pulmonary thromboembolism

pulmonary thromboembolism


 PULMONARY TROMBOEMBOLISMO



Department of Cardiovascular Diseases and Division of Surgery.
Faculty of Medicine. Pontificia Universidad Católica de Chile INTRODUCTION
Deep venous thrombosis and its major complication, pulmonary embolism, constitute the clinical picture that we call pulmonary thromboembolism. It is a serious and potentially fatal clinical condition that complicates the hospital evolution of severe patients, but occasionally it also affects outpatients and in good health. In the United States an estimated 200,000 people die each year from pulmonary embolism. About half of them occur in association with terminal or incurable diseases, however, in the rest they can be saved if appropriate prophylactic measures are taken to avoid pulmonary embolism.

The factors predisposing to deep venous thrombosis were enunciated last century by Virchow. Today we understand more intimately the intimate mechanisms in their genesis.

disorders of coagulation,
damage of the vascular wall
venous stasis
I) COAGULATION ALTERATIONS
The process of coagulation follows a series of biochemical reactions schematized in a cascade and leading to the formation of a fibrin clot. Both the intrinsic pathway that is activated when the blood comes into contact with a surface with its altered endothelium, and the extrinsic pathway that is stimulated by blood exposure to tissue thromboplastin, meet at a common point which is the activation of factor X, which in the presence of calcium, phospholipids and factor V converts prothrombin to thrombin, and this in turn interacts with fibrinogen and converts it to fibrin. Genetic or acquired defects in the levels of natural anticoagulants (antithrombin III, proteins C and S), antiphospholipid antibodies or elevated levels of homocysteine, determines a state of hypercoagulability or thrombophilia.



2) DAMAGE TO THE VASCULAR WALL

Normal endothelium has a resistance to thrombogenesis and does not react with platelets or other blood coagulation proteins. Once the vascular wall is damaged, endothelium disruption occurs and exposure of the subendothelial tissue occurs. Platelets adhere to the collagen and the subendothelial basement membrane releasing ADP and thromboxane A2, substances that in turn generate greater platelet aggregation.



3) ESTASIS

Stasis prevents liver clearance of activated clotting factors and facilitates the interaction of figurative elements of the blood with the vascular wall. The most frequent cause of stasis is the immobilization that occurs in the perioperative period of patients, but also prolonged bed rest due to various medical causes or the application of an immobilizing gypsum are predisposing factors.

Risk factors for venous thrombosis from situations encountered in our daily clinical practice include:

postoperative and surgical trauma
age
malignant disease
immobilization
cardiac insufficiency
previous venous thromboembolism
varices
obesity
pregnancy and puerperium
oral contraceptives
Miscellaneous: thrombocytosis, polycythemia vera, lupus and nocturnal paroxysmal hemoglobinuria.


DIAGNOSIS
Autopsy studies have shown that:

More than 80% of patients with pulmonary embolism have venous thrombosis that affects the deep veins of the extremities. In all other cases there is thrombosis of pelvic veins, in the right heart cavities or in the veins of the upper extremities.
50% of patients with symptomatic lower extremity deep venous thrombosis develop pulmonary embolism, which is usually subclinical
70-80% of patients with postoperative pulmonary embolism demonstrated by ventilation / perfusion scintigraphy have deep venous thrombosis in their extremities.
Deep venous thrombosis clinic
Only one-third of patients with deep vein thrombosis of the lower limbs present clinical manifestations. The most frequent are:

pain and tenderness of the lower extremity, especially in the muscular masses of the compromised segment
distal edema, superficial venous distention
increase of superficial venous weft by collateral circulation
signs of venous congestion with a cyanotic aspect of the limb
occasionally erythema in relation to areas of vascular or perivascular inflammation
palpation of a venous cord, corresponding to the thrombosed vein segment.
The clinical picture of pulmonary embolism depends on:number and size of the pistons
the location of the plunger
the patient's previous respiratory and cardiovascular condition.
The pathophysiological consequences of pulmonary embolism can be categorized into:

Effects on lung parenchyma
The pulmonary parenchyma obtains its oxygen through the bronchial circulation, the arterial pulmonary circulation and directly from the alveolar oxygen. Since oxygen comes from multiple sources, an obstruction of the arterial pulmonary circulation usually does not produce ischemia of the pulmonary parenchyma. However, the oxygen supply to the distal lung parenchyma may be impeded in:
patients with chronic lung disease, since these patients frequently have altered their bronchial circulation;
patients with congestive heart failure due to pulmonary venous congestion and
if the plunger reaches a critical extent and is located in a distal pulmonary vessel. Pulmonary infarction occurs when there is pulmonary parenchymal necrosis due to insufficient oxygen supply.
Effects on gas exchange
The hypoxemia that accompanies pulmonary embolism frequently in its initial stage is not always proportional to the size of the embolism, its mechanism is multiple and is due to
alterations in the ventilation / perfusion balance due to lack of perfusion of areas that are normally ventilated.
In turn, humoral agents such as serotonin and prostaglandins released from platelets and pulmonary parenchyma exposed to embolism may produce airway constriction in normally perfused regions.
Finally, hyperperfusion and edema of non-embolized areas
hypoventilation of the lung caused by pleuritic pain.
Effects on the function of the right heart
Embolism can produce pulmonary hypertension due to mechanisms of mechanical obstruction and pulmonary arterial constriction. The combination of these two phenomena leads to an increase in pulmonary vascular resistance, which in turn can lead to right heart failure and peripheral circulatory collapse or shock if cardiac output is significantly compromised.
The clinical signs for the diagnosis of a pulmonary embolism are:

dyspnoea
chest pain of the pleuritic type,
hemoptysis,
syncope,
apprehension and anxiety,
alterations of consciousness.
The signs to physical examination are:

tachypnea,
tachycardia,
hypotension,
cyanosis
elevation of jugular venous pressure,
prominent right ventricle,
increased lung component of the second noise,
rhythm in gallop,
suggestive signs of a pleural effusion and occasionally bronchoconstriction in the pulmonary examination, although frequently it may be normal.
Despite all these signs, the clinical diagnosis of pulmonary embolism is quite difficult (there are many differential diagnoses) and in turn low sensitivity. (Many pulmonary embolisms are asymptomatic.)



COMPLEMENTARY EXAMS
Due to the difficulty of the clinical diagnosis of pulmonary embolism, laboratory tests should be used to confirm or rule out the diagnosis of pulmonary embolism.Arterial blood gases:
A normal paO2 does not rule out pulmonary embolism, but makes the diagnosis less likely.
Electrocardiogram.
The ECG may have nonspecific alterations, affecting the ST segment or the T wave, appearing images suggestive of acute right ventricular overload (Sl-Q3-T3). The major utility of the ECG is in the differential diagnosis of myocardial infarction.
Chest X-ray:
Chest x-ray is normal or shows nonspecific abnormalities. It is essential to correctly interpret a pulmonary scintigraphic study. Just remember the Westermark sign consisting of an area of ​​hypertranslucency secondary to occlusion of the vascular weave.
Pulmonary scintigraphy.
The perfusion scintigram detects areas in which there is decreased blood flow and is the most useful noninvasive test in the diagnostic process of this pathology. If it is normal, it practically excludes the diagnosis of pulmonary embolism. If abnormal it can not be used as evidence of pulmonary embolism strictly since other lung conditions exist that can be associated to alterations of this examination. However, the association of pulmonary perfusion abnormalities in the scintigram and the normal chest X-ray has a greater sensitivity for the diagnosis of TEE. Pulmonary ventilation scintigraphy should always be associated with perfusion scintigraphy as it increases specificity by demonstrating areas that are hypoperfused are well ventilated, which is characteristic of pulmonary embolism when this test is performed early. If a perfusion defect associated with a ventilation defect is found, it probably does not correspond to a recent pulmonary embolism or other lung disease.
Pulmonary angiography.
Pulmonary angiography is the definitive examination in the objective diagnosis of this condition. However, it is an invasive and non-risk free examination. Angiographic images can now be obtained by helical computed tomography, which avoids the introduction and manipulation of catheters (AngioTAC). It is not always necessary to obtain an angiogram to start the appropriate treatment. However, in some cases, it is essential to confirm or definitively rule out the diagnosis, especially when considering the possibility of anticoagulant treatment in patients at high risk.
No laboratory test, other than positive pulmonary angiography, is specific for diagnosis in pulmonary embolism.



PREVENTION
It is important to discuss the prevention of deep venous thrombosis and its complications in the short and long term.



