Search Journal-type in search term and press enter
In Memoriam
Social Media-Follow Southwest Journal of Pulmonary and Critical Care on Facebook and Twitter

Pulmonary

Last 50 Pulmonary Postings

(Click on title to be directed to posting, most recent listed first, CME offerings in Bold)

September 2019 Pulmonary Case of the Month: An HIV Patient with a
   Fever
Adherence to Prescribed Medication and Its Association with Quality of Life
Among COPD Patients Treated at a Tertiary Care Hospital in Puducherry
    – A Cross Sectional Study
June 2019 Pulmonary Case of the Month: Try, Try Again
Update and Arizona Thoracic Society Position Statement on Stem Cell 
   Therapy for Lung Disease
March 2019 Pulmonary Case of the Month: A 59-Year-Old Woman
   with Fatigue
Co-Infection with Nocardia and Mycobacterium Avium Complex (MAC) 
   in a Patient with Acquired Immunodeficiency Syndrome 
Progressive Massive Fibrosis in Workers Outside the Coal Industry: A Case 
   Series from New Mexico
December 2018 Pulmonary Case of the Month: A Young Man with
   Multiple Lung Masses
Antibiotics as Anti-inflammatories in Pulmonary Diseases
September 2018 Pulmonary Case of the Month: Lung Cysts
Infected Chylothorax: A Case Report and Review
August 2018 Pulmonary Case of the Month
July 2018 Pulmonary Case of the Month
Phrenic Nerve Injury Post Catheter Ablation for Atrial Fibrillation
Evaluating a Scoring System for Predicting Thirty-Day Hospital 
   Readmissions for Chronic Obstructive Pulmonary Disease Exacerbation
Intralobar Bronchopulmonary Sequestration: A Case and Brief Review
Sharpening Occam’s Razor – A Diagnostic Dilemma
June 2018 Pulmonary Case of the Month
May 2018 Pulmonary Case of the Month
Tobacco Company Campaign Contributions and Congressional Support of
   Tobacco Legislation
Social Media: A Novel Engagement Tool for Miners in Rural New Mexico
April 2018 Pulmonary Case of the Month
First-Line Therapy for Non-Small Cell Lung Cancer Including Targeted
   Therapy: A Brief Review
March 2018 Pulmonary Case of the Month
February 2018 Pulmonary Case of the Month
January 2018 Pulmonary Case of the Month
Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia in a Patient
   with Multiple Pulmonary Nodules: Case Report and Literature Review
Necrotizing Pneumonia: Diagnosis and Treatment Options
December 2017 Pulmonary Case of the Month
First Report of Splenic Abscesses Due to Coccidioidomycosis
November 2017 Pulmonary Case of the Month
Treatment of Lymphoma and Cardiac Monitoring during Pregnancy
October 2017 Pulmonary Case of the Month
September 2017 Pulmonary Case of the Month
August 2017 Pulmonary Case of the Month
Tip of the Iceberg: 18F-FDG PET/CT Diagnoses Extensively Disseminated 
   Coccidioidomycosis with Cutaneous Lesions
July 2017 Pulmonary Case of the Month
Correlation between the Severity of Chronic Inflammatory Respiratory
   Disorders and the Frequency of Venous Thromboembolism: Meta-Analysis
June 2017 Pulmonary Case of the Month
May 2017 Pulmonary Case of the Month
April 2017 Pulmonary Case of the Month
March 2017 Pulmonary Case of the Month
February 2017 Pulmonary Case of the Month
January 2017 Pulmonary Case of the Month
December 2016 Pulmonary Case of the Month
Inhaler Device Preferences in Older Adults with Chronic Lung Disease
November 2016 Pulmonary Case of the Month
Tobacco Company Campaign Contributions and Congressional Support
   of the Cigar Bill
October 2016 Pulmonary Case of the Month
September 2016 Pulmonary Case of the Month
August 2016 Pulmonary Case of the Month

 

For complete pulmonary listings click here.

The Southwest Journal of Pulmonary and Critical Care publishes articles broadly related to pulmonary medicine including thoracic surgery, transplantation, airways disease, pediatric pulmonology, anesthesiolgy, pharmacology, nursing  and more. Manuscripts may be either basic or clinical original investigations or review articles. Potential authors of review articles are encouraged to contact the editors before submission, however, unsolicited review articles will be considered.

-------------------------------------------------------------------------------------  

Saturday
Aug252018

Infected Chylothorax: A Case Report and Review

Louis Eubank1, Luke Gabe1, Monica Kraft1, and Dean Billheimer2

1Departments of Medicine and Biostatistics, College of Medicine

2Department of Biostatistics, College of Public Health

University of Arizona Health Sciences Center

Tucson, AZ USA

 

Abstract

Infected chylothorax is a rare complication of a rare pathology with limited literature entirely consisting of case reports, meeting abstracts, and letters to the editor. The case of a 56-year-old male with a spontaneous infected chylothorax successfully treated and discharged to home without any residual effects is described. A systematic review of the literature revealed 11 prior cases of infected chylothoraces. Their etiologies (when known), initial pleural fluid values, and treatment are described. These cases show that while infected chylothorax has a varied presentation and affects a broad range of patients, conservative management including antibiotics, pleural fluid drainage, and symptomatic relief is a safe and appropriate starting point.

Introduction

Chylothorax, a pleural effusion caused by chyle accumulation from obstruction or disruption of the thoracic duct (please see SWJPCC’s Image of the week: chylothorax for an image of non-infected chyle fluid), is a rare condition that may arise from a diversity of etiologies broadly categorized as traumatic or non-traumatic/spontaneous (1). Traumatic causes commonly include iatrogenic injury and chest trauma, although insults as minor as sneezing, light exercise and emesis have been reported (1-3). Non-traumatic chylothorax has been linked to several immunologic and infectious etiologies (1). Regardless of the underlying mechanism, chyle has classically been considered inherently bacteriostatic (1). We present a case of spontaneous infected chylothorax and the first review of infected chylothoraces reported in the literature.

Case Report

A 56-year-old man with alcoholic cirrhosis and remote right-sided hepatic hydrothorax presented to the emergency department complaining of shortness of breath. Patient reported slowly worsening dyspnea over the last six weeks without any other symptoms that had acutely worsened on morning of presentation

Initial vital signs were temperature 38.0°C, heart rate 115, blood pressure 81/60mmHg, and respiratory rate 30 breaths/min on 4L O2 by nasal cannula; labs significant for white blood cell count of 3100/mm3 and lactate 5.0 mmol/L (normal <2.0 mmol/L).  Physical exam demonstrated a fatigued patient with accessory muscle use on inspiration and absent breath sounds at the left lung base. Computed tomography (CT) study of the chest showed a large free-flowing left-sided pleural effusion (Figure 1A&B) as well as subacute rib fractures (Image 1C).

Figure 1. Thoracic CT on the day of presentation. Panel A: Axial view showing pleural effusion. Panel B: Sagittal view showing pleural effusion. Panel C: Coronal view showing rib fractures (white arrows).

Chart review demonstrated an emergency department visit five months previously for a fall with acute left-sided rib fractures and minimal left-sided pleural effusion.

Thoracentesis removed two liters free-flowing, brown, milky, purulent fluid; analysis significant for 58,880 total nucleated cells (32,800 RBCs), 94% neutrophils, glucose <5, LDH 573 IU/dL (serum 193 IU/dL), triglycerides 191 mg/dL, albumin 1.8 g/dL (serum albumin 2.6 g/dL, laboratory lower limit of normal 3.4 g/dL).

The patient remained hypotensive despite fluid boluses, tachypneic with increasing oxygen requirements, and a repeat lactate was 6.4 mmol/L. Norepinephrine and broad-spectrum antibiotics were started and patient was admitted to the intensive care unit.

Pleural fluid and blood cultures grew Escherichia coli resistant to fluoroquinolones. Chest x-ray showed persistent pleural effusion; a chest tube was placed which drained an additional 1.6 L over the following 24 hrs. The patient subsequently improved: serum lactate normalized within 24 hours, vasopressors were weaned within 36 hours, and supplemental oxygen was discontinued within 72 hours.

