asthma gowry
DESCRIPTION
asthmaTRANSCRIPT
It is a chronic inflammatory disorder of airways in which many cellular elements – lymphocyte, neutrophil, mast cell, and macrophages are involved .It results in exaggerated airway hyper responsiveness which leads to reversible airway obstruction and intermittent symptoms of Wheeze, cough, SOB and tightness of chest.
Airflow limitation is due to
a. Bronchial smooth muscle constriction
b. Swelling of bronchial mucosa
c. Mucus plug
d. Airway remodeling
When exposed to allergen,At mucosa
• 1. Immediate reaction – allergen (Ag) bind with IGE AB in the mast cell and eosiniphil and release
Leukotriene, Histamine, PG
Platelet activating factor.
.2. Late reaction – Allergen activate the
Maccrophages, B lymphocytes,
CD4 Ly, Thymocyte, Eosinophil
All these cells release same mediators and IL4 & IL5
Effects of these mediators1. Contraction of the smooth muscle2. Increase in microvascular leakage – secretions
increasess3. Activate different neurones – constricti4. mucosal oedema All these leads to bronchoconstriction
When this inflamation is chronic1. Hypertrophy and hyperplasia of airway smooth
muscle2. Increase in number of goblet cells
3. Enlargement of submucus glands
4. Activation of fibroblasts
5. Remodelling of airway connective tissue – fibrosis will lead to some componant of permanent obstruction.
What is Hyperresponsiveness?- (Infamed airway)
Instability of the airways due to an exagerated bronchoconstrictor response to endohenous + Exogenous stimuli
Why? Due to air way inflammation. Once the airway is inflamed lot of inflammation cells will be there at mucosa for few weeks
Eg: Mast cells, Eosinophilia CD4 cells
Macrophages recurrited to mucosa
Secret
Mediators *Cytokines, Interleukins
*Histamine, seratonin *PAF, Pro-GF
All these Stimulate smooth muscle directly
And Stimulate nerveRapid + Brisk airway constriction
- Br. Asthma is common in Atopic people- 10-30% people suffer from wheeze at one stage of their
life
Risk factors and triger factors for Asthma
1. Host factors: Genetic, Atopy, Gender, Hyper-responsiveness
Gender M>F (childhood) IgE, Race
2. Environmental
- In door allergens- mite, animal allergens, cockroach, fungi, molds, yeasts, tobacco/ wood/ mosquito coil smok
Food
- Out door allergens – Pollens, fungi, molds, yeast, passive smooke
- Air pollution – gases, fumes, dust
- 3.Respiratory tract infections=> viral/bacterial/RSV/influenxa fungal infections, parasitic
- 4.Socioeconomic
Developed > Developing countries
- 5.Family size few> large members
- 6. Drugs + diet – NSAID, beta blockers, cocaine, heroin IL2, Vinblastin, Dipridamole,
- 7.Obesity
More in BMI > Less MBI
8. Exercise + hyperventilation dry & cold air9.Weather changes – cold, high humidity10.Sinusitis, nasal polyp, gastro eosophagal reflux
All triger factors will not cause symtoms in all pt How to diagnose Bronchial AsthmaSymptoms for 2-3 weeks1. Wheeze with or without difficulty in breathing2. Chest tightness3. Cough cough variant asthma All these symptomes are worse at night , after exercise,
exposture to dust, allergen or other trigers.These symtomes gets better with or without treatment.4. H/o eczema/ rhinitis/ Hay fever in the past or family
2.Signs in Br. Asthma
May be normal
Tachypnoea,
wheeze(rhonchi) is the important sign.
