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.

Medical Image of the Month: Stercoral Colitis

Figure 1. Non-contrast CT acquired at the time of admission demonstrating diffusely dilated large bowel loops from cecum to rectum measuring up to 8 cm. Image on the left (Panel A) shows a near-complete intrathoracic sliding-type herniation of stomach adjacent to a herniated portion of transverse colon through the diaphragm into the chest. The image on the right (Panel B) shows a markedly distended rectum with impacted stool with circumferential rectal wall thickening consistent with stercoral colitis. 

 

Figure 2. Non-contrast CT thorax demonstrating on the left (Panel A) large hiatal hernia with intrathoracic herniation of stomach and transverse colon. The image on the right (Panel B) shows mild mass effect upon the left atrium related to the herniated transverse colon.

 

A 78-year-old- man with cerebral palsy requiring an in-home caregiver presented to the emergency room in hypovolemic shock post-sudden cardiac arrest in the setting of hematemesis. The caregiver noticed the patient become unresponsive after having one episode of bright red emesis. EMS arrived and found the patient to be pulseless and performed three rounds of CPR and gave 1 mg of epinephrine before return of spontaneous circulation was obtained. The caregiver reported the patient had been complaining of diarrhea for the past few days after being started on magnesium citrate for constipation by his PCP. In the ED patient was intubated, sedated, and started on pressors due to undifferentiated shock. CT abdomen pelvis demonstrated diffuse dilation of the colon with massive stool burden and markedly distended rectum with impacted stool and circumferential rectal wall thickening consistent with stercoral colitis (Figures 1 and 2). In addition, there was a large hiatal hernia with intrathoracic herniation of the stomach and a portion of the transverse colon, but it did not appear to represent a point of high-grade obstruction. The patient was deemed a poor surgical or endoscopic candidate due to high perioperative mortality. Manual disimpaction was attempted with minimal stool output, mineral oil enemas were given, and OG tube decompression of stomach. The patient had a ST segment elevated myocardial infarction (STEMI) noted on EKG and despite pressors and aggressive IV fluid resuscitation patient’s condition continued to decline with family deciding to pursue comfort care. The patient’s profound constipation, large hiatal hernia, and stercoral colitis were contributing factors to his shock.

Stool impaction can occur secondary to chronic constipation as the colon absorbs salt and colitis is colonic perforation which has a mortality rate between 32-57 percent (1). The modality of choice for diagnosis is CT and the common findings are colonic wall thickening, pericolonic fat stranding, mucosal discontinuity, pericolonic abscess, and free air indicating perforation. A small retrospective study found that the most consistent findings in stercoral colitis were rectosigmoid colon involvement, dilation of the colon >6 cm, and bowel wall thickening >3 mm in the affected segment. It also suggests that colonic involvement of >40 cm and perforation indicate increased mortality (2,3). Stercoral colitis most commonly occurs in the elderly, those who are bedridden due to cerebrovascular events or severe dementia, chronic opioid use, malignancy, and those with motor disabilities, such as this patient with cerebral palsy.  In patients without signs of peritonitis or who are poor surgical candidates can be managed non-operatively with laxatives, enemas, and manual/endoscopic disimpaction (4). Early diagnosis and treatment are imperative to avoid perforation. Patients with signs of perforation require surgical treatment which involves resection of the affected bowel segments.

Kirstin H. Peters MSIV, Angela Gibbs MD, Janet Campion MD

University of Arizona School of Medicine, Banner University Medical Center-Tucson, Tucson, AZ USA

References

  1. Serpell JW, Nicholls RJ. Stercoral perforation of the colon. Br J Surg. 1990 Dec;77(12):1325-9. [CrossRef] [PubMed]
  2. Ünal E, Onur MR, Balcı S, Görmez A, Akpınar E, Böge M. Stercoral colitis: diagnostic value of CT findings. Diagn Interv Radiol. 2017 Jan-Feb;23(1):5-9. [CrossRef] [PubMed]
  3. Wu CH, Wang LJ, Wong YC, et al. Necrotic stercoral colitis: importance of computed tomography findings. World J Gastroenterol. 2011 Jan 21;17(3):379-84. [CrossRef] [PubMed]
  4. Hudson J, Malik A. A fatal faecaloma stercoral colitis: a rare complication of chronic constipation. BMJ Case Rep. 2015 Sep 3;2015:bcr2015211732. [CrossRef] [PubMed]

Cite as: Peters KH, Gibbs A, Campion J. Medical Image of the Month: Stercoral Colitis. Southwest J Pulm Crit Care. 2021;23(3):73-5. doi: https://doi.org/10.13175/swjpcc027-21 PDF 

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

Medical Image of the Month: Bleomycin-Induced Pulmonary Fibrosis in a Patient with Lymphoma

Figure 1. Representative images from the thoracic CT in lung windows showing scattered bilateral ground glass opacities with areas of fibrosis consistent with multifocal pneumonia superimposed on pulmonary fibrosis.

Figure 2. Representative image from the thoracic CT in lung windows done just prior to lung transplantation.

Abstract

Interstitial pulmonary fibrosis is the most feared complication of bleomycin therapy and occurs in up to ten percent of patients that receive the drug. The risk of bleomycin-induced pulmonary fibrosis is related to the age of the patient, the dose of medication given, the patient’s kidney function, and whether the patient smokes cigarettes. Current screening guidelines for bleomycin-induced lung injury are limited, but most clinicians screen high risk and symptomatic patients with pulmonary function testing. This case report is of a patient with lymphoma who received bleomycin as a part of his chemotherapy regimen, and later developed pulmonary fibrosis complicated by bouts of eosinophilic multifocal pneumonia. The case highlights the importance of close monitoring of patients taking bleomycin for signs and symptoms of pulmonary fibrosis and the need for major medical societies to issue concrete screening guidelines.

Introduction 

Bleomycin’s labeled indications include treatment of squamous cell carcinomas of the head and neck, Hodgkin lymphoma, non-Hodgkin lymphoma, malignant pleural effusions, and testicular cancer (1). The most feared complication of bleomycin is interstitial pulmonary fibrosis (2). Pathogenesis is not fully clear but involves oxidative damage secondary to reactive oxygen species (2). Risk factors include age > 40, renal insufficiency (CrCl < 80 mL/min), bleomycin dose > 300 units, and cigarette smoking (2). Symptoms present within one to six months of starting the medication and often begin with dyspnea and auscultatory crackles on physical exam (2). Associated signs and symptoms include cough, chest pain, opacities on chest radiographs, or an asymptomatic decline in diffusing capacity for carbon monoxide (2,3).

Screening for pulmonary fibrosis in patients taking bleomycin is controversial and no clear guidelines exist. Most physicians agree that it is appropriate to get baseline pulmonary function tests (PFTs) in patients receiving bleomycin, and thereafter screen with PFTs intermittently throughout the course of treatment (3). FDG-PET has also been used as a screening tool, but the evidence for its efficacy is mixed (4).

This is a case of a 56-year-old man with a presumed diagnosis of multifocal eosinophilic pneumonia superimposed on pulmonary fibrosis who had to be admitted to the ICU for respiratory distress. The patient recovered and underwent a lung transplant.

Case Presentation 

A 56-year-old man with a history of lymphoma diagnosed 11 years prior and treated with chemotherapy, including bleomycin, presented to the emergency department with fever, chills, and productive cough. A CT of the chest with IV contrast was performed which revealed scattered bilateral ground glass opacities with areas of fibrosis (Figure 1). Next, the patient underwent a bronchoalveolar lavage (BAL) and shortly thereafter developed respiratory distress with respiratory failure that required non-invasive ventilation and admission to the ICU. In the ICU, the patient responded to ceftriaxone, azithromycin, prednisone, and fluconazole. The bronchoalveolar lavage was significant for elevated levels of eosinophils and neutrophils. There were also possible fungal elements on touch prep but no fungal growth. The presumed diagnosis on admission was multifocal pneumonia superimposed on pulmonary fibrosis.  

After recovering, the patient was discharged. Four months later, he underwent a bilateral lung transplant. At explant, the final pathology report confirmed a mixed pattern of fibrosing interstitial lung disease, clinically due to bleomycin. Figure 2 shows the patient’s pulmonary fibrosis just prior to transplant.

The patient’s lung transplantation was successful, and he is currently doing well.

Discussion

Pulmonary fibrosis is a dangerous and relatively common complication of bleomycin. The differential diagnosis includes pulmonary infection, cardiogenic pulmonary edema, radiation-induced pulmonary fibrosis, metastatic disease, and adverse reaction to other medications. Presented here is a case where a patient received bleomycin as a part of his chemotherapy regimen for lymphoma, and subsequently developed pulmonary fibrosis. When the patient presented 11 years after his lymphoma diagnosis, he had eosinophilic multifocal pneumonia superimposed on his already existing pulmonary fibrosis.

This case illustrates the difficulty of managing the pulmonary manifestations of bleomycin in patients taking the drug. There are currently no screening guidelines in place for patients that take the medication (3). Shippee et al. suggest patients undergo PFTs at baseline before starting treatment, followed by PFTs every 3 weeks during therapy (3). They suggest bleomycin should be discontinued in patients who have a linear decline in DLCO of 40-60% from baseline (3).

It is unclear if our patient had been screened for pulmonary fibrosis while he was receiving bleomycin. Regardless, it would be prudent and appropriate for a major medical society to issue clear guidelines regarding screening for pulmonary fibrosis. Standardizing screening protocols will lead to better patient outcomes.

Martin A. Dufwenberg, BS  

University of Arizona College of Medicine – Tucson

Tucson, AZ, USA

Acknowledgments

The author thanks Dr. Michael Larson, M.D., Ph.D., for mentorship, discussion, and help in making this case report become reality.