Chest tube output decreased to less than 200 ml/day within 48 hours of placement; however, repeat thoracic CT demonstrated a persistent multi-loculated left pleural effusion. Surgical evacuation and pleurodesis were considered given the lack of literature regarding intrapleural lytic therapy in infected chylothorax (a single case report described use of streptokinase in a persistent non-infected chylothorax, 1).  However, the patient’s operative risk was considered prohibitively high. He was managed conservatively with a fat-free diet to reduce chyle leak.

Eleven days after initial presentation fluid studies were significant for triglyceride 45mg/dL with negative cultures. Given that a pleural fluid triglyceride level <50mg/dL yields a less than 5% likelihood of being chylous and the clinical stability of the patient, the chylothorax was felt to be resolved (1). The patient was discharged to home twelve days after initial presentation.

The etiology of patient’s infected chylothorax was never fully elucidated. The most likely explanation is the trauma causing rib fractures also caused a traumatic chylothorax that later became infected. The thoracic duct lies alongside the vertebrae until it drains into the left brachiocephalic vein (Figure 2).

Figure 2. Thoracic duct anatomy (black arrows).

A blow to the posterior left thorax sufficient to fracture multiple ribs is more than sufficient to damage the nearby thoracic duct (1-4).  Arguing against this is most patients with large traumatic chylothoraces present within 10 days of injury (1,2).

Another explanation is the patient developed bacterial empyema secondary to hepatic hydrothorax (ascites that has passed through diaphragm from the peritoneal cavity) followed by non-traumatic chylothorax. These empyemas can demonstrate an indolent course and Escherichia coli is one of the most common causative pathogens isolated (1). Arguing against this is the patient’s previous hepatic hydrothorax was right-sided.

Finally, the chylothorax may have arisen from one of the many known causative medical pathologies (2). Chylous ascites secondary to cirrhosis that migrates into the pleural space via diaphragmatic leaks defects is a known phenomenon, albeit extremely rare (2).

In follow-up two months after discharge the patient had total resolution of respiratory symptoms and no recurrence of the effusion.

Systematic Review

Methods

A MEDLINE search (PubMed) from January 1975 to January 2018 and a Google Scholar search (all years) was conducted to identify eligible studies using the following terms: “Infected Chylothorax” (all fields) OR “Infection AND Chylothorax” (all fields) OR “Chylothorax AND Empyema” (all fields) OR “Chylous Empyema” (all fields). The inclusion criteria for studies were patients with infected non-traumatic chylothorax. A triglyceride level > 110 mg/dL or the presence of chylomicrons in pleural fluid was used to confirm the diagnosis of chylothorax; pleural fluid culture speciation was used to confirm the infection. The exclusion criteria were a lack of laboratory data and duplicate data. Two reviewers (LE, LG) independently reviewed the titles, abstracts, and, when necessary, the full text regarding the inclusion/exclusion criteria. Data extraction was performed independently by two reviewers (LE, LG) using data extraction forms defined beforehand. Discrepancies were resolved by consensus discussion with a third reviewer (MK).

Results

Eight case reports, two published abstracts, and one letter to the editor met the inclusion criteria; all eleven were included in the analysis (Figure 3, 13-23). 

Figure 3. Flow diagram of the literature review.

The general characteristics, demographics, and etiology of infected chylothorax are summarized in Table 1, the initial pleural fluid values are reported in Table 2.

Table 1. Population data.

Table 2. Initial pleural fluid values.

There were 11 patients total: six males and five females; age range 5 days-78 years, mean age 40.5 years (standard deviation 28.5 years). One patient was pharmacologically immunosuppressed while others had chronic diseases known to reduce immune system function including diabetes, excessive alcohol intake, and obesity (24-26). Four (36%) were iatrogenic. Three patients (27%) were infected with Streptococcus viridans and five (45%) were infected with Streptococcus genus. In those with available data, three of ten patients (30%) required intravenous vasopressors. No patients required ventilator management for their chylothorax (two patients were already intubated, one for acute respiratory distress syndrome, the other for unstable hemodynamics secondary to large subarachnoid hemorrhage). Two patients (18%) were managed surgically – one was specifically noted to have failed conservative management (17). Of the known outcomes, eight of nine (89%) survived to discharge and all eight remained asymptomatic at follow-up. The mean follow-up duration was 13.3 months (range 6-24 months).

Discussion

Given the paucity of published experience regarding infected chylothoraces, we believe a descriptive summary is warranted. First, there is a large variation in patient characteristics, including age range, immune competence, comorbid medical conditions, and infectious organism (eight different bacterial species and one parasite).

Second, many of the reviewed cases had a more benign presentation than might be anticipated in the context of a large, infected intrathoracic fluid collection.  Seven of the patients (73%) were hemodynamically stable on presentation and the majority of these patients had very mild chief complaints.

Third, the available data suggest a surprisingly good prognosis considering a previously estimated morality of 10-25% in non-infected chylothoraces, depending on etiology (27). The one patient who did not survive to discharge died due to brain herniation. Those with documented outpatient follow-up were asymptomatic up to 16 months post-discharge. 

Fourth, conservative management was frequently efficacious. Eight patients (73%) were medically managed without complication and did not require extensive antibiotic duration, intrapleural lytic therapy, or surgical intervention. The decision to pursue surgical intervention is not well defined given the very limited number of cases requiring surgical management. A brief discussion of non-infected chylothoraces and their management is therefore warranted.

Non-infected chylothorax is universally described as a rare event, although its exact incidence has not been described. Chylous ascites, which sometimes shares pathogenesis with chylothorax and is one of the causes of spontaneous chylothorax, has an occurrence of one in 20,000 hospital admissions (12). Trauma accounts for approximately 50% of chylothoraces, with esophagectomy being the most common iatrogenic cause (28). Thirty percent are due to malignancy; lymphoma accounts for 70-75% of malignant cases (11). While there are no consensus guidelines on how to treat chylothoraces, many authors agree that first line treatment is conservative management with thoracentesis or chest tube drainage, fat free or medium chain triglyceride diet, and consideration of somatostatin or octreotide (1,5,11,27-29). Although somatostatin or octreotide are used at many institutions, data regarding indications & efficacy of these medications are limited and/or inconsistent – some institutions use these medications at the beginning of treatment, others only if/when initial management has failed (5,27).

Additional treatments may depend on the etiology of the chylothorax: it is suggested that earlier surgical intervention in iatrogenic traumatic chylothoraces, especially post-esophagectomy, may be beneficial (30). Conservative management is likely to fail and surgical intervention is recommended in the following situations: 1) daily drainage greater than 1000 mL chyle (adults) or greater than 100mL chyle/kg body weight (children); 2) chyle leak that persists for more than 14 days; 3) unchanged chest tube output for 7-14 days; 4) clinical deterioration (27,28).

Conservative management for infected chylothoraces appears efficacious in our small sample size with the obvious modification of treating the infection. Most antibiotics adequately penetrate the pleural space, although aminoglycosides should be avoided as they appear to be inactivated by the low pH and relative anaerobic conditions (31).

Limitations

The limitation of this systematic review was the inclusion of only case reports, abstracts, and letters to the editor and the small sample size. Unfortunately, given the rarity of infected chylothoraces, studies with sufficient sample size are unlikely to be available.

Conclusion

Infected chylothorax is a rare complication of an already rare pathology. Our case report and literature review show that it can affect any age group, can be caused by several different organisms, and has a variable presentation. Our data suggests that an initial conservative management strategy in infected chylothoraces can be a safe and effective option.

