the pulmonary artery, which will increase blood flow to the lungs until your child is big enough for the final procedure.

What are the signs and symptoms of Tetralogy of Fallot?
Children with this heart condition often have a blue tint to their skin, lips and fingernails. This is called cyanosis and means that not enough oxygen-rich blood is reaching the child’s body.
Sometimes, a baby only shows signs of cyanosis after crying or feeding. These episodes are called “Tet spells.”
Other symptoms of tetralogy of Fallot are:
Trouble feeding
Poor growth and weight gain
Fainting
Clubbed fingers
If your child is having any of these symptoms, especially cyanosis, contact us immediately.

Diagnosing Tetralogy of Fallot
If us suspects your child has a congenital heart defect, he or she will want to do more tests to examine the heart. These tests will help your cardiologist identify the problem affecting your child and create a treatment plan.
Tests that help cardiologists diagnose tetralogy of Fallot are:
Chest x-ray
EKG
Holter and event monitors
ECHO

Helpful resources
If you’d like to learn more about tetralogy of Fallot, visit:

The American Heart Association

The National Heart, Lung and Blood Institute

U.S. National Library of Medicine

Tetralogy of Fallot Program at the Children’s Hospital Colorado
Reprinted with permission from Children’s Hospital Colorado 2012, All rights reserved.

Thyroid Problems

What is hypothyroidism?
What causes hypothyroidism?
Who gets hypothyroidism?
How does hypothyroidism cause disease?
What are the common findings?
How is hypothyroidism diagnosed?
How is hypothyroidism treated?
What are the complications?
How can hypothyroidism be prevented?
What research is being done?
Links to other information

Thomas P. Foley, Jr., M.D.
Professor of Pediatrics, School of Medicine, Professor of Epidemiology
Graduate School of Public Health, University of Pittsburgh
and Children’s Hospital of Pittsburgh, Pittsburgh, PA
What is hypothyroidism?
Hypothyroidism is a deficiency in thyroid hormone secretion and a reduction of action of its hormones on the cells of the body. In children, there are two forms: (1) congenital hypothyroidism, present at birth; and (2) acquired hypothyroidism, a disease with an onset at any time after birth, usually after six months of age. In each of these two forms, there are two categories: (1) primary hypothyroidism, a failure of secretion by a damaged, defective, or absent thyroid gland; and (2) hypothalamic/pituitary hypothyroidism, a failure of the mechanism that stimulates the thyroid gland from the base of the brain, called the hypothalamus and the pituitary gland.
The thyroid hormones are called thyroxine, or T4, and triiodothyronine, or T3. The pituitary hormone that stimulates the thyroid gland is called thyroid stimulating hormone, or TSH.

What causes hypothyroidism?
In most cases, the cause of congenital hypothyroidism is not known. A few cases of inherited hypothyroidism are caused by mutations in the genes producing specific proteins (known as enzymes) that are required to make thyroid hormones. These mutations are inherited as autosomal recessive traits, i.e., the parents are unaffected, and the child is affected because the child receives a mutation from each parent. The parents have a one-in-four chance of having an affected child. Occasionally, a maternal disease or a medication can interfere with the thyroid gland of the unborn child. In certain areas of the world, a dietary lack of iodine causes hypothyroidism.
Most cases of acquired hypothyroidism are caused by autoimmune thyroiditis, a self-inflicted destruction of the thyroid by the body’s immune system. The processes that cause this condition are poorly understood. An inappropriate immune response is directed against the thyroid; the body does not recognize its own thyroid gland and generates an immune response against the normal thyroid cells to cause inflammation, irritation, or damage. Infrequently, surgical removal of the thyroid, certain medications or chemicals, or damage by radiation treatment for cancer may cause hypothyroidism.

Who gets hypothyroidism?
In most cases, congenital hypothyroidism is sporadic. It occurs worldwide, once in every 4,000 newborn infants, and affects girls twice as often as boys. In the inherited forms, an equal number of males and females are affected. An infant born to a mother with iodine deficiency, or an infant receiving, or exposed to a mother given, excessive amounts of iodine for antiseptic reasons may have hypothyroidism. The problem will continue until exposure to deficient or excessive iodine is corrected.
The majority of cases of acquired hypothyroidism occur in females with autoimmune diseases. It may occur: (1) as autoimmune thyroid disease only; (2) in association with other autoimmune diseases, such as insulin-dependent diabetes mellitus, alopecia (hair loss), rheumatoid arthritis, and lupus erythematous; or (3) in association with other diseases, such as Down syndrome and Turner’s syndrome.

How does hypothyroidism cause disease?
Thyroid hormones regulate metabolism, i.e., the amount of energy that is available for body functions. The production of proteins, especially those called enzymes, is controlled by thyroid hormones. They regulate how much sugar is converted to energy, how much protein is converted into muscle, and how much fat is stored and available for energy. From early in fetal life through two to three years of age, thyroid hormones acquired from the mother and those produced by the unborn child in the second and third trimesters of pregnancy are essential for normal brain development.

