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| CASE REPORT |
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| Year : 2019 | Volume
: 17
| Issue : 2 | Page : 38-41 |
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Formic acid poisoning: The vital role of endoscopy in assessment and follow-up
Henna Puthiyaveetil Sabeerali1, Krishna Prasad2
1 Department of Internal Medicine, Sree Gokulam Medical College and Research Foundation, Thiruvananthapuram, Kerala, India
2 Department of Emergency Medicine, Sree Gokulam Medical College and Research Foundation, Thiruvananthapuram, Kerala, India
| Date of Submission | 18-Jun-2019 |
| Date of Acceptance | 02-Aug-2019 |
| Date of Web Publication | 29-Aug-2019 |
Correspondence Address:
Dr. Krishna Prasad
Department of Emergency Medicine, Sree Gokulam Medical College and Research Foundation, Venjaramoodu, Thiruvananthapuram - 695 607, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/cmi.cmi_17_19
Formic acid poisoning, especially intentional, carries a high risk of mortality and morbidity. Unavailability of antidote and rapid deterioration after consumption is an important factor in the management of these types of poisoning. Here, we report a case of suicidal formic acid poisoning which presented to our emergency department. Our objective is to review the literature on formic acid poisoning with emphasis on the role and utility of endoscopy in determining its severity and prognosis. Keywords: Corrosive, endoscopy, formic acid, poisoning
How to cite this article:
Sabeerali HP, Prasad K. Formic acid poisoning: The vital role of endoscopy in assessment and follow-up. Curr Med Issues 2019;17:38-41 |
| Introduction | |  |
Formic acid, otherwise known as methanoic acid, is a commonly used ingredient for coagulating latex as it is cost-efficient. It also guarantees a consistent high-quality natural rubber product, making it one of the best coagulants for latex coagulation in dry rubber production. It is seen commonly in households where rubber tree is cultivated, especially in South India. Due to this reason, it is also misused for deliberating self-harm. The concentrated form being pungent is mixed with country liquor and consumed for suicidal purposes while the dilute form being colorless and odorless is consumed accidentally.[1],[2] Here, we describe a case of acute formic acid poisoning, which presented to our hospital and was managed successfully. We would also like to stress upon the role of endoscopy as a prudent tool in risk assessment and patient follow-up.
| Case Report | | |
A 30-year-old male patient presented to our emergency department with an alleged history of intentional consumption of formic acid (approximately 60 mL) mixed with alcohol. He was brought to the hospital 1½ h after the consumption. He had complained of throat pain, chest pain, and epigastric discomfort of severe nature. On presentation, he had difficulty to talk as well as to swallow, and also, dribbling of the saliva was present. At triage, vitals recorded were respiratory rate - 40/min, SpO2-99% (at room air), blood pressure - 160/90 mmHg, and temperature - 98.6°F. On examination, he was conscious and showing signs of respiratory distress. On bladder catheterization, his urine bag revealed dark-colored urine suggestive of hemoglobinuria and intravascular hemolysis. Point-of-care testing arterial blood gases showed metabolic acidosis (pH - 7.196, pCO2-58.7 mmHg, pO2-92.5 mmHg, cHCO3-15.6 mmol/L, lactates - 0.99 mmol/L). He was immediately intubated and mechanically ventilated; started on intravenous (IV) fluids, pantoprazole, and sodium bicarbonate infusion; and shifted to the medical intensive care unit for emergency hemodialysis. He was kept nil per orally (NPO); neither gastric lavage nor nasogastric tube was inserted. Endoscopy performed on the next day [Figure 1] showed Grade 2B corrosive injury in the esophagus, Grade 3A corrosive injury over the esophago-gastric junction, Grade 3B corrosive injury in the stomach, and Grade 2B corrosive injury over the first part of duodenum. He was then put on total parenteral nutrition (TPN) till the 7th day when a feeding jejunostomy tube was placed. He later developed acute respiratory distress syndrome (ARDS) and was on ventilator support for another 8 days. Gastrografin swallow under fluoroscopy was performed on the 15th day and was reported as mildly dilated cervical and mid-esophagus (possibly inflammatory). Subsequently, another endoscopy [Figure 2] was done on the 16th day after admission which showed erythematous and edematous mucosal changes over esophagus and edematous contracted polypoidal mucosa in the stomach. The first and second part of the duodenum appeared normal. He was started on sips of water followed by clear fluids gradually and later on soft diet. He was discharged with a feeding jejunostomy tube in situ. The patient was regularly followed up at 2 weeks' intervals till the 8th week postdischarge. | Figure 1: Endoscopic pictures of the patient on day 1. (a) Esophagus: Grade 2B corrosive injury. (b) Fundus of stomach: Grade 3B corrosive injury. (c) Body of stomach: Grade 3B corrosive injury. (d) Antrum of stomach: Grade 3B corrosive injury. (e) First part of duodenum: Grade 2B corrosive injury. (f) Second part of duodenum: Minimal edematous mucosa with blood stained fluid.
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 | Figure 2: Endoscopic pictures of the patient on day 16. (a) Esophagus: Erythematous edematous mucosa seen. (b) Fundus of stomach: Erythematous edematous mucosa seen. (c) Antrum of stomach: Contracted polypoidal mucosal changes seen. (d) Pylorus of stomach: Normal. (e) First part of duodenum: Normal. (f) Second part of duodenum: Normal.
