May 2018 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: A 79-year-old man with a past medical history significant for mild, intermittent asthma since childhood and mild aortic stenosis presents to the Emergency Room with fevers and chills for 5 days, associated with dry cough and dyspnea on exertion. His past medical history was otherwise relatively unremarkable, with coronary artery disease as evidenced by coronary artery calcium at a calcium scoring CT, hypothyroidism, and dyslipidemia. The patient has allergies to dust and penicillin, and his only medications included thyroid replacement, aspirin, and an albuterol inhaler as needed. He was a 15-pack-year smoker, quitting 30 years ago. His past surgical history was remarkable only for tonsillectomy, inguinal hernia repair, meniscal repair, and sigmoid colon resection for diverticular abscess 14 years earlier. The patient was afebrile, his heart rate was 96 beats / minute and regular, decreased breath sounds at the lung bases was noted, and the white blood cell count was normal. Electrocardiography showed no abnormalities. Oxygen saturation was 92% on room air. Frontal chest radiography (Figures 1A and B) was performed.

Figure 1. Frontal (A) and lateral (B) chest radiography.

Which of the following represents the most accurate assessment of the frontal chest imaging findings? (Click on the correct answer to proceed to the second of nineteen pages)

1. Chest frontal imaging shows bilateral pleural fluid collections
2. Chest radiography shows bilateral lower lobe bronchial wall thickening and patchy consolidation
3. Chest radiography shows cavitary lung disease
4. Chest radiography shows numerous small nodules
5. Chest radiography shows peribronchial and mediastinal lymphadenopathy

Cite as: Gotway MB. May 2018 imaging case of the month. Southwest J Pulm Crit Care. 2018;16(5):254-78. doi: https://doi.org/10.13175/swjpcc062-18 PDF 

Medical Image of the week: Chronic Pulmonary Histoplasmosis

Figure 1. Chest radiography showing upper lobe fibrosis and cavitation secondary to chronic histoplasmosis.

Histoplasmosis is endemic to the Midwest US and commonly causes an acute infection that presents as a subacute pneumonia.  In patients with underlying lung disease, particularly COPD, a subacute pneumonia can evolve into chronic pulmonary histoplasmosis and is characterized by persistent or recurrent pulmonary symptoms, progressive lung infiltrates, fibrosis, and cavitation. Upper lobe infiltrates and cavities are characteristic, resembling the findings in tuberculosis (Figure 1). Progression is manifested by cavity enlargement, increased fibrosis and bronchopleural fistulae.  Misdiagnosis delays therapy and can be catastrophic.  Histoplasmosis titers and sputum cultures are useful tests.  Bronchoscopy with bronchoalveolar lavage and transbronchial biopsy for culture may be needed when diagnosis remains elusive.

Kenneth S. Knox, MD¹ and Veronica A. Arteaga, MD²

¹Professor of Medicine

University of Arizona College of Medicine- Phoenix

Phoenix, AZ USA

²Associate Professor of Medicine

Medical Imaging

University of Arizona College of Medicine- Tucson

Tucson, AZ USA

Cite as: Knox KS, Artega VA. Medical image of the week: chronic pulmonary histoplasmosis. Southwest J Pulm Crit Care. 2017;14(3):88. doi: https://doi.org/10.13175/swjpcc022-17 PDF

Medical Image of the Week: Extrapleural Pneumolysis for Tuberculosis

Figure 1. PA (A)/Lateral (B) chest films showing a mass like opacity of the left upper lung field.

Figure 2. Representative image from the thoracic CT in soft tissue windows showing a well-circumscribed, oval-shaped, heterogeneous density within the left upper and mid anterior chest with some expansion and destruction of overlying ribs.

The advent of antibiotics revolutionized the management of tuberculosis, a disease that even in the 1950s was a top 10 cause of death in the United States. The first drug to be developed was streptomycin, approved after a clinical trial in 1946. The following decade saw the addition of ethambutol, rifampin, and isoniazid (1). Though we take for granted the use our multidrug regimens nowadays, physicians once had limited interventions for this frequent and devastating infection. Such interventions included surgical techniques to collapse the affected lobes, starving the mycobacterium of their preferred oxygen rich environment. One such technique was known as plombage, or extrapleural pneumolysis. Plombage is a term derived from the Latin for lead or plumbum and entails the insertion of a space occupying material into the pleural space with subsequent compression of the affected lung portion. This was seen as an alternative to the use of thoracoplasty, which required removal of multiple ribs allowing the chest wall to collapse, leading to deformity and a loss of lung function (2). Though rarely seen now, we present the imaging of an elderly female with endometrial cancer with lung metastasis who interestingly had undergone such a procedure when she developed cavitary tuberculosis as a teenager in 1952.