What are the common findings?
The common findings of hypothyroidism are summarized in the table. The appearance of a specific symptom and sign depends upon the age when hypothyroidism develops and its severity. Often, the findings in a child may not be obvious to the parents or the physician.
Congenital hypothyroidism Acquired hypothyroidism
Findings during first two weeks of life – Prolonged yellow jaundice – Swelling of the eyelids, hands, and feet – Gestation more than 42 weeks – Birth weight more than 4 kg – Poor feeding – Low body temperature – An enlarged, swollen abdomen – Large midline fontanelles
Findings beyond age one month – Darkening and mottling of the skin – Stressful, frequent, and labored breathing – Failure to gain weight; poor sucking ability – Decreased stool frequency – Decreased activity and lethargy
Findings after age three months – Swollen and protuberant umbilicus – Infrequent and hard stools – Dry skin with yellow coloration – Large tongue – Generalized swelling – Hoarse cry Findings between six months and three years – Deceleration of linear growth – Coarse facial features – Dry skin with yellow coloration – Hoarse cry and large tongue – Swollen and protuberant umbilicus – Enlargement of the arm and leg muscles
Findings during childhood – Slow growth and short stature – Delay in eruption of teeth and in shedding primary teeth – Muscle weakness; enlargement of the arm and leg muscles – Infrequent and hard stools – Dry skin with yellow coloration – Generalized swelling – Early sexual development
Findings during adolescence – Late onset of puberty – Slow growth and short stature – Delay in eruption of teeth and in shedding primary teeth – Infrequent and hard stools – Dry skin with yellow coloration – Discharge from the breasts (in girls) – Generalized swelling
Table. Common findings of hypothyroidism.

How is hypothyroidism diagnosed?
For newborns in many areas of the world, there are routine, mandated screening programs for congenital hypothyroidism. An elevated TSH on the newborn screening test requires that a repeat TSH test be performed. Other tests are performed to define the cause (inherited or sporadic) and the severity of hypothyroidism. In older infants and children, hypothyroidism is suspected by: (1) the presence of a large thyroid gland, or goiter, on examination of the neck; (2) a failure to maintain a normal rate of growth in height; (3) the symptoms and signs of hypothyroidism (see table); (4) a suspicion of it because members of the family have thyroid diseases; or (5) a routine screening for TSH in children at increased risk for hypothyroidism.
Hypothyroidism is diagnosed by blood tests for TSH and free T4. An elevated TSH is the most sensitive test for thyroid gland failure. A low free T4 is the diagnostic test for hypothalamic/pituitary hypothyroidism, and, usually, it is low in primary hypothyroidism, except in mild cases. Typically, the cause of thyroid gland failure is autoimmune thyroiditis, which is diagnosed by finding thyroid antibodies from a blood test. When the TSH value is increased and the T4 value is decreased, treatment with thyroxine is started. Thyroxine treatment usually is started when the TSH value is increased, yet the T4 value still is normal, as long as the cause of hypothyroidism is known.
In patients with hypothalamic/pituitary hypothyroidism, there usually are other pituitary hormone deficiencies, such as low levels of growth hormone (when the patient is subjected to growth hormone secretion tests); low levels of the sex hormones at the pubertal ages; and, less often, low levels of hydrocortisone and high levels of prolactin, which is the pituitary hormone that stimulates the secretion of milk in the mother after delivery.

How is hypothyroidism treated?
Treatment for hypothyroidism is easy and inexpensive. Typically, levothyroxine (L-thyroxine) is prescribed, and the tablets should be given at least 30 minutes before a meal or infant feeding. The daily dose per body weight steadily decreases from early infancy to childhood to an adult dose in adolescence. Treatment must be individualized; the amount that is absorbed and handled by the body differs among individuals. Careful monitoring of blood tests (TSH and free T4 or T4) until the values are normal, and then annually after three years of age once the tests become normal, is essential for optimal management.

What are the complications?
There are no complications from L-thyroxine treatment when the proper dose is taken and the blood tests are monitored on a regular basis. There are complications associated with unrecognized or inadequately treated hypothyroidism, and the worst outcome occurs if treatment is delayed in early infancy. Severe hypothyroidism before birth, and a delay of treatment after birth, is associated with an impaired intellect (as determined by IQ tests) and other neuropsychological abnormalities. After two or three years of age, there are adverse effects of untreated hypothyroidism; however, in most cases, they are reversible with adequate treatment.
Usually, if hypothyroidism is not adequately treated within approximately the first 6 to 12 months after its onset, a decrease in the rate of growth and, in many instances, shortness of stature occur. If prolonged into the adolescent years, the final adult height may be less than expected despite appropriate treatment. Prolonged hypothyroidism also is associated with high levels of cholesterol, slowing of mental function and school performance, an occasional episode of hip or knee pain from a slippage of the growth center of the hips (usually requires surgical intervention), and chronic constipation. Except for the normalization in growth, these abnormalities should disappear with appropriate treatment.