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| Discussion | | |
Formic acid is the simplest carboxylic acid-methanoic acid. It is a colorless pungent acid used in the production of leather tanning as well as a coagulant in rubber production. In majority of the formic acid poisoning cases reported so far, it is mostly consumed with suicidal intent. Most victims mix formic acid with alcohol while swallowing it for suicidal purpose. Dilute forms of formic acid, being colorless and odorless, are often consumed accidentally. Accidental ingestion of concentrated formic acid is rare. The fatal dose of formic acid poisoning is 50–200 mL. Males of the middle age group are usually affected.[1] Formic acid reaches systemic circulation by various routes including inhalation, through skin, and through ingestion.[3],[4]
Clinical features of formic acid poisoning include oral cavity burns, vomiting, dysphagia, hematemesis, esophageal strictures, gastrointestinal perforation, respiratory distress, aspiration pneumonia, chemical pneumonitis, ARDS, hematuria, acute kidney injury, septicemia, hypotension, and shock. The corrosive effect of formic acid on oral mucosa is manifested as burning pain, excessive salivation, intense vomiting, ulceration, hematemesis, and gastric erosions. Coagulative necrosis of the gastrointestinal mucosa occurs as a result of its corrosive action.[5],[6] It also damages the clotting factors and causes hemolysis which can lead to acute kidney injury.
Treatment goals should be primarily focused on the airway, breathing, and circulation. Vomiting should not be induced and neither gastric lavage be attempted. There is no role of activated charcoal in formic acid poisoning.[7] Since there is no specific antidote available, treatment is mainly supportive.[8] Metabolic acidosis should be promptly managed with IV sodium bicarbonate. This can significantly tide off the mortality before shifting to the intensive care set-up.[8] NPO must be maintained and parenteral nutrition should be initiated.[7] If the electrolyte imbalance is uncorrectable by IV supplementation, hemodialysis should be considered.[9] Exchange transfusion should be considered in case of severe intravascular hemolysis.[2]
Endoscopy is usually recommended in the first 12–48 h although it is safe up to 96 h after corrosive ingestion. Endoscopy should be performed with caution and gentle insufflation. Zargar's modified endoscopic classification of corrosive ingestion is useful in grading endoscopic lesions. Grade 0 is normal, Grade 1 shows mucosal edema and hyperemia, Grade 2A shows superficial ulcers, Grade 2B shows deep focal and circumferential ulcers, Grade 3A shows focal necrosis, Grade 3B has extensive necrosis, and Grade 4 shows perforation.[10]
Patients with injuries up to Grade 2A have excellent prognosis and can be discharged after 24–48 h of observation. Patients with Grade 2B and 3A injury develop strictures in 70%–100% cases. All patients with Grade 2B and 3A injuries can be managed conservatively; they require nutritional support for 6–8 weeks by TPN or feeding jejunostomy. The strictures usually develop within 8 weeks in 80% of patients but can develop as after 3 weeks or as late as 1 year after caustic ingestion. Patients with Grade 3B and 4 injuries have high early mortality rate up to 65%. Patients with Grade 4 injury should be subjected to surgery. All patients after 3–4 weeks of conservative treatment for Grade 2B injury and above are subjected to barium studies for the esophagus and stomach to evaluate the length, number, degree of esophageal stricture, shape of gastric outlet stricture, and evaluation of gastric body and fundus.[11] ARDS, aspiration pneumonitis, and shock lung are the other fatal complications manifested in severe poisoning.[12] This case emphasizes the vital role of endoscopy in classifying the severity of injury and determining further management and prognosis.
| Conclusion | | |
Immediate intervention with anticipation of complications of formic acid poisoning reduces the mortality drastically. Metabolic acidosis corrected with IV sodium bicarbonate during the initial hours reduces morbidity and mortality significantly. Early endoscopy is helpful in assessing the extent of injury to plan future management of the patient. Even if the patient survives, they may have long standing problems such as strictures of the esophagus and stomach; hence, follow-up with serial endoscopy is essential.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Acknowledgment
We would like to thank Dr. Sanjay Zachariah, Dr. Phiji Mathew Philipose (Department of Internal Medicine), Dr. T. S. Prashanth (Department of Gastroenterology), and the nursing staff of the Department of Emergency Medicine, Sree Gokulam Medical College and Research Foundation, Thiruvananthapuram, for their valuable contribution and support in this endeavor.
Financial support and sponsorship
Nil.
Conflicts of interest
Nil.
| References | | |
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| 2. | Malizia E, Reale C, Pietropaoli P, De Ritis GC. Formic acid intoxications. Acta Pharmacol Toxicol (Copenh) 1977;41 Suppl 2:342-7. |
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| 8. | Naik SM, Ravishankara S, Appaji MK, Goutham MK, Devi NP, Mushannavar AS, et al. Acute accidental formic acid poisoning: A common problem reported in rubber plantations in Sullia. Int J Head Neck Surg 2012;3:101-5. |
| 9. | Moore DF, Bentley AM, Dawling S, Hoare AM, Henry JA. Folinic acid and enhanced renal elimination in formic acid intoxication. J Toxicol Clin Toxicol 1994;32:199-204. |
| 10. | Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc 1991;37:165-9. |
| 11. | Chiu HM, Lin JT, Huang SP, Chen CH, Yang CS, Wang HP, et al. Prediction of bleeding and stricture formation after corrosive ingestion by EUS concurrent with upper endoscopy. Gastrointest Endosc 2004;60:827-33. |
| 12. | Wiernikowski A, Guzik E. Acute poisoning with formic acid. Przegl Lek 1973;30:395-6. |
[Figure 1], [Figure 2]
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