Tuffler first developed extrapleural pneumolysis in 1891; he placed fat into the pleural cavity reporting successful control of tuberculosis infection. The technique over the subsequent decades became popular especially as a response to the endemic tuberculosis seen post- the Second World War. Many attempts were made to designate an ideal inert material for use. Though unclear in our patient given the remote history of the procedure, published reports include placement of muscle, fat, air, mineral oil, gauze, paraffin, rubber sheeting, and even inflated Lucite balls. Fortunately, complications of the procedure, even decades later, are rarely seen now. Complications listed in the literature, however, do include infection, hemorrhage, fistula formation, migration of material, and even malignancy. Despite its popularity, there were mixed results in effectiveness and variable complication rates, in one series nearly 50% of patients developed an infection (3). In our patient, it was successful, with no history of recurrence with negative sputum and serologic testing. She did notably report having been treated with a long course of antibiotics as well.

Kareem Ahmad, MD

Department of Internal Medicine

Division of Pulmonary, Critical Care, Sleep, and Allergy Medicine

University of Arizona

Tucson, AZ, USA

References

1. Zumla A, Nahid P, Cole ST. Advances in the development of new tuberculosis drugs and treatment regimens. Nat Rev Drug Discov. 2013 May;12(5):388-404. [CrossRef] [PubMed]
2. Young FH. Extraperiosteal plombage in the treatment of pulmonary tuberculosis. Thorax. 1958; 13(2):130-5. [CrossRef] [PubMed]
3. Murphy JD, Elrod PD, et al. Surgical treatment of residual cavities following thoracoplasties for tuberculosis. Dis Chest. 1948 Sep-Oct;14(5):694-706. [CrossRef] [PubMed]

Cite as: Ahmad K. Medical image of the week: extraplerural pneumolysis for tuberculosis. Southwest J Pulm Crit Care. 2016;13(5):244-5. doi: https://doi.org/10.13175/swjpcc106-16 PDF

Medical Image of the Week: Pott’s Disease

Figure 1. Axial CT scan showing a heterogeneous dense mass-like consolidation in the medial aspect of the right lung apex (arrow).

Figure 2. MRI C-spine (axial T2-weighted images). Panel A: soft tissue marrow edema surrounding the posterior process of the C7 vertebral body and it’s contiguous with a heterogeneous infiltrative process of the right medial lung apex (arrow).  Panel B: C7 vertebral body compression (arrow).

Figure 3. Right upper lung biopsy showing necrotizing granulomas (arrow) and histiocytes aggregates.

A 22 year-old man with a history of asthma presented with a two-month history of progressive right upper extremity weakness with back pain, weight loss, and night sweats. CT scan of the chest revealed mass-like infiltrative mass in the right lung apex with mediastinal and hilar lymphadenopathy (Figure 1). An MRI cervical spine showed a large infiltrating process at the right medial lung apex with vertebral body compression (Figure 2).

A CT-guided lung biopsy was performed and it showed necrotizing granulomatous inflammation (Figure 3). Pott’s disease was diagnosed and the patient started on anti-tuberculous treatment with a good recovery.

Pott’s disease is a common cause of spinal infection and its clinical presentations are nonspecific. Early findings on imaging may reveal loss of vertebral body height, bone sequestration, sclerosis, and paraspinal mass with calcification (1).  A diagnosis of this condition must be made early as prompt treatment may reduce significant morbidity such as spine deformities to neurologic deficits.

