Respiratory diagnosis+management Flashcards
6 Ps of dyspnea
pulmonary bronchial contriction possible foreign body pulmonary embolus pneumonia pump failure pneumothorax
orthoponea
breathlessness while lying flat. Results from abdominal contents pushing on the diaphragm and redistributing blood from lower extremities to the lungs
paraoxysmal nocturnal dysponea
wakes up gasping for breath and is relieved slightly from sitting upright; is a manifestation of left heart failure
acute breathlessness investigations
usually a medical emergency. First line investigations are always ABCDE; if stable, include; CXR, pulse oximetry, ABG. second line; ECG, FBC, U+E, BG, Troponin, DDIMER
acute breathlessness common causes
Acute asthma PE COPD exacerbation Pneumothorax Pulmonary embolism Pneumonia Hypersensitivity pneumonia Upper airway obstruction: inhaled foriegn body or anaphylaxis Left heart failure Cardiac tamponade Panic (hyperventilation)
chronic breathlessness investigations and common causes
investigation include; CXR, FBC, Lung function tests, pulse oximetry, echocardiography Asthma COPD Diffuse parenchymal lung disease Pleural effusion Cancer of bronchus/trachea Heart failure Severe anaemia
auscultation of vesicular breathing and indications
Vesicular breathing - normal but can also be heard in PE, anxiety, metabolic acidosis, anaemia, shock, drugs e.g. salicylates
auscultation stridor sounds and indications
Stridor - heard during inspiration indicates upper airway obstruction. Long sound. More common in children. Foreign Body or tumour, acute epiglottitis (children), anaphylaxis or trauma e.g. laryngeal fracture. Typically loudest over the anterior neck. Sounds like owl hoot.
Auscultation wheez/rhonchi sounds and indications
Wheeze/Rhonchi - continuous high pitch whistling sound indicates asthma, COPD (both acute severe), heart failure, anaphylaxis.
Wheeze - high pitched.
Rhonchi - low pitch rumbling
Auscultations of crepitations/crackles/rales and indications
Crepitation/Crackles/Rales - heard during inspiration indicates pneumonia, pulmonary oedema (and acute cardiogenic heart failure via this), bronchiectasis and pulmonary fibrosis.
Can be heard during both in and expiration. Early during inspiration indicates chronic bronchitis.
Late inspiratory indicates pneumonia, CHF or atelectasis.
Best auscultated at the lung bases. Sounds like wood burning or a fireplace.
Crackles are caused by mucus or pus in lungs - think of conditions that cause this
Pleural rub auscultations and indications
Pleural rub - sound of inflamed pleura rubbing on one another during breathing. Harsh grating, gurgling or creaking sound. Potential causes are TB and pneumonia. Best heard in lower anterior lungs and lateral chest in both exp and inspiration
Cough overview
Most common sign of lower respiratory tract disease
Management of cough = management of the cause
Stimuli:
Mechanical (touch or displacement)
Chemical (noxious fumes etc)
Causes of persistent cough:
Postnasal drip
Asthma
Gastro-oesophageal reflux disease
Post-viral cough
Lung airway disease: COPD, bronchiectasis, tumour, foreign body
Lung parenchyma disease: interstitial lung disease, lung abscess
Drugs: ACEi
Recent cough: few weeks; most commonly due to acute respiratory tract infection (URTI/LRTI)
PND and symptoms
Due to rhinitis, acute nasopharyngitis or sinusitis
Symptoms: cough, nasal discharge, sensation of liquid dripping back into throat and frequent throat clearing
smokers cough
Chronic cough sometimes with phlegm production
Worsening cough may be presenting symptoms of bronchial carcinoma and needs investigation
common causes of dry cough
Asthma
Gastro reflux disease: chronic acid reflux causes cough from excess acid
Viral infection; cough usually lingers post infection due to irritation in airway
Environmental irritants
Smoking; toxant irritations and damage
Bronchitis; acute bronchitis can develop 3-4 days after flu/cold starting with dry cough
haemotysis and common causes
Coughing up blood
Always pathologic
Common causes: Bronchiectasis Bronchial carcinoma PE Bronchitis Pneumonia Lung abscess TB Pulmonary oedema (pink frothy sputum in cough - not always considered haemotysis)
haemotysis investigations
CXR 1st line
2nd line; bronchoscopy, CT thorax, V/Q scan
Perfusion scan shows almost absence in right lung
Ventilation shows normal in both
massive haemoptysis overview
Massive haemoptysis: Greater than 200mL/d May be life-threathening due to asphyxiation and/or massive bleeding and shock Causes: TB Bronchiectasis Lung abscess Lung cancer Management: Admission to hospital Oxygen; two large bore catheter Blood samples; FBC, U+E, clotting screen and ABG CXR Early referral to respiratory physician (pulmonologist) and thoracic surgeon
pulmonary investigations
Macroscopy: yellow/green sputum indicates inflammation/infection such as pneumonia or allergy
Microbiology: gram stain and culture in pneumonia, auramine stain in TB
Cytology: for malignant cells
sputum indications
mucoid - chronic bronchitis green or yellow - infection bloody/transparent with blood fibres - bronchogenic carcinoma, TB bright red - pulmonary infarction rusty colour - pneumonia pink and frothy - pulmonary oedema foul smelling - anaerobic infection
spirometry and obstructive/restrictive pattern
measure functional lung volumes by breathing into a spirometer. Can calculate capacities from volumes recorded
Used to measure FEV and FVC; normal breathing; forced full inspiration and forced full expiration
First volume expired is one second is FEV1
Total volumes expired determines FVC
Obstructive pattern = FEV1/FVC ratio less than 75% due to physical obstruction preventing air being expelled as fast; asthma or COPD
Restrictive pattern = FEV1/FVC greater than 75%; but lower individual measurements than normal; connective tissue disease; pleural effusion; obesity; kyphoscoliosis; neuromuscular problems.
indications for spirometry use
Chest pain Orthopnoea Cough or phlegm production Dyspnea or wheezing Chest wall abnormalities Cyanosis Decreased breath sounds Finger clubbing Blood gas abnormality Chest radiography abnormality
Peak expiratory flow record PEFR and indications for use
Measured by maximal force expiration through peak flow meter
Correlates well with FEV1
Used to estimate airway calibre
More effort dependent than FEV1
Indications for use:
Daily assessment/monitor of pts with asthma and response to treatment
Cheap and user friendly
Can test at home and bring results to clinic themselves
Spirometry procedure overview
Document age, height, weight, sex, ethnicity of pt to predict standardised expected result
Ask NOT to take bronchodilator
Sit pt in chair warn for feeling dizzy etc. from breathing
Wear nose clip to ensure mouth breathing only
Following deep inspiration perform full forced expiration
PEFR procedure overview
Wash hands
Introduce self
Check ID
Explain and gain consent
Insert mouthpiece and set dial to 0
Sit straight and take deep breath in
Seal mouth around mouthpiece
Full breath out as hard and fast as possible
Look at reading on dial and note reading
Teach this to patients to do at home; make them repeat this back to you and show you how they would do it.
Repeat 3 times and take best of three readings
Common respiratory symptoms
Shortness of breath Lung sounds Cough Haemoptysis Chest pain
Asthma, symptoms and signs
Chronic respiratory condition associated with airway inflammation and hypersensitivity responsiveness
Can present in many forms (heterogeneous)
Hygiene hypothesis - immune response is not as developed due to increased hygiene with standard of living
Migration to urban areas from rural tends to be associated with this too
Symptoms: can resolve spontaneously or in response to medication, may sometimes be absent for weeks or months at a time
Cough
Wheeze
Tight chest
SoB
Signs:
Variable expiratory airflow limitation can vary over time and in intensity
Asthma potential triggers
Exercise Allergen or irritant exposure e.g. hayfever or animal fur Changes in weather Night time or early morning Viral infection exposure Strong emotion (children)
Asthma risk factors
Personal or family history of atopic disease (asthma, eczema, allergic rhinitis or allergic conjunctivitis)
More common in boys before puberty and girls post puberty
Respiratory infections in infancy - early antibiotics exposure
Passive or prenatal smoke
Premature birth and associated low birth weight
Obesity
Social deprivation
Exposure to inhaled particles - occupation is important!
Asthma protective factors
varying evidence not conclusive Vaginal birth (not C section) Increasing sibship - exposure to allergens etc Farming environment - animal exposure Breastfeeding
common history in asthma
Episodic symptoms
Diurnal (worse at night or early morning)
Triggered or exacerbated by exercise, viral infection and exposure to cold air or allergens)
In children; may be triggered by emotion or laughter
In adults; triggered by non-steroidal anti-inflammatory drugs and beta blockers
Onset is typically under 35 years old
Asthma investigations
Spirometry on anyone above age 5; FEV1/FVC less than 70% shows airflow limitation. Can be normal for asymptomatic pts. Results can be impaired by inhaled corticosteroids
Bronchodilator reversibility (BDR): anyone over age 17 (but can be considered in 5-16) due to need to follow instructions well. Improvement of FEV1 of 12% or more together with an increase in volume of at least 200mL in response to beta-2 agonists or corticosteroids is regarded as +ve result
Variable peak expiratory flow: compare predictive with actual fo height, age and gender. 20% variability after monitoring at least twice daily for 2-4weeks
FeNO test (fractional exhaled nitric oxide); used to confirm eosinophilic airway inflammation in ages 17 and above (consider in ages 5-16). Result of above 40 parts per billion is considered positive
Asthma differential diagnosis
-Bronchiectasis •Chronic obstructive pulmonary disease (COPD) •Ciliary dyskinesia •Cystic fibrosis •Dysfunctional breathing •Foreign body aspiration •Gastro-oesophageal reflux •Heart failure •Interstitial lung disease (asbestosis, pneumoconiosis, fibrosing alveolitis, sarcoidosis) •Lung cancer •Pertussis •Pulmonary embolism (PE) •Tuberculosis •Upper airway cough syndrome •Vocal cord dysfunction
Asthma long term management
Step 1:
•Beta2-agonist inhaler – short term relief for those with very mild, intermittent asthma. Salbutamol.
Step 2:
•ICS (fluticasone propionate; 16+ 100-500mcg 2xdaily max per dose 1mg, beclometasone diproprionate; 12+ 200-400mcg 2xdaily ).
Prompts for starting inhaled corticosteroids:
An exacerbation in the previous two years.
Use of a beta2-agonist inhaler >3x/week.
Symptomatic of asthma >3x/week.
Waking due to asthma >1x/week.
Step 3:
•a leukotriene receptor antagonist (LTRA) before treatment + a long-acting beta2 agonist (LABA).
** LABA must be used with ICS <800ug/day. +/- sustained release (SR) theophylline. Or MART regimen.
Step 4:
•ICS - < 2g/day + LTRA + SR theophylline or beta2-agonist tablet.
Step 5:
•Regular use of oral steroids + ICS
Asthma long term management in children
Step 1 Low paediatric dose ICS: fluticasone propionate; 5-15year 50-100mcg 2xdaily max per dose 200mcg; beclometasone diproprionate; 5-11 years 100-200mcg 2xdaily; 12+ 200-400mcg 2xdaily OR LTRA such as montelukast for 6months-5years 4mg once in evening; review in 4-8 weeks Step 2 paediatric dose ICS + inhaled LABA (salmeterol 5+ years; 50mcg 2xdaily; in 12+ can increase up to 100mcg 2xdaliy) or LTRA for children (montelukast; 5-14 years; 5mg once in evening) In under 5 years add LTRA Step 3 Consider increasing ICS dose 5+ years adding LTRA/LABA If no response consider stopping LABA Step 5 Specialist therapies referral
when to review asthma patients
review 2 weeks after starting treatments and 2 weeks post every change after
safety net always to come back if breathing gets worse or changes at all
ensure you teach the correct inhaler method to all patients
Inhaler colours
Blue inhaler - short acting beta 2 agonists (salbutamol) for relief of symptoms taken as and when
Brown inhaler - inhaled corticosteroids ( fluticasone, budesonide and beclometasone) taken morning and night as preventatives
Pink/purple - MART; maintenance and relieving therapy regiment (symbicort, fostair, duoresp spiromax, fobumix easyhaler) is combination of ICS and fast acting LABA used for both daily prevention and symptomatic relief (usually used in moderate to severe cases based on patient preference or if other drugs not working etc.)
Asthma drugs overview
Bronchodilators:
Via beta2- agonist receptors
•Short-acting beta2-agonists (SABA): salbutamol and terbutaline.
•Long-acting beta2-agonists (LABA): formoterol, salmeterol (twice daily) and (once daily) indacaterol, olodaterol and vilanterol.
Leukotriene receptor antagonists (LTRAs): Montelukast
Steroids:
•Inhaled corticosteroids (ICS): fluticasone, budesonide, and beclometasone.
•Oral corticosteroids: Prednisolone – risk of DM, osteoporosis, hyperlipidaemia.
Asthma management overview
Add short-acting beta 2 agonist inhaler (e.g. salbutamol) as required for infrequent wheezy episodes.
Add a regular low dose inhaled corticosteroid.
Add an oral leukotriene receptor antagonist (i.e. montelukast).
Add LABA inhaler (e.g. salmeterol). Continue the LABA only if the patient has a good response.
Consider changing to a maintenance and reliever therapy (MART) regime.
Increase the inhaled corticosteroid to a “moderate dose”.
Consider increasing the inhaled corticosteroid dose to “high dose” or oral theophylline or an inhaled LAMA (e.g. tiotropium).
Refer to a specialist.
Additional management:
Individual asthma self management plan
Yearly flu jab
Yearly asthma review
Advice exercise and avoid smoking
asthma additional advice
Individual asthma self management plan
Yearly flu jab
Yearly asthma review
Advice exercise and avoid smoking
asthma complications
Death
Respiratory complications: irreversible airway changes, pneumonia, pulmonary collapse (atelectasis caused by mucus plugging of airways), respiratory failure, pneumothorax and status asthmaticus (repeated asthma attacks without respite, or non-response to appropriate treatment).
Imparied quality of life from suboptimal control of asthma including fatigue and underperformance at work/school etc.
Acute asthma exacerbation and symptoms
Onset of severe symptoms can be life threatening
Refer the same day to the hospital for review by the respiratory team. Or send via A+E
Symptoms:
Exhaustion (inability to complete sentences)
Cyanosis
Use of accessory muscles at rest
Reduced PEFR:
moderate (PEFR more than 50-75% predicted, at least 50% in children and normal speech with no features of acute asthma);
acute severe (PEFR 33-50% predicted, less than 50% in children, or RR of at least 25/min in people over age 12, over 30/min in ages 5-12 and 40/min between 2-5 years. Pulse rate at least 110/min over 12 years, 125 between 5-12 years and 140/min between 2-5 years. Inability to complete sentences in one breath or accessory muscle use or inability to feed (infants) with O2 sats of at least 92%
Life threatening (PEFR less than 33% predicted or O2 sats less than 92%, altered consciousness, exhaustion, cardiac arrhythmia, hypotension, cyanosis or poor respiratory effort or silent chestor confusion
In children: monitor for signs of agitation and behavioural changes as may indicate hypoxia
Acute asthma exacerbation management
O SHIT! -
Oxygen, Salbutamol, Hydrocortisone, Ipratropium, Theophylline!
Oxygen
SABA via nebuliser 5mg to all over age 5 years and 2.5mg to children ages 2-5 years. Ideally oxygen driven usually 6L/min
SABA via metered dose inhaled with large volume spacer - 4 puffs initially followed by 2 puffs every 2 mins for up to 10 puffs. Repeat every 10-20 minutes. For children give every 30-60 seconds up to 10 puffs
Excessive salbutamol can cause tachycardia and fine tremors
Review all pts 48 hours after admission or conservative management
Also consider:
Oral prednisolone 40-50 mg for adults (once a day for 5days ) – also available as soluble tablet ( 5 mg)
Intramuscular (IM) methylprednisolone 160 mg
Hydrocortisone (IV) 100 mg in people aged over 5 years
COPD aeitology and presentation
Persistent respiratory symptoms (SoB, cough and sputum) and airflow obstruction
Aetiology:
Chronic bronchitis - cough and sputum production for 2-3 years
Emphysema - loss of parenchymal lung texture
Chronic obstructive airway disease
Presentation:
Tend to be over 35 years
Breathlessness; typically persistent and progressively worse over time
Chronic cough
Sputum production regularly
Wheeze
Frequent LRTI
COPD risk factors
Smoking - including marijuana and passive smoke
Occupational exposure to dusts, fumes, chemicals
Air pollution
Genetics - alpha1 antitrypsin deficiency (typically present in younger pts under 45 years)
Lung development - in utero factors affecting lung development such as maternal smoking and preterm birth. In childhood severe RTI and passive smoking can affect lung development and increase risk of COPD developing
COPD investigations
CXR: cancers, bronchiectasis, TB, heart failure FBC: anaemia, polycythaemia (increase in RBC) Spirometry Reversibility test: not routine Sputum culture Serial home PFM ECG Echo Serum natriuretic peptides CT thorax: fibrosis or bronchiectasis Serum alpha1 antitrypsin
COPD diagnosis differentials
- Asthma — may co-exist and can be difficult to distinguish clinically.
- Consider asthma if the person has a family history, other atopic disease, or nocturnal or variable symptoms, is a non-smoker, or experienced onset of symptoms at younger than 35 years of age.
- Bronchiectasis
- Heart failure
- Lung cancer
- Interstitial lung disease (asbestosis, pneumoconiosis, fibrosing alveolitis, or sarcoidosis)
- Anaemia
- Tuberculosis (TB)
- Cystic fibrosis
- Upper airway obstruction (tumour)
COPD diagnosis
Spirometry - post bronchodilator FEV1/FVC less than 0.75 confirms persistent obstruction
Calculate FEV1/predicted FEV1 score for severity (more than 80% is mild, 50-80% moderate, 30-50% severe, less than 30% is very severe); if at the higher end of scale then can classify mild-moderate etc.
