scholarly journals Management Dilemmas in Patients with Traumatic Brain Injury on Anticoagulants

2020 ◽  
Vol 17 (02) ◽  
pp. 095-103
Author(s):  
Srinivas Dwarakanath ◽  
Harsh Deora
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Thrombus Formation ◽  
Vitamin K Antagonists ◽  
Head Injuries ◽  
Antiplatelet Agents ◽  
Coagulation Cascade ◽  
Therapeutic Drugs ◽  
Coagulation Mechanism ◽  
Normal Hemostasis

Abstract Introduction A normal individual with normal hemostasis maintains a balance between thrombus formation and destruction using a complex interaction between the smooth vascular endothelium, the coagulation cascade, the platelet aggregation system, and the fibrinolysis mechanism. However, in patients who are on either antiplatelet drugs (APDs) or anticoagulants (ACDs), this normal homeostasis is altered. This is further altered with traumatic brain injury (TBI) and thus, we need specific guidelines to address this subpopulation to decide the length of observation, avoid unnecessary hospitalization, and relieve the economic burden. There exists a very few randomized controlled trials (RCTs) for this clinical question and a thorough risk–benefit analysis for each patient is prudent before making clinical decisions. Materials and Methods This is a review article based on available evidence published in literature. Results There are multiple therapeutic drugs which act on various stages of the coagulation mechanism. These include antiplatelet agents, Vitamin K antagonists, Heparin, Antithrombin III, and Glycoprotein IIb/IIIA inhibitors. While the initial management of head injuries depends on the severity of head injuries, management of head injuries in patients on anticoagulants needs to be approached with care and caution. There are multiple dilemmas including role of CT scans, duration and reason for admission, when to restart anticoagulation, etc. We suggest the recommendations based on available literature; however, no evidence can be given as these are not based on any RCTs, due to paucity of such studies. Conclusion The guidelines are based on previously conducted trials and consensus. We have attempted to provide a pragmatic and practical approach to such cases with the hope that it will ensure minimum risks with the best possible patient outcomes. The entire journey from patient presentation to follow-up has been covered in this article and we hope this would be useful to all practicing in the field of neurotrauma.

New agents for thromboprotection

2015 ◽  
Vol 35 (04) ◽  
pp. 338-350 ◽  
Author(s):  
L. Labberton ◽  
E. Kenne ◽  
T. Renné
Keyword(s):  
Current Knowledge ◽  
Thrombus Formation ◽  
Coagulation Cascade ◽  
Factor Xii ◽  
Bleeding Tendency ◽  
New Agents ◽  
Mechanistic Basis ◽  
Normal Hemostasis ◽  
Coagulation Pathway

SummaryBlood coagulation is essential for hemostasis, however excessive coagulation can lead to thrombosis. Factor XII starts the intrinsic coagulation pathway and contact-induced factor XII activation provides the mechanistic basis for the diagnostic aPTT clotting assay. Despite its function for fibrin formation in test tubes, patients and animals lacking factor XII have a completely normal hemostasis. The lack of a bleeding tendency observed in factor XII deficiency states is in sharp contrast to deficiencies of other components of the coagulation cascade and factor XII has been considered to have no function for coagulation in vivo. Recently, experimental animal models showed that factor XII is activated by an inorganic polymer, polyphosphate, which is released from procoagulant platelets and that polyphosphate-driven factor XII activation has an essential role in pathologic thrombus formation. Cumulatively, the data suggest to target polyphosphate, factor XII, or its activated form factor XIIa for anticoagulation. As the factor XII pathway specifically contributes to thrombosis but not to hemostasis, interference with this pathway provides a unique opportunity for safe anticoagulation that is not associated with excess bleeding.The review summarizes current knowledge on factor XII functions, activators and inhibitors.

scholarly journals Management of Traumatic Brain Injury: A review Update

2017 ◽  
Vol 6 (2) ◽  
pp. 87-89
Author(s):  
ATM Ashadullah ◽  
Monirul Islam ◽  
Fazley Elahi Milad ◽  
Abdullah Alamgir ◽  
Md Shafiul Alam
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injuries ◽  
Skull Fracture ◽  
Traumatic Injury ◽  
Loss Of Consciousness ◽  
Extradural Haematoma ◽  
Inner Surface ◽  
Injury Patient ◽  
Extradural Haematomas