References

  1. U.S. Food and Drug Administration. Blenoxane (bleomycin sulfate for injection, USP). Updated April 2010. Accessed June 8, 2021. https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/050443s036lbl.pdf
  2. Sleijfer S. Bleomycin-induced pneumonitis. Chest. 2001 Aug;120(2):617-24. [CrossRef] [PubMed]
  3. Shippee BM, Bates JS, Richards KL. The role of screening and monitoring for bleomycin pulmonary toxicity. J Oncol Pharm Pract. 2016 Apr;22(2):308-12. [CrossRef] [PubMed]
  4. Groves AM, Win T, Screaton NJ, Berovic M, Endozo R, Booth H, Kayani I, Menezes LJ, Dickson JC, Ell PJ. Idiopathic pulmonary fibrosis and diffuse parenchymal lung disease: implications from initial experience with 18F-FDG PET/CT. J Nucl Med. 2009 Apr;50(4):538-45. [CrossRef] [PubMed]

Cite as: Dufwenberg MA. Medical image of the month: bleomycin-induced pulmonary fibrosis in a patient with lymphoma. Southwest J Pulm Crit Care. 2021;23(2):49-51. doi: https://doi.org/10.13175/swjpcc024-21 PDF 

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

Medical Image of the Month: Hepatic Abscess Secondary to Diverticulitis Resulting in Sepsis

 

Figure 1. An axial, post-contrast CT of the abdomen and pelvis demonstrates an ill-defined, multiloculated, hypodense lesion in the right hepatic lobe most consistent with a hepatic abscess (red circle).

 

       Figure 2. Coronal and axial reconstructions of the post-contrast CT of the abdomen and pelvis demonstrate extensive diverticulosis of the descending and sigmoid colon (blue arrows) with a focal area of fat-stranding in the descending colon consistent with diverticulitis (red arrow) – likely the source of the patient’s hepatic abscess.

 

Clinical Scenario: A 73-year-old man with a previous history of hypertension presented to the hospital with a 4-day history of malaise, myalgias, syncope, nausea, and vomiting. He denied having any fevers, chills, diarrhea, abdominal pain, or recent travel. Upon arrival to the hospital, he was found to be febrile to 103.4°F, and hypotensive with systolic blood pressures in the 80’s. His baseline documented systolic blood pressures from numerous outpatient clinics were in the 110’s. In addition, he was hypoxemic requiring 6 L/min of supplemental oxygen to maintain an adequate oxygen saturation. Physical examination was significant for alteration of his mental status. He denied any abdominal pain with palpation, and there was no rebound tenderness or guarding. His lab work was significant for a leukopenia and thrombocytopenia - new from his previous lab work in our system. A CT of the abdomen and pelvis with contrast demonstrated a multiloculated abscess in the right hepatic lobe (Figure 1). He also had extensive diverticular disease of the descending and sigmoid colon with a focal area of diverticulitis in the descending colon (Figure 2). A CT-guided, percutaneous drain was placed in the right hepatic lobe abscess which grew Streptococcus anginosus and Bacteroides fragilis. With the combination of antibiotics and drainage of the abscess, his clinical condition markedly improved. He was discharged approximately 1 week after admission at his normal baseline.

Discussion: Liver abscess is the most common type of visceral abscess (1). Clinical manifestations include a broad spectrum of symptoms, but the most common are fever (70%–90% of patients) and abdominal pain, usually in the right upper quadrant (50%–75%) (2-4). Liver abscesses can occur because of multiple etiologies to include ascending cholangitis, hematogenous spread from the gastrointestinal tract via portal venous drainage of infectious entities such as diverticulitis and appendicitis, and from hematogenous spread via the hepatic artery. Other etiologies for the development of hepatic abscesses include penetrating trauma or after an invasive procedure (for example biliary instrumentation, transcatheter arterial chemoembolization, percutaneous liver biopsy, or abdominal surgery) (5).

Many bacteria have been described in the pathogenesis of pyogenic abscesses, reflecting the variability among patients and geographic areas. Many aspirated fluid cultures are positive, whereas blood cultures are positive in only 50% of cases (4). Most pyogenic liver abscesses are polymicrobial (4). Traditionally, Escherichia coli has been reported as the most common isolated microbe; however, recent data show that Klebsiella pneumoniae is the most common pathogen in pyogenic liver abscesses (3,4,6).

Management of pyogenic liver abscesses includes imaging-guided drainage and antibiotic therapy. There is considerable variation in clinical practice regarding total antibiotic duration (7). It is recommended that antibiotic therapy be continued for at least 4–6 weeks, but the optimal duration is still unclear (7). Although drainage of single abscesses with a diameter of 5 cm or less can be achieved in some cases, it may not improve outcomes compared with antibiotic treatment alone. In isolated abscesses with a diameter greater than 5 cm, catheter drainage should be considered and is preferred over needle aspiration, although some favor surgical intervention (8). Prompt diagnosis and imaging-guided drainage have been reported to reduce mortality from 65% to 2%–12% (2-4).

Reubender Randhawa MD1, Alan Nyquist MD2, and Tammer El-Aini MD2

1Banner University Medical Center – South Campus, Department of Internal Medicine, Tucson, AZ USA

2Banner University Medical Center – Tucson Campus, Department of Pulmonary and Critical Care

References

  1. Altemeier WA, Culbertson WR, Fullen WD, Shook CD. Intra-abdominal abscesses. Am J Surg. 1973 Jan;125(1):70-9. [CrossRef] [PubMed]
  2. Mohsen AH, Green ST, Read RC, McKendrick MW. Liver abscess in adults: ten years experience in a UK centre. QJM. 2002 Dec;95(12):797-802. [CrossRef] [PubMed]
  3. Rahimian J, Wilson T, Oram V, Holzman RS. Pyogenic liver abscess: recent trends in etiology and mortality. Clin Infect Dis. 2004 Dec 1;39(11):1654-9. [CrossRef] [PubMed]
  4. Huang CJ, Pitt HA, Lipsett PA, Osterman FA Jr, Lillemoe KD, Cameron JL, Zuidema GD. Pyogenic hepatic abscess. Changing trends over 42 years. Ann Surg. 1996 May;223(5):600-7; discussion 607-9. [CrossRef] [PubMed]
  5. Wisplinghoff H, Appleton DL. Bacterial infections of the liver. In: Weber O, Protzer U, eds. Comparative hepatitis. Basel, Switzerland: Birkhäuser, 2008; 143–160. [CrossRef]
  6. Liu Y, Wang JY, Jiang W. An Increasing Prominent Disease of Klebsiella pneumoniae Liver Abscess: Etiology, Diagnosis, and Treatment. Gastroenterol Res Pract. 2013;2013:258514. [CrossRef] [PubMed]
  7. Molton J, Phillips R, Gandhi M, Yoong J, Lye D, Tan TT, Fisher D, Archuleta S. Oral versus intravenous antibiotics for patients with Klebsiella pneumoniae liver abscess: study protocol for a randomized controlled trial. Trials. 2013 Oct 31;14:364. [CrossRef] [PubMed]
  8. Zerem E, Hadzic A. Sonographically guided percutaneous catheter drainage versus needle aspiration in the management of pyogenic liver abscess. AJR Am J Roentgenol. 2007 Sep;189(3):W138-42. [CrossRef] [PubMed]

Cite as: Randhawa R, Nyquist A, El-Aini T. Medical image of the month: hepatic abscess secondary to diverticulitis resulting in sepsis. Southwest J Pulm Crit Care. 2021;23(1):5-7. doi: https://doi.org/10.13175/swjpcc019-21 PDF 

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

Medical Image of the Month: Metastatic Spindle Cell Carcinoma of the Breast

Figure 1. A coronal reconstruction of the patient’s CT of the chest with contrast in lung windows demonstrates extensive, bilateral metastatic disease, with the greatest burden of disease situated in the right lower lobe. Areas of cystic change (blue arrows) and cavitary disease (red arrow) are present.

Clinical Scenario: A 71-year-old woman with primary malignancy of the breast in remission post bilateral mastectomy in 2005 and 2008, presented to the emergency room with progressive shortness of breath for the past 6 months. Upon arrival to the emergency room, she described localized sharp chest pain along the right thoracic wall which had gradually worsened over the past three months. The pain was exacerbated with movement and with deep inspiration. She also endorsed significant hemoptysis, expectorating approximately 500 ml of bloody sputum on the morning of her presentation. Pertinent vitals revealed that she was both tachycardic and tachypneic, saturating 94% on room air with an increased work of breathing. Physical examination was significant for coarse breath sounds and diminished right sided lung sounds. Initial labs demonstrated a normal troponin and an unremarkable EKG. A chest radiograph demonstrated a large left mediastinal and hilar mass with numerous parenchymal nodules bilaterally. A CT of the chest with contrast (Figure 1) demonstrated widespread lung nodules, most notably in the right lung with a confluent mass in the right base. No significant focal lesions were seen in the chest wall or breast regions. A biopsy of the left mediastinal mass was performed and confirmed metastatic spindle cell carcinoma originating from her primary breast cancer.

Discussion: Spindle cell carcinoma of the breast, a variant classified under metaplastic carcinoma, is a rare entity occurring in less than 1% of all incidences of primary breast cancer, and most commonly seen in postmenopausal women (2,5). Treatment is primarily surgical resection. The role of radiation and chemotherapy is unclear and varies per patient treatment plan. Tumors are typically triple-negative, limiting therapeutic options (1,2,5). Primary tumor diameter and grade may be the most important prognostic factors, although prognosis regarding spindle cell carcinoma is generally poor. At the time of diagnosis, incidence of axillary lymph node metastasis was 40 – 56% with a high grade of recurrence at 57% - 63% (1,4,5). Most common extra nodal metastasis was to the lungs. In addition to the poor prognosis of spindle cell carcinomas and high rates of local recurrence, metastatic disease is also frequently seeing in patients, such as the metastatic disease seen with our patient (2-4).

Our patient’s primary breast cancer was treated with a bilateral mastectomy followed by neither chemotherapy nor radiation therapy based on patient’s preference and discussion with her oncology team. The primary tumor was in the left breast with recurrence to the right breast and metastasis to bilateral lungs. Like other cases, a biopsy revealed a triple-negative tumor. She was discharged on supplemental oxygen and is expected to receive P13K inhibitor therapy for targeted palliative treatment.

