Embolus

 EMBOLUS

PKGhatak, MD

The word embolus is derived from Greek: en + ballein = in + to throw. In short, it means a wedge or plug. Obstruction of blood vessels by a wedge or plug may result from any of these - a piece of a detached blood clot, a fat globule, air bubble, a broken piece of the indwelling venous catheter, amniotic fluid and IV drug addicts injected contaminated drugs, and in rare instances broken piece of bones and metal fragments during orthopedic surgery.

What happens with the venous embolus/ emboli.

Venous blood returns to the right side of the heart then goes to the lungs. All formed substances having a size larger than an RBC (red blood cell) are caught in the pulmonary capillaries. The living tissues beyond the site of obstruction suffer severe oxygen lack, undergo various degrees of structural damage or die (infarction).

In patients, with an open foramen ovale or right atrial septal defect, the emboli enter the left atrium, pushed to the left ventricle, from there into the general circulation. Clots can block arteries of the brain, kidneys, GI tract, etc. and result in substantial damage to the organs.

Fat embolism.

Bone marrow contains a large amount of fat and may release fat globules in the blood. Fractured bone or orthopedic surgery fat molecules are released in the circulation. The fat globules, like venous blood clots, get tangled up in the lung capillaries or go via an open foramen ovale and enter the arterial side bypassing the lungs. In addition, the fat molecules can flatten out and may enter the arterial side of the circulation by one of these mechanisms. 1. The cells of the alveoli are disrupted and allow fat to enter pulmonary veins. 2. Fat molecules thinned out and assume elongated narrow shapes and go past the capillary bed to the venous side and then to the left heart and travel everywhere with the arterial blood,

Air embolism.

In an underwater dive, in a submarine or scuba diving, the nitrogen of air dissolves in large volume in the blood due to higher pressure – the deeper the depth the higher the pressure. In a rapid ascend, the nitrogen emerges from blood as gas and forms bubbles in the arteries and veins. Air bubbles obstruct blood circulation and deprive organs of oxygen. In the lungs, the rapid release of dissolved nitrogen can produce enough pressure to rupture the lungs and the lungs may collapse.

In high altitude flying, if the cabin pressure is lost suddenly, then air bubbles form in the blood vessels.

The intravenous line attached to the Porto Cath in the central vein may get disconnected and air can enter. In some instances, the air from the IV tubing is not purged completely; a small amount of air can enter, in most such cases the air will diffuse out via the alveoli and expired breaths but in other instances may produce serious consequences.

Chance of air embolism is a concern in every case involving direct access to central veins - like coronary bypass operation, heart-lung machine, extracorporeal membrane oxygenation, etc.

In childbirth, the freshly separated placental site may allow air to enter the veins of the mother.

Amniotic Fluid Embolism.

In late pregnancy, the placental membrane along and veins can tear open allow amniotic fluid to enter the mother's circulation. Amniotic fluid carries cellular debris, hair and urine and meconium of the fetus. In spontaneous miscarriage/abortion/ Caesarean section, amniotic fluid embolism may happen.

Foreign Body Embolism.

IV drug users inject crushed tablets, some of the ingredients of tablets are kaolin-a kind of earth, gum and inert substances. All these are pushed into the vein.

Many of these chemicals produce inflammation and granuloma in the lungs. Repeated exposures produce pulmonary fibrosis. Broken needles, at times, find their way into the lungs causing hemorrhage, pneumothorax and hemothorax.

Venous Thrombus and Pulmonary Embolism.

Blood contains several clotting factors and also clot preventing factors. Blood circulates constantly, that movement prevents blood from clotting. Just like concrete carrying tucks constantly rotates the cement drum to prevent the concrete to solidify.

Tissue clot promoting factors.

Deep vein thrombosis is seen frequently in these conditions - post surgical patients, multiple fractures, pregnancy and childbirth, cancer chemotherapy. These conditions produce tissue damage and release the Tissue clotting factor.

Stasis of blood in veins.

A prolonged period of sitting, as happens on a long flight on airlines, and in certain jobs, like watching monitors screens constantly, promotes venous clots in the leg and pelvic veins. When blood is stagnant, the tissues use up oxygen and produce anorexic injury to the endothelium of veins and release clot promoting factors. In congestive heart failure, return of venous blood from below the diaphragm is delayed due to higher pressure in the right atrium. Immobilized fracture of the leg is another risk factor, so also varicose veins.

Antithrombotic protein Thrombomodulin and Endothelial Protein Receptors are downregulated in infections, injuries and hypoxia. The same mechanism also up-regulates the Leukocyte adhesion molecule - P-selectin.

Blood viscosity.

In blood diseases, like polycythemia vera and leukemia, the blood cell volume is elevated. In multiple myeloma the globulins levels are high. These conditions result in high viscosity which slows circulation and promotes blood clots.

Congenital absence/ deficiency of anticoagulants.

Protein C in association with V Leiden is a potent anticoagulant. About 5% of the Caucasian population of North America has a congenital deficiency of V Leiden. Several other anticoagulation factors like Protein S, protein C, antithrombin, and prothrombin are also inherited. Congenital deficiency of vitamin K dependent factors occurs due to mutation of the VKORC-1 gene.

Acquired clotting factor abnormalities.

Anti-phospholipid syndrome, Nephrotic syndrome, Lupus antibodies to antiphospholipid and in homocysteinemia, Paroxysmal Nocturnal hemoglobinuria promote blood clots. Carcinoma produces various coagulation factor abnormalities. Central venous indwelling catheters - the tip of the catheter often form clots and a clot can propagate. Estrogen therapy - increases liver production of several clotting factors.

Infected Blood clots.

