Disseminated Intravascular Coagulation: A Case-Based Approach

Transcription

1 Disseminated Intravascular Coagulation: A Case-Based Approach Thursday, May 17 9:45 11 am Note one action you ll take after attending this session: Rebecca Martin, BSN, RN, OCN, BMTCN Staff RN/Educator Froedtert Hospital rebecca.martin@froedtert.com Key Session Takeaways 1. Attendees will be able to identify the early signs and symptoms of oncology-related disseminated intravascular coagulation (DIC). 2. Attendees will learn about treatment options for oncology-related DIC. 3. Attendees will be able to develop a nursing plan of care for the patient with oncology-related DIC. Clinical Practice Oncology Nursing Society 43nd Annual Congress May 17 20, 2018 Washington, DC 1

2 Disseminated Intravascular Coagulation: A Case-Based Approach Rebecca Martin BSN RN OCN BMTCN Staff RN/Educator Froedtert Hospital/Medical College of Wisconsin I have no disclosures Disclosures Clinical Practice 1

3 Objectives List risk factors of DIC in oncology patients Recognize signs and symptoms of DIC in oncology patients Discuss treatment strategies of DIC in oncology patients DIC An acquired syndrome characterized by the the simultaneous presence of thrombin and plasmin It can originate from and cause damage to the microvasculature If sufficiently severe, can produce organ dysfunction -subcommittee on DIC of the International Society on Thrombosis and Haemostasis Over activation of clotting cascade and fibrinolysis Thachil, et. al Pathophysiology Monocytes and endothelial cells are activated or injured Their response is to generate tissue factor on the cell surface, activating the coagulation cascade Clinical Practice 2

4 Toh, 2013 DIC Always occurs secondary to an underlying disorder Must recognize and treat the underlying disorder so that effective therapy can be instituted DIC DIC may occur in 30-50% of patients with sepsis Difficult to estimate frequency in oncology patients frequently diagnosed on autopsy A high mortality rate associated with DIC, however typically due to the underlying disease Clinical Practice 3

5 Cancer Related DIC First described by Trousseau in 1865 Most common malignancies APL Adenocarcinoma Breast, lung, prostate, colorectal Most commonly in stage III-IV Increased incidence with liver mets and increased age APL and DIC Most present with a coagulopathy Overproduction of plasmin and fibrinolysis Initiate all-trans-retinoic-acid immediately Will control DIC Keep platelets >20K Keep fibrinogen >100mg/dL Liver Disease and DIC Can decrease the production and function of platelets and fibrinogen Plays a significant role in treatment plan due to potential prognosis implications Clinical Practice 4

6 Solid Tumors and DIC Large prospective study in DIC and solid tumors (n=1117) Sallen, et.al. (2001) Significant independent factors Age, male, higher staged cancer, breast cancer, presence of necrosis in tumor specimen Management varied Feinstein, 2015 Solid Tumors and DIC Patients with advanced disease and DIC Median survival 9 months vs. 14 months without DIC Patients with stage I/II disease and DIC Median survival 16 months vs. 44 months without DIC Sallen, et.al. (2001) Solid Tumors and DIC Typically chronic and slow moving May lead to a normalized fibrinogen due to liver compensatory strategies Difficult to diagnose Serial lab observation Treatment of underlying disorder Clinical Practice 5

7 Solid Tumors and DIC Mechanism of action Generation of tissue factor by tumor cells Increased tissue factor binds to factor VII, activating factors IX and X Tissue factor is expressed by endothelial cells Endothelial cells regulate coagulation Procoagulant Hyperfibrinolytic Subclinical Cancer Related DIC Procoagulant DIC Increased thrombin leading to thrombosis Adenocarcinoma and pancreatic Symptoms Related to intravascular thrombosis Treatment Treat underlying disorder Consider anticoagulation Clinical Practice 6

