Acute Sinusitis

Acute Sinusitis
Presentation by:Michael E. Prater, MD
Francis B. Quinn, MD

ANATOMY

* There are four paired paranasal sinuses, the maxillary, ethmoid, frontal and sphenoid sinuses
* “Anterior” and “posterior” sinuses
* Lining of the sinuses is pseudostratified, columnar epithelium (respiratory epithelium) which is continuous with the nasal epithelium
* The muocsa secretes a mucous which traps bacteria
* The mucous is naturally extruded through sinus ostia to be expectorated or swallowed
* The drainage of the maxillary and frontal sinuses follows a circular pattern through the natural ostia

The Ethmoid Sinus
The Maxillary Sinuses
Frontal Sinus
Sphenoid Sinuses
Pathophysiology of Sinusitis

* Lined by respiratory epithelium
* Mucous blanket is in two layers: a superficial viscous layer and an underlying serous layer.
* Cilia beat in the serous layer, moving the blanket towards the natural ostia
* Normal function depends on patent ostia, ciliary function and quality of mucous
* Most important pathologic process in disease is obstruction of natural ostia
* Obstruction leads to hypooxygenation
* Hypooxygenation leads to ciliary dysfunction and poor mucous quality
* Ciliary dysfunction leads to retention of secretions
* Local factors can impair ciliary function. Cold air “stuns” the epithelium, resulting in retained secretions. Dry air dessicates the blanket.
* Anatomical factors, ie, polyps, tumors, foreign bodies and rhinitis, block the ostia
* Kartagener’s Syndrome (immotile cilia syndrome)
* Acute sinusitis is defined as disease lasting less than one month
* Subacute sinusitis is defined as disease lasting 1 to 3 months
* Chronic sinusitis is defined as disease lasting more than three months, and is usually due to inadequately treated acute or subacute disease
* Acute sinusitis and subacute sinusitis are treated medically
* Chronic sinusitis is considered irreversible by medical therapy alone, and it is currently believed oxygenation of the sinuses through opening of the ostia is the primary treatment

History and Physical Exam

* Acute sinusitis presents as pain over infected areas, with or without headache
* Pain to palpation is common with anterior sinusitis, but is usually absent with the posterior sinuses
* Posterior sinuses present as bitemporal or vertex headaches
* Fever, malaise, nasal discharge present
* Chronic sinusitis usually seen with a mucopurlent discharge, but fever is usually not present
* Acute sinusitis is often imposed on chronic disease
* Note any facial edema, tenderness, mucosal edema, septal perforations and deviations
* Diagnosis is primarily clinical, but radiographs can be used
* Transillumination of the sinuses can sometimes be used, but due to differences in sinus size and patency , these tests are not reliable
* Antral lavage can be performed in select cases where the diagnosis is in doubt

Acute Bacterial Sinusitis
Acute Fungal Sinusitis
Complications: Mucoceles
Complications: Orbital
Complications: Cavernous Sinus Thrombosis
Complications: Intracranial
Radiology
Radiology: Plain Films

Acute Sinusitis.ppt

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Carotid Cavernous Fistula

Carotid Cavernous Fistula
Presentation by: Laura S Gilmore, MD
Department of Ophthalmology, TTUHSC

Discussant: Kenn Freedman, MD

Case Presentation

* 26yo AAM s/p MVA
* CHI, L zygoma fracture
* Consulted for proptotic, red OS
* CT: proptosis OS. No basilar skull fracture. no retrobulbar hematoma, no superior ophthalmic vein enlargement, no ocular muscle enlargement

Differential Diagnosis

Cavernous Sinus Thrombosis
* Retrobulbar Hematoma
* Unrecognized intra-orbital FB, with possible cellulitis
* Carotid Cavernous Sinus Fistula
* Tumor

Physical Exam

* General: sedated, intubated
* Lids: edematous, margins intact
* Pupils: 2.5mm->2mm, 7->NR
* Conj: chemosis, OS>OD; SCH OS
* IOP: 16, 28
* Cornea 2+ edema OS, clear OD
* + gross proptosis OS
* + bruit OS on auscultation, no neck bruit
* DFE: discs flat with sharp edges, vessels normal, retina flat OU

MRI of CC Fistula
Carotid Cavernous Fistula

* Abnormal communication between previously normal carotid artery and cavernous sinus
* Characterized as:

-Direct vs. Indirect
-High vs. Low Flow
-Traumatic vs. Spontaneous

Types of CC Fistula
Mechanisms of CCSF

* Trauma
* Spontaneous causes:
o rupture of intracavernous aneurysms
o neurofibromatosis
o atherosclerotic disease
o collagen vascular disease
* Iatrogenic

Direct Carotid Cavernous Fistula

* Arterial blood passes directly through a defect in the wall of intracavernous portion of ICA
* Blood in vein becomes arterialized
* Venous pressure increases
* Arterial pressure and perfusion decreases

Signs of Direct CCSF

* Ptosis
* Very red, chemotic conj
* Increased IOP from increased episcleral venous pressure
* Anterior segment ischemia in 20%
o Corneal edema, cell/flare, iris atrophy, rubeosis, cataract
* Proptosis is pulsatile
* Bruit and thrill
* Muscle palsies
* Visual loss

