RBC Morphology

Red blood cell morphologyJ. FORD

Division of Hematopathology,

BC Children’s Hospital, Faculty

of Medicine, University of

British Columbia, Vancouver,

BC, Canada

Correspondence:

Jason Ford, BC Children’s

Hospital, 4500 Oak St,

Vancouver V6H 3N1, BC,

Canada. Tel.:604-875-2044;

Fax: 604-875-2815;

E-mail: [email protected]

doi:10.1111/ijlh.12082

Received 31 December 2012;

accepted for publication 21

January 2013

Keywords

Anemia, morphology, red blood

cell, poikilocytosis, peripheral

smear

SUMMARY

The foundation of laboratory hematologic diagnosis is the complete

blood count and review of the peripheral smear. In patients with

anemia, the peripheral smear permits interpretation of diagnostically

significant red blood cell (RBC) findings. These include assessment

of RBC shape, size, color, inclusions, and arrangement. Abnormali-

ties of RBC shape and other RBC features can provide key informa-

tion in establishing a differential diagnosis. In patients with

microcytic anemia, RBC morphology can increase or decrease the

diagnostic likelihood of thalassemia. In normocytic anemias, mor-

phology can assist in differentiating among blood loss, marrow fail-

ure, and hemolysis—and in hemolysis, RBC findings can suggest

specific etiologies. In macrocytic anemias, RBC morphology can help

guide the diagnostic considerations to either megaloblastic or non-

megaloblastic causes. Like all laboratory tests, RBC morphologies

must be interpreted with caution, particularly in infants and chil-

dren. When used properly, RBC morphology can be a key tool for

laboratory hematology professionals to recommend appropriate

clinical and laboratory follow-up and to select the best tests for

definitive diagnosis.

INTRODUCTION

Medical school educators around the world emphasize

the importance of teaching future physicians the

correct approach to the history and physical examina-

tion. These basic skills are widely understood to be

the foundation of medical practice, even in the face of

technological change.

For laboratory hematology professionals, the com-

plete blood count (CBC) and the peripheral smear are,

respectively, our history and physical examination.

Despite quantum leaps in technological development

in the clinical laboratory, with evolutions and revolu-

tions in flow cytometry and point of care testing and

molecular analysis, review of a patient’s CBC and

peripheral smear morphology is still the mainstay of

hematologic diagnosis.

For patients with anemia, the peripheral smear

morphology provides key information to create the

differential diagnosis. Review of the peripheral smear

has three main components:

• To confirm the CBC findings. It is unusual for labo-

ratory error to affect any of the measurements in the

CBC, but spurious findings may include the following

[1, 2]:

(i) low counts due to faulty aspiration of whole

blood by the automated counter;

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© 2013 Blackwell Publishing Ltd, Int. Jnl. Lab. Hem. 2013, 35, 351–357 351

International Journal of Laboratory HematologyThe Official journal of the International Society for Laboratory Hematology

(ii) macrocytosis due to RBC agglutination or

rouleaux, hyperleukocytosis, or severe hyperglyce-

mia;

(iii) microcytosis due to the blood counter’s mis-

identification of giant platelets as RBCs.

• To review relevant white blood cell (WBC) and

platelet (PLT) findings. For example, a high platelet

count is expected in anemia due to iron deficiency

and a low platelet count is expected in anemia due to

microangiopathic hemolysis.

• To review RBC morphology. There are five impor-

tant aspects:

(i) Shape. What is/are the dominant poikilocyte(s)?

(ii) Size. Is there anisocytosis or a dual population?

(iii) Color. Is there hypo- or hyperchromasia? Is

there anisochromia or polychromasia?

(iv) Inclusions. Are there Howell–Jolly bodies,

malaria parasites, nucleated RBCs, etc.?

(v) Arrangement. Is there agglutination or rou-

leaux?

A list of RBC morphologies, their definitions, and

their associated clinical states is shown in Table 1 [3].

