Review Article

Disseminated Intravascular Coagulation in Children: An Update

*Kamal N1, Hossain MM2

Disseminated Intravascular Coagulation (DIC) is a complex syndrome causing generalized micro

thrombi formation, which causes consumption of coagulation factors resulting in secondary
fibrinolysis. It is not uncommon in children. Due to its highly complex and variable
pathophysiology and interrelationship with hemostatic system, DIC does not show any uniformity
in presentation. Although, there are many forms of DIC, clinical picture of DIC is dominant with
bleeding. Besides, there is no gold standard investigation to diagnose DIC. Many therapeutic
approaches are not validated and controversial. Prompt diagnosis and correct treatment depends on
understanding of underlying pathology. Treatment should be individualized depending on the
nature of DIC to correct the underlying pathology, as complexity and variation of presentation
suggests.

[Mymensingh Med J 2025 Jul; 34 (3): 942-949]

Key words: Disseminated intravascular coagulation (DIC), Blood transfusion, Children, Fresh frozen
plasma (FFP), Neonate

Introduction system of children is profoundly influenced by

D isseminated intravascular coagulation

(DIC) is acute, sub-acute, or chronic
thrombo - hemorrhagic disorder
characterized by the activation of coagulation
cascade excessively and the formation of
age and the concentrations of coagulation proteins
are dependent on both the gestational and
postnatal age of the infant3. At birth,
concentrations of the vitamin K dependent and
contact factors are reduced to about 50.0% of
thrombus in the microvasculature of the body1. normal adult values4. Similarly, concentrations of
Activation of the coagulation system can occur in the naturally occurring anticoagulants,
many clinical conditions. A robust and strong antithrombin, protein C and protein S are low at
activation of this system complicating clinical birth and which leads to reduction of thrombin
settings may result in the occurrence of generation and thrombin inhibition in this period.
disseminated intravascular coagulation (DIC). It is So, for correct management of the DIC, we have
considered to be fatal. Although newer data are to understand children’s haemostatic system,
lacking, older publications shows an alarming underlying pathophysiology and perfect
prevalence of DIC in children2. As established interpretation of different investigations.
clinical scoring systems for DIC are not routinely
employed in clinical practice, overall prevalence
of DIC in hospitalized patients was remain
unknown. DIC as a clinical syndrome is full of 1. *Dr Nusrat Kamal, Junior Consultant,
dilemma starting from pathogenesis, types, Paediatrics, National Center for Control of
diagnosis, investigations and treatment. There is Rheumatic Fever and Heart Diseases, Dhaka,
no gold standard laboratory test to diagnose it. Bangladesh; E-mail: [Link]@ [Link]
Cumulative interpretation of several investigations 2. Professor Dr Mohammad Monir Hossain,
results help to identify the type of DIC and correct Professor & Head, Department of Neonatology
treatment protocol. But, it has been seen that, yet & NICU; Head, Division of Paediatric Medicine
today, we rely on traditional Prothrombin time and Academic Head, Bangladesh Shishu
(PT), Activated partial thromboplastin time Hospital & Institute
(APTT) which has different normal ranges
depending upon reagent used, and age. But we *for correspondence
rarely consider this. Depending on these values,
frequency of inappropriate blood transfusion
increases. On the other hand, the haemostatic

