Nasopharyngeal Carcinoma Therapy

Hello Mbah Dukun Bagong, modern shaman comes again. today mbah dukun will explains about how to therapy the cancer of nasopharyngeal, following last post. There are 2 therapies for this disease. what are they? okey check it out

  

A. Primary Therapy

1. radiotherapy
Until recently, radiotherapy still plays an important role in the management of nasopharyngeal carcinoma. Management of nasopharyngeal carcinoma is the first to radiotherapy with or without chemotherapy.
2. chemotherapy
Chemotherapy as an adjunct therapy in nasopharyngeal carcinoma was found to improve therapeutic outcomes. Especially, given the advanced stage or on the state of relapse.
Various combinations are developed, the best to date is combined with Cis-platinum as the core
Giving chemotherapy anjuvan Cis-platinum, bleomycin and 5-fluororacil with interim results that are satisfactory. Similarly, studies have been conducted of chemotherapy praradiasi with epirubicin and cis-platinum, although there are side effects severe enough, but it gives hope of a better cure.
3. operation
Surgery in patients with nasopharyngeal carcinoma are, radical neck dissection and nasopharyngectomy. Neck dissection is performed if there is still residual gland after radiation or a recurrence of the gland with the proviso that the primary tumor has been cleared as evidenced by radiological examination and serology. Nasopharyngectomy is a palliative operation is performed in relapse cases or the presence of residues that are not successful in the nasopharynx treated by other ways.
4. immunotherapy
By knowing the possible causes of nasopharyngeal carcinoma is the Epstein-Barr virus, So patients can be administered immunotherapy.

Radiotherapy
Radiotherapy is a method of treatment of malignant diseases using lawyer-ion beam, aiming to kill tumor cells as much as possible and maintain the healthy tissue around the tumor so as not to suffer the damage is too severe. Nasopharyngeal carcinoma is radioresponsif that radiotherapy remains an important therapy.
Radiation on tissue, can cause ionization of water and electrolytes from the body fluids both intra-and extra-cellular, so that the resulting very reactive H + and OH-. Ions that can react with a molecule of DNA in the chromosomes, so
can occur:
1. DNA double chain break
2. Changes in cross-linkage in the DNA chain
3. Base changes that cause degeneration or cell death.
Lethal dose and the ability to repair damage to cancer cells is lower than normal cells, so the effect of radiation, the cancer cells more likely to die and remain damaged compared with normal cells.
The cells that still survive, will hold its DNA damage repair on their own. DNA repair ability of normal cells better and faster than the cancer cells. This situation is used as a basis for radiotherapy in cancer.
At the VIII International Congress of Radiology in 1953, set RAD (radiation absorbed Dose) as the amount of energy absorbed per unit of tissue. Currently the International System units (SI) of dose on absorption has been changed to Gray (Gy) and the unit often used is the unit of centi gray
(cGy).
1 Gy = 100 rad
1 rad = 1 cGy = 10-2 Gy.,
Treatment outcomes are expressed in numbers in response to irradiation is highly dependent on tumor stage. The more advanced tumor stage, the less response. For stage I and II, obtained a complete response 80% - 100% with radiation therapy. Whereas stage III and IV, found the numbers
failure of local response and distant metastases is high, namely 50% - 80%. Survival rate of patients with nasopharyngeal carcinoma depends on several factors, foremost among which is the stage of disease.
a.    Preparation / planning prior to radiotherapy
Before, were given radiation therapy, clinical staging was made, histopathologic diagnosis, as well as determined the purpose of radiation, curative or palliative. Patients also prepared mentally and physically. To the patient, if necessary, the family also provided information regarding the necessity of this action, the purpose of treatment, side effects that may arise during the treatment period.
Physical examination and laboratory before starting radiation is absolute. Patients with poor general condition, malnutrition or fever are not allowed to radiation, except in patients with life-threatening circumstances, such as track digestivum obstruction, massive bleeding from the tumor, radiation still starts while improving the general state of the patient. As a benchmark, Hb levels should not be less than 10 g%, the number of leukocytes can not be less than 3000 per mm3 and platelets 100,000 per uL.
b. Determination of the limits of the radiation field
This action is one of the most important step to ensure the success of the radiotherapy. Radiation field included the primary tumor and the surrounding area / potential to continue spreading and lymph-regional lymph nodes.For tumor stage I and II, the following areas should be illuminated:
1. The entire nasopharynx
2. The entire base of the sphenoid and occiput
3. cavernosal sinuses
4. Cranial base, a minimum width 7 cm 2 covering the foramen ovale, carotid canal and jugular foramen laterally.
5. Rear half of nasal cavity
6. Posterior Etmoid sinus
7. 1 / 3 posterior orbit
8. 1 / 3 posterior maxillary sinus
9. fossa pterygoidea
10. Lateral and posterior pharyngeal wall as high as midtonsilar fossa
11. gland retrofaringeal
12. Bilateral cervical glands including the posterior jugular, spinal accessory and supraclavicular
If there is an extension to the nasal cavity or oropharynx (T3) the entire cavity and oropharynx nasal should be included in the radiation field. If the extension through the skull base has reached the cranial cavity, the upper limit of the radiation field is located above the pituitary fossa. If the spread of tumor to the maxillary sinus and Etmoid or orbit, around the sinuses or the orbit should be irradiated. Submental and occipital lymph nodes are not routinely included, unless a massive cervical lymphadenopathy was found or if there is metastasis to the sub-maxillary glands.
irradiation field boundaries are:
- Superior: covering the cranial base, sella tursika included in the radiation field.
- Anterior: located behind the eyeball and choana
- Posterior: right behind the external acoustic meatus, except when there is enlargement of the gland the rear boundary should be located 1 cm beyond the palpable glands.
- Inferior: located on the top edge of thyroid cartilage, these limits change when obtained enlarged neck glands, which is 1 cm lower than the gland is palpable. This field of radiation received from the left and right of the patient.
In patients with neck glands are very large so that the radiation in the above methods can not be done, then the radiation field is given by the front and rear.
The upper limit includes all the cranial base. The lower limit is the bottom edge of the clavicle, the left and right limits are 2 / 3 of the distal clavicle, or follow the magnitude of the gland.
Gland supra clavicle and lower neck received radiation from the field in front, the upper limit of the radiation field is coincident with the lower limit of the radiation field to the primary tumor.
c.    Rays to radiotherapy
Rays used for radiotherapy are:
1. Alpha rays
Alpha rays are corpuscular rays or particles from the nucleus. The nucleus consists of protons and neutrons. This light can not penetrate the skin and are not widely used in radiotherapy.
2. Beta rays
Beta rays is the electron ray. These rays emitted by radioactive substances that have low energy. Power breakdown of the skin is limited, 3-5 mm. Used for the treatment of superficial lesions.
3. Gamma rays
Gamma rays are electromagnetic rays or photons. These rays can penetrate the body. Depending on the power breakdown of the energy that causes the beam. The higher energy or higher voltagenya, the bigger and more power breakdown in the location of the maximum dose.
d.     radioisotopes
1. Caecium137! gamma rays
2. Cobalt60! gamma rays
3. Radium226! alpha rays, beta, gamma.
e. Radiotherapy technique
There are three main ways of radiotherapy, namely:
1. External radiation / teletherapy
Ray sources in the form of X-ray apparatus or a radioisotope which is placed outside the body. Beam is directed into the tumor to be given radiation. Much energy is absorbed by a tumor depends on:
a. The amount of energy emitted by energy source
b. The distance between the source of energy and the tumor
c. Density of the tumor mass.
Teletherapy fractional generally administered at a dose of 150-250 rad per time, in 2-3 series. Among the series 1-2 or 2-3 given 1-2 weeks to break the person's condition so that recovery takes 4-6 weeks of radiotherapy.
e.    2. International Radiation / Brachytherapy
Energy source is placed inside the tumor or adjacent to the tumor in the body cavity. There are several types of internal radiation:
a. interstitial
Radioisotopes in the form of needle inserted into the tumor, for example, radium needles or needle irridium.
b. Intracavitair
The provision of radiation can be done by:
- After loading
An empty applicator is inserted into the body cavity to
the tumor. After the applicator is located right, enter new
radioisotope into the applicator.
- Installation
Radioisotope solution injected into the body cavity, for example:
pleura or peritoneum.
3. intravenous
Radioisotope solution injected into a vein. For example, I131 is injected IV will be absorbed by the thyroid to treat thyroid cancer.
f.    radiation dose
There are two types of radiation, namely:
1. Curative radiation
Awarded to all levels of disease, except in patients with distant metastases. Target of radiation is the primary tumor, lymph nodes of the neck and supra clavicle. Total radiation dose given was 6600-7000 rad to 200 rad fractions, 5 x delivery per week. After a dose of 4000 rad to the spinal cord in the block and after 5000 rad irradiation supraclavicular field were excluded.
2. Palliative radiation
Given for metastatic tumors in bone and local recurrence. The dose of radiation to bone metastases with 3000 rad 300 rad fractions, 5 x per week. For local recurrence, radiation field is limited to local relapse.
g. radiation response
After the radiation is given, then the evaluation of response to radiation. Assessed the response of cervical lymph node reduction and downsizing of the primary tumor in the nasopharynx. Assessment of radiation response based on WHO criteria:
- Complete Response: remove all the lymph nodes are large.
- Partial Response: downsizing of the lymph nodes to 50% or more.
- No Change: the size of lymph nodes that persist.
- Progressive Disease: size of enlarged lymph nodes of 25% or
more.
h. complications of radiotherapy
Complications of radiotherapy can be:
1. early complications
Usually occur during or several weeks after radiotherapy, such as:
- Xerostomia - Nausea, vomiting
- Mukositis - anorexia
- dermatitis
- Erythema
2. further complication
Usually occurs after 1 year of radiotherapy, such as:
- Contractures
- Impaired growth
- etc.

