standard treatment guidelines - kerala

Respiratory diseases

GOVERNMENT OF KERALA

STANDARD TREATMENT GUIDELINES

DEPARTMENT OF HEALTH AND FAMILY WELFARE

STANDARD TREATMENT GUIDELINES INRESPIRATORY DISEASES

Section I

Asthma

Section II

Allergic rhinitis

Section III

Diagnosis & Managementof Chronic Obstructive Pulmonary Disease

Section IV

Community acquired Pneumonia

Section V

Bronchiectasis

Section VI

Pleural Diseases

Section VII

Sleep disordered breathing

Section VIII

Hemoptysis

Section IX

Pumonary embolism

Section X

Interstitial Lung Disease

Section XI

Long term oxygen therapy

Fourteen sections

Section XII

Tuberculosis

Section XIII

Lung cancer

Section XIV

Upper airway obstruction

Convener

Dr. Sanjeev Nair, Department of Pulmonary Medicine,

Medical College, Trivandrum

Members

1. Prof. Dr. C Ravindran, Department of Pulmonary Medicine,

WIMS, Wayanad

2. Prof. Dr. K Anitha Kumari, Department of Pulmonary Medicine, Medical College, Trivandrum

3. Prof. Dr. Rajagopal TP, Department of Pulmonary Medicine, Medical College, Kozhikode

4. Prof. Dr. Fathahudeen A, Department of Pulmonary Medicine, Medical College, Ernakulam

5. Prof. Dr. Suraj KP, Department of Pulmonary Medicine, Medical College, Kozhikode

6. Prof. Dr. Thomas George, Department of Pulmonary Medicine, Medical College, Thrissur

7. Prof. Dr. Santhosh PV, Department of Pulmonary Medicine, Medical College, Manjeri

8. Prof. Dr. Venugopal P, Department of Pulmonary Medicine, Medical College, Alappuzha

9. Dr. Ameer KA, Department of Pulmonary Medicine, KIMS, Trivandrum

10. Dr. Jayaprakash B, Department of Pulmonary Medicine,Medical College, Trivandrum

11. Dr. Ronaldwin B, Department of Pulmonary Medicine, Medical College, Trivandrum

12 Dr. Sreekala C, Department of Pulmonary Medicine, Medical College, Trivandrum

13. Dr. Reshmi S Nair, Department of Pulmonary Medicine,Medical College, Trivandrum

14. Dr. Kamala R, Department of Pulmonary Medicine, Medical College, Trivandrum

Committee for Development of Standard Treatment Guidelines Respiratory diseases

15. Dr. Praveen GS, Department of Pulmonary Medicine, Medical College, Trivandrum

16. Dr. KGR Mallan, Department of Pulmonary Medicine, Medical College, Ernakulam

17. Dr. Jyothi E, Department of Pulmonary Medicine, Medical College, Kollam

Additional Chief Secretary, Department of Health and Family Welfare, Government

of Kerala, the process of preparation of Standard Treatment Guidelines (STG) was

initiated by the Director of Medical Education Dr. Remla Beevi A. The process of

developing and finalizing the STG’s were coordinated by Dr. Sreekumari K. Joint

Director Medical education and Dr. Suma T K, Professor of Medicine and ably

supported by a dedicated team of experts, including external faculty”.

“Driven by the inspiration drawn from Shri. Rajeev Sadanandan IAS,

TABLE OF CONTENTS

Message by Chief Minister 11

Message by Health Minister 13

Foreword by Additional Chief Secretary 15

Abbreviations 17

Section - I

1.Asthma 21

1.1. When to suspect asthma 23

1.2. Making the diagnosis of asthma in special

populations 24

1.3. General principles of asthma management 25

1.4. Categories of asthma medications 26

1.5. Control-based asthma management 27

1.6. Assessment of risk factors 28

1.7. Treatment 28

1.8. Reviewing response and adjusting treatment 30

1.9. Other therapies 32

1.10. Acute exacerbation of Asthma 34

1.11. Management of Asthma in special situations 35

1.12. Acute exacerbation of Asthma 36

1.14. Discharge following IP treatment of patient with

acute Asthma 42

Section - II

2. Allergic rhinitis 43

2.1. Classification of allergic rhinitis 45

2.2. References 49

Section - III

3. Diagnosis & managementof chronic obstructive

pulmonary disease (COPD) 51

3.1. When to suspect COPD 53

3.2. Risk factors for COPD 53

3.3. Diagnosis of COPD 54

3.4. Additional investigations in COPD 55

3.5. Treatment options 56

3.5.1. Management of stable COPD 56

3.5.2. Non pharmacological therapies 60

3.5.3.. Other treatments 61

3.6. Follow-up pharmacological management 62

Section - IV

4. Community acquired pneumonia 65

4.1. Introduction 67

4.2. Definition 67

4.3. Diagnosis of pneumonia 67

4.4. Investigations 68

4.5. Risk stratification 69

4.6. Diagnosis and management of hospital-acquired

pneumonia (HAP) / ventilator-associated pneumonia (VAP) 76

4.7. References 87

Section - V

5. Bronchiectasis 89

5.1. Clinical features 91

5.2 Investigations 91

5.3.Investigations to determine the underlying

Cause of bronchiectasis 92

5.4. Management 93

5.5. Patient education 94

5.6. Role of surgery 98

Section - VI

6. Pleural diseases 101

6.1. Pleural effusion 103

6.2. Management of unilateral pleural effusion 103

6.3. Invasive investigations 106

6.4. Specific conditions and tests 106

6.5. Indications for pleural fluid drainage in pleural infection 109

6.6. Pneumothorax 110

6.7. Treatment Options For Pneumothorax 111

Section - VII

7.1. Overlap syndrome, obesity-hypoventilation and

Pickwickian syndromes 117

7. Sleep disordered breathing 115

6.4. Specific conditions and tests

7.2. Diagnosis of OSA 117

7.3. Various levels of sleep studies 118

7.4. Diagnostic criteria for OSA 119

7.5. Medical management of OSA 120

7.6. Surgical treatment of OSA 122

Section - VIII

8.1. Management 127

8.2. Airway protection and resuscitation 127

8.3. Drugs used 128

Section - IX

9. Pumonary embolism 129

9.1 Treatment 132

Section - X

10. Interstitial lung disease 141

10.1. Diagnosis and management of interstitial lung diseases 143

10.2. Classification of interstitial lung diseases 143

10.3. Diagnosis of interstitial lung diseases 144

10.4. Physiological evaluation 144

10.5. General management strategies in ILD 150

10.6. Treatment recommendations 152

10.7. Connective tissue disease related ILD 154

10.8. Polymyositis-dermatomyositis 155

10.9. Pulmonary langerhan's cell histiocytosis 157

Section - XI

11. Long term oxygen therapy 161

11.1. Use of long-term oxygen therapy in patients with chronic

Obstructive pulmonary disease 163

11.2. LTOT in patients with ild 163

11.3. Assessment of patients for ltot 164

Section - XII

12. Tuberculosis 167

8. Haemoptysis 125

12.1. Treatment of drug sensitive TB 171

Section - XIII

13. Lung Cancer 175

13.1. Introduction 177

13.2. Diagnosis and staging 178

13.3. Treatment 180

13.4.

13.5. References 185

Section - XIV

14. Upper Airway Obstruction 187

14.1 Major Airway Obstruction 189

14.1. Causes of benign and malignant airway obstruction 189

14.2. Malignant 189

14.3. Management 191

Managing brain metastases 184

Message

The Government is taking many initiatives to ensure providing quality

health care to all. Out of the five missions launched by the Government, the

Aardram mission is primarily focussed to improve Primary Health Care to

provide standard health care facilities to people at grassroots. This initiative is

complemented by strategic investment for the improvement of infrastructure in

secondary and tertiary health care institutions to provide quality health care

services.

I am happy to note that the Department of Health is also taking

initiatives to bring standardization in treatment for various disciplines like

Cardiology, Critical care, Diabetes Mellitus, Cancer Care, etc. It is a noteworthy

initiative to improve the qualitative aspects of the health service delivery. I

appreciate the efforts taken by the experts from Government sector and private

sector from Kerala and also the subject experts from outside the state. I am

hopeful that the introduction of standard guidelines for diagnosis and

treatment will ensure better quality and consistency in health care.

I wish all the success to this endeavour.

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Pinarayi VijayanChief Minister

SecretariatThiruvananthapuram

Pinarayi VijayanChief Minister

Message

13

Foreword

Patient care has moved away from management by an

individual based on personal knowledge and skill to an evidence

based, team managed operation. Decisions are reviewed more

rigorously post facto and their alignment verified with standard

practice. With the mode of payment for care moving from out of

pocket payments to third party payers there will be a demand for

rigorous documentation and evidence of having conformed to

standard practice. When analysis of big data and machine learning

becomes the norm it will require a standard set of procedures to act

as the baseline from which to measure deviations and differences in

impact.

To meet the requirement of these developments in the field

of medicine, it is necessary to have explicit, objectively verifiable set

of standard operating procedures. They have to be prepared based

on international guidelines with the highest acceptance, but have to

be modified to suit local knowledge and practice, so that there is

local ownership. Government of Kerala has been trying to get the

guidelines prepared for some time now. I would like to thank and

congratulate Dr. Sreekumari, Joint Director of Medical Education

and Dr. T.K.Suma, Professor of Medicine, T.D. Medical College,

Alappuzha who took on the task of preparing standard treatment

guidelines and completed it through a long, consultative process. I

also thank the conveners of the different thematic groups who

coordinated the work in their field as well as the innumerable

number of participants, in government and private sector, who

contributed their effort and knowledge to improve the guidelines.

Professional associations have also contributed in their fields. Their

efforts have resulted in a product they and Kerala can be proud of.

Treatment guidelines cannot be static if they are to remain

relevant. They must be updated based on new knowledge and the

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experience of treatment based on these guidelines. To do this the

group which prepared the guidelines has to remain active and have

a system for collecting data on the results of practice based on

these guidelines. I hope such an activity is institutionalised and

periodic revisions of the guidelines are prepared and published.

I wish that these guidelines contribute to raising the quality of

patient care in Kerala.

Rajeev Sadanandan IAS

Addl Chief Secretary

Health & Family Welfare

Department

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6MWT 6 Minute Walk Test

ABG Arterial Blood Gas

ACOS Asthma COPD overlap syndrome

ADA Adenosine deaminase

AEC Absolute Eosinophil Count

AFB Acid Fast Bacilli

AHI Apnoea Hypopnoea Index

ANA Anti Nuclear Antibody

BMI Body Mass Index

BPAP Bilevel Positive Airway Pressure

CAT COPD Assessment Tool

CBNAAT Cartridge based nucleic acid amplification test

CF Cystic Fibrosis

CHF Congestive Heart Failure

COP Cryptogenic Organising Pneumonia

COPD Chronic obstructive pulmonary disease

COX2 Cyclo oxygenase - 2

CPAP Continuous Positive Airway Pressure

CT Computed Tomography

DIP Desquamative Interstitial Pneumonia

DLCO Diffusion capacity of the lung for carbon monoxide

DR TB Drug resistant TB

DST Drug susceptibility testing

EBUS Endo bronchial Ultrasound

EDS Excessive Daytime Sleepiness

EP TB Extra pulmonary TB

ESS Epworth Sleepiness Scalest

FEV1 Forced expiratory volume 1 second

FEV1 Forced Expiratory Volume in 1 second

FiO2 Fraction of O2 in inspired air

FNMM Fibre-optic nasopharyngoscopy with Mueller's

manoeuvre

FL-LPA First line Line Probe Assay

FVC Forced Vital Capacity

Abbreviations

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FQ Fluoroquinolone

GERD Gastro esophageal reflux disease

GINA Global initiative for asthma

HST Home Sleep Testing

ICS Inhaled corticosteroids

ILD Intersititial lung disease

LABA Long acting beta agonist

LAM Lymphangioleiomyomatosis

LAMA Long Acting Muscarinic Antagonist

LCH Langerhan' Cell Histiocytosis

LDH Lactate Dehydrogenase

LIP Lipoid interstitial pneumonia

LPA Line probe assay

LTOT Long Term Oxygen Therapy

LTRA Leukotriene receptor antagonists

Mcg/ μg Microgram

MDR Multi-drug resistant TB

MGIT Mycobacterial growth indicator tube

mMRC Modified Medical Research Council

MRA Mandibular Repositioning Appliances

MRI Magnetic Resonance Imaging

NIV Non-invasive ventilation

NSCLC Non Small Cell Lung Cancer

NSIP Non Specific Interstitial Pneumonia

OCS Oral corticosteroids

OCST Out of Centre Sleep Testing

OHS Obesity Hypoventilation Syndrome

OSA Obstructive Sleep Apnoea

PaO2 Partial pressure of Oxygen in arterial blood

PAP Positive Airway Pressure

PBD Post Bronchodilator

PDE4 Phosphodiesterase 4

PEEP Positive End Expiratory Pressure

PEFR Peak expiratory flow rate

PET Position Emission Tomography

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PM Portable Monitoring

pMDI Pressurized Metered Dose Inhaler

PSG Polysomnography

PSP Primary Spontaneous Pneumothorax

RAST Radio allergosorbent test

RB ILD Respiratory Bronchiolitis Interstitial Pneumonia

RDI - Respiratory Disturbance Index

RERA Respiratory Effort Related Arousal

RR TB Rifampicin resistant TB

RS TB Rifampicin sensitive TB

SABA Short acting beta agonist

SAMA Short Acting Muscarinic Antagonist

SCLC Small Cell Lung Cancer

SDB Sleep Disordered Breathing

SDGs Sustainable deveolpment goal

SLE Systemic lupus erythematosus

SLI Second line injectable

SLIT Sublingual immunotherapy

SL-LPA Second line Line Probe Assay

SMART Single maintainance and reliever therapy

Spo2 Peripheral capillary Oxygen saturation

SSP Secondary Spontaneous Pneumothorax

TBNA Trans Bronchitis Needle Aspiration

TRA Tongue Retaining Appliances

UAO Upper Airway Obstruction

UIP Usual Interstitial Pneumonia

ULCT Unattended Limited Channel Testing

UPPP UvuloPalatoPharyngoPlasty

USG Ultrasonography

VATS Video Assisted Thoracoscopic Surgery

WRDT WHO approved rapid diagnostic test

XDR Extremely drug resistant TB

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Section I

Asthma

Section I

1. Asthma

1.1. When to suspect asthma

Asthma is a heterogeneous disease characterized by chronic airway

inflammation and is defined by variable symptoms of wheeze, shortness of breath,

chest tightness and/or cough, and is associated with variable expiratory airflow

limitation. Both symptoms and airflow limitation characteristically vary over time and

in intensity. The usual triggering factors are exercise, allergen or irritant exposure,

change in weather or viral respiratory infections.

Asthma is suspected in a person with history of wheeze, shortness of breath,

chest tightness and cough that is often worse at night or in the early morning. It may

be associated with a triggering factor. The symptoms may improve spontaneously or

with treatment. There may be similar history of respiratory symptoms or allergic

rhinitis or eczema in the family.

Diagnostic criteria for asthma

1. More than one type of the characteristic respiratory symptoms (wheeze,

shortness of breath, chest tightness, cough)

• Vary over time and in intensity.

• Often worse at night or on waking.

• Triggered by exercise, laughter, allergens, cold air, strong smells,

drugs.

• May appear or worsen with viral infections.

2. Evidence of variable expiratory airflow limitation

• A fixed cut off of FEV1/FVC <0.75 for older subjects and <0.8 for

younger individuals (lower 5th percentile of values from reference

population) may be used to diagnose airflow obstruction.

• An increase in FEV1 of >12% and >200 mL from baseline, 10–15

minutes after 200–400 mcg salbutamol or equivalent in adults and

increase in FEV1 of >12% predicted in children.

• An average daily diurnal PEF variability >10% in adults and

average daily diurnal PEF variability >13% in children.

• A fall in FEV1 from baseline of ≥ 20% on bronchial provocation

test.

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Bronchodilator reversibility may be lost during severe exacerbations or viral

infections. If bronchodilator reversibility is not present at initial presentation, the next

step depends on the urgency of the need for treatment. In a situation of clinical

urgency, asthma treatment may be commenced and diagnostic testing arranged

within the next few weeks.

Athletes

The diagnosis of asthma in athletes should be confirmed by positive

exercise challenge test. (Adults: fall in FEV1 of >10% and >200 mL from

baseline, Children: fall in FEV1 of >12% predicted, or PEF variability

>15%)

Cough Variant Asthma

Patients with cough-variant asthma have chronic cough as their principal, if

not the only symptom, and is associated with airway hyper-

responsiveness. It is more common in children and often more problematic

at night. Lung function may be normal. For these patients, documentation

of variability in lung function is important.

Differential Diagnosis

Differential diagnosis of Asthma include

v Chronic upper airway cough syndrome/ Post nasal drip

v GERD

v Vocal cord dysfunction

v Cardiac failure

v Bronchiectasis

v COPD

v Medication related cough

v Parenchymal lung disease

v Pulmonary embolism

v Hyperventilation dysfunctional breathing

v Obstructive sleep apnea

1.2. making the diagnosis of asthma in special populations

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Figure 1.1.

Diagnosis of Asthma

Adapted from: Global Initiatives for Asthma guidelines

1.3. general principles of asthma management

The long-term goals of asthma management are to

• Achieve good symptom control (day to day, occupational and

recreational) without any functional impairment

• Minimize future risk of exacerbations and mortality from

exacerbation, fixed airflow limitation and side-effects of treatment.

• Achieve and maintain control of daytime as well as nocturnal

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symptoms.

• Maintain normal activity levels, including exercise, with normal or

near normal pulmonary function.

The pharmacological options for long-term treatment of asthma fall into three

main categories.

• Controller medications are used for regular maintenance

treatment. They reduce airway inflammation, control symptoms,

and reduce future risks of exacerbations and decline in lung

function.

• Reliever (rescue) medications are provided to all patients for as-

needed relief of symptoms during worsening asthma or

exacerbation (also recommended for short-term prevention of

exercise-induced bronchoconstriction). Success of asthma

treatment aims at reducing and, ideally, eliminating the need for

reliever treatment.

• Add-on therapies may be considered when patients have

persistent symptoms and/or exacerbations despite optimized

treatment with high dose controller medications and treatment of

modifiable risk factors.

1.4. Categories of asthma medications

Table 1.1. Dosage of commonly used inhaled corticosteroids

Drug dosage (mcg) Drug Low Medium High

Beclomethasone dipropionate

100 -

200 >200-400

>400

Budesonide

200-400

>400-800 >800

Fluticasone furoate

100

200

Fluticasone propionate

100-250

>250-500

>500

Ciclosonide

80-160

>160-320

>320

Momentasone

110-220

>220-440

>440

Triamcinolone

400-1000

>1000-2000

>2000

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1.5. Control-based asthma management

In control-based asthma management, step wise assessment of

pharmacological and non-pharmacological treatment should be done, that includes

assessment, treatment and review of both symptom control and future risk (of

exacerbations and side-effects).

Assessment

Before initiating controller treatment,

• Record evidence for the diagnosis of asthma.

• Record the patient's level of symptom control and risk factors,

including lung function.

• Schedule an appointment for a follow-up visit. After initiating

controller treatment

• Review patient's response after 3 months, or earlier depending on

clinical urgency.

• Step up / down treatment based on symptom control.

Once symptom control is achieved for 3 months, treatment may be

stepped down in order to find the patient's minimum effective

treatment.

Symptom control assessment

There are several numerical scores to assess the severity of asthma, most

commonly used being asthma control questionnaire. As per the GINA

guidelines 2018, the symptom control is assessed by the table below.

Asthma symptom control:

In the past 4 weeks, did the patient have

l Daytime asthma symptoms more than twice a week?

l Any night waking due to asthma?

l Reliever needed for symptoms more than twice/week?

l Any activity limitation due to asthma?

Well controlled – none of these

Partly controlled – 1-2 of these

Uncontrolled – 3-4 of these

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1.6. Assessment of risk factors

1.7. Treatment

Potentially modifiable independent risk factors for flare-ups

(exacerbations)

l Uncontrolled asthma symptoms

l High SABA use (with increased mortality if >1 x 200-dose

canister/month)

l Inadequate ICS: not prescribed ICS; poor adherence; incorrect

inhaler technique

l Low FEV1, especially if <60% predicted

l Major psychological or socioeconomic problems

l Exposures: smoking; allergen exposure if sensitized

l Co morbidities: obesity; rhinosinusitis; confirmed food allergy

l Sputum or blood eosinophilia

l Pregnancy

Other major independent risk factors for exacerbations

l Ever intubated or in intensive care unit for asthma

l

Risk factors for developing fixed airflow limitation

l Lack of ICS treatment

l Exposures: tobacco smoke; noxious chemicals; occupational

exposures

l Chronic mucus hypersecretion; sputum or blood eosinophilia

Risk factors for medication side-effects

l Systemic: frequent OCS; long-term, high dose and/or potent ICS;

also taking P450 inhibitors

l Local: high-dose or potent ICS; poor inhaler technique

Recommended options for initial controller treatment in adults and adolescent

Patients need no controller medication or as required reliever medications

(SABA) when

l Asthma symptoms or need for SABA less than twice a month;

l There is no waking due to asthma in last month;

l There are no risk factors for exacerbations,including no

exacerbations in the last year

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≥1 Severe exacerbation in last 12 months


Patients need low dose Inhaled Corticosteroids and as required reliever

medications (SABA) when

1) Asthma symptoms are infrequent, but the patient has one or more risk

factors for exacerbations

2) Asthma symptoms occur or there is need for SABA between atleast

twice a month

Patients need Medium to high dose Inhaled Corticosteroids or Low dose ICS +

LABA when

1) Patient has troublesome asthma symptoms most days

2) There is waking up due to asthma once a week or more(especially if any

risk factors exist)

Patients need a Short course of Oral Corticosteroids and start of regular

controller medications; High dose Inhaled Corticosteroids or moderate dose

ICS + LABA when

1) Initial asthma presentation is with severely uncontrolled asthma, or with

an acute exacerbation

Add-on tiotropium improves lung function and increases the time to severe

exacerbation

l Sputum-guided treatment: for patients with persisting symptoms

and/or exacerbations despite high-dose ICS or ICS/LABA,

treatment may be adjusted based on eosinophilia (>3%) in induced

sputum where facility is available.

Chest X ray is not routinely recommended in the diagnosis of

asthma.

In severe asthma, this strategy leads to reduced exacerbations

and/or lower doses of ICS.

Assess risk factors at diagnosis and periodically, particularly for

patients experiencing exacerbations.

Measure FEV1 at start of treatment, after 3–6 months of controller

treatment to record the patient's personal best lung function, then

periodically for ongoing risk assessment

l Methylxanthines may be used as an add-on therapy in patients who

remain uncontrolled on the moderate to high ICS/LABA

combination. Whenever used as an add-on to ICS, low-dose

(200-400 mg/day) sustained release formulations of theophylline is

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preferred.

l SABA is the agent of choice for rescue medication in asthma.

SAMA is a less preferred alternative/add-on to SABA as reliever

medication

l Oral beta agonists should not be used as rescue medications. Use

of SiT (single inhaler therapy)/ SMART using an ICS/LABA

combination (formoterol-based) as both maintenance and reliever

medication is preferred whenever feasible.

l Inhaler technique and adherence must be ensured.

The frequency of visits depends upon the patient's initial level of control and their

response to treatment. For most controller medications, improvement begins within

days of initiating treatment, but the full benefit may only be evident after 3–4 months.

In severe and chronically under-treated disease, it may take longer.

Ideally, patients should be seen 1–3 months after starting treatment and every

3–12 months thereafter. After an exacerbation, a review visit within 1 week should be

scheduled.

Stepping up asthma treatment

Asthma is a variable condition, and periodic treatment adjustments by the

clinician and/or the patient may be needed. It can either be a sustained or

short term step up or can be day to day adjustment

l Sustained step up (for at least 2–3 months) can be tried when the

initial treatment has failed (provided, inhaler technique and

adherence are satisfactory; and modifiable risk factors such as

smoking have been addressed) any step-up should be regarded as

a therapeutic trial, and the response reviewed after 2–3 months.

