Mastoid air cell system

1. Mastoid air cell system: Is considered to be an important contributor to the physiology of middle ear function. According to Tumarkin the mastoid air cell system served as an reservoir of air and serves as buffer system to replace air in the middle ear cavity temporarily in case of eustachean tube dysfunction. The mean volume of air in the mastoid air cell system could be about 5-8 ml. CT scan evaluation of temporal bone is considered to be the best modality to assess mastoid air cell system.
   The penumatization of mastoid air cell system can be divided into
   3 types:
   Sclerotic mastoid – Pneumatization is absent
   Diploic mastoid – Pneumatization partial
   Pneumatic mastoid – Full and complete pneumatization
   The mastoid air cell system is covered with highly vascular cuboidal epithelium. The contact between the blood vessels and the basement membrane is rather close resembling that of alveoli where extensive gaseous exchange takes place.

The mastoid air cell system is categorized according to various

regions of temporal bone. These include:

a. Squamo mastoid – This area include air cells around antrum, central mastoid tract and peripheral air cell tract.

b. Perilabyrinthine cells – These can be divided into supra labyrinthine and infralabyrinthine air cells

c. Petrosal air cells – Petrosal air cells and petrous apex air cells

d. Accessory air cells – These cells include zygomatic air cells, occipital air cells, squamous air cells and styloid air cells.

Patients with poor pneumatization of mastoid air cell system are more prone to develop adhesive otitis media following middle ear infections as the normal buffering system of the mastoid pneumatization is not adequate in them. Treatment of secretory otitis media with effusion is more effective in a patient with well developed mastoid air cell system when compared to that of patients with sclerosed ones.

2. Describe the anatomy of the tympanic membrane and ossicles of the ear. Describe the role of these structures in the mechanism of hearing.

Tympanic membrane is also known as the ear drum. Anatomically it could be considered to be a part of the external ear since it is attached to the medial terminal end of the bony meatus. Functionally speaking it is part of the tympanic cavity.
It is more or less oval in shape (egg shaped). It is 9mm in diameter. Its broad portion lies superiorly. It is pearly white in color, thin and semitransparent. When viewed under illumination a trianglular cone of light (reflected light) is seen extending from the centre forwards and downwards. This reflection, or cone of light is due to the sectional shape of the membrane. The ear drum is set with an obliquity of about 55 degrees to the floor of the external meatus. The centre of the ear drum appears retracted, and is known as the umbo. This umbo lies at the apex of the cone of light. Visible as an ivory colored extension upwards from the umbo is the handle of the malleus. If the posterior portion of the membrane is transparent, then the image of the long process of the incus, and occasionally the stapedial tendon may also be seen.

Figure showing anatomy of ear drum

The ear drum is composed of 3 layers. The outer layer is formed by stratified squamous epithelium, and is continuous with that of the external auditory canal. Any condition affecting the skin of the external canal will also affect the outer layer of the ear drum. Common conditions like dermatitis involving the skin of the external canal can also involve the outer layer of the ear drum. Embryologically outer layer of the ear drum developed from the ectoderm. Myringitis granulosa a common condition affecting the ear drum affects only the outer layer of the tympanic membrane. The middle and inner layers are not involved in this condition. It is commonly caused by infections arising from the external canal. Constant irritation of the ear drum due to presence of wax may also predispose to this condition. Another condition which involves the outer layer of the ear drum is Bullous myringitis. In this condition blebs may be seen in the outer layer of the ear drum. It is commonly caused by viral infections, or mycoplasma pneumonia. It may also be associated with middle ear effusion.

The middle fibrous layer from which the ear drum derives its strength and resilience is derived from the mesoderm. This portion is infact sandwiched between the outer squamous lining derived from the ectoderm and inner mucosal lining of the middle ear cavity derived from the endoderm. The ectodermal and mesodermal components of the ear drum arise from the first branchial cleft, while the endodermal component is derived from the pharyngotympanic recess. The middle fibrous layer has two components: 1. radial and 2 circular fibres. The handle of the malleus lie between the middle fibrous layer and the inner mucosal layer of the ear drum. From the handle of the malleus the radial fibres of the middle fibrous layer radiate towards the circumferance of the ear drum. The circular fibres are more prominent and thickened along the circumference of the ear drum. The condensation of the circular fibres are fixed to the tympanic sulcus at the medial end of the external auditory canal. This middle firbous layer is absent in the attic area of the ear drum. The fibrocartilagenous ring and the fibrous layer of the ear drum are deficient superiorly. This deficient area is known as the notch of Rivinus. The attic portion of the ear drum which lack the middle layer is known as the pars flaccida, while the rest of the drum which has all the three layers is known as pars tensa. The chorda tympani nerve which is a branch of the facial nerve run between the middle fibrous and inner mucosal layers of the ear drum.

