Diagnostic Hierarchy for Chronic Headache and OroFacial pain free download

Diagnostic Hierarchy for Chronic Headache and OroFacial pain

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Diagnosis Chart for Oral Mucosal Lesions

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Notes on Sialolithiasis-Clinical features, Investigations, Histopathology and Treatment

Sialolithiasis

Thereis presence of one or more round or oval calcified structures in the duct ofthe major or minor salivary glands( salivary stones)

Howthe stone is formed:

Itis assumed that mucin proteins and desquamated ductal epithelial cells form asmall nidus on which the calcium salts are precipitated, this nidus then allowsconcentric lamellar crystallizations to occur and thus sialolith increases insize as a layer by layer gets deposited on it

Clinicalfeatures of sialolithiasis:

About80%of sialolith affects the major salivary glands and there is more predilectionsfor the submandibular gland.

Stonesare rare in children the average age is the 4^th decade with no sex preference.

Theyare asymptomatic discovered on dental radiographs.

Ifsymptomatic the chief complains are pain and swelling . Swelling is results asthere is ductal dilatation caused by the ductal blockade.

Thepain is described as pulling drawing or stinging.

SialolithiasisInvestigations:

Panoramicradiograph.

Ultrasound imaging

orsailography

Histopathologyof sialolithiasis:

Stone: On gross examination moststones are yellow or white in colour. they may be round to oval

  - some of the stones are nodular

  - after decalcification the stone showsconcentric rings as of the annual rings of a tree trunk

   -The stone is acellular and amorphous innature and may contain microbial colonies.

Ducts: the ductal lining thatsurrounds sialolith shows variety of reactive changes.

   - there is squamous and mucus cell

     metaplasia and changes to stratifiedsquamous epithelium with numerous mucous goblet cells

Sialolithiasistreatment:

• Manyof the major salivary gland sialoliths can be removed by manipulation of thestone through major duct orifice
• Whenmanipulation fails then a surgical cut is made into the main duct
• Intriangular, or multiple stones and long standing obstructions removal of thestone and sialadenectomy is done.

Notes on Mucocele and Mucous Retention cyst-Etiology,Clinical Features,Differential Diagnosis and Treatment

Salivary glands react to injury or obstruction by undergoing atrophic degeneration and necrosis with replacement of the parenchyma byinflammatory cells and ultimately fibrous scar formation

Mucocele

It is a tissue swelling composed of pooled mucus thatescapes into the connective tissue from several excretory ducts

Mucocele

Whensalivary duct is severed the acinar cells will continue to secrete saliva intothe severed duct.

Atthe site of the cut/severance the secretory product escape into the connectivetissue forming a pool of mucus that distends the surrounding tissue.

Etiology:

Minorglands of the lip are most prone to severance as a result of injury or bitingthe mucosa.

Intraoral minor salivary can also be effected as result of some irritation as well.

Clinicalfeatures

Mostlyencountered in children and young adults.

Twothird of the mucoceles occur in the 3^rd decade of life.

Bothmales and females are effected equally.

Site:mucosal surface of the lower lip

              buccal mucosa

              floor the mouth

              ventral of the tongue and palate

Clinicalappearance of the mococele depends on its location within the submucosa

Moresuperficial zones of mucous extravasations presents a fluctuant mass withbluish translucent appearance.

Patientusually feels the mucocele and the fluctuation in its size

Painis quite rare .

Initiallythe mucocels are well circumscribed but with repeated truma they become nodular,more diffuse and firm on palpation.

Themucoceles have finely vascularized and distended, appearance often referred toas frogs belly that’s why they are also called Ranulas

Whenpart of this ranula is deep seated in to the sumental or submandibular spacethen the term used is the” Plunging Ranula”

Differentialdiagnosis

• Mucoepidermoidcarcinoma
• Cavernoushemangeoma (when there is hemorrhage)
• Blistersseen in some bullous and desqumative disease.

