Teaching Case

An alcoholic 31-year-old man, otherwise healthy, was admitted to the Emergency Department 4 hours after ingesting an herbicide to commit suicide. Digestive decontamination and haemodialysis were immediately performed and the patient survived. He was discharged 2 months later. One year later he gradually became increasingly breathless on effort.

The chest radiograph at the time of admission was clear. Seven days later there was a diffuse pattern of consolidation on radiography (Fig. 1) but the patient remained asymptomatic.
He missed all follow up chest radiographs and medical appointments until the day he started to experience shortness of breath. He underwent radiography (Fig. 2) that disclosed a reticular appearance.
Subsequently performed high resolution CT demonstrated extensive lung fibrosis with alveolar destruction, distributed predominantly in the central regions of the lung. The honeycombing resulted in thick walled, air-filled cysts measuring not more than 1cm and arranged in several layers (Fig. 3).

Paraquat is an herbicide highly toxic used in agriculture and causes damage to the lungs, liver and kidneys [1]. Exposure usually results in death, either due to gastrointestinal caustic lesions, shock, acute respiratory distress syndrome or related to the progressive development of pulmonary fibrosis associated with refractory hypoxemia. The cytotoxic effects of paraquat have been attributed to the generation of superoxide radicals after reduction of paraquat by intracellular oxidases [2]. Ingestion of a large quantity of paraquat leads to rapid onset of pulmonary edema. Ingestion of smaller doses results in delayed onset of pulmonary abnormalities, which may progress to respiratory failure. The radiographic appearance of paraquat pneumonitis varies widely and is non-specific [1].
On chest radiographs, initially there is diffuse air-space consolidation (first 7 days) indicative of pulmonary edema, followed by diffuse cystic and linear shadows (next 7 days). Consolidation or diffuse haziness evolves later to a pattern of focal interstitial opacities that contained small cysts – honeycombing (one month after paraquat ingestion) [2, 3]. Pneumomediastinum occurs frequently and may result from pulmonary interstitial emphysema or esophageal perforation.
On high resolution CT early abnormal findings include thickening of alveolar walls and septa, microatelectasis and alveolar hemorrhage that appear as bilateral and diffuse areas of ground-glass attenuation and evolves into consolidation with bronchiectasis, irregular lines, and traction bronchiectasis. Late findings are pulmonary fibrosis and microcyst formation. In this stage lung structure is entirely disorganized and replaced by many small (0.5- 2.0 mm) cysts lined by fibrous tissue [2, 3]. An interesting finding is that in most cases paraquat-induced pulmonary fibrosis involves the central regions of the lung, whereas idiopathic pulmonary fibrosis primarily involves the lung periphery.
At pathologic analysis, an exudative phase of diffuse alveolar damage is often initially seen in individuals who survive for several days, followed by interstitial fibrosis in the later phase [1].
Paraquat poisoning should be considered in the differential diagnosis of patients who have unexplained renal failure or progressive pulmonary changes, particularly if there is a history of a persistent sore throat or unexplained painful dysphagia [4].
Paraquat toxicity in the lung is more severe than in other organs because of the delayed effect of paraquat [3]. Its concentration is high in the lungs for 7 days, whereas in other organs there is a rapid decrease in concentration 24-36 hours after ingestion.
There is no specific treatment for paraquat poisoning. The goal is to relieve symptoms and treat complications.