Critical Care

SESSION TITLE: Hematology and Oncology Disorders

SESSION TYPE: Affiliate Case Report Poster
PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM

It’s Not Jungle Fever: Autoimmune Hemolytic Anemia and Lupus

Nandini Mehta* Kevin Lazo Sanjeev Sharma Van Pham and Kambo Varinder Lenox Hill Hospital, Northwell Health,
New York, NY

INTRODUCTION: Autoimmune Hemolytic Anemia (AIHA) is an acquired disorder due to antibody destruction of RBCs. With
an incidence of one to three cases in 100,000 per year, AIHA is relatively rare. We report on a young female whose diagnosis was
complicated by jungle travel and who was ultimately found to have AIHA due to systemic lupus erythematosus (SLE).
CASE PRESENTATION: A 28-year-old Swedish female presented with three weeks of worsening fatigue, cyclical fevers, sweats,
and cough. The symptoms started one week after a seven-day trip to Colombia, South America, where she participated in a jungle
hike. Traveling family members did not have similar symptoms. Family history was significant for rheumatoid arthritis in her
mother, brother, and maternal cousin and Graves’ disease in her maternal aunt. Upon return, she was treated for presumed
community acquired pneumonia with levofloxacin. Persistent symptoms prompted her ED visit. On admission, T was 103 F, and
exam was notable for pallor, two aphthous ulcers, and splenomegaly. Labs revealed a Hb of 5.8 g/dL, which downtrended to 4.1 g/
dL, WBC of 1.6 K/mL, and ANC of 252 K/mL. Non-contrast CT chest showed bibasilar patchy ground glass opacities and probable
bilateral hilar and mediastinal adenopathy. The patient was admitted to the ICU step-down unit due to severe anemia and febrile
neutropenia. She was started on empiric antibiotics and received multiple blood transfusions. Hemolytic markers, reticulocytosis,
and peripheral smear supported hemolysis, and abdominal US confirmed splenomegaly. Broad workup for tropical diseases, such
as malaria, and other infectious etiologies remained negative. Given her family history and exam, an autoimmune cause was
considered. Concurrent investigation was positive for direct Coomb’s IgG, ANA (1:2560, homogeneous pattern), and antibodies
for dsDNA, anti-cardiolipin, and b-2 glycoprotein-1. She was started on steroids for warm AIHA due to SLE and clinically
improved.
DISCUSSION: AIHA is diagnosed by hemolytic markers and direct antiglobulin (direct Coomb’s) testing. Of the four serologic
forms, warm/IgG-mediated AIHA represents 65-70% of the disease. AIHA may be a primary or, as in our case, a secondary
disorder. AIHA has been described in 4-10% of adult SLE. It is generally treated with immune modulation, namely
CRITICAL CARE

glucocorticoids. Nevertheless, if not recognized early, AIHA can result in cardiovascular collapse, thrombosis, infection, or splenic
infarcts.
CONCLUSIONS: Determining the cause of anemia in a critical patient can be formidable in the midst of complex history and
pathologic processes. Correct diagnosis of the type and cause of AIHA takes precedence for proper treatment and avoidance of
fatal complications.
Reference #1: Liebman HA, Weitz IC.Autoimmune Hemolytic Anemia.Med Clin North Am. 2017 Mar;101(2):351-359.
Reference #2: Gormezano NW et al.Autoimmune hemolytic anemia in systemic lupus erythematosus at diagnosis: differences
between pediatric and adult patients.Lupus.2017 Apr;26(4):426-430.
DISCLOSURE: The following authors have nothing to disclose: Nandini Mehta, Kevin Lazo, Sanjeev Sharma, Van Pham, Kambo
Varinder
No Product/Research Disclosure Information
DOI: http://dx.doi.org/10.1016/j.chest.2017.08.348
Copyright ª 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

322A [ 152#4S CHEST OCTOBER 2017 ]