Pulmonary Hantavirus Syndrome: Case Report and Brief Review

Charles J. VanHook, MD

Britt Warner, PA

Angela Taylor, MD

Longmont United Hospital

Longmont, Colorado

A 31-year-old white man presented to the emergency department complaining of fever, headache, mild confusion, and muscle aches. Approximately three days earlier he had developed non-quantified fever and diffuse muscle aches and pains. He was employed as a feedlot worker. He had visited an urgent care center one day earlier and had been advised to increase his oral fluid intake and to use non-steroidal anti-inflammatory agents as needed. Upon arrival to the emergency department he was found to have a temperature of 103.6º Fahrenheit, blood pressure of 125/72 mm Hg, respiratory rate of 40 breaths per minute, and room-air oxygen saturation of 84% by pulse oximetry. Auscultation of the chest disclosed diffuse rales. Heart sounds were rapid and regular. Abdominal exam was benign. There was no skin rash. Central nervous exam demonstrated agitation and confusion, but was otherwise non-focal. Laboratory examination revealed a white blood count of 11.7 K/uL, hemoglobin of 21.5 g/DL, hematocrit of 66.8%, platelet count of 73 K/uL, partial thromboplastin time of 36 seconds, lactic acid of 2.4 mm/L, and procalcitonin of 43 ng/mL. Chest radiograph disclosed extensive bilateral infiltrates (Figure 1).

Figure 1. Chest x-ray showing bilateral infiltrates

The patient precipitously declined, with severe respiratory distress, and was emergently intubated. Despite aggressive measures, including mechanical ventilation with an FIO2 of 1.0 and PEEP of 18 cm H2O, vigorous intravenous intravenous fluid resuscitation with normal saline, and pressor support with intravenous norepinephrine and vasopressin, the patient developed refractory hypoxemia. This was followed by a bradycardic arrest and death 2 hours after presentation. Serology sent at the time of admission later returned as IgM positive for hantavirus, with subsequent testing positive for Sin Nombre IgM.

Hantaviruses are RNA viruses of the family Bunyaviridae that are transmitted to humans by contact with the saliva, urine, or feces of infected rodents, which serve as persistently infected hosts (1). Patients who work in proximity to rodents, such as animal trappers, farmers, and forestry workers are at highest risk for infection. In the Western Hemisphere, there are approximately 200 cases per year of Hantavirus Pulmonary Syndrome (HPS), which was first identified in the Four Corners area of the Southwestern United States in 1993 (2). In the United States, HPS is most commonly caused by the Sin Nombre subfamily of hantavirus. A two-week incubation period precedes a 3-6 day prodromal period during which fever and myalgia are prominent features. The cardiopulmonary phase of HPS follows, with the development of acute non-cardiogenic pulmonary edema and multi-organ dysfunction. Typical laboratory abnormalities are leukocytosis and thrombocytopenia. Elevations in hematocrit and partial thromboplastin time are strong predictors of mortality, which approaches 40%. Definitive diagnosis depends on the serologic identification of IgM antibody to hantavirus using ELISA technology.  Immunochromatographic technology may allow for same day diagnosis (3). Treatment is supportive, and varies with the severity of disease. It may include volume resuscitation, ventilatory support, and renal replacement therapy. There is no established anti-viral therapy for Hantavirus infection, although ribavirin is often used in Asia. Corticosteroids have also been used sporadically with some success, but their use remains controversial (3).

Although Hantavirus remains a rare disease, prodromal symptoms in a patient with associated epidemiologic risk factors should heighten clinical suspicion.

References

1. Lednicky JA. Hantavirus: A short review. Arch Pathol Lab Med. 2003;127:30-35. [PubMed]
2. Duchin JS, Koster FT, Peters CJ, Simpson GL, Tempest B, Zaki S, Ksiazek TG, Rollin PE, Nichol S, Umland E, Moolenaar RL, Reef SE, Nolte KB, Gallaher MM, Butler JC, Breiman RF. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. N England J Med 1994;330:949-55 [CrossRef] [PubMed]
3. Bi Z, Formenty P, Roth C Hantavirus infection: A review and global update. J Infect Developing Countries. 2008;2(1):3-23. [CrossRef] [PubMed]

Cite as: VanHook CJ, Warner B, Taylor A. Pulmonary hantavirus syndrome: case report and brief review. Southwest J Pulm Crit Care. 2015;11(3):121-3. doi: http://dx.doi.org/10.13175/swjpcc122-15 PDF

September 2015 Pulmonary Case of the Month: Holy Smoke

Samir Sultan, DO

David M. Baratz, MD

Banner University Medical Center Phoenix

Phoenix, AZ

History of Present Illness

A 43-year-old woman presents to the office for second opinion of her dyspnea. She has very mild dyspnea with exertion which she notices when she cannot keep up with people going up stairs. She also has a "smoker’s cough".