References

  1. McGrath E, Blades Z, Anderson P. Chylothorax: aetiology, diagnosis and therapeutic options. Respir Med. 2010;104:1-8. [CrossRef] [PubMed]
  2. García-Tirado J, Landa-Oviedo HS, Suazo-Guevara I. Spontaneous bilateral chylothorax caused by a sneeze: an unusual entitiy with good prognosis. Arch Bronconeumol. 2017 Jan;53(1):32-3. [CrossRef]
  3. Torrejais JC, Rau CB, de Barros JA, Torrejais MM. Spontaneous chylothorax associated with light physical activity. J Bras Pneumol. 2006 Nov-Dec;32(6):599-602. [CrossRef] [PubMed]
  4. Rodrigues AL, Romaneli MT, Ramos CD, Fraga AM, Pereira RM, Appenzeller S, Marini R, Tresoldi AT. Bilateral spontaneous chylothorax after severe vomiting in children. Rev Paul Pediatr. 2016 Dec;34(4):518-521. [PubMed]
  5. Bender B, Murthy V, Chamberlain RS. The changing management of chylothorax in the modern era. Eur J Cardiothorac Surg. 2016 Jan;49(1):18-24. [CrossRef] [PubMed]
  6. Verma SK, Karmakar S. Hodgkin's lymphoma presenting as chylothorax. Lung India. 2014 Apr-Jun; 31(2):184-6. [CrossRef] [PubMed]
  7. Kuan YC, How SH, Ng TH, Abdul Rani MF. Intrapleural streptokinase for the treatment of chylothorax. Respir Care. 2011 Dec;56(12):1953-5. [CrossRef] [PubMed]
  8. Nair SK, Petko M, Hayward M. Aetiology and management of chylothorax in adults. Eur J Cardiothorac Surg. 2007 Aug;32(2):362-9. [CrossRef] [PubMed]
  9. Pillay TG, Singh B. A review of traumatic chylothorax. Injury. 2016 Mar;47(3):545-50. [CrossRef] [PubMed]
  10. Tu CY, Chen CH. Spontaneous bacterial empyema. Curr Opin Pulm Med. 2012 Jul;18(4):355-8. [CrossRef] [PubMed]
  11. Skouras V, Kalomenidis I. Chylothorax: diagnostic approach. Curr Opin Pulm Med. 2010 Jul;16(4):387-93. [CrossRef] [PubMed]
  12. Tsauo J, Shin JH, Han K, Yoon HK, Ko GY, Ko HK, Gwon DI.Transjugular intrahepatic portosystemic shunt for the treatment of chylothorax and chylous ascites in cirrhosis: a case report and systemic review of the literature. J Vasc Interv Radiol. 2016 Jan;27(1):112-6. [CrossRef] [PubMed]
  13. Bensoussan AL, Braun P, Guttman FM. Bilateral spontaneous chylothorax of the newborn. Arch Surg. 1975 Oct;110(10):1243-5. [CrossRef] [PubMed]
  14. Asnis DS, Saltzman HP, Iakovou C, Byrns DJ. Anaerobic empyema and chylothorax. Inf Dis Clin Pract. 1994;3(5):368-70. [CrossRef]
  15. Natrajan S, Hadeli O, Quan SF. Infected spontaneous chylothorax. Diagn Microbiol Infect Dis. 1998 Jan;30(1):31-2. [CrossRef] [PubMed]
  16. Guarracino JF, Murruni A; Basílico H, Villasboas RM, Halabe K, Barroso S, Demirdjian G. Chylothorax: Unusual complication presented in a burned child with an inflation injury under the effects of mechanical ventilation (Originial title Quilotórax: Complicación pocofrecuente en un ni-o quemado en asistencia respiratoria mecánica por síndrome inhalatorio). Revista Argentina de Burns 2000:15 (1). Available at: http://www.medbc.com/meditline/review/raq/vol_15/num_1/text/vol15n1p30.htm  (accessed 8/24/18).
  17. Wang JT, Hsueh PR, Sheng WH, Chang SC, Luh KT. Infected chylothorax caused by Streptococcus agalactiae: a case report. J Formos Med Assoc. 2000 Oct;99(10):783-4. [PubMed]
  18. Biswas A, Ghosh JK, Chatterjee A, Basu K, Chatterjee S. Infected chylothorax caused by escherichia coli in a non-immunocompromised child. Indian J Pediatr. 2008 Feb;75(2):192-3. [CrossRef] [PubMed]
  19. Alkassis SH, Bou Khalil BK. Infected chylothorax [abstract]. Presented at American Thoracic Society international meeting 2010 https://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A4591 (accessed 8/24/18).
  20. Epelbaum O, Kazianis J. Chylous empyema or empyematous chylothorax? [Abstract] Presented at American Thoracic Society international meeting 2011. https://www.atsjournals.org/doi/pdf/10.1164/ajrccm-conference.2011.183.1_MeetingAbstracts.A6460 (accessed 8/24/18)
  21. Wright RS, Jean M, Rochelle K, Fisk D. Chylothorax caused by paragonimus westermani in a native Californian. Chest. 2011 Oct;140(4):1064-6. [CrossRef] [PubMed]
  22. Bakar B, Pampal K, Tekkok IH. Infected bilateral chylothorax in a problematic case. Curr Surg. 2012 April;2(2):62-5. [CrossRef]
  23. Di Marco Berardino A, Inchingolo R, Smargiassi A, Re A, Torelli R, Fiori B, d'Inzeo T, Corbo GM, Valente S, Sanguinetti M, Spanu T. Empyema cause by prevotella bivia complicating an unusual case of spontaneous chylothorax. J Clin Microbiol. 2014 Apr;52(4):1284-6. [CrossRef] [PubMed]
  24. Geerlings SE, Hoepelman AI. Immune dysfunction in patients with diabetes mellitus. FEMS Immunol Med Microbiol. 1999 Dec;26(3-4):259-65. [CrossRef] [PubMed]
  25. Boule LA, Ju C, Agudelo M, et al. Summary of the 2016 Alcohol and Immunology Research Interest Group (AIRIG) meeting. Alcohol. 2018 Feb;66:35-43. [CrossRef] [PubMed]
  26. Milner JJ, Beck MA. The impact of obesity on the immune response to infection. Proc Nutr Soc. 2012 May;71(2):298-306. [CrossRef] [PubMed]
  27. Schild HH, Strassburg CP, Welz A, Kalff J. Treatment options in patients with chylothorax. Dtsch Arztebl Int. 2013 Nov 29;110(48):819-26. [CrossRef]
  28. Rudrappa M, Paul M. Chylothorax. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan. [PubMed]
  29. Nadolski G. Nontraumatic Chylothorax: diagnostic algorithm and treatment options. Tech Vasc Interv Radiol. 2016 Dec;19(4):286-90. [CrossRef] [PubMed]
  30. Misthos P, Kanakis MA, Lioulias AG. Chylothorax complicating thoracic surgery: conservative or early surgical management? Updates Surg. 2012 Mar;64(1):5-11. [CrossRef] [PubMed]
  31. Sahn SA. Diagnosis and management of parapneumonic effusions and empyema. Clin Infect Dis. 2007 Dec 1;45(11):1480-6. [CrossRef] [PubMed]

Cite as: Eubank L, Gabe L, Kraft M, Billheimer D. Infected chylothorax: a case report and review. Southwest J Pulm Crit Care. 2018;17(2):76-84. doi: https://doi.org/10.13175/swjpcc097-18 PDF

Wednesday
Aug012018

August 2018 Pulmonary Case of the Month

Arooj Kayani, MD

Richard Sue, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

 

Pulmonary Case of the Month CME Information

Completion of an evaluation form is required to receive credit and a link is provided on the last page of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Arooj Kayani, MD. All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity.

Learning Objectives: As a result of completing this activity, participants will be better able to:

  1. Interpret and identify clinical practices supported by the highest quality available evidence.
  2. Establish the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Translate the most current clinical information into the delivery of high quality care for patients.
  4. Integrate new treatment options for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine at Banner University Medical Center Tucson

Current Approval Period: January 1, 2017-December 31, 201

Financial Support Received: None

 

History of Present Illness

A 59-year-old woman referred because of worsening dyspnea over the past 2 months along with cough and wheezing. She has a history of chronic obstructive pulmonary disease (COPD) and is on continuous oxygen @ 2 L/min.

