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Handbook of Pediatric Hematology
and Oncology
Handbook
of Pediatric
Hematology
and Oncology
Children’s Hospital &
Research Center Oakland
Third Edition
This edition first published 2021
© 2021 John Wiley & Sons Ltd
Wiley‐Blackwell (1e, 2012)
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted,
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Library of Congress Cataloging‐in‐Publication Data
Names: Hastings, Caroline, 1960– author. | Torkildson, Joseph C., author. |
Agrawal, Anurag K. (Anurag Kishor), author. | Children’s Hospital &
Research Center Oakland (Oakland, Calif.)
Title: Handbook of pediatric hematology and oncology : Children’s Hospital
& Research Center Oakland / Dr Caroline A. Hastings, Dr Joseph C.
Torkildson, Anurag K. Agrawal.
Description: Third edition. | Hoboken, NJ : Wiley-Blackwell, 2020. |
Includes bibliographical references and index.
Identifiers: LCCN 2020023659 (print) | LCCN 2020023660 (ebook) | ISBN
9781119210740 (paperback) | ISBN 9781119210764 (adobe pdf) | ISBN
9781119210757 (epub)
Subjects: MESH: Hematologic Diseases | Child | Neoplasms | Handbook
Classification: LCC RJ411 (print) | LCC RJ411 (ebook) | NLM WS 39 | DDC
618.92/994–dc23
LC record available at https://lccn.loc.gov/2020023659
LC ebook record available at https://lccn.loc.gov/2020023660
Cover Design: Wiley
Cover Images: © Billion Photos/Shutterstock
Set in 9.25/11.5pt Minion Pro by SPi Global, Pondicherry, India
10 9 8 7 6 5 4 3 2 1
On a day‐to‐day basis, the patients and their families continue to show us how to live gracefully
in even the most unbearable of times and inspire us to endeavor for improved outcomes. Our
experiences have taught us the magnitude of remembering our roles: “to cure sometimes, to
relieve often, to comfort always.” (anonymous, fifteenth century)
Contents
Preface, ix
Acknowledgments, xi
2 Hemolytic Anemia, 15
4 Thalassemia, 51
5 Transfusion Medicine, 63
6 Chelation Therapy, 79
9 Hemophilia, 103
10 Thrombophilia, 111
12 Thrombocytopenia, 133
19 Neuroblastoma, 245
viii Contents
Formulary, 409
Index, 489
Preface
The pace of change in the field of pediatric and observing the myriad variations in dis-
hematology, oncology, and hematopoietic ease and individual nuances that are not
cell therapies is staggering. Molecular biol- addressed in large studies or case reports,
ogy, genomics, and biochemistry have accel- all the while expanding foundational
erated the knowledge and understanding of knowledge.
disease states and further highlight the com- This handbook represents the work of
plex interplay of clinical, genetic, and social our colleagues at Children’s Hospital &
factors that constantly challenge us in the Research Center Oakland toward this
rapid application of novel findings to treat endeavor. The guidelines offered here have
patients with the goal of improved outcomes. been used to instruct medical students,
This translation of knowledge to the unique pediatric residents, nurses, pediatricians,
patient before us, the true art of the physi- and hematology/oncology fellows for over
cian, encompassing experience, knowledge, 25 years. This handbook provides clinical
intuition, and understanding of the individ- approaches for common problems in pedi-
ual needs and goals of patients and families, atric hematology, oncology, hematopoietic
can be overwhelming. What is needed is a stem cell transplant, and newer cellular ther-
practical, tested approach to analyze and apies; knowledge to organize and evaluate
address these problems to ensure timely the care of your patients; and a framework
evaluation, competent clinical care, and to incorporate ever‐expanding psychosocial
avoidance of pitfalls that might negatively needs, clinical studies, medical treatments,
impact the patient or future treatment and science. All of these are essential com-
options. This practical approach is achieved ponents that encompass the care of the child
by spending time with patients and families with blood disorders and cancer.
Acknowledgments
We are grateful to Yoram Unguru, MD, MS, Coleman Abadi, Assistant Professor of pedi-
MA, for submission of the expert case and atrics at UCSF Benioff Children’s Hospital
teaching guide in Chapter 29. Dr. Unguru is an Oakland; Dr. Cheryl Peretz, senior research
attending physician in the Division of Pediatric fellow and clinical instructor at UCSF
Hematology/Oncology at the Herman & Benioff Children’s Hospital Oakland; and
Walter Samuelson Children’s Hospital at Sinai Dr. Monica Davini, attending physician in
and Chairman of the Sinai Hospital Ethics the Division of Pediatric Hematology/
Committee, as well as attending at the Johns Oncology at Banner—University Medical
Hopkins Berman Institute of Bioethics. Center, Tucson Campus in Tucson, Arizona.
