vein lecture
TRANSCRIPT
Lecture
The subject of the lecture:
Vein diseases: Thrombosis, Embolia of magistral vessels; PTPhS; Pulmonary
embolism.
Thrombosis, Embolia of magistral vessels; PTPhS.
Difinition.
Venous thrombosis of the deep veins is a serious life-threatening condition
which may lead to sudden death in the short term or long-term morbidity due to the
development of a post-thrombotic limb and venous ulceration. The most frequent
location of deep vein thrombosis is in the lower limb.
Deep venous thrombosis and pulmonary embolism are frequent causes of
hospital admission, and an understanding of the complex mechanisms of
thrombosis and thrombolysis is important in the prevention and management of
patients with these disorders.
Anatomy of the venous system in the limbs:
In communicating system are responsible for unidirectional blood flow toward
the heart.
In lower limb, communicating veins are most prominent along the medial
aspect of the calf, where they are called perforating veins. The names of these
veins come from their course from the superficial to the deep venous system
in which they perforate the deep fascia of the leg. Near the ankle are the
Cockett perfopating veins, near the knee the Boyd perforators and the
thigh the Hunterian perforating vein.
All veins in the upper and lower limbs contain valves every few centimeters
which ensure that blood flows towards the heart.
Venous pathophysiology: Blood from the skin and superficial tissues,
external to the deep fascia, drains via the long and short saphenous veins – SFJ and
SPJ – and communicating veins into the deep veins. Valves prevent the flow of
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blood from the deep to the superficial system. During the muscle relaxation phase,
the pressure within the calf falls to a low level and blood from the superficial veins
flows through the perforating veins into the deep veins. The consequence of this is
that the pressure in the superficial veins falls during walking. Normally the
pressure in the superficial veins of the foot and ankle falls from a resting level of
80-100 mmHg to about 20 mmHg. This ability to reduce the pressure in the
superficial venous system is crucial to the health of the lower limb. Patients with
damage to the veins in whom the superficial venous pressure does not fall during
exercise may develop varicose eczema, skin damage and leg ulceration.
One of the most common problems with the veins of the leg is failure of their
valves.
Occasionally complications of varicose veins may develop. These include
thrombosis, which is referred to as superficial thrombophlebitis. Sometimes
thrombosis extends into the deep venous system to cause deep vein thrombosis,
although this is infrequent. The most serious problem is venous ulceration which
complicates varicose veins in less than 5 per cent of patients.
Historical aspects. While pathologists had known for many years that thrombi at
times formed in the peripheral veins, Virchow introduced the embolism concept as
a result of his very cogent findings at autopsy. He observed that patients with
pulmonary embolism often also had thrombi in the veins of the legs and pelvis.
These thrombi were the same histological age as those found in the lungs.
Virchow concluded that thrombi formed in the systemic veins and that
thrombosis was caused primarily by three factors (Virchow's triad):
reduced blood flow in the systemic veins,
injury to the veins,
a state of hypercoagulability.
These factors remain important in the pathogenesis of pulmonary embolism. It
is worth reviewing Virchow's original comments concerning the formation of
thrombi in the peripheral veins.
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Etiology and pathogenesis of thrombosis. Thrombolysis: in the peripheral veins
the danger proceeds chiefly from the small branches. Thrombosis is usually
initiated when alterations in the vascular endothelium cause platelets to adhere to
subendothelial connective tissue. Collagen binds to platelet receptors to activate
enzymes that catalyse the release of arachidonic acid. Platelets release a variety of
mediators after activation, including adenosine diphosphate which modifies the
platelet surface, allowing fibrinogen to attach and link to adjacent platelets.
Platelet-derived growth factor is also released, stimulating the growth and
migration of fibroblasts and smooth muscle cells within the vessel wall.
The primary haemostatic plug is strengthened after several minutes by
activation of the coagulation pathway which causes the production of thrombin and
conversion of plasma fibrinogen to fibrin. The reactions require formation of a
surface-bound complex and the activation of proteases by proteolysis: they are
regulated by plasma and cellular cofactors and by calcium.
Thrombolysis begins immediately after formation of the haemostatic plug.
