Cardiovascular system pathology

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GLOSSARY

 

Anemia Refers to a decrease in the amount of oxygen-carrying hemoglobin in the peripheral blood. This reduction can be attributable to improper formation of new red blood cells, an increased rate of red blood cell destruction, or a loss of red blood cells as a result of prolonged bleeding. Regardless of the cause, a hemoglobin deficiency causes the anemic person to appear pale. This is best appreciated in the mucous membranes of the mouth and conjunctiva, and in the nail beds. A decrease in the oxygen-carrying hemoglobin impairs the delivery of an adequate oxygen supply to the cells and tissues, leading to fatigue and muscular weakness, and often to shortness of breath on exertion (dyspnea). To meet the body’s need for more oxygen, the respiratory rate increases and the heart beats more rapidly.

Iron deficiency anemia is the most common cause of anemia. It most frequently results from chronic blood loss, as from an ulcer, a malignant tumor, or excessive bleeding during menstruation (menorrhagia). Other causes of iron deficiency anemia include inadequate dietary intake of iron and increased iron loss caused by intestinal parasites. Iron deficiency anemia also may develop during pregnancy because the mother’s iron supply is depleted by red blood cell development in the fetus.

Hemolytic Anemia The underlying abnormality in hemolytic anemia is a shortened life span of the red blood cells with resulting hemolysis and the release of hemoglobin into the plasma. Most hemolytic anemias are caused by a hereditary defect that may produce abnormal red cells or abnormal hemoglobin. Less commonly, hemolytic anemia is acquired and related to circulating antibodies from autoimmune or allergic reactions (e.g., drugs such as sulfonamide) or the malarial parasite.

Spherocytosis, sickle cell anemia, and thalassemia are the major hereditary hemolytic anemias.

Hemolytic anemia of the newborn (erythroblastosis fetalis) can result when the mother is Rh negative and the fetus has Rh-positive blood inherited from the father. The mother thus becomes sensitized to the Rh factor of the fetus and makes antibodies against it. Any antibodies reaching the fetal blood through the placenta in future pregnancies cause hemolysis of the fetal red blood cells. The severity of the disease ranges from mild anemia with jaundice to fetal death.

The hemolytic anemias produce a variety of radiographic abnormalities. Although the radiographic findings are similar in the various types of hemolytic anemia, they tend to be most severe in thalassemia and least prominent in spherocytosis.

Bone infarcts commonly occur in infants and children. These most frequently involve the small bones of the hands and feet. In older children and adults, bone infarction may initially appear as an ill-defined lucent area that becomes irregularly calcified. Acute osteomyelitis, often caused by Salmonella infection, is a common complication in sickle cell disease.

The most common extraskeletal abnormality in the hemolytic anemias is cardiomegaly caused by severe anemia and increased cardiac output. Increased pulmonary blood flow produces engorgement of the pulmonary vessels, giving a hypervascular appearance to the lungs. Pulmonary infarction, pulmonary edema and congestive failure, and pneumonia are frequent complications.

The cause and type of hemolytic anemia must be determined to successfully begin treatment. For spherocytosis, a splenectomy is curative.

For sickle cell anemia, no cure currently exists. Therefore treatment consists of management and control of symptoms. The most invasive treatment, a bone marrow transplant, offers a possible cure.

If an Rh-negative mother delivers or aborts an Rh-positive infant, she is given a vaccine of Rh immunoglobulin within 24 hours to prevent the production of antibodies against the Rh factor. An Rh-positive baby born to an Rh-negative mother receives a blood transfusion within 24 hours after birth.