We are also extremely appreciative of These cases appear in Chapters 18, 15,
patient cases submitted by Dr. Christina and 11, respectively.
1 Approach to the
Anemic Child
Anemia is the condition in which the cell indices are very helpful in the diagnosis
concentration of hemoglobin or the red
and classification of anemia. They allow for
cell mass is reduced below normal. Anemia classification by the cell size (mean corpus
results in a physiological decrease in the cular volume [MCV]), give the distribution
oxygen‐carrying capacity of the blood and of cell size (red cell distribution width
reduced oxygen supply to the tissues. Causes [RDW]), and may give important diagnos
of anemia are increased loss or destruction tic clues if specific morphological abnor
of red blood cells (RBCs) or a significant malities are present (e.g., sickle cells, target
decreased rate of production. When evalu cells, and spherocytes). The MCV, RDW,
ating a child with anemia, it is important and reticulocyte count are helpful in the
to determine if the problem is isolated to differential diagnosis of anemia. A high
one cell line (e.g., RBCs) or multiple cell RDW, or anisocytosis, is seen in stress
lines (i.e., RBCs, white blood cells [WBCs], erythropoiesis and is often suggestive of
or platelets). When two or three cell lines iron deficiency or hemolysis. A normal or
are affected, it may indicate bone marrow low reticulocyte count is an inappropriate
involvement (e.g., leukemia, metastatic dis response to anemia and suggests impaired
ease, and aplastic anemia), sequestration red cell production. An elevated reticulo
(i.e., hypersplenism), immune deficiency, cyte count suggests blood loss, hemolysis,
or an immune‐mediated process (e.g., or sequestration.
hemolytic anemia and immune thrombocy The investigation of anemia requires
topenic purpura). the following steps:
1. The medical history of the anemic child
(Table 1.2), as certain historical points
Evaluation of anemia may provide clues as to the etiology of the
anemia.
The evaluation of anemia includes a com 2. Detailed physical examination (Table 1.3),
plete medical history, family history, physi with particular attention to acute and
cal examination, and laboratory assessment chronic effects of anemia.
(see Figure 1.1). 3. Evaluation of the complete blood count
The diagnosis of anemia is made after (CBC), RBC indices, and peripheral blood
reference to established normal controls for smear, with classification by MCV, reticu
age (Table 1.1). The blood smear and red locyte count, and RBC morphology.
Handbook of Pediatric Hematology and Oncology – Children’s Hospital & Research Center Oakland,
Third Edition. Caroline A. Hastings, Joseph C. Torkildson, and Anurag K. Agrawal.
© 2021 John Wiley & Sons Ltd. Published 2021 by John Wiley & Sons Ltd.
2 Chapter 1
History
Physical examination
Complete blood count
Reticulocyte count
Peripheral blood smear examination
Figure 1.1 Diagnostic approach to the child with anemia (abbreviations: DBA, Diamond–Blackfan
anemia; TEC, transient erythroblastopenia of childhood; RDW, red cell distribution width; FEP, free
erythrocyte protoporphyrin; TIBC, total iron‐binding capacity; G6PD, glucose‐6‐phosphate dehydro
genase deficiency; DAT, direct antiglobulin test).
*Refer to Table 1.1 for age‐based normal values.
^Microcytosis with lead toxicity has been noted secondary to concomitant iron deficiency; see text.
