Hematology in the Athlete
William B. Adams
INTRODUCTION
Athletes as a group tend to be healthier, but they are still susceptible to the same hematologic diseases as nonathletes. However, symptoms from hematologic disturbances may manifest earlier and at lower severity, often presenting as impaired physical performance (12,14).
Maximal or prolonged exertion efforts typically cause transient changes in several hematologic indices (4,7,9,19,25,31,37,41). Regular endurance and altitude training generally results in more sustained alterations of hematologic parameters (2,34). Dietary inadequacies, not uncommon in athletes, may cause hematologic problems because of a deficit of calories or critical nutrients (2,18,29,32).
ANEMIA
Anemia is a deficiency of total red blood cell (RBC) mass that manifests as RBC volume (hematocrit [Hct]) or hemoglobin (Hb) concentration below normal values. Symptoms and physical manifestations depend on reduction in RBC volume, the decrement in oxygen delivery to tissues, the rate at which these changes occur, and compensatory capacity of the cardiopulmonary system (23,24).
Prevalence in U.S. males: 2.9% overall, 0.7% in those ages 19-40, but 9.4% in men older than 60 (15).
Prevalence in U.S. women of all ages is 7.5%, with a higher proportion (24%) of black women having anemia. Prevalence in all women ages 19-40 is 8% (6,15).
Anemia arises from either excessive loss or inadequate production of RBCs or a combination of both (13,23,24).
ATHLETIC PSEUDOANEMIA
Regular consistent aerobic or endurance-level training causes an increase in both RBC production and plasma volume; however, plasma volume expansion typically exceeds the increase in RBC mass, causing a slight reduction in Hb and Hct in the resting state. This condition, common in athletes, is not a true anemia but rather a physiologic adaptation that promotes increased cardiac output and enhanced oxygen delivery to tissues and protects against hyperviscosity (8,11,14,34).
Plasma volume can decrease 5%-20% with endurance exercise (sweat losses and intravascular fluid shifts) (34).
Conditioned endurance athletes tend to have greater transient reductions in plasma volume as a result of greater sweat losses.
Hb values typically run 0.5 g · dL−1 lower for athletes regularly pursuing moderate-intensity training and 1.0 g · dL−1 lower for elite-level athletes (8).
Diagnosis may be confirmed by the following:
□ Retesting the athlete after several days of rest from training as the hemodilution of conditioning reverses within days of terminating endurance-level training (34).
□ Inferred from laboratory testing yielding are the following:
Normal RBC indices and reticulocyte distribution width (RDW) on complete blood count (CBC)
Normal reticulocyte count
Normal serum ferritin level
IRON DEFICIENCY ANEMIA
Deficiency of iron in the body is the most common cause of true anemia in the athlete, as in the nonathlete (8,11). It may arise from inadequate dietary intake, excess losses through blood loss, or a combination of both.
Occurs more often in female athletes mostly because of menstrual losses coupled with inadequate consumption of meat or other sources of iron (5,11).
Laboratory testing reveals a low Hb and Hct with low mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH).
RDW is increased, unless iron deficiency is longstanding.
Peripheral smear reveals hypochromic microcytic cells with a low to normal reticulocyte count.
Serum ferritin levels are low, typically < 12 µg · L−1 (note, however, that ferritin levels of 12-35 µg · L−1 may reflect inadequate iron stores with associated decrement in athletic performance without anemia manifesting) (29,31).
Total iron binding capacity (TIBC) tends to be elevated.
In evaluation of iron deficiency anemia, it is imperative to determine the cause of the deficiency in order to choose the best therapy and to avoid overlooking potentially serious conditions. Iron replacement should continue until 6-12 months after anemia has resolved (35).
ANEMIA FROM BLOOD LOSS
Anemia may arise from acute bleeding or massive hemolysis, as well as chronic cumulative losses from insidious bleeding or persistent accelerated destruction of RBCs. Acute hemorrhage is typically obvious from history or examination findings of gross blood, melena, or manifestations of hypovolemia. Bleeding contained within tissues or the body cavity may be less obvious, particularly in the retroperitoneal space. Characteristics of rapid blood loss include the following:
Hb and Hct (both concentration values) are initially normal in the absence of any fluid administration (22,23).
Platelet counts initially drop with hemorrhage but become elevated within 1 hour if hemorrhage stops (22,23).
Hb and Hct values decline over the ensuing days with plasma volume expansion.
RBC indices are initially normal. After 3-5 days, MCV and RDW start to increase because of reticulocyte response (22,23).
Bilirubin levels are normal unless bleeding is internal. Similar to hemolysis, internal bleeding causes a rise in unconjugated bilirubin and lactate dehydrogenase (LDH) but without evidence of hemolysis on peripheral smear.
If blood loss is slow and insidious, as in chronic low-grade gastrointestinal (GI) bleeding or menstrual blood loss in women, anemia may not manifest until iron stores are depleted. This situation may be revealed by a reticulocytosis with concomitant increase in RDW well before iron stores are depleted and MCV becomes low.
GI blood loss: GI bleeding is a very common and often serious cause of anemia. It may arise from peptic ulcer disease, vascular anomalies, inflammatory bowel diseases, ischemic bowel syndromes, infection, diverticula, or tumors. Thus, stool occult blood testing is indicated in any anemia evaluation (28). Note that it is not uncommon for athletes to manifest mild transient GI bleeding from marathons and similar endurance events (exercise-associated GI bleeding).
Features of exercise-associated GI bleeding include the following:
Source of bleeding is seldom detectable; it is theorized to arise from acute transient ischemia or mechanical contusion (e.g., cecal slap syndrome) (5,34,35).
In the absence of this or other pathology, bleeding is seldom significant enough to cause anemia (14).
Note that regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is common among athletes. In addition to NSAID-induced acute GI bleeding, chronic use may cause enough insidious blood loss over time to impact RBC mass (5Related posts:
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