Vinita Kusupati MD, MBA and Stefano Natali DO

Department of Internal Medicine,

Banner University Medical Center-Tucson Campus

Tucson, AZ USA

References

  1. Adem C, Reynolds C, Ingle JN, Nascimento AG. Primary breast sarcoma: clinicopathologic series from the Mayo Clinic and review of the literature. Br J Cancer. 2004 Jul 19;91(2):237-41. [CrossRef] [PubMed]
  2. Alaoui M'hamdi H, Abbad F, Rais H, Asmouki H, Soumani A, Khouchani M, Belbaraka R. Rare variant of metaplastic carcinoma of the breast: a case report and review of the literature. J Med Case Rep. 2018 Feb 21;12(1):43. [CrossRef] [PubMed]
  3. Carter MR, Hornick JL, Lester S, Fletcher CD. Spindle cell (sarcomatoid) carcinoma of the breast: a clinicopathologic and immunohistochemical analysis of 29 cases. Am J Surg Pathol. 2006 Mar;30(3):300-9. [CrossRef] [PubMed]
  4. Khan HN, Wyld L, Dunne B, Lee AH, Pinder SE, Evans AJ, Robertson JF. Spindle cell carcinoma of the breast: a case series of a rare histological subtype. Eur J Surg Oncol. 2003 Sep;29(7):600-3. [CrossRef] [PubMed]
  5. Tse GM, Tan PH, Putti TC, Lui PC, Chaiwun B, Law BK. Metaplastic carcinoma of the breast: a clinicopathological review. J Clin Pathol. 2006 Oct;59(10):1079-83. [CrossRef] [PubMed]
  6. Tse GM, Tan PH, Lui PC, Putti TC. Spindle cell lesions of the breast--the pathologic differential diagnosis. Breast Cancer Res Treat. 2008 May;109(2):199-207. [CrossRef] [PubMed]

Cite as: Kusupati V, Natali S. Medical image of the month: metastatic spindle cell carcinoma of the breast. Southwest J Pulm Crit Care. 2021;22(6):114-5. doi: https://doi.org/10.13175/swjpcc021-21 PDF 

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

Medical Image of the Month: Superior Vena Cava Syndrome

Figure 1. Large mediastinal lymph nodes (red arrow) causing compression of the superior vena cava (blue arrow). Numerous enlarged lymph nodes can also be seen in the axillary, cervical, and upper abdominal regions (green arrows).

History: A 74-year- old man with a history of diastolic heart failure, chronic kidney disease (CKD), and chronic lymphocytic leukemia (CLL) presented with a complaint of dyspnea. He has had several hospitalizations in the last year for heart failure exacerbation and his home bumetanide was recently increased from twice to three times daily due to persistently increasing weight. His CLL was diagnosed two years prior and treatment was stopped three months ago due to side effects. In the emergency department he reported three weeks of worsening dyspnea especially when lying flat, as well as increased swelling in his legs, abdomen, arms, and face. His weight was up to 277lbs from 238lbs the month before. His diuretics were transitioned to IV, but over the next few days he remained clinically volume overloaded. A noncontrast chest CT was obtained to help evaluate his ongoing respiratory distress (Figure 1). It demonstrated innumerable lymph nodes involving the cervical, axillary, mediastinal, and upper abdominal regions, which had significantly increased in size and number from prior exam several months before. The CT also showed several particularly bulky lymph nodes which appeared to be compressing the superior vena cava.

Discussion: The superior vena cava (SVC) is responsible for about one-third of the venous return to the heart. Because of its thin walls relative to arterial vasculature, it is susceptible to compression from adjacent structures which may subsequently impair venous return to the heart, a process known as SVC syndrome. Intrathoracic malignancy is responsible for 60-85% of cases of SVC syndrome, and common symptoms include facial or neck swelling, swelling of the arms, and dyspnea (1). In this case, the patient’s apparent resistance to diuresis was felt to be partially secondary to SVC syndrome. In stable patients, contrast-enhanced CT is the preferred imaging modality if SVC syndrome is suspected, which can define the extent of SVC blockage. Duplex ultrasound may be used first to exclude thrombus. In this patient with acute kidney injury on CKD it was decided to forgo the contrast study to avoid further kidney damage. Management of SVC syndrome depends on severity, with emergent treatment focused on maintaining the airway and endovenous recanalization. Definitive treatment is directed at the underlying cause (2).

After about a week of aggressive IV diuresis, the patient’s breathing and volume status improved and he was transitioned back to oral diuretics. He was discharged home with plans for hospice.

Matthew R. Borchart MD, Daniel Yu MD, and Indrajit Nandi MD

University of Arizona College of Medicine, Phoenix

Phoenix, AZ USA

References

  1. Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome: clinical characteristics and evolving etiology. Medicine (Baltimore). 2006 Jan;85(1):37-42. [CrossRef] [PubMed]
  2. Wilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med. 2007 May 3;356(18):1862-9. [CrossRef] [PubMed]

Cite as: Borchart MR, Yu D, Nandi I. Medical Image of the Month: Superior Vena Cava Syndrome. Southwest J Pulm Crit Care. 2020;21(6):136-7. doi: https://doi.org/10.13175/swjpcc060-20 PDF

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

Medical Image of the Month: Buffalo Chest Identified at the Time of Lung Nodule Biopsy

Figure 1. Buffalo chest, peripheral cavitary lesions, and pneumothorax contralateral to the biopsy site. A) Outpatient CT scan showing a right pneumothorax (blue arrow) and right-sided cavitary lesion (blue arrowhead). B) Subsequent pre-procedural planning CT scan done right lateral decubitus, showing again the cavitary lesion (blue arrowhead) but now with left pneumothorax (red arrow), suggesting buffalo chest. C) Intra-procedural CT showing needle at the periphery of the cavitary lesion (blue arrowhead) and similar-sized left pneumothorax (red arrow). D) 5-minute post-procedural CT demonstrating expected alveolar hemorrhage in the site of the biopsied cavitary lesion (blue arrowhead), but worsening left pneumothorax (red arrow). E & F) Multiple peripheral left lung cavitary lesions (red arrowheads) felt to be possible culprits for the worsened pneumothorax following coughing from the right-sided biopsy.

 

A gentleman in his late 50s with a past medical history of squamous cell carcinoma at the base of the tongue had numerous slowly-growing pneumocyst-like lesions despite clinical remission status post surgery and chemoradiation. Biopsy of one of these lesions was recommended by a multidisciplinary tumor board.

An outpatient pre-procedural supine chest CT revealed a right pneumothorax above the lesion targeted for biopsy. A subsequent pre-procedural right lateral decubitus chest CT three weeks later demonstrated a left-sided pneumothorax, raising concern for buffalo chest. (A less likely possibility would be spontaneous resolution of the right pneumothorax and development of a new left pneumothorax in the less than 4-week interval.) Intraprocedural imaging continued to demonstrate the left-sided pneumothorax. A biopsy touch preparation of the first sample obtained did not demonstrate malignancy. Therefore, an attempt was made at obtaining another sample. However, the patient developed a brief but forceful coughing fit, resulting in the termination of the procedure after only 2 passes of a 20g needle. Post-procedural scans demonstrated expected right-sided alveolar hemorrhage near the biopsy tract but slight worsening of the contralateral pneumothorax. The patient was again scanned five minutes later for concerns of a worsening pneumothorax. CT imaging demonstrated stable right-sided alveolar hemorrhage near the biopsy tract, but also severe left sided pneumothorax with multiple peripheral cavitary lesions. A left anterior chest tube was placed and the patient was discharged a few days later. Biopsy results showed granulomatous tissue only and cultures were negative.

Buffalo chest refers to the abnormal presence of a pleuro-pleural communication in humans. This phenomenon derives its name from the fact that buffalo and similar species possess one contiguous pleural space, while humans ordinarily have two independent pleural spaces corresponding to each lung (1). This pleuro-pleural communication can develop iatrogenically, congenitally, or as a result of trauma. Cases of buffalo chest developing after median sternotomy, laparoscopic surgery and heart-lung transplantation have been described in the literature (2). It is unknown if the worsening of our patient’s left-sided pneumothorax occurred in the setting of underlying buffalo chest, with biopsy producing a right sided pneumothorax that subsequently communicated with the left pleural space. Alternatively, our patient’s episode of forceful coughing could have increased the intrathoracic pressure and caused barotrauma to one of the many peripheral cavitary lesions previously described, leading to a worsening of the left-sided pneumothorax. Cases of bilateral pneumothoraces where interpleural connections exist have been successfully treated with a unilateral chest tube (2, 3). A second chest tube may be necessary in cases where the contralateral lung fails to re-expand. Our patient was able to be discharged after placement of a unilateral chest tube (contralateral to the biopsy side), reaffirming the general recommendation to treat pneumothoraces this patient population with a unilateral pleural catheter.

Phillip Belone MS4, Jason Lee MD, and Michael Craig Larson MD PhD

University of Arizona/Banner University Medical Center-Tucson

Department of Medical Imaging

Tucson, AZ USA

References

  1. Jacobi A, Eber C, Weinberger A, Friedman SN. Bilateral Pneumothoraces after Unilateral Lung Biopsy. A Case of "Buffalo Chest"? Am J Respir Crit Care Med. 2016 Apr 15;193(8):e36. [CrossRef] [PubMed]
  2. Sawalha L, Gibbons WJ. Iatrogenic "buffalo chest" bilateral pneumothoraces following unilateral transbronchial lung biopsies in a bilateral lung transplant recipient. Respir Med Case Rep. 2015 May 16;15:57-8. [CrossRef] [PubMed]
  3. Groarke J, Breen D, O'Connell F, O'Donnell R. Bilateral pneumothorax resulting from a diagnostic thoracentesis. Eur Respir J. 2007 Nov;30(5):1018-9; diagnosis 1020. [CrossRef] [PubMed]

Cite as: Belone P, Lee J, Larson MC. Medical Image of the Month: Buffalo Chest Identified at the Time of Lung Nodule Biopsy. Southwest J Pulm Crit Care. 2020;21(5):121-3. doi: https://doi.org/10.13175/swjpcc056-20 PDF

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

Medical Image of the Month: Severe Left Ventricular Hypertrophy

Figure 1. An electrocardiogram demonstrates left ventricular hypertrophy by voltage and non-voltage criteria.


Figure 2. Parasternal long view of the heart demonstrates marked left ventricular hypertrophy with partial obstruction of the left ventricular outflow tract.

