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.