 

Angina Pectoralis (Angina) Temporary oxygen insufficiency causes angina pectoris. Attacks of angina pectoris are often related to a sudden increase in the demand of the myocardium for oxygen. When physical exertion, strong emotions, extreme temperatures, or eating increase the demand on the heart, a person with angina feels temporary pain, pressure, fullness, or squeezing in the center of the chest or in the neck, shoulder, jaw, upper arm, or upper back. This is angina, especially if the discomfort is relieved by removing the stressor and/or taking sublingual nitroglycerin. The discomfort of angina is temporary, meaning a few seconds or minutes, not lasting hours or all day. An episode of angina is not a heart attack. Having angina means you have an increased risk of having a heart attack. The longer the patient experiences chest pain from angina, the more the heart muscle is at risk of dying or malfunctioning.

Angina is classified as one of the following two types: stable angina and unstable angina.

Stable angina is the most common angina, and the type most people mean when they refer to angina. People with stable angina usually have angina symptoms on a regular basis. The episodes occur in a pattern and are predictable. For most people, angina symptoms occur after short bursts of exertion. Stable angina symptoms usually last less than five minutes. They are usually relieved by rest or medication, such as nitroglycerin under the tongue. Nitroglycerin is a sublingual medication that relieves angina symptoms by expanding blood vessels and decreasing the muscle’s need for oxygen. This allows more blood to flow through the coronary arteries. Nitroglycerin is taken only when the patient actually has symptoms or expects to have them. Slow – or long-acting nitroglycerin can be used as a preventative treatment for angina.

Unstable angina is less common. Angina symptoms are unpredictable and often occur at rest. This may indicate a worsening of stable angina, but sometimes the first time a person has angina it is already unstable. The symptoms are worse in unstable angina – the pains are more frequent, more severe, last longer, occur at rest, and are not relieved by nitroglycerin. Unstable angina is not the same as a heart attack, but it warrants an immediate visit to the healthcare provider or a hospital emergency department. The patient may need to be hospitalized to prevent a heart attack.

The most common cause for the heart not getting enough blood is coronary heart disease, also called coronary artery disease. Another cause of unstable angina is coronary artery spasm.

Risk factors for atherosclerosis and angina include the following. Some of these are reversible.

  • High blood pressure (hypertension)
  • High levels of cholesterol and other fats in the blood
  • Diabetes
  • Smoking
  • Male gender
  • Inactive (sedentary) lifestyle
  • Family history of coronary heart disease
  • Aging
  • Regular use of stimulants, especially nicotine, cocaine, or amphetamines, theophyllines, inhaled beta-agonists, caffeine, diet pills, and decongestants

Other symptoms may occur with an angina attack, as follows:

  • Shortness of breath
  • Lightheadedness
  • Fainting
  • Anxiety or nervousness
  • Sweating or cold, sweaty skin
  • Nausea
  • Rapid or irregular heart beat
  • Pallor (pale skin)
  • Feeling of impending doomArrhythmias (or dysrhythmias) Are problems that affect the electrical system of the heart muscle, producing abnormal heart rhythms. They can cause the heart to pump less effectively.Many arrhythmias have no known cause. However, a number of factors can contribute to arrhythmias. They include coronary artery disease, high blood pressure, diabetes, smoking, excessive use of alcohol or caffeine, drug abuse and stress. Certain substances, including some over-the-counter and prescription medications, dietary supplements and herbal remedies, caffeine, cocaine, amphetaminses and beta-blockers are known to cause arrhythmias in some people. Sometimes anti-arrhythmic medications prescribed to treat one type of arrhythmia can actually cause another type of arrhythmia.
  • The normal beating of the heart is controlled by electrical signals sent from a particular segment of heart muscle tissue called the sinus node. This natural pacemaker is located near the top of the right atrium. In a normal heartbeat, an electrical pulse travels down the muscle tissue, activating the ventricles a split-second after the atria. In arrhythmias, there’s a problem with this signal. There are many different kinds of arrhythmias, but those that affect the ventricles are generally more serious than arrhythmias of the atria.
  • An electrocardiogram (ECG) will be done. The patient may have a chest x-ray. This will show any fluid buildup in the lungs. It can also rule out some other causes of chest pain.

