Resident Physician Harlingen, Texas, United States
Disclosure(s):
Hema S. Vemulapalli, MD: No financial relationships to disclose
Background: Shock due to profound anemia is rare in young patients and may rapidly progress through multiple shock phenotypes. We present a previously healthy young woman with fulminant autoimmune hemolytic anemia (AIHA) complicated by progressive Society for Cardiovascular Angiography and Interventions (SCAI) stage C–E shock and fatal multi-organ failure.
Methods: This is a single-patient case report. A 21-year-old previously healthy female presented with three weeks of progressive weakness, jaundice, abdominal pain, nausea, and anorexia. Initial evaluation demonstrated profound anemia (hemoglobin 3.4 g/dL), marked hyperbilirubinemia (total bilirubin 16.1 mg/dL), and lactic acidosis, consistent with impaired oxygen delivery and SCAI stage C shock. Shortly after ICU admission, she developed severe metabolic acidosis and escalating lactatemia, progressing to SCAI stage D shock.
Her course was complicated by cardiac arrest requiring prolonged cardiopulmonary resuscitation with return of spontaneous circulation, representing episodic SCAI stage E shock. Direct antiglobulin testing confirmed autoimmune hemolytic anemia. Management included high-dose corticosteroids, intravenous immunoglobulin, transfusion of compatible packed red blood cells, mechanical ventilation, and vasopressor support. Broad-spectrum antimicrobials were initiated while evaluating for secondary causes. Serial imaging, laboratory studies, and multidisciplinary consultations were used to guide ongoing critical care management.
Outcome: Following resuscitation, the patient developed shock liver, disseminated intravascular coagulation, and worsening metabolic acidosis. She was found to be influenza A positive and treated with antiviral therapy. Despite transient hemodynamic stabilization, she developed progressive abdominal distention. Imaging revealed mesenteric ischemia with pneumatosis intestinalis, necessitating emergent exploratory laparotomy with extensive small bowel resection, partial colectomy, ileostomy creation, and subsequent splenectomy for refractory hemolysis.
Postoperatively, she experienced recurrent severe anemia requiring transfusions and was initiated on total parenteral nutrition. Over the ensuing days, vasopressors were weaned and she was successfully extubated, corresponding to transient regression to SCAI stage C shock. However, she later deteriorated with recurrent hemolysis, severe electrolyte derangements, and progressive hyperkalemia, consistent with renewed SCAI stage D shock. She suffered multiple recurrent cardiac arrests with transient return of spontaneous circulation, culminating in refractory SCAI stage E shock. Despite maximal supportive care, sustained resuscitation was unsuccessful, and she died following family-directed cessation of resuscitative efforts.
Conclusion: Profound anemia can precipitate catastrophic oxygen delivery failure and progressive SCAI stage C–E shock in young patients. Correction of hemoglobin alone may be insufficient once metabolic and microcirculatory collapse occurs, underscoring the need for early recognition of evolving shock phenotypes.