The skin of the external canal and the outer lining of the tympanic membrane are unique in a sense that they lack frictional and abrasive contacts which is common with the skin lining elsewhere in the body. Desquamated keratin does not accumulate on the surface of the tympanic membrane, or in the deep external meatus, because the skin lining here is endowed with a peculiar feature known as Migration. The surface layers of the skin of the ear drum, and the surface keratin move towards the periphery of the membrane, and then slowly along the external meatus to the exterior. Derangements of this unique feature is associated with some of the diseases of the external ear.

The inner layer of the ear drum derived from the endoderm of the pharyngotympanic recess is continuous with that of the mucosal lining of the middle ear cavity.

Blood supply:

The external surface of the ear drum receives its blood supply from the deep auricular branch of the maxillary artery. This small artery leaves the first part of the maxillary artery behind the neck of the mandible and gains access into the external canal by piercing the anterior wall behind the mandibular joint. It sends small branches into the membrane from the whole circumference of the pars tensa and one or more manubrial branches that descend on the handle of mandible from above. The internal surface of the ear drum is supplied from behind by the stylomastoid branch of the posterior auricular artery, and from the front by the tympanic branch of the maxillary artery. The superficial veins open into the external jugular vein; and those on the internal surface drain into the transverse sinus and veins of the dura mater, and partly into the venous plexus on the eustachean tube.

Nerve supply:

The innervation of the posterior half of the ear drum is by the auricular branch of the X nerve and the anterior half is by the auriculotemporal branch of the Vth nerve. The inner surface of the ear drum is supplied by the tympanic branch of the IXth nerve.

The middle ear contains three ossicles which play a very important role in sound transmission. These ossicles are:

1. Malleus
2. Incus
3. Stapes
   
   
   
   
   
   
   Malleus: This bone is shaped like a hammer hence the name. This is the largest of the three ossicles of the middle ear cavity. It has a head, neck and three processes arising from below the neck. The overall length of the malleus ranges between 7.5 - 9 mm. Its head lies in the attic region of the middle ear effectively dividing the attic into an anterior portion and a posterior one. The anterior portion lie anterior to the handle of the malleus, while the posterior portion lie behind the handle of the malleus. During surgical procedures for attic cholesteatoma clipping of this head will improve the exposure in the attic region. The head of the malleus on its posteriomedial surface has an elongated saddle shaped cartilage covered facet for articulation with the incus. This articular surface is constricted near its middle dividing the articular facet into a larger superior and a smaller inferior portions. The inferior portion of the articular facet lies at right angles to that of the superior portion. This projecting lower portion is also known as the cog or spur of the malleus. Below the neck the bone broadens and gives rise to the following: the anterior process from which a slender anterior ligament arises to insert into the petrotympanic fissure; the lateral process which receives the anterior and posterior malleolar folds from the annulus tympanicum, and the handle which runs downwards, medially and slightly backwards between the mucous and fibrous layers of the tympanic membrane. On the deep medial surface of the handle there is a small projection into which the tendone of the tensor tympani muscle inserts. Additionally the malleus is supported by the superior ligament which runs from the head to the tegmen tympani.
    
   
   
   
   
   
   
   

 

Figure showing the malleus

Incus: This bone is shaped like an anvil. It articulates with the malleus and has a body and two processes. The body lies in the attic and has a cartilage covered articular facet corresponding to that of the malleus. The short process projects backwards from the body to lie in the fossa incudis. It is infact attached to the fossa incudis by a short ligament. The long process of the incus descends into the mesotympanum behind and medial to the handle of the malleus. At its tip there is a small medially directed lenticular process which articulates with the stapes. The long process of the incus has precarious blood suppy. This portion of the incus is prone for undergoing necrosis in disease conditions.

Figure showing the incus

The stapes: The stapes consists of a head, neck, two crura and a base (footplate). The head of the stapes points laterally and has a small cartilage covered depression for articulation with the lenticular process of the incus. The tendon of the stapedius muscle attaches to the posterior part of the neck and the upper part of the posterior crura. The neck of the stapes gives rise to two crura, the anterior crura is thinner and less curved than the posterior crura. The two crura join the foot plate which closes the oval window during life. The average dimensions of the foot plate is 3mm x 1.4mm. The long axis of the foot plate is almost horizontal, with the posterior end being slightly lower than the anterior.

