Sharpening Occam’s Razor – A Diagnostic Dilemma

Payal Sen, MD¹

Uddalak Majumdar, MD²

Patrick Rendon, MD¹

Ali Imran Saeed, MD¹

Akshay Sood, MD¹

¹University of New Mexico

Albuquerque, NM US

²Cleveland Clinic Foundation

Cleveland, OH USA

Abstract

Objective: Physicians often search for Occam’s Razor, that is, to have a single diagnosis explain all clinical manifestations in an individual patient. Herein, we describe a case which was significant for a dual clinical diagnosis, thus proving that Occam’s razor may not always hold true. 

Case Summary: A 22-year-old Caucasian man presented with 4 days history of fever, and dry cough. Chest x-ray revealed a right middle lobe pneumonia. Mycoplasma IgM antibody titer was significantly elevated (>1:320), using the rapid diagnosis enzyme-immunoassay (EIA) test, and clinical course was complicated by rhabdomyolysis. He was treated with oral azithromycin for 5 days. The patient however returned to the ER in 2 weeks with similar symptoms and repeat chest x-ray revealed a persistent right middle lobe infiltrate. Endobronchial biopsy revealed necrotizing granulomatous inflammation which stained positive for Histoplasma capsulatum. Serum complement fixation antibody test for Histoplasma demonstrated an elevated titer of 1:64. The patient was diagnosed to have an ‘atypical pneumonia due to sub-acute Histoplasma capsulatum and acute Mycoplasma Pneumoniae infections, complicated by rhabdomyolysis.’

Discussion: This case is unusual because the patient had an acute community-acquired atypical pneumonia from Mycoplasma pneumoniae, complicated by rhabdomyolysis, and also had subacute Histoplasma pneumonia. Physicians often search for Occam’s Razor. However, following Hickam’s dictum, we made the unusual diagnosis of concomitant lung infection in an immunocompetent host with Mycoplasma pneumoniae and Histoplasma capsulatum. 

Conclusion: This was an immunocompetent patient who ran a complex, protracted, and unusual course of community acquired pneumonia. Often, the pursuit of additional or alternative diagnoses may require repeated and multiple invasive diagnostic sampling. Occam’s razor may not always hold true.

Introduction

Occam's razor proposes that the simplest explanation is usually the correct one. However, in the science of medicine, simple solutions may be elusive. Often there is an incredibly complex constellation of symptoms co-occurring with one another, thereby confounding the scientific community. We described the diagnostic conundrums in managing our patient who ran a complex protracted course of community acquired pneumonia.

Case

A 22-year-old Caucasian male college student with no significant past medical history, initially presented to the University hospital in New Mexico, United States, with 4 days’ history of fever, dry cough, and dyspnea. He had recently returned from a family vacation in Illinois and had spent several weeks fishing on the Mississippi river. Review of systems was negative for chest pain, headache, fever, chills, or night sweats. He denied any sick contacts. He did not smoke and did not use recreational drugs. His grandfather, who had been a heavy cigar smoker, had died of lung cancer.

His vital signs were significant for a body temperature of 100.6° Fahrenheit, respiratory rate of 32 breaths per minute, pulse rate of 94 bpm, blood pressure of 130/82 millimeters of mercury, and pulse oximetry of 90 percent on room air. Physical examination demonstrated that he was in mild respiratory distress. Chest auscultation revealed decreased breath sounds over the right mid to lower lung field. The rest of his physical examination was otherwise unremarkable. 

His laboratory tests revealed a normal complete blood count with a hematocrit of 40.5%, white blood cell count of 8,200 cells per microliter, and platelet count of 263,000 per microliter.  His electrolyte levels showed a serum sodium of 136 mEq per liter, potassium of 3.4 mEq per liter, chloride of 100 mEq per liter, bicarbonate of 21 mEq per liter, blood urea nitrogen of 15 mg/dL and creatinine of 0.9 mg/dL. His blood glucose was normal at 98 mg/dL. His urine analysis revealed 3+ blood without red blood cells. His liver function tests demonstrated an elevated aspartate aminotransferase at 244 units per liter, elevated alanine aminotransferase at 72 units per liter, with normal total bilirubin, albumin, and alkaline phosphatase levels. His serum creatinine kinase (CK) was highly elevated at 26,000 units per liter (normal reference range 39-308 units per liter). His arterial blood gas at rest on room air at an elevation of 5500 feet above sea level showed acute respiratory alkalosis with a normal alveolar arterial gradient with a pH of 7.57, PaCO2 of 28 mmHg, PaO2 of 77 mmHg, and bicarbonate of 22 mEq per liter.  His mycoplasma IgM antibody titer was significantly elevated (> 1:320) using the rapid diagnosis enzyme-immunoassay (EIA) test. Anti-mycoplasma pneumoniae IgA was also elevated. The urinary legionella and pneumococcal antigen levels, sputum culture, blood cultures, and urine toxicology screen were negative. Chest radiograph revealed a right middle and lower lobe pneumonia (Figure 1). 

Figure 1. CXR revealed right mid and lower lobe pneumonia.

The patient was diagnosed with sepsis secondary to Mycoplasma pneumoniae infection of the lungs, with the added complication of rhabdomyolysis. He was treated with intravenous followed by oral azithromycin 500 mg daily for 5 days and given intense hydration therapy. Within 48 hours, his low-grade fever subsided, CK decreased to 1000 units per liter, and the patient felt better. He was then discharged on Day 3 of hospitalization.

The patient however returned to the emergency department 2 weeks after discharge with persistent cough, chest discomfort, and loss of wellbeing. Repeat chest radiograph revealed a persistent right lower lobe infiltrate. Computed tomography (CT) scan of the chest revealed a right lower lobe consolidation with surrounding nodular opacities with a possible endobronchial lesion in the right lower lobe (Figure 2).

Figure 2. Panel A: Coronal view of thoracic CT scan showing right lateral basilar segment consolidation. Panel B: Axial view showing consolidation in the right lower lobe with surrounding nodular opacities.

He underwent bronchoscopy which revealed a mass-like endobronchial lesion in the lateral basilar segmental bronchus of the right lower lobe (Figure 3).

Figure 3. Bronchoscopy revealing a mass-like endobronchial lesion in a lateral segmental bronchus of the right lower lobe.

Endobronchial biopsy revealed necrotizing granulomatous inflammation and stained positive for the yeast form of Histoplasma capsulatum.  Serum complement fixation antibody test for Histoplasma demonstrated an elevated titer of 1:64. Acid fast bacilli were not seen on smear or culture and cytology and histopathology tests did not reveal malignancy.

The patient was diagnosed with an atypical pneumonia due to sub-acute Histoplasma capsulatum and acute Mycoplasma Pneumoniae infections, complicated by rhabdomyolysis. The mycoplasma infection and rhabdomyolysis had already been treated and resolved. For the subacute pulmonary histoplasmosis, the patient was treated with 10 weeks of oral itraconazole. Post treatment clinic follow-up revealed resolution of symptoms and radiological abnormalities.

Discussion

Mycoplasma pneumoniae is a common causative pathogen for community-acquired pneumonia in both children and adults (1).  Apart from respiratory tract symptoms, it is associated with a variety of extra-pulmonary manifestations (2). Recognizing this association can lead to timely diagnosis and treatment of both the mycoplasma infection and its complications. In this case report, we also want to highlight the fact that infection with endemic mycoses can often be mistaken for community acquired pneumonias, and thus having a high index of suspicion for fungal infection is very important, even in immunocompetent patients (3), to prevent a delay in treatment. Physicians often search for Occam’s Razor, i.e., to have a single diagnosis explain all clinical manifestations in an individual patient. This case is significant because of a dual clinical diagnosis, thus proving that Occam’s razor may not always hold true in an individual patient.