B. Palliative care
Palliative care is any active measures to ease the burden of cancer patients especially those that can not be cured. Said to be mainly on the unlikely cure because these actions are not only performed on patients who can not be cured but it worked well in patients who still have hope of recovery together - together with the action - the action or curative treatment, with a view to alleviate or eliminate symptoms - symptoms that disrupt or even aggravate the suffering of patients.

Active measures in question are, among others, relieve pain and complaints - other complaints, improvements in aspects of psychology, social and spiritual. All this aims to improve the quality of life is maximized, for patients and families.
The first attention should be given to patients with radiation treatment. Mouth dryness is caused by damage to major or minor salivary glands during irradiation. Not much can be done in addition to advise patients to eat with lots of sauce, bring drinks to go anywhere and try to eat and chew the material so that the sour taste stimulates saliva. Other disorders of the oral cavity is mukositis because mushrooms, stiffness in the neck because fibrotic tissue caused by irradiation, headache, loss of appetite and sometimes vomiting or nausea.

Difficulties arising in the care of patients post-treatment where the tumor remains incomplete (residual) or relapse (residif). Can also arise post-treatment metastatic far as to bone, lung, liver, brain. In the second condition mentioned above is not much action that can be given medical treatment other than simtimatis to improve the quality of life of patients. The patient eventually died of poor general condition, bleeding from the nose and nasopharynx that can not be stopped and the undermining of vital equipment due to tumor metastasis.

Nasopharyngeal Carcinoma (Nasopharyngeal Cancer)

Be carefull if you smoke ciggaret and eat saltfish too much, because they make deadly disease called Nasopharyngeal Carcinoma or Nasopharyngeal Cancer. Today Mbah Dukun Bagong, Indonesian Modern Shaman special author from Medical and Health Information explains about this cancer. wish it is so usefull for us.

DEFINITION

Carcinoma or cancer is a malignant growth of new cells, composed of epithelial cells that tend to infiltrate surrounding tissues and cause metastases.

Nasopharyngeal carcinoma is a malignant tumor arising in the epithelial coating the space behind the nose (nasopharynx).

ETIOLOGY

The link between Epstein-Barr virus and the consumption of salted fish said to be the main cause of this disease. Epstein-Barr virus can enter the body and remain there without causing an abnormality in a long time. To activate this virus requires a mediator. The habit of eating salted fish are constantly starting from childhood, is the main mediator that can activate the virus causing nasopharyngeal carcinoma.

Mediator below are considered influential to the onset of carcinoma

nasopharyngeal namely:

1. Salted fish, preserved foods and nitrosamines.

2. State of low socio-economic, environmental and lifestyle habits.

3. Frequent contact with substances that are considered carcinogens, such as:

- benzopyrenen

- benzoanthracene

- Chemical gases

- Industrial smoke

- Wood smoke

- Some plant extracts

4. Race and ancestry

5. Chronic inflammation of the nasopharynx

6. HLA profile

 Saltfish causes nasopharyngeal carcinoma

HISTOPATHOLOGIC

Microscopically, nasopharyngeal carcinoma can be divided into three forms, namely:

1. ulcerative forms

This form is most often found on the posterior wall and the area around the fossa rosenmulleri. Can also be found on the lateral wall in front of the tube and on the roof eustachius nasopharynx. These lesions are usually accompanied by smaller necrotic tissue and is very easy to conduct infiltration into surrounding tissue. Histopathologic picture is a form of squamous cell carcinoma with good differentiation.

2. nodular / lubuler / proliferative forms

Nodular form or lobuler very often found in the area around the estuary eustachius tube. This type of tumor shaped like grapes or polypoid rarely, found the existence of ulceration, but is sometimes found a small ulceration. Histopathologic picture of carcinoma usually without differentiation.

3. exophytic forms

exophytic forms usually grow on one side of the nasopharynx, found no presence of ulceration, stemmed and sometimes slippery surface. This type of tumor usually grows from the roof of the nasopharynx and can fill the entire cavity of the nasopharynx. These tumors can encourage the palate mole down and coana grow toward and into the nasal cavity. Histopathologic picture is a limphosarcoma

Nasopharyngeal Cancer

Nasopharyngeal Carcinoma

Nasopharyngeal Cancer

Classification of histopathologic picture of Nasopharyngeal cancer recommended by the Organization

World Health Organization (WHO) before the year 1991, divided into three types, namely:

1. Keratinizing Squamous Cell Carcinoma.

This type of differentiation can be subdivided into good, moderate and bad.

2. Non-keratinizing carcinoma.

In this type of differentiation is found, but no cell differentiation

Squamous intersel without bridges. In general, the cell boundary is quite clear.

3. Undifferentiated carcinoma.

In this type of individual tumor cells showed a vesicular nucleus,

oval or round with a clear nukleoli. Generally, the cell boundaries are not clearly visible.

Types without differentiation and without keratinization typically have the same are radiosensitive. While the type with keratinization is not so radiosensitive.

Histopathological picture of the latest classification recommended by WHO

in 1991, just divided into two types, namely:

1. Keratinizing Squamous Cell Carcinoma.

2. Non-keratinizing carcinoma.

This type can be subdivided into differentiated and not differentiated.

SYMPTOMS AND SIGNS 

Epistaxis

The main symptoms are:

1. Nasal sign:

· Colds that do not heal

· Epistaxis. Blood discharge is usually over and over again, few in number and often mixed with mucus, so it appears pink · Snot may like pus, watery or thick and smelly.

2. Ear sign:

· Tinnitus. Suppress tumor eustachii estuary causing tubal tubal occlusion, because the tube eustachii estuary, close to the fossa rosenmulleri. The pressure in the tympanic cavity is lowered, resulting in tinnitus.

· Conductive hearing loss

· Discomfort in the ear until the ear pain (otalgia).

3. Eye sign:

· Diplopia. Tumor crept laseratum foramen and cause disruption N. IV and N. VI. When exposed Chiasma optic would cause blindness.

4. Tumour sign:

Enlarged neck glands lymphoid · this is the spread or metastases near the lymphogen of nasopharyngeal carcinoma.

5. cranial sign

Cranial symptoms occur when the tumor has spread to the brain and is felt in people. These symptoms include:

· Constant headaches, pain is a metastasis in

haematogenous.

· Sensitibilitas of Regional cheeks and nose reduced.