Histopathology:

Underlyingpool of mucin distends the sarface epithelium.

Themucin is walled of by the rim of granulation tissue or in long standing casesby condensed collagen.

Anepithelial lining is lacking

Themucinous material  basophilic oracidophillic and contains  neutrophilsand large oval foam cells the histocytes .

Thebase of the mucocele will reveal feeder duct.

Longstanding mucoceles will show acinar degeneration with fibrosis and minimalinflammation .

Treatment:

Minorsalivary gland mucocele will not resolve on its own it must be surgicallyexcised.

Tominimize the chances of recurrence the feeder gland should also be removed.

Postsurgical parasthesia might occur when the branches of the mental nerve aresevered

Surgical Removal of Mucocele-Video

Mucusretention cyst

Itis a swelling caused by an obstruction of a salivary gland excretory ductresulting in an epithelial lining cavity containing mucus. Mucus retention cystis sometimes also referred as Sialocyst

Themucus retention cyst is lined by epithelium and rarely occur in the majorsalivary gland, when they do occur they are multiple i.e. poly cystic diseaseof the parotid gland

Clinicalfeatures:

Encounteredin adults from 3^rd -5^th decade.

Thelesion is painless and fluctuant and at times bluish in appearance.

Site:parotid cysts are located in the   superficial lobe as fluctuant well defined mass.

    -with in the oral cavity the floor of themouth is the most common place.

    -this is followed by the lip and the buccalmucosa

Histopathology:

Theepithelium of the cyst is stratified cuboidal or columnar duct like epithelium.

Thecytoplasm in the of these cells is either clear or eosinophlic and my show somefeatures mucous differentiation

70%of these cyst are unilocular rest of the 30% have multilocular pattern.

 

Treatment:

Simpleexcision is the treatment of choice with caution of rupturing the cystic sacs.

Recurrenceis rare.

Howeverdamage to the adjacent gland may result in a mucocele formation.

Notes on Developmental defects of the oral and maxillofacial regions

Developmental defects of the jaws

1. Orofacial clefts
2. Coronoid hyperplasia
3. Condylar hyperplasia
4. Condylar hypoplasia
5. Bifid condyle
6. Exostoses
7. Torus palatinus
8. Torus mandibularis
9. Eagle syndrome
10. Stafne defect
11. Hemihyperplasia
12. Progressive hemifacial atrophy
13. Segmental odontomaxillary dysplasia
14. Crouzon syndrome
15. Apert syndrome
16. Mandibulofacial dysostosis
17. Pierre Robin syndrome

Orofacial clefts

• Most common major congenital defects in humans
• Frequency of CL +/- CP : Native americans,Asians, Whites,Blacks
• CL+CP 45%, CPO 30%, CLO 25%
• More common in males than in females
• CL: 80%-unilateral (70%-left side), 20%-bilateral
• 70% of unilateral CLs are associated with CP
• Minimal manifestation of CP is a bifid uvula
• Submucosal palatal-the surface mucosa is intact, but adefect exists in the underlying musculature of the soft palate

 

Coronoid hyperplasia

• Rare, unknown cause
• Male-to-female ratio = 5:1
• Endocrine influence, heredity
• Bilateral CH is more common than unilateral CH*
• Restricts mandibular opening and causes deviation towardaffected side*

Condylar hyperplasia

• Excessive growth of one of the condyles
• Endocrine disturbances and trauma
• Facial asymmetry, prognathism, crossbite and open bite
• Most commonly found in adolescents and young adults
• Self limiting condition

Condylar hypoplasia

• Underdevelopment of the mandibular condyle
• Congenital
•    (mandibulofacialdysostosis, hemifacial microstomia)
• Acquired
•   (trauma to thecondylar region during infancy or childhood, infection, radiation therapy, RA,OA)