Mycoplasma infection can cause several unusual extra-pulmonary manifestations such as hemolytic anemia, immune thrombocytopenic purpura, transverse myelitis, Guillain-Barre syndrome, acute hepatitis and arthritis (4). Another lesser known complication of mycoplasma infection is rhabdomyolysis (5). Rhabdomyolysis is a syndrome caused by injury to the skeletal muscles, thereby resulting in leakage of myoglobin into blood (6). The classic triad of mycoplasma infection consists of myalgias, pigmenturia, and generalized muscle weakness, but this classic triad is seen in less than 10 percent of infected patients (7). Acute renal failure due to acute tubular necrosis as a result of mechanical obstruction by myoglobin is the most common complication, in particular if the serum CK level is >16,000 IU/l, which may be as high as 100,000 IU/l (8). In addition to mycoplasma infection, more common causes of rhabdomyolysis are trauma, immobilization, and recreational drug and alcohol use (9). 

Other organisms known to cause rhabdomyolysis are Influenza A and B virus, Coxsackie virus, Epstein-Barr virus, Primary Human Immunodeficiency virus, Legionella species, Staphylococcus aureus, and Streptococcus pyogenes (9). With respect to Mycoplasma pneumoniae infection, a possible mechanism for rhabdomyolysis is the induction of inflammatory cytokines, such as tumor necrosis factor-alfa (TNF-α) and interleukin-1 (IL-1), which may cause proteolysis of skeletal muscles (10). 

The rapid and reliable diagnosis of Mycoplasma pneumoniae (Mp) enables the correct and prompt use of antibiotics. Methods for identifying Mp infection include culture, molecular detection of pathogen specific antigen or nucleic acid, and serological analysis (11). Each of these methods has its pros and cons. Culture is the definitive method for diagnosis and is critical for monitoring trends in epidemiology but is slow and requires specialized media and trained personnel (11). Although molecular methods for nucleic acid or antigen detection have emerged as the primary techniques for identification of MP pneumoniae in surveillance programs, adoption of these methods is still lagging behind in USA.

Serologic analysis can prove to be problematic due to poor sensitivity and specificity, and the inability to characterize the specific Mp strain. Having said that, most physicians in the United States continue to rely on serological testing in concordance with the IDSA guidelines (11). It is well known that a single serologic test is of limited value in the early diagnosis of mycoplasma pneumoniae since there are often no IgM antibodies in the early stage of infection, and these IgM antibodies may persist long after the infection (12). However, if these IgM antibodies are present along with anti-Mycoplasma pneumoniae IgA, it is usually indicative of recent primary mycoplasma pneumoniae infection (13). A single high Mp-specific antibody titer (> 1:320) has been regarded as a diagnostic marker of mycoplasma pneumoniae, although it is present in only about 30 percent of the patients (12). Since our hospital relies on serological testing, we tested for the specific Mycoplasma pneumoniae IgM and IgA, both of which were positive. The MP-specific antibody titer was also greater than 1:320, thus signifying it indeed was early MP infection.

Symptoms of Mp infection generally resolve within 3–4 weeks after disease onset but can be shortened with antibiotic therapy; macrolides and doxycycline are the mainstay of this treatment (14). The mainstay for the prevention of pigment-induced acute kidney injury is the correction of volume depletion, prevention of intratubular cast formation, and the treatment of the underlying cause of rhabdomyolysis (4). This is done by aggressive fluid resuscitation resulting in increased renal blood flow and thus increasing the urinary flow with consequential wash out of partially obstructing tubular casts (4). Physicians will be served well to watch out for mycoplasma associated rhabdomyolysis in patients with atypical pneumonia and manifestations like myalgia, elevated aminotransferase levels, and myoglobinuria. 

Moving on to the second teaching point, endemic mycoses like coccidioidomycosis, histoplasmosis, and blastomycosis are often overlooked causes for community acquired pneumonia, particularly when immunocompetent patients travel out of the endemic zones (15). Often, testing is not even performed until the patient has failed to improve on antibacterial therapy. Delays in recognition, diagnosis and proper treatment may lead to disastrous outcomes (3). Performance of fungal antigen testing on bronchial washings or lavage fluid may improve the sensitivity for diagnosis over microscopic examination and the speed of diagnosis over culture even though isolation of the fungus by culture remains the gold standard method for definitive diagnosis (16). In this case, our patient was previously treated as mycoplasma pneumonia, thus leading to prolonged symptom course from histoplasmosis.

