Coughing? Flashcards
Mrs Virginia is a 78-year-old lady who presents with a persistent cough. What questions would you ask her when taking a history?
Open questions:
* The British Thoracic Society (BTS) defines acute as
<3 weeks and chronic as >8 weeks. Between 3 and 8 weeks the cough may be
due to recovering acute illness or developing chronic illness.
Constant or intermittent?* A cough that is intermittent may suggest an extrin-
sic trigger (e.g. if the patient only coughs at work there may be an allergy to
something in the workplace). A cough that is constant suggests an intrinsic
cause.
Productive or dry?* The presence of sputum indicates inflammation and/
or infection. Patients with chronic obstructive pulmonary disease (COPD)
have chronically inflamed airways and often produce white or clear sputum.
Patients with infection have yellow or green sputum. Asthmatics may also
produce yellow sputum. Particularly large volumes of green or rusty sputum
may be coughed up in bronchiectasis and lung abscesses.
- Tiiming? Asthma is classically worse at night. Pulmonary oedema or
gastro-oesophageal reflux disease (GORD) can also be worse at night
due to the positional effects of lying flat. Patients often report sleeping
propped up on pillows to mitigate these effects. Trigger factors such as
pets, cold weather, or exercise indicate asthma, as does a worsening in
spring/summer. COPD by contrast is persistent.
Character?* A wheezy cough suggests airway obstruction due to asthma
or COPD. A bovine cough (breathy) is characteristic of vocal cord paralysis.
A dry cough is suggestive of pulmonary fibrosis. A gurgling cough is sugges-
tive of bronchiectasis. Pertussis infection causes a ‘whooping’ cough.
Then ask more directions about triggers of the cough: smoking, asthma, allergies, recent rhinitis or sinusitis, GORD Hx, drugs, travel (TB).
Then ask about associated symptoms: fevers, night sweats, rigors or weight loss (infection), breathlessness (Asthma, COPD, penumonia or pulmonary oedema), chest pain esp. pleuritic (pneumonia, PT, PE, viral pleurisy, or muscle strain, fractured rib) and wheeze (obstructuve disease or tumours compressing the airway).
Mrs Virginia says that she has had a cough for months but that over the last few days she has been
‘coughing more, and more muck has been coming up’. She says that the sputum is yellow-green, but there has been no blood. There appear to be no triggers or periodicity.
In her history she reveals that she is a long-term smoker (60 years smoking 10 a day = 30 pack years). She says she walks a mile a day to the shops and back, and has no history of asthma, allergies, or reflux. Reassuringly, she has had no
night sweats, rigors, or weight loss, and is no more breathless than usual. However, she says she has felt a little hot over the last day. She has not been abroad ‘since the war’, although she went on a Saga
holiday in Eastbourne the previous summer.
What are distinguishing features of asthma and COPD?
A history can help distinguish between asthma and COPD, along with bronchodilator reversibility testing/post-bronchodilator spirometry.
Asthma is typically associated with atopy (hayfever or eczema), female, GORD irritation, nasal symptoms, pneumonia, sinusitis, and aspirin. A wheeze can rule in asthma but does not rule it out.
Symptoms of asthma can include an expiratory wheeeze, shortness of breath, chest tightness and cough. COPD has similar symptoms but also includes the production of sputum.
List differential diagnoses of a cough. State what you think Mrs. Virginia’s diagnosis is and why
Differential diagnoses in an acute setting, if cough is productive, include:
- LRT infections including pneumonia, and bronchitis, and COPD, with TB less likely
- if dry: asthma, rhinitis/sinusitis ans URTs (pharyngitis and laryngitis). Less likely includes inhaled foreign body, P OED second to HF, smoke or toxin inhalation, lung cancer with obstruction of major bronchus
- if chronic and dry: asthma, GORD and post-nasal drip, less likely to be smoking, lung cancer, COPD, pulmo oed second, non-asthmatic eosinophilic bronchitis
- chronic and productive: bronchiectasis, TB, lung cancer, (congenital: CF and K’s syndrome).
More likely to be COPD, less likely to be asthma. Cough is non-productive in asthma. Condition has been persistent for several months. Recent worsening likely due to recent infection e.g. pneumonia. Need to investigate further.
What examinations and investigations would you undertake, and what findings would you expect?
General observations: diaphoresis? febrile? tachycardic? - indicates infection, upregulation of SNS
- barrel chest/hyperexpansion
- increased work of breathing
- CONFUSION OR DISORIENTATION
- CYANOSIS
- Complete sentences, few words at a time …?