Mymensingh Med J 2025 Jul; 34 (3) 942

 Review Article
Terminology Causes of DIC
In earlier literature, it was known as a a) Sepsis and severe infections: i) Gram-negative
defibrination syndrome5. Many author suggested organisms (including Neisseria meningitidis,
“defibrinogenation syndrome” as a better term6. Haemophilus influenza, coliforms), ii) Gram-
Different text books have also used “consumptive positive organisms (including group B
coagulopathy” for DIC7. As per clinical symptom Streptococcus), iii) Viruses (including Dengue
it is now a days known as thrombo hemorrhagic fever), iv) Rickettsiae (including Rocky Mountain
disorder1. spotted fever, typhus), v) Malaria and vi) Fungal
infections (including Aspergillus,
Types of DIC Histoplasmosis).
It can be categorized into: i) Bleeding or hyper b) Tissue injury: i) Massive trauma/surgery and
fibrinolysis predominance type, ii) Massive crush injury, ii) Tissue infarction/hypo perfusion,
bleeding or consumptive type, iii) Organ failure or iii) Fractures with fat emboli Asphyxia and
hyper coagulation predominance or hypo profound shock, iv) Extensive burns and v)
fibrinolysis type and iv) Non-symptomatic type or Electrocution
pre-DIC8. c) Malignancy: i) Acute leukaemias (including
It can again divided into: i) Non-overt DIC- when
acute promyelocytic, acute monoblastic or
hemostatic system is both stressed and
myelocytic leukaemia) and ii) Solid tumours
compensated and often remain unrecognized and
d) Toxins: i) Snake or insect venoms and ii)
ii) Overt DIC-when hemostatic system is stressed,
Recreational drugs
decompensated and often associated with clinical
consequences9. e) Microangiopathic processes: i) Thrombotic
thrombocytopenic purpura, ii) Haemolytic-
uraemic syndrome and iii) Giant haemangioma
(Kasabach–Merritt syndrome)
f) Hereditary or acquired thrombotic disorders: i)
Protein S or C deficiency
g) Miscellaneous: i) Acute haemolytic transfusion
reactions and other intravascular haemolysis and
ii) Acute thrombosis
h) Obstetrics: i) Amniotic fluid embolus, ii)
Placental abruption and iii) Pre-eclampsia

Figure 1: Types of DIC8

Pathophysiology of DIC
DIC usually was triggered by either (1) release of tissue factor or other, poorly characterized pro
coagulants into the circulation, and (2) widespread injury to the endothelial cells. 1Tissue factor (TF)
pathway is the primary triggering factor which produces thrombin10.

Figure 2: Pathophysiology of DIC 1

Mymensingh Med J 2025 Jul; 34 (3) 943
 Review Article
DIC causes consumption of endogenous anticoagulants- antithrombin (AT), protein C and down
regulation of thrombomodulin and tissue factor pathway inhibitor (TFPI) activity, to promote thrombus 8.
In physiological state, well-controlled thrombus formation leads to minimization of blood loss at the site
of tissue injury; but when the inciting insult (e.g. sepsis) is persistent or severe, the amount of thrombin
generated becomes excessive, causing thrombus formation and hemorrhagic state at a same time 7.
Thrombin also causes commencement of fibrinolytic pathway generating a large amount of fibrin
degradation products11. Anti-fibrinolytic pathway also activates to control the unlimited amount of
fibrinolysis, which can further aggravate the prothrombotic state7. Again, cytokines such as interleukin-1
(IL-1) elevated and it is along with tissue necrosis factor-α (TNF- α) in bloodstream stimulate the
production of plasminogen activator inhibitor type 1 which further impair the fibrinolytic process. 8
Recent advances in DIC have focused on inflammation-coagulation cross-link also. In Covid-19
infection, the development of thrombovasculitis is the most important pathogenic mechanism for the
development of micro thrombi and hemorrhage which leads to DIC9.

Figure 3: Role of thrombin in DIC7

Whatever the pathogenic mechanism, DIC has two consequences: i) There is widespread fibrin
deposition within the microcirculation and ii) Depletion of platelets, clotting factors and the secondary
release of plasminogen activators leads to superimposed bleeding tendency1.

