Croup (or laryngotracheobronchitis) is a respiratory condition that is usually triggered by an acute viral infection of the upper airway.

The infection leads to swelling inside the throat, which interferes with normal breathing and produces the classical symptoms of a "barking" cough,stridor, and hoarseness. It may produce mild, moderate, or severe symptoms, which often worsen at night. It is often treated with a single dose of oral steroids; occasionally epinephrine is used in more severe cases. Hospitalization is rarely required. Croup is diagnosed on clinical grounds, once potentially more severe causes of symptoms have been excluded (i.e. epiglottitis or an airway foreign body). Further investigationssuch as blood tests, X-rays, and culturesare usually not needed. It is a relatively common condition that affects about 15% of children at some point, most commonly between 6 months and 56 years of age. It is almost never seen in teenagers or adults. Signs and symptoms Croup is characterized by a "barking" cough, stridor, hoarseness, anddifficult breathing which usually worsens at night.[1] The "barking" cough is often described as resembling the call of a seal or sea lion.[2] The stridor is worsened by agitation or crying, and if it can be heard at rest, it may indicate critical narrowing of the airways. As croup worsens, stridor may decrease considerably.[1] Other symptoms include fever, coryza (symptoms typical of thecommon cold), and chest wall indrawing.[1][3] Drooling or a very sick appearance indicate other medical conditions.[3] [edit]Causes Croup is usually deemed to be due to a viral infection.[1][4] Others use the term more broadly, to include acute laryngotracheitis, spasmodic croup, laryngeal diphtheria, bacterial tracheitis, laryngotracheobronchitis, and laryngotracheobronchopneumonitis. The first two conditions involve a viral infection and are generally milder with respect to symptomatology; the last four are due to bacterial infection and are usually of greater severity.[2] [edit]Viral Viral croup/acute laryngotracheitis is caused by parainfluenza virus, primarily types 1 and 2, in 75% of cases. Other viral etiologies includeinfluenza A and B, measles, adenovirus and respiratory syncytial virus (RSV).
[2] [5]

Spasmodic croup is caused by the same group

of viruses as acute laryngotracheitis, but lacks the usual signs of infection (such as fever, sore throat, and increased white blood cell count).
[2]

Treatment, and response to treatment, are also similar.

[5]

[edit]Bacterial Bacterial croup may be divided into laryngeal diphtheria, bacterial tracheitis, laryngotracheobronchitis, and laryngotracheobronchopneumonitis.
[2]

Laryngeal diphtheria is due to Corynebacterium diphtheriae while bacterial tracheitis,

laryngotracheobronchitis, and laryngotracheobronchopneumonitis are usually due to a primary viral infection with secondary bacterial growth. The most common bacteria implicated are Staphylococcus aureus, Streptococcus pneumoniae, Hemophilus influenzae, and Moraxella catarrhalis. Steroids Corticosteroids, such as dexamethasone and budesonide, have been shown to improve outcomes in children with all severities of croup. Significant relief is obtained as early as six hours after administration. While effective when given orally, parenterally, or by inhalation, the oral route is preferred. safe.
[4] [4] [7] [7] [2]

A single dose is usually all that is required, and is generally considered to be quite
[8]

Dexamethasone at doses of 0.15, 0.3 and 0.6 mg/kg appear to be all equally effective.

[edit]Epinephrine Moderate to severe croup may be improved temporarily with nebulized epinephrine.[4] While epinephrine typically produces a reduction in croup severity within 1030 minutes, the benefits last for only about 2 hours.[1][4] If the condition remains improved for 24 hours after treatment and no other complications arise, the child is typically discharged from the hospital.
[1][4

Celiac disease is a chronic digestive disorder in which damage to the lining of the small intestine leads to the malabsorption of minerals and nutrients.

