Upper Airway Cough Syndrome

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Upper Airway Cough Syndrome Dr . Arnab Maji 2 nd yr PGT Chest Medicine N.R.S.M.C.H., Kolkata An ACCP guideline based approach

Upper Airway Cough Syndrome:

Types of Cough ACUTE: <3 weeks SUBACUTE: 3-8 weeks CHRONIC: >8 weeks Respiratory tract infection, aspiration event, or inhalation of noxious chemicals or smoke Residuum from a tracheobronchitis , such as in pertussis or "post-viral tussive syndrome

Types of Cough:

CAUSES OF CHRONIC COUGH Upper Airway Cough Syndrome Asthma GERD Post-infectious Meds (ACEI esp.) Airway Diseases (bronchitis, bronchiectasis , neoplasm, foreign body) Parenchymal Disease (ILD, lung abscess) Others VERY COMMON

CAUSES OF CHRONIC COUGH:

The term “cough” itself says its causes

The term “cough” itself says its causes:

In prospective studies in adults, chronic cough is most commonly due to 6 disorders : Upper Airway Cough Syndrome ( UACS ) Ast hma G ERD Chronic Bronchitis Bron chiectasis Non- ast h mati c E o sinophilic Bronchitis Guidelines Writing Committee. Chest 2006; 129 (Suppl. 1): 1S-292S

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10 12 13 12 16 6 4 ASTHMA PNDS GERD Chest 1999;116:279-284 1. Gastro esophageal refl ux disease (21-41%) 2. Cough variant asthma (24-59%) 3. Post nasal drip syndrome (41-58%)

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Percentage of cases presenting one, two, three and four causative factors Palombini BC et al. Chest 1999; 116: 2 PNDS GERD ASTHMA OTHERS

Percentage of cases presenting one, two, three and four causative factors:

İmmunocompetent patients Not exposed to enviromental irritants Chest radiograph is normal Not taking an ACE inhibitor Not a current smoker Ast hma and/or G ERD , PN D S responsible for 93.6% of the cases of chronic cough Harding SM .Chest 2003;123:659-660

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Commonest causes of chronic cough in patients investigated in specialist clinics Reference Diagnosis % of total Asthma Syndrome Oesophageal Disease Rhinitis IRWIN et al . 1981 25 10 29 POE et al . 1982 36 0 8 POE et al . 1989 35 5 26 IRWIN et al . 1990 24 21 41 HOFFSTEIN et al . 1994 25 24 26 O ’ CONNELL et al . 1994 6 10 13 SMYRNIOS et al . 1995 24 15 40 MELLO et al . 1996 14 40 38 MARCHESANI et al . 1998 14 5 56 MCGARVEY et al . 1998 23 19 21 PALOMBINI et al . 1999 59 41 58 BRIGHTLING et al . 1999 31 8 24 SIMPSON G et al . 1999 6 22 28 Total n 317 250 430 Mean % 25 20 34 Morice AH. Eur Respir J 2004; 24: 481–492

Commonest causes of chronic cough in patients investigated in specialist clinics:

Spectrum and frequency of reasons why patients with chronic cough sough medical care * Adverse occurrence Frequency, % Needs reassurance nothing is serious 77 Concerned something is wrong 72 Frequent retching 56 Expaustion 54 Others think something is wrong with me 53 Embarassment 49 Self-consciousness 46 Difficulty spekaing on the telephone 39 Hoarseness 39 Had to change lifestyle 36 Cannot sleep at night 34 Can no longer sing in church 31 Spouse cannot tolerate cough 30 Wetting pants 30 Concerned something is seriously wron 28 Dizziness 21 Excessive sweating 21 Achiness 21 French CL. Arch Intern Med 158(10): 1657-1661, 1998 * N= 39. The relative frequencies for the 28 patients used in the major analyses of this study were similar. AIDS indicates acquired immunodeficieny syndrome; TB: tuberculosis.