In infections of the heart valves and endothelium (inner layer of the heart) the bacteria produce colonies known as vegetation. These vegetations are fragile and break loose. Arterial blood carries these infected vegetations to the brain, kidney, liver, spleen and other organs.

Detached arterial plaques.

In coronary angiogram/angioplasty procedures, the catheter tips may knock off arterial plaques. These plaques are made up of calcium-cholesterol-cellular derbies and these travel downstream to the pelvis, legs, kidney, etc. Carotid artery plaques may go directly to the brain and cause strokes. Similarly, during surgical repairs of Atrial aneurysms emboli can easily happen.

Consequences of Pulmonary Embolism.

Pulmonary embolism (PE) from breaks away clots from the deep veins is the most common cause of pulmonary embolism. About 400,000 cases are recorded each year in the USA and 40,000 patients die from PE.

The symptoms, diagnosis and treatment.

It is easier to discuss this aspect as 1. Massive pulmonary emboli, 2. Recurrent small multiple pulmonary emboli and, 3. Mixed type.

1. Massive pulmonary emboli.

 It is a life ending event if immediate treatment is not available. Sudden acute onset of shortness of breath, chest pain followed by loss of consciousness and ventricular arrhythmia result from lack of oxygen to vital organs. A chest x-ray may show a lack of the usual darkness of blood in the lung and is called an oligemic lung. EKG shows sinus tachycardia in excess of 120/ min, right axis, RBBB, right ventricular strain and ventricular premature beats or tachycardia. Marked hypoxemia, cyanosis, shock, feeble /absent pulse at the wrist, altered consciousness, and poor renal output are usual findings. Angio CT/ angiogram shows clots in the pulmonary trunk/ main branch and sudden tapering of the caliber of the pulmonary artery.

Treatment is very urgent. A pulmonary artery catheter is inserted and advanced to the site of obstruction. Thrombolytic agents are infused. Otherwise, open chest operation and removal of clots have to be undertaken. A six month direct oral anticoagulant or vitamin K dependent \ clotting factors (factor VII, IX, X, protein C, protein S, and Prothrombin inhibition) coumadin are recommended. Underlying clotting factor modification where possible should be done.

2. Chronic small repeated Pulmonary emboli.

The initial episodes of pulmonary emboli may be misdiagnosed as mild asthma attacks, undetermined chest pain, and anxiety attacks. Shortness of breath with mild physical activities develops. Evidence of Pulmonary hypertension develops. Long term anticoagulation is essential to prevent future emboli. In recurrent PE an Inferior vena cava filter is inserted that block the upward movements of clots.

3. Mixed types are the combination of these classes. Thrombolytic therapy and long term direct acting anti-coagulation is appropriate therapy.

Fat embolism.

Fat embolism is underreported. The risk factors of fat embolism are - all major multiple bone fractures, crush injuries, bone marrow transplantation, orthopedic surgery of major joints, IV hyperalimentations, liposuction, acute and chronic pancreatitis, prolonged CPR, splitting sternum in open heart surgery, major burn victims, prolonged use of corticosteroid, fatty liver, sickle cell anemia, thalassemia, etc. When a small amount of fat globules enters the circulation, it may not produce any adverse effect on the body. When intermediary pins were used in hip fractures fat embolism was common.

More than occasionally the fat embolism is misdiagnosed as something else and only by autopsy examination the fat embolism is established. 15 % of all autopsies show fat embolism. Fat is a neurotoxin. Cerebral fat embolism produces significant CNS symptoms. Skin petechiae are very characteristic of fat emboli of the skin. A fluoroscopic eye examination is one direct evidence of fay embolism.

 A chest x-ray may show only nonspecific vascular congestion. MRI of the brain is most helpful for cerebral fat emboli. Centrum putamen and subarachnoid show edema due to the toxic effect of fat.

Treatment of fat embolism has gone through many therapeutic trials, but none are specific. General vascular support and adequate oxygenation of vital organs decide the treatment outcomes. Mortality is about 10%.

Air Embolism.

Air embolism produces two distinct groups of medical problems.

One that produces pain in joints is known as caisson disease or bends. The other is major symptoms due to blockage of blood flow to vital organs. Occasionally air can block blood entry to the heart chambers. These incidences are not common but time is short for the reversal of the block. Less severe but significant symptoms are due to cerebral anoxia.

Treatment consists of giving oxygen immediately and then oxygen delivered in Hyperbaric chambers. This aspect is discussed in an earlier blog.

Amniotic Fluid Embolism.

Amniotic fluid embolism is a near fatal complication during childbirth and in the 48 hours postpartum period. Sudden cardiovascular collapse, air hunger, loss of consciousness and disseminated intramuscular coagulation are usual presentations. Acute pulmonary hypertension from arterial obstruction is complicated by the release of cytokines and complements that produce multisystem failure. Complement C3 and C4 are low in serum, and zinc coproporphyrin levels are elevated. There is no specific therapy for amniotic fluid embolism. Extracorporeal membrane oxygenation and correction of acidosis and other metabolic derailments are therapeutically maintained as well as possible under the circumstance. The pregnancy is terminated by C-section and the prognosis of the newborn is good. Air embolism happens in about 4 per 100,000 childbirths. The mortality is 60 to 80%.

 Embolisms are of several kinds and emboli can originate from various sources. Deep vein thrombosis resulting in pulmonary embolism is common among various groups and in a selected population, like nursing homes, cancer hospitals and ICU units, the incidence is high.

The current nursing practice of early mobilization following surgery, trauma, and childbirth has substantially lowered the incidence of PE. The direct acting anticoagulant improved patients' compliance with therapy.

  

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