IJHNS
10.5005/jp-journals-10001-1104
Acute Accidental Formic Acid Poisoning: A Common Problem Reported in Rubber Plantations in Sullia
CASE REPORT
Acute Accidental Formic Acid Poisoning: A Common
Problem Reported in Rubber Plantations in Sullia
Sudhir M Naik, S Ravishankara, Mohan K Appaji, MK Goutham, Nonthombam Pinky Devi
Annapurna S Mushannavar, Sarika S Naik
ABSTRACT their friends and neighbors. In this territory, the common
Background: Ingestion of formic acid, accidentally or with methods of suicide are by hanging, drowning, ingestion of
suicidal intention is a common problem among the workers in pesticides and different corrosives. As formic acid is easily
rubber plantations in Sullia. The diluted form of formic acid is available to the rubber growing population suicidal ingestion
used in coagulation of rubber latex. Sullia, a small town in South
and accidental ingestion is commonly seen in this region.
India, is well known for its rubber plantations. Easy accessibility
to formic acid makes it susceptible to be used for committing Apart from its use in rubber industry as a latex
suicide in this region. Also accidental ingestion are very common coagulating agent, formic acid is also used in electroplating,
in these workers. tanning and paper industries. It is also used in production
Aim: To study a case report of accidental formic acid poisoning of disinfectants and decalcifying agents.1 Formic acid is
and its management. pungent and corrosive, so it is rarely swallowed acci-
Intervention: The patient was managed successfully by medical dentally.1 It is mixed with alcohol and consumed while
line of treatment. No gastric lavage or antidote was used in committing suicide.1
treatment and no vomiting induced. Nasogastric tube feeding Complications of ingestion of formic acid, the diluted
was done and electrolyte imbalance was corrected.
form of which is used in coagulation of rubber latex, are
Conclusion: Easy availability of formic acid should be curtailed common in this rubber growing belt.2 This is a case study
by enforcing statutory limitations in its distribution and the
complication of formic acid poisoning should be educated to
of a patient who had accidental formic acid poisoning and
these rubber workers. Patients with hematemesis or melena, was managed successfully in our KVG Medical College
after successful treatment, should be followed up with serial Hospital. This case study aims at studying the patterns of
esophagogastroduodenoscopy for diagnosis and early presentation and identifying the predictors of morbidity and
treatment of strictures.
mortality of acute formic acid poisoning and their successful
Keywords: Formic acid, Hematemesis, Esophagogastro- management.
duodenoscopy, Metabolic acidosis.
How to cite this article: Naik SM, Ravishankara S, Appaji CASE REPORT
MK, Goutham MK, Devi NP, Mushannavar AS, Naik SS. Acute
Accidental Formic Acid Poisoning: A Common Problem A 40-year-old patient presented to our ENT, Head and Neck
Reported in Rubber Plantations in Sullia. Int J Head Neck Surg OPD with history of accidental consumption of formic acid.
2012;3(2):101-105. He complained of severe pain in the throat with absolute
Source of support: Nil dysphagia. The patient had accidental consumption of nearly
Conflict of interest: None declared
20 ml of concentrated formic acid which is used in preparing
rubber latex. The patient immediately felt the mistake and
INTRODUCTION spitted it out. Later, he induced vomiting to clear his throat.
He cleansed the throat with water and tried to consume cold
Sullia is a small town situated in the southern region of the milk. He could not drink the cold milk because of dysphagia.
Indian subcontinent and has a total population of nearly He immediately came to a doctor where he was given first
1 lakh. The economy is predominantly agricultural. aid and referred to us. The patient was managed in accident
Arecanut farming and growing rubber are the major and emergency casualty. The airway of the patient was
agricultural produce. The labor is family-based and those maintained and saturation was well above 96%.
engaged in rubber production collect the latex from the trees Oral cavity examination showed intense corrosion of the
by tapping, harden it at once by admixture with formic acid tongue (Fig. 1) and the oral mucosa (Fig. 2). Indirect
and then bring it to the homestead for further processing laryngoscopic examination was not possible. The serum
prior to sale in sheet form. electrolyte concentration levels were; serum sodium –143.0
The formic acid required for this purpose is readily meq/liter and serum potassium – 4.2 meq/liter. Blood reports
available commercially, with the minimum of control of showed Hb% – 13.0 gm%, total RBC count 5.56 cells/mm3,
sale and supply. So, it is easily accessible to all members of total WBC count 18,600 cells/mm3, platelet count—2.68
those families working with rubber industry, as well as to lakh cells/mm3, polymorohs—94%, lymphocytes—4%,
International Journal of Head and Neck Surgery, May-August 2012;3(2):101-105 101
Sudhir M Naik et al
Fig. 1: Corrosion of the tongue due to accidental Fig. 3: Epiglottis and posterior pharyngeal wall swollen due to
formic acid ingestion accidental formic acid ingestion
Fig. 2: Corrosion of the tongue and oral cavity due to Fig. 4: Chest X-ray showing normal lung shadow
accidental formic acid ingestion
eosinophils – 2%. In the peripheral smear RBC’s are normo- dexamethasone 8 mg thrice daily for a week and IV
cytic normochromic in picture having a few macrocytic pantoprazole 40 mg twice daily for a week. The patient was
normochromic cells. Total count appears to be having mild maintained on parenteral IV fluids for 12 hours. After 24
leukocytosis. hours when no severe damage to the GIT was suspected
Differential count shows severe neutrophilic nasogastric tube was inserted and feeding was continued.