Traumatic Brain Injury leads to serious consequences. Approximately half of all deaths is related to traumatic injury and the main cause of head trauma. Extradural haematomas (EDH) develops in all major head injuries. A head injury patient who is only temporary loss of consciousness and is left asleep may sometimes be found dead in the bed next morning due to extradural haematoma. Extradural haematoma which lies in between the inner surface of skull and stripes of dural membrane, are nearly always caused by, and located near a skull fracture. The collection takes several forms in terms of size, location, speed of development and effects they exert on patient. Immediate management is necessary to decrease the bad consequences. In this review the management of traumatic brain injury is highlighted.J Shaheed Suhrawardy Med Coll, 2014; 6(2):87-89

scholarly journals Steroids for delayed cerebral edema after traumatic brain injury

2021 ◽  
Vol 12 ◽  
pp. 46
Author(s):  
G. Lakshmi Prasad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Head Injuries ◽  
Experimental Studies ◽  
Symptomatic Improvement ◽  
High Dose ◽  
The Mean ◽  
Key Aspects

Background: Brain edema is a common phenomenon after traumatic brain injury (TBI) resulting in increased intracranial pressure and subsequent neurological deterioration. Experimental studies have proven that brain edema is biphasic (cytotoxic followed by vasogenic). Till date, all studies, including the corticosteroid randomization after significant head injury (HI) trial, have used high-dose steroids in the acute period during which the edema is essentially cytotoxic in nature. No clinical data exist pertaining to delayed cerebral edema (vasogenic) and steroids. Methods: Patients who had received steroids for delayed cerebral edema after TBI were retrospectively analyzed over a 2-year period. Steroid dose, timing of steroid prescription, time to improvement of symptoms, and complications were noted. Results: There were six males and three females. Mean age was 41.1 years. There were no severe HI cases. All subjects had cerebral contusions on imaging. Dexamethasone was the preferred steroid starting with 12 mg/day and tapered in 5–7 days. The mean interval to steroid administration after trauma was 7 days. The mean duration of steroid prescription was 6.3 days. All patients had complete symptomatic improvement. The mean time to symptom resolution was 3.8 days. No patients experienced any complications pertinent to steroid usage. Conclusion: This is the first study to document efficacy of steroids for delayed cerebral edema after TBI, at least in mild/moderate head injuries. The timing of steroid usage and dose of steroids is key aspects that might determine its efficacy in TBI which was the drawbacks of the previous studies. Future prospective trials with the above factors in consideration may confirm/refute above findings.

scholarly journals Disability as a result of craniocerebral trauma in Russia: actuality and forecasts

2020 ◽  
Vol 23 (2) ◽  
pp. 33-41
Author(s):  
Ilya V. Borisov ◽  
Valeriya A. Bondar ◽  
M. M. Kanarskiy ◽  
Julia Y. Nekrasova ◽  
Dmitriy S. Yankevich ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injuries ◽  
Craniocerebral Trauma ◽  
World Health ◽  
Federal State ◽  
The World ◽  
The Russian Federation ◽  
External Causes ◽  
Health Organization

According to the World Health Organization, injuries take first place among the causes of death among the population under 40 years of age. In the Russian Federation, in 2019, death from external causes, including injuries, was in third place in all deaths. Among the causes of disability first place. Mortality from severe traumatic brain injury is over 70%. The most common cause of disability and mortality is head injuries. Annually, 1.5 million people die from traumatic brain injury (TBI) in the world, and 2.4 million are disabled. According to the Federal State Budgetary Scientific Institution National Institute of Public Health named after N.A. Semashko, the annual damage from the head injury is estimated at 500 billion rubles. This is a serious socio-economic and state problem requiring complex and multidisciplinary intervention.

scholarly journals COMPLEX FORENSIC MEDICAL EVALUATION OF THE TRAUMATIC BRAIN INJURY: CASE OF PRACTICE

2021 ◽  
Vol 121 (1) ◽  
pp. 65-69
Author(s):  
Svіtlana Diachenko ◽  
Roksolana Dіduk ◽  
Nailia Kashapova ◽  
Alina Pletenetska
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injuries ◽  
Medical Examination ◽  
Simultaneous Occurrence ◽  
Craniocerebral Injuries ◽  
Medical Evaluation ◽  
High Incidence ◽  
Traumatic Effect ◽  
The Brain