Symptoms include:

Some of the most common arrhythmias include:

  1. Premature beats – the most common arrhythmia, is basically harmless. Every once in a while, the heart’s electrical signals fire early. The heart beats twice quickly, then pauses and returns to normal. The premature beat may come from the ventricle or the atrium.
  1. Atrial fibrillation (AF) is where disordered signals are fired off in rapid succession, causing fibrillation, an uncoordinated quivering of the muscle. This has often been described as looking like a “bag of worms”. The atria stop pumping blood effectively, yet enough blood still reaches the ventricles to allow the heart to function. Atrial fibrillation is potentially dangerous, however, because blood can pool in the atrium predisposing to clot formation. If one of these travel to the brain, it causes a stroke. AF is the most common form of harmful arrhythmia, affecting almost 1% of the population. It is more common in elderly people.
  1. Ventricular fibrillation is the most dangerous arrhythmia. The ventricles twitch but don’t pump blood. If the twitching does not stop on its own or by a shock from a defibrillator, it is always fatal.
  1. Problems can occur with initiation of the electrical signal; either the sinus node fires abnormally or there is a competing impulse elsewhere in the heart. Problems with the conduction of the electrical impulse can also occur; connections from the atria to ventricles are hindered; this is often termed a heart block.
  2. Artificial pacemakers can take over the job of generating the electrical signals. Defibrillators are devices that restart arrested hearts with jolts of electricity to the chest. Defibrillators are effective at stopping ventricular fibrillation, but since ventricular fibrillation can be fatal in less than four minutes, they are most useful when used early. Most defibrillators are external devices, but now there are automatic implantable cardiovertors/defibrillators (AICD).


Atherosclerosis Occurs when arteries become marked by thickening, hardening, and loss of elasticity in the arterial wall. Atherosclerosis is one form of arteriosclerosis. The major cause of vascular disease of the extremities is atherosclerosis, in which fatty deposits called plaques develop in the intima and produce progressive narrowing and often complete occlusion of large and medium-size arteries. In the abdomen, the disease primarily involves the aorta and the common iliac arteries, often sparing the external iliac vessels. In the lower extremities, atherosclerotic narrowing most commonly affects the superficial femoral artery just above the knee. Plaque formation and luminal narrowing often involve the coronary and cerebral arteries, thus decreasing the blood flow to the heart muscle and the brain and leading to a myocardial infarction or stroke (cerebrovascular accident).

Atherosclerotic plaques often calcify and appear on plain radiographs as irregularly distributed densities along the course of an artery. Small vessel calcification, especially in the hands and feet, is often seen in patients with accelerated arteriosclerosis, especially those with diabetes mellitus.

Doppler ultrasound is an effective and preferred noninvasive technique for screening patients with clinically suspected peripheral arteriosclerotic disease. Evidence of arteriosclerosis includes diffuse vascular narrowing, irregularity of the lumen, and filling defects. In patients with severe stenosis or obstruction, arteriography demonstrates the degree and source of collateral circulation and the status of the vessels distal to an area of narrowing. Three dimensional MRA has become the method of choice and replaced catheter angiography.

Percutaneous transluminal angioplasty (PTA) using a balloon catheter is now a recognized procedure for the alleviation of symptoms of peripheral ischemia in patients with arteriosclerosis. In addition, a stent may be placed to aid in keeping the vessel open. PTA is of special value in patients who are extremely ill and in those who would not benefit from reconstructive arterial surgery.

Coarctation Refers to a narrowing, or constriction, of the aorta that most commonly occurs just beyond the branching of the blood vessels to the head and arms. The blood supply and the pressure to the upper extremities are higher than normal. As a result, there is decreased blood flow through the constricted area to the abdomen and legs. Classically the patient has normal blood pressure in the arms, but very low blood pressure in the legs.