PMH, SH, and FH

In addition to her COPD she has a history of hypothyroidism, pneumonia, tonsillectomy, hip lipoma resection, hysterectomy, and a herniorrhaphy. She has a 30 pack-year history of smoking. She currently smokes half pack/day. No family history of lung disease or cancer.

Medications

  • Fluticasone/salmeterol
  • Tiotropium
  • Albuterol
  • Levothyroxine

Physical Examination

  • Vitals: HR 79/min, BP 100/69 mmHg, RR 16/min, SpO2 92% on 2 L/min.
  • General: Alert and oriented. Healthy appearing in no distress.
  • Lungs: Expiratory stridor and expiratory wheezing loudest over left lung. No crackles.
  • Cardiac: Regular rhythm with no murmurs. No edema.
  • The remainder of physical examination was unremarkable.

Which of the following should be performed? (Click on the correct answer to proceed to the second of four pages)

  1. Spirometry
  2. Sputum Gram stain, AFB stain, and fungal stain with cultures
  3. Thoracic CT scan
  4. 1 and 3
  5. All of the above

Cite as: Kayani A, Sue R. August 2018 pulmonary case of the month. Southwest J Pulm Crit Care. 2018;17(2):47-52. doi: https://doi.org/10.13175/swjpcc093-18 PDF 

Sunday
Jul012018

July 2018 Pulmonary Case of the Month

Anjuli M. Brighton, MB, BCh, BAO

Mayo Clinic Arizona

Scottsdale, AZ USA

 

Pulmonary Case of the Month CME Information

Completion of an evaluation form is required to receive credit and a link is provided on the last page of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Anjuli M. Brighton, MB. All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity.

Learning Objectives: As a result of completing this activity, participants will be better able to:

  1. Interpret and identify clinical practices supported by the highest quality available evidence.
  2. Establish the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
  3. Translate the most current clinical information into the delivery of high quality care for patients.
  4. Integrate new treatment options for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine at Banner University Medical Center Tucson

Current Approval Period: January 1, 2017-December 31, 2018

Financial Support Received: None

 

History of Present Illness

An 81-year-old gentleman was admitted for syncope. He had felt unwell for one month. His recent illness started with the “flu”. He had lingering productive cough, low volume hemoptysis and felt very fatigued. After a coughing episode he apparently lost consciousness and was taken to the emergency department.

Past Medical History, Social History and Family History

He has a past medical history of hypertension, glaucoma, diverticulosis and COPD. He was taking only antihypertensives including a diuretic. He has a 30 pack-year history of smoking but quit 10 years ago.

Physical Examination

  • Normotensive
  • Tachypneic
  • SpO2 96% on 2L NC
  • Afebrile
  • Diffuse wheezing, diminished at L base
  • Irregularly irregular heart rate

Which of the following are indicated at this time? (Click on the correct answer to be directed to the second of six pages)

  1. Chest x-ray
  2. Complete blood count (CBC)
  3. Electrocardiogram (EKG)
  4. 1 and 3
  5. All of the above

Cite as: Brighton AM. July 2018 pulmonary case of the month. Southwest J Pulm Crit Care. 2018;17(1):1-6. doi: https://doi.org/10.13175/swjpcc073-18 PDF 

Thursday
Jun282018

Phrenic Nerve Injury Post Catheter Ablation for Atrial Fibrillation

Payal Sen, MD1 

Uddalak Majumdar, MD2 

Ali Imran Saeed, MD1

1University of New Mexico

Albuquerque, NM USA

2Cleveland Clinic Foundation

Cleveland, Ohio USA

 

Abstract

Objective: Phrenic nerve injury (PNI) is a complication of catheter ablation treatment of atrial fibrillation (AF). This condition can mimic that of comorbid conditions like congestive heart failure (CHF) and chronic obstructive pulmonary disease (COPD).

Case details: A 77-year-old woman with past medical history of heart failure with preserved ejection fraction and mild COPD, presented with dyspnea for 8 days. One week ago, she had undergone radiofrequency catheter ablation for persistent symptomatic AF. After the ablation, she reported dyspnea during PCP and pulmonary office visits and was given increasing doses of diuretics and inhalers since her symptoms were attributed to acute exacerbation of heart failure in the setting of COPD. However, a chest x-ray showed elevation of the right hemidiaphragm, and she had a positive sniff test. She was thus diagnosed with right sided phrenic nerve palsy and was treated with oxygen therapy.

Discussion: Phrenic nerve injury can be diagnosed via clinical exam, chest x-ray and sniff test. A sniff Test which shows paradoxical elevation of the paralyzed hemidiaphragm with inspiration, compared with the rapid descent of the normal hemidiaphragm.

Conclusion: Phrenic nerve palsy is a complication which occurs in 6.6 percent of cases, post catheter ablation procedure for atrial fibrillation. This condition can mimic pulmonary conditions like acute exacerbation of COPD. Not keeping this complication in mind can lead to biased diagnostic reasoning and missed or delayed diagnosis.

Introduction

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia (1). In the past decade, catheter ablation of AF has evolved from an investigational procedure to a frequent therapeutic one (2). Phrenic nerve injury (PNI) is a complication of ablation that pulmonologists should be familiar with, due to its increasing incidence (3). This condition can mimic that of comorbid conditions like congestive heart failure (CHF) and chronic obstructive pulmonary disease (COPD). Hence it is important to develop clinical suspicion of phrenic nerve injury, and correlate onset of symptoms to the ablation, to prevent missed or delayed diagnosis, and to avoid falling prey to availability bias.

Case Report

History of Present Illness: A 77-year-old Caucasian woman with past medical history of heart failure with preserved ejection fraction and mild COPD (GOLD Stage 1), presented with dyspnea and right sided chest discomfort for 7 days. One week ago, she had undergone radiofrequency catheter ablation at the University of New Mexico, for persistent symptomatic AF. After the ablation, she reported dyspnea during PCP and pulmonary office visits, which was attributed to acute exacerbation of heart failure in the setting of COPD. She had been given increasing doses of diuretics which did not relieve her symptoms. A short course of azithromycin and prednisone had also been prescribed for possible acute exacerbation of COPD, but her symptoms had remained unchanged. Review of systems were negative for fever, chills, cough, leg swelling and hemoptysis. She led an active lifestyle, did not require oxygen, and had quit smoking 10 years ago. There was no history of cardio- respiratory diseases in the family.

Physical Examination:

Vitals: Temperature: 97.1°F, Pulse – 88/minute, RR 22/minute, BP –

140/70 mm Hg., Spo2 – 90% in Room air (baseline >95 percent).

She appeared to be in mild distress. Baseline dry weight had not increased. She had no clinical signs of heart failure- no peripheral edema, no JVD, no S3, no bibasilar crackles. There were decreased breath sounds in the base of the right lung but no rales or rhonchi. No significant wheezing was heard in any of the lobes of the lungs.

No clubbing or cyanosis was noted. The rest of the exam was unremarkable with a normal abdominal, and skin exam. There was no lymphadenopathy.

Laboratory: White blood cell count 10,000/mm3, hemoglobin 11 g/dL, with normal electrolytes, liver function tests and negative troponins. Arterial blood gases on room air showed a pH 7.38, paO2 of 62 mm Hg, pCO2 41 mm Hg and HCO3- 25.

EKG: negative for signs of ischemia.

Radiography: Chest radiography showed an elevated right diaphragm (Figure 1).

Figure 1. A: PA chest radiograph and B: 3 weeks earlier for comparison.

Sniff test performed under fluoroscopy showed paradoxical elevation of the right hemidiaphragm with inspiration, compared with rapid descent of the left hemidiaphragm, confirming right hemidiaphragm paralysis (Figure 2).

Figure 2. Static images from sniff test under fluoroscopy: A: pre-sniff. B: post-sniff. When the patient sniffs in, the left hemidiaphragm moves downwards but right hemidiaphragm does not (actually moves upwards very slightly).

