INTRODUCTION — Disseminated intravascular coagulation (DIC) is a pathologic disruption of the finely balanced process of hemostasis. The systemic activation of coagulation is characterized by generation and deposition of fibrin and formation of microvascular thrombi (thrombosis) in the small blood vessels throughout the body, eventually leading to multiple organ dysfunction. Widespread clotting depletes platelets and clotting factors that are needed to control bleeding, which often leads to excessive bleeding. Activation of plasmin-mediated fibrinolysis by intravascular fibrin is another component of the process.
Identification and treatment of the underlying cause are critical to resolution of the hemostatic abnormalities. Any patient with DIC presents a major management challenge, and this challenge is further complicated when the patient is carrying a fetus at a stage of fetal maturity when there is a reasonable chance of extrauterine survival. For example, delaying delivery to transfuse a pregnant patient with DIC who is bleeding heavily may not be in the best interest of a fetus with a category III heart rate tracing, whereas performing an emergency cesarean birth on this patient may not be in their best interest. Even in the setting of fetal demise, labor and vaginal birth of a pregnant patient with DIC carries the potential for catastrophic hemorrhage.
This topic will review DIC related to pregnancy, focusing on clinical findings, etiology, and diagnosis. The management and prognosis of pregnant patients with DIC or another severe coagulopathy are discussed separately. (See "Disseminated intravascular coagulation (DIC) during pregnancy: Management and prognosis".)
Broader discussions of the pathogenesis, clinical manifestations, diagnosis, and treatment of DIC can be found elsewhere (see "Evaluation and management of disseminated intravascular coagulation (DIC) in adults"). Other causes of pregnancy-associated thrombocytopenia and obstetric hemorrhage are also presented elsewhere. (See "Thrombocytopenia in pregnancy" and "Evaluation and differential diagnosis of vaginal bleeding before 20 weeks of gestation".)
●Pregnancy-associated DIC accounts for approximately 1 to 5 percent of all cases of DIC in resource-abundant countries; this proportion appears to be higher in resource-limited countries .
●The prevalence of pregnancy-associated DIC ranges from 0.03 to 0.35 percent of delivery hospitalizations in population-based studies [2-4]. A study from the United States reported a prevalence of 12.5 per 10,000 delivery hospitalizations (0.13 percent) .
●Although the overall prevalence of pregnancy-associated DIC is low, patients with specific pregnancy complications, such as placental abruption or amniotic fluid embolism, can be at very high risk (eg, prevalence >20 percent) [5-7].
PATHOPHYSIOLOGY — The pathogenesis and consequences of DIC are shown in the figure (figure 1) and discussed in detail separately. In pregnancy, impaired uterine contractility is an additional important clinical consequence [8-10]. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Pathogenesis'.)
DIC is a secondary manifestation of an underlying condition that has led to uncontrolled activation of clot formation and breakdown. In pregnant patients, the underlying condition is often placental abruption, amniotic fluid embolism, or fetal demise with necrosis. These conditions result in generation of, or exposure to, tissue factor (TF) [11-13]. TF interacts with circulating factor VIIa to rapidly initiate the clotting cascade via the extrinsic pathway (figure 2).
●Pregnancy-related – The type and frequency of pregnancy-related conditions that triggered DIC in a review of 49 cases from a tertiary maternity hospital included :
•Placental abruption – 37 percent (See "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences" and "Acute placental abruption: Management and long-term prognosis".)
•Postpartum hemorrhage – 29 percent (See "Overview of postpartum hemorrhage".)
There is some debate about the relationship between severe postpartum hemorrhage (PPH) and DIC. There is evidence that severe tissue hypoxia in the setting of shock may result in release of tissue factor (TF) from damaged cells and supraphysiologic activation of coagulation, leading to DIC [14,15]. The counterargument is that coagulopathy in the setting of PPH is simply due to depletion of clotting factors and platelets by blood loss, which results in dilutional coagulopathy.
•Preeclampsia/eclampsia/HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome – 14 percent. These cases were likely complicated by coexistent abruption or liver failure, as most preeclampsia is associated with thrombocytopenia without changes in prothrombin time (PT), activated partial thromboplastin time (aPTT), and fibrinogen . (See "Preeclampsia: Clinical features and diagnosis" and "Preeclampsia: Antepartum management and timing of delivery" and "Eclampsia" and "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)".)
