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Dr. Mohammed Alhamdany
Venous thromboembolism (VTE) :
The majority (80%) of pulmonary emboli arise from the propagation of
lower limb DVT. Rare causes include 1-septic emboli (from endocarditis
affecting the tricuspid or pulmonary valves),2- tumour (especially
choriocarcinoma), 3-fat, 4-air, 5-amniotic fluid and 6-placenta.
Risk factors for venous thromboembolism:
In general there are 3 pathological factor cause thrombosis (in vein)
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Alterations in blood flow: immobilization.
 Factors in the vessel wall: surgery, catheterizations causing direct
injury ("endothelial injury").
 Factors affecting the properties of the blood (procoagulant state).
The risk factor include:
1-Surgical
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Hip/knee surgery
Major abdominal/pelvic surgery
Post-operative intensive care
2-Obstetrics
Pregnancy/puerperium
3-Cardiorespiratory disease
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COPD
Congestive cardiac failure
Other disabling disease
4-Lower limb problems
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Fracture
Varicose veins
Stroke/spinal cord injury
5-Malignant disease
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Abdominal/pelvic
Advanced/metastatic
Concurrent chemotherapy
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6-Miscellaneous
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Increasing age
Previous proven VTE
Immobility
Thrombotic disorders
Trauma
Type of pulmonary embolism:
1-Acute massive PE: in which there is occlusion of main pulm. artery or
its major branches causing decrease cardiac output and acute right heart
failure.
2-Acute small/medium PE: Occlusion of segmental pulmonary artery
causing infarction with or without effusion.
3-Chronic PE: Chronic occlusion of pulmonary microvasculature
causing pulmonary hypertension and right heart failure.
Clinical features
Acute massive PE : Faintness or collapse, crushing central chest pain,
apprehension, severe dyspnea, tachycardia, hypotension, increase JVP,
right ventricular gallop rhythm, loud P2, severe cyanosis, decrease urinary
output.
Acute small/medium PE: Pleuritic chest pain, restricted breathing,
hemoptysis, Tachycardia, pleural rub, raised hemidiaphragm, crackles,
effusion (often blood-stained), low-grade fever.
Chronic PE: Exertional dyspnea. Late symptoms of pulmonary
hypertension or right heart failure, may be minimal signs early in disease,
Later: RV heave, loud P2. Terminal: signs of right heart failure(systemic
fluid over load).
Investigations
Chest radiography
The chest X-ray is most useful in excluding key differential diagnoses,
e.g. pneumonia or pneumothorax. Normal appearances in an acutely
breathless and hypoxemic patient should raise the suspicion of PE.
The changes include:
1-Pulmonary opacities (any size or shape, rarely lobar or segmental , can
cavitate).
2-Wedge – shaped opacity.
3-Horizontal linear opacities (bilateral and usually in lower zones).
4- Pleural effusion.
5-Oligaemia of lung field.
6-Enlarged pulmonary artery.
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7-Elevated hemidiaphragm.
It depend on the type of PE and as following:
1-acute massive PE: Usually normal. May be subtle oligaemia
2-acute small/medium PE: Pleuropulmonary opacities, pleural effusion,
linear shadows, raised hemidiaphragm.
3-chronic PE: Enlarged pulmonary artery trunk, enlarged heart,
prominent RV.
Electrocardiography
1-acute massive PE: S1Q3T3 anterior T-wave inversion, right bundle
branch block (RBBB).
2-acute small/medium PE: Sinus tachycardia.
3-chronic PE: RV hypertrophy and strain.
Arterial blood gases
1-acute massive PE: Markedly abnormal with ↓PaO2 and ↓PaCO2.
Metabolic acidosis .
2-acute small/medium PE: May be normal or ↓PaO2 or ↓PaCO2.
3-chronic PE: Exertional ↓PaO2 .
D-dimer and other circulating markers:
D-dimer is a specific degradation product released into the circulation
when cross-linked fibrin undergoes endogenous fibrinolysis. An elevated
D-dimer is of limited value, as it occurs in a number of conditions
including PE, myocardial infarction, pneumonia and sepsis. However,
low D-dimer levels (< 500 ng/mL measured by ELISA), particularly
where clinical risk is low, have a high negative predictive value and
further investigation is unnecessary. The D-dimer result should be
disregarded in high-risk patients, as further investigation is mandatory
even if it is normal.
Imaging:
CT pulmonary angiography is the most commonly first-line diagnostic
test. It has the advantage of visualizing the distribution and extent of the
emboli, or highlighting alternative diagnoses such as consolidation,
pneumothorax or aortic dissection. It should be avoided in patient with
renal impairment as contrast may be nephrotoxic, and also should be
avoided in those with a history of allergy to iodinated contrast media.
Ventilation-perfusion scanning is less commonly used, as its utility is of
limited value in patients with pre-existing chronic cardiopulmonary . It is
most useful in patients without significant cardiopulmonary disease and a
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normal chest X-ray; interpretation should be informed by clinical
probability.
Color Doppler ultrasound of the leg veins remains the investigation of
choice in patients with suspected DVT, but may also be applied to
patients in whom PE is suspected, particularly if there are clinical signs in
a limb, as many will have identifiable proximal thrombus in the leg veins.
Echocardiography:
Bedside echocardiography is extremely helpful in the differential
diagnosis and assessment of acute circulatory collapse. Acute dilatation
of the right heart is usually present in massive PE, and thrombus
(embolism in transit) may be visible. Alternative diagnoses, including left
ventricular failure, aortic dissection and pericardial tamponade, can also
be established.
Pulmonary angiography:
Conventional pulmonary angiography has been largely superseded by
CTPA but may still be used in selected settings or for delivering catheterbased therapies.
