Approach to Anaemia in the ED
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This document discusses the approach to anaemia in the emergency department. It begins with definitions and an overview of the main causes of anaemia: blood loss, decreased red blood cell production, and increased red blood cell destruction. Two case studies are then presented to illustrate anaemia due to blood loss and decreased production. The remainder of the document covers the specific causes, clinical presentations, investigations, and treatments for anaemia resulting from blood loss, decreased production, and increased destruction. It emphasizes that the treatment depends on identifying the underlying cause of the anaemia. Asymptomatic stable cases can be discharged with follow-up, while symptomatic or unstable patients generally require admission.
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Approach to Anaemia in the ED
- 1. THE APPROACH TO ANAEMIA IN THE EMERGENCY DEPARTMENT Dr Sinéad Taylor – CME 20/07/2017
- 2. Definition An absolute decrease in the number of circulating red blood cells
- 3. Overview 1. Blood loss 2. Decreased RBC production 3. Increased RBC destruction Anaemia is not a diagnosis; it is a finding
- 4. Case 1 • 40 year old woman presents with 2/24 Hx severe vomiting and epigastric pain. • PMHx: Ankle ORIF 1/12 ago • Rx: Paracetamol, Celebrex. Implanon. • SHx: Accountant, non-smoker, minimal ETOH. • Looks pale. HR 92, BP 98/50mmHg, RR 22, SaO2 99%RA, afebrile. Patient’s result Normal range Hb 120 115-165 g/L Haematocrit 41 37-47% MCH (mean corpuscular haemoglobin) 30 27-32 pg MCV (mean corpuscular volume) 83 80-100 fL Reticulocytes 0.8% 0.2-2% White blood cells 15 4-11 x 109/L Platelets 250 150-400 x 109/L
- 5. Case 1 • Given some ondansetron and buprenorphine. • Continues to vomit in ED, complaining of worsening abdominal pain. • HR 130, BP 85/40mmHg • FBP repeated 4 hours later Patient’s result Normal range Hb 81 115-165 g/L Haematocrit 41 37-47% MCH (mean corpuscular haemoglobin) 30 27-32 pg MCV (mean corpuscular volume) 83 80-100 fL Reticulocytes 3% 0.2-2% White blood cells 14.5 4-11 x 109/L Platelets 380 150-400 x 109/L Dx: GI bleed from peptic ulcer, complicated by perforation
- 6. Anaemia due to blood loss
- 7. Causes • Trauma • Blunt trauma to mediastinum • Pulmonary contusion/ haemopneumothorax • Intraperitoneal injury • Retroperitoneal injury • Pelvic disruption • Long bone injury • Non-trauma • GI haemorrhage • Oesophageal varices • Peptic ulcer • Gastritis • Mallory-Weiss tear • Colonic/rectal bleeding • Obstetric/gynae • Ruptured ectopic pregnancy • Menorrhagia • Threatened miscarriage • Antepartum haemorrhage • Other • Epistaxis • Post-op • Secondary to bleeding diathesis
- 8. Investigation • Hyperacute blood loss may have a normal Hb • Acute haemorrhage: • MCV: Macrocytic or normocytic • MCH: Normochromic • Reticulocytes: Reticulocytosis • Chronic haemorrhage often GI – may present as microcytic anaemia with iron deficiency
- 9. Treatment • DRABCD • Find the source of bleeding and control it • Trauma: blood on the floor and 4 more • Correct coagulopathy • Beware the lethal triad! • Hypothermia • Acidosis • Coagulopathy • Restore blood volume • Crystalloid fluids • Blood products • Damage control resuscitation/permissive hypotension (controversial) – aim SBP 80- 100mmHg, or MAP >65mmHg
- 13. Case 2 • 30 year old man • Referred by GP with 6 month history of fatigue • No PMHx, regular medications • SHx: Medical student. No ETOH, non-smoker. • Haemodynamically normal and stable. Looked paler than me.
