Asthma Management

DEFINITION

  • Chronic inflammatory airway disease characterized by variable reversiblemairway obstruction, airway hyper-responsiveness and bronchial inflammation.

AETIOLOGY

  • Genetic factors: Positive family history, twin studies. Almost all asthmatic patients show some atopy (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens). Linkages to multiple chromosomal locations point to ‘genetic heterogeneity’.
  • Environmental factors: House dust mite, pollen, pets (e.g. urinary proteins, furs), cigarette smoke, viral respiratory tract infection, Aspergillus fumigatus spores, occupational allergens (isocyanates, epoxy resins).

PATHOLOGY/PATHOGENESIS

  • Early phase (up to 1 h): Exposure to inhaled allergens in a presensitized individual results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.
  • Late phase (after 6–12 h): Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness.
  • Structural cells (bronchial epithelial cells, fibroblasts, smooth muscle and vascular endothelial cells), may also release cytokines, profibrogenic and proliferative growth factors, and contribute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts (‘airway remodeling’).

EPIDEMIOLOGY

  • Affects 10% of children and 5% of adults. The prevalence of asthma appears to be increasing. ,¼<. Acute asthma is a very common medical emergency and still responsible for 1000–2000 deaths/year in the UK.

HISTORY

  • Episodes of wheeze, breathlessness, cough; worse in the morning and at night.
  • Ask about interference with exercise, sleeping, days off school and work.
  • In an acute attack it is important to ask whether the patient has been admitted to hospital because of his/her asthma, or to ITU, as a gauge of potential severity.
  • Precipitating factors: Cold, viral infection, drugs (b-blockers, NSAIDs), exercise, emotions.
  • May have a history of allergic rhinitis, urticaria, eczema, nasal polyps, acid reflux and family history.

EXAMINATION

  • Tachypnoea, use of accessory muscles, prolonged expiratory phase, polyphonic wheeze, hyperinflated chest.
  • Severe attack: PEFR <50% predicted, pulse > 110/min, respiratory rate > 25/min, inability to complete sentences.
  • Life-threatening attack: PEFR < 33%, silent chest, cyanosis, bradycardia, hypotension, confusion, coma.

INVESTIGATIONS

  • Acute : Peak flow, pulse oximetry, ABG, CXR (to exclude other diagnoses, e.g. pneumothorax, pneumonia), FBC (” WCC if infective exacerbation), CRP, U&Es, blood and sputum cultures.
  • Chronic : PEFR monitoring: There is often a diurnal variation with a morning ‘dip’.
  • Pulmonary function test: Obstructive defect, with improvement after a trial of a b2-agonist.
  • Blood: Eosinophilia, IgE level, Aspergillus antibody titres (see allergic Aspergillus lung disease).
  • Skin prick tests: May help in the identification of allergens.

MANAGEMENT

 

Acute:

 

  • Resuscitate, monitor O2 sats, ABG and PEFR.
  • High-flow oxygen.
  • Nebulized b2-agonist bronchodilator salbutamol (5 mg, initially continuously, then 2–4hourly), ipratropium (0.5mg qds).
  • Steroid therapy (100–200mg IV hydrocortisone, followed by 40mg oral prednisolone for 5–7 days).
  • If no improvement : IV magnesium sulphate. Consider IV aminophylline infusion or IV salbutamol.
  • Summon anaesthetic help if patient is getting exhausted (PCO2 increasing).
  • Treat any underlying cause (e.g. infection, pneumothorax). Give antibiotics if there is evidence of chest infection (purulent sputum, abnormal CXR, ” WCC, fever). Monitor electrolytes closely (bronchodilators and aminophyline).
  • May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early.
  • Discharge : When PEF >75% predicted or patient’s best, diurnal variation < 25%, inhaler technique checked, stable on discharge medication for 24 h, patient owns a PEF meter and has steroid and bronchodilator therapy. Arrange follow-up.
  • Chronic ‘stepwise’ therapy: Start on the step appropriate to initial severity and step up or down to control symptoms. Treatment should be reviewed every 3–6 months.

COMPLICATIONS

  • Growth retardation, chest wall deformity (e.g. pigeon chest), recurrent infections, pneumothorax, respiratory failure, death.

Pharyngitis/Tonsillitis

Inflammation of the pharynx or tonsils. Pharyngitis accounts for 1% to 2% of visits to outpatient clinics, physicians’ offices, and emergency rooms.
Between 10% and 20% of these cases are caused by infection with group A β-hemolytic streptococcus (GABHS).

