Background

Paraquat, which also has the chemical name 1,10 -dimethyl-4,40 –bipyridinium dichloride, is an organic heterocyclic contact herbicide that is widely used in agriculture for weed and grass control throughout the world and especially in China. The main toxokinetic mechanism of paraquat toxicity involve the formation of superoxide anions during the ’redox cycling process’ which then leads to the formation of toxic reactive oxygen species such as hydrogen peroxide and hydroxyl radical in the presence of NADPH and cytochrome P450 reductase.1 2 3 The accumulation of reactive oxygen species leads to cell death in different organs. The clinical complications that arise from paraquat poisoning are; acute renal failure, liver toxicity, respiratory failure, and mucosal injury. 4 5 Early mortality can occur within 1–4 days due to multiple organ failure, while delayed mortality can occur after as long as 3 weeks as a result of respiratory failure secondary to pulmonary fibrosis. The prognosis of paraquat poisoning is poor, and this is elicited by its high mortality rate of 36-90%. 6 7
Oral ingestion of paraquat is accompanied by severe oral mucosal injuries (ulcerations of the oral mucosa and the tongue) and corrosive esophageal injuries. Paraquat exposure leads to the over accumulation of reactive oxygen species and oxidative stress exerted to the mucosa.8 9 The body produces a strong emergency response by the production pro-inflammatory cytokines and stress responders. This amplified response causes a cycle of constant production of cytokines that result in further damage and ulceration of the mucosa. 10 The early manifestations of mucosal injury are erythema, congestion and edema of the mucosa, which then progresses to erosion, inflammation, ulceration, coating, bleeding, and sloughing of the oropharyngeal mucosa. These changes are observable within hours to several days after the ingestion of paraquat.11 12
Patients with oral mucosal injury experience unbearable pain that most describe as a severe burning sensation. The pain associated with paraquat induced mucosal injury significantly compromises nutritional intake, mouth care, and quality of life. The severity of mucosal injury can also be exacerbated by local factors, such as trauma from overzealous oral hygiene, improper nutrition or microbial colonization leading to infections. Infections associated with mucosal injury not only increases the intensity of pain experienced by the patients but may also end up causing life threatening systemic sepsis.13 Decreased nutritional intake also lead caloric deficits that compromise the patients nutritional status, reduce treatment response, increase treatment complications, and further elongate hospital stays.
Literature concerning paraquat induced mucosal injury is sparse and not detailed. Through this systematic review, we hope to evaluate and highlight the correct techniques to achieve proper oral care, nutritional support and possible clinical-therapeutic interventions that have proven to be effective in managing paraquat mucosal injuries, with the aim of reducing patient discomfort and overall improving the patients’ quality of life.