Anemia can be seen in the emergency department both as a primary pathological process or secondary to both medical and surgical diseases. Moreover, acute anemia can occur in children who have been otherwise healthy, who have systemic disease, or who have known hematologic disorders. Anemia may indicate a disorder with a single hematopoietic cell line (eg, red blood cells) or may be associated with changes in multiple cell lines indicative of bone marrow involvement, immunologic disease, peripheral destruction of erythrocytes, or sequestration of cells. Independent of the etiology, prompt diagnosis is predicated on understanding the classifications of anemia, the associated presenting symptoms, and the proper ordering and interpretation of laboratory studies. This article will discuss the evaluation, proper classification, differential diagnosis, and initial management of acute anemia using cases representative of those that might be seen in the pediatric emergency department.

1. Acute Anemia In Children
Dr.Osama Arafa Abd EL Hameed
M. B.,B.CH - M.Sc Pediatrics - Ph. D.
Consultant
of
Pediatrics & Neonatology
Head of Pediatrics Department - Port-Fouad Hospital
By

3. Anemia:
is characterized by a reduction in the number of
circulating red blood cells (RBCs), the amount of
hemoglobin, or the volume of packed red blood
cells (hematocrit).
Anemia is classified as acute or chronic.
Acute anemia denotes a sudden drop in the RBC
population due to hemolysis or acute hemorrhage.
In the emergency department (ED), acute
hemorrhage is by far the most common etiology.

4. Etiology
• The common pathway in life-threatening acute
anemia is a sudden reduction in the oxygen-carrying
capacity of the blood.
• Depending on the etiology, this may occur with or
without reduction in the intravascular volume.
• It is generally accepted that an acute drop in
hemoglobin to a level of 7-8 g/dL is symptomatic,
whereas levels of 4-5 g/dL may be tolerated in
chronic anemia, as the body is able to gradually
replace the loss of intravascular volume.

5. Bloodloss
• Blood loss is the most common cause of acute
anemia seen in the emergency department (ED).
• Iron deficiency anemia is due to chronic slow
bleeding and nutritional deficits.
• Some life-threatening causes include:
• Traumatic injury
• Massive upper or lower gastrointestinal (GI)
hemorrhage, ruptured aneurysm, and disseminated
intravascular coagulation

6. Hemoglobinopathy
• Sickle cell anemia is caused by a point mutation on
the DNA of the beta-globin chain. Valine is
substituted for glutamine in the sixth position of
the amino acid sequence. In response to oxidative
stress, hemoglobin S polymerizes, leading to
sickling and hemolysis .
• Patients with sickle cell anemia may have life-
threatening complications during acute splenic
sequestration and aplastic crisis. An aplastic crisis
is due to cessation of erythropoiesis, which is
caused by the human parvovirus B19

7. • Thalassemias
are characterized by
decreased production of
globin (alpha and beta)
chains. Patients with
thalassemia major
(homozygous for beta
thalassemia) develop severe
anemia that requires
transfusion in the first year
of life. Other forms of
thalassemia may cause
acute anemia during periods
of oxidative stress.

8. Red blood cell enzyme abnormality
• Glucose-6-phosphate dehydrogenase (G6PD) and
pyruvate kinase (PK) deficiency are the 2 most common
enzyme defects that cause hemolytic anemia.
• The 2 variants of G6PD deficiencies are African and
Mediterranean. The Mediterranean variant has
decreased enzyme activity in nearly all circulating RBCs.
When cells are exposed to oxidant stress, a life-
threatening hemolytic crisis ensues. In the African
variant, only a limited portion of the RBC population is
vulnerable at a given time; therefore, life-threatening
complications are rare.

9. Congenital coagulopathy
• Von Willebrand disease
• is the most common congenital bleeding disorder.
The disease is characterized by deficient or defective
von Willebrand factor (vWF), which is essential for
platelet adhesion. Transmission is by an autosomal
dominant pattern.
• Hemophilia A
• (classic hemophilia) is caused by factor VIII
deficiency. Severe bleeding is common. Transmission
is autosomal recessive. Hemophilia B(Christmas
disease) is due to a factor IX deficiency. Only males
are affected.

10. Autoimmune hemolytic anemia
• Autoimmune hemolytic anemia may be life
threatening. The disorder is seen in association with
autoimmune diseases (eg, lupus, certain types of
lymphomas and leukemias), or it may be drug
induced.
• Hemolysis is caused when immunoglobulin G (IgG)
autoantibody binds to RBCs, which then lose part of
the plasma membrane because of the interaction of
the autoantibodies with macrophages. With loss of
their plasma membrane, affected RBCs become
spherocytes.