Respiratory exam:
- increased respiratory rate
- hands and asterixis
- impacted oxygen saturation
- bronchial sounds
- dullness in percussion
- reduced expansion
- increased JVP
- expiratory wheeze?
- crepitations
Spirometry
- reduced FEV1/FVC (<LLN or <70%)
- slow PEF
ABG:
- in respiratory failure?
- impaired gas exchange
- asterixis
FBC, CRP: WBC elevated, infection (neutrophils especially indicative of bacterial infection)
Sputum culture - identify infectious agent
CXR/CT- consolidation? PT?
ECG- rule out cardiac causes e.g. AFib, ischaemia
Define respiratory failure and discuss the two types
Acute respiratory failure occurs when the pulmonary system is no longer able to meet the metabolic demands of the body.
There are two types of respiratory failure:
- Type 1 or hypoxaemic respiratory failure: a failure of gas exchange
- signs include: PaO2 less or equal to 60 mmHg when breathing room air; dead space ventilation: a problem of parenchyma causing defect in gas exchange; diffusion abnormality due to thickening of gas exchange surface e.g. due to pulmonary oedema, fibrosis; perfusion without ventilation or shunting- producing low O2 in blood
- Type 2 - hypercapneic respiratory failure or pump failure
- due to central depression or a mechanical defect (kyphoscoliosis) or fatigue (after prolonged SOB)
- ## signs include: PaCO2 greater than 45, hypoventilation due to inadequate TV (COPD), low RR (opiates, benzos)
N.B. total vent = TV x RR
On examination, Mrs Virginia looks sweaty and unwell. She is cachectic and has a ‘barrel chest’. Her
fingers are tar-stained. She is tachycardic and tachypnoeic with a pulse of 107 bpm and a respiratory
rate of 22/min. Her temperature is 38.5ºC. She has poor chest expansion, an expiratory wheeze, hyper-
resonant percussion note throughout but with dullness at the right lung base, and bronchial breath
sounds in the same place. Vocal resonance is increased over the area of percussion dullness. You find
no lymphadenopathy in the neck. She is not confused, with an AMTS of 9/10.
Interpret her AP CXR.
Patient details, rotation, exposure: Mrs. Virginia, portable AP CXR, adequate exposure. No rotation
A- airwaysclear, midline. Increased opacity over right main bronchus
Bones - no significant fractures
C-cardiac shadow normal : note that AP projection can overestimate size. All contours visule, though right heart border slightly more opaque
D- diaphragm: both hemi-diaphragms visible
E- effusion- not likely, as costophrenic angles (L and R) are still sharp
Fields- not equal. Increased diffuse opacity over right lung, especially in right middle and (lower) lobes. Appears to be consolidation. Location consistent with findings on auscultation
G-no gastric bubble visible
H-both hula visible, increased opacity over right hilum
In Mrs. Virginia’s case, would you conduct pulse oximetry or ABG? Why?
Ideally you would do both. In the immediate, pulse oximetry. Then ABG. Pulse oximetry works to estimate arterial oxygen saturation using absorption of two different wavelengths of infrared light. Note: arterial oxygen saturation does not have a linear relationship with PaO2.
Below 90%, PaO2 of 60 mmHg drops very quickly.
There are many sources of SaO2 error, including:
* Poor peripheral perfusion
* Darker skin
* Bright, ambient light
* Poorly adherent probe, excessive motion
* Carboxyhaemoglobin (SpO2 > SaO2)
* Carbon monoxide poisoning (e.g. after a fire) - carboxyhemoglobin gets recorded in oxygen
saturation but isn’t oxyhaemoglobin so SaO2 much higher than actual
* Hyperlipidemia
* Lipid infusion for TPN
* Propolol infusion (general anaesthesia agent)
Therefore it is best to rely on ABG results.
Mrs Virginia’s CRP and white cell count are raised, with a neutrophilia. Her saturations are 95% (on 28%
oxygen) and her ABG shows Pa
O 2 (arterial partial pressure of oxygen) = 12.4 kPa, Pa
CO2 (arterial partial
pressure of carbon dioxide) = 6.2 kPa, pH 7.42, HCO3
– = 32 mM. Her U&Es show Na 142 mM, K 4.7 mM,
Cl 103 mM, urea 9.2, creatinine 122 μM. An ECG showed sinus tachycardia but no other changes.
Is Mrs. Virginia in respiratory failure?
Not really. High PaO2 ~ 93mmHg.
High/borderline PaCO2 ~ 46.
O2 sats 95%, acceptable.