How can hypothyroidism be prevented?
Hypothyroidism cannot be prevented unless it is caused by a nutritional deficiency of iodine; excessive iodine intake; certain drugs, like lithium, that block the ability of the thyroid gland to produce thyroid hormones; or drugs that impair the absorption of thyroxine in those individuals who are taking it for hypothyroidism. If taken with thyroxine, iron medications and high fiber in food will prevent the absorption of thyroxine. Calcium tablets also may interfere with its absorption.

What research is being done?
In congenital hypothyroidism, research is being focused on the mutations that cause the familial thyroid disorders, the cause(s) of the sporadic disease, and the effects of maternal hypothyroidism on the unborn child. There is considerable interest in discovering the mechanisms that cause autoimmune diseases, with a focus on autoimmune thyroid diseases, the occurrence of diabetes mellitus in specific families with autoimmune thyroid diseases, and an understanding of those antibodies that injure thyroid cells and other antibodies that bind to and block the TSH receptor.

Links to other information
American Thyroid Association www.thyroid.org
Complete textbook available entitled “The Thyroid and Its Diseases” www.thyroidmanager.org
Lawson Wilkins Pediatric Endocrine Society www.lwpes.org

References
Familial Thyroid Diseases Including Hypothyroidism
Vassart G, Dumont JE, Refetoff S. Thyroid disorders. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The Metabolic and Molecular Bases of Inherited Disease. New York: McGraw-Hill, 1995:2883-2928.
Hypothyroidism
Fisher DA. Management of congenital hypothyroidism. J Clin Endocrinol Metab 1991;72:523.
Foley TP Jr. Congenital hypothyroidism. In: Braverman LE, Utiger RD, eds. Werner and Ingbar’s The Thyroid. 8th ed. Philadelphia: Lippincott-Raven, 2000:chap 82, part B, 977-983.
Foley TP Jr. Acquired hypothyroidism in infants, children and adolescents. In: Braverman LE, Utiger RD, eds. Werner and Ingbar’s The Thyroid. 8th ed. Philadelphia: Lippincott-Raven, 2000:chap 82, part C, 983-988.
Foley TP Jr. Hypothyroidism. In: Hoekelman RA, Friedman SB, Nelson NM, Seidel HM, Weitzman M, eds. Primary Pediatric Care. 4th ed. St. Louis: Mosby-Year Book, Inc., 2000:chap 218. In press.
LaFranchi S, Dussault JH, Fisher DA, Foley TP Jr, Mitchell ML. Newborn screening for congenital hypothyroidism: recommended guidelines. Pediatrics 1993;91:1203-1209.
About the Author
Thomas P. Foley, Jr. MD is Professor of Pediatrics in the School of Medicine and Professor of Epidemiology in the Graduate School of Public Health at the University of Pittsburgh and a member of the Medical Staff of the Children’s Hospital of Pittsburgh since 1971. Areas of scientific interest include (1) pediatric thyroidology with specific interests in congenital hypothyroidism, acquired hypothyroidism, hyperthyroidism and thyroid cancer; (2) auxology; and (3) international pediatrics with specific interests in radiation-induced thyroid cancer associated with the Chernobyl accident, autoimmune thyroid diseases, iodine deficiency disorders, newborn screening, toxicology and the effects of maternal hypothyroidism on fetal development. My personal interests are my family (wife, son and step-children), music (opera, classical music and traditional bluegrass music as lead vocal and guitar for The Allegheny River Boys, Revonah RS-506, 1978), sports (spectator and participant) and humanitarian assistance for children and child health through Child Health International (web site of a subsidiary: trfn.clpgh.org/orgs/bach).
Copyright 2012 Thomas P. Foley, Jr., M.D., All Rights Reserved

Tinea (ringworm infection)

What is tinea (or a ringworm infection)?
What causes tinea?
Who gets tinea?
How do dermahytes cause disease?
What are the common findings?
How is tinea diagnosed?
How is tinea treated?
What are the complications?
How is tinea prevented?

Leslie Capin, M.D.
Aurora/Parker Skin Care Center
Aurora, Colorado
What is tinea (or a ringworm infection)?
Tinea, also referred to as ringworm, is a common fungal infection of the skin. Fungi are widespread in the environment. There are thousands of fungal species, but only approximately 200 species regularly infect humans, causing either superficial or deeper infections, and, occasionally, both.
The body area affected by the infection classifies tinea. “Tinea capitis” is a superficial fungal infection involving the scalp, while “tinea corporis” is a superficial fungal infection involving the trunk, limbs, and face. “Tinea manuum,” or ringworm, is an infection of the hands, whereas “tinea pedis” is a fungal infection the feet. “Tinea unguium,” or “onychomycosis,” affects the nails.

What causes tinea?
Dermahytes, a group of fungi, cause superficial fungal infections, also known as fungal dermatosis, dermahytosis, ringworm, or tinea.

