Background:
Leukemoid reaction is defined as a leukocyte count above 50 cells x 109/L with “left shift” that arises in the absence of a myeloproliferative neoplasm. The most common causes include infection and nonhematopoietic neoplasm. Other etiologies include toxin exposure, hemorrhage, acute hemolysis, and growth factor exposure. This case of leukemoid reaction following status epilepticus is unique and points to another stressor capable of provoking leukemoid reaction.
Design/Methods:
PubMed search for “leukemoid reaction” and “status epilepticus” as well as patient chart review.
Results:
A 21yo male with a known history of epilepsy and prior medication non-adherence presented to the emergency department in convulsive status epilepticus along with significant lactic acidosis. The patient was treated with midazolam by EMS and loaded with levetiracetam on arrival to the hospital. He was intubated for airway protection in the setting of tachycardia to the 170s and tachypnea to the 40s. Presenting lacosamide and cenobamate levels were subtherapeutic. Urinalysis, RVP, chest xray, and UDS were negative on admission. WBC count on admission was significant for a leukemoid reaction with 53.19 cells x 109/L (32% neutrophils). A peripheral blood smear was reflexively performed and showed neutrophilia, lymphocytosis, eosinophilia, basophilia, and no blasts which was suspicious for a reactive or infectious process. The patient’s hospital course lasted 4 days for supportive treatment of seizure-induced rhabdomyolysis with CPK peaking at 25,000. Over the 4 days, the patient’s leukocytosis down trended to 8.18 despite early discontinuation of empiric antibiotics. Bronchoalveolar lavage culture demonstrated 10,000 colonies of MSSA along with mixed respiratory flora 1 day after discharge, but the patient never demonstrated infectious respiratory symptoms.
Conclusions:
Status epilepticus is an emergent condition that yields considerable physiologic stress as evidenced by this patient’s severe lactic acidosis and CPK elevations. It should be recognized as an etiology for leukemoid reaction due to inflammatory leukocyte margination.