Respiratory Flashcards

(72 cards)

1
Q

Pleural effusion definition and presentation

A

Abnormal accumulation of fluid in the pleural cavity

Dyspnea
Reduced exercise tolerance
Chest pain

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2
Q

Pleural effusion examination findings

A

Tachypnoea
Cyanosis
Lymphadenopathy
Stony dull percussive sound on affected side
Reduced/absent breath sounds
Bronchial breathing at upper border
Vocal resonance reduced over the effusion
Reduced chest expansion

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3
Q

Exudative pleural effusions

A

Protein content >35g/l

More likely to be unilateral
Caused by diseases that increase capillary permeability, such as:

Infections (parapneumonic effusion)
Malignancy
Inflammatory conditions
Pulmonary infarction
Pancreatitis
Chylothorax (collection of lymph in pleural space, usually secondary to trauma to the lymphatic system)

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4
Q

Transudative pleural effusions

A

Protein content <35g/l

Caused by imbalance in Starling forces governing interstitial fluid:

Heart failure (most common transudate cause)
Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)
Hypothyroidism
Meigs’ syndrome

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5
Q

Light’s criteria

A

Developed to help distinguish between a transudate and an exudate

Exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L
If the protein level is between 25-35 g/L, Light’s criteria should be applied

An exudate is likely if at least one of the following criteria are met:
Pleural fluid protein divided by serum protein >0.5
Pleural fluid LDH divided by serum LDH >0.6
Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH

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6
Q

Pleural effusion investigations

A

Bloods - FBC, U&E, LFT, clotting
CXR (first line)
Thoracic ultrasound
CT scan with contrast
Pleural fluid sampling:

sent for biochem, cytology and microbiology
Also Glucose - most commonly low in rheumatoid arthritis or empyema
pH – <7.2 in empyema
Amylase – raised in pancreatitis
Cholesterol and triglycerides – raised in chylothorax
Immunology

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7
Q

Recurrent pleural effusion management

A

Recurrent aspiration
Pleurodesis
Indwelling pleural catheter
Drug management to alleviate symptoms e.g. opioids to relieve dyspnoea

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8
Q

Asthma pathophysiology

A

Reversible airway obstruction

Often associated with family history of atopy, which includes the atopic triad of asthma, allergic rhinitis, and atopic eczema

Involves a type 1 hypersensitivity reaction, with allergens stimulating Type 2 helper T cells to produce cytokines like IL-4, IL-5, and IL-13. The inflammation of the respiratory airways results in bronchial hyperresponsiveness and reversible bronchoconstriction

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9
Q

Asthma risk factors

A

Family history
Personal history of atopy
Maternal smoking
Viral infections
Lower socioeconomic status

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10
Q

Asthma symptoms/signs

A

Wheeze
Dyspnoea
Cough (may be nocturnal)
Chest tightness
Diurnal variation (symptoms worse in the morning)

Symptoms may worsen following exercise, weather changes or following the use of nonsteroidal anti-inflammatory drugs (NSAIDs)/beta blockers

Tachypnoea
Hyperinflated chest
Hyper-resonance on chest percussion
Decreased air entry
Wheeze on auscultation

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11
Q

Chronic asthma investigations

A

Peak flow diary (readings will be lower in variation the morning due to diurnal - variability >20% is diagnostic)

Bloods - total IgE and eosinophils
CXR to exclude other causes
Spirometry - FEV1/FVC <0.7, reversible with bronchodilator
FeNO - >40 in adults or >35 in children

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12
Q

Chronic asthma management - non-pharmacological

A

Smoking cessation
Avoidance of precipitating factors (eg. known allergens)
Review inhaler technique

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13
Q

Chronic asthma management - pharmacological

A

Step 1: short-acting inhaled β2 agonist (eg. salbutamol)

Step 2: add low-dose inhaled corticosteroid steroid (ICS)

Step 3: add long-acting β2 agonist (eg. salmeterol).

if no benefit, stop this and increase ICS dose
if benefit but inadequate control, continue and increase ICS dose

Step 4: trial of oral leukotriene receptor antagonist, high-dose steroid, oral β2 agonist, oral theophylline

Patients escalated to steps 3 and 4 should be referred to a respiratory specialist.

