Imaging

Those who care for patients with pulmonary, critical care or sleep disorders rely heavily on chest radiology and pathology to determine diagnoses. The Southwest Journal of Pulmonary, Critical Care & Sleep publishes case-based articles with characteristic chest imaging and related pathology.

The editor of this section will oversee and coordinate the publication of a core of the most important chest imaging topics. In doing so, they encourage the submission of unsolicited manuscripts. It cannot be overemphasized that both radiologic and pathologic images must be of excellent quality. As a rule, 600 DPI is sufficient for radiographic and pathologic images. Taking pictures of plain chest radiographs and CT scans with a digital camera is strongly discouraged. The figures should be cited in the text and numbered consecutively. The stain used for pathology specimens and magnification should be mentioned in the figure legend. Those who care for patients with pulmonary, critical care or sleep disorders rely heavily on chest radiology and pathology to determine diagnoses. The Southwest Journal of Pulmonary, Critical Care & Sleep publishes case-based articles with characteristic chest imaging and related pathology. The editor of this section will oversee and coordinate the publication of a core of the most important chest imaging topics. In doing so, they encourage the submission of unsolicited manuscripts. It cannot be overemphasized that both radiologic and pathologic images must be of excellent quality. As a rule, 600 DPI is sufficient for radiographic and pathologic images. Taking pictures of plain chest radiographs and CT scans with a digital camera is strongly discouraged. The figures should be cited in the text and numbered consecutively. The stain used for pathology specimens and magnification should be mentioned in the figure legend.

Rick Robbins, M.D. Rick Robbins, M.D.

March 2023 Medical Image of the Month: Spontaneous Pneumomediastinum as a Complication of Marijuana Smoking Due to Müller's Maneuvers

Figure 1. PA chest radiograph obtained at the time of admission (A) demonstrating gas densities (arrows) along left heart border, left paratracheal stripe, upper mediastinum and neck extending into the right supraclavicular fossa in keeping with pneumomediastinum. Follow-up PA chest radiograph performed just before discharge (B) demonstrates resolution of pneumomediastinum.

Figure 2. Two axial images through the anterior mediastinum obtained from a contrast-enhanced chest CT demonstrating gas densities (arrows) in the mediastinum anterior to the heart and around the esophagus in-keeping with pneumomediastinum.

A 35-year-old woman with a medical history notable for celiac disease, ulcerative colitis, and bipolar disorder presents to the Emergency Department for evaluation of a strange sensation in the chest and neck associated with nausea and vomiting for one day. The patient also reports persistent nausea and markedly decreased oral intake for the last four days. She reported no concomitant symptoms such as shortness of breath, wheezing, fever, or chills. She denies diarrhea or constipation. Socially, she admits to smoking marijuana daily, and alcohol occasionally.

Vital sign shows blood pressure 147/97 mmHg, pulse 92 BPM, temperature 37.3°C, SpO2 96% breathing ambient air. She appears nontoxic and well-nourished, and the lungs are clear to auscultation bilaterally without any wheezes, rales, or rhonchi. The heart examination reveals a regular rate and rhythm, with normal S1 and S2 heart sounds and no murmurs, rubs, or gallops. The abdomen is soft, non-tender, and not distended. Her extremities do not exhibit any clubbing, cyanosis, or edema. CBC and CMP were unremarkable, and the drug screen test was positive for THC. An ECG is obtained (not shown here), which reveals a normal sinus rhythm with a heart rate of 55 beats/min and no ST-segment or T-wave abnormalities. Chest x-ray and CTA chest, CT abdominal with oral contrast were obtained (Figures 1 and 2). Upon further questioning of the patient’s social history, it was discovered that she smokes marijuana daily using water pipes, and while utilizing a water pipe she attempted a full inspiration against a closed mouth and nose, a technique known as the Müller’s maneuver.

Spontaneous pneumomediastinum (SPM) is a rare condition in which air escapes from the lungs and collects in the mediastinum, the space between the lungs. SPM is almost always a benign, self-limited condition. While SPM can be caused by a variety of factors, including coughing, vomiting, and physical trauma, this case report presents a rare instance of SPM caused by marijuana smoking. Spontaneous pneumomediastinum (SPM) was reported in 1939 by Johns Hopkins clinician Louis Hamman for whom the Hamman sign is named. It is defined as free air or gas contained within the mediastinum, which almost originates from the alveolar space or the conducting airways. Many authors distinguish spontaneous pneumomediastinum as a form of pneumomediastinum that is not associated with blunt force or penetrating chest trauma, endobronchial or esophageal procedures, neonatal lung disease, mechanical ventilation, chest surgery, or other invasive procedures.