Spectrum and frequency of reasons why patients with chronic cough sough medical care*:

Impact of Chronic Cough on Quality of Life Arch Intern Med. 1998;158(15):1657-1661. doi:10-1001/pubs. Cynthia L French et al Sickness Impact Profile

Impact of Chronic Cough on Quality of Life :

French CL. Arch Intern Med 158(10): 1657-1661, 1998 Total Physical Psychosocial Ambulation Mobility Body Care and Movement Social Interaction Communication Alertness Behavior Emotional Behavior Sleep and Rest Eating Work Home Management Recreation and Pastimes SIP Score, % 0 10 20 30 40 * * * * * * Sickness Impact Profile (SIP) scores at baseline in patient with chronic cough

Sickness Impact Profile (SIP) scores at baseline in patient with chronic cough:

French CL. Arch Intern Med 158(10): 1657-1661, 1998 6 4 2 0 Before After Treatment Total SIP Score, % p=.003 6 4 2 0 Before After Treatment Physicososyal Score, % p<.02 6 4 2 0 Before After Treatment Physical Score, % p=.05 Sickness Impact Profile (SIP) scores before and after successful treatment of chronic cough at baseline in patient with chronic cough

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Problems with UACS UACS or PNDS? Syndrome? Symptom? Lack of objective testing “Wastebasket” symptom complex? American invention? Upper airway cough syndrome

Problems with UACS:

UACS or PNDS?? Postnasal drip syndrome Vs UACS. Two hundred years of controversy between UK and USA A. Sanu and R. Eccles . Common Cold Centre and Healthcare Clinical Trials, Cardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom, Rhinology , 46, 86-91, 2008

UACS or PNDS??:

What American thought? What British thought? In nineteenth century – American Catarrah American chest physicians adopted PNDS as the most common cause of chronic cough. In 2006 ACCP recommendation - ‘ that the term upper airway cough syndrome (UACS) be used in preference to postnasal drip syndrome (PNDS) when discussing cough that is associated with upper airway conditions because it is unclear whether the mechanism of cough is post-nasal drip, direct irritation, or inflammation of the cough receptors in the upper airway ’. British use the term ‘ rhinosinusitis ’ instead of PNDS. A relationship between PNDS and chronic cough was not accepted by UK chest physicians. In the UK the term PNDS has recently been criticised, and both chest physicians and otolaryngologists recommend that PNDS be replaced by the term ‘ rhinosinusitis ’.

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In patients with chronic cough related to upper airway abnormalities, the committee considers the term UACS to be more accurate, and therefore it should be used instead of PNDS. ACCP RECOMMENDATION, 2006

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Overview Postnasal drip (PND) is the drainage of secretions from the nose or paranasal sinuses into the pharynx . Clinically, the diagnosis of PND syndrome (PNDS) largely rests on the reporting of the patient of this sensation of having something drip down into the throat, nasal discharge, or frequent throat clearing. The presence on examination of the nasopharynges or oropharynges of mucoid or mucopurulent secretions, or cobblestoning of the mucosa also is suggestive .

Overview:

The problem , however, encountered when trying to diagnose PNDS is that There is no objective test for it No way to quantify the amount of PND No way to directly prove that it is causing cough.

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Therefore, because we are actually defining a syndrome and because no pathognomonic findings exist, the diagnosis of PNDS-induced cough is best determined by considering a combination of criteria, including symptoms, physical examination, radio-graphic findings, and, ultimately, the response to specific therapy.

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Upper airway cough syndrome diagnosis history physical exam laboratory treatment

Upper airway cough syndrome:

Pathogenesis Clinical studies have suggested that the pathogenesis of cough from UACS is due to the mechanical stimulation of the afferent limb of the cough reflex in the upper airway

Pathogenesis:

There is, however, also some evidence that suggests that in patients with UACS-induced cough that the cough reflex in the upper airway is more sensitive than normal and that this increased sensitivity can be a contributing factor to the pathogenesis of cough.

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Clinical Presentation Cough + Complaints (or at least an affirmative response to questioning) A sensation of something draining into the throat A need to clear the throat A tickle in the throat Nasal congestion Nasal discharge Hoarseness wheeze These clinical findings are relatively sensitive but are not specific .

