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INFECTIOUS
RHINOSINUSITIS
References-
•Cummings Otolaryngology Head & Neck Surgery 6th edition
•Scott-brown’s Otolaryngology, Head & Neck Surgery 7th edition
•Infectious Diseases Society of America (IDSA) Guideline for ABRS: CID. March 20, 2012
•European Position Paper on Rhinosinusitis and Nasal Polyps(EPOS) March 2012
Dr Vikas
 Rhinosinusitis is a group of disorders characterized
by inflammation of the lining of the nose and
paranasal sinuses.
 The ciliated respiratory mucosal lining of the nose
and paranasal sinuses are contiguous and it would
be rare for one to be affected without the other.
Scott-brown
Pathophysiology
 Acute rhinosinusitis develops in conjunction with an acute viral upper
respiratory tract infection.
 Occur more commonly in predisposed individuals
 The infection results in mucosal swelling with occlusion or
obstruction of the sinus ostia.
 A reduction in oxygen tension occurs which can reduce mucociliary
transport and transudation of fluid into the sinuses.
 The inflammation also results in changes in the mucous that
become more viscous and alterations in cilia beat frequency often
occurs.
 These changes in the nasal-sinus environment lead to mucostasis
and bacterial colonization.
 If the sinuses remain obstructed or the mucociliary. transport system
does not return to normal, a bacterial infection can ensue.
Scott-brown
Classification of infectious rhinosinusitis
Report of the Rhinosinusitis Task Force Committee Meeting. Otolaryngology and Head and Neck Surgery. 1997; 117:
51-68.
Conventional Criteria for Diagnosis of Sinusitis
Based on Presence of at Least 2 Major or 1 Major and 2 Minor Symptoms
IDSAGuideline for ABRS: CID.March 20, 2012
 Acute rhinosinusitis-
◦ Acute onset of symptoms
◦ Duration of symptoms < 4
weeks
◦ Symptoms resolve
completely
◦ Streptococcus
pneumoniae (20%-45%)
and Haemophilus
influenzae (22%-35%) are
the predominant
organisms in adults,
whereas
◦ S. pneumoniae (30%-
43%), H. influenzae (20%-
28%), and Moraxella
catarrhalis (20%-28%) are
the predominant
organisms in children
 Subacute rhinosinusitis
◦ Duration of symptoms >4 weeks to < 12 weeks
◦ Pathogens are same as ARS
 Recurrent acute rhinosinusitis
◦ 4 or more episodes of acute rhinosinusitis per year, with each
lasting longer than 7 to 10 days,
◦ Complete recovery between attacks
◦ Symptom-free period of > 8 weeks between acute attacks in
absence of medical treatment
◦ Bacteriology and pathophysiology would be similar to those of
individual episodes of ABRS
Chronic rhinosinusitis
 Duration of symptoms> 12 weeks
 Persistent inflammatory changes on imaging > 4 weeks after
starting appropriate medical therapy
 no intervening acute episodes
 Unlike for ABRS, the role of bacteria in CRS is not well supported
 CRS is an inflammatory disease, and it may or may not involve
pathogenic microbes.
 Therefore, bacteria, fungi or viruses may be involved in some
cases
 In those patients with CRS who do have potential pathogenic
bacteria, the most common organisms are Staphylococcus
species (55 percent) and Staphylococcus aureus (20 percent).
 Some studies have shown a high prevalence of
Enterobacteriaceae organisms, anaerobes, Gram-negative
bacteria and fungi.
