Bronchiectasis & URTI

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Bronchiectasis & Infections of the Upper Respiratory Tract:

Bronchiectasis & Infections of the Upper Respiratory Tract By: Chest Department Ainshams University

Definition::

Definition: Bronchiectasis ( broncos, airways; ectasia, dilatation) is a morphological term used to describe abnormal irreversibly dilated and often thick-walled bronchi. This is an anatomic definition and is thought to have evolved from Laennec ’ s original description in 1819 of ectatic bronchi in pathological specimens. Bronchiectasis represents the end stage of a variety of pathologic processes that cause destruction of the bronchial wall and its surrounding supporting tissues.

PREVALENCE:

PREVALENCE Bronchiectasis was a common disabling and fatal condition in the pre-antibiotic era. It remains an important cause of suppurative lung disease in the developing world. More recently, the declining incidence of this disease in the developed world has led to repeated suggestions that it be considered an orphan disease. The decline has been variously attributed to : Improved living conditions Frequent and early use of antibiotics Improved sanitation and nutrition Introduction of childhood immunization, particularly against measles and pertussis.

PATHOPHYSIOLOGY:

PATHOPHYSIOLOGY The abnormal bronchial dilatation in bronchiectasis principally affects the medium-sized bronchi, but often extends to the more distal bronchi and bronchioles. On gross examination of surgically resected or autopsied lungs, the affected bronchi and bronchioles are so prominent as to be visible all the way to the pleural surface. These dilated and ectatic bronchi are commonly filled with purulent secretions. The affected bronchi show transmural inflammation, mucosal edema, ulceration, and neovascularization. Dilated and tortuous bronchial arteries may be seen secondary to the development of extensive bronchial-pulmonary anastomoses.

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Microscopically , bronchiectasis is associated with: Loss of cilia, Cuboidal and squamous metaplasia, Hypertrophy of bronchial glands, Lymphoid hyperplasia. Intense infiltration of the bronchial wall with neutrophils, lymphocytes, and monocytes is seen. It has long been recognized that these changes are associated with chronic bacterial infection. This theory proposed that chronic bacterial endobronchial infection and inflammation damage or destroy mucociliary defenses, leading to secretion stasis, which in turn propagates furthers bacterial infection, and increases airway inflammation and bronchial dilatation. It seems likely that focal disturbances resulting in airway obstruction or impairment of drainage and/or systemic conditions, resulting in uncoordinated airway clearance or impaired immune response are required in addition to airway colonization and/or infection.

CLINICAL FEATURES:

CLINICAL FEATURES The classic clinical manifestations of bronchiectasis are : Daily cough and mucopurulent sputum production. Cough is invariably present and often may be the only symptom for years. Purulent, tenacious sputum production, frequently worse in the morning. Sputum production may be intermittent, being affected by recurrent infections, bronchial plugging, and antibiotic therapy. “ Dry bronchiectasis ” presenting as cough, minimal sputum expectoration, and/or hemoptysis is occasionally described. Hemoptysis may be seen in 40 to 70 percent of patients and may vary from blood streaks to large clots. Increasing cough, dyspnea, and volume of sputum production, fever, hemoptysis, and chest pain are hallmarks of acute exacerbations.

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Most patients have abnormalities on physical examination. Chest auscultation usually reveals findings of early and mid-inspiratory crackles as well as diffuse rhonchi and prolonged expiration. Bronchial breath sounds may be heard in severe cases or patients with a complicating pneumonia. Digital clubbing and hypertrophic pulmonary osteoarthropathy,although common in the pre-antibiotic era, are rarely seen now. In severe advanced cases, there may be evidence of respiratory insufficiency and cor pulmonale.

CLASSIFICATION USING RADIOLOGY :

CLASSIFICATION USING RADIOLOGY Bronchiectasis may be classified by predisposing factors, pathological features, and radiographic appearance. In c ylindrical bronchiectasis, the bronchi are regularly outlined (tubular), dilated in diameter, with straight walls, often coming to a straight abrupt end, instead of a tapering end, due to obstruction of the peripheral bronchial tree by secretions, casts, and inflammatory wall edema. Varicose bronchiectasis (illusion to varicose veins) is marked by the presence of irregular dilatations, outpouchings, and tortuosity of the airways. Saccular (cystic) bronchiectasis is characterized by the presence of cystic distortion of the distal airways that may be focal or more generalized, resulting in saccules that appear as a cluster of grapes.

