EMBOLISM

          EMBOLISM

Definition and Types

Embolism is the process of partial or complete obstruction of some part of the cardiovascular system by any mass carried in the circulation; the transported intravascular mass detached from its site of origin is called an embolus. Most usual forms of emboli (90%) are thromboemboli i.e. originating from thrombi or their parts detached from the vessel wall. 

Emboli may be of various types:

A. Depending upon the matter in the emboli:

i) Solid e.g. detached thrombi (thromboemboli), athero-matous material, tumour cell clumps, tissue fragments, parasites, bacterial clumps, foreign bodies. 

ii) Liquid e.g. fat globules, amniotic fluid, bone marrow.

iii) Gaseous e.g. air, other gases.

B. Depending upon whether infected or not:

i) Bland, when sterile.

ii) Septic, when infected.

C. Depending upon the source of the emboli:

i) Cardiac emboli from left side of the heart e.g. emboli

originating from atrium and atrial appendages, infarct in the

left ventricle, vegetations of endocarditis.

ii) Arterial emboli e.g. in systemic arteries in the brain, spleen,

kidney, intestine.

iii) Venous emboli e.g. in pulmonary arteries.

iv) Lymphatic emboli can also occur.

D. Depending upon the flow of blood, two special types of emboli are mentioned: 

i) Paradoxical embolus. An embolus which is carried from the venous side of circulation to the arterial side or vice versa is called paradoxical or crossed embolus e.g. through arteriovenous communication such as in patent foramen ovale, septal defect of the heart, and arteriovenous shunts in the lung. 

ii) Retrograde embolus. An embolus which travels against the flow of blood is called retrograde embolus e.g. metastatic deposits in the spine from carcinoma prostate. The spread occurs by retrograde embolism through intraspinal veins which carry tumour emboli from large thoracic and abdominal veins due to increased pressure in body cavities e.g. during coughing or straining. 

Some of the important types of embolism are tabulated in table and described below. 

 TABLE: Important Types of Embolism.

           Type                                  Common Origin

1. Pulmonary embolism                         Veins of lower legs

2. Systemic embolism                       Left ventricle (arterial)

3. Fat embolism                                      Trauma to bones/soft tissues

4. Air embolism                                 Venous: head and neck                                                                operations,  obstetrical                                                                      trauma

                                                              Arterial: cardiothoracic

                                                                  surgery, angiography

5. Decompression                       Descent: divers

sickness                                        Ascent: unpressurised flight

6. Amniotic fluid embolism          Components of amniotic                                                                     fluid

7. Atheroembolism                     Atheromatous plaques

8. Tumour embolism                 Tumour fragments

Pulmonary Thromboembolism

DEFINITION. Pulmonary embolism is the most common and fatal form of venous thromboembolism in which there is occlusion of pulmonary arterial tree by thromboemboli. Pulmonary thrombosis as such is uncommon and may occur in pulmonary atherosclerosis and pulmonary hypertension. Differentiation of pulmonary thrombosis from pulmonary thromboembolism is tabulated in 

ETIOLOGY. Pulmonary emboli are more common in  hospitalised or bed-ridden patients, though they can occur in ambulatory patients as well. The causes are as follows: 

i) Thrombi originating from large veins of lower legs (such  as popliteal, femoral and iliac) are the cause in 95% of pulmonary emboli. 

ii) Less common sources include thrombi in varicosities of  superficial veins of the legs, and pelvic veins such as peri￾prostatic, periovarian, uterine and broad ligament veins. 

PATHOGENESIS. Detachment of thrombi from any of the  above-mentioned sites produces a thrombo-embolus that flows through venous drainage into the larger veins draining into right side of the heart. 

   •If the thrombus is large, it is impacted at the bifurcation  of the main pulmonary artery (saddle embolus), or may be found in the right ventricle or its outflow tract. 

   •More commonly, there are multiple emboli, or a large embolus may be fragmented into many smaller emboli which are then impacted in a number of vessels, particularly affecting the lower lobes of lungs. 

    •Rarely, paradoxical embolism may occur by passage of an embolus from right heart into the left heart through atrial or ventricular septal defect. In this way, pulmonary emboli may reach systemic circulation.

CONSEQUENCES OF PULMONARY EMBOLISM.