Acute exacerbations chronic rhinosinusitis
 AECRS is a sudden worsening of the baseline CRS symptoms or
appearance of new symptoms
 Complete resolution of acute (but not chronic) symptoms between episodes
 There may be a change in the bacteriology of the disease
Acute Rhinosinusitis
Acute rhinosinusitis in adults
 Inflammation of nose and paranasal sinuses
 ≥ 2 symptoms, one of nasal
blockage/obstruction/congestion or nasal discharge
(ant/post nasal drip):
 ± facial pain/pressure
 ± reduction or loss of smell
EPOS March 2012
 And either
endoscopic signs of:
◦ nasal polyps, and/or
◦ mucopurulent discharge from middle meatus and/or
◦ edema/mucosal obstruction in middle meatus
 and/or
◦ CT changes:
◦ mucosal changes within ostiomeatal complex and/or
sinuses
 For <12 weeks
4/26/12
Acute rhinosinusitis in children
 Inflammation of nose and paranasal
sinuses
 ≥ 2 symptoms one of nasal
blockage/obstruction/congestion or
nasal discharge (ant/post nasal drip):
 ± facial pain/pressure
 ± cough
EPOS March 2012
Acute rhinosinusitis in children
 And either
 endoscopic signs of:
 nasal polyps, and/or
 mucopurulent discharge from middle meatus and/or
 edema/mucosal obstruction in middle meatus
And/or
 CT changes:
 mucosal changes within the ostiomeatal complex and/or sinuses
 For < 12 weeks
EPOS March 2012
Severity of disease in adult and children
 Define disease severity:
 Mild: VAS 0-3
 Moderate: VAS 4-7
 Severe: VAS 8-10
Acute rhinosinusitis can be divided into CommonCold
and post- viral rhinosinusitis. A small subgroup of post-viral
rhinosinusitis is caused by bacteria (ABRS).
EPOS March 2012
Classification of ARS in
adult/children
 Common cold/ acute viral rhinosinusits :
◦ duration of symptoms for< 10 d
 Acute post-viral rhinosinusitis:
◦ increase of symptoms after 5 d or persistent symptoms after 10 d with < 12 wk
duration.
 ABS: ≥ 3 symptoms/signs
◦ Discoloured discharge (unilat predominance) and purulent secretion in nasi
◦ Severe local pain (unilat predominance)
◦ Fever (>38 °C)
◦ Elevated ESR/CRP
◦ ‘Double sickening’ (deterioration after initial milder of illness)
EPOS March 2012
Signs ofABS
At least 3 of:
-Discoloured d/c
-Severe local pain
-Fever
-Elevated ESR/CRP
-Double sickening
Postviral acute rhinosinusitis
Increase in symptoms after 5 d
Persistent symptom after 10 d
EPOS March 2012
Any of following clinical presentations are recommended for
identifying patients with acute bacterial vs viral rhinosinusitis
 Onset with persistent S/S compatible with ARS ≥ 10 d without any
evidence of clinical improvement.
 Onset with severe S/S of high fever ≥ 39 °C and purulent nasal
discharge or facial pain at least 3–4 consecutive d at beginning of
illness.
 Onset with worsening S/S characterized by new onset of fever,
headache, increase in nasal discharge following typical viral URI
that lasted 5–6 d and were initially improving (‘‘doublesickening’’).
IDSAGuideline for ABRS: CID.March 20, 2012
Associated Factors
◦ Environmental Exposures( dampness in home ,air
pollution, irritants)
◦ Anatomical factors
 septal deviation, paradoxical turbinate; nasal polyps, and choanal
obstruction by benign adenoid tissue, or odontogenic sources of
infection
◦ Allergy
 individuals with allergies have a higher incidence of
developing both acute and chronic rhinosinusitis
EPOS March 2012
◦ Ciliary impairment
 Ciliary function diminished during viral and bacterial rhinosinusitis.
 Exposure to cigarette smoke and allergic inflammation has been
shown to impair ciliary function.
 Impaired mucociliary clearance in Allergic Rhinitis patients
predisposes patients to ARS
◦ Primary Ciliary Dyskinesia
◦ Smoking
◦ Laryngopharyngeal reflux
 Pacheco-Galvan et al. 1997-2006 have shown significant associations between
GERD and sinusitis.
 Recent systematic review, Flook and Kumar showed only poor association
between acid reflux, nasal symptoms, and ARS
EPOS March 2012
◦ Anxiety and depression
 Poor mental health, anxiety, or depression is associated with susceptibility
to ARS
 Mechanisms are unclear.
◦ Drug resistance
◦ Concomitant Chronic Disease
 Concomitant chronic disease (bronchitis, asthma, CVS disease, DM,) in
children has been associated with increased risk of developing ARS
secondary to influenza.
◦ Iatrogenic factors
 Including surgery, medications, nasal packing or nasogastric tube
placement. EPOS March 2012
Pathophysiology
 Acute rhinosinusitis develops in conjunction with an acute viral upper
respiratory tract infection.
 Occur more commonly in predisposed individuals
 The infection results in mucosal swelling with occlusion or
obstruction of the sinus ostia.