PREVENTION TECHNIQUES:
Miniheparin
The miniheparin is administered subcutaneously, initiating treatment with heparin 5,000 units 2 hours before the surgery and then every 8 to 12 hours postoperatively until the patient begins to walk.
Currently available fractional heparin preparations of low molecular weight with anticoagulant activity but with low hemorrhagic activity, for subcutaneous use every 12 or 24 hours according to the anti factor X activated concentration. (enoxaparin, fraxiparin, etc.)
Intermittent pneumatic compression
This methodology applies intermittent cycles of compression and decompression by means of an inflatable boot on both lower extremities.
Oral anticoagulants (Acenocumarol, Warfarin)
It is important to double prothrombin time, they are quite effective in preventing the formation of deep venous thrombosis. However, they are associated with a higher incidence of postoperative haemorrhagic complications.
Dextran
If dextran is administered intraoperatively and then 500 ml. daily for the first 4 to 5 days, it is possible to reduce the incidence of deep venous thrombosis postoperatively. It is also associated with a greater number of hemorrhagic complications.TREATMENT OF THE PULMONARY EMBOLIA (EP)
Cardiopulmonary massage
In cases of a massive PF: with hemodynamic compromise, cardiac massage allows the fragmentation of the thrombus and sending the fragments to the more peripheral pulmonary bed, resulting in a decrease in peripheral vascular resistance for purely mechanical reasons.
Fibrinolytics
Fibrinolytics allow vascular occlusions to be unblocked non-surgically. The treatment is very effective in a few hours, which allows its use in severe embolism, re-establishing pulmonary perfusion. It requires the introduction of a catheter directly into the thrombus, for the infusion of high doses of Urokinase (initial 250,000 IU) followed by infusion of new doses according to the angiographic result. It is possible to associate mechanical methods of endoluminal fragmentation to accelerate the fibrinolytic action. The use of heparin should be associated with the use of devices for definitive discontinuation of the inferior vena cava when emboli originate in the veins of the lower extremities.
Anticoagulation
Continuous heparin infusion treatment ensures consistent levels of use at a low risk of bleeding complications.
a) We started treatment with 5,000 units of intravenous heparin
b) Simultaneously, the administration of heparin in continuous infusion at the rate of 1 000 U / hour was initiated. (eg 25,000 IU of heparin in 250 ml of serum at 10 cc / hr).
Monitoring is done by determining the TTPK and the goal is to extend the control time to 2 l / 2 times the original value. Treatment with heparin should be continued for 5 to 10 days, initiating oral anticoagulants from the first day, whose duration will depend on the initial clinical picture. It is intended to reach INR prothrombin levels between 2 and 3 following the patient with serial controls to adjust the dose of anticoagulant.
Deep vein thrombosis of the lower extremities infragenicular should be treated for 3 months with oral anticoagulants and if there is iliofemoral thrombosis and / or a pulmonary embolus, treatment is continued for a period of 6 months.
Interruption of the Lower Cava Vein
In patients are contraindicated relative or absolute for anticoagulant treatment, partial interruption of the inferior vena cava can be used by means of devices that act as filters housed inside the cava (Greenfield filter and others).
Contraindications to anticoagulant therapy include:
a) current or recent gastrointestinal bleeding,
b) malignant hypertension,
c) recent postoperative especially in neurosurgical patients,
d) ocular haemorrhage,
e) subarachnoid or cerebral haemorrhage,
f) stroke,
g) recent trauma
h) bleeding diathesis.
Polytraumatism is a relative indication for interruption of the vena cava, given the enormous frequency of associated thromboembolism, especially in spinal cord injuries, pelvic fractures and long bones of the lower extremities.
In patients with septic pelvic processes with septic thrombophlebitis, the risk of embolization and secondary pulmonary abscess is very high. This clinical condition is the only one that justifies a complete ligation of the infra-renal inferior vena cava, despite the late sequels that this implies.
Pulmonary thromboembolism surgery
In very few cases where there is a frank hemodynamic compromise due to recurrent chronic thromboembolism, there is still the surgical indication of a pulmonary thromboembolectomy.
Long-term treatment
Once the acute stage of the thromboembolic problem is handled, it is necessary to warn the patient about the need to use elastic support for permanence (averages or ad hoc bandages), especially in those cases that have presented proximal deep vein thrombosis, that is thigh or iliac sector, to prevent long-term complications known as the post-phlebitis syndrome: ulcers, varicose veins, etc.


VENOUS THROMBOEMBOLISM IN PEDIATRICS
It is most often seen as a complication of catheterization for intravenous (parenteral) or umbilical vessel treatments in newborns and may give rise to pulmonary embolisms.Deep venous thrombosis in the pediatric patient is exceptional and includes:

heart disease with left to right shunt,
chronic rheumatic heart disease,
atrial fibrillation
primary or secondary pulmonary hypertension.
Also the drainage of cerebrospinal fluid in hydrocephalus may give rise to pulmonary embolisms.