Case 3: Chronic Breathlessness Flashcards
Sympathetic innervation of bronchiolar smooth muscle is mediated by
noradrenaline
Sympathetic innervation of bronchiolar smooth muscle is mediated by noradrenaline acting on beta receptors to cause
bonchodilation
parasymp on lungs
bronchoconstriciton
parasymp receptor and agonist in lungs
acH on muscarinic causes bronchoconstriction
type 1 alveolar cells
simple squamous cells where gas exchange occurs
type 11 alveolar cells
synthesis of surfactant ….10% of cells in alveolar small cuboidal
Pneumocytes
alveolar cells
pulmonary arteries supply
deoxygenated blood from the right ventricle to the alveolar capillary network
Pulmonary veins carry
oxygenated blood from lungs to left atrium
the bronchial arteries supply oxygenated blood from the thoracic aorta to the
lung tissues
the bronchial veins drain deoxygenated blood to the
pulmonary and systemic venous systems
what conditions do you see breathlessness Variation in symptoms at different times of day
Answer(s): Asthma, Asthma/COPD overlap syndrome, Anxiety
Explanation: Diurnal variation in symptoms is a classic feature of asthma
what conditions do you see Night time symptoms breathlessness
Answer(s): Asthma, Asthma/COPD overlap syndrome
Explanation: Nocturnal symptoms are a classic feature of asthma
what conditions do you see symptoms when lying flat breathlessness
cardiac pathology
Explanation: Orthopnoea is a feature of congestive cardiac failure. The doctor could also have asked about paroxysmal nocturnal dyspnoea.
what conditions do you see ankle swelling breathlessness
Answer(s): Cardiac pathology, Pulmonary embolism
Explanation: Bilateral ankle swelling is a sign of cardiac pathology, especially congestive cardiac failure. Unilateral ankle swelling may be an indication of DVT/PE.
what conditions do you see chest pain breathlessness
Answer(s): Cardiac pathology, Pulmonary embolism
Explanation: If the patient answered ‘yes’ to this, you would want to explore this symptom further (for example using a SOCRATES approach) to help determine the likely cause of this pain
what conditions do you see Faintness/lightheadedness breathlessness
Answer(s): Cardiac pathology, Anxiety
Explanation: Cardiac pathology and very classically aortic stenosis can cause breathlessness with lightheadedness. Anxiety may result in lightheadedness or hyperventilation with tingling numbness around the mouth.
what conditions do you see Occupational history breathlessness
Answer(s): Occupational diseases, Asthma, Hypersensitivity pneumonitis
Explanation: There are a number of lung diseases associated with occupational exposure that need to be considered where appropriate. For example, coal miner’s pneumoconiosis, silicosis, beryllisosis, Farmer’s lung (a hypersensitivity pneumonitis). Occupational asthma is a type of asthma caused by exposure to inhaled irritants in the workplace.
what conditions do you see if you have had exposure to asbestos breathlessness
Answer(s): Asbestosis, Malignancy
Explanation: It is well documented that women exposed to asbestos by laundering their husband’s work clothes are at risk of asbestosis and mesothelioma. Asbestos exposure also increases the risk of lung cancer, in particular adenocarcinoma.
what conditions cause breathlessness due to pets
Answer(s): Asthma, Hypersensitivity pneumonitis
Explanation: Asking about pets and exposure to potential asthma-triggering allergens is important in a breathlessness history. Exposure to birds can also cause hypersensitivity pneumonitis in some people.
what condition causes breathlessness due to birds
Answer(s): Hypersensitivity pneumonitis
Explanation: A type of hypersensitivity pneumonitis due secondary to repeated inhalation of avian antigens is seen in bird keepers (sometimes known as ‘Pigeon Fancier’s Lung’).
what conditions causes breathlessness due to smoking
Answer(s): COPD, Malignancy, Cardiac Pathology
Smoking is a risk factor for many respiratory and cardiac pathologies and should always be asked about.