Mean −2 SD Mean −2 SD
Birth (cord blood) 16.5 13.5 108 98
1–3 d (capillary) 18.5 14.5 108 95
1 wk 17.5 13.5 107 88
2 wk 16.5 12.5 105 86
1 mo 14.0 10.0 104 85
2 mo 11.5 9.0 96 77
3–6 mo 11.5 9.5 91 74
0.5–2 y 12.0 11.0 78 70
2–6 y 12.5 11.5 81 75
6–12 y 13.5 11.5 86 77
12–18 y female 14.0 12.0 90 78
12–18 y male 14.5 13.0 88 78
18–49 y female 14.0 12.0 90 80
18–49 y male 15.5 13.5 90 80
*Compiled from the following sources: Dutcher TF. Lab Med 2:32–35, 1971; Koerper MA, et al. J
Pediatr 89:580–583, 1976; Marner T. Acta Paediatr Scand 58:363–368, 1969; Matoth Y, et al. Acta
Paediatr Scand 60:317–323, 1971; Moe PJ. Acta Paediatr Scand 54:69–80, 1965; Okuno T. J Clin
Pathol 2:599–602, 1972; Oski F, Naiman J. Hematological Problems in the Newborn, 2nd ed.,
Philadelphia: WB Saunders, 1972, p. 11; Penttilä I, et al. Suomen Lääkärilehti 26:2173, 1973; and
Viteri FE, et al. Br J Haematol 23:189–204, 1972. Cited in: Rudolph AM (ed). Rudolph’s Pediatrics,
16th ed., Norwalk, CT: Appleton & Lange, 1977.
Abbreviation: MCV, mean corpuscular volume.
History of Consider
perceived safer) f ormulations including fer in pediatric patients, total iron replacement
ric gluconate and iron sucrose. Three addi is feasible in 1–2 doses of LMW iron
tional compounds have been approved, one dextran and has been shown safe. Refer to
only in Europe (iron isomaltoside) and two the Formulary for calculation of LMW iron
in the United States (ferumoxytol and fer dextran dosing.
ric carboxymaltose). These newer agents Severe allergic reactions can occur with
have the potential benefit of total dose iron dextran and therefore a LMW product
replacement in a very short and single infu should be preferentially utilized. A test dose
sion as compared to ferric gluconate and (10–25 mg) should be given prior to the
iron sucrose which require multiple doses. first dose with observation of the patient
Low‐molecular‐weight (LMW) iron dextran for 30–60 minutes prior to administering
is approved as a total dose infusion for the remainder of the dose. A common side
adults in Europe but not the United States. effect is mild to moderate arthralgias the
Due to the smaller dose generally required day after drug administration, especially
6 Chapter 1
Figure 1.2 Evaluation of the child with microcytic anemia (abbreviations: FEP, free erythrocyte proto
porphyrin; TIBC, total iron‐binding capacity; DAT, direct antiglobulin test; IBD, inflammatory bowel
disease).
Low
Elevated or normal
reticulocyte
reticulocyte count Infection
count
TORCH
Coombs test (DAT) Congenital hypoplastic anemia
Transcobalamin II deficiency
Microcytic
α-thalassemia syndrome
Normocytic
Macrocytic Chronic intrauterine blood loss
Iron deficiency
Blood loss
Peripheral smear Iatrogenic
Traumatic delivery
Internal hemorrhage
Normal Twin-twin transfusion
Fetal-maternal transfusion
Abnormal Infection
TORCH
Membrane defect
Hereditary spherocytosis
Hereditary elliptocytosis
Red cell enzyme deficiency
G6PD
Pyruvate kinase
Figure 1.3 Approach to the full‐term newborn with anemia (abbreviations: DAT, direct antiglobulin
test; G6PD, glucose‐6‐phosphate dehydrogenase deficiency; TORCH, toxoplasmosis, other, rubella,
cytomegalovirus, herpes simplex virus).
the benefit of total dose replacement given regarding utilization in pediatric patients
as a rapid infusion due to slow release of are limited regarding appropriate per kg
elemental iron. Neither is immunogenic and dosage, although the infusions appear safe and
therefore no test dose is required. Studies therefore will likely replace use of iron
8 Chapter 1
a. What are some common diagnostic viral or secondary to TEC. Coombs is vital
considerations? to help determine if this is an underlying
b. What are the next laboratory steps? warm autoimmune hemolytic anemia, not
Microcytic causes of anemia, notably iron ing that the Coombs will not be positive in
deficiency anemia and secondary lead toxic all cases. Complete metabolic panel will
ity as well as thalassemia syndromes, have look at many important aspects including
generally been ruled out with a history of a renal function (to rule out aHUS), as well
normal recent hemoglobin as well as a reas as bilirubin and AST which may be ele
suring dietary history. Congenital causes of vated along with the LDH if there is ongo
anemia, especially Diamond–Blackfan ane ing hemolysis. Similarly, the urinalysis will
mia, a pure red cell aplasia, have also been help rule out blood loss as well as hemoly
ruled out with a previous normal hgb. sis. Parvovirus PCR is not vital given the
Megaloblastic anemias are also less likely to lack of clinical history, but this infection
develop in the preceding 3 months after a should remain in the differential diagnosis.