•Acute fatty liver – 8 percent (See "Acute fatty liver of pregnancy".)
•Amniotic fluid embolism – 6 percent (See "Amniotic fluid embolism".)
•Pregnancy-related sepsis – 6 percent. Examples include septic abortion, severe chorioamnionitis, and postpartum endometritis. (See "Unsafe abortion", section on 'Morbidity and mortality' and "Pregnancy loss (miscarriage): Clinical presentations, diagnosis, and initial evaluation", section on 'Septic abortion' and "Clinical chorioamnionitis" and "Postpartum endometritis".)
There were no cases of prolonged retention of a dead fetus because these cases are generally identified early and delivered without significant delay in contemporary obstetric practice . (See "Stillbirth: Maternal care".)
●Nonpregnancy-related – DIC may also be caused by conditions that may occur in the nonpregnant population. The most common events that initiate DIC in the general population are sepsis, trauma, and cancer (table 1). The possibility of these nonobstetric causes of DIC should be considered in pregnant patients with DIC, especially when an obvious pregnancy-associated cause is absent [18,19]. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Causes of DIC'.)
Presentation — DIC typically occurs in the setting of one of the pregnancy complications described above (see 'Causes' above). It may present in either of two ways, depending on the underlying etiology, intensity of coagulation activation, and the deficiency of natural anticoagulation mechanisms:
●Overt DIC – Overt fulminant DIC is the more common scenario in pregnancy. Coagulation and fibrinolysis are both increased, and both overt bleeding and thrombosis are present. Patients may present with severe vaginal bleeding and/or diffuse oozing from skin (eg, at intravenous sites) or mucosa (eg, from a bladder catheter). Signs of shock (eg, tachycardia, hypotension, weak peripheral pulses, altered mental status, cool extremities, narrow pulse pressure [<25 mmHg]) and/or organ dysfunction (eg, acute renal failure, hepatic dysfunction, acute lung injury, neurologic dysfunction) may be present. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Clinical manifestations'.)
Importantly, patients with abruption may not have vaginal bleeding early in the course of the disorder if most of the blood is initially retained in utero behind the placenta (called "concealed abruption"). Patients with intraabdominal bleeding also do not present with vaginal bleeding. Severe intraabdominal bleeding is uncommon but can occur in the setting of hepatic rupture related to preeclampsia, eclampsia, or HELLP syndrome-associated hepatic disease.
●Latent and compensated activation of coagulation – In this situation, there is subtle hemostatic dysfunction and increased thrombotic risk without obvious clinical symptoms or signs. It is characterized by imbalance between activation and inhibition of the coagulation system and can be rapidly normalized by removing the procoagulant stimulus and enhancing the inhibitory mechanisms. This state may become a chronic condition, which is rare in pregnancy, or it may progress to overt DIC. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Acute versus chronic DIC'.)
Laboratory findings — No single laboratory test is sensitive and specific for DIC. Laboratory findings generally include abnormal coagulation studies and thrombocytopenia. These findings need to be interpreted within the context of normal reference values in pregnancy (table 2), which are sometimes different from values in nonpregnant patients. Normal pregnancy is a hypercoagulable state. Changes include marked increases in most coagulation factors, increased platelet reactivity, decreased endogenous anticoagulation, and decreased fibrinolysis. This shift in the hemostatic and fibrinolytic systems serves to prevent excessive bleeding during placental separation. (See "Normal reference ranges for laboratory values in pregnancy".)
Major findings in DIC include:
●Thrombocytopenia – The platelet count is typically mildly to moderately reduced; platelet counts below 20,000/microL are uncommon .
In normal pregnancy, the mean platelet count is slightly lower than in nonpregnant patients (called gestational thrombocytopenia) but usually remains within the normal range. Because platelet counts may be within the normal range in the early stages of DIC, the trend in platelet count should be monitored when DIC is suspected. In a clinical scenario that includes DIC in the differential diagnosis, a falling platelet count may be a sign of developing DIC even if the absolute count is in the normal range.
