Case Presentation: An 84-year-old woman with a medical history of asthma and hypertension presented with generalized weakness and poor oral intake. Initial vital signs showed heart rate of 108 beats/minute, blood pressure 146/77 mmHg, temperature of 105.5 F and respiratory rate of 15 breaths/minute. Admission labs showed a leukocytosis (78.56 K/uL cells) with blasts, thrombocytopenia (platelet count 64 K/uL), anemia (hemoglobin 10.2 g/dL), and an acute kidney injury (creatinine 1.51 mg/dL). Duplex of the lower extremities showed right popliteal and peroneal deep vein thrombosis. CT pulmonary angiography showed a pulmonary embolism (PE) and IVC filter. Transthoracic echocardiogram showed right ventricular (RV) enlargement with normal systolic function. The patient developed hypotension, reflecting a mixed picture shock. Her Pulmonary Embolism Severity Index (PESI) score was 164 consistent with very high risk of clinical deterioration. Further lab testing for risk stratification showed an elevated lactate of 2.4 mmol/L, brain natriuretic peptide of 34,080 pg/mL, troponins 137 ng/L, and d-dimer of 15,247 ng/mL. The patient was started on a heparin drip and empiric antibiotics with meropenem and vancomycin. Subsequent bone marrow biopsy confirmed acute myeloid leukemia (AML) with FLT3-mutation. Due to concern for tumor lysis syndrome (TLS), rasburicase and allopurinol were initiated. Hyperkalemia was treated with insulin and dextrose. Decision was made to transfer the patient to the MICU for leukapheresis and continuous renal replacement given RV strain and concern for precipitating RV failure with aggressive fluid resuscitation for sepsis and concurrent TLS. The patient was started on decitabine, venetoclax, and midostaurin with significant improvement of her AML, although with risk of recurrence. The PE was treated successfully with heparin infusion, which was intermittently held for platelet counts < 50 K/uL. Her hospital course was complicated by pleural effusion requiring a chest tube. The patient was successfully discharged on therapeutic enoxaparin.
Discussion: Venous thromboembolism is a common complication of hematologic malignancy. However, patients in a blast crisis can have significant thrombocytopenia, conferring greater bleeding risk.1-3 Our case represents the challenge of managing PE in a patient with new onset AML complicated by sepsis and thrombocytopenia. Initial management of her embolism involved anticoagulation with heparin infusion alongside close monitoring of her declining platelet count. However, the patient’s heparin was held due to declining platelet count. Her shock state was likely multifactorial in nature having components of obstructive (PE), hypovolemic (tumor lysis syndrome (TLS) and distributive (sepsis) shock with an unclear primary driver.
Conclusions: Here, we present the nuance in managing high-risk pulmonary embolism while balancing the hypercoagulable state and bleeding risks of acute myeloid leukemia with thrombocytopenia and acute renal failure. A platelet-count guided strategy allowed us to strike the balance of therapeutic anticoagulation and bleeding risk.3 This case further illustrates the importance of prudence with fluid resuscitation in the setting of PE with concurrent TLS and sepsis as well as identifying when ICU-level of care is necessary for considerations such as leukapheresis and continuous renal replacement.