August 2011 Case of the Month

Michael B. Gotway, M.D.

Associate Editor, Imaging

Reference as: Gotway MB. August 2011 case of the month. Southwest J Pulm Crit Care 2011;3:54-7. Click here for PDF version

Clinical History

A 60-year-old woman with no significant previous medical history complains of shortness of breath. Chest radiography was performed (Figure 1).

Point to the lesion on the chest X-ray on the chest x-ray to proceed.

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. 

Ground-Glass Opacities

Reference as: Gopal V, Robbins RA. Ground-glass opacities. Southwest J Pulm Crit Care 2011;2:67-70. (Click here for PDF version)

A 54-year-old male was admitted to the medical intensive care unit complaining of abdominal pain, nausea, and vomiting for 2 days. He had a past medical history of pancreatitis in 2009, treated as outpatient, and asthma treated with albuterol inhaler as needed. His medication list included gemfibrizol, gabapentin, and amitriptyline. He drank 6-8 beers per day and smoked 1 pack-per-day for the past 40 years.

On physical examination is the patient was afebrile, his lungs are clear to auscultation, but tenderness was present in both lower quadrants. The remainder of the physical examination was normal.

Laboratory examination revealed a normal complete blood count and normal basic metabolic panel. Abnormal laboratory values included an elevated total bilirubin of 2.7 mg/dL (normal 0.2-1 mg/dL); alkaline phophatase 169 U/L (normal 10-40 U/L);  alanine aminotransferase 286 U/L (normal 10-35 U/L); amylase 468 U/L (normal 25-125 U/L), and lipase 1580 U/L (normal 8-78 U/L). Arterial blood gasmeasurements showed PaO_{2 =} 91 mm Hg, PaCO₂ = 26 mm Hg, pH = 7.52, and oxygen saturation = 98% while breathing room air.

Chest radiography (Figure 1, Panel A) was interpreted as showing a “right upper lobe infiltrate which could represent an acute pneumonia”.  No distinct abnormalities were identified on abdominal radiographs (Figure 1, Panel B).

 Figure 1. Panel A. Frontal chest radiography.  Panel B. Abdominal radiography.

To further evaluate the possibility of a right upper lobe abnormality at chest radiography, thoracic CT was performed and as showing patchy ground-glass opacities throughout the lungs bilaterally (Figure 2).

Figure 2. Representative images from thoracic CT.

Question 1. What’s the most likely diagnosis?

1. Hypersensitivity pneumonitis
2. Acute inhalational injury secondary to “huffing”.
3. Drug-induced lung disease
4. Valley Fever
5. Ground-glass opacities associated with pancreatitis

Question 2. What would you do next?

1. Hypersensitivity panel
2. Bronchoscopy with bronchoalveolar lavage
3. Begin Diflucan
4. Broaden his antibiotic coverage
5. Repeat the thoracic CT scan in 3-4 days.

The thoracic CT was repeated four days later and the ground-glass opacities seen previously had largely resolved (Figure 3).

Figure 3.  Representative images from thoracic CT performed four days following the initial study Figure 2).

These ground-glass opacities likely represent subclinical non-cardiogenic pulmonary edema in the setting of acute pancreatitis. Ground-glass opacities are foci of increased lung attenuation that do not obscure underlying vessels or bronchial margins (1). Ground-glass opacities often represent parenchymal abnormalities below the spatial resolution of high-resolution CT of the lung. Although the differential diagnosis of ground-glass opacities at high-resolution CT is large, these etiologies may be broadly divided into acute or chronic causes. Table 1 lists some of the more common causes of ground-glass opacities at high-resolution CT.

Table 1: Common Etiologies for Ground-Glass Opacity at Thoracic CT

Acute	Chronic
Pulmonary edema (cardiogenic or non-cardiogenic)	Interstitial diseases (hypersensitivity pneumonitis, desquamative interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease, nonspecific interstitial pneumonia, sarcoidosis, others)
Infectious pneumonitis (PJP, CMV, HSV, RSV, others)	Bronchoalveolar carcinoma
Noninfectious pneumonitis (hypersensitivity pneumonitis, acute inhalational exposures, drug-induced lung diseases)	Other causes (drug toxicity, pulmonary alveolar proteinosis, organizing pneumonia, chroic eosinophilic pneumonia, others)

Our patient had no apparent cause, other than subclinical non-cardiogenic pulmonary edema secondary to pancreatitis. Pulmonary edema is a well known complication of pancreatitis and can be severe (2). It seems likely that, as more sensitive methods for the detection of pulmonary abnormalities, such as thoracic CT, are increasingly applied to patients with pancreatitis, that subclinical pulmonary injury may be increasingly detected.

Venu Gopal, M.D.

Chief, Infectious Disease, Phoenix VA Medical Center

Richard A. Robbins, M.D.

Chief, Pulmonary and Critical Care, Phoenix VA Medical Center

Slide Set

References

1. Miller WT Jr, Shah RM.  Isolated diffuse ground-glass opacity in thoracic CT: causes and clinical presentations.  AJR Am J Roentgenol 2005;184:613-22.
2. Raghu MG, Wig JD, Kochhar R, Gupta D, Gupta R, Yadav TD, Agarwal R, Kudari AK, Doley RP, Javed A. Lung complications in acute pancreatitis. JOP. 2007;8:177-85.

