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Acute myeloid leukemia
Symptoms and signs

AML is usually diagnosed in adults after a few days of nonspecific symptoms which are due to abnormal blood cell number, such as fatigue, weakness, bruises, small rash-like spots, gum and nose bleeds or infection. In some patients, particularly younger ones, present with acute symptoms over a few days to 1-2 weeks. Others have a longer course, with fatigue or other symptoms lasting from weeks to months. A longer course may suggest an antecedent hematologic disorder such as MDS.

Generally speaking, manifestations result from either bone marrow failure, organ infiltration with leukemic cells or both.

Effects on hematopoeisis

Most of the symptoms associated with AML (such as fatigue, weakness, bruises, small rash-like spots, gum and nose bleeds or infection) are all reflections of the anemia, thrombocytopenia, and decrease in functional neutrophils associated with marrow replacement by malignant cells.

So, whereas, classically elevated WBCs are expected in leukemia this only happens in about 10% of the patients and constitutes a bad prognostic sign as they are at increased risk of CNS disease, tumor lysis syndrome, and leukostasis due to impedance of blood flow from intravascular clumping of blasts, which are “stickier” than mature myeloid cells. More commonly patients present with pancytopenia and a decrease in WBCs as a result of a decrease in functional neutrophils associated with marrow replacement by malignant cells.

Physical findings

Physical findings in AML are usually minimal.

• Pallor (anemia).
• Increased ecchymoses or petechiae, retinal hemorrhage (thrombocytopenia, coagulopathy).
• Fever may occur due to infection (leukopenia).
• Signs relating to leukostasis include respiratory distress and altered mental status (leukocytosis).
• Patients with a high leukemic cell burden may present with bone pain caused by increased pressure in the bone marrow.

• Manifestations of organ infiltration include: Gingival hypertrophy, and cutaneous involvement (leukemia cutis). Visceral involvement (hepatosplenomegaly and, to a lesser degree, lymphadenopathy) is also rare, occurring as an initial manifestation of AML in < 5% of cases, but it may be more frequent during subsequent relapses.
  These focal collections of blasts, called chloromas or granulocytic sarcomas, can present as soft-tissue masses, infiltrative lesions of the small bowel and mesentery, or obstructing lesions of the hepatobiliary or genitourinary system. Organ inflitration is generally more common with monocytic (M4 or M5) variants of AML than with other variants of AML.

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Hyperuricemia

Hyperuricemia with possible interstitial or ureteral obstruction is seen predominantly in AML with moderate leukocytosis; this condition may be exacerbated by a rapid response to chemotherapy and the “tumor lysis syndrome” (hyperuricemia with renal insufficiency, acidosis, hyperphosphatemia, and hypocalcemia), which may occur within the first 24-48 hours after initiating chemotherapy. To prevent this complication, all patients should receive allopurinol (Zyloprim) and urine alkalinization before marrow-ablative chemotherapy is initiated.

Coagulopathies

Coagulopathies can also complicate the hemostatic defects associated with thrombocytopenia. Disseminated intravascular coagulation (DIC) is most often seen in APL (French-American-British Cooperative group [FAB] subtype M3) due to release of procoagulants from the abnormal primary granules, which activate the coagulation cascade, leading to decreased factors II, V, VIII, and X, and fibrinogen, as well as rapid platelet consumption. Lysozyme released from monoblasts in M4 and M5 subtypes of AML can also trigger the clotting cascade.

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