Almost everyone has had this problem once in his or her childhood. First, you got a cold, then an earache and fever, and the pediatrician told you that you had an “ear infection.” Whatever virus or bacterial infection was causing your cold-like symptoms had inflamed the lining of the middle ear cavity and Eustachian tube. Your Eustachian tube swelled and closed, fluid from the inflammation (pus) formed in the ear, pushed on the eardrum, and you got one heck of an earache. You actually had developed an abscess in the ear.
Adults with AOM will experience fever, general malaise, reduced hearing in the infected ear, and perhaps dizziness or even ringing in that ear.
Children with AOM will complain of earache and will have fever, but they rarely become dizzy or complain of ringing in the infected ear.
Infants with AOM will have a high fever, be irritable, and pull at or otherwise fidget with their ears.
Treating Acute Otitis Media (AOM)
The single most important goal of the treatment of AOM is the elimination of infection from the middle ear cavity Antibiotic medications play the most important role in accomplishing this goal. Amoxicillin (Amoxil, Polymox, Trimox, Wymox) is very often the first antibiotic used, and is commonly taken for 10 to 14 days. However, it should never be used when one is allergic to penicillin. Other antibiotics used to treat AOM include amoxicillin with clavulanate (Augmentin), erythromycin with sulfisoxazole (Pediazole), any erythromycin product (EES, Eryc, Pediamycin, etc.), trimethoprim-sulfamethoxazole (Bactrim, Septra), and cefaclor (Ceclor).
Caution: Up to 15 percent of people allergic to penicillin who take cefaclor-type antibiotics react to those antibiotics. That is because these antibiotics have a chemical structure similar to that of penicillin. If you are allergic to penicillin and cefaclor-type antibiotics, your doctor will likely treat you with erythromycin, erythromycin with sulfisoxazole, or trimethoprim-sulfamethoxazole.
When AOM complicates chronic rhinitis, decongestants in the form of nasal sprays/drops, or pills, capsules, or liquids by mouth are also commonly used.
A basic component of every form of rhinitis is inflammation, the degree of which varies from person to person. When the nose is inflamed, it is common for the Eustachian tube and ear to become involved in that inflammation. When that happens, the Eustachian tube swells, sometimes to the point of complete closure, trapping air behind. When this happens two other important events take place:
The air trapped in the middle ear cavity gets absorbed into the blood stream via the rich network of tiny blood vessels surrounding the middle ear. The absorption of this air produces a relative vacuum in the middle ear. This change in pressure within the ear causes fluid to ooze from the walls of blood vessels into the ear cavity. The swelling of the Eustachian tube also blocks the circulation of blood and tissue fluid from the ear and provides another means by which fluid accumulates in the middle ear. If the process stopped here, you would have otitis media with effusion (ОМЕ) – i.e., fluid in the ear, but no infection associated with it.
If an infection-causing agent such as a virus or a bacteria is trapped in the middle ear cavity, the result will be an infected middle ear, otitis media (OM).
The alarming increase in the prevalence of type 2 diabetes and prediabetes is accompanied by a comparable increase in the number of overweight (BMI > 25kg/m2) or obese (BMI > 30kg/m2) people. In 1991, 12.3% of the U.S. population was obese and 45% was overweight. These rates rose to 19.8% and 56.4%, respectively, by 2000. Thus, over 75% of the U.S. adult population was overweight in 2000, and over 25% had altered glucose metabolism. Similar trends are seen in people under 18 years of age, and type 2 diabetes is now recognized with increased frequency in overweight or obese children and adolescents.
The prevalence of type 2 diabetes is higher among African Americans, Hispanic Americans, Mexican Americans, and Native Born Americans compared with Caucasians. Increases in the U.S. pppulation of some of these ethnic groups have contributed to the overall rise in prevalence of diabetes in the U.S. in the past decade. Thus, the trends shown in older surveys are likely to be magnified with modern data.
Estimates of the prevalence of type 1 diabetes in the U.S. are about 1.7 per 1000 people aged 1-19, and about 1.2 per 1000 people of all ages. In 2000, this suggests close to 350,000 people with type 1 diabetes in the U.S. Other estimates suggest that the prevalence is about 0.3% of adults over the age of 30, or close to 500,000 older people with type 1 diabetes in 2000. In any case, relative to type 2 diabetes, type 1 is a rare disease and probably accounts for less than 5% of the entire population
of close to 20 million people with diabetes in the U.S. However, there are about 30,000 new cases of type 1 diabetes each year, and it is said to be the most frequent chronic childhood disease.
1. Previously it was known as Insulin Dependent or Juvenile Diabetes Mellitus (IDDM)
2. It constitutes about 5% of the diabetes in our country. The incidence of this type is very high in European and Western population.
3 Type-1 diabetes mellitus or Juvenile diabetes results from cellular mediated auto-immune destruction of B-Cells of pancreas that means sell destruction of body’s own insulin producing B-cells in pancreas by the defence system of body cue to failure of differentiation between invading viruses and body’s own cells.
4. Type-1 diabetes mellitus commonly occurs in childhood and adolescence but it can occur at any age even in the 8th and 9th decades of life.
5. In Type-1 diabetes rate of destruction of Beta Cells (insulin producing) is quite variable being rapid in some individuals (mainly infants and childhood) and slow in others (adults).
6. Onset of Type-1 diabetes is usually acute and develops within a short period of time, generally at an age of 5-6 years and 11-14 years. Some Type-1 patients, particularly children and adolescents, may present with ketoacidosis as first presentation of diabetes.
7. As in Type-1 diabetes mellitus, insulin producing Beta-cells in pancreas are totally destroyed and thus insulin is not produced at all. For their survival they are dependent on insulin from external site. Withdrawal of insulin in these patients leads to a serious complication which is acute in nature, known as diabetic Ketoacidosis or diabet;c coma. These are the patients who are advised not to discontinue their insulin injections and should remain under medical supervision.
8. Type-1 diabetes has a strong H.L.A. (Human Leucocytie Antigen) association.
9. This type of diabetes can be diagnosed by markers of immune destruction of beta cells and includes (1) ICAs ”Islet Ce!ls Antibodies) (2) IAAS (Autoantibodies to Insulin) (3) GAD Antigen (Glutamic Acid Decarboxylase
Although patients are very obese, when they present with this type of diabetes the presence of diabetes is not incompatible with the diagnosis. This type of diabetes is also prone to other auto-immune disorder.