Clinical Presentation:

Silent UACS/PNDS A minority of patients with cough will have no upper respiratory signs or symptoms that are suggestive of PND Y et they will respond to therapy with first-generation antihistamine/decongestant (A/D) agents. The authors of one prospective study interpreted this response to treatment as implying that silent PND caused the cough. Pratter MR, Bartter T, Akers S, et al. An algorithmic approach to chronic cough. Ann Intern Med 1993; 119:977–983

Silent UACS/PNDS:

Physical and FOL finding

Physical and FOL finding:

Differential Diagnosis of UACS-Induced Cough Allergic rhinitis Nonallergic rhinitis Post-infectious UACS NARES Bacterial sinusitis Allergic fungal sinusitis Rhinitis due to anatomical abnormalities Rhinitis due to physical or chemical irritants Occupational rhinitis Rhinitis medicamentoza Gestational rhinitis

Differential Diagnosis of UACS-Induced Cough:

Allergic Rhinits : Definition Allergic rhinitis is clinically defined as a symptomatic disorder of the nose induced by an IgE-mediated inflammation after allergen exposure of the membranes lining the nose ARIA Report 2001

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Causes of AR

Causes of AR:

How are the symptoms caused? Irritation of free nerve endings---- Itching and sneezing Increased mucus production ------ Rhinorrhoea Vasodilation -------- Congestion Increased vascular permeability---- Oedema

How are the symptoms caused?:

Clinical Manifestations Nasal congestion Postnasal drainage Nasal pruritus Ear symptoms Watery rhinorrhea Eye symptoms Repetitive sneezing Others

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Moderate-severe one or more items abnormal sleep impairment of daily activities, sport, leisure abnormal work and school troublesome symptoms Persistent ≥ 4 days per week and ≥ 4 weeks Mild normal sleep & no impairment of daily activities, sport, leisure & normal work and school & no troublesome symptoms Intermittent < 4 days per week or < 4 weeks ARIA Classification ARIA Report 2001

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Minimal Persistent Inflammation An underlying cause of chronicity An inflammatory process which is actually present even in asymptomatic subjects who are exposed to allergens

Minimal Persistent Inflammation An underlying cause of chronicity:

Concept of "minimal persistent inflammation" Threshold level for symptoms 0 , 1 1 1 0 1 0 0 0 2 4 6 8 1 0 1 2 M o n t h s mite allergen (µg/g of dust) Minimal persistent inflammation Symptoms inflammation Ciprandi et al, J Allergy Clin Immunol 1996

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Diagnosis of AR History Physical / Nasal Examination Laboratory Testing - Skin Prick Test - Peak Nasal Inspiratory Flow Rate - Rhinomanometry

Diagnosis of AR:

History in allergic rhinitis Nature of symptoms Timing of symptoms Duration of symptoms Family history - If a child has one parent with allergies, chances are 30% that a child will have allergic rhinitis. This increases to 50-70% if both parents have allergies or atopic asthma Related medical history – sply asthma and eczema Social and environmental history

History in allergic rhinitis:

Symptoms of allergic rhinitis C.van Drunen et al. Allergy 2005;60:5-19

Symptoms of allergic rhinitis:

PHYSICAL EXAMINATION Allergic shiner Dennie Morgan line Allergic crease Allergic salute Nasal mucosa may appear normal or pale bluish, swollen with watery secretions but only if patient is symptomatic Exclude structural problems (polyps, deflected nasal septum) Others : nasal voice, constant mouth breathing, frequent snoring, coughing, repetitive sneezing, chronic open gape of the mouth, weakness, malaise, irritability

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Dennie Morgan line Allergic shiners Allergic Salute

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Marked erythema of palpebral and bulbar conjunctivae Chemosis of the conjunctivae

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Hypertrophied turbinates and pale mucosa due to oedema Dried blood is commonly observed secondary to trauma from rubbing the nose

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Cobblestoning in the posterior pharynx is also a sign of follicular hypertrophy of mucosal lymphoid tissue secondary to chronic nasal congestion and postnasal drainage.

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DENTAL MALOCCLUSION DUE TO CHRONIC MOUTH BREATHING IN ALLERGIC RHINITIS

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Nonallergic rhinitis: Vasomotor rhinitis Excessive,thin watery secretions often in reponse to odors, changes in temperature or humidity, eating, or alcohol ingestion It has been postulated that this is related to an autonomic imbalance Allergy testing is negative DIAGNOSIS : History and exclusion of other diseases TREATMENT : Ipratropium bromide

Nonallergic rhinitis: Vasomotor rhinitis:

Nonallergic rhinitis: NARES Nasal symptoms similar to those of vasomotor rhinitis Additionally, pruritus of nasal and ocular mucosae and lacrimation are common Clinical findings Eosinophils in nasal secretions The absence of allergic skin testing and asthma DIAGNOSIS Nasal c orticosteroids . TREATMENT Pratter MR. Chest 2006; 129:63S-71S

Nonallergic rhinitis: NARES:

Postinfectious UACS Persistent cough lasting >3 weeks after experiencing the acute symptoms of an upper respiratory tract infection DIAGNOSIS : A history of a upper respiratory tract infection Mycoplasma , Chlamydia pneumoniae and especially pertussis in its catarrhal stage may also result in cough of sufficient duration to fall into this category. TREATMENT : Antihistamine/decongestant combination Systemic cs? Ipratropium bromide?

