Pleuritic chest pain Flashcards
1
Q
Define pleuritic chest pain
A
Pleuritic chest pain = sharp pain caused by irritation of the pleura, worse on deep inspiration, coughing or movement.
2
Q
What are the differential diagnoses for pleuritic chest pain?
A
- Pneumothorax
- Pneumonia
- Pulmonary embolism
- Pericarditis : retrosternal
3
Q
Anatomy of the pleura:
What are the two layers?
What is the potential space?
What is in this space?
what is the function of this substance?
A
- Two pleura - one associated with each lung –> consist of serous membrane (layer of simple squamous cells supported by connective tissue)
-
Visceral pleura- covers outer surface of the lungs
- extends into the interlobar fissures, continuous w parietal at the hilum of each lung
-
parietal pleura - covers the internal surface of the thoracic cavity
-
named according to region it contacts
- mediastinal
- cervical
- costal
- diaphragmatic
-
named according to region it contacts
- The two parts are continous at the hilum of each lung
-
potential space between the two layers = pleural cavity
- contains small volume of serous fluid
- lubricates surfaces of pleurae allowing them to slide over each other
- also produces surface tension, pulling parietal and visceral pleura together –> ensures when thorax expans lung also expands
- If air enters pleural cavity surface tension is lost – > pneumothorax
4
Q
What is the neurovascular supply of the pleura?
A
- Parietal pleura:
- sensitive to pressure, pain and temperature
- produces well localised pain
- innervated by phrenic and intercostal nerves
- Blood supply = intercostal arteries
- Visceral pleura:
- sensory fibres only detect stretch
- Visceral pleura –> not sensitive to pain, temperature/touch
- autonomic innervation from pulmonary plexus (sympathetic trunk and vagus nerve)
- arterial supply via bronchial arteries
5
Q
Causes of pleuritic chest pain:
Pneumonia
What type of pneumonia are there?
A
- Pneumonia = inflammation of the lungs with consolidation or interstital lung infiltrates
Three types of pneumonia:
- Community acquired CAP
- Hospital acquired HAP - contracted w/in 48 hours after hosp admission
- Ventilator associated VAP - contracted w/in 48 hrs mechanical ventilation
- HAP/VAP - often gram negative bacilli (E.coli, klebsiella) and gram positive cocci (staphylococcus, streptococcus)
6
Q
Pneumonia: pathophysiology
A
- Normally the branching anatomy of resp tract, ciliared epithelium and mucociliary escalator prevent pathogens from invading the lungs
- pathogens that evade these barriers and reach the alveoli are recognised and phagocytosed by alveolar macrophages
- When alveolar macrophages are overwhelmed by large invasion of pathogens –> cytokine release and initate inflammatory cascade
- leukocytes invade the lung tissue, filling infected alveoli with purulent exudates –> impairs effective gas exchange
7
Q
Risk factors of pneumonia?
A
-
increased aspiration risk –>
- seizures/ delerium/ dementia/stroke/neuromuscular disorder/ endotracheal intubation/ alcoholism
-
Decreased clearance of inhaled pathogens –>
- mechanical ventilation
- COPD/ asthma (impaired mucociliary clearance w mucus hypersecretion and airway inflammation)
- smoking (destruction of cilia)
- obstruction of bronchial tree –> tumours/ lymph nodes/ foreign bodies
- Cystic fibrosis
-
Immunocompromised
- iatrogenic –> chemoT/ steroids
- HIV infection
- malignancy (particularly haematological)
- alcoholism
8
Q
What organisms cause CAP?
A
- most commonly caused by bacteria / viruses
- viral (25-40%)
- bacterial:
- streptococcus penumonia
- haemophilus influenzae
- mycoplasma pneumonia (atypical)
- legionella pneumophila (atypical)
- chlamydophilia pneumoniae (atypical)
- staphylococcus aureus (including methicillin resistant)
9
Q
what organisms cause HAP?
A
HAP most commonly caused by gram negative bacilli - (E.coli, enterobacter, klebsiella, pesudomonas aeruginosa)
Gram positive cocci - S. aureus and streptococcus
Aspiration of large volumes of oral secretions/ gastric contents also more common in hospitalised patients
10
Q
What are the key features in the history for pneumonia?
