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Bronchial asthma

Asthma is a chronic inflammatory airway disease characterized by bronchial hyperresponsiveness and reversible airflow limitation. The document traces the history of asthma from its first description in ancient Greek texts to modern recognition of its inflammatory pathophysiology. It then provides details on the definition, epidemiology, classification, pathogenesis, clinical features, investigations and management of asthma.

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ASTHMA
History  Asthma : derived from the Greek aazein, meaning "sharp breath." The word first appears in Homer's Iliad.  In 450 BC. Hippocrates: more likely to occur in tailors, anglers, and metalworkers.  Six centuries later, Galen: caused by partial or complete bronchial obstruction.  1190 AD, Moses Maimonides: wrote a treatise on asthma, describing its prevention, diagnosis, and treatment  17th century, Bernardino Ramazzini: connection between asthma and organic dust.  1901: The use of bronchodilators started.  1960s: inflammatory component of asthma was recognized and anti-inflammatory medications were added to the regimens.
What is known about asthma?
ASTHMA  Chronic inflammatory condition of the airways characterized by; - airflow limitation (reversible with treatment) - airway hyper-responsiveness to a wide range stimuli - inflammation of the bronchi  In chronic asthma, inflammation maybe accompanied by irreversible airflow limitation  Symptoms are cough, wheeze, chest tightness, and shortness of breath which often worse at night
Simple Definition A reversible chronic inflammatory airway disease which is characterized by bronchial hyper- responsiveness of the airways to various stimuli, leading to widespread bronchoconstriction, airflow limitation and inflammation of the bronchi causing symptoms of cough, wheeze, chest tightness and dyspnoea.
Epidemiology  Common disease with unacceptably high morbidity and mortality  Commonly underdiagnosed and undertreated  Only 36.1% of adult asthmatics ever had their peak flow measured  Higher prevalence in rural (4.5%) than in urban areas (4%),lower educational status(5.6%) and lower income  Majority of patients(87.3%) had mild asthma; 9.9% had moderate asthma and 2.7% had severe asthma  Among severe asthmatics, only 19.4% were on inhaled corticosteroids 87% 10% 3% Asthmatic patient Mild Moderate Severe
Epidemiology
EPIDEMIOLOGY  The prevalence of asthma has increased 61% over the last two decades.  Asthma is the leading chronic illness among children.  Asthma results in 10 million lost school days and 3 million lost work days.  Deaths from asthma have increased by 31% since 1980.
Classification  Extrinsic – implying a definite external cause  more frequently in atopic inviduals  (atopic – individual which tends to develop hypersensitivity by contact with allergens)  often starts in childhood - accompanied by eczema  Intrinsic/cryptogenic – no causative agent can be identified  starts in middle age
Types of Asthma According to the severity: helpful for treatment and management. Very mild Mild Moderate Moderately Severe Severe
Types of Asthma According to pathophysiology Allergic asthma Intrinsic (Non-Allergic) Exercise-induced Occupational (allergic) Steroid-resistant ABPA (allergic)
Pathogenesis  Complex, not fully understood  numbers of cells, mediators, nerves, and vascular leakage -activated by expose to allergens or several mechanism Inflammation  Eosinophils, T-lymphocytes, macrophages and mast cell Remodeling  Deposition of repair collagens and matrix proteins- damage  Loss of ciliated columnar cells- metaplasia – increase no of secreting goblet cells
Pathologic features of asthma i. Inflammatory cell infiltration of the airways ii. Increased thickness of the bronchial smooth muscle iii. Partial or full loss of the respiratory epithelium iv. Subepithelial fibrosis v. Hypertrophy and hyperplasia of the submucosal glands and goblet cells vi. Partial or full occlusion of the airway lumen by mucous plugs vii. Enlarged mucous glands and blood vessels
Pathophysiology  Smooth muscle contraction  Thickening of airway –cellular infiltration and inflammation  Excessive secrection of mucus Genetic factor Cytokine gene complex (chromosome 5)-IL-4 gene cluster control IL-3, IL-4 , IL-5 and IL-13 Environment factor Childhood expose irritants or childhood infection
Pathophysiology  Extrinsic asthma: Atopic/allergic, occupational, allergic bronchopulmoary aspergillosis.  Atopic or allergic  Dust, pollens, animal dander, food etc. Family history of atopy.  ↑ serum IgE.  Skin test with Ag  wheal, flare ( Classical IgE mediated response)  Exposure of pre-sensitised mast cells to the Ag stimulates chemical mediators from these cells. Type 1 hypersensitivity.
1.Early phase  Inhaled Antigen  Sensitised mast cells on the mucosal surface  mediator release.  Histamine bronchoconstriction, increased vascular permeability.  prostaglandin D 2  bronchoconstriction, vasodilatation.  Leucotriene C4,D4, E4  Increased vascular permeability, mucus secretion and bronchoconstriction.  Direct subepithelial parasympathetic stimulation  bronchoconstriction.
2.Late phase  starts 4 to 8 hours later  Mast cell release additional cytokine  Influx of leukocytes(neutrophil,eosinophil)  Eosinophils are particularly important- exert a variety of effect
Pathophysiology  Atopic Asthma Trigger Eg.dust,pollen, animal dander TH2 cell IL5 IL4 Eosino phil IgE B cell Mast cell IgE antibody Mediators Eg.Histamine, leukotrines Bronchospasm Increase vascular permeability Mucus production Immediate phase(minutes)
Bronchial inflammation Environment factor Genetic prediposition Bronchial hyperreactivity + trigger factors Cough, Wheeze, Breathlessness, Chest tightness Oedema BronchoC Mucus production Airways narrowing
Aetiology and triggers  Complex and multiple environmental and genetic determinant a) Genetic factors b) Allergen exposure house dust mite, household pets, grass pollen c) Atmospheric polution sulphur dioxide, ozone, ciggerate smoke, perfume d) Dietary deficiency of antioxidants  vit E and selenium may protect asthma in children(freshfruits and vegetables)
Aetiology and triggers e) Occupational sensitizers  isocyanates(from industrial coating, spray painting)  colophony perfumes(electronic industries) e) Drugs  NSAIDS  B-blocker(B1 adrenergic blocker drug such as atenolol is avoided to treat HPT and angina in asthmatic pt f) Cold air g) Exercise  exercise-induced wheeze is driven by histamin and leukotrienes which are release from mast cells when epithelial lining fluid of the bronchi become hyperosmolar owing to drying and cooling during exercise h) Emotion
History Presenting symptoms:  Cough ± sputum - time: become worse at night - duration: chronic / acute - associated with wheezing - fever? URTI  Wheeze - max during expiration and accompanied by prolonged expiration
Cough History 1.Ask specifically about the symptoms: -Cough?how is the cough? more severe at night or on day? associated symptoms like dyspnea & wheezing? how long is the cough? Recurrent?Any previous similar episode? Aggravated factor?like cough become severe after exercise?or the cough is initiated after exercise?
Cough History 2.If the cough is associated with dyspnea and wheezingis it relieved by bronchodilator? 3.Ask for any precipatating factors -whether the symptoms(cough,dyspnea,wheezing) started after exposure to weather changes, dust, exercise, infection or drugs? 4.Is there any pets,carpet or feather pillow in home?(easily trapped dust and the dust or animal fur will cause exacerbation of asthma)
Dyspnoea History  Dyspnoea - onset: after exercise? cold? dust? animal fur? emotion? - severity and pattern: varies from day to day or from hour to hour - no chest pain
History Clinical features  Recurrent episodes of wheezing,chest tightness,breathlessness and cough  Precipitants- cold,allergen,pollutant,viral urti  Exercise tolerance  Disturbed sleep  Other atopic disease  Home-Pet?Carpet?  Occupation
History Clinical features  Display diurnal pattern,symptoms and PEF worse in the morning Mild intermittent asthma- asymptomatic between exacerbation Persistent asthma-chronic wheeze and breathlessness
History 5.Any history of atopy(eczema,hay fever) or allergic rhinitis? 6.Any family history of asthma?Any childhood asthmatics? 7.Whether he is a smoker or any family members is a smoker? 8.What is his occupation? Exposure to chemicals?
History Past medical history:  Experienced asthma attack before  Taking any medications: NSAIDs / β-blocker / aspirin (non atopic asthma) Family history:  Has family history of asthma
History Social history:  Occupation: expose to fumes/organic/chemical dust  House: near to factory? Pets? Dust? Carpet? Feather pillow?  Smoking in any family members
known asthmatic  When he was diagnosed with asthma?  How the asthma was diagnosed?  Who diagnosed it?  Whether he is on prophylaxis?  What type of prophylaxis?  How he get the drugs and how many dosage of the drugs?  Whether he know how to deliver the drugs properly?  How is his compliance to drugs?