Thrombocytopenia in pregnancy is not specific for DIC; it is observed in several pregnancy-related disorders. (See "Thrombocytopenia in pregnancy".)
●Prolongation of the activated partial thromboplastin time (aPTT), prothrombin time (PT), and thrombin time (TT) – The aPTT and PT measure the time taken, in vitro, for blood to form fibrin. The PT/international normalized ratio (INR) evaluates the extrinsic pathway, and the aPTT measures the time taken to form fibrin via the intrinsic pathway.
Both PT/INR and aPTT are prolonged. In a normal gestation, the aPTT and PT/INR may be slightly shorter than that in nonpregnant patients due to normal changes in coagulation factors. This can cause a delay in the recognition of ongoing coagulopathy since prolongation/increase in the aPTT and PT/INR may not become obvious until the causative pathology is well advanced . Thus, it is essential to note any prolongation/increase of the aPTT and PT/INR, even if the starting point is within the normal range and the current aPTT and PT/INR are still within that normal range. A widening differential between baseline and repeat tests in either the aPTT or the PT/INR may indicate clinical worsening . (See "Maternal adaptations to pregnancy: Hematologic changes", section on 'Coagulation and fibrinolysis'.)
The TT is another coagulation test that measures the final step in the coagulation cascade (conversion of fibrinogen to fibrin). The TT is not routinely measured in pregnancy or DIC, but if measured, it tends to follow the same pattern as the aPTT and PT/INR (ie, it is shorter than normal in normal pregnancy and prolonged in DIC) .
●Hypofibrinogenemia – Fibrinogen levels fall in DIC. In a normal pregnancy, the fibrinogen level is >300 mg/dL in the third trimester, a level that is substantially higher than in nonpregnant individuals, since fibrinogen is an acute phase reactant . Reduction in the fibrinogen level from the patient's baseline is concerning even if the absolute level remains in the normal range, as the fall in fibrinogen in DIC can be a relatively late finding .
In a study of patients with persistent uterine atony, a fibrinogen level <200 mg/dL had a positive predictive value of 100 percent for progression to severe postpartum hemorrhage, whereas a level >400 mg/dL had a negative predictive value of 79 percent . The greatest concern for bleeding generally occurs when the fibrinogen level is <100 mg/dL; this is also the typical level below which the aPTT and PT/INR become prolonged/increased.
●Increased D-dimer – D-dimer is increased in DIC. In a normal pregnancy, D-dimer is higher than in nonpregnant individuals [27,28]. In one study of 760 healthy patients with singleton pregnancies, the D-dimer median value was 316 ng/mL at 24 weeks, gradually increasing to 668 ng/mL at 40 weeks; the 95th percentiles at 24 and 40 weeks were 704 ng/mL and 1538 ng/mL, respectively . D-dimer is further increased in DIC, but because of the higher baseline values in pregnancy, a positive D-dimer test and the absolute D-dimer value are difficult to interpret.
●Variable white blood cell (WBC) count – The WBC count is increased in pregnancy, particularly during labor. In DIC, it may be normal, increased, or decreased (eg, due to sepsis). (See "Maternal adaptations to pregnancy: Hematologic changes", section on 'White blood cells'.)
DIAGNOSTIC EVALUATION — Evaluation for DIC may need to occur concurrently with initial management before the diagnosis is completely established, especially if there is ongoing hemorrhage, shock, or an abnormal fetal heart rate pattern. (See "Disseminated intravascular coagulation (DIC) during pregnancy: Management and prognosis", section on 'Initial preparation and assessment of all patients'.)
Many pregnancy-associated causes of DIC are obvious from the history and physical examination. Because the absence of external bleeding does not exclude overt DIC, any pregnant patient with features consistent with DIC should be evaluated for intraabdominal (intraperitoneal and retroperitoneal) hemorrhage and large vaginal or vulvar hematomas. Pregnant patients who have been involved in trauma can lose large amounts of blood into the soft tissues (eg, a fractured femur can bleed into the thigh).
Laboratory testing includes the following:
●Complete blood count (CBC) with differential.
●Coagulation studies including prothrombin time (PT) and international normalized ratio (INR), activated partial thromboplastin time (aPTT), fibrinogen level, and D-dimer.
