Venous and Arterial Thromboembolic Disorders

What is the difference between a thrombus and an embolus?

A thrombus is a blood clot that forms and stays within a vessel, possibly partially or completely obstructing flow; an embolus is a clot or other material that breaks free, travels through circulation, and lodges in another vessel, impairing perfusion

What is venous thromboembolism (VTE), and what are its two main forms?

A condition involving abnormal clot formation in the venous system; it includes deep vein thrombosis (DVT), where a thrombus forms in a deep vein, and pulmonary embolism (PE), where an embolus travels to and obstructs a pulmonary artery

What is Virchow's triad, and what three factors does it include?

The three major mechanisms contributing to venous thrombosis: venous stasis (slowed blood flow from immobility, bed rest, or prolonged travel), endothelial injury (vessel wall damage from surgery, trauma, or catheters), and hypercoagulability (increased tendency to clot from inherited thrombophilia, cancer, or pregnancy)

What is thrombus formation made of, and what does it do to circulation?

Platelets, fibrin, and red blood cells combine to form a clot, which obstructs circulation and impairs blood flow

How can a DVT lead to a pulmonary embolism?

A DVT can dislodge, travel through the venous system to the lungs, and cause a potentially life threatening arterial blockage in the pulmonary arteries, called a PE

What is deep vein thrombosis (DVT)?

Thrombus formation in a deep vein, most commonly in the lower extremities

What is the pathophysiology of DVT once a clot forms?

The thrombus obstructs venous flow, increasing venous pressure; impaired venous return causes swelling, pain, and inflammation; the thrombus may also dislodge and cause a pulmonary embolism

What are two major complications of DVT?

Pulmonary embolism from embolization to the pulmonary circulation, and post thrombotic syndrome from venous valve damage causing chronic edema, pain, and skin changes or ulcers

What are the risk factors for DVT?

Immobility (bed rest, hospitalization, prolonged travel), surgery or trauma (especially orthopedic procedures), hypercoagulable conditions (cancer, pregnancy, estrogen therapy, inherited thrombophilia), and other risks such as previous DVT/PE or obesity

What are the clinical manifestations of DVT?

Unilateral leg swelling, pain or tenderness commonly in the calf, warmth/erythema/discoloration, though it may also be asymptomatic

What are the nursing priorities when DVT is suspected?

Assess and compare both extremities, do not massage the affected leg, and notify the provider to anticipate a diagnostic ultrasound

What is the Wells score used for in DVT diagnosis?

It estimates the likelihood of DVT based on symptoms and risk factors, guiding further laboratory testing and imaging

What is the role of D dimer testing in diagnosing DVT?

D dimer measures fibrin degradation products; a negative D dimer helps exclude DVT in appropriately selected low risk patients, while an elevated D dimer is nonspecific and does not confirm DVT

What is the first line imaging test for DVT, and what does it show?

Venous duplex ultrasound; a thrombus is suspected when the vein does not compress normally

When are CT or MR venography used in DVT diagnosis?

In selected cases when ultrasound is inconclusive or pelvic DVT is suspected

What is the first line pharmacologic treatment for most confirmed DVTs, and what is its purpose?

Anticoagulation; it prevents clot extension and new clot formation, but it does not remove the existing clot

Which anticoagulants are commonly used for DVT, and which are generally preferred?

DOACs such as apixaban and rivaroxaban are preferred for many eligible patients; UFH/LMWH are alternatives based on clinical circumstances, and warfarin is used in selected patients and requires INR monitoring

What is the typical duration of anticoagulation for DVT?

At least 3 months, longer if the DVT is recurrent or the patient has a high bleeding risk

What nonpharmacologic measures are used in DVT management?

Early ambulation once anticoagulated and clinically stable, avoiding massage of the affected limb, and urgent vascular evaluation with possible catheter directed treatment or clot removal for limb threatening DVT

What should be monitored for safety during DVT treatment?

Bleeding (bruising, hematuria, GI bleeding, severe headache), aPTT or anti Xa for UFH, platelet counts for HIT when indicated, PE warning signs (sudden dyspnea, chest pain, tachycardia), and patient education on medication adherence and bleeding precautions

What strategies help prevent a first DVT?