8 Hyperfibrinolytic DIC Increased fibrinolysis APL and metastatic prostate Symptoms Bleeding Treatment Treat underlying cause Support Subclinical DIC Lab changes without bleeding or clotting Many solid cancers Symptoms None Treatment Treat underlying cause Monitor/trend labs Consider prophylactic anticoagulation Laboratory Findings Platelet PT/PTT/INR Fibrinogen FDP D Dimer RBC Morphology Decreased Prolonged Decreased Increased Increased Presence of Schistocytes Clinical Practice 7

9 Platelet Count An increased platelet count is a negative prognostic indicator in patients with DIC Short life span especially in DIC PT/PTT/INR May not be prolonged in cancer-related DIC Initial activation of the coagulation system by a malignancy can even shorten the PTT Potential for mild decrease in Subclinical DIC Abnormal in only 50% of sepsis-related DIC PT/PTT/INR Other causes of impairment in cancer patients Liver impairment Vitamin K deficiency Dysfibrinogenemia Paraproteinemias Acquired inhibitors of coagulation factors Clinical Practice 8

10 Fibrinogen Soluble protein Broken down by thrombin to form clots Procoaculant DIC Rarely decreased Hyperfibrinolytic DIC Extreme and rapid decrease D-Dimer Protein present in the blood after a blood clot is degraded by fibrinolysis Present once the coagulation system has been activated Normal value <0.5 Trend value in patients at risk for DIC D-Dimer False positives Liver disease Inflammation Malignancy Ascitis Pleural effusion Soft tissue picture Trauma Pregnancy Recent surgery Advanced age Insufficiently filled tube Clinical Practice 9

11 D-Dimer Hyperfibrinolytic DIC Very high Can be decreased with appropriate therapy Procoagulant and Subclinical DIC Varying leveles The International Society of Thrombosis and Hemostasis DIC Score Platelet Count >100K 0 points <100K 1 point <50K 2 points Fibrinogen >100 mg/dl 0 points <100 mg/dl 1 point Prothrombin Time Prolonged < 3 seconds 0 points Prolonged 3 5 seconds 1 point Prolonged 6 seconds 2 points D Dimer or FDP No increase 0 points Moderate increase 2 points Strong increase 3 points Clinical Manifestations Bleeding Renal dysfunction Hepatic dysfunction Respiratory dysfunction CNS involvement Other systemic signs/symptoms due to underlying pathophysiology Clinical Practice 10

12 Nursing Assessment Frequent physical assessments Watch for and report subtle changes Trend lab values Monitor vital signs every 1-2 hours Monitor I & O to avoid complications of dehydration Nursing Assessment Neuro HEENT Cardiovascular Respiratory Gastrointestinal Genitourinary Musculoskeletal Skin Pain Treatment Early recognition Treat the underlying problem Supportive care Inhibition of excess thrombin Per the ISTH-SCC (International Society on Thrombosis and Haemostasis, Scientific and Standardization Committee) Clinical Practice 11

13 Supportive Care DIC and active bleeding Keep platelets >50K Keep fibrinogen >100 mg/dl High risk for DIC APL keep platelets >30K Other keep platelets >20K Supportive Care What if volume is an issue? Consider use of Prothrombin Complex Concentrates Factor IX Beriplex, Octaplex, Kcentra Black box warning could stimulate DIC by activating the clotting cascade Supportive Care Cryoprecipitate Given if fibrinogen <100 mg/l Centrifuge FFP and collect the precipitate Factor VIII ABO compatible whenever possible Clinical Practice 12

14 Inhibition of Excess Thrombin Prothrombotic DIC Prophylactic anticoagulation Monitor platelet count and signs and symptoms of bleeding Subclinical DIC Anticoagulation has shown benefit Hyperfibrinolytic Avoid anticoagulation Anticoagulation Not contraindicated due to abnormal coags, without bleeding Heparin frequently preferred over LMWH Especially if high risk of bleeding or renal failure Easier to reverse Monitor anti-fxa activity (UFH level) not PTT Antifibrinolytic Agents Tranexamic Acid (Lysteda) or Animocaproic Acid (Amicar) Not shown to be effective in APL May be useful in therapy-resistant bleeding in Hyperfibrinolytic DIC Increase risk of DVT Recombinant Factor VIIa Uncertain efficacy Definite increase in thrombotic events Clinical Practice 13