Who gets tinea?
A dermahyte infection of the scalp (tinea capitis) and of the general skin surface (tinea corporis) is very common during childhood. Because tinea capitis is no longer reportable to the Health Department, the true incidence is unknown. Probably, the highest incidence of tinea capitis occurs among children who are 1 to 10 years of age.
A dermahyte infection of the hands (tinea manuum) and of the feet (tinea pedis) is more common in adulthood than in childhood. Tinea pedis is probably the most common dermahytosis worldwide; up to 70% of the population has had this infection. Tinea pedis occurs in males and in females, and the incidence of the infection increases with age. Most cases of tinea pedis occur after puberty. Nail infection (tinea unguium) is unusual during the first two decades of life.
Tinea most commonly occurs in warm, humid, tropical climates. Certain risk factors may increase the likelihood of a person developing an infection. These predisposing risk factors include some systemic disorders and certain environmental and occupational sources. Systemic diseases that may predispose individuals to tinea infections include diabetes mellitus and those with compromised immune systems.
Environmental and occupational risk factors include animal contact, especially with kittens, puppies, and horses; contact sports; use of gymnasiums and swimming pools; and outdoor occupations.

How do dermahytes cause disease?
Dermahytes cause infection by invading keratin, which is a protein in the outermost layer of the skin, in the hair, and in the nails. Direct contact with infected animals, soil, or humans causes tinea.

What are the common findings?
Many patients with a mild tinea infection may have no symptoms. Symptoms include itching and burning, especially when the body, hands, or feet are involved. Patients also may complain of tenderness, swelling, and pain in the affected area. The more severe the infection, the worse the symptoms may become.
Tinea capitis appears as a combination of hair breakage and loss, redness, and scaling of the scalp. The extent of scalp redness and scaling varies from person to person. There can be minimal scaling and redness that resembles a mild form of dandruff, or there can be marked redness, swelling, puss formation, and hair loss.
Some patients have a strong reaction in their scalp to the dermahyte, and may develop tenderness, pain, and swelling of the lymph nodes in their neck. Rarely, patients have an elevated white blood cell count. A long-term, severe case of tinea capitis that is not treated adequately may lead to permanent hair loss and scarring.
Tinea corporis is a dermahyte infection of the general body surface. Physical examination reveals individual and grouped round patches of red, scaly skin. These round patches, or “rings,” (hence the term, “ringworm”) progressively enlarge and migrate outwards from the center of the ring to form expanding rings. As the ring expands, the center of the ring often becomes clear. Tinea corporis is similar in its appearance virtually anywhere on the body. Tinea faciei appears on the face, and tinea cruris is an infection that involves the upper thigh and groin area.
A tinea infection of the hands primarily involves the palms, with a dry scale often looking like small circular areas of scale. Occasionally, a tinea infection of the hands can have small blisters on the palms. For unknown reasons, a tinea infection of just one hand, in conjunction with an infection of both feet, is the most common pattern.
Usually, tinea pedis is red and scaly between the toes and on the soles. The skin of the web spaces between the toes can become red, softened, and swollen. The redness and scaling can spread to the side of the foot. Blister formation is more common on the feet than with the other tinea infections.
A tinea infection of the nails (tinea unguium or onychomycosis) invades the nail plate, and causes the nail to lift, thicken, discolor, and become fragile.

How is tinea diagnosed?
An appointment should be made with a primary care provider or a dermatologist for diagnosis and treatment, if an individual experiences the following: hair loss, accompanied by redness and scaling of the scalp; patches of red, circular, scaly skin on the body, hands, or feet; blisters on the palms and soles; or nail changes.
The health care provider will sample a small piece of scale or blister, hair, or nail, and analyze it under the microscope for a fungal organism to establish the diagnosis. This test is called a potassium hydroxide preparation (KOH). Occasionally, the fungal branches and spores characteristic of the infection cannot be seen under the microscope, and a fungal culture will be sent to the laboratory to establish the correct diagnosis. It may take two to four weeks to obtain the fungal culture results.

How is tinea treated?
Tinea infections are treated with ical or systemic oral antifungal medications, and, occasionally, both. Anytime the infection involves the hair or the nails, an oral antifungal medication must be used. When only the skin is involved, a ical antifungal medication is usually sufficient, if the infection does not cover a large body area.
If a large percentage of the body surface is involved, an oral and ical antifungal medication may be prescribed. Antifungal drugs have become increasingly effective in the treatment of tinea infections, especially the newer antifungal drugs on the market. Experience with most of the newer antifungal drugs is limited to patients over 12 years of age.
Griseofulvin was the first significant oral antifungal on the market used to treat tinea infections. It continues to be the preferred drug in the pediatric population because of its long history of effectiveness, its low cost, and its proven safety profile. Griseofulvin is used frequently to treat tinea capitis and tinea corporis in children. It also is used to treat tinea manuum and tinea pedis.
Common side effects of griseofulvin include headaches and gastrointestinal upset. Rarely, allergic rashes from griseofulvin occur. Griseofulvin may make a patient more sensitive to the sun, and the patient is at risk of developing a photosensitive rash or a sunburn.
Many very effective ical antifungal medications are available over the counter, and they can be used one to two times daily to clear infections (except tinea capitis and onychomycosis). Blistering skin eruptions on the palms and soles should be treated with cool compresses, such as Burrow’s solution. Large blisters should be opened and drained for comfort.
The newer antifungal medications on the market, namely Itraconazole and Terbinafine, are very effective for nail infections. Your primary care provider will help you to decide which ical and/or oral antifungal medication is most appropriate for your child.