 

The patient is a 56-year-old man with a history of hypertension who was admitted to ICU after the administration of nitroglycerin for chest pain in the setting of hypertensive emergency resulted in a sudden drop in systolic BP drop from 220 to 106. The above images depict LVH on EKG (Figure 1) along with severe concentric LVH (End-diastolic-wall-thickness = 22mm) with significant apical and septal thickening resulting in partial obstruction of the left ventricle outflow tract concerning for HCM vs HHD (Figure 2).

Significant morphological overlap between HCM and HHD makes establishing a diagnosis difficult and often requires more advanced tissue characterization in the form of cardiac MR. In a patient with severe LVH, a diagnosis of HCM should be considered if ≥ 1 myocardial segment has a LV end-diastolic wall thickness (EDWT) ≥ 15mm on transthoracic echo1. Additional features such as systolic anterior motion of the mitral valve (SAM) are also useful in establishing a diagnosis of HCM, especially in those with concomitant hypertension. A large majority of patients with HCM have elongated mitral valve leaflets which can protrude into the LV cavity. During systole, the mitral valve leaflet moves towards the interventricular septum which is thickened in patients with LVH. This creates a left ventricular outflow obstruction (LVOTO) that causes shortness of breath, chest pain, and syncope. This ultimately increases the risk of arrhythmias and sudden cardiac death.

Treatment of LVOT obstruction is indicated in all symptomatic patients. First line medical management functions to increase preload with negatively inotropic medications such as beta-blockers, disopyramide and verapamil. In patients who are persistently symptomatic despite optimal medical therapy, septal reduction therapy via alcohol septal ablation (ASA) or septal myomectomy (SM) are standard of care2. Long-term data suggests there is no difference in cardiovascular mortality when comparing ASA and SM. However, those receiving ASA have lower periprocedural complications but more often require implantation of pacemakers or reintervention in the future.

April L. Olson MD MPH, Nicholas G. Blackstone MD, Benjamin J. Jarrett MD, and Janet M. Campion MD MPH

University of Arizona College of Medicine at South Campus

Tucson, AZ USA

References

  1. Rodrigues JC, Rohan S, Ghosh Dastidar A, Harries I, Lawton CB, Ratcliffe LE, Burchell AE, Hart EC, Hamilton MC, Paton JF, Nightingale AK, Manghat NE. Hypertensive heart disease versus hypertrophic cardiomyopathy: multi-parametric cardiovascular magnetic resonance discriminators when end-diastolic wall thickness ≥ 15 mm. Eur Radiol. 2017 Mar;27(3):1125-1135. [CrossRef] [PubMed]
  2. Osman M, Kheiri B, Osman K, Barbarawi M, Alhamoud H, Alqahtani F, Alkhouli M. Alcohol septal ablation vs myectomy for symptomatic hypertrophic obstructive cardiomyopathy: Systematic review and meta-analysis. Clin Cardiol. 2019 Jan;42(1):190-197. [CrossRef] [PubMed]

Cite as: Olson AL, Blackstone NG, Jarrett BJ, Campion JM. Medical Image of the Month: Severe Left Ventricular Hypertrophy. Southwest J Pulm Crit Care. 2020;21(4):80-1. doi: https://doi.org/10.13175/swjpcc052-20 PDF

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

Medical Image of the Month: Glioblastoma Multiforme

Figure 1. Non-contrast CT axial views of what was later identified as glioblastoma multiforme demonstrates heterogeneous left frontal lobe mass with foci of hemorrhage (black arrows, A), mass effect (gray arrow, A & B), central necrosis (gray arrowhead, C), invasion of the corpus callosum (gray arrowhead, C), and vasogenic edema (white arrow, D).

A patient in their 60's presented with headaches for approximately 2 weeks followed by acutely worsening mental status with confusion. CT of the head is shown (Figure 1). Glioblastoma multiforme was high on the differential diagnosis.

Glioblastoma multiforme (GBM) is classified as a grade IV astrocytoma and is the most common malignant primary brain tumor. It has an incidence of 3.19 cases per 100,000 persons per year. Astrocytomas are the most invasive type of glial tumor, directly reflecting the remarkably poor prognosis with a 5-year survival rate of approximately 4% and a 26-33% survival rate at 2 years in clinical trials. Symptoms develop relatively rapidly due to edema and mass effect of the tumor. Increased intracranial pressure and swelling manifests as nausea, vomiting, seizures and headaches that are typically worse in the morning. Neurological symptoms are dependent on the location of the cerebrum that is affected (ex. sensory, motor, visual changes, gait disturbances). Conventional gadolinium-enhanced MR imaging is the standard technique for the evaluation of GBM. GBM is characterized by a large, heterogeneous mass in the cerebral hemisphere exhibiting hemorrhage, necrosis and enhancement. In addition, magnetic resonance tomography (MRS) and positron emission tomography (PET) can be used to examine the chemical profile and assist in detecting tumor recurrence, respectively. The current gold standard treatment for GBM is temozolomide in combination with radiation therapy. Two potential new treatment modalities currently under investigation are gene therapy and immunotherapy.

Biopsy of the patient’s mass confirmed glioblastoma multiforme, which was successfully treated without recurrence on MRI 18 months later.

Cassandra Ann Roose and Michael Craig Larson MD, PhD

Medical Imaging Department

Banner University Medical Center/University of Arizona

Tucson, AZ UA

References

  1. Stoyanov GS, Dzhenkov DL. On the Concepts and History of Glioblastoma Multiforme - Morphology, Genetics and Epigenetics. Folia Med (Plovdiv). 2018;60(1):48-66. [CrossRef] [PubMed]
  2. Altman DA, Atkinson DS Jr, Brat DJ. Best cases from the AFIP: glioblastoma multiforme. Radiographics. 2007;27(3):883-888. [CrossRef] [PubMed]
  3. American Association of Neurological Surgeons. Glioblastoma Multiforme. Available from: https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Glioblastoma-Multiforme (accessed 8/24/20).

Cite as: Roose CA, Larson MC. Medical image of the month: glioblastoma multiforme. Southwest J Pulm Crit Care. 2020;21(3):64-5. doi: https://doi.org/10.13175/swjpcc046-20 PDF 

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

Medical Image of the Month and Brief Review: Aspiration Pneumonia in an Intubated Patient with COVID-19

 

Figure 1. Severe aspiration changes on CT. Bronchial wall thickening (white arrow) could barely be perceived elsewhere given the dense layering secretions (black arrows) in bilateral mainstem bronchi and filling the dependent segmental bronchi. Atelectatic collapse (black arrowhead) can be seen distal to the obstructed bronchi. Rounded consolidation (white arrowhead) as seen later in the course of SARS2 COVID-19.

A woman in her 60’s likely acquired COVID-19 through community transmission. When she developed respiratory distress, she came to the emergency department, was found to have abnormalities on chest x-ray and was intubated, testing positive on COVID-19 PCR. She developed worsening hypoxia over the course of one night after a fairly stable ICU course. CT was obtained and demonstrated severe aspiration changes including bronchial filling and collapse of the dependent lower lobes. Increased attention to suctioning helped with the desaturations, and she eventually recovered and was extubated. This case serves as a reminder to ensure adequate suctioning while patients are intubated to prevent aspiration, obstruction and related ventilator-associated pneumonia.

Discussion

Aspiration is a relatively common event which typically resolves with no clinical sequelae. In fact, recent studies have estimated that up to 50% of healthy adults aspirate while in their sleep (1). Pulmonary symptoms of aspiration generally only occur when there is compromise to the usual defenses that protect the lower airways (cough reflex, glottis closure, etc.) and when an inoculum is introduced which has a direct toxic effect on the lower airways, resulting in inflammation. Common predisposing conditions which can lead to aspiration include reduced consciousness (commonly seen in patients with alcohol abuse or IV drug use), dysphagia from neurologic deficits, disorders of the upper GI tract, or mechanical disruption of glottis closure due to endotracheal intubation, bronchoscopy, endoscopy, or NG feeding (2,3). Endotracheal intubation is a key risk factor in ventilator associated pneumonia (4). This brief review will focus on ventilator-associated pneumonia.

Overview and epidemiology: Ventilator-associated pneumonia is defined as new onset pneumonia at least 48 hours following intubation. Despite being frequently thought of as partially protective, the presence of an endotracheal tube may actually serve as a mechanism of transport of organisms from the oropharyngeal tract (most commonly) or GI tract (less commonly) to the lung (5,6). Recent data from 2012 to 2013 suggest that the percentage of patients on ventilator support who go on to acquire aspiration pneumonia is 9.7% (7).  Common pathogens associated with this condition include aerobic gram-negative bacilli (Escherichia coliKlebsiella pneumoniaeEnterobacter spp, Pseudomonas aeruginosaAcinetobacter spp) or gram-positive cocci including MRSA and Streptococcus Pneumoniae.

Prevention: Patients should be placed in the semi-recumbent position (45 degrees) and have intermittent (every 3-6 hours) or continuous subglottic drainage (8,9). Studies have found there isn’t a significant difference in clinical outcomes between intermittent and continuous drainage and that intermittent drainage may be associated with less adverse effects (10). The use of acid reducing agents should also be avoided, although sucralfate use decreased ICU-acquired pneumonia (11). Gastric volume monitoring had long been the standard of clinical practice with an aim to prevent vomiting and subsequent aspiration, however recent studies have suggested that gastric volume monitoring correlates poorly with aspiration risk and may lead to a decrease in caloric delivery (12,13).

Symptoms/Signs

  • Important signs include fever, tachypnea, increased purulent secretions or hemoptysis; systemic signs including encephalopathy or sepsis may also be present (12).
  • Ventilator: Reduced tidal volume, increased inspiratory pressures
  • Labs: worsening hypoxemia, leukocytosis
  • Imaging:
    • New or progressive infiltrates on CXR commonly with alveolar infiltrates or silhouetting of adjacent solid organs
    • Air bronchograms are common

Treatment

Empiric treatment choices should be guided by local distribution of pathogens and susceptibility of those pathogens to antimicrobials (14-16). Treatment options should also take into consideration the likelihood of MDR organisms or MRSA. In a meta-analysis of 15 studies, factors associated with an increased risk of MDR VAP were IV antibiotics in the last 90 days, >5 days of hospitalization prior to onset of symptoms, septic shock on presentation of VAP, ARDS before VAP, and renal replacement therapy prior to VAP. Risk factors for MRSA include treatment in units where >10 to 20% of S. Aureus isolates are methicillin resistant, treatment in a unit where prevalence of MRSA is not known, or prior history of MRSA infection. In the absence of risk factors for MDR or MRSA, patients with VAP should receive one agent that has activity against Pseudomonas, other gram-negative bacilli, and MSSA. Patients with risk factors for MDR or MRSA should receive two agents with activity against P. Aeruginosa and other gram-negative bacilli and one agent with activity against MRSA (15). An algorithm guiding specific regimens for treatment of VAP can be found on UpToDate’s article: Treatment of hospital-acquired and ventilator-associated pneumonia in adults (17).

