Asian Cardiovasc Thorac Ann 2008;16:298-300
© 2008 Asia Publishing EXchange Ltd
Esophageal Injuries Due to Aluminum Phosphide Tablet Poisoning in India
Anshuman Darbari, MCh,
Shekhar Tandon, MCh,
Sushant Chaudhary, MS,
Manu Bharadwaj, MBBS,
Ambrish Kumar, MS,
Gyan P Singh, MD1
Department of Thoracic & Cardiovascular Surgery
1 Department of Anesthesia KGM University Lucknow, India
For reprint information contact: Shekhar Tandon, MCh, Tel: 91 522 239 1919, Fax: 91 522 225 5394, Email: darbari1{at}indiatimes.com, Thoracic & Cardiovascular Surgery Department, KGM University, Lucknow – 226 003, India.
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ABSTRACT
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Aluminum phosphide is a lethal systemic poison with 80%–90% mortality. Survivors have taken either a very small amount or the tablet had been exposed to air, rendering it less toxic, but often causing severe esophageal injuries. The presentation and treatment of 11 cases of esophageal injury due to aluminum phosphide are described. Ten patients had esophageal stricture, and 1 had tracheoesophageal fistula with stricture. Endoscopic bougie dilatation was sufficient in 7 patients, and surgical intervention was required in 4 who underwent definitive repair via gastric tube or feeding jejunostomy with a 2nd stage repair planned in 2. There was no mortality but significant morbidity. Mortality and morbidity might be prevented by withdrawing this pesticide from the market, making its sale difficult, or modifying the packaging.
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INTRODUCTION
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Suicidal poisoning with aluminum phosphide (AlP), a solid fumigant pesticide, is seen with increasing frequency in the mid and northern regions of India. This lethal and cheap pesticide has become very easily available. Its toxic effects are due to the liberation of phosphine gas (PH3).1–5 There is no specific antidote; timely and effective supportive treatment is crucial for survival. Aluminum phosphide poisoning results in 90% mortality in patients admitted to our Department of Medicine. In survivors, residual esophageal damage causes significant morbidity, with associated nutritional complications. There are only 8 previous cases of survival documented in reports from India.6–8
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PATIENTS AND METHODS
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Eleven cases of esophageal injury due to attempted suicide with AlP tablets were managed in our department in the 15 months between June 2005 and August 2006. Seven (63.6%) patients were female, and ages ranged from 20 to 35 years. Onset of symptoms from time of ingestion ranged from immediate to 4 hours. All patients had 1–2 episodes of hematemesis, 10 presented with increasing dysphagia and odynophagia, and 1 had dysphagia and respiratory distress with a positive Ono’s sign (immediate coughing, choking, and respiratory distress following ingestion). All cases were referred to us by physicians after initial conservative measures. Diagnosis of AlP poisoning was made by clinical suspicion, proper history taking, a bedside silver nitrate test, and biochemical examination of the gastric aspirate and viscera. Conservative treatment consisted of early gastric lavage, vasopressors, and supportive care. Specific therapy with intravenous magnesium sulphate was also given. Diagnosis of esophageal injury was established clinically and confirmed by contrast radiography of the esophagus, flexible and rigid esophagoscopy, and by bronchoscopy if needed (Table 1
). Flexible endoscopy was undertaken under mild sedation, but due to the lack of availability of guidewire and balloon dilator systems, further intervention was carried out under general anesthesia. Rigid esophagoscopy with bougie dilatation in the same sitting was attempted in 10 cases of stricture. All patients were followed up regularly after discharge from the hospital.
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RESULTS
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Rigid esophagoscopy revealed a stricture in all 11 patients, which was measured as the distance from the incisor teeth (Table 1
). There was no other pathology in 10 patients, and the strictures in 7 of them were amenable to bougie dilatation as they involved a short segment and the rest of the esophagus was normal. These patients were able to manage a soft diet on the following day, and a normal diet after 1 or 2 days. Three of them underwent successful repeat dilatation within 6 months of the initial procedure. The other 4 have not needed repeat dilatation, and are doing well on regular follow-up. In 3 cases of dense stricture, this simple procedure failed. In one of these patients, a forceful attempt led to esophageal perforation, which was managed conservatively, and later, with feeding jejunostomy. This patient and another with failed dilatation have a planned 2nd stage of esophageal replacement by gastric tube. The 3rd case of failed dilatation was managed by retrosternal reverse peristaltic gastric tube replacement and bypass of the diseased esophagus. The patient with tracheoesophageal fistula was directly managed by esophageal exclusion with replacement. In this case, esophagoscopy revealed an impenetrable esophageal stricture and proximal fistulous communication with the trachea. Tracheal repair was performed under general anesthesia via a cervical approach, with retrosternal bypass by reverse peristaltic stomach tube. The tracheal fistulous opening was closed using interrupted sutures of nonabsorbable 3/0 polypropylene monofilament suture, with an interposition muscle flap. The postoperative period was uneventful. There was no intraoperative or postoperative mortality among the 11 cases, but significant morbidity.