Poikilocytosis must be interpreted in its appropriate

context: finding a rare poikilocyte in an otherwise

normal smear is likely clinically insignificant, while

finding extensive poikilocytosis in a normocytic

anemia may indicate specific causes of hemolysis. In

the neonatal period and in patients on chemotherapy,

poikilocytosis must be interpreted with special

caution: these patients may be expected to have a

background level of mild or moderate nonspecific

poikilocytosis, and only the finding of a dominant or

extensive poikilocytosis in combination with anemia

is likely clinically relevant.

Most clinicians and laboratory professionals use an

approach to anemia centering on the mean cell

volume (MCV). This review of RBC morphology will

follow the MCV approach.

Morphology in the assessment of microcytic anemia

Medical students often learn that there are five main

causes of microcytic anemia, which together form the

easily remembered acronym TAILS:

T = Thalassemia.

A = Anemia of chronic disease.

I = Iron deficiency.

L = Lead poisoning.

S = congenital Sideroblastic anemia.

Only three of these are common in most parts of

the world, namely iron deficiency, anemia of chronic

disease (ACD), and thalassemia. Lead poisoning is not

usually considered a common cause of anemia, but it

may be seen in pediatrics particularly in areas where

paint, toys, or jewelry containing lead can be eaten by

small children. Lead can also be consumed by infants

in formula made with contaminated water [4] and

may rarely cause anemia in adults with extensive

industrial exposure. Congenital sideroblastic anemia is

vanishingly rare.

In classic cases, the morphological differentiation of

the three common microcytic anemias is straightfor-

ward. The classic morphology in ACD is of unremark-

able RBCs, while iron deficiency shows anisocytosis,

anisochromia, and elliptocytosis, and thalassemia trait

demonstrates target cells and coarse basophilic

stippling.

Regrettably, these so-called classic presentations

are unreliable in practice. Elliptocytes and anisocyto-

sis are often seen in thalassemia, target cells may

occur in iron deficiency, and both iron deficiency

and thalassemia may appear as ‘unremarkable’ as

ACD. The red blood cell distribution width (RDW),

classically taught as a key differentiator of iron

deficiency from thalassemia, is also unreliable [5];

far better than the RDW is the RBC count [5, 6],

although even a high RBC count is not proof of

thalassemia.

The only ‘reliable’ classic morphologic finding that

can separate these three conditions is the presence of

coarse basophilic stippling. Coarse stippling is seen in

some cases of thalassemia and is never seen in

uncomplicated iron deficiency or ACD. A microcytic

patient with coarse basophilic stippling likely has

thalassemia—although the patient should be in an

ethnically at-risk group, and there should not be

another reasonably likely cause of basophilic stippling.

Even a likely diagnosis of thalassemia must still be

confirmed by hemoglobin HPLC, H body staining,

molecular testing, or some other reliable method.

Morphology is essentially never diagnostic of thalasse-

mia: it can only suggest whether thalassemia is more

or less likely.

© 2013 Blackwell Publishing Ltd, Int. Jnl. Lab. Hem. 2013, 35, 351–357

352 J. FORD | RED BLOOD CELL MORPHOLOGY

Table 1. Common RBC morphological findings

RBC morphology Morphological definition Clinical associations

Acanthocyte(spur cell)

RBC has irregularly distributed, variablysized, pointy projections off its surface

Advanced liver disease, hyposplenism, somedyslipidemias, pyruvate kinase deficiency,McLeod phenotype

Anisochromia Variation in the amount of central palloramong a population of RBCs

Iron deficiency, myelodysplasia, hypochromicanemia post transfusion

Anisocytosis Variation in size among a population ofRBCs

Common nonspecific finding. Seen in irondeficiency, moderate or severe thalassemia,megaloblastic anemia, partially treated anemiaof several causes, post transfusion

Basophilicstippling: coarse

RBC has variably sized (up to large)basophilic ‘granular’ discolorationsacross its entire cytoplasm, on aWright-stained film

Thalassemia, lead poisoning, myelodysplasia,pyrimidine 5′ nucleotidase deficiency,post chemotherapy

