Biopolymers, often used to fill certain areas of the body, are not completely inert and can generate local or systemic complications, such as infection, necrosis, foreign body reaction, lymphadenopathy and febrile syndrome [3, 5, 8, 9]. Non-thrombotic pulmonary embolism is uncommon, and it frequently occurs with no clinical characteristics, that's why it requires peculiar diagnostic measures, as well as treatment options [3, 5, 6, 7]. Different components, whether ubiquitous in the human body, foreign bodies, or liquids, can be transported through the bloodstream and embolize the pulmonary circulation.

In contrast to pulmonary thromboembolism, the effects of non-thrombotic pulmonary embolism are not purely mechanical; these are also related to the nature of the embolic agent, which is why its pathogenesis is more complex [1, 3]. In 1987, Jean Chastre and his team described that injections of biopolymers are a risk factor at the respiratory level, since they are capable to induce acute pneumonitis, which can evolve, in some patients, to acute respiratory failure; in turn, pneumonitis can also be induced if there is a trauma in the site where it was applied, even though many years have passed since its application; there is latent pneumonitis, which is seen in patients who develop inflammation at the injection site. [3, 4, 5, 8]. There are reports of patients who died after injection of biopolymers due to severe pulmonary edema, which reinforces the theory that biopolymers induce acute pneumonitis [6, 8, 9, 10]. The application of a non-ubiquitous substance to the body in large quantities and directly to body tissues, under high pressure, results in tissue damage which, through inflammation, allows the substance to enter the bloodstream [2, 3]. Cases have been described where biopolymer embolisms are deposited in the arterioles which increases pulmonary arterial pressure causing cor pulmonale. [6, 9]. Alveolitis in biopolymer pneumonitis is characterized by an increase in the number of macrophages, neutrophils, and eosinophils. [3, 4]. Acute pneumonitis consists of phagocytosis of the biopolymer carried out by macrophages, neutrophils, and lymphocytes, secondary to the liquid biopolymer reaching the alveolar space after pulmonary embolization, causing cell-mediated cellular                 inflammation.      Schmid's                group      described               that when macrophages phagocytose the biopolymer, an inflammatory response occurs, which activates endothelial cells, increasing capillary permeability, therefore modulating, and regulating the alveolar response [7].

Two types of post-injection pneumonitis have been described by biopolymers; an acute form which can occur from the application of the biopolymer until a few days after application and presents with sudden dyspnea, fever, mild to moderate hypoxemia, tachycardia and sometimes acute respiratory failure; X-rays typically show a bilateral alveolar pattern with an area of consolidation in patches, as is the case of the patient, which, given the current global health context, led to COVID-19 infection being considered first-instance within the differential diagnoses. The most common abnormalities seen biopolymer pneumonitis were the same as in COVID-19; ground glass opacities, vascular enlargement, bilateral abnormalities, lower lobe involvement, and posterior predilection, that's why the diagnosis of this entity was based on the antecedent of biopolymer injection and PCR negative for SARS CoV-2 [14].

The pulmonary histologic findings of COVID-19 are characterized by acute and organizing diffuse alveolar damage, while biopolymer pneumonitis characterized by silicon emboli, hemorrhage-congestion, acute pneumonitis, as is the case previously described, and diffuse alveolar hemorrhage. [8, 12-14]. There is also a latent form of pneumonitis which appears six months after the last biopolymer injection, usually presenting with inflammation of the injection site and moderate respiratory symptoms; the patient described in the case had a previous session of injections 6 months before, so it can be considered at a given time that he was predisposed to presenting pneumonitis [3]. The usual treatment is rest, high-flow oxygen, and mechanical ventilation in some cases; There is still no consensus regarding the use of corticosteroids, however there are several case reports where when started early are useful to reverse the clinical course in a favorable way; patients generally recover without sequelae, but there are reports where patients have presented pulmonary fibrosis. [4, 9, 10, 12, 13]. Although the clinical and imaging findings of pneumonitis due to biopolymers and COVID-19 are similar, treatment is quite different because use of steroids in the first case are crucial and high doses recommended while in COVID-19 is only recommended in severe cases with a standard dose [5, 9, 15].