 

Figure showing the stapes

Role played by the ear drum and ossicles in hearing:

Sound which impinges on the ear drum sets it into vibrations. These vibrations are transmitted by the middle ear ossicles to reach the round window membrane which conduct it to the inner ear fluids. Initially the vibrations of the ear drum belong to the low pressure high displacement variety. These vibrations are not capable of vibrating the inner ear fluids. For vibrating the inner ear fluids the stimulus should be of low displacement high pressure variety. This change in the type of vibration is brought about by the impedance matching mechanism of the middle ear cavity.

Two processes are involved in the impedance matching mechanism of middle ear. They are:
1. The area of the tympanic membrane is larger than that of the stapes foot plate in the cochlea. The forces collected over the ear drum are concentrated over a smaller area, thus increasing the pressure over oval window. The pressure is increased by the ratio of these two areas i.e. 18.75 times.
2. The second process is the lever action of the middle ear bones. The arm of the incus is shorter than that of the malleus, and this produces a lever action that increases the force and decreases the velocity at the stapes. Since the malleus is 2.1 times longer than the incus, the lever action multiplies the force by 2.1 times. 

Buckling effect of ear drum: The ear drum curves from its rim

to its attachment to the manubrium. The buckling effect causes

greater displacement of the curved ear drum and less

displacement for the handle of the malleus. This causes high

pressure low displacement system. 

Role of ear drum in sound conduction:

The ear drum conducts sound from the external ear to the middle ear.

Bekesy postulated that the ear drum moved like a stiff plate up to

frequencies of 2 kHz. He also suggested that the inferior edge of the drum is

flaccid and moves the most. At frequencies above 6 kHz the vibrating

pattern becomes more complex and chaotic. This reduces the efficiency of

sound transfer mechanism.

The handle of the malleus is attached to the centre of the ear drum. This

allows sound vibrations on any portion of the ear drum to be transmitted to

the ossicles.

 

Describe the mechanism and disorders related to the process of swallowing in humans.

Introduction:

The act of swallowing can be considered as a complex activation of the muscles involved in an orderly sequence as orderly like that of the muscles of a Balle dancer.

Swallowing is initiated either by voluntary cortical drive or via sensations via the peripheral nervous system. Once the act of swallowing is initiated it continues in an orderly manner. After the initiation the whole act of swallowing is not under voluntary control. The neural network responsible for this reflexive phase of swallowing is known as the central pattern generator.

Components of central pattern generator:

Brain stem

Tractus solitarius

Nucleus ambiguus

Reticular formation

Deglutition is defined as the act of swallowing which causes the food bolus / liquid to the stomach via the mouth, pharynx, and oesophagus. Normal deglutition involves a complex series of voluntary and involuntary muscular contractions. For better understanding the process of deglutition is divided into three phases:

Oral

Pharyngeal

Oesophageal

Oral phase:

This phase of swallowing is voluntary in nature. This phase is subdivided into oral preparatory phase, and oral propulsive phase.

During the oral preparatory phase the bolus is processed in such a way that it is rendered swallowable. This phase involves chewing of the food mixed with saliva making it into a bolus which can be smoothly swallowed.

During the oral propulsive phase the muscles of the tongue plays an important role in in propelling the food into the oropharyx. When the bolus reaches the oropharynx the involuntary phase of deglutition begins.

Cranial nerves involved during the oral phase of deglutition include:

Trigeminal, Facial and Hypoglossal nerves. The cerebellum controls these cranial nerve inputs.

Disorders involving oral phase of swallowing:

Disorders involving this phase of swallowing is usually due to impaired tongue control. These patients have difficulty in chewing food and initiating swallow. These patients also have difficulty in holding liquids inside the oral cavity. Excess liquid inside the oral cavity starts to drool. When attempt is being made to swallow liquid the oropharyngeal reflexes are not initiated causing aspiration.

In patients with paralysis involving the facial nerve the lip closure is not precise and complete causing difficulties in holding the bolus inside the oral cavity. These patients also have food stasis in the lateral sulcus due to poor cheek muscle tone.