11. Acquiredplateletdisorder
• Thrombotic thrombocytopenic purpura (TTP) is
rare. Arteriolar lesions with localized platelet
thrombi and fibrin deposits lead to
thrombocytopenia and hemolytic anemia.
• Idiopathic thrombocytopenic purpura (ITP) is an
autoimmune disease often precipitated by viral
infections.IgG autoantibodies bind to platelets,
which then undergo destruction in the spleen. The
platelet count may fall as low as 10,000/µL, leading
to bleeding.

12. Hemolytic-uremicsyndrome
• Acute anemia from hemolytic-uremic
syndrome (HUS) is characterized by
microangiopathic hemolytic anemia,
thrombocytopenia, and renal failure. The disorder is
similar to TTP, but arteriolar lesions are limited to
the kidney. In children, the disease is sometimes
seen after diarrheal illness caused byEscherichia
coli, Shigella and Salmonella species, or viral
gastroenteritis.
• Uremia may also lead to bleeding as a consequence
of abnormal platelet function.

13. Disseminatedintravascularcoagulation
• DIC can be caused by systemic infection, massive
transfusions, severe head injury, trauma, thermal
injury, sepsis, or cancer.
• It initially causes thrombosis due to excess release
of thrombin; this is followed by bleeding due to
consumption of coagulation factors.

14. History
• In the critically ill patient, the emergency physician
should attempt to obtain a focused history per the
mnemonic AMPLE (A llergies; M edications, including
over-the-counter drugs such as nonsteroidal anti-
inflammatory drugs [NSAIDs]; P ast medical and
surgical history;L ast meal; and E vents preceding
incident).
• For noncommunicative patients, caretakers,
paramedics, or primary physicians are a valuable source
of information. For injured patients, paramedics should
be questioned about the circumstances of the accident,
mechanism of the injury, initial vital signs, estimated
blood loss in the field, prehospital treatment initiated,
and response.

15. • Important specific queries should address
gastrointestinal (GI) and menstrual histories
(where applicable)..
• When concern for GI hemorrhage exists, obtain a
full GI history including stool color, consistency,
and frequency. Black, tarry, malodorous, and
frequent stools characterize upper GI bleeding
proximal to the ligament of Treitz. Maroon, lumpy,
irregular stools characterize lower GI bleeding.
• Consider constitutional symptoms of chronic
illnesses (eg, weight loss, night sweats, rashes,
bowel changes). Consider family history of
malignancy or hematologic problems.

16. Physical examination
• Monitor initial vital signs and address any
abnormality. Periodic measurement of vital signs
and examinations of appropriate organ.
• In patients with multiple traumas, presume that
every body cavity contains blood until investigation
suggests otherwise. The chest, abdomen, pelvis,
and extremities must undergo thorough physical
examination with imaging, as clinically indicated.
• In early hemorrhagic shock, capillary refill time may
increase and the skin may feel cool to the touch.
With progressive shock, the skin is cold to the
touch, and it appears pale and mottled.

17. • Patients with jaundice may have liver disease,
hemoglobinopathies, or other forms of hemolysis.
Purpura and petechiae suggest platelet disorders, and
hemarthrosis may be due to hemophilia. Diffuse
bleeding from intravenous (IV) sites and mucous
membranes may be due to disseminated intravascular
coagulation (DIC). In patients with alcoholic liver
disease, spider angiomata, caput medusae, umbilical
hernias, and hemorrhoids may be appreciated.
• Agitation may present secondary to acute blood loss.
When blood loss exceeds 40% of total volume, the
patient may lose consciousness.
• With chronic anemia, a hyperdynamic heart, with a
prominent point of maximal impulse (PMI), a systolic
flow murmur, and occasionally an S3, may be present.

18. • Advanced trauma life support classifies shock into 4
levels; particular findings are associated with each
level, as follows.
• In class I (< 15% blood loss), mild tachycardia may be
present, but blood pressure is normal.
• In class II (15-30% blood loss), tachycardia, tachypnea,
and a decreased pulse pressure are seen.
• Class III (30-40% blood loss) always leads to a
measurable decrease in blood pressure as well as a
significant tachycardia and a narrow pulse pressure.
• Class IV (≥40% blood loss) leads to patient demise
unless prompt resuscitative measures are taken.
Marked tachycardia and significantly decreased blood
pressure are common findings.

19. • Patients with exacerbations of chronic anemia
occasionally may present with signs and symptoms
of congestive heart failure.
• Organomegaly is a common finding in patients with
chronic blood disorders. A palpable spleen and an
enlarged hepatic inferior border (more than 3 cm
below the right midclavicular costal margin) may
suggest chronic anemia.

20. CBC
• The most important index is the mean corpuscular
volume (MCV), on the basis of which anemias can be
classified as microcytic, normocytic, or macrocytic.
• Microcytic anemias (usually defined as MCV < 80)
include anemias of chronic disease, iron deficiency, lead
poisoning, and the hemoglobinopathies (ie, sickle cell
disease, sideroblastic anemia, thalassemias).
• Normocytic anemias (MCV 80-100) include anemias of
acute blood loss, hemolysis, uremia, and cancer
• Macrocytic anemias (usually defined as MCV >100)
include anemias related to alcoholism, folate and
vitamin B-12 deficiencies (pernicious anemia), and
some preleukemic conditions.

