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Acute Myelogenous Leukemia (AML)

 

Internist's overview of AML

  • Pathophysiology: clonal proliferation of myeloid precursors with impaired differentiation
  • Most common acute leukemia in aduts
  • Diagnosis: greater than 20% blasts in periphery and bone marrow, with myeloid lineage confirmed
  • Treatment options:
    • For patients younger than 60, induction with anthracycline and cytarabine is the standard of care
    • Patients older than 60 (such as our patient) are at greater risk of treatment-related complications
    • At Stanford, standard is to enroll these patients on protocol or to treat with alternative agents such as decitabine, which induces differentiation

 

Complications of AML

  • Cytopenias
  • Infection: in hematologic malignancies, pts with normal number of neutrophils may still be predisposed to infection, given infiltration of marrow with blasts
    • Febrile neutropenia
      • Definition: fever to 38.3 or to 38 sustained for one hour, with PMN count <500 or <1000 with predicted nadir of <500
      • Pathogenesis: enteric translocation, from chemotherapy-induced mucositis
        • Primarily GNRs, though specific pathogen is identified in only 30% of cases
        • Rarely anaerobes, though GPCs becoming more common with indwelling lines and instrumentation
      • Empiric therapy: should be directed at GNRs, including pseudomonas (e.g. cefepime, pip/tazo)
      • Indications for gram positive coverage (e.g. vancomycin)
        • Mucositis (for PCN-resistant oral anaerobes)
        • Hypotension
        • Skin or catheter infection
        • Hx MRSA colonization
        • Presence of GPC on gram stain
        • Hx quinolone prophylaxis
  • Tumor lysis syndrome
    • Pathophysiology: results from massive tumor cell lysis with release of potassium, phosphate, nucleic acids
      • Metabolism of nucleic acids --> uric acid, which is poorly water soluble
    • Due to high metabolic demands, phosphorus concentration in malignant cells is 4x that of normal cells
    • Precipitation of uric acid and calcium phosphate in renal tubules leads to kidney injury
    • Signs and symptoms: arrhythmia, renal failure, heart failure, tetany/cramping (from hypocalcemia), seizure
    • Treatment:
      • Frequent electrolyte monitoring
      • Hydration with goal of robust urine output (100 cc/hr) to prevent crystallization
      • Allopurinol: blocks xanthine oxidase, thus reducing uric acid production
        • Does not reduce preexisting hyperuricemia
      • Rasburicase: recombinant urate oxidase to metabolize uric acid to allantoin, which is water soluble
      • Phosphate binders, kayexalate
      • Renal replacement therapy if necessary
  • Leukostasis: elevated blast count with symptoms of compromised tissue perfusion
    • Pathophysiology: WBCs plug microvasculture, typically occurs with blast crisis
      • Increased viscosity (blasts less deformable)
      • Local hypoxemia from increased metabolic demands of blasts
      • Cytokine release and endothelial damage
    • Signs and symptoms: dyspnea, neuro changes, fever, tissue ischemia, DIC
    • Treatment:
      • Cytoreduction: induction chemotherapy, hydroxurea, leukapheresis, total brain irradiation
      • Supportive care: hold pRBC transfusions, as they can increase viscosity, correct thrombocytopenia to prevent reperfusion hemorrhage

 

 

(Christopher Woo MD, 12/14/10)