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Sleep apnea in children

While many people tend to associate sleep apnea only with adults, a surprising 1-3% of children suffer from the condition as well. OSA is now the most common reason tonsils and adenoids are removed in children. Sleep apnea in children typically appears between ages two-six, but it can occur from infancy to adolescence. It is believed that the disease affects girls and boys equally, yet often remains undiagnosed. As in adult sleep apnea, pediatric sleep apnea is a serious condition that can have significant consequences for a child's physical, emotional and intellectual health. Untreated OSA in children has been linked to behavior problems, impaired growth, learning difficulties, poor school performance, bedwetting, high blood pressure, heart disease, and more. In fact, many children with pediatric OSA are diagnosed with attention-deficit hyperactivity disorder (ADHD) before they are diagnosed with OSA. The risk factors associated with an increased incidence of OSA in children include:
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Family history of snoring or OSA Physical abnormalities in the skull or facial structures Cerebral palsy Muscular dystrophy Down syndrome Sickle cell disease Excess weight Mouth breathing Any condition that may narrow the upper airway

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(http://www.itonsil.com/tonsils_apnea_children.html) Symptoms Although snoring is a common symptom in children with obstructive sleep apnea, it is important to remember that between 10-20 percent of normal children snore (primary snoring) on a regular or intermittent basis. In addition to continuous loud snoring, other symptoms of obstructive sleep apnea in children include: failure to thrive (weight loss or poor weight gain) mouth breathing enlarged tonsils and adenoids problems sleeping and restless sleep excessive daytime sleepiness daytime cognitive and behavior problems, including problems paying attention, aggressive behavior and hyperactivity, which can lead to problems at school Diagnosis The diagnosis of OSA in children is usually based on the characteristic symptoms and evidence of adenotonsillar hypertrophy (big tonsils and adenoids) and mouth breathing. Children suspected of having OSA should usually be evaluated by a Pediatric ENT specialist for further evaluation. If necessary, further testing might include polysomnography (a pediatric sleep study).

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Treatments Although most younger children with OSA are not overweight, if a child is overweight, that might contribute to his symptoms. Weight loss is therefore important for overweight children with obstructive sleep apnea. Other underlying medical conditions, especially allergies, should also be treated. A nasal steroid might help improve nasal obstruction and OSA symptoms in children that also have allergies. The main treatment for kids with OSA is surgery, with removal of the child's enlarged tonsils and adenoids (tonsillectomy and adenoidectomy or T&A). (http://pediatrics.about.com/cs/sleep/a/sleep_apnea.htm) Sleep apnea treatment must depend on the individual child's current physical condition, medical history, and pertinent test results. There are some behavioral and mechanical approaches to treating pediatric OSA. However, since enlarged adenoids and tonsils cause the majority of pediatric OSA cases, surgical methods to reduce or remove the adenoids and tonsils are the most common and effective form of treatment. Behavioral treatments

Parents of children with OSA are advised to reduce their child's weight, if necessary, since obesity is often associated with pediatric OSA. In addition, children with OSA should not be given sedatives or medications that relax the airway and/or reduce respiratory function. Mechanical treatments

Some children can be treated by wearing a CPAP device (continuous positive airway pressure) while sleeping. The device maintains an open airway by

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physically blowing air through the nasal passages. However, this option is not as feasible with young children and is rarely prescribed. Surgical treatments

The most common procedure to treat pediatric OSA is a tonsillectomy and adenoidectomy (T&A). A T&A is generally 90-95% effective, yet different methods for performing this surgery can vary the amount of post-surgical pain and length of recovery time. More and more surgeons are also reducing the size of turbinates in addition to removing tonsils and adenoids. For more information on reduction of the inferior turbinates please visit (www.ObstructedNose.com.)

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Complications of AIDS
I. Neurologic complications:

AIDS-related disorders of the nervous system may be caused directly by the HIV virus, by certain cancers and opportunistic infections (illnesses caused by bacteria, fungi, and other viruses that would not otherwise affect people with healthy immune systems), or by toxic effects of the drugs used to treat symptoms. Other neuro-AIDS disorders of unknown origin may be influenced by but are not caused directly by the virus. AIDS dementia complex (ADC), or HIV-associated dementia (HAD), occurs primarily in persons with more advanced HIV infection. Symptoms include encephalitis (inflammation of the brain), behavioral changes, and a gradual decline in cognitive function, including trouble with concentration, memory, and attention. Persons with ADC also show progressive slowing of motor function and loss of dexterity and coordination. When left untreated, ADC can be fatal. It is rare when anti-retroviral therapy is used. Milder cognitive

complaints are common and are termed HIV-associated neurocognitive disorder (HAND). Neuropsychologic testing can reveal subtle deficits even in the absence of symptoms. Central nervous system (CNS) lymphomas are cancerous tumors that either begin in the brain or result from a cancer that has spread from another site in the body. CNS lymphomas are almost always associated with the Epstein-Barr virus (a common human virus in the herpes family). Symptoms include

headache, seizures, vision problems, dizziness, speech disturbance, paralysis, and mental deterioration. lymphomas. Prognosis is Individuals may develop one or more CNS poor due to advanced and increasing

immunodeficiency, but is better with successful HIV therapy.