 A reduction in oxygen tension occurs which can reduce mucociliary
transport and transudation of fluid into the sinuses.
 The inflammation also results in changes in the mucous that
become more viscous and alterations in cilia beat frequency often
occurs.
 These changes in the nasal-sinus environment lead to mucostasis
and bacterial colonization.
 If the sinuses remain obstructed or the mucociliary. transport system
does not return to normal, a bacterial infection can ensue.
Scott-brown
Investigations
Bacterial Culture
 Microbiological investigations are not required for diagnosis of
ARS in routine practice. ( EPOS March 2012)
 May be required in research settings, or in atypical or
recurrent disease
 Maxillary sinus tap with culture is the gold standard for the
diagnosis of ABRS,
 There is increasing interest in the role of endoscopic-guided
middle meatal cultures, but their reliability in children has not
been established
 Nasopharyngeal cultures are unreliable and are not
recommended for microbiologic diagnosis of ABRS
 Current accepted reference standard for culture is more than
10,000 colony forming units (CFU)/mL in sinus aspirate.
IDSA Guideline for ABRS: CID.March 20, 2012
Nasal endoscopy
 Nasal endoscopy may be used to
 visualize nasal and sinus anatomy
 provide biopsy and microbiological samples.
 confirm drainage
 Evaluate treatment response
EPOS March 2012
C-Reactive Protein (CRP)
 Raised in bacterial infection.
 ARS: low or normal CRP may identify low
likelihood of positive bacterial infection
 Limiting unnecessary antibiotic use.
 CRP levels are significantly correlated with
changes in CT scans.
EPOS March 2012
ESR
 ESR levels correlated with CT changes
in ARS
 ESR >10 is predictive of sinus fluid levels
or sinus opacity on CT scan.
 Raised ESR is predictive of positive
bacterial culture on sinus puncture or
lavage
EPOS March 2012
Procalcitonin
 Indicates More severe bacterial
infection
 There is no evidence of its
effectiveness as a biomarker in ARS.
EPOS March 2012
Nasal Nitric Oxide (NO)
 Sensitive indicator of presence of
inflammation and ciliary dysfunction.
 Very low levels: primary ciliary
dyskinesia, significant sinus obstruction.
 Elevated levels: inflammation provided
ostiomeatal patency maintained
EPOS March 2012
Imaging
 CT scan
◦ Modality of choice to confirm extent of pathology and
anatomy.
◦ Very severe disease, immuno-compromised pt, suspicion
of complications.
◦ Routine CT scan in ARS little useful information
 Plain sinus X Rays
◦ Insensitive & limited usefulness
 Ultrasound
◦ Insensitive & limited usefulness
EPOS March 2012
XVII. Which Imaging Is Most Useful for Severe
ABRS who suspected to have Suppurative
complication?
 CT rather than MRI is recommended to
localize infection and to guide further
treatment.
IDSAGuideline for ABRS: CID.March 20, 2012
Algorithm for the management of acute bacterial rhinosinusitis
IDSAGuideline for ABRS: CID.March 20, 2012
Algorithm for the management of acute bacterial rhinosinusitis
IDSAGuideline for ABRS: CID.March 20, 2012
Algorithm for the management of acute bacterial rhinosinusitis
IDSAGuideline for ABRS: CID.March 20, 2012
CHRONIC
RHINOSINUSITIS
Definition
 Chronic Rhinosinusitis (with or without NP) in
adults
 ≥ 2 symptoms
 one of which should be either nasal
blockage/obstruction/congestion or nasal
discharge(ant/post drip) or
 ± Facial pain/pressure
 ± reduction or loss of smell
for ≥12 weeks
EPOS 2012
 CRSwNP: bilateral, endoscopically
visualised polyps in middle meatus.
 CRSsNP: no visible polyps in middle
meatus
Definition
EPOS 2012
CRS in children
 ≥ 2 symptoms
◦ one of which should be either nasal
blockage/obstruction/congestion or nasal
discharge(ant/postnasal drip) or
◦ ± Facial pain/pressure
◦ ± Cough
 for ≥12 weeks
EPOS 2012
Factor associated with CRS
 Ciliary impairment
 Allergy
 Asthma
 Aspirin sensitivity
 Immunocompromised state
 Genetic factor
 Pregnancy and endocrine state
 Local host factor
 Biofilm
 Environmental factor
 Iatrogenic factor
 H.pylori and laryngopharyngeal reflux
 Osteitis
Pathophysiology
Scott-brown
 The role of allergies has been strongly
suggested but not proven
 Antigen-antibody reactions result in the
release of histamine and other mediators of
inflammation.
