The definition of anemia is either a decreased amount of circulating red blood cells (RBCs), the amount of hemoglobin (Hgb), or volume of packed RBCs (hematocrit). The World Health Organization defines anemia as a hemoglobin level less than 13 g/dL in men and less than 12 g/dL in women.
Anemia classifies as either acute or chronic:
Anemia can result from many events.
One way to classify hemolytic anemias is intracorpuscular (the defect is within the RBC itself) versus extracorpuscular (the problem is external to the RBC).
Disseminated intravascular coagulation (DIC}: a condition in which systemic activation of coagulation occurs, resulting in the formation of intravascular fibrin, which initially causes thrombosis then is followed by bleeding due to consumption of coagulation factors.
Toxic agents and Drugs: hyperbaric oxygen (or 100% oxygen), methyldopa, nitrates, chlorates, methylene blue, dapsone, cisplatin, and numerous aromatic (cyclic) compounds; other chemicals include arsine, stibine, copper, and lead
Anemia is common, affecting one-fourth of the population overall, approximately 50% of hospitalized patients, and up to 75% of elderly hospitalized patients. Data collected during the year 2000 on over 81000 health plan members show that the highest rates of anemia are in patients with chronic kidney disease (34.5%), cancer (21%), chronic heart disease (18%), inflammatory bowel disease (13%), rheumatoid arthritis (10%), and infection with human immunodeficiency virus (10%).
The common causes in acute anemia are hemolysis or hemorrhage, which results in a sudden reduction in RBCs. When the drop is quick, hemoglobin of 7 to 8 g/dL is usually symptomatic since the body has inadequate time to compensate and replace the volume lost. Healthy individuals can tolerate 20% loss of their blood volume without significant symptoms, due to reflex vasospasm and redistribution of blood flow. With greater losses, patients develop the signs and symptoms of hypovolemia. Compensatory mechanisms such as redistribution of blood flow are no longer sufficient to maintain blood pressure, and clinical signs include postural hypotension, altered mental status, cool and/or clammy skin, tachycardia, and hyperventilation. In acute hemorrhage, hemoglobin and hematocrit levels can be normal, owing to concomitant loss of both red cells and plasma, which becomes apparent after patient’s plasma volume is restored, either spontaneously or with intravenous fluids.
Viewing the peripheral blood smear under a microscope
Get a thorough but focused history if possible, but priority assessment should include the ABCs (Airway, Breathing, Circulation) and if necessary, initiating resuscitation.
If patients are unable to communicate, obtain as much history as possible from EMS or those at the bedside.
History should also focus on the possible source of bleeding, such as a more complete gastrointestinal (GI) history if there is a concern for GI hemorrhage, and likewise a focused menstrual and/or pregnancy history if concern for gynecological causes.
Vital signs should undergo frequent monitoring. As above, the initial exam should focus on the organ thought to be the cause of the patient’s bleeding. If trauma is suspected, then the chest, abdomen, pelvis, and extremities must be both physically examined and imaged, as clinically indicated.
Below are the various stages of presentation of hemorrhagic shock:
Other useful skin examination findings include:
Further workup is essential in learning the etiology and acuity.
Other tests that merit consideration include:
Sickle cell anemia
The decision to begin transfusion depends on the rate of fall of the hemoglobin and the patient’s clinical condition. Blood transfusion is necessary for aplastic crisis indicated by low reticulocyte counts. In the case of vaso-occlusive crisis, exchange transfusion is warranted to reduce the number of sickle cells and to lower the viscosity of the blood. Hydroxyurea can be used to reduce the incidence of sickle cell crisis.
Patients with thrombocytopenia with clinical evidence of bleeding should receive a platelet transfusion. Patients with platelet count lower than 10,000/microliter are at risk for spontaneous cerebral hemorrhage and thus require a prophylactic transfusion. Large-volume plasmapheresis with FFP replacement is the preferred treatment for HUS and TTP. Many patients will require daily plasmapheresis. Goals include increasing platelet count, decreasing lactate dehydrogenase (LDH), and decreasing red blood cell (RBC) fragments, which will indicate a positive response to treatment. Many patients also receive high-dose glucocorticoids in addition to antiplatelet agents (e.g., aspirin). Patients with a poor response to plasmapheresis can receive with splenectomy or immunosuppression.
