Iodine quantification to assess inflammation in patients with COVID-19

75-year-old man with prior history of hypertension, coronary and chronic obstructive pulmonary disease was admitted for sudden onset of dyspnea. Laboratory examinations showed lymphopenia, increased C-reactive protein, D-dimer and troponin T levels. Pulmonary CT angiography to rule out pulmonary embolism was performed, after findings; COVID-19 was confirmed with RT-PCR test.

A dual-energy CT (DECT) pulmonary angiography ruled out pulmonary embolism (PE) and showed bilateral, diffuse ground glass opacities (GGO), lacking a specific distribution (Fig. 1, A-B). Visual inspection of the iodine maps (Syngo.via, Siemens Healthineers, Forchheim, Germany) revealed higher iodine content within the GGO (Fig. 1, C-D). Quantitative analysis of the iodine concentration demonstrated average iodine concentrations (IC) of 3.1 mg/ml in the GGO and 0.3 mg/ml in the non-affected lung parenchyma, respectively (Fig. 1, E-F). This finding allowed to consider an acute inflammatory lung injury likely secondary to an atypical infection. Even if indeterminate in appearance [1], COVID-19 was suggested, which was later confirmed with PCR test.

The novel Severe Acute Respiratory Syndrome-Coronavirus (SARS-CoV-2) outbreak that emerged in Wuhan (China) in December 2019 is the responsible of the most important viral infection in the last 100 years. In March 2020, the World Health Organization (WHO) declared the infection as Pandemic and COVID-19 (Coronavirus Disease 2019) as the official acronym to refer to the disease caused by the viral infection.

Clinically, COVID-19-infected pneumonia is characterised by fever, fatigue, dry cough and dyspnea. Chest CT is of great value in the diagnosis and prognosis of COVID-19. The pattern of bilateral and predominantly peripheral ground glass and consolidative pulmonary opacities is emerging as a CT hallmark of COVID-19 pneumonia [1,2]. However, some CT imaging findings in COVID-19 may not be specific or may even overlap with other entities, such as cardiogenic pulmonary oedema.

In our patient, the acute clinical presentation raised the clinical suspicion of PE or congestive heart failure. For this purpose, a dual-energy CT pulmonary angiography was performed. The exam ruled out PE but showed diffuse bilateral GGO involvement. Quantitative determination of the IC within the affected lung allowed to establish the inflammatory nature of lung involvement. In our case, the IC was higher in the affected lung areas (3.1 mg/ml) with respect to the normal parenchyma (0.3 mg/ml). This increase in IC within the areas of GGO probably reflects the increased blood flow due to the high permeability of the capillary wall in the acutely inflamed tissue (inflammation and reactive hyperemia). This observation has been previously described in the context of acute interstitial lung disease (AILD) [3]. In a cohort of patients undergoing dual-energy CT to exclude PE, Takeuchi et al. were able to differentiate AILD from cardiogenic pulmonary oedema based on the IC. Similar to our case, these authors observed significantly higher IC values within the affected areas in patients with AILD than in patients with cardiogenic pulmonary edema [3]. In the latter, the IC tends to be homogeneously increased within the entire lung parenchyma. It is reasonable to think AILD and acute inflammatory changes due to infection very likely share a common mechanism and physiopathology originated by a pulmonary insult that produces marked hyperemia and inflammatory cascade.

In challenging cases, when alternate diagnoses are suspected, patients with COVID-19 may benefit from a dual-energy CT pulmonary angiogram. In addition to confirming or ruling out pulmonary embolism, the quantification of the iodine content within the affected lung helps to establish the inflammatory nature of the radiological findings and to differentiate them from other entities, such as cardiogenic pulmonary oedema.