Jeremy P. Head BS and Michael C. Larson MD

Department of Medical Imaging

University of Arizona

Tucson, AZ USA

References

  1. Huxley EJ, Viroslav J, Gray WR, Pierce AK. Pharyngeal aspiration in normal adults and patients with depressed consciousness. Am J Med. 1978;64(4):564-568. [CrossRef] [PubMed]
  2. Lo WL, Leu HB, Yang MC, Wang DH, Hsu ML. Dysphagia and risk of aspiration pneumonia: A nonrandomized, pair-matched cohort study. J Dent Sci. 2019;14(3):241-247. [CrossRef] [PubMed]
  3. Mandell LA, Niederman MS. Aspiration Pneumonia. N Engl J Med. 2019;380(7):651-663. [CrossRef] [PubMed]
  4. Rouzé A, Jaillette E, Nseir S. Relationship between microaspiration of gastric contents and ventilator-associated pneumonia. Ann Transl Med. 2018;6(21):428. [CrossRef] [PubMed]
  5. Garrouste-Orgeas M, Chevret S, Arlet G, et al. Oropharyngeal or gastric colonization and nosocomial pneumonia in adult intensive care unit patients. A prospective study based on genomic DNA analysis. Am J Respir Crit Care Med. 1997;156(5):1647-1655. [CrossRef] [PubMed]
  6. Jaillette E, Girault C, Brunin G, et al. Impact of tapered-cuff tracheal tube on microaspiration of gastric contents in intubated critically ill patients: a multicenter cluster-randomized cross-over controlled trial. Intensive Care Med. 2017;43(11):1562-1571. [CrossRef] [PubMed]
  7. Metersky ML, Wang Y, Klompas M, Eckenrode S, Bakullari A, Eldridge N. Trend in Ventilator-Associated Pneumonia Rates Between 2005 and 2013. JAMA. 2016;316(22):2427-2429. [CrossRef] [PubMed]
  8. Wang L, Li X, Yang Z, et al. Semi-recumbent position versus supine position for the prevention of ventilator-associated pneumonia in adults requiring mechanical ventilation. Cochrane Database Syst Rev. 2016;2016(1):CD009946. [CrossRef] [PubMed]
  9. Caroff DA, Li L, Muscedere J, Klompas M. Subglottic Secretion Drainage and Objective Outcomes: A Systematic Review and Meta-Analysis. Crit Care Med. 2016;44(4):830-840. [CrossRef] [PubMed]
  10. Mao Z, Gao L, Wang G, et al. Subglottic secretion suction for preventing ventilator-associated pneumonia: an updated meta-analysis and trial sequential analysis. Crit Care. 2016;20(1):353. Published 2016 Oct 28. [CrossRef] [PubMed]
  11. Alquraini M, Alshamsi F, Møller MH, et al. Sucralfate versus histamine 2 receptor antagonists for stress ulcer prophylaxis in adult critically ill patients: A meta-analysis and trial sequential analysis of randomized trials. J Crit Care. 2017;40:21-30. [CrossRef] [PubMed]
  12. Meduri GU. Diagnosis and differential diagnosis of ventilator-associated pneumonia. Clin Chest Med. 1995;16(1):61-93. [PubMed]
  13. McClave SA, Lukan JK, Stefater JA, et al. Poor validity of residual volumes as a marker for risk of aspiration in critically ill patients. Crit Care Med. 2005;33(2):324-330. [CrossRef] [PubMed]
  14. Kalil AC, Metersky ML, Klompas M, et al. Executive Summary: Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society [published correction appears in Clin Infect Dis. 2017 May 1;64(9):1298] [published correction appears in Clin Infect Dis. 2017 Oct 1;65(7):1251]. Clin Infect Dis. 2016;63(5):575-582. [CrossRef] [PubMed]
  15. Beardsley JR, Williamson JC, Johnson JW, Ohl CA, Karchmer TB, Bowton DL. Using local microbiologic data to develop institution-specific guidelines for the treatment of hospital-acquired pneumonia. Chest. 2006;130(3):787-793. [CrossRef] [PubMed]
  16. Jones RN. Microbial etiologies of hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia [published correction appears in Clin Infect Dis. 2010 Nov 1;51(9):1114]. Clin Infect Dis. 2010;51 Suppl 1:S81-S87. [CrossRef] [PubMed]
  17. Klompas M. Treatment of hospital-acquired and ventilator-associated pneumonia in adults. UpToDate. July 31, 2020. Available at: https://www.uptodate.com/contents/treatment-of-hospital-acquired-and-ventilator-associated-pneumonia-in-adults (requires subscription).

Cite as: Head JP, Larson MC. Medical image of the month and brief review: aspiration pneumonia in an intubated patient with COVID-19. Southwest J Pulm Crit Care. 2020;21(2):35-8. doi: https://doi.org/10.13175/swjpcc040-20 PDF 

 

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

Medical Image of the Month: Diaphragmatic Eventration

Figure 1. An upright PA chest radiograph demonstrates marked elevation of the left hemidiaphragm with associated superior migration of the gas-filled colon and mild mediastinal shift towards the right.

 

Figure 2. A: frontal. B: sagittal. A non-contrasted reconstruction of the chest demonstrates marked elevation of the left hemidiaphragm with associated superior migration of the abdominal viscera along with preservation of the integrity of the hemidiaphragm. These findings are consistent with a left hemidiaphragm eventration.

 

Clinical Presentation: A 66-year-old woman presented with a three-year history of progressive postprandial dyspnea and left-sided abdominal pain.  Physical exam revealed normal vital signs and bowels sounds over left lung fields on auscultation. Laboratory work revealed a mild normocytic anemia.  Imaging demonstrated marked left hemidiaphragm elevation with ipsilateral lung parenchyma volume loss and atelectasis along with a mild contralateral mediastinal shift.  A sniff test was consistent with left hemidiaphragm paralysis.

The patient underwent a left video-assisted thoracoscopy, and the left hemidiaphragm was noted to be so thin that the abdominal organs could be visualize through it. The central tendon of the left hemidiaphragm was extremely attenuated and larger than normal. The left hemidiaphragm muscle fibers were noted to be situated around the periphery and not providing any significant tension. The redundant left hemidiaphragm central tendon was excised, and the patient was discharged without symptoms one week later.

Discussion: Eventration of a hemidiaphragm is a rare condition where there is non-paralytic weakening and thinning of a hemidiaphragm resulting in elevation of the hemidiaphragm with retained attachments to the costal margins (1). An eventration usually results from a congenital failure of the fetal diaphragm to muscularized. It is usually unilateral, occurs more on the right than the left, affects the anteromedial portion of the hemidiaphragm, occurs more often in women, and is found after the age of 60 in the adult population. A total eventration of a hemidiaphragm may be indistinguishable from diaphragmatic paralysis and result in a false-positive sniff test – as in this case. When symptomatic, it can pose a diagnostic challenge as it may be confused with a traumatic diaphragmatic rupture in the right clinical setting. Asymptomatic adults do not require treatment.

Leslie Littlefield MD and Mohamed Fayed MD

Department of Pulmonary and Critical Care

University of California San Francisco Fresno

Fresno, CA USA

Reference

  1. Black MC, Joubert K, Seese L, et al. Innovative and Contemporary Interventions of Diaphragmatic Disorders. J Thorac Imaging. 2019;34(4):236-247. [CrossRef] [PubMed]

Cite as: Littlefield L, Fayed M. Medical image of the month: diaphragmatic eventration. Southwest J Pulm Crit Care. 2020;21(1):9-10. doi: https://doi.org/10.13175/swjpcc036-20 PDF 

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

Medical Image of the Month: Aspergilloma – Monod’s Sign

Figure 1 (A) Contrast-enhanced CT of chest showing irregular shape, thick wall cavity with oval heterogeneous soft tissue lesion (black arrow) at the posterior inferior aspect of this cavity. Figure 1 (B) Computed tomography of the chest in the prone position showing the mass moving to dependent region of the cavity (black arrow), known as Monod sign.

A 58-year-old man with a history of human immunodeficiency virus on antiretroviral therapy, bullous emphysematous lung with right upper lobe cavity presented with hemoptysis for three days. On presentation, he was afebrile, with normal oxygen saturation on room air and reduced bilateral breath sounds. Computed tomography (CT) of the chest showed a thick wall cavity at the right upper lobe, with a 3 cm heterogeneous mass at the posterior aspect of the cavity (Figure 1 A). When the patient was placed in the prone position, the soft tissue lesion displaced anteriorly (Figure 1B) showing gravity-dependency (Monod's sign). His serum Aspergillus fumigatus antibodies were also positive. The patient was diagnosed with aspergilloma and started on voriconazole initially. However, because of recurrent hemoptysis, the patient was scheduled to undergo surgical excision. Saprophytic aspergillosis is the causative organism for the development of an aspergilloma (1). It results from colonization of fungus in a preexisting pulmonary cavity which can lead to the formation of a fungus ball within the cavity (1,2). Hemoptysis is the most common presentation. CT scan should be performed in the supine as well as in the prone position to help differentiate from other conditions. In the case of recurrent or life-threatening hemoptysis, surgical excision remains the gold standard option (1).  