This case is unusual because the patient had an acute community-acquired atypical pneumonia from Mycoplasma pneumoniae, complicated by rhabdomyolysis, and also had subacute Histoplasma pneumonia. Physicians often search for Occam’s Razor, a principle from philosophy that when presented with competing hypothetical answers to a problem, one should select the one that makes the fewest assumptions.  Countering

Occam’s Razor, Dr. John Hickam said “Patients can have as many diseases as they damn well please!” (17). Following Hickam’s dictum, we made the unusual diagnosis of concomitant lung infection in an immunocompetent host with Mycoplasma pneumoniae and Histoplasma capsulatum.

Conclusion

With this case report, the authors wish to highlight two important teaching points. The first being that rhabdomyolysis is a serious but treatable extrapulmonary complication of Mycoplasma pneumoniae infection of the lungs. Having a high index of suspicion can limit treatment delay for rhabdomyolysis caused by mycoplasma infection and will therefore limit consequential morbidity like renal insufficiency. The second point that the authors wish to emphasize is that endemic fungal infection can often be mistaken for bacterial and viral community-acquired pneumonia in an immunocompetent host, particularly when they present with symptoms outside the endemic zone, thus delaying timely management. Hence one should have a high suspicion for fungal infection in immunocompetent hosts with unusual presentations such as history of travel to endemic zone, chronicity of symptoms, lack of response to therapy for community-acquired pneumonia, nodular lung lesions, and endobronchial abnormalities.

References

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15. Valdivia L, Nix D, Wright M, Lindberg E, Fagan T, Lieberman D, Stoffer T, et al. Coccidioidomycosis as a common cause of community-acquired pneumonia. Send to Emerg Infect Dis. 2006 Jun;12(6):958-62. [CrossRef] [PubMed]
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Cite as: Sen P, Majumdar U, Rendon P, Saeed AI, Sood A. Sharpening Occam's razor-a diagnostic dilemma. Southwest J Pulm Crit Care. 2018;16(6):324-31. doi: https://doi.org/10.13175/swjpcc061-18 PDF 

Interval Development of Multiple Sub-Segmental Pulmonary Embolism in Mycoplasma Pneumoniae Bronchiolitis and Pneumonia

Peter V. Bui¹

Sapna Bhatia²

Ali I. Saeed²

¹Department of Internal Medicine

²Division of Pulmonary, Critical Care, and Sleep Medicine

The University of New Mexico

Albuquerque, NM, USA

Abstract

Introduction: Cases of pulmonary embolism (PE) concurrent with Mycoplasma pneumoniae infection are rare in the medical literature. We describe a patient with M. pneumoniae bronchiolitis and pneumonia who developed multiple right-sided, sub-segmental PE.

Case Description: A 54-year-old man presented following one week of respiratory and constitutional symptoms. He was admitted for respiratory distress and started on ceftriaxone, azithromycin, and oseltamivir. Because of a lack of clinical improvement, antibiotics were escalated to vancomycin and piperacillin-tazobactam. M. pneumoniae IgM and IgG serologies returned positive, and antibiotics were narrowed to azithromycin, with clinical improvement and gradual decrease in supplemental oxygen requirement. One week into the hospitalization, the patient abruptly developed an increased oxygen requirement. Computed tomography angiography (CTA) of the chest found stable M. pneumoniae bronchiolitis and pneumonia and the interval development of multiple right-sided, sub-segmental PE. He was treated with unfractionated and then low-molecular-weight heparin as a bridge to warfarin, azithromycin, and a prednisone taper. In the outpatient setting, repeat CTA revealed resolution of M. pneumoniae infection and PE. 

Discussion: Although the mechanism and association are unclear, other case reports have proposed that M. pneumoniae infection promotes hypercoagulability or a prothrombotic state, predisposing patients to thromboembolism. In a patient with M. pneumoniae infection who develops sudden respiratory distress or failure despite appropriate treatment, clinicians should have a high suspicion for PE, and a CTA should be considered as part of further evaluation.

