Running head: CLOTTING 1

Clotting: A Concept for Nursing Practice

Michelle A. Stimson

Ferris State University

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Abstract

Clotting involves a wide range of physiological processes making the concept of clotting a

complex and multifaceted phenomenon. Normal physiological clotting is a life saving

mechanism intended to stop bleeding. However, clotting can be harmful. Conversely, when

clotting is needed but is not sufficient, bleeding can result. The concept of clotting encompasses

both ends of the hemostasis continuum; unintended clot formation and the inability to clot. The

author provides an overview of the physical assessment findings, pharmacological treatments,

and physiological processes related to the concept of clotting. Clotting-specific patient exemplars

are explored.
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Clotting: A Concept for Nursing Practice

Clotting involves a wide range of physiological processes making the concept of clotting

a complex and multifaceted phenomenon. When physiologically balanced, clotting saves lives.

However, death can ensue when too much or too little clotting exists. The clotting continuum

includes several harmful deviations; unintended clot formation at one end of the spectrum,

bleeding at the other (Wilson, 2017). The professional nurse plays an important role in managing

the care of individuals on the clotting continuum (Wilson, 2017). The purpose of this paper is to

provide an overview of the exam findings, pharmacological treatments, and physiological

processes related to the concept of clotting. Clotting-specific patient exemplars are explored.

Pathophysiology

Cells need a constant flow of oxygen-rich blood to survive and remain healthy (McCance

& Huether, 2014). Generally, diminished blood flow results in cellular injury and/or death

(McCance & Huether, 2014). Lack of supply (bleeding) and obstruction in flow (clot) brings

harm to cells. If blood flow is reestablished quickly, cells may be able to adapt and reverse the

injury (McCance & Huether, 2014). Normal physiological clotting is a life saving mechanism

intended to stop bleeding; however, unintended clotting can be harmful (Wilson, 2017).

Conversely, when clotting is needed but is not sufficient, bleeding ensues (Wilson, 2017).

Normal Clotting

When veins and arteries become injured, the clotting process is activated in an attempt to

stop bleeding. Two mechanisms are put into motion; platelet aggregation and the release of

plasma clotting factors (Wilson, 2017). Vasoconstriction at the site of the injury also occurs

(Wilson, 2017). All three entities work together to seal the cut or break in the vessel wall leading

to hemostasis (National Heart, Lung, and Blood Institute [NHLBI], 2011).

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Platelets become activated by cell mediators at the site of injury (Dressler, 2009). Once

activated, platelets develop spine-like exteriors allowing for fibrinogen receptor exposure

(Dressler, 2009). At the site of injury, platelets link to tissue collagen by bonding to von

Willebrand factor (Dressler, 2009). Tissue collagen is found on the surface of damaged blood

vessels (Burchum & Rosenthal, 2016). After collagen linking occurs, platelets release adenosine

diphosphate (ADP) and thromboxane A2 to attract more platelets (Dressler, 2009). Platelet

aggregation ensues. Eventually, a platelet plug forms after activated glycoprotein (GP) IIb–IIIa

receptors bond to available fibrinogen molecules (Dressler, 2009). Platelet plugs generate

quickly; in approximately three to seven minutes (Wilson, 2017). Platelet plug formation via

platelet aggregation is referred to as primary hemostasis and creates the base for further clot

formation (Burchum & Rosenthal, 2016; Dressler, 2009).

Secondary hemostasis begins when multiple plasma clotting factors are released through

the activation of the clotting cascade (Dressler, 2009). The clotting cascade has two pathways;

extrinsic and intrinsic (Dressler, 2009; Wilson, 2017). Both lead to fibrin formation (Burchum &

Rosenthal, 2016). The extrinsic pathway is activated by tissue factor (TF) and materializes after

external blood vessel injury (Dressler, 2009). The extrinsic pathway produces thrombin, a

powerful procoagulant, which is formed through the interaction of many numbered clotting

factors including factor VII (Overbey, Jones, & Robinson, 2014). Eventually the interactions

lead to fibrin formation after factor X is converted into factor Xa (Dressler, 2009; Overbey,

Jones, & Robinson, 2014). The intrinsic pathway is activated during periods of blood stasis, in

the presence of inflammatory mediators, or when damage to the surface of the vessel wall

(internal lining) occurs; the intrinsic pathway is not activated by external tissue trauma (Dressler,

2009). Pooled blood allows for procoagulant factors to be in close proximity of one another
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leading to factor XII activation (Dressler, 2009). Factor XII converts into factor XIIa eventually

leading to the creation of factor Xa (Overbey, Jones, & Robinson, 2014).