y y y

The destruction of the inner lining of the small intestine in celiac disease is caused by an immunological (allergic) reaction to gluten. Gluten is a family of proteins present in wheat, barley, rye, and sometimes oats. Individuals with celiac disease may developdiarrhea, steatorrhea, weight loss, flatulence, iron deficiency anemia, abnormal bleeding, or weakened bones. However, many adults with celiac disease may have either no symptoms or only vague abdominal discomfort such as bloating, abdominal distension, and excess gas. Children with celiac disease may have stunted growth, and if untreated, childhood celiac disease can result in short stature as an adult. Small intestinal biopsy is considered the most accurate test for celiac disease. Blood tests can be performed to diagnose celiac disease; these include endomysial antibodies, anti-tissue transglutaminase antibodies, and anti-gliadin antibodies. There is no cure for celiac disease. The treatment of celiac disease is agluten free diet. In most individuals, a gluten free diet will result in improvement in symptoms within weeks. Many individuals report symptom improvement within 48 hours. In children with celiac disease, successful treatment with a gluten free diet can lead to the resumption in growth (with rapid catch up in height). Failure to respond to a gluten free diet can be due to several reasons; the most common reason is failure to adhere to a strict gluten free diet.

y y y y y y y

phenylketonuria Phenylketonuria (commonly known as PKU) is an inherited disorder that increases the levels of a substance called phenylalanine in the blood. Phenylalanine is a building block of proteins (an amino acid) that is obtained through the diet. It is found in all proteins and in some artificial sweeteners. If PKU is not treated, phenylalanine can build up to harmful levels in the body, causing intellectual disability and other serious health problems. What are the symptoms of PKU? The signs and symptoms of PKU vary from mild to severe. The most severe form of this disorder is known as classic PKU. Infants with classic PKU appear normal until they are a few months old. Without treatment with a special low-phenylalanine diet, these children develop permanent intellectual disability. Seizures, delayed development, behavioral problems, and psychiatricdisorders are also common. Untreated individuals may have a musty or mouse-like odor as a side effect of excess phenylalanine in the body. Children with classic PKU tend to have lighter skin and hair than unaffected family members and are also likely to have skin disorders such as eczema. What genes are related to phenylketonuria? Mutations in the PAH gene cause phenylketonuria. The PAH gene provides instructions for making an enzyme called phenylalanine hydroxylase. This enzyme converts the amino acid phenylalanine to other important compounds in the body. If gene mutations reduce the activity of phenylalanine hydroxylase, phenylalanine from the diet is not processed effectively. As a result, this amino acid can build up to toxic levels in the blood and other tissues. Because nerve cells in the brain are particularly sensitive to phenylalanine levels, excessive amounts of this substance can cause brain damage. Classic PKU, the most severe form of the disorder, occurs when phenylalanine hydroxylase activity is severely reduced or absent. People with untreated classic PKU have levels of phenylalanine high enough to cause severe brain damage and other serious medical problems. Mutations in the PAH gene that allow the enzyme to retain some activity result in milder versions of this condition, such as variant PKU or non-PKU hyperphenylalaninemia.

y y y y y

Changes in other genes may influence the severity of PKU, but little is known about these additional genetic factors. The main phenylketonuria treatment is a strict diet with very limited intake of phenylalanine, which is mostly found in foods containing protein. Which foods to avoid Because the amount of phenylalanine adults can safely eat is so low, it's crucial they avoid all high-protein foods, including:

Milk Eggs Cheese Nuts Soybeans Beans Chicken Steak and other beef products Pork Fish Chocolate candy Peas Beer Children and adults should also avoid foods, including many diet sodas, and medications made with aspartame (NutraSweet, Equal). Aspartame, found in many artificial sweeteners, releases phenylalanine when digested. Recently, sapropterin has been approved by the US Food and Drug Administration (FDA) as a treatment for PKU. It seems to be effective in a subset of patients.

Scoliosis Scoliosis (from Ancient Greek: skolios "crooked")

[1]

is a medical condition in which a person's spine is curved from side to side.

Although it is a complex three-dimensional deformity, on an X-ray, viewed from the rear, the spine of an individual with scoliosis may look more like an "S" or a "C" than a straight line. Scoliosis is typically classified as either congenital (caused by vertebral anomalies present at birth), idiopathic (cause unknown, subclassified as infantile, juvenile, adolescent, or adult, according to when onset occurred), or neuromuscular (having developed as a secondary symptom of another condition, such as spina bifida, cerebral palsy,spinal muscular atrophy, or physical trauma). Signs and symptoms Patients having reached skeletal maturity are less likely to have a worsening case. Some severe cases of scoliosis can lead to diminishing lung capacity, putting pressure on the heart, and restricting physical activities. The signs of scoliosis can include:

   