Bifid condyle

• Double-headed mandibular condyle
• Medial and lateral head divided by an anteroposterior groove
• Trauma, abnormal muscle attachment, teratogenic agents,persistence of a fibrous septum within the condylar cartilage
• Popping or clicking sound when opening the mouth

Exostoses

• Localized bony protuberances that arise from the corticalplate
• Adults
• A bilateral row of bony hard nodules along the facial aspectof the maxillary and mandibular alveolar ridge

Torus palatinus/mandibularis

Torus palatinus

• Common exostosis that occurs in the midline of the vault ofthe hard palate
• Genetics vs environmental or both
• Asian and Inuit
• Female:Male = 2:1

Torus mandibularis

• A bony protuberance along the lingual aspect of the mandibleabove the mylohyoid line in the region of the premolars
• Bilateral
• May appear on periapicalradiographs as a radiopacity superimposed on the roots of the tooth

Eagle syndrome

• Elongation of the styloid process or mineralization of thestylohyoid ligament complex
• Adults, Most commonly unilateral
• Vague, radiated facial pain while swallowing, turning thehead or opening the mouth
• Classic Eagle syndrome – After tonsillectomy
• Stylohyoid syndrome – impinge on the internal or externalcarotid arteries and associated sympathetic nerve fibers

Stafne defect

• An asymptomatic radiolucency below the mandibular canal inthe posterior mandible, between the molar teeth and the angle of the mandible
• Typically well-circumscribed with a sclerotic border
• Mostly unilateral
• Reported in middle-aged and older adults, children is rarelyaffected
• Normal submandibular gland tissue
• No treatment required

Hemihyperplasia

• Asymmetric overgrowth of one or more body parts (right side)
• 2:1 female-to-male predilection
• Asymmetry may be noted at birth
•  The enlargementbecomes more accentuated with age especially atpuberty
• Skin on the affected side: thickened, increasedpigmentation, hypertrichosis, telangiectasias or nevus flemmeus
• Oral: Macroglossia, larger mandibular canal-crowns
• Differentiated from Proteus syndrome, NF1

 

Progressive hemifacial atrophy

• Atrophic changes affecting one side of the face
• ?trophic malfunction of the cervical sympathetic nervoussystem, trauma, hereditary
• Close relationship with localized scleroderma
• Starts during the first 2 decades of life
• Atrophy of the skin and subcut. Affecting the dermatome ofCNV, osseous hypoplasia
• Oral: mouth deviated toward the affected side, unilateralatrophy of the tongue, unilateral posterior open bite, deficient root formationor resorption

Segmental odontomaxillary dysplasia

• Childhood
• Painless, unilateral enlargement of the maxillary bone alongwith fibrous hyperplasia of the overlying gingival soft tissues
• Missing developing maxillary premolars, hypoplastic primaryteeth
• X-Ray: thickened trabeculae-relatively radiopaque, granularappearance

Crouzon syndrome

• Craniosynostosis : premature closing of the cranial sutures
• FGFR2 gene mutation on chromosome 10q26
• Brachy-scapho-trigonocephaly
• Shallow orbit-visual impairment or total blindness
• Headaches, beaten metal skull
• Underdeveloped maxilla

Apert syndrome

• Characterized by craniosynostosis
• FGFR2 gene on chromosome 10q26
• Autosomal dominant, paternal origin
• Tower(clover leaf) skull, ocular proptosis withhypertelorism, visual loss, hypoplastic middle face – mandibular prognathism,open- mouth appearance, syndactyly*, mental retardation, cleft soft palate

Mandibulofacial dysostosis

• Defects of structures derived from the first and secondbranchial arches
• Autosomal dominant
• TCOF1 gene mapped to chromosome 5q32-q33.1
• Hypoplastic zygoma, narrow face, depressed cheeks, coloboma, tongue-shaped sideburns, anomalies ofears, underdeveloped mandible

