Hyperleukocytosis and leukostasis in hematologic malignancies

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©2022 UpToDate®

Hyperleukocytosis and leukostasis in hematologic

malignancies
Author: Charles A Schiffer, MD
Section Editor: Richard A Larson, MD
Deputy Editor: Alan G Rosmarin, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Aug 2022. | This topic last updated: Nov 18, 2021.

INTRODUCTION

Hyperleukocytosis refers to a laboratory abnormality that has been variably defined as a

total leukemia blood cell count greater than 50 x 109/L (50,000/microL) or 100 x 109/L
(100,000/microL). In contrast, leukostasis (also called symptomatic hyperleukocytosis) is a
medical emergency most commonly seen in patients with acute myeloid leukemia or
chronic myeloid leukemia in blast crisis. It is characterized by an extremely elevated blast
cell count and symptoms of decreased tissue perfusion.

Leukostasis is a pathologic diagnosis in which white cell plugs are seen in the
microvasculature. Clinically, leukostasis is typically diagnosed empirically when a patient
with leukemia and hyperleukocytosis presents with respiratory or neurological distress.
Prompt treatment is indicated since, if left untreated, the one-week mortality rate is
approximately 20 to 40 percent.

The epidemiology, clinical presentation, diagnosis, and management of hyperleukocytosis

and leukostasis in hematologic malignancies will be reviewed here. Other complications of
leukemia are presented separately. (See "Overview of the complications of acute myeloid
leukemia" and "Overview of the complications of chronic lymphocytic leukemia".)

EPIDEMIOLOGY
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Hyperleukocytosis and leukostasis in hematologic malignancies

The incidence of hyperleukocytosis and leukostasis vary by leukemia type and patient
population. In general, symptoms of leukostasis are more common in leukemias with
large, poorly deformable blasts, such as acute myeloid leukemia.

● Acute myeloid leukemia – Hyperleukocytosis is present in 10 to 20 percent of

patients with newly diagnosed acute myeloid leukemia (AML). It is more common in
patients with myelomonocytic (FAB-M4) leukemia, monocytic (FAB-M5) leukemia, or
the microgranular variant of acute promyelocytic leukemia (FAB-M3) [1,2]. Symptoms
of leukostasis occur less frequently and typically affect patients with white blood cell
(WBC) counts over 100 x 109/L (100,000/microL).

● Acute lymphoblastic leukemia – Hyperleukocytosis is seen in 10 to 30 percent of

patients with newly diagnosed acute lymphoblastic leukemia (ALL) [3]. The incidence
appears to be highest in infants, patients between the ages of 10 and 20 years,
males, and those with a T cell phenotype [3,4]. Symptoms of leukostasis are rarely
seen in patients with ALL and hyperleukocytosis. Tumor lysis syndrome and
disseminated intravascular coagulation are more common complications related to
the elevated WBC count.

● Chronic lymphocytic leukemia – A significant proportion of patients with chronic

lymphocytic leukemia (CLL) present with hyperleukocytosis. Symptoms of leukostasis
are rare unless the WBC count exceeds 400 x 109/L (400,000/microL).

● Chronic myeloid leukemia – Patients with chronic myeloid leukemia (CML) typically
present with leukocytosis and a median WBC count of approximately 100 x 109/L
(100,000/microL). Most often, these are segmented neutrophils, metamyelocytes, and
myelocytes. Symptoms of leukostasis are very uncommon in patients in chronic
phase but can be seen occasionally in patients with myeloid blast crisis and very
elevated blast counts.

PATHOPHYSIOLOGY OF LEUKOSTASIS

The pathophysiology of leukostasis is not well understood. There are two main theories,
which are not mutually exclusive:

● Leukostasis may be due to increased blood viscosity as a direct complication of a

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large population of leukemic blasts that are considerably less deformable than
mature leukocytes [5,6]. With increasing blast counts, plugs of these more rigid cells
can develop in the microcirculation, thereby impeding blood flow (leukostasis) [1,7].
This situation can be worsened by red blood cell transfusions or the use of diuretics,
both of which can increase whole blood viscosity.

● Local hypoxemia may be exacerbated by the high metabolic activity of the dividing
blasts and the associated production of various cytokines [8,9]. These cytokines can
result in endothelial damage and subsequent hemorrhage that add to the hypoxic
damage already present from reduced blood flow [8,9]. Leukemic blasts can migrate
into the surrounding tissues, causing additional damage [10]. Thus, the lower
incidence of clinically significant leukostasis and vascular injury in patients with
chronic lymphocytic leukemia (CLL) and acute lymphoblastic leukemia (ALL) may be
related to the lower metabolic and mitotic rate in the former and the lack of catabolic
enzymes and cytokines in both.