The mechanism by which marijuana smoking leads to pneumomediastinum is not well understood, but it is thought to involve increased intra-alveolar pressure and alveolar rupture. This can result in the escape of air into the mediastinum, leading to the development of pneumomediastinum. SPM has been associated with the inhalation of drugs such as cocaine, amphetamines, and marijuana (1-4). Attempted inspiration through a closed glottis or Muller’s maneuver results in a drop in intrathoracic pressure, which increases alveolar air volume, causing alveolar distension and rupture which can cause shear damage and air leakage along a bronchovascular bundle into the mediastinum.

The patient, in this case, was a 35-year-old woman with a history of marijuana smoking who presented with symptoms of chest pain, shortness of breath, and dysphagia. Physical examination revealed subcutaneous emphysema and a chest x-ray confirmed the presence of SPM. This case highlights the potential respiratory complications associated with marijuana smoking, which can lead to SPM and other adverse outcomes. While marijuana use is becoming increasingly common and accepted, it is important for healthcare providers to be aware of the potential risks and to educate their patients about the potential consequences of marijuana use. Further research is needed to understand the full extent of the respiratory effects of marijuana smoking and to develop appropriate interventions and treatments.

Mohammad Abdelaziz Mahmoud DO

Doctors Medical Center of Modesto and Emanuel Medical Center

Modesto and Turlock, CA USA

References

  1. Weiss ZF, Gore S, Foderaro A. Pneumomediastinum in marijuana users: a retrospective review of 14 cases. BMJ Open Respir Res. 2019 Feb 12;6(1):e000391. [CrossRef] [PubMed]
  2. Al-Mufarrej F, Badar J, Gharagozloo F, Tempesta B, Strother E, Margolis M. Spontaneous pneumomediastinum: diagnostic and therapeutic interventions. J Cardiothorac Surg. 2008 Nov 3;3:59. [CrossRef] [PubMed]
  3. Puri C, Rhee K, Harish VK, Slack D. Marijuana induced spontaneous pneumomediastinum. J Community Hosp Intern Med Perspect. 2021 Jun 21;11(4):516-517. [CrossRef] [PubMed]
  4. Motes A, Laoveeravat P, Thongtan T, Nugent K, Islam S, Islam E. Marijuana use-induced spontaneous pneumomediastinum. Proc (Bayl Univ Med Cent). 2020 Dec 7;34(2):274-275. [CrossRef] [PubMed]

Cite as: Mahmoud MA. March 2023 Medical Image of the Month: Spontaneous Pneumomediastinum as a Complication of Marijuana Smoking Due to Müller's Maneuvers. Southwest J Pulm Crit Care Sleep. 2023;26(3):31-33. doi: https://doi.org/10.13175/swjpccs058-22 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

September 2022 Medical Image of the Month: Epiglottic Calcification

Figure 1. Lateral (A) and frontal (B) topogram from a neck CT demonstrates linear calcifications in the expected location of the epiglottis (black arrows).  Sagittal multiplanar reconstructions demonstrate prominent calcification of the epiglottis (white arrow).

In consideration of dysphagia, most cases predominate in the oropharyngeal region with the remainder caused primary by esophageal causes. Lesser known and studied is the development of dysphagia and globus sensation from epiglottic pathology, namely epiglottic calcification. With less than a dozen published cases in literature, very little data exists on identification, diagnosis, and treatment of this known cause of morbidity. Here we present a case of oropharyngeal dysphagia arising from a rare cause, epiglottic calcification.

An 81-year-old man with a history of aortic stenosis and carotid artery stenosis presented with worsening dysphagia over the course of one month. The patient reported significant dysphagia, initially to solids and subsequently to liquids causing a weight loss of over 50 pounds. Physical exam of the oropharynx and neck were unremarkable. A bedside swallow evaluation suggested mildly decreased hyolaryngeal movement, but no other significant abnormalities.  A barium swallow study revealed incomplete epiglottic excursion during the pharyngeal phase of swallowing. The patient then underwent evaluation with a contrast-enhanced esophagogram, which showed severe esophageal dysmotility and gastroesophageal reflux. A CT of the neck demonstrated calcification of the epiglottis without epiglottal enlargement. ENT was consulted, the patient underwent flexible fiberoptic laryngoscopy and also EGD with biopsy.  No other esophageal or gastric pathology were identified other than the epiglottic calcification. As no effective treatment is known at this time, the patient was changed to a modified diet with ongoing speech and swallow therapy as an outpatient.

