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 — 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 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 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 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 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:
●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 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.
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.
●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'.)
●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 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'.)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Beyond the Basics topics (see "Patient education: Acute myeloid leukemia (AML) treatment in adults (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Descriptions – Key terms:
•Hyperleukocytosis – A laboratory abnormality variably defined as a total white blood cell (WBC) count >50 x 109/L (50,000/microL) or >100 x 109/L (100,000/microL).
•Leukostasis – A medical emergency characterized by an extremely elevated WBC count and symptoms of decreased tissue perfusion, most often seen in patients with acute myeloid leukemia (AML) or chronic myeloid leukemia (CML) in blast crisis.
●Presentation – The main symptoms of leukostasis relate to involvement of the central nervous system (CNS; eg, visual changes, headache, dizziness, tinnitus, gait instability, confusion, somnolence, coma) and lungs (eg, dyspnea). (See 'Signs and symptoms' above.)
●Diagnosis – Leukostasis should be considered in a patient with leukemia and hyperleukocytosis who has respiratory distress or neurologic findings. (See 'Diagnosis' above.)
Leukocytosis is a clinical diagnosis supported by clinical evaluation and WBC count >50 to 100,000/microL.
●Management – Initial management is directed at rapidly lowering the WBC count. (See 'Management' above.)
•Preferred approach – For patients with symptomatic or asymptomatic hyperleukocytosis, we suggest initial cytoreduction with induction chemotherapy, rather than hydroxyurea or leukapheresis (Grade 2B). (See 'Induction chemotherapy' above.)
•When chemotherapy must be delayed:
-Symptomatic – 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). (See 'Cytoreduction' above.)
-Asymptomatic – For patients with asymptomatic hyperleukocytosis who must have induction chemotherapy delayed, we suggest cytoreduction with hydroxyurea, rather than leukapheresis (Grade 2C). (See 'Hydroxyurea' above.)
●Supportive care – For all patients with hyperleukocytosis, the following supportive care should be considered (see 'Supportive care' above):
•Transfusions – Red blood cell transfusions should be withheld, if possible, until the blast count is reduced. If a transfusion is necessary, it should be administered slowly.
•Tumor lysis syndrome prophylaxis – 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 – 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'.)