Uneven musculature on one side of the spine A rib prominence and/or a prominent shoulder blade, caused by rotation of the ribcage in thoracic scoliosis Uneven hips/leg lengths Slow nerve action (in some cases)

Cause It has been estimated that approximately 65% of scoliosis cases are idiopathic, approximately 15% are congenital and approximately 10% are secondary to a neuromuscular disease.[4] Idiopathic scoliosis is a condition which lasts a lifetime, but it does not increase the risk of mortality.[5] In adolescent idiopathic scoliosis, there is no clear causal agent and it is generally believed to be multifactorial, although genetics are believed to play a role.[6] Various causes have been implicated, but none of them have consensus among scientists as the cause of scoliosis, though the role of genetic factors in the development of this condition is widely accepted.[7] Still, at least one gene, notably CHD7, has been associated with the idiopathic form of scoliosis.[8][7] In some cases, scoliosis exists at birth due to a congenital vertebral anomaly. Another cause in the past was when the father had ether in his blood stream when the baby was conceived. This would happen if the man was a busy anaesthetist using ether daily in hosptal operating rooms. It no longer happens because ether is not used for anaesthetic any more. [9] Scoliosis often presents itself, or worsens, during the adolescence growth spurt and is more often diagnosed in females versus males.

One of the first treatments of scoliosis is the attempt to prevent further curvature of the spine. Depending on the size of the curvature, this is typically done in one of three ways: bracing, surgery, or postural positioning through customized cushioning.
[32][33][34]

Stopping the progression of the scoliosis can prevent the loss of function in many activities of daily living by

maintaining range of motion, preventing deformity of the rib cage, and reducing pain during activities such as bending or lifting. Occupational therapists are often involved in the process of selection and fabrication of customized cushions. These individualized postural supports are used to maintain the current spinal curvature, or they can be adjusted to assist in the correction of the curvature. This type of treatment can help to maintain mobility for a wheelchair user by preventing the deformity of the rib cage and maintaining an active range of motion in the arms.
[32]

A back brace is a device designed to limit the motion of the spine in cases of fracture or in post-operative fusions. Limiting the motion of the spine enhances the healing process and minimizes the patient's discomfort. Common back braces include:

 

Rigid (Hard) braces : These braces are form-fitting plastic molds that restrict motion by as much as 50%; and Soft braces : Elastic braces that limit forward motion of the spine and assist in setting spinal fusions or supporting the spine during occasions of stress (for example, employment requiring the lifting of heavy loads).

 

Boston brace This is the most commonly-used brace in the United States. It is a symmetrical brace. It corrects curvature by pushing with small pads placed against the ribs, which are also used for rotational correction (here it tends to be slightly less successful, however). These pads are usually placed in the back corners of the brace so that the body is thrust forward against the brace's front, which acts to hold the body upright. The brace opens to the back, and usually runs from just above a chair's seat (when a person is seated) to around shoulder-blade height. Because of this, it is not particularly useful in correcting very high curves. It also does not correct hip misalignment, as it uses the hips as a base point. This brace is typically worn 2023 hours a day.

  

[edit]Milwaukee brace Main article: Milwaukee brace The Milwaukee brace was a very common brace towards the earlier part of the twentieth century in the United States. It is a largely symmetrical brace. The brace is made with a harness-like hip area and metal strips rising to the chin, where a collar is. Between the hips and chin, there are corrective thrusts given with large pads. There is little rotational correction. Today this brace is generally used for very high thoracic curves that are severe and out of range of the Boston. This brace is typically worn 2023 hours a day.

 

[edit]Charleston bending brace This brace was designed with the idea that compliance would increase if the brace were worn only at night. It is asymmetrical. The brace fights against the body's curve by over-correcting. It grips the hips much like the Boston, and rises to approximately the same height, but pushes the patient's body to the side. It is used in single, thoracolumbar curves in patients 1214 years of age (before structural maturity) who have flexible curves in the range of 2535 Cobb degrees.

 

[edit]SpineCor brace This is the only widely-used soft brace currently.

[citation needed]

The brace has a pelvic unit from which strong elastic bands wrap

around the body, pulling against curves, rotations, and imbalances. It is most successful when the patient has relatively small and simple curvatures, is structurally young, and compliantit is usually worn 20 hours a day. The patient is not to have it off for more than two hours at a time. While it is expected that patients can participate in activities as strenuous as competitive gymnastics while in brace, it also pulls down against shoulder misalignments which compresses the spine. Long-term results

are also, largely, in the making. SpineCor is also the only scoliosis brace for adults.