Figure 4: Process in DIC14

[

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 Review Article
Clinical features of DIC International Society for Thrombosis and
The common clinical picture in DIC is bleeding Haemostasis (ISTH) diagnostic scoring system for
with signs of shock out of proportion to the DIC14-
amount of blood loss. In neonate, it may manifest International Society for Thrombosis and
as poor perfusion, cold extremities and poor tone. Haemostasis (ISTH) diagnostic scoring system for
Bleeding may occur as petechiae, purpura, DIC-
subconjunctival or mucosal hemorrhages, A. Risk assessment: Patient has an underlying
extravasation from past venipuncture or surgical disorder that can leads to DIC.
sites, GI hemorrhage, pulmonary hemorrhage or i) If yes, proceed and ii) If no: do not use this
severe life-threatening hemorrhage. Haemorrhagic algorithm
diathesis being the predominant manifestation of B. Order global coagulation tests (PT, platelet
DIC in acute leukaemia. count, fibrinogen, fibrin related marker)
Typical hemorrhagic features11: i) Bleeding C. Score the test result: i) Platelet count
venipuncture site, ii) Oozing of blood from (>100X109/L=0, <100X109/L=1, <50X109/L=2);
indwelling catheter, iii) Spontaneous or minimum ii) Elevated fibrin marker (no increase = 0,
trauma related generalized ecchymosis, iv) moderate increase = 2, strong increase = 3); iii)
Development of large bullous hemorrhagic skin Prolonged PT (<3s=0, >3s but <6s=1, >6s=2)
lesion on previous viral exanthemata’s site, v) and iv) Fibrinogen level ( >1g/l = 0, <1g/l =1)
Mucosal bleeding and vi) Unexpected or major D. Calculate score: >5 compatible with overt DIC
bleeding from postoperative site. and <5 suggestive of non-overt DIC.
Typical thrombotic features11: i) Thrombophlebitis
at unusual site, ii) Renal impairment in absence of Laboratory test
other explanation, iii) Confusion & seizure, iv) DIC is a clinico-laboratory diagnosis. There is no
Respiratory distress with no obvious explanation, gold standard test or single test that can diagnose
v) Dermal infarct & skin necrosis and vi) Acral DIC.
cyanosis. 1. Prothrombin time (PT): It is defined as time
needed to clot plasma that is platelet poor after
Diagnosis of DIC adding tissue factor, calcium and phospholipid. It
To establish or rule out DIC, currently there is no is initiated by tissue factor and involves extrinsic
specific sign-symptoms or diagnostic test12. (V, VII, X) and common (fibrinogen,
Separate guidelines have been published by The prothrombin) coagulation pathways. Usually not
British Committee for Standards in Haematology, prolonged until levels of one or more factor is
Japanese Society of Thrombosis and Hemostasis, <30.0%.
and the Italian Society for Thrombosis and 2. Activated partial thromboplastin time (APTT):
Haemostasis (ISTH)8. As some variation presents Time to clot platelet-poor plasma with addition of
in their recommendations, the International kaolin (or similar reagent) followed by calcium
Society on Thrombosis and Hemostasis (ISTH) and phospholipid. It is initiated by contact
Subcommittee harmonized these dissimilarities activation and involves intrinsic (V, VIII, IX, X,
and recommended a standardized DIC scoring XI, XII) and common (fibrinogen, prothrombin)
system14. coagulation pathways. Usually not prolonged until
ISTH score showed sensitivity, specificity, factor VIII level <35.0% normal.
positive and negative predictive value of 91.0%, 3. Fibrinogen: Kinetic assay for clottable
97.0%, 96.0% and 97.0% respectively15. One of fibrinogen. Sensitivity is 12.0% when, fibrinogen
the advantages of this scoring system is that it value is less than 1.5 g/L and specificity 98.0% to
uses simple, widely available routine coagulation detect increase generation of thrombin and
assay15. In children, to predict mortality and plasmin18. As, fibrinogen is an acute phase
morbidity, ISTH scores have been used16. The cut- reactant, it is also raised in other infective
off value of DIC score in children is lower than condition.
adult ISTH DIC score which called for an increase 4. D-dimer: Agglutination test for factor XIII
awareness of severity of illness in children with crosslinked fibrin subunit. It is small fibrin
DIC score17. degradation product. It demonstrates that plasmin