Etiologies of Direct CCSF

* From trauma in 75% of all cases
o Basal skull fracture tears ICA within cavernous sinus
o Traumatic fistulae-high flow rates, sudden and dramatic onset of symptoms
* Spontaneous rupture of aneurysm or atherosclerotic artery in 25%
o Post-menopausal, hypertensive females
o Lower flow rates, less severe symptoms


Mechanisms of Traumatic CCSF

* direct injury from basilar skull fracture
* injury from torsion or stretching of the carotid siphon upon impact
* impingement of the vessel on bony prominences

Indirect Carotid Cavernous Fistula

* Fistulous connection is within the wall of the cavernous sinus
* Tend to be low-flow
* Small meningeal arteries supplying dural wall of cavernous sinus can rupture spontaneously, while ICA itself remains intact
* Insidious onset, mild orbital congestion, proptosis, low or no bruit
* Lesions may fluctuate, and may resolve spontaneously

Clinical Presentation of CCSF

* Ophthalmic consequences of CCSF are caused by compression and ischemia related to increased venous pressure and reduced arterial pressure
o flow reversal leads to engorged ophthalmic veins causing proptosis, conjunctival injection, chemosis.
o Patients complain of retro-orbital headache, or a bruit. Facial pain with V1 and V2 involvement
* Other manifestations:
o congestion of the opposite orbit
o diplopia
o ptosis, mydriasis
o corneal ulceration
o loss of visual acuity
o transient neurological deficits
o subarachnoid hemorrhage

Radiological Evaluation of CCSF

* Angiography is the definitive diagnostic examination
* CT and MRI may show
o Enlarged superior ophthalmic vein
o Enlarged muscles
o Enlarged cavernous sinus with a convex shape to the lateral wall

Treatment of CCSF

* Most are not life-threatening
o Only involved eye is at risk typically
* Main indicators for treatment
o Glaucoma
o Diplopia
o Intolerable bruit or HA
o Severe proptosis causing exposure keratopathy
o Spontaneous closure from thrombosis of cavernous sinus is unlikely (as in trauma, high-flow)

Treatment of CCS Fistulas

* 99% of treatment is done by interventional neuroradiologists
o Intravascular approach-placement of thrombogenic materials, eg coils
* Other therapies include:
o carotid artery ligation
o surgical exposure with clipping of the fistula

Summary

* Direct CCSF usually results from trauma
* Patients typically present with proptosis, conjunctival injection, and a bruit
* Angiography when pt stable
* Transarterial embolization

Carotid Cavernous Fistula.ppt

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Restorative Materials in Pediatric Dentistry

Restorative Materials in Pediatric Dentistry
Presentation by: S.Lal, DDS
Course Director

Preventive Materials
• Fluoride gels, foam and varnish:
• Used for remineralisation of decalcified enamel and incipient caries.
• Sealants:
• Indicated for preventing and arresting incipient lesions.
• Available as clear or white, filled or unfilled, containing Fluoride or not.

Resin based composites(RBC)
Resin matrix (Bis-GMA) with inorganic filler particles.
1. Filler content-
Filled vs Unfilled
Flowable vs packable
Anterior vs posterior composite
• Particle size-
• macro, microfilled and hybrids


Resin Restorations
• Steps:
• Etch, wash, dry or dessicate?
• Enamel and Dentin adhesives
• Composite selection and placement
• Curing tools and techniques
• Disadvantages:
• Polymerization shrinkage
• Technique sensitive
• Performance of posterior composites in large, stress bearing preparations is questionable

Dentin/Enamel adhesives in Pediatric Dentistry
• Dentin bonding agents or Primers:
• Smear layer
• Etch
• Hydrophillic and hydrophobic component (HEMA)
• Enamel adhesives or bonding agents:
• Hydrophobic resin such as Bis-GMA
• Hybrid layer- copolymerized layer of primer, bonding resin and collagen

Dentin/Enamel adhesives in Pediatric Dentistry
• 3-step total etch
• Total etch using prime and bond
• Self etch primers with bonding agent
• All-in-one adhesives e.g.- prompt L-pops

Glass Ionomer cements
• Fluorosilicate glass powder(base) combined with a water soluble polymer(acid)
e.g. - Ketac cement
• Resin-modified glass ionomer cements:
are glass ionomers with a light polymerised resin component.
e.g.- Vitrebond and Vitremer
Resin-modified glass ionomers
Advantages:
• Increased mechanical properties
• Physiochemically bonds to tooth structure
• Biocompatible, moisture forgiving
• Similar coefficient of thermal expansion as dentin therefore a good dentin replacement material. (sandwich technique)
• Ion lechability - Fluoride release(anticariogenic action)
• Minimal polymerization shrinkage

Compomers
• Polyacid-modified, resin based composite with fluoride releasing glass fillers.
e.g.- compoglass, dyract
• Better results after etch and bond
• Good mechanical properties and polishability

Amalgam
• No polymerization shrinkage
• Moisture forgiving
• Excellent mechanical properties
• Mercury toxicity
• Esthetics


Research trends
• Polymerization shrinkage
• Mechanical properties
• More ‘forgiving’ materials
In summary….
“ Primary teeth are a temporary dentition with known life expectancies of each tooth. By matching the ‘right’ restoration with the expected lifespan of the tooth, we can succeed in providing a ‘permanent’ restoration that will never have to be replaced.”
Restorative Materials in Pediatric Dentistry.ppt

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