[citation needed]

This brace was invented in

[1]

Montral, Canada but is not use in other parts of it, instead being widely used in other countries.

 

[edit]SPoRT brace SPoRT stands for "Symmetric, Patient-oriented, Rigid, Three-Dimensional active," which it intends to be. The brace is symmetrical, built with a plastic frame reinforced with aluminum rods. The brace corrects hip misalignments through padding. Large, sweeping, thick pads push the spine to a corrected position. To prevent overcorrection, however, the brace also has "stop" pads holding the spine from moving too far in the other direction. The brace runs from just above the chair to T3 in many instancesit is successful at correcting high thoracic curves. In front, it goes around the patient's breast and up, even to pushing against the collar bone. Though it sounds restricting, it has been tested for comfort while participating in athletics. The theory holds that the support that the brace gives will help the patient's body learn to work as though it had no curve muscularly. Then the muscles would be able to support the spine, preventing further collapse. This brace is used for all curve patterns and types, even ones considered past brace treatment by other schools. The brace is typically worn 22 hours a day, and often coupled with a physical therapy program.

 

[edit]Cheneau brace This brace is designed for use with the Schroth physical therapy method. It utilizes large, sweeping pads to push the body against its curve and into blown out spaces. The Schroth theory holds that the deformity can be corrected through retraining muscles and nerves to learn what a straight spine feels like, and breathing deeply into areas crushed by the curvature to help gain flexibility and to expand. The brace helps patients keep doing their exercises throughout the day. This brace is asymmetrical, and is used for patients of all degrees of severity and maturity. It is often worn 2023 hours a day. The brace principally contracts to allow for lateral and longditutal rotation and movement.

Hypospadia Hypospadia is a common congenital disease of the penis with an abnormal ventral opening of the meatus of the urethra. Hypospadia are often associated with a ventral curvature of the penis (chordee) and/or a deficient ventral prepuce (foreskin) with a dorsal "hood". The classification of hypospadias depends on the position of the urethral meatus:

Glanular,Coronal,Penile (distal-middle-proximal).Scrotal,Perineal

Causes (Etiology) of Hypospadias Embryology of the Male Urethra:

The urethra emerges from the urethral folds, which fuse ventrally under the influence of androgens. The fusion begins proximally in the 11th week of gestation and proceeds distally. The fusion involves endodermal and ectodermal tissue. The androgen effect is mediated by the 5 -reductase. In hypospadias, malformations concern the endodermal and ectodermal tissue. An example of an ectodermal abnormality is the deficient ventral foreskin with a dorsal "hood". Endodermal abnormalities include the position of the meatus, a deficient urethra distal to the meatus and chordee formation (urethral plate).

Androgen Deficiency:

An absolute (low concentration) or relative (decreased sensitivity of the target tissue) androgen deficiency is a major cause for the development of hypospadias. Many enzyme deficiencies which cause hypospadias are known, such as 5 -reductase deficiency or defects of the androgen receptor. In 1070% of severe proximal hypospadias, an enzyme deficiency or hormonal disease affecting the androgens can be found.

Genetics: Hypospadias have a multifactorial etiology involving several known genes (polygenic disease). This can be concluded from the family history and twin studies. In addition to the known enzyme defects (see above), most genes involved in the etiology of hypospadias are still unknown.

Environmental Factors: A variety of substances with estrogenic activity contaminates the environment and is enriched through the food chain. Substances with estrogenic activity are insecticides, natural estrogens from plants and chemicals from the plastics industry. The impact on wildlife is well documented: thin egg shells in birds or penis malformations in alligators. The worldwide increase in hypospadias in humans is also attributed to these environmental factors.

Orthoplasty Assessment and management of penile curvature is done after artificial erection of the penis. In the majority of cases, the curvature of the penis can be corrected using the technique of Nesbit. In severe cases, grafting of the tunica albuginea helps in straighting the penis. Resection of the chordee is only rarely performed. For tubularized incised plate (TIP) urethroplasty, conservation of the urethral plate is mandatory.

