Anemia is defined as a reduction of the body's total red cell mass (RCM) or it be defined as a deficiency of hemoglobin in the blood, which can be caused by either too few red blood cells or too little hemoglobin in the cells (Table 2.1). Clinical symptoms and signs include feel tired with minimal exertion to dyspnea at rest depending on severity, tachycardia, and pallor of nail beds, palmar creases, conjunctivae and tongue. Both hematocrit (Hct) level and hemoglobin (Hgb) concentration measurements reflect the RCM present in the body. The Hct level, defined as the fractional volume of sampled blood that erythrocytes occupy, is an indirect measurement of the body's RCM. The Hct is a simple, inexpensive, commonly used test to indirectly assess the severity of anemia as well as whole-blood viscosity, oxygen-carrying capacity, and RCM. Hgb, the predominant component of a red blood cell, serves as the major carrier to transport oxygen within the blood. Hgb concentration is a directly measured value that is also used to indirectly assess RCM.

Table 2.1 The Normal Value of Hgb and Hct

Hemoglobin gm/dl Hematocrit percent
Adult male 13.5 -17.5 41-53
Adult female 12 -16 36 -46
New born 14 - 20 49-61

Anemia in pregnancy: Anemia in pregnancy defined as hemoglobin (Hgb) level of < 10 gm/dL, hematocrit level of 30 % or is a qualitative or quantitative deficiency of Hgb or red blood cells in circulation resulting in reduced oxygen carrying capacity of the blood. In addition to causes of anemia listed below and increased requirement for enlarged uterus and growing fetus anemia in pregnancy can be caused by plasma volume expansion increment in excess of red blood cell volume resulting in hemodilution and consequent physiological anemia of pregnancy.

Causes of Anemia

Anemia is the result of a wide variety of causes, globally the most significant contributor to the onset of anemia is iron deficiency from low intake of iron, poor absorption of iron and period of life when requirement are high (small children and pregnancy).

  • Blood loss anemia: After rapid hemorrhage, the body replaces the fluid portion of the plasma in 1 to 3 days, but this leaves a low concentration of red blood cells. In chronic blood loss, a person frequently cannot absorb enough iron from the intestines to form hemoglobin as rapidly as it is lost.
  • Aplastic anemia: Bone marrow aplasia means lack of functioning bone marrow. For instance, a person exposed to radiation from a nuclear bomb blast can sustain complete destruction of bone marrow, followed in a few weeks by lethal anemia. Likewise, excessive x-ray treatment, certain industrial chemicals, and even drugs to which the person might be sensitive can cause the same effect.
  • Megaloblastic Anemia: Lack of vitamin B12, folic acid, and intrinsic factor from the stomach mucosa can lead to slow reproduction of Hgb in the bone marrow. As a result, the red cells grow too large, with odd shapes, and are called megaloblasts (an abnormally large). Thus, atrophy of the stomach mucosa, or loss of the entire stomach after surgical total gastrectomy can lead to megaloblastic anemia. These cells rupture easily, leaving the person in dire need of an adequate number of red cells.
  • Hemolytic anemia: is a form of anemia due to hemolysis, an abnormal break down of red blood cells, Even though the number of red blood cells formed may be normal, or even much greater than normal in some hemolytic diseases, the life span of the fragile red cell is so short that the cells are destroyed faster than they can be formed, and serious anemia results.
Physiologic Response of Acute Anemia

Baroreceptor reflexes mediate the initial response to acute blood loss. Heart rate and minute ventilation initially increase after hemorrhage in the absence of volume replacement. Hyperventilation and tachycardia serve to increase cardiac output, which, in turn, increases blood flow to tissues

Concurrent with the baroreceptor mediated response to acute blood loss is the near-immediate release of catecholamines, angiotensin II, and vasoactive hormones. These biochemical mediators increase systemic vascular resistance and thereby increase systemic blood pressure. The increase in systemic vascular resistance is selective in that blood flow is increased to a lesser extent to gut, skin, muscle and renal tissue than to the heart and brain, so these organs receive preferential blood flow. The increase in catecholamines will also confer a positive inotropic (increase the force of myocardial contractility) and chronotropic (increase heart rate) effects on the heart that will further augment cardiac output.

Decreased intravascular volume stimulates the renin-angiotensin- aldosterone axis, which contributes to increasing cardiac output and improving tissue oxygen delivery by water retention. Water retention augments cardiac preload. Acute hemorrhage is associated with redistribution of water from the extravascular space into the intravascular space, accompanied by decreased Hgb concentration. As intravascular volume is replenished, Hgb concentration and Hct level decline, producing decreased blood viscosity. The resulting lower blood viscosity serves to reduce resistance to blood flow and increase venous return to the right heart; these changes help maintain or increase cardiac output. Reduced resistance to blood flow reduces myocardial work and oxygen consumption despite the overall increase in cardiac output.

Increased erythropoietin concentration and an increase in the circulating reticulocyte count can be detected in as little as 2 days after a hemorrhagic event. The Hgb concentration will start to increase within 7 days after a major hemorrhage. This continuum of physiologic responses occurs in the healthy surgical patient. An individual patient's ability to mount these physiologic responses largely depends on the patient's ability to increase cardiac output and augment tissue oxygen delivery.

Physiologic Response of Chronic Anemia

Chronic anemia is associated with expansion of plasma volume, hyperventilation, and an increased cardiac output. In determining whether to transfuse a chronically anemic patient the clinician should inquire about signs and symptoms of anemia (e.g., fatigue, decreased exercise capacity, and increased frequency of angina in patients with ischemic cardiac disease.

Simultaneously restoring normovolemia and maintaining oxygen delivery are principal goals of treating surgical blood loss. A patient's requirement for RBC transfusion should only be considered after intravascular volume status has been restored to normal. The ability to tolerate a lower Hgb concentration in the perioperative period is integrally dependent on an adequate intravascular volume.

Anesthesia and Physiologic Compensation

The compensatory physiologic response to acute, unreplaced volume loss is reduced under general anesthesia, emphasizing the importance of maintaining intravascular volume. The extent of the sympathetic stimulatory response to acute anemia is impaired during general anesthesia in that the heart rate does not increase to the same degree as in unanesthetized patients and the systemic vascular resistance is lower. The inability to appropriately increase heart rate and augment cardiac output during general anesthesia, or because of medications, must also be considered when determining an individual patient's transfusion threshold.

Anesthetized patients with marked impairment of their compensatory responses to anemia should be treated with transfusion.

Last modified: Sunday, 20 November 2016, 12:59 PM