In atypical HUS (aHUS), the initial management is supportive and similar to the approach used for STEC-HUS. However, in patients with severe complement-mediated HUS who are at risk for death or ESRD, use of eculizumab, a humanized monoclonal antibody to C5 is recommended. Evidence suggests that early initiation can improve renal and nonrenal recovery.
The goal in ITP is to provide a safe platelet count to prevent clinically significant bleeding rather than normalizing the platelet counts. Bleeding risk is highest when the platelet counts are less than 10,000/microL. For all patients with severe bleeding (e.g., intracranial, gastrointestinal) and a platelet count less than 30,000/microL, immediate platelet transfusion along with ITP-specific therapy including intravenous immune globulin (IVIG), glucocorticoids, and romiplostim is recommended.
Congenital bleeding disordersTreatment of von Willebrand disease is with desmopressin (DDAVP), recombinant von Willebrand factor (rVWF), or von Willebrand factor/factor VIII (vWF/FVIII) concentrates; Factor VIII and IX concentrates are used for the treatment of hemophilia A and B respectively, and the dosage is based on the site of the bleeding.
Disseminated intravascular coagulation (DIC)
A primary principle in the management of DIC is the treatment of the underlying cause to eliminate the stimulus for ongoing coagulation and thrombosis; as long as the platelet count is greater than or equal to 10,000/microL, prophylactic transfusion of platelets and coagulation factors are not recommended. Treatment is justified in patients with severe bleeding, are at high risk for bleeding, or require invasive procedures. Antifibrinolytic agents, such as tranexamic acid (TXA), epsilon-aminocaproic acid (EACA), or aprotinin are generally contraindicated.
Do Not Miss
The most severe complication occurs from hypovolemic shock from hemorrhage. Tissue hypoxia can occur, resulting in end-organ damage, including a heart attack, heart failure, renal failure, acute hypoxic respiratory failure, or other end-organ damage.
Interdisciplinary care in acute anemia results in improved outcomes. Education should focus on compliance with any medications (such as iron, steroids, etc.), avoiding triggers (such as alcohol, NSAID use) and a solid understanding of what caused the anemia and how best to avoid another episode. The prognosis of acute anemia largely depends on the etiology and is highly variable — rapid stabilization and treatment results in a better prognosis.
|||Vieth JT,Lane DR, Anemia. Hematology/oncology clinics of North America. 2017 Dec; [PubMed PMID: 29078923]|
|||Cappellini MD,Motta I, Anemia in Clinical Practice-Definition and Classification: Does Hemoglobin Change With Aging? Seminars in hematology. 2015 Oct; [PubMed PMID: 26404438]|
|||Joly BS,Coppo P,Veyradier A, Thrombotic thrombocytopenic purpura. Blood. 2017 May 25; [PubMed PMID: 28416507]|
|||Webster K,Schnitzler E, Hemolytic uremic syndrome. Handbook of clinical neurology. 2014; [PubMed PMID: 24365375]|
|||Picard C,Burtey S,Bornet C,Curti C,Montana M,Vanelle P, Pathophysiology and treatment of typical and atypical hemolytic uremic syndrome. Pathologie-biologie. 2015 Jun; [PubMed PMID: 25845294]|
|||Levi M, Diagnosis and treatment of disseminated intravascular coagulation. International journal of laboratory hematology. 2014 Jun; [PubMed PMID: 24750668]|
|||Liebman HA,Weitz IC, Autoimmune Hemolytic Anemia. The Medical clinics of North America. 2017 Mar; [PubMed PMID: 28189175]|
|||Nissenson AR,Wade S,Goodnough T,Knight K,Dubois RW, Economic burden of anemia in an insured population. Journal of managed care pharmacy : JMCP. 2005 Sep; [PubMed PMID: 16137214]|
|||The Lancet Haematology, Updates on blood transfusion guidelines. The Lancet. Haematology. 2016 Dec; [PubMed PMID: 27890071]|
|||Napolitano LM, Anemia and Red Blood Cell Transfusion: Advances in Critical Care. Critical care clinics. 2017 Apr; [PubMed PMID: 28284299]|