Postinfectious UACS:

Bacterial Sinusitis Cough + sinus infection + chronic sputum production May be silent also Traditionally, the presence of sinus mucosal thickening, and in particular of opacification , and/or air-fluid levels in the presence of chronic cough has been considered to be predictive evidence for bacterial sinus infection and is the basis for antibiotic treatment . The most common etiologic agents for chronic bacterial sinusitis, based on specimens obtained during endoscopic surgery or needle aspiration, are Staphylococcus aureus , coagulase -negative staphylococci, anaerobic bacteria, Haemophilus influenzae , Moraxella catarrhalis , and a variety of Gram-negative bacillary organisms

Bacterial Sinusitis:

Allergic Fungal Sinusitis Diagnosis of this disease should be considered in atopic patients with chronic sinusitis with purulent expectoration or nasal drainage that is refractory to antibiotic treatment. The key feature of the disease is a thick allergic fungal mucin that contains eosinophils and fungal elements, which may occlude the sinuses. The inflammatory response to fungal antigen (not fungal invasion) can cause bony destruction and ocular disorders.

Allergic Fungal Sinusitis:

Rhinitis medicamentosa A term that is specific for the nasal congestion caused, paradoxically, by the persistent use of a drug, the immediate effect of which is the relief of nasal congestion via local vasoconstriction . The most common cause of rhinitis medicamentosa is the long-term use of topical alfa -agonists that are specifically designated for the treatment of nasal congestion, although it can also be a side effect of nasal cocaine usage. Other drugs such as beta-blockers Treatment – discontinuation of that drug and topical vasoconstrictor

Rhinitis medicamentosa:

UACS mimicker - GERD When do we suspect???? Patient giving history of dry cough specially in supine posture, during night , with food intake, Associated with heartburn Cough may be the sole presentation – SILENT GERD

UACS mimicker - GERD:

1. Chronic cough for at least 2 months 2. Immunocompetent patients 3. Chest radiograph is normal 4. Not exposed to enviromental irritants nor a present smoker 5. Not taking an ACE inhibitor 6. Symptomatic asthma has been ruled out 7. Rhinosinus diseases has been ruled out: 8. ‘Silent sinusitis’ has been ruled out 9. Nonasthmatic eosinophilic bronchitis has been ruled out: BPT is negative Cough has not improved with asthma therapy First generation H 1 antagonists has been used Eo 3%  in induced sputum Cough has not improved with steroids Irwin RS. Chest 2006;129:80S-94S İrwin RS. AJRCCM Vol 165; 1469-1474, 2002 Clinical Profile That Chronic Cough İs Likely Due To ‘Silent GERD’

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According to updated guidelines from the American College of Gastroenterology , GER is defined by symptoms or by mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. Esophageal pH testing Acidic GER Non-acid GER A GER event occurs when the pH is less than 4. Non-acid GER can be identified by combining esophageal impedence with pH monitoring. A non-acid liquid GER event is defined by the presence of a drop in esophageal impedence without a drop in pH (<4) Non-acid GER occurs in patients who are on acid suppressive therapy.

According to updated guidelines from the American College of Gastroenterology , GER is defined by symptoms or by mucosal damage produced by the abnormal reflux of gastric contents into the esophagus.:

GERD-related cough incidence 5 - 55% May be the sole presenting symptom(1/3) Thorax 2003:58;1092-1095) (Chest 1997; 111: 1389-1402) Irwin RS. Chest 2006;129:80S-94S Association between cough and r efl ux is important Esophageal-tracheal-bronchial reflex Microaspiration Pathogenesis ARRD 1981;123:413-417 Arch Intern Med 1996;156:997 Chest 1993;104:1511-1517 El Hennawi, 2004 OHNS Nonacidic factors? Esophageal d y smotility ?