Urethroplasty Urethroplasty is reconstruction of the missing distal urethra. The below described surgical techniques differ primarily in the technique of urethroplasty: application of flaps, incision of the urethral plate or free oral mucosa transplants.

Neourethral coverage: A second layer of tissue covers the neourethra and prevents the formation of fistulas. Most often, a pedicled subcutaneous (dartos) flap is raised from preputial, penile or scrotal skin.

Meatoplasty and glanuloplasty: Reconstruction of the meatus and the glans to achieve meatus at the tip of the penis with a vertical slit.

Skin closure: Skin coverage of the penile shaft is achieved with various techniques (e.g. transfer of penile skin).

MAGPI Hypospadia Operation:

MAGPI is Meatal advancement and glanuloplasty (Duckett, 1981b). The MAGPI-technique is only suitable for distal hypospadias. Technique and complications see Chapter Urologic Surgery/MAGPI-technique for hypospadia repair.

Tubularized incised plate (TIP) Urethroplasty TIP urethroplasty is suitable for distal and proximal penile hypospadias (Snodgrass, 1994). The TIP urethroplasty is considered technically simple and has a low complication rate, the cosmetic result of the glans and the meatus is good. Furthermore, the TIP urethroplasty is an useful option for re-operations with preserved urethral plate. The urethral plate is not removed but deeply and longitudinally incised. After mobilization and tubularization, the urethral plate is closed around a catheter. A ventral curvature is corrected using the Nesbit technique. For a description in detail, please see Chapter Urologic Surgery/Tubularized incised plate (TIP) urethroplasty.

Mathieu Hypospadia Repair The Mathieu hypospadia repair is a good option for distal penile hypospadias (Mathieu, 1932). An rectangle of skin over the proximal urethra is raised and folded distally. To avoid a horizontal meatus, a modification of the original technique with V-incision of the flap exists (MAVIS = Mathieu and V incision sutured). Technique and complications see Chapter Urologic Surgery/Mathieu hypospadia repair. The most common complications are unfavorable meatal cosmetics, skin flap necrosis with fistula or stricture of the urethral meatus.

Island Flaps Hypospadia Repair Island flap hypospadia repair is suitable for distal and middle penile hypospadias (Duckett, 1981a). The island flap is raised from the prepuce: the pedicled flap consists of the inner leaf of the prepuce with Tunica dartos. The flap is rotated around the penis and used in onlay technique with a preserved urethral plate. If a resection of a chordee has been necessary, a tubular island flap is necessary. Technique and complications see ChapterUrologic Surgery/Island flaps hypospadia surgery.

Two-stage Hypospadia Repair Indications for a two-stage hypospadia repair are severe proximal hypospadias and situations after failed hypospadia surgery. Technique and complications see Chapter Urologic Surgery/Two-stage hypospadia repair.

Hypospadia Repair with a Free Oral Mucosa Graft Indications for the use of a free oral mucosa graft are situations after failed hypospadias surgery. Tonsillitis Tonsillitis (ton-sil-lie-tiss) is an inflammation of the tonsils caused by an infection. In tonsillitis, the tonsils are enlarged, red, and often coated (either partly or entirely) by a substance that is yellow, gray, or white. Tonsillitis usually occurs as part of a pharyngitis (throat infection). Tonsillitis usually begins with sudden sore throat and painful swallowing. Sometimes, tonsillitis reoccurs, and may cause difficulty breathing. If this occurs, your doctor may recommend taking them out. This procedure of removing tonsils from the throat is called a tonsillectomy. Causes

The most common causes of tonsillitis are the common cold viruses (adenovirus, rhinovirus, influenza, coronavirus, respiratory syncytial virus).
[1][2][3][4]

It can also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus, or HIV.