Mrs. Virginia appears to have a bacterial infection of the lung. Describe some organisms which could be the source of her infection
Common caues of community-acquired pneumonia in COPD patients include S. pneumoniae and H. influenzae.
Other causes include P. aeruginosa, S. aureus. Aspiration pneumonia is typically caused by S. pnemonia (facultative), Fusobacterium, Bacteroides and Prevotella (obligate ans).
S. pneumoniae as an Endogenous Pathogen
- alpha haemolytic, gram positive, diplococcus, facultative anaerobes
- A commensal of the URT of healthy people
- More common in children (40 %) than adults (10 %)
- Children initially colonized ~ 6 months of age
- Highest concentration of organisms usually in nasopharynx
- Children are transiently colonized by different serotypes (sometimes simultaneously)
- 91 known capsular serotypes
- Endogenous pathogen of the URT, can cause otitis media, mastoiditis, sinusitis
- Can disseminate into the LRT or other parts of the body, causing pneumonia, bacteremia, meningitis
- Note: Risk of developing these infections appears highest immediately after colonization because patients have not yet produced specific antibodies to the organism
Produces abrupt onset lobar pneumonia, high fever with rigors, productive cough with usual purulent sputum, pleuritic chest pain. Age is a risk factor, along with asplenia/hyposplenia, HIV infection, CLL, impaired or reduced antibody production.
-
Haemophilus influenzae
- Gram-negative coccobacillus ^[may look like a bacillus or a short bacillus which is almost coccus]
- Unencapsulated - less invasive and less virulent
- Capsulated - a, b, c, d, e, f
- H. influenzae B (Hib) most virulent
Haemophilus influenzae Non-Invasive Infection
i.e. not on mucosal surfaces
- Sinusitis
- Otitis media
- Conjunctivitis
- Pneumonia
Invasive Infection (Hib) ^[very rare since vaccination introduced]
- Epiglottis
- Bacteremia
- Meningitis
- Septic arthritis
Describe the pathophysiology of pneumonia, including factors that predispose to infection, classification of pneumonia, distribution of bacterial pneumonia and stages of bacterial pneumonia
Infection is down to three factors:
- virulence of pathogens
- factors affecting resistance in general
- factors affecting airway defences
Airway Defenses
- Normal lung contains no bacteria.
- Local defense mechanisms.
- Systemic resistance of the host.
Local Defense Mechanisms
- Nasal clearance
- Tracheobronchial clearance (Muco-ciliary action)
- Alveolar clearance (Alveolar macrophages)
Systemic Resistance of Host
- Innate immunity
- Humoral immunity
Factors affecting resistance in general
- Extremes of age
- Other conditions: chronic diseases, immunodeficiency (immunosuppressive treatment, leukopenia)
Factors affecting airway defenses (local defense)
- Altered cough reflex (anaesthesia, coma, drugs)
- Injury to mucociliary apparatus (cigarette smoking, immotile cilia syndrome)
- Interference of macrophage activity (alcohol, tobacco smoke)
- Accumulations of airway secretions (cystic fibrosis, bronchial obstruction)
Classification of Pneumonia
Anatomic Distribution
- Bronchogenic
- Lobar
Aetiologic Agent
- Bacteria
- Virus
- Fungus
Mechanism
- Aspiration
- Community acquired
- Hospital acquired
2 Patterns of Anatomical Distribution
1. Bronchopneumonia
- Patchy consolidation of the lung.
- - Common at the extremes of life.
- - Extension of a preexisting bronchitis.
2. Lobar pneumonia
- Consolidation of a large portion of a lobe or of an entire lobe.
- Acute infection of an entire lobe.
- Usually due to a virulent organism.
- Abrupt onset.
- Now infrequent due to antibiotic treatment.
Pathological Findings in Lobar Pneumonia
- Morphologic changes in the lung tend to follow a classic sequence.
- Four stages:
Congestion
- Enlarged lobe.
- Heavy and congested with blood.
- Blood-stained fluid from the cut surface.
- Dilated alveolar capillaries.
- Air spaces filled with pale fluid.
- Scattered red blood cells and neutrophils
- Occasional bacteria
Red hepatisation
- Cut surface is dry and red.
- Resembles liver macroscopically
microscopically:
- Fluid containing fibrinogen has clotted in alveolar spaces.
- Increased numbers of neutrophils.
- Bacteria more numerous.
Grey hepatisation
- macroscopically: After 2-3 days, loss of the red color; Starts at the hilum and moves out
- Migration of large numbers of neutrophils.
- Decrease in capillary congestion.
- Virtual cessation of blood flow through the unventilated lobe.