The principal physiological factor, tissue plasminogen activator, diffuses from
endothelial cells to convert plasminogen absorbed to the thrombus into plasmin,
which degrades the fibrin polymer. Plasmin can also degrade fibrinogen, but
systemic fibrinolysis does not occur because tissue plasminogen activator activates
plasminogen more effectively when it is absorbed to fibrin thrombi.
A variety of factors may be responsible for the development of thrombosis in
the absence of endothelial injury. Low blood flow increases local concentrations of
coagulation reactants. This may result from venous varicosities, prolonged bed
rest, or stasis during and after an operation or illness. Factors that diminish arterial
blood flow include cardiac disease or shock. Congenital or acquired abnormalities
in the fibrinolytic system and certain dysfibrinogenaemias also predispose to
intravascular thrombosis. While the last two specific disorders are of extreme
interest and help to elucidate the complex mechanisms of thrombosis formation,
they are identified in only 10 per cent of patients with thrombosis.
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Risk factors of the profound veins thrombosis/pulmonary embolism:
Pulmonary embolism/profound veins thrombosis in anamnesis,
Varicose veins,
Oncological diseases,
Character and duration of the surgery,
Postoperative complications,
General anesthesia,
Age over 40,
Obesity,
Diabetes,
Dehydratation/polycythemia,
Infection/sepsis,
Treatment with estrogens,
Blood circulation insufficiency,
Respiratory insufficiency,
Bed regime (for more then 4-6 days),
Immobilization,
Trauma,
Postoperative period.
Age is an important factor in the development of thrombosis, and pulmonary
embolism primarily affects the middle-aged and elderly.
Cardiac disorders, especially congestive heart failure, acute myocardial
infarction, and atrial fibrillation, are particularly conducive to the development of
pulmonary embolism.
Metastatic malignancy, particularly carcinoma of the pancreas and prostate,
is also associated with an increased incidence of pulmonary embolism.
Patients undergoing major surgical procedures or suffering major trauma or
burns also have an increased risk of venous thrombosis (Table 1). Factors
produced in damaged or ischaemic tissues or in patients with metastatic disease,
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together with venous stasis and endothelial injury, induce the formation of venous
thrombi.
Pregnancy increases the risk of pulmonary embolism because pressure from
the gravid uterus retards venous flow from the legs and pelvis.
Postpartum infection may also predispose to septic thrombophlebitis and
embolism, and oral contraceptives, which lower antithrombin III levels, are also
associated with the occurrence of pulmonary embolism. Table 1:
Risk of postoperative venous thromboembolic complications (C.Samama and
M.Samama, 1999, modificated):
Risk Risk factors from:Surgery Patient’s comditions
Low (I А) I. Uncomplicated interferences, lasting no more then 45 min (appendectomy, hernia section, delivery, abortion, transurethral adenectomy etc.)
А. No
Moderate (IВ, IС, IIА, IIВ
II. Larger interferences(cholecystectomy, stomach resection, complicated appendectomy, Cesarean section, uterus amputation etc)
В. Over 40, varicose veins, prescription of estrogens, blood circulation insufficiency, bed regime longer then 4 days, infection, obesity, postpartum period (6 weeks)
High IIС, IIIА, IIIВ,
IIIС
III. Expanded
surgeries(gastrectomy,
pancreatectomy,
colectomy, uterus
extirpation etc)
С. Oncological diseases,
profound veins thrombosis,
pulmonary embolism in
anamnesis, paralysis of
lower extremities,
thrombophilia
Venous thrombosis: Haemostatic thrombi that form in veins when blood flow is
reduced are richly endowed with fibrin and entrapped blood cells and contain
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relatively few platelets. These are often called red thrombi. The friable ends of
these thrombi which form in leg veins often break off and cause emboli in the
pulmonary circulation.
Thrombus formation is typically asymptomatic and the site does not usually
become inflamed. Inflammation of a thrombus in a vein is called
thrombophlebitis. The acute inflammatory response makes the developing
thrombus firmly adherent to the intima of the vessel wall, making embolization
uncommon.
Venous thrombosis may involve the superficial or deep venous systems of the
leg. When both systems are affected, thrombus formation usually begins in the
deep veins and extends to the superficial system. Varicose veins are often
associated with superficial thrombophlebitis of the lower extremities; other causes
include occult malignant neoplasms, local trauma, and parenteral drug abuse. In a
substantial number of patients the condition may be idiopathic.
