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Post-Abortion Vaginal Hemorrhage with Disseminated Intravascular Coagulopathy (DIC)

Case Introduction

A 23-year-old G3P2 woman presented to the emergency department (ED) early in the morning for heavy vaginal bleeding approximately 24 hours after an elective dilation and curettage (D&C) for twin gestation at 13 weeks. This procedure was performed at an outside facility and was unremarkable according to the patient. Post procedure, she had light spotting which became increasingly heavy during the evening prior to presentation. At the time of presentation to the ED, the patient stated that she was using at least one pad per hour. Her medical history was significant for iron deficiency anemia.
On initial evaluation, her blood pressure was 86/53, her heart rate was 100, she was diaphoretic and pale. The patient was mentating well. She had mild suprapubic tenderness. A pelvic examination was notable for bright red blood pooling in the vaginal vault, and she had a syncopal event during the examination. The patient was subsequently moved to the resuscitation area, a massive transfusion protocol (MTP) was initiated empirically.
Her initial laboratory values were notable for the following:
  • Hemoglobin of 7.3 g/dL (normal 12 – 16.0)
  • Platelet count 84 thou/cu mm (normal 140 – 440)
  • INR 4.0 (normal 0.9 – 1.1)
  • D-dimer > 20,000 ug/mL (normal 0.00 – 0.49)
  • Fibrinogen < 60 mg/dL (normal 186 – 461)
Her emergency department resuscitation included fresh frozen plasma (FFP), cryoprecipitate, packed red blood cells (PRBC), and platelets. She was intubated and received blood products in the emergency department. She was Rh+ and RhoGAM was not administered. The obstetrics and gynecology service was consulted emergently.

Discussion

Disseminated intravascular coagulation (DIC) is a widespread hypercoagulable state characterized by widespread activation of coagulation leading to fibrin deposition in the vasculature, organ dysfunction, consumption of clotting factors and platelets and life threatening hemorrhage1Papageorgiou, Chrysoula, et al. “Disseminated intravascular coagulation: an update on pathogenesis, diagnosis, and therapeutic strategies.” Clinical and applied thrombosis/hemostasis 24.9_suppl (2018): 8S-28S. The definition of DIC emphasizes that DIC originates, develops within, and affects the microvasculature and is not restricted to the site of insult, but spreads throughout the body.2 Popescu, Narcis I., Cristina Lupu, and Florea Lupu. “Disseminated intravascular coagulation and its immune mechanisms.” Blood, The Journal of the American Society of Hematology 139.13 (2022): 1973-1986.
pathogenesis of DIC
Pathogenesis of disseminated intravascular coagulation. DIC is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to microvascular thrombi contributing to multi-organ dysfunction. Furthermore, consumption of clotting factors and platelets can result in life-threatening hemorrhage.1Polimeni, Alberto, et al. "Differences in coagulopathy indices in patients with severe versus non-severe COVID-19: a meta-analysis of 35 studies and 6427 patients." Scientific Reports 11.1 (2021): 10464.

Differential Diagnosis:

  • Dysfibrinogenemia
  • Hemolytic uremic syndrome
  • Heparin-induced thrombocytopenia
  • Immune thrombocytopenia (ITC) in emergency medicine
  • Thrombotic Thrombocytopenic Purpura (TTP)

In terms of clinical presentation, DIC is invariably associated with high acuity presentations with a severe or life threatening diagnosis. A 1996 study in Japan found that a DIC accompanied about 1% of admissions to university hospitals.3Matsuda T. Clinical aspects of DIC–disseminated intravascular coagulation. Pol J Pharmacol. 1996 Jan-Feb;48(1):73-5. In patients with acute lymphoblastic leukemia, 12% of cases presented with DIC before starting chemotherapy and 78% of cases during remission induction.4Okajima K, Sakamoto Y, Uchiba M. Heterogeneity in the incidence and clinical manifestations of disseminated intravascular coagulation: a study of 204 cases. Am J Hematol. 2000 Nov;65(3):215-22.

