Embolism Classification Notes

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 common forms of emboli (90%) are thromboemboli i.e. originating from thrombi or their parts detached from the vessel wall.

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Emboli may be of various types:

• Depending upon the matter in the emboli:
  • Solid for example, Detached thrombi (thromboembolic), atheromatous material, tumour cell clumps, tissue fragments, parasites, bacterial clumps, and foreign bodies.
  • Liquid for example, Fat globules, amniotic fluid, bone marrow.
  • Gaseous for example, Air, other gases.
• Depending upon whether infected or not:
  • Bland, when sterile.
  • Septic, when infected.
• Depending upon the source of the emboli:
  • Cardiac emboli from left side of the heart for example, Emboli originating in the atrium and atrial appendages, infarct in the left ventricle, and vegetations of endocarditis.
  • Arterial emboli for example, In systemic arteries in the brain, spleen, kidney, intestine.
  • Venous emboli for example, In pulmonary arteries.
  • Lymphatic emboli in the draining area of a cancer contain tumour cells.

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

1. Paradoxical embolus: An embolus which is carried from the venous side of circulation to the arterial side or vice versa, is called a paradoxical or crossed embolus for example, Through arteriovenous communication such as in patent foramen ovale, septal defect of the heart, and arteriovenous shunts in the lungs.
2. Retrograde embolus: An embolus which travels against the flow of blood is called retrograde embolus. For example, metastatic deposits in the spine from carcinoma prostate in which case the spread occurs by retrograde embolism through intraspinal veins (which normally do not carry the blood from the prostate) which carry tumour emboli from large thoracic and abdominal veins because of increased pressure in body cavities such as during coughing or straining. Lists common types of embolism are described below

Thromboembolism:

A detached thrombus or part of a thrombus constitutes the most common type of embolism. These may arise in the arterial or venous circulation:

Arterial (systemic) thromboembolism:

Arterial emboli may be derived from the following sources:

• Causes within the heart (80-85%): These are mural thrombi in the left atrium or left ventricle, vegetations on the mitral or aortic valves, prosthetic heart valves and cardiomyopathy.
• Causes within the arteries: These include emboli developing in relation to atherosclerotic plaques, aortic aneurysms, pulmonary veins and paradoxical arterial emboli from the systemic venous circulation.

The effects of arterial emboli depend upon their size, site of lodgement, and adequacy of collateral circulation.

Important types of embolism:

If the vascular occlusion occurs, the following ill-effects may result:

• Infarction of the organ or its affected part e.g. ischaemic necrosis in the lower limbs (70- 75%), spleen, kidneys, brain, intestine.
• Gangrene following infarction in the lower limbs if the collateral circulation is inadequate.
• Arteritis and mycotic aneurysm formation from bacterial endocarditis.
• Myocardial infarction may occur following coronary embolism.
• Sudden death may result from coronary embolism or embolism in the middle cerebral artery.

Venous Thromboembolism:

Venous emboli may arise from the following sources:

• Deep vein thrombosis (DVT) of the lower legs, is the most common cause of venous thrombi.
• Thrombi in the pelvic veins.
• Thrombi in the veins of the upper limbs.
• Thrombosis in cavernous sinus of the brain.
• Thrombi in the right side of heart.

The most significant effect of venous embolism is obstruction of pulmonary arterial circulation leading to pulmonary embolism described below.

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.

In contrast, pulmonary thrombosis is uncommon and may occur in pulmonary atherosclerosis and pulmonary hypertension. Differentiation of pulmonary thromboembolism from pulmonary thrombosis is tabulated in the given table.

Pulmonary Thromboembolism Etiology:

Pulmonary emboli are more common in hospitalised or bedridden patients, though they can occur in ambulatory patients as well.

The Pulmonary Thromboembolism causes are as follows:

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

Contrasting features of pulmonary thrombosis and pulmonary thromboembolism:

Pulmonary Thromboembolism Pathogenesis:

The risk factors for pulmonary thromboembolism are stasis of venous blood and hypercoagulable states. Detachment of thrombi from any of the above-mentioned sites produces thrombo-emboli that flow 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 the 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.