Pulmonary embolism occurs more commonly as a complication in patients of acute or chronic debilitating diseases who are immobilised for a long duration. Women in their reproductive period are at higher risk such as in late pregnancy, following delivery and with use of contraceptive pills. The effects of pulmonary embolism depend mainly on the size of the occluded vessel, the number of emboli, and on the cardiovascular status of the patient. The following consequences can result. 

i) Sudden death. Massive pulmonary embolism results in instantaneous death, without occurrence of chest pain or dyspnoea. However, if the death is somewhat delayed, the clinical features resemble myocardial infarction i.e. severe chest pain, dyspnoea and shock.

ii) Acute cor pulmonale. Numerous small emboli may obstruct most of the pulmonary circulation resulting in acute right heart failure. Another mechanism is by release of vasoconstrictor substances from platelets or by reflex vasoconstriction of pulmonary vessels. 

iii) Pulmonary infarction. Obstruction of relatively small sized pulmonary arterial branches may result in pulmonary  infarction . The clinical features include chest pain due to fibrinous pleuritis, haemoptysis and dyspnoea due to reduced functioning pulmonary parenchyma. 

iv) Pulmonary haemorrhage. Obstruction of terminal branches (endarteries) leads to central pulmonary haemorrhage. The clinical features are haemoptysis, dyspnoea, and less commonly, chest pain due to central location of pulmonary haemorrhage. Sometimes, there may be concomitant pulmonary infarction. 

v) Resolution. Vast majority of small pulmonary emboli (60-80%) are resolved by fibrinolytic activity. These patients are clinically silent owing to bronchial circulation so that lung parenchyma is adequately perfused. 

vi) Pulmonary hypertension, chronic cor pulmonale and  pulmonary arteriosclerosis. These are the sequelae of multiple small thromboemboli undergoing healing rather than resolution. 

Systemic Embolism

This is the type of arterial embolism that originates comm￾only from thrombi in the diseased heart, especially in the left ventricle. These diseases of heart include myocardial infraction, cardiomyopathy, RHD, congenital heart disease, infective endocarditis, and prosthetic cardiac valves. These arterial emboli invariably cause infarction at the sites of lodgement which include, in descending order of frequency, lower extremity, brain, and internal visceral organs (spleen, kidneys, intestines). Thus, the effects and sites of arterial emboli are in striking contrast to venous emboli which are often lodged in the lungs. 

Fat Embolism

Obstruction of arterioles and capillaries by fat globules constitutes fat embolism. If the obstruction in the circulation is by fragments of adipose tissue, it is called fat-tissue embolism. 

ETIOLOGY. Following are the important causes of fat embolism: 

i) Traumatic causes:

•Trauma to bones is the most common cause of fat embolism e.g. in fractures of long bones leading to passage of fatty marrow in circulation, concussions of bones, after orthopaedic surgical procedures etc.

•Trauma to soft tissue e.g. laceration of adipose tissue and in puerperium due to injury to pelvic fatty tissue.

ii) Non-traumatic causes:

•Extensive burns

•Diabetes mellitus

•Fatty liver

•Pancreatitis

•Sickle cell anaemia

•Decompression sickness

•Inflammation of bones and soft tissues

•Extrinsic fat or oils introduced into the body

PATHOGENESIS. The following mechanisms are proposed to explain the pathogenesis of fat embolism. These may be acting singly or in combination. 

i) Mechanical theory. Mobilisation of fluid fat may occur following trauma to the bone or soft tissues. The fat globules released from the injured area may enter venous circulation and finally most of the fat is arrested in the small vessels in the lungs. Some of the fat globules may further pass through into the systemic circulation to lodge in other organs. 

ii) Emulsion instability theory. This theory explains the pathogenesis of fat embolism in non-traumatic cases. According to this theory, fat emboli are formed by aggrega￾tion of plasma lipids (chylomicrons and fatty acids) due to disturbance in natural emulsification of fat. 

iii) Intravascular coagulation theory. In stress, release of  some factor activates disseminated intravascular coagulation (DIC) and aggregation of fat emboli. 

iv) Toxic injury theory. According to this theory, the small  blood vessels of lungs are chemically injured by high plasma levels of free fatty acid, resulting in increased vascular permeability and consequent pulmonary oedema. 

