Disseminated Intravascular Coagulation (DIC)


Article Author:
Ryan Costello


Article Editor:
Sara Nehring


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
5/3/2019 7:31:58 PM

Introduction

Disseminated intravascular coagulation (DIC) can be defined as a widespread hypercoagulable state that can lead to both microvascular and macrovascular clotting and compromised blood flow, ultimately resulting in multiple organ dysfunction syndrome or MODS. As this process begins consuming clotting factors and platelets in a positive feedback loop, hemorrhage can ensue, which may be the presenting symptom of a patient with DIC. Disseminated intravascular coagulation typically occurs as an acute complication in patients with underlying life-threatening illnesses such as severe sepsis, hematologic malignancies, severe trauma, or placental abruption. Determining the consequences of DIC and the overall mortality rate of DIC remains difficult as patients with this condition also have additional diagnoses that can cause many of the signs and symptoms consistent with DIC, particularly if they are also suffering from acute or chronic liver failure. While concomitant disease states can obscure a patient’s prognosis, mortality rates have been shown to double in septic patients or those with severe trauma if they are also suffering from DIC.[1][2][3][4][5]

Etiology

Multiple medical conditions can lead to the development of disseminated intravascular coagulation either through a systemic inflammatory response or the release of procoagulants into the bloodstream. The pathological process of DIC has been estimated to occur in up to 30% to 50% of cases of severe sepsis, which is the most common cause of DIC. Classically, DIC has been associated with gram-negative bacteria sepsis, though the prevalence of this disorder in sepsis due to gram-positive organisms may, in fact, be similar. Other causes of sepsis, including parasites, can also lead to DIC. Up to 20% of patients with metastasized adenocarcinoma or lymphoproliferative disease also suffer from DIC in addition to one to five percent of patients with chronic diseases like solid tumors and aortic aneurysms. Obstetrical complications such as placental abruption, hemolysis, elevated liver enzymes, and low platelet count (HELLP syndrome), and amniotic fluid embolism have also been known to lead to DIC. Other causes of DIC include trauma, pancreatitis, malignancy, snake bites, liver disease, transplant rejection, and transfusion reactions. About 15.5% of cases of DIC have also been linked to complications occurring after surgery.[6][7][8][9][10][11]

Epidemiology

Because DIC is a complication of other medical diagnoses, the prevalence of DIC remains greater in higher acuity settings as opposed to lower acuity settings. Almost invariably, a severe or life-threatening diagnosis is associated with the disease. A 1996 study in Japan found that a diagnosis of DIC complicated about 1.0% percent of admissions to university hospitals. Similarly, a 1992 study showed DIC complicated 12% of cases of acute lymphoblastic leukemia before starting chemotherapy, and DIC was detected in 78% of cases during remission induction. Furthermore, HELLP syndrome was associated with DIC in approximately one in five cases, according to a 1993 study. [12][13][14][15]

Pathophysiology

Also referred to as consumptive coagulopathy, DIC involves the homeostatic imbalance between coagulation and bleeding. Tissue factor (TF), which may be released into the circulation from vascular endothelial damage from trauma or certain cancer treatments, bacterial endotoxins, or cytokine exposure, activates coagulation factor VII to VIIa in the coagulation pathway. Via the extrinsic pathway, thrombin and fibrin are formed and result in the formation of clots in the circulation. As this process continues, thrombin and fibrin further impair the coagulation cascade through positive feedback loop stimulation and coagulation inhibitor consumption. Clotting factors, as a result, are consumed due to clotting, which can lead to excessive bleeding. Platelets also may become trapped and consumed in this process. Additionally, pathways including the protein C system and antithrombin III appear to be dysregulated in DIC. Furthermore, an increase in plasma activator inhibitor-1 (PAI-1) can prevent the inhibition of fibrinolysis. [11][5]

History and Physical

Components of a patient’s history that may be consistent with disseminated intravascular coagulation include a recent history of severe infections or trauma as well as hepatic failure, obstetric complications, and malignancy. A remote history of deep vein or arterial thromboses may also be suggestive of DIC. Patients may experience bleeding from multiple sites including gingiva, areas of trauma or surgery, the vagina, the rectum, or through devices such as urinary catheters. Symptoms such as hematuria, oliguria, and anuria may be seen if concomitant renal failure from DIC results. Likewise, end-organ damage to the lungs may lead to dyspnea and hemoptysis if pulmonary hemorrhage or pulmonary embolism is occurring and a patient may have mental status change if either thrombi or hemorrhage to areas of the brain arise. A patient could also experience chest pain if arterial occlusion of a coronary artery develops. Regarding signs of DIC on physical exam, obvious bleeding, or frank hemorrhage in various areas of the body may be noted. Skin lesions including ecchymosis, hematomas, jaundice from liver failure, necrosis, and gangrene may also arise. Excessive coagulation may lead to widespread purpura, petechiae, and cyanosis. A patient in DIC may also experience acute respiratory failure or neurological deficits based on the location of bleeding or clots. [16][17][11]