OTHER DEFINITION

_ Streptococcal tonsillitis is manifested as acute onset of fever, headache, neck pain, odynophagia, sore throat, otalgia, red tongue with enlargement of papillae, sore throat, red swollen uvula, and tender anterior cervical adenitis.

_ Peritonsillar abscess (accumulation of pus between the tonsil and its capsule) is the most common complication of acute tonsillitis. Clinical signs include deformed posterior pharynx, medial displacement of the uvula, trismus, and muffled voice (hot-potato voice).

SEVEN DANGER SIGNS IN PATIENT WITH SORE THROAT

  1. Persistence of symptoms longer than 1 wk without improvement
  2. Respiratory difficulty, particularly stridor
  3. Difficulty in handling secretions
  4. Difficulty in swallowing
  5. Severe pain in the absence of erythema
  6. A palpable mass
  7. Blood, even in small amounts, in the pharynx or ear

CAUSES

VIRUSES

  • Respiratory syncytial virus
  • Influenza A and B
  • Epstein-Barr virus
  • Adenovirus
  • Herpes simplex

BACTERIA

  • Group A streptococci (GAS)
  • Neisseria gonorrhoeae
  • Fusobacterium necrophorum (10% of pharyngitis)

OTHER ORGANISM

  • Mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Arcanobacterium haemolyticum

PHYSICAL & CLINICAL FINDING

  • May appear normal to severely erythematous
  • Tonsillar hypertrophy and exudates commonly seen but do not indicate etiology
  • Rhinorrhea
  • Conjunctivitis
  • Cough
  • High fever
  • Systemic signs of infection
  • Herpes simplex or enterovirus infection: vesicles
  • Streptococcal infection

WORKUP

The Centor criteria to identify patients at risk for GAS consists of:

  1. Fever subjective or measured >38.1° C (100.5° F)
  2. Absence of cough
  3. Tonsillar exudates
  4. Tender anterior cervical lymphadenopathy

Rapid streptococcal antigen test

LABORATORY TESTS

  • CBC
  • Viral cultures, serologic studies rarely needed
  • Monospot if diagnosis is unclear

TREATMENT

NONPHARMACOLOGIC THERAPY

  • Fluids
  • Salt water gargles

PHARMACOLOGIC THERAPY

  • Analgesics: aspirin (adults) or acetaminophen or ibuprofen (adults and children)
  • If streptococcal infection proven or suspected: (1). Penicillin V 500 mg PO bid for 10 days or benzathine penicillin 1.2 million U IM once (adults). Children: penicillin V 250 mg bid or tid. (2). Erythromycin 500 mg PO bid or 250 mg qid for 10 days or azithromycin if penicillin allergic.
  • If gonococcal infection proven or suspected: ceftriaxone 250 mg IM once
  • Amoxicillin 500 mg tid for 10 days is the primary antibiotic treatment of streptococcal tonsillitis. Macrolides or clindamycin can be used in penicillin allergic patients.
  • Treatment of peritonsillar abscess is drainage through needle or incision

Allergic Rhinitis (Hay Fever)

Definition

  • Rhinitis characterized by an IgE-mediated hypersensitivity to foreign allergens
  • Acute-and-seasonal or chronic-and-perennial
  • Perennial allergic rhinitis often confused with recurrent colds


Etiology

  • When allergens contact the respiratory mucosa, specific IgE antibody is produced in susceptible hosts
  • Concentration of allergen in the ambient air correlates directly with the rhinitis symptoms


Epidemiology

  • Age at onset usually <20 yrs
  • More common in those with a personal or family history of allergies/atopy

Clinical Features

  • Nasal: obstruction with pruritus, sneezing
  • Clear rhinorrhea (containing increased eosinophils)
  • Itching of eyes with tearing
  • Frontal headache and pressure
  • Mucosa – swollen, pale, lavender colour, “boggy”
  • Seasonal (summer, spring, early autumn)
  • Pollens from trees
  • Lasts several weeks, disappears and recurs following year at same time
  • Perennial
  • Inhaled: house dust, wool, feathers, foods, tobacco, hair, mould
  • Ingested: wheat, eggs, milk, nuts
  • Occurs intermittently for years with no pattern or may be constantly present


Complications

  • Chronic sinusitis/polyps
  • Serous otitis media

Diagnosis

History

Direct exam

Allergy testing

Treatment

Education: identification and avoidance of allergen

Nasal irrigation with saline

Antihistamines e.g. diphenhydramine, fexofenadine

Oral decongestants e.g. pseudoephedrine, phenylpropanolamine

Topical decongestant (may lead to rhinitis medicamentosa)