Introduction

Mycoplasma pneumoniae is one of thirteen Mycoplasma species isolated from humans and less commonly causes lower respiratory tract infections, of which atypical pneumonia occurs at higher rates (1). These lower respiratory tract infections have been reported to present similarly to other disease processes such as asthma and pulmonary embolism (PE) (2, 3). M. pneumoniae pneumonia typically has a benign course with low mortality. A study by von Baum et al. found a mortality of 0.7% in patients with M. pneumoniae pneumonia, with the deaths occurring in hospitalized patients (4). Despite this low mortality, rare complications may contribute to morbidity and mortality, although to what degree, if any, is unclear. A case report in the medical literature describes a PE and a hypercoagulable state associated with M. pneumoniae pneumonia in an adult during the peri-infectious period (5). We present a case with radiographic evidence of the interval development of multiple segmental PE in a patient with M. pneumoniae bronchiolitis and pneumonia.

Case Description

A 54-year-old man with a 15-pack-year smoking history, positive purified protein derivative treated with isoniazid, occupational exposures including asbestos and dust, and a current history of ethanol abuse presented to the emergency department with a one-week history of a productive cough with yellow sputum, weakness, shortness of breath, and dyspnea on exertion. He also noticed diffuse papular cutaneous lesions over his back.

In the emergency department, he was hypoxic with a need for supplemental oxygen. Cardiopulmonary examination was unremarkable. Initial laboratory studies including complete blood count, chemistry panel, and hepatic function panel were notable for a leukocytosis of 13.6 k/μL with a neutrophilia of 83%, aspartate transaminase of 108 units/L, alanine transaminase of 152 units/L, alkaline phosphatase of 175 units/L, and total bilirubin of 1.5 mg/dL, and creatine kinase of 563 units/L. Conventional chest radiograph (Figure 1) showed a left lower lobe infiltrate.

Figure 1. Conventional chest radiograph on day zero of the hospitalization. The images show a left lower lobe infiltrate.

The patient was admitted to the hospital and started on ceftriaxone and azithromycin for community-acquired pneumonia as well as oseltamivir over concerns for influenza.

During the initial hospitalization, the patient required supplemental oxygen for hypoxia with a rapid increase in fractional inspired oxygen (F_iO₂) to maintain oxygen saturation above 90%. Because of a lack of clinical improvement, antibiotics were broadened to include vancomycin and piperacillin-tazobactam. Since he continued to require a F_iO₂ of 60% on day four of the hospitalization, additional workup for atypical bacterial, viral, and fungal pathogens were performed after consultation with pulmonology. Acid-fast bacillus cultures and stains were negative. Sputum cultures were not obtained. An arterial blood gas prior to evaluation by Pulmonology found a pH of 7.42, partial pressure of carbon dioxide of 38 mmHg, partial pressure of oxygen of 86 mmHg, HCO₃ of 24 mmol/L, and F_iO₂ of 95%. Computed tomography (CT) of the chest (Figure 2) showed extensive bronchiolitis with focal areas of consolidation involving bilateral lower lobes.

Figure 2. Computed tomography of the chest on day four of the hospitalization. The image shows an extensive bronchiolitis with focal areas of consolidation involving bilateral lower lobes.

Oseltamivir was discontinued after the respiratory viral panel returned negative. Broad spectrum antibiotics were narrowed to azithromycin after M. pneumoniae IgM and IgG serologies returned positive. His oxygen requirement gradually improved over the next two days, and he was transitioned to nasal cannula.

On day seven of his hospitalization, the patient suddenly developed moderate respiratory distress with an increase in oxygen requirement. CT angiography (CTA) of the chest (Figure 3) done at this juncture showed unchanged parenchymal findings with interval development of multiple sub-segmental pulmonary emboli in the right lung.

Figure 3. Computed tomography angiography of the chest on day five of the hospitalization. The images show unchanged parenchymal findings with interval development of multiple sub-segmental pulmonary emboli in the right lung (see white arrows in Figure 3A).