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Traction bronchiectasis, a term used to describe the dilated airways seen in diffuse pulmonary fibrosis secondary to fibrous tissue traction and elevated negative intrathoracic pressure, should be distinguished from usual bronchiectasis, because of the lack of intrinsic airway pathology and paucity of sputum expectoration. Congenital bronchial cysts (central and peripheral) are developmentally abnormal cystic bronchial structures, often filled with mucus and lined with respiratory epithelium. While usually lacking connection with the parent bronchus and distal alveoli, if infected they may communicate and mimic localized bronchiectasis. Intralobar bronchopulmonary sequestration too, may become infected and communicate with the bronchial tree, mimicking localized bronchiectasis.

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Chest computed tomography. A . (Left chest) Cylindrical bronchiectasis: Dilated and thickened airways. B. (Right chest) Saccular or cystic bronchiectasis: Very dilated airways clustered into saccules, cysts, or grape like clusters

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Chest computed tomography shows varicose bronchiectasis: dilated airways with irregular thickened mucosa

PREDISPOSING OR ASSOCIATED FACTORS:

PREDISPOSING OR ASSOCIATED FACTORS Previously bronchial damage secondary to childhood respiratory tract infections such as pneumonia, pertussis, complicated measles, and tuberculosis were implicated as common causes of bronchiectasis. However, with the early use of antibiotics and childhood immunizations, the focus has shifted from postinfectious to intrinsic causes. Infections: A number of pulmonary infections have been associated with the development of bronchiectasis. The association of measles with bronchiectasis has been considered a complication secondary to the intense bronchial and peribronchial inflammation and epithelial proliferation. Complicating secondary infections with adenovirus, herpesvirus, and bacteria such as Staphylococcus aureus, Klebsiella pneumoniae, and P. Aeruginosa.

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Primary necrotizing bacterial pneumonias due to S. aureus, K. pneumoniae , and P. aeruginosa may result in bronchiectasis. Necrotizing anaerobic pneumonias secondary to aspiration or bronchial obstruction are often complicated by parenchymal destruction and bronchiectasis. Tuberculosis can result in bronchiectasis by several mechanisms. Bronchial Obstruction Bronchial obstruction may result in the development of localized bronchiectasis. Localized bronchiectasis may also been seen in middle lobe syndrome.

Aspiration/Inhalation Airway Injury:

Aspiration/Inhalation Airway Injury Aspiration or inhalation of foreign matter, such as noxious fumes or particulates into the airways, may result in bronchiectasis. This may involve aspiration of oropharyngeal secretions containing microaerophilic and anaerobic bacteria, which may result in a necrotizing pneumonia. Refluxed material from the esophagus or stomach containing food particles, gastric, biliary, and pancreatic secretions, and gut microbes may enter and damage airways, especially if the aspiration events are large and repeated. Depressed sensorium (stroke, alcohol and drug use, seizure, postanesthetic), brain stem dysfunction, defective laryngeal function (postsurgery, postirradiation), esophageal disorders (dysmotility, gastroesophageal reflux disease [GERD], achalasia,tracheoesophageal fistula), and gastric disorders (gastric outlet obstruction) influence the likelihood and frequency of aspiration. Bronchiectasis may present years after foreign body aspiration

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Cystic Fibrosis Cystic fibrosis (CF) and its variants are a common cause of bronchiectasis in the United States and other developed countries. Young ’ s Syndrome Young ’ s syndrome consists of a combination of obstructive azoospermia (with normal spermatogenesis) and chronic sinopulmonary infections (bronchiectasis and sinusitis). This syndrome is distinguished from ciliary dyskinesia by its lack of ultrastructural ciliary abnormalities. Primary Ciliary Dyskinesia Primary ciliary dyskinesia (PCD) is phenotypically and genetically a heterogeneous group of conditions. It has an autosomal-recessive inheritance pattern . Clinical findings include respiratory distress in neonates, recurrent respiratory tract infections, bronchiectasis, situs inversus, heterotaxia, infertility, and hydrocephalus, singly or in various combinations.