[1][2][3][4]

The second

most common causes are bacterial. The most common bacterial cause is Group A -hemolytic streptococcus (GABHS), which causes strep throat.
[1][2][3][4]

Less common bacterial causes include: Staphylococcus aureus, Streptococcus pneumoniae, Mycoplasma
[1][2][3][4]

pneumoniae, Chlamydia pneumoniae, pertussis, Fusobacterium, diphtheria, syphilis, and gonorrhea.

y y y y

What are the symptoms of Tonsillitis? Each person with tonsillitis may not experience all of the symptoms. Some of the major symptoms of tonsillitis are: a very sore throat,fever,redder-than-normal tonsils,chills;;a yellow or white coating on the tonsils a funny-sounding voice swollen glands in the neck bad breath Tests that may be done include:

y y y

Blood count Mononucleosis test Rapid strep test

y Throat swab culture Treatment

If bacteria such as strep are causing the tonsillitis, antibiotics are given to cure the infection. The antibiotics may be given once as a shot, or taken for 10 days by mouth. If antibiotic pills are used, they must be taken for the entire amount of time prescribed by the doctor. DO NOT stop taking them just because the discomfort stops, or the infection may not be cured. Other treatments include: Drink cold liquids or suck on popsicles Drink fluids, especially warm (not hot), bland fluids Gargle with warm salt water Suck on lozenges (containing benzocaine or similar ingredients) to reduce pain (these should not be used in young children because of the choking risk) Take over-the-counter medications, such as acetaminophen (Tylenol) or ibuprofen to reduce pain and fever. Do NOT give a child aspirin. Aspirin has been linked to Reye syndrome.

y y y y y

Hemophilia B Hemophilia B is a hereditary bleeding disorder caused by a lack of blood clotting factor IX. Without enough factor IX, the blood cannot clot properly to control bleeding. Causes Hemophilia B is caused by an inherited X-linked recessive trait, with the defective gene located on the X chromosome. Males, however, have only one X chromosome, so if the factor IX gene on that chromosome is defective, they will have Hemophilia B. Therefore, most people with hemophilia B are male. If a woman has a defective factor IX gene, she is considered a carrier. This means the defective gene can be passed down to her children. Boys born to a woman who carries the defective gene have a 50% chance of having hemophilia B, while their daughters have a 50% chance of being a carrier. All female children of men with hemophilia carry the defective gene. Risk factors for hemophilia B include: Family history of bleeding

Being male

Gene. F9 is the only gene in which mutations are known to cause hemophilia B. Treatment Treatment (bleeding prophylaxis) is by intravenous infusion of factor IX. Factor IX has a longer half life than factor VIII (Deficient in Haemophilia A) and as such factor IX can be transfused less frequently. Symptoms can include:

y y y y y y y y

Bleeding into joints and associated pain and swelling Blood in the urine or stool Bruising Excessive bleeding following circumcision Gastrointestinal tract and urinary tract hemorrhage Nosebleeds Prolonged bleeding from cuts, tooth extraction, and surgery

Spontaneous bleeding Exams and Tests If the patient is the first person in the family to have a suspected bleeding disorder, he or she will undergo a series of tests called a coagulation study. Once the specific defect has been identified, other family members will need less testing to diagnose the disorder. Tests results may include: Prolonged partial thromboplastin time (PTT) Normal prothrombin time Normal bleeding time Normal fibrinogen level Low factor IX

y y y y y

Hepatitis B vaccine is recommended for individuals with hemophilia B because they are at increased risk of developing hepatitis due to exposure to blood product

Hemophilia A Hemophilia A is a hereditary bleeding disorder caused by a lack of blood clotting factor VIII. Without enough factor VIII, the blood cannot clot properly to stop bleeding. Alternative names Factor VIII deficiency Causes Hemophilia A is caused by an inherited X-linked recessive trait, with the defective gene located on the X chromosome. Females have two copies of the X chromosome, so if the factor VIII gene on one chromosome doesn't work, the gene on the other chromosome can do the job of making enough factor VIII. Males, however, have only one X chromosome, so if the factor VIII gene on that chromosome is defective, they will have hemophilia A. Thus, most people with hemophilia A are male. If a woman has a defective factor VIII gene, she is considered a carrier. This means the defective gene can be passed down to her children. In a woman who carries the defective gene, any of her male children will have a 50% chance of having hemophilia A, while any of her female children will have a 50% chance of being a carrier. All female children of men with hemophilia carry the defective gene. Genetic testing is available for concerned parents.