Symptoms and Sings: The common clinical presentation of superficial
thrombophlebitis is local pain, erythema, and induration, with tenderness of the
thrombosed vein.
Classic triad of profound veins thrombosis of the lower extremities:
Pain.
Edema.
Increased skin temperature of the extremity.
When thrombophlebitis occurs below the knee, management consists of bed
rest, leg elevation, and local application of heat to the affected veins. The disorder
is usually self-limiting as obliteration of the affected part of the superficial venous
system precludes subsequent attacks. The risk of thromboembolism is minimal and
anticoagulation is not indicated. When thrombophlebitis extends above the knee,
embolization may occur: such patients should be closely observed for cephalad
progression of thrombus. Anticoagulation to prevent thromboembolism is
indicated if the response to conservative management is poor.
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Deep venous thrombosis is serious since the thrombus is much more likely to
embolize to the lungs: when the thrombosis is proximal to the calf, there is a 50 per
cent likelihood of pulmonary embolism, and up to 30 per cent of thrombi isolated
to the calf veins embolize to the lungs. As many as 40 to 50 per cent of patients
with deep venous thrombosis who develop pulmonary embolism have no
symptoms of deep venous disease, causing a delay in the administration of
appropriate prophylactic and therapeutic measures.
In patients who develop symptoms, mild oedema, superficial venous
dilatation, and pain in the calf are usually present. Palpation of the calf may
disclose tenderness and occasionally a thrombosed vein can be felt at any site from
the plantar aspect of the foot to the femoral triangle in the groin. A thrombosed
vein is usually best identified by palpation in the popliteal space.
Homans' sign (tenderness and tightness in the calf with hyperextension of the
foot) provides further evidence of thrombosis, but it may be present with any type
of calf muscle irritation and is not pathognomonic for thrombotic disease.
Most forms of deep venous thrombosis involve the popliteal vein and its
tributaries, but occasionally the thrombosis extends proximally to the femoral or
iliac veins. Swelling and pain in the distal thigh are more prominent if femoral vein
thrombosis is present, but these signs may be absent.
Phlegmasia caerulea dolens is the condition found when ileofemoral
thrombosis is associated with massive swelling of the entire extremity to the
inguinal ligament, severe pain, tenderness, and cyanosis.
Ileofemoral arterial thrombosis with spasm is frequently present and is
characterized by a pale cool extremity with diminished or absent pulses. Disease
confined to the popliteal vein and its tributaries may be occult or confused with
other conditions such as rupture of the gastrocnemius muscle or disorders
involving the knee, particularly a ruptured Baker's cyst. It is therefore important to
confirm objectively the presence of suspected deep venous thrombosis.
Diagnostic tests:
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The most specific test for confirmation of the diagnosis of deep venous
thrombosis is venography, in which contrast medium is injected into a vein on the
dorsum of the foot to demonstrate the venous drainage through the popliteal,
femoral, and iliac veins.
A normal result nearly always excludes the presence of venous thrombosis.
However, venography may be complicated by venous thrombosis and
extravasation of contrast media produces perivasculitis, cellulitis, and occasionally
ulceration of the skin. Patients are, therefore, often initially screened with a non-
invasive technique and undergo venography if the diagnosis remains in doubt.
Venography using radioisotopes instead of contrast medium avoids complications,
but although results with this technique are improving it is not in widespread use.
Real-time B-mode ultrasonic imaging combined with Doppler ultrasound
(duplex scanning) is a practical, non-invasive method of assessment of blood flow
in veins and valve cusp movement, and can differentiate between acute and
chronic thrombosis.
Plethysmography is another non-invasive technique which is useful in the
diagnosis of deep venous thrombosis. A calf plethysmograph measures volume
changes and may detect the oedematous changes associated with thrombus
formation.
Like duplex scanning, plethysmography is helpful in demonstrating proximal
thrombotic disease than that occurring in the calf.
Intravenous administration of radioactive fibrinogen is another sensitive
non-invasive technique used to diagnose deep venous thrombosis. Following
intravenous injection of fibrinogen, the legs are scanned with a gamma-camera to
detect the developing thrombus, which incorporates radioactive fibrinogen. This
test is particularly accurate for detecting thrombosis in the calf, but high
background radiation from the pelvic bones and urinary bladder means that it is not
useful in assessing veins in the upper thigh.