What are the complications?
Tinea infections may lead to secondary bacterial infections, hair loss, and scarring. Occasionally, patients will have swollen lymph nodes that may persist

How is tinea prevented?
A cool, dry environment, as well as avoiding exposure to infected animals, soil, and humans, may help reduce infections. Good personal hygiene, thorough drying of the hands and feet, absorbent socks, and wearing breathable natural materials may help prevent infection. For patients that experience recurrent tinea pedis infections, light, ventilated footwear or sandals and a medicated foot powder may be helpful. Sprays or powders with antifungal activity applied into footwear also may help prevent reinfection. Treatment is usually permanent, although the infection may recur.

References
Buttaro, T., Trybulski, J., Bailey, P., Sandberg-Cook, J.: Primary Care: A Collaborative Practice, ed. 1, St. Louis, 1999, Mosby, Inc.
Hurwitz, S.: Clinical Pediatric Dermatology, ed. 2., Philadelphia, 1993, W.B. Saunders Company
Weston, W.L., Lane, A.T., and Morrelli, J.G.: Color Textbook of Pediatric Dermatology, ed. 2, St. Louis, 1996, Mosby, Inc.
About the Author
Dr. Capin received her medical education and completed her dermatology residency at the University of Colorado. A Fellow of the American Academy of Dermatology, she is board certified in Dermatology.
She has been in practice at the Aurora/Parker Skin Care Center for twelve years, and recently opened CARA MIA Medical Day Spa in Parker, Colorado. She enjoys teaching, and often has students with her during office hours.
She is experienced in medical and surgical dermatology, as well as cosmetic dermatology. She is often asked to participate in conferences, and speaks internationally.
Copyright 2012 Leslie Capin, M.D., All Rights Reserved

Toxic Shock Syndrome

What is Toxic Shock Syndrome?
What causes Toxic Shock Syndrome?
Who gets Toxic Shock Syndrome?
How does the toxin cause disease?
What are the common findings?
How is Toxic Shock Syndrome diagnosed?
How is Toxic Shock Syndrome treated?
What are the complications?
How can Toxic Shock Syndrome be prevented?
What research is being done?
Links to other information

by James K. Todd, M.D.
Professor of Pediatrics, Microbiology and Preventive Medicine
University of Colorado School of Medicine
Denver, Colorado
What is Toxic Shock Syndrome?
Toxic Shock Syndrome (TSS) is an acute, severe disease that is characterized by fever, shock, and a sunburn-like rash. TSS is commonly associated with females who are menstruating and using tampons, but it can occur in boys and girls of any age. Fortunately, if recognized early, TSS can be successfully treated.

What causes Toxic Shock Syndrome?
TSS is caused by a toxin (i.e., a poison) at the site of an infection in the body produced by a bacterial organism called Staphylococcus aureus. This organism commonly causes wound infections and abscesses in children. The growth conditions at the site of the infection (which also can occur in adolescent girls who are menstruating and using tampons) provide the organism with the proper nutrients to produce a potent toxin that circulates throughout the body.

Who gets Toxic Shock Syndrome?
Boys and girls of any age can get TSS. It is not just a disease associated with tampons; however, any tampon brand or type, or other inserted vaginal device (e.g., a contraceptive sponge or a diaphragm), can cause the disease if it catches the right patient at the right time. Even so, most children will never be at risk of getting TSS, because they have already developed immunity to the toxin.

How does the toxin cause disease?
A toxin produced at the site of the infection can get into the bloodstream and then go to all of the organs of the body. It damages the blood vessels, and they leak fluid into the tissues. This fluid loss can lead to shock, as well as injury to many organs, including the skin, kidney, liver, brain, and heart.

What are the common findings?
TSS begins with a fever, nausea and vomiting, diarrhea, and a sore throat. The symptoms of TSS are very similar to many other less severe and more common childhood illnesses. However, TSS then progresses to a sunburn-like rash, with signs of early shock, which may be characterized by dizziness, fainting, or confusion.

How is Toxic Shock Syndrome diagnosed?
Doctors diagnose TSS by examining the patient and noting the common signs of the disease in the presence of menstruation and tampon use, or a possible site of bacterial infection, such as a wound infection or an abscess. TSS should be suspected in boys and girls of any age who have a fever or a possible Staphylococcus infection (e.g., a wound infection, an abscess, or a boil), and any of the following symptoms: sunburn-like rash; fainting, dizziness, or confusion; or menstruation and tampon use.

