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

19. Clinical Pathway: Microcytic
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

25. Clinical Pathway: Macrocytic
anaemia

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

33. Clinical Pathway: Haemolytic
anaemia

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.