The problem of studying the mechanisms of the occurrence of traumatic brain injury remains a very urgent issue for forensic medicine. The high incidence and high mortality rate of head injuries underlines its importance to experts. The article presents a case from the practice of a forensic medical examination of a traumatic brain injury. This case is indicative, since it clearly demonstrates the difficulties that forensic doctors face when examining craniocerebral injuries, when determining the mechanism of damage and the severity of bodily injuries. In this case, there is damage to the head and a concussion. The cited several conclusions of the experts of the bureau of forensic medical examination and the commission examination of the Main Bureau of Forensic Medical Examination of the Ministry of Health of Ukraine regarding the forensic medical assessment in the case of traumatic brain injury with damage to the head. When conducting an investigative experiment, it was determined that the simultaneous occurrence of an abrasion and a concussion of the brain with one traumatic effect in the glabellar region is unlikely. After all, a concussion of the brain and abrasions in the glabellar area were formed by different mechanisms. The results of this assessment of the characteristics of traumatic brain injury can be useful for preventing difficulties in establishing the mechanism of damage in further expert practice.

Incidence of head injury and traumatic brain injury among people with Alzheimer’s disease

2019 ◽  
Vol 73 (5) ◽  
pp. 451-454 ◽  
Author(s):  
Sarianna Ilmaniemi ◽  
Heidi Taipale ◽  
Antti Tanskanen ◽  
Jari Tiihonen ◽  
Sirpa Hartikainen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Head Injuries ◽  
Community Dwelling ◽  
University Hospital ◽  
Health Concern ◽  
Increased Risk

BackgroundInjuries caused by falling are a major health concern among older population. For older people, falls are the leading cause of head injuries; especially, persons with cognitive disorders have an increased risk of falling.ObjectiveTo compare the incidence of head injury and traumatic brain injury (TBI) among persons with Alzheimer’s disease (AD) with persons without AD.MethodsThis register-based study was conducted on a nationwide cohort, which includes all community-dwelling persons diagnosed with AD in Finland in 2005–2011. Persons with previous head injuries were excluded, leaving 67 172 persons with AD. For each person with AD, a matching person without AD and previous head injury were identified with respect to age, sex and university hospital district. The Cox proportional hazard model and competing risk analyses were used to estimate HR for head injury and TBI.ResultsPersons with AD had 1.34-fold (95% CI 1.29 to 1.40) risk of head injuries and 1.49-fold (95% CI 1.40 to 1.59) risk of TBIs after accounting for competing risks of death and full adjustment by socioeconomic status, drug use and comorbidities.ConclusionPersons with AD are more likely to have a head injury or TBI incident than persons without AD.

The Effect of Antiplatelet Agents on the Progression of Traumatic Brain Injury: Does Injury Pattern Matter?

2020 ◽  
Vol 231 (4) ◽  
pp. e252
Author(s):  
Catsim Fassassi ◽  
Daniel Dove ◽  
Juliette Hernandez ◽  
Heath Walden ◽  
Krishan Patel ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Antiplatelet Agents ◽  
Injury Pattern

scholarly journals Noncanonical Effects of Oral Thrombin and Factor Xa Inhibitors in Platelet Activation and Arterial Thrombosis

2020 ◽  
Author(s):  
Amin Polzin ◽  
Lisa Dannenberg ◽  
Manuela Thienel ◽  
Martin Orban ◽  
Georg Wolff ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Arterial Thrombosis ◽  
Thrombus Formation ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Factor Xa ◽  
Coagulation Cascade ◽  
Platelet Activity ◽  
Vein Thrombosis

AbstractNonvitamin K oral anticoagulants (NOACs) or direct oral anticoagulants comprise inhibitors of factor Xa (rivaroxaban, apixaban, edoxaban) or factor IIa (dabigatran). Both classes efficiently interfere with the final or penultimate step of the coagulation cascade and showed superior net clinical benefit compared with vitamin K antagonists for prevention of thromboembolic events in patients with AF and for prevention and therapy of deep vein thrombosis and pulmonary embolism. None the less, accumulating data suggested, that there may be differences regarding the frequency of atherothrombotic cardiovascular events between NOACs. Thus, the optimal individualized NOAC for each patient remains a matter of debate. Against this background, some basic and translational analyses emphasized NOAC effects that impact on platelet activity and arterial thrombus formation beyond inhibition of plasmatic coagulation. In this review, we will provide an overview of the available clinical and translational evidence for so-called noncanonical NOAC effects on platelet activation and arterial thrombosis.

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