Surgical Management of Poisoning by a Corrosive Arsenic-Based Depilatory Agent

Mohsen Hojjati MD, M. Saleh MD, Kh. Osanlou MD, N. Salehi MD, E. Hajnasrollah MD, R. Yeganeh MD, M. Ghofrani MD, Mehrnaz Hojati MD, Mojgan Hojati MD

Department of General Surgery, Loghman Hakim Hospital, Shaheed Beheshti University of Medical Sciences, Tehran, Iran

Introduction

Despite numerous reports that demonstrate a much lower incidence of drug poisoning in Iran compared to developed countries, a traditional depilatory agent with corrosive properties is increasingly used in this country as a means of suicide.^1,2 Since the use of this depilatory agent is limited to Iran and a few other Middle Eastern countries, not many references exist in the international medical literature describing the effects of the oral use of this corrosive compound. On the other hand, many investigators have studied arsenic (the major poisonous element of this depilatory agent) as a source of acute and chronic poisoning.^3-6

Although this corrosive arsenic-based depilatory agent (CABD) is produced with various compositions, it has been shown to consist of approximately 65% calcium bicarbonate (Ca(HCO₃)₂), 25% arsenic sulfide (As₂S₃), and 10% clay and moisture.⁷ When dissolved in water, As₂S₃ produces arsenous and arsenic acid. Ca(HCO₃)₂, arsenous acid and arsenic acid are the corrosive components, leading to severe damage of the digestive tract following ingestion,^8-10 while the arsenic compounds cause the signs and symptoms of arsenic poisoning. CABD is inexpensive and easily accessible in Iran and is therefore increasingly used as a means of suicide, even in prison settings, as a powder, paste, or liquid solution.

Arsenic poisoning is seen in four distinct clinical forms; hyperacute, acute, subacute and chronic.¹¹ Hyperacute manifestations of arsenic poisoning include distal cyanosis, tachycardia, cardiac arrhythmias, abdominal cramps and watery diarrhea, leading to dehydration, hypotension, and shock.¹² These reactions usually occur within 30-60 minutes after poison ingestion, and may be due to immunologic hypersensitivity, poison composition, co-ingestion of other poisons, or accelerated absorption due to gastrointestinal corrosion. Acute reactions manifest a few hours after poison ingestion, and may lead to multi-organ system failure 4 to 10 days later.¹³ Subacute poisoning is characterized by the later onset of cardiac and neurological disorders.^14,15 Chronic intoxication manifests as skin lesions, neuropathy, and fatty infiltration of the liver and kidney, 2 to 8 weeks after exposure.^16,17

Treatment of arsenic poisoning is based on aggressive gastrointestinal decontamination, chelator therapy, diuresis, fluid replacement, and supportive measures.^18,19 The benefit of dialysis therapy is subject to debate.^20,21 In the case of CABD poisoning, precautions must be made to prevent re-exposure of the esophagus to the caustic poison.²² Steroids and antibiotics are administered for the medical management of corrosive lesions, and surgery is considered if necessary.^23-27

A unique feature of CABD poisoning is that previous autopsies of patients who had ingested a large amount of poison with suicidal intent revealed a large doughy mass in the gastric fundus and an adhesive layer lining the gastric mucosa which could not be washed out by nasogastric catheterization. A protocol was therefore agreed upon in Loghman Hospital in which patients with evidence of severe poisoning were sent to the operating room for laparotomy and manual removal of the poison from the stomach to prevent further systemic absorption of arsenic.

Patients and Methods

In this prospective study, all patients referred to Loghman Hakim Hospital with a diagnosis of severe poisoning with CABD during a one-year period beginning in January 1993 were included. The hospital poison center is a referral center for the near 10-million population of Tehran. According to hospital protocol, patients with CABD poisoning were admitted to the poison center for initial medical management, then a consultation was made with surgery residents to determine the need for laparotomy. If laparotomy was required, the patient was managed by the Surgical Service. Required inclusion criteria were:

- ingestion of at least one complete pack of depilatory agent (regardless of its form: powder, liquid solution, or paste), and

- patient consent.

Also, at least one of the following criteria was deemed necessary:

- abdominal findings indicating gastrointestinal corrosion, gangrene and necrosis, including signs of peritoneal irritation (tenderness, rebound, guarding, rigidity and diminished bowel sound);

- evidence of oropharyngeal, esophageal or gastric corrosion on endoscopy, including mucosal erythema, edema, bullae, hemorrhage and necrosis, along with dyspnea, stridor, dysphonia, dysphagia, or odynophagia, or signs of esophageal perforation, such as crepitation, cervical tenderness or chest pain;²⁸ or

- evidence of an arsenic-based foreign body in the plain abdominal film,²⁹ indicating ingestion of the poison in the powder or paste form, which adheres to the gastric mucosa and cannot be removed by simple irrigation.