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Magnetic resonance imaging (MRI) is a reliable method of diagnosing
venous thrombosis and can demonstrate thrombi in the pelvic veins. MRI does not
require the administration of intravenous contrast agents and can be used safely in
patients with allergies to dye or with impaired renal function.
Treatment:
Anticoagulation prevents the propagation of the original thrombus and the
development of new thrombi while the existing thrombus is lysed by naturally
occurring fibrinolysis.
Classification of the antithrombotic medications:
1. Antiaggregants (antithrombotic drugs):
Acetylsalicylic acid (Aspirin).
Dipiridamol (Curantyl).
Indobuphen (Ibustrin).
Tiklopidin (Ticlid).
Clopidogrel (Plavix).
Inhibitors of glycoprotein receptors (GP) II b/III a:
Abximab (Rheo-pro).
Lamifiban.
Integrilin.
2. Anticoagulants:
Direct:
Heparin.
Low-molecular heparins:
Dalteparin (Fragmin).
Nadroparin (Fraksiparin).
Parnoparin (Fluxum).
Reviparin (Clivarin).
Enoxaparin (Cleksan).
Sulodeksid (Vessel due F).
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Indirect inhibitors of prothrombine:
Girudin (Lepirudin).
Indirect:
Acenocoumarol (Syncumar).
Caumarin (Varfarin).
Phenindione (Phenilin).
3. Thrombolytic medications:
Streptokinase (Cabikinase, Streptase).
Streptodekase.
Urokinase.
Anisoisolated plasminogen-streptokinase activated complex (Anistreplase).
Tissue plasminogen activator (Alteplase, TPA).
Intravenous heparin has rapid action and can be discontinued, or its effects
reversed rapidly with protamine sulphate, to decrease the possibility of bleeding
complications. Subcutaneous heparin is also effective.
Indication for prescription of heparin:
Treatment of acute arterial thrombosis.
Treatment of acute thrombosis and superficial veins.
Prevention and treatment of acute thrombosis in patients, which are in shock
(nonhemorrhagical).
Prevention of reocclusion after angioplasty
Prevention of thrombosis and embolism during valves prosthesis in cardio-
vascular surgery.
Decrease of the risk of thrombosis of profound veins and pulmonary embolism
after surgeries, during prolonged immobilization or other risk factors.
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Prevention of reocclusion in patients receiving Thrombolytic therapy with the
help of tissue-type plasminogen activator.
Positive moments of heparin prescription:
Accessibility.
Treatment with heparin is physiological (substitution therapy).
Effectiveness and relative safety of heparin (proved by multiple randomized
studies).
Successive clinical use of heparin.
Disadvantages of ungraded heparin in prevention and treatment of thrombosis:
Relatively low bioavailability.
Rapid elimination from the organism.
Multiple introduction of heparin.
Significant number of hemorrhagic complications (up to 10%).
Necessity of thorough laboratory monitoring of the system of coagulation.
No reliable direct correlation between the quantity and effect expression.
No clinically valuable effect on thrombin, connected with thrombi.
Increased sensitivity reaction, where heparin is an allergen.
Model of heparin indication due to the initial time of blood coagulation:
Time of blood coagulation, min (Lee-White)
Heparin dose, Units
Less then 5 20 0005-10 15 00011-18 10 00019-25 500
More then 25 Injection isn’t prescribedIndirect anticoagulants:
Neodicumarin 0,1 (N. 30). 1pill 2-3 times a day, controlling prothrombin
time (PT).
Tab. Phepromaron 0,01 (N. 20).
Tab. Nitropharini 0,005 (N. 30).
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Tab. Syncumari 0,004 (N. 50) /syncoumar or acenocoumarol/ – from the 2-
nd day of treatment the medicine is prescribed in the supporting dose of 2
mg/daily once a day in the morning.
Tab. Phenylini 0,03 (N. 30) /phenylin, or phenindione/.
Tab. Omephini 0,05 (N. 30).
Advantages of low-molecular heparins over upgraded heparin:
Prolong effect.
Introduced 1-2 times a day.
No need for the frequent laboratory control.
Less expressed influence on thrombocytes.
Less frequency of the side effects and complications development.