If there is no response, treatment should be reduced to the previous level,

and alternative treatment options or referral considered.

l Short-term step up (for 1–2 weeks)by increasing maintenance

ICS dose for 1–2 weeks; for example, during viral infections or

seasonal allergen exposure.

l Day-to-day adjustment: for patients prescribed combination

budesonide/formoterol or beclometasone/formoterol as

maintenance and reliever treatment, the patient adjusts the

number of as-needed doses of ICS/formoterol from day to day

1.8. Reviewing response and adjusting treatment

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according to their symptoms, while continuing the maintenance

dosage.

Step1 – As needed SABA as reliever

Step2 - Low dose ICS (controller) with as needed SABA (reliever)

Leucotriene receptor antagonists and low dose theophylline (as other

controllers)

Step3 – Low dose ICS/LABA (controller) plus as needed SABA (reliever)

Or

Medium or high dose ICS or Low dose ICS + LTRA/ theophylline (as other

controllers)

Step 4 – Low dose ICS/LABA or as needed SABA (reliever)

And medium or high dose ICS/LABA (controller)

Add tiotropium or high dose ICS + LTRA/ theophylline (as other controllers)

Step 5 –Consider add-on treatment (tiotropium, anti IgE, anti IL-5) as

controller

Add low dose oral corticosteroids (as other controllers)

Low dose ICS / LABA or as needed SABA (reliever)

Figure 1.2. Treatment of patients diagnosed with Asthma

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Stepping down treatment when asthma is well controlled

Once good asthma control has been achieved and maintained for 3

months and lung function has reached a plateau, treatment can often be

successfully reduced, without loss of asthma control.

l Choose an appropriate time (no respiratory infection, patient not

travelling, not pregnant).

l Stepping down ICS doses by 25–50% at 3 month intervals is

feasible and safe for most patients, while continuing the second

controller.

l Actively engage the patient in the process; ask them to document

their asthma status (symptom control, lung function and risk

factors),and schedule a follow-up visit.

l Provide a written asthma action plan and instructions for how and

when to resume their previous treatment if their symptoms

worsen.If treatment is stepped down too far or too quickly,

exacerbation risk may increase even if symptoms remain Q

reasonably controlled

l Complete cessation of ICS is associated with a significant risk of

exacerbations; hence ICS need to be continued long term.

Controller medication may be stopped only if patient has been

totally asymptomatic for 6 – 12 months and there are no risk factors

for exacerbation. This requires close follow up.

Allergen Immunotherapy

Allergen-specific immunotherapy may be an option if allergy plays a

prominent role, e.g. asthma with allergic rhino-conjunctivitis. Sublingual

immunotherapy (SLIT) can be considered in house dust mite sensitive

patients with allergic rhinitis (FEV1>70%) who have exacerbations despite

ICS treatment.

Vaccinations

Influenza causes significant morbidity and mortality in the general

population, and the risk can be reduced by annual vaccination. Patients

with moderate-severe asthma are advised to receive an influenza

vaccination every year, or when vaccination of the general population is

advised.

1.9. Other therapies

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Treating other modifiable risk factors

Some patients continue to experience exacerbations even with maximal

doses of current treatment. If a patient gets one exacerbation, there is high

risk of getting another in next one year. Hence optimising asthma

management includes addressing modifiable risk factors.

Table 1.2. Managing risk factors for optimal control of Asthma

Risk factor Treatment strategy

Exposure to tobacco smoke

• Encourage smoking cessation by patient/family; provide advice and resources • Consider higher dose of ICS if asthma poorly.

Low FEV1, especially if <60% Predicted

Consider trial of 3 months’ treatment with high-dose ICS and/or 2 weeks’ OCS • Exclude other lung disease, e.g. COPD • Refer for expert advice if no improvement

Obesity

•Document BMI

Strategies for weight reduction • Distinguish asthma symptoms from symptoms due to deconditioning, mechanical restriction, and/or sleep apnea.

Major psychological problems

Arrange mental health assessment Help patient to distinguish between symptoms of anxiety and asthma; provide advice about management of panic attacks

Major socio economic problems

Identify

most cost-effective ICS-based regimen

Confirmed food allergy

Appropriate food avoidance; injectable epinephrine

Allergen exposure if sensitized

Consider trial of simple avoidance strategies; consider cost

Consider step up of controller treatment.The efficacy of allergen immunotherapy in asthma is limited.

Sputum eosinophilia

Increase ICS dose independent of level of symptom control

Medications

Avoid the medications triggering the asthma attack.

Gastro esophageal reflux disease Empirical trial of anti-reflux medication, such as a proton pump inhibitor or motility agent, may be considered.If the symptoms do not resolve, specific investigations such as 24-hour pH monitoring or endoscopy may be considered.

Allergic rhinitis Treatment with Intranasal corticosteroids

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1.10. Evaluation of difficult to treat ASTHMA

l Patients whose asthma symptoms are inadequately controlled,

despite optimal step 4 therapy for a period of 1-3 months, can be

considered to have difficult to treat asthma.

l Check inhaler technique and adherence, and environmental

exposures, smoking, address comorbidities.

l Avoidance of exposure to allergens.

Role of Anti- IGE and anti IL-5 in Asthma

These agents have a role to play in the management of difficult to control

Asthma, not responding to all other steps described above. However in

view of extremely high cost, their use may be initiated only after

consultation and concurrence with an expert committee at a Government

Medical College.

Role of Bronchial Thermoplasty in Asthma

As of now, good quality evidence is lacking for recommending bronchial

thermoplasty in the routine management of bronchial asthma.

Role of Immunotherapy in Asthma

Single allergen immunotherapy may provide a modest benefit to patients

with mild-to-moderate asthma with demonstrable skin allergy to that

antigen. To be decided upon only after approval of institute's expert

committee. It is contraindicated in patients with poorly controlled asthma

and in those with FEV1< 70%.

Role of Patient Education and Pulmonary Rehabilitation

l Optimal self management which involves a combination of

patient education, self-monitoring, regular physician review, and

self management using a written asthma action plan is strongly

recommended in the management of asthma.

l Pulmonary rehabilitation therapy in asthmatics reduces

symptoms, improves exercise capacity and quality of life.

Role of Vaccination and Antibiotics in the prevention of Asthma

Exacerbation

l Current evidence is insufficient to routinely recommend influenza

or pneumococcal vaccination for patients with asthma.

l Antibiotics are not recommended in the prevention of asthma

exacerbations

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1.11. Management of Asthma in special situations

Asthma & Pregnancy

l Most medications used for asthma have negligible effects on the

foetus.

l Adequate asthma control in pregnancy should be attempted with

routinely available asthma medications as in the non-pregnant

state (including systemic steroids whenever indicated).

l It is advisable to delay the objective confirmation of the diagnosis

until after delivery.

l Asthma during lactation should be managed similar to asthma

during pregnancy.

l Caution should be exercised while using theophylline during

pregnancy and lactation.

Exercise induced asthma

l Pre-treatment with bronchodilator agents (SABA,SAMA, and

LABA) as well as anti-inflammatory agents (LTRA but not ICS) is

effective in attenuating the fall in FEV1 associated with EIA.

l Regular use of ICS or LTRAs is effective in prevention of

exercise-induced bronchospasm.

l Regular use of LABA as prophylaxis for EIA should be avoided as

long-term regular administration of LABA induces tolerance and

may cause increase in adverse effects.

Aspirin-exacerbated respiratory disease

l It starts with nasal congestion and anosmia, and progresses to

chronic rhinosinusitis with nasal polyps that re-grow rapidly after

surgery. An acute asthma attack develops within minutes to 1–2

hours of ingestion of Aspirin or other NSAID.

l Aspirin challenge (oral, bronchial or nasal) is the gold standard for

diagnosis. Bronchial (inhalational) and nasal challenges with

lysine aspirin are safer than oral challenges and may be safely

performed in allergy centers.

l Avoid aspirin or NSAID-containing products and other medications

that inhibit cyclooxygenase-1 . Where an NSAID is indicated, a

COX-2 inhibitor (e.g. celocoxib,oretoricoxib), or paracetamol

(acetaminophen), may be considered with appropriate health care

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provider supervision and observation for at least 2 hours after

administration.

l ICS are the mainstay of asthma therapy in AERD, but OCS are

sometimes required; LTRA may also be useful

Occupational Asthma

l Asthma may be induced or aggravated by exposure to allergens or

other sensitizing agents. Hence a detailed history about work

history, exposures and hobbies should be taken. PEF monitoring at

and away from work is often used to help confirm the diagnosis.

l Both removal of exposure and reduction of exposure improve

symptoms of occupational asthma.

l Removal of exposure appears to be better than reduction of

exposure.

Elderly

l It is difficult to diagnose asthma in elderly due to poor perception of

airflow limitation; acceptance of dyspnea as being 'normal' in old

age; and reduced activity.

l The presence of co-morbid diseases also complicates the

diagnosis.

l In older people with a history of smoking or biomass fuel exposure,

a diagnosis of COPD and asthma–COPD overlap syndrome

(ACOS) should be ruled out.

Asthma action plan

l Identify and avoid asthma triggers

l Monitor your breathing

l Identify and treat attacks early

l Take your medication as prescribed.

l Pay attention to increasing quick-relief inhaler use

l Get vaccinated for influenza and pneumonia.

Evaluation and management

Exacerbations of asthma are episodes characterised by acute aggravation

in symptoms of shortness of breath, cough, wheezing or chest tightness

and progressive decline in lung function. It represents a change from the

patient's usual status that is sufficient to require a change in treatment.

1.12. Acute exacerbation of Asthma

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Exacerbation may occur in a patient with previous diagnosis of asthma or

occasionally the first presentation.

Mimickers of an acute asthmatic attack

1) Acute exacerbation of COPD

2) Acute left heart failure

3) Pulmonary thromboembolism

4) Pneumothorax

5) Hyperventilation

6) Vocal cord dysfunction

7) Foreign body inhalation

Assessment of severity of asthmatic attack

Objective assessments

1) Measurement of lung volumes

2) Oxygen saturation

3) Arterial oxygen saturation not routinely recommended

4) Chest x-ray not routinely recommended unless there is suspicion of

cardiac involvement or pneumothorax.

The severity of an asthma exacerbation is defined on a combination of

signs and symptoms and the extent of accompanying cardio-respiratory

dysfunction into non-severe, severe and life-threatening.

Factors that increase the risk of asthma-related death

Patients with one or more of these risk factors should be encouraged to

seek urgent medical care early in the course of an exacerbation.

v A history of near-fatal asthma requiring intubation and mechanical

ventilation

v Hospitalization or emergency care visit for asthma in the past year

v Currently using or having recently stopped using oral

corticosteroids (a marker of event severity)

v Not currently using inhaled corticosteroids

v Over-use of SABAs, especially use of more than one canister of

salbutamol (or equivalent) monthly

v A history of psychiatric disease or psychosocial problems

v Poor adherence with asthma medications and/or poor adherence

with (or lack of) a written asthma action plan

v Food allergy in a patient with asthma

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Table 1.3. Site of management of patients with exacerbation of Asthma

Severity Symptoms Sign/investigations Place of management

Non- severe Not fulfilling criteria for severe or life-threatening asthma

Out-patient

Severe (presence of two or more of the following)

Inability to complete a sentence, agitation.

Use of accessory muscles of respiration,

Respiratory rate more than 30/min

Heart rate >110/min

Pulses paradoxus>25mmHg

Silent chest

PEF <60% of predicted

PaO2<60% of predicted

Or SPo2 < 92%

ED/ ward

Life threatening

Alteration in mental status , orthopnea

Cyanosis,

Paradoxical breathing,

PaCO2>40mmhg with worsening of PH, heart rate <60/min

ICU

Figure 1.3 Treatment

Assess the patient

Rule out alternate diagnosis.Assess the severity

Mild or moderate

Severe or life threatening

If worsening

ED / ward/ ICU

Inhaled SABA, SAMA and steroids

Controlled oxygen therapy

SABA 4-10 puffs by MDI with

spacer to be repeated every

20 min for one hour. Steroids-

prednisolone 1mg/kg max 50mg

in adultsControlled oxygen therapy

To continue SABA as required

To reassess after one hour

If worsening

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Controlled oxygen therapy (if available)

Oxygen therapy should be titrated against pulse oximetry (if available) to

maintain oxygen saturation at 93–95% (94–98% for children 6–11 years,

>95% in pregnancy). Controlled or titrated oxygen therapy gives better

clinical outcomes than high-flow 100% oxygen therapy .Patient should be

monitored for deterioration, somnolence or fatigue.

Inhaled short-acting beta2-agonists

Inhaled SABA ( Salbutamol) therapy should be administered frequently for

patients presenting with acute asthma. The most cost-effective and

efficient delivery is by pMDI with a spacer. Evidence is less robust in severe

and near-fatal asthma. (Salbutamol 4-6 puffs of 100 μg every 15 min or

nebulisation 2.5mg salbutamol every 15 min or >4 nebulisation per hour or;

levosalbutamol 1.25mg)

Levosalbuamol has similar efficacy and safety as compared to salbutamol

in acute asthma.

In patients unable to use MDI with spacer, drugs can be delivered via a

nebulizer.

Once stabilized patient should be switched over to spacer from nebulizer.

Systemic corticosteroids

Oral cortico steroids should be given promptly, especially if the patient is

deteriorating, or had already increased their reliever and controller

medications before presenting. The recommended dose for adults is 1 mg

prednisolone/kg/day or equivalent up to a maximum of 50 mg/day, and 1–2

mg/kg/day for children 6–11 years up to a maximum of 40 mg/day. OCS

should usually be continued for 5–7 days.

Inhaled corticosteroids

Inhaled steroids do not provide any additional benefit when used along

with systemic corticosteroids and hence not recommended in

management of acute asthma.

Other treatments

Antibiotics

Evidence does not support a role of antibiotics in asthma exacerbations unless

there is strong evidence of lung infection (e.g. fever and purulent sputum or

radiographic evidence of pneumonia). Aggressive treatment with corticosteroids

should be implemented before antibiotics are considered.

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Epinephrine

Intramuscular epinephrine (adrenaline) is indicated in addition to standard

therapy for acute asthma associated with anaphylaxis and angioedema. It

is not routinely indicated for other asthma exacerbations.

Ipratropium bromide( SAMA)

l For adults and children with moderate-severe exacerbations,

treatment in the emergency department with both SABA (

Salbutamol or levosalbutamol) plus ipratropium (2 puffs of 20 μg

every 4hourly ; nebulization with 500 μg once then 250 μg four to

six hourly)

l Use of SAMA was associated with fewer hospitalizations and

greater improvement in PEF and FEV1 compared with SABA

alone.

l No benefit noted with SAMA in children.

Aminophylline and theophylline

Intravenous aminophylline and theophylline should not be used in the

management of asthma exacerbations, in view of their poor efficacy and

safety profile, and the greater effectiveness and relative safety of SABA.

But they may be used in exceptional circumstances such as type 2 brittle

asthma or patients on mechanical ventilation with intense bronchospasm

causing ineffective delivery of nebulized drugs.

Magnesium

Intravenous magnesium sulphate is not recommended for routine use in

asthma exacerbations.

When administered as a single 2 g infusion over 20 minutes, it reduces

hospital admissions in some patients, including adults with FEV1

<25–30% predicted at presentation; adults and children who fail to

respond to initial treatment and have persistent hypoxemia; and children

whose FEV1 fails to reach 60% predicted after 1 hour of care.

Leukotriene receptor antagonists

There is limited evidence to support a role for oral or intravenous LTRAs in

acute asthma, hence not recommended.

ICS/LABA combinations

The role of these medications in the emergency department or hospital is

unclear hence not recommended.

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Sedatives

Sedation should be strictly avoided during exacerbations of asthma

because of the respiratory depressant effect of anxiolytic and hypnotic

drugs. An association between the use of these drugs and avoidable

asthma deaths has been reported.

Heliox

Not routinely used in acute asthma exacerbation.

Non-invasive ventilation (NIV)

There is no recommendation for NIV in asthma exacerbation. If NIV is

tried, the patient should be monitored closely (Evidence D). It should not be

attempted in agitated patients, and patients should not be sedated in order

to receive NIV.

Mechanical ventilation in management of acute severe asthma

The absolute indications of MV in severe acute asthma include coma,

respiratory or cardiac arrest and refractory hypoxemia while the relative indications

include inadequate response to initial management, hypercapnia, fatigue,

somnolence and cardiovascular compromise.

Setting Recommendation Mode 8 -12/min Tidal volume 4 -6ml/Kg I:E ratio

1:4 or lower

Waveform

Square waveform

Inspiratory flow

100 -120 l/min

FiO2

Titrate to maintain PaO2>

60m m Hg or SpO2 >/= 89%

Avoid hyperoxia

PEEP

Upto 5cm H2O

Plateau pressure

<30 cm H20

Table 1.4.

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1.14. Discharge following IP treatment of patient with acute Asthma

l A patient with severe acute asthma is considered fit for discharge

from the medical facility when he/she is clinically stable for at least

24 hours.

l PEF has improved to more than 60-80% of baseline.

l The patient should be able to eat and get adequate sleep, should be

able to comfortably use the inhaled medication with requirement of

inhaled short-acting drugs no more than every 4 hours

l Oxygen saturation has improved to >94%.

l Adequate home support.

At the time of discharge, step up or initiate the controller medication after

checking the inhaler technique. Continue the reliever as and when required. Steroids

may be continued orally for 5-7 days. Advise follow-up after a week.

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Section II

Allergic rhinitis

Section II

2. Allergic rhinitis

2.1. Classification of allergic rhinitis

Rhinitis is defined as inflammation of the nasal mucosa and is characterized by

sneezing, nasal congestion, nasal itching, and rhinorrhea. The eyes, ears, sinuses,

and throat can also be involved. It is an extremely common condition, affecting

approximately 20% of the population. Allergic rhinitis, even though not a life

threatening condition can significantly impair quality of life. Systemic effects,

including fatigue, sleepiness, and malaise, can occur from the inflammatory

response. Allergic rhinitis can frequently lead to significant impairment of quality of

life. Symptoms such as fatigue, drowsiness, and malaise can lead to impaired work

and school performance, missed school or work days, and traffic accidents.

Allergic rhinitis involves inflammation of the mucous membranes of the nose,

eyes, eustachian tubes, middle ear, sinuses, and pharynx. The nose invariably is

involved, and involvement of other organs may vary according to severity.

Inflammation of the mucous membranes is triggered by immunoglobulin E (IgE) in

response to an extrinsic allergen.

Duration

1 Intermittent – symptoms are present less than 4 days a week or for less

than 4 weeks.

2 Persistent – symptoms are present at least 4 days a week and for at

least 4 weeks.

Severity

1 Mild – none of the following is present.

2 Moderate-severe – at least one of the following is present.

a) Sleep disturbance

b) Impairment of daily activities, leisure and/or sport

c) Impairment of school or work

d) Troublesome symptoms

Obtaining a detailed history is important in the evaluation of allergic rhinitis.

Important elements include an evaluation of duration, and time course of symptoms;

possible triggers, response to medications, comorbid conditions, family history of

2.1.1Evaluation

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allergic diseases, environmental and occupational exposures. A thorough history

may help identify specific triggers, suggesting an allergic etiology for the rhinitis.

Symptoms that can be associated with allergic rhinitis include sneezing, itching

of nose, eyes, ears and palate, rhinorrhea, postnasal drip, congestion and

headache. Significant complaints of congestion, particularly if unilateral, might

suggest the possibility of structural obstruction, such as a polyp, foreign body, or

deviated septum.

This might include exposure to pollen outdoors, mold spores while doing yard

work, specific animals, or dust while cleaning the house. Irritant triggers such as

smoke, pollution, and strong smells can aggravate symptoms in a patient with

allergic rhinitis.

Response to treatment with antihistamines supports the diagnosis of allergic

rhinitis, although sneezing, itching, and rhinorrhea associated with nonallergic

rhinitis can also improve with antihistamines. Response to intranasal corticosteroids

supports the diagnosis of allergic rhinitis, although some cases of nonallergic rhinitis

(particularly the nonallergic rhinitis with eosinophils syndrome [NARES]) also

improve with nasal steroids.

The mucosa of the nasal turbinates may be swollen and have a pale, bluish-

graycolor. Some patients may have predominant erythema of the mucosa, which

can also be observed with rhinitis medicamentosa, infection, or vasomotor rhinitis.

While pale, boggy, blue-gray mucosa is typical for allergic rhinitis, mucosal

examination findings cannot definitively distinguish between allergic and nonallergic

causes of rhinitis.Thin and watery secretions are frequently associated with allergic

rhinitis, while thick and purulent secretions are usually associated with

sinusitis.Nasal examination may reveal deviation of septum or polyps.

Allergy testing provides knowledge of the degree of sensitivity to a particular

allergen. The most commonly used methods of determining allergy to a particular

substance are allergy skin testing and in vitro diagnostic tests. Testing for reaction to

specific allergens can be helpful to confirm specific allergic triggers. If specific

Trigger factors

Response to treatment

Physical Signs

Laboratory Studies

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allergic triggers are known, then appropriate avoidance measures can be

recommended. It is essential to know which allergens a patient is sensitive to in

order to perform allergen immunotherapy (desensitization treatment).

In vitro allergy tests, ie, RAST, allow measurement of the amount of specific IgE

to individual allergens in a sample of blood. The amount of specific IgE produced to a

particular allergen approximately correlates with the allergic sensitivity to that

substance. When selecting allergens, identify allergens that are present locally and

are known to cause clinically significant allergic disease.

This is a measurement of the total level of IgE in the blood. While patients with

allergic rhinitis are more likely to have an elevated total IgE level than the normal

population, this test is neither sensitive nor specific for allergic rhinitis. As many as

50% of patients with allergic rhinitis have normal levels of total IgE, while 20% of

nonaffected individuals can have elevated total IgE levels. Total blood eosinophil

count. As with the total serum IgE, an elevated eosinophil count supports the

diagnosis of allergic rhinitis, but it is neither sensitive nor specific for the diagnosis.

Radiography

While radiographic studies are not needed to establish the diagnosis of

allergic rhinitis, they can be helpful for evaluating possible structural

abnormalities or to help detect complications or comorbid conditions, such

as sinusitis or adenoid hypertrophy.

CT scanning

Coronal CT scan images of the sinuses can be very helpful for evaluating

acute or chronic sinusitis. CT scanning may also help delineate polyps,

turbinate swelling, septal abnormalities (eg, deviation), and bony

abnormalities (eg, concha bullosa).

MRI

For evaluating sinusitis, MRI images are generally less helpful than CT

scan images, largely because the bony structures are not seen as clearly

on MRI images. However, soft tissues are visualized quite well, making

MRI images helpful for diagnosing malignancies of the upper airway.

Total serum IgE

Imaging Studies

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Other Tests

Treatment

Nasal cytology

Rhinoscopy:

Nasal provocation testing

The management of allergic rhinitis consists of 3 steps

(1) Environmental control measures and allergen avoidance,

(2) Pharmacological management, and

(3) Immunotherapy.

Environmental Control

Environmental control measures and allergen avoidance involve both

the avoidance of known allergens and avoidance of nonspecific, or irritant,

triggers.

Pharmacotherapy

Pharmacologic options for the treatment of allergic rhinitis include

intranasal corticosteroids, oral and topical antihistamines, decongestants,

intranasal cromolyn (Nasalcrom), intranasal anticholinergics, and

leukotriene receptor antagonists. Intranasal corticosteroids are the

mainstay of treatment of allergic rhinitis. The adverse effects most

commonly experienced with the use of intranasal corticosteroids are

headache, throat irritation, epistaxis, stinging, burning, and nasal dryness.

The second-generation oral antihistamines such as desloratadine,

levocetirizine, fexofenadine, and loratadine are effective in controlling

symptoms and have better side effect profile. Compared with oral

antihistamines, intranasal antihistamines offer the advantage of delivering

a higher concentration of medication to a specific targeted area, resulting in

fewer adverse effects. Oral and topical decongestants improve the nasal

congestion associated with allergic rhinitis. There is a chance thatpatients

may develop rhinitis medicamentosa or have rebound or recurring

congestion.