Evidence of hyperinflation of lung-
Impaired cardiac + liver dullness
In severe cases
Cyanosis, drowsiness, difficult to talk, tachycardia, use of accessory muscle, intercostal + subcostal recession –All evedence of repiratory distress
3.Investigations in a stable patient
1. Bedside test – PEFR through PEFM
Highest of three value is taken
Effort dependent,
Affected by airway narrowing, respira Muscle weakness
Easily learned
Reduced In Asthma, COPD, tracheal / broncheal
obstruction
Expiratory muscle weakness
Poor effort
PEF variability: PEFR in the morning and evening
Usually morning dips
If the patient is having symptoms
1.Morning and evening PFR measurements to show the variability > 20% atleast on 3occations or
PEFR before and after nebuliser with beta 2 agonist(15mt)
Demonstrate 15-20 % improvement in PFR
If the patient is not having the symptoms
PEFR before and after provocation –- physical exercise for 6 mts- Pharmacological – methacholin/ histamin
Demonstrate 15-20% decrement in PFR
2.FEVI/ VC Ratio with exercise or B2 agonist
3.Chest x ray
4.Full blood count
To find out eosinophilic conditions 5-7 % eosinophils in asthmatics
In tropical pulmonary eosinophilia 10-70%
PAN, Eosinophilic vasculitis also high
5.ESR – To detect any infections, vasculitis
6. Skin prick tests to detect allergens
Positive test just indicate the allery to particullary Ag
7. Diffusing capacity of the lung is normal
Differential Diagnosis
1.Tropical pulmonary Eosinophilia
Noct cough & wheeze
Eosinophil count > 3.000 cu mm3
Respond to Diethylcarbamazepine 100mg tds for two weeks
2.COPD : Present with cough progressive SOB
Need exclusion in old + wheeze patients with h/o smoking
FEV1 or FEV1/FVC or PER does not improve
Significantly with beta 2 agonist or short course of steroids
3. Bronchiectasis Cough with purrulent sputum They can have bronchospasm4. Gastro-oesophageal reflux Mimic nocturnal asthma / or worse existing
asthma h/o hart burn, symptoms related to posture
5. Upper airway obstruction Inspiratory wheeze & stridor6. Left ventricular failure / Pulmonary oedema In old people need exclusion Commonly they will have crepts but may have
wheeze alone
Classification of Asthma according to overall disease severity ( in stable stage)
1. Mild Intermittent Asthma: step 1 Rx Brief exacerbations only Asymptomatic between attacks Daytime symptoms < once/week Nocturnal symptoms twice / month FEV1 or PEF > 80% predicted PEF or FEV1 variability < 20% highest – Lowest reading * 100PFR variability = Highest PRF
2. Mild Persistant Asthma: Step II Rx
Exacerbations may affect activity & sleep
Day time symptoms > once/week But < daily
Night symptoms > twice / month
FEV1 or PEF > 80% predicted
PEF or FEV1 variability 20 – 30%
3. Moderate Persistant Asthma: Step III Rx
Daily symptoms (daily use of salbutamol inhaler)
Exacerbations afect activities & sleep
Nocturnal symptoms > once/week
FEV1 or PEF 60-80% predicted
PEF or FEV! Variability greater than 30%
4. Severe Persistant Asthma – Step IV Continuous symptoms Frequent exacerbations/frequent nebulization or
hospitalisations Frequent nocturnal symptoms Limitation of physical activities FEV1 or PEF 60% of predicted Variability > 30%
The patient should be considered to the most severe grade in which any feature occurs
Eg: Noct sym – 3 times/months Day sym – once / 2 weeks mild persistant
Primary prevention –* Breast feeding *Fish oil & Vit C in diet *Avoidance of maternal and paternal smoking during pregnancy
Secondary Prevention:1. Avoiding triger factors and optimum Rx2. Regular physical activity3. Weight reduction in obese4. Early Rx of respiratory tract infection and gastro
oesophageal reflux,sinusitis.
