Case report: left atrial Myxoma causing elevated C-reactive protein, fatigue and fever, with literature review.

BACKGROUND: A cardiac myxoma in a young person may pose a diagnostic challenge as symptoms may be variable and the differential diagnosis is wide. The differential diagnosis can include rheumatic mitral valve disease, pulmonary hypertension, endocarditis, myocarditis and vasculitis. CASE PRESENTATION: This case report involves a 49 years old female with a 2.8 cm × 3.4 cm myxoma in the left atrium causing mitral valve obstruction. She presented with fatigue, fever of unknown origin, transient ischemic attack and shortness of breath. Prompt surgery is often recommended due to the risk of embolic complications or complete obstruction. Due to her symptoms, patient underwent successful cardiothoracic surgery to excise the myxoma within 2 weeks of confirmation by cardiac echocardiography. CONCLUSION: This case also emphasizes the diagnostic challenge as symptoms may be variable, ranging from fatigue, fever and shortness of breath to transient ischemic attack and at worst, sudden cardiac death. In conclusion, if a cardiac mass is suspected, echocardiography should be performed early. Surgical resection is curative and recurrence rate is very rare in sporadic isolated myxomas, however, recurrence can be higher in genetic diseases associated with increased frequency of myxomas such as Carney complex. This subpopulation of patients may present further research opportunity to learn more about the perioperative management of patients with myxomas such as determining the optimal time to surgical intervention and decision to anticoagulate.

Diffuse Exfoliative Rash with Sepsis and Eosinophilia: A Case of Erythroderma?

BACKGROUND Erythroderma is an exfoliative dermatitis that manifests as generalized erythema and scaling that involves 90% of the body surface. If untreated, erythroderma can be fatal because of its metabolic burden and risk of secondary infections. CASE REPORT The patient was a 56-year-old male with prior rash attributed to group A Streptococcal cellulitis and discharged on Augmentin, Clindamycin with hydrocortisone cream, and Bactrim, but he had been noncompliant. He was admitted again for rash involving the face, torso, and extremities characterized by diffuse, desquamative, dry scales in morbilliform pattern. The patient was septic with Staphylococcus aureus bacteremia and compromised skin barrier. He was started on vancomycin and switched to Cefazolin IV due to concern for drug reaction. Autoimmune workup included antibodies for anti-Jo-1, anti-dsDNA, anti-centromere, and ANCA. However, only antinuclear antibody and scleroderma antibody were positive. Given the unclear workup results and lack of response to antibiotics, the patient was started on prednisone 60 mg PO and topical Triamcinolone 0.1% cream. A skin biopsy revealed psoriasiform hyperplasia with atypical T cell infiltrate and eosinophils, but negative for T cell gene rearrangement. The rash resolved after day 12 of application of topical Triamcinolone. CONCLUSIONS This case is unique in terms of the rarity of erythroderma and the diagnostic challenge given confounding factors such as noncompliance and drug reaction. Serious causes, such as SLE and cutaneous T cell lymphoma, were ruled out. Fortunately, the rash responded well to steroids; however, given the adverse effects of long-term use of topical steroids, the patient will need follow up with Dermatology.

Pancytopenia as a Consequence of Sepsis and Intravenous Antibiotic Drug Toxicity.

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.

Ventricular fibrillation associated with Graves' disease and amiodarone induced thyrotoxicosis.

This case involves a 55-year-old male patient with systolic heart failure and refractory atrial fibrillation due to thyrotoxicosis, who was electrically cardioverted but then developed torsade de pointes and ventricular fibrillation. Rate control was unsuccessful with digoxin, cardizem, labetalol, esmolol and amiodorone. Patient was externally cardioverted after which ECGs showed prolonged QT with frequent premature ventricular contractions. ECGs also showed 'R-on-T' phenomenon leading to torsades and ventricular fibrillation. Atrial overdrive pacing was used to terminate the dangerous arrhythmia and the patient returned to sinus rhythm. Interestingly, he was found to have new onset thyrotoxicosis and started on methimazole.

Elevated corticosterone in the dorsal hindbrain increases plasma norepinephrine and neuropeptide Y, and recruits a vasopressin response to stress.

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.