Immunotherapy (desensitization)

Immunotherapy is a long-term process. Therapy should be continued

for 3-5 years. Success rates have been demonstrated to be as high as 80-

90% for certain allergens. Sublingual immunotherapy (SLIT) is currently

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increasing in use, particularly in Europe. SLIT can produce significant

clinical improvement in elderly patients with allergic rhinitis caused by

house dust mites (HDMs). [13]

Surgical care is not indicated for allergic rhinitis but may be indicated for co

morbid or complicating conditions, such as chronic sinusitis, severe septal deviation

(causing severe obstruction), nasal polyps, or other anatomical abnormalities. The

value of turbinectomy is not established.

1. Skoner DP. Allergic rhinitis: definition, epidemiology, pathophysiology,

detection, and diagnosis. J Allergy ClinImmunol. Jul 2001;108(1

Suppl):S2-8.

2. Meltzer EO. The prevalence and medical and economic impact of

allergic rhinitis in the United States. J Allergy ClinImmunol. Jun

1997;99(6 Pt 2):S805-28.

3. Bozek A, Ignasiak B, Filipowska B, Jarzab J. House dust mite

sublingual immunotherapy: a double-blind, placebo-controlled study in

elderly patients with allergic rhinitis. ClinExp Allergy. Feb

2013;43(2):242-8.

Surgical Care

2.2. References

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Section III

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Section III

3. Diagnosis & managementof chronic obstructive pulmonary disease

3.1. When to suspect COPD?

3.2. Risk factors for COPD

Chronic Obstructive Pulmonary Disease (COPD) - is a common, preventable

and treatable disease that is characterized by persistent respiratory symptoms and

airflow limitation that is due to airway and/or alveolar abnormalities usually caused by

significant exposure to noxious particles or gases.

A diagnosis of COPD should be considered in persons having chronic symptoms of

cough, sputum production, shortness of breath, and/or wheezing, especially among

those with prolonged exposure to risk factors for the disease. COPD in Indian

females are increasing due to exposure to biomass fuels. Females are more

susceptible to effects of tobacco smoke than males.

Table 3.1. Risk factors for COPD

Established Probable

Tobacco smoking

Environmental tobacco smoke

Exposure to biomass fuel

Occupational exposure to dust/ smoke

Alpha-1 antitrypsin deficiency

Indoor air pollution

Outdoor air pollution

Genetic factors

Advancing age

Intrauterine growth retardation

Low Socioeconomic

Poorly controlled long standing Asthma

Severe childhood respiratory infection

Tuberculosis

Poor nourishment

HIV

A diagnosis of COPD should not be excluded in the absence of physical signs

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3.3. Diagnosis of COPD

Spirometry should be performed in all patients of age > 35 yrs with

symptoms suggestive of COPD

A Post-bronchodilator FEV1/FVC < 0.7 should be used as the criteria for

diagnosis of COPD.

Spirometry should not be used as a screening tool in asymptomatic

individuals to detect airflow obstruction

PEF should not be routinely used for screening, diagnosis, or monitoring of

COPD

Classification of severity of COPD

Classification of severity of the disease should be done for all COPD

patients based on the FEV1 and exacerbation frequency

Level of patient's disability due to symptoms should be assessed using

modified Medical Research Council (mMRC) dyspnoea questionnaire or

the COPD assessment test (CAT)

Classification of Severity of Airflow Limitation in COPD

In patients with post bronchodilator FEV 1/FVC < 0.70

GOLD 1: Mild - FEV1 >/= 80% predicted

GOLD 2: Moderate - 50%=/< FEV 1 < 80% predicted

GOLD 3: Severe - 30%=/< FEV 1< 50% predicted

GOLD 4: Very Severe - FEV1< 30% predicted

*Based on Post-Bronchodilator FEV 1

Combined COPD assessment

In the GOLD -2019 revised assessment scheme (see Figure), the impact of

COPD on an individual patient is assessed by combining the symptomatic

assessment using mMRC or COPD Assessment Tool (CAT), with the

patient's spirometric classification and/or risk of exacerbations.

The number provides information regarding severity of airflow limitation

(spirometric grade 1 to 4) while the letter (groups A to D) provides

information regarding symptom burden and risk of exacerbation which can

be used to guide therapy

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Figure 3.1. Diagnosis of COPD

Gold 1

Gold 2

Gold 3

Gold 4

>/=80

50-79

30-49

<30

FEV1 (% predicted)GRADE

exacerbration history groups

Atleast one exacerbration requiring

hospitalisation or

2 or more exacerbration a year

Maximun of one exacerbraion a year

which does not require hospitalisation

C

A

D

B

SYMPTOMSmMRC 0-1 mMRC OF 2 OR MORE

Cat score less than 10 Cat score of 10 or more

3.4. Additional investigations in COPD

1. All new COPD suspects with cough of more than 2 weeks' duration

should undergo sputum AFB examination as per RNTCP.

2. Pulse Oximetry & ABG – To screen for hypoxemia especially when there

is clinical suspicion and FEV1 < 50%. ABG recommended if SPO2 <

92%.

3. Chest X-ray

Diagnosis of COPD should not be made on the basis of a chest

radiograph.

Chest radiograph may be done during the initial evaluation of COPD to

look for comorbidities, complications, and alternative diagnosis.

4. Special investigations like HRCT scan, lung volumes, DLCO, and

exercise testing should be done in situations of diagnostic difficulty or

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whenever clinically indicated.

5. 6MWT may be used for monitoring of exercise capacity in COPD.

6. Testing for alpha-1 antitrypsin deficiency is not routinely recommended.

It may be done in young patients with lower lobe emphysema. COPD

patients should be routinely evaluated and appropriately treated for

comorbid conditions such as Cardiovascular diseases, Osteoporosis,

Skeletal muscle dysfunction, Cachexia, Respiratory infections, Anxiety

and Depression, Diabetes, Lung cancer and Bronchiectasis

These comorbid conditions may influence the mortality and hospitalizationsand

should be looked for routinely, and treated appropriately

Includes Pharmacological and Non-Pharmacological therapies

Pharmacotherapy –

l Inhaled therapy is now established as the mainstay of treatment for

patients with stable COPD.

l The choice of inhaler device will depend on availability, cost, the

prescribing physician, and the skills and ability of the patient.

l It is essential to ensure that inhaler technique is correct and to

recheck this at each visit.

A .bronchodilators –

a) Antimuscarinic agents

Generally, Antimuscarinic agents are preferred over beta-2 agonists, in

COPD, because they have found to be superior in symptom relief as

well as reducing number of exacerbations.

l Short-acting antimuscarinic agent (SAMA) like iptratropium can be

used as rescue medication to relieve patient symptoms.

l Long term SAMA monotherapy on regular basis is not

recommended.

l Long-acting antimuscarinic agents (LAMA) are useful in stable

COPD (FEV1 < 80%) to control symptoms and decrease the risk of

exacerbations. Eg tiotropium, aclidinium, glycopyrronium bromide

and umeclidinium

l ·LAMA should be preferred over SAMA

3.5. Treatment options

3.5.1. Management of stable COPD

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Inhaled anticholinergic drugs are well tolerated.

l The main side effect is dryness of mouth.

l Occasional urinary symptoms have been reported

b) Beta2 -Agonists

l Short-acting beta-agonist (SABA) can be used to relieve

symptoms of dyspnea as and when needed. The effect of SABAs

usually wears off within 4-6hrs

l Long term SABA monotherapy on regular basis is not

recommended

l Long-acting beta-agonist (LABA) monotherapy is not

recommended.

Long acting Beta 2 agonists, salmeterol and formetrol need to be given twice

daily

Ultra long acting Indacaterol is given once daily

B. Inhaled Corticosteroids

COPD-associated inflammation has limited responsiveness to

corticosteroids. Regular treatment with ICS does not modify the long-term

decline of FEV1 nor mortality in patients with COPD.So use of ICS in

COPD have a beneficial effect in subgroup of COPD patients with

l one exacerbation per year & AEC ≥300 eos inophils / μL

l ≥2 moderate exacerbation spery ear or atleast one severe

exacerbation requiring hospitalization in the prior year & eos inophil

counts ≥ 100cel ls/μL

Prolonged use of ICS has shown to increases risk of pneumonia in COPD

l Long-term monotherapy with oral or inhaled corticosteroids is not

recommended in COPD.

Dosage of inhaled corticosteroids has already been described in chapter 1.

Please see table 1.1.

In patients of severe COPD (FEV1 < 60%), triple therapy (ICS + LABA + LAMA )

may be used in those who are symptomatic despite single or dual bronchodilator

therapy and has shown to have better symptom control and reduction of

exacerbations.

Blood eosinophil count & Inhaled Corticosteroid use

l Recent studies have shown that blood eosinophil counts predict

the magnitude of the effect of ICS in preventing future

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exacerbations

l GOLD 2019 guidelines suggest that that an absolute eosinophil

count (AEC) > 300 cells/μL identifies the patients with the greatest

likelihood of treatment benefit with ICS

l ICS containing regimens have little or no effect at a blood

eosinophil count < 100 cells/μL

Methylxanthines

l There is only evidence for a modest bronchodilator effect

compared with placebo in stable COPD.

l Clearance of the drug declines with age.

l Addition of theophylline to salmeterol produces a greater

improvement in FEV1 and breathlessness than salmeterol alone.

l Adverse effects. Toxicity is dose-related, which is a particular

problem with xanthine derivatives because their therapeutic ratio is

small and most of the benefit occurs only when near-toxic doses

are given

l Methylxanthines are not recommended as first line

They can be used

l As alternative in patients noncompliant with inhalers for any

reason.

l As add-on therapy in patients continuing to have symptoms despite

optimum inhaled therapy. Sustained release preparations are

preferred.

Roflumilast (PDE 4 Inhibitor)may be used in frequent to ICS, when FEV1 <50%

and chronic bronchitis.

PDE 4 Inhibitors should always be used in combination with a bronchodilator

Combination of ICS/Bronchodilator Therapy

l ICS + LABA -more effective than individual components in

improving lung function,health status, decreasing exacerbations in

moderate exacerbations.

An ICS/LABA combination prescribed once daily does not show relevant

differences in efficacy compared to BD dosing. Sustained release preparations

are preferred.

May be used in frequent exacerbators as an add-on or substitute to ICS, and in

patients with chronic bronchitis.

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Combination of bronchodilators

3.5.1. Other pharmacological treatments

Available combinations:

SABA + SAMA – Salbutamol + ipratropium

LABA + LAMA - Formeterol + Tiotropium

Ultra LABA + Ultra LAMA - Inadacaterol + Glycopyronium

Combining bronchodilators with different mechanisms and durations of

action may increase the degree of bronchodilation with a lower risk of side-

effects compared to increasing the dose of a single bronchodilator.

Combinations of a LABA and LAMA in a single inhaler improve lung

function greater than long acting bronchodilator monotherapy effects.

Such a combination is found to decrease exacerbations to a greater

extent than an ICS/LABA combination.

Combination of ICS/Bronchodilator Therapy

More effective than individual components in improving lung functions,

health status, decreasing exacerbations in moderate to severe COPD with

frequent exacerbations.

An ICS/LABA combination OD does not show relevant differences in

efficacycompared to BD dosing

a. Vaccines

Influenza and Pneumococcal vaccination. Influenza vaccination can

reduce serious illness and death in COPD patients. The strains are

adjusted each year for appropriate effectiveness and should be given once

each year.

l Pneumococcal polysaccharide vaccine is recommended for

COPD patients 65yrs and older and also in younger patients with

significant comorbid conditions such as cardiac disease.

l Vaccines reduce the incidence of community acquired pneumonia

in COPD patients younger than 65yrs with an FEV1<40%

predicted

b. Alpha 1 Antitrypsin Augmentation Therapy

l Young patients with severe hereditary alpha 1 antitrypsin

deficiency and established emphysema may be candidate for

alpha 1 augmentation therapy. Very expensive and is not

recommended for patients with COPD that is unrelated to alpha 1

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antitrypsin deficiency

l It should be prescribed only after discussion with an expert

committee.

c.Antibiotics

May be prescribed for treating all exacerbations of COPD especially when

patients present with purulent expectoration.

Recent studies have shown that regular use of some antibiotics may

reduce exacerbation rate.

Azithromycin (250 mg/day or 500 mg three times per week) or

Erythromycin (500 mg two times per day) for one year in patients prone to

exacerbations reduced the risk of exacerbations. But patients on long term

azithromycin should be cautioned about increased incidence of bacterial

resistance, prolongation of QTc interval, and impaired hearing tests

d. Mucolytics:

In COPD patients not receiving inhaled corticosteroids, regular treatment

with mucolytics such as erdosteine, carbocysteine and N-acetylcysteine

may reduce exacerbations and modestly improve health status

e. Antitussives

Regular use not recommended

f. Vasodilators

Nitric oxide contraindicated in stable COPD

Others drugs - Nedocromil, leukotriene modifiers like montelukast not

adequately tested in COPD

Symptom control and palliative care

Even when receiving optimal medical therapy many patients with COPD

continue to experience distressing breathlessness, impaired exercise

capacity, fatigue, and suffer panic, anxiety and depression. Such patients

should be referred to palliative care. Treatment with opioids (low dose

morphine) has been found to be beneficial.

1. Smoking Cessation

Most important intervention for COPD patients who smoke regardless of

disease severity . Greatest capacity to influence natural history

2. Physical activity

Daily physical activity recommended for all COPD patients.

3.5.2. Non pharmacological therapies

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3. Pulmonary Rehabilitation

Improves exercise tolerance and decreases dyspnoea and fatigue

Components of Pulmonary Rehabilitation Programme

l Exercise training.

l Smoking Cessation

l Patient Education

l Assessment and Follow-up

l Nutritional support

4. Identify and reduce the exposure to risk factors like environmental,

occupational and indoor and outdoor air pollution.

l Oxygen therapy

l Ventilatory Support

l Surgical treatments

3.5.3. . Other treatments

Table 3.2. INITIAL Pharmacological treatment of stable COPD

>2 moderate

exacerbations or >1

leading to

hospitalisation

Gp C

LAMA

Gp D LAMA or

LAMA+LABA* or

ICS+LABA**

0 or 1 moderate

exacerbations

(not leading to

hospitalisation)

Gp A

A bronchodilator

Gp B

A long acting

Bronchodilator

(LAMA or LABA

mMRC 0 – 1; CAT<10 mMRC > 2; CAT > 10

* For highly symptomatic patients** If Eosinophils > 300

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3.6. Follow-up pharmacological management

Patient on maintenance treatment should be periodically followed up and treatment

options altered, on the basis of improvement or worsening of dyspnea/exercise

limitation and frequency of exacerbations.

If a change in treatment is considered necessary then select the corresponding

algorithm for dyspnea or exacerbations

Follow up pharmacological management should be guided by the principles of first

review and assess, then adjust if needed:

Review- Review symptoms (dyspnea) and exacerbation risk.

Assess - Assess inhaler technique and adherence, and the role of

non-pharmacological approaches

Adjust Adjust pharmacological treatment, including escalation or

de-escalation.

Any change in treatment requires a subsequent review of the clinical

response, including side effects.

Ø

Ø

Ø

Ø

Dyspnea

Table 3.3. Adjusting the medications for COPD based on symptoms

Current treatment Action advised

Symptomatic on LABA or LAMA LABA + LAMA

Not better with LABA + LAMA

Switching inhalerdevice ormolecules can also be consideredDyspnea due to other causes should be investigated

On LABA + ICS Consider triple combination LABA + LAMA + ICS

Stopping ICS:This can be considered if there are adverse effects (such as pneumonia) or areported lack of efficacy

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Exacerbations

Table 3.4 Management of COPD exacerbations

Current treatment Action advised

Persistent exacerbationson LABA / LAMA alone

Patients with one exacerbationper year &

≥ 300 eosinophils/μL

Escalation to either LABA/LAMA or LABA/ICS

History or findingssuggestive of asthma /ACO

≥ 2 moderate exacerbations per year or at least one severe exacerbation requiring hospitalization in the prior year& eosinophil counts ≥ 100 cells/μL

Persistent exacerbations on LABA + LAMA

AEC > 100 cells/μL

AEC < 100 cells/μL with an FEV1 < 50% predicted and chronic bronchitis

AEC < 100 cells/μL And former smokers

Add roflumilast

Long term macrolides

LABA+ ICS + LAMA

LABA/ICS

LABA/ICS

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Section IV

Community acquired Pneumonia

Section IV

4. Community acquired Pneumonia

4.1. Introduction

4.2. Definition

4.3. Diagnosis of pneumonia

These guidelines refer to the management of adults with pneumonia in Indian

settings.

There is a need for a guideline in Indian setting because our social and

economic factors are different from western setting, population affected by

pneumonia is different, microbial pathogens differ and resistance pattern of

organisms to drugs vary considerably.

Pneumonia is defined as inflammation of lung parenchyma due to an infectious

agent. It is broadly classified as.

1) Community acquired (CAP).

2) Hospital acquired pneumonia (HAP).

3) Pneumonia in immune-compromised Host

4) Aspiration pneumonia

Community acquired pneumonia is the pneumonia that develops in a

community setting or is diagnosed within 48 h of admission to a hospital.Hospital

acquired pneumonia is defined as pneumonia that occurs 48 hours or more after

hospital admission, which was not incubating the infection at the time of admission.

Pneumonia in immune-compromised hosts is considered separately as these hosts

are infected with rarer and unusual organisms apart from infection with common

organisms. Aspiration pneumonia is the pneumonia that develop after a witnessed

aspiration.

Patients with pneumonia usually presents with fever, rigor and chills, cough,

sputum production, pleuritic chest pain and dyspnea. Extra pulmonary symptoms

include headache, diarrhoea, myalgia, arthralgia and other gastro intestinal

symptoms. On examination tachypnea, findings of consolidation, crackles, pleural

friction rub may be observed. Chest radiographic patterns are nonspecific but a

lobar consolidation is usually associated with acute bacterial pneumonia. The

presence of radiological infiltrate in a patient presenting with typical clinical features

is diagnostic of pneumonia.

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Table 4.1: Common pathogens causing pneumonia and their clinical and epidemiological features are summarized below.

4.4. Investigations

l Routine Chest X-ray and microbiological investigations are not

required for Out Patients. But may be required if they fail to respond

to therapy.

l All hospitalized patients should have a chest X-ray taken, since a

diagnosis of pneumonia cannot be reliably established in the

absence of infiltrates.

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l Laboratory tests like complete blood count including ESR, Blood

urea Nitrogen, creatinine, Blood glucose, Serum electrolytes, Liver

Function Tests, O2 Saturation and ABG are also done.

l Gram stain and culture of sputum- If patients are unable to bring

adequate sputum then induction of sputum should be done with

hypertonic saline. Fewer than 10 squamous epithelial cells and

>25 polymorphonuclear neutrophils per low power (×100) field are

required in a Gram stain for subsequent culture.

l Sputum can also be testedwith Acid-fast stain for mycobacteria

and Immunofluorescence for Legionella, Pneumocystis and

viruses.

l Blood culture- It is taken in cases of severe CAP and in cases of

host defect like chronic liver diseases, asplenia, leucopenia. It

should be taken before starting antibiotics. Ideally 2 samples of 20

ml blood 30 min apart should be taken from 2 separate body sites.

l Acute and convalescent serum sample after 3-6 weeks if the

patient responds poorly- Useful in case of infections with atypical

pathogens.

l ·Other cultures: Pleural fluid gram stain and culture, Endotracheal

aspirate culture, Bronchoscopic retrieval of specimen ( PSB and

BAL).

l Antigen testing: Urinary antigen detection for S. pneumoniae and

L. pneumophila serogroup-1 in cases of severe pneumonia.

l Patients with CAP should be risk stratified.

l Initial assessment should be done with CRB-65.

l Accordingly, patients can be managed as either out-patient or in-

patient (ward or ICU).

4.5. Risk Stratification

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Table 4.2: CRB 65 Scoring system for risk stratification of pneumonia

CRB-65

Criteria Score*

Confusion 1

Respiratory rate ≥30/min 1

Low blood pressure(Diastolic blood pressure ≤60 mmHg or Systolic blood pressure ≤90 mmHg)

Age ≥65 years

1

1

*If the score is >1, patients should be considered for admission.

l Clinical judgement should be applied as a decision modifier in all

cases.The following features may indicate severity necessitating

hospitalization.

l Leukopenia (WBC count<4000 cells/mm3)

l Thrombocytopenia (platelet count<100,000 cells/mm3)

l Hypothermia (core temperature< 36ºC)

l Hypoxemia (SaO2 < 90% and PaO2 < 60 mm Hg)

l Presence of multilobar infiltrates

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Figure 4.1: Algorithmic approach for the diagnosis and management of CAP.

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Criteria for admission to ward or ICU

l Patients selected for admission can be triaged to the ward (non-

ICU / ICU) based upon the major / minor criteria. (ATS criteria )

l If any major criterion or ≥ 3 minor criteria are fulfilled, patients

should generally be admitted to the ICU.

Table 4.3. Criteria for admission

Major criteria

Minor criteria

Invasive mechanical ventilation

Septic shock with the need for vasopressors

Respiratory rate > or = 30 breaths/min

PaO2/FiO2 ratio < or = 250

Multi-lobar infiltrates

Confusion/disorientation

Uremia (BUN level > or = 20 mg/dL)

Leukopenia (WBC count < 4000 cells/mm 3)

Thrombocytopenia (platelet count <100,000 cells/mm3

Hypothermia (core temperature <36 0 C)

Hypotension requiring aggressive fluid resuscitation

Antibiotics

l Antibiotics should be administered as early as possible;

l Timing is more important in severe CAP.

l For those patients referred to hospital with suspected CAP and

where the illness is considered to be life threatening, general

practitioners should administer antibiotics in the community.

l Amoxicillin 1 g orally is the preferred agent

Antibiotic Therapy in the Out-patient Setting

l Therapy should be targeted towards coverage of the most

common organisms, namely Streptococcus pneumoniae

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l Out-patients should be stratified as those with or without

comorbidities.

Recommended antibiotics

A) for out-patients without comorbidities

l oral β-lactams e.g. Amoxicillin 500-1000 mg thrice daily or

l oral macrolides (preferably Azithromycin)

B) For out-patients with comorbidities

l ·Oral combination therapy is recommended:- β-lactams plus

macrolides.

l ·Duration of antibiotic treatment in out-patients is for five days.

l ·Fluoroquinolonesshould be kept as reserve drug and not be

used for empirical treatment in view of the high prevalence of

tuberculosis in this country.

Antibiotic in the Hospitalised non-ICU Setting

l The recommended regimen is combination of aβ-lactam plus a

macrolide

l (preferredbetalactams include crystalline penicillin, cefotaxime,

ceftriaxone andamoxicillin-clavulanic acid)

l treatment duration for in-patients is for seven days

l In case of hypersensitivity to β-lactams, respiratory

fluoroquinolones (e.g. Levofloxacin 750mg daily) may be used if

tuberculosis (TB) is not a diagnostic consideration.

Antibiotic Therapy in ICU Setting

1. For patients without risk factors for Pseudomonas aeruginosa,

the recommended regimen is

l β-lactam (cefotaxime, ceftriaxone or amoxicillin-clavulanicacid)

plus

l a macrolide

2. If P. aeruginosais an aetiological consideration,

l an anti-pneumococcal antibiotic should be given

l (e.g. cefepime, ceftazidime, cefoperazone, piperacillin -

tazobactam, Cefoperazone - sulbactam, imipenem or

meropenem).

l Combination therapy may be considered with the addition of

aminoglycosides / ant ipseudomonalf luoroquinolones

(e.g.ciprofloxacin).

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3.For community-acquired methicillin-resistant Staphylococcus

aureusinfection addvancomycin or linezolid.

l The use of linezolid in India should be reserved because of its

potential use in extensively drug-resistant TB.