acute and chronic findings of hypersensitivity pneumonitis
Inhaled antigenic organic dusts: Farmer’s lung (moldy hay). Humidifier lung (thermophilic bacteria). Bird-fancier’s lung (avian proteins). Acute and chronic forms. Chronic disease findings: Interlobular and intralobular interstitial thickening. Honeycombing, Traction bronchiectasis. May spare costophrenic angles.
hemoptysis respiratory history
Haemoptysis is always useful to ask about when taking a respiratory history and is associated with a number of pathologies including lung cancer, tuberculosis and pulmonary embolism.
smoking history
Mrs Smith may well have a smoking-related lung disease, therefore it is very important to take a smoking history and to take the opportunity to make every contact count (I.e. have opportunistic conversations about behaviour change). Taking a detailed smoking history entails finding out the following information.
- Are they a current smoker?
- What age did they start smoking?
- Do they smoke cigarettes or roll-ups?
- How many cigarettes a day do they smoke? (If they smoke roll-ups, how much tobacco is used in a week? - half an ounce of tobacco is around 20 cigarettes.)
- Have they ever smoked more or less than they do now?
- Any breaks from smoking?
- Have they ever tried to give up? What was helpful? What were the challenges? Why did they start again?
- Have they tried nicotine replacement therapy before?
- Does anyone else in the house smoke, i.e., are they a passive smoker (living with other people who smoke also makes it more difficult to quit)?
- Is quitting smoking something they would consider now?
In consultations where smoking is important, but time is very short, we recommend the approach of ‘Ask, Advise, Act.’ For more information and a short e-learning package see the National Centre for Smoking Cessation and Training’s ‘Very Brief Advice on Smoking’.
what causes hyper inflated chest and conditions you see it in
Hyperinflated lungs can be caused by blockages in the air passages or by air sacs that are less elastic, which interferes with the expulsion of air from the lungs. Hyperinflated lungs are often seen in people with chronic obstructive pulmonary disease (COPD) — a disorder that includes emphysema.
polyphonic expiratory wheeze
Polyphonic wheezing consists of multiple musical notes starting and ending at the same time and is typically produced by the dynamic compression of the large, more central airways. Polyphonic wheeze is confined to the expiratory phase only.
Asthma vs COPD
Asthma usually involves acute (temporary) increases in airway resistance whereas COPDs are associated with chronic (long-lasting) increases in airway resistance
findings in COPD CXR
hyperinflation, flattened diaphragm, enlarged retrosternal space, dec. pulmonary vascular markings
LFT and COPD
Lung function tests (spirometry) are the only investigations that can definitively diagnose COPD, and can also determine whether there is any element of reversibility and enable classification of severity of COPD. It might alternatively reveal another diagnosis such as asthma or restrictive lung disease.
D-dimer test
is a global marker of coagulation activation and measures fibrin degradation products produced from fibrinolysis (clot breakdown). The test is used for the diagnosis of DVT when the patient has few clinical signs and stratifies patients into a high-risk category for reoccurrence. Useful as an adjunct to noninvasive testing, a negative D-dimer test can exclude a DVT without an ultrasound.