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Why cough in GERD? Vagal reflex Local axonal reflexes Heightened bronchial reactivity Micro-aspiration inflammation: Substance P Tachykinins Interleukin-8

Why cough in GERD?:

Pharyngeal pHmetry + - Not GERD Clinical GERD symptoms ? Nonacid, weakly acid reflux? Increase dose PPI + alginate İmproved Not improved Continue pHmetry under treatment Consider  Simultaneously dual probes 24 hours pHmonitoring and intraesophageal impedance Irwin RS.AJRCCM 165:1469-74,2002 McGarvey LPA.Thorax 59:342-346,2004

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3 cm 5 cm 7 cm 9 cm 15 cm 17 cm pH - 5 cm 6 impeda nce channels 1 pH electrode + Adult Standard Model ZAN-S61C01E Multichannel intraluminal impedance-pH catheter

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Therapy in Esophageal-pulmonary reflux Conservative and lifestyle measures E mpirical therapy : Acid suppression Proton pump inhibitors  PPI x 2 / 3 months Therapy failure  24 hour intraesophageal pHmetry ( pharyngeal pHmetry )  GERD (+) High dose PPI + H 2 blocker agent Surgery(Fundoplication) Fundoplication is the only option for non-acid GER Pulmonary and Crit Care Update 1994 ; Vol 9 2004;24:481-492

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Weeks of antireflux therapy Patients responded No No (%) 2 16 (41) 4 38 (86) 6 42 (95) 8 43 (99) 12 weeks 44 (100) Poe RH.Chest 2003;123:679-684 Cumulative Response to GERD Therapy

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MANAGEMENT of UACS In general – Avoidance Treatment to block or reduce inflammation and secretions Treatment of infection Correction of structural alterations

MANAGEMENT of UACS:

Management of AR Allergen Avoidance Pharmacotherapy Immunotherapy

Management of AR:

Pharmacotherapy Medications used to treat allergic rhinits : Antihistamines Decongestants AH-D combinations Corticosteroids Mast Cell stabilizers Anticholinergics Antileukotrienes

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Actions of Various Nasal Preparations in the Treatment of Rhinitis Nasal Preparation Sneezing Itching Rhinorrhoea Congestion Antihistamines +++++ ++++ +++ 0 Anticholinergics 0 0 +++++ 0 Corticosteroids +++++ +++++ +++ +++ Decongestants 0 0 + +++++ Mast cell stabiliser +++++ +++ + 0 Antileukotrienes +++ ++ 0 ++++

Actions of Various Nasal Preparations in the Treatment of Rhinitis:

Anti-Histamines Act by preventing histamine from binding to the H 1 -receptors Primarily helpful in controlling Sneezing, itching & rhinorrhoea; ineffective in releiving nasal blockage 1 st generation anti-histamines - chlorpheniramine - diphenylhydramine 2 nd generation anti-histamines - cetrizine - azelastine - fexofenadine - loratadine

Anti-Histamines:

Intranasal corticosteroid therapy Potent topical activity Administration of low doses directly at site of action Considerable efficacy at low doses High topical: systemic activity ratios Rapid first-pass hepatic metabolism of any systemically absorbed drug, to compounds with negligible activity

Intranasal corticosteroid therapy:

The “Ideal” Drug For Allergic Rhinitis Should Have The Following Features: Inhibit both early and late phases Be an H1 blocker Counter effects of other mediators Fast-acting, to control the early phase Dosing- od or bd for compliance No side effects Manage all symptoms Intranasal administration JACI 1999; 103:S388

The “Ideal” Drug For Allergic Rhinitis Should Have The Following Features::

The “Ideal” Drugs Are…… “Corticosteroids are undoubtedly the pharmacotherapeutic agents with the broadest application for the treatment of many types of rhinitis” Otolaryngol Head Neck Surg 1992, 107, 855-60

The “Ideal” Drugs Are……:

Management of Allergic Rhinitis Allergen Avoidance Intermittent Symptoms Persistent Symptoms Mild Moderate-severe Mild Moderate-severe Oral H1 blocker Intranasal H1blocker and/or decongestant No Improvement : switch or add LTRA Oral H1 blocker and/or LTRA Intranasal H1 blocker and/or decongestant Intranasal CS Oral H1 blocker and/or LTRA Intranasal H1 blocker and/or decongestant Intranasal CS Review patient after 2-4 weeks No improvement step up Improved: continue for 1 month If intranasal CS reduced by1/2 Intranasal CS If nose very blocked add oral CS or decongestant or LTRA Improved Not improved Step-down and continue treatment for > 3 month Review diagnosis, compliance, or other causes Blockage: add LTRA or decongestant or oral CS (short term) or increase INCS Rhinorrhea: add ipratropium Itch/sneeze/rhinorrhea add H1 blocker No improvement: refer to specialist

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Management of vasomotor rhinitis Use of an older-generation antihistamine plus a decongestant is usually effective Ipratropium bromide nasal spray may also be effective for this condition specially in when patients did not respond to the older-generation A/D preparation Where A/D preparation contraindicated such as in a patient with glaucoma or symptomatic benign prostatic hypertrophy.