normal hemoglobin. Hemolytic anemia, Type and screen is important as the child
especially warm autoimmune hemolytic may require blood transfusion depending
anemia (AIHA), remains a possibility even on the level of anemia and the potential
without a clinical history of jaundice in presence of hemolysis.
patients with slow hemolytic rates. Many
Lab results include the following:
other diagnostic possibilities remain at this
point including viral suppression secondary 4.7 retic 11.9%
to infections such as parvovirus, syndromes 10.4 279
14.2
that may have bicytopenia or pancytopenia
in addition to the clinical presentation of Normal LDH, total, and indirect bilirubin
anemia including severe aplastic anemia Normal UA
and acute leukemias, as well as transient Negative direct Coombs
erythroblastopenia of childhood (TEC). Normal CMP
Atypical hemolytic uremic syndrome c. What is the likely diagnosis?
(aHUS) is an unlikely possibility, but should The elevated reticulocyte count in the set
be in the differential diagnosis in addition to ting of a low hemoglobin should always
occult blood loss. make the practitioner first think of a hemo
The initial laboratory workup should lytic anemia, either a warm antibody or cold
include labs which will help make the diag agglutinin. Yet, in this case, there are no
nosis and potentially treat the patient: other supporting laboratories for a hemo
CBC/diff, reticulocyte count, Coombs test, lytic process. With a slow hemolytic process,
complete metabolic panel (CMP), LDH, it is possible that the UA, LDH, and indirect
type and screen, fecal occult blood, parvo bilirubin could be normal but the direct
virus PCR, and urinalysis (UA). CBC will Coombs should be helpful in the majority of
help evaluate the level of anemia noted warm antibody‐mediated cases. In the case
clinically as well as determine if there are of a cold agglutinin (usually associated with
more cytopenias which will help direct the Mycoplasma infection), it is possible there
differential diagnosis. The reticulocyte would be no other positive lab findings.
count will be helpful in determining if the The most likely diagnosis here is TEC in
bone marrow is responding correctly to the recovery phase. TEC occurs due to unclear
anemia, as it should be high with a hemo reasons and may present with concomitant
lytic process and suppressed if this is post neutropenia leading to workup for acute
Approach to the Anemic Child 11
lymphoblastic leukemia and aplastic anemia. 2. You are seeing a patient in the hospital
Patients will have a decrease in erythroid admitted at two months of age for sepsis
precursors in the bone marrow and therefore rule out secondary to high fever with asso
a decrease in peripheral reticulocytes. TEC ciated decreased feeds and decreased urine
is an indolent process and thus patients will output. The child has a urinary tract infec
generally present with a well‐compensated tion. A CBC is checked the hgb is 9.0 g/dl.
but often severe normocytic anemia. Spon There is no relevant family history, the
taneous recovery occurs with reticulocyto mother received good prenatal care and
sis, and thus TEC in the recovery phase can was not anemic during pregnancy and the
be mistaken for a hemolytic anemia. baby was born full term. What is the next
best step?
a. Empirically start iron therapy
Multiple choice questions b. Plan to repeat the CBC prior to
discharge
1. You are seeing a patient at their one year c. Plan to repeat the CBC in 1‐2 months
clinic visit and perform a finger stick hemo as an outpatient
globin. The hgb is 9.2 g/dl. The child has d. Provide reassurance to the family
been well without any recent illnesses or Explanation: Although anemia in a young
significant findings on exam. What is the infant with an underlying infection can be
next best step? due to bone marrow suppression, this level
a. Empirically start iron therapy of hemoglobin is normal for age. The physi
b. Obtain further history ologic nadir of infancy occurs around 2‐3
c. Check a full CBC/diff months of age as fetal hemoglobin goes
d. Plan to repeat in one month away (fetal hemoglobin lives 60‐90 days as
e. Perform a lead level compared to hemoglobin A which lives
Explanation: It is first important to under 90‐120 days). A certain level of anemia
stand underlying risk factors for anemia. occurs prior to the bone marrow ramping
These could include a dietary intake of sig up production of hemoglobin A red blood
nificant milk consumption which would cells. Choice a. is incorrect as iron deficiency
lead to iron deficiency or a family history of would be unlikely in this age although can
thalassemia. Also it is important to ask occur in a very preterm infant or if the
about a bleeding history to determine if mother had severe anemia during preg
there are ongoing losses. It important to ask nancy. Choice b. and c. are not necessary
about any history of jaundice or scleral since the hb is normal for age. The answer is d.