Regardless of which pathway is activated, both pathways meet at the same endpoint; the

creation of factor Xa (Wilson, 2017). The pathways then merge into one common pathway

resulting in clot formation (Wilson, 2017). At the end of the process, factor Xa catalyzes the

formation of thrombin, which in turn, leads to the formation of fibrin (Burchum & Rosenthal,

2016). Clot stabilization results achieving the end goal of secondary hemostasis (Wilson, 2017).

Clots are meant to be temporary; the body has the natural ability to break down clots

(Dressler, 2009). This process is called fibrinolysis. Fibrinolysis begins when natural tissue

plasminogen activator (tPA) changes plasminogen into plasmin (Dressler, 2009). Plasmin

dissolves clots allowing blood flow to be reestablished (Dressler, 2009). The body can be aided

in fibrinolysis by pharmacological agents (Burchum & Rosenthal, 2016).

Altered Clotting

Normal clotting physiology becomes impaired during times of inflammation, altered

pathology, and clotting factor absence (Wilson, 2017). For example, sepsis, an inflammatory

process, activates the clotting cascade by releasing endotoxins; clots emerge (Dressler, 2009).

Another example includes clot activating factors expelled by tumor cells as a result of cancer;

cancer magnifies clotting risk (Dressler, 2009). Notably, the body contains natural anticoagulants

including protein C, tissue factor pathway inhibitor, and antithrombin (Dressler, 2009). These

anticoagulants help maintain blood fluidity (Dressler, 2009). When altered, as in the case of

endothelial inflammation and injury, the anticoagulants are halted expediting clot formation

(Dressler, 2009). Clots generated during sepsis, in the presence of cancer, and endothelial injury
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can lead to tissue harm and/or death (Dressler, 2009). Genetic alterations, comorbid conditions,

and medications also lead to unintended clot formation (Dressler, 2009).

Conversely, when necessary clotting factors are missing in the blood, prolonged bleeding

results. Patients with hemophilia, for example, have a deficiency in clotting factors VIII

(hemophilia A) and IX (hemophilia B) (Burchum & Rosenthal, 2016). Without clotting factors

VIII and IX, factor X cannot be converted into factor Xa hindering fibrin synthesis (Burchum &

Rosenthal, 2016). Clot formation is delayed resulting in prolonged bleeding (Burchum &

Rosenthal, 2016). Platelets play an important role in clot formation. Some medical conditions

lead to thrombocytopenia (decreased platelets). Cancer and chemotherapy suppress

hematopoietic growth factors resulting in decreased platelet production (Burchum & Rosenthal,

2016). Thrombocytopenia can lead to excessive bleeding especially in cases of tissue injury.

Assessment

Alterations in clotting are identified during the physical assessment. Depending on

severity, findings may be subtle or drastic (Wilson, 2017). Because clotting affects every area of

the body, changes may occur locally or systemically (Jarvis, 2016). Normal physiological

clotting includes the following exam findings: brisk capillary refill, adequate pulse strength,

warm, dry skin, and age appropriate blood pressure and pulse readings (Jarvis, 2016; Wilson,

2017). Needed information can be gained from subjective and diagnostic data, therefore, the

physical assessment also includes the health history and diagnostic findings (Jarvis, 2016).

Exam Findings

When assessing an individual for clots (thrombus), many factors need to be considered.

Clots can form in both arteries and veins; likewise, clots can form anywhere in the body (Wilson,

2017). Most often, venous clots manifest in the lower extremities (Wilson, 2017). Typical signs
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and symptoms include pain, swelling, and redness (Jarvis, 2016). If dislodged (embolus), a

venous clot will most likely lodge in the pulmonary artery (Wilson, 2017). A pulmonary embolus

(PE) is a life-threatening medical condition (Wilson, 2017). Symptoms of a PE include chest

pain, dyspnea, cyanosis, and hemoptysis (Wilson, 2017).

Arterial clots can manifest anywhere in the body. When an arterial clot occludes blood

flow, signs of decreased perfusion will surface (Wilson, 2017). In the case of a peripheral clot,

pulses in the extremity may be absent; pallor and severe pain will develop (Jarvis, 2016). If an

arterial clot travels through the carotid circulation, blood flow to the brain will become impaired.