●Liver biochemical and function tests (alanine aminotransferase, aspartate aminotransferase, albumin, bilirubin) – Normal results in the setting of coagulopathy suggests DIC, whereas very abnormal results suggest that at least part of the pathology leading to the coagulopathy may be liver failure and failure to produce adequate coagulation factors.
●Thromboelastography (TEG)/Rotational thromboelastometry (ROTEM). This information provides a global assessment of hemostasis in whole blood that includes contributions of platelets, fibrinogen, fibrinolysis, and coagulation factors. TEG/ROTEM can be particularly useful in diagnosing dilutional coagulopathy . (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Viscoelastic testing'.)
●Blood urea nitrogen and creatinine, as acute kidney injury occurs in 25 to 40 percent of patients with acute DIC.
●Blood and urine cultures in patients with suspected sepsis. In cases where intrauterine infection is suspected, aspiration of amniotic fluid for culture is appropriate.
Prior to the return of the first set of laboratory results, a crude clotting time may be performed using any of a variety of methods . One method is to determine the clotting time of 5 mL of blood in a red top tube (ie, no additives) at room temperature; if the blood in the tube clots within 8 to 10 minutes and the clot remains intact, the patient likely has adequate fibrinogen stores. If the blood in the tube does not clot or an initial clot dissolves, it is likely that the patient is markedly deficient in key clotting factors. However, such tests are highly subjective, insensitive, imprecise, and not validated in pregnancy.
Although serial coagulation testing is rarely necessary to diagnose DIC in the obstetric setting (where DIC is typically fulminant), serial laboratory assessments over a few hours in less fulminant cases may show progressively prolonged coagulation times, decreasing platelet counts, increasing values for D-dimer, and falling fibrinogen levels. In challenging cases, this pattern can help distinguish mild DIC from normal pregnancy-related changes in these laboratory values. Serial CBCs, fibrinogen levels, and coagulation tests are important for guiding management (eg, coagulation factor replacement). (See "Disseminated intravascular coagulation (DIC) during pregnancy: Management and prognosis", section on 'Measure blood loss'.)
DIAGNOSIS — We make the diagnosis of acute DIC in a pregnant patient when the clinical setting is appropriate (eg, placental abruption, amniotic fluid embolism, acute fatty liver, sepsis) and there is laboratory evidence of thrombocytopenia, coagulation factor consumption (eg, prolonged prothrombin time and activated partial thromboplastin time; low fibrinogen), and fibrinolysis (eg, increasing D-dimer), as long as another etiology for these findings does not become apparent. No single laboratory test is highly sensitive or specific for the diagnosis.
Early involvement of a hematology specialist is advised when the cause is not thought to be one of the more common obstetric causes described above. (See 'Causes' above.) Specific steps to evaluate the likelihood of DIC and eliminate other possibly life-threatening causes of the findings, such as thrombotic thrombocytopenic purpura, can then be taken. (See 'Differential diagnosis' below.)
Scoring systems — Scoring systems for diagnosis of DIC in pregnant patients have been developed, but are neither widely used nor well-validated.
●One group adapted the International Society of Thrombosis and Hemostasis (ISTH) DIC scoring system for diagnosis of overt DIC for use in pregnant patients. The revised system includes platelet count, prothrombin time (PT) difference (difference between the PT value of the patient and laboratory control in seconds), and fibrinogen levels . The parameters are assigned a score of 0, 1 (platelet count <50,000 or 100,001 to 185,000 or fibrinogen 400 to 450 mg/dL), 2 (platelet count 50,000 to 100,000), 5 (for PT difference 0.5 to 1), 6 (for fibrinogen 300 to 400 mg/dL), 12 (for PT difference 1 to 1.5), or 25 (for PT difference >1.5 or fibrinogen ≤300 mg/dL). In a study of 684 patients with abruption, of whom 150 needed blood transfusion and 43 had DIC, a score ≥26 had 88 percent sensitivity and 96 percent specificity to identify those who needed blood and blood product transfusion.
