Page 78 - Proceeding of Plenary Abstract of Parallel Symposim

HEMATOLOGI

Management of Blood Disorders in Childhood Covid-19

Susi Susanah
Department of Child Health, Faculty of Medicine, Universitas Padjadjaran/Dr. Hasan Sadikin General Hospital, Bandung, West Java, Indonesia
Abstract
Background Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can impact all of the body
systems, including causing hematological disruption. The hematologic manifestation was vary and changes in
hematological parameters involving blood cells and hemostatic disorder. Clinical and laboratory parameter findings
are needed to predict disease progression, management, and prognosis. Methods Identified the manifestation and
management of blood disorders in childhood Covid-19. Results Manifestation of hematological abnormalities in
children with Covid-19 can be in the form of lymphopenia, neutrophilia, thrombocytopenia, monocytopenia,
elevated LDH, elevated ferritin, and Covid-19 associated coagulopathy, such as elevated D-dimers, prolonged
prothrombin time (PT), prolonged partial thromboplastin time (PTT), and elevated fibrinogen. The basic
principle of management is to treat the underlying infection while the management of hematological disorders is
based on the complexity of these impairment. Covid-19 pediatric patients show mildly altered coagulation and
inflammatory parameters; on the other hand, Multisystem Inflammatory Syndrome in Children (MIS-C) cases
showed laboratory signs of an inflammatory driven pro-coagulant status. Universal anticoagulant prophylaxis in
hospitalized children with SARS-CoV-2–related manifestations is not warranted, but may be offered to patients
with other pro-thrombotic risk factors in the context of a multi-modal therapeutic approach. In some cases
hematologigal disorders present a significant management challenge. A comprehensive review of the literature
on Covid-19 in children, multicenter of clinical trial, the experience and expertise of pediatric hematologists
and pediatric critical care physicians from various centers, and specific committee were performed to formulate
consensus-based recommendations management blood disorders in childhood Covid-19, especially on the use
of anticoagulant in children with Covid-19. Conclusion A better understanding of Covid-19 pathogenesis
and pathophysiology, in particular hematological disorders, will help to choose appropriate treatment strategies.
Currently, the national guideline for the management of Covid-19 in health facilities is available then priorities
for future research will be updated as high-quality evidence emerges.

Mechanism of Hemostasis and Coagulopathy in Covid-19

Pustika Amalia Wahidiyat
Department of Child Health, Faculty of Medicine Universitas Indonesia/Dr. Cipto Mangunkusumo Hospital, Jakarta, Indonesia

Abstract
Background The predominant underlying cause of mortality in Covid-19 is tissue damage and endothelial injury.
Normal activation of coagulation cascade is initiated by the disruption of the endothelial lining, which causing
the release of collagen and tissue factor (TF). Discussion The adhesion of platelets at the site of injury leads to
platelet activation. Activated TF will form a complex with FVIIa and activate FIX, FX, and FVII. Generated
thrombin will activate FXI, FVIII, and FV. Factor IXa, binds to its cofactor FVIIIa to form the intrinsic complex,
leading to activation of FX. Factor Xa and FVa complex converts prothrombin to thrombin, which further
activates fibrinogen to fibrin. Fibrin will make a crosslink with activated FXIIIa to form stable thrombi. Fibrin
formation is counterbalanced by tissue-type plasminogen activator (tPA), which cleaves plasminogen to plasmin.
Plasmin limits the thrombus formation by degrading fibrin. The network between the coagulation system and the
innate immune system was called immunothrombosis. It describes the participation of the innate immune system
in thrombus formation via distinct cellular and molecular interactions. Leukocyte activation leads to platelet
activation by releasing platelet-activating factor. Following exposure to pathogens, neutrophils undergo the
formation of neutrophil extracellular traps (NETs) via a process termed NETosis. NETs play a fundamental role
in providing a scaffold for platelets, vWF, TF, and fibrinogen. It also binds factor XII (Hageman factor), generating
its activation to FXIIa.Cytokines are secreted by activated leukocytes and endothelial cells (ECs). The cytokines
exert a procoagulant effect by increase platelet activation, release TF from monocytes and ECs, downregulate the
anticoagulant pathways, and inhibit fibrinolysis. Conversely, the production of pro-inflammatory cytokines (IL-
6 and TNF-a) by monocytes is enhanced by thrombin generation.Viral-mediated coagulation is hypothesized
to occur in 4 pathways: endothelial disruption, leukocyte–platelet interaction, cytokine release, and release of
intravascular TF. Direct viral infection may cause endothelial dysfunction and apoptosis. Viruses can also directly
infect the cells of the innate immune system, which lead to immune dysregulation.
Keywords: hemostasis, coagulopathy, Covid-19, immunothrombosis

Kongres Nasional Ilmu Kesehatan Anak XVIII 63