 These mediators cause changes in vascular
permeability, destabilization of lysosomal
membranes and other reactions that produce
inflammation, mucosal swelling and ostia
obstruction
Pathophysiology
Scott-brown
 Many cells and proteins that are involved with inflammatory
response have been implicated and are being investigated to
their roles in rhinosinusitis, particularly CRS.
 These include, but are not limited to, eosinophils, neutrophils,
mast cells, T and B celis, immunoglobulins, interleukins,
tumour necrosis factor, major basic protein and a number of
other mediators of inflammation.
 Other factors have also been identified that may play a role
in the development or perpetuation of CRS, including,
superantigens, biofilms and osteitis.
•Superantigens are
exotoxins that are
able to activate T
lymphocytes
Immune barrier hypothesis of CRS
EPOS 2012
 Biofilms
◦ Artificial or damaged biologic surface that formed
communicating organization of microorganisms surrounded
by a glycocalys
◦ Biofilms is relatively impervious to antibiotics and is never
eradicated
◦ Mechanical debridement- the only way to resolve biofilms
 Osteitis
◦ Inflammatory bone changes were noted on
contralateral side in 52% of the animals (Khalid et al.
laryngoscope 2002)
Eosinophilic and noneosinophilic form of sinusitis
Spencer C et al. J Allergy Clin Immunol 2011;128:710-20
Mucosa in CRS characterized by basement membrane thickening, goblet cell
hyperplasia, subepithelial edema, and mononuclear cell infiltration with few
eosinophils
Middleton’s Allergy,principal & practice. Seventh edition.
Numerous subepithelial eosinophils in luminal compartment
of early-stage polyp.
Middleton’s Allergy,principal & practice. Seventh edition.
Eosinophils accumulated subepithelially and diffusely
in tissue of mature polyp.
Middleton’s Allergy,principal & practice. Seventh edition.
Type of CRS
Stepwise evaluation of CRS
EPOS 2012
EPOS 2012
EPOS 2012
THANK YOU

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Infectious rhinosinusitis

  • 1. INFECTIOUS RHINOSINUSITIS References- •Cummings Otolaryngology Head & Neck Surgery 6th edition •Scott-brown’s Otolaryngology, Head & Neck Surgery 7th edition •Infectious Diseases Society of America (IDSA) Guideline for ABRS: CID. March 20, 2012 •European Position Paper on Rhinosinusitis and Nasal Polyps(EPOS) March 2012 Dr Vikas
  • 2.  Rhinosinusitis is a group of disorders characterized by inflammation of the lining of the nose and paranasal sinuses.  The ciliated respiratory mucosal lining of the nose and paranasal sinuses are contiguous and it would be rare for one to be affected without the other.
  • 4. Pathophysiology  Acute rhinosinusitis develops in conjunction with an acute viral upper respiratory tract infection.  Occur more commonly in predisposed individuals  The infection results in mucosal swelling with occlusion or obstruction of the sinus ostia.  A reduction in oxygen tension occurs which can reduce mucociliary transport and transudation of fluid into the sinuses.  The inflammation also results in changes in the mucous that become more viscous and alterations in cilia beat frequency often occurs.  These changes in the nasal-sinus environment lead to mucostasis and bacterial colonization.  If the sinuses remain obstructed or the mucociliary. transport system does not return to normal, a bacterial infection can ensue. Scott-brown
  • 5. Classification of infectious rhinosinusitis Report of the Rhinosinusitis Task Force Committee Meeting. Otolaryngology and Head and Neck Surgery. 1997; 117: 51-68.