petechiae and purpura on exam as seen in DIC
petechiae and purpura on exam as seen in DIC (not our patient)2healthjade.net, "Disseminated intravascular coagulation"
The etiology can be either infectious or non-infectious. Not only limited to severe systemic infections, DIC can be seen with malignancy, trauma, obstetric complications as is the case with our patient, vascular malformations, severe immunological reactions, and heat stroke. Essentially, DIC follows exposure to or production of procoagulants insufficiently balanced by endogenous anticoagulant and fibrinolytic mechanisms. In patients with severe post abortion bleeding, as is the case with our patient, DIC should be considered. The incidence is estimated to be between 180 and 200 cases per 100,000 second trimester abortions5 Pazol K, Gamble SB, Parker WY, et al. Abortion surveillance—United States, 2006. MMWR Surveill Summ. 2009 Nov 27;58(8):1–35.

The clinical presentation of DIC can vary widely, from asymptomatic, to mild, to overwhelming thrombosis or bleeding. Most patients will have a clear underlying condition which prompted the development of DIC such as severe infection, trauma, malignancy, etc. Patients may experience bleeding from multiple unexpected sites such as the mouth, areas of trauma or recent surgery, vagina, rectum, indwelling catheters or devices. DIC can affect the kidneys, resulting in hematuria or even anuria. Other end organ dysfunction can present accordingly such as dyspnea or respiratory failure if pulmonary hemorrhage or pulmonary embolism is present or neurological symptoms if thrombosis or hemorrhage occur in the brain. Patients may also have skin lesions, ecchymosis and hematomas from seemingly innocuous contact. Jaundice from liver failure, necrosis and gangrene can occur. Patients may have purpura, petechiae and cyanosis.

example of massive transfusion protocol
Example of massive transfusion protocol.3blood.gov.au, "Massive transfusion protocol template"
Diagnosing DIC requires a combination of subjective, objective and laboratory findings. Typical laboratory findings include an increased prothrombin time (PT) and an increased partial thromboplastin time (PTT). Fibrinogen is decreased as the body consumes clotting factors while d-dimer is typically elevated due to clot turnover. Platelets and hemoglobin are typically reduced. On peripheral blood smear, schistocytes and fragmented erythrocytes can be seen. The ISTH criteria for DIC can be used to help confirm the diagnosis and uses platelet count, fibrin related markers (d dimer or fibrin degradation products), prolonged PT and fibrinogen level.6https://www.mdcalc.com/calc/10203/isth-criteria-disseminated-intravascular-coagulation-dic
Treatment of DIC involves both addressing the underlying condition which triggered the cascade as well as supportive therapy to help reverse the excessive clotting and bleeding. For example, a patient in septic shock would require antibiotics or delivery for placental abruption. Blood products should be administered in patients who are unstable with significant changes in normal laboratory values. Patients often require some combination of packed red blood cells, platelets, fresh frozen plasma and cryoprecipitate. Heparin may need to be considered if the clot burden is extensive or prophylactically if they are not actively bleeding.

Case Conclusion

She was resuscitated in the ED using a massive transfusion protocol. She was taken emergently to the operating room for a suction D&C with OBGYN and uterine artery embolization with Interventional Radiology. A point-of-care ultrasound in the OR did not identify any free fluid in the pelvis and the decision was made to forego an exploratory laparotomy. The patient also received misoprostol, oxytocin and methergine perioperatively. She did well postoperatively and was discharged on post op day 3 in good condition. The patient did not follow up as an outpatient and was subsequently lost to follow up after discharge.

3 Key Points

  1. DIC is characterized by a widespread activation of coagulation leading to fibrin deposition in the vasculature, organ dysfunction, consumption of clotting factors and platelets and life threatening hemorrhage
  2. Diagnosis involves the clinical picture as well as laboratory abnormalities (low platelets, low hemoglobin, high PT/INR, low fibrinogen, high d dimer, high fibrinogen degradation products)
  3. Treatment is directed at the underlying condition as well as supportive measures typically involving blood products and clotting factors

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