Management
General measures
Prompt recognition and treatment are potentially life-saving. Oxygen
should be given to all hypoxemic patients at a concentration necessary to
maintain arterial oxygen saturation above 90%. Circulatory shock should
be treated with intravenous fluids or plasma expander, but inotropic
agents are of limited value, as the hypoxic dilated right ventricle is near
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maximally stimulated by endogenous catecholamines. Diuretics and
vasodilators should also be avoided, as they will reduce cardiac output.
Opiates may be necessary to relieve pain and distress but should be used
with caution in the hypotensive patient. Resuscitation by external cardiac
massage may be successful in the moribund patient by dislodging and
breaking up a large central embolus.
Anticoagulation
Anticoagulation should be commenced immediately in patients with a
high or intermediate probability, but may be safely withheld in patients
with low clinical probability pending investigation. Heparin reduces
further propagation of clot, the risk of further emboli, and lowers
mortality.low molecular weight heparin is most easily administered as
subcutaneous route. The dose is 100 unit x kg x2 and there is usually no
requirement to monitor tests of coagulation. The duration of LMWH
treatment should be at least 5 days, during which time oral warfarin is
commenced. LMWH should not be discontinued until the (INR) is greater
than 2.
Newer thrombin or activated factor X inhibitors offer more predictable
dosing and have no requirement for coagulation monitoring; they may
ultimately replace warfarin.
The duration of treatment :
1-Patients with a persistent prothrombotic risk (such as antiphospholipid)
or a history of previous emboli (recurrent) should be anticoagulated for
life.
2-patient with an identifiable and reversible risk factor usually require
only 3 months of therapy.
3-For patients with unprovoked VTE (idiopathic), the appropriate
duration of anticoagulation should be at least 3 months, but prolonged
therapy should be considered in: a-males (who have a higher risk of
recurrent VTE than females), b-those in whom the D-dimer remains
elevated when measured 1 month after stopping anticoagulation, c-those
with post-thrombotic syndrome, and d-those in whom recurrent PE may
be fatal.
4-In patients with cancer associated VTE, LMWH should be continued
for at least 6 months before switching to warfarin.
Thrombolytic therapy
Thrombolysis is indicated in 1-any patient presenting with acute massive
PE accompanied by cardiogenic shock. In the absence of shock, the
benefits are less clear but 2- it may be considered in patients presenting
with right ventricular dilatation and hypokinesis or 3-severe hypoxaemia.
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Patients must be screened carefully for haemorrhagic risk, as there is a
high risk of intracranial haemorrhage. Surgical pulmonary embolectomy
may be considered in selected patients but carries a high mortality risk.
Caval filters
A patient in whom 1-anticoagulation is contraindicated, who has2suffered massive haemorrhage on anticoagulation, or 3-recurrent VTE
despite anticoagulation, should be considered for an inferior vena caval
filter.
Prognosis
The risk of recurrence is highest in the first 6-12 months after the initial
event. The immediate mortality is greatest in those with
echocardiographic evidence of right ventricular dysfunction or
cardiogenic shock. The vast majority of patients attain normal right heart
function by 3 weeks but persisting pulmonary hypertension may be
present in around 4% of patients by 2 years. A minority progress to overt
right ventricular failure.
Pulmonary hypertension:
Pulmonary hypertension (PH) is defined as a mean pulmonary artery
pressure > 25 mmHg at rest or 30 mmHg with exercise.
Classification of pulmonary hypertension
1-Pulmonary arterial hypertension
A-Primary pulmonary hypertension: sporadic and familial
B-Related to: connective tissue disease (limited cutaneous systemic
sclerosis), portal hypertension, HIV infection, and exposure to various
drugs or toxins.
2-Pulmonary venous hypertension
a-Left-sided atrial or ventricular heart disease
b-Left-sided valvular heart disease
3-Pulmonary hypertension associated with disorders of the respiratory
system and/or hypoxaemia
a-COPD
b-Interstitial lung disease
c-Sleep-disordered breathing
d-Chronic exposure to high altitude
e-Severe kyphoscoliosis
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4-Pulmonary hypertension caused by chronic thromboembolic disease
a-Thromboembolic obstruction of the proximal pulmonary arteries
b-Sickle cell disease
5-Miscellaneous
a-Inflammatory conditions
b-Extrinsic compression of central pulmonary veins
Further classification is based on the degree of functional disturbance,
assessed using the New York Heart Association (NYHA) grades I–IV.
Clinical features
breathlessness, chest pain, fatigue, palpitation and syncope. Important
signs include elevation of the JVP (with a prominent 'a' wave if in sinus
rhythm), a parasternal heave (RV hypertrophy), accentuation of the
pulmonary component of the second heart sound and a right ventricular
third heart sound.
Investigations
Pulmonary hypertension may be suspected if an ECG show a right
ventricular 'strain' pattern or a chest X-ray shows enlarged pulmonary
arteries, and right ventricle enlargement. Confirmation is by transthoracic
echocardiography; Doppler assessment of the tricuspid regurgitant jet
provides a non-invasive estimate of the pulmonary artery pressure.
Further assessment should be undertaken in specialist centres that can
perform right heart catheterisation to assess pulmonary haemodynamics
and measure vasodilator responsiveness, to guide further therapy.
Management
Pulmonary hypertension is incurable but new treatments have delivered
significant improvements in exercise performance, symptoms and
prognosis. All patients should be anticoagulated with warfarin, and
oxygen, diuretics and digoxin prescribed as appropriate. Specific
treatment options include high-dose calcium channel blockers,
prostaglandins such as epoprostenol (prostacyclin) or iloprost therapy, the
PDE5 inhibitor sildenafil, and the oral endothelin antagonist bosentan.
With best regard
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