· Difficulty on swallowing

· Aphonia

· Syndrome or syndrome reptroparotidean jugular Jackson on N. IX, N. X,

N. XI, N. XII. With signs of paralysis on:

o tongue

o palate

o Pharynx or larynx

o M. sternocleidomastoideus

o M. trapezeus

PATHOGENESIS and PATHOPHYSIOLOGY

1) Epstein-Barr Virus

Epstein-Barr virus replicate in epithelial cells and becomes latent in B lymphocytes Epstein-Barr virus infection occurs in two main places of salivary gland epithelial cells and lymphocytes. EBV infection of B lymphocytes initiate by binding to virus receptors, namely the complement component C3d (CD21 or CR2). Glycoprotein (gp350/220) to the capsule EBV binds to the CD21 protein on the surface of lymphocytes B3.

This activity is a series of chain starting from the entry of EBV into B lymphocytes and subsequent DNA causes B lymphocytes to be immortal. In the meantime, until now the mechanism of EBV entry into nasopharyngeal epithelial cells can not be explained with certainty. However, there are two receptors are thought to play a role in entry of EBV into epithelial cells of the nasopharynx and PIGR CR2 (Polimeric Immunogloblin Receptor). Cells infected by Epstein-Barr virus can cause several possibilities, namely: cell to die when infected with Epstein-Barr virus and virus replication conduct, or Epstein-Barr virus that can lead to cell death meninfeksi virus so that the cells return to normal or transformation can occur namely cell interactions between cells and viruses that result in changes in properties of the cell resulting in cell transformation into malignant cancer cells forming.

EBV genes expressed in patients with Nasopharyngeal Carcinoma is a latent gene, namely Ebers, EBNA1, LMP1, LMP2A and LMP2B. EBNA1 protein plays a role in maintaining the virus in latent infection. Transmembrane protein LMP2A and LMP2B inhibits tyrosine kinase signaling that is believed to inhibit viral lytic cycle. Among those genes, genes that were most responsible for cell transformation is the LMP1 gene. structure

LMP1 protein consists of 368 amino acids that is divided into 20 amino acids at the N terminus, six transmembrane protein segments (166 amino acids) and 200 amino acids at the carboxy end (C). LMP1 transmembrane protein mediates the signal for TNF (tumor necrosis factor) and improve the regulatory cytokine IL-10 which memproliferasi B cells and inhibit the local immune response.

2) Genetic

Although nasopharyngeal carcinoma tumor does not include genetic, but susceptibility to nasopharyngeal carcinoma in a particular community group has a relatively prominent and familial aggregation. Correlation analysis showed HLA (human leukocyte antigen) and cytochrome P450 enzyme gene pengode 2E1 (CYP2E1) is the possibility of gene susceptibility to nasopharyngeal carcinoma. Cytochrome P450 2E1 is responsible for metabolic activation of nitrosamines and related carcinogens.

3) Environmental factors

A large number of case studies conducted in populations residing in different regions in asia and north america, has confirmed that the fish sauce and other foods that contain large amounts of preserved nitrosodimethyamine (NDMA), Nitrospurrolidene (NPYR) and nitrospiperidine (NPIP), which may be a factor carcinogenic nasopharyngeal carcinoma. Also smoking and exposure to secondhand smoke who smoke cigarettes that contain formaldehyde and wood dust tepapar recognized risk factors for nasopharyngeal carcinoma by means of reactivating EBV infection.

DIFFERENTIAL DIAGNOSIS

1. adenoid hyperplasia

Usually found in children, rare in adults, in children

hyperplasia occurs Because repeated infections. On the plain will be seen a mass of soft tissue on the upper side of the nasopharynx generally demarcated and generally symmetrical and surrounding structures did not appear the signs look bleak infiltration in carcinoma.

2. Angiofibroma juenilis

Usually found in relatively young age with symptoms resembling nasopharyngeal carcinoma. The tumor is rich in blood vessels and the bias is not infiltrative. On the plain will get a mass on the roof nasofairng demarcated. The process can be extended seperrti on the spread of carcinoma, although rarely cause bone destruction

erosion simply because tumor suppression. Usually there is bending toward the front of the rear wall of the maxillary sinus is known as the antral sign. Because these tumors are rich in the vascular external carotid arteriography is necessary because the picture is very characteristic. Sometimes it is also hard to distinguish angiofibroma juvenils with nasal polyps on the plain.

3. Sinus tumors sphenooidalis

Primary malignant tumors sphenoidalis sinus is extremely rare and usually the tumor had reached somewhat advanced stage when the patient came to the first examination.

4. neurofibroma

Group of these tumors often arise in the lateral pharyngeal space that resembles a malignancy in the lateral wall of the nasopharynx. the C.T. Scan, pendesakan space medially toward the pharynx can help distinguish this group of tumors with nasopharyngeal carcinoma.

5.  parotid gland tumor

Parotid gland tumors, especially those from the lobe that lies somewhat in the space of the pharynx and protruding towards the lumen of the nasopharynx. in most cases seen pendesakan parafaring space medial direction that appears on CT scan examination.

6. Chordoma

Although Chordoma is a major sign of bone destruction, but in view of nasopharyngeal carcinoma

too often cause bone destruction, it is often made ​​it difficult to

membedakanya. With a plain, visible calcification or destruction, especially in the clivus region. CT can help to see if there is enlargement of the upper cervical glands because Chordoma typically do not pay attention to an abnormality in the gland, while nasopharyngeal carcinoma frequently metastasize to lymph nodes.

7. Menigioma cranial base

Although these tumors are somewhat rare, but the picture is sometimes resemble

nasopharyngeal carcinoma with sclerotic signs in the area of ​​the cranial base. CT picture of meningioma is quite characteristic that is a bit hyperdense before injecting a contrast agent and will

become very hyperdense after administration of intravenous contrast agent. Arteriography examination also greatly aid in the diagnosis of this tumor.

STADIUM

Most recent staging based on an agreement between the UICC (Union

Internationale Contre Cancer) in 1992 are as follows:

T = Tumor, describes the state of the primary tumor, large and expansion.

T0: No visible tumor

T1: Tumor limited to one location in the nasopharynx

T2: Tumor extends more than one location, but still inside the cavity of the nasopharynx

T3: Tumor extends into the nasal cavity and / or oropharynx

T4: Tumor extends to the skull and / have about the brain's nerve

N = nodule, described the state of regional lymph nodes

N0: No enlargement of the gland

N1: There homolateral gland enlargement can still be driven

N2: There is enlargement of the gland contralateral / bilateral still be driven

N3: There is enlargement of both glands homolateral, contralateral or bilateral, which already

attached to the surrounding tissue.

M = metastases, distant metastases describe

M0: No distant metastasis

M1: There is distant metastasis.

Based on the above TNM, stage of disease can be determined:

Stage I: T1 N0 M0

Stage II: T2 N0 M0

Stage III: T3 N0 M0

T1, T2, T3 N1 M0

Stage IV: T4 N0, N1 M0

Any T N2, N3 M0

Any T Any N M12

According to the American Joint Cancer Committee in 1988, staging of tumors

nasopharynx are classified as follows:

Tis: Carcinoma in situ

T1: The tumor is found on one side of the nasopharynx or tumor that can not be seen, but

can only be known from the biopsy results.

T2: The tumor that attacks the two places, the wall of the postero-superior and lateral walls.

T3: tumor extension up into the nasal cavity or oropharynx.

T4: The tumor that spread to invade the skull or cranial nerves (or both).

PROGNOSIS

Overall, the 5-year survival rate was 45%. Prognosis is worsened by

several factors, such as:

· Stadium further.

Age of more than 40 years

· Men than women

· China than in whites

The enlargement of the gland neck ·

· Existence of damage to brain nerve palsy skull

· Presence of distant metastases

COMPLICATIONS

1. Petrosphenoid syndrome

The tumor grows upward into the base of the skull through the foramen laserum until sinus

cavernosal nerves pressing N. III, N. IV, N. VI also suppress N.II. which gives abnormalities:

· Trigeminal neuralgia (N. V): Trigeminal neuralgia is a pain in the

sesisi face marked with flavors such as exposed electrical flow is limited

on the distribution of the trigeminal nerve.

· Ptosis palpebra (N. III)

· Ophthalmoplegia (N. III, IV N., N. VI)

2. Retroparidean syndrome

The tumor grows forward toward the nasal cavity can then infiltrate into the surrounding. Tumor to the side and back toward the area where there retropharing parapharing and lymph nodes. The tumor is pressing against a nerve N. IX, N. X, N.