Kulothungan Gunasekaran MD, Nageshwari Palanisamy MBBS, Sandra Patrucco Reyes MD, Safal Shetty MD

Division of Pulmonary Diseases and Critical Care

Yale New Haven Health Bridgeport Hospital

Bridgeport, CT USA

References

  1. Sharma S, Dubey S, Kumar N, Sundriyal D. 'Monod' and 'air crescent' sign in aspergilloma. BMJ Case Rep. 2013 Sep 13;2013:bcr2013200936. [CrossRef] [PubMed]
  2. Grech R. Images in clinical medicine. Aspergilloma. N Engl J Med. 2010 Mar 18;362(11):1030. [CrossRef] [PubMed]

Cite as: Gunasekaran K, Palanisamy N, Patrucco Reyes S, Shetty S. Medical image of the month: aspergilloma – Monod’s sign. Southwest J Pulm Crit Care. 2020;20(6):188-9. doi: https://doi.org/10.13175/swjpcc032-20 PDF 

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

May 2020 Imaging Case of the Month: Still Another Emerging Cause for Infiltrative Lung Abnormalities

Prasad M. Panse MD

Clinton E. Jokerst MD

Michael B. Gotway MD

 

Department of Radiology

Mayo Clinic, Arizona

Scottsdale, Arizona 85054

 

Clinical History: A 46-year-old man with a history of well-controlled asthma presented to the Emergency Room with complaints of worsening non-productive cough for 4-5 days followed by fever to 104°F over the previous 3 days. The patient also complained of some chills and loose stools. The patient denied rhinorrhea, sore throat, congestion, and nausea or vomiting. The patient also denied illicit drug use, and drinks alcohol only occasionally and denied smoking.

The patient’s physical examination showed a pulse rate of 79 / minute and a respiratory rate of 18 / minute, although his blood pressure was mildly elevated at 149/84 mmHg; he was afebrile with a temperature of 97.7 °F (36.5 °C). The patient’s room air oxygen saturation was 98%. The physical examination showed some mild expiratory wheezes bilaterally, but was otherwise entirely within normal limits.

Which of the following represents the most appropriate step for the patient’s management? (Click on the correct answer to be directed to the second of twelve pages)

  1. Obtain a complete blood count
  2. Obtain a travel history
  3. Obtain serum chemistries
  4. Perform chest radiography
  5. All of the above

Cite as: Panse PM, Jokerst CE, Gotway MB. May 2020 imaging case of the month: still another emerging cause for infiltrative lung abnormalities. Southwest J Pulm Crit Care. 2020;20(5):147-62. doi: https://doi.org/10.13175/swjpcc027-20 PDF 

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

Medical Image of the Month: Coccidioidal Pneumatocele Complicated by Pulmonary Hemorrhage

Figure 1. Axial CT of the chest without contrast 12 years prior to this hospitalization demonstrates an irregularly-marginated right upper lobe cyst measuring 1.5 x 1.6 cm (red arrow).

 

Figure 2. Axial CT of the chest without contrast obtained 4 months prior to this admission demonstrated a cavitary lesion now measuring 6.3 x 8.2 cm, thin-walled, with small internal air-fluid level and adjacent small pleural effusion without any internal debris (red arrow).

 

Figure 3. An axial CT angiogram of the chest in lung windows demonstrated a right upper lobe pulmonary cavitary lesion increased in size to 10.5 cm in largest dimension with almost complete opacification (red star) concerning for a superimposed infection.

 

A 77-year-old man with emphysema, hypertension, hypothyroidism, and diabetes mellitus presented with two days of worsening cough that progressed to massive hemoptysis. His hemoptysis included clots the size of golf balls and multiple episodes of frank blood, measuring half a cup each. His symptoms included dyspnea at rest, fatigue, and a 15-20-pound weight loss in three weeks. He denied fevers, night sweats, chest pain, hematemesis, and prior hemoptysis. Additionally, he had a history of coccidioidomycosis complicated by a cavitary lung lesion. Per chart review, 12 years prior to this hospitalization the patient had an irregularly-marginated right upper lobe cyst measuring 1.5 x 1.6 cm (Figure 1). A CT scan obtained 4 months prior to admission showed the cavity to be 6.3 x 8.2 cm thin-walled and clear of debris (Figure 2) – consistent with a pneumatocele. The patient was referred to thoracic surgery for possible resection at that time but was lost to follow up.

Admission labs showed a decrease in hemoglobin to 13.4 from a baseline of 15.1 g/dL and white blood cells of 10,300 cells/µL. Blood cultures were negative. CT angiography now demonstrated an increase in the right upper lobe pulmonary cavitary lesion to 10.5 cm in largest dimension with almost complete opacification of the lesion - concerning for a superimposed infection. Imaging also showed tree-in-bud nodules in right middle and lower lobes without evidence of a pulmonary embolism (Figure 3). Coccidioidomycosis serologies by EIA showed a non-reactive IgM with reactive IgG. Acid fast bacilli staining of the sputum was negative. Bronchoscopy performed in the hospital showed fresh blood present in the trachea and in the visualized tracheobronchial tree. Active bleeding was noted only from the posterior segment of the right upper lobe. A bronchoalveolar lavage was performed confirming alveolar hemorrhage centered in the right upper lobe. Lidocaine with epinephrine was instilled to stop bleeding. No endobronchial lesion was seen.

The case was evaluated by an interventional radiologist and cardiothoracic surgeon at our institution. They both felt the patient would benefit from transfer to a larger medical center for definitive management of his hemorrhage. He was transferred to a tertiary academic center for a right upper lobectomy, which he tolerated well.  Surgical pathology and bronchoscopy cultures ultimately grew coccidioides immitis and the patient was discharge on a treatment course of oral fluconazole.

Pulmonary pneumatoceles are thin-walled, air-filled cystic structures. Most pneumatoceles are encountered in infancy; however, they can appear at any age (1). Pneumatoceles are known sequelae of pneumonia but can also occur due to blunt thoracic injury or as a rare side effect of chemotherapy (2,3). While the mechanism of pneumatocele formation is unclear, several theories have been postulated including check-valve bronchial obstruction and narrowing or from parenchymal necrosis with accompanying focal collections of air within the interstitial tissue (5). Such cases are typically asymptomatic and do not require intervention as they resolve within weeks to months (6). While many pneumatocele resolve on their own without additional intervention, complex pneumatoceles may result in uncontrolled hemorrhage, as portrayed in this case, or infected lesions unresponsive to antibiotics - necessitating surgical intervention (7). Other complications of pneumatoceles are rare and may include a tension pneumatocele with cardiorespiratory compromise or pneumothorax (8). 

Staphylococcal pneumonia is frequently complicated by pneumatocele development, with pneumatoceles thought to occur in 61% of cases of staphylococcal pneumonia (9). However, the literature of pneumatocele development following cocci infection is scant. In immunocompetent hosts, infections from coccidiosis are transient, with pulmonary complications (often nodules and self-limited thin-walled cavities) occurring in less than 10% of patients (10).  Complications from coccidiosis infection are usually brief fatigue, dyspnea, cough, and arthritis, with chronic infection or severe complication being rare. Here, we report a case of a gradually enlarging pneumatocele in the setting of cocci infection that eventually eroded into the pulmonary vasculature. The resulting massive hemoptysis was refractory to epinephrine injection and not amenable to catheter embolization. Upper lobectomy was required for definite treatment of the pulmonary hemorrhage.

Sylvester Moses MD, Gregory Gardner MD, Ella Starobinska MD, and Arthur Wolff MD

Department of Internal Medicine

University of Arizona

Tucson, AZ USA

References

  1. Flaherty RA, Keegan JM, Sturtevant HN. Post-pneumonic pulmonary pneumatoceles. Radiology. 1960;74:50-3. [CrossRef] [PubMed]
  2. Aissaoui O, Alharrar R. Traumatic pulmonary pseudocyst: a rare complication of blunt thoracic injury. Pan Afr Med J. 2019 Apr 11;32:180. [CrossRef] [PubMed]
  3. Sangro P, Bilbao I, Fernández-Ros N, Iñarrairaegui M, Zulueta J, Bilbao JI, Sangro B. Pneumatocele during sorafenib therapy: first report of an unusual complication. Oncotarget. 2017 Dec 22;9(5):6652-6. [CrossRef] [PubMed]
  4. Quigley MJ, Fraser RS. Pulmonary pneumatocele: pathology and pathogenesis. AJR Am J Roentgenol. 1988 Jun;150(6):1275-7. [CrossRef] [PubMed]
  5. Zuhdi MK, Spear RM, Worthen HM, Peterson BM. Percutaneous catheter drainage of tension pneumatocele, secondarily infected pneumatocele, and lung abscess in children. Crit Care Med. 1996 Feb;24(2):330-3. [CrossRef] [PubMed]
  6. Kaira K, Ishizuka T, Yanagitani N, Sunaga N, Hisada T, Mori M. Pulmonary traumatic pneumatocele and hematoma. Jpn J Radiol. 2009 Feb;27(2):100-2. [CrossRef] [PubMed]
  7. Kesieme EB, Kesieme CN, Akpede GO, Okonta KE, Dongo AE, Gbolagade AM, Eluehike SU. Tension pneumatocele due to Enterobacter gergoviae pneumonia: a case report. Case Rep Med. 2012;2012:808630. [CrossRef] [PubMed]
  8. Dines DE. Diagnostic significance of pneumatocele of the lung. JAMA. 1968 Jun 24;204(13):1169-72. [CrossRef] [PubMed]
  9. Nayeemuddin M, Jankowich MD, Noska A, Gartman EJ. A strange case of coccidioidomycosis: utilization of bronchoscopy to diagnose a chronic cavitary lesion. Am J Resp Crit Care Med. 2018;197:A5427 [Abstract].

Cite as: Moses S, Gardner G, Starobinska E, Wolff A. Medical image of the month: coccidioidal pneumatocele complicated by pulmonary hemorrhage. Southwest J Pulm Crit Care. 2020;20(3):84-6. doi: https://doi.org/10.13175/swjpcc008-20 PDF 

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

Medical Image of the Month: Idiopathic Right Lower Lobe Pulmonary Vein Thrombus

Figure 1. CT angiogram chest sagittal view: showing low density filling defect consistent with pulmonary vein thrombus (yellow arrow).

 

Figure 2. A: CT angiogram chest axial view showing right lower lobe pulmonary vein thrombus. B: the vein (red arrow) is well differentiated by his lower contrast than the adjacent artery (blue arrows).