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Allergic Bronchopulmonary Aspergillosis ABPA is a hypersensitivity lung disease caused by the ubiquitous fungus Aspergillus fumigatus and usually occurs as a complication of persistent asthma or cystic fibrosis. ABPA is characterized by a marked local and systemic eosinophilia, an elevated level of Aspergillus fumigatus – specific IgG and IgE antibodies, as well as a nonspecific elevation of total IgE. Clinically, ABPA manifests as recurring episodes of asthma, pulmonary infiltrates, and central bronchiectasis that may progress to fibrosis.

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Inflammatory Disorders Inflammatory and fibrotic processes affecting large and small airways may be seen in several rheumatic diseases and idiopathic inflammatory states. Significantly higher frequencies of bronchiectasis (20 to 35 %) have been found in rheumatoid arthritis patients undergoing HRCT, both in symptomatic (30 % ) and asymptomatic (8 %) patients, and was independent of smoking status. Bronchiectasis may precede or follow the development of rheumatoid arthritis, and the coexistence of both conditions is considered to portend a reduced survival. Sj¨ogren ’ s syndrome may also be complicated by bronchiectasis presumed to be secondary to the effects of inspissated bronchial secretions causing atelectasis and bronchial wall destruction. Relapsing polychondritis may be complicated by bronchiectasis in regions of recurring pneumonia as well as regions free of infection. It is not clear whether the chondritis itself or the recurrent infections predispose to bronchiectasis. While pulmonary involvement in systemic lupus erythematosus is diverse, bronchiectasis by HRCT findings is less frequent than in patients with RA.

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Idiopathic ulcerative colitis has been reported to be associated with bronchiectasis. The pathogenesis remains unknown, although autoimmune and immune complex deposition theories have been proposed. This variant of bronchiectasis does not respond to colectomy and has been known to appear and progress after colectomy. Response to steroids is said to be dramatic. Bronchiectasis seen in sarcoidosis is usually traction bronchiectasis secondary to parenchymal and peribronchial fibrosis. Endobronchial sarcoid may result in localized bronchiectasis secondary to obstruction, atelectasis, and bronchial wall destruction. Hypogammaglobulinemia Recurrent sinopulmonary infections and bronchiectasis are clearly associated with hypogammaglobulinemia. Several forms of antibody deficiency have been linked with the development of bronchiectasis, including X-linked agammaglobulinemia, common variable immunodeficiency, IgA deficiency, and IgG subclass deficiency (usually IgG-G2 and IgG-G4).

DIAGNOSIS OF BRONCHIECTASIS:

DIAGNOSIS OF BRONCHIECTASIS The diagnosis of bronchiectasis is based on: history, clinical features, and radiology. The diagnostic evaluation in these patients is largely aimed at identifying potentially treatable underlying causes of bronchiectasis. Thus, esophageal pH monitoring and ciliary analysis may be evaluated depending on the age of presentation; family history; other organ system involvement and level of clinical suspicion; total white blood cell count and differential for eosinophilia; immunoglobulin G, A, M, and E levels; serumα1-antitrypsin levels; sputum cultures for bacteria, mycobacteria, and fungi; sweat chloride levels; skin prick tests or precipitins to Aspergillus spp.

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Chest Radiograph The chest x-ray may be abnormal and show the presence of increased pulmonary markings, ring like structures, atelectasis, dilated and thickened airways (tram lines), and mucus plugging (finger-in-glove) appearance; however, the chest radiograph may be normal even in the presence of bronchiectasis. High-Resolution Computed Tomography The HRCT has been proved to be a reliable and noninvasive method for assessment of bronchiectasis. HRCT can accurately (sensitivity of 97 %): Diagnose bronchiectasis Localize and describe areas of parenchymal abnormality Identify bronchiolar abnormalities and mucus plugging to the level of fifth- and sixth-order bronchi. It also can identify focal areas of air trapping as an indicator of small airway disease.