Mymensingh Med J 2025 Jul; 34 (3) 945

 Review Article
has digested fibrin clot. It is also elevated in 2. Supportive care with blood products: There are
thrombosis, embolism, tissue injury, after birth2. lots of different practices and controversies related
5. Platelets: Platelet count is a key early indicator to blood product management. Transfusion should
of DIC19. A drop in platelet count below be reserved for bleeding patients with DIC and not
150×109/L showed a sensitivity of 39.0%, a to transfuse primarily based on laboratory result14.
specificity of 88.0%, and positive and negative Depending on underlying requirements and
predictive values of 81.0% and 54.0%, treatment guideline, Platelet, FFP,
respectively, to indicate increased generation of Cryoprecipitate, prothrombin complex concentrate
thrombi as well as plasmin18. Thrombocytopenia (PCC) can be given22.
present in the majority of cases and 50.0% of 3. Thrombin generation modulation:
cases having a count <50×109/L19. a) Heparin: When DIC developed due to
6. Thrombin time: It is defined as, time to form thrombotic condition, Heparin was used to treat it.
fibrin gel when thrombin added to platelet-poor However, they are contraindicated when bleeding
plasma. It measures time needed for fibrin occurs. Unfractionated heparin (UFH) has short
formation. life which leads to better use of it in pediatric
7. Molecular marker like: i) Soluble fibrinogen, ii) population as continuous infusion23. JAMA has
Thrombin- antithrombin (TAT) complex, iii) approves Low molecular weight (LMW) heparin
Plasminogen activator-inhibitor complex, iv) Daltaperin for use in DIC, where chances of
Protein C and v) Clot Fibrnoysis Waveform venous thromboembolism is high24. A randomized
Analysis (CFWA)- novel assay to assess ongoing controlled trial done on severe trauma patients
hemostatic mechanism20. found beneficial use of LMW heparin for the
[Link] / rotational thrombo- treatment of DIC25.
elastometry: New and point of care (POC) test. b) Anticoagulant concentrate: especially effective
Mechanical or optical assessment of the speed of in sepsis associsted DIC17.
clot formation and lysis and clot strength and i) Antithrombin (AT): One of natural
elasticity is performed. It involves all coagulation anticoagulant that is depleted early during
pathways, platelet function and fibrinolysis. To excessive thrombin generation. It is approved in
assess formation of clot, it is usually used at Japan25. Although retrospective data shows good
bedside in cardio-pulmonary bypass or outcome on pediatric population, no RCT has
anaesthesia. Where DIC is suspected in trauma or been found27.
massive transfusion, this test is of much useful to ii) Recombinant Activated protein C: Protein C
detect early DIC. Utility is best documented in found to be low in various septic condition, which
CPB as predictor of bleeding8. leads to use of Recombinant Activated Protein C
(rAPC) in DIC. Several studies demonstrate, early
Management of DIC recovery, less morbidity with it; but, subsequent
Although much of DIC management is centered large trial found no benefit of it in adult or
on use of FFP and other blood products, there are pediatrics group, rather causes excess bleeding.
many other options remaining; whilst use of blood So, rAPC usage is not recommended in children27.
product remains minimal. iii) Thrombomodulin (TM): It is a vascular
1. Treatment of underlying disease: The key to endothelial glycoprotein which enhances the
DIC treatment is vigorous management of Protein C activity. It has similar pharmacological
underlying condition with optimal care8,14 like mechanism like APC. Even though, TM seems to
empiric broad-spectrum intravenous therapy with be safe and effective in pediatric population, more
one or more antimicrobials (bacterial, fungal or RCT are needed to confirm the efficacy as PC is
viral coverage) as soon as possible after required for optimal action28.
recognition and within one hour for those with c) Modulating pro fibrinolytic activity: Hyper
sepsis or septic shock21. Without correcting fibrinolysis in DIC is secondary to excess
underlying pathology, DIC will not resolve by thrombin generation and is a natural reactionary
using of any blood product. Various studies process to deal with the uncontrolled generation of
concluded that, treatment should be directed to thrombin. If we use, antifibrinolytic agent to
correct pathology rather than using various drugs prevent this excess fibrinolysis, it would further
