Friday, 26 September 2014

Pulmonary Embolism

PEs are the big diagnosis that we never want to miss, but we haven't yet decided the significance of all these tiny PEs we're picking up.


Statistics
PEs are very common: 60 to 70 per 100 000 population. They have an untreated mortality of about 30%, cause 15% of all postoperative deaths and are the most common cause of maternal death in the UK. 35 - 45% of thrombi are DVTs and up to 50% embolise.  65% of below knee DVTs are asymptomatic.

Pathogenesis:
Virchow's Triad:
    Stasis:    Immobility, surgery, casts
    Vessel wall injury: trauma, sepsis, IVDA
    Hyper-coaguable state: Primary    Antithrombin and heparin cofactor II deficiencies
                        Protein C and S deficiencies
                        Factor V Leiden   
                        Disorders of the fibrinolytic system
                        Lupus
                        Anticardiolipin antibodies
                        Prothrombin gene variant
                Secondary    Dehydration
                        Pregnancy
                        OCP
                        Malignancy
                        HONK

Risk Factors
*    Major risk factors (relative risk increased 5-20-fold) include:
-    Surgery - major and/or abdominal surgery
-    Lower limb orthopaedic surgery, fracture or varicose veins.
-    Obstetrics - late pregnancy (higher incidence with multiple births), caesarian section, pre-eclampsia
-    Malignancy - pelvic, abdominal, metastatic (occult in 7 - 12% of patients)
-    Previous proved VTE
-    Reduced mobility - any major illness with prolonged bed rest.

*    Minor risk factors (relative risk increased 2-4-fold) include:
-    Cardiovascular - congenital heart disease, congestive cardiac failure, hypertension, central venous access
-    Oestrogens - OCP (especially "third generation" pills), HRT (risk greatest in first year)
-    Miscellaneous - occult malignancy, neurological disability, obesity, thrombotic and myeloproliferative disorders, nephrotic syndrome, inflammatory bowel disease.

*    Inherited thrombophilias -  need to interact with an additional risk factor to cause venous thromboembolism.

Clinical Signs & Symptoms
-     Circulatory collapse in a previously well patient - happens in 5%.
    Massive PE causes RHF.

Tachycardia in 30%.
-     Pulmonary infarction syndrome (60%) -
    pleuritic pain, with or without haemoptysis. Pleural rub.
-     Isolated dyspnoea (25% - 73%) - sudden onset SOB
-     Collapse, poor reserve (10%) -
    In elderly patient with limited cardiorespiratory reserve. Small PE can be catastrophic.

-    New onset AF and chest wall pain
-    Prominent JVP “a” waves
-    Right heart failure
-    Pulmonary area murmur
    May be completely normal, but tachycardia (classically with a loud P2 and splitting of the second heart sound) with tachypnoea are common
-    Signs of a deep vein thrombosis are present in about 25%

Pregnancy
The diagnosis can be difficult to make in women who are pregnant. The standard pre-test clinical probability score should be used, recognising that pregnancy is a major risk factor for venous thromboembolism. The D-dimer test is of no use in this situation because it is raised (in the absence of PE) from about six weeks' gestation, until about three months post-partum.
The risk of pulmonary embolism increases throughout pregnancy, with more pulmonary emboli occurring after delivery than before. The risk of pulmonary embolism in pregnancy increases with maternal age and multiple births.
Pregnancy women normally have a mild compensated respiratory alkalosis.
Penicillins and cefalosporins safe in pregnancy. Avoid co-amox.

Pulmonary oedema higher risk in pregnant women because they have a lower serum osmotic pressure, and increased vascular permeability. Causes include pre-eclampsia, beta adrenergic agonists used to postpone premature labour, cardiac disease, amniotic fluid embolism.

Amniotic fluid embolism is typically associated with rapid changes in coagulation and evidence of DIC. PE does not cause such changes.

Investigations
*    SI QIII TIII  pattern - deep S wave in lead I, Q wave in III, inverted T wave in III.
    20% of patients with PE.