In paralysis involving the hypoglossal nerve the patient is unable to form bolus inside the mouth. Unless a bolus is formed swallowing act is not possible / becomes difficult. Due to reduction in tongue thrust the bolus cannot be propelled into the oropharynx. Due to incomplete contact between the tongue and palate the bolus cannot be efficiently propelled to the oropharynx.

In Parkinson's disease repeated tongue rolling may cause difficulty in propelling the bolus into the oropharynx.

Disorders involving oral phase of swallowing may cause a delay in the oral phase of swallowing.

Pharyngeal phase:

This phase involves a rapid sequence of overlapping events. This phase involves propulsion of bolus from the pharynx into the upper oesphagus through the cricopharyngeal sphincter. This phase is totally involuntary and reflexive capable of progressing as soon as it is initiated.

Critical events involved in this stage include the laryngeal protective sphinteric mechanism which is vital in preventing aspiration of bolus. These events include:

a. The soft palate rises

b. The hyoid bone and larynx moves upwards and forwards

c. The vocal folds adducts and come close to midline

d. The epiglottis folds backwards protecting the airway

e. The tongue pushes backwards pushing the bolus towards the cricopharyngeal sphincter

f. The pharyngeal wall constricts to facilitate backward movement of bolus

g. The cricopharyngeal sphincter relaxes due to forward movement of hyoid bone and larynx facilitating easy passage of bolus into the upper oesophagus.

This phase of swallowing lasts for about a second and it involves the motor and sensory components of 9^th and 10^th cranial nerves.

Disorders involving this phase of swallowing could case severe feeding impairments. In normal persons during swallow, small amounts of ingested food could be retained in the vallecula and pyriform sinus. In patients with disorders involving the pharyngeal phase of swallowing large amounts of food material may get retained in the vallecula / pyriform fossa causing aspiration when the patient attempts a clearance swallow.

Velopharyngeal closure which occurs during this stage helps in preventing nasal regurgitation of food. Imperfect velopharyngeal closure as it occurs due to palatal paralysis / cleft palate / submucosal cleft palate may cause nasal regurgitation during this phase of swallowing. This scenario could also occur when the posterior pillar of tonsil is injured while performing tonsillectomy.

Presence of severe cervical osteophytes could cause severe swallowing disability involving this phase.

In patients with imapired laryngeal elevation due to paralysis of the elevators could lead to cricopharyngeal muscle spasm leading on to aspiration.

Reduced laryngeal closure will cause food spillage into the larynx.

Pharyngeal muscle paralysis on both sides will cause coating of the lateral pharyngeal wall thereby hindering the swallowing process. Ultimately this could lead to an increase in the pharyngeal bolus transit time.

Esophageal phase:

In the esophageal phase of swallowing the bolus after crossing the cricopharyngeal sphincter traverses the oesophagus facilitated by the peristalsis of oesophageal musculature. The lower esophageal sphincter relaxes on initiation of the swallowing process. When the bolus enters the stomach the lower esophageal sphincter closes preventing reflux of gastric contents into the oesophagus. This phase of swallowing is involuntary and reflexive being controlled by the medulla. This phase usually lasts less than 20 seconds.

Disorders involving this phase could lead to retention of food inside the oesophagus. This retention could be caused by:

1. Mechanical obstruction due to presence of tumors
2. Motility disorders
3. Lower oesophageal sphincter failure

1. Describe the clinical features, diagnosis and management of cancer oesophagus.

Patients with cancer oesophagus manifest with:

a.Difficulty in swallowing

b. Painful swallowing.

Usually dysphagia is the most common symptom. Initially dysphagia is pronounced for solid food. Fluids and semisolid diet are better tolerated.

c. These patients manifest with excessive loss of weight which could be due to:

Difficulty in swallowing

Reduced appetite due to malignancy.

d. Heart burns – These patients characteristically complain of burning pain in the midline of the chest. This type of pain progressively gets worse and is made still worse by the act of swallowing.

e. Voice change – This is usually due to involvement of recurrent laryngeal nerves causing paralysis of vocal folds. Right recurrent laryngeal nerve is commonly involved in these patients. During early stages these patients may have varying degrees of aspiration. Sometimes aspiration may be severe enough to cause aspiration pneumonitis.

f. Disruption of peristalsis – The sheer bulk of tumor present intraluminally within the oesophagus may cause disruption of normal peristalsis. This could cause nausea, vomiting and food regurgitation.

g. Haematemesis – If the tumor is friable it can cause intraluminal bleeding leading on to hematemesis.

h. Compression symptoms – Increasing bulk of oesophageal mass can cause compression of local structures. It can cause compression to trachea leading on to upper airway obstruction. Another area of compression is at the level of superior vena cava causing superior vena caval syndrome. Erosion of trachea may lead to troublesome tracheo oesophageal fistula.