CONSEQUENCES OF FAT EMBOLISM. The effects of fat embolism depend upon the size and quantity of fat globules, and whether or not the emboli pass through the lungs into the systemic circulation. 

i) Pulmonary fat embolism. In patients dying after frac￾tures of bones, presence of numerous fat emboli in the capillaries of the lung is a frequent autopsy finding because the small fat globules are not likely to appreciably obstruct the vast pulmonary vascular bed. However, widespread obstruction of pulmonary circulation due to extensive pulmonary embolism can occur and result in sudden death.

ii) Systemic fat embolism. Some of the fat globules may  pass through the pulmonary circulation such as via patent foramen ovale, arteriovenous shunts in the lungs and vertebral venous plexuses, and get lodged in the capillaries of organs like the brain, kidney, skin etc.

Gas Embolism

Air, nitrogen and other gases can produce bubbles within the circulation and obstruct the blood vessels causing damage to tissue. Two main forms of gas embolism—air embolism and decompression sickness are described below.

Air Embolism

 Air embolism occurs when air is introduced into venous or arterial circulation.

VENOUS AIR EMBOLISM. Air may be sucked into systemic veins under the following circumstances:

i) Operations on head and neck, and trauma. The accidental opening of a major vein of the neck like jugular,or neck wounds involving the major neck veins, may allow air to be drawn into venous circulation.

ii) Obstetrical operations and trauma. During childbirth by normal vaginal delivery, caesarean section, abortions and other procedures, fatal air embolism may result from the entrance of air into the opened-up uterine venous sinuses and endometrial veins.

iii) Intravenous infusion of blood and fluid. Air embolism may occur during intravenous blood or fluid infusions if only positive pressure is employed.

iv) Angiography. During angiographic procedures, air may be entrapped into a large vein causing air embolism.

The effects of venous air embolism depend upon the following factors:

i) Amount of air introduced into the circulation. The volume of air necessary to cause death is variable but usually 100-150 ml of air entry is considered fatal.

ii) Rapidity of entry of a smaller volume of air is important determinant of a fatal outcome.

iii) Position of the patient during or soon after entry of air is another factor. The air bubbles may ascend into the superior vena cava if the position of head is higher than the trunk(e.g. in upright position) and reach the brain. 

iv) General condition of the patient e.g. in severely ill patients, as little as 40 ml of air may have serious results. 

 The mechanism of death is by entrapment of air emboli  in the pulmonary arterial trunk in the right heart. If bubbles of air in the form of froth pass further out into pulmonary arterioles, they cause widespread vascular occlusions. If death from pulmonary air embolism is suspected, the heart and pulmonary artery should be opened in situ under water so that escaping froth or foam formed by mixture of air and blood can be detected. 

ARTERIAL AIR EMBOLISM. Entry of air into pulmonary  vein or its tributaries may occur in the following conditions: 

i) Cardiothoracic surgery and trauma. Arterial air  embolism may occur following thoracic operations, thoracocentesis, rupture of the lung, penetrating wounds of  the lung, artificial pneumothorax etc. 

ii) Paradoxical air embolism. This may occur due to passage of venous air emboli to the arterial side of circulation through a patent foramen ovale or via pulmonary arteriovenous shunts. 

iii) Arteriography. During arteriographic procedures, air  embolism may occur.

 The effects of arterial air embolism are in the form of certain characteristic features: 

i) Marble skin due to blockage of cutaneous vessels.

ii) Air bubbles in the retinal vessels seen ophthalmoscopically.

iii) Pallor of the tongue due to occlusion of a branch of lingual  artery. 

iv) Coronary or cerebral arterial air embolism may cause  sudden death by much smaller amounts of air than in the venous air embolism. 

Decompression Sickness

This is a specialised form of gas embolism known by various  names such as caisson’s disease, divers’ palsy or aeroembolism. 

PATHOGENESIS. Decompression sickness is produced  when the individual decompresses suddenly, either from high atmospheric pressure to normal level, or from normal pressure to low atmospheric pressure. 

  •In divers, workers in caissons (diving-bells), offshore drilling and tunnels, who descend to high atmospheric pressure, increased amount of atmospheric gases (mainly nitrogen; others are O2, CO2) are dissolved in blood and tissue fluids. When such an individual ascends too rapidly i.e. comes to normal level suddenly from high atmospheric pressure, the gases come out of the solution as minute bubbles, particularly in fatty tissues which have affinity for nitrogen. These bubbles may coalesce together to form large emboli. 