Epiglottic calcification is a rare cause of dysphagia that is poorly understood in its etiology, clinical course and outcome (1). This case demonstrates that despite consultant team recommendations, no clear evaluation pathway or treatment currently exists. Currently, diagnosis can be accomplished with radiologic evaluation along with exclusion of other causes; however, no definitive treatments are available for this rare condition. Although the condition itself is rare, epiglottic calcification should be considered when other more common causes of significant dysphagia are ruled out.  

Shil Punatar DO1, Dayoung Song MD1, Azkaa Zaman DO1, Benjamin Jiao DO2, and Tilemahos Spyratos DO1,3

1Department of Internal Medicine, Franciscan Health, Olympia Fields, IL

2Department of Radiology, Franciscan Health, Olympia Fields, IL

3Department of Gastroenterology, Franciscan Health, Olympia Fields, IL

Reference

1. Günbey HP, Günbey E, Sayit AT. A rare cause of abnormal epiglottic mobility and dyspagia: calcification of the epiglottis. J Craniofac Surg. 2014 Nov;25(6):e519-21. [CrossRef[[PubMed]

Cite as: Punatar S, Song D, Zaman A, Jiao B, Spyratos T. September 2022 Medical Image of the Month: Epiglottic Calcification. Southwest J Pulm Crit Care Sleep. 2022;25(3):41-42. doi: https//doi.org/10.13175/swjpccs031-22 PDF
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Rick Robbins, M.D. Rick Robbins, M.D.

Medical Image of the Month: Mounier-Kuhn Syndrome

Figure 1. AP chest x-ray showing significant tracheomegaly (diameter 30.8 mm), bilateral interstitial infiltrates with dense consolidation more at the lower lobes (left>right).

 

Figure 2. Axial thoracic CT in lung windows (A-D) and soft tissue windows (E-F). Sagittal CT in soft tissue windows (G-H). A: tracheal diameters in 2 dimensions (coronal 30.4 mm, sagittal 37.6 mm), para-septal emphysema (yellow arrows). B: showing tracheomegaly (23.2 x 34.3 mm) and para-septal emphysema changes (yellow arrows. C: enlarged mainstem bronchi diameters (right mainstem 22.3 x 30.6 mm, left mainstem 24.4 x 16.0 mm). In addition to central bronchiectatic changes (red arrows), left lower lobe consolidative changes (blue arrow). D: dense left lower lobe consolidation and para-septal emphysema. E: Significant tracheomegaly (31.5 x 41.a mm) and dilated esophagus (orange arrow). F: Significant tracheomegaly and dilated esophagus.

 

Figure 3. A: Sagittal CT scan (soft tissue window) showing significant tracheomegaly (sagittal diameter 35.8 mm). B: Sagittal CT chest (lung window) showing significant tracheomegaly, multiple tracheal diverticuli (green arrows) on the upper posterior tracheal wall.

 

Figure 4. Pulmonary function testing.

 

A 52-year-old non-smoking, Caucasian male patient with a past medical history of reported chronic obstructive pulmonary disease (COPD), recurrent lower respiratory tract infections, prior history of pneumothorax, and dysphagia presented with fevers and shortness of breathing associated with a productive cough for one week. Clinically, he was mildly tachypneic and chest auscultation revealed crackles bilaterally - more prominent at the left base. A chest radiograph (Figure 1) showed bilateral lower lobe pulmonary opacities (left more than right). Computed tomography (CT) of the chest demonstrated airspace disease in the lower lobes in addition to significant tracheobronchomegaly along with paraseptal emphysema and central bronchiectatic changes (Figures 2 and 3). Upper posterior tracheal wall diverticulae were also noted (Figure 3). Serum α1-antitrypsin level and serum immunoglobulins, including IgE levels, were normal. Our patient declined performing diagnostic bronchoscopy. He had a pulmonary function test performed few months prior to his hospital admission which showed combined mild obstructive/restrictive pattern (Figure 4). He responded well to empiric antibiotics and chest percussion therapy. He was discharged in stable condition.