Symptoms caused by superior vena cava syndrome include:

1. Dyspnoea
2. Swelling of the face / upper extremities
3. Headache
4. Orthopnoea
5. Nasal stuffiness
6. Light headedness

Symptoms caused by metastatic lesions:

Hepatic metastasis can lead to jaundice, ascitis.

Lung metastasis could cause shortness of breath, pleural effusion.

Diagnosis:

Radiology:

Barium swallow / meal can reveal occlusal mass in the oesophagus.

CT scan imaging will reveal the extent of the lesion, compression to adjacent structures if any.

Metastatic lesions can also be identified by performing CT scan.

PET scans can be used to identify and ascertain whether the lesion is active and metabolically active.

Upper GI endoscopy:

This is the standard in the diagnosis of oesophageal cancer. It helps in identifying the exact location of the lesion, biopsying the lesion. The location of the tumor is generally measured from the incisor.

Histopathology:

This offers the final diagnosis. Adenocarcinoma is common in the lower oesophagus while squamous cell carcinoma is prevalent in the upper third of oesophagus.

Management:

The ideal management modality is determined by:

1. Cellular type of cancer
2. Stage of the disease
3. General condition of the patient

Priority should be given to the nutritional needs of the patient.

Manitenance of good oral hygiene.

As a first step in ensuring adequate nutrition to the patient naso gastric feeding can be resorted to.

To alleviate oesophageal obstruction stenting could be resorted to. Stents are usually used to keep the lumen of oesophagus patent. They also play a vital role in occluding tracheo oesophageal fistulas if present.

Surgical management:

This can be classified into therapeutic and palliative procedures.

If the tumor is resectable then segemental resection of the involved segment of the oesophagus can be performed. The shortened oesophagus can be corrected by interposing stomach / jejunal flaps.

Types of oesophagectomy:

Types of esophagectomy:

• Thoracoabdominal approach- which opens the abdominal and thoracic cavities together.
• Two stage Ivor Lewis (also called Lewis-Tanner) approach- with an initial laparotomy and construction of a gastric tube, followed by a right thoracotomy to excise the tumor and create an esophagogastric anastomosis.
• Three stage McKeown approach- where a third incision in the neck is made to complete the cervical anastomosis.Describe the clinical features, diagnosis and management of cancer oesophagus.

Endoscopic resection of oesophageal tumors:

1. This procedure is safe
2. Less invasive
3. Useful to treat early lesions

Patients who can undergo endoscopic resection are those with early lesions which does not involve the muscularis mucosa. Lasers can be used to assist in these resections.

Chemotherapy is reserved for advanced lesions. It also depends on the histological type of the tumor. The drugs used include:

Cisplatin

5-flurouracil.

 