XI, N. XII with the manifestation of symptoms:

· N. IX: difficulty swallowing because of hemiparesis and the superior constrictor muscle

Taste disturbance at the rear third of the tongue

· N. X: hyper / hipoanestesi moles palate mucosa, pharynx and larynx with

respiratory disorders and salivary

° N XI: paralysis / atrophy bibs trapezius, SCM muscles as well as the palate hemiparese

mole

· N. XII: hemiparalisis and atrophy of the tongue side.

· Horner's syndrome: paralysis of the N. simpaticus servicalis, a narrowing of the fissure palpebralis, onoftalmus and miosis.

3. Cancer cells can contribute to flow with the lymph nodes or blood, the organ that is located far from the nasopharynx. That often is the bones, liver and lungs. This is the end result and a poor prognosis. In another study found that nasopharyngeal carcinoma metastases can hold a lot, to lung and bone,

20% respectively, whereas the liver 10%, 4% of the brain, kidney 0.4%, 0.4% for the thyroid.

Chronic Supurative Otitis Media (CSOM)

3 days ago Mbah Dukun posted about Ear disease, Acute Otitis Media. Today, Mbah Dukun posts about complication of Acute Otitis Media. Yes from the title all of you know what Mbah Dukun means, Chronic Supurative Otitis Media. Is it dangerous? find the answer below.

1. Definition

2. Classification

3. Etiology

4. Pathology

5. Clinical manifestations

6. Management (treatment and therapy)

7. Complications

DEFINITION

CSOM is chronic inflammation of the middle ear cavum, mastoid and tympanic membrane is intact (perforated) also found an intermittent purulent secretions (othorea).  Secretions may be watery or thick, clear or in the form of pus and lasted more than 2 months. 

.

CLASSIFICATION

CSOM can be divided into two types :

1.  Tubotympany = benign type = rhinogen safe.

Tubotympany characterized by the presence of a central perforation or pars Tens and clinical symptoms that vary depends on wide and severity of disease.  Clinically divided into:

a.  active

In this type, there are secretions of the ear and deafness.  Usually preceded by the expansion of the upper respiratory tract infections through the eustachius tube or after swimming where germs enter through the outer ear canal.  Secretions varied from mucoid to mucopurulent.

b.  not active

From examination the ear found total dry perforation with middle ear mucosa is pale.  Symptoms encountered a mild conductive deafness.  Other symptoms are encountered, such as vertigo, tinnitus, or a feeling of fullness in the ear.

2.  Type aticoantral = wild type = danger =  bone type

In this type were found Cholesteatoma and dangerous.  Aticoantral type is more often about flaccida pars and the trademark is the formation of retraction pockets, which is where the accumulation of keratin to produce Cholesteatoma.

Cholesteatoma can be divided

above two types, namely:

a.  Congenital

b.  Obtained.

In general, there Cholesteatoma in chronic otitis media with perforation marginal, but some are located in the pars flaccida (Attic retraction cholesteatom).

ETIOLOGY

CSOM occurs almost always starts with recurrent otitis media in children, rarely in the adult.  Infection factor usually comes from the nasopharynx (adenoiditis, tonsillitis, rhinitis, sinusitis), reaching the middle ear through the tube of Eustachius.  Eustachius tube abnormal function are predisposing factors which found in children with cleft palate and Down's syndrome.  Presence of tubal pathology, causing reflux of contents nasopharynx which is a factor of the high incidence of CSOM in the United States.  Humoral abnormalities (such as hipogammaglobulinemia) and cell-mediated (such as HIV infection) can manifest as chronic ear secretion.

Causes of CSOM among others:

1.  Environment

2.  Genetic

3.  history of otitis media.

4.  Infection

5.  Upper respiratory tract infection

6.  Autoimmune

7.  Allergy

8.  Eustachius tube disfunction.

Some of the factors that cause persistent tympanic membrane perforation in CSOM:

• Infections that persist in the middle ear mastoid resulting in the production of purulent ear discharge persists.

• The continued obstruction Eustachius tube which reduces the spontaneous closure of the perforation.

• Several large perforations suffered through the mechanism of spontaneous closure of epithelial migration.

• At the edge of the perforation of squamous epithelium can experience rapid growth over the medial side of the tympanic membrane.  This process also prevents the spontaneous closure of the perforation.

Factors that cause middle ear infections become chronic suppurative compound, among others:

1.  Eustachius tube dysfunctions chronic or recurrent.

a.  Nose and throat infections are chronic or recurrent.

b.  Partial or total anatomic obstruction tube Eustachius

2.  Persistent tympanic membrane perforation.

3.  The occurrence of squamous metaplasia or other permanent pathological changes in the middle ear.

4.  Persistent obstruction of the aeration of the ear or mastoid cavity.

5.  There are areas with sekuester or persistent osteomyelitis in the mastoid.

6.  Basic constitutional factors such as allergies, general weakness or changes in the body's defense mechanisms.

Pathogenesis

CSOM Patogensis not yet fully known, but in this case is the chronic stage of acute otitis media (OMA) with a perforation that has been formed, followed by the release of secretions that keep menerus1.  OMA perforation can occur secondary to chronic uneventful middle ear infection in eg dry perforations.  Some authors claim this as an inactive state of chronic otitis media.

PATHOLOGY

CSOM is more often a recurrent disease.  This chronic condition is more time-based rather than pathology, and staging.  In general, the picture found is:

1.  There is a perforated tympanic membrane in the central part.

2.  Mucosa varies according to disease stage

3.  The bones of hearing can be damaged or not, depending on the severity of infection

previously.

4.  Mastoid pneumatization

CSOM most often in childhood.  Most recent mastoid pneumatization occurs between 5-10 years.  When chronic infection persists, the mastoid had sclerotic process, thereby shrinking the size of the mastoid processes.

CLINICAL MANIFESTASIONS

1.  Discharge Ear (Otorrhoe)

Purulent or mucoid secretions is dependent stage of inflammation.  In CSOM benign type, the liquid that comes out muco pus that do not stink, often as a reaction to irritation of the mucosa of the middle ear by the tympanic membrane perforation and infection.

The exit discharge is usually intermittent.  In the inactive stage CSOM not found adannya ear secretions.  In CSOM wild type, element and mucoid middle ear secretions reduced or lost due to widespread destruction of the mucosal lining.  Secretions are mixed with blood-related presence of granulation tissue and ear polyps and a sign of Cholesteatoma.  If secretions are watery watery without the possibility of tuberculosis leads to pain.

2.  Hearing Loss

Conductive deafness is usually encountered but can also be mixed.  Severity of deafness depends on the magnitude and location of tympanic membrane perforation and mobility sound delivery system into the middle ear.  In CSOM malignant type, usually obtained severe conductive deafness.

3.  Otalgia (Ear Pain)

In CSOM, complaints of pain caused dammed pus drainage.  Pain may mean the threat of complications due to drainage constraints secretions, exposure durameter or lateral sinus wall, or the threat of brain abscess formation.  Pain is a sign of developing complications such as Petrositis CSOM, subperiosteal abscess or lateral sinus thrombosis.

4.  Vertigo

vertigo often appears, is a sign of labyrinthine fistula caused by the occurrence of erosion of the walls of the maze by Cholesteatoma.  Vertigo that arises usually due to a sudden change in air pressure or the sensitive patient.  vertigo can occur simply because a large perforation of tympanic membrane, causing a maze more easily aroused by the temperature difference.  The spread of infection into the labyrinth will also be led to complaints of vertigo.  Vertigo can also occur from complications of the cerebellum.

CLINICAL SIGNS

Clinical signs of malignant type CSOM

1.  Presence of abscess or fistula retroauricular

2.  Granulation tissue or polyps in the ear canal from the tympanic cavity.

3.  Pus is always active or foul smelling (smell Cholesteatoma)

4.  X-ray mastoid Cholesteatoma the picture.

CLINICAL EXAMINATION

To complete the examination, clinical examination can be performed as

follows:

Audiometric examination

In patients with CSOM audiometric examination is usually found to conductive deafness.  But it can also be found there sensorineural deaf, deafness severity depending on the size and location of the tympanic membrane perforation as well as the integrity and mobility

The degree of hearing loss threshold of hearing

Normal: -10 dB to 26 dB

Mild : 27 dB to 40 dB

Moderate: 41 dB to 55 dB

Moderat to Severe: 56 dB to 70 dB

Severe: 71 dB to 90 dB

Total deafness: more than 90 dB.