The relative obstruction of aortic blood flow leads to the progressive development of collateral circulation—the enlargement of normally tiny vessels in an attempt to compensate for the inadequate blood supply to the lower portion of the body.

Coarctation of the aorta is often seen radiographically as rib notching (usually involving the posterior fourth to eighth ribs) resulting from pressure erosion by dilated and pulsating intercostal collateral vessels, which run along the inferior margins of these ribs. Notching of the posterior border of the sternum may be produced by dilation of mammary artery collaterals. Coarctation of the aorta often causes two bulges in the region of the aortic knob that produce a characteristic figure-3 sign on plain chest radiographs and a reverse figure-3 (or figure-E) impression on the barium-filled esophagus.

Using echocardiography to evaluate the aortic arch, the severity of the coarctation can be determined. Aortography can accurately localize the site of obstruction, determine the length of the coarctation, and identify any associated cardiac malformations. More recently, MRI has been used to demonstrate aortic narrowing and to evaluate the appearance of the aorta after corrective surgery.

Uncorrected aortic coarctation has a dismal prognosis, and surgical repair is required for patient survival. Currently, three surgical repairs are being used: (1) end-to-end anastomosis, (2) patch aortoplasty, and (3) left subclavian flap aortoplasty (surgical reformation of the aorta).

Coronary Artery Disease Narrowing of the coronary arteries causes oxygen deprivation of the myocardium and ischemic heart disease. In most patients, narrowing of the lumen of one or more of the coronary arteries is attributable to the deposition of fatty material on the inner arterial wall (atherosclerosis). Factors predisposing to the development of coronary artery disease include hypertension, obesity, smoking, a high-cholesterol diet, and lack of exercise.

Occlusion of a coronary artery deprives an area of myocardium of its blood supply and leads to myocardial infarction in the area of vascular distribution. The size of the coronary artery that is occluded determines the extent of heart muscle damage. The greater the area affected, the poorer the prognosis because of the increased loss of pumping function that may result in congestive heart failure (CHF). A favorable prognostic factor is the development of collateral circulation, through which blood from surrounding vessels is channeled into the damaged tissue. If the patient survives, the infarcted region heals with fibrosis. Long-term complications include the development of thrombi on the surface of the damaged area and the production of a local bulge (ventricular aneurysm) at the site of the weakness of the myocardial wall.

Radionuclide thallium perfusion scanning is the major noninvasive study for assessment of regional blood flow to the myocardium. Radionuclide scanning (single-photon emission computed tomography, or SPECT), is a new noninvasive technique for detecting, localizing, and classifying myocardial necrosis. On CT, areas of myocardial ischemia appear as regions of decreased attenuation because of the increased water content resulting from intramyocardial cellular edema. MRI also is of value in detecting early signs of muscular necrosis in myocardial infarction and may help determine whether the infarction is acute or remote.

Plain chest radiographs are usually normal or nonspecific in most patients with ischemic heart disease. Calcification of a coronary artery, although infrequently visualized on routine chest radiographs and usually requiring cardiac fluoroscopy, strongly suggests the presence of hemodynamically significant coronary artery disease. Plain chest radiographs are also entirely normal in many, if not most, patients after myocardial infarction. They are primarily of value in detecting evidence of pulmonary venous congestion in patients who develop CHF as a result of an inability of the remaining heart muscle to propel blood through the circulation adequately.

Coronary arteriography is generally considered the definitive test for determining the presence and assessing the severity of coronary artery disease. About 50% of coronary artery disease occurs in the left coronary artery. Arteriography has been the procedure of choice for demonstrating the patency and functional efficiency of aortocoronary bypass grafts.

Aortocoronary bypass grafting, usually using sections of saphenous vein, is an increasingly popular procedure in patients with ischemic heart disease. Patent functioning grafts demonstrate prompt clearing of contrast material and adequate filling of the grafted artery. Stenotic or malfunctioning grafts demonstrate areas of narrowing, filling defects, and slow flow with delayed washout of contrast material.