Pierre Robin syndrome

• Triad: CP, mandibular micrognathia and glossoptosis
• The retruded mandible results in: Posteriordisplacement of the tongue
  

                                Lackof support of the tongue    musculature

                                Airwayobstruction

*             Respiratorydifficulty in supine position noted from birth

*             Thepalatal cleft is often U0shaped and wider than isolated CP

The Temporomandibular System and Temporomandibular Disorders

Temporomandibular disorder or TMD is a broad term referring to problemswith the jaws and their functioning. It is commonly referred to as"TMJ".This system is very complex and problems are caused by avariety of factors. This web page will attempt to give you a general overviewof TMD so you can better understand the problems you may have been having.

The TemporomandibularSystem

The temporomandibularsystem consists of three basic components; the temporomandibular joint or TMJ,the teeth, and the neuromuscular system. 

Muscles of Mastication and TMJ

TMJ- This is the term often used to describe TMD, but itspecifically refers to the joints that work your lower jaw, or mandible. Thesetwo joints are found just in front of the ears. Their close proximity to theear is why some patients experience ear symptoms and can often hear the jointpop or crack. These two joints never act alone, that is, when your jawfunctions, both joints will be working. There is a small cartilage disc betweenyour lower jaw and skull in the joint. Some TMD problems are caused bydysfunction of this disk. When healthy it acts as a sort of "shockabsorber" for the joint.

Teeth- The teeth are like the third leg of a tripod, theTMJ’s being the other two legs. The alignment of your bite and the functioningof the TMJ’s are intimately connected. Problems in any of the three areas mayaffect the other two.

Neuromuscular- This system is the nerves and muscles whichwork the temporomandibular system. It is important to realize that only thelower jaw, or mandible, moves during jaw function. The upper jaw, or maxilla,does not move; it is firmly attached to the skull. Therefore, the nerves andmuscles are involved in moving the lower jaw only. The nerves transmit themessages for the muscles to move the jaw. They also transmit pain signals tothe brain causing you to feel discomfort. The muscles are fairly large and arefound from the side of your head down to your neck. Other related muscles thatdo not specifically work the jaw, but are sometimes symptomatic are found inthe neck, face, and upper back.

What Defines TMD 

A wide spectrum of specific and non specific disorders thatproduce symptoms of pain and dysfunction of muscles ofmastication,Temporomandibular joint and other associated structures.

Symptoms andsigns of TMD can include some or all of the following.

Jaw pain and/or stiffness

Headaches, usually at the temples and side of head

Vague tooth soreness or toothaches which often move around the mouth

Sensitive teeth

Painful or tender jaw joint

Difficulty opening jaw

Pain and fatigue when eating hard or chewy foods

Clicks, pops, or grinding sound in jaw joint

Ear pain

Cervical neck tension and pain

Tooth wear

Diagnostic classification of Temporomandibular Disorders

Congenital or Developmental Disorders

• Aplasia 
• Hypoplasia 
• Hyperplasia 
• Neoplasia

Disc Dearrangement Disorders

• Disc displacement with reduction 
• Disc displacement without reduction

TMJ dislocation

Inflammatory disorders

• Capsulitis/Synovitis 
• Polyarthritides

Osteoarthritis

• Primary osteoarthritis 
• Secondary osteoarthritis

Masticatory Muscle disorders

• Myofacial Pain 
• Myositis 
• Myospasm 
• Myofibrotic contracture 
• Neoplasia

Temporomandibular disorders come in many forms and varyingdegrees of severity. Basically TMD is a problem when you either experience painand/or a loss of jaw function. The pain can range from a mild ache in themorning to a chronic debilitating pain. Loss of function can be mild jawstiffness to being unable to open the jaw barely at all.