- Resolution
- Liquefaction of the previously solid exudate.
- Fibrinolytic enzymes.
- Apoptosis of neutrophils.
- Fluid contents removed:
- Expectoration
- Lymphatics.
- Takes several weeks
Since the introduction of antibiotics, this sequence is often altered.
Describe S. pneumoniae in detail
Endogenous Upper Respiratory Tract Pathogens
Streptococcus species are commensals and common causes of respiratory tract infections. (lobar pneumo if microaspiration into LRT)
Streptococci: General Characteristics
- Gram-positive cocci in chains
- Streptococcus pneumoniae classically in pairs (diplococci)
- **Facultative anaerobes
S. pneumoniae as an Endogenous Pathogen
- A commensal of the URT of healthy people
- More common in children (40 %) than adults (10 %)
- Children initially colonized ~ 6 months of age
- Highest concentration of organisms usually in nasopharynx
- Children are transiently colonized by different serotypes (sometimes simultaneously)
- 91 known capsular serotypes
- Endogenous pathogen of the URT, can cause otitis media, mastoiditis, sinusitis
- Can disseminate into the LRT or other parts of the body, causing pneumonia, bacteremia, meningitis
- Note: Risk of developing these infections appears highest immediately after colonization because patients have not yet produced specific antibodies to the organism
Pneumonia:
- Abrupt onset
- High fever +/- rigors
- Productive cough with usu. purulent sputum
- Shortness of breath
- Pain on breathing (pleuritic)
- Lobar consolidation (or anat segments of lobe) on CXR
Host Risk Factors for Invasive Pneumococcal Infection
- Age: Young and old
- Asplenic/hyposplenic
- HIV infection
- CLL
-
Impaired or reduced antibody production
- Hypogammaglobulinemia
- Multiple myeloma
S. pneumoniae Capsule - Virulence Factor
enables evasion
- Prevents entrapment in mucus, allowing access to epithelial surfaces
- Protects against phagocytosis and complement-mediated lysis: bacteria persist and multiply
- Anti-S. pneumoniae capsule antibodies (generated through acquired immune response) are protective, but typically not cross-protective
- Vaccine contains purified capsular polysaccharide antigen from many different S. pneumoniae serotypes ^[hence why acquiring one does not necessarily confer immunity against another]
Describe the complications of bacterial pneumonia
- Complications may be seen in either bronchopneumonia or lobar pneumonia.
- Bronchopneumonia:
- Healing by fibrosis.
- Lobar pneumonia:
- Pleuritis
- Empyema
- Abscess formation
- Haematogenous seeding
- Death
Organisation / Fibrosis
- Healing by fibrosis rather than resolution is more common in bronchopneumonia.
- Leads to organizing pneumonia.
- Polyps of fibrous granulation tissue within alveoli.
- ‘Masson Bodies’.
Pleuritis
- Inflammation extends to involve the pleura.
- Gives rise to typical pleuritic pain.
- Initially may just be an effusion.
- Followed by fibrinous pleuritis +/- bacteria.
- Healing leads to fibrous adhesions between visceral and parietal pleura.
Abscess Formation
- Localized suppurative process characterized by necrosis of lung tissue.
- Associated with Staphylococcus Aureus and Klebsiella pneumoniae.
- Ranges from millimeters to centimeters.
- Can be single or multiple.
- Macro: Cavities filled with suppurative debris.
Abscess Formation Histology
- Florid inflammation.
- Destruction of alveolar walls.
- Liquefactive necrosis.
- Chronic abscess surrounded by fibrous tissue.
Empyema
- Collection of pus in the pleural cavity is called an empyema.
- Collection usually loculates, followed by scarring.
- Requires drainage.
- Heals by fibrosis.
Haematogenous Spread
- Dissemination of bacterial organisms throughout the lungs or other organs.
- Bacteraemia/septicaemia.
- Seeding to heart valves (bacterial endocarditis), meninges (meningitis), kidneys (pyelonephritis).
Haematogenous Seeding Examples
- Bacterial endocarditis with vegetations on the aortic valve.
- Brain with surface purulent exudate.
- Kidney with surface petechial haemorrhages.
- Meninges (Meningitis).
- Kidneys (Acute pyelonephritis).
Death
- Still one of the commonest causes of death.
- Especially in the very young and old.
- Often represents the terminal event secondary to some other debilitating process.