Pharmacological Mx
Relievers PreventorsRelieve acute symptoms Prevent symptoms1.2 adreno recepto 1. Corticosteroid stimulant(short acting) 2. Cromoglycates rapid action – last 4h mild acting Symptoms controler Long acting 2 agonist/long act theophillin2. Theophyllines3. Anti-muscarinic agents - Ipratropium Oxitropium4. MgSO4
Other drugs
1. Ketotifen – Non selective antihistamine with mast cell stabilizing action. Useful in children
2. Leukotrien modifier -> Zileuton or receptor antagonst Montelekast
Zafirlukast
( Bronchodilator + antiinflammatory)
Useful in aspirin induced and exercise induced asthma
Goals of Rx1. Good control of symptoms at all times2. Maximize lung function3. Identify triger factors4. Minimize side effects of medication5. Prevention of Exacerbations
Management targets1. Assess the severity2. Establish appropriate step Mx3. Health education including inhaler technique4. Maintaining good lung function5. Plans for managing exacerbation6. Providing regular follow up
Appropriate step management
1. Mild intermittent asthma - step 1
as needed short acting beta 2 agonist
Inhaler / oral
2. Mild persistant asthma - Step 2
as needed short acting beta 2 agonist and
low dose regular inhaled steroid
Beclamethasone 100-400 g bd
Budesonide 100 - 400g bd
Fluticazone 50 – 200 g bd one of these
Moderate persistant Asthma: step III
As needed inhaled short acting beta 2 agonist
AND- Regular moderate dose of inhaled steroids
Beclamethazone 250-500g bd
Fluticazone 125 – 250 g bd one of these
AND- Long acting beta 2 agonist salmeterol 50 g bd regularly
can try slow release theophyllin inspite of long acting beta 2 agonists
OR
As needed short acting beta 2 agonist + AND High dose regular steroids Beclamethasone 800 – 1000 g bd Fluticazone 200 – 500 g bd one of these
Severe persistant Asthma: step 4 As needed short acting beta 2 agonist AND Regular high dose steroids ANDRegular long acting beta 2 agonist salmeterole 50g bd Or oral salmeterole / orl slow release theophyllinIf still symptomatic Step 5 With other drugs add oral steroids morning dose 5-7.5 mg
When higher doses of inhaled steroids are prescribed It should be prescribed with spacer
As the inhaled steroids take time (1-3/52) to show the benefit. May need to give short course of oral steroids for 2/52
Education on these aspects
1. What is asthma
2. What are the triger factors, how to prevent
3. Methods of inhaler medication
4. How to monitor asthma with PEFR
5. How to treat acute wheeze at home with first aid
6. Written action plan
Maintaining good lung function
Once it is controlled maintain the same Medication at least for 3-6/12
Monitor lung function with PFR/ FEV1/ VC
If good x 3/12
step down the treatment
Regular follow up care at clinic
1. Look at PEFR chart, also do at clinic
2. Examin inhaler technique and look for side effects of Rx
3. Check the compliance of Rx
4. Find new triger factors and whether they can recognise exacerbation
Management of Acute AsthmaInitialAssessment History brief Physical examination rapidlyTreatment should be started immediately while the
initial assesement is going onOnce the patient is better detail history & examination
Acute asthma should be classified according to its severity
This classification is important to decide whether patient need treatment at outdoor or ward Rx or ICU/EU
mild-moderate severe lifethreatening1.Physical No + + also have Exhaustion paradoxical chest movement2. Talk in sentense in words can’t talk- agitated
3.Pulse rate <120 >120 Bradyccardia BP4.Pulsus para Not present present present- doxus5.Cyanosis No May +ve present6.Wheeze + + silent chestPEF/FEV1 >50% <50% cannot performSPO2 > 92% <92% very low drowsy&confusedABG To do not necessary Yes Yes
FeaturesAcute severe Life threatening1. Can’t complete a sentense 1. Can’t talk2. RR>= 25/mt 2. Cyanosed3. Pulse >120 3. silent chest with poor respiratory effort4. PEF < 50% of predided 4. Hypotension,bradycardia5. Pulse paradoxus 5. Exhausted, confused comatouseBlood gas makers of life threatening Asthma1. PaO2 < 8kPa or 60 mmHg irrespective of O2 Rx2. Normal or high PaCO2 > 45 mmHg3. Low PH
In acute asthma they will have type I failure PaO2 PaCO2
But
When they are having life threatening asthma they will develop type II failure PaO2
But PaCO2
Management of Acute Asthma
1. Mild Acute Asthma
1. Rxed at OPD
2. Ventolin nebuliser 5mg stat
+
Oral prednisolone 30-60 mg stat 2/52 tailoff
Inhalers introduced or double the dose of inhalers
Once PEFR > 70% D
Moderate acute Asthma
a. Rx at ward
b. O2 40-60% prop up
c. Salbutamole 5 mg nebuliser + 4 hourly
d. Oral prednisolone 30-60 mg and
e. If poor response – do CXR
continue inhaler
PEFR > 70% D
Management of acute severe / life threatening asthma
1. Prop up, O2 via face mask (exclude COPD)
40 –60%(connect pulse oxymeter)
2. Salbutamole 5 mg / Terbutaline 10 mg via O2 driven nebuliser
can repeat every 15 minutes 3-4 times if needed
3. If pt can take oral Prednisolone 30-60 mg stat daily