Choua Thao MD¹, David G. Kuykendall MD², Matthew P. Schreiber MD, MHS⁴, and Carmen Luraschi MD³

University of Nevada School of Medicine: Las Vegas

¹Department of Internal Medicine

²Department of Family Medicine

³Division of Pulmonary and Critical Care

Las Vegas, NV

⁴MedStar Georgetown University Hospital/Washington Hospital Center, Washington, DC

Reference

1. Rivas-Garcia A, Sarria-Estrada S, Torrents-Odin C, Casas-Gomila L, Franquet E. Imaging findings of Pott's disease. Eur Spine J. 2013;22:567-78. [CrossRef] [PubMed]

Reference as: Thao C, Kuykendall DG, Schreiber MP, Luraschi C. Medical image of the week: Pott's disease. Southwest J Pulm Crit Care. 2015;11(1):36-7. doi: http://dx.doi.org/10.13175/swjpcc066-15 PDF 

A Bad Back Needs Help

Reference as : Gopal V, Robbins RA, Gotway MB. A bad back needs help. Southwest J Pulm Crit Care 2011;3:19-24. (Click here for a PDF version)

Case Presentation

History of Present Illness

A 61-year-old man was admitted to the hospital with a 2 month complaint of atraumatic back pain, worsening over the previous two weeks. The patient described his pain as sharp, 10/10 in intensity, radiating to his ribs, right hip, and right groin, and aggravated by coughing, weight lifting, and movement. His pain was worse in the supine and prone positions, with some relief provided by sitting, and relieved with high doses of pain medications, topical lidocaine, menthol-containing skin ointments, and chiropractic adjustments. Over the 2 days prior to admission, the patient became increasingly desperate as a result of his pain, and drank several pints of vodka.

Past Medical and Social History

The patient is a retired machinist whose medical history includes fibromyalgia and binge drinking. He smokes three-quarters of a pack of cigarettes per day.

Physical Examination

Physical examination showed normal vital signs and there was pain to palpation over the thoracic spine but no pinpoint tenderness or vertebral abnormalities. Back extension was limited, although flexion was 100 degrees. Lateral flexion was limited by pain equally bilaterally. Neurological examination was normal.

Laboratory Evaluation

Admission laboratory values included complete blood count, showing a normal white blood cell count but a normocytic, normochronic anemia, with a hemoglobin of 8.4 mg/dL and an elevated platelet count of 454,00 cells/µL. Serum chemistries showed an elevated glucose of 295 mg/dL and modest hypokalemia of 3.4 mmol/L. Liver enzymes were all modestly elevated. Urine analysis showed glycosuria of 150-200 mg/dL and microscopy showed 13 red blood cells per high-power field. Cultures of blood and urine were negative. Material obtained for sputum specimen was deemed inadequate for evaluation.

Radiographic Evaluation

Admission chest radiography (Figure 1, lateral projection) and thoracic spine magnetic resonance imaging (Figure 2) was performed.

Figure 1: Lateral projection from a frontal and lateral chest radiographic examination shows compression fractures involving the mid-thoracic spine.

 

Figure 2: Thoracic spine sagittal T2-weighted magnetic resonance imaging shows loss of normal height of approximately one-third of the normal vertebral body height at T8-T9.

The patient was taken to the operating room for drainage of a paraspinal abscess, and biopsies and cultures from material obtained at the T8-T9 levels were performed- these cultures were negative. Nearly one month later, the spine was stabilized with rods and screws and the biopsies and cultures were repeated. These cultures eventually grew Mycobacterium tuberculosis and anti-tuberculous therapy was initiated.

Questions and Discussion

Which of the following drug regimens would be appropriate therapy for this patient?

1. Stop the isoniazid
2. Continue the present regimen
3. Add a fluoroquinolone
4. Add an aminoglyoside
5. Add linezolid

Tuberculous spondylitis, also known as Pott’s disease, results from hematogenous spread of tuberculosis from an extraspinal source (1).  The infection typically involves the anterior aspect of the vertebral body, beginning within the subchondral plate, and spreads within the subligamentous space to involve an adjacent vertebral body. In adults, because the intervertebral disc is relatively avascular, the intervening disc space is typically secondarily involved by infection, resulting in discitis in addition to osteomyelitis. In contrast, in children, the intervertebral disc space is relatively vascular and may be the primary site of infection. Disc space involvement in patients with tuberculous spondylitis typically occurs late in the disease course, in contrast to pyogenic discitis and osteomyelitis. As the vertebral body becomes progressively destroyed, loss of vertebral height ensues, producing the development of the kyphosis, or gibbus deformity, typical of this disorder. Tuberculous spondylitis typically involves several vertebral body levels and relatively spares the discs spaces and posterior elements, in contrast to pyogenic discitis and osteomyelitis. Spread of infection into the adjacent psoas muscles is common, often producing fluid collections that are detectable on cross sectional imaging. Calcification may develop within these collections and is pathognomonic of tuberculous infection.   