including transfusion. deteriorate the condition. However, when acute
Mymensingh Med J 2025 Jul; 34 (3) 946
 Review Article
coagulopathy due to trauma or postpartum of the human coagulation system in the full-
hemorrhage where, hyper fibrinolysis is pre term infant. Blood. 1987;75(1):165-72.
dominant, only in those condition, anti-fibrinolytic 4. Andrew M, Vegh P, Johnston M, Bowker J,
is found beneficial29. It has been reported that Ofosu F, Mitchell L. Maturation of the
Tranexamic acid is effective in hyper fibrinolytic hemostatic system during childhood.
state30. Blood. 1982;80(8):1998-2005.
Over the past few decades, several studies have 5. Merskey C, Johnson AJ, Kleiner GJ, Wohl H.
demonstrated the efficacy of antithrombin (AT) The defibrination syndrome: clinical features
and protein C concentrates (PrCC), recombinant and laboratory diagnosis. British Journal of
activated protein C (APC) and recombinant Haematology. 1967;13:528-49.
thrombomodulin (rTM) for the management of 6. Bick RL, Arun B, Frenkel EP. Disseminated
DIC in children31. intravascular coagulation. Clinical and
d) Combination Therapy: Different combination Pathophysiological mechanisms and
therapy has been trialed. Like a RCT done on 80 manifestations. Haemostasis. 1999;29(2-3):
PICU patients on sepsis / septic shock and non- 111-34.
overt DIC. Intervention group had FFP, low dose 7. Thachil J, Toh CH. Current concepts in the
UFH and tranexamic acid. Compared with this management of disseminated intravascular
group, the non-intervention group had a coagulation. Thrombosis Research. 2012;129:
significantly higher mortality rate, a significantly 54-9.
higher rate of progression to overt DIC (45.0% vs. 8. Wada H, Matsumoto T, Yamashita Y.
10.0%, p<0.0001), and significantly higher DIC Diagnosis and treatment of disseminated
risk assessment scores on the second and fifth intravascular coagulation (DIC) according to
day32. four DIC guidelines. Journal of Intensive
Combination therapy like FFP + AT-III, rTM + Care. 2014;2(1):1-8.
FFP + At-III, APC + LMW heparin has also been 9. Vorobyev PA, Momot AP, Krasnova LS,
used in different studies and found effective33 Vorobiev AP, Talipov AK. Pathogenesis,
e. Others: Studies reported using of plasma diagnosis, prevention and treatment of
exchange and newer therapeutic approaches like disseminated intravascular coagulation
eculizumab, but no proven beneficial role has syndrome in Covid-19 infection. Ter Arkh.
been established34. 2020;92(11):51-6.
10. Squizzato A, Hunt BJ, Kinasewitz GT, Wada
Conclusion H, Ten Cate H, Thachil J et al. Supportive
Though DIC is itself encompass a vast underlying management strategies for disseminated
pathology, clinical manifestation, diagnostic intravascular coagulation. An international
dilemma, treatment options, updated knowledge consensus. Thromb Haemost. 2016;115(5):
emphasized on understanding this 896-904.
pathophysiology and to treat accordingly; rather 11. Rajagopal R, Thachil J, Monagle P.
than blindly transfusing blood product. Disseminated intravascular coagulation in
paediatrics. Archives of Disease in Childhood.
References 2017;102(2):187-93.
1. Kumar V, Abbas AK, Fausto N, Aster JC. 12. Wada H. Disseminated intravascular
Robbins and Cotran pathologic basis of coagulation. Clinica Chimica Acta. 2004;
disease. 9th ed. Canada: Elsevier Inc. 2014. 344(1-2):13-21.
p.663-4. 13. Di Nisio M, Baudo F, Cosmi B, D'Angelo A,
2. Veldman A, Fischer D, Nold MF, Wong FY. De Gasperi A, Malato A et al. Diagnosis and
Disseminated intravascular coagulation in treatment of disseminated intravascular
term and preterm neonates. Seminars in coagulation: guidelines of the Italian Society
Thrombosis and Hemostasis. 2010;36(4):419- for Haemostasis and Thrombosis
28. (SISET). Thrombosis Research. 2012;129(5):
3. Andrew M, Paes B, Milner R, Johnston M, 177-84.
Mitchell L, Tollefsen DM et al. Development 14. Levi M, Toh CH, Thachil J, Watson HG.
Guidelines for the diagnosis and management
Mymensingh Med J 2025 Jul; 34 (3) 947
 Review Article
of disseminated intravascular coagulation. 24. Sakuragawa N, Hasegawa H, Maki M,
British Journal of Haematology. 2009;145(1): Nakagawa M, Nakashima M. Clinical
24-33. evaluation of low-molecular-weight heparin
15. Bakhtiari K, Meijers JC, de Jonge E, Levi M. (FR-860) on disseminated intravascular
Prospective validation of the International coagulation (DIC)-a multicenter co-operative