If cannot take oral Hydrocortisone 200mg stat 6 hrly
Insert IV canula and take blood for investigations
FBC, BU,SC,ESR,RBSIf Patient is not improving
do chest X’ray pneumothorax
pneumoniaMonitor SPO2, pulse, RR,BPIf SPO2 92% ABG from femoral artery *Not to give sedation* Hydrate the patientIf Hypokalaemia – treat itIf evidense of infection, give broad spectram of AB
If improving If not improving
Send to wardSteroid inhaler ICU MxRegular ventolin 1. Ipratropium bromide Nebuliser 2 hourly 500 g + Salbutamol+ oral steroid 2/52 Also try a. Salbutamol 250 g PEFR > 70% IV bolus infusion 5 g/kg D OR+ Plan
2. IV Aminophylline 250 mg bolus 0.5 mg/kg/hr OR c. MgSO4 2 gm in 100ml N. saline in 20 mts
If deteriorating any life threatening signs or low PaO2, high PcO2 (Repeat blood gas analysis)
Ventilate the patient if PCO2 high or acidosis or low O2
Once they are improving
Regular salbutamole 5 mg 4 hrly nebuliser
+
Inhaled steroids appropriate for their severity
+
Oral steroids 30 mg daily x 2/52
+
Inhaled salbutamole sos
Once PEFR > 70%
Plan for D
1. Re-examin the inhaler technique
2. Advice about triger factors + disease
3. Advice to buy peak flow meter
4. Give written action plan Know best PEF best/predicted eg: 500l/mt If low 400 l/mt - double steroid If low 300l/mt – start oral steroids If very low 200l/mt - need hospital admission If acute exacerbation at home 10 puffs of
salbutamole through spacer + oral prednisolone 30 mg on stat
If mild attacks respond well
Tell about side effects of oral steroidsAdvice to take inhalers regularly
Inhaled drug delivery devices:
Types Metered dose inhaler MDI
Dry powder inhaler
Nebuliser
MDI Delivers given dose of drug as aerosol
How Remove the cap, shake canister
Hold canister upright
Breath out until the end of normal breath
Keep the mouth piece into the mouth,
close lips tightly around
As you start to take a slow deep breath in through the mouth sqeeze once to actuate (press canister)
Hold the breath for 10 secondsRepeat the inhalations as neededWash mouth and gargle with water and spit out
15 – 20 % of the drug only deposits in the bronchial system
Balance is wasted or deposit in the throat
Disadvantage
Need good cordination with hand + breathe
If large doses of steroid is prescribed
Prescribe with spacer
How
1. Select compatible MDI
2. Shake the MDI well & insert to the mouth piece into socket of spacer
3. Hold the spacer mouth piece into mouth and close lips tightly
4. Actuate the inhaler and breath in and out normally through the mouth peice 3-4 times
repeat same if large dose is taken
Advantages with Spacer
1. Increases lung deposition of drug up to 30%
2. Cordination of actuation and breathing not necessary
3. No need to have good breathing effort- tidal breathing is enough
Who need spacer
1. People with difficulty in coordinating , old, children < 5 yrs( with faces mask).
2. Who need steroid > 800 g Beclamethasone x 24 hours
• Spacer should be cleaned once in 2-4 days
• Washed with soap water, drip dried
• Should not be wiped with other materials
• Change every year
Dry powder inhalersRelease drug – as powder in capsules or in blister
(dischaler)Ex: Cyclohaler, D-P haler Dipihaler, Rota haler Disk haler, Accuhaler and Turbuhaler low inspiratory effort enough (preloaded dry powder) Deposition rate 20 – 30%For optimum use of dry powder1. Load the capsule or card and break it accordingly2. Breathout until the end 3. Keep the mouth piece & close lips tightly4. Breath in as fast as and as deep as possible
5. Hold breath for 10 seconds
6. Patient should not breathout through the mouth piece of DPI
For most of these drypowder inhalers good inspiratory effort is needed
Exceptions are Turbuhaler x accuhaler
While on Inhaler
Poor control of Asthma may be due to
1. Poor compliance 2. Improper technique
3. Inadequate dosage 4. Inappropriate Rx
5. Poor environmental control
Local side effects of steroids with inhaler
1. Oral candidiasis
2. Steroid induced pharyngeal myopathy – voice change - which is reversible
Asthma & Surgery
1. Life threatening bronchospasm can occur during and after Sx and during anaesthesia.
specially if the asthma was poorly controlled at the time of Sx
It is due to
Severe Bronchospasm occurs with intubation, induction drugs, + maintenance drugs and extubation
2. So, careful pre-op control of symptom of asthma is important before the elective surgery
3. Make sure, there was no lung infection Or asthmatic exacerbation during last 2-3/52, Do PEFR or FEV1 > 70% of predicted If there was post pone Sx by 2-3 /52 x Rx it Repeat PEFR or FEV1 4. Continue inhaled drugs until be the time and after Sx5. If they are on systemic steroids continue it until Sx and give
parenteral steroid during Sx then ct oral.6. Pre op give prednisolone 10mg noct, day before ventolin nebuliser – just before Sx7.Continue the same RX after surgery on which she was on before surgery.8. If connot take inhaler or oral,- cover that time with paranteral steroid.
