Disease Process With blood loss, blood volume diminishes, hemodilution occurs, and oxygenation of the tissues declines.

Symptoms The rate of blood loss determines the signs and symptoms, which may include dizziness; faintness; weakness; pallor; thirst; sweating; rapid, weak pulse; rapid respiration; and orthostatic hypotension.

Potential Complications Lack of prompt treatment or failure to control the bleeding results in shock, coma, and death.

Diagnostic Tests

Complete blood count
RBCs, Hgb, and Hct are deceptively high during initial period of hemorrhage because of vasoconstriction; values begin to decline within hours of the onset of bleeding if hemorrhage is not controlled

Peripheral smear
Normocytic cells, agranulocytosis

Coagulation time
Reduced

Treatments

Surgery – If indicated to control hemorrhage.

Drugs – Iron replacement.

General – Control of bleeding; blood transfusions; IV fluids, oral fluids as tolerated; oxygen; absolute bed rest; diet high in protein and iron.

Disease Process Most commonly, the gastric mucosa develops a defect caused by an unknown factor and atrophies. This inhibits the secretion of intrinsic factor (IF), which binds and transports dietary vitamin B12 to the ileum for absorption. The lack of IF prevents vitamin B12 from entering the body, and existing stores of the vitamin are depleted, leading to the production of enlarged, immature RBCs.

Symptoms Usual signs and symptoms associated with anemia (pallor, fatigue, weakness, dyspnea) plus symptoms that stem from the physiologic changes in the gastrointestinal tract (e.g., glossitis, gingivitis, indigestion, epigastric pain, loss of appetite, diarrhea, constipation, weight loss). Peripheral neurologic changes occur, with paresthesia in the hands and feet.

Potential Complications If the condition goes untreated, the neurologic changes become more profound, with involvement of the spinal cord and loss of vibratory sense, ataxia, spasticity, and disturbances in bowel and bladder function. Depression, paranoia, and delirium may follow. Splenomegaly and hepatomegaly occur, as well as organ failure, neurologic degeneration, or infection, eventually causing death.

Diagnostic Tests

Peripheral blood smear
Oval macrocytes, hypersegmented neutrophils, enlarged platelets

Schilling test
Radioactive-tagged vitamin B12 is not excreted in urine

Complete blood count
Decreased Hgb, leukocytes, erythrocytes, and thrombocytes

Bone marrow aspiration
Hyperplasia; increased large-cell megaloblasts

Gastric analysis
Lack of free hydrochloric acid

Treatments

Surgery – None.

Drugs
Lifelong parenteral vitamin B12 replacement (dietary vitamin B12 replacement is not effective); oral iron if Hgb does not rise.

General
Treatment of underlying cause of gastric atrophy, if possible; oxygen to increase arterial levels; oral hygiene; orientation if confused; safety precautions for neurologic effects; instruction about vitamin B12 replacement as a life change.

Disease Process Some factor (e.g., chronic blood loss, a decrease in iron intake) leads to iron deficiency. This occurs in orderly steps. Initially, iron loss exceeds intake, and the iron stores in the bone marrow are used and depleted. A compensatory mechanism increases absorption of dietary iron but depletion continues, and insufficient iron is available for RBC formation. This leads to a decrease in Hgb production, microcytosis, and a decrease in oxygenation of the tissues.

Symptoms Usual signs and symptoms associated with anemia (pallor, fatigue, weakness) plus symptoms specific to the iron deficiency, such as glossitis, cheilosis, koilonychia (spoon-shaped fingernails), and pica.

Potential Complications Exhaustion, infection, and respiratory and cardiac complications are possible if the condition goes untreated.

Diagnostic Tests

CBC
Decreased RBCs, Hgb, and Hct

Peripheral blood smear
Decreased mean corpuscular volume and mean corpuscular Hgb concentration; microcytosis; hypochromia

Iron capacities
Decreased serum iron, serum ferritin, and iron ferritin; increased iron-binding capacity

Bone marrow aspiration
Erythrocyte:granulocyte ratio 1:1 (normal, 1:3-1:5); lack of marrow iron; ringed sideroblasts

Treatments

Surgery – None.

Drugs – Iron replacement PO or parenterally.

General
Correction of underlying cause (e.g., treatment of bleeding, increased dietary intake of iron); nutritional education.

Disease Process The precipitating factor results in a shortened life span for erythrocytes and an increase in erythrocyte destruction by the reticuloendothelial system. The bone marrow is unable to produce sufficient replacement cells to keep pace with the destruction, and anemia ensues.

Symptoms Hemolysis can be acute or chronic. The symptoms of chronic hemolysis resemble those of other anemias: fatigue, weakness, dyspnea, and pallor. Individuals with chronic symptoms may suffer from a physiologic or emotional stressor that triggers a hemolytic crisis. Acute hemolytic crisis, which is rare, is characterized by chills; fever; headache; pain in the back, abdomen, and joints; splenomegaly; hepatomegaly; lymphadenopathy; and reduced urinary output.

Potential Complications Chronic symptoms can lead to jaundice, arthritis, renal failure, and other organ failure. Crisis can lead to paresthesia, paralysis, chills, vomiting, shock, and organ failure.

Diagnostic Tests

Sickle cell test
To rule out sickle cell anemia

CBC
Decreased Hgb and hematocrit (Hct)

Serum tests
Elevated lactate dehydrogenase and bilirubin

Bone marrow aspiration
Hyperplasia

Reticulocyte count
Elevated

Urine/fecal urobilinogen
Elevated

Treatments

Surgery – Splenectomy.

Drugs
Corticosteroids to depress extracorpuscular factors and diminish inflammatory response; diuretics to prevent tubular necrosis; folic acid to increase RBC production.

General
Elimination of causative agent; erythrocytopheresis (RBC exchange); transfusion; oxygen therapy for hypoxemia; fluid and electrolyte management.

Disease Process Exposure to a known or unknown toxin depresses production of erythrocytes, platelets, and granulocytes in the bone marrow. Common toxins include ionizing radiation, chemical agents (e.g., benzene, DDT, carbon tetrachloride), and drugs (e.g., antitumor or antimicrobial agents).

Symptoms The onset is usually insidious, occurring weeks or months after exposure to the toxin. Fatigue, weakness, dyspnea, and waxy pallor of the skin and mucous membranes are characteristic. Thrombocytopenia causes hemorrhage into mucous membranes, skin, and optic fundi. Agranulocytosis leads to severe infection.

Potential Complications Chronic anemia leads to increasing hemorrhage and repeated infections, which result in death in about half of those diagnosed.

Diagnostic Tests

Complete blood count (CBC)
Decreased RBCs (normochromic, normocytic), WBCs, and hemoglobin (Hgb)

Platelet count
Decreased

Serum iron
Increased

Bone marrow biopsy
Hypocellular/hypoplastic; fatty, fibrous tissue

Reticulocyte count
Markedly decreased

Treatments

Surgery – None.

Drugs – Corticosteroids to stimulate granulocyte production; antibiotics for infection; androgens to stimulate bone marrow.

General
Removal of causative agent; bone marrow transplant from a human leukocyte antigen (HLA)-matched donor (sibling); blood transfusions; hemorrhage precautions.