Past Medical History, Family History, Social History

Her past medical history, family history and social history are unremarkable other than she smokes 1 ppd for the past 20 years and had a "collapsed lung" about 15 years ago.

Physical Examination

Her physical examination was unremarkable except for a small scar on her right chest.

Radiography 

A chest x-ray (Figure 1) was performed. 

 

Figure 1. PA (Panel A) and lateral (panel B) chest radiography.

Which of the following are true regarding the chest x-ray? (Click on the correct answer to proceed to the second of five panels)

1. The chest -ray shows a widened mediastinum
2. The chest x-ray is normal
3. The chest x-ray shows a diffuse reticulonodular infiltrate
4. The chest x-ray shows bilateral hilar adenopathy
5. The chest x-ray shows small bilateral pleural effusions

Cite as: Sultan S, Baratz DM. September 2015 puilmonary case of the month: holy smoke. Southwest J Pulm Crit Care. 2015;11(3):90-6. doi: http://dx.doi.org/10.13175/swjpcc112-15 PDF

August 2015 Pulmonary Case of the Month: Holy Sheep

Jennifer M. Hall, DO

David M. Baratz, MD

Banner University Medical Center Phoenix

Phoenix, AZ

History of Present Illness

A 42-year-old woman presented to the emergency department with chest pain and dyspnea. The onset of symptoms was acute, initially endorsing left-sided sharp chest pain which then progressed with dyspnea. Chest radiograph was read as normal. Laboratory evaluation was notable for an elevated D-Dimer which prompted a thoracic CT scan to be obtained.

Past Medical History, Family History, Social History

• She had well-controlled rheumatoid arthritis (on no medical therapy) and was diagnosed with emphysema by her PCP two years earlier.
• Her mother died from pulmonary embolism secondary to underlying lung cancer.
• She quit smoking 2 years ago with a total of 20-pack-years.

Physical Examination

Patient was in mild distress with heart rate of 105, respiratory rate of 22, but otherwise stable, SpO2 was 95% while breathing ambient air. She had diminished breath sounds in both bases, but otherwise her chest was clear to auscultation. The remainder of the exam was unremarkable.

Radiography 

A chest x-ray (Figure 1) and a thoracic CT scan (Figure 2) were performed.

Figure 1. Initial PA of the chest.

Figure 2. Thoracic CT scan in lung windows. Panels A-F: representative static images. Lower panel: video.

A chest tube was placed for the left-sided pneumothorax.

What is the next step in management? (Click on the correct answer to proceed to the second of five panels)

1. Bronchoscopy
2. Consider pleurodesis
3. Observation with repeat CT in 3 months
4. Open lung biopsy
5. 1 and 3
6. 2 and 4

Reference as: Hall JM, Baratz DM. August 2015 pulmonary case of the month: holy sheep. Southwest J Pulm Crit Care. 2015;11(2):53-8. doi: http://dx.doi.org/10.13175/swjpcc103-15 PDF

Reducing Readmissions after a COPD Exacerbation: A Brief Review

Richard A. Robbins, MD¹

Lewis J. Wesselius, MD²

¹The Phoenix Pulmonary and Critical Care Research and Education Foundation

Gilbert, AZ

²Mayo Clinic Arizona

Scottsdale, AZ

Abstract

CMS' Hospital Readmissions Reduction Program (HRRP) was extended to chronic obstructive pulmonary disease (COPD) exacerbations in October 2014. HRRP penalizes hospitals if admissions for COPD exacerbations exceed a higher than expected all-cause 30-day readmission rate. Recently, a review of 191,698 Medicare readmissions after a COPD exacerbation reported that COPD explained only 27.6% of all readmissions. Patients were more likely to be readmitted if they were discharged home without home care, dually enrolled in Medicare and Medicaid, and had more comorbidities (p<0.001 compared to patients not readmitted). Data on interventions is limited but recently a study of bundled interventions of smoking cessation counseling, screening for gastroesophageal reflux disease and depression or anxiety, standardized inhaler education, and a 48-h postdischarge telephone call did not result in a lower readmission rate. We conclude that there is limited evidence available on readmission risk factors, reasons for readmission and interventions that might reduce readmissions. In the absence of defined, validated interventions it seems likely that CMS's HRRP will be unsuccessful in reducing hospital readmissions after a COPD exacerbation.