To evaluate, the following observations :

1.  Perforation usually cause deafness conductive generally no more than 15-20 dB

2.  Damage to the bones of the circuit causing deafness conductive hearing loss 30-50 dB when accompanied by perforation.

3.  Discontinuity of bone behind of intact tympanic membrane causing conductive deafness 55-65 dB.

4.  Weaknesses and low discrimination speech, no matter what the conductive of bone, showed severe damage cochlea.

Radiological examination.

1.  Projection Schuller

Shows the extent of mastoid pneumatization of the lateral direction and over.  This photo is useful for surgery because it shows the position of the lateral sinus and the tegmen.

2.  Projection Mayer or Owen,

Taken from the middle ear and anterior direction.  Will look picture the bones of hearing and tweaking so it can be known whether the bone damage has on structures.

3.  Projection Stenver

Shows a picture along the petrosal pyramid and more clearly shows the internal auditory canal, vestibule and semicircular canals.  These projections put the antrum in cross section so as to show the existence of enlargement.

4.  Projection Chause III

Give an especial longitudinally so that it can show early damage to the lateral wall of tweaking.  Politomografi and or CT scans can depict bone damage because Cholesteatoma.

Bacteriology

Bacteria are often found in CSOM are Pseudomonas aeruginosa, Staphylococcal aureus and Proteus.  While the OMSA streptococcus bacteria pneumonie, H.  influenza, and Morexella kataralis.  Other bacteria found in CSOM E.  Coli, Difteroid, Klebsiella, and anaerobes are Bacteriodes sp.

1.  Specific bacteria

Eg Tuberculosis.  Otitis tuberculosis is very rare (less than 1%).  In adults is usually caused by advanced lung infection.  These infections enter the middle ear through the tube.  Tuberculous otitis media can occur in children who are relatively healthy as a result of drinking milk that is not pasteurized

2.  Non-specific bacteria both aerobic and anaerobic.

Aerobic bacteria are often met by Pseudomonas aeruginosa, Staphylococcus aureus and Proteus sp.  Antibiotics are sensitive to ceftazidime and Pseudomonas aeruginosa is ciproflokxacin, and is resistant to penicillins, cephalosporins and macrolides.  While Proteus mirabilis sensitive to antibiotics except for macrolides.  Staphylococcus aureus resistant to sulphonamides and trimethoprim and sensitive to cephalosporin generations I and gentamicin

MANAGEMENT

The principle of treatment depends on the type and extent of infectious diseases, where treatment can be divided into:

1.  Conservative

2.  Surgery

CSOM benign INACTIVE

This situation does not require treatment, and advised not to scrape the ears, the water should not enter the ear during bathing, swimming is prohibited and immediately seek treatment when suffering from upper respiratory tract infection.  If the facility allows reconstruction surgery should be performed (miringoplasty, tympanoplasty) to prevent recurrent infections and hearing loss.

CSOM benign ACTIVE

The principle of treatment of CSOM is:

1. Clean ear canal and tympanic cavity.

2. antibiotics:

- Topical antibiotics (antimicrobial)

- Systemic.

Topical antibiotics

Antibiotics topically in the ear and a lot of secretions without cleaning first, is not effective.  If the discharge is reduced / no longer progressive but given

drops containing antibiotics and topical drug delivery kortikosteroid.4 Given meant to go to the middle ear, it is not recommended that antibiotics such as neomycin and duration ototoxic not more than 1 week.  How to best selection of antibiotics based on culture, and resistency test.

Ear powder used as:

a.  Acidum boricum with or without iodine

b.  Terramycin.

c.  Asidum borikum chloromicetin 2.5 grams mixed with 250 mg

Topical antibiotic treatment can be widely used for active CSOM combined with ear cleaning.  Topical antibiotics that can be used in chronic otitis media is:

1.  Polymyxin B or polymyxin E

These drugs are bacterisid against gram-negative bacteria, Pseudomonas, E.

Koli Klebeilla, Enterobakter, but the resistant gram-positive, Proteus, B.  fragilis Toxic to kidneys and nervous system.

2.  Neomycin

bactericid drugs on gram-positive and negative, for example: Staphylococcal aureus, Proteus sp.  Resistant to all anaerobes and Pseudomonas.  Toxic to the kidneys and ears.

3.  Chloramphenicol

These drugs are bactericid

Systemic antibiotics

Antibiotics are not more than 1 week and must be accompanied cleaning profus secretions.  In the event of treatment failure, keep in mind that there are reasons of failure in these patients.  Antimicrobials can be divided into 2 groups.  The first class of power killed him dependent measure.  The higher levels of the drug, the more germs were killed, for example with the quinolone class of aminoglycosides.

The second category is a particular concentration of antimicrobial that killed her best resources.  Elevation does not increase the dose of killing power of this class of antimicrobials, such as beta-lactam class.

Systemic antibiotic therapy is recommended in chronic otitis media is.

Pseudomonas: Aminoglycosides ± carbenicillin

P.  mirabilis: Ampicillin or cephalosporin

P.  morganii, P.  vulgaris: Aminoglycosides ± carbenicillin

Klebsiella: Cephalosporin or aminoglycosides

E.  coli: Ampicillin or cephalosporin

S.  Anti-stafilikokus aureus: penicillin, cephalosporin, erythromycin, aminoglycosides

Streptococci: Penicillin, cephalosporin, erythromycin, aminoglycosides

B.  fragilis: clindamycin

Class of quinolone antibiotics (ciprofloxacin and ofloxacin) are able to nalidixic acid derivate that has anti-pseudomonal activity and can be administered orally.  But it is not recommended for children under the age of 16 years.  Cephalosporin Group III generation (cefotaxime, and ceftriaxone seftazidinm) are also active against Pseudomonas, but must be administered parenterally.  This therapy is very good for the OMA, while for CSOM is uncertain enough, although it can cope with CSOM.  Have the effect of metronidazole for anaerobic bactericid.  According to Browsing et al metronidazole can be given with and without antibiotics (cephalexin and cotrimoxazol) on active CSOM, a dose of 400 mg per 8 hours for 2 weeks or 200 mg per 8 hours for 2-4 weeks.

Malignant CSOM

Treatment for Malignant CSOM is surgery.  Conservative medical treatment is only a temporary treatment before surgery.  If there is a subperiosteal abscess, the abscess incision should be done separately before then performed mastoidektomy.

There are several types of surgery or surgery techniques that can be done in CSOM with chronic mastoiditis, either benign or malignant type, among others:

1.Mastoidektomy simple (simple mastoidectomy)

2. radical Matoidectomy

3.radical with modifications mastoidectomy

4.Miringoplasty

5.Timpanoplasty

6. Combined approach tympanoplasty)

The goal is to stop operating permanently infection, tympanic membrane perforation repair, prevent complications or more severe hearing damage, and improve hearing.

COMPLICATIONS

Tendency of complications of otitis media gets depends on the pathological abnormalities that cause otorrhoea.  Nevertheless resistant organisms and lack of effective treatment, would lead to complications.  usually obtained in patients with CSOM complications malignant type, but an acute otitis media or an acute exacerbation by a virulent bacteria in CSOM benign type can cause complications.

Serious intra-cranial complications more often seen in acute exacerbation of CSOM associated with Cholesteatoma.

A.  Complications of middle ear:

1.  Persistent tympanic membrane perforation

2.  Erosion of bone loss

3.  Facial nerve paralysis

B.  Ear complications in

1.  Labyrinth fistula

2.  Labyrinitis suppurative

3.  Nerve deafness (sensorineural)

C.  Complications of Extradural

1.  Extradural abscess

2.  Lateral sinus thrombosis

3.  Petrositis

D.  Complications to the central nervous system

1.  Meningitis

2.  Brain abscess

3.  Hindrocephalus otitis

Complication of middle ear infections trip to the intra-cranial must pass through three kinds of trajectories:

1.  From the middle ear cavity to the brain membrane

2.  Penetrate the lining of the brain.

3.  brain expansion.