hallmark symptoms of COPD
Shortness of breath
Chronic cough
Sputum production
Other features include:
Winter exacerbations
Wheeze
extra signs of COPD
Tar-staining (fingers) – in developed countries, COPD is caused almost entirely by smoking but may also first present after an individual has stopped smoking
Chest hyperexpansion – a typical ‘barrel-shaped’ chest develops over time due to air trapping
Pursed lip breathing – this enables a patient to reduce their respiratory rate by increasing their period of expiration; it creates resistance to expiratory airflow and development of a positive expiratory pressure in the airways, reducing airway collapse and aiding ventilation
Accessory muscle use (neck/shoulder) – air trapping and hyperinflation impede effective chest expansion by the diaphragm and intercostal muscles, so the patient uses accessory muscles including the sternocleidomastoid, scalene, trapezius and abdominal muscles to aid ventilation
Peripheral oedema (ankles) – indicates right-sided heart failure due to cor pumonale
Palpable liver – may be due to hyperinflation of the lungs or congestive heart failure
Auscultation – you may hear reduced breath sounds, reduced heart sounds, tachypnoea and wheeze; during an exacerbation there may also be crepitations
Chest wall movement – reduced lateral (‘bucket handle’) chest expansion and increased vertical (‘pump handle’) chest expansion
alpha-1 antitrypsin deficiency
Panacinar emphysema
Intrahepatic accumulation of AAT molecules leading to cirrhosis
PAS stain +
COPD inflammation
Inhalation of noxious particles
Mediators released cause damage to lung tissue.
Airways inflamed
Parenchyma destroyed
goblet cell hyperplasia
causes sputum. COPD, also ariway narrowing and alveolar destruction - breathlessness and wheeze
gold standard for diagnosing COPD
Spirometry is the gold standard investigation for diagnosing COPD and grading severity of COPD. Spirometry machines measure the volume and flow rate of inspiration and expiration, and can therefore be used to diagnose obstructive and restrictive lung diseases. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) developed a classification system for severity of COPD disease based on spirometry. NICE guidelines were updated in 2018 to mirror this classification system.
mild >80%
moderate 50-80%
severe 30-50%
very severe <30%
cardinal feature of COPD
airway obstruction
COPD FEV1/FVC
<70%
why does Premature airway collapse happen in copd
structure damaged - airway not mantained
COPD staging
GOLD Criteria
FEV1/FVC of less than 70%
Then FEV1 of:
I (mild)- more than 80
II (mod)- 50-79
III (severe)- 30-50
IV (very severe)- less than 30
Obstructive flow volume loop in spirometry
short and wide loop
Restrictive flow volume loop
skinny and tall
COPD normal progression
Progressive decline in lung function
Progressive dyspnoea and disability
Right ventricular failure (‘cor pulmonale’)
Exacerbations become more frequent and contribute to morbidity and disability
cor pulmonale
right ventricular hypertrophy and heart failure due to pulmonary hypertension
fundamentals of COPD care
no smoking
vaccinations
physio
personalized plan
comorbities treat
COPD care
inhaled therapy oral add on
surgical therapy
oxygen
smoking cessation drugs
Drugs that blunt cravings for nicotine, including buproprion and varenicline
buproprion moa
inhibits reuptake of NE and dopamine
nicotinic antagonist
varenicline moa
partial agonist and antagonist at a4B2 nicotinic ACh receptors in the brain
inhaled therapies for COPD
SABA beta two receptors - bronchodilation
name some SABAs given to COPD patients
Albuterol
Levalbuterol
Pirbuterol
name a SAMA given to COPD patients
Ipratropium - Short acting muscarinic antagonist
what do we give for COPD treatment for those with no ashmatic features
LABA and LAMA
LABAs given to COPD patients
Salmeterol
Formoterol
LAMAs given to COPD patients
Tiotropium
Aclidinium
Umeclidinium
Glycopyrrolate
what do we give COPD patients with asthmatic features
LABA and ICS
name some ICS inhalers
beclamethasone, fluticason, budesonide
Step 3 COPD Treatment
LABA + LAMA + ICS
oral add ons COPD
theophylline, mucolytic
name a mucolytic
Carbocisteine
what is Theophylline
bronchodilator
name some oral corticosteroids
prednisone, methylprednisolone
oral corticosteroids MOA
Decrease inflammation by reducing the activity of the immune system
Oxygen therapy for COPD
PaO2 < 55 mmHg (70%) or right hear failure, polycythemia, or impaired neuropsychiatric function, pulmonary hypertension