Basophilicstippling: fine

RBC has small, uniform, punctatebasophilic dots across its entirecytoplasm, on a Wright-stained film

Reticulocytosis, normal finding

Bite cell/blistercell

RBC has a semi-circular indentation inits outer cytoplasmic border. There maybe a ‘roof’ to this indentation(blister cell) or no roof (bite cell)

Oxidative hemolysis

Dimorphism Two distinct populations of RBC arepresent, for example, microcytic andnormocytic, or hypochromic andnormochromic

Myelodysplasia, post transfusion,partially treated iron deficiency

Echinocyte (burr cell) RBC has regularly distributed, equallysized, rounded projections off its surface

Artifact, renal failure, post transfusion,phosphate deficiency, burns

Elliptocyte RBC is oval shaped Iron deficiency, megaloblastic anemia,hereditary elliptocytosis, post chemotherapy

Heinz body RBC has a submembranous orepimembranous small round mass, whichcan only be seen by supravital orspecialized Heinz body stains. This body isnot visible on a routine Wright-stainedfilm

Oxidative hemolysis, hyposplenism

Howell–Jollybody

Solitary round mass, relatively large(e.g., approximately 10–20% of thediameter of the RBC), within thehemoglobinized portion of the RBC.Appears dark blue or purple on aWright-stained film

Hyposplenism, erythroblastosis, myelodysplasia,megaloblastic anemia, post chemotherapy

Hypochromia The zone of central pallor is > 1/3 thediameter of the RBC

Iron deficiency, thalassemia, anemia of chronicdisease

Irregularlycontracted cell

The RBC is small, dark, and lacks azone of central pallor. Its outermargin is not spherical: it may appeardented, compressed, or otherwise‘contracted’

Nonspecific finding seen in a variety of conditionsincluding G6PD deficiency, hemoglobinopathies,and normal neonates

Pappenheimerbody

Usually multiple small dark blue or purplegranular inclusions, all within thehemoglobinized portion of the RBC.These occupy only one portion or regionof the RBC, unlike basophilic stipplingwhich is more ‘global’ throughout theentire RBC

Iron overload, hyposplenism, myelodysplasia


J. FORD | RED BLOOD CELL MORPHOLOGY 353

The ethnicities that are not at high risk of thalasse-

mia include northern Europeans, American Indians,

Canadian First Nations, Inuit, and patients from Japan

[7]. Everyone else should be considered at risk.

Coarse basophilic stippling is not pathognomonic

for thalassemia: it can also be seen in lead poisoning,

myelodysplastic syndrome, post chemotherapy, and in

rare other conditions (see Table 1). Coarse stippling

does not help differentiate a- from b-thalassemia, as it

may be seen in either condition. It must not be con-

fused with fine basophilic stippling, which is a normal

finding.

The morphology of H bodies [8], which are consis-

tent with (if not pathognomonic for) a-thalassemia, is

well known: using supravital stains, these precipitates

of b-globin tetramers appear as innumerable dark

spots distributed in a geometric fashion across the

entire cytoplasm of the RBC like the pits on the

Table 1. (Continued)

RBC morphology Morphological definition Clinical associations

Polychromasia RBCs show color variability as apopulation: some (usually themajority) are the usual red color,while others are bluish

Reticulocytosis, normal neonate

RBCagglutination

Some RBCs aggregate intomulticellular masses resemblinga bunch of grapes

Cold agglutinin, cold autoimmune hemolyticanemia

Rouleaux Some RBCs aggregate into linearpatterns, said to resemble a stackof coins

Normal finding in the thick part of the bloodsmear, hypergammaglobulinemia (monoclonalor polyclonal)

Schistocyte The RBC appears to have beenfragmented: it lacks the usualcircular shape, instead showing atriangular or other angulatedmorphology. The zone of centralpallor is often missing

RBC fragmentation syndromes, for example,microangiopathic hemolytic anemia andhemolysis secondary to cardiac valve