There are also now biologic therapies in the form of monoclonal antibodies

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14
Q

Acute asthma presentation - severe attack

A

inability to speak in complete sentences
respiratory rate >25 breaths per minute
peak flow 33–50% predicted
heart rate >110 bpm

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15
Q

Acute asthma presentation - life-threatening attack

A

peak flow <33% of predicted
silent chest
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

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16
Q

Acute asthma investigations

A

Routine bloods inc FBC and CRP to look for underlying cause
CXR to exclude other diagnoses
ABG:

in a tachypnoeic patient
respiratory alkalosis is expected – owing to hyperventilation causing low paCO2
paO2 will likely be high

a falling respiratory rate is a sign of patient fatigue
paCO2 will return towards normal – this is a very concerning sign and the patient requires urgent escalation
type 2 respiratory failure (low paO2 and high paCO2) due to hypoventilation is a sign of a life-threatening attack

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17
Q

Management of acute asthma

A

ABCDE approach

Ensure a patent airway
Ensure oxygen saturations of 94–98%
Nebulisers (eg. salbutamol, ipratropium)
Steroids – oral prednisolone or IV hydrocortisone (if severe asthma or unable to swallow)

If severe
Single dose of IV magnesium sulphate
IV aminophylline (if inadequate response to nebulised bronchodilator)

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18
Q

Pneumonia definition

A

inflammatory condition of the lungs caused by infection. This leads to fluid and blood cells leaking into the alveoli. The infection spreads across the alveoli and eventually the lung tissue becomes consolidated, impairing the gas exchange due to reduced ventilation

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19
Q

Common causes of pneumonia

A

streptococcus pneumonia (usually community acquired)
Haemophilus influenzae
Mycoplasma pneumoniae

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20
Q

Pneumonia symptoms

A

Fever
Malaise
Rigors
Cough
Purulent sputum
Pleuritic chest pain
Haemoptysis

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21
Q

Pneumonia signs

A

Tachypnoea
Tachycardia
Hypotension
Cyanosis
Pyrexia
Dull percussion
Increased vocal resonance/ tactile vocal fremitus
Bronchial breathing - this is a higher pitch and inspiration and expiration are equal. There is an audible pause between inspiration and expiration
Pleural rub is an audible sound heard in patients with pleurisy. It is caused by the layers of pleura rubbing against each other

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22
Q

Hospital acquired pneumonia definition

A

lower respiratory tract infection that develops more than 48 hours after hospital admission. The most common organisms are Pseudomonas aeruginosa, Staphylococcal aureus, and Enterobacteria

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23
Q

Aspiration pneumonia definition

A

occurs in patients with an unsafe swallow. Risk factors include stroke, myasthenia gravis, bulbar palsy, alcoholism, and achalasia. On chest x-ray the right lung is most commonly affected, as the right bronchus is wider and more vertical than the left bronchus, making it more likely to facilitate the passage of aspirate.

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24
Q

Staphylococcal pneumonia

A

A bilateral cavitating bronchopneumonia due to staphylococcal aureus, a gram-positive cocci found in clusters.
It is found in intravenous drug users, elderly patients, or patients who already have an influenza infection.