Management of vasomotor rhinitis:

Management of post-viral rhinitis A+D comibination A+D combination dex-brompheniramine maleate (6 mg bid) or azatadine maleate (1 mg bid) + terfenadine or loratadine + sustained-release pseudo-ephedrine sulfate (120 mg bid) sustained-release pseudo-ephedrine sulfate (120 mg bid) Based on these data, the older generation of antihistamines should be used preferentially in patients with UACS that is non-histamine-mediated. The older-generation ( ie , first-generation) antihistamines probably work because of their anti-cholinergic properties. In most patients, some improvement in cough will be seen within days to 2 weeks of the initiation of therapy

Management of post-viral rhinitis A+D comibination:

Severe side effects have usually not been a major problem with the first-generation A/D preparations in the context of treating cough Sedation is the primary side effect due to the antihistamine whether the sedation effect seen with first-generation antihistamines is really significantly greater than with the newer non-sedating preparations? ANSWER IS - ACCP recommendation – initiating therapy once a day at bedtime for a few days before going to twice-daily therapy can sometimes obviate this problem Problems with anti-histamines and solution

Severe side effects have usually not been a major problem with the first-generation A/D preparations in the context of treating cough:

Problems with decongestants Insomnia Difficulty with urination (primarily in older men) Jitteriness Tachycardia or palpitations, Worsening of hypertension, and Increased intraocular pressures in patients with glaucoma

Problems with decongestants:

Management of sinusitis Although sinusitis is usually thought of as being caused by bacterial infection, acute sinusitis (generally defined as being of ≤ 3 weeks duration ) is probably most often caused by acute viral rhinosinusitis ( Ie , “the common cold” ) because it is clinically often difficult to distinguish acute viral rhinosinusitis from acute bacterial sinusitis it may be reasonable to hold off the use of antibiotics and instead to first prescribe a first-generation A/D preparation for 1 week.

Management of sinusitis:

Therapy for acute bacterial sinusitis includes - Antibiotics Intranasal corticosteroids to decrease inflammation Decongestants such as oxymetazoline hydrochloride. Antibiotics of mainly beta- lactam groups considering Streptococcus pneumonia, H. influenzae

Therapy for acute bacterial sinusitis includes - :

Management of chronic sinusitis EVEN LESS CLEAR-CUT The role of bacterial infection and the importance of antibiotic therapy are controversial . RECENT RECOMMENDATION A minimum of 3 weeks of treatment with an antibiotic effective against H influenzae , mouth anaerobes, and S. pneumoniae A minimum of 3weeks of oral treatment with an older-generation A/D twice per day 5 days of treatment with a nasal decongestant twice per day When cough disappears with this therapy, intranasal corticosteroids should be continued for 3 months Refractory to medical therapy and in whom anatomic obstruction is present that is thought to be amenable to endoscopic sinus surgery

Management of chronic sinusitis:

So what are the recommendations? In patients in whom the cause of the UACS-induced cough is apparent, specific therapy directed at this condition should be instituted. For patients with chronic cough, an empiric trial of therapy for UACS should be administered because improvement or resolution of cough in response to specific treatment is the pivotal factor in confirming the diagnosis of UACS as a cause of cough. A patient who is suspected of having UACS-induced cough who does not respond to empiric A/D therapy with a first-generation antihistamine should next undergo sinus imaging. Although chronic sinusitis may cause a productive cough, but it may also be clinically silent in that the cough can be relatively or even completely non-productive and none of the typical findings associated with acute sinusitis may be present.

So what are the recommendations?:

In patients for whom a specific etiology of chronic cough is not apparent, empiric therapy for UACS in the form of a first-generation A/D preparation should be prescribed before beginning an extensive diagnostic workup. So what are the recommendations?

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After successful treatment thank you doc SIP improves a lot

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