Sickle cell There are several sickle RBCmorphologies, including the classicsickle (crescentic with two sharplypointed ends) or boats (linear withtwo tapered if somewhat roundedends)

Severe sickling syndrome, for example, SS,SC and SD

Spherocyte The RBC is smaller and darker thannormal. There is no zone of centralpallor. The outer edge must be almostperfectly round (to differentiate thiscell from irregularly contracted cells)

Autoimmune hemolytic anemia, alloimmunehemolytic anemia (e.g., hemolytic disease ofthe newborn), hereditary spherocytosis

Stomatocyte The zone of central pallor is linear,rather than circular. Usually the‘line of pallor’ runs parallel to thelong axis of the RBC, if the latter isovoid, but in certain variants (e.g.,South East Asian ovalocytosis), theline may run across the long axis ormay be nonlinear, for example,bifurcated or trifurcated

Artifact, obstructive liver disease, hereditarystomatocytosis, South East Asian ovalocytosis,Rh null syndrome

Target cell The RBC has a central red area withinthe zone of central pallor

Thalassemia, liver disease, hyposplenism, HgbC disease or SC disease, hereditary xerocytosis.May be seen in iron deficiency

Teardrop cell The RBC is tapered to a point atone end, resembling the classicartist’s rendition of a drop of water

Nonspecific finding seen in several conditionsincluding myelofibrosis



surface of a golf ball. Patients with a single or double

a-gene deletion may show a single H body RBC in

many high-power fields, while patients with hemo-

globin H disease (a-/-) demonstrate H bodies in the

majority of their RBCs. Unfortunately, the sensitivity

of H body staining is variable, ranging from approxi-

mately 40% up to approximately 90% depending on

the pattern of a-deletions [8] and the laboratory’s

technical expertise. H bodies also usually require the

presence of exclusively normal b-globin chains (i.e.,

bA-chains): if a patient has both a-thalassemia and a

simultaneous b-variant, such as hemoglobin E, it may

be much more difficult to find H bodies. This variable

sensitivity means that although the presence of H

bodies can indicate a-thalassemia, their absence does

not rule this diagnosis out.

In the right context (e.g., microcytic anemia with

a high RBC count, in a patient from a high-risk

ethnicity such as South East Asian), H bodies are in

general considered diagnostic of a-thalassemia. How-

ever, even in this context, H bodies are not ‘proof’ of

a-thalassemia: H-like bodies can be formed by other

unstable hemoglobins besides b4, such as Hemoglobin

J-New York.

The analogous RBC inclusion in b-thalassemia,

consisting of precipitates of a4, may be designated

‘Fessas bodies’ [9]. These are solitary large round

deposits within the cytoplasm of an RBC: like the

surrounding soluble hemoglobin, the precipitated

a-chains are red on a Wright stain, so Fessas bodies

are generally not visible in routine peripheral smears.

They can sometimes be seen as red cytoplasmic inclu-

sions in polychromatophilic RBCs or in nucleated

RBCs in the peripheral blood, and in RBC precursors

in marrow aspirate specimens.

One helpful morphological clue in microcytic ane-

mias is the broad range of poikilocytosis seen in many

cases of thalassemia, compared to iron deficiency. In

some patients with thalassemia, there are not only

target cells but also numerous teardrop cells and schis-

tocytes. Among the poikilocytes seen in thalassemia

are the ‘fish cells’ described by Barbara Bain [Bain,

personal communication]. These are generally not

seen in patients with iron deficiency or ACD. Fish

cells resemble teardrop cells, with one rounded end

and one tapered end: unlike teardrops, the tapered

end flares out into two buds resembling a fish’s tail.

One fish cell is seen at the center of Figure 1. This

image also shows examples of the teardrops and schis-

tocytes which can be seen in thalassemia trait.