How is Toxic Shock Syndrome treated?
TSS is treated by administering antibiotics to kill the organism, and cleansing the site of the infection (i.e., removal of a tampon or other vaginal device in girls who are menstruating, or surgical drainage if an abscess or a wound infection is present). Patients are admitted to the hospital and given intravenous fluids. If organ failure occurs, patients may be treated with other medications.

What are the complications?
Most children with TSS survive, especially if the disease is treated early in its course. Less than 5% of cases are fatal. Most patients will have peeling of the skin on their fingers and toes after several weeks, and, a month later, some transient hair loss may occur. Adolescent girls may experience increased swelling of the hands and feet during menstruation for several months. Some girls may have recurrences of TSS if they use tampons during menstruation in the six months after their first episode.

How can Toxic Shock Syndrome be prevented?
Early recognition and treatment is important. Adolescent girls should be encouraged to use the lowest absorbency tampon that will still control their flow, to change tampons frequently (every four to six hours), and to use pads instead of tampons at night. Although it has been claimed that “all-cotton” tampons have a lower risk of TSS, this is probably not true. A menstruating girl who develops any of the symptoms of TSS (see Table 1) should remove the tampon and immediately seek medical attention.

What research is being done?
Current research shows that TSS is being recognized earlier in its course; therefore, it is being treated more effectively. This has resulted in a decreased fatality rate and less complications. Adolescent girls should be encouraged to read and heed the information regarding TSS on tampon boxes, to learn the warning signs, and to always remove a tampon. If adolescent girls have any symptoms or concerns, they should seek medical attention. Tampon manufacturers are working to make product improvements that will further minimize the already low risk of contracting TSS.

Links to other information
For more information on TSS, log on to the following Web sites:
http://Toxic Shock on MedicineNet
Tampax.com, Toxic Shock
http://www.kidshealth.org/parent/common/toxic_shock.html

References
Kurtz B, Combs P, Todd A, Anderson J, Todd J. Epidemiology of toxic shock syndrome in Colorado, 1970-1996. Royal Society of Medicine Int Congress Symp. 1998; 229: 24-26.
Todd JK, Todd BH, Franco-Buff A, Smith C, Lawellin DW. Influence of focal infection conditions on the pathogenesis of toxic shock syndrome. J Infect Dis 1987;155:673-81.
Todd JK. Toxic shock syndrome. In: Principles & Practice of Pediatric Infectious Diseases, 1996.
Copyright 2012 James K. Todd, M.D., All Rights Reserved

Toxoplasmosis

http://www.cdc.gov/parasites/toxoplasmosis/

Turner Syndrome

What is Turner Syndrome?
What causes Turner Syndrome?
How does it cause disease?
Clinical Findings in Turner Syndrome?
Clinical Findings in Turner Syndrome and Their Incidence
Skeletal Growth Disturbances?
Lymphatic Development
Ovarian Failure?
Heart Abnormalties?
Kidney Abnormalties?
Otitis Media (middle ear infections) and hearing loss?
Other Medical Conditions?
Neuro-psychological Findings
How Do You Diagnose Turner Syndrome
Follow-up Studies
Treatments
Research
Links

Sharon H. Travers, M.D.
Assistant Professor of Pediatrics
University of Colorado Health Sciences Center
What is Turner Syndrome?
Turner syndrome is a genetic disorder that occurs exclusively in girls and results from an abnormality of a chromosome. Chromosomes are material in the cells of the body which contain genes that determine each person’s characteristics.
Everyone has 22 pairs of chromosomes in addition to a pair of sex chromosomes, called X and Y. A female has two X chromosomes (referred to as a XX karyotype), and a male has one X and one Y chromosome (XY karyotype).
In Turner syndrome, one of the X chromosomes is missing (XO karyotype) or is structurally abnormal (XX(abnormal)). This results in a variety of physical manifestations (findings) with the most common being short stature.

What causes Turner Syndrome?
There is no known cause of why this chromosomal abnormality occurs. Neither parent is responsible for this happening nor can they prevent it.
It is not associated with parental age or environmental factors such as maternal drug abuse, alcohol consumption, medication, cigarette smoking, etc. Parents who have one daughter with Turner syndrome do not have an increased risk of having additional daughters with this syndrome.
The incidence of Turner syndrome is approximately 1:2000 live female births. However, the chromosomal abnormality is actually more common than this as 99% of XO fetuses do not survive beyond 28 weeks gestation, and the XO karyotype occurs in 1 out of 15 miscarriages.
Girls with Turner syndrome may have some normal cells in their body (46,XX) with other cells showing the abnormal karyotype 45, XO or 46, XX(abnormal). These girls are described as Turner mosaics and generally have less manifestations of the syndrome.

How does it cause disease?
The X chromosome contains important genes for traits like stature and ovarian function. Consequently, by having a missing or abnormal X chromosome, girls with Turner syndrome will have findings that relate to what those genes code (for example, short stature and ovarian dysfunction).

