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Wednesday, September 22, 2010

DVT, PE and pulmonary infarction

One of the biggest concerns among nurses and physicians is the prevention of deep vein thrombosis (DVT) and Pulmonary Embolism (PE). Collectively, these two diseases are referred to as venous thromboembolism (VTE).

This is important because DVTs may lead to PEs, and, according to Karen Ruffin, "The latest on preventing venous thromboembolism," Nursing Critical Care, March, 2009, research from autopsies has shown that 60% of patients who die in a hospital bed had an undiagnosed PE, and a diagnosis was missed in about 70% of those cases.

She writes that the CDC, federal Department of Health and Human services, FDA, and the surgeon general all note that the 100,000 people die each year from a PE, and this is among the most preventable -- which is why emphasis is on prevention, also known as prophylaxis.

Thus, with no prophylaxic care, and depending on the acuity of the diagnosis, Ruffin notes that any patient has a 10 to 48% chance of developing a DVT.'

The main reason that prevention is the main emphasis is because DVTs and PEs are so darn hard to diagnose because symptoms mimic so many other disease states.

What is a DVT?

Basically, a DVT is a blood clot that most commonly forms in the deep veins of the legs and thighs. When this clot breaks off, it can travel to the arteries of the lungs and cause a PE, which can be lethal.  According to a blood clot that forms in a blood vessel or the heart is called a thrombus

What is a PE?

According to Medscape Reference, pulmonary embolism was first described by Loschner in 1860.  Most PEs develop due to free floating thrombus.  How large the thrombus is will determine how far into the lungs it will travel before it becomes lodged, thus forming the PE. 

The PE will then occlude the blood vessel it is traveling in, and this will prevent blood flow from traveling to the portions of the lungs supplied by that blood vessel.  This results in ventilation/ perfusion (V/Q) mismatching, where that portion of the lung is ventilated but lacks circulation.

Medscapes describes taht mild PEs usually don't present with oxygenation problems. However, if oxygenation presents as a problem, clinical practitioners may be correct in assuming that the PE is massive and causing significant obstruction.  Your body will compensate for this type of V/Q mismatching with tachypnea (rapid breathing). 

If the PE is large this may result in increased pulmonary artery pressure which will result in right heart failure.  This is the result because the right heart will have to pump extra hard to push blood through that part of the lung. 

Generally speaking, as is noted in "Respiratory Disease: Principles of patient care," (Wilkins and Dexter, 1993, page 93), a small PE may be cause "little or no injury to the distal lung tissue, whereas large PEs may desrupt blood flow enough to destroy lung parenchyma" and thus cause an infarction (pulmonary infarction)of the lung. Although pulmonary infarction generally only occurs with COPD or those with left heart failure (CHF).

A PE will resolve itself in time as shortly after it's formed fibrinolysis occurs, and this is the "process of clot destruction in which blood-borne and vascular endothelial factors act to dissolve the clot," according to "Respiratory Disease." The authors further note that "clot resolution involves organization of the thrombus, attachment to the vascular wall, and return of blood flow."

Yet if the PE is too large, or compromise to risky or great, medical treatment will be necessary.

Normally conditions are ripe for smooth blood flow through vessels, although, according to experts, there are there main events that may causes DVTs:
1. Decreased flow of blood: Anything that may result in decreased mobility can cause blood to pool and clot off. Examples of this include:
  • Prolonged bed rest
  • Long flights or car rides
  • Paralysis
  • Atrial Fibrilation (blood pools in heart)
  • Venous obstruction secondary to obesity
  • Tumor
  • Anesthesia that can cause venous dilation and decreased blood flow which can result in venous stasis and clotting.
  • Age over 40
  • Mycardial Infarction (heart attack) causes decreased cardiac output
  • Stroke (less mobility)
2. Damage to blood vessel wall (inflammation): Damage to the endothelial lining of blood vessels can cause platelet activation.
Events that might cause cause inflammation or damage the vessel walls are:
  • Past VTE
  • Smoking
  • Atherosclerosis
  • Varicose veins
  • Trauma
  • Surgery
  • Venipuncture
  • Indwelling venous catheters
  • Vasculitis
  • Elevated blood glucose
3. Changes in blood composition: Any condition or state that decreases blood volume or increases blood viscocity (thickness).
Examples include:
  • Dehydration
  • Thrombocytosis
  • Oral contraceptives
  • Hormone replacement therapy
  • Cancer
  • Sepsis
  • Inflammatory bowel disease
  • Hematologic disorder
  • Blood glucose over 200 mg/dl
  • Blood transfusions
  • Obesity (greater than 30 BMI)
  • High estrogen states (pregnancy, post partum)
  • Advanced age (over 40)
  • Family history of VTE
  • Smoking
Of course you can see, as Ruffin notes, "Risk factors for VTE are cumulative -- the more the patient has, the greater his risk for developing VTE.
How do blood clots form?

While blood normally flows freely through vessels, there are times when your bodies defense mechanism need to shut off flow by causing a clot. The two mechanisms are the clotting mechanism (platelets) and the thrombin system.