Early and regular mobility (ambulation, ankle pumps, frequent walks), mechanical prophylaxis (sequential compression devices or compression stockings when indicated), and pharmacologic prophylaxis (low dose UFH or LMWH) for eligible at risk patients

What is a pulmonary embolism (PE), and what commonly causes it?

A condition in which an embolus, usually from a DVT, obstructs pulmonary arterial blood flow; it can also arise from fat, air, or amniotic fluid

What is the pathophysiologic sequence of PE leading to obstructive shock?

Pulmonary artery obstruction increases pulmonary vascular resistance, which increases right ventricular afterload, causing RV dilation and dysfunction and decreased left ventricular filling, which decreases cardiac output and can cause hypotension and obstructive shock

How does PE affect oxygenation?

Obstructed pulmonary blood flow causes ventilation perfusion mismatch and impaired gas exchange, potentially resulting in hypoxemia

What are the major complications of PE?

Acute right ventricular failure, obstructive shock and cardiac arrest, and chronic thromboembolic pulmonary hypertension causing persistent dyspnea

What are the common clinical manifestations of PE?

Sudden dyspnea and tachypnea, pleuritic chest pain that worsens with inspiration, tachycardia with possible hypoxemia, and possible hemoptysis, anxiety, or syncope

What are the high risk findings in PE that suggest hemodynamic instability?

Hypotension from decreased cardiac output, altered mental status from impaired cerebral perfusion, cool skin with poor perfusion or syncope, and in severe PE, obstructive shock or cardiac arrest

What are the nursing priorities for a patient with suspected PE?

Assess airway, breathing, and circulation; monitor oxygen saturation, blood pressure, heart rate, and mental status; and recognize hemodynamic deterioration to activate the emergency response

What is the Wells score used for in PE, and what guides further testing?

It estimates the likelihood of PE; clinical probability and hemodynamic stability guide which laboratory tests and imaging are obtained

How is D dimer used in diagnosing PE?

It helps exclude PE in appropriately selected low or intermediate risk patients, but an elevated D dimer is nonspecific and does not confirm PE

What is the primary confirmatory imaging test for most eligible patients with suspected PE?

CT pulmonary angiography (CTPA)

When is a ventilation/perfusion scan used in PE diagnosis, and what does echocardiography assess?

A V/Q scan is used as an alternative when CTPA is unsuitable; echocardiography evaluates right ventricular dysfunction, especially in unstable patients

What do troponin and natriuretic peptides indicate in PE evaluation?

They may indicate right ventricular strain and assist with risk assessment

What do ECG and ABGs show in PE, and what is their diagnostic limitation?

ECG may show sinus tachycardia and ABGs may show hypoxemia or respiratory alkalosis, but neither test alone can confirm or exclude PE

What is the first line pharmacologic treatment for most PE patients, and what does it prevent?

Anticoagulation; it prevents recurrent VTE but does not dissolve the existing clot

Which anticoagulants are preferred for PE treatment?

DOACs are preferred when eligible for oral therapy; LMWH is preferred over UFH when injectable/parenteral treatment is needed; warfarin is preferred in thrombotic antiphospholipid syndrome

When is thrombolytic therapy such as alteplase considered for PE, and what is generally avoided?

It is considered for high risk PE with hemodynamic instability and acceptable bleeding risk; routine thrombolysis should be avoided in stable PE

What safety monitoring applies during PE anticoagulation or thrombolytic therapy?

Watch for major bleeding (GI or intracranial), review contraindications/renal function/drug interactions, monitor BP/oxygenation/mental status/response, and reassess the need for extension after the initial 3 to 6 months of treatment

What is the role of an inferior vena cava (IVC) filter in PE management?

It is considered when acute VTE is present and anticoagulation is contraindicated; it traps emboli to prevent new PE but does not dissolve the existing clot, and it should be removed when appropriate, typically within 3 months

What are catheter directed therapy and surgical embolectomy used for in PE?

Catheter directed therapy delivers a thrombolytic, with or without mechanical clot removal, directly into the pulmonary arteries; surgical embolectomy provides urgent clot removal when indicated, both reserved for select patients

What supportive measures are used for oxygenation in PE?

