PE & pneumothorax Flashcards
Pulmonary embolism
The blockage of the pulmonary artery or one of its branches by a embolus
usually a venous embolus from the deep leg veins (80%) but can be septic emboli (endocarditis), malignant emboli, fat, air or amniotic fluid.
Risk factors for a PE
Post operative or lower limb fracture
Pregnancy, Coagulopathy or previous DVT/PE
Malignancy or Reduced mobility
Oestrogen containing contraceptive pill/HRT
COPD or congestive heart disease
Risk stratification for PE
Clinical features + (a) major risk factor OR (b) absence of other cause –> if both high risk, if one intermediate, if neither then low
For high risk proceed directly to CTPA, low and intermediate then D-dimers, and if +ve proceed to CTPA
Pneumothorax
An abnormal collection of air in the pleural space which may interfere with normal breathing
Different types can occur and have different treatment
If symptomatic a chest drain can be placed underwater to assist the lung in re-inflating or a pleurodesis can be performed
Types of pneumothorax
A primary has no apparent cause, while a secondary occurs in the presence of an existing lung pathology
Simple/open–> open route from outside to the pleural space
Closed–> a fixed, closed volume of air in the pleural space
Tension–> a 1-way valve such leading to increasing pressure
Tension pneumothorax
When a 1-way valve which leads to increasing pressure in the pleural space which leads to mediastinal shift and death
This will present with chest pain and respiratory distress, leading to tachycardia, tachypnoea and hypotension, hypoxia and tracheal deviation away from the affected side
Treatment of a tension pneumothorax
Emergency
Large bore cannulae into 2nd intercostal space at midclavicular line
Insert chest drain
Treatment of pneumothorax
A pneumothorax showing a radiological rim of 2cm, the patient >50yrs or it hasn’t responded to aspiration then a chest drain should be placed.
Otherwise discharge w/outpatient X-ray
Radiological appearance of pneumothorax
Can be small and hard to spot
Check if the lung markings extend fully to the margin
A 2cm rim on an CXR occupies 49% of the hemithorax
Risk factors for spontaneous pneumothorax
Being a tall thin young man Lung pathology such as COPD or lung cancer Smoking, and particularly cannabis Family history Previous pneumothorax
Treatment of PE
Emergency Give O2 Consider 50mg bolus alteplase LMWH heparin (tinzaparin 175u/kg/24h SC) Stabilise patient (? Fluid challenge) and commence warfarin INR 2-3 (3.5 if recurrent) for 3mo
Symptoms of PE
Vary depending on if it is an acute massive, small or medium or chronic PE. Generally include:
SOB, pleuritic chest pain,haemoptysis, palpitations, tachycardia and tachypnoea eventually leading to hypotension and death
Incidence of VTE
Unknown in the community but 1% of all hospital admission and causes 5% of in hospital deaths - particularly in patients with stroke, cancer or pregnancy
Acute Massive PE
Significant reduction in CO causing right HF leading to severe dyspnoea, collapse and crushing chest pain.
Signs: shock, tachycardia, RV gallop rhythm, loud P2, S1Q3T3 (or ant T-wave inversion or RBBB)
Differentials: MI, pericardial tamponade and aortic dissection
Small to Medium PE
Segmental artery occluded leading to infarction (+effusion) causing pleuritic pain, restricted breathing & haemoptysis.
Signs: low fever, effusion, creps, pleural rub, tachycardia and raised hemidiaphragm. No specific ECG changes,
Differential: pneumothorax, pnuemonia or MS chest pain
Chronic PE
Chronic blockage of pulmonary microvasculature leading to right HF causing exertional dyspnoea and late symptoms of pulmonary hypertension or HF
Signs: RV heave and loud P2 in late disease, signs of HF in end stage. CXR may show enlarged pulmonary trunk, heart or right ventricle.
Differential: pulmonary hypertension from other causes
Role of D-Dimers in diagnosing PE
Useful as a negative predictor – low D-Dimers broadly rule out PE (if high risk second line investigations may be necessary to exclude PE).
Raised D-Dimer in high risk pts are sufficient for a provisional diagnosis but in low risk pts further test are still needed
ECG changes in PE
Generally –> non-specific sinus tachycardia or anterior T-wave inversion
In large PEs Right heart strain can produce S1Q3T3 pattern and the appearance of RBBB.
Definitive diagnostic tests for PE
CT pulmonary angiography is first line
VQ scans are now rarely used except in special cases (pregnancy - can shield the fetus)
Doppler scans are useful to identify clots in limbs.
Echos can be used to assess heart damage.
Management of PE
Treatment of hypoxia and shock are most important (inotropes are of limited use as the heart is near maximal distension, and diuretics and vasodilators should also be avoided) - external cardiac massage can be useful in extreme cases.
Mainstay of treatment is anticoagulation
Anti coagulation in PE
At least five days of LMWH - reduces clot growth, embolisation and mortality
After this Warfarin should be started to maintain INR for as long as necessary – 3months for reversable risk or life if permanent RFs or repeated thrombous. (also longer in men)