If possible do Sx under local
If GA do intubation + extubation under deep anaesthesia
Post OP
1. Good pain control with Fentanyl / Pethedine
Don’t give morphine
2. Avoid NSAID
3. Good Hydration
Exercise induced Asthma
Exercise
Drying Sympathetic Activity
Cooling
1-2 mnt
CatacholamineMast cells short act broncho
constriction Dilate bronchi
1 –2 Hours 2-6mt constrict
mediater destruction in 20 mt
Depleted mast cells
1. Any one with poorly controled asthma can get wheeze after exercise
2. In some people it occurs only after exercise
3. Symptoms starts 5-10 mts after stopping the Ex
Exercise:
• During exercise both
Dilators + constriction together
So usually no symptoms
But * after exercise when catachalamine is reduced wheeze
4. Once the released mediater is destroyed they will be free of symptoms and there is a refractory period( 2-6 hours) during which they will not develop wheeze even if they exercise due to PG which cause Bronchodilatation.
How to RX
1. Short acting beta 2 agonist just before exercise
OR
Na cromoglycate just before exercise
2. Long acting beta 2 agonist 2 hr before exercise
3. Warming up exercise within last 30 mts.
Brittle Asthma
• Unusual variant, patients are at risk of sudden severe unexpected acute attacks over minutes hours
• Emergency drugs should be with the patient all the time , Nebuliser at home and work place and
• Self injectable epinephrine – Epi pens 0.3 0.5mg pre loaded in syringe x 2 with patient.
• Prednisolone 60 mg with patient
• Medical alert brakelet
Pregnancy & Asthma
- 1/3 gets better
- 1/3 same
- 1/3 gets bad during pregnancy
• Should be monitored carefuly
• Severe asthmatics usually get worse
• Non of the drugs including steroids are contraindicated except leakotrine modifferes
• Theophyllin may cause foetal tackycardia
Hypoxia during acute attacks of asthma cause damage to mother & foetus then drugs so priority is to control asthma
Optimum medication is given with inhaled steroids and beta agonists long + short
Avoid oral salbutamol Treatment is same like other patientsEven if they get acute attacks, Rx is as like others
patients with foetal monitoring + O2They can continue same medication during
pregnancy & lactationDuring Labour All drugs continued
If they were on oral steroids > 7.5 mg/d need to give hydrocortisone 6 hourly
No special indication for LSCS other than Obs indicationIf anaesthesia is needed, local anaesthesia better specially if
they are symptomaticProstaglandin F2 alpha should be avided, if necessary used
with extreme caution.
Anaphylaxis
If Acute Bronchospasm is due to Anaphylaxis
Adrenalin 0.5 mg should be used instead of selective beta 2 agonists
Other drugs that could be used as steroid sparing drugs in Asthma
1. Methotrixate
2. Cyclosporins
3. Gold
4. IV Immunoglobulin
5. Anti IgE monoclonal antibody – Omalizumab
If you see a patient with Asthma with Acute exacerbation
1. Find out what was the precipitatory factor this time
2. Find out the severity prior to this
* How many attacks
* Functional state – dependant/nondepedant
* How often taking salbutamol
* How often absent from work / school
3. No. of hospital admission
Last admission
Any life threatening asthma- need of ventilation.
4. Other precipitating factor
5. allergy history, drug allergy, eczema, rhinitis
6. If already on medication
- compliance, side effcts of drugs – Ex prednisol.