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Cryptococcal meningitis is seen in about 10 percent of untreated individuals with AIDS and in other persons whose immune systems have been severely suppressed by disease or drugs. It is caused by the fungus Cryptococcus neoformans, which is commonly found in dirt and bird droppings. The fungus first invades the lungs and spreads to the covering of the brain and spinal cord, causing inflammation. Symptoms include fatigue, fever, headache, nausea, memory loss, confusion, drowsiness, and vomiting. If left untreated, patients with cryptococcal meningitis may lapse into a coma and die. Cytomegalovirus (CMV) infections can occur concurrently with other infections. Symptoms of CMV encephalitis include weakness in the arms and legs, problems with hearing and balance, altered mental states, dementia, peripheral neuropathy, coma, and retinal disease that may lead to blindness. CMV infection of the spinal cord and nerves can result in weakness in the lower limbs and some paralysis, severe lower back pain, and loss of bladder function. It can also cause pneumonia and gastrointestinal disease. This is rarely seen in HIVtreated individuals since advanced immunity is required for CMV to emerge. Herpes virus infections are often seen in people with AIDS. The herpes zoster virus, which causes chickenpox and shingles, can infect the brain and produce encephalitis and myelitis (inflammation of the spinal cord). It commonly

produces shingles, which is an eruption of blisters and intense pain along an area of skin supplied by an infected nerve. In people exposed to herpes zoster, the virus can lay dormant in the nerve tissue for years until it is reactivated as shingles. This reactivation is common in persons with AIDS because of their weakened immune systems. Signs of shingles include painful blisters (like those seen in chickenpox), itching, tingling, and pain in the nerves. People with AIDS may suffer from several different forms of neuropathy, or nerve pain, each strongly associated with a specific stage of active

immunodeficiency disease. Peripheral neuropathy describes damage to the

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peripheral nerves, the vast communications network that transmits information between the brain and spinal cord to every other part of the body. Peripheral nerves also send sensory information back to the brain and spinal cord. HIV damages the nerve fibers that help conduct signals and can cause several different forms of neuropathy. Distal sensory polyneuropathy causes either a numbing feeling or a mild to painful burning or tingling sensation that normally begins in the legs and feet. These sensations may be particularly strong at night and may spread to the hands. Affected persons have a heightened sensitivity to pain, touch, or other stimuli. Onset usually occurs in the later stages of the HIV infection and may affect the majority of advanced-stage HIV patients. Neurosyphilis, the result of an insufficiently treated syphilis infection, seems more frequent and more rapidly progressive in people with HIV infection. It may cause slow degeneration of the nerve cells and nerve fibers that carry sensory information to the brain. Symptoms, which may not appear for some decades after the initial infection and vary from person to person, include weakness, diminished reflexes, unsteady gait, progressive degeneration of the joints, loss of coordination, episodes of intense pain and disturbed sensation, personality changes, dementia, deafness, visual impairment, and impaired response to light. The disease is more frequent in men than in women. Onset is common during mid-life. Progressive multifocal leukoencephalopathy (PML) primarily affects individuals with suppressed immune systems (including nearly 5 percent of people with AIDS). PML is caused by the JC virus, which travels to the brain, infects multiple sites, and destroys the cells that make myelin the fatty protective covering for many of the bodys nerve and brain cells. Symptoms include various types of mental deterioration, vision loss, speech disturbances, ataxia (inability to coordinate movements), paralysis, brain lesions, and, ultimately, coma. Some individuals may also have compromised memory and cognition, and seizures

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may occur. PML is relentlessly progressive and death usually occurs within 6 months of initial symptoms. However, immune reconstitution with highly active antiretroviral therapy allows survival of more than half of HIV-associated PML cases in the current treatment era. Psychological and neuropsychiatric disorders can occur in different phases of the HIV infection and AIDS and may take various and complex forms. Some illnesses, such as AIDS dementia complex, are caused directly by HIV infection of the brain, while other conditions may be triggered by the drugs used to combat the infection. Individuals may experience anxiety disorder, depressive disorders, increased thoughts of suicide, paranoia, dementia, delirium, cognitive

impairment, confusion, hallucinations, behavioral abnormalities, malaise, and acute mania. Toxoplasma encephalitis, also called cerebral toxoplasmosis, occurs in about 10 percent of untreated AIDS patients. It is caused by the parasite Toxoplasma gondii, which is carried by cats, birds, and other animals and can be found in soil contaminated by cat feces and sometimes in raw or undercooked meat. Once the parasite invades the immune system, it remains there; however, the immune system in a healthy person can fight off the parasite, preventing disease. Symptoms include encephalitis, fever, severe headache that does not respond to treatment, weakness on one side of the body, seizures, lethargy, increased confusion, vision problems, dizziness, problems with speaking and walking, vomiting, and personality changes. Not all patients show signs of the infection. Antibiotic therapy, if used early, will generally control the

complication. Vacuolar myelopathy causes the protective myelin sheath to pull away from nerve cells of the spinal cord, forming small holes called vacuoles in nerve fibers. Symptoms include weak and stiff legs and unsteadiness when walking. Walking becomes more difficult as the disease progresses and many patients

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eventually require a wheelchair. Some people also develop AIDS dementia. Vacuolar myelopathy may affect up to 30 percent of untreated adults with AIDS and its incidence may be even higher in HIV-infected children. (http://www.ninds.nih.gov/disorders/aids/detail_aids.htm) II. Kaposi's sarcoma (KS)

is a tumor caused by Human herpesvirus 8 (HHV8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV). It was originally described by Moritz Kaposi (KA-po-she), a Hungarian dermatologist practicing at the University of Vienna in 1872.[1]It became more widely known as one of the AIDS defining illnesses in the 1980s. The viral cause for this cancer was discovered in 1994. Although KS is now well-established to be caused by a virus infection, there is widespread lack of awareness of this even among persons at risk for KSHV/HHV-8 infection. (http://en.wikipedia.org/wiki/Kaposi's_sarcoma)