Percutaneous transluminal angioplasty (PTA) using a balloon catheter is now a recognized procedure for the treatment of patients with narrowing of one or more coronary arteries. As in other types of PTA, a catheter is placed under fluoroscopic guidance into the affected coronary artery, and an arteriogram is performed for localization. The angioplasty balloon is then positioned at the level of the stenosis and inflated. After dilation, coronary arteriography is repeated to illustrate the resulting appearance of the stenosis and to detect any complications of the procedure. Symptomatic improvement occurs in 50% to 70% of dilations. Other interventional procedures include endovascular stent, atherectomy, and laser-assisted angioplasty.


Embolus and Thrombus The blood-clotting mechanism is the major protective device of the body in response to the escape of blood from a vessel (hemorrhage). This same mechanism can occur in intact blood vessels, leading to the development of an intravascular clot called a thrombus. Three factors lead to the development of intravascular thrombosis. Clots tend to form where blood flow is slow and thus develop much more commonly in veins than in arteries. Thrombi occur especially in areas of stasis (slow circulation) in patients who are inactive or immobilized, as after abdominal surgery.

The second factor is a change in the wall of blood vessels, leading to thrombosis. Normally, the inner wall of a blood vessel has a very smooth lining (endothelium), and platelets cannot stick, or adhere, to it. However, when the endothelium is destroyed by injury or inflammation, platelets rapidly adhere to the rough spot, and a clot begins to form from the blood as it flows past. Arteriosclerosis is the major cause of endothelial irregularity and subsequent thrombosis. Nodules of vegetation on heart valves caused by rheumatic heart disease are also important predisposing factors for thrombus formation.

The third factor is a change in the blood itself, which leads to thrombosis. A low level of oxygen within the blood, as in some forms of heart disease, forces the body to compensate by increasing the number of red blood cells (polycythemia). This causes the blood to become more viscous and increases the risk of thrombosis. Changes in the clotting and fibrinolytic mechanisms also may increase the risk of thrombus formation.

Once a thrombus is formed, it may follow one of three courses. The thrombus may contract or become canalized so that blood can once again flow through the lumen. The thrombus may continually enlarge or become converted into fibrous tissue, resulting in permanent occlusion of the vessel. A potentially catastrophic event is the production of an embolus, which refers to part or all of a thrombus that becomes detached from the vessel wall and enters the bloodstream. Embolization is especially likely to occur if there is infected tissue around the thrombus or if there is a sudden movement caused by rough handling of the involved area. An embolism may lodge at any of several points, depending on the size of the vessels through which it travels. Since veins become larger as they approach the heart, an embolism arising from a thrombus in a leg vein flows easily to the heart and typically gets stuck in a pulmonary artery (pulmonary embolism). Fat emboli are the result of trauma, especially leg fractures, in which marrow fat enters torn peripheral veins and is trapped by the pulmonary circulation. An air embolism refers to bubbles of air introduced into a vein during surgery, trauma, or an improperly administered intravenous injection.

Regardless of its type or source, an embolism blocks the vascular lumen and cuts off the blood supply to the organ or parts supplied by that artery. The effect of an embolism depends on the size of the embolus and on the extent of collateral circulation, which can bring blood to an affected part by an alternate route, and the location of the embolus.

Acute embolic occlusion of an artery most commonly affects the lower extremities. Arteriography is the procedure of choice to confirm the clinical diagnosis and to demonstrate the extent of occlusion, the degree of collateral circulation, and the condition of the distal vessels. Embolic occlusion typically appears as an abrupt termination of the contrast column, along with a proximal curved margin reflecting the nonopaque embolus protruding into the contrast-filled lumen.

