COVID-19 Hematologic Complications: Difference between revisions
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To go to the COVID-19 project topics list, click '''[[COVID-19 Project Topics|here]]'''. | To go to the COVID-19 project topics list, click '''[[COVID-19 Project Topics|here]]'''. | ||
{{CMG}} {{AE}} {{RG}}, [https://www.wikidoc.org/index.php/User:ShakibaHassanzadeh Shakiba Hassanzadeh, MD.][[User:Fausatadogba|Oluwabusola Adogba, MD]][mailto:fausat.adogba@gmail.com] | {{CMG}} {{AE}} {{RG}}, [https://www.wikidoc.org/index.php/User:ShakibaHassanzadeh Shakiba Hassanzadeh, MD.][[User:Fausatadogba|Oluwabusola Fausat Adogba, MD]][mailto:fausat.adogba@gmail.com] | ||
==Overview== | ==Overview== | ||
Revision as of 21:44, 18 June 2020
To go to the COVID-19 project topics list, click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2], Shakiba Hassanzadeh, MD.Oluwabusola Fausat Adogba, MD[3]
Overview
Recent pandemic of COVID-19 infection is shown to have multi-systemic complication. Hematologic complication of COVID-19 include Lymphopenia, Neutrophilia, Thrombocytopenia. some articles suggest that Hemoglobin may decrease in the event of disease.
Complications
Lymphopenia
There is an assosiation between sever COVID-19 infection and lymphopenia.[1]
Neutrophilia
The human body fights infections by recruiting neutrophils early to the sites of infection by oxidative burst and phagocytosis. [2] New evidence suggests that the severe symptoms of COVID-19, including Acute Respiratory Distress Syndrome (ARDS), could be caused by Neutrophil Extracellular Traps (NETs). Acute Respiratory Distress Syndrome (ARDS), pulmonary inflammation, thick mucus secretions in the airways, extensive lung damage and blood clots are suggested to be as a result of the action of Neutrophils. When neutrophils detect pathogens, they can expel their DNA in a web laced with toxic enzymes (called a NET- Neutrophil Extracellular Trap) to attack them. These NETs capture and digest the unwanted pathogen but in cases of ARDS (Covid-19 manifestation) they cause damage to the lungs and other organs. [3] The neutrophil-to-lymphocyte ratio (NLR) has been identified as the independent risk factor for severe illness in patients with the 2019 novel coronavirus disease.[4] A higher NLR at hospital admission in patients has been associated with a more severe outcome. A NLR of >4 has been identified as a predictor of admission to the ICU.[5]
Thrombocytopenia
There is an association between severe COVID-19 infection and thrombocytopenia.[6] Thrombocytopenia is seen in 57.7% of patients with severe COVID-19 infection compared to 31.6 % of patients with non-severe infection.[7]
The pathogenesis of thrombocytopenia in COVID-19 infection is due to several factors:[8]
- Decrease in primary platelet production due to infection of bone marrow cells by coronaviruses[9] and inhibition of bone marrow growth,[10] which lead to abnormal hematopoietic function.[8]
- Decrease in circulating platelet due to lung injury which causes megakaryocyte fragmentation and decreases platelet production, because lung is a reservoir for megakaryocyte and hematopoieitic progenitor cells and has a role in platelet production.[8][12] In addition, decrease in platelets may be due to activation of platelets that result in platelet aggregation and formation of micro-thrombus which increase platelet consumption.[8][13]
Hemoglobin decrease
Coagulopathy
Pathophysiology
COVID-19 induces a hypercoagulable state in the body. An increased risk of mortality has been noted in patient’s with coagulopathy in COVID-19. [14]The factors that contribute to this state are-
- Virchow’s triad [15]
- Vascular endothelial damage
- Endothelitis- direct invasion of endothelial cells by SARS-CoV-2
- Complement mediated damage to pericytes
- Pro-inflammatory cytokines- IL-1, IL-6, and TNF- α, that activate the coagulation pathway and the fibrinolytic system
- Stasis- Prolonged hospital admissions causing immobilization of the patient
- Hypercoagulabe state- Evidenced by elevated fibrinogen, prothrombotic factors and hyperviscosity [16]
- Some patients have been found to have Lupus anticoagulant (anti-cardiolipin) and anti-β2GP1 antibodies that may be contributory. [17]
Clinical Features
Thrombotic complications like: [15] [18]
- Deep Vein Thrombosis
- Pulmonary Embolism
- Ischemic stroke
- Myocardial infarction
- Ischemic limbs
- Systemic arterial events
- Other features like clotting of central venous catheters, dialysis catheters, and dialysis filters were also seen.