●Pregnancy-specific scoring systems for nonovert DIC have also been developed to predict patients likely to require blood product transfusion. The parameters include fibrinogen, antithrombin III, protein C, prothrombin time, platelet count, thrombin-antithrombin (TAT) complex, and D-dimer . In one study, a score ≥3 had a sensitivity and specificity of 71.4 and 77.9 percent to identify patients at risk for obstetrical hemorrhage requiring blood product transfusion.
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of DIC in pregnancy includes other causes of bleeding, thrombosis, and/or organ damage. In some cases, these conditions may coexist with DIC or contribute to the pathogenesis of DIC. Treatment of the underlying cause typically leads to resolution of DIC (see "Disseminated intravascular coagulation (DIC) during pregnancy: Management and prognosis", section on 'Identify and address the triggering event'):
●Postpartum hemorrhage (PPH) with dilutional coagulopathy – Severe bleeding from PPH may result in dilutional coagulopathy. The reduced levels of coagulation factors can prolong the prothrombin time (PT) and activated partial thromboplastin time (aPTT) as in DIC. The blood smear is useful because there is no evidence of microangiopathy (no schistocytes) in PPH, while schistocytes should be evident in fulminant DIC. However, some patients with PPH may have elements of suggestive of coagulation factor consumption consistent with DIC. (See "Overview of postpartum hemorrhage", section on 'Criteria for diagnosis'.)
●Primary thrombotic microangiopathy – Primary thrombotic microangiopathies such as thrombocytopenic purpura (TTP) are rare during pregnancy, but the physiologic stress of pregnancy may trigger clinical manifestations of hereditary or acquired TTP. Pregnancy (including the postpartum period) is also a major precipitating factor for complement-mediated hemolytic uremic syndrome. (See "Thrombotic microangiopathies (TMAs) with acute kidney injury (AKI) in adults: CM-TMA and ST-HUS", section on 'Pregnancy or postpartum'.)
Like DIC, patients with TTP may have Coombs-negative hemolytic anemia with schistocytes on the blood smear, thrombocytopenia, and organ damage. In contrast to DIC, the coagulation studies in TTP typically are normal, and the ADAMTS13 (A disintegrin and metalloproteinase with thrombospondin-like repeats-13) activity is severely reduced (eg, activity <10 percent). Mild decreases in ADAMTS13 activity (eg, between 10 and 60 percent) are often seen in acutely ill pregnant patients (eg, preeclampsia, HELLP syndrome) and are not thought to be pathophysiologically or clinically significant . (See "Diagnosis of immune TTP" and "Diagnostic approach to suspected TTP, HUS, or other thrombotic microangiopathy (TMA)".)
●von Willebrand disease (VWD) – VWD is the most common inherited bleeding disorder, and many pregnant patients with VWD are already aware of their diagnosis. Pregnancy is generally well-tolerated in most cases of VWD (in particular type 1, which may be asymptomatic or associated with mild bleeding symptoms), partly due to the physiologic increases in von Willebrand factor (VWF) levels. However, VWF levels decline in the postpartum period, and it is possible for a patient who has not had a prior hemostatic challenge to have marked postpartum bleeding as the initial manifestation of VWD [33-35].
Like DIC, some types of severe VWD may be associated with thrombocytopenia and/or prolongation of the aPTT. Unlike DIC, VWD does not cause prolongation of the PT, a low fibrinogen level, or elevated D-dimer; and patients with VWD will have low levels of VWF, VWF activity (ristocetin cofactor activity), and factor VIII. (See "Clinical presentation and diagnosis of von Willebrand disease".)
●Antiphospholipid syndrome (APS) – APS is caused by autoantibodies to proteins bound to anionic phospholipid-protein complexes (the dominant protein target is beta2-glycoprotein I); it can occur in the setting of systemic lupus erythematosus or independently.
Like DIC, patients can have thrombosis and elevated D-dimer, and the aPTT is frequently prolonged. Unlike DIC, in APS, the PT and fibrinogen levels are normal, and bleeding typically does not occur. Furthermore, the autoantibodies in APS can sometimes cause prolongation of the aPTT as a laboratory artifact (ie, lupus anticoagulant); they are actually prothrombotic. (See "Clinical manifestations of antiphospholipid syndrome".)