Natural history of pulmonary embolism may have following consequences:

• 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.
• 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.
• 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.
• 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.
• 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.
• Pulmonary hypertension, chronic cor pulmonale and pulmonary arteriosclerosis: These are the sequelae of multiple small thromboemboli undergoing organisation rather than resolution.

Pulmonary Thromboembolism Systemic Embolism:

This is the type of arterial embolism that originates commonly from thrombi in the diseased heart, especially in the left ventricle. These heart diseases include myocardial infarction, cardiomyopathy, RHD, congenital heart disease, infective endocarditis, and prosthetic cardiac valves.

The emboli are arterial and invariably cause infarction at the sites of lodgement.

These sites, in descending order of frequency, are:

• 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 and Bone Marrow 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 Causes of fat embolism may be traumatic and non-traumatic:

Traumatic causes:

• Trauma to bones is the most common cause of fat embolism for example 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, for example, Laceration of adipose tissue and in puerperium due to injury to pelvic fatty tissue.

Pulmonary Thromboembolism 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
• Hyperlipidaemia
• Cardiopulmonary bypass surgery

Pulmonary Thromboembolism Pathogenesis:

Pathogenesis of fat embolism is explained by the following mechanisms which may be acting singly or in combination:

• Mechanical obstruction theory: Mobilisation of fluid fat may occur following trauma to the bone or soft tissues. 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 the lungs and enter into the systemic circulation to lodge in other organs.
• Biochemical injury theory: This theory is based on proinflammatory changes. Following trauma, fat globules break down into free fatty acids which enter into venous circulation.

This causes toxin injury to the endothelium, particularly of the pulmonary capillary bed, which is followed by platelet activation and infiltration by neutrophils. This sequence causes release of free radicals, proteases and prostaglandins that damages the pulmonary capillary bed.

These biochemical events result in chemical pneumonitis, pulmonary oedema and acute respiratory distress syndrome (ARDS).

Pulmonary Thromboembolism 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. Fat embolism syndrome is an uncommon life-threatening clinical syndrome occurring in orthopaedic trauma cases manifesting within 24-72 hours and is characterised by classic clinical triad of hypoxaemia, neurologic manifestations and petechial rash.

1. Pulmonary Fat Embolism:

In patients dying after fractures of bones, the 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.

• Microscopically: The lungs show hyperaemia, oedema, petechial haemorrhages and changes of adult respiratory distress syndrome (ARDS). Pulmonary infarction is usually not a feature of fat embolism because of the small size of globules.

In routine stains, the fat globules in the pulmonary arteries, capillaries and alveolar spaces appear as vacuoles. Frozen section is essential for confirmation of globules by fat stains such as Sudan dyes (Sudan black, Sudan III and IV), oil red O and osmic acid.

2. 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.

• Brain:  The pathologic findings in the brain are petechial haemorrhages on the leptomeninges and minute haemorrhages in the parenchyma.
• Microscopically: Microinfarcts of the brain, oedema and haemorrhages are seen. The CNS manifestations include delirium, convulsions, stupor, coma and sudden death.
• Kidney:  Renal fat embolism present in the glomerular capillaries, may cause decreased glomerular filtration. Other effects include tubular damage and renal insufficiency.
• Other organs:  Besides the brain and kidneys, other findings in systemic fat embolism are petechiae in the skin, conjunctivae, serosal surfaces, fat globules in the urine and sputum.

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:

• Operations on the 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.
• 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.
• Intravenous infusion of blood and fluid: Air embolism may occur during intravenous blood or fluid infusions if only positive pressure is employed.
• Angiography: During venous angiographic procedures, air may be entrapped into a large vein causing air embolism.

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

• 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.
• Rapidity of entry of a smaller volume of air is important determinant of a fatal outcome.
• 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 (for example in, Upright position) and reach the brain.
• General condition of the patient for example, 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 underwater 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:

• 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.
• Paradoxical air embolism: This may occur due to the passage of venous air emboli to the arterial side of circulation through a patent foramen ovale or via pulmonary arteriovenous shunts.
• Arteriography: During arteriographic procedures, air embolism may occur.