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Preventive measures against venous thromboembolism complications:Risk stages Preventive measures
Low Early exercising of patients Elastic compression of low extremities
Moderate LMH /НМГ/ (Clexan 20 мг) * once a day subcutaneously or
NFH /НФГ/ 5000 Units * 2-3 times a day subcutaneously or
Prolonged interrupted compression of extremities
High LMH /НМГ/ (Clexan 20 мг) * once a day subcutaneously or
NFH /НФГ/ 5000-7500 units * 3-4 times a day subcutaneously
+ methods of acceleration of venous circulation
Special cases Medical doses of LMH /НМГ/ or
NFH /НФГ/
+ Partial occlusion of inferior vena cava
(implantation of filter, plication)
Fibrinolytic therapy:
Activators of the fibrinolytic system are frequently used to accelerate lysis of
thrombi. These agents are either naturally occurring products or chemically
modified derivatives, and they differ with respect to fibrin specificity and
complications. Current indications for fibrinolytic therapy include patients with
massive pulmonary embolism complicated by hypotension, severe hypoxaemia,
and right heart strain or failure.
In addition, fibrinolytic agents have been successfully administered to patients
with extensive iliofemoral thrombophlebitis. While such therapy often resolves
venous thrombi, there is no firm evidence that lytic therapy reduces the incidence
of long-term complications. Fibrinolytic therapy may be of benefit in patients with
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thrombosis of the axillary vein, which does not respond well to conventional
anticoagulation.
Streptokinase is a soluble product of the metabolism of Streptococcus pyogenes
(Lancefield Group A) which indirectly activates plasminogen. Patients who have
suffered previous streptococcal infections may be allergic to streptokinase,
clinically manifest as toxic reactions such as pyrexia, dyspnoea, tachycardia, and
anaphylaxis. Urokinase is a product of renal epithelial and tubular cells which
directly activates plasminogen.
Streptokinase is usually given with a loading dose of 250000: this may need to
be repeated since patients may have antistreptococcal antibodies. Urokinase is
given with a loading dose of 4400 units/kg body weight, administered over 10 to
30 min. After the initial loading dose, 100000 units of streptokinase or 4400 units
of urokinase/kg body weight are administered hourly for 24 to 72 h. Heparin
therapy can be started after 6 h and is continued for 7 to 10 days.
Fibrinolytic therapy should be initiated as soon as possible after the onset of
thrombosis or embolism.
The systemic fibrinolysis associated with the fibrinolytic agents may cause
haemorrhage since essential haemostatic plugs are attached as well as pathological
thrombi.
Lytic therapy is therefore not recommended for patients with recent surgery or
those with a history of a neurological lesion, gastrointestinal bleeding, or
hypertension.
Recombinant tissue plasminogen activator is now available for general use.
The surgical extraction of venous thrombi has been almost completely
discontinued since the recurrence rate is high. Venous thrombectomy still has a
role in the management of patients with extensive iliofemoral disease in which
limb loss is imminent, such as in phlegmasia alba dolens.
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PTPhS:
Valvular incompetence of the deep veins develop in the same way as in the
superficial venous system, with the degeneration of the valve cusps resulting in
reverse flow in these veins. In other patients it may develop following a deep vein
thrombosis. When the deep veins fill with thrombus a new channel appears
(recanalisation) after a number of weeks or months (6 months). However, the deep
vein valves are destroyed by this process and, although the veins carry blood, the
valves no longer work and reverse flow is allowed. Some veins are severely
scarred by the recanalisation process so that they also become very narrow and
ineffective at carryng blood. Occasionally veins fail to recanalise at all. This is
sometimes seen following a venous thrombosis in the iliac veins. Under these
conditions the blood must find an alternative way round the blockage and collateral
veins develop. In the leg the long and short saphenous veins may act as collateral
channels and may double in size to accommodate the additional blood flow. In
patients with chronic iliac vein occlusion large suprapubic or abdominal varices
may be seen carrying the collateral flow.