The symptoms of TMD can be an obvious jaw pain in themuscles near the mouth, but can also often exhibit as headache at the temples("temporal headache"). This is due to inflammation in the large jawclosing temporalis muscle which is on either side of your head. To find thismuscle place your hands on your temples and clench your teeth hard and you willfeel this powerful muscle contract. Patients often feel this symptom is atension headache or sinus headache but it can be easily differentiated during aTMD exam. Patients understandably (and many doctors) fail to make thisconnection between TMD and headaches.

The pain of TMD can come from either the muscles or the TMjoint itself; often it comes from a combination of the two. The muscles canache due to causes discussed below. Pain in the joint is usually due toinflammation within the structure itself. Sometimes the symptoms are found inother facial structures; such as dull ear pain, toothache, neck pain, etc. Thisreferred pain is fairly common but it is important to rule out medical and/ordental causes of these pains prior to TMD treatment.

Loss of jaw function can be due to muscular and/or jointproblems as well, just as pain can. The degree to which each is involved isdetermined through thorough history and exam.

Causes of TMD

Temporomandibular disorders rarely have a single cause. Anyone of the following factors may contribute to TMD. Each patient presents withan individual combination of factors that are determined during history takingand clinical exam.

Trauma - Acute trauma to the jaws such as a car accident, afall, a punch, etc. can cause damage to the muscles and/or joint. The acutepain and loss of function is usually responsive to conservative treatment.Sometimes trauma to the joint can cause chronic damage which may eventuallycontribute to a TMD problem at a later time.

Bruxism - Bruxism refers to a non functional grinding andclenching of the teeth. Some do this while awake but more often it is donewhile sleeping. Most people grind their teeth while sleeping to some degree.For whatever reason some people do this very hard to the point where they wearthe enamel from their teeth. This bruxing is done by the jaw muscles and by themorning they can be painful due to fatigue. This constant pressure also candamage the TMJs over time. Bruxism is the most common factor found in TMD.

Malocclusion - This term means "bad bite".Sometimes when the teeth do not bite together in harmony with the shape and positionof the joints it can place pressure on the joints. Missing teeth can sometimescontribute to this as well. The misalignment can also put strain on the jawmuscles. This factor can be mild to severe. Though the bite is an importantpart of the whole system it is only altered after conservative measures andonly if it is felt improvement will result. In some patients discrepancies(known as interferences) become apparent after wearing the NTI device for a fewmonths and a bite adjustment is recommended. Treatment of the bite for TMD isusually not needed but its contribution to the whole must be examined.

Emotion - Emotional stress often plays an integral role inthe development of TMD. This occurs due to two basic reasons. Stress increasesboth the severity and duration of bruxism while asleep. Also, many willsubconsciously clench and/or grind their teeth more while awake during times ofstress. The other way stress contributes to TMD is that during times of stressyour adaptability and pain threshold will go down. As a result you are morelikely to experience symptoms of TMD if other factors already exist (bruxing,joint damage, etc.).

Emotional conditions beyond daily life stress can contributeto TMD as well. Depression, anxiety disorders, and the like can often have TMDproblems arise. These conditions are quite stressful and it is not hard toimagine why TMD would develop.

Ergonomic - Your job and how you do it can contribute to TMDand related problems. If you work at a computer all day, for example, you maybe holding your head in such a way that places strain on your TM system.

TMD Treatment

Treatmentplans for TMD are as varied as the patients that present with it. Each patientmust be treated differently depending on the uniqueness of their problems andthe contributing factors. Pain Relief Info.

It is veryimportant to realize that the goal of TMD treatment is to minimize pain andestablish a return to function. TMD conditions are not "cured" butare managed instead. The basic goal is to allow the muscles and joints to healthrough rest and care. Often damage to the joint itself can not be reversed,but the body can often heal it enough to return to function without pain. Wealso want to teach you to recognize the symptoms early and manage them yourselfonce we give you the tools to do so. This condition can often recur later onbut early care can minimize the severity.