Physical examination  General inspection: - tachypnoeic, sign of respiratory distress, effort of breathing, cyanosis (life-threatening)  Inspection: - fingers: tar staining - pulse rate: tachycardia and pulsus paradoxus, bradycardia (life- threatening) - used of accessory muscles or recession - wheezing
Chest  Inspection: - shape: hyperinflated in severe asthma - movement of chest/silent chest (life-threatening) - chest deformity: - recession:  Palpation: - chest expension may be reduce (hyperinflated)/ normal - apex beat: may be displaced -vocal fremitus: decrease  Percussion: - may be hyperresonance / normal  Auscultation: - breath sound: vesicular - ronchi in expiratory phase, may be both in severe asthma - prolonged expiratory phase -vocal resonance decrease / normal
Clinical features Sign • Tachypnoea,audible wheeze,hyperinflated chest,hyperresonant percussion note,diminished air entry,widespread polyphonic wheze • Severe attack – inability to complete sentences, pulse >110bpm, RP>25/min, PEF 33-50% • Life-threatening attack- silent chest,cyanosis,bradycardia,exhaustion, PEF < 33%,confusion • Pulsus paradoxus (exaggeration of the normal variation in the pulse volume with respiration, becoming weaker with inspiration and stronger with expiration )
Correlation + The symptoms of asthma consist of a triad of dyspnea, cough, and wheezing. + At the onset of an attack, patients experience a sense of constriction in the chest, often with a nonproductive cough. + Respiration becomes audibly harsh; wheezing in both phases of respiration becomes prominent; expiration becomes prolonged; and patients frequently have tachypnea, tachycardia, and mild systolic hypertension. + The lungs rapidly become overinflated. + If the attack is severe or prolonged, there may be a loss of adventitial breath sounds, and wheezing becomes very high pitched. + The accessory muscles become visibly active, and a paradoxical pulse often develops.
Diagnosing asthma
Diagnosing asthma  Reversible and variable airflow limitation-as measured by a peak expiratory flow (PEF) meter in any of the following ways:  PEF increases more than 15% and 200mls 15 to 20 mins after inhaling a short acting beta2 agonist, or  PEF varies more than 20% from morning measurement upon arising to measurement 12 hours later in patients who are taking a bronchodilator, or  PEF decreases more than 15% after 6 mins of running or exercise
Differential diagnosis + Upper airway obstruction – Tumor – Epiglottitis – Vocal cord dysfunction – Obstructive sleep apnea + Bronchomalacia + Endobronchial lesion + Foreign body + Congestive heart failure + Gastroesophageal reflux + Sinusitis + Adverse drug reaction – Aspirin – Beta-adrenergic antagonist – ACE inhibitors – Inhaled pentamidine + Allergic bronchopulmonary aspergillosis + Hyperventilation with panic attacks
Non-specific investigation  Non-specific: - full blood count and differential count: increase number of eosinophils number - arterial blood gases - sputum test: number of eosinophils - chest X-ray: hyperinflated
Specific investigation  Specific: - respiratory function test: 1. peak expiratory flow 2. spirometry - exercise tests -histamine/methacholine bronchial provocation test - trial of corticosteroids
Reversibility Test + This test is done to see whether the obstruction can be relieved by the use of a short-acting bronchodilator eg salbutamol + An improvement of 15% or more (as measured on the peak flow meter) is diagnostic of asthma. + However, in severe chronic disease or patient who has treated with long-acting bronchodilators, little reversibility will be demonstrated.
Reversibility test Forced expiratory manoeuvres before 20 minutes after inhalation of a beta-2- adrenoceptor agonist. Note the increase in FEV1 from 1.0 to 2.5 litres.
Peak expiratory flow rate  Simple and cheap  Subject take full inspiration then blow out forcefully into peak flow meter.  Best used to monitor progression of the asthma and its treatment.  To access possible occupational asthma  PEFR value varies with sex, age and height.
Peak Expiratory Flow Rate (PEFR)  The maximum rate of air breathed out as hard as possible through a measuring device called a peak flow meter, (after a full breath taken in).  Reading is measured in litres/minute (l/min).  Take 3 readings and choose the best  Reading < 80% - presense of obstruction, but not diagnostic of asthma
 Require to take a series of reading - on waking up - prior taking bronchodilator - after taking bronchodilator (before sleep)
PEF measurements 1. During periods of well-being: provides measurement of the patients best PEF value which will provide the target for the doctor and the patient to aim for.Twice daily measurements before any inhaled bronchodilator tx will determine the diurnal variability of airway calibre.Good control of asthma means PEF variability is maintained at less than 10%. 2. During symptomatic episodes: During an attack of asthma PEF fairly accurately measures the degree of bronchospasm.A PEF of less than 50% of normal or best suggests a very severe attack and a PEF of less than 30% suggests a life-threatening attack
Response to treatment
Occupational asthma
Spirometry Test + It is the single best diagnostic test for patients with airflow limitation. + A Spirometry Test + - measures the volume of air blown out against time + - gives more specific information about lung function. + A value is calculated for the amount of air blown out in one second - “Forced Expiratory Volume” or FEV1). + This is divided by the total amount of air blown out until all air is expired - Forced Vital Capacity or FVC). + FEV1/FVC expressed as a percentage value
+ Reading is affected by age, gender and height + Male Spirometry reading range Mild reduction: 2.5 litres or more Moderate reduction :1.5 to 2.49 litres Severe reduction :Less than 1.5 litre + Female Spirometry reading range Mild reduction :2.0 litres or more Moderate reduction: 1.0 to 1.99 litres Severe reduction: Less than 1.0 litre + In asthma, the readings will be reduced, returning to normal between episodes
TLC VC RV IC FRC IRV ERV RV TV TLC : total lung capacity VC : vital capacity RV : reserve volume IC : inspirational capacity FRC : functional residual capacity IRV : inspirational reserve volume TV : tidal volume ERV : expiratory reserve volume  Normal:75-80%  Obstructive airway disease: reduced ratio  Restrictive lung disease: ratio normal or increase (enhanced elastic recoil).
Exercise Test + Done especially in children + Peak flow reading measured before hand + Ask patient to run for 6 min, to increase HR > 160 beats/min + Cannot run – use cold air challenge, isocapnoiec (CO2) hyperventilation, aerosol challenge with hypertonic solution + After exercise – take readings at intervals of 5, 10 and 15 minutes. + Diagnosed asthma - fall in peak flow of 15% or more, after exercise.
Exercise test
histamine/methacholine bronchial provocation test
Chest X-ray Showed lung hyperinflation. Not diagnostic of asthma Useful to rule out other causes eg. Pneumothorax ----------------------------------------------- Hyperinflation and increased bronchovascular markings
Allergies & Atophy Allergen Provocation Test  In suspected occupational asthma and food-allergy related asthma Skin-Prick Test  To identify allergens  A drop of allergen is placed on skin , site is marked and pricked with needle, measured any weals
Approach to management
Management
Severity assessment for acute setting of AEBA Mild Moderate Severe Breathless Walking Talking At rest Can lie down Prefer sitting Hunched forward Talk in Sentences Phrases Words Alertness May be Usually agitated Agitated Central cyanosis Absent Absent Present Use of accessory muscle Absent Moderate Marked Sternal retraction Absent Moderate Marked Wheeze on auscultation Moderate, often end expiratory Loud Loud  Silent Chest Pulsus paradoxus Not palpable May be palpable Often palpable Initial PEF More than 80% 60 – 80% Less than 60% Oximetry on presentation More than 95% 91 – 95% Less than 90%
Severity of AEBA 1
Severity of AEBA 2
Severity of AEBA 3
Management of Chronic Asthma  Aims of management • to recognize asthma • to abolish symptoms • to restore normal or best possible long term airway function • to reduce morbidity and prevent mortality
Approach of chronic asthma  Education of patient and family  Avoidance of precipitating factors  Use of the lowest effective dose of convenient medications minimizing short and long term side effects.  Assessment of severity and response to treatment.
1) Education of patient and family i. Nature of asthma ii. Preventive measures/avoidance of triggers iii. Drugs used and their side- effects iv. Proper use of inhaled drugs v. Proper use of peak flow meter vii. Knowledge of the difference between relieving and preventive medications vii. Recognition of features of worsening asthma  increase in bronchodilator requirement  development of nocturnal symptoms  reducing peak flow rates). viii. Self management plan for selected, motivated patients or parents. ix. The danger of non prescribed self medication including certain traditional medicines.
2) Avoidance of precipitating factors The following factors may precipitate asthmatic attacks: • Beta blockers  contraindicated in all asthmatics • Aspirin and nonsteroidal anti- inflammatory drugs  if known to precipitate asthma, these drugs should be avoided. • Allergens  e.g. house dust mites, domestic pets, pollen should be avoided whenever possible. • Occupation  should be considered as a possible precipitating factor. • Smoking  active or passive. • Day to day triggers  such as exercise and cold air. It is preferable to adjust treatment if avoidance imposes inappropriate restrictions on lifestyle. • Atmospheric pollution. • Food  if known to trigger asthma, should be avoided.