 

A 62-year-old man with a medical history notable only for a seasonal allergy, presented to the emergency department with complaints of shortness of breath with productive cough for 2 months which were worsening for the last 2 weeks. CTA chest revealed low density filling defect in the RLL vein consistent with RLL vein thrombus (Figures 1 and 2). After a comprehensive work up to rule out malignancy and hypercoagulable disorders, a diagnosis of idiopathic pulmonary vein thrombosis was made. The patient received heparin and was discharged with rivaroxaban.

Pulmonary vein thrombosis is a rare disease but can be fatal, usually patient presents with non-specific symptoms such as cough and shortness of breath (1). The etiology in most of cases is hypercoagulable disorders, malignancies, atrial fibrillation, post lung operations such as lobectomy and lung transplantation, or could be idiopathic as in our patient.

Timothy Jon Rolle MD1 and Mohammad Abdelaziz Mahmoud MD, DO2
1Department of Radiology and the 2Internal Medicine Residency

Midwestern University Arizona College of Osteopathic Medicine

Canyon Vista Medical Center
Tucson, AZ USA

Reference

  1. Chaaya G, Vishnubhotla P. Pulmonary vein thrombosis: a recent systematic review. Cureus. 2017 Jan 23;9(1):e993. [CrossRef] [PubMed]

Cite as: Rolle TJ, Mahmoud MA. Medical image of the month: idiopathic right lower lobe pulmonary vein thrombus. Southwest J Pulm Crit Care. 2020;20(1):7-8. doi: https://doi.org/10.13175/swjpcc048-19 PDF

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

Medical Image of the Month: Radiation-induced Organizing Pneumonia

Figure 1. Axial contrast enhanced CT depicting marked skin thickening of the right breast with fibrotic changes in the adjacent costal lung parenchyma.

 

Figure 2. Axial/Coronal CT images in lung window showing central ground glass attenuation with surrounding consolidation areas in both lung fields involving regions beyond the radiation field.

 

Radiotherapy post breast conserving surgery has been in vogue for the treatment of early breast cancer. Organizing pneumonia is one of the responses the lung has to acute lung injury. However, an unusual organizing pneumonia is being recognized with peculiarity of involving the lung zones beyond the actual irradiated parenchyma. Clinically patients may be asymptomatic or present with fever, nonproductive cough, dyspnea, malaise, fatigue and weight loss. The “reverse halo” sign describes the central ground glass haze surrounded by consolidation. Subsequent imaging may reveal migratory infiltrates.

The recognition of this entity is important as a differential with a good prognosis. Though the response to steroids is marked, radiation-induced organizing pneumonia can quickly relapse once the steroid is withdrawn (1,2).

Saika Amreen MD, Nidha Nazir MBBS, Naseer A. Choh MD, and Tariq Gojwari MD.

Department of Radiodiagnosis

Sher-i-Kashmir Institute of Medical Sciences (SKIMS)

Soura, Srinagar, India

References

  1. Takigawa N, Segawa Y, Saeki T, et al. Bronchiolitis obliterans organizing pneumonia syndrome in breast-conserving therapy for early breast cancer: radiation-induced lung toxicity. Int J Radiat Oncol Biol Phys. 2000 Oct 1;48(3):751-5. [CrossRef] [PubMed]
  2. Otani K, Seo Y, Ogawa K. Radiation-induced organizing pneumonia: a characteristic disease that requires symptom-oriented management. Int J Mol Sci. 2017 Jan 27;18(2). pii: E281. [CrossRef] [PubMed]

Cite as: Amreen S, Nazir N, Choh NA, Gojwari T. Medical image of the month: radiation-induced organizing pneumonia. Southwest J Pulm Crit Care. 2019;19(6):167-8. doi: https://doi.org/10.13175/swjpcc014-19 PDF

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

Medical Image of the Month: Penicillium Pneumonia Presenting as a Lung Mass

Figure 1. Representative image from thoracic CT scan in lung windows.

 

Figure 2. Panel A: Culture plate showing growth on culture plate. Panel B: Photomicrograph showing the dimorphic fungus taken from the culture plate.

 

A 72-year-old woman who is a non-smoker was referred for evaluation of a suspected lung cancer. She had progressive shortness of breath at rest for 5 months associated with right-sided chest pain, cough and yellowish sputum. She failed multiple courses of antibiotics.

Her past medical history was significant for hypertension, dyslipidemia, hypothyroidism and poorly controlled diabetes mellitus type 2. She also had mild coronary artery disease for which she was on dual antiplatelet therapy. On physical examination, her oxygen saturation was 94% on room air her other vital signs also being unremarkable. Her physical exam revealed decreased breath sounds on the right associated with dullness to percussion.

Her chest radiograph demonstrated right middle lobe opacities. Her chest CT showed a right hilar mass surrounded by multiple nodules along with interlobular septal thickening, a right middle lobe consolidation with air bronchograms, and multiple mediastinal lymph nodes – all suggestive of malignancy (Figure1).

The patient underwent bronchoalveolar lavage and multiple transbronchial biopsies from the right upper and right middle lobes. The lung biopsy showed nonspecific lymphocytic inflammatory infiltrates. Her bronchoalveolar lavage was positive for fungus on PAS stain. The BAL culture showed germ tube negative yeast, which were identified to be Penicillium species (Figure 2).

Fungi are uncommon causes of pneumonia in the general population, but they are more prevalent in immunocompromised hosts with HIV infection, bone marrow transplant, patients on steroids, or patients with neutropenia (1). Penicillium are thermally dimorphic fungi, widely spread in the environment (2). They found especially in soil or where decaying organic material is present. They are saprophytic and capable of causing food spoilage. Patients usually inhale the spores of penicillium present in soil, and so lungs are the primary site of infection. However, disseminated Penicilliosis with lymphadenopathy and organomegaly (especially in immunocompromised patients) can be seen. There was no evidence of disseminated Penicilliosis in our patient. She was not immunocompromised, and her only risk factor was poorly-controlled diabetes mellitus. If not recognized early, Penicillium pneumonia can be fatal. The diagnosis depends on obtaining tissue, sputum and/or BAL samples for fungal cultures. Use of a serum galactomannan antigen assay may facilitate earlier diagnosis of Penicillium infections, however it is not specific for this pathogen as it is a polysaccharide cell wall component of most Aspergillus species as well (3).

There is no consensus about the treatment of Penicillium pneumonia, however standard therapy consists of intravenous amphotericin B, followed by oral itraconazole for several weeks. The optimal duration of treatment is unknown as several cases of relapse have been reported in the literature.

The patient received two weeks of intravenous amphotericin B deoxycholate followed by 12 months of oral itraconazole. The patient improved significantly with resolution of the consolidation seen on her previous chest radiography.

Hasan S. Yamin MD1, Amro Alastal MD2, Abbas Iter MD1, Murad Azamttah1

1Pulmonary and Critical Care, An-Najah University Hospital, Nablus, Palestine

2Pulmonary and Critical Care, Marshall University, WV, USA

References

  1. Kang Y, Feitelson M, de Hoog S, Liao W. Penicillium marneffei and its pulmonary Involvements. Current Respiratory Medicine Reviews. 2012;8(5):356-64. [CrossRef]
  2. Visagie CM, Houbraken J, Frisvad JC, Hong SB, Klaassen CH, Perrone G, Seifert KA, Varga J, Yaguchi T, Samson RA. Identification and nomenclature of the genus Penicillium. Stud Mycol. 2014 Jun;78:343-71. [CrossRef] [PubMed]
  3. Hung CC, Chang SY, Sun HY, Hsueh PR. Cavitary pneumonia due to Penicillium marneffei in an HIV-infected patient. Am J Respir Crit Care Med. 2013 Jan 15;187(2):e3-4. [CrossRef][PubMed]

Cite as: Yamin HS, Alastal A, Iter A, Azamttah M. Medical image of the month: Penicillium pneumonia presenting as a lung mass. Southwest J Pulm Crit Care. 2019;19:164-6. doi: https://doi.org/10.13175/swjpcc033-19 PDF 

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

Medical Image of the Month: Pneumoperitoneum with Rigler’s Sign

Figure 1. CT of the abdomen with contrast showing a large quantity of free air within the peritoneal cavity. The etiology of her free intraperitoneal air was not evident on this imaging study.

 

Figure 2. An upright chest radiograph performed six months later again demonstrates a large amount of free air under the hemidiaphragms, outlining both the spleen and the superior surface of the liver. Rigler’s sign (air on both the peritoneal and luminal side of bowel wall (arrows) - which clearly delineates the bowel wall) is in noted and supports the diagnosis of free intraperitoneal air.

 

Clinical Presentation: A 70-year-old Asian-American woman presented to the hospital with a distended and tympanic abdomen. She was otherwise asymptomatic. Her past medical history was significant only for an uncomplicated colonoscopy the previous summer. A CT scan showed free air within the peritoneal cavity (Figure 1). She was managed conservatively without a surgical intervention. After six months without a chest x-ray continued to show free air (Figure 2). She underwent an elective exploratory laparotomy without identification of a cause for her free intraperitoneal air. Her pneumoperitoneum completely resolved on follow up imaging.

Discussion: Pneumoperitoneum is a condition which commonly presents as an acute abdomen (1). Causes are numerous and include penetrating and blunt abdominal trauma, perforation of viscus, diaphragmatic rupture, fistula formation – among other etiologies. Work-up of pneumoperitoneum varies depending on the suspected etiology. In the presence of hemodynamic instability or peritoneal signs, the patient should proceed to an exploratory laparotomy immediately following airway maintenance and resuscitation. In the setting of a perforation or sepsis, broad-spectrum intravenous antibiotics are indicated. Stable patients are managed expectantly with NPO status, intravenous fluids resuscitation, serial vitals/abdominal imaging/labs, and nasogastric tube decompression if indicated for obstructive etiologies.

Rigler’s sign is well-demonstrated in the abdominal radiograph (figure 2). Rigler’s sign is the presence of air on both the luminal and peritoneal side of the bowel wall – which clearly delineates the bowel wall (1). This sign is highly suggestive of free intraperitoneal air. Rigler’s sign can be seen on a supine abdominal radiograph and can be helpful in the identification of free intraperitoneal air in a patient who may be too ill for upright radiographs or CT imaging.