Symptoms?
key part of the hx?
A
-
Symptoms:
- fever
- chills
- dysponea
- cough productive w purulent sputum
- extension of inflammation into adjacent pleura –> sharp pleuritic pain
- 15% haemoptysis
- malaise + rigors
- Recent travel hx? –> TB in south america/ SE asia/ subsaharan africa
11
Q
Examination features - Pneumonia
A
- Fever or hypothermia (> 38 oC or < 35oC)
- (normal temp range 35.9 - 37.8)
- tachycardia
- tachypnea
- hypoxaemia
- laboured breathing/ accessory muscle use
- asymmetric chest expansion - rare
- abnormal lung sounds –> bronchial breath sounds, crackles, egophony (increase vocal resonance - consolidation/ fibrosis)
- dullness chest percussion –> consolidation
- flatness chest percussion –> effusion
12
Q
Investigations - pneumonia
A
- Bedside:
- Observtions - O2 sats / temp/ RR/ HR /BP
- ECG
- Diagnostic –> CXR
- may reveal lobar or diffuse consolidation
- Chest CT –> for additional details in atypical presentations/ recurrent infection/ failure to improve w tx
- look for structural defects/ effusion/ obstructing masses/abscesses / enlarged lymph nodes
- Bloods:
- FBC –> ↑ WBC’s (leukopenia may occur in sepsis) (White blood cells : WCC> 12,000/ uL or WCC< 4000/uL or 10% immature WCC)
- Inflammatory markers –> ↑ CRP
- U+ E’s (baseline & sepsis)
- LFT’s (Baseline)
- ABG –> hypoxia/ hypercapnia / ensure not in respiratory failure
- Sputum culture –> gram stain and culture
- Blood cultures only +ve in 5-14% pts
- Thoracocentesis –> pleural fluid culture
13
Q
What scores can be used to triage pneumonia patients?
A
- Pneumonia severity index (PSI) or CURB- 65 score
- triage patients & determine overall risk
- PSI –> patient demographics/ comorbidities/vital sign abnormalities/ lab values/ radiographic findings
- CURB 65 score –> 1 point for confusion, uraemia (BUN > 19), RR > 30 BP < 90/60 mmHg, age > 65 yrs
- Patients w score of 1 - outpatient care
- patients w score of 2 - inpatient care
- score of 3 - ITU
14
Q
Management of pneumonia?
A
- ABCDE
- Sepsis six –> Take: Blood cultures, serum lactate, urine output, give: empirical Abx, O2 therapy, IV fluids
- Analgesics
- Low severity –> Amoxicillin, Flucoxacillin or macrolide (Azithromycin/ clarithromycin/ erythromycin)
- if Staph aureus –> Vancomycin for MRSA
- if suspected or proven influenza –> oseltamivir
- Severe –> Amoxicillin + macrolide or B lactam (Ceftriaxone) + macrolide
- HAP –>
- need to cover for MRSA/ pesudomonas aeruginosa –> vancomycin
- Co-amoxiclav + gentamicin
15
Q
Pulmonary embolism:
Definition
Pathophysiology
A
Definition:
- Obstruction in the pulmonary arterial tree (either in pulmonary artery or distal arteriole) by: thrombus/ air/ fat/ amniotic fluid. V> Q
Pathophysiology:
- Thrombus forms when Virchow’s triad is present:
- Stasis
- Endothelial injury
- hypercoaguability
- Thrombus originating in venous system (normally legs, can be R side of heart) obstructs pulmonary artery
- pulmonary arterial occlusion –> increase in pulmonary artery pressure & vasospasm distal to clot
- alveolar collapse and atelectasis occur in lung distal to obstruction
- Lung has dual circulation (pulmonary and bronchial arteries directly off descending aorta) therefore infarction not common - occurs w large clots
- Risk factors:
- Pregnancy
- active cancer
- immobilisation (e.g. post surgical)
- Trauma
- DVT - in > 95% emboli originate as DVT
16
Q
Pulmonary embolism:
Demographics/ RF’s?