The basicphilosophy of treatment is to do the conservative and reversible treatmentsfirst. Irreversible treatments, such as surgery or orthodontics, are onlyconsidered if conservative steps have failed to bring lasting relief. Thesemore radical treatments are rarely used. Most patients respond well to simplercare.

Thefollowing treatment modalities may be used in each case.

Conservativetreatment

• Patienteducation and self care 
• Rest andrelaxation 
• Cognitive behavioralintervention 
• Pharmacotherapy 
• Occlusaltherapy 
• Occlusal therapy 
• Orthopedic appliances 
• Physiotherapy 
• Rehabilitationof Denatal deficits 
• Managementof trigger points

SurgicalTreatment

• Arthrocentesis 
• Arthroscopy 
• Arthroplasty 
• Discectomy 
• Condylectomy

Occlusal Splint - Also called a night guard is designed toprotect the teeth from further wear. These also will reduce the severity ofgrinding at night and allow the muscles to rest. In more severe cases it needsto be worn all day as well to allow the TMJ and muscles to rest.

Anatomy and Physiology of the Salivary Glands and Sialography

Types of salivaryglands

The Major Salivary Glands

• Parotid
• Submandibular
• Sublingual

The Minor SalivaryGlands

 

Embryology

• 6th-8th Weeks ofGestation
• Parotid
• First to develop
• Last to becomeencapsulated
• Autonomic NervousSystem Crucial

Anatomy of ParotidGland

• Wedge shaped with 5processes
• 3 Superficial
• 2 Deep
• Parotid Compartment
• Superior – Zygoma
• Posterior – EAC
• Inferior – Styloid,ICA, Jugular Veins
• 80% overlies
• Masseter &Mandible
• 20% Retromandibular
• Stylomandibular,Tunnel,Isthmus of Parotid
• Tail of Parotid

Parapharyngeal Space

• Prestyloid Compartment
• PoststyloidCompartment (Paragangliomas)

Stensen’s Duct

• Arises from anteriorborder
• 1.5 cm inferior toZygomatic arch
• Pierces Buccinator at2nd Molar
• 4-6 cm in length
• 5 mm in diameter

Parotid Capsule

• Superficial layer DeepCervical Fascia
• Superficial layer
• Deep layer

 

CN VII-Facial nerve

• 2 Surgical zones
• 3 Motor branches
• immediately
• Pes Anserinus – 1.3 cm
• Temperofacial Division
• Cervicofacial Division
• 5 Terminal branches

Localization of CN VII

• Tragal pointer
• Tympanomastoid suture
• Posterior bellyDigastric
• Styloid process
• Retrograde dissection
• Mastoidectomy

• Great Auricular nerve
• Auriculotemporal nerve
• Superficial Temporalvessels
• Frey’s Syndrome

Neural compartment-VII, Great Auricular,Auriculotemporal

Venous compartment-Retromandibular vein

Arterial compartment-SuperficialTemporal/Transverse Facial

Lymphatics

• Paraparotid &Intraparotid nodes
• Superficial & DeepCervical nodes

Submandibular Gland-Anatomy

 

• The ‘Submaxilla’
• Submandibular Triangle
• Mylohyoid ‘C’
• Marginal Mandibular branch
• Capsule fromsuperficial layer of Deep Cervical fascia

Wharton’s duct

• Exits medial surface
• Between Mylohyoid &Hyoglossus
• 5 cm in length
• Lingual nerve & CNXII

Innervation

Superior CervicalGanglion (symp)

Submandibular Ganglion(para)

Artery: Submentalbranch of Facial a.

Vein: Anterior Facial Vnerve.

Lymphatics: DeepCervical and Jugular chains

Facial artery nodes

Between Mandible &Genioglossus

No capsule

Ducts of Rivinus +/-Bartholin’s duct

Sialogram not possible

Innervation: Same asSubmandibular

Artery/Vein: Sublingualbranch of Lingual & Submental branch of Facial

Lymphatics:Submandibular nodes

Minor Salivary Glands

• 600-1,000
• Simple ducts
• Buccal, Labial,
• Palatal, Lingual
• Tumor sites:
• Palate, upper lip,cheek
• Lingual & Palatinenn.