Discussion

On the basis of above findings, a diagnosis of Mounier-Kuhn syndrome complicated by pneumonia was made. The syndrome was first described by P. Mounier-Kuhn in 1932 (1). The diagnosis is usually made when the tracheal diameter is greater than 3 cm on a CT chest (measured 2 cm above the aortic arch) (2). Other diagnostic criteria include a mainstem bronchial diameter of 20-24 mm (right) and 15-23 mm (left) (3). Our patient’s tracheal diameter was around 37 mm. Both mainstem bronchi were dilated.

The abnormal tracheobronchial dilatation in this syndrome is attributed to atrophy of the muscular and elastic tissues in the tracheal and the bronchial walls (3). Hence, in addition to tracheobronchomegaly, these patients can also develop tracheal diverticulosis along with varicose and cystic bronchiectasis (3). These patients usually present in the 3rd or 4th decade of life with nonspecific respiratory symptoms including recurrent bronchitis and subsequently end up being misdiagnosed with COPD (3).

Three subtypes of this syndrome had been described. Subtype 1 has symmetric dilation of the trachea and mainstem bronchi. Subtype 2 demonstrates tracheal dilation and tracheal diverticula. Subtype 3 has diverticular and saccular structures extending to the level of the distal bronchi (3). Our patient likely fits subtype 3 of this syndrome. Overall, treatment is supportive - usually with antibiotics, physiotherapy and postural drainage. In rare instances, tracheal stenting has been used (4). Special consideration should be taken post intubation as achieving good cuff seal can be potentially challenging.

Dysphagia has not been well documented in this syndrome and could be a coincidental finding in our case. However, theoretically, the etiology of this patient’s dysphagia could be secondary to extrinsic compression of the anterior esophageal wall by his markedly dilated trachea. Historically, he underwent multiple esophageal dilatations and at least one Botox injection over the last 5 years without any significant improvement.

Abdulmonam Ali MD and Naga S. Sirikonda MD

Pulmonary and Critical Care

Good Samaritan Hospital

Mount Vernon, Illinois

References

  1. Mounier-Kuhn P. "Dilatation de la trachee: constatations, radiographiques et bronchoscopies." Lyon Med. 1932;150:106-9.
  2. Menon B, Aggarwal B, Iqbal A. Mounier-Kuhn syndrome: report of 8 cases of tracheobronchomegaly with associated complications. South Med J. 2008;101(1):83-7. [CrossRef] [PubMed]
  3. Falconer M, Collins DR, Feeney J, Torreggiani WC. Mounier-Kuhn syndrome in an older patient. Age Ageing. 2008;37(1):115-6. [CrossRef] [PubMed]
  4. Schwartz M, Rossoff L. Tracheobronchomegaly. Chest 1994;106(5):1589-90. [CrossRef] [PubMed]

Cite as: Ali A, Sirikonda NS. Medical image of the month: Mounier-Kuhn syndrome. Southwest J Pulm Crit Care. 2019;19(2):73-5. doi: https://doi.org/10.13175/swjpcc044-19 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

Medical Image of the Month: Double Aortic Arch

Figure 1. A chest radiograph performed after endotracheal intubation of the patient demonstrated prominence of the upper mediastinum in the region of the right paratracheal strip (red arrow).

 

Figure 2. A non-contrasted CT of the chest demonstrates a complete vascular ring secondary to the patient’s double aortic arch (outlined in red) surrounding the trachea (T) and esophagus (E).

 

Case Presentation: A 78-year-old gentleman presented to the hospital via EMS with altered mental status. An urgent CT of the head performed in the emergency room demonstrated a large, right intraparenchymal hemorrhage with intraventricular extension into the right lateral ventricle. His Glascow Coma Scale score was 6, and he was intubated for airway protection.  A chest radiograph performed to verify placement of the endotracheal tube demonstrated prominence of the upper mediastinum in the region of the right paratracheal strip (Figure 1). A CT of the chest (Figure 2) demonstrated a double aortic arch corresponding to the upper mediastinal abnormality noted on the chest radiograph. In speaking with the patient’s family after acquiring the CT of the chest, they stated that the patient had long-term issues with dysphagia – specifically choking with solid foods. Unfortunately, the patient passed away from complications of his large intraparenchymal hemorrhage.

A double aortic arch results from persistence of both the right and left embryonic arches with each arch giving rise to the ipsilateral, separate carotid and subclavian arteries (1). A double aortic arch is the most common cause of a symptomatic vascular ring with the trachea and esophagus being compressed by the two arches (1). Symptoms usually arise in childhood with good outcomes with surgical repair of this abnormality in pediatric populations. A few case series exist describing repair of this anomaly in adult populations (2).