leukocytosis and platelets were adequate in number and The patient was comfortable after 48 hours with no pain
normal in size. Overall the peripheral smear was showing and tendency to frequently clear the throat had subsided.
severe neutrophilia. X-ray lateral view of the neck showed Nasogastric tube was (Fig. 5) removed after 5 days and oral
swelling of the epiglottis with inflammatory edema of the cavity examined. A layer of oral mucosa came out after
posterior pharyngeal wall and laryngeal inlet structures oral rinsing. X-ray of the lateral view of the neck was
(Fig. 3). Chest X-ray posterior-anterior view was clear with repeated, which showed reduction in swelling of the
no signs of aspiration pneumonitis (Fig. 4). epiglottis (Fig. 6).
The patient was put on high-dose of intravenous (IV) The barium swallow (Fig. 7) of the patient was done
hydrocortisone 100 mg twice daily for 3 days as the patient after removal of the nasogastric tube which showed normal
did not have severe GIT bleeding. Other treatment given contour of the esophagus. The pharyngeal lumen showed
were IV antibiotic ceftriaxone 1 g twice daily for a week, irregularity. The patient complained of mild dysphagia at
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Acute Accidental Formic Acid Poisoning: A Common Problem Reported in Rubber Plantations in Sullia
Fig. 8: Corroded oral mucosa peeled out
Fig. 5: Nasogastric tube inserted the time of discharge. Oral cavity examination showed a
red congested mucosa (Fig. 8). Esophagogastro-
duodenoscopy was done on the 7th day after accidental
ingestion, the mucosal pattern showed erythema of the upper
one-third esophagus and no hemorrhagic areas seen. The
patient was discharged after 7 days with minimal dysphagia.
The patient was followed up for 4 months with serial
esophago-gastroduodenoscopy and no complications were
observed. The patient did not complain of dysphagia and
was symptom free after 4 months.
DISCUSSION
Formic acid is a colorless liquid with pungent penetrating
odor.2 The fatal dose is 50 to 200 ml.2 Usually, the victims
are males in the middle age group.2 Nearly 90% of cases of
formic acid poisoning are with intention of suicide and only
Fig. 6: Swelling of the epiglottis and posterior pharyngeal wall 10% are accidental consumption.2 It is observed that most
reduced after 5 days of treatment of the victims mix formic acid with alcohol while
swallowing it for suicidal purpose.2
Most common clinical features at the time of
presentation are vomiting, respiratory distress, hematemesis
and hematuria.3 Fresh blood vomitus and frank fresh blood
per rectum may start early with 30 to 40 ml of ingestion of
formic acid.3,4 Patient will complain of acute abdominal pain
and pass dark red urine.3,4 Most common complications of
the poisoning observed were oral cavity burns, metabolic
acidosis, septicemia, dysphagia, esophageal stricture,
gastrointestinal perforation, aspiration pneumonia, acute
respiratory distress syndrome (ARDS), acute renal failure,
chemical pneumonitis and shock.3,4 Erythema and blisters
are common, if the formic acid is accidentally splashed on
to the face or the skin at the time of the suicidal attempt.3,4
Rare complications were tracheoesophageal fistula,
pneumomediastinum and chemical injury to the cornea.3,4
The corrosive effect of the formic acid on the oral
Fig. 7: Normal barium swallow on 7th day mucosa is manifested as burning pain, excessive salivation,
International Journal of Head and Neck Surgery, May-August 2012;3(2):101-105 103
Sudhir M Naik et al
intense vomiting, mucosal corrosion and ulceration, levels, urine output and serum potassium levels to detect
hematemesis and also as gastric ulcerations.3,4 It is readily early onset of acute renal failure.8 Earlier acute renal failure
absorbed from the gastrointestinal tract.3,4 Coagulative were corrected by peritoneal dialysis 8 nowadays
necrosis of the gastrointestinal mucosa occurs as a result of hemodialysis is preferred.9 Hypovolemia due to blood loss
its corrosive action.3,4 It also damages the clotting factors was corrected by whole blood transfusions.9
and causes hemolysis leading to acute renal failure.3,4 At In cases of shock intubation and ventilatory support are
the cellular level, it has inhibitory action on aerobic essential to maintain oxygen saturation.9 Correction of
glycolysis with consequent dimunition of ATP synthesis.3,4 metabolic acidosis and renal failure, if it sets in should be
Blood examination may show varying degree hemolysis and done.9 Fatal intoxication after oral ingestion of high doses
disseminated intravascular coagulation. Severe clotting of formic acid are frequently due to acid induced severe