  •In aeroembolism, seen in those who ascend to high altitudes or air flight in unpressurised cabins, the individuals  are exposed to sudden decompression from low atmospheric pressure to normal levels. This results in similar effects as in divers and workers in caissons.

EFFECTS. The effects of decompression sickness depend upon the following:

 •Depth or altitude reached

 •Duration of exposure to altered pressure

 •Rate of ascent or descent

 •General condition of the individual

  Pathologic changes are more pronounced in sudden decompression from high pressure to normal levels than in those who decompress from low pressure to normal levels.The changes are more serious in obese persons as nitrogen gas is more soluble in fat than in body fluids.

Clinical effects of decompression sickness are of 2 types—acute and chronic.

•Acute form occurs due to acute obstruction of small blood vessels in the vicinity of joints and skeletal muscles. The condition is clinically characterised by the following:

i) ‘The bends’, as the patient doubles up in bed due to acute pain in joints, ligaments and tendons.

ii) ‘The chokes’ occur due to accumulation of bubbles in the lungs, resulting in acute respiratory distress.

iii) Cerebral effects may manifest in the form of vertigo, coma,and sometimes death.

•Chronic form is due to foci of ischaemic necrosis throughout body, especially the skeletal system. Ischaemic necrosis may be due to embolism per se, but other factors such as platelet activation, intravascular coagulation and hypoxia might contribute. The features of chronic form are as under:

i) Avascular necrosis of bones e.g. head of femur, tibia,humerus.

ii) Neurological symptoms may occur due to ischaemic necrosis in the central nervous system. These include paraesthesias and paraplegia.

iii) Lung involvement in the form of haemorrhage, oedema,emphysema and atelactasis may be seen. These result in dyspnoea, nonproductive cough and chest pain.

iv) Skin manifestations include itching, patchy erythema,cyanosis and oedema.

v) Other organs like parenchymal cells of the liver and pancreas may show lipid vacuoles.

Amniotic Fluid Embolism

This is the most serious, unpredictable and unpreventible cause of maternal mortality. During labour and in the immediate postpartum period, the contents of amniotic fluid may enter the uterine veins and reach right side of the heart resulting in fatal complications. The amniotic fluid components which may be found in uterine veins, pulmonary artery and vessels of other organs are: epithelial squames,vernix caseosa, lanugo hair, bile from meconium, and mucus.The mechanism by which these amniotic fluid contents enter the maternal circulation is not clear. Possibly, they gain entry either through tears in the myometrium and endocervix, or the amniotic fluid is forced into uterine sinusoids by vigorous uterine contractions.

     The clinical syndrome of amniotic fluid embolism is characterised by the following features:

 •Sudden respiratory distress and dyspnoea

 •Deep cyanosis

 •Cardiovascular shock

 •Convulsions

 •Coma

•nexpected death

 The cause of death may not be obvious but can occur as a result of the following mechanisms:

i) Mechanical blockage of the pulmonary circulation in extensive embolism.

ii) Anaphylactoid reaction to amniotic fluid components.

iii) Disseminated intravascular coagulation (DIC) due to liberation of thromboplastin by amniotic fluid.

iv) Haemorrhagic manifestations due to thrombocytopenia and afibrinogenaemia.

Atheroembolism

Atheromatous plaques, especially from aorta, may get eroded to form atherosclerotic emboli which are then lodged in medium-sized and small arteries. These emboli consist of cholesterol crystals, hyaline debris and calcified material, and may evoke foreign body reaction at the site of lodgement.

Tumour Embolism

Malignant tumour cells invade the local blood vessels and may form tumour emboli to be lodged elsewhere, producing metastatic tumour deposits. Notable examples are clear cell carcinoma of kidney, carcinoma of the lung, malignant melanoma etc. 

Miscellaneous Emboli

Various other endogenous and exogenous substances may act as emboli. These are:

i) Fragments of tissue

ii) Placental fragments

iii) Red cell aggregates (sludging)

iv) Bacteria

v) Parasites

vi) Barium emboli following enema

vii) Foreign bodies e.g. needles, talc, sutures, bullets, catheters etc.