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Hematologic Disorders in the ICU

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Hematologic Disorders in the ICU Powered By Docstoc
					Hematologic Disorders
     in the ICU

  Bradley J. Phillips, M.D.
     Burn-Trauma-ICU
     Adults & Pediatrics
                     CASE # 1
   78 yom with rest pain R foot, ABI’s L 0.6, R 0.25
   PMH - PVD, COPD, HTN, ? Cirrhosis (EtOH)
   PSH - R CEA ‘97, R 1st Toe Amp ‘98
   Meds - Trental, Spirolactone, Inhalers
   SH - EtOH quit ‘90, Smoker 50 pk yrs. quit ‘95
   PE - ruddy complexion, L CEA scar, distant BS,
    mildly distended abd, R foot cool
   Pulses 1+ R fem, doppler only R Pop/DT/PT
                      CASE # 1

   Angiogram - severe plaque R ext iliac, occluded
    SFA, patent AK popliteal artery with marginal
    runoff via posterior tibia artery
   Labs - Plts 100K, Hct 30, INR 1.4, PTT 40, Tbil 2.1
   OR - exploration of R iliac with endarterectomy,
    femoral to AK popliteal bypass with reversed vein
   Blood Loss (intraop) 3 liters, given 6 units PRBC
   Postop - transferred to ICU, pulmonary toilet,
    heparin qtt for graft patency
                      CASE # 1
   Uneventful recovery until day 5, plt count dropped to
    60 K, then 30 K the next day
   Developed protracted bleeding from venopuncture
    sites and mild hematuria
   HO transfused 6 units plts, but bleeding continued
   ? Cause of hemorrhage ?
   ? Evaluation (ie. exam, labs) ?
   ? Plan of treatment ?
                          CASE # 1
   Plan
       Coagulation studies
         • R/O DIC
         • Exclude excessive anticoagulation with heparin
       LFT’s - R/O worsening liver dysfunction
       R/O Sepsis
         • Blood cultures
         • ? Broad-spectrum antibiotics
       R/O drug reaction
       ? Dilutional or consumptional thrombocytopenia
       ? Bone marrow aspiration
             Case # 1 - Workup

   Blood smear - thrombocytopenia, no
    fragmentation RBC
   Coags - PTT 13 s, PTT 50 s, FDP < 4 mg/l
   LFT’s - no significant changes from pre-op
   Blood cultures draw - initial read negative
   DX : HIT confirmed by heparin antibody
                               Hemostasis

Liver Disease                                                Nature of Abnormalities
Decreased and abnormal                                       Underlying liver disease
proteinsIntravascular consumption of      Liver              Severity of disease
factors Delayed clearance of activated                       Speed of onset of impairment
products




                                     Minimal generation of
                                     thrombin and plasmin




            Endothelium                                           Bone Marrow
           Thrombocytopenia (ICU)

   Causes (Common)                    Causes (Uncommon)
       Lab error - clumping               Liver Disease
        secondary to EDTA in               Hypersplenism
        test tube, need smear to           Bone marrow failure
        exam
                                           Drugs ( ie heparin,
       Sepsis                              immunosuppressives,
       Peripherial consumption             antibiotics)
       Dilutional                         Viruses
       Disseminated                       Rare diseases in surgical
        intravascular coagulation           patients (TTP, ITP)
        (DIC)
                  DIC

 Intravascular thrombin generated leads to
  consumption of both coagulation factors
  and platelets with secondary fibrinolysis
  releasing fibrin degradation products
 Severe thrombocytopenia, coagulopathy
                             DIC - Etiology
   Increased Tissue Factor               Thrombogenic
       Injured tissue                     Phospholipids
         • trauma                             Obstetric disorders
         • tissue necrosis                      • abruptio placentae
         • burns                                • eclampsia
       Stimulated monocytes or                 • amniotic fluid embolism
        endothelial cells                     Intravascular hemolysis
         • endotoxin                            • transfusion reactions
         • cell wall polysaccharides            • infections
         • immune complexes
                                              Ascitic fluid
       Endothelial sloughing from              • Leveen or Denver shunts
        acidosis ( pH < 7.2 , fully
        heparinized blood clots)
                  Clinical Presentation

   Bleeding                          Thrombosis
       More pronounced in liver       (microvascular)
        disease                           Organs at risk
       Wound bleeding                      •   Lungs (ARDS)
       Waterhouse-Friderichsen             •   Kidneys (ARF)
        Syndrome                            •   Liver
                                            •   Cardiac (MI)
                                            •   Brain (stroke)
                                          Purpura fulminans
                                            • gangrene of digits or
                                              skin necrosis
               DIC – Lab Findings

 Lab findings
    Procoagulant and fibrinolytic activation

    Reduced protein C and S activity

    Fibrin degradation products (FDP)

    Biochemical evidence of end organ dysfunction

 Low-grade DIC - near normal labs
    Trousseau’s syndrome

    Subacute bleeding (qualitative platelet defect from

     FDP)
                            DIC

   Laboratory findings
       Fribinolysis
         • FDP - measures fibrinogen and fibrin ( 85-100%)
         • D-dimer - measures plasmin degradation of cross-
           linked fibrin only ( 90%)
       PT (unreliable) - prolonged in 50 - 75%
       PTT (unreliable) - prolonged in 50%
       Platelets usually low
       Blood smear (schistocytes)
                                 DIC
 Management
    Identify and treat underlying condition
    Supportive care
    If condition rapidly reversible, watch and wait, use
     FFP and platelets as needed
    Stop microvascular thrombosis
      • consider heparin, tPA, or urokinase
            surgical intact vascular system
            actual or potentially serious bleeding or clotting
            Not rapidly reversible
    Control bleeding, use FFP and platelets as needed
    Heparin Induced Thrombocytopenia
                  (HIT)
   Heparin-dependent IgG antibodies which bind
    platelet-bound heparin through specific antigen
    binding
   Antibody Fc region then either binds complement
    or receptor on platelet membrance causing
    platelet activation and in vivo aggregation, in
    some causing thrombus formation
   Thrombocytopenia >> thrombosis
   Thrombosis = higher mortality
   Incidence 0.5 to 5.0 %
                     HIT - Diagnosis

 Seen 5-12 days or more after treatment
 Not dose-dependent, increased risk with length of
  treatment
 Platelet count < 100 K
 Diagnosis
       follow platelet count daily 3-5 days
       in vitro platelet aggregation studies (heparin antibody)
                     HIT - Treatment

   Treatment
       Stop heparin
       Danaparoid - immediate anticoagulant
         • cross reacts with plt factor 4 in 10% of cases
       Ancrod - snake venom enzyme
         • no cross-reactivity, take 12 hours to onset
         • contraindicated in sepsis and DIC
                         CASE # 2
 46 yom motorcyle vs car, + EtOH
 Hypotension in the field BP 90/P
 Arrival to trauma bay
       Airway patent, Breath sounds ok (RR 22)
       BP 90/P, HR 110
       Alert and oriented
       Given 2L of saline, BP 95/P
       Complaining of L sided abdominal pain
       FAST - positive fluid LUQ
       OR - exploratory lap, 1.5 L of blood, shattered spleen,
        omental bleeding, liver laceration L lat lobe
                      CASE # 2
   Perform splenectomy, controlled bleeding, repair
    liver lac, place JP under L liver lobe, EBL 4 L
   Given intraop - 10 u PRBC, 3 FFP
   Transferred to SICU, Hgb 10, P 76, BP 120/75
   Blood stain fluid from liver bed JP drain, next 3 hrs
    400 cc
   Pulse gradually increased to 110, BP 100/60 despite
    2 u PRBC
   Labs
      Hgb 8.0, PT 32 sec, PTT 65 sec, Platelets 70K


   ? Plan ?
                     CASE # 2

   Blood products given
       10 U FFP
       2 U PRBC
   Two hours
       450 ml of blood-stained fluid from abdominal
        drain
 ? Etiology of Bleeding ?
 ? Plan ?
                     CASE # 2

 Further coagulation test ordered
 Patient reexamined
 Labs
       Hgb 8.0, PT 17, PTT 42, FDP 4, Plt 84K
       Cr 1.7, BUN 32
   ? PLAN ?
                     CASE # 2

   Given
       10 U FFP
       6 U Cryoprecipitate
       6 U Platelets
       2 u PRBC
 Continued bleeding from abdominal drain
 ? PLAN ?
        Evaluation and Management