Consider other causes in older people without typical COPD symptoms
Consider COPD in younger people with symptoms of COPD even with ratio above 0.7
Medical research council MCR dyspnoea scale
grade 0-Not troubled by breathlessness except during strenuous exercise
grade 1-SoB when hurrying or walking up slight hill
grade 2-Walks slower than contemporaries on level due to SoB or has to stop for breath when walking at own pace
grade 3-Stops for breath after walking roughly 100m or after few mins on same level
grade 4-Too breathless to leave house or breathless when dressing/undressing
COPD management overview
Inhalers
Oral medicines
Oxygen therapy
Lifestyle modifications
COPD drugs management
SABA or SAMA to reduce breathlessness and improve exercise capacity
With asthmatic features: LABA plus ICS; Without asthmatic features: combined LABA and LAMA
Triple inhaled therapy (LAMA + LABA + ICS) to people with COPD with asthmatic features suggesting steroid responsiveness who remain breathless or have exacerbations despite taking LABA+ICS = trimbow
In both groups only consider combination inhalers if non-pharmacological options, vaccinations and smoking cessation have been addressed
COPD preventor drugs
Theophylline - relaxes smooth muscle and relieves bronchial spasm
Mucolytic therapy - chronic productive cough; an adjuntive therapy for excessive viscous mucus - carbocisteine (mucolytic that helps you cough up phlegm. It works by making your phlegm less thick and sticky)
Prophylactic antibiotics - discussion with respiratory specialist
COPD oxygen therapy
For the management of hypoxic patients – not breathlessness
Usually with severe COPD
•MRC score: 4-5
•FEV1: Stage 3 (severe) 30–49% of predicted value – 4 (very severe) less than 30% of predicted value or FEV1 less than 50% with respiratory failure.
Under the direction of a respiratory specialist.
Flammable - need to be made aware
Can’t smoke near!!
COPD lifestyle management
Smoking cessation - offer multiple times
Pulmonary rehabilitation - individually tailored, MD care program for people with COPD which aims to optimize physical and psychological condition through exercise training, education and nutritional, psychological and behavioural interventions
Vaccinations - influenza and pneumococcal as are high risk for LRTI
TRAVEL advice: MCR score of 1-2 and stable oxygen levels do not need to inform DVLA
Unstable oxygen sats air exceeding 4L/min at sea level cannot travel on planes.
Acute exacerbation of COPD
•Exacerbations are acute episodes of worsening COPD symptoms (such as increased breathlessness, cough and sputum) which are beyond normal day-to-day variations.
Acute exacerbation of COPD symptoms
Symptoms:
•Worsening breathlessness.
•Increased sputum volume and purulence.
•Cough.
•Wheeze.
•Fever without an obvious source.
•Upper respiratory tract infection in the past 5 days.
•Increased respiratory rate or heart rate >20% above baseline.
In severe cases
•Pursed-lip breathing and/or use of accessory muscles at rest.
•New-onset cyanosis or peripheral oedema.
•Acute confusion or drowsiness.
•Marked reduction in activities of daily living.
acute COPD management
Be prepared to refer the same day !
•If managing in clinic:
•Maximise dose of short-acting bronchodilator inhalers.
•Prednisolone 30 mg PO once daily for 5/7. SE – osteoporosis.
•Antibiotics: Amoxicillin 500 mg TDS 5/7; Doxycycline 200 mg on first day, then 100mg OD for 5/7; Clarithromycin 500 mg BD for 5/7.
•Send a sputum sample for MCS if no resolution.
•Follow up within a week or sooner if needed, then in 6/52.
•Consider CXR, pulmonary rehab/respiratory referral, as well as a rescue pack (antibiotics + steroid at home).
Complications of COPD
Progressive pulmonary HTN; development of RV hypertrophy leading to cor pulmonale (RHF secondary to lung disease) Pneumothorax Respiratory failure Arrhythmias including AF Infection Secondary polycythaemia (too many RBCs) Depression
Obstructive sleep apnoea/hypopnoea syndrome
OSAHS: The coexistence of excessive daytime sleepiness with irregular breathing at night
Irregular breathing from upper airway collapse during sleep
Collapse can be partial (hypopnoea) or full (aponea)
Leads to transient arousal from deep sleep to wakefulness; allowing restoration of normal airway muscle tone
Cycle repeats once in deep sleep again
Broken sleep pattern results in reduced sleep quality, excessive daytime sleepiness and reduced concentration and alertness
OSAHS presentation in adults
Excessive daytime sleepiness and snoring and/or impaired concentration
Witnessed apneas or choking noises while sleeping
Feel unrefreshed when waking
Mood swings, personality changes or depression
Nocturia - weeing lots at night time
Rarely, nocturnal sweating, reduced libido and gastro-oesophageal reflux disease (GORD)
OSAHS presentation in children
Snoring and pauses in breathing often followed by a gasp or a snort
Restlessness and sudden arousals from sleep, laboured breathing, unusual sleep posture (head bent back) and bedwetting
Daytime symptoms: changes in behaviour, irritability, poor concentration, decreased performance at school, tiredness and sleepiness, failure to gain weight or grow and mouth breathing
OSAHS red flags and referral
Unilateral nasal bleeding and/or severe nasal obstruction
Change in voice character and/or unexplained hoarseness
Dysphagia
Rapid onset symptoms without significant weight gain
Any red flag symptoms need 2 week referral
OSAHS risk factors
•Male (2–3:1). •Middle aged/increasing age •Obesity. •Neck circumference greater than 43 cm. •Family history. •Smoking. •Alcohol intake before bed. •Sleeping supine. •Hypothyroidism. •Craniofacial abnormalities. •Acromegaly (abnormal growth due to excess growth hormone). OSAS in children is around 1–2%, and this may be increasing due to increasing obesity. The incidence in children with congenital conditions (for example Down's syndrome, neuromuscular disease, and craniofacial abnormalities) is higher. Adenotonsillar hypertrophy is also a risk factor.
OSAHS diagnosis
Epworth sleepiness questionnaire. •Eight questions •Assessing likelihood of dozing off. •A score greater than 10 represents abnormal sleepiness •Range: •Mild (11–14) •Moderate (15–18) •Severe (more than 18)
OSAHS management
•Referral to a sleep center for sleep studies to confirm diagnosis.
•Polysomnography (PSG) measures sleep and breathing patterns simultaneously. Five or more episodes of apnoea/hypopnoea episodes per hour needed to confirm the diagnosis.
•Scale of mild, moderate & severe.
•Continuous Positive Airway Pressure (CPAP) – highly effective.
•Intra oral mandibular advancement devices and weight loss may also be appropriate.
Urgent refer: Severe OSAS, respiratory failure/CHF, people sleepy whilst driving or operating machinery at work. Advise the person not to drive until they have been assessed by a specialist.
Routine refer: Symptomatic patients with an Epworth sleepiness questionnaire score >10.
Refer children to paediatric ENT specialist if they have features of OSAS/persistent snoring as well as adenotonsillar hypertrophy.
Children management - mouth breathing, nasal obstructions, large tonsils, can resolve apnea, advise weight loss if necessary
PE signs and symptoms
tachypnoea of 20 breaths per minute or greater (in 70% of people with PE), crackles (51%), tachycardia (30%), signs of DVT (11%). Hypoxia, pyrexia, elevated JVP, widely split second heart sound, tricuspid regurgitation murmur, pleural rub, hypotension and cardiogenic shock may also occur.
symptoms:
acute-onset breathlessness (in 73% of people with PE), pleuritic pain (66%), cough (37%), haemoptysis (13%). Severe cases may lead to dizziness or syncope.
PE risk factors
immobilization, surgery, cancer, acute medical illness, obesity, prolonged travel, symptoms or signs of deep vein thrombosis (DVT), previous DVT, thrombophilia, or age over 60 years.
Pleural effusion signs and symptoms
signs:
reduced chest wall movements on the affected side, stony dull percussion note, diminished or absent breath sounds, decreased tactile vocal fremitus/vocal resonance and bronchial breathing just above the effusion. There may be signs of the underlying condition.
symptoms:
progressive breathlessness, pleuritic pain and symptoms of the underlying condition
Lung or pleural cancer signs and symptoms
signs
chest examination is often normal but there may be unilateral wheeze, decreased breath sounds, or signs of pleural effusion. Other signs include finger clubbing, and supraclavicular or cervical lymphadenopathy.
symptoms
cough, shortness of breath, haemoptysis, chest pain, weight loss, appetite loss, fatigue, hoarseness, persistent chest infections, symptoms relating to bone or brain metastases.
Lung or pleural cancer risk factors
smoking
asbestos exposure
Causes of pleural effusion
heart, liver, or renal failure, pneumonia, pulmonary embolism, cancer (including mesothelioma), tuberculosis, pleural infection (empyema), and autoimmune disease.
Acute pulmonary oedema pathology
Acute: accumulation of fluid in lung parenchyma leading to decreased gaseous exchange
Pathophysiology:
as heart begins to fail; compensatory mechanisms maintain BP and CO
increased sympathetic tone increases SVR and stimulates renin release
RAAS increases salt and fluid retention, initially increasing preload and EDV, but overtime leads to cardiac dilation and reduced contractility (and CO)
leading to congestion of pulmonary and systemic veins with associated tissue oedema (pitting/ankle and sacral oedema)
alveolar oedema increases causing dyspnoea
venous return increases when patient lies flat causing orthopnoea and paroxysmal dyspnoea (PND)
Acute pulmonary oedema causes
cardiac: ACS arrhythmia valvular heart disease HTN cardiomyopathy cardiac tamponade Non-cardiac: non-compliance with medication negatively inotropic medication fluid overload high output cardiac failure: anaemia, thyrotoxicosis, sepsis ARDS acute respiratory distress syndrome renal artery stenosis RAS Chest trauma Infections e.g. sepsis
Acute pulmonary oedema signs and symptoms
fatigue
worsening dyspnea progressing from exercise tolerance of dyspnoea on exertion to at rest
Orthopnoea; shortness of breath worsens when lying down
PND
cough producing pink, frothy sputum
ankle swelling (pitting oedema)
Acute pulmonary oedema investigations
ABG FBC U+Es Mg Ca TFTs 12 lead ECG: shows ischaemia, infarction, LVH, arrhythmia CXR: ABCDE signs (alveolar oedema, bats wings and kerley B lines, cardiomegaly, diversion to upper lobes, effusions; blunting of costophrenic angles) echocardiogram if needed
Acute pulmonary oedema management
Initial management:
assess patient ABCDE
sit upright and attach monitoring: BP, oximeter, 3 lead cardiac monitor
maintain airway; suctions
oxygen if needed; 15L non-rebreathing mask
IV access and blood tests
consider troponin if concerned about cardiac event
Furosemide 40mg IV (diuretic)
Morphine 2.5-10mg IV (dilate venous system; decrease preload and improve breathing)
GTN 1mg/ml at 2ml/hour or give sublingually if fails IV
start CPAP if severe oedema (continuous positive airway pressure)
Further management:
continuing CPAP or inotropic support needs referral to HDU for continuous BP, ABG, CVP, oxygen, cardiac monitoring and urine output monitoring
Common respiratory tract infections
URTI LRTI Sinusitis - nasal passages Cold Pharyngitis (sore throat) Laryngitis (voice change) Influenza Bronchitis (acute/chronic) Pneumoniae
acute bronchitis risk factors and causes
Cough lasting 10 days to 3 weeks (acute infection)
Chronic is inflammation and cough lasting longer than this; usually due to irritants such as smoking
Cause:
Viruses cause 85-95% of acute bronchitis in adults
Can be same virus as common cold etc.
Rare cases can develop bacterial bronchitis after viral infection of bronchitis
Risk factors:
Smoking
Immunocompromised
Reflux
Exposure to irritants
Age 50 and over
Influenza and causes
Acute respiratory illness
Often self-limiting although acutely debilitating
In vulnerable individuals can be fatal
Symptoms usually last 3-5 days but cough and tiredness may last 1-2 weeks
Cause:
Caused by influenza A or B viruses (also C)
influenza signs and symptoms
Upper and/or lower respiratory tract involvement
Indications of systemic illness e.g. fever
Headache
Myalgia - muscle pain involving tendons, ligaments and fasica
Weakness
High risk groups for influenza
Young children under 5, especially under 6 months
Adults above age 65
Residents of nursing homes and other long-term care facilities
Pregnant women and women up to two weeks after giving birth
People with weakened immune systems
People who are very obese, with a body mass index (BMI) of 40 or higher
Native Americans
People who have chronic illnesses, such as asthma, heart disease, kidney disease, liver disease and diabetes, neurological disease, immunosuppression,pregnancy etc.
Influenza transmission and infectious rate
Droplet coughing and sneezing
Direct nasal or eye contact with hands carrying virus
Infectiveness continues for 5 days from onset, although children can remain infectious for 2 weeks and severely immunocompromised can shed virus for weeks
Influenza diagnosis
usually not needed only for formal stats etc. Clinical Nasopharyngeal swabs/aspirates PCR Antigen testing
Influenza treatments
Advice:
Do not prescribe antiviral drugs for otherwise healthy people
Reassure person worst symptoms of uncomplicated influenza resolve after 1 weeks, although cough, headache, insomnia, loss of appetite etc. may persist for longer than 2 weeks
Treatments:
Oseltamivir (tammiflu) and zanamivir reduce replication of influenza A and B
They are most effective if started within a few hours of the onset of symptoms. In otherwise healthy individuals they reduce the duration of symptoms by about 1-1.5 days.
When influenza is circulating in the community, either oseltamivir or zanamivir is recommended for the treatment of influenza in at-risk patients who can start treatment within 48 hours (within 36 hours for zanamivir in children) of the onset of symptoms
Influenza complications
Acute bronchitis (20% cases with increased risk in elderly and chronic disease sufferers)
Secondary bacterial pneumonia (especially staph. aureus)
Primary viral pneumonia
Exacerbations of asthma and COPD
Empyema
Pulmonary aspergillosis
Sinusitis
Risk factors for pneumonia
Age: especially infants, young children and the elderly.
Lifestyle: smoking, alcohol.
Preceding viral infections - eg, influenza predisposing to Streptococcus pneumoniae infection.
Respiratory: asthma, chronic obstructive pulmonary disease (COPD), malignancy, bronchiectasis, cystic fibrosis.
Immunosuppression, AIDS, cytotoxic therapy - increased risk of infection with Staphylococcus spp., tuberculosis, Gram- negative bacilli and P. jirovecii.
Intravenous drug abuse, often associated with Staphylococcus aureus infection.
Hospitalisation - often involving Gram-negative organisms.
Aspiration pneumonia: patients with impaired consciousness, neurological disease such as cerebrovascular or Parkinson’s disease, or patients with oesophageal obstruction are at risk of aspiration pneumonia which usually affects the right lung and is caused by anaerobes from the oropharynx.
Underlying predisposing disease: diabetes mellitus, cardiovascular disease.
Community acquired bacterial pneumonia
Defined as the presence of symptoms and signs consistent with acute lower respiratory tract infection in association with new radiographic shadowing for which there is no alternative explanation.
The most likely (TYPICAL) organisms are: S. pneumoniae, S. aureus, Mycoplasma pneumoniae, Haemophilus influenzae, Chlamydophila pneumoniae and respiratory viruses[3]. Mixed pathogens occur up to 25% of the time.
0.5-1% of people develop community-acquired pneumonia (CAP) in the UK every year.
The mortality rate is between 5% and 14%.
Hospital acquired bacterial pneumonia
defined as onset of infection in a patient admitted more than 48 hours
Occurs mostly in pts severely debilitated, immunocompromised or mechanically ventilated
Infection occurring less than five days after admission is usually strep. Pneumonia
Infection occuring after this time usually caused by H. influenzae, MRSA, pseudomonas aeruginosa and other non-pseudomonal gram -ve bacteria
Often caused by multiple organisms
Complications of bacterial pneumonia
Pleural effusion
Emphysema
Pneomothorax
Lung abscess (due to S. pneumoniae classically seen in pts with klebsiella or staphycoccal pneumonia
Pyopneumothorax e.g. following rupture of Staphylococcal lung abscess in pleural cavity
AKI - acute kidney injury; stage 1; creatinine baseline 1.5x higher; check pts previous creatinine values if possible but if not; assume normal kidney function range
DVT - less mobile while ill
Septicaemia
Pericarditis
Endocarditis
Osteomyelitis
Septic arthritis
Cerebral abscess
Meningitis (particularly pneumococcal pneumonia)
Bacterial pneumonia prognosis
Mortality from CAP is less than 1% in those well enough to be managed within community
Mortality in those admitted to hospital is 5-10% in those not requiring ICU admission
As high as 25% in intubated pts
Nearly 50% in ICU pts
Legionella has most severe course and may cause significant morbidity if not treated early
Bacterial pneumonia typical presentation
Symptoms: cough, purulent sputum which may be blood- stained or rust-coloured, breathlessness, fever, malaise.
Signs: tachypnoea, bronchial breathing, crepitations, pleural rub, dullness with percussion.
Diagnosis is unlikely if there are no focal chest signs and heart rate, respiratory rate and temperature are normal. Would instead call this a LRTI as pneumonia usually has these features
The elderly may present with mainly systemic complaints of malaise, fatigue, anorexia and myalgia.
Young children may present with nonspecific symptoms or abdominal pain.