Introduction 

To address rising costs and quality concerns, the Hospital Readmissions Reduction Program (HRRP) was enacted, targeting inpatient discharges in the Medicare fee-for-service population for congestive heart failure (CHF), acute myocardial infarction (AMI), and pneumonia in 2012. HRRP was extended to chronic obstructive pulmonary disease (COPD) exacerbations in October 2014.

Correlation of Readmissions with Outcomes

There were about 800,000 hospitalizations for COPD exacerbations annually, with about 20% of patients needing to be rehospitalized within 30 days of discharge (2,3). The cost of readmissions is about $325 million for the U.S. Centers for Medicare and Medicaid Services (CMS) (4). Therefore, it is hardly surprising that CMS is attempting to reduce COPD readmission to reduce costs. The implication is that care was incomplete or sloppy on the first admission, and that better care might reduce readmissions.

However, a number of concerns have been raised questioning the wisdom of the HRRP. Hospitals with better mortality rates for heart attacks, heart failure and pneumonia had significantly greater penalties for readmission rates (5). If this correlation is found to be true with randomized trials, then CMS is financially encouraging hospitals to perform an action with potential patient harm and suggest that CMS continues to rely on surrogate markers that have little or no correlation with patient-centered outcomes. Until this question is resolved, we cannot recommend programs that discourage hospital readmissions.

Differences between COPD Exacerbations and CHF, AMI and Pneumonia Methodology

Several aspects of COPD exacerbations differentiate it from other conditions included in HRRP. AMI, CHF, pneumonia and COPD exacerbations are all defined by discharge ICD-9 codes. Examination of ICD-9 coding against physician chart review found profound underestimation of COPD exacerbations, with sensitivities ranging from 12% to 25% and positive predictive values as low as 81.5% (6). In contrast, coding data to identify pneumonia and AMI have a sensitivity and positive predictive value of over 95% (7,8). Therefore, there is a high probability of misclassification of COPD exacerbations used to calculate the readmissions penalty.

COPD exacerbations are clinically defined while AMI and CHF are defined by biomarkers (plasma troponin, B-type natriuretic peptide) and pneumonia is defined by not only a compatible clinical situation but by consolidation on chest radiography. Because COPD symptoms overlap with many other diseases, biomarker and radiograph evidence can make accurate diagnosis difficult. Furthermore, this uncertainty in diagnosis may provide an opportunity for hospitals to game the system by excluding sicker patients who present with COPD from the readmission measure (9).

COPD may also require prolonged times for recovery as opposed to AMI, CHF, and pneumonia patients who seem to require shorter recovery times. One quarter of patients with a COPD exacerbation had not returned to preexacerbation peak expiratory flow rate by day 35 (10).

There is also a suggestion of a frequent exacerbation phenotype of COPD independent of disease severity (11). The single best predictor of exacerbations was a history of exacerbations, although a history of gastroesophageal reflux (GERD) was also associated with increased exacerbations. A hospital with higher numbers of patients with the frequent exacerbation phenotype or with GERD would be expected to have a higher readmission rate but would be penalized under CMS' HRRP.

Causes for Readmission after a COPD Exacerbation

Most patients readmitted after a COPD exacerbation are not readmitted for COPD. Shah et al. (9) recently examined nearly 200,000 COPD exacerbation hospital readmissions in the Medicare population. Only 27.6% were classified as being readmitted for COPD. There were a variety of readmission diagnosis with respiratory failure, pneumonia, CHF, asthma, septicemia, cardiac dysrhythmias, fluid and electrolyte disorders, intestinal infection, and non-specific chest pain and other accounting for the rest. This data is consistent with previous studies by Jencks et al. (12) who found 36.2% of exacerbation patients were readmitted for COPD. Not surprisingly, the sickest patients (as defined by the Charlson sum) are more likely to be readmitted (9). This would also be consistent with causes of readmission being diverse rather than limited to COPD.

