Case Presentation: A 21-year-old man presented with two weeks of progressive dyspnea. He denied chest pain, lower extremity edema, orthopnea, melena, hematochezia, hemoptysis, cough, or fever. He had a previous presentation with similar symptoms of unknown etiology a few weeks before treated with steroids, blood transfusions, and antibiotics with improvement in symptoms. He was on no medications, was a former cigarette smoker, and smoked marijuana daily. He worked in construction and spray painting.
On presentation, he was afebrile and normotensive. Heart rate was 140 beats per minute, respiratory rate 30 per minute, and oxygen saturation 82% on room air. He had fine crackles bilaterally without wheeze and a regular rhythm with no extra heart sounds. Hemoglobin was 6.4 g/dL (13.5-17.5 g/dL), LDH 1142 IU/L (110-210 IU/L), and reticulocytes 6% (0.5-2.5%). Haptoglobin was undetectable. A Coombs test was negative, and peripheral smear revealed neither schistocytes nor spherocytes. Serum creatinine was 0.6 mg/dL (0.6-1.5 mg/dL), and urinalysis had few dysmorphic red blood cells with no protein. Chest CT revealed bilateral ground glass opacities. Lung biopsy revealed diffuse alveolar hemorrhage (DAH). Serologies included negative ANCA and positive anti-glomerular basement membrane antibodies. The patient was diagnosed with Goodpasture Syndrome and was treated with solumedrol, rituximab, and plasmapheresis with good response.
Discussion: Hospitalists commonly encounter patients with dyspnea from anemia. However, hypoxemia is is not an expected finding with anemia, and its presence should spark further investigation into a pulmonary pathology. Classically, DAH causes hemoptysis, which often helps identify the correct diagnosis. However, as with our patient, hemoptysis may be absent in up to one-third of patients, even with severe hemorrhage.
Reconciling hypoxemia with the patient’s picture of hemolytic anemia (elevated LDH and reticulocytes and low haptoglobin) created further diagnostic confusion during our patient’s evaluation. Several causes of hemolysis were considered, including the patient’s recent blood transfusion. However, our patient’s peripheral smear without abnormal cells and negative Coombs test suggested the absence of true hemolysis. Case reports in the pediatrics literature have shown that pulmonary hemorrhage can mimic hemolytic anemia. As red blood cells are deposited into the alveoli, hemoglobin is rapidly absorbed, binding haptoglobin and releasing LDH. In the absence of a second, hypoproliferative process, reticulocyte production increases, mimicking hemolysis (“pseudo-hemolysis”). The patient’s biopsy and serologies supported DAH from Goodpasture Syndrome as the etiology of both his anemia and hypoxemia.
Conclusions: DAH should be in the differential diagnosis of patients presenting with anemia and hypoxemia even in the absence of hemoptysis. DAH may also be associated with “pseudo-hemolysis” with elevated LDH and low haptoglobin but a normal Coombs and unremarkable peripheral smear.