The gastric juice aspiration syndrome (Mendelson syndrome)

Abstract

The gastric juice aspiration syndrome (GJA-S, Mendelson syndrome) was studied experimentally in pigs. Following instillation of gastric juice into the right main bronchus necrosis of pneumocytes and bronchiolar epithelium occurred with activation of complement and a prostaglandin E releasing system (possibly the kinin system). Cell necrosis was followed by loss of surfactant and formation of hyaline membranes, rich in immunoglobulin M. The alveolar damage organized, resulting in intraalveolar and interstitial fibrosis. The causative agents were found to be both gastric hydrochloric acid and pepsin. Pretreatment with H2-, or acetylcholine-receptor-antagonists (cimetidine or pirenzepin) as well as buffering of the gastric juice to a neutral pH did not prevent lung fibrosis. If a mixture of aluminium hydroxide, magnesium carbonate and oxethazaine was added to the aspirate, development of lung fibrosis was prevented, but severe granulomatous reaction with foreign body giant cells within both lungs evolved. Kallikrein inhibitor, when administered intravenously not later than 3 min after artificial aspiration, protected the left lung completely and large areas of the right. If infused within 60-90 s complete protection of the left lung and the right upper lobe was achieved. In the majority of the animals a mild focal fibrosis developed in the right lower lobe; in one experiment both lungs were devoid of fibrotic areas. If Kallikrein inhibitor was infused 5 min prior to aspiration, lung fibrosis was not prevented.

High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis

“…Pulmonary fibrosis (PF) has been induced by direct instillation of acid into the airways of animals in experimental models of PF [16][17][18]. In a pilot study, abnormal acid GER was documented in 16 out of 17 patients with IPF [19].…”

Bronchiolitis, an update

“…Some acidic aerosols can cause this bronchiolitis. This is the case in Mendelson's syndrome, where hydrochloric acid together with pepsin are the actors [43]. Due to the fact that the basal lamina is destroyed or at least interrupted, this kind of bronchiolitis will never heal 'ad integrum' and can progress into BO-organizing pneumonia (BOOP) [43].…”

“…For example, particulate matter between 200 µm and 5 µm of aerodynamic diameter will primarily cause bronchitis and bronchiolitis but rarely inflammation in the alveolar region. Gases, aerosols, or particulate matter <5 µm will easily pass the larger airways, causing either no or only mild inflammatory reactions, whereas the major inflammatory reaction will be seen in the bronchioles and the alveoli [43,44]. Viral infection in an otherwise immunocompetent patient will present as a lymphocytic inflammation in the bronchi, bronchioles, and alveoli, whereas bacteria early on causes a granulocytic inflammatory response.…”

“…Respirotropic viruses, for example, preferentially dock to ciliated and Clara cells, whereas bacteria preferentially dock to ciliated and secretary columnar cells [26,31,32,46]. Inorganic toxic substances show an order of susceptibility of ciliated > Clara > secretory cells [43,53]. Therefore, if early stages of the inflammatory process are carefully examined, one can tell viral infection apart from bacterial infection and infection from toxic injury by analyzing the main targeted cells, the reaction of the cells and, very importantly, the types of leukocytes entering the inflammatory focus, i.e., lymphocytes in early viral and macrophages and neutrophils in early bacterial infection.…”

“…3). In addition, these acidic compounds characteristically cause constriction of smooth muscle cells [43]. Endogenous noxes primarily act on endothelial cells and cause interstitial edema and leakage of capillaries.…”