4. For suspected influenza

l Early treatment (within 48 h of the onset of symptoms) with

oseltamivir or zanamivir is recommended.

l Antimicrobial therapy should be changed according to specific

pathogen isolated.

l For those with high severity microbiologically-undefined

pneumonia, 7–10 days treatment is proposed.

l This may need to be extended to 14 or 21 days according to clinical

judgement and development of complications.

l Diagnostic/therapeutic interventions should be done for

complications, e.g. thoracentesis, chest tube drainage, etc., as and

when required

Switch from intravenous to oral therapy (De-escalation)

l Patients should be switched from intravenous to oral therapy when

they are hemodynamically stable and improving clinically, are able

to ingest medications, and have a normally functioning

gastrointestinal tract.

l Patients should be discharged as soon as they are clinically stable.

Amoxicillin 0.5-1 g thrice daily (PO or IV)

Co-amoxiclav 625 mg thrice a day to 1 g twice daily (PO) / 1.2 g thrice daily (IV)

Azithromycin 500 mg daily (PO or IV)

Ceftriaxone 1-2 g twice daily (IV)

Cefotaxime 1 g thrice daily (IV)

Cefepime 1-2 g two to three times a day (IV)

Ceftazidime 2 g thrice daily (IV)

Piperacillin-tazobactam 4.5 g four times a day (IV)

Imipenem 0.5-1 g three to four times a day (IV)

Meropenem 1 g thrice daily (IV)

Table 4.4. Dosages of antibiotics

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Duration of Antibiotics

CAP should be treated be treated for a minimum of 5 days. For patients with

severe pneumonia, 10 days of treatment is proposed. This should be extended to 14-

21 days where Legionella, Staphylococcal or Gram negative enteric bacilli

pneumonia are suspected or confirmed.

Patients can be switched over from parenteral to oral therapy when they are:

l Hemodynamically stable

l Improving clinically

l Able to ingest medications

l Have a normally functioning gastrointestinal tract.

Adjunctive Therapies

l Correction of dehydration with IV fluids, correction of hypoxemia

with oxygen administration important supportive therapies to be

considered in appropriate settings.

l Steroids are not recommended for use in non-severe CAP.

l Steroids should be used for septic shock or acute respiratory

distress syndrome (ARDS) secondary to CAP according to the

prevalent management protocols for these conditions.

l No role of other adjunctive therapies (anticoagulants,

immunoglobulin, granulocyte-colony-stimulating factor, statins,

probiotics, chest physiotherapy, antiplatelet drugs, over-the

counter cough medications, β2-agonists) in the routine

management of CAP.

l CAP-ARDS and CAP leading to sepsis and septic shock should be

managed according to the standard management protocols for

these conditions.

l Non-invasive ventilation may be used in patients with CAP and

acute respiratory failure.

Role of Immunisation and Smoking Cessation for Prevention of CAP

l Routine use of pneumococcal vaccine among healthy

immunocompetent adults for prevention of CAP is not

recommended.

l Pneumococcal vaccine may be considered for the prevention of

CAP in special populations who are at high risk for invasive

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pneumococcal disease.

l Influenza vaccination should be considered in adults for the

prevention of CAP.

l Smoking cessation should be advised for all current smokers.

Non responding pneumonia is a situation in which an inadequate clinical

response is present despite adequate antibiotic treatment. There will be persistence

of symptoms and <50% radiological clearance after 2 weeks with radiological

infiltrates persisting after 30 days.

Failure to respond may be due to agent factors, host factors or due to extend of

disease. At this stage a review of diagnosis should be done. Other causes which

should be evaluated include:

l Resistant microorganism

l Nosocomial superinfection

l Spread of pneumonia

l Drug fever

l Non-infectious etiologies

l Post obstructive pneumonia.

In addition to microbiologic diagnostic procedures Chest CT, thoracocentesis

and bronchoscopy should be considered at this stage.

Hospital Acquired Pneumonia (HAP)

Pneumonia diagnosed 48 hrs or more after hospital admission.

Ventillator Associated Pneumonia(VAP)

Pneumonia diagnosed 48 hrs or more after endotracheal intubation

Clinical diagnosis of HAP/VAP can be done using modified Centers for Disease

Control and Prevention (CDC) criteria.

Failure to respond

Definition

4.6. Diagnosis and management of hospital-acquired pneumonia (HAP) /

ventilator-associated pneumonia (VAP)

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Table 4.5: Modified Centers for Disease Control and Prevention (CDC) criteria for diagnosis of HAP/VAP

Chest radiographic opacities (new, progressive or persistent infiltrate or cavitation)

AND

At least two of the following:

1. Fever >38 °C or >100.4 °F

2. Leukopaenia (<4000 WBC/μL) or leukocytosis (≥12000 WBC/μL)

3. Altered mental status with no other recognised cause in the elderly

4. New onset of purulent sputum, or change in character of sputum, or increased

respiratory secretions, or increased suctioning requirements

5. Worsening gas exchange (e.g., desaturations, increased oxygen requirements,

or increased ventilator demand)

6. New onset or worsening cough, or dyspnoea, or tachypnoea

7. Rales or bronchial breath sounds

Risk stratification

l Gram-negative bacteria are the most common pathogens causing

HAP/VAP in the Indian setting

l The risk stratification regarding acquisition of multidrug-resistant

(MDR) pathogen should be individualized

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Figure 4.2: Approach to HAP

Risk Factors for Multi drug- Resistant Pathogens

Risk factors for MDR VAP

l Prior intravenous antibiotic use within 90 d

l Septic shock at time of VAP

l ARDS preceding VAP

l Five or more days of hospitalization prior to the occurrence of VAP

l Acute renal replacement therapy prior to VAP onset

Risk factors for MDR HAP or MRSA VAP/HAP or MDR Pseudomonas

VAP/HAP

l Prior intravenous antibiotic use within 90 d

Microbiological methods to diagnosis of HAP and VAP

VAP:-

1. Non-invasive sampling with semi-quantitative cultures are

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recommended to diagnose VAP

l Non-invasive respiratory sampling refers to endotracheal

aspiration.

l Invasive respiratory sampling includes bronchoscopic techniques

(ie, bronchoalveolar lavage [BAL], protected specimen brush

[PSB]) and blind bronchial sampling (ie, mini-BAL).

HAP:-

Patients with suspected HAP has to be treated according to the results of

microbiologic studies performed on respiratory samples obtained

noninvasively, rather than being treated empirically.

Use of bio markers for initiation of antibiotic therapy

1. To decide whether or not to initiate antibiotic therapy, clinical criteria

alone is recommended rather than using serum PCT plus clinical

criteria .

2. Where available, serum procalcitonin levels<0.5 ng/mL may help in

differentiating bacterial HAP/VAP from other non-infective aetiologies,

and may help in decisions for antibiotic cessation.

Initial treatment of HAP and VAP

l All hospitals should regularly generate and disseminate a local

antibiogram, ideally one that is specific to their intensive care

population.

VAP :- Antibiotics Recommended for Empiric Treatment of Clinically

Suspected VAP

l In patients with suspected VAP, coverage for S. aureus,

Pseudomonas aeruginosa, and other gram-negative bacilli is

recommended in all empiric regimens.

l an agent active against MRSA recommended only in patients

withany of the following:

i. a risk factor for antimicrobial resistance

ii. patients in units where the prevalence of MRSA is not known

l An agent active against methicillin sensitiveS. aureus (MSSA)

is recommended for the empiric treatment of suspected VAP

I. in patients without risk factors for antimicrobial resistance

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l For MRSA:- either vancomycin or linezolid is recommended.

l for MSSA :-a regimen including piperacillin-tazobactam, cefepime,

levofloxacin, imipenem or meropenem is recommended.

l Two anti -pseudomonal antibiotics from different classes are

recommended only in patients with any of the following:

i. a risk factor for antimicrobial resistance

ii. patients in an ICU where local antimicrobial susceptibility

rates are not available.

l One antibiotic active against P. aeruginosa is recommended

i. in patients without risk factors for antimicrobial resistance

l Aminoglycosides is to be avoided if alternative agents with

adequate gram-negative activity are available.

l Colistin to be avoided if alternative agents with adequate gram-

negative activity are available.

Table 4.6. Antibiotics With MRSA Activity

Glycopeptides

Vancomycin 15 mg/kg IV q 8– 12h

(consider a loading dose of 25–30 mg/kg × 1 for severe illness)

Or

Oxazolidinones

Linezolid 600 mg IV q 12h

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Table 4.7. Antibiotics WithAntipseudomonal Activity

β-Lactam–Based Agents

Antipseudomonalpenicillins

Piperacillin-tazobactam 4.5 g IV q6h

Cephalosporins

Cefepime 2 g IV q8h

Ceftazidime 2 g IV q8h

Carbapenems

Imipenem500 mg IV q6h

Meropenem1 g IV q8h

Monobactams

Aztreonam2 g IV q8h

Fluoroquinolones

Ciprofloxacin 400 mg IV q8h

Levofloxacin 750 mg IV q24h

Aminoglycosides

Amikacin 15–20 mg/kg IV q24h

Gentamicin5–7 mg/kg IV q24h

Tobramycin5–7 mg/kg IV q24h

Polymyxins

Colistin5 mg/kg IV × 1 (loading dose)

followed by 2.5 mg × (1.5 × CrCl + 30) IV q12h (maintenance dose)

Polymyxin B2.5–3.0 mg/kg/d divided in 2 daily IV doses

Table 4.8. Gram-Negative coverage With AntipseudomonalActivity

- Non-β-Lactam–Based Agents

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HAP:- Antibiotics Recommended for Empiric Treatment of Clinically

Suspected HAP (Non-VAP)

Recommendations

1. For patients being treated empirically for HAP, an antibiotic with activity

against S. aureus is recommended

l an antibiotic with activity against MRSA is recommended for

patients with HAP who are being treated empirically and have

either a risk factor for MRSA infection

l For patients with HAP who are being treated empirically and have

no risk factors for MRSA infection and arenot at high risk of

mortality, we suggest prescribing anantibiotic with activity against

MSSA.

l For patients with HAP who are being treated empirically,

antibiotics with activity against P. aeruginosa and other

gram-negative bacilli is recommended.

Recommended Initial Empiric Antibiotic Therapy for Hospital-Acquired

Pneumonia (Non-Ventilator-Associated Pneumonia)

Table 4.9. Treatment for those not at High Risk of Mortality and no

suspicion of MRSA

One of the following:

·Piperacillin-tazobactam 4.5 g IV q6h

·Cefepime 2 g IV q8h

·Levofloxacin 750 mg IV daily

·Imipenem 500 mg IV q6h

·Meropenem 1 g IV q8h

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Table 4.10. Not at High Risk of Mortality but With Factors Increasing the

Likelihood of MRSA

One of the following:

· Piperacillin-tazobactam 4.5 g IV q6h

OR

· Cefepime or ceftazidime 2 g IV q8h

OR

· Levofloxacin 750 mg IV daily

· Ciprofloxacin 400 mg IV q8h

OR

· Imipenem 500 mg IV q6h

· Meropenem 1 g IV q8h

OR

· Aztreonam 2 g IV q8h

Plus:

· Vancomycin 15 mg/kg IV q8–12h with goal to target 15–20 mg/mL trough level

(consider a loading dose of 25–30 mg/kg × 1 for severe illness)

OR

· Linezolid 600 mg IV q12h

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Table 4.11. High Risk of Mortality Or Receipt of IV Antibiotics During the

Prior 90 days

Two of the following, but avoid 2 β-lactams:

· Piperacillin-tazobactam 4.5 g IV q6h

OR

· Cefepime or ceftazidime 2 g IV q8h

OR

· Levofloxacin 750 mg IV daily

· Ciprofloxacin 400 mg IV q8h

OR

· Imipenem 500 mg IV q6h

· Meropenem 1 g IV q8h

OR

· Amikacin 15–20 mg/kg IV daily

· Gentamicin 5–7 mg/kg IV daily

· Tobramycin 5–7 mg/kg IV daily

OR

· Aztreonam 2 g IV q8h

Plus:

· Vancomycin 15 mg/kg IV q8–12h with goal to target 15–20 mg/ml trough level

(consider a loading dose of 25–30 mg/kg IV × 1 for severe illness)

OR

· Linezolid 600 mg IV q12h

Role of Inhaled Antibiotics in the Treatment of VAP

l Aerosolised antibiotics (colistin and tobramycin) may be a useful

adjunct to intravenous antibiotics in the treatment of MDR

pathogens

l Aerosolised antibiotics should not be used as monotherapy and

should be used concomitantly with intravenous antibiotics.

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Pathogen specific therapy

Treatment for HAP/VAPdue to MRSA

l either vancomycin or linezolid rather than other antibiotics

HAP/VAP due to P. aeruginosa

l the choice of an antibiotic for definitive therapy has to be based

upon the results of antimicrobial susceptibility testing

HAP/VAP Due to Extended-Spectrum β-Lactamase (ESBL)–Producing

Gram- Negative Bacilli

l the choice of an antibiotic for definitive (not empiric) therapy has to

be based upon the results of antimicrobial susceptibility testing

and patient-specific factors.

HAP/VAP Due to Acinetobacter Species

l Treatment with either a carbapenem or ampicillin/ sulbactamif the

isolate is susceptible to these agents.

l if caused by Acinetobacter species that is sensitive only to

polymyxins, intravenous polymyxin (colistin or polymyxin B) , and

adjunctive inhaled colistin.

HAP/VAP Due to Carbapenem-Resistant Pathogens

l If caused by a carbapenem-resistant pathogen that is sensitive

only to polymyxins, intravenous polymyxins (colistin or polymyxin

B) and adjunctive inhaled colistin are recommended

Length of therapy

l For patients with VAP, a 7-day course of antimicrobialtherapy

rather than a longer duration is recommended.

l For patients with HAP, a 7-day course ofantimicrobial therapy is

recommended.

l For patients with HAP/VAP,antibiotic therapy should be de-

escalated rather than fixed.

l If cultures are sent after initiation of antibiotics,and there is clinical

improvement with subsequent cultures being sterile, antibiotics

should be continued for seven days followed by the assessment of

clinical pulmonary infection score (CPIS) on the 7th day.

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Table 4.12. CPIS scoring for pneumonia

l If CPIS is <6, antibiotics can be stopped while if it is ≥6,treatment

should be continued for 10 to 14 days.

Other Good Practices to be followed in the ICU

l Stress ulcer prophylaxis:

l Early enteral feeding:

l Enteral feeding is superior toparenteral nutrition and should be

usedwhenever tolerated and in those without anycontraindications

to enteral feeding.

Deep venous thrombosis (DVT) prophylaxis:

l DVTprophylaxis with unfractionated heparin (5000U thrice a day)

or a low molecular weight heparin should be used if no

contraindications.

Glucose control:

l A plasma glucose target of 140-180 mg/dL is recommended in

most patients with HAP/VAP, rather than a more stringent target

(80-110 mg/dL) or a more liberal target (180 -200 mg/dL).

Blood products:

l ·Red cells should be transfused at ahaemoglobin threshold of <7

gm/dL except inthose with myocardial ischaemia and pregnancy.

l Platelet transfusion is indicated in patients withplatelet count

<10,000/μL, or <20,000/μL if there is active bleeding.

l Fresh frozen plasma is indicated only if there is a documented

abnormality in the coagulation tests and there is active bleeding or

if a procedure is planned.

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4.7.References

1) Guidelines for Diagnosis and Management of Community and Hospital

Acquired Pneumonia in Adults: Joint ICS/ NCCP (I) Recommendations

2012

2) BTS guidelines for the management of community acquired pneumonia in

adults: update 2009

3) Infectious Diseases Society of America/American Thoracic Society

Consensus Guidelines on the Management of Community-Acquired

Pneumonia in Adults 2007

4) Management of Adults With Hospital-acquired and Ventilator-associated

Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases

Society of America and the American Thoracic Society

5) Guidelines for Diagnosis and Management of Community and Hospital

Acquired Pneumonia in Adults: Joint ICS/ NCCP (I) Recommendations

2012

6) BTS guidelines for the management of community acquired pneumonia in

adults: update 2009

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Section V

Bronchiectasis

Section V

5. Bronchiectasis

5.1. Clinical features

5.2. Investigations

Bronchiectasis refers to abnormal, irreversibly dilated and thickened airways. It

represents the end stage of a variety of pathologic processes that cause destruction

of bronchial wall and its surrounding supporting tissue.

l Chronic cough with sputum production (occur in more than 90%),

Dyspnea (72%), hemoptysis (45-51%), fever, chest pain

l Exacerbation of bronchiectasis : either a change in one or

more of the common symptoms of bronchiectasis (increasing

sputum volume or purulence, worsening dyspnea, increased

cough, declining lung function, increased fatigue/malaise) or the

appearance of new symptoms (fever, pleurisy, hemoptysis,

requirement for antibiotictreatment)

l The number of infective exacerbations per annum should be

noted including frequency and nature of antibiotic usage

l Psychosocial symptoms : patients have increased anxiety and

depression scoresincreased fatigue , lower quality of life.

Investigations are done to confirm the diagnosis of bronchiectasis and also to

identify theunderlying cause of it. In approximately 40-50% patients even after

extensive evaluation nospecific cause is found (Idiopathic). Investigations into

underlying cause can changemanagement, while sometimes have important

treatment and /or prognostic implications(eg: cystic fibrosis, immune deficiency,

ciliary dyskinesia).

l Complete blood count with differential count, ESR, CRP

l Respiratory tract specimen for microbiology: Send sputum for

bacterial, mycobacterial and fungal culture & sensitivity, Gram

staining accordingly based onclinical suspicion, before starting

antibiotics.

l When atypical mycobacterial infection is suspected, bronchoscopy

with bronchial washings may be done if sputum culture negative.

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Chest x-ray

l A baseline chest x-ray should be done in all patients.

HRCT chest

l HRCT CHEST is the gold standard investigation for diagnosis of

bronchiectasis

l Routine repeat chest x-ray or HRCT is not necessary; repeat

imaging should beconsidered when there is clinical need.

l In cases of humoral immune deficiency, repeat HRCT at intervals

may be necessary todetect asymptomatic progression.

l Raised Serum IgE , skin prick testing , peripheral blood eosinophilia

positive specific IgE and IgG to aspergillus and aspergillus

precipitins to rule out ABPA .

l To rule out underlying connective tissue disorder: RA, ANA and

ANCA (if clinically relevant).

l To rule out primary Immunodeficiency:

v Screening measurement of serum IgG, IgA, IgM levels with

electrophoresis in allpatients.

l Second line immunological investigations are performed in

appropriate clinicalcircumstances.

Cystic fibrosis should be evaluated

a) Unless a confident alternative cause can be identified, all children

withbronchiectasis will need investigation to exclude Cystic fibrosis

b) In adults, investigations should also be considered in those with:–

l age at presentation <40 years and no other identified cause

l persistent isolation of S aureus in the sputum

l features of malabsorption

l male primary infertility

l upper lobe bronchiectasis

l a history of childhood steatorrhoea.

c) The screening investigations should include two sweat chloride

measurement and CFTR genetic mutation analysis.

5.3. Investigations to determine the underlying cause of bronchiectasis

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Ciliary dyskinesia should be evaluated

a) Ciliary investigations should be considered in adults only if there is a history

of chronic upper respiratory tract problems or otitis media.

Factors favouring investigation include:

l symptoms since childhood

l childhood chronic otitis media

l predominantly middle lobe bronchiectasis

l infertility or situs anomalies.

a) Screening tests is nasal nitric oxide test. Nasal niric oxidelevels< 100

parts per billion indicates need to test further ciliary function test

b) Confirmatory test to assess the structure and function of cilia(ciliary

beatfrequency / pattern tests and electron microscopy studies)

Gastro intestinal investigations

If gastric aspiration is suspected as a cause

l Investigations chosen normally include one or more of 24 h

oesophageal pHmonitoring, barium studies,or the identification of

foam-laden macrophages onbronchoscopic samples.

Bronchoscopy

l Bronchoscopy can identify and be used to remove foreign bodies

in the endobronchialtree and can show anatomical abnormalities of

the bronchi.

l In adults with localized disease, bronchoscopy may be indicated

to exclude proximalobstruction

l When atypical mycobacterial infection is suspected,

bronchoscopy with bronchialwashings significantly increases the

yield of mycobacterial cultures above that ofsputum culture alone.

Lung function tests

l Pre and post bronchodilator spirometry . All adults with

bronchiectasis should havemeasures of FEV1, FVC and PEF.

l Repeat lung function may be done annually.

l General approach and treatment of the specific underlying

cause

l Education for patients and parents of children with

bronchiectasis

5.4. Management

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l Airway clearance

v Physiotherapy and exercise

v Mucolytic and hyperosmolar therapies

l Pulmonary rehabilitation

l Immunisation

l Airway drug therapy

v Bronchodilators

v Anti-inflammatory therapy

l Antibiotic therapy

l Surgical management

Management of complications

General approach and treatment of the specific underlying cause

l Identify and treat underlying cause(immunodeficiency, foreign

body, aspiration)

l To maintain or improve pulmonary function and reduce

exacerbations and improvequality of life

l Patients with primary or secondary immune deficiency should be

under joint care with a clinical immunologist.

l Patients with CF should be referred to a CF specialist centre.

l Explain treatment approaches including airway clearance

techniques, airway therapiesand management of infections.

l Explain how to recognise an exacerbation

l Explain the usefulness of sending a sputum sample for culture and

sensitivity to aidappropriate management with antibiotics.

Patients who should have regular follow-up in secondary care Include:

l All children with bronchiectasis

l Patients with chronic P aeruginosa, opportunist mycobacteria or

methicillin-resistant Saureus colonisation

l Deteriorating bronchiectasis with declining lung function

l Recurrent exacerbations (>3 per year)

l Patients receiving prophylactic antibiotic therapy (oral or

nebulised)

l Patients with bronchiectasis and associated rheumatoid arthritis,

immune deficiency, inflammatory bowel disease and PCD

5.5. Patient education

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l Patients with ABPA

l Patients with advanced disease and those considering

transplantation

Chest physiotherapy and postural drainage

(Airway clearance techniques & exercise)

l All patients with bronchiectasis should be taught chest

physiotherapy and posturaldrainage of secretions accordingly

based on anatomical segments affected.

l The active cycle of breathing techniques and oscillating positive

expiratory devices (plus postural drainage and the forced

expiration technique) may be considered

l Airway clearance therapy should be for 20-30 min once or twice

daily. This may alterwith periods of infective exacerbation.

l Effectiveness and acceptability to the patient of the airway

clearance technique shouldbe reviewed within approximately3

months of the initial visit

Adjuncts to airway clearance

l Sterile water inhalation, nebulized hypertonic saline may be used

before airwayclearance to facilitate clearance. When nebulised

hyper ton ic sa l ine i s f i r s t admin is te red ,watch fo r

bronchoconstriction in susceptible patients

l Nebulization with beta 2 agonists enhance sputum clearance.

l NIV/intermittent positive pressure breathing may be used to

augment tidal volume and reduce the work of breathing in those

patients who are becoming fatigued and finding their standard

airway clearance difficult.

Pulmonary rehabilitation

l Pulmonary rehabilitation should be offered to individuals who have

breathlessness affecting their activities of daily living. Inspiratory

muscle training can be used in conjunction with conventional

pulmonary rehabilitation to enhance the maintenance of the

training effect

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Vaccination

l Pneumococcal vaccination and yearly influenza vaccination are

advised

Airway pharmacotherapy

Bronchodilators and anti inflammatory drugs

1. Beta 2 agonist: if PFT shows airway obstruction which is reversible with

betaagonist may be used. May also be used in management of coexistent

asthmaand bronchiectasis

2. Anticholinergics : no evidence of benefits of its use in children, some adults

maygain a useful response

3. Methylxanthines : have no routine role in bronchiectasis

4. Inhaled steroids : should not be used in chi ldren with

bronchiectasis(outside of use for those patients with additional asthma). In

adults, may be used in a selected subset of patients

5. Oral steroids and Leukotriene receptor antagonist: no evidence of role of

oralsteroids in bronchiectasis without other indications like ABPA, chronic

asthma, COPD andinflammatory bowel disease.