Importantly, two observations were made which may have major implications for care after COPD exacerbations (9). First, patients dually enrolled in Medicare and Medicaid had higher readmission rates. These patients tend to be poorer and seek care at "safety net" hospitals. A penalty for readmissions would be largest at these hospitals which may most in need of financial help. Second, patients discharged home without home care were more likely to be readmitted. This will likely influence more discharges to either an extended care facility or with home care which may actually increase costs rather than result in the cost savings that CMS hopes to collect.

Interventions that Reduce COPD Readmissions

Jennings et al. (13) used a "bundle" for patients with COPD exacerbations in hopes of reducing readmissions and emergency department visits. The bundle consisted of smoking cessation counseling, screening for gastroesophageal reflux disease and depression or anxiety, standardized inhaler education, and a 48 hour postdischarge telephone call. It is easy to criticize these interventions. A single session of smoking cessation counseling is usually inadequate (14). Although gastroesophageal reflux disease has been associated with COPD, there is only a single trial with lansoprazole demonstrating a reduction in COPD exacerbations (15). To our knowledge there is no data on screening for depression or anxiety, standardized inhaler education and a single phone call in preventing COPD readmissions. Not surprisingly, the bundle did not work. However, it underscores that interventions to prevent COPD readmissions are unknown. Until these are defined, it seems unlikely that any program will be successful in reducing COPD readmissions.

Potential COPD Readmission Reduction Strategies

Discharge and Follow-Up

Discharge to an extended care facility or with home care reduces readmissions (9). Approximately one third of readmissions after hospitalization for COPD occur within 7 days of discharge and 60% occur within 15 days (9). Therefore, even close outpatient followup within 2 weeks of discharge from the hospital, may not prevent a majority of readmissions. However, we would recommend that close follow-up of patients be liberal which seems likely to have some impact on readmissions. Follow-up telephone calls may be reasonable but probably need to be more than a single call at 48 hours (13). We offer some additional suggestions below that have not been subjected to randomized trials, but seem reasonable based on the current state of knowledge.

Pharmacologic Therapy

1. Bronchodilators. Many of the therapies that treat COPD exacerbations have been tested to determine if chronic use might prevent exacerbations. The best evidence is for the long-acting bronchodilators. Two large randomized controlled trials have confirmed that a combination of a long-acting beta agonist (salmeterol) with an inhaled corticosteroid (fluticasone) or a long-acting anticholinergic (tiotropium) reduce exacerbations (16,17). Given that only about one-third of readmissions are due to COPD, the impact, if any, with addition of long-acting bronchodilators after a COPD exacerbation would likely be small. The newer long-acting beta agonists and anticholinergics would also be expected to reduce exacerbations and might prevent readmissions.
2. Inhaled corticosteroids. Addition of inhaled corticosteroids to long-acting bronchodilators in COPD remains controversial. A meta-analysis by Spencer et al. (18) recommended regular inhaled corticosteroid therapy as an adjunct in patients experiencing frequent exacerbations. However, the data supporting this recommendation is unclear. It is also unclear if their addition would prevent readmissions.
3. Antibiotics. Continuous or intermittent treatment with some antibiotics, particularly macrolides, reduces exacerbations. Treatment with azithromycin for one year lowered exacerbations by 27% (19). Although the mechanism(s) accounting for the reduction in exacerbations is unknown, current concepts suggest the reduction is likely secondary to the macrolides’ anti-inflammatory properties. However, concern has been raised about a very small, but significant, increase in QT prolongation and cardiovascular deaths with azithromycin (20). In addition, the recent trial with azithromycin raised the concern of hearing loss which occurred in 25% of patients treated with azithromycin compared to 20% of control (19). An alternative to the macrolides may be tetracyclines such as doxycycline, which also possess anti-inflammatory properties but do not lengthen QT intervals nor cause hearing loss (21). Similar to the long-acting bronchodilators, antibiotics might reduce readmissions, but since most readmissions are not due to COPD, the effect would likely be small.
4. Medication Compliance. Poor compliance with inhaled therapies has been implicated as a factor contributing to COPD exacerbations (22). The role of COPD medication noncompliance has not been specifically assessed in hospital readmissions, although it seems likely to be a contributing factor. Socioeconomic factors influence medication compliance and could lead to greater readmission rates in hospitals caring for patients with limited financial and social resources. Poor compliance with COPD medications as well as medications for comorbid conditions may both be important as most readmissions are not due to COPD.