ACUTE OTITIS MEDIA

Today Mbah Dukun share information about kind of ear disease. what is that, mbah? it's called ACUTE OTITIS MEDIA. maybe you've never heard about this disease, but you might have it before. Okey mbah dukun start to explain. Just click options below

 1. DEFINITION

2. ETIOLOGY 

3. PATHOGENESIS

4. DIAGNOSIS

5. TREATMENT AND THERAPY

6. COMPLICATIONS

DEFINITION
 Acute otitis media is an inflammation of the mucosa of the middle ear cavity, eustachius tube, and aditus ad antrum caused by bacterial or viral infection with clinical symptoms of ear pain, fever, and even hearing loss, tinnitus and vertigo.  generally takes place within 3-6 weeks.


Etiology
The main cause of acute otitis media (AOM) is the invasion of pyogenic bacteria into the middle ear in a state that is normally sterile.  Common bacterial causes of AOM include hemolytic streptococcus, Staphylococcal aureus, Pnemococcus.  In addition, occasionally found also Haemofilus influenza, Escherichia coli, Streptococcus anhemolitikus, Proteus vulgaris and Pseudomonas aurogenosa.  Haemofilus influenza is often found in children aged under 5 years old.  Upper respiratory tract infections are recurrent and tubal dysfunction eustachii also be the cause of the AOM in children and adults.

Incidence
Acute otitis media most commonly suffered by children ages 3 months-3 years.  But not infrequently also the adults.  Children are more often exposed to AOM due to several things, including:
1.  Child's immune system is not perfect
2.  Tuba eusthacius children are shorter, wider and lies horizontally
3.  Adenoid children relatively larger and situated adjacent to the mouth of the fallopian tubes so that disrupt the opening of the eustachii tube eusthachii.  Adenoids are easy to track the spread of infected bacteria and viruses into the middle ear.

Pathogenesis
AOM trigger factors can be initiated by the occurrence of upper respiratory tract infection accompanied by the repeated disruption of the body by the cilia of the tubal mucosa eusthachii, enzymes and antibodies that cause negative pressure resulting in bacterial invasion of the mucosa of the nasopharynx into the middle ear through the eustachii tube and settled in  in the middle ear becomes acute otitis media.

There are 5 stages of acute otitis media (AOM) based on changes in middle ear mucosa, namely:
1.  tubal occlusion Stadium
Marked with a picture of the tympanic membrane retraction due to negative middle ear pressure.  Sometimes the tympanic membrane appears normal or pale cloudy color.  Effusions may have occurred but difficult to detect.

2.  Hiperemia Stadium

 


Dilated blood vessels that appear in some or all of the tympanic membrane accompanied by edema.  Secretions are beginning to form serous exudate is still so difficult to assess.




3.  Suppuration Stadium

 
Severe edema of the mucosa of the middle ear accompanied by the destruction of superficial epithelial cells and the formation of purulent exudate in the tympanic cavity causing the tympanic membrane protruding toward the outer ear canal (bulging).  Clinical symptoms, the patient seems to ache, pulse, fever, and pain in the ear intensified.  In the circumstances further, ischemia can occur due to the pressure of growing purulent exudate, thrombophlebitis in the veins of small even to necrosis of the mucosa and submucosa.


4.  Perforation Stadium
Rupture of the tympanic membrane so that the pus out of the middle ear into the outer ear canal.  Sometimes the secret expenditures are pulsation.  This stage is often caused by late delivery of antibiotics and the high virulence of germs.







5.  Resolution Stadium
Characterized by a gradual normal tympanic membrane perforation of the tympanic membrane to close the back and no purulent secretions.  This occurs if the tympanic membrane was intact, good endurance and low-virulence bacteria.

DIAGNOSIS
Diagnosis AOM should meet the following 3 things:
1.  sudden onset (acute)
2.  The discovery of signs of effusion (effusion: fluid collection in a body cavity) in the middle ear.  Effusions evidenced by observing the following signs:
a.  Deployment tympanic membrane
b.  Limited / lack of movement of the tympanic membrane
c.  The existence of the shadow of fluid behind the tympanic membrane
d.  Discharge from the ear
3.  Signs / symptoms of inflammation of the middle ear as evidenced by the presence of either one of the following signs:
a.  Redness of the tympanic membrane
b.  Ear pain that interferes with sleep and normal activity
Children with AOM may experience ear pain, discharge from the ear, decreased hearing, fever, difficulty eating, nausea and vomiting and cranky.  However these symptoms are not specific to that diagnosis AOM AOM can not be based on history alone.  Middle ear effusions examined with otoscope to see clearly the situation in the tympanic membrane / tympanic membrane is bulging, erythema and even yellow and dingy and the presence of yellowish fluid in the ear canal.  If confirmation is required, generally performed with a pneumatic otoscope (an instrument used to see the tympanic membrane which is equipped with a small air pump to assess tympanic membrane response to changes in air pressure).  Movement of the tympanic membrane is less visible with this examination.  This examination can be used as additional tests to confirm the diagnosis of AOM.  But generally AOM can already be enforced by ordinary otoscope examination.  Middle ear effusions can also be proved by tympanosyntesis (stabbing of the tympanic membrane).  But this examination is not performed on any child.  Among other indications of the need tympanosyntesis AOM in infants younger than 6 weeks with a history of intensive care in hospital, children with immune disorders, children who are not members of the response to some antibiotics or with very severe symptoms and complications.

TREATMENT of  ACUTE OTITIS MEDIA
1.  Antibiotics
AOM is generally a disease that will heal by itself. About 80% of AOM cured in 3 days without antibiotics.  Use of antibiotics does not reduce complications, including decreased hearing.
If symptoms do not improve within 48-72 hours or there is worsening of symptoms, antibiotic given.  American Academy of Pediatrics (APP) which categorize AOM observable and should be treated with antibiotics as following;
a. <6 months of Antibiotics
b. 6 months - 2 years of Antibiotics
c. > 2 years of antibiotics if symptoms are severe. if symptoms are mild, do observations

Mild Symptoms if mild ear pain and fever <39 C in 24 last hour.  While the severe symptoms are moderate to severe ear pain or fever 39 C.
Options observation for 48-72 hours can only be performed on children age 6 months-2 years with mild symptoms during the examination or diagnosis of doubtful in children over 2 years.  Analgesia should still be given during the observation.
The first choice of antibiotics in AOM is amoxycilin. American Academy of Family Physicians (AAFP) recommends dosing 40mg/kgweight/daystandards in children with low risk (age> 2tahun, not in intensive care, had not received antibiotic treatment within 3 last month).  While high doses administered 80mg/kgweight/day in children with high risk (age <2 years, in treatment, there is a history antibiotics in the last 3 months and are resistant to giving amoxycilin low dose).  Meanwhile, The Centre for Disease Control and Prevention (CDC) recommends antibiotic therapy on the AOM as follows:

CONDITIONS OF TREATMENT
Otitis media with bulging tympanic membrane  High-dose amoxycilin (80 - 100mg/kgweight/day per oral) for 7 days
Otitis media without bulging tympanic membrane  Delays antibiotics, (Spontaneously cured)
recurrent otitis media  delays antibiotics, used influenza vaccine
Otitis media bacterial resistance e.c against high-dose amoxycilin  High-dose clavulanate amoxycilin (80-90 mg / kg / day orally for 7 days), cefuroxime axetil (30 mg / kg 2 times / day orally); ceftriaxone (IM 50mg/kgweight/day during 3 days)

Delays antibiotics and antibiotic treatment settings performed to otitis media without bulging because, generally, it recover spontaneously without antibiotic treatment. Setting prescribing can be done by administering acetaminophen in case of otalgia and fever, and if after giving it, a fever still on going and no improvement of clinical symptoms for 3 days, so amoxycilin just given in high doses.  Antibiotics in the AOM will produce symptAOMtic improvement in 48-72 hours.  In the first 24 hours occurred stabilization, while the 24 second hours began repairs.  If the patient does not improve in 3 days or re-emerged in 14 days there may be other diseases or treatment provided is not adequate / inadequate or has even happened bacterial resistance to antibiotics. If the patient is allergic to alternative antibiotics Penicilin class used were cefuroxime axetil, ceftriaxone injection (2-3x50mg/kgweight/day) or second-generation cephalosporins such as cefdinir, cefpodoxime or cefuroxime. Another option is a class of macrolides such as azithromycin and clarithromicyn.
2.  Analgesia / pain relief
Besides antibiotics, treatment should be accompanied AOM pain relievers. Analgesia is commonly used is simple analgesia such as paracetamol or ibuprofen.  However, it should be noted that the use of ibuprofen should be ensured that the children do not have indigestion Since the granting of ibuprofen can aggravate the situation.

