EMS Recap: Disseminated Intravascular Coagulation (DIC)

It’s 2:30 in the morning. You and your partner have been called to the parking lot of the local hot spot just after closing for a shooting. The police secured the scene prior to your arrival and you find a 32-year-old male with multiple gunshot wounds to the chest, abdomen and right leg lying between two cars. He is hypotensive and tachycardic with labored respirations. Your partner starts two large bore IVs, begins giving fluids and darts his chest as you perform your initial assessment. You see bright red blood steadily draining from the chest darts; the abdominal dressing rapidly soaks with blood and his IV sites are oozing blood. After intubating the patient you suction his endotracheal tube and find blood-tinged secretions. En route to the trauma center your patient’s limbs begin to feel cool, and his mucous membranes are becoming cyanotic. Based on the signs, symptoms and gunshot trauma, you suspect your patient may be experiencing disseminated intravascular coagulation, or DIC.

DIC is a bleeding and clotting condition with activation of the coagulation system, causing intravascular clots compromising blood supply to organs and bleeding from the exhaustion of platelets and coagulation factors.¹ The excessive clotting depletes clotting factors faster than the liver and bone marrow can replace them. The blood clots cause hypoperfusion of tissues and organs leading to ischemia, while the anticoagulants released to dissolve the clots trigger hemorrhages in other locations.² The sudden hemorrhages to the tissues beneath the skin and mucous membranes produce bruises.³

During the initial phase of DIC microvascular clots develop in the kidneys and lungs, causing acute renal failure and acute respiratory distress syndrome. Left untreated, wide-spread activation of fibrinolysis to dissolve the micro-clots also eliminates coagulation factors and platelets, leading to uncontrolled bleeding from wounds and spontaneous hemorrhage into the tissues, abdomen and the brain. Organ failure occurs as a result of hypercoagulopathy.¹

DIC never occurs alone. It is important to recognize whether your patient has a disorder that could result in development of DIC and manage your patient appropriately.³ DIC often occurs in patients with sepsis, malignancy, trauma, liver and vascular pathologies, arterial hypotension, and hypoxemia.² Underlying diseases frequently associated with DIC are acute promyelocytic leukemia, fulminant hepatitis, and sepsis.⁴ DIC is also possible in pregnancies complicated by placental abruption or amniotic fluid embolism. And finally, DIC may complicate poisoning, envenomation and major transfusion reactions.³ Mortality rates for DIC are the same for trauma and sepsis patients, with those who progress to late stage DIC and develop multiple organ dysfunction syndrome (MODS) having the lowest recovery prognosis.

Increased tissue factor production is the primary cause and septicemia is the most common clinical condition associated with DIC. Platelet destruction occurs in almost all cases of DIC.³ High tissue factor production and release results in the transformation of prothrombin to form clots, and bacterial infection is most often the cause of sepsis.¹ Vascular conditions that may precipitate DIC include large aortic aneurysms, giant hemangiomas and pathogenic pathways producing thrombin.⁵ Patients experiencing sepsis and DIC are two times more likely to die than someone experiencing sepsis without DIC.³

In trauma patients, there will always be tissue factor released and activation of the extrinsic coagulation pathway. Unchecked DIC will progress from a bleeding event to a clotting event sans sepsis, with severity of bleeding and organ dysfunction being a good predictor of progression to MODS.⁴ The first 24 to 48 hours after a traumatic injury is primarily a bleeding event. During the change to a hypercoagulable state, patients have an increased risk for clotting events leading to MODS.⁴ Multiple traumas in a patient precipitate DIC due to a combination of hemolysis, endothelial activation, releasing of tissue material in the circulation and acidosis from hypoperfusion.^1,5 Severity of DIC and organ dysfunction in the first 24 to 48 hours post traumatic injury is a good predictor of progression to late-phase DIC.⁴

Preeclampsia is the most common obstetric condition associated with the activation of blood coagulation and DIC with large clots in multiple organs in severe cases. Acute onset DIC occurs with placental abruption and amniotic fluid emboli. A woman surviving an acute amniotic fluid emboli is 50% more likely to develop DIC within four hours of the emboli.^1,5

With pediatric patients, DIC mortality rates are increased for children experiencing shock, regardless of their hemodynamic status. With children, DIC is the result of inflammation and damaging of the microvasculature that paves the way for the progression to MODS.⁶

When evaluating your patient in the prehospital environment, be alert for abrupt bleeding that quickly became severe, with blood oozing from venipuncture sites, surgical incisions, drainage tubes and partially healed wounds. Patients may also experience a GI bleed, genitourinary bleed, CNS bleed and have fingers, nose, toes and ears that may become cyanotic.² When assessing the skin, look for bruises and hemorrhages that do not blanche when pressed. Be alert for respiratory insufficiency, abdominal pain, confusion and seizures indicating poor perfusion.

Management of DIC in the field involves finding and treating your patient for the underlying disease or trauma, and providing supportive care.^1,3 DIC can spontaneously resolve when the underlying disorder is properly managed. Monitor pulse oximetry and provide ventilator assistance and oxygen as needed. Remove the triggering mechanism if possible. This may be intravenous fluids if the patient is hypovolemic or hypotensive, treating for hypoxemia, acidosis, or a transfusion reaction.

Avoid unnecessary needle sticks, use of manual and automatic BP cuffs, and other procedures that could cause bleeding, bruising or hematomas. Consider using low suction for tracheal or oral suctioning, and comfort measures with pain management.² For blood pressure control, Dopamine and other vasopressors are effective and the administration of low molecular weight heparin helps to block the formation of new clots if the patient has not had recent surgery, or a CNS or GI bleed.²

If blood products are available, packed red blood cells help to restore oxygen carrying capacity, fresh frozen plasma replaces clotting factors, cryoprecipitate can be given to replenish depleted fibrinogen, and platelet concentrate helps to correct thrombocytopenia.²

Be aware that if you are doing a critical care transport of a patient with DIC your patient has a high risk for venous thromboembolic events (VTEs) if they are older, have had recent surgery, have been immobilized, have an in-dwelling vascular catheter or have had previous VTEs.

References

1. Dalainas I. Pathogenesis, diagnosis, and management of disseminated intravascular coagulation: A literature review. European Review for Medical and Pharmacological Sciences, 2008; 12: 19–31.
2. Dressler DK. Coping with a coagulation crisis. Nursing, 2004; 34(5).
3. British Society for Haematology. Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Journal of Haematology, 2009; 145: 24–33.
4. Murakami H, Satoshi G, Hayakawa M, Sawamura A, Sugano M, Kubota N, Uegaki S, Jesmin S. Disseminated intravascular coagulation (DIC) at an early phase of trauma continuously proceeds to DIC at a late phase of trauma. Clinical and Applied Thrombosis/Hemostasis, 2012; 18(4): 364–369.
5. Levi M. Disseminated intravascular coagulation. Journal of Coagulation Disorders, 2011 Oct; 3(1).
6. Khemani RG, Bart RD, Alonzo TA, Hatzakis G, Hallman D, Newth CJL. Disseminated intravascular coagulation score is associated with mortality for children with shock. Intensive Care Medicine, 2009; 35: 327–333.

Robert E. Sippel, Major, USAF (Ret.), MS, MAEd, NREMT-P, LP is an assistant professor and clinical coordinator in the Emergency Health Science Department at the University of Texas Health Science Center, San Antonio, TX.