CURB65 score for pneumonia
scoring system to determine severity of pneumonia and if it can be managed within the community or needs hospital admission. One point for each factors
Should also be admitted with delirium (acute confusion) or hypoxia
Confusion (AMTS above 8 or disorientated to person, place, time)
Raised serum Urea over 7mmol/L (U+Es tests)
Raised Respiratory rate over 30bpm
Low Blood pressure
Over 65 years of age
Risk of death:
0-1: low risk (less than 3% mortality risk)
2: intermediate risk (3-15%)
3-5: High risk (more than 15%)
Low-moderate severity CAP management
CURB65 score 0-1:
COVID UPDATE: Doxycycline 1st line 200mg day one then 100mg once daily for four days
Offer 5 day course of amoxicillin 500mg 3xdaily; 125mg 1-11months old; 250mg 1-4years; 500mg 4+years all 3xdaily
Reserve clarithromycin (500mg 2xdaily for 5 days; weight based in under 12 years; 250-500mg 2xdaily for 12-18 years), erythromycin (pregnancy; 500mg 4x daily for 5 days; 8-17 years 150-500mg 4xdaily) or doxycycline (for pts allergic to penicillin or if atypical pathogen suspected)
Stop ABs after 5 days unless microbiology results suggest longer course or pt is not clinically stable
If atypical add clarithromycin to amoxicillin
MOD severity CAP as above pending microbiology results
High severity CAP management
Co-amoxiclav (broad spectrum; 500/125mg 3xdaily orally or 1.2g 3xdaily IV for 5 days; 1-11months 0.5ml/kg of 125/31 3x daily; 1-5 years 10ml of 125/31 3xdaily; 6-11 years 10ml of 250/62 3xdaily; 12-17 500/125mg 3xdaily orally) with clarithromycin (atypical forms; 500mg 2xdaily orally or IV for 5 days; 1month-11 years weight based; 12-17 years 250-500mg 2xdaily 5 days orally) or erythromycin (pregnancy; 500mg 4xdaily orally for 5 days; 8-17 years 250-500mg 4xdaily orally 5 days) should be offered
Levofloxacin orally or IV (500mg 2xdaily) for pts allergic to penicillin
Follow local guidelines
Bacteria Pneumonia management in hospitals
Oxygen: for hypoxia
IV fluids: for pts with hypotension, tachycardic, signs of sepsis etc. 0.9% saline/Hartmann’s 250mL, 500mL , 1L bolus then 1L over 4/6 hrs. Use with caution in heart failure pts
Nebulised saline might help expectoration
Failure to improve within 72hrs should seek medical attention
Community pts should be advised to return is symptoms persist for more than 3 weeks
Atypical pneumonia
Atypical organisms might be implicated in approx. 20% of CAP:
Mycoplasma pneumoniae - spread by person-person contact most commonly in closed populations e.g. schools and offices
Chlamydia pneumoniae - spread by person-person contact most commonly in closed populations e.g. schools and offices
Legionella pneumophila - found most commonly in freshwater and man made systems
Wont respond to broad spectrum ABs like amoxicillin, but often give both ABs before lab results arrive to cover for both possibilities
Mycoplasma pneumoniae presentation
Vague and slow onset history over few days or weeks of fever, upset, headache, dry cough with tracheitic +/- pleuritic pain, myalgia, malaise and sore throat
Persistence and progression helps determine this diagnosis
In otherwise healthy individuals, it usually resolves spontaneously over a few weeks.
Mycoplasma pneumoniae symptoms and complications
SYMPTOMS:
The hacking, dry cough can be very persistent.
COMPLICATIONS:
Extra-respiratory features include rashes such as erythema multiforme, erythema nodosum and urticaria;
neurological complications like Guillain- Barré syndrome, transverse myelitis, cerebellar ataxia and aseptic meningitis;
haematological complications such as cold agglutinin disease and haemolytic anaemia; joint symptoms like arthralgia and arthritis;
cardiac complications such as pericarditis and myocarditis; rarely, may cause pancreatitis.
Chlamydia pneumoniae and complications
Gradual onset, which may show improvement before worsening again; incubation period is 3-4 weeks.
Where it causes significant problems, this may be due to secondary infection or co-existing illness - eg, diabetes.
Chlamydia pneumoniae symptoms
Initial nonspecific upper respiratory tract infection symptoms lead on to bronchitic or pneumonic features.
Most of those infected remain quite well or are asymptomatic. Cough with scanty sputum is a prominent feature. Hoarseness is a common feature.
Headache affects the majority of symptomatic sufferers.
Fever is relatively unusual.
Symptoms may drag on for weeks or months, despite a course of appropriate antibiotics.
Legionella pneumophila
This tends to be the most severe of the pneumonias due to atypical pathogens
Focal outbreaks centred around poorly maintained air- conditioning or humidification systems (although this is often noted retrospectively by public health physicians).
2-10 days’ incubation period.
Legionella pneumophila symptoms
Initial mild headache and myalgia leading to high fever, chills and repeated rigors; non-chest symptoms often predominate early on.
Cough is nearly always present, initially unproductive but may lead to expectoration later.
Dyspnoea, pleuritic pain and haemoptysis (coughing up blood) are not uncommon.
Gastrointestinal upset, such as diarrhoea, nausea and vomiting or loss of appetite/anorexia, may occur.
Legionella pneumophila complications
There may be neurological complications such as confusion, disorientation and focal neurological deficit.
Arthralgia and myalgia are often reported.
Severe complications include pancreatitis, peritonitis, pericarditis, myocarditis, endocarditis and glomerulonephritis.
Atypical pneumonia history tips
Legionella pneumoniae - water cooled air condition
Strep pneumonia - most likely in adults with rusty sputum
Staphylococcus areus - most likely following influenza and IV drug users
Mycoplasma pneumonia - atypical flu like sympts, dry cough, people living close together, rash (erythema multiforme)
Bacterial pneumonia investigations
Routine bloods; FBC, U+Es, LFT, CRP
Blood cultures - determine strain
Pneumococcal and legionella urinary antigen tests
CXR with 6 week post recovery repeat as follow up
Sputum culture
Pulse oximetry or ABC
Aspiration of pleural fluid
Sepsis 6
High flow oxygen Take blood cultures Give IV antibiotics Give fluid challenge Measure lactate Measure urine output
Aspiration pneumonia
Results from inhalation of stomach contents or secretions of oropharynx, leading to LRTI.
In many healthy adults very small quantities of aspiration occur frequency but normal defences (cough) remove material with no ill effects
Usual site for aspiration pneumonia is apical and posterior segments of lower lobe of right lung
If pt is supine then may aso enter posterior segment of upper lobes
aspiration pneumonia symptoms and signs
non-specific symptoms e.g. fever, heachache, nausea, vomiting, anorexia, myalgia, weight loss Cough SoB Pleuritic chest pain Purulent sputum Signs may include: Tachycardia Tachyponea Decreased breath sounds Dullness to percussion over areas of consolidation Pleural friction rub
aspirations pneumonia risk factors and complications
Impaired consciousness; drug, alcohol misuse, general anaesthesia, seizures, sedation, acute stroke, CNS lesions, head injury
Poor mobility
Increasing age
Nil-by-mouth
COPD
Male gender
Increasing number of medications
Swallowing disorders: oesophageal stricture, dysphagia, stroke, bulbar pasly
Other: tracheo-oesophageal fistula, ventilator associated pneumonia, periodontal disease, GORD
Complications:
Severe infection may lead to hypoxia and septic shock
Aspiration pneumonia Community acquired pathogens
Pathogens of community-acquired aspiration pneumonia are often the normal flora of the oropharynx, including:
Streptococcus pneumoniae.
Staphylococcus aureus.
Haemophilus influenzae.
Anaerobes - eg, Peptostreptococcus, Fusobacterium and Prevotella spp.
‘Streptococcus milleri’ group.
Klebsiella pneumoniae - increasingly seen in those with a history of alcohol misuse.
Nosocomial aspiration pneumonia pathogens and treatment
Pathogens of nosocomial (occurring within hospital) aspiration pneumonia include:
Oral anaerobes - as above.
Gram-positive cocci - eg, Peptostreptococcus spp., Peptococcus spp.
Gram-negative bacilli - eg, enterobacteria
(K.pneumoniae, Escherichia coli, Enterobacter spp.), Pseudomonas aeruginosa.
Methicillin-resistant S. aureus (MRSA).
Treated the same as pneumonia; but ensure there is no airway compromise first (suction, ABCDE etc.)
signs of life threatening asthma
silent chest,
oxygen saturation below 92%,
bradycardia
poor respiratory effort
Acute asthma investigations
ABG
FBC - raised WCC and CRP indicate infection causing exacerbation
U+Es - dehydration
Blood Cultures for suspected infections
CXR
ECG if indicated - other comorbidities present
Sputum sampling for culture if productive cough
acute asthma discharge planning
Assess and reassuring PEFR is >75% of predicted upon discharge
Patient education and training to use PEF meter and other medications at home for more information on asthma
Advice to keeping diary recorded PEFR measurements
To see their GP within 2 days
To complete the oral steroid course , and /or oral antibiotics if prescribed .
Signs of respiratory distress
Increased breathing rate Colour changes - cyanosis Grunting (mainly in children) Retractions (children) Use of accessory muscles Sweating Wheezing Body position - leaning forward etc.
Breathlessness definitions
Acute breathlessness: onset develops over minutes
Subacute breathlessness: onset over hours or days
Chronic breathlessness: onset develops over weeks or months
When should you consider hospital admission for respiratory admissions
Heart rate more than 130 beats per minute
Respiratory rate of more than 30 breaths per minute
Altered level of consciousness
Systolic blood pressure less than 90 mmHg or diastolic blood pressure less than 60 mmHg
Oxygen saturation less than 92%, or central cyanosis
PEFR less than 33% of predicted ( refer to asthma severity criteria )
PE and VTE
Pulmonary embolism
blockage in one of the pulmonary arteries in your lungs. In most cases, pulmonary embolism is caused by blood clots that travel to the lungs from deep veins in the legs or, rarely, from veins in other parts of the body (deep vein thrombosis).
Venous thromboembolism VTE: term used to describe both PE and DVT
PE risk factors
Family history of DVT, clotting conditions or PE
Heart disease
Cancer: especially brain, ovary, pancreas, colon, stomach, lung and kidney cancers, and cancer metastases — can increase the risk of blood clots, and chemotherapy further increases the risk. Women with a personal or family history of breast cancer who are taking tamoxifen or raloxifene also are at higher risk of blood clots.
Surgery
Clotting disorders: APS
COVID-19
Prolonged immobility
Smoking
obesity/overweight
Supplemental oestrogen: birth control pills
Pregnancy
Provoked and unprovoked PE
Provoked PE: associated with acquired risk factors, either transient or persistent. These risk factors can be removed therefore reducing risk of recurrence.
Unprovoked PE: aka idiopathic PE; associated with no apparent clinical risk factors, or risk factors that are persistent and not easily correctable (such as active cancer or thrombophilia). Because these factors cannot be removed, they are at increased risk of recurrence.
PE investigations
ECG: most commonly see sinus tachycardia. “S1Q3T3” pattern of acute cor pulmonale is classic (McGinn-White Sign). A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain.
Two level PE wells score: 0-4 order DDIMER; if positive arrange immediate CTPA or offer interim therapeutic anticoagulation (apixaban or LMWH) try to choose drug that can be continued if PE confirmed
If DDIMER is negative; stop anticoagulation and consider alternative diagnosis
Above 4: PE is highly likely; arrange hospital admission for an immediate computed tomography pulmonary angiogram (CTPA) and, where necessary, carry out other tests
ABG
CXR
Lower limb ultrasound - useful in pregnancy to avoid harmful irradiation
Echocardiography - for hypotension (clinically massive PE) to assess RV function and thrombus
PE prevention
Anticoagulants Compression stockings Leg elevation Physical activity Pneumatic compression: thigh/calf-high cuffs that inflate to squeeze veins and improve blood flow in lower limbs
PE management
Arrange immediate admission for people with suspected PE if:
They have signs of haemodynamic instability (including pallor, tachycardia, hypotension, shock, and collapse).
They are pregnant or have given birth within the past 6 weeks.
Pharmacological treatment options for confirmed pulmonary embolism (PE) include:
Low molecular weight heparin (LMWH).
Fondaparinux.
Unfractionated heparin.
Oral anticoagulant treatment (warfarin, apixaban, or rivaroxaban).
LMWH followed by an oral anticoagulant (dabigatran or edoxaban).
Thrombolytic therapy may be used to remove the embolic material from the pulmonary arteries by promoting lysis of blood clots.
*Treatment choice and duration made by consultant decision, based on overall assessment of the patient and associated comorbidities.
In some cases, mechanical or physical interventions may be considered; IVC filters - designed to trap fragmented thromboemboli from deep leg veins en route to pulmonary circulation (whilst preserving blood flow) can be put in on temporary or permanent basis
PE follow up management
Adequate monitoring of specific anticoagulant treatments
Ensure they’re provided with all relevant info on anticoagulants, PE, specific requirements of treatment they’re on etc.
For people with unprovoked PE; review medical history and baseline blood test results including FBC, renal and hepatic function, prothrombin time etc.
Offer physical exam for people not known to have cancer
If planned to stop anticoagulation; consider testing for APS and hereditary thrombophilia in people with first degree relative with DVT or PE
pneumonia signs and symptoms
Increased effort to breathe
Increased respiratory rate
Dullness to percussion
Tactile vocal fremitus - more vibrations from persons back on vocal tactile test due to sound travelling better in fluid
Late inspiratory crackles
Bronchial breath sounds
Bronchophony
Egophony
CXR: bronchopneumonia showing patchy areas spread throughout of fluid.
Lobar pneumonia showing fluid localised to single lobe/lobes
Atypical pneumonia; concentrated in the perihilar region in reticular pattern (stripes of fluid around the hilum)
classification of pneumonia by locations
Bronchipneumonal throughout the lungs, bronchial and alveoli CXR: showing patchy areas spread throughout of fluid.
Atypical interstitial in lung interstitium CXR showing fluid concentrated in the perihilar region in reticular pattern (stripes of fluid around the hilum)
Lobar is consolidation of a whole lung lobe CXR showing fluid localised to single lobe/lobes
Pneumonia causes classification
Viral pneumonia: mostly caused by influenza
Fungal pneumonia: candida, aspergillus and mucor species tend to cause
Mycobacteria: Mycoplasma pneumoniae
Bacterial pneumonia: pneumococcal, staphylococcal, pseudomonas, legionella pneumophila, chlamydophila pneumoniae
Antibiotics for pneumonia overview
Fluoroquinolones effective against 3 common infective organisms (ciprofloxacin, levofloxacin)
Amoxicillin - COVID-19 guidelines suggest doxycycline first line treatment!
clarithromycin/erythromycin for ATYPICAL STRAINS
With ABs - after 72 hrs there should be some kind of improvement in pts suggesting its working such as no tachycardia, BP restoring; if they are the same or worse; then may need other kind of ABs/treatment etc.
Pneumocystis pneumonia (PCP)
serious fungal infection caused by pneumocystis jirovecii
Most suffers have weakened immune systems from immunosuppressive conditions such as HIV/AIDS or medicines such as corticosteroids
Less likely to contract due to availability of antiretroviral therapy (ART)
Transmission is airborne from healthy carriers
PCP symptoms
fever, cough, difficulty breathing, chest pain, chills, fatigue
PCP risk factors and prevention
fungus can live in the lungs asymptomatically in 20% adults and is removed naturally after several months in healthy individuals
30-40% of people with this infection have HIV/AIDS
People on corticosteroids
chronic conditions such as; chronic lung diseases,
cancer,
inflammatory or autoimmune diseases (rheumatoid arthritis) or
solid organ/stem cell transplant
PREVENTERS:
Given to individuals more likely to suffer from PCP infection
trimethoprim/ sulfamethoxazole (TMP/SMX)
PCP diagnosis and treatment
sputum/mucus sample Lung biopsy Blood test to detect beta-D-glucan TREATMENT: TMP/SMX given orally or via IV for 3 weeks Side effects: rash and fever
TB
Caused by Mycobacterium tuberculosis in humans, (MTB, M.Tb)
Chronic granulomatous disease.
Can be inactive for decades similar to HIV etc.
Can affect every organ of the body but only transmitted via the lungs (airborne): meaning that only lung and occasionally laryngitis TB is transmissible, aside from in 3rd world countries where can also be spread via polluted cows milks
TB epidemiology and how it spreads
Globally 9.6 million new cases/yr. Roughly 37% are unreported/undiagnosed
12% of new cases show co-infection with HIV
UK 8000/yr; 73% born outside UK (immigration)
It is most commonly spread by inhalation of infected droplets (accounts for almost all
cases in the UK).
Infectious patients cough up huge numbers of mycobacteria, which can survive in the
environment for long periods of time.
TB pathophysiology
Mycobacterium tuberculosis, MTB has slow metabolism in the body and is resistant against the immune system
Aerobic metabolism»_space; prefers the more oxygenated areas of the organs i.e. areas with richer blood vessels e.g. apex of the lung, anterior part of vertebral column, …
BK is swallowed by PMNs (polymorphonuclear cells; phagocytosis), but it is not digested/killed (like other bacteria)»_space; it survives and proliferates inside the cell + it is transferred to the Lymph Nodes by the PMN»_space; Lymphadenopathy (disease of the lymph nodes, in which they are abnormal in size or consistency)
Usually, specially-trained CMI (Cell-mediated immunity, trained T-cells/Macrophages) are able to kill the MTb.
Cell mediated immunity (trained T-cells/Macrophages) can kill MTb.
Tubercle in the lung/Granuloma in the body, is an organized collection of macrophages and is a special defensive cell arrangement.
Body/TB interaction results in a special type of necrosis ‘Caseous necrosis
Caseous necrosis
Cavitation [evacuation of necrotic materials] and/or
Calcification [Ca deposition on necrotic materials].
TB may cause Cold Abscess.
[Classic 4 signs of inflammation: swelling, warmth, redness, ~pain.]
Morphological patterns of caseous necrosis
Liquefactive necrosis, the dead tissue appears as a liquid viscous mass.