Antibiotic therapy

l Antibiotics should be given for exacerbations that present with an

acute deteriorationwith worsening symptoms ( cough, increased

sputum volume or change in viscosity,increased sputum purulence

with or without increasing wheeze, breathlessness,hemoptysis )

and/or systemic upset

l Patients with an infective exacerbation of bronchiectasis should be

assessed for the need for inpatient or outpatient treatment.

Inpatient treatment recommendations

a) Unable to cope at home

b) Development of cyanosis or confusion

c) Breathlessness with respiratory rate ≥25/min

d) Circulatory failure

e) Respiratory failure

f) Temperature ≥ 38˚C

g) Unable to take oral therapy

h) IV therapy required in patients with clinical failure with oral therapy

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Recommendations for antibiotic usage

l Before starting antibiotics, a sputum sample should be sent off for

culture.

l Empirical antibiotics should be started whilst awaiting sputum

microbiology.

l If there is no previous bacteriology, first-line treatment is amoxicillin

500 mg three times a day or clarithromycin500 mg twice daily (in

patients that are penicillin-allergic) for 14days

l High-dose oral regimens (eg, amoxicillin 1 g three times a day or

amoxicillin 3 g twice daily) may be needed in patients with severe

bronchiectasis chronically colonised with H influenzae.

l Antibiotics can be modified subsequently once the pathogen is

isolated only if there isno clinical improvement and the treatment

should then be guided by antibioticsensitivity results.

l Failure to respond to an antibiotic course should prompt a repeat

sputum culture.

l Intravenous antibiotics should be considered when patients are

particularly unwell, have resistant organisms or have failed to

respond to oral therapy (this is most likely toapply to patients with P

aeruginosa).

l There is no evidence to support the routine use of antiviral drugs in

exacerbations

l In patients who culture Psuedomonas aeruginosa that is sensitive

to ciprofloxacin, monotherapy with oral respiratory flouroquinolone

can be used as first-line treatment if tuberculosis has been ruled

out

l In patients who have not responded to oral ciprofloxacin,

monotherapy with an antipseudomonal intravenous antibiotic

should be considered

l Combination antibiotics should be used for infections due to strains

of Psuedomonas aeruginosa that are resistant to one or more

antipseudomonal antibiotics (including ciprofloxacin) or if the

clinician suspects the patient will require many subsequent

antibiotic courses to reduce the development of drug resistance.

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Third generation cephalosporin (ceftazidime) and aminoglycoside

(gentamycin) for 14 days

Long term antibiotics

l Patients having ≥ 3 exacerbations per year requiring antibiotic

therapy or patients with fewer exacerbations that are causing

significant morbidity should be considered for long term antibiotics.

P aeruginosa colonised patients: Use inhaled colistin for patients with chronic

P aeruginosa infection. Inhaled gentamycin may be considered as a

second line alternative.

Azithromycin or Erythromycin may be considered as alternative if the

patient does not tolerate inhaled antibiotics.

Macrolides may also be considered as an additive treatment to inhled

antibiotics for patients with high exacerbation frequency.

Non P. aeruginosa colonised patients. Use Azithromycin or Erythromycin as

first choice. Consider inhale gentamycin as an alternative.

Consider doxycycline as an alternative in patients intolerant of macrolides

or in whom they are ineffective.

Eradication algorithm for psuedomonas aeruginosa in adults

For patients with new or first isolation of P. aeruginosa, eradication treatment

may be considered. First line treatment is ciprofloxacin 500-750 mg bd for 2

weeks. Alternative choice is intravenous antipseudomonal beta lactum ± an

intravenous aminoglycoside for 2 weeks. This should be followed by a 3 month

course of nebulised colistin, gentamycin or tobramycin. Risk and benefits of an

eradication treatment should be discussed, like likelihood of achieving

sustained eradication, risk of developing chronic infection and the risk of

adverse events to eradication treatment.

l Lung resection surgery may be considered in patients with

localised disease in whomsymptoms are not controlled by medical

treatment.

l Surgical option decided by expert committee in a tertiary care

centre

5.6. Role of surgery

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Lung transplantation for bronchiectasis

l Consider transplant referral in bronchiectasis patients below 65

years, if the FEV1 is < 30% with significant clinical instability or if

there is rapid clinical deterioration despite optimal medical

management.

l Earlier referral for transplant may be considered in patients with

poor lung function and the following additional factors- massive

hemoptysis, severe secondary pulmonary hypertension, ICU

admissions or respiratory failure requiring NIV.

Massive hemoptysis

l Haemoptysis is a potentially life-threatening complication of

bronchiectasis.

l Bronchial artery embolisation and/or surgery may be required in

the management of massive haemoptysis.

Treatment of Respiratory Failure

Consider long term oxygen therapy for patients with respiratory failure,

using the same eligibility criteria as for COPD.

Consider domiciliary NIV with humidification for patients with associated

hypercapnia, especially where it is associated with recurrent

hospitalisation.

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Section VI

Pleural Diseases

Section VI

6. Pleural disease

6.1. Pleural effusion

Management of unilateral pleural effusion

Pleural effusion is abnormal collection of fluid in the pleural cavity.

Clinical assessment and history

Initial diagnostic imaging

1. Chest x ray preview

The posteroanterior (PA) chest x-ray is abnormal in the presence of about

200 ml of pleural fluid. However, only 50 ml of pleural fluid can produce

detectable posterior costophrenic angle blunting on a lateral film.

2. Ultrasonography

Bedside ultrasound guidance significantly increases the likelihood of

successful pleural fluid aspiration and reduces the risk of iatrogenic

pneumothorax ,organ puncture.

Pleural aspiration

A diagnostic pleural fluid sample should be aspirated with a fine-bore

(21G) needle and preferably USG guided.

Pleural fluid studies sent for protein, LDH, Gram stain, cytology and

microbiological culture, ADA andsugar

Appearance : The appearance of the pleural fluid and any odour should be

noted.

Investigations to be sent for all aspiration

1. Biochemistry: LDH and protein

2. Microscopy and culture

3. Cytological examination and differential cell count.

4. Pleural fluid ADA

5. Sugar

Tests sent only in selected cases

1. pH in non-purulent effusions when pleural infection is suspected.

2. Acid-fast bacilli and TB culture when there is clinical suspicion of TB

pleuritis.

3. Triglycerides and cholesterol to distinguish chylothorax from

pseudochylothorax in milky effusions.

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4. Amylase useful in suspected pancreatitis-related effusion.

5. Haematocrit Diagnosis of haemothorax.

Differentiation into exudative and transudative causes

Light's criteria: pleural fluid is an pleural fluid is an exudate if one or

more of the following criteria are met:

1. Pleural fluid protein divided by serum protein is >0.5

2. Pleural fluid lactate dehydrogenase (LDH) divided by serum LDH is

>0.6

3. Pleural fluid LDH >2/3 the upper limits of laboratory normal value for

serum LDH.

Transudative pleural effusion e.g are: Left ventricular failure, liver

disease, renal disease

Treat the cause in a transudative effusion

l Exudative pleural effusion common causes are Tuberculosis,

malignancy, parapneumonic effusions, pulmonary embolism,

rheumatoid arthritis

Differential count

Lymphocytic pleural effusion

If differential count of lymphocytes more than 50%, Causes of lymphocytic

pleural effusion are Tuberculosis, Malignancy, Lymphoma, Cardiac

failure, Rheumatoid effusion.

Neutrophil-predominant pleural effusion

when differential count of neutrophils is more than 80% of the total

common causes-parapneumonic effusion, Pulmonary embolism, Acute

tuberculosis, empyma.

Eosinophilic pleural effusion

When eosinophil count more than or equal to 10%.

Causes are: Air or blood in the pleural space, Parasitic disease ,Churg

strauss syndrome, Pulmonary infarction, Lymphoma.

pH

In non-purulent effusions, when pleural infection is suspected, pleural fluid

pH should be measured. In a parapneumonic effusion, a pH of <7.2

indicates the need for tube drainage.

Malignant effusion low pH is associated with shorter survival, more

extensive disease, lower chance of successful pleurodesis.

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Glucose

A low pleural fluid glucose level (<3.4 mmol/l) may be found in complicated

parapneumonic effusions, empyema, rheumatoid pleuritis , oesophageal

rupture.

Amylase

Routine measurements of pleural fluid amylase or its isoenzymes are not

warranted. It can be useful in suspected cases of oesophageal rupture or

effusions associated with pancreatic diseases.

Cytology

Malignant effusions can be diagnosed by pleural fluid cytology in about

60% of cases. The yield from sending more than two specimens (taken on

different occasions) is very low and should be avoided.

Immunocytochemistry should be used to differentiate between malignant

cell types and can be very important in guiding oncological therapy.

Immunohistochemistry useful to differentiate between pleural

mesothelioma, and metastatic adenocarcinoma as both are

morphologically similar. But if possible pleural tissue should be obtained by

biopsy.

Computed tomography (ct)

CT scans should be performed in the investigation of all undiagnosed

exudative pleural effusions and can be useful in distinguishing malignant

from benign pleural effusion

A CT scan should be requested for complicated pleural infection when

initial tube drainage has been unsuccessful and surgery is to be

considered.

In a pleural effusion, a contrast-enhanced CT scan taken before full

drainage of the fluid as pleural abnormalities will be better visualised.

CT also distinguishes empyemas from lung abcesses.

Magnetic resonance imaging (mri)

MRI is not used as a routine investigation of pleural effusion, but may be

used to accurately assess pleural disease. Distinction of morphological

features of pleural malignancy by MRI is equal CT and assessment of

diaphragmatic and chest wall involvement is superior.

In patients for whom contrast is contraindicated and to assess response of

pleural mesothelioma to chemotherapy.

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6.3. Invasive investigations

6.4. Specific conditions and tests

Percutaneous pleural biopsy

When investigating an undiagnosed effusion where malignancy is

suspected pleural biopsy can be done

Thoracoscopy

Thoracoscopy is the investigation of choice in exudative pleural effusions

where a diagnostic pleural aspiration is inconclusive and malignancy is

suspected.

Local anaesthetic thoracoscopy and video assisted thoracoscopy are

avaliable

Bronchoscopy

Diagnostic bronchoscopy is performed for undiagnosed pleural effusion,

whose radiology suggests the presence of a mass or loss of volume or

when there is a history of haemoptysis, possible aspiration of a foreign

body or a trapped lung with a suspicion of a proximal lung mass., it should

be done after pleural drainage

Tuberculous pleurisy

Lymphocytic pleural effusion with high ADA is highly suggestive of

tuberculosis. Pleural biopsies can be taken if still inconclusive, they

should be sent for both histological examination and culture to improve

the diagnostic sensitivity.

Connective tissue diseases

Rheumatoid arthritis and systemic lupus erythematosus (SLE) are the

most common causes.

Rheumatoid arthritis-associated pleural effusions: very low glucose

level of <1.6 mmol/l (29 mg/dl).

Elevated pleural fluid antinuclear antibodies (ANA) and an increased

pleural fluid to serum ANA ratio is suggestive of SLE pleuritis, is also

seen in malignant effusion. But not routinely done.

l Pleural effusions due to pulmonary embolism: in appropriate

clinical setting pulmonary embolism should be ruled out with the

help of other specific investigation.

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Chylothorax and pseudochylothorax:

If a chylothorax or pseudochylothorax is suspected, pleural fluid should

be tested for cholesterol crystals and chylomicrons and the pleural fluid

triglyceride and cholesterol levels measured. Chylothorax causes

occurs due to the thoracic duct involvement trauma, tumor etc

Pseudochylothorax causes are Tuberculosis, rheumatoid arthritis.

Figure 6.1 Diagnostic algorithm for the investigation of a unilateral pleural effusion

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Figure 6.2. Diagnostic algorithm for the management of patients with

pleural infection

Involve respiratory physiciannutrition and DVT prophylaxis

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6.5. Indications for pleural fluid drainage in pleural infection

1. Patients with frankly purulent or turbid/cloudy pleural fluid on sampling

2. The presence of organisms identified by Gram stain and/or culture from a

non-purulent pleural fluid sample.

3. Pleural fluid pH <7.2 in patients with suspected pleural Infection.

4. Poor clinical progress during treatment with antibiotics alone should lead to

prompt patient review, repeat pleural fluid sampling and probably chest

tube drainage.

5. Patients with a loculated pleural collection should receive early chest tube

drainage.

6. Large non-purulent effusions could be drained by aspiration and/or chest

tube if required for symptomatic benefit.

Antibiotics

l All patients should receive antibiotics targeted to treat the bacterial

profile of modern pleural infection and based on local antibiotic

policies and resistance patterns.

l Antibiotics to cover anaerobic infection should be used in all

patients except those with culture proven pneumococcal infection.

l Macrolide antibiotics are not indicated unless there is objective

evidence for or a high clinical index of suspicion of 'atypical'

pathogens.

l Where possible, antibiotic choice should be guided by bacterial

culture results and advice from a microbiologist.

l Penicillins, penicillins combined with b-lactamase inhibitors,

metronidazole and cephalosporins penetrate the pleural space

well. Aminoglycosides should be avoided.

l Empirical antibiotic treatment for hospital-acquired empyema

should include treatment for MRSA and anaerobic bacteria.

l Intravenous antibiotics should be changed to oral therapy once

there is clinical and objective evidence of improvement in sepsis.

l Intrapleural antibiotics are not recommended.

l Prolonged courses of antibiotics may be necessary and can often

be administered as an outpatient after discharge

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Intrapleural fibrinolytics

Not recommended routinely

l Patients with persistent sepsis and a residual pleural collection

should undergo further radiological imaging.

l Patients should receive surgical treatment if they have persisting

sepsis in association with a persistent pleural collection, despite

chest tube drainage and antibiotics.

Malignant Pleural Effusion

Malignant pleural effusions are generally managed by oncologist

respiratory opinion may be seeked if a pleurodesis or a indwelling

pleural catheter needed.

CLASSIFICATION:

1. PRIMARY SPONTANEOUS PNEUMOTHORAX [PSP]: occurring in

healthy people

2. SECONDARY SPONTANEOUS PNEUMOTHORAX [SSP];occur in those

with underlying lung pathology

Imaging

Initial diagnosis

v Standard erect PA chest x-ray

Standard erect chest x-rays in inspiration are recommended for the initial

diagnosis of pneumothorax, rather than expiratory films.

v Supine and lateral decubitus x-rays.

These imaging techniques have mostly been employed for trauma patients

who cannot be safely moved.

v Ultrasound scanning

Specific features on ultrasound scanning are diagnostic of pneumothorax

but, to date, the main value of this technique has been in the management

of supine trauma patients.

v CT scanning

l small pneumothoraces and in size estimation.

l surgical emphysema and bullous lung disease

l aberrant chest drain placement or additional lung pathology

6.6. Pneumothorax

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6.7. Treatment Options For Pneumothorax

If the patient is severely dyspnoeic, hypoxic or with underlying lung pathology an

immediate intercostal tube drainage insertion should be done

Other modalities are needle aspiration, high flow oxygen,

Failure of a pneumothorax to re-expand or a persistent air leak should prompt

early referral to a respiratory physician, preferably with in 24hr. Such patients may

require prolonged chest drainage with complex drain management (suction, chest

drain repositioning) and liaison with thoracic surgeons.

Management Of SSP

All patients with SSP should be admitted to hospital for at least 24 h and receive

supplemental oxygen

Those with a persistent air leak should be discussed with a thoracic surgeon.

Patients with SSP but unfit for surgery, medical pleurodesis may be appropriate.

Discharge And Follow-up

l Patients should be advised to return to hospital if increasing

breathlessness develops.

l All patients should be followed up by respiratory physicians until full

resolution.

l Air travel should be avoided until full resolution.

l Diving should be permanently avoided unless the patient has

undergone bilateral surgical pleurectomy and has normal lung

function and chest CT scan postoperatively.

Medical Chemical Pleurodesis

Chemical pleurodesis can control difficult or recurrent pneumothoraces but,

since surgical options are more effective, it should only be used if a patient is either

unwilling or unable to undergo surgery.

Agents:

l Tetracycline: dose is 1500mg

l Doxycycline

l Minocycline

l Talc

l Betadine

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Referral To Thoracic Surgeons

In cases of persistent air leak or failure of the lung to reexpand, an thoracic

surgical opinion should be sought.

Indications are:

l Second ipsilateral pneumothorax.

l First contralateral pneumothorax.

l Synchronous bilateral spontaneous pneumothorax.

l Persistent air leak (despite 5-7 days of chest tube drainage) or

failure of lung re-expansion.

l Spontaneous haemothorax.

l Professions at risk (eg, pilots, divers).

l Pregnancy

Tension Pneumothorax

Tension pneumothorax is a medical emergency that requires heightened

awareness in a specific range of clinical situation eg ventilated patients on

ICU,trauma patient,. Resuscitation patients acute presentations of asthma and

chronic obstructive pulmonary disease, blocked, clamped or displaced chest drain.

Treatment is with oxygen and emergency needle decompression or a chest

drain may need to be inserted if there is an initial treatment failure

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Figure 6. 3. Management of spontaneous pneumothorax

Ref : BTS pleural disease guidelines 2010

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Section VII

Sleep disordered breathing

Section VII

7. Sleep-disordered breathing (SDB)

7.1. Overlap syndrome, obesity-hypoventilation and Pickwickian syndromes

7.2. Diagnosis of OSA

Sleep disordered breathing refers to abnormal respiratory pattern during sleep,

characterised by apnoea, hypopnea or respiratory effort related arousals (RERAs)

or central sleep apnoea which includes Cheyne-Stokes breathing or central

hypoventilation leading to an altered gas exchange.

Obstructive sleep apnoea (OSA) is defined as the occurrence of an average 5 or

more episodes of obstructive respiratory events (apneas, hypopnoeas or RERAs)

per hour of sleep with either sleep related symptoms or comorbidities or 15 such

episodes without any sleep related symptoms or co-morbidities.

Overlap syndrome is defined as the co-occurrence of both

chronic obstructive pulmonary disease and OSA in the same

individual.

Obesity-hypoventilation syndrome consists of obesity, sleep-

disordered breathing, hypoxia and chronic hypercapnia during

wakefulness in the absence of other known causes of

hypercapnia.

Historically, OHS was first described as Pickwickian syndrome

in a case report in 1956. This patient resembled a character

depicted by Charles Dickens in “The Posthumous Papers of the

Pickwick Club as he was obese and had hyper-somnolence.

When to suspect OSA

Patients undergoing routine health check-up with snoring, daytime

sleepiness, obesity, hypertension and motor vehicular accidents

need to be screened

High risk cases such as congestive heart failure, diabetes mellitus,

coronary artery disease, stroke, metabolic syndrome, nocturnal

dysrhythmias should undergo a comprehensive sleep evaluation.

Pulmonary hypertension and preoperative cases should also have

a comprehensive sleep evaluation.

Those suspected to have OSA on comprehensive sleep evaluation

should be referred for a sleep study.

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High risk cases, even if asymptomatic, can be referred for a sleep

study.

Medical examiners evaluating drivers, air pilots, railway drivers and

heavy machinery workers should be educated about OSA and

should comprehensively evaluate applicants for OSA, if snoring,

daytime sleepiness or obesity irrespective of the presence or

absence of co morbidities are noted

The role of ESS and pre-test screening questionnaires in the

diagnosis of OSA

ESS Epworth sleepiness scale can be used as a tool to measure

the quality of life with regard to Excessive Daytime Sleepiness

(EDS), likelihood of long-term compliance to continuous positive

airway pressure (CPAP) and to evaluate the treatment response

rather than to screen for OSA .

Both Berlin questionnaire and modified Berlin questionnaire are

moderately accurate to screen for OSA .

STOP Bang questionnaire is the most appropriate questionnaire

for screening preoperative cases.

It may also be used for pre-test probability assessment before

portable monitoring because of ease of administration and high

sensitivity.

Level 1: Fully attended polysomnography (7 channels) in a laboratory

setting

Level 2: Unattended polysomnography (7 channels)

Level 3: Limited channel study (using 4–7 channels)

Level 4: One or two channels usually using oximetry as one of the

parameters

“Gold standard” for diagnosis for OSA

Level 1 study or in-hospital, in-laboratory, technician-attended,

overnight polysomnography (PSG) is the “Gold standard” for

evaluation of sleep-disordered breathing .

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Portable monitoring (PM) / out of center sleep testing (OCST) / home

sleep testing (HST)/ unattended limited channel testing (ULCT) in

diagnosis of OSA

Laboratory attended PSG is not necessary in all patients suspected

to have OSA.

Portable monitoring or OCST with type 3 or type 4 devices (which

should at least include airflow, oxygen saturation and respiratory

effort) is adequate for diagnosis when used in conjunction with

comprehensive sleep evaluation and in patients with high pre-test

probability of moderate to severe OSA without co-morbid sleep

disorders or medical disorders like pulmonary disease,

neuromuscular disease, or congestive heart failure.

Sleep study in preoperative evaluation

The incidence of postoperative desaturation, respiratory failure,

postoperative cardiac events and intensive care unit transfers is

higher in patients with OSA

Portable monitoring is preferable as it reduces the likelihood of

delay in surgery, inconvenience and high cost of in-laboratory PSG.

Alternatively, in a case with high likelihood of OSA, sleep study may

be deferred if it is not feasible or causes delay in surgery.

Instead, a standby CPAP with a close monitoring may be advised.

Patients with known OSA must be advised to use CPAP in the

perioperative period.

The diagnostic criteria for OSA are the presence of (A and B) or C

A. Presence of one or more of the following:

a. Complaints of sleepiness, non refreshing sleep, fatigue, or

symptoms of insomnia.

b. Waking up with breath holding, gasping or choking.

c. Habitual snoring, interruptions in breathing, or both during sleep

as reported by patient's bed partner or other observer.

d. Co-existing morbidities such as hypertension, type 2 diabetes

mellitus, coronary artery disease, congestive heart failure, atrial

fibrillation, stroke, mood disorder, or cognitive dysfunction.

B. PSG or OCST (out of center sleep testing) demonstrates

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a. Five or more obstructive respiratory events (apneas,

hypopneas, or RERAs) per hour of sleepduring a PSG or per

hour of monitoring with OCST.

OR

C. PSG or OCST demonstrates

a. Fifteen (15) or more obstructive respiratory events (apneas,

hypopneas, or RERAs) per hour ofsleep during a PSG or per

hour of monitoring with OSCT, even in the absence of

symptoms.

OSA Severity Grading

OSA severity, based on the frequency of abnormal respiratory

events during sleep is graded as

Up to 5 apnoea / hypopnoea events per hour is normal

a) mild: 5 to <15 events/hr of sleep

b) moderate: 15–30 events/hr of sleep and

c) severe: > 30 events/hr of sleep.

Methods to prescribe PAP (Positive airway pressure) therapy

Full-night PSG with attended manual CPAP titration is regarded as

the gold standard for prescription of CPAP.

However, split-night study, i.e., initial PSG followed by 3 hours of

continuous positive airway pressure (CPAP) titration may be

performed if AHI is >40 events/hr during first 2 hours or between

20-40 events/hr with clinical judgment regarding definitiveness of

prescribing CPAP therapy

The process of BPAP titration in OSA management is initiated in

two situations, i.e., after maximal CPAP has not resolved the

respiratory events or less commonly as a primary PAP strategy.

Certain autoPAP devices can be tried during attended titration with

PSG or in an unattended way to determine a fixed PAP level in

patients with moderate to severe OSA without significant co-

morbid illness such as CHF, COPD, central sleep apnea or

hypoventilation syndromes.

The role of behavioural therapy in OSA

The following measures have shown modest improvement in OSA and

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should be considered as adjuncts to PAP therapy:

Smoking cessation

Avoidance of alcohol, sedatives and nicotine

Treatment of nasal obstruction

Weight loss

Positional therapy during sleep

Sleep hygiene, avoidance of sleep deprivation

The role of pharmacotherapy in OSA

There is no role of pharmacotherapy in OSA, however modafinil

and armodafinil are the only agents approved for EDS for poor

response despite use of adequate PAP therapy.

PAP therapy and its role in OSA

PAP therapy is the mainstay of treatment of OSA, however, patient

compliance is a major issue. Therefore, proper patient counselling

is necessary to ensure adequate compliance.