21. Reticulocyte count
• The reticulocyte count may suggest an inadequate bone
marrow response to anemia, which can occur in patients
with aplastic anemia or hematologic cancers or can be due
to drugs or toxins.
• For patients with hemolytic anemias, use a Finch
reticulocyte count, which corrects for the anemia and the
2-day lifespan (versus 1-d lifespan, typically) of immature
reticulocytes. The Finch count is the measured reticulocyte
count multiplied by the measured hematocrit level, divided
by 45, and then divided by 2.
• A simple corrected reticulocyte count is sufficient in
patients with sickle cell disease. This is the measured
reticulocyte count multiplied by the measured hematocrit
level, divided by 45. Normal reticulocyte counts are 0.5-
1%.

22. Additional Laboratory Studies
• Other studies that may be helpful in evaluating anemia
but may not be applicable to the acute ED setting
include the following:
• Iron studies
• Folate and vitamin B-12 levels
• Lead levels
• Hemoglobin electrophoresis
• Factor deficiency tests
• Bleeding time
• Bone marrow aspiration
• Coombs test

23. Urine & stool studies
•Urinalysis should be
performed for
detection of
hemoglobinuria or
urobilinogen could
indicate hemolysis.
•Stool analysis for
fresh & occult blood

24. Ultrasonography
• Ultrasonography is a quick, noninvasive, and relatively
simple bedside test useful for diagnosing
intraperitoneal bleeding. The focused abdominal
sonography for trauma (FAST) examination is
commonly performed to diagnose intra-abdominal
hemorrhage in unstable trauma patients. When
performed by experienced providers.
• In pregnant females with suspected ectopic pregnancy,
correlate the sonogram with the serum beta human
chorionic gonadotropin (β-hCG) level. It is important to
remember that most ectopic pregnancies occur 5-8
weeks after the last normal menses.

25. Principles of Therapy
• Therapeutic approaches to treat anemia include
blood and blood products, immunotherapies,
hormonal/nutritional therapies, and adjunctive
therapies.
• The goal of therapy in acute anemia is to restore
the hemodynamics of the vascular system and to
replace lost red blood cells (RBCs). To achieve
this, the practitioner may use mineral and
vitamin supplements, blood transfusions,
vasopressors, histamine (H2) antagonists, and
glucocorticosteroids.

26. Use of blood and blood products
• Correction of acute anemia often requires blood, blood products, or both.
• Multiple studies have reported worse outcomes (eg, higher mortality and
morbidity rates) in transfused patients compared with non-transfused (or
less-transfused) patients.
• Consequently, a conservative approach is indicated. Although the specific
threshold is uncertain, restricting transfusion to patients with hemoglobin
levels <6-8 g/dL may be associated with better outcomes.
• Whole blood contains RBCs, platelets, and coagulation factors; however, it is
rarely used as a treatment option. Packed red blood cells (PRBCs) are the
remaining components of whole blood after the plasma and platelets are
removed.
• One unit of PRBCs is the product of 1 unit of whole blood and has a volume
of 250-300 mL. Each unit of PRBCs is expected to raise the hematocrit level
by 3 points.

27. • Each unit of platelets contains 50 mL of plasma and has
normal amounts of fibrinogen and coagulation factors. Some
decrease in factors V and VII is noted in comparison with
whole blood. Each unit of platelets raises the platelet count
by approximately 10,000/µL. The usual pediatric dose is 10-20
ml /kg do not exceed 300 ml .
• Fresh frozen plasma (FFP) is the medium that suspends RBCs
and platelets and contains all the coagulation factors. The
coagulation factors are diluted. Patients with factor V and XI
deficiency and those with coagulopathies due to liver disease
are the best candidates for FFP administration; most of the
other coagulation factors are now available in concentrated
forms.
• Cryoprecipitate is derived from the precipitate collected from
thawed FFP. It contains fibrinogen, factor VIII, von Willebrand
factor (vWF), and factor XIII. It is ideal for treatment of mild
hemophilia A and conditions that lead to afibrinogenemia.

28. Management of Acute Anemia by Etiology
• In the emergency department (ED), the first steps
are to evaluate the ABCs (Airway, B reathing,
and C irculation) and to treat any life-threatening
conditions immediately. Crystalloid is the initial
fluid of choice.
• Transfer may be considered for patients who are
hemodynamically and neurologically stable or
when a higher level of care is required. The
benefits of transfer must outweigh the risks.

29. Patients with ongoing
hemorrhage or
ongoing hemolysis
are unstable and
should not be
transferred unless the
initial facility cannot
adequately care for
the patient.
Specific management
varies, depending on
the etiology of the
acute anemia and the
patient’s condition.

30. THANKYOU