3) Medication 2 major groups of drugs: Bronchodilator drugs •to relieve bronchospasm and improve symptoms. Anti inflammatory drugs •to treat the airway inflammation and bronchial hyperresponsiveness, the underlying cause of asthma, i.e. to prevent attacks.
Drug Delivery  The inhaled route is preferred for beta2- agonists and steroids as it produces the same benefit with fewer side effects  Inhaled medications exert their effects at lower doses  pMDI is suitable for most patients as long as the inhalation technique is correct  Alternative methods include spacer devices,dry powder inhalers and breath- actuated pMDI  Nebulised route is preferred in the management of acute attacks
3 main groups of bronchodilators [β2 agonists] Inhaled β2agonist •Salbutamol (Ventolin, Respolin) •terbutaline (Bricanyl) •fenoterol (Berotec) •salmeterol (Serevent) - long acting Oral long acting β2 agonist: •salbutamol (Volmax) •terbutaline (Bricanyl durules) •bambuterol (Bambec) Oral short acting β2 agonist: •salbutamol •terbutaline etc.
2. Anti-Inflammatory Drug • Corticosteroids Examples: Beclomethasone dipropionate (Becotide, Becloforte, Beclomet, Aldecin, Respocort) Budesonide (Pulmicort) • Sodium cromoglycate (Intal) • Other treatments Anti-histamines including ketotifen  Anticholinergics Examples: Ipratropium bromide (Atrovent)  Methylxanthines Examples: Nuelin SR, Theodur, Euphylline
Approach To Drug Therapy - "Stepwise Approach" [step 1] Start at the step most appropriate to severity, moving up if needed or down if control is good for > 3 months. Rescued courses of prednisolone may be needed STEP 1 MILD EPISODIC ASTHMA • Infrequent symptoms • No nocturnal symptoms • PEF 80-100% predicted Treatment: inhaled beta2 agonist "as needed" for symptom relief. If needed more than once a day, advance to Step 2
Approach To Drug Therapy - "Stepwise Approach" [step 2] STEP 2 MODERATE ASTHMA • Frequent symptoms • Nocturnal symptoms present • PEF 60-80% predicted Treatment • inhaled steroids, e.g. beclomethasone or budesonide 200-800 mcg/day • inhaled sodium cromoglycate plus • inhaled beta2 agonist "as needed"
Approach To Drug Therapy - "Stepwise Approach" [step 3] STEP 3 SEVERE CHRONIC ASTHMA • Persistent symptoms • Frequent nocturnal symptoms • PEF 60% predicted or less Treatment: • inhaled beclomethasone or budesonide 800-2000 mcg/day plus • inhaled beta2 agonist as needed plus, if necessary • oral beta2 agonist preferably long acting, or • inhaled long acting beta2 agonist, or • inhaled ipratropium bromide 40 mcg 3-4 times a day, or • oral theophylline (sustained release), or
Approach To Drug Therapy - "Stepwise Approach" [step 4] STEP 4 VERY SEVERE ASTHMA • Persistent symptoms not controlled by step 3 medications Treatment: • as in step 3, plus oral steroids (the lowest dose possible) STEP DOWN • Patients should be reviewed regularly. • When the patient’s condition has been stable for 3-6 months, drug therapy may be stepped down gradually. • The monitoring of symptoms and peak flow rate should be continued during drug reduction.
Management of acute severe asthma •RR >50/min •PEFR <50% •Pulse >140 beats/min •breathlessness •10 puffs Bronchodilator and Metered Dose Inhaler •High flow 02, bronchoD •MDI, nebulizer(1-2h) •Oral prednisolone (3-5d) •Monitore PEFR/O2 •B2 agonist / 02 if required •PEFR <33% •Tiredness •Cyanosis •Decrease respiratory effort •Silent chest •iv aminophylline •Iv hydrocortisone •Salbutamol •Ipratropium bromide •Adequate hydration •antibiotic •ICU •Artificial ventilation•Wean iv •Β2 Agonist •Oxygen if required •Oral prednisolone •Monitor PEFR •Patient’s education •Review maintenance medication •Review inhaler technique •Follow up •PEFR monitor DISCHARGE PLAN response Give treatment improve
Management Of Acute Asthma Aims Of Management i. To prevent death ii. To relieve respiratory distress iii. To restore the patient’s lung function to the best possible level as soon as possible. iv. To prevent early relapse
1. Assess severe attack Severe attack: a) Unable to complete sentences b) RR>25/min c) PR>110 bpm d) PEF< 50% of predicted or best Life-threatening attack: a) PEF<33% of predicted or best b) Silent chest, cyanosis, feeble respiratory effort c) Bradycardia/ hypotension d) Exhaustion, confusion, or coma e) ABG : normal/high PaCO2>5kPa (36mmHg) PaO2< 8kPa (60mmHg) low pH, e.g. <7.35
2. Start treatment immediately • Sit patient up & give high dose O2 in 100% via non-rebreathing bag • Salbutamol 5mg (or terbutaline 10mg) + ipratropium bromide 0.5 mg nebulized with O2 • Hydrocortisone 100mg IV/prednisolone 30 mg PO (both if very ill) • CXR to exclude pneumothorax If life threatening features (above) present: • Inform ITU, and seniors • Add MgSO4 1.2-2g IV over 20 min • Give Salbutamol nebulizers every 15 min, or 10mg continuously per hour
Further management If improving • 40-60% O2 • Prednisolone 30-60mg/24h PO • Nebulized salbutamol every 4 h • Monitor peak flow and O2 saturations If not improving after 15-30min • Continue 100% O2 and steroids • Hydrocortisone 100mg IV or prednisolone 30mg PO if not already given • Give Salbutamol nebulizers every 15 min, or 10 mg continuously per hour • Continue ipratropium 0.5 mg every 4-6h
Post-attempt…. If patient still not improving • Discuss with seniors and ITU. • Repeat salbutamol nebulizers every 15 mins • MgSO4 1.2-2g IV over 20 min, unless already given. • Consider aminophylline, if not already on a theophylline. Alternatively, give salbutamol IVI. Monitoring the effects of treatment • Repeat PEF 15-30min after initiating treatment • Pulse oximeter monitoring: maintain SaO2 >92 %. • Check blood gases within 2h if:initial PaO2 was normal/ raised or initial PaO2 <8 kPa (60mmHg) or patient deteriorating • Record PEF pre- and post- β-agonist in hospital at least 4 times.
Once patient improving… Once patient is improving • Wean down and stop aminophylline over 12-24 h. • Reduced nebulized salbutamol and switch to inhaled β-agonist. • Initiate inhaled steroids and stop oral steroids if possible • Continue to monitor PEF. Look for deterioration on reduced treatment and beware early morning dips in PEF • Look for the cause of the acute exacerbation and admission
Component 1: Patient-Doctor relationship
Component 2: Identify and Reduce Exposure to Risk Factors
Follow-Up and Monitoring Include review of symptoms and measurement of lung function o PEF monitoring at every visit along with review of symptoms helps in evaluating the patient’s response to therapy and adjusting tx.PEF consistently >80% of the patient’s personal best suggests good control. o Regular visits (at 1 to 6 month interval as appropriate) is essential even after control of asthma is established
Asthma Management Plan  When PEF >80%: continue current dose of inhaled corticosteroids  When PEF 60-80%:double the dose of inhaled corticosteroids  When PEF 40- 60%:start rescue course prednisolone  When PEF persists below 60% despite rescue course prednisolone with worsening symptoms,advised to come to EMERGENCY DEPT immediately
Management of asthma in pregnancy  In general during pregnancy,asthma becomes worse in a third of women,is stable in another third and improves in the remaining third.  Women should be reassured that their asthma medication carries less risk to the foetus than a severe asthma attack  Inadequately treated asthma can cause maternal and foetal hypoxaemia,which leads to complications during pregnancy and poorer birth outcomes
Management: Pregnancy in asthmatics  Treatment should be aggressive,with the aim of eliminating symptoms and restoring and maintaining normal lung function  Beta2 agonists: No evidence of a teratogenic risk with the commonly used inhaled beta2 agonists  Ipratropium bromide: appears to be safe for use during pregnancy  Salmeterol/formoterol: not been tested extensively in pregnant women
Management: Pregnancy in asthmatics  Theophyllines: may aggravate the nausea and GERD and can caause transient neonatal tachycardia and irritabilityTeratogenicity has been shown in animals.  Sodium cromoglycate: no adverse foetal effects  Inhaled corticosteroids: mainstay of tx in persistent asthma,good safety profile in pregnancy  Oral corticosteroids: necessary for severe asthma in pregnancy but usually only for short periods.Increased risk of cleft palate in animals given huge doses of oral steroids  Anti-leukotrienes: no data available
Labour and Breastfeeding  Women with very severe asthma may be advised to have an elective caesarean section at a time when their asthma control is good  Breastfeeding should be continued in women with asthma  In general,asthma medications are safe during pregnancy and lactation and the benefits outweigh any potential risks to the foetus and baby
Allergic Rhinitis and Asthma  80% of patients with asthma have allergic rhinitis  When allergic rhinitis is undetected or untreated,patients have frequent exacerbations not responding to conventional treatment  Nasal inhalation of corticosteroids are mainstay of treatment with or without oral antihistamine
Status Asthmaticus Acute exacerbation of asthma that does not respond to standard treatment of bronchodilators and corticosteroids. Symptoms include chest tightness, rapidly progressive dyspnoea, dry cough and wheezing The lung failure means that oxygen can no longer be provided, carbon dioxide can no longer eliminated. Hence, leading to acidosis.