7. Drug compliance and technique of inhaler
8. Detail occupational history -
Chronic Obstructive Pulmonary DiseaseClinical syndromes that leads to destruction of lung
and irreversible airway obstructionAirway obstruction is progressive and associated with
abnormal inflammatory response to noxious agentsFollowing conditions are included:a. Mainly Emphysema and chronic bronchitis usually both co- exist togetherb. Other diseases - bronchiectasis - Cystic fibrosis - Persistant chronic uncontrolled asthma - Bronchiolitis obliterans
It is characterized by followinga. Inflammatory narrowing of respiratory
bronchiolesb. Proteolytic destruction of connective tissue of lungc. Loss of alveolar surface area and vascular bedd. Lung hyperinflation with loss of Elastic recoile. Increased vascular resistance
Risk Factors1. Smoking active + passive proportionate to number of cigarette, cigar, house-hold smoke Increased with number of pack per year
2. Environmental factors
Air pollution
Occupational exposure to toxic gas
3. Genetic
1 Antitrypsin deficiency(proteolytic enzme inhibitor
4. Old age, F/H of COPD, Male sex
5. Low birth weight and recurrent childhood infection or at infant stage
Emphysema Pathological defiition
Dilatation & Destruction of air spaces distal to the terminal bronchole without obvious fibrosis
There is reduction of elastic recoil of lungCollapse of airways in early Expiration Air
traping expiration +ve p
pleural
pressure
Normal recoil recoil pressure is less
pressure
Chronic bronchitis
Clinical Diagnosis
Def: Chronic cough and sputum production on most of the days for at least 3 consecutive months of succesive 2 years
Here obstruction is due to narrowing of airways by mucosal thickening excess mucus & structural narrowing
Exacerbations are due to- Respiratory tract infection- Bronchospasm- Mucus plugging
PresentationChronic BronchitisBlue Bloated Symptoms Signs Complications * cough with *cyanosis * Iiry polycythe— sputum * peripheral * pul. HT oedema cor pulmonale * SOB usually mild * wheeze Ix: PO2 + PCO2 cracles
Emphysema – pink & puffing
Symptoms signs complicationsSOB Tachypnoeic pneumothorax Pink weight lossCough pursed lip breathingmild accessory muscle use Cackectic PO2 Barrel chest PCO2 or Breath soundsUsually both components will be there together in
patients. Main symptoms and signs depends on the predominant component
Ix:1. Chest X’ray Laterl - Increased AP diameter. Increased Retrosternal space.
PA - flat hemidiaphragm on PA. Elongated Cardiac shadow. prominent Pu A. Reduced Peripheral marking . When cor- pulmonalae Cardiomegaly with
prominent PA
2. PEFR very low not improved with Bronchodilators or steroids x 2/52 30 mg oral daily
3. FEV1 VC FEV1 / VC ratio
RV & TLC both are increased
FEV1/VC
5 VC normal 4.5/5 = > 90%
4.5
3.5 VC of PT
2.5 1.5/3 = 50%
1.5
FEV1
COPD 1.5/3 = 50%
COPD Gold criteria with FEV1
1.mild - FEV1 > 80% variable SOB
2.moderate - FEV1= 50-70% SOB on mild exertion
3.Severe - FEV1= 30 – 49 % SOB ++
4. Very severe – EFV1= < 30% limitd all activities
4. Flow volume Loop Normal & early COPD Late COPD 7lFlOw second4.5l recidual volume Increased Recidual volume
PFR 75 50 25% of lung volume In early COPD PEFR may be normal But rate at 50%,
25% of lung volume is very low5.Diffusing capacity of lung is low but in early
Bronchitis may be normal
Management of COPDManagement of COPD
Usually they present to us with exacerbations
– infections or CCF
By the time when they present with SOB, their lung function is badly affected
I. Etablish the diagnosis with history / Ix & examinations
after 30 y, in normal people FEV1 decreases by 20 ml/year but in COPD 50 ml/year
II. Once diagnosis is made
1. Stop smokiong
2.7 stoped smoking
FEV1 contined to smoking
a. Set up a date for stoping
b. Make group discussion & councelling
c. If they are dependant – nicotine patches
Nicotine chuingum
2. Rx of Exacerbations:-
Treatmetn is as like as exacerbation of bronchial Asthma