COMPLICATIONS
Acute otitis media is not treated promptly with antibiotics can be continued become chronic otitis media (COM) and mastoiditis.  Another complication that can periosteal abscess occurs as up to meningitis and brain abscess even can also result in permanent hearing loss due to rupture tympanic membrane and if it has to disrupt auditory function will also cause problems in speech and language in children.

Laryngeal Papilloma

Inul Daratista, dangdut singer, came to Mbah Dukun,s house. She complained to mbah dukun about her voice. use laryngoscope direct methode, mbah dukun found something in Inul's laryng. what is that? it called Laryngeal Papilloma. Do you wanna know about Laryngeal Papilloma? just click options below.

1. Definition
2. Etiology
3. Histopatology
4. Clinical manifestations
5. Diagnose
6. Therapy and treatment (management)
7. Complications
 





definition
Laryngeal papilloma is a benign proliferative squamous epithelial cell larynx which most often found. Papillomavirus is the type of tumor that develops rapidly, although not malignant. These tumors can migrate to the oral cavity, nose, trachea and lungs, but the most common location is larynx.



There are two types of laryngeal papillomas: one is the laryngeal papilloma juvenilis usually multiple and tend to be aggressive. The other is a solitary senile larynx papilloma and less aggressive but can develop into malignant.

etiology
The cause of laryngeal papilloma is a " human papilloma virus ' ( HPV ) types 6.11 which infect epithelial cells. It is estimated that the spread of the disease is present at birth from mothers exposed by " genital warts ".
In the normal mucosa cells adjacent to the papilloma, also contain viral DNA that can be activated recurrent lesions. Papilloma in children is more often multiple and recur than adults. While the papilloma in adults is usually single but it tends to become malignant with a specific subtype found that HPV 16.

histopathology
Macroscopic : eksofitik lesions, such as cauliflower, gray or red and bleed easily. This type of lesion is aggressive and easily relapse, but may disappear  spontaneously.
Microscopic: showing a group of connective tissue stroma and blood vessels such as the fingers are coated with a layer of squamous epithelial cells or parakeratotik keratotic surface. Sometimes a picture appeared that bermitosis cells.

clinical manifestations
Initial symptoms are the form of hoarse voice phonation disorders, disfoni even afoni. If the papilloma is large enough can cause respiratory problems such as cough, shortness, and stridor inspiration. In children, the bias occurs misdiagnosis, because often show symptoms of hoarseness, stridor, and respiratory distress after failed treatment of severe asthma or bronchitis.

diagnosis
anamnesis:
Found symptoms of hoarseness until afoni arise even respiratory distress. At the sound of crying children can appear abnormal. Found also a history of progressive hoarseness changes slowly, especially in patients who have a history of the parents had suffered Condyloma akuminata.
physical examination
Usually there is stridor on inspiration and direct laryngoscopy examination of the tumor that resembles the picture looks cauliflower, red, brittle, and bleed easily

Differential Diagnoses
1. Vocal cord polyp.
2. Vocal cord cyst.
3. Vocal cord nodules
4. bronchial asthma
5. bronchitis
6. laryngomalaise

Management
Laryngeal papilloma therapeutic goal is to maintain the airway, maintaining voice quality and eliminates the mass of papilloma and prevent recurrence.
a. Surgery
Some techniques used include: tracheostomy, laryngofissure, microlaryngoscope and extirpation by forceps, microcauter, microlaryngoscope with diathermy or ultrasound, cryosurgery, CO2 surgical laser.
b. medical
Drugs used: antivirus, hormone ( diethylstilbestrol ), steroids, and topical podophyllin
c. immunologically
using interferon
d. photodynamic therapy
This therapy uses dihematoporfirin ether which are activated with the appropriate wavelength (630 nm ).

Post-operative care including total voice rest during the first week, spoke softly during the second week, and gradually to normal in the third week. To speed healing and prevent mucosal dryness is important given the cold mist inhalation (cool mist ) during the first week.

complication
In general, laryngeal papillomas in children may heal spontaneously when puberty, but can be extended to the trachea, bronchus, and lung, believed to tracheostomy or extirpation due to action is not perfect.

prognosis
Prognosis is generally good, early diagnosis and appropriate treatment is a factor thought to affect recurrence. The cause of death is usually due to spread to the lungs.

TONSILITIS

Today, Mbah Dukun Bagong Lee, the shaman medical, visit his blog. He reads comment from visitor. Please post about tonsillitis!!! Before mbah dukun explains about tonsillitis, we must know what tonsil is.

Definition
The palatine tonsil represents the largest accumulation of lymphoid tissue in the head and neck region. Each tonsil has a compact body with a definite thin capsule on its deep surface. A stratified squamous epithelium lines the outer surface of the tonsil and invaginates deeply into the lymphoid tissue to form multiple crypts.

Anatomy of the tonsils
The tonsillar fossa is composed of three muscles: the palatoglossus muscle, the palatopharyngeal muscle, and the superior constrictor muscle. The palatoglossus muscle forms the anterior pillar and the palatopharyngeal muscle forms the posterior pillar. The tonsillar bed is formed by the superior constrictor muscle of the pharynx. The arterial blood supply of the tonsil enters primarily at the lower pole and is derived from the tonsillar branch of the dorsal lingual artery, the scending palatine artery and the tonsillar branch of the facial artery. The ascending pharyngeal artery and the lesser palatine artery also contribute to the vascular supply at the upper pole. Venous blood drains through the peritonsillar plexus around the capsule. The plexus then drains into the lingual and pharyngeal veins, which in turn drain into the internal jugular vein.
The nerve supply of the tonsillar region is through the tonsillar branches of the glossopharyngeal nerve and the descending branches of the lesser palatine nerves. The cause of referred otalgia with tonsillitis is through the tympanic branch of the glossopharyngeal nerve. The lymphatic drainage courses through the upper deep cervical lymph nodes.

What function do tonsils serve?
The tonsils are predominantly ß-cell organs with ßlymphocytes comprising 50% to 65% of all tonsillar lymphocytes. T-cell lymphocytes comprise approximately 40% of tonsillar lymphocytes and 3% are mature plasma cells. Tonsils are involved in inducing secretory immunity and regulating immunoglobulin production. The tonsils are favourably located to mediate immunologic protection of the upper aerodigestive tract as they are exposed to airborne antigens. Moreover, there are 10 to 30 crypts in each tonsil that are ideally suited to trapping foreign material and transporting it to the lymphoid follicles. The proliferation of ß cells in the germinal centres of the tonsils in response to antigenic signals is one of the most important tonsillar functions.
The human tonsils are immunologically most active between the ages of four and 10. Involution of the tonsils begins after puberty, resulting in a decrease in the ß-cell population and a relative increase in the ratio of T- to ß-cells.
Although the overall immunoglobulin production is reduced, there is still considerable ß-cell activity if seen in clinically healthy tonsils. The immunologic consequences of tonsillectomy are unclear. It is evident, however, that tonsillectomy does not result in a major immunologic deficiency.

What are tonsils and what is tonsillitis?
Tonsils are made of soft glandular tissue and are part of the immune system. You have two tonsils, one on either side at the back of the mouth. The picture shows normal non-infected tonsils.
Tonsillitis is an infection of the tonsils. A sore throat is the common symptom. In addition, you may also have a cough, fever, headache, feel sick, feel tired, find swallowing painful, and have swollen neck glands. The tonsils may swell and become red. Pus may appear as white spots on the tonsils.

