Clinical Emergencies Presented by Anemia Tridip Chatterjee 1,2* and Annesha Das 2 1 Suraksha Genomics (R & D Division of Suraksha Diagnostics), Kolkata, West Bengal, India 2 Institute of Genetic Medicine and Genomic Science, Kolkata, West Bengal, India * Corresponding author: Tridip Chatterjee, Suraksha Genomics (R & D Division of Suraksha Diagnostics), DD-18/1, Sector 1, Salt Lake, Kolkata-700064, West Bengal, India, Tel: +91-033-6619-1000; +91-09831325280; E-mail: ctridip@gmail.com, tridip.academic@gmail.com Received date: May 20, 2016; Accepted date: May 28, 2016; Published date: June 04, 2016 Copyright: © 2016 Chatterjee T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Anaemia affects 24.8% of the population worldwide. It has wide variety in terms of clinical manifestation of the disease severity. It can also ranges from almost asymptomatic to severe haemolytic anaemia. In contrast to all other nucleated cells, RBCs show very interesting biology. An alteration in any of the major factors in RBCs (eg. shape, size, and structural or functional or quantitional abnormalities in haemoglobin) usually results in compensatory changes in the other compensatory factors. Sometimes, the compensatory responses may fail because of severity of disease or due to underlying pathologic conditions. The result of failed compensatory responses is cellular dysfunction, tissue hypoxia and eventual cell death, which ultimately leads to severity in anaemia and emergency situations due to it. In this paper, we have concentrated to focus on how the extrinsic and intrinsic defects on RBCs cause severe haemolytic anaemia, leading to emergencies. We have also discussed the destructions of RBCs in both extra and intra vascular regions, contributing to severe haemolysis. Other than haemolytic anaemia, other structural and functional defects of haemoglobin, which can lead to life threatening conditions (e.g.: β thalassemia major and transfusion dependent haemoglobinopathies) are also being discussed here. In nutshell, this paper is an exclusive review on all forms of clinical emergencies due to anaemia’s and other haemoglobinopathies. Keywords: Anaemia; Haemolysis; Haemoglobinopathies Introduction Anaemia is defned by an absolute decrease in the number of red blood cells (RBCs), circulating in the blood. Te diagnosis of anaemia is based on the laboratory measurements of RBC indices. If that found to fall below accepted normal values (Table 1) [1], then it is considered as anaemia. Age Haemoglobin (g/dL) Hematocrit (%) Red Blood Cell Count (x106/mcL) 3 months 10.4-12.2 30-36 3.4-4.0 3-7 years 11.7-13.5 34-40 4.4-5.0 Adult man 14.0-18.0 40-52 4.4-5.9 Adult woman 12.0-16.0 35-47 3.8-5.2 Table 1: Normal values of RBC indices. In worldwide scale, anaemia afects 24.8% of the population. It is more prevalent in children and pregnant women [2], than the adult men and women. It is also seen to be more prevalent in women than men. Te prevalence of anaemia varies depending on the RBC indices used to defne it. Anaemias in most cases are chronic, but it can also give rise to emergency in some special cases or clinical conditions. It can be presented as an emergency is mainly due to some clinical causes like acute blood loss or more rarely acute haemolysis or marrow involvement by hypoplasia or malignancy. More chronic types of anaemia can also be presented as an emergency, when the Haemoglobin (Hb) level falls to much lower than the normal level (Table 1), whereby the patient him or herself develops symptoms or when other disorders, e.g. myocardial insufciency or respiratory disease co-exist. Erythropoesis and Anaemia Te pluripotent stem cells of bone marrow diferentiate into erythroid, myeloid, megakaryocytic and lymphoid progenitors. Erythropoietin stimulates the growth and diferentiation of erythroid progenitors, resulting in production of RBCs. When the normoblast extrudes its nucleus, it retains its ribosomal network, which identifes the reticulocyte. Te reticulocyte keeps its ribosomal network for approximately four days, three of which are normally spent in the bone marrow and remaining one in the peripheral circulation. Te RBC develops as the reticulocyte loses its ribosomal network, and the mature RBC circulates for 110 to 120 days. Te old erythrocytes are destined for phagocytosis by macrophages that can detect senescence signals. Under steady-state conditions, the rate of RBC production is equal to the rate of RBC destruction, resulting the constant amount of production of RBCs. Te mass of RBCs remains constant because equal numbers of reticulocytes replace the destroyed senescent erythrocytes [3]. Anaemia ofen can stimulate the erythropoiesis, mainly controlled by the hormone erythropoietin. Erythropoietin is a glycoprotein, produced primarily in the kidney. It regulates the diferentiation of the committed erythroid stem cell and thereby controlling the production of RBCs. Tissue hypoxia and by products of RBC destruction pathway Emergency Medicine: Open Access Chatterjee and Das, Emerg Med (Los Angel) 2016, 6:4 DOI: 10.4172/2165-7548.1000327 Review Article Open Access Emerg Med (Los Angel) ISSN:2165-7548 EGM, an open access journal Volume 6 • Issue 4 • 1000327 E m e r g e n c y M e d i c i n e : O p e n A c c e s s ISSN: 2165-7548