factors defect may be seen and should be monitored by damage to the gastric wall with perforation.9 In cases without
bleeding time and clotting time.3,4 They are confirmed by severe local lesions, death is caused by massive acidosis,
prothrombin time, thrombin time, serum fibrinogen and excessive hemolysis and bleeding.9 The majority of the
serum fibrinogen degradation products. Serial platelet lesions were evident in the gastrointestinal tract, with facial
counts are monitored.3,4 (typically circumoral) burns and ulceration of the oral and
Patient may present with drowsiness, weakness all over pharyngeal mucosa.9 Abdominal pain was accompanied by
the body, with pupils completely dilated.3,4 The patient may hematemesis and dysphagia.9
present with tachycardia or bradycardia, hypertension or Later complications included contractures and keloid
hypotension.3,4 The changes in the cardiovascular system formation on the affected area of the skin and notably,
are nonspecific, both brady- and tachyarrhythmias being esophageal stricture, for which reparative surgery should
observed, frequently accompanied by profound vascular be done.10 Progress should be monitored by the usual
hypotension.1,3,4 biochemical and hematological investigations, including
Acute respiratory distress syndrome, aspiration bleeding and clotting times.10 In cases where severe gastro-
pneumonitis and shock lung are the fatal respiratory intestinal hemorrhage was seen, barium swallow and serial
complications manifested in severe poisoning.5 Inhalation OGD were performed during follow-up.10 OGD sometimes
pneumonitis which manifests as cough, dyspnea and reveals florid hemorrhagic esophagitis.10
cyanosis, can complicate as chemical pneumonitis and In a study where a retrospective analysis of 15 deaths
respiratory failure.5 They usually present on the 3rd to 4th due to formic acid poisoning were done,6 had succumbed
days later and may need ventilatory support.5 to severe vascular hypotension and respiratory arrest, four
Metabolic acidosis may be profound with pH nearing died of acute renal failure and five failed to recover from
7, this should be treated intensively with IV sodium gastrointestinal hemorrhage. Ten milliliters by mouth could
bicarbonate.5 Nill per orally should be maintained and total prove lethal, death then taking place within hours, regardless
parenteral nutrition advised.6 If severe gastrointestinal of treatment. Those believed to have taken 15 ml to a
hemorrhage is seen, no steroids should be given as it may mouthful were likely to be found dead.
precipitate impending perforation of the gut wall.6 OGD No specific antidote is available and so treatment is
should not be done.6 essentially supportive.10 Antacids, milk and egg—white
The patient should be immediately admitted.6 Vomiting were cautiously administered orally, if no gastrointestinal
should not be induced and gastric lavage should not be hemorrhage is suspected. If GIT hemorrhage is suspected,
attempted.6 No role of activated charcoal exists in formic patients should be maintained nil orally. Intravenous fluids
acid poisoning management.6 High doses of folinic acid and electrolytes were infused to counter ‘shock’ and
(1 mg/kg IV bolus followed by 6 doses of 1 mg/kg IV doses antibiotics10 were indicated prophylactically to prevent
at 4th hourly intervals) should be given in severe poisoning. infection.10 Diuretics promote renal function in acute renal
Folinic acid acts by enhancing formate degradation in the failure.10 Hydrocortisone counters stress and inflammation
liver. 7 If electrolyte imbalance is uncorrectable by but should be only be given in case where no GIT
intravenous supplementation hemodialysis should be hemorrhage is seen otherwise perforation results.10
considered.7 Exchange transfusion should be considered in When the acute emergency of gastrointestinal
conditions of severe intravascular hemolysis.1 Devastating hemorrhage, metabolic acidosis, renal failure are all settled,
changes may be seen in the renal system, with hematuria pain relief should be given to the patient preferably with
usually appearing within a few hours of ingestion of the diamorphine.11 If the patient is anxious and irritable sedation
acid.8 An intense watch should be kept on serem creatinine can be given in low doses of diazepam.11 Local pain relief
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Acute Accidental Formic Acid Poisoning: A Common Problem Reported in Rubber Plantations in Sullia
can be given by local irrigations of 5% lignocaine viscous 5. Wiernickowski A, Guzik E. Ostre zatrucie kwasem mr6wkowym
or 15% lignocaine spray.11 [Acute poisoning with formic acid.] Przeglad Lekarski
1973;30:395.
