C51-18 Shock Without Hypotension: Severe Anemia Leading to Global Ischemic Injury

Abstract Introduction Severe anemia, especially from blood loss, typically presents with hemodynamic instability. However, multiorgan ischemic injury can occur in a setting of preserved blood pressure. This reflects a state of inadequate oxygen delivery despite maintained perfusion, leading to tissue hypoxia as the etiology of organ injury. As a result, clinical features and markers of ischemic injury may resemble shock, even without accompanying hypotension. Case 77-year-old female with CAD, type 2 diabetes, hypertension, hyperlipidemia, and HFrEF (EF 35-40%11/2024), living alone, found down at home for an unspecified amount of time. She was minimally responsive, demonstrating agonal breathing. EMS vitals: BP 135/58 mmHg, HR 92 bpm, RR 8 breaths/min, SpO2 80%,and GCS E2M1V1. She was intubated in the field for airway protection. On arrival demonstrated underlying pallor and markedly pale conjunctiva; lungs were clear. Labs showed Hgb 2.9 g/dL, Hct 13%, MCV 77.8 fL, WBC 29.65 K/µL, lactate 11.8 mmol/L, creatinine 2.2 mg/dL, BUN 41 mg/dL, pH 7.31, pCO2 18mmHg, pO2 499 mmHg, CK 1,140 U/L, troponin-T 4,391 ng/L, NT-proBNP 16,305 pg/mL, AST 1,471 U/L, ALT 944 U/L. Head CT negative for acute pathology. She received four units of PRBCs, increasing Hgb to 10.9 g/dL, later stabilizing at 11.2 g/dL. EGD revealed two non-bleeding gastric ulcers (Forrest IIc and III) treated with clips, and a small hiatal hernia with non-bleeding erosions. Vitals remained stable without hypotension. Despite hemoglobin correction, mental status did not improve. MRI obtained on hospital day 3 demonstrated diffuse acute bilateral watershed infarcts. Patient was extubated and transferred out of the ICU. Due to persistent neurologic deficits, she was discharged to long-term care, Percutaneous Endoscopic Gastrostomy-dependent, with residual aphasia, dysphagia, and requiring significant assistance Discussion Despite normal blood pressure and oxygenation, this patient developed multiorgan injury from critically reduced oxygen delivery from profound anemia. Oxygen delivery depends on cardiac output and arterial oxygen content, largely determined by hemoglobin. With a hemoglobin of 2.9 g/dL, oxygen-carrying capacity was markedly reduced. Despite the patient’s high PaO2 and normal ventilation, tissue oxygenation was inadequate. Once compensatory mechanisms failed, global hypoxia led to lactic acidosis, myocardial injury consistent with demand ischemia, acute kidney injury, hepatic injury, and diffuse watershed infarcts. This case shows that severe anemia can produce shock-like multiorgan failure without hypotension. Markers of tissue perfusion, including lactate and organ dysfunction, are essential, and early recognition with prompt transfusion is critical to prevent or mitigate irreversible injury. This abstract is funded by: n/a