Laboratory Findings
Coagulation testing: Pro-coagulant profile: [19]
- Platelet counts- normal or increased
- Prothrombin time (PT)- normal or slightly prolonged
- Activated partial thromboplastin time (aPTT)- Normal or slightly prolonged (can be due to Lupus Anticoagulant)[17]
- Fibrinogen- increased, especially in nonsurvivors
- D-dimer - increased - The level of D‐dimer has shown to reflect the severity and is associated with adverse outcomes.
TEG findings: [20]
- Reaction time (R)- decreased
- Clot formation time (K)- decreased
- Maximum amplitude (MA) increased
- Clot lysis at 30 minutes (LY30) reduced
Other findings:
- Factor VIII activity- increased
- VWF antigen- increased
- Protein C- increased
- Antithrombin and Protein S- decreased
COVID- 19 Coagulopathy and DIC
The main feature of COVID-19 coagulopathy is thrombosis while the acute phase of DIC presents with bleeding. [21]
- Similar laboratory findings are- marked increase in D-dimer and normal/slightly low platelets, prolonged PT.
- Findings distinct in COVID 19- high fibrinogen and high factor VIII activity
- The scoring system of the International Society on Thrombosis and Hemostasis should be used to detect DIC (platelet count, PT, fibrinogen, D‐dimer, antithrombin and protein C activity monitoring), but the diagnosis and subsequent treatment should be done clinically. [22]
Other hematological findings
References
- ↑ Tan, Li; Wang, Qi; Zhang, Duanyang; Ding, Jinya; Huang, Qianchuan; Tang, Yi-Quan; Wang, Qiongshu; Miao, Hongming (2020). "Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive study". Signal Transduction and Targeted Therapy. 5 (1). doi:10.1038/s41392-020-0148-4. ISSN 2059-3635.
- ↑ "Targeting potential drivers of COVID-19: Neutrophil extracellular traps | Journal of Experimental Medicine | Rockefeller University Press".
- ↑ "Severe COVID-19 symptoms may be caused by overactive neutrophils".
- ↑ Akagi Y, Itoi M, Sano Y, Andonian MR, Barrett AS, Vinogradov SN, Moroi K, Sato T, Gheorghescu B, Baghurst PA, Nichol LW, Rainsford KD, Akagi Y, Itoi M, Sano Y (August 1980). "[Monoaminergic neurons of monkey retina (author's transl)]". Nippon Ganka Gakkai Zasshi (in Japanese). 84 (8): 771–80. doi:10.1016/0005-2795(75)90035-5. PMID 7211594.
- ↑ Lippi G, Plebani M, Henry BM (2020). "Thrombocytopenia is associated with severe coronavirus disease 2019 (COVID-19) infections: A meta-analysis". Clin Chim Acta. 506: 145–148. doi:10.1016/j.cca.2020.03.022. PMC 7102663 Check
|pmc=value (help). PMID 32178975 Check|pmid=value (help). - ↑ Guan WJ, Ni ZY, Hu Y, Liang WH, Ou CQ, He JX; et al. (2020). "Clinical Characteristics of Coronavirus Disease 2019 in China". N Engl J Med. 382 (18): 1708–1720. doi:10.1056/NEJMoa2002032. PMC 7092819 Check
|pmc=value (help). PMID 32109013 Check|pmid=value (help). - ↑ 8.0 8.1 8.2 8.3 Xu P, Zhou Q, Xu J (2020). "Mechanism of thrombocytopenia in COVID-19 patients". Ann Hematol. 99 (6): 1205–1208. doi:10.1007/s00277-020-04019-0. PMC 7156897 Check
|pmc=value (help). PMID 32296910 Check|pmid=value (help). - ↑ Yang M, Ng MH, Li CK (2005). "Thrombocytopenia in patients with severe acute respiratory syndrome (review)". Hematology. 10 (2): 101–5. doi:10.1080/10245330400026170. PMID 16019455.