Doppler ultrasound found no evidence of deep venous thrombosis (DVT) in both lower extremities. He was subsequently started on therapeutic anticoagulation with unfractionated heparin and then low-molecular-weight heparin as a bridge to warfarin. The patient subsequently improved on a 14-day course of azithromycin 500 mg orally once daily and 3-month tapered course of prednisone 60 mg orally once daily for M. pneumoniae infection, a 3-month course of warfarin for the PE, and supplemental oxygen. During follow-up in the outpatient setting, CTA of the chest showed the infection and PE to have resolved, and all therapies related to the infection and PE were discontinued.

Discussion

We herein describe a case of M. pneumoniae bronchiolitis and pneumonia complicated by right-sided PE. The reported occurrences of venous thromboembolism (VTE) during M. pneumoniae infection are limited to case reports. In our review of the literature, we found one case of M. pneumoniae infection associated with PE in the adult population. Ascer et al. (5) presented the case of a 28-year-old male with right-sided pneumonia and right-sided PE who was found to have antiphospholipid antibodies. For the PE, this patient was successfully treated with recombinant tissue-type and plasminogen activator and heparin and was discharged with hydroxychloroquine sulphate, aspirin, and warfarin. However, Ascer did not publish additional follow up for this seemingly prothrombotic state. In a case without PE, Senda et al. (6) reported on a 21-year-old patient with a left middle cerebral artery embolus and DVT in bilateral femoral veins in the setting of a M. pneumoniae infection. This patient had a transient increase in prothrombin time, partial thromboplastin time, fibrin/fibrinogen degradation products, thrombin-antithrombin III-complex, antiphospholipid antibodies, and IgM anticardiolipin antibodies and decrease in protein C activity.

The pediatric medical literature has additional case reports linking M. pneumoniae to PE. Brown et al. (7) described a 6-year-old male child with M. pneumoniae pneumonia, right-sided ileofemoral thrombosis, and right-sided PE found to have anticardiolipin IgG and IgM antibodies, lupus anticoagulant, and acquired activated protein C resistance. This prothrombotic state subsequently resolved after treatment of the infection with antibiotics and the PE with unfractionated heparin and then dalteparin. In another case report, during workup for a 13-year-old male child with right-sided PE in the setting of a left lower lobe M. pneumoniae pneumonia, Graw-Panzer et al. (8) found lupus anticoagulant, anticardiolipin IgG and IgM antibodies, and an underlying protein S deficiency. The transient prothrombotic markers returned to normal levels during subsequent follow-up for his acute illness.

M. pneumoniae pulmonary infections have been reported in the pediatric medical literature to be associated with an underlying hypercoagulability. Creagh et al. (9) reported on a left femoral vein thrombosis in a 10-year-old female with M. pneumoniae pneumonia who was found to have type I familial antithrombin III deficiency. In another case report of two children describing splenic infarcts associated with M. pneumoniae pneumonia, Witmer et al. (10) found elevated D-dimer, lupus anticoagulant, and elevated anticardiolipin and β2-glycoprotein antibodies that resolved following successful treatment of the infection with antibiotics and a three-month course of anticoagulation and, in one patient, an additional course of aspirin (10). No specific etiology was found for the infarctions, but Witmer et al. attributed the infarctions to possible thrombosis. Other case reports in the pediatric literature that found antiphospholipid antibodies include a patient with cardiac thrombus and internal carotid artery occlusion (11, 12). However, in their report of right popliteal artery thrombosis in a 5-year-old male child with M. pneumoniae pneumonia and right popliteal artery thrombosis, Joo et al. (13) did not find abnormalities in their limited hypercoagulability workup.

Our lack of hypercoagulability workup limits comparison with the available medical literature. We did not perform a hypercoagulability workup because the patient did not meet any Wells criteria and did not have a family history of hypercoagulability. Based on the available case reports, the underlying pathophysiology can be inferred to be related to a transient formation of antiphospholipid antibodies during a M. pneumoniae infection. Additionally, the thromboembolism can be expected to occur within a short period of time following the onset of symptoms. The rate that hypercoagulability occurs in infected patients and the practical clinical relevance of such a prothrombotic state without or without an inherited or congenital deficiency are unknown at this time. These questions would benefit from further investigation.