- 15. Anaemia due to decreased RBC production
- 16. Causes Microcytic (MCV <80) Normocytic (MCV 80- Macrocytic (MCV > 100 Iron deficiency Chronic disease Vitamin B12 deficiency Thalassaemia Chronic renal infufficiency Folate deficiency Sideroblastic anaemia Hypothyroidism Liver disease Lead intoxication Bone marrow suppression Reticulocytosis Chronic disease (late) Aplastic anaemia Myelodysplastic syndromes ETOH abuse Drugs (hydroxyurea, AZT, chemoTx like MTX)
- 17. Microcytic anaemia • Iron deficiency • Most common nutritional disorder in the world • 15-20% TBI stored – bound to haemosiderin or ferritin • Rest of TBI complexed with functional proteins (80% with Hb) • Causes: • Low dietary intake - rare in developed nations • Chronic blood loss – most important. HUNT FOR THE BLOOD LOSS. • Malabsorption • Excessive demand (infancy, pregnancy) • Blood cell morphology • Hypochromic, microcytic • Poikilocytosis • Increased RBC central pallor • Plummer-Vison Triad • Hypochromic, microcytic • Atrophic glossitis • Oesophageal webs
- 18. Microcytic anaemia • Thalassaemia • Genetic autosomal defect • Thalassaemia major (homozygous) – severe anaemia, hepatosplenomegaly, jaundice, abnormal childhood development, premature death • Requires blood transfussions • Patients often die from iron toxicity • Thalassaemia minor (heterozygous) – mild microcytic, hypochromic anaemia • Usually asymptomatic. No treatment needed. • Sideroblastic anaemia • Defect in porphyrin synthesis • Pallor, splenomegaly • Idiopathic: pre-leukaemic state • Secondary: Toxins, haemolytic + megaloblastic anaemia, infection, leukaemia, rheumatoid arthritis. • Lead intoxication – reversible cause of sideroblastic anaemia
- 20. Normocytic anaemia • Chronic disease • Common • Haematocrit rarely <25% to 30% patients often asymptomatic; therapy rarely required • May be microcytic • Iron studies: Low TIBC, normal ferritin • Chronic renal insufficiency • Multifactorial • Insufficient erythropoietin production • Effectively treated with recombinant erythropoietin • Hypothyroidism • Bone marrow failure – low reticulocytes
- 21. Normocytic anaemia • Aplastic anaemia – pancytopaenia secondary to failure of pluripotent myeloid stem cells • 50-65% idiopathic • Toxic exposures • Drugs, chemicals – benzene, alkylating agents, antimetabolic agents (vincristine), chloramphenicol, chlorpromazine, streptomycin, NSAIDs • Radiation • Viral infections – seronegative hepatitis, EBV, CMV • Inherited diseases • Fanconi anaemia • Defects in telomerase activity • Needs BMAT for diagnosis. • Treatment with stem cell transplant, or immunosuppression
- 22. Clinical Pathway: Normocytic anaemia Normocytic anaemia due to reduced RBC production should have normal or low reticulocytes (elevated in acute blood loss, haemolytic anaemia)
- 23. Macrocytic anaemia • Vitamin B12 deficiency • Pernicious anaemia, due to autoimmune impairment of intrinsic factor secretion • Malabsorption – gastritis, gastric bypass, parasites. • Dietary deficiency (less common) • Folate deficiency • Malabsorption/intrinsic intestinal disease, e.g., coeliac disease • ETOH • Haemodialysis (increased loss) • Folic acid antagonsists or metabolic inhibitors of metabolism (e.g., methotrexate) • Vit B12 and folate co-enzymes for thymidine synthesis • Deficiency inadequate DNA synthesis defective nuclear maturation of rapidly proliferating cells -> abnormally large RBCs and megaloblasts (erythroid precursors)
- 24. Macrocytic anaemia • Liver disease • Reticulocytosis • Myelodysplastic syndromes • Group of syndromes affecting the elderly • No reduction of bone marrow cellularity, but mature RBCs, granulocytes and platelets are disordered and dysfunctional • 1/3 progress to AML • ETOH abuse • Drugs – hydroxyurea, azathioprine, methotrexate and other chemotherapy drugs
- 26. Management • Depends on the cause! • Anaemia caused by decreased RBC have an insidious onset • Associated with low reticulocytes. RBC indices and peripheral blood film smear morphology useful for diagnosis • May require bone marrow examination • Definitive diagnosis often not made in ED refer to GP or haematologist • Replacement should not be initiated except in circumstances that require transfusion • Supplemental iron especially should be avoided
- 27. Anaemia due to increased RBC destruction
- 28. Haemolysis • Intravascular • Typically acute, dramatic • Large numbers of RBCs lysed in circulation • Initially free Hb binds to haptoglobin + haemopexin transported to liver converted to bilirubin, conjugated, and excreted. • Binding and transport overwhelmed free Hb in blood • Clinical picture: • Mild chronic anaemia • Transfusion reaction: Fever, abdominal and back pain, mental state changes • Jaundice