2.1 Prop up, monitor, SPO2, pulse, BP
If SPO2 < 85% - arterial blood gas analysis
2.2 O2- 24 – 28 % Just to maintain SaO2 88-90%
If we over treat with more O2 patient will develop CO2 Narcosis
2.3 Bronchodilators SALBUTAMOL / Terbutalin
& Anticholinergics (Iprotropium) 4 hourly
Although bronchodilatation is very minimal
*High in crosectional area * in resistance to air flow
Helps Symptomatically (lung function not much improved)
2.4 IV cannula - Take blood samples – BU, Se, FBC, RBS - Sputum – DS - Culture & ABST - Do chest X’ray, ECG. - In young patients 1 Antitrypsin level
2.5 Give IV Hydrocortisone 200 mg / 6 hourly or oral prednisolone to reduce mucosal oedema
2.6 If still symptomatic Aminophyllin 250mg bolus followed with
infusion
Aminophillin act as
-Resp. stimulant, Bronchodilator,mild diuretic
& mild positive Ionotrope
2.7 If poor response Try with Doxopram (Resp.stimulant)
2.8 If precipitant is infection start broad spectrum antibiotics Ampicillin / Cefuroxine
Need to repeat arterial Blood gas after 1-2hours
2.9 If arterial blood gas shows severe hypoxia
PO2 < 55 mm Hg
PCO2 > 55 mm Hg
pH < 7.26(acidosis)
If the patients living status prior to this acute problem is OK. (at least the patient was able to look after themselves)
ET tube & Ventilation – Artificial
Ventilation• Noninvasive with continuous positive
airway pressure is prefered
-No ET tube
- tightly fitting Mask that covers the nose or nose and mouth, is used
• Invasive ET tube with + ve pressure ventilation
Clinical judgement is very important before ventilation
Rationalae for ventilation giving time for the acute
problem to settle, so the pt can get back to previous stage
3. Once the patient is recovered follow up
3.1 Regular bronchodilators
inhaled – salbutamol 200 microgram 6 hourly
MILD –(FEV1 > 80%) or
COPD Salmeterole 50 microgram bd
AND
MODERATE Anticholinergic
FEV1 50-70 % Ipratropium Bromide 40micro.g6hly
Oral slow release theophyllin 150-250 mg Bd
• SEVERE COPD PFR < 50%, FEV1< 30%
Together with other Rx
• Optional Inhaled steroids- with spacer higher dose– only in severe cases. Ex
If there is improvement in FEV1 / PEFR
After Rx with oral prednisolone 30-60 mg/daily for 2 weeks
Very SEVERE COPD FEV1, PEFR < 30%
Add Oral steroid 5- 7.5 mg daily together
3.2 Mucolytics- if difficult to cough out sputum
3.3 If Right heart failure due to cor-Pulmonalae
Diuretics, ACEI, Digoxin, theophyllin
3.4 Avoid Sedatives
3.5 Good nutrition, Calori intake
3.6 Regular limb exercise
3.7 Regular vaccination – Pneumococcus
Haemophilus
Influenza virus
3.8 Home O2 treatment
3.9 Surgical options
3.10 If treatable eg: Antitrypsin replace it
3.11 Cor-pulmonalae with polycythemia regular
venesection
Home O2 Rx (Domicilliary O2)
Indicationsshould not smoke at present(COHb <3%)
• PaO2 < 55 mm Hg When the patient is
• PaCO2 > 38 mm Hg stable after 6/52
• Previous Corpulmonalae of Exacerbation
• FEV1 < 1.5 L
O2 could be delivered with O2 concentrator or O2 cylinders
It is given for 15 hours / day
Given through nasal catheter
Step Rx in COPD Lung reducing surgery
FEV1 Home O2 Pulmonary rehabilitation
combination of steroid inhaler
long act beta 2 agonist
long acting theophyllin
Symptoms combination of Ipratropium inhalar with
beta2 agonist
Long acting bronchodilator regularly
short acting bronchodilators vaccination Stop smoking Regular lung function
The rate of O2 should be titrated at hospital usually 1.5 – 2 L / mt
When they are going out they could be given with O2 cylinder on wheel
*If they have severe hypoxia at night CPAP with mask
continuous positive airway pressure
(Durig REM sleep all muscles are relaxed–more weak)
Surgical Options:
1. Bullectomy
2. Lung reduction surgery
3. Single Lung transplantation
Complications of COPD
1. Low effort tolerance
2. Type II respiratory failure
- Hypoxia
- High CO2
3. Pulmonary hypertension loud P2
4. Right heart failure cor pulmonalae
5. Polycythemia
6. Severe hypoxic cachexia
Cor pulmonalae – Heart disease2ry to disease of Lung