15 IVC Filter Use only if evidence of LE DVT and anticoagulation is not an option Could activate the coagulation system Case Study JB 27 year old female Past Medical History Large T-cell lymphoma Diagnosed November Upon Diagnosis DVT right upper extremity Left lower lobe PE Clinical Practice 14

16 Presenting signs and symptoms Typical Painless swelling in the neck, arm pit or groin, loss of appetite or tiredness B symptoms JB s presenting signs and symptoms Right axillary and supraclavicular lymphadenopathy Swelling of the right arm, breast and neck Diagnosis Typical Lymph node biopsy Blood tests, x-rays, scans, bone marrow biopsy JB MRI Right supraclavicular node biopsy Negative bone marrow biopsy Diagnosis At time of diagnosis JB had compression of the right subclavian and axillary veins as well as DVT of right upper extremity 14 weeks pregnant Therapeutic pregnancy termination Clinical Practice 15

17 Treatment Timeline Martin, 2017 Transplant Transplant statistics: No transplant-15% long term survival Transplant % long term survival 2% TRM Conditioned with BEAM: carmustine, etoposide, ara-c, melphalan Auto transplant December Transplant course unremarkable-discharged on Day +12 with good engraftment Post-Transplant Readmission February Admitted after 48 hours of nausea, vomiting, diarrhea, fever, cough and rhinorrhea at home Clinical Practice 16

18 Pancytopenia Influenza Diarrhea Menorrhagia Back pain Skin rash Hospitalization Issues Readmission Week One 5 Admit with URI symptoms, fever and diarrhea Vanco and Cipro started February Afebrile, decreased diarrhea Vanco and Cipro dc d Febrile and CT new increased sites of diarrhea ground glass infiltrates Repeat Vanco and Cipro BAL restarted Vanco dc d Readmission Week Two Diarrhea and rash February Coagulopathy Colonoscopy noted Steroids FFP and Vitamin K Clinical Practice 17

19 Readmission Week Three February All Fevers Evidence DIC Decreased LOC Herniation biopsies Cultures of DIC continues Increased oxygen and negative NGTD Fluid Large right needs minimal Spleen and overload MCA DIC Continues brain Kidney Negative Decreased activity Infarcts Echo LOC Steroid taper Vanco restarted Lasix Supportive Care Blood Products Heparin drip Intubation Mannitol Hyperventilation Heparin drip increased Comfort Measures Kidney Infarct Used with permission from Froedtert Hospital Splenic Infarct Clinical Practice 18

20 Key Takeaways Identification of early signs and symptoms of oncology-related DIC Treatment options of oncology-related DIC Development of a nursing plan of care for the patient with oncology-related DIC References Thachil J, Falanga A, Levi M, Liebman H, Di Nisio M. Management of cancer-associated disseminated intravascular coagulation: guidance from the SCC of the ISTH. J Thromb Haemost 2015; 13:671-5 Feinstein, D. Disseminated intravascular coagulation in patients with solid tumors. Oncology-Journal 2015; 2. Sallah S, Wan JY, Hguyen NP, et al. Disseminated intravascular coagulation in solid tumors: clinical and pathologic study. J Thromb Haemost. 2001; 86: Anselmo M, Nobre de Jesus G, Lopes, J et al. Massive bleeding as the first clinical manifestation of metastatic prostate cancer due to disseminated intravascular coagulation with enhanced fibrinolysis. Case Reports in Hematology Toh CH, Alhamdi Y. Current consideration and management of disseminated intravascular coagulation. American Society of Hematology. 2013; 1: Clinical Practice 19