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INDICATIONS for HRCT: It is indicated in the evaluation of bronchiectasis when surgical resection is considered. bronchiectasis is strongly suspected clinically and routine chest radiographs are normal. Findings: Airway dilatation can be detected by finding tram lines or end-on-ring appearance. A luminal diameter more than 1.5 times the adjacent vessel is indicative of bronchiectasis. Bronchial wall thickening may also be seen. Evidence of small airway plugging with debris (tree-in-bud) may also be seen

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Chest computed tomography. A . Extensive peripheral branching opacities of tree-in-bud. B . Extensive peripheral branching dilated and thickened airways.

Pulmonary Function::

Pulmonary Function: The degree of impairment depends on the extent abnormalities of bronchiectasis, & if associated conditions are present. Thus, findings of spirometry vary from normal lung function tests to variable degrees of airways obstruction, with normal or reduced (FVC), reduced (FEV1), and reduced FEV1/FVC ratio. In some patients with accompanying atelectasis, parenchymal and pleural scarring, restrictive or mixed/obstructive and restrictive physiology may be seen with reduced FVC and normal FEV1/FVC ratios. Lung volumes may help identify restriction, as the total lung capacity (TLC), functional residual capacity, and residual volume (RV) are reduced. With mainly obstruction, air trapping is evident with increased residual volume and increased RV/TLC.

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BACTERIOLOGY Patients with bronchiectasis are frequently found to be colonized by potentially pathogenic microorganisms. Thus even in stable conditions 60 to 80 % of patients with bronchiectasis are known to be colonized. The most frequent microorganisms isolated are H. influenzae and P. aeruginosa and are often implicated as the cause of periodic exacerbations.

TREATMENT::

TREATMENT: The treatment of bronchiectasis is aimed at : Controlling infection , reducing inflammation, and improving bronchial hygiene. Surgical resection of affected areas being useful in selected patients. Control of Infection : Since infection plays a major role in the causation and perpetuation of bronchiectasis, reducing the microbial load and associated inflammatory mediators remains a cornerstone of therapy. Antibiotics are indicated to treat an acute exacerbation.However, they have been used variably to prevent recurrent infections by suppression and/or elimination of attendant flora. Antibiotics are directed at commonly isolated pathogens such as H. influenzae, S. pneumoniae, and P. aeruginosa. Oral fluoroquinolones are often used as initial antibiotic choices for treatment durations of 10 to 14 days.

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The role of prophylactic/suppressive antibiotics remains controversial. Several approaches to the prescription of suppressive antibiotics exist, including daily antibiotics, antibiotics given for 1 to 2 weeks each month, as well as more prolonged courses lasting weeks to months. Bronchial Hygiene: Airway mucus clearance is a problem in bronchiectasis. Chest percussion and postural drainage have been the traditional method of facilitating mucus clearance. The labor intensive nature of physical therapy procedures such as chest wall percussion and postural drainage, and potential issues of hypoxemia and chest discomfort may result in poor patient compliance and search for alternative therapies. Autogenic drainage, mechanical vibration with ultrasonic devices, positive expiratory pressure, and Flutter valve use without the assistance of another caregiver have been shown to achieve good chest clearance provided the patient has motivation, breath control, and the neuromuscular function to perform.

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Mucus Clearance: Mucus hypersecretion is a prominent feature of chronic inflammatory airways disease and little is known about the effects of current therapies for airways disease, because of the difficulties in quantifying mucus hypersecretion in clinical studies, both at baseline and in response to treatment. Maintenance of hydration with oral and/or intravenous fluids is considered useful in preventing inspissated sputum retention. Humidification of inhaled air or oxygen as an adjunct to chest physical therapy has been shown to significantly increase the sputum produced. The use of nebulized normal or hypertonic saline and acetylcysteine may be considered .