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25
Klebsiella pneumonia
Primarily affects the upper lobes resulting in a cavitating pneumonia, presenting with “red-currant” sputum. It is caused by a gram-negative anaerobic rod. Furthermore, there is an increased risk of developing complications including empyema, lung abscesses and pleural adhesions. Patients at risk of Klebsiella pneumonia are those with weakened immune systems such as elderly, alcoholics, and diabetics. Additional at-risk groups include patients with malignancy, chronic obstructive pulmonary disease, long term steroid use and renal failure.
26
Mycoplasma pneumonia
Presents with flu like symptoms consisting of flu, arthralgia, myalgia, dry cough and headache. It primarily affects younger patients. Additional features include auto-immune manifestation due to cold agglutinins causing an autoimmune haemolytic anaemia. Complications that are associated with this pneumonia include: erythema multiforme; Stevens-Johnson Syndrome; Guillain-Barre Syndrome and meningoencephalitis
27
Legionella pneumonia
Fever, myalgia and malaise followed by a dyspnoea and a dry cough. It is associated with Legionnaire's disease, usually in patients who have been exposed to poor hotel air conditioning. Look for hyponatraemia and deranged LFTs on blood tests. Legionella antigen may be present in the urine
28
Chlamydophila psittaci pneumonia
Chlamydophila psittaci is an intracellular bacteria that results in psittacosis. It is acquired from contact with infected birds such as parrots, cattle, horse and sheep. Features include lethargy, arthralgia, headache, anorexia, dry cough and fever. Additional features include: hepatitis; splenomegaly; nephritis; infective endocarditis; meningoencephalitis and a rash
29
Pneumocystis pneumonia
This is associated with patients who are immunosuppressed (malignancy or chemotherapy) or HIV positive. The causative organism is known as pneumocystis jiroveci and is a fungus. In patients who are HIV-positive the risk of PCP increases when the CD4+ <200 cells/uL. Symptoms include exertional dyspnoea, dry cough, and fever
30
Pneumonia investigations
ABG Bloods – FBC, U&E, LFT, ESR, CRP Blood culture Sputum for microscopy & culture Polymerase chain reaction: for mycoplasma pneumonia Urine antigen: for legionella and pneumococcal pneumonia Chest X-ray: identify lobar, multi-lobar, cavitation and signs of pleural effusion
31
Pneumonia scoring severity
CURB-65 C – confusion: An abbreviated mental test of ≤8 U – urea: >7mmol/L R - Respiratory rate: ≥30/ min B - blood pressure <90 systolic and/ or <60mmHg diastolic 65 - age: >65year old
32
Pneumonia management
Oxygen to keep O2 saturations above 94% Fluid management Analgesia if patients have pleuritic chest pain. Paracetamol 1g/6 hours (Max. 4g 24hours) Antibiotics can be given orally for patients who are not nil by mouth and are managed in the community. However, for severe pneumonia Intravenous route is required Follow up appointments are organized for 6 weeks and CXR could be repeated at this time if there are complications or symptoms have not resolved
33
Pneumothorax definition
the presence of air in the pleural space
34
Pneumothorax signs/symptoms
Sudden onset shortness of breath Pleuritic chest pain Tachypnoea Respiratory distress Reduced chest expansion on affected side Hyper-resonant percussion on affected side Vocal resonance reduced on affected side Tachycardia Hypotension Tracheal deviation to contralateral side
35
Pneumothorax investigations
CXR
36
Pneumothorax management - primary
rim of air <2cm and patient not short of breath then discharge or aspirate If fails, insert chest drain
37
Pneumothorax management - secondary
if patient >50 year old and/or rim of air is >2cm and/or patient short of breath insert chest drain and admit for 24 hours
38
Tension pneumothorax definition
Life-threatening emergency ongoing, one-way leak into pleural space as the pressure in this space increases, it will begin to displace the mediastinum, impeding venous return and cardiac output this will eventually cause cardiovascular collapse and cardiac arrest in a simple pneumothorax, air does not continue entering the pleural cavity in this way, so it does not cause tension
39
Tension pneumothorax management
Initially ABCDE High flow oxygen 15l/min via a non-rebreather mask open thoracostomy followed by a chest drain otherwise a needle decompression can be used with a 16-gauge cannula, which is inserted at the second intercostal space, mid-clavicular line, on the affected side
