Infectious rhinosinusitis

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 SinusitisBased on Presence of at Least 2 Major or 1 Major and 2 Minor

Symptoms

IDSA Guideline 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 smellEPOS March 2012

And eitherendoscopic 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

EPOS March 2012

Acute rhinosinusitis can be divided into Common Coldand postviral 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 of ABSAt 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’’).


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 rhinosinusitisEPOS 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.


Nasal endoscopyNasal 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

ProcalcitoninIndicates 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.


Algorithm for the management of acute bacterial rhinosinusitis






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 weeksEPOS 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 weeksEPOS 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.


Eosinophils accumulated subepithelially and diffusely in tissue of mature polyp.


Type of CRS

Stepwise evaluation of CRS

Daniel L et al. J Allergy Clin Immunol 2011;128:693-707

EPOS 2012

EPOS 2012

EPOS 2012

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Infectious rhinosinusitis

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