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Bronchodilators: Bronchodilators such as beta agonists, anticholinergics, or theophyllines are frequently used in patients with bronchiectasis, since these patients show signs of airway obstruction and hyperreactivity.There are few reports documenting efficacy in bronchiectasis. Anti-inflammatory Therapy: Persistent endobronchial inflammation is known to play a significant role in the pathogenesis of bronchiectasis, and anti-inflammatory therapy may be beneficial. The role of inhaled steroids (fluticasone) in bronchiectasis was evaluated and reduced sputum volume ,purulence and reduced rates of exacerbations was found in some studies.

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Surgery: Bronchiectasis generally is a diffuse disease and surgical removal of affected areas is often not feasible. However, in selected cases surgical resection of the most severely affected segments, bleeding segments, or areas harboring resistant tuberculosis or atypical mycobacteria may confer significant benefits in terms of symptom control, reduction of tenacious sputum production, elimination of large-volume bronchial bleeding, reduction of acute infective episodes, and improved quality of life. The surgical approach varies: video-assisted thoracoscopy approach the lateral thoracotomy approach. Complications include: spread of infection, bleeding, prolonged air leak, and poor lung expansion following surgery.

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Lung transplantation is now considered a viable option in advanced cases. The outcomes of patients receiving lung transplantation in non-CF bronchiectasis were recently reported. Overall 1-year survival was 68 %, and overall 5-year survival was 62 %. Survival was higher in patients receiving two lungs, as was the FEV1 and FVC. Miscllaneous: V accinations against S. pneumoniae and influenza should be considered in these patients. Smoking cessation should be emphasized as a matter of routine. oxygen supplementation for patients with advanced bronchiectasis with evidence of exercise and/or nocturnal desaturation should be considered to delay the onset of pulmonary hypertension and cor pulmonale and improve exercise tolerance. Pulmonary rehabilitation and inspiratory muscle training may be considered, as these modalities have been documented to improve exercise tolerance.

Infections of the Upper Respiratory Tract:

Infections of the Upper Respiratory Tract Upper respiratory tract infections are the most common infections. Most upper respiratory infections are minor and self-limiting, but some (e.g., peritonsillar abscess, epiglottitis, invasive fungal sinusitis) may be life-threatening. THE COMMON COLD: The common cold is a mild, self-limiting infection. Six major viral families are responsible: rhinovirus (30 to 40 % of cases); influenza virus (25 to 30 %); coronavirus (10 to 15 %); adenovirus (5 to 10 %); parainfluenza virus (5 percent); and respiratory syncytial virus (5 %). Each virus has several serotypes; (rhinovirus has 100). Adults have an average of two to four colds and children six to eight colds per year. Transmission probably occurs either by inhalation of infectious droplets or by hand-to-nose “ self-inoculation ” after touching infectious secretions. .

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The pathogenesis of rhinovirus infections is thought to include viral entry into the nose followed by infection of the epithelial cells of the upper airway. Symptoms (sneezing, nasal discharge and congestion, and a “ scratchy ” throat) develop 16 to 72 h after inoculation, and last for 1 to 2 weeks. The peak of rhinoviral excretion in nasal secretions coincides with the peak of clinical illness. Complications of the common cold include bacterial superinfections of the upper respiratory tract, such as acute otitis media and acute sinusitis, and exacerbations of asthma. Treatment of the common cold is symptomatic, with non steroidal anti-inflammatory drugs (NSAIDs) and antihistamines providing some benefit. Development of a vaccine is unlikely given the number of viral pathogens and serotypes. Antiviral agents such as pleconaril have not provided sufficient benefit

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PHARYNGITIS: Over 6 million adults visit primary care physicians annually for sore throats, and three-fourths receive antibiotics. Most cases of acute pharyngitis occur as part of the common cold and are caused by viruses such as rhinovirus, coronavirus, and parainfluenza virus. These cases are mild, nonexudative, and self-limiting. A severe, usually exudative pharyngitis occurs in about half of patients with either adenovirus infection or Epstein-Barr virus mononucleosis. Group A streptococcus (Streptococcus pyogenes) is the most important bacterial cause of pharyngitis because of its suppurative (e.g., peritonsillar abscess) and nonsuppurative complications (e.g., rheumatic fever, acute poststreptococcal glomerulonephritis). It causes 15 to 30 % of cases of pharyngitis in children and 5 to 10 % in adults . Diagnosis of streptococcal pharyngitis is made by culture or by rapid antigen detection test (RADT). The latter is 95 % specific but not as sensitive as culture. A peritonsillar abscess (quinsy) may follow untreated streptococcal pharyngitis or may be due primarily to mouth anaerobes.