Generally stage IV
2 L/min
polycythemia
A disorder characterized by an abnormal increase in the number of red blood cells in the blood
Surgery for COPD
lung reduction surgery to remove damaged lung tissue or lung transplant
Bullectomy
Used for emphysema
Large bullae are resected to improve lung function
phenotype of patients who get exacerbations of COPD
can be pneumonia on CXR or not
bacteria or virus
AE of COPD symptoms
runny nose
breathlessness
cough
sputum
sputum purulence
ankle swelling
Coryzal symptoms
snotty/runny nose
ae of COPD investigations
CXR ECG
gas exchange
FBC, U+E
CRP
Management of COPD Exacerbations
SABAs (specifically inhaled, either alone or in combination with inhaled anticholinergics) are preferred for bronchodilation during COPD exacerbations
Systemic glucocorticoids
Antibiotics if purulent
Supplemental oxygen to maintain an oxygen saturation of 88% to 92%
COPD blood gases
Arterial Blood Gases (ABGs)
- Arterial pO2 (80-100 mm Hg)
- Arterial pCO2 (35-45 mm Hg)
Hemoglobin O2 saturation
- SaO2 (95-100%)
type 1 and type 2 resp failure
Type 1 respiratory failure
failure of oxygenation
PaO2 <8 (SaO2 <90%)
increased resp drive leads to increased ventilation
PCO2 drops
Causes include diffusion abnormalities, v/q mismatch, low inspired O2
ONE = Oxygen low, Not Equal V/Q
Type 2 respiratory failure
failure of ventilation, cannot increase ventilation
PaO2 <8, pCO2 rises >6.7, pH falls <7.35
CO2 dissolves in blood to produce carbonic acid
Causes include airway obstruction, hyperexpanded lungs, thoracic cage problems, weaknesss of resp muscles
TWO = Thoracic cage probs/hyperexpansion, Weakness in muscles, Obstruction
type 2 resp failure and copd
In COPD the elastic recoil of the lungs is lost. This causes gas trapping and reduced excretion of carbon dioxide. Sputum retention also means there is less surface area for gas exchange. In the blood, the carbon dioxide combines with water to form carbonic acid.
In an acute setting, the increased acid levels in the blood would lower the pH levels and the patient would become unwell very quickly.
However, when carbon dioxide retention is slowly progressive, as is often the case in chronic COPD, the body can compensate for this by utilising the bicarbonate buffer system of the blood. The kidneys are stimulated to reabsorb more bicarbonate, which acts as a base and neutralises the carbonic acid, thus restoring the pH back to the normal range.
clinical features of hypercapnia
dilated pupils
altered mental state
asterixis
bounding pulse
tachyopnea
raised JVP
flushed skin
nipple shadows
May be visible at the level of the fourth or fifth anterior rib spaces and may occasionally mimic nodules or masses in the chest. May be differentiated with markers or oblique projections of the chest
- google the image
COPD on CXR
hyperinflation, flattened diaphragm, enlarged retrosternal space, dec. pulmonary vascular markings
- check google
P pulmonale
RA enlargement, almost always related to pulmonary system; usually causes backup into the ventricle & atria, causing enlargement of atria
COPD and cancer
The presence of emphysema has been shown to confer a significant risk of developing lung cancer, particularly squamous cell carcinoma and SCLC (20). Overall, people with COPD have an increased risk (4- to 6-fold) of developing lung cancer, independent of smoking history, age and sex
nail clubbing associated with
Nail clubbing can be seen in lung cancer, suppurative lung diseases (bronchiectasis, cystic fibrosis) and interstitial lung diseases.
nail clubbing mechanism
An increase in hypoxia may activate local vasodilators, consequently increasing blood flow to the distal portion of the digits; however, in most cases, hypoxia is absent in the presence of clubbing, and many diseases with noted hypoxia are not associated with clubbing
interstitial lung disease
refers to a group of almost 200 disorders that cause inflammation and scarring of the alveoli and their supporting structures
suspected interstitial lung disease investigations
HRCT and spirometry
what is FEV1/FVC
Ratio that is useful in distinguishing between restrictive & obstructive diseases
High FEV1/FVC indicates
restrictive disease
Transfer factor
converts normal lymphocytes into antigen-sensitized cells
FEV1 ILD
In ILD a restrictive pattern of lung function is seen. FVC and FEV1 are low but proportionally so, so that the FVC/FEV1 ratio remains normal. Lung volumes are also reduced, as is the transfer factor, which measures the lungs’ ability to ‘soak up’ oxygen.