Society of Thrombosis and Haemostasis double-blind trial in comparison with heparin.
scoring system for disseminated intravascular Thrombosis Research. 1993;72(6):475-500.
coagulation. Critical Care Medicine. 2004; 25. Wen JM, Sun YX, Pan XH, Chen HS. Effects
32(12):2416-21. of low-molecular-weight heparin and
16. Khemani RG, Bart RD, Alonzo TA, Hatzakis unfractionated heparin on traumatic
G, Hallam D, Newth CJ. Disseminated disseminated intravascular coagulation.
intravascular coagulation score is associated Tropical Journal of Pharmaceutical Research.
with mortality for children with 2018;7(5):961-6.
shock. Intensive Care Medicine. 2009;35(2): 26. Iba T, Saito D, Wada H, Asakura H. Efficacy
327-33. and bleeding risk of antithrombin
17. Slatnick LR, Thornhill D, Davies SJ, Ford JB, supplementation in septic disseminated
Scott HF, Manco-Johnson MJ et al. intravascular coagulation: a prospective
Disseminated Intravascular Coagulation Is an multicenter survey. Thrombosis Research.
Independent Predictor of Adverse Outcomes 2012;130(3):129-33.
in Children in the Emergency Department 27. Nadel S, Goldstein B, Williams MD, Dalton
with Suspected Sepsis. The Journal of H, Peters M., Macias WL et al. Drotrecogin
Pediatrics. 2020;225:198-206. alfa (activated) in children with severe sepsis:
18. Schmidt B, Vegh P, Johnston M, Andrew M, a multicenter phase III randomized controlled
Weitz J. Do coagulation screening tests detect trial. The Lancet. 2007;369(9564):836-43.
increased generation of thrombin and plasmin 28. Yagasaki H, Kato M, Shimozawa K, Hirai M,
in sick newborn infants? Thrombosis and Nishikawa E, Okuma H et al. Treatment
Haemostasis. 1993;69(05):418-21. responses for disseminated intravascular
19. Morley SL. Management of acquired coagulation in 25 children treated with
coagulopathy in acute paediatrics. Archives of recombinant thrombomodulin: a single
Disease in Childhood-Education and Practice. institution experience. Thrombosis Research.
2011;96(2):49-60. 2012;130(6):289-93.
20. Onishi T, Ishihara T, Nogami K. Coagulation 29. ASH-2 trial collaborators, Shakur H, Roberts
and fibrinolysis balance in disseminated I, Bautista R, Caballero J, Coats T et al.
intravascular coagulation. Pediatrics Effects of tranexamic acid on death, vascular
International. 2021;63(11):1311-8. occlusive events, and blood transfusion in
21. Levy MM, Evans LE, Rhodes A. The trauma patients with significant haemorrhage
surviving sepsis campaign bundle: 2018 (CRASH-2): a randomized, placebo-
update. Intensive Care Medicine. 2018;44(6): controlled trial. Lancet. 2010;376(9734):23-
925-8. 32.
22. Kunwar S, Alam M, Ezekwueme F, Yasir M, 30. El-Nawawy AA, Elshinawy MI, Khater DM,
Lawrence JA, Shah S et al. Diagnostic Scores Moustafa AA, Hassanein NM, Wali YA et al.
and Treatment Options for Acute Outcome of early hemostatic intervention in
Disseminated Intravascular Coagulation in children with sepsis and non overt
Children. Cureus. 2021;13(9):e17682. disseminated intravascular coagulation
23. Toh CH, Hoots WK. SSC on Disseminated admitted to PICU: a randomized controlled
Intravascular Coagulation of the ISTH. The trial. Pediatric Critical Care Medicine. 2021;
scoring system of the Scientific and 22(3):e168-77.
Standardization Committee on Disseminated 31. Kongstad C, Mikkelsen TS, Hvas AM.
Intravascular Coagulation of the International Disseminated intravascular coagulation in
Society on Thrombosis and Haemostasis: a 5- children with cancer: a systematic review.
year overview. Journal of Thrombosis and Pediatric Hematology and Oncology. 2020;
Haemostasis. 2007;5(3):604-6. 37(5):390-411.
Mymensingh Med J 2025 Jul; 34 (3) 948
 Review Article
32. Go H, Ohto H, Nollet KE, Kashiwabara N, coagulation. International Journal of
Ogasawara K, Chishiki M et al. Risk factors Hematology. 2002;75(5):540-7.
and treatments for disseminated intravascular 34. Galic S, Csuka D, Prohászka Z, Turudic D,
coagulation in neonates. Italian Journal of Dzepina P, Milosevic D. A case report of a
Pediatrics. 2020;46(1):1-7. child with sepsis induced multiorgan failure
33. Aoki N, Matsuda T, Saito H, Takatsuki K, and massive complement consumption treated
Okajima K, Takahashi H et al. A comparative with a short course of eculizumab: a case of
double-blind randomized trial of activated crosstalk between coagulation and
protein C and unfractionated heparin in the complement? Medicine (Baltimore). 2019;98:
treatment of disseminated intravascular e14105.

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