A Case of Mislabeled Identity

Reference as: Singarajah C, Park K. A case of mislabeled identity. Southwest J Pulm Crit Care 2010;1:22-27. (Click here for PDF version)

A 60-year-old man in the surgical intensive care unit for atrial fibrillation with rapid ventricular response, on his second post-operative day following colectomy, complained of worsening shortness of breath. A chest radiograph (Figure 1) was obtained. A chest radiograph performed one day previous to Figure 1 showed clear lungs, no pleural effusions, and no volume loss.

Question 1 and Figure 1: What are the abnormal findings on the chest radiograph? In particular, what technical error has occurred? 

The frontal chest radiograph shows increased opacity in the bases bilaterally, greater on the side labeled left (see “L” in the image- this is the technologist’s marker). Note the shift of the trachea towards the side labeled left. However, note also the opacity along the superior mediastinum on the right side; this opacity has the appearance of the aortic arch. Note the appearance of the stomach below the diaphragm, ipsilateral to the aortic arch. Also, the opacity at the left lung base shows a configuration resembling the heart. Taken together, these findings raise the possibility that the radiograph is mislabeled, with the “Left” marker (“L”, Figure 1) improperly placed on the patient’s right side. Prior chest radiographs not shown) confirm the patient did not have situs inversus.

There is evidence of volume loss in the right thorax (labeled incorrectly as left in this image). Note the shift of the trachea towards the side with increased lung opacity. The entire left right thorax (again, incorrectly labeled left in this image) is small, and the air column in the right mainstem bronchus abruptly terminated, suggesting endobronchial obstruction.

Furthermore, the patient had no clinical reasons for a new large pleural effusion, and recent prior films showed no pleural fluid.

Surgery was consulted and a procedure was performed. The results of this procedure are shown in Figure 2.

Question 2: What procedure was performed by the surgery team?

The surgery team improperly placed a thoracostomy tube in the left thorax because they misinterpreted Figure 1 as showing a large left pleural effusion. Figure 2 shows the tip of the thoracostomy tube in the medial superior left thorax, associated with subcutaneous emphysema. Progressive volume loss is seen on the right side, again suggesting endobronchial obstruction- note that the residual air in the right upper thorax in Figure 1 is no longer present in Figure 2. The surgery team then improperly placed a thoracostomy tube on the right side, mistaking the small, opacified right thorax for pleural effusion on that side. Figure 3 shows the new right thoracostomy tube tip located over the cranial right thorax.

The surgical team was concerned that the thoracostomy tube showed little fluid output and a second thoracotomy tube was placed on the contralateral side (Figure 3).

 

This tube also did not show significant output. The pulmonary / critical care medicine team was then consulted. The pulmonary / critical care medicine physician performed a procedure which partially corrected the cause of the patient’s original complaints. The chest radiograph following this procedure is shown in Figure 4. 

Question 3: What procedure (s) was performed by the pulmonary / critical care medicine team?

Bronchoscopy was performed, and showed significant mucous plugging. The mucous plugs were removed resulting in improved right lung aeration (Figure 4).

Learning Points:

• Physical exam would have identified improperly labeled chest radiograph
• The chest radiograph shows volume loss, suggesting endobronchial obstruction due to mucous plugging- the side of the thorax showing increased attenuation shows reduced volume. In contrast, pleural effusion would show increased opacity associated with mass effect and shift of the cardiomediastinal structures away from the side of the thorax showing increased attenuation
• Time-outs are no substitute for clinical skills.The patient had two thoracostomy tubes, both placed for incorrect reasons, one of which was placed on the wrong side all together.
• Therapy for atelectasis and mucous plugging includes the following:
  •  Patient mobilization, ambulation, sitting up;
  • Minimize anti-tussive meds (narcotics, etc), minimizes sedation;
  • Chest physiotherapy for the affected lung;
  • Continuous lateral rotation therapy for patients with altered mental status who cannot mobilize  (for example, a Triadyne bed  made by KCI or manual turning);
  • Bronchoscopy, and;
  • Mucolytics are of equivocal benefit

Clement Singarajah MD.  Associate Chief Pulmonary and Critical Care Fellowship, Phoenix VA Hospital and Good Samaritan Regional Medical Center, Phoenix AZ.

Kevin Park, MD, Pulmonary and Critical Care Medicine fellow, Phoenix VA Hospital and Good Samaritan Regional Medical Center, Phoenix AZ.

Email csingarajah@earthlink.net

Painful Necrotic Fingers

  

Reference as: Raschke RA. Painful necrotic fingers. Southwest J Pulm Crit Care 2010;1:8-9. (Click here for PDF version)

A 38-year-old woman, an active smoker, presents with complaints of finger pain and changes in skin color. A photograph of the patients fingers is shown above. This photo was taken in 1989, before the hospital instituted a no smoking policy.  Prior to that time, patients were allowed to smoke in their hospital rooms.

Catheter angiography was performed and showed a corkscrew configuration of the small arteries of the hand and fingers. Evaluation for connective tissue diseases was negative.

What is your diagnosis?

Answer: Buerger's disease (thombangitis obliterans).

Discussion

First described by Leo Buerger in 1908, Buerger’s disease (thrombangitis obliterans) is characterized by an inflammatory thrombosis of small to medium-sized arteries and veins, predominantly affecting the distal extremities.  The disorder is unusual in women, but is extremely strongly associated with use of tobacco products.  The only proven therapy for Buerger's disease is smoking cessation.

Robert A. Raschke, M.D.