(Chest. 2001;119:1956-1957.)
© 2001
American College of Chest Physicians
Tracheal Injury Caused by Ingested Paraquat*
Manuel Ruiz-Bailén, MD;
María del Carmen Serrano-Córcoles, MD and
José Ángel Ramos-Cuadra, MD
*
From the Intensive Care Unit (Drs. Ruiz-Bailén and Ramos-Cuadra) and Emergency Unit (Dr. Serrano-Córcoles), Critical Care and Emergencies Department, Hospital de Poniente, El Ejido, Almería, Spain.
Correspondence to: Manuel Ruiz-Bailén, MD, C/. Las Torres 57, 23650 Torredonjimeno, Jaén, Spain; e-mail: MRB1604{at}teleline.es
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Abstract
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Paraquat is a potent herbicide of lethal toxicity. Its injury
mechanism is attributed to the generation of very-reactive oxygen
species, such as superoxide radicals, through which multiple injuries
are produced on mucosa, although there have been no reports of injuries
on the trachea. We describe a case of fatal paraquat poisoning with
tracheal injuries, where the clinical debut was acute respiratory
insufficiency and a spontaneous pneumothorax.
Key Words: paraquat • pneumothorax • poisoning • trachea
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Case Report
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A 20
-year-old man came to our emergency department with a 1-day history of
odynophagia, pharyngeal pruritus, general malaise, and fever, but
without presenting severe symptomatology. He denied any history of
suicide attempts and received a diagnosis of pharyngotonsillitis. He
received outpatient treatment with amoxicillin and paracetamol. After
16 h, he returned to the emergency department with acute
respiratory insufficiency; on this occasion, he admitted the ingestion
3 days earlier of approximately 100 mL of a 20% paraquat compound,
because of a transient suicidal impulse. The examination showed major
bilateral subcutaneous emphysema (from mandible to lower extremities).
Radiography revealed right pneumothorax of 35%, pneumopericardium, and
pneumomediastinum. He presented with hyperthermia, hypotension,
tachycardia, tachypnea, and a low level of consciousness. Basal
analytical findings were as follows: leukocytosis; prothrombin
activity, 47%; urea, 148 mg/dL; serum creatinine, 8.8 mg/dL; direct
bilirubinemia, 8.8 mg/mL; aspartate aminotransferase, 175 mg/dL; plasma
amylase, 5,349 U; hyponatremia and hyperkalemia;
PaO2/fraction of inspired oxygen
ratio, 95; and metabolic acidemia. The concentration of paraquat in
blood was 1.25 µg/mL, determined at the time of hospital admission (3
days after the ingestion) by spectrophotometry. Findings of culture
analyses were all negative. The chest CT scan revealed right
pneumothorax, pneumomediastinum, and pneumopericardium, and ruptured
continuity of the posterior tracheal wall (Fig 1 ). The bronchoscopy findings were as follows: multiple pearly
ulcerations in the oral cavity, friable and hyperemic tracheal mucosa
with abundant material of purulent appearance, necrotic ulcers in the
trachea and entire bronchial tree, and a necrotic lesion that permitted
visualization of a break in the continuity of the posterior tracheal
wall. The patient developed ARDS and distributive shock that progressed
to hyperacute multiorgan failure, with hepatic, renal, neurologic,
respiratory, hemodynamic, and hematologic failures that caused the
death of the patient 24 h after his admission.
