This case involves a 62-year-old male with a prior history of epidural abscess and L1-L2 osteodiscitis who was admitted because of low back pain. The patient was previously treated for methicillin-susceptible Staphylococcus aureus (MSSA) discitis in the L1/L2 vertebral region with intravenous (IV) nafcillin through a peripherally inserted central catheter (PICC). However, he returned after four months with recurrent low back pain along with chills and fever. He was admitted for severe sepsis related to the L1-L2 region osteomyelitis and discitis. The Infectious Disease department initially started the patient on IV vancomycin and cefepime; however, routine labs on the second day of IV antibiotics showed concern for pancytopenia with white blood cell count (WBC) decreased to 2.5 thou/mm 3 , Hgb to 6.2 g/dL, Hct to 20.8%, and platelets to 82 thou/mm 3 from baseline values of WBC 3.9 thou/mm 3 , Hgb 8.3 g/dL, Hct 28%, and platelets 126 thou/mm 3 . Due to concern for pancytopenia in the setting of severe sepsis, extensive hematologic workup was pursued to evaluate for disseminated intravascular coagulation (DIC) and bone marrow suppression. The patient also had a positive fecal occult blood test, so the Gastroenterology department was consulted for esophagogastroduodenoscopy (EGD) and colonoscopy. Furthermore, despite appropriate outpatient treatment for MSSA osteodiscitis, the patient was bacteremic with Staphylococcus aureus. Hence, the Cardiology department was consulted to rule out cardiac valvular vegetation. This case presents a unique case of pancytopenia involving elements of drug-induced aplastic anemia as well as DIC-related sepsis. The agranulocytosis may have been a consequence of drug reaction to IV vancomycin. The anemia and thrombocytopenia may have been caused by DIC. Repeat computed tomography (CT) guided spinal aspiration confirmed pan-sensitive Staphylococcus aureus infection of the L1/L2 vertebral region. Treatment was reverted to nafcillin monotherapy and fortunately his hematologic function normalized, avoiding the need for advanced treatments such as intravenous immunoglobulin infusion therapy (IVIG) or high dose steroids.

The hallmarks of myxedema coma are decreased mental status and hypothermia; but hypotension, bradycardia, hyponatremia, hypoglycemia, and hypoventilation may also be present. This case involves a 74-year-old female, with arthritis and dementia, who presented with weakness and failure to thrive. Physical exam was significant for altered level of consciousness, lethargy, pretibial pitting edema and hypotension. Since friends and family were absent, history was obtained per chart review. Initial labs showed severe hypokalemia of 2.0 mmol/L and associated changes of prolonged QT interval and T wave flattening on electrocardiogram (ECG). The family later revealed additional history of thyroidectomy and clarification that the patient had been noncompliant with her medications for at least 6 months. Hypothyroidism was confirmed with a thyroid stimulating hormone (TSH) level of 82.2 U/mL and a free thyroxine (T4) level below normal threshold. Endocrinology was consulted and care was taken when reinstituting her thyroid supplementation after checking cortisol level as well as reviewing her ECGs. This case report illustrates the importance of checking for thyroid dysfunction especially in the elderly who present with altered mental status and unclear history as most symptoms of myxedema coma may be reversible. Furthermore, myxedema coma occurring in the setting of decompensated hypothyroidism is a medical emergency. In this case, despite timely diagnosis and appropriate treatment, her cognitive function failed to improve, and as a result, palliative care was consulted. Ultimately, the family elected for hospice care due to severe dementia, bed-bound status, and failure to thrive.