Coagulative necrosis, the dead tissue appears as a soft and white proteinaceous mass [something like a boiled egg]
Fat necrosis
Caseous necrosis, the dead tissue appears as a cheese-like appearance. Caseous [‘keɪsiəs’, Latin]: Cheese
Caseous necrosis can be considered a combination of coagulative and liquefactive
Necrosis.
Active TB
When containment by the immune system (T-cells/macrophages) is inadequate.
It can arise from primary infection, or re-activation of previously latent disease.
Transmission is through inhalation of aerosol droplets containing bacterium.
Only active pulmonary TB is contagious.
Latent TB
Persistent immune system containment, i.e. granuloma formation prevents bacteria growth and spread.
Positive skin/blood testing shows evidence of infection.
But the patient is asymptomatic and not contagious (normal sputum/CXR).
Lifetime risk of reactivation is 5–10%.
Risk factors for TB reactivation
new infection (<2y), HIV, organ transplantation, immunosuppression (incl. corticosteroids), elderly, young children, silicosis, illicit drug abuse, malnutrition, high-risk settings (homeless shelter, prison), low socio-economic status, haemodialysis, etc.
TB mechanism
M. tuberculosis is first encountered (Primary infection)
Host macrophages in the lung engulf the organisms and carry them to hilar lymph nodes in an attempt to control the infection.
Some organisms may disseminate via the lymphatics or bloodstream to distant sites (Extra-pulmonary TB).
Small granulomas (tubercles) are formed around the body to contain the mycobacteria.
These may heal spontaneously and the bacteria are eliminated (in 80% of cases)
Or bacteria are encapsulated in a defensive barrier but persist in an otherwise healthy individual where the disease is considered dormant (Latent TB).
Only a small proportion of patients progress to overt disease (Active TB).
Types of TB
Pulmonary TB, Tuberculous Pneumonia
Cardiac TB»_space; Constrictive Pericarditis
Tuberculous cervical lymphadenitis»_space; Scrofula
Gastrointestinal TB
Spinal TB, Tuberculous Spondylitis, Pott’s disease
Miliary TB, Disseminated Tuberculosis
Urogenital TB: Tuberculous Nephritis, Tuberculous Cystitis, etc.
Genital TB»_space; “Beading” of Vas/F. tube
Cutaneous TB, Lupus vulgaris
Tuberculous Osteomyelitis
Tuberculous Meningitis (CNS TB)
TB general presentation
Systemic features/General presentations Low-grade Fever, POU pyrexia of unknown origin Night Sweats Anorexia, Weight Loss Fatigue, Malaise Clubbing, Erythema Nodosum Symptoms of involved organ
Pulmonary TB presentation
Pulmonary TB accounts for 60% of TB cases in the UK.
Presentation varies and may be silent or atypical, especially with immunosuppression, e.g. HIV, post-transplantation.
Symptoms:
Chronic, productive Cough >2–3 weeks, dry then productive: purulent ± bloodstained sputum.
May result in lobar collapse, bronchiectasis, pleural effusion, pleurisy, or pneumonia, ± cavities
Haemoptysis - Uncommon, seen with bronchiectasis, not always shows an active disease
Tuberculosis lymphadenitis, Scrofula
Enlargement of cervical or supraclavicular lymph nodes (LAP). Axillary and inguinal node involvement is less common.
Systemic symptoms in only 40–50%.
Can occur with or without pulmonary disease.
Node is typically firm and painless and not acutely-inflamed (Cold abscess).
Skin can adhere to the underlying mass with risk of rupture and Sinus formation.
Diagnosis is fine-needle aspiration (FNA), AFB staining, and culture.
Miliary TB
Haematogenous dissemination leads to the formation of discrete foci (~2mm) of granulomatous tissue throughout the lung (‘millet’ seed appearance).
Dissemination is throughout the body, TB meningitis ~25%.
Diagnosis - Sputum may be negative for AFB, as spread is haematogenous.
Have a low threshold for LP.»_space; NAAT
IGRAS
Treatment - Untreated mortality is assumed to be close to 100%.
Do not delay treatment while test results are pending.
Gastrointestinal TB
Most disease is in the ileocaecal area.
Bowel obstruction (colicky abdominal pain and vomiting) due to bowel wall thickening, stricture formation, or inflammatory adhesions.
Biopsy is required for diagnosis and to differentiate from Crohn.
Cardiac TB
Usually involves pericardium: pericarditis, pericardial effusion, and/or constrictive
pericarditis.
Diagnosis is CXR (pulmonary TB, mediastinal lymph nodes), Echo., IGRAS, ± biopsy
Treatment is Anti-TB medications
Pericardiectomy, if persistent constriction despite anti-TB med.
TB differential diagnosis
Based on the presentation/s
Cancer, like lymphoma
Pneumonia
PUO pyrexia of unknown origin (FUO)
Fibrotic lung disease (e.g., Sarcoidosis, Hypersensitivity Pneumonitis,
Pneumoconiosis, Silicosis)
Chronic diseases such as Anorexia nervosa (AN) and Diabetes (DM).
Indications of latent TB
Been in close contacts of [active] pulmonary or laryngeal TB patients, those with immune dysfunction, healthcare workers, and high-risk populations, e.g. elderly, children, prison, homeless, vulnerable migrants, etc.
Investigations for latent TB
• Tuberculin skin testing, TST, Mantoux test, PPD
Intradermal injection of purified protein derivative (PPD) tuberculin. Assess skin reaction to the injection.
Positive result: Skin induration >5mm if risk factors; >15mm if no risk factors
It is dependent on BCG (bacillus Calmette-Guérin) vaccination history, and the immune status. Reaction will be false positive in pts with BCG vaccine. Not a very sensitive test.
• Interferon-gamma release assays, IGRAS (newer test):
exposure to TB»_space; release of interferon-gamma (IFN-γ), from T-cells, reacting to TB
antigen.
More Specific test»_space; If history of BCG vaccination (unlike TST) won’t give a positive result.
These tests are mainly for screening.
Neither test can diagnose or exclude active disease (false negative in 20–25%) and clinical evaluation is required.
Immune-suppressed states reduce the sensitivity of both tests
Investigations for active TB
Active Pulmonary TB
Offer HIV, HBV, HCV test for all.
CXR - can be normal so does not rule out TB. Typically shows Non-specific Fibronodular/Linear Opacity (tubercle) in Upper lobe, Ipsilateral Hilar Lymphadenopathy, Cavitation, Calcification, Effusion, Miliary disease
Ghon lesion/focus - Upper lobe opacity, usually sub-pleural. Ipsilateral hilar LAP. It is sometimes seen in TB. It is noy pathognomonic of TB.
Sputum smear - Sputum can be spontaneously produced or induced (with nebulized saline and precautions to prevent transmission). 3 specimens are needed, including an early-morning sample. It is stained for the presence of acid-fast bacilli (AFB). If AFB are seen, Tx should be commenced, and Pt. isolated (hospital/home).
Sputum culture - More sensitive than smear testing. Provides Drug sensitivity. Takes 1–3 weeks (liquid media) or 4–8 weeks (solid media). [other bacteria 2 days!]
NAAT - Nucleic acid amplification test. Direct detection of M. tuberculosis in sputum [or other fluid samples] by DNA or RNA amplification. Quick (<8hrs). Can detect drug resistance.
AFB - acid fast bacilli; staining technique for gram staining resistant bacteria; will colour red with acid staining
Active TB extra-pulmonary investigations
Offer HIV tests for all. [PCR, ‘Fourth-generation test (detection of HIV antibody and p24 antigen), ‘IgG sensitive’ tests, etc.]
Investigate for coexisting pulmonary disease. [CXR, Sputum, …]
Obtain material from aspiration or biopsy (lymph node, pleura, bone, synovium, GI, GU tract.»_space; AFB staining, histological examination (caseating granuloma) and/or culture.
NAAT»_space; on any sterile body fluid [interact with other bacteria]: CSF, pericardial fluid,
Investigate for co-existing pulmonary disease»_space; CXR, Sputum smear and culture
Involved Organ-related test e.g. CSF
Lumbar Puncture»_space; CSF»_space; AFB staining (Acid-Fast staining, Ziehl-Neelsen staining)
NAAT in CSF:
- Nucleic acid amplification test (NAAT)
- Direct detection of M. tuberculosis, in sputum/CSF/…, by DNA/RNA amplification
- Rapid diagnosis (< 8 hrs)
Tests are time-consuming»_space; Start treatment on suspicion
latent TB treatment considerations
Balance the risk of development of active disease, with the possible side-effects of Tx, like hepatotoxicity.
Consider Tx in all at high risk of active disease: HIV, transplantation, chemotherapy, etc.
Offer HIV, hepatitis B and C testing prior to treatment.
Active TB treatment considerations
All forms of active TB are statutorily notifiable in the UK. Notification»_space; www.gov.uk/health-protection-team
Treatment is given under the care of a specialist TB clinician/service
Offering HIV, hepatitis B and C testing, prior to treatment.
Patient’s compliance and Patient tracking is of extreme importance.
Pulmonary TB treatment
2 antibiotics (isoniazid and rifampicin) for 6 months 2 additional antibiotics (pyrazinamide and ethambutol) for the first 2 months of the 6-month treatment period). If you have TB in areas like your brain or the sac surrounding your heart (pericardium), you may initially be prescribed a corticosteroid (Links to an external site.) such as prednisolone (Links to an external site.) for several weeks to take at the same time as your antibiotics. This will help reduce any swelling in the affected areas
Bronchiectasis
Abnormal permanent dilation of the airways
Leads to impaired clearance of bronchial secretions with secondary bacterial infections and bronchial inflammation
May be localised to a lobe or generalised throughout the bronchial tree
Bronchiectasis is usually a complication of other conditions like pneumonia.
Bronchiectasis itself has important and dangerous complications, like recurrent Infections.
Bronchiectasis causes
common causes:
Cystic fibrosis (CF)
Post-infectious - After Pneumonia, Whooping cough (Pertussis), TB, HIV, Measles, Bronchiolitis etc.
Idiopathic
Rarer causes
Immunodeficiency (Hypogammaglobulinaemia,…)
Congenital ciliary defect e.g. Kartagener’s syndrome: immotile cilia, situs invertus, chronic sinusitis
Airway obstruction (tumor, inhaled FB)
RA (rheumatoid arthritis, UC (ulcerative colitis)
Bronchiectasis presentation
Chronic productive Cough
Recurrent chest infections
Severe cases - copious amounts of thick, foul-smelling green sputum.
Haemoptysis (which may be massive and life-threatening)
SOB (breathlessness)
Wheeze [as a symptom]
Clubbing
Coarse Crackles/crepitations, over the affected area (usually the lung bases)
Wheeze
Bronchiectasis investigations
CXR - Normal, Dilated bronchi with thickened bronchial walls, multiple cysts, containing fluid.
High resolution CT scan (GOLD STANDARD) - airway dilatation, bronchial wall thickening, bronchial wall cysts
Sputum culture»_space; essential during an infective exacerbation. The common organisms: Staphylococcus aureus, Pseudomonas aeruginosa and Haemophilus influenzae.
Where an underlying cause is suspected:
Serum immunoglobulins
Sweat test (CF)
Spirometry»_space; shows an obstructive pattern
Bronchoscopy»_space; to locate site of haemoptysis, exclude obstruction, and obtain samples for culture.
Bronchiectasis management
Smoking cessation
Respiratory physiotherapy and mucolytics, to promote mucociliary clearance and sputum production.
Annual influenza vaccination, pneumococcal vaccination
Prompt Antibiotic therapy for exacerbations.
Bronchodilators (β2 agonists [nebulized Salbutamol] and/or anticholinergics)
Inhaled or oral Steroids»_space; can decrease the rate of disease progression. [vicious cycle]
Surgery/Resection is reserved for the very small minority with localized disease or severe haemoptysis.
Severe disease sometimes requires lung or heart–lung transplantation.
Antibiotic treatment for bronchiectasis exacerbations
Patients with increased cough, sputum production, or purulence of sputum.
Mild: Cefaclor, 500 mg three times daily.
If Staph. is isolated on sputum culture»_space; Flucloxacillin
If the sputum remains yellow or green despite regular physiotherapy and antibiotics»_space; it is probable that there is infection with P. aeruginosa Ceftazidime, by aerosol or parenterally.
Ciprofloxacin, oral
≥3 exacerbations a year consider»_space; Long-term antibiotics
Bronchiectasis complications
Haemoptysis Pneumonia Empyema (Pyothorax) Pleural effusion Pneumothorax Respiratory failure Cerebral abscess Amyloidosis
Cystic fibrosis
One of the commonest life-threatening autosomal recessive conditions (1:2000 live
births) affecting Caucasians.
1:25 people carry a copy of the faulty gene. [Carrier]
All UK babies are screened at birth.
CF pathology
Mutated CFTR (chromosome 7) → absent or dysfunctional chloride channel → dysfunctional transport of chloride → abnormal secondary transport of sodium and water In sweat glands: inability to reabsorb chloride from the lumen → reduced reabsorption of sodium and water → sweat with elevated levels of sodium chloride + excessive loss of salt In rest of exocrine glands: inability to secrete chloride into the lumen → accumulation of intracellular chloride → increased sodium and water reabsorption → formation of hyperviscous mucus → accumulation of secretions → blockage of small passages → chronic inflammation → multiple organ damage
The lungs of babies born with CF are structurally normal at birth, frequent respiratory infections soon develop and are the presenting feature.
The resultant inflammatory response damages the airway, leading to progressive bronchiectasis, airflow limitation and eventually respiratory failure.
20% develop ABPA (allergic bronchopulmonary aspergillosis).
Mycobacterial colonization affects up to 20% of children, making a rapid deterioration
of condition.
In the newborn, thick tenacious intestinal secretions cause small bowel obstruction
(meconium ileus), an early manifestation of CF.
CF presentation in neonates
Meconium ileus [obstruction due to impaction of thick meconium] FTT (Failure to thrive) Rectal prolapse Fatty stool Cyanosis Finger clubbing Bilateral lung crackles
CF presentation in young adult s and children
Respiratory: cough, wheeze, recurrent infections, bronchiectasis, pneumothorax, haemoptysis, respiratory failure, cor pulmonale - nasal polyps, sinusitis Bilateral lung crackles Fatty stool Cyanosis Finger clubbing
CF presentation GI related and other signs
Pancreatic insufficiency (DM, Steatorrhoea), Malabsorption
Intestinal obstruction (content impaction),
Gallstones, Cirrhosis, GORD, …
Other
Male Infertility
Osteoporosis, Arthritis, Hypertrophic pulmonary osteoarthropathy (HPOA)
Vasculitis
CF diagnosis
Usually based on Sweat test and Genetic assessment.
Sweat test - Sweat Na and Cl >60mmol/L. Initial investigation.
Genetics - Blood DNA analysis. Genetic screening and counselling [family]
Faecal elastase - It is a simple and useful screening test for exocrine pancreatic dysfunction.
CF investigations
Sweat test genetic assessment Bloods: FBC, U&E, LFT, Clotting screen - vitamin A, D, E levels Annual glucose tolerance test, OGTT from 12yrs Bacteriology: Cough swab, sputum culture Imaging CXR: hyperinflation, bronchiectasis Abdominal ultrasound: Fatty liver, cirrhosis, chronic pancreatitis DEXA bone scanning (osteoporosis) Spirometry: Obstructive lung disease Aspergillus serology/skin test (20% develop ABPA, allergic bronchopulmonary aspergillosis) Biochemistry: Faecal fat analysis
CF management
Holistic management (psychosocial + physical wellbeing):
MDT: physician, GP, physiotherapist, specialist nurse, and dietician
Chest:
Respiratory Physiotherapy (postural drainage, airway clearance techniques). Abx
(Antibiotics) for acute infective exacerbations and prophylactically.
Mucolytics, Bronchodilators
Chronic Pseudomonas infection is an important predictor of survival.
Annual CXR surveillance
GI
Pancreatic enzyme replacement, vitamin supplements (A, D, E, K) …
Other:
Mx of CF-related DM
Screening (DEXA scan)»_space; treatment of osteoporosis
Advanced lung disease:
Oxygen
Diuretics (cor pulmonale)
Non-invasive ventilation
Lung or heart/lung transplantation
CF complications
Pseudomona
Lung damage associated with persistent infection with P. aeruginosa is a major cause of
morbidity and mortality in patients with CF.
Nebulized anti-pseudomonal antibiotic therapy, e.g. Tobramycin, improves lung
function, slows the rate of respiratory decline and decreases the risk of infective
exacerbations and hospitalization in these patients.
Regular sputum culture for Pseudomonas allows early detection and treatment.
CF prognosis
Today: Median survival is now ~ 41yrs in the UK.
In future: A baby born today would expect to live longer.
Post-lung-transplant survival = 5 years.
Occupational lung disease: pneumoconiosis
Exposure to dusts, gases, vapours and fumes at work can lead to the following types of lung
disease:
1. Acute bronchitis and pulmonary oedema by irritants - sulphur dioxide, chlorine, ammonia or
oxides of nitrogen
2. Pulmonary fibrosis, Pneumoconiosis - inhalation of inorganic dust: coal, silica, asbestos, iron,
tin
3. Occupational asthma –the commonest industrial lung disease in the more-developed world
4. Hypersensitivity pneumonitis
5. Bronchial carcinoma (Lung cancer) due to Asbestos, polycyclic hydrocarbons and radon in
mines.
6. Mesothelioma (neoplasm of pleura), due to Asbestosis
Coal workers pneumoconiosis CWP pathology
Underground coal-mines, inhalation of coal dust particles over 15–20yrs.
Particles are ingested by macrophages»_space; cell death»_space; releasing enzymes»_space; Fibrosis
Normally, particles are destroyed by clearance mechanisms. (trapped in the nose, removed by the mucociliary clearance system, destroyed by alveolar macrophages). But these particles are small and scape from this mechanism.