Anticoagulants, such as Heparin and Coumadin, are often used to prevent intravascular clotting. Heparin prevents platelets from sticking together and to the vessel wall, helping prevent thrombus formation. Coumadin acts by antagonizing the action of vitamin K, which is necessary for blood clotting. However, these medications also interfere with the person’s normal ability to stop bleeding and may lead to severe hemorrhage from relatively minor trauma or to potentially fatal bleeding in the brain and gastrointestinal tract. Although emergency surgery to remove the embolus (embolectomy) has been the traditional treatment for acute arterial occlusion, the intraarterial infusion of streptokinase by means of a catheter placed immediately proximal to the occlusion is becoming a more common alternative therapy, especially in patients who are poor surgical risks.

Hypertension High blood pressure is the leading cause of strokes and CHF. The blood pressure is a function of cardiac output (the amount of blood pumped per minute by the heart) and the total peripheral resistance, which reflects the condition of the walls of the blood vessels throughout the body. Although the peripheral resistance and cardiac output may fluctuate rapidly, depending on such factors as whether a person sits or stands and is quiet or excited, the systemic blood pressure remains remarkably constant in a healthy person.

A blood pressure reading consists of two parts. The systolic pressure is the highest pressure in the peripheral arteries that occurs when the left ventricle contracts. The diastolic pressure is the pressure in the peripheral arteries when the left ventricle is relaxing and filling with blood from the left atrium. High blood pressure is defined as elevation of the systolic pressure above 140 millimeters of mercury (mm Hg) and of the diastolic pressure above 90 mm Hg. In patients older than 40 years, the systolic pressure may be somewhat higher and still be considered within normal limits. As a rough rule of thumb, a person is allowed an additional 10 mm Hg in systolic pressure for each decade over 40 years of age.

Most patients with elevated blood pressure have essential, or idiopathic, hypertension. The benign form of essential hypertension is characterized by a gradual onset and a prolonged course, often of many years. In the much less common malignant form, the elevated blood pressure has an abrupt onset, runs a rapid course, and often leads to renal failure or cerebral hemorrhage.

About 6% of patients have secondary hypertension resulting from another disease. Although some patients in this group have adrenal abnormalities (e.g. Cushing’s syndrome) in which there is an abnormality of the regulation of salt and water content (and thus the blood volume), and others have an abnormality involving the secretion of a substance that increases vascular tone and peripheral arterial resistance, most have renal parenchymal or vascular disease as the underlying cause of hypertension.

Prolonged high blood pressure forces the heart to overwork, causing the left ventricle to enlarge and eventually fail. Since high blood pressure affects all arteries of the body, including the coronary and carotid vessels, this condition increases the risk of coronary occlusion, myocardial infarction, and carotid narrowing leading to a stroke.

Decreased function of the kidneys leads to the retention of water and salt, which increases the blood volume and elevates the blood pressure. Long-standing hypertension causes atherosclerosis of the renal artery, which reduces blood flow to the kidneys and causes further damage.

Medical treatment includes some combination of diuretics and beta, alpha, and calcium blockers to control blood pressure.

Patent Ductus Arteriosus (PDA) The third major type of left-to-right shunt. The ductus arteriosus is a vessel that extends from the bifurcation of the pulmonary artery to join the aorta just distal to the left subclavian artery. It serves to shunt blood from the pulmonary artery into the systemic circulation during intrauterine life. Persistence of the ductus arteriosus (a temporary vessel that is used during in utero life), which normally closes soon after birth, results in a left-to-right shunt. The flow of blood from the higher pressure aorta to the lower pressure pulmonary artery causes increased pulmonary blood flow, and an excess volume of blood is returned to the left atrium and left ventricle. Radiographically, there is enlargement of the left atrium, the left ventricle, and the central pulmonary arteries, along with a diffuse increase in pulmonary vascularity. The increased blood flow through the aorta proximal to the shunt produces a prominent aortic knob in contrast to the small- or normal-size aorta seen in atrial and ventricular septal defects.

This condition is more common in premature infants, occurring in approximately 80% of infants born before 28 weeks of gestation, especially in those who have respiratory distress syndrome.