Clinical Findings in Turner Syndrome?
There are multiple findings in girls with Turner syndrome and they occur with varying frequencies. Consequently, not all features will necessarily be present in each affected girl. In fact, short stature in many girls may be the only manifestation. A list of the common findings are presented in the Table and discussed in the following sections.

Clinical Findings in Turner Syndrome and Their Incidence

Finding Approximate Incidence(%)
Short stature 100
Short neck 40
Scoliosis 35
Characteristic facial features 35
Webbed neck 25
Low posterior hairline 42
Edema of hands/feet 22
Ovarian failure 95
Infertility 99
Moles 25
Heart abnormalities 55
Kidney abnormalities 39
Thyroid disease 35
Skeletal Growth Disturbances?
The most common physical abnormality in girls with Turner syndrome is short stature. This is thought to be primarily a result of an abnormality of the growth response of the skeleton. Affected girls usually show an early decline in their growth within the first few months of life followed by a normal or near normal growth velocity until between 3 and 5 years of age. After 3 to 5 years, growth becomes increasingly abnormal (see Figure) so that the height of a Turner girl falls further and further below the normal curve. The average Turner adult height reached is 4 feet 8 inches, compared to an average adult female height of 5 feet 41/2 inches. There are genetic influences so that Turner girls who have tall parents typically will be taller than the average Turner height and likewise girls with short parents will be shorter.

Figure. Growth curve for girls with Turner Syndrome. (Provided as a service of Genentech, Inc. � Genentech, Inc., 1987. All rights reserved.)
Some girls with Turner syndrome have a distinctive facial appearance, and this is due in part to abnormal development of the bones in the face. Characteristic features include a small chin, downward droop of the outer corners of the eyes, and an abnormally arched palate (roof of mouth)

Lymphatic Development
Many girls with Turner syndrome have maldevelopment of their lymphatic system. The lymphatic system is a collection of vessels that bring fluid from body tissues back to the heart. As a result of lymphatic obstruction, there is extra fluid in a Turner fetus referred to as lymphedema. There is often a large collection of fluid in the neck, and when this fluid eventually decompresses, the skin remains stretched and can appear “webbed”. The stretching of the neck skin also results in a low posterior hair line, low-set and rotated ears, and extended growth of the eyebrows. Lymphedema of the hands and feet in a Turner fetus may cause abnormal development of fingernails and toenails. If this edema is present in a newborn, there is the appearance of “puffy” hands and feet. This typically resolves within the first few weeks/months after birth.

Ovarian Failure?
The ovaries in girls with Turner syndrome initially develop normally in the fetus. However, if there are not two normal X chromosomes in the ovarian cells, there is early egg loss and scarring of the ovaries. This process can occur entirely prenatally or within the first few months or years of life. The ovaries also produce the hormone estrogen which is responsible for sexual development in girls. Consequently, the majority of girls with Turner syndrome do not show spontaneous puberty such as breast development and menstrual periods. Most girls are also infertile.
In approximately 10 to 20% of Turner girls, there will be some ovarian function at puberty that allows for a little bit of breast development. A small percent of this group will also have normal periods, and an even smaller percent (less than 1% of all girls with Turner syndrome) will actually be fertile. Pregnancy has been reported in a small number of girls with Turner syndrome; however, there is an increased risk of chromosomal abnormalities in the children of these women. Girls who are Turner mosaic have a greater chance of retaining some or all of their ovarian function.

Heart Abnormalties?
There is an increased risk of heart abnormalities in Turner girls. Coarctation of the aorta is a condition where there is a narrowing of the aorta (the main blood vessel coming from the heart). This occurs in 15 to 20% of Turner girls and is more common in girls with a webbed neck. If found, this abnormality requires surgical treatment. A more common abnormality that occurs in up to 30% of girls is a bicuspid aortic valve. The normal valve of the aorta has three leaflets whereas a bicuspid valve only has two. Girls with bicuspid valves need cardiology follow-up but do not require surgical repair. High blood pressure may also occur in Turner girls but is not typically evident until adulthood. There is also a risk of dilation of the aorta that if not diagnosed and treated can rupture and cause significant morbidity and/or mortality. It is not clear whether girls who have normal hearts are at risk for dilation of the aorta or if it only occurs in those with abnormal hearts (i.e., coarctation or bicuspid valve). Because of this uncertainty, it is the opinion of this author that girls with normal hearts have a cardiology evaluation every 4-5 years.

Kidney Abnormalties?
Kidney abnormalities occur in 30-40% of girls with Turner syndrome. These abnormalities typically involve the structure, position, or blood vessels of the kidneys. Usually there are no health consequences of these abnormalities. Rarely patients require surgery or have any kidney impairment.