Conclusions

Prevention of COPD readmissions after a COPD exacerbation represents a challenge with no straight-forward strategies to reduce readmissions other than discharge to an extended care facility or home with home health. Readmissions come from heterogeneous causes but most are not due to COPD suggesting that comprehensive care for disorders other than just COPD is likely important.

References

1. Centers for Medicare and Medicaid Services. Readmissions reduction program. Available at: http://www.cms.gov/Medicare/Medicare-Fee-for-Service-Payment/AcuteInpatientPPS/Readmissions-Reduction-Program.html (accessed 6/4/15).
2. Wier LM, Elixhauser A, Pfuntner A, Au DH. . Overview of hospitalizations among patients with COPD, 2008: Statistical Brief #106. Healthcare Cost and Utilization Project (HCUP) Statistical Briefs [Internet]. Rockville, MD: Agency for Health Care Policy and Research (US); 2006–2011 Feb. Available from: http://www.hcup-us.ahrq.gov/reports/statbriefs/sb106.pdf (accessed 5/4/15)
3. Elixhauser A, Au DH, Podulka J. . Readmissions for chronic obstructive pulmonary disease, 2008: Statistical Brief #121. Healthcare Cost and Utilization Project (HCUP) Statistical Briefs [Internet]. Rockville, MD: Agency for Health Care Policy and Research (US); 2006–2011 Sep. Available from: http://www.hcup-us.ahrq.gov/reports/statbriefs/sb121.pdf (accessed 6/4/15).
4. Medicare Payment Advisory Commission (MEDPAC). Report to the Congress: promoting greater efficiency in Medicare, 2007.
5. Robbins RA, Gerkin RD. Comparisons between Medicare mortality, morbidity, readmission and complications. Southwest J Pulm Crit Care. 2013;6(6):278-86.
6. Stein BD, Bautista A, Schumock GT, Lee TA, Charbeneau JT, Lauderdale DS, Naureckas ET, Meltzer DO, Krishnan JA. The validity of International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis codes for identifying patients hospitalized for COPD exacerbations. Chest. 2012;141(1):87-93. [CrossRef] [PubMed]
7. Skull SA, Andrews RM, Byrnes GB, et al. ICD-10 codes are a valid tool for identification of pneumonia in hospitalized patients aged ≥ 65 years. Epidemiol Infect. 2008;136(2):232-40. [CrossRef] [PubMed]
8. Kiyota Y, Schneeweiss S, Glynn RJ, Cannuscio CC, Avorn J, Solomon DH. Accuracy of Medicare claims-based diagnosis of acute myocardial infarction: estimating positive predictive value on the basis of review of hospital records. Am Heart J. 2004;148(1):99-104. [CrossRef] [PubMed]
9. Shah T, Churpek MM, Coca Perraillon M, Konetzka RT. Understanding why patients with COPD get readmitted: a large national study to delineate the medicare population for the readmissions penalty expansion. Chest. 2015;147(5):1219-26. [CrossRef] [PubMed]
10. Seemungal TA, Donaldson GC, Bhowmik A, Jeffries DJ, Wedzicha JA. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2000;161(5):1608-13. [CrossRef] [PubMed]
11. Hurst JR, Vestbo J, Anzueto A, Locantore N, Müllerova H, Tal-Singer R, Miller B, Lomas DA, Agusti A, Macnee W, Calverley P, Rennard S, Wouters EF, Wedzicha JA; Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) Investigators. Susceptibility to exacerbation in chronic obstructive pulmonary disease. N Engl J Med. 2010;363(12):1128-38. [CrossRef] [PubMed]
12. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418-28. [CrossRef] [PubMed]
13. Jennings JH, Thavarajah K, Mendez MP, Eichenhorn M, Kvale P, Yessayan L. Predischarge bundle for patients with acute exacerbations of COPD to reduce readmissions and ed visits: a randomized controlled trial. Chest. 2015;147(5):1227-34. [CrossRef] [PubMed]
14. Rigotti NA, Munafo MR, Stead LF. Smoking cessation interventions for hospitalized smokers: A systematic review. Arch Intern Med. 2008;168:1950-60. [CrossRef] [PubMed]
15. Sasaki T, Nakayama K, Yasuda H, Yoshida M, Asamura T, Ohrui T, Arai H, Araya J, Kuwano K, Yamaya M. A randomized, single-blind study of lansoprazole for the prevention of exacerbations of chronic obstructive pulmonary disease in older patients. J Am Geriatr Soc. 2009;57(8):1453-7. [CrossRef] [PubMed]
16. Calverley PM, Anderson JA, Celli B, Ferguson GT, Jenkins C, Jones PW, Yates JC, Vestbo J; TORCH investigators. Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease. N Engl J Med. 2007;356:775-89. [CrossRef] [PubMed]
17. Tashkin DP, Celli B, Senn S, Ferguson GT, Jenkins C, Jones PW, Yates JC, Vestbo J; TORCH investigators. A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Engl J Med. 2008;359:1543-54. [CrossRef] [PubMed]
18. Spencer S, Karner C, Cates CJ, Evans DJ. Inhaled corticosteroids versus long-acting beta(2)-agonists for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2011 Dec 7;(12):CD007033. [PubMed]
19. Albert RK, Connett J, Bailey WC, Casaburi R, Cooper JA Jr, Criner GJ, Curtis JL, Dransfield MT, Han MK, Lazarus SC, Make B, Marchetti N, Martinez FJ, Madinger NE, McEvoy C, Niewoehner DE, Porsasz J, Price CS, Reilly J, Scanlon PD, Sciurba FC, Scharf SM, Washko GR, Woodruff PG, Anthonisen NR; COPD Clinical Research Network. COPD Clinical Research Network. Azithromycin for prevention of exacerbations of COPD. N Engl J Med. 2011; 365:689-98. [CrossRef] [PubMed]
20. Ray WA, Murray KT, Hall K, Arbogast PG, Stein CM. Azithromycin and the risk of cardiovascular death. N Engl J Med. 2012;366:1881-90. [CrossRef] [PubMed]
21. Rempe S, Hayden JM, Robbins RA, Hoyt JC. Tetracyclines and pulmonary inflammation. Endocr Metab Immune Disord Drug Targets. 2007;7:232-6. [CrossRef] [PubMed]
22. Ismaila A, Corriveau D, Vaillancort J, Parsons D, Dalal A, Su Z, Sampalis JS. Impact of adherence to treatment with tiotropium and fluticasone propionate/salmeterol in chronic obstructive pulmonary disease patients. Curr Med Res Opin. 30(7);1427-36, 2014. [CrossRef] [PubMed] 