It is not just asthma CASE PRESENTATION / UMMC
MIBMH  10.5 years old boy, known case of mild intermittent asthma presented to HSB with:  Fever, cough and runny nose ----- 1 wk.  Hemoptysis and loss of appetite ---- 5d  No night sweating .  Seen by GP and managed with oral antibiotic and symptomatic treatment but the patient did not improve.
Review of symptoms  The patient is unable to lie flat for the past 2 weeks due to feeling of breathlessness.
 In HSB  respiratory distress upon admission  CXR:  mediastinal mass on right perihilar region  multiple cannon ball lesions in both lung fields, so  CT thorax, abdomen and pelvis done  Huge anterior mediastinal mass encasing great vessels with lung metastasis and lymphadenopathy.  Referred to UMMC for possibility of malignancy.
Past history  Asthma  since age of 7 years  not on regular follow-up or treatment/prophylaxis  mild infrequent diurnal symptoms  no interference with general activity or school attendance.  acute exacerbation: twice a year and precipitated mainly by coldness.  No hospital admission
 Perinatal history: uneventful.  Developmental history: attends school, average level, very shy.  Immunization: full schedule.  Allergy: allergic to dust.  Family and social history:  No ill family member.  No H/O contact with T.B
O/E  Looks lethargic, dyspneic RR 32/min with recessions, HR 120/min, SpO2 96% on face mask O2 5l/min, temp 36.4C  No lymphadenopathy.  Lungs: -reduced breath sounds on right medial and lower zones with crepitations on the right side  CVS: S1 + S2 , no murmur.  Abdomen: soft, liver 2cm firm.
 Genitalia: pubic hair stage 3, penile length 7.5cm, testes 2 ml each.  Breast tissue: gynaecomastia.
Growth parameters
 Height: 166 cm  Upper/lower segment ratio = 1
investigations  FBC: Hb 11.9gm/dl wbc 12,600/ul plt 397,000/ul ANC 9,500/ul.  BUSE: Na 131mmol/l K 3.9mmol/l Cl 95mmol/l urea 2.4mmol/l creat 77umol/l  LFT: alb 29gm/l t-bili 4umol/l ALP 146u/l ALT 41u/l AST 58u/l  Ca 2.37mmol/l PO4 1.23mmol/l Mg 0.83mmol/l  PBF: normal findings.
 ESR: 110mm/hr  CRP: 14.8mg/dl  LDH: 511U/L
Radiological investigations
 BhCG: <2 mu/ml (L) (0-10)  AFP: 397040.9 (H) (0-6.7)
 LH 11 mu/ml (H) (<0.1-6)  FSH 33 mu/ml(H) ( 1.2-2.5)  Estradiol <37 pmol/l (0-198)  Testosterone 2.3 nmol/l (L) (8.4-28.7)  DHEAS 0.5 umol/l (L) (2.2-15.2)  Karyotyping: 47 XXY, how many cells? Any evidence of mosaic Klinefelter? (waiting formal report).
diagnosis  Mediastinal germ cell tumor with bilateral lung metastasis and pseudoprecocious puberty.  Klinefelter syndrome.
Management and progress  Respiratory support, required BiPAP .  Required neb Salbutamol 4 hourly.  Had spikes of fever, covered with Erythromycin and Ceftriaxone.  After 4 days in PICU transferred to P6.  Started chemotherapy(UKCCSG).  Had NNF covered with piptazocin then imipenem and later on Ampho-B.
 Became neutropenic.  All blood and respiratory cultures have no growth.
Discussion
Klinefelter syndrome  In 1942 Klinefelter et al published a paper on 9 men with large breasts, minimal sexual and body hair, small testes and inability to produce sperms.  It is the most common syndrome assoc with male hypogonadism and infertility.  Classically 47XXY, but many variants like 48 XXXY, 48XXYY,49XXXXY,49XXXYY,50XXXXYY.  It is due to meiotic non-disjunction. mosaic patients may be fertile .
Features  Hypogonadism (small testes and azoospermia-hyalinzation and fibrosis of seminiferous tubules).  Gynaecomestia in late puberty (30-50%) due to increase estradiol/testosterone ratio.  Psychosocial problems.  Elevated urinary gonadotrophins.  Mental retardation is affected by number of X chromosomes (decreased IQ 15 points for each X chromosome) [most males with 47XXY have normal intellegence, 70% have minor developmental and learning disability]
Other features:  Pes cavus, genu valgus, fifth finger clinodactily.  Taurodontism (prominent molar teeth): 40% in Klinefelter, 1% in general population.  Radio-ulnar synostosis---- 49XXXXY.
Increased risk of:  DM.  CVS: varicose veins, venous ulcer, DVT , pulm embolism, mitral valve prolapse.  Cancer: breast, leukemia, mediastinal germ cell tumors.  Osteoporosis.  Autoimmune disease (SLE, RA, Sjogren with increased mortality).
Mortality  40% of conceptions with Klinefelter survive fetal period.  Mortality is not significantly higher in healthy individuals.
 Prevalence: in USA 1:500-1000  Race: no race difference.  Age: it goes undetected in most affected males until adulthood. the common indication for karyotyping is hypogonadism and infertility.
investigations  Mid-puberty: increase FSH and LH, decrease testosterone.  Increase estradiol/testosterone ratio-----gynaecomastia 80%.  Cortisol should be checked (47% have low cortisol).  Decrease osteocalcin---- bone resorption.  Coagulation profile because of increased risk of DVT and pulm embolism.  Karyotyping:47 XXY 80-90 % - 10% mosaic.
Germ cell tumors  Classification:  -suppressed differentiation: seminoma, dys- germinoma.  -differentiation: Initial embryonal carcinoma Embryonic mature and immature teratoma Extra-embryonic(choriocarcinoma-yolk sac tumor{endodrermal sinus tumor})  -mixed histology: mixed GCT.
Primary mediastinal germ cell tumors  Comprise only 1-3% of germ cell tumors.  Overall teratoma is the most common variant, seminoma is the most common malignant variant.  Malignant variants are uncommon and more in males.  Benign variants are equally disributed among males and females.  Testicular examination, U/S and CT are mandatory to rule out testicular primary cancer.
Serum markers  Alpha-fetoprotein: indicates malignant non- seminomatous type.  BhCG: suggests trophoblastic component. Malignant non-seminomatous and mixed GCTs carry worse prognosis than other GCTs.
Association of M- GCTs with Klinefelter syndrome  Klinefelter syndrome is present in 20% of patients with M-GCT.  The incidence of M-GCT is 50 fold increased in patients with Klinefelter syndrome.  M-GCT mask the usual clinical signs of Klinefelter syndrome by inducing puberty by BhCG.
Comparison of GCT between KS and general population  Klinefelter syndrome:  All contain non-seminominatous elements  Present at younger age (mean 17 years)  Precocious puberty is seen more often.  Almost exclusively extragonadal.  General population:  Pure seminoma is the most common malignant variant.  Older age at presentation (mean 29 years)  Precocious puberty is less often.  Only 2-5% extragonadal.
references  http://emedicine.medscape.com/  Ann Thorac Surg 1998;66:547-548
THANK YOU

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Bronchial asthma

  • 1.
  • 2.
    History  Asthma :derived from the Greek aazein, meaning "sharp breath." The word first appears in Homer's Iliad.  In 450 BC. Hippocrates: more likely to occur in tailors, anglers, and metalworkers.  Six centuries later, Galen: caused by partial or complete bronchial obstruction.  1190 AD, Moses Maimonides: wrote a treatise on asthma, describing its prevention, diagnosis, and treatment  17th century, Bernardino Ramazzini: connection between asthma and organic dust.  1901: The use of bronchodilators started.  1960s: inflammatory component of asthma was recognized and anti-inflammatory medications were added to the regimens.
  • 3.
    What is knownabout asthma?
  • 4.