Imaging of SalivaryGland-Important things to remember

• CT – Inflammatory
• MR – Tumor
• Children: U/S & MR
• NO sialogram duringactive infection
• Parotid is fatty

The Secretory Unit

• Acinus (serous, mucous,mixed)
• Myoepithelial cells
• Intercalated duct
• Striated duct
• Excretory duct

Microanatomy of Salivary glands

• Striated &Intercalated ducts well developed in serous, NOT mucous glands
• Striated duct: HCO3into, Cl from lumen
• Intercalated duct: Kinto lumen, Na from lumen, producing hypotonic fluid
• Excretory ducts do NOTmodify saliva

 

The Bicellular Theory

• Intercalated duct
• Excretory duct

The Multicellular Theory

Parotid: serous &fatty

Submandibular: mixed serous

Sublingual: mixed mucous

Stroma: Plasma cells

Function of Saliva

1. Moistens oral mucosa
2. Moistens & cools food
3. Medium for dissolvedfood
4. Buffer (HCO3)
5. Digestion (Amylase,Lipase)
6. Antibacterial (Lysozyme, IgA, Peroxidase, FLOW)
7. Mineralization
8. Protective Pellicle

 

Effects of Salivaryhypofunction

• Candidiasis
• Lichen Planus
• Burning Mouth
• Aphthous ulcers
• Dental caries
• Xerostomia not reliable

 

Production of Saliva

• Primary secretion
• Ductal secretion
• The “secretory potential”
• (hyperpolarizes)
• Increased flow rate yieldsdecreased
• hypotonicity & K

Autonomic Innervation

Parasympathetic

• Abundant, waterysaliva
• Amylase down

Sympathetic

• Scant, viscous saliva
• Amylase up

Salivary Flow

• 1-1.5 L/day (1 cc/min)
• Unstimulated state
• Submandibular
• Stimulated state
• Parotid
• Sublingual & minor
• Mucin

Effects of Aging

Total salivary flowindependent of age

Acinar cellsdegenerate with age

Submandibular glandmore sensitive to metabolic/physiologic change

Unstimulated salivaryflow more greatly affected by physiologic changes

Sialography

Radiologic examinationof the salivary glands

The submandibular andparotid glands are investigated by this method

The sublingual glandis usually not evaluated this way-Difficulty incannulation

Indications

• Ductal obstruction-Stonesor tumors
• Inflammation of a ductor gland

Contraindications

• Severe infection of agland
• Known allergies tocontrast media

Equipment

• Fluoroscopic unitw/spot film capabilities
• Cannula forintroducing contrast
• Connecting tubing
• Lemons
• Dilators for duct
• 5 mL syringe
• Overhead light
• Gauze
• Contrast

Preliminary andProcedure Radiographs

• Parotid-Tangential
• Perpendicular tocassette, directed to lateral surface of mandibular ramus
• Submandibular-Lateral
• Perpendicular tocassette, directed to 1 in. superior to mandibular angle to demonstrate parotidgland

• Inferior margin ofmandibular angle to demonstrate the submandibular gland

Patient Preparation

1. Thorough explanationof examination
2. Any removable dentalwork, jewelry, and other artifact causing opaque items must be removed
3. Consent must be signed

Procedure

• The patient firstsucks on a lemon wedge to open the ducts
• An overhead lamp isused to provide adequate light
• The duct iscannulated, not punctured, and contrast is introduced with fluoroscopicguidance
• Radiographs are obtained
• After the radiographs,the patient then sucks on a lemon wedge to evacuate the contrast
• Obtain post-procedureradiographs as indicated

Lateral Parotid GlandRadiograph

 

Lateral SubmandibularGlands