Individuals can lose motor function, develop slurred speech, have vision changes, become dizzy,

and develop a facial droop (Jarvis, 2016). In the coronary circulation, arterial clots cause chest

pain, cardiac arrhythmias, and alterations in blood pressure and pulse readings (Jarvis, 2016).

Symptoms of bleeding can manifest locally, systemically, or both. Systemic bleeding

causes widespread pallor, weak or thready pulses, dizziness, tachycardia, and low blood pressure

readings (Jarvis, 2016; Wilson, 2017). The skin may have large amounts of bruising or petechiae

(Wilson, 2017). Bloody stools, bleeding gums, and hematuria may also develop (Wilson, 2017).

Local symptoms include swelling, pain, and warmth (Wilson, 2017). Frank blood from previous

wounds or puncture sites may erupt. Bleeding in the brain reveals identical symptoms of clot-

related tissue damage, however, pupils may change in shape and headaches are common (Jarvis,

2016).

Health History

Certain medical conditions, lifestyle choices, and medications exacerbate alterations in

clotting (Wilson, 2017). Genetic predisposition, age, surgical history, and special considerations

such as pregnancy also need to be considered (Wilson, 2017).

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Medications can drastically alter an individual's ability to maintain hemostasis.

Anticoagulants such as aspirin and warfarin increase bleeding risk; conversely, oral

contraceptives increase clotting risk (Burchum & Rosenthal, 2016). Over-the-counter

medications and herbal supplements also need explored. Niacin, omega-3 fatty acids, ginko

biloba, ginseng, black cohosh, and turmeric have the ability to affect clotting (Wilson, 2017).

Prolonged periods of sitting or bed rest increase clotting risk due to venous stasis

(Wilson, 2017). Atrial fibrillation potentiates clot formation when blood pools in the top

chambers of the heart (Wilson, 2017). Nicotine smoking leads to endothelial damage and later to

atherosclerosis enhancing clotting potential (Wilson, 2017). Hypertension, obesity, and

pregnancy also increase the risk for clots (Jarvis, 2016; Wilson, 2017).

When assessing for bleeding, information regarding excessive or frequent nose bleeds,

blood in stool, and bleeding gums should be pursued (Wilson, 2017). Reports of prolonged

bleeding after tissue trauma or excessive fatigue are significant findings (Wilson, 2017). Medical

conditions that enhance bleeding risk include hemophilia and leukemia (Wilson, 2017).

Diagnostic Tests

Several laboratory tests can provide information regarding clotting or bleeding risk.

Specific laboratory tests include prothrombin time (PT), international normalized ratio (INR),

partial thromboplastin time (PTT), fibrinogen, platelet count, and D-dimer (Wilson, 2017). The

PT and INR speak to the extrinsic pathway of the clotting cascade; values will increase when

extrinsic pathway clotting factors are decreased (Wilson, 2017). Increased values equate to

prolonged clotting time and both are used to monitor warfarin therapy (Wilson, 2017). The PTT

measures the clotting time of the intrinsic pathway (Wilson, 2017). A prolonged PTT (greater

than 70 seconds) means clotting is delayed and is used to guide heparin therapy (Wilson, 2017).
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Platelet counts measure the number of platelets in the blood. Low platelet counts (less

than 150,000) increase bleeding risk whereas high platelet counts (greater than 400,000) increase

clotting risk (Wilson, 2017). D-dimers tell about thrombin and plasmin activity (Wilson, 2017).

An elevated D-dimer makes note of fibrin degradation; this occurs during clot breakdown

(Wilson, 2017). Values also elevate during disseminated intravascular coagulation (DIC) and

after surgery (Wilson, 2017). Measuring hemoglobin, hematocrit, and red blood cell counts

provide valuable information regarding anemia and blood loss (Wilson, 2017). Radiological tests

include ultrasound and arteriograms; both diagnose clot size and location (Wilson, 2017).

Pharmacology

Often times, alterations in clotting can be addressed by pharmacological means.

Anticoagulant, antiplatelet, and thrombolytic medications prevent, suppress, and degrade clots;

conversely, procoagulants intensify clotting potential (Burchum & Rosenthal, 2016).

Anticoagulant, antiplatelet, and thrombolytic medications interfere with normal

hemostasis. Both anticoagulants and antiplatelets suppress clot formation (Burchum &

Rosenthal, 2016). Anticoagulants either activate antithrombin, impair vitamin K synthesis, or

directly inhibit thrombin and factor Xa formation (Burchum & Rosenthal, 2016). Regardless of

the mechanism, anticoagulants inhibit fibrin formation and are used to prevent venous thrombi

(Burchum & Rosenthal, 2016). Examples of anticoagulant medications include heparin, warfarin,

dabigatran, and rivaroxaban (Burchum & Rosenthal, 2016).

