A Challenging Case of Acute Mercury Toxicity

Background Mercury exists in multiple forms: elemental, organic, and inorganic. Its toxic manifestations depend on the type and magnitude of exposure. The role of colonoscopic decompression in acute mercury toxicity is still unclear. We present a case of acute elemental mercury toxicity secondary to mercury ingestion, which markedly improved with colonoscopic decompression. Clinical Case A 54-year-old male presented to the ED five days after ingesting five ounces (148 cubic centimeters) of elemental mercury. Examination was only significant for a distended abdomen. Labs showed elevated serum and urine mercury levels. An abdominal radiograph showed radiopaque material throughout the colon. Succimer and laxatives were initiated. The patient had recurrent bowel movements, and serial radiographs showed interval decrease of mercury in the descending colon with interval increase in the cecum and ascending colon. Colonoscopic decompression was done successfully. The colon was evacuated, and a repeat radiograph showed decreased hyperdense material in the colon. Three months later, a repeat radiograph showed no hyperdense material in the colon. Conclusion Ingested elemental mercury can be retained in the colon. Although there are no established guidelines for colonoscopic decompression, our patient showed significant improvement. We believe further studies on this subject are needed to guide management practices.


Introduction
Mercury exists in multiple forms: elemental, organic, and inorganic. Its toxic manifestations depend on the type and magnitude of exposure which can range from a minor to a life-threatening presentation. In this article, we present a case of mercury toxicity due to elemental mercury ingestion. We discuss the human use of elemental mercury and its exposure, routes of absorption, and clinical manifestations of its toxicity. We will also discuss the assessment and management of elemental mercury toxicity.

Case Presentation
A 54-year-old male with past medical history of degenerative joint disease, major depressive disorder, polysubstance dependence, and history of childhood burn presented to the Emergency Department (ED) complaining of imbalance, irritability, outburst of temper, fatigue, and weakness for the last ve days after he ingested ve ounces (oz) (148 cc) of mercury as a suicidal attempt. In the ED, the patient denied any changes in vision, hearing impairment, or tremors. He also denied shortness of breath, abdominal pain, nausea, vomiting, or diarrhea.
On physical examination, the patient appeared to be in no obvious distress. He seemed well developed, alert, and oriented to time, place, and person. Vital signs (BP 144/96, HR 74, RR 16, and temperature 96.3). A neurological examination yielded intact cranial nerves, with normal motor function and no sensory de cits. Abdominal examination showed a distended and nontender abdomen with normoactive bowel sounds. e rest of the physical examination showed no abnormalities.
Due to the patient's toxic mercury levels and worrying neurological signs and symptoms, the patient was admitted to the intensive care unit with a one on one sitter available at his bedside. Vital signs, neurological checks, and electrolytes were measured on regular basis. e poison-control team was consulted upon admission and recommended starting the patient on succimer, as a chelating agent, to be given in a dose of 500 mg every eight hours for the rst 5 days then every twelve hours for the 14 days.
e patient was also started on polyethylene glycol 17 gm twice a day and magnesium citrate to enhance GI motility along with intravenous uids and continuous replacement of electrolytes. e neurology team was consulted for further evaluation of the patient neurological complaints. ey agreed with the current plan of care; head computed tomography (CT) was performed and showed no intracranial abnormalities. e psychiatry team was asked to assess the patient for his suicidal attempt and was evaluated as nonsuicidal at that time and was started on escitalopram 10 mg. Bedside sitter was discontinued. e patient was showing slow progress in term of feeling weak, fatigue, and imbalance during his stay but remained hemodynamically stable. e patient was transferred out of the ICU to the oor, and serial abdomen X-rays were done. e patient was having recurrent bowel movements on daily basis, and X-rays showed continued decrease in the amount of mercury in the descending colon with interval increase in the hyperdense materiel in the cecum and ascending colon. Mercury levels were trended during the patient's hospitalization, and results are shown in Table 1.
e gastroenterology team was consulted and recommended placing a nasogastric tube and to give 4 liters of polyethylene glycol through the tube and magnesium citrate every 8 hours in an attempt to enhance gastrointestinal motility and hasten mercury clearance. Repeated X-rays showed no advancement of the hyperdense material which remained in the cecum and ascending colon. e decision was made to do a colonoscopy for an attempt of colonoscopic decompression (Figure 2). e colon was evacuated with copious amount of washing, and a repeat abdominal X-ray showed decreased hyperdense material in the colon with a nonobstructive gas pattern (Figure 3). e patient was discharged in a good condition after a 10-day hospital stay and followed up after 3 months; at that time, he had a mercury level of 33, and an abdominal X-ray showed no hyperdense material in the colon (Figures 4 and 5). e patient followed up again 1 month later. His neurological symptoms resolved, and kidney function preserved. Also, his mercury level was trending down at 18.

