disseminated intravascular coagulation: a case-based approach
TRANSCRIPT
Oncology Nursing Society 43nd Annual CongressMay 17–20, 2018 • Washington, DC 1Clinical Practice
Rebecca Martin, BSN, RN, OCN, BMTCNStaff RN/Educator Froedtert Hospital [email protected]
Key Session Takeaways1. 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.
Disseminated Intravascular Coagulation: A Case-Based ApproachThursday, May 17 • 9:45–11 am
Note one action you’ll take after attending this session: ____________________________________________________
________________________________________________________________________________
ONS 43rd Annual Congress
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Disseminated Intravascular Coagulation: A Case-Based ApproachRebecca Martin BSN RN OCN BMTCN
Staff RN/Educator Froedtert Hospital/Medical College of Wisconsin
Disclosures
• I have no disclosures
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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 fibrinolysisThachil, et. al. 2014
Pathophysiology• Monocytes and endothelial cells are activated or
injured• Their response is to generate tissue factor on
the cell surface, activating the coagulation cascade
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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
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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
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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 variedFeinstein, 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
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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
Cancer Related DIC• Procoagulant• Hyperfibrinolytic• Subclinical
Procoagulant DIC• Increased thrombin leading to thrombosis• Adenocarcinoma and pancreatic• Symptoms
– Related to intravascular thrombosis• Treatment
– Treat underlying disorder– Consider anticoagulation
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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 Decreased
PT/PTT/INR Prolonged
Fibrinogen Decreased
FDP Increased
D‐Dimer Increased
RBC Morphology Presence of Schistocytes
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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
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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
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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
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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 AssessmentNeuro
HEENT
Genitourinary
Gastrointestinal
Cardiovascular
Respiratory
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)
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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
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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
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Clinical Practice 14
IVC Filter• Use only if evidence of LE DVT and
anticoagulation is not an option• Could activate the coagulation system
Case StudyJB
27 year old female
Past Medical History• Large T-cell lymphoma
– Diagnosed November
• Upon Diagnosis– DVT right upper extremity– Left lower lobe PE
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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
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Treatment Timeline
Martin, 2017
Transplant• Transplant statistics:
– No transplant-15% long term survival– Transplant- 40-50% 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
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Hospitalization Issues• Pancytopenia• Influenza• Diarrhea• Menorrhagia• Back pain• Skin rash
Readmission Week One
February5
Admit with URI symptoms, fever and diarrhea
6 7 8 9Afebrile, decreased diarrhea
10Febrile and increased diarrhea
11CT –new sites of ground glass infiltrates
Vanco and Cipro started
Vanco and Cipro dc’d
Vanco and Cipro restarted
Repeat BAL
Vanco dc’d
Readmission Week Two
February12 13
Diarrhea and rash
14 15Coagulopathy noted
16Colonoscopy
17 18
SteroidsFFP and
Vitamin K
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Readmission Week ThreeFebruary
19All biopsies negative
20Fevers Cultures NGTDSpleen and Kidney Infarcts
21Evidence of DICFluid overloadNegative Echo
22 23DIC continuesLarge right MCADecreased LOC
24Decreased LOCIncreased oxygen needsDIC Continues
25Herniation and minimal brain activity
Steroid taper
Vanco restarted
Lasix
Supportive Care –Blood
Products
Heparin drip
IntubationMannitol
HyperventilationHeparin drip
increased
Comfort Measures
Kidney Infarct
Used with permission from Froedtert Hospital
Splenic Infarct
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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; 86:828-33• 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 2016.
• Toh CH, Alhamdi Y. Current consideration and management of disseminated intravascular coagulation. American Society of Hematology. 2013; 1:286-91