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ORAL CAVITY INFECTIONS: The oral cavity extends from the lips to the circumvallate papillae of the tongue. Various streptococci (e.g., S. mutans,S. mitis, S. salivarius ) and anaerobes (e.g., Peptostreptococcus, Veillonella, Lactobacillus, Bacteroides, Prevotella ) heavily colonize this area, and are the main pathogens in dental and oral cavity infections. Gingivitis and periodontitis are associated with anaerobic gram-negative rods such as Prevotella intermedia and Porphyromonas gingivalis. Mouth anaerobes are the major cause of Vincent ’ s angina (acute necrotizing ulcerative gingivitis, or trench mouth). Patients have gingival pain, cervical adenopathy, and ulcerations of the interdental papillae. Treatment is with oral clindamycin or penicillin plus metronidazole.

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Ludwig ’ s angina is a rapidly spreading cellulitis of the sublingual and submandibular spaces. It usually begins in the floor of the mouth from an infected mandibular molar tooth. The sublingual area becomes edematous, pushing the tongue to the roof of the mouth. The infection can cause acute airway obstruction. Patients present with fever, difficulty swallowing, and prominent submandibular and sublingual swelling. They should be admitted for airway monitoring, as intubation or tracheostomy may be necessary. Intravenous antibiotics against streptococci and anaerobes should be given. Surgical incision of the infected soft tissue compartment may be necessary. Primary herpes simplex infection may cause painful vesicles on the buccal mucosa as well as the lips and tongue, and should be treated with hydration and acyclovir.

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LARYNGITIS: Laryngitis, or inflammation of the larynx, is characterized by hoarseness. Acute laryngitis is usually caused by the same viruses that cause the common cold, and treatment is symptomatic. Hoarseness may accompany infections with human metapneumovirus, a virus identified in 2001 and primarily associated with bronchiolitis in young children. Herpes simplex virus may cause acute laryngitis; ulcerations or vesicles are typically seen. Streptococcal pharyngitis may be associated with laryngitis and should be treated with penicillin. Streptococcal pharyngitis may be associated with laryngitis and should be treated with penicillin. Corynebacterium ulcerans has been a rare cause of a membranous laryngopharyngitis that may mimic diphtheria.

EPIGLOTTITIS::

EPIGLOTTITIS: Acute epiglottitis (supraglottitis) is a medical emergency, as it can rapidly lead to airway obstruction. It begins as a cellulitis between the base of the tongue and the epiglottis, pushing the epiglottis posteriorly. It then involves the epiglottis itself, with rapid swelling and airway compromise. Broad-spectrum intravenous antibiotics with activity against H. influenzae , such as ampicillin-sulbactam, should be given. If the patient with epiglottitis due to H. influenzae has household contacts that include an unvaccinated child under age 4, the patient and all members of the household should receive rifampin prophylaxis to eradicate carriage of the organism.

SINUSITIS::

SINUSITIS: The most common cause of inflammation leading to acute sinusitis is a viral upper respiratory infection. Most adults with common colds have (CT) evidence of ostial obstruction and sinus abnormalities, although only about 0.5 % of all colds are complicated by acute sinusitis. Viral infections increase the amount of mucus produced and may damage ciliated cells. Another predisposing factor for sinusitis is allergic rhinitis, which may cause ostial obstruction by mucosal edema or polyps. Dental infections, especially of the upper teeth that adjacent to the maxillary sinus, may cause some cases of maxillary sinusitis. Anatomic obstruction of the sinus ostia due to a deviated septum, tumor, granulomatous disease (e.g., Wegener ’ s granulomatosis), or nasotracheal or nasogastric tubes may also lead to sinusitis. Barotrauma from deep-sea diving or airplane travel, chemical irritants, and mucus abnormalities (e.g., cystic fibrosis) are other risk factors for sinusitis.