CT of interstitial lung disease
basal fibrosis
honeycombing
honeycombing
small (6 to 10 mm) cystic spaces with thick (1 to 3 mm) walls. usually have shared walls . Usually in posterior subpleural regions. End-stage pulmonary fibrosis: IPF (UIP). Chronic hypersensitivity pneumonitis. Occasionally sarcoidosis. (google)
what is pulmonary function test for ILD
FEV1
transfer factor measurement
Normal DLCO: >75% of predicted, up to 140% Mild: 60% to LLN (lower limit of normal) Moderate: 40% to 60% Severe: <40
A gas transfer test measures how your lungs take up oxygen from the air you breathe. The result of the test is called the transfer factor, or sometimes the diffusing capacity.
is Fibrosis is a cardinal feature of Interstitial Lung Disease?
No Different forms ILD can be categorised as primarily inflammatory or primarily fibrotic. The inflammatory conditions may eventually lead to fibrosis if left unchecked. Distinguishing between the two is important with respect to the treatments available.
diagnosis of exclusion
elimination of all competing possibilities
name some Idiopathic ILD
Idiopathic pulmonary fibrosis
sarcoidosis
cryptogenic organising pneumonia
Known causes of interstitial lung disease
Occuptaional - asbestosis/silicosis
enviromental - hypersensitivities - pigeons
immune - connective tissue disease
smoking - DIP (Desquamative Interstitial Pneumonia) and RBILD (Respiratory bronchiolitis–associated interstitial lung disease)
ILD patient history
Occupational history – asbestos exposure, stone working (silicosis), farmers (mould exposure)- Other environmental exposures – birds, hot tubs- Smoking history- Medication history – a thorough medication history is very important as a number of drugs are known precipitants of lung fibrosis- Symptoms and signs of connective tissue disease – Raynaud’s, swollen/stiff joints, dry eyes, dry mouth, mouth ulcers, photosensitive rash, skin changes, sclerodactyly, telangiectasia, periungal erythema, dysphagia- Their perspective: exploring what they think might be going on, any worries they have, or hopes for treatment – this provides space for this patient to be known as an individual, may give clues to uncovered aspects of the history and indicates how sharing information about diagnosis/next steps should be tailored. Gathering the patient perspective increases patient satisfaction, enables better treatment adherence, reduces medication prescribed, and reduces likelihood of mistakes.
drugs that can cause ild
amiodarona, ntrifurantoin, digoxin
Nitrofurantoin moa
Inhibits various bacterial enzymes and damages bacterial DNA
treatment for ILD
antifibrotics, pulmonary rehabilitation, oxygen assesment
drugs extend life by 2-3 yrs
antifibrotics
prevent lysis of fibrin. (Amicar)
pirfenidone, nintedanib
antifibrotics side effects
Patients treated with pirfenidone or nintedanib have reported a number of different side-effects, the vast majority being gastrointestinal (nausea, dyspepsia, diarrhoea) and skin-related events (rash, photosensitivity reaction) in the case of pirfenidone, and mainly gastrointestinal (diarrhoea and vomiting)
lymphadenopathy cxr
swollen
check google
Sarcoidosis
chronic inflammatory disease in which small nodules (granulomas) develop in lungs, lymph nodes, and other organs
lymphoma
malignant tumor of lymph nodes and lymph tissue
sit lamp examination
stereoscopic magnified view of the anterior eye structures in detail, includes cornea
uveitis
inflammation of the uvea causing swelling and irritation
Uveoparotid fever
Heerfordt’s syndrome
acute uveitis, fever, parotid gland swelling
features of neurosarcoidosis
4%- 7% of pts; CN lesions most common; Facial palsy (7th Cranial Nerve) most frequent presentation
It represents a form of neurosarcoidosis, and in some patients a facial palsy is also seen. It is a relatively rare acute presentation of sarcoidosis, although involvement of the eyes, nervous system or salivary glands in isolation all occur frequently in sarcoidosis.
