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OTORHINOLARYNGOLOGY
SYMPOSIUM
DEPARTMENT OF ENT
CHENGLEPET MEDICAL COLLEGE
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OVERVIEW OF SINUSITIS COMPLICATIONS
INTRACRANIAL COMPLICATIONS
ORBITAL COMPLICATIONSVASCULAR COMPLICATIONS
OSTEOMYELITIS
ASTHMA
LOSS OF SMELL AND TASTE
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COMPLICATIONS OF SINUSITIS
CAVERNOUS SINUS THROMBOSIS
MENINGITIS
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Cavernous sinus communicates with the valveless facial veins,Cavernous sinus communicates with the valveless facial veins,
pterygoid plexus, lateral sinus, IJV.pterygoid plexus, lateral sinus, IJV.
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CAVERNOUS SINUS THROMBOSIS
NASAL SINUSES
ORBIT AND EYEBALL
DANGER TRIANGLE OF FACE
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CLINICAL HISTORY
NON SPECIFIC
MID FACE INFECTION,FURUNCLE IS COMMON
HEADACHE
SHARP,PROGRESSIVELOCALISED TO OPTHALMIC AND MAXILLARY N
ORBITAL PAIN AND FULLNESS
BLURRED VISION-DIPLOPIA
PERIORBITAL OEDEMA
UNILATERAL BECOMIN BILATERAL IN 24-48HRS
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PHYSICAL FINDINGS
1. PERIORBITAL OEDEMA
2. LATERAL GAZE PALSY
3. PTOSIS, MYDRIASIS AND EYE MUSCLE WEAKNESS
4. CHEMOSIS
5. EXOPHTHALMOS AND OPTHALMOPLEGIA
6. SLUGGISH PUPIL RESPONSE AND DEC. VISUAL ACUITY
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1. HYPER OR HYPOAESTHESIA OF V1,V2 BARNCHES OF V TH
NERVE
2. APPEARANCE OF SIGNS IN CONTRALATERAL EYE
3. NUCHAL RIGIDITY AND BRUDZINSKI SIGNS
4. SEPSIS- CHILLS ,FEVER ,SHOCK
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TREATMENT
Critical medical emergency
Intravenous antibiotics
Cefotaxime 1.5 to 2 g IV q4h
Metronidazole 15 mg/kg load followed by 7.5 mg/kg IV q6hvancomycin in methicillin resistant organisms
Remove septic focus from sinuses
Steroids-hydrocortisone
ANTICOAGULATION
Based on limited observation, anticoagulation may be beneficial after
exclusion of hemorrhagic complications by CT scan. [1] [2] [13]
Anticoagulation is thought by some to be dangerous in patients with
bilateral CST and/or concurrent intracranial hemorrhage.
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PROGNOSIS
100 % mortality prior to antimicrobials
30 % now
Morbidity-1/6 th have decreased vision
-half of them have cranial nerve deficits
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Acute purulent infection within subarachnoid space
Bacterial meningitis commonly
Mostly spreads from the ethmoid and sphenoid sinuses
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EPIDEMIOLOGY
Strep.pneumoniae 50 %
N.meningiditis-25%
Group b streptococci-15 %
Listeria monocytogenes-10%
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1. bacterial colonisation
2. Transport across epithelial cells3. Transport in blood stream
4. Intraventricular choroid plexus
5. S.pneumoniae-affinity for cerebral capillary endothelium
6. CSF-decreased leucocytes,complement and IG
7. Host immune response
8. Bacterial degradation products are released9. Inflammatory reaction
10.purulent
PATHOGENESIS
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CLINICAL PRESENTATION
Classical triad-fever,headache,nuchal rigidity
Seizures-focal or generalised
Raised ICP features-Kernigs sign and brudzinskis sign
Maculopapular rash
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DIAGNOSISclinical diagnosis
blood and csf cultures can be taken
Lumbar spinal puncture
aseptic precaution sCT and Fundoscopy prior to CSF tap
l3 and l4 vertebrae for 4 to 6 cms
CSF escapes at the rate of 1drop/sec
if pressure is raised it escapes as a jet
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CSF findings
Increased opening pressure
WBC count> 1000 per cu.mm
DLC count predominance of polymorphonuclear lymphocytes
Protein- mild to marked elevation
CSF glucose is decreased
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TREATMENT
Start empirical antibiotic therapy wit cephalosporins & metroinidazole
1. Specific antimicrobial therapy
2. Pneumococcal-cephalosporins & vancomycin
3. Listeria-ampicillin &gentamycin4. Staphylococcal-vancomycin &nafcillin
5. Gram ve bacteria-3rd generation cephalosporins
6. Meningococcal-penicillin&icillin
ADJUNCTIVE THERAPY
Dexamethasone To decrease ICP
-tilt head at 30 to 45
-intubate
-hyperventilate
-iv mannitol
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