Kelly Wickstrom DO, Steven P. Sears DO, and Laura Meinke MD

Division of Pulmonary, Critical Care, Allergy and Sleep Medicine

University of Arizona College of Medicine

Tucson, AZ USA

References

  1. Hanneman K, Newman B, Chan F. Congenital variants and anomalies of the aortic arch. Radiographics. 2017 Jan-Feb;37(1):32-51. [CrossRef] [PubMed]
  2. Noguchi K, Hori D, Nomura Y, Tanaka H. Double aortic arch in an adult. Interact Cardiovasc Thorac Surg. 2012 Jun;14(6):900-2. [CrossRef] [PubMed]

Cite as: Wickstrom K, Sears SP, Meinke L. Medical image of the month: Double aortic arch. Southwest J Pulm Crit Care. 2019;18(5):120-1. doi: https://doi.org/10.13175/swjpcc019-19 PDF 

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Rick Robbins, M.D. Rick Robbins, M.D.

Medical Image of the Week: Esophageal Perforation

Figure 1. Axial, non-contrast CT of chest demonstrates wall thickening of the mid-thoracic esophagus with an extra-luminal focus of gas (blue arrow) in the mediastinum in addition to a small amount of right peri-esophageal fluid (red arrow).

 

Figure 2. Sagittal, non-contrast CT of chest demonstrates extra-luminal air posterior to the mid-thoracic esophagus (blue arrows).

 

A 74 year old man with a past medical history of esophageal strictures status post dilatation, coronary artery disease status post CABG, and atrial fibrillation presented to hospital with complaints of severe chest pain that began after the consumption of tortilla chips one hour prior to presentation. Electrocardiogram and cardiac enzymes were not consistent with acute coronary syndrome. Chest X-ray was consistent with a widened mediastinal silhouette. Contrast esophogram was negative for extra luminal extravasation. CT scan of the chest with oral contrast demonstrated thickening of the mid-thoracic esophagus with an extra-luminal focus of gas in the mediastinum along with fluid along the inferior aspect of the esophagus (Figures 1 and 2). These findings were concerning for esophageal perforation. The patient was taken to the operating room for endoscopy which showed micro perforation in mid-esophagus.

Esophageal perforation remains a highly morbid condition. Mortality rates are based predominantly on time of presentation and the etiology of perforation. Symptoms of esophageal perforation are non-specific and include neck or chest pain, dysphagia, odynophagia, difficulty breathing, vomiting, drooling, hematemesis, and abdominal rigidity (1) Initial diagnostic assessment includes conventional radiography, which can be normal in up to 10% of patients. Follow-up contrast esophograms are used to determine the presence and precise location of an esophageal perforation. However, false negative rates of 10% have been reported (2). CT scan of the chest or abdomen is indicated when contrast esophogram cannot be performed or all other diagnostic modalities have not been helpful in diagnosing esophageal perforation despite high clinical suspicion. Extra-luminal air in the mediastinum or surrounding the esophagus is the most reliable sign and when taken in conjunction with the clinical presentation, has 92% accuracy. Other common findings include obliteration of fat planes in the mediastinum resulting from inflammation, peri-esophageal or mediastinal fluid (92% accuracy), esophageal thickening, pleural effusions, extravasation of oral contrast material into the peri-esophageal tissues, and a tract at the site of the tear (3).

Jawad Bilal MD, David Testa MD, Irbaz bin Riaz MD and Ryan Nahapetian MD MPH

University of Arizona

Tucson, AZ

References

  1. Aronberg RM, Punekar SR, Adam SI, Judson BL, Mehra S, Yarbrough WG. Esophageal perforation caused by edible foreign bodies: A systematic review of the literature. Laryngoscope. 2015;125(2):371-8. [CrossRef] [PubMed]
  2. Bladergroen MR, Lowe JE, Postlethwait RW. Diagnosis and recommended management of esophageal perforation and rupture. Ann Thorac Surg. 1986;42(3):235-9. [CrossRef] [PubMed]
  3. Lee S, Mergo PJ, Ros PR. The leaking esophagus: CT patterns of esophageal rupture, perforation, and fistulization. Crit Rev Diagn Imaging. 1996;37(6):461-90. [PubMed] 

Reference as: Bilal J, Testa D, Riaz I, Nahapetian R. Medical image of the week: eosphageal perforation. Southwest J Pulm Crit Care. 2015;10(4):201-2. doi: http://dx.doi.org/10.13175/swjpcc033-15 PDF

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