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Discussion
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Paraquat (1,1 dimethyl-4,4-bipyridilium chloride) has been used as
a herbicide since 1962 and is the most widespread weed killer among the
group of bipyridilium compounds with quaternary structures. Paraquat is
heavily used in greenhouse cultivation in our region (Almería,
Spain). It is a potent herbicide that rapidly destroys plants in the
presence of light and oxygen. Poisoning in humans is normally produced
by ingestion because of accident or suicide attempt (although
percutaneous absorption has also been reported), which produces, as in
the present case, a multisystemic involvement, with injuries to the
lungs, kidneys, liver, brain, heart, suprarenal gland, or
muscles1
until multiorgan failure, ARDS, or lung fibrosis
develops.2
A large ingestion of this toxin, as in our
case, is rapidly followed by the onset of a major inflammatory process
in the oropharynx, esophagus, and stomach that translates into nausea,
vomiting, abdominal pain, and diarrhea,1
and normally
generates toxic hepatitis with centrolobular necrosis and myocarditis,
occasionally with a reduced level of consciousness. Very rarely,
spontaneous extra-alveolar air appears (pneumothorax,
pneumomediastinum, pneumopericardium, subcutaneous emphysema), which
has been ascribed to a direct provocation by the toxin of acute lung
injury, with the formation of subpleural bullae followed by
rupture.3
We present a case of massive paraquat poisoning, with the peculiarity
that the corrosive effects of the paraquat itself also caused injuries
to the trachea and principal bronchi. Although there have been reports
that the local corrosive effect of paraquat produces ulcerated lesions
in the oropharynx, esophagus, and stomach,4
the tracheal
injuries seen in the present patient have not previously been
described. These injuries appeared on the trachea and bronchial tree
and ruptured the posterior tracheal wall. They were directly caused by
the caustic action of the toxin, probably after its aspiration. The
effects at cell level, especially on tracheal epithelial cells, which
have shown experimentally a greater sensitivity to paraquat, could be
produced by the generation of very-reactive oxygen species, such as
superoxide radicals. These radicals have deleterious effects on the
cells by attacking the proteins and membranous organelles, inhibiting
macromolecular synthesis, and enhancing lipid
peroxidation.5
The tracheal injuries contributed to the development of extra-alveolar
air and to the demise of the patient. Although there has been no
previous report of a similar injury, the Toronto Lung Transplant
Group6
described a patient with acute paraquat poisoning
who required a lung transplant, with death caused by complications
derived from a trachea-innominate artery fistula. The fistula was
initially described as a complication of the tracheotomy, although the
deleterious effect of the paraquat could also have influenced the
genesis of this tracheal injury. There is no efficacious treatment for
paraquat poisoning in the clinical setting, but it has been
experimentally demonstrated that a reduction in the intracellular
nicotinamide adenine dinucleotide phosphate can protect the
tracheal cells against paraquat poisoning,5
which suggests
that future studies may show more satisfactory results.
Received for publication June 13, 2000.
Accepted for publication November 15, 2000.
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References
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Rusell, LA (1981) Paraquat poisoning: toxicologic and pathologic findings in three fatal cases Clin Toxicol 18,915-928[ISI][Medline]
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Miro, JM, Nogue, S, Mas, A, et al (1983) Fatal paraquat poisoning: presentation of 2 new cases and review of the literature Med Clin (Barc) 81,350-354[Medline]
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Chen, KW, Wu, MH, Huang, JJ, et al (1994) Bilateral spontaneous pneumothoraces, pneumopericardium, pneumomediastinum, and subcutaneous emphysema: a rare presentation of paraquat intoxication. Ann Emerg Med 23,1132-1134[ISI][Medline]
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Im, JG, Lee, KS, Han, MC, et al (1991) Paraquat poisoning: findings on chest radiography and CT in 42 patients AJR Am J Roentgenol 157,697-701[Abstract/Free Full Text]
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Lee, TC, Lai, GJ, Kao, SL, et al (1993) Protection of a rat tracheal epithelial cell line from paraquat toxicity by inhibition of glucose-6-phosphate dehydrogenase. Biochem Pharmacol 45,1143-1147[CrossRef][ISI][Medline]
-
. The Toronto Lung Transplant Group. (1985) Sequential bilateral lung transplantation for paraquat poisoning: a case report. Thorac Cardiovasc Surg 89,734-742
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Abstract
Case Report
