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BRONCHIAL ASTHMA

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BRONCHIAL ASTHMA

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 -

COPD

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

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

1. Severe life threatening haemoptysis – usually from

bronchial artery

- Rest

- Antibiotics

- Blood transfusion

If still not improved Embolise, surgical

resection