It is likely that both of these mechanisms, and additional yet unidentified mechanisms, are
involved in the development of leukostasis. In vitro studies have demonstrated a dramatic
rise in viscosity when leukocyte suspensions exceed a fractional volume of leukocytes (ie,
leukocrit) of 12 to 15 mL/dL [11]. Attainment of such a high leukocrit requires an acute
myeloid leukemia (AML) blast count of approximately 300 x 109/L (300,000/microL) or an
ALL blast count of approximately 600 x 109/L (600,000/microL). This observation is
consistent with the increased incidence of leukostasis in AML compared with ALL. It also
suggests that factors other than white blood cell count are important in the pathogenesis
of leukostasis, since symptoms of leukostasis commonly occur at blast concentrations
below these predicted thresholds.

SIGNS AND SYMPTOMS

Although pathologic evidence of leukostasis can be found in most organs in patients with
extremely high white blood cell (WBC) counts, the main clinical symptoms of leukostasis
and causes of early death are related to involvement of the central nervous system
(approximately 40 percent) and lungs (approximately 30 percent) [1,3,7].

● Pulmonary signs and symptoms include dyspnea and hypoxia with or without diffuse

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interstitial or alveolar infiltrates on imaging studies. Measurement of the arterial pO2

can be falsely decreased in patients with hyperleukocytosis, since the WBCs in the
test tube utilize oxygen. Pulse oximetry provides a more accurate assessment of O2
saturation in this setting. (See 'Laboratory abnormalities' below.)

● Neurological signs and symptoms include visual changes, headache, dizziness,

tinnitus, gait instability, confusion, somnolence, and, occasionally, coma. In addition,
patients who present with hyperleukocytosis have an increased risk of intracranial
hemorrhage that persists for at least a week after the reduction of white cell count,
perhaps from a reperfusion injury as areas of the brain that were ischemic from
leukostasis regain blood flow. Because there can be other structural causes of central
nervous system symptoms, brain imaging with noncontrast CT or MRI is indicated in
patients with neurologic abnormalities. Clinicians must be cautious about using
intravenous contrast dye at a time when renal function may be compromised by
leukostasis or tumor lysis syndrome, and dehydration.

● Approximately 80 percent of patients with leukostasis are febrile, which may be due
to inflammation associated with leukostasis or concurrent infection. Since an
infectious cause cannot be easily excluded, we treat empirically for infection in all
such patients. (See "Overview of neutropenic fever syndromes" and "Treatment of
neutropenic fever syndromes in adults with hematologic malignancies and
hematopoietic cell transplant recipients (high-risk patients)" and "Treatment and
prevention of neutropenic fever syndromes in adult cancer patients at low risk for
complications".)

● Less common signs or symptoms of leukostasis include electrocardiographic signs of

myocardial ischemia or right ventricular overload, worsening renal insufficiency,
priapism, acute limb ischemia, or bowel infarction [3].

Occasionally, patients develop dyspnea and worsening hypoxemia following the initiation
of chemotherapy due to the lysis of leukemic cells trapped in the lungs (eg, acute lysis
pneumopathy) [12-15].

LABORATORY ABNORMALITIES

Hyperleukocytosis may result in laboratory abnormalities, which can be due to interference

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with laboratory assays or may be a consequence of the high number of circulating blasts.

● Arterial pO2 can be falsely decreased because of the enhanced metabolic activity of
the malignant cells, even when the specimen is appropriately placed on ice during
transport to the laboratory. Pulse oximetry provides a more accurate assessment of
O2 saturation.

● The platelet count may be overestimated by automated blood cell counters because
fragments of blasts on blood smear can be mistakenly counted as platelets. A manual
platelet count and careful review of the peripheral smear is appropriate in such
settings. (See "Approach to the patient with thrombocytosis", section on 'Blood
smear'.)

● Serum potassium can be spuriously elevated due to its release from leukemic blasts
during the in vitro clotting process. Potassium levels measured from heparinized
plasma samples, rather than serum, can circumvent this effect. (See "Causes and
evaluation of hyperkalemia in adults", section on 'Pseudohyperkalemia'.)

