1 / 47

A stem cell transplant patient with cough and SOB.

A stem cell transplant patient with cough and SOB. ID Case Conference Wednesday September 26 th , 2007 David Fitzgerald, MD. History of Present Illness.

fabian
Download Presentation

A stem cell transplant patient with cough and SOB.

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. A stem cell transplant patient with cough and SOB. ID Case Conference Wednesday September 26th, 2007 David Fitzgerald, MD

  2. History of Present Illness • 23 year old white male with h/o Hodgkin's disease s/p allogenic matched sibling stem cell transplant 4/16/2007 complicated by cutaneous GVHD who is now admitted for acute SOB and hypoxia. • He was at his baseline state until a few days PTA when he developed a non-productive cough and rhinitis. He became progressivly more SOB and was having increasing difficulty with ADLs due to DOE, • Was referred by oncology for PFT evaluation on 9/3/07 – this demonstrated markedly reduced FEV1, FVC and DLCO with a pulse oximetry reading in the mid 80s on RA. • Patient was admitted to BM transplant unit for further evaluation.

  3. HPI • Cough is non-productive with no hemoptysis. • Increasing fatigue over last 2 weeks. • He denies any fever, chills, NS, chest pain, leg swelling. • No unusual activity or exposure • Sick contacts – father with a “cold” several weeks prior. No TB contacts.

  4. PMH • Hodgkin's disease - diagnosed in 2000 treated with combined chemotherapy and XRT with prolonged remission relapse in 2004. • Relapsed and treated with salvage gemcitabine and vinorelbine and then autologous SCT. • Relapse again in 10/06 with mediastinal and neck disease treated with etoposide and Ara-C + steroids. • Allogenic matched sibling SCT in 4/07 – campath conditioning and fludarabine, busulfan • History of glucose intolerance/diabetes mellitus due to steroids • Skin GVHD • History of Klebsiella pneumoniae bacteremia/sepsis

  5. Social History No tobacco, no EtOH, no drugs. Lives with father. No recent travel. No pets. Not sexually active Family History Mother died of an accident. Father and sister are well.

  6. Meds • Voriconazole 200 mg po BID • Septra DS once daily • Cellcept 1000 mg bid • Prednisone 50 mg qd • Prograf 1 mg BID • Synthroid 100 mcg qd

  7. Tm 36.5 P 117 BP 108/81 R 18 Sat 100% ON 40 FiO2 Chronically ill appearing with mild respiratory distress HEENT – Perrla, eomi, anicteric, OP without exudate or lesions Neck supple No LAN CV – tachy, but reg with no murmur Lungs bibasilar crackles R>L Abd – soft, NT, ND, no HSM Skin – diffuse scaly eruption on forearms c/w GVHD Neuro – A+O x 3, grossly non-focal Physical

  8. WBC 5.1 ANC 4.9 Hgb 9.7 Plt 33 Basic panel WNL Bun/Cr 30/1.3 T bili 0.6 AST 74 ALT 108 Alk phos 342 GGT 1716 LDH 3117 Alb 2.9 BCx pending Ucx pending Data

  9. Imaging

  10. Imaging

  11. CT read • Numerous nodular groundglass opacities scattered throughout all segments of the lungs. There are scattered foci of confluent ground glass consolidation. There are no pleural effusions.

  12. Further testing • Urine histo ag negative • Serum crypto negative • Aspergillus Ag negative • Serum PCR • CMV <500 copies (repeat negative) • EBV neg • Adeno neg • HHV6 neg • Parvo neg

  13. Bronch • Quant cx - < 10,000 organism • PCP DFA neg • Bacterial Culture neg • AFB cx negative • Fungal cx negative • PCR on BAL • HSV ½ neg • CMV neg

  14. Diagnosis • BAL viral culture positive for • Parainfluenza virus type 3 • Transbronchial biopsy results suggestive of DAD with type II pneumocyte, hyperplasia, fibrin, hemorrhage, sparse acute inflammation and focal edema.- Bronchial wall shows essentially no inflammation, making graft versus host disease unlikely.- No fungal or AFB organisms seen by fungus or AFB stains.

