RESUMO
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/mm3, Hgb to 6.2 g/dL, Hct to 20.8%, and platelets to 82 thou/mm3 from baseline values of WBC 3.9 thou/mm3, Hgb 8.3 g/dL, Hct 28%, and platelets 126 thou/mm3. 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.
RESUMO
Repeated stress and chronically elevated glucocorticoids cause exaggerated cardiovascular responses to novel stress, elevations in baseline blood pressure, and increased risk for cardiovascular disease. We hypothesized that elevated corticosterone (Cort) within the dorsal hindbrain (DHB) would: 1) enhance arterial pressure and neuroendocrine responses to novel and repeated restraint stress, 2) increase c-Fos expression in regions of the brain involved in sympathetic stimulation during stress, and 3) recruit a vasopressin-mediated blood pressure response to acute stress. Small pellets made of 10% Cort were implanted on the surface of the DHB in male Sprague-Dawley rats. Blood pressure was measured by radiotelemetry. Cort concentration was increased in the DHB in Cort-treated compared with Sham-treated rats (60 ± 15 vs. 14 ± 2 ng Cort/g of tissue, P < 0.05). DHB Cort significantly increased the integrated arterial pressure response to 60 min of restraint stress on days 6, 13, and 14 following pellet implantation (e.g., 731 ± 170 vs. 1,204 ± 68 mmHg/60 min in Sham- vs. Cort-treated rats, day 6, P < 0.05). Cort also increased baseline blood pressure by day 15 (99 ± 2 vs. 108 ± 3 mmHg for Sham- vs. Cort-treated rats, P < 0.05) and elevated baseline plasma norepinephrine and neuropeptide Y concentrations. Cort significantly enhanced stress-induced c-Fos expression in vasopressin-expressing neurons in the paraventricular nucleus of the hypothalamus, and blockade of peripheral vasopressin V1 receptors attenuated the effect of DHB Cort to enhance the blood pressure response to restraint. These data indicate that glucocorticoids act within the DHB to produce some of the adverse cardiovascular consequences of chronic stress, in part, by a peripheral vasopressin-dependent mechanism.