A
Risk factors: Virchow’s triad
Vessel wall damage:
- Trauma or recent fracture
- previous DVT
- surgery
Venous stasis:
- Age >40 years
- Pregnancy
- general anaesthesia
- immobilisation (e.g. post surgical, long travel/ stroke/ paralysis/ spinal cord injury)
- prior MI or stroke
- varicose veins
- advanced CHD/COPD
Hypercoagulability:
- active cancer
- high oestrogen states –> oral contraceptives/HRT/obesity/ pregnancy
- sepsis
- IBD
- blood transfusion
- inherited thrombophilias - factor V ledien, protein C/S deficiency/ antithrombin deficiency
DVT - in > 95% emboli originate as DVT –> having PMH of previous DVT/ PE increases risk too, Family Hx of VTE increases risk.
20
Q
What tools can be used to assess the clinical probability of PE?
A
- WELLS criteria or Geneva score
- Wells: (in simplified score one for each)
- clinical signs DVT
- alternative diagnosis less likely than PE
- Previous PE/DVT
- HR > 100
- surgery/immobilisation last 4 weeks
- haemoptysis
- active cancer
- Likely –> If score greater than 1, unlikely if less
21
Q
What are the appropriate investigations for PE?
A
-
If PE likely –> CTPA or V/Q lung scan if CTPA contraindicated
- Direct visualisation of thrombus in pulmonary artery
-
PE unlikely –> either low or intermediate score –> D dimer testing
- Haemodynamically stable with intermediate score –> D dimer test
- Patients w initial risk low but do not meet all the PERC criteria
- PERC criteria = PE Rule out Criteria –> used to find patients where risk of PE lower than risk of further testing
- PERC criteria = less than 50 yrs, HR less than 100 bpm, O2 sats 94%, no leg swelling/haemoptysis/surgery or trauma/ hx VTE/ oestrogen
- If D dimer levels abnormal –> CTPA (or V/Q lung scan)
- Normal D dimer –> almost 100% negative predictive value (can exclude PE)
- raised D dimer –> non specific therefore further testing
-
Other imaging:
-
CXR –> cannot confirm diagnosis but can support
- Fleischner sign – >enlarged Pulm artery
- pleural effusion
- knuckle sign –> abrupt tapering or cut off of pulmonary artery
- westermark sign –> decreased vascularisation at lung periphery (Hypoxic vasoconstriction / obstruction of distal arterioles).
- Ultrasound scanning — > check for clots in pelvic or iliofemoral veins
- echocardiography –> assess right ventricular dysfunction, may show thrombus
- Radionuclide V/Q scanning --> Pulmonary scintigraphy demonstrates under perfused areas (pt inhales radioactive xenon gas)
-
CXR –> cannot confirm diagnosis but can support
-
Other bedside:
- ABG –> may be normal, may show hypoxia w significant PE
-
ECG –> assess right ventricular function
- sinus tachycardia
- R atrial dilatation –> tall peaked P waves lead II
- R ventricular strain –> R axis deviation and R BBB
-
Bloods:
- Cardiac troponin –> may be elevated, associated with adverse outcome
- Coagulation studies –> INR/PT/aPTT
- U+ E –> dose of anticoag/ renal impairment
- FBC –> Thrombocytopenia + [Plasma D dimer]
23
Q
Causes of pleuritic chest pain:
Pneumothorax Pathophysiology?
A
- Normally alveolvar pressure is greater than Intrapleural pressure.
- Intrapleural pressure is normally negative (less than atmospheric pressure) due to inward lung and outward chest wall recoil –> lung tissue elastic recoil in, chest wall expands out water, surface tension between parietal and visceral pleura expands lung out.
- therefore if communication develops between alveolus and pleural space or atmosphere and pleural space, gases will follow pressure gradient into the pleural space.
- Air enters pleural space from outside chest or lung itself via mediastinal tissue planes or direct pleural perforation.
29
Q
CXR signs of pneumothorax?
A
- Visible visceral pleural edge seen as thin sharp white line between lung margin and chest wall
- no lung markings seen peripheral to this line
- peripheral space radiolucent compared to adjacent lung
- lung may completely collapse
- mediastinum should not shift unless tension pneumothorax
30
Q
Physical signs of tension pneumothorax?