Risk factors for hemophilia A include: Family history of bleeding,Being male Bleeding into joints, with associated pain and swelling.Blood in the urine or stool,Bruising,Gastrointestinal tract and urinary tract hemorrhage,Nosebleeds Prolonged bleeding from cuts, tooth extraction, and surgery Spontaneous bleeding Tests to diagnose hemophilia A include: Low serum factor VIII activity Normal prothrombin time Normal bleeding time Normal fibrinogen level

y y

Symptoms may include:

y y y y

y Prolonged partial thromboplastin time (PTT) Treatment

Standard treatment involves replacing the missing clotting factor. The amount of factor VIII concentrates needed depends on the severity of the bleeding, the site of the bleeding, and the size of the patient. Mild hemophilia may be treated with desmopressin (DDAVP), which helps the body release factor VIII that is stored within the lining of blood vessels. otitis media? Otitis media is an inflammation of the middle ear (the air-filled space located behind the eardrum). There are two types of otitis media. acute otitis media is a painful infection of the middle ear. otitis media with effusion is fluid in the middle ear. What causes otitis media? Acute otitis media is usually a complication of a cold, sore throat, or other infection of the upper respiratory tract. The eustachian tube connects the ear to the back of the throat. When a child has a stuffy nose, the tube gets blocked. Bacteria (or viruses) become trapped in the middle ear and cause an infection. Fluid and pressure build up behind the eardrum, causing ear pain, swelling, and redness. Bacteria are responsible for most cases of acute otitis media. Acute otitis media is not contagious, but the upper respiratory illnesses that can lead to it may be. Otitis media with effusion is a build-up of fluid in the middle ear that can happen in two ways. When a child has a cold, the middle ear may produce fluid just as the nose does; however, the fluid does not run out as easily from the middle ear because of blockage of the eustachian tube. Or, when a child has recently had acute otitis media, fluid may remain in the middle ear even after the infection clears. Acute otitis media is an infection that can cause pain, fever, or an inflamed eardrum. It can occur in one or both ears. Symptoms in infants and toddlers include: y Tugging or scratching at the ear,Hearing problems,Crying, irritability,Fever,Vomiting y Ear drainage treatment for otitis media? y Acute otitis media is treated with oral antibiotics. Amoxycillin is the first-line antibiotic for treatment of acute otitis media. Cleft lip (cheiloschisis) and cleft palate (palatoschisis), which can also occur together as cleft lip and palate, are variations of a type of clefting congenital deformity caused by abnormal facial development during gestation. A cleft is a fissure or openinga gap. It is the non-fusion of the body's natural structures that form before birth. Approximately 1 in 700 children born have a cleft lip and/or a cleft palate. An older term is harelip, based on the similarity to the cleft in the lip of a hare. Clefts can also affect other parts of the face, such as the eyes, ears, nose, cheeks, and forehead. In 1976, Paul Tessier described fifteen lines of cleft. Most of these craniofacial clefts are even more rare and are frequently described as Tessier clefts using the numerical locator devised by Tessier.[1] A cleft lip or palate can be successfully treated with surgery, especially so if conducted soon after birth or in early childhood. Cleft lip and palate If the cleft does not affect the palate structure of the mouth it is referred to as cleft lip. Cleft lip is formed in the top of the lip as either a small gap or an indentation in the lip (partial or incomplete cleft) or it continues into the nose (complete cleft). Lip cleft can occur as a

one sided (unilateral) or two sided (bilateral). It is due to the failure of fusion of the maxillary and medial nasal processes (formation of the primary palate). mild form of a cleft lip is a microform cleft.[2] A microform cleft can appear as small as a little dent in the red part of the lip or look like a scar from the lip up to the nostril.[3] In some cases muscle tissue in the lip underneath the scar is affected and might [4] require reconstructive surgery. It is advised to have newborn infants with a microform cleft checked with a craniofacial [5 team as soon as possible to determine the severity of the cleft. Cleft palate Cleft palate is a condition in which the two plates of the skull that form the hard palate (roof of the mouth) are not completely joined. The soft palate is in these cases cleft as well. In most cases, cleft lip is also present. Cleft palate occurs in about one in 700 live births worldwide.[6] Palate cleft can occur as complete (soft and hard palate, possibly including a gap in the jaw) or incomplete (a 'hole' in the roof of the mouth, usually as a cleft soft palate). When cleft palate occurs, the uvula is usually split. It occurs due to the failure of fusion of the lateral palatine processes, the nasal septum, and/or the median palatine processes (formation of the secondary palate). The hole in the roof of the mouth caused by a cleft connects the mouth directly to the nasal cavity. the most common procedure to repair a cleft lip is the Millard procedure pioneered by Ralph Millard.