Heparin products enhance antithrombin activity, which in turn, subdues the formation of

thrombin and factor Xa (Burchum & Rosenthal, 2016). Low-molecular-weight heparin primarily

inactivates factor Xa; unfractionated heparin inactivates both thrombin and factor Xa equally

(Burchum & Rosenthal, 2016). Heparin peaks quickly and works well in medical emergencies
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(Burchum & Rosenthal, 2016). Warfarin, a vitamin K antagonist, suppresses the synthesis of

prothrombin and factors VII, IX, X (Burchum & Rosenthal, 2016). Warfarin is slow to peak,

therefore, best suited for long-term therapy (Burchum & Rosenthal, 2016). Warfarin is used to

prevent venous and pulmonary thrombi, prosthetic heart valve-related clots, and clots caused by

atrial fibrillation (Burchum & Rosenthal, 2016).

Direct thrombin inhibitors directly inhibit thrombin by binding to free and bound

thrombin throughout the body (Burchum & Rosenthal, 2016). One example is dabigatran

[Pradaxa]. Alternately, direct factor Xa inhibitors bind to factor Xa resulting in blocked thrombin

production (Burchum & Rosenthal, 2016). Benefits of both classifications include quick onset,

minimal food and drug interactions, and no required laboratory monitoring (Burchum &

Rosenthal, 2016). Dabigatran is used to prevent strokes and nonvalvular atrial fibrillation-related

clots (Burchum & Rosenthal, 2016). Rivaroxaban [Xarelto], a direct factor Xa inhibitor, prevents

deep vein thrombi, pulmonary emboli, and stroke (Burchum & Rosenthal, 2016).

Antiplatelet medications such as aspirin, clopidogrel [Plavix], and Tirofiban [Aggrastat]

suppress platelet aggregation (Burchum & Rosenthal, 2016). Antiplatelet therapy targets arterial

thrombi (Burchum & Rosenthal, 2016). Aspirin suppresses platelet aggregation by inhibiting

cyclooxygenase; cyclooxygenase synthesizes TXA2 which is necessary for platelet activation

(Burchum & Rosenthal, 2016). The effects of aspirin are irreversible; once inhibited, platelets

can no longer produce cyclooxygenase (Burchum & Rosenthal, 2016). Clopidogrel blocks

platelet P2Y12 ADP receptor sites limiting ADP-stimulated platelet aggregation; the effects are

similar to aspirin and are also irreversible (Burchum & Rosenthal, 2016). Clopidogrel reduces

incidence of stroke, heart attack, and coronary stent occlusion (Burchum & Rosenthal, 2016).

Tirofiban, a GP IIb/IIIa receptor antagonist, blocks platelet GP IIb/IIIa receptors, the final step in
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platelet aggregation (Burchum & Rosenthal, 2016). These medications typically work in

conjunction with aspirin and low-dose heparin (Burchum & Rosenthal, 2016). Treatment is

costly, therefore, GP IIb/IIIa receptor antagonists are typically reserved for medical emergencies

such as pre and post coronary artery revascularization (Burchum & Rosenthal, 2016).

Thrombolytic medications remove clots instead of prevent them. Alteplase, identical to

human tPA, works by binding with plasminogen which produces plasmin; plasmin digests clots

(Burchum & Rosenthal, 2016). Thrombolytics carry substantial hemorrhage risk, therefore,

thrombolytics are reserved for medical emergencies specifically ischemic stroke and acute

coronary syndrome (ACS) (Burchum & Rosenthal, 2016).

Anticogulants, antiplatelets, and thrombolytics significantly increase bleeding risk

(Burchum & Rosenthal, 2016). All three classifications demand caution and careful monitoring

of mental status, blood pressure and pulse readings, and medication-specific laboratory results

(Burchum & Rosenthal, 2016). Blood in stool and urine may develop (Burchum & Rosenthal,

2016). Warfarin and heparin are reversible, however, dabigatran, rivaroxaban, and aspirin are not

(Burchum & Rosenthal, 2016). Several of the aforementioned medications need withdrawn prior

to an invasive procedure; several should not be administered together (Burchum & Rosenthal,

2016). Multiple food and drug interactions are plausible. Withholding clot suppressing

medication in the case of significant thrombocytopenia or uncontrolled bleeding is paramount to

patient safety (Burchum & Rosenthal, 2016).