● Disseminated intravascular coagulation (DIC) occurs in up to 40 percent of patients

[3]. DIC presents with various degrees of thrombin generation (eg, decreased
fibrinogen) and increased fibrinolysis (eg, elevated fibrin degradation products and D-
dimer). DIC may develop or worsen following chemotherapy. (See "Evaluation and
management of disseminated intravascular coagulation (DIC) in adults".)

● Spontaneous tumor lysis syndrome (TLS) is present in up to 10 percent of patients

with leukostasis [3]. Laboratory evidence of tumor lysis syndrome includes increased
elevated serum concentrations of uric acid, potassium, and phosphate, often
accompanied by hypocalcemia. TLS may develop or worsen following chemotherapy.
(See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology
and risk factors".)

DIAGNOSIS

Leukostasis (symptomatic hyperleukocytosis) is diagnosed empirically when a patient with

leukemia and a white blood cell (WBC) count over 100 x 109/L (100,000/microL) presents
with symptoms thought to be due to tissue hypoxia, most commonly respiratory or

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neurological distress. The diagnosis requires a high degree of suspicion, and some
patients have pathologically proven leukostasis at WBC counts below this level.

Pathologically, leukostasis is diagnosed when a biopsy of involved tissue demonstrates

white cell plugs in the microvasculature [1,5-7]. A pathologic diagnosis of leukostasis is
rarely obtained because of the risks associated with biopsy of affected tissues.

MANAGEMENT

Leukostasis (symptomatic hyperleukocytosis) constitutes a medical emergency, and efforts

should be made to rapidly stabilize the patient and lower the WBC count. In most cases,
rapid cytoreduction can be achieved with induction chemotherapy, which should be
administered in conjunction with prophylaxis for tumor lysis syndrome. Because clinical
deterioration can sometimes occur rapidly, most clinicians also advocate prompt initiation
of cytoreductive therapy in patients with asymptomatic hyperleukocytosis. Adequate fluid
resuscitation to prevent dehydration and ensure good urine output is important. (See
"Tumor lysis syndrome: Prevention and treatment", section on 'Clinical impact of tumor
lysis syndrome'.)

Cytoreduction — Twenty to 40 percent of patients with symptomatic hyperleukocytosis

die within the first week of presentation [16-22]. The mortality rate appears to be unrelated
to the level of the WBC count, but patients with symptoms (eg, respiratory distress or
neurological compromise) have a significantly worse prognosis when compared with
patients who have hyperleukocytosis alone.

Cytoreduction can be achieved through the use of chemotherapy (hydroxyurea or

remission induction chemotherapy) or leukapheresis. While both modalities rapidly
decrease the circulating WBC count, chemotherapy also destroys leukemia cells in the
bone marrow and is the only treatment proven to improve survival. No randomized trials
have compared addition of leukapheresis to chemotherapy for the treatment of
hyperleukocytosis (with or without symptoms of leukostasis). Two multi-institutional
retrospective analyses concluded that there was no clearcut evidence supporting routine
addition of leukapheresis for such patients [23,24].

In general, we propose the following approach to patients with hyperleukocytosis:

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● For patients with symptomatic or asymptomatic hyperleukocytosis, we suggest initial
treatment with induction chemotherapy rather than hydroxyurea or leukapheresis.
This should be accompanied by tumor lysis syndrome prophylaxis with aggressive
hydration and allopurinol. (See 'Induction chemotherapy' below and "Tumor lysis
syndrome: Prevention and treatment", section on 'Clinical impact of tumor lysis
syndrome'.)

Our preference for induction chemotherapy is primarily based upon the knowledge
that such therapy is also a necessary step toward the successful treatment of patients
with leukemia. There is little evidence to confirm that decreasing the WBC count with
leukapheresis will reduce the early mortality rate [25]. In addition, clinical
deterioration may occur even after the WBC count has been significantly reduced.

An exception to this approach may occur in patients who cannot start induction
chemotherapy immediately. Such patients include those who have poor venous
access, renal insufficiency, or other severe metabolic disturbances, and those with
delays in initiating prophylaxis for tumor lysis syndrome (TLS). If induction
chemotherapy must be delayed, our approach to hyperleukocytosis depends on
whether or not the patient is having symptoms of hyperleukocytosis (ie, leukostasis).

● For patients without symptoms of leukostasis who must have induction

chemotherapy delayed, we suggest cytoreduction with hydroxyurea rather than
leukapheresis. Cytoreduction with hydroxyurea can precipitate or exacerbate
hyperuricemia and occasionally precipitate TLS, therefore such patients also need
intravenous hydration and TLS prophylaxis. (See 'Hydroxyurea' below.)