- 29. Haemolysis • Extravascular • More common • Clinically better tolerated • Clinical picture: • Mild-mod anaemia • Jaundice • Splenomegaly • Signs and symptoms vary with severity and chronicity
- 30. Intravascular haemolysis: causes IMMUNE • ABO or Rhesus incompatibility • Haemolytic disease of the newborn • Transfusion mismatch • Warm antibody type AIHA (most common) • IgG mediated • Drugs: Methyldopa, penicillin, cephalosporins, erythromycin, probenecid, paracetamol, ibruprofen • Autoimmune diseases: SLE, RA • Lymphoproliferative diseases • Idiopathic • Cold agglutinin type • Complement mediated • Infections: Mycoplasma, EBV • Lymphoproliferative • Idiopathic
- 31. Intravascular haemolysis: causes NON-IMMUNE • Mechanical • March haemoglobinaemia • Infection – severe sepsis, malaria, babeosis, Clostridium perfringens, CMV, EBV, HSV, HIV, measles, varicella, • Drugs: antimalarials, arsine, copper, dapsone, lead, local anaesthetics (lignocaine, benzocaine), nitrates, nitrites, sulphonamides • Microangiopathic haemolytic anaemia • Envenoming • HUS • TTP • HELLP • Liver disease – Wilson’s disease
- 32. Extravascular haemolysis: Causes • G6PD deficiency • Genetic: X-linked. African or Mediterranean descent. • Exposure to fava beans • Drugs: dapsone, primaquine, nitrofurantoin • Membrane abnormalities • Hereditary spherocytosis • Hereditary eliptocytosis • Paroxysmal nocturnal haemoglobinuria • Haemoglobinopathies • Sickle cell • Thalassaemia • Hypersplenism
- 34. Management • Again, depends on the cause • DRABCD • Haematology input • Find and remove/treat underlying cause, if possible • Targeted blood product replacement • Splenectomy may be considered for extravascular causes • Plasmapheresis for temporary treatment of fulminant acute haemolysis, but will not treat the underlying problem • Warm AIHA • First line: corticosteroids (decrease IgG production) • Second line: Splenectomy (site of ab production) • Third line: cyclophosphamide or azathioprine • Cold AIHA • Keep them warm! • Corticosteroids and splenectomy ineffective
- 35. Summary
- 38. Disposition • Symptomatic acute anaemia generally requires admission • If patient discharged, they need very clear instructions regarding when and why they should represent • Don’t discharge people requiring RBC transfusions in ED • Unless they receive chronic outpatient transfusions • Asymptomatic stable chronic anaemia • Can be safely discharged • Acute/newly diagnosed stable anaemia • Can be discharged, but need clear follow up arranged
- 39. References 1. Janz TG, Johnson RL, Rubenstein SD. Anemia in the Emergency Department: Evaluation and Treatment. Emergency Medicine Practice. 2013;15(11):1-16. 2. Braunstein EM. Anaemias Caused by Deficient Erythropoiesis Merck; 2016 [cited 2017. Available from: http://www.merckmanuals.com/professional/hematology-and-oncology/anemias-caused-by-deficient- erythropoiesis. 3. Cadogan M. Investigations - Anaemia [cited 2017. Available from: https://lifeinthefastlane.com/investigations/anaemia/. 4. Cameron P, Jelinek G, Kelly A-M, Brown A, Little M, editors. Textbook of Adult Emergency Medicine. 4 ed: Elsevier; 2015. 5. Janz TG, Johnson RL, Rubenstein SD. Anemia in the Emergency Department: Evaluation and Treatment. Emergency Medicine Practice. 2013;15(11):1-16. 6. Nickson C. Anaemia 2014 [cited 2017. Available from: https://lifeinthefastlane.com/ccc/anaemia/. 7. Nickson C. Major Haemorrhage in Trauma 2015 [cited 2017. Available from: https://lifeinthefastlane.com/ccc/major- haemorrhage-in-trauma/. 8. Nickson C. Haemolytic Anaemia 2016 [cited 2017. Available from: https://lifeinthefastlane.com/ccc/haemolytic- anaemia/. 9. Kumar V, Abbas AK, Fausto N, Aster JC. Pathologic Basis of Disease. 8 ed. Robbins, Cotran, editors. Philadelphia: Saunders Elsevier; 2010.
Editor's Notes
- If a patient is anaemic, they are doing one of three things: Bleeding Not producing enough red blood cells Destroying blood cells too quickly
- Damage control resuscitation – 3 components: permissive hypotension early haemostatic resuscitation damage control surgery Aim of this: maintain volume Control haemorrhage Correct lethal triad
- Low haemoglobin Low reticulocytes MCV high MCH high Macrocytic, hyperchromic anaemia But low reticulocytes, and suppression of all lineages
- Chronic blood loss – most important cause. E.g., menstruation, GI bleeding.
- Chronic blood loss – most important cause. E.g., menstruation, GI bleeding.
- Antibodies bind to RBCs and cause their premature destruction
- Antibodies bind to RBCs and cause their premature destruction