Other topicals: steroids (fluticasone), disodium cromoglycate, antihistamines, ipratropium bromide

Oral steroids if severe

Desensitization by allergen immunotherapy

Sinusitis Inflammation

DEFINITION
Sinusitis is infl ammation of the mucous membranes lining one or more of the paranasal sinuses. The various presentations are as folllows:
● Acute sinusitis: infection lasting less than 30 days, with complete resolution of symptoms
● Subacute infection: lasts from 30 to 90 days, with complete resolution of symptoms
● Recurrent acute infection: episodes of acute infection lasting less than 30 days, with resolution of symptoms, which
recur at intervals of at least 10 days apart
● Chronic sinusitis: infl ammation lasting more than 90 days, with persistent upper respiratory symptoms
● Acute bacterial sinusitis superimposed on chronic sinusitis:
new symptoms that occur in patients with residual symptoms from prior infection(s). With treatment, the new
symptoms resolve but the residual ones do not.
PHYSICAL FINDINGS AND CLINICAL PRESENTATION
● Patients often give a history of a recent upper respiratory illness with some improvement, then a relapse.
● Mucopurulent secretions in the nasal passage
● Purulent nasal and postnasal discharge lasting more than 7 to 10 days
● Facial tightness, pressure, or pain
● Nasal obstruction
● Headache
● Decreased sense of smell
● Purulent pharyngeal secretions, brought up with cough, often worse at night
● Erythema, swelling, and tenderness over the infected sinus in a small proportion of patients
● Diagnosis cannot be excluded by the absence of such findings.
● These fi ndings are not common, and do not correlate with number of positive sinus aspirates.
● Intermittent low-grade fever in about one half of adults with acute bacterial sinusitis
● Toothache is a common complaint when the maxillary sinus is involved.
● Periorbital cellulitis and excessive tearing with ethmoid sinusitis
● Orbital extension of infection: chemosis, proptosis, impaired extraocular movements.
Characteristics of acute sinusitis in children with upper respiratory tract infections:
● Persistence of symptoms
● Cough
● Bad breath
● Symptoms of chronic sinusitis (may or may not be present)
● Nasal or postnasal discharge
● Fever
● Facial pain or pressure
● Headache
● Nosocomial sinusitis is typically seen in patients with nasogastric tubes or nasotracheal intubation.

CAUSE
● Each of the four paranasal sinuses is connected to the nasal cavity by narrow tubes (ostia), 1 to 3 mm in diameter; these drain directly into the nose through the turbinates. The sinuses are lined with a ciliated mucous membrane (mucoperiosteum).
● Acute viral infection
● Infection with the common cold or infl uenza
● Mucosal edema and sinus infl ammation
● Decreased drainage of thick secretions, obstruction of the sinus ostia
● Subsequent entrapment of bacteria
a. Multiplication of bacteria
b. Secondary bacterial infection
 Other predisposing factors
● Tumors
● Polyps
● Foreign bodies
● Congenital choanal atresia
● Other entities that cause obstruction of sinus drainage
● Allergies
● Asthma
● Dental infections lead to maxillary sinusitis.
● Viruses recovered alone or in combination with bacteria (in 16% of cases):
● Rhinovirus
● Coronavirus
● Adenovirus
● Parainfluenza virus
● Respiratory syncytial virus
● The principal bacterial pathogens in sinusitis are Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis.
● In the remainder of cases, fi ndings include Streptococcus pyogenes, Staphylococcus aureus, alpha-hemolytic streptococci, and mixed anaerobic infections (Peptostreptococcus, Fusobacterium, Bacteroides, Prevotella).

Infection is polymicrobial in about one third of cases.
● Anaerobic infections seen more often in cases of chronic sinusitis and in cases associated with dental infection; anaerobes are unlikely pathogens in sinusitis in children.
● Fungal pathogens are isolated with increasing frequency in immunocompromised patients but remain uncommon
pathogens in the paranasal sinuses. Fungal pathogens include Aspergillus, Pseudallescheria, Sporothrix, phaeohyphomycoses, Zygomycetes.
● Nosocomial infections occur in patients with nasogastric tubes, nasotracheal intubation, cystic fi brosis, or those who are immunocompromised.
● S. aureus
● Pseudomonas aeruginosa
● Klebsiella pneumoniae
● Enterobacter spp.
● Proteus mirabilis
Organisms typically isolated in chronic sinusitis:
● S. aureus
● S. pneumoniae
● H. infl uenzae
● P. aeruginosa
● Anaerobes

