It's a clinical picture characterized by chest pain
with dyspnoea, very serious: patients in 10% of
cases patients may have an exitus.
It is characterized by the partial or complete acute occlusion of one or more
branches of the pulmonary arteries, determined by the presence of emboli or
thromboemboli, or much more rarely, by emboli of fat, bone marrow, gaseous and
neoplastic.
In current European guidelines for the diagnosis and treatment of EP, the
clinical classification is based on the level of risk of early mortality,
defined as intra-hospital or 30-day mortality.
This stratification allows to distinguish two forms of embolism:
- high risk EP with presence of cardiogenic shock or persistent hypotension
- Non-high risk EP in the absence of shock or hypotension at the entrance.
In the case of cardiogenic shock and hypotension, it is clear that the patient
must be treated with regards to hemodynamic parameters, which must be supported
with appropriate treatments (see below); in case of pulmonary embolism, if the
pressure and hemodynamic conditions are satisfactory, it is possible to treat
the patient in a semi-intensive therapy, also a good, well-equipped internal
medicine department is fine.
In situ thrombosis of the pulmonary artery is rare.
notes by dr Claudio Italiano
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The problem is understanding when a patient presents the picture of pulmonary embolism, which is not easy.
The doctor suspects polmonary embolism when a subject presents respiratory distress (dyspnoea), cyanosis, EGA with values altered by hypoxemia, chest pain that mimics a myocardial infarction. If the D-Dimer is high, ie emboli are formed and degraded fibrin products are found in the bloodstream, ie the coagulated blood has been brought into the circulation, for example during a venous thrombosis and brought to the right heart and into the pulmonary artery.
Therefore it is difficult to talk about casuistry and
epidemiology with an incidence that varies from 30 cases / 100,000 inhabitants /
year in our country. Other authors, according to Heit for example, say that the
incidence of venous thromboembolism (VTE), which include
deep vein thrombosis (DVT)
and E.P., is 117 cases per year per 100,000 inhabitants.The 2/3 remain
undiagnosed and are found in 12-15% of the autopsies on hospitalized patients.
30% of subjects with DVT develop PE.
An embolus is a formation not part of the blood stream, to understand something, as
if a gummy ball moved in the blood vessels to occlude a vase. The embolus can be:
solid (mainly originating from a thrombus placed distally in the circulation),
liquid (eg amniotic fluid) or gaseous (underwater activity, penetrating wounds
of the neck). In the vast majority of cases, however, there must be a lesion of
the blood vessel or of an altered vein and a venous stasis.
-Parietal injury
- Venous stasis
These are conditions already present in the subject that pose a risk in the
onset of pulmonary embolism and not only.
Risk factors for EP are divided into congenital and acquired:
- Mutation of the V Leiden factor
-
Prothrombin gene mutation
-
Antithrombin III deficiency
of protein C or of protein S
- Hyperhomocysteinemia
- old age
- smoke
- obesity
- active neoplasms
- antiphospholipid antibody syndrome
- hyperhomocysteinemia
- contraceptive pill or hormone replacement therapy
- atherosclerosis
- trauma
- recent surgical interventions or hospitalizations
- acute infections
- recent long air travels
- pacemaker
- intracardiac defibrillators or venous catheters
The clinical suspicion is based on the finding of symptoms such as dyspnoea,
ie the hunger of air; the patient is agitated, sweating, with sudden onset,
chest pain, syncope, coughing in particular with a blood spittle (hemoptysis)
and fever above 38 ° C. By engagement of the myocardial right sections, due to lack of
blood discharge, a turgidity of the jugular veins is observed, that can be seen at the
neck, with turgid and serpiginose vessels; the patient will have cyanosis of the
lips, tachycardia, that is fast beating, will breathe
with difficulty and engaging the belly, besides the pulse will be barely
perceptible, and the low pressure, up to the dramatic picture of myocardial
shock. At this point eye the lower limbs if they show signs of DVT
The most frequent differential diagnoses are:
- myocardial infarction,
- the pneumothorax,
- the dissecting aortic aneurysm,
- pneumonia.
What to do? Call the doctor, but if the doctor is you and you are in a hospital staff and beds cut, with relatives on, what can you do ?
You must immediately request
laboratory examinations, start with the simplest:
Dimer Test: D-Dimerum is a degradation product of fibrinogen, the main
coagulation protein, and this is an indication of consumption coagulopathy,
and is very specific for EP;
ECG: it provides information about the state of the right ventricle, which may
undergo acute decompensation due to sudden pulmonary hypertension. Execution
of the ECG in patients with suspected PE is useful for excluding the presence
of a myocardial infarction. In patients with PE, this instrumental examination
is frequently normal or demonstrates non-specific abnormalities of the ST
segment or the T wave;
CHEST X-RAY: The chest X-ray is a very useful test, above all because it
allows to exclude some of the morbid conditions with which the differential
diagnosis arises, for example a lobar pneumonia, but most of the times it is
an examination that says little: it is a chest CT scan is more useful;
EGA: means using a special syringe to take a radial or femoral artery sample,
to measure oximetry, that is, how much oxygen and carbon dioxide are present
in the blood, its pH and other parameters. In the EP will give information
that does not allow diagnosis.
POLMONARY SPECT: the ventilatory-perfusional Scintigraphy allows to establish
the hypoperfused areas and to compare them with the hypoventilated ones, see
below.