Mohammad A. Mahmoud MD DO, Jonathon P. Mahn DO, and Alexander E. Brahmsteadt, MSIV.

Midwestern University | Arizona College of Osteopathic Medicine

Canyon Vista Medical Center

Sierra Vista, AZ USA

Reference

  1. Levine MS, Scheiner JD, Rubesin SE, Laufer I, Herlinger H. Diagnosis of pneumoperitoneum on supine abdominal radiographs. AJR Am J Roentgenol. 1991 Apr;156(4):731-5.

Cite as: Mahmoud MA, Mahn JP, Brahmsteadt AE. Medical image of the month: pneumoperitoneum with Rigler's sign. Southwest J Pulm Crit Care. 2019;19(6):156-7. doi: https://doi.org/10.13175/swjpcc047-19 PDF 

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

Medical Image of the Month: Hampton Hump and Palla Sign

Figure 1. A chest radiograph demonstrates a wedge-shaped opacity in the right lung base (red circle) and enlargement of the right descending pulmonary artery branch (blue arrow) consistent with a Hampton hump and Palla sign, respectively.

 

Figure 2. A computed tomography angiogram (CTA) of the chest in a lung window demonstrates a wedge-shaped opacity in the right middle lobe consistent with a Hampton hump (red circle).

 

Figure 3. A CTA of the chest demonstrates an embolus in the right main pulmonary artery which appears slightly dilated (red circle).

 

Figure 4. A CTA of the chest demonstrates extension of the pulmonary embolus into the right lower lobe pulmonary arterial branch (blue circle) along with a right middle lobe pulmonary infarction (red circle) which is better demonstrated in Figure 2.

 

A 51-year-old lady presented to emergency room with acute, severe, right-sided pleuritic chest pain, mild cough and dyspnea at rest. She underwent a lumbar spine laminotomy and foraminotomy twelve days prior to her presentation with limited mobility after her operation. On examination, she was tachypneic and tachycardic. Her blood pressure and oxygen saturations on room air were normal. Chest auscultation revealed a few crackles in the right lung base. There was no pedal edema or calf tenderness.

A chest radiograph demonstrated a right lower lobe wedge-shaped opacity along with right hilar prominence (Figure 1). She was initially diagnosed with a right lower lobe pneumonia and was admitted to step-down unit for further management. However, her history, clinical examination, and chest radiograph findings suggested the high likelihood a pulmonary embolism. A computed tomography angiogram (CTA) of the chest confirmed the diagnosis of a pulmonary embolism (Figures 2-4).

Based her clinical presentation and radiology results, the patient was diagnosed with a sub-massive pulmonary embolism (PE). She was treated with an intravenous heparin drip. She was hemodynamically stable throughout the hospital admission. Her echocardiogram showed no evidence of right ventricular strain. Eventually, she was transitioned to oral anticoagulation and was discharged home in good condition.

Discussion

The wedge-shaped right lower lobe opacity and right hilar prominence correspond to a Hampton hump and Palla sign, respectively. A Hampton hump represents a pulmonary infarction secondary to PE, and it was named by the radiologist Aubrey Hampton in 1940 (1). The Palla sign is an enlarged right descending pulmonary artery, an observation made in 1983 by a radiologist, Antonio Palla (2). Both signs can be seen on chest radiography and may aid in the diagnosis of a PE.

Although these radiologic findings of PE are rare, practicing physicians should be aware of these findings as they can be extremely helpful and expediate the diagnosis of a PE. On the other hand, misinterpretation of these findings can lead to a delay in the diagnosis of other significant chest pathologies.

Abdulmonam Ali MD and Naga S Sirikonda MD

SSM Health

Mount Vernon, IL USA

References

  1. Hampton AO, Castleman B. Correlation of postmortem chest teleroentgenograms with autopsy findings with special reference to pulmonary embolism and infarction. Am J Roentgenol. 1940;43:305–26.
  2. Palla A, Donnamaria V, Petruzzelli S, Rossi G, Riccetti G, Giuntini C. Enlargement of the right descending pulmonary artery in pulmonary embolism. AJR Am J Roentgenol. 1983;141:513-7. [CrossRef] [PubMed]

Cite as: Ali A, Sirikonda NS. Medical image of the month: Hampton hump and Palla sign. Southwest J Pulm Crit Care. 2019;19(5):144-5. doi: https://doi.org/10.13175/swjpcc041-19 PDF

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

Medical Image of the Month: Air Bronchogram Sign

Figure 1. Chest radiograph showing bilateral dense airspace disease with air bronchograms. Veno-venous ECMO catheter is visible tracking from the right internal jugular vein to the inferior vena cava.

 

Figure 2. Chest radiograph on day 5 of ECMO after 4 days of induction chemotherapy demonstrating marked improvement of his airspace disease.

 

An 18-year-old man without any known past medical history presented with a one-day history of progressive shortness of breath. He reported a sudden onset of symptoms the morning of presentation, and an accompanying sensation of confusion with difficulty concentrating. Initial laboratory evaluation was significant for leukocytosis over 60 K/mm3. Due to his increased work of breathing and worsening lethargy, the patient was intubated and sedated for airway protection and ventilatory support. The patient was admitted to the ICU, and his initial chest radiograph was concerning for acute respiratory distress syndrome. Subsequent hematologic analyses from his admission CBC were consistent with a new diagnosis of acute myelogenous leukemia.

Despite aggressive alveolar recruitment maneuvers and maximum ventilator support, the patient’s oxygen saturation remained poor and his respiratory reserve continued to decline. The decision was made to place the patient on veno-venous extracorporeal membrane oxygenation (ECMO) prior to initiating therapy with doxorubicin and cytarabine (7+3 induction protocol). A dual-lumen ECMO catheter was placed in the right internal jugular vein. His initial chest radiograph demonstrated complete bilateral air bronchograms (Figure 1). The patient was started on chemotherapy while on ECMO and was successfully decannulated after five days on the circuit. His chest radiograph on day 5 of ECMO was significant for marked improvement in bilateral airspace disease (Figure 2).

In patients with hematologic malignancy, an inflammatory response can be generated by either the malignant cells themselves, or more commonly as a reaction to subsequent infection. This inflammation often results in protein-rich fluid infiltrating the alveoli. When this process becomes severe enough to cause hypoxic respiratory failure, it can progress to acute respiratory distress syndrome (ARDS) (1). The chest radiograph demonstrates dense airspace disease which developed in this patient. The fluid-filled alveoli in this extreme example of ARDS created a volume of uniform opacities throughout his lung parenchyma which make the conducting airways stand out clearly (2). Segmental air bronchograms can be seen in localized airspace disease, such as atelectasis or pneumonia, but a full-pulmonary air bronchogram of this clarity can only be seen on a patient undergoing ECMO as there are effectively no functional alveoli to participate in gas exchange.

Eric Brucks, MD and Richard Young, MD

Department of Internal Medicine

Banner University Medical Center

University of Arizona

Tucson, AZ USA

References

  1. Papazian L, Calfee CS, Chiumello D, Luyt CE, Meyer NJ, Sekiguchi H, Matthay MA, Meduri GU. Diagnostic workup for ARDS patients. Intensive Care Med. 2016 May;42(5):674-85. [CrossRef] [PubMed]
  2. Natt B, Raz Y. Air Bronchogram. N Engl J Med. 2015 Dec 31;373(27):2663. [CrossRef] [PubMed]

Cite as: Brucks E, Young R. Medical image of the month: air bronchogram sign. Southwest J Pulm Crit Care. 2019;19(4):119-20. doi: https://doi.org/10.13175/swjpcc036-19 PDF 

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

Medical Image of the Month: Large Complex Cerebral Arteriovenous Malformation

Figure 1. Computed tomography angiography of the head showing the large complex arteriovenous malformation near the midline of the brain. A: sagittal plane the malformation is fed predominantly by the anterior circulation more on the right and the left. B: coronal plane.

A 70-year-old woman with a history of hypertension presented with left-sided weakness, headache, nausea, and vomiting. She denied loss of consciousness or seizure activity. On examination, she had receptive aphasia. Pupils were equal, round and reactive. She had neck pain on flexion. Her left upper extremity was plegic. Computed tomography of the brain showed acute hemorrhage involving the right thalamus, extending into the ventricular system, and a midline mass. She underwent a computed tomography angiogram, which showed a large, complex arteriovenous malformation (AVM) with a dilated branch of the right suprasellar internal carotid artery feeding the AVM, which then drained into the vein of Galen and straight sinus (Figure 1). She was monitored in the intensive care unit without worsening neurological deficit. She was discharged to a rehabilitation facility, having had no intravascular or surgical intervention.

AVMs are intracranial vascular anomalies which occur in 0.1% of the population (1). Clinical presentations include intracranial hemorrhage, seizures, headaches and neurological deficits, with hemorrhage being the most common and significant manifestation (2). The gold standard imaging modality is conventional cerebral angiography (1). Treating an AVM is a challenging clinical problem, as the risk of treatment has to be weighed against the natural history of the condition. Treatment modalities include observation with medical management, surgical resection, stereotactic radiosurgery, and endovascular embolization (1,2).

Vedhapriya Srinivasan MD, Piruthiviraj Natarajan MD, Reuben De Almeida, Safal Shetty MD, and Kulothungan Gunasekaran MD.

Bridgeport Hospital

Yale New Haven Health

New Haven, CT USA

References

  1. Ajiboye N, Chalouhi N, Starke RM, Zanaty M, Bell R. Cerebral arteriovenous malformations: evaluation and management. ScientificWorldJournal 2014;2014:649036. [CrossRef] [PubMed]
  2. Geibprasert S, Pongpech S, Jiarakongmun P, Shroff MM, Armstrong DC, Krings T. Radiologic assessment of brain arteriovenous malformations: what clinicians need to know. RadioGraphics. 2010;30:483-501. [CrossRef] [PubMed]

Cite as: Srinivasan V, Natarajan P, De Almeida R, Shetty S, Gunasekaran K. Medical image of the month: large complex cerebral arteriovenous malformation. Southwest J Pulm Crit Care. 2019;19(3):97-8. doi: https://doi.org/10.13175/swjpcc027-19 PDF 

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