  • 6. Conventional Criteria for Diagnosis of Sinusitis Based on Presence of at Least 2 Major or 1 Major and 2 Minor Symptoms IDSAGuideline for ABRS: CID.March 20, 2012
  • 7.  Acute rhinosinusitis- ◦ Acute onset of symptoms ◦ Duration of symptoms < 4 weeks ◦ Symptoms resolve completely ◦ Streptococcus pneumoniae (20%-45%) and Haemophilus influenzae (22%-35%) are the predominant organisms in adults, whereas ◦ S. pneumoniae (30%- 43%), H. influenzae (20%- 28%), and Moraxella catarrhalis (20%-28%) are the predominant organisms in children
  • 8.  Subacute rhinosinusitis ◦ Duration of symptoms >4 weeks to < 12 weeks ◦ Pathogens are same as ARS  Recurrent acute rhinosinusitis ◦ 4 or more episodes of acute rhinosinusitis per year, with each lasting longer than 7 to 10 days, ◦ Complete recovery between attacks ◦ Symptom-free period of > 8 weeks between acute attacks in absence of medical treatment ◦ Bacteriology and pathophysiology would be similar to those of individual episodes of ABRS
  • 9. Chronic rhinosinusitis  Duration of symptoms> 12 weeks  Persistent inflammatory changes on imaging > 4 weeks after starting appropriate medical therapy  no intervening acute episodes  Unlike for ABRS, the role of bacteria in CRS is not well supported  CRS is an inflammatory disease, and it may or may not involve pathogenic microbes.  Therefore, bacteria, fungi or viruses may be involved in some cases  In those patients with CRS who do have potential pathogenic bacteria, the most common organisms are Staphylococcus species (55 percent) and Staphylococcus aureus (20 percent).  Some studies have shown a high prevalence of Enterobacteriaceae organisms, anaerobes, Gram-negative bacteria and fungi.
  • 10. Acute exacerbations chronic rhinosinusitis  AECRS is a sudden worsening of the baseline CRS symptoms or appearance of new symptoms  Complete resolution of acute (but not chronic) symptoms between episodes  There may be a change in the bacteriology of the disease
  • 12. Acute rhinosinusitis in adults  Inflammation of nose and paranasal sinuses  ≥ 2 symptoms, one of nasal blockage/obstruction/congestion or nasal discharge (ant/post nasal drip):  ± facial pain/pressure  ± reduction or loss of smell EPOS March 2012
  • 13.  And either endoscopic signs of: ◦ nasal polyps, and/or ◦ mucopurulent discharge from middle meatus and/or ◦ edema/mucosal obstruction in middle meatus  and/or ◦ CT changes: ◦ mucosal changes within ostiomeatal complex and/or sinuses  For <12 weeks 4/26/12
  • 14. Acute rhinosinusitis in children  Inflammation of nose and paranasal sinuses  ≥ 2 symptoms one of nasal blockage/obstruction/congestion or nasal discharge (ant/post nasal drip):  ± facial pain/pressure  ± cough EPOS March 2012
  • 15. Acute rhinosinusitis in children  And either  endoscopic signs of:  nasal polyps, and/or  mucopurulent discharge from middle meatus and/or  edema/mucosal obstruction in middle meatus And/or  CT changes:  mucosal changes within the ostiomeatal complex and/or sinuses  For < 12 weeks EPOS March 2012
  • 16. Severity of disease in adult and children  Define disease severity:  Mild: VAS 0-3  Moderate: VAS 4-7  Severe: VAS 8-10
  • 17. Acute rhinosinusitis can be divided into CommonCold and post- viral rhinosinusitis. A small subgroup of post-viral rhinosinusitis is caused by bacteria (ABRS). EPOS March 2012
  • 18. Classification of ARS in adult/children  Common cold/ acute viral rhinosinusits : ◦ duration of symptoms for< 10 d  Acute post-viral rhinosinusitis: ◦ increase of symptoms after 5 d or persistent symptoms after 10 d with < 12 wk duration.  ABS: ≥ 3 symptoms/signs ◦ Discoloured discharge (unilat predominance) and purulent secretion in nasi ◦ Severe local pain (unilat predominance) ◦ Fever (>38 °C) ◦ Elevated ESR/CRP ◦ ‘Double sickening’ (deterioration after initial milder of illness) EPOS March 2012
  • 19. Signs ofABS At least 3 of: -Discoloured d/c -Severe local pain -Fever -Elevated ESR/CRP -Double sickening Postviral acute rhinosinusitis Increase in symptoms after 5 d Persistent symptom after 10 d EPOS March 2012
  • 20. Any of following clinical presentations are recommended for identifying patients with acute bacterial vs viral rhinosinusitis  Onset with persistent S/S compatible with ARS ≥ 10 d without any evidence of clinical improvement.  Onset with severe S/S of high fever ≥ 39 °C and purulent nasal discharge or facial pain at least 3–4 consecutive d at beginning of illness.  Onset with worsening S/S characterized by new onset of fever, headache, increase in nasal discharge following typical viral URI that lasted 5–6 d and were initially improving (‘‘doublesickening’’). IDSAGuideline for ABRS: CID.March 20, 2012
