DIC/anticoagulation reversal Flashcards
(32 cards)
What is the Pathophysiology of HIT?
HIT - thrombocytopenia but causes thrombotic problems, occurs w LMWH too; usually in 1st week
What are the findings in HIT?
Thrombocytopenia: < 150, 50% decrease from baseline
Thrombosis: arterial or venous
Timing: generally 5-10 days after starting heparin
No other explanation
Necrotic skin lesions, skin necrosis
What is the treatment for HIT?
Tx : stop heparin/LMWH; start alternative anticoagulant ( lepirudin, bivalirudin or argatroban), reverse warfarin. Avoid warfarin and avoid platelet transfusions
Presentation of TTP-
10-40 yo female, thrombocytopenia, microangiopathic hemolytic anemia (schistocytes, frag RBC’s), fluctuating neuro sx, renal dz, fever.
Findings in TTP-
Fever, anemia (microangiopathic hemolytic- Increased unconjugated bili, LDH, decreased haptoglobin), thrombocytopenia, renal abnormalities, neurologic
(thrombosis)
Low platelets, normal coagulation factors, normal fibrinogen, MAHA, platelet plugs
Treatment of TTP-
Tx: Steroids, dialysis if renal failure, Plasma exchange dramatically ↓ mortality, FFP (gives back ADAMTS13)
-avoid plts
Presentation of ITP?
ITP
Acute: 2-6 yo, prior viral prodrome, self-limited with in few weeks to months
Adults if have, usually present with platelets < 10,000
Treatment of Acute ITP?
Tx : supportive care; if severe bleeding (platelets < 50,000) or platelet < 20,000
RBCs for resuscitation and anemia
Steroids: impaired clearance of Ab coated platelets
IVIG (1 gm/kg): <5,000 platelets and completed steroid course
Treatment of Acute Pediatric ITP?
Pediatrics: controversial, usually self resolves, consider if concern for ICH- need to discuss with hematologist
Treatment of Chronic ITP?
Chronic: mostly adult female, insidious onset, r/o other dz (SLE, lymphoma, etc)
Tx: consider steroids and splenectomy; life threatening bleed IV IgG and plt transfusion, immunosuppression, rituximab, thrombopoietin agonist
<50,000 and asymptomatic- no treatment
<50,000 and symptomatic- steroids
<20,000- IV methylpred
<20-30,000 with active bleeding- IVIG
Treatment of ITP in pregnancy?
Pregnancy: count should be maintained > 30,000 and 50,000 near term
Presentation of Hemolytic Uremic Syndrome
HUS - similar to TTP, less CNS, more renal (child w E Coli 0157:H7); age 6 mo-4yo;
Treatment of Hemolytic Uremic Syndrome
Tx: supportive care and admit; plasma exchange, Abx may worsen; dialysis if renal failure
-avoid plts
What is the pathophysiology of Hemophilia A -
Hemophilia A - ↓VIII, prolong PTT
What is the treatment of Hemophilia A?
Tx : recomb VIII, VIII conc: Mild bleeding (hematuria, early hemarthrosis, laceration) 12.5 units/kg, Moderate (oral lacerations, dental, late hemarthrosis) 25 units/kg,
severe (CNS, GI, major trauma/surgery) 50 units/kg. Each unit/kg increases plasma factor VIII level by 2%
-Cryo if no recombinant VIII- one bag has 80-100 units of factor VIII
-FFP increases by 3-5%- limited use
-DDAVP for acute bleeding or prophylaxis (0.3mcg/kg/dose IV)
-Ice, compression, and splinting
-Consult Heme
Pathophysiology of Von Willebrand’s Dz -
Von Willebrand’s Dz - ↓VIII:vwf (need for plt adhesion and causes plt malfunction) (also ↓VIII) nl PT, PTT but bleeding time increased; most common hereditary
blood d/o.
Type 1 (decreased vWF), type II (abnormal or dysfunctional vWF), type III (no vWF)
Treatment of Von Willebrand’s Dz-
Tx : DDAVP 0.3mcg/kg
-Humate P- factor VIII conc
-Cryo- 10 units/kg
-FFP- limited use due to volume overload
Pathophysiology of Hemophilia B (Xmas Dz) -
Hemophilia B (Xmas Dz) - ↓IX, sex linked; Inc PTT, nl PT
Treatment of Hemophilia B (Xmas Dz)-
Tx : recomb IX or IX conc : minor 25 units/kg, moderate 50 units/kg, severe 100 units/kg. Increases activity by 1%
-FFP if no recomb IX
Pathophysiology of DIC -
DIC - ↓plt, schistocytes, ↑PT/PTT/TT, ↓fibrinogen, ↑or↓ D-dimer, inc FSP.
1. Thrombin generation, small vessel thrombosis and consumption of clotting factors and platelets.
2. Concomitant activation of fibrinolytic system–>breakdown of fibrin clots and subsequent bleeding
Trigger → loss of localization or compensated control in the intravascular activation of coagulation
Causes of DIC-
Causes: Sepsis (most common), leukemia, carcinoma, trauma, pancreatitis, liver disease, pregnancy, snake bite, ARDS, transfusion, transplant
DIC Clinical Findings-
Clinical findings:
Sepsis: hypercoagulation may predominate (cutaneous gangrene, thrombotic purpura)
Inflammation induces synthesis of fibrinogen→ normal or elevated levels of fibrinogen→ more hypercoagulable
Avoid blood products unless bleeding, purpura fulminans may require plasma exchange
Leukemia: hyperfibrinolysis (petechiae, ecchymosis, oozing, hematuria)
Trauma/OB: hypercoagulation and hyperfibrinolysis (major bleeding complications)
Some maybe subclinical
DIC Lab Findings:
Lab findings:
Thrombocytopenia (Most common), prolonged PT, low fibrinogen, elevated D dimer
Tx: tx underlying cause (infx, obstetric pathology, trauma, malignancy, drugs, transfusion) and predominant sx
DIC Treatment:
