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Hematology/Oncology Emergencies. Ali Mullah-Ali Oct 8 th , 2011. Tumor Lysis Syndrome Bleeding & Coagulation Abnormalities Anemia (neonates & older) including hemolytic Thrombocytopenia (neonates & older ) Thrombocytosis Pancytopenia Leukocytosis Fever & neutropenia Typhlitis

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hematology oncology emergencies

Hematology/Oncology Emergencies

Ali Mullah-Ali

Oct 8th, 2011

slide2
Tumor Lysis Syndrome
  • Bleeding & Coagulation Abnormalities
  • Anemia (neonates & older) including hemolytic
  • Thrombocytopenia (neonates & older)
  • Thrombocytosis
  • Pancytopenia
  • Leukocytosis
  • Fever & neutropenia
  • Typhlitis
  • Mediastinal mass +/- SVC obstruction
tumor lysis syndrome1
Tumor Lysis Syndrome
    • Oncological emergency
    • Release of large amounts
      • Potassium Hyperkalemia
      • Phosphate Hyperphosphatemia
      • Nucleic acids Hyperuricemia
  • Results from tumor necrosis OR fulminant apoptosis
    • Spontaneous
    • Treatment-related
  • Comlications:
    • Hypocalcemia
    • ARF
      • Due to uric acid & Calcium phosphate deposition in renal tubules
slide7
Pre TLS
    • Rapid cell breakdown Nucleic acid Catabolized to uric acid
    • Hyperuricaemia
  • Established TLS
    • Urate nephropathy + ARF
    • Hyperphosphataemia
    • Hyperkalaemia
    • Hypocalcaemia
  • Prevention is best management
slide8
Typically starts after induction of Rx
    • May occur prior to Rx to 5/7 after Rx
  • Risk factors:
    • High cell count leukemia (WBC >100)
    • Burkitt’s lymphoma
    • Large tumour bulk
    • Bulky T celllymphoma
    • Bulky lymphoproliferative disease
    • Evidence of renal infiltration with tumor
    • Evidence of renal impairment
    • Cancer with high sensitivity to chemoRx
    • High uric acid
    • High LDH
prevention of tls
Prevention of TLS
  • Hydration
    • 3 L/m2/day (0.45% NaCl/2.5% Glu)
    • No potassium additives
  • If no evidence of fluid overload
    • Tachycardia
    • Tachypnoea
    • Gallop rhythm
    • Desaturation
    • O2 requirement

 May increase to 4 L/m2/day

slide11
Allopurinol
    • If no high risk features
    • 100 mg/m2 8 hrly PO
    • Reduce dose by 50% or more in renal failure
  • Rasburicase
    • If
      • High risk
      • Poor response to allopurinol
    • 200 mcg/kg once per day
    • Risk of haemolysis in G6PD deficiency
    • For very high risk patients with rapid tumourlysis
      • May increase the frequency (18 hrly, max 12 hrly) for 2-3 days
slide12
Review pt clinically at least q 4 hrs
  • Check v/s
  • Look for oliguria / fluid overload
  • Fluid balance
  • Biochemistry
    • Na, K, Ca, PO4, TCO2, urate, urea and creatinine (q 4-6 hrs)
    • If very high risk, monitor biochemistry 2-3 hrly
  • If signs of fluid overload
    • Furosemide 1-2mg/kg (up to 5 mg/kg)
  • Cardiac monitor
    • Peaked T waves and dysrhythmias
treatment
Treatment
  • Established TLS:
    • Haemodialysis (HD) preferred in acute phase
  • Absolute indications for HD include:
    • Potassium > 5 mmol/l
    • Phosphate > 4 mmol/l
    • Pulmonary oedema
      • Oxygen and consider ventilation
    • Anuria
  • Relative indications for HD include:
    • Rapid rise in K, phos or urate
    • Oliguria unresponsive to furosemide
    • Urea > 15 mmol/L OR creatinine > 150 μmol/L
definition of clinically significant bleeding
Definition of Clinically Significant Bleeding
  • Recurrent nose bleeds (> 30 min)
  • Oral Bleeds (>30 min)
    • Restarting over next days
  • Bleeding from skin laceration (> 30 min)
  • Prolonged bleeding related to dental extraction
  • Menorrhagia requiring Rx
  • Spontaneous GI bleeding
  • Hemarthrosis
    • Spontaneous or after minor trauma
  • Petechiae, Ecchymosis
    • Unusual sites
    • With minor trauma
hemostasis overview
Hemostasis Overview
  • Primary phase  Platelet plug
    • Adhesion
    • Activation
    • Aggregation
  • Secondary phase  Cross-linked fibrin clot
slide17
Coagulation Cascade

Contact Factors,

XI, XII

Tissue Factor

Extrinsic

Pathway

Intrinsic

Pathway

IX

VIII

VII

X, V, Phospholipids

Common

Pathway

Common

Pathway

Thrombin

Prothrombin

Fibrinogen

Fibrin

clot

XIII

Cross Linked Fibrin Clot

duration quantity
Duration / Quantity
  • Beyond “routine” bleeding episodes
  • Previous surgery or dental extractions without bleeding complications

 Unlikely underlying congenital hemorrhagic disorder

family history
Family History
  • Most children not encountered severe challenges
  • Inherited disorders ? undiagnosed / misdiagnosed for generations, especially when mild
  • Family members
    • Hemophilia (X-linked) may also result in abnormal bleeding symptoms in female carriers
  • Previous
    • Surgical procedures
    • Dental extractions
    • Transfusions
    • Menstrual and obstetric Hx of female relatives
      • Up to 20% of girls with menorrhagia beginning at menarche have an underlying bleeding disorder
type of bleeding
Type of Bleeding
  • Platelet & vWD
    • Mucosal bleeding
      • Gingival hemorrhage
      • Epistaxis
      • Menorrhagia
    • Petechiae
    • Bruising
  • Factor deficiencies (hemophilia)
    • Spontaneous, deep muscle, and joint bleeding
time of onset
Time of Onset
  • No rule
  • Acute onset (days/weeks)  Acquired disorder:
    • Immune (previously idiopathic) thrombocytopenic purpura (ITP)
    • Vitamin K deficiency
  • Longer duration are indicative of a congenital disorder:
    • VWD
    • Coagulation-factor deficiencies
  • Infants with congenital coagulation disorders
    • At birth (following circumcision)
    • 1st months of life (with immunizations)
    • When mobile and begin to experience mild trauma (most common)

 Severe inherited bleeding disorder may not manifest until 6-12 months of age

slide23
Significant challenges to hemostatic system
    • Surgery, dental extractions, trauma, or menstruation
  • Good initial hemostasis followed by persistent oozing
      • Due to failure to form a firm clot

 Characteristically is seen with ??

overall health
Overall Health
  • Otherwise well
    • Congenital bleeding disorders
    • ITP
  • Sick individuals +/- comorbid conditions
    • DIC
  • Liver disease
    • Impaired factor production
  • Malabsorbtion / GI disease
    • Impaired vit K absorption
    • Impaired factor synthesis
  • Renal disease
    • ?Platelet function
physical examination
Physical Examination
  • Petechiae
    • Almost pathognomonic of platelet-related bleeding

+/- Involvement of the mucosal membranes with purpura or hemorrhage

  • Nares
    • Gently examined in epistaxis cases
    • Excoriations and damaged vessels may be indicative of trauma
  • Ecchymoses ,,,,, unusual sites
  • Bruises
    • Excessively large for degree of trauma
  • Joint swelling without h/o significant trauma
  • Deep tissue and intramuscular bleeds

** Physical abuse

pt and aptt
PT and aPTT
  • Screening tests for the second phase of hemostasis
  • PT
    • Extrinsic and common pathways
    • Reported as an international normalized ratio (INR)
      • A standard allowing for comparison of results between different laboratories
  • aPTT
    • Intrinsic and common pathways
  • Factor level at which PT or aPTT prolonged varies:
    • Usually ~ 40% N pooled plasma level
slide27
PT

VII

X

V

II

Fgn

slide28
PTT

XII

XI

IX

VIII

X

V

II

Fgn

aptt pt mixing studies
aPTT & PT Mixing Studies
  • For abnormal PT or aPTT
  • Mixing pt's plasma with N plasma
    • Factor deficiency corrects ~ 50%
    • Normalization Factor deficiency
    • Persistent prolongation  Inhibitors
  • If factor deficiency
    • Measure
      • FVIII
      • FIX
      • FXI

 Associated with clinical bleeding

thrombin clotting time
Thrombin Clotting Time
  • Time required to form a clot when thrombin added to plasma
  • A measure of fibrin formation
  • If prolonged
    • Low fibrinogen activity
    • Presence of fibrin split products
    • Heparin contamination
  • Reptilase clotting time
    • Similar to thrombin time
    • Not inhibited by heparin
slide31
TCT

Fgn

management of bleeding disorder
Management of Bleeding Disorder
  • Laboratory Investigations:
    • CBC
    • Platelet morphology
    • INR, PT, APTT
    • Mixing study
    • Bleeding time
    • TCT
    • Clotting Factor assay
    • Factor XIII assay
    • Platelet Aggregation studies
management
Management
  • ABC
  • Local measures whenever possible
  • Plts + PRBCs as needed
  • Tranexemic acid (cyklokapron):
    • PO 20-25 mg/kg (max 1.5 g) q8hr
    • IV 10 mg/kg (max 1g) q8hr
  • As indicated:
    • FFP
    • Factor replacement
    • Cryo
    • Novoseven
slide35
Fresh Frozen Plasma (FFP)
    • Frozen within 8 hrs of separation, at ≤ -18ْ C
      • Frozen Plasma (FP)  Frozen within 24 hrs
    • Contain all clotting factors (low fibrinogen)
    • Dose 10-15 ml/kg over 30-120 min
    • Transfuse slowly in 1st 15 min (50ml/hr)
  • Cryoprecipitate
    • Contains all clotting factors
    • Contains 150mg fibrinogen/unit
    • Dose 1 unit / 5-10 kg
slide36
FVIII
    • 1 unit incease level by 2%
    • Half-life
      • 1st dose 6-8 hrs ,,, Subsequent doses 8-12 hrs
    • Dose
      • Minor bleeds .. Increase level to 20-30 % of normal
      • Major bleeds .. Increase level to 70-100 % of normal
  • FIX
    • 1 unit incease level by 1%
    • Half-life
      • 1st dose 4-6 hrs ,,, Subsequent doses 18-24 hrs
    • Dose
      • Minor bleeds .. Increase level to 20-30 % of normal
      • Major bleeds .. Increase level to 70-100 % of normal
novoseven
NovoSeven
  • rFVII
  • Dose 90 mg/kg IV every 2 hrs
  • Rarely …. Risk of thrombosis
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