Pneumothorax is an uncommon presentation with these symptoms. Describe what PT looks like on CXR
Pneumothorax, commonly abbreviated to PTX, (plural: pneumothoraces) refers to the presence of gas (often air) in the pleural space. When this collection of gas constantly enlarges with resulting compression of mediastinal structures, it can be life-threatening and is known as a tension pneumothorax (if no tension is present it is a simple pneumothorax). An occult pneumothorax refers to one missed on initial imaging, usually a supine/semierect AP chest radiograph.
Presentation is variable and may range from no symptoms to severe dyspnea with tachycardia and hypotension. In patients with a tension pneumothorax, presentation may include distended neck veins and tracheal deviation, cardiac arrest, and death in the most severe cases.
It is interesting to note that some generalizations can be made regarding the clinical presentation in primary versus secondary spontaneous pneumothoraces:
- primary spontaneous: pleuritic chest pain usually present, dyspnea mild or moderate - secondary spontaneous: pleuritic chest pain often absent, dyspnea usually severe
A pneumothorax is, when looked for, usually easily appreciated on erect chest radiographs. Typically they demonstrate:
visible visceral pleural edge is seen as a very thin, sharp white line no lung markings are seen peripheral to this line peripheral space is radiolucent compared to the adjacent lung lung may completely collapse mediastinum should not shift away from the pneumothorax unless a tension pneumothorax is present (discussed separately) subcutaneous emphysema and pneumomediastinum may also be present
Describe other less frequent causes of typical as well as atypical pneumonia
Neisseria meningitidis
- Gram-negative diplococcus
- Unencapsulated - not often associated with infection - 10-25% of young people carry in pharynx
- Capsulated - A, B, C, W, Y
- Invasive disease
- Vaccination: Previously only C but now also combined tetravalentA, C, W, Y and standalone B
Neisseria meningitidis Invasive Disease
- Risk factors for invasive disease
- Age <5 years and 15-25 years ^[living in close quarters]
- Asplenia/hyposplenia
- Deficiency or **impairment of complement membrane attack complex (C5-C9)
- Invasive disease:
- Bacteremia (meningococcemia)
- Meningitis
Moraxella catarrhalis
- Gram-negative diplococcus
- Diseases
- Sinusitis
- Otitis media
- Pneumonia
- Infective exacerbations of chronic obstructive pulmonary disease
Atypical Respiratory Tract Infections
“Atypical” Pneumonia
- “Atypical” bacteria
- Not detectable by Gram stain or cultured by standard methods
- **Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila, L. longbeachae
- “Atypical” symptoms and signs
- Constitutional symptoms (headache, fever, malaise, nausea) may predominate over respiratory symptoms (dry cough)
- Less likely to have lobar changes on CXR, diffuse or non-specific infiltrates
- Most cases are milder, but some, especially Legionella pneumophila, C. psittacii, can be severe and life-threatening
Mycoplasma species
- Smallest and simplest bacteria
- Lack of cell wall
- Unable to Gram stain
- Resistant to cell wall antibiotics e.g. blactam
Mycoplasma pneumoniae
Respiratory
- Pharyngitis
- Otitis media
- Pneumonia
Extrapulmonary
- Meningitis/encephalitis
- Erythema multiforme, tathet lesions
- Autoimmune hemolytic anemia/thrombocytopenia
- Pericarditis/myocarditis
Legionellosis pnumophila and serotypes, longbeachae
- Gram-negative bacillus
- Difficult to see on Gram stain
- Difficult to culture
- Specific growth factors
- Slow - missed in routine cultures
- Antibody response may take several weeks )(false negative)
- Urinary antigen (Legionella pneumophila) ^[not all subtypes, not longbeachae]
- Nucleic acid amplification ^[not lab validated]
Describe COPD classes, treatment and overall treatment aims
Aims:
- Relieve symptoms
- Prevent exacerbations
- Maximize exercise capacity
- Limit further damage
- Minimize treatment adverse effects
COPD classification
* Spirometry-confirmed diagnosis → assessment of airflow limitation →
assessment of symptoms/risk of exacerbations
* Group A: don’t have symptoms or risk of exacerbations ∴ SABA
* Group B: more symptoms, no risk of exacerbations - LAMA, LABA and ICS
* Combining will increase bronchodilator response and exercise capacity
* Bronchodilators improve symptoms but increase exacerbations likely due to
dynamic hyperinflation (struggle to generate enough expiratory capacity to
blow out any mucous)
* LAMA decrease mucous secretion and maintain airway calibre - decrease
symptoms
* Group C: LAMA and if exacerbations occur then LAMA + LABA or LABA + ICS
* Group D: LAMA + LABA or LABA + ICS → LAMA + LABA + ICS → roflumilast if
FEV1<50% or consider macrolide for former smokers