CWP includes a wide range in pathology and presentation (asymptomatic – col pulmonale)
CWPs presentation
Asymptomatic
SOB
Cough, with black sputum
Chronic bronchitis (co-existing CB)
PMF (Progressive massive fibrosis) progression of CWP»_space; progressive dyspnoea, fibrosis»_space; cor pulmonale.
Unlike simple CWP, even after stopping exposure to coal dust, PMF may progress.
CWP investigations
CXR: round opacities (1–10mm), especially in upper zone
PMF: fibrotic masses (1–10cm), bilateral, upper-mid zone
CWPs management
There is no specific treatment:
Smoking cessation (if smoker)
Avoid exposure to coal dust
Treatment of co-existing chronic bronchitis
Claiming compensation (Industrial Injuries Act).
Asbestos
Cause: inhalation of asbestos fibres.
Asbestos was used in the building trade (fire-proofing, pipe-lagging, electrical wire insulation, roofing felt, …), shipyard workers and ship engineering, etc.
Degree of asbestos exposure is related to the degree of pulmonary fibrosis.
Asbestos presentations
A long latency period (20–40 years) Progressive dyspnoea, productive cough and wheezing Clubbing Bilateral Lung Crackles Presentations of cor pulmonale.
Asbestos diagnosis
Based on History of exposure + typical CXR Fx
Sometimes»_space; CT, lung function tests (restrictive pattern), pleural biopsy
CXR:
Normal
Pleural plaques, pleural thickening, benign pleural effusions
Presentations of lung cancer, or mesothelioma
Asbestos complications
Pulmonary fibrosis
Risk of bronchial adenocarcinoma and mesothelioma
Asbestos management
Symptomatic Tx, smoking cessation, … Avoid (further) asbestos exposure Claiming compensation (UK Industrial Injuries Act)
Sarcoidosis
A multi-system granulomatous disorder of unknown cause
Women, 20–40yrs, African–Caribbean
Two main forms: Pulmonary Sarcoidosis, Non-Pulmonary Sarcoidosis
Pulmonary sarcoidosis
Asymptomatic 20–40%»_space; is discovered incidentally by a routine CXR shows bilateral (B/L) hilar lymphadenopathy (BHL) ± pulmonary infiltrates or fibrosis
Symptomatic: Constitutional: fever, night sweats, malaise, fatigue, weight loss. Respiratory: dry cough, progressive dyspnoea, ↓exercise tolerance, chest pain
Progressive disease in 20% of cases results in Pulmonary Fibrosis
Non-pulmonary sarcoidosis and signs
Any organ can be affected: skin, lymph nodes, eye, heart, brain, kidney, joint etc.
signs:
enlarged lymph nodes, scarring and granulomas
Eyes: dry and blurry vision
Heart: complications
Liver and spleen: enlargement
Joints: pain, arthritis, knee swelling
Skin: rashes, lupus pernio, erythema nodosum, skin lesions on back, subcutaneous nodules
Sarcoidosis differential diagnosis
TB
Lymphoma
Pneumoconiosis
Metastatic disease
Diagnosis of sarcoidosis
Diagnosis: a matter of exclusion, as there is no specific test for the condition.
As an example, to exclude sarcoidosis in a case presenting with pulmonary symptoms, might involve:
CXR
CT scan of chest
PET scan
CT-guided biopsy
Mediastinoscopy open lung biopsy bronchoscopy with biopsy endobronchial ultrasound, and endoscopic ultrasound with fine-needle aspiration of mediastinal lymph nodes (EBUS FNA).
Sarcoidosis variants
Acute sarcoidosis often presents with erythema nodosum ± polyarthralgia.
Usually self-limited»_space; Tx: bed rest, NSAIDS
BHL (only) is usually self-limited»_space; No Tx needed, just follow up
Sarcoidosis management and prognosis
Corticosteroids: Prednisolone
Antimetabolites: Methotrexate, Azathioprine, Leflunomide, Mycophenolate
Anti-tumour necrosis factor (TNF) monoclonal antibodies: Infliximab, Adalimumab
Prognosis:
response over 2 yr Tx: 60% resolve of disease
20% get better
20% no response – progressive disease
Pulmonary fibrosis types
Three types
- Replacement fibrosis- secondary to lung damage in a medical condition - infarction [PE],TB, pneumonia.
- Focal fibrosis - in response to irritants - e.g., coal dust and silica. (Pneumoconiosis)
- Diffuse parenchymal lung disease (DPLD) - in Idiopathic pulmonary fibrosis (IPF), and Hypersensitivity pneumonitis.
Idiopathic interstitial pneumonias and pathology
accounts for ~40% of diffuse parenchymal lung disease.
The most common interstitial lung disease (7.4/100,000)
Men, median age of presentation: 70
Most, smoker or ex-smoker
Often co-existing COPD
- No underlying causes can be identified.
- IPF (previously, cryptogenic fibrosing alveolitis) is the commonest type.
IPF, Pathology
patchy fibrosis of the interstitium
minimal or absent inflammation,
acute fibroblastic proliferation
collagen deposition.
Idiopathic interstitial pneumonias risk factors
Smoking
Industrial exposure (Pneumoconiosis): asbestos, heavy metals, silica, …
Environmental factors: pigeon breeding, contaminated ventilation systems.
Chronic viral infections: HCV, EBV (Epstein-Barr virus)- COVID-19 (?)
GORD, with micro-aspiration.
Idiopathic interstitial pneumonias presentation
Any patient, with breathlessness, + pre-existing medical condition or environmental exposure >> pulmonary fibrosis But: If Persistent/Progressive breathlessness \+ Age >45 Persistent non-productive/dry cough B/L inspiratory basal crackles Finger clubbing Normal spirometry or restrictive spirometry No Hx of med. Condition/environmental exposur >> IPF End sage IFP: respiratory failure, pulmonary hypertension cor pulmonale.
Idiopathic interstitial pneumonias investigations
CXR
Initially, ground-glass appearance,
Later, fibrosis and honeycomb lung. most prominent in the lower zones.
HRCT (High-resolution CT scan)»_space; the most sensitive imaging technique
bilateral irregular linear opacities and honeycombing
Respiratory function tests [spirometry]: Restrictive defect, lung volumes↓, gas transfer↓
ABG: O2↓, CO2 normal - [decreases O2 absorption but no issue losing CO2]
Histological confirmation is necessary in some patients.
» video-assisted thoracoscopic [VATS] lung biopsy
Idiopathic interstitial pneumonias diagnosis, treatmet and prognosis
detailed Hx, including Past medical History Drug history Occupational exposure (past and present) Treatment: Multidisciplinary team Pulmonary rehabilitation Pirfenidone (NICE, in some), Nintedanib, etc. Lung transplantation Prognosis - There is no cure - Poor prognosis (2.5 years survival from the time of diagnosis)
Kerley B lines and how to distinguish on CXR
caused from fluid in interlobular fissures (heart failure causes leakages etc.) found on the PERIPHERY of lung fields so can differ from pulmonary vessels which will remain more visible closer to the lung hilum.
Normal CXR
Cardiac shadow -Normal heart takes up less than 50% cardiothoracic volume on PA projection!
Lung fields - can see pulmonary vessels (spidery), no lung edges, no shadowing or opacity, nice clear costophrenic angles (diaphragm meeting lung angle)
Mediastinum (middle mediastinum - great vessel roots etc.)- no more than 6cm width on PA, no more than 8cm width on AP
Systemic approach to CXR
Date and name Side labelling and projection markers - no projection make judgment (usually PA) Lung fields - ABCDE? Any consolidation? Hilum - any consolidation? Mediastinum Diaphragm and costophrenic angles - lifted? Gas underneath? Fluid in angles? Sharp angles? Trachea - side deviation? Bones - broken? Alignment? dislocations? Soft tissues
common CXR pathologies and how to distinguish
Pneumothorax - can see lung edge due to air pushing it into chest space; can be so subtle but if in doubt get a CT scan!
Tension pneumothorax - can see trachea being pushed to one side by this air
Put needle into 2nd ICS to drain air
Pleural effusion
upside down meniscus shape suggests fluid in the lungs not consolidation as this will be more solid looking! Sounds like Stony dullness on percussion. Can be unilateral or bilateral (heart failure characteristic)
Takes a lot of fluid to be able to be seen on CXR! To get better view can take a lateral view
Consolidation:
lower lobe consolidation - less meniscus shape more defined edging to mass.
upper lobe consolidation
middle lobe consolidation
Consolidation doesn’t always occur at the base of the lung and can follow bronchial tubes while pleural effusion only fills the lungs from the bottom up. Also less likely to see other chest structures with consolidation as more XR absorbing
Mediastinal widening
if extends over the apexes of the lung is very bad sign. What disease?? google
Tumors:
cannonball metastases. Secondary tumors - tend to be round and discrete
calcium deposits seen in the mass in the lung, left upper lobe mass, often at the root of consolidation seen in CXRs so often see consolidation after. Can see bronchial vessels within consolidation but only Ca deposits in tumor mass. Masses have more defined edges usually. This is primary tumor is usually larger and less defined edges.
Pectus excavatum - on CXR heart is missing right side border, ribs are ‘7’ shaped and heart is displaced more to the left
red flag symptoms for coughing
Systemic symptoms: fever, night sweats, weight loss (TB, lymphoma, bronchial carcinoma)
Haemoptysis (TB, bronchial carcinoma)
Significant dyspnea (HF, COPD, fibrotic lung disease)
History taking for cough symptoms
Sound: barking, hacking, whooping etc.
Duration: acute less than 3 weeks, subacute (3-8 weeks), chronic more than 8 weeks
Timing: nocturnal, diurnal (asthma), trigger response to allergens or weather etc.
Secretion: dry, productive, moist cough (smokers)
Associated symptoms: SoB, fever, vomiting, blood, chest pain, weight loss
cough timing and indications
acute - less than 3 weeks: allergic rhinitis, asthma, COPD exacerbations, irritant exposure, pneumonia, PE, viral URTI
subacute - 3-8 weeks: postinfectious cough and bacterial sinusitis
chronic - longer than 8 weeks: asthma, beta blockers, chronic LVF, CHF, COPD, cystic fibrosis, GORD, lung cancer, postnasal drip, sarcoidosis, tobacco use, ACEi use
haemoptysis and indications
Haemoptysis:
Coughing up blood. Streaks or clots in sputum (lung Cancer) if mixed with green sputum (infection)
Other causes: TB, lung abscess, bronchiectasis
Duration and frequency: intermittent over years (bronchiectasis), more than one week (lung cancer), single episode with pleuritic chest pain (PE).
cough medications
OTC medicines:
Cough expectorant
Cough suppressant - decrease cough reflex to normal levels, most common OTC suppressant is dextromethorphan
Clinical use: dry cough with little phlegm needs cough suppressant (antitussive drugs)
Productive cough needs cough expectorant or mucolytic to help bring up phlegm. Designed to force cough reflex and propel phlegm out of airway. No evidence they have any effect!
Sedating antihistamines used as suppressant component of many compound cough preps on sale in public.
Acute and chronic bronchitis
Acute bronchitis:
Cough lasting 10 days to 3 weeks (acute infection)
Chronic is inflammation and cough lasting longer than this; usually due to irritants such as smoking
Chronic bronchitis:
Daily productive cough that lasts for 3 months of the year and for at least 2 years in a row.
Mostly affects those under age 40
Main causative factor is smoking
Causes of bronchitis
Viruses cause 85-95% of acute bronchitis in adults
Breathing irritant substances such as dust, smoke or occupational exposure to them
Rare cases can develop bacterial bronchitis after viral infection of bronchitis
Most common complication is pneumonia, especially in high risk groups(1 in 20 cases get pneumonia)
Most common in children under 5
More common in winter with common colds and flu
bronchitis symptoms
Sore throat Headache Runny nose/blocked nose Aches and pains in muscles Fatigue Cough - may persist several weeks post infection/after other symptoms have gone; may bring up clear/yellow or greenish mucus Fever Wheezes or Rhonchi may be heard on auscultation SoB
Bronchitis risk factors
Smoking Immunocompromised Reflux Exposure to irritants Age 50 and over
Bronchitis (acute and chronic) treatments
Mostly self-limiting will go away by itself within a few weeks without need for treatment
Home-care: hydration, bed rest, warm drinks, paracetamol or ibuprofen for headaches and pain relief, OTC cough suppressant medications (little evidence that these actually work however)
There’s no cure for chronic bronchitis, but some lifestyle changes can help ease your symptoms, such as:
eating a healthy diet
regular moderate exercise
avoiding smoking
Can also give bronchodilators and oral steroids to open up airway (inhalers or tablets)
Mucolytic medicines to help expectoration
Fungal pneumonia and common pathogens
Fungi from soil/bird droppings can cause pneumonia
Usually caused in those with compromised immune systems
Cannot spread from person to person; comes from contaminated environment
Pathogens:
Cryptococcus species
Histoplasmosis species
Pneumocystis jirovecii (HIV related)
fungal pneumonia presentation and treatments
Presentation:
Dry cough (no sputum)
SoB on exertion
Night sweats
Treatment:
Co-trimoxazole
Low CD4 pts are given prophylactic oral co-trimoxazole to protect against fungal pneumonia infection
Anti-fungal treatments may need longer periods of treatment
mortality can be as high as 90% in immunocompromised pts
Pneumocystis pneumonia
HIV related pneumonia
serious fungal infection caused by pneumocystis jirovecii
Most suffers have weakened immune systems from immunosuppressive conditions such as HIV/AIDS or medicines such as corticosteroids
Less likely to contract due to availability of antiretroviral therapy (ART)
Transmission is airborne from healthy carriers
Pneumocystis pneumonia symptoms
fever, Dry cough SoB chest pain, chills, Fatigue Night sweats
Pneumocystis pneumonia risk factors
fungus can live in the lungs asymptomatically in 20% adults and is removed naturally after several months in healthy individuals
30-40% of people with this infection have HIV/AIDS
People on corticosteroids
chronic conditions such as; chronic lung diseases,
cancer,
inflammatory or autoimmune diseases (rheumatoid arthritis) or
solid organ/stem cell transplant
Pneumocystis pneumonia prophylactics and treatment
PREVENTERS:
Given to individuals more likely to suffer from PCP infection
trimethoprim/ sulfamethoxazole (TMP/SMX or co-trimoxazole)
TREATMENT:
TMP/SMX aka co-trimoxazole given orally or via IV for 3 weeks
Side effects: rash and fever
Pneumocystis pneumonia diagnosis
sputum/mucus sample
Lung biopsy
Blood test to detect beta-D-glucan
Viral pneumonia
Is a complication of viruses causing colds or the flu
Accounts for roughly one third of pneumonia cases
Virus invades the lungs causing swelling and blocking oxygen flow
Many cases of viral pneumonia are self-limiting and resolve on their own within a few weeks
Severe cases can be life-threatening
Transmitted via coughing or sneezing or touching contaminated surfaces
Symptoms usually persist for 1-2 weeks but cough and headaches may last longer
Viral pneumonia Causes
Adenoviruses (common cold or bronchitis causing)
Chickenpox (varicella zoster virus)
Influenza virus
Respiratory syncytial virus (cold-like symptoms)
Viral pneumonia symptoms
Cough with yellow or green mucus Fever Shaking or chills Fatigue Sweating Blue lips Weakness Headaches SoB Muscle pain Worsening cough Children may show symptoms more gradually and less severe, may also lose appetite or eat poorly
viral pneumonia risk factors
Working in hospital or care setting Age 65 + Age 2 or under Pregnancy Autoimmune diseases Immunosuppression such as cancer pts Recent viral infection Smoking
Viral pneumonia investigations and diagnosis
CXR Sputum culture Nasal swab FBC ABC CT scan Blood culture Bronchoscopy - look into airways; rarely needed Diagnosis: Decreased airflow Crackling sounds Wheezing Rapid HR
Viral pneumonia treatment
Usually self-limiting and goes away by itself.
Home-care: bed rest, good hydration, OTC cough suppressant medications, warm drinks and herbal teas etc.
Antiviral medications are given to pts with severe illness or not otherwise healthy individuals (eg also immunocompromised) to help reduce symptoms and speed recovery
In some cases can develop secondary bacterial pneumonia from primary viral pneumonia and so will need to follow treatment for bacterial pneumonia (AB courses)
Advise flu vaccine yearly in vulnerable pts
General respiratory safety netting symptoms
New onset confusion Rapid breathing BP drop SoB Constant fever Chest pain
Pneumothorax
Also called collapsed lung
Air gets between the pleura of one lung
The pressure can cause the lung to give way
Causes decreased chest expansion
Can be caused by blockage or lack of pressure inside the lung instead of outside (atelectasis)
Pneumothorax signs and symptoms
Symptoms: SoB Chest pain - pleuritic one sided, sudden and stabbing Signs: Reduced air entry in auscultation Reduced vocal resonance and fremitus Hyperresonance on affected side
Pneumothorax investigations
CXR
CT scan
Pneumothorax types
Primary - no clear cause
Secondary - underlying lung conditions
Tension pneumothorax
Traumatic pneumothorax
Pneumothorax risk factors
Male gender
Ruptured air blisters more likely to occur between ages 20-40 years
Tall and thin body structure
Smoking
Family history/genetics
Lung diseases such as COPD, mechanical ventilation, previous pneumothorax
define haemothorax and haemopneumothorax
Haemothorax - pleural space fills with blood
Haemopneumothorax - blood fills pleura and lung filling from the bottom up
Tension pneumothorax
Occur when intrapleural air accumulates progressively exerting positive pressure on mediastinal and intrathoracic structures PUSHING the trachea
Develops when a lung or chest wall injury is such that it allows air into the pleural space but not out of it (a one-way valve)
The pressure decreases venous return to the heart causing shock.
