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.