  • 21. Associated Factors ◦ Environmental Exposures( dampness in home ,air pollution, irritants) ◦ Anatomical factors  septal deviation, paradoxical turbinate; nasal polyps, and choanal obstruction by benign adenoid tissue, or odontogenic sources of infection ◦ Allergy  individuals with allergies have a higher incidence of developing both acute and chronic rhinosinusitis EPOS March 2012
  • 22. ◦ Ciliary impairment  Ciliary function diminished during viral and bacterial rhinosinusitis.  Exposure to cigarette smoke and allergic inflammation has been shown to impair ciliary function.  Impaired mucociliary clearance in Allergic Rhinitis patients predisposes patients to ARS ◦ Primary Ciliary Dyskinesia ◦ Smoking ◦ Laryngopharyngeal reflux  Pacheco-Galvan et al. 1997-2006 have shown significant associations between GERD and sinusitis.  Recent systematic review, Flook and Kumar showed only poor association between acid reflux, nasal symptoms, and ARS EPOS March 2012
  • 23. ◦ Anxiety and depression  Poor mental health, anxiety, or depression is associated with susceptibility to ARS  Mechanisms are unclear. ◦ Drug resistance ◦ Concomitant Chronic Disease  Concomitant chronic disease (bronchitis, asthma, CVS disease, DM,) in children has been associated with increased risk of developing ARS secondary to influenza. ◦ Iatrogenic factors  Including surgery, medications, nasal packing or nasogastric tube placement. EPOS March 2012
  • 24. Pathophysiology  Acute rhinosinusitis develops in conjunction with an acute viral upper respiratory tract infection.  Occur more commonly in predisposed individuals  The infection results in mucosal swelling with occlusion or obstruction of the sinus ostia.  A reduction in oxygen tension occurs which can reduce mucociliary transport and transudation of fluid into the sinuses.  The inflammation also results in changes in the mucous that become more viscous and alterations in cilia beat frequency often occurs.  These changes in the nasal-sinus environment lead to mucostasis and bacterial colonization.  If the sinuses remain obstructed or the mucociliary. transport system does not return to normal, a bacterial infection can ensue. Scott-brown
  • 26. Bacterial Culture  Microbiological investigations are not required for diagnosis of ARS in routine practice. ( EPOS March 2012)  May be required in research settings, or in atypical or recurrent disease  Maxillary sinus tap with culture is the gold standard for the diagnosis of ABRS,  There is increasing interest in the role of endoscopic-guided middle meatal cultures, but their reliability in children has not been established  Nasopharyngeal cultures are unreliable and are not recommended for microbiologic diagnosis of ABRS  Current accepted reference standard for culture is more than 10,000 colony forming units (CFU)/mL in sinus aspirate. IDSA Guideline for ABRS: CID.March 20, 2012
  • 27. Nasal endoscopy  Nasal endoscopy may be used to  visualize nasal and sinus anatomy  provide biopsy and microbiological samples.  confirm drainage  Evaluate treatment response EPOS March 2012
  • 28. C-Reactive Protein (CRP)  Raised in bacterial infection.  ARS: low or normal CRP may identify low likelihood of positive bacterial infection  Limiting unnecessary antibiotic use.  CRP levels are significantly correlated with changes in CT scans. EPOS March 2012
  • 29. ESR  ESR levels correlated with CT changes in ARS  ESR >10 is predictive of sinus fluid levels or sinus opacity on CT scan.  Raised ESR is predictive of positive bacterial culture on sinus puncture or lavage EPOS March 2012
  • 30. Procalcitonin  Indicates More severe bacterial infection  There is no evidence of its effectiveness as a biomarker in ARS. EPOS March 2012
  • 31. Nasal Nitric Oxide (NO)  Sensitive indicator of presence of inflammation and ciliary dysfunction.  Very low levels: primary ciliary dyskinesia, significant sinus obstruction.  Elevated levels: inflammation provided ostiomeatal patency maintained EPOS March 2012
  • 32. Imaging  CT scan ◦ Modality of choice to confirm extent of pathology and anatomy. ◦ Very severe disease, immuno-compromised pt, suspicion of complications. ◦ Routine CT scan in ARS little useful information  Plain sinus X Rays ◦ Insensitive & limited usefulness  Ultrasound ◦ Insensitive & limited usefulness EPOS March 2012
  • 33. XVII. Which Imaging Is Most Useful for Severe ABRS who suspected to have Suppurative complication?  CT rather than MRI is recommended to localize infection and to guide further treatment. IDSAGuideline for ABRS: CID.March 20, 2012
  • 34. Algorithm for the management of acute bacterial rhinosinusitis IDSAGuideline for ABRS: CID.March 20, 2012
  • 35. Algorithm for the management of acute bacterial rhinosinusitis IDSAGuideline for ABRS: CID.March 20, 2012
  • 36. Algorithm for the management of acute bacterial rhinosinusitis IDSAGuideline for ABRS: CID.March 20, 2012
  • 37.