● For patients with symptoms of leukostasis who must have induction chemotherapy
delayed, we suggest initial cytoreduction with leukapheresis in combination with
hydroxyurea to lower or stabilize the WBC count. (See 'Leukapheresis' below.)

The use of these three approaches to cytoreduction is presented in more detail in the
following sections.

Induction chemotherapy — Induction chemotherapy is an essential component of the

successful treatment of patients with leukemia. In the setting of hyperleukocytosis,
induction chemotherapy serves to both rapidly decrease the circulating WBC count and
target the leukemia cells in the bone marrow. Induction therapy typically substantially
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reduces the WBC count within 24 hours. Details regarding the administration of induction
therapy are presented separately. (See "Induction therapy for acute myeloid leukemia in
medically-fit adults" and "Acute myeloid leukemia: Management of medically-unfit adults"
and "Induction therapy for Philadelphia chromosome negative acute lymphoblastic
leukemia in adults".)

Patients with hyperleukocytosis are at higher risk of developing tumor lysis syndrome with
induction chemotherapy. This syndrome is best prevented via appropriate treatment with
intravenous hydration to ensure adequate urine flow, allopurinol or rasburicase to reduce
serum uric acid levels, and correction of any electrolyte disturbances or causes of
reversible renal failure. (See "Tumor lysis syndrome: Prevention and treatment", section on
'Clinical impact of tumor lysis syndrome'.)

Hydroxyurea — We typically reserve hydroxyurea for patients with asymptomatic

hyperleukocytosis who are unable to receive immediate induction chemotherapy.
Hydroxyurea, given at a total dose of 50 to 100 mg/kg per day orally, reduces the WBC
count by 50 to 80 percent within 24 to 48 hours [26]. The usual hydroxyurea dose is 2 to 4
grams orally every 12 hours, which is continued until the WBC count is below 50 x 109/L
(50,000/microL).

Side effects of hydroxyurea are usually minimal and are typically limited to patients who
are exposed to hydroxyurea for a prolonged period. Rare complications include fever and
abnormal liver function tests.

Leukapheresis — The role of leukapheresis as an adjunct to the treatment of all patients

with hyperleukocytosis is controversial. It is not clear whether survival is improved in
patients treated with leukapheresis when compared with patients who receive
cytoreductive chemotherapy promptly.

Although intensive leukapheresis, with procedure times often lasting many hours, has
been reported to produce improvement in pulmonary and central nervous system
symptoms, there are theoretical and practical limitations to its benefits. It is precisely the
patient in whom leukostasis is most likely to occur, that is, the patient with a high and
rapidly rising blast count, in whom the technical limitations of leukapheresis are relevant. It
is often difficult, even with highly efficient cell separators, to reduce the rapidly rising
count. Cycle-specific chemotherapeutic agents (eg, induction chemotherapy) are more
likely to be most rapidly effective.
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Although some clinicians advocate its use for patients with asymptomatic
hyperleukocytosis, we typically reserve leukapheresis for patients with symptomatic
hyperleukocytosis who must have induction chemotherapy postponed. Our preference to
reserve leukapheresis for this selected patient population is primarily based upon the
known risks associated with leukapheresis described below and an unclear benefit.
Anecdotal reports have claimed dramatic responses [27-31], but larger retrospective
analyses have demonstrated conflicting effects on early mortality rates [19,22-24,32].
Given the paucity of data concerning the efficacy of leukapheresis in reducing early
mortality and/or improving overall survival, leukapheresis cannot be recommended for
routine therapy as a form of tumor "debulking" in patients with high blast counts.

However, patients with symptomatic leukocytosis have an extremely high mortality rate
without immediate therapy [16-22]. When both respiratory failure and neurologic
compromise are present, the death rate at one week reaches 90 percent [22]. Therefore, if
facilities are available, we suggest leukapheresis for patients with leukemic blast counts
greater than 50 to 100 x 109/L (50 to 100,000/microL) and associated symptoms as a
temporizing measure until chemotherapy can be initiated. It is difficult to predict the
percent leukocyte count reduction in individual patients, but sessions are usually planned
for four- to five-hour collections with repeat sessions as needed.