Life threatening as can cause cardiorespiratory arrest Usually caused my trauma
tension pneumothorax signs and symptoms and investigations
Hypotension & Hypoxia
Deviated trachea
Hyperresonant, Jugular venous distention Tachycardia, tachypnoea
investigations: CXR
tension Pneumothorax treatment
Immediate needle decompression insert large bore (14-16 gauge) needling into 2nd ICS in mid clavicular line
Air released and this will result in simple pneumothorax so chest drain should be inserted immediately after
tension pneumothorax follow up advice
Patients should be advised to return to hospital if increasing breathlessness develops.
All patients should be followed up by respiratory physicians until full resolution.
Flying with a pneumothorax can be dangerous. This is because air in the pleural space in your chest will expand at the lower cabin pressure during the flight. This can compress the lung and can be dangerous. Until full resolution.
Diving should be permanently avoided unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively.
Pleural effusion
Also called water on the lung, is an excessive buildup of fluid in the space between your lungs and chest cavity.
➤ The pleura creates too much fluid when it’s irritated, inflamed, or infected. This fluid accumulates in the chest cavity outside the lung, causing what’s known as a pleural effusion.
➤ A pleural effusion is a collection of fluid next to the lung. There are various causes. The effusion may cause you to become breathless. The fluid can be drained if necessary. Treatment is mainly aimed at the underlying cause.
Pleural effusion causes
Lung infections (pneumonia) TB Cancers Heart failure Liver cirrhosis/ kidney disease Arthritic conditions may cause inflammation of the pleura e.g Systemic Lupus Erythematosis (SLE), Rheumatoid Arthritis (RA)
Pleural effusion signs and symptoms
Usually painless, but may have some chest pain
Fluid amount varies - but with a larger effusion, it presses on the lung which cannot expand fully when you breath and therefore may cause breathlessness
Symptoms relating to the underlying cause
Pleural effusion may be the first sign of an underlying cause
Signs:
Reduced or absent breath sounds on the side or area of pleural effusion
Stony Dull percussion
Reduced vocal resonance or fremitus - vibrations transmitted through the body
Transudate pleural effusions
Protein less than 30g/L Caused by factors that alter hydrostatic pressure, pleural permeability and oncotic pressure such as: CCF Liver cirrhosis Severe hypoalbuminemia Nephrotic syndrome
Exudate pleural effusions
Protein greater than 30g/L
Caused by changes to local factors influencing formation and absorption of pleural fluid such as:
Malignancy
Infection (empyema due to bacterial pneumonia)
Trauma
PE
Pleural effusion management
Directly mostly to correcting underlying cause
If underlying causes persists or there is recurrent pleural effusions, draining the fluid can help to manage
Small pleural effusion that cause no or mild symptoms are usually left and ‘observed’
Treatment is usually only needed if the effusion causes breathlessness
Large effusions can be drained using a pleural fluid aspiration or pleural tap.
Repeated draining of the fluid when symptoms become a problem for a patient is one option.
Depending on the underlying cause, other treatment options that are sometimes considered include:
Pleurodesis - chemical injection into pleural space
Leaving permenant drain in
Surgery to insert shunt for fluid
pleurectomy - remove pleura only last resort once all else fails
Pleurisy
Inflammation of the pleura usually causing pleuritic chest pain for a patient - sharp/ stabbing pain worse when breathing in or cough
May feel pleuritic chest pain anywhere in the chest depending on the site of the inflammation or problem with the pleura.
Two parts of the inflamed pleura rub over each other.
Pleurisy causes
Viral infection is the most common cause - pain typically lasts a few days and goes as the virus clears away and the inflammation settles
Bacterial Pneumonia PE
Chest injuries Pneumothorax
Lung Cancer
Inflammation with some forms of arthritis
Pleurisy diagnosis and management
Clinical diagnosis
Rule out other serious causes of pleuritic chest pain
Most common viral pleurisy - no signs on a chest x ray; viral
Management:
Painkillers for viral pleurisy
Otherwise treat for underlying cause pneumonia, PE, other causes
Empyema
Aka pyothorax
Pus gathers in pleural space
Can’t be coughed out, needs to be drained
Empyema causes
Develops after pneumonia - most common causative organisms are strep. Pneumoniae and staph. Aureus.
Occasionally caused by post surgical compilation
Empyema pathology
The pleural space naturally has some fluid, but infection can cause fluid to build up faster than it can be absorbed.
The fluid then becomes infected with the bacteria that caused the pneumonia or infection.
The infected fluid thickens. It can cause the lining of your lungs and chest cavity to stick together and form pockets. This is called an empyema.
Your lungs may not be able to inflate completely, which can lead to breathing difficulties.
Empyema investigations
CXR shows curved line across lung
Simple empyema:
Early stages of illness - pus is free flowing
SoB
Dry cough
Fever
Pleuritic chest pain
Systemic symptoms of headache, loss of appetite and confusion
Complex empyema:
SOB, Decreased breath sounds, weight loss chest pain
Complex empyema
Complex empyema occurs in the later stage of the illness. In complex empyema, the inflammation is more severe. Scar tissue may form and divide the chest cavity into smaller cavities. This is called loculation, and it’s more difficult to treat.
If the infection continues to get worse, it can lead to the formation of a thick peel over the pleura, called a pleural peel. This peel prevents the lung from expanding. Surgery is required to fix it.
Symptoms: SOB, Decreased breath sounds, weight loss chest pain
Empyema management
Treatment is aimed at removing the pus and fluid from the pleura and treating the infection. Antibiotics are used to treat the underlying infection.
The method used to drain the pus depends on the stage of the empyema.
In simple cases, a needle can be inserted into the pleural space to drain the fluid. This is called
percutaneous thoracentesis.
In the later stages, or complex empyema, a drainage tube must be used to drain the pus - thoracostomy/ chest drain; video assisted thoracic surgery; open decortication.
Near drowning
Drowning is the process of experiencing respiratory impairment from submersion/immersion in liquid. Drowning outcomes should be classified as: death, morbidity, and no morbidity.
Epidemiology:
4th most common injury.
2/3rd most common cause of accidental death in children in UK, Australia and USA
Incidence peaks for toddlers and teenage boys
Near drowning pathophysiology
Initial gasp with possible aspiration or period of breath hold
Apnoea eventually exceeds breaking point stimulating hyperventilation, causing aspiration and variable degree of laryngospasm
Leads to hypoxia and acidosis
85% cases asphyxia leads to relaxation of airway before inspiratory efforts have ceased and lungs filled with water
In young children immersion in cold water (less than 10 degrees) can stimulate protective diving reflex and produce apnoea, bradycardia and preferential shunting of blood to coronary and cerebral circulation which increases survival chance
Near drowning complications
Pulmonary oedema
Foreign body aspiration,
laryngospasm or bronchospasm may worsen the hypoxia.
Hypothermia, if it occurs, leads to a slowing of the metabolic rate but respiration is slowed even more so and hypoxia and hypercapnia develop. Prolonged hypoxia can lead to CNS and renal damage. Cold water immersion may also cause life-threatening cardiac arrhythmias.
Haemolysis occasionally occurs after freshwater drowning. Freshwater drowning can be much faster than saltwater drowning. This can also induce hyperkalemia that can stop the heart.
Near drowning risk factors
Unattended children under 5 years
People who can’t swim
Alcohol use
Water sports
Unsupervised swimming particularly in open water
Underlying risk factors such as epilepsy, cardiac dysrhythmias, hyperventilation, hypoglycemia, hypothermia and illicit drug use
Near drowning important history
Mechanism and duration of submersion
Type and temperature of water
Time until CPR started
Time of first spontaneous breath
Time of return of spontaneous cardiac output
Vomiting
Likelihood of associated trauma and other conditions like arrhythmias, MI, seizure etc.
Near drowning examination and investigations
ABCDE Vitals - oxygen Treat hypothermia or other associated conditions Immediate action Basic life support at scene - remember cervical spine may be injured Hospital action: Treat underlying or associated conditions Oxygen if needed CPAP if needed ECMO for severe pulmonary oedema Nasogastric tube +/- urinary catheter Dialysis for acute kidney injury?
Near drowning prognosis and prevention
Prognosis: Ultimately related to duration and magnitude of hypoxia Poor survival related with need for continued CPR Prevention: Education and water safety Safety barriers PPE such as buoyancy aids Pool coverings and safety signs etc.
Pneumothorax treatment
If no SOB and there is a < 2cm rim of air on the chest CXR then no treatment required as it will spontaneously resolve. Follow up in 2-4 weeks is recommended.
Give safety netting advice !!
If SOB and/or there is a > 2cm rim of air on the chest xray then it will require aspiration and reassessment.
If aspiration fails twice it will require a chest drain.
Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain
Chest drain insertion
inserted into the “triangle of safety”. This triangle is formed by:
The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)
The needle is inserted just above the rib to avoid the neurovascular bundle that runs just below the rib. Once the chest drain is inserted obtain a chest xray to check the positioning.
Normal MABP systemic and pulmonary (PAP) ranges and how to calculate
MABP normal systemic: 70-100mmHg
MABP (PAP) normal pulmonary: 10-14mmHg
To calculate: double diastolic BP, + systolic BP then divide by 3
Pulmonary HTN
PAP above 25mmHg at rest.
Progressive complication of many heart, lung or systemic diseases
Rarely idiopathic
Is a haemodynamic and pathophysiological condition with wide range of aetiologies
Finding the cause is important for the management!
More common in severe respiratory and cardiac diseases such as in acute PE; 0.5-4% show chronic thromboembolic PH
In US most common PH cause is left heart disease
Pulmonary HTN pathology
Pulmonary vascular resistance increases
Pulmonary blood flow increases causing further increased pulmonary resistance
Injury to pulmonary endothelium causes tendency for in-situ thrombosis (thrombotic pulmonary arteriopathy).
Disease process continues through vascular scarring, endothelial dysfunction and proliferation of smooth muscle cells within intima and media of pulmonary arterial tree
Causing progressive pulmonary arterial HTN
Obliteration of small pulmonary arterial vessels leads to right ventricular hypertrophy, progressive right heart strain and eventually right heart failure (COR PULMONALE)
pulmonary arterial HTN causes
Idiopathic
Hereditary
Drug-induced, toxin induced
Secondary causes: HIV, congenital heart disease, portal HTN, chronic haemolytic anaemia
Connective tissue disorders: rheumatoid arthritis, systemic lupus erythematosus, CREST syndrome etc.
WHO PH classifications:
Secondary to chronic lung disease or environmental hypoxaemia
Secondary to left heart disease, valvular disease (eisenmenger syndrome), restrictive cardiomyopathy
Secondary to chronic thrombotic disease, embolic disease or both
Secondary to metabolic disorders, systemic disorders, haematological diseases and other causes such as sarcoidosis
Idiopathic
Idiopathic Pulmonary arterial HTN
Rare
Severe
Often rapidly progressive
Diagnosis based on exclusion of other possible causes of PAH
Pulmonary HTN presentation
Early: Progressive exertional dyspnea Weakness Fatigue Loud pulmonary S2 Right parasternal have (due to RVH) Late: Abdominal pain (hepatic congestion - RVH) Angina Tachyarrhythmia (AF) Increased JVP Hepatojugular reflux Hepatomegaly (enlarged liver) Pulsatile liver Ascites Peripheral oedema Pleural effusion Will also show presentations of underlying disease
Differential diagnosis for pulmonary HTN
Cor pulmonale (secondary to PH) Cardiomyopathies Primary RV failure eg after MI CHF Recurrent PE Valvular disease Portal HTN Obstructive sleep apnea Hypothyroidism Sickle cell disease
Pulmonary HTN investigations
CXR:enlarged proximal pulmonary arteries +/- cause in heart or lung such as emphysema, calcified mitral valve etc.
ECG: shows RVH pattern (may be normal) also may show P pulmonale signs; right axis deviation, peaked P waves higher than 2.5mm and right bundle branch block.
Echo: RV hypertrophy/dilation (may be normal) +/- causes such as CHD can also estimate pulmonary artery pressure
Raised NT-proBNF blood test indicated RVF
MRI
Lung biopsy
Right heart catheterisation to confirm diagnosis by directly measuring pulmonary pressure
Pulmonary HTN management
Provided by specialist units:
Manage underlying cause
Medications can significantly help symptoms and exercise tolerance in short term
Specific treatments exist for PAH and chronic thromboembolic PH
Cardiosupportive therapy:
Oxygen increases exercise tolerance
Diuretics, digoxin lessens RHF and peripheral oedema
CCB (pulmonary vasodilators) for idiopathic PAH
Warfarin - reduce risk of intrapulmonary thrombosis; needs bleed risk assessment
Intravenous prostacyclin (potent vasodilator and inhibitor of platelet aggregation)
Bosentan, Ambrisentan (endothelin-A receptor antagonists; vasoconstrictor)
Heart and lung transplantations
Primary pulmonary hypertension can be treated with:
IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphodiesterase-5 inhibitors (e.g. sildenafil)
Secondary pulmonary hypertension is managed by treating the underlying cause such as pulmonary embolism or SLE.
Supportive treatment for complications such as respiratory failure, arrhythmias and heart failure.
The prognosis is quite poor with a 30-40% 5 year survival from diagnosis. This can increase to 60-70% where specific treatment is possible.
Cor pulmonale
Right heart failure caused by chronic PAH
Difficult to assess how common it is
In the UK, COPD is most common causative
Four main aetiologies:
Chronic lung disease; COPD, bronchiectasis, pulmonary fibrosis, severe chronic asthma, lung restriction
Pulmonary vascular disorders; pulmonary emboli, pulmonary vasculitis, primary PH, ARDS, sickle-cell disease, parasite infection
Neuromuscular disease; Myasthenia gravis, poliomyelitis, motor neuron disease
Skeletal diseases; scoliosis, kyphosis
Cor pulmonale most common causes
COPD Pulmonary embolism Interstitial lung disease CF Primary pulmonary HTN
Cor pulmonale presentation
Non-specific (especially in early disease)
Peripheral oedema
Raised CVP/JVP
Systolic parasternal heave
Loud pulmonary S2
Worsening tachypnea, exertional dyspnea, fatigue
Angina type chest discomfort (often non-responsive to GTN)
Haemoptysis
Exertional syncope
Cyanosis (worsening)
Tachycardia
SoB and increased difficulty breathing
Hepatomegaly
Usually chronic and progressive
However massive PE usually from acute PH and acute cor pulmonale
NICE guidelines for diagnosis - cor pulmonale diagnosis only made clinically after excluding other causes for peripheral oedema
Cor pulmonale investigations
FBC, Hb, haematocrit (secondary polycythaemia)
ABG; hypoxia with or without hypercapnia
CXR: enlarged right heart, prominent pulmonary arteries
ECG: P pulmonale (peaked P waves and right axis deviation), right ventricular hypertrophy
Spirometry/lung function tests
CT/MRI
Bronchoscopy
Lung biopsy
Cor pulmonale management
Treat underlying cause
Treat respiratory failure; acute situation (massive PE) give 24% oxygen, if PaO2 is less than 8kPa
In COPD; long term oxygen therapy 16hrs/day/nocturnal oxygen therapy (NOT)
Diuretics for HF
Venesection if Haematocrit is above 55%
heart/lung transplant in younger pts may be possible
Cor pulmonale complications
Exertional syncope Hypoxia Significant reduction in exercise capacity Peripheral oedema Peripheral venous insufficiency Tricuspid regurgitation Hepatic congestion and cardiac cirrhosis Death
Emphysema
Irreversible lung disease
Primarily caused by smoking
Alveoli and lung tissue are destroyed.
Alveoli cannot support the bronchial tubes. The tubes collapse and cause an obstruction, which traps air inside the lungs.
Too much air trapped in the lungs can give some patients a barrel-chested appearance.
Less oxygen will be able to move into the bloodstream.
Emphysema risk factors
Male Ages 50-70 Smoking Genetics (alpha-1 antitrypsin deficiency) Frequent respiratory infections
Emphysema symptoms
can be almost asymptomatic until up to 50% of lung tissue has been destroyed! Cough (long term ‘smokers cough’) Wheezing SoB Long term mucus problems Fatigue ‘Hollow’ sound on resonance
Investigations for emphysema
Clinical examination
CXR; moderate to severe cases can be detected
Pulse oximetry - low O2 sats
Spirometry and PFTs
ABGs
ECGs; rule out heart problems as cause of SoB
emphysema management
No known cure so treatment focussed on reducing rate of decline:
Smoking cessation
Bronchodilator medications
Anti-inflammatory meds; long term side effects include osteoporosis, HTN, high blood sugar and fat redistribution
Oxygen therapy for hypoxic pts
Lung volume reduction surgery: remove portions of diseases lung and join remaining tissues may help relieve pressure on breathing muscles and improve elasticity
emphysema good additional advice for pts
Good hand hygiene to prevent other infections
Brush and floss teeth daily and use antibacterial mouthwash
Keep breathing equipment clean
Keep house clean and tidy
Yearly flu shots
Following Dr prescribed exercise program
Avoid irritants such as smoking, exhaust fumes, perfumes, dust etc.
Type 1 respiratory failure (hypoventilation with V/Q mismatch
PINK PUFFERS cause: - pneumonia - PE - pulmonary oedema - Fibrosing alveolitis symptoms: ABCD - agitation - breathlessness - confusion - drowsiness and fatigue
Signs: central cyanosis
PaO2 less than 8kPa (or less than 10 of whatever O2 conc. if pt on Oxygen)
PaCO2 normal or low (4.7-6kPa)
Treatment:
- oxygen replacement therapy
- treatment of underlying cause
Complications:
- nosocomial infections like pneumonia
- HF
- Arrhythmia
- pericarditis
Type 2 respiratory failure: hypoventilation with or without V/Q mismatch
BLUE BLOATERS cause: - COPD and asthma - cerebrovascular disease - opiate overdose - myasthenia gravis - motor neuron disease Symptoms: ABCD: - agitation - breathlessness - confusion - Drowsiness and fatigue
Signs: ABC - A flapping tremor -bounding pulse - cyanosis PaO2 below 8 kPa (or 10 less than whatever O2 conc. pt is on if on oxygen) PaCO2 above 6kPa (hypercapnia)
treatment:
- noninvasive ventilation
- treatment of underlying cause
complications:
- nosocomial infections like pneumonia
- HF
- arrhythmias
- pericarditis
Silicosis
aka Potters rot
caused by inhaling silica particles unable to be removed by respiratory defenses
Macrophages engulf silica particles releasing TNF and cytokines inducing fibroblasts resulting in fibrosis and collagen deposition
Associated with increased TB infection
Acute: Symptoms happen a few weeks up to 2 years after exposure to a large amount of silica.