  • 38.
  • 40. Definition  Chronic Rhinosinusitis (with or without NP) in adults  ≥ 2 symptoms  one of which should be either nasal blockage/obstruction/congestion or nasal discharge(ant/post drip) or  ± Facial pain/pressure  ± reduction or loss of smell for ≥12 weeks EPOS 2012
  • 41.  CRSwNP: bilateral, endoscopically visualised polyps in middle meatus.  CRSsNP: no visible polyps in middle meatus Definition EPOS 2012
  • 42. CRS in children  ≥ 2 symptoms ◦ one of which should be either nasal blockage/obstruction/congestion or nasal discharge(ant/postnasal drip) or ◦ ± Facial pain/pressure ◦ ± Cough  for ≥12 weeks EPOS 2012
  • 43. Factor associated with CRS  Ciliary impairment  Allergy  Asthma  Aspirin sensitivity  Immunocompromised state  Genetic factor  Pregnancy and endocrine state  Local host factor  Biofilm  Environmental factor  Iatrogenic factor  H.pylori and laryngopharyngeal reflux  Osteitis
  • 44. Pathophysiology Scott-brown  The role of allergies has been strongly suggested but not proven  Antigen-antibody reactions result in the release of histamine and other mediators of inflammation.  These mediators cause changes in vascular permeability, destabilization of lysosomal membranes and other reactions that produce inflammation, mucosal swelling and ostia obstruction
  • 45. Pathophysiology Scott-brown  Many cells and proteins that are involved with inflammatory response have been implicated and are being investigated to their roles in rhinosinusitis, particularly CRS.  These include, but are not limited to, eosinophils, neutrophils, mast cells, T and B celis, immunoglobulins, interleukins, tumour necrosis factor, major basic protein and a number of other mediators of inflammation.  Other factors have also been identified that may play a role in the development or perpetuation of CRS, including, superantigens, biofilms and osteitis.
  • 46. •Superantigens are exotoxins that are able to activate T lymphocytes
  • 47. Immune barrier hypothesis of CRS EPOS 2012
  • 48.  Biofilms ◦ Artificial or damaged biologic surface that formed communicating organization of microorganisms surrounded by a glycocalys ◦ Biofilms is relatively impervious to antibiotics and is never eradicated ◦ Mechanical debridement- the only way to resolve biofilms  Osteitis ◦ Inflammatory bone changes were noted on contralateral side in 52% of the animals (Khalid et al. laryngoscope 2002)
  • 49. Eosinophilic and noneosinophilic form of sinusitis Spencer C et al. J Allergy Clin Immunol 2011;128:710-20
  • 50. Mucosa in CRS characterized by basement membrane thickening, goblet cell hyperplasia, subepithelial edema, and mononuclear cell infiltration with few eosinophils Middleton’s Allergy,principal & practice. Seventh edition.
  • 51. Numerous subepithelial eosinophils in luminal compartment of early-stage polyp. Middleton’s Allergy,principal & practice. Seventh edition.
  • 52. Eosinophils accumulated subepithelially and diffusely in tissue of mature polyp. Middleton’s Allergy,principal & practice. Seventh edition.
  • 54.
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  • 62.