Assess ABGs and monitor respiratory status, give supplemental oxygen for hypoxemia (SpO2 below 90%), manage hypotension and impaired perfusion with vasopressors if needed, and escalate care for worsening respiratory distress

What strategies help prevent a first PE?

Early and regular ambulation to reduce venous stasis, mechanical prophylaxis with sequential compression devices, and risk based pharmacologic prophylaxis with LMWH or UFH during hospitalization

What is an ischemic stroke?

Cerebral artery obstruction causing decreased cerebral blood flow, leading to neuronal injury and infarction

What are the three major etiologic types of ischemic stroke?

Atherosclerotic (large artery) stroke from plaque formation or rupture causing thrombosis or embolization; cardioembolic stroke from a clot forming in the heart (such as with atrial fibrillation) that travels to cerebral circulation; and small vessel (lacunar) stroke from occlusion of small penetrating cerebral arteries, often linked to chronic hypertension and diabetes

What is the underlying mechanism of neuronal injury in ischemic stroke?

Arterial obstruction decreases oxygen and glucose delivery, and prolonged ischemia causes irreversible brain injury

What happens at the cellular level during cerebral ischemia?

Arterial occlusion decreases oxygen and glucose, decreasing ATP production and causing failure of cellular ion pumps; this leads to cellular sodium and water accumulation, causing cytotoxic edema, and prolonged ischemia leads to neuronal injury and infarction

What is the difference between the infarct core and the ischemic penumbra?

The infarct core is irreversibly injured brain tissue; the ischemic penumbra is hypoperfused tissue that may still be salvageable, but without reperfusion it may progress to infarction

Why does the saying time is brain apply to ischemic stroke treatment?

Rapid reperfusion may restore blood flow and preserve the threatened ischemic penumbra, while delayed treatment carries a greater risk of permanent neurological deficits

What are the modifiable risk factors for ischemic stroke?

Hypertension (a major risk factor), diabetes mellitus, dyslipidemia, smoking, obesity, physical inactivity, and atrial fibrillation (which increases cardioembolic stroke risk)

What are the nonmodifiable risk factors for ischemic stroke?

Increasing age, family history, prior transient ischemic attack (TIA) or stroke, and sex related differences in risk and outcomes

What are the clinical manifestations of ischemic stroke?

Sudden unilateral weakness or numbness, facial droop and arm weakness, aphasia (difficulty speaking or understanding language), and visual loss, dizziness, ataxia, or impaired balance

What does the BE FAST acronym stand for in stroke recognition?

Balance difficulty, Eyes (sudden vision loss, usually in one eye), Facial droop, Arm weakness, Speech difficulty, and Time to call 911 immediately

What is assessed in the immediate evaluation of a suspected ischemic stroke?

Identify the last known well time, assess ABCs/vital signs/blood glucose, and use the NIHSS to quantify neurologic deficits and monitor changes

What brain imaging is obtained urgently in suspected ischemic stroke, and why?

Non contrast CT of the brain within about 20 minutes of arrival to urgently exclude intracranial hemorrhage; MRI within about 60 minutes is more sensitive for early ischemic injury

What vascular imaging is used in ischemic stroke evaluation?

CT angiography within about 30 minutes to detect large vessel occlusion, and CT or MR perfusion within about 60 minutes to help identify potentially salvageable tissue in selected patients

What additional evaluation is obtained in suspected ischemic stroke?

Early ECG to detect atrial fibrillation or arrhythmias, echocardiography within 24 hours to evaluate possible cardiac embolic sources, and labs including glucose, CBC, and coagulation studies (PT, INR, aPTT, with fibrinogen and platelet count as indicated)

What is the eligibility window and key action for IV thrombolysis with alteplase or tenecteplase in ischemic stroke?

Treatment is generally given for eligible disabling stroke within 4.5 hours of last known well, using alteplase or tenecteplase for fibrinolysis; selected extended or unknown onset cases may be eligible based on imaging

What must be confirmed before giving IV thrombolysis for ischemic stroke?

CT or MRI showing no intracranial hemorrhage, NIHSS assessment of baseline stroke severity, review of anticoagulant use, checking glucose and bleeding risk, and ensuring blood pressure is below 185/110 mmHg

What monitoring is required in the first 24 hours after thrombolysis for ischemic stroke?

