Acute Blood Loss. Severe anemia may result from a deficiency of all the circulating elements, following acute blood loss. This occurs with post traumatic hemorrhage, ruptured duodenal ulcer, ectopic pregnancy and in hemophilia. The etiology of the condition is exsanguination and the symptomatology is that of shock. The blood volume is first replaced by plasma, and there is a lowering of the hemoglobin, marked increase in the platelet count and a leukocytosis. Rapid loss of one third of the blood volume (1500-2000 CC.) is usually fatal, but 50 per cent may be lost more slowly, over a period of more than 24 hours, without death. The administration of plasma or transfusions may be life saving.
Iron Deficiency. Patients of either sex with chronic iron deficiency usually give a history of chronic blood loss (melena, hemoptysis, epistaxis or metrorrhagia). Iron deficiency may also develop during periods of maximum growth in childhood, puberty and pregnancy because of its increased utilization. The blood picture is of the hypochromic, microcytic type. Because of the iron deficiency the red cells contain less hemoglobin and there is a low mean corpuscular hemoglobin concentration. Fatigability, headache, weakness or dyspnea on exertion are outstanding symptoms. The finger nails may be brittle and spoon shaped. This type of anemia responds to iron therapy.
Deficiency of Anti-Anemic Principle (B12,) in Pernicious Anemia. The liver Under normal conditions stores an antianemic factor which is absorbed from food of high protein content, such as liver, yeast and eggs. Absorption of this extrinsic factor is aided by a factor in gastric secretion, formerly called the intrinsic factor. The intrinsic factor is apparently absent in patients suffering achylia in pernicious anemia and in certain stomach disorders. The essential extrinsic factor is apparently vitamin B 12. The interaction of these two factors and their absorption from the gastrointestinal tract provides the antianemic principle stored in the liver. Its formation and absorption may be interfered with in cases of diarrhea or steatorrhea (sprue or celiac disease), or its storage in the liver may be reduced in hepatic diseases, such as cirrhosis, with resultant macrocytic anemia. This anti-anemic principle, which is necessary for the maturation of red blood cells, has been designated vitamin B 12.
In pernicious anemia caused by vitamin B12 deficiency the patients have a characteristic lemon color tint. Neurologic symptoms, such as parathesias and difficulty in walking, may be prominent, and the anemic triad, pallor, weakness and dyspnea, is present. In sprue, celiac disease and pellagra, there are diarrhea and loss of weight. All patients with macrocytic anemia may suffer with sore tongue and a variety of gastrointestinal disturbances. The blood findings in this type of anemia are characterized by macrocytosis, hyperchromia and marked variation in the size and shape of the red blood cells. Following specific therapy, signs of blood regeneration (reticulocytosis) are seen. There is leukopenia in which large multisegmented neutrophilic leukocytes are conspicuous. The platelet count may be lowered. In relapse, the icteric index may be raised to 20 or more units (normal, from 5 to 7) and circulating normoblasts are numerous. There is a marked hyperplasia of the bone marrow in which the count of nucleated red blood cells may reach 50 per cent or more with megaloblasts predomi nating. This group of anemias responds specifically to liver therapy or vitamin B 12.
