Paraquat Poisoning Complicated by Pneumothoraces and Pneumomediastinum: Two Cases
Corresponding Author: Samanvitha Vengaldas, Department of Respiratory Medicine, Prathima Institute of Medical Sciences, Karimnagar, Telangana, India, Phone: +91 9663863988, e-mail: email@example.com
Received on: 01 March 2023; Accepted on: 04 July 2023; Published on: 30 October 2023
Aim and background: The present study on paraquat poisoning gives a detail about the compound, presentation of patient to emergency, management and complications. Paraquat is a bipyridylium compound that, when ingested, has a corrosive action locally and organ injury caused by free radicals. Pneumothorax and pneumomediastinum cause respiratory distress, eventually increasing the mortality.
Case description: Herein we report two young males who presented with history of consumption of paraquat. Gastric lavage was done at a local hospital for both patients and presented to us in a hemodynamically stable state for further management. Both the patients underwent ICD insertion and were treated with steroids, cyclophosphamide and antioxidants and one of patient requiring mechanical ventilator support. In spite of aggressive treatment both the patients have succumbed.
Conclusion: In case of history of exposure or ingestion of paraquat early presentation may help in aggressive decontamination reducing further complications. Whereas patients presenting with pneumomediastinum pose a 100% risk of mortality.
How to cite this article: Vengaldas S, Chenimilla NP, Israel J, et al. Paraquat Poisoning Complicated by Pneumothoraces and Pneumomediastinum: Two Cases. Indian J Respir Care 2023;12(3):259–262.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.
Keywords: Case report, Free radical injury, Mortality, Paraquat, Pneumomediastinum, Pneumothorax
Paraquat (1,1’-Dimethyl-4,4’-bipyridinium dichloride) is a nonselective contact herbicide,1 available as a brown liquid of dichloride salt in 10–30% strength (Gramoxone) or as brown 5% granules (Weedol).2 Under anaerobic conditions, the paraquat cation is reduced by nicotinamide adenine dinucleotide phosphate hydrogen-dependent microsomal flavoprotein reductase to form reduced radically, which reacts with molecular oxygen-producing superoxides.3 Reactive oxygen species formed cause free radical damage to the epithelial cell of the lung.2
There is a structural similarity between diamine and polyamine compounds which is the reason for the accumulation of Paraquat in the lung.3
Proliferative phase: Fibroblasts that appear in alveolar spaces undergo proliferation and differentiation to mature fibroblasts forming extensive fibrosis, impairing gas exchange, and leading to the death of alveoli.6
A 29-year-old male farmer presented to the casualty with a history of consumption of 50–100 mL of Paraquat (24%) under the influence of alcohol. Initially, the patient was treated with gastric lavage at a local hospital. The patient developed vomiting and was referred to a higher center. At presentation, he was conscious, coherent, and hemodynamically stable with saturation of peripheral oxygen (SpO2) of 100% at room air. Chest X-ray (CXR) was normal; serum creatinine was 1.1 mg/dL, raised bilirubin, and elevated liver enzymes. He was planned for hemodialysis for decreasing urine output, raising creatinine compared to baseline, and metabolic acidosis. He was managed with intravenous (IV) methylprednisolone 1 gm/day for 3 days, N-acetyl cysteine, and vitamin C 1.5 gm. After 48 hours, he developed respiratory distress with SpO2: 86%, thus started on 6 L of O2via an oro-nasal mask. Subcutaneous emphysema was noted over the anterior chest wall, face, and neck. Computerized tomography (CT) of the chest revealed bilateral pneumothoraces and pneumomediastinum (Figs 1 and 2). Chest tube insertion was done on the left side (Fig. 3). Repeat liver function tests showed a fourfold increase in liver enzymes and serum creatinine of 4.3 mg/dL with blood urea of 229 mg/dL; a second session of hemodialysis was done. The patient left against medical advice to another hospital where intercostal drainage (ICD) tube insertion was done on the right side but succumbed after 4 days.
