Related Experiment Video

Updated: Mar 24, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

1.8K

Spontaneous subdural hematoma and antiplatelet therapy: Does efficacy of Ticagrelor come with added risk?

Pattanagere Manjunatha Suryanarayana Sharma1, Aniruddha Tekkatte Jagannatha2, Mahendra Javali3

  • 1Senior Resident, Department of Neurology, M.S. Ramaiah Medical College, Bangalore 560054, India.

Indian Heart Journal
|March 21, 2016
PubMed

Insights

Antiplatelet therapy, including aspirin and ticagrelor, can increase bleeding risk. This case highlights spontaneous subdural hematoma, emphasizing early recognition and management for good outcomes.

Area of Science:

  • Neuroscience
  • Cardiology
  • Pharmacology

Background:

  • Antiplatelet therapy is crucial for cardiovascular outcomes after percutaneous coronary intervention.
  • Major bleeding, particularly intracranial hemorrhage (ICH), is a significant risk associated with these therapies.
  • Ticagrelor is a P2Y12 receptor antagonist with proven benefits but potential bleeding risks.

Observation:

  • A case of spontaneous acute subdural hematoma is presented.
  • The patient was concurrently on antiplatelet therapy with aspirin and ticagrelor.
  • This event occurred despite no apparent trauma, suggesting a spontaneous etiology.

Findings:

  • Early identification and cessation of antiplatelet medications were key.
  • Appropriate medical management led to hematoma resolution.
  • The patient achieved a favorable clinical outcome.

Implications:

  • Judicious use and risk stratification are essential when prescribing antiplatelet agents.
  • Neurophysicians must be aware of the potential for ICH with newer antiplatelet drugs.
  • This case underscores the importance of prompt diagnosis and intervention in managing antiplatelet-associated intracranial bleeding.

Keywords:
Acute coronary syndromeAntiplatelet therapyIntracranial hemorrhageSubdural hematomaTicagrelor

More Related Videos

Ferric Chloride-induced Murine Thrombosis Models10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

23.4K
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

1.2K

Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
1.5K
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
459
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
2.3K
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
2.7K
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
10.6K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
10.1K