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What lies beneath: poking a hole in the diagnosis
  1. Natalya Kozlova1,
  2. Anna Rozenshtein2,
  3. Soumya Mikkilineni3,
  4. Yevgeniy Linnik4,
  5. Oleg Epelbaum1
  1. 1Pulmonary, Critical Care and Sleep Medicine, Westchester Medical Center Health Network, Valhalla, New York, USA
  2. 2Department of Radiology, Section of Cardiac and Thoracic Imaging, Westchester Medical Center Health Network, Valhalla, New York, USA
  3. 3Department of Pathology, Westchester Medical Center Health Network, Valhalla, New York, USA
  4. 4Department of Pathology, Vanderbilt University Medical Center, Nashville, Tennessee, USA
  1. Correspondence to Dr Natalya Kozlova, Pulmonary, Critical Care and Sleep Medicine, Westchester Medical Center Health Network, 100 Woods Road, Macy Pavilion, Valhalla, NY 10595, USA; natalya.kozlova{at}wmchealth.org

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Natalya Kozlova (NK), respiratory specialist trainee

A man aged 77 years was referred to the emergency department (ED) of our hospital by his primary physician for evaluation of dyspnoea and hypoxaemia. On presentation to the ED, he reported 2 months of progressively worsening dyspnoea and non-productive cough. He also endorsed weight loss and fatigue. He had been prescribed a recent course of clarithromycin after an episode of fever, but this did not ameliorate either the dyspnoea or the cough. On the day he was referred to the ED, his primary physician found him to be hypoxemic, which is what prompted the referral.

The patient’s medical history was significant for hypertension and coronary artery disease with myocardial infarction and coronary stenting 4 years prior to admission. His usual home medications included aspirin, carvedilol, losartan, rosuvastatin, sertraline and zolpidem. He was a former smoker who quit 25 years earlier after accumulating 40 pack-years. He had no occupational or environmental exposures.

On admission, his hypoxaemia was confirmed with an oxygen saturation by pulse oximetry on room air of 76%. The patient was visibly dyspnoeic and had diffuse bilateral crackles on auscultation. His jugular venous pulse was normal. There was no clubbing or oedema. Routine laboratory evaluation was remarkable for a brain natriuretic peptide level of 557 pg/mL (normal <100 pg/mL). There was no blood eosinophilia. Testing of a nasopharyngeal swab specimen for the most common respiratory viral pathogens and Bordetella pertussis by PCR was negative. Frontal chest radiograph (CXR) obtained in the ED demonstrated extensive bilateral airspace opacification (figure 1A), which was new compared with a CXR taken 18 months earlier. There were no pleural effusions. Intravenous furosemide was administered for a presumptive diagnosis of cardiogenic pulmonary oedema. However, the patient’s symptoms and oxygenation failed to improve. Transthoracic echocardiography showed focal left ventricular wall motion abnormalities. However, systolic function …

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Footnotes

  • Contributors NK prepared the manuscript, formatted it for publication and reviewed it in its final form. AR provided content input, formatted the radiology figures, edited the manuscript and reviewed it in its final form. YL and SM provided content input, formatted the pathology figures, edited the manuscript and reviewed it in its final form. OE oversaw the conception, writing, formatting, editing and review of the manuscript in its final form.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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