40
Recurrent pneumothorax management
Smoking cessation Avoid scuba diving pleurodesis bullectomy
41
Lung cancer risk factors
Smoking (tobacco and cannabis) Passive smoking Occupational exposure (asbestos, silica, welding fumes, coal) HIV Organ transplantation Radiation exposure (X-ray, gamma rays) Beta-carotene supplements in smokers
42
Lung cancer symptoms
Cough Haemoptysis Dyspnoea Chest pain Weight loss Nausea and vomiting Anorexia
43
Lung cancer signs
Cachexia Finger clubbing Hypertrophic pulmonary osteoarthropathy Anaemia Horner syndrome (if the tumour is apical) Examination of the chest: consolidation (pneumonia) collapse (absent breath sounds, ipsilateral tracheal deviation) pleural effusion (stony dull percussion, decreased vocal resonance and breath sounds) Enlargement of supraclavicular and axillary lymph nodes Paraneoplastic syndromes: Cushing syndrome – suggests small cell syndrome of inappropriate ADH production (SIADH) – suggests small cell Lambert–Eaton syndrome – suggests small cell hyperparathyroidism – suggests squamous cell
44
Features of squamous cell carcinoma
most common presents as obstructive lesions of the bronchus leading to infection occasionally cavitates Hypercalcaemia (high PTHrp) Clubbing hypertrophic pulmonary osteoarthropathy
45
features of adenocarcinoma
Commonly invades the mediastinal lymph nodes and the pleura, and spreads to the brain and bones Does not usually cavitate Proportionally more common in nonsmokers, women and people from the Far East – least likely to be related to smoking Most likely to cause pleural effusion
46
Features of small cell carcinoma
Arises from endocrine cells (Kulchitsky cells, which are APUD cells), so these tumours secrete many polypeptides, mainly adenocorticotrophic hormone (ACTH) Can cause various presentations, such as Addison's disease and Cushing syndrome Spread very early – almost always inoperable at presentation Do respond to chemotherapy, but the prognosis is generally poor
47
Lung cancer investigations
Sputum cytology CXR: nodules lung collapse pleural effusion consolidation bony metastases contract CT including adrenals and liver to check for metastases Bronchoscopy – used to obtain a sample for histology Endobronchial ultrasound transbronchial needle aspiration (EBUS-TBNA) – allows biopsy of lymph nodes, paratracheal and bronchial lung lesions for histology Cardiovascular review and lung function tests should also be performed to assess the patient's suitability for different treatment options
48
COPD definition
Irreversible, usually progressive airway obstruction Encompasses chronic bronchitis (hypertrophy and hyperplasia of the mucus glands in the bronchi) and emphysema (enlargement of the air spaces and destruction of alveolar walls)
49
COPD symptoms
Productive cough Recurrent respiratory infections Wheeze Dyspnoea Reduced exercise tolerance Weight loss
50
COPD signs
Accessory muscle use for respiration Prolonged expiratory phase Pursed lip breathing Tachypnoea Hyperinflation – reduction of the cricosternal distance Reduced chest expansion Hyper-resonant percussion Decreased/quiet breath sounds Wheeze Cyanosis Cor pulmonale (signs of right heart failure)
51
COPD investigations
Bloods FBC – polycythaemia due to chronic hypoxia ABG – reduced paO2 +/– raised paCO2 (may be acute or compensated type 2 respiratory failure) ECG P-pulmonale (right atrial hypertrophy) Right ventricular hypertrophy, if there is cor pulmonale Chest X-ray Hyperinflated chest (>6 anterior ribs) Bullae Decreased peripheral vascular markings Flattened hemidiaphragms Spirometry – can be performed at diagnosis or to monitor progression FEV1/FVC ratio <0.7 Increased TLC Low TLCO – seen in patients who have significant emphysema without a significant chronic bronchitis element Reversibility testing is not required unless history/examination fails to differentiate between asthma and COPD Other tests: Sputum culture – to identify exacerbating organisms Brain natriuretic peptide (BNP) + echocardiogram – to assess for heart failure Serum alpha-1 antitrypsin – to assess for genetic cause in young patients Consider high-resolution CT (HRCT) scan if the diagnosis remains ambiguous
52
COPD pharmacological management