Bronchiectasis
Destructive lung disease associated with
chronic localised dilatation of bronchi
persistant but variable inflamation of the lung
Should suspect, when there is chronic productive cough
Pathollogy: any part of lung is affected, commonly lower lobes
Dilatation of the bronchi
Ulceration of the Mucosa
Squamous metaplasia
Inflammatory infiltration & excess
Mucus secretion due to high Goblet cells
Conditions associated with bronchiectasis
1. Host defects
a. Immunodeficiency IgG , IgM abnormal phagocytic function
Reduced complement levels
Leucocyte adhereace defect
b. Mucociliary clearance defect
Immotile cilia syndrome
Young syndrome, cystic fibrosis
Katageners syndrome
2. After infection: -Aspiration pneumonia or TB, Measles, whooping cough, poorly
treated pneumonia, septic emboli, HIV, Allergic aspergilosis
3. Post Inflammatory – aspiration, neurological weakness-achalasia
Gastric reflex aspiration IV heroin, Rheumatoid arthritis Fibrosing alveolitis4. Others: 1, Antitrypsin deficiency Yellow nail syndrome5. 2ry to obstruction by LN, adenoma, Foreign body
Clinical features
• Usually present with acute exacerbations,
• Chronic cough with purulent sputum,fever
• Haemoptysis with pleuritic chest pain Sputum production is continuous or intermitent
Sputum production, cough is changed with position
H/O post nasal drip, infertility, chronic ear discharge
Chronic sisusitis& frequent chest infections
H/O - HIV, RA, Reflux disease
F/H cystic fibrosis p/h TB, pneumonia
Exacerbation
1. Large amount of sputum production
2. Fever and worsening cough
3. Change is colour of sputum
O/E
Clubbing + Halitosis
Coarse crepts & rhonchi
Signs of consolidation
Investigations:
1. Chest X’ray: Tram line shadow
Cystic shadow
Areas of minor collapse
and fibrotic changes
2. Sputum examination is necessary during excerbation: Direct smear, culture, ABST & fungal study
3.FBC – high N
4.ESR - High
3. High resolution CT Chest – Non invasive
Diagnostic investigation
Demonstrate the dilated bronchi & distribution
4. Bronchogram
1. Invasive
2. But confirm the diagnosis
5. Lung function test
To asses the lung damage & degree of obstruction
- Spirometry
- flow volume loop
6. To find out underlying cause for bronchiectasis 1. X’ray sinus 2. Aspergilus test 3. BA swallow 4. IgG, IgM complement level 5.Cilliary function, Neutrophil function test, sweat Na+, 1 antitrypsin level
ManagementWhen they come with acute exacerbationGeneral – 1.Bronchodilator –inhaled beta 2 agonist
–2. chest physiotherapy postural drinage(Important
- 3. Mucolytic agents - 4. O2 If needed
2. Antibiotics If not very ill short courses of Amox 500 mg tds/cotrim 2 bdOr erythromycin 500 mg 6h / cephalexin 500 mg 10 – 14 days
If severe infectionIV 2nd or 3rd generation cephalosporin or AugmentinIf sputum is offensive Metronidazole is addedOnce sputum culture, ABSt is available change
accordingly
Follow up Rx
Very important
1. Continue chest physio regularly Bd at home
2. Ct Bronchodilators,
3. Good nutritionVitamin A & D
4. If cor pulmonalae – diuretics
5. If needed – Antibiotic prophylaxix / Rx
< 2/52 every 2/12 continuous purulent sputum
Give antibiotic Rx frequent excerbation Amox 3g Bd
Only for Exacerbation Rx Exacerbation Rx with high dose antibiotics
Prophylaxix Continuous Rx
Amox 500mg D 500 mg tds
Cotrim 960mg D If pseudomonas ceftazidine or Cipro.
or Inhaled antibiotics
5. If needed – Antibiotic prophylaxix / Rx
Over 2 months disability
< 2/52 > 2/52 continuous purulent sputum
SOS Rx Prophylaxic Rx Continuous Rx
Give antibiotic Rx frequent excerbation Amox 3g Bd
Only for Exacerbation Rx Exacerbation Rx with high dose
antibiotics
Prophylaxix Continuous Rx
Amox 500mg D 500 mg tds
Cotrim 960mg D If pseudomonas
ceftazidine or Cipro.
or Inhaled antibiotics
6. Surgical Rx
If Bronchiectasis is Localised - lobectomy
7. Steroids may be useful in some patients-Optional
Complications:
1. Pneumonia
2. Pneumothorax
3. Empyema
4. Metastatic abscess, Amyloidosis