features of Acute sarcoidosis
- Erythema Nodosum
- Bilateral Hilar Lymphadenopathy
- Arthritis
- Uveitis, parotitis
- Fever
Sarcoidosis epidemiology
Younger black females in their 30s-40s
Erythema nodosum
painful nodules on anterior shins due to subcutaneous inflammation
Lofgren’s syndrome (presentation and epidemiology)
Presentation of Sarcoidosis
- Hilar lymphadenopathy
- Erythema nodosum
- Polyarthritis
- Fever
females
scandinaivan or irish women
HLA-B8 gene
will settle with NSAIDS
sarcoidosis systems
order of commoness
resp
skin
eye
thoracic lymp
liver
spleen
neuro
cardiac
Sarcoidosis dermatological symptoms
Dermatologic signs include rash, lesions, color change, and nodule formations just under the skin.
sarcoidosis - ophthalmic manifestations
uveitis, corneal deposits, iritis, vitritis, synechiae
reticuloendothelial sarcoidosis
peripheral lymphadenopathy, hepato and splenomegaly
sarcoidosis musculoskeletal
arthitis acute, chronic with periosteal bone resoprtion
exorcrine sarcoidosis
enlarged salivary glands, xerostomia
xerostomia
dry mouth
Sarcoidosis Cardiac Manifestations
arrythmia, pulonary hypertension, cor pulmonale
renalsarcoidosis
hypercalculria, hypercalcaemia, neprhocalcinosis
sarcoidosis nervous system
meningitis, cranial nerve pals, central DI, hypothalamic hypopituitarism
hypothalamic hypopituitarism
Hypothalamic hypopituitarism is relatively rare cause of secondary adrenal deficiency which is often accompanied by severe hypoglycemia. Hydrocortisone replacement therapy is essential for this condition, but gastrointestinal symptom such as nausea and vomiting is not well-recognized adverse effect of hydrocortisone
sarcoidosis staging
- Normal
- Hilar/Mediastinal Nodes only
- Nodes + Parenchyma Dz
- Parenchyma Only
- End stage fibrosis
clinical presentation of sarcoidosis
persistent dry cough, eye and skin manifestations, weight loss, fatigue, night sweats, and erythema nodosum.
lab tests for sarcoidosis
ESr raised
hypercalcaemia
ACE raised
hypercalcinuria
leukopenia
transbronchial biopsy
A pulmonologist performs a diagnostic bronchoscopy with biopsy. The endoscope was introduced into the bronchus, and attachments were used to perforate the bronchial wall. Tissue was obtained and submitted to the pathologist, who identified it as “lung parenchyma.” What type of biopsy was performed?
weaning off steroids
administering exogenous steroids causes suppression of endogenous cortisol production by the adrenal glands. Abrupt withdrawal of exogenous steroids can therefore precipitate an adrenal crisis. A gradual reduction in exogenous steroid dose enables the adrenal glands to resume their normal function.
aims of sarcoidosis treatment
prevent organ damage
need to do LFT, ECG, eye check, neur test, calcium 24 hour
first line treatment sarcoidosis
observational if mild. 0.5mg prednisolone 2-4 weeks, taper according to response
Methotrexate moa
inhibits dihydrofolate reductase
What is methotrexate?
antineoplastic, immunosuppressant to treat malignancies
chemotherapy, rheumatoid arthritis, psoriasis, and for abortions
Bronchiectasis
Bronchiectasis is a chronic condition in which the bronchial tree becomes abnormally and irreversibly dilated. The bronchial walls become thickened and inflamed, leading to a build-up of excess mucus which can make the lungs vulnerable to infection.