Chronic: Problems may not show up until decades after you’re exposed to low or moderate amounts of silica. It’s the most common type of silicosis. Symptoms may be mild at first and slowly worsen.
Accelerated : You’ll notice signs about 5 to 10 years after heavy exposure to silica. They’ll worsen quickly.
Silicosis risk factors
Most people get silicosis because they’re exposed to silica dust at work. Jobs in these fields may put you at higher risk:
Mining
Steel industry
Construction
Plaster or drywall installation
Glass manufacturing
Road repair
Sandblasting
Masonry
Roofing
Farming
Silicosis symptoms
A nagging cough
Phlegm
Trouble breathing as an early symptom of silicosis.
Later symptoms include:
Trouble breathing
Fatigue
Weight loss
Chest pain
Fever that comes on suddenly
Shortness of breath
Swollen legs
Blue lips
Silicosis investigations
CXR shows eggshell calcification of hilar lymph nodes with nodular lesions in upper lobes
bronchoscopy
Lung biopsy
Sputum test
Silicosis treatment
Medications: inhaled steroids to reduce mucus and bronchodilators
Oxygen therapy
Lung transplant
Berylliosis
caused by inhalation of Beryllium
causes granuloma formation made of giant cells, macrophages and epitheliod cells
Acute beryllium disease is very rare today. Current workplace safety regulations prevent the massive quantities of beryllium that cause acute beryllium disease from being released into the air. Chronic beryllium disease (CBD, berylliosis) is associated with inhaling beryllium powder or fumes An exposed person usually gets sensitized (allergic) to beryllium prior to progressing to CBD. Beryllium sensitivity (BeS) and CBD can develop soon after exposure or many (30-40) years later. Of those working around beryllium, about 10% get sensitized to it and about half of those progress to develop CBD.
There is no health threat associated with contact with solid beryllium; however, both the solid and powder forms can cause irritation if they come in contact with broken skin
Berylliosis symptoms
Difficulty breathing/shortness of breath
Weakness
Fatigue
Loss of appetite
Weight loss
Joint pain
Cough
FeverBerylliosis treatment
While there is no cure, commonly adopted management options involve cessation of beryllium exposure and use of systemic corticosteroids 4. Early treatment with corticosteroids may lead to disease regression and prevent further progression. If fibrosis has developed, the lung damage is irreversible.
symptoms of sinusitis
pain, swelling and tenderness around your cheeks, eyes or forehead
a blocked nose
a reduced sense of smell
green or yellow mucus from your nose
a sinus headache
a high temperature
toothache
bad breath
Signs of sinusitis in young children may also include irritability, difficulty feeding, and breathing through their mouth.
sinusitis treatment
mild sinusitis - home care: rest, fluids, taking painkillers, such as paracetamol or ibuprofen (do not give aspirin to children under 16), avoiding allergic triggers and not smoking, cleaning your nose with a salt water solution to ease congestion
OTC drugs: should not be used for more than 1 week:
decongestant nasal sprays or drops to unblock your nose (decongestants should not be taken by children under 6)
salt water nasal sprays or solutions to rinse out the inside of your nose
GP treatment:
steroid nasal sprays or drops – to reduce the swelling in your sinuses
antihistamines – if an allergy is causing your symptoms
antibiotics – if a bacterial infection is causing your symptoms and you’re very unwell or at risk of complications (but antibiotics are often not needed, as sinusitis is usually caused by a virus)
You might need to take steroid nasal sprays or drops for a few months. They sometimes cause irritation, sore throats or nosebleeds.
A GP may refer you to an ear, nose and throat (ENT) specialist if, for example, you:
still have sinusitis after 3 months of treatment keep getting sinusitis only have symptoms on 1 side of your face
They may also recommend surgery in some cases ( functional endoscopic sinus surgery (FESS).)
widen your sinuses by either:
removing some of the blocked tissue inflating a tiny balloon in the blocked sinuses, then removing it
Sinusitis
Sinusitis is swelling of the sinuses, usually caused by an infection. It’s common and usually clears up on its own within 2 to 3 weeks. But medicines can help if it’s taking a long time to go away.
Restrictive lung disorders and spirometry results
pneumoconiosis Disorders such as sarcoidosis, asbestos, pulmonary fibrosis, silicosis etc.
FEV1/FVC will be above 75% but individual FEV1 and FVC measurements will be less than predicted
Calculate FEV1/predicted FEV1 score for severity (more than 80% is mild, 50-80% moderate, 30-50% severe, less than 30% is very severe); if at the higher end of scale then can classify mild-moderate etc.
Lung cancers
arise from malignant epithelial cells in lungs.
globally is most common cancer (11.6% new diagnoses) and leading cause of cancer deaths
Poor prognosis with 5 year survival rate of 17%
Neoplastic pulmonary disease divisions:
Bronchogenic carcinoma - primary lung cancer
SCLC (oat cell)
NSCLC (adenocarcinoma, large cell)
Metastatic tumours - secondary lung tumours
Carcinoid tumours (wannabes)
Pulmonary nodules (coin lesions/SPN)
solitary Pulmonary nodules SPN
aka coin lesions
solitary nodules with no other clinical presentation; presents as a round/oval shadow usually less than 3cm on CXR
Can also have calcification present
Wide range of causes benign (80%) and malignant (20%)
SPN causes
Benign:
infectious granuloma eg TB
other infections eg localised pneumonia, abscess, hydatid cyst, benign neoplasms, arteriovenous malformations, bronchogenic cyst, pulmonary infarct, inflammatory conditions like rheumatoid nodule or Wegeners granuloma
Malignant: bronchial carcinoma single metastasis lymphoma pulmonary carcinoid
SPN/coin lesion differentials
Primary lung tumour (95% malignant; 5% benign) Secondary malignancy Carcinoid tumour Arteriovenous malformation (AVM) -Hamartoma^ -Chondroma -Abscess -Granuloma: TB, Non-tuberculous mycobacteria (NTM), Fungi, Sarcoidosis, RA,) -Encysted effusion (fluid, blood, pus) (e.g. Vanishing tumor/Phantom tumor) -Cyst -Foreign body (FB) -Hydatid cyst Not all spots are SPN/Coin lesions: Nipple Skin lesion/tumour ECG monitoring leads Encysted pleural fluid Healing rib fracture (callous)
General lung cancer risk factors
main risk factor is tobacco smoking, which is associated with 80% of lung cancer cases.
Passive smoke inhalation
Air pollution
Family history of cancer, especially lung cancer
Male sex (3:1 ratio)
Radon gas (typically affects miners) and ionising radiation
General lung cancer investigations
Pulse oximetry ECG preoperatively FBC: anaemia LFTs: raised ALP and GGT indicate hepatic or bone metastases U+Es: baseline before treatment Serum Calcium: elevation of PTH-related protein common in SCC CXR PET/CT-scan for staged imaging bronchoscopy+/- biopsy if indicated CYTOLOGY of sputum, pleural fluid etc.
all Pts with NSCLC considered for radical treatment should have a staging PET.CT scan to detect occult distant metastasis in brain, bone and liver
Lung cancer staging summary
Begins with TNM staging classification then to I-IV staging below:
I - one small tumour (less than 4cm) localised to lung
II - larger tumour (more than 4cm) may have spread to nearby lymph nodes
III - tumour spread to contralateral lymph nodes or grown into nearby structure eg trachea
IV - tumour spread to lymph nodes outside of chest or other organs eg liver
Non-small cell lung carcinoma management
Stage I-III:
surgery: lobectomy/pneumonectomy in pts with intact lung functions
wedge resection in pts with reduced lung function
Preoperative chemotherapy
Postoperative chemo and radiotherapy (Neoadjuvant preoperative chemo: may downstage tumours to render them operable . Adjuvant postoperative chemo and radio: improves survival chance reducing risk of tumour recurrence after resection)
Stereotactic ablative radiotherapy in pts unsuitable for surgery
Stage IV:
Targeted therapy: target specific mutated cells
Immunotherapy: drugs target immune checkpoints preventing pts immune cells from killing tumour cells (emerging therapy)
Chemotherapy: especially important for those who do not have mutations for targeting via other methods
Palliative care: palliative radiotherapy for metastases and symptoms control
Small cell lung carcinoma treatments
Chemotherapy and radiotherapy
Surgery: rare in small cell lung cancer, as most patients present with advanced disease.
Prophylactic cranial irradiation: since small cell lung cancer is associated with a high risk of brain metastases, radiotherapy is directed at the brain to prevent brain metastases.
SPN/coin lesion investigations and management
CXR approach: based on risk factors for malignancy:
Age above 40 years
Smoker
Occupational exposure to carcinogens etc.
Suspicious CXR features:
Lesion size greater than 3cm
Irregular border (spiculated margin)
Eccentric calcification (eg popcorn calcification)
Increasing size in follow up CXR
PET-CT scan/CT-guided biopsy
Excision if suspicious
Based on clinical judgement in MDT
In Pts with high risk excision could precede all steps after CXR
In cases of benign looking lesions and very low risk pt. Follow ups could also feature in approach to see if there are any changes etc.
Hamartoma overview
Type of coin lesion
Is not a neoplasm, just a mass of disarranged normal lung tissue
benign and rare condition
Diagnosed by CT scan shows lobulated mass with flecks of calcification
Treatment is often excision to exclude malignancy
Vanishing tumour overview
Localised fluid in interlobular fissue, secondary to chronic heart failure
treatment is to treat the CHF and tumour appearance on CXR should also ‘vanish’
aka phantom tumour
Metastatic lung cancer
Most common lung cancer: due to lungs receiving venous blood from whole body, therefore likely to pick up metastases spread from other sites in body is 2nd most common site for distant metastases (1st is liver for same reason)
Typical sites for primary tumour: kidneys, prostate, breast, GIT, cervix, ovary
Metastases usually develop in parenchyma
Metastatic lung carcinoma presentation and investigation
Presentations:
Relatively asymptomatic even if extensive
Carcinoma of the stomach, pancreas and breast may involve mediastinal lymph nodes, causing progressive and severe breathlessness
Investigations:
CXR: multiple and bilateral ‘cannonball lesions’ appearance
CT scan
Biopsy if indicated
Metastatic lung carcinoma management
Management of primary tumour
Lung metastases is usually sign of stage 4 cancer; indicating start of palliative chemo-radiotherapy
Metastasectomy can be performed in exceptions like colon cancer, Wilms tumour, oligometastatic breast cancer. These have slow growth characteristics meaning that it may be useful to remove primary and secondary metastases if there is only one/few metastases. May help to improve survival chances or alleviate symptoms.
Bronchogenic lung carcinoma
most common Primary lung carcinoma (95% cases)
less common cancer than secondary
arises from bronchus
Leading cause of cancer death - very very aggressive
Peak incidence between 55-65 years
SCLC and NSCLC primary lung carcinomas
Small cell lung cancers: (15% cases)
Approach from beginning is palliative
Cancer is incredibly aggressive with very poor prognosis
Non-small cell lung cancers (85% cases)
Squamous cell carcinoma SCC (37%) thought to arise from proximal airway
Adenocarcinoma (35%) more distal airway origins
Large cell carcinoma (7%)
Carcinoid tumours (6%)
SCLC summary
arise from endocrine cells (kulchitsky cells)
secretes polypeptide hormones causing paraneoplastic syndromes
More common in elderly smokers
located centrally
cells are poorly differentiated (multiply too fast to specialize)
early development of widespread metastases
responds to chemotherapy but has poor prognosis
NSCLC summary
adenocarcinoma: located peripherally in smaller airways. Glandular differentiation. Associated with asbestos exposure. more common in NON SMOKERS and ASIAN WOMEN
Metastases early but responds well to immunotherapy
SCC: located centrally (bronchi), squamous cell differentiated (KERATINISATION). more common in smokers. Secrete PTHrP causing hypercalcaemia
metastases late via lymph nodes.
Large cell: Poorly differentiated cells, metastases early. located peripherally. more common in smokers
Lung carcinoma presentations
Often no physical signs on clinical examination
Tumours located in the periphery tend to give earlier signs (like adenocarcinoma): pleural and chest wall invasion:
Signs of pleuritic chest pain - parietal pleural irritation or invasion
Constant chest wall pain - rib/muscle involvement, intercostal nerve involvement etc.
Pleuritic friction rub
Pleural effusion
Tumours localised in central areas tend to give later signs (like SCC, carcinoid): bronchus invasion:
Cough - bronchial irritation or compression
Hemoptysis - tumor erosion or irritation
Chest pain
Breathlessness - obstruction or compression of airway
Recurrent infections (pneumonia, lung abscess)
Clinical examination features of lung carcinomas
Needs FULL RESP. EXAM if cancer suspected
Cachexia: increased resting energy expenditure and lipolysis
Finger clubbing
Dullness to percussion: tumour
Cervical lymphadenopathy: metastases in lymphatics
Wheeze on auscultation: tumour obstructing airway
RED FLAGS for respiratory system
Patient above age 40 with two of following symptoms (or is smoker with one of following symptoms): cough weight loss appetite loss dyspnoea chest pain fatigue
Consider urgent referral for anyone above 40 with one of follwing:
persistent or recurrent chest infections
finger clubbing
supraventricular lymphadenopathy or persistent cervical lymphadenopathy
chest signs consistent with lung cancer
thrombocytosis
Unexplained haemoptysis or CXR suggestive of carcinoma
Urgernt referral for 2 week wait CXR and follow ups
General lung carcinoma management approach
General approach:
Confirm diagnosis via tissue sample
Assess spreading to other areas of body (image staging CT/PET scan)
Refer to MDT
Management then based on TNM staging and MDT decision
Pancoast syndrome
pancoast tumour: unique due to apical location causing many VESSEL COMPLICATIONS!
Apical lung cancer
non-SCLC (mostly, but can be SCLC rarely)
Invasion to adjacent structures: subclavian vessels, lymphatic system, brachial plexus, spine, 2-3rd ribs, stellate ganglion, SNS
Mass effect: local inflammation due to tumour site causes compression of surrounding vessels
Difficult to treat
Typical symptoms of lung cancer usually absent
Pt is usually a smoker with rapid deterioration symptoms and signs in the eye, face, neck, shoulder, arm and vocals (whatever vessels are invaded)
Mass seen in apex of lung in CXR
Pancoast syndrome symptoms
Severe shoulder pain or paraesthesia towards axilla and scapula (brachial plexus)
Atrophy of hand or arm muscles (nerve invasion)
Horner syndrome(occurs on same side of face as the nerve affected!!)- caused from T1 sympathetic nerves compression! These supply the head, neck and eyes so will cause; ptosis (drropy eyelids), miosis (constricted pupils), anhydrosis (failure to sweat), hemianhidrosis, enophthalmos (SNS invasion)
Compression of blood vessels with oedema in face and arms, flushed face, shortness of breath (SVC invasion)
Hoarse voice (recurrent laryngeal nerve invasion)
Bovine (non-exposive) cough (recurrent laryngeal nerve invasion)
General symptoms: malaise, fever, weight loss, fatigue etc.
DIagnosis and treatment of pancoast syndrome
Diagnosis: CT scan/CXR Biopsy to confirm cell type Treatment: Preoperative chemo/raidotherpy to shrink tumours make them operable Surgery
SCC/epidermoid carcinomas
Usually starts on bronchus (central area) on lung and doesn’t present clinically until later
Produces airway obstruction symptoms: cough, hemoptysis, chest pain, SoB, recurrent infections
Strongly associated with smoking
May show cavitation (diagnosis similar to TB)
Most common in elderly men
Doesn’t tend to metastasis early
Better prognosis
Adenocarcinoma
More common in women
Most common cancer in non-smokers
Most common cancer with asbestos exposure
Starts near lung periphery: gives earlier signals in development
Invasion of pleura, mediastinal lymph nodes are common with later chest wall invasion
In later stages can often spread to brain and bone
Asbestosis:
In lung causes adenocarcinoma
In pleura causes mesothelioma (range of benign to malignant tumours)
Large cell carcinoma
Start in any part of lung
Poor prognosis; undifferentiated (high grade) tumours that spread early in the body
Small cell lung carcinomas
Aka oat cell carcinoma
Usually starts in central lung in proximal/central bronchi: signals occur in later disease; cough, chest pain, haemoptysis, SoB, recurrent pneumonia, lung abscess
Grows rapidly and spreads to lymph nodes and other organs quickly
Usually only palliative treatment of chemo-radiotherapy
Response to chemotherapy better than others
Arises from endocrine cells: causing hormone secretion producing Paraneoplasic syndromes
Highly proliferative
Accounts of 10-20% all lung cancer
Strongest associated with smoking (only 1% occur in non-smokers)
Mostly males
Diagnosis common at age 60
Onset of symptoms is rapid
Endobronchial biopsy to confirm
Lung carcinoma paraneoplastic syndromes
Endocrine: PTHrP causing hypercalcemia ACHT Cushings syndrome ADH (inappropriate secretion) Carcinoid syndrome Gynecomastia etc.
