Case Study Number One

HPI:
JS: 74 y/o man with a history of COPD and HF following an MI 6 years ago presenting in clinic with sudden onset of:

• Shortness of breath and fever.
• No change in his alertness or mental status (per wife)
• Unable to speak in full sentences for the past several hours (per wife)
• He has a productive cough with sputum of unknown color
• Audible wheezing since last night.
• Mild chest tightness
• Dyspnea

COPD usual manifestation in this patient:

• Cough, worse in the morning, productive of gray sputum,
• Gets short of breath if he walks more then 10 feet,
• Episodes of wheezing if he gets sick (e.g. with an upper respiratory infection).
• Usually able to help around the house with light work and fixing things.

Past Medical/Surgical History

• Heart failure following myocardial infarction at age 68 years
• COPD (on 2 L home oxygen)
• Hypertension
• Appendectomy

Family History

• Father died of myocardial infarction at age 59 years (diabetes, hypertension, smoker)
• Mother alive (atrial fibrillation, heart failure)
• Healthy siblings

Social History

• Married, 3 adult children
• 30 pack year smoking history (quit after MI)
• Worked on a farm
• No alcohol or illicit drug use

Medications / Allergies

• Lisinopril 20 mg twice daily
• Metoprolol 50 mg twice daily (Beta Blocker!)
• Spironolactone 25 mg daily
• Furosemide 40 mg daily (Diuretic)
• Salmeterol/fluticasone 50/500 dry powdered inhaler (DPI) one puff inhaled twice daily
• Tiotropium DPI one cap inhaled daily                
• Albuterol/ipratropium metered dose inhaler (MDI) or solution for nebulization every 6 hours as needed
• Levalbuterol – a beta2 agonist.  MDI two puffs every 4 to 6 hours as needed
• Home oxygen
• Beta blocker
• Pt confused about when to take which medicine; compliance unknown
• No known allergies.

JS Past Record Review  (brought by wife)

• Echocardiogram with EF of 25%
• Spirometry with FEV1 35% predicted that does not change significantly after inhaled bronchodilator
• Unable to determine when last pneumoccal vaccine was give.
• Patient and wife don’t recall “a pneumonia shot”.
• Does know he got his “flu shot” last month at a grocery store.
• An arterial blood gas (ABG): pH 7.17, PCO2 55, PO2 62, HCO3- 25

Physical examination

• Vital Signs: BP 128/74; P 68, reg; RR 32; Ht 5ft 6 in; Wt 132 lbs; T 101.5 °F oral.
• Unable to speak in full sentences, audible wheezing, alert and oriented

Pertinent positives:

General:  audible wheezing, no accessory muscle use
Nails: tar stains, clubbing
Chest: increased anteroposterior (AP) diameter; diffuse wheezing to auscultation
Heart: regular, no murmurs

 

 

Case Report Questions

At this point, can you think of at least two diagnoses?  What is your most likely diagnosis? 

• It is possible that the patient has pneumonia leading to an exacerbation of his COPD or heart failure.  The most likely diagnosis is pneumonia with exacerbating COPD

Explain the main reasons for your diagnosis.   

• The main reason for this diagnosis is the worsening in underlying COPD symptoms such as the “unknown” sputum color as well as the worsening dyspnea. There lack of evidence of a pneumococcal vaccine.

How would you interpret his clinical picture?  Hint:  Use the GOLD criteria for COPD (Look this up)

Normal: FEV1/FEV: 0.7-0.8 (NOTE: a ratio less than 0.7 is indicative of COPD)
Restrictive lung disease: FEV1/FEV >0.7 with decreased FVC and decreased or normal FEV1
Moderate COPD: FEV1/FVC <0.70; FEV1: 50 to 79% of predicted value
Mild COPD: FEV1/FVC <0.70; FEV1:  ≥80% of predicted value
Severe COPD: FEV1/FVC <0.70; FEV1: 30 to 49% of predicted value
Mild asthma: FEV1/FEV: <0.7 but is reversible/FEV1 increases with bronchodilator

• According to the GOLD criteria for COPD the patient has Stage 3 COPD (severe)[1]

In a patient with COPD, assessment of symptoms should include the following?

Severity of breathlessness:
Sputum production
Wheezing
Weight loss/anorexia

• All of the above

All of the above are symptoms of COPD and worsening or changes of those symptoms could be indicative of mismanagement or worsening of COPD.  COPD usually manifests as chronic bronchitis and emphysema. Often caused by smoking, in COPD the body is unable to clear the mucus from the lungs due to damaged cilia. Since the mucus cannot move the only way to clear it is through coughing which often produces sputum. If all of the mucus cannot be cleared it causes an obstruction. Since there is airway obstruction breathlessness occurs along with wheezing, the severity of this needs to be determined to see if the patient’s symptoms are getting worse. Weight loss/anorexia is indicative of the difficulty a patient might be taking to breathe in and out due to COPD. Patients with COPD have to work harder to breathe and therefore to maintain oxygenation within their bodies, an increase in weight loss may be indicative of a worsening of symptoms[2][3]

Which of the following is the least likely cause of patient’s symptoms?

COPD exacerbation

• Recurrent aspiration

Heart failure
Pneumonia
Asthma exacerbation

• There are no symptoms that point towards recurrent aspiration, nor is there any history of aspiration for this patient. The other four are possible causes of the patient’s current symptoms and aligns with the patient’s past medical history. Heart failure, pneumonia or an asthma exacerbation could cause the COPD exacerbation. The exacerbation symptoms look very similar to pneumonia symptoms (sputum color change) or asthma exacerbation symptoms (increase difficulty breathing). Since the patient has underlying COPD many of these diseases manifest the same way. Since the patient has had a previous MI and has a family history of MI, heart failure cannot be ruled out either[4][5]

Which other further investigations do you think would be appropriate?  Why? What results would you expect? What might be expected on this patient’s chest Xray?