Ludwig's angina

Introduction: Ludwigs angina is described as rapidly spreading cellulitis involving the
floor of the mouth. It was first described by Wilhelm Friedrich von Ludwig in 1836.
This disorder has a potential for airway obstruction.
Synonyms: Cynanche, Carbuculus gangraenosus, Morbus strangulatorius, and Angina
maligna.
Anatomy:
This infection involves the submandibular space. The submandibular space can be divided
into two spaces: submaxillary and sublingual space. These two spaces are separated from each
other by the mylohyoid muscle. These two spaces are connected posteriorly through a cleft
known as the mylohoid cleft. The mylohyoid cleft contains the following structures:
1. Tail of submandibular gland
2. wharton's duct
3. Lingual nerve
4. Hypoglossal nerve
5. Lymphatics
6. Arteries and veins
The floor of the submandibular space is formed by the superficial layer of deep cervical
fascia. It is attached from the hyoid bone to the mandible. This space communicates across the
midline with that of the space on the opposite side.
Pathophysiology:
Commonest cause of Ludwig's angina is dental infections. One important factor to be
considered is the relationship of mandibular dentition to the attachment of mylohoid
muscle (mylohyoid ridge). The anterior teeth and first molars regularly attach
superior to this line, and infections arising from these roots commonly result in a
limited sublingual abscess. The second and third molar roots are attached routinely
below this line. Infections involving these roots cause infections of submaxillary
space. One other important relationship is that the roots of the anterior teeth and first
molar approximate the lateral mandibular surface, whereas the second and third
molar roots approach the lingual surface of the mandible.
Criteria for diagnosing Ludwig's angina:
To diagnose Ludwig's angina the following features should be present:
1. Rapidly spreading cellulitis with no specific tendency to form abscess.
2. Involvement of both submaxillary and sublingual spaces, usually bilaterally
3. Spread by direct extension along facial planes and not through lymphatics
4. Involvement of muscle and fascia but not submandibular gland or lymph nodes
5. Originates in the submaxillary space with progression to involve the sublingual
space and floor of the mouth.
Etiology:
1. Ludwigs angina is commonly caused as a sequlae to dental infections. In fact it is
very common in young adults with periodontal disease. Dental causes account for
75% to 80% of these cases.
2. Penetrating injuries involving the floor of the mouth (stab wounds, gun shot
wounds etc)
3. Mandibular fractures
Bacteriology of Ludwig's angina:
Since a majority of cases of Ludwig's angina are caused by dental infections, cultures
from this infected area show oral cavity flora. The most common aerobes isolated are
alpha haemolytic streptococci followed by staphylococci. Anaerobic cultures are
difficult to interpret. The anaerobes isolated are peptostreptococcus, peptococcus,
fusobacterium nucleatum, and bacteroids. The combination of aerobic and anaerobic
organisms has a synergistic effect due to production of endotoxins like collagenase,
hyaluranidase, and proteases. These endotoxins contribute to the rapidly spreading
cellulitis.
Clinical features:
1. Patient has c/o increasing oral cavity and neck pain.
2. These patients have poor oral hygiene
3. Symptoms are at first unialteral but soon become bilateral
4. The soft tissues of the floor of the mouth swells
5. Tongue gets pushed posteriorly causing air way obstruction
6. These patients are usually febrile
On examination:
These patients have tachycardia, fever, and variable degrees of respiratory obstruction
with dysphagia and drooling. The submandibular and submental regions are tense,
swollen and tender. The floor of the mouth may become tense swollen and indurated.
Fluctuation is not present. The tongue is seen to be pushed backwards.
Diagnosis of Ludwigs angina is based on the clinical features enumerated above.
These patients may show leukocytosis. X ray soft tissue neck may show soft tissue
oedema. CT scan neck is to be considered in all persistent cases to rule out
complications. Xray chest must also be considered to rule out mediastinitis.
Management:
Airway management: Since the airway is threatened insertion of oral airway is to be
considered. If the patient does not tolerate an oral airway then tracheostomy is to be
considered.
Intravenous antibiotics with broad spectrum features (chloramphenicol)may be
administered. The drug of choice is amoxycillin with clavulanic acid. Metronidazole
must also be administered. Clindamycin can be administered in resistant cases.
Role of surgical drainage: Wide decompression of the supra hyoid region may be
considered. The approach is through a median horizontal incision three to four finger
breadths below the mandibular margin. The mylohoid muscle is split in the midline,
and drainage is established both medially and laterally. Pus is very rarely encountered
during this procedure, but starts to drain several days after the procedure.
Complications:
1. Airway compromise
2. Extension to mediastinum causing mediastinitis. This can be suspected if there is
persistent swelling in the neck with pain, spiking fever and persistent leukocytosis.
3. Extension into the carotid sheath and retropharyngeal space.

Image courtesy drtbalu.com

Onodi cell

Axial CT nose and paranasal sinuses showing Onodi air cell marked "O" close to the optic nerve.

Onodi cell is also known as spheno ethmoidal air cell.  This air cell lies posterior and superior to the sphenoid sinus.

This air cell lies close to the optic nerve sheath.  Infections involving this air cell can lead to blindness.  Surgery in this

area can cause blindness if care is not exercised.

Lesions involving retropharyngeal space

Introduction:

Lesions involving the retropharyngeal space can be best classified according to the lesions involving its various contents. A good knowledge of the anatomical contents of this space will make the diagnosis of lesions involving this space a bit easier.