After obtaining proper imaging, the patient was finally diagnosed with right-sided diaphragmatic paralysis due to phrenic nerve injury from the catheter ablation procedure done to treat AF. She was discharged with home oxygen and her symptoms have resolved. Follow up clinic visits revealed complete resolution of symptoms.

Discussion

Ectopic discharges from pulmonary veins are an important cause of atrial fibrillation, the most common sustained cardiac arrhythmia (1). Calkins et al. (4) carried out a study in 2009, where they showed statistically significant improvement in symptoms and quality of life in patients receiving ablation therapy versus those patients who received anti arrhythmic drugs (4). Traditionally, isolating the pulmonary vein by point-by-point radiofrequency catheter ablation was the cornerstone of catheter ablation strategies for the treatment of atrial fibrillation (2). However, this procedure had various complications such as thromboembolism, cardiac perforation, injury to adjacent structures and pulmonary vein stenosis (5). Hence, with the hope of finding an effective alternative approach with less complications, cryothermal ablation was started. This particular procedure involves electrically isolating pulmonary veins, by creating circumferential lesions by means of a cryoballoon catheter (6). Nonetheless, in both techniques, the most common complication is hemi‐diaphragmatic paralysis, due to phrenic nerve injury. This especially occurs whilst trying to isolate the right superior pulmonary vein (3). The approximate incidence of this complication is close to 3–11% (7). It is thought that the phrenic nerve gets injured due to the close anatomic relationship of the phrenic nerve to the heart (Figure 3).

Figure 3. Thoracic CT scan showing anatomical relationships (yellow star is the right phrenic nerve).

Both the right and the left phrenic nerves can get damaged - the right phrenic nerve is specifically at risk when ablations are carried out in the superior caval vein and the right superior pulmonary vein, and the left phrenic nerve is liable to damage during lead implantation into the great cardiac and left obtuse marginal veins (8). In our patient, the right phrenic nerve, which runs along the lateral surfaces of the superior vena cava and right atrium, was injured by energy delivered to the adjacent area during ablation.

In 2005 Bunch et al. (9) investigated the specific mechanism of phrenic nerve injury. Their study revealed that the phrenic nerve tended to retain heat after ablation. This phenomenon resulted in higher local temperatures with subsequent energy deliveries, causing early transient injury. Andrade et al. (3) in 2014, were the first to define this phrenic nerve injury histopathologically. According to them, phrenic nerve injury consisted of Wallerian degeneration characterized by loss of large myelinated axons with variable degrees of endoneural edema, vacuolated macrophages, myelin ovoids, and myelin digestion chambers (6).

Phrenic nerve injury can be diagnosed on clinical exam, and via a chest X-ray. Thereafter one can confirm the diagnosis with the sniff test or phrenic nerve stimulation/diaphragm electromyography. An upright chest x-ray will reveal an elevated diaphragm on the affected side. This test is sensitive, but not specific for the diagnosis of unilateral diaphragmatic paralysis (10). Another frequently done test is the sniff test which shows paradoxical elevation of the paralyzed hemidiaphragm with inspiration, compared with the rapid descent of the normal hemidiaphragm (11). The sniff test has more than 90 percent sensitivity (11). In 2014, Linhart et al. (12) performed studies to show that fluoroscopic assessment of diaphragm movement during spontaneous breathing was more sensitive for the diagnosis of phrenic nerve injury as compared to SVC pacing (12). It has also been seen that EMG‐guided approach results in less damage to the phrenic nerve and a significant reduction in hemi‐diaphragmatic paralysis as compared to current methods of abdominal palpation and fluoroscopy (13).

In unilateral diaphragmatic paralysis, patients are usually asymptomatic, have good prognosis and do not always need treatment. This is specifically true in the absence of underlying lung disease (14). Another procedure often done is the surgical plication of the affected hemidiaphragm (15). In bilateral diaphragm paralysis, ventilatory failure often occurs and these patients may require continuous positive airway pressure or mechanical ventilation and tracheostomy (16). According to Kauffman (17) in 2014, functional restoration of the paralyzed diaphragm should also be part of the standard treatment algorithm in managing symptomatic patients.

Conclusion

Phrenic nerve palsy is a complication which occurs in about 6 percent of cases post catheter ablation procedure for atrial fibrillation. This condition can mimic pulmonary conditions like acute exacerbation of COPD. It is important to develop clinical suspicion and correlate onset of symptoms to the ablation. Not keeping this complication in mind can lead to biased diagnostic reasoning and missed or delayed diagnosis.

References

  1. Yamazaki M, Filgueiras-Rama D, Berenfeld O, Kalifa J. Ectopic and reentrant activation patterns in the posterior left atrium during stretch-related atrial fibrillation. Prog Biophys Mol Biol. 2012 Oct-Nov;110(2-3):269-77. [CrossRef] [PubMed]
  2. Pedrote A, Acosta J, Jauregui-Garrido B, Frutos-Lopez M, Arana-Rueda E. Paroxysmal atrial fibrillation ablation: Achieving permanent pulmonary vein isolation by point-by-point radiofrequency lesions. World J Cardiol. 2017 Mar 26;9(3):230-40. [CrossRef] [PubMed]
  3. Andrade JG, Dubuc M, Ferreira J, Guerra PG, Landry E, Coulombe N, et al. Histopathology of cryoballoon ablation-induced phrenic nerve injury. J Cardiovasc Electrophysiol. 2014 Feb;25(2):187-94. [CrossRef] [PubMed]
  4. Calkins H, Reynolds MR, Spector P, et al.  Treatment of atrial fibrillation with antiarrhythmic drugs or radiofrequency ablation: two systematic literature reviews and metaanalyses. Circ Arrhythm Electrophysiol. 2009 Aug;2(4):349-61. [CrossRef] [PubMed]
  5. Sarabanda AV, Bunch TJ, Johnson SB, et al. Efficacy and safety of circumferential pulmonary vein isolation using a novel cryothermal balloon ablation system. J Am Coll Cardiol. 2005 Nov 15;46(10):1902-12. [CrossRef] [PubMed]
  6. Andrade JG, Khairy P, Guerra PG, et al. Efficacy and safety of cryoballoon ablation for atrial fibrillation: a systematic review of published studies. Heart Rhythm. 2011 Sep;8(9):1444-51. [CrossRef] [PubMed]
  7. Omran H, Gutleben KJ, Molatta S, et al. Second generation cryoballoon ablation for persistent atrial fibrillation: an updated meta-analysis. Clin Res Cardiol. 2018 Feb;107(2):182-92. [CrossRef] [PubMed]
  8. Sanchez-Quintana D, Cabrera JA, Climent V, Farre J, Weiglein A, Ho SY. How close are the phrenic nerves to cardiac structures? Implications for cardiac interventionalists. J Cardiovasc Electrophysiol. 2005 Mar;16(3):309-13. [CrossRef] [PubMed]
  9. Bunch TJ, Bruce GK, Mahapatra S, et al. Mechanisms of phrenic nerve injury during radiofrequency ablation at the pulmonary vein orifice. J Cardiovasc Electrophysiol. 2005 Dec;16(12):1318-25. [CrossRef] [PubMed]
  10. Chetta A, Rehman AK, Moxham J, Carr DH, Polkey MI. Chest radiography cannot predict diaphragm function. Respir Med. 2005 Jan;99(1):39-44. [CrossRef] [PubMed]
  11. Alexander C. Diaphragm movements and the diagnosis of diaphragmatic paralysis. Clin Radiol. 1966 Jan;17(1):79-83. [CrossRef] [PubMed]
  12. Linhart M, Nielson A, Andrie RP, et al. Fluoroscopy of spontaneous breathing is more sensitive than phrenic nerve stimulation for detection of right phrenic nerve injury during cryoballoon ablation of atrial fibrillation. J Cardiovasc Electrophysiol. 2014 Aug;25(8):859-65. [CrossRef] [PubMed]
  13. Miyazaki S, Ichihara N, Nakamura H, et al. Prospective evaluation of electromyography-guided phrenic nerve monitoring during superior vena cava isolation to anticipate phrenic nerve injury. J Cardiovasc Electrophysiol. 2016 Apr;27(4):390-5. [CrossRef] [PubMed]
  14. Piehler JM, Pairolero PC, Gracey DR, Bernatz PE. Unexplained diaphragmatic paralysis: a harbinger of malignant disease? J Thorac Cardiovasc Surg. 1982 Dec;84(6):861-4. [PubMed]
  15. Kuniyoshi Y, Yamashiro S, Miyagi K, Uezu T, Arakaki K, Koja K. Diaphragmatic plication in adult patients with diaphragm paralysis after cardiac surgery. Ann Thorac Cardiovasc Surg. 2004 Jun;10(3):160-6. [PubMed]
  16. Davis J, Goldman M, Loh L, Casson M. Diaphragm function and alveolar hypoventilation. Q J Med. 1976 Jan;45(177):87-100. [PubMed]
  17. Kaufman MR, Elkwood AI, Colicchio AR, et al. Functional restoration of diaphragmatic paralysis: an evaluation of phrenic nerve reconstruction. Ann Thorac Surg. 2014 Jan;97(1):260-6. [CrossRef]