   First step
       Resuscitation and establish cause of bleeding
 Blood volume should be increased to
  maintain tissue perfusion, rather than a
  normal hemoglobin concentration
 Hgb useful as an index of hemorrhage as
  some blood loss may be concealed
                              Etiology
   Surgical Cause (missed injury, local hemostatic failure)
   Acquired disorder of hemostasis
       Drugs ( ie. ASA, heparin flushes)
       Uremia
       Dilutional effect ( massive blood loss or transfusion)
       Consumption (sepsis or poor tissue perfusion)
       Anemia
       DIC
   Liver disease
   Pre-existing herditary hemorrhagic disorder
       Mild hemophilia (Christmas factor)
       von Willebrand;s disease
       variety of platelet defects
                       CASE # 2
   Bleeding is prolonged by anemia
      progressive anemia may contribute to the bleeding

       tendency
      ? Related to platelet-endothelial interaction at high

       shear rates with less interaction at low hematocrits
   No clinical evidence of pre-existing coagulapathy
   No drugs given to impair hemostasis
   Protracted bleeding from isolated site - no bleeding at
    venipuncture sites, ET tube, abdominal wound
   Mild coagulopathy documented with prolongation of PT
    and PTT but corrected with FFP
   DX: Surgical bleeding, re-exploration revealed 2 L of
    blood, bleeding short gastric artery
                    CASE # 3
   53 yof with a three -year h/o menorrhagia
    admitted for elected TAH
   On admission her Hgb was 9.0 with MCV 75
   She was taken FeSO4 200 mg/d but no other
    medications
   No significant PMH
   Three healthy children
   In view of her anemia, her OB/GYN postponed her
    surgery and transfused her 3 u PRBC
                      Case # 3

   On the day of surgery, she was found to be unwell,
    T 39.0 , pulse 105 and BP 105/60.
   On PE no apparent vaginal blood loss or
    hemorrhage elsewhere
   IVF were started and patient transferred to SICU
    where she was noted to have macroscopic
    hematuria
                   CASE # 3
   Given 1.5 L of saline, HR 90, BP 115/60
   LAB’s
      Hgb 6.2, normal PT and PTT

      Creatinine 1.2

   Urology was consulted for cystoscopy
   4 U of PRBC were cross-matched for
    transfusion, but two where found incompatible
    and the cystoscopy was cancelled
   ? DX ?
   ? Incidence ?
                         CASE # 3
 DX - delayed hemolytic transfusion reaction
  with intravascular hemolysis causing
  hemoglobinuria
 Blood sample should be taken
       direct coomb’s
       determination of specificity of the antibody for
        incompatibility
       serum bilirubin
   Moderate hypochromic anemia on admission
    likely result of iron deficiency
            Indications for Transfusions
   Hemoglobin concentration is a determinant of
    arterial oxygen concentration
       CaO2 = HGB x O2 sat x 1.34 + PaO2 x 0.0031
   RBC infusion used to improve oxygen delivery
       DO2 = CI x CaO2 x 10
   Animal experiments show that tissue oxygen
    extraction is maintained with an 80% reduction in
    red cell mass, so long as blood volume and blood
    flow are maintained
        Indications for Transfusions

 In critical ill patients impaired tissue oxygen
  extraction may occur and red cell transfusion
  may not result in any improvement in tissue
  oxygen metabolism
 Traditionally, patient for elective surgery
  transfused for Hgb< 10, Now data shows no
  difference in mortality if Hgb > 7 if euvolemic
            Risks of Transfusion of RBC

              Infectious                   Non-infectious
   Hepatitis A      Rare           Fever             1-2%
   Hepatitis B      1/100,000      Urticaria         1%
   Hepatitis C      1/120,000      Hemolytic         1/6000
   HIV              1/1,000,000    Fatal hemolytic 1/100,000

   Creutzfeld-Jacob none
   CMV              1/4,000,000
   Bacterial        1/1,000,000
   Syhillis         Rare
         Hemolytic Transfusion Reaction
   Signs and symptoms
       fever, chills, headache, chest pain, anxiety, respiratory
        distress
   Laboratory results
       free Hgb in plasma
       Hemoglobinuria
       Decreased haptoglobin
       Increased creatinine and ARF ( lysis of RBC membranes
        in golmerulus)
   Fatal transfusion reactions are usually secondary to
    clerical error that results in giving the wrong blood
    to a particular patient
Questions…?

				
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posted:3/7/2011
language:English
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