  15. Diagnosis • Parainfluenza virus type 2 pneumonia

  16. Parainfluenza virus • RNA virus • Family of Paramyxoviridae • 5 types – 1, 2, 3, 4a, 4b • Initially described 1950s as cause of croup layrngotracheobronchitis in children

  17. Parainfluenza virus • Virus has a tropism for the respiratory tract, replicating only in cells of the respiratory epithelial layer • Causes acute respiratory tract infections • Repeated infections occur thoughout life • Reinfection usually involves only the upper respiratory tract in immunocompetent adults • LRI more common with type 3 infection • Immunity wanes quickly

  18. Parainfluenza virus • Types • 1 and 2 cause seasonal fall epidemics that often will alternate years • 3 is endemic but has an April May spring peak • Most common isolate in children • More common to cause pneumonia • Types 4a and 4 b are rare

  19. Clinical manifestations • Children – PIV causes 60% of croup cases • barking cough , hoarseness and stridor • Adults – causes 15% of URIs • Immunocompromised adults – common cause of URIs and also LRIs

  20. Diagnosis • Cell culture – grows in cell culture • PCR also available

  21. Parainfluenza in immunocompromised hosts • Significant cause of morbidity and mortality among HSCT recipients • Limited data available on its presentation and treatment

  22. Clinical Trial Data • Large study from Fred Hutchinson Cancer center • Evaluated data on 3577 HSCT recipients 1990-1999 • All pts with URI sxs received Nasopharyngeal swab • Also cxs done on all bronch specimens, lung bxps and autopsy • Ribavirin was used at discretion of treating physician but was a standardized dose and course • Nichols W, et al. Parainfluenza virus infections after hematopoietic stem cell transplantation: rick factors, response to antiviral therapy and effect on transplant outcome. Blood 2001;98:573-78.

  23. Epidemiology in SCT pts • PIV was isolated from 7.1% of the 3577 patients • PIV3 was most common form (90%) • Occurred year round but in clusters

  24. Results • Clinical presentation • 81% of PIV 3 infections were URI, 7% with pneumonia and 6% both • No real difference in clinical characteristics of the patients who did and did not develop PIV 3

  25. Results • Risk factors for progression to LRI • Receipt of corticosteroids was the only dependent risk factor

  26. Corticosteroid use and progression to LRI • Association present for both autologous and allogenic transplants • Dose dependent

  27. Copathogens • 53% of pts with PIV3 LRI had copathogens • Aspergillus fumigatus was most common copathogen - 24% • Similar to association of Staph aureus with influenza • PIV3 infection may damage the epithelium and allow other organisms to penetrate or may exert an immunosuppressive effect

  28. Mortality • Overall mortality in PIV3 LRI was 35% at 30 days and 75% at 180 days after dx of pneumonia • The majority died with persistent radiographic or clinical evidence of pneumonia

  29. Mortality • Risk factors for mortality • Presence of co-pathogens on BAL at time of PIV3 diagnosis was associated with increased mortality • 48% vs 19% at 30 days • 96% vs 50 % at 180 days • Need for mechanical ventilation also mortality risk

  30. Treatment • Aerosolized ribavirin +/- IVIG were used in 33 of 55 patients with PIV3 pneumonia • Characteristics of the two groups were similar but treated group had more intubated patients and more pts requiring O2

  31. Treatment and Viral Shedding • No difference in duration of viral shedding • 35% of treated pts continued to shed at 3 weeks compared to 33% of untreated patients • Only 35% of treated patients shed for < 10 days compared to 50% of untreated patients

  32. Treatment and Mortality • No difference in 30 day mortality between the treated and untreated groups • Even after stratification by presense of copathogen

  33. Conclusions • PIV infections were relatively common after SCT • Associated with increased mortality • Overall 24.1% of patients with PIV3 infection developed pneumonia • Development of LRI was driven by administration of steroids for GVHD • Copathogens were commonly isolated from Pts with PIV pneumonia • Copathogens were associated with increased mortality

  34. No real benefit seen with ribavirin and IVIG although not a randomized trial

  35. Further course • Initially covered with broad spectrum antibiotics including imipenim, vanco, voriconazole, bactrim, doxy. • Received increasing doses of steroids due to concern that may be GVHD • When cx + for PIV pt begun on oral ribavirin and IVIG • Had a worsened course and received several days of pulse dose steroids 850 mg bid with some improvement • Steroids weaned to 125 mg BID • Rebronch 12 days later still with viral cx + for PIV3. No other copathogens identified • Remains on broad spectrum abx with relatively stable O2 requirement at 4 L • Could not obtain aerosolized ribavirin since not used at UNC for 5 years • Difficult to use as it is teratogenic and mutagenic and aerosol gets everywhere

  36. Search PubMed • Parainfluenza Virus Type 2 • Case Reports • Reviews • Differential Diagnosis • Drug Therapy

More Related