A49-45 Sepsis-Induced Absolute Neutropenia From Toxic Shock Syndrome in an Immunocompetent Patient

Introduction Hematologic abnormalities are well recognized in sepsis, with leukocytosis often serving as an early indicator. However, sepsis-associated leukopenia is frequently overlooked despite being linked to a markedly higher mortality rate of about 40-50%. We present a case of sepsis complicated by absolute neutropenia and toxic shock syndrome secondary to Streptococcus dysgalactiae. Case Presentation An 86-year-old man with hypertension, hyperlipidemia, chronic right lower extremity lymphedema, osteoarthritis, and benign prostatic hyperplasia presented with generalized weakness, dyspnea, urinary retention, and worsening right leg swelling. On arrival, he was febrile (101.7 °F) and profoundly hypotensive (53/36 mmHg) despite aggressive fluid resuscitation, requiring norepinephrine and vasopressin support. Examination revealed new ascending ecchymosis and bullae on his chronically edematous right leg. Laboratory evaluation showed a white blood cell count of 0.97 × 10³/µL, absolute neutrophil count of 0.49 × 10³/µL, platelet count of 125 × 10³/µL, and a bandemia of 25%. Basic metabolic panel demonstrated acute kidney injury, an anion gap metabolic acidosis, and lactic acid of 10.7 mmol/L. CT imaging showed no focal infectious source. Broad-spectrum antibiotics (piperacillin-tazobactam and vancomycin) were initiated empirically. Despite escalation of vasopressor therapy and endotracheal intubation, he developed progressive mottling, purpura, and hemorrhagic bullae, consistent with streptococcal toxic shock syndrome. After multidisciplinary discussion, the patient’s code status was transitioned to do-not-resuscitate (DNR). He subsequently expired. Blood cultures later grew Streptococcus dysgalactiae (SDSE). Discussion Staphylococcus aureus or Streptococcus pyogenes most commonly causes toxic shock syndrome (TSS), a fulminant toxin-mediated illness. SDSE-associated TSS is increasingly recognized in elderly or immunocompromised patients. Superantigen-mediated immune activation triggers a cytokine storm, leading to shock and multiorgan failure. Clindamycin or Linezolid, in combination with β-lactam therapy, can be used as an adjunctive therapy to suppress toxin production, though Clindamycin resistance among SDSE strains is rising and data to support use of Linezolid is limited. Sepsis-induced neutropenia, as observed in this case, is a well-documented but underappreciated marker of poor prognosis. Mechanisms include increased neutrophil apoptosis, impaired granulopoiesis, and myeloid maturation arrest. Recognition of this hematologic pattern should prompt early and aggressive management. This abstract is funded by: none