    ASTHMA  Chronic inflammatorycondition of the airways characterized by; - airflow limitation (reversible with treatment) - airway hyper-responsiveness to a wide range stimuli - inflammation of the bronchi  In chronic asthma, inflammation maybe accompanied by irreversible airflow limitation  Symptoms are cough, wheeze, chest tightness, and shortness of breath which often worse at night
  • 5.
    Simple Definition A reversiblechronic inflammatory airway disease which is characterized by bronchial hyper- responsiveness of the airways to various stimuli, leading to widespread bronchoconstriction, airflow limitation and inflammation of the bronchi causing symptoms of cough, wheeze, chest tightness and dyspnoea.
  • 6.
    Epidemiology  Common diseasewith unacceptably high morbidity and mortality  Commonly underdiagnosed and undertreated  Only 36.1% of adult asthmatics ever had their peak flow measured  Higher prevalence in rural (4.5%) than in urban areas (4%),lower educational status(5.6%) and lower income  Majority of patients(87.3%) had mild asthma; 9.9% had moderate asthma and 2.7% had severe asthma  Among severe asthmatics, only 19.4% were on inhaled corticosteroids 87% 10% 3% Asthmatic patient Mild Moderate Severe
  • 7.
  • 8.
    EPIDEMIOLOGY  The prevalenceof asthma has increased 61% over the last two decades.  Asthma is the leading chronic illness among children.  Asthma results in 10 million lost school days and 3 million lost work days.  Deaths from asthma have increased by 31% since 1980.
  • 9.
    Classification  Extrinsic –implying a definite external cause  more frequently in atopic inviduals  (atopic – individual which tends to develop hypersensitivity by contact with allergens)  often starts in childhood - accompanied by eczema  Intrinsic/cryptogenic – no causative agent can be identified  starts in middle age
  • 10.
    Types of Asthma Accordingto the severity: helpful for treatment and management. Very mild Mild Moderate Moderately Severe Severe
  • 11.
    Types of Asthma Accordingto pathophysiology Allergic asthma Intrinsic (Non-Allergic) Exercise-induced Occupational (allergic) Steroid-resistant ABPA (allergic)
  • 12.
    Pathogenesis  Complex, notfully understood  numbers of cells, mediators, nerves, and vascular leakage -activated by expose to allergens or several mechanism Inflammation  Eosinophils, T-lymphocytes, macrophages and mast cell Remodeling  Deposition of repair collagens and matrix proteins- damage  Loss of ciliated columnar cells- metaplasia – increase no of secreting goblet cells
  • 13.
    Pathologic features ofasthma i. Inflammatory cell infiltration of the airways ii. Increased thickness of the bronchial smooth muscle iii. Partial or full loss of the respiratory epithelium iv. Subepithelial fibrosis v. Hypertrophy and hyperplasia of the submucosal glands and goblet cells vi. Partial or full occlusion of the airway lumen by mucous plugs vii. Enlarged mucous glands and blood vessels
  • 14.
    Pathophysiology  Smooth musclecontraction  Thickening of airway –cellular infiltration and inflammation  Excessive secrection of mucus Genetic factor Cytokine gene complex (chromosome 5)-IL-4 gene cluster control IL-3, IL-4 , IL-5 and IL-13 Environment factor Childhood expose irritants or childhood infection
  • 15.
    Pathophysiology  Extrinsic asthma:Atopic/allergic, occupational, allergic bronchopulmoary aspergillosis.  Atopic or allergic  Dust, pollens, animal dander, food etc. Family history of atopy.  ↑ serum IgE.  Skin test with Ag  wheal, flare ( Classical IgE mediated response)  Exposure of pre-sensitised mast cells to the Ag stimulates chemical mediators from these cells. Type 1 hypersensitivity.
  • 16.
    1.Early phase  InhaledAntigen  Sensitised mast cells on the mucosal surface  mediator release.  Histamine bronchoconstriction, increased vascular permeability.  prostaglandin D 2  bronchoconstriction, vasodilatation.  Leucotriene C4,D4, E4  Increased vascular permeability, mucus secretion and bronchoconstriction.  Direct subepithelial parasympathetic stimulation  bronchoconstriction.
  • 17.
    2.Late phase  starts4 to 8 hours later  Mast cell release additional cytokine  Influx of leukocytes(neutrophil,eosinophil)  Eosinophils are particularly important- exert a variety of effect
  • 18.
    Pathophysiology  AtopicAsthma Trigger Eg.dust,pollen, animal dander TH2 cell IL5 IL4 Eosino phil IgE B cell Mast cell IgE antibody Mediators Eg.Histamine, leukotrines Bronchospasm Increase vascular permeability Mucus production Immediate phase(minutes)
  • 19.
    Bronchial inflammation Environment factorGenetic prediposition Bronchial hyperreactivity + trigger factors Cough, Wheeze, Breathlessness, Chest tightness Oedema BronchoC Mucus production Airways narrowing
  • 22.
    Aetiology and triggers Complex and multiple environmental and genetic determinant a) Genetic factors b) Allergen exposure house dust mite, household pets, grass pollen c) Atmospheric polution sulphur dioxide, ozone, ciggerate smoke, perfume d) Dietary deficiency of antioxidants  vit E and selenium may protect asthma in children(freshfruits and vegetables)
  • 23.
    Aetiology and triggers e)Occupational sensitizers  isocyanates(from industrial coating, spray painting)  colophony perfumes(electronic industries) e) Drugs  NSAIDS  B-blocker(B1 adrenergic blocker drug such as atenolol is avoided to treat HPT and angina in asthmatic pt f) Cold air g) Exercise  exercise-induced wheeze is driven by histamin and leukotrienes which are release from mast cells when epithelial lining fluid of the bronchi become hyperosmolar owing to drying and cooling during exercise h) Emotion
  • 28.
    History Presenting symptoms:  Cough± sputum - time: become worse at night - duration: chronic / acute - associated with wheezing - fever? URTI  Wheeze - max during expiration and accompanied by prolonged expiration
  • 29.
    Cough History 1.Ask specificallyabout the symptoms: -Cough?how is the cough? more severe at night or on day? associated symptoms like dyspnea & wheezing? how long is the cough? Recurrent?Any previous similar episode? Aggravated factor?like cough become severe after exercise?or the cough is initiated after exercise?
  • 30.
    Cough History 2.If thecough is associated with dyspnea and wheezingis it relieved by bronchodilator? 3.Ask for any precipatating factors -whether the symptoms(cough,dyspnea,wheezing) started after exposure to weather changes, dust, exercise, infection or drugs? 4.Is there any pets,carpet or feather pillow in home?(easily trapped dust and the dust or animal fur will cause exacerbation of asthma)
  • 31.
    Dyspnoea History  Dyspnoea -onset: after exercise? cold? dust? animal fur? emotion? - severity and pattern: varies from day to day or from hour to hour - no chest pain
  • 32.
    History Clinical features  Recurrentepisodes of wheezing,chest tightness,breathlessness and cough  Precipitants- cold,allergen,pollutant,viral urti  Exercise tolerance  Disturbed sleep  Other atopic disease  Home-Pet?Carpet?  Occupation
  • 33.
    History Clinical features  Displaydiurnal pattern,symptoms and PEF worse in the morning Mild intermittent asthma- asymptomatic between exacerbation Persistent asthma-chronic wheeze and breathlessness
  • 34.
    History 5.Any history ofatopy(eczema,hay fever) or allergic rhinitis? 6.Any family history of asthma?Any childhood asthmatics? 7.Whether he is a smoker or any family members is a smoker? 8.What is his occupation? Exposure to chemicals?
  • 35.
    History Past medical history: Experienced asthma attack before  Taking any medications: NSAIDs / β-blocker / aspirin (non atopic asthma) Family history:  Has family history of asthma
  • 36.
    History Social history:  Occupation:expose to fumes/organic/chemical dust  House: near to factory? Pets? Dust? Carpet? Feather pillow?  Smoking in any family members
  • 37.
    known asthmatic  Whenhe was diagnosed with asthma?  How the asthma was diagnosed?  Who diagnosed it?  Whether he is on prophylaxis?  What type of prophylaxis?  How he get the drugs and how many dosage of the drugs?  Whether he know how to deliver the drugs properly?  How is his compliance to drugs?
  • 38.
    Physical examination  Generalinspection: - tachypnoeic, sign of respiratory distress, effort of breathing, cyanosis (life-threatening)  Inspection: - fingers: tar staining - pulse rate: tachycardia and pulsus paradoxus, bradycardia (life- threatening) - used of accessory muscles or recession - wheezing
  • 39.
    Chest  Inspection: - shape:hyperinflated in severe asthma - movement of chest/silent chest (life-threatening) - chest deformity: - recession:  Palpation: - chest expension may be reduce (hyperinflated)/ normal - apex beat: may be displaced -vocal fremitus: decrease  Percussion: - may be hyperresonance / normal  Auscultation: - breath sound: vesicular - ronchi in expiratory phase, may be both in severe asthma - prolonged expiratory phase -vocal resonance decrease / normal
  • 41.
