Sex: F
Vaccine: FLU3
Symptoms: Pyrexia, Rheumatoid factor
Clinical narrative: Pt received flu vax on 11/29/99. The pt was receiving weekly methotrexate to treat rheumatoid arthritis at the time of immunization. She became ill on 12/3/99. On 12/7/99, she was seen by her physician and hospitalized in the ICU. She required mechanical ventilator on 12/12/99. The pt died on 1/6/00. The treating physicians reportedly attributed this event to the methotrexate therapy. The husband attributed this event to an interaction between the flu vax and methotrexate. On Follow-up pt had a history of Parkinsonism. Medical records were recieved on 7/12/00. The pt had increasing shortness of breath and fatigue for months prior to hospitalization. On 12/7/99, she was hospitalized because of fatigue, shortness of breath, nausea, and possible low-grade fever. Medical history included allergies to metoclopramide, ibuprofen, and salsalate. During hospitalization, her rheumatoid factor was positive; ANA titer was negative, ESR was 106mm/hr. Chest x-ray revealed "severe bilateral parenchymal disease since December 12, 1999." Follow up info was received from a medical center on 8/17/00, 9/28, and 10/25/00.The pt is a non-smoker and abstains from alcohohl. She has a past hisotry of bilateral silicone breast implant with subsequent removal, partial vaginal hysterectomy, tubal ligation. She also had problems with occasional choking and gasping while eating and drinking, though no recent episodes of aspiration were reported. the pt's medical history includes a recent treatment with Mirapex and requip, which were discontinued due to "intolerance." Therapy with Methotrexate 15mg weekly for rheumatoid arthritis began in 1997 and ceased after 12/5/99. The pt received her 1999-2000 formula influenza virus vaccine on 11/29/99, approximately 14 hrs afte her methotrexate dose. A chest x-ray revealed bialteral infiltrates with the greatest concentration int he left perihilar and righ tupper lobe region. The differential diagnosis at this time included congestive heart failure, aspiration, connective tissue disease, drug reaction, atypical community acquired pneumonia, and other atypical infections. Immunosuppresive therapy, including methotrexate, was withdrawn. A bronchoscopy examination on 12/10/99 was unremarkable; however, microscopic analysis of pooled bronchoalveolar levage revealed acute and chronic inflammation with rare atypical squamous and bronchial epithelial cells. Bronchial lavage cultures were negative. The pt was inturbated and ventilated on 12/12/99. A chest x-ray on 12/13/99, revealed progressive RUL infiltrate with no improvement in severe bilateral lparenchymal disease compared to 12/12/99. The pt was also treated with piperacillin/tazobactam and imipenem/cilastatin. Additional therapy included furosemide, propofol and lorazempam. Physical examination on 12/13/99 revealed lungs iwth bialteral rhonchi and rales. A chest x-ray on 12/15/99 revealed significant improvement since 12/14. Lab test results in December 1999 included: rheumatoid factor, positive; ANA negaitve; and ESR 106. Based on these lab results and the fact that the pt remained afebrile, the neurologist suggested htat an autoimmune process should be considered. ON 12/10/99, C-ANCA and P-ANCA were both negtive. The pt's WBC count rose steadily from 14,400 cells/mm^3 on 12/10/99 to 40,700 cells/mm^3 on 1/6/00. Amantadine was discontinued due to the pt's fatigue. Findings during a lung biopsy on 12/21/99 were a severely diffuse process with ver friable weak lung prenchyma incapable of holding either stapling devices and/or sutures. The lung was extremely abnormal and did not appear to be ventilating or aerating well. Microscopic analysis revealed rapidly progressive diffuse alveolar damage considdtent with acute interstitial pneumonitis of unknown etiology. The abnormalities were temporally uniform and reflected an episode of massive acute lung injury occurring at a single point in time. The pt continued to have a persisitent broncho-alveolar fistula following thoracic surgery. Cultures of lung tissue were negative for bacteria, virus and fungi. Blood cultures on 12/20/99 were positive for coagulase-negative Staphylococci and sputum cultures were positive for presumptive Candida albicans. A sputum culture on 1/4/00 was positive for P. seruginosa. A PPD performed during the hospital stay was negative. On 12/23/99, a chest x-ray revealed a small apical pneumothorax and development of what appeared tobe pneumopericardium and neumomediastinum since 12/22/99, with persistent bilateral pulmonary densities consistent with severe pulmonary edema. The impression was that ARDS was a consideration. Corticosteroid therapy with subsequently initiated. The consumer reported that the pt had lost "50% of her then reduced lung capacity" and she required an increase in her oxygen from "60% to 100% and requiring paralyzing drugs." A chest x-ray on 1/6/00 revealed a reduced right apical pneumothorax with dense infiltrates bilaterally. There appeared to be increase in air within the right basilar pleural space compared to prior film. Subcutaneous emphysema is increased in the right axillary region. She died on 1/6/00, from respiratory failure secondary to acute interstitial penumonitis. The consumer reported that the event was a result of a compromised immune system, which the consumer felt was exacerbated by the influenza virus vaccine. The pulmonologist confirmed the pneumonitis, but due to its uncertain etiology, could not confirm that the pt had pneumonia. Further medical records recieved on 9/28/00, provided additional medical history of bone mass decreased (osteopenia), gastro-oesophageal reflux disease; los of balance resulting in falls, and headaches NOS. Medications included /Relafen, Sinemet. On 12/7/99, the pt's flu-like illness included scratchy, then sore throat, cough and chills. Hematology results on 12/7/99,included WBC and absolute neutrophil count which rose from 7.3 x 10^3 and 6.12 x 10^3 respectively, to 12.4 x 10^3 and 10.68 x 10^3 on 12/9/99. Seurm osmolarity was 253 and potassium was 2.4 on 12/7/99. Lab test results on 12/8/99 were creatinine 0.4; sodium 125; and chloride 94. Blood, pleural fluid, and urine cultures were negative. A chet x-ray on 12/7/99, revealed a dense upper lobe consolidation (lung infiltration NOS) with focal areas at the right base and mid-lung. A chest x-ray on 12/9/99 revealed worsening bialteral air-space consistent with pneumonia, pulmonary hemorrhage, or atypical pulmonary edema. A CT scan of the chest showed a predominatly alveolar process with marked areas of consolitation involving the lungs bilaterally; a moderately large right-sided pleural effusion; right lobe volume loss; and atherosclerotic aortic disease. An abdominal x-ray on 12/8/99 was suggestive of ileus. Her diagnosis at this time was RUL infiltrate and pleural effision, thought to be secondary to aspiration. She also had ileus and hyponatremia secondary to SIADH, both considered secondary to the pulmonary proces. The pt also had increased lower extremity weakness. (Reference methotrexate case number HQ7226113JUN2000).