In Sullia town, accidental poisoning, suicide and 6. Estresa A, Taylor W, Miller LJ, et al. Corrosive burns of the
attempted suicide with formic acid are all treated as medico- esophagus and stomach: A remainder for aggressive surgical
legal cases and suicide and attempted suicide as crimes. All approach. Ann Thoracic Surg 1986;41:276-83.
the patients are reported to the police authorities except 7. Moore DF, Bentley AM, Dawling S, Hoase AM, Henry JA.
Formic acid and enhanced renal elimination in formic acid
accidental cases. intoxication. Clinical Toxicol 1994;32:199-204.
8. Krishna Kumar S, Rajan N, Mathew Roy, VC. Peritoneal dialysis
CONCLUSION in acute renal failure following viper bite. Kerala Med J
Hematemesis and melena had significant association with 1975;15:1975.
9. Westphal F, Rochholz G, Ritz-Timme S, Bilzer N, Schütz HW,
esophageal stricture. Hematuria, respiratory distress,
Kaatsch HJ. Fatal intoxication with a decalcifying agent
hematemesis and gastrointestinal perforation at presentation containing formic acid. Int J Leg Med 2001 Feb;114(3):
were significantly associated with mortality. Metabolic 181-85.
acidosis with pH <7.3, hematemesis and age more than 40 10. Webb WR, Koutran P, Ecker RR, et al. An evaluation of steroids
and antibiotics in corrosive burns of esophagus. Ann Thoracic
are independent predictors of morbidity. Even if the patients
Surg 1970;9:95-102.
survives the patient may have long standing problems of 11. Berlyne GM, Henry Jones J, Hewitt V, Nilwarangkur S. Protein
esophageal stricture which may need serial dilatations later. loss in peritoneal dialysis. Lancet 1964;1:738.
Skin scarring and disfigurement should be corrected by
cosmetic surgery. ABOUT THE AUTHORS
Education about safe handling of the formic acid and
dangers of consumption should be educated to the rubber Sudhir M Naik (Corresponding Author)
growing population of Sullia. Associate Professor, Department of ENT and Head and Neck Surgery
KVG Medical College and Hospital, Kurunjibag, Sullia, Karnataka
SUMMARY India, Phone: 919916807109, e-mail: [email protected]
Since, formic acid is so readily accessible to the laborers of
S Ravishankara
the rubber cultivating community in Sullia, it is the easiest
means of corrosive poisoning in this region. Easy availability Associate Professor, Department of ENT and Head and Neck Surgery
of formic acid should be curtailed by enforcing statutory KVG Medical College and Hospital, Kurunjibag, Sullia, Karnataka, India
limitations in its distribution and spreading the knowledge
Mohan K Appaji
of its side-effects.
Metabolic acidosis, if taken care of by administration Professor and Head, Department of ENT and Head and Neck Surgery
KVG Medical College, Hospital, Kurunjibag, Sullia, Karnataka, India
of sodium bicarbonate intravenously at the local medical
centers, before referring the patient to a tertiary setup, may
MK Goutham
reduce mortality and morbidity in acute formic acid
poisoning. Patients with hematemesis or melena, if they Senior Resident, Department of ENT and Head and Neck Surgery, KVG
survive, should be followed up with serial OGD for Medical College and Hospital, Kurunjibag, Sullia, Karnataka, India
diagnosis and early treatment of strictures.
Nonthombam Pinky Devi
REFERENCES Senior Resident, Department of ENT and Head and Neck Surgery, KVG
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intoxications. Acta Pharmacologica et Toxicologica (Suppl.)
1977;41:342. Annapurna S Mushannavar
2. Rajan N, Rahim R, Krishna S Kumar. Formic acid poisoning
with suicidal intent: A report of 53 cases. Postgrad Med J Senior Resident. Department of ENT and Head and Neck Surgery, KVG
1985;61:35-36. Medical College and Hospital, Kurunjibag, Sullia, Karnataka, India
3. Naik RB, Stephens WP, Wilson DJ, Walker A, Lee HA.
Ingestion of formic acid-containing agents: Report of three fatal Sarika S Naik
cases. Postgrad Med J 1980;56:451.
4. Sujathan G, Jayapalan VK. Formic acid poisoning. J Ind Acad Senior Resident, Department of Anesthesia and Critical Care
Forensic Med 1991;13:29-31. Narayana Hrudayalaya, Bengaluru, Karnataka, India
International Journal of Head and Neck Surgery, May-August 2012;3(2):101-105 105