Evaluation

No single history, physical exam, or laboratory component can lead to a diagnosis of or rule out DIC; therefore, a combination of both subjective, objective, and laboratory findings should be utilized to make a diagnosis of DIC. Laboratory findings suggestive of DIC include both an increased prothrombin time (PT) and an increased partial thromboplastin time (PTT), as well as a decreased fibrinogen level as widespread activation and consumption of the clotting cascade occurs. The overall platelet count and hematocrit level may be reduced as well. Schistocytes or fragmented erythrocytes are also commonly seen on a peripheral blood smear. The presence of fibrin split products additionally has a high sensitivity but low specificity for the presence of DIC. A specific scoring system to assess for the presence of DIC was established in 2007. This score includes platelet count, fibrin markers such as D-dimer, prolonged PT, and fibrinogen level with a score over five indicating a high likelihood for overt DIC. [18][19][20][21]

Treatment / Management

The treatment for DIC centers on addressing the underlying disorder, which ultimately led to this condition. Consequently, therapies such as antibiotics for severe sepsis, possible delivery for placental abruption, and possible exploratory surgical intervention for trauma represent the mainstays of treatment for DIC. Platelet and plasma transfusions should only be considered in patients with active bleeding or a high risk of bleeding or those patients requiring an invasive procedure. A common threshold utilized for platelet transfusions in this patient population is less than 50 x 10^9 platelets per liter for actively hemorrhaging patients and 10-20 x 10^9 platelets per liter for those not actively bleeding but at high risk of future bleeding. Likewise, fresh frozen plasma, typically at a dose of 15 mL/kg to 30 mL/kg, and cryoprecipitate can be transfused to replenish coagulation factors. Prothrombin complex concentrate may also be considered; however, this formulation only contains some coagulation factors and will only somewhat correct a patient’s hemostasis. Heparin may also become necessary if a patient has extensive clotting as this medication may prevent further activation of the clotting cascade. Patients with DIC who are not actively bleeding should receive prophylactic anticoagulation with heparin or low molecular weight heparin (LMWH). Other treatment options with human activated protein C, particularly in severe sepsis, may also be effective. [11][19][20][22][5]

Pearls and Other Issues

Disseminated intravascular coagulation can quickly lead to multi-organ failure and death, particularly if early recognition and treatment fail to occur. A high index of suspicion of this high mortality disease in critically ill patients remains paramount to improve outcomes in patients with DIC.

Enhancing Healthcare Team Outcomes

The diagnosis and management of DIC is complex and challenging. The condition is best managed by a multidisciplinary team that possibly consists of a hematologist, surgeon, intensivist, infectious disease consultant, pathologist, and an internist. The key is to address the underlying disorder that ultimately led to this condition developing. Consequently, therapies such as antibiotics for severe sepsis, possible delivery for placental abruption, and possible exploratory surgical intervention for trauma represent the mainstays of treatment for DIC. Platelet and plasma transfusions should only be considered in patients with active bleeding or a high risk of bleeding or those patients requiring an invasive procedure. Despite optimal treatment, DIC carries a very high mortality rate. Because DIC affects many organ systems, most survivors have a prolonged recovery period. [16][23](Level V)

 

 

 


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Disseminated Intravascular Coagulation (DIC) - Questions

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A 71-year-old patient undergoes surgery for colorectal cancer. Postoperatively, the patient develops an intra-abdominal abscess. Despite antibiotic therapy, the patient has persistent fever and develops hematemesis and melena in association with a purpuric skin rash. Laboratory tests reveal 70,000 platelets/microliter, prolonged prothrombin time (PT), and decreased fibrinogen. What is the appropriate treatment for this patient's suspected condition?



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Which of the following is not a feature of disseminated intravascular coagulation (DIC)?



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What is the most appropriate initial treatment regimen in a patient with disseminated intravascular coagulation secondary to bacterial sepsis?



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Which of the following is not commonly seen with disseminated intravascular coagulation (DIC)?



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A 76-year-old female on Day 8 of her hospitalization for a car accident was transferred to the ICU overnight due to bleeding, elevated aPTT and INR, thrombocytopenia, and an elevated D-dimer. Which of the following physical exam findings would be most likely in this scenario?



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A 28-year-old female is one day postpartum and is noted to have purpura, widespread petechiae, and mucocutaneous bleeding on morning rounds. Which of the following laboratory findings is least likely in this patient based on her most likely current condition?