ANGIOGRAPHY: Pulmonary angiography has been the gold standard in the diagnosis
of PE as well as phlebography for diagnosis of deep vein thrombosis until a
few years ago. Injection of contrast medium into the main pulmonary artery by
catheterization in fact allows direct visualization of the arterial occlusion
responsible for the clinical manifestations. Perfusion lung scintigraphy with
Tc99-labeled macroaggregates performed within 48 hours of onset excludes the
diagnosis of pulmonary embolism if normal. A defect of segmental or lobar
uptake may not be specific as secondary to any infiltrate (pneumonia, TB,
tumors, atelectasis); it is useful in these cases to associate a ventilatory
scintigraphy with Xe33. Ninety percent of patients with impaired ventilation /
perfusion ratios have vascular obstruction in the lung.
COMPUTERIZED SPIRAL TOMOGRAPHY: The computerized tomography (CT) spiral, which
has now completely replaced the traditional equipment, allows the direct
display of the embolus after injection of contrast medium.
ULTRASONOGRAPHY TO LOWER LIMBS: Since many of the patients with established PE
have a proximal DVT, venous ultrasound with compression tests but especially
with ecodoppler technique has been widely used especially in patients with
non-diagnostic pulmonary scintigraphic pattern.
ECOCARDIOGRAM: It is an examination that allows to evaluate the right
ventricular function and that rarely allows the direct display of the embolus,
the latter is however the only finding that allows to diagnose EP with a good
accuracy.
The goals of therapy are basically three:
- Guarantee a good oxygenation of the blood through oxygen therapy;
- Keep blood pressure through the administration of liquids and vasopressor
drugs: beta-agonists (dopamine, dobutamine and adrenaline)
- Correction of respiratory alkalosis.
- Stop the formation of the clot and prevent any embolic recurrence by
administering anti-coaugulants and / or heparinics.
- Anticoagulants.
Current European guidelines recommend in most cases of acute low-risk EP not
complicated by severe renal failure, treatment with low molecular weight
heparins (LMWH) enoxaparin sodium or fondaparinux subcutaneously, which do not
require laboratory monitoring , and are preferred over unfractionated heparin
because of the lower risk of bleeding complications and heparin-induced
thrombocytopenia.
Another main drug was once calcium heparin; it is administered in non-critical
EP but above all already in case of strong clinical suspicion of the pathology.
A bolus of calcium heparin generally of 5-10,000 U is administered. Subsequently,
calcium heparin is infused in drip which allows a good level of anticoagulation
to be reached quickly. It is recommended to start IV heparin therapy (10,000 U
bolus followed by a continuous infusion at the rate of 800-1200 U / hour) even
without formal diagnostic confirmation.
The activated partial thromboplastin (PTT) values regulate the dosage,
considering as a therapeutic value of 2-2.5 times the basal one. The treatment
lasts 7-14 days, and is followed by dicumarolics for a minimum of 6 weeks.
During heparin therapy, bed rest is maintained. The treatments generally last
from a minimum of 3 months, to a life-long treatment, with oral anticoagulants,
especially if there are basic diseases that predispose to the recurrence of
embolism.
Today, 2020, in consideration of the results of the main clinical trials on NAO
treatment in the acute phase of EP, these drugs have been indicated by current
guidelines as an alternative to standard treatment with heparin and vitamin K
antagonists.
The trials conducted conclude, in fact, for the "non-inferiority" of rivaroxaban,
dabigatran and apixan (currently approved in the EU for the treatment of acute
EP) and a potential safety profile greater than the standard treatment.
- Lysing the thrombus with thrombolytic drugs. Thrombolytics, on the other hand,
are drugs capable of lysing the thrombus, among which urokinase, streptokinase
or the tissue activator of plasminogen (t-PA) are currently used.
As for the comparison between different thrombolytic drugs, 100 mg of rtPA or
Alteplase, produced with the recombinant technique, in 2h resulted in a faster
hemodynamic and angiographic improvement
Due to the high risk of bleeding, these drugs are used only in selected cases of
hemodynamically unstable patients. However recent studies have shown that the
use of thrombolytics allows to avoid permanent deficiencies of perfusion of the
pulmonary capillary bed and of alveolus-capillary diffusion thus preventing
chronic pulmonary hypertension.
- Thromboembolectomy. Surgical embolectomy, the role of which has lost
importance with the use of thrombolytics and transvenous unclogging which allows
the removal of the thrombus by the endovascular route. Bilateral pulmonary
embolectomy requires cardiopulmonary bypass. When an extracorporeal circuit is
not available, a unilateral pulmonary embolectomy can be performed. It is
indicated in the refractory shock to treatment and if contraindications to
heparin are present. The survival of patients undergoing acute embolectomy
varies from 40 to 70%.
In the presence of a contraindication to thrombolysis or, as an additional
therapy in the event that this has not led to an improvement in hemodynamic
conditions, percutaneous thrombectomy can be used to reopen the partially
occluded pulmonary trunk or the main pulmonary arteries, as a valid life-saving
option in centers that do not have surgery.
The mechanical unclogging of thrombi in the pulmonary arteries involves the use
of various devices, with four main mechanisms of action:
1) mechanical fragmentation through guides, catheters, pigtails, balloons,
insertion of stents, with devices that allow to fragment the thrombus with
embolization of the thin fragments in the most distal areas of the lung tree,
2) aspiration,
3) rheolithic thrombectomy,
4) rotational thrombectomy.
Other therapeutic measures, especially important in the case of
contraindications to the aforementioned drugs, are: caval filters, implantable
supports that prevent the migration of emboli to the pulmonary arterial system