PAP creates a pneumatic splint in the upper airway which prevents

collapse of the pharyngeal airway, acting at all potential levels of

obstruction.

PAP therapy improves quality of life in terms of significant

reduction in daytime sleepiness, improvement in quality of life,

driving performance, neuro-cognitive performance and

cardiovascular outcomes including overall mortality

The indications for PAP therapy

PAP is indicated based on PSG results showing:

AHI or RDI> or = 15 events/hour

Or

AHI or RDI > or = 5 but <15 events/hour with any one of the

following symptoms:

Excessive daytime sleepiness

Neurocognitive impairment

Hypertension

Coronary artery disease

Cardiac arrhythmias

Pulmonary hypertension

History of stroke

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Role of oral appliances in OSA

OAs are indicated for use in patients with mild to moderate OSA

who prefer oral appliances to CPAP

or

who do not respond to CPAP or who fail treatment attempts with

CPAP or behavioural measures

Types of oral appliances

Two types of oral appliances are available

Mandibular repositioning appliance (MRA) and

Tongue retaining appliances (TRA).

These have defined indications and contra-indications with modest efficacy.

Who should undergo surgical treatment for OSA?

Surgical treatment is recommended in patients who have failed or

are intolerant to PAP therapy. 2Patients with BMI > or = 35kg/m should undergo bariatric surgery

rather than site directed surgery

How is the level of obstruction evaluated preoperatively?

Of the various methods available, fibre-optic nasopharyngoscopy

with Mueller's manoeuvre (FNMM) is found to predict response to

UPPP.

Other investigations like cephalometry, acoustic analysis,

somnofluoroscopy are outdated.

CT and MRI do not predict level of obstruction consistently and

hence are not recommended for routine use

Role of nasal and nasopharyngeal surgery

Nasal surgery (correction of anatomical defects) alone is not a

useful method of treatment of moderate to severe sleep apnea

Nasal surgery improves the compliance with PAP and also

enhances its effectiveness in patients who have nasal obstruction

Maxillo-mandibular surgery

Maxillo-mandibular surgeries which include maxillo-mandibular

advancement, genioglossus advancement, distraction

osteogenesis are recommended only in the subset of patients with

the specific anatomical abnormalities and intolerance to PAP

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therapy .

Uvulopalatopharyngoplasty (UPPP)

It is recommended in patients with retropalatal obstruction and PAP

therapy intolerance

Multi-level surgery

Multi-level surgery is done in patients who have failed PAP therapy

and other conservative measures with documented multi-level

obstruction

Bariatric surgery 2Bariatric surgery is indicated in patients with BMI > or = 35kg/m .

Gastric bypass is the most successful procedure and gastric

banding is the least effective procedure for treating OSA

Epworth sleepiness scale

Epworth sleepiness scale (ESS) is a simple, self-administered

measurement of sleep propensity during daytime in adults that

requires the subject to rate the probability of dozing off in eight

different situations that are met in day-to-day life on a scale of 0–3.

Thus, the sum of the score can vary from 0 to 24.

ESS score >10 is defined as excessive daytime sleepiness and

has a sensitivity of 49% and specificity of 80% for predicting OSA.

Situation

Watching TV

Sitting and reading

Sitting, inactive in a public place (e.g. a theatre or a meeting)

As a passenger in a car for an hour without a break

Lying down to rest in the afternoon when circumstances permit

Sitting and talking to someone

Sitting quietly after a lunch without alcohol

In a car, while stopped for a few minutes in the traffic

0 = would never doze 1 = slight chance of dozing 2 = moderate chance

of dozing 3 = high chance of dozing

References:

1. INOSA guidelines 2014

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Section VIII

Hemoptysis

Section VIII

8. Haemoptysis

8.1. Management

8.2. Airway protection and resuscitation

Hemoptysis or spitting / coughing out of blood is a life threatening emergency which

also creates a lot of anxiety in patients and bystanders.

The various common causes of Hemoptysis include

1. Tuberculosis / Post – TB sequelae

2. Bronchiectasis

3. Lung cancer

4. Pneumonias and other infections (e.g. fungal)

5. Pulmonary embolism

6. Lung trauma

7. Systemic diseases like bleeding disorders

Always differentiate between hemoptysis and hemetemesis before starting

the management

Initial approach – resuscitation and protecting the airway

Second step – localizing the site and cause of bleeding,

Final step – application of definitive & specific treatments to prevent

recurrent bleeding.

Hemoptysis should be monitored in an intensive care unit if massive (>100ml per

hour or >500ml in 24 hrs)

l Airway - Suction to prevent asphyxia & aspiration.

l If large volume bleeding continues or the airway is compromised -

Intubation with as large an endotracheal tube as is possible to allow

adequate suctioning and access for bronchoscopy

l Breathing – Correct / Prevent Hypoxia

l Circulation – Connect IV lines, Blood loss should be treated with

volume resuscitation, blood transfusion, and correction of

coagulopathy.

When the site of bleeding is known, one simple, initial bedside manoeuvre is to

place the involved side in a dependent position in order to protect the uninvolved

lung

If the bleeding can be localised to the right or left lung, unilateral lung

intubation may protect the non-bleeding lung.

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It may be possible to protect the nonbleeding lung from spillage by using of one

of the following techniques for intubation and mechanical ventilation: unilateral lung

ventilation using a standard, single-lumen endotracheal tube advanced into the right

or left mainstem bronchus or independent lung ventilation using a double-lumen

endotracheal tube.

l Sedatives and anti-tussives – preferred drugs are morphine /

pethedine as these are very good antitussives. However in case of

non-availability of morphine a codeine containing cough syrup can

be given.

l The antifibrinolytic agent IV/Oral tranexamic acid( 1 gm TDS) or

ethamsylate 500mg QID may be used.

l All patients with massive hemoptysis should have known or

suspected coagulation abnormalities rapidly reversed.

l For patients with massive hemoptysis, flexible bronchoscopy at the

bedside as the initial intervention to assess and attempt to control

the bleeding.

l Bronchoscopic strategies to control pulmonary hemorrhage

include balloon tamponade, iced saline lavage, administration of a

topical vasoconstrictor or a topical coagulant, laser therapy, APC

and electrocautery.

l When FOB fails Rigid bronchoscopy can be tried with ballon

tamponade,electrocutery or APC

l For patients with massive hemoptysis who continue to bleed

despite a bronchoscopic intervention and are stable enough to

leave the intensive care unit for a procedure, bronchial artery

embolization rather than surgery during active bleeding episode.

8.3. Drugs used

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Section IX

Pumonary embolism

Section IX

9. Pulmonary embolism

The diagnostic approach to PE should be targeted toward the patient population

being studied.

For outpatients, the use of a clinical prediction rule coupled with D-dimer testing

or the use of the PERC criteria can prioritize patients for imaging studies.

In patients with a low or intermediate clinical likelihood of PE, a negative D-

dimer study is sufficient to exclude the diagnosis, assuming a highly sensitive assay

is used.

PERC = Pulmonary Embolism Rule-out Criteria

l age < 50 years.

l pulse < 100 beats min.

l SaO2 >or= 95%

l no hemoptysis.

l no estrogen use.

l no surgery/trauma requiring hospitalization within 4 weeks.

l no prior venous thromboembolism (VTE)

l no unilateral leg swelling.

Variable Score

Age>65y 1

Previous DVT or PE 3

Surgery (GA) or lower limb fracture within 1m

2

Active malignancy

2

Symptom

·

Unilateral lower limb pain

3

·

Hemoptysis

2

Clinical Signs

·

Heart rate: 75-94/min

3

·

>95/min

5

·

Pain on lower limbdeep venous palpitation or unilateral oedema

4

Total score

0-3

Low

4 to 10

Moderate

>10 High

Table 9.1 The Revised Geneva Clinical Prediction

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Table 9.2. The Wells' Clinical Prediction Score

Variable Score

DVT symptoms/signs 3

PE like or more likely than alternative

diagnosis

3

Heart rate> 100

1.5

Immobilisation / surgery previous 4 wk

1.5

Previous DVT or PE

1.5

Hemoptysis

1

Malignancy

1

Total score

<2

Low

2 to 6

Moderate

>6

High

Dichotomized score

<=4 PE unlikely

>4 PE likely

An imaging study (CT pulmonary angiogram) should be performed in all

patients with a high probability of disease without going for D-dimer test,

And in those with a low or intermediate probability having positive D-dimer test.

Initial approach to patients with suspected PE (Pulmonary Embolism) is to

stabilize the patient while clinical evaluation and definitive diagnostic testing are

ongoing.

Stratify the risk

Assess hemodynamic stability.

Hemodynamically Stable PE

A heterogenous group ranging from patients with small PE and stable BP(low

risk) to patients with larger PE who have RV dysfunction and borderline BP

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(submassive PE).

Obtain peripheral intravenous access with or without intravenous fluidsGive

oxygen supplementation

Start empiric anticoagulation depending upon the clinical suspicion for PE, risk

of bleeding, and expected timing of definitive diagnostic tests

Hemodynamically Unstable PE(Massive PE)

Presenting with hypotension defined as systolic pressure <90 mmHg for a

period >15 minutes, hypotension requiring vasopressors, or clear evidence of shock.

A small percentage of patients with PE present with hemodynamic instability or

shock (approximately 8 percent; ie, “massive” PE).

Initial support should focus upon restoring perfusion with intravenous fluid

resuscitation and vasopressor support, as well as oxygenation and, if necessary,

stabilizing the airway with intubation and mechanical ventilation.

When portable perfusion scanning or CTPA is not available or is unsafe,bedside

echocardiography (transthoracic or transesophageal) to obtain a presumptive

diagnosis of PE (right ventricle enlargement/hypokinesis, regional wall motion

abnormalities that spare the right ventricular apex [McConnell's sign], or

visualization of clot) prior to the empiric administration of systemic thrombolytic

therapy (ie, reperfusion therapy).

If bedside echocardiography is delayed or unavailable, the use of thrombolytic

therapy as a life-saving measure should be individualized; if not used, the patient

should receive empiric anticoagulation.

Hemodynamic support

The precise threshold that warrants hemodynamic support depends upon

the patient's baseline blood pressure and whether there is clinical evidence

of hypoperfusion (eg, change in mental status, diminished urine output).

Small volumes of intravenous fluid (IVF), usually 500 to 1000 mL of normal

saline, followed by vasopressor therapy, should perfusion fail to respond to

IVF.

Intravenous fluid

IV Fluid isthe first-line therapy for patients with hypotension. However, in

patients with right ventricular (RV) dysfunction, limited data suggest that

aggressive fluid resuscitation is not beneficial, and may be harmful. The

rationale for limiting IVF administration comes from preclinical studies and

one small observational study in humans, which reported that small

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volumes of IVF increase the cardiac index in patients with PE, while

excessive amounts of IVF result in RV overstretch (ie, RV overload), RV

ischemia, and worsening RV failure. The patient's volume status should be

carefully assessed as this could influence the approach to fluid

administration.

Vasopressors

Intravenous vasopressors are administered when adequate perfusion is

not restored with IVF.

Norepinephrine is generally preferred.

Empiric anticoagulation (Initiation of anticoagulation before confirmation)

The administration of empiric anticoagulation depends upon the risk of

bleeding, clinical suspicion for PE and the expected timing of diagnostic

tests

Low risk for bleeding – Patients without risk factors for bleeding, having a

three-month bleeding risk of <2 percent; empiric anticoagulation to be

considered in the following patient groups:

l A high clinical suspicion for PE (eg, Wells score >6)

l A moderate clinical suspicion for PE (eg, Wells score 2 to 6), in

whom the diagnostic evaluation is expected to take longer than four

hours

l A low clinical suspicion for PE (eg, Wells score <2), if the diagnostic

evaluation is expected to take longer than 24 hours

Unacceptably high risk for bleeding

For patients with absolute contraindications to anticoagulant therapy

(eg, recent surgery, hemorrhagic stroke, active bleeding) or those

assessed by their physician to be at an unacceptably high risk of bleeding

(eg, aortic dissection, intracranial or spinal cord tumors), empiric

anticoagulation should not be administered. The diagnostic evaluation

should be expedited so that alternate therapies (eg, inferior vena cava

filter, embolectomy) can be initiated if PE is confirmed.

Typically, menstruation, epistaxis, and the presence of minor hemoptysis

are not contraindications to anticoagulation but should be monitored

during anticoagulant therapy.

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The optimal agent for empiric anticoagulation

Depends upon the presence or absence of hemodynamic instability, the

anticipated need for procedures or thrombolysis, and the presence of risk factors

and comorbidities.

As an example, low molecular weight heparin(LMWH) may be chosen for

patients with hemodynamically stable PE who do not have renal insufficiency in

whom rapid onset of anticoagulation needs to be guaranteed (ie, therapeutic levels

are achieved with four hours).

In contrast, unfractionated heparin is preferred by most experts in patients who

are hemodynamically unstable in anticipation of a potential need for thrombolysis or

embolectomy.

Direct thrombin and factor Xa inhibitors should not be used in hemodynamically

unstable patients.

DEFINITIVE THERAPY

For patients in whom the diagnostic evaluation excludes pulmonary embolism

(PE)), anticoagulant therapy should be discontinued if it was initiated empirically,

and alternative causes of the patient's symptoms and signs should be sought.

For patients in whom the diagnostic evaluation confirms PE, an approach that is

stratified according to whether the patient is hemodynamically stable or unstable. At

any time, the strategy may need to be redirected as complications of PE or therapy

arise.

Hemodynamically stable patients

For those in whom the risk of bleeding is low, anticoagulant therapy is indicated.

For those who have contraindications to anticoagulation or have an unacceptably

high bleeding risk, placement of an inferior vena cava (IVC) filter should be

performed.

For hemodynamically stable (ie, normotensive) patients with intermediate-

risk/submassive PE who are anticoagulated, should be monitored closely for

deterioration. Thrombolysis and/or catheter-based therapies may be considered on

a case-by-case basis when the benefits are assessed by the clinician to outweigh

the risk of hemorrhage. Examples of such patients include those who have a large

clot burden, severe RV enlargement/dysfunction, high oxygen requirement, and/or

are severely tachycardic.

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Options for anticoagulation

Unfractionated heparin (UFH)

Low molecular weight (LMW) heparin

Fondaparinux

Oral factor Xa inhibitors or direct thrombin inhibitors

Direct oral anticoagulants – Rivaroxaban and apixaban are the only direct oral

anticoagulants that have been studied and approved by regulatory agencies as

monotherapy (ie, no pre-treatment with heparin is necessary) for the treatment of

patients with VTE.

They may be preferred in those who wish to avoid the burden of injections in

whom convenience or oral medication is a personal preference. Importantly, LMW

heparin (or UFH) should be administered if there is a delay in obtaining these

anticoagulants (eg, availability needs to be assured).

When prescribing the direct thrombin inhibitor

dabigatran, or the factor Xa inhibitor edoxaban, a short course of heparin

(typically LMW heparin) be administered for five days prior to transitioning

to oral therapy (ie, dual therapy) since their efficacy as monotherapeutic

agents has not been studied or approved.

LMW heparin

Subcutaneous LMW heparin may be preferred in those in whom oral

anticoagulation is not feasible (eg, poor oral intake, malabsorption) or for

those in whom rivaroxaban or apixaban are unavailable (eg, too costly).

-Fondaparinux – Subcutaneous fondaparinux is an acceptable alternative

to subcutaneous LMW heparin (eg, for those who prefer once daily

injections; heparin induced thrombocytopenia [HIT]).

Warfarin -When chosen as the long term anticoagulant it must be co-

administered with heparin so that full anticoagulation is assured.

Heparin stopped when INR reaches 2.5 and warfarin alone to be

continued.INR periodically monitored warfarin dose adjusted to maintain

INR between 2-3.

Dosing

LMWH

Dosing is typically weight-based and renally-adjusted, and all are

administered subcutaneously.

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Typical starting doses are:

Enoxaparin 1 mg/kg twice daily (preferred); alternatively, 1.5 mg/kg

once daily can be used in selected non-obese inpatients; for home

treatment, the twice daily regimen is better studied and therefore

preferred by many experts.

Dalteparin 200 units/kg once daily

Fondaparinux

As an alternative to LMW heparin, fondaparinux is an acceptable

anticoagulant for most nonpregnant patients with newly diagnosed VTE

(eg, patients with HIT).

Dosing

Fondaparinux is typically dosed according to patient weight as 5 mg once

daily (<50 kg), 7.5 mg once daily (50 to 100 kg), and 10 mg (>100 kg). The

dose should be reduced to 1.5 mg once daily in patients with creatinine

clearance (CrCl) in the range of 20 to 50 mL/minute. No dosage reduction

is required for patients with mild renal impairment (CrCl >50 mL/minute)

Dosing oral drugs

Typical initial doses in those with normal renal function are:

Rivaroxaban 15 mg twice daily (for the first three weeks) then 20 mg daily to

complete 3 months

Apixaban 10 mg twice daily (for first seven days) then 5 mg bd to complete

3months.

Edoxaban 60 mg once daily (and 30 mg once daily in patients with a body

weight below 60 kg) (after an initial 5 to 10 days of parenteral

anticoagulation)

Dabigatran 150 mg twice daily (after an initial 5 to 10 days of parenteral

anticoagulation)

Duration of anticoagulation

Typically three months (eg, transient VTE risk factors), or up to 6 or 12

months in some cases (eg, persisting risk factors, or unprovoked VTE).

Indefinite anticoagulation

Select patients with PE are candidates for indefinite anticoagulation.

Patient selection depends upon the nature of the event (ie, provoked or

unprovoked), the presence of risk factors (eg, transient or persistent), the

estimated risk of bleeding and recurrence, as well as patient preferences

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and values (eg, occupation, life expectancy, burden of therapy)

Outpatient anticoagulation

In select patients with PE, outpatient therapy can be administered by

giving the first dose of anticoagulant in the hospital or urgent care center,

with the remaining doses given at home. The decision to treat as an

outpatient should be made in the context of the patient's clinical condition,

understanding of the risk-benefit ratio, and their preferences.

-No requirement for supplemental oxygen

-No requirement for narcotics for pain control

-No respiratory distress

-Normal pulse and blood pressure

-No recent history of bleeding or risk factors for bleeding

-No serious comorbid conditions (eg, ischemic heart disease, chronic lung

disease, liver or renal failure, thrombocytopenia, or cancer)

-Normal mental status with good understanding of risk and benefits, are

not needle averse (if low molecular weight (LMW) heparin chosen), and

have good home support (eg, do not live alone, have access to a telephone

and physician, can return to the hospital quickly if there is clinical

deterioration)

-Absence of concomitant deep venous thrombosis (a high clot burden in

the lower extremities may increase the risk of death or warrant additional

therapy)

Inferior vena cava filter

For most patients with PE in whom anticoagulation is contraindicated, or

patients in whom the risk of bleeding is unacceptably high, IVC filter should

be placed.

Similarly, an IVC filter is appropriate in patients who develop

contraindications while on anticoagulation; however, placement in this

population depends upon the planned duration of anticoagulation and risk

of recurrence when anticoagulation is discontinued.

Retrievable filters are preferred, such that once the contraindication has

resolved, the filter can be removed and patients should be anticoagulated.

Hemodynamically unstable patients

In patients with PE who are hemodynamically unstable or who become unstable

due to recurrence despite anticoagulation

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Thrombolytic therapy is indicated provided there is no contraindication

Embolectomy is appropriate for those in whom thrombolysis is either

contraindicated or unsuccessful (surgical or catheter-based)

Thrombolytic therapy — Systemic thrombolytic therapy is a widely accepted

treatment for patients with PE who present with, or whose course is complicated

by, hemodynamic instability.

Continuous infusions — Intravenous thrombolytic infusion regimens are the

most common method of administering thrombolytics.

Common regimens that are approved by the FDA include:

tPA (alteplase) – 100 mg intravenously over two hours.

-Streptokinase – 250,000 units intravenously over the initial 30 minutes,

then 100,000 units/hour for 24 hours. Monitor closely for hypotension,

anaphylaxis, asthma, and allergic reactions. Mild adverse reactions may

respond favorably to a decreased infusion rate.

-Urokinase – 4400 units/kg intravenously over the initial 10 minutes, then

4400 units/kg per hour for 12 hours.

The FDA-approved infusion duration for tPA of two hours, being much

shorter than for SK or UK, has been the main reason why this drug is

commonly chosen.

An activated partial thromboplastin time (aPTT) can be measured when

infusion of the thrombolytic therapy is complete. Heparin should be

resumed without a loading dose when the aPTT is less than twice its upper

limit of normal. If the aPTT exceeds this value, the test should be repeated

every four hours until it is less than twice its upper limit of normal, at which

time heparin should be resumed.

Catheter-directed thrombus removal

with or without thrombolysis can also be administered in select patients

(eg, those at high risk of bleeding, those with shock who will likely die

before systemic thrombolysis can take effect (eg, within hours), and those

who have failed systemic thrombolysis

For those in whom systemic thrombolysis is unsuccessful, the optimal

therapy is unknown. Options include repeat systemic thrombolysis,

catheter-directed thrombolysis, or catheter or surgical embolectomy, the

choice of which is dependent upon available resources and local expertise.

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Embolectomy

Embolectomy is indicated in patients with hemodynamically unstable PE

in whom thrombolytic therapy is contraindicated. It is also a therapeutic

option in those who fail thrombolysis.

Emboli can be removed surgically or using a catheter. The choice between

these options depends upon available expertise, the presence or absence

of a known diagnosis of PE, and the anticipated response to such

therapies.

Special populations

In general, the initial approach to the treatment of PE as well as the treatment of life-

threatening PE in special populations are similar to that in the general population.

However, definitive therapy may differ in hemodynamically stable patients with

malignancy, pregnancy, and heparin-induced thrombocytopenia.

Patients with malignancy

In hemodynamically stable patients with malignancy and PE, LMW

heparin is the preferred agent for all phases of anticoagulation.

Patients who are pregnant

For most pregnant women with hemodynamically stable PE, adjusted-

dose subcutaneous LMW heparin is the preferred agent for initial and

long-term anticoagulation due to its favorable fetal safety profile .

Patients with heparin-induced thrombocytopenia

For patients with PE and heparin-induced thrombocytopenia (HIT), all

forms of heparin are contraindicated (eg, unfractionated and LMW

heparin).

Fondaparinux can be used.

Immediate anticoagulation with a fast-acting non heparin anticoagulant

(eg, argatroban) is indicated.

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Section X

Interstitial Lung Disease

Section X

10. Interstitial Lung Disease

10.1. Diagnosis and management of interstitial lung diseases

10.2. Classification of interstitial lung diseases

ILD (interstitial lung diseases) refers to a heterogeneous collection of distinct

lung disorders that tend to be grouped together because they share clinical,

radiological, and pathologic features.

Broadly classified into

1. Aetiology known

2. Aetiology unknown

Aetiology known

l Inorganic exposure – Asbestos, Silica, Hard Metals, Coal

Dust

l Organic exposure- Birds, Hay, Mould, Mycobacteria

l Connective tissue disease- Scleroderma, Polymyositis,

Dermatomyositis, Rheumatoid Arthritis, Sjogrens Syndrome

l Drugs- Amiodarone, Methot rexate , N i t ro furanto in ,

Chemotherapy.

l Smoking- DIP, RB-ILD, LCH

Aetiology unknown

1. Idiopathic interstitial pneumonias

l Major idiopathic interstitial pneumonias

Chronic fibrosing-

l Idiopathic pulmonary fibrosis

l Idiopathic nonspecific interstitial pneumonia

Smoking related

l Respiratory bronchiolitis–interstitial lung disease

l Desquamative interstitial pneumonia

Acute or sub acute

l Cryptogenic organizing pneumonia

l Acute interstitial pneumonia

l Rare idiopathic interstitial pneumonias

v Idiopathic lymphoid interstitial pneumonia

v Idiopathic pleuroparenchymal fibroelastosis

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l Unclassifiable idiopathic interstitialpneumonias

2. GRANULOMATOUS- SARCOIDOSIS.

3. RARE FORMS OF ILD- LAM, VASCULITIS

The multidisciplinary approach is now considered the ''gold standard'' for

diagnosing interstitial lung disease.