DIFFERENTIAL DIAGNOSIS
● Migraine headache
● Cluster headache
● Dental infection
● Trigeminal neuralgia
WORKUP
● Water’s projection: sinus radiograph
● CT scan
● Much more sensitive than plain radiographs in detecting acute changes and disease in the sinuses
● Recommended for patients requiring surgical intervention, including sinus aspiration; it is a useful adjunct to
guide therapy.
● Transillumination
● Used for diagnosis of frontal and maxillary sinusitis
● Place transilluminator in the mouth or against cheek to assess maxillary sinuses, and under the medial aspect of the supraorbital ridge to assess frontal sinuses.
● Absence of light transmission indicates that sinus is filled with fluid.
● Dullness (decreased light transmission) is less helpful in diagnosing infection.
● Endoscopy
● Used to visualize secretions coming from the ostia of infected sinuses
● Culture collection via endoscopy often contaminated by nasal flora; not nearly as good as sinus puncture
● Sinus puncture
● Gold standard for collecting sinus cultures
● Generally reserved for treatment failures, suspected intracranial extension, nosocomial sinusitis.
TREATMENT
Nonpharmacologic therapy
● Sinus drainage
● Nasal vasoconstrictors, such as phenylephrine nose drops, 0.25% or 0.5%

● Topical decongestants should not be used for more than a few days because of the risk of rebound congestion.
● Systemic decongestants
● Nasal or systemic corticosteroids, such as nasal beclomethasone, short-course oral prednisone
● Nasal irrigation, with hypertonic or normal saline (saline may act as a mild vasoconstrictor of nasal blood fl ow)
● Use of antihistamines has no proved benefi t, and the drying effect on the mucous membranes may cause crusting,
which blocks the ostia, thus interfering with sinus drainage.
● Analgesics, antipyretics.
Antimicrobial therapy
● Most cases of acute sinusitis have a viral cause and will resolve within 2 weeks without antibiotics.
● Current treatment recommendations favor symptomatic treatment for those with mild symptoms.
● Antibiotics should be reserved for those with moderate to severe symptoms who meet the criteria for diagnosis of
bacterial sinusitis.

● Antibiotic therapy is usually empirical, targeting the common pathogens.
● First-line antibiotics include amoxicillin, TMP-SMZ.
● Second-line antibiotics include clarithromycin, azithromycin, amoxicillin-clavulanate, cefuroxime axetil, loracarbef, ciprofloxacin, levofloxacin.
● For patients with uncomplicated acute sinusitis, the less expensive first-line agents appear to be as effective as the
costlier second-line agents.

Surgery
● Surgical drainage indicated
● If intracranial or orbital complications suspected
● For many cases of frontal and sphenoid sinusitis
● For chronic sinusitis recalcitrant to medical therapy
● Surgical débridement imperative for treatment of fungal sinusitis

Asthma Attack

Introduction
Asthma is a syndrome with a chronic but variable clinical course and presentation. Its main features are (1)
reversible airflow obstruction, (2) nonspecific airways hyper-reactivity, and (3) airways inflammation. The nonspecific nature of the hyper-reactivity is perhaps a reflection of airway inflammation. Symptoms are triggered
by nonallergic stimuli such as smoke and strong odors and quantifi ed by sensitivity to inhalational challenge
to nonallergic stimuli such as histamine. Airway hyperreactivity predisposes patients to symptoms in a variety
of environments.

Both children and adults develop asthma. The remission rate in adults is 10% to 15% but is more than 50%
in children. Despite advances in the understanding of asthma and better medications, asthma morbidity and
mortality have increased. During the past 110 years, our understanding of asthma has changed greatly. It was
long considered a disease of “twitchy” airways and a minor ailment that, according to Osler, allowed the patient
to “pant into old age.” Now, asthma is considered a disease of chronic fl uctuating airways infl ammation with
a lethal potential of 5000 deaths annually in the United States. It is a major public health problem that results
in 1.8 million emergency room visits per year, with about 10% of patients requiring hospitalization at a cost
of $12 billion annually in the United States.