Morphology in the assessment of normocytic anemia

Most cases of normocytic anemia are caused by blood

loss, suppressed production of RBCs, or hemolysis. In

hemorrhage the RBC morphology is entirely unre-

markable, except for the polychromasia that typically

arises after the first twelve to 24 h. In patients with

reduced RBC production, red cell morphology may be

normal where the cause is extrinsic to the red cell

itself: for example, because of low erythropoietin in a

patient with renal failure. But where erythropoiesis is

intrinsically disordered (e.g., myelodysplasia) and in

cases of hemolysis, RBC morphology may be diagnos-

tically significant.

Patients with disordered RBC production (such as

myelodysplastic syndrome, MDS, or congenital dysery-

thropoietic anemia, CDA) may have a dual population,

elliptocytes, teardrop cells, or other poikilocytes. There

may also be circulating nucleated RBCs (nRBCs), show-

ing dysplastic features including asymmetric nuclear

budding, multinuclearity, megaloblastoid changes, or

karyorrhexis. In children, particularly infants, ‘reactive’

(transient) dysplastic nRBCs are frequently seen in

many patients with brisk reticulocytosis following

hemorrhage or hemolysis. ‘Reactive’ dysplasia in chil-

dren will abate after correction of the patient’s anemia.

The most common role of RBC morphology in

patients with normocytic anemia is in the assessment

Figure 1. A ‘fish cell’ and other poikilocytes in a case

of thalassemia trait. Wright stain, 9100.



of patients with hemolysis. Poikilocytosis will often

suggest a specific cause or mechanism of hemolysis

(Table 1):

• Bite and blister cells, as well as irregularly contracted

cells, are the classic findings in oxidative hemolysis: for

example, because of G6PD deficiency. Oxidative

hemolysis may also lead to (less prominent) schisto-

cytosis and spherocytosis.

• Acanthocytes are rarely the dominant finding in a

hemolytic patient, but may suggest pyruvate kinase

deficiency (where they will be accompanied by irregu-

larly contracted cells) or the McLeod phenotype.

Acanthocytes are more commonly observed in

patients with hyposplenism, liver disease, a variety of

dyslipidemias, and even anorexia nervosa.

• Sickle cells will suggest a diagnosis of sickle cell anemia

or any of the severe sickling syndromes (including

Sb0, SD and SO-Arab). In essentially every patient

with sickle cell anemia by the age of 2 years, there

will also be evidence of hyposplenism including tar-

gets, acanthocytes, and Howell–Jolly bodies. Patients

with SC disease and any of the sickle thalassemia

compound disorders (including Sb0 and SS-a thalasse-

mia) may have considerably more target cells than

patients with uncomplicated SS. Patients with SC

disease may also demonstrate C crystals in some RBCs

[10]. C crystals and targets by themselves, without

sickle cells, of course may suggest homozygosity for

hemoglobin C.

• Spherocytes have two common causes: immune-mediated

hemolysis and hereditary spherocytosis (HS). Some patients

with HS will demonstrate occasional ‘mushroom cell’

or ‘pincer cell’ variants: these cells resemble sphero-

cytes with mirror-image indentations, resulting in an

appearance similar to a button mushroom. RBC mor-

phology is not usually very helpful in differentiating

immune hemolysis from HS: further testing (such as

direct antiglobulin testing and flow cytometry [11])

may be required. It should be noted that spherocytosis

may also be seen in neonates with gram-negative sepsis

and in patients with thermal burns, as well as in other

hemolytic anemias including G6PD deficiency.

• Elliptocytosis is most commonly due to iron deficiency

or hereditary elliptocytosis (HE). Although there are

several other causes of elliptocytosis, as a practical

matter if iron deficiency is excluded then elliptocytosis

is most likely due to HE. Parents with typical HE may

have newborns with a much more abnormal pheno-

type, featuring severe microschistocytosis as well as

elliptocytosis. These infants may have either heredi-

tary elliptocytosis with infantile poikilocytosis (HEIP)

or hereditary pyropoikilocytosis (HPP) [12]. In South

East Asian ovalocytosis (SEAO), the elliptocytes show

a transverse (as opposed to longitudinal) zone of cen-

tral pallor, or two zones of pallor separated by a trans-

verse bar of cytoplasm, or even a zone of central

pallor divided into two or three spokes like the open

spaces on a sleigh bell. SEAO is considered hemato-

logically benign, although there is a suggestion that

it may be responsible for transient anemia in the

newborn period [13].