Neurology:
encephalopathy
subacute cerebellar degeneration
progressive multifocal leukoencephalopathy
peripheral neuropathy
Eaton-lambert syndrome (esp. associated with SCLC)
Skeletal:
finger clubbing
Haem:
anaemia
Thrombocytosis
many more
Carcinoid tumours
Carcinoid tumour of lung.GIT, phyllodes tumour of breast, mesothelioma of pleura, desmoid tumour of abdominal wall, mucinous/serous adenoma of pancreas
Tumour between adenoma and adenocarcinoma in terms of grading
All are malignant but with very low grade
Slow growing with good prognosis
Carcinoid: means Tumour-like:
1-2% lung malignancies uncommon
Low grade malignant very slow spreading
Often in central airways of lung
One of the neuroendocrine tumours of lung originating from Kulchitsky cells
Pathology shows ‘rosette’ formation
Carcinoid tumour presentations
Cough Wheeze Haemotpysis Chest pain SoB Recurrent infections Carcinoid syndrome (flushing, sweating, abdominal cramps, oedema, diarrhoea etc.) is rare (unlike in GI carcinoids) as not enough hormones made to produce these symptoms
Carcinoid tumour diagnosis and treatment
Diagnosis: 2wk referral CXR PET-CT scan Treatment: Referral to MDT Surgery if advised
Lambert-Eaton Myasthenic Syndrome
Lambert-Eaton myasthenic syndrome is a result of antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones. This leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). This weakness gets worse with prolonged used of the muscles.
This syndrome has similar symptoms to myasthenia gravis although the symptoms tend to be more insidious and less pronounced in Lambert-Eaton syndrome. In older smokers with symptoms of Lambert-Eaton syndrome consider small cell lung cancer.
ABG key values and normal ranges
PH 7.35-7.45 PaCO2 4.7-6.0kPa Bicarbonate 22-26 mEq/L Base excess +2 - -2mmol/L PaO2 11-13kPa
ABG steps for analysis overview
How is the patient? assess history eg vomiting likely loss of acidity etc.
Assess oxygenation (can rely on ABG for this, not VBG): less than 8kPa on air is resp failure but if pt on oxygen; anything less than 10kPa of inspired air is resp. failure (type 1 just hypoxia; type 2 hypoxia and hypercapnia)
Determine pH or H+ (between 7.35-7.45) acidosis is low; alkalosis is high
Determine respiratory component (CO2 between 4.6-6kPa)
Determine metabolic component (bicarb between 22-26; BE between -2 to 2)
ROME = respiratory opposite (to pH) Metabolic equal (to pH) eg if CO2 is high then is low pH (acidosis) and if bicarb/base excess is high then pH also high (alkalosis)
Respiratory acidosis and causes
Caused by increased CO2 CAUSES: Hypoventilation sedatives/sedation/opiates due to respiratory depression Depression of respiratory centre in brain stem via trauma Pneumonia Asthma COPD
Respiratory alkalosis and causes
Caused by hyperventilation blowing off too much CO2 CAUSES: Anxiety Hypoxaemia (HF) PE Pneumothorax Pain
Metabolic acidosis and causes
Increase in circulating acids or loss of HCO3- CAUSES: Renal failure (unable to excrete H+) Lactic acidosis (increased acids) Keto acidosis (increased acid) Diarrhoea (HCO3- loss)
Metabolic alkalosis and causes
Increase in HCO3- Or loss of metabolic acids CAUSES: Prolonged vomiting (acid loss) GI suctioning (acid loss) Hypokalaemia (H+ excretion)
ABG compensation and determining primary insult
primary insult will reflect the pH, while compensatory system will reflect the OPPOSITE (high pH with high bicarb is primary insult, but CO2 also raised in order to compensate for alkalosis by developing resp. acidosis!!)
Always go by pH to determine primary cause and match to bicarb or CO2
Compensatory mechanism always state ‘partial’ or ‘full’ to describe if it is correcting the problem or not
For cases of FULL COMPENSATION: look at patient and assess which is primary insult based on history OR based on results alone; use judgement on if pH looks more on the acidic or alkali side (low or high) the one it’s closer to is probably primary insult
Lactate normal values and indications for abnormal values
Less than 2 normally
High lactate = disease with lactate accumulation
In general, the higher the lactate the more severe the condition
When associated with hypoxia, lactate increase can indicate organs aren’t functioning properly
Separated into two groups:
Type A: most common type may be due to hypoxia from hypoventilation or reduced blood flow
Conditions include: shock from trauma or hypovolaemia, sepsis, MI, CHF, severe lung disease or resp. Failure, pulmonary oedema, severe anaemia
Type B: reflects excess demand for O2 or metabolic problems including: liver disease, kidney disease, uncontrolled diabetes, drugs like salicylates and metformin, exposure to toxins like cyanide and methanol, variety of rare inherited metabolic and mitochondrial diseases that are forms of MD and affect ATP productions or strenuous exercise like marathon runners
Anion gap
Derived variable used for evaluation of metabolic acidosis to determine presence of unmeasured anions
To work out if acidosis is from increased acid production vs decreased acid excretion can calculate anion gap
Na+ - (CL- + HCO3-)
Increased gap indicated increased acid production or ingestion such as diabetic ketoacidosis, lactic acidosis or aspirin overdose
Decreased gap indicates decreased excretion or loss of HCO3- such as diarrhoea, ileostomy, proximal colostomy, renal tubular acidosis (retaining H), addison’s disease etc.
respiratory syncytial virus
Causes respiratory tract and lung infections
So common that most children have been infected by age 2
Can also infect adults
In adults and healthy children RSV is usually mild and typically mimics the common cold
Self care measures are usually all that’s needed
Spread via droplet infection
Contagious for a few days post infection but can be up to few weeks
Respiratory syncytial virus symptoms
SYMPTOMS: most commonly appear 4-6 days after viral exposure Congested or runny nose Dry cough Low grade fever Sore throat Mild headache Severe cases: Fever Severe cough Wheezing Tachypnea Cyanosis In severe cases in infants: Short, shallow and rapid breathing Cough Poor feeding Fatigue Irritability
Resp. syncytial virus risk factors
Premature infants
Young children with congenital heart or lung defects
Children with immunosuppression
Older adults
Adults with asthma, CHF or COPD
Immunodeficient pts (HIV, transplants/chemotherapy)
Resp. syncytial virus complications
Pneumonia
Middle ear infection
Asthma
Repeated infections
Resp. syncytial virus investigation and diagnosis
Usually diagnosed via auscultation and exam
Wheeze in chest
Blood tests for infection (WCC, RBC, FBC, CRP)
CXR for lung inflammation
Swab of mouth or nose for culture
Pulse oximetry to detect hypoxia
Resp. syncytial virus management and prevention
TREATMENT:
Generally self care is all that’s needed; stay hydrated
OTC meds like acetaminophen (tylenol) to reduce fever, nasal saline drops
Antibiotics if there is a bacterial complication (pneumonia)
Hospital care includes IV fluids, humidified O2 and mechanical ventilation PRN
Preventative medications:
Palivizumab (Synagis) can help protect children at high risk of RSV complications
Medication recommended for children born prematurely with or without chronic lung disease, infants under 12 months with congenital heart disease, under age 2 who needed supplemental O2 at birth for at least 1 month and continue to have lung treatments or children under 2 who are immunocompromised during RSV season (winter)
Medication usually given monthly for five months during peak RSV season
Does not help symptoms once virus has been caught, only helps prevent
bronchiolitis
Common LRTI affecting infants under 2 years
Most cases (90%) are mild and clear up within 2-3 weeks without need for treatment
Caused by virus called respiratory syncytial virus (RSV)
Spread via droplet infection (coughs n sneezes)
Causes bronchioles to become inflamed reduced air intake in lungs and causing dyspnea
Around 1 in 3 children in UK develop during 1st year of life (most common between 3-6 months old)
By age 2 almost all infants have been infected with RSV and up to half have had bronchiolitis
Possible to get more than once - more common from Nov to March
bronchiolitis symptoms and red flags
usually worst between days 3-5. Cough usually resolves around 3 weeks.
Runny nose
Cough (dry and persistent)
Fever
Difficulty feeding typically after 3-5 days of illness
Rapid or noisy breathing (wheezing or crackles on auscultation)
WHEN TO SEEK HELP:
Child taken less than half their usual amount during last 2-3 week feeds
Have had dry nappy for 12 hours or more
Persistent fever above 38 degrees
Seems irritable or tired
RED FLAGS:
Severe respiratory distress e.g.:
grunting,
marked chest recession
Nasal flaring
RR over 70bpm
Persistent O2 sats under 92% on air
Clinical dehydration (fluid intake is 50-75% or normal or no wet nappy for 12 hours
Central cyanosis (blue lips or tongue)
Aponea
Exhaustion (not responding to social cues normally, wakes only with prolonged stimulation)
bronchiolitis risk factors
for developing severe bronchiolitis:
Chronic lung diseases
Hemodynamically significant congenital heart disease
Infants under 3 months old
Premature birth particularly under 32 weeks
Neuromuscular disorders
Immunodeficiency
take into account social risk factors (housing, ability and availability of carer to monitor child while unwell; as other factors for referral to secondary care while unwell
bronchiolitis investigations and differentials
INVESTIGATIONS:
Clinical assessments: RR, auscultations etc.
Oxygen saturation
DIFFERENTIALS:
Asthma (consider in infants with recurrent or persistent episodic wheeze or crackles and family history of atopy)
Bronchiolitis diagnosis
Based on clinical assessment of child’s symptoms and respiratory rate:
Persistent cough AND
Either tachypnea or chest recession (or both) AND
Either wheeze or crackles on chest auscultation (or both)
Young infants (especially under 6 weeks) may present with apnea without other clinical signs
Bronchiolitis management
Mostly mild will clear up within 2-3 weeks without treatment
Self care; good hydration, paracetamol or ibuprofen PRN
2-3% admitted to hospital for serious symptoms of breathing difficulties (more common in premature babies and those with congenital heart or lung conditions)
Give supplemental O2 for hypoxia
Fluids by nasogastric or orogastric tube (if cant take fluids by mouth)
Fluids IV isotonic for children not tolerating above or have impending resp. failure
Chest physiotherapy assessment for children with relevant comorbidities (spinal muscular atrophy etc)
Consider CPAP with respiratory failure
Capillary blood gas testing if worsening respiratory distress (when supplemental O2 is greater than 50%)
Bronchiolitis prevention and discharge
PREVENTION:
Good hygiene
Clean toys and surfaces
Keep infected children at home until better
Avoid smoking near children
High risk children for severe bronchiolitis can have monthly antibody injections to help limit severity of infection
DISCHARGE:
Clinically stable
Taking adequate oral fluids
Maintained O2 above 92% for 4 hours including period of sleep
Croup/laryngotracheobronchitis
Common childhood disease usually caused by virus
Most common in children aged 6 months - 6 years; peak incidence at age 2
Usually self limiting resolves in around 48 hours
Croup symptoms
Sudden onset barking cough Usually with stridor (inspiratory) on auscultation Symptoms usually worse at night Mild: Seal like barking cough Moderate: Cough With stridor And sternal recession at rest Severe: Cough With stridor And sternal recession at rest Associated with agitation and lethargy Symptoms of impending respiratory failure: Increasing upper airway obstruction sternal/intercostal recession Asynchronous chest wall Abdominal movement Fatigue Pallor or cyanosis Altered conscious levels Respiratory rate over 70bpm
Croup differentials
Bacterial tracheitis: fever, sudden onset stridor and resp. Distress, following viral like illness
Epiglottitis: high fever, dysphagia, drooling, anxiety, cough, sit upright head extended preferred
Foreign body in upper airway: stridor, dyspnoea, history in inhalation
Allergic reaction: rapid onset dysphagia, stridor, rash, family history of allergies
Croup management
All children with mod-severe presentation should be admitted immediately to hospital
All children should be given single dose of oral dexamethasone (0.15mg per kg body weight)
If child too unwell for this; give inhaled budesonide (2mg nebulised single dose) or intramuscular dexamethasone (0.6mg/kg single dose)
Mild croups can be managed at home however admission considerations include: chronic lung disease, congenital heart disease, neuromuscular disorders, immunodeficiency, under 3 months old, dehydration, social factors meaning care would not benefit etc.
Mild home management includes paracetamol or ibuprofen for fever distress, good hydration, regularly check child’s wellbeing and monitor signs, advise parents symptoms usually resolve within 48 hours and safety net to come back/phone ambulance if signs of respiratory distress or persists longer than this
Pertussis/whooping cough
Highly contagious bacterial infection
Caused by bacteria bordetella pertussis
Incubation time roughly 5-10 days but symptoms may not appear for up to 3 weeks
Infectious from 6 days - 3 weeks post infection
Antibiotics can help reduce this infective window
Infants are at highest risk of death even after starting treatment
Children and adults generally recover quickly with early medical intervention
pertussis/whooping cough symptoms
Early symptoms mimic the common cold; runny nose, cough and fever
Coughing bouts lasting a few minutes
Worse at night
Makes ‘Whoop’ sound with gasps for breath in between coughing (may not if infants)
Thick mucus
Can cause vomiting
Red flushed face (more common in adults)
pertussis/whooping cough complications
Complications in infants under 6 months: Dehydration Breathing difficulties Pneumonia Seizures Complications in children and adults: Nosebleeds Sore ribs Hernia
COMPLICATIONS: Brain damage Pneumonia Seizure Bleed on brain Apnea Convulsions Death Urinary incontinence Rib fractures Sleeping difficulty
red flags for pertussis
URGENT 111 CALL IF:
Baby under 6 months
Cough is worsening
Been in contact with someone with whooping cough and are pregnant
Been in contact with someone with whooping cough and are immunocompromised
best to call GP before coming in as is very very contagious
CALL 999 for:
Apnoea
Cyanosis
Shallow breathing (resp. Rate over 70)
Pain worsening with breathing or coughing (pneumonia)
Seizures
pertussis/whooping cough investigations
Sputum cultures/samples
Pulse oximetry
Blood tests and cultures
Pertussis/whooping cough management and prevention
Severe cases or under 6 months old:
Hospitalisation: IV fluids, respiratory support, antibiotics for infection but do not treat the cough (may persist for long time post infection)
If diagnosed within 3 weeks of infection will be given antibiotics to help reduce spread to others
If diagnosed after 3 weeks of infection antibiotics are not needed
For mild cases: self care; rest, hydration, paracetamol or ibuprofen for discomfort/fever
PREVENTION:
Vaccination in infants and young children
Usually given as part of the 6 in 1 vaccination for infants aged 8, 12 and 16 weeks and the 4 in 1 pre school booster for pre school children
Should also be vaccinated if pregnant ideally between 16-32 weeks
acute epiglottitis
Inflammation and swelling of the epiglottis
Often caused by infection
Can occur from throat trauma/injury
Can be fatal if throat becomes completely blocked
With prompt treatment most recover from condition within a week and can be discharged within 5-7 days
acute epiglottitis cause
Haemophilus influenzae type b bacteria
Pneumonia
Meningitis
Spread by droplet infection and contaminated surfaces
Less common causes include strep. Pneumonia, fungal infections (in immunosuppressed) and viral infections like chickenpox.
acute epiglottitis symptoms
Severe sore throat
Dysphagia and pain while swallowing
Difficulty breathing (may improve when leaning forward)
Stridor on auscultation
Fever
Irritability and restlessness
Muffled or hoarse voice
Drooling
main symptoms in children are breathing difficulties, stridor, dysphagia and drooling
main symptoms in adults and older children are dysphagia and drooling
acute epiglottitis management and prevention
Hospitalisation
Intubation and oxygenation
In severe and urgent cases tracheostomy needed for oxygen access
Nasal oxygenation tube inserted once patient is more stable
Once the patient is stable; tests can be carried out:
Fiberoptic laryngoscopy (flexitube with camera to examine throat)
Throat swab to test for infection
CXR or CT scan to check level of swelling
PREVENTION:
Vaccination for HiB, particularly in children who are most vulnerable to this infection
Babies vaccinated in 6 in 1 vaccination
Should receive 3 doses at 8, 12 and 16 weeks of age followed by booster vaccine at age 1
Due to this vaccination, most child cases are rare and now only really occur in adults
Asthma BTS diagnosis guidelines
High probability asthma: typical clinical assessment, recurrent symptoms, wheeze heard, historical record of variable airflow obstruction and +ve history of atrophy without features to suggest alternative diagnosis
Record pt as likely having asthma and commence carefully monitored inhalation treatment (typically 6wks ICS)
Assess lung function and daily life (questionnaires)
With good symptomatic relief and objective response can confirm asthma diagnosis
If response is poor or equivocal check inhaler technique and adherence, arrange further tests and consider alternatives
Intermediate probability: spirometry with bronchodilator reversibility tests if appropriate, FeNO for eosinophilic inflammation if spirometry is normal, ‘watch and wait’ technique if children are asymptomatic or careful monitoring with symptomatic child
Low probability asthma: undertake further tests into alternative diagnoses or further lung function tests to widen clinical picture
Respiratory causes of finger clubbing
Clubbing Til Pulmonary Bronchi Burst
Cystic fibrosis Tuberculosis Pulmonary fibrosis Bronchiectasis Bronchial carcinoma
CF impact on organ systems
Lung
Ineffective mucociliary clearance; obstruction of the alveoli/bronchioles with an increased risk of infection
Destruction of the lung and reformation into a honeycomb parenchymal pattern due to chronic inflammation
Pancreas
Blockage of the exocrine gland’s secretion outlets
Fibrotic and cystic mutation
Loss of exocrine function
Gallbladder
Obstruction of bile drainage
Development of biliary cirrhosis
Intestines
Obstipation
asthma pathology
Chronic inflammatory disease of the middle to small sized airways
Hypersensitivity reaction causing increased goblet cell secretion increases mucus build up lining the airways
This blocks the mid to small sized airways due to the mucus taking up too much of the lumen (as the lumen is smaller) and so creates obstruction of air
This can cause high pitched wheeze noises classic presentation of asthmatics