It is generally agreed that leukapheresis should not be used for patients with acute
promyelocytic leukemia because it may worsen the intrinsic coagulopathy associated with
this subtype of leukemia [2]. Placement of large intravenous leukapheresis catheters in
these patients has been associated with venous thrombosis or hemorrhage. (See "Clinical
manifestations, pathologic features, and diagnosis of acute promyelocytic leukemia in
adults", section on 'Coagulopathy and APL'.)

Additional considerations include:

● Leukapheresis usually requires the placement of a large bore, central venous

catheter, is only available at select medical centers, and lacks standardization. The
procedure can also be done using antecubital veins if they are adequate for
placement of large bore needles bilaterally.

● A small number of platelets are inevitably removed with the leukemic blasts, resulting
in worsening thrombocytopenia.
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● Some patients require multiple sessions to control their WBC count, while many
others, presumably those with the most rapidly proliferating acute myeloid leukemia
(AML), do not respond to multiple sessions of leukapheresis [33].

● The effect is generally transient with WBC counts typically rebounding after
leukapheresis is discontinued unless chemotherapy is begun.

● It is unclear whether leukapheresis can reverse vascular damage already sustained

from leukostasis. In addition, symptomatic leukostasis can still develop after the WBC
count has been lowered by leukapheresis.

Supportive care — The following supportive care measures should be considered for all
patients with hyperleukocytosis:

● Symptomatic leukostasis can be precipitated by increases in whole blood viscosity

following red blood cell transfusions. Such transfusions should be withheld, if
possible, until the blast count is reduced. If a transfusion is necessary, it should be
given slowly, administering a single unit of red blood cells over a few hours, or during
the leukapheresis procedure. Hydration is encouraged and diuretics are discouraged.

● Patients with hyperleukocytosis are at risk of tumor lysis syndrome (TLS), although
this syndrome is less common in patients with AML than in those with acute
lymphoblastic leukemia (ALL) or Burkitt leukemia/lymphoma. TLS is best prevented
with intravenous hydration to ensure adequate urine flow, allopurinol or rasburicase
to reduce serum uric acid levels, and the correction of any electrolyte disturbances or
causes of reversible renal failure. (See "Tumor lysis syndrome: Prevention and
treatment", section on 'Clinical impact of tumor lysis syndrome'.)

Although intravenous hydration is recommended for the management and

prevention of tumor lysis syndrome, care should be taken to avoid overhydration and
hypervolemia which could exacerbate pulmonary symptoms.

● Coagulation abnormalities, including disseminated intravascular coagulation (DIC),

further increase the risk of local hemorrhage. Specific treatment aimed at the DIC
should be considered. (See "Evaluation and management of disseminated
intravascular coagulation (DIC) in adults" and "Initial treatment of acute
promyelocytic leukemia in adults", section on 'Control of coagulopathy'.)

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Hyperleukocytosis and leukostasis in hematologic malignancies
● Patients should also receive prophylactic platelet transfusions to maintain a count of
greater than 20 to 30,000/microL until the WBC count has been reduced and the
clinical situation has been stabilized. The risk of intracranial hemorrhage is greatest
after the WBC count has been markedly reduced, suggesting that a reperfusion injury
may occur when the circulation is restored to previously hypoxemic or ischemic
capillary beds. Thus, aggressive platelet transfusion support and correction of
coagulopathy should continue for several days during the remission induction period.

In addition, patients with leukostasis often require specialized, symptom-directed

supportive care including mechanical ventilation for respiratory failure and/or stroke. (See
"Initial assessment and management of acute stroke" and "Overview of initiating invasive
mechanical ventilation in adults in the intensive care unit".)

Is there a role for cranial irradiation? — Some centers have advocated low dose cranial
irradiation (eg, 400 cGy in a single fraction), including treatment of the retina, to prevent
further proliferation of leukemic cells in central nervous system sites, where drug delivery
may theoretically be compromised. However, there are no comparative studies to
determine whether the results with cranial irradiation are superior to those with
chemotherapy alone, and we do not advocate the routine use of cranial irradiation in this
setting. Nevertheless, it could be considered for patients with serious central nervous
system symptoms related to leukostasis.

PROGNOSIS

The prognostic impact of hyperleukocytosis and leukostasis (symptomatic

hyperleukocytosis) depends on the type of leukemia (acute myeloid leukemia or acute
lymphoblastic leukemia) and the presence of symptoms.

