Platelets and coagulation basics for EMS

To keep from bleeding to death each time we scratch ourselves, we need to form clots or coagulate

Editor's Note: Be sure to check out Jim's article "Anticoagulation fundamentals for EMS" as a follow-up to this article.

To clot means to change from a liquid to a solid. So, to keep from bleeding to death each time we scratch ourselves, we need to form clots or coagulate.

The initial ingredient for a blood clot or thrombus is the platelet or thrombocyte, which is created and released by large bone marrow cells called megakaryocytes. Platelets float around in the blood looking for damaged tissue or damaged blood vessels. When they find damage they change shape and get sticky, becoming 'activated' platelets that stick to the damaged area and to each other to build a platelet plug.1

The platelet plug then attracts and activates more platelets and initiates the coagulation cascade following one or both pathways that leads to a common final pathway to produce thrombin which then splits fibrinogen into fibrin.1 (Fig 1)

Figure 1: Coagulation Cascade

Fibrin forms a web throughout the platelet plug to snag red blood cells to finish the clot. We circulate 150,000 to 450,000 platelets per microliter of blood (one thousand microliters = one milliliter).2 If you have too few platelets you can bleed too much, if you have too many platelets you can clot too much.

This life-saving process can become life-threatening when a thrombus forms in an artery, not because it is injured and at risk of losing life-sustaining blood, but because it has a narrowed and/or irregular inner surface caused by hardening of the arteries (arteriosclerosis) or an arterial wall dissection or the rupture of an arterial plaque.1 The location of the obstructed artery will determine whether the ischemia or infarct occurs in the heart muscle, brain or extremities.

An abnormal blood clot may also form in the venous system. Two causes are blunt trauma and stasis.3 Blunt trauma may injure deep veins in the extremities and cause irregularities of the inner surface of the vein, triggering platelet adhesion and coagulation. Inactivity can result in stasis or sluggish venous blood flow that can also stimulate clot formation. Prolonged bed rest or extended travel on planes, trains or automobiles are common examples of risky inactivity. Clots may also form in the superficial veins but it is the deep venous thrombi that can dislodge and travel to the lungs.

Abnormal blood clots may also form during atrial fibrillation when the atria cannot pump the blood into the ventricles and the blood pools in the atria. These clots may break off and travel to the lungs or the brain.

Most of the time our blood does not coagulate without just reason. This is due to adequate movement of blood and the action of antithrombin III, a molecule that floats around in the blood stream and destroys excess circulating coagulation factors including thrombin, thus preventing unwanted fibrin formation and clot.4

There are times when we want to prevent clots from forming in the first place and there are times when we want to stop an already forming clot from getting bigger. Anti-platelet medication is fundamental in the battle against abnormal thrombus formation. There are three classes of platelet inhibitors, each working through a different mechanism.

The first and best known is acetylsalicylic acid or ASA, better known as aspirin. When aspirin is ingested it blocks thromboxane from activating platelets and decreases their desire to stick together. Taking an aspirin a day is recommended for patients at risk for coronary artery disease or with a history of transient ischemic attacks (TIAs) or stroke.

Aspirin inhibits the development of the platelet plug that ends up as a clot. And, if you have already started a clot in a coronary artery, aspirin is effective in slowing thrombus growth and delaying total occlusion. Of course we would not use aspirin in the suspected stroke patient without a CAT scan since we don't know if we're dealing with a thrombotic stroke or a brain bleed.

Next is clopidogril (Plavix) which blocks platelet activation in a different way by blocking the platelet adenosine diphosphate receptor. Clopidogril may be used if the patient with suspected cardiac chest pain is allergic to aspirin. Clopidogril may also be prescribed with aspirin after a heart attack or after coronary artery bypass surgery. However, clopidogril should not be given to the patient who may require early coronary artery bypass surgery as it increases post-operative bleeding.5 Prasugrel is a newer adenosince diphosphate receptor blocker that you may see prescribed for your patient.6

Glycoprotein IIB IIIA inhibitors
And third are the only intravenously administered platelet inhibitors, the glycoprotein IIB IIIA inhibitors. There are three available: Abciximab (ReoPro), Eptifibatide (Integrilin) and Tirofiban (Aggrastat). These anti-platelet medications work by (you guessed it) inhibiting the glycoprotein IIB IIIA receptors to block platelet activation. They are used when a patient has a non-ST elevation myocardial infarct (NSTEMI) or unstable angina to discourage the clot from getting any bigger. Several years ago an oral form of glycoprotein IIB IIIA inhibitors were studied but were determined unsafe.

So we have three different medications that prevent platelet activation (stickiness) at three different sites on the platelet. And sometimes we use all three.

But wait, there's one more in the wings undergoing investigational studies. Atopaxar blocks platelet activation from thrombin at a separate receptor site. So there may be four types of platelet inhibitors for you to remember in the near future.7

In summary, the important field indication for anti-platelet medication is the early administration of aspirin for the patient with an acute coronary syndrome. Aspirin is clearly effective in stalling clot progression in the coronary arteries. In addition, knowledge of the other platelet inhibitors is important if your prehospital patient is taking them or if your interfacility transport patient is getting them.

1. Furie B, Furie BC. Mechanisms of Thrombus Formation. New Engl J Med 2008:359:938-949.
2. Lab Tests Online. Retrieved from
3. University of Maryland Medical College, Division of Nuclear Medicine. Pathophysiology and Diagnosis of Deep Venous Thrombosis. Semin Nucl Med 2001;31:90-101.
4. Butenas S, Mann KG. Blood Coagulation. Biochemistry(Moscow) 2002; 67:3-12.
5. Kang W, Theman TE, Reed JF, Stoltzfus J, Weger N. The Effect of Clopidogrel on Bleeding after Coronary Artery Bypass Surgery. J Surg Educ 2007;64:88-92.
6. Baker WL, White CM. Role of Prasugrel, a Novel P2Y(12) Receptor Antagonist, in the Management of Acute Coronary Syndromes. Am J Cardiovasc Drugs 2009;9:213-229.
7. O'Donoghue ML, Bhatt DL, Wiviott SD, Goodman SG, Fitzgerald DJ, Angiolillo DJ, Goto S, et al. Safety and Tolerability of Atopaxar in the Treatment of Patients With Acute Coronary Syndromes: The Lessons From Antagonizing the Cellular Effects of Thrombin-Acute Coronary Syndromes Trial. Circulation 2011;123:1843-1853.

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