A 19-year male farmer presented to the casualty with an alleged history of consumption of 70–80 mL of Paraquat. After gastric lavage at a local hospital, the patient was referred to a higher center. On presentation, the patient was irritable with a history of vomiting. The patient was hemodynamically stable with a SpO2 of 98% at room air. CXR was normal, and serum creatinine was 0.6 mg/dL. He has managed with IV dexamethasone 8 mg, then IV methylprednisolone 500 mg/day for 2 days, cyclophosphamide 500 mg stat dose, and antioxidants such as N-acetylcysteine (NAC) 1.2 gm IV, vitamin C 1.5 gm IV. Later the same day, in view of the severe metabolic acidosis and oliguria, the patient was planned for hemodialysis. The patient had cardiac arrest, revived after one cycle of cardiopulmonary resuscitation, followed by which he was given mechanical ventilatory support with 40% fraction of inspired oxygen, 4 mL/kg of tidal volume, and positive end-expiratory pressure of 6 cm of H2O, plateau pressure of 25 cm of H2O. After 24 hours, respiratory distress ensued with subcutaneous emphysema over the neck and anterior chest wall. CT chest revealed left pneumothorax and pneumomediastinum (Figs 4 and 5). ICD insertion was done on the left side (Fig. 6). After 24 hours patient again had a cardiac arrest and expired.
Self-poisoning by Paraquat is common in many parts of South Asia, including India.7 Acute respiratory distress syndrome after Paraquat ingestion is known to occur after 24–48 hours.2 In our study, the patients presented with repeated episodes of vomiting and presented with pneumothorax and pneumomediastinum after 48 and 24 hours, respectively. According to Zhou et al., 93.8% of patients with pneumomediastinum die within 3 days.4 Deng et al. demonstrated the mortality rate with pneumomediastinum to be 100%.5
Paraquat poisoning is by direct ingestion or by cutaneous contact. If ingested causes a mucosal burning sensation leading to vomiting (100%), diarrhea (24%), and oral ulceration (53%); direct contact causes dermatitis and skin burns.8 Patients ingesting <7.5 mL of 20% (m/v) concentrate are usually asymptomatic or have mild symptoms with full recovery. Consuming 7.5–15 mL of 20% (m/v) presents with moderate to severe symptoms, with death occurring in 2–4 weeks. Ingestion of Paraquat of >15 mL of 20% (m/v) concentrate is associated with multi-organ failure, with death occurring in 24 hours to a few days.6 Paraquat injury leads to oxygen-free radical release, which causes the destruction of cell membranes of type 1 and 2 pneumocytes leading to impaired gas exchange and loss of surfactant, causing an increase in surface tension within alveolar cells and rupture of cells, pneumothorax, and pneumomediastinum. This phenomenon is referred to as Daisley-Barton syndrome.9,10 Redox cycling has been shown to occur in microsomal preparations from the liver, lung, and kidney.3 In our cases, the initial imaging was normal with no respiratory distress, but after a period of 48 hours, patients developed sudden respiratory distress, which ultimately revealed the presence of pneumothorax and extensive pneumomediastinum.
Gastric lavage with activated charcoal is recommended for presentation within 1 hour.11 In our cases, immediately after ingestion, gastric lavage was done. Later, they were treated with parenteral methylprednisolone, cyclophosphamide, NAC, and vitamin C. In animal studies, dexamethasone has been shown to decrease paraquat accumulation in lung tissue and reduce lipid peroxidation.11 Antioxidants such as vitamin E, vitamin C, NAC, desferrioxamine, and salicylic acid act as potential antidotes in paraquat poisoning. Vitamin C neutralizes by donating a free radical, whereas NAC reduces paraquat-induced apoptosis and inflammatory response by limiting replenishing cysteine in the synthesis of glutathione.11
Several researchers have used combination regimens of cyclophosphamide, dexamethasone or methylprednisolone, vitamin C, and NAC and showed mortality benefits compared to standard treatment.1 Hemodialysis as a part of treatment is considered in patients with acute kidney injury, which was done in our cases. Oxygen supplementation should be avoided as it increases free radical injury; hence to be given with caution.9
Two patients, after paraquat ingestion, developed respiratory distress. These two cases can be labeled as Daisley Barton syndrome as alveolar injury secondary to paraquat poisoning led to pneumothorax with pneumomediastinum, followed by death in both cases.
5. Deng P, Chen Y, Li H, et al. Pneumomediastinum caused by occult paraquat poisoning: case report. Medicine 2018;97(51). DOI: 10.1097%2FMD.0000000000013745
6. Dinis-Oliveira RJ, Duarte JA, Sánchez-Navarro A, et al. Paraquat poisonings: mechanisms of lung toxicity, clinical features, and treatment. Crit Rev Toxicol 2008;38(1):13–71. DOI: 10.1080/10408440701669959
8. Sandhu JS, Dhiman A, Mahajan R, et al. Outcome of paraquat poisoning-a five year study. Indian J Nephrol 2003;13(2):64–68. https://www.researchgate.net/publication/228705717_Outcome_of_paraquat_poisoning_A_five-year_study
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