    Clinical features Sign • Tachypnoea,audiblewheeze,hyperinflated chest,hyperresonant percussion note,diminished air entry,widespread polyphonic wheze • Severe attack – inability to complete sentences, pulse >110bpm, RP>25/min, PEF 33-50% • Life-threatening attack- silent chest,cyanosis,bradycardia,exhaustion, PEF < 33%,confusion • Pulsus paradoxus (exaggeration of the normal variation in the pulse volume with respiration, becoming weaker with inspiration and stronger with expiration )
  • 42.
    Correlation + The symptomsof asthma consist of a triad of dyspnea, cough, and wheezing. + At the onset of an attack, patients experience a sense of constriction in the chest, often with a nonproductive cough. + Respiration becomes audibly harsh; wheezing in both phases of respiration becomes prominent; expiration becomes prolonged; and patients frequently have tachypnea, tachycardia, and mild systolic hypertension. + The lungs rapidly become overinflated. + If the attack is severe or prolonged, there may be a loss of adventitial breath sounds, and wheezing becomes very high pitched. + The accessory muscles become visibly active, and a paradoxical pulse often develops.
  • 43.
  • 44.
    Diagnosing asthma  Reversibleand variable airflow limitation-as measured by a peak expiratory flow (PEF) meter in any of the following ways:  PEF increases more than 15% and 200mls 15 to 20 mins after inhaling a short acting beta2 agonist, or  PEF varies more than 20% from morning measurement upon arising to measurement 12 hours later in patients who are taking a bronchodilator, or  PEF decreases more than 15% after 6 mins of running or exercise
  • 46.
    Differential diagnosis + Upperairway obstruction – Tumor – Epiglottitis – Vocal cord dysfunction – Obstructive sleep apnea + Bronchomalacia + Endobronchial lesion + Foreign body + Congestive heart failure + Gastroesophageal reflux + Sinusitis + Adverse drug reaction – Aspirin – Beta-adrenergic antagonist – ACE inhibitors – Inhaled pentamidine + Allergic bronchopulmonary aspergillosis + Hyperventilation with panic attacks
  • 47.
    Non-specific investigation  Non-specific: -full blood count and differential count: increase number of eosinophils number - arterial blood gases - sputum test: number of eosinophils - chest X-ray: hyperinflated
  • 48.
    Specific investigation  Specific: -respiratory function test: 1. peak expiratory flow 2. spirometry - exercise tests -histamine/methacholine bronchial provocation test - trial of corticosteroids
  • 49.
    Reversibility Test + Thistest is done to see whether the obstruction can be relieved by the use of a short-acting bronchodilator eg salbutamol + An improvement of 15% or more (as measured on the peak flow meter) is diagnostic of asthma. + However, in severe chronic disease or patient who has treated with long-acting bronchodilators, little reversibility will be demonstrated.
  • 50.
    Reversibility test Forced expiratorymanoeuvres before 20 minutes after inhalation of a beta-2- adrenoceptor agonist. Note the increase in FEV1 from 1.0 to 2.5 litres.
  • 51.
    Peak expiratory flowrate  Simple and cheap  Subject take full inspiration then blow out forcefully into peak flow meter.  Best used to monitor progression of the asthma and its treatment.  To access possible occupational asthma  PEFR value varies with sex, age and height.
  • 52.
    Peak Expiratory FlowRate (PEFR)  The maximum rate of air breathed out as hard as possible through a measuring device called a peak flow meter, (after a full breath taken in).  Reading is measured in litres/minute (l/min).  Take 3 readings and choose the best  Reading < 80% - presense of obstruction, but not diagnostic of asthma
  • 53.
     Require totake a series of reading - on waking up - prior taking bronchodilator - after taking bronchodilator (before sleep)
  • 54.
    PEF measurements 1. Duringperiods of well-being: provides measurement of the patients best PEF value which will provide the target for the doctor and the patient to aim for.Twice daily measurements before any inhaled bronchodilator tx will determine the diurnal variability of airway calibre.Good control of asthma means PEF variability is maintained at less than 10%. 2. During symptomatic episodes: During an attack of asthma PEF fairly accurately measures the degree of bronchospasm.A PEF of less than 50% of normal or best suggests a very severe attack and a PEF of less than 30% suggests a life-threatening attack
  • 57.
  • 59.
  • 60.
    Spirometry Test + Itis the single best diagnostic test for patients with airflow limitation. + A Spirometry Test + - measures the volume of air blown out against time + - gives more specific information about lung function. + A value is calculated for the amount of air blown out in one second - “Forced Expiratory Volume” or FEV1). + This is divided by the total amount of air blown out until all air is expired - Forced Vital Capacity or FVC). + FEV1/FVC expressed as a percentage value
  • 61.
    + Reading isaffected by age, gender and height + Male Spirometry reading range Mild reduction: 2.5 litres or more Moderate reduction :1.5 to 2.49 litres Severe reduction :Less than 1.5 litre + Female Spirometry reading range Mild reduction :2.0 litres or more Moderate reduction: 1.0 to 1.99 litres Severe reduction: Less than 1.0 litre + In asthma, the readings will be reduced, returning to normal between episodes
  • 62.
    TLC VC RV IC FRC IRV ERV RV TV TLC : totallung capacity VC : vital capacity RV : reserve volume IC : inspirational capacity FRC : functional residual capacity IRV : inspirational reserve volume TV : tidal volume ERV : expiratory reserve volume  Normal:75-80%  Obstructive airway disease: reduced ratio  Restrictive lung disease: ratio normal or increase (enhanced elastic recoil).
  • 63.
    Exercise Test + Doneespecially in children + Peak flow reading measured before hand + Ask patient to run for 6 min, to increase HR > 160 beats/min + Cannot run – use cold air challenge, isocapnoiec (CO2) hyperventilation, aerosol challenge with hypertonic solution + After exercise – take readings at intervals of 5, 10 and 15 minutes. + Diagnosed asthma - fall in peak flow of 15% or more, after exercise.
  • 64.
  • 65.
  • 66.
    Chest X-ray Showed lunghyperinflation. Not diagnostic of asthma Useful to rule out other causes eg. Pneumothorax ----------------------------------------------- Hyperinflation and increased bronchovascular markings
  • 67.
    Allergies & Atophy AllergenProvocation Test  In suspected occupational asthma and food-allergy related asthma Skin-Prick Test  To identify allergens  A drop of allergen is placed on skin , site is marked and pricked with needle, measured any weals
  • 68.
  • 69.
  • 70.
    Severity assessment foracute setting of AEBA Mild Moderate Severe Breathless Walking Talking At rest Can lie down Prefer sitting Hunched forward Talk in Sentences Phrases Words Alertness May be Usually agitated Agitated Central cyanosis Absent Absent Present Use of accessory muscle Absent Moderate Marked Sternal retraction Absent Moderate Marked Wheeze on auscultation Moderate, often end expiratory Loud Loud  Silent Chest Pulsus paradoxus Not palpable May be palpable Often palpable Initial PEF More than 80% 60 – 80% Less than 60% Oximetry on presentation More than 95% 91 – 95% Less than 90%
  • 71.
  • 72.
  • 73.
  • 74.
    Management of ChronicAsthma  Aims of management • to recognize asthma • to abolish symptoms • to restore normal or best possible long term airway function • to reduce morbidity and prevent mortality
  • 75.
    Approach of chronicasthma  Education of patient and family  Avoidance of precipitating factors  Use of the lowest effective dose of convenient medications minimizing short and long term side effects.  Assessment of severity and response to treatment.
  • 76.
    1) Education ofpatient and family i. Nature of asthma ii. Preventive measures/avoidance of triggers iii. Drugs used and their side- effects iv. Proper use of inhaled drugs v. Proper use of peak flow meter vii. Knowledge of the difference between relieving and preventive medications vii. Recognition of features of worsening asthma  increase in bronchodilator requirement  development of nocturnal symptoms  reducing peak flow rates). viii. Self management plan for selected, motivated patients or parents. ix. The danger of non prescribed self medication including certain traditional medicines.
  • 77.
    2) Avoidance ofprecipitating factors The following factors may precipitate asthmatic attacks: • Beta blockers  contraindicated in all asthmatics • Aspirin and nonsteroidal anti- inflammatory drugs  if known to precipitate asthma, these drugs should be avoided. • Allergens  e.g. house dust mites, domestic pets, pollen should be avoided whenever possible. • Occupation  should be considered as a possible precipitating factor. • Smoking  active or passive. • Day to day triggers  such as exercise and cold air. It is preferable to adjust treatment if avoidance imposes inappropriate restrictions on lifestyle. • Atmospheric pollution. • Food  if known to trigger asthma, should be avoided.