CXR signs of tension pneumothorax?
A
Physical signs –> hypotension, hypoxia, absent breath sounds on affected side, tracheal deviation to contralateral side, thorax hyperressonant, JVP distended and tachycardia.
On CXR –> ipsilateral increased intercostal spaces, contralateral shift of mediastinum, depression of the ipsilateral hemidiaphragm
(image shown 1) significant mediastinal shift to left 2) depressed R hemidiaphragm 3) widened IC spaces, marked asymmetric expansion R hemithorax
31
Q
Management of a tension pneumothorax?
A
- Immediate cardiac arrest call
- high flow oxygen - target sats 100% unless patient at risk of hypercapnic RF (88-92%)
-
immediate decompression required:
- large bore cannula (14/16G) into second intercostal space Midclavicular line OR 4th/5th IC space midaxillary line (standard cannula for needle decompression may be too short in 2nd IC space, therefore 4th/5th IC space alternative site for decompression, can also be used as a site of chest drain insertion).
- “hiss” of air confirms diagnosis
- insert chest drain immediately after needle decompression - to prevent block of air drainage if needle becomes blocked
- if tension pneumothorax secondary to trauma use open thoracostomy for decompression
32
Q
Anatomy of needle compression insertion?
Insertion site - at 4th IC midaxillary line
A
- Sternal angle (angle of luis) –> level T4/54, marks 2nd rib
- below is the 2nd IC space
- Count down two ribs to find the 4th IC space
- Abduct patients arm to reveal anterior axillary line -> lateral edge of pectoris major, posterior axillary line –> lateral edge of latissimus dorsi
- Midaxillary line inbetween the two –> insertion site just anterior to Midaxillary line, behind lateral edge of pectoris major
- Needle enters above superior border of the 5th rib (avoiding the neurovascular bundle at lower portion of rib- avoid damage of intercostal nerve and vessels in subcostal groove).
- Advance needle through: skin/superficial fascia/ subcutaneous fat/ pectoralis muscle/ intercostal muscles (external intercostal, internal intercostal, innermost intercostal)/ parietal pleura –> pleural cavity
- Note if in 2nd IC space –> upper border 3rd rib, again goes through skin/superficial fascia/subcut fat/ serratus anterior/ external intercostal/internal intercosta./innermost intercostal/parietal pleura.
Needle may become blocked, therefore for definitive treatment need to insert a chest drain - hence why recommended in 4th IC space now.
33
Q
Surface anatomy of the pleura?
A
34
Q
Management of spontaneous pneumothorax
(not tension pneumothorax)
A
- Treat according to the type of pneumothorax and clinical presentation
- If primary spont PneumoT –>
- if no visible rim > 2m or breathlessness – > consider discharge and review
- If visible rim > 2cm plus breathless –> aspirate <2.5L using 16018 G cannula –> repeat CXR –> visible rim smaller and breathing improved then discharge
- if no improvement - insert chest drain, give O2
- If secondary spont PneumoT –>
- Again visibile rim > 2cm/ breathless -> insert chest drain and O2
- If visible rim between 1-2 cm –> aspirate < 2.5L and repeat CXR –> high flow O2 & observation 24 hrs
- visible rim <1cm –> high flow o2 and observation
- Surgery –> may be needed if persistent air leak or failure of lung to re-expand –> open thoracotomy.
40
Q
What investigations would you do for pericarditis?
A
Bedside:
- Observations - HR/RR/BP/Temp
-
ECG: changes occur in 90% of pateints
- 1) Global upwardly concave ST elevation with PR segment depression in most leads
- ECG may show 4 stages:
- ST elevated and upright T waves
- resolves to normal over days or
- evolves to T wave inversion
- then normal
-
Bloods:
- FBC –> raised WBC –> infectious
- Urea –> raised urea think uraemic cause
- ESR –> elevated ESR consistent with inflammatory state
- CRP --> inflammation
- Serum tropnins (initial and serial) –> elevated levels may represent myocaridal involvement
- CXR –> often nromal but can see large pericardial effusions (water bottle shape enlarged cardiac silhouette)
- echocardiography --> when cardiac tamponade suspected