Keep blood pressure below 180/105 mmHg for 24 hours, monitor for intracranial hemorrhage, perform frequent neurologic and blood pressure checks, and hold antiplatelets/anticoagulants for 24 hours until follow up CT/MRI

When is aspirin started after an ischemic stroke, and what is the exception?

Generally within 48 hours after CT excludes bleeding; if a thrombolytic was given, wait 24 hours and repeat CT/MRI first before starting aspirin

What other secondary prevention measures are started after ischemic stroke?

Anticoagulation for selected cardioembolic indications, and statins to reduce future vascular risk

What is mechanical thrombectomy (endovascular thrombectomy, EVT), and when can it be performed?

Endovascular removal of a clot from an occluded artery, recommended for appropriately selected large vessel occlusions, and can be performed up to 24 hours after last known well in selected patients, with eligibility guided by imaging and clinical assessment

What supportive care measures help prevent secondary brain injury after ischemic stroke?

Maintain airway, oxygenation (SpO2 at least 94%), and circulation; perform a swallow screen before oral intake to prevent aspiration; manage fever, glucose, and hydration; and position appropriately to prevent immobility complications

What are the target ranges for blood pressure, temperature, and glucose in post stroke supportive care?

Avoid hypotension and follow reperfusion specific BP targets; treat fever at or above 38.0 degrees C and investigate the cause; correct hypoglycemia and manage persistent hyperglycemia (around 140 to 180 mg/dL) while avoiding overly intensive control

When is early rehabilitation started after ischemic stroke?

Once the patient is medically stable, beginning multidisciplinary rehabilitation assessment with physical, occupational, and speech language therapy as indicated

How does cerebral edema develop after an ischemic stroke?

Ischemia causes cellular injury and cytotoxic edema; later blood brain barrier disruption causes vasogenic edema; severe swelling increases intracranial pressure

What are the effects of increased ICP on cerebral perfusion after stroke?

Increased ICP decreases cerebral perfusion; severe edema may cause brain herniation, and large cerebellar infarcts may cause hydrocephalus and brainstem compression

What are the warning signs of worsening cerebral edema or increased ICP after stroke?

Declining level of consciousness, new or worsening neurological deficits, headache/vomiting/pupillary changes, and Cushing's triad (hypertension, bradycardia, irregular respirations) as a late sign of severe increased ICP

How is cerebral edema managed after ischemic stroke?

Urgent neurological reassessment and brain imaging, general measures (head of bed at 30 degrees, maintain oxygenation and euvolemia and normothermia), osmotherapy (hypertonic saline or mannitol) to reduce ICP, and decompressive surgery for selected patients with life threatening swelling

What are the key components of primary prevention for a first ischemic stroke?

Controlling medical risks (treating hypertension to a goal below 130/80 mmHg for most treated adults, optimizing diabetes, treating high cholesterol with a statin when indicated, and anticoagulating atrial fibrillation when indicated), maintaining healthy daily habits (Mediterranean style diet, at least 150 minutes per week of moderate exercise, smoking cessation, healthy weight and sleep), and regular screening for blood pressure, glucose, lipids, and atrial fibrillation risk

Is aspirin routinely recommended to prevent a first stroke?

No, aspirin is not routinely recommended solely to prevent a first stroke

What is the mechanism of action, examples, and indication for antiplatelet drugs?

They inhibit platelet aggregation to prevent platelet rich clots; examples include aspirin and clopidogrel; they are indicated for noncardioembolic ischemic stroke prevention

What is the mechanism of action, examples, and indication for anticoagulant drugs?

They inhibit coagulation factors to prevent clot formation and extension; examples include heparin, apixaban, and warfarin; they are indicated for DVT, PE, and atrial fibrillation related stroke prevention

What is the mechanism of action, examples, and indication for thrombolytic drugs?

They activate plasmin to break down fibrin clots; examples include alteplase and tenecteplase; they are indicated for selected acute ischemic strokes and high risk PE

What is the overall distinction between antiplatelets, anticoagulants, and thrombolytics, and their shared major risk?

Antiplatelets prevent platelet aggregation, anticoagulants prevent clot formation and extension, and thrombolytics actively break down existing clots; all three increase bleeding risk, with major hemorrhage being a particular concern with thrombolytics