Bio International Society on Thrombosis and Haemostasis

Jonathan Mieog^*
*Correspondence: Jonathan Mieog, Department of Internal Medicine, Leiden University Medical Centre, Netherlands, Email:

Commentary

Patients who have been resuscitated after a cardiac arrest have a pathophysiological condition known as "post cardiac arrest syndrome" (PCAS). It's a complicated global condition involving global ischemia, cardiac arrest, and subsequent reperfusion and reperfusion damage. Surprisingly, post-cardiac arrest syndrome shares numerous characteristics with sepsis's systemic inflammatory response syndrome. Multiple organs, such as the brain, heart, and blood arteries, are all involved in the same way. The pathophysiology includes an intensified inflammatory response with the production of inflammatory markers, as well as abnormal coagulation system activation and deactivation. Disturbances in the microcirculation may potentially be a common denominator in sepsis and PCAS. Disturbed microcirculation, despite adequate perfusion pressure, high cardiac output, and adequately oxygenated blood, has been postulated to be a cause of cardiovascular disease. Patients who have been resuscitated after a cardiac arrest have a pathophysiological condition known as "post cardiac arrest syndrome" (PCAS).

It's a complicated global condition involving global ischaemia, cardiac arrest, and subsequent reperfusion and reperfusion damage. Surprisingly, post-cardiac arrest syndrome shares numerous characteristics with sepsis's systemic inflammatory response syndrome. Multiple organs, such as the brain, heart, and blood arteries, are all involved in the same way. The pathophysiology includes an intensified inflammatory response with the production of inflammatory markers, as well as abnormal coagulation system activation and deactivation. Disturbances in the microcirculation may potentially be a common denominator in sepsis and PCAS. Disturbed microcirculation, despite adequate perfusion pressure, high cardiac output, and adequately oxygenated blood, has been postulated to be a cause of cardiovascular disease.

They looked back on 273 OHCA patients who were eligible included 253 people for whom laboratory measurements were taken right away. The DIC score could be calculated after admission to the hospital. The study cohort includes OHCA with a variety of etiologist. Only one of these arrests was due to respiratory reasons or trauma third, due to a cardiac reason On admission, the DIC score was displayed be an independent predictor of survival that includes a number of well-known variables Survival predictors and treatments that influence survival with the exception of time, which is subject to spontaneous circulation (ROSC). Unfortunately, the number of patients in the study was modest (only 28 [11 %]). Patients' thromboelastometry during and after cardiopulmonary resuscitation (CPR).8,9 They pointed out that the time it takes for blood to clot is important lysis was reduced in patients who did not achieve ROSC and in those who did patients who take longer to reach ROSC.

This would imply a tense situation hyper fibrinolysis. It's been suggested that this hyperfibrinolytic enzyme is to blame. It's possible that condition is a defence mechanism to keep tissue oxygenated. Thrombosis and tissue hypoxia However, past research suggests otherwise. It's been suggested that the decrease in endogenous anticoagulants like after cardiac collapse, protein C prevents clot lysis. At times, birth might result in cord haemorrhage or cephalohaematomas. Bruising and joint bleeding is usually not visible until 6–12 months after exercise and mobility have been restored. Patients with severe haemophilia (FVIII 1% of the population) recruitment joint bleeding are common and appear to be spontaneous, and they can cause lasting joint injury. This could be the case. The administration of prophylactic factor VIII or IX concentrates can avoid this. A rare yet life-threatening consequence is intracranial haemorrhage. Patients with mild haemophilia (FVIII >5% normal) have a higher risk of bleeding. Rather than spontaneous joint bleeds, have haemorrhage caused by trauma or surgery. Moderate haemophiliacs (FVIII 1–5%) have a clinical profile ranging from severe to moderate [1-5].

REFERENCES

1. Bouwmans, Clazien, Krol Marieke, Severens Hans and Koopmanschap Marc, et al. “Targeted Next Generation Sequencing for Human Papillomavirus Genotyping in Cervical Liquid-Based Cytology Samples.” Value Health 18 (2015): 753-758.

Google Scholar, Crossref, Indexed at

2. Walboomers, J.M.; Jacobs, M.V.; Manos, M.M.; Bosch, F.X.; Kummer, J.A.; Shah, K.V.; Snijders, P.J.; Peto, J.; Meijer, C.J.; Muñoz, N. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J. Pathol. 1999, 189, 12–19.

Google Scholar, Crossref, Indexed at

3. Jack Cuzicka,⁎ and Cosette Wheeler. “Need for expanded HPV genotyping for cervical screening.” Value Health 17 (2014): 112–115.

Google Scholar, Crossref, Indexed at

4. Jesper H. Bonde, Maria-Teresa Sandri, Devin S. Gary, and Jeffrey C. Andrews. “Clinical Utility of Human Papillomavirus Genotyping in Cervical Cancer Screening: A Systematic Review.” J Low Genit Tract Dis 2020 Jan1–13.

Google Scholar, Crossref, Indexed at

5. Dana Hashim, Birgit Engesæter, Gry Baadstrand Skare, Philip E. Castle, Tone Bjørge, Ameli Tropé and Mari Nygård. “Real-world data on cervical cancer risk stratification by cytology and HPV genotype to inform the management of HPV-positive women in routine cervical screening.” British Journal of Cancer volume 122, 1715–1723 (2020).

Google Scholar, Crossref, Indexed at