Prediction model for mortality after intracranial hemorrhage in patients with leukemia

Dayyani, Farshid; Mougalian, Sarah Schellhorn; Naqvi, Kiran; Shan, Jianqin; Ravandi, Farhad; Cortes, Jorge; Weinberg, Jeffrey S.; Jabbour, Elias; Faderl, Stefan; Wierda, William G.; Thomas, Deborah A.; O’Brien, Susan; Pierce, Sherry; Kantarjian, Hagop M.; Garcia‐Manero, Guillermo

doi:10.1002/ajh.22031

Cited by 33 publications

(34 citation statements)

References 19 publications

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“…101,102 In older patients, in whom the risk of rebleeding is significantly high and allogeneic transplantation is not a practical option, we consider less myeloablative therapy, such as hydroxyurea, low-dose cytarabine, or hypomethylating agents. 100,103 This patient has a high risk for CNS involvement based on the myelomonocytic lineage morphology and leukocytosis [104][105][106] but there is no firm evidence to suggest a connection between ICH and CNS involvement of leukemia. 107 Although ICH preceded the diagnosis of leukemia by 6 weeks and the patient has poorly controlled hypertension For personal use only.…”

Section: Questionsmentioning

confidence: 99%

How I treat acute myeloid leukemia presenting with preexisting comorbidities

Ofran

Tallman

Rowe

2016

Blood

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Acute myeloid leukemia (AML) is a devastating disease with an incidence that progressively increases with advancing age. Currently, only ∼40% of younger and 10% of older adults are long-term survivors. If untreated, the overall prognosis of AML remains dismal. Initiation of therapy at diagnosis is usually urgent. Barriers to successful therapy for AML are the attendant toxicities directly related to chemotherapy or those associated with inevitable aplasia. Organ dysfunction often further complicates such toxicities and may even be prohibitive. There are few guidelines to manage such patients and the fear of crossing the medico-legal abyss may dominate. Such clinical scenarios provide particular challenges and require experience for optimal management. Herein, we discuss select examples of common pretreatment comorbidities, including cardiomyopathy, ischemic heart disease; chronic renal failure, with and without dialysis; hepatitis and cirrhosis; chronic pulmonary insufficiency; and cerebral vascular disease. These comorbidities usually render patients ineligible for clinical trials and enormous uncertainty regarding management reigns, often to the point of withholding definitive therapy. The scenarios described herein emphasize that with appropriate subspecialty support, many AML patients with comorbidities can undergo therapy with curative intent and achieve successful long-term outcome.

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Section: Questionsmentioning

confidence: 99%

How I treat acute myeloid leukemia presenting with preexisting comorbidities

Ofran

Tallman

Rowe

2016

Blood

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“…53 In a survey of 2421 patients with acute leukemia, 4 factors were identified predicting the outcome of ICH: low albumin, elevated LDH, age more than 60 years, and relapsed disease. 54 The most common presenting symptom is mental status change; and at the first such clinical sign, patients need to be monitored closely by repeat radiologic imaging (CT/ MRI). We maintain the platelet count more than 50 000/L.…”

Section: What Is the Best Prophylaxis And Emergent Management Of Coagmentioning

confidence: 99%

How I treat hematologic emergencies in adults with acute leukemia

Zuckerman

Ganzel

Tallman

et al. 2012

Blood

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Acute myeloid leukemia and acute lymphoblastic leukemia remain devastating diseases. Only approximately 40% of younger and 10% of older adults are long-term survivors. Although curing the leukemia is always the most formidable challenge, complications from the disease itself and its treatment are associated with significant morbidity and mortality. Such complications, discussed herein, include tumor lysis, hyperleukocytosis, cytarabine-induced cellebellar toxicity, acute promyelocytic leukemia differentiation syndrome, thrombohemorrhagic syndrome in acute promyelocytic leukemia, L-asparaginase-associated thrombosis, leukemic meningitis, neutropenic fever, neutropenic enterocolitis, and transfussion-associated GVHD. IntroductionAlthough inadequate for the cure of most patients, the initial therapeutic approach to acute myeloid leukemia (AML) is standardized. However, the management of hematologic emergencies is challenging and may be controversial. We present clinical vignettes describing 10 emergencies encountered in practice and the questions such emergencies generate. We then provide our view of how to treat adults supported by studies if available and, if not, by clinical experience and consensus. The approach to these emergencies is as important as the antileukemia therapy, and in no clinical setting is it fairer to say that "the devil is in the details." Tumor lysis syndromeA 23-year-old man with a history of G6PD deficiency is diagnosed with pre-B acute lymphoblastic leukemia (B-ALL). At presentation, his white blood cell count (WBC) is 160 000/L with 90% lymphoblasts and 450/L neutrophils; the hemoglobin is 7.5 g/dL and platelet count is 10 000/L. His electrolytes and renal function are normal, the uric acid is 11.0 mg/dL, and lactate dehydrogenase (LDH) is 1500 IU/L (normal, 100-250 IU/L). Remission induction chemotherapy is planned. Questions What is the risk of tumor lysis syndrome (TLS)? What is the optimal treatment for preventing TLS? What is the role of rasburicase and urine alkalinization?TLS can appear before starting treatment (primary TLS) as a result of high turnover of the malignant cells or, more commonly, a short time after the beginning of treatment (secondary TLS). 1 The risk of developing TLS and its severity is influenced by many factors, including tumor burden, potential for rapid cell lysis, and preexisting nephropathy. 2 In acute leukemias, the risk is dependent on the WBC and the rate of response to therapy. In ALL with WBC Ͼ 100 000/L, the risk for TLS is high. With lower WBC, the risk is moderate and low. 3 A classification system has been developed, 4 which is based on separate definitions for laboratory and clinical TLS. Laboratory TLS loosely is defined as the presence of 2 or more abnormal laboratory values of uric acid, potassium, phosphorus, or calcium at presentation or a 25% change in values from the pretreatment measurements. Clinical TLS is defined as the presence of laboratory TLS plus renal dysfunction, seizures, cardiac arrhythmia, or sudden death. An expert TLS pane...

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“…Several retrospective studies consistently show that the overall incidence of ICH in acute leukemia patients is 5% [4,5,6]. These studies included patients with ICH at the time of AML diagnosis, after therapy commenced, and at later time points.…”

Section: Tablementioning

confidence: 99%