Procoagulants intensify clotting potential. Examples include clotting factor concentrates,

antifibrinolytic agents, and thrombopoietic growth factors (Burchum & Rosenthal, 2016).

Procoagulant medications include recombinant factor VIII, desmopressin, tranexamic acid, and

oprelvekin [Neumega] (Burchum & Rosenthal, 2016). Factor concentrates either derive from
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human plasma or recombinant DNA; recombinant DNA derivatives are deemed safer because no

contact with animal proteins occurs (Burchum & Rosenthal, 2016). Factor VIII concentrates

replace factor VIII; with hemophilia A routine infusions are common (Burchum & Rosenthal,

2016). Desmopressin, an antidiuretic hormone analog, assists the vascular endothelium in

releasing stored factor VIII (Burchum & Rosenthal, 2016). If bleeding is expected, prophylactic

desmopressin can be administered prior to an invasive procedure (Burchum & Rosenthal, 2016).

Because desmopressin does not release factor IX, it is ineffective for hemophilia B (Burchum &

Rosenthal, 2016). Antifibrinolytic agents prevent plasmin synthesis inhibiting fibrin breakdown

(Burchum & Rosenthal, 2016). Tranexamic acid, an antifibrinolytic agent, is used to stop

recurrent bleeding episodes (Burchum & Rosenthal, 2016). Oprelvekin, a thrombopoietic growth

factor, increases platelet production by stimulating hematopoietic stem cell growth and

maturation (Burchum & Rosenthal, 2016). Chemotherapy-related myelosuppression decreases

platelet production (Burchum & Rosenthal, 2016).

Many procoagulants carry the risk of severe allergic reaction (Burchum & Rosenthal,

2016). Symptoms include hives, fever, and wheezing (Burchum & Rosenthal, 2016). Plasma

derived factors carry the risk of viral contamination including human immunodeficiency virus

(HIV) and hepatitis B (Burchum & Rosenthal, 2016). Regular treatments require permanent

intravenous catheters which increase thrombus and infection risk (Burchum & Rosenthal, 2016).

Both desmopressin and oprelvekin cause fluid retention and need discontinued in the presence of

heart failure or fluid overload (Burchum & Rosenthal, 2016).

Patient Exemplars

As previously discussed, the clotting continuum includes normal and abnormal

pathology. Abnormal pathology manifests as unintended clots and/or bleeding. Examples of

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clotting-specific disease processes include venous thromboembolism, arterial embolism, DIC,

hemophilia, and heparin-induced thrombocytopenia (HIT) (Wilson, 2017). Severity depends on

the location and vastness of the problem; in many cases, outcomes can be tragic.

Venous Thromboembolism

Venous thrombi form in veins. Deep vein thrombosis (DVT) and PE are two common

examples. Venous thrombi occur in conjunction with surgical procedures, bed confinement, oral

contraception, pregnancy, cancer, and inherited clotting disorders (Centers for Disease Control

and Prevention [CDC], 2016b). Clots are common around valve cusps and bifurcations in the

deep veins of the lower extremities (Dressler, 2009). When venous thrombi travel to other parts

of the body, a PE can result. A PE is a clot embedded in the pulmonary circulation; PEs can

result in death (Wilson, 2017). Up to 600,000 DVTs occur every year; reoccurrence is common

(CDC, 2016b). Prevention includes early and frequent ambulation, compression stockings,

anticoagulants, and maintaining a healthy weight (CDC, 2016b). Ultrasound, computed

tomography (CT), and D-dimer testing help diagnose venous thrombi; treatment includes short

and long-term anticoagulant therapy and thrombolytics in severe cases (CDC, 2016b).

Arterial Embolism

Arterial emboli form in arteries. Common locations include the brain, heart, and

extremities (Wilson, 2017). Arterial emboli become medical emergencies if blood flow is

obstructed (Wilson, 2017). Severe tissue impairment or death may occur; the magnitude depends

on the extent, duration, and location of the clot (Wilson, 2017). When lodged in cranial

circulation, an arterial embolus becomes an ischemic stroke (National Stroke Association [NSA],

2016). Approximately 80% of strokes are ischemic with African Americans having twice the risk

of stroke than other racial groups (NSA, 2016). Likewise, an arterial clot embedded in the
CLOTTING 14

coronary circulation becomes a myocardial infarction (MI) (Dressler, 2009). Prevention includes

adequate blood pressure management, tight glycemic control, abstaining from smoking,

maintaining a healthy weight, favorable cholesterol levels, and atrial fibrillation-related

anticoagulant therapy (NSA, 2016). An electrocardiogram, CT, ultrasound, or arteriogram may

be used to diagnose an arterial clot (NSA, 2016). Treatment includes aspirin, anticoagulants,

thrombolytics, clot removal, and stenting (Dressler, 2009). Timely treatment is necessary for

optimal outcomes (NSA, 2016).