- ↑ Yeager CL, Ashmun RA, Williams RK, Cardellichio CB, Shapiro LH, Look AT; et al. (1992). "Human aminopeptidase N is a receptor for human coronavirus 229E". Nature. 357 (6377): 420–2. doi:10.1038/357420a0. PMC 7095410 Check
|pmc=value (help). PMID 1350662. - ↑ Nardi M, Tomlinson S, Greco MA, Karpatkin S (2001). "Complement-independent, peroxide-induced antibody lysis of platelets in HIV-1-related immune thrombocytopenia". Cell. 106 (5): 551–61. doi:10.1016/s0092-8674(01)00477-9. PMID 11551503.
- ↑ Lefrançais E, Ortiz-Muñoz G, Caudrillier A, Mallavia B, Liu F, Sayah DM; et al. (2017). "The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors". Nature. 544 (7648): 105–109. doi:10.1038/nature21706. PMC 5663284. PMID 28329764.
- ↑ Liu X, Zhang R, He G (2020). "Hematological findings in coronavirus disease 2019: indications of progression of disease". Ann Hematol. doi:10.1007/s00277-020-04103-5. PMC 7266734 Check
|pmc=value (help). PMID 32495027 Check|pmid=value (help). - ↑ Tang N, Li D, Wang X, Sun Z (2020). "Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia". J Thromb Haemost. 18 (4): 844–847. doi:10.1111/jth.14768. PMC 7166509 Check
|pmc=value (help). PMID 32073213 Check|pmid=value (help). - ↑ 15.0 15.1 Becker RC (2020). "COVID-19 update: Covid-19-associated coagulopathy". J Thromb Thrombolysis. doi:10.1007/s11239-020-02134-3. PMC 7225095 Check
|pmc=value (help). PMID 32415579 Check|pmid=value (help). - ↑ Maier CL, Truong AD, Auld SC, Polly DM, Tanksley CL, Duncan A (2020). "COVID-19-associated hyperviscosity: a link between inflammation and thrombophilia?". Lancet. 395 (10239): 1758–1759. doi:10.1016/S0140-6736(20)31209-5. PMC 7247793 Check
|pmc=value (help). PMID 32464112 Check|pmid=value (help). - ↑ 17.0 17.1 Bowles L, Platton S, Yartey N, Dave M, Lee K, Hart DP; et al. (2020). "Lupus Anticoagulant and Abnormal Coagulation Tests in Patients with Covid-19". N Engl J Med. doi:10.1056/NEJMc2013656. PMC 7217555 Check
|pmc=value (help). PMID 32369280 Check|pmid=value (help). - ↑ Barrett CD, Moore HB, Yaffe MB, Moore EE (2020). "ISTH interim guidance on recognition and management of coagulopathy in COVID-19: A comment". J Thromb Haemost. doi:10.1111/jth.14860. PMID 32302462 Check
|pmid=value (help). - ↑ Ranucci M, Ballotta A, Di Dedda U, Bayshnikova E, Dei Poli M, Resta M; et al. (2020). "The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome". J Thromb Haemost. doi:10.1111/jth.14854. PMID 32302448 Check
|pmid=value (help). - ↑ Panigada M, Bottino N, Tagliabue P, Grasselli G, Novembrino C, Chantarangkul V; et al. (2020). "Hypercoagulability of COVID-19 patients in Intensive Care Unit. A Report of Thromboelastography Findings and other Parameters of Hemostasis". J Thromb Haemost. doi:10.1111/jth.14850. PMID 32302438 Check
|pmid=value (help). - ↑ Levi M, Thachil J, Iba T, Levy JH (2020). "Coagulation abnormalities and thrombosis in patients with COVID-19". Lancet Haematol. 7 (6): e438–e440. doi:10.1016/S2352-3026(20)30145-9. PMC 7213964 Check
|pmc=value (help). PMID 32407672 Check|pmid=value (help). - ↑ Levi M, Toh CH, Thachil J, Watson HG (2009). "Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology". Br J Haematol. 145 (1): 24–33. doi:10.1111/j.1365-2141.2009.07600.x. PMID 19222477.