Clinical features of deep vein incompetence. A number of patients with severe
deep vein damage has little to show for their problems. In patients with venous
valvular incompetence the calf muscle increases in size, apparently in response to
the greater work in returning blood from the leg. There may be some ankle
oedema, especially in those patients who have persistent venous obstruction. A
proportion of patients develops skin complications. These may range from mild
eczema to severe ulcerations. An early sing of sing injury is brown pigmentation
due to haemosiderin deposition in the skin. This occurs because the high venous
pressures which result from damage to the muscle pumping mechanism cause red
blood cells to be forced out of capillaries in the skin where their haemoglobin
breaks down to form haemosiderin. A later and more serious stage is
lipodermatosclerosis in which palpable induration develops in the skin and
subcutaneous tissues. This particularly affects the gaiter area of the leg, just above
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the malleoli, and may be the precursor of the leg ulceration. Atrophie blanche may
also develop. In this condition the superficial blood vessels are lost from the skin
and white patches develop. These indicate that the skin has been severely damaged
by the venous valvular incompetence. Venous ulceration may develop in these
areas.
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Pulmonary embolism (Acute).
Difinition.
Pulmonary embolism is a common and sometimes fatal complication of deep
venous thrombosis.
Etiology and pathogenesis of pulmonary embolism.
Although it is recognized in the postoperative period, most patients develop
pulmonary embolism secondary to non-surgical disorders, including congestive
heart failure, cerebrovascular accidents, chronic pulmonary disease, systemic
infections, carcinomatosis, and many chronic disorders.
Emboli that prove fatal are generally 1.5 cm or more in diameter and 50 cm or
more in length, and are often fragmented. The right pulmonary artery is more
commonly affected than the left, and the lower lobes more often than the upper
lobes. Emboli originate primarily in the systemic venous circulation; most arise in
the iliac and femoral veins, but up to 20 per cent originate from other sources,
including the inferior vena cava, the subclavian, axillary, and internal jugular
veins. Emboli due to neoplasms should also be considered in the differential
diagnosis.
Physiological changes following pulmonary embolism are related to the size
of the emboli and can be divided into those that produce microembolism
(obstruction of terminal small arteries and arterioles) and those that produce
macroembolism (occlusion of the large pulmonary vessels). Considerable
reduction in the diameter of the main pulmonary artery and the primary branches
(at least 50 per cent) is required to reduce pulmonary blood flow significantly or to
produce pulmonary hypertension.
Symptoms, sings and clinical manifestations.
A clinical diagnosis of pulmonary embolism may be difficult because of its
similarity to a number of other cardiorespiratory disorders. Dyspnoea, chest pain,
and haemoptysis are classic symptoms but are not sufficiently specific to establish
a definite diagnosis. It should be emphasized that many patients have underlying
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cardiac disease, and dyspnoea and tachypnoea are the most frequent clinical
findings. Accentuation of the pulmonary second sound is also common.
Haemoptysis, pleural friction rub, gallop rhythm, hypotension, cyanosis, and chest
splinting are present in no more than one-quarter of patients. Clinical evidence of
venous thrombosis occurs in only one-third of patients.
Special examinations :
In patients with acute pulmonary embolism and no other pulmonary disease,
the plain chest radiograph is usually normal. Diminished pulmonary vascular
marking at the site of embolism may be present (Westermark's sign).
The ECG is not specific but significant changes can be confirmatory. No
more than 10 to 20 per cent of patients subsequently proven to have pulmonary
embolism show any alterations in the ECG, including disturbance of rhythm (atrial
fibrillation, ectopic beats, heart block), enlargement of P waves, S-T segment
depression, and T-wave inversion. The most common abnormality is S-T segment
depression due to myocardial ischaemia, reduced cardiac output, and low systemic
arterial pressures, as well as increased right ventricular pressure.
Arterial blood gases are often normal, especially in young patients. Because
clinical findings and routine examinations are non-specific, radioactive pulmonary
scanning and pulmonary angiography are used to diagnose pulmonary embolism.
Radioactive pulmonary scanning: Radioisotope perfusion and ventilation
pulmonary scans remain the most frequently employed technique in the diagnosis
of pulmonary embolism. The method involves the detection of intravenously
injected particles such as technetium that become lodged in the pulmonary
capillary bed.
The results of ventilation/perfusion scans are usually described in terms of
the probability of embolism. High probability is indicated by segmental or greater
perfusion defects with a normal ventilation scan (V/Q mismatch). Moderate
probability is indicated by multiple subsegmental perfusion defects with a normal
ventilation scan or segmental perfusion defects without a ventilation scan.
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Venograms or other non-invasive tests may be useful in establishing a
definitive diagnosis of deep venous thrombosis, particularly in patients in whom
the diagnosis is in doubt or when insertion of a vena caval umbrella is being
considered.
