Pulmonary Embolism

Pulmonary Embolism

Write a brief on embolism.
Answer:

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 a fat-tissue embolism.

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 orthopedic surgical procedures, etc.
• Trauma to soft tissue, e.g. laceration of adipose tissue and in puerperium due to injury to pelvic fatty tissue.;

Pulmonary embolism symptoms

Non-traumatic Causes

• Extensive burns
• Diabetes mellitus
• Fatt liver
• Pancreatitis
• Sickle cell anemia
• Decompression sickness
• Inflammation of bones and soft tissues
• Extrinsic fat or oils introduced into the body
• Hyperlipidemia
• Cardiopulmonary bypass surgery.

Embolism Pathogenesis

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

• Mechanical theory: Mobilization 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.
• Emulsion instability theory: This theory explains the pathogenesis of fat embolism in non-traumatic cases. According to this theory, fat emboli are formed by aggregation of plasma lipids (chylomicrons and fatty acids) due to disturbance in the natural emulsification of fat.
• Intravascular coagulation theory: In stress, the release of some factors activates disseminated intravascular coagulation (DIC) and aggregation of fat emboli.
• Toxic injury theory: According to this theory, the small blood vessels of the lungs are chemically injured by high plasma levels of free fatty acid, resulting in increased vascular permeability and consequent pulmonary edema.

CTPA in PE diagnosis

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 are air embolism and decompression sickness.

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
• Obstetrical Operations and trauma during childbirth
• Intravenous infusion of blood and fluid
• Angiography

Arterial Air Embolism

Entry of air into a pulmonary vein or its tributaries may occur in the following conditions:

• Cardiothoracic surgery and trauma
• Paradoxical air embolism
• Arteriography

Decompression Sickness

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

Pathogenesis

Decompression sickness is produced when the individual decompresses suddenly, either from high atmospheric pressure to a normal level or from normal pressure to low atmospheric pressure. In divers, workers in caissons (diving-bells), of shore drilling and tunnels, who descend to high atmospheric pressure, increased amount of atmospheric gases are dissolved in the 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 that have an 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 unpressurized 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.

Clinical Effects

The clinical effects are acute or chronic.

Acute Form

It occurs due to acute obstruction of small blood vessels in the vicinity of joints and skeletal muscles. The condition is clinically characterized 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

The chronic form is due to foci of ischemic necrosis throughout the body, especially the skeletal system. Ischemic necrosis may be due to embolism per se, but other factors such as platelet activation, intravascular coagulation, and hypoxia might contribute.

The features of the chronic form are as under:

• Avascalar necrosis of bones, For Example. head of the femur, tibia, and humerus.
• Neurological symptoms may occur due to ischemic necrosis in the central nervous system. These include paresthesia and paraplegia.
• Lung involvement in the form of hemorrhage, edema, emphysema, and atelectasis may be seen. These result in dyspnea, nonproductive cough, and chest pain.
• Skin manifestations include itching, patchy erythema, cyanosis, and edema.
• 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 labor 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.
• Its onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock which is followed by seizures and coma.
• 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.
• It has a mortality rate of 20 to 40% of cases.

Embolism Atheroembolism

Atheromatous plaques, especially from the 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 reactions at the site of lodgement.

Tumor Embolism

Malignant tumor cells invade the local blood vessels and may form tumor emboli to be lodged elsewhere, producing metastatic tumor deposits. 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
• Foreignbodies, For Example. needles, talc, sutures, bullets, catheters, etc