Otitis Media (middle ear infections) and hearing loss?
One of the most common medical problems in girls with Turner syndrome is recurrent ear infections. Abnormal development of the bones of the face leads to an abnormal relationship between the middle ear and eustation tube, which creates a predisposition to fluid collection in the middle ear and infection. Hearing loss may be a consequence of recurrent ear infections and fluid in the middle ear. This is referred to as conductive hearing loss.
Hearing loss that is not associated with ear infections (referred to as sensorineural hearing loss) also occurs in a high percentage (about 64%) of Turner girls. This hearing loss can become worse with age; consequently, girls with Turner syndrome should have regular assessments of their hearing.

Other Medical Conditions?
Other disorders that are seen with increased frequency in girls with Turner syndrome include hypothyroidism and gastrointestinal disorders. Diabetes mellitus may also occur but generally not until adolescence or adulthood.

Neuro-psychological Findings
The intelligence of girls with Turner syndrome is normal; however, there is often impairment in motor skills, visual-motor coordinating, and visualizing objects in relation to each other. This type of impairment is termed nonverbal learning disability (NVLD), often manifested by a discrepancy between verbal and performance IQ scores with verbal scores being higher.
Girls with Turner syndrome and NVLD have difficulty with mathematics, tasks requiring manual dexterity, and poor directional sense (i.e., difficulty with left and right). These girls may also show social immaturity as they have difficulty understanding social and nonverbal cues.
These neuro-psychological findings are seen in a high percentage of, but not all Turner girls. Consequently, it may be beneficial for girls to have neuro-psychological testing early on so parents and teachers can help girls compensate for this problem.

How Do You Diagnose Turner Syndrome
A girl who has the clinical findings suggestive of Turner syndrome should have a chromosomal analysis done by a simple blood draw. The blood is sent to a laboratory where specialists separate the chromosomes in the white blood cells and count and examine them carefully.
Since poor growth may be the only finding in many girls with Turner syndrome, this test should be strongly considered in any girl who has unexplained short stature.

Follow-up Studies
Once the diagnosis of Turner syndrome has been established by chromosome analysis, additional studies and tests are indicated. Because of the risk of hypothyroidism, thyroid tests should be done on a yearly basis.
In girls who are older than 10 years, blood studies can also be done to assess for ovarian function. An ultrasound of the kidney allows for detection of any abnormality. If this study is normal, it does not need to be repeated.
A cardiology consultation should be obtained in all girls, and part of this evaluation generally includes an echocardiogram (ultrasound of the heart). Girls with Turner syndrome should also be referred to a pediatric endocrinologist as soon as the diagnosis is made.

Treatments
Growth hormone therapy has been shown in several studies to increase final height in girls with Turner syndrome by up to 3-4 inches. Turner syndrome is one of the three FDA approved indications for growth hormone treatment in children.
At this time, growth hormone therapy should be considered as soon as a Turner girl has dropped below the fifth percentile of the normal female growth curve.
Growth hormone is safe and has only a few rare adverse side effects. A pediatric endocrinologist monitors girls on growth hormone therapy every 3-4 months for response and possible side effects. Currently, patients receive growth hormone as a daily subcutaneous injection (just under the skin).
In girls who have ovarian failure, estrogen is started sometime between ages 12 and 14 years to allow for pubertal development. Progesterone (another important hormone that the ovary makes) is typically added 1 to 2 years after estrogen is started. Both of these hormones can be taken orally as tablets; estrogen is also available as a patch preparation.
Although the majority of Turner girls are infertile, they can be the recipient of an embryo (donated egg which is fertilized in vitro) and can carry a pregnancy successfully to term.
Other treatments are indicated according to the clinical findings, i.e., hypothyroidism, heart abnormalities, etc.

Research
There is currently a national multi-center study giving growth hormone to toddler girls (ages 9 months to 4 years) to see if it can prevent the early fall off in growth that girls with Turner’s syndrome have. Frequency of ear infections, and hearing and development assessments are also monitored in this study. The Turner’s Syndrome Society web site has information on this study and others.

Links
http://turnersyndrome.org/
http://members.tripod.com/tsmagicmom/index.html

References
Lippe BM: Turner Syndrome. In Sperling MA (ed): Pediatric Endocrinology. Philadelphia, WB Saunders, 1996, pp. 387-421.
Rosenfeld RG, Attie KM, Frane J, et al: Growth hormone therapy of Turner’s syndrome: Beneficial effect on adult height. J Pediatr 132:319, 1998.
Rosenfeld RG, Tesch LG, Rodriguez-Rigau LJ, et al: Recommendations for diagnosis, treatment, and management of individuals with Turner syndrome. The Endocrinologist 4:351. 1994.
About the Author
Dr. Travers is an Assistant Professor of Pediatrics at the University of Colorado Health Sciences Center. She is board certified in both Pediatrics and Pediatric Endocrinology.
She is a clinician at The Children’s Hospital of Denver and sees children with a variety of endocrine disorders. Her clinical and research interests include Turner Syndrome and obesity in childhood.
Copyright 2012 Sharon H. Travers, M.D., All Rights Reserved