The most definitive test for the diagnosis of pulmonary embolism is
pulmonary arteriography. It is important that the appearance of the normal
pulmonary angiogram is familiar in order that morphological and physiological
changes can be appreciated. The arteries in the lower areas of the lung are normally
larger because of a greater volume of pulmonary tissue. In most patients who
survive the initial embolic episode the obstruction in the pulmonary arteries
involves lobar or segmental branches. The defect should remain constant on
several successive films in the series, and the flow may be sluggish, shown by a
small pool of contrast medium that may persist in the artery above the obstruction
after the venous phase of the angiogram. When pulmonary arteriography is
performed later in the course of embolism, contrast medium may pass around the
obstruction, causing delayed opacification of the artery distally. In some areas
avascular segments resulting from unresolved thromboembolism may be seen.
Oblique views of the pulmonary arteriogram should be obtained for maximal
visualization and diagnostic accuracy. Pulmonary arteriography is safe when
experienced radiologists use small diameter catheters and low osmolarity contrast
agents.
The most reliable means of achieving absolute diagnosis are pulmonary
scanning and arteriography (scanning is a simple, safe, and reliable technique, it is
generally performed initially).
If the pulmonary scan is to be used for definitive diagnosis, a concomitant
plain chest film must show a normal pulmonary appearance in the area in which
the scan demonstrates pulmonary arterial occlusion.
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Treatment:
Surgical management
While anticoagulant therapy of pulmonary embolism is usually successful, it
may fail, and in this event the need for surgical management should be reviewed
on an individual basis.
Venous thrombectomy was previously recommended but is now rarely
performed because of the high incidence of recurrent postoperative thrombosis.
The presence of phlegmasia caerulea dolens with secondary arterial spasm is a
rare indication for thrombectomy. Although thrombosis may recur in such patients,
the venous lumen may remain patent for long enough to relieve the arterial spasm
and prevent gangrene developing.
Pulmonary embolectomy: In 1908, Trendelenburg performed the first
pulmonary embolectomy. In 1924, Kirschner performed the first successful
pulmonary embolectomy. The first successful pulmonary embolectomy performed
using extracorporeal circulation was reported in 1961: this is currently the
preferred technique, since it permits continuous oxygenation of the body while the
emboli are safely removed from the pulmonary arteries.
Persistent and refractory hypotension despite maximal resuscitation is the
primary indication for pulmonary embolectomy, especially in a patient with
massive embolism clearly documented by either a pulmonary scan or pulmonary
arteriogram. Treatment includes systemic heparinization and the administration of
vasopressors, inotropic agents, and endotracheal oxygen. The primary management
should be by this approach, since many patients previously thought to require
embolectomy respond favourably with intensive resuscitation. Usually, 1 or 2 h
may be spent attempting to restore acceptable cardiopulmonary function, unless
the clinical situation is desperate. An appropriate blood pressure should be
maintained and embolectomy may be postponed, especially if renal and cerebral
function is acceptable.
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If pulmonary embolectomy is indicated, it is usually performed using
cardiopulmonary bypass.
A median sternotomy is made for exposure of the pulmonary artery. The main
pulmonary artery is usually found to be free of emboli, although partial obstruction
may be present. The emboli are removed from the right and left pulmonary arteries
and from their major branches. Smaller emboli may be removed by passage of a
Fogarty catheter and irrigation with saline. The pulmonary artery is closed and
cardiopulmonary bypass is gradually discontinued, allowing the heart and lungs to
resume normal function.
Patients with acute and severe cardiopulmonary collapse can be supported by
partial cardiopulmonary bypass by a circuit from femoral vein to femoral artery for
immediate resuscitation. If extracorporeal circulation is not available, a right or left
thoracotomy with exposure of the most severely involved pulmonary artery can be
performed, the side of predominant occlusion being determined by a scan or
arteriogram. An anterior thoracotomy is appropriate for exposure of either the right
or left pulmonary artery, which can be opened distally for removal of emboli while
normal circulation to the opposite lung is maintained.
Methods of embolectomy in patients with pulmonary embolism:
Trendelenburg’s position with extrapleural approach, cross-clamping of aorta
and pulmonary artery (it is nor used nowadays).