Reference as: Robbins RA, Wesselius LJ. Reducing readmissions after a COPD exacerbation: a brief review. Southwest J Pulm Crit Care. 2015;11(1):19-24. doi: http://dx.doi.org/10.13175/swjpcc089-15 PDF

July 2015 Pulmonary Case of the Month: A Crazy Case

Lewis J. Wesselius, MD

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 23-year-old woman presented in 2008 at outside institution with dyspnea and diffuse pulmonary infiltrates. She required intubation. After a surgical lung biopsy, she was transferred to the Mayo Clinic Hospital for further care.

Past Medical History

She has had a history of progressive dyspnea for several months, otherwise negative 

Physical Examination

Vital signs are stable. SpO2 94% on FiO2 of 0.4. She is intubated and there is a chest tube in her right chest. Otherwise the physical examination is unremarkable.

Radiography

A thoracic CT scan was performed (Figure 1).

Figure 1. Representative images from the thoracic CT in lung windows.

Which of the following are present on the thoracic CT scan? (click on the correct answer to proceed to the second of five panels)

1. Diffuse ground-glass opacities
2. Interlobular septal thickening and intralobular reticular thickening
3. Right-sided pneumothorax
4. 1 and 3
5. All of the above

Reference as: Wesselius LJ. July 2015 pulmonary case of the month: a crazy case. Southwest J Pulm Crit Care. 2015;11(1):3-10. doi: http://dx.doi.org/10.13175/swjpcc079-15 PDF