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A 28-year-old pregnant female in her third trimester presents to the ED for fever, confusion, and vaginal bleeding, epigastric pain, and hypertension. On physical examination, she is noted to have gingival bleeding and a petechial rash. You initially order labs for fibrin degradation products, aPTT, INR, CBC, CMP, and a peripheral blood smear. Which of the following conditions should the patient also be screened for at this time?



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A 28-year-old pregnant female in her third trimester presents to the ED for fever, confusion, and vaginal bleeding, epigastric pain, and hypertension. On physical examination, she is noted to have gingival bleeding and a petechial rash. You initially order labs for fibrin degradation products, aPTT, INR, CBC, BMP, and a peripheral blood smear. What is the next step in the management of this patient?



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An 86-year-old female begins to develop petechiae and an elevated aPTT and INR. The patient developed pneumonia in the recent past and had failed to respond to successfully yo the management. Her Foley catheter output this morning was also noted to be bloody. In addition to the activation of factor VII via tissue factor, what other pathways may be affected in the above condition?



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Which of the following physical exam finding is not consistent with disseminated intravascular coagulation (DIC)?



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In which of the following patients with schistocytes on the peripheral blood smear, a petechial rash, and an elevated aPTT as well as INR should the administration of platelets be highly considered?



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A 63-year-old female is brought to the emergency room with a febrile illness for two days that has not improved. The patient is in shock and has purple, non-blanching skin papules that vary in size over the extremities and trunk. There are also petechiae noted. The peripheral blood smear shows thrombocytopenia and fragmented red blood cells. Which of the following additional laboratory findings would be most likely in this patient?



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An 11-year-old female is brought to the emergency department with epistaxis and hematochezia. Laboratories show INR is 1.5 (0.9-1.2), activated partial thromboplastin time of 48 seconds (control 36 seconds), platelet count of 45,000/microliter, and factor VIII level at 16% (50%-200%). What is a feared complication of the most likely diagnosis in this patient?



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A patient with multiple abdominal stabbings is taken to the operating room for surgery. He has major lacerations to the liver, spleen, small bowel, pancreas, and stomach. During the prolonged surgery, which is massively contaminated with gastric and intestinal contents, the surgeon notes profuse bleeding from all the cut edges. Immediate blood work reveals prolonged coagulation times, thrombocytopenia, elevated fibrin degradation products, and elevated D-dimer levels. What finding on a peripheral blood smear will strengthen the diagnosis of this suspected pathology?



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A patient with multiple abdominal stabbings is taken to the operating room for surgery. He has major lacerations to the liver, spleen, small bowel, pancreas, and stomach. During the prolonged operation, where gastric and intestinal contents massively contaminated the surgical area as well, the surgeon notes profuse bleeding from all the cut edges. Immediate blood work reveals prolonged coagulation times, thrombocytopenia, elevated fibrin degradation products, and elevated D-dimer levels. What is the most important goal in the management of this patient?



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A 77-year-old female was admitted to the intensive care unit three days ago for septic shock secondary to pyelonephritis. This morning, she was found to have gross hematuria in her urinary catheter as well as petechiae on her lower extremities. Laboratory studies revealed a white blood cell count of 27.6, a hemoglobin of 7.8 g/dL, a platelet count of 37, an elevated PT and PTT, a sodium of 135, a potassium of 4.9, a chloride of 101, a bicarbonate of 23, a BUN of 76, and a creatinine of 5.9. What is the pathophysiology of the most likely concomitant disease this patient is now suffering?



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A 52-year-old male who was recently diagnosed with colon cancer underwent a right hemicolectomy 3 days prior. As the night doctor, you receive a call from the floor nurse that the patient is having new onset altered mental status. You order a CT of the head, EKG, and chest x-ray that are all negative for any acute findings. Of note, his WBC has increased from 13.2 to 20. His hemoglobin has remained stable at 9.2, but his platelet count has dropped to 72 from 290 on the day of admission. A urinalysis is positive for leukocyte esterase, nitrites, mild hematuria, and WBCs. You check PT/INR and PTT, and they are slightly elevated. On physical exam, you note the presence of some petechiae that have not been mentioned in prior daily progress notes. At this time, how will you manage this patient?



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An on-call physician receives a call that he is soon to receive an ICU transfer from an outside facility. The charge nurse informs the physician that the patient is being transferred with anemia, thrombocytopenia, prolonged aPTT, and INR, and schistocytes noted on a peripheral blood smear. Before the patient arrives, the physician develops an action plan for the patient while considering the additional medical problems the patient is likely to have. What is the most likely additional disease process occurring in this patient?



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You are caring for a woman with a diagnosis of placental abruption on the mother-baby unit. During your 0400 rounds, signs of disseminated intravascular coagulation emerge. Which of the following assessment findings and clinical data would support the diagnosis? Select all that apply.



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Disseminated Intravascular Coagulation (DIC) - References

References

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