Embolectomy through the branches of pulmonary artery (Marion P., Estanove
K., 1956).
Embolectomy from the pulmonary artery in conditions of temporary (more then
3 min) cross-clamping of veins cava (Vosschulte K., 1959). It is advised to
perform a surgery in conditions of artificial lung ventilation. It is rather well
spread method of surgery.
Transvenous embolectomy is the most perspective.
A serious complication which may follow pulmonary embolectomy is massive
endobronchial haemorrhage. Successful management involves endotracheal
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intubation for selective collapse of the lung and entrapment of the haemorrhage
into the involved lung. Reperfusion pulmonary oedema may occur after pulmonary
artery thromboendarterectomy, and prolonged mechanical ventilation is often
required. This syndrome is a cause of postoperative hypoxaemia with local
pulmonary infiltrate.
Although vena caval interruption was previously recommended for selected
patients with pulmonary embolism, it is seldom performed today. A stainless steel
umbrella designed by Greenfield, Michna, Amplatz, Gunther and «Birds nest» can
be inserted under local anaesthesia through the femoral or jugular vein. With this
device a filter is fixed to the wall of the inferior vena cava by hooks.
Complications include distal migration to the bifurcation of the inferior vena
cava, protrusion of the struts through the caval wall, formation of thrombus on the
filter, misplacement of the device, retroperitoneal haemorrhage, perforation of the
duodenum or ureter, and development of a thrombus proximal to the umbrella,
producing emboli. The filter may also migrate into the iliac vein, renal vein, right
atrium, right ventricle, or pulmonary artery, and such migration is occasionally
fatal. The filter may also stimulate distal thrombosis in the vena cava and late
occlusion may occur.
Anticoagulation therapy:
Anticoagulation with heparin is the standard treatment for pulmonary
embolism and acute thrombosis (Treatment of thrombosis).
Prevention of pulmonary embolism:
Prophylaxis of deep venous thrombosis and pulmonary embolism is an
important aspect of postoperative care.
Nevertheless, no method or combination of methods completely prevents
thromboembolism.
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Factors which reduce the risk include physical activity and elevation of the
lower extremities for gravity drainage of venous return. Some consider
compression of the legs by stockings or mechanical devices and prophylactic
anticoagulation to be useful, but many disagree and these issues remain
controversial. Early ambulation and resumption of physical activity after operation
or bed rest for any reason has long been recommended.
Antiplatelet agents: antiplatelet drugs play a role in the management of
patients with thromboembolism.
Non-steroidal anti-inflammatory drugs, including aspirin and dipyridamole,
have also been shown to inhibit the platelet-release reaction secondary to ADP-
induced platelet aggregation and adherence to collagen in vitro. Dipyridamole
inhibits phosphodiesterase and raises intracellular cyclic AMP levels. The usual
dose of 50 to 100 mg four times daily has no effect on platelet function, and it is
usually administered in a combination with aspirin.
Aspirin reduces the incidence of thrombosis too.
Dextran has also been used as an antiplatelet drug to prevent deep venous
thrombosis.
Position and compression devices: elevation of the legs with flexion of the
knee causes a rapid runoff of the blood in the veins of the leg and thigh due to
gravity (this is a simple, effective, and broadly applicable prophylactic measure).
Pneumatic compression devices also decrease stasis and increase venous blood
flow but are not widely used.
Prophylactic anticoagulation: while prophylactic anticoagulation may be
beneficial, especially after trauma and in patients with orthopaedic disorders, the
concept of low-dose heparin as a prophylactic measure remains controversial. The
usual regimen is an initial dose of 5000 units subcutaneously, repeated every 8 to
12 h until the patient is fully ambulatory. Coagulation times are prolonged
minimally, if at all, with a low risk of bleeding. Although low-dose heparin
continues to be recommended by some to prevent thromboembolism, it is not
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frequently used. It appears to have limited value after prostatectomy, after
myocardial infarction, and in major orthopaedic procedures, particularly repair of
femoral fractures and reconstructive surgery of the hip and knee.
Low-dose heparin prophylaxis is also inadequate for patients with an active
thrombotic process. Finally, it may lead to heparin sensitivity and cause
disseminated intravascular coagulation, a condition in which platelets aggregate
into thrombi and which may result in gangrene of the extremities.
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