Etiology and Pathogenesis
Asthma manifests as inflammation in the lower airways. Over time, structural changes in the airway called remodeling result (i.e., muscle hypertrophy and thickening of the basement membrane) . Acute asthma exacerbations cause airway muscle contraction, edema and sloughing of the airway mucosa, and the accumulation of mucus, cellular debris, and exudative secretions in the airway lumen. These changes degrade airway function, causing respiratory symptoms and even death by suffocation.
There are clinical and epidemiologic links between asthma and immunoglobulin E (IgE). Transcription
factors, such as nuclear factor-KB and members of the signal transduction-activated transcription (STAT) factor
family, act on genes encoding for infl ammatory cytokines, such as interleukins (ILs), and appear to initiate and sustain airway  inflammation. Corticosteroids are the most effective controllers of asthma. They inhibit these
transcription factors and airway infl ammation. Asthma refractory to corticosteroids has been linked to the tumor
necrosis factor axis. However, the newly described subset of natural killer T (NKT) cells, CD1d-restricted NKT
cells, with potent immunoregulatory functions and associated with asthma, are also resistant to modulation by
corticosteroids.

A widely held mechanistic explanation is that inhaled antigen activates mast cells and T helper type 2 (Th2)
lymphocytes, causing mediator release that promotes a persistent eosinophilic airway infl ammation. There is no
clear understanding of which biologic infl uences lead to chronic eosinophilic airway infl ammation and hyperresponsiveness in asthma. Genetic factors (e.g., polymorphism for the IgE receptor, β receptor, matrix
metalloproteinase, and CD14), environmental factors (e.g., excessive hygiene, vaccinations), and triggers (e.g., viral
infection, exposures to tobacco smoke, pollutants, allergens) have all been implicated in the pathogenesis of asthma . Most asthmatic patients are atopic and have IgE-mediated disease, although there is evidence suggesting that intrinsic or nonatopic asthmatic patients may produce local, as opposed to circulating, IgE. Inflammation in atopic asthma can be demonstrated when the patient is challenged with inhaled allergen.

The sensitive patient will show decline in pulmonary function demonstrated by obstruction of airflow with spirom-etry and decrease in the forced expiratory fl ow at 1 second (FEV1) and in the peak expiratory fl ow rate (PEFR). There is an initial decline within about 20 minutes associated with histamine release from mast cells that is stimulated by allergen binding to IgE on the mast cell surface. This immediate reaction is blocked by antihistamines but not by steroids. Classically, a spontaneous recovery occurs, only to be followed by a second, later decline in fl ow rates. Steroid pretreatment inhibits this late phase reaction, which is manifest by the recruitment of inflammatory cells into and around the lower airway.

Salivary Gland Tumor

Salivary gland neoplasms are benign or malignant tumors of a salivary gland (parotid, submandibular, or sublingual).

PHYSICAL FINDINGS AND CLINICAL PRESENTATION

  • Parotid gland
  • Painless swelling overlying the masseter muscle (under the temporomandibular joint)
  • Pain
  • Facial nerve palsy
  • Cervical lymph nodes
  • Mass in oral cavity
  • Submandibular gland: swelling under anterior portion of the mandible
  • Sublingual gland: intraoral swelling under the tongue, medial to the mandible
  • Salivary gland neoplasms most often present as slowgrowing, well-circumscribed masses. Pain, rapid growth, nerve weakness, fi xation to skin or underlying muscle, and paresthesias usually are indicative of malignancy.

DIFFERENTIAL DIAGNOSIS

Benign tumors

  • Mixed tumor (usually parotid)
  • Adenolymphoma (Warthin’s tumor)
  • Pleomorphic adenoma
  • Capillary hemangioma, lymphangioma (in children)
  • Intraductal papilloma
  • Other (e.g., myoepithelioma, canalicular adenoma, basal cell adenoma)

Malignant tumors

  • Mucoepidermoid carcinoma (most common malignant tumor of the parotid gland)
  • Adenoid cystic carcinoma
  • Adenocarcinoma
  • Malignant mixed tumor
  • Squamous cell carcinoma
  • Other

WORKUP

  • Fine-needle aspiration. The sensitivity, specificity, and accuracy of parotid gland aspirates are approximately 92%, 100%, and 98%, respectively
  • Imaging by CT scan or MRI
  • Open biopsy

TREATMENT

Malignant tumors

  • Surgery is the mainstay of treatment; gland resection and neck dissection if lymph nodes are involved
  • A lateral lobectomy with preservation of facial nerve should be considered for tumors confined to the superficial lobe of the parotid gland. Gross tumor should not be left in situ, but if the facial nerve is able to be preserved by “peeling” the tumor off the nerve, it should be attempted, followed by radiation therapy for microscopic disease.
  • Postoperative radiation is indicated for high-grade malignancies demonstrating extraglandular disease, perineural invasion, direct invasion of surrounding tissues, or regional metastases.
  • Chemotherapy

Benign tumors

  • Surgery for tumor resection