Contents of retropharyngeal space:

1. Fat
2. Lymph nodes – Lateral retropharyngeal group (Rouviere) and medial retropharyngeal group.


Pseudomass lesions involving retropharyngeal space include:

1. Tortuous internal carotid artery
2. Mucosal oedema involving the space. This is common in venous obstruction.
3. Lymph spilling into this space due to obstruction to the lymphatic circulation


Congenital mass lesions:

1. Hemangioma
2. Lymphangioma


Inflammatory lesions involving retropharyngeal space:

1. Reactive lymphadenitis
2. Suppurative lymphadenopathy also known as intranodal abscess
3. Cellulitis / abscess

Benign tumor:

Commonest benign tumor involving this space is the lipoma

Malignant tumors involving retropharyngeal space:

1. Nodal metastasis from carcinoma of head and neck
2. Melanoma
3. Lymphomas (Non Hodgekins type is common)
4. Direct invasion of tumors like meningioma and chordoma

Lingual thyroid and its management

This e book discusses Lingual thyroid and its management.

Lingual Thyroid

Lesions involving the prestyloid compartment of parapharyngeal space

Anatomical contents of prestyloid compartment of parapharyngeal space include:

1. Fat
2. Pterygoid venous plexus
3. Internal maxillary artery and its branches
4. Ascending pharyngeal artery
5. Branches of mandibular division of trigeminal nerve

The presence of fat in this compartment is clearly visualized in the axial CT scan images of this space. Obliteration of this fat plane indicates sinister lesions ? Malignancies.

Asymmetric pterygoid venous plexus can be visualized as mass lesion in coronal CT scan images. Hence this asymmetry is also known as pseudotumor.

Congenital lesions involving this space include the rare second branchial cleft cyst.

Inflammatory lesions involving this space:

1. Spreading infections from adjacent spaces: Pharyngeal mucosal space infections like pharyngitis, adenoiditis, tonsillitis, peritonsillar abscess and retromandibular venous thrombosis.
   Parotid space infections like parotid calculus, parotid abscess
   Massticator space infections commonly caused due to dental infections, 3^rd molar tooth extraction with violation of pterygomandibular raphae
2. Infections due to penetrating lesions of lateral pharyngeal wall

Benign lesions involving this space include:

1. Pleomorphic adenoma parotid gland
2. Lipoma
3. Schwannoma

Malignant tumors involving this space include:

1. Mucoepidermoid cancer of parotid
2. Adenoid cystic carcinoma parotid
3. Malignant mixed tumor of parotid
4. Metastatic lesions from kidney & prostate

Cloisson sagittale

Cloisson sagittale are small, bilateral,sagittally oriented slips of fascia extending from the buccopharyngeal fascia anteriorly to the prevertebral fascia posteriroly close to their attachment to the transverse process of cervical vertebrae.  These slips separate the retropharyngeal space which is present medially from the laterally placed retrostyloid compartment of the parapharyngeal space.  These slips are also known as alar fascia.

Radiological anatomy of nasopharynx

1 - Nasopharynx

2 - Tensor veli palatini

3 - Levator veli palatini

4 - Temporalis muscle Medial / deep head

5 - Temporalis muscle lateral / superficial head

6 - Coronoid process of mandible

7 - Lateral pterygoid muscle

8 - Condylar process of mandible

11 - Pterygomaxillary fissure

Viral sialadenitis

Introduction:

Viral infections involving salivary glands are rather common in children.  These infections lead to acute inflammation of the involved salivary gland.  The most common viral infection involving salivary glands is Mumps infection.

Mumps infection:

This is the most common viral infection involving the salivary glands. Submandibular and sublingual salivary glands are very rarely involved.   This is rather common in children aged between 4-6 years.  This scenario is likely to change with popularisation of the Mumps vaccine.  Mumps are not common in adults due to the common presence of neutralizing antibodies.

Features of Mumps infection:

Parotid glands are commonly involved.  Incubation period ranges between 2-3 weeks.   Parotid swelling is invariably preceded by the development of fever, malaise, and myalgia.

Diagnosis is usually by demonstrating mumps s antigen, mumps v antigen and haemagglutination antigen.

Mumps virus can be isolated from the urine of affected individuals.  It may be present in the urine about 6 days prior to infection and may persist up to 2 weeks after the infection has subsided.

Majority of mumps infection may remain subclinical.

Complications:

1. Sudden deafness
2. Pancreatitis
3. Meningitis
4. Orchitis

Other viral infections involving the salivary glands include:

1. Cytomegalovirus – Involves new borns. This can lead to physical and mental retardation.  These patients manifest with hepatosplenomegaly and thrombocytopenia.
2. Coxakie virus
3. Echo virus
4. Lymphocytic choriomeningitis virus