  • 78.
    3) Medication 2 majorgroups of drugs: Bronchodilator drugs •to relieve bronchospasm and improve symptoms. Anti inflammatory drugs •to treat the airway inflammation and bronchial hyperresponsiveness, the underlying cause of asthma, i.e. to prevent attacks.
  • 79.
    Drug Delivery  Theinhaled route is preferred for beta2- agonists and steroids as it produces the same benefit with fewer side effects  Inhaled medications exert their effects at lower doses  pMDI is suitable for most patients as long as the inhalation technique is correct  Alternative methods include spacer devices,dry powder inhalers and breath- actuated pMDI  Nebulised route is preferred in the management of acute attacks
  • 80.
    3 main groupsof bronchodilators [β2 agonists] Inhaled β2agonist •Salbutamol (Ventolin, Respolin) •terbutaline (Bricanyl) •fenoterol (Berotec) •salmeterol (Serevent) - long acting Oral long acting β2 agonist: •salbutamol (Volmax) •terbutaline (Bricanyl durules) •bambuterol (Bambec) Oral short acting β2 agonist: •salbutamol •terbutaline etc.
  • 81.
    2. Anti-Inflammatory Drug •Corticosteroids Examples: Beclomethasone dipropionate (Becotide, Becloforte, Beclomet, Aldecin, Respocort) Budesonide (Pulmicort) • Sodium cromoglycate (Intal) • Other treatments Anti-histamines including ketotifen  Anticholinergics Examples: Ipratropium bromide (Atrovent)  Methylxanthines Examples: Nuelin SR, Theodur, Euphylline
  • 82.
    Approach To DrugTherapy - "Stepwise Approach" [step 1] Start at the step most appropriate to severity, moving up if needed or down if control is good for > 3 months. Rescued courses of prednisolone may be needed STEP 1 MILD EPISODIC ASTHMA • Infrequent symptoms • No nocturnal symptoms • PEF 80-100% predicted Treatment: inhaled beta2 agonist "as needed" for symptom relief. If needed more than once a day, advance to Step 2
  • 83.
    Approach To DrugTherapy - "Stepwise Approach" [step 2] STEP 2 MODERATE ASTHMA • Frequent symptoms • Nocturnal symptoms present • PEF 60-80% predicted Treatment • inhaled steroids, e.g. beclomethasone or budesonide 200-800 mcg/day • inhaled sodium cromoglycate plus • inhaled beta2 agonist "as needed"
  • 84.
    Approach To DrugTherapy - "Stepwise Approach" [step 3] STEP 3 SEVERE CHRONIC ASTHMA • Persistent symptoms • Frequent nocturnal symptoms • PEF 60% predicted or less Treatment: • inhaled beclomethasone or budesonide 800-2000 mcg/day plus • inhaled beta2 agonist as needed plus, if necessary • oral beta2 agonist preferably long acting, or • inhaled long acting beta2 agonist, or • inhaled ipratropium bromide 40 mcg 3-4 times a day, or • oral theophylline (sustained release), or
  • 85.
    Approach To DrugTherapy - "Stepwise Approach" [step 4] STEP 4 VERY SEVERE ASTHMA • Persistent symptoms not controlled by step 3 medications Treatment: • as in step 3, plus oral steroids (the lowest dose possible) STEP DOWN • Patients should be reviewed regularly. • When the patient’s condition has been stable for 3-6 months, drug therapy may be stepped down gradually. • The monitoring of symptoms and peak flow rate should be continued during drug reduction.
  • 87.
    Management of acutesevere asthma •RR >50/min •PEFR <50% •Pulse >140 beats/min •breathlessness •10 puffs Bronchodilator and Metered Dose Inhaler •High flow 02, bronchoD •MDI, nebulizer(1-2h) •Oral prednisolone (3-5d) •Monitore PEFR/O2 •B2 agonist / 02 if required •PEFR <33% •Tiredness •Cyanosis •Decrease respiratory effort •Silent chest •iv aminophylline •Iv hydrocortisone •Salbutamol •Ipratropium bromide •Adequate hydration •antibiotic •ICU •Artificial ventilation•Wean iv •Β2 Agonist •Oxygen if required •Oral prednisolone •Monitor PEFR •Patient’s education •Review maintenance medication •Review inhaler technique •Follow up •PEFR monitor DISCHARGE PLAN response Give treatment improve
  • 88.
    Management Of AcuteAsthma Aims Of Management i. To prevent death ii. To relieve respiratory distress iii. To restore the patient’s lung function to the best possible level as soon as possible. iv. To prevent early relapse
  • 89.
    1. Assess severeattack Severe attack: a) Unable to complete sentences b) RR>25/min c) PR>110 bpm d) PEF< 50% of predicted or best Life-threatening attack: a) PEF<33% of predicted or best b) Silent chest, cyanosis, feeble respiratory effort c) Bradycardia/ hypotension d) Exhaustion, confusion, or coma e) ABG : normal/high PaCO2>5kPa (36mmHg) PaO2< 8kPa (60mmHg) low pH, e.g. <7.35
  • 90.
    2. Start treatmentimmediately • Sit patient up & give high dose O2 in 100% via non-rebreathing bag • Salbutamol 5mg (or terbutaline 10mg) + ipratropium bromide 0.5 mg nebulized with O2 • Hydrocortisone 100mg IV/prednisolone 30 mg PO (both if very ill) • CXR to exclude pneumothorax If life threatening features (above) present: • Inform ITU, and seniors • Add MgSO4 1.2-2g IV over 20 min • Give Salbutamol nebulizers every 15 min, or 10mg continuously per hour
  • 91.
    Further management If improving •40-60% O2 • Prednisolone 30-60mg/24h PO • Nebulized salbutamol every 4 h • Monitor peak flow and O2 saturations If not improving after 15-30min • Continue 100% O2 and steroids • Hydrocortisone 100mg IV or prednisolone 30mg PO if not already given • Give Salbutamol nebulizers every 15 min, or 10 mg continuously per hour • Continue ipratropium 0.5 mg every 4-6h
  • 92.
    Post-attempt…. If patient stillnot improving • Discuss with seniors and ITU. • Repeat salbutamol nebulizers every 15 mins • MgSO4 1.2-2g IV over 20 min, unless already given. • Consider aminophylline, if not already on a theophylline. Alternatively, give salbutamol IVI. Monitoring the effects of treatment • Repeat PEF 15-30min after initiating treatment • Pulse oximeter monitoring: maintain SaO2 >92 %. • Check blood gases within 2h if:initial PaO2 was normal/ raised or initial PaO2 <8 kPa (60mmHg) or patient deteriorating • Record PEF pre- and post- β-agonist in hospital at least 4 times.
  • 93.
    Once patient improving… Oncepatient is improving • Wean down and stop aminophylline over 12-24 h. • Reduced nebulized salbutamol and switch to inhaled β-agonist. • Initiate inhaled steroids and stop oral steroids if possible • Continue to monitor PEF. Look for deterioration on reduced treatment and beware early morning dips in PEF • Look for the cause of the acute exacerbation and admission
  • 95.
  • 97.
    Component 2: Identifyand Reduce Exposure to Risk Factors
  • 99.
    Follow-Up and Monitoring Includereview of symptoms and measurement of lung function o PEF monitoring at every visit along with review of symptoms helps in evaluating the patient’s response to therapy and adjusting tx.PEF consistently >80% of the patient’s personal best suggests good control. o Regular visits (at 1 to 6 month interval as appropriate) is essential even after control of asthma is established
  • 100.
    Asthma Management Plan When PEF >80%: continue current dose of inhaled corticosteroids  When PEF 60-80%:double the dose of inhaled corticosteroids  When PEF 40- 60%:start rescue course prednisolone  When PEF persists below 60% despite rescue course prednisolone with worsening symptoms,advised to come to EMERGENCY DEPT immediately
  • 101.
    Management of asthmain pregnancy  In general during pregnancy,asthma becomes worse in a third of women,is stable in another third and improves in the remaining third.  Women should be reassured that their asthma medication carries less risk to the foetus than a severe asthma attack  Inadequately treated asthma can cause maternal and foetal hypoxaemia,which leads to complications during pregnancy and poorer birth outcomes
  • 102.
    Management: Pregnancy in asthmatics Treatment should be aggressive,with the aim of eliminating symptoms and restoring and maintaining normal lung function  Beta2 agonists: No evidence of a teratogenic risk with the commonly used inhaled beta2 agonists  Ipratropium bromide: appears to be safe for use during pregnancy  Salmeterol/formoterol: not been tested extensively in pregnant women
  • 103.
