Hematology · Coagulation Disorders
The facts most likely to be tested
DIC is a pathologic activation of coagulation characterized by the systemic formation of fibrin thrombi leading to the consumption of platelets and clotting factors.
The most common obstetric trigger for DIC is abruptio placentae, which releases tissue factor into the maternal circulation.
Laboratory findings in DIC include prolonged PT and PTT, thrombocytopenia, and hypofibrinogenemia.
The most sensitive and specific laboratory marker for DIC is an elevated D-dimer, reflecting secondary fibrinolysis.
Peripheral blood smear in DIC classically reveals schistocytes (fragmented red blood cells) due to microangiopathic hemolytic anemia.
The primary management strategy for DIC is the treatment of the underlying cause (e.g., sepsis, trauma, or obstetric emergency).
Blood product replacement in DIC is reserved for patients with active bleeding or those requiring invasive procedures, prioritizing platelets, cryoprecipitate, and fresh frozen plasma.
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A 32-year-old G2P1 woman at 36 weeks gestation presents to the emergency department with severe abdominal pain and vaginal bleeding. Physical examination reveals a firm, tender uterus and fetal heart rate decelerations. Shortly after admission, she develops oozing from her IV sites and petechiae on her extremities. Laboratory studies show a low platelet count, prolonged PT and PTT, and a markedly elevated D-dimer.
What is the most appropriate next step in the management of this patient's coagulopathy?
Emergent delivery of the fetus
The patient is presenting with DIC secondary to abruptio placentae; the most critical step is treating the underlying cause, which in this obstetric emergency is immediate delivery.
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High yield triage
Etiology / Epidemiology
Triggered by sepsis, obstetric complications, or malignancy. Pathologic activation of coagulation leads to systemic microthrombi and consumption of clotting factors.
Clinical Manifestations
Simultaneous bleeding and thrombosis. Look for purpura fulminans and oozing from venipuncture sites.
Diagnosis
Diagnosis via coagulation profile: low platelets, prolonged PT/PTT, and low fibrinogen. Elevated D-dimer is the most sensitive marker.
Treatment
Treat the underlying cause. Replace platelets and FFP only if active bleeding occurs. Avoid heparin in most cases.
Prognosis
High mortality rate. Multi-organ failure is the primary cause of death.
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Epidemiology & Etiology
DIC is a secondary complication of systemic disease, most commonly Gram-negative sepsis. Other high-yield triggers include Abruptio placentae, acute promyelocytic leukemia, and severe trauma. It represents a systemic breakdown of the coagulation-fibrinolysis balance.
Pertinent Anatomy
The systemic vasculature is the primary site of pathology. Microvascular thrombosis leads to end-organ ischemia in the kidneys, lungs, and brain.
Pathophysiology
Excessive tissue factor release activates the extrinsic coagulation pathway, causing widespread microvascular fibrin deposition. This consumes platelets and coagulation factors, leading to a paradoxical hemorrhagic state. Secondary fibrinolysis further degrades clots, producing high levels of fibrin degradation products.
Clinical Manifestations
Patients present with oozing from IV sites, mucosal bleeding, and purpura fulminans. End-organ failure (renal, hepatic, respiratory) is a critical red flag. Thrombotic complications may manifest as digital gangrene or deep vein thrombosis.
Diagnosis
The coagulation profile is the diagnostic standard. Expect thrombocytopenia (<100k), prolonged PT/PTT, and hypofibrinogenemia (<100 mg/dL). An elevated D-dimer or fibrin split products confirms the presence of excessive fibrinolysis.
Treatment
Management focuses on the underlying trigger (e.g., antibiotics for sepsis, delivery for obstetric causes). Replace platelets for counts <20k or FFP for prolonged PT/PTT if active bleeding is present. Heparin is strictly reserved for cases with prominent thrombosis or purpura fulminans.
Prognosis
Prognosis is dictated by the severity of the underlying disease. Multi-organ failure is the leading cause of mortality. Serial monitoring of fibrinogen levels is required to assess disease progression.
Differential Diagnosis
TTP: characterized by the pentad of fever, anemia, thrombocytopenia, renal failure, and neuro symptoms without coagulopathy
ITP: isolated thrombocytopenia without prolonged PT/PTT
Vitamin K deficiency: normal platelet count and fibrinogen levels
Liver failure: prolonged PT/PTT but usually normal or elevated fibrinogen
HELLP syndrome: specific to pregnancy with elevated liver enzymes and hemolysis