The indolent nature of tuberculous osteomyelitis and septic arthritis often leads to delayed or overlooked diagnoses. The most common symptom of tuberculous spondylitis is local pain, becoming increasingly over weeks to months, and occasionally associated with muscle spasm and rigidity. Constitutional symptoms, fever, and weight loss are present in less than 40% of patients (1). The most important potential complication of tuberculous spondylitis is spinal cord compression during the active phase of the infection, resulting in paraplegia. In countries where the incidence of tuberculosis is low, the diagnosis of tuberculous spondylitis is often significantly delayed due to a low index of suspicion (2). Unfortunately, the presentation of tuberculous spondylitis also tends to be late in highly endemic areas as a result of poor access to medical care and/or poverty; in this setting, 40-70% of patients with tuberculous spondylitis have symptoms and signs of spinal cord compression at the time of diagnosis.

The American Thoracic Society, Centers for Disease Control, and Infectious Disease Society of America recommends 4 drug therapy for initial treatment of tuberculous spondylitis (1). Therefore in the question above, response #4 is correct. Treatment for tuberculous spondylitis for a minimum of 6 months is recommended, but usually 12-18 months is typical, with even longer treatment for slowly responding patients.

This patient responded well to therapy, although his wife, a naturopath, felt he was taking too much medication. After several months of therapy, drug sensitivity results became available, showing that the organism in this patient was resistant to isoniazid at 0.2 micrograms/ml, but sensitive at 1.0 microgram/ml.

What should be done next?

1. Stop the isoniazid
2. Continue the present regimen
3. Add a fluoroquinolone
4. Add an aminoglyoside
5. Add linezolid

Some experts favor continuing isoniazid in the setting of "low-level" isoniazid resistance, i.e., resistant to a concentration of 0.2 micrograms/mol but sensitive to 1.0 micrograms/mL (2). Others favor addition of fluoroquinolone to this regimen for the duration of therapy (3). Regardless, close observation, usually with directly observed therapy, is probably prudent. Therefore, either answers #2 or #3 is correct. The patient was continued on his present regimen and continues to make slow clinical progress.

Venu Gopal, MD

Chief, Infectious Disease

Phoenix VA

Richard A. Robbins, MD

Phoenix Pulmonary and Critical Care Medicine

Research and Education Foundation

Michael B. Gotway, MD

Scottsdale Medical Imaging

References

1. McDonald M, Sexton DJ. Skeletal tuberculosis. UpToDate (accessed 7-28-11).  Available at http://www.uptodate.com
2. Nussbaum ES, Rockswold GL, Bergman TA, Erickson DL, Seljeskog EL. Spinal tuberculosis: a diagnostic and management challenge. J Neurosurg 1995;83:243-7.
3. Blumberg HM, Burman WJ, Chaisson RE, et al. American Thoracic Society/Centers for Disease Control and Prevention/Infectious Diseases Society of America: treatment of tuberculosis. Am J Respir Crit Care Med 2003;167:603-62.
4. Berning SE, Peloquin CA. Antimycobacterial agents: Isoniazid. In: Antimicrobial Therapy and Vaccines, Yu V, Merigan T, Barriere S (Eds), Williams and Wilkins, Baltimore 1998.
5. Dorman SE, Johnson JL, Goldberg S, Muzanye G, Padayatchi N, Bozeman L, Heilig CM, Bernardo J, Choudhri S, Grosset JH, Guy E, Guyadeen P, Leus MC, Maltas G, Menzies D, Nuermberger EL, Villarino M, Vernon A, Chaisson RE, Tuberculosis Trials Consortium. Substitution of moxifloxacin for isoniazid during intensive phase treatment of pulmonary tuberculosis. Am J Respir Crit Care Med 2009;180:273-80.