It is based on the following:

1. Detailed history & clinical examination

2. Physiological evaluation

3. Radiology

4. Serologic evaluation

5. Pathologic evaluation

Detailed history include chronology of symptoms, smoking history, occupation,

hobbies, travel, family history, drugs, past medical history, connective tissue

symptoms, h/o radiotherapy

Spirometry

l All patients with ILD should have a baseline spirometry.

l For evaluation, prognostication, & assessment of treatment

response.

l FVC & DLCO are reliable measures of disease severity.

Exercise testing

l 6 Minute Walk test (6MWT) - distance covered during 6MWT and

desaturation to 88%- prognostic indicators.

l For monitoring and assessment of treatment response

Radiology

Chest radiography

l Specificity 50%

l It is widely used for monitoring patients with ILD.

High resolution computed tomography (HRCT)

l Most essential component in diagnosis of ILD.

l Specificity and positive predictive value > 90%

10.3. Diagnosis of interstitial lung diseases

10.4. Physiological evaluation

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l In the appropriate clinical setting, appearances on the HRCT

scan may be sufficiently characteristic to preclude the need

for BAL or lung biopsy and histopathological confirmation.

Blood investigations

l Initial tests in cases of suspected ILD should include a

l full differential blood cell count,

l serum urea, electrolytes and creatinine,

l Liver function tests.

l Erythrocyte sedimentation rate(ESR), C-reactive protein (CRP)

Baseline cardiac investigations

l ECG

l ECHO

Based on clinical context:

l Autoantibody testing,creatine kinase

l Serum calcium, serum angiotensin converting enzyme (ACE),

urinary calcium,tuberculin test

l Precipitating antibodies

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Table 10.1. Hrct patterns for making diagnosis

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Probable UIPUIPIndeterminate for

UIP Alternate Dignosis


Table 10.2. Histopathological patterns & features

Table 10.3. Auto antibody testing in evaluation of ILD

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UIP Probable UIP Indeterminate for UIP

Alternate Dignosis


Table 10.4. Diagnosis of IPF

Role of bronchoscopy in ILD

Bronchoalveolar lavage (BAL), trans bronchial lung biopsy (TBLB),

endobronchial biopsy

l Diagnosis is uncertain after clinical assessment and HRCT

scanning.

l BAL helpful in diagnosis of ILDs like sarcoidosis,

h y p e r s e n s i t i v i t y p n e u m o n i t i s , L C H , a l v e o l a r

proteinosis,eosinophi l ic pneumonia and to exclude

infection/malignancy.

l TBLB – helpful in diseases with Bronchocentric involvement like

sarcoidosis,HP

l Endobronchial biopsy: in suspected sarcoidosis

l BAL/TBLB should be performed before the initiation of

treatment.

Role of surgical lung biopsy in ILD

l Surgical lung biopsy is required in cases of ILD, ifintegration of

clinical, radiological and, where appropriate, BAL/TBLB data don't

lead to a confident diagnosis.

l The principal factors influencing the decision to proceed to a

surgical biopsy are the degree of confidence in the clinical

diagnosis including the HRCT appearances and the patient's age,

functional status and wish to proceed once informed about the

risks versus benefit of the procedure.

l In appropriate clinical setting, patients may be referred to a tertiary

care centre for decision regarding surgical biopsy.

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l Surgical lung biopsy, when required, should be performed before

the initiation of treatment. It can be done either by VATS or Open

lung biopsy.

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Figure 10.1. Algorithm for diagnosis of ILD


10.5. General management strategies in ILD

l All patients with ILD should have access to a multidisciplinary

team based in a regional centre with expertise in ILD.

l Referral to a regional ILD clinic should be made if there are

perceived difficulties in diagnosis and/or management, but a

tailored shared care model is advocated.

l Patients with ILD who are current smokers should receive

opportunistic smoking cessation advice from healthcare

professionals and this advice should be recorded in the clinical

notes.

l Patients with ILD should have access to a local pulmonary

rehabilitation programme.

l Patients with clinically significant resting hypoxemia (resting

SpO2<88%) should receive long term oxygen therapy.

l Adult immunisation with annual influenza vaccine and

pneumococcal vaccine is also recommended.

Table 10.5. Treatment approach and monitoring strategy

Pulmonary hypertension in ILD:

Pulmonary hypertension should be considered in patients with ILD who have either

breathlessness or lung dysfunction (reduced TLCO or desaturation on exercise) that

seem disproportionate to the extent of parenchymal lung disease.

Transthoracic echocardiography is a suitable screening tool.

Long-term warfarin therapy may be prescribed in patients with CTD-associated

pulmonary artery hypertension.

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ILD presenting with acute respiratory failure

The two most common scenarios in which ILD presents with acute respiratory

failure are

1. Rapid deterioration in a patient with previously diagnosed ILD. Eg:

acute exacerbation of IPF

2. Initial presentation with rapidly progressive disease.

Eg: acute interstitial pneumonia, fulminant COP

Decision on admission to ICU

On a case by case basis.

Compare previous CXRs and HRCT; Evidence of extensive fibrotic

change or a pattern of disease typical of IPF usually indicates that

invasive ventilation is highly unlikely to have a successful outcome.

Pre-emptive counselling of patients that palliation or non-invasive

supportive therapy rather than invasive ventilation is appropriate is an

important component of management.

In management of pre-existing ILD, non ILD processes such as

pulmonary oedema, malignancy, drug induced lung disease and

infection has to be excluded.

Pharmacological management

l Intravenous corticosteroid therapy is the initial treatment of choice.

v Methyl prednisolone 750mg or 1g given on three

consecutive days and maintanence therapy of 0.5-1mg/kg

depending on clinical response.

v Assess response after 5-7 days.

l Intravenous cyclophosphamide- second line.

v Dose: 600-650mg/m2

l In suspected vasculitis – IV cyclophosphamide first choice.

Follow up

Follow up of ILD patients is recommended every 3 -6 months with clinical

assessment, spirometry, DLCO and 6MWT.Timing of follow up HRCT to be

decided by the treating physician.

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Management of specific ILDs

Idiopathic pulmonary fibrosis (IPF)

IPF is defined as a specific form of chronic, progressive fibrosing interstitial

pneumonia of unknown cause, occurring primarily in older adults, limited to the

lungs, and associated with the histopathology and/or radiologic pattern of UIP.

Diagnostic criteria

The diagnosis of IPF requires: multidisciplinary discussion

1. Exclusion of other known causes of interstitial lung disease (ILD) (e.g.,

domestic and occupational environmental exposures, connective

tissue disease, and drug toxicity).

2. The presence of a UIP pattern on high-resolution computed

tomography (HRCT) in patients not subjected to surgical lung biopsy.

3. Specific combinations of HRCT and surgical lung biopsy pattern in

patients subjected to surgical lung biopsy.

A. Pirfenidone- dose: 400 to 800 mg TID,

l A/E: photosensitivity, fatigue, stomach discomfort, and anorexia.

B. Anti- Acid Therapy-Proton pump inhibitors/H2 receptor blockers

C. Nintedanib – dose: 150 mg BD,

l Adverse effect - Diarrhoea

Treatment Not Recommended

l Anticoagulation with Warfarin

l Imatinib

l Combination prednisone,azathioprine, and N-acetylcysteine

l Selective endothelin receptor antagonist (Ambrisentan)

l Phosphodiesterase-5 inhibitor (sildenafil).

l Dual endothelin receptor antagonists (macitentan, bosentan)

l N-acetylcysteinemonotherapy.

Nonpharmacologic Therapies

Long term oxygen therapy-In patients with clinically significant resting

hypoxemia (SpO2 of < 88%)

Lung transplantation

Referral to a transplant centre should be made if the disease is advanced

(TLCO <40% predicted) or progressive (>10% decline in FVC or >15% decline in

10.6. Treatment recommendations

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FVC) during 6 months of follow-up.

Decision regarding transplantation should be made by an expert panel in a

tertiary care centre.

Pulmonary Rehabilitation

Pulmonary rehabilitation recommended in majority of patients.

Mechanical Ventilation

may be used as a bridge therapy prior to lung transplantation.

Pulmonary hypertension

In patients with moderate to severe pulmonary hypertension documented by

right heart catheterization (i.e., mean pulmonary artery pressure >35 mm Hg), a trial

of vaso-modulatory therapy may be indicated.

Acute exacerbation of IPF

Criteria

l Previous or concurrent diagnosis of IPF

l Unexplained worsening or development of dyspnoea within 30

days.

l HRCT with new B/L GGO and/or consolidation superimposed on a

background consistent with UIP pattern

l No evidence of pulmonary infection by ET aspirate or BAL

l Exclusion of alternative causes including: left heart failure,

pulmonary embolism and identifiable cause of lung injury.

Treatment

High dose corticosteroid with or without immunosuppressive agents in

combination with a broad spectrum of antimicrobial coverage.

Non specific interstitial pneumonia (NSIP)

For exposure related NSIP related to drugs or inhalations, cessation of the

offending agent is the treatment.

Idiopathic NSIP can have 3 clinical profiles

1) NSIP /IPF

Clinical presentation and the distribution of disease on HRCT scanning is

similar to that of IPF but ground glass attenuation tends to be more

extensive than in IPF and honeycombing is rarely present. Treatment is

similar to that of IPF and is based on the hope of slowing orpreventing

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disease progression in most cases rather than achieving regression of

disease.

2) NSIP/COP

Initial high-dose steroid regimen is recommended.Steroid dose of 1 mg/kg

of oral prednisolone for several months and then assessed for evidence of

objective response on PFT or HRCT.

Long-term treatment may be required to prevent progression of

fibroticdisease.

3) NSIP/HSP

Similar to that of HSP; the introduction and continuation of treatment

calibrated against disease behaviour.

Immunosuppresants l ike Azath iopr ine,Cyclophosphamide,

mycophenolate mofetil may be considered in a minority of cases.

Rheumatoid arthritis is the most common CTD associated with ILD, while

systemic sclerosis is much less prevalent than RA but is more commonly

complicated by ILD. NSIP is the predominant histological diagnosis in CTDs.

In the diagnosis of CTD ILD, a rheumatologist should also be included in the

multidisciplinary discussion team

Rheumatoid arthritis

ILD in RA may result from the disease itself or as a consequence of its

treatment (eg: methotrexate-induced pneumonitis). A significant smoking

history also increase the risk of developing ILD.

Treatment

1. Oral corticosteroids (Tab prednisolone 0.5 mg/kg/day)

a. May be started at a dose of 0.5mg/kg/day

b. May be tapered off to 10mg /day or 20mg alternate day as a

maintenance dose.

2. Immunosuppressant –

a. Cyclophosphamide (1 – 1.5mg/kg)

b. Azathioprine (2.5mg/kg/day)

c. D-penicillamine (125-250mg/day)

In case of non-responsiveness to steroid.

3. Cyclosporin A (5mg/kg/day)has been useful as a steroid-sparing

agent.

10.7. Connective tissue disease related ILD

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4. Anti-TNF alpha therapy in severe case of RA-ILD

Treatment of methotrexate induced pneumonitis

Withdrawal of methotrexate

Oxygen therapy

Corticosteroids

Cyclophosphamide is used in severe cases.

Treatment

l Corticosteroids, usually with oral prednisolone (0.75–1.0

mg/kg/day) with gradual tapering.

l Fulminant disease may require high-dose intravenous

methylprednisolone (1.0 g/day for 3 days).

l Immunosuppressant or cytotoxic agents, cyclophosphamide (1 -

1.5mg/kg), tacrolimus (0.075mg/kg daily), mycophenolatemofetil

(dose 1-3gm/d)

l Rituximab

v If not responding to steroids.

Systemic sclerosis

1) Low-dose corticosteroid therapy (prednisolone 10 mg daily)

2) Immunosuppressive agent- oral cyclophosphamide, at a dose of

1.0–1.5 mg/kg.

Sjogren's syndrome

Treatment

1. Corticosteroids are the main mode of treatment.

2. Cytolytic therapy such as Azathioprine (2.5mg/kg/day) or

Cyclophosphamide (1 -1.5mg/day) may be used.

3. Cyclosporine (5mg/kg/day) is recommended in steroid – resistant

cases.

4. Rituximab, an anti- CD20 antibody may be recommended in selected

patients.

10.8. Polymyositis-dermatomyositis

Treatment

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Systemic lupus erythematosis

Treatment –

1) Low dose steroids

2) Azathioprine (2.5mg/kg/d) &mycophenolatemofetil (1-3g/d)-

depending upon underlying histology)

Sarcoidosis

Sarcoidosis is a multisystem disorder characterized by noncaseating

granulomatous inflammation at sites of disease.

Treatment

Tr e a t m e n t s h o u l d b e c o n s i d e r e d f o r p a t i e n t s w i t h :

a) Deteriorating lung function over 3–6 month intervals;

b) Deteriorating radiological changes;

c) Significant pulmonary symptoms of cough, shortness of breath,

chest pain or haemoptysis.

Treatment

1. Corticosteroids is the main form of treatment.

Treatment varies from between 15–40 mg prednisolone / prednisone

and 4– 32 mg methylprednisolone given for 3–24 months.Alternate

day therapy is also used

2. Bisphosphonates should be given to prevent and treat steroid

induced osteoporosis

3. Immunosuppressive drugs can be used both as treatment and as

steroid-sparing agents. These include methotrexate, cyclosporin A,

h y d r o x y c h l o r o q u i n e , a z a t h i o p r i n e , c h l o r a m b u c i l ,

cyclophosphamide, leflunamide, pentoxifylline, thalidomide,

infliximab and etanercept.

4. Lung transplantation- lung transplantation has been considered in

end stage sarcoidosis.

Cryptogenic Organising Pneumonia (COP)

Corticosteroid therapy has been the rule, with the occasional addition of

azathioprine, Cyclophosphamide or cyclosporine in refractory cases.

Recommended corticosteroid regimen is

Prednisolone 0.75 mg/kg for 4 weeks followed by 0.5 mg/kg for 4 weeks, 20 mg

daily for 4 weeks; 10 mg daily for6 weeks; 5 mg daily for 6 weeks and gradually

tapered off

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Hypersensitivity pneumonitis

Avoidance of allergen is most important mode of treatment

Persisting symptoms despite antigen withdrawal are an indication to introduce

oral corticosteroids (0.5 mg/kg/day) until symptoms and radiographic changes have

resolved.

Pulmonary langerhan's cell histiocytosis

An uncommon smoking related ILD that primarily affects young adults and is

characterised by abnormal organ infiltration by Langerhans's cells. It may be

associated wi th systemic mani festat ions l ike aneurysmal bone

cyst,diabetesinsipidus etc.

l Investigations- Apartfrom routine Investigations for

ILD(HRCT,PFT,DLCO), Bronchoscopy and BAL Langerhans cell >

5%

l Birbeck granule in EMS, CD 1a/S100 Ag +ve. Langerin in Birbeck

granule: (CD 207+).

Definitive diagnosis:

Based on clinicopathological evidence with microscopic examination and

atleast one of the following Immunological staining

LANGERIN, CD1a ,Birbeck granules on EMF

Treatment:

l Smoking cessation – first step

l Watchful waiting in a- or minor symptomatic patient.

l Systemic steroid therapy in symptomatic patients.

l Chemotherapy (eg: cladribine) in progressive disease.

l RADIOTHERAPY for symptomatic bone lesions may be palliative

l LUNG TRANSPLANTATION: for selected patients with end stage

disease or severe pulmonary hypertension.

l PLEURODESIS: in patients with recurrent pneumothorax.

LAM is a multisystem disorder, predominantly affecting women, which is

characterised by cystic lunglesions,abdominalangiomyolipomas[AML],

lymphatictumours and chylous effusions.

10.9. Pulmonary lymphangioleiomyomatosis

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l Investigations-In addition to the usual investigations for ILD,

VEGF D > 800 pg/mm in blood.

l Circulating LAM cell - (in blood, pleural fluid etc.) react with HMB

45.

Treatment:

LAM is considered to be a low-grade malignancy and drugs targeting

signalling pathways that are considered important in the pathogenesis of

the disease may turn out to be effective.

General measures

l Educate patient.

l Weight control.

l Avoidance of sports martial arts.

l Avoidance of oestrogen containing drugs & phytoestrogen food.

Targeted therapies

l Anti estrogen therapy: oopherectomy, progesterone and

gonadotropin releasing hormone analogues

l Mtor C1 Inhibitors: Sirolimus, Everolimus

l Starting dose of sirolimus is 2mg/d

l Mtor C2 Inhibitors: Simvastatin

l Matrix Metalloproteinase Inhibitors: Doxycycline

l Inhibitors Of Autophagy: Hydroxychloroquine

l Aromatase inhibitor: LETROZOLE

l VGEF inhibitors

Treatment of complications

Pneumothorax: Chemical sclerosis, pleurectomy, mechanical abrasion and talc

poudrage are most effective

Chylous Effusion and Lymhangioleiomyomas:

Low fat diet, pleura peritoneal or peritoneal-venous shunts, sirolimus

Angiomyolipomas: Selective embolization of tumor, sirolimus

Lung Transplantation: considered when FEV1 and DLCO are less than

30% predicted and the patient is on continuous supplemental oxygen and

unable to carry out activities of daily living or surgical pleurodesis by video

assisted thoracoscopy.

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Respiratory bronchiolitis interstitial lung disease

Diagnosis is based on typical HRCT finding in a current smoker or who recently

quit smoking.

Investigations- in addition to radiology and spirometry

BAL: pigment laden macrophages.

TREATMENT

l Smoking cessation

Desquamative interstitial pneumonia

Rare disease

Affect smokers in 4th to 5th decade.

Association with Infection, Organic dust exposure, Marijuana addicts, mutation

in SP-C,SP-B. TREATMENT

l Good prognosis on smoking cessation.

l Progressive & symptomatic cases - Corticosteroids x 6-9 m.

l Macrolide as steroid sparing agent.

l Lung transplantation

Lymphoid interstitial pneumonia

l Female >50 yr.

l Associations: Immune deficiency, HIV, Autoimmune diseases

(Sjogrens,thyroiditis), Idiopathic (<20%).

Treatment

l Idiopathic /CTD-LIP -potential benefit for Corticosteroids (1mg/kg

over 8-12 weeks and taper over several months)

&Immunosuppressive (cyclosporine or azathioprine)

l HIV LIP – HAART,

Corticosteroids trial may be given

General management strategies in ild

l All patients with ILD should have access to a multidisciplinary

team based in a regional centre with expertise in ILD.

l Patients with ILD who are current smokers should receive

opportunistic smoking cessation advice from healthcare

professionals and this advice should be recorded in the clinical

notes.

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l Patients with ILD should have access to a local pulmonary

rehabilitation programme.

l Patients with clinically significant resting hypoxemia (resting

SpO2<88%) should receive long term oxygen therapy.

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Section XI

Long Term Oxygen Therapy

Section XI

11. Long-term Oxygen Therapy

11.1. Use of long-term oxygen therapy in patients with chronic obstructive pulmonary disease

11.2. LTOT in patients with ILD

LTOT can be defined as oxygen used for at least 15 h per day in chronically

hypoxemic patients.

Chronic hypoxaemia is defined as a PaO2 ≤ 54.75 mmHg or, in certain clinical

situations, PaO2 ≤60kPa.

LTOT is delivered via an oxygen concentrator.

LTOT addresses specific physiological inclusion criteria as outlined below:

Ø Patients with stable chronic obstructive pulmonary disease

(COPD) and a resting PaO2 ≤ 54.75 mmHg or SaO2 at or

below 88% should be assessed for long-term oxygen therapy

(LTOT) which offers survival benefit and improves pulmonary

haemodynamics

Ø LTOT should be ordered for patients with stable COPD with a

resting PaO2 between 55mmHg and 60 mmHg or SaO2 88%

with evidence of peripheral oedema, polycythaemia

Ø (Haematocrit >55%) or pulmonary hypertension.

Ø LTOT should be ordered for patients with resting hypercapnia if

they fulfil all other criteria for LTOT.

Ø LTOT should be ordered for patients with interstitial lung disease

(ILD) with a resting PaO2 ≤54.75 mmHg.

Ø LTOT should be ordered for patients with ILD with a resting PaO2

≤60 mmHg in the presence of peripheral oedema, polycythaemia

(haematocrit ≥55%) or evidence of pulmonary hypertension.

Ø Patients with ILD who experience severe breathlessness could be

considered for palliative oxygen therapy.

LTOT in patients with pulmonary hypertension

Ø LTOT should be ordered for patients with pulmonary hypertension,

including idiopathic pulmonary hypertension, when the PaO2 is ≤60 mmH.

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LTOT in patients with neuromuscular or chest wall Disorders

Ø Non-invasive ventilation (NIV) should be the treatment of choice for

patients with chest wall or neuromuscular disease causing type 2

respiratory failure. Additional LTOT may be required in case of

hypoxaemia not corrected with NIV

Patients with a resting stable oxygen saturation (SpO2) of ≤ 92% should be

referred for a blood gas assessment in order to assess eligibility for LTOT.

In patients with clinical evidence of peripheral oedema, polycythaemia

(haematocrit ≥55%) or pulmonary hypertension, referral for LTOT assessment may

be considered at SpO2 levels ≤94% to identify patients with a resting PaO2 ≤60

mmHg

Patients should undergo formal assessment for LTOT after a period of stability

of at least 8 weeks from their last exacerbation.

Patients should not normally have LTOT ordered at the time of an acute

exacerbation of their underlying condition. However, if home oxygen is ordered (e.g.

at hospital discharge), it should be limited to patients with a SpO2 of ≤92%, who are

breathless, and unable to manage off oxygen.

Assessment using arterial blood gases and capillary blood gases

Ø Patients being assessed for LTOT should undergo initial

assessment for suitability using arterial blood gases (ABG)

sampling.

Ø Patients assessed for LTOT during a period of apparent clinical

stability should undergo two ABG measurements at least 3 weeks

apart, before the need for LTOT can be confirmed.

Ø Patients undergoing LTOT assessment should be reassessed with

ABG after oxygen titration is complete to determine whether

adequate oxygenation has been achieved without precipitating

respiratory acidosis and/or worsening hypercapnia.

Ø For oxygen titration during LTOT assessment, capillary blood

gases (CBG) sampling can be used in place of ABG sampling for

re-measuring PaCO2 and pH at different oxygen flow rates.

Ø For oxygen titration during LTOT assessment, cutaneous

capnography can be used in place of ABG sampling for re-

11.3. Assessment of patients for LTOT

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measuring PaCO2 alone but not pH at different oxygen flow rates.

Assessment using pulse oximetry

Ø Patients potentially requiring LTOT should not be assessed using

pulse oximetry alone.

Ø Ambulatory and nocturnal oximetry may be performed to allow

more accurate flow rates to be ordered for exercise and sleep,

respectively.

LTOT hours of use

Ø LTOT should be ordered for a minimum of 15 h per day, and up to

24 h per day may be of additional benefit.

LTOT flow rates

Ø Patients eligible for LTOT should be initiated on a flow rate of 1

L/min and titrated up in 1 L/min increments until SpO2 >90% at 20

minutes intervel. An ABG should then be performed to confirm that

a target PaO2 ≥60 mm Hg at rest has been achieved.

Ø Non-hypercapnic patients initiated on LTOT should increase their

flow rate by 1 L/min during sleep in the absence of any

contraindications.

Ø Patients initiated on LTOT who are active outdoors should receive

an ambulatory oxygen assessment to assess whether their flow

rate needs increasing during exercise.

Follow-up of LTOT patients

Ø LTOT patients should receive follow-up at 3 months after LTOT has

been ordered, which should include assessment of blood gases

and flow rate to ensure LTOT is still indicated and therapeutic.

Ø LTOT patients should receive follow-up visits at 6– 12 months after

their initial 3-month follow-up, which can be either home based or

in combination with hospital visits.

Ø Follow-up visits should be conducted by a specialist home oxygen

assessment team with the necessary skills to deliver patient

education and manage withdrawal of home oxygen.