Acute Community-Acquired Bacterial Sinusitis :

Acute Community-Acquired Bacterial Sinusitis Symptoms of acute bacterial sinusitis include purulent nasal or postnasal drainage, nasal congestion, and sinus pain or pressure. The location of this pain depends on the sinus affected. Patients usually complain of pain in their cheek or upper teeth in maxillary sinusitis, the sides of the bridge of the nose in ethmoid sinusitis, supraorbital or frontal pain in frontal sinusitis, and retro-orbital, frontal, occipital, or vertex pain in sphenoid sinusitis. Fever occurs in about half of adults with acute sinusitis. The diagnosis of acute bacterial sinusitis is often difficult on the basis of history and physical examination alone. Identical symptoms may occur in patients with viral upper respiratory infections, although bacterial sinusitis should be suspected if the patient has had persistent symptoms for more than 7 days.

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The bacteriology of sinusitis has been well defined only for acute, community-acquired maxillary sinusitis. Sinus puncture studies of adults with this infection have revealed that over 50 % of cases are due to S. pneumoniae or H. influenzae . Other pathogens include other streptococci, anaerobes, Moraxella catarrhalis , and rarely S. aureus . Anaerobes are more common in adults and M. catarrhalis is more common in children. Studies of sinuses other than the maxillary sinus are hindered by the difficulty of obtaining culture material that is not contaminated by nasal flora. Treatment should be empiric and target the bacterial pathogens noted above. Oral therapy (e.g., amoxicillin clavulanate, cefuroxime, levofloxacin) for 10 days is sufficient except in severe disease or in patients who also have a complication of sinusitis (e.g., orbital sinusitis).

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Nosocomial Bacterial Sinusitis Nosocomial bacterial sinusitis is usually seen in patients in the intensive care unit, and typically considered in those with fever of unknown origin. The incidence is higher in patients with nasotracheal tubes. It is also higher in patients with nasogastric tubes vs. those without. A sinus CT scan showing sinus opacification or an air-fluid level suggests the diagnosis. Bedside nasal endoscopy performed by an otolaryngologist may be helpful in obtaining cultures, either by endoscopically directed cultures of purulent meatal secretions or by maxillary sinus (antral) puncture. The pathogens in nosocomial sinusitis are usually S. aureus and gram-negative bacilli, and often include antibiotic-resistant organisms. Empiric treatment should be directed against these organisms (e.g., intravenous vancomycin plus cefepime) until culture results are known.

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Chronic Bacterial Sinusitis Chronic sinusitis is characterized by symptoms that last for weeks to months. Patients complain of persistent dull pain, postnasal drainage, foul odor and taste, and fatigue. True fever is rare. Most patients have stable, low-grade symptoms punctuated by episodes of acute sinusitis. The bacteriology of chronic sinusitis is not well defined. Most patients with chronic disease will have sinus cultures positive for bacteria, but whether these are colonizers or pathogens is not always clear. Patients without sinus disease also have positive cultures when cultures are obtained intranasally. Sinus cultures cannot be obtained without contamination by nasal flora, and since S. aureus is a nasal colonizer in 30 % of the normal population, recovery of this organism is particularly difficult to interpret in the patient with chronic sinusitis.

Complications of Bacterial Sinusitis:

Complications of Bacterial Sinusitis Orbital Cellulitis Fungal Sinusitis There are three forms of fungal sinusitis: allergic fungal sinusitis,sinus aspergilloma, and invasive fungal sinusitis. EAR AND MASTOID INFECTIONS Auricular Cellulitis and Perichondritis Otitis Externa Acute Otitis Media Otitis Media with Effusion Chronic Suppurative Otitis Media Acute Mastoiditis

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