Pulse oximetry
Spirometry
Alpha-1-antitrypsin level
None of the above

• The pulse oximeter looks at if oxygen is bound to hemoglobin whereas the ABG looks at oxygen that is not bound to hemoglobin (PO2 vs. PaO2). A pulse oximetry reading would be easy to administer in a clinic and would provide information for if supplemental oxygen is needed (although the ABG shows a previous low PaO2, it is not known what the current oxygenation state of the patient is). The pulse oximeter would probably show that supplemental oxygen is needed.
• Spirometry is usually used to initially diagnose COPD, but since it is already documented that the patient has COPD this would not be as helpful. However previous spirometry levels could be used to compare with current levels to see if there is a difference after interventions are taken but this would not be done immediately.
• Similarly, alpha-1-antitrypsin levels are used to determine if COPD is caused due to a deficiency in alpha-1-antitrypsin. This would not be helpful in treating the acute nature of this case and would have only been helpful in the initial COPD diagnosis.
• This patient’s chest x-ray would probably show hyperinflation due to the increased AP diameter; x-ray could also potentially show evidence of pneumonia (opaque areas within the lungs due to infection, also shows degree/spread of infection) or heart failure seen as cardiomegaly)

Does JS present with clinical factors that increase risk of severe COPD exacerbations? If so, can you list at least two?

• There are several clinical factors that increase the risk for severe COPD exacerbations. One of them is the fact that the COPD that the patient already in a severe stage. Furthermore, the patient has a marked increase in his regular COPD symptoms (worsening shortness of breath and sputum production of unknown color), and is also presenting with factors that point to comorbidity factors with COPD (possible pneumonia or heart failure).

What would be the best option to improve his symptoms and slow progression?  Would you treat JS as an outpatient or inpatient? Explain your choices.

• The best option for this patient is to go to the hospital (treat as an inpatient). I would do this because of the marked increase in symptoms as well as the possible comorbidities in question.  I would provide supplemental oxygen and also probably give a bronchodilator (beta 2 agonist) in order to increase oxygenation. If the patient is positive for pneumonia an antibiotic would also be taken.

Would you be concerned that the patient takes a beta blocker? Why?  Advise the patient to stop taking the beta blocker? (Look it up)

• The fear with beta-blockers is a cross reaction with beta agonists that are being taken. This is largely dependent on what type of beta-blocker is being taken. As long as the beta-blocker is cardio-specific there shouldn’t be any issue. Currently, according to the medication list, the patient is taking Metoprolol, which is cardio-specific and therefore is not a problem. However an additional beta-blocker is listed on the medications list as just “beta blocker.” It needs to be further investigated if this medication is the different than the Metoprolol  (in which cardio-specificity needs to be investigated) or if this was just a mistake due to the fact that the patient was confused when providing the history and medications and did not know that Metoprolol was the beta-blocker he was taking.[6]

What do you think about the possibility of using non-invasive positive pressure ventilation (bi-level positive airway pressure or BiPAP) in this patient?

• Using BiPAP in this patient would most probably have positive effects on this patient as BiPAP is frequently used in patients with pulmonary issues such as COPD, especially during exacerbations like this patient is having.

What is the main difference between bi-level positive airway pressure (BiPAP) and continuous positive airway pressure (CPAP)?  What are the indications for using these different modes of non-invasive mechanical ventilation?

• The main difference between BiPAP and CPAP is that BiPAP delivers two different level of air pressure (one higher for breathing in and one lower when breathing out) at varying intervals and CPAP only delivers one air pressure continues.  CPAP has been used to treat issues such as sleep apnea, pneumonia, and pulmonary edema. BiPAP is more common for lung issues such as COPD, or instances when CPAP has failed. [7] [8]

References:

[1] Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease  (2011). Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute].

[2] MacNee, W. (2006). Pathology, pathogenesis, and pathophysiology. BMJ : British Medical Journal, 332(7551), 1202–1204.

[3] Ali Al Talag, MD, Pearce Wilcox, MD. Clinical physiology of chronic obstructive pulmonary disease. BCMJ, Vol. 50, No. 2, March, 2008, page(s) 97-102 — Articles.

[4] Hawkins, N. M., Petrie, M. C., Jhund, P. S., Chalmers, G. W., Dunn, F. G., & McMurray, J. J. V. (2009). Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology. European Journal of Heart Failure, 11(2), 130–139. http://doi.org/10.1093/eurjhf/hfn013

[5] The Relationship between COPD and Heart Problems. (n.d.). Retrieved from https://lunginstitute.com/blog/the-relationship-between-copd-and-heart-problems/

[6] Ghanei, M., & Taheri, S. (2013). β-Blockers or β–Agonists. That’s the Question in the COPD Management. J Pulmon Resp Med S, 4.

[7] Brochard, L., Mancebo, J., & Elliott, M. W. (2002). Noninvasive ventilation for acute respiratory failure. European Respiratory Journal, 19(4), 712–721. http://doi.org/10.1183/09031936.02.00295502

[8] Renston, J. P., DiMarco, A. F., & Supinski, G. S. (1994). REspiratory muscle rest using nasal bipap ventilation in patients with stable severe copd. Chest, 105(4), 1053–1060. http://doi.org/10.1378/chest.105.4.1053