Cite as: Sen P, Majumdar U, Saeed AI. Phrenic nerve injury post catheter ablation for atrial fibrillation. Southwest J Pulm Crit Care. 2018;16(6):362-7. doi: https://doi.org/10.13175/swjpcc070-18 PDF 

Tuesday
Jun262018

Evaluating a Scoring System for Predicting Thirty-Day Hospital Readmissions for Chronic Obstructive Pulmonary Disease Exacerbation

Vanessa Yap, MD1

Diahann Wilcox, APRN, DNP1

Richard ZuWallack, MD2

Debapriya Datta, MD1

 

1Division of Pulmonary & Critical Care Medicine

University of CT Health Center

Farmington, CT USA

2Division of Pulmonary & Critical Care Medicine

St Francis Hospital & Medical Center

Hartford, CT USA

 

Abstract

Introduction: Chronic obstructive pulmonary disease (COPD) results in 700,000 hospitalizations annually in the United States and 12-25% of patients are readmitted within 30 days of hospital discharge. A simple scoring system to risk-stratify these patients would be useful in allocating scarce resources.

Objective: The objectives of this study were to identify possible predictor variables to develop a clinically-useful instrument that can predict 30-day hospital readmissions in COPD patients.

Methods: Fifty patients hospitalized for a COPD exacerbation at two hospitals over a one-month period were studied prospectively. Demographics, disease severity, symptoms, functional status, psychological, and co-morbidity variables were assessed during the hospitalization. Patients were contacted telephonically thirty days post-discharge to determine readmission. Baseline variables were tested as predictors of 30-day readmissions.

Results: Mean age was 71 ± 11 years; 77% were female, 60% had Medical Research Council dyspnea 3 or 4; mean FEV1 was 41 ± 13% of predicted. Mean length of stay was 4.3 ± 3.2 days. Sixty percent had ≥ 1 clinical exacerbations in the preceding year, 52% had been hospitalized at least once for a respiratory exacerbation; 61% had been hospitalized at least once; 26% were on chronic prednisone. Thirty-day readmission rate was 24%. Three variables were found to be predictive of hospitalization: Clinical exacerbations in the previous year, chronic prednisone use, and functional limitation from dyspnea predictive of hospitalization.

Conclusions: Exacerbations in the previous year, chronic prednisone use, and functional limitation from dyspnea hold promise in a scoring system used to predict 30-day re-hospitalization and could be quickly assessed from a review of hospital record or a brief interview.

Introduction

Chronic obstructive pulmonary disease (COPD) is a common disease and is a leading cause of mortality in the United States (1). Much of the cost of care in COPD involves expenses related to exacerbations of this disease (2). Hospital readmissions within 30 days in COPD are frequent – with approximately 9-20% being readmitted (3-6). Hospitals will soon be financially penalized for 30-day readmissions for COPD. Risk stratification would be useful in directing scarce medical resources toward those patients most likely to be readmitted. The objectives of our study were: 1. To evaluate predictors of 30-day hospital readmission in patients hospitalized for an exacerbation of COPD and 2. To develop a simple, clinically-useful instrument that can predict any-cause 30-day hospital readmissions in COPD patients. To this end, the final tool would have to be brief (taking < 10 minutes to complete), convenient to use and have sufficient predictive power to predict hospital readmission.

Methods

This was a prospective study, performed by means of review of medical records and patient interview. Approval for the study was obtained from the IRBs of both participating institutions. There was no extramural funding for the study.

Fifty patients admitted with acute exacerbation of COPD over a 3-month period were studied. The primary inclusion criterion was a clinical diagnosis of a COPD exacerbation resulting in hospitalization. Patients with primary diagnosis of acute exacerbation of COPD exacerbation but with concomitant diagnosis of heart failure or pneumonia were included in the analysis. Inability to effectively communicate with the investigator, including language barrier or cognitive defect was the exclusion criterion.

The hospitalist physician, after receiving verbal approval from the hospitalized COPD patient of his/her potential willingness to see an investigator for a clinical research study, was then seen by an investigator, and informed consent was obtained. Following this, an interview and review of medical records were performed to obtain demographic and disease variables. Variables (from interview or record review) included: demographics (age, gender), disease severity, all-cause and respiratory-related hospitalizations over the preceding year, outpatient treated respiratory exacerbations over the preceding year, functional status, co-morbidities, psychological status, treatment upon admission. COPD assessment test (CAT) (7), Charlson Comorbidity Index (CCI) (8) and LACE Index (9) were determined for all patients. We also measured the treating physician’s “gut feeling” of the likelihood of a 30-day readmission. The treating physician was blinded as to the specific variables we measured. (All variables tested are detailed in Appendix. Post-bronchodilator forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and FEV1/FVC ratio were obtained from previous spirometry (within 3 years), if available. The patients without a historical spirometric diagnosis of COPD had spirometry before hospital discharge. Consented patients were then contacted at 30-days to determine whether they had readmissions and if so, for what cause.

General statistics are reported as means ± standard deviations (SD). Univariate logistic regression analyses were used to determine which of our tested variables predicted 30-day admission for exacerbation of COPD. Following this, multivariate forward logistic regression, incorporating variables that were predictive in univariate analyses, was utilized to determine which variables were predictive of 30-day hospitalization for COPD exacerbations.

Hospitalizations were analyzed as binary variables (yes-no). Based on the univariate analysis, two scoring systems were developed to predict readmission. The 2 scoring systems, each including three variables, significantly predicted 30-day readmissions.

The first scoring system (scoring system I) was as follows:

  1. MRC dyspnea. This score ranges from 0 (least) to 4 (greatest) dyspnea. Our scoring was dichotomized to 0 (MRC 0, 1, 3, or 3) or 1 (MRC 4: “too short of breath to leave the house or short of breath dressing/undressing.”
  2. Exacerbation history: Those with 1 or more hospitalizations for exacerbations in the preceding year were given a score of 1; those below this threshold had a score of 0.
  3. Chronic prednisone use prior to admission: Chronic prednisone use was defined as prednisone used on all or most days for at least three months prior to admission. Those meeting this criterion were given a score of 1, those without chronic prednisone use had a score of 0.

The second scoring system (scoring system II) was as follows:

  1. MRC dyspnea. This was identical to # 1 in the first scoring system.
  2. Exacerbation history: Those with 2 or more outpatient -treated exacerbations (some of these could result in hospitalization) in the preceding year were given a score of 1; those below this threshold had a score of 0.
  3. Chronic prednisone use prior to admission: This was identical to # 3 in the first scoring system.

Scores for each of the above scoring systems could, therefore, range from 0-3. The relationship between the above scores and 30-day hospital readmissions were evaluated using receiver operating characteristic (ROC) curves, which plot the true-positive rate (sensitivity) versus the false-positive rate (1-specificity).

A receiver operating characteristic (ROC) curve, plotting the true-positive rate (sensitivity) versus the false-positive rate (1-specificity) was used to characterize the relation. The ROC model was used to predict the likelihood of readmission for scoring system I and scoring system II.

