It is uncommon to detect abnormalities by thoracic radiographic examination at the early stages of the paraquat-induced respiratory syndrome; however, thoracic radiographs may provide useful information during the later stages. In people, thoracic abnormalities that are detectable by radiography the first week after paraquat ingestion include a bilateral ground-glass pulmonary shadow, diffuse consolidation, pneumomediastinum with or without pneumothorax, and cardiomegaly with widening of the superior mediastinum.^18-20

Histopathologic lesions

Histologic evidence of widespread pulmonary alveolar damage, hemorrhage, and edema are typical of the early stages of paraquat poisoning in dogs.^2,3 The classic progression of lung changes in people starts with detachment or necrosis of alveolar type I and type II cells, edema, and hemorrhage. These changes are followed by the proliferation of fibroblasts and polymorphic cells, the loss of surfactant secretion, attempts at re-epithelialization of the alveolar surface, and eventual thickening of the alveolar septa from interstitial fibrosis. In people that survive the acute phases of paraquat toxicosis, marked pulmonary fibrosis usually develops two or three weeks after ingestion.²

Diagnosis

Paraquat toxicosis is usually diagnosed through a combination of clinical history, the results of a histologic examination of affected tissues, and detection of paraquat in tissue or bait samples. Spectrophotometry, gas and liquid chromatography, and radioimmunoassay have all been used to measure paraquat concentrations in biologic fluids; however, because prompt recognition of paraquat poisoning is a key factor in its treatment, using fast qualitative tests based on the dithionite reaction (i.e. dithionite spot test) may offer an important advantage.³ In the acute stages of paraquat poisoning, vomitus, gastric contents, bait or concentrate samples, feces, and lung and renal tissue are ideal samples. Blood or plasma may be tested, but circulating paraquat concentrations are much lower in blood and plasma than concentrations in the lungs.

Treatment

Currently, no specific antidote for paraquat poisoning is available. The most important determinant of survival after ingestion is early treatment.² Treatment must be instituted within hours of exposure to be effective. The initial treatment priorities for paraquat poisoning are administering an adsorbent to neutralize ingested paraquat and removing the poison by emesis or gastric lavage. Traditionally, fuller's earth (i.e. attapulgite clay, calcium montmorillonite) or bentonite (i.e. sodium montmorillonite) adsorbents have been used. Keep in mind that the adsorbent capacity of fuller's earth varies among manufacturers and that only highly adsorbent, pharmaceutical-grade preparations should be used.²²

Experimental studies have demonstrated that activated charcoal is an effective in vivo paraquat adsorbent. Activated charcoal's in vitro binding of paraquat is equivalent to that of fuller's earth.²³ Thirty percent activated charcoal administered as an aqueous oral slurry is as effective as 30% fuller's earth administered as an aqueous oral slurry in reducing the systemic absorption of paraquat up to one hour after ingestion.²⁴ In cases of experimental paraquat poisoning in rodents, concomitantly administering activated charcoal and magnesium citrate improved the survival rate.²³ Since fuller's earth and bentonite are usually not on hand, it's better to go ahead and administer activated charcoal.²⁵ In an emergency, pulverized clay-based cat litter has also been suggested as an alternative adsorbent.²⁵ Cation exchange resins, such as sodium polystyrene sulfonate (Kayexalate—Sanofi-Synthelabo), have much higher paraquat-binding capacities than other adsorbents, increase the LD₅₀ up to 2.1 times in rats, and improve survival rates in people.²⁶ Unfortunately, these materials are not routinely available in veterinary practice. Because of the risk of esophageal perforation, use extreme care when administering adsorbents through a stomach tube.