An alternative interpretation is a preexisting hypercoagulability may predispose patients to M. pneumoniae infection, which can exacerbate the hypercoagulability, further increasing the risk of VTE. This interpretation may be relevant for the patients of Graw-Panzer et al. (8) and Creagh et al. (9) who had underlying hypercoagulable conditions and subsequently suffered M. pneumoniae infection and then developed VTE. The Worcester Venous Thromboembolism study found an association between infection and VTE, and Rosendaal’s review of the literature found an association between hypercoagulability and increased risk of thrombosis (14-16). With the available case reports and epidemiological studies, this alternative interpretation has not been elucidated.

In this report, we described the interval development of PE in a patient with M. pnuemoniae bronchiolitis and pneumonia. The mechanism for the hypercoagulability during M. pneumoniae infection is unclear. A CTA of the chest should be obtained if a patient with M. pneumonia infection fails to show clinical improvement or suddenly develops clinical worsening of his or her respiratory status, so as to exclude PE. However, clinicians should take into account that Mycoplasma pneumonia may present with the symptoms of PE (3).

Acknowledgements

We would like to acknowledge Cecelia Kieu for assisting in the preparation of the figures for this manuscript.

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16. Spencer FA, Emery C, Lessard D, Anderson F, Emani S, Aragam J, Becker RC, Goldberg RJ. The Worcester Venous Thromboembolism study: a population-based study of the clinical epidemiology of venous thromboembolism. J Gen Intern Med. 2006;21(7):722-7. [CrossRef] [PubMed]

Cite as: Bui PV, Bhatia S, Saeed AI. Interval development of multiple sub-segmental pulmonary embolism in Mycoplasma pneumoniae bronchiolitis and pneumonia. Southwest J Pulm Crit Care. 2015;11(6):277-83. doi: http://dx.doi.org/10.13175/swjpcc152-15 PDF 

December 2014 Pulmonary Case of the Month: Bronchiolitis in Adults

Kashif Yaqub, MD

Lewis J. Wesselius, MD

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 61-year-old man was admitted to the hospital with cough, dyspnea and hypoxemia. He had some prior respiratory symptoms about a month prior to admission, but his symptoms worsened recently. He was seen in Family Medicine Clinic on the day of admission and noted to have saturations of 88 – 89%.

A thoracic CT scan was done shortly after his initial symptoms but was negative for lung consolidation or pulmonary embolus. He currently was having fever with temperatures of 99 to 103 degrees and cough that was only slightly productive.

PMH, FH, SH

He had a history of hypertension and obstructive sleep apnea although he was not using continuous positive airway pressure (CPAP).

Medications

• nifedipine
• lisinopril/hydrochlorothiazide
• cough medication

Physical Examination

      General: SpO2 95% on 2l/min by nasal cannula

      Chest: his breath sounds were coarse, but there were no wheezes or crackles.       

      Cardiovascular: regular rate and rhythm with no murmur noted

      Extremities: no clubbing, cyanosis or edema.

      Skin: no rashes noted.

Laboratory

      CBC: Hemoglobin 15.1 d/dL,  WBC 15.3 x 10³ cells/µL, no eosinophilia.

      Procalcitonin: 0.22 ng/mL (normal < 0.15 ng/mL).    

      Nasopharyngeal swab: PCR negative for pertussis, chlamydophila and           mycoplasma pneumonia.

Radiography

His thoracic CT scan at the initial presentation of his illness about a month prior to admission was reviewed (Figure 1).

Figure 1. Representative images from thoracic CT scan in lung windows done about one month prior to admission.

Which of the following are appropriate at this time? (Click on the correct answer to proceed to the next panel)

1. Cocci serology
2. Empirically begin antibiotics for community-acquired pneumonia
3. Repeat the thoracic CT scan
4. Sputum culture
5. All of the above

Reference as: Yaqub K, Wesselius LJ. December 2014 pulmonary case of the month: bronchiolitis in adults. Southwest J Pulm Crit Care. 2014;9(6):297-301. doi: http://dx.doi.org/10.13175/swjpcc149-14 PDF