What are the types of tonsillitis?
o Acute Tonsillitis – those affected usually have fever, sore throat, foul breath, difficulty or painful swallowing, and tender, enlarged lymph nodes. These symptoms usually resolve in 5 – 7 days, but may persist up to two weeks despite therapy
o Recurrent Tonsillitis – same symptoms, with multiple episodes over time
o Chronic Tonsillitis – chronic sore throat, bad breath, soreness with swallowing, perhaps, enlarged and tender neck lymph nodes
o Peritonsillar Abscess – severe sore throat, fever, bad breath, difficulty opening the mouth, usually with a muffled (hot potato) voice. This is due to infection around the tonsil, and typically occurs seven to ten days after the onset of symptoms

Etiology
Many viruses and many bacteria can cause tonsillitis. The most common include:
o Herpes simplex virus
o Streptococcus pyogenes – “strep throat”
o Epstein-Barr virus – the cause of infectious mononucleosis (mono)
o Adenovirus
o Cytomegalovirus
Bacteria cause between 15 and 30 percent of cases of acute tonsillitis. To determine the cause, many tests are commonly performed. While most episodes are viral in origin, only a throat culture helps determine whether the infection is viral or bacterial in origin. The symptoms and signs of viral versus bacterial tonsillitis are very similar. To the observer, the condition looks the same in most individuals.

Symptoms
The Following are the most common symptoms dor tonsillitis include  the following however, individuals may experience symptoms differently:
a.    Swollen, red tonsils (often coated with a yellow, gray, or white membrane)
b.    Blisters or painful ulcerated areas on the throat
c.    Sudden onset of sore throat
d.    Pain while swallowing
e.    Headache
f.    Malaise
g.    Chills
h.    Fever
i.    Swollen and tender lymph nodes in the neck or jaw area
 Also you will find these symptoms when repeated infections or irritation causes enlargement, You may notice:
a.    Difficulty breathing through the nose
b.    Mouth breathing
c.    A muffled sound to the voice (hot potato voice)
d.    Noisy breathing
e.    Snoring while sleeping
f.    A chronic sensation of drainage in the back of the nose and upper throat

What are the complications of tonsillitis?
The complications of tonsillitis may be classified into suppurative and nonsuppurative complications. The nonsuppurative complications include scarlet fever, acute rheumatic fever, and post-streptococcal glomerulonephritis. Suppurative complications include peritonsillar, parapharyngeal and retropharyngeal abscess formation.
Scarlet fever is secondary to acute streptococcal tonsillitis or pharyngitis with production of endotoxins by the bacteria. Clinical signs include an erythematous rash, severe lymphadenopathy, fever, tachycardia, and a yellow exudate overlying erythematous tonsils. Acute rheumatic fever is a syndrome that follows Group A Streptococcal Pharyngitis for one to four weeks. Certain proteins found in heart muscle appear to be antigenetically similar to protein found on the streptococcus.
This is believed to be the method of infection of cardiac tissue. Post-streptococcal glomerulonephritis may be seen after both pharyngeal and skin infections. The typical patient develops an acute nephritic syndrome one to two weeks after a streptococcal infection. The infection is secondary to the presence of a common antigen in the glomerulus and in the streptococcus. Antibiotic therapy may not necessarily alter the natural history of glomerulonephritis. A tonsillectomy may be necessary to eliminate the source of infection.
Peritonsillar abscess most commonly occurs in patients with recurrent tonsillitis or in those with chronic tonsillitis who have been inadequately treated. The spread of infection is from the superior pole of the tonsil with pus formation between the tonsil bed and the tonsillar capsule. peritonsillar cellulitis and abscess respectively. This infection usually occurs unilaterally and the pain is quite severe.
Drooling is caused by odynophagia and dysphagia. Trismus is frequently present as a result of irritation of the pterygoid musculature by the pus and inflamma on. There is gross unilateral swelling of the palate and anterior pillar with displacement of the tonsil downward and medially with deviation of the uvula toward the opposite side. Cultures of peritonsillar abscess usually show a polymicrobial infection, both aerobic and anaerobic.
An abscess in the parapharyngeal space can develop if infection or pus drains from either the tonsils or from a peritonsillar abscess through the superior constrictor muscle. The abscess is located between the superior constrictor muscle and the deep cervical fascia and causes displacement of the tonsil on the lateral pharyngeal wall toward the midline.
Involvement of the adjacent pterygoid and paraspinal muscles with the inflammatory process results in trismus and a stiff neck. Progression of the infection of the abscess may spread down the carotid sheath into the mediastinum. As with most softtissue infections of the neck, lateral pharyngeal space infections are polymicrobial and reflect the oropharyngeal flora.
A retropharyngeal abscess may also result from a peritonsillar abscess. The source of the abscess is a chain of lymph nodes on either side of the midline in the retropharyngeal space. These lymph nodes receive drainage from the nose, paranasal sinuses, pharynx and Eustachian tube. Children usually present with irritability, fever, dysphagia, muffled speech, noisy breathing, stiff neck, and cervical lymphadenopathy.


What is the treatment for tonsillitis?
•    Not treating is an option as many tonsil infections are mild and soon get better.
•    Have plenty to drink. It is tempting not to drink very much if it is painful to swallow.
•    You may become mildly dehydrated if you don't drink much, particularly if you also have a fever. Mild dehydration can make headaches and tiredness much worse.
•    ANALGESIC include Paracetamol or ibuprofen to remove pain, headache, and fever. To keep symptoms to a minimum it is best to take a dose at regular intervals as recommended on the packet of medication rather than 'now and then'. For example, take paracetamol four times a day until symptoms ease.
•    Aspirin gargles may ease the soreness. (There is little research evidence that confirms this. However, it is a popular treatment and may be worth a try.) Dissolve some soluble aspirin in water and gargle for 3-4 minutes. You can do this 3-4 times a day. Spit out the aspirin after gargling. (You should not give aspirin to children under 16.)
•    Other gargles, lozenges, and sprays that you can buy at pharmacies may help to soothe a sore throat. However, they do not shorten the illness.

What are indications for tonsil removed or tonsillectomy
Tonsillectomy is still commonly performed in children, occasionally in adults. The actual
procedure performed does not vary with the age of the patient.
Reasons tonsils are removed – tonsillectomy -- include:
A. Infection
1. Recurrent tonsillitis (more than seven per year or five per year for two years or three per year for three years).
2. Persistent, chronic tonsillitis.
3. Recurrent otitis media unresponsive to medical or previous placement of PETubes.
4. Chronic/recurrent nasopharyngitis.
5. Chronic/recurrent sinusitis.

B. Obstruction
1. Hypertrophy with obstruction unresponsive to antibiotics with or without obstructive apnea, severe
dysphagia, and failure to thrive.
-If adenoids enlarged only.
-If tonsils enlarged only.
-If tonsils and adenoides are enlarged.
2. Nasal obstruction with speech abnormalities, orodental abnormalities.

C. Miscellaneous
1. Recurrent peritonsillar abscess or peritonsillar abscess with previous history of recurrent or persistent
tonsillitis.
2. Unilateral tonsillar hypertrophy.
3. Hemorrhagic tonsillitis.
4. Chronic tonsillolithiasis.


Why are adenoids removed – adenoidectomy?
Reasons adenoids are removed – adenoidectomy -- include:
1.    Often removed at the same setting as tonsils in children with chronic upper airway obstruction;
2.    Chronic mouth breathing;
3.    Chronic, recurrent sinus infections in children, under age 10;
4.    Abnormalities in dental growth – high arched palate;
5.    Need for more than one set of eardrum tubes for recurrent ear infections

About tonsillectomy & adenoidectomy
1.    The surgery is performed under general anesthesia, that is, the patient is put to sleep for  short time
2.    The duration of surgery is generally 20 – 30 minutes, and is performed in an outpatient surgical facility or hospital operating room
3.    The adenoids are removed through the back of the throat, with the surgeon seated at the patient’s head. No external skin incisions are made.
Ue a technique called Coblation® Tonsillectomy. I feel this technique results in less discomfort after surgery. Most patients resume a normal diet in 3 – 5 days after surgery, compared to 7 – 10 days using the outdated electrocautery technique.


refferences
1. http://www.homoeopathyclinic.com/articles/diseases/Tonsillitis.pdf
2. ttp://www.woodlandsmedicalcentre.com/Portals/0/Tonsilitis.pdf

3. http://farm3.static.flickr.com
4. http://www.stacommunications.com/journals/diagnosis/2003/02_February/tonsilitis.pdf