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DISCUSSION
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Aluminum phosphide is now perhaps the most common suicide agent in mid and northern India, where it is freely used as grain preservative and easily available over the counter. The toxic product, phosphine gas, is liberated on exposure to moisture. Phosphine is a systemic poison that causes severe congestion and evokes a significant inflammatory response. It is similar to cyanide, but acts slowly. It has been found to inhibit cytochrome oxidase, a respiratory chain enzyme. Systematic toxic effects appear 1–60 min after ingestion. Acute cardiovascular collapse is the most frequent mode of presentation, seen in 60%–100% of cases. There is a "dose-toxicity" and "dose-time to death" correlation. Even 1.5 g (1/2 tablet) can prove fatal within a few hours. Tablets exposed to air lose their toxicity. The mortality is highly variable, depending on factors such as fresh or damp tablets, duration and severity of poisoning, severity of shock, and response to resuscitative measures. There is no specific antidote.1,2 Intravenous magnesium sulphate, probably due to its membrane stabilizing action and antioxidant effect, helps in reducing mortality from 90% to 50%. It has also been suggested that hypomagnesemia might be responsible for the high mortality with this poison, so correction is beneficial.3–5 Most survivors had taken a small amount, taken very little water with it, or it had been exposed to air. These factors, with possible impaction of the tablet in the esophagus, lead to local injuries (similar to "pill esophagitis"). Easy availability, preventable at the primary level or by proper management, is the major difference between this and other caustic substance injury.
For such patients, the most important investigatory tool is contrast-enhanced radiography of the esophagus, which in almost all cases demonstrates the pathology. Supplementary investigations are flexible or rigid esophagoscopy and bronchoscopy, which not only directly visualize but assess the mucosa of both tracts, and determine any other pathology. Flexible esophagoscopy is easy and can be carried out under mild sedation; this was the first choice of intervention in earlier series.6–8 Important aspects of management are preoperative preparation, which should be planned to improve the nutritional status of the patient, and careful use of appropriate antibiotics to control any infection.9 Our policy is intervention after stabilizing medical management in all cases.
Initially, bougie dilatation was attempted in all 10 cases of established esophageal stricture, which was successful in 7 but failed in 3 due to a very tight stricture with no opening. One of these patients suffered perforation during attempted dilatation. We did not perform esophagectomy for fear of aggravating the mediastinitis due to esophageal perforation. Esophageal bypass with transverse colon or gastric tube is generally needed for an irreparably damaged esophagus or dense non-dilatable esophageal stricture. The preferred route is a retrosternal approach which is safer and easier if dense adhesions are suspected in the mediastinal region. In our case, a reverse peristaltic stomach tube was formed and anastomosed to the esophagus above the site of damage. There was no risk of mucocele formation because only esophageal bypass was undertaken, not esophagectomy. In one case, a tracheoesophageal fistula developed due to impaction of the tablet, and the subsequent slow release of phosphine gas caused local damage with excessive inflammation and corrosion of the esophagus and tracheal walls. Clinically, Ono’s sign suggested the diagnosis; later, contrast esophagography, flexible and rigid esophagoscopy, and bronchoscopy confirmed it. Although spontaneous healing has been reported, direct surgical repair should be undertaken for this rare pathology.8,9 The avoidance of mortality was attributed to early intervention, improved nutrition, and the fact that pulmonary infection was mild to moderate only, which all predispose to a good overall outcome.6–9
The message from this and earlier series is that we should be vigilant for these complications of AlP poisoning because they may cause significant morbidity.6–8 Prevention of AlP poisoning is only possible by ceasing or restricting supply, or by packaging the tablets in plastic tubes with some modifications, such as spikes, to render them unsuitable for swallowing. Recently, some social organizations have voiced support for the implementation of restrictive measures.
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ACKNOWLEDGMENTS
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We are highly thankful to Prof. Hari Gautam, MS, Vice-Chancellor of KGMU, Lucknow, who gave us strong motivation and kind permission for this manuscript.
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REFERENCES
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ABSTRACT
INTRODUCTION