The initial mortality rate for patients with acute myeloid leukemia (AML) and leukostasis
has been estimated at 20 to 40 percent and appears to be unrelated to the severity of the
hyperleukocytosis [16-19,22]. If patients survive the initial period, they tend to have
somewhat lower remission rates. Remission durations are also shorter, possibly because of
a larger initial tumor mass, but more likely related to the biology and intrinsic
chemotherapy resistance of the leukemia [16,18].

Risk factors for mortality in patients with AML and hyperleukocytosis were identified in a
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Hyperleukocytosis and leukostasis in hematologic malignancies

retrospective analysis [22]. When compared with patients who lived more than one week
after presentation, patients who died within the first week of presentation had significantly
higher rates of coagulopathy (64 versus 18 percent), respiratory distress (100 versus 15
percent), renal failure (43 versus 29 percent), and neurologic symptoms (64 versus 12
percent) [22].

In patients with acute lymphoblastic leukemia (ALL), hyperleukocytosis is rarely

complicated by leukostasis and the early death rate is less than 5 percent in childhood ALL
[4]. The challenge of leukostasis management in ALL involves preventing tumor lysis
syndrome, disseminated intravascular coagulation, and the higher risk of relapse
(approximately 50 percent by four years) [3]. (See "Prognostic factors and risk group
stratification for acute lymphoblastic leukemia/lymphoblastic lymphoma in children and
adolescents" and "Evaluation and management of disseminated intravascular coagulation
(DIC) in adults" and "Tumor lysis syndrome: Prevention and treatment", section on 'Clinical
impact of tumor lysis syndrome'.)

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Here are the patient education articles that are relevant to this topic. We encourage you to
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● Beyond the Basics topics (see "Patient education: Acute myeloid leukemia (AML)
treatment in adults (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

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Hyperleukocytosis and leukostasis in hematologic malignancies
● Hyperleukocytosis is a laboratory abnormality that has been variably defined as a
total white blood cell (WBC) count greater than 50 x 109/L (50,000/microL) or 100 x
109/L (100,000/microL). In contrast, leukostasis (also called symptomatic
hyperleukocytosis) is a medical emergency that is most commonly seen in patients
with acute myeloid leukemia (AML) or chronic myeloid leukemia (CML) in blast crisis
and is characterized by an extremely elevated WBC count and symptoms of
decreased tissue perfusion.

● The main clinical symptoms of leukostasis and causes of early death are related to
involvement of the central nervous system and lungs. (See 'Signs and symptoms'
above.)

● Clinically, leukostasis is diagnosed empirically when a patient with leukemia and a

blast cell count over 50 to 100 x 109/L (100,000/microL) presents with respiratory or
neurological distress. (See 'Diagnosis' above.)

● The initial management of a patient with hyperleukocytosis is directed at rapid

lowering of the WBC count. (See 'Management' above.)

• For patients with symptomatic or asymptomatic hyperleukocytosis, we suggest

initial cytoreduction with induction chemotherapy rather than hydroxyurea or
leukapheresis (Grade 2B). (See "Induction therapy for acute myeloid leukemia in
medically-fit adults" and "Acute myeloid leukemia: Management of medically-unfit
adults" and "Induction therapy for Philadelphia chromosome negative acute
lymphoblastic leukemia in adults".)

• For patients with asymptomatic hyperleukocytosis who must have induction

chemotherapy delayed, we suggest cytoreduction with hydroxyurea rather than
leukapheresis (Grade 2C).

• For patients with symptoms of leukostasis who must have induction

chemotherapy delayed, we suggest initial leukapheresis in addition to
hydroxyurea (if possible) to lower or stabilize the WBC count (Grade 2C).

● The following supportive care measures should be considered for all patients with
hyperleukocytosis (see 'Supportive care' above):

• Red blood cell transfusions should be withheld, if possible, until the blast count is
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Hyperleukocytosis and leukostasis in hematologic malignancies

reduced. If a transfusion is necessary, it should be administered slowly.

• Most patients with hyperleukocytosis are candidates for tumor lysis syndrome
prophylaxis with aggressive intravenous hydration and allopurinol or rasburicase
to decrease serum uric acid levels. (See "Tumor lysis syndrome: Prevention and
treatment", section on 'Clinical impact of tumor lysis syndrome'.)

• Coagulation abnormalities require aggressive treatment with platelet transfusions

and coagulation factors. (See "Evaluation and management of disseminated
intravascular coagulation (DIC) in adults" and "Initial treatment of acute
promyelocytic leukemia in adults", section on 'Control of coagulopathy'.)

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