Brief Introduction, Sources, and Exposure.
Elemental mercury is a silver-colored liquid that is volatile at room temperature and causes pulmonary, neurological, and renal toxicity [1]. It is used in many technical and medical instruments including sphygmomanometers, manometers, thermometers, barometers, and compact uorescent light bulbs as well [2,3]. Mercury has been used widely in amalgam dental lling, which can also be a source of elemental mercury exposure to patients, dental technicians, and dental practitioners. However, studies have not correlated any symptoms or clinically signi cant health e ects with absorption from dental amalgams [2]. Other sources of exposure can be from ingestion of herbal medications for vertigo management, inhalation of mercury vapor for pain relief of arthralgia, and inhalation of mercury vapor for hemorrhoid treatment [2].

Absorption.
e major route of absorption is by di usion through the respiratory tract where up to 80% of inhaled mercury vapor is expected to di use into the bloodstream. Absorption from the gastrointestinal tract is very poor with a bioavailability of less than 0.01% and most of the ingested mercury is eliminated in feces [2]. Absorption through the skin is limited as well [2]. Although ingestion of elemental mercury is poorly absorbed through the gastrointestinal tract, mercury globules in the gastrointestinal tract can release vapor at body temperature and this can be absorbed by the lungs. Moreover, the metal can be absorbed more readily in cases of diverticulitis or GI abscesses where there is intense in ammation and mucosal breakdown causing increased bioavailability and systemic manifestations. Also in cases of diverticulosis and GI abscesses, there is a possibility of conversion of elemental mercury to the organic form by bacteria, leading to systemic toxicities [2,4].

Distribution and Metabolism.
e oral lethal dose 10 is approximately 100 grams for a 70 kg adult [5]. In our case, the patient ingested 5 ounces of elemental mercury which is  Case Reports in Medicine equivalent to around 141.75 grams causing a higher level of absorption. Also, the patient presented ve days after ingestion of elemental mercury which we believe increased the chance of the metal to volatilize and di use into the bloodstream. is was demonstrated by the patient's neurological symptoms and the high levels of blood and urine mercury.

Clinical Manifestations (Acute and Chronic), Diagnosis, and Management.
e clinical manifestations depend on the magnitude of elemental mercury exposure and whether it was acute or chronic. Acute toxicity can be seen in the setting of industrial exposure in which the inhalation of mercury vapor results in hypoxia, permanent lung damage, and even death (2). Inhaled mercury vapor can cause several neurological manifestations due to its ability to di use through the blood brain barrier. ese manifestations can be reversible once the metal is cleared out of the body and include tremors, paresthesia, memory loss, hyperexcitability, and delayed re exes [2,6]. Other symptoms occurring with mercury toxicity include cough, dyspnea, stomatitis, excessive salivation, nausea, vomiting, diarrhea, conjunctivitis, and dermatitis.
With chronic exposure to elemental mercury, central nervous system and kidneys are the main a ected organs. e major clinical features of chronic mercury poisoning include tremors, psychological disturbances, erethism, and gingivitis [2,7]. Tremor, either intentional or resting, is considered to be an early neurological sign of poisoning. Erethism is the hallmark of mercury poisoning where features include a change in personality, anxiety, excitability, fearfulness, pathologic shyness along with insomnia, memory loss, depression, fatigue, and outbursts of temper. Proteinuria is the most common sign of kidney e ects due to    Case Reports in Medicine 3 tubular damage. Nephrotic syndrome can occur in severe cases. In addition, peripheral nerve abnormalities can occur but are not very common [2]. Diagnosing elemental mercury toxicity depends on exposure history and clinical manifestations. Blood mercury level is a useful test especially if the level of exposure was high (2). However, once absorbed into the blood, the serum half-life is relatively short lasting for approximately three days as the level deceases due to redistribution in the body [8].
e overall half-life of mercury in the body is approximately 1-3 months [8].
e 24-hour urine mercury level is the best biomarker for chronic long-term exposure. Chest X-ray may be needed in the case of presence of respiratory symptoms especially with inhalational toxicity. Abdominal X-ray may show the deposition of mercury in the GI tract in cases of oral ingestion as in our patient.
When managing cases of mercury toxicity, treatment starts with eliminating the source of exposure and initiating supportive measures including oxygen, bronchodilators, and uid resuscitation. Lowering the body level concentration is fundamental in selected cases by using chelating agents especially if the blood and urine concentrations are above 100 mcg/L [9]. (Chelating agents increase the urinary excretion of mercury [9] which includes thiol-based agents such as dimercaprol (British anti-Lewisite (BAL)), penicillamine, unithiol (2,3-dimercaptopropane-1-sulfonate (DMPS)), and succimer (dimercaptosuccinic acid (DMSA)).
Retained mercury in the colon can be removed using agents that increase GI motility and colonoscopy. Although the role of colonoscopy is not an established evidence-based recommendation, there are previously reported cases of colonoscopic decompression and evacuation [10].

Conclusion
Ingestion of elemental mercury can be retained in the colon. Vigorous GI cleansing via motility enhancing medications and colonoscopy can be used to hasten elimination. e role of colonoscopic decompression in elemental mercury ingestion is not established, but there are previously reported cases where colonoscopy was used for evacuation.