Because the left ventricle contracts with more force than the right ventricle, the arterial blood within the aorta is shunted into the pulmonary trunk via the open ductus arteriosus instead of out into the systemic circulation. This increases the volume of blood propelled into the lungs, thus increasing pulmonary vascular congestion and the volume of blood returning to the left atrium. Infants with this condition generally have a heart murmur and display cyanotic features resulting from the shunting.

Echocardiography is the imaging method of choice for evaluating the severity of this anomaly and usually demonstrates a left atrial diameter larger than the aortic root. Chest radiographs of the infant demonstrate cardiomegaly with prominence of the left side of the heart and ascending aorta and increased pulmonary vascular congestion.

In premature infants, treatment includes fluid restriction and diuresis, the use of drugs, or surgical intervention. Surgery is used as a last resort in premature infants and generally is not performed until the infant is 1 to 2 years of age. In full-term infants, surgical ligation is necessary in cases of heart failure. In full-term infants without distress, elective surgery is generally performed between the ages of 6 months and 3 years to decrease the chance that the infant will develop infective endarteritis.


Pericardial Effusion Accumulation of fluid within the pericardial space surrounding the heart. The effusion may result from bacteria, viruses, or neoplastic involvement. In some cases, the cause cannot be determined (idiopathic pericardial effusion). Rapid accumulation of effusion interferes with cardiac function because of an increase in pericardial pressure. A slow accumulation of fluid allows the pericardium to expand, so that the pericardial pressure usually remains within the normal range.

Echocardiography is the most effective imaging technique for demonstrating pericardial effusions and has largely replaced other methods. Plain chest radiographs show a pericardial effusion as an enlargement of the cardiac silhouette when at least 200 ml of fluid is present before the effusion can be detected. Rapid enlargement of the cardiac silhouette, especially in the absence of pulmonary vascular engorgement indicating CHF, is highly suggestive of pericardial effusion. CT can detect loculated pericardial effusions as small as 50 ml, whereas MRI may be able to characterize the fluid as serous or hemorrhagic by characteristic changes in the signal intensity and identify an accumulation of as little as 30 ml.

The treatment depends on the cause. Pericardiocentesis is performed to remove fluid buildup, and insertion of a drain may be required. If the pericardial effusion recurs, a pericardiectomy may be necessary. An interventional technique includes administration of drugs into the pericardial sac.

Phlebitis Inflammation of a vein. Thrombophlebitis is the term used when a blood clot in the vein causes the inflammation. Thrombophlebitis usually occurs in leg veins, but it may occur in an arm. The thrombus (clot) in the vein causes pain and irritation and may block blood flow in the veins. Phlebitis can occur in both the surface (superficial) or deep veins.

Phlebitis may occur spontaneously or as a complication of a medical procedure. Local trauma and injury to a vein also increase the risk of forming a blood clot. Some risk factors for deep venous thrombophlebitis include the following:

  • Prolonged inactivity. Blood returns from the extremities to the heart by the contraction of muscles. Situations in which a person sits or reclines for long periods of time can allow blood to pool and clot. Examples include long trips in a car or airplane or bed rest after an operation or illness.
  • Sedentary lifestyle – inactivity with little or no exercise
  • Smoking cigarettes
  • Hormone replacement therapy or birth control pills
  • Pregnancy or Obesity
  • Certain medical conditions, such as cancer or blood disorders, that increase the clotting potential of the blood
  • Injury to the arms or legs
  • Varicose veins may be associated with superficial phlebitisThere is usually a slow onset of a tender red area along the superficial veins on the skin. A long, thin red area may be seen as the inflammation follows the path of a superficial vein. This area may feel hard, warm, and tender. The skin around the vein may be itchy and swollen. The area may begin to throb or burn. Symptoms may be worse when the leg is lowered, especially when first getting out of bed in the morning. A low-grade fever may occur. Sometimes phlebitis may occur at the site where a peripheral intravenous line was started. The surrounding area may be sore and tender along the vein. If an infection is present, symptoms may include redness, fever, pain, swelling, or breakdown of the skin.
  • Superficial phlebitis affects veins on the skin surface. The condition is rarely serious and, with proper care, usually resolves rapidly. Sometimes people with superficial phlebitis also get deep vein thrombophlebitis, so a medical evaluation is necessary.
  1. Deep vein thrombophlebitis affects the larger blood vessels deep in the legs. Blood clots (thrombi) can form, which may break off and travel to the lungs. This is a potentially life-threatening condition called pulmonary embolism.Deep vein thrombophlebitis requires immediate medical care. If the patient has any of these signs and symptoms, go to a hospital emergency department for evaluation:
  2. Deep vein thrombophlebitis can be similar in presentation to superficial phlebitis, but some people may have no symptoms. The classic signs and symptoms include redness, warmth, swelling, and pain in the leg. One may have pain and swelling throughout the entire limb. For example, one side of the lower leg may swell for no apparent reason.
  • High fever with any symptoms in an arm or leg
  • Lumps in a leg
  • Severe pain and swelling in an arm or leg
  • Chest pain and shortness of breath, which could be the first symptom that a blood clot has already traveled to the lung
  • Patients may be put on a anticoagulant such as Warfarin, Coumadin or Heparin to prevent the production of a thrombus.


Tetralogy of Fallot The most common cause of cyanotic congenital heart disease. It consists of four (thus “tetra”) abnormalities: (1) high ventricular septal defect, (2) pulmonary stenosis, (3) overriding of the aortic orifice above the ventricular defect, and (4) right ventricular hypertrophy. Pulmonary stenosis causes an elevation of pressure in the right ventricle and hypertrophy of that chamber. Because of the narrow opening of the pulmonary valve, an inadequate amount of blood reaches the lungs to be oxygenated. The ventricular septal defect and the overriding of the aorta produce right-to-left shunting of unoxygenated venous blood into the left ventricle and then into the systemic circulation, thus increasing the degree of cyanosis.

Enlargement of the right ventricle causes upward and lateral displacement of the apex of the heart. This results in the classic coeur en sabot appearance resembling the curved-toe portion of a wooden shoe. In about one fourth of patients with Tetralogy of Fallot, the aorta is on the right side.

Currently, echocardiography is the modality of choice to demonstrate the four abnormalities comprising Tetralogy of Fallot. However, pulmonary stenosis is better demonstrated on a cine MRI.

Without surgical repair, most patients die before reaching puberty. Although operative repair provides some chance of recovery, the outcome depends on the severity of the defect and other extenuating circumstances. In some cases, surgery provides only a palliative supportive role.

Transposition of Great Vessels Is an anomaly in which the aorta arises from the right ventricle instead of the left ventricle and the pulmonary trunk arises from the left ventricle instead of the right ventricle. This serious congenital defect does not allow the pulmonary and systemic subsystems to communicate and comprises over 5% of all cardiac anomalies. Deoxygenated blood returns to the right atrium, travels through the right ventricle, and is pumped through the aorta back into the systemic subsystem without becoming oxygenated. The oxygenated blood returns to the left atrium, travels through the left ventricle, and is pumped through the pulmonary trunk back to the lungs for gas exchange to occur.

A conventional chest radiograph demonstrates a narrow mediastinum because the vessels are superimposed and the main pulmonary trunk is not in the usual location. Pulmonary congestion is also visible in the lung fields. Obviously, this anomaly is incompatible with life. Because immediate recognition and treatment of this defect are imperative, echocardiography is performed to confirm the diagnosis.

Emergency cardiac catheterization and balloon septostomy must be performed to enlarge the opening between the atria to increase mixing of venous and arterial blood and to decompress the left atrium. Surgical correction of this anomaly is indicated within the first 10 days of life.

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