*    Chest x-ray:    wedge shaped infarction or infection
            regional oligaemia (Westermark sign)
            pleural effusions
*    ABG: Hypoxia results from reduced cardiac output and a low mixed PaO2 with ventilation/perfusion mismatching. A normal PaO2 and alveolar arterial gradient is possible in a young, healthy person.
           
Definitions
Massive PE:    Acute PE with obstructive shock or SBP <90mmHg: at least 1 of the following:
    - Sustained hypotension from PE itself (SBP < 90 mmHg for = 15 min, or requiring inotropic support)
    -  Pulselessness
    - Persistent profound bradycardia (HR < 40 bpm with signs/symptoms of shock)

Submassive PE: Acute PE without systemic hypotension (SBP = 90 mmHg) but with either:
*    RV dysfunction (of at least 1 of the following):
        - RV dilation
        - BNP > 90 pg/mL
        - N-terminal pro-BNP > 500 pg/mL
        - ECG changes: New complete or incomplete right BBB, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion
•     Myocardial necrosis is defined as either of the following:
        - Troponin I > 0.4 ng/mL, or
        - Troponin T > 0.1 ng/mL

Low Risk PE: Acute PE and the absence of the clinical markers of adverse prognosis
that define massive or sub-massive PE.

Scoring Systems
The original ‘PERC’ study excluded patients:
*    patients in whom shortness of breath is not the most important, or equally most important, presenting complaint
*    cancer
*    thrombophilia or strong FHx
*    beta blockers that may mask tachycardia
*    transient tachycardia
*    patients with amputations
*    massively obese and in whom leg swelling cannot be reliably ascertained
*    baseline hypoxemia


PERC rule can’t be used on:    HAD CLOTS
Hormone, Age >50, DVT/PE history, Coughing blood, Leg swelling, O2 >95%, Tachycardia 100+, Surgery/trauma <28 d



Treatment
Massive PE - Alteplase 50mg ASAP.

Anticoagulation for three or six months for a first idiopathic pulmonary embolism. A British Thoracic Society trial comparing three and six months' treatment is ongoing. Some trusts use PESI  to work out whether outpatient anticoagulation is suitable.


Flight prophylaxis. Current British guidelines suggest considering aspirin or LMWH, or formal anticoagulation for those at high risk of pulmonary embolism. Limited evidence to support this. Compression stockings may be beneficial.


Differentials
Venous air emboli may cause:
    Raised venous pressure
    Cyanosis
    Hypotension
    Tachycardia
    Syncope.

Treatment is by lying the patient on their right side, with head down and feet up, to allow air to collect and stay at the cardiac apex. From here it can be aspirated. This may be done by ultrasound guided needle aspiration.

Fat embolism

This occurs in association with long bone fractures, with bone marrow fat droplets released into the venous circulation at fracture. It is more common in non-immobilised fractures.

It typically presents with:
    Hypoxia
    Coagulopathy
    Transient petechial rash on neck, axillae, and skin folds
    Neurological disturbance, such as confusion.
    Fat globules can be identified in the urine.
Treatment is supportive.




References
http://www.enlightenme.org/knowledge-bank/cempaedia/pulmonary-embolism

http://lifeinthefastlane.com/education/ccc/pulmonary-embolism/
http://lifeinthefastlane.com/ecg-library/pe/
http://lifeinthefastlane.com/cicm-saq-2012-2-q5/
http://lifeinthefastlane.com/education/ccc/thrombolysis-submassive-pulmonary-embolus/
http://lifeinthefastlane.com/cardiovascular-curveball-011/
http://lifeinthefastlane.com/pulmonary-puzzle-016/
http://lifeinthefastlane.com/hematology-hoodwinker-001/

http://www.enlightenme.org/the-curriculum-zone/node/2091http://www.enlightenme.org/the-curriculum-zone/node/11779http://m.eurheartj.oxfordjournals.org/content/early/2014/09/17/eurheartj.ehu283

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