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Ambulatory Oxygen Therapy in patients eligible for LTOT

AOT assessment should only be offered to patients already on LTOT if they are

mobile outdoors.

Ø AOT should be offered to patients for use during exercise in a

pulmonary rehabilitation programme or during an exercise

programme following a formal assessment demonstrating

improvement in exercise endurance.

Nocturnal oxygen therapy

l Only in those with CF, Neuro-muscular disorders, OSA & ILD in

ventilatory failure

l Should be used along with NIV.

Mode of delivery

l Long term oxygen therapy may be delivered via oxygen

concentrator or oxygen cylinder.

l For long term use, oxygen concentrators pose definite advantage

over cylinders.

l In areas where electric supply is erratic, oxygen concentrator with

battery backup & supportive high power UPS may be considered.

l Accessories to be used – pulse oxymeter, UPS.

l Nasal cannula is the first choice for oxygen administration.

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Section XII

Tuberculosis

Section XII

12. Tuberculosis

Tuberculosis is not dealt in detail in this document as the RNTCP

guidelines extensively cover the diagnosis and treatment of TB and it is

expected that all doctors follow the RNTCP guidelines. A brief summary of the

diagnosis and treatment of TB is provided in this chapter.

Tuberculosis remains a major public health problem in India and the

World with about 10.4 million new cases in the world every year. India is the

highest TB country in the world with an incidence of 2.79 million and with

435,000 mortality every year. Kerala state has an annual notification of total

TB patients of 20969 in the government sector and the private sector notified

26324 cases (TB India 2017).

Worldwide the TB control strategy is now moving to the END TB strategy,

and as part of this and the sustainable development goals (SDGs), many

countries in the world, including India, are now moving towards TB

elimination. One of the key targets for the END TB strategy is reduction of

mortality due to TB. For this, early diagnosis of TB as well as early diagnosis of

Rifampicin resistance is believed to be crucial. As such, the country is now

moving towards “Universal DST”, which in the Indian context means offering

at least Rifampicin resistance testing, primarily through CBNAAT, to all TB

patients.

Pulmonary TB is the major form of TB, however extrapulmonary TB is also

not too uncommon. TB is suspected in persons with cough more than two

weeks. However other symptoms like fever, weight loss, night sweats,

hemoptysis, etc should also be kept in consideration.

The diagnostic algorithm for Pulmonary and extra-pulmonary TB are

given in the following pages. This is followed by an algorithm on evaluation for

drug resistance.

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Figure 12.1. Diagnosis of Pulmonary TB

Figure 12.2. Diagnosis of Pulmonary TB

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12.3. Diagnosis of pediatric TB

12.1. Treatment of drug sensitive TB

Only a single regime now. All patients with new or retreatment TB, if found to

have drug sensitive TB, are started on a 6 month regime with two months (eight

weeks) of INH, Rifampicin, pyrazinamide and ethambutol followed by four months

(16 weeks) of INH, Rifampicin and ethambutol

Table 12.1 Drug dosages for drug sensitive TB

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This dosing schedule is likely to change in the 2019 update, hence please refer

to the updated dosing schedule in the current RNTCP guidelines. 4

Regimes for drug resistant TB

INH mono / poly resistant TB

l For patients who are found to have H resistant and R sensitive TB,

the regimen recommended regimen is Lfx R Z E for a period of 6

months. (injection free regimen-no separate IP and CP, for

Pulmonary as well as Extra-pulmonary H mono/poly DR-TB

patients)

l Baseline SL-LPA must be done for all patients with H resistance to

check for additional FQ resistance. Substitution of drug with Lzd,

Cfz + Cs.

MDR TB – short MDR regime

1. Inclusion criteria

1. RR-TB patients with no resistance to FQ/SLI

2. Exclusion criteria

1. FL-LPA (inhA), DST (Mfx 2.0 and Z) to be done and switch to longer

regimen if any resistance detected.

2. Other exclusion criteria: Intolerance to drugs being used in the

regimen, pregnancy, EPTB in PLHIV, Disseminated, Meningeal or

CNS-TB.

3. In any early signs of failure or ADR observed, switch to longer

regimen

Regime

Intensive phase h h(4-6) Mfx Km Eto Cfz Z H E

Continuation phase h

(5) Mfx Cfz Z E

Conventional regime

Intensive phase

(6-9) Km Lfx Eto Cs Z E

Continuation phase

(18) Lfx Eto Cs E

This regime is likely to change in the 2019 RNTCP guidelines, hence please refer to

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the 2019 RNTCP guidelines when these are released.

Patients are eligible for the two new drugs, Bedaquiline and Delamanid in the

following scenarios

l Patient not eligible for a shorter MDR-TB regimen for reasons of

resistance, contraindication or tolerability

l MDR/RR-TB with resistance to any/all FQ OR any/all SLI

l XDR-TB

l Mixed Pattern DR-TB including patients who are

v failing any DR-TB regimen or

v have drug intolerance or contraindications or

v who return after interruption or

v emergence of any exclusion criteria for shorter MDR-TB

regimen or

v with extensive or advanced disease and

v others deemed at higher baseline risk for poor outcomes.

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Figure 12.4. Drug sensitivity / resistance based regimes for TB


Section XIII

Lung cancer

Section XIII

13. LUNG CANCER

13.1. Introduction

Preamble

Lung cancer is usually managed by the oncologist in most institutions. Advanced

centres use the services of tumour board for decision making in which a

pulmonologist is a member. These guidelines are intended to provide information to

the Pulmonologist on early diagnosis and proper referral to the concerned specialist.

About 90% of lung cancers are caused by smoking. Now that fewer men smoke,

lung cancer deaths in men have decreased by more than a quarter. However, the

number of women who smoke has risen and deaths from lung cancer in women have

increased.

Only about 5.5% of lung cancers are currently cured. Although the cure rate is

rising slowly, the rate of improvement has been slower than for other common

cancers. There is evidence that outcomes vary in different countries, which among

other factors may be explained by variations in the standard of care.

Recommendations are included on communication, diagnosis and staging,

selection of patients with non-small-cell lung cancer (NSCLC) for treatment with

curative intent, treatment for small-cell lung cancer (SCLC) with curative intent,

managing endobronchial obstruction, managing brain metastases, smoking

cessation, and follow-up and patient perspectives.

Patient-centred care

People with lung cancer should have the opportunity to make informed decisions

about their care and treatment, in partnership with their healthcare professionals. If

patients do not have the capacity to make decisions, healthcare professionals should

interact with his close relatives.

Good communication between healthcare professionals and patients is

essential. It should be supported by evidence-based written information tailored to

the patient's needs. Treatment and care, and the information patients are given about

it, should be culturally appropriate. It should also be accessible to people with

additional needs such as physical, sensory or learning disabilities.

If the patient agrees, families and carers should have the opportunity to be

involved in decisions about treatment and care. Families and carers should also be

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given the information and support they need.

l Choose investigations that give the most information about

diagnosis and staging with least risk to the patient. Think carefully

before performing a test that gives only diagnostic pathology when

information on staging is also needed to guide treatment.

l Sputum cytology is rarely indicated and should be reserved for the

investigation of patients who have centrally placed nodules or

masses and are unable to tolerate, or unwilling to undergo,

bronchoscopy or other invasive tests.

l An X-ray should be performed in the first instance for all patients

presenting with symptoms and signs suggestive of a primary or

metastatic tumour. If the results are negative or inconclusive, either

a bone scan or an MRI scan should be offered. Avoid bone

scintigraphy when PET-CT has not shown bone metastases.

l Patients with known or suspected lung cancer should be offered a

contrast-enhanced chest CT scan to further the diagnosis and

stage the disease. The scan should also include the liver and

adrenals.

l In the assessment of mediastinal and chest wall invasion CT alone

may not be reliable. Other techniques such as ultrasound should be

considered, where there is doubt. Surgical assessment may be

necessary if there are no contraindications to resection.

l Magnetic resonance imaging (MRI) should not routinely be

performed to assess the stage of the primary tumour (T-stage) in

NSCLC. MRI should be performed, where necessary to assess the 3extent of disease, for patients with superior sulcus tumours .

l EBUS-guided TBNA for biopsy of paratracheal and peri-bronchial

intra-parenchymal lung lesions is a relatively safe choice. Ensure

adequate samples are taken without unacceptable risk to the

patient to permit pathological diagnosis including tumour

sub-typing and measurement of predictive markers.

l CT- or ultrasound-guided transthoracic needle biopsy is done in

patients with peripheral lung lesions when treatment can be

planned on the basis of this test. Biopsy any enlarged mediastinal

13.2. Diagnosis and staging

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nodes (≥ 10 mm maximum short axis on CT) or other lesions in

preference to the primary lesion if determination of stage affects

treatment.

l Fibreoptic bronchoscopy is to be considered in patients with central

lesions on CT where nodal staging does not influence treatment.

Enlarged lymph nodes (≥ 10 mm maximum short axis on CT) may

be simultaneously sampled with TBNA (non-ultrasound-guided) if

required for diagnosis.

l PET-CT is the preferred first test after CT showing a low probability

of mediastinal malignancy (lymph nodes 10 mm maximum short

axis on CT) for patients who are potentially suitable for treatment

with curative intent.

l Consider neck ultrasound with sampling of visible lymph nodes or

non-ultrasound-guided TBNA to patients with a high probability of

mediastinal malignancy (lymph nodes > 20 mm maximum short

axis on CT). If neck ultrasound is negative, follow with non-

ultrasound-guided TBNA, EBUS-guided TBNA or EUS-guided

FNA. If non-ultrasound-guided TBNA is negative follow with

EBUS-guided TBNA or EUS-guided FNA.

l Evaluate PET-CT-positive mediastinal nodes by mediastinal

sampling (except when there is definite distant metastatic disease

or a high probability that N2/N3 disease is metastatic [for example,

if there is a chain of lymph nodes with high 18F-deoxyglucose

uptake]).

l Confirm negative results obtained by EBUS-guided TBNA and/or

EUS-guided FNA using surgical staging if clinical suspicion of

mediastinal malignancy is high.

l Confirm the presence of isolated distant metastases/synchronous

tumours by biopsy or further imaging (for example, MRI or PET-CT)

in patients being considered for treatment with curative intent.

Consider MRI or CT of the head in patients selected for treatment

with curative intent, especially in stage III disease.

Multidisciplinary teams

The care of all patients with a working diagnosis of lung cancer should be

discussed at a lung cancer MDT meeting (Tumour board). Rapid access clinics

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should be provided where possible for the investigation of patients with suspected

lung cancer, because they are associated with faster diagnosis and less patient

anxiety.

Smoking cessation

Inform patients that smoking increases the risk of pulmonary complications

after lung cancer surgery. Advise patients to stop smoking as soon as the

diagnosis of lung cancer is suspected and tell them why this is important.

Offer nicotine replacement therapy and other therapies to help patients to

stop smoking in line with Smoking cessation services and Varenicline for

smoking cessation.

Assessment before radiotherapy

A clinical oncologist's in thoracic oncology should determine suitability for

radiotherapy with curative intent, taking into account performance status

and comorbidities.

Surgery for non-small-cell lung cancer

In patients with NSCLC who are medically fit and suitable for treatment with

curative intent, lobectomy is the treatment of first choice. For patients with

borderline fitness and smaller tumours (T1a–b, N0, M0), consider lung

parenchymal-sparing operations (segmentectomy or wedge resection) if a

complete resection can be achieved. More extensive surgery

(bronchoangioplastic surgery, bilobectomy, pneumonectomy) are

considered only when needed to obtain clear margins. Perform hilar and

mediastinal lymph node sampling or en bloc resection for all patients

undergoing surgery with curative intent.

For patients with T3 NSCLC with chest wall involvement who are

undergoing surgery, complete resection of the tumour should be the aim by

either extrapleural or en bloc chest wall resection.

Radiotherapy for non-small-cell lung cancer

Radical radiotherapy is indicated for patients with stage I, II or III NSCLC

who have good performance status (WHO 0,1) and whose disease can be

encompassed in a radiotherapy treatment volume without undue risk of

normal tissue damage.

All patients should undergo pulmonary function tests (including lung

volumes and transfer factor) before having radical radiotherapy for

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NSCLC. Patients who have poor lung function but are otherwise suitable for

radical radiotherapy should still be offered radiotherapy, provided the

volume of irradiated lung is small.

Chemotherapy for non-small-cell lung cancer

Chemotherapy should be offered to patients with stage III or IV NSCLC and

good performance status (WHO 0,1 or a Karnofsky score of 80–100), to

improve survival, disease control and quality of life.

Chemotherapy for advanced NSCLC should be a combination of a single

third-generation drug (docetaxel, gemcitabine, paclitaxel or vinorelbine)

plus a platinum drug. Either carboplatin or cisplatin may be administered,

taking account of their toxicities, efficacy and convenience. Patients who

are unable to tolerate a platinum combination may be offered single-agent

chemotherapy with a third-generation drug.

Docetaxel monotherapy should be considered if second-line treatment is

appropriate for patients with locally advanced or metastatic NSCLC in

whom relapse has occurred after previous chemotherapy.

Biological agents such as gefitinib or erlotinib may be considered for non-

small-cell lung cancer having EGRF mutation detected in the

histopathological specimen.

Combination treatment for non-small-cell lung cancer

Patients with stage I–III NSCLC who are not suitable for surgery need to be

assessment by a clinical oncologist specialising in thoracic oncology for

radiotherapy with curative intent. Consider chemoradiotherapy for patients

with stage II or III NSCLC who are not suitable for surgery. Consider

potential benefit in survival with the risk of additional toxicities before this

treatment.

Consider postoperative chemotherapy in patients with good performance

status (WHO 0 or 1) and T2–3 N0 M0 NSCLC with tumours greater than 4

cm in diameter. Offer a cisplatin-based combination chemotherapy

regimen for adjuvant chemotherapy. Ensure eligible patients have the

benefit of detailed discussion of the risks and benefits of adjuvant

chemotherapy.

Treat Pancoast tumours in the same way as other types of NSCLC. Offer

multimodality therapy according to resectability, stage of the tumour and

performance status of the patient.

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Assessing patients with small-cell lung cancer

All patients with small-cell lung cancer (SCLC) should be assessed by a

thoracic oncologist within 1 week of deciding to recommend treatment.

First-line treatment for limited-stage disease small-cell lung cancer

Patients with limited-stage disease (T1–4, N0–3, M0) should receive four

to six cycles of cisplatin-based combination chemotherapy. Consider

substituting carboplatin in patients with impaired renal function, poor

performance status (WHO 2 or more) or significant comorbidity.

Concurrent chemoradiotherapy may be offered to patients with limited-

stage disease (T1–4, N0–3, M0) and a WHO performance status of 0 or 1 if

they present with disease that can be encompassed in a radical thoracic

radiotherapy volume. Start the radiotherapy during the first or second cycle

of chemotherapy.

Sequential radical thoracic radiotherapy is given to patients with limited-

stage disease SCLC (T1–4, N0–3, M0) who are unfit for concurrent

chemoradiotherapy but who respond to chemotherapy.

Surgical treatment for patients with small-cell lung cancer

Consider surgery in patients with early-stage SCLC (T1–2a, N0, M0).

First-line treatment for extensive-stage disease of small-cell lung cancer

Platinum-based combination chemotherapy is preferred in patients with

extensive-stage disease SCLC (T1–4, N0–3, M1a/b – including cerebral

metastases) if they are clinically fit. Assess the patient's condition before

each cycle of chemotherapy for extensive-stage disease SCLC and offer

up to a maximum of six cycles, depending on response and toxicity.

For patients with extensive-stage disease SCLC, thoracic radiotherapy

should be considered after chemotherapy if there has been a complete

response at distant sites and at least a good partial response within the

thorax.

Prophylactic cranial irradiation in small-cell lung cancer

Prophylactic cranial irradiation is offered at a dose of 25 Gy in 10 fractions

to patients with limited-stage disease SCLC and WHO performance status

2 or less, if their disease has not progressed on first-line treatment.

Prophylactic cranial irradiation is given to patients with extensive-stage

disease SCLC and WHO performance status 2 or less, if their disease has

not progressed on first-line treatment.

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Second-line treatment for patients with small-cell lung cancer that has

relapsed after first-line treatment

SCLC that has relapsed after first-line treatment is assessment by a

thoracic oncologist. Inform patients whose disease has not responded to

first-line treatment that there is very limited evidence that second-line

chemotherapy will be of benefit. Treatment with an anthracycline-

containing regimen or further treatment with a platinum-based regimen to a

maximum of six cycles is the choice in such situations. Offer radiotherapy

for palliation of local symptoms to these patients.

Supportive and palliative care

Supportive and palliative care of the patient should be provided by general

and specialist palliative care providers. Patients who may benefit from

specialist palliative care services should be identified and referred without

delay.

Palliative radiotherapy

Patients who cannot be offered curative treatment, and are candidates for

palliative radiotherapy, may either be observed until symptoms arise and

then treated, or be treated with palliative radiotherapy immediately.

Managing endobronchial obstruction

When patients have large airway involvement, monitor (clinically and

radiologically) for endobronchial obstruction to ensure that treatment is

g i ven ea r l y. O f fe r ex te rna l beam rad io the rapy and /o r

endobronchialdebulking or stenting to patients with impending

endobronchial obstruction.

Other palliative treatments

Pleural aspiration or drainage should be performed in an attempt to relieve

the symptoms of a pleural effusion. Patients who benefit symptomatically

from aspiration or drainage of fluid should be offered talc pleurodesis for

longer-term benefit.

Non-drug interventions based on psychosocial support, breathing control

and coping strategies should be considered for patients with

breathlessness.

Non-drug interventions for breathlessness should be delivered by a

multidisciplinary group, coordinated by a professional with an interest in

breathlessness and expertise in the techniques (for example, a nurse,

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physiotherapist or occupational therapist). Although this support may be

provided in a breathlessness clinic, patients should have access to it in all

care settings.

Opioids, such as codeine or morphine, should be considered to reduce

cough.

Patients with troublesome hoarseness due to recurrent laryngeal nerve

palsy should be referred to an ear, nose and throat specialist for advice.

Patients who present with superior vena cava obstruction should be

offered chemotherapy and radiotherapy according to the stage of disease

and performance status.

Stent insertion should be considered for the immediate relief of severe

symptoms of superior vena caval obstruction or following failure of earlier

treatment.

Offer dexamethasone to patients with symptomatic brain metastases and

reduce to the minimum necessary maintenance dose for symptomatic response.

Consider palliative whole-brain radiotherapy for patients with symptomatic brain

metastases with good performance status (WHO 0 or 1).

Hypercalcaemia, bone pain and pathological fractures

For patients with bone metastasis requiring palliation and for whom standard

analgesic treatments are inadequate, single-fraction radiotherapy should be

administered. Managing other symptoms: weight loss, loss of appetite, difficulty

swallowing, fatigue and depression.

Other symptoms, including weight loss, loss of appetite, depression and difficulty

swallowing, should be managed by multidisciplinary groups that include supportive

and palliative care professionals.

Follow-up and patient perspectives

Offer all patients an initial specialist follow-up appointment within 6 weeks of

completing treatment to discuss ongoing care. Offer regular appointments

thereafter, rather than relying on patients requesting appointments when they

experience symptoms.

Offer protocol-driven follow-up led by a lung cancer clinical nurse specialist as

an option for patients with a life expectancy of more than 3 months.

Ensure that patients know how to contact the lung cancer clinical nurse

13.4. Managing brain metastases


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specialist involved in their care between their scheduled hospital visits.

The opinions and experiences of lung cancer patients and carers should be

collected and used to improve the delivery of lung cancer services. Patients should

receive feedback on any action taken as a result of such surveys.

1. Jaklitsch MT, Jacobson FL, Austin JHM, et al. The American association for

thoracic surgery guidelines for lung cancer screening using low-dose

computed tomography scans for lung cancer survivors and other high-risk

groups. J ThoracCardiovascSurg 2012;144:33-8 [PubMed] [Google

Scholar]

2. 4. Brodowicz T, Ciuleanu T, Crawford J, et al. Third CECOG consensus on

the systemic treatment of non-small-cell lung cancer. Ann Oncol

2012;23:1223-9 [PubMed] [Google Scholar]

3. Sørensen M, Pijls-Johannesma M, Felip E, et al. Small-cell lung cancer:

ESMO clinical practice guidelines for diagnosis, treatment and follow-up.

Ann Oncol 2010;21Suppl 5:v120-5 [PubMed] [Google Scholar]

4. National Collaborating Centre for Cancer. eds. Lung cancer. The diagnosis

and treatment of lung cancer. London: National Institute for Health and

Clinical Excellence, 2011. [Google Scholar]

13.5. References


Section XIV

Upper airway obstruction

Section XIV

14. Upper airway obstruction

14.1. Major Airway Obstruction

14.2. Causes of Benign and malignant airway obstruction

14.3. Malignant

Major airway obstruction is an uncommon and potentially life threatening

condition. It may be caused by a luminal compromise due to intrinsic pathology or by

extrinsic compression. The upper airway is conventionally described as being made

up of all the structures that conduct air between the carina and the nares. Within the

upper airway pharyngeal airway do not have a bony support and is susceptible to

collapse during sleep.

Benign

l Post-intubation

l Post-tracheostomy

l Anastomotic stricture (lung transplant, sleeve resection, airway

resection)

l Intrinsic airway tumors

l Extrinsic airway tumors

l Infalmmatory

l Infectious

l Foreign body

l Adjacent malignancies

v Lung cancer

v Thyroid cancer

v Esopahgeal cancer

v Mediastinal tumors

l Primary airway tumors

v Carcinoid tumor

v Adenoid cystic carcinoma

v Mucoepidermaoid carcinoma

v Squamous cell carcinoma

l Metastatic tumors

v Breast cancer

v Renal cell carcinoma

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v Melanoma

v Colorectal

v Others

Clinical presentation:

UAO can have acute life threatening presentation resulting in asphyxia.

Sometimes the manifestation is chronic with noisy breathing often misdiagnosed

and treated as asthma. It can also be asymptomatic for long period of time.

Commonest symptoms are breathlessness, noisy breathing. By the time exertional

dyspnea develops UA diameter is already reduced to 8 mm. It becomes around 5

mm when the patient is having stridor. Stridor is more predominant on inspiration

and louder over the neck.

History:

l Dyspnea, onset and progression

l Stridor

l Positional variation of symptoms

l Whether patient wakes at night with difficulty in breathing

l Dysphagia, Drooling

l H/o foreign body aspiration/ Recentintubation

l Any h/o suggestive of anaphylaxis/ infection

l H/o cancer

l Drug overdose

Examination:

l Examine the patient in the position in which they are most

comfortable.

l Check vitals

l Examine neck and oral cavity

l Check for stridor, its respiratory phase and change with

position.Inspiratory stridor suggests extrathoracic airway

obstruction at or above the vocal cords while expiratory stridor

may be due tointrathoracic obstruction. Biphasic stridor is present

in subglottic or tracheal stenosis.

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14.4. Management

Initial management of UAO focus on securing the airway and stabilizing the

patient.

Adequate oxygenation

Sometime bypassing the obstruction by translaryngeal intubation or

tracheostomy is required.

Fibre optic bronchoscope helps to assess the site of obstruction and its

extend. It helps to clear out blood clot or mucous plug obstructing the major

airway. Foreign bodies causing luminal obstruction can be taken out using

grasping forceps or by cryoprobe. During the procedure there can be

desaturation as the bronchoscope further compromises the already

narrowed airway.

With regard to securing the airway , maintaining ventilation, and controlling

hemoptysis rigid bronchoscope is more useful than fibre optic

bronchoscope. The UAO due to PITS can be dilated by serial passage of

bronchoscopes. Intraluminal lesions can be mechanically debulked.

Ablative procedures like endobronchial laser can be performed through

rigid scope. UAO due to extraluminal lesion can treated by airway stent.

For benign causes silicone stents are preferred.

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Figure 14.1 Management of upper airway obstruction

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Annexe II, Secretariat Thiruvananthapuram

Kerala-695001

Department Of Health And Fa ily WelfaremGovernment Of Kerala

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standard treatment guidelines - kerala

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