●Pulmonary embolism (PE) – PE is a leading cause of death in pregnant/postpartum persons and is often underappreciated due to the wide range of presenting symptoms.
Like DIC, patients with PE may present with shock and elevated D-dimer. Unlike DIC, PE generally is not associated with bleeding, prolongation of the clotting times, or low fibrinogen. (See "Pulmonary embolism in pregnancy: Clinical presentation and diagnosis".)
●Heparin-induced thrombocytopenia (HIT) – HIT is a potentially life-threatening disorder in which autoantibodies cause activation of platelets in the presence of heparin (ie, the antibodies are prothrombotic). HIT is extremely rare in pregnancy.
Like DIC, HIT can present with thrombocytopenia, thrombosis, and/or organ damage; bleeding may be present due to the heparin. Unlike DIC, HIT has a temporal relationship to heparin exposure; patients with HIT have positive testing for HIT antibodies and do not have coagulation abnormalities (except for those due to their anticoagulant). (See "Clinical presentation and diagnosis of heparin-induced thrombocytopenia".)
●Transfusion reaction – Severe transfusion reactions, especially due to ABO incompatibility, can mimic or cause DIC.
Like DIC, a severe transfusion reaction from ABO mismatch can cause anemia, thrombocytopenia, oozing from mucocutaneous sites, and bleeding. Unlike DIC, transfusion reactions have a history of antecedent transfusion and often are associated with a positive direct antiglobulin (Coombs) test. (See "Approach to the patient with a suspected acute transfusion reaction", section on 'Acute hemolytic transfusion reaction (AHTR)'.)
Additional discussion of the differential diagnosis in nonobstetric patients is reviewed separately. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Differential diagnosis'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Obstetric hemorrhage".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Disseminated intravascular coagulation (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Pathophysiology – Disseminated intravascular coagulation (DIC) is a secondary manifestation of an underlying primary cause of uncontrolled activation of coagulation and fibrinolysis. (See 'Pathophysiology' above.)
●Underlying cause – DIC typically occurs in the setting of one of the following pregnancy complications:
•Preeclampsia with severe features/eclampsia/HELLP syndrome (hemolysis, elevated liver enzymes, low platelets)
•Amniotic fluid embolism
•Acute fatty liver of pregnancy
•Pregnancy-related sepsis (eg, septic abortion, severe chorioamnionitis, or severe postpartum endometritis)
Postpartum hemorrhage (PPH) by itself usually does not cause consumptive coagulopathy unless associated with increased release of tissue factor but can lead to a dilutional coagulopathy. Prolonged retention of a dead fetus over several weeks is now a rare cause of DIC because these cases are identified early and delivered without significant delay. (See 'Causes' above.)
●Prevalence – The prevalence of DIC in pregnancy ranges from 0.03 to 0.35 percent in population-based studies or 12.5 per 10,000 delivery hospitalizations (0.13 percent). Although the overall prevalence of DIC is low in pregnancy, the frequency of DIC in patients with specific pregnancy complications, such as amniotic fluid embolism or placental abruption, can be very high. (See 'Prevalence' above.)
●Diagnosis – The diagnosis of acute DIC in a pregnant patient is made when the clinical setting is appropriate and there is laboratory evidence of consumptive coagulopathy characterized by thrombocytopenia, coagulation factor consumption (eg, prolonged prothrombin time [or international normalized ratio] and activated partial thromboplastin time; low fibrinogen), and fibrinolysis (eg, increasing D-dimer, thromboelastography evidence of accelerated fibrinolysis). Bleeding is often present but is not required for diagnosis. (See 'Clinical findings' above and 'Diagnostic evaluation' above and 'Diagnosis' above.)
●Differential diagnosis – The differential diagnosis of DIC in pregnancy includes other causes of bleeding, thrombosis, and/or organ damage, which may coexist with DIC or contribute to its pathogenesis. These include PPH with dilutional coagulopathy, primary thrombotic microangiopathy, von Willebrand disease, antiphospholipid syndrome, pulmonary embolism, heparin-induced thrombocytopenia, and transfusion reaction. (See 'Differential diagnosis' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Kirk D Ramin, MD, and Susan Ramin, MD, who contributed to earlier versions of this topic review.
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