Results

Of the 50 studied patients, 77% were female; mean age was 71 ± 11 years. The body mass index (BMI) was 29.65 + 9 kg/m2. Clinical characteristics of subjects are shown in Table 1.

Table 1. Clinical characteristics of studied subjects.

Sixty percent had Medical Research Council (MRC) dyspnea 3 or 4 (moderate to severe). Mean length of stay was 4.3 ± 3.2 days. Thirty-four percent lived alone at home.  

In our study, all patients readmitted within thirty days had respiratory exacerbations of COPD as principal diagnoses (i.e., the frequency of respiratory-related and all-cause 30-day readmissions was identical). Thirty-day readmission rate for exacerbation of COPD was 24%. Of the studied parameters, the ones that did not predict rehospitalization in univariate logistic regression analyses are shown in Table 2.

Table 2. Variables that did not predict 30-day readmission.

Variables that significantly predicted or tended to predict readmission included: 1) two or more clinical exacerbations (not necessarily resulting in hospitalization) in the previous year (OR 4.6, p= 0.04); 2) prednisone use (chronic or prior to admission) (OR 4.4, p< 0.04); 3) MRC = 4 (OR 2.7, p = 0.16); 4) one or more respiratory hospitalizations in the preceding year (OR 3.1, p = 0.08).

Using scoring system I, 16 patients had a score of 0; 16 had a score of 1, 14 patients had a score of 2, and 4 had a score of 3. Readmission rates for each of these categories were as follows: 13%, 19%, 29%, and 75%, respectively. Using the ROC model (Figure 1), odds ratios for readmission for- Score 0 versus 3 was 18; (2) odds ratios for readmission for score 1 versus 3 was 16 and (3) odds ratios for readmission for score 2 versus 3 was 6.7.

Figure 1. Receiver operating characteristic (ROC) curve for scoring system I, showing odds ratio for readmission for Score 0 versus 3, Score 1 versus 3 and Score 2 versus 3.

In scoring system II, 19 had a score of 0, 16 had a score of 1, 11 had a score of 2, and 4 had a score of 3. Readmission rates for each of these categories were as follows: 11%, 19%, 36%, and 75%, respectively.  Using the ROC model (Figure 2), odds ratios for readmission for- Score 0 versus 3 was 24; (2) Score 1 versus 3 was 15 and (3) Score 2 versus 3 was 4.5.

Figure 2. Receiver operating characteristic (ROC) curve for scoring system II, showing odds ratio for readmission for score 0 versus 3, score 1 versus 3 and score 2 versus 3.

In both scoring systems, the combined score of 3, with all 3 variables present, was associated with a high rate of readmission. The odds ratio was calculated for the clinical scores as it provides a valid effect measure and allows comparison of the clinical scores with regards to outcome, i.e. the readmission for COPD exacerbation, in a small study such as this.

The closer AUC is to 1, the better the predictive performance of the test, with the practical lower limit for the AUC of a predictive test being 0.5. In this study, scoring system I with an AUC of 0.69 (Figure 1) and scoring system II, with an AUC of 0.73 (Figure 2), indicate fair strength as predictors for COPD readmission.

Discussion

The purpose of our study was to create a simple scoring system that might predict 30-day readmissions in patients hospitalized with COPD exacerbations. Data regarding factors which predisposes to hospital readmissions within 30 days of discharge after hospitalization for acute exacerbations of COPD is variable and remains limited (4-6, 10,11). Our study aimed at identifying potential risk factors and evaluating probable predictors of hospital re-admission in COPD patients within a month of discharge.

In our study, three variables held promise in a scoring system used to predict re-hospitalization within 30 days: exacerbations (either clinically-treated or hospitalized), chronic prednisone use, and functional limitation from dyspnea. These three variables could be assessed within a few minutes from a review of the inpatient hospital record or from a brief interview.

Previous studies evaluating readmission risk factors in COPD up to one year have identified several variables. These include: a lower FEV1 (12- 16), reduced physical activity, functional limitation and poor health-related quality of life (2,4,17-19), need for self-care assistance, active/ passive smoking, long term supplemental O2-requirement (12,16-18), and presence of selected co-morbid conditions (20, 21).

More recent studies found low physical activity to be a significant factor (5,18). Minutes of physical activity per day in the first week following discharge was lower in those readmitted (42 + 14 minutes vs. 114 + 19 minutes, p = 0.02) (5). Ngyuen et al. (19) reported an 18% readmission rate in 4000 patients, with independent predictors of increased readmission including reduced activity, anemia, prior hospitalizations, longer lengths of stay, more comorbidities, receipt of a new oxygen prescription at discharge, use of the emergency department or observational stay before the readmission. In another retrospective study, multivariate analysis showed the following risk factors to be associated with early readmission within 30 days of discharge- male gender, history of heart failure, lung cancer, osteoporosis, and depression; no prior prescription of statin within 12 months of the index hospitalization and no prescription of short-acting bronchodilator, oral steroid and antibiotic on discharge; length of stay, <2 or >5 days and lack of follow-up visit after discharge (10). Another study found these variables to have a significant association with 30-day readmissions: age, diastolic blood pressure, COPD severity score, length of stay, pH, paCO2, FEV1< 50%, number of previous days until exacerbation (6). This study also found an increased mortality at 6 months and one year in patients readmitted within 30 days of discharge (6).

In our study, the most influential variable 30-day readmission was the history of two or more exacerbations in the preceding year (OR: 2.47, CI= 1.51-4.05, p< 0.001). This variable was also found in our study to be significantly associated with 30-day readmission, following discharge for a COPD exacerbation hospitalization.

Our study found steroid use (chronic or prior to admission) to be a significant predictor of COPD readmissions. Steroid use has been associated with a significantly increased risk of readmission in a few other studies (12,13,16,22). We hypothesize chronic prednisone use reflects instability and variability in the chronic respiratory disease or a recent exacerbation prior to the index hospitalization- hence its relatively strong relationship to re-hospitalization.

The second significant predictor in our study, exacerbations resulting in hospital admission in the preceding year, has been found to be a risk factor readmission in prior studies (6,12,13,23). Three admissions in the year preceding recruitment was found to increase risk for readmission for COPD exacerbation (12,13,23). Frequent exacerbations in the preceding year likely reflect the severity of disease in these patients. A retrospective study found no association between the number of previous hospital COPD admissions and readmission (24).

Our third significant predictor, the severity of dyspnea has also been reported in some studies to be an independent risk factor for hospital admission for an acute exacerbation of COPD. Kessler et al. (14) reported that COPD patients with a dyspnea of grade 3, 4 or 5 (defined as breathlessness with mild, minimal or limited exertion respectively), had a significant risk of hospitalization at one year but those with dyspnea of grade 2 did not. Patients with “severe dyspnea” have been found to be more likely to be readmitted to hospital in studies (15,18). Our study using the MRC rating for dyspnea and found patients with an MRC rating of 4, which is equal to the most severe grading of dyspnea in this scale. The severity of dyspnea by MRC dyspnea being a predictor for readmission in COPD indicates that the severity of the disease predisposes to exacerbations of COPD and consequent readmissions.

A systematic review of studies on risk factors for readmission for patients with COPD exacerbation found 3 predictive factors similar to our study, namely- previous hospital admission, dyspnea and oral corticosteroids (25). This review also identified other variables including use of LTOT, having low health status or poor health related quality of life and reduced routine physical activity as risk factors for admission and readmission for COPD exacerbation (25).

A scoring system similar to ours, using 3 the significant predictors of COPD readmission (chronic prednisone use, MRC dyspnea rating and prior exacerbations, either clinical or requiring hospitalizations) has not been studied in predicting the 30 day- readmission for COPD exacerbation. This scoring system was a fairly strong predictor of readmission for COPD and may serve as a useful tool in risk-stratifying patients and directing medical resources toward those patients most at risk for readmission. This is especially of relevance at the present time when hospitals will face financial penalties for 30-day readmissions for COPD.