Step 1: short-acting β2 agonist/short-acting muscarinic antagonist – these are continued as the patient goes up the management steps Step 2: for patients with persistent exacerbations but no asthmatic features or evidence of steroid responsiveness add a long-acting β2 agonist AND a long-acting muscarinic antagonist for patients with persistent exacerbations with asthmatic features or evidence of steroid responsiveness increase management to a combination of long-acting β2 agonist and ICS Step 3: for patients on a long-acting β2 agonist + long-acting muscarinic antagonist combination who are still getting daily symptoms that affect their activities of daily living consider a 3-month trial of long-acting muscarinic antagonist + long-acting β2 agonist + ICS (triple therapy) if this does not work, revert back to long-acting β2 agonist + long-acting muscarinic antagonist for any patient on step 2 who is getting more than one severe or two moderate exacerbations in a year start long-acting muscarinic antagonist + long-acting β2 agonist + ICS Step 4: if patients are still symptomatic, consider specialist referral
53
COPD acute exacerbation management
Ensure a patent airway Ensure oxygen saturations of 88–92% (if there is a history of CO2 retention) Oral prednisolonw Nebulisers – salbutamol, ipratropium Steroids – oral prednisolone or IV hydrocortisone (if severe) Antibiotics if any evidence of infection (eg. fever or raised inflammatory markers) Monitor closely for signs of type 2 respiratory failure: drowsiness, asterixis, agitation as this may indicate the need for non-invasive ventilation (BiPaP)
54
Chronic bronchitis pathophysiology
Chronic exposure to noxious particles such as smoking or air pollutants causes hypersecretion of mucus in the large and small bronchi Airway inflammation and fibrotic changes result in narrowing of the airways and subsequently chronic airway obstruction Cigarette smoke interferes with the action of cilia in removing noxious particles Cigarette smoke also dampens the ability of leukocytes in eliminating the bacteria in the airways
55
Emphysema pathophysiology
Abnormal irreversible enlargement of the airspaces distal to the terminal bronchioles, due to destruction of their walls This reduces the alveolar surface area thus impeding efficient gaseous exchange Cigarette smoke stimulates accumulation of neutrophils and macrophages which produce neutrophil elastase that destroys alveolar walls In a normal lung, α1-antitrypsin is responsible for inhibiting excessive activity of neutrophil elastase. However, in emphysema, the normal balance of proteases and antiproteases is lost. The stimulated neutrophils release free radicals that inhibit the activity of α1-antitrypsin This results in loss of elastic recoil and subsequently airway collapse during expiration and air trapping
56
COPD FEV1 severity scale
Stage 1 (mild): FEV1 more than 80% of predicted Stage 2 (moderate): FEV1 50-79% of predicted Stage 3 (severe): FEV1 30-49% of predicted Stage 4 (very severe): FEV1 less than 30% of predicted
57
Ratio of FEV1 to FVC below 70%
Obstructive lung disease
58
Ratio of FEV1 to FVC above 70%
Restrictive lung disease
59
Obstructive vs restrictive lung disease
Obstructive = difficulty with exhalation Restrictive = difficulty with inhalation
60
Type 1 respiratory failure
Pa O2 <8kPa, PaCO2 normal Due to V/Q mismatch - volume of air passing in and out of the lungs is comparatively smaller than the volume of blood perfusing the lungs Asthma Congestive Cardiac Failure Pulmonary embolism Pneumonia Pneumothorax Low V/Q: areas that have poor ventilation with oxygen but are well perfused by blood. E.g. bronchoconstriction (Asthma), airway collapse in emphysema, mucus plug, congestive cardiac failure High V/Q: areas of the lung with adequate ventilation but are lacking blood perfusion E.g. Pulmonary embolism
61
Type 2 respiratory failure
PaO2 <8kPa, PaCO2 >6kPa Due to alveolar hypoventilation - lungs fail to effectively oxygenate and blow off carbon dioxide Obstructive lung diseases – Chronic obstructive pulmonary disease Restrictive lung diseases - idiopathic pulmonary fibrosis Depression of the respiratory center – opiates Neuromuscular disease – Guillan-Barre syndrome, motor neuron disease Thoracic wall disease – rib fracture
62
PE definition
formation of a blood clot in the pulmonary arterial vasculature, typically stemming from an underlying deep vein thrombosis (DVT) in the lower limbs
63
PE risk factors
Immobility (eg. bed-rest, long-haul flights) Pregnancy Oestrogen-containing medications – combined oral contraceptive pill, hormone replacement therapy (HRT) Obesity Age Malignancy Thrombophilia Recent lower limb surgery or injury Smoking
64
PE signs/symptoms