Patients typically present with recurrent chest infections, persistent cough with sputum production, and shortness of breath.
CXR features of bronchiectasis
ring shadow
consolidation
mucus plugging
tram track opacity
google or check onemed to see
causes of non-CF bronchiectasis
Idiopathic (most common)
Post-infective – e.g., bacterial pneumonia, mycobacterial infection
Allergic – e.g., to mould or fungus, especially in allergic bronchopulmonary aspergillosis (ABPA)
Autoimmune – associations with connective tissue diseases and inflammatory bowel disease
Immunodeficiency – e.g., primary ciliary dyskinesia, primary immunodeficiency disorders, HIV/AIDs
Obstruction – secondary to severe asthma or COPD, or distal to a neoplasm or inhaled foreign body
UK epidemiology bronchiectasis
An estimated 212,00 people in the UK are living with non-CF bronchiectasis
There is a female to male predominance
Incidence increases with age, with 60% of diagnoses made in the over-70 age group
Interestingly, bronchiectasis is more commonly diagnosed in the least deprived sections of the UK population, in contrast to other respiratory disorders
bronchiectasis treatments
Physiotherapy and airway clearance techniques
Cough assist devices
Smoking cessation: it is important for healthcare professionals to know what services are available to refer patients to, do you know how to find this information?
Pneumococcal and annual influenza vaccinations
Treatment with short courses of antibiotics for exacerbations or chest infections
In rare cases surgery, for example a lobectomy if bronchiectasis is localised and symptoms are debilitating
active cycle of breathing technique
Involves the pt going through phases of breathing control, thoracic expansion exercises, and a huff cough
sail sign
The CXR shows volume loss of the left lung field and a dense triangular opacity overlying the cardiac shadow: this is known as the ‘sail sign’
Mucus plugging
Retention of secretions resulting in full airway obstruction that can result in atelectasis and impaired oxygenation due to shunting
atelectasis
collapsed lung; incomplete expansion of alveoli
Exacerbation of bronchiectasis
An exacerbation of bronchiectasis is defined as deterioration in three or more of the following key respiratory symptoms for at least 48 hours:
- Cough- Sputum volume and/or consistency- Sputum purulence- Breathlessness and/or exercise tolerance- Fatigue and/or malaise- Haemoptysis
They are not always the result of acute infection, and antibiotics are not always indicated.
prognosis of bronchiectasis
depends on the underlying cause/associated conditions
Bronchiectasis is an extremely variable disease, but most patients have few day-to-day symptoms and a normal life expectancy. Some patients have frequent chest infections or exacerbations, which may severely effect quality of life. More severe disease results in daily symptoms, progressive loss of lung function and a reduced life expectancy. Uncommon complications are the development of pulmonary hypertension and cor pulmonale. A rare but serious complication of bronchiectasis is massive haemoptysis.
Signet ring sign
Bronchiectasis. Cross section of pulmonary artery branch adjacent to dilated, ring-shaped bronchus.Bronchus diameter exceeds adjacent artery’s
Image: Signet ring sign
Bronchoscopy with biopsy EBUS
EBUS (endobronchial ultrasound) bronchoscopy is a procedure used to diagnose different types of lung disorders, including inflammation, infections or cancer. Performed by a pulmonologist, EBUS bronchoscopy uses a flexible tube that goes through your mouth and into your windpipe and lungs.
LTOT
Long term oxygen therapy
Aminophylline
Bronchodilator - Decreases SOB
Therapeutic levels 10-20 mcg/dl
TOXIC > 20
CANT MIX WITH ANYTHING