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

• Marble skin due to blockage of cutaneous vessels.
• Air bubbles in the retinal vessels seen ophthalmoscopically.
• Pallor of the tongue due to occlusion of a branch of the lingual artery.
• 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.

Decompression Sickness 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 O If the vascular occlusion occurs, the following ill-effects may result:, CO If the vascular occlusion occurs, the following ill-effects may result:) 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 an affinity for nitrogen. These bubbles may coalesce together to form large emboli.

In aeroembolism occurring 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
• The 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:
  • ‘The bends’, as the patient doubles up in bed due to acute pain in joints, ligaments and tendons.
  • ‘The chokes’ occur due to the accumulation of bubbles in the lungs, resulting in acute respiratory distress.
  • Cerebral effects may manifest in the form of vertigo, coma, and sometimes death.

Chronic form: This 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:

• Avascular necrosis of bones for example, Head of femur, tibia, humerus.
• Neurological symptoms may occur due to ischaemic necrosis in the central nervous system.
• These include paraesthesia and paraplegia.
• Lung involvement in the form of haemorrhage, oedema, emphysema and atelectasis may be seen. These result in dyspnoea, nonproductive cough and chest pain.
• Skin manifestations include itching, patchy erythema, cyanosis and oedema.
• Other organs like parenchymal cells of the liver and pancreas may show lipid vacuoles.

Amniotic Fluid Embolism:

This is the most serious, unpredictable and unpreventable cause of maternal mortality. During labour and in the immediate postpartum period, the contents of amniotic fluid may enter the uterine veins and reach the right side of the heart resulting in fatal complications.

The amniotic fluid components which may be found in uterine veins, pulmonary arteries and vessels of other organs are epithelial squames, vernix caseosa, lanugo hair, bile from meconium, and mucus.

These amniotic fluid contents gain entry either through tears in the myometrium and endocervix, or due to vigorous uterine contractions, the amniotic fluid is forced into uterine sinusoids.

Morphologic Features:

Notable changes are seen in the lungs such as haemorrhages, congestion, oedema and changes of ARDS, and dilatation of right side of the heart. These changes are associated with identifiable amniotic fluid contents within the pulmonary microcirculation.

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

• Sudden respiratory distress and dyspnoea
• Deep cyanosis
• Cardiovascular shock
• Convulsions
• Coma
• Unexpected death

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

• Mechanical blockage of the pulmonary circulation in extensive embolism.
• Anaphylactoid reaction to amniotic fluid components.
• Disseminated intravascular coagulation (DIC) due to liberation of thromboplastin by amniotic fluid.
• 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.

Morphologic Features:

Pathologic changes and their effects in atheroembolism are as under:

• Ischaemia, atrophy and necrosis of tissue distal to the occluded vessel.
• Infarcts in the organs affected such as the kidneys, spleen, brain and heart.
• Gangrene in the lower limbs.
• Hypertension, if widespread renal vascular lesions are present.

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 the kidney, carcinoma of the lung, malignant melanoma etc.

Miscellaneous Emboli:

Various other endogenous and exogenous substances may act as emboli. These may include the  following:

• Fragments of tissue
• Placental fragments
• Red cell aggregates (sludging)
• Bacteria
• Parasites
• Barium emboli following enema
• Foreign bodies, for example, Needles, Talc, Sutures, Bullets, Catheters etc.

Embolism:

• Embolism is the process of partial or complete obstruction of some part of the cardiovascular system by any mass carried in the circulation.
• Most common forms of emboli (90%) are thromboemboli originating from thrombi or their detached parts within the heart, arteries or veins.
• Pulmonary thromboembolism is common and fatal form of venous thromboembolism, most often originating from deep vein thrombosis of the lower legs.
• Most common form of arterial embolism arises in the thrombi from the left ventricle due to heart diseases.
• Fat embolism may be traumatic (most often from surgical or accidental trauma to the bones) or from non-traumatic causes.
• Gas embolism may be air embolism (arterial or venous) or decompression sickness (in divers or in high altitude).
• Amniotic fluid embolism is the most serious, unpredictable and unpreventable cause of maternal mortality occurring during labour and in the immediate postpartum period.
• Other forms of embolism include atheroembolism, tumour embolism etc.