• Schistocytes generally reflect intravascular hemolysis.

When seen with thrombocytopenia, schistocytes sug-

gest microangiopathic hemolytic anemia (MAHA), a

group of conditions consisting primarily of thrombotic

thrombocytopenic purpura (TTP), hemolytic uremic

syndrome (HUS), and disseminated intravascular

coagulopathy (DIC). Morphology is not useful in dif-

ferentiating among these three conditions, nor among

their subtypes (such as congenital vs. acquired TTP or

typical vs. atypical HUS). Morphology is also unreli-

able in predicting the severity of a case of MAHA: a

patient with more schistocytes is not necessarily ‘more

sick’ than a patient with fewer schistocytes. There are

other important causes of schistocytosis, including

vasculitis, intracardiac hemolysis (e.g., due to a septal

defect or prosthetic cardiac valve), thermal burn,

march hemoglobinuria, the HELLP syndrome in preg-

nancy, and the Kasabach–Merritt phenomenon in

infants. All of these lesions share the common patho-

genetic step of extrinsic mechanical injury to the red

blood cell.

Many hemolytic anemias show multiple poikilo-

cytes: G6PD deficiency, for example, often shows not

only bite and blister cells but also schistocytes and

spherocytes. The RBC morphology may not so much

suggest a single diagnosis as several relevant avenues

for clinical and laboratory follow-up. A patient with

bite cells and spherocytes may benefit from G6PD

screening and a direct antiglobulin test, for example.

This problem is particularly notable in neonates, in

whom the usual hemolytic morphologies may not be

clearly evident. Neonatal hemolysis may lead to a

very broad range of poikilocytosis, without the same



‘classic’ patterns as are relied upon in adults: oxidative

hemolysis, for example, may lead to more schistocyto-

sis than bite/blister cells. The morphologic differential

diagnosis for hemolysis in a neonate must therefore

be broader than in an adult.

Morphology in the assessment of macrocytic anemia

The usual approach to macrocytosis is to differentiate

between megaloblastic and nonmegaloblastic causes:

megaloblastosis is seen with B12 and folate deficiency,

MDS and CDA, HIV infection, and rare inborn errors

of metabolism, while nonmegaloblastic causes include

liver and thyroid disease, alcohol, Down syndrome,

aplastic anemia, and reticulocytosis. Medications can

be responsible for both megaloblastic and nonmega-

loblastic anemia, while RBC agglutination may lead to

spurious macrocytosis.

Red blood cell morphology usually plays a small

but important role in this differentiation of megalob-

lastic from nonmegaloblastic causes. Important preli-

minary findings include agglutination, polychromasia

(reticulocytosis), target cells (liver disease or alcohol),

and a dual population (MDS or post transfusion).

Oval macrocytosis and severe macrocytosis (e.g.,

>115 fL) are both classically found in megaloblastic

anemia, while round macrocytosis is seen in non-

megaloblastic anemia. Circulating nRBCs may show

dysplastic features suggesting megaloblastic change:

that is, large immature nuclei within mature red

cytoplasm.

In many patients with macrocytic anemia, the RBC

morphology is quite bland: for example, marrow fail-

ure (e.g., Diamond–Blackfan anemia, idiopathic aplas-

tic anemia, etc.) may produce morphologically

unremarkable RBCs.

CONCLUSION

The review of red blood cell morphology is a critical

step in the evaluation of a patient with anemia. It can

be very useful in evaluating microcytic, normocytic,

and macrocytic anemias and is especially helpful in

the work-up of patients with hemolysis. Assessment

of RBC morphology can be the best tool for laboratory

hematology professionals to recommend clinical and

laboratory follow-up in a patient with anemia and to

select the right tests for definitive diagnosis.

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