Disseminated Intravascular Coagulation

Disseminated intravascular coagulation, a unique pathology, includes both clotting and

bleeding (Wilson, 2017). Caused by septicemia, severe trauma, and malignant cancer, DIC

generates numerous, widespread thrombi (Wilson, 2017). Inflammatory processes fuel DIC

making DIC difficult to control and reverse; DIC is exacerbated as hypoxia, shock, and acidosis

worsen (Dressler, 2009). The prolific amount of thrombi consume circulating platelets and

clotting factors; internal and external bleeding results (Wilson, 2017). Damage occurs to the

microcirculation resulting in multisystem organ failure (NHLBI, 2011). Treatment includes

managing the underlying cause, anticoagulants, and blood transfusions aimed at replacing

platelets and clotting factors (NHLBI, 2011). Complete blood counts, PT/INR, and D-dimer

testing help diagnose DIC (Wilson, 2017). A true medical emergency, DIC carries very high

mortality rates and requires aggressive and timely treatment (Dressler, 2009).

Hemophilia

Hemophilia, an inherited bleeding disorder, potentiates spontaneous bleeding (Wilson,

2017). Individuals with hemophilia have low levels of factor VIII (hemophilia A) or factor IX

(hemophilia B) (CDC, 2016a). Even though females may carry the gene, hemophilia is a
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recessive disorder and is typically expressed in males (Wilson, 2017). Hemophilia severity is

determined by the amount of clotting factors available in the blood; low levels increase bleeding

risk and complication severity (CDC, 2016a). Bleeding in joints is common (CDC, 2016b).

Trauma and/or surgery can lead to profuse bleeding and treatment includes clotting factor

replacement (Burchum & Rosenthal, 2016). Hemophilia is diagnosed via genetic testing and

clotting factor assays (CDC, 2016a).

Heparin-Induced Thrombocytopenia

Heparin exposure can lead to HIT, an immune-mediated disorder characterized by

thrombocytopenia and thrombotic events (Sparks, 2009). Antibodies form against heparin–

platelet protein complexes resulting in platelet aggregation, aggressive clot formation, and severe

platelet depletion (Burchum & Rosenthal, 2016). Pulmonary emboli, MI, and stroke may occur;

limb amputations may be necessary (Burchum & Rosenthal, 2016). All heparin-related

treatments need replaced with non-heparin products (Burchum & Rosenthal, 2016). Diagnosis is

confirmed through platelet counts (50% decrease from baseline) and heparin antibody assays

(Sparks, 2009). A potentially fatal disorder, mortality rates reach as high as 30% (Sparks, 2009).

Special Considerations

Special considerations such as diet, positioning, and cultural aspects of care need

observed. Certain foods can hinder pharmacological treatments. For example, individuals

undergoing warfarin therapy should avoid foods rich in vitamin K (Wilson, 2017). Patient

education is paramount. In the case of positioning, DVT affected extremities need elevated; for

arterial clots, the limb should stay dependant (Wilson, 2017). After a stroke, the head of the bed

needs positioned at 30 degrees or greater to prevent cerebral edema (Wilson, 2017). Jehovah

Witnesses may refuse needed blood transfusions or plasma-derived products based on religious
CLOTTING 16

beliefs; seeking alternatives may be necessary (JW.org, 2016). Heparin may contain porcine or

bovine products (Eriksson, Burcharth, & Rosenberg, 2013). Hindus and Muslims do not accept

porcine-based drugs (Eriksson, Burcharth & Rosenberg, 2013). Lastly, a diagnosis of HIT

requires permanent abstinence from all heparin products (Sparks, 2009).

Conclusion

The concept of clotting involves a wide range of physiological processes. When

functioning as intended, clotting saves lives. Alterations in clotting include excessive clotting

and inadequate clotting. Both lead to tissue damage and/or death. The professional nurse plays an

important role in managing the care of individuals on the clotting continuum. Performing

clotting-specific assessments, understanding pharmacological treatments, recognizing individuals

at risk, and intervening appropriately will generate the best possible outcomes for individuals

with clotting abnormalities.

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