According to, platelets are made in the bone marrow and float around in the blood waiting for a time when they are needed. When bleeding occurs, chemicals are released that change the composition of platelets, causing them to stick to the vessel wall. When enough platelets are present, a clot is formed to stop the bleeding. This is called a white clot. also notes that as far as the thrombin system is concerned, several proteins become activated when bleeding occurs, and this results in chemical reactions that produce a substance called fibrin that sticks to the walls of the exposed vessels forming what is called a red clot.
Conditions that can cause a DVT are:
  • Compression of veins (sitting or lying for a long time)
  • Trauma
  • Cancer
  • Infections
  • Stroke (increases inflammation)
  • Heart Failure (increases inflammation)
  • Nephrotic Syndrome (increases inflammation)
Things that increase risk for DVT include:
  • Surgery
  • Hospitalization
  • Immobilization
  • Smoking
  • Obesity
  • Over age 40
  • Certain drugs (like estrogen)
  • Certain contraceptives
  • Thrombophilia
  • Pregnancy
  • High glucose (increases inflammation)
Tests used to diagnose DVTs are:
  • D-Dimer
  • Doppler Ultrasound of effected vein
A key for hospitals is to have an order set to make sure no patient is overlooked. This way all patients at risk can obtain the appropriate prophylactic therapy. An order set for one hospital looks something like this:
  • PT, PTT on admission: These show the ability of the body to clot, and are usually rise as the blood becomes thinner and loses its ability to clot. This must be monitored because one of the preventative measures for clots is giving blood thinners. Both may be therapeutically high if patient is on a blood thiner. Critical would be a PT greater than 60, or a PTT greater than 40, and this would basically mean blood thinners should be scaled back.
  • CBC and CMP on admission: Complete Blood Count (CBC) provides the doctor with a baseline level of white blood cells and red blood cells so this can be monitored during the course of the stay. Complete Metabolic Panel (CMP) are lab tests that provide the doctor with kidney function, liver function, electrolyte and acid base balance. For a list of lab values, click here.
  • Leg elevated while in bed and pressure off heals: This keeps blood from pooling.
  • No IM injections: Prevents trauma to the vessels
  • Heparin IV protocol: This is a naturally occuring anti-coagulant to prevent the formation of clots. According to Wikepedia, it does not bust apart already formed clots, but "it allows the body's natural clot lysis mechanisms to work normally to break down clots that have formed."
  • lovenox: According the, this is "used to prevent and treat harmful clots." This lowers the activity of clotting factors in your blood to keep your blood flowing smoothly. It's called a blood thinner, but it's more correctly termed an anti-coagulant like Heparin.
  • Coumadin: An anticoagulant (blood thinner). It blocks the synthesis of certain clotting factors, and thus makes the blood thinner. It makes it so blood clots are unable to form.
  • Surfak 1 capsule PO BID (hold if having loose stools): Used to prevent constipation. Hard stools can actually scrape the skin and cause bleeding and infection.
  •, Suddenly increased and decreased blood flow
  • Compression stockings: They are stockings meant to prevent DVTs by preventing blood from pooling.
  • Intermittent Pneumatic Compression (see picture): According to, "a technique to prevent thrombosis in bedridden patients. It uses an inflatable device that squeezes the calf when it inflates, preventing pools of blood forming behind the valves in the veins, thus mimicking the effects of walking."
Regardless of prophylaxis, some patients will get DVTs which may progress at some point to PEs. Since it's hard to differenciate PEs from other disorders, it's important to think ahead.
Signs of PE are:
  • Tachypnea: increased rate and depth (70% of cases)
  • Rales (50% of cases)
  • ABG may be normal, but may appear as thought patient is hyperventilating (low CO2) yet the patient is not hyperventilating
  • Dyspnea (shortness of breath) at rest
  • Diaphoretic
  • Chest pain occurs suddenly and may worsen with deep breath, cough, movement
  • Cough began suddenly
  • May be bloody sputum
  • Tachycardia (30% of cases)
  • Anxiety
  • Bluish or dusky skin
  • D-Dimer is abnormal (70% false positive)
  • V/Q scan (best indicator 87%)
Again, the best treatment is preventative, although you'll want to support ventilation and provide anticoagulants as noted above.
An interesting thing I'd like to add to this post is that, according to "Respiratory Disease," a PE is also associated with localized bronchoconstriction. The author's note, "the release of chemical mediators such as serotonin, histamine, and prostaglandins from platelets causing the bronchoconstriction, although the exact etiology is unknown. This causes ventilation perfusion mismatching and hypoxemia to go along with the shunting (blood shunted away from area PE is located) that is already occurring as a result of the PE.
So one would wonder if this might be the reason some doctors choose to treat PEs with regularly scheduled bronchodilator breathing treatments such as Albuterol.
Another pathological condition "Respiratory Disease" notes is associated with a PE is a reduction in surfactant 24 hours after the PE is formed, "which leads to decreased pulmonary compliance (lungs become stiffer), atelectasis, further ventilation/ perfussion mismatching, and hypoxemia.
A PE can also cause hemodynamic compromise, yet this is usually reserved for those patients who are already hemodynamically compromised, had a PE in the past, or have COPD. These patients may develop pulmonary hypertension.
So, several studies have shown that as VTE prophylaxis therapies and VTE protocols have increased the number of patients diagnosed with DVTs and PEs has steadily declined.

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