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.
11
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
15
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
17
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
18
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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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
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>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
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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
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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
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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
STANDARD TREATMENT GUIDELINES - RESPIRATORY DISEASES
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
13.3. Treatment
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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
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the systemic treatment of non-small-cell lung cancer. Ann Oncol
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13.5. References
STANDARD TREATMENT GUIDELINES - RESPIRATORY DISEASES
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
Ke HEALTHrala
Feb
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021