icterus which would point to a hemolytic
anemia as well as other inflammatory condi 3. You are seeing a patient in follow up. At
tions which could lead to anemia of chronic the one year visit the finger stick hemoglobin
disease. Choice a. would likely be correct was 9.4 g/dl. Given a nutritional history
after obtaining more history; choice c. is of significant milk intake you previously
reasonable in cases where the history is not decided to empirically start iron therapy at a
suggestive or the hgb does not increase with dose of 3 mg elemental iron daily and see the
empiric iron therapy; choice d. would not be child today, one month later for a repeat finger
correct without other interventions; choice e. stick hemoglobin. The repeat hemoglobin is
is important to do but lead toxicity itself now 10.2 g/dl. What is the next best step?
does not lead to anemia, rather it is concom a. Stop iron therapy
itant iron deficiency. The answer is b. b. Send a full CBC/diff
12 Chapter 1
c. Continue iron therapy and see the Explanation: As iron deficiency is the most
patient back in one month likely cause of anemia, an empiric trial of
d. Continue iron therapy and see the iron is the correct first step. Assessing com
patient back in 2‐3 months pliance with iron therapy and nutritional
Explanation: Given the level of hemoglobin recommendations is very important in fol
and nutritional history, iron deficiency is low up especially if the hgb is not improved.
the most likely diagnosis. Reticulocyte counts In many cases the family is unable to give
should increase in 1‐2 days after commence the iron well and the excessive milk intake
ment of iron therapy and hemoglobin continues. Assuming a reliable family as in
should rise within one week. A rise in hb in the case above, it is important to now check
one month is reassuring that the diagnosis a CBC/diff to further characterize the ane
and treatment plan are correct. Choice a. is mia. It would also be important to test for
incorrect because it is important to continue ongoing losses at this point with a urinalysis
iron therapy for 2‐3 months after resolution and fecal occult blood test. Choice a. is
of anemia to replete liver iron stores; as this incorrect since iron therapy should show
child is still anemic it is too early to stop iron improvement in the hgb in 1 week and if
therapy. Choice b. is unnecessary at this that is not the case it is best to avoid iron
point since the hgb is appropriately increas overload by unnecessarily continuing iron.
ing with therapy but may be necessary at a Choice b. though correct is not as good a
later point if the anemia persists on iron choice as choice c. Choice d. is reasonable
therapy. Choice c. is reasonable although although it would be first important to
given the amount of time of iron therapy check for microcytosis on the full CBC—if
required to replete stores and the improve microcytic then it would be reasonable to
ment seen to date, it is not necessary to see test iron studies (ferritin, TIBC) in addition
the patient so frequently. The answer is d. to checking hemoglobin electrophoresis for
β‐thalassemia trait given the non‐respon
4. You are seeing a patient in follow up. At siveness to iron therapy. The answer is c.
the one year visit the finger stick hemo
globin was 9.4 g/dl. Given a nutritional his 5. You are seeing a 15-month-old for a rou
tory of significant milk intake you previously tine clinic visit. The family notes the child
decided to empirically start iron therapy at a has been more tired and pale recently. There
dose of 3 mg elemental iron daily and see the was an antecedent viral illness about one
child today, one month later for a repeat fin month prior but the child is now otherwise
ger stick hemoglobin. The repeat hemo well. The child had a normal finger stick hb
globin is now 9.2 g/dl. The mother states at one year of age, eats a varied diet, has had
that the child is taking the iron well, with no noted blood loss and had no signs of
vitamin C, and she has decreased milk jaundice. The child is pale and tachycardic
intake to 16 oz (480 ml) on average in a but otherwise well appearing without LAD
24 hour period. What is the next best step? or HSM. A finger stick hemoglobin is 5.4 g/
a. Continue iron therapy for another dl. Follow up CBC shows a normocytic ane
month and recheck hb at that time mia with normal WBC/diff and platelet
b. Check a CBC/diff count. The retic count is very low. What is
c. Stop iron therapy and check a CBC/ the most likely diagnosis?
diff a. Transient erythroblastopenia of
d. Stop iron therapy and check iron childhood
studies in addition to a CBC/diff b. Iron deficiency anemia
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