The risk factors identified for COPD readmission in this study are not modifiable. However, if patients more at risk for readmissions can be identified based on these risk factors, more resources can be directed to these group of patients- such as closer outpatient follow-up, VNA services, inpatient and outpatient pulmonary rehabilitation, more gradual steroid taper and institution of anti-inflammatory therapy such as azithromycin.

One limiting factor of this study is the small number of patients. The scoring system generated by the study using the 3 identified predictors, though fairly predictive of readmissions for COPD exacerbations, cannot be used without corroboration. The validity of the scoring system using needs to be established in a larger group of patients. Based on the results of this study, we intend to assess these variables as part of a quality assurance study on a larger number of hospitalized COPD patients. We plan to attempt to refine the scoring system, if possible, with an emphasis on simplicity in assessing data, brevity in data collection and predictive power for 30-day and subsequent hospitalization.

Conclusions

A simple 3-point scoring system, incorporating three variables: 1) chronic prednisone use; 2) MRC dyspnea rating; and 3) prior exacerbations (either clinical or requiring hospitalizations) has a fairly high predictive value for 30 -day readmission due to COPD exacerbation. This can be easily assessed within a few minutes from a review of the inpatient hospital record or from a brief patient interview. It can serve as a useful tool in risk-stratifying patients and directing medical resources toward those patients most at risk for readmission. This scoring system using these three variables holds promise for future validation studies.

References

  1. Celli BR, Barnes PJ. Exacerbations of chronic obstructive pulmonary disease. Eur Respir J. 2007;29:1224-38. [CrossRef] [PubMed]
  2. Steer J, Gibson GJ, Bourke SC. Predicting outcomes following hospitalization for acute exacerbations of COPD. QJM. 2010;103:817-29. [CrossRef[ [PubMed]
  3. Johannesdottir SA. Hospitalization with acute exacerbation of chronic obstructive pulmonary disease and associated health resource utilization: a population-based Danish cohort study. J Med Econ. 2013;16:897-906. [CrossRef] [PubMed]
  4. Tan WC. Factors associated with outcomes of acute exacerbations of chronic obstructive pulmonary disease. COPD. 2004;1(2):225-47. [CrossRef] [PubMed]
  5. Sharif R, Parekh TM, Pierson KS, Kuo YF, Sharma G. Predictors of early readmission among patients 40 to 64 years of age hospitalized for chronic obstructive pulmonary disease. Ann Am Thorac Soc. 2014;11:685-94. [CrossRef] [PubMed]
  6. Guerrero M, Crisafulli E, Liapikou A, Huerta A, Gabarrus A, Chette A, Soler N, Torres A. Readmission for acute exacerbation within 30 days of discharge is associated with a subsequent increase in mortality risk in COPD patients: A long-term observational study. PLoS ONE. 2016;11:e0150737. [CrossRef] [PubMed]
  7. Jones PW, Harding G, Berry P, Wiklunf I, Chen WH, Kline Leady N. Development and first validation of the COPD assessment test. Eur Respir J. 2009;34:648-54. [CrossRef] [PubMed]
  8. Charlson M, Szatrowski TP, Peterson J, Gold J. Validation of a combined comorbidity index. J Clin Epidemiol. 1994:47:1245-51. [CrossRef] [PubMed]
  9. Walraven C, Dhalla IA, Bell C, Etchells E, Stiel IG, Zarnke K, Austin PC, Foster AJ. Derivation and validation of an Index to predict early death or unplanned readmission after discharge from hospital to community. CMAJ. 2010; 182: 551-7. [CrossRef] [PubMed]
  10. Garcia-Aymerich J, Monso E, Marrades RM, Escarrabill J, Felez MA, Sunyer J, Anto JM. Risk factors for hospitalization for a chronic obstructive pulmonary disease exacerbation. EFRAM study. Am J Respir Crit Care Med. 2001;164:1002-7. [CrossRef] [PubMed]
  11. Garcia-Aymerich J, Farrero E, Félez MA, Izquierdo J, Marrades RM, Antó JM. Risk factors of readmission to hospital for a COPD exacerbation: a prospective study. Thorax. 2003;58:100-5. [CrossRef] [PubMed]
  12. Gudmundsson G, Gislason T, Janson C, et al. Risk factors for rehospitalisation in COPD: role of health status, anxiety and depression. Eur Respir J. 2005;26:414–19. [CrossRef] [PubMed]
  13. Cao Z, Ong KC, Eng P, Tan WC, Ng TP. Frequent hospital readmissions for acute exacerbation of COPD and their associated factors. Respirology. 2006;11(2):188-95. [CrossRef] [PubMed]
  14. Lau AC, Yam LY, Poon E. Hospital re-admission in patients with acute exacerbation of chronic obstructive pulmonary disease. Respir Med. 2001;95:876-84. [CrossRef] [PubMed]
  15. Kessler R, Faller M, Fourgaut G, Mennecier B, Weitzenblum E. Predictive factors of hospitalization for acute exacerbation in a series of 64 patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1999;159:158-64. [CrossRef] [PubMed]
  16. Wang Q, Bourbeau J. Outcomes and health-related quality of life following hospitalization for an acute exacerbation of COPD. Respirology. 2005;10:334-40. [CrossRef] [PubMed]
  17. Almargo P, Barriero B, DeEchaguen AO, Quintana S, Rodriguez CM, Heredia JL, Garau J. Risk factors for hospital re-admission in patients with chronic obstructive pulmonary disease. Respiration. 2006;73:311-7. [CrossRef] [PubMed]
  18. Chawla H, Bulathsinghala C, Tejada JP, Wakefield D, ZuWallack R. Physical activity as a predictor of thirty-day hospital re-admission after a discharge for a clinical exacerbation of COPD. Ann Am Thorac Soc. 2014;11:1203-9. [CrossRef] [PubMed]
  19. Ngyuen HQ, Chu L, Liu ILA, Lee JS, Suh D, Korotzer B, Yuen G, Desai S, Coleman KJ, Gould MK. Associations between physical activity and 30-day readmission risk in chronic obstructive pulmonary disease. Ann Am Thorac Soc. 2014;11(5): 695-705. [CrossRef] [PubMed]
  20. Kessler R, Faller M, Fourgaut G, Mennecier B, Weitzenblum E. Predictive factors of hospitalization for acute exacerbation in a series of 64 patients with Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 1999;159:158–164. [CrossRef] [PubMed]
  21. Miravitlles M, Guerrero T, Mayordomo C, Sanchez-Agudo L, Nicolau F, Segu JL. Factors associated with increased risk of exacerbation and hospital admission in a cohort of ambulatory COPD patients: a multiple logistic regression analysis. Respiration. 2000;67:495–501. [CrossRef] [PubMed]
  22. Groenewegen KH, Schols AM, Wouters EF. Mortality and mortality-related factors after hospitalization for acute exacerbation of COPD. Chest. 2003; 124:459-67. [CrossRef] [PubMed]
  23. Connolly MJ, Lowe D, Anstey K, Hosker HSR, Pearson MG, Roberts CM. Admissions to hospital with exacerbations of chronic obstructive pulmonary disease: effect of age related factors and service organization. Thorax. 2006;61:843-8. [CrossRef] [PubMed]
  24. Pouw EM, Ten Velde GP, Croonen BH, Kester AD, Schols AM, Wouters EF. Early non-elective readmission for chronic obstructive pulmonary disease is associated with weight loss. Clin Nutr. 2000;19:95–99. [CrossRef] [PubMed]
  25. Bahadoori K, Fitzgerald JM. Risk factors of hospitalization and readmission of patients with COPD exacerbation-systematic review. Int J Chron Obstruct Pulmon Dis. 2007:2(3) 241-51. [PubMed]

Cite as: Yap V, Wilcox D, ZuWallack R, Datta D. Evaluating a scoring system for predicting thirty-day hospital readmissions for chronic obstructive pulmonary disease exacerbation. Southwest J Pulm Crit Care. 2018;16(6):350-9. doi: https://doi.org/10.13175/swjpcc054-18 PDF