triad of symptoms, although all three features are rarely present: Sudden-onset shortness of breath Pleuritic chest pain Haemoptysis Syncope is a concerning symptom indicating massive PE A small PE may be asymptomatic Tachypnoea Tachycardia – may be the only presenting sign Hypoxia Low-grade pyrexia (possibly) A massive PE may present with: Hypotension Cyanosis Signs of right heart strain (eg. a raised JVP, parasternal heave and loud P2)
65
PE investigations
ECG findings: Normal or sinus tachycardia In a massive PE, there may be evidence of right-heart strain – P pulmonale, right axis deviation, right bundle branch block, and nonspecific ST/T wave changes The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III and inverted T waves in lead III) is relatively uncommon – <20% of patients Bloods: D-dimer - is highly nonspecific but has a 95% negative predictive value (ie. it is useful in ruling out a PE if negative) FBC – the patient may be anaemic if the PE has caused haemoptysis CRP – may be raised U&E – to assess renal function before a CTPA Clotting function – important if the patient is to be started on low-molecular weight heparin (LMWH)/warfarin ABG - may be normal or show a type 1 respiratory failure and/or a respiratory alkalosis (from hyperventilation secondary to hypoxia) Chest X-ray -typically normal in PE but helpful in ruling out differentials (eg. pneumonia, pneumothorax) possible findings include: Fleischner sign – an enlarged pulmonary artery Hampton's hump – a peripheral wedge shaped opacity Westermark sign – regional oligaemia CT pulmonary angiogram (CTPA) – the diagnostic test of choice for a PE, will show a filling defect in the pulmonary vasculature V/Q scan – preferred if the patient has renal impairment, contrast allergy or is pregnant Lower limb Duplex – helpful if a DVT is thought to be the cause of the PE (note: this investigation is first-line – before a CTPA – in pregnancy) Bedside echocardiogram – used to check for signs of right heart strain/hypotension in intermediate to high-risk PE, done to assess suitability for thrombolysis
66
Well's coring system
3 points clinical signs and symptoms of a DVT if no alternative diagnosis is more likely than a PE 1.5 points tachycardia (heart rate >100 beats/minute) if the patient has been immobile for more than 3 days or has had major surgery within the last month if the patient has had a previous PE or DVT 1 point if the patient presents with haemoptysis if there is an active malignancy If 4 or less, measure D-dimer to rule out PE If more than 4, diagnostic imaging required
67
PE general management
Oxygen if hypoxic Consider fluids if hypotensive Analgesia Consider IV fluids if the systolic blood pressure is <90 mmHg
68
PE anticoagulation
administered if there is high clinical suspicion can be started while awaiting confirmation on CTPA First-line treatment = direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban if neither suitable, dabigatran, edoxaban or warfarin (with low molecular weight heparin bridging), LMWH or unfractionated hepartin can be considered In inpatient/emergency setting, low molecular weight heparin is usually started instead as it is shorter acting provoked PE (identifiable risk factors, such as surgery or peripartum) should be treated for 3 months An unprovoked PE should be treated for 6 months If there is an ongoing cause (eg. thrombophilia), the patient should be treated for life recurrence of venous thromboembolism in a patient already on warfarin requires an increase in the target INR (to 3–4)
69
Massive PE management
defined as systolic blood pressure <90 mmHg (or >40 mmHg below patient's baseline BP) for >15 minutes treatment is thrombolysis (an IV bolus of Alteplase®) there is an associated risk of haemorrhage but this it lower than the risk of death from PE There is ongoing debate over whether Alteplase® should be administered in an intermediate–high risk (or submassive) PE This should be considered on a case-by-case basis
70
In COPD acute exacerbation give
Prednisolone for 5 days Amoxicillin if purulent sputum or clinical signs of pneumonia
71
Pneumectomy definition and CXR findings
Surgical procedure to remove a lung opacified hemithorax with mediastinal and tracheal shift towards the affected side Crowding of the ribs over the affected side with compensatory overinflation of normal lung is also seen NB. filled with air for first ~6 months then fills with fluid
72
The Centor criteria
presence of tonsillar exudate tender anterior cervical lymphadenopathy or lymphadenitis history of fever absence of cough to determine if a sore throat is bacterial in origin and should be treated via antibiotics (if 3 or more are met)