Thirty patients fulfilling the above-mentioned criteria underwent laparotomy and therefore formed the study group.

In patients with hyperacute reactions, surgery was not considered to be of much benefit and the mortality rate was high despite medical treatment with chelator agents and fluid replacement. Also, in cases in which at least 6-12 hours had passed since the ingestion of poison and signs of peritoneal irritation or digestive tract perforation were not evident, the patient was managed by medical treatment. If such findings were recorded on subsequent consultations, laparotomy was performed. This "golden time" was determined by the fact that the arsenous and arsenic acid in the depilatory agent causes spasm of the pylorus, thereby containing the poison in the stomach for 4-6 hours. After that, the poison is emptied into the duodenum, leading to possible bowel necrosis and perforation.

Prompt pre-operative studies including a complete history and physical examination, complete blood count (to document hemoconcentration, anemia, leukopenia or leukocytosis), urinalysis (arsenic-induced hemolysis), chest X-ray and plain abdominal films (intraluminal radiopacities with metal density) and arterial blood gas (metabolic acidosis and hypoxemia) were completed. Routine preparations were made for the laparotomy.

A midline incision was used. In cases where no gross pathology was observed, a long gastrotomy was performed along the greater curvature of the stomach. Separating the poison from the gastric mucosa usually required scrubbing the region, often leading to hemorrhage of the corroded tissue. Biopsies were usually obtained from the posterior fundus as it was often the site of maximal necrosis and gangrene. Signs of patchy gangrene were inspected and gangrenous portions were resected. Biliary secretions emulsified poison passing the pylorus, preventing its adherence to the mucosa. Therefore, saline infusion and suction with a long nasogastric tube through the gastrotomy was performed to clear the bowels of any poison that may have passed into the duodenum. Finally a tube gastrostomy or jejunostomy was inserted and the abdominal layers were sutured. In 2 cases transmural gangrene of the stomach was observed, justifying a total gastrectomy and roux-en-y esophagojejunostomy.

Results

During the study period, 2,894 cases of drug poisonings were referred to the hospital poison center, with 30 cases (1.04%) of CABD poisoning requiring surgical management. Eleven cases proved fatal. Therefore, although CABD poisoning ranked only eighteenth among the various drug poisonings, its mortality ranked fourth.³⁰

The age and sex distribution of the patients are shown in Fig. 1. Twenty-five cases (83.33%) were suicide attempts, 1 case (3.33%) was a homicidal poisoning, and in the remaining 4 cases (13.33%) the motive was unknown. In all cases the poison was ingested orally. The form of poison ingested and the mortality associated with each form are shown in Fig. 2. The relationship between the amount of poison ingested and mortality is shown in Fig. 3. As shown in Fig. 4 and Fig. 5, time was an important determinant of survival.

The presenting signs and symptoms are shown in Table 1.

Discussion

Due to its traditional origin, CABD poisoning has not been reported in developed countries. On the other hand, Iranian investigators have reported cases of accidental or deliberate poisoning with this compound.

In our study, patients with a strong intent to commit suicide ingested CABD as a liquid solution, which is associated with the highest mortality. Ingesting the powder followed by water has a similar effect. If the dry powder is not removed from the GI tract as soon as possible, it may become emulsified by biliary secretions, leading to rapid absorption. On the other hand CABD paste is associated with the least mortality, since the arsenic-containing solution is discarded and does not enter the body, and surgical removal of the poison is most effective.

The age distribution of poisoning with CABD differs from other drug poisonings. Although drug poisonings are generally more frequent in the third decade, CABD poisoning peaks in the fourth, fifth and sixth decades. This may be attributed to the fact that CABD is recognized among the older generation who are more familiar with traditional customs. Sex distribution showed an unexpected 4 to 1 preponderance of poisoning in males, probably due to the fact that most cases occurred in male convicts during their sentence in prison, where they usually do not have access to other means of suicide.

Early surgical removal of the poison is not only effective in preventing the systemic effects of the toxin, but also local resection of corroded gangrenous tissue, and if necessary total gastrectomy, can save patients with life-threatening gangrene.³¹ Especially, insertion of a feeding gastrostomy or jejunostomy to initiate early enteral feeding in patients unable to feed orally due to upper gastrointestinal corrosion is very effective. It should be noted that surgical management is most effective if medical therapy, especially the administration of sufficient doses of British anti-Lewisite (BAL), is initiated as soon as possible to reduce the systemic effects of the toxin.

The utmost importance of prompt treatment in reducing mortality due to the poisonous effects of arsenic and corrosion of the gastrointestinal mucosa was evident in our study. This demonstrates the need for creating a greater number of poison centers to facilitate access to medical and surgical care.

References

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