    Management: Pregnancy in asthmatics Theophyllines: may aggravate the nausea and GERD and can caause transient neonatal tachycardia and irritabilityTeratogenicity has been shown in animals.  Sodium cromoglycate: no adverse foetal effects  Inhaled corticosteroids: mainstay of tx in persistent asthma,good safety profile in pregnancy  Oral corticosteroids: necessary for severe asthma in pregnancy but usually only for short periods.Increased risk of cleft palate in animals given huge doses of oral steroids  Anti-leukotrienes: no data available
  • 104.
    Labour and Breastfeeding Women with very severe asthma may be advised to have an elective caesarean section at a time when their asthma control is good  Breastfeeding should be continued in women with asthma  In general,asthma medications are safe during pregnancy and lactation and the benefits outweigh any potential risks to the foetus and baby
  • 105.
    Allergic Rhinitis andAsthma  80% of patients with asthma have allergic rhinitis  When allergic rhinitis is undetected or untreated,patients have frequent exacerbations not responding to conventional treatment  Nasal inhalation of corticosteroids are mainstay of treatment with or without oral antihistamine
  • 106.
    Status Asthmaticus Acute exacerbationof asthma that does not respond to standard treatment of bronchodilators and corticosteroids. Symptoms include chest tightness, rapidly progressive dyspnoea, dry cough and wheezing The lung failure means that oxygen can no longer be provided, carbon dioxide can no longer eliminated. Hence, leading to acidosis.
  • 107.
    It is notjust asthma CASE PRESENTATION / UMMC
  • 108.
    MIBMH  10.5 yearsold boy, known case of mild intermittent asthma presented to HSB with:  Fever, cough and runny nose ----- 1 wk.  Hemoptysis and loss of appetite ---- 5d  No night sweating .  Seen by GP and managed with oral antibiotic and symptomatic treatment but the patient did not improve.
  • 109.
    Review of symptoms The patient is unable to lie flat for the past 2 weeks due to feeling of breathlessness.
  • 110.
     In HSB respiratory distress upon admission  CXR:  mediastinal mass on right perihilar region  multiple cannon ball lesions in both lung fields, so  CT thorax, abdomen and pelvis done  Huge anterior mediastinal mass encasing great vessels with lung metastasis and lymphadenopathy.  Referred to UMMC for possibility of malignancy.
  • 111.
    Past history  Asthma since age of 7 years  not on regular follow-up or treatment/prophylaxis  mild infrequent diurnal symptoms  no interference with general activity or school attendance.  acute exacerbation: twice a year and precipitated mainly by coldness.  No hospital admission
  • 112.
     Perinatal history:uneventful.  Developmental history: attends school, average level, very shy.  Immunization: full schedule.  Allergy: allergic to dust.  Family and social history:  No ill family member.  No H/O contact with T.B
  • 113.
    O/E  Looks lethargic,dyspneic RR 32/min with recessions, HR 120/min, SpO2 96% on face mask O2 5l/min, temp 36.4C  No lymphadenopathy.  Lungs: -reduced breath sounds on right medial and lower zones with crepitations on the right side  CVS: S1 + S2 , no murmur.  Abdomen: soft, liver 2cm firm.
  • 114.
     Genitalia: pubichair stage 3, penile length 7.5cm, testes 2 ml each.  Breast tissue: gynaecomastia.
  • 115.
  • 116.
     Height: 166cm  Upper/lower segment ratio = 1
  • 117.
    investigations  FBC: Hb11.9gm/dl wbc 12,600/ul plt 397,000/ul ANC 9,500/ul.  BUSE: Na 131mmol/l K 3.9mmol/l Cl 95mmol/l urea 2.4mmol/l creat 77umol/l  LFT: alb 29gm/l t-bili 4umol/l ALP 146u/l ALT 41u/l AST 58u/l  Ca 2.37mmol/l PO4 1.23mmol/l Mg 0.83mmol/l  PBF: normal findings.
  • 118.
     ESR: 110mm/hr CRP: 14.8mg/dl  LDH: 511U/L
  • 119.
  • 121.
     BhCG: <2mu/ml (L) (0-10)  AFP: 397040.9 (H) (0-6.7)
  • 122.
     LH 11mu/ml (H) (<0.1-6)  FSH 33 mu/ml(H) ( 1.2-2.5)  Estradiol <37 pmol/l (0-198)  Testosterone 2.3 nmol/l (L) (8.4-28.7)  DHEAS 0.5 umol/l (L) (2.2-15.2)  Karyotyping: 47 XXY, how many cells? Any evidence of mosaic Klinefelter? (waiting formal report).
  • 123.
    diagnosis  Mediastinal germcell tumor with bilateral lung metastasis and pseudoprecocious puberty.  Klinefelter syndrome.
  • 124.
    Management and progress Respiratory support, required BiPAP .  Required neb Salbutamol 4 hourly.  Had spikes of fever, covered with Erythromycin and Ceftriaxone.  After 4 days in PICU transferred to P6.  Started chemotherapy(UKCCSG).  Had NNF covered with piptazocin then imipenem and later on Ampho-B.
  • 125.
     Became neutropenic. All blood and respiratory cultures have no growth.
  • 126.
  • 127.
    Klinefelter syndrome  In1942 Klinefelter et al published a paper on 9 men with large breasts, minimal sexual and body hair, small testes and inability to produce sperms.  It is the most common syndrome assoc with male hypogonadism and infertility.  Classically 47XXY, but many variants like 48 XXXY, 48XXYY,49XXXXY,49XXXYY,50XXXXYY.  It is due to meiotic non-disjunction. mosaic patients may be fertile .
  • 128.
    Features  Hypogonadism (smalltestes and azoospermia-hyalinzation and fibrosis of seminiferous tubules).  Gynaecomestia in late puberty (30-50%) due to increase estradiol/testosterone ratio.  Psychosocial problems.  Elevated urinary gonadotrophins.  Mental retardation is affected by number of X chromosomes (decreased IQ 15 points for each X chromosome) [most males with 47XXY have normal intellegence, 70% have minor developmental and learning disability]
  • 129.
    Other features:  Pescavus, genu valgus, fifth finger clinodactily.  Taurodontism (prominent molar teeth): 40% in Klinefelter, 1% in general population.  Radio-ulnar synostosis---- 49XXXXY.
  • 131.
    Increased risk of: DM.  CVS: varicose veins, venous ulcer, DVT , pulm embolism, mitral valve prolapse.  Cancer: breast, leukemia, mediastinal germ cell tumors.  Osteoporosis.  Autoimmune disease (SLE, RA, Sjogren with increased mortality).
  • 132.
    Mortality  40% ofconceptions with Klinefelter survive fetal period.  Mortality is not significantly higher in healthy individuals.
  • 133.
     Prevalence: inUSA 1:500-1000  Race: no race difference.  Age: it goes undetected in most affected males until adulthood. the common indication for karyotyping is hypogonadism and infertility.
  • 134.
    investigations  Mid-puberty: increaseFSH and LH, decrease testosterone.  Increase estradiol/testosterone ratio-----gynaecomastia 80%.  Cortisol should be checked (47% have low cortisol).  Decrease osteocalcin---- bone resorption.  Coagulation profile because of increased risk of DVT and pulm embolism.  Karyotyping:47 XXY 80-90 % - 10% mosaic.
  • 135.
    Germ cell tumors Classification:  -suppressed differentiation: seminoma, dys- germinoma.  -differentiation: Initial embryonal carcinoma Embryonic mature and immature teratoma Extra-embryonic(choriocarcinoma-yolk sac tumor{endodrermal sinus tumor})  -mixed histology: mixed GCT.
  • 136.
    Primary mediastinal germcell tumors  Comprise only 1-3% of germ cell tumors.  Overall teratoma is the most common variant, seminoma is the most common malignant variant.  Malignant variants are uncommon and more in males.  Benign variants are equally disributed among males and females.  Testicular examination, U/S and CT are mandatory to rule out testicular primary cancer.
  • 137.
    Serum markers  Alpha-fetoprotein:indicates malignant non- seminomatous type.  BhCG: suggests trophoblastic component. Malignant non-seminomatous and mixed GCTs carry worse prognosis than other GCTs.
  • 138.
    Association of M-GCTs with Klinefelter syndrome  Klinefelter syndrome is present in 20% of patients with M-GCT.  The incidence of M-GCT is 50 fold increased in patients with Klinefelter syndrome.  M-GCT mask the usual clinical signs of Klinefelter syndrome by inducing puberty by BhCG.
  • 139.
    Comparison of GCTbetween KS and general population  Klinefelter syndrome:  All contain non-seminominatous elements  Present at younger age (mean 17 years)  Precocious puberty is seen more often.  Almost exclusively extragonadal.  General population:  Pure seminoma is the most common malignant variant.  Older age at presentation (mean 29 years)  Precocious puberty is less often.  Only 2-5% extragonadal.
  • 140.
  • 141.

Editor's Notes

  • #23 Allergen exposure- e.g. house dust mite, household pets(cats and dogs), Atmospheric pollution- e.g. Antioxidants- e.g.